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■RAC GP Guidelines for preventive
Royal Australian College 0/General Practitioners

activities in general practice
9th edition
Over
25
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of preventive health
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Healthy Profession.
racgp.org.au
Healthy Australia.
Guidelines for preventive activities in general practice, 9th 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 (RACGP) 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
The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice.
9th edn. East Melbourne, Vic: RACGP, 2016.
The Royal Australian College of General Practitioners

100 Wellington Parade
East Melbourne, Victoria 3002 Australia
Tel 03 8699 0414

Fax 03 8699 0400
www.racgp.org.au
ISBN: 978-0-86906-451-1 (Print)

ISBN: 978-0-86906-452-8 (Web)
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
Eighth edition published 2012
Ninth edition published 2016
Cover image © istockphoto/skodonnell

© The Royal Australian College of General Practitioners, 2016.
We recognise the traditional custodians of the land and sea on which we work and live.
jbracgp Guidelines for preventive
Royal Australian College of General Practitioners
activities in general practice
9th edition
Guidelines for preventive activities in general practice
9th edition
Acknowledgements
The Royal Australian College of General Practitioners (RACGP) gratefully acknowledges the generous contribution
of the following authors, contributors and reviewers of the Guidelines for preventive activities in general practice
(Red Book), 9th edn.
Red Book Editorial Committee

Professor Nicholas Zwar Professor Claire Jackson
Chair, Red Book Editorial Committee Director, Centres for Primary Care Reform
School of Public Health and Community Medicine, Research Excellence
University of New South Wales, New South Wales Professor in Primary Care Research, Chair,
Metro North Primary Health Network
Dr Evan Ackermann
Past President, The Royal Australian College of
Chair, RACGP Expert Committee - Quality Care
General Practitioners (2010-12)
Professor Mark Harris
Associate Professor John Litt
Centre for Primary Health Care and Equity,
Department of General Practice,
University of New South Wales
Flinders University, South Australia
RACGP Expert Committee - Quality Care
Deputy Chair, RACGP Expert Committee -
Dr Meredith Arcus Quality Care
Deputy Executive Director, Medical Services,
Professor Danielle Mazza
Sir Charles Gairdner and Osborne Park Health Care
Group, Western Australia
School of Primary Care,
Associate Professor Pauline Chiarelli Monash University, Victoria
School of Health Sciences, University of Newcastle, RACGP Expert Committee - Quality Care
New South Wales
Professor Dimity Pond
Professor Chris Del Mar Professor of General Practice,
Faculty of Health Sciences and Medicine, School of Medicine and Public Health,
Bond University, Queensland University of Newcastle, New South Wales
Professor Jon Emery Associate Professor Jane Smith

Department of General Practice, Head of General Practice Discipline,
University of Melbourne, Victoria Faculty of Health Science and Medicine,
Bond University, Queensland
Associate Professor Michael Fasher
Adjunct Associate Professor, University of Sydney, Professor Nigel Stocks
New South Wales; and Conjoint Associate Professor, Head of Discipline - General Practice,
University of Western Sydney, New South Wales University of Adelaide, Adelaide
Associate Professor John Furler Dr Christine Walker

Department of General Practice, Executive Officer, Chronic Illness Alliance
University of Melbourne, Victoria
Professor Tania Winzenberg
Dr Caroline Johnson Chair, RACGP Expert Committee - Research
Department of General Practice, Professor of Chronic Disease Management,
University of Melbourne, Victoria Menzies Institute for Medical Research and Faculty
RACGP Expert Committee - Quality Care of Health, University of Tasmania, Tasmania
9th edition
Conflicts of interest
This publication has been produced in accordance with the rules and processes outlined in the RACGP Conflict of
Interest (COI) Policy. The RACGP COI Policy is available at www.racgp.org.au/support/policies/organisational
Contributors
Associate Professor Lena Sanci Professor Lindy Clemson
Department of General Practice, Professor in Ageing and Occupational Therapy,
University of Melbourne, Victoria University of Sydney, New South Wales
Dr Magdalena Simonis
Reviewers
We gratefully acknowledge the expert reviewers Dr Chris Bourne
and representatives from the organisations who Sydney Sexual Health Centre,
contributed scholarly feedback. Sydney Hospital, New South Wales
Members of RACGP Aboriginal and Torres Strait Professor Hanny Calache
Islander Health Centre for Population Health Research,
Deakin University, Victoria
Associate Professor Anne Abbott
School of Public Health and Preventive Medicine, Professor Henry Brodaty
Monash University, Victoria Dementia Collaborative Research Centre,
University of New South Wales and Prince of Wales
Dr Stuart Aitken
Hospital, New South Wales
Gold Coast Sexual Health Clinic, Queensland
Professor Ian Caterson
Professor Craig Anderson
Boden Institute, Charles Perkins Centre,
George Institute for Global Health, New South Wales
University of Sydney, New South Wales
Associate Professor Nick Antic
Professor Derek Chew
Clinical Director of the Adelaide Institute
Professor of Cardiology, Flinders University,
for Sleep Health
Flinders Medical Centre, South Australia
President Australasian Sleep Association,
South Australia Professor Rufus Clarke
Faculty of Public Health Medicine,
Professor Kaarin Anstey
Royal Australasian College of Physicians,
ANU College of Medicine, Biology & Environment,
New South Wales
Australian Capital Territory
Professor Jacqueline Close
Associate Professor Kristine Barlow-Stewart
Consultant Geriatrician, Prince of Wales Hospital,
Genetic Medicine, Northern Clinical School,
Director, Falls and Injury Prevention Group, NeuRA,
Sydney Medical School, New South Wales
University of New South Wales, New South Wales
Professor Adrian Bauman
Professor Stephen Colagiuri
School of Public Health, University of Sydney,
Director, Boden Institute, University of Sydney,
New South Wales
New South Wales
Dr Glenise Berry
Dr Gary Deed
Australian & New Zealand Society for Geriatric
Chair, RACGP Specific Interests - Diabetes Network
Medicine, New South Wales
Dr Joanne Dixon
Associate Professor Mark Bolland
National Clinical Director, Clinical Leader Genetic
School of Medicine, University of Auckland,
Services, Genetic Health Service New Zealand
New Zealand
9th edition
iii
Professor Jenny Doust Associate Professor Warrick Inder

Faculty of Health Sciences and Medicine, Department of Diabetes and Endocrinology,
Bond University, Queensland Princess Alexandra Hospital, Queensland
Professor Peter Ebeling Professor Stephen Lord
Head of the Department of Medicine, Senior Principal Research Fellow, Neuroscience
Monash Medical Centre, Victoria Research Australia, New South Wales
Associate Professor Matt Edwards Professor Finlay Macrae
Department of Paediatrics, Head, Colorectal Medicine and Genetics,
University of Western Sydney, New South Wales Royal Melbourne Hospital, Victoria
Professor, Department of Medicine, University of
Professor John Eisman
Melbourne, Royal Melbourne Hospital, Victoria
Director of Clinical Translation and Advanced
Education, Garvan Institute of Medical Research, Dr Catherine Mandel
Darlinghurst, New South Wales MRI Radiologist, Swinburne University of Technology
Honorary Senior Fellow, Department of Radiology,
Dr Ben Ewald
Senior Lecturer in Epidemiology and General
Practitioner, Centre for Clinical Epidemiology Professor Rebecca Mason
and Biostatistics, University of Newcastle, Professor of Endocrine Physiology,
New South Wales School of Medical Sciences, Sydney Medical School,
University of Sydney, New South Wales
Professor Kwun Fong
Prince Charles Hospital, Department of Clinical Professor Richard Mendelson
Thoracic Medicine, Queensland Royal Perth Hospital, University of Western Australia,
Western Australia
Professor Peter Frith
Respiratory Medicine, Flinders University, Professor Sylvia Metcalfe
South Australia Genetics Education & Health Research,
Murdoch Childrens Research Institute, Victoria
Clinical Professor Jack Goldblatt
School of Paediatrics and Child Health, Dr Mark Morgan
University of Western Australia, Western Australia General Practitioner, South Australia
Senior Lecturer, Discipline of General Practice,
Professor Jonathon Golledge
University of Adelaide, South Australia
Head of the Vascular Biology Unit, School of Medicine
and Dentistry, James Cook University, Queensland Professor Paul Norman
Winthrop Professor of Vascular Surgery,
Professor Paul Glasziou
University of Western Australia, Western Australia
Professor of Evidence-Based Medicine, Faculty of
Health Sciences and Medicine, Bond University, Professor Mark Nelson
Queensland Chair, Discipline of General Practice,
University of Tasmania, Tasmania
Associate Professor Jane Halliday
Professional Research Fellow, Menzies Research
Public Health Genetics, Murdoch Childrens Research
Institute, University of Tasmania, Tasmania
Institute, Victoria
Mark Nevin
Dr James Harvey Senior Executive Officer, Faculty of Clinical Radiology,
Council member of Royal Australian and New Zealand
Royal Australian and New Zealand College of
College of Obstetricians and Gynaecologists,
Radiologists, New South Wales
South Australia
Professor Doug McEvoy
Associate Professor Kelsey Hegarty
Senior Director, Adelaide Institute for Sleep Health;
Staff Consultant in Sleep and Respiratory Medicine
at Repatriation General Hospital and Flinders Medical
Ms Cristy Henderson Centre, South Australia
Assistant Director, Bowel Screening Section, Cancer
Dr Nicki Murdoch
and Palliative Care Branch, Population Health & Sport
President, Paediatrics & Child Division, Royal
Division, Department of Health
Australasian College of Physicians, New South Wales
Dr Elizabeth Hindmarsh
Professor Frank Oberklaid
General Practitioner, New South Wales
Director, Centre for Community Child Health,
Royal Children’s Hospital, Victoria
iv 9th edition
Dr Jan Orman Clinical Associate Professor Liz Wylie

GP Services Consultant, Black Dog Institute, Medicine and Pharmacology Royal Perth Hospital
Prince of Wales Hospital, New South Wales Unit, University of Western Australia, Western Australia
Professor Kelly Phillips Professor Graeme Young
Peter MacCallum Cancer Centre, Victoria Flinders Centre for Innovation in Cancer,
Flinders University, South Australia
Professor Matthew Peters
Head of Respiratory Medicine, Professor Helen Zorbas
Concord Hospital, New South Wales Chief Executive Officer, Cancer Australia,
New South Wales
Professor Ian Reid
Deputy Dean, Faculty of Medical and Health Australian & New Zealand Society for Geriatric
Sciences, University of Auckland, New Zealand Medicine Council
Professor Ann Roche Australasian Sleep Association
National Centre for Education and Training on
Australian Diabetes Society
Addiction, Flinders University, South Australia
Australian Dental Association
Professor John Saunders
Consultant Physician in Internal Medicine and Cancer and Palliative Care Branch, Population
Addiction Medicine, New South Wales Health & Sport Division, Department of Health
Professor Virginia Schmied Cancer Australia
School of Nursing and Midwifery,
Cancer Council Victoria
University of Western Sydney, New South Wales
Centre for Population Health, NSW Ministry of
Associate Professor Jonathan Shaw
Health, Harm Reduction and Viral Hepatitis Branch
Baker IDI Heart & Diabetes Institute, Victoria
Continence Foundation of Australia
Professor Maria Fiatarone Singh
Chair of Exercise and Sport Science, Exercise, Health Haemochromatosis Society Australia
and Performance Group, Faculty of Health Sciences,
Human Genetics Society of Australasia
Sydney Medical School, New South Wales
Dental Health Services Victoria
Associate Professor John Slavotinek
Gastroenterologist Exercise & Sports Science Australia
Honorary Senior Associate,
Cancer Council Victoria, Victoria
Kidney Health Australia
Professor Denis Spelman National Stroke Foundation

Deputy Director, Clinical Infectious Diseases Unit National Heart Foundation of Australia
and Head, Microbiology Department,
Monash University, Victoria NSW STI Programs Unit, Sydney Sexual Health
Centre, Sydney Hospital, New South Wales
Professor James St John
Gastroenterologist Optometry Australia
Honorary Senior Associate, Royal Australian and New Zealand College of
Cancer Council Victoria, Victoria Obstetricians and Gynaecologists
Dr Michael Tam Representatives from Cancer Council Victoria
Staff Specialist, General Practice,
University of New South Wales, New South Wales Royal Australian and New Zealand College of
Radiologists
Dr Wendy Tsui
RACGP Fellow, Family & Sports Medicine Centre, Royal Australian College of Ophthalmologists
New South Wales SANE Australia
Dr Angela Taft Urological Society of Australia and New Zealand
Professor and Director, Judith Lumley Centre,
La Trobe University, Victoria
Dr Brendan White
Australian Dental Association (NSW Branch),
New South Wales
9th edition
v
Acronyms
CEITC Centre for Excellence in Indigenous
13vPCV 13-valent pneumococcal conjugate vaccine
Tobacco Control
23vPPV 23-valent pneumococcal polysaccharide
CF cystic fibrosis
vaccine
CHD coronary heart disease
AAA abdominal aortic aneurysm
CKD chronic kidney disease
ABCD asymmetry, border, colour, diameter
CDK-EPI Chronic Kidney Disease Epidemiology
ABI ankle:brachial index
Collaboration
ABS Australian Bureau of Statistics
COPD chronic obstructive pulmonary disease
ACE angiotensin converting enzyme
CRC colorectal cancer
ACIR Australian Childhood Immunisation Register
CRP C-reactive protein
ACR albumin-to-creatinine ratio
CT computed tomography
ACS asymptomatic carotid artery stenosis
CVD cardiovascular disease
ADHD attention deficit hyperactivity disorder
DALY disability-adjusted life year
AEDC Australian Early Development Census
DASH dietary approaches to stop hypertension
AF atrial fibrillation
DBP diastolic blood pressure
ALA alpha-linolenic acid
DNA deoxyribonucleic acid
AMD aged-related macular degeneration
DLCN Dutch Lipid Clinic Network (criteria)
APC adenomatous polyposis coli
DPA docosapentaenoic acid
ApoE apolipoprotein E
DRE digital rectal examination
ARB angiotensin receptor blocker
DT diphtheria, tetanus
ASCIA Australasian Society of Clinical Immunology
DTPa diphtheria, tetanus, acellular pertussis
and Allergy
(child version)
AUDIT-C Alcohol Use Disorders Identification Test -
dTpa diphtheria, tetanus, acellular pertussis
Consumption
(adolescent/adult version)
AUSDRISK Australian type 2 diabetes risk assessment
DXA dual-energy X-ray absorptiometry
tool
ECG electrocardiogram
BCG Bacillus Calmette-Guerin
EFG elevated, firm, growing for more than
BMD bone mineral density
one month
BMI body mass index
eGFR estimated glomerular filtration rate
BNP B-type natriuretic peptide
EPDS Edinburgh Postnatal Depression Scale
BP blood pressure
ESRD end-stage renal disease
BRCA1 breast cancer susceptibility gene 1
FAP familial adenomatous polyposis
BRCA2 breast cancer susceptibility gene 2
FH familial hypercholesterolaemia
BUA broadband ultrasound attenuation
FHSQ family history screening questionnaire
CA cancer antigen
FOBT faecal occult blood test
CA125 cancer antigen 125
GP general practitioner
CAD coronary artery disease
GPCOG general practitioner assessment
CALD culturally and linguistically diverse of cognition
CCTA coronary computed tomography angiography HbA1c glycated haemoglobin
CEA carotid endarterectomy HCG human chorionic gonadotrophin
HDL high-density lipoprotein

vi 9th edition
HDL-C high-density lipoprotein-cholesterol OSA obstructive sleep apnoea
HHC hereditary haemochromatosis PBS Pharmaceutical Benefits Scheme
Hib haemophilus influenzae type b PCR polymerase chain reaction
HIV human immunodeficiency virus PEDS parents’ evaluation of developmental status
HNPCC hereditary non-polyposis colon cancer PET-CT positron emission tomography - computed
tomography
HPV human papillomavirus
PLCO Prostate, Lung, Colorectal and Ovarian trial
hsCRP high sensitivity C-reactive protein
PND postnatal depression
HSIL high-grade squamous intraepithelial lesion
PVD peripheral vascular disease
IADL instrumental activities of daily living
RACGP The Royal Australian College of General
IBIS International Breast Cancer Intervention Study
Practitioners
IFG impaired fasting glucose
RCT randomised controlled trial
IGT impaired glucose tolerance
SBP systolic blood pressure
IPV inactivated polio vaccine
SCC squamous cell carcinoma
IS intussusception
SES socioeconomic status
KICA Kimberley Indigenous Cognitive Assessment
SIDS sudden infant death syndrome
tool
SMMSE standardised mini-mental state examination
LDL low-density lipoprotein
SNAP smoking, nutrition, alcohol, physical activity
LDL-C low-density lipoprotein-cholesterol
SNP single nucleotide polymorphism
LSIL low-grade squamous intraepithelial lesion
SOS speed of sound
LUTS lower urinary tract symptoms
SPF sun protection factor
LVH left ventricular hypertrophy
SSRI selective serotonin reuptake inhibitor
MBS Medicare Benefits Schedule
STI sexually transmissible infection
MCH mean corpuscular haemoglobin
SUDI sudden unexpected death in infancy
MCV mean corpuscular volume
T2D type 2 diabetes
MI myocardial infarction
TB tuberculosis
MMR measles, mumps and rubella
TG triglyceride
MMRV measles, mumps, rubella and varicella
TGA Therapeutic Goods Administration
MMSE mini-mental state examination
TIA transient ischaemic attack
MRI magnetic resonance imaging
TUGT timed up and go test
MS multiple sclerosis
UACR urine albumin-to-creatinine ratio
MSM men who have sex with men
UKCTOCS UK Collaborative Trial of Ovarian Cancer
MSU mid-stream urine
Screening
MTHFR methylenetetrahydrofolate reductase
USPSTF US Preventive Services Task Force
MUKSB Modified UK Simon Broome (criteria)
UV ultraviolet
NAAT nucleic acid amplification test
VIVAS Vaccination Information and Vaccination
NHMRC National Health and Medical Research Administration System
Council
VV varicella vaccination
NIP National Immunisation Program
VZV varicella zoster virus
NIPS National Immunisation Program Schedule
WHO World Health Organization
NIPT non-invasive prenatal test
NMSC non-melanocytic skin cancer
NTD neural tube defect

Pap test Papanicolaou test
9th edition
vii
1. Contents
Acknowledgements i
Red Book Editorial Committee i
Conflicts of interest ii
Contributors ii
Reviewers ii
Acronyms v
I. Introduction 1
The Red Book 3
The Australian experience 3
Benefits and harms of preventive health activities 4
Prevention in the practice population 5
Screening versus case finding 6
Opportunistic versus systematic prevention 6
Screening principles 7
II. Patient education and health literacy 8

Impact of patient education 8
Approaches to patient education 8
Health inequity 9
Supporting patient education and health literacy in disadvantaged groups 10
III. Development of the Red Book 11

Recommendations 11
IV. How to use the Red Book 12

Organisational detail 12
References - Chapters I-IV 14
V. What’s new in the 9th edition? 16
1. Preventive activities prior to pregnancy 18

References 22
2. Genetic counselling and testing 24

References 28
Appendix 2A. Family history screening questionnaire 29
Appendix 2B. Dutch Lipid Clinic Network Criteria for making a diagnosis of familial
hypercholestrolaemia in adults 30
3. Preventive activities in children and young people 32

References 38
Appendix 3A ‘Red flag’ early intervention referral guide 41
4. Preventive activities in middle age 42

References 44
viii 9th edition
5. Preventive activities in older age 45

5.1 Immunisation 46
5.2 Physical activity 46
5.3 Falls 47
5.4 Visual and hearing impairment 50
5.5 Dementia 51
References 53
6. Communicable diseases 57
6.1 Immunisation 57
6.2 Sexually transmissible infections 61
References 64
7. Prevention of chronic disease 66

7.1 Smoking 67
7.2 Overweight 69
7.3 Nutrition 73
7.4 Early detection of at-risk drinking 75
References 80
8. Prevention of vascular and metabolic disease 85

8.1 Assessment of absolute cardiovascular disease risk 86
8.2 Blood pressure 87
8.3 Cholesterol and other lipids 89
8.4 Type 2 diabetes 92
8.5 Stroke 94
8.6 Kidney disease 95
8.7 Atrial fibrillation 97
References 98
Appendix 8A. Australian cardiovascular disease risk charts 102
9. Early detection of cancers 104

9.1 Prostate cancer 104
9.2 Colorectal cancer 105
9.3 Breast cancer 109
9.4 Skin cancer 113
9.5 Cervical cancer 117
9.6 Ovarian cancer 121
9.7 Testicular cancer 121
References 122
10. Psychosocial 126

10.1 Depression 127
10.2 Suicide 129
10.3 Intimate partner violence 130
References 132
9th edition
ix
11. Oral health 134

References 136
12. Glaucoma 137

References 137
13. Urinary incontinence 138

References 139
Appendix 13A. The 3 Incontinence Questions (3IQ) 140
14. Osteoporosis 141

References 145
15. Screening tests of unproven benefit 147

References 153
Lifecycle chart 158

9th 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 137 million general practice consultations take place annually in Australia and 85% of the
Australian population consult a general practitioner (GP) at least once a year.1 Preventive healthcare is an important
activity in general practice. It includes the prevention of illness, the early detection of specific disease, and the
promotion and maintenance of health. The partnership between GP and patient can help people reach their goals
of maintaining or improving health. Preventive care is also critical in addressing the health disparities faced by
disadvantaged and vulnerable population groups.
Prevention of illness is the key to Australia’s future health - both individually and collectively. About 32% of
Australia’s total burden of disease can be attributed to modifiable risk factors (Figure I.1 and Table I.1).2
Figure I.1. Leading risk factors contributing to the burden of disease3
*Total burden of disease and injury measured by disability-adjusted life year (DALY)
A healthy lifestyle is vital for preventing disease, including prevention of cancer. Cancer Australia4 summarises the
recommendations for adults to reduce their risk of cancer and stay healthy as the following:
• Do not smoke
• Maintain a healthy weight
• Be active
• Eat a balanced and nutritious diet
• Limit alcohol consumption
• Be sun smart
• Protect against infection
The evidence of associations between behavioural and biomedical risk factors and chronic diseases is summarised
in Table I.1.
2 9th edition
Table I.1. Strong evidence of direct associations between selected chronic diseases and
behavioural and biomedical risk factors5
Chronic Behavioural Behavioural Behavioural Behavioural Biomedical Biomedical Biomedical
disease Tobacco Insufficient Excessive Dietary risks Obesity High blood Abnormal
smoking physical alcohol pressure blood lipids
activity consumption
*
CVD • • — • • • •
Stroke • • • — • • •
*
Type 2 diabetes • • — • • — —
Osteoporosis • • • •' — — —
Colorectal
• — • •» • — —
cancer
Oral health •§ — •II •# — — —
CKD • — — — • • —
Breast cancer **
— — • — • — —
(female)
Depression — — — — • — —
Osteoarthritis — — — — • — —
Rheumatoid
• — — — — — —
arthritis
Lung cancer • — — — — — —
Cervical cancel • — — — — — —
COPD • — — — — — —
Asthma • — — — — — —
• Strong evidence in support of a direct association between the chronic disease and risk factor
— There is either not a direct association or the evidence for a direct association is not strong
*For coronary heart disease and type 2 diabetes, dietary risks relate to high intake of saturated fat
tRor osteoporosis, dietary risks relate to insufficient calcium and vitamin D. The recommendation is to enhance vitamin D levels through
adequate sun exposure and/or supplements if required
* For colorectal cancer (CRC), dietary risks relate to high intakes of processed (preserved) meat. In addition, a high intake of red meat
is associated with an increased risk of CRC. The Australian dietary guidelines (ADG) therefore recommend that processed meat intake
should be limited (also because of its high saturated fat content). In addition, to enhance dietary variety and reduce some of the health
risks associated with consuming red meat, the ADG recommend Australian adults should consume up to a maximum of 455 g per week
(one serve [65 g] per day) of lean red meats
The evidence for tobacco smoking and oral health relate to oral cancer and adult periodontal diseases
§
“The evidence for excessive alcohol consumption and oral health relate to oral cancer
#For oral health, dietary risks relate to amount and frequency of free sugars for dental caries, soft drinks and fruit juices for dental erosion,
excess fluoride for enamel developmental defects, and deficiency of vitamin C for periodontal disease
“The evidence for obesity and breast cancer is for postmenopausal women
tt Persistent infection with the human papillomavirus (HPV) is a central cause of cervical cancer. HPV infection is not identified in Table I.1
as it only includes those risk factors that are implicated in more than one chronic disease and have the greatest prevalence within the
population. It is important to recognise that the behavioural risk factors of multiple sexual partners and early age at initiation of sexual
activity reflect the probability of being infected with HPV
The chronic diseases included in Table I.1 are those that currently contribute the most to burden of disease and/or are the focus of
ongoing national surveillance efforts
The behavioural and biomedical risk factors included in Table I.1 are those that are implicated in more than one chronic disease and
have the greatest prevalence within the population
ADG, Australian dietary guidelines; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; CRC, colorectal cancer;
CVD, cardiovascular disease; HPV human papillomavirus
Reproduced with permission from Australian Institute of Health and Welfare. Chronic disease risk factors. Canberra: AIHW, 2016
9th edition
3
The Red Book

The Royal Australian College of General Practitioners (RACGP) has published the Guidelines for preventive activities
in general practice (Red Book) since 1989 to support evidence-based preventive activities in primary care. The Red
Book is now widely accepted as the main guide to the provision of preventive care in Australian general practice.
Purpose
The Red Book is designed to provide the general practice team with guidance on opportunistic and proactive
preventive care. It provides a comprehensive and concise set of recommendations for patients in general practice
with additional information about tailoring advice depending on risk and need. The Red Book provides the evidence
and reasons for the efficient and effective use of healthcare resources in general practice.
The Red Book’s companion publication, National guide to a preventive health assessment for Aboriginal and Torres
Strait Islander people, 2nd edn, is intended for all health professionals delivering primary healthcare to Aboriginal
and Torres Strait Islander peoples.
Scope
The Red Book covers primary (preventing the initial occurrence of a disorder) and secondary (preventive early
detection and intervention) activities. These guidelines focus on preventive activities applicable to substantial portions
of the general practice population rather than specific subgroups. This means, in general, recommendations apply
to asymptomatic (low-risk) people. However, there is an emphasis on equity, with recommendations aimed at major
disadvantaged groups at higher risk of disease and those who are less likely to receive preventive care.
These guidelines do not include:

• detailed information on the management of risk factors or disease (eg what medications to use when treating
hypertension)
• information about the prevention of infectious diseases. This information has been limited largely to immunisation
and some sexually transmissible infections (STIs).
There is limited advice about travel medicine. This information can be obtained from the Centers for Disease
Control and Prevention at wwwnc.cdc.gov/travel or World Health Organization (WHO) International Travel and
Health at www.who.int/ith/en
The Australian experience

The role of general practice in prevention has been recognised by the Council of Australian Governments (COAG)6
and in the Australian Government’s National Preventative Health Strategy and National Primary Health Care
Strategic Framework.2,7
Deaths and hospitalisations from preventable illness have continued to decline in Australia. However, the leading
causes of death and disability in Australia are preventable or able to be delayed by early treatment and intervention
(Figure I.2).8
4 9th edition
Figure I.2. Age-standardised death rates for potentially avoidable deaths,

1997-2010
* 9
*Deaths among people <75 years of age that are potentially avoidable within the present healthcare system
Potentially avoidable deaths are divided into potentially preventable deaths (cases amenable to screening and primary prevention) and
treatable deaths (cases from potentially treatable conditions amenable to therapeutic interventions). There were 32,919 potentially avoidable
deaths in Australia in 2010; 62% were classified as potentially preventable and 38% as potentially treatable.8 Preventable death rates fell from
142 to 91 deaths per 100,000 between 1997 and 2010 (36%), and treatable death rates fell by 41% (from 97 to 57 deaths per 100,000)
Reproduced with permission from Australian Institute of Health and Welfare. Australia’s health 2014. Canberra: AIHW, 2014.
An Australian review10 concluded that lifestyle interventions could have a large impact on population health. The
absolute cardiovascular disease (CVD) 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, preventive interventions in general practice remain
underused, being the primary reason for the consultation in only seven of every 100 clinical encounters.11 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.12
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 its foundation, and encourages all general practices, GPs and
their teams to prioritise evidence-based preventive health activities.
Benefits and harms of preventive health activities

‘Prevention is better than cure’ makes intuitive sense. Yet there is evidence that some preventive activities are not
effective, some are actually harmful. It has been said ‘all screening programs do some harm; some do good as
well’.13 Screening of asymptomatic patients may lead to overdiagnosis, causing needless anxiety, appointments,
tests, drugs and even operations, and may leave the patient less healthy as a consequence. Therefore, it is crucial
that evidence clearly demonstrates that benefits outweigh those harms for each preventive activity.
Determining whether a preventive activity is beneficial, harmful or of indeterminate effect (ie there is not enough
evidence on which to base a decision) requires a consistent, unbiased, evidence-based approach.
Cancer screening, in particular, can polarise different sectors of the health profession and broader community.
The objective interpretation of evidence, balancing harms and benefits, and considering overdiagnosis and
overtreatment is a goal of the Red Book.
9th edition
5
In the Red Book, the RACGP provides information to assist GPs in caring for their patients, including in areas
where the evidence is uncertain or contentious. Screening activities are only recommended where evidence
demonstrates that benefits outweigh harms. Chapter 15 provides some guidance on common tests where this is
not the case or where the evidence is either unclear or not available.
Prevention in the practice population

The risk of illness and disease is associated with a range of factors that operate on the individual across the
lifecycle. For example, poor nutrition and lack of antenatal care during pregnancy are associated with later risk
of chronic diseases in the child. Risk behaviours in childhood may become entrenched, leading to progressive
physiological changes that can cause chronic diseases in later life. All these factors are in turn influenced by the
social determinants of health, which operate at the local community and broader societal levels; these are poverty,
housing, education and economic development (Figure I.3). Thus, it is highly desirable for general practice to
think beyond the preventive healthcare needs of the individual patient, towards a practice population approach to
primary prevention.
Figure I.3. The determinants of health and illness9
______ y_____
Broad features of Socioeconomic Health Biomedical
society characteristics behaviours factors
Culture Education Tobacco use Birth weight
Affluence Employment Alcohol Body weight
Social cohesion Income and consumption Blood pressure
Social inclusion wealth Physical activity Blood cholesterol
Political Family, Dietary behaviour Glucose tolerance
structures neighbourhood Use of illicit drugs Immune status
Media Housing Sexual practices
Access to
A
Language Vaccination
Environmental services
Psychological _____ Ï______v
factors Migration/ factors
Health and wellbeing
Natural refugee status
Stress over time
Built Food security
Trauma, torture Life expectancy, mortality
Geographical Knowledge,
Safety factors Subjective health
location attitudes and
Risk taking, Functioning, disability
beliefs
Remoteness violence Illness, disease
Health literacy
Latitude Occupational Injury
health and safety
\ \______ _______ \__________ _________
M M M
Individual physical and psychological make-up

Genetics, antenatal environment, gender, ageing, life course and intergenerational influences
Note: Bold highlights selected social determinants of health
Reproduced with permission from Australian Institute of Health and Welfare. Australia’s health 2014. Canberra: AIHW, 2014.
6 9th edition
General practice has a practical role to play in addressing these determinants and helping to break the cycle that
may exist linking social and economic factors to illness and injury. This requires a systematic approach across
the whole practice population, not just for those who seek out or are most receptive to preventive care. This may
include auditing medical records to identify those who are missing out, using special strategies to support patients
with low literacy, and being proactive in following up patients who are most at risk. It will usually require teamwork
within the practice as well as links with other services.
General practice also has a broader role in facilitating health improvement for vulnerable and disadvantaged groups
in the local community, in association with other services and providers. In some cases, this may involve advocacy
for their needs. Information on local vulnerable and disadvantaged groups and their access to healthcare can be
obtained from local Primary Health Networks (PHNs) or state and territory health networks. Measures to improve
access to preventive healthcare by Aboriginal and Torres Strait Islander peoples are especially important given their
higher burden of disease and the barriers that exist to preventive healthcare. More information is available in the
National guide to preventive health assessment for Aboriginal and Torres Strait Islander people, 2nd edn.
Screening versus case finding

Many clinicians confuse screening and case-finding tests. Screening is defined as ‘the examination of
asymptomatic people in order to classify them as likely or unlikely to have a disease’.14 The primary purpose of
screening tests is to detect early disease in apparently healthy individuals.
Case finding is the examination of an individual or group suspected of having, or at risk of, the condition. Case
finding is a targeted approach to identifying conditions in select patients who may already have symptoms.15
A diagnostic test is any kind of medical test performed to establish the presence (or absence) of disease as a basis
for treatment decisions in symptomatic or screen-positive individuals (confirmatory test). Examples include taking
a mid-stream urine (MSU) sample for evaluation of a urinary tract infection and performing a mammogram for a
suspicious breast lump.
Screening and case finding carry different ethical obligations. If a clinician initiates screening in asymptomatic
individuals, there needs to be conclusive evidence that the procedure can positively affect the natural history of
the disorder. Moreover, the risks of screening 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.
It could be argued that there is at least some implied exposure to risk (eg performing colonoscopy to investigate
abdominal pain).
Opportunistic versus systematic prevention

Most preventive activities are undertaken in Australia opportunistically - that is when patients present for other
reasons, and the preventive activity is an add-on.16 This approach is supported by evidence, which shows that
visits just for ‘a general check-up’ are not effective or necessary.17
However, systematic approaches to register and recall patients for some specific targeted conditions are
worthwhile - including childhood immunisations; and screening for cervical, breast and colorectal cancers (CRC),
and diabetes. Proactive recall of patients for screening is warranted for high-risk groups, those who may have
difficulty accessing services and for conditions where population coverage has been identified by the government
as a public health priority.15
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Screening principles
The World Health Organization (WHO) has produced guidelines18,19 for the effectiveness of screening programs.
These and the National Health Service’s (NHS) guidelines20 in the UK have been kept in mind in the development of
recommendations about screening in the Red Book.
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.
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 they should be treated.
Outcome
• There should be evidence of improved mortality, morbidity or quality of life as a result of screening, and the
benefits of screening should outweigh the harm.
• The cost of case finding (including diagnosis and treatment of patients who are 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 they can make an informed choice about participation.
In Australia, there is an increasing number of Medicare Benefits Schedule (MBS) items for health assessments in
particular population groups: Aboriginal and Torres Strait Islander children and adults, refugees, people with an
intellectual disability, those aged 45-49 years (with a risk factor), and those aged >75 years. There is evidence that
these assessments improve the likelihood of preventive care being received.21 However, it is important that such
‘health checks’ involve preventive interventions where there is clear evidence of their effectiveness.
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II. Patient education and health literacy
Impact of patient education

Patient education and counselling contribute to behaviour change for the primary prevention of disease.21 More
broadly, they may also help to 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.22
Patients view the general practitioner (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 literacy23
• the patient’s sense of trust in their GP24
• face-to-face delivery25
• patient involvement in decision making26-28
• highlighting the benefits and costs29,30
• strategies to help the patient remember what they have been told31
• tailoring the information to the patient’s interest in change32
• strategies that address the difficulty in adherence28,33
• the use of decision aids.34
Many preventive activities involve a change in health-related behaviour. In general practice, it may take at least six
to eight sessions to discuss and see changes to diet, physical activity or weight loss. This will often require referral,
which should be followed up by the general practice. 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 support strategies35,36 and has the potential to increase the patient’s responsibility for their health. In
addition, it:
• enhances the quality of communication37,38
• enhances the doctor-patient consultation26
• can reduce the cost of aspects of care through better informed patients27
• increases the demand and use of appropriate referral to other health professionals and agencies38
• increases adherence to recommended preventive activities and therapeutic regimens.38,39
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 cervical cancer screening test, patients weigh up the perceived benefits and
costs.40 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.
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There are a number of theoretical approaches to understanding and supporting behaviour change including the:
• Theory of planned behaviour41
• Health belief model42
• capability, opportunity and motivation (COM-B) system, which has been proposed by Michie et al as a way of
representing the necessary conditions for behaviour change to occur43
• ‘stages of change model’,44 which proposes five 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. Although there is a lack of evidence for greater effectiveness of stage-based approaches,45
this model provides a useful framework for clinicians to identify patients’ interest in behaviour change in the
consultation and to provide tailored support in a way that is time efficient and likely to be well received.46
Support from the GP and/or practice nurse may involve motivational interviewing. This is an evidence-based
counselling technique based on a therapeutic partnership that acknowledges and explores the patient’s
ambivalence about a behaviour in a way that allows them to clarify what goals are important to them and to
organise their reasons in a way that supports actions.
Motivational interviewing is a counselling philosophy that values patient autonomy and mutual respect, and the use
of open-ended questions, affirmations, reflection and summarising.47
Further information about motivational interviewing and its application in general practice can be found in The Royal
Australian College of General Practitioners’ (RACGP) Smoking, nutrition, alcohol and physical activity (SNAP): A
population health guide to behavioural risk factors in general practice (www.racgp.org.au/your-practice/guidelines/
snap) and Putting prevention into practice: Guidelines for the implementation of prevention in the general practice
setting (Green Book; www.racgp.org.au/your-practice/guidelines/greenbook ).
Health inequity
It is well recognised that socioeconomic disadvantage has a profound impact on people’s health, and GPs are
often in a good position to confront this.48
However, poverty is not evenly spread across Australia, and it is likely that GPs who see some patients with
socioeconomic disadvantage will see many. Similarly, GPs are not evenly spread with respect to poverty. The
Australian Bureau of Statistics (ABS) have shown that, in 2006, 11% of GPs worked in the most disadvantaged
areas, while 24% worked in the least disadvantaged.49
Healthcare in communities that are socioeconomically deprived is often complex. As well as having more chronic
health conditions, and more health behaviours leading to increased risk, there may be a lack of local support and
infrastructure to improve the situation. General practices are often one of the few resources patients have to call on.
There are often significant personal and social barriers to achieving change. As well as good communication skills,
GPs may need to help patients navigate health, housing, welfare and legal systems. This often makes for more-
frequent, longer, more-complex consultations. However, the long-term relationships GPs develop with patients are
significant enablers for patients who are socioeconomically deprived to be able to make changes.
Health equity issues are more complex than just socioeconomic factors. There are specific issues for Aboriginal and
Torres Strait Islander peoples, where an ongoing history of colonisation, dispossession and racism interact with a
lack of economic opportunity. The National guide to a preventive health assessment for Aboriginal and Torres Strait
Islander people, 2nd edn50 provides extensive detail on specific preventive care issues facing Aboriginal and Torres
Strait Islander peoples, and the health equity material canvassed here should be read in conjunction with those
guidelines. They provide much more in-depth and important guidance on preventive healthcare strategies that are
recommended for practitioners working with Aboriginal and Torres Strait Islander peoples and communities. In
addition, GPs should optimise their use of Medicare Benefits Schedule (MBS) Item 715 that supports health checks
in Aboriginal and Torres Strait Islander peoples and their use of Close the Gap provisions in ensuring affordable
access to medicines. GPs should also proactively address cost barriers to referral to other services faced by
Aboriginal and Torres Strait Islander peoples.
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Supporting patient education and health literacy in

disadvantaged groups
What are the key equity issues and who is at risk?
• 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.
• Socioeconomic disadvantage and low health literacy are linked. Health literacy is a key factor in how patient
education leads to patient empowerment. It allows individuals to access, understand and use information to
negotiate the health system and support self-management.51 Health literacy is important as low health literacy is
associated with poorer health outcomes and lower utilisation of health services such as screening and preventive
care.
• Other groups that require particular focus in patient education include Aboriginal and Torres Strait Islander
peoples and culturally and linguistically diverse (CALD) groups.52
What can GPs do?

A range of strategies can be used by GPs to help patients with low health literacy and to promote health-related
behaviour changes.51,53 These include:
• specific communication techniques such as asking patients to ‘teach back’ what has been taught to them and
the ‘ask me 3’ health education program based on three patient-led questions54 (https://npsf.site-ym.com/
default.asp?page=askme3)
• motivational interviewing and counselling techniques
• plain-language and culturally appropriate written materials (explicitly asking about reading skills may be important)
• use of web-based or computer-based programs (explicitly asking about internet access, eg at home or through a
library may be important)
• helping patients navigate the healthcare system to improve access to care, for example, by working in
collaboration with other services such as community health centres and consumer organisations to access
community health and group education programs.
Effective patient education for CALD populations means ensuring that health services and messages are accessible
and relevant. GPs should:
• offer interpreter services during consultations. There is good evidence that interpreter services improve care
experience and clinical outcomes55
• use patient education materials in plain English or those that are culturally and linguistically sensitive (eg have a
range of patient material in relevant different languages in your practice)
• link individuals to specific community-based health programs.56,57
Cultural competence is important in providing appropriate patient education to all communities. This is particularly
important in working with Aboriginal and Torres Strait Islander communities.58 It is important for GPs to better
appreciate Aboriginal and Torres Strait Islander peoples’ perspectives on health, culture and history, and provide
services within a culturally appropriate framework.59 This could be facilitated through:
• reading about the history and impact of colonisation on Aboriginal and Torres Strait Islander peoples and their
health, nationally and locally60
• arranging Aboriginal and Torres Strait Islander cultural awareness training for themselves and practice staff
(www.racgp.org.au/yourracgp/faculties/aboriginal/education/resources-for-gps-and-practice-staff/cultural-
awareness)
• linking your practice and Aboriginal and Torres Strait Islander patients to local Aboriginal community controlled
health services61
• developing relationships with your local Aboriginal and Torres Strait Islander community, and resources, people
and services that can provide you with assistance and cultural mentorship.
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III. Development of the Red Book

The Red Book, 9th edn, has been developed by a team of general practitioners (GPs) and experts to ensure
that the content is the most valuable and useful for GPs and their teams. The content broadly conforms to the
highest evidence-based standards according to the principles underlying the Appraisal of Guidelines Research and
Evaluation (AGREE) tool.62,63
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, and relevance and applicability to general
practice.
Recommendations
The recommendations in the Red Book are based on current, evidence-based guidelines for preventive
activities. Focus has been 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).
Where NHMRC guidelines are not available or recent, other sources have been used, such as guidelines from the
National Heart Foundation of Australia, Canadian or US preventive guidelines, or the results of systematic reviews.
References to support these recommendations are listed. However, particular references may relate only to part of
the recommendation (eg 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.
These recommendations are based on the best available information at the time of writing (May 2015 to May 2016).
Any updated information will be posted on The Royal Australian College of General Practitioners’ (RACGP) website.
More information and guidelines can be found on the NHMRC website www.nhmrc.gov.au/guidelines-publications,
the Australian Government clinical guidelines portal (www.clinicalguidelines.gov.au) and the Cochrane Collaboration
website (www.cochrane.org).
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IV. How to use the Red Book

The Red Book is 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 establish 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, todemonstrate to patients the evidence that exists for preventive activities
• study guide - a comprehensive list of references is provided in each chapter. This allows more in-depth
information on a particular topic.
Organisational detail
The information in the Red Book 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. Activities to be performed only in patients with risk factors or where the evidence is
not as strong are shaded in light red or pink.
A copy of this chart can be downloaded and attached to the patient record as a systematic reminder for preventive
activities. General practitioners (GPs) can also use it as a wall chart or keep it handy on the 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 existing National Health and Medical Research Council (NHMRC) levels of evidence and grades of
recommendations.64 Future editions will consider adopting the GRADE system (www.gradeworkinggroup.org) for
evaluating the quality of evidence for outcomes reported in systematic reviews.
Recommendations in the tables are graded according to the levels of evidence and 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. Refer to Table IV.1 for more
information.
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Table IV. 1. Coding scheme used for levels of evidence and grades of recommendation64
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 (ie alternate allocation or some other method)
Evidence obtained from a comparative study with concurrent controls:

• non-randomised, experimental trial
III-2 • cohort study
• case-control study
• interrupted time series with a control group
Evidence obtained from a comparative study without concurrent controls:

• historical control study
III-3
• 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 Opinions of respected authorities, based on clinical experience, descriptive studies or reports of expert
Point 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 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.
14 9th edition
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44. Cassidy C. Using the transtheoretical model to facilitate competence adequately considered? BMC Med Educ
behaviour change in patients with chronic illness. J Am 2014;14:167.
Acad Nurse Pract 1999;11(7):281. 59. Vass A, Mitchell A, Dhurrkay Y. Health literacy and
45. Cahill K, Lancaster T, Green N. Stage-based interventions Australian indigenous peoples: An analysis of the role
for smoking cessation. Cochrane Database Syst Rev of language and worldview. Health Promot J Aust
2010;11:CD004492. 2011;22(1):33-37.
46. Prochaska JO, Velicer WF, Redding C, et al. Stage 60. Eckermann A, Dowd T, Chong E, Nixon L, Gray R. Binan
based expert systems to guide a population of primary Goonj: Bridging cultures in Aboriginal health. 3rd edn.
care patients to quit smoking, eat healthier, prevent skin Chatswood, NSW: Elsevier Australia, 2010.
cancer, and receive regular mammograms. Prev Med 61. Ware VA. Improving the accessibility of health services
2005;41(2):406-16. in urban and regional settings for Indigenous people.
47. Miller WR, Rollnick S. Motivational interviewing - Helping Canberra: Australian Institute for Health and Welfare,
people change. 3rd edn. New York: Guildford Press, 2013.
2012. 62. Harris MF, Bailey L, Snowdon T, et al. Developing
48. Watt G, Brown G, Budd J, et al. General practitioners the guidelines for preventive care - Two decades of
at the deep end: The experience and views of general experience. Aust Fam Physician 2010;39(1-2):63-65.
practitioners working in the most severely deprived areas 63. Development and validation of an international appraisal
of Scotland. Occasional paper. Edinburgh: Royal College instrument for assessing the quality of clinical practice
of General Practitioners, 2012. guidelines: The AGREE project. Qual Saf Health Care
49. Australian Bureau of Statistics. Australian social trends, 2003;12(1):18-23.
Mar 2010. Canberra: ABS, 2010. Available at www.abs. 64. National Health and Medical Research Council.
gov.au/AUSSTATS/abs@.nsf/Lookup/4102.0Main+Featur NHMRC additional levels of evidence and grades for
es30Mar+2010 [Accessed 29 April 2016]. recommendations for developers of guidelines. Canberra:
50. National Aboriginal Community Controlled Health NHMRC, 2009. Available at www.nhmrc.gov.au/guidelines-
Organisation and The Royal Australian College of General publications/information-guideline-developers/resources-
Practitioners. National guide to a preventive health guideline-developers [Accessed 6 January 2016].
16 9th edition
V. What’s new in the 9th edition?
Chapter Change
1. Preventive activities prior to Advice on nutrition, weight assessment and oral health has been included in
pregnancy Table 1.1
Information on health inequity is presented under ‘What are the key equity issues
and who is at risk?’ and ‘What can GPs do?’, highlighting the key issues and
strategies
2. Genetic counselling and testing Information on referral to clinical genetic services has been added
Inclusion of the use of a simple family history screening questionnaire to identify

individuals in general practice who may require a more detailed assessment of their
family history of cancer, heart disease or diabetes (Appendix 2A. Family history
screening questionnaire)
Additional advice added regarding Down syndrome - for all pregnant women -
hereditary haemochromatosis, haemoglobinopathies and thalassaemias (Table 2.1)
Non-invasive prenatal test now included
3. Preventive activities in children Content has been edited and layout simplified to enable faster appreciation of the
and young people recommendations ‘at a glance’
strategies
4. Preventive activities in middle Information on health inequity is presented under ‘What are the key equity issues
age and who is at risk?’ and ‘What can GPs do?’, highlighting the key issues and
strategies
5. Preventive activities in older age Falls and physical activity are now in separate sections
Physical activity recommendations relevant to the Australian environment are

included
6. Communicable disease Inclusion of new information on the consent process before vaccination
New information on the prevalence of chlamydia, gonorrhoea, syphilis and human

immunodeficiency virus (HIV) in Australia
strategies
7. Prevention of chronic disease Additional information on identifying nutrition-related complications in children and
adolescents (Table 7.3.1)
Change of title of Section 7.4 from ‘Problem drinking’ to ‘Early detection of at-risk
drinking’. Additional advice and information on effective interventions
Section 7.5. Physical activity includes assessment advice and referral information for
different age groups, and those at increased risk
Consumption of red meat and processed meat recommendations modified to align

with World Health Organization (WHO) recommendations
strategies
9th edition
17
8. Prevention of vascular and Information added on assessing need for anticoagulation (Table 8.5.2)
metabolic disease
New information on atrial fibrillation
New advice about screening for diabetes based on US Preventive Services Task
Force (USPSTF) guidelines
Information on health inequity is presented under ‘What are the key equity issues and
who is at risk?’ and ‘What can GPs do?’, highlighting the key issues and strategies
9. Early detection of cancer Sections rearranged in order of incidence - that is, most commonly reported in
Australia (www.aihw.gov.au/cancer/cancer-in-australia-overview-2012/ch2/#t3)
After reviewing information from recent large trials of prostate cancer screening,
population screening for prostate cancer by prostate-specific antigen (PSA) testing
continues to not be recommended. Therefore, GPs have no obligation to offer
prostate cancer screening to asymptomatic men. Reference included to a decision
aid to assist discussion of possible benefits and harms of screening with PSA in men
who have individual concerns about prostate cancer
Inclusion of information on the cervical cancer screening program to commence in

May 2017
New information about the risks and benefits of screening mammogram; in

particular, the risk of over-diagnosis
Oral cancer section moved to Chapter 11. Oral health
who is at risk?’ and ‘What can GPs do?’ highlighting the key issues and strategies
10. Psychosocial Additional information on adolescents and those at average risk included for intimate
partner violence (Table 10.3.1)
who is at risk?’ and ‘What can GPs do?’, highlighting the key issues and strategies
11. Oral health Title of chapter has changed from ‘Oral hygiene’ to ‘Oral health’ to include
information on both oral hygiene and cancer
14. Osteoporosis Inclusion of an additional section on quantitative ultrasound as an alternative imaging

technique for assessing fracture risk
15. Screening tests of unproven Additional screening tests not recommended:

benefit • Coronary computed tomography (CT) angiography for coronary artery disease
• Cardiac calcium scoring for coronary heart disease
• Thermography and single nucleotide polymorphisms testing for breast cancer
• Optical colonoscopy and CT colonography for colorectal cancer
• Heel ultrasound for osteoporosis
• Carotid artery ultrasound for asymptomatic carotid artery stenosis
• Enquiry about sleep for obstructive sleep apnoea
• Bimanual pelvic exam during a routine Pap smear in asymptomatic women
• Genetic testing for methylenetetrahydrofolate reductase (MTHFR)
• Genetic testing for apolipoprotein E (ApoE)
‘Genetic profiling’ has been renamed ‘genomic sequencing’
18 9th edition
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 of reproductive age should be considered for preconception care (C). This consists 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.1 Preconception care should include reproductive planning and the
effective use of contraception to prevent unplanned pregnancy (A), smoking cessation (A)2 and advice to consider
abstinence from alcohol (especially if planning a pregnancy, or if the woman could become pregnant or is in the
early stages of pregnancy),3 folic acid and iodine supplementation (A),4,5 nutrition and weight assessment,6 review of
immunisation status (C),7 medications (B),8 oral health,9 and chronic medical conditions, especially glucose control
in patients with diabetes (B).10
There is evidence to demonstrate improved birth outcomes with preconception healthcare in women with diabetes,
phenylketonuria and nutritional deficiency,11 as well as benefit from the use of folate supplementation12 and a
reduction in maternal anxiety.13 Below is information about all the potential interventions in preconception care that
expert groups have recommended (C).
What does preconception care include?

Medical issues
Reproductive life plan
Assist your patients to develop a reproductive life plan that includes whether they want to have children. If they do,
discuss the number, spacing and timing of intended children, and provide effective contraception to enable the
implementation of this plan and reduce the risk of an unplanned pregnancy. If relevant, discuss reduction in fertility
with advancing maternal age.
Reproductive history
Ask if there have been any problems with previous pregnancies such as infant death, fetal loss, birth defects
(particularly neural tube defects [NTD]), low birth weight, preterm birth, or gestational diabetes. Also, if there are 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? Consider if current management is
optimal for early pregnancy given that early embryogenesis will occur prior to any consultation in pregnancy.
Medication use
Review all current medications for teratogenic effects, including over-the-counter medications, vitamins and
supplements.
9th edition
19
Genetic/family history (also refer to Chapter 2. Genetic counselling and testing)

Increased frequency of intellectual disability, multiple pregnancy losses, stillbirth or early death, and children with
congenital abnormalities may suggest the presence of genetically determined disease. Patients of particular
ethnic backgrounds may be at increased risk and can benefit from genetic testing for specific conditions. Possible
consanguinity (eg 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?’ General practitioners (GPs) should
consider referral to, or consultation with, a genetic service 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. The time on waiting lists for genetic services is usually longer than one month, so direct consultation
and liaison by telephone are necessary when the genetic advice could affect a current pregnancy. Provide
opportunity for carrier screening for genetic conditions (eg cystic fibrosis, haemoglobinopathies) and referral for
genetic counselling based upon risk factors.
General physical assessment

Conduct a breast examination and, if it is due, perform a cervical screening test (eg Papanicolaou [Pap] test) before
pregnancy. Also assess body mass index (BMI) and blood pressure (BP), and check the oral cavity.
Substance use
Ask about tobacco, alcohol and illegal drug use. Offer counselling and referral for specialised assistance when use
is identified.
Vaccinations
The need for vaccination, particularly for hepatitis B, rubella and varicella, should be assessed as part of any pre
conception health check. Vaccinations can prevent some infections that may be contracted during pregnancy,
and relevant serological testing can be undertaken to ascertain immunity to hepatitis B and rubella. Routine
serological testing for varicella does not provide a reliable measure of vaccine-induced immunity; however, it can
indicate whether natural immunity has occurred due to prior infection. Women receiving live viral vaccines such
as measles, mumps and rubella (MMR) and varicella should be advised against becoming pregnant within 28
days of vaccination. It is also important that women of child-bearing age who present for immunisation should
be questioned regarding the possibility of pregnancy as part of the routine pre-vaccination screening, to avoid
inadvertent administration of a vaccine(s) not recommended in pregnancy (refer to Section 2.1.4 Pre-vaccination
screening in the Australian immunisation handbook, 10th edn). Recommended preconception vaccinations are:
• MMR
• varicella (in those without a clear history of chickenpox or who are non-immune on testing)
• influenza (recommended during pregnancy)
• diphtheria, tetanus, acellular pertussis (dTpa; to protect newborn from pertussis).
Lifestyle issues
Family planning
Based on the patient’s reproductive life plan (refer to above), discuss fertility awareness and how fertility reduces
with age, chance of conception, the risk of infertility, and fetal 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 per day supplement of folic acid for at least one month prior to pregnancy,
and for the first three months after conception. Where there is a known increased risk of NTD (ie patients
taking anticonvulsant medication, or with pre-pregnancy diabetes mellitus, previous child or family history of
NTD, 5-methyltetrahydrofolate deficiency or BMI >30 kg/m2) or a risk of malabsorption, a 5 mg daily dose is
recommended.14
20 9th edition
Iodine supplementation
Women who are pregnant, breastfeeding or considering pregnancy should take an iodine supplement of 150 pg
each day.5
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 (eg vegan diet, lactose intolerance, and
calcium, iron or vitamin D deficiency due to lack of sun exposure).
Psychosocial health
Discuss perinatal mental health, including anxiety and depression, pre-existing mental health conditions,
psychological or psychiatric assessment and treatment, use of medication, and the risk of exacerbation of mood
disorders in pregnancy and postpartum. Mental health screening should include a psychosocial assessment.
Smoking, alcohol and illegal drug cessation (as indicated)

Smoking,15 illegal drug16 and excessive alcohol use17 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 (eg syphilis, varicella, mumps, parvovirus and human immunodeficiency virus [HIV], listeriosis), Rubella,
Cytomegalovirus and Herpes simplex.
• Toxoplasmosis: Avoid cat litter, garden soil, raw/undercooked meat and unpasteurised milk products; wash all
fruit and vegetables.
• Cytomegalovirus, parvovirus B19 (fifth disease): Discuss the importance of frequent hand-washing. Those who
work with children or in the healthcare sector can further reduce risk by using gloves when changing nappies.
• Listeriosis: Avoid paté, soft cheeses (eg feta, brie, blue vein), prepackaged salads, deli meats and chilled/
smoked seafood. Wash all fruit and vegetables before eating. Refer to Food Standards Australia New Zealand
(www.foodstandards.gov.au/consumer/generalissues/pregnancy/Pages/default.aspx) regarding folate, listeria
and mercury.
• Fish: Limit fish containing high levels of mercury. Refer to www.betterhealth.vic.gov.au/health/healthyliving/
mercury-in-fish
9th edition
21
Table 1.1. Preconception: Preventive interventions

Intervention Technique References
Folate Most women: 0.5 mg/day supplementation, beginning ideally at least one month 4, 18-20
supplementation prior to conception and continuing for the first trimester
High-risk women: 5 mg/day supplementation, ideally beginning at least one month

prior to conception and continuing for the first trimester
Iodine All women who are pregnant, breastfeeding or considering pregnancy should take 5, 14
supplementation an iodine supplement of 150 pg each day
Nutrition All women, especially those who become pregnant in adolescence or have closely- 6, 21
and weight spaced pregnancies (interpregnancy interval less than six months), require nutritional
assessment assessment and appropriate intervention in the preconception period with an
emphasis on optimising maternal body mass index (BMI) and micronutrient reserves
Check oral cavity Ask the woman if she has bleeding gums, swellings, sensitive teeth, loose teeth,
and referral holes in teeth, broken teeth, toothache, or any other problems in the mouth
Check oral cavity to confirm. Reassure the patient that it is safe to have a range of
dental treatments during pregnancy
Smoking Inform women who smoke that tobacco affects fetal growth and advise them to 22
cessation stop smoking. Evidence exists to suggest improved cognitive ability in children of
mothers who quit smoking during gestation (III, A). Consider pharmacotherapy 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 1
drug use option. The risk of harm to the fetus is highest when there is high, frequent maternal
alcohol intake. The risk of harm to the fetus is likely to be low if a woman has
consumed only small amounts of alcohol before she knew she was pregnant. Inform
pregnant women that illicit drugs may harm the fetus and advise them to avoid use
Interpregnancy Perinatal outcomes are worse with interpregnancy intervals <18 months or >59 23
interval months; the outcomes affected are preterm birth, low birth weight and small size for
gestational age
Chronic diseases Optimise control of existing chronic diseases (eg diabetes, hypertension, epilepsy). 18
Avoid teratogenic medications
BMI, body mass index

22 9th edition
Health inequity
Preconception care is especially important to adolescents and young women in vulnerable populations.24
Adolescent parenthood is more common in low socioeconomic groups and Aboriginal and Torres Strait Islander
communities, and is associated with poor birth outcomes and adverse health effects, including mental health
issues and substance misuse.25-29
Decreased folate supplementation is associated with being a woman from a lower socioeconomic group, being
an Aboriginal and Torres Strait Islander person, or being younger or from a rural area.30 Awareness of folic acid is
related to income, educational level and younger age.31,32 Other dietary supplements may follow similar gradients.
Smoking and alcohol use in pregnancy show socioeconomic gradients. Women who are young, on a low
income and of low socioeconomic status, Aboriginal and Torres Strait Islander women, single mothers, and
women experiencing addiction, violence and mental health issues are all more likely to smoke during pregnancy.33,34
Women from culturally and linguistically diverse (CALD) backgrounds are more likely to experience poorer perinatal
outcomes.36-38
What can GPs do?

• Provide youth-friendly care to adolescent parents through non-judgemental, competent, considerate and
respectful advice and services.39
• Offer women culturally appropriate resources, including in the mother’s own language, about health issues
and the health system, and consider the use of interpreters.
• Link women into English language and perinatal education courses, and offer cultural brokerage through
maternity liaison officers or bilingual health workers wherever possible.39
• Refer to ‘Antenatal care for Aboriginal and Torres Strait Islander women’ in the Australian Health Ministers’
Advisory Council’s Clinical practice guidelines: Antenatal care - Module 1.39
• Refer to the general principles of providing patient education and supporting health literacy in disadvantaged
groups.
References
1. Johnson K, Posner SF, Biermann J, et al. 6. Dean SV, Lassi ZS, Imam AM, Bhutta ZA. Preconception
Recommendations to improve preconception health care: Nutritional risks and interventions. Reprod Health
and health care - United States. MMWR Recomm Rep 2014;11 Suppl 3:S3.
2006;55(RR-6):1-23. 7. Australian Technical Advisory Group on Immunisation
2. Lumley J, Chamberlain C, Dowswell T, Oliver S, Oakley (ATAGI). The Australian immunisation handbook. 10th edn
L, Watson L. Interventions for promoting smoking (2015 update). Canberra: Department of Health, 2015.
cessation during pregnancy. Cochrane Database Syst 8. Australian Department of Health and Aged Care.
Rev 2009;3:CD001055. Prescribing medicines in pregnancy. 4th edn. Canberra:
3. National Health and Medical Research Council. Australian Therapeutic Goods Administration, 1999.
guidelines to reduce health risks from drinking alcohol. 9. Rogers JG. Evidence-based oral health promotion
Canberra: NHMRC, 2009. resource. Melbourne: Prevention and Population Health
4. Lumley J, Watson L, Watson M, Bower C. Periconceptual Branch, Department of Health, 2011.
supplementation with folate and/or multivitamins for 10. Korenbrot CC, Steinberg A, Bender C, Newberry S.
preventing neural tube defects. Cochrane Database Syst Preconception care: A systematic review. Matern Child
Rev 2001;3:CD001056. Health Journal 2002;6(2):75-88.
5. National Health and Medical Research Council. Iodine 11. Gjerdingen DK, Fontaine P. Preconception health care: A
supplementation for pregnant and breastfeeding women. critical task for family physicians. J Am Board Fam Pract
Canberra: NHMRC, 2010. Available at www.nhmrc. 1991;4(4):237-50.
gov.au/_files_nhmrc/file/publications/synopses/new45_ 12. Hodgetts VA, Morris RK, Francis A, Gardosi J, Ismail
statement.pdf [Accessed 8 December 2015]. KM. Effectiveness of folic acid supplementation in
9th edition
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pregnancy on reducing the risk of small-for-gestational low and middle income countries. BMC Public Health
age neonates: A population study, systematic review and 2012;12.
meta-analysis. BJOG 2015;122(4):478-90. 25. Hodgkinson S, Beers L, Southammakosane C, Lewin
13. de Jong-Potjer LC, Elsinga J, le Cessie S, et al. GP- A. Addressing the mental health needs of pregnant and
initiated preconception counselling in a randomised parenting adolescents. Pediatrics 2014;133(1):114-22.
controlled trial does not induce anxiety. BMC Fam Pract 26. Payne NA, Anastas JW. The mental health needs of
2006;7:66. low-income pregnant teens: A nursing-social work
14. The Royal Australian and New Zealand College of partnership in care. Research on Social Work Practice
Obstetricians and Gynaecologists. Vitamin and mineral 2015 Sep;25(5):595-606.
supplementation and pregnancy (C-Obs 25), November 27. Penman-Aguilar A, Carter M, Snead MC, Kourtis AP.
2014, amended May 2015. East Melbourne, Vic: Socioeconomic disadvantage as a social determinant of
RANZCOG, 2015. Available at www.ranzcog.edu.au/ teen childbearing in the US Public Health Reports 2013;
doc/vitamin-and-mineral-supplementation-in-pregnancy. 128:5-22.
html [Accessed 5 September 2015].
28. Hilder L, Zhichao Z, Parker M, Jahan S, Chambers
15. The Royal Australian and New Zealand College of G. Australia’s mothers and babies 2012. Canberra:
Obstetricians and Gynaecologists. Women and smoking Australian Institute of Health and Welfare, 2014.
(C-Obs 53). East Melbourne, Vic: RANZCOG, 2011.
29. Middleton P. Preventing infant deaths among Aboriginal
Available at www.ranzcog.edu.au/college-statements-
and teenage women in South Australia. Adelaide: The
guidelines.html [Accessed 27 May 2016].
Strategic Health Research Program Team, The University
16. The Royal Australian and New Zealand College of
of Adelaide, 2009.
Obstetricians and Gynaecologists. Substance use in
30. Australian Institute of Health and Welfare. Mandatory folic
pregnancy (C-Obs 55). East Melbourne, Vic: RANZCOG,
acid and iodine fortification in Australia and New Zealand:
2013. Available at www.ranzcog.edu.au/college-
Baseline report for monitoring. Canberra: AIHW, 2011.
statements-guidelines.html [Accessed 27 May 2016].
31. Hage CN, Jalloul M, Sabbah M, Adib SM. Awareness
17. The Royal Australian and New Zealand College of
and intake of folic acid for the prevention of neural tube
Obstetricians and Gynaecologists. Alcohol in pregnancy
defects among Lebanese women of childbearing age.
(C-Obs 54). East Melbourne, Vic: RANZCOG, 2014.
Matern Child Health 2012;16(1):258-65.
Available at www.ranzcog.edu.au/college-statements-
guidelines.html [Accessed 27 May 2016]. 32. Rasmussen MM, Clemmensen D. Folic acid
supplementation in pregnant women. Dan Med Bull
18. National Institute for Health and Care Excellence.
2010;57(1):A4134
Diabetes in pregnancy: Management of diabetes and
its complications from preconception to the postnatal 33. Borland T, Babayan A, Irfan S, Schwartz R. Exploring the
period. London: NICE, 2015. adequacy of smoking cessation support for pregnant and
postpartum women. BMC Public Health 2013;13:472
19. Wilson RD, Johnson JA, Wyatt P, et al. Pre-conceptional
vitamin/folic acid supplementation 2007: The use 34. Cui Y, Shooshtari S, Forget EL, Clara I, Cheung KF.
of folic acid in combination with a multivitamin Smoking during pregnancy: Findings from the 2009
supplement for the prevention of neural tube defects 2010 Canadian Community Health Survey. PLOS ONE
and other congenital anomalies. J Obstet Gynaecol Can 2014;9(1):e84640
2007;29(12):1003-26. 35. Burns L, Breen C, Bower C, O’ Leary C, Elliott EJ.
20. US Preventive Services Task Force. Guide to clinical Counting fetal alcohol spectrum disorder in Australia:
preventive services: Report of the US Preventive Services The evidence and the challenges. Drug Alcohol Rev
Task Force. 2nd edn. Alexandria, VA: Williams & Wilkins, 2013;32(5):461-67.
2002. 36. Laws P, Li Z, Sullivan E. Australia’s mothers and babies
21. Opray N, Grivell RM, Deussen AR, Dodd JM. Directed 2008. Canberra: Australian Institute of Health and
preconception health programs and interventions for Welfare, 2010.
improving pregnancy outcomes for women who are 37. O’Mahony JM, Donnelly TT. How does gender influence
overweight or obese. Cochrane Database Syst Rev immigrant and refugee women’s postpartum depression
2015;7:CD010932. help-seeking experiences? J Psychiatr Ment Health Nurs
22. The Royal Australian College of General Practitioners. 2013;20(8):714-25.
Supporting smoking cessation: A guide for health 38. O’Mahony JM, Donnelly TT, Bouchal SR, Este D. Cultural
professionals. Melbourne: RACGP, 2011. background and socioeconomic influence of immigrant
23. Conde-Agudelo A, Rosas-Bermudez A, Kafury- and refugee women coping with postpartum depression.
Goeta AC. Birth spacing and risk of adverse perinatal J Immigr Minor Health 2013;15(2):300-14.
outcomes: A meta-analysis. JAMA 2006;295:1809-23. 39. Australian Health Ministers’ Advisory Council. Clinical
24. Hanson MA, Gluckman PD, Ma RCW, Matzen P, Biesma practice guidelines: Antenatal care - Module 1. Canberra:
RG. Early life opportunities for prevention of diabetes in Department of Health and Ageing, 2012.
24 9th 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
Genetic testing can be used for various purposes, from preconception planning (refer to Chapter 1. Preventive
activities prior to pregnancy), during pregnancy, for neonates (newborn screening), during childhood and right
through to adult-onset familial diseases (eg cancer, cardiac and neurodegenerative diseases).
In order to identify patients who may be at risk of a genetic disorder, a comprehensive family history must be taken
from all patients, and this should be regularly updated. A family history should include first-degree and second-
degree relatives on both sides of the family and ethnic background. Age of onset of disease and age of death
should be recorded where available.
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 congenital
abnormalities may suggest the presence of genetically determined disease. Patients of particular ethnic
backgrounds may be at increased risk and may benefit from genetic testing for specific conditions. Possible
consanguinity (eg 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?’ General Practitioners (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. The time on waiting lists for genetic services is usually longer than
one month, so direct consultation and liaison by telephone are necessary when the genetic advice could affect a
current pregnancy. On the basis of current evidence, whole genome sequencing is not recommended in low-risk
general practice populations (refer to Chapter 15. Screening tests of unproven benefit).
Clinical genetic services provide testing, diagnosis, management and counselling for a wide range of genetic
conditions. Reasons for referral include:
• diagnosis of a genetic condition
• family history of a genetic condition
• recurrence risk counselling (eg risk of recurrence in a future pregnancy)
• pregnancy counselling (eg preconception, consanguinity)
• prenatal screening and testing
• presymptomatic and predictive testing for adult-onset disorders (eg cancer)
• discussions surrounding genetic testing
• arranging of genetic testing.
Services such as paternity testing or genetic testing/management of very common genetic conditions (eg
haemochromatosis) are not provided by clinical genetic services.
Use of a simple family history screening questionnaire (FHSQ) can help identify individuals who may require a
more detailed assessment of their family history of cancer, heart disease or diabetes (refer to Appendix 2A. Family
history screening questionnaire for a published and validated FHSQ).1 This tool can be used as part of the patient
assessment at their first visit to a practice. If a patient is uncertain about their family history, they can be asked
to discuss the FHSQ with their relatives prior to completing the questionnaire. For patients with low literacy,
the FHSQ may need to be completed with the support of a healthcare professional. A positive response to any
question requires follow-up with a more detailed assessment of the family history. As family history can change, it is
recommended that the FHSQ be repeated at least three every years.
9th edition
25
Table 2.1. Genetic testing: Identifying risks

Who is at risk? What should be done? How often? References
Cystic fibrosis (CF)
Increased probability: Offer referral for genetic Test couple for carrier 2-5
• Northern European or Ashkenazi counselling and carrier testing status if planning
Jewish ancestry (III, B) pregnancy or in first
• Family history of CF or a relative with a trimester
If patient is pregnant, contact
known CF mutation genetic services to organise
• Where partner is affected or a known screening in first trimester
carrier of CF
• Partners from Northern European
or Ashkenazi Jewish backgrounds
who are consanguineous (eg cousins
married to each other)
• Men with infertility suspected or due to
congenital absence of the vas deferens
Down syndrome
Probability: Combined maternal serum and First or second 3, 6-11

• All pregnant women ultrasound screening in first trimester
trimester
*
Maternal serum screening in

second trimester1' (C)
Non-invasive prenatal test (NIPT)*
Significantly increased probability: Fetal diagnostic genetic testing First or second 10

• Women who had a previous Down (C) trimester
syndrome pregnancy Offer referral for genetic
• Women with positive maternal serum counselling
screening/nuchal translucency
ultrasound, NIPT in first trimester
or maternal serum screening in
second trimester
• Parent with a chromosomal
rearrangement (eg balanced
translocation of chromosome 21)
Fragile X syndrome
Increased probability Deoxyribonucleic acid (DNA) Any age for diagnosis 3, 12, 13
test for fragile X and karyotype/
Children or adults of either sex with one or Prior to pregnancy to
comparative genomic
more of the following features: ascertain carrier status
hybridisation by microarray
• developmental delay including and reproductive risk
for other possible causes of
intellectual disability of unknown cause developmental delay
• autistic-like features
Refer to genetic services for
• attention deficit hyperactivity disorder
genetic counselling and testing
(ADHD)
at-risk family (I, A)
• speech and language problems
• social and emotional problems, such as
aggression or shyness
• a female with a history of primary
ovarian insufficiency or premature 14-16
menopause (aged <40 years) (IV B)
• adults with ataxia, balance problems
(IV A) 17
and parkinsonism
• relative with a fragile X mutation
26 9th edition

Haemoglobinopathies and thalassaemias
Increased probability: Test for mean corpuscular Test couple for 3, 18-20
• People from any of the following ethnic volume (MCV), mean corpuscular carrier status prior to
backgrounds: Southern European, haemoglobin (MCH) and ferritin pregnancy or in first
African, Middle Eastern, Chinese, Indian trimester
Haemoglobin electrophoresis
subcontinent, Central and South-east (III, B)
Asian, Pacific Islander, New Zealand
Maori, South American, Caribbean, and Blood for deoxyribonucleic acid
some northern Western Australian and (DNA) studies
Northern Territory Aboriginal and Torres Arrange partner testing if: MCV
Strait Islander communities <80 fL and/or MCH <27 pg and/
or abnormal haemoglobin (Hb)
electrophoresis
Breast and ovarian cancer Refer to Section 9.3. Breast cancer
Colon cancer Refer to Section 9.2. Colorectal cancer
Familial hypercholesterolaemia (FH)
Increased probability: Assess their probability of First presentation 21,22

• Premature ischaemic heart disease (ie having FH using the Dutch
ischaemic heart disease in men aged Lipid Clinic Network (DLCN)
<55 years and women aged <60 years) criteria or Modified UK Simon
• First-degree relative with premature Broome (MUKSB) criteria (III,
ischaemic heart disease (men aged B) (Appendix 2B. Dutch Lipid
<55 years and women aged <60 years) Clinic Network Criteria for
making a diagnosis of Familial
• Total cholesterol >7.5 mmol/L or low
Hypercholestroloaemia in adults)
density lipoprotein-cholesterol (LDL-C)
>4.9 mmol/L Offer referral to a lipid disorders
• First-degree relative with a total clinic if DLCN score >3 or the
cholesterol >7.5 mmol/L or LDL-C MUKSB suggests possible FH
>4.9 mmol/L
• Tendon xanthomata or arcus cornealis
at <45 years of age
9th edition
27

Hereditary haemochromatosis (HHC)
Increased probability: Positive family history - Aged >18 years at first 9, 23-29
• All first-degree relatives of patients with asymptomatic and symptomatic presentation
HHC who are C282Y homozygous or For patients aged >18 years, test Although
C282Y/H63D compound heterozygous for HFE mutations, transferrin abnormalities in
saturation and serum ferritin to transferrin saturation
simultaneously assess future and serum ferritin may
and current risk of iron overload occur at <18 years
(C). Medicare Benefits Schedule of age in patients
(MBS) rebate applies if affected with HHC, morbidity
relative is first-degree relative; from significant
no MBS rebate applies for more iron overload is
distant relatives exceedingly rare
before the age of 18
If HFE mutation tests show
years
C282Y homozygous or C282Y/
H63D compound heterozygous
result, arrange for all of that
patients first degree relatives
aged >18 years to have tests for
HFE mutations and transferrin
saturation and serum ferritin (C).
MBS rebate applies
Consider in these patients: Other patients - asymptomatic

• Patients with conditions that could be and symptomatic
a complication of haemochromatosis For patients aged >18 years, test
(eg arthritis, chronic fatigue, erectile transferrin saturation and serum
dysfunction, early menopause, ferritin
cirrhosis, hepatocellular carcinoma,
cardiomyopathy, diabetes mellitus) If transferrin saturation >45%
or serum ferritin >250 pg/L on
• Patients with liver disease of unknown
repeated testing, test for HFE
cause, including those with suspected
mutations. MBS rebate applies
alcoholic liver disease
• Patients with a family history of The ideal sample for testing
haemochromatosis, liver cancer, transferrin saturation and serum
unexplained early death from liver or ferritin is early morning fasting
heart failure blood test with iron supplements
• Patients with porphyria cutanea tarda withheld for 24 hours
and chondrocalcinosis (‘pseudogout’)
*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 and Edwards syndrome)
• nuchal translucency screen at 11 weeks, 3 days to 13 weeks, 6 days
• NIPT* from 10 weeks for trisomy 21, 18 and 13; not available for MBS rebate. Tests for fetal DNA in maternal blood
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
neural tube defects (NTDs)
ADHD, attention deficit hyperactivity disorder; GF, cystic fibrosis; DLCN, Dutch Lipid Clinic Network; DNA, deoxyribonucleic acid; FH,
familial hypercholesterolaemia; Hb, haemoglobin; HCG, human chorionic gonadotrophin; HHC, hereditary haemochromatosis; LDL-C,
low density lipoprotein-cholesterol; MCH, mean corpuscular haemoglobin; MOV, mean corpuscular volume; MUKSB, Modified UK
Simon Broome; NIPT non-invasive prenatal test; NTD, neural tube defect
28 9th edition
References
1. Emery JD, Reid G, Prevost AT, Ravine D, Walter FM. 15. Laml T, Preyer O, Umek W, Hengstschlager M. Genetic
Development and validation of a family history screening disorders in premature ovarian failure. Hum Reprod
questionnaire in Australian primary care. Ann Fam Med Update 2002;8(5):483-91.
2014;12(3):241-49. 16. Better Health Channel. Menopause - Premature (early
2. Southern KW, Merelle MM, Dankert-Roelse JE, menopause). Melbourne: Better Health Channel,
Nagelkerke AD. Newborn screening for cystic fibrosis. 2003. Available at www.betterhealth.vic.gov.au/bhcv2/
Cochrane Database Syst Rev 2009;1:CD001402. bhcarticles.nsf/pages/Menopause_premature_early_
3. The Royal Australian and New Zealand College of menopause [Accessed 15 April 2016].
Obstetricians and Gynaecologists. Prenatal screening 17. Jacquemont S, Hagerman RJ, Leehey MA, Hall DA.
and diagnosis of chromosomal and genetic abnormalities Penetrance of the fragile X-associated tremor/ataxia
in the fetus in pregnancy (C-Obs 59). East Melbourne, syndrome in a premutation carrier population. JAMA
Vic: RANZCOG, 2011. Available at www.ranzcog.edu.au/ 2004;291(4):460-69.
college-statements-guidelines.html [Accessed 19 April 18. Dormandy E, Bryan S, Gulliford MC, et al. Antenatal
2016]. screening for haemoglobinopathies in primary
4. Ioannou L, McClaren BJ, Massie J, et al. Population care: A cohort study and cluster randomised trial
based carrier screening for cystic fibrosis: A to inform a simulation model. The Screening for
systematic review of 23 years of research. Genet Med Haemoglobinopathies in First Trimester (SHIFT) trial.
2014;16(3):207-16. Health Technol Assess 2010;14(20):1-160.
5. Delatycki M, Burke J, Christie L, et al. Population based 19. Cunningham F, Bowden D. Suggested protocol
carrier screening for cystic fibrosis. Position statement. for pre-conceptual and antenatal carrier testing for
Alexandria, New South Wales: Human Genetics Society haemoglobinopathies. Clayton, Vic: Monash Medical
of Australasia, 2013. Centre, 2013.
6. The American College of Obstetricians and Gynecologists 20. Pagon RA, Bird TD, Dolan CR, Stephens K AM, editors.
Committee on Genetics and The Society for Maternal- GeneReviews. Seattle: University of Washington, 2010.
Fetal Medicine Publications Committee. Committee 21. Sullivan D, Watts G, Hamilton-Craig I, and members
opinion no. 545: Noninvasive prenatal testing for fetal of the Cardiovascular Genetic Diseases Writing Group.
aneuploidy. Obstet Gynecol 2012;120(6):1532-34. Guidelines for the diagnosis and management of familial
7. Woolcock J, Grivell R. Noninvasive prenatal testing. Aust hypercholesterolaemia. Sydney: Cardiac Society of
Fam Physician 2014 Jul;43(7):432-34. Australia and New Zealand, 2013.
8. Bianchi DW, Parker RL, Wentworth J, et al. DNA 22. Watts GF, Sullivan DR, Poplawski N, et al. Familial
sequencing versus standard prenatal aneuploidy hypercholesterolaemia: A model of care for Australasia.
screening. N Engl J Med 2014;370(9):799-808. Atheroscler Suppl 2011;12(2):221-63.
9. Genetics Education in Medicine Consortium. Genetics 23. Crawford D, Macdonald D. Haemochromatosis. 3rd edn.
in family medicine: The Australian handbook for general Mount Waverley, Vic: Digestive Health Foundation and
practitioners. Canberra: Biotechnology Australia, 2008. the Gastroenterological Society of Australia, 2007.
Available at www.nhmrc.gov.au/_files_nhmrc/file/ 24. Powell LW, Dixon JL, Ramm GA, Purdie DM.
your_health/egenetics/genetics_in_family_mdicine.pdf Screening for hemochromatosis in asymptomatic
[Accessed 15 April 2016]. subjects with or without a family history. Arch Int Med
10. Facher J, Robin N. Genetic counselling in primary care. 2006;166(3):294-303.
What questions are patients likely to ask, and how should 25. Delatycki MB, Powell LW, Allen KJ. Hereditary
they be answered. Postgrad Med 2000;107(3):59-66. hemochromatosis genetic testing of at-risk children:
11. Dick P. Periodic health examination, 1996 update. 1. What is the appropriate age? Genet Test 2004;8(2):98-
Prenatal screening for and diagnosis of Down syndrome. 103.
Canadian Task Force on the Periodic Health Examination. 26. Whitlock EP, Garlitz BA, Harris EL, Beil TL, Smith PR.
CMAJ 1996;154(4):465-79. Screening for hereditary hemochromatosis: A systematic
12. Cohen J, Lennox N. Fragile X syndrome. In: Lennox N, review for the US Preventive Services Task Force. Ann
Diggens J, editors. Management guidelines: People with Intern Med 2006 Aug 1;145(3):209-23.
developmental and intellectual disabilities. Melbourne: 27. EASL clinical practice guidelines for HFE
Therapeutic Guidelines Limited, 1999. hemochromatosis. J Hepatol 2010;53(1):3-22.
13. Mefford HC, Batshaw ML, Hoffman EP. Genomics, 28. Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS,
intellectual disability, and autism. N Engl J Med American Association for the Study of Liver Diseases.
2012;366(8):733-43. Diagnosis and management of hemochromatosis: 2011
14. Murray A, Schoemaker MJ, Bennett CE, et al. practice guideline by the American Association for the
Population-based estimates of the prevalence of Study of Liver Diseases. Hepatology 2011;54(1):328-43.
FMR1 expansion mutations in women with early 29. Goot K, Hazeldine S, Bentley P, Olynyk J, Crawford D.
menopause and primary ovarian insufficiency. Genet Med Elevated serum ferritin - What should GPs know? Aust
2014;16(1):19-24. Fam Physician 2012;41(12):945-49.
9th edition
29
Appendix 2A. Family history screening questionnaire

The use of a simple family history screening questionnaire (FHSQ) can help identify individuals who may require a
more detailed assessment of their family history of cancer, heart disease or diabetes.1
This tool can be used as part of the patient’s assessment at their first visit to a practice. If patients are uncertain about
their family history, they can be asked to discuss the FHSQ with their relatives prior to completing the questionnaire.
For patients with low literacy, the FHSQ may need to be completed with the support of a healthcare professional.
A positive response to any question requires follow-up with a more detailed assessment of the family history. As
family history can change it is recommended that the FHSQ be repeated at least every three years.
This risk assessment focuses on your close relatives including parents, children,
brothers and sisters who are either living or dead. Yes No
Have any of your close relatives had heart disease before 60 years of age?
‘Heart disease’ includes cardiovascular disease, heart attack, angina and bypass surgery.
Have any of your close relatives had diabetes?
‘Diabetes’ is also known as type 2 diabetes or non-insulin dependent diabetes.
Do you have any close relatives who had melanoma?
Have any of your close relatives had bowel cancer before 55 years of age?
Do you have more than one relative on the same side of the family who had bowel cancer at
any age?
Please think about your parents, children, brothers, sisters, grandparents, aunts, uncles, nieces,
nephews and grandchildren.
*
Have any of your close male relatives had prostate cancer before 60 years of age?
Have any of your close female relatives had ovarian cancer?
Have any of your close relatives had breast cancer before 50 years of age?
Do you have more than one relative on the same side of your family who has had breast cancer
at any age?
Please think about your parents, children, brothers, sisters, grandparents, aunts, uncles, nieces,
nephews and grandchildren.
*
‘Only first-degree and second-degree relatives need be considered in this screening questionnaire
Reproduced with permission from Emery JD, Reid G, Prevost AT, Ravine D, Walter FM. Development and validation of a family
history screening questionnaire in Australian primary care. Ann Fam Med 2014;12(3):241-49. Available at www.annfammed.org/
content/12/3/241.long
30 9th edition
Appendix 2B. Dutch Lipid Clinic Network Criteria for making

a diagnosis of familial hypercholestrolaemia in adults
Score
Family history
First-degree relative with known premature coronary and/or vascular disease (men aged <55 years and 1
women aged <60 years)
or
First-degree relative with known low-density lipoprotein-cholesterol (LDL-C) above the 95th percentile
for age and sex
First-degree relative with tendinous xanthomata and/or arcus cornealis 2
or
Children aged <18 years with LDL-C 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 45 years of age 4
LDL-C (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
Deoxyribonucleic acid (DNA) analysis: Functional mutation in the low-density lipoprotein receptor (LDLR), 8
apolipoprotein B (APOB) or proprotein convertase subtilisin/kexin type 9 (PCSK9) gene
Stratification Total score

Definite familial hypercholesterolaemia (FH) >8
Probable FH 6-7
Possible FH 3-5
Unlikely FH <3
ApoB, apolipoprotein B; DNA, deoxyribonucleic acid; FH, familial hypercholesterolaemia; LDL-C, low-density lipoprotein-cholesterol;
LDLR, low-density lipoprotein receptor; PCSK9, proprotein convertase subtilisin/kexin type 9
Reproduced with permission from Elsevier from Watts GF, Sullivan DR, Poplawski N, 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.
9th edition
31
Modified UK Simon Broome criteria

1. Deoxyribonucleic acid (DNA) mutation
2. Tendon xanthomas in patient or first-degree or second-degree relative
3. Family history myocardial infarction (MI) <50 years of age in second-degree relative or <60 years of age in
first-degree relative
4. Family history of cholesterol >7.5 in first-degree or second-degree relative
5. Cholesterol >7.5 (adult) or >6.7 (aged <16 years)
6. Low-density lipoprotein-cholesterol >4.9 (adult) or >4.0 (aged <16 years)

Definite: (5 or 6) + 1
Probable: (5 or 6) + 2
Possible familial hypercholesterolaemia: (5 or 6) + (3 or 4)

32 9th edition
3. Preventive activities in children and

young people
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
■
Early intervention
Prevention and health promotion in the early years, from conception to 5 years of age, is important for an
individual’s lifelong health and wellbeing.1 It may also be an opportunity to redress health inequalities.2,3 In
adolescence, neurodevelopmental studies support the value of early intervention to prevent ongoing harm.4
Many infants and children visit their general practitioner (GP) frequently, and adolescents visit at least once a year.5
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’.6 There is also evidence that supports the beneficial impact of similar care for
children without special healthcare needs.7,8
Health inequity
• Low socioeconomic status (SES) is associated with increased childhood morbidity and mortality.9 This includes
higher rates of death from neonatal hypoxia, sudden unexpected death in infancy (SUDI), prematurity-related
disorders, and accidental and non-accidental injury;10,11 hospitalisations related to asthma;12 and risk of child
abuse.13 Low SES is also associated with overweight and obesity in children.14
• While there has been a decline in infant mortality since the 1990s, infant mortality in Aboriginal and Torres
Strait Islander peoples is more than twice that of non-Indigenous children,10 in part due to pregnancy, labour
and delivery complications, and trauma and congenital malformations.15 Aboriginal and Torres Strait Islander
infants have higher rates of death from SUDI.16 They are also more likely to be born premature or with low birth
weight17,18 and are more likely to be hospitalised before 1 year of age.19
• Aboriginal and Torres Strait Islander peoples and people from socioeconomically disadvantaged backgrounds
are more likely to experience low immunisation rates.20
What can GPs do?

• Refer to the general strategies for supporting patient education and health literacy in disadvantaged groups.
• Consider advocating for and supporting community-based strategies or policies for health promoting changes
within the environments in which families live (eg school-based programs targeting nutrition and physical
activity).21-27
• Use resources supporting the provision of culturally competent care to adolescents from culturally diverse
backgrounds.28
9th edition
33
Table 3.1. Age-related health checks in children and young people

Age What should be done? References
Neonatal • Promote immunisation as per recommendations in the Australianimmunisation handbook
at www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/Handbook10-
home
• Vitamin K as per recommendations by the National Health and Medical Research Council
(NHMRC) at www.nhmrc.gov.au/guidelines-publications/ch39
Assessment
• Metabolic screen (IV, B) 29
• Universal hearing screen 30
• Physical exam as outlined in the Child Personal Health Record (C; refer to Practice Point 31
a in Table 3.2)
• Identify family strengths, elicit concerns and promote parental confidence, competence 32
and mental health (C)
Preventive counselling and advice
Injury prevention: Promote protection from accidental and non-accidental injury. This 31,33
includes protecting against the risks of:
• passive smoking
• sudden unexpected death in infancy (SUDI)
• use of appropriate restraints in motor vehicles
2, 4, 6, • Immunisation as per the Australian immunisation handbook at www.immunise.health.gov.

12 and 18 au/internet/immunise/publishing.nsf/Content/Handbook10-home (A)
months; and • Immunisation includes seeking informed consent and identifying Aboriginal and Torres
3 years Strait Islander babies, infants and toddlers
Assessment
• Physical exam as outlined in the Child Personal Health Record (C; refer to Practice Point a in
Table 3.2). This includes regular measurement, plotting and interpreting of length, weight and 31
head circumference on growth charts. Include body mass index (BMI) from 2 years of age
• When a baby or child is presented as a ‘problem’, assessment should include parental
mental health, family functioning, the possibility of domestic violence and adequacy of 34
social support (C; refer to Practice Point b in Table 3.2)
• From 12 months, ‘Lift the lip’ dental check (C; refer to Practice Point e in Table 3.2)
Health promotion
• Support breastfeeding (refer to Practice Point c in Table 3.2 for introduction of solids and 35, 36
reduction of food allergy)
• Promote healthy eating in the second year of life as per Australian dietary guidelines at
www.nhmrc.gov.au/guidelines-publications/n55
• Promote physical activity as per Australian recommendations for children aged 0-5 years
• Promote healthy sleep
• www.sleephealthfoundation.org.au
• http://raisingchildren.net.au
• Enquire about developmental progress including behaviours that suggest normal hearing
and vision (refer to Practice Point d in Table 3.2)
• From 6 months of age, consider the use of tools such as Parents’ evaluation of
developmental status (PEDS) and the Early intervention referral guide (refer to Appendix
3A. ‘Red flag’ early intervention referral guide)
• Promote early interactive reading with children 37, 38
• Promote secure attachment
Preventive counselling and advice 31
• Injury prevention: Promote protection from accidental and non-accidental injury
• The Royal Children’s Hospital Melbourne has advice for parents and carers of children from
birth to 5 years at www.rch.org.au/uploadedFiles/Main/Content/safetycentre/fact_sheets/
Growing%20Safely%20DL%20brochure_WEB%20secure.pdf
• Promote sun protection (refer to Section 9.4. Skin cancer)
34 9th edition

3.5-5 years • Promote immunisation as per recommendations in the Australian immunisation
handbook at www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/
Handbook10-home
• Recommendations include seeking informed consent and identifying Aboriginal and
Torres Strait Islander babies, infants and toddlers 39
• Use the Australian Early Development Census (AEDC) to determine the vulnerabilities of
children 0-5 years of age in your community
Available at www.aedc.gov.au/resources/resources-accessible/aedc-user-guide-local-
government
Assessment
• Physical exam (include checking vision and calculating BMI; refer to Practice Point g and
j in Table 3.2)
• ‘Lift the lip’ dental check (C; refer to Practice Point e in Table 3.2) 40, 41
• Promote healthy eating, drinking and physical activity (refer to Practice Point f in 36
Table 3.2)
• Promote healthy sleep as per advice from 6 months of age 42
• If behaviour is a concern, consider the quality of family functioning and the possible
contribution of factors in the child’s wider social environment (C; refer to Practice Point h
and i in Table 3.2)
• Elicit concerns regarding development, social and emotional wellbeing (refer to Practice
Point l in Table 3.2)
• Injury prevention: Promote protection from accidental and non-accidental injury
6-13 Assessment
years • Measure growth and BMI routinely (B; refer to Practice Point k in Table 3.2).
• Promote oral health 40, 41
• Promote healthy eating and drinking 36
• ‘Lift the lip’ dental check (C; refer to Practice Point e in Table 3.2). Encourage regular
dental reviews
• Promote healthy physical exercise and reduction of sedentary behaviour 43
• Enquire about progress at school as an index of wellbeing (C)
• When behaviour is a concern, explore possible contributing factors within the family and
the wider social environment
• Injury prevention - Harm minimisation (II). The Royal Children’s Hospital Melbourne has
advice for parents of children 6-12 years of age at
www.rch.org.au/uploadedFiles/Main/Content/safetycentre/ChildSafetyHandbook.pdf
• Promote social and emotional wellbeing (C)
9th edition
35

14-19 • Promote immunisation as per the Australian immunisation handbook at
www.immunise.health.gov.au (A). Note the electronic version of the handbook is regularly
years
updated in between editions of the hardcopy
Assessment
• Measure growth and BMI routinely (B; refer to Practice Point k in Table 3.2) 44, 45
• Promote healthy eating, drinking, physical activity and sleep 36, 43
• Screen sexually active young people for Sexually Transmissible Infections (STIs; refer to
Section 6.2.1. Chlamydia and other STIs)
• Assess for risky behaviours (refer to Practice Point m in Table 3.2). In one study, risky 32,46,47
behaviours occurred in 90% of young Australians attending a general practice
• Promote oral health (also refer to Chapter 11. Oral health)
• Use 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. The NSW Agency for Clinical Innovation has models of care for transition
for most paediatric centres across Australia
• www.trapeze.org.au/content/gps
• www.aci.health.nsw.gov.au/networks/transition-care
• Ask about smoking and provide a strong anti-smoking message (III, C; refer to Section
64
7.1. Smoking)
AEDC, Australian Early Development Census; BMI, body mass index; NHMRC, National Health and Medical Research Council;
PEDS, parents’ evaluation of developmental status; SUDI, sudden unexpected death in infancy
36 9th edition
Table 3.2. Explanatory notes for Practice Points

Practice
Point Comment
a Physical exam
• Complete the Child Personal Health Record, which is given at birth in New South Wales,31 or refer to
relevant programs in individual states and territories
Note: parents value reviewing completed growth charts
b 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 PND48 and improving the quality of mother-infant interaction
adversely affected by PND.49,50 GPs should be alert to the possibility of impaired parental mental health and
family dysfunction. Visit www.beyondblue.org.au/the-facts/pregnancy-and-early-parenthood
Table 10.1.2 and Section 10.3. Intimate partner violence
c The Australasian Society of Clinical Immunology and Allergy’s (ASCIA) 2016 Guidelines for allergy prevention
in infants supports the introduction of complementary ‘solid’ foods within four to six months of age and
preferably while breastfeeding.51 The introduction of allergenic food should not be delayed. However,
the ASCIA position is in conflict with the 2012 National Health and Medical Research Council (NHMRC)
guideline, which recommends exclusive breastfeeding until 6 months of age35
The new ASCIA guidelines provide:

• good *evidence that introducing peanut into the diet of infants who already have severe eczema and/or
egg allergy before 12 months of age can reduce the risk of these infants developing peanut allergy
• moderate evidence1 that introducing cooked egg into an infant’s diet before 8 months of age, where there
is a family history of allergy, can reduce the risk of developing egg allergy. Raw egg is not recommended
Also refer to Table 7.3.2
* High/good/strong evidence means convincing evidence from well-conducted studies, or many well-
conducted studies results pooled into a large analysis (meta-analysis)
1 Moderate evidence means evidence from reasonably well-conducted studies or well-conducted single
studies
d Developmental progress
Early intervention presupposes early detection. Prior to 3 years of age, 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 3 years of age
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 progress52,53
Developmental milestone assessments are outlined in the Child Personal Health Record, which is provided
at birth in New South Wales
A tool, such as the Parents’ evaluation of developmental status (PEDS), can be used on a regular basis
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/peds
The value of the PEDS may be increased if used in conjunction with:

• Learn the signs - Act early at www.cdc.gov/ncbddd/actearly/index.html
• Red flags early intervention guide at www.health.qld.gov.au/cq/child-development/docs/red-flag-a3-
poster-banana.pdf (refer to Appendix 3A. ‘Red flag’ early intervention referral guide). Information on the
Ages and Stages Questionnaire is available at http://agesandstages.com
9th edition
37
Practice
Point Comment
e ‘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 their child, looking for signs of tooth decay
(eg white lines on top of the teeth below the 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 <17 months of age and low fluoride toothpaste up
to 5 years of age
• Encourage dental visits annually after 12 months of age
Also refer to Chapter 11. Oral health
f The latest Australian recommendations for healthy eating, drinking and physical exercise are summarised in
The Royal Australian College of General Practitioners’ (RACGP) Smoking, nutrition, alcohol and physical activity
(SNAP): A population guide to the behavioural risk factors in general practice, 2nd edn, in particular, Table 1554
Nutrition for babies:
www.eatforhealth.gov.au/sites/default/files/files/the_guidelines/n55e_infant_brochure.pdf
Nutrition for children:
www.eatforhealth.gov.au/sites/default/files/files/the_guidelines/n55f_children_brochure.pdf
g The American Academy of Pediatrics has recommended the annual plotting of body mass index (BMI) for all
patients aged >2 years. Be aware that small errors in measuring either height/length or weight cause large
errors in the position of the calculated BMI on the BMI percentile chart. This is because percentile lines are
crowded together in the preschool ages
h An Australian randomised controlled trial (RCT) demonstrated that a coordinated cross-agency system of
parenting support, which included general practice, produced meaningful effects at the population level56
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 adolescence32,56
j The US Preventive Services Task Force (USPSTF) concludes with moderate certainty that vision screening
for all children at least once between 3 and 5 years of age to detect the presence of amblyopia or its risk
factors has a moderate net benefit.57 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
k The USPSTF recommends that clinicians screen children aged >6 years for obesity and offer them or refer
them to comprehensive, intensive behavioural interventions to promote improvement in weight status (B)45
• 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’45
• ‘Overweight’ is having a BMI between the 85th and 94th percentiles for the individual’s age and gender
• ‘Obesity’ is having a BMI >95th percentile for age and gender
l Mental, emotional, behavioural disorder in Australian young people

• Fifty per cent of adult disorders have onset by 14 years of age
• Between 14% and 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 years58
• The USPSTF recommends the 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-up (B)59
• Risk factors for major depressive disorder include parental depression, having comorbid mental health or
chronic medical conditions, and having experienced a major negative life event59
38 9th edition
Practice
Point Comment
m Assess for risky behaviours
Promoting health and minimising harm is a whole-of-community opportunity and responsibility. Celebrating
strengths, explaining confidentiality (including its limits) and using the HE2ADS3 framework60 (refer to below)
to explore with young people the context in which they live are strategies that are likely to improve the
clinician’s capacity to promote health and minimise morbidity (C):61,62
- Home
- Education/employment
- Eating and exercise
- Activities
- Drugs
- Sexuality
- Suicide
- Safety
• Young people who present frequently are at higher risk of having a mental health problem63
• 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 those who are sexually active)
• Be familiar with the resources in the community that provide harm reduction programs for substance
abuse, pregnancy prevention, injury prevention and road safety
• 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)
ASCIA, Australasian Society of Clinical Immunology and Allergy; BMI, body mass index; NHMRC, National Health and Medical
Research Council; PEDS, parents’ evaluation of developmental status; PND, postnatal depression; RCT, randomised controlled trial;
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childhood intervention. 2nd edn. New York: Cambridge
University Press, 2000; p. 549-88.
9th edition
41
Appendix 3A ‘Red flag’ early intervention referral guide

Changing Uves for the better
Central Queensland Hospital and Health Service
The “Red Flag”

Early Intervention Referral Guide
for children 0 - 5 years
How to use this resource When to be concerned? Who helps with these Red Flags?
This resource is a tool to help you to determine One or more Red Flags (in any area) is a sign Children aged 0 - 5 years who have a
whether a child may have developmental of delayed development. developmental concern, may benefit from the
delays. It will allow you to refer early before the services from any of the following:
child begins to struggle to achieve tasks usually • Paediatrician
Who to go to?
managed by children of the same age.
• Speech Pathologist
Parents: • Occupational Therapist
Step 1: If you have concerns about your child’s • Physiotherapist
Find the child’s age across the top of the development, please contact your • Social Worker
table below. Family Doctor or • Psychologist
Child Health Nurse Phone: (07) 4992 7000
Step 2: • Dietitian
Read through the list and identify if the child is

demonstrating any of the Red Flags ® at their
Health Professionals: Local Child Development Service
age level. If you have screened and identified any
Banana Community and Allied Health Services
Red Flags, please contact your local Child Phone (07) 4992 7000
Step 3: Development Service. Office Hours 8.00 am to 4.30 pm
If the child is between age levels (e.g. 2 yrs 5 Monday to Friday
months) check the lower age level for Red Flags
(ie. 2 yrs) www.health.qld.gov.au/cq/child-development
Developed by: Child Development Program, Children’s Health Services in conjunction with GPpartners.
Adapted by Central Queensland Hospital and Health Service 2015. Print ID P1000 05052015 v1.0
Red Flag referral guidelines

Red Flags at
6 months 9 months 12 months 18 months 2 years 3 years 4 years 5 years
any stage
pm No interest in
Rl Does not notice im When playing pretend play or
with toys tends other children
someone new
|H Not sharing to bang, drop,
■■ Does not smile Rl Lacks interest
enjoyment with or throw them pm Difficulties in pm Unwilling / pm Play is different
or squeal in pH Does not play in playing and
others using eye rather than use noticing and unable to play than their
response to early turn taking interacting with
contact or facial them for their understanding cooperatively friends pm Not achieving
people games (e.g. others
Social / expression purpose (e.g feelings in indicated
peekaboo,
cuddle doll, themselves developmental
Emotional rolling a ball)
build blocks) and others (e.g. milestones
happy, sad)
Lack of or limited eye contact pm Strong parent

pm Does not have at concerns
pm No gestures least 50 words pm Difficulty telling
P® No babbled pm No clear words
(e.g. pointing, pm Speech difficult pm Speech difficult a parent what is
phrases that pm Significant loss
showing, pm Not putting to understand to understand wrong
•1 Not starting sound like pm Cannot of skills
waving) words together
to babble (e.g talking understand
eg. ‘push car’ M Not using simple pM Unable to follow pm Cannot answer
adah; oogoo) short requests
pm Not using 2 part sentences e.g. directions with 2 questions
pm No response to eg. ‘Where is the pm Lack of response
babble (e.g. pm Most of what is big car go steps in a simple
Communication familiar words ball?’ to sound or
gaga, arma) said is not easily conversation
understood visual stimuli
|m Majority of pm Concerns from

pm Difficulty
nutrition still teacher about
helping with pm Poor interaction
liquid/puree school readiness with adults or
pm Unable to hold pm Not holding or self care skills
M Not reaching other children
and/or release scribbling with a (e.g. feeding, pm Not toilet trained
for and holding ■m Cannot chew pm No interest in pm Not independent
toys ~ solid food crayon dressing) by day
(grasping) toys self care skills with eating and
eg. feeding, dressing
pH Cannot move toy pm Does not pm Difficulty pm Unable to draw pm Difference
M Hands frequently pm Unable to pick dressing
from one hand attempt to tower manipulating lines and circles between right
Fine Motor clenched up small items pm Cannot draw
to another blocks small objects and left sides of
using index simple pictures body in strength,
and Cognition e.g. threading
finger and (e.g. stick movement or
beads
thumb person) tone
pm Awkward
|m Not sitting pm Not running well when walking,
pm Cannot pedal a
without support pm Not crawling or running, pm Loose and floppy
tricycle
bottom shuffling pm Unable to run pm Cannot walk up climbing and movements (low
M Not rolling pm Not attempting
pm Not moving and down stairs using stairs tone) or stiff
to walk without pm Cannot catch,
eg. creeping or pm Not pulling to pm Unable to use and tense (high
M Not holding support throw or kick a
crawling motion stand stairs holding on pm Cannot kick or pm Ball skills are tone)
head and ball
throw a ball very different to
shoulders up pm Not standing
pm Does not take pm Not standing pm Unable to throw their peers
when on tummy alone pm Cannot balance
weight well on holding on to a ball pm Cannot jump
well standing on
legs when held furniture with 2 feet Unable to hop
Gross Motor one leg
by an adult together 5 times on each
foot
Parents - If there are Red Flags call your Family Doctor or Child Health Nurse
Professionals - REFER EARLY - DO NOT WAIT
Queensland
Government
Reproduced with permission from Queensland Health from Central Queensland Hospital and Health Service. The Red Flag: Early intervention
referral guide for children 0-5 years. Brisbane: Central Queensland Hospital and Health Service, 2016. Available at www.health.qld.gov.au/cq/
child-development/docs/red-flag-a3-poster-banana.pdf [Accessed 15 July 2016].
42 9th 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 in Table 4.1.
Patients should be offered these opportunistically, or at two-year to five-year intervals.
Planned health checks in general practice of middle-aged adults have been demonstrated to improve the
frequency of the management of smoking, nutrition, alcohol and physical activity (SNAP) behavioural risk factors;
screening for cervical and colorectal cancer (CRC); and hyperlipidaemia.1-3
There is also evidence that Aboriginal and Torres Strait Islander health checks improve early detection of diabetes
and provision of preventive care.4 However, there is mixed evidence for the effectiveness of interventions to address
multiple risk factors.5 These checks may be facilitated by the involvement of practice nurses.6-8 Interventions should
be tailored to the level of risk, and the use of the 5As framework (Ask, Assess, Advise and agree, Assist, Arrange
follow-up) is recommended as a guide to their delivery in primary healthcare.9
Health inequity
• Midlife, between 45 and 64 years of age, is particularly a time of determining patient risk factors and offering
screening for health conditions. Multimorbidity, particularly physical-mental health comorbidity, is an important
issue in middle aged populations. Social disadvantage can hasten the onset of multimorbidity by about 10-15
years, suggesting screening should start earlier in high-risk populations, including Aboriginal and Torres Strait
Islander peoples (eg at 30 years of age). This may be a critical time for preventive interventions to reduce later
life chronic illness.10
• The impact of income-related inequalities on the prevalence of common mental health disorders and
psychological distress is particularly seen in middle aged people.11
What can GPs do?

groups.
• Be aware that disadvantaged groups may be less likely to access health checks,12 so proactive efforts to go
outside the practice (eg to workplaces) may be needed or preventive care may be built in opportunistically to
routine consultations.
• Actively manage vulnerable patients by recalling patients by phone or text messages for preventive care.
9th edition
43
Table 4.1. Age-related health checks for low-risk patients in middle age
Age What should be done Chapters
45-49 years Ask about:
• Smoking, nutrition, alcohol and physical activity (SNAP), and readiness to change Chapter 7
• possible depression but do not routinely screen unless staff-assisted depression care Chapter 10
supports are in place
• early signs of skin cancer Section 9.4
• preconception care Chapter 1
• completing a family history screening questionnaire Chapter 2
Measure:
• weight, height (to calculate body mass index [BMI]) and waist circumference Section 7.2
• blood pressure (BP) Section 8.2
• fasting lipids Section 8.3
Perform:
• Papanicolaou (Pap) test every two years (until April 2017)
Section 9.5
• Human papillomavirus (HPV) test every five years (from May 2017)
Section 9.3
• mammogram for women dependent on her individual degree of risk
• 23-valent pneumococcal polysaccharide vaccine (23vPPV) and influenza vaccination Chapter 6
for all Aboriginal and Torres Strait Islander peoples
• Influenza and diphtheria, tetanus, and acellular pertussis (dTpa adolescent/adult Chapter 6
version) vaccination for pregnant women
• genetic testing as part of preconception planning Chapter 2
Calculate:
• risk of diabetes using the Australian type 2 diabetes risk assessment tool (AUSDRISK) Section 8.4
• review fracture risk factors for osteoporosis for women aged >45 years of age Chapter 14
• absolute cardiovascular risk Section 8.1
50-64 years Ask about:

• SNAP and readiness to change Chapter 7
• possible depression but do not routinely screen unless staff-assisted depression care Chapter 10
supports are in place
• early signs of skin cancer Section 9.4
• completing a family history screening questionnaire Chapter 2
Measure:
• weight, height (to calculate BMI) and waist circumference Section 7.2
• BP Section 8.2
• fasting lipids Section 8.3
Perform:
• Colorectal cancer (CRC) screening with faecal occult blood testing (FOBT) at least
Section 9.2
every two years
• Pap test every two years (until April 2017) Section 9.5
• HPV test every five years (from May 2017)
• mammography for women dependent on individual degree of risk Section 9.3
• 23vPPV and influenza vaccination for all Aboriginal and Torres Strait Islander peoples Chapter 6
• vaccination for diphtheria, tetanus (DT); dTpa should be used in place of DT when Chapter 6
providing booster tetanus immunisations
Calculate:
• risk of diabetes using AUSDRISK Section 8.4
• review fracture risk factors for osteoporosis for women aged >45 years and men aged Chapter 14
>50 years
• absolute cardiovascular risk Section 8.1
23vPPV 23-valent pneumococcal polysaccharide vaccine; AUSDRISK, Australian type 2 diabetes risk assessment tool; BMI, body
mass index; BP, blood pressure; DT, diphtheria, tetanus; dTpa, diphtheria, tetanus, and acellular pertussis(adolescent/adult version);
HPV human papillomavirus; Pap, Papanicolaou; SNAP smoking, nutrition, alcohol and physical activity
44 9th edition
Table 4.2. Preventive interventions in middle age

Intervention Technique
Health education Tailor health advice or education to the patient’s risk, stage of change and health literacy
(Chapter II. Patient education and health literacy)
Practice organisation Use clinical audit to identify patients who have not had preventive activity. Recall to
practice or opportunistically arrange a 45-49 years health assessment
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9th edition
45
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, with difficulties accessing healthcare, with poor mobility and with limited financial support are particularly
vulnerable.1 Their health problems may be exacerbated by poor nutrition, poor oral health,2 lack of physical activity,3
taking multiple medications4,5 and lack of sun exposure,6 all of which can be addressed in preventive activities.
Older people may rely on the help and support of carers and family. 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.7-11 Their need for support should be assessed when possible (C) and
appropriate referral instituted.12 Carer support resources are helpful for carer wellbeing and may delay the need for
the older person who is receiving care to be relocated to a residential facility.7,13-15
People should be advised to plan as much as possible for their care as they get older to prevent family disruption
in episodes of illness as well as unpleasant and undesired acute care interventions. This includes organising
wills, financial enduring power of attorney, and the equivalent documentation for health and care (called enduring
guardianship in some jurisdictions), and an advance care plan.16 The Royal Australian College of General
Practitioners’ (RACGP) position statement on the incorporation of advance care planning into routine general
practice is available at www.racgp.org.au/download/documents/Policies/Clinical/advancedcareplanning_
positionstatement.pdf
Medication-related problems may cause unnecessary hospital admissions, adverse drug reactions and other
adverse outcomes for older people living in the community.17 General practitioners (GPs) should review medications
in older people, particularly for vulnerable groups. Vulnerability factors include:
• recent discharge from hospital or other facility
• significant changes made to medication treatment regimen in the past three months
• high-risk drug groups (eg those with a narrow therapeutic index and those that cause xerostomia)
• confusion/cognitive impairment or dementia
• other causes of difficulty managing medications including literacy, language issues, dexterity problems, sight
impairment
• inability to manage therapeutic devices
• history of falls
• currently taking five or more regular medications
• taking >12 doses of medication per day
• patients attending multiple doctors including GPs and specialists
• disease states where medication management is an important process of care (chronic kidney disease,
congestive cardiac failure)18
• multiple chronic medical problems
• regular use of alcohol
• previous adverse drug reaction
• anticholinergic load.
GPs may consider a medication review, in particular focusing on reducing medications and anticholinergic load.
The most successful interventions were delivered by small numbers of pharmacists working in close liaison with
primary care doctors (III, C).19 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 and sedative loads of the medications may also be done, as anticholinergic
and sedative loads increase the rate of confusion and other adverse side effects.20-23 This process is often referred
to as ‘deprescribing’.24
46 9th edition
5.1 Immunisation
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
I I I I I I I I I I
Influenza immunisation is recommended for adults aged >65 years, according to the Australian immunisation
handbook (which is regularly updated and available at www.immunise.health.gov.au/internet/immunise/publishing.
nsf/Content/Handbook10-home). However, the benefits are modest, with a number needed to treat of 71 people in
the general population for influenza vaccination to prevent a single episode of influenza in older age.25
Table 5.1. Immunisation: Preventive interventions in older age

Vaccination: Influenza Annual influenza vaccination in the pre-flu season months (III, C) 26
Vaccination: Pneumococcal 23-valent pneumococcal polysaccharide vaccine (23vPPV) is 27

recommended for the 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
Refer to www.health.gov.au/internet/immunise/publishing.nsf/content/
older-australians
Vaccination: Herpes zoster A single dose of zoster vaccine is recommended for adults aged >60 28
years (II, B)
Also refer to Section 6.1. Immunisation
23vPPV 23-valent pneumococcal polysaccharide vaccine
5.2 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 people (A).29 In addition, vigorous physical
activity offers additional benefits for those without specific contraindications such as unstable, advanced or terminal
illness. For the older person, physical activity provides many benefits, as well as minimising some of the limitations
of later life.30
Benefits include:
• maintaining or improving physical function and independent living
• improving social interactions, quality of life, sleep and reducing depression
• building and maintaining healthy bones, muscles and joints, reducing the risk of injuries from falls
• reducing the risk of heart disease, stroke, high blood pressure, type 2 diabetes, some cancers and vascular
disease and Alzheimer’s dementia
• improving management of lung disease, heart disease, arthritis, osteoporosis, kidney disease, stroke, cancer,
and other chronic conditions.
9th edition
47
The following are Australia’s physical activity and sedentary behaviour guidelines for older people31
(www.health.gov.au/internet/main/publishing.nsf/Content/health-pubhlth-strateg-phys-act-guidelines#chba ):
Older people:
• should do some form of physical activity, no matter what their age, weight, health problems or abilities
• should be active every day in as many ways as possible, doing a range of physical activities that incorporate
fitness, strength, balance and flexibility
• should accumulate at least 30 minutes of moderate intensity physical activity on most, preferably all, days
• who have stopped physical activity, or who are starting a new physical activity, should start at a level that is
easily manageable and gradually build up to the recommended amount, type and frequency of activity
• who continue to enjoy a lifetime of vigorous physical activity should carry on doing so in a manner suited to their
capability into later life, provided recommended safety procedures and guidelines are adhered to.
Refer to falls risk reduction in Table 5.3.2 for more information on specific exercises.
5.3 Falls
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
Approximately 30% of people aged >65 years report one or more falls in the past 12 months.32 Most falls are
caused by an interaction of multiple risk factors. Having one fall puts you at risk of another fall, and the more risk
factors, the greater the chance of falling. You can help your patients manage their risk and prevent further falls by
regularly asking them about falls.
Table 5.3.1. Falls: Identifying risks

Who is at risk of falls? What should be done? How often? References
Average risk:
• All people aged >65 years Screen for falls (I, A) Every 12 months 29, 33
Moderately high risk:

• Older people presenting with one or more falls, Case find for risk factors Every six months 32, 33
who report recurrent falls or with multiple risk and involve in preventive
factors (refer to Table 5.3.2) activities (I, A)
48 9th edition
Table 5.3.2. Falls: Preventive interventions |

Screening for Ask the following three screening questions: 32, 34-36
falls risk 1. Have you had two or more falls in the past 12 months?
Case finding 2. Are you presenting following a fall?
questions 3. Are you having difficulty with walking or balance?
about risk
If the answers to any of these are positive, complete a multifactorial risk
factors to be
assessment including obtaining relevant medical history, completing a physical
used in those
examination, and performing cognitive and functional assessments
at moderately
• History should include: 29, 32, 33, 37
high risk
- detailed history of falls (eg how many falls?, at home or outdoors?,
patient perception of causes, any fear of falling)
- multiple medications, and specific medications (eg psychotropic
medications)
- impaired gait, balance and mobility
- foot pain and deformities, and unsafe footwear
- home hazards
- bifocal or multifocal spectacle use
- incontinence
- recent discharge from hospital
- chronic illness such as stroke, multiple sclerosis (MS), Parkinson’s
disease, cognitive impairment/dementia
- vitamin D deficiency/poor sun exposure if housebound or in a care
facility
• Physical examination should include:
- impaired visual acuity, including cataracts
- reduced visual fields
- muscle weakness
- neurological impairment
- cardiac dysrhythmias
- postural hypotension
*
- six-metre walk, balance, sit-to-stand
• Cognitive and functional impairments should include:
- dementia/cognitive impairment assessment (eg General Practitioner
Assessment of Cognition [GPCOG])
- activities of daily living and home assessment as appropriate (eg by
occupational therapist)
- falls risk-assessment tools
- if unsteady, gait and mobility assessment by physiotherapist 29
There are many fall risk-assessment tools. However, reports from researchers
are variable, so no single tool can be recommended for implementation in all 38, 39
settings or for all subpopulations within each setting
Also refer to Chapter 13. Urinary incontinence

9th edition
49

Falls risk Prescribe or refer for a home-based exercise program and/or encourage 40-47
reduction participation in a community-based exercise program, particularly targeting
29, 33
balance and which may include strength and endurance (I)
For specific exercises to reduce the risk of falls, refer to www.racgp.org.au/

your-practice/guidelines/handi/interventions/musculoskeletal/exercises-for-
falls-prevention
Patients who report unsteadiness or are at higher risk of falls should be

referred to a health professional for individual exercise prescription. Referral
should specify fall prevention
Exercise programs targeting non-English-speaking patients may need to 41

address cultural norms about appropriate levels of physical activity
Exercise guidelines for fall prevention recommend the following:

48, 49
• Exercise that specifically challenges balance is the most effective physical
activity intervention to prevent falls
• Exercise needs to be done for at least two hours per week and continue as
a lifetime activity
• Fall prevention exercises can be home-based or a group program.
• Walking or strength training as a single intervention does not appear to
prevent falls
Regularly review medication. Encourage patients to keep a medication review 33
card. Reduce dose to address side effects and dose sensitivity, and stop
medications that are no longer needed
Medications that can promote falls include psychotropic medications, and

medications with anticholinergic activity, sedation effects and hypotensive
effects or orthostatic hypotensive side effects
Also refer to Chapter 14. Osteoporosis
A home assessment should be considered for those at moderately high to

29, 33
high risk of falls. Occupational therapy interventions can reduce fall hazards,
raise awareness of fall risk and implement safety strategies. Referral should
specify fall prevention
Other risk factors should be managed actively including:

29, 33
• using a multidisciplinary team (eg podiatrist regarding foot problems,
optometrist regarding avoidance of multifocal lenses, physiotherapist or
nurse regarding urge incontinence)
• referring to relevant medical specialists (eg ophthalmologist for cataract
surgery, cardiologist for consideration of pacemaker)
• investigating the causes of dizziness
*Two simple tests are the repeated chair standing test and 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, includes these tests as well
as simple assessments of medication use, vision, sensation and balance. This is available at www.neura.edu.au/wp-
content/uploads/2016/05/QuickScreen-Information-Order-Form_1.pdf
GPCOG, General Practitioner Assessment of Cognition; MS, multiple sclerosis
50 9th edition
5.4 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 65 years of age 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.50,51
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 (B).
In some states and territories, there are legal requirements for annual assessment (eg driving aged >70 years).52
Eye disease and visual impairment increase three-fold with each decade of life after 40 years of age. They are often
accompanied by isolation, depression and poorer social relationships, and are strongly associated with falls and hip
fractures.53 It should be determined whether the patient is wearing up-to-date prescription spectacles, and whether
there is a possibility of falls because the patient is 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; such history should be sought. Smoking (current or previous) increases the risk of age-related
macular degeneration.54 Cataracts are the most common eye disease in Australians aged >65 years (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%).55,56
Table 5.4.1. Visual and hearing impairment: Identifying risks

What should be
Who is at higher risk of hearing loss? done? How often? References
People >65 years of age Screen for hearing Every 12 months 57
impairment (II, B)
Table 5.4.2. Visual and hearing impairment: Preventive interventions

Visual impairment: Case finding Use a Snellen chart to screen for visual impairment in the elderly 50
if requested, or indicated by symptoms or history. There is no
evidence that screening asymptomatic older people results in
improvements in vision
Also refer to Chapter 12. Glaucoma
Hearing impairment screening A whispered voice out of the field of vision (at 0.5 m) or finger 58
rub at 5 cm has a high sensitivity for hearing loss, as does a
single question about hearing difficulty
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51
5.5 Dementia
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
With people aged >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, current work situation, driving, and advance care planning.59
Table 5.5.1. Dementia: Identifying risks

Average risk:
• Those without symptoms No evidence of benefit from N/A 60, 61
screening (II, C)
Moderate risk: Case finding and early N/A 62-64

• Those with symptoms (refer to Table 5.5.2) intervention (III, C)
• Risk increases with increasing age
• A family history of Alzheimer’s disease
• People with history of repeated head trauma 65
• People with Down syndrome
• Those with elevated cardiovascular risk (eg heart
66-69
disease, stroke, hypertension, obesity, diabetes,
elevated homocysteine, elevated cholesterol,
smoking, sedentary lifestyle)
• Those with depression or a history of depression 64
• People with low levels of education
• Aboriginal and Torres Strait Islander peoples Note that culturally safe 70-74
practices should be adopted
with this community
52 9th edition
Table 5.5.2. Dementia: Preventive interventions

Case • Ask ‘How is your memory?’ and obtain information about dementia and other 75-77
finding and cognitive problems from others who know the person (eg repeating questions,
confirmation forgetting conversations, double buying, unpaid bills, social withdrawal)
• 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 or dressing. Falls may
also be an indication of cognitive impairment
• Over several consultations, obtain the history from the person and family/carer, and
perform a comprehensive physical examination. Undertake cognitive assessment
using:
- Standardised Mini-Mental State Examination (SMMSE) available at www.ihpa.
gov.au/publications/standardised-mini-mental-state-examination-smmse
- General Practitioner Assessment of Cognition at www.gpcog.com.au 75
- clock drawing test 78
- Rowland Universal Dementia Assessment Scale at www.fightdementia.org.au/ 79
understanding-dementia/rowland-universal-dementia-assessment-scale.aspx
which is a multicultural cognitive assessment scale that has been used to detect
dementia across cultures
- The Kimberley Indigenous Cognitive Assessment tool (KICA) dementia
assessment instrument (available at www.healthinfonet.ecu.edu.au/key-
resources/programs-projects?pid=509), may be used as a component of
dementia assessment for Aboriginal and Torres Strait Islander peoples living in
remote areas; and the modified KICA, may be used as a component of dementia
assessment in more urban Aboriginal and Torres Strait Islander peoples
- The Mini-Mental State Examination (MMSE), is the most widely used and
evaluated scale. However, as it is now copyrighted, it should be replaced by
the SMMSE
A suite of recommended rating tools is available at www.dementia-assessment.com.au
• Assess functional status. The Instrumental activities of daily living at
www.abramsoncenter.org/media/1456/instrumental-activities-of-daily-living. 80, 81
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. Reassessment after 6-12 months may be helpful
Assessment should include relevant blood tests and imaging to a exclude space
occupying lesion or other brain disorder
Relevant tests are recommended in the Clinical practice guidelines for dementia in
Australia available at http://sydney.edu.au/medicine/cdpc/documents/resources/
LAVER_Dementia_Guidleines_recommendations_PRVW5.pdf
9th edition
53

Early Evidence is growing that attention to cardiovascular disease (CVD) risk factors may 68, 69, 82-87
intervention improve cognitive function and/or reduce dementia risk. There is sufficient evidence
and now for clinicians to recommend the following strategies for early intervention and
prevention prevention of dementia: 88
• increased physical activity (eg 150 minutes per week of moderate-intensity walking
or equivalent)
• social engagement (increased number of social activities per week) 89, 90
• cognitive training and rehabilitation 91,92
• diet - the Mediterranean and the Dietary Approaches to Stop Hypertension (DASH)
67
diets have been shown to be protective against cognitive decline
• smoking cessation 66, 68
• management of vascular risk factors (refer to Chapter 8. Prevention of vascular and
metabolic disease)
• use of the risk assessment tool developed by the Collaborative Research Centre,
which is based on dementia prevention, and takes about 15 minutes to fill out and
provides a good overview for all the possible risks for dementia, for discussion with
the GP available at http://anuadri.anu.edu.au
Refer to Chapter 7. Prevention of chronic disease, Chapter 8. Prevention of vascular
and metabolic disease, and Chapter 10. Psychosocial
CVD, cardiovascular disease; DASH, Dietary Aproaches to Stop Hypertension; KICA, Kimberley Indigenous Cognitive Assessment;
MMSE, Mini-Mental State Examination; SMMSE, Standardised Mini-Mental State Examination
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on exercise and falls prevention in older people. J Sci J Neurol Neurosurg Psychiatry 2003;74(7):857-62.
Med Sport 2011; 14(6):489-95. 66. Anstey KJ, Eramudugolla R, Hosking DE, Lautenschlager
50. Smeeth L, Iliffe S. Community screening for visual NT, Dixon RA. Bridging the translation gap: From
impairment in the elderly. Cochrane Database Syst Rev dementia risk assessment to advice on risk reduction. J
2006;3:CD001054. Prev Alzheimers Dis 2015;2(3):189-98.
51. US Preventive Services Task Force. Impaired visual acuity 67. Anstey KJ, von Sanden C, Salim A, O’Kearney R.
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acuity-in-older-adults-screening#consider [Accessed 23 68. Alzheimer’s Disease International. World Alzheimer
May 2016]. report 2014. Dementia and risk reduction. An analysis
52. Austroads. Assessing fitness to drive for commercial of protective and modifiable risk factors. London:
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(as amended up to 30 June 2014). Available at www. 69. Beydoun MA, Beydoun HA, Gamaldo AA, Teel A,
onlinepublications.austroads.com.au/items/AP-G56-13 Zonderman AB, Wang Y. Epidemiologic studies of
[Accessed 15 December 2015]. modifiable factors associated with cognition and
53. Taylor H, Keeffe J. Updates in medicine: Ophthalmology. dementia: Systematic review and meta-analysis. BMC
Med J Aust 2002;176(1):29. Public Health 2014;14:643.
54. Smith W, Mitchell P, Leeder SR. Smoking and age-related 70. Flicker L, Holdsworth K. Aboriginal and Torres Strait
maculopathy. The Blue Mountains Eye Study. Arch Islander people and dementia: A review of the research.
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55. Australian Institute of Health and Welfare. Australia’s Alzheimer’s Australia, 2014.
health 2006. Canberra: AIHW, 2006. 71. Broe T, Wall S. The Koori dementia care project (KDCP):
56. Tapp RJ, Shaw JE, Harper CA, et al. The prevalence of Final report. Sydney: Dementia Collaborative Research
and factors associated with diabetic retinopathy in the Centres, 2013. Available at: www.dementiaresearch.org.
Australian population. Diabetes Care 2003;26(6):1731-37. au/images/dcrc/output-files/1288-cb55_final_report_
57. US Preventive Services Task Force. Screening for hearing with_amendments.pdf
loss in older adults. Rockville MD: USPSTF, 2011. 72. Smith K, Flicker L, Lautenschlager NT, et al. High
Available at www.uspreventiveservicestaskforce.org/ prevalence of dementia and cognitive impairment in
uspstf/uspshear.htm#top [Accessed 15 December 2015]. Indigenous Australians. Neurology 2008;71(19):1470-73.
58. Moyer VA. Screening for hearing loss in older adults: 73. Australian Health Ministers’ Advisory Council. Standing
US Preventive Services Task Force recommendation Committee on Aboriginal and Torres Strait Islander Health
statement. Ann Intern Med 2012;157(9):655-61. Working Party. AHMAC cultural respect framework for
59. The Royal Australian College of General Practitioners, Aboriginal and Torres Strait Islander health, 2004-2009.
NSW Health. Care of patients with dementia in general Canberra: AHMAC, 2004.
practice: Guidelines. Sydney: Department of Health, 74. Smith K, Flicker L, Shadforth G, et al. ‘Gotta be sit down
2003. and worked out together’: Views of Aboriginal caregivers
60. Boustani M, Peterson B, Hanson L, et al. Screening for and service providers on ways to improve dementia
dementia in primary care: A summary of the evidence for care for Aboriginal Australians. Rural Remote Health.
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2003;138(1):927-37. subviewnew.asp?ArticleID=1650 [Accessed 26 January
61. National Collaborating Centre for Mental Health. 2016].
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with dementia and their carers in health and social L. The GPCOG: A new screening test for dementia
care. London: National Institute for Health and Care designed for general practice. J Am Geriatr Soc
Excellence, 2007. 2002;50(3):530-34.
62. Gao S, Hendrie HC, Hall KS, Hui S. The relationship 76. DeLepeleire J, Heyrman J, Baro F, Buntinx F. A
between age, sex and the incidence of dementia and combination of tests for the diagnosis of dementia
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had significant diagnostic value. J Clin Epidemiol

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77. Dementia Collaborative Research Centre - Assessment
and Better Care 2011. 14 Essentials for good dementia
care in general practice. Sydney: University of New South
Wales, 2011.
78. 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.
79. 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.
80. Laver K, Cumming RG, Dyer SM, et al. Clinical practice
guidelines for dementia in Australia. Med J Aust
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81. Guideline Adaptation Committee. Clinical practice
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82. Farooki A. Central obesity and increased risk of
dementia more than three decades later. Neurology
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83. Helzner EP, Luchsinger JA, Scarmeas N, et al.
Contribution of vascular risk factors to the progression in
Alzheimer disease. Arch Neurol 2009;66(3):343-48.
84. Peila R, White LR, Petrovich H, 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(12):2882-89.
85. 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(1):70-74.
86. 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.
87. 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(3 Suppl 2):S79-83.
88. Mortimer JA, Ding D, Borenstein AR, et al. Changes
in brain volume and cognition in a randomized trial of
exercise and social interaction in a community-based
sample of non-demented Chinese elders. J Alzheimers
Dis 2012;30(4):757-66.
89. Sitzer DI, Twamley EW, Jeste DV. Cognitive training in
Alzheimer’s disease: A meta-analysis of the literature.
Acta Psychiatr Scand 2006;114(2):75-90.
90. Lampit A, Hallock H, Moss R, et al. Dose-response
relationship between computerized cognitive training
and global cognition in older adults. J Nutrit Health Aging
2013;17(9):803-04.
91. Lourida I, Soni M, Thompson-Coon J, et al.
Mediterranean diet, cognitive function, and dementia: A
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92. Tangney CC, Li H, Wang Y, et al. Relation of DASH- and
Mediterranean-like dietary patterns to cognitive decline in
older persons. Neurology 2014;83(16):1410-6.
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6. Communicable diseases
General practitioners (GPs) have an important role in the prevention and management of communicable diseases.
This includes advice on prevention, immunisation, early detection and management.
The use of immunisation information systems1 such as the Australian Childhood Immunisation Register (ACIR) and
Vaccination Information and Vaccination Administration System (VIVAS) in Queensland helps raise immunisation
rates. The available information in these databases helps to create recall-and-reminder systems and individual
immunisation records within GP electronic medical records. An adult immunisation register is planned from
September 2016.2
Updates on communicable diseases and notification requirements are available from the Department of Health at
www.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-nndss-casedefs-distype.htm
Notification of particular infectious diseases to state public health units is mandatory (the law overrides all privacy
regulations). This is almost completely automated by pathology laboratories, but for clinically diagnosed infections
such as varicella and herpes zoster, the GP is required to notify the relevant authority.
6.1 Immunisation
Age Birth <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 from birth for all children, and at particular ages throughout life, according to the
Australian immunisation handbook (this is updated regularly at www.health.gov.au/intemet/immunise/publishing.
nsf/Content/Handbook10-home).
Consent
Consent should be sought from someone with legal capacity before each vaccination. The individual providing
consent should have the intellectual capacity to understand specific information and agree voluntarily without
pressure, coercion or manipulation. The consent process should include written advice about benefits and harms
of the vaccines, risk of not having the vaccine, and what to do after receiving the vaccine. Information on providing
valid consent is available at www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/Handbook10-
home~handbook10part2~handbook10-2-1#2-1-3
The National Immunisation Program Schedule (NIPS) lists the recommended funded vaccines for all Australian
residents. There may be other vaccines that are not funded but are recommended in the Australian immunisation
handbook, depending on occupation or travel. There may be variability in vaccines recommended/funded (eg
hepatitis A vaccine).
Vaccination for special high-risk groups

Adults or children who develop asplenia, human immunodeficiency virus (HIV) infection or a haematological
malignancy, or who have received a bone marrow or other transplant, may not be fit for some vaccinations, or may
require additional or repeat vaccinations.
58 9th edition
Health inequity
GPs need to be aware of groups with lower levels of age-appropriate immunisation.3 Socioeconomic
characteristics associated with lower immunisation rates at 12 months4 include:
• being Aboriginal or Torres Strait Islander
• being born overseas
• no private health insurance
• being in the highest or lowest socioeconomic quintile
• being of low birth weight and singleton birth.
All of these factors were also associated with lower immunisation coverage at 24 months, with the exception of low
birth weight, which was only significant in the very low birth weight category.
What can GPs do?

Evidence supports a number of strategies in improving immunisation rates that could reduce inequities if efforts
were focused on at-risk groups:
• audit of immunisation coverage of at-risk groups in the practice
• use of recall-and-reminder systems and catch-up plans, with a focus on at-risk groups
• integrating vaccination status checks into routine health assessments for those target population groups.
Table 6.1.1. Summary of the main requirements from the National Immunisation Program
Schedule
Age Vaccine
Birth
* Hepatitis B (hep B)
6-8 weeks Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), haemophilus
influenzae type b, inactivated poliomyelitis (polio; hepB-DTPa-Hib-IPV)
Pneumococcal conjugate (13vPCV)
Rotavirus (dose 1 of Rotarix or RotaTeq)'
4 months Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), haemophilus

Rotavirus (dose 2 Rotarix or RotaTeq)'
6 months Hepatitis B, diphtheria, tetanus, acellular pertussis (whooping cough), haemophilus

Rotavirus (dose 3 for RotaTeq recipients only)'
>6 months Influenza annually (for those at risk of serious complications of influenza - eg Aboriginal
and Torres Strait Islander peoples)
12 months Haemophilus influenzae type b and meningococcal C (Hib-MenC)
Measles, mumps and rubella (MMR)
Pneumococcal conjugate (13vPCV) booster (only for medically at-risk groups)

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Age Vaccine
12-18 months Hepatitis A (for Aboriginal and Torres Strait Islander peoples in the Northern Territory,
Queensland, South Australia and Western Australia only)
Pneumococcal conjugate (13vPCV; for Aboriginal and Torres Strait Islander peoples in
the Northern Territory, Queensland, South Australia and Western Australia only)
18 months Measles, mumps, rubella and varicella (chickenpox; MMRV)
Diphtheria, tetanus, acellular pertussis (whooping cough; DTPa)
18-24 months Hepatitis A (for Aboriginal and Torres Strait Islander peoples in the Northern Territory,
Queensland, South Australia and Western Australia only)
4 years* Diphtheria, tetanus, acellular pertussis (whooping cough) and inactivated poliomyelitis
(polio; DTPa-IPV)
Measles, mumps and rubella (MMR; if MMRV vaccine was not given at 18 months of
age)
Pneumococcal polysaccharide (23vPPV; only for medically high-risk groups)
10-15 years Hepatitis B (two adult doses for those not vaccinated against hepatitis B)
School-based programs +/- Varicella (catch up until all immunised)

GP catch-up
Human papillomavirus (HPV; three doses over six months)
Diphtheria, tetanus and acellular pertussis (dTpa is the adult/adolescent vaccine)
15-49 years Influenza annually (for Aboriginal and Torres Strait Islander peoples)
Pneumococcal polysaccharide (23vPPV; for Aboriginal and Torres Strait Islander people
who are medically at risk)
Pregnant women Influenza
Diphtheria, tetanus and acellular pertussis (dTpa) from 28 weeks (up to 38 weeks
acceptable). Note that this is recommended for all but funding is variable
50 years and over Influenza (for Aboriginal and Torres Strait Islander peoples)
Pneumococcal polysaccharide (23vPPV; for Aboriginal and Torres Strait Islander

peoples)
65 years and over Influenza
Pneumococcal polysaccharide (23vPPV)
*Hep B vaccine (dose 1 or 0) should ideally be given to all infants within 24 hours of birth, but at most within seven days of birth.
Infants born to hepatitis B surface antigen (HBsAg)-positive mothers should be given hepatitis B immune globulin (HBIG) and a
dose of monovalent hepatitis B vaccine on the day of birth (preferably within 12 hours of birth and certainly within 48 hours). Further
information at www.health.gov.au/internet/immunise/publishing.nsf/Content/Handbook10-home
Rotavirus vaccines are contraindicated in infants with a history of intussusception (IS), or predisposing abnormality to IS, or severe
t
combined immunodeficiency. Rotavirus vaccines are time limited and differ in number of doses and timing: catch-up may not be possible
MMR dose 2 remains at 4 years of age for children not immunised with MMRV at 18 months
*
60 9th edition
Table 6.1.2. Vaccines recommended but not funded in National Immunisation Program
Age Vaccine
Soon after birth Bacillus Calmette-Guerin (BCG; Aboriginal and Torres Strait Islander peoples in higher risk areas
of the Northern Territory, Queensland, and parts of northern South Australia). Infants born to
migrants from country with high risk of tuberculosis (TB) - look up individual state and territory
guidelines
<2 years and Meningococcal B vaccine recommended for highest incidence age groups from 6 weeks of age
between 15 and 19
years of age
Any age from 12 Varicella - A second dose of vaccine, at least one month after first dose, provides improved
months protection from varicella
Parents and carers Diphtheria, tetanus and acellular pertussis (dTpa) is recommended to protect the infant from
of infants aged <6 pertussis. To maximise the protection of infants, parents and carers should get immunised before
months the birth. The dTpa vaccine can be given at any time after vaccination with diphtheria, tetanus
(DT), and may be given again five years after previous dTpa
50 years and >65 dTpa should be used in place of DT when providing booster tetanus immunisations >50 years of
years age. This booster dose is recommended if no tetanus immunisation was received in the previous
10 years, or no previous dTpa
Travellers of any age
>60 years A single dose of zoster vaccine is recommended for prevention of shingles
All healthcare dTpa

workers
Hepatitis B (and hepatitis A in some jurisdictions)
Annual influenza
Measles, mumps and rubella (MMR; if not immune)
Varicella (if not immune)
Men who have sex Hepatitis A and B

with men
People who inject

drugs
Immunisation information resources include:

• NIPS, available at
www.immunise.health.gov.au/internet/immunise/publishing.nsf/Content/national-immunisation-program-schedule
• Australian immunisation handbook, available at www.immunise.health.gov.au/internet/immunise/publishing.nsf/
Content/Handbook10-home
• Australian Childhood Immunisation Register (ACIR), available at www.humanservices.gov.au/customer/services/
medicare/australian-childhood-immunisation-register, by email (acir@humanservices.gov.au) or telephone (1800
653 809). The ACIR can be used to obtain information on the vaccination history of individuals from birth to 7
years of age given since 1 January 1996
• National Centre for Immunisation Research & Surveillance, available at www.ncirs.edu.au
Notification of adverse events

The reporting of adverse events following vaccinations varies geographically. It is possible to report directly to the
Therapeutic Goods Administration (TGA) from anywhere in Australia by telephone on 1800 044 114, or online at
www.tga.gov.au/hp/problem-medicine-reporting-reactions.htm
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6.2 Sexually transmissible infections

Sexually transmissible infections (STIs) are frequently seen in general practice, especially chlamydia, which is
typically asymptomatic.5,6 It is important to detect it early in order to prevent transmission to others and minimise
potential complications, such as infertility. It may also be appropriate to screen for other STIs. The individual’s age,
sexual behaviour and community HIV or STI prevalence all influence the level of risk, and should influence the
choice of STI screening tests. For additional resources specific to Aboriginal and Torres Strait Islander peoples, The
Royal Australian College of General Practitioners’ (RACGP) National guide to a preventive health assessment for
Aboriginal and Torres Strait Islander people, 2nd edn, includes information about sexual health and blood-borne
viruses (www.racgp.org.au/your-practice/guidelines/national-guide).
Sexual health consultation

Many patients and doctors feel uncomfortable discussing sexual histories even when indicated or the patient is
requesting STI testing. Taking a sexual history is an important part of the assessment and management of STIs,
and it should not be a barrier to offering STI testing.7
A non-judgmental attitude and environment will facilitate disclosures on sexual matters.8 It is important to ask open-
ended questions and to avoid assumptions about sexual orientation, by using the term ‘partner’. Gentle enquiry
about recent sexual activity, gender, number of partners, contraception (including use of condoms), travel history,
and immunisation status helps to inform decision making. Additionally, ask about the risk for blood-borne viruses
(hepatitis B, C, and HIV), such as injecting drug use, tattooing and piercing. Investigations should be explained, and
patients should be asked for consent before tests such as HIV or hepatitis C are ordered.
Contact tracing
Contact tracing is essential in reducing the transmission of STIs and HIV. It is the responsibility of the diagnosing
clinician to facilitate the process of notifying current and past partners. This may be through a direct approach from
the patient, their treating health professional, or by using online partner notification services available such as:
• www.letthemknow.org.au
• www.thedramadownunder.info/notify (for men who have sex with men [MSM])
• www.bettertoknow.org.au (for Aboriginal and Torres Strait Islander youths).
For more information and to determine ‘how far back to trace’, refer to the contact tracing manual at the
Australasian Society of HIV, Viral Hepatitis and Sexual Health Medicine’s (ASHM) website at http://contacttracing.
ashm.org.au or the Contact Tracing Tool for General Practitioners at NSW STI Programs Unit's website at http://
stipu.nsw.gov.au/wp-content/uploads/GP-Contact-Tracing-Tool.pdf
For HIV contact tracing, seek assistance from local sexual health services.
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 set by the department of health in the relevant state or territory.
62 9th 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
More than 80% of chlamydia infections occur in people <29 years of age.9 Screening for chlamydia infection in
all sexually active people up to 29 years of age is recommended because of increased prevalence and risk of
complications.10 In asymptomatic, sexually active people up to 29 years of age, the overall absolute risk of infection
is approximately 5% for chlamydia and 0.5% for gonorrhoea.
The ranked risk for specific infections per 100,000 in general population/Aboriginal and Torres Strait Islander
populations:11
• Chlamydia (371/1341)
• Gonorrhoea (49/858)
• Hepatitis B (23/50)
• Syphilis (8/32)
• HIV (4/6)
A large proportion of young people will attend primary care clinics each year, and this presents the opportunity
to normalise sexual health care as part of usual general practice.10 Younger sexually active youths should not be
excluded from case finding, or identifying any safety or abuse issues. This may involve a complete psychosocial
(HE2ADS3)12 risk assessment as discussed in Table 3.2.
Women with untreated chlamydia infections have a 2-8% risk of infertility.13 Other STIs to consider screening for
in higher risk individuals are gonorrhoea, HIV and syphilis.14 The risk for gonorrhoea, HIV and syphilis is low for
heterosexuals in all major cities in Australia and New Zealand,15 but rates of gonorrhoea and syphilis are higher
among MSM. The individual’s age and sexual habits, and community STI prevalence all influence the level of risk
and should guide STI testing recommendations for patients (refer to Tables 6.2.1.1 and 6.2.1.2 for guidance).
MSM should be screened for gonorrhoea, chlamydia, syphilis and HIV every 12 months. Screening should be
performed more often if they have multiple sexual contacts. Most MSM with STIs have no symptoms.16
Aboriginal and Torres Strait Islander peoples are at higher risk and should also be screened for gonorrhoea,
chlamydia, syphilis and HIV.
Screening for hepatitis C should be provided if the patient is HIV positive or there is a history of injecting drug use,
as this increases the risk of transmission.16
All pregnant women should be screened for hepatitis B, C, HIV and syphilis.14,17,18 Consider screening pregnant
women up to 29 years of age for chlamydia (and also gonorrhoea, if the patient is at high risk).17-20
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Table 6.2.1.1. Sexually transmissible infections: Identifying risks

Risk assessment of asymptomatic
sexually active person What should be done? How often? References
Low-average risk: Urine, cervical or genital swab Opportunistically if 5
• Heterosexual asymptomatic up to 29 years polymerase chain reaction indicated (evidence
of age requesting sexually transmissible (PCR; or self-collected) for is unclear on testing
infection (STI) check up chlamydia interval)
Consider other infections

based on risk assessment
Medium-high risk: As above Opportunistically if 6, 10, 11,

• <20 years of age indicated (evidence 21-26
Consider other infections,
• Rural and remote is unclear on testing
particularly gonorrhoea
interval)
and syphilis, based on risk
assessment
Higher risk: Testing for chlamydia, Every 12 months 27

• Aboriginal or Torres Strait Islander peoples gonorrhoea, syphilis (evidence is unclear
on testing interval)
Serology for human
immunodeficiency virus (HIV),
syphilis and, if the person is
not vaccinated or immune,
hepatitis A and B (III)
Offer hepatitis A and B

vaccination (III, B)
Other higher risk: Testing for chlamydia, Every 12 months

• People who inject drugs gonorrhoea, syphilis; Serology (evidence is unclear
• Sex workers for HIV, syphilis; if the person on testing interval)
is not vaccinated or immune,
hepatitis A and B

vaccination (III, B)
Hepatitis C testing if the

patient injects drugs
Highest risk: Urine, throat and rectal swab Every 12 months 5, 16, 28
• Asymptomatic men who have sex with men for chlamydia PCR and three to six
• Highest risk in those who: monthly in higher
Throat and rectal swab for
risk men
- have unprotected anal sex gonorrhoea PCR (III, B)
- had >10 partners in past six months Serology for HIV, syphilis and,
- participate in group sex or use if the person is not vaccinated
recreational drugs during sex or immune, hepatitis A and B

vaccinations (III, B)
Sexual contacts from the last six months of Test and treat contacts If chlamydia 29-32
women and men with an STI presumptively (II, A) infection found (and
treated), repeating
For how far back to trace, refer to Consider other infections
testing to check for
Contact Tracing Tool for General Practice based on risk assessment
re-infection after
such as gonorrhoea, hepatitis
3-12 months may
B (if not vaccinated), syphilis
be appropriate
and HIV (III, B)
HIV human immunodeficiency virus; PCR, polymerase chain reaction; STI, sexually transmissible infection
64 9th edition
Table 6.2.I.2. Tests to detect sexually transmissible infections

Test Technique References
Nucleic acid The first 20 mL of urine passed at any time of day, and at least 20 minutes 33
amplification test since last voiding
most commonly by
PCR testing can be performed on urine, throat, endocervix rectum, or 5, 15, 30, 34
polymerase chain
vagina (whichever are indicated)
reaction (PCR)
Gonorrhoea If the suspected clinical diagnosis is gonorrhoea, an MCS is required to 11

microscopy, culture guide antibiotic treatment
and sensitivity (MCS)
MCS, microscopy culture and sensitivity; PCR, polymerase chain reaction
Implementation
Chlamydia is the most common and curable STI in Australia. Notification rates per 100,000 increased from 35.4 in
1993 to 363 in 2011, and has been steady since; 78% of those infected are aged 15-29 years.11 Young Aboriginal
and Torres Strait Islander peoples have higher infection rates especially in regional and remote areas, with a
substantially increased risk of chlamydia, gonorrhoea and syphilis.10
Screening sexually active women <25 years of age for chlamydia on an annual basis has been shown to halve the
infection and complication rates.11,13,35
Treatment of partners and contact tracing

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.36 There is no single optimal strategy for contact tracing. Getting assistance from
the local sexual health services is recommended for HIV and syphilis because it leads to more contacts being tested
and treated.35 Referral to sexual health services should be considered for problematic or repeated infections.37
It is important to ensure current sexual partners are treated simultaneously. Untreated pregnant women infected
with chlamydia have a 20-50% chance of infecting their infant at delivery.38
References
1. Community Preventive Services Task Force (USA). 6. Kong FY, Guy RJ, Hocking JS, et al. Australian general
Recommendation for use of immunization information practitioner chlamydia testing rates among young people.
systems to increase vaccination rates. J Public Health Med J Aust 2011;194(5):249-52.
Manag Pract 2015;21(3):249-52. 7. Pavlin NL, Parker R, Fairley CK, Gunn JM, Hocking
2. Department of Health. Update: Expansion of Australia’s J. Take the sex out of STI screening! Views of young
immunisation registers. Canberra: DoH, 2015. Available women on implementing chlamydia screening in general
at www.immunise.health.gov.au/internet/immunise/ practice. BMC Infect Dis 2008;8:62.
publishing.nsf/Content/news-20152310 [Accessed 13 8. Preswell N, Barton D. Taking a sexual history. Aust Fam
May 2016]. Physician 2000;29(5):533-39.
3. Ward K, Chow MYK, King C, Leask J. Strategies to 9. Department of Health. Third national sexually transmissible
improve vaccination uptake in Australia, a systematic infections strategy 2014-2017. Canberra: DoH, 2014.
review of types and effectiveness. Aust N Z J Public Available at www.health.gov.au/internet/main/publishing.
Health 2012;36(4):369-77. nsf/Content/ohp-bbvs-sti [Accessed 23 May 2016].
4. Haynes K, Stone C. Predictors of incomplete 10. Guy RJ, Ali H, Liu B, Hocking J, Donovan B, Kaldor J.
immunisation in Victorian children. Aust N Z J Public Genital chlamydia infection in young people: A review of
Health 2004;28(1):72-79. the evidence. Sydney: The Kirby Institute, 2011.
5. Australasian Society for HIV, Viral Hepatitis and Sexual 11. The Kirby Institute. HIV, viral hepatitis and sexually
Health Medicine. HIV, viral hepatitis and STIs: A guide for transmissible infections in Australia: Annual surveillance
primary care. Sydney: ASHM, 2014. report 2015. Sydney: The Kirby Institute, 2015.
9th edition
65
12. Goldenring J, Rosen D. Getting into adolescent trachomatis infection in young women: Results
heads: An essential update. Contemp Pediatrics of a multicenter cohort study. Sex Transm Dis
2004;21(64):64-90. 2001;28(2):117-23.
13. Hocking J, Fairley C. Need for screening for genital 30. Orr DP, Johnston K, Brizendine E, Katz B. Subsequent
chlamydia trachomatis infection in Australia. Aust N Z J sexually transmitted infection in urban adolescents
Public Health 2003;27(1):80-81. and young adults. Arch Pediatr Adolesc Med
14. Meyers D, Wolff T, Gregory K, Marion L. USPSTF 2001;155(8):947-53.
recommendations for STI screening. Am Fam Physician 31. Guy R, Wand H, Franklin N, et al. Re-testing for
2008;77(6):819-24. chlamydia at sexual health services in Australia, 2004-08.
15. Cook RL, Hutchison SL, Ostergaard L. Systematic Sex Health 2011;8(2):242-47.
review: Noninvasive testing for Chlamydia trachomatis 32. Centers for Disease Control and Prevention. Sexually
and Neisseria gonorrhoeae. Ann Intern Med transmitted diseases treatment guidelines. MMWR
2005;142(11):914-25. 2006;55:38-40.
16. Templeton DJ, Read P, Varma R, Bourne C. Australian 33. Kwan B, Ryder N, Knight V, et al. Sensitivity of
sexually transmissible infection and HIV testing guidelines 20-minute voiding intervals in men testing for Chlamydia
for asymptomatic men who have sex with men 2014: A trachomatis. Sex Transm Dis 2012;39(5):405-06.
review of the evidence. Sex Health 2014;11(3):217-29. 34. Watson E, Templeton A, Russell I, Paavonen J. The
17. Australian Health Ministers’ Advisory Council. Clinical accuracy and efficacy of screening tests for Chlamydia
practice guidelines: Antenatal care - Module II. Canberra: trachomatis: A systematic review. J Med Microbiol
AHMAC, 2014. 2002;51(12):1021-31.
18. The Royal Australian and New Zealand College of 35. Ferreira A, Young T, Mathews C, Zunza M, Low N.
Obstetricians and Gynaecologists. Routine antenatal Strategies for partner notification for sexually transmitted
assessment in the absence of pregnancy complications. infections, including HIV. Cochrane Database Syst Rev
East Melbourne, Vic: RANZCOG, 2016. Available at 2013;10:CD002843.
www.ranzcog.edu.au/college-statements-guidelines. 36. Trelle S, Shang A, Nartey L, Cassel J, Low N. Improved
html#obstetrics [Accessed 28 April 2016]. effectiveness of partner notification for patients with
19. Cheney K, Wray L. Chlamydia and associated factors sexually transmitted infections: Systematic review. BMJ
in an under 20s antenatal population. Aust NZ J Obstet 2007;334(7589):354.
Gynaecol 2008;48(1):40-43. 37. Burnet Insitute. Partner notification of sexually transmitted
20. Chen MY, Fairley CK, De Guingand D, et al. Screening infections in New South Wales: An informed literature
pregnant women for chlamydia: What are the predictors review. Melbourne: Centre for Population Health, 2010.
of infection? Sex Transm Infect 2009;85(1):31-35. Available at http://stipu.nsw.gov.au/wp-content/uploads/
21. Scholes D, Stergachis A, Heidrich FE, Andrilla H. NSW_STI_PN_PDF.pdf [Accessed 28 January 2016].
Prevention of pelvic inflammatory disease by screening 38. Honey E, Augood C, Templeton A, et al. Cost
for cervical chlamydial infection. N Eng J Med effectiveness of screening for Chlamydia trachomatis:
1996;334(21):1362-66. A review of published studies. Sex Transm Infect
22. Queensland Health. Indigenous sexual health service 2002;78(6):406-12.
report for Brisbane Southside. Brisbane: Communicable
Disease Unit, 2004.
23. 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.
24. Heal C, Jones B, Veitch C, Lamb S, Hodgens S.
Screening for chlamydia in general practice. Aust Fam
Physician 2002;31(8):779-82.
25. Hayman N. Chlamydia PCR screening in an Indigenous
health general practice clinic in Brisbane 2002-3.
Brisbane, 2004.
26. 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):65-68.
27. The Kirby Institute. Bloodborne viral and sexually
transmitted infections in Aboriginal and Torres Strait
Islander people: Surveillance and evaluation report.
Sydney: The Kirby Institute, 2014.
28. Whiley DM, Garland SM, Harnett G, et al. Exploring
‘best practice’ for nucleic acid detection of Neisseria
gonorrhoeae. Sex Health 2008;5(1):17-23.
29. Whittington WL, Kent C, Kissinger P, Oh MK.
Determinants of persistent and recurrent chlamydia
66 9th edition
7. Prevention of chronic disease

The lifestyle risk factors of smoking, nutrition, alcohol and physical activity (SNAP) are common among patients
attending general practice.1 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 General practitioners (GPs) and their teams can make an important
contribution to managing each of the SNAP lifestyle behaviours, including smoking,3,4 dietary change,5 hazardous
drinking,6 physical activity7,8 and weight.9,10
Each of these risk factors may interact with the others throughout the lifecycle and need to be considered together
rather than separately.11 The 5As is an internationally accepted framework for organising the assessment and
management of behavioural risk factors in primary healthcare.12-14 It consists of the following:
• Ask - A systematic approach to asking all patients about their SNAP, 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.
• Assist/agree - Work with the patient to set agreed goals for behaviour change; provide motivational
interviewing; refer to telephone support services, group lifestyle programs or individual providers (eg dietitian or
exercise physiologist); consider pharmacotherapy.
• Arrange - Regular follow-up visits to monitor maintenance and prevent relapse.
Progress along the pathway from assessment and advice to goal setting, referral and follow-up is associated with
increased patient motivation and behaviour change.15 A number of evidence-based preventive care guidelines are
based on the 5As framework.9
Health inequity
• The greatest burden of chronic illness is experienced by socioeconomically disadvantaged groups, including
Aboriginal and Torres Strait Islander peoples, who access preventive healthcare less frequently than other
groups.16-18 Aboriginal and Torres Strait Islander peoples have a significantly lower life expectancy at birth than
non-Indigenous Australians. This is attributable, to a significant extent, to inequities in prevalence and care for
chronic diseases.19,20 This gap appears to be widening and is the widest seen globally between Indigenous and
non-Indigenous populations.21 Multimorbidity is more common in disadvantaged groups and is associated with
higher levels of psychosocial stress.22,23
• The uptake of preventive and screening services in primary healthcare is significantly related to higher levels of
education, health motivation, and self-rated health, as well as to particular cultural groups. Immigrant groups
undergo fewer preventive consultations and screening tests, and have overall less primary care utilisation.24
Aboriginal and Torres Strait Islander peoples and socioeconomically deprived people have higher risks of
disease, but are less likely to be offered preventive interventions.25
• Socioeconomic disadvantage is associated with higher rates of smoking and alcohol use, poorer diets and
lower levels of physical activity. The higher rates are a product of social, environmental and individual factors.
• Smoking rates show significant inequities across groups. Most disadvantaged groups continue to have higher
smoking rates. Smoking status varies by education level, employment status, socioeconomic status (SES),
geographic location and Indigenous status.26,27 Nationally, the prevalence of smoking among Aboriginal and
Torres Strait Islander peoples (45%) is more than double that of non-Indigenous Australians, and is up to 82% in
remote communities.28,29 Smoking is also more prevalent in people with long-term mental illness.30
9th edition
67
• Overweight and obesity rates are higher in socioeconomically disadvantaged groups and the gap is
widening.31-33 Aboriginal and Torres Strait Islander peoples have higher rates of being overweight and obese
as well as a higher incidence of vascular disease.34 Aboriginal and Torres Strait Islander communities in remote
regions face significant access barriers to nutritious and affordable food.35,36 Nutritious food tends to cost more
in rural and remote areas, and cost may also be an issue in low SES groups.37,38 Low-income groups are less
likely to be offered interventions to prevent being overweight.39
• Alcohol may produce a greater burden of harm in more socially disadvantaged groups partly through the more
hazardous pattern of drinking and partly through reduced access to resources to mitigate harm.40-43 Recognition
and treatment are also impeded by the social stigma associated with problematic use of alcohol.44-46
What can GPs do?

• Interventions targeting Aboriginal and Torres Strait Islander peoples could include individual and group
interventions delivered in primary healthcare and community settings to promote improved health literacy and
awareness of behavioural risk factors.47 Financial assistance to enable healthier food choices may be effective.48
The Centre for Excellence in Indigenous Tobacco Control (CEITC) provides resources and strategies at
www.ceitc.org.au 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.34,49
• Provide motivational interviewing for at-risk patients with low SES.50-52 Individual behavioural counselling is
more likely to be effective for patients from disadvantaged backgrounds if linked to community resources, and
if financial and access barriers are addressed.53,54 Interventions to improve physical activity among socially
disadvantaged patients would ideally be linked to community programs that improve the physical environment,
are culturally acceptable and address cost barriers.55-57 Supportive provider attitudes are also important in
building self-efficacy among patients from these groups.58
• Be aware that behavioural risk factors are not simply a matter of ‘individual lifestyle choices’. For example,
racism and stress may be drivers of smoking for Aboriginal and Torres Strait Islander peoples and dietary
choices may be shaped significantly by availability, cost and distribution of healthy food.
• Quality improvement activities, especially clinical audit and practice plans, can help improve the assessment and
recording of behavioural risk factors.59
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 and documented in the medical record for every patient
>10 years of age.3,13,60 All patients who smoke, regardless of the amount they smoke, should be offered smoking
cessation advice. This should include the following actions:
• Ask about their interest in quitting (B).
• Advise to stop smoking (A), agreeing on quit goals and offer pharmacotherapy to all patients smoking more than
10 cigarettes per day unless contraindicated, especially if there is evidence of nicotine dependence (A).
• Offer referral to a proactive telephone call-back cessation service (eg Quitline 13 7848; A).
• Follow up to support maintenance and prevent relapse using self-help or pharmacotherapy (A).
To assess nicotine dependence, ask about the:60

• number of minutes between waking and smoking the first cigarette
• 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)
• type of craving or withdrawal symptoms experienced in previous quit attempts.
68 9th edition
Table 7.1.1. Smoking: Identifying risks

Average risk: Ask about quantity and frequency of smoking Opportunistically
* (III, C) 60
• Everyone >10 (I, A). Offer smoking cessation advice, set quit
years of age goals, offer pharmacotherapy, referral and
follow-up as appropriate (II, A)
High risk of Offer smoking cessation advice. Agree on quit Opportunistically, ideally
complications: goals, offer pharmacotherapy and culturally at every visit
* (III, C)
appropriate referral and support
• Aboriginal and
(II, A)
Torres Strait 61
Islander peoples
• People with (I, A)
smoking-related
disease
Patients requiring different interventions to those at average risk

• People with mental Make careful use of pharmacotherapy, because Opportunistically, ideally 62
illness of the significant impact of nicotine and nicotine *
every visit (III, C)
• People with other withdrawal on drug metabolism (I, A)+
drug-related Add mood management to behavioural support in
dependencies those with current or past depression
• Pregnant women Offer smoking cessation advice, agree on quit At each antenatal visit
goals, offer referral to a quit program (I, A). Also (III, C)
refer to Chapter 1. Preventive activities prior to
pregnancy
• Parents of young Offer smoking cessation advice. If the parent is Opportunistically, ideally
babies and unable to quit, advise to: *
every visit (III, C)
children • smoke away from children
• not smoke in confined spaces with children
(eg when driving) (I, A)
• Adolescents and Ask about smoking and provide a strong Opportunistically (III, C) 63
young people antismoking message (III, C)
*Refer to Appendix 9. Effect of smoking abstinence on medications in the New Zealand smoking cessation guidelines 2007 at
www.treatobacco.net/de/uploads/documents/Treatment%20Guidelines/New%20Zealand%20treatment%20guidelines%20in%20
English%202007.pdf
While enquiry about smoking should occur at every opportunity, be aware of patient sensitivity. Non-judgmental enquiry about
smoking is associated with greater patient satisfaction64-66
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.67 Where this is insufficient,
other effective treatment strategies include referral to the Quitline,68 pharmacotherapy69,70 and motivational
interviewing.71,72 Tobacco use is most effectively treated with a comprehensive approach involving behavioural
support and pharmacotherapy. Combined pharmacotherapy and behavioural support increases the success of
smoking cessation.73
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. Higher smoking rates in
disadvantaged individuals reflect greater neighbourhood disadvantage, less social support, greater negative effect
9th edition
69
and lower self-efficacy.21,28 Removing access barriers and providing incentives to motivate patients to quit may
improve quit rates.
Patients should be reviewed within one week and again after one month of stopping smoking in order to help
increase the long-term chance of quitting.
There is a lack of consistent, bias-free evidence that acupuncture, acupressure or laser therapy have sustained
benefit on smoking cessation for longer than six months.74 There is insufficient evidence that electronic cigarettes
(e-cigarettes) help smokers to stop smoking when compared with nicotine patches or placebo.75
The CEITC provides resources and strategies at www.ceitc.org.au
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
Body mass index (BMI) and waist circumference should be measured every two years and recorded in the
medical record (A). On its own, BMI may be misleading, especially in older people and muscular individuals, and
classifications may need to be adjusted for some ethnic groups.9 Waist circumference is a stronger predictor of
CVD and diabetes than weight alone.76,77
Patients who are overweight or obese should be offered individual lifestyle education and skills training (A).9
Restrictive dieting is not recommended for children and most adolescents who have not completed their growth
spurt.9 A modest loss of 5-10% of starting body weight in adults who are overweight is sufficient to achieve some
health benefits.9,78
70 9th edition
Table 7.2.1. Obesity-related complications: Identifying risks

Average risk:
Adults Assess body mass index (BMI) and waist Every two years (IV, D) 78
circumference in all adults >18 years of age (I, A)
Offer education on nutrition and physical activity (I, A)
Adolescents Assess weight and height using age-specific BMI Every two years 9
charts (either Centers for Disease Control and
Prevention [CDC] or World Health Organization
[WHO]; Practice Point)
Involve parents, carers and families in lifestyle change

(Practice Point)
Children Aged >2 years: Assess weight and height using age At times of child 9
specific BMI charts (either CDC or WHO; health surveillance or
Practice Point) immunisation
Aged <2 years: Monitor growth using WHO growth

charts (Practice Point)
Involve parents, carers and families in lifestyle change
Increased risk: Assess BMI and waist circumference in all adults Every 12 months 49
• Aboriginal and aged >18 years (I, B) (IV D)
Torres Strait Offer individual or group-based education on nutrition
Islander peoples and physical activity (II, A)
and people from
the Pacific Islands
• Patients with
existing diabetes
or cardiovascular
disease, stroke,
gout or liver
disease
Identified risk: Assess weight and waist circumference (I, B) Every six months+ 9, 79
• Adults who are (III, C)
Develop weight management plan
* (II, B)
overweight or
obese Offer behaviour-oriented interventions to assist with
weight loss (I, B)
Consider referral for:

• self-management support
• coaching in an individual or group-based diet
• physical activity program
• allied health provider (eg dietitian, exercise
physiologist, psychologist)
• Children and Recommend lifestyle change including reducing 80

adolescents who energy intake and sedentary behaviour, and
are overweight or increased physical activity and measures to support
obese behaviour change (II, B)
*Refer to the National Health and Medical Research Council’s (NHMRC) Clinical practice guidelines for the management of overweight
and obesity in adults, adolescents and children in Australia .9 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 two weeks

t
BMI, body mass index; CDC, Centers for Disease Control and Prevention; NHMRC, National Health and Medical Research Council;
WHO, World Health Organization
9th edition
71
Table 7.2.2. Overweight and obesity: Assessment and preventive interventions

Assessment Technique References
Body mass BMI = body weight in kilograms divided by the square of height in metres. BMI of >25 kg/m2
index (BMI) conveys increased risk
Waist An adult’s waist circumference is measured halfway between the inferior margin of 9
circumference 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 Ask patients what concerns they have about their weight and if they tried to lose weight 9, 81
reduction in in the past
adults (5As
Assess BMI, waist circumference, diet, physical activity, motivation to change and
approach)
health literacy
Advise that weight loss can have health benefits, including reduced blood pressure and
prevention of diabetes in high-risk patients. Advise the risks of being overweight and a
lifestyle program that includes reduced caloric intake (aiming for 600 kcal or 2500 kJ energy
deficit) and increased physical activity (increasing to 60 minutes at moderate intensity five
days per week), supported by behavioural counselling
Assist/Agree: Discuss goals, including a realistic initial target of 5% weight loss and
specific measurable changes to diet and physical activity. Make contact (eg visit, phone)
two weeks after commencing weight loss to determine adherence and if goals are
being met. If no response (<1 kg weight or <1 cm waist reduction) after three months,
consider alternative approaches, including referral to lifestyle programs or coaching.
These programs may be face to face or delivered by phone
Arrange: After achieving initial weight loss, advise that patients may regain weight
without a maintenance program that includes support, monitoring and relapse
prevention
Consider very low energy diets if there is no response to lifestyle programs. Bariatric
surgery may be considered in patients who fail lifestyle interventions and who have
a BMI >35 kg/m2 with comorbidities, such as poorly controlled diabetes, who are
expected to improve with weight reduction

72 9th edition
Table 7.2.3. Nutrition: Healthy weight: Body mass index (kg/m2)82

Classification Body mass index (BMI; kg/m2) Risk of morbidities
Underweight <18.5 Increased
Normal weight 18.5-24.9 Low
Overweight 25.0-29.9 Increased
Obese I 30.0-34.9 Moderate
Obese II 35-39.9 Severe
Obese III >40.0 Very severe
Implementation
Consider and offer adult patients a range of treatment options. Individual education and simple behavioural
interventions are appropriate for some patients, while behavioural approaches may be more appropriate for those
with disordered eating patterns. Behaviour change techniques include goal setting, self-monitoring of behaviour
and progress, stimulus control (eg recognising and avoiding triggers that prompt unplanned eating), cognitive
restructuring (modifying unhelpful thoughts or thinking patterns) or problem-solving, and relapse prevention and
management.9
Telephone coaching has been demonstrated to be comparable with face-to-face techniques and is available in
most states.83,84
For adolescents and children, lifestyle programs should focus on parents, carers and families. Advise that weight
maintenance is an acceptable approach in most situations for children who are overweight or obese. Recommend
lifestyle changes, including reducing energy intake and sedentary behaviour, and increasing physical activity based
on current Australian dietary and physical activity guidelines.9
For more information, refer to The Royal Australian College of General Practitioners’ (RACGP) Smoking, Nutrition,
Alcohol and Physical activity (SNAP): A population health guide to behavioural risk82 and National Health and
Medical Reserach Council’s (NHMRC) Clinical practice guidelines for the management of overweight and obesity in
adults, adolescents and children in Australia.9
9th edition
73
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 they eat in a day and advise to follow the NHMRC’s Australian
dietary guidelines (B).85 Brief advice should be given to eat two serves of fruit and five serves of vegetables per day
(2 + 5 portions), and to limit sugar, saturated fat, salt and alcohol.
Breastfeeding should be promoted as the most appropriate method for feeding infants (and one that offers
protection against infection and some chronic diseases).85 Refer to Chapter 3. Preventive activities in children and
young people for nutrition-related recommendations.
Table 7.3.1. Nutrition-related complications: Identifying risk

Average risk:
Adults Ask about the number of portions of fruits and Every two years 9, 86
vegetables eaten per day, and the amount of (IV D)
sugar (including sweetened drinks), salt and
alcohol, and saturated fat intake (II, B)
All patients should be advised to follow the

Australian dietary guidelines (www.nhmrc.gov.
au/guidelines-publications/n55), and eat at
least five serves of vegetables and two serves
of fruit per day (II, B)
Children and adolescents Assess growth using the World Health At times of 85
Organization (WHO) weight-for-age and child health
height-for-age charts up to 2 years of age, surveillance or
and body mass index (BMI) for age charts immunisation
from 2 to 16 years of age until 5 years of
age then every
Advise patients to follow Australian dietary
two years
guidelines, including eating high quantities of
vegetables, fruit, wholegrain cereals, poultry,
fish, eggs and low fat milk, yoghurt and
cheese products, and less discretionary food
choices including sugary soft drinks
High risk: Provide lifestyle advice to limit intake of foods Every six months 85, 87
• Overweight or obese containing saturated fat, added salt, added (Practice Point)
• High cardiovascular disease sugars (including sugary drinks) and alcohol,
(CVD) absolute risk (>15%) and increase serves of fruit and vegetables.
(Refer to Section 7.2. Overweight for dietary
• A past or first-degree family
recommendations for overweight and obesity;
history of CVD (including stroke)
II, B)
before 60 years of age. For
personal history the age does Provide self-help nutrition education materials
not matter and refer to a dietitian, group diet program or
• Type 2 diabetes or high risk for phone coaching (II, B)
diabetes
BMI, body mass index; WHO, World Health Organization

74 9th edition
Table 7.3.2. Nutrition-related complications: Preventive interventions

Vitamin supplements Vitamin supplementation is not of established value in asymptomatic 85
individuals
* (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, including: 85

recommendations • five serves of vegetables (of different types and colours, and legumes/
beans) and two serves of fruit
• grain or cereals (mostly wholegrain and/or high fibre varieties such as
breads, rice, pasta, noodles, polenta, couscous, oats, quinoa and barley)
• lean meats, fish, poultry, eggs, tofu, nuts and seeds
and
• drink plenty of water.
Take care to:
• limit saturated fat and reduce salt
• limit alcohol intake
• avoid sugary beverages including soft drink and limit fruit juices
• limit sugars and foods containing added sugars
88
• limit red meat (three to four times per week) and limit or avoid
processed meat
• care for food: prepare and store it safely
• encourage and support breastfeeding
For specific advice, especially patients with specific conditions, refer to a
dietitian
The National Heart Foundation of Australia has a number of nutrition position

statements at http://heartfoundation.org.au/for-professionals/food-and-
nutrition/position-statements
In children, overweight or obesity is associated with sweet drink consumption,

and dental problems are associated with consumption of fatty foods and 89
sweet drinks
Encourage Encourage and support exclusive breastfeeding until 4 to 6 months of age 85

breastfeeding (there is current controversy about when to introduce foods; refer to Practice
Point c in Table 3.2). It is recommended that breastfeeding continue until 12
months of age and thereafter as long as is mutually desired
*Prevalence of nutritional deficiency is high in certain groups, such as people with alcohol dependence and the elderly living alone
or in institutions.
For further information, refer to the RACGP’s SNAP guide, 2nd edn,82 and NHMRC’s Australian dietary guidelines.85
9th edition
75
7.4 Early detection of at-risk 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 15 years of age (A).6 Those
with at-risk patterns of alcohol consumption should be offered brief advice on the risk in drinking (A).90 Motivational
interviewing is both a useful and effective counselling strategy to facilitate a decrease of alcohol intake to low-risk
drinking (I, B).91-94
Table 7.4.1. Alcohol-related complications: Identifying risk

*
Low risk: Ask about the quantity and frequency of Every two to four years 6, 95
• All patients aged >15 years alcohol intake (II, B) (III, C)
The alcohol use disorder identification
test-consumption (AUDIT-C) tool can be
used to assess this (II, B)
Advise if drinking alcohol to drink two

drinks or less per day or less and no
more than four drinks on any one
occasion (II, B)
Increased risk: Advise children aged <15 years not to Opportunistically (III, C) 6, 96, 97
• Children and adolescents drink (III, B)
Advise young people aged 15-17 years

to delay drinking as long as possible
(III, B)
• Older people4 Inform that there is an increased risk of Opportunistically (III, C) 98, 99
potential harm from drinking (III, B)
• Young adults, who have 100, 101

a higher risk of accidents
and injuries
• People with a family history 102, 103

of alcohol dependence
• Individuals who are Advise that non-drinking is the safest Opportunistically (III, C) 104-106
participating in or option: driving (I, A), other areas (III, C)
supervising risky activities
(eg driving, boating,
extreme sports, diving,
using illicit drugs)
• Women who are pregnant Advise that non-drinking is the safest At each antenatal visit (III, C) 107, 108
or planning a pregnancy option
(refer to Chapter 1.
Preventive activities prior
to pregnancy)
76 9th edition

• People with a physical Advise that non-drinking is the safest Opportunistically (III, C)
condition made worse by option (II-IV, B)
alcohol:
Advise those with hypertension, or taking
- pancreatitis antihypertensive medication, to limit 6
- diabetes alcohol intake to no more than two (for 109
- hepatitis/chronic liver men) or one (for women) standard drinks 110, 111
disease per day (II, B)
- hypertension 6, 112
- sleep disorders 6, 113
- sexual dysfunction 114, 115
- other major organ
disease
• People with a mental Assess whether there are possible Opportunistically (III, C) 116-118
health problem made harmful interactions between their
worse by alcohol (eg medications and alcohol (II, A)
anxiety and depression)
• People taking multiple Opportunistically (III, C) 119, 120

medications
*There is some variability between the levels of low-risk drinking in the drinking guidelines for each country. The Australian
guidelines, to be updated in 2016, represent the modal (or most common) recommendation. Refer to www.iard.org/wp-content/
uploads/2016/02/Drinking-Guidelines-General-Population.pdf
Older people who have a higher risk of falls and are more likely to be taking medication.121
+
AUDIT-C, alcohol use disorder identification test-consumption
Table 7.4.2. What advice, and to whom, should be provided?

What advice should be given to adults who drink alcohol? References
• Advise to limit their drinking to two drinks or less per day, and no more than four drinks on any one 6
occasion (II, B)
• Counsel everybody who consumes alcohol about the dangers of operating a motor vehicle or
performing other potentially dangerous activities after drinking (II, B)
• Provide simple advice to reduce alcohol consumption to all patients drinking at potentially risky or
high-risk levels (I, A)
• Advise pregnant women not to drink alcohol (ie there are no safe drinking levels)
9th edition
77
Table 7.4.3. Strategies to increase effectiveness

Screening • Early detection of at-risk drinking may be improved by asking patients about their 122, 123
drinking more frequently. New patient registration, health assessment, chronic
disease or mental health assessments and care planning are acceptable times for
enquiry
Brief • Screening and brief advice in general practice has been demonstrated to have 90, 124-126
intervention resulted in a reduction in drinking of about four to six standard drinks per week
for men
• While there is no clear dose-response curve for spending more time counselling
subjects who are drinking at risky levels, the minimum time to achieve some
impact is between five and 15 minutes. Although some have argued that 126-129
screening, of itself, constitutes a brief intervention, the impact of interventions of
less than five minutes is less clear
• Components of effective interventions include: 124, 130, 131
- motivational interviewing, especially being more person-centred and eliciting
change talk
- asking about drinking and its consequences
- personalised feedback about impact on health
- goal setting
Management of • Brief interventions and routine GP care are likely to be insufficient for patients 132
dependence or with alcohol dependence or heavy drinking. Such patients should be referred to a
heavy drinking drug and alcohol service
Implementation
There is some evidence from earlier systematic reviews that for every 10 hazardous drinkers treated using brief
interventions, one will reduce drinking to low-risk levels.102,133,134 For more information, refer to the RACGP’s SNAP
guide, 2nd edn.82

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 about the patient's current level of physical activity and sedentary behaviour, and assess against current
guidelines.
Provide age-specific advice on meeting recommended levels of sedentary behaviour and physical activity.
The message that any physical activity is better than none is important. If a patient does not already engage in regular
physical activity, they can be encouraged to start by doing some, and then gradually build up to the recommended
amount.135 Advice, written physical activity materials and referral should be tailored to age (refer to Table 7.5.1).
78 9th edition
Table 7.5.1. Physical activity: Assessment, advice and referral

Age and risk group What should be done? How often? References
Children 0-5 years of age From birth, encourage physical activity, At times of child 136
particularly supervised floor-based play in safe health surveillance
environments or immunisation
(Practice Point)
Toddlers and pre-schoolers should be physically
active every day for at least three hours, spread
throughout the day (Practice Point)
Recommend children <2 years of age not

spend time in front of screens. From two to five
years of age recommend limiting screen time to
one hour per day (Practice Point)
Children 5-17 years of age Ask questions regarding current level of activity Opportunistically 136
and sedentary behaviour, and assess against
current guidelines (II, A)
Recommend accumulating 60 minutes of a

variety of moderate or vigorous aerobic physical
activity per day (I, A) and muscle strengthening
activity three days a week (II, A)
Recommend limiting or breaking up sitting time

and use of screens to no more than two hours
a day (Practice Point)
Adults 18-64 years of age Ask questions regarding current level of activity Every two years 135
and sedentary behaviour, and assess against (III, C)
Recommend doing some activity on most

days of the week. Accumulate 2.5-5 hours of
moderate intensity physical activity, 1.25-2.5
hours of vigorous intensity physical activity, or
a combination of these per week (III, A). Do
muscle strengthening activities at least two days
a week (I, A)
Avoid prolonged sitting and break up periods of

sitting (III, C)
People >65 years of age Ask questions regarding current level of activity Every two years 137, 138
and sedentary behaviour, and assess against
Recommend some physical activity every day

that improves fitness, strength, balance and
flexibility (III, C)
Gradually increase amount and frequency

(Practice Point)
Accumulate at least 30 minutes of moderate

activity on most days (III, C; refer to Section 5.2.
Physical activity)
9th edition
79
Age and risk group What should be done? How often? References
Increased risk
• Those at higher risk include Ask questions regarding current level of activity At least two 139-141
teenage girls, older adults, and sedentary behaviour and assess against yearly and
office workers, Aboriginal current guidelines (III, C) opportunistically
and Torres Strait Islander (IV D)
Provide brief interventions (refer to below)
peoples, and people from
and age-appropriate written physical activity
low socioeconomic and
materials (III, C)
non-English-speaking
backgrounds Refer to an exercise or physical activity 142, 143
• Those with or at high risk professional or program if appropriate brief
of a chronic condition or interventions within the general practice cannot
cancer (refer to Chapter 8. be offered (I, D) or if preferred by the patient
Prevention of vascular and (Practice Point)
metabolic disease, and Programs with additional behaviour change
Chapter 9. Cancer) support may be more beneficial (III, C)
Table 7.5.2. Physical inactivity interventions

Assessment and
intervention Technique References
Brief interventions to Some of the components of interventions in general practice that have
increase levels of physical been shown to have short-term benefit in changing behaviour related to
activity physical activity include:
• at least two sessions of face-to-face provision of brief advice or
counselling on exercise with supporting written materials
• written prescription for exercise and/or supplementary advice or
counselling by telephone
• pedometer step target that is incremental and agreed with the patient 142, 144
Physical activity program Structured programs of physical activity education and exercise may 145, 146
be delivered as individual or group program and over several sessions.
The National Heart Foundation of Australia’s program is available 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
Non-face-to-face programs using telephone or internet have been

demonstrated to be effective in adults >50 years of age 143, 147
It should be noted that there is limited research examining the effectiveness

of exercise referral and none comparing exercise referrals to general
practice-based physical activity interventions
Implementation
Physically inactive patients may be referred to physical activity programs or classes run by local community
organisations. Those who have a chronic medical condition and complex needs may benefit from referral to an
accredited exercise physiologist or physiotherapist. For more information, refer to the RACGP’s SNAP guide,
2nd edn.82
80 9th edition
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122. Tam CW, Leong LH, Zwar N, Hespe C. Consultation 137. Sims J, Hill K, Hunt S et al. National physical activity
contexts and the acceptability of alcohol enquiry from 84 recommendations for older Australians: Discussion
Guidelines for preventive activities in general practice 9th document. Canberra: Department of Health and Ageing,
edition general practitioners - A survey experiment. Aust 2006.
Fam Physician 2015;44(7):490-96. 138. Michael YL, Whitlock EP, Lin JS, Fu R, O’Connor EA,
123. Tam CW, Leong L, Zwar N, Hespe C. Alcohol enquiry by Gold R. Primary care - Relevant interventions to prevent
GPs - Understanding patients’ perspectives: A qualitative falling in older adults: A systematic evidence review for
study. Aust Fam Physician 2015;44(11):833-38. the US Preventive Services Task Force. Ann Int Med
124. Kaner EF, Beyer F, Dickinson HO, et al. Effectiveness of 2010;153(12):815-25.
brief alcohol interventions in primary care populations. 139. Bauman A, Bellew B, Vita P, Brown W, Owen N.
Cochrane Database Syst Rev 2007;2:CD004148. Getting Australia active: Towards better practice for the
125. Moyer VA, US Preventive Services Task Force. Screening promotion of physical activity. Melbourne: National Public
and behavioral counseling interventions in primary care Health Partnership, 2002.
to reduce alcohol misuse: US Preventive Services Task 140. LeFevre ML. Behavioral counseling to promote a healthful
Force recommendation statement. Ann Intern Med diet and physical activity for cardiovascular disease
2013;159(3):210-18. prevention in adults with cardiovascular risk factors:
126. McCambridge J, Kypri K. Can simply answering research US Preventive Services Task Force recommendation
questions change behaviour? Systematic review and statement. Ann Int Med 2014;161(8):587-93.
meta analyses of brief alcohol intervention trials. PLOS 141. Mammen G, Faulkner G. Physical activity and the
ONE 2011;6(10):e23748. prevention of depression. A systematic review of
127. Jonas DE, Garbutt JC, Amick HR, et al. Behavioral prospective studies. Am J Prev Med 2013;45(5):649-57.
counseling after screening for alcohol misuse in primary 142. Orrow G, Kinmonth AL, Sanderson S, Sutton S.
care: A systematic review and meta-analysis for the Effectiveness of physical activity promotion based in
US Preventive Services Task Force. Ann Intern Med primary care: Systematic review and meta-analysis of
2012;157(9):645-54. randomised controlled trials. BMJ 2012;344:e1389.
128. Gaume J, McCambridge J, Bertholet N, Daeppen JB. 143. Pavey TG, Anokye N, Taylor AH, et al. The clinical
Mechanisms of action of brief alcohol interventions effectiveness and cost-effectiveness of exercise referral
remain largely unknown - A narrative review. Front schemes: A systematic review and economic evaluation.
Psychiatry 2014;5:108. Health Technol Assess 2011;15(44):i-xii, 1-254.
129. McCambridge J, Rollnick S. Should brief interventions in 144. Kolt GS, Schofield GM, Kerse N, Garrett N, Ashton T,
primary care address alcohol problems more strongly? Patel A. Healthy Steps trial: Pedometer-based advice and
Addiction 2014;109(7):1054-58. physical activity for low-active older adults. Ann Fam Med
130. Riper H, van Straten A, Keuken M, Smit F, Schippers 2012;10(3):206-12.
G, Cuijpers P. Curbing problem drinking with 145. Muller AM, Khoo S. Non face-to-face physical activity
personalizedfeedback interventions: A meta-analysis. Am interventions in older adults: A systematic review. Int J
J Prev Med 2009;36(3):247-55. Behav Nutr Phys Act 2014;11(35).
131. O’Donnell A, Anderson P, Newbury-Birch D, et al. The 146. Goode AD, Reeves MM, Eakin EG. Telephone-delivered
impact of brief alcohol interventions in primary healthcare: interventions for physical activity and dietary behavior
A systematic review of reviews. Alcohol Alcohol change: An unpdated systematic review. Am J Prev Med
2014;49(1):66-78. 2012;42(1):81-88.
132. Saitz R. Alcohol screening and brief intervention in 147. Pavey T, Taylor A, Hillsdon M, et al. Levels and predictors
primary care: Absence of evidence for efficacy in people of exercise referral scheme uptake and adherence:
with dependence or very heavy drinking. Drug Alcohol A systematic review. J Epidemiol Community Health
Rev 2010;29(6):631-40. 2012;66(8):737-44.
133. Ballesteros J, Duffy JC, Querejeta I, Arino J, Gonzalez-
Pinto A. Efficacy of brief interventions for hazardous
drinkers in primary care: Systematic review and meta
analyses. Alcohol Clin Exp Res 2004;28(4):608-18.
134. Beich A, Thorsen T, Rollnick S. Screening in brief
intervention trials targeting excessive drinkers in general
practice: Systematic review and meta-analysis. BMJ
2003 6;327(7414):536-42.
135. Brown W, Bauman A, Bull F, et al. Development of
evidence-based physical activity recommendations for
adults (18-64 years). Canberra: Department of Health,
2012.
136. Okely AD, Salmon J, Vella SA, et al. A systematic review
to inform the Australian sedentary behaviour guidelines
for children and young people. Canberra: Department of
Health and Ageing, 2012.
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8. Prevention of vascular and

metabolic disease
Cardiovascular disease (CVD) occurs in 18% of Australians. It accounts for 36% of all deaths and 6.9% of all
disability.1 The most important behavioural and physiological risk factors for CVD are smoking, diabetes, raised
blood pressure (BP), dyslipidaemia, obesity, physical inactivity and poor diet.2 These risk factors are common in
the Australian population: 90% of adults aged >45 years have at least one modifiable risk factor and 66% have
three or more risk factors for CVD.3 In addition to these, a family history of premature heart disease in a first-degree
relative,4 history of depression, social isolation and lack of quality social support are recognised risk factors for
coronary heart disease (CHD).5
Health inequity
• CVD: Socioeconomic disadvantage is associated with higher rates of CVD.6 Aboriginal and Torres Strait Islander
peoples, people living in rural and remote areas, and people in lower socioeconomic groups, all have an
increased risk of cardiovascular disease.6 Minority groups have high risk factor rates of cardiovascular disease
globally.6,7
• Type 2 diabetes (T2D): There is a higher prevalence of T2D among Australians in the lower socioeconomic
groups.8 T2D is more than twice as common in the most disadvantaged communities.9 Certain ethnic groups
are more at risk.10 Aboriginal and Torres Strait Islander peoples are three times more likely to have diabetes than
non-Indigenous Australians, and T2D is a direct or indirect cause for 20% of Aboriginal and Torres Strait Islander
deaths.11
• CVD risk factors: Biological and behavioural risk factors play a role in increasing cardiovascular risk (refer
to Chapter 7. Prevention of chronic disease). However, while smoking, nutrition, alcohol and physical activity
(SNAP) risk factors exhibit clear socioeconomic gradients,10,12 the higher prevalence of vascular and metabolic
disease is only partly mediated by behavioural risk factors and is more consistently observed in women.13
Diabetes and CVD are more common in rural populations, and this is exacerbated by poorer access to
healthcare.14 There is evidence that men from socioeconomically disadvantaged backgrounds may be less likely
to be offered statins.15
• Chronic kidney disease (CKD): Disadvantaged groups have higher rates of CKD for which type 2 diabetic
nephropathy is a common cause.16,17 Over the past 25 years, the number of Aboriginal and Torres Strait Islander
peoples commencing renal replacement therapy was 3.5 times greater than the majority of the population.
CKD has an earlier onset in Indigenous peoples.18-20 Aboriginal and Torres Strait Islander peoples are 10 times
more likely than non-Indigenous Australians to be hospitalised for CKD, and, from 2008 to 2012, CKD was
responsible for or associated with 16% of Aboriginal and Torres Strait Islander deaths.11
What can GPs do?

• Inequities in diabetes care can be ameliorated using a structured systems-based approach to care targeting at-
risk and minority populations using diabetes registries.21
• Social disadvantage may be a factor in poor medication adherence in patients with chronic disease.22,23
Interventions that can help improve medication adherence include those that target the barriers created by
socioeconomic status (SES) and the treatment itself.23 Underuse of cardiovascular medications is common in
older adults at high risk of CVD, and may be a factor in inequity in cardiovascular outcomes.24
86 9th edition
• Effective chronic disease interventions are likely to be those that address the determinants of behavioural risk
factors that arise from root social causes such as poverty and low health literacy.6 Interventions delivered in
community settings that target families and are multifaceted to incorporate the social context are generally the
most successful.25,26
• Trust is an important element in the delivery of culturally competent health service to patients with chronic
diseases, particularly Aboriginal and Torres Strait Islander peoples. Key ways to improve healthcare delivery
are to respond to social complexity; promote empowerment, trust and rapport; and reduce discrimination and
racism. To do so requires not only practice-system change but also Aboriginal and Torres Strait Islander cultural
training of health professionals to build culturally safe environments.27,28 Continuity of care and patient-centred
care are also important. Culturally specific interventions are needed and there are ongoing initiatives to develop
these.29-33
8.1 Assessment of absolute cardiovascular

disease 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
Aboriginal and Torres

Strait Islander peoples
Absolute CVD risk assessment combines risk factors to calculate the probability that an individual will develop
a cardiovascular event (eg myocardial infarction, stroke) or other vascular disease within a specified time frame
(usually five years). Absolute CVD risk assessment should be conducted at least every two years in all adults aged
>45 years who are not known to have CVD or to be at clinically determined high risk (B).34 This calculation requires
information on the patient’s age, sex, smoking status, total and high-density lipoprotein-cholesterol (HDL-C),
systolic blood pressure (SBP) and whether the patient is known to have diabetes or left ventricular hypertrophy
(LVH). In adults at low absolute CVD risk, blood test results within five years may be used for review of absolute
CVD risk unless there are reasons to the contrary.34
Adults >74 years of age may have their absolute CVD risk assessed with age entered as 74 years. This is likely to
underestimate five-year risk but will give an estimate of minimum risk.35 Patients with a family history of premature
CVD (in a first-degree relative - men aged <55 years, women aged <65 years)4 or obesity (body mass index [BMI]
above 30 kg/m2 or more) may be at greater risk.36-38 Similarly, patients with depression and atrial fibrillation (AF) may
also be at increased risk.34
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Table 8.1.1. Cardiovascular disease: Identifying risk

Population group What should be done? How often? References
Adults aged >45 years Calculate absolute CVD risk
* Every two years+ 34
not known to have 45-74 years (II, B) (IV, C)
cardiovascular disease (CVD)
or not clinically determined
to be at high risk
Aboriginal and Torres Strait Assess absolute CVD risk Every two years
Islander peoples aged (may underestimate risk; IV, C) (IV, C)
> 35 years not known to
have CVD or not clinically
determined to be at high risk
‘Calculate risk using the National Heart Foundation of Australia’s risk charts (refer to Appendix 8A. Australian cardiovascular disease risk
charts) or online at www.cvdcheck.org.au Blood lipid results within five years can be used in the calculation of absolute CVD risk, but
blood pressure (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 electrocardiogram
(ECG) is not required to determine left ventricular hypertrophy (LVH) if it is not previously known. Other absolute CVD risk calculators have
been developed but most should not be applied to the Australian population.
fiAdults with any of the following do not require absolute CVD risk assessment using the absolute risk calculator, because they are
already known to be at clinically determined high risk of CVD (IV D):
• diabetes and >60 years of age

• diabetes with microalbuminuria (>20 pg/min or urine albumin-to-creatinine ratio (UACR) >2.5 mg/mmol for males, >3.5 mg/mmol for
females)
• moderate or severe chronic kidney disease (CKD; persistent proteinuria or estimated glomerular filtration rate [eGFR] <45 mL/min/1.73 m2)
• previous diagnosis of familial hypercholesterolaemia (FH)
• Systolic blood pressure (SBP) >180 mmHg or diastolic blood pressure (DBP) >110 mmHg
• serum total cholesterol >7.5 mmol/L
• Aboriginal or Torres Strait Islander peoples aged >74 years (Practice Point)
BP blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP diastolic blood pressure; ECG,
electrocardiogram; eGFR, estimated glomerular filtration rate; FH, familial hypercholesterolaemia; LVH, left ventricular hypertrophy; SBP,
systolic blood pressure; UACR, urine albumin-to-creatinine ratio
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
I I I I I
BP should be measured in all adults from 18 years of age (A) at least every two years. BP should be interpreted in
the context of an absolute CVD risk assessment after 45 years of age (35 years of age for Aboriginal and Torres
Strait Islander peoples; B). Secondary causes of hypertension and ‘white coat’ hypertension should be considered.
88 9th edition
Table 8.2.1. Hypertension: Identifying risk

How
Who is at risk? What should be done? often? References
Low absolute risk: Provide lifestyle advice and education (I, B) BP every 34, 39-41
• <10% cardiovascular disease two years
Offer pharmacotherapy if blood pressure (BP)
(CVD) risk (III, C)
persistently over 160/100 mmHg
Review BP of 140-159 mmHg after two months of

lifestyle advice
Moderate risk: Provide intensive lifestyle advice (II, B) BP every 34, 38, 42
• 10-15% absolute CVD risk 6-12
Consider pharmacotherapy if systolic blood 11,36, 37,
months
pressure (SBP) is 140-159 mmHg or diastolic 41,43
(III, C)
blood pressure (DBP) is 90-99 mmHg. If SBP is
130-139 mmHg or DBP is 85-89 mmHg, review
BP in six months
Offer pharmacotherapy simultaneously with lifestyle

intervention if BP persistently over 160/100 mmHg
or if family history of premature CVD or patient is
of South Asian, Middle Eastern, Maori, Aboriginal,
Torres Strait Islander or Pacific Islander descent
(III, C)
High risk: Provide intensive lifestyle advice (II, B) BP every 34, 43

• >15% absolute CVD risk 6-12
Commence pharmacotherapy (simultaneously with
• Clinically determined high risk: weeks
lipid therapy unless contraindicated)
(III, C)
- diabetes and >60 years of age
Treatment goal is BP <140/90 mmHg in adults
- diabetes with microalbuminuria 44, 45
without CVD, or lower (SBP <120 mmHg) in some
(>20 gg/min or urine the urine individuals who tolerate more intensive treatment,
albumin-to-creatinine ratio * <130/80 mmHg
and those with CKD (I, B to III, D;
[UACR] >2.5 mg/mmol for in people with diabetes or microalbuminuria or
males, >3.5 mg/mmol for macroalbuminuria UACR >2.5 mg/mmol in males
females) and >3.5 mg/mmol in females)
- moderate or severe chronic
kidney disease (CKD)
(persistent proteinuria or
estimated glomerular filtration
rate [eGFR] <45 mL/min/
1.73 m2)
- previous diagnosis of familial
hypercholesterolemia (FH)
- SBP >180 mmHg or DBP
>110 mmHg
- serum total cholesterol >7.5
mmol/L
- Aboriginal and Torres Strait
Islander peoples aged >74
years
• Existing CVD (previous event, Provide lifestyle risk factor counselling and Every six 43, 46
symptomatic CVD), stroke or commence pharmacotherapy to lower risk (I, A). months
transient ischaemic attacks There is some evidence that a treatment goal (SBP (III, C)
(TIAs) or CKD <120 mmHg) in some individuals who tolerate
more intensive treatment provides additional
benefit. Adverse effects need to be monitored
*D recommendation for clinically determined high risk

BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; DBP, diastolic blood pressure; eGFR, estimated
glomerular filtration rate; FH, familial hypercholesterolaemia; SBP, systolic blood pressure; TIA, transient ischaemic attack;
UACR, urine albumin-to-creatinine ratio
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89
Table 8.2.2. Hypertension: Preventive interventions

Measure Measure BP on at least two separate occasions with a calibrated mercury 34, 40
blood sphygmomanometer, or automated device that is regularly calibrated against a mercury
pressure (BP) 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
47
hypotension (eg elderly, those with diabetes), measure BP in sitting position and repeat
after the patient has been standing for at least two minutes
If possible, use ambulatory BP monitoring or self-measurement for patients with:

• unusual variation between BP readings in the clinic
• suspected white coat hypertension
• hypertension that is resistant to drug treatment
• suspected hypotensive episodes (eg in elderly or diabetic patients)
Risk calculation should be performed using clinical BP measurements (as the algorithms
are based on these)
Lifestyle Lifestyle risk factors should be managed at all risk levels 34, 40, 48
modification
All people, regardless of their absolute cardiovascular disease (CVD) risk assessment,
should be given dietary advice. Those at low to moderate absolute CVD risk should be
given dietary and other lifestyle advice (refer to Chapter 7. Prevention of chronic disease)
Advise to aim for healthy targets:

• Encourage any physical activity and aim for at least 30 minutes of moderate-intensity
physical activity on most, if not all, days
• Recommend smoking cessation
• Suggest a target waist measurement <94 cm for men and <80 cm for women, and a
body mass index (BMI) <25 kg/m2
• Recommend dietary salt restriction <4 g/day (65 mmol/day sodium)
• Encourage limiting 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): 34, 49
• <140/90 mmHg for adults without CVD (including those with chronic kidney disease [CKD])
• <130/80 mmHg for adults with diabetes or with microalbuminuria or macroalbuminuria
(urine albumin-to-creatinine ratio urine albumin-to-creatinine ratio [UACR] >2.5 mg/
mmol for males, >3.5 mg/mmol for females)
• In patients at high absolute risk there is some evidence that a lower treatment goal
(systolic blood pressure [SBP] <120 mmHg) in individuals who tolerate more intensive
treatment provides additional benefit. Adverse effects need to be monitored
BMI, body mass index; BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; SBP, systolic blood pressure;
UACR, urine albumin-to-creatinine ratio
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

Adults should have their blood lipids (a fasting sample should be used when assessing elevated triglycerides [TG])50
assessed every five years starting at 45 years of age (A for males, C for females). Lipid levels should be interpreted in
the context of an absolute CVD risk assessment after 45 years of age (35 years of age for Aboriginal and Torres Strait
Islander peoples; B). Aboriginal and Torres Strait Islander adults should have lipid tests performed every five years
from 35 years of age (B).
90 9th edition
Table 8.3.1. Cholesterol and lipids: Identifying risk

Low risk: Provide lifestyle advice (I, A) Repeat lipids 34
• Absolute cardiovascular disease (CVD) risk <10% every five years
*
Moderate risk: Provide intensive lifestyle Repeat lipids 34, 36-38, 42

• Absolute CVD risk 10-15% advice (II, B) every two years
Consider pharmacotherapyt
if not reaching target after
six months (I, A) or if family
history of premature CVD
or patient is of Aboriginal or
Torres Strait Islander, South
Asian, Middle Eastern, Maori
or Pacific Islander descent
(II, C)
High risk: Provide intensive lifestyle Every 12 34, 42

• Absolute CVD risk >15% advice (II, C) months (III, C)
• Patient with the following clinically determined Commence cholesterol
high-risk factors: lowering therapy
- diabetes and >60 years of age (simultaneously with
- diabetes with microalbuminuria (>20 pg/min antihypertensive unless
or urine albumin-to-creatinine ratio [UACR]) contraindicated) (II, C to III,
>2.5 mg/mmol for males, >3.5 mg/mmol for D)§
females)
- Chronic kidney disease (CKD); persistent
microalbuminuria or stage 4 renal failure
(estimated glomerular filtration rate [eGFR]
<30 mL/min/1.73 m2) or stage 3a renal failure
eGFR <45 mL/min/1.73 m2)
- previous diagnosis of familial
hypercholesterolaemia
- Systolic blood pressure (SBP) >180 mmHg or
diastolic blood pressure (DBP) >110 mmHg
- serum total cholesterol >7.5 mmol/L*
- Aboriginal and Torres Strait Islander peoples
aged >74 years
Refer to Section 8.2. Blood pressure
• Existing CVD (previous event, symptomatic CVD) Provide lifestyle risk factor Every 12 51
counselling and commence months (III, C)
pharmacotherapy to lower
risk
*Lipid blood test results within five years can be used to calculate absolute CVD risk every two years. Patients with diabetes, cardiac
disease, stroke, hypertension or kidney disease should have their lipids tested every 12 months (III, C)
fin Australia, pharmacotherapy with statins are only subsidised on the pharmaceutical benefits scheme (PBS) for limited criteria at
www.pbs.gov. au/info/news/2006/09/Eligibility-cholestl-lwring-meds
:Those with low-density lipoprotein cholesterol (LDL-C) >4.0 or total cholesterol >7.5 should be reviewed for family history and clinical
features of FH52
§D recommendation for clinically determined high risk
CKD, chronic kidney disease; CVD, cardiovascular disease; DBP diastolic blood pressure; eGFR, estimated glomerular filtration rate;
FH, familial hypercholesterolaemia; low-density lipoprotein cholesterol, LDL-C; PBS, Pharmaceutical Benefits Scheme; SBP systolic
blood pressure; UACR, urine albumin-to-creatinine ratio
9th edition
91
Table 8.3.2. Cholesterol and lipids: Preventive interventions

Blood lipids Total cholesterol, low-density lipoprotein-cholesterol (LDL-C), high-density 50, 53-55
lipoprotein-cholesterol (HDL-C) and triglycerides (TGs)
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. A fasting sample should be used when
assessing elevated TGs
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 with low absolute cardiovascular disease (CVD) risk, blood test
results within five years may be used for review of absolute CVD risk unless
there are reasons to the contrary
Lifestyle modification Lifestyle risk factors should be managed at all risk levels 34, 40
All people, regardless of their absolute CVD risk level, should be given
dietary advice. Those at low to moderate absolute CVD risk should be
given dietary and other lifestyle advice (refer to Chapter 7. Prevention of
chronic disease)
Advise to aim for healthy targets:

• Encourage any physical activity and aim for at least 30 minutes of
moderate-intensity physical activity on most, if not all, days
• Recommend smoking cessation
• Suggest a target waist measurement <94 cm for men and <80 cm for
women, and a body mass index (BMI) <25 kg/m2
• Recommend salt restriction <4 g/day (65 mmol/day sodium
• Encourage limiting alcohol intake to <2 standard drinks per day for
males and <1 standard drink per day for females
Pharmacotherapy Lipid-lowering therapy for primary prevention should (while balancing risks 34, 49
and 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
Refer to the Australian medicines handbook for pharmacotherpy options
BMI, body mass index; CVD, cardiovascular disease; HDL-C, high-density lipoprotein-cholesterol; LDL-C, low-density lipoprotein
cholesterol; TG, triglyceride
92 9th edition
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

Abnormal blood glucose is a modifiable risk factor for CVD and a diagnosis of diabetes substantially increases
a person’s absolute CVD risk score. The Australian type 2 diabetes risk assesment tool (AUSDRISK) is useful in
assessing risk of diabetes. Preventive interventions (refer to Table 8.4.3) have been shown to reduce progression to
diabetes in patients with impaired fasting glucose.
Patients at high risk should be screened for diabetes every three years from 40 years of age. Aboriginal and
Torres Strait Islander peoples should have their risk of diabetes assessed every three years from 18 years of age.
Screening should be part of a comprehensive CVD assessment including BP, lipids, smoking, physical activity, diet,
overweight and obesity.
Table 8.4.1. Type 2 diabetes: Identifying risk

What should
Who is at risk? be done? How often? References
Increased risk: AUSDRISK
* Every three 56
• >40 years of age (III, B) years (III, C)
• Aboriginal and Torres Strait Islander peoples aged >18 years
High risk: Fasting blood Every three 57-59

• >40 years of age and being overweight or obese glucose (III, B) years (III, C)
(refer to Section 7.2. Overweight) OR
• AUSDRISK score of 12 or more glycated
• Consider screening the following groups because they may be haemoglobin
at increased risk for diabetes at an earlier age or lower body (HbA1c)
mass index (BMI):
- first-degree relative with diabetes
- high-risk race/ethnicity (Indian subcontinent or Pacific
Islanders)
- all people with a history of a previous cardiovascular event
(eg acute myocardial infarction or stroke)
- women with a history of gestational diabetes mellitus
- women with polycystic ovary syndrome
- patients on antipsychotic drugs
• Those with impaired glucose tolerance test or impaired fasting Fasting blood Every 12 58
glucose (not limited by age) glucose (III, B) months (III, C)
or HbA1c
*The Australian type 2 diabetes risk assessment tool (AUSDRISK) is available at www.health.gov.au/preventionoftype2diabetes
BMI, body mass index; HbA1c, glycated haemoglobin
9th edition
93
Table 8.4.2. Tests to detect diabetes

*
Fasting blood Measure plasma glucose levels on a fasting sample: 58
glucose • <5.5 mmol/L: Diabetes unlikely
• 5.5-6.9 mmol/L: May need to perform an oral glucose tolerance test
• >7.0 mmol/L (>11.1 non-fasting): Diabetes likely; repeat fasting blood sugar on
a separate day to confirm
The test should be performed on venous blood and tested in a laboratory to confirm
a diagnosis
Impaired fasting glucose is diagnosed on the basis of a result between 6.1 and
6.9 mmol/L
Glycated HbA1c may be used as a diagnostic test for diabetes. HbA1c of >48 mmol/mol (6.5%) 60, 61
haemoglobin is diagnostic of diabetes
(HbA1c)
Oral glucose Measure the plasma glucose before (fasting) and two hours after a 75 g glucose load 58
tolerance test is taken orally. Diabetes is diagnosed if fasting plasma glucose is >7.0 mmol/L or two-
hour plasma glucose is >11.1 mmol/L. If the two-hour plasma glucose is between 7.8
and 11.0 mmol/L, there is impaired glucose tolerance. A two-hour result <7.8 mmol/L
is considered normal
*Cut off levels for classifications vary by national and World Health Organization (WHO) guidelines, and are subject to change as more
evidence is developed
HbA1c, glycated haemoglobin; WHO, World Health Organization
Table 8.4.3. Type 2 diabetes: Preventive interventions

Target group Intervention References
Impaired glucose tolerance, • Increasing physical activity (eg 30 minutes brisk walking five 62-65
impaired fasting glucose and those times a week) and/or weight loss reduces risk of developing
with an elevated Australian type diabetes by 40-60% in those at high risk
2 diabetes risk assesment tool • Give advice on healthy low-fat diet (<30% kcal or kilojoules
(AUSDRISK) score or with other from fat and <10% from saturated fat; high fibre, low
specific high-risk factors glycaemic index with cereals, legumes, vegetables and
fruits), weight loss and increased physical activity (refer
to Smoking, nutrition, alcohol, physical activity (SNAP): A
population health guide to behavioural risk factors in general
practice, 2nd edn)
• Refer patients to a dietitian and a physical activity program
• Provide pre-conception advice to women with a history of
gestational diabetes
AUSDRISK, Australian type 2 diabetes risk assessment tool
The RACGP and Diabetes Australia’s publication General practice management of type 2 diabetes - 2016-18
provides guidance for the management of patients diagnosed with T2D.
94 9th edition
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 transient ischaemic attacks (TIAs) in those aged >45 years and they should
assess these patients 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 CVD risk assessed and the cause of their AF determined and treated according to cardiovascular
and thromboembolic risk (II, B).
Table 8.5.1. Stroke: Identifying risk

High absolute risk: Question about symptoms of TIA. If TIA, stratify Every 12 34, 51
• Calculated >15% absolute risk, risk of stroke and consider anticoagulation
* (I, A) months (IV, C)
66-68
clinically determined high risk If AF, determine cause of AF and treat according
or pre-existing cardiovascular to cardiovascular and thromboembolic risk (II, B)
disease (CVD)
Manage behavioural and physiological risk
• Previous stroke (especially with
factors actively. Treat with antihypertensive
co-existent atrial fibrillation
and lipid-lowering medications unless
[AF] or high grade [70-99%]
contraindicated or clinically inappropriate (II, B)
symptomatic carotid stenosis)
• Previous transient ischaemic
attack (TIA)
Auscultation for carotid bruit Auscultating for carotid bruit in asymptomatic 67, 69-71
people is not recommended in the general adult
population as a screening tool for stroke risk.
Screening with duplex ultrasonography in this
population is not cost-effective (yields many false
positive results). In addition, the 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 67

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 therapy for long-term secondary prevention should be used in people with ischaemic stroke or TIA who have
documented atrial fibrillation or cardio-embolic stroke
+Antiplatelet therapy should be considered for non-cardio-embolic stroke or TIA

AF, atrial fibrillation; CVD, cardiovascular disease; TIA, transient ischaemic attack
9th edition
95
Table 8.5.2. Tests to detect stroke risk

Question about Question patient or carer regarding symptoms of sudden onset of loss of focal 68, 72
transient ischaemic neurological function such as weakness or numbness of arms or legs, speech
attack (TIA) disturbance, double vision or vertigo
ABCD2 tool All patients with suspected TIA should have stroke risk assessment, which may
include 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 minutes (2 points), 10-59 minutes (1 point)
• Diabetes (1 point)
Important additional information required:
• presence of atrial fibrillation (AF)
• signs that might indicate carotid disease (eg anterior circulation signs),
in people who are candidates for carotid surgery
• >2 TIAs within the previous seven 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 low risk (ABCD2 tool = 0-3 without AF, potential carotid
disease or crescendo TIA): Refer for computed tomography (CT) of brain (and
carotid ultrasound where indicated) as soon as possible (ie within 48-72 hours)
Assess the need for A decision to anticoagulate someone with AF can be assisted by stroke 73, 74
anticoagulation (CHA2DS2-VASc) and bleeding (HAS-BLED) scores
AF, atrial fibrillation; CT, computed tomography; TIA, transient ischaemic attack
For further information about secondary prevention after stroke or TIA, refer to https://strokefoundation.com.au
Also refer to Chapter 15. Screening tests of unproven benefit.
96 9th edition
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
lililí!
Approximately 1.7 million Australians aged >18 years have reduced kidney function and/or albumin in the urine,75
but only 10% are aware of this.76 CKD may be a stronger risk factor for future coronary events and all-cause
mortality than diabetes.77 Early management of CKD includes CVD risk factor reduction, lifestyle changes and
prescription of angiotensin-converting-enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).78 Patients
should be screened for kidney disease if they are at high risk (B).
Table 8.6.1. Kidney disease: Identifying risk

High risk: Blood pressure (BP), Every one to two 79-88,
• Smoking albumin-to-creatinine *years (IV, C) 92-94
• Obesity (body mass index [BMI] >30 kg/m2) ratio (ACR) and estimated
glomerular filtration rate
• Family history of kidney failure
(eGFR; III, A)
• Diabetes
• Hypertension If ACR is positive, arrange 57, 88-91
two further samples for urine
• Aboriginal or Torres Strait Islander peoples
ACR over two months (III, B)
aged >30 years
• Established cardiovascular disease (CVD), If eGFR <60 mL/min/1.73 m2,
coronary heart disease (CHD) or peripheral repeat within seven days
vascular disease (PVD)
• History of acute kidney injury
*One year for patients with hypertension or diabetes
ACR, albumin-to-creatinine ratio; BMI, body mass index; BP, blood pressure; CHD, coronary heart disease; CVD, cardiovascular
disease; eGFR, estimated glomerular filtration rate; PVD, peripheral vascular disease
9th edition
97
Table 8.6.2. Tests to detect kidney disease

Albuminuria Estimation of urine albumin-to-creatinine ratio (UACR), preferably on a first morning void. 88, 90
Note: Dipstick urine test is not adequate to identify microalbuminuria
Albumin-to-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
Estimated This is currently automatically reported with every test for serum creatinine using 78, 89, 95
glomerular the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula (staging
filtration rate is based on both eGFR level and UACR [normoalbuminuria, microalbuminuria or
(eGFR) macroalbuminuria]):
• Stage 1: >90 mL/min/1.73 m2 with microalbuminuria, proteinuria or haematuria with
the presence of structural or pathological abnormalities
• Stage 2: 60-89 mL/min/1.73 m2 with microalbuminuria, proteinuria or haematuria with
the presence of structural or pathological abnormalities
• Stage 3a: 45-59 mL/min/1.73 m2
• Stage 3b: 30-44 mL/min/1.73 m2
• Stage 4: 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 a renal unit or nephrologist, and consider referral at
Stage 3 or earlier if:
• persistent significant albuminuria (UACR >30 mg/mmol)
• a sustained decrease in eGFR of 25% or more OR a sustained decrease in eGFR of
15 mL/min/1.73 m2 within 12 months
• chronic kidney disease (CKD) with hypertension that is hard to get to target despite at
least three antihypertensive agents
Visit www.kidney.org.au/cms_uploads/docs/ckd-management-in-gp-handbook-3rd-
edition.pdf
Note: eGFR and the presence and severity of albuminuria reflects the risk of
cardiovascular disease (CVD) progression and future cardiovascular events
The eGFR may be unreliable in the following situations:

• acute changes in renal function
• patients on dialysis
• certain diets (eg 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 of age
• severe liver disease
ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease; CKD-EPI, Chronic Kidney Disease Epidemiology Collaboration; CVD,
cardiovascular disease; eGFR, estimated glomerular filtration rate; UACR, urine albumin-to-creatinine ratio
8.7 Atrial fibrillation

AF is the most common heart arrhythmia; it increases in incidence with age,96,97 affecting less than 1% of patients
aged <60 years and between 5% and 15% of patients aged >80 years.98
Systematic screening for AF is not recommended; however, opportunistic screening when taking a blood pressure
or at other times appears to be cost effective.99
98 9th edition
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102 9th edition
Appendix 8A. Australian cardiovascular disease risk charts
People without diabetes
Women Men
Non-smoker Non-smoker Smoker
179’
I60
■■ 179’
160
140 140
120 120
E
E 179
* g
■■■
M
2 II»
^■■■B ■■■■■ 120
T
n
S 179>BBBH ■■■■ ■■■M

(J)
« "B
,20
II«. ■■■■■ 120 W
■■■■ mil Charts in this age
160
140
■ ■ ■■■«O
|16O bracket are for use in
Abongmal and Torres
Strait Islander
:,20BBBBB ■■MB ■BB”° populations only.
4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8
Total cholesterokHDL 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 clinically determined high absolute risk of CVD.
Risk level tor 5-year cardiovascular (CVD) risk

High risk Moderate risk Low risk
I ^30% Q IO-I5% H 5-9%
■ 25-29% | <5%
j 20-24%
16-19%
How to use the risk charts

I Identify the chart relating to the person's sex, diabetes (1C):HDL ratio, f-or example, the lower left cell contains
status, smoking history and age. The charts should all non smokers without diabetes who are 34 -44 years
be used tor all adults aged 45 years or over (and all and have a TCtHDL ratio of less than 4.5 and a SBP ot
Aboriginal and Torres Strait Islander adults aged 35- 74 less than 130 mmHg.
years) without known history of CVD and not already
3. The colour of the cell that the person falls into provides
known to be at clinically determined high risk. their 5-year absolute cardiovascular risk level (see legend
2. Within the chart, choose the cell nearest to the person's for risk category). People who fall exactly on a threshold
age. systolic blood pressure (SBP) and total cholesterol between cells are placed in the cell indicating higher risk.
9th edition
103
People with diabetes
Women Men
Non smoker Smoker Non smoker Smoker
Adults over the age of
160 ■ Age 60 with diabetes are
65-74 H 140 equivalent to high risk
140
(>15%). regardless
120 of their calculated risk
E level. Nevertheless,
■■■■■ ■■■■ 179’ E
e reductions in risk
■■■■■
■in Age
55-64
nm 160
140
120
i
factors in this age
group can still lower
overall absolute risk.
Age
140
■■ 45-54
120
■■■ 120
Charts in this age

bracket are for use in
Strait Islander
populations only.
Total cholesterol:HDL ratio

* Total cholesterokHDL ratio
*
______________________________________________________________________________
* In accordance with Australian guidelines, patients with systolic blood pressure s180 mm Hg, or a
total cholesterol of >7.5 mmol/L, should be considered at clinically determined high absolute risk of CVD.
Risk level for 5-year cardiovascular (CVD) risk

High risk Moderate risk Low risk
| >30% H 10-15% H 5-9%
| 25 29% H <5%
■ 20-24%
16-19*X,
Notes: The risk charts include values for SBP alone as this is the most informative of • The predictive value of the Framingham Risk Equation has not been
conventionally measured blood pressure parameters for cardiovascular risk. specifically assessed in adults who are overweight or obese (EBR Grade D).
For specific groups, additional guidance includes: • The increased risk of cardiovascular events and all-cause mortality, in
addition to thromboembolic disease including stroke, should be taken into
The Framingham Risk Equation has not been validated for all population groups,
account for adults with atrial fibrillation (particularly those aged over 65 years) (PP).
the assessment score should be interpreted with caution in the following groups:
• The Framingham Risk Equation may underestimate CVD risk in Aboriginal Charts are based on the NVDPA’s Guidelines for the assessment of absolute
and Torres Strait Islander peoples (EBR Grade D); adults with diabetes aged cardiovascular disease risk and adapted with permission from New Zealand
between 45 and 60 years (EBR Grade C); adults aged over 74 years (CBR), Guidelines Group. New Zealand Cardiovascular Guidelines Handbook: A Summary
however, available evidence suggests that this approach will provide an estimate Resource for Primary Care Practitioners. Second edition. Wellington, NZ: 2009.
of minimum cardiovascular risk. www.nzgg.org.nz.
• The Framingham Risk Equation is likely to underestimate CVD risk in adults
with socioeconomic deprivation (an independent risk factor for cardiovascular
disease) (PP) or depression (PP).
Reproduced with permission from the National Heart Foundation of Australia from National Vascular Disease Prevention Alliance. Absolute
cardiovascular disease risk management. Quick reference guide for health professionals. Melbourne: NVDPA, 2012.
104 9th edition
9. Early detection of cancers

General practitioners (GPs) can play a key role in identifying patients who may be at increased risk of cancer, and
giving tailored advice and cancer screening. There are many risk factors for cancers that GPs can explore - most
are specific to each cancer.
9.1 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 of asymptomatic (low-risk) men for prostate cancer by prostate specific antigen (PSA) testing is not
recommended because the benefits have not clearly been shown to outweigh the harms.1 This remains the case
following recent large trials.1 Therefore, GPs have no obligation to offer prostate cancer screening to asymptomatic men.
Some men may have individual concerns about prostate cancer and may put a higher value on the possible
benefits of prostate cancer screening. This requires specific discussion to address the benefits and harms
(from overdiagnosis and overtreatment) of prostate cancer screening.2 The Royal Australian College of General
Practitioners (RACGP) has produced a patient decision aid that may assist this discussion (www.racgp.org.au/
your-practice/guidelines/prostate-cancer).
If after an informed process, perhaps using a decision aid, a man still requests prostate cancer screening, a PSA
blood test is acceptable.3 Digital rectal examination (DRE) is no longer recommended as it is insufficiently sensitive
to detect prostate cancers early enough.4
Clinicians should not test for asymptomatic prostate cancer (eg by adding the PSA test to a battery of other tests)
without counselling about possible harms as well as possible benefits, and obtaining informed consent.
Table 9.1.1. Prostate cancer: Identifying risk

Average risk: Respond to requests for On demand 5, 6
• The risk of developing prostate cancer increases screening by informing (Practice Point)
with age and positive family history. However, patients of risks and benefits
because prostate cancer is normally slow of screening using a decision
growing, men aged >75 years or with a life support aid (I, A)
expectancy of <10 years are at 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 for On demand 5-7

• Men with one or more first-degree relatives screening by informing (Practice Point)
diagnosed <65 years of age patients of risks and benefits of
• Men with a first-degree relative with familial screening (Practice Point)
breast cancer (BRCA1 or BRCA2)
LUTS, lower urinary tract symptoms

9th edition
105
Table 9.1.2. Screening for prostate cancer in asymptomatic men

Not
recommended Justification References
Prostate specific The most common adverse effect of radical prostatectomy is erectile dysfunction,
antigen (PSA) which affects most men (it is less common in younger men, those with a lower 4, 8-11
screening PSA, and when nerve-sparing surgical techniques are used)
Other complications are common as well, including urinary incontinence (which

is very common in the months after treatment; however, this returns to normal in 12
75-90% men after two years, depending on treatment type). To a lesser extent,
urinary irritation and bowel symptoms can occur. General feelings of ‘vitality’ are
lost in about 10% of men
Both suicide and cardiovascular disease (CVD) increase enormously (eight and
13, 14
11 times more respectively) in the week after men are given their diagnosis of
prostate cancer
Even diagnostic procedures performed following positive screening can be 15

harmful, with Australian data showing that the risk of life-threatening sepsis
needing intensive care admission is about 1% after biopsy
Despite large trials, two meta-analysis suggests that prostate cancer screening
does not save lives
For more information on benefits and harms, visit the Clinical practice guidelines 2, 8
PSA testing and early management of test-detected prostate cancer at
http://wiki.cancer.org.au/australia/Guidelines:PSA_Testing/About_this_guideline
CVD, cardiovascular disease; PSA, prostate specific antigen
Implementation
Strategy
Patients who request testing should be informed about the risks and benefits of tests for prostate cancer, and
should be assisted to make their own decision using an acceptable decision aid.16
9.2 Colorectal 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
Average risk
High risk
■■■■■ 10 years prior to age of onset of affected family member
■■
Biennial faecal occult blood test (FOBT) can reduce colorectal cancer (CRC) mortality by 16%.17 The original trials
of FOBT screening used the guaiac-based FOBT but this has been superseded by the more sensitive and specific
faecal immunochemical test. Organised screening by FOBT is recommended for the asymptomatic (average risk)
population from 50 years of age every two years (A) until 75 years of age with repeated negative findings.18,19
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.
Colonoscopy is not recommended as a screening test for people at average risk of CRC. No randomised
controlled trials (RCTs) have evaluated the effect of colonoscopy on CRC mortality, although trials are in progress in
Spain, Sweden and the US. Colonoscopy has indirect and direct harms, including, rarely, death from the procedure
106 9th edition
(1 in 10,000-14,000 colonoscopies).20'21 Harm may be caused by the bowel cleanout prior to the procedure (eg
dehydration and electrolyte imbalances), the sedation used during the procedure (eg cardiovascular events), or
the procedure itself (eg infection, colonic perforations, bleeding). There is insufficient evidence about the use of
computed tomography (CT) colonography (also refer to Chapter 15. Screening tests of unproven benefit), faecal
deoxyribonucleic acid (DNA) or plasma circulating DNA tests to recommend them as alternatives to FOBT for CRC
screening.22 There is insufficient evidence to recommend the use of low-dose aspirin in people at average risk of
CRC.23
Table 9.2.1. Colorectal cancer: Identifying risk

Category 1 - Average or slightly Faecal occult blood test Every two years from 17, 19, 24
increased risk: (FOBT; I, A) 50 years of age
(Practice Point)
Asymptomatic people with:
• no personal history of bowel cancer,
colorectal adenomas, inflammatory bowel
disease or family history of colorectal cancer
(CRC)
or
• one first-degree or second-degree relative
with CRC diagnosed aged >55 years
Category 2 - Moderately increased risk Colonoscopy Every five years from 19, 25, 26
(1-2% of the population): 50 years of age, or
Sigmoidoscopy plus
at an age 10 years
Asymptomatic people with: double-contrast barium
younger than the age
• one first-degree relative with CRC diagnosed enema or computed
of first diagnosis of
aged <55 years tomography (CT)
CRC in the family,
colonography (performed
or whichever comes first
by an experienced
• two first-degree or one first-degree and one (Practice Point)
operator) are acceptable
second-degree relative(s) on the same side if colonoscopy is
of the family with CRC diagnosed at any age contraindicated
(without potentially high-risk features as in
Consider offering FOBT In intervening years
Category 3)
(III, B)
9th edition
107

Category 3 - High risk Refer for genetic screening Those at risk for: 25, 26
(relative risk of ~4-20%; <1% of the of affected relatives • FAP (no APC
*
population): mutation defined):
Refer to bowel cancer
Asymptomatic people with: specialist to plan Every 12 months
appropriate surveillance from 12-15 to
• three or more first-degree or second-
(III, B) 30-35 years of age
degree relatives on the same side of the
and every three
family diagnosed with CRC (suspected FAP: flexible years after 35 years
Lynch syndrome, also known as hereditary sigmoidoscopy of age#
non-polyposis CRC [HNPCC]or other Lynch
syndrome-related cancers* or • Lynch syndrome:
one to two yearly
or Colonoscopy in
from 25 years of
attenuated FAP*
• two or more first- or second-degree relatives age or five years
on the same side of the family diagnosed earlier than the
with CRC, including any of the following youngest affected
high-risk features: member of the
- multiple CRC in the one person family (whichever is
- CRC aged <50 years earliest)
- a family member who has or had Lynch Aspirin 100 mg/day is
syndrome-related cancer effective prophylaxis§
or
• at least one first-degree 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 high-risk mutation in the adenomatous HNPCC: In intervening years
polyposis coli (APC) or one of the mismatch
- colonoscopy
repair genes has been identified
• Members of proven FAP11 and Lynch
syndrome families who are shown not to carry
the family mutation are no longer at high risk Consider offering FOBT (Practice Point)
and revert to the average-risk group and still (III, B)
require population-based screening
*Age of starting screening varies in high-risk groups: 25 years of age for those with Lynch syndrome or five years earlier than the
earliest age of onset in the family
* Lynch syndrome-related cancers include colorectal, small bowel, endometrial, ovarian, gastric, brain and urothelial cancers
Âttenuated FAP is characterised by a significant risk for colon cancer but fewer colonic polyps (average of 30), more proximally
located polyps, and diagnosis of CRC 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
Aspirin at 600 mg/day reduced Lynch syndrome cancer incidence by 50-68% in the Colorectal Adenoma/Carcinoma Prevention
§
Programme 2 (CAPP2) trial.27 Follow-up of the low-dose aspirin randomised controlled trials (RCTs)28, 29 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
“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 50 years of age in untreated subjects. FAP, however, accounts for less than 1% of all CRC cases. HNPCC
(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, the risk for colorectal or other syndrome cancers is 70-90%19
# Bi-annual (six-monthly) or annual sigmoidoscopy for APC gene carriers of diagnosed FAP (colonoscopy in attenuated FAP)
APC, adenomatous polyposis coil; CAPP2, Colorectal Adenoma/Carcinoma Prevention Programme 2; CRC, colorectal cancer; CT,
computed tomography; FAP familial adenomatous polyposis, FOBT, faecal occult blood test; HNPCC, hereditary non-polyposis
colorectal cancer; RCT, randomised controlled trials
108 9th edition
Patients who have adenomatous polyps removed at colonoscopy are then at above-average risk for the
development of metachronous adenomatous polyps and CRC. Table 9.2.2 relates to the follow up of people after
polypectomy. It is important to try and obtain information about the histology, size and number of polyps removed
as this determines the future risk of adenomas and CRC, and therefore frequency of recommended surveillance
colonoscopy.30
Table 9.2.2. Follow up after polypectomy

Polyp type and number Recommended colonoscopy screening interval
Small pale distal hyperplastic polyps only (not No follow up required as no increased risk of metachronous colorectal
adenomas) neoplasia
One to two small tubular (<10 mm) Repeat colonoscopy at five years
adenomas
If that colonoscopy is normal, repeat colonoscopy at 10 years or faecal
occult blood test (FOBT) every two years
High-risk adenomas (three or more Three-year intervals

adenomas, >10 mm, or with tubulovillous or
villous histology, or high-grade dysplasia)
Large and sessile adenomas removed Three to six months and again at 12 months to ensure complete removal
piecemeal
Multiple adenomas, which is a strong

determinant of risk of metachronous
advanced and non-advanced neoplasia:
• >5 adenomas • 12 months
• >10 adenomas • Sooner than 12 months (because of the likelihood of missed
synchronous polyps)
Family history in addition to adenomas Intervals determined by adenoma characteristics, unless a syndromic risk
mandates more frequent surveillance
If advanced adenomas are found during Three-yearly schedule is prudent, but the choice should be individualised.
subsequent surveillance The interval can be lengthened if advanced adenomas are not found
People aged >75 years No surveillance as lead time for progression of an adenoma to cancer is
around 10-20 years
FOBT, faecal occult blood test
Table 9.2.3. Test to detect colorectal cancer

Faecal occult Two main types of FOBT are available: Guaiac and faecal immunochemical tests 31,32
blood test (FOBT)
Immunochemical tests are preferred as they have greater sensitivity and higher
screening
uptake (A).31 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 colonoscopy (such people being at least 12 times
more likely to have colorectal cancer [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
CRC, colorectal cancer; FOBT, faecal occult blood test

9th edition
109
Implementation
Strategy
Measures to increase screening in these groups include organised approaches such as employing recall
and reminders;32,33 recommendations by the GP for the screening;33,34 addressing capacity issues, including
convenience;33,35 and minimising barriers such as cost.33,35,36 Refer to the RACGP’s Putting prevention into practice:
Guidelines for the implementation of prevention in the general practice setting (Green Book) for more information
(available at www.racgp.org.au/your-practice/guidelines/greenbook).
The National Bowel Cancer Screening Program, using a faecal immunochemical test, is being expanded and by
2020 will offer biennial screening for people aged 50-74 years. GPs are critical, not just in maximising participation,
but managing participants with a positive FOBT.34,37
Participation is under-represented by Aboriginal and Torres Strait Islander, and culturally and linguistically diverse
(CALD) peoples.38
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
i i i i i i i i i
Increasing age is a major risk factor for developing breast cancer. Other major risk factors include a personal history
of atypical hyperplasia or lobular carcinoma in situ, a strong family history of the disease or mutation in a breast
cancer predisposition gene, and previous radiotherapy (eg for previous cancer). Breast cancer risk factors that
reflect hormonal exposures in the distant past, such as age at menarche or age at first birth, are less predictive of
late-life breast cancer than factors indicating recent hormonal exposures such as high bone mass or obesity (refer
to https://canceraustralia.gov.au/clinical-best-practice/breast-cancer/breast-cancer-risk for further information).
Breast cancer risk is not normally distributed: most women have a low (<4%) lifetime risk; and the remainder 4% to
more than 80%.39,40
Prevention of breast cancer

Physical activity,41 adequate folate,42 a Mediterranean diet,43 normal BMI (in postmenopausal women only) and
decreased alcohol consumption44 are associated with a decreased risk of breast cancer in observational studies.
For women at moderate (ie 1.5-3 times the population risk) or high (ie >3 times the population risk) risk, additional
interventions such as risk-reducing medication45 (moderate and high risk) and risk-reducing surgery46 (high risk) are
available. Referral to specialist genetic assessment is available for women assessed at high risk.
Screening
The screening strategy employed for an individual woman depends on her individual degree of risk. Validated tools
are available that can assess an individual woman’s breast cancer risk (eg International Breast Cancer Intervention
Study [IBIS] tool, available at www.ems-trials.org/riskevaluator).47 For asymptomatic, low-risk women, BreastScreen
Australia recommends screening mammograms every two years for women aged 50-74 years (B).48
The benefits of screening are obvious. However, the risks must not be forgotten: assuming that screening reduces
breast cancer mortality by 15%, and that overdiagnosis and overtreatment is at 30%, then for every 2000 women
invited for screening over 10 years, one will avoid dying of breast cancer and 10 healthy women, who would not
have been diagnosed if there had not been screening, will be treated unnecessarily.49,50 An extra 200 women will
experience important psychological distress including anxiety and uncertainty from false positive findings. The
substantial advances in treatment, and greater breast cancer awareness since the trials were carried out, mean
110 9th edition
that presented breast cancers are detected earlier and survive better, so screening today is less effective than at
the time of the trials. Recent observational studies show more overdiagnosis than in the trials and very little or no
reduction in the incidence of advanced cancers with screening.51
The decision to start screening mammogram should be an individual one. This is especially for women aged <50
years, where the benefits-harms ratio is less favourable.48
Some points:
• Screening mammogram in women aged 40-49 years may reduce the risk of dying of breast cancer, but the
number of deaths averted is much smaller than in older women, and the number of false-positive tests and
unnecessary biopsies are larger (C). Some women put a higher value on the potential benefit than the potential
harms, and may choose to begin screening between the ages of 40-49 years (C).48
• For women at average risk (ie <1.5 times population risk) of breast cancer, most of the benefit of a mammogram
will result from biennial screening during ages 50-74 years of age.48
• Of all age groups, women aged 60-69 years are most likely to avoid a breast cancer death through
mammogram screening (C).48
• All women undergoing regular screening mammogram are at risk of overdiagnosis - the detection (and then
treatment) of non-invasive and invasive breast cancer that would otherwise not have become a threat to their
health, or even apparent, during her lifetime (C).48
• Women with a parent, sibling, or child with breast cancer may benefit more than average-risk women from
beginning screening between 40 and 49 years of age (C).48
• Cancer Australia recommends considering annual mammograms from 40 years of age if the woman has a first-
degree relative <50 years of age diagnosed with breast cancer (refer to Table 9.3.1).48
• There is insufficient evidence to assess the balance of benefits and harms of screening mammogram in women
aged >75 years (I).48 Randomised trials of the benefits of screening mammogram did not include women >74
years of age. However observational studies favour extending screening mammogram to older women who
have a life expectancy of not less than 10 years.52
• There is insufficient evidence to recommend that clinical breast examination offers any benefits to women, of any
age (C).48 However, it is recommended that all women, whether or not they undergo mammogram 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, pain in a breast) to their GP. No one method for
women to use when checking their breasts is recommended over another.
The recommended screening strategy for women at different individual degrees of risk is outlined in Table 9.3.1.
Cancer Australia recommends that women at any age at increased risk (ie >1.5 times population risk) are offered
an individualised surveillance program by their GP and/or specialist.53 This might include regular clinical breast
examination and breast imaging with mammography and/or ultrasound and magnetic resonance imaging (MRI).
There is government funding available for MRI screening for women <50 years of age at high risk of developing
breast cancer.54
9th edition
111
Table 9.3.1. Breast cancer: Managing risk

Average or only slightly higher
* risk Clarify risk at http://canceraustralia. 55
(>95% of the female population): gov.au/clinical-best-practice/
gynaecological-cancers/familial-risk-
assessment-fra-boc
No confirmed family history of breast cancer Mammogram Every two years

• One first-degree relative diagnosed with from 50 to 74
Breast awareness (I, A)
breast cancer aged >50 years years of age
• One second-degree relative diagnosed Regular
with breast cancer at any age (Practice Point)
• Two second-degree relatives on the
same side of the family diagnosed with
breast cancer aged >50 years
• Two first-degree or second-degree
relatives diagnosed with breast cancer,
aged >50 years, but on different sides
(ie on each side) of the family
As a group, risk of breast cancer up to 75
years of age is between 1:11 and 1:8
Moderately increased risk1' (<4% of the Clarify risk at http://canceraustralia. 55

female population): gov.au/clinical-best-practice/
• One first-degree relative diagnosed with gynaecological-cancers/familial-risk-
breast cancer aged <50 years (without assessment-fra-boc
the additional features of the potentially Mammogram (III, C) At least every
high-risk group) two years from
Breast awareness
• Two first-degree relatives, on the same 50 to 74 years
side of the family, diagnosed with breast Consider referral to or consultation of age
cancer (without the additional features of with a family cancer clinic for further
Annual
the potentially high-risk group) assessment and management plan
mammograms
• Two second-degree relatives, on the
from 40 years
same side of the family, diagnosed with
of age may be
breast cancer, at least one aged <50
recommended
years (without the additional features of
if the woman
the potentially high-risk group)
has a first-
As a group, the relative risk of breast cancer degree relative
up to 75 years of age is between 1:8 and 1:4 aged <50 years
diagnosed with
breast cancer
(Practice Point)
112 9th edition

Potentially high risk* or carrying a Clarify risk at http://canceraustralia. Individualised 55
mutation (<1% of the female population): gov.au/clinical-best-practice/ surveillance
• Women who are at potentially high risk of gynaecological-cancers/familial-risk- program
ovarian cancer assessment-fra-boc
This may
• Two first-degree or second-degree Advise referral to a cancer specialist include regular
relatives on one side of the family or family cancer clinic for risk clinical breast
diagnosed with breast or ovarian cancer, assessment, possible genetic testing examination,
plus one or more of the following features and management plan, which might and annual
on the same side of the family: include treatment with chemo breast
- additional relative(s) with breast or prevention with selective oestrogen- imaging with
ovarian cancer receptor modulators (SERMs [eg mammography,
- breast cancer diagnosed before age tamoxifen or raloxifene] or aromatase MRI or
40 years inhibitors [Als; eg exemestane and ultrasound
- bilateral breast cancer anastrozole]), which reduce the risk of (Practice Point)
cancer in women at moderate or high
- breast and ovarian cancer in the same
risk of breast cancer. Tamoxifen has
woman
greater efficacy (and can be used in
- Ashkenazi Jewish ancestry
premenopausal women), but raloxifene
- breast cancer in a male relative has fewer adverse effects
• One first-degree or second-degree
relative diagnosed with breast cancer An alternative treatment is mastectomy
aged <45 years plus another first-degree or salpingo-oophorectomy (which has
or second-degree relative on the same a greater effect on ovarian cancer risk
side of the family with sarcoma (bone/ reduction), which also reduces the risk
46-56
soft tissue) aged <45 years of breast cancer
• Member of a family in which the These decisions requires careful

presence of a high-risk breast cancer assessment of risk and benefits
gene mutation has been established for individual women. Information
• Refer to the Cancer Australia guidelines tailored for GPs is available at https://
at http://canceraustralia.gov.au/clinical- canceraustralia.gov.au/sites/default/
best-practice/gynaecological-cancers/ files/publications/rrm-risk-reducing-
familial-risk-assessment-fra-boc for medication-for-women-at-increased-
further information risk-of-breast-cancer-due-to-family-
history_504af03f31630.pdf
As a group, risk of breast cancer up to 75
years of age is between 1:2 and 1:4 Ongoing surveillance strategies
may include regular clinical breast
examination, breast imaging with
mammography, magnetic resonance
imaging (MRI) or ultrasound, and
consideration of ovarian cancer risk
(Ill, C)
*About 1.5 times the population average

+About 1.5-3 times the population average
* More than three times the population average. Individual risk may be higher or lower if genetic test results are known
Implementation of breast cancer screening

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.57
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113
9.4 Skin cancer

Primary prevention is being ‘sun smart’ (refer to Table 9.4.1.2). Everyone, particularly children, should be advised
to adopt protective measures when ultraviolet (UV) levels are >3. An RCT in Queensland showed that sunscreen
applied daily reduces the incidence of melanoma and squamous cell carcinoma (SCC) in adults with a previous
history of skin cancer.58,59
Screening of asymptomatic (low-risk) people for melanoma or non-melanocytic skin cancer (NMSC) is not
recommended as there is insufficient evidence available to show that this reduces death.60 A skin cancer screening
program in one region of Germany reported temporary reductions in melanoma mortality; however, this ecological
study may be subject to several biases.61,62
Instead of screening, providing education that raises awareness of the early signs of skin cancer, particularly in
people aged >40 years is recommended. Patients can be assessed opportunistically, or when concerned generally,
or about a specific skin lesion.
9.4.1 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-risk
and high-risk patients
Clinical assessment of future risk of melanoma should take into account:60

• patient’s age and sex
• history of previous melanoma or NMSC
• number of naevi (common and atypical)
• family history of melanoma
• skin and hair pigmentation
• response to sun exposure
• evidence of actinic skin damage.
There are no sufficiently well-validated risk models to assess the combined effects of all these factors.63
Skin self-examination should be encouraged for high-risk individuals every three months and clinical examination
every six months (B).63,64
114 9th edition
Table 9.4.1.1. Melanocytic skin cancer: Identifying risk

Average risk: Primary preventive Opportunistically 60
• Medium/dark skin colour and no other risk factors advice (III, B)
Increased risk: Primary preventive Opportunistically 60, 65

• Family history of melanoma in first-degree relative advice and examination
(relative risk [RR] = 1.7) of skin (III, B)
• Fair complexion, a tendency to burn rather than tan,
the presence of freckles, high naevus count (>100),
light eye colour, light or red hair colour
• Presence of actinic damage (RR = 2)
• Past history of non-melanocytic skin cancer (NMSC)
(<40 years of age higher risk)
• People with childhood high levels of ultraviolet (UV)
exposure and episodes of sunburn in childhood
(RR = 2)
High risk (Risk >6 times normal): Preventive advice, Every 6-12 66
• Previous history of melanoma (RR >10) examination of skin (with months (Practice
64
• >5 atypical (dysplastic) naevi (RR = 6) or without photography) Point)
and advice on self
Frequency
examination (III, C)
of follow-up
examinations for
people who have
had melanoma
is based on
disease stage
RR, relative risk; NMSC, non-melanocytic skin cancer; UV ultraviolet

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115
Table 9.4.I.2. Melanocytic skin cancer: Preventive interventions

Sun All people (especially children aged <10 years) should be advised to be ‘sun smart’: 60, 67
protection Adopt protective measures during sun protection times (when ultraviolet [UV] levels are
advice >3). These measures include use of shade; broad-brimmed, bucket or legionnaire-style
hats; protective clothing; sunglasses; and sunscreens with a sun protection factor (SPF)
> 30 (which need to be reapplied every two hours)
Sun protection times are available from the Bureau of Meteorology. Apps for Apple and
Android tablets and smartphones or desktops provide real-time electronic alerts on
recommended sun protection times, current and maximum UV levels, and information
on recommended exposure for vitamin D. They are adjustable to specific geographic
locations around Australia, and is available at www.sunsmart.com.au
Skin Before examining the skin, it is worth asking about any new, or changes in old skin 60, 68-70
examination lesions. Characteristics of suspicious naevi include asymmetry, border irregularity,
variable colour (including a surrounding coloured halo) and diameter >6 mm (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’)
The 7-point checklist is an alternative method to assess pigmented skin lesions 71-73
and is the only one to have been validated and shown to improve the identification
of melanoma in primary care. A score of >3 is associated with an increased risk of
melanoma
Major features of the lesions (scoring 2 points each):

• change in size
• irregular shape
• irregular colour
Minor features of the lesions (scoring 1 point each):
• largest diameter 7 mm or more
• inflammation
• oozing
• change in sensation
Excision biopsy or referral should be considered for lesions where there is clear suspicion
of melanoma
Training in the use of dermatoscopy and monitoring lesions for three months where
there is diagnostic uncertainty can reduce excision rates of benign skin lesions while
maintaining sensitivity to detect melanoma
Photography aids in monitoring skin lesions by detecting changes over time, and may 74-76
reduce the excision rate of benign lesions
Self- Advise patients to be aware of the specific skin changes that suggest melanoma, be 65, 77
examination encouraged to become familiar with their skin, and be alert for new or changing skin
lesions
Encourage high-risk individuals to perform self-examination, potentially with the aid of

a partner or carer, especially of naevi. Those at high risk may benefit from the use of 78
self-photography. At present, the role of ‘melanoma apps’ on smart phones to support
self-monitoring is not advised given uncertainties about their image quality and accuracy
SPF, sun protection factor; UV ultraviolet
Implementation
GPs over-excise pigmented lesions in people who are younger (aged <40 years) or female, in whom they excise
more benign lesions.75 GPs should be more suspicious of skin lesions in men aged >50 years.75
116 9th edition
9.4.2 Non-melanocytic skin cancer (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
Prevention advice
Opportunistic
case finding
High-risk individuals aged >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 (A).
An RCT in Queensland showed that sunscreen applied daily reduces the incidence of melanoma and SCC in adults
with a previous history of skin cancer.58 In northern Australia and some parts of southern Australia, UV exposure is
sufficiently high to require daily use of sunscreen. For daily information about UV levels, visit the SunSmart widget at
www.sunsmart.com.au/uv-sun-protection/uv/uv-widget
Table 9.4.2.I. Non-melanocytic skin cancer: Identifying risk

Average risk: Preventive advice (III, B) Opportunistically 79
• Those with fair to lighter than
olive skin colour, aged <40 years
without any risk factors
Increased risk: Preventive advice, educate Opportunistically 79

• Fair complexion, a tendency to patients to present to their
burn rather than tan, the presence GP if changes occur in a skin
of freckles, light eye colour, light lesion, and examination of
or red hair colour skin (III, B)
• Family history of skin cancer
• Aged >40 years
• Male
• Presence of multiple solar
keratoses
• People with high levels of
ultraviolet (UV) exposure such as
outdoor workers
High risk: Preventive advice, educate If initial opportunistic 80

• Previous non-melanocytic skin patients to present to their assessment indicates the
cancer (NMSC; up to 60% of GP if changes occur in a need. Every 12 months, or
patients grow another in three skin lesion, examination of when patient develops new
years' time) skin, and advice on self skin lesion (Practice Point)
• Immunosuppressed (eg post examination (III, B)
renal or heart transplant)
• Past exposure to arsenic
NMSC, non-melanocytic skin cancer; UV, ultraviolet

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117
Table 9.4.2.2. Non-melanocytic skin cancer: Preventive interventions

Sun protection Advise all people (especially children aged <10 years) to adopt protective measures 60, 67
advice when ultraviolet (UV) levels are >3. These measures include use of shade; broad
brimmed, bucket or legionnaire-style hats; protective clothing; sunglasses; and use of
sunscreen with sun protection factor (SPF) >30 (which need to be reapplied every two
hours)
Sun protection times are available from the Bureau of Meteorology. ‘SunSmart’
applications for Apple and Android tablets and smartphones or desktops provide real
time electronic alerts on recommended sun protection times, current and maximum UV
levels, and information on recommended exposure for vitamin D. They are adjustable to
specific geographic locations around Australia, and is available at www.sunsmart.com.
au
Skin Precede skin examination by enquiring for relevant history (eg of lesions of concern to 70, 75
examination 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. Consider incision, shave or excision biopsy for histology (or
referral). There are many suitable means to treat non-melanocytic skin cancer (NMSC);
these include surgery, cryotherapy, curettage and cytotoxic and immune modulating
creams
Training in the use of dermoscopy can assist in diagnosis
Self Advise patients to be alert for skin lesion changes 79

examination
NMSC, non-melanocytic skin cancer; SPF, sun protection factor; UV, ultraviolet
9.5 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
Prevention
Human papillomavirus vaccination (B)
For maximal effect, the vaccination should be given prior to the onset of sexual activity. It has no modifying effect
on already acquired human papillomavirus (HPV) infections. It is available as part of the National Immunisation
Program Schedule for girls and boys in year 7.81,82 HPV-vaccinated women still require cervical screening as the
HPV vaccine does not protect against all the types of HPV that cause cervical cancer.
118 9th edition
Screening
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 Papanicolaou (Pap) test or been inadequately screened
in the past 10 years. Women aged >50 years are still under-screened.83
Australia’s National Cervical Cancer Screening Program will change from May 2017. As of that date, women aged
25-74 years, both HPV vaccinated and unvaccinated, will be invited to undertake an HPV test every five years.84
Women of any age who have symptoms (including pain or bleeding) should have appropriate clinical assessment,
which may include a cervical cytology test and an HPV test. Women between 70 and 74 years of age who have
had a regular screening test will be recommended to have an exit HPV test before leaving the cervical screening
program.
A comparison between the current program and the one starting in May 2017 is given in Box A. In the interim,
the National Cervical Cancer Screening program continues to recommend Pap test screening every two years
for women who have ever had sex and have an intact cervix, commencing from 18-20 years of age (or up to two
years after first having sexual intercourse, whichever is later).85
Box A. Comparison of the key aspects of the current national cervical screening program with
that commencing from May 2017
Current recommendations From May 2017
Who? Human papillomavirus (HPV) vaccinated and HPV vaccinated and unvaccinated women
unvaccinated women
What? Pap test screening HPV test
How often? Every two years Every five years
Commencing? From 18-20 years of age From 25 years of age
(or two years after first having sexual intercourse, (or two years after first having sexual
whichever is later) intercourse, whichever is later)
Ending? At 70 years of age for women who have had two Between 70 and 74 years of age
normal Papanicolaou (Pap) tests within the last five
years. Women >70 years of age who have never
had a Pap test, or who request a Pap test, should
be screened
HPV human papillomavirus; Pap, Papanicolaou

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119
Table 9.5.1. Cervical cancer: Identifying risk

What should
Who is at risk? be done? How often? References
Average risk: Papanicolaou All women who have ever been sexually active should 85
• All women who have (Pap) test start having Pap tests between 18 and 20 years of
ever been sexually active (III-2, B) age (or two years after first having sexual intercourse,
whichever is later)
Routine screening with Pap tests should be carried

out every two years for women who have no
symptoms or history suggestive of cervical pathology
(Practice Point)
Pap tests may cease at 70 years of age for women

who had two normal Pap tests within the last five
years. Women aged >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
Increased risk: Pap test It is important to ensure the patient always receives
• Persistent infection (Practice Point) the results of her test
86, 87
with high-risk human Low-grade squamous intraepithelial lesion (LSIL):
papillomavirus (HPV)
• A woman with a Pap test report of possible/definite
types is necessary for the
LSIL should have a repeat Pap test in 12 months
development of cervical
(Practice Point). If the repeat test at 12 months
cancer. Other risk factors
shows LSIL (definite or possible) the woman should
include:
be referred for colposcopy
- immunosuppression
• A woman aged >30 years with a Pap test report
- cigarette smoking of LSIL, without a history of negative smears in the
- use of combined oral preceding two to three years, should be offered
contraception >5 either colposcopy or a repeat Pap test at six
years months (Practice Point)
High-grade squamous intraepithelial lesion (HSIL):
• Refer for colposcopy 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
HPV human papillomavirus; HSIL, high-grade squamous intraepithelial lesion; LSIL, low-grade squamous intraepithelial lesion;
Pap, Papanicolaou
120 9th edition
Table 9.5.2. Tests to detect cervical cancer risk

Papanicolaou A sample of the ectocervix (using an extended tip spatula) then the endocervix (using a 88
(Pap) test 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 five
seconds. If the smear is reported as technically unsatisfactory, it should not be repeated
before six weeks
In postmenopausal women with atrophic changes, it may be necessary to use vaginal

oestrogen for 14-21 days prior to the test. Refer to Chapter 15. Screening tests of
unproven benefit regarding evidence related to bimanual vaginal examination
Human As a primary screening tool: 85, 89, 90

papillomavirus • Current national guidelines do not support the use of HPV testing as a primary
(HPV) testing screening tool. This will change from May 2017
In triage of low-grade squamous intraepithelial lesion (LSIL):
• The use of HPV testing in the triage of LSIL remains under investigation and is not 85, 91-93
currently recommended by the National Cervical Cancer Screening guidelines
In follow-up of high-grade squamous intraepithelial lesion (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 94, 95
cytology not as a substitute. Its addition may be useful when repeating an unsatisfactory smear,
or added if requested by the woman
Self-collection If patients do not agree to undergo Pap (or HPV) testing by a clinician, they can be 84, 96
assisted to collect the sample themselves
HPV human papillomavirus; LSIL, low-grade squamous intraepithelial lesion; HSIL, high-grade squamous intraepithelial lesion
The following resources provide helpful advice:

• Recommended screening tests and the visual appearance of the cervix, www.papscreen.org.au/downloads/
resources/other/cervical_sampling_card.pdf
• HPV: A guide for practitioners, www.papscreen.org.au/downloads/resources/other/hpv-a-guide-for-
practitioners.pdf
Pelvic examination
Screening pelvic examinations for the detection of pathology in asymptomatic, non-pregnant, adult women is not
recommended because there is no evidence of benefit.98 Also refer to Chapter 15. Screening tests of unproven benefit.
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.97
9th edition
121
9.6 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
Screening in asymptomatic, low-risk women is not recommended. Screening methods for ovarian cancer employ
blood tests for cancer antigen (CA) 125, or transabdominal or transvaginal ultrasound. There are three large
randomised trials on ovarian cancer screening: the United States Prostate, Lung, Colorectal and Ovarian trial (PLCO),
which reported in 2011;99 the United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) in late
2015;100 and a European trial, which commenced in 2005 and has not reported yet. The UK trial found a small
reduction in ovarian deaths from CA125, and transvaginal ultrasound for routine population-based screening for
ovarian cancer. However, the results are regarded as preliminary, requiring confirmation and longer follow-up100 and, in
the meantime, the US Preventive Services Task Force (USPSTF) recommends against ovarian cancer screening.101
Table 9.6.1. Ovarian cancer: Identifying risk

Lower risk: No screening 102
• Those who have used the oral
contraception or carried a pregnancy to
term (risk of about half the population
average)
Higher risk: No screening 103

• Family history of ovarian cancer, Consider increased frequency of
especially first-degree relatives and screening for breast and colorectal
more than one relative (risk of about 3 cancer (CRC)
times the population average)
• Presence of the genes BRCA1 or
104
BRCA2
CRC, colorectal cancer
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.105,106 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 106-108
(Practice Point) (Practice Point)
Those with a history of cryptorchidism (relative
risk [RR] = 3.5-17 above average), orchidopexy,
testicular atrophy, or previous testicular cancer
(RR = 25-28)
RR, relative risk

122 9th edition
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comparing trends in melanoma mortality in regions with Dermatol 2001;45(2):260-76.
and without screening. Cancer 2012;118(21):5395-402. 78. Kassianos AP, Emery JD, Murchie P, Walter FM.
63. Usher-Smith JA, Emery J, Kassianos AP, Walter FM. Risk Smartphone applications for melanoma detection by
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Cancer Epidemiol Biomarkers Prev 2014;23(8):1450-63. review. Br J Dermatol 2015;172(6):1507-18.
64. Watts CG, Dieng M, Morton RL, Mann GJ, Menzies SW, 79. National Health and Medical Research Council. Clinical
Cust AE. Clinical practice guidelines for identification, practice guidelines non-melanoma skin cancer:
Guidelines for treatment and management in Australia.
screening and follow-up of individuals at high risk of
Canberra: NHMRC, 2002.
primary cutaneous melanoma: A systematic review. Br J
Dermatol 2015;172(1):33-47. 80. Czarnecki D, Mar A, Staples M, Giles G, Meehan C.
The development of non-melanocytic skin cancers
65. MacKie R, McHenry P, Hole D. Accelerated
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detection with prospective surveillance for cutaneous
1994;189(4):364-67.
malignant melanoma in high-risk groups. Lancet
1993;341(8861):1618-20. 81. Australian Technical Advisory Group on Immunisation.
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66. New Zealand Dermatological Society. New Zealand
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82. Skinner SR, Garland SM, Stanley MA, Pitts M, Quinn MA.
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Human papillomavirus vaccination for the prevention of
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cervical neoplasia: Is it appropriate to vaccinate women
67. Baade PD, Balanda KP, Stanton WR, Lowe JB,
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Del Mar CB. Community perceptions of suspicious
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84. Australian Government Department of Health. National
68. Kelly J, Chamberlain AJ, Staples MP, McAvoy B. Nodular
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melanoma. No longer as simple as ABC. Aust Fam
Health, 2015. Available at www.cancerscreening.gov.
Physician 2003;32(9):706-09.
au/internet/screening/publishing.nsf/Content/future-
69. Scope A, Dusza SW, Halpern AC, Rabinovitz H. The changes-cervical [Accessed 15 November 2015]
‘ugly duckling’ sign: Agreement between observers. Arch
85. National Health and Medical Research Council.
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Screening to prevent cervical cancer: Guidelines for
70. Zalaudek I, Kittler H, Marghoob AA, Balato A. Time the management of asymptomatic women with screen
required for a complete skin examination with and detected abnormalities. Canberra: NHMRC, 2005.
without dermoscopy: A prospective, randomized 86. EUROGIN. Conclusions: Cervical cancer control,
multicenter study. Arch Dermatol 2008;144(4):509-13. priorities and new directions: International charter.
71. National Institute for Health and Care Excellence. France, 2003.
Suspected cancer: Recognition and referral. London: 87. Monsonego J, Bosch FX, Coursaget P, et al. Cervical
NICE, 2015. cancer control, priorities and new directions. Int J Cancer
72. Walter FM, Prevost AT, Vasconcelos J, et al. Using the 2004;108:329-33.
7-point checklist as a diagnostic aid for pigmented skin 88. Buntinx F, Brouwers M. Relation between sampling
lesions in general practice: A diagnostic validation study. device and detection of abnormality in cervical smears:
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adding a diagnostic aid to best practice to manage 89. Mayrand MH, Duarte-Franco E, Rodrigues I, et al.
suspicious pigmented lesions in primary care: Canadian Cervical Cancer Screening Trial Study Group.
Randomised controlled trial. BMJ 2012;345:e4110. Human papillomavirus DNA versus papanicolaou
74. Hanrahan P, CAD’Este SW, Plummer T, Hersey P. screening tests for cervical cancer. N Engl J Med
A randomised trial of skin photography as an aid to 2007;357(16):1579-88.
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90. Koliopoulos G, Arbyn M, Martin-Hirsch P, Kyrgiou M, 103. Kerlikowske K, Brown JS, Grady DG. Should women
Prendiville W, Paraskevaidis E. Diagnostic accuracy with familial ovarian cancer undergo prophylactic
of human papillomavirus testing in primary cervical oophorectomy? Obstet Gynecol 1992;80:700-07.
screening: A systematic review and meta-analysis of non 104. Ford D, Easton DF. The genetics of breast and ovarian
randomized studies. Gynecol Oncol 2007;104(1):232-46. cancer. Br J Cancer 1995;72:805-12.
91. Safaeian M, Solomon D, Wacholder S, Schiffman M, 105. Elford RW. Screening for testicular cancer. Canadian
Castle P. Risk of precancer and follow-up management Task Force on the Periodic Health Examination Canadian
strategies for women with human papillomavirus-negative Guide to Clinical Preventive Health Care. Ottawa: Health
atypical squamous cells of undetermined significance. Canada, 1994; p. 892-98.
Obstet Gynecol 2007;109(6):1325-31. 106. US Preventive Services Task Force. Screening for
92. Arbyn M, Paraskevaidis E, Martin-Hirsch P, Prendiville testicular cancer: Recommendation statement. Rockville,
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of minor cervical lesions, follow-up of women treated for 107. Dieckmann KP, Pichlmeier U. Clinical epidemiology of
high-grade CIN: An update of pooled evidence. Gynecol testicular germ cell tumors. World J Urol 2004;22(1):2-14.
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Martin-Hirsch P, Dillner J. Virologic versus cytologic triage 2012. Available at www.cancer.gov/cancertopics/pdq/
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Randomised controlled trial. BMJ 2007;335(7609):28.
95. Davey E, Barratt A, Irwig L, 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.
96. Arbyn M, Verdoodt F, Snijders PJ, et al. Accuracy of
human papillomavirus testing on self-collected versus
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97. Everett T, Bryant A, Griffin MF, Martin-Hirsch PPL, Forbes
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126 9th edition
10. Psychosocial
General practitioners (GPs) play an important role in the detection and management of mental illness, especially
with prevalent conditions such as depression and anxiety, and social conditions such as intimate partner violence.1
The prevalence of gender-based violence has been estimated at 27.4%.2 In the most recent (2007) 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, 6.2% for affective disorders and 5.1% for substance use
disorders.3 Patients, especially women, who experience underlying intimate partner violence, often present with
depression and anxiety.4
Health inequity
• Socioeconomic disadvantage - The National Survey of Mental Health and Wellbeing 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.3 The likelihood of depression
among low socioeconomic status (SES) persons is almost double that of high SES persons (most marked for
persistent depression).3,5-7 Anxiety and affective disorders are more common in unemployed people.8,9 In patients
with chronic disease and disability, lower educational level and unemployment are predictive of depression.10,11
- Practices in disadvantaged areas have a higher prevalence of depression to identify and manage. Mental
health services overall are used at lower rates by the socioeconomically disadvantaged, possibly related to
low health literacy and stigma.12-14
- Suicide and attempted suicide are consistently associated with markers of SES disadvantage including
limited educational achievement and homelessness.15,16
• Aboriginal and Torres Strait Islander peoples - Aboriginal and Torres Strait Islander peoples are known to be
at greater risk of morbidity and mortality from mental health-related conditions affecting social and emotional
wellbeing. Aboriginal and Torres Strait Islander peoples are hospitalised for mental health problems at twice the rate
of non-Indigenous Australians and experience twice the rate of suicide, rising to five times the rate in the 15-19
years age group.17 Very high psychological distress in Aboriginal and Torres Strait Islander communities may be
related to the risk factors of chronic stress and exposure to violence, racism (including within the health system18
where all concerned have a role to ensure this does not happen), and marginalisation and dispossession.19
• Culturally and linguistically diverse patients (CALD) - 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.20
• Age - Income-related inequalities in the prevalence of psychological distress and common mental health
conditions are particularly common in midlife.21 With advancing age, socioeconomic inequities lead to an
increase in anxiety and depression. Young people with a low level of education have the greatest likelihood of
experiencing chronic depression and progression from anxiety to depression. Socioeconomic disadvantage is
associated with both the incidence and chronic nature of depression and anxiety symptoms in older adults.22
• Childbirth - Postpartum depression and poor childbirth outcomes are associated with socioeconomic
disadvantage.23 Postpartum depression is more common in women from CALD backgrounds and these women
are less likely to receive help.24 Immigrant women experience many barriers to accessing high-quality, equitable
care and are especially vulnerable to stress in the postpartum period, which may result in postnatal depression.25,26
9th edition
127
What can GPs do?

groups (refer to preamble).
• Be aware of the associated stigma of mental illness if offering opportunistic screening for depression to
disadvantaged groups.
• Refer to The Royal Australian College of General Practitioners’ (RACGP) National guide to a preventive health
assessment for Aboriginal and Torres Strait Islander people for important information on offering mental health
care to Aboriginal and Torres Strait Islander patients.27
• Assist women to achieve optimal postpartum health by linking them into social and medical supports, improving
their health literacy and self-efficacy, and promoting positive coping strategies and realistic expectations.28 Early
screening and treatment of women with perinatal mental illness can alleviate symptoms and decrease comorbid
disease risk.29 Culturally appropriate, individual-level interventions may be important.30
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 (eg via practice
nurses; B).31 There is insufficient evidence to recommend routine screening in adults or adolescents where case
management and coordination is not available (C).31 There is insufficient evidence to recommend screening in
children.32 Clinicians should maintain a high level of awareness for depressive symptoms in patients at high risk of
depression and make appropriate clinical assessments wherever the risk is high.33
Table 10.1.1. Depression: Identifying risk

Average risk: Be alert to possible depression, but Opportunistically 31
• Adult population aged >18 years, do not routinely screen unless staff-
where no risk factors for depression assisted depression care supports
are identified are in place (C)
Increased risk: Recurrent screening may be more Opportunistically 31

• Past history of depression useful in people deemed to be
33
• Family history of depression at higher risk of depression (B);
however, in the case of people with
• Other psychiatric disorders,
chronic diseases (eg diabetes, heart
including substance misuse 34
failure, coronary heart disease),
• Chronic medical conditions
a screen-and-treat strategy for
• Unemployment depression has not been shown to
35
• Low socioeconomic status (SES) improve chronic disease symptoms
• Older adults with significant life nor reduce health service use
events (eg illness, cognitive decline, 36
Maintain a high level of clinical
bereavement or institutional
awareness of those at high risk of
placement)
depression and consider depression
• All family members who have when a person presents with
experienced family violence suggestive symptoms such as low
• Lesbian, gay and bisexual peoples mood, insomnia, anhedonia, suicidal
• Experience of child abuse thoughts
128 9th edition

Increased risk Recurrent screening may be more Opportunistically 31
• Pregnant and postpartum women useful in people deemed to be at
higher risk of depression (B)
Risk factors for depression during
pregnancy and postpartum include
poor self-esteem, child care
stress, prenatal anxiety, life stress,
decreased social support, single/
unpartnered relationship status,
history of depression, difficult infant
temperament, previous postpartum
depression, lower SES, and
unintended pregnancy
• Adolescents aged 12-18 years, The benefits of screening alone have At every encounter 32, 37-39
particularly with: not been established, but screening
- family history of depression is recommended where access to
- deliberate self-harm effective treatment and follow up is
available 40, 41
- comorbid mental health or
chronic medical conditions Be alert for signs of depression in this
- experience of a major negative age group (B)
life event (including being bullied)
Consider use of HE2ADS3
assessment tool (refer to Practice
Point m in Table 3.2)
SES, socioeconomic status
Table 10.1.2. Test to detect depression

Question Asking two simple questions may be as effective as longer instruments:
regarding mood • ‘Over the past two weeks, have you felt down, depressed or hopeless?’ 42
and anhedonia • ‘Over the past two 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 33
improves the specificity of a GP diagnosis of depression (IV)
43
In adolescents, consider use of HE2ADS3 assessment tool (refer to Chapter 3.
Preventive activities in children and young people)
In women in the perinatal period, the Edinburgh Postnatal Depression Scale

(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/who-does-it-affect/
pregnancy-and-early-parenthood/edinburgh-postnatal-depression-scale
Refer to Section 10.3. Identification of intimate partner violence, as depression is a

common reason for presentation in those experiencing violence
EPDS, Edinburgh Postnatal Depression Scale

9th edition
129
10.2 Suicide
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 these patients. There is evidence that detecting and
treating depression has a role in suicide prevention.44,45 For example, the incidence of suicide has decreased in
older men and women in association with exposure to antidepressants.31,46
Table 10.2.1. Suicide: Identifying risk

What should be
Who is at risk? done? How often? References
Average risk: No routine screening N/A 47, 48
• General population for suicide (III, C)
Increased risk: Be aware of risk factors Opportunistically 31,44, 48,

• Attempted suicide is a higher risk in the for suicide (III, C) 49
following factors:
- mental illness, especially mood disorders,
and alcohol and drug 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 50
- widowed
51
- living alone or in prison
- chronic and terminal medical illness 35
- in the 12 months following discharge from a

psychiatric hospital
- women experiencing intimate partner
violence
- lesbian, gay and bisexual people
130 9th edition
Table 10.2.2. Tests to detect suicide risk

Evaluate the risk of Assessment of risk involves enquiring into the extent of the person’s 41
suicide in the presence of suicidal thinking and intent, including the following:
risk 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
For all patients with suicidal ideation, enquiry should be made regarding
preparatory actions (eg obtaining a weapon, making a plan, putting affairs
in order, giving away prized possessions, preparing a suicide note)
Screening for The HE2ADS3 tool has questions that can assist in assessing suicide risk. 40
psychological distress in For example:
young people • 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 (eg cutting,
burning or putting yourself in unsafe situations, such as 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 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
Abused women use healthcare services more than non-abused women. They also identify healthcare providers
as the professionals they would most trust with disclosure of abuse.52 Consider asking all pregnant adult and
adolescent women about partner violence during antenatal care.1 There is insufficient evidence for screening
the general population;53 however, there should be a low threshold for asking about abuse, particularly when
the GP suspects underlying psychosocial problems.1 Training GPs to identify violence has resulted in increased
identification and referral to services.54 Inviting women who are fearful of a partner to attend counselling by trained
GPs has resulted in increased safety discussions with women and less depressive symptoms.55 There is some
evidence for the effectiveness of interventions in clinical practice to reduce partner violence.56
9th edition
131
Table 10.3.1. Intimate partner violence: Identifying risk

Average risk: Be alert to possible partner Opportunistically 53
• Adult population aged >18 years, where no violence, but do not routinely
risk factors for intimate partner violence are screen (II, B)
identified
• Adolescents aged 12-18 years, particularly Consider use of HE2ADS3 At every 57

with: assessment tool (refer to encounter
- family history of violence Chapter 3. Preventive activities in
- comorbid mental health conditions children and young people; III, B)
- pregnancy
Increased risk: Screen all pregnant women Opportunistically 1,52, 53

• Pregnant women Maintain a high level of clinical
• People who were abused or witnessed awareness of those at high risk
intimate partner violence as a child of intimate partner violence
• People with psychiatric disorders, especially and consider intimate partner
substance misuse violence when a person presents
• Unemployed people with suggestive symptoms such
• People suffering poverty as symptoms of mental ill health,
chronic unexplained physical
symptoms, and unexplained
injuries (II, B)
Table 10.3.2. Tests to detect intimate partner violence

Ask about Victimised women stress the importance of a trusting doctor-patient relationship, 52
partner confidentiality, and respectful and non-judgemental attitudes to achieving disclosure, as well
violence as 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 >2 years of age 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 World Health Organization (WHO) guidelines recommend that GPs should ask women
who are ‘symptomatic’ (eg show symptoms of mental ill health, chronic unexplained
physical symptoms, unexplained injuries, frequent attendance) about partner violence
Questions and statements to make if you suspect domestic violence:

• Has your partner ever physically threatened or hurt you?
• Is there a lot of tension in your relationship? How do you resolve arguments? 1
• 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
WHO, World Health Organization
These recommendations might apply to people in same-sex relationships and male victims, but there has been
insufficient research in these areas.
132 9th edition
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31. Siu AL, US Preventive Services Task Force. Screening for Association between antidepressant prescribing and
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recommendation statement. JAMA 2016;315(4):380-87. 2003;326(7397):1008-12.
32. Siu AL, US Preventive Services Task Force. Screening for 47. Goldney RD. Suicide prevention. Oxford, UK: Oxford
depression in children and adolescents: US Preventive University Press, 2008.
Services Task Force recommendation statement. Ann Int 48. LeFevre ML, US Preventive Services Task Force.
Med 2016;164(5):360-66. Screening for suicide risk in adolescents, adults, and
33. National Collaborating Centre for Mental Health. older adults in primary care: US Preventive Services
National Institute for Health and Clinical Excellence: Task Force recommendation statement. Ann Intern Med
Guidance. Depression: The treatment and management 2014;160(10):719-26.
of depression in adults (updated edition). Leicester 49. US Preventive Services Task Force. The guide to clinical
(UK): British Psychological Society and Royal College of preventive services 2014: Recommendations of the
Psychiatrists, 2010. US Preventive Services Task Force. Rockville, MD:
34. Health Quality Ontario. Screening and management US Preventive Task Force. 2014. Available at www.
of depression for adults with chronic diseases: An ahrq.gov/professionals/clinicians-providers/guidelines-
evidence-based analysis. Ont Health Technol Assess Ser recommendations/guide/index.html [Accessed 1
2013;13(8):1-45. November 2015].
35. King M, Semlyen J, Tai SS, et al. A systematic review 50. Large MM, Nielssen OB. Suicide in Australia: Meta
of mental disorder, suicide, and deliberate self harm analysis of rates and methods of suicide between 1988
in lesbian, gay and bisexual people. BMC Psychiatry and 2007. Med J Aust 2010;192(8):432-37.
2008;8:70. 51. World Health Organization, Department of Reproductive
36. Canadian Task Force on Preventive Health Care, Joffres Health and Research London School of Hygiene and
M, Jaramillo A, et al. Recommendations on screening for Tropical Medicine, South African Medical Research
depression in adults. CMAJ 2013 Jun 11;185(9):775-82. Council. Global and regional estimates of violence against
37. Lereya ST, Copeland WE, Zammit S, Wolke D. Bully/ women. Prevalence and health effects of intimate partner
victims: A longitudinal, population-based cohort study violence and non-partner sexual violence. Geneva: WHO,
of their mental health. Eur Child Adolesc Psychiatry 2013.
2015;24(12):1461-71. 52. World Health Organization. Responding to intimate
38. Sanci L, Lewis D, Patton G. Detecting emotional disorder partner violence and sexual violence against women.
in young people in primary care. Curr Opin Psychiatry WHO clinical and policy guidelines. Geneva: WHO, 2013.
2010;23(4):318-23. 53. O’Doherty LJ, Taft A, Hegarty K, Ramsay J, Davidson LL,
39. Thapar A, Collishaw S, Pine DS, Thapar AK. Depression Feder G. Screening women for intimate partner violence
in adolescence. Lancet 2012;379(9820):1056-67. in healthcare settings: Abridged Cochrane systematic
40. Chown P, Kang M, Sanci L, Newnham V, Bennett DL. review and meta-analysis. BMJ 2014;348:g2913.
Adolescent health: Enhancing the skills of general 54. Feder G, Davies RA, Baird K, et al. Identification and
practitioners in caring for young people from culturally referral to improve safety (IRIS) of women experiencing
diverse backgrounds - GP resource kit; 2nd edn. domestic violence with primary care training and support
Sydney: NSW Centre for the Advancement of Adolescent programme: A cluster randomised controlled trial. Lancet
Health and Transcultural Mental Health Centre, 2008. 2011;378(9805):1788-95.
41. McDermott B, Baigent M, Chanen A, et al. Clinical 55. Hegarty K, O’Doherty L, Taft A, et al. Screening and
practice guidelines: Depression in adolescents and young counselling in the primary care setting for women
adults. Hawthorn, Vic: beyondblue, 2010. who have experienced intimate partner violence
42. Arroll B, Goodyear-Smith F, Kerse N, Fishman T. Effect (WEAVE): A cluster randomised controlled trial. Lancet
of the addition of a ‘help’ question to two screening 2013;382(9888):249-58.
questions on specificity for diagnosis of depression 56. Bair-Merritt MH, Lewis-O’Connor A, Goel S, et al. Primary
in general practice: Diagnostic validity study. BMJ care-based interventions for intimate partner violence: A
2005;331(7521):884. systematic review. Am J Prev Med 2014;46(2):188-94.
43. Austin MP, Highet N, the Guidelines Expert Advisory 57. Sanci L, Chondros P, Sawyer S, et al. Responding
Committee. Clinical practice guidelines for depression to young people’s health risks in primary care:
and related disorders - anxiety, bipolar disorder and A cluster randomised trial of training clinicians in
puerperal psychosis - in the perinatal period. A guideline screening and motivational interviewing. PLOS ONE
for primary care health professionals. Hawthorn, Vic: 2015;10(9):e0137581.
beyondblue, 2011.
44. Gaynes B N, 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.
134 9th edition
11. Oral health

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
Good oral hygiene and a diet low in sugar help to prevent dental decay and periodontal disease, and improves oral
health in children and adults. There is evidence that the use of fluoride in water, or topically, reduces dental decay in
children.1-3 Although there is insufficient evidence to screen for oral cancer, opportunistic examination of the mouth
and lips is encouraged in increased risk groups.4
Table 11.1. Oral health: Identifying risk of dental decay, periodontal disease and oral cancer
Increased risk: Examination of the mouth, At least every 12
• Lower socioeconomic groups with teeth and lips (IV, C) months (more frequent
5-7
difficulty accessing dental care dental check-ups as
Education regarding prevention
• Elderly (including residential care) determined by dentist
(I, B)
and other dental health
• Aboriginal and Torres Strait Islander
Recommendation of professionals; Practice
peoples
professional or home Point)
• Rural and remote populations application of topical fluoride
• Migrant groups (especially refugees); pastes, gels or mouth rinses
more information is available at (I, A)
http://refugeehealthnetwork.org.au/
category/oral-health
• People with reduced saliva flow (eg
head and neck radiation therapy,
Sjögren syndrome, multiple drug
therapy including psychotropic
medications) 8, 9
*
• Smokers aged >50 years, heavy Opportunistic examination of
drinkers, patients chewing tobacco or the mouth and lips (Practice
betel nut Point)
• Patients exposed to excessive
sunlight (lip cancer)
*Oral cancer references

9th edition
135
Table 11.2. Oral health: Preventive interventions

Education • Advise about the hazards of snacks and sweetened drinks containing high levels of
carbohydrate and acid between meals
• Advise against the use of baby bottles with any fluid apart from water at night 10, 11
• Advise patients to brush teeth twice daily with fluoride toothpaste. A small pea
sized amount of low-fluoride toothpaste should be used from 18 months to 6 years
of age. Encourage to spit not rinse
• Advise patients that adult supervision of tooth-brushing is recommended for 12
children until 8 years of age
• Encourage home use of high-fluoride toothpastes, gels or mouth rinses for children
>10 years of age and adults at high risk
• Advise the use of dental floss daily to prevent gingivitis and periodontal disease 13
• Advise the use of mouthguards for contact sports
• Advise patients of the risks of smoking, chewing tobacco, excessive alcohol
consumption and sunlight exposure 9
• Recommend regular dental check ups 13

• Additional advice can be obtained from the findings of a national consensus
workshop conducted in 2011, available atwww.adelaide.edu.au/arcpoh/oral-
health-promotion/resources/national-consensus-workshop
Oral • Inspect mouth for dental decay, stained, worn or broken teeth, and inflamed or
examination swollen gums
• Advise pregnant women to visit a dentist for treatment of all active dental decay
and periodontal disease
• Inspect mouth for xerostomia (dry mouth). It may present as dry and reddened
gums and increased decay rate particularly on root surfaces
• ‘Lift the lip’ of children 0-5 years of age for early identification of oral problems (also 14, 15
refer to Chapter 3. Preventive activities in children and young people)
• Inspect the oral cavity - buccal mucosa, gums, tongue, floor of mouth and palate
(looking for white or red patches, ulceration or induration)
• Examine the extra-oral areas - neck lips and facial areas - looking for lumps and 9, 16
swellings
Fluoridation • Fluoridation of public water supplies has improved dental health and reduced 1,2
dental decay
• Approximately 90% of Australians now drink fluoridated water. Details regarding
fluoride levels in Australian water supplies and recommended dosages of fluoride 17
are provided atwww.nhmrc.gov.au/health-topics/health-effects-water-fluoridation
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.18
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 locations. People who hold healthcare cards are less likely to receive
preventive dental care and more likely to receive extractions when visiting the dentist.18,19 Aboriginal and Torres
Strait Islander peoples are at higher risk of poor oral health.20
136 9th edition
References
1. Iheozor-Ejiofor Z, Worthington HV, Walsh T, et al. Water 11. Walsh T, Worthington HV, Glenny AM, Appelbe P,
fluoridation for the prevention of dental caries. Cochrane Marinho VC, Shi X. Fluoride toothpastes of different
Database Syst Rev 2015;6:Cd010856. concentrations for preventing dental caries in children
2. McDonagh MS, Whiting PF, Wilson PM, et al. Systematic and adolescents. Cochrane Database Syst Rev
review of water fluoridation. BMJ 2000;321(7265):855- 2010;1:Cd007868.
59. 12. Marinho VC, Worthington HV, Walsh T, Chong LY.
3. World Health Organization. Sugars intake for adults and Fluoride gels for preventing dental caries in children
children. Geneva: WHO, 2015. and adolescents. Cochrane Database Syst Rev
4. US Preventive Services Task Force. The guide to clinical 2015;6:Cd002280.
preventive services: Recommendations of the US 13. National Oral Health Promotion Clearing House. Oral
Preventive Services Task Force. Rockville, MD: USPSTF, health messages for the Australian public. Findings
2014. Available at www.ahrq.gov/professionals/clinicians- of a national consensus workshop. Aust Dent J
providers/guidelines-recommendations/guide/index.html 2011;56(3):331-35.
[Accessed 1 November 2015]. 14. Department of Health. Evidence-based oral health
5. National Health and Medical Research Council. Review promotion resource. Melbourne: Prevention and
of water fluoridation and fluoride intake from discretionary Population Health Branch, 2011.
fluoride supplements. Canberra: NHMRC, 1999. 15. NSW Health. Early childhood oral health guidelines for
6. Ahovuo-Saloranta A, Forss H, Hiiri A, Nordblad A, Makela child health professionals. Sydney: Centre for Oral Health
M. Pit and fissure sealants versus fluoride varnishes Strategy, 2014. Available at www0.health.nsw.gov.au/
for preventing dental decay in the permanent teeth of policies/gl/2014/GL2014_020.html [Accessed 21 March
children and adolescents. Cochrane Database Syst Rev 2016].
2016;1:Cd003067. 16. Sugerman PB, Savage NW. Current concepts in oral
7. Sievers K, Silk H. Fluoride varnish for preventing dental cancer. Aust Dent J 1999;44(3):147-56.
caries in children and adolescents. Am Fam Physician 17. Neil A. The extent of water fluoridation coverage in
2016;93(9):743-44. Australia. Aust N Z J Public Health 2011;35(4):392-93.
8. US Preventive Services Task Force. Oral cancer: 18. Sanders A. Social determinants of oral health: Conditions
Screening. Rockville, MD: USPSTF, 2014. Available at linked to socioeconomic inequalities in oral health in the
www.uspreventiveservicestaskforce.org/Page/Document/ Australian population. Canberra: Australian Institute of
UpdateSummaryFinal/oral-cancer-screening1 [Accessed Health and Welfare, 2007.
1 November 2015]. 19. Chrisopoulos S, Harford J. Oral health and dental care in
9. Smith RA, Cokkinides V, Brooks D, Saslow D, Shah M, Australia: Key facts and figures 2012. Canberra: AIHW,
Brawley OW. Cancer screening in the United States, 2013.
2011: A review of current American Cancer Society 20. National Aboriginal Community Controlled Health
guidelines and issues in cancer screening. CA Cancer J Organisation and The Royal Australian College of General
Clin 2011;61(1):8-30. Practitioners. National guide to a preventive health
10. Marinho VC, Higgins JP, Sheiham A, Logan S. Fluoride assessment for Aboriginal and Torres Strait Islander
toothpastes for preventing dental caries in children people. 2nd edn. South Melbourne, Vic: RACGP, 2012.
and adolescents. Cochrane Database Syst Rev
2003;1:Cd002278.
9th edition
137
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
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). General practitioners (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.1,2
Table 12.1. Glaucoma: Identifying risk

Increased risk: Refer for ocular Frequency of follow 1,2
• Family history of glaucoma (first-degree relatives) examination 5-10 years up determined by the
• Caucasian and Asian patients aged >50 years earlier than the age of individual patient’s eye
onset of glaucoma in the assessment
• Patients of African descent aged >40 years
affected relative (A)
Higher risk: Refer for examination Frequency of follow 1,2

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

Patient education Educate patients about glaucoma and alert them to associated risk factors, 1,2
with advice to attend regular, fully comprehensive eye examinations
Tonometry Applanation or puff 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 of 1,2
(ophthalmoscopy) choice
References
1. National Health and Medical Research Council. A guide to 2. National Health and Medical Research Council. Guidelines
glaucoma for primary health care providers - A companion for the screening, prognosis, diagnosis, management and
document to NHMRC Guidelines for the screening, prevention of glaucoma. Canberra: NHMRC, 2010.
prognosis, diagnosis, management and prevention of
glaucoma. Canberra: NHMRC, 2010.
138 9th 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 for urinary incontinence in the general population. Instead, GPs should case-find
those at higher risk (B).
Within the general population, up to 19% of children,1 13% of men and 37% of women may be affected by some
form of urinary incontinence.2 While urinary incontinence is most common in women and increases with age,
bedwetting (enuresis) is common in children (5.5% of children also report daytime wetting).1 In men, uncomplicated
lower urinary tract symptoms do not appear to be associated with an increased risk of prostate cancer.3 Of those
sitting in a GP waiting room, 65% of women and 30% of men report some type of urinary incontinence, yet only
31% of these people report having sought help from a health professional.4 Primary care professionals are in a
position to take a more proactive approach to incontinence treatment by asking about 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.5
Table 13.1. Urinary incontinence: Identifying risk

Who is at higher risk of urinary
incontinence? What should be done? How often? References
Average risk: There is no evidence to support N/A
screening (IV)
Higher risk: Case finding (IV, B) Every 12 2

• Prenatal and postnatal women months
Ask about the occurrence of urinary
• Women who have had children incontinence
• Women who are overweight
• Women reporting constipation
• People with respiratory conditions,
diabetes stroke, heart conditions,
recent surgery, neurological disorders
• Frail elderly people or long-term care In residential aged care facilities,
residents residents are automatically assessed
Table 13.2. Urinary incontinence: Preventive interventions

Case finding Probing questions such as ‘Other people with ... [state conditions of higher risk here] 6
have had problems with their waterworks [bladder control] ...'
Simple patient survey assessment tools have been shown to be valid and reliable (A)
9th edition
139

Assessment 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 and/or overflow
There are four common types of incontinence:

1. Stress incontinence is the leaking of urine that 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
2. Urge incontinence is a sudden and strong need to urinate. It is often associated
with frequency and nocturia, and is often due to having an over-active or unstable
bladder, neurological condition, constipation, enlarged prostate or history of poor
bladder habits
3. Mixed incontinence is a combination of stress and urge incontinence, and is most
common in older women
4. Overflow incontinence as a result of bladder outflow obstruction or injury. Its
symptoms may be confused with stress incontinence
Because treatments differ, urge incontinence should be distinguished from stress
incontinence (A)
To make this distinction, the International Continence Society guidelines recommend an 7

extensive evaluation that is too time-consuming for primary care practice
However, the 3 Incontinence Questions (3IQ) questionnaire is a simple, quick, and

8, 9
non-invasive test with acceptable accuracy for classifying urge and stress incontinence,
and may be appropriate for use in primary care settings (A). The questionnaire is
provided in Appendix 13A
The Continence Foundation of Australia (CFA) has a helpline available for consumers and healthcare professionals at
1800 33 00 66. Consumers can ask for specific help or for contact details of their nearest continence professional. The
CFA website has many evidence-based resources available for consumers at www.continence.org.au/resources.php
References
1. Bower W, editor. An epidemiological study of enuresis in 7. Staskin D, Kelleher C, Avery K, et al, editors. Committee
Australian children. Sydney: Wells Medical, 1995. 5: Initial assessment of incontinence. Proceedings of the
2. Continence Foundation of Australia. What is fourth international consultation on incontinence. Paris:
incontinence: Key statistics. Brunswick, Vic: CFA, 2015. Health Publication Ltd, 2009.
Available at www.continence.org.au/pages/key-statistics . 8. Brown J, Bradley C, Subak L, Richter H, Kraus S,
html [Accessed 2015 September]. Brubaker L. The sensitivity and specificity of a simple test
3. Martin RM, Vatten L, Gunnell D, Romundstad P, Nilsen to distinguish between urge and stress incontinence. Ann
TI. Lower urinary tract symptoms and risk of prostate Intern Med 2006;144:715-23.
cancer: The HUNT 2 Cohort, Norway. Int J Cancer 9. Hess R, Huang AJ, Richter HE, et al. Long-term efficacy
2008;123(8):1924-28. and safety of questionnaire-based initiation of urgency
4. Byles J, Chiarelli P, Hacker A, Bruin C. Help seeking for urinary incontinence treatment. Am J Obstet Gynecol
urinary incontinence: A survey of those attending GP 2013;209(3):244, e1-9.
waiting rooms. Aust Continence J 2003;9(1):8-15.
5. 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.
6. 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.
140 9th edition
Appendix 13A. The 3 Incontinence Questions (3IQ)

1. During the last three months, have you leaked urine (even a small amount)?
d Yes d No —► Questionnaire completed.

2. During the last three months, did you leak urine (check all that apply):
a. d When you were performing some physical activity, such as coughing, sneezing, lifting, or exercise?
b. d When you had the urge or feeling that you needed to empty your bladder, but you could not get to the
toilet fast enough?
c. d Without physical activity and without a sense of urgency?
3. During the last three months, did you leak urine most often (check only one):
a. d When you are performing some physical activities, such as coughing, sneezing, lifting, or exercise?
b. d When you had the urge or feeling that you needed to empty your bladder, but you could not get to the
toilet fast enough?
c. d Without physical activity or a sense of urgency?
d. d About equally as often with physical activities as with a sense of urgency?
Definitions of the type of urinary incontinence are based on responses to Question 3

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
Reproduced with permission from Brown JS, Bradley CS, Subak LL, et al. The sensitivity and specificity of a simple test to distinguish
between urge and stress incontinence. Ann Intern Med 2006;144(10):715-23.
9th edition
141
14. Osteoporosis
Age 0-9 10-14 20-24 15-19 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-79 >80
Women
Men
The goal of the prevention and treatment of osteoporosis is to reduce a person’s overall fracture risk, not just to
maintain bone density.
Review of fracture risk factors for postmenopausal women aged >45 years and men aged >50 years is
recommended (Practice Point). Those with increased risk should have bone density assessed (Practice Point).
Osteoporosis is a disease characterised by low bone mass and micro-architectural deterioration of bone tissue,
leading to bone fragility and increased fracture risk.1 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 bone mineral density (BMD) as a T-score of <-2.5. However, age, lifestyle factors, family history, and
some medications and diseases contribute to bone loss and increased risk of fragility fractures. Furthermore, it is
important to note that in an individual who has sustained a fragility fracture, a T-score of <-2.5 is not also required
to make the diagnosis of osteoporosis, the presence of a fragile fracture is sufficient. Thus, the goal of prevention
and treatment is to reduce a person’s overall fracture risk (not just maintain bone density).
Two of the most widely validated methods to estimate absolute fracture risk for osteoporotic fractures relevant to
the Australian population are available at:
• www.shef.ac.uk/FRAX
• www.garvan.org.au/promotions/bone-fracture-risk/calculator
These calculators can be used with and without measuring BMD, though the Garvan fracture risk calculator
has not been validated in an external cohort when BMD has not been used in the calculator.2 Risk estimation is
imperfect, with the tools being modest predictors of fracture risk.3,4 Risk factors (eg falls, glucocorticoid use) not
included in one or the other risk algorithm require clinical judgement to modify the risk estimate.
To date, there are no randomised controlled trials (RCTs) directly evaluating screening effectiveness, harms and
intervals, and whether screening is performed by bone density screening by dual-energy X-ray absorptiometry
(DXA) or by estimating absolute fracture risk.4 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.
142 9th edition
Table 14.1. Osteoporosis: Identifying risk

Average risk: Clinical assessment for Every 12 months (Practice 1,3, 5
• Postmenopausal women (aged >45 risk factors (Practice Point)
years) Point)
• Men aged >50 years Preventive advice (II, C)
Increased risk: Dual X-ray absorptiometry The optimal timing of 3, 5-8

• Aged >60 years for men and >50 years (DXA) to measure bone repeated DXA for screening
for women plus any of: mineral density (BMD) is unknown but is likely to
- family history of fragility fracture and management of vary depending on baseline
risk factors (II, A to III, D BMD
- smoking
depending on risk factor)
- high alcohol intake (>4 standard drinks Women with baseline
per day for men and >2 for women) Investigate for causes of T-score >-1.0 may take
- vitamin D deficiency <50 nmol secondary osteoporosis longer than 15 years to
(screening for vitamin D not indicated if indicated by history, transition to osteoporosis
just for risk assessment)
* examination findings or
Repeat only when it is likely
BMD result (Practice
- low body weight (body mass index to change management
Point)
[BMI] <20kg/m2) (II, C)
- recurrent falls
Where there is a specific
- low levels of physical activity2 condition or medication
- immobility (to the extent that person present likely to lead to
cannot leave their home or cannot do accelerated bone loss (eg
any housework) corticosteroid use [refer
• Medical conditions and medications to causes of secondary
that may cause secondary osteoporosis osteoporosis]), consider
including: more frequent repeat of
- endocrine disorders DXA (Practice Point)
(eg hypogonadism, Cushing
syndrome, hyperparathyroidism,
hyperthyroidism)
- premature menopause
- anorexia nervosa or amenorrhea for
>12 months (unrelated to pregnancy)
before 45 years of age
- inflammatory conditions
(eg rheumatoid arthritis)
- malabsorption (eg coeliac disease)
- chronic kidney or liver disease
- multiple myeloma and monoclonal
gammopathies
- human immunodeficiency virus (HIV)
and its treatment
- Type 1 and type 2 diabetes mellitus
- drugs, especially corticosteroids
(eg 7.5 mg for >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 (SSRIs)
9th edition
143

High risk of further fracture: DXA to measure BMD DXA at presentation and no 1
• Patients aged >45 years who have and management of risk more than every two years
sustained a low-trauma fracture factors (II, A) (II, B).
• Postmenopausal women, and older men Investigate for causes of It is appropriate to
with a vertebral fracture. Such fractures secondary osteoporosis recommend a repeat
should be ruled out if clinically suspected if indicated by history, BMD by DXA after two
(eg from loss of height >3 cm, kyphosis, examination findings or years for patients at risk of
back pain) BMD result (Practice developing osteoporosis,
Point) to assist in re-evaluation of
fracture risk
Recommend that such
individuals are initiated on In patients with confirmed
effective anti-osteoporosis osteoporosis, repeat BMD
therapy unless there are is generally not required;
specific contraindications however, it may be
conducted before initiating
a change in, or cessation of,
anti-osteoporotic therapy
(Practice Point)
Where there is a specific

condition or medication
present likely to lead to
accelerated bone loss (eg
corticosteroid use [refer
to causes of secondary
osteoporosis]), consider
more frequent repeat of
DXA (Practice Point)
*Assessment of the potential clinical importance of a given serum vitamin D level should take into consideration the season in which
the test was done, as levels in an individual will be higher from late spring to autumn than in winter to early spring6,9 (Practice Point)
There is no accepted cut-off or standard definition for defining low levels of physical activity as a risk factor for osteoporosis. Those at
+
risk would include people with higher levels of sedentary behaviour, (eg those who participate in no recreational exercise,10 or who are
sitting and lying for more than 20 hours per day).11 It also includes those who perform relatively low levels of weight bearing physical
activity (eg people who walk less than 60 minutes per day,11 less than 12 km per week,12 or do not walk for exercise)10
BMD, bone mineral density; BMI, body mass index; DXA, dual X-ray absorptiometry; HIV human immunodeficiency virus; SSRI,
selective serotonin reuptake inhibitor
144 9th edition
Table 14.2. Osteoporosis: Preventive interventions

Assessment of risk Take a thorough history, paying particular attention to the risk factors above plus:
factors • vertebral deformity (if has occurred within 5-10 years, this creates an
equivalent risk to any other fragility fracture)
• loss of height (>3 cm) and/or thoracic kyphosis (consider lateral spine X-ray
for vertebral deformity)
Preventive actions Encourage a daily dietary calcium intake that meets the age-appropriate 13-19
Australian recommended daily intake (1000 mg for adult men until 70 years of
age and women until 50 years of age, 1300 mg after this age; prevention of
bone loss [I, A] but not for fracture prevention [III-2, D])
Encourage healthy lifestyle (eg smoking cessation and limiting alcohol intake) (D)
Education and psychosocial support for risk factor modification (Practice Point)
Falls reduction strategies: Falls (I, A), and fracture risk reduction (Practice Point)
Encourage regular weight-bearing and resistance exercise for the prevention of

falls (I, A), bone loss (I, A) and fracture risk reduction (I, C)
Advise on appropriate sun exposure levels (which minimise the risk of skin
cancer) as a source of vitamin D (II, C)
*
Discuss absolute risk of fracture (Practice Point)
Bone mineral BMD should be measured by dual X-ray absorptiometry (DXA) scanning 8, 20
densitometry (BMD) performed on two sites, preferably antero-posterior spine and hip. Without
bone-losing medical conditions (eg hypogonadism, anti-gonadal therapy or
corticosteroid use), BMD is unlikely to change significantly in <2 years (II, B)
DXA should generally be repeated only when patient is at risk of reaching

treatment thresholds (average decrease in T-score is usually approximately
0.1/year if no specific bone-losing medical conditions; Practice Point)
*Population screening for vitamin D deficiency is not recommended, but targeted testing of people who are at risk of osteoporosis
and/or 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 (ie <30 nmol/L) and so is less
likely to be corrected by low-risk levels of sun exposure 21 (Practice Point)
BMD, bone mineral density; DXA, dual X-ray absorptiometry
Quantitative ultrasound
An alternative imaging technique for assessing fracture risk is quantitative ultrasound, which measures parameters
such as speed of sound (SOS) and broadband ultrasound attenuation (BUA), with these values being combined
into composite parameters such as stiffness index. These parameters predict fracture to a similar degree as
DXA measures of BMD. However, there is no agreed definition of osteoporosis using quantitative ultrasound,
and it cannot be used to assess the response to osteoporosis treatment.22 Moreover, intervention trials have
predominantly been based on cases identified through DXA assessment, so their results cannot readily be applied
to individuals identified by other means.1,3 For this reason, DXA remains the recommended method of assessment.
9th edition
145
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.23,24 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. This is unlikely given the range of treatments now available.
Optimal treatment necessitates the use of a specific anti-osteoporosis treatment such as a bisphosphonate, but
also includes ensuring adequate calcium intake and correcting vitamin D deficiency.
There are inequities in the use of BMD measurement with relative underuse in men and people from rural and
remote locations.25
There is insufficient evidence to support population screening of younger women by DXA. However, if a DXA is
performed for a clinical indication, the results could be used opportunistically to improve bone health via feedback
of relative fracture risk. In women aged 25-45 years, written feedback of being at high risk compared to not at
high risk of fracture in later life (based on mean DXA hip and lumbar spine T-score being less than or greater than
or equal or zero) resulted in improved osteoporosis preventive behaviours and femoral neck BMD at two26 and 12
years.27
References
1. The Royal Australian College of General Practitioners. Osteoporotic Fractures Research Group. N Engl J Med
Clinical practice guideline for the prevention and 1995;332(12):767-73.
treatment of osteoporosis in postmenopausal women 11. Coupland C, Wood D, Cooper C. Physical inactivity is an
and older men. South Melbourne, Vic: RACGP, 2010. independent risk factor for hip fracture in the elderly. J
2. Marques A, Ferreira RJ, Santos E, Loza E, Carmona L, Epidemiol Community Health 1993;47(6):441-43.
da Silva JA. The accuracy of osteoporotic fracture risk 12. Krall EA, Dawson-Hughes B. Walking is related to
prediction tools: A systematic review and meta-analysis. bone density and rates of bone loss. Am J Med
Ann Rheum Dis 2015;74(11):1958-67. 1994;96(1):20-26.
3. Nelson HD, Haney EM, Chou R, Dana T, Fu R, 13. National Osteoporosis Foundation. Clinician’s guide to
Bougatsos C. Screening for osteoporosis: Systematic prevention and treatment of osteoporosis. Washington,
review to update the 2002 US Preventive Services Task DC: National Osteoporosis Foundation, 2014.
Force Recommendation. Rockville, MD: USPSTF, 2010. 14. Ebeling PR, Daly RM, Kerr DA, Kimlin MG. Building
4. Rubin KH, Friis-Holmberg T, Hermann AP, Abrahamsen healthy bones throughout life: An evidence-informed
B, Brixen K. Risk assessment tools to identify women strategy to prevent osteoporosis in Australia. Med J Aust
with increased risk of osteoporotic fracture: Complexity 2013;199(7 Suppl):S1.
or simplicity? A systematic review. J Bone Miner Res 15. Bolland MJ, Leung W, Tai V, et al. Calcium intake and risk
2013;28(8):1701-17. of fracture: Systematic review. BMJ 2015;351:h4580.
5. US Preventive Services Task Force. Screening for 16. Tai V, Leung W, Grey A, Reid IR, Bolland MJ. Calcium
osteoporosis: Clinical summary of US Preventive Services intake and bone mineral density: Systematic review and
Task Force Recommendation: Rockville, MD: USPSTF, meta-analysis. BMJ 2015;351:h4183.
2011.
17. Gillespie LD, Robertson MC, Gillespie WJ, et al.
6. Nowson CA, McGrath JJ, Ebeling PR, et al. Vitamin D Interventions for preventing falls in older people living
and health in adults in Australia and New Zealand: A in the community. Cochrane Database Syst Rev
position statement. Med J Aust 2012;196(11):686-87. 2012;9:CD007146.
7. Maurel DB, Boisseau N, Benhamou CL, Jaffre C. Alcohol 18. Howe TE, Shea B, Dawson LJ, et al. Exercise
and bone: Review of dose effects and mechanisms. for preventing and treating osteoporosis in
Osteoporos Int 2012;23(1):1-16. postmenopausal women. Cochrane Database Syst Rev
8. Gourlay ML, Fine JP, Preisser JS, et al. Bone-density 2011;7:CD000333.
testing interval and transition to osteoporosis in older 19. Kemmler W, Haberle L, von Stengel S. Effects of exercise
women. N Engl J Med 2012;366(3):225-33. on fracture reduction in older adults: A systematic review
9. Bolland MJ, Grey AB, Ames RW, et al. The effects of and meta-analysis. Osteoporos Int 2013;24(7):1937-50.
seasonal variation of 25-hydroxyvitamin D and fat mass 20. Frost SA, Nguyen ND, Center JR, Eisman JA, Nguyen TV.
on a diagnosis of vitamin D sufficiency. Am J Clin Nutr
Timing of repeat BMD measurements: Development of
2007;86(4):959-64. an absolute risk-based prognostic model. J Bone Miner
10. Cummings SR, Nevitt MC, Browner WS, et al. Risk Res 2009;24(11):1800-07.
factors for hip fracture in white women. Study of
146 9th edition
21. Winzenberg T, van der Mei I, Mason RS, Nowson C, by sex and rural versus urban location. Med J Aust
Jones G. Vitamin D and the musculoskeletal health of 2009;190(3):126-28.
older adults. Aust Fam Physician 2012;41(3):92-99. 26. Winzenberg T, Oldenburg B, Frendin S, De Wit L, Riley
22. Schousboe JT, Shepherd JA, Bilezikian JP, Baim S. M, Jones G. The effect on behavior and bone mineral
Executive summary of the 2013 International Society for density of individualized bone mineral density feedback
Clinical Densitometry Position Development Conference on and educational interventions in premenopausal women:
bone densitometry. J Clin Densitom 2013;16(4):455-66. A randomized controlled trial [NCT00273260]. BMC
23. Barrack CM, McGirr EE, Fuller JD, Foster NM, Ewald Public Health 2006;6:12.
DP. Secondary prevention of osteoporosis post minimal 27. Wu F, Laslett L, Wills K, Oldenburg B, Jones G,
trauma fracture in an Australian regional and rural Winzenberg T. Effects of individualised bone density
population. Aust J Rural Health 2009;17(6):310-15. feedback and educational interventions on osteoporosis
24. National Institute of Clinical Studies. Evidence - Practice knowledge and self-efficacy in young women: A 12-yr
gaps report. Melbourne: NICS, 2005. prospective study. Plenary poster P11, ANZBMS
23rd Annual Scientific Meeting; Hilton on the Park,
25. Ewald DP, Eisman JA, Ewald BD, et al. Population rates
of bone densitometry use in Australia, 2001-2005, Melbourne, 2013.
9th edition
147
15. Screening tests of unproven benefit

The following are not recommended as screening tests in low-risk or asymptomatic general practice populations.
These tests may have a separate 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
Genomic sequencing Genetic risk Limited evidence on the balance of benefits and harms, 1-5
ethical issues and uncertain utility in an asymptomatic
adult
Genetic testing - Venous The MTHFR test has minimum clinical utility and is 6
thrombo not recommended in the evaluation of thrombophilia,
methylenetetrahydrofolate
embolism recurrent pregnancy loss, or assessment of risk of
reductase (MTHFR)
coronary artery disease or any other condition
Genetic testing - Alzheimer’s ApoE testing is not recommended to assess risk of 6

disease Alzheimer’s disease due to its poor predictive value and
apolipoprotein E (ApoE)
the lack of preventive options
Vascular
Coronary computed Coronary No randomised controlled trial (RCT) evidence. RCTs of 7-11
*
tomography angiography artery disease therapy show no effect on coronary artery progression
(CCTA) (CAD)
May be of benefit in those at moderate risk of CAD -
but not in:
• asymptomatic persons
• subjects with known significant CAD
• subjects with a high pre-test probability of CAD
Computed tomography (CT) Coronary heart Usually not appropriate in a low-risk asymptomatic 8, 9, 11-13
calcium scoringt disease (CHD) population, but may be of possible value in risk
reclassification in those at moderate risk
Serum homocysteine CHD Value as a risk factor for CHD is uncertain and 14-18
published RCTs show no evidence of benefit by
lowering levels
Exercise electrocardiogram CHD Low yield and high false-positive rate given low 14, 19-22
(ECG) prevalence in asymptomatic population
High sensitivity C-reactive Cardiovascular Insufficient evidence to support the role of hsCRP in 14, 22-29
protein (hsCRP) disease (CVD) preventive screening of asymptomatic patients
Ankle:brachial index (ABI) Peripheral Current evidence is insufficient to assess benefits 28, 30-37
vascular and costs of using ABI to screen for peripheral
disease vascular disease
148 9th edition

Carotid artery ultrasound Asymptomatic It is no longer justifiable to screen for the presence of 38-43
carotid artery asymptomatic carotid artery stenosis to select patients
stenosis for carotid procedures. There is no current evidence
of patient benefit. However, there is evidence of harms
from screening, including significant procedural risk
and cost
Carotid stenting cannot be recommended because

it causes about twice as many strokes or deaths as
carotid endarterectomy (CEA), a risk that is not offset
by the CEA risk of myocardial infarction
Also, asymptomatic carotid artery stenosis patients

with particularly high ipsilateral stroke risk who benefit
from CEA, in addition to current optimal medical
treatment alone, have not been identified. Evidence
is insufficient to allow reliable risk stratification. For
example, degree of stenosis within the 50-99%
range, asymptomatic stenosis progression, plaque
echolucency and transcranial Doppler embolus
detection are not specific enough to identify patients
likely to benefit from CEA
A research priority is to find out if screening to detect

asymptomatic carotid artery stenosis improves medical
treatment and patient outcomes over screening for,
and optimal treatment of, other established vascular
risk factors
Cancer
Magnetic resonance Breast cancer Ongoing surveillance strategies for women at high 44-51
imaging (MRI) risk of breast cancer may include imaging with MRI.
A Medicare rebate is available for MRI scans for
asymptomatic women <50 years of age at high risk of
breast cancer
There is no evidence for MRI as a stand-alone

screening test for women at average risk of breast
cancer
Thermography Breast cancer Thermography is associated with high false-positive 52, 53

and false-negative rates. There is insufficient evidence
to support the use of thermography in breast cancer
screening or as an adjunctive tool to mammography
Single nucleotide Breast cancer Use of a SNP-based breast cancer risk assessment 46, 54-56
polymorphism (SNP) testing test should only be undertaken after an in-depth
discussion led by a clinical professional familiar with the
implications of genetic risk assessment and testing,
including the potential insurance implications
Genetic testing should be offered only with pre-test

and post-test counselling to discuss the limitations,
potential benefits, and possible consequences
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149

Cancer antigen (CA)125/ Ovarian cancer There is no evidence to support the use of any 46, 57-61
transvaginal ultrasound test - including 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
The recently reported UK Collaborative Trial of Ovarian

Cancer Screening (UKCTOCS) trial of transvaginal
ultrasound +/- CA125 found no significant difference in
mortality over 0-14 years
Secondary analyses suggest a possible benefit of

screening using transvaginal ultrasound and CA125,
but further follow-up is needed before firm conclusions
can be reached on the long-term efficacy and cost
effectiveness of ovarian cancer screening
Optical colonoscopy or Colorectal These have good sensitivity for cancer and advanced 62-69
computed tomography (CT) cancer (CRC) polyps, and are more acceptable than colonoscopy,
colonography* but there is no current evidence of the reduction of
CRC mortality. There are several trials under way to
assess effectiveness and cost effectiveness of this as a
screening strategy
Neither optical colonoscopy nor CT colonography are

recommended for primary screening because there is
no current RCT evidence of effectiveness in relation to
any harms
Whole-body CT or MRI Cancer Whole-body imaging has not been shown to improve 70-77
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
Lung disease
Spirometry Chronic Screening with spirometry in the absence of symptoms 78-83

obstructive has no net benefit
pulmonary
Opportunistic case-finding should be considered in
disease
high-risk individuals. These include those aged >40
(COPD)
years, plus either:
• symptoms (chronic cough, increased sputum
production, wheezing or dyspnoea)
• history of exposure to relevant environmental factors
such as cigarette smoke
Several questionnaires§ are useful and if positive,
should be followed by spirometry by a trained
professional (consensus statement)
150 9th edition

Endocrine
Thyroid function tests Thyroid Despite the relatively high incidence of subclinical 84-89
dysfunction hypothyroidism 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
There is no evidence supporting an increased risk for

stroke associated with subclinical thyroid dysfunction
More research is needed to determine the clinical

benefits associated with thyroid screening
Chronic disease prevention
Vitamin D Vitamin D Current evidence is insufficient to assess the balance 90-97

deficiency of benefits and harms of screening for vitamin D
deficiency in asymptomatic adults
Heel ultrasound Osteoporosis While there is some evidence that heel ultrasound in 98-103
combination with femoral neck bone densitometry
better predicts hip fracture, there are no RCTs showing
any benefit of using heel ultrasound as the primary
screening tool for osteoporosis, nor is its usefulness as
a pre-screening tool in tandem with dual-energy X-ray
absorptiometry (DXA) proven
Infection
Mid-stream urine (MSU) Asymptomatic Identifying and treating non-pregnant adults with 104, 105
culture bacteriuria asymptomatic bacteriuria does not improve outcomes
(elderly) and may increase antibiotic resistance. The only two
exceptions to this are pregnancy and a patient who is
about to undergo a urological procedure
Other tests
Enquiry about sleep Obstructive The prevalence of undiagnosed OSA is high and it is 106-109
sleep apnoea associated with considerable morbidity. While there are
(OSA) some screening tools that are available, there are no
large-scale RCTs showing the benefit or cost-benefit of
routine screening for OSA in primary care
Case-finding for OSA may be beneficial in commercial

vehicle drivers and pilots, but it has not been mandated
by any government authority
Bimanual pelvic exam During a A bimanual examination performed as part of routine 110-113
routine Pap smear examination is of no proven benefit, but
Papanicolaou studies are limited
(Pap) test in an
It has been shown to be not an effective screening
asymptomatic
method for ovarian cancer detection
woman
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151
*CCTA involves the use of multi-slice CT and intravenously administered contrast material to obtain detailed images of the blood vessels
of the heart. It has been used as an alternative to conventional invasive coronary angiography for evaluating CAD and coronary artery
anomalies. CCTA requires high doses of ionizing radiation, with an average dose of 8.1 milliSieverts for patients weighing 75 kg. This
dose is approximately two to three times higher than the average radiation dose administered to patients during conventional coronary
angiography
+ CT calcium scoring (also known as Coronary Calcium Scan and Coronary Artery Calcium Scoring). A good summary on CT calcium
score can be found at www.aetna.com/cpb/medical/data/200_299/0228.html [Accessed 26 May 2016]
There are no current Medicare Benefits Schedule (MBS) rebates for performing cardiac CT in asymptomatic individuals.
*
§Refer to the Lung Foundation website at http://lungfoundation.com.au/health-professionals/clinical-resources/copd/targeted-copd-

case-finding-using-copd-screening-devices-in-the-community
ABI, ankle:brachial index; ApoE, apolopoprotein E; CA, cancer antigen; CAD, coronary artery disease; CCTA, coronary computed
tomography angiography; CEA, carotid endarterectomy; CHD, coronary heart disease; CT, computed tomography; CVD,
cardiovascular disease; DXA, dual-energy X-ray absorptiometry; hsCRP high sensitivity C-reactive protein; MBS, Medicare Benefits
Schedule; MRI, magnetic resonance imaging; MSU, mid-stream urine; MTHFR, methylenetetrahydrofolate; OSA, obstructive sleep
apnoea; Pap, Papanicolaou; RCT, randomised controlled trial; SNP, single nucleotide polymorphism; UKCTOCS, UK Collaborative Trial
of Ovarian Cancer Screening
Table 15.2. Screeningt tests of indeterminate value

Vitamin D Pregnancy Pregnant women with one or more risk 92, 114-17
factors for low vitamin D levels should have
their serum 25-hydroxy vitamin D levels
measured at their first antenatal visit
Risk factors for low vitamin D levels are

lack of skin exposure to sunlight, dark
skin, southerly latitude, conditions affecting
vitamin D metabolism and storage (including
obesity) and, for infants, being born to
a mother with low vitamin D levels and
exclusive breastfeeding combined with at
least one other risk factor.
Vascular
Ultrasound Abdominal aortic National screening of men aged 65 years 118-23

aneurysm (AAA) has been successfully introduced in the UK
and parts of Scandinavia for AAA. However,
it is unclear what the impact of the lower-
than-expected prevalence (<2%) of AAAs
will be on the long-term benefit
The US Preventive Services Task Force

(USPSTF) recommends screening of older
male smokers. Limiting screening to this
sub-group has raised some ethical issues
and may influence cost-effectiveness
Unpublished recent data from the Western

Australian trial of screening for AAA suggests
that the magnitude of the benefit from
screening men aged >65 years does not
warrant the introduction of a national AAA
screening program in Australia at this stage
152 9th edition

B-type natriuretic peptide Congestive The evidence for screening for heart failure 25, 124-30
(BNP) cardiac failure using BNP is mixed despite its sensitivity
and prognostic significance. It may be useful
in excluding the condition in suspected
heart failure. A recent, pragmatic, un
blinded randomised controlled trial (RCT)
has shown some benefit for BNP screening
in high-risk groups, but large scale trials
are needed to confirm these findings and
establish feasibility and cost effectiveness
Cancer
Low-dose chest Lung cancer A large trial in the US has shown that 131-38
computed tomography patients selected for high lung cancer
risk have reduced lung cancer and total
mortality within a carefully conducted LDCT
screening program in the context of a
structured program of selection, screening,
evaluation, and management of the relatively
high number of benign abnormalities
Performing CT scans in high-risk

individuals outside well-designed and
conducted research programs may lack
any benefit and may be harmful. Low-risk
persons should not have screening CT as
the reasonably foreseeable benefits are
lower and may be substantially outweighed
by harms. More accurate data on the
identification of the appropriate target
group including the threshold for absolute
lung cancer risk, are required before any
recommendation on LDCT
Positron emission Lung cancer There is no current evidence of benefit for 135, 139, 140
tomography - PET screening for lung cancer
computed tomography
(or PET CT scan)
Elderly
Visual acuity Visual impairment Current evidence is insufficient to assess the 141-43
balance of benefits and harms of screening
for impaired visual acuity in older adults
AAA, abdominal aortic aneurysm; BNP B-type natriuretic peptide; LDCT, low-dose computed tomography; PET, positron emission
tomography; RCT, randomised controlled trial ; USPSTF, US Preventive Services Task Force
9th edition
153
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Guidelines for preventive activities in general practice 9th edition 159
Preventive activities over the lifecycle — Adults Patient name: Date of birth: Date:
Activity/topic Frequency Notes Reference Age group

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
Prevention of chronic disease

Smoking Opportunistically It would be ideal to offer smoking cessation advice at every visit for those p 67, Section 7.1
at high risk of complications
Women who are pregnant or planning Each antenatal visit p 67, Section 7.1 and
a pregnancy p 18, Chapter 1.
Overweight Every two years Every 12 months for Aboriginal and Torres Strait Islander patients, or those p 69 Section 7.2
with existing diabetes, cardiovascular disease, stroke, gout or liver disease.
Every six months for adults who are overweight or obese
Nutrition Every two years Every six months for patients who are overweight or obese, or have high p 73 ................
cardiovascular absolute risk, a family history cardiovascular disease, type 2
diabetes or high risk of type 2 diabetes .
Alcohol: Early detection of at-risk drinking Every two to four years for low-risk groups and All patients 15 years of age and older should be asked about the quantity p 75, Section 7.4
opportunistically for higher risk groups and frequency of alcohol intake
Women who are pregnant or planning Each antenatal visit No drinking is the safest option p 18, Section 1
a pregnancy
Physical activity Every two years Opportunistically for those at higher risk, including teenage girls, older p 77 7.5
adults, office workers, Aboriginal and Torres Strait Islander patients, patients
with low socioeconomic status and non-English speaking background, or
those at high risk of a chronic condition or cancer
Pre-conception care Opportunistically Consider for all women aged 15-49 years p 18, Chapter 1
Sexual health - Chlamydia and other Opportunistically if indicated All sexually active patients up to 29 years of age. Test every 12 months for p 62, Section 6.2.1
sexually transmissible diseases higher and highest risk groups
Prevention of vascular disease
Absolute cardiovascular disease Every two years Aged >35 years for Aboriginal and Torres Strait Islander patients p 86, Section 8.1
risk assessment
Blood pressure Every two years Every 6-12 months for patients with moderate risk and every 6-12 weeks p 87, Section 8.2
for patients with high risk.
Cholesterol and other lipids Every five years Every two years for those with increased risk, and 12 months with p 89, Section 8.3
increased cardiovascular risk and existing chronic disease. Aged >35 years
for Aboriginal and Torres Strait Islander patients
Type 2 diabetes Every three years Every 12 months for those with impaired glucose tolerance or impaired p 92, Section 8.4
fasting glucose. Aged 18 years and older for Aboriginal and Torres Strait
Islander patients
Stroke Assess patients with high absolute risk every 12 months p 94, Section 8.5
Kidney disease Every one to two years for those at high risk Aged >30 years for Aboriginal and Torres Strait Islander patients p 96, Section 8.6
Cancer
Colorectal cancer Every two years from 50 years of age Earlier for those with high risk p 105, Section 9.2
Breast cancer Every two years p 109, Section 9.3
Melanocytic skin cancer Opportunistically for average and increased risk Examine every 6-12 months for those at high risk. p 113, Section 9.4.1
Non-melanocytic skin cancer Opportunistically Opportunistically for patients with increased risk including those >40 years p 116, Section 9.4.2
of age, and every 12 months for high-risk patients
Cervical cancer (to April 2017) Every two years p 117, Section 9.5
Cervical cancer (commencing May 2017) Every five years p 117, Section 9.5
Psychosocial
Depression Every encounter for those aged 12-18 years and
opportunistically for those aged >18 years
Intimate partner violence Opportunistically; maintain a high level of clinical Every encounter for adolescent women and screen all pregnant women p 130, Section 10.3
awareness for patients at increased risk
Elderly
Immunisation Refer to Section 5.1 or the Australian immunisation p 46, Table 5.1
handbook
Physical activity Every two years Advise moderate physical activity p 46, Section 5.2 and
p 78, Table 7.5.1
Falls risk Every 12 months Every six months if the patient has a history of falls or multiple risk factors p 47, Section 5.3
Vision and hearing Every 12 months
Oral health At least every 12 months and encouraged to attend More frequently for those at increased risk p 134, Chapter 11
annual dental visits
Glaucoma Frequency of follow-up determined by the patient’s Patients at increased risk p 137, Chapter 12
eye assessment
Osteoporosis
Postmenopausal women Every 12 months for average risk Increased risk for women aged >50 years with risk factors p 141, Chapter 14
Men Every 12 months for average risk Increased risk for women aged >50 years with risk factors p 141, Chapter 14
Family history screening questionnaire First visit to a practice and then at least every three years p 24, Chapter 2 ■
Low-average risk Increased risk
160 Guidelines for preventive activities in general practice 9th edition
Preventive activities over the lifecycle — Children Patient name: Date of birth: Date:
Activity/topic Frequency Reference Age group

Neonatal 2,4,6 & 12 months 18 months & 3 years 3.5-5 years 6-13 years 14-19 years
Immunisation Refer to the Australian immunisation handbook p 58, Table 6.1.1
Assessment
Metabolic screen p 33, Chapter 3, Table 3.1
Hearing p 33, Chapter 3, Table 3.1
Physical examination As outlined in the Child Personal Health Record (Blue Book) p 33, Chapter 3, Table 3.1
Body mass index Measure routinely from 2 years of age p 37, Table 3.2 Practice Point k
Vision At least once between 3 and 5 years of age p 37, Table 3.2 Practice Point j
Oral health Lift the lip’ check from 12 months of age and encourage p 37, Table 3.2 Practice Point e
annual dental visits. Opportunistic examination of higher
risk groups
Chlamydia and other sexually Patients who are sexually active p 62, Section 6.2.1
transmissible infections
Family and social environment When a child presents with behavioural or emotional p 33, Table 3.1
problems
Depression Every encounter p 38, Table 3.2 Practice Point m
Risky behaviours p 38, Table 3.2 Practice Point m
Intimate partner violence Opportunistically at every encounter for adolescent women p 131, Table 10.3.1
Health promotion
Support breastfeeding p 74, Table 7.3.2
Nutrition p 32, Chapter 3, Table 3.1
Physical activity p 37, Table 3.2 Practice Point f
Healthy sleep p 32, Chapter 3, Table 3.1
Interactive reading p 32, Chapter 3, Table 3.1
Developmental progress As outlined in the Child Personal Health Record (Blue Book) p 36, Table 3.2 Practice Point d
Smoking Ask about passive smoking during the neonatal period. p 67, Section 7.1
It should be asked oportunistically in adolescents and
young people
Sudden unexpected death in infancy p 32, Chapter 3, Table 3.1
Social/emotional wellbeing p 32, Chapter 3, Table 3.1
Injury prevention p 32, Chapter 3, Table 3.1
Sun protection Opportunistically
Early detection of at-risk drinking Every two to four years all patients aged >15 years p 75, Section 7.4
Opportunistically for children aged <15 years (increased risk)
Low-average risk Increased risk

A RACGP
Healthy Profession.
Healthy Australia.
Diarrhoea • THEME
Acute gastroenteritis
in children
BACKGROUND Gastroenteritis (GE) is G astroenteritis (GE) is inflammation of the mucous
inflammation of the mucous membranes of the membranes of the gastrointestinal tract, and is
gastrointestinal tract, and is characterised by characterised by vomiting and/or diarrhoea. Acute
vomiting and/or diarrhoea. The most common diarrhoea is defined as the abrupt onset of increased
causes are viruses, but bacterial, protozoal and fluid content of stool above the normal value of 10
helminthic GE occur, particularly in developing mL/kg/day.1 In practical terms it is associated with Annette Webb,
countries. Vomiting and diarrhoea can be increased frequency and fluid consistency of stools. MBBS, FRACP, is a
nonspecific symptoms in children, and the consultant paediatrician
General practitioners commonly manage GE in
diagnosis of viral GE should be made after careful and Gastroenterology
children. Parents or carers will consult a GP in up to Fellow, Department of
exclusion of other causes.
75% of cases of childhood GE.2,3 A United Kingdom Gastroenterology and
OBJECTIVE This article outlines the assessment study estimated that an average of 10 100 new Clinical Nutrition, Royal
Children’s Hospital,
and management of children with acute GE. episodes of infectious intestinal disease in children Victoria.
DISCUSSION The most important complication aged less than 5 years of age are seen in general
of GE is dehydration. The amount of weight loss practice each week.4
as a percentage of normal body weight provides In Australia, there are approximately 4000 episodes
the best estimate of degree of dehydration. of diarrhoea per 1000 children less than 15 years
Clinical signs are not present until the child of age per year.5 In the United States there are 1-2
has lost at least 4% of their body weight. The episodes of acute diarrhoea per child below 5 years
best signs for identifying dehydration include of age annually, with 220 000 hospital admissions
decreased peripheral perfusion, abnormal skin
(approximately 10% of all admissions for children in
turgor, and an abnormal respiratory pattern. Fluid
this age range) and 325-425 deaths per year.6,7
replacement is the mainstay of management and
Over the past 2 decades, worldwide mortality
most infants and children can be rehydrated safely
from viral GE has fallen, mostly as a consequence of
with oral rehydration solution. Antiemetics and Mike Starr,
widespread use of oral rehydration solutions (ORS).8
antidiarrhoeals are not indicated in children with MBBS, FRACP, is a
acute GE. general paediatrician,
Aetiology infectious diseases
Viruses account for approximately 70% of episodes of physician, and
Consultant in
acute infectious diarrhoea in children, with rotavirus
Emergency Medicine,
(Figure 1) being the most common cause. Rotavirus Royal Children’s
infection is associated with approximately half Hospital, Victoria.
mike.starr@rch.org.au
of acute GE hospitalisations in children,9 peaking
in the 6-24 months age group. Rotavirus also
causes the majority of cases of severe viral GE in
developing countries.10
Reprinted from Australian Family Physician Vol. 34, No. 4, April 2005 4 227
Theme: Acute gastroenteritis in children
GE, but tends to be associated with more persistent

diarrhoea. Other protozoa include cryptosporidium spp.
and Entamoeba histolytica.
Clinical features
Children with viral GE typically present with watery
diarrhoea without the presence of blood, with or
without vomiting, low grade fever and anorexia. Most
are less than 5 years of age. The typical peak period is
in the autumn or winter months. A history of contact
with GE may be present.
Bacterial GE may be associated with food or water
borne infections. It is usually characterised by the
presence of bloody diarrhoea, mucous in the stools
Figure 1. Negatively stained rotavirus particles seen by electron
microscopy in faecal extract. Reproduced with permission: and a high fever. A travel history should be sought.
Professor Ruth Bishop Haemolytic uraemic syndrome should be considered
in any child with bloody diarrhoea, pallor, and poor
Bacteria account for approximately 15% of episodes; urine output. It is characterised by acute renal
bacterial GE is generally more common in the first few impairment, thrombocytopenia and microangiopathic
months of life, and then in the school aged child.1 The haemolytic anaemia.11
most common bacterial causes are salmonella spp., It must be noted that GE is a diagnosis of exclusion
Campylobacter jejuni, Escherichia coli, and shigella spp. as vomiting and diarrhoea can be nonspecific symptoms
Giardia lamblia is the most common protozoal cause of in young children, and it is important to exclude other
Table 1. Guidelines to the assessment and management of dehydration14
Assessment of dehydration Signs Treatment
No/mild dehydration No signs or decreased peripheral ORS/water/usual fluids if no dehydration.

<4% body weight loss perfusion,' thirsty, alert and restless ORS only is preferred in high risk patients,
particularly those <6 months of age.
Child should be assessed regularly,
especially if <6 months and should
be seen again within 8 hours
Moderate 4-6% body weight loss Decreased peripheral perfusion, thirsty, Infants in this group may require
alert and restless, rapid pulse, sunken rehydration via the nasogastric route
eyes and fontanelle, dry mucous
membranes, deep acidotic breathing,'
pinched skin retracts slowly' (1—2 seconds)
Severe >7% body weight loss All of the above plus Intravenous rehydration is required until
In infants: drowsy, limp, cold, sweaty, organ perfusion is restored. ORS can
cyanotic limbs and altered conscious then be given
level Check electrolytes
In older children: apprehensive, cold,
sweaty, cyanotic limbs, rapid weak pulse,
low blood pressure
* These are the only signs proven to discriminate between hydration and dehydration (>4%)
228 3Reprinted from Australian Family Physician Vol. 34, No. 4, April 2005
Figure 2a-c. Assessment of capillary refill. Reproduced with permission: Advanced Paediatric Life Support 4th ed: instructor materials.
Advanced Life Support Group, 2005
Figure 2a. Press for 5 seconds Figure 2b. Release. Colour should return Figure 2c. A delay of more than 2 seconds
within 2 seconds in the well perfused, in association with other signs of shock
warm child and in a warm child suggests poor
peripheral perfusion
causes for these symptoms. Other causes of these • abnormal respiratory pattern (deep acidotic
symptoms include: breathing).12
• surgical conditions (acute appendicitis/pelvic These are the only signs proven to discriminate
abscess, malrotation with volvulus of the midgut, between hydration and dehydration (4% or greater).13
intussusception)
Which children require hospital admission?
• inflammatory bowel disease
• systemic infections (eg. urinary tract infections, Children without dehydration can be managed at
pneumonia, meningitis), and home and should be offered their normal fluids (see
• metabolic conditions (eg. diabetes mellitus). Resources). These can be given as small volumes
but more frequently. Children with mild to moderate
Assessment of dehydration dehydration should be observed for 4-6 hours to ensure

successful rehydration (2-4 hours) and maintenance
The most important complication of GE is dehydration. of hydration (1-2 hours). Children at high risk of
The risk of dehydration is increased with younger age, dehydration on the basis of age (<6 months), high
and is most common in: frequency of stools (>8 per 24 hours) or vomits (>4 per
• infants less than 6 months of age 24 hours) should be observed for at least 4-6 hours to
• those with anatomical abnormalities of their gut (eg. ensure adequate maintenance of hydration, and hospital
short gut syndrome), and admission should be considered.
• those on hyperosmolar feeds (eg. polyjoule). Hospital admission is required for children:
The amount of weight loss as a percentage of normal • with severe dehydration (>7% body weight loss)
body weight provides the best estimate of degree • whose carers or parents are thought to be unable to
of dehydration, however, it is not always practical to manage the child’s condition at home.
calculate this. If a child is seen early in the episode, Hospital admission should be considered for:
it is important to measure weight accurately for later • children with significant comorbidity (eg. short bowel
comparison if required. Clinical signs are not present until syndrome, diabetes, congenital heart disease).15
the child has lost at least 4% of their bodyweight (Table
What fluids to use?
1). The best signs for identifying dehydration include:
• decreased peripheral perfusion as evidenced by Several studies have shown that ORS correct
prolongation of capillary refill time (Figure 2a-c) dehydration more quickly and with fewer adverse
• abnormal skin turgor (pinched skin retracts slowly in effects than intravenous therapy.16,17 Most infants and
1-2 seconds), and children can be rehydrated safely with ORS. This may
be given orally or if this is unsuccessful, via nasogastric based on evidence that the risks of adverse effectsof
administration. The use of ORS is based on the principle loperamide outweigh its limited benefit in reducing
of glucose facilitated sodium transport in the small stool frequency.15,19 Antiemetics have no proven
intestine. The compositions of ORS currently available benefit and the risk of adverse effects such as acute
in Australia are listed in Table 2 and suitable fluids dystonic reactions preclude their use in children.20
for nondehydrated children in Table 3. The preferred Patients with invasive bacterial infections with
ORS are those that are hypotonic with an osmolarity Salmonella typhi, shigella, cholera, and those with
between 200-250 mOsm/L.17 Children who refuse to amoebiasis and giardiasis should be treated with
drink can sometimes tolerate ORS icy-poles. antibiotics. Consider antibiotic use in infants less than
6 months of age with other salmonella infections,
Which children require investigation?
those who are systemically unwell, and the
All children requiring intravenous rehydration should immunocompromised.15
have blood taken for electrolytes, urea and creatinine.
Breast and formula feeding
Stool cultures should be obtained if there is a history
of bloody diarrhoea, recent travel, or if the history is Breastfed children should continue to breastfeed
suggestive of food poisoning. through the rehydration and maintenance phases
Damage to the intestinal villi can cause transient of their acute GE.21 Additional ORS can be given if
lactose malabsorption. In any child with prolonged required. In the dehydrated child who is normally
watery diarrhoea (>7 days) associated with signs of fed with formula, formula feeds should stop during
carbohydrate malabsorption (excoriation of buttocks), rehydration and restart as soon as the child is
faeces should be tested for reducing substances. If rehydrated.15 Dilution of formula is unnecessary when
confirmed lactase deficiency (reducing substances in formula is reintroduced.19
stool >0.5%) lactose free feeds may be indicated for
When should solids be restarted?
2-4 weeks. Lactose free feeds can be given in the
form of soy based preparations; low lactose feeds by Studies have shown that an early return to feeding
reduced lactose cow's milk based preparations.18 shortens the duration of diarrhoea and improves weight
gain without increasing vomiting or diarrhoea.20,22,23
When should medications be used?
Often the child will refuse food initially. In general,
Antidiarrhoeal agents such as loperamide should not food should not be stopped for more than 24
be used to treat acute diarrhoea in children. This is hours, and children should be offered solid food if
hungry. The complete resumption of a child's 'normal'
Table 2. Oral rehydration preparations available in Australia
* feeding (including lactose containing formula) after 4
hours of rehydration with ORS, has led to significantly
Na K Cl Citrate Glucose higher weight gain and does not result in worsening of
Gastrolyte 60 20 60 10 90 diarrhoea or lactose intolerance after rehydration and
Hydrolyte 60 20 60 10 90 during hospitalisation.21
Repalyte 45 20 35 30 80
Conclusion
* Concentrations expressed as mmol/L of prepared solution
Vomiting and diarrhoea can be nonspecific symptoms
in children, and the diagnosis of viral GE needs to
be made after excluding other causes. Children need
to be assessed carefully for signs of dehydration.
Children without dehydration can be managed
Table 3. Suitable fluid for nondehydrated children14
at home and should be offered their normal
fluids. Most infants and children can be rehydrated
Solution Dilution
safely with ORS. Children with severe rehydration
Sucrose (table sugar) 1 teaspoon in 200 mL boiled water
(>7%) require hospital admission and those with
Fruit juice 1 part in 6 parts water
Cordials 1 part in 16 parts water lesser degrees of dehydration require observation
Lemonade 1 part in 6 parts water and early review to ensure rehydration is

occurring appropriately.
230 3Reprinted from Australian Family Physician Vol. 34, No. 4, April 2005
Summary of important points lence and molecular diversity. J Med Virol 2003;71:82-93.
10. Doan LT, Okitsu S, Nishio O, Pham DT, Nguyen DH,
Ushijima H. Epidemiological features of rotavirus infection
• Diagnosis of acute gastroenteritis is made after a among hospitalised children with gastroenteritis in Ho Chi
careful exclusion of other causes. Minh City, Vietnam. J Med Virol 2003;69:588-94.
• Dehydration is the most important complication.
11. Cleary TG. The role of Shiga-toxin-producing Escherichia coli
in hemorrhagic colitis and hemolytic uremic syndrome. Semin
• The best signs for identifying dehydration are Pediatr Infect Dis 2004;15:260-5.
decreased peripheral perfusion as evidenced by 12. Mackenzie A, Barnes G, Shann F. Clinical signs of dehydration
prolongation of capillary refill time, abnormal skin
in children. Lancet 1989;2:605-7.
13. Steiner MJ, Dewalt DA, Byerley JS. Is this child dehydrated?
turgor and abnormal respiratory pattern. JAMA 2004;291:2746-54.
• Children at high risk (<6 months or significant 14. Oliver M, Lubitz L. Gastrointestinal conditions. In: Marks
comorbidity) should be referred for paediatric care. M, Munro J, Paxton G, editors. Paediatric handbook. 7 th ed.
Blackwell Science 2003;371-3.
• Antiemetics and antidiarrhoeals are not indicated in
15. Armon K, Stephenson T, MacFaul R, Eccleston P, Wernecke U.
children with acute gastroenteritis. An evidence and consensus based guideline for acute diarrhoea
management. Arch Dis Child 2001;85:132-42.
Resources 16. Sharifi J, Ghavami F, Nowrouzi Z, Fouladvand B, Maelk M,
Royal Children’s Hospital fact sheets
Rezaeian M. Oral versus intravenous rehydration therapy in
severe gastroenteritis. Arch Dis Child 1985;60:856-60.
www.rch.org.au/kidsinfo/factsheets.cfm?doc_id=5353
(Please note that the correct fluid recipe for lemonade and
17. Fontaine O. Multicentre evaluation of reduced-osmolarity
oral rehydration salts solution. International Study Group on
water is 1:6. The ratio given in the fact sheet is now outdated).
reduced-osmolarity ORS solutions. Lancet 1995;345:282-5.
Royal Children’s Hospital. Clinical practice guidelines: 18. Therapeutic Guidelines. Gastrointestinal. Version 3. Transient
diarrhoea and vomiting lactose intolerance in children with acute gastroenteritis. North
www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5192 Melbourne: Therapeutic Guidelines Ltd, 2002;120.
Royal Children’s Hospital. Paediatric handbook. 19. Practice parameter: the management of acute gastroenteritis in
7th ed. Blackwell Publishing, 2003. (Available from RCH Child
young children. American Academy of Pediatrics, Provisional
Information Centre 03 9345 6429)
Committee on Quality Improvement, Subcommittee on Acute
Gastroenteritis. Pediatrics 1996;97:424-35.
20. Tait PA. Supraglottic dystonic reaction to metoclopramide in a
Conflict of interest: none declared.
child. Med J Aust 2001;174:607-8.
21. Khin MU, Nyunt-Nyunt-Wai, Myo-Khin, et al. Effect on
References clinical outcome of breastfeeding during acute diarrhoea. BMJ
1. Guandalini S. Acute diarrhoea. In: Walker WA, et al editors. 1985;290:587-9.
Paediatric gastrointestinal disease. 4th ed. BC Decker, 22. Sandhu BK, Solauri E, Walker-Smith JA, et al. A multicen
2004;166-79. tre study on behalf of the European Society of Paediatric
2. Elliot EJ, Backhouse JA, Leach JW. Pre-admission management Gastroenterology and Nutrition Working Group on Acute
of acute gastroenteritis. J Paediatr Child Health 1996;32:18-21. Diarrhoea. Early feeding in childhood gastroenteritis. J Pediatr
3. O’Loughlin EV, Notaras E, McCullogh C, Halliday J, Henry Gastroenterol Nutr 1997;24:522-7.
RL. Home based management of children hospitalised with 23. Brown KH, Gastranaduy AS, Saaredra JM, et al. Effect of con
acute gastroenteritis. J Paediatr Child Health 1995;31:189-91. tinued oral feeding on clinical and nutritional outcomes of acute
4. Djuretic T, Ramsey M, Gay N, Wall P Ryan M, Fleming D. An diarrhoea in children. J Pediatr 1988;112:191-200.
estimate of the proportion of diarrhoeal disease episodes seen by
general practitioners attributable to rotavirus in children under
5 years of age in England and Wales. Acta Paediatr 1999;88:38-
41.
5. Mathers C. Diarrhoeal diseases and gastroenteritis: Australia.
Australian Institute of Health and Welfare. Burden of disease
and disease expenditure. Available at: www.aihw.gov.au/bod/
bod_yld_by_disease/a_infectious/a4_diarrhoea.xls). Accessed
February 2005.
6. Glass R, Lew J, Gangarosa RE, LeBaron CW, Ho MS. Estimates
of morbidity and mortality rates for diarrheal diseases in
American children. J Pediatr 1991;118:S27-33.
7. Herikstad H, Yang S, Van Gilder TJ, et al. A population-based
estimate of the burden of diarrhoeal illness in the United States:
FoodNet 1996;7. Epidemiol Infect 2002;129:9-17.
8. Kosek M, Bern C, Guerrant RL. The global burden of diar
rhoeal disease, as estimated from studies published between
1992 and 2000. Bull World Health Organ 2003;81:197-204.
9. Oh DY, Gaedicke G, Schreier E. Viral agents of acute gastroen
teritis in German children: prevalence and molecular diversity. Email: afp@racgp.org.au afp
Viral agents of acute gastroenteritis in German children: preva
o Short report •RESEARCH
Screening for social anxiety

disorder in first year university
students
A pilot study
Ian Wilson, MBBS, PhD, FRACGP, FACPsycMed, is Associate Professor, Department of General Practice,
University of Adelaide, South Australia. ian.wilson@adelaide.edu.au
S ocial anxiety disorder (SAD) is Table 1. Numbers of students and prevalence of SAD using Mini-SPIN
characterised by fear of negative evaluation.1
Sufferers become anxious when they perceive
Bachelors degree n Number of screen positive responses
themselves as the centre of attention, finding for given Mini-SPIN cut score, n (%)
it difficult to speak in public, attend social 6 7 8 9
events and deal with authority figures. It is Arts 69 26 (38) 19 (28) 15 (22) 12 (17)
common, with an annual prevalence of 2.7% Commerce 17
in Australia,2 but elsewhere in the western Computing science 8
world it is higher (3-4%) and has a lifetime Economics 3
incidence of 7-13%.3 It has significant Engineering 216 61 (28) 32 (15) 24 (11) 13 (6)
impact on education and employment, with Environmental studies 1
lower levels of educational achievement and Finance 3
lower incomes.4 Food tech and management 1
There are several screening tests for social Health science 33 12 (36) 8 (24) 5 (15) 3 (9)
anxiety disorder. The 24 question Liebowitz International studies 8
Social Anxiety Scale is reliable, but requires Law 17
a significant verbal introduction.5,6 The Social Mathematics and computer science 15
Anxiety Scale for Adolescents is a 13 question Media 5
self report scale but has no documented
Medicine 49 8 (16) 6 (12) 5 (10) 2 (4)
cut-scores.7 The abbreviated version of the
*
Psychology (Hons) 21
Social Phobia Inventory (Mini-SPIN) needs
Science 184 55 (30) 30 (16) 20 (11) 8 (4)
only three questions, making it suitable for
Social science 9
clinical practice.8 Each response can range 0
Not stated 8
4 (from 'not at all' to 'extremely'). A cut-score
Total 666 202 (30) 118 (18) 87 (13) 49 (7)
of 6 (out of a possible 12) is used to indicate
social anxiety disorder (although it cannot * 4 year undergraduate degree resulting in honours degree in psychology
differentiate different types) with a sensitivity

of 88.7% and specificity of 90.0%. These questions. Responses from students who
were derived in only one study of adults
Method indicated that this was not their first year
(where the positive predictive was 52.5%, and I wrote to the executive deans of each of the at university, and those over the age of 25
negative predictive value 98.5%), so validation five faculties, seeking access to first year years were discarded.
has not been adequately established.8 students. At the end of introductory lectures Analysis was carried out using SPSS
I wondered if it was feasible to screen for I briefly introduced the project, and invited (version 12 for Windows). Mini-SPIN scores
social anxiety disorder among adolescents, first time university students to complete were dichotomised to presence or absence
and settled on first year university students a one page questionnaire which contained of SAD, using scores of 6 and higher as
as a convenient sample. demographic data and the three Mini-SPIN indicative of SAD, and after examining the
Reprinted from Australian Family Physician Vol. 34, No. 11, November 2005 4 983
Research: Screening for social anxiety disorder in first year university students — A pilot study
results, higher cut-scores. Prevalence of SAD References

was calculated for each degree and gender. 1. American Psychiatric Association. Diagnostic and
Comparisons between groups were made Statistical Manual of Mental Disorders. 4th ed.
using the Mann-Whitney U test.
Washington DC: American Psychiatric Association,
1994.
The Human Research Ethics Committee of 2. McLennan W. Mental Health and wellbeing: profile
the University of Adelaide granted approval. of adults, Australia. Canberra: Australian Bureau of
Statistics, 1997.
Results 3. Furmark T. Social phobia: overview of community
surveys. Acta Psychiatr Scand 2002;105:84-93.
Of the 4368 commencing undergraduate 4. Patel A, Knapp M, Henderson J, Baldwin D. The
students, responses were received from 710 economic consequences of social phobia. J Affect
Disord 2002;68:221-33.
(16.3%) students aged 16-46 years (almost
5. Fresco DM, Coles ME, Heimberg RG, et al. The
80% 17 or 18 years of age). After discarding Liebowitz Social Anxiety Scale: a comparison of the
ineligible students, the total was 666 psychometric properties of self report and clinician
adolescents. Of these 348 (52.3%) were male.
administered formats. Psychol Med 2001;31:1025-
35.
The overall prevalence using a cut-score 6. Baker SL, Heinrichs N, Kim HJ, Hofmann SG. The
of 6 was just over 30% (Table 1). Higher rates Liebowitz Social Anxiety Scale as a self report instru
were seen in students studying for degrees in
ment: a preliminary psychometric analysis. Behav Res
Ther 2002;40:701-15.
arts (38%) and health sciences (36%), while 7. Myers MG, Stein MB, Aarons GA. Cross validation
lower rates were seen in science (28%), of the Social Anxiety Scale for Adolescents in a high
engineering (28%) and medicine (16%). school sample. J Anxiety Disord 2002;16:221-32.
8. Connor KM, Kobak KA, Churchill LE, Katzelnick
The differences between students studying
D, Davidson JR. Mini-SPIN: a brief screening assess
medicine versus health science and versus ment for generalised social anxiety disorder. Depress
arts were significant (p<0.05). Anxiety 2001;14:137-40.
There was a large difference in the number
of respondents reporting Mini-SPIN scores of
6 and 7. Using the cut-score of 7 reduced the
prevalence to 18.3% (Table 1).
Discussion
These results confirm that the Mini-SPIN still
requires further work to set the cut-point and
validate the instrument: the cut-point of 6
or 7 seems to overestimate the prevalence
of social anxiety disorder, although I used
no gold standard to test this. Until a reliable
instrument is validated, it will be difficult to
mass screen in general practice.
Implications of this study

for general practice
• Social anxiety disorder is common in

adolescents.
• It may have important impact on educa
tion and employment.
• The Mini-SPIN screening instrument
seemed to grossly overestimate its preva
lence in university students.
• A suitable screening test has yet to be
developed.
Correspondence
■ Email: afp@racgp.org.au
984 3Reprinted from Australian Family Physician Vol. 34, No. 11, November 2005
THEME
Gynaecological
malignancies
The woman with
postmenopausal
bleeding
Alison H Brand
MD, FRCS(C), FRANZCOG, CGO,
BACKGROUND
is a certified gynaecological Postmenopausal bleeding is a common complaint from women seen in general practice.
oncologist, Westmead
Hospital, New South Wales.
OBJECTIVE
alisonb@westgate.wh.usyd. This article outlines a general approach to such patients and discusses the diagnostic possibilities and their
edu.au management.
DISCUSSION
The most common cause of postmenopausal bleeding is atrophic vaginitis or endometritis. However, as 10% of women
with postmenopausal bleeding will be found to have endometrial cancer, all patients must be properly assessed to rule
out the diagnosis of malignancy. Most women with endometrial cancer will be diagnosed with early stage disease when the
prognosis is excellent as postmenopausal bleeding is an early warning sign that leads women to seek medical advice.
Postmenopausal bleeding (PMB) is defined as bleeding • cancer of the uterus, cervix, or vagina (Table 1).
that occurs after 1 year of amenorrhea in a woman Endometrial or vaginal atrophy is the most common cause
who is not receiving hormone therapy (HT). Women of PMB but more sinister causes of the bleeding such
on continuous progesterone and oestrogen hormone as carcinoma must first be ruled out. Patients at risk for
therapy can expect to have irregular vaginal bleeding, endometrial cancer are those who are obese, diabetic and/
especially for the first 6 months. This bleeding should or hypertensive, nulliparous, on exogenous oestrogens
cease after 1 year. Women on oestrogen and cyclical (including tamoxifen) or those who experience late
progesterone should have a regular withdrawal bleeding menopause1 (Table 2).
after stopping the progesterone.
Assessment
Patients requiring investigation include: The majority of women diagnosed with endometrial cancer
• women with any postmenopausal bleeding, spotting or present with vaginal bleeding or discharge. Most women
vaginal discharge if not on HT recognise that this is abnormal and seek medical advice as
• women on continuous combined HT who have bleeding a result. Abnormal postmenopausal bleeding should always
6 months after starting treatment, and be taken seriously and investigated, no matter how minimal
• women on cyclical HT who have bleeding outside the or insignificant it may appear.
expected time of withdrawal bleed. Initial assessment by the general practitioner
Postmenopausal bleeding may be caused by the following: should include a complete history with assessment of
• hormone (oestrogen) therapy risk factors, as well medication history covering use of
• atrophy of the vagina or uterus oestrogen, tamoxifen or anticoagulants. It is also important
• uterine or cervical polyps to inquire about any nonprescription medications such
• endometrial hyperplasia as phytoestrogens.
116 Reprinted from Australian Family Physician Vol. 36, No. 3, March 2007
Examination
Table 1. Causes of postmenopausal bleeding14
Clinical examination should include abdominal examination,
looking for abdominal masses. A speculum examination Cause of bleeding Frequency (%)
should be performed to allow assessment of atrophic Endometrial or cervical polyps 2-12

vaginitis and to rule out tumours of the cervix, vagina or
Endometrial hyperplasia 5-10
vulva, or cervical polyps. A Pap smear should be taken if
Endometrial carcinoma 10
there is any suspicion of an abnormality on the cervix (note:
this is a diagnostic test not a screening test and therefore Exogenous oestrogens 15-25
the presence of blood is irrelevant). The finding of atrophic Atrophic endometritis and vaginitis 60-80
vaginitis or an endocervical polyp should not be accepted as Other
the explanation of the bleeding without further assessment (vaginal trauma, urethral caruncle, uterine sarcoma,
of the endometrial cavity. cervical cancer, anticoagulants)
Bimanual examination should be performed to assess
uterine size, mobility and position before performing
endometrial biopsy. Cervical or vaginal masses that were Table 2. Relative risks for endometrial cancer14
not seen on speculum examination may be palpated,
Characteristic Relative risk
as well as detection of adnexal masses. Rectovaginal
examination allows detection of nodularity in the cul de Nulliparity 2-3
sac. Abnormal bleeding should NEVER be an excuse, on Late menopause (>age 52 years) 2.4
the part of either the patient or the doctor, not to perform Obesity
an examination, as it is usually indicative of a problem.
15-25 kg overweight 3
Biopsy >25 kg overweight 10
Diabetes mellitus 2.8
The gold standard for diagnosis of any malignancy is
tissue biopsy. Endometrial office biopsy can be easily Unopposed estrogen therapy 4-8
performed in most patients (with the exception of those Tamoxifen 2-3
with cervical stenosis) with only minor discomfort Atypical endometrial hyperplasia 8-29
or cramping in most cases. (An antiprostoglandin
administered 1 hour before the procedure can reduce
cramping.) Endometrial office biopsies are usually Ultrasound
performed by a gynaecologist rather than the GP. Transvaginal ultrasound is often recommended as
Technically, it is not a difficult procedure to learn or do, a preliminary ‘noninvasive’ technique for assessing the
however, there is always the chance of complications endometrium in women with PMB. Unfortunately, it cannot
such as perforation and infection (which the operator give a definitive answer as to the presence or absence
must then be able to deal with), and of course the of malignancy, although it can sometimes be helpful in
GP must be confident in his/her ability to interpret the assessment of uterine polyps. There is no consensus
the results. General practitioners could potentially in the literature as to what the cut-off value for normal
undertake this procedure if they were interested in office endometrial thickness should be. It has been reported
gynaecological procedures, had appropriate training and as anywhere from 4-8 mm. Obviously the lower the cut
medical defence cover. off, the higher the sensitivity for detection of endometrial
The diagnostic accuracy of office endometrial biopsy cancers and its precursors but at a cost of lower specificity
for endometrial cancer is over 90% when compared to and increased false positives.3 A normal endometrial
dilatation and curettage (D&C). A review of 13 598 D&Cs thickness on ultrasound does not exclude endometrial
and 5851 office biopsies showed that adequacy of the cancer, especially in those with significant risk factors. A
specimens were comparable, but that D&C had a high suggested algorithm for the management of abnormal
complication rate.2 vaginal bleeding is presented in Figure 1.
Hysteroscopy and biopsy should be reserved for cases
Differential diagnosis
in which office endometrial sampling cannot be performed
due to cervical stenosis or patient discomfort, or where Atrophic vaginitis/endometritis
bleeding persists after negative office biopsy or where an The diagnosis of atrophic vaginitis is made when speculum
inadequate specimen is obtained. examination reveals a thin, friable vaginal wall that may
Reprinted from Australian Family Physician Vol. 36, No. 3, March 2007 117
THEME The woman with postmenopausal bleeding
bleed upon opening the speculum. visualisation. Saline infusion sonograms have been used
Women with atrophic endometritis usually have been to identify the polyps that show up as filling defects. Pelvic
postmenopausal for over 10 years. There is often minimal ultrasound usually does not reveal endometrial polyps unless
tissue or just mucous and blood on endometrial biopsy. they are particularly large. Treatment is removal during
Treatment is topical or systemic oestrogens. The addition of hysteroscopy. The specimen should always be sent for
progesterone is needed if using systemic oestrogens with pathological assessment.
an intact uterus.
Endometrial hyperplasia
Cervical polyps
Endometrial hyperplasia covers a range of pathological
Endocervical polyps are more common than ectocervical changes in the uterine glands and stroma. Hyperplasia
polyps. They appear as red protrusions from the cervical can be simple or complex, with or without atypia. The
os. They can usually be easily removed in the office by presence of atypia is the most worrisome feature as
grasping with sponge forceps and twisting on their pedicle. approximately 20% of those with atypical hyperplasia will
Any bleeding can usually be stopped with cautery have a concomitant endometrial carcinoma and a further
or Monsel’s solution. The polyp should be sent for 25-30% will develop endometrial hyperplasia within 2 years
pathological examination. if the condition is left untreated.6
Hyperplasia without atypia can be treated with
Endometrial polyps
progesterone, with an expected response rate of 80%.7
The incidence of endometrial polyps varies with age, Hyperplasia with atypia responds less well to progesterone
reaching a peak in the fifth decade of life.4 Because they treatment and definitive treatment in the postmenopausal
are oestrogen sensitive, their incidence declines after woman should be hysterectomy with or without
menopause. They are also associated with tamoxifen use oophorectomy because of the risk of concomitant and future
and are the most common abnormality seen with tamoxifen malignancy. Those patients medically unfit for surgery can
use.5 Rarely, endometrial polyps may undergo malignant be treated with high dose progesterone but need to be
change into a carcinoma or sarcoma. reassessed frequently with endometrial sampling to ensure
Hysteroscopy can identify endometrial polyps by direct reversal of changes.
Abnormal vaginal bleeding
'Ir
Office endometrial biopsy
Abnormal Unsatisfactory or Negative but Negative, no

unable to do continued symptoms
sympto
▼
Appropriate Low risk for High risk for Repeat biopsy Follow up
management cancer cancer or perform
transvaginal
ultrasound
Transvaginal
ultrasound
Negative Positive
(If negative and if
symptoms persist)
Hysteroscopy
▼ and biopsy
Follow up
Figure 1. Algorithm for the management of abnormal vaginal bleeding3
The woman with postmenopausal bleeding THEME
Endometrial carcinoma
Over 90% of women with endometrial carcinoma present Case study 1
with vaginal bleeding. Other symptoms include irregular A woman, 59 years of age, presents with complaints of spotting per
vagina. On examination, a large 2 cm infarcted endocervical polyp
perimenopausal bleeding or heavy irregular bleeding in
is seen protruding from the endocervical canal. This is removed with
patients with anovulatory cycles. Rarely, abnormal a sponge forceps. Pathology is reported as a benign endocervical
endometrial cells are seen on a routine Pap smear in polyp. The bleeding continues and 3 months later she re-presents
asymptomatic postmenopausal women. to her GP. An endometrial biopsy shows grade 2 endometroid
adenocarcinoma.
Uterine cancer is the fifth commonest cancer in women
Practice point: It is important to rule other serious causes of
in Australia and is the commonest cancer of the female
postmenopausal bleeding even if a seemingly obvious cause is noted.
genital tract. In 2001, there were 1537 new cases of uterine
cancer in Australia and 299 deaths from uterine cancer,
accounting for approximately 2% of all cancer deaths.8
Case study 2
Treatment
A woman, 52 years of age, presents with complaints of
Treatment of endometrial carcinoma is almost always postmenopausal bleeding while on continuous combined HT
surgical. Staging is carried out at the same time and allows after 1 year. Office endometrial biopsy reveals inadequate tissue.
Hysteroscopy and D&C reveals atrophic endometrium with no
accurate assessment of extent of disease. Complete
polyps. Currettings are negative. Six months later, she represents
surgical staging should include peritoneal cytology, total with ongoing complaints of vaginal spotting. She remains on the HT
abdominal hysterectomy, bilateral salpingo-oophorectomy, She has no risk factors for endometrial cancer. Endometrial biopsy is
and bilateral pelvic and para-aortic lymphadenectomy. again negative with minimal tissue. Transvaginal ultrasound shows
In reality, patients with low grade, noninvasive tumours
thin endometrium. The most likely explanation for the bleeding is felt
to be the HT and she is switched to sequential HT. She has a regular
have an extremely low risk of lymph node spread and do
withdrawal bleed and no irregular spotting.
not routinely require lymphadenectomy. Unfortunately, Practice point: Ongoing spotting on HT, especially if it is continuous
although the grade of tumour is usually known before combined HT with adequate progesterone dose, is unlikely to be
definitive surgery, myometrial invasion is not, and a due to hyperplasia or malignancy. This should be investigated
decision regarding need for lymphadenectomy will need to
appropriately in the first instance, but in the absence of risk factors
for endometrial cancer, switching the patient to sequential HT will
be made intra-operatively. As the ability to perform lymph
usually alleviate the troublesome irregular spotting.
node dissection is outside the usual skill set of a general
gynaecologist, referral to a gynaecological oncologist should
be considered. The performance of lymphadenectomy trial looking at the benefit of adjuvant radiotherapy showed a
allows accurate assessment of lymph node status and may decrease in the risk of pelvic recurrence but no improvement
avoid the necessity for adjuvant radiotherapy should the in overall survival.11
lymph nodes be negative. The most common histological type of endometrial
In recent years there has been a move toward cancer is endometroid, accounting for over 75% of all
laparoscopic management of early stage endometrial endometrial carcinomas. Other histological types include
carcinoma, primarily because of the benefits associated papillary serous, clear cell and carcinosarcoma (malignant
with laparoscopic surgery in general (ie. shorter hospital mixed mullerian tumour) which all exhibit a much more
stay and quicker recovery). This is especially true for obese aggressive behaviour.
patients in whom open surgery can be difficult. To date, Prognosis for endometrial carcinoma is usually good
trials comparing open versus laparoscopic surgery have as most patients are diagnosed at an early stage. Those
shown, as would be expected, shorter hospital stay, quicker patients with stage 1 disease (ie. confined to the uterus)
return to normal activities, decreased requirements for would be expected to have a greater than 85% 5 year
analgesics and less overall complications.9 No trials as survival (Table 3).
yet, have been large enough to answer the question as to Screening for endometrial carcinoma, with either office
whether prognosis is the same although there is an ongoing endometrial biopsy or transvaginal ultrasound, has not been
trial in Australia attempting to address this question.10 shown to be cost effective for the general population. It
Complete surgical staging reduces the need for may confer some benefit for those patients with extreme
adjuvant radiotherapy. In surgically staged patients, adjuvant risk, ie. hereditary nonpolyposis colon cancer carriers who
radiotherapy would be reserved only for patients with high have up to a 40% life time risk of endometrial cancer.12 The
grade, deeply invasive tumours, those with cervical spread or Australian Cancer Network recommends that such patients
those with involvement of lymph nodes. The only randomised at very high risk for endometrial cancer consider either
Reprinted from Australian Family Physician Vol. 36, No. 3, March 2007 119
THEME The woman with postmenopausal bleeding
Table 3. FIGO staging of endometrial cancer and prognosis15

FIGO stage Extent of disease 5 year survival
IA: tumour limited to endometrium

Stage I IB: invasion to less than half of the myometrium } 85%
IC: invasion to greater than half the myometrium
IIA: endocervical gland involvement only

Stage II } 70%
IIB: cervical stromal invasion
IIIA: tumour invades serosa of uterus and/or adnexae, and/or

positive peritoneal cytology
Stage III } 40-60%
IIIB: vaginal metastases
IIIC: metastases to pelvic and/or para-aortic lymph nodes
IVA: tumour invades bladder and/or bowel mucosa

Stage IV IVB: distant metastases including intra-abdominal spread or inguinal } 10-20%
lymph nodes
prophylactic surgery or screening with annual transvaginal 700 patients treated with tamoxifen for breast cancer. Gynecol Oncol
2000;78:181-6.
ultrasound, although the efficacy of such screening has
6. Kurman RJ, Kaminski PF, Norris HJ. The behavior of endometrial hyperpla
not been determined.13 It is acknowledged that this sia: A long term study of ‘untreated’ hyperplasia in 170 patients. Cancer
1985;56:403-12.
recommendation is based on expert opinion rather than
7. Ferenczy A, Gelfand M. The biologic significance of cytologic atypia in
definitive scientific evidence. progestogen-treated endometrial hyperplasia. Am J Obstet Gynecol
1989;160:126-31.
Summary of important points 8. Australian Institute of Health and Welfare (AIHW) and Australasian
Association of Cancer Registries (AACR) 2004. Cancer in Australia 2001.
• Postmenopausal bleeding should always be AIHW Cat No. 23. Canberra: AIHW (Cancer Series No. 28).
investigated, as 10% of patients will have endometrial 9. Tollund L, Hansen B, Kjer JJ. Laparoscopic assisted vaginal vs. abdominal
surgery in patients with endometrial cancer stage 1. Acta Obstet Gynecol
carcinoma.
Scand 2006;85:1138-41.
• The commonest cause of postmenopausal bleeding is 10. Janda M, Gebski V, Forder P, Jackson D, Williams G, Obermair A. LACE
an atrophic vaginitis or endometritis. Trial Committee. Total laparoscopic versus open surgery for stage 1 endo
metrial cancer: the LACE randomised controlled trial. Contemp Clin Trials
• Assessment of the endometrium with tissue pathology 2006;27:353-63.
is essential, even if the presence of obvious atrophic 11. Aalders J, Abeler V, Kolstad P, Onsrud M. Postoperative external irradia
tion and prognostic parameters in Stage 1 endometrial carcinoma. Obstet
vaginitis or cervical polyp.
Gynecol 1980;56:419-46.
• The prognosis for endometrial carcinoma is usually 12. Burke W, Petersen G, Lynch P, et al. Recommendations for follow up care
good as most patients present with early stage disease of individuals with an inherited predisposition to cancer. I. Hereditary
nonpolyposis colon cancer. Cancer Genetics Studies Consortium. JAMA
due to the early symptom of postmenopausal bleeding.
1997;277:915-9.
13. Australian Cancer Network Colorectal Cancer Guidelines Revision
Committee. Guidelines for the prevention, early detection and manage
ment of colorectal cancer. The Cancer Council Australia and Australian
Cancer Network, Sydney 2005.
References 14. Lurain J. Uterine cancer. In: Berek JS, Adashi EY, Hillard PA,
1. Brinton LA, Berman ML, Mortel R, et al. Reproductive, menstrual and editors. Novak’s Gynecology 12th ed. Baltimore: Williams & Wilkins,
medical risk factors for endometrial cancer: Results from a case control 1996;1057-110.
study. Am J Obstet Gynecol 1992;167:1317-25. 15. Hacker N. Uterine cancer. In: Berek JS, Hacker NF, editors. Practical
2. Chambers JT, Chambers SK. Endometrial sampling. When? Where? Why? Gynaecological Oncology 3rd ed. Lippincott Williams and Wilkins.
With what? Clin Obstet Gyecol 1992;35:28-39.
3. Brand A, Dubuc-Lissior J, Ehlen T, Plante M. Diagnosis of endometrial
cancer in patients with abnormal vaginal bleeding. SOGC clinical practice
guidelines. J Soc Obstet Gynecol Can 2000;22:102-4.
4. Van Bogaert LJ. Clinicopathologic findings in endometrial polyps. Obstet
Gynecol 1988;71:771-3.
CORRESPONDENCE email: afp@racgp.org.au
5. Deligdisch L, Kalir T, Cohen C, et al. Endometrial histopathology in
THEME
Travel medicine
Travel vaccination
BACKGROUND
Immunisation is very cost effective. It provides high level immunity against a range of general and travel specific
pathogens. There are more vaccines available as research and development of vaccines progresses. Some vaccines
require multiple doses to induce long lasting protective immunity, and some will only induce protective immunity for a
limited period of time.
OBJECTIVE
This article outlines the principles of travel immunisation and reviews the use of each individual vaccine.
DISCUSSION
Sonny Lau
Pre-travel consultation is interactive and must be individualised. A systematic approach is required, as well as
knowledge of disease risks and vaccine details. Recommendation of vaccines should be based on travel illness
MBBS, MRCP(UK), MPH&TM,
is Medical Director, Travel epidemiology, and be appropriate to the traveller’s needs and budget. We need to update routine vaccinations relevant
Doctor-TMVC, Melbourne, in Australia, recommend vaccines relevant to the traveller’s usual lifestyle and occupation, and travel vaccines based on
Victoria. sonny.lau@ specific needs.
traveldoctor.com.au
Tony Gherardin
MBBS, MPH, FRACGP, is
National Medical Adviser, Pre-travel vaccinations are an integral part of the travel • Ideally separate administration of live vaccines
Travel Doctor-TMVC, medical consultation. The consultation is interactive by more than 4 weeks; otherwise give on the
Melbourne, Victoria.
and must be ‘individualised’, not ‘cookbook’ (reading off same day
a list of tables). Vaccination requirements are specific • If required, perform and read a tuberculin (Mantoux)
for both the individual and the trip to be undertaken. A skin test before giving live vaccines
systematic approach is required, as well as knowledge • Multiple vaccines can be co-administered, but
of disease risks and vaccine details. Some travellers increases the rate of local side effects
have a limited budget, therefore prioritising indicated • It is critical to ensure a robust ‘cool chain’
vaccines may be necessary. For complex situations, • Good documentation of vaccination is essential;
referral to a specialist centre is appropriate. record batch numbers.
We need to update routine vaccinations relevant in
Principles of travel immunisation
Australia, recommend vaccines relevant to the traveller’s
Immunisation is probably the most cost effective medical usual lifestyle and occupation, and give travel vaccines
intervention. It provides a high level of immunity against based on specific needs.
a range of general and travel specific pathogens. There It is essential to issue travellers with an International
is an increasing range of vaccinations available as Certificate of Vaccination - the vaccination record book
research and development of vaccines progresses. Some (‘yellow book’). All vaccines administered should be clearly
vaccines require multiple doses to induce long lasting detailed with date, vaccine type (including brand name),
protective immunity, and some will only induce protective dose, name of clinic, and signed by the administrator.
immunity for a limited period of time. Practitioners need When referring to a specialist travel clinic, encourage the
to understand the differences and consider booster traveller to attend with their full vaccination record. Table
immunisation where appropriate. 1 and 2 provides a general overview of travel vaccines in
adults and children.
Underlying principles of immunisation
Updating routine immunisation (Australia)
• Every single dose counts
• If courses have been interrupted, continue where left Diphtheria/tetanus/pertussis (DTPa)
off, regardless of the time interval since the last dose Travellers may have a booster for tetanus (and diphtheria)
(we do not have to restart an immunisation schedule if it is more than 10 years since the last dose, or 5
all over again) years in the case of travellers undertaking prolonged
304 Reprinted from Australian Family Physician Vol. 36, No. 5, May 2007
Table 1. Dosage and route of administration of routine background vaccines in adult travellers
Vaccine Brand Main constituents Dose Route Primary schedule Duration of immunity/booster recommendations
Cholera Dukoral Kills 1/ cholerae 01 1 sachet oral 0, 1-6 weeks Cholera protection starts to wane in adults after 2 years,
organisms and B subunit a single dose booster is recommended at 2-3 years for
of cholera toxin adults and after 6 months for children <5 years
Avoid oral typhoid for 8 hours
Hepatitis A Avaxim 160 EIA U inactivated 0.5 mL IM 0,6-12 months Although not yet demonstrated, a completed 2 dose
HAV antigen series of any hepatitis A vaccine provides >20 years
protection; possibly lifetime immunity
Havrix 1440 1440 EIA U inactivated 1.0 mL IM 0,6-12 months

HAV antigen (16+years)
VAQTA 50 U inactivated HAV 1.0 mL IM 0,6-18 months

Adult antigen (18+years)
Hepatitis Vivaxim S. typhi polysaccharide 1mL IM Single dose A dose of monovalent hepatitis vaccine given 6-12
A/typhoid 0.25 mg and 160 EIA combined months later will provide long term (possibly lifetime)
combined inactivated HAV antigen vaccine immunity. Duration of protection against typhoid is
probably 3 years
HepatitisA/ Twinrix 720 EIA U inactivated 1 mL(16+ IM 0,1,6months A completed series may give lifetime immunity to
B combined (720/20) HAV antigen and 20 pg years) or *0 6-12 months hepatitis A and B
recombinant hepatitis B or 7, 21 days and 12
virus surface antigen
a months
Hepatitis B Engerix B Hepatitis B surface 1.0 mL IM 0, 1,6 months A completed series may give lifetime immunity
antigen (rys) protein, (20+years) or
20 pg/mL
H B-Vax II Hepatitis B surface 1.0 mL ** 7, 21 days and 12

0,
antigen (recombinant) (20+years) months
R
e
protein, 10 pg/mL
prin
tedfro
Influenza Fluvax 15 pg haemagglutinin of 0.5 mL SC/IM Single dose As different strains circulate from year to year,
m AustralianFam
Vaxigrip two current influenza A annual vaccination with appropriate formulation is

piuad and 1 influenza B strains recommended
Fluarix
ilyPhysicianV
Influvac
Measles/ Priorix Live attenuated measles/ 0.5 mL IM/SC Ideally two doses Travellers born during or since 1966 who have not
ol.3
mumps/ mumps/rubella vaccine separated by at least 1 received a second dose of MMR vaccine or a'catch up'
6,N
o.5
rubella month dose during the 1998 campaign should be vaccinated

,Ma
A single dose will protect before travelling

y2007 305
95% of adults
306
Table 1. Dosage and route of administration of routine background vaccines in adult travellers (continued)
R
eprin
tedfro
Vaccine Brand Main constituents Dose Route Primary schedule Duration of immunity/booster
m
recommendations
AustralianFam
Poliomyelitis IPOL Inactivated virus strains 0.5 mL SC In unimmunised 3 doses A single dose given as an adult in previously
at 1-2 month intervals immunised individuals confers lifetime
ilyP
If >10 years since last protection
THEME Travel vaccination

hysicianV
primary course, single

dose required
ol. 3
6,N
o.5
ADT Tetanus toxoid 6 Lf, 0.5 mL IM Single dose Provides good protection for 10 years
,M
Tetanus and
a
y2
diphtheria diphtheria toxoid 2 Lf providing pertussis immunity is preferred

0
07
(+/- pertussis)
Boostrix Tetanus toxoid 5 Lf, 0.5 mL IM Single dose
(includes diphtheria toxoid 2.5 Lf,
pertussis) purified antigen of B.
pertussis
Adacel
Tetanus/diphtheria/ Boostrix IPV As per individual 0.5 mL IM Single dose As per individual components
pertussis/polio components
Adacel polio Adacel-IPV will soon be available in Australia
Typhoid Vivotif oral Live attenuated typhoid Single Oral Days 1,3 and 5 (+/- day Repeat course after 3 years if 3 dose series
bacteria capsule *7) given; after 5 years if 4 dose series given
Typherix 25 pg purified Vi capsular 0.5 mL IM Single dose 3 yearly

polysaccharide
Typhim Vi 25 pg purified Vi capsular 0.5 mL IM Single dose 3 yearly

polysaccharide
Japanese J E-VAX Inactivated Japanese 1 mL SC 0,7,21-28 days Single booster dose after 2-3 years
encephalitis encephalitis virus
^Meningococcal Mencevax 50 pg capsular 0.5 mL SC Single dose Revaccinate 3-5 yearly if at ongoing risk
(tetravalent ACWY polysaccharides from
polysaccharide) N. meningitidis serogroups
A, C,W135andY
Menomune 50 pg capsular 0.5 mL SC Single dose Revaccinate 3-5 yearly if at ongoing risk
polysaccharides from
N. meningitidis serogroups
A, C,W135andY
Varicella Varilrix Live attenuated Oka strain 0.5 mL SC 0, 6 weeks or later Duration of protection is unknown, possibly
virus >2000 pfu lifetime immunity
Varivax Live attenuated Oka/merck 0.5 mL SC 0, 4-8 weeks

strain virus >1350 pfu
Rabies Merieux 2.5 IL! inactivated rabies 1 mL IM 3 doses on 0, 7 and If at ongoing high risk of exposure, measure
(pre-exposure inactivated virus antigens 21-28 days
* ***
** rabies antibody titres 2 yearly
prophylaxis) rabies If reported as inadequate, give booster
vaccine
(human
diploid cell)
Rabipur 2.5 IL! inactivated rabies 1 mL IM 3 doses on 0, 7 and

(purified virus antigens 21-28 days
chick
embryo cell)
Tick borne FSME- Inactivated whole cellTBE 0.5 mL IM 0,1-3 months, 9-12 Boost 3 yearly
encephalitis Immun virus months
***0, 7, 21 days with Available through SAS only
booster at 12-18 months
Yellow fever Stamaril Live attenuated yellow fever 0.5 mL IM/SC Single dose 10 yearly boosters if at ongoing risk
virus
*This schedule is not recommended if prompt protection against hepatitis B is required

**This 'rapid' schedule should only be used if there is very limited time until departure to endemic regions
***This 'rapid' schedule should only be used if there is very limited time until departure to endemic regions
ft Young adult travellers who intend staying more than a month in either Europe or North America should be vaccinated against meningococcal group C disease, using either the conjugate
or polysaccharide vaccine
t A fourth capsule of oral typhoid vaccine on day 7 is recommended as it confers more prolonged immunity than the 3 capsule regimen as well as providing higher level of protection.There
Travel vaccination
are 3 capsules in each Vivotif oral pack.Travel clinic may dispense 3 or 4 capsules. Dispensing 4 capsules through retail pharmacies may incur cost of a second pack
R
ep
# Intradermal (ID) course of 0.1 mL on days 0, 7 and 21-28 may be used for travellers with budget constraints and if travelling in at risk countries for <1 year. Postvaccination serology check
rin
te
is recommended. ID route should only be used by experienced practitioners skilled in giving ID injection
dfro
m
NB: Routine use of cholera vaccine is not recommended, as the risk to travellers is very low
AustralianFam
IM = intramuscular injection
THEME
SC = subcutaneous injection
ilyPhysicianV
ol.36,N
o.5
,Ma
y2007 307
or remote travel. This avoids travellers having to seek a Measles/mumps/rubella and varicella zoster
routine booster after an injury during travel when hygiene These common childhood illnesses circulate widely in
standards, cost and access may be problematic. developing countries. The illnesses tend to be more
New dTpa vaccines are available for boosting, severe in adults. The highest risk cohort for measles are
particularly for individuals who have close contact with those born after 1966 and before 1986, where only partial
children, in view of the ever increasing incidence of immunity might have been achieved.1 A history of the
pertussis in older people in recent years. illness or two vaccinations should be sought. Antibody
Table 2. Travel vaccines for children

Vaccine Lower age limit Dose/route Primary schedule Comments
Cholera
Dukoral 2 years 1 sachet orally 3 doses over 2-6 Boost after 6 months in children <5 years
weeks Rarely indicated
Hepatitis A
Avaxim 2 years 0.5 mL IM 0, 6-12 months Recommended for travel to developing
Havrix Junior 2 years 0.5 mL IM 0, 6-12 months countries
VAQTA paediatric/ 1 year 0.5 mL IM 0, 6-18 months
adolescent
Hepatitis A and B
Twinrix Junior (360/10) 1 year 0.5 mL IM 0, 1, 6 months Recommended for travel to developing
Twinrix (720/20) 1 year 1.0 mL IM 0, 6-12 months countries
Japanese encephalitis
JE-VAX 1 year 1-3 years of age: 0, 7, 21-28 days Only for travellers spending more than
0.5 mL SC 4 weeks in high risk rural areas or those
Over 3 years of staying in urban areas of Asia (except
0, 7, 21-28 days
age: 1.0 mL SC Singapore) for more than 1 year
Meningitis ACWY
Menomune 2 years 0.5 mL SC Single dose Revaccinate 3-5 yearly if at continuing
Mencevax risk
Should be preferably preceded by
MenCCV by at least 2 weeks or MenCCV
delayed for at least 6 months after
4vMenPV
Rabies
MIRV (HDCV) 1 year 1.0 mL IM 0, 7, 21-28 days Children are at greater risk of disease
Rabipur (PCECV) than adults
Rotavirus
Rotateq 2 months 2.0 mL orally 2, 4, 6 months Minimum interval between doses 4
Rotarix 1.0 mL orally 2, 4 months weeks
Typhoid
Vivotif oral (oral live 6 years Oral capsule One capsule on 1, 3, Children often cannot swallow capsules
vaccine) 5 (and 7) days
Typherix or Typhim Vi 2 years 0.5 mL IM Single dose Do not give live oral vaccine with
(injectable killed) antibiotics, sulphonamides or proguanil
Yellow fever
Stamaril 9 months 0.5 mL IM/SC Single dose Yellow fever vaccine should not be given
to infants aged under 9 months due to
the risk of encephalitis
IM = intramuscular injection SC = subcutaneous injection
Travel vaccination THEME
levels can guide when unsure, and those with inadequate children cannot take the capsules, therefore injectable
protection should be offered vaccination. vaccine is preferred for children. Oral typhoid vaccine
comes in a three dose pack, so a fourth dose means
Influenza
that the patient needs to purchase a second pack, and
Influenza vaccination should be offered to all international therefore incurs additional cost.
travellers as influenza is the commonest vaccine
Hepatitis B
preventable disease encountered by travellers, and
influenza virus circulates all year in tropical zones. Airports, Long term and frequent travellers should be immunised
lounges and waiting areas are common sites of infection. against hepatitis B, which can be transmitted through
Annual vaccine should be encouraged. The overlap of sexual contact and accidental body fluid exposure.
content of the two hemisphere influenza vaccines is often Accessing medical interventions in developing countries is
high, so our vaccine is usually adequate. The vaccine does a risk factor for hepatitis B.
not protect against avian influenza. Pneumococcal vaccine
Poliomyelitis
should be offered to travellers in high risk categories.
Restricted to a few countries until 2003, recent spread has
Choosing travel vaccinations
increased the number of infected countries, notably Africa
Hepatitis A and the Indian subcontinent. There was an outbreak in
Hepatitis A is a common illness for travellers, distributed Indonesia in 2005. Travellers to endemic countries should
widely across the developing world. The severity of have a booster if it is more than 10 years since their last
hepatitis A infection is highly correlated with the increasing dose. Current international recommendations are that a
age of the subject (and previous liver disease). All travellers single booster of inactivated polio vaccine (IPV) given in
to developing countries should be vaccinated. adult life to those fully vaccinated in childhood will confer
Modern vaccines are very immunogenic and protection lifetime immunity.4,5
is probably 100% and lifetime after two doses, although
Cholera
anecdotal cases of vaccine failure have been reported. The
vaccine offers immediate protection after a single dose, so Cholera is not generally a disease of travellers, despite its
can be given up to the day of departure, with the second widespread distribution. Most travellers simply need to be
dose given after 6 months, or years later.2 All brands of counselled to avoid drinking local water and basic hygiene
vaccine are interchangeable. Routine postimmunisation measures. Cholera vaccination is not required of any
serological surveillance is not recommended. traveller for border crossings.
Hepatitis A vaccine is also presented as a combination For specific individuals vaccine may be required, and
vaccine with typhoid or hepatitis B. Hepatitis A protection oral vaccine is now available. It is an efficacious vaccine
is achieved after two doses of Twinrix given 4 weeks against cholera and is well tolerated, protecting against
apart, or three doses given over 3 weeks. A single dose cholera for 2 years.2 It has a protective effect of about 3
of Twinrix may not be adequate for hepatitis A protection months against enterotoxigenic Escherichia coli (ETEC), a
(see product information). In cases of time constraint, a common cause of traveller’s diarrhoea. In view of the rarity
single dose of hepatitis A vaccine should be given instead of cholera affecting travellers, but for its action against
of Twinrix. ETEC, the indications for vaccination are:
• water scientists, health or aid workers likely to be
Typhoid
working in disaster areas where cholera is possible
Typhoid fever from Salmonella typhi infection is less • travellers to endemic areas who have a condition or
common than hepatitis A. A high level of endemicity exists treatment likely to reduce gastric acidity or where
in south Asia, Africa, South America and other developing traveller’s diarrhoea is unacceptable.
countries, and travellers make up approximately 70% of
Meningococcal disease
cases reported in industrialised countries.3 Multi-drug
resistant strains are now reported in Asia, the Middle In developing countries, outbreaks of meningococcal
East and Latin America.3 Risk is generally low to travellers disease are mainly caused by serogroup A, W135 and
who are cautious with food and water precautions. Both C. Tetravalent vaccine, not the monovalent group C
injectable and oral vaccines are available and are of similar vaccine, is indicated for those where an increased risk of
efficacy; in the order of 50-70%. Oral vaccine provides meningococcal disease exists. This includes:
better and longer protection if four doses are given.2 Small • the meningococcal belt of sub-Saharan Africa
Reprinted from Australian Family Physician Vol. 36, No. 5, May 2007 309
• pilgrims on the Hajj for children under 5 years of age who may be at high risk,
• those in isolated, crowded conditions (remote and for selected adults where tuberculosis risk is high (eg.
trekking, refugee camps), and health workers). Tick borne encephalitis vaccine is available
• those entering areas of existing outbreaks. through the special access scheme.
Yellow fever
Yellow fever vaccination is the only mandatory vaccination
References
and protects against disease where it is prevalent. A valid 1. National health and Medical Research Council. Australian Immunisation
vaccination certificate is required for entry from infected Handbook. 8th ed, 2003. Available at www.immunise.health.gov.au/
internet/immunise/publishing.nsf/Content/handbook03.
areas into countries vulnerable to introduction of yellow 2. Yung A, Ruff T, Torresi J, Leder K, O’Brien D. The manual of
fever, including Australia. The vaccine must be administered travel medicine: a pre-travel guide for health care professionals. 2nd
edn. Melbourne: IP Communications, 2004.
at an approved yellow fever vaccination centre. Vaccination
3. World Health Organisation. Typhoid fever. Available at www.who.
is contraindicated or problematic in the following individuals int/topics/typhoid_fever/en/ [Accessed 16 March 2007].
4. World Health Organisation. International travel and health, 2007.
and specialist advice should be sought:
Available at www.who.int/ith/en/.
• elderly patients (>65 years of age) 5. CDC, US Department of Health and Human Services. Health informa
• infants <1 year (particularly <9 months) tion for international travel, 2006-2007. Available at www.cdc.gov.
• those with impaired immune status or anaphylactic

type of hypersensitivity to eggs or previous yellow
fever vaccination, and
• those with a past history of thymus gland problems.
Japanese encephalitis
Japanese encephalitis is transmitted by mosquitoes in
many countries across Asia and into Oceania. It is relatively
rare, and is generally resticted to rural areas. Vaccine is
indicated for people living in endemic areas or travellers
spending more than 1 month in rural areas.
The vaccine is associated with high rates of adverse
reactions; local reactions in 20% of vaccinated individuals,
and systemic symptoms in 10%. Urticarial reactions
have been reported and observation recommended
postvaccination for 30 minutes. Hypersensitivity reactions
occur in 0.5% of cases.
Rabies
Rabies is transmitted through the bite or scratch of
animals, mainly dogs, in many countries of the world,
especially Africa and Asia, and travellers are at risk
from exposure in an unpredictable way. While all
travellers to endemic areas should be counselled
about prevention, vaccines should be considered for
long term travellers and expatriates. Children are at
higher risk. The vaccines are expensive, but are safe
and effective, and pre-immunised individuals can be
managed by vaccine only after subsequent exposure.
Routine boosters for travellers previously immunised are
no longer recommended.
Other vaccines
Rotavirus vaccine is relevant to infants travelling to the
developing world. BCG (TB) vaccine may still have a role
THEME
Arrhythmias
Emergency
management of acute
cardiac arrhythmias
Hugh JM Grantham BACKGROUND
MBBS, FRACGP, is Medical
Anything other than normal sinus rhythm can be classified as an arrhythmia. However not all arrhythmias need
Director, SA Ambulance acute intervention.
Service, Adelaide, South
Australia. grantham.hugh@
OBJECTIVE
saambulance.com.au This article reviews which arrhythmias need intervention in an acute setting, and the various options available
for intervention.
DISCUSSION
The impact of an arrhythmia upon perfusion determines what intervention should be considered. Conscious level,
cardiac ischaemia secondary to poor perfusion of the coronary arteries and blood pressure need to be assessed.
Patients with bradycardias with adequate perfusion are treated initially with oxygen and observation. Sinus bradycardia
not responding to increased oxygenation is treated with atropine. For other bradycardias the two alternatives are to
drive the inherent rate with a sympathomimetic drug or to pace the patient with an external or internal pacer. Usually
supraventricular tachycardias are not life threatening. Unconscious patients with wide complex tachycardia should be
treated in a standard cardiac arrest approach. Conscious patients in ventricular fibrillation however, can be treated either
chemically or with synchronised cardioversion. If a patient is in cardiac arrest the approach is to establish effective
resuscitation and early defibrillation as per Australian Resuscitation Council guidelines.
Not all arrhythmias need acute intervention. Some are probably the best marker of perfusion in this
relatively benign and as such are best not addressed situation. Although blood pressure has always
in the acute setting. For instance, atrial fibrillation been considered as a key marker it is probably less a
(AF) should not be addressed in the acute setting useful than conscious level, as a marker of adequate
unless of very recent origin. Other arrhythmias - while perfusion. Mean arterial pressure is the key measure
looking dramatic - are still managing to perfuse the of perfusion but unfortunately is not well related to
brain and are better than the alternatives that might measured blood pressure particularly at the extremes of
result from an attempt to correct them. An approach heart rate. The hardest decisions regarding intervention
to arrhythmias that are still perfusing is to provide are for patients who, while conscious, are obviously
support with oxygen and ventilation while observing not perfusing well and for whom the consequences
the patient. The alternative approach of more active of intervention may include an even worse rhythm.
management sometimes runs the risk of creating a For example, a complete heart block with a junctional
situation that is worse than the current one. escape rhythm may generate perfusion that, although
not optimum, is adequate. If in doubt, an approach
The criteria for deciding that an arrhythmia of maximising oxygenation, optimising preload and
needs intervention vary with the situation adopting an attitude of optimistic expectancy is the
and the support available. Conscious level is safest strategy.
492 Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007
Too slow
Bradycardia can be a sinus bradycardia often associated
with increased vagal tone (Figure 1) or secondary to
a failure of the sinoatrial (SA) node or atrioventricular
(AV) block. Atrioventricular block is a problem of the
conduction system with a block at the AV node. Complete
Figure 1. Sinus bradycardia
AV block results in the failure to transmit any impulses
from atria to ventricle (Figure 2) while the partial AV
block will result in either a slower transmission or an
intermittent transmission.
The degree of bradycardia and the impact upon
perfusion determine whether or not intervention should be
considered. Conscious level is a good guide of perfusion,
as is evidence of ischaemic chest pain secondary to poor
perfusion of the coronary arteries. Blood pressure and
other indirect measures of perfusion (the ability to provide
a pulse wave detected by a pulse oximeter) are useful
adjuncts when assessing perfusion status.
Evidence of ischaemia in the right coronary artery
territory (inferior leads) in a patient who is not yet
bradycardic raises the possibility of bradycardia secondary
Figure 2. Bradycardia (complete block)
to failure of the SA node or AV node. A patient with
evidence of ischaemia in this area should have an
intravenous (IV) inserted and preparations available for
pacing or drug intervention.
The initial approach to sinus bradycardia should be to
increase oxygenation and ensuring an adequate preload
(Figure 3). Simply lying the patient down and raising
the legs will improve venous return and improve the
preload. If the jugular venous pulse (JVP) or pressure can
be assessed and is found to be low, a little additional IV
fluid judiciously given is appropriate. If however the JVP
is already elevated, then increasing the preload further
would be harmful as it is likely to lead to acute pulmonary
oedema. Sinus bradycardia will often respond to atropine
as atropine effectively removes the parasympathetic brake
on the SA, and to a much lesser extent the AV node. The
dose of atropine should be at least 1 mg as small doses
have been known to paradoxically reduce the heart rate
by interfering with the sympathetic system. In reality this
means two ampoules of 600 pg of atropine for an adult.
Bradycardia that is not sinus rhythm is running on Figure 3. Bradycardia improving with oxygen
either a junctional or a ventricular pace maker (Figure
4). Although atropine tends to be given as an automatic
response it is not logical to expect it to be very effective
as there is only a slight parasympathetic innovation of
the AV node. If the patient is symptomatic and oxygen
and optimising the preload with posture has already been
tried, the two alternatives are to drive the inherent rate
with a sympathomimetic drug or to pace the patient with
Figure 4. Bradycardia
an external or internal pacer arrangement. Adrenaline is
Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007 493
THEME Emergency management of acute cardiac arrhythmias
an excellent choice of sympathomimetic drug, although

isoprenaline is often the drug of choice. Whichever drug
is used the route should be IV and ideally by a low dose
infusion gradually increasing the infusion rate until a desired
response is achieved. The issue here is balancing improved
oxygenation of the coronary muscle with increased oxygen
demand. Although improving the heart rate improves
coronary artery perfusion pressure and thus oxygenation,
oxygen demand rises as heart rate and force of contraction
increase. Usually the predominant effect is beneficial from
the increase in coronary artery perfusion pressure.
Externally applied pacemakers are becoming
Figure 5. Supraventricular tachycardia commonplace and can be easily used as an alternative.

The self adhesive pads should be placed on the anterior
chest wall and between the shoulder blades for optimum
current transmission. The patient should be warned that
this will be uncomfortable. The pacing function is selected
at an initial rate of about 60 bpm. It is not a good idea
to select too high a rate initially as an increase in heart
Figure 6. Ventricular tachycardia rate increases the oxygen demand. The current delivered
should be quickly increased to a point where capture
occurs. Capture will be confirmed by the presence of
a complex after each pacing spike and hopefully by the
presence of a palpable pulse. At this point, the increased
perfusion will be improving the patient’s conscious state to
the point where they will be aware of the distress caused
by the repeated muscle contractions. Once perfusion has
been achieved it is appropriate to give midazolam (and
possibly an opiate in a small dose) to relieve the patient’s
discomfort and reduce their memory of the event. In a
more intensive setting, formal pacing with an internal wire
can be considered.
Too fast
Tachycardias can also reduce cardiac output as ventricular
filling becomes ineffective; they also increase myocardial
oxygen demand making ischaemia worse.
A supraventricular tachycardia (SVT) arises above
the ventricles (Figure 5) and, with the exception of atrial
fibrillation/flutter, has an atrial contraction preceding each
ventricular contraction. This means that the SVT is likely
to have better ventricular filling and hence better cardiac
output. Usually SVTs are not life threatening and the patient
remains conscious, although distressed, by palpitations.
Initial management is to increase the vagal stimulus to
the AV node by performing a Valsalva manoeuvre. To do
this properly the patient should be supine and a forced
expiration against a blocked airway needs to be maintained
for at least 15 seconds. The vagal stimulus occurs after
Figure 7. Basic life support flowchart
letting go. Rubbing the carotid sinus will also produce
Reproduced with permission: Australian Resuscitation Council
vagal stimulation, however this is considered dangerous
Emergency management of acute cardiac arrhythmias THEME
in anyone over 50 years of age because of the risk of

disturbing atherosclerotic plaque. If a Valsalva manoeuvre
has failed, the usual drug treatment is adenosine given in
increasing doses of 6, 12, and if still not effective, 18 mg
as sharp IV pushes into a running line (at least 18 gauge).
This gives a 'chemical defibrillation' giving the heart an
opportunity to restart in sinus rhythm. Some patients
find this sensation distressing and so should be warned
beforehand.
Rapid AF is a common supraventricular arrhythmia
characterised by a rapid irregular QRS, which is often best
heard by listening to the rhythm of the beat via the audible
alarm. Long term AF should not be reverted in the acute
setting without first excluding the possibility of mural
thrombosis in the atria which might then become the
source of an embolus. Management of AF is discussed in
a separate article in this issue.
Ventricular tachycardia (VT) arises below the atria and
is characterised by a broad complex tachycardia that often
has an unusual axis (Figure 6). The unconscious patient
should be treated as if in ventricular fibrillation (VF) with
a standard cardiac arrest approach. Conscious patients
can be treated either chemically or with synchronised
cardioversion. The advantage of cardioversion is that there
is no after effect persisting after treatment and lowering
of cardiac output. Any antiarrhythmic drug used will also
reduce myocardial contractility. For this reason, drug
treatment of VT should be reserved for patients with a
reasonable initial cardiac output despite the VT. In the past, Figure 8. Adult cardiorespiratory arrest
Reproduced with permission: Australian Resuscitation Council
lignocaine (1.5 mg/kg=100 mg for adults) was commonly
used but is now being displaced by amiodarone (150
mg slowly in an IV infusion over 30 minutes and share • the presence of P waves independently timed to
the call with a cardiologist) as a drug of choice; sotalol the ventricular complexes in VT. These are seen as
and magnesium have also been used in this role. If the irregularities behind the QRS complexes that appear
patient is not well perfused, cardioversion is preferable on a regular basis but are not there on all beats
to drug therapy. For this procedure the patient is given a • the presence of fusion beats where a P wave has
small dose of midazolam to ensure that they have little or transmitted through the AV node and then the
no memory of the event, but not enough to significantly ventricular depolarisation has been subsumed by the
sedate them (up to 3 mg in an adult). Once the drug has VT wave in VT
circulated, which will take time in a compromised patient, • an abnormal axis (often seen as failure of the chest,
a synchronised DC shock is given via the defibrillator pads leads to progress from negative to positive; often
or paddles. Most patients will revert at 50 J but starting seen in VT)
at 100 J gives a high probability of first shock success. • the patient’s age and perfusion status are a guide,
The shock is delivered ‘synchronised’ - this means you with elderly patients with poor perfusion status being
avoid defibrillating in the middle of the T wave which might more likely to be VT.
provoke VF.
Ventricular ectopics
Supraventricular tachycardias in patients with a wide
electrocardiogram (ECG) complex can be confused with VT. The presence of more than the odd ventricular ectopic
If the patient is poorly perfused or unconscious it is safer used to be a trigger to reach for an antiarrhythmic drug
to treat them as a VT. The criteria that help to differentiate because of a fear of the ‘R on T phenomenon’. This brought
between a broad complex ST and a VT are: with it the consequences of decreased contractility and
THEME Emergency management of acute cardiac arrhythmias
in the chest compression rhythm and a steadily escalating

level of adjuncts.
Basic life support

Once cardiac arrest has been observed and the airway
confirmed as clear with no respiratory effort, two gentle
breaths are administered. Try not to overinflate the
stomach as this may cause reflux and airway soiling.
The pulse check is only one of the signs of life, and in
a patient who has allowed two ventilations without
objection, is probably not indicated. Compressions should
be commenced as soon as possible at a rate of 100 per
minute (ie. almost two per second) and at a depth of one-
third of the chest anterior posterior measurement. A ratio
of 30 compressions to two ventilations is appropriate for all
adults and children regardless of the number of operators.
In a specialist advanced life support setting, children can be
managed with a 15:2 ratio and neonates with a 3:1 ratio.
However, a ratio of 30:2 will suffice in most circumstances
encountered outside a specialist unit.
Defibrillation and drugs

Defibrillation should occur as early as possible and
confined to a single shock at a high energy setting. This
means 360 J in an older monophasic defibrillator, and
200 J in a modern biphasic defibrillator. Children receive 2
J/kg followed by 4 J/kg rounded to the next higher setting,
regardless of the defibrillator type.
Figure 9. Child cardiorespiratory arrest
Reproduced with permission: Australian Resuscitation Council Once the shock has been delivered it is important to
go straight back to compressions and not waste time
sometimes a proarrhythmic effect of the drug. Ectopics watching the rhythm develop. After 2 minutes of CPR
are better treated with attention to oxygenation and (which will be 5 cycles of 30:2) it is time to see what
perfusion and preparation to defibrillate should any VF that rhythm the defibrillation produced. No harm will be done
occur. Oxygen is a wonderful antiarrhythmic that does not to the heart if compressions are delivered on top of a
decrease myocardial contractility. developing rhythm. 1 mg of IV adrenaline is given every 3
minutes to maintain peripheral vascular tone.
Cardiac arrest
Advanced airway techniques are used as soon as
Patients presenting in cardiac arrest will have an underlying possible, however if intubation is used there should not be
rhythm of: an interruption to compressions of more than 20 seconds
• VF/VT which is treatable with defibrillation and a maximum of two attempts is reasonable. Failing
• pulseless electrical activity (PEA) which cannot be this, a laryngeal mask airway provides an airway that is far
treated with defibrillation and where an underlying superior to an ordinary oropharyngeal airway.
cause should be sought, or If the patient still remains in VF despite repeated
• asystole which will not respond to defibrillation but cycles of CPR, defibrillation, adrenaline and improved
can occasionally be encouraged into a more favourable oxygenation/ventilation then an anti-arrhythmic drug
rhythm with oxygen and CPR with adrenaline. is appropriate and the preferred choice is amiodarone
If a patient is in cardiac arrest, the approach is to establish 300 mg IV. If amiodarone is not available, lignocaine
effective resuscitation and early defibrillation. The 100 mg IV is an acceptable alternative. Persistent VF in
Australian Resuscitation Council Basic and advanced life this situation can only be treated with more CPR and
support guidelines (www.resus.org.au) are described in oxygen once an adequate dose of antiarrhythmic has
Figures 7-9. The key issues are a focus on minimal gaps been given.
Emergency management of acute cardiac arrhythmias THEME
PEA and asystole

The presence of PEA should prompt a review of the
reversible causes - the ‘Hs and Ts’ (Figure 8):
• hypoxia
• hypovolaemia
• hypo-/hyper-thermia
• hypo-/hyper-kalemia and other metabolic disorders
• tamponade
• tension pneumothorax
• toxins, and
• thrombosis (pulmonary or coronary).
Asystole can be treated with oxygen CPR and adrenaline.
It is acceptable to give at least 1 mg of atropine in this
situation as vagal tone can produce asystole.
Postresuscitation
Postresuscitation care focuses on maintaining a safe
airway, adequate ventilation and oxygenation, supporting
perfusion, and facilitating transport to hospital.
Conclusion
The management of arrhythmias is not as daunting
as initially seems. For rhythms that are still perfusing,
administration of high concentrations of oxygen,
attention to optimising preload (JVP) and patience are
good first responses which then allow plenty of time to
share the problem with a cardiologist before embarking
on drug therapy. For rhythms not perfusing, the
response is as per a standard cardiac arrest following
the ARC directions included in this article.
RESEARCH
Macrocytosis
An Australian general practice perspective Stella Elisabeth Rumsey
MBBS FRACGP, is a general
practitioner, Morisset East,
New South Wales. srumsey@
baysurgery.com.au
BACKGROUND Bevan Hokin

Clinicians’ approaches to identifying and investigating red blood cell macrocytosis are variable. There is little literature MSc, MAppSc, PhD, is Director
on the Australian primary care approach. of Pathology, Sydney Adventist
Hospital, Wahroonga, New
METHODS South Wales.
Mean corpuscular volume (MCV) in blood counts from an urban Australian general practice were calculated and general
Parker John Magin
practitioners in the surrounding division were surveyed on their experience of and approach to investigating macrocytosis.
MBBS, PhD, FRACGP, is
RESULTS Senior Lecturer, Discipline of
Mean corpuscular volume above 100 fL was found in 1.7% of patients, and 7.3% had an MCV above 96 fL. Ninety-four General Practice, University of
percent of responding GPs replied they would further investigate this clinical finding, particularly at levels above 100 fL. Newcastle, New South Wales.
Alcohol excess and vitamin B12 deficiency were the most common single causes of macrocytosis in their experience. Dimity Pond
DISCUSSION MBBS, PhD, FRACGP, is

Macrocytosis can be a marker for disease and it is important to identify and investigate its presence. Further research Professor, Discipline of
General Practice, University of
is needed to clarify the reference range for healthy adults in general practice and to formulate evidence based clinical
Newcastle, New South Wales.
guidelines for investigating isolated macrocytosis.
The average volume of red blood cells in a sample is especially alcohol abuse, may have been overlooked’.
expressed as the mean corpuscular volume (MCV) The authors sought to explore this subject in an
and is measured in femtolitres (fL). Mean corpuscular Australian primary care setting. Funding was provided by
volume is routinely reported as part of a full blood the Commonwealth Department of Health and Ageing’s
count along with other red blood cell indices. An Primary Health Care Research Development Program;
elevated MCV is referred to as (erythroid) macrocytosis. ethics approval was obtained from the University of
The upper reference limit for MCV quoted varies from Newcastle Human Research Ethics Committee.
95-100 fL.1-3
Phase 1: frequency of macrocytosis in a
general practice
Macrocytosis may or may not be associated with anaemia;
isolated macrocytosis refers to an elevated MCV in the Method
absence of associated abnormalities of the haemoglobin, Mean corpuscular volume values were obtained for 2801
white cell and platelet counts. Guidelines exist for patients aged over 16 years at time of testing who were
investigating macrocytic anaemia, but it is unclear whether referred to the main pathology provider for a full blood
these guidelines can be used for isolated macrocytosis. count by a single urban group practice over a 5 year time
The presence of macrocytosis can be an indicator period. There was no upper age limit. Initial blood counts
of underlying disease. Potential causes of macrocytosis were used so that each patient was included only once.
are listed in Table 1;1,2,4,5 several have serious health
Results
consequences. The investigation of macrocytosis may
provide an opportunity to identify and manage these The MCV values had a normal distribution with a mean of
conditions. However, hospital based research suggests 90.3 fL and standard deviation of 4.8. This is comparable
that primary care clinicians’ approaches to identifying with another population based Australian study8 as well as
and investigating macrocytosis are variable.6 Seppa et al7 the laboratory's mean that sets an upper reference limit of
stated that ‘evaluation of macrocytosis, when undertaken, 100 fL for MCV.
was well done by general practitioners. However, it The proportion of initial blood counts with an MCV above
was performed too seldom and, thus, several diseases, 96, 100 and 105 fL is shown in Table 2.
RESEARCH Macrocytosis - an Australian general practice perspective
Phase 2: GP questionnaire disease, folate deficiency and age were reported

less frequently.
Method When asked to consider an otherwise
A one page survey was sent to the 408 well adult with isolated macrocytosis, 94%
members of an urban Australian division of of respondents indicated that they would
general practice in 2005. An item was placed investigate this finding. Figure 1 shows the
in the division newsletter advising the intended frequency with which these GPs reported they
(n=132) (n=138) (n=141) (n=142)
research so as to increase the rate of completion would investigate an otherwise well adult with Mean corpuscular volume
and return of the questionnaire. A second copy differing MCV levels given a reference range of
Figure 1. Number of responses investigating
of the survey was mailed with a modified cover 80-100 fL. macrocytosis at different MCV levels
letter asking GPs to disregard the survey if they Respondents raised some important issues
had replied the first time. One hundred and fifty in regard to macrocytosis: limit of normal for MCV.1-3 Laboratories often
of 408 (37%) surveys were returned. • the value of ‘watchful waiting’, repeating quote an upper reference limit of 100 fL5,
The survey employed both open ended and the blood count after a period of time however this does not necessarily reflect the
multiple choice questions asking about the most • the role of history, medication use and upper limit of MCV in healthy adults and therefore
common cause of macrocytosis in the GP’s alcohol assessment the level beyond which investigations should be
experience, investigating isolated macrocytosis • the importance of the patient’s general considered; 96 fL may be a more appropriate
in an otherwise well adult patient, frequency of health reference limit.3 A number of the GPs surveyed
investigation of macrocytosis at various MCV • discussing the case with a haematologist replied that they would investigate patients with
levels, and general comments. • a request for a cost effective approach to an MCV below 100 fL.
investigating persistent macrocytosis with Patients need to obtain the right tests at the
Results
no clear underlying cause right time if they are to receive quality primary
Eighty-one percent of respondents identified • the importance of clinical judgment and health care. We question the appropriateness of
excessive alcohol intake or vitamin B12 deficiency ‘treating the patient, not the numbers’. using 100 fL as a universal upper reference limit
as the most common causes of macrocytosis in Information on respondent demographics was for MCV and suggest that guidelines for the
their clinical experience. ‘Idiopathic’ causes, liver not collected. Limitations to this phase of the investigation of isolated macrocytosis in primary
research include the low overall response rate care be developed.
Table 1. Potential causes of macrocytosis and the potential for responder bias. This limits
Vitamin B12 and folate deficiency the generalisability of the findings.
Alcohol References
Discussion 1. Eastham RD. Clinical haematology. 5th edn. Bristol: John
Liver disease Bright & Sons, 1977.
Bone marrow disorders The variability between doctors’ investigations 2. Beutler E, Marshall AL, Coller BS, Kipps TJ, Seligsohn U.
(myelodysplasia, aplastic, of macrocytic patients reported in the literature6

Williams hematology. 6th edn. New York: McGraw-Hill,
dyserythropoietic and sideroblastic 2001.

was reflected in the stated practices of 3. Metz J. Appropriate use of tests for folate and vitamin
anaemias and leukaemia)
B12 deficiency. Aust Prescr 1999;22:16-18.
Medications respondents to the questionnaire.
4. Rozenberg G. Microscopic haematology: a practical guide
Physiological (neonates, pregnancy) Guidelines exist for the investigation of for the laboratory. 2nd edn. London: Martin Dunitz, 2003.
5. The Royal College of Pathologists Australasia. RCPA
Hypothyroidism macrocytic anaemia. However, there is little
manual. 4.0 edn. Available at: www.rcpamanual.edu.
Artifact (cold agglutinins, clinical information on investigating isolated au/sections/pathologytest.asp?s=33&i=285 [Accessed 24
hyperglycaemia) macrocytosis where an elevated MCV exists May 2006].
Hyperlipidaemia 6. Wymer A, Becker DM. Recognition and evaluation of red

without associated abnormalities of other full blood cell macrocytosis in the primary care setting. J Gen
Reticulocytosis blood count indices. Intern Med 1990;5:192-197.
Postrenal transplant 7. Seppa K, Heinila K, Sillanaukee P, Saarni M. Evaluation
An elevated MCV may be a useful indicator
of macrocytosis by general practitioners. J Stud Alcohol
of alcoholic liver disease and B12 deficiency 1996;57:97-100.
Table 2. Proportion of patients with MCV although in the latter the MCV elevation may
8. Tsang CW, Lazarus R, Smith W, Mitchell P, Koutts J,
Burnett L. Hematological indices in an older population
over 96, 100 and 105 fL rise only once the B12 levels are quite low.7,9 sample: derivation of healthy reference values. Clin Chem
To estimate the reference range on normally 1998;44:96-101.

MCV (fL) Number of patients (%) 9. Metz J, McNeil AR, Levin M. The relationship between
N=2801 distributed data, laboratories usually take the two serum cobalamin concentration and mean red cell volume
standard deviations either side of the mean, which at varying concentrations of serum folate. Clin Lab
96.0-99.9 205 (7.32) Haematol. 2004;26:323-5.
includes 95% of all results. The range determined
100.0-104.9 48 (1.71)
may then be modified to reflect clinical utility.
105+ 15 (0.54) CORRESPONDENCE email: afp@racgp.org.au
There are differing opinions regarding the upper
THEME
Nausea and
vomiting
Nausea and
vomiting in adults
A diagnostic approach
BACKGROUND
Most people experience nausea and vomiting at some stage, but when these symptoms recur frequently they can
Andrew Metz significantly reduce quality of life. In most cases, a thorough history, examination and simple investigations can yield a
MBBS(Hons), is a diagnosis. Chronic nausea is a more challenging problem with its many potential causes and with a significant number
gastroenterology advanced
of patients remaining undiagnosed despite extensive investigation.
trainee, The Royal Melbourne
Hospital, Victoria. OBJECTIVE
Geoff Hebbard This article discusses the assessment and management of acute and chronic nausea and vomiting in adults.
MBBS, BMedSci, PhD, FRACP, DISCUSSION

is Director of Gastroenterology,
Gastrointestinal infections and food poisoning are the most common causes of acute nausea and vomiting. Medication
The Royal Melbourne Hospital,
side effects and pregnancy should always be suspected. Hospitalisation may be required for severe metabolic
Victoria. geoff.hebbard@
mh.org.au abnormalities, dehydration or surgical causes. There are many potential causes of chronic nausea and vomiting and
a comprehensive history and examination is required. Symptoms are poor predictors of functional versus pathological
illness. Type and extent of investigation must be tailored to the individual patient.
Only one-quarter of people affected by acute nausea mouth, usually without nausea, and may be a symptom of
and vomiting visit their general practitioner. Of these, gastro-oesophageal reflux disease or rumination syndrome.
two-thirds cite the severity of their symptoms as the The causes and plan for investigation of nausea and
reason, while the remainder fear serious disease and vomiting can be conveniently divided into whether the
seek reassurance from their doctor.1 The economic symptoms are acute or chronic. Chronic symptoms are
burden for the community is also significant with defined as those lasting 1 month or more.
a British study demonstrating a loss of 8.5 million
Acute nausea and vomiting
working days per year.2
Aetiology
Vomiting is controlled by the brainstem that coordinates The most common cause of acute nausea/vomiting (Table
a series of actions involving the gut and skeletal muscle, 1) is viral gastroenteritis or bacterial food poisoning.
resulting in the forceful ejection of the contents of the Gastrointestinal infections are more common in autumn
upper gut. Essentially, vomiting is a reflex designed to and winter and in children and young adults. Viruses include
expel potentially harmful substances from the body. rotavirus, adenovirus and norovirus (especially during
It is important to distinguish between the various epidemics). Preformed bacterial toxins ingested in food
symptoms that may be described as ‘vomiting’. Nausea may cause vomiting alone, and are often due to ingestion of
is the unpleasant sensation of being about to vomit and poorly cooked and inappropriately stored food contaminated
is often associated with mouth watering. Vomiting is with Staphylococcus aureus or Bacillus cereus.
the forceful expulsion of gastric contents via the mouth. An infective cause is supported by the presence of
Retching is contraction of the abdominal muscles without diarrhoea, mild abdominal pain, fever, malaise, a potential
the expulsion of gastric contents. In contrast, regurgitation cause/contact (eg. travel, sick family member, ‘dodgy’
is the effortless appearance of gastric contents into the meal) and an absence of significant abdominal tenderness.
688 Reprinted from Australian Family Physician Vol. 36, No. 9, September 2007
Toxin mediated vomiting develops 1-6 hours after ingestion
Table 1. Causes of acute nausea and vomiting
of the offending food. Other infections such as otitis media,
urinary tract infections (UTI), meningitis and hepatitis can Common
also result in vomiting as part of the overall clinical picture, • Gastroenteritis
but rarely present with nausea and vomiting alone except • Nongastrointestinal infections (eg. UTI in elderly/institutionalised patients)
in elderly or institutionalised individuals. • Medications
Medication side effects usually present acutely soon Not to be missed
after commencing the drug, but may be delayed or go • Surgical causes
unrecognised and present subacutely. A full medication • Pancreatitis
history including vitamins, herbs and over-the-counter - cholecystitis
drugs should be sought, as well as an alcohol and drug - appendicitis
history. Recent changes in medication are particularly - small bowel obstruction
relevant. Any recently commenced drug should be • Diabetic ketoacidosis
considered as a potential cause of nausea/vomiting, • Addisonian crisis
however, some are particularly prone to cause this side • Raised intracranial pressure (usually with other neurological features)
effect (Table 2). • Hepatitis
Mechanical gastrointestinal obstruction causes vomiting • Ingestion of irritants/allergens
often without nausea as a prominent symptom, at least
initially. The nature of the vomitus may give a clue to the
Examination
level of the obstruction; undigested food and saliva in
acute oesophageal obstruction, partially digested food in Dehydration is assessed clinically by examining for dry
gastric outlet obstruction, and bile or faeculent vomiting mucous membranes, reduced skin turgor, tachycardia and
with more distal obstructions. Small bowel obstruction is postural hypotension.
usually acute, persistent and associated with colicky pain; The abdomen should be examined for tenderness
but may occasionally be intermittent or subacute. (particularly localised tenderness), distension or a succussion
Vertigo, neurological symptoms, neck stiffness or splash - a splashing sound heard with a stethoscope when
headache hint at a neurological cause and should prompt the abdomen is shaken in intestinal or pyloric obstruction.
appropriate investigation. Pregnancy should not be Particular attention should be paid to areas where hernias
forgotten in women of childbearing age, particularly those are common. Bowel sounds may be tinkling in mechanical
with early morning nausea. obstruction or absent in an ileus. The presence of abdominal
signs should prompt a surgical opinion.
Initial assessment
Investigations
In the acute setting, history, examination and simple
investigations can often yield a diagnosis. The illness In many cases nil investigations may be appropriate. Basic
is commonly self limiting. The diagnostic approach biochemistry may include (as appropriate):
focuses on identifying the cause (or at least excluding • electrolytes and renal function
significant underlying diseases) with a view to expectant • full blood count
management or directing specific treatment. • pancreatic and liver enzymes
Complications of nausea and vomiting should be • glucose.
identified and acute emergencies should be excluded. Most If small bowel obstruction is suspected, erect and supine
cases are not severe enough to require hospitalisation, abdominal radiographs should be considered. However,
however intravenous (IV) therapy may be required for: it should be remembered that these are neither sensitive
• severe dehydration (inability to tolerate oral fluids) nor specific.2 They can be normal in patients with partial/
• significant metabolic abnormalities related to subacute obstruction and acute gastroenteritis may cause
vomiting (including hypokalaemia, metabolic alkalosis a degree of small bowel dilation and some fluid levels.
or uraemia)
Management
• surgical emergencies (eg. mechanical obstruction,
perforation or peritonitis) Once surgical and major medical causes have been
• other medical or social factors increasing the excluded, rehydration with oral fluids is preferred with
likelihood of complications (eg. underlying renal, oral or intramuscular antiemetic therapy. Patients may
cardiac or hepatic impairment). be discharged with instructions to return if symptoms
Reprinted from Australian Family Physician Vol. 36, No. 9, September 2007 689
THEME Nausea and vomiting in adults - a diagnostic approach
deteriorate or do not improve. If outpatient management remembered that nausea itself can delay gastric emptying.
is not tolerated, admission for IV fluids and parenteral Gastroparesis may occur following gastric surgery (an
antiemetic treatment (IV or IM) is required. Antiemetic increasingly rare cause) or be due to diseases such as
choices include: metaclopramide (oral or parenteral [should longstanding diabetes or scleroderma. In younger patients
be used with caution in young females due to the risk of gastroparesis is commonly idiopathic, often presumed
an occulogyric crisis]); prochlorrperazine (oral, suppository to be due to ‘a virus’ as it may follow an acute episode
or parenteral); or ondansetron (oral or parenteral). Usually suggestive of infection.
no specific follow up is required for a self limiting episode
Underlying medical conditions
of nausea/vomiting unless there are public health issues.
Neurological conditions include increased intracranial
Chronic nausea and vomiting
pressure, migraines, seizures and labyrinthine disorders.
Aetiology Vertigo, neurological symptoms, neck stiffness or headache

hint at a neurological cause. Endocrine causes include
Table 3 outlines the many potential causes of chronic hypercalcaemia, hypothyroidism and Addison disease.
nausea and vomiting. Many gastrointestinal diseases Severe cardiac failure can cause nausea due to liver and
present with nausea, often with associated symptoms. gut congestion. Fever, night sweats and weight loss may
Postprandial nausea and vomiting suggest upper occur with malignancy.
gastrointestinal causes including gastro-oesophageal
Functional nausea and vomiting
reflux disease, functional dyspepsia, gastroparesis or
gastrointestinal obstruction. Vomiting in gastric outlet Unexplained nausea and vomiting may be functional in
obstruction commonly occurs about an hour after eating origin. This is covered in detail in the article ‘Functional
(although timing can be variable). Coeliac disease, nausea and vomiting’ by Nicholas Talley in this issue.
peptic ulcer, upper gastrointestinal malignancy, hepatitis
Assessment and diagnosis
or pancreatic carcinoma may present with nausea or
vomiting as part of the symptom complex, or occasionally A comprehensive history and examination is required.
as the major symptom. Uncomplicated Helicobacter pylori
History
infection is not a cause of chronic nausea.3
The history can be suggestive of the aetiology, but it
Gastroparesis
is important to note that symptoms can be poor
Gastroparesis is a poorly understood condition in which predictors of pathological versus functional illness as
gastric emptying is delayed, presumably due to disordered even significant weight loss may occur in functional
gastric or duodenal motility. The stomach is unable to illness.4 Epidemiologically, the best predictors of
clear food and secretions leading to gastric distension, significant pathology are male gender and increasing
discomfort, nausea and vomiting. The relationship age.4 Exhaustion, number of doctor visits, time off work,
between the severity of gastroparesis and symptoms is associated ‘functional’ symptoms such as headaches and
relatively poor for reasons that are unclear, and it should be chronic pain, ingestion of psychotropic drugs, and negative
H. pylori status are all predictors of functional disease.4
Table 2. Common medications causing nausea and vomiting Patients might volunteer an initiating event. A relationship
to changes in medication should be sought with any drug
• Cancer chemotherapy
considered a potential cause, including over the counter,’
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
natural medications’, vitamins or herbs, and health or
• Digoxin (nausea can occur at therapeutic levels)
nutritional supplements. Common medication causes include
• Antiarrythmics
opiates, NSAIDs, dopaminergic agents (eg. levadopa),
• Oral antidiabetics (especially metformin)
digoxin, antibiotics (eg. doxycycline and sulphonamides) oral
• Antibiotics (especially erythromycin, bactrim)
hypoglycaemics and gastrointestinal drugs (eg. sulfasalazine),
• Sulfasalazine
but any drug should be considered as a potential cause
• Nicotine patches
(Table 2). Chronic heavy alcohol or marijuana use should be
• Narcotics
specifically enquired for. Nausea due to chronic marijuana
• Antiparkinsonian drugs
use is characteristically improved by a hot shower.5
• Anticonvulsants (including at therapeutic doses)
Early morning vomiting is associated with pregnancy,
• High dose vitamins
uraemia, alcohol use and raised intracranial pressure.
Nausea and vomiting in adults - a diagnostic approach THEME
Neurogenic vomiting is often projectile and positional, while may be found or strongly suspected and the appropriate
functional disorders often result in continuous symptoms. therapy commenced. Withdrawal or substitution of a
suspect medication or treatment of depression/anxiety
Examination
should be trialed early as if this results in improvement,
Examination focuses on the general medical and no further investigation may be required. If no cause
gastrointestinal conditions listed in Table 3, along with a is found on initial evaluation, a decision will need to be
nutritional and neurological assessment. It is rare in adults made as to how far it is appropriate to investigate and
for intracranial pathology to present with vomiting alone.1 this will depend on the clinical circumstances. In the
If other symptoms are absent, neurological causes should interim, a therapeutic trial with an antiemetic may be
only be considered if severe and prolonged vomiting is considered if there are no alarming symptoms, although
otherwise unexplained. the cost effectiveness of this technique has not been
evaluated. Dietary modification may also be beneficial,
Investigations
with frequent small meals, reduction of fat content
Following a comprehensive clinical assessment and initial and avoidance of spicy foods or other foods noted to
investigations the aetiology of a patient’s symptoms cause symptoms.
Investigation needs to be tailored to the clinical
Table 3. Causes of chronic nausea and vomiting situation, focusing on the potential causes and the
Drug induced metabolic/nutritional consequences and may include the
• Prescribed medications investigations listed in Table 4.
• Alcohol Upper gastrointestinal endoscopy is the most sensitive
• Illicit drugs and specific test for mucosal lesions and a duodenal biopsy
- marijuana should be taken to assess for Coeliac disease, infection
- opiates or eosinophilic enteritis. Gastroparesis is suggested
Gastrointestinal conditions by retained food at the time of the endoscopy. Further
• Gastro-oesophageal reflux disease investigation may involve computerised tomography

(CT) of the abdomen looking for obstruction, masses
• Functional dyspepsia
pancreatic or hepatobiliary pathology. A small bowel series
• Gastroparesis
is rarely helpful, but may be of value if done during acute
• Peptic ulcer disease
symptoms to diagnose internal herniation (CT with oral
• Gastric/small bowel, Crohn disease
contrast is probably superior in these circumstances).
• Intermittent internal herniation
Referral to a gastroenterologist or neurologist for further
General medical conditions
investigation may be required, including barium follow
• Uraemia
through, gastric emptying study (to formally evaluate
• Hyper-/hypothyroidism
gastroparesis - during euglycaemia in diabetics as a high
• Hypercalcaemia
blood glucose may delay gastric emptying) and magnetic
• Addison disease
resonance imaging (MRI) of the brain if there is a concern
• Cardiac failure
about intracranial pathology.
Occult malignancy
Psychological or psychiatric evaluation may be helpful
• Pancreas
if the symptoms are still unexplained, but will need to be
• Lung
carefully explained and negotiated with the patient. Some
• Endocrine
patients with chronic nausea and vomiting have seen many
• Gastrointestinal
doctors and are very sensitive to their symptoms being
Neurological
trivialised or to being told ‘it is all in your head’.
• Raised intracranial pressure
It is often helpful to explain to patients in whom a
• Migraine
psychiatric or functional cause is suspected that
• Labyrinthine disorders
the gut contains a complete nervous system and that
Psychiatric/functional/idiopathic
this communicates extensively with the ‘big brain’. It
• Depression/psychosis
is then relatively easy to introduce the concept that
• Anxiety
communications can ‘go wrong’ and that this might be
• Functional nausea
a cause of the symptoms. Every day language is full of
• Cyclic vomiting syndrome
expressions indicating the close relationship between the
Reprinted from Australian Family Physician Vol. 36, No. 9, September 2007 691
THEME Nausea and vomiting in adults - a diagnostic approach
• Pregnancy should be considered in women of

Table 4. Investigations to consider in chronic nausea and/or vomiting
childbearing age.
Pathology testing • Hospitalisation may be required for severe metabolic
• Full blood count abnormalities, dehydration or suspected surgical
• Inflammatory markers causes.
• Urea and electrolytes • In chronic nausea and vomiting, with many potential
• Calcium/phosphate causes, a comprehensive history and examination is
• Liver function tests, including albumin required.
• Nutrition screen, iron • Symptoms are poor predictors of functional versus
• Thyroid function tests pathological illness.
• Drug levels, especially for medications such as digoxin or anticonvulsants • The type and extent of investigation is heavily
• Fasting cortisol +/- synacthen test for Addison disease influenced by the clinical circumstances and
• Tissue transglutaminase and total IgA presentation and must be tailored to the individual.
Imaging studies • A therapeutic trial of antiemetic or dietary
• Upper GI endoscopy modification can be undertaken while investigation
• CT abdomen and further referral is made.
brain and gut at the time of emotion or stress: ‘You make Conflict of interest: none declared.
me sick!’ ‘I’ve had it up to here!’ ‘You give me the shits!’
References
I’ve had a gutful!’ ‘He was gutted.’ ‘These examples can be 1. Quigley EM, Hasler WL, Parkham HP. American Gastroenterological
used to demonstrate to patients that emotion and stress Association. Technical review on nausea and vomiting.
Gastroenterology 2001;120:264.
can be associated with gastrointestinal sensations.
2. Hasler WL, Chey WD. Nausea and vomiting. Gastroenterology
Management 2003;125:1860-7.
3. Review article: current and emerging therapies for functional dyspep
Antiemetic therapy in patients with chronic nausea and sia. Alimentary Pharmacology & Therapeutics 2006;24:475.
4. Spiller RC. ABC of the upper gastrointestinal tract: anorexia, nausea,
vomiting where a specific cause has not been identified
vomiting, and pain. BMJ 2001;323:1354-7.
can be extremely challenging, particularly where symptoms 5. Wallace D, Martin AL, Park B. Cannabinoid hyperemesis: marijuana
are severe. Intermittent use of Ondansetron wafers (for puts patients in hot water. Australas Psychiatry 2007;15:156-8.
rapid absorption not dependent on gastric emptying),

although expensive, may be useful as rescue therapy
where symptoms are intermittent. A trial of maxalon,
Stemetil, or domperidone is useful. These therapies
are available for prolonged use in this setting on the
Pharmaceutical Benefits Scheme (Authority required).
However, there is an increased risk of extrapyramidal side
effects in this setting. Chronic nausea and vomiting may
respond to a low dose of a tricyclic (eg. amitrytaline 30 mg
at night, commencing at 10 mg and built up slowly).
Summary of important points

• Most cases of acute nausea and vomiting are self
limited and the aims of assessment are to reduce
complications and screen for important treatable
causes (especially surgical). In many cases, a
diagnosis can be made following a thorough history,
examination and/or simple investigations.
• Gastrointestinal infections and food poisoning make
up the majority of acute presentations.
• Medication side effects should always be suspected
with recent commencement or change in dose of
medication.
CLINICAL
PRACTICE
Lead Update
Toxicology and assessment Greg Cunningham

MBBCh, BAO, BA, DCH,
FRACGP, DOccMed, DAvMed,
in general practice is a practitioner, Brisbane

Industrial Health Services,
Brisbane, Queensland.
bihs@bigpond.net.au
BACKGROUND
Despite a consistent fall in the number of reported cases of inorganic lead toxicity, lead remains an important toxicant.
While much of the pathology caused by lead is known, much remains to be established regarding its mutagenicity and
teratogenicity.
OBJECTIVE
This article briefly outlines aspects of lead toxicity relevant to general practice, and provides an outline for taking a
workplace exposure medical history.
DISCUSSION
Recent trends show a continuous decline in the number of lead toxicity cases among workers and nonoccupational
cases in adults and children. The protean manifestations of lead toxicity make it difficult for doctors to consider it as
a differential diagnosis. A basic understanding of lead toxicology is helpful when assessing its clinical presentation,
ordering laboratory tests, advising patients how to avoid workplace exposure, and in understanding why it remains a
major concern as a mutagen and teratogen.
Fortunately there has been a steady fall in the (contained in paint) during demolitions, renovations and
incidence of lead toxicity in recent decades. Lead maintenance. Occupational exposures occurred most
toxicity is a notifiable condition, with laboratories commonly in battery manufacturing, foundry work, and
undertaking the notification process. radiator manufacture and repair.2
Toxicology
Nonoccupational toxicity is notifiable at a lower level
(0.73 pmol/L) than for occupational cases (2.41 pmol/L), In order to suffer the ill effects of a toxicant, one must
the latter being stipulated by the National code of be exposed to a sufficient dose, which must in turn be
practice for the control and safe use of inorganic lead absorbed into the blood. Ingestion and inhalation are
at work.1 These levels are the equivalent of 15 pg/dL both important. Approximately 10-15% of the ingested
and 50 pg/dL set by the American National Institute for quantity is absorbed, although this can be higher in the
Occupational Health and Safety. presence of iron deficiency, pregnancy, and fasting.3,4
Annual occupational exposure notifications in For lead to be absorbed by inhalation, the dose must be
Queensland have fallen from 32 in the year 2000 to 12 delivered in a form that is respirable, ie. can be delivered
in 2005, with nonoccupational notifications falling from to the alveolus. The particulate size of fume can be as
54 to 29. Nonoccupational notifications included childhood small as 0.1 micron, and almost all of this is absorbed.
notifications, which fell from 11 to one in the same Lead dust is also respirable as particles may be as small
period.2 There has been an increase in the number of as 0.5-1 microns, well within the range capable of
specimens tested by laboratories (both from occupational alveolar deposition.5 It is estimated that approximately
and nonoccupational sources) but a fall in the incidence 35-40% of inhaled lead dust is actually absorbed into the
of lead toxicity, despite well publicised environmental blood.3
concerns in a few Australian industrial cities. Upon absorption, lead binds to erythrocytes, and over
Recent nonoccupational exposures in Queensland a period of weeks is distributed predominantly to bone,
occurred most commonly by exposure to old lead liver, kidney, marrow and brain. Over 90% of the body
Reprinted from Australian Family Physician Vol. 36, No. 12, December 2007 1011
CLINICAL PRACTICE Lead - toxicology and assessment in general practice
burden of lead is stored in the compact bone buffing, rotary brushes or grinding. include a blue line on the dental margins of
matrix and trabecular bone from which lead Other points to consider in seeking a the gums and ‘saturnine’ gout6,7 (named after
may be mobilised. workplace history include: the miserable and dull Roman god Saturn, who
Lead’s primary toxicity is due to its affinity • workplace hygiene - cleaning should not was reputedly irritable enough to eat his own
for sulfhydryl groups allowing alteration of be performed in a manner that generates children).
protein and enzymatic function. Lead is similar dust (appropriate vacuuming is required) Lead’s adverse effect on neurological
to calcium in its physiochemical properties, • kitchen and meal areas - food should not development in children is long established.
accounting for its osseous deposition be taken into the workplace. Kitchen and There is recent evidence that, in addition to
and its effect within mitochondria where it meal rooms should be dust free its other neurological effects, lead causes
competitively antagonises the action of • personal hygiene - adequate measu res cognitive abnormalities in adults which are
calcium. Lead also appears to affect nucleic are needed to remove dust before donning demonstrable on neuropsychological testing.3
acids, through mechanisms which are not clear, nonworkplace clothing It is worth noting that the onset of
giving rise to concerns about chromosomal • smoking and nail biting are common symptoms or signs following lead exposure
abnormalities.6 sources of ingestion may be highly variable depending on the
Lead causes anaemia, both by inhibiting • overalls should be left at work and not intensity of the exposure as well as host
haeme synthesis and accelerating erythrocyte taken home for cleaning. A ‘take home’ factors. For example, a high intensity dose
destruction. Enzyme inhibition leads to a range dose may be delivered to family members may increase blood level concentration
of changes including the accumulation of zinc by lead contaminated clothing.5 rapidly with the early onset of accompanying
protoporphyrin (ZPP), which forms the basis of Larger workplaces tend to have better symptoms. Levels of 4-5 pmol/L may occur
a laboratory test. workplace procedures and compliance with over the course of 1-3 days. With subacute
Renal toxicity may be reversible with lower statutory health surveillance. Most cases and chronic exposure symptoms may take
exposure, as early pathological changes affect of toxicity now arise from smaller, poorly time to develop. There is also a significant
only the proximal tubules. Higher exposure managed workplaces. degree of individual variability in susceptibility
leads to interstitial fibrosis and progressive Biological monitoring of exposed workers to overt lead intoxication. The reasons for this
nephropathy. It is thought that lead affects must be performed. Legislation in the various are uncertain, but are thought to be associated
the renin-angiotensin system, causing states is based on a national standard requiring with specific lead binding proteins made in
hypertension.3 that employers have a blood lead level test response to lead exposure.7
There is no active elimination of lead. within the first month of employment, after 3 It should be noted that the toxicity of
Elimination occurs through skin desquamation, months, and then every 6 months.2 inorganic lead is very different to that of
nail growth, biliary secretion and glomerular The aims of biological monitoring are early organic lead (found in some petrochemicals),
filtration. detection, minimisation of risk of significant which causes an organic psychosis.6
exposure, reduction in overall exposure, and
Points to seek in a workplace Laboratory assessment
identification of affected workers for exclusion
history
from further lead exposure. It is also a useful Elevation of zinc protoporphyrin (ZPP), in
Details of job tasks undertaken are important source of information when assessing a addition to serum blood lead levels, may be
in assessing potential lead exposure. For worker with elevated lead levels. used as an indicator of lead toxicity. Increases
example, in automotive radiator repair, the in ZPP lag behind the increase in blood lead
Clinical presentation
radiator core is connected to the top and level by 2-6 weeks. Therefore, the finding of
bottom tanks by lead solder, which is also A difficulty with the presentation of lead a normal ZPP with elevated levels suggests
used to repair holes in the radiator. Lead fume toxicity is the nonspecific nature of symptoms. acute exposure. Elevation of ZPP may occur
is not normally produced by this process as These symptoms range from fatigue, with lead levels as low as 1.45 pmol/L.
the solder is not hot enough. Soldering is by concentration difficulties, sleep disturbances, However, the ZPP test is not 90% sensitive
definition the joining of metals at temperatures headache, weight loss, nausea and myalgia until blood lead levels exceed 2.41 pmol/L.7
of less than 430°C (brazing or welding occurs with mild to moderate toxicity to the classic
Mutagenicity and teratatogenicity
above this temperature). Lead fume is only features of severe toxicity of abdominal
produced above 550°C, but may be generated cramps, renal disease, encephalopathy, Lead’s reproductive toxicity is well recognised
if excessive heat is used during a soldering convulsions and peripheral neuropathy. Motor in both males and females. It is associated
task (eg. when soldering is performed with neuropathy leads to the classic lead palsy, with sperm abnormalities and miscarriage.
an oxyacetylene torch [which should not be affecting the long extensor muscles of the Carcinogenesis has been demonstrated in
permitted]).5 Exhaust systems should be in limbs. Lead induced Fanconi syndrome is more laboratory animals.3 The International Agency
operation when lead dust is generated by likely to occur in children. Unique features for Research on Cancer has classified
1012 Reprinted from Australian Family Physician Vol. 36, No. 12, December 2007
Lead - toxicology and assessment in general practice CLINICAL PRACTICE
inorganic lead in group 2A, concluding that

on current evidence inorganic lead is probably
carcinogenic to humans.8
The Center for Disease Control has
established 0.48 pmol/L as the blood level
of concern in children. Because lead crosses
the placental barrier readily, fetal blood levels
are directly proportional to maternal levels
(usually 80% of the maternal level). Thus, the
maternal blood level should be no greater than
0.63 pmol/L. Pregnancy and breastfeeding
are both indications for workplace exclusion,1
although lead excretion in breast milk is a less
important means of transmission.
It is known that lead can exert toxic effects
at levels well below 2.41pmol/L, which is
the level at which a male worker must be
excluded. For example, sperm morphology
abnormalities and abnormal sperm counts
have been demonstrated to occur at levels
of 1.93 pmol/L. The reproductive effects of
paternal levels below 1.9 pmol/L are unknown.
This remains a significant issue and further
epidemiological research is needed.7
References
1. Australian Safety and Compensation Council.
National code of practice for the control and safe use
of inorganic lead at work. Available at: www.ascc.
gov.au/NR/rdonlyres/1CE63D01-C21F-4F2B-84EB-8-
B7924FC224A/0/LeadCOP_NOHSC2015_1994.pdf.
2. Queensland Health. Blood lead levels in Queensland
2005. Available at www.health.qld.gov.au/phs/docu-
ments/ehu/31749.pdf.
3. DeRoos FJ. Smelters and metal reclaimers. In:
Greenberg MI, Hamilton RJ, Phillips SD, McCluskey
GJ, editors. Occupational, industrial and environmental
toxicology. 2nd edn. Philadelphia: Mosby, 2000;388-97.
4. Harrington J, Gill F, Aw T, Gardiner K. Chemicals,
gases, dusts and particles. In: Occupational health. 4th
edn. Oxford: Blackwell Science Ltd, 2002;94.
5. Frumkin H. Toxins. In: Levy BS, Wegman DH, editors.
Occupational health: recognising and preventing work-
related disease and injury. 4th edn. Philadelphia:
Lippincott Willimas & Wilkins, 2000;319-22.
6. Morgan L, Scott A. Metals. In: Baxter PJ, Adams PH,
Aw TC, Cockcroft A, Harrington JM, editors. Hunter’s
diseases of occupations. 9th edn. London: Arnold,
2000;82-9.
7. Hipkins KL, Kosnett MJ. Lead poisoning. In: Bowler
RM, Cone JE, editors. Occupational medicine secrets.
Philadelphia: Hanley & Belfus Inc, 1999;53-60.
8. International Agency for Research on Cancer. Inorganic
and organic lead compounds. Available at http://mono-
graphs.iarc.fr/ENG/Meetings/vol87.php.
Reprinted from Australian Family Physician Vol. 36, No. 12, December 2007 1013
THEME URINARY INCONTINENCE O®
Stanley K Santiagu Mohan Arianayagam Audrey Wang

MBBCh, is resident medical officer, Department BSc, MBBS, is a registrar, Department of FRACS, is Clinical Fellow, Department of
of Urology, Port Macquarie Base Hospital, Port Urology, Port Macquarie Base Hospital, Urology, Westmead Hospital, Sydney, New
Macquarie, New South Wales. stanleyk@ Port Macquarie, New South Wales. South Wales.
hotmail.com
Urinary incontinence
Pathophysiology and management outline
■ The International Continence Society (ICS) defines urinary
Background
incontinence (UI) as the complaint of any involuntary leakage of
Urinary incontinence is common in the community and may
urine.1 It is a distressing and debilitating condition that is
impact significantly on quality of life; yet only one-third of
sufferers seek medical attention. There are many treatment
becoming more prevalent as our population ages. It significantly
options for patients suffering with urinary incontinence. impacts on quality of life, both physically and psychosocially and
has major economic ramifications. The incidence of UI is higher
Objective
in women and is currently estimated to affect 4 million
This article aims to aid general practitioners in the managment
Australians.2 While UI is common, only one-third of sufferers
urinary incontinence. We outline the pathophysiology of urinary
seek medical attention, possibly due to social stigma or
incontinence in women and provide a primary care treatment
paradigm. Suggestions for when specialist referral would be of ignorance regarding available treatments.3 Furthermore, one in 5
benefit are also discussed. women with UI also experiences some degree of faecal
incontinence. By effectively identifying and treating incontinence
Discussion
it is possible to significantly improve patients' quality of life.
Most urinary incontinence can be evaluated and treated in the
primary care setting after careful history and simple clinical
It is essential that general practitioners understand the manifestations
assessment. Initial treatment, for both urge urinary incontinence
and stress urinary incontinence, is lifestyle modification and of this condition and its treatments to be able to broach this sensitive
pelvic floor muscle treatment. Urinary urgency responds to subject with their patients.4
bladder training and pharmacotherapy with anticholinergic
Continence mechanisms in women
medication. Pharmacotherapy has a limited place in stress
incontinence. If there is complex symptomatology or primary Continence is maintained by a coordinated effort between the bladder,
management fails, then referral to a specialist is suggested. urethra, pelvic muscles and the surrounding connective tissue. The
function of the lower urinary tract is to either store (storage phase) or
expel (voiding phase) urine. This is dependent upon a bladder that is
able to expand while maintaining a relatively constant low pressure
in the absence of involuntary contractions. The body of the bladder is
innervated by parasympathetic nerves while the bladder neck receives
sympathetic innervation (Figure 1). Normal urine storage is dependent
on a closed outlet and a relaxed bladder.5
Outlet closure is dependent on the bladder neck and urethral
smooth muscle with a skeletal muscle rhabdosphincter, which is
under voluntary control (somatic). The outlet remains closed during
urine storage and the rhabdosphincter and pelvic floor respond to
rises in intra-abdominal pressure. Intact urethral mucosal is also
important for a watertight seal. Continence is maintained while the
urethral pressure exceeds intravesical pressure.
106 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 3, March 2008
Prem Rashid
Figure 1. Anatomy and innervation of the bladder
MBBS, FRACGP, FRACS(Urol), PhD, is a urological surgeon, Port
Macquarie Base Hospital, and Conjoint Associate Professor,
Rural Clinical School, University of New South Wales, Port
Macquarie, New South Wales.
The voiding phase starts with relaxation of the outlet with a

sustained detrusor contraction. The micturition reflex is normally
under voluntary control and coordinated by the pontine micturition
centre with various relays in the spinal cord (Figure 1). Details of
voiding and storage phases are listed in Table 1.
Pathophysiology and terminology

Urinary incontinence occurs when there is dysfunction in either the
storage function or occasionally, in the emptying function of the lower
urinary tract. Urethral sphincter dysfunction and bladder dysfunction and give them the opportunity to discuss their symptoms. The type of
can co-exist and various components of the continence mechanism UI can most often be diagnosed by history alone. Storage symptoms
may compensate one another. For example, women may experience include frequency, nocturia, urgency and incontinence. Voiding
anatomical or neuromuscular injury during childbirth but remain symptoms include hesitancy, poor or interrupted stream, straining
asymptomatic until there is a loss of urethral sphincter function due and terminal dribbling. Frequency of incontinent episodes, pad usage,
to aging. The ICS has defined nomenclature for UI as: stress (SUI), degree of bother, circumstances of loss, time of day (or night) and
urge (UUI) and mixed (MUI) (Table 2). relationship to drug treatments (eg. diuretics, alpha blockers), voiding
habits and fluid intake need to be evaluated. A history of urinary tract
Stress urinary incontinence
infection or poorly controlled diabetes can also impact on lower urinary
Stress urinary incontinence occurs when vesical pressure exceeds tract function and constipation needs to be excluded. Haematuria
urethral pressure in the setting of sudden increases in intra (microscopic or macroscopic) or irritative symptoms require assessment
abdominal pressure. This can be due to weakness of the pelvic floor to exclude malignancy.
or sphincter. Loss of bladder neck support is referred to as bladder A bladder diary or frequency and volume chart is simple and useful
neck hypermobility and treatments target the restoration of that for initial assessment and quality of life evaluation.8,9
support. Sphincter dysfunction is referred to as intrinsic sphincter Examinations are focused on organ systems that could be
deficiency. It is believed that most patients have elements of both implicated in UI. Initial assessment includes general observation
disorders in varying degrees. Risk factors for SUI include childbirth, for mobility, cognitive status, peripheral oedema and body habitus;
postmenopausal involution of the urethra, or as a complication of abdominal examination for pelvic masses and focused neurological
pelvic surgery or trauma. examination for upper motor neuron lesions (eg. multiple sclerosis,
Parkinson disease) or lower motor neuron lesions (eg. sacral nerve
Urge urinary incontinence
root lesion) if suspected. Vaginal examination is performed to
Urge urinary incontinence can be caused by detrusor overactivity or assess oestrogen status, the presence of pelvic organ prolapse,
low compliance. Detrusor overactivity is a urodynamic observation urethral meatal abnormality, pelvic floor muscle tone and leakage
characterised by involuntary detrusor contractions during the filling during coughing or Valsalva manoeuvre. The strength of the pelvic
phase. Detrusor overactivity may be neurogenic or idiopathic. floor muscles can be assessed during the bimanual examination
Detrusor overactivity can originate from the bladder epithelium or by asking patients to contract the muscles around the fingers of
detrusor muscle itself. The myogenic theory6 suggests that age related examining physician.
changes in smooth muscle lead to hyperexcitability. The neurogenic Urine microscopy and culture is required to exclude infection
theory7 suggests that detrusor overactivity can be due to denervation at as well as postvoid residual volume by ultrasound. In patients with
the spinal or cortical level, leading to hyperactive voiding secondary to suspected voiding difficulties or neuropathy, previous failed treatment
the spinal micturition reflexes. Parkinson disease or stroke may cause a or when considering surgical treatment, cystometry or urodynamic
loss of inhibitory neurons, leading to neurogenic detrusor overactivity. studies, can be performed.10,11 In cases where central nervous system
pathology is suspected, the opinion of a neurologist may be required.
History and examination
Assessment of UI is discussed in further detail in the article
As up to two-thirds of UI sufferers may not seek medical treatment ‘Urinary incontinence - assessment in women: stress, urge or both?’
for their symptoms, it is important to broach the subject with women by Karen McKertich in this issue of AFP.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 3, March 2008 107
Urinary incontinence - pathophysiology and management outline
Table 1. Summary of the functions of the autonomic and somatic nervous systems and urge suppression techniques with
distraction or relaxation. A Cochrane
Storage phase Voiding phase
review suggests bladder training may be
Somatic (Onuf’s nucleus) Contracted rhabdosphincter Relaxed rhabdosphincter
more effective than placebo, however,
Sympathetic Contracts bladder neck and inhibits Relaxes bladder neck there was not enough data to determine
contraction of bladder body
whether bladder training was a useful
Parasympathetic No action Contracts bladder
supplement to other therapies.19 The World
Sensory (afferent) fibres run with the autonomic nerves Health Organization and the International
Consultation on Incontinence recommended
Treatment that initial bladder training involves a voiding interval of 1 hour during
The aims of treatment are to reduce symptoms and improve quality of waking hours with a gradual increase by 15-30 minutes per week
life through nonsurgical and surgical therapies. until a 2-3 hour voiding interval is reached.20
Pelvic floor muscle training and bladder training are best undertaken
Nonsurgical therapy
with the assistance of a continence therapist (see Resources). The role
Lifestyle intervention of the physiotherapist in PFMT and bladder training is discussed in the
Weight loss and exercise in morbidly obese patients reduces SUI, article 'Physiotherapy for urinary incontinence' by Patricia Neumann and
and to a certain extent, UUI.12,13 Fluid and caffeine restriction may Shan Morrison in this issue of AFP.
also reduce UI,14 while the effect of smoking on UI is unclear.15,16
Pharmacotherapy
Constipation and straining may increase the risk of pelvic organ
prolapse and SUI. Anticholinergic medications form the basis of pharmacological
treatment in UUI by reducing involuntary detrusor contractions
Pelvic floor exercise
mediated by acetylcholine. A Cochrane review showed anticholinergic
Pelvic floor muscle training (PFMT) involves strengthening the pelvic medications are effective in reducing symptoms of urgency and
floor muscles. It needs to be continued for 3-4 months before improve quality of life and symptoms during treatment when
determining its success. It should be done with three sets of 8-12 compared with, or combined with, bladder training alone.21,22 In
slow maximal contractions sustained for 6-8 seconds and repeated Australia, the most commonly used anticholinergic drug is oxybutynin.
3-4 times per week. A 2001 Cochrane review has shown that women Newer uroselective anticholinergic medications including tolterodine,
undergoing PFMT were seven times more likely to be cured and 23 solifenacin and darefenacin have similar efficacy to oxybutynin but
times more likely to show improvement.17 It can be combined with an improved side effect profile. As yet they are not available on the
biofeedback equipment such as intravaginal resistance devices or Pharmaceutical Benefits Scheme (Table 3).
weighted vaginal cones. However, these have not been shown to Medical treatments are less effective for SUI. However, there is
improve the efficacy of PFMT.17,18 evidence that serotonin noradrenaline re-uptake inhibitors (SNRIs)
may be effective in SUI.23 Duloxetine, a SNRI, relaxes the bladder and
Bladder training
increases outlet resistance. However, adverse effects are common
Bladder training is the initial treatment for UUI, being noninvasive, including nausea, fatigue, dry mouth and constipation.24
inexpensive and easy. This includes PFMT, a scheduled voiding
Other medications
program with gradual increases in the duration between voids,
Imipramine, a tricyclic antidepressant, may reduce detrusor
contractility and increases outlet resistance and can be used in
Table 2. International Continence Society definition of the
conjunction with anticholinergics. There is little evidence to support
symptoms of urinary incontinence1,26
the use of oestrogen replacement for UI.25
Stress urinary The complaint of involuntary leakage
incontinence (SUI) on effort or exertion, or on sneezing or Surgical therapy
coughing
If symptomatology is complex or pharmacotherapy unsuccessful, then
Urge urinary The complaint of involuntary leakage
specialist referral is warranted for further assessment and treatment.
incontinence (UUI) accompanied by, or immediately
preceded by, urgency. (Urgency is a For detrusor overactivity refractory to oral medications, intravesical
sudden compelling desire to pass urine, botulinum toxin A injections or neuromodulation can be performed,
which is difficult to defer) usually in specialist units. More invasive options include detrusor
Mixed urinary The complaint of involuntary leakage myomectomy or bladder augmentation, which reduce the efficacy of
incontinence (MUI) associated with urgency and also with detrusor contraction and thus improve continence. As a last resort,
exertion, effort, sneezing or coughing
ileal conduit urinary diversion may be performed.
Urinary incontinence - pathophysiology and management outline THEME
Table 3. Anticholinergic medications for urge urinary incontinence
Medication/formulation Uroselective Usual dosage Comments

Oxybutynin (Ditropan) No 2.5-5 mg orally • Effective and inexpensive
2-4 times per day • Side effects include constipation, dry mouth, blurred vision
(geriatric dose 2.5
• May precipitate acute urinary retention
mg)
• In the elderly may cause confusion and sedation
• Available on the PBS
Oxybutynin transdermal No 39 cm2 patch 2 • Side effects of oxybutynin are due to metabolites which may
patch (Oxytrol) times/week be reduced by newer transdermal delivery system
(3.9 mg/day • Not available on the PBS
Tolterodine (Detrol) Yes 2-4 mg orally per • Comparable efficacy to oxybutynin
day • Improved side effect profile
• No PBS listing as yet
Darifenacin hydrobromide Yes 7.5-15 mg orally • Comparable efficacy to oxybutynin
(Enablex) once per day • Improved side effect profile
Solifenacin (Vesicare) Yes 5 mg/day orally • Comparable efficacy to oxybutynin
• Improved side effect profile
Figure 2. Demonstration of midurethral sling placed via pelvic surgery or neurological disorders. Most UI can be evaluated
a retropubic approach and treated in the primary care setting after careful history and
simple clinical assessment. This can include lifestyle modification,
PFMT, bladder training and/or pharmacotherapy. If there is complex
symptomatology or primary management fails, then referral to a
specialist is suggested. Urinary incontinence can be very distressing
both physically and psychologically and impacts on quality of life and
health. As primary care providers, it is essential that GPs evaluate,
treat and refer high risk patients.
Resource
Continence Foundation of Australia
Freecall 1800 33 00 66 www.continence.org.au.
References
1. Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology of lower
urinary tract function: report from the Standardisation Sub-committee of the
International Continence Society. Am J Obstet Gynecol 2002;187:116-26.
Stress urinary incontinence can be treated with colposuspension,
2. Continence Foundation of Australia. Available at www.continence.org.au.
pubovaginal sling with rectus fascia or midurethral tapes. There 3. Holst K, Wilson PD. The prevalence of female urinary incontinence and reasons
are various midurethral tape kits available using a retropubic or for not seeking treatment. N Z Med J 1988;101:756-8.
4. O’Donnell M, Viktrup L, Hunskaar S. The role of general practitioners in the initial
transobturator route. These slings aim to reduce bladder neck
management of women with urinary incontinence in France, Germany, Spain and
hypermobility (Figure 2). Periuretheral bulking agents may also be the UK. Eur J Gen Pract 2007;13:20-6.
used and work well for some patients. 5. Morrison A, Levy R. Fraction of nursing home admissions attributable to urinary
incontinence. Value in Health 2006;9:272-4.
Further details of these procedures for treating both SUI and UUI are
6. Brading AF. A myogenic basis for the overactive bladder. Urology 1997;50(6A
available in the article ‘Urinary incontinence: procedural and surgical Suppl):57-67; discussion 8-73.
treatments for women’ by Karen McKertich in this issue of AFP. 7. de Groat WC. A neurologic basis for the overactive bladder. Urology 1997;50(6A
Suppl):36-52; discussion 3-6.
Conclusion 8. van der Vaart CH, de Leeuw JR, Roovers JP, Heintz AP. The effect of urinary incon
tinence and overactive bladder symptoms on quality of life in young women. BJU
Urinary incontinence is common in women but it is under-reported Int 2002;90:544-9.
and undertreated. Generally UI is caused by aging, childbirth, 9. Coyne KS, Zhou Z, Thompson C, Versi E. The impact on health-related quality of
life of stress, urge and mixed urinary incontinence. BJU Int 2003;92:731-5.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 3, March 2008 109
THEME Urinary incontinence - pathophysiology and management guideline
10. Artibani W, Cerruto MA. The role of imaging in urinary incontinence. BJU Int
2005;95:699-703.
11. Homma Y. The clinical significance of the urodynamic investigation in inconti
nence. BJU Int 2002;90:489-97.
12. Subak LL, Whitcomb E, Shen H, Saxton J, Vittinghoff E, Brown JS. Weight loss: a
novel and effective treatment for urinary incontinence. J Urol 2005;174:190-5.
13. Bo K, Borgen JS. Prevalence of stress and urge urinary incontinence in elite ath
letes and controls. Med Sci Sports Exerc 2001;33:1797-802.
14. Swithinbank L, Hashim H, Abrams P. The effect of fluid intake on urinary symp
toms in women. J Urol 2005;174:187-9.
15. Bump RC, McClish DM. Cigarette smoking and pure genuine stress incontinence
of urine: a comparison of risk factors and determinants between smokers and
nonsmokers. Am J Obstet Gynecol 1994;170:579-82.
16. Hannestad YS, Rortveit G, Daltveit AK, Hunskaar S. Are smoking and other
lifestyle factors associated with female urinary incontinence? The Norwegian
EPINCONT Study. BJOG 2003;110:247-54.
17. Hay-Smith EJ, Bo Berghmans LC, Hendriks HJ, de Bie RA, van Waalwijk van Doorn
ES. Pelvic floor muscle training for urinary incontinence in women. Cochrane
Database Syst Rev 2001;(1):CD001407.
18. Aksac B, Aki S, Karan A, Yalcin O, Isikoglu M, Eskiyurt N. Biofeedback and pelvic
floor exercises for the rehabilitation of urinary stress incontinence. Gynecol Obstet
Invest 2003;56:23-7.
19. Wallace SA, Roe B, Williams K, Palmer M. Bladder training for urinary incon
tinence in adults. Update of Cochrane Database Syst Rev. 2000;(2):CD001308;
PMID: 10796768. Cochrane Database Syst Rev 2004;(1):CD001308.
20. Wilson P. Incontinence. Plymbridge Distributors; 1999, p. 579-634.
21. Nabi G, Cody JD, Ellis G, Herbison P, Hay-Smith J. Anticholinergic drugs versus
placebo for overactive bladder syndrome in adults. Cochrane Database Syst Rev
2006; Issue 4. Art. No.: CD003781.
22. Alhasso AA, McKinlay J, Patrick K, Stewart L. Anticholinergic drugs versus
non-drug active therapies for overactive bladder syndrome in adults. Cochrane
Database Syst Rev 2006; Issue 4. Art. No.: CD003193.
23. Hashim H, Abrams P. Pharmacological management of women with mixed urinary
incontinence. Drugs 2006;66:591-606.
24. Mariappan P, Alhasso A, Ballantyne Z, Grant A, N’Dow J. Duloxetine, a serotonin
and noradrenaline reuptake inhibitor (SNRI) for the treatment of stress urinary
incontinence: a systematic review. Eur Urol 2007;51:67-74.
25. Grady D, Brown JS, Vittinghoff E, et al. Postmenopausal hormones and incon
tinence: the Heart and Estrogen/Progestin Replacement Study. Obstet Gynecol
2001;97:116-20.
26. Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology in lower
urinary tract function: report from the standardisation sub-committee of the
International Continence Society. Urology 2003;61:37-49.
CORRESPONDENCE afp@racgp.org.au
THEME ALLERGY ®
Wendy Hu Constance H Katelaris Andrew S Kemp

MBBS, DipPaeds, MHA, PhD, FRACGP, is MBBS, PhD, FRACP, is Professor MBBS, PhD, FRACP, is Professor of Paediatric
Senior Lecturer, Western Clinical School, of Immunology and Allergy, Allergy and Clinical Immunology, Department of
University of Sydney, New South Wales. University of Western Sydney, Allergy and Immunology, The Children’s Hospital at
wendyhu@med.usyd.edu.au New South Wales. Westmead, New South Wales.
Allergic rhinitis
Practical management strategies
■ ‘You know how they did those 12 prick tests... what have
Background
you, they have the pollen, the bed mites and things like that.
Allergic rhinitis is a common condition associated with
I’m a bit blasé when it comes to things like that... I mean, if
significant effects on quality of life. Readily available treatments
[my son] sneezes, he sneezes, you know? What can you do?
can improve outcomes in rhinitis as well as associated
allergic diseases such as asthma. Yet allergic rhinitis remains And that’s just part of life. And, unless it gives him chronic,
underdiagnosed and undertreated. chronic symptoms, I really don’t think it’s much of a worry.
[It] was just general house dust that he was sensitive to -
Objective
unfortunately you have to live with that. You’re never going to
This article outlines practical strategies and evidence based
get away from it. We don’t live in a sterile environment.'
management of allergic rhinitis.
Discussion Allergy and allergic conditions such rhinitis (‘hayfever’) arouse a

Allergic and nonallergic rhinitis often co-exist. Thorough history
range of community responses from indifference to heightened
of allergen exposure and its relationship to symptoms is vital
concern.1 The above quote is from a qualitative study on parental
for the ordering and interpretation of investigations and for
views of their children’s allergies2 and typifies attitudes held by
management decisions. Some allergen avoidance measures
many. Interestingly, the parent has also highlighted key issues in
may be ineffective and may cause an unnecessary burden.
Demonstrated effective strategies are patient education, recent research; quality of life, undertreatment, allergen avoidance
intranasal steroids and immunotherapy (‘desensitisation’). and the importance of patient education.
General practitioners play a vital role in all three strategies, and Allergic rhinitis has tended to be seen as an annoying nuisance
in supporting patients and families to self manage what is often rather than a serious disease. However recent studies have
a chronic condition. documented its impact on quality of life,3-5 with significant effects
on sleep, cognitive and psychomotor function, participation in social
activities, and learning impairment in children. Economic impact
analysis shows the estimated financial cost of allergy in Australia
in 2007 was $7.8 billion, with $5.6 billion due to lost productivity.6
While this estimate includes all allergic conditions, allergic rhinitis
is the most common allergic disorder, and often coexists with
asthma, sinus disease, eczema and conjunctivitis. Treating rhinitis
can improve outcomes for asthma and vice versa.7,8 Yet, despite the
morbidity, availability of over-the-counter treatments and evidence
that intranasal steroids and immunotherapy are effective, rhinitis is
often underdiagnosed and undertreated.9
Clinical assessment
Rhinitis is usually classified into nonallergic and allergic. Allergic
rhinitis is further divided into seasonal (‘hayfever’) and perennial
214 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 4, April 2008
Table 1. Types of rhinitis - characteristic features14, 28, 29
Rhinitis type Key features

Allergic rhinitis
Seasonal allergic rhinitis ‘hayfever’ Associated with spring and early summer
Triggered by pollens, timing dependent on plant species and geographical location
Perennial allergic rhinitis Symptoms occur year round
Triggered by house dust mite, pollens and pet animals
Allergic and nonallergic rhinitis
Occupational Symptoms abate away from workplace
Triggered by chemicals and irritants (eg. in manufacturing processes, laboratories, hair and
nail salons) and allergens (eg. work with animals)
Nonallergic rhinitis
Idiopathic Triggered by strong smells and changes in temperature
Infective Most commonly repeated viral infections causing episodes every 4-8 weeks of mucousy
nasal discharge lasting 5-7 days
Vasomotor rhinitis Sudden onset and offset of watery discharge
Nonallergic with eosinophilia (NARES) Negative allergy tests but >20% eosinophils on nasal smears
Hormonal Associated with pregnancy, hypothyroidism and acromegaly
Drug induced Beta blockers, chlorpromazine, oral contraceptives, aspirin, rebound symptoms from topical
decongestants
(all year round) types (Table 1).

Figure 1. Functional classification of allergic rhinitis13
While this classification is useful for
specific treatments such as allergen
avoidance and immunotherapy, in
practice, nonallergic and allergic
rhinitis often co-exist.10 These may be
difficult to differentiate as skin prick
tests can be positive in 25-30% of
healthy young adults and 30-35% of
healthy children.11,12 An alternative
classification system based on
symptom severity and frequency
has been proposed and is useful in
treatment decision making (Figure 1).
Rhinitis symptoms characteristically include nasal obstruction Skin prick testing
and rhinorrhoea, with allergic rhinitis also featuring sneezing, itchy Skin prick tests are the principal investigation for assessing the
nose, eyes and throat. However, the presentation can be more allergic basis of symptoms in patients of all ages, but their reliability
nonspecific, with features such as ‘fuzzy’ head, tiredness and day is highly dependent on the use of correct technique, reliable extracts,
time sleepiness, constant ‘colds’, and in children, sniffing, blinking and positive and negative control tests. Adequate training and safety
and eye rubbing, speech problems, snoring, and dark circles under precautions are essential and Australasian practice guidelines are
the eyes. Once rhinitis is suspected, take a directed history to available.15 It is important to remember that positive results (a skin
assess the patient’s environment and likely exposure to allergens wheal >3 mm) do not prove that the allergen is causing the patient’s
and irritants, the type and timing of symptoms and their relationship symptoms, only that there is sensitisation or IgE antibodies to the
to exposure, and the effect of symptoms on quality of life.14 This allergen. Additionally, patients and parents often interpret skin
history will underpin decisions about investigations and future wheals as proof of allergy. Investigations therefore need to be guided
management. Key features on history and physical examination are by history and their limitations carefully explained to patients. Limit
set out in Table 2. the allergens to be tested to what appears to be likely or to what can
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 4, April 2008 215
Allergic rhinitis - practical management strategies
be excluded, as the indiscriminate ordering of ‘panels’ with large This should cover the practical implications of test results, allergen
numbers of allergens can lead to confusion and unnecessary allergen avoidance measures, benefits, risks and side effects of treatments,
avoidance. Interpret tests together with the history. For example, techniques for administering topical medications, and follow up. As
symptoms restricted to early spring with negative tests to rye grass an adjunct, patients can be directed to internet based information
and positive tests to house dust mite suggests that symptoms are sources (see Resources). Common questions include:
nonallergic as house dust mite is a year round allergen.16 A mismatch
Do I really need to buy dust mite covers?
between test results and history, or failure to respond to treatment
should prompt consideration of other diagnoses (Table 3). Allergy While avoidance of proven or likely allergens is a cornerstone
testing is further reviewed in the article by Robinson and Smart in of allergy management, in reality it can be difficult to achieve,
this issue of AFP. particularly for house dust mite. There is little evidence that mite
reduction strategies are effective in relieving perennial rhinitis and
Management
bedding covers used alone appear to be ineffective.17 The decision
Evidence based guidelines confirm that patient education improves to implement avoidance strategies such as impermeable covers,
treatment effectiveness and quality of life; intranasal steroids are replacement of soft furnishings, high filtration vacuum cleaners
the treatment of choice; and that immunotherapy (‘desensitisation’) and frequent washing will depend on the severity of symptoms, the
is highly effective in selected cases.14 motivation of families to trial strategies, and the cost.
Parent and patient education Should I get rid of the cat?

The chronic nature of rhinitis symptoms and consequent need for Removal of a pet can be very upsetting, so clear demonstration of
self management underline the importance of patient education. sensitivity to the animal is required before such advice is given. It
Table 2. Key features in clinical assessment
Important points in the history

At what age did the symptoms start? Seasonal rhinitis is more common in school aged children and young adults
Perennial rhinitis is more common in preschool children
Does the rhinitis occur all year round or at a Rye grass is the most common cause of hayfever. Grass pollination usually extends for
particular time of the year? 6-8 weeks in spring and early summer
Is there a nasal discharge? Is it unilateral or Watery, bloody, discoloured or unilateral discharge suggests diagnoses other than
bilateral? What is it like? allergic rhinitis
Does the patient have cough, wheeze, itchy red Asthma (50% of rhinitis patients have asthma), rhinoconjunctivitis (70% of rhinitis
eyes and skin? patients) and eczema frequently co-exist with allergic rhinitis
What drugs does the patient take? Medications may cause symptoms
Response to previous treatment and capacity to follow long term treatment regimen
influence subsequent management
What allergens is the patient exposed to? Ask about housing conditions, occupational exposure, and pets
Diet in young children as food allergies may co-exist
What effect do the symptoms have on quality of Ask about sleep, snoring, day time somnolence, school and work performance,
life? participation in social activities
Important points on physical examination
Inspect the face Signs of allergic rhinitis include ‘shiners’ (dark circles under the eyes) and transverse
nasal crease caused by the ‘allergic salute’, an upward rubbing of the nose with the
hand
Assess nasal airflow by asking patient to close The area of condensation indicates air flow
mouth then breathe normally through the nose Unequal airflow suggests partial obstruction, most likely due to swollen turbinates
onto a metal surface such as a stethoscope arm and/or a deviated nasal septum
Look up each nostril with an auriscope Assess inferior turbinate size, nasal mucosal appearance, nasal septum position,
presence of polyps
If the patient has had epistaxis, dilated vessels may be apparent in Little’s area
Examine the throat Large tonsils indicate lymphoid hypertrophy which may involve the adenoids
Mucus in the oropharynx (‘postnasal drip’) indicates upper airways pathology such as
rhinosinusitis
Allergic rhinitis - practical management strategies THEME
Table 3. When to suspect nonallergic causes
Clinical feature Possible cause

Mismatch between allergy test results and Nonallergic rhinitis (Table 1)
clinical presentation Any of the causes listed below
Mismatch between degree of airflow Adenoidal hypertrophy (eg. inferior turbinates do not appear swollen and airway appears
obstruction and diameter of nasal airway on patent, but airflow is restricted)
inspection
Unilateral obstruction Structural causes such as deviated septum, enlarged turbinates, nasal polyps
Persistent unilateral discharge In children, foreign body
Rarely, watery unilateral discharge may indicate cerebrospinal fluid leak
Persistent mucopurulent discharge +/- facial Chronic rhinosinusitis or superimposed infection
pain
Nasal crusting Staphylococcal aureus infection, nose picking
In adults, severe crusting is rare and suggests connective tissue disease
Loss of sense of smell Chronic sinusitis or polyps
Failure to respond to medical treatment for Nonadherence to treatment regimen
allergic rhinitis Reconsider diagnosis, including any of the causes listed above
These clinical scenarios should prompt review of the diagnosis and possible referral to specialist allergist or ENT services, as appropriate
These conditions may co-exist with allergic rhinitis
is difficult to adequately control symptoms if the pet remains in the

Table 4. Instructions for administering intranasal sprays14
house. After removal of the pet, symptoms may not resolve promptly
as cat allergens in particular, may persist in furnishings. Thorough Patients should:
cleaning may be beneficial. 1. Shake the bottle
How do I avoid pollen? 2. Look DOWN at the floor

3. Use the right hand for the left nostril, put the nozzle just
Strategies such as staying indoors in an airconditioned environment inside the nose and aim to the side
or wearing a mask outdoors have low acceptability and are generally 4. Squirt once or twice as directed
impractical. Pre-treatment with antihistamines before outdoor exposure 5. Change hands and repeat for the other side
may give some protection. Using a clothes dryer to finish drying
Note: it is not necessary to sniff hard
washed bedding may reduce exposure to pollen deposits. Wearing of
sunglasses has been suggested for reducing ocular deposition, but is
of unproven efficacy and may be impractical in children. asthma.8 Intranasal steroids should be commenced before referring
patients with nasal obstruction to an allergist or ear, nose and throat
When do I use antihistamines?
surgeon (Table 3).
Oral and topical antihistamines are effective in allergic Intranasal steroids appear safe for long term use, although it
rhinoconjunctivitis and histamine related symptoms such as itching, is prudent to use the lowest dose that will control symptoms.18,19
rhinorrhoea and sneezing, but are less effective for nasal blockage. The total steroid dose should be considered, for example if used
Ideally they should be given before allergen exposure. Impairment for intercurrent asthma. Systemic absorption of intranasal steroids
in learning and concentration have been demonstrated with older occurs, but side effects typical of systemic steroids such as
antihistamines, therefore newer oral formulations (cetirizine, osteoporosis, diabetes and hypertension have not been reported.
loratadine, fexofenadine) are preferred. Intranasal antihistamines Triamcinolone, budesonide, fluticasone and mometasone have lower
(levocabastine, azelastine) are as effective as oral antihistamines systemic bioavailability.20 Beclomethasone used for 1 year has
and have a rapid onset of action. been shown to affect children’s growth, but this has not been
demonstrated with fluticasone or mometasone.21,22 For this reason,
Intranasal steroids
children should be prescribed these newer generation formulations
Intranasal steroids are the treatment of choice for persistent in low doses and have their growth monitored.
moderate to severe allergic rhinitis (Figure 1) and may also improve A common reason for treatment failure is nonadherence due
nonallergic rhinitis.18 Where there is coexisting asthma, intranasal to local side effects such as dryness, irritation and epistaxis from
steroid use is associated with fewer emergency presentations for spraying Little’s area in an ‘upward’ direction. Demonstrate and
Allergic rhinitis - practical management strategies THEME
check the patient’s technique (Table 4). Where patients find it indiscriminate ‘panel’ testing.
difficult to use sprays on a daily basis, intermittent ‘when necessary’ • Evidence of the effectiveness of allergen avoidance measures,
dosing has been shown to be effective for beclomethasone and particularly for house dust mite, is limited.
fluticasone over the short term (4-6 weeks).23 Used before the • Antihistamines are useful for itching, rhinorrhoea and sneezing
steroid, nasal saline spray can clear mucus, thus improving mucosal but are not effective for nasal obstruction, for which intranasal
contact with the steroid and potentially reducing the dose required steroids are required.
to be effective. • Newer generation intranasal steroids are preferred due to their
lower systemic bioavailability, particularly in children.
Immunotherapy
• A common reason for treatment failure with intranasal steroids is
Systematic reviews of randomised controlled trials have incorrect administration technique.
demonstrated Level I evidence for the effectiveness of • Immunotherapy can lead to sustained improvement in symptoms;
immunotherapy in improving symptoms and medication use in patients should be referred to a qualified allergist or practitioner
allergic rhinitis and asthma.24,25 The decision to start immunotherapy trained in the prescription of immunotherapy if this is being
should be carefully considered (with an allergist referral) as 3-5 considered.
years of treatment is required for sustained effects. Immunotherapy • Patient and parent education is essential for effective
may be recommended where symptoms are severe and medications management.
have been ineffective, inappropriate or have intolerable side effects.
Resources
Systemic reactions to injection immunotherapy are rare; a general • Australasian Society of Clinical Immunology and Allergy (ASCIA)
practitioner treating 10 patients can expect one systemic reaction A comprehensive range of information sheets for health professionals
every 7 years.24 As reactions can be unpredictable, patients should and patients. ASCIA is the peak professional body for specialist allergists
wait in the surgery for 30 minutes following injections. More in Australasia and the site also lists members and their contact details
www.allergy.org.au
recently, oral or sublingual immunotherapy has been shown to be
• HealthInSite
effective for allergic rhinitis.26 This may be more acceptable to
Australian Government endorsed site for health consumer information.
children and those wishing to avoid injections and waiting time Ask patients to search under ‘rhinitis’ not ‘hayfever’, as the latter will
as it can be given at home. There have been no reports to date yield mostly product information
of systemic reactions to sublingual immunotherapy where single www.healthinsite.gov.au/index.cfm
inhalant allergens are administered. • American Academy of Allergy, Asthma and Immunology
www.aaaai.org/patients.stm
Conclusion • American College of Allergy, Asthma and Immunology
www.acaai.org/public/.
Allergic rhinitis tends to be chronic and relapsing, so it may be
difficult to see treatment effects and adhere to therapy. Conflict of interest: none declared.
Complementary and alternative therapies are a current research
Acknowledgment
focus but evidence is inconclusive.27 Advise patients to be cautious The authors wish to thank the parents who participated in the study and
with advertisements for ‘allergy cures’. Nonetheless, there is much gave permission to be quoted.
that can be done to improve symptoms and quality of life - for the
parent quoted earlier, the GP can inquire about other symptoms,
References
1. Jackson M. Allergy: the history of a modern malady. London: Reaktion, 2006.
inform about the relationship between asthma and rhinitis, confirm 2. Hu W, Grbich C, Kemp A. Parental food allergy information needs: a qualitative
their views on allergen avoidance and discuss treatment options, study. Arch Dis Child 2007;92:771-5.
3. Blaiss MS. Cognitive, social, and economic costs of allergic rhinitis. Allergy
including allergist referral if immunotherapy is to be considered. As
Asthma Proc 2000;21:7-13.
with other chronic diseases, a long term partnership between GP, 4. Blaiss MS. Allergic rhinitis and impairment issues in schoolchildren: a consensus
report. Curr Med Res Opin 2004;20:1937-52.
parent and patient is more likely to result in satisfactory outcomes.
5. Laforest L, Bousquet J, Pietri G, et al. Quality of life during pollen season in
patients with seasonal allergic rhinitis with or without asthma. Int Arch Allergy
Immunol 2005;136:281-6.
6. Access Economics. The economic impact of allergic disease in Australia: not to
• Allergic rhinitis is often chronic but readily available treatments
be sneezed at. Sydney: Access Economics; 2007 13 November 2007. Available at
are effective in relieving both rhinitis and associated conditions www.allergy.org.au/content/view/327/274/ [Accessed 23 December 2007].
such as asthma. 7. Taramarcaz P, Gibson PG. The effectiveness of intranasal corticosteroids in com
bined allergic rhinitis and asthma syndrome. Clin Exp Allergy 2004;34:1883-9.
• Patients presenting with rhinitis should be assessed for asthma,
8. Rimmer J, Ruhno JW. 6: Rhinitis and asthma: united airway disease. Med J Aust
rhinoconjunctivitis and eczema. 2006;185:565-71.
• Positive skin prick and RAST tests can be misleading to patients, 9. Meltzer EO. Allergic rhinitis: the impact of discordant perspectives of patient and
physician on treatment decisions. Clin Ther 2007;29:1428-40.
parents and doctors. Ordering and interpretation of tests should 10. Bachert C. Persistent rhinitis - allergic or nonallergic? Allergy 2004;59(Suppl
be guided by likelihood of allergens on history rather than 76):11-5; discussion 5.
Allergic rhinitis - practical management strategies
11. Ponsonby AL, Dwyer T, Kemp A, Lim L, Cochrane J, Carmichael A. The use of
mutually exclusive categories for atopic sensitization: a contrasting effect for
family size on house dust mite sensitization compared with ryegrass sensitiza
tion. Pediatr Allergy Immunol 2003;14:81-90.
12. Mygind N. Diagnosis of allergy. In: Mygind N DR, Pedersen S Theshrup-Pedersen
K, editor. Essential Allergy. Oxford Blackwell Science, 1996.
13. Bachert C, van Cauwenberge P, Khaltaev N. Allergic rhinitis and its impact on
asthma. In collaboration with the World Health Organization. Executive summary
of the workshop report. 7-10 December 1999, Geneva, Switzerland. Allergy
2002;57:841-55.
14. Scadding GK, Durham SR, Mirakian R, et al. BSACI guidelines for the manage
ment of allergic and non-allergic rhinitis. Clin Exp Allergy 2008;38:19-42.
15. ASCIA Sptwp. Skin prick testing for the diagnosis of allergic disease: a manual
for practitioners. 2007 4 November 2007. Available at www.allergy.org.au/
images/stories/pospapers/ASCIA_SPT_manual_Sep-06.pdf [Accessed 23
December 2007].
16. Douglass JA, O’Hehir RE. Diagnosis, treatment and prevention of allergic
disease: the basics. Med J Aust 2006;185:228-33.
17. Sheikh A, Hurwitz B, Shehata Y. House dust mite avoidance measures for peren
nial allergic rhinitis. Cochrane Database Syst Rev 2007:CD001563.
18. Walls RS, Heddle RJ, Tang ML, Basger BJ, Solley GO, Yeo GT. Optimising
the management of allergic rhinitis: an Australian perspective. Med J Aust
2005;182:28-33.
19. Al Sayyad JJ, Fedorowicz Z, Alhashimi D, Jamal A. Topical nasal steroids for
intermittent and persistent allergic rhinitis in children. Cochrane Database Syst
Rev 2007:CD003163.
20. Cave A, Arlett P, Lee E. Inhaled and nasal corticosteroids: factors affecting the
risks of systemic adverse effects. Pharmacol Ther 1999;83:153-79.
21. Allen DB, Meltzer EO, Lemanske RF Jr, et al. No growth suppression in children
treated with the maximum recommended dose of fluticasone propionate aqueous
nasal spray for one year. Allergy Asthma Proc 2002;23:407-13.
22. Schenkel EJ, Skoner DP, Bronsky EA, et al. Absence of growth retardation in chil
dren with perennial allergic rhinitis after one year of treatment with mometasone
furoate aqueousnasal spray. Pediatrics 2000;105:E22.
23. Price D, Bond C, Bouchard J, et al. International Primary Care Respiratory
Group (IPCRG) Guidelines: management of allergic rhinitis. Prim Care Respir J
2006;15:58-70.
24. Weiner JM. Allergen injection immunotherapy. Med J Aust 2006;185:234.
25. Calderon MA, Alves B, Jacobson M, Hurwitz B, Sheikh A, Durham S. Allergen
injection immunotherapy for seasonal allergic rhinitis. Cochrane Database Syst
Rev 2007:CD001936.
26. Wilson DR, Lima MT, Durham SR. Sublingual immunotherapy for allergic rhinitis:
systematic review and meta-analysis. Allergy 2005;60:4-12.
27. Passalacqua G, Bousquet PJ, Carlsen KH, et al. ARIA update: I--Systematic
review of complementary and alternative medicine for rhinitis and asthma. J
Allergy Clin Immunol 2006;117:1054-62.
28. Saleh HA, Durham SR. Perennial rhinitis. BMJ 2007;335:502-7.
29. Wheeler PW, Wheeler SF. Vasomotor rhinitis. Am Fam Physician
2005;72:1057-62.
AFP CORRESPONDENCE afp@racgp.org.au
CLINICAL PRACTICE O®
Chih-Hung Kuo Leo Pang Robert Chang

BSc(Med), MBBS, is an intern, Royal Prince BSc(Med), MBBS, is an advanced trainee in FRCS(Edin), DLO(Lond), is Head, ENT
Alfred Hospital, Sydney, New South Wales. ENT, Liverpool Hospital, Sydney, New South Department, Liverpool Hospital, Sydney,
chihhung.kuo@gmail.com Wales. New South Wales.
Vertigo
Part 1 - Assessment in general practice
■ The word vertigo is derived from the Latin ‘vertere’ meaning
Background
to turn and ‘-igo’ meaning a condition. Medically, vertigo refers
Vertigo is a common and diagnostic challenge faced by clinicians.
to a specific symptom describing a false sense of motion,
Objective usually spinning or rotatory, in the surroundings or within
This article discusses the assessment of patients with vertigo. oneself despite the absence of physical movement. In clinical
Discussion practice, the term ‘vertigo’ is not usually volunteered by patients.
The clinical assessment aims to: establish the presence of true Instead, a nonspecific complaint of ‘feeling dizzy’ is commonly
vertigo, differentiate between vertigo of central or peripheral used and clinicians are therefore faced with the challenge of
origins, and to evaluate the need for urgent investigations and deciphering the actual meaning of such a complaint.
referrals. Peripheral causes of vertigo are more common, but
central causes such as transient ischaemic attack or stroke The need for medically meaningful interpretations of ‘dizziness’ has
should always be considered and ruled out appropriately. Presence resulted in a classification system with four different subtypes.1
of syncope excludes the peripheral causes of vertigo. Vertigo in
Features and clinical implications of these subtypes are summarised
the elderly population is likely to be multifactorial and warrants
in Table 1. Out of the four subtypes of ‘dizziness’, vertigo accounts for
careful evaluation. Online videos of the head impulse test and the
around 32% of all cases2,3 and up to 56.4% in the elderly population.4
Dix-Hallpike manoeuvre are valuable as these tests are of great
diagnostic value. Audiological testing and neuroimaging can provide Causes of vertigo
further information to guide patient management.
The labyrinth is an inner ear neurosensory organ made up of two
components: semicircular canals (for balance) and cochlear (for hearing)
(Figure 1). Typically, vertigo is caused by an imbalance of sensory
inputs into the two vestibular nuclei from overactivity or underactivity
of either or both sides of the labyrinth.5 The brain interprets such input
differences as a sensation of movement. However, any disturbances
to the labyrinth, visual-vestibular interaction centres in the brain stem
and cerebellum, and sensory pathways to or from the thalamus, can
result in vertigo. Conventionally, causes of vertigo are separated into
central or peripheral origins as shown in Table 2. Such classification
serves to guide further investigations and management of the patient.
In the general practice setting, the three most common causes of
vertigo (accounting for 93% of all patient presentations)6 are:
• benign paroxysmal positional vertigo (BPPV)
• acute peripheral vestibulopathy (vestibular neuritis or labyrinthitis),
and
• Meniere disease.
Central causes of vertigo, although not as common, are generally
more serious and should always be considered. In the elderly
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 5, May 2008 341
Vertigo - Part 1 - Assessment in general practice CLINICAL PRACTICE
Table 1. Subtypes of dizziness and their clinical signficance1
Vertigo Presyncope Disequilibrium Light headedness

Description Illusion of movement, Sensation of impending loss of Postural unsteadiness, Also called ‘dizziness’,
usually rotatory of self or consciousness imbalance ‘giddiness’ or
surrounding ‘wooziness’. No clear
definition
Clinical A wide range of possible Reduction of total cerebral blood Neurological disorder, This term is now used
significance causes requiring further flow, usually of cardiovascular origin musculoskeletal interchangeably with
assessment Presence of syncope exclude weakness or visual presyncope
peripheral causes of dizziness impairment
Table 2. Classification for causes of vertigo8
Peripheral vertigo (labyrinth, vestibular nerves) Central vertigo (central nervous system) Other
Causes Common
Acute vestibulopathy: vestibular neuritis or Transient ischaemic attack or stroke, Psychogenic vertigo
labyrinthitis especially if vertebrobasilar system affected
Medication induced
vertigo
Benign positional paroxysmal vertigo Cervical vertigo
Meniere disease Migrainenous vertigo
Multiple sclerosis
Rare
Perilymphatic fistula Cerebellopontine angle tumour
Cholesteatoma erosion
Herpes zoster oticus
Otosclerosis
population, the causes of vertigo may be multifactorial and can be Figure 1. Structure of the ear
more difficult to assess.
Clinical assessment
The clinical assessment is aimed at determining if the patient has true
vertigo, whether the vertigo is of central or peripheral origin, and to
rule out life threatening conditions such as cerebellar haemorrhage.
An algorithm to guide initial history taking is summarised in Figure 2.
History
Whether the patient has vertigo or not can be checked by asking the
simple question, ‘When you have dizzy spells, do you just feel light
headed or do you see the world spinning around you?’ vestibular neuritis or labyrinthitis. Past history of head trauma or
Features of an attack such as duration, onset, frequency, severity ear surgery makes perilymphatic fistula more likely. Medication
and aggravating factors should be explored. Typically, an attack such as aminoglycoside, frusemide, antidepressants, alcohol
of central vertigo has a longer duration but is milder in severity. and antipsychotics can all cause vertigo. Patients with migraine
Associated features such as nausea and vomiting, headache, hearing or Meniere disease might have a strong family history. Anxiety
loss, ear discharge, ear fullness and tinnitus should be elicited. disorders and depression can also manifest as dizziness and vertigo.
The presence of cardiovascular risk factors increases the likelihood
Examination
of cerebrovascular ischaemia causing vertigo, especially in an
elderly person with a spontaneous and mild attack. History of recent A detailed examination of the patient starts with a general inspection
upper respiratory tract or ear infection suggests the possibility of looking for patterns of facial asymmetry suggesting either peripheral
Figure 2. Algorithm to guide initial history taking
t Recently recognised disease entity caused by congenital breakage in the bony labyrinth capsule. The breakage leads to hypersensitivity of
vestibular labyrinth to changes in pressure and sound causing vertigo. There are only about 100 reported cases
facial nerve involvement or a cerebrovascular event. The vesicles of the head still, observations for subtle nystagmus-like movements of
herpes zoster on the external ear might also be visible. Otoscopic the optic disc or optic blood vessels can be made.9
examination may reveal signs of inflammation associated with acute
Clinical tests
vestibulopathy, scarring of the eardrum from chronic suppurative otitis
media, or an erosive cholesteatoma. The Hennebert sign is positive Four clinical tests are useful tools for evaluating vestibular function:
when the symptom of vertigo is reproduced by applying external • the head impulse test
pressure on the tragus. The positive sign suggests the presence of a • the Romberg test
perilymphatic fistula. • the Fukuda-Unterberger test, and
Careful observation for features of nystagmus such as spontaneity, • the Dix-Hallpike manoeuvre.
direction, and associated changes with eye movements, convey Suitability of these tests should be considered, especially in patients
valuable diagnostic information. The direction of the nystagmus is with severe nausea and vomiting during the acute phase of illness.
determined by the ‘fast phase’ of the eye movement. Horizontal and
Head impulse test
torsional nystagmus, which beats to a unilateral direction regardless
of whether the eyes are gazing to the left or right, suggests the vertigo The head impulse test is both sensitive and specific to detect
is of peripheral origin.7 Conversely, if the direction of nystagmus unilateral hypofunction of the peripheral vestibular system, which
changes when the eyes are gazing toward a different direction, a is commonly due to acute vestibulopathy.10 Usually, a functional
central cause of vertigo is more likely.7,8 vestibular system can detect small changes in the head position
Vertical nystagmus also implies centra l and brainstem and rapidly adjust eye movements so the centre of vision remains
involvement. In peripheral vestibulopathy, central adaptation can lead on a target. In patients with acute vestibulopathy, when the head is
to a reduction of the magnitude of nystagmus within 24-48 hours. turned toward the affected side there will be a delay in vestibular
One way to observe for attenuated nystagmus during this period is to adjustment. Such a delay will manifest as a brief and fixed gaze
use an ophthalmoscope to examine one eye while blocking or closing toward the affected side followed by a corrective saccadic eye
the other eye to remove the external visual fixation. While keeping movement back to the centre.
CLINICAL PRACTICE Vertigo - Part 1 - Assessment in general practice
Figure 3. Dix-Hallpike manoeuvre
1. Sit patient on examination couch and explain procedure

2. Reassure the patient that, although they may feel dizzy, they will not be allowed to fall
3. Turn the patient’s head 45 degrees to one side
4. Lie patient supine with their head over the end of the examination bed, supporting their
head with a hand on each side of head. Maintain the 45 degree head turn as you lie the
patient down
5. Inspect the eyes for nystagmus, and ask the patient if they feel dizzy
6. Hold this position for at least 30 seconds, and for 1 minute if there is no reponse
7. The result is positive if the patient develops symptoms (vertigo) and nystagmus
8. Repeat on the opposite side
One important role of the head impulse test is to differentiate dysfunctions such as dysdiadochokinesia, dysmetria, dysarthria and
between cerebellar infarction and acute vestibular neuritis. In ataxia should also be sought. Cardiovascular examination and testing
patients with acute vertigo but a normal head impulse test, acute for postural hypotension can also provide useful clues.
vestibulopathy is ruled out and cerebrovascular causes of vertigo such
Investigations
as ischaemia or infarction should be considered.5
An excellent video of the head impulse test can be found at the A thorough history and examination can usually reveal the underlying
Journal of Neurology, Neurosurgery, and Psychiatry website (see causes of vertigo in the majority of patients. Investigations without a
Resources). Note: the head impulse test is usually performed with the proper clinical reasoning are unlikely to help in reaching a diagnosis.
clinician sitting face-to-face with the patient and holding the patient’s For example, routine blood tests are not recommended as they usually
head from the front. Due care should be taken when performing this fail to identify an underlying cause of vertigo.12
test on patients with neck pathology as the manoeuvre requires a Audiological testing can check for the presence of hearing loss
rapid repositioning of the head. and quantify it. Bilateral low frequency sensorineural or conductive
hearing loss is typical of Meniere disease. Caloric testing evaluates
Romberg test
the vestibular labyrinth function, however this test should only be
A Romberg test assesses the integrity of peripheral proprioception, done in a specialist centre and the results interpreted by a clinician
cerebellar and vestibular functions. A Romberg test is positive when with expertise in the field.5
the patient can maintain their balance with both feet placed close Neuroimaging is an important investigative tool if there is a
together with visual input, but not when the eyes are closed. concern of a central pathology. Clinical features that warrant urgent
neuroimaging are summarised in Table 3. Magnetic resonance
Fukuda-Unterberger test
imaging is the preferred imaging modality when conditions such
In the Fukuda-Unterberger test, the patient is asked to march on the as multiple sclerosis, vascular infarction or cerebropontine tumour
spot with their eyes closed. The test is positive when the patient are suspected. Computerised tomography is superior to detect any
deviates from the midline; usually toward the side with a relatively petrous bone abnormality or cerebellar haemorrhage, and as a follow
lower vestibular activity. up tool for trauma induced vertigo.13
Dix-Hallpike manoeuvre Conclusion

The Dix-Hallpike manoeuvre should be performed if the history is Dizziness and vertigo can present a diagnostic challenge because
suggestive of BPPV or if the nystagmus is inducible. The manoeuvre of confusion in the nomenclature and a vast number of diagnostic
is easy to perform and has a positive predictive value of 83.3% possibilities. During the initial assessment, the role of the clinician
and a negative predictive value of 52%11 (Figure 3). A short video is identifying benign and treatable underlying causes and to rule
demonstrating the Dix-Hallpike manoeuvre as the first part of the
Table 3. Warning clinical features warranting neuroimaging14
Epley manoeuvre can be found at the Australian Prescriber website
(see Resources). Explanations of the Dix-Hallpike manoeuvre and • Very sudden onset (seconds) of vertigo that persists and not
provoked by position
constant reassurance during the process can help reduce patient
• Association with new onset of (occipital) headache
discomfort and anxiety. It is also important to wait for at least 30
• Association with deafness but no typical Meniere history
seconds to observe for nystagmus or symptoms of vertigo before
testing the other side. • Acute vertigo with normal head impulse test
If symptoms are more suggestive of central vertigo, a thorough • Associated with central neurological signs such as severe gait
neurological examination should be performed. Signs of cerebellar and truncal ataxia
346 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 5, May 2008
out serious conditions. This can usually be achieved by using a

systemic approach with careful history, physical examination and
appropriate investigations.
Resources
• Journal of Neurology, Neurosurgery, and Psychiatry
http://jnnp.bmj.com/content/vol0/issue2007/images/data/
jnnp.2006.109512/DC1/78101113webonlymedia.mpg
• Australian Prescriber
www.australianprescriber.com/upload/issue_files/2804_epley.mov .
References
1. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology
1972;22:341-54.
2. Hanley K, O’Dowd T, Considine N. A systematic review of vertigo in primary care. Br
J Gen Pract 2001;51:666-71.
3. Colledge NR, Barr-Hamilton RM, Lewis SJ, Sellar RJ, Wilson JA. Evaluation of
investigations to diagnose the cause of dizziness in elderly people: a community
based controlled study. BMJ 1996;313:788-92.
4. Bird JC, Beynon GJ, Prevost AT, Baguley DM. An analysis of referral patterns for diz
ziness in the primary care setting. Br J Gen Pract 1998;48:1928-32.
5. Sloane P, Blazer D, George L. Dizziness in a community elderly population. J Am
Geritr Soc 1989;37:101-8.
6. Halmagyi GM, Cremer PD. Assessment and treatment of dizziness. J Neurol
Neurosurg Psychiatry 2000;68;129-34.
7. Labuguen R. Initial evaluation of vertigo. Am Fam Physician 2006;73:244-51.
8. Baloh RW. Superior semicircular canal dehiscence syndrome: Leaks and squeaks can
make you dizzy. Neurology 2004;62:684-5.
9. Baloh RW. Differentiating between peripheral and central causes of vertigo.
Otolaryngol Head Neck Surg 1998;119:55-9.
10. Paine M. Dealing with dizziness. Australian Prescriber 2005;28:94-7.
11. Jorns-Häderli M, Straumann D, Palla A. Accuracy of the bedside head impulse test in
detecting vestibular hypofunction. J Neurol Neurosurg Psychiatry 2007;78:1113-8.
12. Hanley K, O’Dowd T. Symptoms of vertigo in general practice: a prospective study of
diagnosis. Br J Gen Pract 2002;52:809-12.
13. Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. Am J Med
1999;107:468-78.
14. Seemungal B. Neuro-otological emergencies. Curr Opin Neurol 2007;20:32-9.
15. Bruzzone MG, Grisoli M, De Simone T, Regna-Gladin C. Neuroradiological features
of vertigo. Neurol Sci 2004;24:S20-3.
CLINICAL PRACTICE
Patient education
Management of benign
positional vertigo
Benign positional vertigo is caused by abnormal clumps of debris exercises for any benefit to occur. If the exercises are done regularly,
collecting in one of the fluid filled balance canals of the inner ear. the symptoms should resolve in most cases over a period of several
Brandt-Daroff exercises are designed to break up this material and days.
unblock the canal. These exercises should be performed three times
per day. The symptoms of dizziness need to be reproduced by the
Step 1 Step 2
Sit on edge of bed, turn head Lie down quickly on right side (so that the back of the
slightly to left side (approximately head rather than the front is resting on the bed). Wait
45 degrees) for 20-30 seconds or for any dizziness to resolve
Step 3 Step 4
Sit up straight, again waiting for Turn head slightly to right side and repeat sequence
20-30 seconds or for any dizziness in opposite direction
to resolve
Continue as above for 10 minutes (five or more repetitions to each side)
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 6, June 2008 415
CLINICAL PRACTICE ®
Andrew Baird
MA, MBChB, DRANZCOG, DA, FRACGP, FACRRM,
is a general practitioner, Brighton, Victoria.
bairdak@gmail.com
Emergency drugs in general practice

■ General practitioners need the knowledge, skills, drugs and
This review article discusses available drugs for the initial
equipment for managing medical emergencies. Clinics need
management of medical emergencies in general practice.
treatment rooms and doctor’s bags that enable emergencies to be
managed onsite and offsite respectively. Rural medical generalists
may provide more advanced emergency management in their local
Table 1. General principles in the management of medical hospitals. In managing emergencies, GPs may be working with
emergencies paramedics, therefore it helps to be familiar with their skills and
with the drugs they carry. General principles that apply in
• Danger, response, airway, breathing, circulation (and
managing medical emergencies are described in Table 1. Relevant
compressions) - DRABC
contraindications should be checked before administering any of
• Activate a crisis resource management plan
the drugs described below (Table 2).
- get help (eg. other practice staff, ambulance professionals
via ‘000’, bystanders) Life threatening medical emergencies
- assign roles (including leader, scribe, and timekeeper)
- facilitate teamwork
Cardiac arrest
Current guidelines1 emphasise the importance of cardiac compressions, and
• Some history is better than no history
prompt defibrillation for ventricular fibrillation (VF) or pulseless ventricular
- any drugs or allergies?
tachycardia (VT). Adrenaline is given every 3 minutes intravenously (IV) until
- any ‘not for resuscitation orders’? (Ideally sighted, and on
standardised forms) return of spontaneous circulation (ROSC):
- if available - ask relatives, check medical records • adult dosage: 1 mg with a saline flush (10-20 mL)
• Give oxygen (8 L/min) via Hudson mask (via bag-valve-mask • paediatric dosage: 0.01 mg/kg (10 pg/kg) (Table 3) with a saline flush (up
system in cardiac arrest) to 5 mL).
• I ntravenous drugs are generally given over 2-5 minutes (but During cardiopulmonary resuscitation, the following drugs may be
as a ‘push’ with saline flush in cardiac arrest) considered:
• Continuous assessment and management until stable • VF or VT: lignocaine 1 mg/kg
• Observe patient once stable (especially if sedative drugs • asystole or severe bradycardia: atropine 1.2-3.0 mg (adult);
have been administered) 20 pg/kg (child)
• Be willing to consult with an emergency department for In the hospital setting amiodarone is the first line drug for treating
advice and patient transfer ventricular arrhythmias. Following ROSC, blood pressure (BP) and adequate
• Practise safe sharps management, and follow infection perfusion should be maintained. This may require IV adrenaline (Table 4).
control procedures
• Take detailed notes, and transcribe these to the patient’s Anaphylaxis2
medical record at the earliest opportunity. Keep copies of
any transfer of care letters • Adrenaline is given every 5 minutes intramuscularly (IM) (anterolateral
• Arrange debriefing as appropriate for the patient (or thigh) until clinical features have improved. Up to 10 doses may be given:
relatives), and for those involved in managing the emergency - adult dosage: 0.5 mg
- paediatric dosage: 0.01 mg/kg (10 pg/kg) (Table 3)
- in adults, if there is a poor response, consider glucagon 1-2 mg
IV over 5 minutes
- consider IV adrenaline if shock persists after two IM doses; use with
extreme caution (Table 4)
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 7, July 2008 541
CLINICAL PRACTICE Emergency drugs in general practice
• Oxygen (8 L/min) • ipratropium 20 pg/dose metered dose inhaler (MDI) via spacer, 2-4
• Normal saline (20 mL/kg) is given for hypotension puffs every 20 minutes in first hour
• Hydrocortisone 250 mg (or 4 mg/kg), single dose IV. • hydrocortisone 4 mg/kg IV.
If there is no response to inhaled salbutamol, then salbutamol
Potentially life threatening emergencies should be given IV as a bolus (250 pg for adults, 5 pg/kg over 10
Asthma and bronchospasm3 minutes for children) followed by an infusion. This may not be
Critical or severe (any of: talking in words, unable to talk, SpO2 <90%, practical in most general practice settings. Consider IV adrenaline in
agitated, confused, drowsy, maximal accessory muscle use and recession). extremis (Table 4).
Adult: Mild/moderate
• oxygen, at least 8 L/min to maintain SpO2 >94% Adult:
• nebulised salbutamol 10 mg driven by oxygen, at least 8 L/min every • oxygen at least 8L/min to maintain SpO2 >94%
15 minutes • salbutamol 100 pg/dose MDI via spacer, 10-20 puffs (4-6 tidal
• nebulised ipratropium 500 pg 2 hourly breaths per puff) every 1-4 hours, or salbutamol 5-10 mg nebulised,
• hydrocortisone 250 mg (or 4 mg/kg) IV driven by oxygen every 1-4 hours
Paediatric: • ipratropium 20 pg/dose MDI via spacer, six puffs every 2 hours,
• oxygen at least 8 L/min to maintain SpO2 >94% OR ipratropium 500 pg nebulised, driven by oxygen every 2 hours
• nebulised salbutamol (5 mg/2.5 mL) driven by oxygen, at least 8 L/min, (ipratropium is optional)
continuous • prednisolone 50 mg orally
Table 2. Emergency drugs: presentation, contraindications, and potential adverse reactions (in emergency use)
Drug presentation Contraindications (other than known allergy) Adverse reactions

Adrenaline: 1 mg/1 mL Nil in cardiac arrest and anaphylaxis Arrhythmia; myocardial and cerebrovascular
(1:1000) ischaemia
Atropine: 600 pg/1 mL Nil in cardiac arrest or hypotensive bradycardia Tachycardia, confusion, nausea
ADT: 0.5 mL vial Children <8 years of age Local: pain, swelling
Systemic: fever, malaise
Benztropine: 2 mg/2 mL Children <3 years of age Tachycardia, confusion
Benzylpenicillin powder: Nil Nil
600 mg or 3 g
Dexamethasone: 4 mg/1 mL Nil in emergency Rare with single dose
Diazepam: 10 mg/2 mL Cardiorespiratory failure Drowsiness, confusion, respiratory
Central nervous system (CNS) depression depression
Dihydroergotamine: 1 mg/1 mL Hemiplegic migraine Vasospasm syndromes (rare)
Use of sumatriptan
Frusemide: 20 mg/2 mL Sulfonamide allergy Nil
Glucagon: 1 mg/1 mL Nil Nil
GTN spray: 400 pg/dose Cardiogenic shock Headache, hypotension
Systolic blood pressure <100 mmHg
Use of phosphodiesterase type 5 (PDE5) inhibitors
Haloperidol: 5 mg/1 mL Cardiovascular collapse Dystonia, confusion, hypotension
CNS depression
Hydrocortisone: 100 mg or Nil in emergency Rare with single dose
250 mg/2 mL
Lignocaine: 100 mg/5 mL Nil Lightheadedness, nausea, agitation
Metoclopramide: 10 mg/2 mL Acute complete bowel obstruction Dystonic reactions (~1%, more common in
children)
Morphine sulphate: 15 mg or Respiratory or CNS depression Sedation, nausea, vomiting
30 mg/1 mL
Naloxone Min-I-Jet: 0.8 mg/2.0 mL Nil Nil
or 2 mg/5 mL
Prochlorperazine: 12.5 mg in 1.0 mL Circulatory collapse Drowsiness
CNS depression
542 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 7, July 2008
Emergency drugs in general practice CLINICAL PRACTICE
Table 2. Emergency drugs: presentation, contraindications, and potential adverse reactions (in emergency use) continued
Drug presentation Contraindications (other than known allergy) Adverse reactions

Salbutamol: Nil Tachycardia, tremor
MDI: 100 pg/dose
Nebuliser: 2.5 mg or 5.0 mg/2.5 mL
Tramadol: 100 mg/2 mL Children, MAOIs, respiratory or CNS depression; Nausea, vomiting, dizziness
caution with SSRI drugs
Verapamil: 5 mg/2 mL Cardiogenic shock, heart block, hypotension, broad Nausea, heart block, bradycardia,
complex SVT, use of beta blocker drugs hypotension
*#:
Aspirin 300 mg tablet Active haemorrhage, active gastrointestinal ulcer; Dyspepsia
caution in asthma
Ceftriaxone
*#: 2 g powder Nil Nil
*:
Diclofenac Active gastrointestinal ulcer or haemorrhage; Nausea, dyspepsia
tablets: 50 mg caution in: renal impairment, anticoagulation,
asthma
suppositories: 100 mg
*#
Glucose 50% (500 mg/mL): 50 mL Diabetic coma Phlebitis
Ipratropium bromide
*#: Nil Nil
MDI: 20 pg/dose
Nebuliser: 500 pg/1 mL
Ketorolac
*: 10 mg/1 mL Active gastrointestinal ulcer or haemorrhage; caution Nausea, dyspepsia
in: renal impairment, anticoagulation, asthma
*#:
Midazolam 5 mg in 1 mL Cardiorespiratory failure Drowsiness, confusion, respiratory
(or 15 mg in 3 mL) CNS depression depression
*:
Olanzapine 5 mg wafer or tablet Nil Hypotension
Sumatriptan
*: Ischaemic heart disease Transient flushing, dizziness, tightness in
tablets: 50 mg, 100 mg Cerebrovascular disease chest or throat, increased BP
injection: 6.0 mg in 0.5 mL Ergotamine <24 hour ago
Caution: taking SSRI, SNRI
Syntometrine
* 1 mL Threatened abortion Hypertension
(oxytocin 5 intra-uterine (IU) plus Severe hypertension Headache
ergometrine 500 pg) Nausea
* Not supplied under PBS emergency drug (doctor’s bag) items # Drugs are carried by MICA paramedics in Victoria
MAOI = monoamine oxidase inhibitor, SSRI = selective serotonin reuptake inhibitor, SNRI = selective noradrenaline reuptake inhibitor
Paediatric: Acute coronary syndrome5

• oxygen at least 8 L/min to maintain SpO2 >94% • Oxygen 8 L/min
• salbutamol 100 pg/dose MDI via spacer, 4-6 tidal breaths per puff, • Aspirin 300 mg orally
• Glyceryl trinitrate (GTN) spray, 1 dose repeated after 5 minutes if no
repeat after 20 minutes for two further doses if not improved
improvement
- over 6 years of age: 12 puffs
• Morphine 2.5 mg IV every 5 minutes as required, titrated to analgesic
- 6 years of age or under: 6 puffs
effect (maximum of 15 mg).
And
All patients with acute coronary syndrome (ACS) should be stabilised
• prednisolone 1 mg/kg orally.
and transferred to hospital as soon as possible.
Acute exacerbation of chronic obstructive pulmonary disease4 Fibrinolysis (for ACS with ST elevation or new left bundle branch
Treat as acute asthma, with the following exceptions: block) in an out-of-hospital setting is controversial. Patients who present
• controlled oxygen therapy to reduce the risk of inducing hyperoxic to a rural hospital less than 12 hours from symptom onset may be
hypercapnia. In practice, oxygen at 2 L/min via nasal prongs is considered for fibrinolysis if percutaneous coronary intervention is not
indicated to achieve oxygen saturation of 90-93% possible within 1-2 hours. A cardiologist should be consulted.
• nebulised bronchodilators should be driven with high flow air,
Severe upper airway obstruction
not oxygen
• start antibiotics for clinical signs of infection (eg. oral doxycycline). • Nebulised adrenaline (1 mg in 1 mL ampoules):
- adult dosage: 5 mL And/or:

- paediatric dosage: 0.5 mL/kg (maximum dose: 5.0 mL); dilute to • Glucose 50% IV at 3 mL/min via large vein
5.0 mL if necessary. - adult and paediatric dosage: 20-50 mL (depending on response).
Acute pulmonary oedema Convulsive status (convulsion for longer than 10 minutes)
• Oxygen 8 L/min - patient must be sitting up • Oxygen 8 L/min
• GTN spray, one dose, repeat every 5 minutes as required • Diazepam
• Frusemide 20 mg IV (consider 40 mg in patients currently taking - adult dosage: 5-10 mg IV or 10-20 mg per rectum (PR) (insert nozzle
frusemide) of syringe PR, can dilute with 5 mL of saline)
• Consider morphine 2.5 mg IV. - paediatric dosage: (Table 3)
Or
Arrhythmias
• Midazolam (dose can be repeated after 15 minutes if there is
Adults persistent or recurrent convulsion)
• Cardiac monitoring is essential. - adult dosage: 5-10 mg IM or 2.5-5.0 mg IV
• Supraventricular tachycardia (SVT): consider verapamil 5 mg IV over - paediatric dosage: 0.2 mg/kg IM or 0.1 mg/kg IV.
1 minute if symptomatic and if vagal manoeuvres have failed
Opioid induced respiratory depression
• Bradycardia and ventricular arrhythmias - as described under
‘cardiac arrest’. • Oxygen 8 L/min
Adenosine by rapid IV bolus (6 mg then 12 mg if required) is now the • Naloxone
drug of first choice for converting SVT, and GPs may consider this. It is - adult dosage:
potentially safer than verapamil, which may result in VF if given to treat - titrated IV bolus (preferred): 0.1 mg at 1-2 minute intervals
VT which has been misdiagnosed as broad complex SVT. - I M (if no IV access): 0.4 mg, repeat every 3 minutes as required (to a
maximum of 10 mg)
Hypovolaemia
- paediatric dosage: 10 pg/kg IM initially; second dose 100 pg/kg if
• Normal saline IV required.6
• Adult dosage: 500 mL-1L bolus then infusion to maintain circulation Titration reduces the risk of precipitating withdrawal symptoms. Patients
• Paediatric dosage: 20 mL/kg bolus then infusion to maintain should be observed for renarcotisation; naloxone infusion may be
circulation. required.
Postpartum haemorrhage and incomplete abortion Meningitis and/or meningococcaemia (suspected)

• Syntometrine 1 mL IM. • Benzylpenicillin, preferably IV but IM acceptable
- adult dosage: 1.2 g
Hypoglycaemia
- paediatric dosage:
• Glucagon IV, IM, or SC - age <1 year: 300 mg
- adult (and children over 8 years of age) dosage: 1 mg - age 1-9 years: 600 mg
- children 8 years or under dosage: 0.5 mg - age >9 years: 1.2 g
Table 3. Paediatric dosage chart for adrenaline and diazepam
Approximate Approximate Adrenaline Adrenaline Diazepam IV Diazepam PR

age weight (kg)
* 1 mg/1mL 1 mg/10 mL 10 mg/2 mL 10 mg/2 mL
0.01 mL/kg* 0.1 mL/kg* 0.04 mL/kg 0.10 mL/kg
6 months 8 0.05 mL 0.5 mL 0.2-0.3 mL 0.5-0.8 mL
1-2 years 10 0.10 mL 1.0 mL 0.4 mL 1.0 mL
2-3 years 15 0.15 mL 1.5 mL 0.6 mL 1.5 mL
4-6 years 20 0.20 mL 2.0 mL 0.8 mL 2.0 mL
7-8 years 25 0.25 mL 2.5 mL 1.0 mL 2.5 mL
9-10 years 30 0.30 mL 3.0 mL 1.2 mL 3.0 mL*
11-12 years 35 0.35 mL 3.5 mL 1.4 mL 3.0 mL*
>12 years 40 0.40 mL 4.0 mL 1.6 mL 3.0 mL*
Note: A useful approximation for a child’s weight is: 9 + (age x 2) kg
t = 0.01 mg/kg (10 pg/kg)
i = maximum recommended dosage
Emergency drugs in general practice CLINICAL PRACTICE
• Ceftriaxone (if known allergy to penicillin)

Table 4. Intravenous adrenaline in low cardiac output states and life threatening asthma
- adult dosage: 2 g IV or IM
- paediatric dosage: 50 mg/kg IV or IM (maximum 2 g) • Ambulance clinical practice guidelines describe the use of diluted incremental
doses of IV adrenaline every 2 minutes as required to maintain blood pressure
• Dexamethasone (0.15 mg/kg IV (maximum 10 mg)) may also be
and perfusion
administered on specialist advice.
• Initial doses 10 pg. If there is inadequate response, doses are increased to
Septicaemia (suspected) 50 pg and then if necessary to 100 pg
• For 10 pg doses, add adrenaline 1 mg to a 1 L bag of normal saline to give a
• Ceftriaxone
solution of adrenaline 1 pg/mL. Ensure that the bag is labelled. Withdraw
- adult dosage: 2 g IV or IM 10 mL for each dose
- paediatric dosage: 50 mg/kg IV or IM (maximum 2 g).
• For 50 pg and 100 pg doses, add an adrenaline 1 mg/mL 1 mL ampoule to 9 mL
of normal saline to give a solution of adrenaline 100 pg/mL. Ensure that the
Nonlife threatening emergencies syringe is labelled. Add the required volume of this solution (0.5 mL or 1.0 mL)
to a syringe with 10 mL of normal saline to give the diluted dose of adrenaline
Nausea and vomiting
Adults: • An infusion of normal saline should be running when adrenaline is used
intravenously
• metoclopramide 10 mg, IV, IM or SC
• prochlorperazine 12.5 mg IM is effective for nausea and vomiting • IV adrenaline should only be used with extreme caution. Cardiac monitoring
is essential
associated with vertigo, related to vestibular system disorders.
Metoclopramide has a higher risk of dystonic reactions in children than
in adults, and its use in children should be avoided. Metoclopramide has Palliative care emergencies
no place in the management of a child with gastroenteritis. Seidel et al7 have written a review on the use of doctor’s bag drugs in the
management of these emergencies.
Severe acute pain
Psychiatric emergencies (adults)
• Pethidine has no place in the management of pain due to its high
potential for dependence and its neurotoxic metabolites Acute psychosis, mania, severe agitation, severe anxiety or panic attack,
• Consider and exclude drug seeking behaviour before administering delirium (pending diagnosis and definitive treatment):
opioids. • diazepam 5-20 mg orally, or
In most contexts, severe pain can be treated with: • olanzapine 5 mg orally, or
• morphine (preferably IV, but can be given IM or SC) • midazolam 2.5-10.0 mg IM or 2.5-5.0 mg IV every 20 minutes as
- adult dosage: 2.5-5.0 mg, titrate to analgesic effect every 5 minutes required (especially for drug induced states), or
up to a maximum of 15 mg • haloperidol 2.5-5.0 mg IM or IV.
- paediatric dosage: 0.1 mg/kg (avoid in infants) With severe disturbance, IV access will be impossible.
• consider an antiemetic Dystonic drug reaction:
Or (for moderate pain in adults): • benztropine IV or IM
• Tramadol 50-100 mg slow IV or IM. - adult dosage: 1-2 mg
- paediatric dosage: 0.02 mg/kg.
Migraine (adult)
Contaminated wounds
• Aspirin 900 mg orally
• Metoclopramide 10 mg IV Cleaning and debridement is the principal management.
• Normal saline 1 L IV over 1-4 hours Adult diphtheria and tetanus (ADT) 0.5 mL IM should be given if:
• Alternatives to aspirin: • tetanus prone wound, if more than 5 years since last dose of tetanus
- dihydroergotamine 1 mg IM toxoid
- diclofenac 50-100 mg orally or PR • any wound, if more than 10 years since last dose of tetanus toxoid
- sumatriptan 50-100 mg orally. • uncertainty that primary course has been completed.
Ureteric colic and biliary colic Emergency drugs provided under the PBS
Nonsteroidal anti-inflammatory drug (NSAID), eg. diclofenac 100 mg PR General practitioners can submit a monthly order form to a pharmacist
or ketorolac 10 mg IM. for the supply of Pharmaceutical Benefits Scheme (PBS) doctor’s bag
drugs at no cost. Alternative drugs may be preferable for managing
Painful wounds
some emergencies.
Consider using plain lignocaine by infiltration, topical application • Chlorpromazine may cause hypotension; should be used with
(eg. eyes, ears) or ring block. extreme caution
• Midazolam is more versatile than diazepam. It can be used to manage References

convulsions and agitated states, and, unlike diazepam, can be given 1. Adult cardiorespiratory arrest flow chart, Australian Resuscitation Council. Available
IM, buccally and intranasally. It can be given IV at half the IM dose at www.resus.org.au/public/arc_adult_cardiorespiratory_arrest.pdf [Accessed 19
December 2007].
• Dihydroergotamine is less effective than sumitriptan for relieving the
2. Emergency management of anaphylaxis in the community. Australian Prescriber
symptoms of migraine 2007;30:115. Available at www.australianprescriber.com/upload/pdf/articles/913.
• Haloperidol may cause significant dystonic reactions. Midazolam is pdf [Accessed 19 December 2007].
3. National Asthma Council. Emergency management of asthma. Available at www.
preferable for managing severe agitated states8
nationalasthma.org.au/html/emergency/print/EMAC.pdf [Accessed 19 December
• Promethazine has no place in the management of anaphylaxis as 2007].
it may cause hypotension and vasodilatation. Oral nonsedating 4. McKenzie DK, Abramson M, Crockett AJ, et al, The COPD-X Plan. Australian and
New Zealand guidelines for the management of chronic obstructive pulmonary
antihistamines are preferable for managing acute urticaria9
disease, 2007.
• Current emergency management guidelines do not include the use of 5. National Heart Foundation. Algorithm for the management of acute coronary syn
either procaine penicillin or terbutaline. drome. Available at www.heartfoundation.com.au/downloads/NHF_ACS_chart0506.
pdf [Accessed 19 December 2007].
Emergency drugs not provided under the PBS 6. Clark SFJ, Dargan PI, Jones AL. Naloxone in opioid poisoning: walking the tightrope.
Emerg Med J 2005;22:612-6.
Doctors may obtain these as private items - at their own expense - by 7. Seidel R, Sanderson C, Mitchell G, Currow DC. Until the chemist opens - palliation
submitting a written order to a pharmacist. In addition to the non-PBS from the doctor’s bag. Aust Fam Physician 2006;35:225-31.
8. Pharmaceutical Benefits Scheme: Doctors bag emergency drugs. Available at www.
items listed in Table 2, the following should be considered:
pbs.gov.au/html/healthpro/browseby/doctorsbag [Accessed 19 December 2007].
• oral drugs: analgesics, antibiotics, prednisolone, diazepam 9. Brown SGA, Mullins RJ, Gold MS. Anaphylaxis: diagnosis and management. Med J
• normal saline, 1 L bags Aust 2006;185:283-9.
10. Hiramanek N, O’Shea C, Lee C, Speechly C, Cavanagh K. What’s in the doctor’s bag?
• normal saline and water for injection. Aust Fam Physician 2004;33:714-20.
Oxygen
Oxygen is essential for managing emergencies and its availability is a
requirement for general practice accreditation. Oxygen cylinders can
be hired and refilled from a medical gas supplier (eg. BOC). A size C
cylinder (490 L) will last for 55 minutes at 8 L/min.
The following are required to administer oxygen: adult and paediatric
Hudson masks and nebuliser masks, nasal prongs, airways, and a bag
valve-mask breathing system (eg. Air Viva 3).
Equipment for managing emergencies

Appropriate supplies of IV infusion sets, cannulas, syringes, and needles
are required. General practitioners should consider the following items
for their practices:
• an automated external defibrillator (AED) with monitor and manual
override. Although a defibrillator is not a requirement for practice
accreditation, its absence may put a practice at clinical and
medicolegal risk
• pulse oximeter
• portable packs to enable equipment to be taken for use offsite.
Equipment for the doctor’s bag is discussed in detail by Hiramanek
et al.10
Managing emergency drugs in general practice

Drugs must be stored in a locked cupboard or a locked bag at less than
25°C. ADT and syntometrine are stored in a refrigerator. Schedule 8
drugs (opioids) must be stored in a locked, fixed, steel safe; although
ampoules may be put in a locked bag for use away from the clinic.
All emergency drugs should be logged in a book or spreadsheet that
includes date received, date administered, recipient, and expiry date.
Systems should be in place for checking drug stocks and expiry dates,
and for auditing the log.
A separate book is required to log Schedule 8 drugs received and
used. A Schedule 8 drug record book is available from The Royal
Australian College of General Practitioners at www.racgp.org.au/
publications/recordkeeping.
Conflict of interest: none declared. AFP CORRESPONDENCE afp@racgp.org.au
RESEARCH
Alison Fogarty Grant Blashki Elle Morrell Graeme Horton

MSocSc(Env&Plan), GreenClinic, is MD, FRACGP, is Senior Research MSocSc (Socio-Environmental FRACGP, FARGP, MEnvStud, is Senior
Coordinator, Australian Conservation Fellow, Department of General Assessment and Planning), GreenHome, Lecturer in Medical Education,
Foundation, Fitzroy, Victoria. Practice, University of Melbourne, is Coordinator, Australian Conservation University of Newcastle, New South
a.fogarty@acfonline.org.au Victoria. Foundation, Fitzroy, Victoria. Wales.
The GreenClinic pilot

Educational intervention for environmentally
sustainable general practice
■ There is an urgent need for our community to live and work
Background
within the capacity of our environment to supply our resources
GreenClinic was a pilot educational program developed by the
and absorb our wastes.1 Human health is already affected by
Australian Conservation Foundation and Doctors for the Environment
Australia. The program ran between October 2006 and March 2007
climate change: examples include the changing distribution of
with the aim of informing and encouraging general practitioners to infectious diseases and allergens, and increases in heat
employ more environmentally sustainable practices in their clinics. related deaths.2 If global temperature increases are to be
curbed, we must take every opportunity to share our collective
Methods
knowledge of how best to involve others in this challenge.
Twenty GPs attended an education meeting at the launch of
GreenClinic in Melbourne in October 2006; 12 registered with
the program and seven followed it to completion. An audit was The direct environmental benefits of employing sustainable practices
undertaken before and after the intervention to determine the usual in general practice clinics include decreased energy consumption and
water and energy consumption and waste disposal practices of the greenhouse gas production. There are increasing calls for doctors to
participating clinics, and how these changed after the program. assume a community leadership role in promoting environmentally
sustainable practices3 and to model ‘carbon literate’ behaviour.4
Results
General practitioners and practice managers are already under
This evaluation suggested that GPs who participated in an
environmental educational initiative were able to make changes pressure to provide health care, run practices and meet bureaucratic
toward sustainability in their practices. requirements. Encouragements to take up sustainable practices in
clinics therefore need to be straightforward and easy to implement,
Discussion
while having tangible and significant environmental outcomes.
There are potential benefits to be gained from employing
The pilot of the GreenClinic program was launched in Melbourne
environmental educational interventions more widely in general
practice and from evaluating their impact.
in October 2006 with the support of Doctors for the Environment
Australia (DEA) and the Australian Conservation Foundation (ACF).
The program was based on the ACF GreenHome program and used a
community based social marketing model to encourage sustainable
behaviours. It involved a multimodal approach to behaviour change
incorporating predisposing, enabling and reinforcing factors.5 In the
GreenClinic program this involved a face to face educational meeting,
a written GreenClinic guide, and follow up phone or email support.
Methods
General practitioners were invited to participate in the GreenClinic
pilot program through advertisements placed in the weekly fax
bulletin of The Royal Australian College of General Practitioners.
Victorian members of DEA were invited by email.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 8, August 2008 681
RESEARCH The GreenClinic pilot - educational intervention for environmentally sustainable general practice
Educational intervention
Table 1. Contents of the ‘action kit’ distributed at GreenClinic
The educational intervention was held in Melbourne at the 60L Green
educational intervention
Building, a building that showcases sustainable design and operation.
The intervention featured presentations on current environmental •Copy of ACF Habitat magazine
issues, the roles of health care professionals, and a discussion of •‘No junk mail’ sticker
the 10 ‘Greening your clinic’ tips outlined in the GreenClinic Guide • Four minute shower timer
supplied to participants (Table 1) and available electronically from the •GreenClinic guide
ACF website.6 - outline of program’s aim
Participants were invited to register for follow up and audit of the - ‘Top 10 tips for greening your clinic’
program. Registrants received three email updates about the program. • Hints for promoting environmentally responsible and healthy
An email address was provided to enable response to queries or lifestyles for patients
concerns raised by participants.
Outcome tools Waste management

Participants completed a self reported baseline survey assessing Six out of seven clinics reported new policies and procedures to
water and energy use and waste disposal in their clinics within 3 reduce paper consumption. Four clinics increased the amount of
weeks of the educational meeting. The surveys followed the format of recycled paper items they purchased, with one moving from 50%
the GreenClinic Guide and covered each of the 10 ‘Greening your clinic’ recycled content to 100% recycled content. One clinic requested being
tips (Table 2). The surveys were repeated 3 months later. Participants removed from direct mailing lists and two clinics reported requesting
received up to four telephone reminders about completing the surveys. that mail be sent to them via email when possible.
One of the clinics had no recycling service at baseline but
Results
introduced recycling after the intervention.
Twenty GPs attended the educational meeting. Of these, 12 agreed to
Discussion
register for the full program and seven completed both baseline and
follow up surveys. The GreenClinic program engaged a number of GPs in working
A descriptive comparison was made of baseline and follow up toward sustainable practices in the running of their clinics. There
survey responses in relation to energy and water usage and waste were improvements in the areas of water, energy use and waste
management. minimisation.
During the intervention period there were five enquiries from Seemingly minor actions can, over time, produce significant
participants: one related to ‘green power’ suppliers, another to types environmental benefits. A tap leaking at a rate of one drip per second
of recycled paper, and two queries related to recycling services for equates to approximately 230 litres per week. Fixing the three leaking
clinics. There was one request for contact details of builders who taps found in our evaluation represented a saving of approximately
observed GreenClinic principles. Available information relating to 36 000 litres of water per year.7
each of these enquiries was distributed to all participating clinics. Clinics that reduced lighting hours by 50 hours per week would
be reducing their greenhouse gas production by 8.7 kg/week, or 450
Changes in reported behaviours
kg/year. The clinic which reduced vehicle travel by 100 km/week
Energy use would be saving approximately 40 kg of greenhouse gas emissions
Reduction in travel was the most significant change in energy use. per week, or 2080 kg/year. Recycling and reducing consumption of
One clinic reported a reduction in the number of pathology pickups. raw materials can also have a positive effect; recycling one shopping
Another clinic reported a change to the ways in which doctors and bag full of containers per week reduces greenhouse gas production by
staff travelled to work, with a reduction of five car trips and an 260 kg/year.8
increase of bike trips amounting to a total saving of 100 km/week in While these figures may sound impressive, the activities of each
motor vehicle transport. Australian, on average, generates 25 000 kg of carbon dioxide per year,
Four out of seven clinics reduced lighting hours; the average and it is estimated that this figure needs to be as low as 4000 kg/year
reduction was 50 hours per week. One clinic switched to green before Australia achieves environmental sustainability.9 In this context,
energy. Between the seven clinics, a total of seven appliances usually the changes reported in this study are modest.
on standby were turned off.
Limitations
Water use
This study involved a self selected sample of GPs who were likely to
Three out of 50 taps checked in the clinics were found to be leaking; already be interested in environmental sustainability. There was no
these were subsequently fixed. control group and no opportunity to account for behaviour changes
682 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 8, August 2008
The GreenClinic pilot - educational intervention for environmentally sustainable general practice RESEARCH
Table 2. Changes in clinic practices measured against the Australian Conservation Foundation ‘Ten tips for greening your clinic’
Tips Changes in clinic practices following intervention

1. Install low energy lighting No change in lighting type. Five clinics reduced the amount of time a light was in use; the
average reduction for these clinics was 50 hours per week per clinic
2. Buy green power for the clinic One clinic changed to green energy; two clinics were already using green energy
3. Turn off computers and appliances to Three clinics reduced the number of appliances left on standby. A total of seven out of 39
save energy appliances were turned off
4. Energy efficient refrigerators No change
5. Aim for a paper free office Three clinics introduced new or additional policies and procedures to reduce paper use
6. Reduce car journeys One clinic reduced pathology pickups by one trip. One clinic reduced staff car trips by five per week
7. Reduce junk mail One clinic requested removal from direct mailing lists; two other clinics had already adopted
this measure. Two clinics requested mail be sent to them electronically; four clinics had already
adopted this measure
8. Recycle paper and plastics A recycling system was introduced by the one clinic which did not already practice recycling
9. Buy recycled paper, stationery and One clinic increased its use of recycled paper, stationery and toilet paper from 50-100%. Three
toilet paper clinics started purchasing recycled toilet paper, and two started purchasing recycled paper towel
10. Save water in the kitchen, Three out of 50 taps were found to be leaking and were fixed
bathroom and consulting room
related to other influences, such as environmental reporting in the media. Acknowledgment

The survey instruments relied on self reports, and claims for The authors thank the ACF, DEA and the doctors, practice managers and staff
who participated in the GreenClinic program.
behaviour change were not verified. The number of respondents to
the invitation was small, and not all initial registrants followed the References
program to completion. 1. Kates RW, Parris TM. Long-term trends and a sustainability transition.
Proceedings of the National Academy of Sciences of the United States of America
However, the authors believe this is the first evaluation of such 2003;100:8062-7.
program in a general practice setting in Australia. Multiplying even 2. Intergovernmental Panel on Climate Change. IPCC fourth assessment report,
working group II report, impacts adaptation and vulnerability. Available at
these modest environmental improvements by the number of general www.ipcc.ch/pdf/assessment-report/ar4/wg2/ar4-wg2-chapter8.pdf [Accessed
practices in Australia suggests that this is an area worthy of further 10 January 2008].
3. Kefford RF. Medical heat for climate change. Med J Aust 2006;184:582.
investigation. Previous educational interventions in the community,
4. Jackson R, Shields KN. Preparing the U.S. health community for climate change.
such as ACF’s GreenHome program, have resulted in significant Annu Rev Public Health 2008;29:1-25.
5. Davis D. Does CME work? An analysis of the effect of educational activi
improvements in sustainable practices.10
ties on physician performance or health care outcomes. Int J Psychiatry Med
1998;28:21-39.
Conclusion 6. Australian Conservation Foundation. Calling all doctors - green your clinic!
Available at www.acfonline.org.au/articles/news.asp?news_id=962.
This study identifies some useful lessons for future programs. Such 7. Australian Conservation Foundation. Greenhome, save water. Available at
programs would do well to involve practice managers. It is also likely www.acfonline.org.au/default.asp?section_id=90.
8. Australian Government Department of Climate Change. Global warming - cool it.
that more incentives will need to be provided to engage general Available at www.greenhouse.gov.au/gwci/transport.html.
practice clinics in adopting environmentally sustainable practices. 9. Australian Conservation Foundation. Greenhome ecocalculator. Available at
www.acfonline.org.au/custom_greenhome/calculator.asp?section_id=86.
Such incentives might include the provision of products such as
10. Banksia Environmental Foundation. 2007 award winners. Available at www.bank-
compact fluorescent light globes and tap aerators, or incentives for siafdn.com/index.php?page=333.
installing rainwater tanks or solar hot water heaters.

A more comprehensive evaluation strategy involving sample in
depth interviews and focus groups would help identify the barriers and
motivations for pro-environmental behaviour within a clinic setting.
The authors recommend that this program be taken up and
developed by other medical organisations to integrate principles of
sustainability in the running of general practice clinics. This will help
to ensure that our profession is part of our community’s transition to
reducing its impact on the environment.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 37, No. 8, August 2008 683
PROFESSIONAL PRACTICE
Jeremy Bunker Narelle Shadbolt

MBBS(Hons), FRACGP, is Director of MBBS, FRACGP, MFM, is Associate Dean (Student
Training, Sydney Institute of General Support), and Senior Lecturer, Discipline of General
Practice Education and Training, New Practice, University of Sydney, Academic General
South Wales. jeremyb@sigpet.com.au Practice Unit, Hornsby Hospital, New South Wales.
Choosing general practice as a career

The influences of education and training
■ This review draws from the conventional literature. It

Background
was performed as part of a larger study that also used
In Australia, most medical students graduate without a firm career
stakeholder interviews, grey literature (reports, position
choice, with this decision being made during their early postgraduate
years. Strategies addressing the current lack of meaningful exposure
papers, planning documents and nonpeer reviewed findings)
to general practice during these formative prevocational years and opinion summaries, and reviews of the marketing and
are likely to be the most effective in increasing the proportion and consumer choice literature, to report on the determinants of
number of entrants to general practice. career choice.
Objective
Databases accessed included PubMed, Medline and Cinahl.
This review summarises the influences of medical student selection
criteria, curriculum, geographical location, timing and duration of Snowballing - identifying further articles identified from the
general practice exposure and experience, prevocational experience, reference lists and associated links of retrieved articles - added to
and vocational training, on an eventual choice of general practice as the yield. Articles citing retrieved literature were also sought. Search
a career. terms included: ‘medical students’, ‘prevocational doctors’, ‘general
practice’, ‘family medicine’, ‘career intention’ and ‘recruitment’, and
Discussion
These are important influences on the complex process of career
these were augmented with keywords associated with previously
choice. Much research has focused on isolated interventions at one retrieved articles.
point along the pipeline. Varied and conflicting conclusions emerge Retrieved peer reviewed articles were examined for relevance
from individual studies. In complex systems it is hard to understand and methodological quality. Australian articles were most relevant,
the influence of an isolated intervention without looking at the system but international studies from countries with similar structures
as a whole. of primary care and general practice, or with similar workforce
and recruitment issues, were deemed relevant. Relevant reports
published by Australian agencies and other institutions were
examined. Articles were reviewed independently by four project
staff, then collectively in a 2 day workshop at which emergent
themes were identified. The workshop generated a further search
and also informed key stakeholder interviews. This iterative search,
the inclusion of material derived from a range of methodologies and
sources, and subsequent descriptive and thematic analysis is best
described as a narrative synthesis.1 This is an appropriate approach
to a complex topic, where the results of qualitative and quantitative
studies, statistics, expert opinion, value judgment and anecdote
need to be related.2 In comparison to traditional systematic reviews,
the steps in narrative synthesis are nonlinear, iterative and the
heterogeneity of opinion and findings is explored descriptively rather
than statistically.
PROFESSIONAL PRACTICE Choosing general practice as a career - the influences of education and training
Influences during primary and secondary education and rural scholarships or cadetships continue to be predictors for
There is consistent evidence that students of rural origin are more likely rural work location for postgraduate doctors.4,12 Compulsory rural
to return to rural areas on graduation, and are more likely to work in placements may increase intentions to ultimately practice in a rural
generalist medical disciplines.3-6 This has translated into current policies location.13 Noncapital city locations are likely to have more generalist
giving priority in medical school entry, or financial and other support opportunities than specialist, but the effect of the establishment of
during study, to students of rural origin. Most of this research, and its new medical schools in regional and rural areas in influencing more
incorporation into policy, has been undertaken to address rural workforce graduates to choose general practice remains unclear.
shortages rather than concentrating on general practice recruitment. There are mixed conclusions about different curricula’s ability
There are potentially significant influences during secondary to influence choice of a primary health care career. There is greater
education which drive career choice, and for some individuals the agreement on the influence of negative and positive experiences of
career die may be cast, with an interest in primary care at the time particular disciplines and the importance of exposure to role models
of matriculation perhaps the strongest predictor of eventual general during medical school.6,9,14-17 There are increasing expectations
practice career.7 regarding the amount of teaching undertaken by general practitioners
within primary care,18 with some evidence that positive student
Influences via selection of medical students
experiences may influence career choice toward general practice.19,20
Selection processes and criteria for entry into medical school have There is also awareness of significant capacity and resource issues that
changed considerably over the past 2 decades, moving away from must be addressed21,22 to produce positive experiences.
selection based exclusively on academic performance to a broader Only a minority of Australasian and British medical students have
assessment of attributes and competencies for medical practice. A a definite career choice at graduation, with it taking 1-2 years after
second change is the growth in graduate entry courses which will graduation before the majority have committed to a discipline.23-26
provide 45% of Australian medical graduates in 2012 (from a base of In contrast, a high proportion of students nearing graduation from
zero in 1996).8 There is also an increase in the proportion of female Canadian and United States medical schools have chosen their career.
entrants; while women have been in the past more likely to choose This reflects the need to select elective terms in medical school in
general practice than their male peers, this appears to be changing.9 preparation for streamed residencies - they make their minds up earlier
The change to graduate entry may have transiently increased the because they have to.
number of students interested in a general practice career but overall
Influences during prevocational training
the changes are not significant.10 Graduate entry has been associated
with an increased average age of entry, but age at entry into medical The attitudes of senior colleagues and peers, positive and negative role
school was not a significant predictor of career choice.11 models, and experience working in disciplines at this stage continue to
Recent articles in the Australian medical press point to differences influence eventual career choice.
in the proportions of alumni choosing general practice as a career, Surveys of participants in the Prevocational General Practice
and relate this to the selection criteria, location and philosophy of the Placements Program (PGPPP), where interns or residents spend a
medical school of graduation. A survey of medical school websites does rotation in general practice, suggest that this experience exposes
suggest that medical schools vary in the extent to which they perceive participants to positive experiences and role models, is clinically
and project themselves as having a focus on producing doctors working useful,27 and a positive formative experience.28 There is little
in primary care. information yet about whether this translates into a higher proportion
A broader consideration of the influence of entry criteria on eventual of doctors choosing a general practice career. Given that an important
career choice would also look at the increasingly complex mixture influence in career choice is experience gained through rotations,23
of financial variables on entry. Entry requirements may be modified it may be essential for graduates to work in general practice for the
according to the financial contribution the student is prepared to make. discipline to successfully compete with other specialties. There are
Bonding or other long term commitments may also impact on the significant challenges already in teaching and supervision in Australian
attributes and qualities of students on entry, and the financial and other general practice.29 Other specialties are also likely to embrace private
commitments on exit. The effect of these changes on the proportion of clinical settings for prevocational training and experience.30
graduates choosing general practice as a career remains unclear. Lessons from the introduction of the foundation framework in the
United Kingdom, which underpin the prevocational years of practice,
Influences during medical school
include the need for changes in career paths and structure to be clearly
Stated and hidden curricula, role models and the physical and communicated and discussed, and adequately resourced.31
professional environments in which education is delivered may all
Influences during vocational training
influence career choice.
Locations of study may predict the ultimate geographical destination The influence of current general practice training programs on
of practice. Rural background, rural education and training experiences, career choice has not been studied and vocational trainees have
Choosing general practice as a career - the influences of education and training PROFESSIONAL PRACTICE
apparently already made their career choice. However, vocational and training and the quality of medical student experiences in general
training experiences may reinforce commitment to general practice as practice influence career choice.
a vocation, or contribute to a decision to change career. How medical Appropriately timed, relevant, positive exposures to general
students and prevocational doctors perceive the structure and rewards practice and its practitioners may lead to more individuals considering
of vocational training for general practice may influence their eventual it as a career. Integrated changes and influences along the pipeline of
career choice. education and training are likely to be the most effective in increasing
Ease of entry into training, and the duration of training, were factors the attractiveness of general practice as a career choice; isolated
that positively influenced a decision to enter general practice.23,25 The interventions without reinforcing changes at other stages of education
positive and negative aspects of general practice training have been and professional development are less likely to bear fruit.
explored,32,33 but there is room for research on the effect of the current In Australia, most medical students graduate without a firm career
configuration of general practice vocational training on career choice. choice, and it is during early postgraduate years that these decisions
are made. Strategies addressing the current lack of meaningful
Discussion
exposure during these formative prevocational years are likely to be
Overall, an individual’s experience of medical education and training the most effective in increasing the proportion and number of entrants
is a significant external influence on eventual career choice but it is to general practice.
challenging to determine the influence of individual components. Only
a small percentage of medical students have firm career intentions
at entry. There is strong evidence that students of rural origin are Acknowledgments
more likely to return to rural areas after graduation and choose more This paper is taken from a report commissioned by General Practice
generalist careers. The influence of other entry criteria, university, and Education and Training Australia. The report, ‘If the job fits... the complexity
of medical career decision making: a review’, was a collaborative under
curriculum is less clear. Meaningful analysis of the degree to which
taking by Sydney Institute of General Practice Education and Training, the
different medical schools produce different practitioners is not yet University of Sydney and the Rural Doctors Network (NSW). The full refer
possible. Potential medical students possibly make largely pragmatic ence list has not been included. The full report is is available at www.agpt.
decisions on where to apply to study medicine. com.au/PoliciesPublications/Research/.
Most decisions about career are made in the prevocational years.

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THEME WEIRD SKIN STUFF @
Belinda Welsh
MBBS, MMed, FACD, is consultant dermatologist,
St Vincent's Hospital, Melbourne and Sunbury
Dermatology and Skin Cancer Clinic, Sunbury,
Victoria. drbwelsh@bigpond.net.au
Blistering skin
conditions
■ Blistering of the skin is a reaction pattern to a diverse
Background
group of aetiologic triggers and can be classified as either:
Blistering of the skin can be due to a number of diverse
• immunobullous (Table 1), or
aetiologies. Pattern and distribution of blisters can be helpful in
• nonimmunobullous (Table 2).
diagnosis but usually biopsy is required for histopathology and
immunofluoresence to make an accurate diagnosis.
Separation of the skin layers leading to acquired blistering
can occur due to loss of cohesion of cells:
Objective
• within the epidermis (Figure 1)
This article outlines the clinical and pathological features of
• between the epidermis and dermis (basement membrane
blistering skin conditions with a particular focus on bullous
zone) (Figure 2), or
impetigo, dermatitis herpetiformis, bullous pemphigoid and
• in the uppermost layers of the dermis.
porphyria cutanea tarda.
Discussion This distinction forms the histologic basis of diagnosing many of the
Infections, contact reactions and drug eruptions should
different blistering diseases. Clinical patterns may also be helpful and
always be considered. Occasionally blistering may represent
are listed in Table 3. Important features include:
a cutaneous manifestation of a metabolic disease such as
• location of the blisters (Figure 3, 4)
porphyria. Although rare, it is important to be aware of the
• the presence or absence of mucosal involvement, and
autoimmune group of blistering diseases, as if unrecognised and
untreated, they can lead to significant morbidity and mortality. • whether the blisters are tense and intact, or fragile resulting in
Early referral to a dermatologist is important as management of erosions and crusting (Figure 5).
blistering skin conditions can be challenging. Generally however, diagnosis relies on biopsy for histopathology and
immunofluoresence to make an accurate diagnosis.
Overall, the immunobullous diseases are rare (Table 1); although
awareness is important as delayed diagnosis can lead to significant
morbidity and mortality. Most patients will require referral to a
dermatologist as diagnosis and management can be challenging.
If you see a patient with blisters it is worth asking yourself:
• Could this be an infection?
• Could this be due to a topical contact reaction or drug eruption?
• Could this be a primary skin disease with:
a) blisters as a secondary phenomenon (due to inflammation), ie.
the small blisters of hand eczema seen in pomphylox?
b) blistering due to an autoimmune mechanism (immunobullous)?
• Could this be due to an underlying systemic disease or process?
Table 3 provides a guide to the features of the blistering disorders,
with bullous impetigo, dermatitis herpetiformis, bullous pemphigoid
Table 1. Immunobullous diseases
and porphyria cutanea tarda discussed in more detail.
Intraepidermal blistering diseases - the Pemphigus group
Bullous impetigo
• Pemphigus vulgaris
The bullous form of impetigo is always caused by coagulase positive • Pemphigus foliaceus
Staphylococcus aureus, which causes separation of the epidermis by • IgA pemphigus (subcorneal pustular dermatosis type)
exotoxin production. It is seen most frequently on the face (around the • paraneoplastic pemphigus
mouth and nose) or at a site of trauma (Figure 6). The blisters tend to Subepidermal blistering diseases - the Pemphigoid group
rupture easily leaving crusted edges and honey coloured crusts. Fever • bullous pemphigoid
may be present but regional lymphadenopathy is uncommon. • mucous membrane (cicatricial) pemphigoid
It is important to confirm the diagnosis by skin swab to define the • pemphigoid (herpes) gestationis
infective organism and establish antibiotic sensitivity. • linear IgA disease (chronic bullous disease of childhood)
Topical treatment is important. It is essential to gently remove • dermatitis herpetiformis
the crusts - which harbor bacteria - with regular, gentle soaks. This • epidermolysis bullosa acquisita
can be done with gauze soaked in saline or aluminium acetate 13%
• bullous systemic lupus erythematosus
(Burow) solution diluted 1:20 with water, or potassium permanganate
(Condy crystals) 0.1% solution diluted 1:10 with water. For very mild
infections, mupirocin 2% ointment topically three times per day may
Table 2. Causes of nonimmunobullous blistering
be sufficient. For severe infections, widespread or recurrent oral
antibiotics are needed, generally either di/flucloxacillin or cephalexin Infection Viral - herpes simplex, varicella zoster
(depending on sensitivities). There is often an associated infective Bacterial - bullous impetigo, bullous erysipelas
dermatitis, so a mild topical corticosteroid such as 1% hydrocortisone Fungal - tinea (dermatophyte infection)
twice per day can be useful.1 Medications Including photosensitive drug eruptions
Because of the contagious nature of impetigo, children should Immunological *
TEN/SJS/EM/vasculitis
not return to day care or school before the lesions clear. As infection
Infiltrates Cellular Sweet syndrome (neutrophils)
is transmitted by direct contact and by fomites, including hygiene
Mastocytosis (mast cells)
items, clothing and toys, parents and carers must know how to
Noncellular Amyloidosis
avoid infection, ie. by encouraging good hygiene and hand washing.
Inflammatory Eczema (pompholyx), lichen planus, lichen
Impetigo tends to occur in mini epidemics, especially within families
skin disease sclerosus
where nasal carriage of pathogens is common. If impetigo is recurrent
Metabolic Porphyria cutanea tarda, renal failure, diabetes
or resistant, suspect chronic nasal carriage of S. aureus. If nose and
Toxic epidermal necrolysis/Stevens-Johnston syndrome/erythema multiforme
or perineal swabs are positive (depending on the location of the
these may be triggered by drugs
impetigo), it is worth treating both the patient and their family with
intranasal mupirocin up each nostril three times per day for 5 days.
Figure 1. Epidermal blistering. Due to the split occurring in the
Practice tip epidermis intact blisters are often not seen in Pemphigus vulgaris. It
more commonly presents with nonhealing crusting and erosions on
If persistent and located around the buttocks and groin (Figure 3),
the head trunk and oral mucosa
consider linear IgA disease (chronic bullous disease of childhood).
Dermatitis herpetiformis
Dermatitis herpetiformis (DH) is an uncommon, autoimmune blistering
disorder associated with a gluten sensitive enteropathy. Onset is
usually in the second to fourth decade of life.
Dermatitis herpetiformis has recently been proposed as a
cutaneous manifestation of asymptomatic to mild coeliac disease.
A genetic predisposition to the development of gluten sensitivity
underlies the disease. In patients with DH, 10-15% of first degree
relatives will have DH or coeliac disease.2 It has been hypothesised
that DH is the resu lt of an immunologic response to chronic
stimulation of the gut mucosa by dietary gluten. It has recently been
suggested that epidermal transglutaminase is the auto-antigen of DH.
THEME Blistering skin conditions
Typically, patients present with intensely itchy, grouped papules be weaned over 4-6 months to maintain the patient on the lowest
and urticarial plaques. Vesicles are often excoriated to erosions by dose of drug required for control of lesions. Although most patients
the time of physical examination and are located on the extensor require 50-150 mg/day, some are controlled on significantly lower
surfaces of the elbows, knees, buttocks and lower back (Figure 5). doses (eg. dapsone 25 mg/week). Haemolysis is the main side effect
Patients may have associated worsening of disease with dietary of dapsone therapy. A gluten free diet takes 6 months to be effective
intake of gluten, although many do not report any gastrointestinal and to allow reduction or discontinuation of medication.
(GI) symptoms until prompted. Gluten is a protein present in grasses of the species Triticeae,
Diagnosis requires routine skin biopsy of a representative lesion, which includes barley, rye, and wheat. Rice and oats belong to
which classical ly shows neutrophil micro-abcesses within the different species and are generally well tolerated. Strict compliance
papillary dermis. A second biopsy of adjacent normal skin for direct with a gluten free diet results in normalisation of the small bowel
immunofluorescence displays deposition of immunoglobulin A (IgA) in a mucosal changes and control of the cutaneous manifestations of DH
granular pattern in the upper papillary dermis.3 Although most patients in most patients.
have no bowel related symptoms, more than 90% have an associated
gluten sensitive enteropathy upon endoscopic examination.4 Practice tip
The mainstays of treatment are dapsone and a life long gluten free Initially patients may need referral to a dermatologist,
diet. Following glucose-6-phosphate dehydrogenase screening, the gastroenterologist and dietician. Patients with DH are at increased
risk of developing lymphoma of the GI tract.5 A gluten free diet will
drug of choice is dapsone 100 mg/day. A dramatic clinical response is
help prevent this complication.
seen usually within 4-5 days. Once control is obtained, dapsone can
Table 3. Distinguishing features of blistering skin disorders
Pemphigus Bullous Linear Mucous membrane Epidermolysis Pemphigoid

vulgaris pemphigoid IgA disease pemphigoid bullosa aquisita (herpes) gestationis
Cutaneous • Crusted, • Large tense Small vesicles • Crusted erosions • Can mimic bullous • Small vesicles and
lesions eroded lesions bullae and/or large on the skin pemphigoid blisters
• Occasional • Urticarial bullae • Scarring alopecia or cicatricial • Urticarial patches/
intact blister patches and pemphigoid plaques
• Oral blisters/
plaques erosions • Skin fragility • Intensely itchy
• Scarring milia • Late pregnancy
formation and immediately
postpartum
Distribution • Scalp • Trunk • Groin • Scalp/head and Sites prone to friction Begins in
• Face • Extremities • Buttocks neck trauma, especially periumbilical region
• Upper trunk hands and feet Palms/soles
• Upper torso • Flexures • Trunk
• Extremities
Mucosal Common Uncommon Occasional Common on eyes, Variable Rare
involvement mouth, genitals
Histology Intra epidermal Subepidermal Subepidermal Subepidermal blister Subepidermal Subepidermal split
loss of cell-cell bullae with bullae with with mixed infiltrate split with variable (similar to bullous
adhesion of eosinophils neutrophilic inflammatory infiltrate pemphigoid)
keratinocytes infiltrate
Direct IgG antibodies Linear IgG and Linear IgA Linear IgG and C3 IgG deposits along C3 along BMZ
immunofluoresence to desmosomes C3 at basement and C3 at along BMZ BMZ (especially on
between membrane zone BMZ dermal side)
keratinocytes (BMZ)
Drug triggers to • Thiol group • Sulphur • Vancomycin • Practalol No No
consider • Amoxycillin containing drugs • Diclofenac • Clonidine Spontaneous
• Ampicillin • Frusemide • Lithium resolution over weeks
(most common) to months following
• Captopril • Phenytoin
• Amoxicillin delivery
• Cephalosporins • Captopril
• Ampicillin
• Penicillin • Amiodarone
• Penicillin
• Amoxicillin
• Beta blockers
Blistering skin conditions THEME
Bullous pemphigoid Although BP is uncommon, it is the most common subepidermal

Bullous pemphigoid (BP) is a chronic, autoimmune, subepidermal, autoimmune blistering disease. Incidence is equal in both genders,
blistering skin disease that rarely involves the mucous membranes. and childhood disease can occur. The generalised bullous form is the
Bullous pemphigoid is characterised by the presence of most common presentation.
immunoglobulin G (IgG) autoantibodies specific for the skin basement Onset may be either subacute or acute, with widespread tense
membrane. The binding of antibodies at the basement membrane blisters (Figure 7). Significant itch is frequently present. Tense blisters
activates complement and inflammatory mediators. arise on any part of the skin surface, with a predilection on the
flexural areas. Blisters can occur on normal appearing, as well as
Figure 2. Subepidermal blistering of linear IgA disease erythematous, skin surfaces.
It is important to recognise that some patients with BP initially
present with persistent urticarial lesions that subsequently convert to
blisters. However, urticarial lesions may be the sole manifestation of
the disease, often delaying the diagnosis if a biopsy is not done.
Drugs associated with triggering BP include: frusemide, ibuprofen
and other nonsteroidal anti-inflammatory drugs (NSAIDs), captopril,
penicillamine, and antibiotics.6
Skin biopsy is required to confirm the diagnosis. A 3 mm punch
biopsy (in formalin for H+E staining) of the edge of a blister is ideal.
A second biopsy of adjacent noninflamed skin in saline soaked gauze
is necessary for direct immunofluorescence. The skin is stained
looking for deposition of antibodies and complement at the basement
Figure 3. Blistering around the buttocks and groin is a site of

membrane zone. This must be sent to a laboratory within 4 hours.
predilection for linear IgA disease, particularly in children In most patients who are treated, BP remits within 1.5 to 5 years.
Because the average age at onset is about 65 years, comorbid
conditions are common, making these patients more vulnerable to the
adverse effects of corticosteroids and immunosuppressive agents.
For localised disease, strong topical corticosteroid treatment
may achieve disease control or topical steroids plus a systemic
anti-inflammatory (doxycycline/minocycline 100-200 mg/day and
nicotinamide [vitamin B3] 500 mg three times per day) may be
sufficient.7 Oral steroid doses can be kept relatively low, ie. 40-60 mg
tapering slowing after 2-3 weeks. Then, over the next 2-3 months,
reduce prednisone to 10-20 mg/day. Once dosing is down to 10
mg/day, reduce by 1 mg/month. For patients treated with systemic
corticosteroid for more than 1 month, a combined supplement of
calcium and vitamin D should be instituted to prevent osteoporosis.
Figure 4. Oral mucosal erosions and blisters, especially common in Bone mineral density testing should be considered early in the course
Pemphigus vulgaris, requiring biopsy for diagnosis of treatment, as often long term corticosteroid use is required.
For more seve re cases, systemic steroids along with
immunosuppressives (eg. azathioprine, methotrexate, mycophenolate
mofetil, cyclosporine or intravenous immunoglobulin) may be needed
to control the disease.8 More recently, the anti-CD20 antibody
(rituximab), which is relatively specific in targeting the antibody
producing B cells, has shown promise in recalcitrant cases.9
Most patients require therapy for 6 months to 4 years, after which
many experience long term remission of the disease.
Practice tip
Other bullous diseases such as epidermolysis bullosa acquisita,
erythema multiforme, and bullous drug eruptions may clinically
resemble pemphigoid and may explain atypical therapeutic responses.
Blistering skin conditions THEME
Porphyria cutanea tarda Some patients are heterozygote for haemochromatosis. It occurs in
Porphyria cutanea tarda encompasses a group of disorders in which both genders and the sporadic form typically manifests in adulthood.
activity of the haem synthetic enzyme uroporphyrinogen decarboxylase Uroporphyrinogen decarboxylase activity is reduced by hepatotoxins
is deficient.10 Porphyria cutanea tarda is the most common porphyria and the metabolic products preceding it in the haem pathway become
and includes familial and acquired types that may occur in individuals elevated. These porphyrins are reddish pigments that accumulate in
with a genetic predisposition (sporadic porphyria cutanea tarda), after the liver and disseminated in plasma to other organs, including the
exposure to hepatotoxins, or rarely in the context of hepatic tumours. skin. Porphyrins are photoactive molecules that efficiently absorb
energy in the visible light spectrum. Photo-excited porphyrins in the
Figure 5. Excoriated papules on the elbows in dermatitis skin mediate oxidative damage causing cutaneous lesions.
herpetiformis. Blisters are fragile and often not seen intact A history of exposure to environmental inducers (eg. ethanol,
oestrogens, hepatitis, human immunodeficiency virus [HIV], iron
overload) can be often elicited. Patients often do not realise the role
of sunlight exposure in the subsequent appearance of lesions.
The most common photocutaneous manifestations are due to
increased mechanical fragility after sunlight exposure; typically
erosions and blisters on the backs of the hands that form painful
indolent sores that heal slowly, with milia, dyspigmentation and
scarring (Figure 8). Other common features of porphyria cutanea tarda
include hypertrichosis around the temples and cheeks, scleroderma
like plaques that may develop dystrophic calcification, and excretion
of discoloured urine that resembles port wine or tea due to the
porphyrin pigments present.
Diagnosis requires samples of blood, urine and faeces for
Figure 6. Bullous impetigo
porphyrin levels. Urinary porphyrin levels are abnormally high and the
faecal isocoproporphyrin is characteristically elevated. Erythrocyte
porphyrin levels are in the reference range.
Skin biopsy findings by light microscopy and direct
immunofluorescence techniques are not unequivocally diagnostic.
Fresh blisters show subepidermal bullae with minimal dermal
inflammatory infiltrate and dermal papillae protruding upward into
the blister cavity (festooning).
A thorough evaluation requires determination of the haematologic
and iron profile, including serum ferritin level, l iver function
profile, and screening for hepatitis viruses and HIV. Assessment of
haemochromatosis genes may be informative. Alpha-fetoprotein
presence in serum is useful to screen for hepatocellular carcinoma.
Patients need to avoid sun exposure where possible (protective
clothing is preferable to sunscreen) and sunscreens need to be
Figure 7. Bullous pemphigoid with blisters and urticarial patches
reflective (titanium or zinc oxide) so as to block visible light. Alcohol,
oestrogens and other hepatotoxins also need to be eliminated.
Therapeutic phlebotomy probably works by increasing the
consumption of iron and porphyrins in the production of new
haemoglobin. The goal of therapy is to reduce serum ferritin levels to
the lower limit of the reference range.11 Venesections are generally
scheduled every 2-3 weeks, as tolerated by the patient. Clinical
remission may not be complete unti l several weeks to months
after biochemical remission has been reached. In patients in whom
phlebotomy is not convenient or is contraindicated, and in those
who have relatively mild iron overload, oral chloroquine phosphate
(77.5 mg twice per week) or hydroxychloroquine sulfate (200 mg 2-3
times per week) is often effective.12-14 Larger doses can cause severe
Blistering skin conditions
10. Porphyria. In: Bologna J, Jorizzo JL, Rapini RP, editors. Dermatology. St Louis:
Figure 8. This type of skin fragility and poor healing can be seen Mosby, 2003; p. 679-83.
in both epidermolysis bullous acquisita (pictured) and porphyria 11. Ratnaike S, Blake D, Campbell D, Cowen P, Varigos G. Plasma ferritin levels as
cutanea tarda a guide to the treatment of porphyria cutanea tarda by venesection. Australas J
Dermatol 1988;29:3.
12. Taljaard JJ, Shanley BC, Stewart-Wynne EG, Deppe WM, Joubert SM. Studies
on low dose chloroquine therapy and the action of chloroquine in symptomatic
porphyria. Br J Dermatol 1972;87:261.
13. Kordac V, Semradova M. Treatment of porphyria cutanea tarda with chloroquine.
Br J Dermatol 1974;90:95.
14. Malkinson FD, Levitt L. Hydroxychloroquine treatment of porphyria cutanea tarda.
Arch Dermatol 1980;116:1147.
15. Anderson KE, Goeger DE, Carson RW, Lee SM, Stead RB. Erythropoietin for the
treatment of porphyria cutanea tarda in a patient on long-term hemodialysis. N
Engl J Med 1990;322:315.
hepatotoxicity (even low dose regimens require careful monitoring).

Oral chloroquine phosphate works by increasing urinary porphyrin
excreti on. For patients with porphyria cutanea tarda who are
anaemic due to other chronic diseases (eg. renal failure, HIV), human
recombinant erythropoietin can be used to stimulate erythropoiesis.15
Practice tip
Other porphyrias or photo-aggravated bullous dermatoses can
manifest with clinical features indistinguishable from those of
porphyria cutanea tarda (Figure 8). Failure to obtain sufficient
biochemical confirmation of the diagnosis can lead to inappropriate
treatment. Drugs such as NSAIDs, tetracyclines and frusomide
can cause a similar clinical picture on photo-exposed sites
(pseudoporphyria).
References
1. Brown J, Shriner DL, Schwartz RA. Impetigo: An update. Int J Dermatol
2003;42:251.
2. Neuhausen SL, Steele L, Ryan S, et al. Co-occurrence of celiac disease and other
autoimmune diseases in celiacs and their first-degree relatives. J Autoimmun
2008;31:160-5.
3. Alonso-Llamazares J, Gibson LE, Rogers RS 3rd. Clinical, pathologic, and immu-
nopathologic features of dermatitis herpetiformis: Review of the Mayo Clinic
experience. Int J Dermatol 2007;46:910-9.
4. Rose C, Armbruster FP, Ruppert J, Igl BW, Zillikens D, Shimanovich I.
Autoantibodies against epidermal transglutaminase are a sensitive diagnostic
marker in patients with dermatitis herpetiformis on a normal or gluten-free diet.
J Am Acad Dermatol 2009; April 1, Epub ahead of print.
5. Viljamaa M, Kaukinen K, Pukkala E, Hervonen K, Reunala T, Collin P. Malignancies
and mortality in patients with coeliac disease and dermatitis herpetiformis:
30-year population-based study. Dig Liver Dis 2006;38:374.
6. Lee JJ, Downham TF 2nd. Furosemide-induced bullous pemphigoid: case report
and review of literature. J Drugs Dermatol 2006;5:562-4.
7. Khumalo NP, Murrell DF, Wojnarowska F, Kirtschig G. A systematic review of
treatments for bullous pemphigoid. Arch Dermatol 2002;138:385-9.
8. Kirtschig G, Khumalo NP. Management of bullous pemphigoid: recommendations
for immunomodulatory treatments. Am J Clin Dermatol 2004;5:319-26.
9. Schmidt E, Hunzelmann N, Zillikens D, Bröcker EB, Goebeler M. Rituximab in
refractory autoimmune bullous diseases. Clin Exp Dermatol 2006;31:503-8. AFP CORRESPONDENCE afp@racgp.org.au
THEME BITES @ft ft
Claire Dendle David Looke

MBBS, FRACP, is an infectious diseases FRACP, FRCPA, MMedSci(Clin Epidemiol), is
physician, Department of Infectious Diseases, an infectious diseases physician and clinical
Southern Health, Melbourne, Victoria. microbiologist, Department of Infectious Diseases,
clairedendle@hotmail.com Princess Alexandra Hospital, and Associate Professor,
Department of Medicine, University of Queensland.
Management of
mammalian bites
■ Australia has one of the highest incidences of pet
Background
ownership in the world1 with the rate of dog ownership by
Mammalian bites are a significant public health problem
household between 35-42%.2,3 Mammalian bites, in
in Australia, with the majority of bites coming from dogs.
particular dog bites, are common. In Australia, it has been
Complications include tissue damage from the bite itself,
estimated that approximately 2% of the population is bitten
infection and post-traumatic stress disorder.
by a dog annually, of which 100 000 will require treatment
Objective and 13 000 will seek treatment in a hospital.4
This article describes the assessment and management of
mammalian bites in the Australian general practice setting
Dog bites constitute the majority (85-90%) of animal bites followed
based on a PubMed search of the English language literature
by cats (5-10%), humans (2-3%) and rodents (2-3%).5,6 However,
from the years 1966 to present.
any animal with teeth can bite and there are reports of bites from
Discussion livestock7-9 and native Australian animals.10
General practitioners need to be familiar with the treatment of
Risk factors for dog bites include3:
animal bites, pitfalls in management, and the need to educate
• children under 5 years of age
patients on ways to avoid future bite injuries. Meticulous wound
• male gender
cleaning, irrigation, exploration and debridement is essential
• households with dogs, and
to bite wound healing. Recognition of complicating fractures
with imaging is important. Risk of infection differs among animal
• male, unsterilised dogs.
species, although most infected bite wounds are polymicrobial. Sixty-six percent of dog bite victims are bitten by their own dog or an
animal that is known to them; about half are unprovoked.11 Certain
breeds are over represented. A study in Adelaide (South Australia)
demonstrated that three-quarters (75%) of dog attacks were caused
by german shepherds, pit bull terriers, blue/red heelers, dobermans,
and rottweilers, despite the fact that these breeds only accounted
for 31% of the dog population.4 Knowledge of these risk factors is
important to help design campaigns with a view to reducing this
significant public health problem.
Complications of mammalian bites

The main complications of mammalian bites are tissue damage from
the bite itself, infection and psychological distress.
Injuries sustained from a bite are dependent on the animal species
and dentition, ferocity of attack and the anatomical location of the
bite. Dog bite wounds are most often crush injuries, lacerations and
abrasions resulting from the high pressures generated from the canine
868 Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 38, No. 11, November 2009
jaw and the associated ripping and tearing motion.12,13
Table 1. Oral flora of mammalian species
In contrast, cats almost always inflict puncture wounds
due to their long, slender incisor teeth. These wounds Animal Organism
may appear minor at the skin surface but can penetrate
Dogs17,48 Pasteurella dagmatis, P canis, Staphylococcus aureus,
deeply and puncture bone, joints and tendons. This S. intermedius, Streptococci, Moroxella spp., Neisseria
is of particular importance on the hand, where joint spp., C. canimorsus, Clostridium spp. including
penetration can easily be missed by clinicians. Clostridium tetani, Anaerobes spp.
The rate of infection of bite wounds differs
Cats17,23 Pasteurella multocida, mixed aerobes and anaerobes
between the animal species due to the oral flora in
the biting animal and injury type. Infecting organisms Rodents28-30 Streptobacillus moniliformis, Spirillum minus,
Salmonella spp.
most commonly arise from the mouth of the biting
animal; however, they can also arise from the host’s Cows, horses, camels9 Polymicrobial, Actinobacillus spp.
own flora or the environment. Animal bite infections
Pigs8 Polymicrobial, Aeromonas spp., P aerogenes,
should be considered to be polymicrobial, but certain Actinobacillus spp.
unusual pathogens can be characteristic of particular
animal species and knowledge of these is useful to Humans16,42,43 Viridans streptococci, S. pyogenes, S. aureus,
Anaerobes, Eikenella corrodens, hepatitis B and C, HIV
guide antibiotic choice (Table 1). Australian antibiotic
guideline recommendations for mammalian bites Monkeys33,49 Mixed aerobes and anaerobes, Streptococci, Neisseria
are shown in Table 2. Deep infection can result in spp., Haemophilus influenzae, Herpes simiae (B virus)
septic arthritis, osteomyelitis, tenosynovitis and
compartment syndrome.12,14
Psychological trauma following animal bites is an Table 2. Australian antibiotic guideline recommendations for mammalian bite
wounds46
under appreciated problem. A study of 3000 people
in Adelaide showed 50% of respondents feared dog Infection not established
attacks and 21% modified their behaviour toward
• Amoxycillin + clavulanate (child: 22.5 + 3.2 mg/kg up to 875 + 125 mg) orally,
dogs.4 There is also evidence that of children who
12 hourly for 5 days
have experienced minor dog attacks, about half (50%)
• If commencement of above is likely to be delayed, procaine penicillin
suffer post-traumatic stress disorder.15 (child: 50 mg/kg up to 1.5 g) IM, as one dose followed by above
Infectious risk according to species Infection established
Dog bites • Metronidazole (child: 10 mg/kg up to 400 mg) orally, 12 hourly for 14 days
Up to 18% of dog bites become infected, however, this PLUS EITHER
increases when the hand is involved.16-18 The microbiology • Cefotaxime (child: 50 mg/kg up to 1 g) IV daily for 14 days
of dog bite wounds is polymicrobial, with a mixture OR
of aerobes and anaerobes. Of particular importance • Ceftriaxone (child: 50 mg/kg up to 1 g) IV daily for 14 days
is the presence of species isolated in 50% of dog bite ALTERNATIVELY USE
wounds.17 Pasteurella species are the predominant • Piperacillin + tazobactam (child: 100 + 12.5 mg/kg up to 4 + 0.5 g) IV, 8 hourly
for 14 days
organism in the oral flora of many animals, and is
noteworthy because it produces a characteristic rapidly OR
progressive skin and soft tissue infection and is generally • Ticarcillin + clavulanate (child: 50 + 1.7 mg/kg up to 3 + 0.1 g) IV,
6 hourly for 14 days
resistant to flucloxacillin, first generation cephalosporins
and clindamycin.19 Capnocytophaga canimorsus is For patients with immediate penicillin hypersensitivity
found in approximately 5% of dog bite wounds and • Metronidazole (child: 10 mg/kg up to 400 mg) orally, 12 hourly for 14 days
may opportunistically invade the host, usually affecting PLUS EITHER
immunosuppressed and asplenic patients (reports of • Doxycycline (child >8 years: 5 mg/kg up to 200 mg) orally for the first dose,
severe sepsis in immunocompetent hosts had a case then (child >8 years: 2.5 mg/kg up to 100 mg) orally, 12 hourly
fatality rate of 28%20). OR
Methicillin resistant Staphylococcus aureus (MRSA) • Trimethoprim + sulphamethoxazole (child: 4 + 20 mg/kg up to 160 + 800 mg)
orally, 12 hourly
appears to be an emerging zoonotic pathogen. It is known
OR
that humans can transmit MRSA to their companion
• Ciprofloxacin (child: 10 mg/kg up to +500 mg) orally, 12 hourly
animals, however there are increasing reports of animal-
Reprinted from AUSTRALIAN FAMILY PHYSICIAN Vol. 38, No. 11, November 2009 869
THEME Management of mammalian bites
to-human transmission in both domestic animals and livestock, and illness developed more than 2 years following the bat bite.38
the emergence of new MRSA strains. Methicillin resistant S. aureus All bats in Australia can potentially transmit ABL, and considering
decolonisation of pets is recommended in the setting of recurrent the almost universal fatality rate of this disease, all bites should
infection of the human, if human household contacts are not colonised or receive postexposure prophylaxis for rabies.34,39 This should
already treated and the pet has been clearly identified as the source of be given irrespective of the time lapsed since the bite. Furthermore,
recurrent infection.21,22 prophylaxis should also be offered to those where there has
been a ‘reasonable probability’ of a bat bite occurring, such as
Cat bites
children exposed to bats in confined setting. Bat bites can be tiny
Twenty-eight to 80% of cat bites may become infected, with and may go unnoticed.40
P. multocida isolated in 75% of cases.23,24 Bartonella henselae
Human bites
(the causative organism of cat scratch disease) can be transmitted
via the scratch or bite of an infected cat or cat flea, and 30% Human bites have a higher complication and infection rate than
of Australian cats are bacteraemic with this organism.25,26 In animal bites.19 Most occur to the fingers, however 10-20% of
normal hosts, this is usually either asymptomatic or a self limiting wounds are ‘love nips’ to the breast and genitals.19 If a bite mark
lymphadenitis but can be a life threatening disseminated infection has an intercanine distance greater than 3 cm, the bite probably
in an immunocompromised host.25 came from an adult and this should raise concerns about child
abuse.41 Infected bites are usually polymicrobial, however the
Rodent bites
fastidious Gram negative Eikenella corrodens is well recognised as
Rodent bites have an infection rate of approximately 10%.27 Rat causing septic arthritis after a penetrating injury of the hand, and
bite fever is a disease caused by Streptobacillus moniliformis or this may be complicated by infective endocarditis.
Sprillum minus and should be considered in a case of systemic Hepatitis B and C can be transmitted by human bites15 and human
sepsis following a rodent bite.28 Following an incubation period immunodeficiency virus (HIV) transmission has occurred on at least
of 10 days to 4 weeks, the patient presents with fever, rash and five occasions, mostly in the setting of bloody saliva and late stage
septic arthritis.29 The diagnosis requires a high index of suspicion HIV disease.43 Although there is only limited evidence to support its
as the organism is fastidious and good communication with the use, HIV postexposure prophylaxis should be considered in high risk
microbiology staff may help isolate the pathogen.29,30 Treatment human bite injuries (ie. from a known HIV positive source).
with penicillin or doxycycline is usually successful, however there
Assessment and management of mammalian bites
are reports of serious complications such as endocarditis where
mortality may be significant.31,32 The management of animal bites is an evidence poor area and most
recommendations are based on small case series, microbiological
Monkey bites
data and expert opinion. The main controversies include whether
Monkey bites can present in returned travellers, zoo or laboratory wounds should or should not undergo primary closure and the use
workers. They pose a high risk of infection as well as serious of prophylactic antimicrobials. The assessment and management of
damage to underlying structures.33 Rabies can be transmitted from animal bites is presented in Table 3.
monkey bites. Prophylaxis should be offered for patients presenting Most animal bite wounds can be managed in the general
with monkey bites sustained in a rabies endemic area, which practice setting. However, it is important to recognise when a
recently has included Bali in Indonesia.33,34 wound is at high risk of infection and when referral to hospital is
Cercopithecine herpesvirus 1 (herpes simiae or B virus) infects required (Table 4). The following factors place wounds at a high risk
old world macaque monkeys, can be transmitted by a bite or of infection:12,44-46
scratch33,35 and human infection causes a fatal encephalitis if • puncture and crush wounds (particularly if inflicted by a cat)
not treated appropriately. There is little data on the efficacy of • wounds that penetrate bone, joint, tendons, vascular structures or
postexposure prophylaxis; nonetheless expert opinion recommends that overly a prosthetic joint
14 days of oral valacyclovir for moderate to high risk macaque • wounds on the hands, feet, face or genitals
monkey bites or scratches.35,36 Referral to an infectious diseases • wounds with a delayed presentation of greater than 8 hours, and
specialist should be considered in these circumstances. • patients who are immunocompromised or have oedema or
lymphoedema.
Bat bites
Prevention of bites
Australia is currently classified as being free of rabies, although
a very similar virus, Australian bat lyssavirus (ABL) has been General practitioners play an important role in primary and
transmitted from bat bites on two occasions.37,38 Both patients secondary prevention of mammalian bites. They can provide
died from encephalitis and the second case was notable as the opportunistic education for patients regarding behaviour around
Management of mammalian bites
Table 3. Assessment and management of mammalian bite wounds
Resuscitation44 • Treat any life threatening injuries according to standard guidelines

• Children with facial or cranial bites need cervical immobilisation until cervical lesions are excluded
History12,47,50 • Circumstances of attack (animal species, provocation, timing)
• Determine if law enforcement has been notified
• Medical comorbidities (particularly immunosuppression)
• Medications
• Allergies
• Immunisation status (tetanus, hepatitis, rabies)
• Occupation
• Hand dominance
Examination • Exploration - even for apparently minor injuries
• Document wound type and measurements
• Identify foreign bodes (eg. animal teeth and debris)
• Assess penetration of bone and joint (put joints through full range of motion)
• Assess nerve, motor and vascular function (for bites in the hand or feet, placement of a proximal tourniquet
may facilitate visualisation of deeper structures)
• Assess for established infection (purulent/nonpurulent, abscess, extent, associated lymphadenopathy)
• Draw diagrams and take photographs as necessary
Imaging13 • Identify foreign bodies (teeth), fractures and penetration of bone and joint
• X-rays for all clenched fist injuries, puncture wounds near bone or joint and penetrating scalp injuries (a
fracture associated with a bite should be managed as a compound fracture with hospital/specialist referral)
• Ultrasonography can be used for diagnosis of suspected soft tissue injury
Important: determine if wound is at high risk of infection (see text and Table 4)
Wound culture • Only take cultures from clinically infected wounds
• Communicate with microbiology staff that the specimen is from a bite wound
Wound • Involves cleaning, irrigation and debridement
management11,12,50,51 • Wound should be cleaned with soap and water or normal saline as this reduces the concentration of bacterial
contamination and may reduce the risk of infection (particularly in rabies bite)
• Remove foreign bodies (dirt, debris, teeth)
• If the wound is clinically infected, open sutures or incise and drain abscess
• Irrigate the wound with copious quantities of normal saline or water. Use enough fluid to remove all visible
dirt and foreign material (usually 250 mL is adequate)
• Irrigate under high pressure using a 19 or 20 gauge needle or plastic catheter on a large syringe
• Debride as necessary
Wound closure52,53 • Evidence is limited so assess on a case-by-case basis
• Primary closure could be considered in carefully selected bite wounds where cosmesis is an issue
• Primary closure of head and neck wounds with antibiotic prophylaxis is associated with low risk of infection
(1%) due to enhanced blood supply and lack of dependent oedema
• Suturing is not recommended in wounds at high risk of infection
Elevation/ • Elevate the injured extremity during the first 48-72 hours
immobilisation50,54 • Significant hand wounds can benefit from 3-5 days of immobilisation in the position of function
Tetanus prophylaxis34 • Tetanus toxoid should be administered if 5 years since the last dose and the patient has completed a full
primary course of tetanus immunisation
• If the patient is unvaccinated, they should receive tetanus toxoid plus tetanus immunoglobulin
Australian bat • Rabies postexposure prophylaxis should be administered to all bat bites and returned travellers from a rabies
lyssavirus/rabies endemic area with a mammalian bite wound
prohylaxis34 • If the patient is unvaccinated, they should receive rabies immunoglobulin plus a full vaccination course with
human rabies diploid cell vaccine. If the patient is vaccinated (documented), then rabies immunoglobulin is not
required however they should receive two doses of rabies vaccination. Contact state public health authorities
for advice and access to rabies vaccine
Management of mammalian bites THEME
Table 3. Assessment and management of mammalian bite wounds (continued)
Postexposure prohylaxis: • For human bites consider hepatitis B prophylaxis if not immune and HIV postexposure prophylaxis if at high
hepatitis B, C risk (seek advice from infectious diseases physician)
Antibiotics46,55,56 • Prophylaxis: this is controversial considering side effects, cost and only marginal benefits demonstrated in
meta-analyses of use in dog bites. Expert opinion recommends prophylaxis for high risk wounds only
• Treatment of established infection: broad spectrum antibiotics should be used, covering aerobes and
anaerobes, in particular Pasteurella spp. Pasteurella spp. should be considered resistant to flucloxacillin, first
generation cephalosporins, erythromycin and clindamycin and these antibiotics should not be used alone for
empirical treatment. This represents a common cause of treatment failure
(See Table 2 for antibiotic recommendations)
Patient education12,57 • Written instructions upon discharge should include:
- general wound care
- daily wound inspection
- emphasis of infection and other complications
- specific signs and symptoms of infection or clinical deterioration
- clear directions when and where to return for re-evaluation
- importance of compliance
Patient review12 24-48 hours
Table 4. Indications for hospital referral12,16,44,47,58 recognise when a wound is at high risk of infection and when
Multiple and severe injuries referral to hospital is required.
Systemic signs of infection Conflict of interest: none declared.

Cellulitis - severe or rapidly spreading or advancement past
one joint
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tonella infections in patients with bacillary angiomatosis-peliosis. N Engl J 55. Cummings P. Antibiotics to prevent infection in patients with dog bite wounds:
Med 1997;337:1876-83. A meta-analysis of randomized trials. Ann Emerg Med 1994;23:535-40.
26. Branley J, Wolfson C, Waters P, Gottlieb T, Bradbury R. Prevalence of Bartonella 56. Medeiros I, Saconato H. Antibiotic prophylaxis for mammalian bites. Cochrane
Database Syst Rev 2001(2):CD001738.
henselae bacteremia, the causative agent of cat scratch disease, in an
Australian cat population. Pathology 1996;28:262-5. 57. Hubler JRZJ. Bite wounds: Don’t let patients leave with the wrong impression.
27. Hodge DTF. Bites and stings. In: Textbook of paediatric emergency medicine. 4th ED Legal Letter 2000;2:21-32.
58. Higgins MA, Evans RC, Evans RJ. Managing animal bite wounds. J Wound Care
edn. Fleisher GR, Ludwig S, 2006, p.1045.
1997;6:377-80.
28. Graves MH, Janda JM. Rat-bite fever (Streptobacillus moniliformis): A potential
emerging disease. Int J Infect Dis 2001;5:151-5.
29. Fordham JN, McKay-Ferguson E, Davies A, Blyth T. Rat bite fever without the
bite. Ann Rheum Dis 1992;51:411-2.
30. Rumley RL, Patrone NA, White L. Rat-bite fever as a cause of septic arthritis: A
diagnostic dilemma. Ann Rheum Dis 1987;46:793-5.
31. Roughgarden JW. Antimicrobial therapy of ratbite fever. A review. Arch Intern
Med 1965;116:39-54.
32. Rupp ME. Streptobacillus moniliformis endocarditis: Case report and review.
Clin Infect Dis 1992;14:769-72.
33. Goldstein EJ, Pryor EP 3rd, Citron DM. Simian bites and bacterial infection. Clin
Infect Dis 1995;20:1551-2.
34. Australian Immunisation Handbook. 9th edn, 2008. Available at www.health-
govau/internet/immunie/publishingnsf/Content/Handbook-home [Accessed 11
May 2009].
35. Weigler BJ. Biology of B virus in macaque and human hosts: A review. Clin
Infect Dis 1992;14:555-67.
36. Cohen JI, Davenport DS, Stewart JA, Deitchman S, Hilliard JK, Chapman LE.
Recommendations for prevention of and therapy for exposure to B virus (cercop-
ithecine herpesvirus 1). Clin Infect Dis 2002;35:1191-203.
37. Hooper P. A new lyssavirus. The first endemic rabies related virus recognised in
Australia. Bull Inst Pasteur 1997;95:209-18.
38. Hanna JN, Carney IK, Smith GA, et al. Australian bat lyssavirus infection: A
second human case, with a long incubation period. Med J Aust 2000;172:597-9.
39. Gould AR, Hyatt AD, Lunt R, Kattenbelt JA, Hengstberger S, Blacksell SD.
Characterisation of a novel lyssavirus isolated from Pteropid bats in Australia.
Virus Res 1998;54:165-87.
40. Gibbons RV. Cryptogenic rabies, bats, and the question of aerosol transmission.
Ann Emerg Med 2002;39:528-36.
41. Prescott P. Child abuse and neglect. In: A practical guide to paediatric intensive
care. Levin DL, editor. St Louis: Mosby, 1984;454.
42. Dusheiko GM, Smith M, Scheuer PJ. Hepatitis C virus transmitted by human
bite. Lancet 1990;336:503-4.
43. Bartholomew CF, Jones AM. Human bites: A rare risk factor for HIV transmis
sion. AIDS 2006;20:631-2.
44. Morgan M, Palmer J. Dog bites. BMJ 2007;334:413-7.
45. Dire DJ, Hogan DE, Riggs MW. A prospective evaluation of risk factors for
infections from dog-bite wounds. Acad Emerg Med 1994;1:258-66. AFP CORRESPONDENCE afp@racgp.org.au
THEME BITES @)©
Stephen L Doggett Richard Russell

BSc, PestContCert, MASM, is Senior Hospital BSc, MSc, PhD, FACTM, is Professor and
Scientist, Department of Medical Entomology, Director of Medical Entomology Department
ICPMR, Westmead Hospital, New South Wales. of Medical Entomology, University of Sydney,
stephen.doggett@swahs.health.nsw.gov.au Westmead, New South Wales.
Bed bugs
What the GP needs to know
■ From an early age, the term ‘bed bug’ is indelibly lodged

Background
into our psyche, yet as one journalist recently suggested, for
Since the mid 1990s, there has been a global resurgence of
most of us, they are just a ‘mythical creature from a childhood
bed bugs ( Cimex spp.), which are blood feeding insects that
nursery rhyme’.1 However, these insects are very much real
readily bite humans. Patients suffering with bite reactions are
increasingly presenting to medical practitioners.
and since the mid 1990s there has been an unprecedented
global bed bug pandemic. Australia has not been excluded
Objective
and infestations have risen by an incredible 4500% between
This article reviews the various clinical consequences of bed
2000 and 2006.2
bug bites and outlines management strategies.
Discussion So why are these insects such a problem? Bed bugs bite and have
Common dermatological responses include the early a propensity for human blood, and this usually produces some form
development of small macular spots that may later progress
of skin reaction and irritation. With the growing resurgence, it is
into prominent wheals accompanied by intense itching. Patients
likely that more patients with bed bug bites will present to general
exposed to numerous bed bugs can present with a widespread
practitioners.
erythematous rash or urticaria. Bullous eruptions are not
uncommon and anaphylaxis has been reported, albeit rarely. Pathophysiology
There is no evidence that bed bugs transmit human pathogens,
but they are responsible for significant psychological distress, Bed bugs belong to the same order of insects (Hemiptera) that
can produce anaemia when abundant, and have been implicated includes common garden plant pests such as aphids and cicadas.
in the triggering of asthmatic reactions. Symptomatic control The difference with bed bugs is that the family that they belong to
involves treatment of the patient with antihistamines and (Cimicidae) has evolved to become exclusively haematophagus, ie.
corticosteroids, and ensuring that the infestation responsible for blood feeders. Bed bugs are wingless, roughly oval in shape and
the problem is effectively eliminated. flattened. The adults have a deep brown colouration, are around
5-6 mm in length when unfed (Figure 1), and not dissimilar to the size
and colour of an apple seed. There are five juvenile stages, with the
youngest being around 1 mm and having a light cream appearance,
but progressively becoming darker and larger as they develop.
There are two species that have been introduced to Australia and
both bite humans: the common bed bug, Cimex lectularius, and the
tropical bed bug, Cimex hemipterus.2
In the early part of the current resurgence, bed bugs were most
likely to be encountered in commercial accommodation with high
guest turnover, such as at popular tourism destinations, with people
often transferring the insects home via luggage. However, since
then, bed bugs have spread to the wider community and infestations
have occurred in such diverse locations as trains, charter boats,
Figure 1. The various life stages of the common Figure 2. One of the most commonly encountered sites for bed bugs
bed bug, C. lectularius (the bar = 5 mm) is, as the name implies, on beds. Insects typically harbour along
mattress beading. Dark faecal spotting is an indication that bed bugs
are or have been present
cinemas, hospital wards and clinic waiting rooms, staff and student
accommodation, and brothels.3 Over the past 3 years, there has Figure 3. Bite marks the morning after being bitten by bed bugs; the
been a large rise in bed bug infestations in low income housing, marks appear as faint, red macular spots
often involving thousands to tens of thousands of bed bugs in a
single infestation. Indications of an infestation include unexplained
bite reactions, dark spotting on the bed from faecal deposition, and
presence of the insects themselves (Figure 2).
With the re-emergence of bed bugs, there have been several recent
reviews of the dermatological reactions caused by bed bugs4-7 and
a contemporary clinical experimental investigation.8 These papers
should be referred to for greater detail.
The mouthparts of bed bugs are especially adapted for piercing
skin and sucking blood. During feeding they inject saliva, which has the cognitive link between the bites and bed bugs, is unknown.
anticoagulant properties and contains protein fractions that can Clearly more research is needed in this area.
produce various allergic reactions in humans. It is not known if the two The most commonly affected areas of the body are the
bed bugs species produce different clinical reactions. Blood feeding arms, shoulders and legs, ie. those that tend to be not covered
typically occurs at night and often the bites are not noticed until the while sleeping. Reactions to bites may be delayed, with up to
appearance of a clinical reaction, which can occur some days later. For 9 days or more before lesions appear.12 Often the first sign of
some, the bite itself is painful and can result in a restless night’s sleep,9 bed bug bites are small indistinct red macular spots (Figure 3),
which can affect the victim’s work performance during the day. which may later develop into the classic bed bug wheal. These
It has often been quoted that around 20% of people will show no wheals are usually greater than 1 cm (up to 20 cm) across,4 and
clinical reaction to the bite;10 however, such figures have been based are accompanied by itching and inflammation (Figure 4); they
on limited data.8 In a recent study by Reinhardt et al,8 it was found usually subside to red spots and can last for several days. It
that 11 out of 24 people had no dermatological reaction to a bed bug is often reported in the literature that lines of bites may occur
bite on first exposure. With further bites, most (18/19) developed an and this can be seen in Figure 4. However, most bites do not
obvious clinical skin reaction and the latency period for those that occur in a linear pattern and when they do, it is not known if
previously reacted decreased substantially. This particular research this is caused by one or by several different bugs. Bites from
focused on acute exposure, yet investigations on chronic exposure a large number of bed bugs can present as a widespread
are virtually nonexistent. In one very small trial, a researcher exposed erythematous rash or urticaria13 (Figure 5, 6), which can be
himself to multiple bed bug feedings over 6 months and failed to chronic if the infestation remains uncontrolled.14 Bullous eruptions
become sensitised.11 From the observations of the first author of this (Figure 7) are not uncommon,15-18 and these may be accompanied
article, many individuals in low income housing who are chronically by a systemic reaction of fever and/or malaise.19 Anaphylaxis has
exposed to bed bugs are often unaware that an infestation is present. been reported in patients with a severe bed bug allergy, although it
Whether this is due to a failure of individuals to become sensitised, appears to be rare.20 Like any skin irritation, constant scratching of
or that many have become desensitised, or that some have not made the bite site can lead to infection and ulceration.21
THEME Bed bugs - what the GP needs to know
For a haematophagus arthropod, bed bugs take a relatively large

Figure 5. Urticarial papular bite reactions from bed bugs 4 days after
blood meal. While it takes many hundreds of bites for even the exposure and involving hundreds of bites over the body
loss of one millilitre of blood, in India, iron deficiency in infants has
been associated with severe infestations,22 and there was a recent
report from Canada of severe anaemia in a man aged 60 years due to
multiple bed bug bites.23
Another medical condition suggested to be associated with bed
bugs is asthmatic reaction brought about by exposure to the allergens
of the insect;24,25 not dissimilar to the situation with dust mites.
However, such studies are limited and require further investigations.
Misdiagnoses of bed bug bites have been well documented and have
included:
Figure 6. This 4 year old girl was bitten by
• scabies26 (which should always be confirmed by a skin scraping)
hundreds of bed bugs. There were so many
• antibiotic reactions
bites on the front lower abdomen that there
• food allergies was the appearance of a broad erythematous
• hives rash rather than individual bites
• mosquito bites
• spider bites
• Staphylococcus infections, and
• chicken pox.27
In one case of a severe allergic reaction that led to anaphylaxis,
the patient was initially diagnosed with a coronary occlusion.20
Misdiagnosis often results in inappropriate medical interventions,
such as the use of scabicides,26 biopsy of the bite site, and
various blood tests,27 with obviously no useful result forthcoming.
Unfortunately, insect bites are generally poorly described and
categorised and the bite reaction can vary tremendously from
individual to individual, even with the same biting pest. Therefore should always be undertaken to confirm the presence of the insect,
diagnoses of bed bug infestations from only the bite reactions are and to exclude other possible biting arthropods such as fleas, mites
unreliable. If bed bugs are suspected, then a thorough inspection of (especially bird and rat mites), mosquitoes, ticks and midges.
the sleeping areas of the patient by an experienced pest manager
Infectious diseases
Figure 4. This is the same patient as Figure As bed bugs are blood feeders, many people have been concerned
3, 4 days later. The classic bed bug wheal that the insects could be capable of transmitting infectious agents
can be seen, along with the linear pattern
like so many other haematophagus arthropods such as mosquitoes
of bites that sometimes is apparent with
multiple bed bug bites and ticks. Indeed, bed bugs have been suspected of the transmission
of more than 40 human pathogens.7 However, the reality is that
currently there has not been a single proven case of an infectious
agent passed on to humans by bed bugs.28
Mental health impact

One aspect of the medical affects of bed bug bites that is almost never
addressed is the significant psychological distress caused by the bites.
This is a very real health problem and should not be ignored. There is
an apparent stigma associated with bed bugs that relates the insect
with poor housekeeping and hygiene,29 even though five star hotels
do not escape infestations. Often when people learn that there is
Photo courtesy Dr Nigel Hill, London School
an insect in their bed that is biting them at night, they are horrified
of Hygiene and Tropical Medicine
and disgusted. This can develop into a delusionary state, whereby
Bed bugs - what the GP needs to know THEME
a major economic imposition on the community. Unfortunately,

Figure 7. Bullous eruptions on the hand and ankle following bed bug bites
such an apathetic stance by health authorities can allow the bed
bug resurgence to continue and become an increasing problem in
more communities. As a result, more medical practitioners will be
consulted by more victims of bed bug bites.

• Bed bug infestations are becoming increasingly common.
• Bed bugs are blood feeders that produce variable skin reactions in
humans.
• Clinical symptoms may include macular spots, wheals,
erthyematous rashes, urticaria and bullous reactions, all
accompanied by intense itching.
• Bed bugs are not known to transmit human pathogens but are
responsible for considerable physical irritation and often
the patient feels bites and insects crawling on them, even if the bed psychological distress.
bugs have been eliminated for some time.30 As bed bugs often bite on • Control invo lves treating both the patient’s symptoms and
the face and neck, the resulting bite marks can affect an individual’s elimination of the infestation.
self esteem and possibly interfere with employment performance
or prospects. Another aspect of how bed bugs impact on the mental
health of people relates to the trauma of the cost of eradication, which Acknowledgment
can be from hundreds to thousands of dollars per infestation. Dr David Mitchell, Senior Staff Specialist, Centre for Infectious Diseases and
Microbiology, Westmead Hospital, kindly reviewed a draft of the paper.
Treatment
References
Despite the dramatic increase in exposure of the human population 1. Tucker J. ‘Don’t let the bedbugs bite’ is apt in Pueblo, Colo. Knight Ridder/Tribune
Business News 2003; May 21:1.
to bed bugs, to date the literature examining treatment of patients
2. Doggett SL, Russell RC. The resurgence of bed bugs, Cimex spp. (Hemiptera:
with bite reactions is extremely limited. Also as noted above, it is cimicidae) in Australia: Experiences from down under. In: Robinson WH, Bajomi
not possible to determine from the bite reaction alone if the cause is D, editors. Proceedings of the 6th International Conference on Urban Pests.
Budapest: Executive Committee of the International Conference of Urban Pests,
actually bed bugs. For this reason, the general recommendation for
2008;407-25.
treatment is similar to that for other biting arthropods, and usually 3. Doggett SL. The resurgence of bed bugs. In: Doggett SL, editor. Bed bug work
involves the use of antihistamines and topical and/or systemic shop, AEPMA course notes. Sydney: The Department of Medical Entomology,
corticosteroids.7 The clinical review by Goddard and de Shazo7 should Westmead Hospital, 2009;39-60.
4. Cleary CJ, Buchanan D. Diagnosis and management of bedbugs. Nurse Practit
be consulted for more information on treatment.
2004;29:47-8.
5. Thomas I, Kihiczak GG, Schwartz RA. Bedbug bites: A review. Int J Dermatol
Bed bug control 2004;43:430-3.
6. Poorten MC, Prose NS. The return of the common bed bug. Ped Dermatol
Bed bugs are considered one of the most challenging of all insect
2005;22:183-7.
pests to control due to the high degree of insecticide resistance they 7. Goddard J, deShazo R. Bed bugs (Cimex lectularius) and clinical consequences of
have developed. The cryptic behaviour of the insects means that their bites. J Am Med Assoc 2009;301:1358-66.
8. Reinhardt K, Kempke D, Naylor R, Siva-Jothy MT. Sensitivity to bites by the
they are difficult to detect and treat, and thus building treatments
bedbug, Cimex lectularius. Med Vet Ent 2009;23:163-6.
can be expensive of labour and chemicals. As such, control should 9. Pinto L. Bed bugs...they’re back. Pest Cont 1999;67:10-2.
only be undertaken by an experienced pest manager who uses the 10. Krueger L. Don’t get bitten by the resurgence of bed bugs. Pest Cont 2000;68:58-
principles of management as set out in ‘A Code of Practice for the 64.

11. Goddard J, de Shazo R. Multiple feeding by the common bed bug, Cimex lectular-
Control of Bed bug Infestations in Australia’.31 This code can be freely
ius, without sensitization. Midsouth Entomol 2009;2:90-2.
downloaded at www.bedbug.org.au. 12. Sansom JE, Reynolds NJ, Peachey RDG. Delayed reaction to bed bug bites. Arch
Derm 1992;128:272-3.
Conclusion 13. Scarupa MD, Economides AE. Letter to the editor: Bedbug bites masquerading as
urticaria. J Allergy Clin Immunol 2008;117:1508-9.
As bed bugs are not known to transmit infectious diseases, most 14. Borts MR. Cimex lectularius (bedbug) bites presenting as chronic urticaria. J Aller
regional and local health authorities do not strictly consider them Clin Immunol 2006;2:S310.
15. Kinnear J. Epidemic of bullous erythema on legs due to bed bugs. Lancet
to be a health issue. Clearly, however, they are a community health
1948;2:55.
problem. Bed bugs produce variable irritating skin reactions and 16. Tharakaram S. Bullous eruption due to Cimex lectularius. Clin Exp Derm
are responsible for considerable mental anguish, as well as being 1999;24:241-2.
Bed bugs - what the GP needs to know
17. Fletcher CL, Ardern-Jones MR, Hay RJ. Widespread bullous eruption due to multi
ple bed bug bites. Clin Exp Derm 2002;27:74-5.
18. Leverkus M, Jochim RC, Schad S, et al. Bullous allergic hypersensitivity to
bed bug bites mediated by IgE against salivary nitrophorin. Soc Invest Dermat
2006;126:91-6.
19. LieboldK, Schliemann-Willers S, Wollina U. Disseminated bullous eruptions with
systemic reaction caused by Cimex lectularius. E Acad Derm Vener 2003;17:461-3.
20. Parsons DJ. Bed bug bite anaphylaxis misinterpreted as coronary occlusion. Ohio
Med J 1955;51:669.
21. Potter M. Battling bed bugs in the USA. In: Robinson WH, Bajomi D, editors.
Proceedings of the 6th International Conference on Urban Pests. Budapest:
Executive Committee of the International Conference of Urban Pests, 2008:401-6.
22. Venkatachalam PS, Belavady B. Loss of haemoglobin iron due to excessive biting
by bed bugs. A possible aetiological factor in the iron deficiency anaemia of
infants and children. Trans R Soc Trop Med Hyg 1962;56:218-21.
23. Pritchard MJ, Hwang SW. Severe anemia from bed bugs. CMAJ 2009;181:287-8.
24. Abou Gamra ESM, El-Shayed FA, Morsy TA, Hussein HM, Shehata ESZ. The rela
tion between Cimex lectularius antigen and bronchial asthma in Egypt. J Egypt
Soc Parasit 1991;21:735-46.
25. WanZhen F, KaiShong Y. A clinical study of the relationship between bed bugs and
allergic asthma. Chin J Vect Biol Cont 1995;6:54-7.
26. Stevens K. Sleeping with the enemy. NY Times 2003;25:5.
27. Gooch H. Editorial: Bed bug issue might separate the professional from the
not-so-professional. Pest Cont Buzz Online News 2008. Available at www.pes-
tcontrolmag.com/pestcontrol/article/articleDetail.jsp?id=109597 [Accessed 24
June 2008].
28. Goddard J. Do bed bugs carry human diseases? A controversy. Pest Cont Tech
2003;31:38-40.
29. Thompson J. Bed bug. Agfacts. New South Wales Department of Agriculture
information leaflet, 1983.
30. Vandam J. Sleep tight, and don’t let...Oh, just forget about it. New York Times
2003; Nov 2:14.6.
31. Doggett SL. A code of practice for the control of bed bug infestations in Australia.
Draft 3rd edn. Sydney: Department of Medical Entomology and The Australian
Environmental Pest Managers Association 2007. Available at http://medent.usyd.
edu.au/bedbug/cop_ed3_draft.pdf [Accessed 1 October 2009].
RESEARCH
Mark A J Morgan James Dunbar Prasuna Reddy

BM, BCh, MA, FRACGP, is Senior Research MD, FRCP(Edin), FRCGP, FRACGP, PhD, MAPS, is Director of Research, Greater
Fellow and general practitioner, Greater FACRRM, is Director, Greater Green Green Triangle, University Department
Green Triangle, University Department Triangle, University Department of Rural of Rural Health, Flinders and Deakin
of Rural Health, Flinders and Deakin Health, Flinders and Deakin Universities, Universities, Victoria.
Universities, Victoria. Victoria. director@greaterhealth.org
Collaborative care
The role of practice nurses
■ In patients with either type 2 diabetes mellitus or coronary
Background
heart disease the presence of depression leads to increased
Comorbid depression can occur with diabetes and heart disease.
morbidity and mortality.1,2 This comorbid depression is often
This article reports on a feasibility study focusing on additional roles
missed in routine general practice.3 To address these
for practice nurses in detecting and monitoring depression with
other chronic diseases.
problems we describe the implementation of collaborative
care based on new roles for practice nurses (PNs),
Method
information technology solutions, and a shift of focus toward
A convenience sample of six practices in southeast Australia was
self care. A similar model of collaborative care has been
identified. Practice nurses received training via a workshop, which
shown overseas to be an effective way to improve the
included training in the use of the Patient Health Questionnaire, to
management of depression in primary care.4
detect depression.
Results Method
The 332 patients who participated in the project each received a
A feasibility study focusing on additional roles for PNs. Six practices
comprehensive health summary to assist with self management.
in southeast Australia were selected by invitation on the basis
Depression was identified in 34% of patients in this convenience
of having PNs available to participate in the study. Patients were
sample. After 18 months implementation, practice nurses were
strongly in favour of continuing the model of care. General
selected by the general practitioner from a disease registry or
practitioners gave highly favourable ratings for effectiveness and opportunistically invited to attend the PN before review by the
willingness to continue this model of care. usual doctor. Regular follow up checks by the PN/doctor team were
organised at 3-6 month intervals according to clinical need. The
Discussion
GP Management Plan template allowed de-identified collection
Practice nurses can include depression monitoring alongside
and feedback of data, as well as prompting review appointments.
systematic care of diabetes and heart disease. A randomised trial is
currently underway to compare the clinical outcomes of this model
Structured interviews were conducted with all PNs and GPs in the
with usual care. study to evaluate the usefulness of the collaborative model.
Ethics approval was obtained from the Flinders University Social
and Behavioural Research Ethics Committee.
The workshops
Nurse training workshops prepared PNs for new roles including:
• use of the Patient Health Questionnaire (PHQ-9)5 to detect and monitor
depression and to assist the GP in clinical treatment of depression
• physical checks and pathology results checklist generated from
National Heart Foundation and Diabetes Australia guidelines
• coordinating and ensuring follow up and appropriate allied health
referrals
• helping patients understand and set goals related to depression,
lifestyle changes, and targets for physical and chemical measures
• drafting a GP Management Plan
RESEARCH Collaborative care - the role of practice nurses
• automated collection and feedback of results References

• ensuring completion of Medicare requirements for chronic disease 1. Lin EH, Katon W, Von Korff M, et al. Relationship of depression and diabetes self
care, medication adherence, and preventive care. Diabetes Care 2004;27:2154-60.
item numbers. 2. Bunker SJ, Colquhoun DM, Esler MD, et al. ‘Stress’ and coronary heart disease:
Psychosocial risk factors. Med J Aust 2003;178:272-6.
Results 3. Harris MF, Zwar NA. Care of patients with chronic disease: The challenge for
general practice. Med J Aust 2007;187:104-7.
For patients 4. Hunkeler EM, Katon W, Tang L, et al. Long term outcomes from the IMPACT ran
The 332 patients who participated in the project each received a domised trial for depressed elderly patients in primary care. BMJ 2006;332:259-63.
5. Kroenke K, Spitzer RL, Williams JBW. The PHQ-9: Validity of a brief depression
comprehensive health summary to assist with self management.
severity measure. J Gen Intern Med 2001;16:606-13.
Patients experienced PN led, systematic, protocol driven care. 6. Morgan M, Dunbar J, Reddy P, Coates M, Leahy R. The TrueBlue study: Is prac
Depression was identified in 34% of patients in this convenience tice nurse-led collaborative care effective in the management of depression for
patients with heart disease or diabetes? BMC Fam Pract 2009;10:46.
sample. In this model, mental health was being addressed as part of
comprehensive care.
For practice nurses

Evaluation of the training workshops showed significant improvement
in knowledge and confidence in the identification and assessment
of depression and significant improvement in undertaking case
management tasks. After 18 months implementation, nurses were
strongly in favour of continuing the model of care. A supportive GP and
protected time of at least 30 minutes to consult were the main enablers.
For GPs
General practitioners had to be willing to accept scrutiny of patient
care by PNs using ‘best practice’ guidelines to highlight gaps. Despite
this barrier, GPs gave highly favourable ratings for effectiveness
and willingness to continue this model of care. Practices were able
to claim Medicare rebates for GP Management Plans, Team Care
Arrangements and completion of Diabetes Annual Cycles of Care.
Discussion
The business case did suggest that, by completing GP Management
Plans or Team Care Arrangements where applicable, and Diabetes
Annual Cycle of Care Medicare item numbers, practices could more
than recoup the additional costs of the PN’s time. It was both feasible
and acceptable for collaborative care to be implemented for the
management of patients with diabetes or coronary heart disease.
Our training package and computer templates can equip PNs to
successfully take on the role of screening for, and monitoring of,
comorbid depression. A randomised trial is currently underway in three
regions of Australia (urban, regional and rural) to compare the clinical
outcomes of this model with usual care.6
Implications for general practice

• Depression in patients with type 2 diabetes or coronary heart
disease is a risk factor for poor outcome, but it is underdiagnosed.
• Practice nurses can include depression monitoring alongside
systematic care of diabetes and heart disease.
• Nurse led chronic disease clinics for diabetes and heart disease are
feasible, acceptable and affordable.
FOCUS Sports injuries
Sports ankle injuries

Drew Slimmon
Peter Brukner
Assessment and management
Background Case study

Sports ankle injuries present commonly in the general Lucia is a female, 16 years of age, who plays netball with the
practice setting. The majority of these injuries are inversion state under 17s netball team. She presents with an ankle injury
and plantar flexion injuries that result in damage to the sustained at training the previous night. She is on crutches
lateral ligament complex. and is nonweight bearing. Examination raises the possibility of
a fracture, but X-ray is negative. You diagnose a severe lateral
Objective ligament sprain and manage Lucia with ice, a compression
The aim of this article is to review the assessment and bandage and a backslab initially. She then progresses through
management of sports ankle injuries in the general practice a 6 week rehabilitation program and you recommend she wear
setting. an ankle brace for at least 6 months.
Discussion
Assessment of an ankle injury begins with a detailed history
to determine the severity, mechanism and velocity of the
injury, what happened immediately after and whether
there is a past history of inadequately rehabilitated ankle
injury. Examination involves assessment of weight bearing,
inspection, palpation, movement, and application of special
examination tests. Plain X-rays may be helpful to exclude
a fracture. If the diagnosis is uncertain, consider second The majority of ankle injuries are inversion and plantar
line investigations including bone scan, computerised flexion injuries that result in damage to the lateral
tomography or magnetic resonance imaging, and referral to a ligament complex (Figure 1). The main ligaments of
sports physician. Manage all lateral ligament complex ankle concern are the anterior talofibular ligament (ATFL),
sprains with ice, compression, elevation where possible and the calcaneofibular ligament (CFL), and the anterior
analgesia. Severe ligament sprains or rupture benefit from tibiofibular ligament (also called the anterior inferior
a brief period of immobilisation. After initial management, tibiofibular ligament or AITFL). The AITFL is the anterior
the athlete should complete a 6 week guided rehabilitation
component of the syndesmosis complex (Figure 2). A
program. Athletes with moderate to severe lateral ankle
thorough history including past history and examination
ligament sprains should wear a semirigid or rigid ankle
orthosis for at least 6 months following injury. will determine the need for investigations and guide
appropriate management.
Keywords: ankle; athletic injuries; soft tissue injuries
MSB History
Injury details
Severe ligament sprains or ruptures occur with high velocity injuries,
such as landing on a player’s foot while jumping or running. Simply
rolling the ankle on an uneven surface while walking is unlikely
to cause a ligament rupture or fracture in the setting of normal
bone density and ligament integrity, ie. there is no history of prior
ligament damage. Dorsiflexion and eversion injuries can cause
damage to the syndesmosis (Figure 2). A syndesmosis injury takes
significantly longer to recover than a lateral ligament injury and, if
unstable, warrants immediate surgical referral.
18 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 1/2, JANUARY/FEBRUARY 2010
Postinjury details Lateral talar tilt test
After a ruptured ligament or fracture, athletes are unlikely to be able This is performed by applying an inversion force to the ankle joint at
to continue training or playing sport, and may be unable to weight the heel, then assessing the degree of talar tilt. A talar tilt of greater
bear (particularly with a fracture). Swelling within minutes or hours than 15 degrees reflects rupture of the ATFL and CFL (Figure 4).3,4
is the result of the bleeding that occurs with a ligament rupture
or fracture/dislocation; swelling from synovitis takes longer to
develop. Reports of a cracking noise or the feeling that the ankle bent
double cannot differentiate between a fracture, ligament rupture or
ligamentous sprain.1
Past history
The past history provides the practitioner with an understanding of the
state of the ankle before the current injury. Inadequate rehabilitation
and a subsequently chronically unstable ankle would be expected
to take significantly longer to completely rehabilitate. It is important
to clarify the extent of any previous injury and any investigations or
treatment. If a rehabilitation program was instituted, the clinician
Figure 1. Lateral ankle ligaments
should seek details of the type and duration of the program. Appropriate
Reproduced from Brukner P Kahn K. Clinical sports medicine,
rehabilitation programs focus on range of motion, proprioception, 3rd edn. Sydney: McGraw-Hill, 2007
strength and sports specific exercises, and are usually a minimum of
6 weeks duration. Asking about previous or current use of a semirigid
brace or tape may offer insight into the adequacy of past rehabilitation
efforts as this is an important component of rehabilitation.
Examination
Examination of the injured ankle includes:
• Weight bearing - if the patient cannot weight bear on the affected
leg for more than four steps unaided, ankle X-rays should be
ordered (Figure 3)2
• Inspection - discoloration haematoma and significant swelling are
suggestive of ligament rupture or fracture
• Palpation - pain on palpation of the posterior aspect of the
medial and lateral malleolus (both sites are void of ligamentous
attachments), the base of the fifth metatarsal and the proximal
fibula are suggestive of fracture (Figure 3).2 Lack of tenderness on
palpation of the ATFL excludes ATFL rupture
• Range of movement - this may not assist diagnosis acutely and is
likely to be limited by acute swelling and pain.
Special examination tests

These may not assist diagnosis acutely as a result of swelling and
pain. In this situation the examination should be repeated 3-5 days
later when pain and swelling have subsided.
Anterior drawer test

This is performed with the knee at 90 degress of flexion and the
muscles relaxed. Increased laxity compared to the contralateral ankle
reflects injury to the ATFL and possibly the CFL. The combination Figure 2. Syndesmosis sprain
of discoloration haematoma, ATFL tenderness and positive anterior Reproduced from Brukner P, Kahn K.
Clinical sports medicine, 3rd edn.
drawer provides sensitivity of 98% and a specificity of 84% of an acute
Sydney: McGraw-Hill, 2007
lateral ligament rupture.1
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 1/2, JANUARY/FEBRUARY 2010 19
FOCUS Sports ankle injuries - assessment and management
C baw or Mi
Figure 3. Ankle X-ray recommendations

Ankle X-rays are only required if there is pain in the malleolar
zone and any of these findings: bone tenderness at A; bone
tenderness at B; inability to bear weight both immediately and
at the clinical assessment. Foot X-rays are only required if there
is pain in the midfoot zone and any of these findings: bone
tenderness at bone tenderness at D; or inability to bear weight
both immediately and at the clinical assessment
Reproduced from Brukner P Kahn K. Clinical sports medicine,
3rd edn. Sydney: McGraw-Hill, 2007
Tests for a syndesmosis injury

External rotation stress test, squeeze test and interosseous membrane Figure 4. Lateral talar tilt test
tenderness length should be performed if the mechanism suggests a

syndesmosis injury, or if there is tenderness on palpation of the AITFL If the patient fails to improve significantly after a well guided
(Table 1). Importantly, following an ankle inversion plantarflexion rehabilitation period of at least 6 weeks then they should be reassessed
injury, 60% of patients will have pain over the medial malleolus in the and the differential diagnosis reviewed. At this stage, plain radiographs
absence of a syndesmosis injury or medial malleolus fracture.1 may be reconsidered to exclude an occult osteochondral lesion.
Consider the commonly missed fractures around the ankle (Table 2). This
Investigations is also an opportune time to consider referral to a sports physician.
Plain X-rays are often unnecessary in the case of uncomplicated lateral While a plain X-ray excludes a fracture in the vast majority of
ligament complex injuries. The Ottawa ankle rules (Figure 3) provide cases, a bone scan or computerised tomography (CT) scan may be
a well validated guide to assessing whether an X-ray is required to helpful if an occult fracture is suspected. These investigations are
exclude a fracture.2 Clinical assessment is usually adequate initially to relatively inexpensive compared to magnetic resonance imaging
assess the severity of ligament damage. There is no evidence based (MRI) and are highly sensitive for bony pathology. Focally increased
role for stress radiographs or ultrasound in acute ankle injuries. radioisotope uptake on the delayed phase of a bone scan confirms
bone damage; CT provides further anatomical detail and assists
determining whether surgery is required.
Table 1. Clinical testing for syndesmosis injury
Magnetic resonance imaging can be useful as a second line
External The patient’s ankle is passively investigation, usually in the specialist setting. It can clarify diagnoses
rotation stress dorsiflexed in maximal external of ligament sprain or rupture, reveal ongoing synovitis, and assess
test rotation (either seated or lying prone
osteochondral damage that may require surgical referral.
with knee flexed to 90 degrees). Pain
at the syndesmosis is regarded as a
positive test Diagnosis and management
Squeeze test With both hands clasp the medial For management purposes, ankle injuries can be considered under the
and lateral aspects of the midcalf and following headings:
squeeze. Pain distally at the site of • Mild to moderate lateral ligament complex sprain - treatable with
the syndesmosis is regarded as a early mobilisation and guided proprioceptive and strengthening
positive test
rehabilitation program
Interosseous Patient sits or lies supine with their
• Severe lateral ligament complex sprain - immobilisation for a
membrane affected leg extended on examination
tenderness table. Palpate between the fibula and period of days in a cast (a simple backslab is sufficient) or cam
length tibia from the ankle joint proximally. walker (walking boot) followed by a guided proprioceptive and
Determine the length of tenderness strengthening rehabilitation program
from the distal tip of the fibula and • Fracture/dislocation or unstable syndesmotic injury requiring
document orthopedic surgeon referral.
Sports ankle injuries - assessment and management FOCUS
mobilisation for all ankle sprains and showed that severe ankle
Table 2. Commonly missed fractures
ligament sprains or ruptures had a better outcome following cast
• Proximal fibula immobilisation for 10 days rather than early mobilisation with
• Base of fifth metatarsal compression alone or an aircast.5 Severe was defined as being
• Anterior process of calcaneus unable to weight bear for at least 3 days without radiological
• Lateral talar process evidence of fracture. It is now generally accepted that following a
severe ligament sprain or rupture, initial protected immobilisation
• Posterior process of talus (also os trigonum fracture)
is likely to be beneficial. A backslab or cam walker usually provides
• Talar dome
adequate protection. A more diagnostic examination is usually
• Tibial plafond possible when pain and swelling have decreased and following
Adapted from Brukner P, Kahn K. Clinical sports medicine, a period of immobilisation the patient can progress to a graded
3rd edn. Sydney: McGraw-Hill, 2007 rehabilitation program.
Rehabilitation
Acute phase management of lateral
ligament complex strains Guidelines for rehabilitation of ankle injuries are shown in Table
3. Ideally, the program should be supervised by a clinician (often
Once a fracture/dislocation or unstable syndesmotic injury is excluded, a physiotherapist); however, in rural settings this may not be
acute phase (1-5 days) management can be instituted. The aim is possible. The aim of a guided rehabilitation program is to improve
to decrease pain and swelling with ice, compression and elevation proprioception and decrease the risk of ongoing pain and recurrent
where possible. Simple analgesia (paracetamol) is useful to allow injury.6,7 Proprioceptive exercises are an essential component (Figure
rehabilitation progression. Nonsteroidal anti-inflammatory drugs 5) and have been shown to reduce the rate of re-injury by up to 80%.8
(NSAIDs) are probably best avoided early due to the increased risk No clinically validated tests have been created to formally
of bleeding early and the impediment of tissue healing. Furthermore, assess proprioception, however, the star excursion balance test is
acute inflammation is a necessary component of injury recovery and a simple dynamic functional task that may be employed by general
there is a lack of supportive data to suggest improved healing time practitioners clinically to assess proprioception during rehabilitation
with use of NSAIDs. (Figure 6).9 A detailed description of this test is beyond the scope of
A recent study published in The Lancet questioned early this article.
Table 3. Rehabilitation guidelines

Phase Time postinjury Goal of phase
Gentle pain free stretching, avoiding 1-2 weeks • Normalise range of motion, perform three times daily
further tissue injury
Progressive weight bearing exercises 1-2 weeks • Walk with normal gait
Proprioception and resistance exercises: 1-6 weeks • Proprioception
commence when weight bearing pain - at least 10 minutes daily
free - 5 days per week
- progress difficulty, eg. increasingly unstable surfaces, then
increase complexity of tasks while balancing on unstable
surface
• Strength - resisted eversion exercises
- theraband
- three sets of 15 daily
- increase resistance if pain free
Return to running: commence when 2-4 weeks • Progression
walking pain free, able to balance on - slow jog - running in straight lines
unstable surface pain free - slow change of direction - high speed zigzags
Return to training: functional exercises 4-6 weeks • Full ankle range of motion
and sports specific drills • Roughly 80% strength compared with contralateral lower limb
• Running and changing direction at pace pain free
• Capable of light controlled skills drills
Return to competition 5-8 weeks • After two full pain free training sessions
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 1/2, JANUARY/FEBRUARY 2010 21
FOCUS Sports ankle injuries - assessment and management
Taping and ankle braces • Manage a lateral ligament complex sprain with ice, compression,
Ankle taping has been shown to be effective for initial support of the elevation where possible and analgesia. Severe ligament sprains or
injured ankle.10 However, it was found that the mechanical support of rupture benefit from a brief period of immobilisation.
tape was reduced by more than two-thirds after approximately 400 • Organise a thorough rehabilitation program of 6 weeks duration
steps.10 Lace-up ankle braces have been shown to be equally, if not postinjury. Athletes with moderate to severe lateral ankle ligament
more effective and more cost effective.10 Athletes with moderate to sprains should wear a semirigid or rigid ankle orthosis for at least 6
severe lateral ankle ligament sprains should wear a semirigid or rigid months.
ankle orthosis for at least 6 months following injury.11 The brace should • If pain persists after a well guided rehabilitation program, revisit
be worn during painful activities and during exercise. the diagnosis and consider further investigations and referral to a
sports physician.
Summary of steps in assessment and
management of ankle injuries Resource
Brukner P, Kahn K. Clinical sports medicine, 3rd edn. Sydney: McGraw
• Take a full history to determine the severity, mechanism and velocity Hill, 2007.
of the injury, what happened immediately afterward and whether
Authors
there is a past history of inadequately rehabilitated ankle injury.
Drew Slimmon BMedSc, MBBS, is a sport and exercise medicine reg
• Examine the patient to determine whether any investigations are istrar, The Sports Medicine Centre Hobart, Tasmania, and Hawthorn
necessary, starting with an X-ray. Football Club. drewslimmon@gmail.com
• Refer any fracture/dislocation or unstable syndesmotic injury to an Peter Brukner OAM MBBS, DRCOG, FACSP, FASMF, FACSM, is Adjunct
orthopaedic surgeon. Associate Professor, Centre for Health, Exercise and Sports Medicine,
University of Melbourne, and a sports physician, Melbourne, Victoria.
Acknowledgment
I would like to thank Dr Steven Reid for his guidance during the prepa
ration of this manuscript.
References
1. Van Dijk CN. Diagnosis of ankle sprain: History and physical examination.
ISAKOS - FIMS World Consensus Conference on Ankle Instability, 2005; p.
21-2.
2. Stiell IG, Greenberg GH, Douglas McKnight R, et al. Decision rules for the use
of radiography in acute ankle injuries. Refinement and prospective validation.
JAMA 1993;269:1127-32.
3. Mabee J, Mabee C. Acute lateral sprained ankle syndrome. The Internet
Journal of Family Practice 2009;7:1.
4. Gaebler C, Kukla C, Breitenseher MJ, et al. Diagnosis of lateral ankle liga
Figure 5. Proprioceptive exercises ment injuries. Comparison between talar tilt, MRI and operative findings in
on an unstable surface 112 athletes. Acta Orthopaedica Scandinavica 1997;68:286-90.
Reproduced from Brukner P, Kahn 5. Lamb SE, Marsh JL, Hutton JL, Nakash R, Cooke MW, on behalf of The
Collaborative Ankle Support Trial (CAST Group). Mechanical supports for
K. Clinical sports medicine, 3rd
acute, severe ankle sprain: a pragmatic, multicentre, randomised controlled
edn. Sydney: McGraw-Hill, 2007 trial. Lancet 2009;373:575-81.
6. Holme E, Magnusson S, Becher K, Bieler T, Aagaard P, Kjaer M. The effect
of supervised rehabilitation on strength, postural sway, position sense and
re-injury risk after acute ankle ligament sprain. Scand J Med Sci Sports
1999;9:104-9.
7. Verhagen E, van der Beek A, Twisk J, Bouter L, Bahr R, van Mechelen W.
The effect of a proprioceptive balance board training program for the pre
vention of ankle sprains: a prospective controlled trial. Am J Sports Med
2004;32:1385-93.
8. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med
1985;13:259-62.
9. Hertel J, Braham R, Hale SA, Olmsted-Kramer LC. Simplifying the star
excursion balance test: analyses of subjects with and without chronic ankle
instability. J Orthop Sports Phys Ther 2006;36:131-7.
10. Beynnon B. The use of taping and bracing in treatment of ankle injury.
ISAKOS - FIMS World Consensus Conference on Ankle Instability, 2005; p.
38-9.
11. Osborne MD, Rizzo TD Jr. Prevention and treatment of ankle sprain in ath
letes. Sports Med 2003;33:1145-50.
Figure 6. Star excursion

balance test
correspondence afp@racgp.org.au
focus Culture and diversity
Using interpreters
Christine Phillips
A guide for GPs
O Australia is one of the most multilingual countries in the

Background
world, but also one of the most monolingual. Four out
Australia is one of the most multilingual countries in
of 5 Australians speak only English; but among the 20%
the world. In their working lives, all doctors will need to
communicate with patients whose languages they do not who speak another language, 400 languages are spoken.1
speak. Although Australia has many bilingual doctors, nearly
80% of consultations are conducted in English, and only
Objective 3% of general practitioners conduct more than half their
To outline Australia’s system for providing interpreters
consultations in a language other than English.2 The
for medical consultations, and to discuss optimal ways of
diversity of languages exceeds the capacity of any doctor
working with these interpreters.
to communicate with all patients using his or her own
Discussion language skills.
Australia has the world’s largest free telephone interpreter
service for doctors. All general practitioners claiming
Fortunately, interpreter services in Australia for doctors are highly
Medicare consultations can contact this service, quote a
accessible compared to those in other countries. However, interpreter
doctor code or Medicare provider number, and generally
services remain underused, and frequently misunderstood, by
receive an interpreter within 3 minutes. Onsite interpreters
can be booked if required. State and territory health GPs.3 Reasons appear to be related to faith in ‘in house’ bilingual
services can also provide onsite and telephone interpreters. staff, beliefs about the preference of patients for family members
Despite this, interpreters are underused in Australia. to interpret, and a lack of practice systems to contact interpreters.
Practices can improve their uptake of interpreters by Numerous studies have demonstrated that interpreters are viewed
establishing routine systems to contact interpreters when as cumbersome to access and challenging to use in day-to-day
needed; however nation wide measures are also needed, practice.3-5 Front office staff often consider accessing interpreters to
including education and providing incentives through the be the doctor’s problem, and GPs in turn are often inexperienced and
Medicare fee structure. Decisions about when to contact unaware of interpreter services.3,4 The fallback position tends to be to
an interpreter will be determined by patient or doctor ‘get by’ in English or by using a family member to interpret.
request, the nature of the illness, and/or the subject of the
Evidence suggests that using interpreters where needed
consultation. The quality of interpreted consultations can
improves both the quality and safety of health care.6,7 Patients
be improved if the GP speaks slowly and speaks to the
are more confident with their care when trained interpreters are
patient, not the interpreter; allows time for the interpreter
to interpret the elements of the consultation to the patient; used.8 Failure to use an interpreter when one was needed has been
and remains in charge of the consultation. Information in determined to be a breach of duty of care in United States of America
many languages is now widely available on the internet, courts.9 It is likely that such an argument could also be mounted in
and can be a useful supplement to the interpreted Australia, where interpreters are readily available to GPs and their
consultation. appropriate use forms part of The Royal Australian College of General
Practitioners Standards for general practices (see Resources), which
Keywords: general practitioners; translating; vulnerable
populations; quality of care; communication barriers are used by Australian General Practice Accreditation Ltd (see
Resources) as part of the accreditation process for general practice
clinics in Australia.
This article outlines Australia’s health care interpreter system,
and discusses key communication issues when using interpreters.
Consultations with interpreters are different from noninterpreted
consultations, but the skills can be readily learned and are likely to
improve communication skills for noninterpreted consultations.
188 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 4, APRIL 2010
Accessing interpreters When to use an interpreter
Interpreters work with the spoken word, while translators work with Decisions about when to contact an interpreter before a consultation
the written word. Most employed interpreters are accredited through will be determined by patient request, the nature of the illness and/
the National Accreditation Authority for Translators and Interpreters or the subject of the consultation. Command over a second language
(NAATI) (see Resources). This body is internationally unique,10 and sets can slip with illness or distress, so even quite competent speakers of
the standards against which interpreters and translators are tested English as a second language may on occasion need an interpreter.
and/or accredited in 57 languages. Complex consultations likely to require an interpreter include:
Access to language support services is a national population • where self management with adjustment of medication is required
based initiative, in contrast to many other countries.11 Doctors can (eg. insulin regimens, asthma management approaches)
access two sets of interpreting services: the national Translating and • where matters that are socially or psychologically complex are
Interpreting Service (TIS) and state or territory health funded services raised (eg. mental health, sexual health matters, personal distress)
(Table 1). Larger hospitals also fund their own in-house interpreters in • where matters of patient safety are concerned (eg. intimate partner
priority languages. violence, risk of harm to self or reported risk of harm to others)
• consultations where patients cannot make decisions without full
The Translating and Interpreting Service information (eg. therapeutic options for serious illness, consent for
TIS, set up by the then Department of Immigration in 1977, is now the interventions).
largest interpreting service in the country, and also provides services Sometimes the need for an interpreter becomes apparent after the
to New Zealand. TIS operates from a call centre in Melbourne and is consultation has started. In these cases, the doctor should state that
linked to 1500 interpreters speaking 160 languages around Australia. they would like to contact an interpreter to understand the problem
Doctors in immediate need of an interpreter should call, or ask their better, and contact TIS. In most cases the 3-5 minutes lost in engaging
receptionist to call, the Doctors Priority Line (see Resources), which an interpreter will be readily compensated for by a more efficient and
undertakes to provide a telephone interpreter within 3 minutes. safer consultation.
The call operator will ask the doctor for their code number. Doctors Face-to-face interpreters may occasionally be preferable to
who have not previously used the service can quote their Medicare telephone interpreters for intimate examinations (where same-gender
provider number and will be given a code number (if you have interpreters are preferable) and for mental health consultations.
forgotten your code number, TIS can locate it by linking it with your
provider number). It is not necessary to disclose the identity of the Working with interpreters
patient to TIS. Working with an interpreter helps to refine GPs’ consultation skills.
Translating and Interpreting Service interpreting services are Detailed guidelines for working with interpreters are available from the
free for any GP providing a Medicare rebateable consultation, and Australian Institute of Interpreters and Translators13 (see Resources).
for their receptionists (who can use the doctor’s code number for The Victorian Transcultural Psychiatry Unit has produced specific
this purpose) for arranging appointments and providing results. From guidelines for working with interpreters in mental health settings,
December 2008, pharmacists can also access TIS services at no cost which are also of relevance to GPs.14 Some simple tips for working
(6 months after the introduction of this initiative 25% of pharmacies with interpreters are:
had registered for this service).12 TIS can also translate key documents, • speak to the patient, not the interpreter. The interpreter
such as immunisation records, into English at no cost. should become part of the background, not the object of your
Onsite interpreters are available through both TIS and state and communication efforts. Use the first person when speaking to the
territory health services. These interpreters can often provide more patient; make eye contact with the patient. The interpreter will also
outreach to patients than the TIS interpreter can. In some states, these use the first person when communicating the patient’s words
services are free to government funded agencies, but in most cases a • allow time for the interpreter to interpret what you say. Health
charge will be levied for profit businesses. care interpreters almost always work in consecutive mode, that
is, they interpret your words to the patient in a turnabout fashion.
Auslan and Indigenous languages
The doctor speaks a few sentences, and then pauses to allow the
Indigenous language support has lagged behind services for interpreter to interpret those sentences. While the interpreter
migrant Australians, and there is no national system akin to TIS for speaks, the doctor can observe the patient, and formulate the next
Indigenous Australians. However, there are local services available question and the direction of the consultation. It is this thinking and
(Table 1). The National Auslan Interpreter Booking and Payment observing time that enables an interpreted consultation to become
Service can arrange free sign interpreters to attend a wide range of as efficient as any other consultation, as there is less ‘wasted’
clinical consults, including those run by allied health practitioners time in the consultation. Learning to use this ‘negative space’
(Table 1, see Resources ). They also provide video sign interpreting when the doctor is silent and observing can lead to more skilled
for GPs in rural areas. communication with all patients15
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 4, APRIL 2010 189
190
Reprintedfrom
Table 1. Publicly funded health interpreting services in Australia

AUSTRALIANFAM
Region Name of service Availability of service Languages covered

Australia wide Translating and Interpreting Service (TIS) 24 hours a day, 7 days a week. Fee free, rapid access Over 160 languages. Does not include
FO C U S
service for GPs charging Medicare rebateable services. Indigenous languages
ILYPH
(Department of Immigration and Citizenship)

Prefer telephone interpreters, but can arrange face-to-
Y
Doctors Priority Line 1300 131 450

SIC
U
face interpreter bookings
IA
singinterpreters aguideforG
NVO
Book online at www.immi.gov.au/living-in-australia/

L.3
9,M
help-with-english/help_with_translating/booking.htm
O.4
(ideally allow 2 weeks)

,A
-
PRIL2010
National Auslan Booking and Payment Service Free booked service for GPs. Provides face-to-face and Auslan
(sign language services) video use of interpreters
Ps
Book online at www.nabs.org.au/03_booking_form.php
Victoria Contractée with Department of Human 24 hours a day, 7 days a week. For services within A list is available at www.
Services (ONCALL Translating and Interpreting the Department of Human Service system, including oncallinterpre ters .com
Ltd) community health
Telephone 03 9867 3788
New South Health Language Services (NSW Health) 24 hours a day, 7 days a week. Free for services within 91 languages. A list is available at www.
Wales (formerly South East Sydney and South West the NSW public health system sswahs.nsw.gov.au/SSWAHS/Interpreter
Sydney area)
Health Care Interpreter Service (NSW Health) 24 hours a day, 7 days a week, business hours.
Illawarra: telephone 02 4274 4211 Available to GPs
Shoalhaven: telephone 1800 247 272
Health Care Interpreter Service (NSW Health) 24 hours a day, 7 days a week. Free for services within 120 languages. A list is available at
Sydney West Area Health Service the NSW public health system and correctional health www.wsahs.nsw.gov.au/services/hcis/
Telephone 02 9840 3456 services languages.htm
Rural Health Care Interpreter Service 24 hours a day, 7 days a week. Fee free for services A list is available at www.hnehealth.
Hunter New England Health Service, covers within the NSW public health system nsw. gov. au/multiculturalhealth/
rural NSW (NSW Health) interpre ter_services
Freecall 1800 674 994 (business hours)
Freecall 1800 674 994 (24 hours)
Northern Non-Indigenous languages: Interpreting and Business hours, Monday to Friday. Fee free for 38 languages. A list is available at www.
Territory Translating Services NT community and nonprofit nongovernment agencies. itsnt.nt.gov.au/countries_and_their_
(Department of Housing, Local Government Fee for services to private businesses languages_spoken
and Regional Services)
www. itsnt. nt. gov. au
Indigenous languages: Booking service, 24 hours. There is a fee for this Over 60 languages. A list is available
Aboriginal Interpreting Service service. Users are requested to brief the interpreter at www. dlgh .nt.gov. au/ais/aboriginal_
(Department of Housing, Local Government beforehand on the topic of the consultation regions_and_languages
and Regional Services)
Darwin: telephone 08 8999 8353
Alice Springs: telephone 08 8951 5576
South South Australian Interpreting and Translating 24 hour service. There is a fee for this service Over 112 languages. Includes provision
Australia Centre (Government of SA) of interpreting services for Fitiantjatjara
Telephone 08 8226 1990 and Yankunytjatjara
Queensland Contractée with Queensland Health 24 hours a day, 7 days a week. For services within the A list is available at www.
(ONCALL Translating and Interpreting Ltd) Queensland health system, including community health oncaHinterpre ters .com
Telephone 07 3018 0333 Queensland has no publicly funded
Indigenous language interpreter services
Tasmania Non-Indigenous languages: uses TIS [See above, Translating and Interpreting Service] for Languages available through TIS
Tasmanian public health services
Western Non-Indigenous languages: uses TIS [See above, Translating and Interpreting Service] for Languages available through TIS
Australia WA public health services
Indigenous languages (Government of WA) Booking service in business hours. There is a fee for 18 Kimberley and Central Desert
Kimberley Interpreting Services this service. Based in Broome languages
Australian Migrant Health Unit (ACT Health) Fee free services to GFs and specialists, as well as Seven languages. A list is available at
Capital Telephone 02 6205 3333 those within the public sector www. health.act.gov.au/c/health?a=da&
Territory did=10040621&template=25
co
Using interpreters - a guide for GPs FOCUS
Barriers to using interpreters Misconceptions

• About access: many doctors continue to believe that there is a cost
Despite Australia’s widespread provision of interpreters, in general
to using interpreters. This is only true of some services, and is not
there is still a reluctance from GPs to use them. This can be
true of TIS. Many are unaware that the service is available after
attributed to: misconceptions about the service, the impact of a
bad experience using an interpreter, and preference for a family or hours (Table 3, Case study 1)
bilingual staff member to be used as the interpreter. • About responsibility to access an interpreter: from a medicolegal
and quality perspective, it is the responsibility of the treating doctor,
not the patient, to ensure an interpreter is present (Table 3, Case
Table 2. Practice level changes to increase uptake of study 2). When making referrals to specialists, the language spoken
interpreters by the patient and the need for an interpreter should be stated.
The referral letter may need to state how to access TIS, as it is not
• List the telephone number(s) for interpreters in the
uncommon for the specialist or their receptionist to state that the
practice telephone directory
referring doctor should book the interpreter (GPs cannot use their
• Ensure all doctors have TIS code numbers which are
readily accessible for receptionists own code number to arrange an interpreter for another doctor)
• Indicate that interpreters are available in signage in • About confidentiality and medicolegal risk: some doctors have
the waiting room and practice pamphlets expressed concern that interpreters pose a risk to patient
• Install speaker telephones for each room confidentiality. Such breaches are more likely among untrained
• Routinely collect language spoken and English interpreters, as professional interpreters work to a code of ethics
competence data for all patients which covers confidentiality.16 Patients from small communities
• Maintain a register of languages spoken by all staff, who are concerned about breaches of confidentiality with onsite
and their proficiency interpreters are often happy to use a telephone interpreter who
• Establish ongoing training for practice staff, including is anonymous and likely to be located in a different city. Table 4
receptionists, in identifying the need for interpreters
outlines a case where having an interpreter protected the doctor
and using them when required
from medicolegal risk
• For practices that have patients from a range of non
English speaking backgrounds for whom staff cannot • That interpreted consultations take longer: despite this widely
identify the language, print out the language identifier held perception, the lengthening of consultations by interpreters
flip chart from the Find Your Language tool at www. is not supported by the literature.17 An interpreted consultation is
healthtranslations.vic.gov.au/bhcv2/bhcht.nsf and keep a skill, but because it uses pared back communication, can usually
it as a resource at the reception desk be conducted without extending the consultation unduly, provided
interpreters are available.
Table 3. Knowledge barriers to using interpreters

Case study 1
Problem: Not knowing how to get an interpreter
An overseas student on a backpacking holiday was brought to the emergency department of a small regional hospital. He
had a malleolar fracture which would need open reduction and internal fixation. His language, Ukrainian, was not spoken
by anyone at the hospital. The staff decided to keep him comfortable overnight by giving him pain relief and deferred
getting consent for the operation until the morning staff came on, when they knew there was an overseas trained doctor
who spoke Ukrainian. The staff expressed some concern about not knowing if he was allergic to morphine, but decided
to go ahead and give it to him.
Comment: The patient was denied information about his treatment for 7 hours, and given a medication without knowing
if it was safe for him. This potentially risky situation could have been avoided by contacting a telephone interpreter from
the Translating and Interpreting Service.
Case study 2
Problem: Not knowing whose responsibility it is to get an interpreter
While talking at a workshop, Dr J said that he was rather surprised that there should be any need for doctors to contact
interpreters. He said that he was perfectly happy for his patients to use interpreters, and stated so in his practice leaflet:
‘This is an interpreter friendly practice. Patients are welcome to bring an interpreter with them whenever they wish’.
He observed that there couldn’t have been much need for interpreters, because it was rare for patients to present to a
consultation with one.
Comment: Patients who organise their own interpreters generally bear the cost, which acts as a disincentive to getting
an interpreter. The GP, on the other hand, is able to access interpreters at no cost.
FOCUS Using interpreters - a guide for GPs
Table 4. Interpreters and quality consultations

Case study 3
Mrs JB had not been seen at the practice before. She presented with subacute onset of pain in the right knee and
hip and left side of her abdomen. She brought a supporter from her community with her, who was very anxious about
Mrs JB’s pain and concerned that Mrs JB might be fobbed off, as she had been at other general practices. Mrs JB
had an anxious demeanour, and requested that her friend interpret, but then appeared to be arguing with the friend.
You decided to request that the friend wait outside and arranged a telephone interpreter. Fortunately, Mrs JB spoke a
language for which TIS could quickly locate an interpreter, and the consultation continued after a break of 5 minutes.
With the aid of the interpreter, it became apparent that the pain was nonanatomical in nature, and followed a period of
some stress. Several times the interpreter pointed out that it was difficult to make sense of the content of the patient’s
speech. It became apparent that Mrs JB had a formal thought disorder and was globally suspicious. You arranged for a
later, longer appointment and also contacted the mental health team.
The patient later formally complained about you to the Medical Board, stating that you had asked for a bribe and that you
had asked inappropriate questions. The interpreter was able to confirm that this was not the case.
Influence of bad experiences (NAATI): www.naati.com.au

• Doctors Priority Line: 1300 131 450
Not all interpreting experiences are good. Some of the newer • Forms to register with the Translating and Interpreting Service (and
languages spoken in Australia currently only have interpreters at get a doctor code number): www.immi.gov.au/living-in-australia/
paraprofessional level, that is, the lowest level of accreditation by help-with-english/help_with_translating/_pdf/doctors-free-inter-
NAATI.18 Interpreters at this level represent a pragmatic solution to preting-registration-form.pdf
• AUSIT Guidelines for health care professionals working with inter
providing language support to the most needy Australians and may not
preters: www.ausit.org/pics/HealthGuide08.pdf
have the level of skills of most health interpreters, who are accredited
• NSW Multicultural Health Communication Service. Patient health
at the professional level. If your interpreting experience has been less information in 63 languages: www.mhcs.health.nsw.gov.au/publica-
than satisfactory, you should alert the employing organisation. tionsandresources/languages.asp
• Victorian Health Translations Directory. Patient health information in
Preference for family or bilingual staff 64 languages: www.healthtranslations.vic.gov.au
members as interpreter • National Auslan Interpreter booking service: www.nabs.org.au.
The ideal situation is for the doctor and patient to speak the same Author
language. Using other clinicians (eg. nurses) as interpreters is Christine Phillips MBBS, MA, MPH, DipEd, FRACGP, is Associate
convenient, but depends on the quality of interpreting the nurse can Professor, Social Foundations of Medicine, Medical School, Australian
National University, Canberra, Australian Capital Territory. christine.
give.19 Using family members introduces a range of family dynamics
phillips@anu.edu.au.
into the consultation, which may not always be beneficial, and has
been shown to result in poorer quality, longer consultations.20 Conflict of interest: Christine Phillips is a member of the ACT Regional
Advisory Committee for the National Accreditation Authority for
Conclusion Translators & Interpreters.
Australia has such linguistic diversity that all doctors will need
References
at some stage to use an interpreter. Australia provides a suite of 1. Australian Bureau of Statistics. Proficiency in spoken English/language
services, including interpreters, and health information resources by age by sex. Australia Cat No. 20680. Canberra: Australian Bureau of
Statistics, 2008.
in community languages,21,22 which is unparalleled in scope and
2. Britt H, Miller GC, Charles J, et al. General practice activity in Australia
availability anywhere in the world. To enable doctors to take up these 2007-8. GP Series No 22. Canberra: Australian Institute of Health and
opportunities, general practices need to become proactive about Welfare, 2008.
3. Huang Y-T, Phillips C. Telephone interpreters in general practice: bridging the
accessing interpreters as an organisational routine,23 and doctors need
barriers to their use. Aust Fam Physician 2009;38:443-6.
to practise and become confident using both onsite and telephone 4. Atkin N. Getting the message across - professional interpreters in general
interpreters. practice. Aust Fam Physician 2008;37:174-6.

5. Centre for Culture Ethnicity and Health - Health Sector Development.
In addition, the Commonwealth Government should underscore the Working effectively with professional interpreters in private general practice.
importance of using interpreters by adding a small Medicare incentive Available at www.multicultural.vic.gov.au/Web24/rwpgslib.nsf/GraphicFiles/
Working+Effectively+with+Interpreters+in+Private+General+Practice/$file/
for consultations where interpreters are used.
Interpreter+report.pdf [Accessed January 2010].
Resources 6. Flores G. The impact of medical interpreter services on the quality of health
care: a systematic review. Med Care Res Rev 2005;62:255-99.
• Australian General Practice Accreditation Ltd: www.qip.com.au
7. Brach C, Fraser I. Can cultural competency reduce racial and ethnic
• RACGP Standards for general practices (3rd edn): www.racgp.org. health disparities? A review and conceptual model. Med Care Res Rev
au/standards 2000;57(Suppl 1):181-217.
• The National Accreditation Authority for Translators and Interpreters 8. Garcia EA, Roy LC, Okada PJ, Perkins SD, Wiebe RA. A comparison of the
Using interpreters - a guide for GPs FOCUS
influence of hospital-trained, ad hoc, and telephone interpreters on perceived
satisfaction of limited English-proficient parents presenting to a pediatric
emergency department. Pediatr Emerg Care 2004;20:373-8.
9. Bird S. Lost without translation. Aust Fam Physician 2008;37:1023-4.
10. Ozolins U, Clyne M. Immigration and language policy in Australia. In: Extra G,
Gorta D, editors. The other languages of Europe. Clevedon: Cromwell Press,
2001.
11. Partida Y. Addressing language barriers: building response capacity for a
changing nation. J Gen Intern Med 2007;22(Suppl 2):347-9.
12. Department of Immigration and Citizenship. Annual report 2008-9. 2.1.5
Free Translating Services. Available at www.immi.gov.au/about/reports/
annual/2008-09/html/outcome2/output2-1-5.htm [Accessed 20 January
2010].
13. Australian Institute of Interpreters and Translators, Inc. AUSIT Guidelines for
health professionals working with interpreters. Available at www.ausit.org/
pics/HealthGuide08.pdf [Accessed 20 January 2010].
14. Victorian Transcultural Psychiatry Unit. Guidelines for working effectively
with interpreters in mental health settings. July 2006. Available at www.
vtpu.org.au/docs/interpreter/VTPU_GuidelinesBooklet.pdf [Accessed 20
January 2010].
15. Buetow SA. Something in nothing: negative space in the clinician-patient
relationship. Ann Fam Med 2009;7:80-3.
16. Australian Institute of Interpreters and Translators. Code of ethics for
interpreters and translators. Available at www.ausit.org/eng/showpage.
php3?id=650 [Accessed January 2010].
17. Thornton JD, Pham K, Engelberg RA, Jackson JC, Curtis JR. Families with
limited English proficiency receive less information and support in interpreted
intensive care unit family conferences. Crit Care Med 2009;37:89-95.
18. National Accreditation Authority for Translators and Interpreters.
Accreditation by testing. Available at www.ausit.org/eng/showpage.
php3?id=650 [Accessed January 2010].
19. Elderkin-Thompson V, Silver RC, Waitzkin H. When nurses double as inter
preters: a study of Spanish-speaking patients in a US primary care setting.
Soc Sci Med 2001;52:1343-58.
20. Karliner LS, Jacobs EA, Chen AH, Mutha S. Do professional interpreters
improve clinical care for patients with limited English proficiency? A system
atic review of the literature. Health Serv Res 2007,42:727-54.
21. NSW Health. NSW Multicultural Health Communication Service. Available at
www.mhcs.health.nsw.gov.au/index.asp [Accessed January 2010].
22. Department of Human Services, Victoria. Health translations directory.
Available at www.healthtranslations.vic.gov.au/bhcv2/bhcht.nsf [Accessed
January 2010].
23. Greenhalgh T, Voisey C, Robb N. Interpreted consultations as ‘business as
usual’? An analysis of organisational routines in general practices. Sociol
Health Illn 2007;29:931-54.
CLINICAL
Postsplenectomy
Penelope Jones
Karin Leder
Ian Woolley
infection
Paul Cameron
Allen Cheng
Strategies for prevention in general practice
Denis Spelman
reasons for surgical removal of the spleen are:

Background trauma (40%), haematological disorders and
The spleen plays a crucial role in human defence against infection. Patients who are
malignancies (35%), and incidental trauma at
asplenic or hyposplenic are at increased risk of severe sepsis due to specific organisms.
the time of intra-abdominal surgery (24%). Less
Overwhelming postsplenectomy infection (OPSI) has a mortality rate of up to 50%.
commonly, an asplenic state may occur in medical
Objective conditions such as coeliac disease or sickle cell
This article describes the causes of OPSI and provides strategies to reduce it. anaemia. Congenital asplenia is rare; screening
Discussion of family members is recommended in affected
Streptococcus pneumoniae is responsible for over 50% of cases of OPSI. Strategies to patients.
prevent OPSI include education; vaccination against S. pneumoniae, Haemophilus
influenzae type b, Neisseria meningitidis and influenza (annually); and daily antibiotics Overwhelming postsplenectomy
for at least 2 years postsplenectomy and emergency antibiotics in case of infection. infection
Asplenic patients should carry a medical alert and an up-to-date vaccination card. Patients who are asplenic or hyposplenic are at
Asplenic patients require specific advice around travel and animal handling as they are increased risk of severe sepsis due to specific
at increased risk of severe malaria, and OPSI (due to Capnocytophaga canimorsus) may
organisms. Overwhelming postsplenectomy
result from dog, cat or other animal bites. The Victorian Spleen Registry was established
infection (OPSI) is defined as ‘septicaemia and/or
to improve adherence to best practice preventive guidelines and thereby reduce the
meningitis, usually fulminant but not necessarily
incidence of OPSI.
fatal, occurring at any time after removal of the
Keywords: splenectomy; antibiotic prophylaxis; immunisation; patient education
spleen’.1 These septic episodes have a mortality
as a topic
of up to 50% and may be associated with
significant long term morbidity.1 Organisms that
< 0^0®
can cause OPSI include:
• Streptococcus pneumoniae (responsible for
# The spleen is the largest lymphatic organ over 50% of cases of OPSI1)
in the body and plays an important role • Haemophilus influenzae type b
in fighting infection. It works to remove • Neisseria meningitidis
micro-organisms and their products • Capnocytophaga canimorsus (acquired by dog
circulating within the bloodstream, or cat bites).
and to produce antibodies to enhance The annual and lifetime risk of OPSI for an
the immune response. The asplenic or asplenic patient varies between reports. An
hyposplenic state can be confirmed by the Australian study reported an incidence of 0.42
detection of Howell-Jolly bodies on a blood cases per 100 person years.2 Another shows that
film or by the demonstration of decreased 4.4% of children less than 16 years of age and
IgM memory B cells in the blood. 0.9% of adults develop postsplenectomy sepsis.3
The risk was assumed to be the greatest in the
Splenectomy is the most common cause of first 2 years after splenectomy; however, reports
asplenia. In patients on the Victorian Spleen indicate that the increased risk of OPSI is lifelong.
Registry, the authors have found the most frequent In a series of 77 OPSI cases, the majority occurred
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 6, JUNE 2010 383
s= sQ
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Table 1. Victorian Spleen Registry recommendations for the prevention of infection in asplenic or hyposplénie adults
and children aged >10 years of age (for children <10 years of age please refer to the Australian Immunisation Handbook11)
Vaccine Which Route Timing Revaccination
Pneumococcal Pneumococcal 23 valent 0.5 mL SC or IM >2 weeks before elective surgery, or First after 5 years It is safe
polysaccharide vaccine polysaccharide vaccine PPV23 7-14 days after emergency *
Second to give
(Pneumovax 23) splenectomy or before discharge these three
vaccines at
Patients previously given pneumococcal conjugate 7 valent vaccine see recommendations below the same
time
Haemophilus influenzae Hib 0.5 mL IM >2 weeks before elective surgery, or No booster required
type b (liquid PedvaxHIB, Hiberix) upper arm/thigh 7-14 days after emergency
splenectomy or before discharge
Meningococcal vaccines • Meningococcal C conjugate 0.5 mL IM >2 weeks before elective surgery, or No booster required
conjugate vaccine upper arm/thigh 7-14 days after emergency
• MenCCV (NeisVac-C, splenectomy or before discharge
Menjugate, Meningitec) Wait 6 months to administer
conjugate meningococcal vaccine
if polysaccharide vaccine was
administered first
Polysaccharide Then 6-8 weeks later: 6-8 weeks after MenCCV First after 5 years
• Meningococcal quadrivalent 0.5 mL SC
polysaccharide ACWY vaccine
4vMenPV (Mencevax ACWY)
Influenza vaccine 0.5 mL IM or Annually (pre-winter) Annually

deep SC
If the patient has a bleeding disorder and there is a concern about giving vaccinations, delay administration until corrected and contact the
Victorian Spleen Registry (email spleenregistry@alfred.org.au, telephone 03 9076 3828) or a hospital haematology department
Antibiotic - prophylaxis • Oral phenoxymethyl penicillin 250-500 mg twice daily, or amoxycillin 250-500 mg once daily
• Penicillin allergy: patient may have roxithromycin 150 mg once daily or erythromycin 250 mg twice daily
• Duration: immunocompromised patients - lifelong; otherwise healthy patients recommend daily antibiotics for at least 2 years
Antibiotic - emergency Emergency supply of antibiotic, irrespective of prophylaxis: all patients to have amoxycillin 3 g sachet, kept at home and taken if
fever occurs. Penicillin allergy: roxithromycin 300 mg/day or erythromycin 1 g four times per day - patients should initiate antibiotics
immediately and then seek medical advice as soon as possible
Pneumococcal • Pneumococcal conjugate 7 valent vaccine PCV7 (Prevenar) is recommended for asplenic children (<18 years). Currently there are
*vaccinations insufficient data to recommend PCV7 for adults
• If PCV7 has been given, the patient should receive the pneumococcal polysaccharide vaccine (Pneumovax 23) 6-8 weeks later
• Second *revaccination
: at age 65 years (50 years for Indigenous Australians), or at least 5 years after first revaccination if >65 years
Patient education Inform patients (and their families) of increased risk of bacterial infection and strategies to prevent these infections. Patients should not
worry about afebrile upper respiratory tract infection symptoms. Discuss OPSI, risk of tick and animal bites/scratches. Immunisation card,
information sheet, laminated health advice card, spleen alert card, fridge magnet and spleen registry details should be given to patient
Blood tests Full blood examination (FBE) and film - lack of splenic function shown by Howell-Jolly bodies on film and lowered IgM memory B cell
markers
Travel recommendations • Seek medical advice before travel

• Where malaria is endemic, antimalarials, insect repellent and barrier precautions should be recommended
• Ensure meningococcal vaccination is current for travel to high incidence countries
Alerts Patients should wear or carry a Medialert medallion or wallet card. Patient's medical notes should display medical alert sticker
Seek medical Possible symptoms of a serious bacterial infection include fever, shivers and/or vomiting. Patients with these symptoms should take
Postsplenectom
attention emergency antibiotics and should call a doctor or present to a local hospital emergency department
i-3
R
yinfection strategiesfor prevention ingeneral practice

ep
§
rintedfrom
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AUSTRALIANFAMILYPHYSICIANVOL.3
9,M
O.6
,JUNE2010
C L IN IC A L
3
385
CLINICAL Postsplenectomy infection - strategies for prevention in general practice
Why a spleen registry? Resources 9. Boone K, Watters D. The incidence of malaria

• Information for patients and GPs about the after splenectomy in Papua New Guinea. BMJ
The listed recommendations are lifelong. 1995;311:1273.
Victorian Spleen Registry: www.spleen.org.au
Unfortunately, most reports document suboptimal 10. Spickett GP, Bullimore J, Wallis J, et al. Northern
• To obtain a copy of the Victorian Spleen region asplenia register - analysis of first two
rates of adherence in this patient group.6
Registry annual newsletter please email years. J Clin Pathol 1999;52:424-9.
Reports proposed that a spleen registry may 11. Department of Health and Ageing and National
spleenregistry@alfred.org.au.
Health and Medical Research Council. The
result in improved adherence to recommended
Australian immunisation handbook. 9th edn, 2008.
guidelines.1,10 Authors Available at www.health.gov.au/internet/immu-
The Victorian Spleen Registry was established Penelope Jones RN, GradDipEpid, is Manager, nise/publishing.nsf/Content/78CDF41C283426A8C
Victorian Spleen Registry, The Alfred, Melbourne, A2574E40020CCAB/$File/handbook-9.pdf.
in 2003 at The Alfred Hospital in Melbourne,
Victoria. p.jones@alfred.org.au
Victoria. This was extended to a state wide
Karin Leder MBBS, FRACP, PhD, MPH, is Head,
service with support from the Victorian
Infectious Diseases, Epidemiology, Department of
Department of Human Services. The role of Epidemiology and Preventive Medicine, Monash
the registry is to ensure that patients, families University, Melbourne, Victoria
and carers have ready access to up-to-date Ian Woolley MBBS, FRACP, DTMH, is Deputy
recommendations for the prevention of OPSI. Once Director, Infectious Diseases Department, Monash
registered, patients receive a copy of the Victorian Medical Centre, Melbourne, Victoria
Spleen Registry recommendations (see Resources) Paul Cameron MBBS, PhD, FRACP, FRCPA, is
and educational resources. Patients also receive Clinical Immunologist, Infectious Diseases Unit,
The Alfred, Melbourne, Victoria
an annual reminder about vaccinations at the time
that the annual influenza vaccine is available. A Allen Cheng MBBS, FRACP, MPH, PhD, is
Associate Professor, Infectious Diseases,
web based online registration process is being
Epidemiology, Infectious Diseases Unit, The
developed and additional funding is being sought
Alfred, Department of Epidemiology and
to expand this service to become an Australia Preventive Medicine, Monash University,
wide service. Melbourne, Victoria.
Data from the Victorian Spleen Registry Denis Spelman MBBS, FRACP, FRCPA, MPH,
annual questionnaire in 2007 shows an overall is Head of Microbiology and Deputy Director,
59% adherence to antibiotics in the first 2 years Infectious Diseases Unit, The Alfred, Department
of Epidemiology and Preventive Medicine,
postsplenectomy and 84% adherence in the
Monash University, Melbourne, Victoria
trauma group. This is significantly better than
those achieved in published data.
Summary of important points References

1. Waghorn DJ. Overwhelming infection in asplenic
• Asplenic or hyposplenic patients are at
patients: current best practice preventive measures
increased risk of OPSI, which has a mortality are not being followed. J Clin Pathol 2001;54:214-
rate of up to 50%. 8.
2. Cullingford G, Watkins D, Watts A, et al. Severe
• S. pneumoniae is responsible for over 50% of late postsplenectomy infection. Br J Surg
cases of OPSI. 1991;78:716-21.
3. Holdsworth R, Irving A, Cuschieri A.
• Strategies to prevent OPSI include education;
Postsplenectomy sepsis and its mortality rate actual
vaccination against S. pneumoniae, H. versus perceived risks. Br J Surg 1991;78:1031-8.
influenzae type b, N. meningitidis and 4. Spelman D, Buttery J, Daley A, et al. Guidelines

for the prevention of sepsis in asplenic and hypos
influenza (annually); daily antibiotics for at plenic patients. Intern Med J 2008;38:349-56.
least 2 years postsplenectomy and emergency 5. EI-Alfy M, El-Sayed M. Overwhelming post-splenec
tomy infection: is quality of patient knowledge
antibiotics in case of infection. enough for prevention? Haematol J 2004;5:77-80.
• Asplenic patients should carry a medical alert 6. de Montalembert M, Lenoir G. Antibiotic pre
vention of pneumococcal infections in asplenic
and an up-to-date vaccination card.
hosts: admission of insufficiency. Ann Hematol
• Asplenic patients require specific advice 2004;83:18-21.
around travel and animal handling as they are 7. Therapeutic guidelines: antibiotic. Version 13.
Postsplenectomy prophylaxis, 2006;181.
at increased risk of severe malaria, and OPSI 8. Working party of the British Committee for
(due to C. canimorsus) may result from dog, cat Standards in Haematology Clinical Haematology
Task Force. Guidelines for the prevention and treat
or other animal bites. ment of infection in patients with an absent or
dysfunctional spleen. BMJ 1996;312:430-4. correspondence afp@racgp.org.au
386 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 6, JUNE 2010
CLINICAL
Hypoglycaemia in
Ching Luen Ng
nondiabetic patients
An evidence based approach
Hypoglycaemia is a medical emergency.

Background It signals an inability of the central
Hypoglycaemia can have serious consequences for patients. Hypoglycaemia in nondiabetic
nervous system to meet its energy needs.
patients is not a common condition, and is often a diagnostic challenge for general
Untreated, hypoglycaemia can result in
practitioners.
permanent neurologic damage and death.1
Objective Hypoglycaemia is a common complication
To search for evidence based guidelines on diagnosis and management of hypoglycaemia of drug treatment for diabetes mellitus.
in nondiabetic adult patients and to see how these guidelines can be applied in general
Reported severe hypoglycaemia ranged
practice.
from 62-320 episodes per 100 patient
Discussion years in patients with type 1 diabetes
The Endocrine Society clinical practice guideline 2009 recommends evaluation and mellitus,2,3 and 3-73 episodes per 100
management of hypoglycaemia only in patients in whom Whipple’s triad is documented: patient years in patients with type 2 4,5
symptoms and/ or signs of hypoglycaemia; low plasma glucose; and resolution of symptoms However, hypoglycaemia is an uncommon
and/or signs after plasma glucose returns to normal. The first step in evaluation is
condition in nondiabetic patients and
to pursue clinical clues to specific aetiologies, ie. drugs, critical illnesses, hormone
a diagnostic challenge for general
deficiencies and nonislet cell tumours. In a seemingly well individual, the differential
practitioners.
diagnosis of hypoglycaemic disorder narrows to drug induced hypoglycaemia; accidental,
surreptitious, or malicious hypoglycaemia; endogenous hyperinsulinism; and idiopathic
postprandial hypoglycaemia. When a spontaneous hypoglycaemic episode cannot be
observed, patients should be referred for a prolonged fasting test or a mixed meal test. Symptoms of hypoglycaemia can be divided into
two categories:
Keywords: hypoglycaemia
• neurogenic (autonomic), and
o • neuroglycopenic symptoms.6
Autonomic symptoms result from sympatho
adrenal discharge triggered by hypoglycaemia.
• Case study They include palpitations, tremor, anxiety,
Mr N is a retired businessman; he is 68 years of sweating, hunger and paraesthesias.6
age and in good health. He had breakfast at 7 Neuroglycopenic symptoms are caused by
am. At 10 am he had sudden onset sweating, compromised central nervous system function
palpitations and tremor. His wife gave him due to brain glucose deprivation. They include
a piece of bread and the symptoms subsided
weakness, fatigue, confusion, unusual or bizarre
within a few minutes. He attends a clinic on the
behaviour, seizures, focal neurologic deficit, and
same afternoon and his physical examination
coma.1'7 There are no genuine hypoglycaemic
is normal. Recent routine fasting blood glucose
disorders characterised solely by autonomic
and renal function tests were normal. The
working diagnosis is hypoglycaemia. Mr N asks, symptoms.8 Although some patients with
‘Doctor, my wife is a diabetic, and she suffers true hypoglycaemic disorder may experience
from hypoglycaemia occasionally. But I’m not a only autonomic symptoms initially, eventually
diabetic and take no antidiabetic medications, episodes of neuroglycopenia will also occur in
how come I have hypoglycaemia?’ subsequent attacks.8
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39' NO. 6' JUNE 2010 399
CLINICAL Hypoglycaemia in nondiabetic patients - an evidence based approach
Classification of hypoglycaemic and is observed more often in women, usually disorder in which autonomic and neuroglycopenic
disorders in adults in a health related occupation.8 Malicious symptoms develop postprandially, accompanied by
Traditionally hypoglycaemic disorders in hypoglycaemia15-17 is due to the malicious low plasma glucose.26 Various mechanisms have
nondiabetics are classified as: administration of insulin or hypoglycaemic agents been shown to cause this disease:
• postabsorptive (fasting) hypoglycaemia, or to others. • high insulin sensitivity
• postprandial (reactive) hypoglycaemia (ie. Insulinomas (pancreatic beta cell tumours) • an exaggerated insulin response, either
hypoglycaemia that occurs within 4 hours after are rare. The estimated incidence is 1 case related to insulin resistance or to increased
food ingestion).7 per 250 000 patient years.18 It is characterised glucagon-like peptide 1
This classification has been criticised for being by neuroglycopenia spells due to endogenous • renal glycosuria, and
unhelpful diagnostically8 For instance, some hyperinsulinaemic hypoglycaemia and occurs • defects in glucagon response.26
causes of hypoglycaemia can present with both primarily in a fasting state, and only occasionally A small case series suggested Helicobacter
postabsorptive and postprandial hypoglycaemia in a postprandial period.19 Diagnosis may require pylori gastritis may contribute to the occurrence
(eg. insulinoma). Other disorders can present with computerised tomography, ultrasonography or of idiopathic postprandial hypoglycaemia.27
erratically occurring symptoms independent of more sophisticated imaging and procedures in a Low carbohydrate/high protein diets, frequent
food ingestion (eg. factitious hypoglycaemia).8 specialist setting.9 feeding and avoidance of simple sugars are
A more useful approach for clinicians is a The noninsulinoma pancreatogenous commonly recommended to patients diagnosed
classification based on clinical characteristics7-10 hypoglycaemia syndrome is an endogenous with idiopathic postprandial hypoglycaemia.
(Table 1). People who appear healthy are likely to hyperinsulinaemia, characterised by attacks of The efficacy of dietary measures has not been
have different hypoglycaemic disorders from those neuroglycopenia, typically, but not invariably, established in controlled clinical trials.7,28
who are ill. Accidental, surreptitious, or malicious after a meal.20 The pathology is diffuse pancreatic In idiopathic postprandial syndrome,
hypoglycaemia; endogenous hyperinsulinism; and islet involvement with nesidioblastosis (islet autonomic symptoms (tremor, tachycardia,
idiopathic postprandial hypoglycaemia will usually hypertrophy, sometimes with hyperplasia, with sweating), appear 2-5 hours after a meal, with
cause hypoglycaemia without the patient appearing enlarged and hyperchromatic beta cell nuclei).21 normal plasma glucose concentration.29,30 There
ill. Hypoglycaemia due to critical illnesses, hormone Patients who have undergone Roux-en-Y is enhanced catecholamine release following
deficiency and nonislet cell tumours will usually gastric bypass for obesity may have endogenous a meal or enhanced sensitivity to normal
cause hypoglycaemic symptoms while the patient hyperinsulinaemic hypoglycaemia most often postprandial noradrenaline and adrenaline
appears ill. Drugs (including alcohol) can cause due to pancreatic islet nesidioblastosis.22 This release. This condition is also known as
hypoglycaemia in both healthy looking and ill condition usually also causes postprandial spells pseudohypoglycaemia.30
appearing clinical presentations.7-10 of neuroglycopenia. In the beta cells of the pancreas, proinsulin is
Drugs are the most common cause of Hypoglycaemia due to anti-insulin antibody cleaved into insulin and C peptide (biochemically
hypoglycaemia,11 with insulin and sulphonylureas is a rare disorder occurring primarily in people inert peptide fragment). Then insulin and C
being the most common of these.7 Many of Japanese or Korean ethnicity,23 often with a peptide are cosecreted from the pancreas in
other drugs have been reported to cause history of autoimmune disease. Symptoms occur equimolar quantities.31 The pattern of plasma
hypoglycaemia but this is usually based only on in the late postprandial period as insulin secreted insulin, C peptide, proinsulin, sulphonylurea
either low or very low quality evidence. Of the in response to the meal is bound to the circulating and anti-insulin antibody can help clinicians to
drugs available in Australia, only indomethacin, antibody, then the insulin dissociates from the differentiate various causes of hyperinsulinaemic
pentamidine and quinine have been associated antibody in an unregulated fashion.9 Whereas hypoglycaemia (Table 2).7
with hypoglycaemia; the evidence is of moderate most autoantibodies against the insulin receptor
Evidence based guidelines
quality.12 are antagonists and cause insulin resistance,
Accidental hypoglycaemia occurs when there some are agonists and cause hypoglycaemia.24 The author used the advanced search function of
are pharmacy errors (eg. wrongly dispensing a Mesenchymal tumours, hepatocellular MEDLINE with the keyword ‘hypoglycemia’ and
sulphonylurea for another medication), medical carcinoma, adrenocortical tumours, carcinoid the article filter set for only practice guidelines;
treatment errors or medication errors.13 An tumours, leukaemia and lymphomas are nonislet 26 items were retrieved. Article abstracts were
example is the outbreak in Singapore in 2008 cell tumours most commonly associated with scanned by the author: 11 were irrelevant and
of severe drug induced hypoglycaemia in 150 hypoglycaemia.1 An incompletely processed 14 were guidelines for diabetic patients only.
nondiabetic patients due to four brands of sexual insulin-like growth factor II (IGF-II) molecule, Only one was a guideline on hypoglycaemia in
enhancement drugs that were contaminated termed 'Big IGF-II', with decreased affinity to nondiabetic adults: ‘Evaluation and management
with glyburide.14 Factitious hypoglycaemia due IGF binding proteins has been established as of adult hypoglycemic disorders: an Endocrine
to surreptitious self administration of insulin or the cause of hypoglycaemia in some of these Society clinical practice guideline', published
hypoglycaemic agent is usually manifested by tumours.25 in 2009 by the Endocrine Society of the United
erratically occurring neuroglycopenic symptoms Idiopathic postprandial hypoglycaemia is a States of America.9 In the guideline there are
Hypoglycaemia in nondiabetic patients - an evidence based approach CLINICAL
healthy individuals as having hypoglycaemia.36,37

Table 1. Causes of hypoglycaemia in adults9,10
Recommendation 2
Well appearing individual Ill appearing individual
Recommendation 2 is to review the history,
• Drugs • Drugs physical findings, and all available laboratory data
- insulin or insulin secretagogue - insulin or insulin secretagogue seeking clues to specific disorders, eg. drugs,
- alcohol - alcohol critical illnesses, hormone deficiencies, nonislet
- other drugs - other drugs cell tumours.
• Accidental, surreptitious, or malicious • Critical illnesses Ill appearing patients presenting with
hypoglycaemia hypoglycaemia are usually managed in hospital.
- hepatic, renal, or cardiac failure
• Endogenous hyperinsulinism History, physical examination and review of
- sepsis
- insulinoma available laboratory data will usually provide
- inanition
clues to a cause of hypoglycaemia or exclude
- functional beta cell disorders • Hormone deficiency
(nesidioblastosis) hypoglycaemia caused by medications, critical
- cortisol
- noninsulinoma pancreatogenous illnesses, hormone deficiencies, or a nonislet
- glucagon and adrenaline (in cell tumour,9 which usually require little or no
hypoglycaemia
insulin deficient diabetes mellitus)
- postgastric bypass hypoglycaemia investigation. Recognition of the association
• Nonislet cell tumour
- insulin autoimmune hypoglycaemia of disease with hypoglycaemia will be most
important.8
- anti-insulin antibody
In a seemingly healthy individual presenting
- anti-insulin receptor antibody
with suspected hypoglycaemia, always look for
• Idiopathic postprandial hypoglycaemia
evidence of hypoglycaemia induced by drugs
or alcohol, even if there is no previous history
six recommendations relevant to hypoglycaemic Furthermore, when insulin secretion is increased of using a relevant drug (given the possibility
disorders in nondiabetic adult patients based on substantially (eg. after a glucose load) the of accidental, surreptitious, or malicious drug
either high or moderate quality evidence (Table antecubital venous plasma glucose concentration administration).7 Careful history taking is crucial
3). Seven relevant original articles listed in the can be as much as one-third lower than arterial for decision making. Among the plethora of
references of this guideline were also reviewed glucose concentrations (which are relevant to symptoms of hypoglycaemia, neuroglycopenic
looking for further evidence. maintain brain glucose metabolism).34 symptoms will be of utmost importance. Patients
Therefore it is not possible to state a single with only autonomic symptoms are unlikely to
Application of evidence based
plasma glucose concentration that unambiguously have true hypoglycaemic disorder. However,
guidelines in general practice
defines hypoglycaemia, hence the diagnosis of even one episode of neuroglycopenia, or single
In the Endocrine Society clinical practice guideline hypoglycaemia is most convincingly established severe adverse event (eg. loss of consciousness,
2009, recommendations 1, 2, 4 and 6 can be when based on Whipple’s triad: traumatic injury) attributable to hypoglycaemia,
applied to guide GPs to formulate diagnostic and • symptoms, signs or both consistent with warrants further investigation to confirm
management plans for hypoglycaemic disorders in hypoglycaemia Whipple’s triad.1,8,9 Timing and duration of
nondiabetic adults.9 • a low plasma glucose concentration, and symptoms, aggravating and relieving factors,
• resolution of those symptoms or signs after and exposure to any medications can greatly
Recommendation 1
the plasma glucose concentration is raised to assist in deciding whether the patient’s history
This recommendation discusses evaluating and normal level. is suggestive of hypoglycaemia or not. For those
managing hypoglycaemia only in patients in whom A normal plasma glucose level, reliably without a strong history of hypoglycaemia, other
Whipple’s triad7 is documented. obtained during the occurrence of spontaneous differential diagnoses need to be considered.
Hypoglycaemia manifestations are nonspecific, hypoglycaemic symptoms, eliminates the In a seemingly well individual, the differential
vary among different people, and can change possibility of a hypoglycaemic disorder; and no diagnosis narrows to drug induced hypoglycaemia;
from time to time in the same person.7 Although further evaluation is required.8 accidental, surreptitious, or malicious
symptoms of hypoglycaemia typically develop To diagnose hypoglycaemic disorders hypoglycaemia; endogenous hyperinsulinism; and
at mean plasma glucose concentration of accurately, hypoglycaemia should be documented idiopathic postprandial hypoglycaemia.7-10
approximately 3.0 mmol/L in healthy individuals, the by laboratory glucose measurement. Blood
Recommendation 3
glycaemic thresholds for response to hypoglycaemia glucose meters are unsuitable for the diagnosis
shift to lower plasma glucose concentrations of hypoglycaemia8,9 as meters may be unreliable The blood tests in this recommendation
in patients with recurrent hypoglycaemia.32,33 in the hypoglycaemic ranges;35 and may mislabel distinguish hypoglycaemia caused by endogenous
(or exogenous) insulin from that caused by other when they consult their GP after experiencing both, with plasma concentrations of glucose less
mechanisms. However, often patients are already suspected hypoglycaemia. To establish that a than 3.0 mmol/L, insulin of at least 3.0 mU/L
asymptomatic when they attend the clinic, so patient has fasting hypoglycaemia, a prolonged (18 pmol/L), C peptide of at least 0.6 pg/L (0.2
this is more applicable to emergency department fasting test is required.38 Similarly, a mixed nmol/L), and proinsulin of at least 5.0 pmol/L
settings. meal test is required to confirm postprandial document endogenous hyperinsulinism.9
hypoglycaemia.38 Since the prolonged fasting In summary, when a spontaneous
Recommendation 4
test may require fasting for up to 72 hours, this hypoglycaemic episode cannot be observed in
When a spontaneous hypoglycaemia episode test should be performed in hospital settings to a nondiabetic patient who complains of typical
cannot be observed, the recommendation is to mitigate the risks if hypoglycaemia develops.1 hypoglycaemic symptoms, they should be referred
formally recreate the circumstances in which The key pathophysiological feature of for a prolonged fasting test or mixed meal test to
symptomatic hypoglycaemia is likely to occur, endogenous hyperinsulinism is that insulin confirm Whipples’ triad and to confirm (or exclude)
ie. during a fast of up to 72 hours or after a secretion is inappropriately high when plasma endogenous hyperinsulinism and hypoglycaemia
mixed meal. glucose concentration is falling to hypoglycaemic induced by oral hypoglycaemic agents.
Often patients are already asymptomatic levels.9 The findings of symptoms, signs, or
Table 2. Biochemical pattern in patients with various causes of hyperinsulinaemic hypoglycaemia7
Insulin C Peptide Proinsulin Sulphonylurea Insulin antibody Diagnosis

t i i - - Exogenous insulin
t t t - - Insulinoma
t t t + - Sulphonylurea
t t t - + Autoimmune anti-insulin antibody
Table 3. Endocrine Society clinical practice guideline 20099 on evaluation and management of adult hypoglycaemic disorders in
people without diabetes mellitus
Recommendation Quality of evidence9
1 Evaluate and manage hypoglycaemia only in patients in whom Whipple’s triad is documented, ie: High
• symptoms, signs, or both, consistent with hypoglycaemia
• a low plasma glucose concentration, and
• resolution of those symptoms or signs after the plasma glucose concentration is raised
2 Review the history, physical findings, and all available laboratory data seeking clues to specific Moderate
disorders, ie:
• drugs
• critical illnesses
• hormone deficiencies
• nonislet cell tumours
3 When the cause of the hypoglycaemic disorder is not evident: Moderate
• measure plasma glucose, insulin, C peptide, proinsulin concentrations
• screen for oral hypoglycaemic agents, during an episode of spontaneous hypoglycaemia, and
• observe the plasma glucose response to IV injection of 1 mg glucagon
4 When a spontaneous hypoglycaemic episode cannot be observed formally recreate the Moderate
circumstances in which symptomatic hypoglycaemia is likely to occur
5 In a patient with documented fasting or postprandial endogenous hyperinsulinaemic Moderate

hypoglycaemia, negative screening for oral hypoglycaemic agents, and no circulating insulin
antibodies, conduct procedures for localising an insulinoma
6 Tailor treatment to the specific hypoglycaemic disorder, taking into account the burden of Moderate
hypoglycaemia on patient wellbeing and patient preferences
Hypoglycaemia in nondiabetic patients - an evidence based approach CLINICAL
investigation and management. Being familiar

with the classification of hypoglycaemic
disorders and the recommendations of evidence
based guidelines enables GPs to carry out
comprehensive initial evaluation and make
appropriate and timely referrals.
In the case of Mr N, there were no
neuroglycopenic symptoms and his symptoms
subsided too quickly (within a few minutes)
after taking a small quantity of food with
low glycaemic load, to suggest a genuine
hypoglycaemic disorder. Moreover, this was
only the first attack of such symptoms, and the
symptoms did not result in significant adverse
events and did not affect his daily activities.
Therefore, he does not currently warrant referral
for a mixed meal test. Indeed, the clinical
features were more compatible with idiopathic
postprandial syndrome. A reasonable approach
is to observe progress at this stage. Anxiety
disorders should be considered. Should he
develop neuroglycopenic symptoms or other
more typical features of a hypoglycaemic
disorder in future, he should then be referred for
further investigation and management.

• Hypoglycaemia typically presents with
autonomic and neuroglycopenic symptoms.
• Evaluation and management of
hypoglycaemia for nondiabetic patients
Figure 1. Approach to adult nondiabetic patients with hypoglycaemia in general practice9 should only be carried out in patients in
whom Whipple’s triad is documented.
• Initial evaluation of nondiabetic patients
Recommendation 5
excision to cure solitary insulinomas. However, with hypoglycaemia is to review the history,
This recommendation suggests conducting GPs can play a valuable role in managing physical findings, and all available laboratory
relevant investigations to confirm insulinoma in some disorders, ie. idiopathic postprandial data to seek clues to specific disorders, ie.
patients with documented fasting or postprandial hypoglycaemia or postgastric bypass drugs, critical illnesses, hormone deficiencies
endogenous hyperinsulinaemic hypoglycaemia hypoglycaemia, where dietary advice can assist and nonislet cell tumours.
(with negative screening for oral hypoglycaemic to manage daily work and activities.7,30 • In seemingly well individuals, the differential
agents and no circulating insulin autoantibodies). A diagnostic algorithm for hypoglycaemia in diagnosis of hypoglycaemic disorders narrows
This is more relevant to secondary and tertiary care nondiabetic adult patients in general practice can to drug induced hypoglycaemia; accidental,
settings. be formulated ( Figure 1 ). surreptitious, or malicious hypoglycaemia;
endogenous hyperinsulinism; and idiopathic
Recommendation 6 Conclusion postprandial hypoglycaemia.
Recommendation 6 is to tailor treatment to the The diagnosis of hypoglycaemic disorders in • When a spontaneous hypoglycaemic
specific hypoglycaemic disorder, taking into nondiabetic patients requires a high level of episode cannot be observed, recreate the
account the burden of hypoglycaemia on patient suspicion, careful patient assessment and circumstances by referral to hospital for a
wellbeing and patient preferences. methodical evaluation on the basis of well prolonged fasting test or a mixed meal test.
Most hypoglycaemic disorders need defined diagnostic criteria and guidelines. These tests can also confirm endogenous
specific specialist treatment, eg. surgical Some patients may need referral for further hyperinsulinism and hypoglycaemia induced by
19. Kar P Price P Sawers S, et al. Insulinomas may moglycaemic range. Practical Diabetes International
oral hypoglycaemic agents.
present with normoglycemia after prolonged 1998;15:133-4.
fasting but glucose-stimulated hypoglycemia. J Clin 38. Service FJ. Diagnostic approach to adults with
Author Endocrinol Metab 2006;91:4733-6. hypoglycaemic disorders. Endocrinol Metab Clin
Ching Luen Ng MBBS, FRACGP, FHKCFP, FHKAM, 20. Won JG, Tseng HS, Yang AH, et al. Clinical features North Am 1999;28:519-32.
is Associate Consultant, Department of Family and morphological characterization of 10 patients
with noninsulinoma pancreatogenous hypoglycaemia
Medicine, Kowloon West Cluster, Hospital syndrome. Clin Endocrinol (Oxf) 2006;65:566-78.
Authority, Hong Kong. chingluen@yahoo.com.hk. 21. Anlauf M, Wieben D, Perren A, et al. Persistent
hyperinsulinemic hypoglycemia in 15 adults with
Conflict of interest: none declared. diffuse nesidioblastosis: diagnostic criteria, inci
dence, and characterization of beta-cell changes. Am
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FOCUS Clots
Deep vein
Wai Khoon Ho
thrombosis
Risks and diagnosis
A Venous thromboembolism (VTE), comprising deep vein

Background thrombosis and pulmonary embolism (PE), is the third
Venous thromboembolism, comprising deep vein
commonest vascular disorder in Caucasian populations.1
thrombosis (DVT) and pulmonary embolism, is common in
In Australia, DVT alone (without concomitant PE) affects
Australia and is associated with high morbidity.
52 persons per 100 000 annually.2 Timely management of
Objective DVT is important as it is a common cause of morbidity.
This article provides a summary of the risk factors for Thromboses of the deep veins in the upper limbs and
DVT of the lower limb and discusses the diagnosis of
‘unusual sites’, such as mesenteric veins, constitute less
the condition using a diagnostic algorithm incorporating
than 10% of DVT cases.2 As they are uncommon, this article
clinical assessment, D-dimer testing and imaging studies.
focuses only on the risks and diagnosis of lower limb DVT.
It also briefly reviews the clinical significance of isolated
distal lower limb DVT and superficial vein thrombosis.
Deep vein thrombosis usually starts in the calf area.3 Most thrombi
Discussion confined to the deep veins below the popliteal trifurcation (distal
Many conditions in the lower limb mimic DVT. Diagnosing
DVT, Figure 1) probably resolve spontaneously without causing any
DVT on clinical grounds without objective testing is
symptoms. Distal DVT can extend to the popliteal and femoral veins
unreliable. Patients incorrectly diagnosed as having DVT
and other proximal veins. (Note that in some imaging reports, the
may be subjected to unnecessary anticoagulation and its
associated risks of bleeding. In contrast, there is a risk of term ‘superficial femoral vein’ is applied to that part of the femoral
thrombus extension and embolisation when DVT is missed vein between the popliteal vein and the confluence with the deep
or inappropriately treated. femoral vein.4 The superficial femoral vein is therefore a part of the
proximal deep venous system.)
Keywords: venous thrombosis; thrombophlebitis; risk
Most patients present with symptoms when there is proximal
factors
vein involvement. About 50% of patients with untreated
symptomatic proximal DVT develop symptomatic PE within 3 months.
Despite adequate treatment, DVT can recur. About 10% of patients
with symptomatic DVT develop severe post-thrombotic syndrome
within 5 years.3
Risk factors for VTE

Venous thromboembolism may be provoked by transient and
reversible clinical risk factors such as surgery or oestrogen exposure,
or long term and permanent factors, such as hemiparesis from stroke
(Table 1).5 In 25% of cases, no clinical cause can be ascertained
(idiopathic VTE).6
About 40-60% of VTE patients in Caucasian cohorts have
thrombophilia - a haemostatic disorder resulting in a thrombotic
tendency.7 This may be heritable (eg. factor V Leiden, prothrombin
gene mutation and deficiencies of protein C, protein S and
antithrombin),7 or acquired (eg. antiphospholipid antibodies).8
468 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 7, JULY 2010
Table 1. Clinical risk factors for venous
Inferior vena cava thromboembolism5
Strong clinical risk factors (odds ratio >10)
• Fracture of the hip or lower limb
Common iliac vein • Hip or knee replacement surgery
• Major general surgery
External iliac vein • Major trauma
Common femoral vein • Spinal cord injury
Moderate clinical risk factors (odds ratio 2-9)
Deep femoral vein • Arthroscopic knee surgery
• Hormonal therapy (eg. oral contraceptives, hormone
replacement therapy)
• Pregnancy - postpartum
Superficial femoral vein
• Paralytic stroke
• Previous venous thromboembolism
Great saphenous vein Weak clinical risk factors (odds ratio <2)
(superficial vein) • Immobilisation (eg. bed rest >3 days, air travel >8
hours)
• Pregnancy - antepartum
Popliteal vein
• Obesity
• Advancing age
Proximal veins
Assessment of the patient with
Distal veins
suspected DVT
Peroneal vein
The diagnosis without objective testing is unreliable as many
Anterior tibial vein common conditions, such as ruptured Baker cyst, haematoma
and venous insufficiency, mimic DVT. In primary care among
Posterior tibial vein adults with suggestive symptoms and/or signs, only 29% have
ultrasonographically proven DVT.21
To better evaluate the clinical probability of DVT before further testing,
scoring systems based on symptoms, signs and risk factors have been
developed. One such system is the modified Wells score (Table 3) which
categorises patients as likely to have DVT (score of 2 or more points) or
Figure 1. Schematic diagram of the deep venous system

not (<2 points).22 This score is reproducible and is used together with
of the lower limb laboratory and/or imaging studies in a diagnostic algorithm.
(Note that the superficial femoral vein - that portion of the
femoral vein between the popliteal vein and the confluence
Laboratory testing
with the deep femoral vein - is part of the proximal deep
D-dimer is a degradation product of cross linked fibrin in thrombi. It is
venous system4)
elevated in many conditions where fibrin is formed and then degraded,
including acute VTE (Table 4).23,24 Various D-dimer assays are now
The prevalence of thrombophilia varies greatly with ethnicity available. They vary in turnaround times and sensitivity and specificity.
(Table 2)7,9-13 In Caucasian populations, the most common heritable Enzyme linked immunosorbent assays (ELISAs) are the most sensitive
thrombophilic defects are factor V Leiden and prothrombin gene (sensitivity >90%) compared with the latex (sensitivity 80-85%) and
mutation but these are absent in Indigenous Australians without whole blood (sensitivity ~87%) agglutination assays.25 The specificity
Caucasian admixture10 and in east Asians.9 of the various assays differ, but in general, the clinical utility of the
Heritable thrombophilia increases the risk of a first VTE14 but does D-dimer assays in diagnosing DVT is limited by their low specificity and
not appear to be a major determinant of the risk of recurrence (Table low positive predictive value (Table 4). In contrast, a negative result
2).13,15-17 In contrast, the antiphospholipid syndrome is a strong risk (normal D-dimer) from a sensitive assay is useful to exclude DVT.
factor for first and recurrent VTE and warrants consideration of long D-dimer levels correlate with the size of the thrombus and clot
term anticoagulation.8,18-20 activity. The sensitivity of an assay may be diminished in cases of
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 7, JULY 2010 469
FOCUS Deep vein thrombosis - risks and diagnosis
Table 2. Thrombophilia: prevalence and risks of venous thromboembolism

Thrombophilia Prevalence in general Prevalence in VTE Odds of first Odds of recurrent
population7,9-11 patients7,12,13 VTE8,14 VTE13,15-18
Factor V Leiden 2.0-4.0% in Australia 10-20% 6.6 1.4
Absent in Indigenous
Australians
Prothrombin G20210A 2.0-3.2% in Australia 5-6% 2.8 1.2-1.7
Absent in Indigenous
Australians
Antithrombin 0.1-0.3% 1-2% 5.0 1.9-2.6
deficiency
Protein C deficiency 0.2-0.5% 2-3% 6.5 1.4-1.8
Protein S deficiency 0.2-0.5% 2-3% 1.6 1.0—1.4
Lupus anticoagulant 3-6% (depending on 6-17% (depending 11.1 2.3-8.5
Anticardiolipin assay and cut off values) on assay and cut off 3.2 (high titre
antibodies (aCL) values) aCL)
been validated in management studies (Table 5). Other methods such

Table 3. Modified Wells score for predicting
as computersied tomography (CT) and magnetic resonance imaging
probability of deep vein thrombosis22
(MRI) are generally limited by availability.28,29
Clinical characteristic1 *
Score
Active cancer (treatment ongoing, administered 1 Diagnostic algorithm
within previous 6 months or palliative) A patient with symptoms and signs consistent with DVT should be
Paralysis, paresis or recent plaster 1 assessed and the clinical (pretest) probability of acute DVT established
immobilisation of the lower extremities
by using a validated scoring system (Figure 2).22,26,30 Thereafter, if
Recently bedridden >3 days or major surgery 1
the clinical probability of DVT is low, a D-dimer assay should be
within previous 12 weeks requiring general or
performed. In the modified Wells score, a pretest probability less than
regional anaesthesia
2 (DVT unlikely) combined with a normal D-dimer assay result, reliably
Localised tenderness along the distribution of 1
the deep venous system excludes DVT without the need for imaging studies. If D-dimer is
Swelling of entire leg 1 raised, CUS is indicated.

A high pretest probability (DVT likely) should be followed up by
Calf swelling >3 cm larger than asymptomatic 1
side (measured 10 cm below tibial tuberosity) CUS. With an abnormal CUS, DVT is diagnosed. However, a normal
Pitting oedema confined to the symptomatic leg 1 CUS does not exclude DVT and then a D-dimer assay should be
performed. Anticoagulation can be withheld if the D-dimer result is
Collateral superficial veins (nonvaricose) 1
normal. In the event of a raised D-dimer, imaging should be repeated
Previously documented DVT 1
within 1 week (or earlier if symptoms are worsening) as isolated
Alternative diagnosis at least as likely as DVT -2
distal DVT that have been missed initially on CUS may extend into the
* A score of >2 indicates that the probability of DVT is proximal veins and be detected on repeated scanning.26,30 In patients
likely; a score of <2 indicates that the probability of
with unexplained swelling of the entire leg but having negative CUS,
DVT is unlikely
the possibility of pelvic vein thrombosis should be considered, in which
1 In patients who have symptoms in both legs, the more
symptomatic leg is used case, CT, MRI or venography may be indicated.30
Figure 2 simplifies the diagnostic process and reduces cost by
small, isolated DVT compared with large proximal thrombosis. Further, decreasing the number of patients undergoing both D-dimer testing
the passage of time and/or the administration of anticoagulation may and imaging studies while allowing room for the clinician to exercise
slow thrombus turnover thereby reducing assay sensitivity, hence, clinical judgment: in the event that confirmatory testing is delayed and
D-dimer testing may not be useful if a patient has already been the clinical suspicion of DVT remains high, empirical anticoagulation
effectively treated.23-26 (eg. low molecular weight heparin) should be started if there are
no contraindications. Note that this algorithm has been developed
Imaging studies
and validated for use predominantly in studies of outpatients. The
Compression ultrasonography (CUS) is the method of choice to evaluate D-dimer assay is frequently positive and has limited usefulness among
the lower limbs for DVT.23,26,27 It is simple, noninvasive and its use has inpatients (because of comorbidities) and pregnant women.26,30
Table 4. Limitations of the D-dimer assay in the Table 5. Imaging studies available for the diagnosis
evaluation of suspected deep vein thrombosis23,24 of deep vein thrombosis
Clinical situations other than acute VTE resulting in Compression ultrasonography27
raised D-dimer (potentially diminishing the specificity • Sensitivity and specificity exceed 95% and 98%
and positive predictive value of the test) respectively for symptomatic proximal DVT
• Surgery and/or trauma • Sensitivity of 11-100% and specificity of 90-100% for
• Haemorrhage and extensive bruises symptomatic distal DVT
• Ischaemic heart disease • Noninvasive: can be performed relatively rapidly
and a portable technique allowing for the bedside
• Cerebrovascular accident (stroke) assessment of critically Hl patients
• Infections • Does not visualise the pelvic veins well and cannot be
• Malignancy used in obese patients or in patients whose limbs are
• Peripheral arterial disease and aneurysms in plaster casts
• Pregnancy Computerised tomography28
• Advancing age of patients (ie. the very elderly) • Sensitivity and specificity of 96% and 95%
• Extensive burns respectively in a meta-analysis of studies
predominantly examining its use for the diagnosis of
Clinical situations resulting in a false-negative proximal DVT
D-dimer assay • Can visualise the pelvic veins, define the upper limit
• Small thrombus (eg. isolated distal deep vein of thrombus extension into the iliac veins and inferior
thrombosis) vena cava
• Time lag between symptom onset and laboratory • Requires the injection of contrast medium, exposes
testing the patient to radiation, may be difficult to interpret
• Concomitant anticoagulation (with heparin or when artefact and insufficient venous filling is
warfarin) present, and is more expensive than ultrasonography
• Limited by availability and technical expertise
Magnetic resonance imaging29
In pregnant women, if a DVT is suspected and initial CUS is negative,
• Sensitivity and specificity for the diagnosis of
repeat scanning in 5-7 days is indicated. If pelvic vein thrombosis is
symptomatic DVT is 96% and 93% respectively
suspected, then MRI is the investigation of choice;31,32 alternatives are
• Sensitivity for distal DVT is much lower (about 62%)
pulsed Doppler study of the iliac vein and CT venography.32
• Can be performed without the use of contrast
medium
Further assessment • Can visualise the pelvic veins, define the upper limit
Evaluation of clinical risk factors for VTE helps determine the duration of thrombus extension into the iliac veins and inferior
of anticoagulation.33 Venous thromboembolism provoked by a vena cava
transient, reversible cause has a low risk of recurrence and short term • Limited by availability and technical expertise
anticoagulation is generally required. If the cause is permanent and Venography (phlebography)27
irreversible (eg. hemiparesis from stroke), or if no provoking factor is • Reference standard technique
identifiable (idiopathic VTE), the risk of recurrence is higher and longer • Reliably detects isolated distal DVT and thrombosis
term anticoagulation may be indicated. in the iliac veins and inferior vena cava
Laboratory testing for heritable thrombophilia among unselected • Cumbersome to perform, requires the injection of
patients is generally not indicated as results do not influence patient
contrast medium, exposes the patient to radiation,
may be difficult to interpret when insufficient venous
management.20,33-35 As long term anticoagulation may be warranted
filling is present
in the antiphospholipid syndrome, testing for lupus anticoagulant
and anticardiolipin and anti-R2 glycoprotein I antibodies should be 0-29%.30 One review estimated that 25% of untreated cases extended
considered in apparently idiopathic cases or among patients with proximally within a week.3
concomitant connective tissue disorder, previous arterial thromboses At diagnosis, up to 40% of cases of symptomatic isolated distal
(eg. stroke or myocardial infarction) particularly if premature, and/or a DVT can have coexisting symptomatic PE.36 Among those with
history of recurrent pregnancy failure or fetal death.19,20 untreated distal DVT, 6.3% developed symptomatic PE within 7 days.37
Because of the variable risk of extension and/or embolisation, the
Isolated distal DVT optimal management of symptomatic distal DVT is uncertain38 but
The risk of symptomatic isolated distal DVT extending into the proximal some authors suggest that anticoagulation for 6 weeks to 3 months
veins if untreated or inadequately managed varies and ranges from is generally adequate.39-41
Deep vein thrombosis - risks and diagnosis FOCUS
Figure 2. Diagnostic algorithm for clinically suspected deep vein thrombosis26,30

CUS = compression ultrasound scan; +ve = positive; -ve = negative
Routine screening of the asymptomatic postoperative patient for Summary of important points
DVT is unwarranted.33 However, if isolated asymptomatic distal DVT • Diagnostic algorithms incorporating clinical assessment, D-dimer
is found incidentally, it is reasonable to withhold anticoagulation testing and imaging studies have been developed and validated for
as many of these thrombi resolve spontaneously and do not cause use in diagnosing DVT.
clinically significant PE.3,42,43 If anticoagulation is withheld, repeat • Anticoagulation is generally indicated in symptomatic lower limb
testing within the next 10 days should be considered to determine if
DVT. This includes thrombosis in the superficial femoral vein, which
the thrombus has extended.44 Repeat testing is also indicated if the
despite its name, is part of the proximal deep venous system.
patient becomes symptomatic.
• The duration of anticoagulation is largely determined by the
Superficial vein thrombosis site of thrombosis and clinical risk factors; testing for heritable
thrombophilia does not generally influence management of the
Concomitant DVT is observed in 2.6-65% of cases of superficial vein
patient and is not warranted.
thrombosis (SVT) whereas symptomatic PE is present in 0.5-4.0%.45 In
case series involving >15 patients with untreated SVT, DVT and/or PE Author
occurred in 1.7% to >11% within 3 months.45,46 Wai Khoon Ho MMedSc, FRACP, FRCPA, is Consultant Haematologist,
Ultrasonography should be performed in cases of SVT to confirm Department of Haematology, Austin Health, Melbourne, Victoria.
the diagnosis and establish its extent, and to look for the presence wai.ho@austin.org.au.
of concomitant DVT. Where the proximal extent of SVT is close to
the sapheno-femoral or sapheno-popliteal junction, some authors
recommend the institution of anticoagulation due to the presumed high Acknowledgment
risk of DVT and/or PE.45,46 I thank Mr Stephen Valentine for the illustration in Figure 1.
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38. Righini M, Paris S, Le Gal G, Laroche JP, Perrier A, Bounameaux H. Clinical
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10. Bennett JA, Palmer LJ, Musk AW, Erber WN. Prevalence of factor V Leiden Haemost 2006;95:56-64.
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41. Pinede L, Duhout P, Chabaud S, et al. Comparison of 3 and 6 months of oral
13. Baglin T, Luddington R, Brown K, Baglin C. Incidence of recurrent venous
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14. Van der Meer FJM, Koster T, Vandenbroucke JP, Briët E, Rosendaal FR. The
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18. Zhu T, Martinez I, Emmerich J. Venous thromboembolism: risk factors for
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22. Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the diagno
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23. Palareti G, Cosmi B, Legnani C. Diagnosis of deep vein thrombosis. Semin
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26. Tan M, van Rooden CJ, Westerbeek RE, Huisman MV. Diagnostic manage
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analysis. Clin Radiol 2008;63:299-304. correspondence afp@racgp.org.au
FOCUS Clots
Pulmonary embolism
Simon McRae
ft More than 150 years after the first Virchow description

Background of his triad of risk factors for venous thromboembolism
Pulmonary embolism remains a common and potentially
(VTE), pulmonary embolism (PE) remains an important
preventable cause of death.
preventable cause of morbidity and mortality. It was
Objective estimated that in 2008 there were approximately
This article reviews the epidemiology, clinical features, 15 000 episodes of VTE in Australia, a substantial
diagnostic process, and treatment of pulmonary embolism. proportion of which were PE.1 Both the diagnosis and
Discussion initial management of PE still largely take place within
Well recognised risk factors include recent hospitalisation, the hospital setting. However an understanding and
other causes of immobilisation, cancer, and oestrogen awareness of PE by the primary care clinician remains
exposure. Diagnostic algorithms for pulmonary embolism important, due to the need for a high diagnostic suspicion
that incorporate assessment of pretest probability and of PE to enable prompt recognition of a potentially
D-dimer testing have been developed to limit the need fatal disease and also the increasing tendency for early
for diagnostic imaging. Anticoagulation should be
discharge of patients being treated for PE.
administered promptly to all patients with pulmonary
embolism with low molecular weight heparin being the Epidemiology
initial anticoagulant of choice, although thrombolysis is
indicated for patients presenting with haemodynamic Venous thromboembolism, consisting of both deep vein thrombosis
compromise. Following initial anticoagulation warfarin (DVT) and PE, has an annual incidence in Caucasian populations of
therapy should be continued for a minimum of 3 months. approximately 1.5 per 1000,2,3 with the incidence increasing with
Long term anticoagulation with warfarin should be age. Approximately 30-40% of patients with VTE will present with
considered in patients with unprovoked pulmonary symptomatic PE.2,3
embolism, due to an increased risk of recurrence Pulmonary embolism will be fatal in up to 25% of patients
after ceasing anticoagulation. The availability of new in whom the diagnosis has been made if left untreated,4 with
anticoagulants is likely to significantly impact on the anticoagulation substantially reducing the risk of fatal PE during
treatment of patients with pulmonary embolism, although the initial treatment period to less than 2%.5 However, in up to
the exact role of these drugs is still to be defined.
25% of individuals with PE the initial presentation will be sudden
Keywords: pulmonary embolism; risk factors; fibrin death before therapy can be initiated.6 The risk of death in patients
fibrinogen degradation products with confirmed PE who have been treated with anticoagulation at 3
months postdiagnosis is approximately 10-15%,7,8 with the majority
being due to comorbid conditions.
Risk factors for pulmonary embolism

There are a number of well defined risk factors for PE (Table 1), the
presence of which will raise the level of diagnostic suspicion in
patients with suggestive symptoms.
Recent hospitalisation
Venous thrombosis occurring after recent hospitalisation accounts
for approximately 50% of cases,6 with recent surgical and medical
admissions accounting for an equal proportion of events. There
is an approximate seventyfold increase in risk of VTE following
inpatient surgery, and a tenfold increase in risk following day
surgery, despite modern surgical practice.9 The risk is maximal at
Table 1. Risk factors for venous thrombosis Extended travel
Much publicity has been given to air travel as a risk factor for VTE.
Recent surgery
However in a recent large cohort study less than 2% of individuals
Joint replacement, cancer surgery, fracture, major
with venous thrombosis had undertaken a prolonged flight within the
gastrointestinal surgery, gynaecological surgery
8 weeks before diagnosis.18 Flights shorter than 4 hours do not appear
Inpatient day surgery
to be associated with any increase in risk of venous thrombosis, with
Acute medical illness
flights between four and 8 hours in duration associated with a twofold
Congestive cardiac failure, acute respiratory failure
increase in the risk of VTE, and flights more than 12 hours a fivefold
Inflammatory conditions (eg. inflammatory bowel risk increase.19 The magnitude of the increase in risk is therefore
disease, rheumatological disease)
substantially less than that associated with recent surgery. While there
Malignancy
is less data, the risk of venous thrombosis with travel of the same
Increased by chemotherapy, hormone therapy, surgery
duration by other modes of transport, including car and rail, appears
Hormonal risk factors similar to that associated with flying.20
Oral contraceptive use, hormone replacement therapy
Pregnancy Other risk factors
Miscellaneous Comorbid medical conditions that have been demonstrated to be
Increased body mass index risk factors for pulmonary embolism include cardiac failure, acute
Prolonged travel or chronic respiratory failure, acute rheumatological disease, acute
Heparin induced thrombocytopenia infection, inflammatory bowel disease, and increased body mass
Antiphospholipid antibody syndrome index.21,22 Recent data suggests that smoking is associated with a
Inherited risk factors 1.5 fold increase in the risk of venous thrombosis.23
‘Strong’ - antithrombin, protein C + S deficiency

Clinical presentation of pulmonary
‘Moderate’ - factor V leiden and prothrombin gene
mutations
embolism
Pulmonary embolism is usually suspected due to acute onset new, or
3 weeks following surgery and remains elevated for up to 12 weeks. worsening, shortness of breath or chest pain. Dyspnoea is present in
Therefore the majority of cases of PE related to surgery will occur 70-80% of patients with confirmed PE,24-26 with chest pain present
following hospital discharge. in 60-70% of cases. Between 10-20% of patients with confirmed PE
report haemoptysis.25,26 Symptoms at presentation vary according to
Cancer thrombus location, with patients with larger pulmonary emboli more
Patients with cancer make up 15-20% of patients with VTE.10 The likely to present with isolated dyspnoea (25% of cases), and those with
risk of venous thrombosis in patients with cancer is increased with more peripheral emboli causing pulmonary infarction with pleuritic
the administration of chemotherapy, hormone therapy and surgical chest pain +/- haemoptysis (60% of cases).26 Five to 8% of patients
procedures.11 Malignancies with a high risk of venous thrombosis with PE who survive long enough to have a diagnostic evaluation,
include brain, ovarian and pancreatic cancer.10 will present with circulatory collapse, as defined by a systolic blood
pressure of <90 mmHg.25,27 A proportion of these patients will not have
Oral contraceptive pill use and pregnancy
symptoms of chest pain nor dyspnoea.25
The use of currently available combined oral contraceptive preparations Clinical features shown to be predictive for the presence of PE
is associated with a 2-7 fold increase in the risk of VTE.12,13 The include concurrent symptoms of DVT, a history of syncope, presence
magnitude of the increase in risk varies according to the type of of pleuritic chest pain, tachypnoea and tachycardia.28,29 However the
progesterone, being lowest with second generation preparations (2-4 presence or absence of any single symptom or sign cannot be used to
fold increase in risk), and higher with either third generation pills or confirm or refute the diagnosis. This fact, along with the consequences
preparations containing cyproterone or drospirenone (4-7 fold increase of a missed diagnosis, mean that the threshold for initiating further
in risk).12,13 Due to the low background annual incidence of VTE in investigation in patients presenting with symptoms known to be
women of reproductive age (~1 in 10 000),14,15 the absolute risk in oral associated with PE, particularly in the absence of an alternative
contraceptive users is still low, being less than 0.1% per year. explanation, should be low.
The incidence of VTE during pregnancy and the postpartum
period is approximately 1 in 1000, ie. approximately tenfold of that in
Diagnostic algorithms for pulmonary
nonpregnant women of similar age. The risk of PE is highest during the
embolism
4-6 weeks postpartum, with more than 50% of episodes of pregnancy The incidence of confirmed PE in patients undergoing investigation has
related PE occurring during this time period.16,17 fallen over time to a current figure of approximately 20%.30
FOCUS Pulmonary embolism
Given that the majority of patients will not have confirmed PE,
diagnostic algorithms have been developed to safely exclude PE while
limiting the need for diagnostic imaging.
Clinical prediction rules for pulmonary

embolism
Experienced clinicians are able to accurately stratify the probability of
PE using unstructured clinical assessment.31 Clinical prediction rules
have been developed to formalise this process, with the assessment
of pretest probability being used to guide further diagnostic testing
(Figure 1).30 The most widely used prediction rule for PE is the Wells
score, in which points are given according to the presence or absence
of risk factors for, and symptoms and signs of, PE (Table 2).32 A
simplified version classifying patients as either PE unlikely (prevalence
of PE 12%) or PE likely (prevalence of PE 47%) is optimal for helping to
exclude PE without diagnostic imaging.33
D-dimer testing *Assess pre-test probability according to simplified Wells score (Table 2)
**Algorithm applies if D-dimer test used is a high sensitivity test (eg.
D-dimer, a degradation product of cross-linked fibrin, is a highly sensitivity >95%)
sensitive test for recent VTE.34 A negative D-dimer test can be used to + VQ scanning can be used as an alternative imaging test in patients
help exclude PE in patients with a low pretest probability. In patients with renal impairment or in whom there are concerns regarding
radiation exposure (eg. young women, particularly during pregnancy).
classified as PE unlikely with a negative highly sensitive D-dimer test, If CTPA is technically inadequate VQ scanning can also be performed
the probability of PE is sufficiently low (<1%) to exclude the diagnosis
without further testing.35 In patients classified as PE likely, the Figure 1. Diagnostic algorithm for the diagnosis of
pulmonary embolism
prevalence of PE in patients with a negative D-dimer is still ~10%.30
Therefore patients in the latter category should proceed directly to
diagnostic imaging without D-dimer testing being performed (Figure 1).
associated with an intermediate probability of PE (10-40%) and further
Diagnostic imaging for pulmonary embolism imaging, normally CTPA, is therefore required.
Computerised tomographic pulmonary angiography (CTPA) has become Ultrasound of the lower limbs can be used as an initial
the most widely used radiological investigation for suspected PE. investigation, particularly where there are concurrent symptoms
Modern multidetector CTPA is highly sensitive for PE, with a single suggestive of DVT. The finding of DVT justifies commencement of
negative study having been shown to safely exclude PE.35,36 A filling anticoagulation, although further investigation is still required if no
defect within a segmental or more proximal vessel confirms PE and evidence of DVT is found. This strategy is useful where there are
justifies commencing therapy. An additional benefit of CTPA is that concerns regarding radiation exposure, such as during pregnancy.
alternative diagnoses will also be detected. Downsides include the
detection of small subsegmental emboli, for which the need for
Limitations of diagnostic algorithms in the
anticoagulation remains unclear, contrast complications, and concerns
primary care setting
regarding the degree of radiation exposure and the subsequent The majority of studies evaluating diagnostic algorithms for PE have
increase in the risk of breast cancer, particularly in women of been performed in the emergency department setting. The Wells score
reproductive age.37 requires the clinician to make a judgment regarding the likelihood of
Ventilation perfusion (VQ) scanning remains an alternative method PE in comparison to alternative explanations, which in most studies
of imaging for PE, particularly in individuals without pre-existing was guided not only by clinical symptoms and signs but also initial
lung disease in whom the incidence of nondiagnostic results is investigations such as chest X-ray and electrocardiogram. Caution
decreased.30 It has the advantage over CTPA of not requiring contrast should therefore be applied in applying diagnostic algorithms for PE
exposure, and therefore is the investigation of choice in patients with when the patient is assessed solely in the primary care setting, and
renal impairment. Breast radiation exposure is also substantially prompt evaluation of such patients in an emergency department,
reduced with VQ scanning in comparison to CTPA, and therefore it particularly in those with a high pretest probability, is recommended.
should be considered as a first line investigation for PE in women of If there is likely to be a substantial delay in definitive investigation, an
reproductive age. A normal VQ scan can be used to exclude PE, while initial therapeutic dose of low molecular weight heparin (LMWH) is
a high probability scan justifies anticoagulation. All other results are warranted in the absence of contraindications.
Pulmonary embolism FOCUS
Table 2. Simplified Wells pulmonary embolism score The role of thrombolytic therapy
Thrombolysis is accepted as being indicated in patients with PE who
Variable Points
present with haemodynamic instability (systolic BP <90 mmHg), due
Clinical signs and symptoms of deep vein 3.0 to a high fatality rate with standard anticoagulant therapy. It has
thrombosis been proposed that patients without haemodynamic compromise with
(minimum of leg swelling and pain on markers of poor prognosis present, such as right ventricular dilatation
palpation of the deep veins)
or elevated troponin, should also be considered for thrombolytic
Alternative diagnosis less likely than 3.0 therapy.42 There are however, no randomised studies that clearly
pulmonary embolism demonstrate that early thrombolysis improves survival in this subgroup
Heart rate >100 bpm 1.5 of PE patients, provided that rescue thrombolysis can be administered
Immobilisation (>3 days) or surgery within the 1.5 in the event of clinical deterioration.
previous 4 weeks
Duration of anticoagulation
Previous pulmonary embolism or deep vein 1.5
thrombosis After the initial treatment period with LMWH, warfarin is usually
used for continued anticoagulation, with a recommended target
Haemoptysis 1.0
International Normalised Ratio (INR) of 2.0-3.0. A minimum of 3 months
Malignancy (receiving treatment, treated in 1.0 anticoagulation is recommended in patients with symptomatic PE, as the
last 6 months or palliative)
risk of recurrent thrombosis is increased in patients receiving a shorter
Clinical probability of PE unlikely: score <4 points duration of therapy. The strongest predictor of the risk of recurrent
Clinical probability of PE likely: score >4 events is the circumstances at the time of the initial event.43 In patients
with PE associated with a definite provoking risk factor, such as recent
major surgery, the risk of recurrence is generally low, and 3-6 months
Treatment of anticoagulant treatment is sufficient. In patients with unprovoked
Anticoagulation has been the mainstay of treatment for PE since PE the recurrence risk is higher, and long term anticoagulation may be
the study of Barritt and Jordan,4 in which 25% of patients receiving indicated. This particularly applies if additional prognostic factors known
placebo died of recurrent PE, with all patients treated with to be associated with an increased recurrence risk including male gender,
anticoagulant therapy surviving. antithrombin, protein C and protein S deficiency or antiphospholipid
antibody syndrome are present. The decision regarding the duration of
Choice of initial anticoagulant anticoagulation in such patients should be made in conjunction with a
Due to the delay in therapeutic effect of warfarin, initial treatment specialist with an interest in venous thrombosis.
with a parenteral anticoagulant is necessary in patients with acute
PE. Subcutaneous weight based LMWH has been found to be at Conclusion
least as effective and safe as intravenous unfractionated heparin in Pulmonary embolism remains a potentially fatal disease for which
the treatment of PE,38 and has the additional benefit of not requiring a high diagnostic suspicion must be maintained. The future is likely
therapeutic monitoring, therefore it can be administered at a fixed to see improved strategies for risk stratification of patients with PE,
weight based dose. Low molecular weight heparin is therefore usually identifying low risk patients able to be managed as outpatients and
the agent of choice for initial treatment of PE. Unfractionated heparin high risk patients likely to benefit from more aggressive intervention.
is still preferred in patients with significant renal impairment, due to The emergence of new oral anticoagulants, such as the direct thrombin
the renal clearance of LMWH, and is also recommended in unstable inhibitor dabigatran44 and the factor Xa inhibitor rivaroxaban,45
patients in whom thrombolytic therapy may still be considered. that have the potential to be used for both initial and long term
anticoagulation without the need for therapeutic monitoring, is likely
Inpatient versus outpatient therapy to simplify management of patients with venous thrombosis. The exact
The ability to give LMWH subcutaneously has meant that outpatient role of these agents is however, still to be determined, and will be
therapy of PE is now theoretically possible. There is limited influenced by drug cost, which in turn will influence any restrictions
observational data supporting the safety of this approach in low that are placed on drug availability.
risk patients with PE.39,40 Tools have been developed to identify a
low risk subgroup of patients with PE potentially best suited for Author
Simon McRae MBBS, FRCPA, FRACP, is Consultant Haematologist,
outpatient therapy.41 However, the safety of inpatient versus complete
Department of Haematology, South Australia Pathology, Royal Adelaide
outpatient therapy has not yet been examined in randomised trials, and Hospital, South Australia. simon.mcrae@health.sa.gov.au.
therefore at least a short period of initial inpatient evaluation is still
recommended for patients with PE until such trials are performed. Conflict of interest: none declared.
FOCUS Pulmonary embolism
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3. White RH. The epidemiology of venous thromboembolism. Circulation sis of acute pulmonary embolism: systematic review and meta-analysis. Q J
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4. Barritt DW, Jordan SC. Anticoagulant drugs in the treatment of pulmonary 30. Huisman MV, Klok FA. Diagnostic management of clinically suspected acute
embolism: a controlled trial. Lancet 1960;1:1309-12. pulmonary embolism. J Thromb Haemost 2009;7(Suppl 1):312-7.
5. Douketis JD, Kearon C, Bates S, et al. Risk of fatal pulmonary embolism in 31. Chunilal SD, Eikelboom JW, Attia J. Does this patient have pulmonary embo
patients with treated venous thromboemblism. JAMA 1998;279:458-62. lism. JAMA 2003;290:2849-58.
6. Heit JA. Venous thromboembolism: disease burden, outcomes and risk 32. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical
factors. J Thromb Haemost 2005;3:1611-7. model to categorize patients’ probability of pulmonary embolism: increas
7. Conget F, Otero R, Jiménez D, et al. Short-term clinical outcome after acute ing the model’s utility with the SimpliRED D-dimer. Thromb Haemost
symptomatic pulmonary embolism. Thromb Haemost 2008;100:937-42. 2000;83:416-20.
8. PIOPED investigators. Value of ventilation/perfusion scan in acute pulmonary 33. Gibson NS, Sohne M, Kruip MJ, et al. Further validation and simplification
embolism: results of the prospective investigation of the pulmonary embolism of the Wells clinical decision rule in pulmonary embolism. Thromb Haemost
diagnosis (PIOPED). J Am Med Assoc 1990;263:2753-9. 2008;99:229-34.
9. Sweetland S, Green J, Liu B, et al; Million Women Study collaborators. 34. Adam SS, Key NS, Greenberg CS. D-dimer antigen: current concepts and
Duration and magnitude of the postoperative risk of venous thromboembo future prospects. Blood 2009;113:2878-87.
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10. Lee AYY. Management of thrombosis in cancer: primary prevention and sec pected pulmonary embolism using an algorithm combining clinical probability,
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11. Heit JA, Silverstein MD, Mohr DN, et al. Risk factors for deep vein thrombo 36. Perrier A, Roy PM, Sanchez O, et al. Multidetector-row computed tomography
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1997;112:974-9. correspondence afp@racgp.org.au
focus Traps for the unwary
Addison disease
Susan O’Connell
Aris Siafarikas
Diagnosis and initial management
# Primary adrenal insufficiency was first described

Background
Adrenal insufficiency is a rare disease caused by either by the English physician Thomas Addison in 1855.1
primary adrenal failure (Addison disease) or by impairment Addison disease is a rare condition with an estimated
of the hypothalamic-pituitary-adrenal axis. Steroid prevalence of 4-11 per 100 000 and an incidence of 0.8
replacement therapy normalises quality of life, however, per 100 000 population/year.2,3 In children, boys constitute
adherence can be problematic. approximately 75% of patients in contrast to adults, where
the majority (70%) are women.4 The underlying pathology is
Objective
This article provides information on adrenal insufficiency a destruction of the cortex of the adrenal gland.5 Secretion
focusing on awareness of initial symptoms and on of cortisol is reduced or absent, with or without associated
risk scenarios, emergency management and baseline reduction or absence of aldosterone. Adrenocorticotrophic
investigations, complete investigations and long term hormone (ACTH) levels are increased.2
management.
Historically, tuberculosis was the most common cause of Addison
Discussion
Early recognition of adrenal insufficiency is essential disease.4,5 Today however, 70-80% of all cases of Addison disease
to avoid associated morbidity and mortality. Initial in the Western world are due to autoimmune adrenalitis;4,6 whereas
diagnosis and decision to treat are based on history and worldwide infectious diseases - such as tuberculosis,7 fungal
physical examination. Appropriate management includes infections (histoplasmosis, cryptococcus), and cytomegalovirus - are
emergency resuscitation and steroid administration. Initial still important causes. Acute haemorrhage (ie. in meningococcal
investigations can include sodium, potassium and blood septicaemia) although uncommon, is also a cause of primary adrenal
glucose levels. However, complete investigations can be insufficiency.5
deferred. Specialist advice should be obtained and long Overall, Addison disease in the paediatric population is most
term management includes a Team Care Arrangement. For commonly attributed to primary adrenal insufficiency, which occurs in
patients, an emergency plan and emergency identification
approximately one in 15 000 births and usually presents in the neonatal
are essential.
period or early childhood.8 Ninety-five percent of cases are due to
Keywords: Addison disease; diagnosis, differential; deficiency of an enzyme (21 hydroxylase) involved in the steroidogenesis
fludrocortisone; hydrocortisone; patient care planning pathway, which also results in impaired aldosterone synthesis. In
SgB o contrast to Addison disease, the adrenal cortex is not destroyed and
hence increased ACTH stimulation causes adrenal hyperplasia.5
Concomitant autoimmune disease is seen in 50% of patients with
Addison disease. These include thyroid disease, hypoparathyroidism
and type 1 diabetes mellitus.5 More complex associations can be found
in two recognised polyglandular autoimmune syndromes (PGA).5,8,9
Secondary forms of adrenal insufficiency, characterised by low
ACTH levels, are caused by hypopituitarism due to pituitary disease,
or suppression of the hypothalamo-pituitary-adrenal axis (HPA)
following steroid therapy or endogenous steroid excess (ie. tumour).
The role of inhaled steroids is controversial. It has been suggested
that therapy with more than 800 pg/day over a prolonged period of
time might result in HPA suppression.10
In secondary adrenal insufficiency, secretion of aldosterone is
not affected. However, with acute hypopituitarism, other hormone
834 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 11, NOVEMBER 2010
deficiencies including growth hormone, thyroxine, oestradiol or What should I do?
testosterone, must be identified and treated. In every scenario the initial diagnosis of acute adrenal insufficiency
and decision to treat are based on history, physical examination, and
When should I consider an adrenal occasionally, laboratory findings (hyponatraemia, hyperkalaemia,
crisis? hypoglycaemia).12 Delay in treatment while attempting to confirm
Adrenal crisis is a medical emergency and should be considered in any this diagnosis can result in poor outcomes and must be avoided
patient presenting with one or more of the following symptoms: (Table 1).13
• altered consciousness
• circulatory collapse
Management of adrenal crisis
• hypoglycaemia This is a medical emergency.12,13 Acute management is based
• hyponatraemia on emergency resuscitation: restoring and maintaining circulation,
• hyperkalaemia administration of IV hydrocortisone, detection and treatment of
• seizures hypoglycaemia, and identification and treatment of precipitating
• history of steroid use/withdrawal, or causes. A specialist should be contacted early. In many cases
• any clinical features of Addison disease. admission to an intensive care unit will be required.12,13
Adrenal crisis may be precipitated by stress, sepsis, dehydration or
trauma; clinical features may be modified accordingly. In patients with
Management of the subacute or chronic
known adrenal insufficiency, nonadherence with therapy, inappropriate
presentation
cortisol dose reduction or lack of stress related cortisol dose In most cases patients are cardiovascularly stable. Electrolyte
adjustment can cause adrenal crisis.11 imbalances and hypoglycaemia can be present. Therapy will focus
on steroid replacement and fluid resuscitation. Basic laboratory
When should I consider Addison investigations include sodium, potassium and blood glucose levels.
disease? Urea, creatinine, calcium and full blood count can be added to
Addison disease can manifest with adrenal crisis. Chronic symptoms specify underlying causes. Referral to an endocrinologist for further
result from cortisol deficiency, aldosterone deficiency and excess ACTH: investigations will be required to confirm primary adrenal insufficiency.
• cortisol deficiency results in weakness (99%), fatigue, weight loss Optional investigations are: serum cortisol, serum ACTH and
(97%), anorexia progressing to nausea, vomiting, diarrhoea (20%), 24 hour urinary cortisol. If considered necessary, a synacthen (ACTH
constipation (19%), flank or abdominal pain (34%), low blood stimulation) test can be performed but this should never result in
glucose levels and hyperthermia.2,4,5 Fasting hypoglycaemia is delayed administration of steroids and should only be performed under
common and occurs because of loss of the gluconeogenic effects of controlled circumstances in the hospital setting.
cortisol.5 In patients with pre-existing type 1 diabetes, deterioration Education of the patient, and their family, on the diagnosis,
of glycaemic control with recurrent hypoglycaemia can be the importance of adherence, and an emergency management plan must
presenting sign of adrenal insufficiency2 be initiated.
• aldosterone deficiency causes hyponatraemia, hyperkalaemia,
acidosis, tachycardia and hypotension. Low voltage
Long term management
electrocardiogram (ECG) and a small heart on chest X-ray are Long term management may include a Team Care Arrangement
not necessarily present.4,5 Suggestive symptoms are postural involving a general practitioner, endocrinologist and clinical nurse
hypotension and salt cravings2,11 specialist. Assistance by social workers and psychologists can be
• excess ACTH is only present in primary adrenal insufficiency. It important. Medical management includes replacement of
causes increased melanin production resulting in generalised cortisol ± aldosterone. Regular specialist reviews are needed to
hyperpigmentation.4,5 Because this resembles a suntan, it is optimise therapy.12,14-16 These include: assessment of growth
essential to inspect areas not exposed to the sun for diffuse and pubertal development, looking for clinical signs of adrenal
hyperpigmentation which can be more obvious in recent scars insufficiency, biochemical analyses of electrolytes, cortisol levels and,
and in areas such as the axillae, nipples, pressure points, depending on the underlying pathology, ACTH, and monitoring for
palmar creases, and mucous membranes. Some patients with other autoimmune conditions.5 Emphasis will be on the importance
autoimmune mediated adrenal insufficiency also present with of adherence with medication and adjustments for illness and stress
vitiligo.2,5 situations to achieve a good quality of life.11,13 As steroid replacement
Chronic unrecognised Addison disease can cause psychiatric symptoms therapy is associated with an increased risk of osteoporosis, further
such as memory impairment, confusion, apathy, depression and investigations including dual energy X-ray absorptiometry scans and
psychosis.5 These features regress on treatment with replacement preventive strategies such as adequate dietary calcium, exercise and
corticosteroids. vitamin D/sun exposure should be considered.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 11, NOVEMBER 2010 835
FOCUS Addison disease - diagnosis and initial management
Emergency plan 5.5 mmol/L. He was given a bolus of 10% dextrose followed
An up-to-date emergency plan and practical teaching in administering by normal saline. He then had a generalised tonic clonic
emergency medication are of paramount importance. At each seizure, was treated with anticonvulsants and intubated,
consultation the physician must ensure that the patient and carer(s) ventilated and transferred to the intensive care unit.
are well versed in the emergency plan and that their ready-to-use vial
In his background history he had an admission at 11 months
of age with profound hypoglycaemia (BGL 0.6 mmol/L)
of emergency hydrocortisone is in-date and available for use at any
following an episode of gastroenteritis. He had presented to
time.11,14 In growing children, the dose may require adjustment and a
the ED unresponsive and pale following 18 hours of profuse,
new appropriate prescription should be issued where indicated. It is
watery diarrhoea and vomiting. At that time, sodium was
recommended that patients wear a MedicAlert bracelet or pendant and
recorded at 126 mmol/L with potassium 4.3 mmol/L. He
have ambulance cover.
became alert and interactive after 10% dextrose bolus.
Case study 1 - An acute presentation On the second admission, the boy was noted to have
Paramedics attended a boy, aged 21 months, at his home. His hyperpigmentation of the buccal mucosa (Figure 1) and
Glasgow Coma Scale was 8/15. He was poorly perfused, with appeared diffusely suntanned.
Sp02 of 76% and capillary blood glucose <2 mmol/L. He had Plasma cortisol was <30 mmol/L with a raised ACTH of
been unwell at home with symptoms of an upper respiratory 492 pmol/L (normal range 2.0-10). A diagnosis of acute
tract infection for the previous 24 hours. He was given oral Addisonian crisis was made and he was treated with 50 mg
glucose gel and IM glucagon with no effect. On arrival at IV hydrocortisone 4 hourly. He made a full recovery.
the hospital emergency department he had spontaneous He was discharged on oral maintenance hydrocortisone
respirations with a heart rate of 126 bpm and cool peripheries. with an emergency plan. A MedicAlert bracelet and
Investigations showed a metabolic acidosis, blood glucose ambulance cover were organised. Further investigations
level (BGL) of 1.6 mmol/L, sodium 134 mmol/L and potassium revealed normal aldosterone levels, negative adrenal
Table 1. Summary of the management and prevention of acute adrenal insufficiency5,11,14

Clinical findings Correction of hypoglycaemia
• Cortisol deficiency: weakness, anorexia, nausea • Neonates or infants: 10% dextrose 5 mL/kg (IV bolus)
and/or vomiting, hypoglycaemia, hypotension • Older children, adolescents and adults: 25% dextrose
(particularly postural) and shock 2 mL/kg (IV bolus)
• Aldosterone deficiency: dehydration, hyperkalaemia, Correction of hyperkalaemia
hyponatraemia, acidosis, low blood pressure
• Potassium usually normalises with fluid and electrolyte
Investigations replacement
• Blood sugar level; serum glucose, urea, sodium and • If K+ >6 mmol/L - perform ECG and apply cardiac monitor
potassium; blood gas analysis as arrhythmias and cardiac arrest may occur
• Keep extra blood for analysis of ACTH and cortisol Identify and treat potential precipitating causes
if possible
• Admit to appropriate inpatient facility
• Do not wait for results to start therapy
When patient tolerates oral intake
Intravenous fluids • Reduce IV hyrocortisone dose, then switch to triple
• Initial fluid resuscitation: NaCl 0.9% 20 mL/kg (severe dose oral hydrocortisone therapy, gradually reducing to
dehydration); 10 mL/kg (moderate dehydration) - maintenance levels (10-15 mg/m2/day)
repeat until circulation restored
• Patients with aldosterone deficiency: start fludrocortisone
• Maintenance fluids: 5-10% dextrose at maintenance doses (usually 0.1 mg/day)11
Steroid replacement (hydrocortisone) Prevention
• If intravenous (IV) access is difficult, give • Emergency plan for susceptible patients, emergency
intramuscularly (IM) while establishing IV line identification (MedicAlert)
• Neonates (1 year): 25 mg stat, then 10-25 mg • Triple normal oral maintenance dose for 2-3 days during
4-6 hourly stress (ie. fever, fracture)
• Toddlers (1-3 years): 25-50 mg stat, then 25-50 mg • Administer IM hydrocortisone if oral medication not
4-6 hourly tolerated (eg. vomiting)
• Children (4-12 years): 50-75 mg stat, then 50-75 mg • Increase parenteral hydrocortisone (1-2 mg/kg) before
4-6 hourly anaesthesia, consider increased dose postoperatively
• Adolescents and adults: 100-150 mg stat, then 100 mg • Ensure patients have ambulance cover and ready-to-use
4-6 hourly IM hydrocortisone preparation (Act-o-vial®) for emergencies
836 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 11, NOVEMBER 2010
Addison disease - diagnosis and initial management FOCUS
antibodies and normal, very long chain fatty acids (to Why is Addison disease easily missed?
exclude adrenoleukodystrophy). Investigations to exclude Addison disease is easily missed due to nonspecific symptoms and
other endocrinopathies were normal, and no cause for
presentations, rarity of the condition, and low index of suspicion.
Addison disease identified.
The consequences of delayed diagnosis and treatment are increased
Ongoing management
morbidity, mortality and medicolegal risk.12,13 Outcomes may be
Ongoing management in this boy includes oral
hydrocortisone maintenance treatment and growth improved with a higher index of diagnostic suspicion, prompt emergency
monitoring. An emergency plan with instructions to increase management with IM or IV hydrocortisone as indicated, early referral,
his dose of hydrocortisone in the event of illness is in place. and good patient education.11,13
In the event of unresponsiveness or persistent vomiting his
parents have been instructed on the administration of IM
Key points in management
• Physical findings are subtle and nonspecific; hyperpigmentation
hydrocortisone and to call the emergency numbers listed
may be seen, particularly in sun exposed areas or pressure points.
on the emergency plan. The importance of adherence with
• Circulatory compromise can range from mild signs of sodium and
regular medications is reiterated and the boy’s emergency
volume depletion to shock.
plan reviewed at each clinic attendance.
• If in doubt give oral/IM/IV hydrocortisone.
• Don’t delay treatment while awaiting laboratory results.
Authors
Susan O’Connell MB, MRCPI, MD, is Fellow in Paediatric
Endocrinology, Princess Margaret Hospital for Children, Western
Australia. susanmary.o’connell@health.wa.gov.au
Aris Siafarikas MD, FRACP, is Consultant Paediatric Endocrinologist,
Princess Margaret Hospital for Children, Clinical Associate Professor,
Institute of Health and Rehabilitation Research, University of Notre
Dame, and Senior Clinical Lecturer, School of Paediatrics and Child
Health, University of Western Australia, Perth, Western Australia.
References
1. Addison T, editor. On the constitutional and local effects of disease of the supra
renal capsules. London: Highley, 1855.
Figure 1. Hyperpigmentation of the buccal mucosa 2. Arlt W, Allolio B. Adrenal insufficiency. Lancet 2003;361:1881-93.
3. Laureti S, Vecchi L, Santeusanio F, et al. Is the prevalence of Addison’s disease
underestimated? J Clin Endocrinol Metab 1999;84:1762.
Case study 2 - Issues in management 4. Brook GD, Brown RS, editors. Handbook of clinical pediatric endocrinology. 1st
edn. Malden, Mass: Blackwell Publishing, 2008.
A girl, 15 years of age, with a diagnosis of Addison disease 5. Kronenburg, editor. Williams textbook of endocrinology. 11th edn. Philadelphia:
made 3 years previously (anti-adrenal antibodies positive) Saunders Elsevier, 2008.
6. Oelkers W. Adrenal insufficiency. N Engl J Med 1996;335:1206-12.
attended her routine endocrinology clinic appointment with
7. Soule S. Addisons disease in Africa - a teaching hospital experience. Clin
her father. She had a history of poor adherence. Regular Endocrinol (Oxf) 1999;50:115-20.
medications were: prednisolone 4 mg morning and evening 8. Perry R, Kecha O, Paquette J, et al. Primary adrenal insufficiency in children:
twenty years experience at the Sainte-Justine Hospital, Montreal. J Clin
and fludrocortisone 100 pg/day. She denied missing her
Endocrinol Metab 2005;90:3243-50.
medications. She had regular menses. She described fair 9. Ahonen P, Myllarniemi S, Sipila I, et al. Clinical variation of autoimmune
energy levels. polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) in a series of 68
patients. N Engl J Med 1990;322:1829-36.
On examination she looked well but appeared diffusely 10. Greenfield JR, Samaras K. Suppression of HPA axis in adults taking inhaled corti
suntanned, not confined to, but more obvious in sun costeroids. Thorax 2006;61:272-3.
exposed areas. Her BP was normal. Records showed that 11. Arlt W. The approach to the adult with newly diagnosed adrenal insufficiency. J
Clin Endocrinol Metab 2009;94:1059-67.
she had not gained weight for the past year. 12. Klauer KM. Adrenal insufficiency and adrenal crisis: differential diagnoses and
The patient was intermittently living between her parents’ workup, 2009. Available at http://emedicine.medscape.com/article/765753-
homes. On review of her emergency plan she was unsure diagnosis [Accessed 21 October 2010].
13. Erichsen MM, Lovas K, Fougner KJ, et al. Normal overall mortality rate in
of what to do should she become unwell. Her father Addison’s disease, but young patients are at risk of premature death. Eur J
appeared to be well informed in the management of any Endocrinol 2009;160:233-7.
illness, however it was revealed that the ready-to-use IM 14. The Royal Children’s Hospital Melbourne. Adrenal crisis. 2010. Available at
www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5121 [Accessed 24 June 2010].
hydrocortisone was only available at her mother’s house. 15. Nieman L. Patient information: adrenal insufficiency (Addison’s disease).
New prescriptions for IM hydrocortisone were issued for UpToDate, (internet serial), 2010.
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plan were also made. The importance of adherence with
regular medication was reiterated. correspondence afp@racgp.org.au
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 11, NOVEMBER 2010 837
focus Chronic heart failure
Acute pulmonary
Andrew Baird
oedema
Management ingeneral practice
0 Acute heart failure (AHF) is a clinical syndrome

Background characterised by the rapid onset and progression of
Acute pulmonary oedema is a life threatening emergency breathlessness and exhaustion. There is usually fluid
that requires immediate intervention with a management overload.1 Acute heart failure typically occurs as ‘acute
plan and an evidence based treatment protocol. decompensated heart failure’ (ADHF) either secondary to
Objective chronic heart failure (CHF) or de novo. The more severe
This article describes the features, causes, prevalence and presentations of acute heart failure are acute pulmonary
prognosis of heart failure and the management of acute oedema (APO) and cardiogenic shock. In the EuroHeart
pulmonary oedema. Failure Survey II2 of patients hospitalised with AHF, 37% had
de novo acute heart failure and 16% had APO.
Discussion
Presentations of acute pulmonary oedema and acute heart
General practitioners are familiar with the clinical presentation of APO
failure to general practice require a coordinated and urgent
- severe dyspnoea, distress, pallor, sweating, tachycardia and poor
response. Initial assessment, management and monitoring
peripheral perfusion. However, in general practice, the presentation of
should occur concurrently and must be modified in
response to clinical changes. AHF may be less dramatic than APO and the clinical features may be
atypical (eg. delirium or falls in the elderly). Differential diagnoses and
Keywords: heart failure; pulmonary oedema; emergencies
potential precipitants for APO are listed in Table 1.
The most common cause of heart failure is impaired myocardial
function (cardiomyopathy) secondary to one or more of the following1:
• hypertension (>60% of patients with heart failure)
• ischaemic heart disease (>50% of patients with heart failure)
• idiopathic dilatation (10% of patients with heart failure)
• diabetes
• alcohol excess
• obesity
• drug toxicity.
Other cardiac causes of heart failure include arrhythmias, valve
dysfunction and pericardial disease. Noncardiac causes of heart failure
are hypovolaemia (dehydration or haemorrhage), pulmonary embolism
and high output states (anaemia, septicaemia and thyrotoxicosis).
On echocardiographic criteria, about one-third to one-half of patients
with a diagnosis of CHF have normal ventricular systolic function with
a left ventricular ejection fraction >40%.1 There is impaired relaxation
of the ventricle in diastole, which is termed ‘diastolic heart failure’ or
synonymously ‘heart failure with normal systolic function’ (HFNSF). The
significance of HFNSF as a distinct clinical entity is uncertain. However,
patients with HFNSF do seem particularly dependent on ventricular filling
for cardiac output and are very sensitive to overdiuresis.3
910 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 12, DECEMBER 2010
Table 1. Acute pulmonary oedema - differential diagnoses and potential precipitants
Consider and manage the following as appropriate
Differential diagnoses of acute dyspnoea Precipitants of acute pulmonary oedema
Primary respiratory causes Primary cardiac causes
• Exacerbation of chronic obstructive pulmonary • Acute coronary syndrome/myocardial infarction
disease (COPD) • Arrhythmia
• Acute asthma • Pericarditis
• Pneumothorax • Acute valve dysfunction (aortic stenosis, mitral regurgitation)
• Pneumonia • Endocarditis
Anaphylaxis Fluid overload
Hyperventilation Drugs (eg. nonsteroidal anti-inflammatory drugs [NSAIDs],
nondihydropyridine calcium channel blockers)
Noncardiogenic acute pulmonary oedema Noncompliance with:
• Drowning • heart failure management medications
• Laryngospasm/upper airway obstruction • restrictions on fluid intake or alcohol intake
• Toxic inhalation
Pulmonary embolus Pulmonary embolus
Acute renal failure Acute renal failure
High output states High output states
• Septicaemia • Septicaemia
• Anaemia • Anaemia
• Thyrotoxicosis • Thyrotoxicosis
Prevalence Table 2 summarises the assessment and management steps for APO.
The prevalence of CHF increases with age. In Australia, the prevalence There are no guidelines or studies which specifically address the
in the 55-64 years age group is estimated at 2.5%, in the over 75 management of APO in the primary care setting. A PubMed search
years age group it is 8.2%. There are twice as many women as men on all fields using the MeSH terms ‘acute heart failure’ and ‘family
with CHF.4 At the age of 40 years, the lifetime risk of developing heart practice’ produced only one relevant article.11
failure is about 20% in both men and women.1 There are no data on The goals of APO management are symptom relief, reduction
the incidence of APO, but it is estimated that most patients with CHF of extracellular fluid excess, improved haemodynamics, improved
will have at least one episode of ADHF or APO.1 arterial oxygenation and satisfactory perfusion of the vital organs.1
General guidelines, approaches and goals must be modified
Prognosis according to clinical setting (eg. rural or metropolitan) and context
Overall, CHF has a poor prognosis with about 50% mortality 5 years (eg. APO in an elderly patient with end stage CHF as opposed to a
from diagnosis.5-7 In-hospital mortality from ADHF ranges from previously healthy patient 50 years of age).
2.1-21.9%, depending on mortality risk stratification.8 The prerequisites for successful management of APO include
Clinical decision tools to predict mortality in ADHF have been appropriate:
developed based on the following recognised indicators of poor • systems (triage, crisis resource management plans, organisation,
prognosis: renal impairment, low systolic blood pressure, tachypnoea, leadership, teamwork, documentation)
hyponatraemia, anaemia and comorbidities.8,9 • resources (personnel, equipment and drugs)
• knowledge and skills.
Management Assessment, management and definitive therapy are concurrent,
The management of ADHF and APO is largely based on clinical continuous and iterative. All patients require hospital admission
experience rather than prospective randomised controlled trials.1,5-7,10 for stabilisation and monitoring unless inappropriate, such as in
Current management described in this article is informed by guidelines the palliative care context. Definitive therapy for acute pulmonary
from Australia,3,6 Europe,5 the United States of America7 and by oedema is outlined in Table 3.
a review.10 The therapeutic interventions recommended by these Once the patient is stable, management progresses to postacute
authorities differ in approach and emphasis but the principles are similar. care planning.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 39, NO. 12, DECEMBER 2010 911
FOCUS Acute pulmonary oedema - management in general practice
Table 2. Assessment and management of acute pulmonary oedema
Initial • Call for help (other GPs, nurses, clinic staff, dial 000)
• Commence oxygen
• Insert 16 gauge intravenous cannula
• Commence definitive treatment while assessing patient
History • Focused cardiorespiratory history (Note: nocturnal dyspnoea and orthopnoea are
specific but not sensitive for heart failure)
• Check past medical history, medications, compliance
• Consider third party information
Examination • Five vital signs

- temperature
- pulse (rate, rhythm)
- blood pressure
- respiration (rate, pattern)
- oxygen saturation
• Focused cardiorespiratory examination, particularly:
- colour
- diaphoresis
- jugular venous pulse
- apex beat (shift, loading)
- heart sounds (gallop rhythm?)
• Murmurs (eg. mitral regurgitation, aortic stenosis)
• Peripheral perfusion and oedema
• Air entry, crepitations, rhonchi
Monitoring • Blood pressure

• Continuous ECG (lead II) - if available
• Oxygen saturation
• Automated external defibrillator on standby
• Consider urinary catheter if managing in rural hospital
Investigations • 12 lead electrocardiogram (ECG) as soon as possible (APO is an acute coronary

(depending on availability) syndrome until proven otherwise)
• Chest X-ray (portable, if available)
• Point-of-care pathology tests (if available)
- troponin
*
- B-type natriuretic peptide (BNP)
• Other pathology tests: urea and electrolytes, liver function tests, glucose, urinalysis, full
blood examination (FBE), arterial blood gases
• Echocardiogram at earliest opportunity (depending on access and patient stability)
Reassurance • Patient and relatives

and explanation
* Useful negative predictive value (if BNP lower than 100 pg/mL, dyspnoea is unlikely to be cardiogenic). This test costs
about $50 and there is a Medicare rebate for the diagnosis of dyspnoea in hospital emergency departments. The role
and utility of this test in APO and in primary care settings is not yet well defined
Acute pulmonary oedema - management in general practice FOCUS
Table 3. Definitive therapy for acute pulmonary oedema

Therapy (action) Dose Notes
Posture Patient supported in sitting up Supine position if unconscious or in cardiogenic
position shock
Oxygen 10-15 L/min via Hudson type When stable, reduce to 2-6 L/min via nasal
(corrects hypoxaemia) mask and reservoir bag12 prongs or 5-10 L/min via Hudson mask
(align centre of flowmeter ball to (This is initial treatment even Patients with COPD should ideally receive
required flow rate) in patients with known COPD controlled oxygen therapy via a 28% Venturi
who are at risk of hyperoxic mask (flow rate 4 L/min)12
hypercapnia as oxygenation is Titrate to achieve oxygen saturation of 94-96%
the priority. Monitor conscious (non-COPD) or 88-92% (COPD)12
state, respiratory rate and
oxygenation)
Glyceryl trinitrate 400 pg sublingual every 5 Maintain systolic blood pressure (SBP) above
(venodilator, reduces preload) minutes (up to three doses) 100 mmHg
Contraindicated within 48 hours of PDE5
inhibitor
Intravenous infusion Double infusion rate every 5 minutes according
commencing at 10 pg/min to clinical response (maintain SBP above 90
mmHg)
Positive airway pressure • Continuous positive airway Contraindicated if:
support (continuous [CPAP] pressure - 10 cmH20 • SBP <90 mmHg
or bi-level [BiPAP] if available) • BiPAP: inspiratory pressure • reduced consciousness
reduces alveolar and pulmonary 15 cmH20, expiratory pressure Clinical improvement may occur within 10
interstitial oedema; reduces 5 cmH20
venous return and preload minutes. Duration of use depends on efficacy
and tolerability. Some evidence BiPAP may be
superior
Frusemide 20-80 mg IV bolus Consider repeating a bolus dose after
(loop diuretic, reduces fluid After bolus, consider continuous 30-60 minutes if there has been no clinical
overload; possible vasodilator IV infusion at 5-10 mg/hour (total improvement and no diuresis
effect) dose <100 mg in first 6 hours, Risk of hypovolaemia; avoid if no clear fluid
and <240 mg in the first 24 hours) overload
Morphine (reduces sympathetic 1-2 mg IV Does not improve pulmonary oedema or cardiac
nervous activity; possible output
venodilator effect) Anxiolytic
Reduces respiratory work
Other drugs that may be used
Low molecular weight heparin Eg. enoxaparin 40 mg SC daily Commence if available
(venous thromboembolism
prophylaxis)
Digoxin 500 pg IV (over 5 or more Only for digoxin naïve patients with rapid atrial
minutes) fibrillation
Spironolactone 25-50 mg orally stat Consider in volume overloaded patient with
poor response to IV frusemide5
Other therapies that may be used in intensive care unit
• Adrenaline infusion
• Vasopressin antagonists (conivaptan, tolvaptan)
• Vasodilators (sodium nitroprusside)
• Inotropes (for cardiogenic shock or hypoperfused state with SBP <90 mmHg)
- beta-adrenergic stimulators (dobutamine, dopamine)
- phosphodiesterase inhibitors (milrinone, enoximone)
• Ultrafiltration
• Mechanical support (eg. intra-aortic balloon pump) for cardiogenic shock
FOCUS Acute pulmonary oedema - management in general practice
Checklist for postacute care Summary of important points

• Structured management plan (Medicare primary care items may • Acute pulmonary oedema is a life threatening emergency requiring
apply): patient and GP define problems, goals and actions immediate intervention with a crisis resource management plan
• Team based care according to needs and access (Medicare primary and an evidence based treatment protocol.
care items may apply). This may involve the GP, practice nurse, • The principal therapies for APO are oxygen, sitting the patient
cardiologist and/or heart failure clinic, pharmacist, Aboriginal upright, glyceryl trinitrate, positive airway pressure, frusemide,
health worker, dietician or exercise physiologist morphine and inotropes.
• Education and support for patient and carers (useful resources are • A key component in the management of APO is postacute care
available at www.heartfoundation.org.au) which presents an opportunity to optimise wellbeing and prognosis
• Home assessment and community support in CHF.
• Lifestyle
Author
- smoking cessation Andrew Baird MBChB, FRACGP, FACRRM, is a general practitioner,
- diet: follow Heart Foundation guidelines, no added salt Melbourne, Victoria. bairdak@gmail.com.
- fluid restriction: maximum 2 L/day (1.5 L/day if severe CHF)
- alcohol: no more than one unit per day
- exercise: individualised program References
• Investigations 1. Krum H, Abraham W. Heart failure. Lancet 2009;373:941-55.
2. Nieminen M, Brutsaert D, Dickstein K, et al, EuroHeart Failure Survey II
- echocardiogram: mandatory for all patients post-AHF
(EHFS II): a survey on hospitalized acute heart failure patients: description
- full cardiac ‘workup’: ECG, lipid profile, glucose, renal function, of population. Eur Heart J 2006;27:2725-36.
liver function, thyroid function, iron studies, FBE 3. Cardiovascular Expert Group. Therapeutic Guidelines: cardiovascular.
Version 5. Melbourne: Therapeutic Guidelines Limited, 2008.
• Monitoring: patient self monitoring (symptoms, weight, BP) 4. Australian Institute of Health and Welfare. Heart failure in Australia.
• GP review (frequency determined by severity and stability of CHF): Available at www.aihw.gov.au/cvd/heart_failure.cfm.
5. Dickstein K. The Task Force for the Diagnosis and Treatment of Acute and
- symptoms, weight, BP, cardiorespiratory status
Chronic Heart Failure of the European Society of Cardiology. ESC guidelines
- risk factor management for the diagnosis and treatment of acute and chronic heart failure 2008. Eur
- comorbidities (especially ischaemic heart disease, diabetes, Heart J 2008;29:2388-442.
6. National Heart Foundation of Australia and the Cardiac Society of Australia
COPD, renal impairment, sleep apnoea, obesity, depression, and New Zealand (Chronic Heart Failure Guidelines Expert Writing Panel).
osteoarthritis) Guidelines for the prevention, detection and management of chronic heart
failure in Australia, 2006. Available at www.heartfoundation.org.au.
- mental state
7. Lindenfeld J, Albert NM, Boehmer JP, et al. Executive summary: Heart
- medication review (Medicare primary care items may apply) Failure Society of America 2010 Comprehensive Heart Failure Practice
- pathology (urea, creatinine, electrolytes, FBE) Guideline. J Card Fail 2010;16:475-539.
8. Fonarow GC, Adams KF Jr, Abraham WT, et al for the ADHERE Scientific
• Medications indicated (*improves prognosis as well as symptoms) Advisory Committee, Study Group, and Investigators. Risk stratification for
- angiotensin converting enzyme inhibitor (ACEI)
*: all patients in-hospital mortality in acutely decompensated heart failure: classification
and regression tree analysis. JAMA 2005;293:572-80.
with CHF (if not tolerated use angiotensin II receptor blocker)
9. Lee DS, Austin PC, Rouleau JL, et al. Predicting mortality among patients
- beta *blocker
: patients with systolic failure; COPD is not a hospitalized for heart failure: derivation and validation of a clinical model.
contraindication (bisoprolol, carvedilol, metoprolol, nebivolol) JAMA 2003;290:2581-7.
10. Allen LA, O’Connor CM. Management of acute decompensated heart
- frusemide: symptoms of fluid overload failure. Can Med Assoc J 2007;176:797-805.
- :
*spironolactone add on if symptom control inadequate 11. Bosomworth J. Rural treatment of acute cardiogenic pulmonary edema:
applying the evidence to achieve success with failure. Can J Rural Med
- digoxin: consider for atrial fibrillation, or as add on therapy for
2008;13:121-8.
sinus rhythm with severe CHF inadequately controlled with the 12. O’Driscoll B, Howard L, Davison A. Emergency Oxygen Guideline Group,
above British Thoracic Society. Guideline for emergency oxygen use in adult
patients. Thorax 2008;63(Suppl 6):849-50.
• Medications (contraindicated or caution):
- verapamil and diltiazem
- NSAIDs or cyclo-oxygenase-2 inhibitors
- corticosteroids
• Vaccinations: influenza, pneumococcal
• Device therapy for patients with moderate or severe CHF
(cardiologist would assess and recommend if appropriate):
- cardiac resynchronisation therapy (eg. if QRS is greater
than 120 ms)
- implantable cardioverter defibrillator. correspondence afp@racgp.org.au
EDITORIAL
Take heart general practice

Rachel Lee
There has been recent passionate email acknowledges the importance of general practice This edition of AFP covers key aspects of
discussion by members of the Australian and primary care.6 The message from recent policy managing patients with heart failure. Baird’s
Association for Academic Primary Care work is clear - primary care is a central part of the article discusses the latest approach to the
about the ‘invisibility’ of general practice health system and the reform solutions. Academic management of acute pulmonary oedema. Sindone
research. general practice is critical to ensure these changes and Naoum consider chronic heart failure, and
and the care delivered is effective and evidence Prior and Coller outline the principles underlying
In a nutshell, this ‘invisibility’ seems to occur at based and the future primary care workforce is echocardiography and how this tool can best
three different levels: within general practice as well taught and supported. assist GPs in managing heart failure. Davidson
general practitioners decline research roles1 and The time is ripe to expand the scope and and colleagues provide guidelines for managing
some eschew evidence based practice; from the increase the presence of Australian academic the palliative phase of cardiac failure, and Stewart
wider medical profession as GPs still produce far general practice. discusses the multidisciplinary team approach
less research than their sub-specialist colleagues2 Just as the causes are complex the solutions to heart failure. Together we hope these articles
and struggle to find appropriate grant categories will also be multifaceted and require significant provide a thorough update about this incredibly
for primary care research; and finally in the co-ordination and collaboration. Australia is well important and common syndrome.
broader arena as departments of general practice supplied with departments of general practice,
Author
and researchers struggle to get their messages to rural clinical schools, regional training providers, Rachel Lee MBBS, BA, MPH, is Medical Editor,
the general public and policy makers. divisions of general practice and many national Australian Family Physician, Board Director, General
Certainly there is a lot of work to be done organisations, including the RACGP, that support Practice Education and Training, and a general prac
until academic primary care gets the funding and different aspects of primary care and general tice registrar, North Yarra Community Health Centre,
Victoria.
recognition it deserves. Yet I find myself optimistic practice. These bodies will need to work together
about the future of general practice and academic to ensure that academic general practice is firmly References
1. Askew DA, Clavarino AM, Glasziou PP, Del Mar CB.
primary care. Indeed, I’m proud of our profession’s on the agenda and will need to develop different
General practice research: attitudes and involvement
recent achievements - take heart general programs and ways of working to adapt to the of Queensland general practitioners. Med J Aust
practice! demands of the new environment. 2002;177: 74-7.
2. Askew DA, Glasziou PP, Del Mar CB. Research
Unlike some other medical specialties, There is a growing base of enthusiastic
output of Australian general practice: a comparison
general practice has a cadre of trained medical registrars who are ready to be engaged. The with medicine, surgery and public health. Med J
educators and supervisors who are passionate presentations from the academic registrars at the Aust 2001;175:77-80.
3. Soos M, Temple-Smith M, Gunn J, Johnson-Ata’Ata,
about teaching. Research practice networks recent General Practice Education and Training Pirotta M. Establishing the Victorian Primary Care
are gathering momentum3 and the quality of convention were outstanding, the two registrars Practice Based Research Network. Aust Fam Physician
2010;39:857-62.
primary care research submitted to Australian working with at AFP as Publications Fellows this
4. The Royal Australian College of General Practitioners.
Family Physician has improved markedly over year have also been fantastic, and I have met a Curriculum for Australian General Practice. 2007.
recent years. The new Royal Australian College increasing number of registrars who have taken on Available at www.racgp.org.au/scriptcontent/
curriculum/pdfdraft/DRAFT_Procedural_skills_curricu-
of General Practitioners (RACGP) curriculum junior medical educator roles. We clearly need to
lum_statement.pdf.
statements now include 'GPs as teachers and nurture this interest and support academic general 5. General Practice Education and Training. GPET wel
mentors’ and 'Critical thinking and research’4 practice activities before, during, and after the comes new training places. [Media release 15 March
2010]. Available at www.gpet.com.au/NewEvents/
and the newly elected RACGP President has training program. As a start we need clear career Media/ [Accessed 8 November 2010].
a very strong academic background. Training pathways for researchers and educators. This 6. Commonwealth of Australia. Primary Health Care
Reform in Australia: Report to Support Australia’s First
places for general practice registrars continue would enhance the visibility of academic general
National Primary Health Care Strategy. Commonwealth
to expand and increasing numbers of junior practice and may increase the attractiveness of a of Australia. Canberra: 2009. Available at www.
doctors will be exposed to a general practice career in general practice for junior doctors. yourhealth.gov.au/internet/yourhealth/publishing.nsf/
Content/nphc-draftreportsupp-toc/$FILE/NPHC-supp.
rotation in their prevocational years,5 enhancing So academic primary care practitioners, there
pdf [Accessed 8 November 2010].
their understanding of what general practice is is good reason to take heart and even better
all about. The Federal Health Reform agenda reason to take action! correspondence afp@racgp.org.au
CLINICAL
Treating common warts

Lawrence Leung
Options and evidence
excellent review has been written by Jablonska

Background et al;5 and a brief summary of the various types of
Nongenital warts are a common condition seen in general practice, affecting patients common warts is given in Table 1 (Figure 1-4).
of all ages. There are many treatment options and patients often self medicate with
remedies from folklore or tradition before presenting to their doctor. Pathogenesis
Objective With a minor breach in the epithelial surface,
This article attempts to summarise the quality of different treatments and to provide HPV enters the epithelial cells via putative
recommendations and a quick reference for treating common warts. surface receptors and proliferates. This results
Discussion in persistent viral infection with metaplasia
Many common warts will resolve spontaneously but others are recalcitrant and often of keratinocytes, which gradually accumulate
require ongoing treatment beyond first line measures. Without definite guidelines for keratohyalin granules6 and are sloughed off.4
treating recalcitrant warts, it is important for the general practitioner to consider the As these virally infected keratinocytes are not
available evidence for efficacy and contraindication of the various treatment options. destroyed, the HPV virions are rarely exposed to
Keywords: warts; skin diseases; treatment; salicylic acid; cryosurgery the Langerhans cells of the skin, and therefore
evade being cleared by systemic immunity. This
facilitates the viral persistence and continual
growth of the wart.
Diagnostic features and

A Nongenital cutaneous warts are commonly differential diagnoses
seen in general practice with an overall Cutaneous warts often present as localised flat
prevalence of 7-10%1 and a peak age of or dome shaped papules with well demarcated
presentation of 12-16 years.1-2 They are edges. Histological findings include epidermal
most commonly found on the hands and acanthosis, papillomatosis, hyperkeratosis
feet but can also be found on the face, and parakeratosis with elongated rete ridges
eyelids and torso. The causative agent is often curving toward the centre of the wart.
human papilloma virus (HPV). Without
treatment, one-third of cutaneous warts
will resolve spontaneously within 3 months
and two-thirds within 2 years.3 Myrmecia
warts often persist despite repeated
treatments and become recalcitrant warts.
There is no consensus on the prevalence
of, and most effective treatment for,
recalcitrant warts.
Classification of nongenital
cutaneous warts
There are over 100 identified types of HPV;4 Figure 1. Myrmecia warts on the ball of
calcaneum. These are painful. Notice the
the most common types of cutaneous warts are
typical round appearance with pitting when
type 1, 2, 3, 4, 7, 10, 27 and 57.2,4 Cutaneous
keratinised plates were removed
warts can present in various forms and sizes. An
CLINICAL Treating common warts - options and evidence
Capillary vessels are often prominent and may are used to feed the wart. While most cutaneous seek treatment. With a record of existence going
be thrombosed, giving the pathognomonic brown warts tend to be exophytic and painless (ie. back to the ancient Greeks and Romans, the
dots at the centre of the lesion when the warts are grow out of and above the skin), those affecting common wart in no way lacks curative options,
pared down. Due to the continuous viral induced the palm and soles are often endophytic (ie. including hypnotherapy;8 garlic;9 duct tape;7 fig
hyperkeratotic changes, the surface papillary grow inwards into the skin) and lead to pain and tree latex;10 oral zinc sulphate;11 oral histamine
lines of the skin are disrupted resulting in a rough discomfort. When several warts with different 2 receptor antagonist;11 cautery;7 hyfrecation;7
surface. Most lesions are of skin colour but can morphologies cluster together, a mosaic wart is surgical removal;12 salicylic acid;2,7 liquid
appear black due to thrombosed capillaries which formed.4 Due to the myriad of morphologies and nitrogen cryotherapy;7 local hyperthermia;13 CO2
wide area of possible distribution, cutaneous laser;3 YAG laser;12 pulsed dye laser;14 intense
warts have to be differentiated from other skin pulsed light (IPL);15 topical imiquimod;16 topical
conditions such as seborrhoeic keratosis, callous, 5-fluorouracil;17 squaric acid;18 intralesional
lichen planus, molluscum contagiosum, mole, injection of bleomycin;19 interferon;2 candida
melanoma, keratoacanthoma and cutaneous horn.7 antigen 1;20 measles, mumps and rubella
(MMR) vaccine;21 and autoimplantation of wart
Treatment options materials.22 Detail of each treatment modality
Most cutaneous warts are self limiting and is beyond the scope of this article and readers
resolve within 2 years. When they pose are referred to Lipke’s excellent reviews.7
discomfort or aesthetic problems, patients often Classification of quality of evidence (Table 2)
Figure 2. Common warts on the sole of the
foot with irregular hyperkeratosis. These are Table 1. Categories of common warts with their HPV subtypes
relatively painless
Type HPV Morphology Mode of regression
type
Myrmecia 1 Round keratinised lesions found Vascular extravasation
warts commonly on pressure point of and haemorrhage
(Figure 1) foot, often painful endophytic with minimal
growth with central pit when inflammatory infiltrate
central hyperkeratotic plate
removed
Common 2, 4, 57 Flat or raised papules or nodules Cellular inflammatory
warts with irregular hyperkeratotic infiltrate involving
(Figure 2) surfaces commonly found on the lymphocytes,
dorsum of hand and periungually, natural killer cells and
and can involve the sole of the macrophages
Figure 3. Butcher’s wart from a food handler
foot or face - often painless.
with the exophytic cauliflower morphology
Lesions can converge to form
on the lateral aspect of the digit. Notice the
coexistence of plane warts on the dorsum
mosaic warts and can be
and base of the finger
endophytic
Butcher’s 7 Found exclusively in butchers Vascular extravasation
warts and meat handlers, cauliflower and minimal
(Figure 3) like exophytic lesions found on inflammation
both sides of the hand but rarely
periungually
Plane warts 3, 10 Multiple flat papules with Simultaneous
(Figure 4) relatively smooth but inflammatory
hyperkeratotic surfaces found on infiltration of
the hand and face, often painless mononuclear cells
and brought on by Koebner
phenomenon
Intermediate 10, 27 Intermediate morphology Simultaneous
Figure 4. Multiple plane warts on dorsum of warts between common and plane inflammatory reaction
hand. Notice the papular appearance which warts found mostly on dorsum of
can be smooth or hyperkeratotic hands in the immunosuppressed
Treating common warts - options and evidence CLINICAL
and recommendations ( Table 3) according to the 3 months and two-thirds disappear in 2 years’ plantar warts and should be used with caution
United States Preventive Services Task Force are rule. Should the wart persist, the best initial for lesions around the eye. When patients
applied to a summary of treatment options and treatment is salicylic acid (evidence I-A), which present with common warts it is likely they
evidence in Table 4. has clear evidence of advantage over placebo. have already tried salicylic acid or even liquid
Next in line would be cryotherapy with liquid nitrogen at home with no result. In such cases,
Fresh warts
nitrogen (evidence I-B), which has not been the GP can pursue more aggressive liquid nitrogen
For lesions that on initial presentation have mild shown to be superior over other treatments cryotherapy, which has longer contact time with
or no symptoms, the general practitioner can such as salicylic acid or placebo. Liquid nitrogen paring down to the base and increased risks of
choose to observe the ‘one-third disappear in may have better efficacy than salicylic acid for pain and blistering. Intralesional immunotherapy
or chemotherapy, laser and electrosurgery are
Table 2. Classification of quality of evidence better reserved as second line treatments and
are not recommended for common warts at initial
Level of Quality of evidence
evidence presentation.
Level I Evidence obtained from at least one properly designed randomised Best practice for treating fresh
controlled trial (RCT) common warts
Level II-1 Evidence obtained from well designed controlled trials without
Nonfacial lesions are best treated with a salicylic
randomisation
acid gel, cream or instant dry film preparation.
Level II-2 Evidence obtained from well designed cohort or case control analytic Commercial brands come in various strengths
studies, preferably from more than one centre or research group
from 15-40%. Apply on alternate days with
Level II-3 Evidence obtained from multiple time series with or without the contact time of 8 hours, adding occlusive dressing
intervention. Dramatic results in uncontrolled trials might also be (adhesive bandage or plastic wrap) if necessary
regarded as this type of evidence
to enhance effects. If no improvement is observed
Level III Opinions of respected authorities, based on clinical experience, after 6 weeks, proceed to liquid nitrogen
descriptive studies, or reports of expert committees application with four sets of five freeze-thaw
Adapted from United States Preventive Services Task Force. Available at www.ahrq. cycles per treatment, to be repeated fortnightly.
gov/clinic/uspstfix.htm Lesions with hyperkeratinisation should either
be pared down with a scalpel or rubbed with a
pumice stone in warm water before treatment.
Table 3. Recommendations: United States Preventive Services Task Force
For facial lesions, salicylic acid application
Level Recommendations is not recommended because of the possibility
Level A Good scientific evidence suggests that the benefits of the of scarring. They are best treated in the practice
clinical service substantially outweigh the potential risks. with liquid nitrogen. Apply the liquid nitrogen
Clinicians should discuss the service with eligible patients with a fine nozzle spray or cottonwool tip with
Level B At least fair scientific evidence suggests that the benefits of two sets of five freeze-thaw cycles to be repeated
the clinical service outweigh the potential risks. Clinicians fortnightly. If lesions do not resolve within 3
should discuss the service with eligible patients months, or after five rounds of liquid nitrogen
Level C At least fair scientific evidence suggests that there are treatment, the warts are considered refractory or
benefits provided by the clinical service, but the balance recalcitrant.
between benefits and risks are too close for making general Lesions that are resolved with initial
recommendations. Clinicians need not offer it unless there are treatments can recur and they are treated as fresh
individual considerations
lesions, albeit with a lower chance of success.
Level D At least fair scientific evidence suggests that the risks of the Lesions with unusual morphology, bleeding
clinical service outweigh the potential benefits. Clinicians or pigmentation should be biopsied to exclude
should not routinely offer the service to asymptomatic patients
possible malignancy.
Level I Scientific evidence is lacking, of poor quality, or is conflicting,
such that the risk versus benefit balance cannot be assessed. Recalcitrant warts
Clinicians should help patients understand the uncertainty
surrounding the clinical service When warts fail to resolve after repeated
treatments, they are considered recalcitrant. There
Adapted from United States Preventive Services Task Force. Available at www.ahrq. is no consensus for the definition of recalcitrant
gov/clinic/pocketgd09/gcp09app.htm#ApA
warts but as a general rule, they can be described
CLINICAL Treating common warts - options and evidence
as warts that fail five rounds of first line human immunodeficiency virus infections.28 immunotherapy (eg. interferon and MMR
treatment (salicylic acid or liquid nitrogen). Plantar There are no definite guidelines for treating vaccine). These are not first line treatments
warts are notorious for becoming recalcitrant. recalcitrant warts and available options for common warts and should be administered
Certain immunosuppressed conditions create a include destruction treatments (eg. laser and only with prior training or in a specialist
higher risk of developing recalcitrant warts, these electrosurgery), intralesional chemotherapy (eg. centre so that possible side effects can be
include acute leukemia,25 organ transplant26,27 and bleomycin and 5-fluorouracil) and intralesional monitored. A preferred option of the author is
Table 4. Summary of treatment and evidence for common warts
Method Level of evidence Comments

Salicylic acid2 I-A Benefits are established as compared to placebo but only modest. Most
trials look at use of salicylic acid in combination with other agents
Liquid nitrogen cryotherapy2,23 I-B Overall evidence is inconclusive to suggest a therapeutic advantage
of cryotherapy over other topical treatments or placebo. Aggressive
cryotherapy may be more effective but is offset by more pain and
blistering
Intralesional interferon2,23 I-C Trials use various forms of interferons (alfa, beta, gamma). Intralesional
injections are often painful and overall evidence of use is insufficient
Intralesional bleomycin I-C Cochrane review of trials used various dosages and concentrations
with different delivery systems, but none show sufficient evidence of
beneficial use2
I-B More recent studies showed significant benefits as compared to
cryotherapy19
Intralesional candida II-3B Data from case series and isolated reports. No RCT yet. Suggested use in
antigen1,20 the more recalcitrant types of warts
Intralesional MMR vaccine21 I-B One RCT and one time series executed with recalcitrant plantar warts.
Efficacy for other types of warts still unknown
Autoimplantation of wart II-3C Only one intention-to-treat series reported significant effects. No RCT
material22 available
Topical 5-fluorouracil2 I-C Efficacy significant with one study using cream preparation in children,
but overall evidence becomes limited when pooled with other studies
Intralesional 5-fluorouracil24 I-B One double blind RCT using a 5-fluorouracil mixture of epinephrine and
lidocaine
Topical podophyllin7 II-2D Good efficacy from older case series in 1970s, not recommended now for
toxicities. No known RCT
Topical imiquimod16 II-2C Approved for use in genital warts, only two case studies of efficacy for
plantar warts. Evidence is still lacking
Topical squaric acid18 II-3C Intention to treat studies showed efficacy in children and cases of
recalcitrant wart, known risks of contact dermatitis
Duct tape2 I-I Perhaps the most controversial of all treatments, modest efficacy from
an RCT in school children is later refuted by another RCT in adults.
Evidence is too conflicting to suggest benefit
Laser (CO2 and YAG)14 I-C Good efficacy from intention to treat case series especially with
recalcitrant warts and in children. The only RCT does not show evidence
of benefit over conventional treatment
Intense pulsed light15,30 I-I One case study combines photosensitiser with IPL and shows efficacy,
another RCT using IPL alone shows no efficacy. Evidence is lacking
Electrosurgery II-1C Good efficacy from case reports with known risks of scarring and deep
(electrodessication, tissue damage. One controlled trial compares electrocoagulation with
electrocoagulation and infrared coagulation with no difference, no known RCT. Often used for
cautery)7 recalcitrant warts
Surgical excision7 II-3D No RCTs so far, generally not recommended as first line treatment due to
scarring, pain and high rate of recurrence - up to 30%
Treating common warts - options and evidence CLINICAL
electrodessication (hyfrecation) of the lesion 2006;3:CD001781. Autoimplantation therapy for multiple warts. Indian J
3. Sterling JC, Handfield-Jones S, Hudson PM. Dermatol Venereol Leprol 2009;75:593-5.
under local anaesthesia, which often results in 23. Damstra RJ, van Vloten WA. Cryotherapy in the
Guidelines for the management of cutaneous warts.
clearance after a single treatment. However, Br J Dermatol 2001;144:4-11. treatment of condylomata acuminata: a controlled
4. Handisurya A, Schellenbacher C, Kirnbauer R. study of 64 patients. J Dermatol Surg Oncol
this option is contraindicated in patients with
Diseases caused by human papillomaviruses (HPV). J 1991;17:273-6.
poor wound healing (eg. uncontrolled diabetes Dtsch Dermatol Ges 2009;7:453-66. 24. Yazdanfar A, Farshchian M, Fereydoonnejad M.
or peripheral vascular diseases), keloid tendency 5. Jablonska S, Majewski S, Obalek S, et al. Cutaneous Treatment of common warts with an intralesional
warts. Clin Dermatol 1997;15:309-19. mixture of 5-fluorouracil, lidocaine, and epinephrine:
or patients with pace makers. It is also not
6. Gross G, Pfister H, Hagedorn M, et al. Correlation a prospective placebo-controlled, double-blind rand
recommended for lesions on the face. between human papillomavirus (HPV) type and his omized trial. Dermatol Surg 2008;34:656-9.
tology of warts. J Invest Dermatol 1982;78:160-4. 25. Tobin AM, Cotter M, Irvine AD, et al. Successful
Best practice for treating recalcitrant 7. Lipke MM. An armamentarium of wart treatments. treatment of a refractory verruca in a child with acute
warts Clin Med Res 2006;4:273-93. lymphoblastic leukaemia with topical cidofovir. Br J
Dermatol 2005;152:386-8.
8. Phoenix SL. Psychotherapeutic intervention for
numerous and large viral warts with adjunctive hyp 26. Sandoval M, Ortiz M, Diaz C, et al. Cutaneous mani
Destructive options include aggressive
nosis: a case study. Am J Clin Hypn 2007;49:211-8. festations in renal transplant recipients of Santiago,
cryotherapy (maximum paring down with Chile. Transplant Proc 2009;41:3752-4.
9. Dehghani F, Merat A, Panjehshahin MR, et al.
scalpel and longer freezing time of 6 seconds Healing effect of garlic extract on warts and corns. 27. Dharancy S, Catteau B, Mortier L, et al. Conversion to
Int J Dermatol 2005;44:612-5. sirolimus: a useful strategy for recalcitrant cutaneous
instead of the usual 3 seconds), hyfrecation
10. Bohlooli S, Mohebipoor A, Mohammadi S, et viral warts in liver transplant recipient. Liver Transpl
with local anaesthesia, laser treatment and al. Comparative study of fig tree efficacy in the 2006;12:1883-7.
thermocoagulation. treatment of common warts (verruca vulgaris) vs 28. Lowe S, Ferrand RA, Morris-Jones R, et al. Skin
cryotherapy. Int J Dermatol 2007;46:524-6. disease among human immunodeficiency virus-
Subject to availability 5-fluorouracil or infected adolescents in Zimbabwe: a strong indicator
11. Stefani M, Bottino G, Fontenelle E, et al. Efficacy
bleomycin can be administered either topically or comparison between cimetidine and zinc sulphate in of underlying HIV infection. Pediatr Infect Dis J
2010;29:346-51.
intralesionally, preferably in a specialist setting. the treatment of multiple and recalcitrant warts. An
Bras Dermatol 2009;84:23-9. 29. Dubina M, Goldenberg G. Viral-associated nonmela
Lesions with unusual morphology, bleeding noma skin cancers: a review. Am J Dermatopathol
12. Tosti A, Piraccini BM. Warts of the nail unit: surgi
or pigmentation should be biopsied to exclude cal and nonsurgical approaches. Dermatol Surg 2009;31:561-73.
30. Kalil CL, Salenave PR, Cignachi S. Hand warts
possible malignancy. 2001;27:235-9.
13. Huo W, Gao XH, Sun XP, et al. Local hyperthermia at successfully treated with topical 5-aminolevulinic
acid and intense pulsed light. Eur J Dermatol
44 degrees C for the treatment of plantar warts: a
Summary randomized, patient-blinded, placebo-controlled trial. 2008;18:207-8.
J Infect Dis 2010;201:1169-72.

Common nongenital warts are common and may
14. Sethuraman G, Richards KA, Hiremagalore RN, et al.
persist despite active treatment. Salicylic acid is Effectiveness of pulsed dye laser in the treatment
the best evidence based treatment for warts on of recalcitrant warts in children. Dermatol Surg
2010;36:58-65.
initial presentation and can be complemented by
15. Togsverd-Bo K, Gluud C, Winkel P et al. Paring and
liquid nitrogen cryotherapy. For recalcitrant warts, intense pulsed light versus paring alone for recalci
choices vary depending on availability and the trant hand and foot warts: a randomized clinical trial
with blinded outcome evaluation. Lasers Surg Med
training of the GP The expected efficacy must be
2010;42:179-84.
balanced against costs and possible side effects. 16. Mitsuishi T, Wakabayashi T, Kawana S. Topical
It is advisable to perform skin biopsy for suspicious imiquimod associated to a reduction of heel hyper
keratosis for the treatment of recalcitrant mosaic
lesions where necessary in order to exclude plantar warts. Eur J Dermatol 2009;19:268-9.
diagnoses such epidermodysplasia verruciformis 17. Moore AY Clinical applications for topical 5-fluoro-
uracil in the treatment of dermatological disorders. J
and verrucous carcinoma, which are HPV induced
Dermatolog Treat 2009;20:328-35.
squamous cell carcinomas of the skin.29 18. Hama N, Hatamochi A, Hayashi S, et al. Usefulness
of topical immunotherapy with squaric acid dibutyl
Author
ester for refractory common warts on the face and
Lawrence Leung MBBChir, BChinMed, MFM(Clin), neck. J Dermatol 2009;36:660-2.
FRACGP, FRCGP(UK), is Assistant Professor, 19. Dhar SB, Rashid MM, Islam A, et al. Intralesional
Department of Family Medicine, Queen’s bleomycin in the treatment of cutaneous warts:
University, Kingston, Ontario, Canada. a randomized clinical trial comparing it with
leungl@queensu.ca. cryotherapy. Indian J Dermatol Venereol Leprol

2009;75:262-7.
Conflict of interest: none declared. 20. Summers P Richards-Altmon P Halder R. Treatment
of recalcitrant verruca vulgaris with candida antigen
References in patient with human immunodeficiency virus. J
1. Clifton MM, Johnson SM, Roberson PK, et al. Drugs Dermatol 2009;8:268-9.
Immunotherapy for recalcitrant warts in children 21. Nofal A, Nofal E. Intralesional immunotherapy of
using intralesional mumps or Candida antigens. common warts: successful treatment with mumps,
Pediatr Dermatol 2003;20:268-71. measles and rubella vaccine. J Eur Acad Dermatol
2. Gibbs S, Harvey I. Topical treatments for cuta Venereol 2010 [Epub ahead of print].
neous warts. Cochrane Database Syst Rev 22. Shivakumar V, Okade R, Rajkumar V. correspondence afp@racgp.org.au
CLINICAL
ç Polymyalgia rheumatica
“ Diagnosis and management
There are occasional familial cases and there is

Background a clear north to south gradient with the highest
Polymyalgia rheumatica (PMR) is a common inflammatory rheumatic disease and an prevalence in Scandinavian countries and in
indication for long term treatment with oral steroids. Its incidence rises progressively
parts of the USA that have a population of a
beyond the age of 50 years. For the most part, PMR is managed in primary care.
similar ethnic background, a lower prevalence
Objective in Mediterranean countries and the lowest
This article highlights the main points in the British Society for Rheumatology and the prevalence in Arabian and Asian countries.7
British Health Professionals in Rheumatology guidelines that may be useful to general Studies report a cyclical yearly pattern of
practitioners in the primary care setting.
incidence and seasonal variations in incidence,
Discussion which might suggest an environmental infectious
Different levels of awareness of the condition between practitioners, and a lack of uniform aetiology7 Polymyalgia rheumatica is twice as
diagnostic criteria may impede correct diagnosis and management of PMR. Updated common in women as in men and is related to
international guidelines produced by the British Society for Rheumatology and the British giant cell arteritis (GCA), although the precise
Health Professionals in Rheumatology can aid diagnosis and direct treatment and disease relationship between the two conditions remains
monitoring.
unknown. Polymyalgia rheumatica is 2-3 times
Keywords: polymyalgia rheumatica; general practice; primary care more common than GCA.7
Clinical features
Polymyalgia rheumatica affects the shoulder
A Polymyalgia rheumatica (PMR) is a and hip girdles causing aching and morning
common rheumatic disease that affects stiffness related to synovitis of proximal joints
patients middle aged and older. Its and inflammation of extra-articular synovial
incidence increases progressively beyond structures.8 Patients may complain of difficulty
the age of 50 years.1 The reported annual getting out of bed or standing from the seated
incidence in Europe and the United position. Typically, morning stiffness lasts for 30
States of America varies between 1.3 minutes or more. The onset is often abrupt and
and 11.3 per 10 000 individuals aged symptoms are usually symmetrical. Pain can also
over 50 years.2-5 This wide variation may involve the neck, upper arms, lower back and
reflect differing levels of awareness of thighs. Distal musculoskeletal manifestations
the condition between practitioners, or may include carpal tunnel syndrome and
a lack of uniform criteria used to make nonerosive, asymmetrical peripheral arthritis
the diagnosis. A United Kingdom study6 (affecting the knees and small joints of the hands
demonstrated that general practitioners and feet) and are seen in about half of patients.9
do not always use established criteria Atypical presentations involving asymmetrical
to diagnose PMR. This may result in proximal joint symptoms or younger patients may
unnecessary further investigation and occasionally occur.
needlessly expose patients to the risks Examination findings may be minimal and
associated with long term steroid use. include painful restriction of active and passive
movements of the shoulder and hip joints, usually
While the aetiology of PMR remains elusive, without detectable proximal joint swelling.
both environmental and genetic risk factors Muscle strength is usually normal, although
are thought to contribute to its development.7 interpretation may be difficult because of pain.
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 5, MAY 2011 303
CLINICAL Polymyalgia rheumatica - diagnosis and management
Systemic signs and symptoms such as low grade Table 1. Polymyalgia rheumatica: core inclusion criteria (all these criteria are
fever, depression, fatigue, anorexia, and weight required for a diagnosis)
loss may occur in up to 40% of patients.7
• Bilateral shoulder or pelvic girdle aching - or both
Diagnosis • Morning stiffness longer than 45 minutes
There are no specific diagnostic tests • Age older than 50 years
for polymyalgia rheumatica. The British • Duration >2 weeks
Society for Rheumatology and the British • Evidence of an acute phase response (raised ESR/CRP)
Health Professionals in Rheumatology have
published joint guidelines on the diagnosis
and management of polymyalgia rheumatica.9 Table 2. Conditions that may mimic polymyalgia rheumatica
Good scientific evidence is currently lacking • Active cancer (eg. multiple myeloma, lymphoma, leukaemia)
and most of the recommendations for diagnosis
• Infections: viral or bacterial
and treatment included in these guidelines are
• Giant cell arteritis
graded at level B or C. The guidelines recommend
• Rheumatic diseases
a stepped diagnostic and management process
- late onset rheumatoid arthritis (symmetrical peripheral synovitis, positive
with diagnosis involving identification of core
rheumatoid factor and anticyclic citrullinated peptide antibodies, joint erosions,
inclusion criteria and exclusion of conditions extra-articular manifestations)
that may mimic PMR - exclusion criteria (Table - remitting seronegative symmetrical synovitis with pitting oedema (RS3PE
1, 2). Inclusion and exclusion criteria should be syndrome)
documented in the patient’s medical record. - late onset spondyloarthopathy (peripheral enthesitis, dactylitis, anterior uveitis,
HLA-B27, and radiological evidence of sacroüiitis)
Suspected giant cell arteritis - late onset systemic lupus erythematosus, other connective disease
Regardless of the presence of PMR, if the - polymyositis (proximal muscular weakness rather than pain, increased muscle
with or without creatine kinase, myopathic electromyogram changes)
acute phase reactants are elevated and this is
- pseudogout
associated with new headache or an unexplained
- fibromyalgia (younger, absence of typical joint stiffness, normal inflammatory
pain located above the neck, it is important to
markers)
consider a diagnosis of GCA. Features of this
• Hypothyroidism
condition include headache, jaw claudication and
• Drug induced (eg. statin myopathy)
visual symptoms. If GCA is suspected, commence
treatment with high dose steroids immediately
• Chronic pain syndrome (osteoarthritis of neck or shoulder, fibromyalgia)
and refer the patient to a hospital emergency • Local shoulder or hip pathology
department without delay.10 The Therapeutic
Guidelines: rheumatology13 suggest steroids and Adapted from Gonzalez-Gay et al10
urgent ophthalmology referral.
cases (range 7-20%).11 C-reactive protein is a imaging (eg. scintigraphy, magnetic resonance
Investigations more sensitive indicator of disease activity than imaging, ultrasonography) to detect synovitis in
So long as there are no features that suggest ESR in PMR as it is less affected by extraneous proximal joints and periarticular structures.
GCA, urgent institution of steroid therapy is not factors such as increasing age.11 Patients in
necessary, and treatment can be delayed to whom evidence of inflammation on blood testing Management
enable further investigation. Suggested initial is equivocal should be referred for specialist
Corticosteroids
laboratory investigations in PMR are listed in assessment.9 Patients with PMR may have a
Table 3. normochromic, normocytic anaemia and raised Once the diagnosis is established, the patient
Laboratory test findings in PMR are alkaline phosphatase but creatinine kinase is should be commenced on low dose steroid
nonspecific and usually indicate the presence invariably normal (in contrast to elevated levels therapy. The dose is then gradually tapered over
of inflammation with elevated erythrocyte in polymyositis, hypothyroidism and other muscle time. It is important to counsel the patient about
sedimentation rate (ESR) and C-reactive protein diseases). potential risk factors associated with long term
(CRP). However, the presence of PMR can be The extent of further investigations steroid therapy (Table 4).
established in the setting of a normal ESR if there will depend on the level of certainty of the Osteoporotic risk with long term steroid
is a classic clinical picture and a good response diagnosis. Secondary investigations may include therapy can be minimised by using the minimum
to steroids; this occurs in up to one-fifth of autoantibody screening, muscle biopsy and effective steroid dose. A recent meta-analysis
304 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 5, MAY 2011
Polymyalgia rheumatica - diagnosis and management CLINICAL
Bone protection
Table 3. Suggested initial laboratory investigation in polymyalgia rheumatica
The decision about the use of a bone sparing
• Full blood count agent (eg. oral biphosphonate) for bone
• ESR/plasma viscosity and/or CRP
protection when initiating steroids for PMR
• Urea and electrolytes
depends on the clinical risk of developing
• Liver function tests
• Calcium, phosphate, albumin, alkaline phosphatase glucocorticoid induced osteoporosis. A recent
• Protein electrophoresis (also consider urinary Bence Jones protein) review suggests that osteoporotic risk in
• Thyroid stimulating hormone PMR varies widely, from 3.6-27%, and from
• Creatine kinase 58-91%.12 However, all individuals with PMR
• Rheumatoid factor (antinuclear antibody and anticyclic citrullinated peptide should commence calcium and vitamin D
antibodies may be considered) supplementation and receive advice about weight
• Dipstick urinalysis
bearing exercise. In patients deemed at high
fracture risk clinically (eg. prior fragility fracture,
showed that starting prednisolone doses of 15 • 10-20 mg orally, daily in the morning initially high steroid dose) or following dual energy X-ray
mg/day or lower was associated with lower for 2-4 weeks absorptiometry (DXA) scan, a bone sparing agent
cumulative steroid dosages than higher starting • then reduce the daily dose by 2.5 mg every (eg. oral biphosphonate) should be considered.
doses and that higher doses of corticosteroids 2-4 weeks until the daily dose is less than Medicare rebates are available for patients
were associated with more adverse effects.12 In 10 mg having DXA scan who are currently on prolonged
addition, higher doses may mask those conditions • then decrease the daily dose by 1 mg every glucocorticoid therapy (such as equivalent to or
whose symptoms mimic PMR (Table 2). 4-8 weeks. greater than 7.5 mg prednisolone daily for a for a
There is no consistent evidence for an ideal Intramuscular methylprednisolone (intramuscular period anticipated to last for at least 4 months).16
steroid regimen that is suitable for all patients. depomedrone) may be used in milder cases Some bisphosphonates are available on the
Therefore, the approach to treatment must be and may reduce the risk of steroid related Pharmaceutical Benefits Scheme for: 'Treatment
flexible and tailored to the individual. Dose complications. Initial dose is 120 mg every 3-4 as the sole PBS subsidised anti-resorptive agent
adjustment may be required for disease severity, weeks, reducing by 20 mg every 2-3 months.14 for corticosteroid induced osteoporosis in a
comorbidity, side effects and patient wishes. The The addition of nonsteroidal anti patient currently on long term (at least 3 months),
British Society for Rheumatology and the British inflammatory drugs to glucocorticoid regimens high dose (at least 7.5 mg per day prednisolone
Health Professionals in Rheumatology consensus for the treatment of patients with PMR has or equivalent) corticosteroid therapy with a bone
regimen suggests using:9 shown no advantage over steroids alone in terms mineral density (BMD) T-score of -1.5 or less.'17
• daily prednisolone: 15 mg for 3 weeks of duration of therapy or daily or cumulative
Follow up and monitoring
• then 12.5 mg for 3 weeks prednisone doses, but produced more adverse
• then 10 mg for 4-6 weeks events.15 In specialist settings, glucocorticoid Early follow up is vital to evaluate response to
• then reduction by 1 mg every 4-8 weeks sparing agents such as methotrexate and other initial therapy and to confirm the diagnosis.18
or alternate day reductions (eg. 10/7.5 mg biological and nonbiological agents may be A patient reported global improvement of
alternate days). considered. >70% within 1 week of commencing steroids is
The Therapeutic Guidelines rheumatology group
suggest a similar regimen:13 Table 5. Indications for referral in polymyalgia rheumatica
Atypical features
Table 4. Risks of long term steroid
therapy • Age younger than 60 years
• Chronic onset more than 2 months
• Osteoporosis • Lack of shoulder involvement
• Weight gain • Lack of inflammatory stiffness
• Skin bruising • Prominent systemic features, weight loss, night pain, neurological signs
• Raised blood pressure • Features of other rheumatic disease
• Impaired blood glucose • Normal or extremely high acute phase response
• Depression
• Cardiac failure Treatment dilemmas
• Increased risk of infection • Incomplete, poorly sustained or nonresponse to corticosteroids
• Cataracts • Inability to reduce corticosteroids
• Glaucoma • Contraindications to corticosteroid therapy
• Cushing syndrome • Prolonged corticosteroid therapy (more than 2 years)
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 5, MAY 2011 305
CLINICAL Polymyalgia rheumatica - diagnosis and management
Polymyalgia rheumatica: a disorder of extraar

consistent with a diagnosis of PMR. Inflammatory • Suspect PMR in the elderly patient with
ticular synovial structures? J Rheumatol
markers usually normalise within 4 weeks. A bilateral shoulder ache and stiffness. 1 999;26:517-21.
lesser response should prompt a search for an • Document inclusion and exclusion criteria 9. Dasgupta B, Borg F, Hassan N, et al. BSR and
BHPR guidelines for the management of polymy
alternative condition. If a relapse of PMR is in the medical record.
algia rheumatica. Oxford: Oxford University Press,
suspected as the steroid dose is being tapered, • Use the minimum effective steroid dose 2009.
the steroid dose can be increased to the initially (15 mg/day prednisolone or less). 10. Gonzalez-Gay M. The diagnosis and management
of patients with giant cell arteritis. J Rheumatol
previously effective dose level and dose reduction • Taper steroids gradually (<1 mg/month); 2005;32:1186-8.
recommenced from that level.13 relapses are common. 11. Cantini F, Salvarani C, Olivieri I, et al. Erythrocyte
sedimentation rate and C-reactive protein in the
Each follow up encounter with the GP should • Assess the need for bone sparing agents
evaluation of disease activity and severity in
try to explore the following: and institute osteoporosis prophylaxis polymyalgia rheumatica: a prospective follow-up
• response to treatment - degree of reduction early, if required. study. Semin Arthritis Rheum 2000;30:17-24.
12. Hernandez-Rodriguez J, Cid M, Lopez-Soto A,
in proximal pain, fatigue and morning • Atypical features and treatment dilemmas
et al. Treatment of polymyalgia rheumatica:
stiffness warrant referral. a systematic review. Arch Intern Med
• complications of disease including symptoms 2009;169:1839-59.

Resource 13. Rheumatology Expert Group. Polymyalgia rheu-
of GCA (eg. headaches, jaw claudication and matica and giant cell arteritis. In: Therapeutic
large vessel disease) The stepped diagnostic and management Guidelines: rheumatology. Melbourne:
Therapeutic Guidelines, 2010.
• steroid related adverse events process recommended by the British Society
14. Dasgupta B, Dolan AL, Fernandes L, et al. An
• atypical features or other mimicking for Rheumatology and the British Health initially double-blind controlled 96 week trial of
conditions Professionals in Rheumatology is available depot methylprednisolone against oral predniso
lone in the treatment of polymyalgia rheumatica.
• laboratory monitoring (full blood count, ESR/ at http://rheumatology.oxfordjournals.org/
Brit J Rheumatol 1998;37:189-95.
CRP, urea and electrolytes, glucose) every 4-6 content/49/1/186/F2.large.jpg. 15. Gabriel S, Sunku J, Salvarani C, et al. Adverse
weeks. outcomes of antiinflammatory therapy among
Author patients with polymyalgia rheumatica. Arthritis
Duration of treatment can vary from 1-3 years,
Oliver van Hecke MBChB, MRCGP, FRACGP, Rheum 1997;40:1873-8.
and some patients will require small doses of is Lecturer, Department of General Practice, 16. Australian Government Department of Health
steroids beyond 3 years.7 Slow prednisolone dose and Ageing. Medicare Benefits Schedule - Note
Monash University, Melbourne, Victoria. oliver.
D1.27. Available at www9.health.gov.au/mbs/
tapering (<1 mg/month) is important as slower vanhecke@monash.edu. fullDisplay.cfm?type=note&qt=NoteID&q=D1.27.
tapering regimens are associated with fewer 17. Australian Government Department of Health
and Ageing. Pharmaceutical Benefits Scheme.
relapses and earlier glucocorticoid treatment Conflict of interest: none declared.
Available at www.pbs.gov.au/browse/body-
cessation than faster tapering regimens.12 system?depth=4&codes=m05ba.
Steroids may be stopped when the patient is References 18. Dasgupta B, Salvaran I, Schirmer M, et al.
1. Salvarani C, Cantini F, Boiardi L, et al. Development of classification criteria for
asymptomatic from their inflammatory symptoms. Polymyalgia rheumatica and giant-cell arteritis. polymyalgia rheumatica (PMR): results from an
Isolated raised ESR or CRP is not an indication for N Engl J Med 2002;347:261-7. expert work group meeting and a wider survey. J
2. Gran J, Myklebust G. The incidence of poly Rheumatol 2008;35:270-7.
continuing steroid therapy but may require further
myalgia rheumatica and temporal arteritis
investigation and referral. in the county of Aust Agder, South Norway:
a prospective study 1987-94. J Rheumatol
When to refer? 1997;24:1739-43.
3. Salvarani C, Macchioni P, Zizzi F, et al.
The British Society for Rheumatology and the Epidemiologic and immunogenetic aspects of
British Health Professionals in Rheumatology polymyalgia rheumatica and giant cell arteritis
in Northern Italy. Arthritis Rheum 1991;34:351-
guidelines advise early specialist referral in 6.
cases with atypical features or when treatment 4. Doran M, Crowson C, O’Fallon W, et al. Trends
in the incidence of polymyalgia rheumatica
dilemmas arise (grade C recommendation)
over a 30 year period in Olmsted County,
(Table 5).9 Minnesota, USA. Rheumatol 2002;29:1694-7.
5. Chuang T, Hunder G, Ilstrup D, et al.
Summary Polymyalgia rheumatica: a 10-year epide
miologic and clinical study. Ann Intern Med
• Polymyalgia rheumatica is a chronic relapsing 1982;97:672-80.
disease, managed for the most part in primary 6. Barraclough K, Liddell WG, du Toit J, et al.
Polymyalgia rheumatica in primary care: a
care. The extended use of steroids in this
cohort study of the diagnostic criteria and
population group places extra emphasis outcome. Fam Pract 2008;25:328-33.
7. Salvarani C, Cantini F, Hunder G. Polymyalgia
on accurate diagnosis, safe management,
rheumatica and giant-cell arteritis. Lancet
ongoing monitoring of disease activity and 2008;372:234-45.
prevention of complications. 8. Salvarani C, Cantini F, Olivieri I, et al. correspondence afp@racgp.org.au
306 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 5, MAY 2011
FOCUS Mental health
@ Anxiety disorders
a a
Michael Kyrios
Richard Moulding
Assessment and management in
Maja Nedeljkovic
general practice
• Anxiety is a normal human physiological mechanism

Background designed to help the body respond to a threat. The
Anxiety is a normal physiological response to a threat.
autonomic changes that occur in anxiety are essential to
Anxiety disorders occur when this normal physiological
response is associated with high levels of autonomic avoid danger and moderate anxiety can actually improve
arousal, erroneous cognitions and dysfunctional coping performance. However, when anxiety is associated
strategies. Anxiety disorders are highly prevalent and with very high levels of autonomic arousal, erroneous
present commonly to general practice. Anxiety disorders cognitions including exaggerated threat perceptions
are often comorbid with other psychiatric and medical and dysfunctional coping strategies, it can result in
disorders and may be associated with significant morbidity. significant distress and impairment in work, school,
Objective family, relationships, and/or activities of daily living.
This article describes the diagnosis, assessment and Patients presenting with anxiety symptoms in the general
management of anxiety disorders in the general practice practice setting do not always fit the criteria for a specific
setting. anxiety disorder. However, it is important for the general
practitioner to know how to assess patients for specific
Discussion
anxiety disorders and the basic principles of management
Assessment in patients presenting with anxiety symptoms
involves excluding a medical cause, identifying features of these disorders. Equally, GPs need strategies to manage
of specific anxiety disorders as well as other coexisting patients with distressing anxiety symptoms who do not
psychiatric disorders, and assessing the degree of fulfil the criteria for the diagnosis of a specific anxiety
distress. Management options include psychoeducation, disorder and/or where the anxiety coexists with another
psychological treatments (particularly cognitive behaviour mental health disorder (such as depression), substance
therapy) and pharmacological treatments. Patients with abuse or medical condition.1
a diagnosis of an anxiety disorder can access Medicare
funded psychological care under a number of Australian Twelve month prevalence rates in Australia indicate that anxiety
government initiatives. Selective serotonin reuptake disorders are the most common mental health problem, affecting
inhibitors and serotonin norepinephrine reuptake inhibitors
14.4% of the population (although some people experienced more
are the first line pharmacological agents used to treat
than one type of anxiety disorder). Post-traumatic stress disorder
anxiety disorders. Regular review is vital to monitor for
(PTSD) is the most widespread affecting 6.4% of the population,
clinical improvement and more complex presentations may
followed by social phobia (4.7%), agoraphobia (2.8%), generalised
require specialist psychological or psychiatric referral.
anxiety disorder (GAD, 2.7%), panic disorder (2.6%), and obsessive
Keywords: anxiety disorders; mental health; treatment
compulsive disorder (OCD, 1.9%).2 Women experienced higher rates
than men (18% and 11% respectively), and the highest rate of anxiety
disorders was in the 35-44 years age group (18%). One in 5 women
and one in 10 men report a specific phobia.3 General practice is often
the first port-of-call for patients with anxiety disorders; one in 10
people experiencing an anxiety disorder within the past 12 months
visited a GP for their mental health problems but did not receive care
from any other provider.4 The Bettering the Evaluation and Care of
Health program showed that GPs treat psychological problems at a
rate of 11.5 per 100 encounters and anxiety is the second commonest disorder such as depression, bipolar disorder or a psychotic disorder.
psychological problem managed after depression.5 It is important to screen for these diagnoses at the initial assessment.
For example, the ruminative thoughts seen in depression can be similar
Assessment to worry, but they usually are more concerned with past events, self
Initial assessment should begin with a focused history. Allow criticism and guilt, rather than future events. If a specific anxiety
the patient to describe the symptoms they find most concerning disorder is diagnosed, there is a high risk that the patient will also have
and enquire about substance use as well as symptoms that may a psychiatric comorbidity or significant substance use. For example, the
be suggestive of a medical condition. Physical examination and presence of GAD increases the likelihood of having depression by an
investigations should concentrate on excluding an underlying medical odds ratio of 28.9.7 Anxiety disorders themselves tend to co-occur and
cause. Medical conditions that can be associated with anxiety include:6 the greater the comorbidity, the greater the likelihood of help seeking.8
• hypoglycaemia Hypochondriasis is another important diagnosis to consider in the
• hyper- or hypo-thyroidism
• cardiac disorders
• chronic respiratory disease
• vitamin B deficiency
• inner ear conditions
• acute reactions to aspartame
• withdrawal from benzodiazepines.
If there is no evidence of a medical cause
for the patient’s symptoms, assessment
should move on to looking for features
of specific anxiety disorders as well as
other coexisting psychiatric disorders,
and assessing the degree of distress.
Symptoms of specific
anxiety disorders
Diagnosis of specific anxiety disorders
involves identification of a specific focus
for the anxiety. For instance, if a patient
has panic attacks and catastrophises
about these as indicating an imminent
heart attack/suffocation, a diagnosis
of panic disorder may be warranted.
However, if anxiety or the panic attacks
occur only on exposure to social
situations, then social phobia may be
the diagnosis (Figure 1). Full diagnostic
criteria are available in the Diagnostic
and Statistical Manual of Mental
Disorders (4th edn, text revision) (DSM-
IV-TR).6 Of course, in the general practice
setting, many patients do not fit neatly
into this framework and have symptoms
of multiple disorders without fulfilling the
criteria for a specific disorder.
Coexisting psychiatric
disorders
Anxiety may be a symptom of, or coexist
Figure 1. Differential diagnosis of anxiety disorders
with, another underlying psychiatric
FOCUS Anxiety disorders - assessment and management in general practice
primary care setting. Hypochondriasis is considered a somatoform feared stimuli in a graded fashion until anxiety reduces. The diagnosis
disorder, not an anxiety disorder, however, there can be some overlap will indicate the stimuli to which the individual will require exposure,
between the symptoms of hypochondriasis and OCD. Both may exhibit for example, bodily sensations in panic disorder or social situations
obsessions about health, with reassurance seeking from medical in social phobia. Usually exposure techniques are coupled with
professionals for short term relief.9 The panic attacks that characterise behavioural strategies to address avoidance behaviour and cognitive
panic disorder and GAD are particularly prominent, with panic attacks strategies that challenge specific maladaptive beliefs (eg. ‘I must
often misattributed to medical symptoms (eg. arriving at a hospital control my horrible thoughts’ in OCD). Other aspects of CBT for anxiety
emergency department with a ‘heart attack’). However, in OCD the include training in problem solving to help patients develop adaptive
patient recognises that their ruminations are irrational, whereas in coping and interpersonal skills and relapse prevention strategies.
hypochondriasis they do not. In addition to in-session exposure practice, home based tasks and
monitoring sheets to help the patient report on their experiences
Assessing the degree of distress between consultations have been shown to be helpful.16-18 Online
An anxiety checklist or self report inventory may be helpful to quantify information and treatments for anxiety disorders may be helpful. These
levels of anxiety and track the severity of symptoms over time and are outlined in more detail in the article ‘Anxiety and depression:
in response to treatment. These include the Depression Anxiety online resources and management tools’ by Reynolds et al in this issue
Stress Scales-21 (DASS)10 (see Resources) and the Penn State Worry of Australian Family Physician.
Questionnaire).11 The Kessler 10 (K-10) questionnaire, which measures
general distress, is also a useful objective measure of distress caused
Pharmacological management
by psychiatric symptoms12 (see Resources). Selective serotonin reuptake inhibitors (SSRIs) and serotonin
noradrenaline reuptake inhibitors (SNRIs) are the first line
Management pharmacological agents used to treat anxiety disorders, however
Psychoeducation not all are available on the Pharmaceutical Benefits Scheme (PBS)
for this indication (Table 1).19 Benzodiazepines are commonly used
Psychoeducation about the nature of anxiety, its purpose and how it in panic disorder and GAD, however, their chronic use is associated
can present is important when dealing with someone with any anxiety with significant potential problems including tolerance, dependence,
disorder. Most individuals with anxiety symptoms will also suffer a withdrawal, relapse, rebound, interactions with other medications
secondary ‘worry about worry’ (eg. that anxiety is dangerous, that they and adverse events.20-22 There is inconsistent data about the long
are going crazy or ‘losing it’), which clearly exacerbates the anxiety.
Psychoeducation is also an important lead in to some treatment Table 1. PBS listing for SSRIs used in anxiety
options (eg. relaxation, cognitive behaviour therapy [CBT], exercise, disorders
*
yoga). As a trusted and authoritative source of information about
Escitalopram Listed as Restricted Benefit for the
health and physiology, GPs are in an excellent position to provide such treatment of major depressive disorder
information. (MDD) and treatment of moderate to
severe GAD in a patient who has not
Psychological treatments responded to nonpharmacological
therapy, AND
Psychological treatments have been shown to be at least as effective
• for whom a GP Mental Health Care
as medication for anxiety disorders, with CBT having the greatest
Plan, as described under Item 2710 of
evidence for efficacy.13,14 Some GPs may have special skills in the the Medicare Benefits Schedule, has
area of CBT but in most cases the patient will need to be referred been prepared, OR
to a psychologist. Patients with a diagnosis of an anxiety disorder • who has been assessed by a
can access Medicare funded psychological care under a number of psychiatrist
Australian government initiatives. These generally involve completion Fluoxetine Listed as Restricted Benefit for MDD and
and billing under Medicare for a GP Mental Healthcare Plan or Review
(items 2710 and 2712) (see Resources).
a OCD
Cognitive behaviour therapy for anxiety disorders starts with Paroxetine Listed as Restricted Benefit for MDD,
OCD and panic disorder
psychoeducation about anxiety, as outlined above, and training
patients in relaxation techniques (such as progressive muscular Sertraline Listed as Restricted Benefit for MDD,
OCD and panic disorder where
relaxation or guided imagery) or increasingly, mindfulness based
other treatments have failed or are
meditation. Preliminary evidence indicates that mindfulness techniques inappropriate
may be of particular benefit.15 Exposure techniques are helpful if there
* Refer to www.pbs.gov.au
is a specific feared stimulus. These involve exposing the patient to
Anxiety disorders - assessment and management in general practice FOCUS
term efficacy of benzodiazepines, however, they have clear short term management to motivate her, an exposure program to
efficacy, quick onset of action and generally good tolerance.20 Ideally,
challenge her avoidance, and a cognitive therapy program
to help Simone with control of her worry. Within two lots
benzodiazepines should be restricted to short term use (eg. up to 4
of six individual sessions, Simone’s anxiety and avoidance
weeks) and at the lowest possible doses.22 Azapirones, a group of
have ameliorated, although her chronic worrying is still a
drugs that work at the 5-HT1A receptor, are also used to treat GAD, but
problem. The psychologist suggests the GP refer Simone to
findings for their efficacy are conflicting.23 Tricyclic antidepressants a 10 session group therapy program run at a local university
and monoamine oxidase inhibitors as well as adjunctive treatment psychology clinic. Subsequently, Simone’s quality of life
with anticonvulsants and atypical antipsychotics may be considered in improves significantly.
treatment resistant cases.19
Case study 2
Pharmacological, nonpharmalogical Jack, aged 46 years, presents with severe dermatitis on
or both his hands. He reports constantly washing his hands and
has always been concerned about ‘catching germs and
It is important to note that the management of anxiety disorders
diseases’. More recently, following an overseas trip where
with concurrent CBT and pharmacotherapy has not been found to
he caught a severe flu, he has become hypervigilant about
be superior in the longer term to either treatment alone, despite ‘avoiding germs’ and can hardly think about anything else.
its continued use in practice.24,25 Some researchers consider the He complains of symptoms of depression, which are severe
concurrent use of CBT and anxiolytic medications to be detrimental to enough for a diagnosis of a major depressive episode,
the extinction phase of exposure based therapies, which is dependent and feels unable to cope with life. He refuses to leave the
on the effects that glucocorticoid activity has on learning of emotional house except under enormous duress and cannot take
material.26 Patients value both CBT and pharmacotherapy, but tend public transport to go to work in the abattoir where he is a
to prefer CBT to medication for the treatment of anxiety disorders, manager. He has a large mortgage and is at risk of losing
and see CBT as more likely to be effective in the long term.27,28 A his job.
Jack’s GP assesses Jack and assesses that the primary
commonly used rule of thumb is to start with CBT and, if patients do
diagnoses are major depression and OCD, with a secondary
not respond or if significant depression levels are present, to consider
dermatitis caused by abrasions from overwashing of hands.
pharmacotherapy. For more severe forms of presentation, starting
He completes a Mental Health Plan and refers Jack to a
off with an evidence based medication is considered prudent before
clinical psychologist who specialises in the treatment of
commencing CBT. Either way, patient preferences and characteristics OCD. The psychologist suggests a CBT program focusing
must be considered in clinical decision making. Regular review is vital on activity management to motivate Jack, a program of
to monitor for clinical improvement. More complex presentations (eg. exposure with response prevention for the OCD, as well
severe, comorbid) or disorders requiring more specialised psychological as a cognitive therapy program. Unfortunately, Jack’s
interventions (eg. OCD, PTSD, GAD) may necessitate referral to a depression makes it difficult for him to undertake any of
psychologist or psychiatrist with a special interest in these areas. the psychological strategies. Jack is started on a SSRI
following consultation between the psychologist and GP.
Case study 1 Jack responds very positively to the combined intervention,
Simone, aged 35 years, reports generally being a ‘worry and within 10 weeks has a moderate severity rating on an
wart’ and details a range of chronic symptoms including OCD measure. The psychologist further suggests that Jack
feeling nervous and jumpy, palpitations, hyperventilating undertake an online treatment for OCD before seeing him
and nausea. More recently, she was caught up in an armed for a further two sessions to discuss relapse prevention
robbery at the local supermarket. Since this event, Simone strategies. The additional treatment produces further
reports insomnia and intrusive worries that it might happen amelioration in OCD and depressive symptoms. Jack is
again. She has avoided going to the supermarket since the able to return to work and function satisfactorily. Jack’s
robbery and is reticent to leave the house at all, even for GP continues to monitor him for another 12 months before
work. She is slowly becoming more isolated and depressed. commencing a process to cease the SSRI.
Simone’s GP suspects that she is suffering from PTSD
with depression following the armed robbery, on the Summary of important points
background of underlying generalised anxiety symptoms.
• Anxiety disorders occur when the normal physiological response
After a full history and examination, the GP completes
to a threat is associated with high levels of autonomic arousal,
a Mental Health Plan and refers Simone to a clinical
psychologist who specialises in the treatment of PTSD. erroneous cognitions and dysfunctional coping strategies.
The psychologist undertakes a thorough diagnostic • Anxiety disorders are highly prevalent, present commonly to
interview and also diagnoses a pre-existing GAD. The general practice and are associated with significant morbidity.
psychologist suggests a CBT program focusing on anxiety • Anxiety disorders are often comorbid with other psychiatric and
management training to decrease Simone’s arousal, activity medical disorders.
FOCUS Anxiety disorders - assessment and management in general practice
• Assessment in patients presenting with anxiety symptoms involves 6. American Psychiatric Association. Diagnostic and statistical manual
of mental disorders. 4th edn. Washington, DC: American Psychiatric
excluding a medical condition, identifying features of specific Association, 2000.
anxiety disorders, as well as other coexisting psychiatric disorders 7. Andrews G, Slade T, Issakidis C. Deconstructing current comorbidity: data
from the Australian National Study of Mental Health and Well-Being. Br J
and assessing the degree of distress.
Psychiatry 2002;181:306-14.
• Management options in anxiety disorders include 8. Issakidis C, Andrews G. Service utilisation for anxiety in an Australian com
psychoeducation, psychological treatments (particularly CBT) and munity sample. Soc Psychiatry Psychiatr Epidemiol 2002;37:153-63.
9. Salkovskis PM, Warwick HMC, Deale AC. Cognitive-behavioral treatment
pharmacological treatments.
for severe and persistent health anxiety (hypochondriasis). Brief Treat Crisis
• Patients with a diagnosis of an anxiety disorder can access Interv 2003;3:353-68.
Medicare funded psychological care under a number of Australian 10. Lovibond PF, Lovibond SH. The structure of negative emotional states: com
parison of the Depression Anxiety Stress Scales with the Beck Depression
government initiatives.
and Anxiety Inventories. Behav Res Ther 1995;33:335-43.
• SSRIs and SNRIs are the first line pharmacological agents used to 11. Meyer TJ, Miller ML, Metzger RL, Borkovec TD. Development and validation
treat anxiety disorders. of the Penn State Worry Questionnaire. Behav Res Ther 1990;28:487-95.
12. Kyrios M, Hegarty K. Self-monitoring and psychometric tools. In: Blashki G,
• Regular review is vital to monitor for clinical improvement and Judd F, Piterman L, editors. General practice psychiatry. North Ryde, NSW:
more complex presentations may require specialist psychological or McGraw-Hill, 2007;356-72.
13. Olatunji BO, Cisler JM, Deacon BJ. Efficacy of cognitive behavioral therapy
psychiatric referral.
for anxiety disorders: a review of meta-analytic findings. Psychiatr Clin North
Am 2010;33:557-77.
Resources 14. Deacon BJ, Abramowitz JS. Cognitive and behavioral treatments for anxiety
disorders: a review of meta-analytic findings. J Clin Psychol 2004;60:429-41.
• The Depression Anxiety Stress Scales-21 is available from the
15. Allen NB, Chambers R, Knight W, Melbourne Academic Mindfulness Interest
University of New South Wales School of Psychology: www2.psy. Group. Mindfulness-based psychotherapies: a review of conceptual founda
unsw.edu.au/groups/dass tions, empirical evidence and practical considerations. Aust N Z J Psychiatry
2006;40:285-94.
• The K-10 questionnaire is available from the Black Dog Institute: 16. Roemer L, Orsillo SM, Salters-Pedneault K. Efficacy of an acceptance-based
www.blackdoginstitute.org.au/docs/5.K10withinstructions.pdf behavior therapy for generalized anxiety disorder: evaluation in a randomized
controlled trial. J Consult Clin Psychol 2008;76:1083-9.
• Information about GP Mental Health Care Medicare Items: www.
17. Kyrios M. Exposure and response prevention in the treatment of obsessive
health.gov.au/internet/main/publishing.nsf/content/health-pcd-gp- compulsive disorder. In: Menzies R, Silva P de, editors. Obsessive-compulsive
mental-health-care-medicare. disorder: theory, research and treatment. Chichester, England: Wiley,
2003;259-74.
Authors 18. Kazantzis N, Deane FP, Ronan KP. Homework assignments in cognitive and
behavioral therapy: a meta-analysis. Clin Psychol 2000;7:189-202.
Michael Kyrios BA(Psych, Phil), DipEd(Psych), MPsych(Clin Psych),
19. Ravindran LN, Stein MB. The pharmacologic treatment of anxiety disorders: a
PhD(Clin Psych), FAPS, is Professor of Psychology and Director of the
review of progress. J Clin Psychiatry 2010;71:839-54.
Brain and Psychological Sciences Research Centre, Faculty of Life 20. Lader MH. Limitations on the use of benzodiazepines in anxiety and insom
and Social Sciences, Swinburne University of Technology, Melbourne, nia: are they justified? Eur Neuropsychopharmacol 1999;9:S399-405.
Victoria. mkyrios@swin.edu.au 21. Kaplan EM, Du Pont RL. Benzodiazepines and anxiety disorders: a review for
the practicing physician. Curr Med Res Opin 2005;21:941-50.
Richard Moulding BSc(Hons), MPsych(Clin Psych), PhD, MAPS, is a
22. Cloos JM, Ferreira V. Current use of benzodiazepines in anxiety disorders.
lecturer, Brain and Psychological Sciences Centre, Faculty of Life and Curr Opin Psychiatry 2009;22:90-5.
Social Sciences, Swinburne University of Technology, Melbourne, 23. Chessick CA, Allen MH, Thase M, et al. Azapirones for generalized anxiety
Victoria. disorder. Cochrane Database Syst Rev, Issue 3. Art. No.: CD006115. DOI:
10.1002/14651858.CD006115. 2006.
Maja Nedeljkovic BSc(Hons), MPsych(Clin Psych), PhD, MAPS, is a
24. Foa EB, Franklin ME, Moser J. Context in the clinic: How well do cognitive-
Lecturer, Brain and Psychological Sciences Centre, Faculty of Life and behavioral therapies and medications work in combination? Biol Psychiatry
Social Sciences, Swinburne University of Technology, Melbourne, 2002;52:987-97.
Victoria. 25. Hofmann SG, Sawyer AT, Korte KJ. Is it beneficial to add pharmacotherapy
to cognitive-behavioral therapy when treating anxiety disorders? A meta-
Conflict of interest: none declared. analytic review. Int J Cogn Ther 2009;2:160-75.
26. Otto MW, McHugh RK, Kantak KM. Combined pharmacotherapy and
cognitive-behavioral therapy for anxiety disorders: medication effects,
References glucocorticoids, and attenuated treatment outcomes. Clin Psychol Sci Pract
1. Teesson M, Slade T, Mills K. Comorbidity in Australia: findings of the 2007
2010;17:91-103.
National Survey of Mental Health and Wellbeing. Aust N Z J Psychiatry
27. Jorm AF, Korten AE, Rodgers B, et al. Belief systems of the general public
2009;43:606-14.
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2. Australian Bureau of Statistics. Survey of Mental Health and Wellbeing:
Psychiatric Epidemiol 1997;32:468-73.
summary of results. Publication 4326.0, 2007.
28. Deacon BJ, Abramowitz JS. Patients perceptions of pharmacological
3. Fredrikson M, Annas P, Fischer H, Wik G. Gender and age differences in the
and cognitive-behavioral treatments for anxiety disorders. Behav Ther
prevalence of specific fears and phobias. Behav Res Ther 1996;34:33-9.
2005;36:139-45.
4. Burgess PM, Pirkis JE, Slade TN, Johnston AK, Meadows GN, Gunn
JM. Service use for mental health problems: findings from the 2007
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5. Harrison C, Britt H. The rates and management of psychological problems in
Australian general practice. Aust N Z J Psychiatry 2004;38:781-8. correspondence afp@racgp.org.au
CLINICAL
Prostate specific
Tom Brett
antigen
This article forms part of our ‘Tests and results’ series for 2011 which aims to provide information is within the ‘normal’ range. Currently universal
about common tests that general practitioners order regularly. It considers areas such as indications,
screening is not recommended but, if proceeding,
what to tell the patient, what the test can and cannot tell you, and interpretation of results.
the combination of PSA and DRE should be
encouraged to improve the predictive value of both
Keywords: prostate-specific antigen as early detection tests.
Monitoring treatment outcomes for

prostate cancer
• What is the prostate specific Surgical removal of the prostate (radical

antigen test? prostatectomy) should stop PSA production; PSA
levels fall then remain at zero. Persistence of PSA
Prostate specific antigen (PSA) is a levels or rising PSA after radical surgery indicates
glycoprotein produced solely by the a failure to remove the gland completely, cancer
prostate. Its function is to liquefy semen. recurrence or metastases.
Small amounts leak into the bloodstream, Similarly, a positive response to radiation or
where it can be measured. Prostate hormone treatment should drop PSA levels while
specific antigen is tissue-specific but not any subsequent increase in PSA would suggest
cancer-specific. Elevated levels can occur disease recurrence or spread.
in men with benign prostatic hypertrophy
Watchful waiting
(BPH), prostatitis, urinary tract infection
or prostatic infarction. Elevation also may Not all prostate cancer requires treatment and
occur after prostate biopsy, aggressive some men with nonaggressive cancers may
digital rectal examination (DRE), be managed by ‘watchful waiting’, including
ejaculation, bicycle riding and physical serial PSA testing every 6-12 months. A gradual
exercise. increase in PSA may suggest disease progression
and urological intervention may be considered.
The use of PSA as a screening test for prostate
Diagnosing and monitoring prostatitis
cancer remains controversial because no double
blind, randomised controlled trial has shown that Prostatitis can be diagnosed by a sudden rise in
early detection reduces mortality.1,2 Despite this PSA levels combined with typical symptoms and
controversy, PSA provides valuable information signs (deep seated pelvic discomfort; tender, boggy
for the general practitioner in everyday clinical prostate). A return to normal PSA levels 6 weeks
practice, including monitoring of treated and after appropriate antibiotic treatment signifies a
untreated prostate cancer and prostatitis. positive response to treatment.
What are the indications? Contraindications

There are no absolute contraindications to PSA
Early detection of prostate cancer
testing. Clinician discretion is required in regards
Men requesting PSA testing should be counselled to if and when to test, and the appropriate interval
about the nature of the test; the information it between testing. Most research suggests that PSA
provides, especially its limitations; and that it is testing is not indicated beyond 75 years unless
possible to have prostate cancer even if their PSA monitoring known cancer.
CLINICAL Prostate specific antigen
Precautions suggests prostatitis, especially in conjunction with Gleason score.7 Potential side effects from biopsy
Patients need to understand that PSA is not dysuria or pelvic discomfort. Early stream urine include pain, infection, prostatitis, haematuria,
a diagnostic test. Careful informed consent is postprostate massage may occasionally yield haematospermia and blood in stools. Adequate
required including explanation that invasive positive culture, but in reality this is uncommon. analgesia is important and prophylactic antibiotic
investigations (transrectal ultrasound [TRUS] and A tender, slightly boggy prostate is more likely to cover is typical.
prostate biopsy) may be needed if PSA levels are confirm the diagnosis. If cancer is diagnosed, further staging tests
elevated. Prostate specific antigen provides no such as a bone scan may be used, especially if
Medications can impact on PSA levels. Anti information about the physical characteristics of PSA levels are >10 ng/mL.8
androgens (eg. finasteride, duasteride) lower PSA the prostate gland. Clinical examination with DRE
Watchful waiting
levels but alpha-adrenergic blockers (eg. prazosin, complements PSA and is minimally invasive. Failure
terazosin) do not. Cyclophosphamide, methotrexate to undertake DRE can result in a failure to diagnose Some patients, especially older men, decline
and some herbal treatments can also affect PSA prostatitis, a hard craggy gland suspicious of cancer specialist opinion and instead opt for 6 monthly
levels. Urology referrals should include details of or an enlarged gland with BPH. monitoring. These patients must be fully
any medications being used. A normal blood level does not exclude cancer counselled about their options and should
and patients should be reminded of this test understand that a tissue diagnosis is necessary
What do I tell the patient?
limitation. to confirm a clinical suspicion of cancer. Patient
Informed consent is essential with careful Methods to heighten the accuracy of PSA autonomy needs to be respected, but regular
explanation of the pros and cons of testing. The testing are highlighted in Table 1. follow up should be encouraged and GPs are
PSA test involves providing a blood sample. No advised to use their recall register for ‘watchful
special preparation is required but the test should What are the next steps in waiting’ patients.
not be taken within 24 hours of ejaculation or after management?
Monitoring disease outcomes
bicycle riding. Medicare funding is available once The next steps depend on the indication and
every 12 months. Men with symptomatic disease clinical setting. Although advisable for all men, General practitioners have an important role for
can have more frequent testing. DRE is essential in assessing a patient with an patients who have locally advanced or metastatic
elevated PSA as it provides valuable additional disease, in close liaison with the radiation
How is PSA measured? information. oncologist and urologist. Regular PSA (eg. 6
The PSA test is based on analysis of a single monthly) can help monitor the impact of treatments
Early detection of prostate cancer
serum sample. Some variations occur between such as brachytherapy, radiation or hormone
pathology providers based on differing assays. Men requesting testing for prostate cancer with treatment. A positive response can see PSA return
Results are expressed in ng/mL with levels of total persistent PSA levels in the ‘normal’ range (and to near zero levels. Although there may be a small
PSA >4.0 ng/mL regarded as abnormal. The test no suspicious DRE), can be offered annual testing transient rise after treatment (termed ‘bounce’),9
should be repeated after 1-3 months if results are with both PSA and DRE. Men with PSA <1.0 serial measurements showing a gradual rise in
markedly different from that expected. ng/mL on serial annual testing are at low risk PSA may mean disease is recurring or progressing
Age specific reference ranges,3 PSA velocity4 of developing prostate cancer and should be and further pulsed treatments may be indicated.
and free-to-total PSA5 can also be useful if reassured. The testing interval could be stretched
Management of prostatitis
considering a diagnosis of prostate cancer. to 2 yearly when these men reach 65 years of age.
Suspicious clinical findings such as induration, A review if symptoms develop could be offered as Treatment with antibiotics and early clinical follow
a nodular prostate or a tender prostate on DRE an alternative. up is indicated. Prostate specific antigen should
may help with interpretation of the PSA result. If the PSA test is unexpectedly elevated and be repeated after 6 weeks to ensure levels are
there are no clinical features demanding more returning to baseline.
What do the results mean?
urgent investigation, it may be wise to repeat PSA
Raised PSA levels occur with BPH, prostate cancer, testing after 1-3 months.
Case study 1
James, aged 51 years, enquired about
prostatitis, prostatic infarction, postaggressive Prostate specific antigen (and DRE) are early
getting tested for prostate cancer. He has
DRE, bicycle riding or postejaculation. detection tests used to facilitate a diagnosis of
an uncle who developed prostate cancer in
Benign enlargement remains the commonest prostate cancer. If abnormal, the patient needs to his mid 60s and his grandfather had a TURP
cause overall for raised PSA levels. Surgery such be counselled about the nature of the findings. If for BPH. His GP explained the increased
as transurethral resection of prostate (TURP) and cancer is suspected, urological referral is indicated risk of a first degree relative developing
less invasive laser treatments can reduce and for further investigation. This will generally consist prostate cancer, what was involved in
complicate the interpretation of PSA and PSA of TRUS guided prostate biopsy where core having a DRE and what the PSA test might
kinetics.6 samples of suspicious areas in the prostate are reveal. A prostate model was used to assist
A sudden unexpected rise in PSA levels obtained and sent for histological analysis and explanation - with examples of a normal
Prostate specific antigen CLINICAL
Table 1. Improving PSA testing Case study 2

Peter was 63 years of age and divorced
The following methods may heighten the accuracy of PSA testing, are also when diagnosed with prostate cancer. Serial
covered by Medicare and are clinically useful in assessment monitoring over the previous 2 years revealed
Age specific PSA ranges3 are an attempt to improve the interpretation of raised normal DRE but PSA increased from 4.1 ng/
PSA levels by allowing for the natural increase found with advancing years. Prostate mL to 4.9 ng/mL. Before diagnosis, his PSA
specific antigen values are adjusted upward with advancing age. Up to 2.5 ng/mL is had reached 5.8 ng/mL and DRE revealed
regarded as normal for men aged 40-49 years; up to 3.5 ng/mL for men aged 50-59 a small nodular area in the left lobe. Peter
years; up to 4.5 ng/mL for men aged 60-69 years; and up to 6.5 ng/mL for men aged
had been counselled both before and after
70-79 years
the annual tests and had initially deferred
Free-to-total PSA ratios5 - patients with prostate cancer have more bound PSA and urology referral.
thus lower free-to-total ratios. Ratios under 15% are regarded as more suspicious of
Peter now accepted urology assessment
cancer. (Note: this can be complex to explain to patients)
which involved TRUS and biopsy. Two foci of
Prostate specific antigen velocity4 is a measure of annual increases in PSA levels of adenocarcinoma were identified with Gleason
more than 0.75 ng/mL over at least 2 years. It seeks to improve the specificity of PSA scores of 7 and 6. The urologist explained
based on the theory that cancer cells produce increased amounts of PSA over time treatment options (radiation treatment,
Note: PSA density10 is the ratio of serum PSA to prostate volume as measured by brachytherapy, radical prostatectomy and
TRUS. It is based on the premise that cancer tissue produces higher volumes of watchful waiting) and Peter sought further
serum PSA than benign hyperplastic disease. However, the measurement of prostate advice from his GP. He elected to undergo
volume by TRUS is not readily available in primary care and is subject to observer nerve sparing radical prostatectomy.
variability; seriously limiting its usefulness in clinical practice
Good urinary continence was achieved after
2 months but no spontaneous erections
prostate, a hard craggy mass, a discrete firm prostate. After the examination, James was returned. He was referred to a sexual health
nodule and a hypertrophied prostate. James asked to provide a first pass urine sample. specialist and trialled intracavernosal
was also advised that the DRE and PSA were Urinalysis was positive for leucocytes injections but decided against continuing
early detection tests and could not diagnose and the sample was sent for culture. A after 6 months. Oral agents provided minimal
or totally exclude prostate cancer. He was provisional diagnosis of prostatitis was made assistance and were also discontinued with
told that a normal finding on DRE combined and James was commenced on ciprofloxacin Peter citing a lack of a partner as a factor in
with a low PSA (<1 ng/mL) would suggest a 500 mg twice per day for 2 weeks. his decisions.
low likelihood of prostate cancer. He agreed On review 2 days later, James’ symptoms had
Six months postoperation his PSA level had
to undertake a PSA test and arranged to slightly improved, his PSA was 8.5 ng/mL
fallen to <0.1 ng/mL and remained there on
return after a week for the result and to have and first pass urine sample grew Escherichia
serial testing over 12 years when he agreed to
a DRE. coli. He completed the full 2 weeks of
discontinue regular testing. His comorbidities
James’ PSA reading was 0.8 ng/mL. Digital antibiotics and his symptoms gradually
from ischaemic heart disease and diabetes are
rectal examination felt normal with a disappeared. A repeat PSA after 6 weeks
now more pressing concerns, while his risk
gland size of about 35 g, smooth regular showed a level of 2.4 ng/mL and a repeat
from prostate cancer recurrence is minimal.
consistency and palpable medial sulcus. In urine culture was normal. A further PSA test
after 6 months was advised.
light of his family history, he was advised Case study 3
to undertake an annual PSA and DRE and Bob, aged 68 years, presented with increasing
encouraged to maintain a low fat diet and Case study learning points nocturia and worsening urinary stream.
regular exercise. Rectal examination confirmed clinical
Prostatitis remains underdiagnosed in primary
Over the next 3 years, James’ PSA levels rose suspicion of prostatic hypertrophy with a
care and may be confused with a urinary tract
slightly (0.9, 1.1, 1.4 ng/mL) while his DRE large, smooth 60 g prostate. The PSA level was
infection. Culture of first pass urine postprostatic
remained normal. He then presented feeling 6.8 ng/mL. Bob was counselled before and
massage is rarely positive. The more common
unwell for 3 days. His symptoms were vague after undertaking the early detection tests
diagnostic findings are a tender, boggy prostate
but included deep-seated pelvic discomfort and accepted urology referral in view of his
on DRE together with a sudden rise in PSA and his wife’s concerns about prostate cancer.
as well as slight discomfort on passing urine.
that returns to normal levels after appropriate
He was afebrile with a blood pressure (BP) Urology assessment supported the clinical
treatment. Remember to undertake the PSA test
of 130/78. Cardiovascular, respiratory and diagnosis of benign prostatic hypertrophy and
superficial abdominal examinations were before undertaking the DRE as a vigorous prostate
conservative management was continued.
normal. The potential for a urinary tract or examination can alter the PSA result! Always At 12 months, Bob’s PSA was 7.1 ng/mL
prostatic problem was discussed and options consider prostatitis in men presenting with vague, falling to 7.0 ng/mL after a further 12
outlined. A PSA test was obtained followed deep seated pelvic pain. You will never find it if months. Digital rectal examination remained
by DRE. The DRE revealed a slightly tender you don’t consider it. nonsuspicious with no suggestion of
CLINICAL Prostate specific antigen
cancerous nodularity or induration. During antigen. Curr Urol Rep 2010;11:224-7.

7. Gleason DF. Histologic grading and staging of pros
this time, his urinary stream had further
tatic carcinoma. In: Urologic Pathology: The Prostate.
deteriorated with minimal benefit from Philadelphia, Lea and Febiger 1977, p. 171-8.
alpha-adrenergic blockers. 8. Oesterling JE. Using PSA to eliminate unnecessary
diagnostic tests: significant worldwide economic
Further urology referral was made as his
implications. Urology 1995;46(Suppl 3A):26-33.
symptoms deteriorated with increasing 9. Mitchell DM, Swindell R, Elliott T, Wylie JP, Taylor
hesitancy and slow stream. Prostate specific CM, Logue JP. Analysis of prostate-specific bounce
antigen level was now 7.4 ng/mL. Bob’s after I(125) permanent seed implant for localised
prostate cancer. Radiother Oncol 2008;88:102-7.
urologist advised TURP which eased his 10. Benson MC, Whang IS, Pontuk A, et al. Prostate
urinary flow problems considerably. Initial specific antigen density: a means of distinguishing
haematuria was followed by 3 months benign prostatic hypertrophy and prostate cancer. J
Urol 1992;147:815-6.
of mild urinary incontinence before full
dryness was achieved. His erectile function
deteriorated and he lost ejaculatory
capacity but declined sexual health review.
Histopathology of prostate chips revealed
benign hyperplasia with no evidence of
cancer. His nocturia is now twice per night
with a good urinary stream.
Resources
• A patient PSA test factsheet is avail
able at Andrology Australia: www.
andrologyaustralia.org/pageContent.
asp?search=PSA&pageCode=PS1
• UK Cancer Research has patient factsheets and
information for GPs: www.cancerresearchuk.
org.uk
• The Mayo Clinic has further information on
prostate cancer: www.mayoclinic.com/health/
prostate-cancer/DS00043/TAB=indepth.
Author
Tom Brett MA, MD, MRCGP, MICGP, FRACGP,
is Professor and Director, General Practice and
Primary Health Care Research, School of Medicine,
The University of Notre Dame Australia, Western
Australia. tom.brett@nd.edu.au.
References
1. Andriole GL, Crawford ED, Grubb RL, et al. Mortality
results from a randomised prostate-cancer screening
trial. N Engl J Med 2009;360:1310-9.
2. Schroder FH, Hugosson J, Roobol MJ, et al. Screening
and prostate-cancer mortality in a randomised
European study. N Engl J Med 2009;360:1320-8.
3. Osterling JE, Jacobsen SJ, Chute CG, et al. Serum
prostate-specific antigen in a community-based popu
lation of healthy men: establishment of age-specific
reference ranges. JAMA 1993;270:860-4.
4. Carter HB, Pearson JD, Metter EJ, et al. Longitudinal
evaluation of prostate-specific antigen levels in
men with and without prostate disease. JAMA
1992;267:2215-20.
5. Beduschi MC, Osterling JE. Percent free prostate
specific antigen: the next frontier in prostate-specific
antigen testing. Urology 1998;51(Suppl 5A):98-109.
6. Modi P, Helfand BT, McVary KT. Modifications and
surgical interventions for benign prostatic hyperpla
sia are potential confounders of prostate-specific correspondence afp@racgp.org.au
f
focus Current issues in alcohol j
Problem drinking
Apo Demirkol
Katherine Conigrave
Management ingeneral practice
Paul Haber
# Problem drinking has similar characteristics to many of

Background
the chronic conditions routinely managed in the general
Management of problem drinking presents the general
practice setting. The management of chronic conditions
practitioner with similar challenges and rewards to
those associated with the management of other chronic can at times be challenging and time consuming.
conditions. However, the majority of Australian general practitioners
find dealing with chronic conditions more rewarding and
Objective satisfactory if they have clear treatment goals.1
This article presents a framework for managing alcohol
problems in general practice based on national guidelines
Management of drinking problems presents the GP with similar
for the treatment of alcohol problems.
opportunities for challenging and rewarding practice.2,3 The
Discussion approach described in this article is based on the Guidelines for
General practitioners are well placed to undertake the treatment of alcohol problems published by the Australian
the management of drinking problems following an
Government Department of Health and Ageing (see Resources).4
assessment of the amount of alcohol taken and the risks
An algorithm for the management of problem drinking is shown
this poses for the individual and the people around them.
in Figure 1.
This assessment starts the process of engagement and
reflection on drinking habits and will inform the appropriate The management of drinking problems starts with an assessment
management approach. Brief interventions can result of the amount of alcohol taken and the risks this poses for both
in reduction in drinking in nondependent drinkers. For the individual and the people around them. This assessment of
dependent drinkers, treatment steps include assessing problem drinking is described in the article ‘Problem drinking:
need for withdrawal management and developing a Detection and assessment in general practice’ in this issue.5 The
comprehensive management plan, which includes degree to which alcohol dependence is present will inform the
consideration of relapse prevention pharmacotherapy appropriate management approach. The ’Drink-less Program’ is
and psychosocial interventions. The patient’s right to also a useful resource to help GPs in the detection and treatment
choose what they drink must be respected, and those who of risky drinking.6 If alcohol dependence is not present, a brief
continue to drink in a problematic way can still be assisted,
intervention may be successful in helping the patient cut down on
with compassion, within a harm reduction framework.
their drinking.7-9
Keywords: alcohol related disorders/management;
general practice Brief intervention
SSÍ] O Brief interventions as short as 5 minutes have been shown to reduce
drinking in nondependent drinkers in randomised controlled trials.7-9
Key components of a brief intervention are summarised by the
acronym FLAGS (Table 1):
• giving individualised Feedback that is relevant and realistic for
them
• Listening to the patient’s response and readiness to change
• providing clear Advice including on benefits they will get out of
change
• helping them identify their Goals, and
• to develop practical Strategies to work toward.
Several sessions may be needed in some patients. On average,
patients reduce their drinking by a few drinks per week from brief
576 AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 8 AUGUST 2011

a
steps for dependent drinkers include
predicting and managing alcohol
withdrawal, preventing nutritional
deficiency, and considering
strategies such as medications to
help prevent relapse, counselling
and group based approaches and
residential rehabilitation. Support
for family and significant others may
be required and follow up is vital.
Importantly, 24 hour specialist
advice, information and support is
available for clinicians managing
withdrawal in patients and any other
aspect of problem drinking from the
Drug and Alcohol Clinical Advisory
Service (DACAS) (see Resources).
An addiction medicine or addiction
psychiatry specialist at a tertiary
hospital may also be able to assist.
Predicting and
managing alcohol
withdrawal
Alcohol withdrawal syndrome is a
period of central nervous system
hyperactivity, which occurs when
an alcohol dependent individual
abruptly stops or significantly
reduces their drinking. Almost half
of dependent drinkers experience
clinically relevant withdrawal
symptoms upon cessation of
alcohol.9 Table 2 describes the
most common signs and symptoms
of uncomplicated and complicated
withdrawal. Management of
Figure 1. Management of problem drinking these symptoms facilitates further
engagement and ensures the
intervention, with associated reductions in harm. The topic of drinking patient’s safety. However, it is only a transitional step toward long
can be revisited at some (but not necessarily every) subsequent visit. term sobriety.4
There is evidence of a cumulative effect of brief interventions,9 but The main predictor of withdrawal severity is the patient’s previous
this should never become confrontational. Tools such as the Australian experience of withdrawal - individuals with a history of severe
Drug Foundation’s ‘Drinking Diary’ may assist GPs to engage patients alcohol withdrawal syndrome are more likely to have a similar
in reflecting their own drinking (see Resources). The focus should be experience in future withdrawal episodes.9 Unplanned withdrawal (eg.
on assisting the patient to identify their own goals and work toward after an emergency admission to hospital or entry to prison) tends to
achieving these goals for optimal health and quality of life. be more severe than in a planned withdrawal (when management is
For a dependent drinker, a brief intervention is not usually enough started promptly). If the patient has never stopped drinking previously,
on its own, but it can be important in initiating the conversation around the timing of the first drink of the day may be a good indicator of
alcohol. In these patients, the goal will usually be abstinence, as loss the likely severity of their withdrawal symptoms. A mild withdrawal
of control over drinking is a typical feature of withdrawal. Treatment overnight might leave the patient feeling tense on waking but they
AUSTRALIAN FAMILY PHYSICIAN VOL. 40, NO. 8 AUGUST 2011 577

Problem drinking - management in general practice FOCUS
could wait several hours before their

Table 1. FLAGS brief intervention structure
first drink, whereas in severe overnight
Feedback withdrawal, marked anxiety and tremors
• Provide individual feedback about the harms already experienced from alcohol or may only resolve with an early morning
the risks associated with continued drinking, based on the current patterns
drink.10-11 Marked morning symptoms
• Outline potential common harms and risks of early stage problem drinking
and early drinking to resolve them can be
including physical, mental health and social problems such as:6
a good predictor of a severe withdrawal
- insomnia; less energy
syndrome.
- poor coordination; less ability to think clearly
Patients who are physically well, and
- high blood pressure
who have had only mild to moderate
- depression; stress
withdrawal symptoms in the past and with
- impotence
no past history of withdrawal seizures,
- risk of injury; danger in driving and operating machinery
can typically be managed effectively and
Listen
safely as an outpatient,12 with or without
Listen to the patient’s response and put their response in context by providing
diazepam. Guidelines for the treatment
information on how their drinking levels relate to levels recommended by NHMRC
guidelines and that of the population average (see the article ‘Problem drinking: of alcohol problems provides a practical
Detection and assessment’ in this issue) approach to the use of diazepam and
Advice other medications for managing alcohol
Provide clear and nonjudgmental advice of about 5-10 minutes duration on the withdrawal symptoms in different settings
importance of changing current drinking patterns. This advice can be supported by and scenarios.4
self help materials, which can inform and motivate the patient further. Examples of If diazepam is required, the dose will
the benefits of reducing drinking include6:
vary, for example from 10 mg at night for
• Better sleep; more energy
3 days for insomnia in the setting of mild
• Better physical shape; reduced weight
withdrawal, through to 10 mg four times
• No hangovers; better memory
daily for moderate withdrawal. The initial
• Improved mood; fewer family problems
amount of diazepam required is decided
• More money
on the basis of past history of withdrawal
• Reduced risk of high blood pressure, liver damage, brain damage, cancer, drink
driving, injury to you and others and ongoing dosing on current withdrawal
symptoms and signs. Withdrawal rating
Goals
scales are used to monitor treatment
Assist the patient to set specific goals for changing their drinking pattern based on
safe drinking levels (see the article ‘Problem drinking: Detection and assessment’ in progress, being careful to exclude other
this issue). The conversation should instil optimism in the patient that these goals conditions, such as pneumonia, that may
can be achieved raise the score (by causing tachycardia,
Strategies fever and anxiety). Diazepam dose should
Ask the patient to choose strategies that may help achieving these goals. Provide be monitored carefully and appropriate
some prompters and help, but make sure that it is the patient’s own strategy for their doses prescribed or ’written up’ daily
own situation. Example of strategies for cutting down alcohol intake include6: according to need. Diazepam should
• Drink only with food be gradually but steadily reduced to
• Have a glass of water between drinks to quench the thirst
nil within a week to avoid dependence
• Switch to smaller glass sizes
to benzodiazepines. More severe
• Switch to low alcohol beer
withdrawals may need to be managed in
• Avoid going to the pub after work
the hospital setting and may require large
• Avoid or limit time spent with friends who drink heavily
• If under pressure to drink, say: ‘My doctor has told me to cut down’ or ‘I’m on a amounts of diazepam or, in the case of
fitness drive’ delirium tremens, a midazolam infusion.
• Alternatives: Offering outpatient withdrawal
- plan other activities or tasks at a time when you usually have a drink management is often greatly appreciated
- when stressed, take a walk or exercise instead of drinking by patients as there is often a waiting list
- explore new interests for inpatient withdrawal beds and many
- spend time with friends who don’t drink people do not like the idea of ’checking
Adapted from Guidelines for the treatment of alcohol problems4 and the Drink-less in to a detox’ facility. Proper assessment
Program6 and screening will ensure that outpatient

FOCUS Problem drinking - management in general practice
withdrawal is a safe and feasible process. The presence of a relative dependence: naltrexone, acamprosate and disulfiram (Table 3). All
or friend at home who can help supervise, or easy access to the can be prescribed by GPs.
GP or skilled nurse for regular reviews, can facilitate a relatively Naltrexone, an orally active opiate antagonist, reduces the rate
straightforward experience for the patient and the doctor. of relapse to heavy drinking by reducing the reward associated with
Patients who have previously experienced complicated and drinking alcohol and by reducing craving.15-16
severe withdrawals11-13 (seizures, delirium tremens), who have Acamprosate reduces cravings by helping reverse the
other significant medical or psychiatric problems,13 and who use overstimulated state resulting from neuroadaptation to alcohol. It
concomitant licit or illicit substances such as benzodiazepines14 are achieves this by modulating brain gamma-aminobutyric acid (GABA)
more likely to experience further complicated and severe withdrawal and glutamate.17,18
symptoms. Their withdrawal is best managed as on inpatient basis. Disulfiram is the oldest among these medications. Disulfiram acts
Multiple failed ambulatory withdrawal attempts, being surrounded as a deterrent to drinking because the patient expects to experience
by heavy drinkers, being unable to initiate abstinence and lacking a severe negative reaction if they drink even a small amount of
support people to monitor withdrawals are other important alcohol.19 This is because disulfiram interferes with the breakdown of
indications for inpatient withdrawal management. alcohol, and the resulting build up of acetaldehyde produces severe
headache, palpitations and vomiting. It is best suited to patients who
When to give thiamine have someone to help supervise them taking the medication and who
All dependent drinkers are prone to thiamine deficiency because of are relatively healthy.20-21
poor diet and damage to the gastric lining, and impaired thiamine Naltrexone and acamprosate are subsidised by the
utilisation. Current consensus is that thiamine should be given to Pharmaceutical Benefits Scheme (PBS) when part of a comprehensive
all dependent drinkers at a dose of at least 300 mg/day.4 Parenteral treatment program. This can mean that the patient has been offered
thiamine is preferred if the person is vomiting, or has extremely poor counselling and measures such as Alcoholics Anonymous (AA),
nutrition or severe alcohol dependence. Parenteral thiamine in doses and that the GP will monitor progress. Disulfiram is not currently
of at least 500 mg/day for 3-5 days should be considered for all subsidised by the PBS, which makes it more expensive for patients,
heavy drinkers who present with memory impairment, hypothermia, but it can be very effective in a well informed and motivated patient.
hypotension or delirium tremens.4 Importantly, the typical triad of Other agents with the potential to help reduce alcohol intake
Wernicke syndrome (confusion, ataxia, eye signs) is rarely seen, and and/or cravings for alcohol are currently being studied. Among
milder and subclinical cases can result in permanent impairment them are baclofen, and topiramate. Baclofen, a GABA-B receptor
of memory if left untreated. Thiamine should be given before agonist, has shown to be a promising agent for controlling alcohol
any carbohydrate load such as intravenous dextrose. In addition withdrawal symptoms as well as reducing alcohol cravings.22 It
to thiamine, an oral multivitamin preparation may be helpful as can be safely used in cirrhosis.22 Topiramate, a relatively new
deficiencies of other B complex vitamins along with vitamin C, zinc anticonvulsant, has been studied for managing alcohol dependence
and magnesium are common in poorly nourished heavy drinkers.9 with a degree of success.8
Medications to help prevent relapse Counselling and group based approaches

Relapse prevention pharmacotherapy should be offered to all Psychosocial interventions such as motivational interviewing
dependent patients following withdrawal management. Currently and cognitive behavioural therapies are important and effective
there are three medications approved for the treatment of alcohol elements in the management of alcohol dependence.23-25 Similarly,
Table 2. Signs and symptoms of alcohol withdrawal

Withdrawal Symptoms and signs of Gastrointestinal symptoms and Cognitive and perceptual
experience autonomic hyperactivity signs symptoms and signs
Uncomplicated Sweating, tachycardia, Anorexia, nausea, vomiting, Poor concentration, anxiety,
withdrawal hypertension, tremor, dyspepsia psychomotor agitation,
fever (generally lower than disturbed sleep
38°C)
Complicated Dehydration and As above Seizures, hallucinations or
withdrawal electrolyte imbalances perceptual disturbances
(visual, tactile, auditory),
delirium
Source: Guidelines for the treatment of alcohol problems4

Problem drinking - management in general practice FOCUS
Table 3. Choice of pharmacotherapies for alcohol dependence

Acamprosate Naltrexone Disulfiram
Once daily dosing No Yes Yes
Reduces cravings Yes Yes No
Stops ‘slips’ becoming relapses May Yes Yes
Assists in anxiety/insomnia Yes No No
Use in cirrhosis *
Yes (except Childs C) No No
Use in renal failure
** No Precaution No
Use in heart disease Yes Yes No
* Childs C refers to advanced decompensated cirrhosis ** If creatinine >120 pmol/L seek advice from a renal physician
mutual help-groups such as AA and cognitive behaviour therapy harm associated with drinking, and perhaps more importantly
based groups such as ‘SMART Recovery’ may help improve the benefits of change. In addition, GPs can encourage patients
outcomes (see Resources). Psychosocial interventions may not be to take thiamine to reduce the risk of memory loss, and manage
acceptable to every patient but should be offered to all. ‘Directline’ complications of drinking.
and Alcohol & Drug Information Service (ADIS) have a 24 hour If a patient continues to drink, it is important to carefully consider
telephone line for information and support for patients including their safety, and the safety of those around them, in relation to
information about locally based counsellors and other services driving and child safety as well as safety in the workplace for
(see Resources). occupations such as professional driving or mining. In some cases,
the GP’s professional obligations to preserve public safety and child
Residential rehabilitation welfare can exceed the requirement for patient confidentiality. If
Patients with refractory drinking problems, or who have tried and/or there is a need to consider reporting the patient to child welfare,
are not suited to home based postwithdrawal care can be referred to workplace authorities or road and traffic authorities, this should be
a residential rehabilitation unit. These units offer intensive programs conveyed to the patient if possible, as some patients will accept the
to stabilise patients and to build resilience to prevent relapse. need to reduce their drinking or accept referral for treatment when
Programs can last from weeks to months. The Drug and Alcohol faced with unpleasant alternatives. Specialist advice from senior
Clinical Advisory Service, ADIS and Directline can provide information colleagues, medical defence organisations or an addiction specialist
about local residential rehabilitation facilities (see Resources). should be sought in these situations.
Follow up Resources
• Australian Government Department of Health and Ageing.
Long term follow up is an important part of a comprehensive Guidelines for the treatment of alcohol problems: www.health.
approach to manage alcohol dependence and provides opportunities gov.au/internet/alcohol/publishing.nsf/Content/treat-guide
to optimise physical and mental health and improve social • Drink-less Program: www.sswahs.nsw.gov.au/sswahs/Drinkless
• The Australian Drug Foundation’s Drinking Diary: http://bookshop.
functioning.
adf.org.au/store
Support for family and significant others • Drug and Alcohol Clinical Advisory Service (DACAS) provides 24
hour advice for healthcare professionals:
Often there will be calls for help from distressed family members - ACT and NSW 1800 023 687
and GPs are well placed to provide this support. In addition to GP - SA 08 8363 8633
support, families and significant others may be able to get help - NT 1800 111 092
- QLD 07 3636 7098
from a psychologist, Al-Anon (a mutual support group for families
- VIC 1800 812 804
of alcoholics), or from other family focused services such as Family
- TAS 1800 630 093
Drug Support (see Resources). - WA 08 9442 5042; 1800 688 847 (WA country)
• Directline and Alcohol & Drug Information Service (ADIS) provide
What to do if the patient keeps 24 hour information and support for patients:
drinking - ACT 02 6205 4545
- NSW 1800 422 599 (NSW country); 02 9361 8000 (Sydney)
There will always be patients who will continue to drink - some
- SA 1300 131 340
because they cannot stop and some because they do not want to. A
- VIC 1800 888 236
compassionate, harm reduction approach is appropriate. Periodically, - NT 08 8948 0087 (Darwin); 08 8951 7580 (Central Australia);
patient encounters can be used as an opportunity to reiterate the 1800 131 350 (Territory wide)

FOCUS Problem drinking - management in general practice
- QLD 07 3837 5989 (Brisbane); 1800 177 833 (QLD country) 15. Rösner S, Hackl-Herrwerth A, Leucht S, et al. Opioid antagonists for
- TAS 1800 811 994 alcohol dependence. Cochrane Database Syst Rev 2010; Issue 12. Art.
No.: CD001867. DOI: 10.1002/14651858.CD001867.pub3.
- WA 08 9442 5000 (Perth); 1800 198 024 (WA country)
16. Rosner, S, Leucht S, Lehert P, et al. Acamprosate supports abstinence,
• Alcoholics Anonymous Australia: www.aa.org.au
naltrexone prevents excessive drinking: evidence from a meta-analysis
• SMART Recovery Australia: www.smartrecoveryaustralia.com.au
with unreported outcomes. J Psychopharmacol 2008;22:11-23.
• Al-Anon Family Groups Australia: www.al-anon.alateen.org/aus-
17. Mann K, Kiefer F, Spanagel R, et al. Acamprosate: recent findings and
tralia
future research directions. Alcohol Clin Exp Res 2008;32:1105-10.
• Family Drug Support: 24 hour support line 1300 368 186;
18. Rösner S, Hackl-Herrwerth A, Leucht S, et al. Acomprosate for alcohol
www.fds.org.au. dependence. Cochrane Database Syst Rev 2010; Issue 9. Art. No.:
CD004332. DOI: 10.1002/14651858.CD004332.pub2.
Authors 19. Heather N. Disulfiram treatment for alcoholism. BMJ 1989;299:471-2.
Apo Demirkol MD, MSc, PhD, FAFPHM, FAChAM, is Staff Specialist, 20. Chick J, Gough K, Falkowski W, et al. Disulfiram treatment of alcoholism.
The Langton Centre, South Eastern Sydney Local Health District, New Br J Psychiatry 1992;161:84-9.
South Wales. demirkolster@gmail.com 21. Hughes J, Cook C. The efficacy of disulfiram: a review of outcome
Katherine Conigrave MBBS, PhD, FAFPHM, FAChAM, is a Senior Staff studies. Addiction 1997;92:381-95.
Specialist and Associate Professor, Royal Prince Alfred Hospital Drug 22. Addolorato G, Leggio L, Ferrulli A, et al. Effectiveness and safety of
Health Services, Sydney, New South Wales baclofen for maintenance of alcohol abstinence in alcohol-dependent
patients with liver cirrhosis: randomised, double-blind controlled study.
Paul Haber MBBS, MD, RACP, FAChAM, is a Senior Staff Specialist
Lancet 2007;370:1915-22.
and Professor and Medical Director, Royal Prince Alfred Hospital
23. Miller W, Rollnick S. Motivational interviewing: preparing people for
Drug Health Services, Sydney, New South Wales.
change. New York: Guilford Press, 2002.
24. Miller WR, Wilbourne PL. Mesa Grande: a methodological analysis
Conflict of interest: none declared. of clinical trials of treatments for alcohol use disorders. Addiction
2002;97:265-77.
References 25. Carroll KM, Onken LS. Behavioural therapies for drug abuse. Am J
1. Olroyd J, Proudfoot J, Infante FA, et al. Providing healthcare for Psychiatry 2005;162:1452-60.
people with chronic illness: the views of Australian GPs. Med J Aust
2003;179:30-3.
2. Weller DP, Litt JC, Polls RG, et al. Drug and alcohol problems in primary
care-what do GPs think? Med J Aust 1992;156:43-8.
3. Ampt AJ, Amoroso C, Harris MF, et al. Attitudes, norms and controls
influencing lifestyle risk factor management in general practice. BMC
Fam Pract 2009;10:59.
4. Haber P, Lintzeris N, Proude E, Lapotko O. 2009. Guidelines for the treat
ment of alcohol problems. The Australian Government Department of
Health and Aging. Canberra. Accessible at www.health.gov.au/internet/
alcohol/publishing.nsf/Content/treat-guide.
5. Demirkol A, Haber P, Conigrave K. Problem drinking: detection and
assessment in general practice. Aust Fam Physician 2011;40:570-4.
6. University of Sydney. Drink-less Program. Available at www.sswahs.nsw.
gov.au/sswahs/Drinkless [Accessed 15 March 2011].
7. Kaner EF, Dickinson HO, Beyer FR, et al. Effectiveness of brief alcohol
interventions in primary care populations. Cochrane Database Syst Rev
2007; Issue 2. Art. No.: CD004148. DOI: 10.1002/14651858. CD004148.
pub3.
8. Latt N, Conigrave K, Saunders J, Marshall EJ, Nutt D. Addiction
Medicine. Oxford University Press, 2009.
9. Proude E, Lapotko O, Lintzeris N, Haber P. The treatment of alcohol prob
lems: a review of the evidence. Canberra: The Australian Government
Department of Health and Aging, 2009.
10. Benzer DG. Quantification of the alcohol withdrawal syndrome in 487
alcoholic patients. J Subst Abuse Treat 1990;7:117-23.
11. Essardas Daryanani H, Santolaria FJ, Reimers EG, et al. Alcoholic with
drawal syndrome and seizures. Alcohol Alcohol 1994;29:323-8.
12. Hayashida, M, Alterman AI, McLellan AT, et al. Comparative effective
ness and costs of inpatient and outpatient detoxification of patients
with mild-to-moderate alcohol withdrawal syndrome. N Engl J Med
1989;320:358-65.
13. Saitz R. Introduction to alcohol withdrawal. Alcohol Health Res World
1998;22:5-12.
14. Wetterling T, Kanitz RD, Veltrup C, et al. Clinical predictors of alcohol
withdrawal delirium. Alcohol Clin Exp Res 1994;18:1100-2. correspondence afp@racgp.org.au

CLINICAL
Lactational mastitis
Leila Cusack
Meagan Brennan
and breast abscess
Diagnosis and management in general practice
Epidemiology
Background
Lactational mastitis affects approximately 20%
Lactational mastitis is common, affecting one in 5 breastfeeding women. As well as
of breastfeeding Australian women in the first 6
causing significant discomfort, it is a frequent reason for women to stop breastfeeding.
months postpartum.7 It is most common in the first 6
Objective weeks of breastfeeding1,5 with the highest incidence
This article outlines an evidence based approach to the diagnosis and management of
occurring during the second and third weeks.6,9 It is
lactational breast infections in general practice.
initially localised to one segment of the breast, but
Discussion untreated can spread to affect the whole breast.5
Lactational mastitis is usually bacterial in aetiology and can generally be effectively Around 3% of lactating women with mastitis will
managed with oral antibiotics. Infections that do not improve rapidly require further develop a breast abscess,1,10 although an incidence
investigation for breast abscess and nonlactational causes of inflammation, including of up to 11% has been reported.10
the rare cause of inflammatory breast cancer. In addition to antibiotics, management of
lactational breast infections include symptomatic treatment, assessment of the infant’s Risk factors and prevention
attachment to the breast, and reassurance, emotional support, education and support
The main risk factor for mastitis is breastfeeding
for ongoing breastfeeding.
during the early postpartum period.6 Milk stasis
Keywords: mastitis; breast abscess; lactation; general practice
and cracked nipples may contribute to the
development of mastitis,1,3-6 although the evidence
for this is inconclusive.1 Other implicated factors
include previous mastitis,6 maternal fatigue1,3 and
ft Lactational mastitis is an inflammatory primiparity9 Reported risk factors for breast abscess
process affecting the lactating breast.1-4 include a past history of mastitis, maternal age over
It is usually bacterial in aetiology. It 30 years and gestational age greater than 41 weeks.5
affects the breast parenchyma, causing There are no interventions that have been
localised pain, tenderness, erythema and consistently proven to prevent mastitis. Encouraging
engorgement,3-6 and may be accompanied emptying of milk from the breast is often
by systemic features such as fever, recommended, however, evidence for its efficacy
malaise, rigors, nausea and vomiting.4-8 is inconclusive.6 The most commonly practised
intervention is the prevention and management of
A breast abscess, a localised collection in the damaged nipples; in some settings this may reduce
breast tissue that results in a painful breast lump, the risk of developing mastitis.3 A Cochrane review
is potentially secondary to bacterial mastitis found that anti-secretory factor cereal, mupirocin
that is rapidly progressive or is not managed ointment, fusidic acid ointment and breastfeeding
expeditiously. Effective management is essential advice had no significant impact on the initiation
to control the discomfort and reduce the likelihood or duration of breastfeeding or the incidence of
of discontinuation of breastfeeding, which may symptoms of mastitis.11
occur as a consequence of mastitis.6,7 Mastitis
Microbiology
and breast abscess may develop in women who
are not breastfeeding; this article will focus on The most common causative organism for mastitis
lactational breast infections. is Staphylococcus aureus8,10 Strains of methicillin
Lactational mastitis and breast abscess - diagnosis and management in general practice CLINICAL
resistant S. aureus (MRSA) have been identified, may distinguish inflammation (mastitis) from a lump remains- no fluid is obtained or fluid is
particularly in hospital acquired infections. Other collection of pus in the breast (abscess) (Figure bloodstained rather than purulent- then core
organisms include streptococci and S. epidermidis. 2). Ultrasound also allows guided aspiration of biopsy is recommended to exclude breast cancer.13
Patients who suffer with recurrent breast abscesses any abscess providing drainage and fluid for Mammography is not a first line investigation
have a higher incidence of mixed flora, including microscopy and culture. A malignant lesion may in lactating women but is indicated if there are
anaerobic organisms.5 On rare occasions Candida mimic an inflammatory collection on ultrasound. clinical- sonographic or biopsy features suspicious
albicans, not an uncommon cause of nipple pain in Hence- following aspiration- if a significant for malignancy.13
lactating women,9 can cause parenchymal infection.12
Clinical assessment
History and physical examination
Breast pain is the primary symptom of mastitis.7

High fever is common, along with other generalised
flu-like symptoms including malaise, lethargy,
myalgia, sweating, headache, sometimes nausea
and vomiting and occasionally rigors.1-^7
Clinical examination of the breast should focus
on looking for signs of inflammation (erythema- Figure 1. Mastitis is characterised by a Figure 2. Ultrasound of a breast abscess.
localised tenderness- heat- engorgement and tender area of localised erythema Image shows a heterogeneous area which
swelling) (Figure 1) and signs of nipple damage. Photo © Science Photo Library, 2011. All has the typical appearance of a breast
rights reserved abscess
General observations including temperature- pulse
and blood pressure are important to exclude sepsis-
which requires hospital admission. Table 1. Common breast problems in the puerperium
Breast abscess is characterised by symptoms Benign conditions
similar to mastitis- with the additional sign of
Conditions related to lactation
a discrete tender lump- which may be tense or
• Engorgement
fluctuant. The mass may have overlying skin
• Breast infection (mastitis or abscess)
necrosis suggesting that the abscess is ‘pointing’
- bacterial infection - usually S. areus
(abscess is sitting close to the surface of the skin).
- fungal infection (C. albicans; uncommon)
Less frequently- breast abscess presents as a non
- viral (herpes; very rare)
tender lump without erythema (‘cold abscess’).
• Galactocoele (noninfected milk-filled cyst)
Examination of the infant and • Nipple pain
attachment to the breast - cracked/damaged nipples
- incorrect attachment: misalignment of mother’s nipple and baby’s mouth
The infant should be examined to ensure adequate
- infant causes: poor sucking, tongue-tie, cleft palate
growth and hydration. Examination of the baby’s
- incorrect use of breast pump
mouth can exclude candida infection (white film
- C. albicans nipple infection
adherent to the buccal mucosa)-2 or anatomical
Other conditions
conditions such as cleft palate or tongue-tie which
• Benign breast disease: fibroadenoma, fibrocystic change, cyst, benign phyllodes
may interfere with attachment.6-9 Observation of
tumour
breastfeeding can determine if there are difficulties
• Musculoskeletal conditions
with attachment to the breast. A lactation
- tender costochondral junctions (Tietze syndrome)
consultant may be helpful.
- sleeping or breastfeeding in an uncomfortable position
• Raynaud disease of the nipple
Investigation
Malignant causes
Mastitis is a clinical diagnosis and investigations
• Breast cancer
are not indicated in the initial assessment.1
- lobular and ductal carcinoma
Breast infection that does not improve
- inflammatory breast cancer (may mimic bacterial mastitis)
with a course of appropriate antibiotics should
- malignant phyllodes tumour
be investigated with breast ultrasound.5 This
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 40- NO. 12- DECEMBER 2011 977
CLINICAL Lactational mastitis and breast abscess - diagnosis and management in general practice
Table 2. Management approach to breast infections
Other less common breast problems may present in
Clinical assessment
the puerperium ( Table 1 ). These differentials should
• Localised inflammatory features (pain, erythema, heat, swelling)
be kept in mind, particularly if the clinical features
• Systemic features (fever, malaise, myalgia)
are not of a classic nature.
• Assessment of infant hydration and weight
Inflammatory breast cancer is a rare
Symptom management
presentation but should be considered if mastitis is
• Simple analgesia
not responding to treatment1,2! Figure 3). Nonbreast
• Hot packs before feeding
causes of fever (such as urinary tract infection
• Cold packs after feeding
or endometritis, ie. following complications of
Antibiotic therapy
Caesarean delivery) should be considered where the
• Flucloxacillin or dicloxacillin 500 mg qid for at least 5 days
presentation is with fever rather than breast pain • For abscess - guided by microbiological culture and sensitivity
and erythema.2
Support continued breastfeeding
• Education and reassurance
Management
• Regular and complete drainage of breast (use breast pump if needed)
The key components of management are symptom • Observe feeding and attachment
control, oral antibiotics and encouraging continued • Referral to lactation consultant
milk flow from the affected breast ( Table 2). The • Referral to Australian Breastfeeding Association
patient should be reassured that antibiotics and Early and frequent review
simple analgesics will not harm her baby. Women • Review in 24-48 hours; investigate if not settling
should be encouraged to continue breastfeeding, to • If not settling, ultrasound to look for breast abscess and rare causes of
rest whenever possible and to drink plenty of fluids. inflammation such as inflammatory breast cancer
Close monitoring is required to ensure that the • Aspiration of abscess collection
infection resolves.
• Biopsy lesions suspicious for malignancy
Management of breast abscess if present
Management of symptoms • Aspiration with antibiotic cover is a safe first line approach where specialist
breast clinics or ultrasound guidance are available
Simple analgesia
• Incision and drainage if not settling or aspiration is unavailable
Regular oral paracetamol is first line treatment.
• Other management (as per mastitis)
Nonsteroidal anti-inflammatory drugs can be added.
Psychological support
Both are safe in breastfeeding.1,2
• Reassurance and support
Hot and cold packs to breast • Evaluation for depression
• Referral to Australian Breastfeeding Association
Evidence is inconsistent, however, breastfeeding
authorities recommend: • application of cold packs after feeding (may help options include cephalexin or clindamycin.15
• gentle massage and warm compress prior to alleviate pain).1,49 Alternatives used overseas include amoxycillin/
feeding (may encourage milk flow)1,4,6 Cabbage leaves have demonstrated inconsistent clavulanic acid and macrolides (erythromycin,
effects; producing postfeeding symptom relief clarithromycin).5 Avoid tetracycline, ciprofloxacin
similar to-ice packs in some studies,5 while and chloramphenicol as they are unsafe for use in
demonstrating no effect in others.9 lactating women.5 Hospitalisation for intravenous
antibiotics is rarely required but is indicated if
Antibiotic therapy
there are systemic signs of sepsis.5,15 Candida is a
Adequate antibiotic therapy is essential. Where rare cause of mastitis and is characterised by the
possible this should be guided by microbiological presence of intense pain, particularly noted after
culture and sensitivity (such as when fluid is the breast empties, and the absence of breast
aspirated from an abscess).14 As S. aureus is the erythema.2,9,12
common causative organism, antibiotic therapy
Figure 3. Inflammatory breast cancer may Support for continued
mimic mastitis. Classically it presents with a of choice at least 5 days of flucloxacillin or
breastfeeding
poorly defined clinical mass with erythema, dicloxacillin in a dose of 500 mg four times per
skin thickening and peau d’orange (‘orange day.15 Due to antibiotic packaging in Australia The aim of therapy is to continue breastfeeding
peel’ appearance to the skin)
this may require two consecutive 6 day courses and to empty the breast as fully as possible with
Photo © Slaven, 2011. All rights reserved
of antibiotics. For patients allergic to penicillin, each feed. This relieves symptoms and reduces
Lactational mastitis and breast abscess - diagnosis and management in general practice CLINICAL
the likelihood of progression to breast abscess. Identification and drainage of breastfeeding women including telephone and
breast abscess email counselling and helpful resources:
There is no evidence of risk of harm to a healthy
• Breastfeeding Helpline 1800 mum 2 mum (1800
infant feeding from an infected breast.1'4'6 If Lactating women with a breast abscess often 686 286)
attachment is painful, a breast pump can be used present late when the abscess is established and • www.breastfeeding.asn.au
to drain the breast until the infection settles of large volume.5 The traditional management of • Lactation Resource Centre www.lrc.asn.au.
enough to allow the baby to feed from the breast breast abscess was surgical incision and drainage
Authors
(Figure 4). Infant attachment to the breast should under general anaesthetic. This has been largely
Leila Cusack BSc, MBBS(Hons) is a junior medical
be checked and corrected. Referral to a lactation replaced by percutaneous (outpatient) aspiration officer, currently living in Europe. leilacusack@
consultant may be helpful. The Australian under local anaesthetic where specialist breast gmail.com
Breastfeeding Association is also useful for clinics or radiology services are available. Meagan Brennan BMed, FRACGP DFM, FASBP
mother-to-mother support (see Resource). Surgery can usually be avoided and outcomes is a breast physician, The Poche Centre, North
Despite support and encouragement, some are better for outpatient clinic management Sydney and Clinical Senior Lecturer, Northern
Clinical School, Sydney Medical School, University
women choose to cease breastfeeding. These than surgical management (including reduced
of Sydney, New South Wales.
women should be supported in their decision and pain and scarring and increased likelihood
encouraged to wean gradually, preferably after of continued breastfeeding).5,10,14 Access to Conflict of interest: none declared.
the infection has resolved. Sudden cessation specialist breast clinics may be limited in some
References
of breastfeeding may exacerbate the infection, areas, particularly in rural areas, so surgical 1. Academy of Breastfeeding Medicine Protocol
increasing the risk of abscess formation.1,4 incision and drainage may be the treatment of Committee. ABM Clinical Protocol #4: Mastitis.
Revision, May 2008. Breastfeed Med 2008;3:177-80.
Medication to suppress milk production is not choice in this setting.
2. Amir LH. Breast pain in lactating women: mastitis or
recommended in this situation. something else? Aust Fam Physician 2003;32:141-5.
Psychological issues 3. Amir LH, Forster DA, Lumley J, McLachlan H. A
Early and frequent review descriptive study of mastitis in Australian breast
As well as the severe physical pain, mastitis
feeding women: incidence and determinants. BMC
Women with mastitis should be reviewed within is often associated with complex emotions. It Public Health 2007;7:62.
24-48 hours to ensure that the inflammation is occurs at a time of great physical, hormonal 4. Betzold CM. An update on the recognition and
management of lactational breast inflammation. J
settling. If minimal improvement occurs, breast and lifestyle change.7 Depression, distress, Midwifery Womens Health 2007;52:595-605.
ultrasound is indicated ( Figure 2). Ultrasound anxiety, tearfulness, helplessness and concerns 5. Dixon JM, Khan LR. Treatment of breast infection.
BMJ 2011;342:d396.
helps detect any abscess and can guide about milk supply have been associated with
6. Spencer JP Management of mastitis in breastfeed
aspiration.1,4,5 Ultrasound can identify or exclude episodes of mastitis.7 By acknowledging the ing women. Am Fam Physician 2008;78:727-31.
other causes of inflammatory breast signs such difficulties involved in breastfeeding, general 7. Amir LH, Lumley J. Women’s experience of lacta
tional mastitis - ‘I have never felt worse’. Aust Fam
as inflammatory breast cancer and can facilitate practitioners can help mothers while providing
Physician 2006;35:745-7.
ultrasound guided biopsy if indicated by the support, encouragement and reassurance that 8. Francis-Morrill J, Heinig MJ, Pappagianis D, Dewey
imaging findings. their milk is extremely valuable to the health of KG. Diagnostic value of signs and symptoms of
mammary candidosis among lactating women. J
their child, and is safe for their baby when they Hum Lact 2004;20:288.
are taking appropriate antibiotics. The Australian 9. Mass S. Breast pain: engorgement, nipple pain and
Breastfeeding Association is an excellent source mastitis. Clin Obstet Gynecol 2004;47:676-82.

10. Amir LH, Forster D, McLachlan H, Lumley J. Incidence
of free information and support and women of breast abscess in lactating women: report from an
should be encouraged to use this resource. Australian cohort. BJOG 2004;111:1378-81.
11. Crepinsek MA, Crowe L, Michener K, Smart NA.
Interventions for preventing mastitis after childbirth.
Summary Cochrane Database Syst Rev 2010;(8):CD007239.
Lactational breast infections are common and 12. Amir LH. Candida and the lactating breast: predis
posing factors. J Hum Lact 1991;7:177.
require prompt and effective management to
13. National Breast Cancer Centre. Investigation of a
minimise associated morbidity. Management new breast symptom: a guide for general practition
of mastitis includes antibiotic therapy and ers. NBCC report: Evidence relevant to guidelines
for the investigation of breast symptoms. 2nd edn.
encouragement of milk flow from the affected February 2006.
breast, ideally with ongoing breastfeeding. Close 14. Elder EE, Brennan M. Nonsurgical management
should be first-line therapy for breast abscess. World
monitoring is important to detect poor responders,
J Surg 2010;34:2257-8.
Figure 4. Continued breastfeeding is trigger investigation and identify breast abscess to 15. Antibiotic Expert Group. Therapeutic Guidelines:
encouraged for women with mastitis and/or allow urgent referral for specialist management. antibiotic. Version 14. Melbourne: Therapeutic
breast abscess. Emptying of the breast can Guidelines Ltd, 2010.
be helped by the use of a breast pump

Resources
The Australian Breastfeeding Association provides
Photo © iStockphoto.com/joakimbkk
advice for health professionals and support for correspondence afp@racgp.org.au
FOCUS Neurology
Multiple sclerosis
Benjamin K-T Tsang
Richard Macdonell
Diagnosis, management and prognosis
A Multiple sclerosis (MS) is a multifocal central nervous
Background system (CNS) disorder characterised by inflammatory
Multiple sclerosis is the most common chronic disabling demyelinating lesions affecting white and grey matter;
disease of the central nervous system in young adults.
thought to be mediated by autoreactive T cells.1,2 In
Objective addition to demyelination, irreversible axonal injury
This article summarises the diagnosis, management and occurs from the outset. It is the steady accumulation
prognosis of multiple sclerosis. of damage to the CNS over time that leads to the
Discussion irreversible disability that characterises the advanced
Multiple sclerosis usually starts with an acute episode stages of the disease.1
of neurological disturbance, termed a ‘clinically isolated
syndrome’, followed by an illness phase punctuated by Aetiology
relapses and remissions which may transition after 10 Multiple sclerosis arises from a complex interaction of environmental
years to a phase of progressive accumulation of disability and genetic factors. Environmental factors include place of residence
without relapses. Fifteen to 20% of patients will have a in pre-adult years, age of exposure to Epstein-Barr virus, and
progressive course from the onset. There is significant
smoking. Later age of exposure to Epstein-Barr virus infection is
interpatient variability in prognosis. The main diagnostic
associated with a higher incidence of the disease while seronegative
criteria are clinical, supported by investigations including
individuals have a very low risk of developing MS.3 Genome wide
magnetic resonance imaging and lumbar puncture and
evoked potentials. First line disease modifying agents for association studies have now identified 52 risk alleles for the
relapsing remitting multiple sclerosis include interferon-B development of MS, but HLA-DRB1 status retains the strongest
and glatiramer. First line treatment for relapses is usually correlation.4
intravenous methylprednisolone for 3 days. Troublesome
symptoms may include spasticity, parasthesias, tremor,
Epidemiology
erectile dysfunction, depression and anxiety, fatigue and The epidemiology of MS in Australia shows that it varies with
pain. After excluding differential diagnoses, symptomatic latitude. It is more common in Tasmania (approximate prevalence 100
management includes pharmacological agents, allied per 100 000 and incidence 4 per 100 000) and becomes progressively
health consultation and continence strategies. Although less common as one travels further north.5 There are approximately
pregnancy reduces disease activity, there is a higher risk of
13 000 people with MS currently in Australia, females comprise
relapse in the postpartum period.
approximately 73% of cases. Mean age at symptom onset and
Keywords: multiple sclerosis diagnosis is the mid 30s.6
SITO O Natural history and disease phases

Clinically isolated syndrome (first
demyelinating event)
Eighty-five percent of people who later develop MS start with an
episode of neurological disturbance, usually evolving over days or
weeks.7 This is known as a ‘clinically isolated syndrome’ (CIS), or
‘first demyelinating event’. A review of a large database of patients
with MS found that 21% started with a clinically isolated syndrome
of optic neuritis, 46% with long tract symptoms and signs (motor
or sensory deficits), 10% with a brainstem syndrome and 23% with
multifocal abnormalities (Table 1 ).8-10
Relapsing remitting multiple sclerosis Investigations and diagnosis
Most patients with MS experience an initial disease phase punctuated Multiple sclerosis remains a clinical diagnosis supported by magnetic
by relapses and remissions. This is termed relapsing remitting MS resonance imaging (MRI), laboratory findings from cerebrospinal fluid
(RRMS). A relapse is defined as symptoms or objective signs typical of an (oligoclonal bands and raised IgG index), and evoked potential studies
acute inflammatory demyelinating event in the CNS which last at least (delayed evoked response with preserved waveform).9,14 Ultimately
24 hours (Table 1).9 Complete resolution may occur, but mild residual it can only be confirmed histopathologically, but the need to resort
symptoms or signs persist in up to 40% of attacks.11 A major increase in to biopsy is rare. Over recent years diagnostic criteria for clinically
disability due to a single relapse is uncommon. In untreated patients new definite, probable and possible MS have evolved from the purely
relapses occur erratically with a mean rate of 0.65 attacks per year.12 clinically based definitions,15,16 which emphasised dissemination in
Fatigue in isolation or transient fever related worsening of symptoms are space and in time of lesions, with exclusion of alternative diagnoses.
not considered to be relapses and are termed pseudorelapses.9 The advent of MRI led to the McDonald criteria9 (most recently
revised in 2010) which are now the accepted criteria for a diagnosis
Secondary progressive multiple sclerosis of MS. These criteria still allow for a diagnosis of clinically definite
After 10 years, 40-45% of patients with RRMS will have transitioned MS if a patient has objective clinical evidence of two lesions
to a phase of progressive accumulation of disability without relapses, that are disseminated in space and time and there is no better
termed, secondary progressive MS (SPMS).12 The lifetime risk of this explanation for the clinical presentation. However in reality, MRI
transition is greater than 80%.12 In this phase, occasional plateaus correlation is usually sought. Importantly, if imaging or other tests (eg.
and temporary minor improvements may be observed, however the cerebrospinal fluid) are undertaken and are negative, extreme caution
overwhelming trend is toward progressively increasing disability. needs to be taken before making a diagnosis of MS and alternative
diagnoses must be considered. The McDonald criteria also allow for
Primary progressive multiple sclerosis a diagnosis of MS without objective clinical evidence of two lesions
Fifteen to 20% of patients have a progressive course from disease disseminated in space and time. If one of these criteria are not met
onset, without relapses or remissions. This is termed, primary the presence of the other can be inferred from contrast enhanced MRI
progressive MS (PPMS).13 The most common presentation of PPMS findings (Figure 1), which has sensitivities in the range of 95% for
is a slowly progressive spastic paraparesis, followed by cerebellar or patients with clinically definite MS.8 Typical locations of MS lesions
hemiplegic syndromes.13 Primary progressive MS does not respond to on MRI are listed in Table 2.8,9 Primary progressive MS is diagnosed
current treatment. by recognising the clinical syndrome of 1 year of disease progression,
Table 1. Common sites, signs and symptoms of acute inflammatory demyelinating events (clinically
isolated syndrome or multiple sclerosis relapses)8-10
Site Condition Symptoms Signs
Optic nerve Optic neuritis Pain on eye movement, blurred Reduced monocular visual
vision acuity, colour desaturation
Cerebellum Cerebellar disease Unsteadiness Limb or gait ataxia;
horizontal or torsional gaze
evoked nystagmus
Spinal cord (usually Partial myelitis affecting Upper or lower limb weakness Pyramidal distribution
multifocal and pyramidal tracts weakness
asymmetric) Partial myelitis affecting Unilateral or bilateral limb numbness Sensory level
spinothalamic tract and or paraesthesias
posterior columns L'Hermitte’s phenomenon (short
electric shock-like sensation on neck
movement)
Brainstem
• Medial longitudinal Internuclear Blurred or double vision Internuclear
fasciculus ophthalmoplegia ophthalmoplegia
• Pyramidal tracts (Similar to conditions
described in spinal cord)
• Spinothalamic (Similar to conditions
tract and posterior described in spinal cord)
columns
Bowel/bladder Loss of upper motor neuron Constipation, urinary frequency, urge
control incontinence, erectile dysfunction
FOCUS Multiple sclerosis - diagnosis, management and prognosis
an MRI showing evidence of inflammatory lesions with dissemination

in space and positive oligoclonal bands in the cerebrospinal fluid.9
Differential diagnoses
The most problematic differential diagnoses are other
demyelinating illnesses such as neuromyelitis optica (Devic
Table 2. Typical sites of lesions on MRI8,9

• Periventricular white matter (if at right angles to the
corpus callosum, these are referred to as ‘Dawson
fingers’)
• Juxtacortical white matter
• Corpus callosum
• Optic nerve (with gadolinium enhancement in acute
neuritis)
Figure 1. Sagittal view of the brain, showing mul • Infratentorial structures (pons, cerebellar peduncles
tiple pericallosal hyperintense lesions (arrow) on and cerebellum)
fluid attenuation inversion recovery (FLAIR) • Spinal cord
Table 3. Disease modifying treatments for multiple sclerosis available on the PBS20,21
Drug Mode of action Indications Route and recommended dose
Interferon-ß-1a Immunoregulatory including antagonism Reduction of relapses in Avonex®: IMI 30 pg once per
(Avonex®, Rebif®) of gamma interferon, reduction of cytokine ambulatory RRMS week
release and augmentation of suppressor T Rebif®: SC 44 pg three times per
cell function week
Interferon-ß-1b Immunoregulatory including antagonism Reduction of relapses in SC 250 pg every 2 days

(Betaferon®) of gamma interferon, reduction of cytokine ambulatory RRMS
release and augmentation of suppressor T SPMS with relapses
cell function
Glatiramer acetate Synthetic polypeptide; possibly blocks Reduction of relapses in SC 20 mg once dally
(Copaxone®) presentation of myelin antigens to T RRMS
lymphocytes
Natalizumab Recombinant humanised monoclonal Reduction of relapses in IV 300 mg over 1 hour, once a
(Tysabri®) antibody to alpha-4 integrins, inhibiting RRMS month
leucocyte migration from blood to CNS
Fingolimod (GHenya®) Sphingosine 1-phosphate receptor Reduction of relapses in Orally 0.5 mg/day
modulator RRMS
Mitoxantrone Anthracenedione derivative that inhibits RRMS IV 12 mg/m2 every 3 months up

(Onkotrone®) DNA and RNA synthesis by intercalation to a total cumulative dose of 140
of DNA base pairs. Prevents DNA repair by mg/m2 (100 mg/m2 in patients
inhibiting topoisomerase II with cardiac risk factors)
Cyclophosphamide Cytotoxic effect on lymphocytes RRMS IV - multiple different regimens
(Endoxan®,
Cycloblastin®)
IV = intravenous; SC = subcutaneous; IMI = intramuscular injection
Multiple sclerosis - diagnosis, management and prognosis FOCUS
disease) and acute disseminated encephalomyelitis. Neuromyelitis • compressive lesions of the spinal cord
optica can present with relapsing CNS demyelinating disease • infections (eg. syphilis, HIV)
characterised by involvement of optic nerves, often severe • amyotrophic lateral sclerosis
myelopathy with MRI evidence of longitudinally extensive • steroid sensitive relapsing disorders (eg. systemic lupus
spinal cord lesions and serum aquaporin-4 autoantibodies.9 erythematosus, neurosarcoidosis)
This phenotype has a different clinical course and prognosis • recurrent infarcts
and is poorly responsive to MS disease modifying therapies • paraneoplastic syndromes
(DMTs). Acute disseminated encephalomyelitis is a monophasic • psychiatric disease/functional symptoms.
autoimmune demyelinating illness of the CNS typically seen in
paediatric populations. However, it is also seen in adults and can Treatment of acute relapses
be indistinguishable from an acute MS attack.17 Typical acute Intravenous methylprednisolone (1 g/day for 3 days) is the treatment
disseminated encephalomyelitis tends to have a more explosive of choice but is only necessary if the relapse impacts significant on
course associated with alterations in mental status. Triggers such quality of life. This treatment has been shown to hasten the recovery
as recent viral infection or vaccination may be present. Other from a relapse but not the likelihood of recovery, frequency of further
important differential diagnoses include1,9,10: attacks or any permanent disability resulting from an attack.18,19 Side
• migraine effects may include mood changes, psychosis, aseptic hip necrosis
• cerebral neoplasms (primary and secondary) and hyperglycaemia.20 Plasma exchange is considered in steroid
• nutritional deficiencies (eg. B12 or copper) unresponsive patients with severe relapse.19 Pseudorelapses may
Precautions Adverse effects Other comments
May worsen seizures, Common: injection site reactions, flu-like illness, headache, Dose titration recommended
depression, psychiatric depression, nausea, abdominal pain, raised liver function tests Paracetamol may reduce flu-like
illnesses, and cardiac (LFTs), anaemia, leucopenia symptoms
disease Uncommon: interferon-ß neutralising antibodies, hypertension Presence of neutralising antibodies
Rare: heart failure, cardiomyopathy, suicidal thoughts, may reduce response
lymphadenopathy, autoimmune disease, hepatotoxicity, Monitor full blood examination,
thyroid dysfunction, hypersensitivity, alopecia LFTs periodically
Asthma, history of Common: injection site reactions, nausea, arthralgia, oedema, Antibodies to glatiramer develop in
anaphylaxis - risk of hypertonia, tremor all patients and are not associated
allergic reactions Rare: anaphylaxis with adverse effects or decreased
efficacy
Caution if history of Common: infusion reactions, (headache, dizziness, fever, Persistent neutralising antibodies
progressive multifocal arthralgia, rigors, flushing), neutralising antibodies associated with reduced efficacy
leukoencephalopathy, Rare: progressive multifocal leukoencephalopathy, and increased risk of allergic
immunosuppression hepatotoxicity reactions
Treatment with other
DMTs contraindicated
Caution in diabetic Common: bronchitis, lymphopenia, bradycardia, LFT
patients due to increased abnormalities
risk of macular oedema Uncommon: prolongation of QT interval, bronchospasm,
macular oedema, disseminated varicella in the nonimmunised
Caution in hepatic disease Common: lassitude
(dose reduction) and Infrequent: taste disturbance, gastrointestinal bleeding,
elderly (increased risk of dyspnoea, rash, nail pigmentation, conjunctivitis,
myelosuppression) cardiomyopathy, acute myeloid leukaemia
Caution in renal Common: myelosuppression, alopecia, anorexia, haemorrhagic Mesna (a cytoprotective agent) is
impairment (dose cystitis, nasal congestion, taste disturbance used for prophylaxis of cystitis
reduction) Rare: heart failure, pulmonary fibrosis
occur as a result of sepsis and fever and treatment should be geared relapses and their surrogates (new lesions on imaging) have been
toward the infectious agent rather than using steroids. used as the endpoints for evaluating efficacy of these drugs.
Suboptimal response is indicated by an unchanged relapse rate or
Disease modifying treatments ongoing MRI activity after continuous therapy for at least 6 months
Disease modifying treatments are approved by the Therapeutic compared with pretreatment. The patient should first be evaluated
Goods Administration for use in patients with clinically isolated to identify secondary causes for suboptimal response including
syndrome and RRMS but are only available on the Pharmaceutical noncompliance or the development of neutralising antibodies to
Benefits Scheme (PBS) for RRMS (Table 3).20,21 Suppression of interferon-R.
Table 4. Therapy directed at the symptoms of multiple sclerosis20,21

Symptom Drug Dosage Common side effects Comments
Spasticity Baclofen If predominantly Weakness, drowsiness, dizziness, If ceased, needs to
nocturnal fatigue, headache, insomnia, be withdrawn slowly
symptoms: confusion, ataxia, frequency, urgency, over 2 weeks to avoid
10-25 mg nocte; dysuria, constipation agitation, delirium,
if continuous convulsions
symptoms: 5-25
mg tds
Diazepam 2-10 mg tds Drowsiness, ataxia, dependency Can be used as add-on
therapy to baclofen
Dantrolene Starting dose 25 Muscle weakness, drowsiness, Mainly useful in bed
mg/day (maximum hypertension, drooling, enuresis, bound patients
50 mg qid) diarrhoea, nausea, abnormal LFTs
Paroxysmal Carbamazepine Initially 100 mg bd Fatigue, weakness, ataxia
symptoms increasing slowly to
of MS
* 300 mg bd
Fatigue Amantadine 100-200 mg/day in Nervousness, depression, nightmares, Should be gradually
two divided doses hallucinations, insomnia, dizziness, withdrawn after 3-4
headache, blurred vision, orthostatic months because of
hypotension, peripheral oedema, dry likely spontaneous
mouth, gastrointestinal side effects improvement
Intention Clonzepam 0.5 mg/day Drowsiness, ataxia, dependency
tremor increasing slowly to
6 mg/day
Propranolol 40 mg bd Nausea, diarrhoea, bronchospasm,
dyspnoea, cold extremities,
bradycardia, hypotension
Carbamazepine 100 mg bd, can be See above Increase slowly until
increased to 300 symptoms resolve
mg bd
Urinary Oxybutynin 2.5-5 mg bd to tds Dry mouth, constipation, nausea,
urgency vomiting, dyspepsia, blurred vision,
dry eyes, tachycardia, facial flushing
Propantheline 15-30 mg tds Dry mouth, constipation, nausea,
vomiting, dyspepsia, blurred vision,
dry eyes, tachycardia
Amitriptyline or 25-75 mg nocte Dry mouth, constipation, nausea,
imipramine vomiting, dyspepsia, blurred vision,
dry eyes, tachycardia
Erectile Sildenafil 25-100 mg 1 hour Rash, diarrhoea, urinary tract
dysfunction before intercourse infections, abnormal vision
* Paroxysmal symptoms of MS include trigeminal neuralgia and paraesthesias
bd = twice per day; tds = three times per day; qid = 4 times per day; nocte = at night
First line treatments Table 5. Early clinical features affecting progno

The interferon-Rs and glatiramer acetate have been used as first sis in multiple sclerosis35-38
line DMTs for RRMS for over a decade. They have roughly equivalent
efficacy; double blind, placebo controlled trials demonstrate a relapse
Better prognosis Poor prognosis
reduction of around 30% and reduction in the number of active • Optic neuritis or isolated • Efferent systems
sensory symptoms as the affected in the CIS
lesions on brain MRI for both groups.22,23 Studies have also shown
CIS or ‘multifocal’ CIS
these drugs delay the progression from clinically isolated syndrome to
• Initial relapsing remitting • High relapse rate in
clinically definite MS.24 However, they are not approved for this use course first 2-5 years
on the PBS. • Long interval to second • Substantial
relapse disability after 5
Second line treatments • No disability after 5 years years
Natalizumab has been demonstrated to reduce the rate of disability • Normal initial MRI • Abnormal initial
progression, the annualised relapse rate and the number of new • Female gender MRI with large
lesions on MRI by 54%, 68% and 92% respectively.25 Although
lesion load
• Younger age at onset
these relative risk reduction figures appear greater than those seen • Complete recovery from the
with interferon-B and glatiramer acetate, its use is limited due to first neurological episode
the potentially devastating complication of progressive multifocal
leukoencephalopathy due to a brain infection with JC virus. The risk
Symptomatic treatment
of progressive multifocal leukoencephalopathy overall is estimated Troublesome symptoms may include spasticity, parasthesias, tremor,
at one case per 600 patients treated26 and an increased risk is erectile dysfunction, depression and anxiety, fatigue and pain.
associated with longer treatment duration, prior immunosuppressant Symptomatic management includes pharmacological agents (Table 4),
use and presence of antibodies against JC virus.27 Natalizumab allied health consultation and continence strategies. It is important
has generally been used to treat patients who have a suboptimal to exclude differential diagnoses before instituting treatment (eg.
response to first line DMTs or in those who have a particularly urinary infection in patients with new urinary symptoms).
aggressive initial disease course. In addition to the medications outlined in Table 4, spasticity
Fingolimod (FTY720), the first oral treatment for RRMS, was listed may respond to physiotherapy and muscle stretching. Cerebellar
on the PBS on 1 September 2011.28 This drug has a unique mode of intention tremor is difficult to treat pharmacologically, however wrist
action through the sphingosine 1-phosphate receptor which prevents weights can be tried. A pre- and post-void bladder scan will help
lymphocyte trafficking through the lymph node and causes a reversible direct continence strategies: urinary urgency due to a small capacity
lymphopenia.29 With regards to the efficacy of fingolimod in clinical ‘spastic’ bladder may respond to anticholinergic drugs. If the bladder
trials, the annualised relapse rate was approximately 50% lower is atonic, intermittent urinary catherterisation is more appropriate.
compared to placebo. Approximately 70-75% of the fingolimod groups Depression and anxiety are very common in MS, but psychoses
were relapse free for 2 years compared with 46% of the placebo are rare. Management options include counselling with a psychologist
group.30 Despite being a 1 year trial, fingolimod has also been shown familiar with MS and antidepressants.21 Fatigue is common and
to have greater efficacy compared to interferon with respect to relapse may respond to amantidine 100 mg in the morning and at midday.
rate and proportion who are relapse-free. However, discontinuation Importantly, depression should always be considered as a cause in
rates were higher in the fingolimod arm.31 The drug is given 0.5 mg/day any MS patient complaining of fatigue. Pain is common and often
and is generally well tolerated. Possible side effects include first dose under-recognised in MS and management includes counselling and
bradycardia, macular oedema, liver function abnormalities and increased medications (eg. amitriptyline, carbamazepine, gabapentin, pregabalin).
risk of infections. It should not be used in patients without prior exposure
to varicella zoster infection or immunisation.
Pregnancy and multiple sclerosis
Other oral therapies currently undergoing preclinical trials include All drugs listed in Table 3 are Australian Drug Evaluation Committee
laquinimod, teriflunomide and BG12. The long term safety and exact pregnancy category D, except glatiramer (Category B1) and
role of these oral therapies in MS are yet to be established. natalizumab (Category C). Pregnancy reduces disease activity,
particularly in the third trimester when it is around 70% lower than
Third line and salvage therapeutic options the year preceding pregnancy.32 In the postpartum period, there is a
In patients with aggressive disease who do not respond to treatment, higher risk of relapses in the first 3 months after delivery when up to
other options include immunosuppression with cyclophosphamide 30% of patients may relapse.32 The decision when to stop treatment
or mitoxantrone, or high dose chemotherapy followed by autologous and when to recommence after delivery should be individualised,
haematopoeitic stem cell transplant. The use of these strategies is depending on disease activity in the months leading up to the time
limited by their lower tolerability and potentially serious adverse events. when the woman plans to conceive.
Prognosis Conflict of interest: Professor Macdonell has served on advisory boards

Multiple sclerosis is characterised by considerable interpatient for Biogen Idec, Novartis, Sanofi-Aventis and Merck-Serono. The MS
variability in prognosis. Less than 5% of patients have very severe service at Austin Health has received honoraria, travel support, and
disability within the first 5 years after onset and 10-20% of patients research and clinical service sponosrhip from Biogen Idec, Novartis,
remain unimpaired without therapy over 20 years.12 In the pre-DMT Sanofi-Aventis, Merck-Serono and Bayer-Schering.
era, the median time from disease onset to cane requirement,
bedbound status and death, was roughly 15, 26 and 41 years
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years shorter for MS patients than for the age matched general mechanism of disease progression in multiple sclerosis. J Neurol
2008;255(Suppl 1):3-11.
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4. Sawcer S, Hellenthal G, Pirinen M, et al. Genetic risk and a primary role
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for cell-mediated immune mechanisms in multiple sclerosis. Nature
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B. Trends in the epidemiology of multiple sclerosis in Greater Hobart,
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Tasmania: 1951 to 2009. J Neurol Neurosurg Psychiatry 2010;82:180-7.
developed mild to moderate disability by time of diagnosis.12 6. Lucas RM, Ponsonby AL, McMichael AJ, et al. Observational analytic
Cognitive impairment occurs at all stages and in all subtypes of studies in multiple sclerosis: controlling bias through study design and
conduct. The Australian Multicentre Study of Environment and Immune
MS, with the more severe levels of cognitive impairment occurring
Function. Mult Scler 2007;13:827-39.
in the progressive phase.39 The typical profile of impairment is in 7. Miller D, Barkhof F, Montalban X, Thompson A, Filippi M. Clinically iso
information processing speed, memory and executive skills. This lated syndromes suggestive of multiple sclerosis. Part I: natural history,
pathogenesis, diagnosis, and prognosis. Lancet Neurol 2005;4:281-8.
often impacts on the employability of the patient with MS, even
8. Lovblad KO, Anzalone N, Dorfler A, et al. MR imaging in multiple scle
when physical disability is low, and should be factored in at the rosis: review and recommendations for current practice. AJNR Am J
other end of the spectrum when end-of-life issues are raised. Neuroradiol 2010;31:983-9.
9. Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for mul
tiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol
Summary of important points 2011;69:292-302.
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11. Lublin FD, Baier M, Cutter G. Effect of relapses on development of
• There is significant interpatient variability in prognosis. residual deficit in multiple sclerosis. Neurology 2003;61:1528-32.
• The main diagnostic criteria are clinical, supported by 12. Scalfari A, Neuhaus A, Degenhardt A, et al. The natural history of mul
tiple sclerosis: a geographically based study 10: relapses and long-term
investigations including MRI and lumbar puncture and evoked disability. Brain 2010;133:1914-29.
potentials. 13. Thompson AJ, Montalban X, Barkhof F, et al. Diagnostic criteria for
primary progressive multiple sclerosis: a position paper. Ann Neurol
• First line disease modifying agents for relapsing remitting MS
2000;47:831-5.
include interferon-B and glatiramer. 14. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multi
• First line treatment for relapses is usually intravenous ple sclerosis: 2005 revisions to the “McDonald criteria”. Ann Neurol
2005;58:840-6.
methylprednisolone for 3 days.
15. Schumacker GA, Beebe G, Kibler RF, et al. Problems of experimental
• Troublesome symptoms including spasticity, parasthesias, tremor, trials of therapy in multiple sclerosis: Report by the Panel on the
erectile dysfunction, depression and anxiety, fatigue and pain Evaluation of Experimental Trials of Therapy in Multiple Sclerosis. Ann
N Y Acad Sci 1965;122:552-68.
can be managed with pharmacological agents, allied health
16. Poser CM, Paty DW, Scheinberg L, et al. New diagnostic criteria for
consultation and continence strategies. multiple sclerosis: guidelines for research protocols. Ann Neurol
• Pregnancy reduces disease activity. However, there is a higher 1983;13:227-31.
17. Menge T, Hemmer B, Nessler S, et al. Acute disseminated encephalo
risk of relapse in the postpartum period.
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18. Beck RW, Cleary PA, Trobe JD, et al. The effect of corticosteroids for
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• Multiple Sclerosis Society of Australia: www.msaustralia.org.au sis. The Optic Neuritis Study Group. N Engl J Med 1993;329:1764-9.
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trolled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med
2006;354:899-910.
26. Yousry TA, Major EO, Ryschkewitsch C, et al. Evaluation of patients treated
with natalizumab for progressive multifocal leukoencephalopathy. N Engl J
Med 2006;354:924-33.
27. Linda H, von Heijne A, Major EO, et al. Progressive multifocal leukoenceph
alopathy after natalizumab monotherapy. N Engl J Med 2009;361:1081-7.
28. Available at www.australianprescriber.com/latest_drug/fingolimod%20
hydrochloride%20/948.
29. Kappos L, Antel J, Comi G, et al. Oral fingolimod (FTY720) for relapsing
multiple sclerosis. N Engl J Med 2006;355:1124-40.
30. Kappos L, Radue EW, O’Connor P, et al; FREEDOMS Study Group. A
placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N
Engl J Med 2010;362:387-401.
31. Cohen JA, Barkhof F, Comi G, et al; TRANSFORMS Study Group. Oral fin-
golimod or intramuscular interferon for relapsing multiple sclerosis. N Engl
J Med 2010;362:402-15.
32. Vukusic S, Hutchinson M, Hours M, et al. Pregnancy and multiple scle
rosis (the PRIMS study): clinical predictors of post-partum relapse. Brain
2004;127(Pt 6):1353-60.
33. Bronnum-Hansen H, Koch-Henriksen N, Stenager E. Trends in survival and
cause of death in Danish patients with multiple sclerosis. Brain 2004;127(Pt
4):844-50.
34. Trojano M, Pellegrini F, Fuiani A, et al. New natural history of inter-
feron-beta-treated relapsing multiple sclerosis. Ann Neurol 2007;61:300-6.
35. Tintore M, Rovira A, Rio J, et al. Baseline MRI predicts future attacks and
disability in clinically isolated syndromes. Neurology 2006;67:968-72.
36. Brex PA, Ciccarelli O, O’Riordan JI, Sailer M, Thompson AJ, Miller DH. A
longitudinal study of abnormalities on MRI and disability from multiple
sclerosis. N Engl J Med 2002;346:158-64.
37. Confavreux C, Vukusic S, Moreau T, Adeleine P. Relapses and progression
of disability in multiple sclerosis. N Engl J Med 2000;343:1430-8.
38. Confavreux C, Vukusic S, Adeleine P. Early clinical predictors and progres
sion of irreversible disability in multiple sclerosis: an amnesic process.
Brain 2003;126(Pt 4):770-82.
39. Langdon DW. Cognition in multiple sclerosis. Curr Opin Neurol
2011;24:244-9.
PROFESSIONAL
A is for aphorism
If ‘a physician who treats himself has a fool
Jane Smith for a patient’ - are we all fools?
How do doctors perform at self
Keywords treatment?
aphorisms and proverbs as a topic; self care; patient acceptance of healthcare
Self referrals and self treatment are significantly
more likely to be judged as inappropriate by
a blinded expert panel than ‘usual care’.6
Sir William Osler was a great physician much (0.4 times a year) and most (75%) do not Formal healthcare is more likely to result in a
and medical educator and many of his visit their GP at all in a year. This is in the United documented history and examination, more
wise teachings have survived the passage Kingdom where all doctors are registered with preventive healthcare, more appropriate referral
of time, including the counsel about self their own GP6 patterns, and more time on sick leave.4 It appears
treatment - the title of this article.1 A systematic review showed that 24-87% of that doctors receive higher quality of healthcare
doctors see their GP in a year, but suggested that using formal arrangements.
Research from around the world shows that the these were mostly corridor consultations, not
majority of doctors self diagnose, self investigate, formal care.4
Moral of the story?
self treat and self prescribe; behaviour advised Although about half the medical profession Osler was right. Doctors are fools not to seek the
as foolish by Osler, frowned upon by most is registered with a GP, the majority self treat, advantages of formal healthcare. We should all
professional medical organisations, and even regardless of whether they have their own doctor have our own GP
legislated against in the state of Victoria.2 Such or not.
Author
statutory prohibition has not been shown to make Jane Smith MBBS, FRACGP, GradDipFM, MHS,
a difference to this pattern of behaviour3
Why don’t doctors access formal
FAICD, is Associate Professor, Faculty of Health
healthcare?
Indeed, self treatment is commonplace among Science and Medicine, Bond University, Gold
the medical profession - from student days onward Qualitative analyses show several reasons why Coast, Queensland. jsmith@bond.edu.au.
- and is an almost universal response among doctors self treat, or avoid seeking healthcare Conflict of interest: none declared.
doctors when illness develops. These findings have from another doctor. They:4,7
been fairly consistent over the past 30 years. • find it embarrassing to be a patient, more so References
1. Osler W. Sir William Osler: Aphorisms from his
So why is it that the default health seeking for mental health issues bedside teachings and writings. Bennett Bean R,
behaviour for most of the medical profession • regard self treatment and self prescribing as Bennett Bean W, editors. Springfield, Ill. Thomas;
1961.
is just the opposite of such wise advice from a normal and okay 2. Kay M, Del Mar CB, Mitchell G. Does legislation
founding father of modern medicine? • feel pressured to stay at work and reduce harm to doctors who prescribe for them
selves? Aust Fam Physician 2005;34:94-6.
Doctors have privileged access to medicines demonstrate their health status
3. Rosvold EO, Tyssen R. Should physicians’
so can choose to self medicate from a range of • like to be in control self-prescribing be restricted by law? Lancet
sources, including sample drugs as well as self • fear loss of privacy/confidentiality. 2005;365:1372-4.
4. Kay M, Mitchell G, Clavarino A, Doust J. Doctors
prescribing pharmacy medicines.4 Nonprescribing It appears reasonable to expect doctors to use
as patients: a systematic review of doctors’ health
patients only have the opportunity to pursue self their expertise to their own advantage. More access and the barriers they experience. Br J Gen
treatment at their local supermarket, pharmacy than 90% of doctors think it acceptable to Pract 2008;58:501-8.
5. Australian Institute of Health and Welfare.
or online. self treat acute minor illnesses, but only one-
Australia’s health 2010. Canberra: AIHW, 2010.
quarter to one-third feel the same about chronic
How often do doctors visit diseases.
6. Chambers R, Belcher J. Self reported health care
over the past 10 years: survey of general practition
their GP? In just the same way as we expect patients to
ers. Br J Gen Pract 1992;42:153-6.
7. Montgomery AJ, Bradley C, Rochfort A,
We know that 85% of Australians attend their manage minor problems, doctors should be able Panagopoulou E. A review of self-medication in
physicians and medical students. Occup Med (Lond)
general practitioner every year at least, visiting to self manage minor illnesses and accidents
2011;61:490-7.
on average about five times per year.5 However, without restriction. But this should not apply
patients who are doctors only consult their GP to the management of chronic diseases, which
a fraction of this number - less than a tenth as affect doctors as much as other people. correspondence afp@racgp.org.au
622 Reprinted from AUSTRALIAN FAMILy PHySICIAN VOL. 41, NO. 8, AUGUST 2012
CLINICAL
Managing undernutrition
in the elderly
Damian Flanagan
Therese Fisher Prevention is better than cure
Michael Murray
Renuka Visvanathan
Karen Charlton
Cathy Thesing
Gerald Quigley
Kerstin Walther
and weight loss.8'9 Ageing is associated with

Background significant impairment in the regulation of food
Undernutrition in the elderly is common and can be associated with adverse intake, which means older people are less likely to
medical consequences, contributing to frailty, morbidity, hospitalisation and want to eat and more likely to feel full, and do not
mortality.
automatically compensate with increased intake
Objective following periods of decrease in energy intake (eg.
This article provides guidelines for screening for undernutrition in general following acute illness).10 Moreover, weight loss in
practice, and suggests strategies to address undernutrition in older patients. the elderly is associated with loss of muscle mass.
Discussion If weight is regained, there is a disproportionate
Screening for undernutrition in general practice helps focus time and resources regain of fat rather than lean body mass (ie. often
on people at greatest risk. Early identification and management of people at risk there is a net loss of muscle mass).11,12 The ensuing
of undernutrition is important because it is difficult to reverse its adverse effects, sarcopaenia is associated with a risk of adverse
once established. outcomes such as physical disability, reduced
Keywords mobility, institutionalisation, poor quality of life and
aged; diet; undernutrition even death.13
If an older patient presents with any of the many
contributing factors for undernutrition or clinical
consequences associated with undernutrition (Figure
Undernutrition is common among elderly 1), it is important to consider how undernutrition
Australians living in the community,1-3 with might affect their clinical outcome and to intervene
an estimated 10-44% of older people being with appropriate management.
at risk.2-4 Acute illness in such individuals
can trigger severe clinical consequences,
Definitions
with recovery likely to be difficult and Malnutrition: A deficiency or excess (or imbalance)
delayed given the lack of nutritional of energy, protein and other nutrients, which
reserve. Yet undernutrition often remains causes measurable adverse effects on tissue/
unrecognised and undermanaged. body form (shape, size, composition), function and
clinical outcome. Can encompass both overnutrition
The potential consequences of undernutrition and undernutrition, but often used to refer to
and risk factors contributing to its development have undernutrition only2
been reviewed elsewhere (summarised in Figure Undernutrition: A clinical syndrome characterised
1 ).1,5-7 This article focuses on: by weight loss associated with significant depletion
• introducing routine screening for undernutrition of fat stores and muscle mass. Also known as
into general practice protein energy undernutrition.3
• interventions to prevent undernutrition in general Frailty: Age related cumulative declines across
practice patients. multiple physiologic systems, with impaired
Prevention and early intervention are key because homeostatic reserves and reduced capability to
it is difficult to reverse the effects of undernutrition withstand stress, resulting in increased vulnerability
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 41, NO. 9, SEPTEMBER 2012 695
CLINICAL Managing undernutrition in the elderly - prevention is better than cure
to adverse health outcomes such as falls, therefore systematic screening within general Screening tools
hospitalisation, institutionalisation and mortality.13 practice is a useful means of identifying those most Validated nutritional screening tools provide an easy and
Sarcopaenia: Progressive and generalised loss at risk. reliable way to identify clinical characteristics associated
of skeletal muscle mass and strength, with a risk with undernutrition.3,16 A more comprehensive nutrition
of adverse outcomes such as physical disability,
Incorporating screening into assessment can be considered (eg. by an accredited
frailty, poor quality of life and death.13
general practice practising dietician) for people identified as malnourished/
Screening for undernutrition among elderly patients high risk or with complex nutritional needs.3 Two screening
Identifying undernutrition
in general practice should be incorporated into tools that can be easily incorporated into Australian
in the elderly
routine practice wherever possible, to help focus general practice are described in Table 1, with suggested
Who is at risk? time and resources on intervention for those interventions outlined in Table 2.
identified as at greatest risk.2,15 A systematic
Identifying and addressing
All elderly people are at potential risk of approach is best, such as:
contributing factors
undernutrition. Obese as well as underweight • weigh elderly patients at every visit or twice
elderly people can experience unintentional weight yearly if a patient is seen frequently, with any A variety of common contributing factors can lead to an
loss due to undernutrition (masked undernutrition). recorded weight loss triggering nutritional increased risk of undernutrition in the elderly. Addressing
The risks associated with rapid loss of muscle mass screening (in the elderly, weight loss over time is these factors early and in the community allows for
remain in both groups of patients.1,14 a better indicator of undernutrition than BMI) improved nutritional health - giving older people the
It is not possible to identify undernourished • for patients aged >75 years, incorporate a simple nutritional reserves that can be counted on during periods
patients simply by their physical appearance, body nutritional status screening tool (discussed of acute illness.
mass index (BMI) or weight at a single time point, below) into the 75+ annual health assessment. Some contributing factors benefit from a
multidisciplinary approach involving dieticians, dentists,
pharmacists, psychologists and other allied health
professionals while for some elderly patients, specialist
advice from geriatricians may also be of benefit.
The challenge for general practitioners is to identify
contributing factors for undernutrition and address them
effectively.
Management strategies
Key factors to address, and management strategies to
consider, are reviewed below. It is important to address
all of these factors concurrently: addressing social factors
without managing contributing medical factors and vice
versa may not be fully effective.
A multidisciplinary approach may assist in managing
these patients.
Identify ‘red flag’ conditions

If a patient presents with undernutrition, the first objective
in general practice is to assess for any potentially life
threatening or serious medical conditions (‘red flags’) that
may have led to unintentional weight loss, such as cancer
or cardiac, hepatic or renal failure.
Manage chronic or reversible medical

conditions
Once ‘red flags’ have been eliminated, many other
medical conditions or their treatments that may contribute
to undernutrition can be addressed within general practice
(Table 3). It is also important to review patient attitudes
Figure 1. Contributing factors and health outcomes associated with undernutrition1,3,5,7,22
toward weight; elderly patients may be confused by
696 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 41, NO. 9, SEPTEMBER 2012
Managing undernutrition in the elderly - prevention is better than cure CLINICAL
Table 1. Screening tools for undernutrition

Screening tool Criteria assessed Outcome categories Validation
Mini Nutritional • Weight loss (of 1-3 kg or >3 kg over • Malnourished Validated in international
Assessment Short Form the past 3 months) • At risk of malnutrition studies for the early detection
(MNA®-SF)
* • Appetite • Normal nutritional of undernutrition and frailty
• Mobility status in community dwelling
individuals aged >65
• Psychological stress or acute illness years15,25,26
• Dementia/psychological problems
• BMI (or calf circumference if BMI not
available)
Malnutrition Screening • Weight loss (of 1-5 kg, 6-10 kg, • High risk Developed and validated for
Tool (MST)' 11-15 kg or >15 kg over the past 6 • Medium risk acute hospital, oncology and
months) • Low risk residential care patients27
• Appetite
* Downloadable in various formats from www.mna-elderly.com23
t Downloadable from www.health.qld.gov.au/nutrition/resources/hphe_mst_pstr.pdf24
Tailor nutritional advice to the individual. Refer

Table 2. Suggested interventions according to outcome category23
to Table 5 for tips on increasing protein in the diet
Category Action
and other general recommendations.
Malnourished • Commence nutritional intervention:
Consider referral to a dietician for patients with
- oral nutritional supplementation (400-600 kcal/day)
complex needs.
- diet enhancement (Table 5)
• Monitor weight closely Encourage exercise
• Carry out further in depth nutritional assessment
(refer to a dietician) While not an intervention for undernutrition,
At risk of With weight loss resistance training is essential to maximise
malnutrition • Commence nutritional intervention: muscle mass and strength in the elderly. Physical
- diet enhancement activity provides an opportunity for linking to social
- oral nutritional supplementation (400 kcal/day)
activities as well, which can improve general
• Monitor weight closely
wellbeing and contribute to better energy intake.
• Carry out further in depth nutritional assessment
No weight loss Encourage physical activity and mobility in addition
• Monitor weight closely to an adequate high protein diet.19
• Rescreen every 3 months
Reinforcement and monitoring
media coverage of obesity and consider any weight what constitutes healthy eating. It can be difficult for elderly patients to change
loss to be beneficial. Management of these issues requires an eating habits, particularly when eating is not
If geriatric syndromes (eg. falls, dementia, individualised approach for each patient. Where triggered by hunger. Regular follow up and
polypharmacy) or functional decline (eg. reduced possible, enlist the help of family and friends; some reinforcement of nutritional messages is needed.
mobility or ability to perform activities of daily living) potential interventions are listed in Table 4. This may include:
are identified, consider referral to a geriatrician. • providing written advice (eg. sticky notes to place
Recommend nutritional support around the kitchen, or a doctor’s prescription of
Address social and functional Nutritional therapy is an important component in dietary advice)
issues
the management of undernourished patients, and • involving family members
Low socioeconomic status, limited functional ability should be provided alongside medical and social/ • telephone prompting/reminders.
and social isolation are often major driving factors functional interventions. It is important to monitor nutritional intervention
for undernutrition in the community. Financial Dietary requirements change in elderly people. regularly. Examples of how this can be achieved
constraints will affect access to basic necessities In particular, protein requirements for older people include:
such as nutritious food. Living or eating alone often are approximately 25% higher than for younger • multidisciplinary team management review
results in lower food intake for older people and adults.17 Based on the limited data available, the • monitoring patients’ weight at each visit
increases their risk of undernutrition.1 recommended dietary intake for people aged >70 • recording changes in food intake.
It is also important to consider patients’ ability years is 81 g per day for men and 57 g for women, As weight gain is achieved, review meal plans and
to shop for and prepare food, and awareness of or approximately 1 g protein per kg body weight.18 dietary supplements. It is important to remember
CLINICAL Managing undernutrition in the elderly - prevention is better than cure
intervention, followed by appropriate management

Table 3. Management of medical conditions that may contribute to
strategies that are implemented once undernutrition
undernutrition1,2
or the risk of undernutrition has been identified.
• Screen for dementia, anxiety and depression (depression is one of the commonest
Assessment and treatment of nutritional risk
causes of undernutrition in the elderly)
• Review polypharmacy and long term medications that may influence appetite or should be part of routine care for the elderly, just
nutrition (eg. those causing side effects such as nausea, constipation, anorexia); as assessment and management of cardiovascular
switch to an alternative medication or eliminate if possible risk factors are standard practice in adults. General
• Review dietary restrictions - refer to a dietician for advice and support as required practice is an ideal setting to identify and manage
• Identify and manage dyspepsia, nausea or constipation
patients at risk of undernutrition.
• Review oral health and encourage regular reviews with the dentist
• Optimise management of chronic conditions that may affect nutrition, such as: Key points
- dysphagia
- gastrointestinal diseases causing malabsorption or maldigestion • Early identification of patients who are at risk of
- infection or inflammation undernutrition is important.
- pain • Monitor weight and incorporate nutritional
- hypermetabolism (eg. hyperthyroidism) screening of elderly patients into routine clinical
practice.
Table 4. Social and functional interventions for undernutrition • Many of the contributing factors for
in the elderly28,29 undernutrition in the elderly are amenable to
medical intervention by GPs.
• Community care services:
• A subset of patients with more complex needs
- centre based day care
- domestic assistance would benefit from referral to a dietician or
- home delivered meals (eg. ‘Meals on Wheels’ or similar) geriatrician.
• Extended Aged Care at Home, Community Aged Care Package Program, Home
and Community Care Program Authors
• Allied healthcare: Damian Flanagan MBBS, MWell, is a general
- consider referral (eg. occupational therapist, dietician) practitioner, West Rosebud, Chair, Peninsula GP
Network and a lecturer, RMIT, Victoria. flanagan@
• Home visit (with nutritional prompts):
pac.com.au
- family and friends
- community nurse Therese Fisher MBBS, is a general practitioner
- service providers in aged care, the Royal Australian Air Force
Association, Merriwa, Western Australia
- general practitioner or practice nurse
• Case management and/or care coordination/planning Michael Murray MBBS, MPH, FRACP, is a geriatri
• Dietary and social support: cian and Director, Geriatric Medicine, St Vincent’s
Hospital, Clinical Associate Professor, University
- dietitian
of Melbourne and Adjunct Associate Professor,
- cooking lessons
Australian Centre for Evidence Based Aged Care, La
- men’s sheds
Trobe University, Melbourne, Victoria
- community meal programs
Renuka Visvanathan PhD, FRACP MBBS, is an aca
demic geriatrician and Director, Aged and Extended
that weight is also influenced by fluid, so some program is considered necessary, attention to Care Services, Queen Elizabeth Hospital, Adelaide,
patients, such as those with cardiac failure, will adequate protein and micronutrient intake, as well South Australia
need their weight assessed in the context of fluid as exercise, is required to preserve muscle mass.8 Karen Charlton PostgradDipNutrDiet, MPhil(Epi),
retention. Close monitoring of the weight loss program is MSc, PhD, APD, is Associate Professor, Public
important to ensure preservation of muscle mass. Health Program, University of Wollongong, New
Intentional weight loss in the South Wales
elderly Summary Cathy Thesing BSc, MND, PostgradDipPublicHealth,
is a dietician and Director, Melbourne Dietetic
Elderly people who are underweight are at Undernutrition can present a significant clinical
Centre, Victoria
greater risk of mortality than those who are and public health problem among older Australians
Gerald Quigley BPharm, MH, is a pharmacist,
overweight,18,20,21 and the optimal BMI range living in the community. Patients with undernutrition
master herbalist and media presenter, Melbourne,
for older people is suggested to be about 22-27 are at increased risk of morbidity, hospitalisation Victoria
kg/m2.1 Intentional weight loss is considered and mortality and therefore early detection and
Kerstin Walther PhD, is Program Manager,
inappropriate unless excess weight is associated intervention is important. Identifying patients at risk Prevention and Chronic Disease Management,
with functional problems.8218 If a weight loss via screening is the first step to providing effective Central Sydney GP Network, New South Wales.
698 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 41, NO. 9, SEPTEMBER 2012
Managing undernutrition in the elderly - prevention is better than cure CLINICAL
MD. Nutritional screening in community-dwelling older

Table 5. Nutritional support and advice for the elderly at risk of adults: a systematic literature review. Asia Pac J Clin
undernutrition3,18,28-30 Nutr 2010;19:440-9.
16. Vellas B, Lauque S, Andrieu S, et al. Nutrition assess
• Liberalise the patient’s diet (review dietary restrictions) ment in the elderly. Curr Opin Clin Nutr Metab Care
• Encourage use of flavour enhancers 2001;4:5-8.
17. Janssen I, Mark AE. Elevated body mass index and mor
• Recommend frequent small meals and snacks: tality risk in the elderly. Obes Rev 2007;8:41-59.
- cheese and crackers 18. Paddon-Jones D, Short KR, Campbell WW, Volpi E,
- scrambled, poached or boiled eggs Wolfe RR. Role of dietary protein in the sarcopenia of
aging. Am J Clin Nutr 2008;87:1562S-6.
- baked beans 19. Flicker L, McCaul KA, Hankey GJ, et al. Body mass index
- fortified soups and survival in men and women aged 70 to 75. J Am
Geriatr Soc 2010;58:234-41.
- milk based puddings and drinks
20. Zunzunegui MV, Sanchez MT, Garcia A, Casado JM,
- sandwiches with high protein fillings (eg. cheese, tuna, ham, chicken) Otero A. Body mass index and long-term mortality in
• Ensure ready availability of nourishing snacks (eg. nuts, yoghurt, cheese and an elderly Mediterranean population. J Aging Health
crackers) 2012;24:29-47.
21. Nestlé Nutrition Institute. MNA Mini Nutritional
• Ensure food texture suits chewing and swallowing ability Assessment. Available at www.mna-elderly.com
• Suggest ways to increase protein and energy intake by fortifying foods: [Accessed 11 November 2011].
- incorporate milk, butter or cheese in foods such as soups, sandwiches 22. Guigoz Y The Mini-Nutritional Assessment (MNA®).
Review of the literature - what does it tell us? J Nutr
or mashed potato
Health Aging 2006;10:466-87.
- add milk based sauces (eg. custard, cheese sauce) to fruit and vegetables 23. Morley JE. Assessment of malnutrition in older persons:
- add powdered nutritional supplements to foods such as soups, cereals, custard, a focus on the mini nutritional assessment. J Nutr
mashed potato Health Aging 2011;15:87-90.
24. Queensland Government. Malnutrition: is your patient
• Consider high energy/protein nutritional supplements (nutritional drinks are a at risk? Available at www.health.qld.gov.au/nutrition/
convenient and effective way to meet requirements when appetite and/or mood resources/hphe_mst_pstr.pdf [Accessed 11 November
are low. They allow an individual to remain well nourished while the causal factors 2011].
can be addressed) 25. van Veenrooij LMW, de Vos R, Borgmeijer-Hoelen
• Ensure sufficient fluid intake AMMJ, Kruizenga HM, Jonkers-Schuitema CF, de Mol
BAMJ. Quick-and-easy nutritional screening tools to
• Where a specific nutrient deficiency has been identified, use of a micronutrient detect disease-related undernutrition in hospital in- and
supplement may be indicated (eg. iron, folate, vitamin D) outpatient settings: a systematic review of sensitivity
and specificity. Clin Nutr 2007;2:21-37.
Conflict of interest: All authors are members of the older Australian recipients of domiciliary care services 26. Aged Care Australia. Description of community care
and its association with outcomes at 12 months. J Am service types. Canberra: Aged Care Australia. Available
Malnutrition in the Elderly Advisory Board, sup
Geriatr Soc 2003;51:1007-11. at www.agedcareaustralia.gov.au/internet/agedcare/
ported by Nestlé Pty Ltd. Karen Charlton and Renuka 5. Norman K, Pichard C, Lochs H, Pirlich M. Prognostic publishing.nsf/content/description+of+community+care+
Visvanathan were members of the international impact of disease-related malnutrition. Clin Nutr service+types [Accessed 11 November 2011].
2008;27:5-15. 27. Aged, Community and Mental Health Division, Victoria.
working group to revise and validate the Mini
6. Kinney JM. Nutritional frailty, sarcopenia and falls Identifying and planning assistance for home-based
Nutritional Assessment (funded by Nestlé Nutrition in the elderly. Curr Opin Clin Nutr Metab Care adults who are nutritionally at risk: a resource manual.
Institute, Switzerland). Renuka Visvanathan partici 2004;7:15-20. Melbourne: Home and Community Care Program, 2001.
7. Visvanathan R, Chapman IM. Undernutrition and ano Available at www.health.vic.gov.au/hacc/downloads/
pated in the 2012 International Consensus Meeting pdf/resourcemanual.pdf [Accessed 11 November 2011].
rexia in the older person. Gastroenterol Clin North Am
for Protein Intake In Older People, which also 2009;38:393-409. 28. Koopman R. Dietary protein and exercise training in
received support from the Nestle Nutrition Institute. 8. Chapman IM. Weight loss in older persons. Med Clin ageing. Proc Nutr Soc 2011;70:104-13.
North Am 2011;95:579-93. 29. Evans C. Malnutrition in the elderly: a multifactorial
9. Miller SL, Wolfe RR. The danger of weight loss in the failure to thrive. The Permanente Journal 2005;9:38-41.
Acknowledgements elderly. J Nutr Health Aging 2008;12:487-91. 30. Milne AC, Potter J, Avenell A. Protein and energy sup
The authors would like to thank Ms Jane Winters 10. Roberts SB. Regulation of energy intake in relation to plementation in elderly people at risk from malnutrition.
and Dr Sue Cripps for their assistance in preparing metabolic state and nutritional status. Eur J Clin Nutr Cochrane Database Syst Rev 2005(2):CD003288.
2000;54(3 Suppl):S64-9. 31. Silver HJ. Oral strategies to supplement older adults’
this review. Preparation of the manuscript was sup dietary intakes: comparing the evidence. Nutr Rev
11. Newman AB, Lee JS, Visser M, et al. Weight change
ported by an independent educational grant from and the conservation of lean mass in old age: the 2009;67:21-31.
Nestlé Pty Ltd. Health Aging and Body Composition Study. Am J Clin 32. Australian Government Department of Health and
Nutr 2005;82:872-8. Ageing and National Health and Medical Research
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1. Sampson G. Weight loss and malnutrition in the elderly regain and effects on body composition: the Health, Zealand. Canberra: NHMRC, 2005. Available at www.
- the shared role of GPs and ADPs. Aust Fam Physican Aging, and Body Composition Study. J Gerontol A Biol nhmrc.gov.au/_files_nhmrc/publications/attachments/
2009;38:507-10. Sci Med Sci 2010:65:78-83. n35.pdf [Accessed 11 November 2011].
2. Dietitians Association of Australia. Evidence-based 13. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al.
practice guidelines for the nutritional management of Sarcopenia: European consensus on definition and
malnutrition in adult patients across the continuum of diagnosis: Report of the European Working Group on
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Medicine. Under-nutrition and the older person. 14. Gallagher D, Ruts E, Visser M, et al. Weight stability
Position statement no. 6. Sydney: ANZsGm, 2007.
masks sarcopenia in elderly men and women. Am J
4. Visvanathan R, Macintosh C, Callary M, Penhall R,
Physiol Endocrinol Metab 2000;279:E366-75.
Horowitz M, Chapman I. The nutritional status of 250 15. Phillips MB, Foley AL, Barnard R, Isenring EA, Miller correspondence afp@racgp.org.au
FOCUS Psychological strategies
A] Motivational interviewing
“ Facilitating
techniques
Tania Gibbie
Dan I Lubman behaviour change in the general
practice setting
Background One of the biggest challenges that primary care practitioners

One of the biggest challenges that primary care practitioners face is helping people change longstanding behaviours
face is helping people change longstanding behaviours that that pose significant health risks. When patients receive
pose significant health risks. compelling advice to adopt a healthier lifestyle by cutting
Objective back or ceasing harmful behaviours (eg. smoking,
To explore current understanding regarding how and overeating, heavy drinking) or adopting healthy or safe
why people change, and the potential role of motivational behaviours (eg. taking medication as prescribed, eating
interviewing in facilitating behaviour change in the general more fresh fruit and vegetables), it can be frustrating and
practice setting. bewildering when this advice is ignored or contested.
Discussion A natural response for a practitioner who encounters
Research into health related behaviour change highlights such opposition (termed ‘resistance’ in the psychological
the importance of motivation, ambivalence and resistance. literature) is to reiterate health advice with greater authority
Motivational interviewing is a counselling method that or to adopt a more coercive style in order to educate the
involves enhancing a patient’s motivation to change by means patient about the imminent health risks if they don’t change.
of four guiding principles, represented by the acronym RULE: When these strategies don’t succeed, the practitioner
Resist the righting reflex; Understand the patient’s own may characterise the patient as ‘unmotivated’ or ‘lacking
motivations; Listen with empathy; and Empower the patient. insight’. However, research around behaviour change shows
Recent meta-analyses show that motivational interviewing
that motivation is a dynamic state that can be influenced,
is effective for decreasing alcohol and drug use in adults and
and that it fluctuates in response to a practitioner’s style.
adolescents and evidence is accumulating in others areas
Importantly, an authoritative or paternalistic therapeutic
of health including smoking cessation, reducing sexual risk
behaviours, improving adherence to treatment and medication style may in fact deter change by increasing resistance.1
and diabetes management.
The Stages of Change model and
Keywords motivational interviewing
communication; doctor-patient relations; patient centred care;
Prochaska and DiClemente2 proposed readiness for change as a
psychotherapy, brief; motivation
vital mediator of behavioural change. Their transtheoretical model
wgi] co of behaviour change (the ‘Stages of Change’) describes readiness to
change as a dynamic process, in which the pros and cons of changing
generates ambivalence. Ambivalence is a conflicted state where
opposing attitudes or feelings coexist in an individual; they are stuck
between simultaneously wanting to change and not wanting to
change. Ambivalence is particularly evident in situations where there
is conflict between an immediate reward and longer term adverse
consequences (eg. substance abuse, weight management). For
example, the patient who presents with serious health problems as a
result of heavy drinking, who shows genuine concern about the impact
of alcohol on his health, and in spite of advice from his practitioner to
cut back his drinking, continues to drink at harmful levels, embodies
this phenomenon.
660 Reprinted From AUSTRALIAN FAMILY PHYSICIAN VOL. 41, NO. 9, SEPTEMBER 2012
The Prochaska and DiClemente Stages of Change model2 offers a
Table 1. Practitioner tasks within the Stages of
conceptual framework for understanding the incremental processes
Change model1,2
that people pass through as they change a particular behaviour. This
change process is modelled in five parts as a progression from an Patient stage Practitioner tasks
initial precontemplative stage, where the individual is not considering Precontemplation Raise doubt and increase the
change; to a contemplative stage, where the individual is actively (Not ready) patient’s perception of the risks
ambivalent about change; to preparation, where the individual and problems with their current
behaviour. Provide harm reduction
begins to plan and commit to change. Successful progression through
strategies
these stages leads to action, where the necessary steps to achieve
change are undertaken. If successful, action leads to the final stage, Contemplation Weigh up the pros and cons of
(Getting ready) change with the patient and work
maintenance, where the person works to maintain and sustain long
on helping them tip the balance by:
term change.3 Relapse is considered an important stage in the change
• exploring ambivalence and
process and is used as an opportunity to learn about sustaining alternatives
maintenance in the future. • identifying reasons for change/
Motivational interviewing (MI) is an effective counselling method risks of not changing
that enhances motivation through the resolution of ambivalence. It • increasing the patient’s
grew out of the Prochaska and DiClemente model described above2 confidence in their ability to
and Miller and Rollnick’s1 work in the field of addiction medicine, change
which drew on the phrase ‘ready, willing and able’ to outline three Preparation - Clear goal setting - help the patient
critical components of motivation. These were:1 action to develop a realistic plan for
• the importance of change for the patient (willingness) (Ready) making a change and to take steps
• the confidence to change (ability)
toward change
• whether change is an immediate priority (readiness). Maintenance Help the patient to identify and use
Using MI techniques, the practitioner can tailor motivational (Sticking to it) strategies to prevent relapse
strategies to the individual’s stage of change according to the *Relapse Help the patient renew the
Prochaska and DiClemente model (Table 1).1,2 (Learning) processes of contemplation and
action without becoming stuck or
Applications and effectiveness of demoralised
motivational interviewing * Relapse is normalised in MI and is used as an
Recent meta-analyses show that MI is equivalent to or better opportunity to learn about how to maintain long term
than other treatments such as cognitive behavioural therapy (CBT) behaviour change in the future
or pharmacotherapy, and superior to placebo and nontreatment
controls for decreasing alcohol and drug use in adults4-6 and • stress management
adolescents.7 Motivational interviewing has also been shown to be • completion of recommended screening or diagnostic tests or
efficacious in a number of other health conditions, such as smoking specialist/allied health/psychologist referral.
cessation,8 reducing sexual risk behaviours,9-11 improving adherence
to treatment and medication,12 as well as diabetes management.13
The spirit of motivational interviewing
In addition, studies support the applicability of MI to HIV care, Motivational interviewing is underpinned by a series of principles
such as improving adherence to antiretroviral therapy14,15 and the that emphasise a collaborative therapeutic relationship in which
reduction of substance use among HIV positive men and women.15 the autonomy of the patient is respected and the patient’s
As such, MI is an important therapeutic technique that has wide intrinsic resources for change are elicited by the therapist.
applicability within healthcare settings in motivating people to Within MI, the therapist is viewed as a facilitator rather than
change. In general practice, possible applications include: expert, who adopts a nonconfrontational approach to guide
• medication adherence the patient toward change. The overall spirit of MI has been
• management of the SNAP (smoking, nutrition, alcohol and described as collaborative, evocative and honouring of patient
physical activity)16 risk factors autonomy.1 Miller and Rollnick1 have commented that the use
• engagement in prevention or management programs for diabetes of MI strategies in the absence of the spirit of MI is ineffective.
or cardiovascular health Although paradoxical, the MI approach is effective at engaging
• management of substance abuse problems apparently ‘unmotivated’ individuals and when considered in
• management of problem gambling or sexual risk taking the context of standard practice can be a powerful engagement
• pain management strategy (Case study, Table 2).
Reprinted From AUSTRALIAN FAMILY PHYSICIAN VOL. 41, NO. 9, SEPTEMBER 2012 661
FOCUS Motivational interviewing techniques - facilitating behaviour change in the general practice setting
Case study - using the spirit of Motivational interviewing in practice

motivational interviewing The practical application of MI occurs in two phases: building
A male patient, 52 years of age, who drinks heavily and has motivation to change, and strengthening commitment to change.
expressed the desire to reduce drinking, but continues to
drink heavily. Building motivation to change
It is easy to conclude that this patient lacks motivation, his In Phase I, four early methods represented by the acronym OARS
judgment is impaired or he simply does not understand (Table 3) constitute the basic skills of MI. These basic counselling
the effects of alcohol on his health. These conclusions techniques assist in building rapport and establishing a therapeutic
may naturally lead the practitioner to adopt a paternalistic
relationship that is consistent with the spirit of MI.
therapeutic style and warn the patient of the risks to his
health. In subsequent consultations, when these strategies Strengthening commitment to change
don’t work, it is easy to give up hope that he will change
his drinking, characterise him as ‘unmotivated’ and drop This involves goal setting and negotiating a ‘change plan of action’.
the subject altogether. In MI, the opposite approach is In the absence of a goal directed approach, the application of the
taken, where the patient’s motivation is targeted by the strategies or spirit of MI can result in the maintenance of ambivalence,
practitioner. Using the spirit of MI, the practitioner avoids where patients and practitioners remain stuck. This trap can be
an authoritarian stance, and respects the autonomy of avoided by employing strategies to elicit ‘change talk’.1 There are many
the patient by accepting he has the responsibility to strategies to elicit ‘change talk’, but the simplest and most direct way
change his drinking - or not. Motivational interviewing is to elicit a patient’s intention to change by asking a series of targeted
emphasises eliciting reasons for change from the patient,
questions from the following four categories:
rather than advising them of the reasons why they should
• disadvantages of the status quo
change their drinking. What concerns does he have about
• advantages of change
the effects of his drinking? What future goals or personal
values are impacted by his drinking? The apparent ‘lack • optimism for change
of motivation’ evident in the patient would be constructed • and intention to change (Table 4).
as ‘unresolved ambivalence’ within an MI framework. The Alternatively, if a practitioner is time poor, a quick method of drawing
practitioner would therefore work on understanding this out ‘change talk’ is to use an ‘importance ruler’.
ambivalence, by exploring the pros and cons of continuing Example: ‘If you can think of a scale from zero to 10 of how
to drink alcohol. They would then work on resolving this important it is for you to lose weight. On this scale, zero is not
ambivalence, by connecting the things the patient cares important at all and 10 is extremely important. Where would you be on
about with motivation for change. For example, drinking this scale? Why are you at _ _ _ _ and not zero? What would it take for
may impact the patient’s values about being a loving
you to go from ___ to (a higher number)?’
partner and father or being healthy and strong. A discussion
This technique identifies the discrepancy for a patient between
of how continuing to drink (maintaining the status quo)
their current situation and where they would like to be. Highlighting
will impact his future goals to travel in retirement or have a
good relationship with his children may be the focus. The this discrepancy is at the core of motivating people to change. This
practitioner would emphasise that the decision to change can be followed by asking the patient to elaborate further on this
is ‘up to him’, however they would work with the patient to discrepancy and then succinctly summarising this discrepancy and
increase his confidence that he can change (self efficacy). reflecting it back to the patient. Next, it is important to build the
Table 2. The spirit of motivational interviewing vs an authoritative or paternalistic therapeutic style

The spirit of motivational interviewing Authoritative or paternalistic therapeutic style
Collaboration: a partnership between the patient and Confrontation: the practitioner assumes the patient has
practitioner is formed. Joint decision making occurs. The an impaired perspective and consequently imposes the
practitioner acknowledges the patient’s expertise about need for ‘insight’. The practitioner tries to persuade and
themselves coerce a patient to change
Evocation: the practitioner activates the patient’s own Education: the patient is presumed to lack the insight,
motivation for change by evoking their reasons for change. knowledge or skills required to change. The practitioner
The practitioner connects health behaviour change to the tells the patient what to do
things the patient cares about
Honouring a patient’s autonomy: although the practitioner Authority: the practitioner instructs the patient to make
informs and advises their patient, they acknowledge the changes
patient’s right and freedom not to change. ‘It’s up to you’
Adapted from Miller and Rollnick, 2002
Motivational interviewing techniques - facilitating behaviour change in the general practice setting FOCUS
Table 3. OARS: The basic skills of motivational interviewing

Ask Open-ended questions
* Example
• The patient does most of the talking I understand you have some concerns about your drinking.
• Gives the practitioner the opportunity to learn more Can you tell me about them?
about what the patient cares about (eg. their values Versus
and goals) Are you concerned about your drinking?
Make Affirmations Example
• Can take the form of compliments or statements of I appreciate that it took a lot of courage for you to discuss
appreciation and understanding your drinking with me today
• Helps build rapport and validate and support the You appear to have a lot of resourcefulness to have coped
patient during the process of change with these difficulties for the past few years
• Most effective when the patient’s strengths and Thank you for hanging in there with me. I appreciate this is
efforts for change are noticed and affirmed not easy for you to hear
Use Reflections
* Example
• Involves rephrasing a statement to capture the You enjoy the effects of alcohol in terms of how it helps you
implicit meaning and feeling of a patient’s statement unwind after a stressful day at work and helps you interact
• Encourages continual personal exploration and helps with friends without being too self-conscious. But you are
people understand their motivations more fully beginning to worry about the impact drinking is having on
• Can be used to amplify or reinforce desire for change your health. In fact, until recently you weren’t too worried
about how much you drank because you thought you had
it under control. Then you found out your health has been
affected and your partner said a few things that have made
you doubt that alcohol is helping you at all
Use Summarising Example
• Links discussions and ‘checks in’ with the patient If it is okay with you, just let me check that I understand
• Ensure mutual understanding of the discussion so far everything that we’ve been discussing so far. You have been
• Point out discrepancies between the person’s current worrying about how much you’ve been drinking in recent
situation and future goals months because you recognise that you have experienced
some health issues associated with your alcohol intake, and
• Demonstrates listening and understand the patient’s
you’ve had some feedback from your partner that she isn’t
perspective happy with how much you’re drinking. But the few times
you’ve tried to stop drinking have not been easy, and you are
worried that you can’t stop. How am I doing?
A general rule-of-thumb in MI practice is to ask an open-ended question, followed by 2-3 reflections
patient’s confidence in their ability to change. This involves focusing • Where do we go from here?
on the patient’s strengths and past experiences of success. Again, a • What do you want to do at this point?
‘confidence ruler’ could be employed if a practitioner is time poor. • How would you like things to turn out?
Example: ‘If you can think of a scale from zero to 10 of how • After reviewing all of this, what’s the next step for you?
confident you are that you can cut back the amount you are drinking. It is common for patients to ask for answers or ‘quick fixes’ during
On this scale, zero is not confident at all and 10 is extremely confident. Phase II. In keeping with the spirit of MI, a simple phrase reminding the
Where would you be on this scale? Why are you at _ _ _ _ and not zero? patient of their autonomy is useful, ‘You are the expert on you, so I’m
What would it take for you to go from ___ to (a higher number)?’ not sure I am the best person to judge what will work for you. But I can
Finally, decide on a ‘change plan’ together. This involves standard give you an idea of what the evidence shows us and what other people
goal setting techniques, using the spirit of MI as the guiding principle and have done in your situation’.
eliciting from the patient what they plan to do (rather than instructing or
advising). If a practitioner feels that the patient needs health advice at this The guiding principles of motivational
point in order to set appropriate goals, it is customary to ask permission interviewing
before giving advice as this honours the patient’s autonomy. Examples of In general practice, the particular difficulties associated with quick
key questions to build a ‘change plan’ include: consultation times can present unique challenges in implementing MI.
• It sounds like things can’t stay the same as they are. What do you Miller and Rollnick17 have attempted to simplify the practice of MI for
think you might do? health care settings by developing four guiding principles, represented
• What changes were you thinking about making? by the acronym RULE:
Table 4. Eliciting ‘change talk’1

Change talk Questions to elicit change talk Example of patient’s change talk
Disadvantages of the • What worries you about your blood ‘I guess, if I’m honest, if I keep drinking,
status quo pressure? I am worried my family are going to stop
• What difficulties have resulted from your forgiving me for my behaviour’
drinking?
• In what way does your weight concern
you?
Advantages of change • How would you like your health to be in 5 ‘If I lose weight, at least I won’t have to
years time? wake up feeling guilty every morning that I
• What are the advantages of reducing your am not taking care of myself’
drinking?
• What would be different in your life if you
lost weight?
Optimism for change • When have you made a significant change ‘I did stop smoking a few years ago for a
in your life before? How did you do it? year and I felt so much healthier. It was
• What strengths do you have that would really hard, but once I put my mind to
help you make a change? something I usually stick at it’
Intention to change • In what ways do you want your life to be ‘I never thought I would be living like this.
different in 5 years? I want to go back to being healthy and
• Forget how you would get there for a strong, with enough energy to enjoy my
moment. If you could do anything, what friends and family’. ‘I want to manage my
would you change? diabetes better’
• Resist the righting reflex Empower your patient

• Understand the patient’s own motivations Patient outcomes improve when they are an active collaborator in their
• Listen with empathy treatment.17 Empowering patients involves exploring their own ideas
• Empower the patient. about how they can make changes to improve their health and drawing
on the patient’s personal knowledge about what has succeeded in
Resist the righting reflex the past. A truly collaborative therapeutic relationship is a powerful
The righting reflex describes the tendency of health professionals to motivator. Patients benefit from this relationship the most when the
advise patients about the right path for good health. This can often have practitioner also embodies hope that change is possible.
a paradoxical effect in practice, inadvertently reinforcing the argument RULE is a useful mnemonic to draw upon when implementing
to maintain the status quo. Essentially, most people resist persuasion the spirit of MI in general practice. If a practitioner has more time,
when they are ambivalent about change and will respond by recalling four additional principles (Table 5) can be applied within a longer
their reasons for maintaining the behaviour. Motivational interviewing in therapeutic intervention.
practice requires clinicians to suppress the initial righting reflex so that
they can explore the patient’s motivations for change. Barriers to implementing motivational
interviewing in general practice
Understand your patient’s motivations Barriers to implementing MI in general practice include time pressures,
It is the patient’s own reasons for change, rather than the practitioner’s, the professional development required in order to master MI, difficulty
that will ultimately result in behaviour change. By approaching a in adopting the spirit of MI when practitioners embody an expert role,
patient’s interests, concerns and values with curiosity and openly patients’ overwhelming desire for ‘quick fix’ options to health issues
exploring the patient’s motivations for change, the practitioner will and the brevity of consultation times. These barriers to implementing
begin to get a better understanding of the patient’s motivations and MI in primary care represent significant cons on a decisional balance.
potential barriers to change. On the other hand, the pros for adopting an MI approach with patients
who are resistant to change are compelling. While we are not
Listen with empathy advocating MI for all patient interactions in general practice, we invite
Effective listening skills are essential to understand what will motivate practitioners to explore their own ambivalence toward adopting MI
the patient, as well as the pros and cons of their situation. A general within their practice, and consider whether they are ‘willing, ready and
rule-of-thumb in MI is that equal amounts of time in a consultation able’. Practitioners who undertake MI training will have an additional
should be spent listening and talking. therapeutic tool to draw upon when encountering patient resistance
FOCUS Motivational interviewing techniques - facilitating behaviour change in the general practice setting
Table 5. Four further principles of motivational interviewing
Express empathy
In practical terms, an empathic style of communication involves the use of reflective listening skills and accurate
empathy, where the practitioner seeks to understand the patient’s perspective, thoughts and feelings without
judgeing, criticising or blaming. Building empathy and understanding does not mean the practitioner condones the
problematic behaviour. Instead, the practitioner seeks to create an open and respectful exchange with the patient,
who they approach with genuine curiosity about their experiences, feelings and values
Develop discrepancy
Assisting patients to identify discrepancies between their current behaviour and future goals or values about
themselves as a person, partner, parent, or worker is a powerful motivator that helps ‘tip the balance’ toward change.
Exploring the pros and cons of change can help a patient develop discrepancy. These ‘decisional balance’ exercises
are used effectively in MI to help patients tease apart their ambivalence and help the patient express their concerns
about the behaviour
Roll with resistance
Often when a practitioner attempts to move a patient toward change too quickly because the risks of the behaviour
are significant or they perceive that there are time pressures for change, they adopt a coercive or authoritative style.
If the patient is ambivalent about change, this approach will commonly be met with resistance from the patient.
Resistance takes many forms but most commonly can be described as interrupting or arguing with the practitioner,
discounting the practitioner’s expertise, excusing their behaviour, minimising the effects of their behaviour, blaming
other people for their behaviour, being pessimistic about their chances to change or being unwilling to change
altogether. In MI, rolling with this resistance involves approaching resistance without judgement and interpreting
these responses as a sign that the patient holds a different perspective to the practitioner. MI then uses strategies
such as simple reflection of the resistance, emphasising the individual’s choice to change or not (‘it’s up to you’),
shifting the focus of the discussion or simply reframing what the person has said, in order to roll with resistance and
prevent resistance from affecting engagement
Support self efficacy
Many people with enduring behaviours that have negative impacts on their health have made their own attempts to
change at some time or other and been unsuccessful. They may have attempted to cease smoking and only lasted
a week, or tried to lose weight but been unable to sustain a diet. They may have attempted to comply with their
medication several times in the past but found it difficult because of side effects or a complicated dosing regimen.
By highlighting the patient’s strengths and reflecting on times in their life when they have successfully changed,
even if just in one small area, self efficacy can be promoted. The practitioner’s belief in a patient’s ability to change
is a powerful way to promote self efficacy. By promoting self efficacy, the practitioner can help the individual develop
the confidence that they are capable of change
to change and a proven method for dealing with a number of common References
1. Miller WR, Rollnick S. Motivational Interviewing. Preparing people
presentations within general practice.
for change. 2nd edn. New York: The Guilford Press, 2002.
2. Prochaska J, DiClemente C. Towards a comprehensive model of
Resource change. In: Miller WR, Heather N, editors. Treating addictive behav
For further information and online motivational interviewing training iours: processes of change. New York: Pergamon, 1986.
opportunities visit www.motivationalinterview.org. 3. DiClemente CC, Velasquez M. Motivational interviewing and the
stages of change. In: Miller WR, Rollnick S, editors. Motivational
Authors interviewing, second edition: Preparing people for change. New

York: The Guilford Press, 2002.
Kate Hall BA(Hons), DPsych(Clin), MAPS, is Senior Lecturer, Deakin
4. Burke BL, Arkowitz H, Menchola M. The efficacy of motivational
University, Department of Psychology and senior clinical psychologist,
interviewing: a meta-analysis of controlled trials. J Consult Clin
Turning Point Alcohol and Drug Centre, Eastern Health, Melbourne,
Psychol 2003;71:843-61.
Victoria. kateh@turningpoint.org.au 5. Hettema J, Steele J, Miller WR. Motivational interviewing. Ann
Tania Gibbie BSc(Hons), MPsych(Health), PhD, is a health psychologist, Rev Clin Psychol 2005;1:91-111.
Barwon Health, Geelong, Victoria 6. Lundahl BW, Kunz C, Brownell C, Tollefson D, Burke BL. A meta
analysis of motivational interviewing: twenty-five years of
Dan I Lubman BSc(Hons), MBChB, PhD, FRANZCP, FAChAM, is Director
empirical studies. Res Soc Work Pract 2010;20:137-60.
and Professor of Addiction Studies, Turning Point Alcohol and Drug 7. Jensen CD, Cushing CC, Aylward BS, Craig JT, Sorell DM, Steele
Centre, Eastern Health and Monash University, Melbourne, Victoria. RG. Effectiveness of motivational interviewing interventions for
adolescent substance use behavior change: a meta-analytic review.
Conflict of interest: none declared. J Consult Clin Psychol 2011;79:433-40.
8. Gray E, McCambridge J, Strang J. The effectiveness of motivational

interviewing delivered by youth workers in reducing drinking, ciga
rette and cannabis smoking among young people: quasi-experimental
pilot study. Alcohol 2005;40:535-9.
9. Fisher J, Fisher W, Cornman D, Amico R, Bryan A, Friedland G.
Clinician-delivered intervention during routine clinical care reduces
unprotected sexual behaviour among HIV-infected patients. J Acquir
Immune Defic Syndr 2006;41:44-52.
10. Kuyper L, de Wit J, Heijman T, Fennema H, van Bergen J,
Vanwesenbeeck I. Influencing risk behavior of sexually transmit
ted infection clinic visitors: Efficacy of a new methodology of
motivational preventive counseling. AIDS Patient Care STDs
2009;23:423-31.
11. Naar-King S, Wright K, Parsons J, et al. Healthy choices:
Motivational enhancement therapy for health risk behaviours in HIV
positive youth. AIDS Educ Prev 2006;18:1-11.
12. Swanson AJ, Pantalon MV, Cohen KR. Motivational interviewing
and treatment adherence among psychiatric and dually diagnosed
patients. J Nerv Ment Dis 1999;187:630-5.
13. West D, Dilillo V, Bursac Z, Gore SA, Greene PG. Motivational
interviewing improves weight loss in women with type 2 diabetes.
Diabetes Care 2007;30:1081-7.
14. Cooperman NA, Arnsten JH. Motivational interviewing for improv
ing adherence to antiretroviral medications. Curr HIV/AIDS Rep
2005;2:159-64.
15. Parsons J, Rosof E, Punzalan JC, Di Maria L. Integration of motiva
tional interviewing and cognitive behavioral therapy to improve HIV
medication adherence and reduce substance use among HIV-positive
men and women: results of a pilot project. AIDS Patient Care STDs
2005;19:31-9.
16. The Royal Australian College of General Practitioners. Available at
www.racgp.org.au/guidelines/snap [Accessed August 2012].
17. Rollnick S, Miller WR, Butler CC. Motivational interviewing in health
care. Helping patients change behavior. New York: The Guilford
Press, 2008.
CLINICAL
Elevated serum ferritin

What should GPs know?
Katie Goot
Simon Hazeldine
Peter Bentley
John Olynyk
Darrell Crawford
While there is interest in iron reduction therapy

Background for cancer risk reduction,3 improvement of insulin
Elevated serum ferritin is commonly encountered in general practice. Ninety sensitivity in metabolic syndrome4 and management
percent of elevated serum ferritin is due to noniron overload conditions, where
of fatty liver disease not responding to lifestyle
venesection therapy is not the treatment of choice.
changes,5 the Australian Red Cross Blood Service
Objective Therapeutic Venesection program is currently
This article aims to outline the role of the Australian Red Cross Blood Service restricted to patients meeting the criteria listed in
Therapeutic Venesection program, to clarify the interpretation of the HFE gene Table 1, and who also meet the general eligibility
test and iron studies, and to describe the steps in evaluating a patient with criteria for volunteer blood donation.
elevated serum ferritin.
Patients meeting therapeutic venesection criteria
Discussion with contraindications to volunteer blood donation
After exclusion of hereditary haemochromatosis, investigation of elevated serum (eg. comorbid angina, hepatitis C, cerebrovascular
ferritin involves identifying alcohol consumption, metabolic syndrome, obesity, disease) need to be referred elsewhere for
diabetes, liver disease, malignancy, infection or inflammation as causative therapeutic venesection. Options include private
factors. Referral to a gastroenterologist, haematologist or physician with an
pathology providers, public hospitals, haematologists
interest in iron overload is appropriate if serum ferritin is >1000 pg/L or if the
and some GPs.
cause of elevated serum ferritin is still unclear.
In the absence of contraindications, patients with
Keywords elevated SF who do not meet eligibility criteria for
haemochromatosis; venesection; iron therapeutic venesection may become volunteer whole
blood donors every 12 weeks.
Potential harms of frequent venesection therapy
for a person without true iron overload include
The Australian Red Cross Blood Service has development of iron deficiency anaemia, reinforcement
experienced a growing number of referrals of a suboptimal management strategy for a biochemical
from general practitioners for therapeutic abnormality, perpetuation of the myth that a genetic
venesection for patients with elevated condition affecting family members exists, and the
serum ferritin (SF) who do not meet the general venesection risks of venous scarring, phlebitis
eligibility criteria of two HFE mutations and vasovagal episodes.
or documented iron overload. Thirty-
six percent of referrals to the Australian Table 1. Eligibility criteria for
Australian Red Cross Blood Service
Red Cross Blood Service Therapeutic
Therapeutic Venesection program
Venesection program in an 8 month period
in 2011 were for patients with elevated SF • Evidence of hereditary
haemochromatosis:
and an HFE genotype not associated with
- C282Y homozygosity
iron overload.1 Venesection therapy, while - C282Y/H63D compound
the mainstay of treatment for iron overload heterozygosity
due to hereditary haemochromatosis (HH), • Clinical iron overload supported by
does not address the underlying reasons for FerriScan® MRI or liver biopsy
elevated SF in patients without true iron • Polycythaemia rubra vera
• Porphyria cutanea tarda
overload.2
CLINICAL Elevated serum ferritin - what should GPs know?
Iron metabolism In HH, total body iron stores can be calculated liver fibrosis, liver cirrhosis, hepatocellular
Approximately 75% of the body’s 3-4 g total iron from the volume of blood removed during weekly carcinoma, cardiac arrhythmias, cardiomyopathy,
is found within haemoglobin in red blood cells, venesections. Removal of 4 g or more of iron (16 diabetes, arthropathy, hypogonadism and skin
10-20% is stored in the protein ferritin and the weekly venesections) without developing iron hyperpigmentation. Organ damage can be averted
remainder is found in the iron transport protein deficiency anaemia indicates iron overload.6 with early diagnosis and appropriate venesection
transferrin, as well as in myoglobin, cytochromes therapy, but this is challenging due to the variable,
and as unbound serum iron.6
Hereditary haemochromatosis subtle and nonspecific symptoms in early disease.
Synthesised by the liver, the hormone hepcidin Hereditary haemochromatosis is an autosomal Whereas the HFE gene test indicates the risk
regulates total body iron levels by controlling recessive condition of progressive iron overload, of eventually developing iron overload, iron studies
intestinal iron absorption.7 Under the strict control usually due to homozygosity for the C282Y mutation indicate if iron overload is currently present. The HFE
of hepcidin, daily iron losses of 1-2 mg from in the HFE gene. This mutation causes inappropriately gene test is performed once, whereas iron studies
sloughed mucosal, gastrointestinal and skin cells increased intestinal iron absorption at a rate 2-3 are performed every time an assessment of current
are accurately offset by daily absorption of 1-2 mg times greater than normal.8 Similar to type 1 diabetes iron overload is required (Table 3). A typical schedule
from dietary sources. Only 10% of daily dietary iron being a metabolic condition of glucose homeostasis of venesections for a patient with HH and iron
intake is absorbed.2 due to insulin deficiency, HH is a metabolic condition overload is presented in Table 4.
of iron homeostasis due to hepcidin deficiency9
Iron overload Approximately 1 in 200 people of Caucasian
Iron studies
The human body lacks an iron excretion mechanism. race are homozygous for the C282Y mutation. This Accurate diagnosis of a patient’s total body iron
Table 2 outlines circumstances in which iron mutation has much higher penetrance than the H63D stores requires careful interpretation of iron studies
overload can develop. mutation. C282Y homozygotes are at highest risk of (Table 5). Serum iron exhibits diurnal variation14
Assessment of iron overload relies on surrogate developing total body iron overload whereas C282Y/ and the ideal specimen for iron studies is a fasting
markers, including serum tests (transferrin H63D compound heterozygotes have much lower morning sample where oral iron supplementation
saturation, serum ferritin), noninvasive magnetic risk.8-10 Even if H63D homozygotes develop elevated has been withheld for at least 24 hours before
resonance imaging (MRI) scans for hepatic iron serum iron indices, they are unlikely to develop total testing.13
concentration (FerriScan®), liver biopsy and body iron overload.10,11 The most useful tests in the evaluation of iron
quantitative phlebotomy2,6 C282Y homozygosity confers risk of the multi overload due to HH are transferrin saturation and
Whole blood contains 250 mg iron per 500 mL. organ consequences of iron overload, including serum ferritin.15 Transferrin saturation >45% is
sensitive and fairly specific for diagnosing HH, with
Table 2. Causes of iron overload increasing specificity when the threshold is increased
Mechanism of iron overload Example to >55%. Serum ferritin is most useful in monitoring
Inappropriately increased • Hereditary haemochromatosis venesection requirement and venesection response
intestinal iron absorption • HFE-haemochromatosis in patients already diagnosed with HH.
- Type 1: HFE mutation (HFE gene)
• Non-HFE haemochromatosis (rare) Serum ferritin
- type 2A: haemojuvelin mutation (HJV gene) While low SF is a sensitive and specific indicator of
- type 2B: hepcidin mutation (HAMP gene)
low total body iron stores, elevated SF is sensitive
- type 3: transferrin receptor 2 mutation (TfR2 gene)
- type 4: ferroportin mutation (FPN1 gene) but very nonspecific for iron overload. While a
Transfusional iron overload • Multiple transfusions to treat anaemia due to: normal SF rules out iron overload, only 10% of cases
1 unit packed red cells «250 - red cell aplasia (congenital or acquired) of elevated SF are due to iron overload (Figure 1).
mg iron - haemoglobinopathies Chronic alcohol consumption, metabolic syndrome,
- myelodysplastic syndrome, leukaemia obesity, diabetes, malignancy, infection and
- cancer or chemotherapy for cancer inflammatory conditions explain 90% of causes of
- severe haemorrhage in haemophUia/surgery/trauma elevated SF6,16
Iron-loading anaemias • a-thalassaemia
Elevations of SF in the range 300-1000 pg/L
• p-thalassaemia
are common, and often reflect the presence of the
• Chronic haemolytic anaemias
• Congenital sideroblastic anaemia previously listed conditions. Mild elevations below
• Congenital dyserythropoietic anaemia 1000 pg/L are ‘tolerable’6 and in the absence of HH,
Hepatocellular chronic liver • Alcoholic liver disease the risk of hepatic iron overload is exceedingly low.17
disease • Hepatitis B or C Australian studies have shown a link between
• Nonalcoholic steatohepatitis alcohol consumption and elevated SF, with beer
Excess parenteral iron • Excess IM or IV iron more so than spirits or wine causing increases
Elevated serum ferritin - what should GPs know? CLINICAL
Table 3. Advice based on HFE genotype and serum ferritin

Genotype Prevalence Advice if serum Advice if serum ferritin is elevated
in Caucasian ferritin is normal
Australians11,12
High risk HFE genotypes
Highest risk 1 in 188 • Increased risk of • Begin venesections - candidate for therapeutic
C282Y homozygous future iron overload venesection
• Check iron studies • Family members need testing13
Lower risk 1 in 46 every 1-5 years • SF >1000 |ig/l,: refer to gastroenterologist, haematologist
C282Y/H63D compound • Family members or physician with an interest in iron overload
heterozygous need testing13
Low risk HFE genotypes
H63D homozygous 1 in 49 • Check iron studies • Not a candidate for therapeutic venesection but can become
every 1-5 years a volunteer blood donor if no contraindications exist
• Look for another cause of elevated SF apart from HH,
especially alcohol consumption, metabolic syndrome,
obesity, liver disease and inflammation
• Consider non-HFE haemochromatosis
C282Y carrier 1 in 8 • No further follow up • Family members don’t need testing13
H63D carrier 1 in 4 needed13 • SF >1000 pg/L: refer to gastroenterologist, haematologist
No mutations 3 in 5 or physician with an interest in iron overload
Table 4. Venesection schedule Table 5. Interpretation of iron studies

Iron unloading phase, target serum Iron study Explanation Iron as an Abnormal values (vary from
ferritin ~50 pg/L test name analogy to laboratory-to-laboratory)
• Weekly venesection of ~7 mL/kg money
Suggestive of Suggestive of high
(maximum 550 mL) whole blood low iron stores iron stores
• Ensure pre-venesection haemoglobin Serum Unbound serum ‘Loose <10 pmol/L >30 pmol/L
>120 g/L iron iron change in
• Monitor Hb and SF your pocket’
- Hb: is it safe to remove more
blood? Delay for 1 week if pre Total iron Ability to bind ‘Greediness >70 pmol/L <45 pmol/L
venesection Hb <120 g/L binding even more iron for more
capacity money’
- SF: is it safe to remove more iron?
Monitor SF every 4-6 venesections, Transferrin • Iron absorbed ‘Money <16% >45%
more often as SF approaches saturation from kept in your
100 pg/L duodenum wallet’
• It may take many months or even bound to a
years to unload excess iron transport
• Oral vitamin B12 and folate protein
supplements support erythropoiesis • One molecule
during frequent venesections of transferrin
Lifelong maintenance phase, target binds two
atoms of iron
SF ~50-100 pg/L
• Venesections to maintain SF Serum • Iron within ‘The <30 pg/L • >200 pg/L pre
~50-100 pg/L ferritin a storage savings you menopausal
• Highly variable between individuals, protein have in your women
often in the range 2-6 venesections • One molecule bank’ • >300 pg/L
per year of ferritin men and
• Monitor SF at least every 12 months binds 4500 postmenopausal
atoms of iron women
in ferritin secretion by the liver.18 Chronic daily • >1000 pg/L
consumption of two or more standard drinks refer to
gastroenterologist,
might explain elevated SF19 Repeat SF testing haematologist or
after a period of alcohol abstinence can clarify the physician with
contribution of a patient’s alcohol intake on their an interest in iron
overload
elevated SF
CLINICAL Elevated serum ferritin - what should GPs know?
There exists a well-established link between LFTs usually requires further investigation.23 elevated SF, assess for potential causes including
elevated SF, metabolic syndrome and fatty Malignancy, infection and inflammatory chronic alcohol consumption, metabolic syndrome,
liver.20,21 With the Australian prevalence of conditions may all cause elevated SF. Normal obesity, diabetes, liver disease, malignancy, infection
metabolic syndrome being 1 in 3,22 the high pre screening tests for C-reative protein (CRP), and inflammation.
test probability of ‘metabolic hyperferritinaemia’ erythrocyte sedimenation rate (ESR) and antinuclear • If SF >1000 pg/L, refer to a gastroenterologist,
is important to consider when evaluating antibody (ANA) can help exclude the presence of haematologist or physician with an interest in iron
patients with elevated SF. Features which may these conditions. overload.
discriminate elevated SF due to HH from metabolic Specialist review is mandatory if SF exceeds • If SF <1000 pg/L, address reversible causes and
hyperferritinaemia are listed in Table 6. 1000 pg/L due to the increased risk of fibrosis repeat iron studies.
Liver disease is a cause of elevated SF. Injured and cirrhosis above this threshold. However, in • Encourage voluntary blood donation every 12 weeks.
hepatocytes leak ferritin into the serum, so in the absence of C282Y homozygosity, hepatic iron
liver disease, SF can be considered as another concentration is usually normal or only mildly
Further information
• Australian Red Cross Blood Service: www.transfu-
type of liver function test (LFT), along with the elevated and fatty liver, hepatitis B, hepatitis C and sion.com.au/high_ferritin
transaminases (alanine transaminase [ALT], alcoholic liver disease may be found.17,24 • Australian Red Cross Blood Service App (which
aspartate aminotransferase [AST]) and gamma provides real-time processing of referrals and current
glutamyl transferase (GGT). Some causes of liver Key points information regarding patients who do not meet eligi
bility criteria): http://highferritin.transfusion.com.au
disease are associated with increased hepatic iron • Of all HFE genotypes, only C282Y homozygotes
• Haemochromatosis Australia resources for GPs:
concentration (hepatitis B, hepatitis C, alcoholic have a high risk of hepatic iron overload.
www.haemochromatosis.org.au/GPResources.htm
liver disease, HH) so elevated SF with abnormal • Once HH has been excluded in a patient with • GESA haemochromatosis clinical practice guidelines:
10%
I
HFE genotype
Highest risk C282Y carrier

C282Y H63D
homozygous homozygous
Lower risk H63D carrier
C282Y/H63D
No mutations
compound
heterozygous --------- 1 ,
Keep looking
Hereditary
haemochromatosis
Explains elevated SF
Commence venesections
Suitable for blood service
therapeutic venesection
program
Figure 1. Algorithm for the investigation and management of elevated serum ferritin in general practice
Elevated serum ferritin - what should GPs know? CLINICAL
Table 6. Comparison between elevated serum ferritin in haemochromatosis and in metabolic syndrome
Feature Elevated serum ferritin due to Metabolic hyperferritinaemia due
hereditary haemochromatosis to metabolic syndrome/fatty liver/
insulin resistance/diabetes/obesity
Genotype C282Y homozygous Not C282Y homozygous
Ancestry Usually Caucasian Variable
Transferrin saturation Usually >45% Usually normal (20-45%)
Serum ferritin Elevated Elevated
C-reactive protein Normal Normal
Hepcidin levels Reduced hepcidin levels Normal or elevated hepcidin levels
(not commercially available)
Serum ferritin over time Progressively more elevated Fluctuations from one test to another
Total body iron levels Raised Normal
Response to weekly 500 mL venesections Patient tolerates >16 weekly venesections Patient becomes anaemic after <16
without becoming anaemic weekly venesections
Hepatic iron concentration Raised Normal
(FerriScan® MRI or liver biopsy)
Pattern of iron deposition on liver biopsy Parenchymal deposition in hepatocytes Nonparenchymal deposition in
sinusoidal and Kupffer cells
Management • Iron depletion • Lifestyle modifications
- venesections - weight control
- iron chelation therapy - correction of insulin resistance
www.gesa.org.au/files/editor_upload/File/ 2. Beaton MD, Adams PC. Treatment of hyperferritine Available at www.cdc.gov/ncbddd/hemochromatosis/
Professional/Haemochromatosis.pdf mia. Ann Hepatol 2012;11:294-300. training/pdf/hemochromatosis_course.pdf [Accessed

3. Zacharski LR, Chow BK, Howes PS, et al. Decreased 11 July 2012].
• FerriScan®: www.resonancehealth.com.
cancer risk after iron reduction in patients with 14. Dale JC, Burritt MF, Zinsmeister AR. Diurnal varia
peripheral arterial disease: results from a randomized tion of serum iron, iron-binding capacity, transferrin
Authors trial. J Natl Cancer Inst 2008;100:996-1002. saturation, and ferritin levels. Am J Clin Pathol
Katie Goot MBBS, BSc, is an ACRRM registrar, 4. Houschyar KS, Ludtke R, Dobos GJ, et al. Effects of 2002;117:802-8.
Biloela, Queensland and GPET academic reg phlebotomy-induced reduction of body iron stores on 15. EASL clinical practice guidelines for HFE hemochro
istrar, UQ Rural Clinical School, Rockhampton, metabolic syndrome: results from a randomized clini matosis. J Hepatol 2010;53:3-22.
Queensland. k.goot@uq.edu.au cal trial. BMC Med 2012;10:54. 16. St John AT, Stuart KA, Crawford DHG. Testing for
5. Valenti L, Moscatiello S, Vanni E, et al. Venesection HFE-related haemochromatosis. Australian Prescriber
Simon Hazeldine MBBS, BSc, MRCP, is Senior for non-alcoholic fatty liver disease unresponsive 2011;34:73-6.
Clinical Fellow, Department of Gastroenterology, to lifestyle counselling: a propensity score-adjusted 17. Olynyk JK, Gan E, Tan T. Predicting iron overload
Fremantle Hospital, Fremantle, Western Australia observational study. QJM 2011;104:141-9. in hyperferritinemia. Clin Gastroenterol Hepatol
6. Adams PC, Barton JC. A diagnostic approach to 2009;7:359-62.
Peter Bentley MBBS, MBA, is Manager, Medical
hyperferritinemia with a non-elevated transferrin 18. Leggett BA, Brown NN, Bryant SJ, Duplock L, Powell
Services (WA), Australian Red Cross Blood Service,
saturation. J Hepatol 2011;55:453-8. LW, Halliday JW. Factors affecting the concentrations
Perth, Western Australia 7. Bridle KR, Frazer DM, Wilkins SJ, et al. Disrupted of ferritin in serum in a healthy Australian population.
John Olynyk BMedSc, MBBS, FRACP, MD, is hepcidin regulation in HFE-associated haemochro Clin Chem 1990;36:1350-5.
Director, Department of Gastroenterology, Fremantle matosis and the liver as a regulator of body iron 19. Rossi E, Bulsara MK, Olynyk JK, Cullen DJ,
homoeostasis. Lancet 2003;361:669-73. Summerville L, Powell LW. Effect of hemochroma
Hospital, Fremantle, Western Australia
8. Allen K. Hereditary haemochromatosis - diagnosis tosis genotype and lifestyle factors on iron and red
Darrell Crawford MBBS, FRACP, MD, is Head, and management. Aust Fam Physician 2010;39:938- cell indices in a community population. Clin Chem
Discipline of Medicine, University of Queensland 41. 2001;47:202-8.
School of Medicine, Brisbane, Queensland. 9. Pietrangelo A. Hemochromatosis: an endocrine liver 20. Brudevold R, Hole T, Hammerstrom J.
disease. Hepatology 2007;46:1291-301. Hyperferritinemia is associated with insulin resist
Conflict of interest: none declared. 10. Gurrin LC, Bertalli NA, Dalton GW, et al. HFEC282Y/ ance and fatty liver in patients without iron overload.
H63D compound heterozygotes are at low risk of PLoS One 2008;3:e3547.
Acknowledgements hemochromatosis-related morbidity. Hepatology 21. Trombini P, Piperno A. Ferritin, metabolic syndrome
The authors thank Dr Barbara Bell, National Medical 2009;50:94-101. and NAFLD: elective attractions and dangerous liai
11. Gochee PA, Powell LW, Cullen DJ, Du Sart D, Rossi sons. J Hepatol 2007;46:549-52.
Services Manager, Australian Red Cross Blood
E, Olynyk JK. A population-based study of the 22. Chew GT, Gan SK, Watts GF Revisiting the metabolic
Service for her assistance in providing referral data.
biochemical and clinical expression of the H63D syndrome. Med J Aust 2006;185:445-9.
Australian governments fully fund the Australian hemochromatosis mutation. Gastroenterology 23. Pietrangelo A. Iron in NASH, chronic liver diseases
Red Cross Blood Service for the provision of blood 2002;122:646-51. and HCC: How much iron is too much? J Hepatol
products and services to the Australian community. 12. Olynyk JK, Cullen DJ, Aquilia S, Rossi E, Summerville 2009;50:249-51.
L, Powell LW. A population-based study of the clinical 24. Wong K, Adams PC. The diversity of liver diseases
References expression of the hemochromatosis gene. N Engl J among outpatient referrals for an elevated serum fer
1. Bell B. Australian Red Cross Blood Service Referrals Med 1999;341:718-24. ritin. Can J Gastroenterol 2006;20:467-70.
Database. National Office, 17 O’Riordan Street 13. Centers for Disease Control and Prevention.
Alexandria NSW [Accessed 20 April 2012]. Hemochromatosis for health care professionals. correspondence afp@racgp.org.au
FOCUS The elderly
Dementia
An update on management
Dimity Pond
Background Dementia is an increasingly common condition with

Dementia is an increasingly common condition in the prevalence expected to rise from just over a quarter of a
community. On average, every general practitioner in Australia million currently to just under 1 million in 2050.1 In Australia,
will see three new cases each year. There are strong reasons the number of new cases (or the incidence) is expected
for making an early diagnosis of dementia, as this may enable to rise from around 75 000 in 2010 to 385 000 by 2050.2
families to plan ahead and to institute management that could This means that, on average, every general practitioner
reduce cognitive impairment and slow disease progression. in Australia will see three new dementia cases each year.
Objective Prevalence may vary, and GPs with a special interest in aged
This article discusses the GP’s role in the identification and care or those practising in areas with a high percentage of
management of dementia in general practice and provides an elderly people may see more cases, as will GPs who make
update on management of this disease. visits to residential aged care facilities.
Discussion
Several new strategies for the management of dementia have Apart from its high prevalence, there are other reasons why GPs should
emerged recently and GPs should be aware that optimal become proficient in the assessment and management of dementia:
management of cardiovascular risk factors will improve • carers of people with dementia are at risk of depression and carer
cognition and may delay onset. Management of exercise, fatigue and can only be fully supported once a diagnosis is made
socialisation and cognitive training may improve cognitive • the burden of caring for a person with dementia is identified in
function in early-diagnosed cases. The GP’s role in initiating funding schemes. For example, the Aged Care Funding Instrument
service delivery is an important one, and the practice nurse (ACFI) allows for extra funding for those with a diagnosis of dementia
may play an important role in coordinating services for
living in residential care and some community services depend on
patients in the early stages of dementia.
the diagnosis in order to provide their services.
Keywords Therefore, in order to provide optimal support for their elderly patients,
dementia; Alzheimer disease GPs should consider making a diagnosis of dementia explicit.
BSD O Update - prevention

We know that older patients should be encouraged to reduce their
cardiovascular risk factors, specifically to prevent dementia - both
vascular and Alzheimer dementia. Reduction in blood pressure, lipid
levels, blood sugar, weight, alcohol intake and smoking may improve
cognitive function and prevent or delay the progression of dementia.3
There is growing evidence that regular exercise, social engagement
and cognitive training (the ‘dose’ and complexity are not yet clear,
but examples include crosswords and Sudoku) also improve cognitive
function,4 both in those without dementia and those who already have it.
Update - stage at which a diagnosis

should be made
There have been strong calls for a more timely diagnosis of dementia.5
How should GPs respond to this call?
The arguments for making an early diagnosis include giving patients
and families time to plan ahead and to allow supports to be put in
place. Patients and carers can be educated about what lies ahead and
make plans to ensure as smooth a pathway into the future as possible.
However, many GPs see patients who do not wish to know the constipation. Renal, hepatic, thyroid or other abnormalities revealed on
diagnosis, or do not have the opportunity to discuss the possibility blood testing should also be corrected or treated. Depression should be
of a diagnosis of dementia with carers who are not their patients, managed with ‘talking treatments’ such as cognitive behaviour therapy
and there may be ethical barriers to such discussions if the patient and counselling and/or antidepressants, and referral to a psychologist
does not agree to it. Some GPs may see the negatives in the slow if appropriate. Co-existing dementia and depression is a difficult and
inevitable decline of dementia and prefer to protect their patients from not uncommon problem, and may require referral to a psychiatrist or
knowledge of it, especially if they have known the patient for many psychogeriatrician. Most cases of dementia are sporadic, without a
years. Each case is different, and the GP’s role in broaching this issue strong genetic basis. However, if there is a strong family history of
will vary from patient-to-patient. However, it is evident that more dementia, especially at early onset, referral for genetic counselling and
information about the disease, its effects and its progression, is a pre testing may be considered.
requisite to better planning. A recent study has shown that awareness The importance of a medication review has recently come to the
of the diagnosis was associated with a higher quality of life compared fore. Such a review may be done by the GP, or in close collaboration
to those who had dementia but were not aware of it.6 This is a strong with a pharmacist, and any medications that can be reduced or
argument for GPs to make the diagnosis early when possible, while stopped should be identified. This is known as ‘deprescribing’ and
keeping in mind patient and carer factors when breaking the news. the optimal approach involves reviewing all current medications,
The assessment
Table 1. Assessments to be made in dementia7,14
How should GPs identify dementia? It has been suggested that all
• Clinical history: cognitive, behavioural and
patients over a certain age (eg. 75 years) should be screened for
psychological symptoms (carer/family input preferable)
dementia using a screening questionnaire such as the Mini-Mental
• Physical examination: causes of cognitive impairment
State Examination (MMSE), the General Practitioner assessment of (eg. urinary tract infection, cardiac failure, visual or
COGnition (GPCOG) or the Rowland Universal Dementia Assessment hearing impairment)
Scale (RUDAS), which is particularly useful for assessing patients • Activities of daily living (include safety issues, eg.
from a non-English speaking background.7 However, screening tests driving, falls, nutrition)
will fail to identify dementia in well educated people and will identify • Depression (eg. Geriatric Depression Scale)
as possible dementia many who do not have the disease.8 Poorer • Medication review
performance on screening questionnaires may be due to depression, • Cognitive screening test (eg. MMSE, RUDAS,
poor education, drug side effects, being unwell or anxious on the day GPCOG)15
or other factors. For this reason, GPs should use clinical judgement as Routine tests
well as screening tests when assessing patients for dementia. • Full blood count (FBC)
A reasonable approach is ‘case finding’, which involves assessing • Erythrocyte sedimentation rate (ESR)
only those with symptoms or signs such as ‘lost prescriptions’ and • Liver function test (LFT)
missed appointments, or other behaviours mentioned by family • Calcium
members, neighbours, the practice receptionists and others. The • Thyroid function
patient’s own subjective memory complaints should be taken seriously, • Vitamin B12, folate
although not all those with memory complaints will have dementia. In • Computed tomography scan of brain without contrast
such cases, the assessments listed in Table 1 should be performed. If indicated (* recommended)
Case study - Helen • Chest X-ray
*
Helen, aged 79 years, presents complaining that it is • Fasting blood sugar levels (BSL)
taking her a long time to cook her dinner and she has • Fasting lipids
*
given up some of her usual activities because she ‘isn’t • Fasting homocysteine level
coping’. On a screening test for cognitive impairment she • Electrocardiogram (ECG)
*
scores only slightly above the cut-off level. This concerns • Mid stream urine (MSU)
*
you because Helen is very well educated and you would • Serology for HIV, syphilis
have expected a higher score.
Special investigations
• Electroencephalogram (EEG)
Update on assessment
• Magnetic resonance imaging (MRI)
• Positron emission tomography (PET)
Physical problems that emerge from the physical examination should be
addressed, including management of hypoxia secondary to heart failure
• Apolipoprotein E (E4 status confers increased risk)
or chronic lung disease, treatment of infection and management of
• Neuropsychological assessment
FOCUS Dementia - an update on management
identifying those to be targeted for cessation and then planning a training, GPs are in an ideal position to manage dementia. They should
slow reduction in the offending drugs, in partnership with the patient also monitor patients for evidence of decreasing functional impairment.
and their family, and monitoring of adverse effects.9 In particular, An activities of daily living scale,12 ideally answered by the patient’s
drugs with anticholinergic or sedative actions may have an additive carer, may assist with this assessment. The GP may need to consider
effect on cognition: with cessation or reduction the patient may ‘wake whether the patient is still fit to drive. Carer support and education
up’ and engage more effectively. A cognitive function test may be should be provided, this may include referral to Alzheimer’s Australia.
used to track improvement. General practitioners should also recommend that legal issues are
addressed while the patient is still competent to do so. This includes a
Case study continued will, power of attorney (for financial matters), guardianship (for health
You assess Helen for depression, perform a physical
decisions) and advance care planning.13
examination, order blood tests and a brain CT scan, and
As the patient’s functional impairment increases, support services
ask the pharmacist for a medication review, with a focus
on medications that may cause cognitive impairment. You will need to be mobilised. In the past, GPs often referred patients to the
treat any reversible factors and recommend a diet and Aged Care Assessment Team (ACAT) for ongoing management. However,
exercise program, informing Helen that these have been workforce shortages and the increasing burden of care of the elderly
shown to improve cognition. You organise a review in 6 mean that ACAT (ACAS in Victoria) teams may not be able to manage
months. patients with early dementia who are not yet eligible for packaged care,
which includes a case manager. General practitioners may therefore need
Next steps for Helen to refer such patients to other support services (Table 3). It is possible that
Having treated the reversible causes of cognitive impairment, the GP the practice nurse may familiarise herself with local service providers and
should review the case and perform another cognitive function test. coordinate care to some extent. As dementia is a chronic disease, a care
Ideally, the family or another informant should be consulted for their plan with regular review is an appropriate way to monitor the patient. The
view on Helen’s progression or decline. The GP should consider which practice nurse may be able to assist with reviews of cognitive function,
subtype of dementia is present (eg. vascular, Alzheimer or other). If depression and activities of daily living scales.
there is some doubt about the diagnosis or the management then
Helen should be referred to a specialist service such as a memory Conclusion
clinic. Table 2 identifies reasons for referral. The number of people with dementia in Australia is growing rapidly.
If cognitive impairment is definite, the GP may continue to manage Inevitably this will increase the dementia patient-load for GPs.
Helen. If a trial of anti-dementia drugs is her wish, then the GP must Additionally, as aged care services are stretched, the management of
prescribe these in consultation with a specialist. These medications, this group with chronic and complex care needs will fall to GPs and
which include acetylcholinesterase inhibitors for mild to moderate the extended primary care team. General practitioners have a role in
Alzheimer disease (donepezil, rivastigmine and galantamine) and an promoting reduction of cardiovascular risk factors and encouragement
NMDA glutamate receptor inhibitor (memantine - available on the of exercise, socialisation and cognitive training in all older patients,
Pharmaceutical Benefits Scheme for moderately severe Alzheimer including those with dementia. Clarification of the diagnosis facilitates
disease) may all have a modest effect in some cases.10,11 These access to services and may increase the support available to patients
medications are available on Authority prescription and rules for and their carers. General practitioners should be aware of the
prescribing are complex and should be checked carefully. There are assessment and management of this disease and ways in which they
currently no clear ‘stopping’ rules for ceasing these medications. can best enable their patients to access available services.
The changing role of the GP in ongoing Table 3. Useful contact numbers and websites
management • Alzheimer’s Australia National Dementia Helpline:
With the emergence of evidence in favour of reducing cardiovascular 1800 100 500 (provides carer support, living with
memory loss programs and other services)
risk factors and encouraging exercise, socialisation and cognitive
• Dementia Behaviour Management Advisory Service:
1800 699 799 (provides strategies to help manage
Table 2. Reasons for referral to specialist services7 behaviour associated with dementia)
• Unsure of diagnosis • Commonwealth Respite and Carelink Centres:
• Patient is young or atypical 1800 200 422
• Symptoms and signs are atypical • Alzheimer’s Australia: www.fightdementia.org.au
(information and support for patients and carers. Tools
• Psychotic or severe behavioural disturbance occur for dementia assessment, such as RUDAS, in people
• Multiple, complex comorbidities exist from a non-English speaking background)
• Considering anti-dementia medication • GPCOG assessment tools: www.gpcog.com.au
Dementia - an update on management FOCUS
Author
Dimity Pond MBBS, FRACGP, PhD, is Professor of General Practice,
Discipline of General Practice, School of Medicine and Public Health,
Faculty of Health, University of Newcastle, Callaghan, New South
Wales. dimity.pond@newcastle.edu.au.
Conflict of interest: Dimity Pond has received NHMRC grant funding

and payment from Pfizer, Novartis, Janssen and Lundbeck (Board
membership) and Pfizer (consultancy).
References
1. Access Economics. Caring places: planning for aged care and demen
tia 2011-2050. Available at http://203.89.197.244/common/files/
NAT/20111014_Nat_Access_DemAcrossAust.pdf [Accessed 30 July 2012].
2. Access Economics. Keeping dementia in front of mind: incidence and
prevalence 2009-2050. Available at http://apo.org.au/research/keeping-
dementia-front-mind-incidence-and-prevalence-2009-2050 [Accessed 30
July 2012].
3. Farrow M. Dementia risk reduction: a practical guide for general practition
ers. Available at www.dementia.unsw.edu.au/images/dcrc/pdf/drrgps.pdf
[Accessed 30 July 2012].
4. 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;24:683-8.
5. Phillips J, Pond D, Goode S. Timely diagnosis of dementia: can we do
better? Available at www.fightdementia.org.au/common/files/NAT/
Timely_Diagnosis_Can_we_do_better.pdf [Accessed 30 July 2012].
6. Mate KE, Pond DC, Magin PJ, Goode SM, McElduff P, Stocks NP. Diagnosis
and disclosure of a memory problem is associated with quality of life
in community based older Australians with dementia. International
Psychogeriatrics 2012. doi:10.1017/S1041610212001111.
7. Brodaty H. Fourteen essentials for good dementia care in general practice.
Available at www.dementia.unsw.edu.au/images/dcrc/pdf/14essentials.
pdf [Accessed 30 July 2012].
8. Boustani M, Petersen B, Hanson L, Harris R, Lohr KN. Screening for
dementia in primary care: a summary of the evidence for the US Preventive
Services Task Force. Ann Int Med 2003;38:927-37.
9. Woodward M. Deprescribing: achieving better outcomes for older people
through reducing medications. Available at http://jppr.shpa.org.au/lib/pdf/
gt/Dec2003.pdf [Accessed 30 July 2012].
10. McShane R, Areosa Sastre A, Minakaran N. Memantine for dementia.
Cochrane Database Syst Rev 2006; Issue 2. Art. No.: CD003154. DOI:
10.1002/14651858.CD003154.pub5.
11. Birks J, Harvey RJ. Donepezil for dementia due to Alzheimer’s disease.
Cochrane Database Syst Rev 2006; Issue 1. Art. No.: CD001190. DOI:
10.1002/14651858.CD001190.pub2.
12. Dementia Outcome Measurement Suite. Function assessment measures.
Available at www.dementia-assessment.com.au/function/index.html
13. The Royal Australian College of General Practitioners. Advance care plans.
Available at www.racgp.org.au/guidelines/advancecareplans [Accessed 31
July 2012].
14. Pond D, Brodaty H. Diagnosis and management of dementia in general
practice. Aust Fam Physician 2004;33:789-93.
15. Dementia Outcome Measurement Suite. Cognition assessment measures.
Available at www.dementia-assessment.com.au/cognitive/index.html
CLINICAL
Prostatitis
Diagnosis and treatment
Gretchen Dickson
gland following intraprostatic reflux of urine

Prostatitis is a spectrum of disorders that impacts a significant number of men. infected with organisms such as Escherichia coli,
Acute bacterial prostatitis may be a life-threatening event requiring prompt
Enterococcus and Proteus species.5,6 Men with
recognition and treatment with antibiotic therapy. Chronic bacterial prostatitis has
chronic indwelling catheters, diabetes mellitus,
a more indolent course and also requires antibiotic therapy for resolution. Chronic
immunosuppression, or who intermittently
prostatitis/chronic pelvic pain syndrome is the most common manifestation of
perform self-catheterisation, are at higher risk
prostatitis and may be the most difficult to treat. Asymptomatic inflammatory
prostatitis is an incidental finding of unclear significance. Understanding the of developing ABP due to their increased risk of
diagnostic and management strategies for each of these entities is critical for bacterial colonisation of the urethra.6,7 There is
general practitioners in caring for their male patients. no evidence that perineal trauma from bicycle or
horseback riding, dehydration or sexual abstinence
Keywords
are risk factors for ABP
prostatitis; bacterial infections; pelvic pain
The clinical presentation of ABP may be highly
variable with symptoms ranging from mild to
severe.6 Classic symptoms include:
Up to 8% of Australian men report having • fever
urogenital pain at any given time, with • chills
15% of men suffering from symptoms • perineal or lower abdominal pain
of prostatitis at some point during their • dysuria
lives.1,2 In addition to causing impaired • urinary frequency
quality of life, men who have a history of • urinary urgency
prostatitis have increased rates of benign • painful ejaculation
prostatic hyperplasia, lower urinary tract • hematospermia8
symptoms and prostate cancer.1,3 Acute bacterial prostatitis should be considered in
the differential diagnosis of any male presenting
Prostatitis encompasses four distinct clinical with urinary tract symptoms. While gentle
entities, which can be described using the National palpation of the prostate gland on physical
Institutes of Health International Prostatitis examination will often reveal a pathognomonic
Collaborative Network classification system. The finding of an exquisitely tender, boggy prostate
four categories of prostatitis are: gland, care should be taken to avoid vigorous
• acute bacterial prostatitis prostate massage as this may precipitate
• chronic bacterial prostatitis bacteremia and sepsis.9
• chronic prostatitis/chronic pelvic pain syndrome Acute bacterial prostatitis can be diagnosed
- inflammatory subtype clinically, although both urine Gram stain and
- non-inflammatory subtype urine culture are recommended to identify
• asymptomatic inflammatory prostatitis.4 causative organisms and guide treatment. While
blood cultures and C-reactive protein may prove
Acute bacterial prostatitis useful, a prostate specific antigen (PSA) test is not
Acute bacterial prostatitis (ABP) accounts indicated. Prostate specific antigen elevations are
for approximately 5% of cases of prostatitis common in the setting of infection and may take
cases.1 Although rare, ABP requires prompt up to 1 month postinfection to resolve. Imaging
recognition and treatment as it may result in is only indicated when prostatic abscess is
sepsis. Acute bacterial prostatitis results from suspected in a patient with ABP who is failing to
proliferation of bacteria within the prostate improve with treatment.
Prostatitis - diagnosis and treatment CLINICAL
Antibiotic therapy for ABP should be based

Table 1. Treatment of acute and chronic bacterial prostatitis40
on the acuity of the patient and the known or
suspected causative organism. Table 1 outlines Acute bacterial Mild or moderate disease while awaiting culture
the Australian Therapeutic Guidelines current prostatitis • Trimethoprim 300 mg orally daily for 14 days, or
treatment recommendations. While ABP is • Cephalexin 500 mg orally twice daily for 14 days, or
usually caused by urinary pathogens, sexually • Amoxicillin and clavulanic acid 500 mg + 125 mg orally twice
transmissible infections such as chlamydia and daily for 14 days
gonorrhoea should be considered, particularly Appears septic or unable to tolerate oral therapy
in young men. If chlamydia is thought to be • Admit to hospital, offer parenteral therapy with ampicillin
and gentamycin or ceftriaxone as per severe pyelonephritis
the causative agent, azithromycin 1 g orally
treatment
stat or doxycycline 100 mg orally twice daily
for 7 days is appropriate. If gonorrhoea is Chronic bacterial First line treatment
suspected, ceftriaxone 500 mg intramuscularly prostatitis • Norfloxacin 400 mg orally every 12 hours for 4 weeks, or
and azithromycin 1 g orally is indicated. Contact • Trimethoprim 300 mg orally daily for 4 weeks
tracing, notification and treatment is also If chlamydia or ureaplasma noted
important in these cases. • Doxycycline 100 mg orally every 12 hours for 2-4 weeks
In addition to antibiotic therapy, non-steroidal
anti-inflammatory drugs (NSAIDs) may offer spread of rectal bacteria, hematogenous spread of both the right and left sides of the prostate gland.
both analgesia and more rapid healing through bacteria from a remote source, undertreated acute More than 20 leucocytes per high powered field
liquefaction of prostatic secretions.6 bacterial prostatitis or recurrent urinary tract on the post-massage urine sample is diagnostic
Urine culture 48 hours post-treatment is infection with prostatic reflux. Causative agents of CBP.19 If urine cultures show no growth,
useful combined with review after 7 days of of CBP are similar to those of ABP include Gram consider a nucleic acid test for C. trachomatis
antibiotic treatment to assess clinical response to negative rods, fungi, mycobacterium, Ureaplasma and culture of prostatic fluid for ureaplasmas.
treatment. urealyticum, Chlamydia trachomatis14 and Occasionally, Mycoplasma genitalium is found in
If the patient fails to improve with antibiotics, Trichomonas vaginalis.15 However, Escherichia prostatic secretions, although its role in prostatitis
a prostatic abscess should be suspected, coli is believed to be the causative organism in is unclear. If these tests are also negative, an
particularly in men who are immunocompromised, 75-80% of CBP cases.14 alternative diagnosis should be considered.
have diabetes mellitus or who have had recent Recognising CBP can be difficult, as the Limited comparative trials exist to guide
instrumentation of the urinary tract.10 Both history and examination are highly variable. All antibiotic regimens for CBP. Table 1 lists current
computed tomography (CT) and transrectal patients note some degree of genitourinary pain recommendations. Patients should be warned
ultrasound may be used to detect a prostate or discomfort. Common presentations include about the common side effects of extended
abscess.11 If perineal puncture of the abscess is recurrent urinary tract infections with no history duration of antibiotic use, such as Achilles tendon
planned, ultrasound may guide the procedure.12 of bladder instrumentation, dysuria and frequency rupture with fluoroquinolones.
However, if surgical debridement of the abscess is with no other signs of ABP or new onset sexual In addition to antibiotics, NSAIDs may
planned, a CT scan may be more helpful to define dysfunction without other aetiology.16,17 alleviate pain symptoms. Alpha-blockers may
borders of the abscess, plan the surgical approach Often the physical examination, including diminish urinary obstruction and reduce future
and to investigate for other abnormalities in the prostate examination, is normal. Prostate occurrences.20 Although less well studied, saw
genitourinary system.12 examination should be performed to document palmetto, quercetin, daily sitz baths, perianal
Acute urinary retention may develop as a any abnormalities such as prostatic calculi, which massage and frequent ejaculation may also
complication of ABP. Suprapubic tap should can serve as a reservoir of infection. Prostate help to clear prostatic secretions and lessen
be performed to alleviate retention as urethral stones may be difficult to palpate, but if found, discomfort. If prostatic stones are present,
catheterisation may worsen infection and is may impact management decisions. prostatectomy may eliminate the nidus of
contraindicated. In addition to acute urinary Although the Meares-Stamey four glass infection.
retention and prostatic abscess, ABP can lead test is the gold standard to diagnose CBP, it is
to sepsis, chronic bacterial prostatitis, fistula rarely used in practice due to time constraints Chronic prostatitis/chronic
formation or spread of infection to the spine or and the difficulty obtaining samples.18 Instead pelvic pain syndrome
sacroiliac joints.6,13 pre- and post-prostatic massage urine samples Chronic prostatitis/chronic pelvic pain syndrome
for analysis and culture may be useful and can (CP/CPPS) is more common than either acute
Chronic bacterial prostatitis guide antibiotic therapy.19 A prostate massage bacterial or chronic bacterial prostatitis.4 Up to
Chronic bacterial prostatitis (CBP) may result is performed by stroking the prostate with firm 18% of Australian men may experience some
from ascending urethral infection, lymphogenous pressure from the periphery to the midline on type of urogenital pain within a 12 month period,
CLINICAL Prostatitis - diagnosis and treatment
2010;105:373-9.
while up to 2% of Australian men may have Additional studies are needed to determine
2. Krieger JN. Classification, epidemiology and impli
prostatitis-like symptoms at any given time.1,21 the role of 5 alpha-reductase inhibitors, cations of chronic prostatitis in North America,
Unlike bacterial prostatitis where a causative glycosaminoglycans, saw palmetto, acupuncture, Europe and Asia. Minerva Urol Nefrol 2004;56:99-
107.
organism can be identified, the aetiology of CP/ physical therapy, and pelvic floor training using
3. Krieger JN, Lee SW, Jeon J, Cheah PY, Liong
CPPS is poorly understood; both inflammatory biofeedback as part of treatment.17,35 ML, Riley DE. Epidemiology of prostatitis. Int J
and infectious mechanisms have been Other treatments that have proven useful in Antimicrob Agents 2008;31(Suppl 1):S85-90.
4. Krieger JN, Nyberg L, Nickel JC. NIH Consensus
postulated.17,22,23 Psychological stress may be a small studies for targeted symptoms include:
definition and classification of prostatitis. JAMA
major contributor to symptom severity.24 Some phosphodiesterase five inhibitors for sexual 1999;282:236-7.
evidence exists of an association between irritable dysfunction,36 cernilton or pollen extract for 5. Cornia PB, Takahashi TA, Lipsky BA. The micro
biology of bacteriuria in men: a 5-year study at a
bowel syndrome, chronic fatigue syndrome urinary symptoms,37 quercetin (500 mg orally veterans affairs hospital. Diagn Microbiol Infect Dis
and fibromyalgia with CP/CPPS, although twice daily for 30 days) for pelvic floor muscle 2006;56:25-30.
6. Brede CM, Shoskes DA. The etiology and
little correlation exists between the amount of spasm,38 and fluoxetine (20 mg orally daily)
management of acute prostatitis. Nat Rev Urol
inflammatory markers detected within the prostate for depression and improved quality of life.39 2011;8:207-12.
gland itself and the degree of symptoms.25,26 Transurethral microwave therapy may be used 7. Wyndaele JJ. Complications of intermittent cath
eterization: their prevention and treatment. Spinal
Symptoms of CP/CPPS can vary widely and as a last resort for men who have failed other
Cord 2002;40:53-41.
include dysuria; urinary frequency; urinary urgency; interventions.17 8. Krieger JN, Egan KJ, Ross SO. Chronic pelvic pains
weak urinary stream; pain in the perineum, lower represent the most prominent urogenital symptoms
abdomen, testicles or penis; hematospermia or Asymptomatic inflammatory of chronic prostatitis. Urology 1996;48:715-21.
9. Nickel JC. Inflammatory conditions of the male
difficulty achieving erection.27,28 Diagnosis requires prostatitis genitourinary tract: prostatitis and related condi
the patient to have had pelvic pain or urinary Asymptomatic inflammatory prostatitis is, by tions, orchitis, and epididymitis. In: Wein AJ,
Kavoussi LR, Novick AC, Partin AW, Peters CA, eds.
symptoms for more than three of the previous definition, asymptomatic. It is often diagnosed
Campbell-Walsh Urology. 9th edn. Philadelphia, Pa.:
6 months with no evidence of ABP or urinary tract incidentally during the evaluation of infertility Saunders, 2007;304-29.
infection in that time.17 or prostate cancer.17 The clinical significance of 10. Tiwari P, Pal D, Tripathi A, et al. Prostatic abscess:
diagnosis and management in the modern antibiotic
Chronic prostatitis/chronic pelvic pain category IV prostatitis is unknown, and is often
era. Saudi J Kidney Dis Transpl 2011;22:298-301.
syndrome is a diagnosis of exclusion and left untreated.17 11. Horcajada JP, Vilana R, Moreno-Martinez A.
laboratory or imaging studies are indicated to rule Transrectal prostatic ultrasonography in acute bac
out other potential causes of symptoms. Elevated Summary terial prostatitis: findings and clinical implications.
Scand J Infect Dis 2003;35:114-20.
PSA should not be attributed to CP/CPPS and A diagnosis of prostatitis encompasses a 12. Schull A, Monzani Q, Boni L, et al. Imaging in
warrants further investigation.29 spectrum of disease: acute bacterial prostatitis, lower urinary tract infections. Diagn Interv Imaging
2012;93:500-8.
Approximately 60% of men affected by CP/ chronic bacterial prostatitis, chronic prostatitis/ 13. Siroky MB, Moylan R, Austen G, Olsson CA.
CPPS will seek treatment for their symptoms.30 chronic pelvic pain syndrome and asymptomatic Metastatic infection secondary to genitourinary
tract sepsis. Am J Med 1976;61:351-60.
Although various treatments have been studied, prostatitis have varying clinical significance,
14. Schaeffer AJ. Clinical practice: chronic prostatitis
methodological problems including lack of causative agents, treatment strategies and long and the chronic pelvic pain syndrome. N Engl J Med
randomisation and small sample size limit the term prognosis. 2006;355:1690-8.
15. Skerk V, Krhen I, Schonwald S, Cajic V, et al. The
ability to apply research findings to the clinical Limited research exists to guide the diagnosis
role of unusual pathogens in prostatitis syndrome.
treatment of CP/CPPS. With the current evidence and management of these entities, making Int J Antimicrob Agents 2004;24(Suppl 1):S53-6.
available, tailoring treatment to individual patient prostatitis a challenging condition to manage. 16. Muller A, Mulhall JP Sexual dysfunction in
the patient with prostatitis. Curr Opin Urol
symptom complexes may be more beneficial than
Author 2005;15:404-9.
attempting to use one treatment as a curative Gretchen Dickson MD, MBA, is Assistant 17. Murphy AB, Macejko A, Taylor A, Nadler RB.
agent in all individuals.31 The National Institute Professor, Department of Family and Community Chronic prostatitis: management strategies. Drugs
2009;69:71-84.
of Health Chronic Prostatitis Symptom Index (NIH- Medicine, University of Kansas School of
18. McNaughton Collins M, Fowler FJ, Elliott DB.
CPSI) provides a validated indicator of disease Medicine, Wichita, Kansas, United States of Diagnosing and treating chronic prostatitis:
America. gdickson@kumc.edu. do urologists use the four glass test? Urology
severity that can be monitored over time to
Competing interests: None. 2000;55:403-7.
determine if a particular treatment is improving a 19. Nickel JC, Shoskes D, Wang Y, et al. How does
patient’s symptoms or overall quality of life.32 Provenance and peer review: Not commissioned; the pre-massage and post-massage 2-glass test
Of the treatments that have been studied, externally peer reviewed. compare to the Meares-Stamey 4-glass test in men
with chronic prostatitis/chronic pelvic pain syn
alpha-adrenergic receptor blockers and antibiotics
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22. Leskinen MJ, Rantakokko-Jalava K, Manninen R, W. Pollen extract for chronic prostatitis-chronic
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with symptoms of chronic pelvic pain syndrome 38. Shoskes DA, Nickel JC. Quercetin for chronic pros-
(CPPS) and localized prostate cancer. Prostate tatitis/chronic pelvic pain syndrome. Urol Clin North
2003;55:105-10. Am 2011;38:279-84.
23. Lee JC, Muller CH, Rothman I, et al. Prostate biopsy 39. Xia D, Wang P, Chen J, Wang S, Jiang H. Fluoxetine
culture findings of men with chronic pelvic pain ameliorates symptoms of refractory chronic pros-
syndrome do not differ from those of healthy con tatitis/chronic pelvic pain syndrome. Chin Med J
trols. J Urol 2003;169:584-7. (Engl) 2011;124:2158-61.
24. Anderson RU, Orenberg EK, Morey A, Chavez 40. Prostatitis. In: eTG Complete. Melbourne:
N, Chan CA. Stress induced hypothalamus Therapeutic Guidelines Limited, 2012 July.
pituitary-adrenal axis responses and disturbances Available at http://online.tg.org.au/complete/
in psychological profiles in men with chronic [Accessed 24 September 2012].
prostatitis/chronic pelvic pain syndrome. J Urol

2009;182:2319-24.
25. Nickel JC, Roehrborn CG, O’leary MP, Bostwick DG,
Somerville M, Rittmaster RS. Examination of the
relationship between symptoms of prostatitis and
histological inflammation: Baseline data from the
REDUCE chemoprevention trial. J Urol 2007;178(3
Pt 1):896-900.
26. Rodriguez MA, Afari N, Buchwald DS. National
institute of Diabetes and Digestive and Kidney
Disease Working Group on urological chronic pelvic
pain. Evidence for overlap between urological and
nonurological unexplained clinical conditions. J
Urol 2009;182:2123-31.
27. Trinchieri A, Magri V, Cariani L, et al. Prevalence of
sexual dysfunction in men with chronic prostatitis/
chronic pelvic pain syndrome. Arch Ital Urol Androl
2007;79:67-70.
28. Krieger JN, Ross SO, Penson DF, Riley DE.
Symptoms and inflammation in chronic pros-
tatitis/chronic pelvic pain syndrome. Urology
2002;60:959-63.
29. Nickel JC. Clinical evaluation of the man with
chronic prostatitis/chronic pelvic pain syndrome.
Urology 2002;60(6 Suppl):20-2.
30. Nickel JC, Downey J, Hunter D, Clark J. Prevalence
of prostatitis like symptoms in a population
based study using the National Institutes of
Health Chronic prostatitis symptoms index. J Urol
2001;165:842-5.
31. Nickel JC, Shoskes DA. Phenotypic approach to
the management of the chronic prostatitis/chronic
pelvic pain syndrome. BJU Int 2010;106:1252-63.
32. Nickel JC, Alexander RB, Anderson R, et al.
Chronic Prostatitis Collaborative Research Network
Study Groups. Category III chronic prostatitis/
chronic pelvic pain syndrome: insights from the
National Institutes of Health Chronic Prostatitis
Collaborative Research Network studies. Curr Urol
Rep 2008;9:320-7.
33. Anothaisintawee T, Attia J, Nickel JC, et al.
Management of chronic prostatitis/chronic pelvic
pain syndrome: a systematic review and network
meta-analysis. JAMA 2011;305:78-86.
34. Cheah PY, Liong ML, Yuen KH, et al. Terazosin
therapy for chronic prostatitis/chronic pelvic pain
syndrome: a randomized, placebo controlled trial. J
Urol 2003;169:592-6.
35. Schiller DS, Parikh A. Identification, pharmacologic
considerations and management of prostatitis. Am
J Geriatr Pharmacother 2011;9:37-48.
36. Shoskes DA. The challenge of erectile dysfunction correspondence afp@racgp.org.au
focus The right upper quadrant : »
Fatty liver disease

A practical guide for GPs
David Iser
Marno Ryan
Background First described in 1980,1 non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD), encompassing both (NAFLD) is now the most common cause of liver disease in
simple steatosis and non-alcoholic steato-hepatitis (NASH), is the industrialised countries.2 Non-alcoholic fatty liver disease
most common cause of liver disease in Australia. Non-alcoholic includes both non-alcoholic steato-hepatitis (NASH), involving
fatty liver disease needs to be considered in the context of the lobular inflammation and fibrosis, and simple steatosis (non
metabolic syndrome, as cardiovascular disease will account for
NASH). This distinction is important, as simple steatosis
much of the mortality associated with NAFLD.
is unlikely to lead to liver related complications, whereas
Objective NASH may lead to increased fibrosis and cirrhosis, and its
To provide an approach to the identification of NAFLD in general complications (Figure 1). The difficulty lies in trying to decide
practice, the distinction between simple steatosis and NASH, whether raised liver functions tests (LFTs) are due to simple
and the management of these two conditions. steatosis, NASH without fibrosis, NASH with severe fibrosis
Discussion or cirrhosis, or another cause of hepatitis altogether.
Non-alcoholic steato-hepatitis is more common in the presence
of diabetes, obesity, older age and increased inflammation, and is Epidemiology
more likely to progress to cirrhosis. Cirrhosis may be complicated The prevalence of NAFLD is estimated to be approximately 30% of
by hepatocellular carcinoma or liver failure. Hepatocellular adults in developed countries such as Australia and the United States,
carcinoma has also been described in NASH without cirrhosis. depending on definition and detection methods.3 However, NAFLD
Assessment and treatment of features of the metabolic syndrome
is also becoming increasingly common in Asia (countries previously
may reduce associated cardiovascular mortality. Numerous
thought to be at low risk of NAFLD), where a prevalence of up to 15%
agents have been evaluated, but weight loss remains the only
has been reported in China.4
effective treatment for NAFLD.
Keywords Natural history
liver diseases; fatty liver
Simple steatosis appears to be a relatively benign condition, although
S£3 O it may progress to NASH over time. Cardiovascular disease is the major
cause of death in patients with NAFLD;5 NAFLD alone is associated with
a slightly higher overall mortality. However, when NAFLD occurs in the
presence of other features of the metabolic syndrome (MetSy), mortality
doubles.6 The MetSy is a clustering of cardiovascular risk factors related to
reduced insulin sensitivity. Diagnostic criteria for the syndrome include:7
• elevated serum triglycerides (TG)
• lowered serum high-density lipoprotein cholesterol (HDL-C)
• impaired glucose tolerance
• central adiposity
• hypertension.
Although NAFLD is not officially included in the definition of the MetSy,
it commonly co-exists with features of this syndrome.
In addition to its association with cardiovascular complications,
NAFLD can lead to liver related morbidity and mortality. The risk of
developing cirrhosis is higher in the presence of NASH, which is more
likely in the presence of the following features:
• type 2 diabetes mellitus (T2DM)
• obesity (body mass index [BMI] >30 kg/m2)
need to be excluded, such as viral hepatitis, autoimmune hepatitis,
haemochromatosis, thyroid disease and coeliac disease (Table 1).
Diagnostic assessment of NAFLD

A definitive diagnosis of NAFLD depends on three factors:
• evidence of fatty infiltration from either imaging (ultrasound,
magnetic resonance imaging [MRI]) or histology (liver biopsy)
• exclusion of significant alcohol consumption
• exclusion of other causes of hepatic steatosis (eg. medications,
surgery, metabolic disorders).
Confirming hepatic fatty infiltration using ultrasound is important.
Specificity is high (95%), but the sensitivity of ultrasound for detecting
fatty infiltration is lower (85%).14 Ultrasound is also useful to look for
signs of cirrhosis, such as irregular liver edge, but has a sensitivity
of only 43-74% (specificity is slightly higher at 54-89%).15 Signs
of cirrhotic complications are also important, eg. signs of portal
hypertension (splenomegaly, increased portal vein size, varices) or
other complications such as HCC, portal vein thrombosis, or ascites.
Cardiovascular Decompensation Hepatocellular The risk of fibrosis and progressive liver disease in NAFLD
disease or liver failure carcinoma increases with severity of insulin resistance. In the absence of simple
available clinical measurements of insulin resistance, the number
Figure 1. The natural history of non-alcoholic fatty liver disease of MetSy features present can be used to estimate risk of insulin
resistance. The presence of three or more features of the syndrome,
• age more than 50 years especially if these include central adiposity and T2DM, are predictive
• serum aminotransferases (ALT or AST) more than two times the of the presence of NASH rather than simple steatosis. In addition,
upper limit of normal. family history plays a role: an individual with a first degree relative
Non-alcoholic steato-hepatitis cirrhosis probably accounts for the vast with T2DM has a 90% chance of developing T2DM, and therefore
majority of what was previously described as ‘cryptogenic cirrhosis’. In NASH.16 Central adiposity can be assessed using waist circumference
one series, 70% of patients with cryptogenic cirrhosis had risk factors measured at the narrowest point mid-way between the lowest rib and
for NAFLD.8 In the US, NASH is an increasingly common indication for the iliac crest at the end of expiration with the patient standing.
liver transplantation.9,10 In the setting of cirrhosis from NASH, the risk Staging liver disease and detecting cirrhosis is the most important
of developing hepatocellular carcinoma (HCC) is between 2.4% over aspect of assessing fatty liver disease. However, it is also difficult and
7 years, and 12.8% over 3 years,11 compared to 21% over 10 years error prone. The traditional gold standard in assessing liver disease is
for hepatitis C cirrhosis.12 Hepatocellular carcinoma has also been liver biopsy. However, biopsy has unfavourable cost, safety, availability,
reported in NASH without cirrhosis, particularly in association with sampling error, inter-observer variability and patient acceptance. Liver
the MetSy.13 biopsy may be considered where cirrhosis is suspected, or where
an alternative diagnosis is considered. At this stage, referral to a
Identifying NAFLD and NASH in gastroenterologist is also suggested.
general practice Non-invasive tools for estimating the degree of fibrosis include
The most common presentation of NAFLD will be incidental finding of transient elastography (FibroScan®), acoustic radiation force impulse
abnormal LFTs. Typical findings in NAFLD are raised ALT and AST, with (ARFI), and non-invasive biomarker algorithms such as NAFLD Fibrosis
a preserved ALT: AST ratio of 1.5, raised gamma glutamyl transferase Score, FibroTest and Hepascore. However, their use in clinical practice
(GGT) and, occasionally, raised alkaline phosphatase (ALP). These is still being evaluated.
findings commonly occur in the setting of features of the MetSy.
There are several features on examination and laboratory values Management of NAFLD
that should raise suspicion of cirrhosis, such as spider naevi, low
Cardiovascular risk factors and lifestyle
or falling platelets, low albumin or reversal in ALT:AST ratio (where modification
AST exceeds ALT), before the features of portal hypertension and
decompensation become obvious. The cornerstone to managing NAFLD is achieving weight control and
Apart from excluding excess alcohol consumption as a potential reduction in cardiovascular risk factors such as smoking, diabetes,
cause, there are several other important causes of raised ALT that hypertension and dyslipidaemia. This may include referral to a dietician,
FOCUS Fatty liver disease - a practical guide for GPs
Table 1. What to consider and how to exclude differential diagnoses

Consideration Test
Excess alcohol consumption Careful, corroborative history
Chronic hepatitis B HBsAg, anti-HBs, anti-HBc
Chronic hepatitis C Hepatitis C antibody
Autoimmune hepatitis Anti-nuclear antibody (ANA)
Anti-smooth-muscle antibody (ASMA)
Anti-mitochondrial antibody (AMA)
Haemochromatosis Iron studies
Thyroid disease Thyroid function tests
Coeliac disease Coeliac antibodies (usually deamidated antigliadin antibody, tissue transglutaminase,
total lgA level)
Medications History of amiodarone, anticonvulsants, methotrexate, tamoxifen, synthetic oestrogens,
corticosteroids, HIV therapy, perhexiline
endocrinologist or cardiologist. Treatment of associated dyslipidaemia

is appropriate with either HMgCo-A reductase inhibitors (‘statins’) or
fibrates where required. Moderate elevations in liver enzymes due
to the use of statins should be tolerated and treatment continued.17
However, severe elevations more than 10 times the upper limit of
normal should prompt cessation of the medication and reassessment.
Dietary manipulation, such as the adoption of a Mediterranean
type diet, has shown promise. The most important feature appears
to be caloric reduction. Where diet and exercise are unsuccessful in
achieving weight reduction, bariatric surgery may be considered.
Novel treatments
Various therapeutic agents have shown some promise in the
management of NAFLD.18-22 However, weight loss remains the only
therapy with proven benefit and safety.23-27
What follow up should be performed?

A pragmatic approach to the investigation and management of NAFLD
is presented in Figure 2.28 Normalisation of LFTs associated with mild
weight loss may be an encouraging sign that the disease activity is
driven by NAFLD. However, it is important to stage the disease initially
(with ultrasound and histology if appropriate). The presence of normal
LFTs does not exclude underlying cirrhosis, nor does a ‘non-cirrhotic’
ultrasound. Monitoring full blood examination (FBE), LFTs, International
Normalised Ratio (INR), blood pressure and lipid profile every 6 months
is a reasonable approach.
Figure 2. Algorithm for management of suspected NAFLD
When to refer for specialist management
Referral for specialist management should be undertaken whenever • NAFLD should be considered when abnormal LFTs are found,
there is a suspicion of severe fibrosis or cirrhosis, whether at initial particularly in the presence of features of the MetSy.
assessment or at any time during monitoring. • Weight reduction via caloric restriction and regular exercise are
important, and no medications can currently be recommended as
Key points specific therapy.
• Non-alcoholic fatty liver disease is increasingly common, and will • General practitioners are vital in identifying patients at risk of
have a significant impact on morbidity and mortality on a growing NAFLD, and encouraging initiation and maintenance of appropriate
number of Australians. lifestyle changes.
Fatty liver disease - a practical guide for GPs FOCUS
Further reading 10. Afzali A, Berry K, Ioannou GN. Excellent posttransplant survival for patients with
nonalcoholic steatohepatitis in the United States. Liver Transpl 2011;18:29-37.
• The diagnosis and management of NAFLD: Practice guideline by 11. White DL, Kanwal F, El-Serag HB. Association between nonalcoholic fatty liver
the American Association for the Study of Liver Diseases, American disease and risk for hepatocellular cancer, based on systematic review. Clin
Gastroenterol Hepatol 2012;10:1342.
College of Gastroenterology and the American Gastroenterological
12. van der Meer AJ, Veldt BJ, Feld JJ, et al. Association between sustained virologi-
Association. Available at www.aasld.org/practiceguidelines/ cal response and all-cause mortality among patients with chronic hepatitis C and
Documents/NonalcoholicFattyLiverDisease2012_25762_ftp.pdf advanced hepatitis fibrosis. JAMA 2012;308:2584-93.
13. Ertle J, Dechene A, Sowa JP, et al. Non-alcoholic fatty liver disease progresses
• Farrell GC, Chitturi S, Lau GK, et al. Guidelines for the assessment
to hepatocellular carcinoma in the absence of apparent cirrhosis. Int J Cancer
and management of NAFLD in the Asia Pacific region: Executive 2011;128:2436-43.
summary. J Gastroenterol Hepatol 2007;22:775-7. Available at 14. Hemaez R, Lazo M, Bonekamp S, et al. Diagnostic accuracy and reliability of
ultrasonography for the detection of fatty liver: a meta-analysis. Hepatology
www.medscape.com/viewarticle/559335_1 2011;54:1082-90.
• Farrell GC, editor. Fatty liver disease: When to suspect it? What to 15. Choong CC, Venkatesh SK, Siew EP. Accuracy of routine clinical ultrasound for
staging of liver fibrosis. J Clin Imagin Sci 2012;2:58.
do about it? GESA guidelines. Available at www.gesa.org.au/files/
16. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepati-
editor_upload/File/Professional/Fatty-Liver-1st-Edition.pdf tis, and the metabolic syndrome. Hepatology 2003;37:917-23.
• Ratziu V, Bellentini S, Cortez-Pinto H, et al. A position statement 17. Athyros VG, Tziomalos K, Gossios TD, et al. Safety and efficacy of long-term
statin treatment for cardiovascular events in patients with coronary heart disease
on NAFLD/NASH based on the EASL 2009 special conference. J
and abnormal liver tests in the Greek Atorvastatin and Coronary Heart Disease
Hepatol 2010;53:372-84. Available at http://f.i-md.com/medinfo/ Evaluation (GREACE) Study: a post-hoc analysis. Lancet 2010;376:1916.
18. Rakoski MO, Singal AG, Rogers MA, Conjeevaram H. Meta-analysis: insulin sensi
material/714/4e113707e4b02d0c1e8d2714/494B559E82E5F1F07D8
tizers for the treatment of non-alcoholic steatohepatitis. Aliment Pharmacol Ther
015701B2ABFC6.pdf 2010;32:1211-21.
• World Gastroenterology Global Guidelines: NAFLD and NASH. 19. Boettcher E, Csasko G, Pucino F, et al. Meta-analysis: pioglitazone improves liver
histology and fibrosis in patients with non-alcoholic steatohepatitis. Aliment
Available at www.worldgastroenterology.org/assets/export/
Pharmacol Ther 2012;35:66.
userfiles/2012_NASH%20and%20NAFLD_Final_long.pdf. 20. Musso G, Gambino R, Cassader M, Pagano G. A meta-analysis of randomized
trials for the treatment of nonalcoholic fatty liver disease. Hepatology 2010;52:79.
Authors 21. Zein CO, Yerian LM, Gogate P, et al. Pentoxifylline improves nonalcoholic steato-
David Iser MBBS(Hons), BMedSc, FRACP, PhD, is a gastroenterologist, hepatitis: a randomized placebo-controlled trial. Hepatology 2011;54:1610.
Department of Gastroenterology, St Vincent’s Hospital, Melbourne and 22. Parker HM, Johnson NA, Burdon CA, et al. Omega-3 supplementation and non
Infectious Diseases Unit, The Alfred Hospital, Melbourne, Victoria. alcoholic fatty liver disease: a systematic review and meta-analysis. J Hepatol
2012;56:944.
david.iser@svhm.org.au
23. Dixon JB, Bhathal PS, Hughes NR, O’Brien PE. Nonalcoholic fatty liver disease:
Marno Ryan MBBS(Hons), FRACP, MD, is a gastroenterologist, Improvement in liver histological analysis with weight loss. Hepatology
Department of Gastroenterology, St Vincent’s Hospital, Melbourne, 2004;39:1647.
Victoria. 24. Hickman IJ, Jonsson JR, Prins JB, et al. Modest weight loss and physical activity
in overweight patients with chronic liver disease results in sustained improve
Competing interests: None. ments in alanine aminotransferase, fasting insulin, and quality of life. Gut
2004;53:413.
Provenance and peer review: Commissioned; externally peer reviewed.
25. Promrat K, Kleiner DE, Niemeier HM, et al. Randomized controlled trial testing the
effects of weight loss on nonalcoholic steatohepatitis. Hepatology 2010;51:121.
References 26. Keating SE, Hackett DA, George J, Johnson NA. Exercise and non-alcoholic fatty
1. Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis:
liver disease: a systematic review and meta-analysis. J Hepatol 2012;57:157.
Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc
27. Chavez-Tapia NC, Tellez-Avila FI, Barrientos-Gutierrez T, et al. Bariatric surgery
1980;55:434-8.
for non-alcoholic steatohepatitis in obese patients. Cochrane Database Syst Rev
2. Younossi ZM, Stepanova M, Afendy M, et al. Changes in the prevalence of
2010;20:CD007340.
the most common causes of chronic liver disease in the United States from
28. Farrell G, et al. Fatty liver disease. GESA guidelines, 2007. Available at www.gesa.
1988 to 2008. Clin Gastroenterol Hepatol 2011;9:524-30.
org.au/files/editor_upload/File/Professional/Fatty-Liver-1st-Edition.pdf [Accessed
3. Browning JD, Szczepaniak LS, Dobbins R, et al. Prevalence of hepatic
7 June 2013].
steatosis in an urban population in the United States: impact of ethnicity.
Hepatology 2004;40:1387-95.
4. Fan JG, Zhu J, Li XJ, et al. Prevalence of and risk factors for fatty liver in a
general population of Shanghai, China. J Hepatol 2005;43:508-14.
5. Ong JP, Pitts A, Younossi ZM. Increased overall mortality and liver-related
mortality in non-alcoholic fatty liver disease. J Hepatol 2008;49:608-12.
6. Gami AS, Witt BJ, Howard DE, et al. Metabolic syndrome and risk of incident
cardiovascular events and death: a systematic review and meta-analysis of
longitudinal studies. J Am Coll Cardiol 2007;49:403.
7. The IDF consensus worldwide definition of the metabolic syndrome.
Available at www.idf.org/webdata/docs/MetS_def_update2006.pdf
[Accessed 16 February 2013].
8. Caldwell SH, Oelsner DH, Iezzoni JC, et al. Cryptogenic cirrhosis: clini
cal characterization and risk factors for underlying disease. Hepatology
1999;29:664.
9. Bugianesi E, Leone N, Vanni E, et al. Expanding the natural history of
nonalcoholic steatohepatitis: from cryptogenic cirrhosis to hepatocellular
carcinoma. Gastroenterology 2002;123:134-40. correspondence afp@racgp.org.au
CLINICAL
The bariatric surgery patient

Nutrition considerations
Caroline Shannon
Ashlee Gervasoni
Trudy Williams
procedures is beyond the scope of this article;

Background information is available online from The Obesity
Bariatric surgery is an effective method of weight loss for the treatment of morbid Surgery Society of Australia and New Zealand.10
obesity. It is more effective when combined with nutritional care, which is
The aim of this article is to explore the
sometimes complex, always ongoing and differs between surgical procedures. In
nutrition and dietary considerations for these
Australia, the three most common bariatric surgical procedures are the adjustable
three surgical procedures.
gastric banding, sleeve gastrectomy and the Roux-en-Y gastric bypass.
Objective Pre-operative assessment
This article introduces the nutritional and dietary considerations for each and advice
procedure, and provides practical advice to support the general practitioner’s role
in managing patients who are considering, or who have had, bariatric surgery. Baseline nutrition-related
Discussion
biochemistry
While bariatric procedures influence the volume of food consumed, none of the Between 35-80% of bariatric candidates are in
procedures necessarily improve the quality of food consumed or compliance a state of ‘high calorie malnutrition’ and show
with recommended supplement usage, leaving nutrition care and food choice
some dietary deficiency pre-operatively,7 with a
important lifelong considerations. Ongoing coordinated care by the GP, that links
reported prevalence of 60-80% for vitamin D,
with the bariatric dietitian and others in the health management team, maximises
24% for folate, 14.5% for selenium and up to 35%
the benefits and health outcomes for the patient through ongoing monitoring of
for iron.11-17 Nutrient-poor food choices, chronic
nutritional status, prevention of nutrient deficiencies and maximising long term
weight loss. dieting cycles, side effects of medications to treat
comorbidities and other factors contribute to this
Keywords state of ‘malnutrition’ masked by an ample energy
bariatrics, bariatric surgery; morbid obesity; nutrition therapy
intake. Therefore, regardless of the bariatric
procedure proposed, a comprehensive screening
is recommended, ideally in sufficient time to
correct deficiencies before surgery.3,15,18,19
Bariatric surgery is currently the most The screening tests and subsequent ongoing
effective and sustainable method of weight monitoring enable the practitioner to recognise
loss for the treatment of morbid obesity.1-3 and distinguish between pre-existing nutritional
Morbid obesity is defined as a body mass concerns and those due to post-operative
index (BMI) greater than 40 kg/m2.4 Bariatric complications, known deficiency risks linked to the
surgery is also recommended for people with specific procedure performed and non-compliance
comorbidities at a BMI of 35 kg/m2 or more.4 with recommended nutrient supplementation.
Table 1 summarises the suggested baseline pre
Morbid obesity reduces life expectancy by 5-20 operative biochemical markers and profiles for all
years.2,5-7 Bariatric surgery not only reduces bariatric surgery candidates, and other nutrients
body weight, it reduces (and sometimes resolves) ‘at risk’ related to medication usage or poor dietary
comorbidities, such as diabetes and obstructive quality. These investigations are in addition to a
sleep apnoea, and improves quality of life.6-8 In full blood count, lipid profile and diabetes markers.
Australia, the three most common bariatric surgical These nutrient marker investigations should be
procedures are the adjustable gastric band (AGB), repeated as depicted in Table 1, unless a higher
sleeve gastrectomy (SG), and the Roux-en-Y gastric frequency is indicated due to the presence of other
bypass (RYGB).9 Details about these surgical comorbidities.3
Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 8, AUGUST 2013 547
CLINICAL The bariatric surgery patient - nutrition considerations
Nutrition and dietary Table 1. Biochemical parameters and suggested monitoring frequency
assessment classified by type of surgical procedure3
To complement the medical nutrition screening, a
Nutrient Pre-operative Post-operative at 6 Annual
*
comprehensive pre-operative dietary assessment marker months
by a bariatric accredited practising dietitian (APD)
Iron studies AGB, SG, RYGB RYGB 6—12 months RYGB, and optional
identifies additional factors that potentially impact AGB, SG
AGB, SG optional at 6
on nutritional status pre and post surgery. These months
include dietary beliefs and behaviours, cultural
Vitamin B12 AGB, SG, RYGB At 3—6 months if AGB, SG, RYGB
background, psychosocial issues (motivation, non- (methylmalonic supplemented (AGB,
hungry eating), economic factors and goal setting.3 acid optional) SG, RYGB)
Folic acid AGB, SG, RYGB RYGB 6—12 months RYGB, and optional
Preparation for surgery (RBC folate, AGB, optional SG at 6 AGB, SG
For 2-4 weeks immediately before surgery, most homocystiene) months
patients are advised to follow a very low energy 25-vitamin D AGB, SG, RYGB Optional AGB, SG, RYGB
diet (VLED). Vitamin A AGB (optional), RYGB RYGB every 6—12
This protocol helps reduce liver volume by SG, RYGB months
up to 25%, which in turn reduces intra-operative Vitamin E AGB (optional), Optional Optional
complications.20 This typically includes three SG, RYGB
VLED meal replacements daily, and is further Zinc AGB (optional), Optional Optional
adjusted to suit each patient’s protein and nutrient SG, RYGB
requirements. Pre-operatively, the dietitian Thiamine AGB (optional), Persistent vomiting Persistent vomiting
advises about VLED product selection, addition SG, RYGB (SG, RYGB) (SG, RYGB)
of low carbohydrate-low joule foods, adequate Parathyroid Optional Optional Optional
hydration, stimulus control, fibre supplementation hormone
and any surgeon-specific requirements. A Magnesium — Optional Optional
medication review and patient assessment for Selenium — Optional RYGB
contraindications and suitability is required before Copper — — Optional persistent
starting the VLED protocol. The low carbohydrate unresolved problems
content of VLED protocols reduces blood glucose with iron levels
levels suddenly. To reduce risk of hypoglycaemia, * At least annually but more frequently if clinically indicated
an active management plan to adjust medication AGB = adjustable gastric band; SG = sleeve gastrectomy; RYGB = Roux-en-Y gastric
and monitor blood glucose is recommended. bypass
Post-operative nutrition care

Table 2. Common suggested texture progressions (classified by type of
The focus during the first 1-8 weeks post-
surgical procedure)
operatively is to maintain adequate hydration,
provide adequate nutrients and protein to support Texture Weeks after surgery for each texture
progression AGB SG RYGB
healing and minimise loss of lean muscle mass,
and progressively return to ‘normal’ food.3,15 Fluids Weeks 1-2 Weeks 1-2 Weeks 1-2
Puree Weeks 2-4 Weeks 2-4 Weeks 2-4
Texture progression Soft solids Weeks 3-4 Weeks 4-6 Weeks 4-6
After all bariatric procedures, a patient’s diet (optional phase)
transitions from liquids to puree/blended foods, Normal solids Weeks 4-5 Weeks 6-8 Weeks 6-8
and then back onto solids.3 The duration of each
transition phase depends on the procedure nutrient requirements match satiation within Eating style
performed and the patient’s tolerance. The the texture permitted. Nutrient supplements While bariatric procedures aim to influence
purpose of the texture progression in the case of and formulated specific food products may be the volume of food consumed, none of the
the SG and RYGB is to preserve the staple line required to ensure nutritional adequacy and procedures necessarily improve the quality
and enhance healing, and in all cases to prevent maintain muscle mass yet maximise fat loss. of food and drinks consumed, nor a patient’s
unnecessary gastrointestinal symptoms.15 Common progressions and durations at each dysfunctional eating and drinking style.
Each phase is designed by a dietitian to ensure phase are shown in Table 2. The different mechanisms of action of each
548 Reprinted from AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 8, AUGUST 2013
The bariatric surgery patient - nutrition considerations CLINICAL
procedure can also have a distinct influence on patient adjust to and establish new eating and Altered absorption or treatment of nutrients
specific eating behaviours.21-23 drinking behaviours.18 Table 4 provides a brief after RYGB and SG add to the potential for
The AGB creates a narrowing near the trouble-shooting guide to some of the more deficiencies.318,26
gastro-oesophageal junction to influence common dietary related complaints/adverse Adjustable gastric banding does not
solid volume consumed and promote early gastro-intestinal symptoms reported after bariatric impact on nutrient absorption or utilisation.
satiety. Specific eating behaviours (Table 3) surgery. These symptoms and common complaints Any nutritional aberrations that occur are due
help minimise problems such as regurgitation may appear early (weeks) or late (years). to dietary choice (food quality, tolerance and
and food blockages, which if left unmanaged, volume limits), drug-nutrient interactions, or
promote the consumption of inappropriate, less
Vitamin, mineral and trace other medical/aging causes.15,22 After AGB,
element monitoring and
satiating food textures.21 After SG and RYGB,
the reduced gastric volume combined with
supplementation a comprehensive multivitamin and mineral
supplement that satisfies the gender and age
hormonal changes, taste changes and, in the Lifelong vitamin and mineral supplementation is specific ‘nutrient reference values’ for the patient
case of SG, increased gastric emptying, influence recommended after all bariatric procedures.3,15,18,25 is recommended.3,15
eating style. Dysfunctional eating behaviour may Supplement selection is influenced by the After SG, early satiety and a gastric volume
result in discomfort, regurgitation and dumping procedure performed, pre-operative status and that is restricted to about 15% of original capacity
syndrome.24-26 the findings during long term nutrition monitoring. impact on dietary intake.24 Although SG does not
Simple changes to a patient’s eating and Poor eating behaviour, low nutrient food choices, cause malabsorption, it appears to alter nutrient
drinking style, as outlined in Table 3, can altered food tolerance and restricted portion size utilisation, in particular of vitamin B12 and iron.11,13
minimise the adverse symptoms and help the can contribute to potential nutrient deficiencies.3 Hence, a complete multivitamin and mineral
Table 3. Eating behaviours to encourage (classified by type of surgical procedure)

Eating behaviour Explanation Practical tip
Eat regular meals - Due to the very small gastric volume, skipping meals results Plan meals ahead of time so appropriate
avoid skipping meals in inadequate nutrition, especially protein, as patients choices are made
cannot eat more to compensate at the next meal (SG, RYGB) Cook in bulk and freeze meals
Going for long periods of time without food can result in
nausea and hunger, therefore patients can be more likely
to eat too fast or too much at the next meal, resulting in
adverse side effects (AGB, RYGB, SG)
Consume smaller Satiety is achieved with smaller serves but external tools/ Serve onto small side plates and child
amounts reminders may be needed to reduce over-serving (AGB, sized bowls to moderate volume
RYGB, SG) Use toddler-sized cutlery to reduce bite
volume and eating pace
Cut food into small Small cut-size aids the thorough mastication of food Use small utensils to pick up smaller
pieces (AGB) and gives perception of more food (AGB, RYGB, amounts of food
SG)
Chew well Poor mastication increases risk of blockages (AGB) and Use the tongue to feel for remaining food
fast eating (AGB, RYGB, SG) lumps before swallowing
Eat slowly Fast eating increases the risk of overeating (AGB, RYGB, Wait at least 30 seconds between each
SG), pain and regurgitation (AGB) swallow (AGB)
Aim to make a meal last 20-30 minutes,
but no longer than an hour
Avoid distraction Distracted eating is linked to overconsumption and poor Make eating a pure behaviour by removing
when eating - practise food appreciation (AGB, RYGB, SG) external stimuli such as the TV, computer
mindful eating and work
Avoid eating and If the patient is not diligent in allowing enough time Do not place drinking vessels at the dining
drinking at the same between swallows, drinking and eating together may area
time wash inadequately chewed food into the stomach and Set a timer as a reminder to commence/
contribute to pain, regurgitation or blockage (AGB) cease drinking
The stomach capacity is small and fluids may displace Carry a sipper bottle of water
capacity for solid foods (SG, RYGB) or contribute to
dumping syndrome (SG, RYGB)
Table 4. Common complaints and solutions for gastrointestinal symptoms (classified by type of surgical procedure)
Symptom Suggested management
Nausea or vomiting • Recurrent vomiting needs to be addressed urgently, particularly in the first 8 weeks after RYGB
and SG surgery, as it may lead to thiamine depletion and dehydration
• Vomiting could be a result of stenosis/anastomic stricture following SG or RYGB, generally occurring
around 8 weeks post-operatively (previously 10%, now 2% of patients with a good anastomosis)
• Long term nausea and vomiting occur after SG and RYGB when stomach capacity is exceeded
• Remind the patient not to rush through texture transition phases
• Reinforce the need to dramatically reduce total volume consumed at any single time after SG and RYGB
• Remind the patient to eat slowly, chew well and keep to recommended portion sizes
• Suggest that eating and drinking together are incompatible, especially following SG and RYGB
Regurgitation or bolus food • Reinforce the eating behaviours listed in Table 3
block (different from vomiting • Recommend follow up with surgeon as band may be too tight and need adjustment (AGB)
and only applies to AGB)
Constipation • Check that the patient is not confusing reduced frequency/volume of bowel output due to
(AGB, RYGB, SG) reduced intake with constipation
• Encourage adequate fluid (1000-1500 mL/day), high fibre intake (25-30 g/day) and exercise
• Recommend fibre supplement to boost intake
Overly decreased appetite • Following SG or RYGB, five or six half volume meals spread over the day are better tolerated and
(common after RYGB and SG) help achieve an adequate protein intake
• Low energy, high protein meal replacements or protein supplements may be necessary to meet
protein requirements
• Avoid unplanned snacking or ‘grazing’ behaviours, especially on ‘poor quality’ foods
Dumping syndrome (not • More common after RYGB, SG
common after AGB) • Encourage adequate protein and low glycaemic index carbohydrate foods
• Remind patient to separate fluid and foods
• Discourage highly refined and processed sugar foods and drinks
Diarrhoea • Review dumping syndrome management
• Consider that it may be a transient post-operative event
• Add soluble fibre in some circumstances
supplement high in B12 is recommended, plus iron Post-operative biochemical to weight loss.27,28 Thus, patients who have had
and others as required.3,13 monitoring either of these latter two higher risk procedures
After RYGB, the changes in gastrointestinal Nutritional deficiencies and aberrations may (with respect to nutrient status) may become
physiology result in altered absorption or persist and/or only present many years post- lost to follow up and not have critical nutritional
treatment of nutrients.3,15 In addition to a complete operatively, even when the person is in weight assessment maintained unless the patient responds
multivitamin and mineral supplement, specific maintenance or a regain cycle. Methodical and to a medical practice recall alert.
vitamin, mineral and trace element supplements frequent lifelong testing for nutrient markers is
in higher doses will be required lifelong.3,15 The recommended following all procedures.3,15,25 In
Expected rates of weight loss
dosage and range will likely change with time in the first year, repeat baseline tests every 6 months Many patients often have unrealistic expectations
response to laboratory results, including injections after RYGB and SG, on the anniversary for AGB, for both the rate and total weight loss expected
of vitamins A, D, B12 and iron when oral therapies and then annually thereafter for all procedures after restrictive surgery. Although the rate
are insufficient.3,15 (Table 1).3,15 Further tests including, but not of weight loss varies between surgeries and
Symptoms of vitamin and mineral deficiency limited to, magnesium, parathyroid hormone, individuals, up to 4 kg weight loss per month
are commonly non-specific, and most characteristic carotenoids, copper and urinary oxalates may be is a reasonable expectation.29 Rates are also
physical findings are seen late in the course of recommended.3,15 Unlike AGB that requires the influenced by time elapsed after surgery, energy
nutrient deficiency. Laboratory confirmation will be patient to return for band adjustment to effect intake relative to energy requirements, gender,
most reliable for early diagnosis. Table 5 provides continued weight loss/maintenance, RYGB or SG age and eating motivation. Bariatric surgeries are
recommendations for each of the vitamin and do not necessarily require further intervention or designed to impact on true physiological hunger.
mineral supplementations.3 specific follow up care to be effective with respect But internal hunger is not the only trigger for
The bariatric surgery patient - nutrition considerations CLINICAL
eating motivation. Myriad external factors trigger dietary and lifestyle changes facilitated by their influence the volume of food consumed, none of
a person to eat and influence food choice and dietitian, as an adjunct to their surgical procedure, the procedures necessarily improve the quality of
eating behaviour; at the surface are factors such have better nutritional and weight loss outcomes food consumed or compliance with recommended
as psychological health, obesogenic environment, than those who have limited follow up.30 supplement usage, leaving nutrition care and
peer influence, belief structure and celebrations. food choice important lifelong considerations.
Table 6 provides specific practical guidelines to Conclusion Ongoing coordinated care by the GP, that links
support sustained weight loss. Bariatric surgery is a reasonably safe and effective with the bariatric dietitian and others in the health
It is not unusual for patients to regain some method of weight loss for the treatment of morbid management team, maximises the benefits and
lost weight after surgery.29 Additional dietary obesity, and is more effective when combined health outcomes for the patient through ongoing
and psychological interventions minimise the risk with nutritional care, which is sometimes monitoring of nutritional status, prevention of
of regain and are highly indicated for those who complex, always ongoing, and differs between nutrient deficiencies and maximising long term
are regaining excessively.15,29 Patients who make surgical procedures. While bariatric procedures weight loss.
Table 5. Recommendations for vitamin and mineral supplementation (classified by type of surgical procedure)3
Daily minimum supplement SG RYGB AGB
Routine adult multivitamin Two chewable initially, then Two chewable initially, then One chewable initially, then
plus mineral (includes iron, solid solid solid
folic acid and thiamine)
Elemental calcium 1 200-1 500 mg (from diet and 1 200-1 500 mg (from diet and 1 200-1 500 mg (from diet and
as citrate supplements in as citrate supplements in as citrate supplements in
divided doses) divided doses) divided doses)
Vitamin D 3 000 IU vitamin D (titrated to 3 000 IU vitamin D (titrated to 3 000 IU vitamin D (titrated to
therapeutic levels) therapeutic levels) therapeutic levels)
Vitamin B12 As needed to maintain B12 As needed to maintain B12 Within routine supplement
levels levels
Total iron 45-60 mg (from multivitamin + 45-60 mg (from multivitamin + If indicated to satisfy NRV if
additional supplements) additional supplements) dietary intake plus routine
supplement insufficient
Other Further variation to the basic supplement recommendation is required to maintain nutritional
status if dietary intake plus routine supplements is insufficient, and for pregnancy planning
Table 6. Guidelines to support healthy long term weight loss and manage suboptimal weight loss
Guideline Specifics
Eat nutrient-dense foods and balanced Encourage adequate amount and variety of lean meat or meat alternative, whole grains,
meals reduced/low fat dairy, vegetables/salad, fruits and a modest amount of unsaturated oil/
nuts/seeds as per dietary guidelines for Australians
Establish a regular eating pattern to Plan for three mealtimes daily with structured mid-meal snacks, as and if required to
avoid meal skipping minimise grazing and impulse eating
Avoid energy-dense, nutrient poor Replace foods such as chips, chocolate, sugar, lollies, biscuits, pastries, fried foods,
foods processed meats with more nourishing core foods
Avoid kilojoule containing drinks Make water the drink of choice in order to minimise non-essential kilojoule sources such
as fruit juice, alcohol, ‘energy’ drinks, sports drinks, cordials, soft drinks, excess milk
Support mindful consumption and Refer to dietitian for advice and/or psychologist to learn mindfulness techniques and
manage ‘non-hungry’ eating manage habitual/emotional/other eating triggers
Take recommended vitamin and Monitor biochemistry and encourage compliance with supplements even if feeling well
mineral supplements or the active weight loss phase has ceased
Exercise and become more active Encourage at least 30 minutes of moderate intensity physical activity on most, preferably
within abilities all days as per the National Physical Activity Guidelines for Adults
Monitor weight to identify relapse early Refer to dietitian and other health professionals for intervention program
Maintain ongoing follow up with Frequency to be individually determined by each health professional
surgeon, dietitian and psychologist
Resources obesity_surgery.htm [Accessed 10 October 2012]. 2012;36:348-55.

11. Papailiou J, Albanopoulos K, Toutouzas KG, Tsigris 28. Laurenius A, Larsson I, Melanson KJ, et al.
Obesity Surgery Society Australia New Zealand
C, Nikiteas N, Zografos G. Morbid obesity and Decreased energy density and changes in food
(OSSANZ). www.ossanz.com.au/nutrition.htm selection following Roux-en-Y gastric bypass. Eur J
sleeve gastrectomy: how does it work. Obes Surg
Find a bariatric dietitian: http://daa.asn.au/for- 2010;20:1448-55. Clin Nutr 2013;67:168-73.
the-public/find-an-apd/. 12. Aasheim ET, Hofso D, Hjelmesaeth J, Birkeland KI, 29. Ames GE, Patel RH, Ames SC, Lynch SA. Weight loss
B0hmer T. Vitamin status in morbidly obese patients: surgery: patients who regain. Obes Weight Manag
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Caroline Shannon BSc, PostGradDipDiet, is an 362-69. 30. Peterli R, Steinert R, Woelnerhanssen B, et al.
13. Damms-Machado A, Friedrich A, Kramer KM, et al. Metabolic and hormonal changes after laparoscopic
Accredited Practising Dietitian, Sydney, NSW.
Pre- and postoperative nutritional deficiencies in Roux-en-y gastric bypass and sleeve gastrectomy:
carolineshannon@gmail.com a randomized, prospective trial. Obes Surg
obese patients undergoing laparoscopic sleeve gas
Ashlee Gervasoni BAppSc(HM), MD, is an trectomy. Obes Surg 2012;22:881-89. 2012;22:740-48.
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nutrient deficiencies in bariatric patients. Nutrition
Trudy Williams BSc, GradDipNutDiet,
2009;25:1150-56.
GradDipComm, is an Accredited Practising 15. Allied Health Sciences Section Ad Hoc Nutrition
Dietitian and Director of FoodTalk, Brisbane, QLD. Committee: Aills L, Blankenship J, Buffington C,
Competing interests: Trudy Williams is the author Furtado M, Parrott J. ASMBS Allied health nutri
tional guidelines for the surgical weight loss patient.
of patient and professional resources for bariatric
Surg Obes Relat Dis 2008;4:S73-108.
surgery and weight management.
16. Kaidar-Person O, Person B, Szomstein S, Rosenthal
Providence and peer review: Not commissioned; RJ. Nutritional deficiencies in morbidly obese
externally peer reviewed. patients: a new form of malnutrition? Part A: vita
mins. Obes Surg 2008;18:870-76.
References 17. Kaidar-Person O, Person B, Szomstein S, Rosenthal
1. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric RJ. Nutritional deficiencies in morbidly obese
surgery: a systematic review and meta-analysis. patients: a new form of malnutrition? Part B: miner
JAMA 2004;292:1724-37. als. Obes Surg 2008;18:1028-34.
2. Sjostrom L, Narbro K, Sjostrom CD, et al. Effects of 18. Mechanick JI, Kushner RF, Sugerman HJ, et al.
bariatric surgery on mortality in Swedish obese sub American Association of Clinical Endocrinologists,
jects. N Engl J Med 2007;357:741-52. The Obesity Society, and American Society for
3. Mechanisk JI, Youdim A, Jones DB, et al. AACE/ Metabolic & Bariatric Surgery medical guidelines
TOS/ASMBS Clinical Practice Guidelines for the for clinical practice for the perioperative nutritional,
perioperative nutritional, metabolic, and nonsurgi- metabolic, and nonsurgical support of the bariatric
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update: cosponsored by American Association of 19. Ernst B, Thurnheer M, Schmid S, Schultes B.
Clinical Endocrinologists, The Obesity Society, and Evidence for the necessity to systematically assess
America Society for Metabolic & Bariatric Surgery. micronutrient status prior to bariatric surgery. Obes
Obesity 2013;21:s1-27. Surg 2009;19:66-73.
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Overweight and obesity in adults: a guide for general Preoperative weight loss with a very-low-energy diet:
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633F62237CA256F190003BC2F/$File/adults_gp.pdf 21. Overs SE, Freeman RA, Zarshenas N, Walton KL,
[Accessed 10 October 2012]. Jorgensen JO. Food tolerance and gastrointestinal
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Surgical options. Available at http://ossanz.com.au/ Roux-en-Y gastric bypass. Int J Obes (Lond) correspondence afp@racgp.org.au
FOCUS Diagnostic challenges
Systemic lupus
Diane Apostolopoulos
Alberta Yik-Bun Hoi
erythematosus
When to consider and management options
Background Systemic lupus erythematosus (SLE) is a chronic

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterised by multi-system
autoimmune disease that sometimes poses a diagnostic manifestations. It is regarded as the prototypal connective
challenge, owing to the wide variety of clinical and tissue disease,1 where the key pathogenesis relates to
immunological presentations. There can be a significant a dysfunctional immune system that results in over
delay between onset of symptoms and the diagnosis of SLE.
production of various autoantibodies. Most of its pathology
Appreciation of its typical presentations and diagnostic
is mediated by either direct or indirect effects of these
process can help general practitioners decide on the timing of
autoantibodies, as well as other components of the innate
specialist referral.
and adaptive immune systems.
Objective
This article describes clinical and immunological The prevalence of SLE can vary greatly depending on race, disease
manifestations that are required in the diagnosis of SLE,
definition and method of validation, but is generally accepted as a rare
and provides an overview of management options.
disease, affecting less than 0.1% of the population.2-4 In Australia,
Discussion SLE is more common and more severe in Indigenous Australians and
Some of the more common clinical and immunological descendants from South-East Asia.5,6 It is nine times more common
manifestations of SLE are discussed and case studies to in females.7 Generally speaking, SLE has a relapsing and remitting
highlight the importance of accurate diagnosis are presented. nature where patients experience episodes of symptom exacerbation
Control of disease activity is crucial in alleviating symptoms,
interspersed with periods of relatively low disease activity.
prevention of damage accrual and early mortality.
Keywords Clinical presentation and diagnosis
lupus erythematosus, systemic; lupus erythematosus, discoid While the clinical presentation of SLE can be quite diverse
BBH — because the disease can affect virtually any organ system, patients
typically present with symptoms relating to joint, skin or mucosal
inflammation, or with a varying degree of haematological abnormality
or constitutional features.8 In some cases, patients may present with
more serious and potentially life-threatening renal, neurological or
cardiopulmonary complications.9 Since the disease most commonly
affects women of childbearing age, it is a diagnosis that should be
considered when such a patient presents with symptoms relating to
multiple systems.
Most SLE manifestations are the result of chronic inflammatory
response at the affected end organ, which can be demonstrated using
laboratory, imaging or histological measures. However, the lack of
a gold standard test to confirm diagnosis often results in delays or
misdiagnosis.
The Systemic Lupus Erythematosus International Collaborating
Clinics (SLICC) group has recently proposed a revised classification
criteria,10 which hopes to replace the 1997 American College of
Rheumatology criteria,11 to improve on the sensitivity and specificity
(Table 1). These criteria are useful and give consistency in the
696 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 10 OCTOBER 2013
Table 1. SLICC classification criteria for Cutaneous manifestations
systemic lupus erythematosus10 The spectrum of cutaneous manifestations of lupus erythematosus (LE)
is broad, but the most classical forms associated with systemic LE are
Clinical criteria Immunologic criteria
the acute malar and chronic discoid lupus erythematosus (DLE) rash.
Acute cutaneous lupus or ANA
Both can be quite photosensitive in nature.15,16
subacute cutaneous lupus
Acute malar rash is a slightly raised erythematous rash of the face,
Chronic cutaneous lupus Anti-dsDNA
particularly cheeks and nose, with nasolabial sparing, known as the
Oral ulcers or nasal ulcers Anti-Sm
‘butterfly’ rash. A worsening of the rash usually accompanies a flare of
Non-scarring alopecia Low complement
systemic disease. Sometimes a more generalised form over the body
Synovitis involving two or more Direct Coombs’ test
is present.
joints
DLE are characterised by slightly raised, scaly lesions that have a
Serositis Antiphospholipid
antibodies potential to scar. They can be found commonly on the scalp and face,
Renal and less commonly over the limbs and trunk. Only 5% of people with
DLE have SLE, but conversely among individuals with SLE, 20% will
Neurologic
have DLE.17
Haemolytic anaemia
Subacute cutaneous lupus erythematosus is another lupus-specific
Leukopenia (<4 000/mm3) or
lymphopenia (1 000/mm3) rash. It is a common skin manifestation in drug-induced lupus. The rash
Thrombocytopenia (<100 000/ is extremely photosensitive. The two main variants look as their names
mm3) suggest: papulosquamous looks psoriasiform, and annular polycyclic
Diagnosis of definitive SLE requires four or more criteria, gives a characteristic ring pattern.
with at least one clinical and one laboratory, with the Other cutaneous manifestations such as alopecia, oral ulcers,
exception of biopsy-proven LN (which requires fewer Raynaud’s phenomenon, urticaria, lichen planus, vasculitis or nail fold
criteria). Criteria are cumulative and need not be present infarcts are LE non-specific, but they often present at times when
concurrently.
patients experience increased lupus disease activity.
classification of the disease, mainly for the purpose of research and

Renal manifestations
surveillance. For clinicians, these criteria also serve as a good guide Lupus nephritis (LN) is one of the more serious manifestations, and
and reminder of the spectrum of disease, but, in clinical practice, many contributes significantly to mortality. It occurs in 30-50% of SLE
patients can present in a more forme fruste or atypical state. patients during their disease course.18,19 It is important to recognise
that LN can be relatively ‘silent’, and symptoms are often driven by
Common clinical manifestations other organ involvement or non-specific constitutional symptoms.
Constitutional Renal involvement can be missed if urinalysis is not performed.

Definitive diagnosis and information on prognosis can be obtained by
Constitutional manifestations such as malaise, fatigue, fever renal biopsy, but presence of glomerular haematuria, proteinuria or
and weight loss affect most patients at some time during their casts, are the key features of LN.
disease. They are, however, non-specific, and other non-SLE or
non-rheumatological conditions (eg. infection and malignancy)
Haematologic manifestations
can present the same way. Fibromyalgia is commonly observed in The most frequent haematological manifestation of SLE is anaemia.20
patients with SLE, but is considered a non-inflammatory complication This is usually due to chronic inflammation, but sometimes an
of the disease. More sinister constitutional symptoms such as fever autoimmune haemolytic anaemia can be demonstrated. Leukopenia,
and weight loss warrant investigation before being attributed to such as lymphopenia or less commonly neutropenia, is also well
lupus. recognised, but it rarely predisposes to infections. Thrombocytopenia
may also be a recurring feature.
Musculoskeletal
Up to 95% of patients with SLE have intermittent arthritis.12 The
Serosal manifestations
most common presentation is a symmetrical polyarthritis, affecting Pleural and pericardial inflammation can occur during active SLE.21
hands, wrists and knees. The degree of swelling is less prominent They can present as pleuritic chest pain, when associated with
than seen in rheumatoid arthritis. Tenosynovitis is a relatively common pleurisy or pericarditis. Less commonly, the presence of pleural or
musculoskeletal manifestation.13 Joint deformities are uncommon, pericardial effusion may present with pleuritic chest pain with or
as are erosive changes on X-rays.14 Myalgia is also a common without exertional dyspnoea. This symptom adds robustness to the
manifestation, even though true myositis is relatively rare. criteria for identifying SLE. Other cardiopulmonary manifestations such
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FOCUS Systemic lupus erythematosus - when to consider and management options
fl
as interstitial lung disease, pulmonary hypertension or Libman-Sacks Complements

endocarditis are less common complications of the disease. Tissue deposition of immune complexes can fix complement in the
classical pathway, and therefore results in a reduction of serum
Common immunological manifestations complement levels. C3 and C4 can be measured readily, and are now
Antinuclear antibodies part of the SLICC classification criteria for SLE.10 Complement levels
are also used to gauge disease activity.26
The antinuclear antibodies (ANA) test is the serological hallmark
of SLE. Up to 98% of patients with SLE will have a positive ANA,22 Management
making it highly sensitive and useful as a screening test. A negative Systemic lupus erythematosus is a chronic inflammatory condition
ANA makes SLE very unlikely and other diagnoses should be sought to driven by a dysfunctional immune system. Sometimes patients are able
explain symptoms. to report known triggers, such as ultraviolet or hormonal exposure.
Both titre and pattern are relevant. A titre of 320 or greater is Avoidance of these triggers would be sensible in preventing flares.
considered clinically significant.23 Low-titre ANA can be found in an The overall aim of therapy is to control disease activity. Mild
otherwise healthy population (Table 2).24 The most common patterns activity can be managed with non-steroidal anti-inflammatory drugs
observed in SLE are homogenous and speckled pattern while other (NSAIDs) or low-dose steroids, but more severe manifestations
patterns may be associated with other connective tissue disease. While require prompt treatment with moderate-to-high doses of steroids
the titre of ANA can fluctuate over time, it is not useful to repeat ANA to minimise organ damage. Steroid-sparing immunosuppressive
testing unless there is still a question regarding the diagnosis. The medications should be considered early to prevent steroid-related
finding of a positive ANA must be taken into context of the clinical morbidities.
manifestations. A positive ANA in the absence of the clinical features Hydroxychloroquine is an effective treatment in SLE, especially for
associated with connective tissue disease may be irrelevant. The test arthritis and rash. Furthermore, it has a protective effect in reducing
has generally poor specificity, and many autoimmune or non-autoimmune damage accrual in the long term, and confers a survival benefit in
conditions can also be associated with a positive ANA (Table 2). SLE patients. Hydroxychloroquine is well tolerated and, when dosed
appropriately, ocular toxicity is very rare.27
Other autoantibodies A range of immunosuppressive medications has been used
Antibodies to double-stranded DNA (dsDNA) are specific for SLE. In as a steroid-sparing agent in SLE, such as cyclophosphamide and
some patients, an increase in anti-dsDNA titre may signify onset of mycophenolate for lupus nephritis, although azathioprine and
disease flare.25 Other autoantibodies, available on the extractable methotrexate are used commonly. Belimumab, which is a human
nuclear antigen-testing panel, can also be associated with SLE or other monoclonal antibody that inhibits the activation of B-cells by
connective tissue diseases. Antibodies to Sm (anti-Smith), for example, interfering with a protein necessary for B-cell activity, has recently
are highly specific autoantibodies in SLE. been approved by the Australian Therapeutic Goods Administration
While antiphospholipid antibodies are not specific for SLE, they are for treatment of moderately severe SLE.28 This therapy is currently
part of the immunological abnormalities that can be associated with not easily accessed, as it has not been listed on the Pharmaceutical
pregnancy morbidities and thrombotic complications. Testing should Benefits Scheme.
include anticardiolipin antibodies, lupus anticoagulant and anti-p2 Other general measures that should be considered in SLE
glycoprotein 1. patients include cardiovascular risk reduction and optimisation of
Table 2. Conditions other than SLE associated with positive ANA23,24

Systemic autoimmune diseases Organ-specific autoimmune diseases Non-autoimmune associations
Scleroderma Autoimmune hepatitis Viral infections
(Infectious mononucleosis, parvovirus,
hepatitis C, HIV)
Sjögrens syndrome Primary biliary cirrhosis Bacterial infections (infective
endocarditis, TB)
Polymyositis or dermatomyositis Grave’s disease Parasitic infections

Rheumatoid arthritis Hashimoto’s thyroiditis Malignancy
Mixed connective tissue disease Idiopathic pulmonary fibrosis Normal population
1:40 (25-30%)
1:80 (10-15%)
1:160 (5%)
698 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 10, OCTOBER 2013
Systemic lupus erythematosus - when to consider and management options FOCUS
bone protection. Patients with SLE are at significantly increased risk Her background history included two episodes of pericarditis
of premature atherosclerosis,29 so smoking cessation and control in her twenties, intermittent arthralgia and occasionally a
of hypertension, dyslipidemia, obesity and hyperglycaemia are low platelet count was noted. She also had two previous
strongly recommended. Strategies to prevent osteoporosis should be
miscarriages. Investigation results:
considered in most patients because many are likely to require long • ANA 320 homogenous, positive anti-dsDNA, ESR 25, low
term glucocorticoid therapies. neutrophil and platelet counts, low C3/4, normal urine
Specialist referral to a rheumatologist is important to establish the sediment and no proteinuria
diagnosis, to gauge disease activity and severity, and to guide disease • Coronary angiogram found an irregular LAD with greater
management. However the role of the general practitioner (GP) is also than 70% stenosis in the mid portion which was treated
imperative for the optimal management of this chronic disease. By with thrombolysis, and a stent was inserted.
better understanding the disease process and management, GPs can She was diagnosed with SLE, but current presentation
help patients comprehend the complexity of disease pathogenesis was probably not due to active disease. She was started on
and priorities in treatment. GPs, working with the treating specialist, hydroxychloroquine. In the next few months, she had an
play a key part in the monitoring and management of the disease and exacerbation of joint pain and was found to have synovitis
associated co-morbidities. Furthermore, they are also well placed to at her wrists. Methotrexate was added to control her
offer patients ongoing support and counselling, especially for those symptoms.
who may find coping with a chronic disease difficult.
The case studies (see below) demonstrate the range and breadth Conclusion
of diagnostic challenges that can occur due to SLE. SLE is a multi-system autoimmune disease that is characterised by
mostly chronic inflammatory effects on a variety of organs. Diagnosis
Case study 1 of SLE can be challenging, but is based on demonstration of a number
A medical student, aged 24 years, presented with
of clinical manifestations as well as immunological abnormalities.
a 3-month history of fatigue and arthralgia. She has
Referral to a rheumatologist is strongly recommended to assist with
occasional mouth ulcers and alopecia. She has a
photosensitive rash on her face. Investigation results: the diagnosis and make treatment recommendations. Management of
SLE depends on the level of disease activity and can include general
• ANA 640 homogenous, positive anti-Ro, ESR 30,
measures, NSAIDs and steroids. Immunosuppression is often required
lymphopenia, low C3
and specific targeted therapy is on the horizon.
• Normal urinary sediment and negative for protein.
She was diagnosed with SLE, and treated with NSAIDs as Authors
Diane Apostolopoulos B BiomedSci, MBBS, Rheumatology Registrar,
required and hydroxychloroquine.
Department of Rheumatology, Monash Health, Melbourne, VIC.
dianeapost@gmail.com
Case study 2 Alberta Yik-Bun Hoi MBBS, FRACP, PhD, Consultant Rheumatologist,
A 35-year-old mother of two, presented with 6-month Department of Rheumatology, Monash Medical Centre, Melbourne,
history of fatigue, lethargy and arthralgia. She has had VIC
intermittent episodes of chest pain with one presentation
Competing interests: Alberta Yik-Bun Hoi is on the Advisory Board of
to emergency department without a specific cause found. Bristol-Myers Squibb and Janssen-Cilag. She has received payments
She has now noticed increased swelling in her legs with for lectures from Mundipharma, Janssen-Cilag, UCB, Pfizer, Abbott and
puffy eyes. Investigation results: Bristol-Myers Squibb.
• Urinary protein to creatinine ratio 0.38 (normal 0.02), Provenance and peer review: Commissioned; externally peer reviewed.
MSU showed glomerular red cells, ESR 40, albumin 32
• ANA 1280 homogenous, positive anti-dsDNA and anti-
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6. Vincent FB, Bourke P, Morand EF, Mackay F, Bossingham D. Focus on sys

temic lupus erythematosus in Indigenous Australians: towards a better
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FOCUS Diagnostic challenges
Fibromyalgia
Emma Guymer
Geoffrey Littlejohn
Background Fibromyalgia is a common and potentially disabling condition

Fibromyalgia is a common and debilitating condition. The affecting 2-5% of the population in developed countries,
cardinal feature of fibromyalgia is musculoskeletal pain, predominantly young to middle-aged women.1 Fibromyalgia
usually accompanied by other problems, such as fatigue, sleep has a varied and fluctuating clinical spectrum. Cardinal
disturbance and cognitive difficulties. Fibromyalgia commonly features include widespread musculoskeletal pain and
coexists with other chronic illnesses and can result in poorer tenderness, poor quality, unrefreshing sleep and significant
outcomes if untreated.
levels of fatigue. Other key features include cognitive
Objective disturbances, particularly problems with concentration and
The objective of this review is to discuss when fibromyalgia memory, and high distress levels.2 Fibromyalgia can be
should be considered as a diagnosis, how it is diagnosed, the considered part of a group of clinical syndromes, including
current understanding of the pathophysiology of fibromyalgia chronic fatigue syndrome, multiple chemical sensitivities
and the management strategies available. and irritable bowel syndrome, whose clinical features reflect
Discussion similar pathophysiological processes - termed by some as
The features of fibromyalgia are similar to those of many ‘central sensitivity syndromes’.3 These different diagnoses
other chronic illnesses, sometimes resulting in diagnostic are used depending on the predominant clinical features. For
confusion. Fibromyalgia can co-exist with other disorders example, patients with fatigue as their most severe symptom
and it is important to consider the possibility of fibromyalgia may receive a diagnosis of chronic fatigue syndrome.
contributing to symptoms in any chronically ill patient.
Keywords
fibromyalgia; central nervous system sensitisation What causes fibromyalgia?
— Fibromyalgia pathophysiology is underpinned by the development
of changes in the central nervous system (CNS)4,5 that alter the
processing of afferent sensory input, and can be grouped together
under the term ‘central sensitisation’.6 Central sensitisation changes
are often triggered by long-standing psychological or physical stress.7
These changes result in the intensity of usually non-painful stimuli
being amplified and experienced as painful. Other effects include
abnormality in the sleep cycle, where patients are unable to achieve
deep, restorative, stage IV non-REM sleep, and disturbances in the
hypothalamic-pituitary axis, with altered levels of serum cortisol,
decreased 24-hour urinary free cortisol and blunted cortisol responses
to dynamic testing.8
Genetic polymorphisms resulting in alteration in CNS serotonergic
and catecholaminergic processes continue to be investigated, and
appear to increase the risk of developing fibromyalgia.9
Aside from any genetic predisposition, clinical fibromyalgia is
frequently triggered. In an internet survey of 2 596 fibromyalgia
patients in North America, 79% described potential triggering events
at the onset of the their fibromyalgia,10 while 88.7% of patients seen in
an Australian public hospital fibromyalgia clinic reported recognisable
triggers.11 A physical or psychological stressor in a susceptible
individual can result in a chronic, maladaptive stress response, which,
in turn, mediates the central changes.12
690 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 42, NO. 10 OCTOBER 2013
How is fibromyalgia diagnosed? chronic pain are also experiencing fatigue, sleep problems, cognitive
Fibromyalgia is diagnosed according to criteria published by the disturbance, depression, headache and/or abdominal pain, then
American College of Rheumatology (ACR). The initial classification fibromyalgia should be considered.
criteria were published in 1990 and included widespread
musculoskeletal pain and tenderness measured by the ‘tender point When is fibromyalgia easy to miss?
count’ on physical examination.13 These criteria were useful in Fibromyalgia is easy to miss when it coexists with another chronic
defining a standard group for research purposes, however did not illness, particularly when it occurs with another condition causing
recognise the broader spectrum or fluctuating nature of fibromyalgia similar symptoms such as arthritis, endocrine disorders, depression or
symptoms. sleep apnoea.
In 2010 the ACR published diagnostic criteria, taking these Fibromyalgia coexists in a significant proportion of patients with
aspects into consideration.14 These criteria now account for chronic rheumatoid arthritis. These patients have worse disease activity,
musculoskeletal pain, as well as fatigue, sleep problems, cognitive joint tenderness and swelling, and psychological distress.18,19
disturbance and some more focal symptoms. In publishing these Concomitant fibromyalgia is also reported in patients with systemic
newer criteria, the authors recognised that fibromyalgia symptoms lupus erythematosis and osteoarthritis, who have significantly higher
fluctuate significantly over time and they aimed to be able to proportion of problems associated with central sensitisation, including
recognise a spectrum of severity in patients with central sensitisation sleep disturbance and fatigue.20-22 In these conditions, there is an
symptoms - rather than just those with the most severe illness who obvious source of nociceptive input to drive central sensitisation
satisfied the traditional definition of fibromyalgia. The severity scale processes. In a subgroup of patients with diabetes there is reported
captured by the new criteria has been termed by some as a degree of coexisting central sensitisation,23 and a significant proportion of
‘fibromyalgianess’ or a ‘polysymptomatic distress scale’.15,16 Recent patients with hyperthyroidism also have features of fibromyalgia.24
research focus uses this gauge of central sensitisation symptom In all of these situations of chronic illness, the possibility of long
severity to investigate the extent of sensitisation syndrome features standing physical or psychological stress exists, so that even when
in patients with fibromyalgia, chronic pain and other associated there is no obvious nociceptive input (such as in thyroid disease),
conditions.16 It is clear, however, that many clinical features of these patients can still develop the changes of central sensitisation.
central sensitisation are also found in a large number of other chronic Therefore, if patients have clinical features out of keeping with general
illnesses. disease activity, then it may be necessary to consider whether central
The diagnosis of fibromyalgia is often not initially considered. sensitisation could be contributing.
In a large North American survey, 46% of fibromyalgia patients had
consulted 3-6 health care providers regarding their symptoms, prior to Management of fibromyalgia
their fibromyalgia diagnosis.10 Team management
When should fibromyalgia be Fibromyalgia is a complex disorder, requiring input from many
considered? different health care providers, including medical, allied health,
Fibromyalgia has multiple, varied and fluctuating symptoms. It should and complementary and alternative medicine practitioners. General
be considered when a patient describes chronic musculoskeletal pain, practitioners are in an ideal position to co-ordinate and monitor these
fatigue and poor sleep. These symptoms are usually accompanied by a multidisciplinary management strategies.
number of other problems such as depression or anxiety, sensitivity to In this vulnerable patient group, psychosocial issues often arise.
chemicals, irritable bowel or restless legs. The symptoms often start or General practitioners are uniquely placed to recognise problems such
worsen during a period of severe psychosocial or physical stress. as financial hardship, social isolation, loss of role and secondary
The key symptoms of fibromyalgia are also commonly found in depression, and can provide essential structured support and validation
many other illnesses, and a thorough examination and investigation for these patients.
needs to be undertaken in order to ensure there is not another
pathological cause for the symptoms - particularly if there are any ‘red Table 1. Red flags
flags’ in the patient’s history suggestive of another serious pathology
• Older age at new symptom onset
(Table 1).
• Weight loss
Care also needs to be taken when interpreting results of
• Night pain
investigations, particularly radiology. Sometimes abnormalities found
• Focal pain
on musculoskeletal imaging are attributed to causing symptoms, when
• Fever or sweats
the clinical picture is much more global.
• Neurological features
Often, screening questions based on the modified 2010 ACR • History of malignancy
criteria17 (Figure 1) are useful. If patients presenting with widespread
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FOCUS Fibromyalgia
Education in fibromyalgia, and can contribute significantly to reduced patient

Following fibromyalgia diagnosis, an in-depth discussion of the clinical wellbeing. Addressing these problems, if present, is essential to any
features and pathological mechanisms of fibromyalgia is essential. improvement in a patient’s overall health.
Patient understanding of the condition and their expectations as to Stress management techniques are an essential part of any
clinical improvement are key to developing a successful management fibromyalgia therapeutic plan and, when combined with the
program. Often the validation and reassurance experienced once a development of other skills such as planning, pacing and coping
diagnosis is made result in improvement.25 strategies as part of cognitive behaviour therapy (CBT), then there is
The chronic and fluctuating nature of fibromyalgia and the demonstrated improvement in pain-related behaviour, self-efficacy and
management goals of symptom reduction and optimising function physical function.26 Other psychological strategies such as mindfulness
need to be explained. The importance of adherence to treatment techniques may also be helpful. Mindfulness-based therapies seem to
plans and realistic expectations regarding progress and outcomes be effective in alleviating symptoms common in fibromyalgia such as
need ongoing reinforcement. Thorough and targeted patient pain, depression and a range of other psychological factors as well as
education also results in increased patient engagement and proactive improving health-related quality of life, although in studies with active
attitude to self management. comparator arms, they have in general, not proven superior.27,28 A
recent randomised controlled trial of an online mindfulness intervention
Psychology targeting socioemotional regulation in fibromyalgia patients resulted
A number of psychological interventions are helpful in the management in significant improvement in social functioning, positive affect and
of fibromyalgia. Concomitant depression and anxiety often occur coping efficacy for pain and stress.29
Fibromyalgia FOCUS
Exercise Antidepressants as pain modulators

Regular exercise improves pain, fatigue and sleep disturbance in Medications that elevate levels of serotonin and noradrenaline
patients with fibromyalgia.30 There is no ‘best’ form of exercise in the descending inhibitory nociceptive pathways of the CNS,
and all types may be considered. Aerobic exercise, in particular, such as low-dose tricyclic antidepressants (TCAs) and serotonin
reduces fibromyalgia symptoms and improves physical capacity.31 noradrenaline reuptake inhibitors (SNRIs), can provide significant
The initiation of any regular exercise program needs to be slow and benefit in patients with fibromyalgia independent of effects on
gradual. Patients who are deconditioned and concerned regarding mood.39 Amitriptyline, duloxetine and milnacipran are the best-
the possible worsening of pain and fatigue will need reassurance; studied agents in these categories, and all have substantial
they may need to start with only a few minutes of gentle exercise evidence for the significant improvement of pain, and other
several times a week. This can be built up very slowly and gradually symptoms of fibromyalgia, although some early studies were short
as tolerance increases. Often a hydrotherapy pool is a good place to term.4 Milnacipran is approved by the Australian Therapeutic
start an exercise regimen, as the warmth of the water and relative Goods Administration for use in fibromyalgia,40 but is not currently
weightlessness relieves symptoms while the resistance provides a available in Australia.
gentle workout.
Membrane stabilisers
Other physical therapies Pregabalin and gabapentin bind to voltage-dependent calcium
Other physical therapies can be helpful in the management of channels, reducing calcium influx into sensitised spinal cord neurons
fibromyalgia, particularly those that can be self administered. There in central pain syndromes such as fibromyalgia. In a meta-analysis of
is evidence to support the use of yoga, qi gong and tai chi in patients randomised, controlled trials in fibromyalgia patients, the use of these
with fibromyalgia.32 Studies in which the use of these therapies agents resulted in reduced pain, improved sleep and better quality of
resulted in improvement in fibromyalgia symptoms and physical life.41
functioning were generally small and unblinded, however, given the
lack of serious adverse effects and the promotion of self-efficacy, Key points
these management modalities are generally useful options. • Fibromyalgia is a clinical syndrome resulting from a process of CNS
sensitisation.
Medication • It has varied and fluctuating symptoms and can be confused with
There are no pharmaceutical agents currently available on other illnesses with similar features.
Australia’s Pharmaceutical Benefits Scheme for specific use to treat • Fibromyalgia can also coexist with other disorders, and identifying
fibromyalgia. the source of clinical complaints can be difficult.
• The possibility of central sensitisation should be considered in
Analgesics all patients with chronic illness when the one particular aspect
Simple analgesia is often the first medication patients with (particularly musculoskeletal pain or fatigue) is not responding to
fibromyalgia will trial. Guidelines published by the European League seemingly adequate treatment.
Against Rheumatism (EULAR) recommend the use of simple analgesics
like paracetamol in the management of fibromyalgia; however, due to Authors
Emma Guymer MBBS, FRACP, is a Rheumatologist and Head of the
insufficient data this is based on expert opinion alone.33 Paracetamol
Fibromyalgia Clinic, Department of Rheumatology, Monash Medical
use has not been studied in fibromyalgia patients, other than in Centre, Melbourne, and Adjunct Lecturer, Department of Medicine,
combination with tramadol, where the combination resulted in a Monash University, Melbourne, VIC. emma.guymer@monash.edu
modest (18%) improvement in pain compared with placebo.34 Geoffrey Littlejohn MD, MPH, FRACP, FRCP[Edin] is Emeritus Director,
Other studies have found some benefit with tramadol use Department of Rheumatology, Monash Medical Centre, and Associate
for fibromyalgia;5,35 the therapeutic benefit was possibly due to Professor, Department of Medicine, Monash University, Melbourne, VIC
tramadol’s serotonin-noradrenaline reuptake inhibition, rather than Competing interests: None.
p-opioid activity. Other opioid use in fibromyalgia is not routinely Provenance and peer review: Commissioned; externally peer reviewed.
recommended. There is reduced opioid receptor availability in
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a narrative review evaluating levels of evidence. ISRN Psychiatry
FOCUS Rheumatology
Ankylosing spondylitis:
Vera Golder
Lionel Schachna
an update
Background Spondyloarthritis (SpA) encompasses a group of rheumatic
Ankylosing spondylitis (AS) affects one in 200 individuals and disorders that share clinical, genetic and radiographic
is usually diagnosed many years after onset of symptoms. features and includes psoriatic arthritis, reactive arthritis
Chronic back pain is common and recognition of early disease and arthritis of inflammatory bowel disease. These
requires clinical experience and a high index of suspicion. disorders affect 2-3% of the population and are twice as
Further, inflammatory markers are not invariably elevated and common as rheumatoid arthritis. As they often cause long
radiographic changes are often late findings. term disability, early recognition is important.
Objective
The objective of this review is to address AS and the recently This review will focus on ankylosing spondylitis (AS) and the recently
defined disorder of non-radiographic axial spondyloarthritis. defined disorder of non-radiographic axial SpA.1 These conditions
The latter is a common early presentation of AS, before the occur in one in 200 individuals but most general practitioners have
development of radiographic sacroiliitis, and will evolve into never identified a new case of AS, suggesting the need for a higher
typical AS in 50% of patients. index of suspicion in primary care.
Discussion
MRI may be particularly useful in evaluating early disease, Clinical features
although chronic changes of sacroiliitis are better seen on
plain X-rays. Nonsteroidal anti-inflammatory drugs (NSAIDs)
Back pain
are first-line therapy and recent studies suggest that regular Approximately 5% of chronic lower back pain is attributable to SpA.
use among patients with AS slows radiographic progression. The presence of inflammatory back pain (IBP), the archetypal feature
Tumour necrosis inhibitor therapy has strikingly improved
of AS, increases the likelihood of SpA to approximately 14%.2 Table 1
quality of life for the more than two-thirds of AS patients with
shows the differentiating features of inflammatory and mechanical
an inadequate response to NSAIDs.
back pain. Two very specific features of IBP are alternating buttock
Keywords pain and awakening only in the second half of the night with spinal
rheumatology; ankylosing spondylitis; spondyloarthritis; pain or stiffness. Clinicians can only assess the activity of IBP by
therapeutics subjective symptoms: fatigue, spinal pain, and severity and duration
of morning stiffness. Identification of IBP should prompt more detailed
BSi] O
evaluation and consideration of a multimodality treatment approach.2
Table 1. Characteristics of inflammatory and

mechanical back pain
Inflammatory Mechanical
Age at <40 years old Any age
symptom onset
Onset Insidious, persists Variable
for >3 months
Activity Improves with Improves with
exercise rest
Morning Moderate, persists Mild, short-lived
stiffness for >45 minutes
Inflammatory Elevated in Normal
markers 50-70%
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Reduced spinal mobility Juvenile SpA
The most common measures of spinal mobility are listed below. It is important to be aware of juvenile SpA and 50% of cases will
• Modified Schober’s test (Figure 1): serial measures are valuable in evolve into typical AS. Asymmetric oligoarthritis, often associated
assessing progression of spinal restriction; may be abnormal with with severe midfoot pain (tarsitis), is a common presentation. HLA-
disc disease and degenerative lumbar disease. B27, tarsitis and hip involvement are predictors of the persistence of
• Lumbar side flexion: the best measure of overall spinal restriction disease as AS into adulthood.
and disease activity.
• Occiput-to-wall distance: should be zero in normal people. Investigations
Chest expansion (at the fourth intercostal space): abnormal (<5 cm) in
Imaging
only a minority of patients during the first few years of disease
It is important to note that in early disease, spinal mobility may be X-ray
normal. A single anteroposterior pelvis X-ray (rather than dedicated sacroiliac
joint views) should be adequate to assess the sacroiliac joints. AS
Extra-axial features is defined by IBP and at least bilateral grade 2 or unilateral grade 3
Peripheral arthritis occurs in all variants of SpA. Up to 50% of AS changes (Figure 2).4
patients develop asymmetric oligoarthritis (<4 joints), often targeting The radiographic findings represent reparative changes in response
the lower limb joints. Enthesitis or inflammation at insertions of to earlier acute inflammation. As such, the appearance of radiographic
tendons, ligaments and joint capsules into bone can present as abnormalities is typically delayed. In the spine, there is progression
Achilles tendinitis, plantar fasciitis and intercostal enthesitis, which from reactive sclerosis (‘shiny corner’ or Romanus lesion), squaring
causes chest wall pain. Dactylitis (‘sausage digit’) is diffuse swelling and erosions at the edge of the vertebral bodies to syndesmophyte
of a finger or toe caused by tenosynovitis of the digital flexor tendon, formation and bony bridging (Figure 3). The classic ‘bamboo spine’ is
and is more common in psoriatic and reactive arthritis. characteristic of advanced AS.
Extra-articular features Magnetic resonance imaging (MRI)

Uniocular anterior uveitis occurs in about 40% of patients and MRI is often considered when X-rays are normal but there is a clinical
typically presents as acute painful red eye, with blurred vision suspicion of SpA. MRI may be particularly helpful in early disease,
and photophobia. In suspected first episodes of anterior uveitis, although it can be normal even in active SpA and the chronic changes
ophthalmology review for slit-lamp examination is mandatory. of sacroiliitis are better seen on plain X-rays. Fat-suppressed short
First-line treatment is a combination of corticosteroid and mydriatic T1 inversion recovery (STIR) sequences demonstrate marrow oedema
eye drops. About 60% of AS patients have mucosal inflammation at the sacroiliac joints and/or vertebral corners. Marrow oedema is
on colonoscopy, while symptomatic inflammatory bowel disease associated with later development of bony sclerosis or fusion, either of
occurs in 10% of patients. Osteopenia and osteoporosis commonly the sacroiliac joints or spine.5
occur, particularly in long-standing persistently active disease, and
Ultrasonography
the risk of vertebral fracture is increased approximately sevenfold.
Importantly, bone densitometry in the spine may be spuriously Ultrasonography can be useful in detecting enthesitis, such as
elevated by the syndesmophytes of AS. Patients with AS are at risk Achilles tendonitis. Its role in the detection of sacroiliitis remains to
of developing apical pulmonary fibrosis (up to 15%) and aortic valve be determined as this modality is largely operator-dependent. There
incompetence (up to 10%). These features usually develop late in the are, however, some suggestions that colour Doppler ultrasound may be
disease and are often asymptomatic. used to diagnose early sacroiliitis and to monitor response to therapy.
A) Patient standing erect. Mark

an imaginary line connecting
both posterior superior iliac
spines (close to the dimples of
Venus).
B) A mark is placed 10 cm above.
C) The patient bends forward
maximally, measure the
difference between the two
marks. Report the increase (in
cm to the nearest 0.1 cm). The
Figure 1. Spinal Mobility - Modified Schober best of two tries is recorded.
Reproduced with permission from ASAS handbook, Ann Rheum Dis 2009; 68 (Suppl II)
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FOCUS Ankylosing spondylitis: an update
Figure 2. Radiographic grading of sacroiliac joints. Grade 1: Suspicious changes, not definitive. Grade 2: Small localised
areas of erosions or sclerosis; normal joint space width. Grade 3: Definite changes of erosions, sclerosis, narrowing or partial
fusion. Grade 4: Complete fusion
Laboratory tests longer among women, who comprise one third of AS patients, perhaps
Acute phase reactants such as erythrocyte sedimentation rate (ESR) and related to a misconception that AS is rare among women.
C-reactive protein are useful markers of inflammation but are elevated in Features of SpA are important to identify early at presentation and
only 50-70% of AS patients. They are more likely to be elevated in patients include alternating buttock pain, asymmetric peripheral arthritis, heel
with concurrent peripheral arthritis and inflammatory bowel disease. pain, uveitis, positive family history and good response to non-steroidal
anti-inflammatory drugs (NSAIDs). The presence of one or two of these
The role of HLA-B27 and other genes features increases the likelihood of SpA to 35-70%, and three or more
The association of HLA-B27 with AS is well established and occurs features increases the likelihood to 80-95%.3
in 85-90% of patients. HLA-B27 is seen in 5-15% of the general
population, with some variability associated with ethnic background, Non-radiographic axial SpA
but only 5% of HLA-B27 positive people develop AS. As such, HLA-B27 Even in the modern era of MRI, X-ray changes at the sacroiliac joints
in the patient with clinical features of SpA can support the diagnosis must be present in order to establish a diagnosis of AS. The delay
but has no role as a general screening test for spinal pain. from symptom onset to X-ray changes, however, can be 10 years
or more. Many but not all patients with early presentations have
Delay in diagnosis active sacroiliitis on MRI scan. If MRI abnormalities are identified,
The delay between onset of symptoms and physician diagnosis of AS is a diagnosis of non-radiographic axial SpA can be established if at
5-7 years on average.6 Chronic back pain is common and recognition of least one clinical feature of SpA is present. If the MRI is normal, then
early disease requires clinical experience and a high index of suspicion. HLA-B27 and two or more SpA features are required. The Assessment
Further, inflammatory markers are not invariably elevated and of SpondyloArthritis International Society (ASAS) has developed and
radiographic changes are often a late finding. The delay in diagnosis is validated these classification criteria (Figure 4).7
Ankylosing spondylitis: an update FOCUS
Although patients with non-radiographic axial SpA patients have and NSAIDs, but not for non-radiographic axial SpA. As such, X-ray
fewer intense inflammatory changes on MRI and have lower levels changes of sacroiliitis are required. Randomised controlled trials,
of inflammatory markers, they have similar levels of disease activity however, suggest better clinical responses in early non-radiographic
and pain as those with established AS. Therefore patients with non disease.
radiographic axial SpA warrant early evaluation and treatment. For IBP, all TNF inhibitors have similar efficacy and the choice
of agent is often determined by extra-articular features and patient
Predictors of outcome preference. Approximately 94% of AS patients commenced on
Several factors associated with poor prognosis are identified in AS, treatment with a TNF inhibitor at Austin Health in Melbourne remain
most importantly juvenile-onset and hip arthritis. Other factors include on long-term treatment (personal communication). To date, there is
persistent active disease, cigarette smoking, inadequate response to little evidence to suggest slowing of spinal fusion with TNF blockers.
NSAIDs and baseline spinal radiographic changes.
Other DMARDs
Management Traditional DMARDs such as methotrexate and sulfasalazine have little
Symptom management effect in spinal disease, but can be useful for an associated peripheral
arthritis. Other biologic agents available for rheumatoid arthritis in
Education and exercise Australia have not been effective in AS.
As with any chronic condition, patient education and support is vital in
the management of AS. Patient disease and medication information, Assessment and monitoring
as well as access to support groups, can be found on the Arthritis In concert with the treating rheumatologist, the general practitioner
Australia website (www.arthritisaustralia.com.au). A tailored exercise has an important part to play in monitoring of AS patients. The goal of
and stretching program is recommended for AS patients and there are AS treatment in 2013 should be to achieve a state of minimal morning
several useful online resources (eg. www.nass.co.uk/exercise) and stiffness and gel phenomenon, stable measures of spinal mobility
mobile apps (eg. iAnkSpond). and optimal functional status. A significant change in any of these
NSAIDs
NSAIDs are first-line therapy for symptomatic AS patients. Recent
studies suggest that regular NSAID use in AS slows radiographic
progression more than on-demand use.8 An individualised assessment
of risk of long-term NSAID use should be made in consultation with the
rheumatologist before long-term daily NSAID use is recommended.
Tumour necrosis factor (TNF) inhibitors

TNF inhibitor therapy has strikingly improved the quality of life for
the more than two thirds of AS patients with an inadequate response
to NSAIDs.9 These agents are listed on the Pharmaceutical Benefits
Scheme (PBS) for active AS not adequately responsive to exercise
Figure 4. ASAS classification criteria for axial

spondyloarthritis.7 These classification criteria have a
sensitivity of 83% and specificity of 84% for detecting
Figure 3. Lumbar spine changes in AS. A) Shiny corners all axial SpA. (IBD = inflammatory bowel disease,
and erosions. B) Early syndesmophytes C) Spinal fusion CRP = C-reactive protein, NSAID = non-steroidal anti
or ankylosis inflammatory drug)
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FOCUS Ankylosing spondylitis: an update
drugs reduce radiographic progression in patients with ankylosing spondy

parameters should prompt semi-urgent review by a rheumatologist.
litis: a randomized clinical trial. Arthritis Rheum 2005;52:1756-65.
General practitioners should familiarise themselves with the risks of 9. van der Heijde D, Sieper J, Maksymowych WP, et al. 2010 Update of the
TNF inhibitors, particularly infection. Among Australian patients, risk international ASAS recommendations for the use of anti-TNF agents in
patients with axial spondyloarthritis. Ann Rheum Dis 2011;70:905-08.
of melanoma and other skin cancers is important to recognise. Before
major surgery, TNF inhibitors are generally withheld for 1-2 half
lives. The treating rheumatologist should be notified of any possible
complications of treatment, to consider whether to withhold or cease
treatment.
Key points
• Inflammatory back pain can be identified only by a targeted medical
history.
• In early disease, spinal mobility may be normal.
• Identification of IBP should prompt more detailed evaluation and
consideration of a multimodality treatment approach.
• The diagnosis of AS is established by IBP and the presence of
definite X-ray changes of sacroiliitis.
• Non-radiographic axial SpA, with or without MRI changes, is often
an early presentation of AS.
• Patient education and a tailored exercise routine are essential
aspects of management.
• NSAIDs are first-line therapy in SpA.
• TNF inhibitors are indicated in AS patients with inadequate
response to exercise and NSAIDs.
• Regular review of IBP symptoms and spinal mobility is important to
determine the effectiveness of treatment.
Authors
Vera Golder MBBS, Advanced Trainee in Rheumatology, Austin Health,
Melbourne, VIC. vera.golder@gmail.com
Lionel Schachna MBBS, FRACP, PhD, Consultant Rheumatologist,
Austin Spondylitis Clinic, Austin Health, Melbourne, VIC
Competing interests: None.
Provenance and peer review: Commissioned; externally peer reviewed.
References
1. Braun J, Sieper J. Ankylosing spondylitis. Lancet 2007;369:1379-90.
2. Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J. How to
diagnose axial spondyloarthritis early. Ann Rheum Dis 2004;63:535-43
3. Kain T, Zochling J, Taylor A, et al. Evidence-based recommendations for the
diagnosis of ankylosing spondylitis: results from the Australian 3E initiative
in rheumatology. Med J Aust 2008;188:235-37.
4. van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria
for ankylosing spondylitis. A proposal for modification of the New York
criteria. Arthritis Rheum 1984;27:361-68.
5. Weber U, Lambert RG, Ostergaard M, Hodler J, Pedersen SJ,
Maksymowych WP. The diagnostic utility of magnetic resonance imaging
in spondylarthritis: an international multicenter evaluation of one hundred
eighty-seven subjects. Arthritis Rheum. 2010;62:3048-58.
6. Reed MD, Dharmage S, Boers A, Martin BJ, Buchanan RR, Schachna
L. Ankylosing spondylitis: an Australian experience. Intern Med J
2008;38:321-27.
7. Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of
SpondyloArthritis international Society (ASAS) handbook: a guide to assess
spondyloarthritis. Ann Rheum Dis 2009;68(Suppl 2):ii1-44.
8. Wanders A, Heijde D, Landewe R, et al. Nonsteroidal antiinflammatory correspondence afp@racgp.org.au
Ulcer dressings and
Geoff Sussman management
Background The most common chronic wounds seen in general

Chronic leg ulcers caused by venous disease, arterial disease practice are venous ulcers, arterial ulcers, mixed
or a combination of both need to be clearly identified before aetiology ulcers (venous and arterial), pressure ulcers,
treatment can be commenced. Their management will depend skin tears and atypical wounds such as vasculitic ulcers.
on the diagnosis, combining direct management of the ulcer The management of ulcers is complex. Current practice
as well as management of patient factors. Other chronic
varies in different clinical settings and treatments are
wounds commonly observed in practice include pressure
often delivered by different healthcare professionals, who
wounds, skin tears, atypical leg ulcers.
may or may not use best practice guidelines. The process
Objective described in this article is that used in the Therapeutic
This paper will outline a simple way to manage people with guidelines: Ulcer and wound management.1
chronic ulcers.
Discussion The issue is not so much the choice of product but the accurate
The prevalence of chronic ulcers in Australia has been diagnosis of the underlying cause of the wound. It is often the case
estimated at 2-5%. Comprehensive assessment of the ulcer, that a product is applied to a wound and when not successful the
the region and the whole person is an important first step in product is considered at fault so a different one is used; when that
treatment. The aim of management is to promote healing and fails, the next product is used. The simple rule is to treat the whole
minimise the impact on the patient.
patient and not the hole in the patient.
Keywords The three principles of wound management are:
skin ulcer; leg ulcer; bandages 1. Define the aetiology.
2. Control factors affecting healing.
wgi] o 3. Select appropriate local environmental management (dressings).
Define aetiology
The most common chronic wounds seen in practice are:
• leg ulcers (venous, arterial, mixed)
• pressure wounds
• skin tears.
Venous leg ulcers

An estimated 400,000 Australians have venous leg ulcers (VLUs;
Figure 1) due to chronic venous insufficiency (CVI). VLUs are managed
in primary care or the community with variation in treatment and
effectiveness,2 which in 2010 translated to healthcare costs of over
$2 billion per year.3 The burden of recurrence is expected to rise
with an ageing population and the growing epidemic of diabetes and
obesity, which will further increase healthcare costs.4
VLUs result from the breakdown of the venous circulation in
the leg and are associated with the inability of the leg to force the
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passage of blood through the various connecting veins via the bicuspid Their edges are often sharply defined and the ulcer is ‘punched out’.
valves by muscular contraction. The increased venous pressure leads The base is often covered with slough. This may deepen to expose
to pitting oedema, which in turn affects perfusion of the skin, so tendons. A history of intermittent claudication (pain on exercise),
when some trauma occurs there is insufficient supply for healing to dependent foot (dusky foot) white on elevation, peripheral vascular
occur and an ulcer develops. Pitting oedema may result not only from disease, lower ankle brachial pressure index, weak/absent pulses,
chronic venous insufficiency but also organ failure, lymph disease or sluggish/poor capillary refilling may be present. Commonly, the
from medication (eg calcium channel blockers). ulcer site is below the ankles and on the foot or toes; however,
Venous ulcers commonly develop in the lower one-third of the leg arterial ulcers may be present on other areas of the body. The skin is
(the gaiter area) and are usually irregular in shape. Pitting oedema often shiny and friable. Poorly controlled diabetes and smoking are
is usually present. The skin is often stained around the ulcer area significant risk factors causing arterial insufficiency.7
because of haemosiderin deposition after leakage of red blood cells Treatment of arterial ulcers may involve surgical intervention for
from the circulation. Typical features of venous ulcers include skin angioplasty, stenting, bypass grafting and, ultimately, amputation.
changes such as eczema or atrophy blanche (white stippled scars on Pain control is an important aspect of the management of arterial
the skin). The three most common risk factors for VLUs are a history of ulcers. Adequate analgesia is required to manage the severe
obesity, past deep vein thrombosis (DVT) and poor mobility resulting in ischaemic pain often experienced with arterial ulcers. These wounds
venous stasis.3,5 should not have compression applied even if there is some associated
In some cases, treatment includes surgery; however, the mainstay venous disease.7
of treatment is the application of graduated compression therapy
toe-to-knee (30-40 mmHg at the ankle). It is, however, essential to
exclude arterial involvement by testing the ankle brachial index or by
ultrasonography. Lower limb exercise and addressing occupational
factors, such as long periods of standing leading to venous stasis,
should be encouraged.
It is important to keep in mind that oedema may result not only
from venous disease (pitting oedema), but also other causes including
organ failure, lymph disease or from medication (eg calcium channel
blockers). Lymphoedema is caused by a reduction in the function of
the lymph vessels to drain extracellular fluid. The resultant oedema Figure 2. Arterial ulcers
will place the patient at risk of ulcer development as a result of minor
trauma and by the hyperkeratotic nature of the skin.6
Venous/arterial or mixed ulcers
It is important to note that 15-20% of leg ulcers are of mixed
aetiology. These ulcers are often difficult to heal because of
associated oedema, cellulitis, thrombophlebitis, rheumatoid diseases,
particularly in patients who are bedridden, and malnourishment-
related conditions of the skin in elderly patients. The most important
issue is to determine whether the predominant cause is venous
or arterial and then treat it. Graduated compression may be
contraindicated, depending on the extent of the arterial component of
the problem. If compression cannot be used it is difficult to address
the venous component of the problem.1,8,9
Figure 1. Venous leg ulcer
Skin tears
Skin tears (Figure 3) are the most common wound type in the elderly
Arterial ulcers population. If treated inappropriately, skin tears can become chronic
The death of skin automatically follows occlusion of its arterial blood wounds, exerting huge costs on the community and deleterious effects
supply unless this is gradual enough to allow a collateral blood supply on the individual’s physical and psychological health.
to be established. Atheroma (thickening) is the most common cause of The ageing process will affect most of the structures of skin
arterial ulcers of an ischaemic nature. through loss of hair follicles, sebaceous glands that supply natural
Ischaemic pain, especially at night, is associated with arterial moisture to the skin, receptors, blood supply and sweat glands.
ulcers (Figure 2). This is as marked in small ulcers as in larger ulcers. The result of these tissue changes is that the skin becomes thinner
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FOCUS Ulcer dressings and management
and brittle, and the blood supply is reduced, fragile and more prone
to injury. It is critical to identify patients at risk and then introduce
prevention strategies. A recent study in Western Australia of 900
patients in 23 nursing homes showed a 50% reduction in skin tears
and a significant cost saving by applying a moisturising lotion twice
daily.10
Figure 4. Pressure wound
Friction
Friction occurs when the top layers of skin are worn away by
continued rubbing against an external surface. This can be caused by
ill-fitting footwear- or even bed linen- and can manifest in a simple
blister or tissue oedema- or an open pressure wound.
Figure 3. Skin tear
Shear
Shear occurs when the skin remains in place- usually unable to
The management of a skin tear will depend on the level of move against the surface it is in contact with- while the underlying
damage. If it is possible to replace the flap, this should be done bone and tissue are forced to move. This force will contribute to
carefully, holding it in place with a few adhesive strips applied with the destruction of microvasculature in a manner similar as direct
no tension and covering with a silicone foam dressing, then covering pressure.
with one or two layers of tubular compression bandages to apply mild The management of a pressure wounds requires the removal of
pressure on the wound. This system is reviewed after 3 days then all pressure on the wound- increased nutrition and- depending on the
redressed every 5-7 days until the wound has healed.1-11 size and depth of the wounds- the use of topical or cavity products.1-13
Other causes of ulcers Control factors that affect healing

In addition to the more common forms of ulceration- there are a Most wounds heal readily but others are slow to heal or remain
number of less common causes. Vasculitic ulcers may develop as a unhealed for a considerable length of time. A number of factors-
result of a number of medical conditions- such as rheumatoid arthritis including intrinsic and extrinsic factors-14-15 affect wound healing
and polyarthritis- which cause damage to the microarterial circulation (Table 1). These should be considered and addressed as part of a
by circulating antibodies. These wounds are often misdiagnosed as holistic approach to wound management.
venous ulcers. If there is a dark wound margin- purple discolouration
in the peri-skin and the wound is painful- suspect vasculitis. These Wound management
wounds need to be treated systemically as well as topically.1-12 The management of the wound environment is now based on the
concept of wound bed preparation (WBP) interventions- which
Pressure ulcers address debridement- bacterial balance- exudate management
Pressure ulcers (Figure 4) are the most preventable of all of the chronic and the local tissue in the wound environment. These important
wounds. assessment elements have led to the development of the concept
Patients who are bedridden- for example- as a result of stroke of the TIME principles (Tissue- Inflammation/Infection- Moisture-
spinal injury- multiple sclerosis or dementia- often develop extensive Edge/Epithelialisation)- overseen by the World Union of Wound
pressure ulcers. These wounds may result from direct pressure- friction Healing Societies.1-16-17 The Therapeutic guidelines: Ulcer and wound
or shear injuries. management uses this approach in guiding wound care in a best
A pressure wound develops when capillary blood flow to the skin practice- evidence-based context.1
and tissue over a bony prominence is decreased for a sufficient period Much of the focus in wound management is on the dressing when-
of time. The consequence of the restricted blood supply is a reduction in fact- this is not the important aspect to address. It is often the
in oxygen supply and nutrition to the tissue- and inadequate excretion case that a product is applied to a wound and when not successful
of the waste products. the product is considered to be at fault so a different one is used and
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Ulcer dressings and management FOCUS
when that fails the next product is used. In general, the dressing does Interactive dressings
not heal the wound, but appropriate contemporary dressings facilitate These dressings help to control the micro-environment by combining
the optimal environment to enhance wound healing. It is critical to with the exudate to form either a hydrophilic gel or, by means of
first determine and address the underlying cause of the wound. The semipermeable membranes, controlling the flow of exudate from
next step is to identify and address those factors affecting healing the wound into the dressing. They may also stimulate activity in the
over which there may be some influence. Finally, the local wound healing cascade and speed up the healing process.
management issues should be considered and dressing selection
There are six classes of interactive dressings, classified according to
based on the function of the dressing (eg exudate management,
their functionality:1,18,19
debriding, cavity filler) and what is needed to optimise the local
• Film dressings
wound environment for healing. Once a venous ulcer is healed then
• Hydroactive dressings
consider the ongoing use of compression stockings for life.1,3,5
• Hydrocolloid dressings
Wound management products • Hydrogel dressings
• Foam dressings
Passive dressings • Alginate absorbent fibre dressings.
For many years the products used were of the ‘passive’ or the ‘plug The choice of dressing will depend on the wound type and depth, level
and conceal’ concept, including gauze, lint, non-stick dressings and of exudate and the presence of bacteria. A comprehensive overview of
tulle dressings. These products fulfill very few of the properties of an wound dressings may be found in Wound Dressing Products Update.18
ideal dressing and have very limited, if any, use as primary dressing, A wound identification and products selection guide can be found on
but some are useful as secondary dressings.1,18,19 the Department of Veterans Affairs website (see Resources).
Table 1. Intrinsic and extrinsic factors affecting wound healing

Intrinsic factors Extrinsic factors
Health status Mechanical stress
• Good arterial and venous circulation: anaemia • Pressure
impairs oxygen transport • Friction
• Shearing forces
Immune function Debris
• Normal immune function helps to cleanse the • Slough
wound • Necrotic tissue
• Reduced function increases the risk of infection • Eschar
• Scab
• Dressing residue
• Sutures
Comorbidities Dessication
• Diabetes • Drying of the wound surface results in death of surface cells
• Rheumatoid arthritis
• Other diseases
Age-related changes to skin Maceration
• Loss of hair follicles, sebaceous glands, receptors • Excess moisture retards healing and damages the
• Reduced blood supply peri-skin
• Increased fragility Temperature
• Dryness • Optimal temperature 37°C
• Thinning
Nutrition Infection
• Balanced diet including proteins (particularly Chemical stress may have an adverse effect on the wound and cells
for the amino acid arginine), carbohydrates, fats • Topical agents (eg antiseptics)
and fluids promotes healing • Smoking20
• Drugs (eg steroids and non-steroidal anti-inflammatory drugs)21-23
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Bandages 8. Humphreys ML, Stewart AH, Gohel MS, Taylor M, Whyman MR, Poskitt
KR. Management of mixed arterial and venous leg ulcers Br J Surg
The use of material to bind the wound is as ancient as medicine 2007;94:1104-07.
itself. Techniques and material have changed little over the centuries, 9. Ghauri AS, Nyamekye I, Grabs AJ, Farndon JR, Poskitt KR. The diagnosis
and management of mixed arterial/venous leg ulcers in community-based
but in the past 15 years there has been an explosion in the types of clinics. Eur J Vasc Endovasc Surg 1998;16:350-55.
bandages available. When choosing and applying a bandage it is 10. Carville K. The cost of preventing and managing skin tears. Australian
Wound Management Association National Conference; 2014, 7-10 May,
important to differentiate between the traditional and the ritual on
Gold Coast, Australia.
one hand and what is best and most cost-effective for the patient on 11. Thomas, S. Wound Management and Dressings. London: Pharmaceutical
the other.11 Press; 1990.
12 Patel GK, Grey JE, Harding KG. Uncommon causes of ulceration. BMJ
The bandage may be needed for several reasons:
2006;332:594-96.
• Retention: keeping a dressing in place 13. Australian Wound Management Association. Pan Pacific Clinical Practice
Guideline for the Prevention and Management of Pressure Injury. Osborne
• Musculoskeletal support: supporting an injured joint
Park: Cambridge Media, 2012.
• Compression: assisting venous return from the lower leg. 14. Thomas Hess C. Checklist for factors affecting wound healing. Adv Skin
Wound Care 2011;24:192.
Conclusion 15. Guo S, Dipietro LA. Factors affecting wound healing J Dent Res
2010;89:219-29.
The prevalence of chronic wounds is expected to rise given that people 16. Falanga V. Classifications for wound bed preparation and stimulation of
are living longer and that the incidence of diabetes is increasing. There chronic wounds. Wound Repair Regen 2000;8:347-52.
17. Sibbald RG, Williamson D, Orsted HL, et al. Preparing the wound bed -
is a need is to clearly identify the underlying cause of any wound, debridement, bacterial balance and moisture balance. Ostomy Wound
including factors that may delay healing, and to treat appropriately. Manage 2000;46:14-22,24-28,30-35.
18. Sussman G, Weller C. Wound Dressings Update. J Pharm Prac Res
Treatment should address the wound environment, tissue base,
2006;36:318-24.
presence of bacteria and the level of slough. If there is no improvement 19. Queen D, Orsted H, Sanada H, Sussman G. A dressing history. Int Wound J
in wound healing after 4 weeks then seek help from a wound specialist. 2004;1:59-77.
20. Sussman G. The role of smoking in wound healing. Aust Pharmacist
2005;24:633-34.
Author
21. Pollack SV. Systemic medications and wound healing. Int J Dermatol
Geoff Sussman OAM, JP, PhC, FACP, FAIPM, FPS, FAWMA, Associate
1982;21:489-96
Professor, Medicine Nursing & Health Sciences, Monash University, 22. Karukonda SR, Flynn TC, Boh EE, McBurney EI, Russo GG, Millikan LE. The
Clayton, VIC. Geoff.Sussman@monash.edu effects of drugs on wound healing: part 1. Int J Dermatol 2000;39:250-57.
23. Karukonda, Flynn TC, Boh EE, McBurney EI, Russo GG, Millikan LE. The
Competing interests: Geoff Sussman has received payment for lectures
effects of drugs on wound healing: part 2. Int J Dermatol 2000;39:321-33.
at Ansmed Conferences.
Provenance and peer review: Commissioned, external review.
Resources
Department of Veterans Affairs. Wound identification and dressing
selection chart resources. Canberra: Commonwealth of Australia; 2012.
Available at www.dva.gov.au/service_providers/resources/Pages/
WoundCareFlashVideo.aspx [Accessed 5 August 2014].
References
1. Ulcer and Wound Management Expert Group. Therapeutic guidelines:
Ulcers and wound management. In: eTG Complete [Internet] Melbourne.
Therapeutic Guidelines Ltd. 2013. Available at tg.org.au [Accessed 4
August 2014].
2. Weller C, Evans S. Venous leg ulcer management in general practice
- practice nurses and evidence based guidelines. Aust Fam Physician
2012;41:331-37.
3. Australian Wound Management Association, New Zealand Wound Care
Society. Australian and New Zealand clinical practice guideline for pre
vention and management of venous leg ulcers. Osborne Park: Cambridge
Publishing; 2011. Available at www.awma.com.au/publications/2011_
awma_vlug.pdf [Accessed 4 August 2014].
4. Gottrup F, Apelqvist J, Price P. Outcomes in controlled and comparative
studies on non-healing wounds: recommendations to improve the quality of
evidence in wound management. J Wound Care 2010;19:237-68.
5. Alexander House Group. Consensus statement: consensus paper on venous
leg ulcers. Phlebology 1992;7:48-58.
6. Rockson SG. Update on the biology and treatment of lymphedema. Curr
Treat Options in Cardiovasc Med 2012;14:184-92.
7. Hopf HW, Ueno C, Aslam R, et al. Guidelines for the treatment of arterial
insufficiency ulcers. Wound Repair Regen 2006;14:693-710. correspondence afp@racgp.org.au
592 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 43, NO. 9, SEPTEMBER 2014
THEME ENT disorders
f
■■ ____ ■ n
Management of
epistaxis in
Dennis Pashen
Maurice Stevens
general practice
BACKGROUND The vast majority of cases of epistaxis can be managed successfully within Dennis Pashen, MBBS,
general practice. MPHTM, FRACGP,
OBJECTIVE To describe a range of clinical interventions in the management of epistaxis FACRRM, is Associate
Professor and Director,
appropriate to general practice.
Mt Isa Centre for Rural
DISCUSSION A number of relatively simple treatments and procedures may provide relief for and Remote Health,
anterior nasal bleeding, which is the site for over 80% of cases of epistaxis. Where more James Cook University,
procedural interventions are necessary, adequate preparation and appropriate tools are Queensland.
required to perform these processes safely. Initial identification of the site of bleeding before Maurice Stevens, MBBS,
commencement of treatment may be difficult but allows the correct treatment to be applied FRACS(ENT), is visiting
with minimal discomfort to the patient. More copious bleeding which constitutes less than 5 medical doctor, Royal
10% of cases, is usually the result of posterior nasal bleeding and is best treated in a facility Brisbane Hospital,
Queensland.
well set up to handle such an eventuality. In cases of chronic epistaxis, a number of
interventions, medical and surgical have been trialled with variable success, and should be
used with caution in general practice.
he majority of cases of epistaxis arise from Examination

T the nasal septum. Exceptions but not neces
sarily exclusions to septal bleeding may occur Initial assessment can be delayed in acute epistaxis
with injury to the turbinates, congenital causes while immediate measures to stem the tide are put
of bleeding such as hereditary haemorrhagic in place. Direct digital pressure to the lower soft
telangiectasia, blood dyscrasias, anticoagulation cartilaginous part of the nose by pinching for
therapy, cardiovascular conditions including approximately 10 minutes is the method of choice.
hypertension and raised venous pressure from The patient should be sitting and leaning forward,
mitral stenosis (Table 1). These are uncommon breathing through the mouth and may suck on ice.
however. This will allow time to prepare for the examination
The blood supply of the nasal septum is from and protect your clothes, self, and the patient.
the internal carotid through the anterior and pos Once the initial flow has stemmed, the nasal
terior ethmoidal arteries, and from the external cavity can be viewed. Persistence of bleeding with
carotid through greater palatine, sphenopalatine adequate anterior control would suggest a more
and superior labial arteries (Figure 1). posterior origin of bleeding.
Some commonalities in epistaxis do exist
however. It is messy for both the patient and treat Light source
ing physician, and if copious, equally distressing. A good hands free light source is essential. A mir
rored head loop, or a headlight that can be
Reprinted from Australian Family Physician Vol. 31, No. 8, August 2002 • 1
n Management of epistaxis in general practice
Table 1. Causes of epistaxis focused. A Thudicum nasal speculum will allow

viewing of the cavity. The sprung speculum is
Local causes General causes looped over the tip of the second finger, the back
Spontaneous: Little’s area (anterior) Cardiovascular conditions of the hand facing the patient, and is actively
Trauma: nasal fractures, septal ulcers, Hypertension closed by compression using the third and fourth
chronic perforations fingers. The speculum is inserted while closed,
allowing the natural spring of the speculum to open
Postoperative bleeding Raised venous pressure
(mitral stenosis) up the anterior nares. A large calibre otic speculum
and otoscope may also be used, but care must be
Tumours (benign and malignant), Coagulation or vessel
granulomas defects taken during insertion into the nostril so as to not
recommence any bleeding from the Little’s area.
Hereditary telangiectasia Haemophilia
This should allow ready access for small anterior
Autoimmune disease Leukaemia septal bleeds necessary to perform cautery.
Others Anticoagulation therapy
Thrombocytopaenia Suction
Fevers, infections (rare) An effective suction device is necessary if the
Typhoid fever bleeding cannot be controlled. An angled Fraser
Influenza sucker, 10-12 French gauge, is preferred to allow
evacuation of the anterior and middle nasal cavity.
Analgesia
Analgesia is most often not required in anterior
cavity bleeding. Topical analgesia may be required
for posterior bleeding, especially if packing is
required. A range of topical agents is available,
either as packaged products or prepared by a phar
macist. Sedation may be effective in bleeding that
is a result of hypertension. Intramuscular mor
Figure 1. Blood supply of nasal septum phine (0.05-0.15 mg/kg) or pethidine (0.5-1.5
mg/kg) have been used for many years and have
proven to be of value. It is best to avoid narcotics
until after control of haemorrhage. However, care
must be taken to maintain airway safety in sedated
patients. An intravenous line should be inserted in
the early treatment phase.
Local anaesthetic agents

• cophenylcaine forte (a mixture of xylocaine and
decongestant) solution or spray
Figure 2. Electrocautery handpiece • xylocaine 10% solution with 1/10 000 adrenaline
or xylocaine 10% CFC free spray
• xylocaine 2% 1/200 000 adrenaline ampoules for
local injection
• cocaine 4% solution
• cocaine 25% in paraffin base ointment.
Equipment
A range of equipment may facilitate the treatment
of epistaxis. This may include:
• Jobson Horne wool carrier, or long handled
Figure 3. Chemical cautery cottonbuds/swabs
2 • Reprinted from Australian Family Physician Vol. 31, No. 8, August 2002
Management of epistaxis in general practice n
• silver nitrate applicator

• electrocautery device (Figure 2)
• Foley’s catheter, sponge foam stay, and clamp
(from an intravenous line or umbilical clamp is
suitable)
• nasal packing forceps
• angled rigid Fraser, 10-12 French gauge sucker
• triamcinolone ointment with and without anti-
septic/antibiotic (Kenacomb ung.). This is also Figure 4. Nasal electrocautery
used following cautery to reduce crusting and
hence reduce bleeding during healing.
Anterior epistaxis
Anterior epistaxis is the commonest form of epis
taxis and constitutes over 80% of all cases of
epistaxis. Primarily this is the result of bleeding
from the Little’s area, which contains the
Kiesselbach plexus of vessels (Figure 1). This is
often triggered by infection to the overlying
Figure 5. Lateral nerve supply of nose
mucosa. In children, the ease with which small
fingers can be inserted and the ensuing satisfaction
that this provides contributes to a large number of
cases, especially when associated with various
organisms such as staphylococci and streptococci.
Treatment
A conservative regimen can be trialled initially. A
once a week application of Triamcinolone 0.025%
cream (Aristocort cream), nemdyn, nasalate or
equivalent cream combined with nightly applica Figure 6. Anterior view of nerve supply of nose
tion of a small quantity of petroleum jelly to the
septum before bedtime.1,2 nostril which can last for approximately three
weeks. The patient shouldn’t blow their nose for a
Chemical cautery few hours to avoid this happening (Figure 3).
Silver nitrate sticks can be applied over the Little’s
area.3 Topical anaesthetic may be applied via spray Electrocautery
or impregnated swabs before this. Electrocautery is performed after suitable anaes
thesia such as topical anaesthetic followed by local
Technique
anaesthetic injection. The red-hot electrocautery
Light application over the area of origin of bleed loop is passed over the mucosal blood vessels
ing may result in cauterisation of the underlying effecting cautery (Figure 4). It must be noted that
vessels. This is achieved by lightly wiping the tip of the cautery is achieved not by direct contact, but
the silver nitrate stick over the Little’s area until it by the approximate application of heat, and that
becomes discoloured to a grey-white. It may also the anterior nares must be protected by a speculum
trigger further bleeding. A clean cottonbud may be or other means as burning can result in scarring.
dabbed gently on the area to remove excess chemi Topical antibiotic ointment and/or petroleum jelly
cal or blood induced from rubbing. Caution must can be used postoperatively.
also be exercised in that ideally, only one side at a
time should be cauterised by any means, as nasal Other forms of bleeding
septal perforation may result from bilateral In other forms of bleeding, obvious sites of haem
cautery. Silver nitrate may stain the skin of the orrhage may not be visualised. This may include
n Management of epistaxis in general practice
Figure 7a, b, c, d. Foley’s catheter
posterior bleeding from fractures or systemic surgically clean bowl and mixed with triamcinolone
causes, or injury to the turbinates. In cases of and antibiotic cream (Kenacomb ointment). Many
various systemic causes, tamponade via nasal alternate mixtures exist, such as paraffin plus neo-
catheters or packing provides the main treatment, tracin, or the traditional bismuth and iodoform
at least initially. paraffin paste (BIPP).
After application of topical and local anaesthetic
(Figure 5, 6) packing can proceed with the patient Anaesthesia
positioned sitting forward, holding a kidney tray, The patient’s nose should be adequately anaes
and breathing through his/her mouth. Adequate thetised, although it may be difficult. A good
splash protection includes the wearing of plastic headlamp and suction is necessary to clear any blood
clothing covers, goggles or glasses, and gloves. from the airway. Using cophenylcaine or cocaine
spray or swabs, the nasal mucosa is anaesthetised as
Balloon catheters much as possible. The use of parenteral premedica
Double balloon catheters, although expensive are tion or sedation should be used with caution as it is
easy to insert. After fully inserting the catheter, the possible to tip the patient over into hypovolemic
posterior balloon is first inflated and brought shock if blood loss has been severe.
forward to close off the postnasopharyngeal space.
Technique
The second and anterior balloon is then inflated to
apply pressure to the internal cavity of the nose. A Foley’s catheter with a foam stay placed on its
Normal saline is the preferred agent for inflation of proximal end is inserted along the floor of the
the balloons as gradual deflation can occur if air is nasal cavity under the inferior turbinate, to the
used, and this may result in recurrence of bleeding. nasopharynx. The part of the catheter beyond the
Do not inflate beyond the capacity of the balloons balloon may be removed to facilitate positioning
as discomfort, rupture of the balloons, or pressure and improve patient comfort. The pharynx is
necrosis of the mucosa may occur. viewed to make sure the catheter has not passed
into the oropharynx. The catheter balloon is then
Nasal packing (anterior and inflated with up to 8 mLs of normal saline, and
posterior bleeds)
should be no larger than the size of the choana (the
Preparation of the pack posterior nasal aperture), and then brought
A six foot strip of Vaseline gauze is placed into a forward by gentle traction.
4 • Reprinted from Australian Family Physician Vol. 31, No. 8, August 2002
Management of epistaxis in general practice n
At this stage there should be no blood in the the author.

• Hamilton Bailey’s Emergency Surgery. Butterworth-
pharynx if the choana is obstructed and the Heinemann, Linnacre House, Jordan Hill, Oxford
catheter is on the correct side. The prepared pack OX2 8DP. ISBN 0 7506 2771 9.
is picked up in a loop, the length of which should
be the length of the packing forceps, which is References
1. Kubba H, MacAndie C, Botma M, Robinson J,
approximately equivalent to the length of the floor
O’Donnell M, Robertson G, Geddes N. A prospec
of the nose (Figure 7a,b). The loop is inserted infe tive, single blind, randomised controlled trial of
riorly to the Foley’s catheter, and subsequent loops antiseptic cream for recurrent epistaxis in childhood.
Clin Otolaryngol 2001; 26(6):465-466.
placed above these parallel to one another and the
2. London S D, Lindsey W H. The American
floor of the nose (Figure 7c). The catheter needs to Laryngological, Rhinological & Otalogical Society. A
be fixed in position by the piece of foam being reliable medical treatment for recurrent mild anterior
applied to the alar margin; this prevents any epistaxis. Laryngoscope 1999; 109(9):1535-1537.
3. Bull P D. Lecture notes on diseases on the ear, nose
erosion of that margin. A suitable clamp is used to and throat. 8th edn. Blackwell Science, 87.
fix the stay in place (Figure 7d). This may be an 4. Viducich R A, Blanda M P, Gereson L W. Posterior
intravenous line or an umbilical clamp, the former epistaxis: clinical features and acute complications.
Ann Emerg Med 1995; 25(5): 592-596.
preferable, as it is more easily adjustable. The
5. Sabba C, Gallietelli M, Palasciano G. Efficacy of
tension on the catheter should be sufficient to keep unusually high doses of tranexamic acid for the treat
it in place but not enough to interfere with the via ment of epistaxis in hereditary hemorrhagic
telangiectasia. N Engl J Med 2001; 345(12):926.
bility of the skin of that region. The pack can then
be left in place for one to three days which is nec
essary to stabilise the haemostasis.3,4 Often the
tension on the catheter is released after 24 hours
but the catheter is left in place.
Continuing bleeding
SUMMARY OF
A range of medical and surgical interventions is IMPORTANT POINTS
required in cases of continuing and/or severe
bleeding. These are best delivered within the • The majority of cases of epistaxis originate
from the anterior septal area (Little’s area).
context of a specialist unit in a tertiary hospital as
• Chemical cautery (silver nitrate) and
often resuscitation may be required. Such medical
electrocautery are treatments of choice for
interventions as intravenous administration of anterior epistaxis and can be delivered with
Tranexamic Acid, 0.5-1.0 gm four times a day in minimal discomfort and cost in general
hereditary haemorrhagic telangiectasia,5 ligation of practice.
internal or external carotids are not for the faint • Adequate preparation includes having the
hearted and are best left to major centres.5 appropriate equipment to enable easy and
effective management of nasal bleeding.
Conclusion • Nasal packing is appropriate management for
posterior and recalcitrant epistaxis. Adequate
Epistaxis is a common presentation with over 60%
analgesia is mandatory. Packing can be
of the population suffering from it at some stage of performed in a well equipped general practice
their lives. It is often influenced by environmental or outpatient department.
conditions. Over 80% of these are attributable to • Do not forget that patients can die from
anterior nasal cavity causes. The general practi epistaxis. Attention to normal resuscitation
tioner may be required to deal with this condition procedures is always appropriate.
and can do so in the majority of cases in an appro
priate and safe manner. With training and REPRINT REQU ESTS
knowledge they may also be able to take appropri Dennis Pashen
ate measures to deal with other causes of bleeding. Mt Isa Centre for Rural and Remote Health
PO Box 2572
Further guidance and reading
Mt Isa, Qld 4825
• Upya nose, Inya Ear and Downya throat. CD-ROM
Email: pashend@micrrh.qld.edu.au
available from the RACGP library, NQ Clinical
School, Mt Isa Health Service District Library, or
CL
‘For men only’

A mental health prompt list in primary care
Suzanne Brownhill, BSW, MPH, is a PhD Candidate, School of Psychiatry,
University of New South Wales.
Kay Wilhelm, MD, FRANZCP, is Associate Professor, School of Psychiatry,
University of New South Wales.
Gregory Eliovson, BSc, MComm, was a research assistant, St Vincent's Hospital,
Sydney, New South Wales.
Merilyn Waterhouse, BA, GradDipPsych, was a research assistant, St Vincent's
Hospital, Sydney, New South Wales.
BACKGROUND Barriers to detecting symptoms of depression in male patients in

primary care include patients’ reticence to self disclose and doctors’ failing to ask
questions that tap into their patient’s emotional distress. Effective consultation is
further hindered by time constraints, undifferentiated and nonspecific symptoms of
depression, differing attribution of symptoms and expectations of the consultation,
and low levels of mental health literacy. These issues, of particular relevance to men,
informed the design of a screening instrument, the ‘For Men Only’ Prompt List (PL).
OBJECTIVE This article reports an evaluation by male patients and their general
practitioners of the PL conducted in the context of primary care. The patients
completed the PL in the waiting room and used it to raise issues during consultation.
The instrument was evaluated using a short questionnaire completed by patients, a
postal questionnaire by GPs, and field notes.
DISCUSSION The PL was useful for those patients who required prompting in raising
issues surrounding depression. Those who already had a good relationship with their
doctor, were at ease discussing issues without prompting, or had a specific physical
problem to be treated, did not find it as useful. All practitioners found the PL
provided extra information about their patients. It also helped them build rapport
with patients and made their job of assessment easier. Doctors depend on patients to
self disclose and patients depend on doctors to provide an accurate diagnosis.
The PL addresses some of the barriers to identifying depressive symptoms in men,
particularly in assisting male patients to ‘open up’ to their doctors.
number of barriers to detection of Differing attributions (where patients may ‘Hidden’ symptoms
A depression in primary care have con
tributed to low detection rates. These
construe their problems as ‘physical’ while
the doctor may see them as ‘psychological’,
Low treatment rates for men have been
linked to social norms of traditional mas
include structural barriers such as the or vice versa) may also hinder recognition culinity that make help seeking more
setting of the clinic,1 and time constraints of symptoms. Other complicating factors difficult for men. The belief that express
(perceived and actual long waiting times include alcohol abuse and where symptoms ing the need for help, for men, is a ‘sign
and short consultation) which can lead to are ‘hidden’ (such as somatic presentations of weakness’4,5 characterised by difficulty
focussed, task orientated enquiry and limit of emotional distress). These barriers are relinquishing control,6 has been known
a broader psychosocial exploration. particularly salient for men whose delayed to inhibit expressiveness and lead to
Interpersonal barriers to detecting depres help seeking and reticence to self disclose symptoms being avoided, denied, camou
sion include sex, age and socioeconomic may also be a reflection of low levels of flaged or hidden.7,8 Furthermore, doctors
bias, and differing expectations of the con mental health literacy (such as knowledge who maintain this same view of mas
sultation between doctors and patients.2 of mental health issues).3 culinity and help seeking in men are
Reprinted from Australian Family Physician Vol. 32, No. 6, June 2003 • 443
n ‘For men only’ - A mental health prompt list in primary care
more likely to overlook, deny or dismiss Another study, formative to this evalua tional health have been found to be pro
symptoms in men.9,10 tion study, recruited a nonclinical group of tective, for the onset of depression.20 The
young and older men to a series of focus question: ‘When was the last time you saw
Differing expectations of groups.5 The group discussions were a doctor?’ was designed to establish
the consultation
designed to elicit ‘new’ information con delayed help seeking and whether an
Accurate assessment is impeded when cerning men’s experience of depression, emotional crisis had precipitated the visit.
doctors and patients approach the consul ways of coping and help seeking.2 The Emotional problems can manifest in phys
tation with differing expectations.11 For qualitative data were used both descrip ical problems due to delayed help seeking,
example, some doctors may attach greater tively, and analysed using a grounded common in men, at which point the
importance to somatic symptoms, and pre theory approach.16,17 The results indicated a problem is likely to be serious. The next
scribing drugs,12 while some patients may high level of mental health literacy in those question: ‘Why are you seeing the doctor
be more oriented to emotional agendas men who identified in themselves, and today?’ was designed for the doctor to
and quality of life issues such as disruption observed in other men, all the commonly quickly identify the patient’s perception of
of normal activities and relationships.13 In accepted symptoms of DSM-IV major the visit. This enables the doctor to
other cases, patients may invite a prescrip depression.18 In addition, they identified respond appropriately and ‘in tune’ with
tion or a ‘quick fix’ to avoid any the need to withdraw, and an escalation the patient thus building rapport.
exploration of sensitive psychosocial and intensification of negative affect Having the patient nominate his ‘best’
issues that may be difficult to raise. In any toward anger.19 These two symptoms in and ‘worst’ life events taps into any signif
case, doctors depend on patients to self men may easily be overlooked in consulta icant issues and acts as a cue for questions
disclose in order to fulfill their profes tion and thus remain ‘hidden’.7,8 surrounding, eg. unresolved grief or loss,
sional task10,12 and patients depend on Furthermore, the men also reported a ten being retrenched from work, etc. ‘Work’
doctors to provide an accurate assess- dency for male patients to wait for doctors and ‘family’ have been found to be major
ment14 and to respond to issues raised.2 to ‘guess’ the problem rather than actively sources of, and buffers against, depression
self disclosing.2 for men.2
Mental health literacy In an attempt to narrow the expecta The last questions on the front page
Patients’ self disclosure and doctors’ tion gap between doctor and male patient ask the patient to identify things the
ability to detect depressive symptoms in the consultation process, the men were doctor needs to know about them and
requires a level of mental health literacy. asked: ‘What questions should general what they would like the doctor to discuss
This has been defined as the knowledge practitioners be asking to detect depres with them. These questions allow the
and beliefs about mental disorders sive symptoms in men?’ The answer to patient to write down sensitive issues that
(including depression) which aid their this question and overall analysis of the may be difficult to articulate, and also
recognition, management and prevention.3 qualitative data informed an instrument encourages the patient to take an active,
A recent Australian study assessing for use by male patients and practitioners rather than passive, approach to the con
knowledge and beliefs about depression in primary care to facilitate discussion on sultation process.
found a community wide lack of recogni issues surrounding depression. The instru Twenty ‘Yes/No’ questions on the
tion of the symptoms of depression and ment, the ‘For Men Only’ Prompt List back page of the PL reflect issues articu
limited understanding of the availability (PL), is the focus for this evaluation study. lated by men in relation to their
and effectiveness of standard treatments, experience of depression and coping
in both depressed and nondepressed The ‘For Men Only’ (Figure 2). These questions also incorpo
Prompt List
groups.15 It remains unclear, however, rate the commonly accepted symptoms of
whether levels of mental health literacy The front page of the PL asks questions DSM-IV major depression18 which
differ between men and women. that relate to perception of health, work include diminished interest, lethargy, and
While numerous studies have sought to and family satisfaction, social support, change in weight or sleep patterns.
understand why depression in men is diffi major life events, and issues the doctor Additional questions focus on the need to
cult to detect in primary care,4 few studies needs to know and discuss (Figure 1). The withdraw and the escalation and intensifi
have engaged men directly. Heifner5 first question asks the patient to rate his cation of negative effect.
recruited a group of men to talk about physical (poor/fair/good/excellent) and The PL has been informed by men for
their experience of depression and found emotional health (lousy/not bad/pretty men. It is in ‘male friendly’ form and lan
that most had very defined traditional good/feeling great). Poor ratings of emo guage style, designed to facilitate
stereotypical gender role identities which tional health have been found to be discussion for men, and to make the
influenced their help seeking behaviour. predictive, while positive ratings of emo doctor’s job easier in detecting symptoms
444 • Australian Family Physician Vol. 32, No. 6, June 2003
]
Copyright © 2001: S. Brownhill & K. Wilhelm

University of New South Wales: Version 2:1
All rights reserved. No part of this instrument may
be reproduced without permission in writing from
the authors.
Please fill in this form and hand it to your doctor at consultation. The
answers you give are building blocks for you and your doctor to
discuss health and related issues. Thank you!
HEALTH WORK
How would you rate your physical health? Are you employed? Yes No
(please circle)
What is your usual occupation?
Poor Fair Good Excellent Years in your present job:
How satisfied are you at work?
How would you rate your emotional health?
Not at all Not very Fairly Very
Lousy Not bad Pretty good Feeling great
FAMILY
When was the last time you saw a doctor?
Do you have a partner?
If so, how is the relationship working for you?
Why are you seeing the doctor today?
It's not Could be better Working well
Do you have kids?

If so, how is your relationship with
him/her/them working for you?
Who are the main people in your life at It's not Could be better Working well
present (family, mates)? [please write their
names on the arrows] Are you having any major problems at
home? If yes, please state:
Are there any other things that the

doctor needs to know about you?
Who is your main support person?
What would you like the doctor to
What have been your best and worst life discuss with you?
events?
Please tick the boxes over the page ü
Figure 1. The ‘For Men Only’ Prompt List

]
‘For men only’ - A mental health prompt list in primary care n
Copyright © 2001: S. Brownhill & K. Wilhelm

University of New South Wales: Version 2:1 Your name: Age:
Take ‘in the past month’ as a guide, but some of YES NO

these issues may be over a longer time period. [Please tick ü]
Is work getting on top of you?
Are you coping with the demands of family life?
Have you had less interest or pleasure in doing things?
Do you use recreational drugs or alcohol to boost your mood or self — —

confidence?
If yes, is your use of drugs or alcohol becoming a problem for you — —

and/or your relationships?
Has anyone commented that you're not your 'normal' self?
Have you been wanting to be on your own, more than usual?
Have you been more angry, resentful, critical, or aggressive towards — —

other people or animals?
Do things easily trigger you to explode with anger or frustration?
Have you been doing things that are ‘out of character’?
Have you been thinking that things are becoming increasingly out of — —
your control?
Have you been taking risks that might injure yourself or others?
Have your sleeping patterns changed for the worse?
Have you been having more 'aches and pains' than usual?
Has your interest in sex decreased?
Have you been lacking energy or just couldn't be bothered?
Have your eating habits changed for the worse?
Have you been thinking a lot about regrets or sad events in — —

the past?
Have you been feeling down, depressed or hopeless?
Please hand to the doctor
Figure 2. Prompt List ‘Yes/No’ questions

of depression in men. The PL also acts as (why/why not?) and whether patients having children and, of those, most
a practical exercise or ‘something for men would change anything about the form (if (82.5%) reported their relationship with
to do’ while waiting to be seen by their yes, what changes?). Space was provided their children was ‘working well’. Most
doctor.5 This article reports the pre-test to allow these men to make additional nominated major life events related to
and evaluation of the PL in the context of comments about their personal experience work, family/relationships and health, and
primary care. of depression, coping or help seeking almost all (91.2%) of the men reported
beyond the scope of the set questions. they were ‘coping with the demands of
Method family life’.
GP postal questionnaire
Recruitment
General practitioners
General practitioners who had been The GPs’ postal questionnaire sought
involved in earlier research with the feedback on whether using the PL helped Fourteen GPs (10 women, 4 men) partici
authors were asked to allow access to doctors to build rapport, elicit extra infor pated in this study, representing five sites
male patients in their waiting rooms. The mation from patients, clarify in the inner west and eastern suburbs of
five practices’ receptionists played a vital understanding of patients’ current emo Sydney (NSW). Even after follow up,
role in recruiting male patients into the tional state, and provide any new only eight of the participating GPs
study. A large poster was displayed in the information about patients’ environment returned their questionnaires, a response
GPs’ waiting rooms and receptionists (relationships/support system/work satis- rate of 57%. Those eight GPs (6 women,
directed the men’s attention to it. The faction/home life). Other questions 2 men) have been in general practice for
male patients were invited to participate invited GPs to comment on any problems an average of 24.7 (SD: 5.1) years.
in the evaluation. For most, the response they had with the PL, to make sugges
Usefulness of the PL
was positive - some older men declined tions on improvement, and to recall any
(because they did not have their reading comments received from their patients Patient responses
glasses) even though they were interested. regarding the PL. Sixty percent of male patients found the PL
The completed forms were placed in the useful in raising issues with their doctor.
patient’s file for the doctor to view during Field notes Patient responses are outlined in Table 1.
the consultation. Field notes were collected detailing While only 60% of patients reported
observations of the interview process with the PL useful, qualitative data shed light
Evaluation
the patients, and are included in the on patients who did not find the PL
The evaluation of the PL was conducted Results section. useful. These were men who already had
using a self report (for men), a postal a good relationship with their doctor (the
questionnaire (for GPs) and field notes of Results doctor knows me/knows my history), or
the interviewer. The patient feedback The men were positive about the doctor’s consulta
questionnaire was completed postconsul Seventy-four men participated in this tion style (the doctor knows what to ask;
tation and the GPs’ feedback form mailed study. Their mean age was 50.3 (SD: at ease talking with the doctor). Other
back shortly thereafter. To ensure 19.02) years. Information derived from reasons given by patients for not (finding
minimal intrusion in terms of time taken, the PL provides a profile of male atten the PL useful) centred around the consul
the GPs’ form required minimal work dees. The majority rated their physical tation being straightforward (having a
(ticking boxes, adding comments) and a health as ‘good’ (52.3%). Ratings of ‘fair’, specific problem to raise, eg. skin, blood
reply paid envelope was provided. ‘excellent’ and ‘poor’ were 30.8%, 9.2% test, ‘sugar levels’), about commonsense
and 7.7% respectively. The majority rated issues or where there were no psychoso
Self report questionnaire their emotional health as ‘pretty good’ cial issues worth raising (not having a
A short questionnaire was completed by (58.5%). The next most common rating need, or not having issues or problems to
patients immediately after the consulta was ‘feeling great’ (20.0%), then ‘not bad’ raise, not being applicable, or not affected
tion. The first question sought patient (15.4%) and ‘lousy’ (6.2%). Most of the by symptoms of depression).
perception of whether the doctor had men were employed (63.1%), with an Field notes provided additional evalua
asked the ‘right’ questions to pick up average 11.1 (SD: 13.6) years spent in tive information from comments made by
symptoms of depression, and if not, what their present job; 75.6% were ‘fairly’ or the men. For example, the comments: ‘The
else needed to be asked; and whether the ‘very satisfied’ at work. Of the men who doctor can read the body signals of the
patient had told the doctor about bother had a partner (77.8%), most (82.2%) patient’ illustrates and reinforces the poten
some issues. They were also asked whether reported their relationship was ‘working tial ‘guesswork’ component to the
the form was ‘useful’ in raising issues well’. Most (67.2%) of the men reported consultation process.5 Another patient com-
‘For men only’ - A mental health prompt list in primary care n
time providing a safe, nonthreatening

Table 1. Patient responses to the PL
environment for men to raise and
He now knows some issues about me and he might be able to help me. respond to important issues.5 Men have
Prompted discussion that would not have been raised otherwise. their own barriers underpinned by the
Reminder, check list, thought beforehand about issues to be raised. belief that expressing emotion or prob
I felt obliged to mention current issues that otherwise I would probably have ignored. lems, or exposing their vulnerabilities is a
It clarified for myself and my doctor what was needed. ‘sign of weakness’2,5 so that the provision
To ensure I spoke openly about the way I have been feeling lately. of task orientated tools to facilitate this
I probably wouldn’t have raised specific queries with the doctor had I not been process may prove invaluable.
prompted. The comments by male patients and
Questions regarding the ‘best/worst’ things in life prompted discussion. their doctors emphasise the importance of
It was a good source of information about myself so the doctor could create friendly effective communication on both sides. In
conversation. this regard, the PL was designed to assist
The form supplies all the necessary questions that you would like to be asked. doctors to ask questions relevant to men,
Opens the ‘emotional floodgates’ to coin a phrase. Would promote honesty and and to assist men to self disclose. All GPs
reflection but in a nonconfrontational way. reported that the PL provided new infor
mation about their patients, and most of
the patients found it useful in ‘opening up’.
They ‘opened up’ about issues that they
Table 2. GP responses to the PL GP responses
may not otherwise have raised with their
All GPs reported the PL provided extra doctors. The PL may be beneficial overall,
Great
information and 71% reported it clarified but is likely to be of most benefit where
The language and layout was good. Easy
information about their patients. Most there is less familiarity and interpersonal
to fill out, easy to get info.
GPs (86%) found it useful in building ease between the doctor and the patient.
The question about ‘main people’ was
very revealing in most cases.
rapport with their patients and 71% The PL may be considered useful as
reported that using the PL made their job part of the move to a more patient centred
Valuable in new, unfamiliar patients.
easier. Supportive comments from GPs approach to health care delivery.22 It pro
The prompt list helped bring to mind new
issues about patients that I’ve been are outlined in Table 2. vides the opportunity for men to take
treating for years. Two problems were raised by GPs: responsibility for their health by giving
The PL is yet ‘another’ form to complete information to their GPs in a structured,
and too many responses on the back page nonthreatening format thus exposing sensi
can be daunting for the GP (even though tive issues that would normally have
mented that he had previously endured the PL was not designed to be completed remained ‘hidden’. The PL has the poten
three months of depression and felt that the by GPs), and it is another issue to field in tial to increase the mental health literacy of
PL ‘would have helped the doctor’ diagnose limited time (even though the PL was men by raising their awareness of such
his depression. He reported not wishing to designed to save GPs time in identifying issues and by providing access to a screen
ask for help, nor to see a doctor during his important issues). Despite these com ing instrument for such purpose. It also
depression despite losing 18 kgs over the ments, the GPs requested copies of the appears to narrow the gap of differing
period. Another issue raised was the PL to use with risk taking behaviours expectations of the consultation by provid
patient’s familiarity with their doctor (if you common to men. ing a focal point for discussion in line with a
know your doctor well then the form plays collaborative approach where patients are
no major part other than letting the doctor Discussion more proactive and informed. While the PL
pick up depression symptoms). Important Task orientated short consultations in covers symptoms of major depression, the
issues were more likely to be raised if the general practice (based on fee-for- aim is to promote a clinical conversation
doctor was seen as easy to talk to or having service) pose barriers to detection of about depression and possible precipitants
an easygoing style. Another comment, that depression in men. Despite this, recent and associated risky behaviours.
people can easily lie about the answers on research has demonstrated that the first
Changes to the PL
the PL, reinforces the view that men may two minutes are important to set the
under report lifestyle habits rather than scene for the consultation.21 It is, there The aim of this pre-test was to allow a
‘look bad’.5 Time constraint on the consul fore, important for doctors to engage men sample of male patients (for whom the
tation process was also raised. in a short space of time while at the same instrument was designed), to have some
input into its utility. The most consistent practitioners were offered additional copies of 13. Campion P, Butler N M, Cox AD. Principle
the PL for use with future male patients. agendas of doctors and patients in general
comment from male patients was about practice consultations. Fam Pract 1992;
the ambiguity of two Yes/No questions Acknowledgments 9(2):181-190.
that sought answers that related to 14. Ong L, de Haes J C J M, Hoose A M,
We thank the patients and GPs who
Lammes F B. Doctor-patient communica
‘change’ in behaviour, eg.: ‘Have you participated in the study, and Dr George
tion: A review of the literature. Soc Sci
been sleeping less, or more, than usual?’ Burkitt for helpful comments on the draft PL.
Med 1995; 40:903-918.
This study was supported by a NHMRC Grant
and ‘Has your interest in sex decreased or No. 993208. 15. Goldney R, Fisher L J, Wilson D H. Mental
health literacy: An impediment to the
increased?’ These questions were aimed
optimum treatment of major depression in
to elicit any ‘change’ in behaviour, but Conflict of interest: none declared. the community. J Affect Dis 2001;
have been misconstrued by users as 64:277-284.
Further reading 16. Glaser B, Strauss A L. The Discovery
‘either/or’ answers therefore not fitting
Morgan H. Depression in men. Aust Fam of Grounded Theory: Strategies for qualita
the Yes/No answer options. The GPs also Physician 2001; 30(30):206-217. tive research. London: Weidenfeld &
suggested that the same questions be Nicolson, 1967.
reworded to avoid ambiguity and the two References 17. Strauss A, Corben J. Basics of qualitative
research: Techniques and procedures for
questions have been modified accordingly 1. Burkitt G. Barriers to men consulting.
developing grounded theory. 2nd edn.
Clinical Skills in Men’s Health Conference.
(Figure 1). Newbury Park, California: Sage
Newcastle, New South Wales, 1999.
Publications, 1998.
2. Brownhill S, Wilhelm K, Barclay L, Parker
Limitations 18. American Psychiatric Association,
G. Detecting depression in men: A matter
Diagnostic and Statistical Manual of Mental
The patients and doctors in this study of guesswork. International Journal of
Disorders. IV edn. Washington, DC:
Men’s Health 2002; 1(3):259-280.
may have been particularly vigilant in 3. Jorm A, Korten A E, Jacomb PA,
American Psychiatric Association, 1995.
focussing on and talking about issues sur 19. Brownhill S, Wilhelm K, Barclay L, The
Christensen H, Rodgers B, Pollitt P. Mental
‘big build’: Men’s experience and expres
rounding depression. Despite this, the health literacy: A survey of the public’s
sion of depression. (in preparation).
ability to recognise mental disorders and
GPs found out more information about their beliefs about the effectiveness of
20. Hoff R, Bruce M L, Kasl S V, Jacobs S C.
their male patients, and male patients Subjective ratings of emotional health as a
treatment. Med J Aust 1997; 166:182-186.
risk factor for major depression in a com
offered additional information that would 4. Moller-Leimkuhler A. Barriers to help
munity sample. Br J Psychiatry 1997;
seeking by men: A review of sociocultural
otherwise not have been forthcoming. 170(2):167-172.
and clinical literature with particular refer
21. Pollack K, Grime J. Patients’ perceptions of
ence to depression. J Affect Dis 2002;
Conclusion 71:1-9.
entitlement to time in general practice
consultations for depression: Qualitative
We set out to pre-test and evaluate a 5. Heifner C. The male experience of depres
study. Br Med J 2002; 325:687-690.
sion. Perspect Psychiatr Care 1997;
screening instrument informed and 33(2):10-18.
22. Clark N, Gong M. Management of chronic
designed by men for men to overcome disease by practitioners and patients: Are
6. Tudiver F, Talbot Y. Why don’t men seek
we teaching the wrong things? Br Med J
some of the barriers in detecting depres help? Family physicians’ perspectives on
help seeking behaviour in men. J Fam
2000; 320:572-575.^^^H^^^R FP
sion in men in primary care. The PL has
Pract 1999; 48(1):47-52.
been found to break down some of those 7. Warren L. Male intolerance of depression:
barriers, particularly in guiding GPs to A review with implications for psychother
apy. Clin Psychol Rev 1983; 3(2):147-156.
ask questions relevant to men’s experi
8. Pollack W. The tortures of job: Diagnosing
ence and expression of depression, and by and treating hidden depression in older
assisting male patients to ‘open up’. The men. J Geriatr Psychiatry 1999;
positive responses from this small sample 32(2):195-222.
9. Ross S, Moffat K, McConnachie A, Gordon
suggest implementation of the PL on a J, Wilson P. Sex and attitude: A ran
larger scale. This includes modification of domised vignette study of the management
the PL for other groups including women, of depression by general practitioners. Br J
Genl Pract 1999; 49(438):17-21.
adolescents and cross cultural studies in
10. Salmon P, Peters S, Stanley I. Patients’ per
primary care. ceptions of medical explanations for
somatisation disorders: Qualitative analy
Ethical issues sis. Br Med J 1999; 318:372-376.
Correspondence
Approval for the pre-test and evaluation was 11. Anstett R. The difficult patient and the Suzanne Brownhill
granted from the University of New South physician-patient relationship. J Fam Pract
Caritas Centre
Wales Ethics Secretariat. Patients were given a 1980; 11:281-286.
Statement of Information that explained the 12. Arborelius E, Timpka T. Comparison of 299 Forbes Street
study and those willing to participate in the patients’ and doctors’ comments on video Darlinghurst, NSW 2010
study gave their informed consent. General recorded consultations. Scand J Prim
Email: sbrownhill@stvincents.com.au
Health Care 1991; 9(2):71-77.

eview
eet syndrome
A clinical review
Ravinder P S Makkar, MD, is Medical Advisor, Department of Medical Assistance, International
SOS, New Delhi, India.
Anju Arora, MD, is attending physician, Department of Medicine, Sitaram Bhartia Institute of
Science and Research, New Delhi, India.
Amitabh Monga, MD, is attending physician, Department of Medicine, Sitaram Bhartia Institute of
Ajay Kr Gupta, MD, is attending physician, Department of Medicine, Sitaram Bhartia Institute of
Surabhi Mukhopadhyay, MD, is attending physician Department of Medicine, Sitaram Bhartia
Institute of Science and Research, New Delhi, India.
BACKGROUND Burning pain in the feet has been known to occur as a distinct clinical symptom for
almost two centuries. Despite being a common and fascinating clinical entity, this syndrome has
received scant attention in the medical literature and has been described only in anecdotal reports.
OBJECTIVE This article describes and discusses the various aspects of this intriguing syndrome.
DISCUSSION Burning feet syndrome (BFS) is a common disorder especially among the elderly and
is frequently encountered in general practice. There is no specific aetiology and it can occur as an
isolated symptom or as part of a symptom complex in a variety of clinical settings. In contrast to
the presence of distressing subjective symptoms, the physical examination is marked by a paucity
of objective signs. The pathophysiology of BFS is not very clear and treatment varies depending on
the aetiology.
urning feet syndrome (BFS), which is be divided into the following categories ciency related neuropathy before frank
B characterised by a sensation of
burning and heaviness in the feet and
(Table 1). neurological signs appear.8 No other vita
mins apart from the B-group have been
Nutritional causes
lower extremities, is a common disorder implicated in the cause of BFS.
frequently encountered by general practi Since its initial descriptions,1-3 BFS has Other conditions associated with
tioners. In the past, this syndrome has been postulated to be caused by vitamin vitamin deficiencies such as chronic alco
been described only in anecdotal reports deficiency. The specific vitamin, however, holism, or patients on chronic
and has received scant attention in the remains obscure, the deficient factor hemodialysis, can develop BFS possibly
medical literature. Grierson1 was, in 1826, being variously attributed as riboflavin2,3 due to associated nutritional deficiencies.8
the earliest to document such a symptom, nicotinic acid,4 thiamine,5 and pyridoxine.6
Metabolic or endocrinal causes
but a detailed description was given by Most patients with burning feet show evi
Gopalan2 in 1946, hence, BFS is also dence of riboflavin deficiency.7 Burning feet is commonly seen with dia
known as Grierson-Gopalan syndrome. It is suggested that vitamin B defi betes. Patients with signs and symptoms
ciency leads to disturbance in cellular of burning feet may be part of diabetes
What causes ‘burning feet’? metabolism in the tissues causing accumu related small fiber or autonomic neu
There is no specific aetiology for BFS. lation of intermediate metabolites which ropathies.9 The development of this
It can occur as an isolated symptom or as may cause abnormal and excessive stimu symptom in diabetics is related to some
part of a symptom complex in association lation, or lower the pain and temperature extent to the severity and duration of the
with a variety of unrelated clinical set threshold of peripheral sensory nerve disease. Functional or organic abnormali
tings. Based on the underlying endings.2 It is also thought that BFS is an ties may be present in small
mechanism, the various causes of BFS can early clinical phase of vitamin B12 defi unmyelinated-C fibers.13 The dysfunc
1006 • Reprinted from Australian Family Physician Vol. 31, No. 12, December 2002
Burning feet syndrome — a clinical review n
tional phase can precede organic struc characterised by burning pain and redness
Table 1. Causes of BFS
tural damage and symptoms may develop of the extremities and may be primary or
without signs of overt neuropathy. secondary to systemic disorders such as Nutritional
Burning feet can also occur in other diabetes, collagen vascular disorders, or • Vitamin B deficiency
endocrine disorders such as hypothy myeloproliferative disorders such as poly • Malabsorption syndrome
roidism, though the mechanism is not cythemia vera or essential thrombo- • Chronic alcoholism
completely understood. cytosis.16 The symptoms of this disorder Metabolic/endocrinal
are probably related to intravascular • Diabetes mellitus
Hereditary • Renal failure (dialysis patients)
platelet aggregation and may involve a
• Hypothyroidism
Familial disorder with an autosomal hyperactive axon reflex in C-nociceptive
dominant inheritance may cause BFS.11 fibers or a mutation of the capsaicin Hereditary
• Autosomal dominant BFS
The clinical picture is that of bilateral receptors.17
symmetrical pain with no muscle weak Other unrelated and less common Mechanical (entrapment neuropathies)
ness, atrophy or foot deformity. Initially, conditions with symptoms of burning feet • Tarsal tunnel syndrome
• Traumatic nerve compression
it was thought that BFS may be the sole are chronic mountain sickness,18 leishma-
manifestation of an hereditary sensory niasis,19 Gitelman syndrome20 (a rare renal Psychosomatic
neuropathy (HSN), but subsequently, tubular disorder), and carnitine deficiency Miscellaneous
molecular genetic studies excluded state.21 Patients who do not reveal any • Erythromelalgia
linkage to HSN locus on chromosome abnormalities even after exhaustive labo • Chronic mountain sickness
• Gitelman syndrome
9q22 and 3qi3-q22.12 Therefore, it is ratory investigations are usually labelled
• Leishmaniasis
concluded that autosomal dominant idiopathic. • Multiple sclerosis
burning feet represents a distinct clinical
Clinical features Idiopathic
entity in itself.
Although no geographical or seasonal
Mechanical causes
variation is known, BFS has been mainly
Burning feet syndrome may occur as a reported in Asian and Far East countries
result of mechanical compression of the during a hot summer.3-5 It is most
peripheral nerves (as seen in tarsal tunnel common in those over 50 years, although warm overlying skin as in erythromelal-
syndrome) and in diseases such as it can occur in any age group. Usually dis gia.16 There is no local tenderness over the
hypothyroidism, diabetes and rheumatoid carded by physicians as vague and affected parts. Neurological examination
arthritis. Nerve entrapment can occur at unimportant, the symptoms characterised is essentially normal in most patients but
the level of the tarsal tunnel adjacent to by a burning sensation, heaviness, numb some may show a varying degree of hypo-
the medial malleolus. Nerve entrapment ness, or a dull ache in the feet, can be or hyper-aesthesia.9 Knee and ankle jerks
due to sciatic mononeuropathy and spinal extremely distressing to the patient. show normal to brisk reaction, but are
arteriovenous malformation can also Burning is usually limited to the soles of never absent or diminished.2-4 There are
cause burning feet.13,14 the feet but may ascend to involve the no signs of upper motor neuron involve
dorsum, ankles or lower legs. The arms ment such as extensor plantars or
Psychosomatic causes
and palms of the hands are spared. A few increased tone. Motor power is main
Burning sensations and paraesthesia are patients occasionally complain of ‘pins tained and there is no atrophy or wasting
among the commonest psychosomatic and needles’ or tingling in the lower of the overlying muscles.
symptoms encountered in the general extremities. Most nutritionally deficient patients
population. In a study by Keshavan et al,15 Symptoms show worsening at night develop signs and symptoms of burning
although many patients with burning feet with day time improvement. Patients with feet after approximately 4-5 months of
had evidence of peripheral neuropathy, underlying psychiatric disorders may deficient diet. Skin manifestations of
few also had psychological disorders. present with a myriad of psychosomatic vitamin deficiency such as scrotal der
signs and symptoms in association with matitis or pellagra-like rash can precede
Miscellaneous causes
burning feet. On examination, there is a the onset of burning sensation in the feet.
Burning feet symptoms have also been paucity of objective signs. The overlying Some patients develop retrobulbar neuri
reported in various unrelated clinical con skin and blood vessels are normal in tis as a part of vitamin deficiency
ditions. Erythromelalgia, also known as most, while in some patients there may be syndrome.3 Physical examination may be
erythermalgia, is an uncommon disorder accompanying erythema of the feet with entirely normal, as in familial BFS.12
Reprinted from Australian Family Physician Vol. 31, No. 12, December 2002 • 1007
n Burning feet syndrome — a clinical review
Approach to the patient

Table 2. Useful diagnostic studies in BFS
with burning feet
As burning feet can occur in a wide spec Suspected clinical condition Test
trum of disorders, the approach to such a In all patients Complete blood count and red blood cell
patient is not simple. A thorough clinical indices, routine biochemistry
history and examination regarding nutri Vitamin B deficiency or malnutrition Serum levels of B group of vitamins like
tional status, vitamin deficiencies, and thiamine, riboflavin, and cyanocobalamin
metabolic disorders such as diabetes and Tests for malabsorption
Malabsorption syndrome (chronic
hypothyroidism, and a detailed family
diarrhea, postgastric surgery) Oral glucose tolerance test
history are required in determining
Diabetes (if signs/symptoms or risk factors
further investigations. Diagnostic tests are for diabetes are present) Thyroid function tests (T3, T4, TSH)
shown in Table 2. Although patients with Hypothyroidism Platelet count, bone marrow aspiration
burning feet should be evaluated for a sec Erythromelalgia (to rule out myeloproliferative diseases
ondary cause, an underlying psycho such as essential thrombocytosis or
somatic illness as the cause of the symp polycythemia vera)
toms should be ruled out by psychiatric Serum and urine electrolytes
assessment. Gitelman syndrome (young patients with (magnesium, sodium, potassium and
fatigue, muscle weakness, cramps and chloride)
Treatment fasciculations or simply asymptomatic
hypokalaemia) Electrophysiological studies (nerve
Treatment of BFS depends on the cause. conduction velocities, electromyography
Neuropathy, if present or strongly
Management can be divided into general suspected or nerve biopsy)
and disease specific measures. Molecular genetic studies
Familial inheritance Imaging studies such as MRI or CT
General measures
Mechanical cause (entrapment
General treatment for all cases of BFS neuropathy)
includes reassurance about the benign
nature of the disorder. Wearing open and
comfortable shoes, especially those with
arch supports, and wearing cotton socks is
Table 3. Suggested treatment regimen for BFS with injectable
vitamin B preparations
helpful. Soaking the feet in cold water
(not ice cold) for around 15 minutes can
Vitamin Dose and duration
bring symptomatic temporary relief.
Avoidance of feet exposure to heat Riboflavin 6-10 mg intramuscularly for 2-3 weeks
should be advised. Tricyclic antidepres Thiamine 50-100 mg intramuscularly for 2-3 weeks
sants or membrane stabilising agents such Pantothenate 20-40 mg intramuscularly for 2-3 weeks
as carbamazepine or gabapentin may be
Nicotinic acid 100 mg intramuscularly for 2-3 weeks
used for symptomatic relief.
Cyanocobalamin 1000 pg 3-4 times a week for one week followed by
Disease specific measures twice a week for another week
As most cases of BFS occur as a conse
quence of malnutrition or vitamin
deficiency, it is important to elucidate nitroglycerine therapy may alleviate pain feet, orthotics may help restore the foot’s
which particular vitamin is responsible and burning.22 In erythromelalgia, treat arch. If inflammation of the nerve is
for the condition. A suggested vitamin B ment with aspirin typically produces causing the compression, nonsteroidal
treatment regimen is shown in Table 3 if rapid but short lived relief of symptoms. anti-inflammatory drugs (NSAIDs) may
a deficiency is detected. In patients with Elevation, cooling of limbs and systemic be prescribed. In patients where pain is
diabetes, small doses of insulin in addi analgaesia may be helpful. In mechanical not relieved by NSAIDs, local injectable
tion to oral hypoglycaemic agents, cases such as tarsal tunnel syndrome, steroids may be beneficial. Surgical
adequate calories and vitamin supple conservative treatment with arch sup decompression to relieve nerve entrap
ments are helpful. Local application of ports and wider shoes may successfully ment may be needed if conservative
capsaicin ointment and percutaneous relieve discomfort. If BFS is due to flat measures fail.
1008 • Reprinted from Australian Family Physician Vol. 31, No. 12, December 2002
Burning feet syndrome — a clinical review n
1999; 67(1):78-81.
Conclusion 13. Galer B S, Lipton R B, Kaplan R, Kaplan J
G, Arezzo J, Portenoy R K. Bilateral
Burning feet is a common complaint burning foot pain: Monitoring of pain, sen
especially in the elderly and can occur in sation and autonomic function during
successful treatment with sympathetic
a variety of unrelated clinical settings.
blockade. Pain Symptom Manage 1991;
Common causes include diabetes melli 6(2):92-97.
tus, psychosomatic disorders and various 14. Sethi P K, Kakar A, Sethi N K. Burning feet
syndrome as the presentation of spinal
vitamin deficiency states, rarely ery-
arteriovenous malformation. J Assoc
thromelalgia or familial disorder. Physicians India 2001; 49:586-587.
Mechanism involves vasomotor distur 15. Keshavan M S, Isaac, Kapur R L. Ill defined
bances or altered pain and temperature somatic symptoms in a South Indian rural
clinic. Some preliminary clinical observa
threshold of peripheral sensory nerve tions. Trop Geogr Med 1980;
endings. Treatment depends on the spe 32(2):163-168.
cific aetiology and includes injectable 16. Kurzock R, Cohen P R. Erythromelalgia;
review of clinical characteristics and
vitamin B preparations, membrane stabil
pathophysiology. Am J Med 1991;
ising agents and cooling measures. 91(4):416-422.
Conflict of interest: none declared. 17. Layzer R B. Hot feet: Erythromelalgia and
related disorders. J Child Neurol 2001;
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21. Cornelio F, Peluchetti D, Remold M, Testa
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drome. Case due to malabsorption and
cal study. Acta Neuropathol Suppl 1981;
responding to riboflavin. BMJ 1970;
7:226-229.
702(2):151-152.
22. Lewis G B. Local percutaneous nitroglyc
P
8. Mathur J G. Burning feet syndrome (letter).
erine therapy for burning feet syndrome
Med J Aust 1980; 2(13):733.
(letter). Med J Aust 1987; 1469(1):56.ff
9. Oda K, Ono Y, Noro H, Kudo M,
Nakayama H, Nagakawa S. Prevalence of
autonomic disturbances in diabetics as
compared with nondiabetics and healthy
subjects. Tohoku J Exp Med 1 983;
141:447-451.
10. Vinik A I, Erbas T, Stansberry K B,
Pittenger G L. Small fiber neuropathy and
neurovascular disturbances in diabetes
mellitus. Exp Clin Endocrinol Diabetes
2001; 109(Suppl 2):S451-S473.
11. Dyck P J, Low P A, Stevens J C. Burning
feet as the only manifestation of domi
nantly inherited sensory neuropathy. Mayo
Clin Proc 1983; 58(7):426-429.
12. Stogbauer F, Young P, Kuhlenbaumer G, et
Correspondence
al. Autosomal dominant burning feet syn
drome. J Neurol Neurosurg Psychiatry Email: makkar_r@yahoo.com
Reprinted from Australian Family Physician Vol. 31, No. 12, December 2002 • 1009
Forensic series • CLINICAL PRACTICE
Writing a police
statement
Helen Louise Parker, MBBS, FACEM, DMJ (clin), is a forensic physician, Division of Clinical
Forensic Medicine, Victorian Institute of Forensic Medicine, and emergency physician, Western
Hospital, Footscray, Victoria.
BACKGROUND Police statements ment of a deceased patient is sought. In this

Requests for police statements regarding a instance, consent for release of the report is
patient’s medical condition or injuries are
Responding to a request not required and an opinion is not appropri
common. A lack of training in their Police may request statements from doctors ate. Many of the following principles
preparation, coupled with ignorance as to for a variety of reasons, but most commonly regarding the preparation of a statement still
their fate, combine to make the task one they are requested when a person has apply however. An important difference is
which is generally viewed as a necessary sought treatment for injuries sustained in an that the doctor’s performance may be
paperwork evil. assault. The request may be in writing or may subject to criticism, thus it is wise to notify
be verbal. It may be a very general request to one’s medical defence provider of the
OBJECTIVE ‘provide a statement regarding injuries’ or request and have them review the statement
This article aims to provide practical may in fact contain a specific issue to be before its release.
guidelines and a suggested format for use addressed. The doctor should receive written
Format for statements
when preparing a police statement. specific consent from the patient (or the
patient’s legal guardian) before releasing the All police statements should be typed rather
DISCUSSION statement to police. The statement will form than handwritten, and it is preferable that
Police statements prepared by medical part of the police ‘brief of evidence,’ which they appear on a professional letterhead, or
practitioners are important documents contains all the information on which the at least contain the professional contact
whose intended audience is overwhelmingly police base their case against the accused. It details of the author.
nonmedical. A small time investment made is a legal requirement that the accused Many advocate the use of a structured
in the preparation of a concise, objective person’s legal representative receives a copy format when preparing a police statement,1-3
report in language likely to be understood of the ‘brief’. This is important to bear in and this has benefits for the recipient includ
by the lay person will assist the courts in mind when sensitive medical information ing ease of locating particular information. A
understanding complex medical issues and may form part of the statement. It is also structured, well presented report conveys a
may obviate the need for the doctor to important to note that consumers of these professional image of its author, and, if a pro
appear in court as a witness. A structured statements are laypersons - police officers, forma is used, it has the additional benefits of
statement ‘proforma’ can be readily lawyers, the judiciary and jurors. saving time in preparation and prompting the
customised and will both reduce time in Another common request for a statement author to include all relevant information.4
preparation of reports and serve as a is that made on behalf of a coroner, in which It is important to distinguish information
prompt for inclusion of essential details. a doctor’s role in the assessment and treat- that is factual from that which is opinion.
Reprinted from Australian Family Physician Vol. 33, No. 11, November 2004 ► 927
Clinical practice: Writing a police statement
Figure 1. Example of a police statement
Smithtown Family Clinic

1 Parkside Way
Smithtown 3006
Ph 9684 4480
Fax 9684 4481
3rd February 2004
Detective Senior Constable Plodd
Smithtown Criminal Investigation Unit
122 Smith’s Road
Smithtown 3006
Re: Mr John Smith DOB: 13th January 1970
I, Mary Nicole Brown of the Smithtown Family Clinic, 1 Parkside Way Smithtown
Hereby state that:

I am a medical practitioner registered in the state of Victoria.
I hold the qualifications of Bachelor of Medicine and Bachelor of Surgery conferred in 1988, and Fellowship of the
Royal Australian College of General Practitioners conferred in 1996. I have worked in the capacity of a general practi
tioner in both rural and metropolitan practice since 1992.
Background
I have received a request from Detective Plodd to detail the injuries received by Mr Smith as a result of an alleged
assault on him on Saturday 12th January 2004. In particular he has asked whether Mr Smith’s head wound could
have ‘resulted from being struck with a baseball bat or could have occurred when he fell to the pavement’. I exam
ined Mr Smith at this clinic on Tuesday 15th January 2004, 3 days after he was allegedly assaulted, and again on
Monday 21st January 2004 to remove his sutures.
I have been provided with a signed consent form from Mr Smith for the release of this report to police. This report
has been prepared from:
• my clinical notes made at the time of the examination
• a letter from the Smithtown Hospital Emergency Department.
History
Mr Smith told me that he had been assaulted on the previous Saturday night (ie. 3 days before the consultation). He
said he was unable to recall much of what had occurred as he had consumed a considerable amount of alcohol. He
stated the following to me:
• he was in a queue outside a nightclub and was shoved from behind
• he turned around and verbally abused the male standing behind him and that male punched him in the face
• he recalled being on the ground and thinks he was struck on the head with a baseball bat
• he was taken to hospital by ambulance.
The letter from the hospital indicated a wound on his scalp was sutured.
Mr Smith attended here requesting review and documentation of his injuries, and a medical certificate for work.
There is no past medical history of relevance to this allegation.
Symptoms of recent injury

Mr Smith complained of headaches and indicated his injuries to me.
Examination
Mr Smith’s upper torso only was examined. He appeared of normal intellect and had a composed demeanour.
928 ◄ Reprinted from Australian Family Physician Vol. 33, No. 11, November 2004
Signs of recent injury

Head
Injury no 1: extensive blue and black bruising surrounding the left eye. In association there was a bruise
involving the white of the eye (subconjunctival haemorrhage). He reported no visual disturbance.
Injury no 2: a sutured irregular ‘Y’ shaped wound was present on the back of the head (occiput). It was
approximately 5 cm in its total length and had dried scab over it.
Investigations
The CT brain performed at Smithtown Hospital was reportedly normal.
Treatment and follow up
Mr Smith was provided with written advice regarding the effects of concussion and advised to use simple
analgesics such as paracetamol for his headache. His sutures were removed from his scalp wound on
Monday 21st January. At that time his black eye was significantly reduced in size.
Opinion
In summary, Mr Smith is a 34 year old man whom I examined 3 days following an incident in which he was
allegedly punched to the face and possibly struck with a baseball bat. He had evidence of a black eye and a
sutured wound on the back of his scalp. With respect to the findings I am of the opinion that:
1. The bruise around the eye is the result of blunt trauma:
• blunt trauma may result from a blow or forceful contact with an object
• it is impossible to accurately age a bruise, however that observed could have occurred within the time
frame of the alleged incident
• it is not possible to state more precisely the cause of this bruising around the eye. It may have resulted
from a punch, however other mechanisms are plausible
• this injury should fully resolve leaving no permanent sequelae, however, a blow to the eye has the
potential to result in permanent serious visual impairment.
2. The sutured wound had the appearance of a laceration, due to the application of blunt trauma to the
region causing the skin to split:
• it had the appearance of a relatively recent wound and could have occurred within the time frame of the
incident
• it is not possible to state more precisely the exact cause of this wound, and in particular I am unable to
differentiate between a fall onto the pavement versus a blow with a baseball bat as the cause. The
doctor who initially treated Mr Smith and sutured his wound may be able to assist you further with this
inquiry
• this wound should heal, leaving a scar that will be barely visible under the hair.
Dr Mary Nicole Brown

MBBS, FRACGP
I hereby acknowledge that this statement is true and correct and I make it in the belief that a person
making a false statement in the circumstances is liable to the penalties of perjury.
Mary N Brown
Acknowledgement taken and signature witnessed by me at 3 pm,

On 6th February 2004
at Smithtown
Signature P Plodd ____________________________________________
Name Peter Plodd____________________________________________
Rank/No D/S/C 31268 _________________________________________
Reprinted from Australian Family Physician Vol. 33, No. 11, November 2004 ► 929
Medical evidence is frequently complex and disease, this may affect the extent of any beyond his or her area of expertise and
requires interpretation for the courts to bruising observed). should not be afraid to refrain from offering
understand its role in a particular case. For an opinion if he or she feels unable to do so.
Examination
this reason, doctors are frequently asked to
express their opinion, which is considered Include the extent of the examination and
The final check
‘expert’ evidence, as distinct from evidence any limitations encountered. A comment Having completed the statement, it is wise to
of fact that is the more usual form of evi regarding the patient’s intellect and check that spelling, names and dates are
dence. demeanour is often appropriate. List the correct. Enlisting the assistance of a col
physical findings in an orderly fashion, league to read over the statement is
Elements of the statement grouped by body region. It is often useful to invaluable for checking its clarity. A copy of
The following is a list of items and headings number each finding particularly when the statement should be kept with the
for inclusion in a statement. Figure 1 gives an several injuries exist - this allows ready refer patient file and the original sent to the
example of a completed police statement. ence in your opinion later in the statement, requesting officer.
and also in any subsequent court appearance. Statements generally require the addition
Addressee
Include any relevant negative findings. Use of a ‘jurat’ before they can be tendered as
The name of person who requested the report. lay terminology (you may include medical ter evidence. The requirements vary between
minology in brackets). jurisdictions, but essentially require the state
Date of preparation of the statement
ment’s author to sign in the presence of a
Investigations and specimens
Patient’s name and date of birth designated person a declaration that the con
Do not include the patient’s address - as If investigations were performed or speci tents of the statement are true and correct.
already stated, a copy of your report may be mens taken, detail why they were done and The requesting police officer can assist in this
provided to the other party’s legal practi what they showed, again, in lay terms. For requirement.
tioner. specimens, detail their handling if required
for evidentiary purposes (eg. glass fragments Summary of important points
Qualifications
removed from a wound and handed to
Give a brief account of your professional police). • Ensure that you have specific written
qualifications and experience as a medical consent from your patient before release
Management
practitioner. of a police statement.
Describe what treatment if any was required • Use terminology that will be understood
Background
including referrals to other health care by a lay audience.
Briefly describe how you came to be prepar providers. Indicate if treatment is ongoing. • Any opinion expressed should be clearly
ing the statement. This should include the delineated as such and must be objective,
Opinion
date, time and place of the consultation, the impartial and based on the facts contained
reason for it, and the nature of the request It is useful to provide a very brief summary of within the statement.
for the statement. You should acknowledge the allegations and principle findings here,
all sources of information used in its prepara particularly if the report is quite lengthy. Conflict of interest: none declared.
tion (eg. your contemporaneous notes, X-ray Follow this with your opinion about the
References
and pathology reports) and that appropriate observed findings. In simple terms, courts
1. Young S, Wells D. The medicolegal report in
consent has been obtained for the release of frequently seek the following information:
emergency medicine. Emerg Med
the statement. • how and when the injury/injuries could 1995;7:233-236.
have been caused 2. Paul D. Writing medicolegal reports. BMJ
History 1981;282:2101-2102.
• how severe the injuries were, and
3. Bird S. How to write a medicolegal report. Aust
Detail the history regarding the incident that • whether the injuries could have occurred Fam Physician 2004;33:66-67.
you obtained from the patient. Indicate if pos in the manner alleged, and what alterna 4. Parker H, Kelly A, Wells D. Improving the
quality of hospital generated police reports
sible what was offered spontaneously, what tive explanations are possible.
using a structured proforma. Emerg Med
was said verbatim, and what you ascertained The opinion should be objective and impartial, 2000;12:317-321.
in response to specific questioning. A brief and based on the facts described earlier in
description of any relevant medical history the statement. Consideration should be given
would be appropriate (eg. if a patient is taking to any possible alternative explanations for Correspondence
aspirin or warfarin, or if they have liver the findings. The author should not stray
930 ◄ Reprinted from Australian Family Physician Vol. 33, No. 11, November 2004
■ Email: helenp@vifm.org
Prescribing drugs of dependence
RACGP in general practice, Part B
Benzodiazepines
www.racgp.org.au Healthy Profession.

Healthy Australia.
Prescribing drugs of dependence in general practice, Part B - Benzodiazepines
Disclaimer
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.
Prescribing drugs of dependence in general practice, Part B - Benzodiazepines. Melbourne: The Royal Australian
College of General Practitioners, 2015.
Published by
East Melbourne Victoria 3002 Australia
Tel 1800 473 247

Fax 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-430-6
Published June 2015

Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
i
Foreword
Benzodiazepines have a chequered clinical history and continue to produce polar opinions in the medical
community. Benzodiazepines have been associated with both benefits and harms for patients, and a clear
guide for accountable prescribing has been requested from multiple agencies.
Drug therapies will only ever have a partial role in managing complex bio-psychosocial issues that
characterise mental health care. In the modern health environment, we have to explore and use non-drug
therapies, and redefine the place of existing medications.
This guide represents a synthesis of the best available evidence for benzodiazepine use in the primary
care setting. Consistent with all medications, prescribing benzodiazepines requires clear patient selection
and ongoing clinical monitoring to optimise outcomes. The risk-benefit ratio of benzodiazepines changes
considerably with concomitant psychoactive drugs, or comorbid alcohol or substance abuse or misuse.
In completing this guide, we acknowledge the work of the key advisers and reviewers, and the many people
who have provided constructive feedback.
The Royal Australian College of General Practitioners (RACGP) welcomes feedback on this guide to
continually improve services at the general practice level. Please use the feedback section on our website
to help co-create this guide.
ii Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
Acknowledgements
The RACGP gratefully acknowledges the generous contribution of the following authors and reviewers of
the RACGP’s Prescribing drugs of dependence in general practice, Part B - Benzodiazepines.
Clinical editor
Dr Evan Ackermann, Chair, RACGP National Standing Committee for Quality Care; University Medical
Centre, Southern Cross University, Queensland
Medical writer
Raquel Newman
Reviewers
Dr Caroline Johnson, Department of General Practice, the University of Melbourne, Victoria; RACGP
National Standing Committee for Quality Care
Dr Simon Holliday, General Practitioner, Taree, New South Wales; Staff Specialist, Drug and Alcohol Clinical
Services, Hunter New England Local Health District, New South Wales
Dr Walid Jammal, Senior Medical Advisor, Avant; Clinical Lecturer, University of Sydney
Dr John Buchanan, Consultant Psychiatrist, Melbourne
Thank you to the following organisations, groups and individuals for feedback and advice:
NPS MedicineWise
Australian Medical Association
RACGP National Standing Committee for Quality Care
RACGP National Standing Committee for Standards
RACGP National Standing Committee for General Practice Advocacy and Support
RACGP Victorian Faculty, Drug and Alcohol Committee
RACGP Queensland Faculty
RACGP South Australia & Northern Territory Faculty
RACGP National Faculty of Aboriginal and Torres Strait Islander Health
RACGP National Rural Faculty
RACGP National Faculty of Specific Interests - Addiction Medicine Network
RACGP National Faculty of Specific Interests - Pain Management Network
RACGP National Faculty of Specific Interests - Aged Care Network
RACGP National Faculty of Specific Interests - Psychological Medicine Working Group
Dr Beres Joyner, General Practitioner, Rockhampton, Queensland; RACGP National Faculty of Specific
Interests - Aged Care Network
Janet Shaw, Manager, Reconnexion, a Service of EACH, Victoria
Dr Sara Bird, Manager, Medico-legal and Advisory Services, MDA National
Dr Mike Civil, Chair, RACGP National Standing Committee for Standards
Dr Jenny James, Substance Misuse Medical Coordinator, Aboriginal Medical Service Western Sydney
Karen Booth, RN, President, Australian Primary Health Care Nurses Association
Benzodiazepines
iii
Dr Mark E Montebello, Senior Staff Specialist and Medical Team Manager, Drug and Alcohol Service, South
Eastern Sydney Local Health District
Peter Boyles, Pharmaceutical Services Branch, Department of Health and Human Services, Tasmania
Dr Adrian Reynolds, Clinical Director, Alcohol and Drug Service, Southern Mental Health and Statewide
Services, Tasmania; Clinical Associate Professor, University of Tasmania
Dr Noel Plumley, Addiction Medicine Specialist, Tasmanian Alcohol and Drug Services
Dr Richard O’Regan, Addiction Medicine Consultant, Drug and Alcohol Office North Metro Community Drug
Service, Department of Health, Western Australia
Dr Chris Holmwood, Director, Clinical Consultation Liaison and Standards, Drug and Alcohol Services,
South Australia
Dr Stephen Christley, Public Health and Clinical Systems, Department for Health and Ageing, Government
of South Australia
Dr Adam Pastor, General Physician and Addiction Medicine Specialist; Director, Addiction Medicine,
Northern Territory
Dr Malcolm Dobbin, Senior Medical Advisor (Alcohol and Drugs), Mental Health, Drugs and Regions
Division, Department of Health, Victoria
Drugs of Dependence Unit, Pharmaceutical Services Branch, Department of Health, Western Australia
Drugs of Dependence Unit, Medicines and Technology Policy and Programs, Department for Health and
Ageing, South Australia
Medicines and Poisons Control, Department of Health, Northern Territory
Pharmaceutical Services Unit, Legal and Regulatory Services Branch, New South Wales Ministry of Health
Medicines Regulation & Quality, Department of Health, Queensland
Pharmacy Board of Australia
Australian Health Practitioner Regulation Agency
Consumers Health Forum of Australia
The Royal Australasian College of Physicians
Laureate Professor Nicholas J Talley, President, The Royal Australasian College of Physicians
Brigitte Cusack, Program Officer, Medication Management, Eastern Sydney Medicare Local
Dr Tim Senior, Chair, RACGP National Faculty of Aboriginal and Torres Strait Islander Health
Dr Ronald McCoy, Education Strategy Senior Advisor, RACGP
Dr Michael Wright, General Practitioner, RACGP National Standing Committee for General Practice
Advocacy and Support
Dr Andrew Byrne, General Practitioner, Redfern, New South Wales
Dr Dennis Gration, General Practitioner, Belgrave, Victoria
Dr John Scopel, General Practitioner, RACGP National Faculty of Specific Interests - Refugee Health Network
Dr Glynn Kelly, Deputy Chair, RACGP National Standing Committee for Standards
Dr Margaret Daley, Advisor, Medical Indemnity Protection Society
Dr Genevieve Hopkins, General Practitioner, Red Hill, Queensland
Dr Brendan Kay, General Practitioner, Warrnambool, Victoria
Dr Michael Tan, General Practitioner, Blacktown, New South Wales
Dr Paul Neeskens, General Practitioner, Board Member, RACGP Queensland Faculty
Dr Cameron Loy, General Practitioner, Deputy Chair, RACGP Victorian Faculty

iv Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
Acronyms
ADIS Alcohol and Drug Information Service
ATODS Alcohol, tobacco and other drugs
AUDIT Alcohol Use Disorders Identification Tool
AWS Alcohol Withdrawal Scale
CAS Clinical Advisory Service
CBT Cognitive behavioural therapy
CIWA-Ar Clinical Institute Withdrawal Assessment of Alcohol State, revised
CNMP Chronic non-malignant pain
CNS Central nervous system
DACAS Drug and Alcohol Clinical Advisory Service
DASAS Drug and Alcohol Specialist Advisory Service
DSM Diagnostic and Statistical Manual of Mental Disorders
GABA Gamma-aminobutyric acid
GAD Generalised anxiety disorder
GP General practitioner
ICD International Classification of Disorders
IDRS Illicit Drug Reporting System
IDU Injecting drug use
MOAI Monoamine oxidase inhibitors
MED Morphine equivalent dose
NHS National Health Service
NPS National Prescribing Service
OCD Obsessive compulsive disorder
OHS Occupational health and safety
OTC Over the counter
PBS Pharmaceutical Benefits Scheme
PSIS Prescription Shopping Information Service
PTSD Post-traumatic stress disorder
S4 Schedule 4
S8 Schedule 8
SAD Social anxiety disorder
SADQ Severity of Alcohol Dependence Questionnaire
SNRI Serotonin-norepinephrine reuptake inhibitor
SSRI Selective serotonin reuptake inhibitor
SUD Substance use disorder
SUSMP Standard for the Uniform Scheduling of Medicines and Poisons
TCAs Tricyclic antidepressants
US United States of America
Benzodiazepines
v
Contents
Foreword i
Acknowledgements ii
Acronyms iv
Summary of recommendations ix
Wording of key principles and recommendations ix
Key principles ix
Treatment of insomnia x
Treatment of anxiety disorders xi
Treatment for alcohol withdrawal xi
Discontinuing benzodiazepines xi
1. Introduction 1
1.1 Aims 1
1.2 How to use this guide 2
1.3 Why do we need this guide? 2
1.3.1 Issues surrounding benzodiazepines 2
1.3.1.1 Variations in prescribing 2
1.3.1.2 Questions about over prescribing 2
1.3.1.3 Questions about safety of prescribing 4
1.3.1.4 Increasing awareness of problematic use, including misuse 6
1.3.2 The factors involved 6
1.3.2.1 Source of benzodiazepine misuse 6
1.3.2.2 Benzodiazepines are often combined with other drugs 7
1.4 Clinical pharmacology of benzodiazepines 7
1.4.1 Properties 7
1.4.2 Speed of onset 7
1.4.3 Metabolism and duration of activity 9
1.4.4 Tolerance 9
1.4.5 Equivalent dosages 10
1.5 Adverse effects of benzodiazepines 10
1.5.1 Adverse effects on mental health and functioning 10
1.5.1.1 Cognitive impairment 10
1.5.1.2 Anxiety 10
1.5.1.3 Depression 10
1.5.1.4 Paradoxical stimulation and disinhibition 10
vi Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
1.5.2 Dependence, withdrawal syndrome and problematic use 11

1.5.2.1 Dependence - A contemporary understanding 11
1.5.2.2 Withdrawal syndrome 11
1.5.2.3 Incidence of withdrawal symptoms 11
1.5.2.4 Cravings and reinforcement 12
1.5.2.5 The spectrum of problematic use 12
1.5.2.6 Low-dose or therapeutic-dose dependence 12
1.5.2.7 Problematic benzodiazepine use 12
1.5.3 Morbidity and mortality 13
1.6 Clinical governance 13
1.6.1 Laws and regulations 13
1.6.2 General practice systems of care 14
1.6.2.1 Staff education and competency 14
1.6.2.2 Balancing patients’ needs with practice capacity (risk stratification) 14
1.6.2.3 Care coordination 15
1.6.2.4 Practice policies and standards 16
1.6.2.5 Using and managing information 16
1.6.2.6 Quality improvement 17
1.6.3 Accountable prescribing of benzodiazepines 17
1.6.3.1 Evidence-based prescribing of benzodiazepines 18
1.6.3.2 Practical prescribing decisions 18
1.6.3.3 Assessing risk 18
1.6.4 Patient focus 21
1.6.4.1 Sharing prescribing decisions 21
1.6.4.2 Clinical responsibility in shared decision making 21
1.6.4.3 Aboriginal and Torres Strait Islander peoples 22
2. Evidence-based guidance for benzodiazepines 23

2.1 Overview 23
2.2 Insomnia 24
2.2.1 Background 24
2.2.2 Management of insomnia in general practice 25
2.2.2.1 Assessment and diagnosis 25
2.2.2.2 Acute insomnia 25
2.2.2.3 Chronic insomnia 26
2.2.2.4 Non-drug interventions 26
2.2.2.5 Drug therapy 26
2.2.3 Resources 27
2.3 Anxiety disorders 28
2.3.1 Background 28
2.3.2 Management of anxiety in general practice 29
2.3.2.1 Assessment and diagnosis 29
2.3.2.2 Cognitive behavioural therapy 29
2.3.2.3 Antidepressants 30
2.3.2.4 Benzodiazepines 30
2.3.3 Resources 31
Benzodiazepines
2.4 Alcohol withdrawal 31

2.4.1 Background 31
2.4.2 Management of alcohol withdrawal in general practice 32
2.4.2.1 Assessment 32
2.4.2.2 Assisted withdrawal approaches 32
2.4.2.3 Benzodiazepines 32
2.4.2.4 Baclofen and carbamazepine 33
2.5 Acute mania (bipolar disorder) 33
2.5.1 Background 33
2.5.2 Management of manic episodes in general practice 33
2.6 Epilepsy 34
2.6.1 Background 34
2.6.2 Management of epilepsy in general practice 34
3. Contraindications and precautions in special groups 35

3.1 Overview 35
3.2 Paediatric patients 35
3.3 Women who are pregnant or breastfeeding 35
3.4 Older patients 36
3.4.1 Patients living in residential aged care facilities 36
3.5 Patients with chronic non-malignant pain 37
3.6 People with comorbidity - Mental illness and problematic drug use 37
3.7 Patients who misuse alcohol and/or other drugs (prescribed and illicit) 38
3.8 Prescribing to patients who drive 39
4. Duration of benzodiazepine therapy 40
4.1 Optimal duration of therapy 40
4.2 Prescribing benzodiazepines for longer than 4 weeks 40
4.3 Rationale for long-term benzodiazepine prescribing 41
4.4 Management of long-term benzodiazepine prescriptions 41
5. Discontinuing benzodiazepines 42
5.1 Discontinuing after short-term use 42
5.2 Discontinuing after longer term use - Withdrawal 42
5.2.1 Patients taking ‘therapeutic doses’ 43
5.2.2 Patient taking high doses of benzodiazepines or who are users of illicit drugs (polydrug users) 43
5.3 General principles for the management of withdrawal of benzodiazepines 43
5.3.1 Resources 44
5.4 Tapering dosing 44
5.5 Additional pharmacotherapies 45
5.6 Should every patient be withdrawn? 45
Resources 46
Resource A. Examples of responses to patient requests for benzodiazepines 46
Resource B. Drug interactions 53
Resource C. State and territory contacts 54
Additional resources for Schedule 4 and Schedule 8 drug information 55
Benzodiazepines
Resource D. Communication with patients 56

D.1 Benzodiazepine fact sheet for patients 56
D.2 Benzodiazepine reduction in the practice population 58
D.2A Practice letter to patients about benzodiazepine reduction 58
D.2B Practice guide to reduction and withdrawal of benzodiazepines (and Z drugs) in the practice
population 58
D.3 Stopping benzodiazepines (benzodiazepine withdrawal) fact sheet for patients 63
D.4 Sleep hygiene and stimulus control fact sheet for patients 65
Resource E. Practice policies and forms 67
E.1 Practice policy example for repeat prescriptions 67
E.2 Prescription plan/agreement for a trial of longer term treatment 68
Resource F. Drug and alcohol assessment tool 71
Alcohol Use Disorders Identification Test 71
AUDIT questionnaire: Screen for alcohol misuse 71
Audit-C questionnaire 71
Resource G. GP guide to behavioural therapy for insomnia 72
Behavioural therapy for insomnia - Information for GPs 72
Sleep hygiene 72
Stimulus control 72
Stimulus control instructions 72
Sleep restriction therapy 73
Relaxation 73
Cognitive therapies 73
Appendix A. Key terms and definitions 74

A.1 Drugs of addiction and drugs of dependence 74
A.2 Tolerance, dependence, substance use disorder and withdrawal 74
A.3 Misuse, non-medical use and abuse 75
A.4 Drug-seeking behaviour 76
A.5 Prescriber behaviour 76
A.6 Staged supply 76
Appendix B. Recommendations and grading 77
B.1 Evidence-based statements and recommendations - Insomnia 77
B.2 Evidence-based statements and recommendations - Anxiety 78
B.3 Evidence-based statements and recommendations - Alcohol withdrawal 79
Appendix C. Process of development 80
References 81
Benzodiazepines
ix
Summary of recommendations
Drugs of dependence have important therapeutic uses, but there is a need to ensure the supply of these
medicines is clinically appropriate. A key measure is accountable prescribing that can be supported by
a range of strategies at the practice level. Please refer to RACGP’s Prescribing drugs of dependence in
general practice, Part A - Clinical governance framework for information about these strategies.
Since 2002, approximately 7 million prescriptions for benzodiazepines have been dispensed in Australia
each year, for conditions such as anxiety and insomnia. There is concern a portion of these prescriptions
is causing or contributing to patient harm. This is a practical guide general practitioners (GPs) can use to
minimise harm and maximise benefits to patients.
Evidence-based recommendations are collated here and there is further information in the body of the guide.
Wording of key principles and recommendations

Within the key principles and recommendations, the term ‘should’ refers to a recommended action, ‘must’
refers to an obligation, ‘must not’ to a prohibition, and ‘may’ refers to a discretionary action.
Recommendations denoted with ‘Rec’ and a number are those taken from existing evidence-based
guidelines and are accompanied by a link to the original source and grading. Each ‘Rec’ has a hyperlink
allowing you to click through to the references. Other links are provided to sections in the body of the
document. Recommendations without a ‘Rec’ are practice points.
For definitions of key terms, refer to Appendix A.
Key principles
Incorporating key principles of accountable prescribing, practice systems of care and patient-focused care:
1. Prescription of benzodiazepines, as with any treatment, should be based on a comprehensive medical

assessment; a diagnosis; thoughtful consideration of the likely risks and benefits of any medication, as
well as alternative interventions; and a management plan derived through shared decision making and
continual clinical monitoring.
2. GPs should be aware of the common concerns associated with benzodiazepines, such as potential
dependence, withdrawal, problematic drug use (including diversion and misuse) and known harmful
effects, including falls, potential cognitive decline and motor vehicle accidents. These risks should be
discussed with patients.
3. Treatment seeks to maximise outcomes for the health and social functioning of the patient while
minimising risks. To minimise risks, benzodiazepines should be prescribed at the lowest effective dose
for the shortest clinical timeframe.
4. Avoid prescribing benzodiazepines to patients with comorbid alcohol or substance use disorders or
polydrug use. GPs should consider seeking specialist opinion in the management of these patients.
Patients who use two or more psychoactive drugs in combination (polydrug use) and those with a
history of substance misuse may be more vulnerable to major harms.
5. Benzodiazepines are generally regarded by clinical practice guidelines as a short-term therapeutic

option. Long-term use, beyond 4 weeks, should be uncommon, made with caution and based on
thoughtful consideration of the likely risks and benefits of benzodiazepines.
- If alternatives to benzodiazepine treatment fail, have limited benefit or are inappropriate (either
psychologically or pharmacologically), supervised benzodiazepine treatment may remain an
acceptable long-term therapeutic option.
x Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
- Long-term benzodiazepine prescriptions should be at the lowest effective dose, preferably given
intermittently, and regular attempts at reduction should be scheduled. Continued professional
monitoring of health outcomes is required.
- Benzodiazepines should be prescribed from one practice and preferably one GP and dispensed from
one pharmacy.
6. GPs may wish to use the diagnosis of substance use disorder (SUD) rather than dependence, addiction
or abuse; this is based on the Diagnostic and Statistical Manual of Mental Disorders, 5th edition’s,
(DSM-5’s) sedative, hypnotic or anxiolytic use disorder criteria. This is a more neutral term that may reduce
stigmatisation of patients with problematic use of benzodiazepines and other drugs or alcohol.
7. GPs should develop strategies to manage inappropriate requests for benzodiazepines by patients.
8. All patients, including those who use benzodiazepines and other drugs or alcohol problematically, have
the right to respectful care that promotes their dignity, privacy and safety.
Treatment of insomnia
Insomnia is a common problem that can cause significant distress and reduced functioning. Chronic
insomnia can be more challenging to manage, as it may be associated with an underlying cause, or be
an independent disorder that can precipitate or worsen other comorbid conditions (eg depression). The
understanding of chronic insomnia is still evolving.
The first step is comprehensive medical assessment, including identification of any underlying issues, and
diagnosis.
Where treatment is indicated:
• First-line therapy should be non-drug interventions. Cognitive behavioural therapy (CBT), which may
include stimulus control, sleep restriction, relaxation techniques and sleep hygiene education is well
supported by evidence. It should therefore be offered to patients, including older adults. (Level A
Evidence) Rec 1.
• Decisions to prescribe pharmacological treatment should be made on an individual basis, after serious
consideration of all risks and possible benefits.
• Effective pharmacological therapies include benzodiazepines and Z drugs (benzodiazepine receptor

agonists), and both should be treated with the same cautions. (Level A Evidence) Rec 2, Rec 3.
• Short-term or intermittent dosing of benzodiazepines should be used to reduce the risk of tolerance and
dependence. (Level B Evidence) Rec 4, Rec 5.
• Pharmacological treatment should be accompanied by specific patient education, regular review and
continued efforts to employ the lowest effective dosage of medication, and to taper medication when
conditions allow.
Note: When access to CBT is an issue, GPs and practice nurses may consider offering brief behavioural
therapy to patients (refer to www.racgp.org.au/your-practice/guidelines/handi/interventions/mental-health/
brief-behavioural-therapy-for-insomnia-in-adults ).
Benzodiazepines
xi
Treatment of anxiety disorders

Anxiety disorders are common and exist as a spectrum of conditions that vary from mild to severe.
Comprehensive clinical assessment is the first step in management. Effective management requires
obtaining a diagnosis and recognising that patients may not present with a single disorder (eg patients may
experience generalised anxiety, panic disorder as well as depression).
Where treatment is indicated:
• First-line therapy for generalised anxiety disorder (GAD), panic disorder, and panic attacks should include
CBT due to its effectiveness at reducing the symptoms of anxiety in the short and long term. (Level A
Evidence) Rec 6.
• Selective serotonin reuptake inhibitor (SSRI) and serotonin-norepinephrine reuptake inhibitor (SNRI)
medications are effective across the range of anxiety disorders and are generally suitable for first-line
pharmacological treatment of anxiety. (Level A Evidence) Rec 7.
• Benzodiazepine use in anxiety disorders is mostly limited to severe or treatment-resistant cases.

• Benzodiazepines have proven benefit for GAD, social anxiety disorder and panic disorder.
Benzodiazepines have not shown benefit for obsessive compulsive disorder (OCD) or post-traumatic
stress disorder (PTSD). (Level A Evidence) Rec 8.
• Short-term benzodiazepine use as occasional adjunctive therapy may be effective at reducing worsening
of symptoms that can occur in the first few days to weeks of initiating antidepressant medication.
Note: When access to CBT is an issue, internet-based or computerised CBT programs have been shown
to be effective (visit www.racgp.org.au/your-practice/guidelines/handi/interventions/mental-health/internet-
based-or-computerised-cbt-for-depression-and-anxiety).
Treatment for alcohol withdrawal

Benzodiazepines are an effective component of an alcohol withdrawal program. However, not every
patient withdrawing from alcohol will require medication. Comprehensive medical assessment (including
assessment of social support and the use of formal assessment tools) is required to determine the most
appropriate approach for alcohol withdrawal (ie in the primary care or specialist alcohol services setting).
Where assisted withdrawal from alcohol is indicated:
• Benzodiazepines (eg diazepam, oxazepam) are the drugs of choice for treatment of acute alcohol
withdrawal (including alcohol withdrawal delirium), but should be limited to a maximum of 7 days. (Level
A Evidence) Rec 9.
Discontinuing benzodiazepines
When discontinuing benzodiazepines, consider using a stepped approach, starting with minimal
interventions and moving to more intensive measures.
• Minimal interventions such as advisory letters or GP’s advice should be considered as an initial step in
benzodiazepine discontinuation.
• The strength of the GP-patient therapeutic alliance is an important positive factor that assists the
successful withdrawal of benzodiazepines.
• If benzodiazepine use disorder has become moderate or severe, it can become a long-term and
distressing problem. However, gradual dose reduction interventions are possible for many patients
titrating the dose reduction against the level of withdrawal symptoms experienced. Additional
psychological therapies increase the effectiveness of gradual dose reduction.
• Switching from a short half-life benzodiazepine to a long half-life benzodiazepine before gradual taper
may assist patients with problematic withdrawal symptoms on reduction.
Benzodiazepines
1
1. Introduction
The arrival of benzodiazepines into clinical practice in the 1960s was met with enthusiasm. It allowed
doctors to offer patients a class of medication with a range of properties (eg sedative/hypnotic, anxiolytic,
anticonvulsant, muscle relaxation) at a time when there were few effective therapeutic alternatives.
Benzodiazepines were effective and appeared safe in comparison to barbiturates, chloral hydrate and other
drugs, which were problematic due to toxicity and overdose.1
Due to the seeming paucity of side effects, rapid onset of effect and a pressing mental health need,
benzodiazepines were quickly used and prescribed short- and long-term for anxiety, depression, insomnia,
mental illness and neuromuscular conditions. By the 1970s, they were the most commonly prescribed
drugs in the world.2 In 1978, more than 2.3 billion doses of diazepam were sold in the US alone.3
In the 1980s, evidence of the addictive nature of benzodiazepines grew and it became generally accepted
that benzodiazepines brought their own problems. In 1988, the Committee on Safety of Medicines (UK)
published the first guideline for benzodiazepine use and recommended limiting the length of treatment
to 2-4 weeks.4 Since then, many international guidelines have advocated for the reduction in prescribing
benzodiazepines, particularly short-acting benzodiazepines for long-term disorders such as anxiety.
However, there has been - and still is - a wide divergence between recommendations and clinical practice.
In Australia, nearly 7 million benzodiazepine prescriptions are currently recorded through the Pharmaceutical
Benefits Scheme (PBS), Repatriation PBS and private scripts each year.5 Benzodiazepines have remained a
major anxiolytic therapy, and given the trend towards larger quantity scripts, not just for short-term use.5
There is growing apprehension in Australia regarding the harms associated with the sanctioned and
unsanctioned use of benzodiazepines.6 The misuse of alprazolam is particularly problematic. It appears to
be disproportionately associated with misuse, fatal and non-fatal overdoses, paradoxical excitation, and
withdrawal and rage responses, as well as traffic accidents and crime-related harms.7
The conditions where benzodiazepines are most commonly prescribed (ie anxiety and insomnia) remain
sources of debate in medical circles. General practitioners (GPs) must consider multiple factors when
prescribing benzodiazepines, including potential prescription abuse. Good clinical governance and an
evidence-based approach remain key to safe and appropriate prescribing (refer to RACGP’s Prescribing
drugs of dependence in general practice, Part A - Clinical governance framework).
1.1 Aims
This guide aims to provide assistance to GPs in the appropriate prescribing of benzodiazepines in the
context of general practice.
It is designed to discourage inappropriate use and reduce harms by providing GPs with:
• evidence of the advantages and disadvantages associated with the use of benzodiazepines
• support for appropriate prescribing of benzodiazepines within regulatory frameworks
• support for safer prescribing within their practices
• alternatives to benzodiazepines, including non-drug options
• tools for managing patients who are prescribed benzodiazepines such as objective goals and time
limited prescribing
• tools for recognising and managing higher risk situations.
Implementing principles from this guide should reduce the risk that GPs will be involved in an adverse
event associated with prescribing benzodiazepines.
2 Prescribing drugs of dependence in general practice, Part B
Benzodiazepines
1.2 How to use this guide

This guide is a reference to assist the management of benzodiazepine prescribing. It is part of a
reference series on drugs of dependence. It is not a set of mandatory rules. Recommendations should
be considered and implemented as required, and where appropriate to the individual practice and
patient.
The appendices contain examples of some practice policies. These examples are not individually
approved or endorsed by the RACGP Council, or by the RACGP Standards for general practices
(4th edition) (the Standards). They are based on policies and practices from national and international
sources. If practices wish to adopt any of these policies, they should be modified for relevance and
applicability to the local context.
1.3 Why do we need this guide?

Drugs of dependence have important therapeutic uses and are highly beneficial to many individuals. The
clinically appropriate supply of these medicines needs to be maintained.8
This guide is a resource to assist with the appropriate and accountable prescribing of benzodiazepines
to prevent and reduce harms to patients, and to prevent medico-legal issues for GPs.
GPs need to be aware of the broad issues around benzodiazepine use in society, as well as specific
problems at a patient level, and how to address these issues with practice-based interventions.
1.3.1 Issues surrounding benzodiazepines

1.3.1.1 Variations in prescribing
Benzodiazepine prescribing rates vary between clinicians and practices. GPs vary in the extent
to which they are willing to prescribe benzodiazepines. Some consider benzodiazepines to be
extremely useful drugs for multiple situations, while others feel they have no place in general
practice. Richard Balon wrote, ‘... benzodiazepines have been hesitantly lauded and frequently
enthusiastically vilified ... ’9
The range of approaches to prescribing benzodiazepines may be explained by the variation in

attitudes to the drugs, the changing context of prescribing, differing perceptions of the role and
responsibility of the GP (and the personal responsibility of the patient), issues around alternative
treatment options, perceptions of patient expectations, non-clinical considerations (eg race,
gender) and the doctor-patient relationship.8
1.3.1.2 Questions about over prescribing

Comparing the prevalence of conditions for which benzodiazepines are indicated and the number
of prescriptions dispensed, the evidence suggests that they may be over-prescribed and/or
prescribed outside published guidelines.10
In 1991, there were an estimated 9.2 million benzodiazepine prescriptions dispensed from
Australian retail pharmacies - enough to provide a daily dose for 3% of the adult population.5
Since then there has been a modest declining trend in prescription numbers, although there are
still approximately 7 million prescriptions for benzodiazepines written each year. Nearly 5 million
prescriptions are subsidised through the PBS, and the rest are private or under co-payment
prescriptions.11 Since 2000, there has been a shift away from the PBS to private scripts.5
The modest decline can be partly explained by the use of selective serotonin reuptake inhibitors
(SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). The use of SSRIs doubled
between 2000-11, and have become the primary pharmacological treatments for anxiety
disorders.5
Benzodiazepines 3
Figure 1. Year-wise total dispensing of benzodiazepine derivatives in Australia between

1992 - 2011
total (Ashton manual) under co-payment (World health

A. Organization (WHO) DDD)
total (WHO DDD)
private (WHO DDD)
Year
Year
A. Defined daily dose (DDD)/1000 people/day
B. Number of prescriptions.
Reproduced with permission from Islam MM, Conigrave KM, Day CA, Nguyen Y, Haber PS. Twenty-year trends in
benzodiazepine dispensing in the Australian population. Intern Med J 2013;44:57-64.
Benzodiazepines
Despite a decrease in the prevalence of benzodiazepine prescriptions overall, diazepam and

alprazolam prescribing increased.5
Figure 2. Dispensing trend of major benzodiazepines in Australia between 1992 - 2011
A. Diazepam Temazepam Alprazolam Oxazepam
Nt Nitrazepam Flunitrazepam Zolpidem Lorazepam
Year
B. Oxazepam Alprazolam Diazepam Temazepam
Clonazepam Nitrazepam — Lorazepam Flunitrazepam
Year
A. Defined daily dose (DDD)/1000 people/day
B. 10 mg diazepam dose/1000 people/day.
Reproduced with permission by Islam MM, Conigrave KM, Day CA, Nguyen Y, Haber PS.
Twenty-year trends in benzodiazepine dispensing in the Australian population. Intern Med J
2013;55:57-64.
1.3.1.3 Questions about safety of prescribing

Coronial data reported in the Australian media have raised public concern about the safety of
prescription medications. Based on Victorian drug-related death data,12 prescription drugs are
associated with 77% of all drug-related deaths.
Benzodiazepines 5
Approximately half (48.8%) of all drug-related deaths are associated with benzodiazepines, which
were identified as causal or contributory.
The number of deaths associated with benzodiazepines as a single drug is uncommon, and less
than that from alcohol.
The most serious adverse events with benzodiazepines occur in the context of polydrug use (the
use of more than one psychoactive substance in combination). The Coroner’s Court of Victoria’s
figures suggest benzodiazepines, when used in conjunction with prescription or illicit opioids, are
associated with a significant number of drug-related deaths.12 Similar findings occur when used
in conjunction with antidepressants and antipsychotic drugs.
In many of the benzodiazepine-related deaths (57%), there was a positive history of substance abuse.12
State coroners have called on the RACGP to address benzodiazepine prescribing by GPs
following these benzodiazepine-related deaths.
Regulatory bodies are also reviewing benzodiazepines and how they are prescribed. As of February
2014, alprazolam has been rescheduled by the Therapeutic Goods Administration (TGA) to a
Schedule 8 (S8) drug, due to concerns about misuse and harms. This followed a dramatic increase
in the prescriptions for alprazolam (especially private prescriptions) - rising from 4.1% of the
population in 1998 to 27.9% in 2010 - and a trend towards higher dose formulations.13-15
Table 1. Drug related deaths in Victoria 201012

1A. Drugs contributing to drug-related deaths
Number Percentage of all drug-related
of deaths deaths
Prescription drugs (alone or in combination with 261 77.2%
other drugs)
Multiple drugs 215 63.6%
Single drug alone 123 36.4%
Prescription drugs alone 137 40.5%
Illicit drugs (alone or in combination with other drugs) 152 45%
Illicit drugs alone 50 14.8%
Alcohol (alone or in combination with other drugs) 82 24.3%
Alcohol alone 21 6.2%
*
Total deaths 338
1B. Drug-related deaths associated with benzodiazepines

Percentage Percentage of
Number
Number of deaths of all drug benzodiazepine-
of deaths
related deaths related deaths
Total (causal or contributory)

* 165 48.8% 100%
Combined with illicit or prescription opioids 136 40.2% 82.4%
Combined with substance abuse history 94 27.8% 57%
Combined with antidepressants 69 20.4% 41.8%
Combined with antipsychotics 47 13.9% 28.5%
Combined with alcohol 42 12.4% 25.5%
Benzodiazepines alone 5 1.5% 3%

*Where an overdose involves more than one drug type, the death is counted under all contributing drug types. Therefore,
individual data does not sum to the total.
Benzodiazepines
1.3.1.4 Increasing awareness of problematic use, including misuse

Problematic use has been identified in men and women of all ages. According to the National Drug
Strategy Household Survey, in 2010:16
• tranquillisers/sleeping pills (including benzodiazepines) were used for non-medical purposes by 3.2%
of the Australian population aged 14 years and older at some stage in their lifetime
• benzodiazepines were used for non-medical purposes by 1.4% of Australians in the 12 months
before the survey
• non-medical use of benzodiazepines is highest in people aged 20-29 (2.9%).
Awareness of diversion is relatively high, with benzodiazepines acknowledged as being among the most
commonly diverted prescription medications (along with opioids) for illicit use.17 However, unintentional
misuse is less known. Australia is likely to have a large, but relatively hidden, population who
unintentionally misuse benzodiazepines and who have developed an iatrogenic dependence.18 Patients
may also intentionally take medications outside of recommended use (eg larger doses) for what they
consider to be a legitimate medical purpose (eg chronic insomnia).
Deliberate misuse of benzodiazepines for non-medical purposes occurs for a variety of reasons. People
use benzodiazepines to:6,7
• enjoy the effects (especially taking large intermittent doses in a binge pattern)
• enhance an opiate effect
• help come down from stimulants

• combat opiate withdrawal symptoms
• substitute for their drug of choice.
The benzodiazepine, flunitrazepam, has been used to facilitate sexual assault.
The true prevalence of benzodiazepine misuse is unknown. However, the harms associated with non
medical prescription drug use, notably dependence and overdose, are well documented.17
1.3.2 The factors involved

1 .3.2.1 Source of benzodiazepine misuse
In contrast to other drugs used for non-medical reasons, medical practitioners are the main source for
benzodiazepine misuse.19
Individuals may obtain prescription medicines for non-medical purpose through a variety of means including:
• multiple doctors (doctor shopping or prescription shopping)
• drug theft (including from pharmacies)
• forgery of prescriptions
• inappropriate prescribing
• illicit market purchases
• procuring medicines from family, friends or acquaintances20
• bartering for sex or other services
• the internet.
In a survey of recent users of tranquilisers and sleeping pills for non-medical purposes, 71% thought these
drugs were easy to obtain.16 Patients are often highly skilled at obtaining prescriptions. They may present
with a range of plausible and compelling reasons for why they should receive benzodiazepines. The most
common is that they are benzodiazepine dependent and at risk of seizures if not prescribed the drug.21
Patients often describe medical reasons for needing to take the medicine (eg epilepsy and anxiety).
Benzodiazepines
7
1.3.2.2 Benzodiazepines are often combined with other drugs

Benzodiazepines are often used in combination with other drugs, including alcohol (polydrug use).
This can dramatically increase the risk of harm (eg road traffic accidents and overdose). This also
presents a medico-legal risk for prescribers (eg if the patient was not warned, concurrent drug or
alcohol use was not assessed, or the risk or presence of substance use disorder [SUD] was not
assessed).
A Melbourne study of adolescents who died of a drug overdose found a pattern of escalating
attendance at general practices in the 6 months before death. The main reason for attendance
was to obtain prescriptions for benzodiazepines.21 Another study found 55% of heroin-related
deaths and 88% of methadone deaths in Victoria involved benzodiazepines.22 More than 90%
of a cohort of heroin users in Sydney reported using benzodiazepines; 35% of the sample had
injected benzodiazepines and 26% of those who had ever used benzodiazepines were diagnosed
as dependent.23 The 2011 Victorian Illicit Drug Reporting System (IDRS) - a sentinel survey of
people who inject drugs - reported 92% of lifetime and 71% recent benzodiazepine use.24
1.4 Clinical pharmacology of benzodiazepines

Numerous benzodiazepines are available. They can be classified according to their main use, speed of
onset, duration of action and drug half-life.
While benzodiazepines differ in their pharmacokinetics (absorption, distribution, metabolism, excretion),

they all have similar pharmacodynamic properties and clinical actions.
1.4.1 Properties
Benzodiazepines have four basic properties that give rise to their clinical use:
• anxiolytic
• sedative/hypnotic
• anticonvulsant
• muscle relaxant.
Benzodiazepines can also produce anterograde and retrograde amnesia. This effect is used peri-
procedurally.
These properties are the result of enhancement of activity of the major inhibitory neurotransmitter
in the central nervous system (CNS), gamma-aminobutyric acid (GABA). Benzodiazepines bind
to receptors on the GABA-A receptor complex causing inhibitory effects throughout the brain,
including drowsiness and cognitive impairment (cerebral cortex), dampening of emotions such as
fear and anxiety (mesolimbic dopamine system), memory impairment and anticonvulsant actions
(hippocampus), and impairment of balance, motor control, muscle tone and coordination (cerebellum
and other motor areas). These effects are non-selective.
Newer Z drugs (eg zolpidem and zopiclone) enhance the activity of GABA by binding at the same
location as benzodiazepines. While these drugs have similar actions to benzodiazepines, they are
marketed for insomnia due to their kinetic profile. High doses are required to produce the other
actions such as decreased anxiety.25 There is evidence Z drugs, which are now the most commonly
prescribed hypnotic agents, share similar risks to benzodiazepines.26-29
1.4.2 Speed of onset

Benzodiazepines are rapidly absorbed orally. After ingestion, peak effects will occur within 30 minutes
to 2 hours (refer to Table 2). The more fat-soluble drugs (eg diazepam) enter the CNS more rapidly.
co
Adapted with permission from Drug and Alcohol Withdrawal Clinical Practice Guidelines
Table 2. Summary of the speed of onset, half-life and equivalent dose

Speed of onset, Approximate
Generic
Benzodiazepines
Trade name time to peak Elimination half-life equivalent dose to Comments
name
concentration diazepam 5 mg
*
Diazepam Antenex, Rapid 30-90 minutes Biphasic: rapid phase 5 mg Risk for accumulation because of long-acting metabolites
Ducene, Valium, 3 hours; elimination (temazepam, desmethyldiazepam, oxazepam)
Valpam half-life 20^18 hours Increased risk for abuse because of quick onset
Alprazolam Alpraz, Kalma Rapid-intermediate, 6-25 hours 0.5 mg Increased risk for abuse because of greater lipid solubility
1 hour Clinically, non-medical users report onset of effects at 20
minutes and lasting up to 6 hours
Bromazepam Lexotan Rapid, 0.5^t hours 20 hours 3 mg
Clonazepam Paxam, Rivotril Intermediate, 2-3 hours 22-54 hours 0.25 mgf Use caution in patients with liver disease
Flunitrazepam Hypnodorm Rapid, 1-2 hours 20-30 hours *
Lorazepam Ativan Intermediate, 2 hours 12-16 hours 1.0 mgi Preferred for patients with liver impairment, as no active
metabolites
Nitrazepam Alodorm, Rapid, 2 hours 16-48 hours 5 mg

Mogadon
Oxazepam Alepam, Slow-intermediate, 4-15 hours 15 mg Preferred for patients with liver impairment, as no active
Murelax, 2-3 hours metabolites
Serepax
Temazepam Euhypnos, Intermediate, 30-60 5-15 hours 10 mg Preferred for patients with liver impairment, as no active
-
NSW. Sydney: Ministry of Health, 2008;
Normison, minutes after tablets or metabolites

Temaze, 2 hours after capsules
Temtabs
Triazolam Halcion Rapid, 1-3 hours Biphasic: rapid 0.25 mg Lacks active metabolites
phase 2.5-3.5 hours;
elimination half-life 6-9
hours
Zolpidem Stilnox Rapid, 0.5-3 hours 2.5 hours 10 mg
Zopiclone Imovane Rapid, 1.75 hours 5 hours 7.5 mg

*A broad review of published equivalents shows inconsistent data. The widely varying half-lives and receptor binding characteristics means that exact equivalence is difficult. +There is a wide variety of reported equivalence
between clonazepam and other benzodiazepines. ^Lorazepam may be relatively more potent at higher doses.
Benzodiazepines 9
1.4.3 Metabolism and duration of activity

Benzodiazepines vary greatly in the speed at which they are metabolised and several different
mechanisms are involved. Depending on their metabolic structure, benzodiazepines are short,
medium or long acting (refer to Table 2).
For the majority of benzodiazepines, the elimination half-life is significantly longer than the duration of
clinical action. As they are rapidly redistributed into fatty tissue after absorption, the noticeable clinical
effects wear off after a few hours. However, the drugs may continue to exert subtle effects and, with
repeated dosing, accumulation within the fatty tissue occurs and a steady state of blood concentration
can be reached in approximately five half-lives. Due to slow leaching from fatty tissue, benzodiazepines
may be detected in urine tests weeks to months after cessation of benzodiazepine use.
Benzodiazepines are metabolised by the liver and excreted renally. Metabolism may be impaired in
patients with liver and/or kidney disease. Lorazepam, oxazepam and temazepam are metabolised
by glucuronidation and therefore do not produce active metabolites. These are rarely susceptible
to medication interactions, although their sedative effects remain synergistic. Some other
benzodiazepines undergo metabolism by the cytochrome P450 (CYP450) 3A4 hepatic enzyme
system and many are weak inhibitors of the CYP enzymes. Therefore, these benzodiazepines may
have significant interactions with other drugs that are metabolised by these enzyme pathways.
Refer to Resource B for common drug-drug interactions.
1.4.4 Tolerance
Tolerance to all drugs of dependence develops with repeated use.31 Steady state plasma
concentrations of benzodiazepines and their metabolites are reached after about five elimination
half-lives, usually a few days to 2 weeks after starting therapy. Within a few days of reaching
a steady state of plasma concentration, patients may start to experience a loss of effect from
benzodiazepines,32 due to a range of neuroadaptive and physiological mechanisms.
Tolerance to the different benzodiazepine effects develops at different speeds and to different
degrees, and may never be complete.2,32-34 The degree of tolerance differs between patients:35
• A high proportion of patients with epilepsy develop tolerance to the anticonvulsant effects within a
few weeks. This is similar to patients with spasticity disorders and the muscular relaxant effects.2
• Tolerance to the hypnotic effects is less clear. Some of the literature claims it develops rapidly,2 while
other authors claim it is slower.25 The evidence is limited by the length of trials.32 Sleep studies have
shown that tolerance develops to the hypnotic effects of some rapidly eliminated benzodiazepines
(eg triazolam) by 2 weeks, whereas for others (eg midazolam) tolerance emerges slowly and
minimally.32,36 Tolerance also appears to develop with the Z drugs, however to a low degree.3,32,36
• Tolerance to the anxiolytic and amnesic effects of benzodiazepines probably does not occur at
all.32 Although, there is some evidence that a slow (years) tolerance may develop.2,37
Long-term use of benzodiazepines may produce chronic changes in benzodiazepine-receptor

functioning, which are thought not to fully return to their pre-addicted state after withdrawal and
abstinence.38
There is a high degree of cross-tolerance between benzodiazepines and other sedative/hypnotic

medications and alcohol.39
The development of tolerance is associated with escalation in dose, binge dosing and is one of the
criteria for dependence31 and SUD40 (refer to Table 3). However, it is unusual for patients to steadily
increase their dosage, even with long-term use, as might be expected with the development of
tolerance.25,41 Patients who are prescribed benzodiazepines for anxiety or sleep problems usually
do not escalate their doses even over a lengthy period of use. However, high-dose benzodiazepine
mono-dependence has been reported.3
Tolerance also makes it difficult to calculate equivalence.
Benzodiazepines
1.4.5 Equivalent dosages

Equivalent doses are primarily used when making a transfer between drugs. Comparative oral doses of
benzodiazepines are described in various sources, such as the Therapeutic Guidelines.35 However, the
clinical potency of different drugs varies among individuals and it is difficult to demonstrate equivalence
with drugs having very different half-lives (refer to Table 2). Due to this and variations in metabolism
among people, these equivalence tables should be used with caution.
1.5 Adverse effects of benzodiazepines

1.5.1 Adverse effects on mental health and functioning
While used commonly for mental illness, benzodiazepines are associated with a range of adverse
effects on mental health and function.
1.5.1.1 Cognitive impairment

Cognitive impairment is a broad term that encompasses several symptoms of benzodiazepine-
induced CNS effects.42
Acute administration may induce dose-related sedation, drowsiness, learning impairment,

psychomotor slowing and anterograde amnesia.33,43-48
Chronic cognitive effects are modified by tolerance to some, but not all of the acute effects.3 A range
of cognitive and psychomotor effects may persist after withdrawal.49
Long-term use of benzodiazepines has been associated with significant long-term cognitive
impairment and increased risk of dementia in various studies.50-52 The difficulty with these studies is
symptoms that may naturally precede dementia for 10 years or more (eg anxiety, sleep disorders)
are the very indications for which benzodiazepines are commonly prescribed.53
Other prospective trials show no association between benzodiazepines and accelerated cognitive
decline.54
One aspect of psychomotor functioning that has received a lot of attention is driving ability.
Benzodiazepines are associated with a 60-80% increase in the risk of traffic accidents, and taking
alcohol and benzodiazepines together increases accident risk more than seven times.55
1.5.1.2 Anxiety
Patients may experience new or worsened anxiety while taking benzodiazepines long term or after
stopping long-term use (rebound anxiety).37,56
1.5.1.3 Depression
Patients taking benzodiazepines may experience aggravated depression or depression that first
appears during benzodiazepine use.37,57 Benzodiazepines may cause and aggravate depression,
possibly by reducing the output of neurotransmitters such as serotonin and noradrenaline.
1.5.1.4 Paradoxical stimulation and disinhibition

Benzodiazepines may have a disinhibitory effect (especially at high doses), leading patients to behave
out of character and potentially placing themselves in dangerous situations because of an impaired
perception of inherent risk. Common scenarios involve high-risk sexual behaviour and reckless driving.42
So called ‘benzo binges’ have been associated with shoplifting and other crimes.30
Patients may also experience paradoxical excitement with increased anxiety, insomnia, talkativeness,
restlessness, mania, and occasionally rage and violent behaviour (known as the ‘Rambo effect’).7
Refer to Precautions in special groups interventions for further precautions and adverse effects.
Benzodiazepines
11
1.5.2 Dependence, withdrawal syndrome and problematic use

1.5.2.1 Dependence - A contemporary understanding
Despite its familiarity and ubiquitous use, the concept of dependence is complex.
Historically, dependence has been defined in pharmacological terms. That is a state that develops
during chronic drug treatment in which cessation elicits an abstinence reaction (withdrawal). This is
time limited and reversible by renewed administration of the drug.
As awareness of problematic use grew, the definition of benzodiazepine dependence changed
to include benzodiazepine addiction and abuse. Various definitions evolved with Diagnostic
and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), International Classification of
Disorders, 10th edition (ICD-10), World Health Organization (WHO) and leading authors describing
it as a cluster of behavioural, cognitive and physiological phenomena that may develop after
repeated substance use. This definition acknowledged that dependence is a complex condition
that involves variable combinations of interacting patient and drug factors (eg reinforcement,
tolerance, withdrawal).
This has created difficulties in determining incidence and prevalence of benzodiazepine
dependence, caused inadvertent changes in reporting levels of adverse drug events58 and
difficulties in comparing dependence and withdrawal reactions in benzodiazepine alternative (eg
SSRIs).
The DSM-5 criteria combine the former DSM-IV categories of substance abuse and substance
dependence into a single condition of SUD, measured on a continuum from mild to severe. The
essential feature of SUD is a cluster of cognitive, behavioral and physiological symptoms indicating
the individual continues using the substance despite significant substance-related problems.
1.5.2.2 Withdrawal syndrome

Benzodiazepine withdrawal syndrome is highly variable. It remains unclear why some long-term
users can withdraw without difficulty, even after years of continuous use, while others undergo
protracted agonies.59
The symptoms of withdrawal usually appear within 2-3 half-lives of the benzodiazepines being
withdrawn.60 They usually lessen and then disappear within a few weeks.60 Sudden withdrawal of
benzodiazepines can be associated with seizures.
The mildest form of withdrawal is rebound.3 Rebound comprises of the original symptoms
recurring transiently at a greater intensity.3 Discontinuation of benzodiazepines is frequently
associated with rebound anxiety and insomnia.36,61-66 Withdrawal symptoms include irritability,
paraesthesia, tinnitus, headaches, dizziness, poor memory, poor concentration, perceptual
distortions, menstrual disturbances and sensory hypersensitivity.38,59,65,67 Withdrawal symptoms
can usually be minimised by gradual reduction.68,69 There is evidence that some patients suffer
protracted withdrawal symptoms that can continue for months to years after cessation.59 There is
debate about whether these persistent symptoms are withdrawal reactions, or simply features of
an underlying disorder or worsening of that condition, which is triggered by treatment withdrawal.25
Short- and intermediate-acting benzodiazepines carry a greater risk of rebound and withdrawal
than long-acting benzodiazepines. Withdrawal syndrome can appear while the patient is still
taking medication. This may be because the patient avoids increasing the dose to cover increased
tolerance,59 or the patient is taking short-acting formulations and experiencing withdrawal as blood
levels drop.
1.5.2.3 Incidence of withdrawal symptoms

The occurrence of withdrawal syndrome is related to high dosage and long-term use.3
Authors argue that based on the incidence of withdrawal symptoms, evidence of benzodiazepine
dependence can be quite high. Withdrawal symptoms from benzodiazepines prescribed for
insomnia can ensue after 4-6 weeks of use in approximately 15-30% of patients.70 Others suggest
Benzodiazepines
much higher incidences of withdrawal: in the order of 30-45% of patients who have used regular
therapeutic doses of benzodiazepines for more than a few months.71
It has been debated whether this is a clinical problem.72 For example, it has been suggested that
in the absence of SUDs, the risk of addiction to benzodiazepines during long-term treatment
of anxiety and related disorders has been exaggerated. In addition, the pharmacological
dependence that develops when benzodiazepines are used long-term does not denote an
all-encompassing preoccupation with and craving for benzodiazepines, nor does it create
compulsive or uncontrollable benzodiazepine-seeking behaviour and adverse health and/or social
consequences.73
1.5.2.4 Cravings and reinforcement

The reinforcement potential of a drug is its ability to maintain or increase the frequency of drug
taking or drug-seeking behaviour. Drugs may have positive reinforcement potential by creating
a reward (or ‘high’) or negative reinforcement potential by alleviating some form of distress (eg
anxiety or withdrawal symptoms).57
Benzodiazepines predominantly demonstrate negative reinforcement effects.71 By alleviating

anxiety and withdrawal symptoms, it can encourage continued use. Used alone, and at
therapeutic doses, they have not been associated with significant positive reinforcement for
most patients (ie the drug itself does not encourage further use or dose escalation). Patients
with a history of alcohol abuse, or even those with moderate alcohol consumption, appear to
experience greater reinforcement effects with benzodiazepines. High doses may have positive
reinforcing effects in some patients, particularly polydrug users.71
1.5.2.5 The spectrum of problematic use

Problematic use rarely develops in patients taking a normal, therapeutic dose for short periods.
However, particular patient populations may be more vulnerable to developing problematic use.
An original US report focusing specifically on the development of physiological dependence,
especially at therapeutic doses, notes that benzodiazepines do not strongly reinforce their own
use and are not widely abused drugs. When abuse does occur, it is almost always among
individuals who are also actively abusing alcohol, opiates or other sedative hypnotics.74
1.5.2.6 Low-dose or therapeutic-dose dependence

In cases of low-dose dependence, benzodiazepines were usually initiated for their anxiolytic or
hypnotic effects. Doses may escalate slightly over years, however, prescriptions usually remain
within therapeutically recommended limits.57
While high-dose dependence may be easier to recognise through drug-seeking behaviours, GPs
should be aware of the more subtle behaviours of patients with low-dose dependence.
Patients with low-dose dependence tend to return at regular intervals to obtain repeat
prescriptions, often before the previous supply has run out. They often carry their tablets around,
and it is not uncommon for them take an extra dose before an anticipated stressful event or a
night in a strange bed. They have difficulty stopping the medication or reducing the dosage due
to withdrawal symptoms.57
In contrast with patients with high-dose dependence (prescribed or recreational), patients with
low-dose dependence tend not to abuse other drugs or alcohol.57
1.5.2.7 Problematic benzodiazepine use

Based on the available epidemiological data, the prevalence of benzodiazepine abuse is generally
low in the therapeutic setting (ie where the drug is correctly medically prescribed). The American
Psychiatric Publishing Textbook of Psychopharmacology quotes prevalence of 0.6% for abuse
and 0.5% for dependence among therapeutic users.75 However, the incidences are much higher
in people who abuse alcohol and other drugs.75
Benzodiazepines
13
Supporting this, a 2013 study found most patients used benzodiazepines according to
guidelines, and only 0.9% ended up as excessive users after 3 years.76 Again, problematic use
occurred mostly in individuals with alcohol and drug histories.
If benzodiazepine use disorder has become moderate or severe, it can become a long-term and
distressing problem. There are several behaviours that indicate a patient may have problematic
benzodiazepine use (eg escalating use patterns, drug-seeking behaviour and doctor or
prescription shopping).77
GPs need to maintain vigilance in identifying SUDs, assist patients in recognising disordered use
where it exists, set goals for recovery and assist patients to seek appropriate treatment.
1.5.3 Morbidity and mortality

Epidemiological studies have demonstrated an excess of consultations for accidents among persons
taking benzodiazepines.78
In Victoria alone, benzodiazepines were involved in 3135 ambulance attendances in 2010-11 and
3440 in 2011-12. In terms of all alcohol and drug related attendances, they were the second most
common only to alcohol. There was a disproportionate increase in the involvement of alprazolam
compared to all benzodiazepines in ambulance attendances.79,80
In older patients, benzodiazepines are associated with higher risk of falls and subsequent injuries.81-83
The harmful effects of benzodiazepines, other than the risk of dependence with long-term use, have
been associated (ie not proven cause and effect) with a 4-6-fold increased risk of death from all
causes.84
Research has found patients prescribed hypnotic drugs (including benzodiazepines, Z drugs,
barbiturates and sedative antihistamines) have an elevated risk of dying compared to those
prescribed with no hypnotics.84 There is a dose-dependent relationship, but even patients prescribed
fewer than 18 hypnotic doses per year experienced increased mortality.84 Note that this research
did not find that hypnotic drugs were the cause of premature death - at best, it found a potential
association.
Large cohort studies refute the relationship between benzodiazepine therapy and premature death.
Emerging evidence suggests underlying psychiatric disorders are the principal determinant driving
the association between hypnotics and mortality risk.85
1.6 Clinical governance

Please refer to RACGP’s Prescribing drugs of dependence in general practice, Part A - Clinical
governance framework for further information on clinical governance and its role in improving safety and
quality for the use of drugs of dependence in general practice.
1.6.1 Laws and regulations

Most benzodiazepines are Schedule 4 (S4) ‘prescription only’ medicines. The exceptions are
flunitrazepam and alprazolam, which are classed as S8 drugs.
Each state and territory has laws regulating the prescription of these medicines. Generally, there
are tighter controls around the prescribing of S8 drugs and for prescribing to patients with known
addiction. For example, GPs must seek a permit or an authority from the relevant state or territory
health department when prescribing an S8 drug to persons who are drug dependent.
Some states have subsets of S4 drugs that involve prescribing restrictions or additional
requirements; benzodiazepines often fall into this category.
Benzodiazepines
GPs must be familiar with the relevant legislative requirements associated with writing prescriptions
for S4 and S8 drugs.
State and territory departments and government-funded drugs of dependence units (or equivalent)
can provide information regarding prescribing. Refer to Resource C.
1.6.2 General practice systems of care

The quality and safety of patient care is no longer confined to the individual practitioner. General
practices have responsibilities to work collaboratively with practitioners to address the safety and
quality of health services provided in their facilities.
Practice systems of care around benzodiazepines can be put in place to maximise health outcomes
and social functioning for patients while minimising drug and alcohol misuse, abuse, diversion and
crime. Systems of care also provide the necessary infrastructure and support for GPs to perform
their job efficiently and effectively.
1.6.2.1 Staff education and competency

Practices should ensure they have the level of knowledge among team members and practice
capacity to address the issues associated with benzodiazepine prescribing (eg identification of
patients with more complex needs and those at higher risk). Prescriber education is particularly
important. The risk of benzodiazepine misuse and dependence is lower when the first-time
prescriber is a specialist in general practice compared to a prescriber without specialty training.76
GPs who are regularly involved in managing patients with problematic use of benzodiazepine
or other drugs and alcohol should consider further training and developing good working
relationships with addiction specialists.
Practices should promote the development of competency in prescribing benzodiazepines.

Where potentially inappropriate and suboptimal prescribing is identified, practices and GPs have
an opportunity to engage in education and support, and improve patient outcomes.
Dependence programs
Access to relevant programs is limited in some areas of Australia. Practices may wish to consider
supporting GP-based benzodiazepine detoxification programs in-house. Benzodiazepine
detoxification typically requires significant and frequent communication with patients, more
regular visits with the GP and other clinical staff, on-call mechanisms and management of
patients who are often highly anxious.86 Suitably qualified staff, organised support and ongoing
quality assurance arrangements may be required. GPs involved in this type of program should
feel comfortable prescribing adjunct medications.86
1.6.2.2 Balancing patients’ needs with practice capacity (risk

stratification)
Patients should be appropriately evaluated to determine the complexity of services required.
One of the goals in the initial assessment of a patient is to obtain a reasonable assessment of
clinical complexity/risk in the context of concurrent SUD or psychopathology. In this context,
patients can be stratified into three basic groups. The following will offer a practical framework
to help determine which patients may be safely managed in the primary care setting, should be
co-managed with specialist support and should be referred on for management in a specialist
setting.
GPs with advanced training in addiction medicine and/or mental health management are suited
to taking on higher responsibilities under this model.
Group I - Managed in primary care: Patients with no evidence of past or current history of
SUD or mental illness, apart from the presenting problem.
Benzodiazepines
15
• Group II - Managed in primary care with specialist support: Patients may have a past
history of a treated SUD or a significant family history of problematic drug use. They may also
have a past or concurrent psychiatric or chronic pain disorder. While not actively addicted,
patients are at increased risk, which may be managed in consultation with appropriate
specialist support.
• Group III - Managed by specialist services: This group of patients represents the most
complex cases to manage because of an active SUD or major, untreated psychopathology.
These patients are either actively misusing prescription drugs or pose significant risk to both
themselves and to the practitioners, who may lack the resources or experience to manage
them.
It is important to remember that all groups can be dynamic. Group II can become Group III
with relapse to active addiction, while Group III patients can move to Group II with appropriate
treatment. In some cases, as more information becomes available to the practitioner, the patient
who was originally thought to be low risk (Group I) may be reclassified as Group II or even Group
III. It is important to continually reassess risk over time.87
1.6.2.3 Care coordination

A key message from inter-professional dialogue is that all health professionals (eg psychiatrists,
pharmacists, GPs, nurses) have difficulties when dealing with high-risk patients and prescribing
benzodiazepines.88 There should be an agreed set of professional standards regarding
communication and transfer of care. In particular, the responsibility of ongoing prescribing duties
should be explicit.
Prescribing may be initiated and recommended by other specialists, or during hospital in-patient
care. When prescribing is transferred from secondary to primary care, the following information
should be relayed to the GP:
• indication for use
• expected length of treatment
• when the treatment will be reviewed and by whom
• advice about withdrawal if indicated
• clear indications of the GP’s role
• clear agreement on roles of all clinicians between GP and secondary care
• clear indications of support and referral pathways to the secondary service.
GPs should take care when patients on high doses of benzodiazepines are transferred from
secondary care without a therapeutic rationale for clinical benefits or planned withdrawal
schedule. GPs are not required to continue prescriptions commenced elsewhere if they are not
comfortable doing so. However, GPs should not undermine the professional advice of colleagues,
and should attempt immediate contact by telephone to clarify the management plan when there
are concerns.
With continued monitoring of care, issues may arise which should prompt specialist review or
immediate transfer to hospital (refer to RACGP’s Prescribing drugs of dependence in general
practice, Part A - Clinical governance framework). The following should prompt consideration for
referral to specialist mental health services:89
• insufficient experience to manage the patient’s condition requiring benzodiazepine therapy, or

insufficient practice infrastructure to provide ongoing recall and review
• multiple attempts at treatment have not resulted in sustained improvement
• severe coexisting depressive symptoms or a risk of suicide
• evidence of problematic drug use

Benzodiazepines
• comorbid physical illness and concomitantly prescribed treatments which could interact with
prescribed psychotropic medication
• proposed interventions are not available within primary care services.
1.6.2.4 Practice policies and standards

General practices should have agreed clinical policies regarding prescribing benzodiazepines to
improve the quality and consistency of prescribing, and improve safety for patients and practice
staff.
Practices should consider having policies regarding:
• the management of patients according to mental illness and use of drugs of dependence to
provide the appropriate level of service internally and externally
• repeat scripts for benzodiazepines (refer to Resource E.1)
• limitations for registrar prescribing of benzodiazepines (refer to RACGP’s Prescribing drugs of

dependence in general practice, Part A - Clinical governance framework).
Simple, practice-based interventions can be quite effective. Practice-based letters sent to a

general practice population have repeated proven effectiveness in reducing benzodiazepine use
in older patients.90 A 10-year follow-up in the Netherlands after such an intervention revealed
60% of these patients remained abstinent of benzodiazepine use.91 Those who returned to
benzodiazepine therapy often did so at lower doses. Simple educational interventions may also
reduce inappropriate benzodiazepine use.90,92
Benzodiazepine misuse might not be a highly visible problem in every practice, however all
practices should be involved in supporting steps to reduce inappropriate benzodiazepine use in
their practice and community. Each general practice should assess their own needs and develop
policies that suit their circumstances.
1.6.2.5 Using and managing information

To help GPs manage prescribing risks, practices should have infrastructure (computer based or
other) that provides:
• standardised patient information on benzodiazepines, including the effects on driving and

operating machinery (refer to Resource D.1)
• a treatment plan when there is a clinical decision to continue benzodiazepines. The plan
should clearly outline the responsibilities of the patient and the practice, and include an
agreement to review and monitor clinical progress against therapeutic goals
• access to high-quality information systems and/or prescription shopping hotlines to assist in

curtailing prescription abuse
• mechanisms/processes within the practice to share information regarding benzodiazepine

abuse/misuse
formalised benzodiazepine withdrawal guidelines within the practice (refer to Resource D.2B)
standardised patient information on sleep hygiene methods (refer to Resource D.4).

Benzodiazepines
17
1.6.2.6 Quality improvement

Quality improvement measures around benzodiazepine prescribing include developing policies or
an audit, communicating with patients and managing risks.
Further information about quality improvement can be found in the RACGP’s Prescribing drugs of
dependence in general practice, Part A - Clinical governance framework.
1.6.3 Accountable prescribing of benzodiazepines

K Key points
• Prescribing benzodiazepines, as with any treatment, should be based on a comprehensive
medical assessment, a diagnosis, thoughtful consideration of the likely risks and benefits of
any medication as well as alternative interventions, and a management plan derived through
shared decision making and continual clinical monitoring.
• GPs should be aware of the concerns associated with benzodiazepines such as potential
dependence, withdrawal, problematic drug use (including diversion and misuse), and known
harmful effects, including falls, potential cognitive decline and motor vehicle accidents.
These risks should be discussed with patients.
• GPs may wish to use the diagnosis of SUD rather than dependence, addiction or abuse.
This is based on the DSM-5 sedative, hypnotic or anxiolytic use disorder criteria. This is
a more neutral term that may reduce stigmatisation of patients with problematic use of
benzodiazepines and other drugs/alcohol.
• Treatment seeks to maximise outcomes for the health and social functioning of the patient
while minimising risks. To minimise risks, benzodiazepines should be prescribed at the
lowest effective dose, for the shortest clinical time frame.
• Once started, some patients find it hard to stop benzodiazepines. Therefore, prescription
should be accompanied with a plan to reduce and cease benzodiazepines.
• Patients who use two or more psychoactive drugs in combination (polydrug use), and those
with a history of substance misuse may be more vulnerable to major harms. Significant
caution should be taken if prescribing benzodiazepines to patients with comorbid alcohol/
substance abuse or polydrug use. GPs should consider seeking specialist opinion in
management of these patients.
• Benzodiazepines are generally regarded by clinical practice guidelines as a short-term

therapeutic option. Long-term use, beyond 4 weeks, should be uncommon, made
with caution and based on thoughtful consideration of the likely risks and benefits of
benzodiazepines.
- If alternatives to benzodiazepine treatment fail, have limited benefit or are inappropriate

(either psychologically or pharmacologically), supervised benzodiazepine treatment may
remain an acceptable long-term therapeutic option.
- Long-term benzodiazepine prescriptions should be at the lowest effective dose,

preferably given intermittently, and regular attempts at reduction should be scheduled.
Continued professional monitoring of health outcomes is required.
- Benzodiazepines should be prescribed from one practice and preferably one G , with
prescriptions dispensed from one pharmacy.
• GPs should develop strategies to manage inappropriate requests for benzodiazepines by

patients.
Benzodiazepines
1.6.3.1 Evidence-based prescribing of benzodiazepines

The evidence base for benzodiazepine use continues to evolve, but despite the length of time
they have been used in clinical practice, the evidence remains incomplete in many areas.93 The
clinical recommendations and practice points presented in this guide are based on the best
available evidence.
With respect to benzodiazepine therapy, recommendations based on these randomised

controlled studies do not always reflect clinical reality. It is recognised that randomised controlled
trials are generally a maximum of 12 weeks and performed in restricted patient groups with little
comorbidity or other features resembling conventional clinical samples.94
1.6.3.2 Practical prescribing decisions

Good prescribing practice involves careful and considered diagnosis; clear therapeutic goals;
the use of non-drug therapies where suitable; prescribing appropriate types, formulations and
amounts of medication; explaining the effects of medications and any risk of dependence; and
implementing regular medication reviews.
The risks of problematic use and diversion make prescribing benzodiazepines more challenging.
The short-term use of benzodiazepines can be helpful for symptomatic relief across a wide range
of clinical conditions. Given the potential for harm with benzodiazepine use, clinical discipline is
required. The immediate relief with benzodiazepines is tempting, yet the best outcomes are often
achieved with non-drug treatment. However, these interventions take time, may not be available
in a timely fashion, and involve engagement and effort from patients.
While the thrust of this guide is that benzodiazepines should generally be prescribed less, care
should be exercised when changing from one psychoactive substance to another or when
using combination therapies. All psychoactive drugs have risks and benefits. Some non
benzodiazepine drugs also have problems with dependence and problematic use (eg quetiapine).
There is consensus that although benzodiazepines have been problematic, when prescribing is
placed in the broader historical context and the types of patients prescribed benzodiazepines are
considered, it is apparent that other psychotropic drugs have raised similar problems.58'95-99
1.6.3.3 Assessing risk

Patients who previously misused drugs (eg opioids, anti-alcohol or smoke cessation treatments)
have a higher risk of becoming excessive users compared to patients who have not previously
misused drugs.76 Greater challenges exist for patients already prescribed benzodiazepines for
some time. Once a benzodiazepine prescription has been started, it may be harder to stop.
To minimise harms associated with prescription drug misuse, GPs need to maintain vigilance
in identifying SUDs, assist patients in recognising disordered use where it exists, set goals for
recovery and assist patients to seek appropriate treatment.
Recognising patients with problematic benzodiazepine use

There are several behaviours that indicate a patient may have problematic benzodiazepine use,
such as escalating use patterns, drug-seeking behaviour and doctor or prescription shopping.77
Drug-seeking behaviours that indicate risk, but are less predictive of problematic use include:
• attending early for prescription renewal
• complaining aggressively about the need for higher doses
• hoarding drugs during periods of reduced symptoms

• requesting specific drugs
• acquiring similar drugs from other medical sources
• escalating unsanctioned doses 1-2 times

Benzodiazepines
19
• using the drug to treat other symptoms
• selling prescription drugs.
Drug-seeking behaviours that are highly predicative of problematic use include:
• forging prescriptions
• stealing or borrowing another patient’s drugs
• injecting oral formulations
• obtaining prescription drugs from non-medical sources
• abusing illicit drugs concurrently
• escalating unsanctioned doses multiple times

• losing prescriptions repeatedly.
Patients may be extremely convincing, using plausible stories and even manipulating a GP’s
discomfort with confrontation to obtain medication.77
For ways to manage patient who may be drug seeking, refer to patient scripts in Resource A.
Patients with previous substance use problems, or those who use antipsychotic medication,
are at increased risk of disordered benzodiazepine use.76 However, any patient can develop
problematic use, and so universal precautions are important when considering prescribing.
Assessment of substance use disorder

The DSM-5 criteria combine the old DSM-IV categories of substance abuse and substance
dependence into a single condition of SUD, measured on a continuum from mild to severe.40
The essential feature of SUD is a cluster of cognitive, behavioral and physiological symptoms
indicating the individual continues using the substance despite significant substance-related
problems.40
Using the term SUD should:
• reduce confusion associated with the terms dependence, addiction and abuse (which have
been inconsistently and often incorrectly used to describe points on a spectrum of disordered
use)
• be more acceptable to patients and their carers - a diagnosis of being ‘drug dependent’ may
be confronting and create stigma.
Diagnosis of SUD requires the presence of at least two of 11 criteria, across four categories:
impaired control, social impairment, risky use and pharmacology. Based on the total number of
criteria the patient has, the substance use disorder can be classified as mild (2-3 symptoms),
moderate (4-5 symptoms) or severe (6 or more symptoms). It is hoped these severity classifiers
may help to clarify treatment options (refer to Table 3).
Although the term SUD is a helpful addition, the term dependence will necessarily be used when
discussing any ‘drug of dependence’.
Benzodiazepines
Table 3. DSM-5 criteria for diagnosing a sedative, hypnotic or anxiolytic use disorder
A problematic pattern of sedative, hypnotic or anxiolytic use leading to clinically significant impairment or
distress, as manifested by at least two of the following 11 criteria, occurring within a 12-month period:
Impaired control 1. Sedatives, hypnotics or anxiolytics are often taken in larger amounts or over a longer
criteria period than was intended
2. There is a persistent desire or unsuccessful efforts to cut down or control sedative,
hypnotic or anxiolytic use
3. A great deal of time is spent in activities necessary to obtain the sedative, hypnotic or
anxiolytic; use the sedative, hypnotic or anxiolytic; or recover from its effects
4. Craving or strong desire or urge to use the sedative, hypnotic or anxiolytic
Social 5. Recurrent sedative, hypnotic or anxiolytic use resulting in a failure to fulfil major role
impairment obligations at work, school or home (eg repeated absences from work or poor work
criteria performance related to sedative, hypnotic or anxiolytic use; sedative-, hypnotic- or anxiolytic-
related absences, suspensions or expulsions from school; neglect of children or household)
6. Continued sedative, hypnotic or anxiolytic use despite having persistent or recurrent social or
interpersonal problems caused by or exacerbated by the effects of sedatives, hypnotics or
anxiolytics (eg arguments with a spouse about consequences of intoxication; physical fights)
7. Important social, occupational or recreational activities are given up or reduced because of
sedative, hypnotic or anxiolytic use
Risky use criteria 8. Recurrent sedative, hypnotic or anxiolytic use in situations in which it is physically
hazardous (eg driving an automobile or operating a machine when impaired by sedative,
hypnotic or anxiolytic use)
9. Sedative, hypnotic or anxiolytic use is continued despite knowledge of having persistent
or recurrent physical or psychological problem that is likely to have been caused or
exacerbated by the sedative, hypnotic or anxiolytic
Pharmacological 10. Tolerance, as defined by either of the following:
criteria a. A need for markedly increasing amounts of the sedative, hypnotic or anxiolytic to
achieve intoxication or desired effect
b. A markedly diminished effect with continued use of the same amount of the sedative,
hypnotic or anxiolytic
Note: This criterion is not considered to be met for individuals taking sedatives,
hypnotics or anxiolytics under medical supervision
11. Withdrawal, as manifested by either one of the following:
a. The characteristic withdrawal syndrome for sedatives, hypnotics or anxiolytics (refer
to Criteria A and B of the criteria set for sedative, hypnotic or anxiolytic withdrawal in
DSM-5 pp 557-558)
b. Sedatives, hypnotics or anxiolytics (or a closely related substance, such as alcohol)
are taken to relieve or avoid withdrawal symptoms
Specifiers:
In early remission: After full criteria for sedative, hypnotic or anxiolytic use disorder were previously met, none of
the criteria for sedative, hypnotic or anxiolytic use disorder have been met for at least 3 months but for less than
12 months (with the exception that criterion 4 may be met)
In sustained remission: After full criteria for sedative, hypnotic or anxiolytic use disorder were previously met,
none of the criteria for sedative, hypnotic or anxiolytic use disorder have been met at any time during a period of
12 months or longer (with the exception that criterion 4 may be met)
In a controlled environment: This additional specifier is used if the individual is in an environment where access
to sedatives, hypnotics or anxiolytics is restricted
Current severity:
Mild: Presence of 2-3 symptoms
Moderate: Presence of 4-5 symptoms
Severe: Presence of 6 or more symptoms
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Copyright 2013).
American Psychiatric Association. All Rights Reserved.
Benzodiazepines
1.6.4 Patient focus
K Key points
• All patients, including those who use benzodiazepines and other drugs and alcohol
problematically, have the right to respectful care that promotes their dignity, privacy and safety.
1.6.4.1 Sharing prescribing decisions

Treatment and care of patients should take into consideration their needs and preferences.
Clinical options and patient information should be culturally appropriate. It should be accessible
to people with individual needs including those with physical, sensory or learning disabilities, and
those who do not speak or read English.
Fully informing patients about the benefits and drawbacks of benzodiazepines may improve
shared decision making between the patient and doctor. While there are time constraints in a
consultation, this approach may reduce GPs’ workload with fewer patients returning for repeat
prescriptions.8
Non face-to-face methods of communication can also be useful. For example, a study involving
direct delivery of an educational tool on benzodiazepines to older patients increased their risk
perception of inappropriate prescriptions.100
Exploring patient preferences, ideas and expectations during a consultation may lead to fewer
benzodiazepine prescriptions. Evidence suggests doctors sometimes assume patients want
drug treatment and/or would be resistant to withdrawal, whereas some patients prefer not to use
medication or wish to discontinue drugs.8
Patients need good information and access to alternative treatments including CBT for insomnia
and anxiety. These interventions may be made available in the practice or through local services.
There are many resources available on the internet (eg computer-based anxiety therapies).
1.6.4.2 Clinical responsibility in shared decision making

While most patients’ involvement with drugs of dependence is clinically driven, there
can be elements of manipulation (and rarely criminal intent) behind patients’ requests for
benzodiazepines.
The important caveat when prescribing drugs of dependence relates to healthcare benefits.
Some patients with drug dependency may request higher doses on the basis that they are
making a choice as an informed patient, or as harm minimisation.
Patients have a right to good healthcare, but not a right to drugs of dependence. Patients need
to be informed of this at the beginning of any trial using drugs of dependence. If the clinician feels
further therapy is detrimental to a patient’s health, then clinical withdrawal of medication should
begin.
Doctors typically have a strong desire to alleviate a patient’s distress and suffering. The
psychological phenomenon of transference in addiction, pain and mental illness can result in
doctors having difficulty in these clinical areas. Some GPs may find it difficult to set boundaries for
patients, and are therefore at risk of being pressured to prescribe inappropriately. Other GPs may
have difficulty saying ‘no’ or believe they are ‘helping’ or taking a harm minimisation approach by
giving in to a patient’s requests for drugs.
All practitioners express difficulty responding to patients who use manipulative behaviour (eg
threatening to self-harm if they do not receive medication). GPs should educate themselves
about appropriate responses to common manipulative behaviours used to access drugs of
dependence. To aid GPs’ negotiation skills, scripted replies have been developed to help with
appropriate responses in difficult situations (refer to Resource A).
Benzodiazepines
1.6.4.3 Aboriginal and Torres Strait Islander peoples

There is very little literature on benzodiazepine use in Aboriginal and Torres Strait Islander
peoples. While the clinical recommendations in this guide are the same for all patients, there is a
need to understand the complex cultural context of Aboriginal and Torres Strait Islander peoples
to build an effective therapeutic alliance. Working with local, respected Aboriginal Health Workers
and/or drug and alcohol workers is crucial for comprehensive bio-psychosocial care.
Resources
The Working Together book is relevant in understanding and providing mental health care to
Aboriginal and Torres Strait Islander peoples. This is available at http://aboriginal.telethonkids.org.
au/media/699863/Working-Together-Book.pdf
The Handbook for Aboriginal Alcohol and Drug Work includes useful information on
benzodiazepines. This is available at http://ses.library.usyd.edu.au/bitstream/2123/8339/6/2012-
handbook_online-version3.pdf
Benzodiazepines
2. Evidence-based guidance for

benzodiazepines
2.1 Overview
The evidence base for benzodiazepine use continues to evolve, but despite the length of time they
have been used in clinical practice, the evidence remains incomplete in many areas.93 The clinical
recommendations and practice points presented in this guide are based on the best available evidence.
Benzodiazepines are used for a broad range of conditions including:
• insomnia
• anxiety disorders
• alcohol withdrawal
• mania/hypomania
• epilepsy
• acute seizures
• arousal/agitation in the in-patient setting
• palliative care
• musculoskeletal disorders.
Insomnia and anxiety disorders are commonly managed in general practice and are the main focus of
this chapter. Alcohol withdrawal may be managed in general practice and is covered briefly. However,
GPs wishing to manage patients withdrawing from alcohol will need to consult other resources.
The following sections demonstrate how benzodiazepines fit into the context of treatment for a range of
conditions, but do not represent comprehensive guidance. Additional resources are provided for each
condition.
Benzodiazepines
2.2 Insomnia
K Key points
• Insomnia is a common problem seen in general practice. The understanding of chronic
insomnia is still evolving.
• In acute insomnia, sleep often returns to normal once the precipitating factor has resolved.
• In chronic insomnia, treatment is focused on addressing underlying comorbid precipitants

(where present), and psychological and behavioural management.
• Pharmacotherapy for acute and chronic insomnia may be necessary for severe or resistant
cases of insomnia. The decision to prescribe should be on an individual basis and involve
serious consideration of all risks and possible benefits.
• Benzodiazepines and Z drugs have been shown to be effective treatments and may be
prescribed for short-term or intermittent use. Harm, such as dependence and adverse events,
may occur with both drug groups.
• Dose reduction and cessation should be discussed with the patient on first prescription and
commenced once sleep patterns return to normal.
• Pharmacological treatment should be accompanied by specific patient education and regular review.
Evidence statements Grade

Rec 1 Cognitive behavioural therapy (CBT) based treatment packages for chronic insomnia, A
including sleep restriction and stimulus control, are effective and therefore should be
offered to patients as first-line treatment.101
Rec 2 Z drugs and short-acting benzodiazepines are efficacious for insomnia.101 A
Rec 3 Prescription of zolpidem and zopiclone should be treated with the same caution as A
benzodiazepines.102
Rec 4 Intermittent dosing may reduce the risk of tolerance and dependence.101 B
Rec 5 If hypnotics are to be used for treating insomnia, it is recommended that treatment is B
short term (not more than 4 weeks) and at the lowest possible dose.103
To see the original source of the recommendations and grading, as well as supporting sources, click on the
recommendation number in the left column.
2.2.1 Background
Sleep disturbance is the third most common psychological reason for patient encounters in general
practice. Population surveys found 13-33% of adult Australians have regular difficulties getting to
sleep or staying asleep.104
Insomnia is defined in DSM-5 as a difficulty in getting to sleep, staying asleep or having non
restorative sleep despite having adequate opportunity for sleep, together with associated impairment
of daytime functioning, with symptoms being present for at least 4 weeks.40
Acute insomnia meets the DSM-5 definition of insomnia, but with symptoms occurring for less than
4 weeks.40 It is experienced by up to 80% of the population at some stage, generally due to one or
more precipitating factors.105
Benzodiazepines
Factors that can precipitate acute insomnia include:104
• physiological - hyperarousal due to stress, being ‘on-call’, caring for a sick child/relative, being in
a strange situation (eg in hospital)
• pharmacological - prescribed drugs (eg newly prescribed diuretic causing nocturia) and non
prescribed drugs
• physical - coughing, environment (eg noise, temperature)
• disruption of circadian rhythm (eg jet lag).
Provided patients adhere to good sleep habits, most will return to normal sleep once the
precipitating factor has resolved or diminished.106
Chronic insomnia was previously viewed as a sleep disturbance that was secondary to a medical
condition, psychiatric illness, sleep disorder or medication, and would improve with treatment of the
underlying disorder.107,108 However, evidence over the last 20 years indicates this view is incorrect. It is
now recognised that insomnia may be an independent disorder.108-110 The understanding of chronic
insomnia continues to evolve. Insomnia may have some similarities with depression in that they both
represent long-term disorders for which many patients require maintenance treatment.
Chronic insomnia may occur in the absence of coexisting conditions. When coexisting conditions exist,
insomnia may persist despite successful treatment of the coexisting condition. Treatment directed
at the insomnia, rather than the comorbidity, may be necessary. Since insomnia can precipitate,
exacerbate or prolong comorbid conditions, treatment of insomnia may in turn improve comorbidities.
Chronic insomnia is unlikely to resolve spontaneously.111
2.2.2 Management of insomnia in general practice

When patients present with insomnia to GPs in Australia, few (0.8%) receive a referral for
specific non-drug therapy.112 All guidelines strongly recommend psychological and behavioural
management. 68,102,108,113
2.2.2.1 Assessment and diagnosis

Assessment and diagnosis of insomnia requires:111
• understanding the patient’s typical sleep pattern over an extended time frame (weeks to
months) - a sleep diary can help assessment
• identifying contributing lifestyle factors (eg caffeine, nicotine, pets in the bedroom)
• understanding the patient’s beliefs and concerns about sleep
• determining the effects of poor sleep on the patient (eg poor memory, fatigue, work absence,
accidents)
• identifying comorbid conditions - this may be aided by the Auckland Sleep Questionnaire,
which is a validated screening tool.114
2.2.2.2 Acute insomnia

Treatment is focused on avoiding or withdrawing the precipitant, if possible. All patients should
receive basic behavioural counselling on sleep hygiene and stimulus control.
Drug treatment may be indicated as an adjuvant to non-drug therapies for acute insomnia that is
severe, disabling and causing distress. Benzodiazepines and Z drugs are the most effective drugs.25
The short-term use of benzodiazepines as hypnotic agents should only be one aspect of general
management,25 with a clear endpoint of drug cessation once sleep patterns return to normal.
Benzodiazepines
2.2.2.3 Chronic insomnia

Management of chronic insomnia starts with addressing any relevant, underlying problems that
are present, such as:
• pharmacological - prescribed drugs (eg some antidepressants, withdrawal of sedatives) and

non-prescribed drugs (eg caffeine, alcohol)
• physical (eg pain, respiratory and cardiovascular disorders, neurological disorders, movement
disorders, restless leg syndrome and other sleep disorders)
• psychiatric disorders (eg depression, anxiety, dementia and substance misuse)
• disruption of circadian rhythm (eg shift work).
2.2.2.4 Non-drug interventions

First-line therapy for chronic insomnia should be non-drug interventions that are supported by
evidence in achieving sustained improvements in sleep parameters.115,116 Interventions include:
• CBTs18,117 (eg stimulus control, sleep restriction therapy, relaxation techniques, cognitive
therapy and sleep hygiene education)111
• brief behavioural therapy (ie modification of waking behaviours that affect the physiological
systems regulating sleep)118-121
• exercise.122
Psychological and behavioural treatments administered weekly over a 4-8- week period have
shown robust and stable improvements in sleep continuity for up to 2 years.123 These therapies
are now available online, which has vastly improved access.
Refer to Resource G for a GP guide to behavioural therapies for insomnia.
2.2.2.5 Drug therapy

For patients who continue to have insomnia that is sufficiently burdensome to warrant other
interventions, reasonable approaches include continued behavioural therapies, medication or
both.108
Recommendations in guideline on the use of medication for chronic insomnia vary. This is
primarily due to the lack of evidence from extended trials that adequately compare long-term
risks and harms of these medications. Some guidelines suggest avoidance of hypnotic drugs as
far as possible,102 while others make a considered judgement on the risks and benefits.68,108,113
The decision to treat chronic insomnia must weigh any potential serious side effects associated
with pharmacologic therapy against potential health risks of not providing treatment. This
includes decreased quality of life, increased risk for psychiatric comorbidities and SUD, and
decreased performance. The approach should be individualised according to the patient’s values
and preferences, the availability of advanced behavioural therapies, the severity and impact of the
insomnia, and the potential benefits versus the risks, costs and inconveniences.108
Pharmacological treatment should be accompanied by specific patient education, regular review

and continued effort to employ the lowest effective maintenance dosage of medication, and to
taper medication when conditions allow.113
• Benzodiazepines - May have a place in the treatment of severe acute insomnia or

treatment-resistant chronic insomnia. For patients with sleep onset insomnia, a short-acting
medication is a reasonable choice for an initial trial of pharmacologic therapy. This may
improve the insomnia with less residual somnolence the following morning. For patients with
sleep maintenance insomnia, a longer-acting medication is preferable for an initial trial of
pharmacological therapy.108
• Z drugs - Have been shown to be effective in the treatment of insomnia in the short term.
However, there is very limited evidence that they retain their efficacy during long-term
Benzodiazepines
treatment.123 Z drugs are associated with issues relating to adverse events, rebound insomnia,
development of tolerance and SUD, and need to be carefully monitored in individual patients.123
Zolpidem’s black box warning states, ‘Zolpidem may be associated with potentially dangerous
complex sleep-related behaviours which may include sleep walking, sleep driving and other
bizarre behaviours. Zolpidem is not to be taken with alcohol. Caution is needed with other CNS
depressant drugs. Limit use to four weeks maximum under close medical supervision’.124
Psychological and behavioural treatments produce comparable outcomes to Z drugs during

active treatment and have better durability beyond the active administration of treatment.123
Prescription of zolpidem and zopiclone should be treated with the same precautions and
patient management as benzodiazepines.102
• Melatonin - An endogenous hormone associated with the control of circadian rhythms and
sleep regulation. Melatonin levels may be reduced in middle-aged and elderly patients with
insomnia. Supplementation with melatonin has been shown to improve limited aspects of
sleep in 30-50% of patients over 55 years of age.106,125,126 Data from clinical trials are variable.
Some showed that some patients gain clinically significant improvements in quality of sleep
and morning alertness with prolonged-release melatonin, but many patients in the clinical trials
did not respond to treatment.35 Melatonin does not appear to be addictive or cause withdrawal
effects when stopped.125 There are a lack of long-term study data.
At the time of writing, melatonin is available in Australia as a prolonged-release formulation for

short-term treatment of primary insomnia, characterised by poor sleep quality in patients aged
55 years or older.35 The recommended dose is 2 mg orally at bedtime, and at present, there is
insufficient evidence to support treatment beyond 3 weeks.35
In a European campaign to reduce benzodiazepine and Z drug usage, the availability of

prolonged-release melatonin was shown to positively contribute to success.127
• Other prescription medications - Includes antipsychotics (eg quetiapine, olanzepine).

Studies demonstrating the usefulness of these medications for either short- or long-term
management of insomnia are lacking. Furthermore, these agents have significant risks and
therefore, their use in the treatment of chronic insomnia (without a relevant comorbid condition)
cannot be recommended.107 Numerous other medications have a sedating effect, but are
not recommended for routine use in patients with insomnia. These include antidepressants,
diphenhydramine and antipsychotics.108
• Over-the-counter (OTC) medications - Such as antihistamines or antihistamine/analgesic

type drugs, and herbal and nutritional substances (eg valerian) are not recommended in the
treatment of chronic insomnia due to the relative lack of efficacy and safety data.
2.2.3 Resources
• Medical Journal of Australia supplement, Sleep Disorders: A practical guide for Australian health
care practitioners, available at www.sleephealthfoundation.org.au/files/MJA%20Supplement/
MJA_Supplement_final.pdf
• Australasian Sleep Association, Insomnia, available at www.sleep.org.au/documents/item/355
• Australian Prescriber, Cognitive behaviour therapy in medical practice, available at www.

australianprescriber.com/magazine/24/2/33/7
• Australian Psychological Society, Managing insomnia: What we’ve learnt in the last 10 years,
available at www.psychology.org.au/inpsych/2014/april/bartlett
• RACGP Handbook of non-drug interventions (HANDI), Brief behavioural therapy for insomnia in
adults, available at www.racgp.org.au/your-practice/guidelines/handi/interventions/mental-health/
brief-behavioural-therapy-for-insomnia-in-adults
• South Australian kit - Insomnia management kit, available at www.sahealth.sa.gov.au/

wps/wcm/connect/public+content/sa+health+internet/clinical+resources/clinical+topics/
substance+misuse+and+dependence/sleep+problems+-+insomnia+management+kit
Benzodiazepines
2.3 Anxiety disorders

K Key points
• Anxiety disorders are common and exist as a spectrum of conditions that vary from mild to
severe.
• Comprehensive clinical assessment is the first step in management. Effective management

requires obtaining a diagnosis, and recognising that patients may not present with a single
disorder (eg patients may experience generalised anxiety, panic disorder as well as depression).
• Where treatment is indicated:
- First-line therapy for generalised anxiety disorder (GAD), panic disorder, and panic attacks
should include CBT (due to its effectiveness at reducing the symptoms of anxiety in the short
and long term.
- SSRI and SNRI medications are effective across the range of anxiety disorders and generally
suitable for first-line pharmacological treatment of anxiety.
- Short-term benzodiazepines as occasional adjunctive therapy may be effective at reducing

worsening of symptoms that can occur in the first days to weeks of initiating antidepressant
medication, and therefore aid adherence
- Benzodiazepine use in anxiety disorders is mostly limited to severe or treatment-resistant cases.
- Patients who use two or more psychoactive drugs in combination (polydrug use) may be
more vulnerable to major harms.

Rec 6 Cognitive behavioural therapy is recommended as one of the treatments of A
choice for generalised anxiety disorder, panic disorder, and panic attacks due to
its effectiveness at reducing the symptoms of anxiety in the short and long term,
although patient preference must be taken into consideration.64
Rec 7 Consider an selective serotonin reuptake inhibitor (SSRI) for first-line drug treatment, A
as SSRIs are effective across the anxiety and related disorders, in short and long
term, and are generally well tolerated.128
Rec 8 Benzodiazepines have evidence of benefit in generalised anxiety disorder, social A/B
anxiety disorder and panic disorder, but not obsessive compulsive disorder or post
traumatic stress disorder.94
To see the original source of the recommendations and grading, as well as supporting sources, click on the
recommendation number in the left column.
2.3.1 Background
Anxiety disorders include GAD, panic disorder, OCD, PTSD, phobias and SAD.
In 2007, anxiety disorders were the most common self-reported mental disorder in Australia,
affecting 14% of people aged 16-85 years.129 Anxiety disorders may be prominent in depressive
conditions and other chronic health diseases. Anxiety and related disorders often become chronic.
Not all patients with anxiety symptoms require treatment. Anxiety symptoms exist on a continuum
and many people with milder degrees of anxiety, particularly recent onset and association with
stressful situations will recover without intervention.89 The need for treatment is determined by the
severity and persistence of symptoms, the presence of comorbid mental or physical illness, the level
of disability and the impact on social functioning. Treatment should aim to achieve full remission of
symptoms and return of function, rather than just symptom improvement and distress reduction.130
Benzodiazepines
Randomised controlled trials across a range of anxiety disorders often demonstrate a high placebo
response, which indicates that non-specific effects can play a large part in improvement.128
Approaching anxiety disorders systematically involves identifying and treating any comorbidities,
providing patient education and appropriate psychological and pharmacological interventions. These
should be evidence-based and patients should receive ongoing monitoring to determine whether
treatment aims are being achieved.130
2.3.2 Management of anxiety in general practice

For a comprehensive review of management of anxiety disorders, GPs are advised to review
individual clinical guidelines.
Benzodiazepine use in anxiety disorders is mostly limited to severe, or treatment-resistant, cases.

Patients with a history of significant mental illness who use two or more psychoactive drugs
(polydrug use) may be more vulnerable to major harms. Significant caution should be taken if
prescribing benzodiazepines to patients with comorbid alcohol or SUDs, or polydrug use. GPs
should consider seeking specialist opinion in the management of these patients.
2.3.2.1 Assessment and diagnosis

Comprehensive clinical assessment is the first step to developing a diagnosis and determining
the patient’s level of disability. In milder, recent onset anxiety disorders, consider ‘watchful waiting’
(support, addressing social factors and monitoring).89
It is important to detect comorbid depression. Depression should be treated if depressive

symptoms are moderate or severe.
Most guidelines recommend CBT as first-line non-drug therapy, while SSRIs and SNRIs are
the drugs of first choice. Benzodiazepine recommendations are generally limited to severe
or treatment-resistant cases. However, the efficacy of psychological and pharmacological
approaches is similar in the acute treatment of mild to moderate anxiety disorders.89,94,131
The selection of an initial treatment modality should be guided by considerations including
the patient’s needs and preferences, the risks and benefits for the patient, the patient’s past
treatment history, the presence of comorbid general medical and other psychiatric conditions,
cost and the local availability of evidence-based psychological interventions.
Where appropriate and available, patients should be offered a choice of evidence-based

treatment approaches.
2.3.2.2 Cognitive behavioural therapy

All major guidelines recommend CBT as the first-line intervention for anxiety disorders.64,89,94,130
CBT is a multimodal intervention. Specific techniques used in the therapy include education,
self-monitoring, relaxation training, cognitive restructuring, exposure to imagery and anxiety
producing situations, and relapse prevention. CBT has been shown to be an effective stand
alone treatment for GAD.132 Comorbidity does not decrease the treatment effects of CBT.
CBT for most anxiety, and related disorders, can be delivered effectively in individual or group
therapy formats.130 There are also an increasing number of self-directed formats that require
minimal or no therapist contact, which have been shown to be effective.130 These include
bibliotherapy (self-help books) and internet or computer-based programs.133,134
A combination of medication and cognitive behaviour or exposure therapy has been shown
to be a clinically desired treatment strategy.94 However, combination therapy results have
been conflicting,135,136 and results vary for different anxiety disorders. While current evidence
does not support the routine combination of CBT and pharmacotherapy as initial treatment
for all anxiety disorders, there is support for combined use in panic disorders, with or without
agoraphobia.137,138
Benzodiazepines
Benzodiazepines are generally avoided in patients with anxiety disorders who are undergoing
CBT. This is due to their potential interference with motivation and learning, which are required
for CBT to be effective. Some authors are now challenging this,73 however there is sparse trial
evidence to support a conclusion. More research is needed to ascertain if these treatment
modalities can be combined effectively.
CBT protocols for anxiety usually involve 10-14 weekly sessions, but briefer strategies of 6-7
sessions have been shown to be as effective. Unfortunately, a lack of access to trained clinicians
may be an issue in some areas and therefore lead to the majority of patients with anxiety being
treated with medications.139 Online CBT programs have shown efficacy, and may be suitable for
patients who cannot access face-to-face therapy, or who prefer treatment in their own homes, in
their own time.
2.3.2.3 Antidepressants
Note that anxiety disorders show a strong placebo response, especially at mild to moderate levels of
symptom severity.89 If pharmacotherapy is indicated, the SSRIs and SNRIs are preferred agents.140
Tricylic antidepressants (TCAs) and monoamine oxidase inhibitors (MOAI) are other alternatives.
Although preferred over benzodiazepines, there are limited studies comparing head-to-head
effectiveness with antidepressants. Reviews of the studies performed suggest comparative
effectiveness of benzodiazepines to older and new antidepressants.141-142
In trials of benzodiazepines and newer antidepressants, benzodiazepines have demonstrated

comparable or greater improvements with fewer adverse events in patients suffering from GAD or
panic disorder.141 Efficacy of benzodiazepines for panic disorder is comparable to SSRIs, SNRIs
and TCAs.143 Similarly, the incidence of withdrawal symptoms from antidepressants seems to
occur at similar levels to benzodiazepines.96
Reviewers have suggested the major change in prescribing pattern from benzodiazepines to
newer antidepressants in anxiety disorders has occurred in the absence of comparative data of
high-level of proof.141,144
However, SSRIs and SNRIs remain recommended first-line treatments by international guidelines
for anxiety disorders.143
Short-term benzodiazepines as occasional adjunctive therapy may be effective at reducing

worsening of symptoms that can occur in the first days to weeks of initiating antidepressant
medication.
2.3.2.4 Benzodiazepines
Benzodiazepines are not indicated for ‘mild’ anxiety.
Benzodiazepines may be used (as monotherapy or in combination with antidepressants) for
patients with very distressing or impairing symptoms whom rapid symptom control is critical.143
Benzodiazepines have evidence of benefit for GAD, social anxiety disorder and panic disorder,
but not for OCD or PTSD.64,94 Trials have been conducted with clonazepam, diazepam and
lorazepam, which have demonstrated the efficacy of these compounds in managing panic
disorder clonazepam for SAD, diazepam and bromazepam for GAD.3
The benefit of a more rapid response to benzodiazepines must be balanced against the
possibilities of troublesome side effects (eg sedation) and physiological dependence that may
lead to difficulty discontinuing the medication.143 Note that:
• Due to its rapid onset and offset of action, alprazolam is the benzodiazepine most commonly
prescribed for panic disorders. However, in a meta-analysis, it has not been shown to have
better efficacy than other benzodiazepines for panic disorders, and it does have a greater risk
of dependence, problematic use and withdrawal.145
• Although tolerance is less of an issue with anxiety, patients are at risk of dependence and
other harms (eg depression, increased anxiety, accidents).
Benzodiazepines
When benzodiazepines are prescribed short term for severe anxiety, they are generally used in
conjunction with other interventions including counselling or antidepressants (where appropriate),
to reduce the risk of symptom recurrence89 or to alleviate and prevent the worsening of anxiety130
that may occur at the start of antidepressant therapy.146
Rarely, ongoing therapy with benzodiazepines may be necessary in patients with severe,
treatment-resistant anxiety. Although concerns have surrounded the risks of tolerance and SUD
with long-term use of benzodiazepines, there is little evidence of tolerance to their anxiolytic
effects.35 Problematic use is a risk in those with a history of SUD, but is otherwise uncommon.147
The decision to treat chronic anxiety with benzodiazepines must weigh the risks and benefits of
benzodiazepine therapy. Concerns about potential problems in long-term use should not prevent
their use in patients with persistent, severe, distressing and impairing anxiety symptoms,147
or in patients who are resistant to, or cannot tolerate, multiple first-line therapies.130 Ongoing
supervision is required.
2.3.3 Resources
• Australian Prescriber, Cognitive behaviour therapy in medical practice, available at www.
australianprescriber.com/magazine/24/2/33/7
• RACGP Handbook of non-drug interventions (HANDI), Depression and anxiety: internet based or
computerised CBT (iCBT or CCBT), includes relevant website links, available at www.racgp.org.
au/your-practice/guidelines/handi/interventions/mental-health/internet-based-or-computerised-
cbt-for-depression-and-anxiety
2.4 Alcohol withdrawal

K Key points
• Benzodiazepines are an important component of alcohol withdrawal programs, but not every
patient requires medication.
• Benzodiazepines are generally only used as first-line options for acute treatment in a controlled
environment for alcohol withdrawal.

Rec 9 Benzodiazepines (eg diazepam, oxazepam) are the drugs of choice for treatment of A
acute alcohol withdrawal (including alcohol withdrawal delirium), but for a maximum
of 7 days.148
To see the original source of the recommendations and grading, as well as supporting sources, click on the recommendation
number in the left column.
2 .4.1 Background
Alcohol dependence is characterised by craving, tolerance, preoccupation with alcohol and
continued drinking in spite of harmful consequences (eg liver disease). From a clinical perspective,
alcohol dependence can be subdivided into mild, moderate or severe categories. People with mild
dependence (based on alcohol dependence assessment tools) usually do not need assisted alcohol
withdrawal. People with moderate dependence usually need assisted withdrawal, which can be
managed in a community setting. People who are severely alcohol dependent need assisted alcohol
withdrawal, typically in an in-patient or residential setting.149
Benzodiazepines
The onset of alcohol withdrawal is usually 6-24 hours after the last drink. In some severely
dependent drinkers, withdrawal can occur while the patient is still intoxicated due to drops in blood
alcohol level.30
About 95% of people with alcohol dependence can stop drinking without major withdrawal
symptoms (ie delirium, seizures).30 Supportive care alone is often effective in minor alcohol
withdrawal. Medication may not be necessary with lower daily alcohol consumption or for periodic
drinkers. Seizures (usually a single episode) occur in approximately 5% of people with alcohol
dependence when withdrawing from alcohol, and delirium tremens are typically seen in the most
severe forms of alcohol withdrawal.30
2 .4.2 Management of alcohol withdrawal in general practice

Alcohol dependence may require complex multidisciplinary therapy, including social support
systems.
2.4.2.1 Assessment
Formal assessment tools can help determine if the patient is best suited to alcohol withdrawal in
the primary care or specialist alcohol services setting.
The routine screening tool is the Alcohol Use Disorders Identification Tool (AUDIT or AUDIT-C)
(refer to Resource F). Other tools include Severity of Alcohol Dependence Questionnaire (SADQ)
to assess the severity of dependence; and the Clinical Institute Withdrawal Assessment of
Alcohol State, revised (CIWA-Ar) or Alcohol Withdrawal Scale (AWS) for severity of withdrawal.
Patients may be suitable for home alcohol withdrawal if they:
• have no history of seizures or delirium tremens
• do not pose a suicide risk
• have social support

• show no significant polydrug misuse
• are not dependent on benzodiazepines.149
2.4.2.2 Assisted withdrawal approaches

When conducting an assisted withdrawal from alcohol, there are three commonly used
approaches:30
• benzodiazepine loading - involves giving a large dose (up to 80 mg of diazepam) on day one
in an in-patient setting, and then no further benzodiazepines
• tapering dose regimes - a predetermined (fixed) dose of benzodiazepine is administered in
tapering doses over 2-6 days
• symptom-triggered sedation - doses of benzodiazepine are administered according to the

severity of withdrawal symptoms.
There is limited evidence for selecting one approach over another, however, the first approach is
more suited to an in-patient setting. In a comparison of fixed schedule and symptom triggered
regimens, the latter two approaches were favoured.150
2.4.2.3 Benzodiazepines
Benzodiazepines have been shown to be one of the most effective drug classes in the
management of alcohol withdrawal syndrome. The rationale of the use of benzodiazepines is to
modulate CNS hyperactivity due to the alcohol withdrawal, by interacting with GABA receptors.150
Benzodiazepines
A 2010 systematic review found benzodiazepines have a protective benefit against alcohol
withdrawal symptoms, in particular seizures (when compared to placebo), and have a potentially
protective benefit for many outcomes when compared with other drugs. This review did not find
a statistical significance among the performance of different benzodiazepines.150
Avoid prescribing benzodiazepines to patients who are dependent on alcohol before enrolling
them in, or referring them to, community withdrawal. Prescribing a ‘small dose of diazepam’ to
help patients who claim to have stopped or reduced their alcohol consumption should also be
avoided. Benzodiazepines can increase alcohol cravings and relapse rates.151
2.4.2.4 Baclofen and carbamazepine

Baclofen has been used to rapidly reduce symptoms of severe alcohol withdrawal syndrome.
However, the evidence for recommending baclofen is insufficient to support its use in most
situations.152 Carbamazepine has been effective in trials, but its role is as yet unclear.153 These,
and several other drugs, may be useful adjuncts but cannot currently be recommended for
clinical monotherapy.
2.5 Acute mania (bipolar disorder)

K Key points
• Benzodiazepines can be used to calm or sedate and control aggressive, overactive or disturbed
behaviour in manic episodes until a mood stabiliser takes effect.
2.5.1 Background
Bipolar disorder is a recurrent, disabling condition. Patients experience periods of mania or
hypomania, depression and mixed episodes or ‘dysphoric mania’ (both manic and depressive
symptoms). Bipolar disorder is commonly subdivided into bipolar disorder I (at least one manic
episode) and bipolar disorder II (hypomania and depression only).154
Bipolar disorder has a lifetime prevalence of up to 1.6%.154
2.5.2 Management of manic episodes in general practice

For acutely manic patients, referral to a specialist psychiatric service for in- or out-patient care is
recommended.154
There are two components to managing acute mania with medication:154
• mood stabilisation with drugs (eg lithium, sodium valproate, carbamazepine) or one of the new
second-generation antipsychotics
• adjunct therapy to control acute agitation while mood stabilisers start to take effect (about 1 week
for most patients).
Adjunct therapy usually consists of an antipsychotic or benzodiazepine (or a combination). This

calms or sedates the person with mania as a temporary measure, until the mood stabiliser starts to
be effective.154
In most cases, the benzodiazepine or antipsychotic would be withdrawn once the acute episode
has resolved, and then only the mood stabiliser continued. It is common practice to taper down and
discontinue benzodiazepines within 2-3 weeks of achieving adequate symptom control in mania.154
Benzodiazepines
2.6 Epilepsy
K Key points
• Clonazepam has been the most commonly used benzodiazepine for the long-term treatment of
epilepsy.

Carbamazepine, sodium valproate, lamotrigine and oxcarbazepine can all be regarded as first- A
line treatments for partial and secondary generalised seizures.155
Sodium valproate and lamotrigine are drugs of choice for primary generalised seizures and A
should also be prescribed if there is any doubt about the seizure type and/or syndrome
classification.155
2.6.1 Background
Epilepsy affects approximately 224,000 Australians (1 in 100) and is the most common chronic brain
disorder. Nearly 10% of Australians will have a seizure during their lifetime, and one-third of those will
be diagnosed with epilepsy.156
2.6.2 Management of epilepsy in general practice

In acute epilepsy, diazepam, lorazepam and midazolam are the drugs most commonly used to
control prolonged seizures.155
In chronic epilepsy, the use of benzodiazepines is now rare. They have limited usefulness in long
term management due to the rapid development of tolerance to anticonvulsant effects and the
associated side effects (eg sedation and psychomotor slowing).155
Benzodiazepines are considered adjunct to standard antiepileptic drugs, and used when these have
failed to achieve acceptable control.155
Benzodiazepines for seizure prophylaxis should only be used on advice from a specialist neurologist
or paediatrician.
Prescription of benzodiazepines for epilepsy within Australia requires an authority prescription. Take
care with monitoring and detecting problematic use.
Benzodiazepines
3. Contraindications and precautions

in special groups
3.1 Overview
Benzodiazepines should not be prescribed, or prescribed with extreme caution, to:
• women who are, or may be, pregnant
• patients with active SUDs, including alcohol (unless it is a part of an alcohol withdrawal program)
• patients with medical or mental health conditions that may be worsened by benzodiazepines (eg
fibromyalgia, chronic fatigue syndrome, depression, bipolar disorder or impulse control disorders)
• patients being treated with opioids for chronic pain or addiction
• patients experiencing grief reactions, as benzodiazepines may suppress and prolong the grieving process.
3.2 Paediatric patients

Benzodiazepines are generally not recommended for use in children.
Benzodiazepines may cause aggression, anxiety, nervousness and disinhibition in children and
adolescents. Routine use for anxiety disorders cannot be recommended.157
The use of benzodiazepines in the paediatric population is clinically limited.158 Control of acute febrile or
epileptic seizures is the primary indication. Seizures commonly occur in the paediatric populations and
while most self-terminate within 5 minutes, those lasting longer may warrant medication to control the
seizure and avoid status epilepticus (and neurological compromise).159 Buccal or intranasal midazolam
and buccal or rectal diazepam are effective for the treatment of acute seizures in children.160
Note that children may have access to benzodiazepines through their parents, their peers or potentially
via the internet.
3.3 Women who are pregnant or breastfeeding

Benzodiazepines should be avoided during pregnancy and breastfeeding. Non-drug approaches for
anxiety and insomnia are preferred.
Women who become pregnant and are already taking benzodiazepines should be tapered down to the
lowest effective dose, or have it completely withdrawn. With good withdrawal management, there is no
evidence that withdrawal is likely to cause problems with the pregnancy.38
As benzodiazepines are highly fat soluble, they rapidly cross the placenta. Benzodiazepines taken early
in pregnancy have been linked to congenital abnormalities (eg oral clefts, pyloric stenosis and alimentary
tract atresia).161 This association is considered controversial, and data published in the last 10 years
do not indicate an absolute contradiction to benzodiazepines in the first trimester.162 However, avoiding
benzodiazepines or tapering off (completely or to the lowest possible dose) is recommended.163
Benzodiazepines taken later in pregnancy (late third trimester), during labour or while breastfeeding are
associated with risks to the fetus/neonate. They can cause neonatal drowsiness, respiratory depression,
poor temperature regulation, poor feeding, hypotonicity (‘floppy baby syndrome’) and neonatal
withdrawal syndrome.35,164
Benzodiazepines
Neonates exposed in utero may benefit from breastfeeding to reduce neonatal withdrawal.165,166
Where a hypnotic is necessary, zolpidem has been suggested.163 However, two studies have reported
an association between zolpidem and an increased risk of adverse pregnancy outcomes, including
small-for-gestational age, low birth weight and preterm deliveries.35
Note that women misusing benzodiazepines during pregnancy may also be using other drugs including
alcohol.
3.4 Older patients

Patients over 60 years of age have the most significant risk of harm with benzodiazepine use (particularly
if the patient has additional risk factors for cognitive or psychomotor adverse events) relating to falls,
fractures and cognitive decline.50,167
Benzodiazepines are used by approximately 15% of people over 65 years of age in Australia.168 Use of
benzodiazepines in this age group is often chronic, despite the combination of harms associated with
long-term, physiological changes with ageing (eg hepatic metabolism impairment) and the potential for
multiple coexisting pathologies and drug interactions.
Older patients are more sensitive to the CNS depressant effects of psychotropic medications including
benzodiazepines. This may result in confusion, night wandering, amnesia, pseudo-dementia38 (refer to
1.5.1.1 Cognitive impairment), ataxia, falls and fractures.
In older patients, all psychotropic medications have been associated with an increased risk of fractures.
The risk increase is moderate and similar across all psychotropic medications. One meta-analysis
demonstrated that the relative risk of fractures was 1.34 (95% CI=1.24-1.45) for benzodiazepines, 1.60
(95% CI=1.38-1.86) for antidepressants, 1.59 (95% CI=1.27-1.98) for antipsychotics and 1.38 (95%
CI=1.15—1.66) for opioids.169
Older people presenting with anxiety symptoms should be treated initially with antidepressants and
psychological therapies, rather than benzodiazepines.170
Sedative use for insomnia has shown statistically significant improvements in sleep, but the magnitude
of effect is small and the benefits of these drugs may not justify the increased risk.167 Clinical judgement
is required.
Zolpidem and other Z drugs have become preferred drugs to manage insomnia. They are widely
used among older adults because of perceived improved safety profiles compared with traditional
benzodiazepines. However, accumulating data in recent years in patients over 65 years of age suggest
possible safety concerns of these medications (zolpidem specifically) including effects on balance and
memory and increased fracture risk. Until better studies or pharmacovigilance data become available
to guide patient selection for prescribing zolpidem and other Z drugs, judicious use of these hypnotic
agents in older adults is warranted.171
Reduction in the use of benzodiazepines in the elderly is a worthwhile goal if this can be achieved
without psychotropic substitution. Older patients require planned interventions including CBT and
stepped-dose reduction to reduce long-term benzodiazepine prescription.
3.4.1 Patients living in residential aged care facilities

Prescribing for patients living in residential aged care facilities (RACFs) (and other residential facilities)
carries all of the risks associated with benzodiazepine use in older patients and presents further
special difficulties.
Accreditation of RACFs has resulted in a heightened awareness of the facility’s responsibilities for
quality use of medicines.
Medication may occasionally be required to control anxiety, agitation or other disturbed behaviours.
Staff should be knowledgeable in the appropriate management of challenging behaviours. Where
staff have received education in geriatric care, and where the organisational culture is supportive,
there is less use of benzodiazepines.170
Benzodiazepines
In a study of sleep quality in patients using benzodiazepines in RACFs, patients who were long-term
users slept more poorly than those who were non-users. The effects were worse in patients taking
long-acting benzodiazepines.172 Although patients, doctors, nursing staff and families often fear the
consequences of benzodiazepine withdrawal in older patients, there is no evidence that patients
experience an ‘unmasking’ of depression or anxiety.173
Successful reduction in the rates of benzodiazepine use in RACF patients results in benefits (eg
increased mobility and alertness, reduced incontinence and improved wellbeing).174 Discontinuation
of benzodiazepines can often be achieved gradually in RACFs, providing patient, family and nursing
staff are cooperative.175
Benzodiazepines have been associated with increased fracture risk in patients living in RACFs.
However, a reduction in benzodiazepine use may not lead to a decrease in fracture risk if substitution
medications are used.176 Reduction in benzodiazepine use for RACF patients is worthwhile if it can
be achieved without psychotropic drug substitution.
3.5 Patients with chronic non-malignant pain

Use of multiple psychoactive medications (including benzodiazepines) is common in people who have
chronic non-malignant pain (CNMP). Where available, it is advisable that a specialist pain or addiction
service becomes involved in the care of these patients.177
The relationship bewteen pain, mental illness, SUD and dependence, and the social environment are
complex. A range of addictive drugs has been misused in the context of CNMP including alcohol,
benzodiazepines, cannabis, opioids and stimulants. Estimates of dependence (on any drug including
alcohol) among people with chronic pain varies. In patients on long-term opioids, prevalence of DSM-5
opioid-use disorder may be as high as 26%.178
Benzodiazepines have little place in the management of chronic musculoskeletal pain. There is sparse
evidence that these are clinically effective as muscle relaxants. The decision to use benzodiazepines
in the context of multiple sclerosis or muscle disorders should be taken on a case-by-case basis with
specialist consultation.
There is a strong association between sleep disturbance and CNMP. Evidence suggests that pain and
sleep exist in a complex relationship in which pain causes sleep disturbance and sleep disturbance
intensifies pain. This association can impair a patient’s daily function and decrease quality of life.179
Assessment of a patient’s sleep disturbance involves review of the contributing impacts of lifestyle,
comorbid anxiety or depression, and uncontrolled pain to focus management on an individualised basis.
Benzodiazepines present additional risk for someone being prescribed opioids in terms of overdose
(fatal and non-fatal) and psychomotor impairment. Driving presents a particular risk.
CBT can be useful in addressing emergent anxiety symptoms. Simple reassurance and attention to
sleep hygiene can be effective with managing the emergent sleep disturbance.
3.6 People with comorbidity - Mental illness

and problematic drug use
For the purposes of this guide, comorbidity will refer to situations where people have problems related
both to their use of substances (from hazardous through to harmful use and/or dependence) and to their
mental health (from problematic symptoms through to highly prevalent conditions such as depression
and anxiety, and to the low-prevalence disorders such as psychosis).177
While it is common to refer to a patient’s psychiatric disorder or SUD as primary or secondary, this may
have limited clinical use. It is important to establish whether substance use may be contributing to the
patient’s psychiatric problems.177
Benzodiazepines
Symptoms of psychiatric disorders (eg depression, anxiety and psychosis) in patients misusing drugs
and/or alcohol are the rule rather than the exception. In addition, these psychiatric disorders increase
the risk of harmful substance use and patients may be physically unwell. These patients are often the
most challenging to engage and treat, and their prognosis is frequently poor.177
The number of placebo-controlled trials is small, and there remains little evidence to guide treatment.177
Available evidence suggests that a substantial proportion of patients with a comorbid SUD mental
illness who are treated with benzodiazepines will develop some form of dependence. Therefore,
benzodiazepines should largely be avoided, except in the context of withdrawal.180
Patients with personality disorders have a higher risk of dependence and dose escalation, hence
benzodiazepines should be avoided in this group.
3.7 Patients who misuse alcohol and/or other

drugs (prescribed and illicit)
Patients who have problematic drug use belong to a complex group at high risk of adverse events.
A common drug combination that should be noted is alcohol and benzodiazepines.180 When
benzodiazepines are combined with other CNS depressants (eg alcohol, opioids), patients are at
risk of respiratory depression, heavy sedation, coma and death. It has been reported that the use of
antidepressant drugs in combination with benzodiazepines may also increase the risk of overdose,
especially in the case of older TCAs.181 Alcohol and benzodiazepines can produce cross tolerance, and
regular use of both can make withdrawal more severe and/or protracted.180
Apart from the risk of overdose, harms associated with polydrug use (particularly among people who
inject drugs) include a higher rate of infectious and metabolic complications, as well as psychiatric,
social and forensic consequences, with an increasing cost to society.182,183 People who are participating
in medication-assisted opioid dependence treatment, and who take benzodiazepines regularly or
intermittently, tend to do very poorly, with a higher risk of adverse outcomes.21
There is little evidence to guide practitioners in the management of this often difficult-to-treat
population. However, when treating polydrug users, it is recommended not to initiate prescription of
benzodiazepines. For polydrug users already taking them, it is recommended to reduce and cease
prescription of benzodiazepines in a supervised manner.153
Therapeutic monitoring and prescribing should only occur if GPs have extensive experience in addiction
medicine, or in conjunction with specialist supervision. When working with known polydrug users, it
is essential to collaborate with local drug and alcohol services, and to provide clear guidelines on the
accepted harm-minimisation strategies. Clear boundaries are crucial.
Maintenance benzodiazepine prescribing in illicit drug users cannot be recommended on the basis of
existing evidence. Although it may reduce illicit benzodiazepine use in some patients,153 it may not be
in the best interests of the patient or the wider community. The very rare exception would be under
explicit agreement concerning specified short-term indications (such as outpatient alcohol withdrawal)
as advised by a drug and addiction medicine specialist with daily, or at most weekly, dosing at a
nominated pharmacy and monitoring with urinary drug test. Drug screens may be useful to monitor
other benzodiazepines and drug use, especially in this population.
Benzodiazepines
3.8 Prescribing to patients who drive

Summarising the extensive literature on benzodiazepines and driving, the risk of accident increases
proportionally to dose. However, there is no dose without increased risk - including stable, longer term
dosing. Risk is highest at initiation, with long-acting benzodiazepines and when benzodiazepines are
taken with other sedatives, especially alcohol.
Benzodiazepines have especially been shown to impair vision, attention, information processing,
memory, motor coordination and combined-skill tasks. All drivers should be advised of increased crash
risk when taking benzodiazepines. Patients who experience any degree of sedation should be cautioned
not to drive.
According to Austroads, a person is not fit to hold an unconditional licence if they have an alcohol
disorder or other SUD (eg substance dependence, heavy frequent alcohol or other substance use) that
is likely to impair safe driving.184
The state or territory driver licensing authority may consider a conditional licence. This is subject to
periodic review, taking into account the nature of the driving task and information provided by the
treating doctor as to whether the following criteria are met:184
• the person is involved in a treatment program and has been in *remission for at least 1 month
• there is an absence of cognitive impairments relevant to driving
• there is absence of ‘end-organ effects’ that impact on driving.
* Remission is attained when there is abstinence from the use of impairing substance(s) or where substance use has
reduced in frequency to the point where it is unlikely to cause impairment. Remission may be confirmed by biological
monitoring for the presence of drugs.
Some patients with SUD will continue to drive after being warned not to do so. If GPs are aware that a
patient continues to drive in a dangerous way, they should:
• more strongly recommend the patient stops
• advise the patient that the GP has an obligation to report behaviours that are dangerous to the
patient and others
• consider reporting dangerous behaviour to state or territory licensing authorities.
This is a difficult situation as it will damage the doctor-patient relationship. However, in some cases the
risk of damaging the relationship is outweighed by the risk of the patient (and others) being hurt or killed.
If in doubt, contact your medical indemnity provider.
Benzodiazepines
4. Duration of benzodiazepine therapy
4.1 Optimal duration of therapy

Guidelines and formularies typically give durations of 1-4 weeks for benzodiazepine therapy, depending
on the indication. Short-term therapy is generally advised to reduce the risk of dependence and
withdrawal, as well as other potential harm such as cognitive impairment. Short-term therapy does not
reduce the risk of accidents or falls.
Dependence is recognised as a risk in some patients who receive treatment for longer than 1 month,
and health professionals should be conscious of this when considering the relative benefits and risks of
treatment.25
The 1-4 week time frame is not based on risk-benefit data; rather that no substantive placebo-
controlled trials of hypnotics have been carried out for longer than a few weeks. The available evidence
does not suggest there is an unfavourable risk-benefit transition at 3-4 weeks for any agent.101
Patients who are prescribed benzodiazepines for problems relating to anxiety or sleep usually do
not escalate their doses even over a lengthy period of use.185 A 2013 study found most patients use
benzodiazepines according to guidelines, and only 0.9% ended up as excessive users after 3 years.76
Excessive use occurred mostly in individuals with alcohol and drug histories.
Lacking the means to determine the optimal duration of therapy, a rational approach is to allow the
duration of treatment to be determined by a series of risk-benefit decisions and shared decision making,
with periodic trials of tapering and discontinuing medication to determine whether continued therapy
is indicated.101,186 This approach provides an ‘exit strategy’ and thereby addresses concerns that once
started, hypnotic therapy could be unending.101
Clinical discipline and accountable prescribing are essential when considering long-term benzodiazepine
therapy.
4.2 Prescribing benzodiazepines for longer

than 4 weeks
While the optimum duration of therapy is not clear from the evidence, there are very few specific
indications for the chronic use of benzodiazepines. The decision to prescribe benzodiazepines longer
term should be uncommon and made with caution. Assume that all patients are at risk of dependence.
Benzodiazepines may be used for longer than 4 weeks in selected cases. Patients who are terminally ill
or severely handicapped, where it is clear that the benefits outweigh the risks and side effects, or where
a detailed individual assessment has been made with a patient and their family or carers.
Benzodiazepines may also be indicated in certain neurological disorders (eg stiff person syndrome) and in
neuromuscular conditions where spasticity is problematic. Increasingly, benzodiazepines are being used
off-label for indications (eg drug-induced movement disorders, restless legs syndrome, acute psychotic
agitation, terminal agitation, nausea and vomiting, intractable pruritus and intractable hiccup).187
Recommendations supporting the long-term use of benzodiazepines for any mental illness or chronic
sleep disorder come from evidence limited to shorter time frames. Hence, longer duration of prescribing
should occur in conjunction with heightened clinical surveillance.
The principles of universal precautions apply. Ensure a clear diagnosis is formed, comprehensive
assessment is undertaken, clear treatment plan is discussed with the patient and information is provided
to the patient to enable informed consent. The negotiated treatment plan will have clearly defined time
limit and goals of treatment.
Benzodiazepines
4.3 Rationale for long-term benzodiazepine

prescribing
Benzodiazepines are generally regarded by clinical practice guidelines as a short-term therapeutic
option. Long-term use, beyond 4 weeks, is not generally advocated by clinical practice guidelines,
hence long-term therapy should be should be uncommon and made with caution.
Prescribing benzodiazepines, like other aspects of clinical practice, should be based on thoughtful
consideration of the likely risks and benefits, and the risks and benefits of alternative interventions. This decision
should be made in conjunction with the patient and their carers, where appropriate.100 Benzodiazepines may
be prescribed longer term where:
• patients do not respond to, or cannot tolerate, numerous first-line therapies130,188
• use is intermittent
• specialists make a recommendation and are able to provide a rationale of therapy.
For some patients, benzodiazepine alternatives fail, have limited benefit, are unavailable or clinically
inappropriate. If there is no history of drug dependence, positive indicative ‘lifestyle’ factors are present
and a clinical decision for benzodiazepine treatment can be justified, then long-term therapy should
not necessarily be regarded as a deviation from good clinical practice.25 Supervised benzodiazepine
treatment may remain an acceptable long-term therapeutic option for some patients.
4.4 Management of long-term benzodiazepine

prescriptions
Many patients are able to safely take short courses of benzodiazepines, or to use them intermittently
longer term, on a ‘as required’ basis and to stop them when no longer needed.25,113
In a situation where the clinical decision is that the ongoing use of a benzodiazepine is the most
appropriate management, this requires ongoing monitoring of health outcomes and continuing vigilance
for potential hazards throughout treatment.25
The responsible specialist or GP should clearly outline a prescribing plan that should be documented in
the patients’ notes or management plan.
The prescribing plan may include instructions that:
• regular prescription reviews take place
• no repeat prescriptions will be made without face-to-face contact
• all prescriptions will be made by one doctor within a single practice
• one pharmacy will dispense all medication.
Benzodiazepine prescriptions should be at the lowest effective dose and given intermittently, with regular
reviews of the treatment plans and regular attempts at withdrawal.
At the time of benzodiazepine prescription renewal or medication review, GPs should continue to
discuss the risks of long-term benzodiazepines and the benefits of discontinuation (eg cognition, mood,
sleep and energy level) and advise the patient to reduce or discontinue the benzodiazepines if there are
issues. GPs should document this communication.
Patients should be monitored closely for problematic use or any therapeutic dose dependence behaviour.
Any escalation of dose or inappropriate use would lead to a complete review of prescribing and attempted
withdrawal of benzodiazepine, along with a review of alternative therapy.
Refer to Resource E.2 for an example of a prescription plan/agreement.
All GPs should develop strategies to manage inappropriate requests for benzodiazepines.
Benzodiazepines
5. Discontinuing benzodiazepines
5.1 Discontinuing after short-term use

For patients on less than 4 weeks of benzodiazepine therapy, it should be possible to stop medication
without tapering. Caution should be exercised with patients who are at risk of seizures.
5.2 Discontinuing after longer term use -

Withdrawal
Withdrawal is possible for most patients on longer term benzodiazepines, although the process of
reduction may be difficult and lengthy. The withdrawal process is aided by a good therapeutic alliance
between the GP and patient, with specialist support where needed. Discontinuation is usually beneficial
as it is followed by improved psychomotor and cognitive functioning, particularly in the elderly.189 Up to
15% of patients who experience withdrawal will go on to have protracted symptoms lasting months to
years.2
Withdrawal strategies will vary with the type of dependence (therapeutic dose, prescribed high dose,
recreational high dose or polydrug). Withdrawal symptoms are highly variable and each patient will need
tailored withdrawal management that will also address any underlying problems. Withdrawal symptoms
may appear in 1-2 days for agents with shorter half-lives, but may not appear until 3-7 days for agents
with longer half-lives.
Table 4. Acute withdrawal symptoms
Anxiety symptoms Major incidents

Distorted perceptions Mainly when high doses
Psychological Physical are stopped abruptly
• Anxiety • Agitation • Hypersensitivity to • Fits (1-2% of patients)

• Panic attacks • Tremor sound, light, touch, • Delirium (rare)
taste
• Insomnia • Headache • Transient
• Abnormal body hallucinations (visual,
• Poor memory • Weakness
sensation eg itching, tactile, auditory) or
• Depression • Dizziness pain, stiffness, blurred illusions (rare)
• Paranoia • Nausea vision, paraesthesia,
• Psychosis (very rare)
• Intrusive memories • Vomiting muscle twitching,
tinnitus, burning
• Cravings • Diarrhoea
sensations
• Nightmares • Constipation
• Feeling self or world
• Excitability • Palpitations to be abnormal
• Agoraphobia • Rashes (depersonalisation or
• Social phobia • Tingling, numbness, derealisation)
• Obsessions altered sensation

• Rage, aggression • Fatigue
• Irritability • Flu-like symptoms
Reproduced with permission from Ford C, Law F. Guidance for the use and reduction of misuse of benzodiazepine
prescribing and other hypnotics and anxiolytics in general practice. 2014.38
Benzodiazepines
Protracted benzodiazepine withdrawal symptoms include:30
• anxiety
• depression
• diarrhoea, constipation, bloating
• insomnia
• irritability
• muscle aches
• poor concentration and memory
• restlessness
• less commonly, perceptual disturbances and panic attacks
• occasionally, seizures and symptoms of psychosis.
The symptoms and duration of benzodiazepine withdrawal can vary, mostly impacted by the level of
dose reduction. Although, other contributing factors can include a history of polydrug dependence,
seizures, anxiety, depression or trauma, or when the total daily dose is not clear (due to doctor shopping
or illegal purchase).
5.2.1 Patients taking ‘therapeutic doses’

For patients who have early/mild dependence, minimal interventions such as advisory letters, other
information provision or GP advice should be offered. Where dependence is established, gradual
dose reduction of prescribed benzodiazepine is recommended (both grade A recommendations from
the British Association for Psychopharmacology).153
Switching from a short half-life benzodiazepine to a long half-life benzodiazepine before gradual
taper should be reserved for patients having problematic withdrawal symptoms on reduction (grade
D recommendation from the British Association for Psychopharmacology).153
Additional psychological therapies increase the effectiveness of gradual dose reduction, particularly
in patients with insomnia and panic disorder. Consideration should be given to targeted use of these
interventions (grade B recommendation from the British Association for Psychopharmacology).153
5.2.2 Patient taking high doses of benzodiazepines or

who are users of illicit drugs (polydrug users)
So called ‘harm-reduction dosing’ or maintenance prescribing of benzodiazepines for patients
using polydrugs cannot be recommended on the basis of existing evidence, as prescribing
benzodiazepines does not appear to prevent use of other drugs.153 There are some evidence that
maintenance dosing of benzodiazepines may reduce high-dose problematic benzodiazepine use in
some patients (grade D recommendation from the British Association for Psychopharmacology).153
5.3 General principles for the management of

withdrawal of benzodiazepines
If dependence on benzodiazepines has become established, it is often difficult to treat and can become
a long-term, distressing problem.25 All patients with dependence should be encouraged to discontinue
the drug and offered a detoxification program at regular intervals. For some patients, discontinuation
will be difficult, but the effort should be made. For other patients, a reduction in dose, rather than
discontinuation, will be the first goal.
Benzodiazepines
Evidence-based recommendations for general practice management of benzodiazepine withdrawal are

difficult due to a lack of data. The following are general principles:
• Review the patients’ prescription records and discuss the situation to those receiving long-term
benzodiazepines.
• Send patients letters suggesting methods of tapering off benzodiazepines (this may be enough to
motivate them to withdraw).
• Teach patients ways to deal with anxiety and insomnia (either as primary conditions or due to
withdrawal).
• Acknowledge that withdrawing from benzodiazepines can be stressful.
• Encourage family and friends to provide encouragement and practical help during withdrawal.
• Refer patients to appropriate services (eg psychologist or support groups). Only refer to drug
or alcohol dependence services if the service has shown specific interest in benzodiazepine
dependence or the patient also has a drug or alcohol problem.
• Advise patients to make changes in lifestyle such as regular exercise.
• Advise patients to avoid alcohol.
• Advise patients to avoid mild stimulants (eg coffee and chocolate [theobromine]) as these can cause
anxiety, panic and insomnia.
• Postpone advice on smoking cessation until after the benzodiazepine has been withdrawn.189
Benzodiazepine reduction requires a team approach with regular communication between the prescriber
and other practitioners involved in the patient’s care (eg pharmacist, counsellor, psychiatrist, addiction
services).
5.3.1 Resources
Specialist services such as Reconnexion, www.reconnexion.org.au, offer free telephone support
(1300 273 266) to help with benzodiazepine withdrawal.
5.4 Tapering dosing

The clearest strategy for withdrawing benzodiazepines in primary care is to taper the medication.189
Slow discontinuation of benzodiazepines is recommended to avoid withdrawal symptoms (eg rebound

anxiety, agitation, insomnia or seizures) particularly when use exceeds 8 weeks. However, clear evidence
for the optimal rate of tapering is lacking. The British National Formulary recommends a minimum of 6
weeks,190 while Lader recommends a maximum of 6 months.189 The exact rate of reduction should be
individualised according to the drug, dose and duration of treatment (refer to Table 5).
Two-thirds of patients can achieve cessation with gradual reduction of dose alone. Others need
additional psychological therapies and a limited number of patients benefit from additional
pharmacotherapy.191 CBT performed in a single, extended (20-minute) consultation with a GP, with
a handout, has been shown to increase non-use at 1 year from 15% to 45%.192 A systematic review
comparing routine care to brief interventions, gradual dose reduction and psychological interventions
found all interventions increased benzodiazepine discontinuation over routine care, with gradual dose
reduction plus psychological interventions the most effective.191
All patients on a reduction regime must obtain prescriptions from one prescriber and through one
pharmacy, where time-limited dispensing may be required (eg once or twice a week at a specified time).
Plans should be in place to cover absences of the usual prescribing doctor from the practice. Consider
working closely with the patient’s pharmacist with staged supply or supervised dosing to assist the
patient with dose reduction and cessation, if they are unable to manage this themselves.
Benzodiazepines
Table 5. Recommendations for tapering benzodiazepines

Recommended taper
Duration of use Comments
length
<6 to 8 weeks Taper may not be required Depending on clinical judgment and patient
stability/preference, consider implementing a taper,
particularly if using a high-dose benzodiazepine or
an agent with a short or intermediate half-life, such
as alprazolam or triazolam
8 weeks to 6 months Slowly over 2-3 weeks Go slower during latter half of taper. Tapering
will reduce, not eliminate, withdrawal symptoms.
6 months to 1 year Slowly over 4-8 weeks Patients should avoid alcohol and stimulants during
>1 year Slowly over 2-4 months benzodiazepine withdrawal
Copyrighted 2015. Frontline Medical Communications. 117258:0515BN
A common first step in withdrawal is to substitute diazepam for the benzodiazepine being taken.189 The
slower elimination of diazepam creates a smoother taper in blood level.102
Refer to Resource D.2B for withdrawal protocols.
5.5 Additional pharmacotherapies

Pharmacotherapy interventions have limited use in benzodiazepine withdrawal. Generally, other drugs
are used to address symptoms rather than substitute for benzodiazepines.
Carbamazepine - Carbamazepine has shown some usefulness, however, there is not enough evidence to
recommend its use.193
Antidepressants - There is limited evidence that antidepressants help in benzodiazepine withdrawal,

unless depression (or anxiety disorders/panic disorders) are present or emerge during withdrawal.191,193
Melatonin - Melatonin may help benzodiazepine reduction in older people with insomnia.194
5.6 Should every patient be withdrawn?

There may be a small number of patients whose quality of life improves with the stable use of
benzodiazepines. This may justify long-term therapy. The decision to continue long-term benzodiazepine
treatment needs to be clearly documented. The decision may also involve a second opinion by a
specialist in an area relevant to the patient’s needs. These patients still require regular, ongoing review
and re-assessment of the risks and benefits of benzodiazepine use.
Attempts at withdrawal are more likely to succeed if the patient is able to contemplate the ultimate
goal of cessation, and the doctor and patient are able to work together in a productive therapeutic
relationship to achieve this.
Some patients struggle to reduce and cease benzodiazepine use. However, this group can often reduce
their daily dose markedly and this is accompanied by a decrease in risk and side effects. They may
continue on low-dose benzodiazepines (eg 2-5 mg diazepam daily) for an extended period. Continued
regular review may assist in the majority who will successfully cease benzodiazepines in the longer term.
This decision should be made on a case-by-case basis.
For patients who have complex, multiple morbidities, GPs should seek advice from mental health and
addiction specialists, as well as other relevant specialists (eg neurologists) to assist with development of
the best plan to assist the patient.
Benzodiazepines
Resources
Resource A. Examples of responses to patient

requests for benzodiazepines
Purpose
To provide GPs with examples of responses to specific inappropriate and maladaptive patient requests for
benzodiazepines.
Reducing the incidence of requests

Before the actual consult, there are a number of things that practices can do to decrease the incidence of
inappropriate and maladaptive requests for medications:
• When new patients make an appointment, ask the receptionist to give the following information, ‘The doctor,
when seeing you for the first time, will do a detailed assessment and may need additional information from
your previous doctors prior to making any treatment decisions, including prescribing medicines’.
• Inform patients of practice-wide policies regarding prescribing, including reviewing prescribing for existing
patients. This may involve a sign in the waiting room.
• Develop clear plans for all staff on how to respond to requests for benzodiazepines using scripted
response.
Example responses to inappropriate requests for medications

Alprazolam and temazepam are frequently used in the scenarios below, but may be substituted for
other benzodiazepines. Some responses are specific for alprazolam or temazepam as both medications
have undergone changes to their Pharmaceutical Benefits Scheme (PBS) listing and Therapeutic Goods
Administration (TGA) scheduling.
Table A.1 gives some examples of responses to patient requests and includes a rationale for the response.
Note that all responses are examples only and should be adapted to individual clinical circumstances.
Table A.1. Sample responses to inappropriate requests for medications

Patient request Sample responses Comments
I need something to Sometimes poor sleep indicates more You need to make a detailed assessment and
help me to sleep. serious underlying problems. Can you tell diagnose the condition rather than treating a
me more about your sleep issues? symptom.
or Don’t assume that if someone asks you to assist
What have you tried to help you sleep? them with sleep that they are looking for sleeping
tablets.
or
Offer a hierarchy of alternatives, including sleep
Sleeping tablets have been used in hygiene and cognitive behaviour therapy (CBT).
the past to help people with sleeping
problems. However, we now know these Give the patient written information.
can have side effects and can be risky so
we don’t always prescribe them.
Ok, you won’t give This is clearly an inappropriate request. You can only legally prescribe drugs for the medical
me alprazolam, We don’t just prescribe the medications treatment of a patient under your care, and must
how about some people ask for. take all reasonable steps to ensure a therapeutic
Serepax or Rivotril? need exists.
My job as a professional is to make a
diagnosis and do what I think is best for You can’t legally prescribe drugs merely to support
my patients. the drug dependence of a person.
Benzodiazepines

No, I’ve tried all this. Have you used medication before? Who A patient asking for medication (especially specific
The only thing that prescribed it to you? medication) is a possible red flag that the patient
works for me is a or is drug seeking.
sleeping pill. I want Ask the patient why they have not returned to the
medication. I am concerned about that, as a request
like this can sometimes be a sign of doctor who previously prescribed medication to
dependence on the medication. Can we them. Stress the advantages of continuity of care.
talk about how much you are taking? Ask the patient about what sleep hygiene
or practices they have tried and gauge their
knowledge. Provide further information about
Sleeping pills are not the first choice in sleep hygiene as needed.
treating insomnia. These come with risks
and limitations. Educate the patient about the problems
associated with sleeping tablets, including
or abnormal sleep often with early awakening, as
Sleeping medicines only provide a short well as the risks.
term benefit. If you’re having trouble Play a broken record on this advice. Remember,
sleeping, it may be because you’ve become patients may no longer derive any relief from the
dependent on them. Using non-drug medication, but they feel very much worse when
methods has been shown to have a better they stop it.
long-term benefit.
If the patient does not accept your advice and
or continues to pressure you, one last resort option
It’s my/our practice’s policy not to prescribe is to stand up from your chair while maintaining
sleeping tablets. eye contact with the patient, walk to and open
or the door of your consulting room and say
something like, ‘Thank you for coming to see me
I am concerned that providing ongoing
... (or) It was nice to meet you ... I am unable to
medication is not good for your overall
prescribe the medications that you request today
health. Can we trial a graduated withdrawal
because I don’t believe it is in your best interest
program, or can I refer you to a specialist?
.... if you decide ... ’
or
Your sleep problems can be a result of your
drug use. Giving tablets is just treating a
symptom. I’d like to get to the cause and
help you with your drug problem.
or
Thank you for coming to see me. It was
nice to meet you. I am unable to prescribe
the medications that you requested today
because I don’t believe it is in your best
interest and that’s not the way we now
practice medicine. I have mentioned
alternative methods of exploring and
treating your problem. Please give my
advice some further thought and if you
decide you would like to avail yourself of the
treatment that I am able to offer you, I look
forward to seeing you again. In that case,
please make another appointment.
Doctor, I need a Let’s first talk about what you have been Panic attacks are a symptom, not a condition,
script for my panic experiencing to ensure we have the right and their cause needs to be diagnosed.
attacks. diagnosis. Then we’ll talk about which
treatment is most likely to help you.
Medication is not necessarily the first
option in treating this condition and in
some cases it can actually be a cause of
anxiety.
Benzodiazepines

I want/need a We don’t prescribe this medication(s). Provide sleep hygiene leaflet and CBT
prescription for Let’s talk about how I can help you with information.
alprazolam (or other your sleep problem without drugs. Alprazolam has been rescheduled as Schedule
benzodiazepines). or 8 (S8) drug.
The rules around these medications have
changed due to the range of harms they
were causing.
or
I’m sorry, it’s my/our practice policy not to
prescribe alprazolam.
or
I don’t prescribe these medications. But
I’d like to know more about why you are
on these medications, and the best way
to manage this. Can we talk about how
you came to be on these tablets?
or
I am concerned about that. Sometimes
a request of this nature is a sign that
someone has become dependent on the
medication. Can we talk about how much
you are using?
Why don’t you We prescribed them in the past, but we It is preferable that you openly and honestly
prescribe sleeping have generally reduced their use (to very communicate your true clinical concerns about
tablets? specific circumstances). the medication requested; advising the patient
or of the time limited ‘benefit’ and the serious risks.
Emphasise your duty of care to ‘first do no
We now realise they only provide short harm’ and help.
term benefits and can lead people to
adopt unhealthy and unsafe ways of If you do not feel confident or able to have this
dealing with their sleep and other life frank discussion with the patient at this time, you
problems. may alternatively provide literature that explains
this clinical perspective. Some clinicians find it
or helpful to provide a letter jointly signed by an
The health department has warned us not authoritative source (‘borrowed protection’*).
to prescribe some benzodiazepines as This may sometimes be necessary when a
they are causing serious problems. patient is demonstrating apparent drug-seeking
If really being pushed inappropriately: behaviour and persisting in their pressure on you
to prescribe inappropriately, especially if they
I am sorry, you are asking me to do
are asking you to do something that is medically
something which I consider to be
unsound or even unethical. This response can
inappropriate or unsafe.
offload the pressure being placed on you and
While I can understand your situation, deflect it back onto the patient.
I cannot prescribe outside legal
frameworks or if I consider that the
medication will not help.
(In a patient with This is a serious problem and There is no evidence that prescribing
substance use benzodiazepines have never been shown benzodiazepines helps heroin or morphine users
disorder [SUD]) to help. control their opioid use. On the contrary, these
But the tablets/ If you have a morphine problem, you drugs are commonly used to supplement, boost
capsules have need proper treatment. I think you need or counteract the effects of other unsanctioned
helped me cut down the best help you can get. I can treat you drug use.
my morphine use. for morphine dependence with a more There is ample evidence that benzodiazepine
effective treatment, or, if after further use by opioid users causes harm.
assessment, I think you need specialised
treatment, I can refer you for specialist help.
Benzodiazepines
49

But Dr X prescribes That’s Dr X’s decision, but the other Discuss this issue with Dr X. Develop a practice
them (Dr X being doctors in this practice don’t prescribe policy (or local area policy) if your ability to
someone in your them. handle requests for drugs is compromised.
practice or one or Dr X can contact the Clinical Director of the
nearby). Alcohol and Drug Services for advice about
That’s Dr X’s decision, but other doctors
in this practice insist on continual appropriate prescribing of benzodiazepine
monitoring of patients they prescribe this medications.
medication. Ask the patient why they have not returned
or to the doctor who previously prescribed the
medication. Stress the advantages of continuity
That’s Dr X’s decision, but other doctors of care.
in this practice have very strict prescribing
criteria.
or
If that doctor prescribed it for you before,
it may be best for you to go back to him/
her. They know your history better than I
do, and it’s best to continue with the one
doctor
Why don’t I am sorry, it’s my/our practice policy not Refer to the guide on prescribing S8 opioids and
you prescribe to prescribe alprazolam. drugs of dependence.
alprazolam? or Remember that alprazolam can only be
Xanax, one of the brands of alprazolam, prescribed as a PBS benefit on an Authority
has been taken off the market in Australia prescription for one indication, ‘Panic disorder
and there have been restrictions placed where other treatments have failed or are
on this medication because of concerns inappropriate’. Other anxiety disorders are not
on safety. Many people have suffered included in that indication.
significant side effects from this drug and
there have been a number of deaths.
If I don’t get That’ll be completely your decision, and It is not possible to establish or maintain a
alprazolam I’ll not something I can support. However, I genuinely therapeutic relationshipt with any
be desperate. I’ll can help you with your drug problem and patient who uses such emotional manipulation
have to go and sleeping/anxiety problem without the need to influence your clinical decision making.
<prostitute myself, for alprazolam. Continue to offer the patient help. There is
do an armed hold If the patient threatens to harm you or your no need to accept responsibility for another’s
up, go back to using staff: behaviour or threat. Be very clear and firm,
drugs>. though empathetic, in your responses.
This practice takes these sorts of threats
seriously and has serious consequences. You may elect to call the police if you consider
Are you sure about what you just said? the threat to be a serious one. You can call staff
or at your local drug of dependence unit to notify
them of the events and your clinical actions.
Activate practice duress alarms or They will provide you with advice and support.
processes.
or
I do not believe it is safe or appropriate to
prescribe the medication you are asking
me to prescribe under these conditions.
or
This practice takes these sort of threats
seriously. I am sorry, I cannot supply the
services that are necessary for your care.
I cannot continue with this consultation,
thank you.
Benzodiazepines

(In a patient with If you’ve got a problem with drug There is no evidence that prescribing
[SUD]) dependence, there’s a very significant, and benzodiazepines for the treatment of heroin or
I’m trying to get off proven, risk of you becoming dependent on morphine addiction is any use at all. There is
drugs and I need other drugs too. Have you seen a specialist ample evidence of the harm, including increasing
some help with about this lately? the risk of overdose, confusion, amnesia, falls
sleep. or and accidents, risky sexual behaviour and
increased needle sharing.
I want to help you get off drugs, but it would
be a breach of my duty of care to you to It is important to say these things to the patient
prescribe this medication. in a firm, unwavering and confident manner so
the patient understands you mean what you say
I wouldn’t be doing the right thing by you if I and there is no room for negotiation.
prescribe this medication.
Drugs can interfere with sleep either as a
Sleeping drugs cause their own problems, result of stimulation (caffeine, nicotine or other
and can make things worse rather than stimulants) or as a response to varying levels
better. of sedation (rebound insomnia) associated with
You will have some sleep problems declining blood levels (trough levels) with alcohol,
when you are withdrawing from opioid opioid or benzodiazepine medications.
medications like morphine, but this will Reinforce the principles of sleep hygiene,
improve with time as your body recovers including never napping during the day no
from the effects of this medication. What matter how tired the patient feels and getting out
you tell yourself, your self-talk, is very of bed to do something relaxing after 30 minutes
important during this time. When you of trying to get to sleep and trying again when
experience difficulties settling off to sleep, feeling ready to sleep.
reframe the situation by reminding yourself
that these symptoms are a result of your Talk to the patient about the use of de-
body repairing itself, like the itch you catastrophising techniques.
experience when a sore is healing. Remind
yourself these are ‘good’ symptoms rather
than ‘bad’ or sinister ones.
Your sleep problem is a common side effect
of using sedative drugs like morphine,
sleeping tablets or alcohol - it’s due to
a rebound effect resulting in increased
alertness after a period of sedation. It’s
much better to treat the cause rather than
the symptom.
You’re going to have this sleep problem
as long as you continue using these
medications or drinking. I can help you (or
refer you for help) with your drug problem if
you like.
If you are unable to sleep, you need to
remain positive. Tell yourself: ‘If I am unable
to sleep tonight, I am not going to let it
worry me because it won’t do me any
serious harm. I will just get up and read or
do something else that relaxes me’.
You prescribed These sorts of drugs are for short-term Prescribing hypnotics for drug-dependent
alprazolam for me use only. If you’re asking for a repeat, patients creates an expectation of further
before, why not we haven’t solved your sleep problem prescribing, and causes hostility and aggression
now? (or anxiety problem) and you are on a when expectations aren’t met.
pathway to developing a new problem.
Alprazolam has been found to be so
problematic that has now been reclassified
to a more dangerous drug group.
We need to find a more effective longer term
solution that is not associated with harm.
Benzodiazepines

(In a patient with If you have a drug addiction problem, Offer help or refer them to Alcohol and Drug
SUD) benzodiazepines are one of the least Information Service (ADIS), for counselling and
I’m trying to cut effective and most dangerous drugs to referral.
down my drug use use. I know you want me to give you the
but you won’t help best treatment, but benzodiazepines will
me. not help.
Why do you I know that I have been prescribing these Doctors often find it difficult to make changes in
want to change medications for you for many years now. their prescribing of analgesic and psychotropic
my medications However, I have been giving a lot of medications, particularly when they are pressed
now? You have thought to your health problems and I for time, and when their patients express strong
been prescribing have been doing some reading on the emotional attachment to these medications and a
alprazolam for latest medical literature and speaking to deep fear of change.
my panic attacks, some experts in the field. While prescribing benzodiazepine medications
temazepam for my in the long term does not generally represent
sleeping problems, As you know, medical research continues
to reveal new things that change the way good clinical practice, prescribing multiple
diazepam for benzodiazepines is poor clinical practice.
my anxiety and we think and practice medicine. I have
clonazepam for realised the medications I am prescribing Doctors need be aware of the evidence and
that seizure that for you are no longer in your best interests. have confidence in their clinical judgement when
I had a long time Because I care about you, I need to do making changes to medications and other
ago. I need these something about that. It is my ethical duty treatments.
medications and I to provide you with nothing but the best Doctors also need to learn to manage their
might die if you stop possible medical care that I can. So, we emotions when responding to the emotions and
them. need to make a number of changes over pressures of patients.
the next several (2-3) months. It can be important to play a broken record of
I’d like to tell you about the reasons we positive reinforcement on the benefits of altering
need to make these changes and how treatment to one that is consistent with evidence
your health will actually improve over time and careful clinical assessment of the patients’
as a result of these changes. circumstances.
I will be there to guide and support you It is important to document changes to a
all the way and a medical colleague treatment plan.
who specialises in making these sorts of A copy of this treatment plan should be provided
medication changes has offered his/her to the patient so there is clarity, transparency
support and advice as we go. Let’s now and certainty in what is to be offered in the new
discuss how we are going to make these treatment plan.
changes to your treatment and map this
out. If the patient declines to comply with this change
of treatment plan, the doctor must then consider
whether to continue providing suboptimal care,
and whether it is possible to maintain a genuine
therapeutic relationship.
While recognising that practical challenges
may arise in rural and remote areas, it may be
appropriate for the doctor to ask the patient to
go away and think about what is proposed and
return when they are ready to embark upon the
new treatment plan.
Please give me I’m sorry but we don’t prescribe those You may use ‘we’ and ‘our practice’ to
<drug name> just drugs in our practice. suggest a collective decision and if you do
this once and I I am concerned about that, as sometimes not have confidence to say ’no’ when under
won’t ask again a request like this can be a sign that a such emotional pressure. This avoids direct
patient has become dependent on the confrontation.
medication. Can we talk about how much However, it is better to own your clinical
you are taking? decisions and to communicate them in a
confident, positive light.
Benzodiazepines

(In a patient with I am sorry you had to wait. I am very Some patients may use waiting time to coerce
SUD) keen to help you, but your treatment doctors. This can be averted by a sign in the
I’ve been waiting depends on finding the best solution to waiting room indicating that particular drugs are
for hours to see you your problem. Now let’s talk about your not prescribed by doctors in the practice.
and you won’t even problem and explore ways I can help you. Never allow yourself to be a ‘victim’ of
help. inappropriate or manipulative patient behaviour.
Ok, if you can’t give I’m sorry, we can help you with your sleep Many drugs prescribed for insomnia, including
me temazepam, problem, but we can’t prescribe other antidepressants such as doxepin and
could you please drugs that might also cause harm. antipsychotic medications like seroquel or zyprexa
prescribe some are misused by injecting drug users (IDUs).
deptran or It is important not to substitute benzodiazepines
seroquel? Another with drugs (eg antidepressants and major
doctor gave me that tranquillisers) that may cause a range of serious
to help me sleep. side effects, especially when misused.
If I don’t get benzos I’m sorry to hear that. But in that case, you Benzodiazepine withdrawal for drug-seeking
I’m going to fit. must be dependent on benzodiazepines. patients requires close supervision. Specialist
I had a seizure We’re not allowed to prescribe drugs withdrawal management is highly advisable
once before when to sustain drug dependence (consider where there is any history of severe or
I was detoxing (or showing the patient the relevant section of complicated withdrawal (eg seizures or delirium)
withdrawing). the legislation). where the patient has been taking diazepam
You need referral for detoxification. I can 50 mg daily or more or its equivalent dose
offer you three options for help: for other benzodiazepine medications, where
there is significant comorbidity, where there is
• I can arrange treatment. unsanctioned or hazardous alcohol or other drug
• I can give you a specialist contact to use in the patient’s present living environment or
call for advice. where there is a past history of failed ambulatory
withdrawal management.
• If, after further assessment, I believe
it is appropriate and safe for you, I
might be able to offer you out-patient
withdrawal.
A note on staff safety

All practices must implement strategies to ensure the occupational health and safety (OHS) of general practitioners (GPs) and other members of
the practice team. This includes having a risk management strategy that details the necessary steps to protect doctors and practice staff from
potential patient violence.
A doctor duress system is recommended in each consulting room and doctors should feel confident to use it in any situation where they feel
under threat.
For tips on minimising risks of violence, practices can refer to General Practice - A safe place: tips and tools, available at www.racgp.org.au/
your-practice/business/tools/safetyprivacy/gpsafeplace
For advice on managing aggressive, violent or threatening patients, refer to www.miga.com.au/library/10RRAR08.pdf
*Borrowed protection
If you have reason to believe you may be at immediate risk, or if you do not feel confident to manage a particular clinical circumstance safely or
effectively, it may be wise to tell the patient that it is not your responsibility for the decision, but defer to a ‘higher’, less identifiable authority. For
example, ‘I can’t prescribe X because of health department regulations.’ Using ‘borrowed protection’ should be limited to when you feel it is
absolutely necessary. It is usually therapeutically more appropriate for you to communicate clearly and with confidence that you will not prescribe
particular medications when you do not believe this is in the best interests of the patient, and then also explain alternative treatment approaches.
This approach lets the patient know that you believe in yourself as a clinician and that you are confident and competent as a doctor.
tThe presence of a therapeutic doctor-patient relationship in a consultation is a key to recognising a patient who wants help and a
person seeking drugs.
The establishment of a therapeutic relationship requires mutual openness and truth telling. A relationship in which a patient tells a doctor what
medications they want, regardless of the clinical circumstances, is not a therapeutic one. A patient who is not open to an honest discussion
about the benefits, risks and harms associated with their prescribed and non-prescribed medications, or to treatment goal setting and planning,
is not engaging in treatment. They are not demonstrating they are ready to join the doctor in a genuine therapeutic relationship.
When this relationship does not exist, the challenge for the GP is to speak and work with the drug-seeking person in a way that is insightful and
sensitive to their circumstances and to encourage and motivate them to accept constructive, safe and appropriate clinical assistance.
This tool has been adapted with permission from the work of Adrian Reynolds, Clinical Director, Alcohol and Drug Service,
Department of Health & Human Services, Tasmania and Dr Malcolm Dobbin, Senior Medical Advisor (Alcohol and Drugs),
Department of Human Services, Victoria.
Benzodiazepines
Resource B. Drug interactions

Clinically significant medication interactions with benzodiazepines.
Drugs that increase serum levels of

Drugs that have sedative effects
benzodiazepines (through action on
significantly enhanced by benzodiazepines
hepatic metabolic pathways)
• Ketoconazole • All full-agonist opioids, including methadone
• Itraconazole • Partial agonist opioids such as buprenorphine
• Macrolides • Alcohol
• Fluoxetine • Antipsychotics or other sedating medication
• Cimetidine • Barbiturates
• Sedating anti-histamines
Benzodiazepines
Resource C. State and territory contacts

24-hour
State/ Legislative clinical
Legislation Contact (web)
territory contact (phone) advisory
services
Australian Medicines, Poisons Pharmaceutical Services Pharmaceutical DACAS -
Capital and Therapeutic http://health.act.gov.au/health- Services Section, ACT Australian
Territory Goods Act 2008 services/population-health/health- Health Capital Territory
protection-service/pharmaceutical-
www.legislation.act.gov. 02 6205 0998 03 9418 1082
services/pharmaceutical-services
au/a/2008-26/default.asp
New South Poisons and Pharmaceutical Services Pharmaceutical DASAS

Wales Therapeutic Goods http://www.health.nsw.gov.au/ Services Unit, Legal and 02 9361 8006
Act 1966 pharmaceutical/pages/default.aspx Regulatory Services (Sydney)
www.austlii.edu.au/au/ Branch, NSW Health
legis/nsw/consol_act/ 1800 023 687
patga1966307
02 9391 9944 (Rural)
Northern Medicines, Poisons Poisons Control Poisons Control Unit, DACAS -

Territory and Therapeutic www.health.nt.gov.au/ Department of Health Northern
Goods Act 2014 Environmental_Health/Medicines_ and Community Territory
and_Poisons_Control/index.aspx
http://notes.nt.gov.au/ Services 1800 111 092
dcm/legislat/legislat.nsf/d9
89974724db65b1482561c
08 8922 7341
f0017cbd2/86a3e80a889a
330369257d4f001810d5?
OpenDocument
Queensland Health (Drugs and Medicines Regulation Medicines Regulation GPs can phone
Poisons) Regulation and Quality and Quality, ADIS 1800
1996 www.health.qld.gov.au Queensland Health 177 833 to be
www.legislation.qld.gov.au/ 07 3328 9890 put through
LEGISLTN/CURRENT/H/ to ATODS for
HealDrAPOR96.pdf
clinical advice
South Controlled Medicines and Technology Drugs of Dependence DACAS -

Australia Substances Act Policy and Progams Unit, Department for South Australia
1984 http://www.sahealth.sa.gov.au/ Health 08 8363 8633
www.legislation.sa.gov. wps/wcm/connect/public+content/
sa+health+internet/about+us/
1300 652 584
au/lz/c/a/controlled%20
substances%20act%20 department+of+health/public+health+
1984.aspx and+clinical+systems/medicines+and
+technology+policy+and+programs
Tasmania Poisons Act 1971 Pharmaceutical Pharmaceutical Services DACAS -

Services Branch Branch, Department Tasmania
http://www.dhhs.tas.gov.au/ of Health and Human 1800 630 093
psbtas/welcome Services
03 6166 0400
Victoria Drugs, Poisons Drugs and Poisons Drugs and Poisons DACAS -
and Controlled Regulation Unit, Department of Victoria
Substances Act 1981 http://www.health.vic.gov.au/dpcs/ Human Services 1800 812 804
www.austlii.edu.au/au/ index.htm
1300 364 545
legis/vic/consol_act/
dpacsa1981422
Western Poisons Act 1964 Pharmaceutical Pharmaceutical CAS

Australia www.austlii.edu.au/au/ Services Branch Services Branch, 08 9442 5042
legis/wa/consol_act/ http://www.public.health.wa.gov. Department of Health
pa1964121 au/1/872/2/pharmaceutical_
services.pm
08 9222 6883
DACAS - Drug and alcohol clinical advisory service; DASAS - Drug and alcohol specialist advisory service; ADIS - Alcohol and drug information
service; CAS - Clinical advisory service; ATODS - Alcohol, tobacco and other drugs
Prescribing drugs of dependence in general practice, Part B 55
Benzodiazepines
Additional resources for Schedule 4 and Schedule 8 drug

information
New South Summary of Controls on the Prescribing and Handling of Drugs of Dependence, www.
Wales health.nsw.gov.au/pharmaceutical/Documents/drugsofdependence-controls.pdf
Northern Remote Health Atlas; Restricted S4 Medicines, http://remotehealthatlas.nt.gov.au/

Territory restricted_schedule_4_medicines.pdf
Regulatory requirements and resources, www.health.qld.gov.au/clinical-practice/

Queensland guidelines-procedures/medicines/drugs-of-dependence/regulation/default.asp
Drugs of Dependence, www.sahealth.sa.gov.au/wps/wcm/connect/Public+Content/

South
SA+Health+Internet/Clinical+resources/Clinical+topics/Medicines+and+drugs/
Australia Drugs+of+dependence/
Things medical practitioners need to know - key prescribing requirements, http://docs.

Victoria health.vic.gov.au/docs/doc/Things-medical-practitioners-need-to-know--key-prescribing-
requirements
Western Requirements for the prescribing of S4 and S8 Medicines in Western Australia, www.
Australia public.health.wa.gov.au/cproot/3565/2/Prescribing_S4_S8_080825.pdf
Benzodiazepines
Resource D. Communication with patients
D.1 Benzodiazepine fact sheet for patients

*
What are benzodiazepines?
Benzodiazepines are a group of prescription-only medicines that have a sedating and calming effect on the
brain and nervous system. They are also known as sedatives or tranquillisers. Examples of benzodiazepines
include medicines containing one of the following active ingredients: diazepam, lorazepam, oxazepam,
temazepam and alprazolam.
They come in tablet and capsule form, and some are available for intravenous use in hospital settings.
How do benzodiazepines work?

Benzodiazepines differ in how quickly the active ingredient starts to work and how long the effect lasts. The
effect of the medicine also depends on the prescribed dose, and on the individual (eg height, weight, health
status and previous experience with benzodiazepines), which can impact on how the medication will work.
Benzodiazepines can help treat symptoms of anxiety and sleeping problems (eg insomnia). As non-medicine
therapies have proven benefit in these conditions, benzodiazepines are generally considered only if these
options are inappropriate or have failed.
If you have been diagnosed with an anxiety disorder, benzodiazepines can make you feel calmer. If you have
insomnia, benzodiazepines may help you fall asleep. They are sometimes used for other reasons, such as a
medication before an operation to alleviate nervousness.
After taking benzodiazepines, people can describe feeling drowsy, relaxed, confused/fuzzy and having a heavy
sensation in their arms and legs. Coordination and reflexes can be effected too, which means you should not
take benzodiazepines if you need to be focused and coordinated (eg drive a car or operate heavy machinery).
Benzodiazepines are usually taken for a set period until the intended therapeutic effect is achieved. Then, the
dose is reduced and plans to stop it are made.
If you take benzodiazepines for a prolonged time, the body may adapt and get used to the effects of
the medication. Stopping the medication can lead to withdrawal symptoms that includes anxiety and
restlessness. Withdrawal symptoms are often mild, but can be severe if you are on high doses of a
benzodiazepine. Serious side effects, including seizures, can occur if you stop taking high doses suddenly.
Can benzodiazepines be addictive?

Although addiction (cravings, abuse, misuse, compulsive or uncontrollable benzodiazepine-seeking behaviour)
is possible with benzodiazepines, it is rare in people who are taking therapeutic doses for a specific reason
over a short period as prescribed by their doctor.
You may be at a greater risk of developing an addiction to benzodiazepines if you have a history of drug
dependence, or if you are currently misusing any substance including alcohol or strong pain killers (opioid drugs).
Before prescribing a benzodiazepine, your doctor will ask you questions about these sorts of things to help
prevent addiction.
Benzodiazepines
What are the possible side effects of benzodiazepines?

Benzodiazepines are associated with a number of side effects including:
• drowsiness and unsteadiness, potentially increasing the risk of a fall

• impairment in judgement and dexterity, making tasks such as driving or using heavy machinery more difficult
• forgetfulness, confusion, irritability
• paradoxical aggression and excitability (although this is rare, it is the opposite effect to what is expected with
these medicines).
Taking benzodiazepines in combination with other drugs or alcohol can be very dangerous, and in some
cases fatal.
Can I take benzodiazepines for a long time?

Benzodiazepines are usually taken for a short length of time. In rare instances, some patients will
require long-term therapy with benzodiazepines. This is after a serious consideration of risks and
benefits of long-term therapy between you and your doctor. If you and your doctor have decided that
benzodiazepines are an important part of your long-term treatment, then you should continue to take
them as prescribed and keep checking in with your doctor for review.
If you have been taking benzodiazepines regularly for longer than 4 weeks and wish to stop them, your
doctor would be happy to advise you on how to do this. Do not stop or significantly alter the dose
abruptly. Many people can stop taking benzodiazepines without difficulty. For others, gradual reduction
helps prevent or reduce any withdrawal symptoms.
Where can I get more information?

• Reconnexion, www.reconnexion.org.au, an Australian not-for-profit organisation that offers programs,
counselling, telephone information and support for people with anxiety, stress, depression and
benzodiazepine dependence and related conditions.
• The Victorian Government’s Better Health Channel website, www.betterhealth.vic.gov.au
• The Australian Drug Foundation’s help and support page, www.druginfo.adf.org.au/contact-numbers/

help-and-support, lists sources of information and advice.
* Kenny T, Harding M. Benzodiazepines and Z Drugs [Internet]. London: patient.co.uk; 2014 [updated October 2014].
Available at http://patient.info/health/benzodiazepines-and-z-drugs [Accessed 11 June 2015].
Benzodiazepines
D.2 Benzodiazepine reduction in the practice population

D.2A Practice letter to patients about benzodiazepine reduction
[Insert practice name]
Address
Date
Dear [Patient name]
We are currently undertaking a review of prescriptions for medications collectively known as benzodiazepines and
sleeping tablets. I am writing to you because our records show that you have received a number of prescriptions
for one or more of these types of medications in the past 12 months.
A growing body of evidence suggests that if these medications are used for long periods, they can have harmful side
effects, including anxiety symptoms, memory and sleep problems, and they can be addictive. We do not recommend
long-term use.
We are writing to ask you to consider cutting down your dose of tablets and perhaps stopping them completely at some
time in the future. As each person is different, we would like to discuss this with you in person within the next 3 months.
The best way to cut down your tablets is to take them only when you feel they are absolutely necessary. It is best to
cut down gradually; otherwise you may have some withdrawal side effects. You should not stop your tablets suddenly.
Once you start to reduce your dose you may start to notice that you feel a lot better and you may be able to think about
stopping altogether.
Please make an appointment with your GP to discuss this further. If you have not attended to discuss this
within the next 3 months, we may not be able to continue to prescribe this medicine for you. If you have already
discussed this with your doctor, or have stopped your medications, this letter does not apply to you.
Yours sincerely,
[Dr name]
D.2B Practice guide to reduction and withdrawal of benzodiazepines

(and Z drugs) in the practice population
• Print a list of patients on repeat prescriptions for benzodiazepines (and Z drugs).
• Identify patients who have repeat prescriptions (including repeat acute prescriptions) of hypnotics
and anxiolytics. In agreement with the general practitioner (GP), remove drug repeats for patients
who have not ordered a prescription within the last 6 months.
• Agree on exclusion criteria (with GP) to identify patients not suitable for withdrawal, for example:
- drug or alcohol problems, unless GP advises otherwise
- terminal illness
- acute crisis
- risk of suicide
- severe mental illness (liaise with psychiatrist)
- organic brain disease
- epilepsy requiring benzodiazepines as part of anticonvulsant therapy
- benzodiazepine prescriptions for muscle spasm.

• The GP(s) should agree on the final list of patients to be included in the scheme.
Benzodiazepines
• Invite the patient to discuss a supported withdrawal regime. If the withdrawal is to be managed by
a GP, then it would be beneficial for the patient to see the same doctor throughout the process.
• Prior to the consultation, use computer records and/or paper notes to gather the required
information to complete the patient clinical summary. Send the patient self-help information on
sleep and relaxation.
• In the initial consultation with the patient, reiterate the benefits of withdrawing from
benzodiazepines and explain the possible treatment withdrawal regimes.
• Find out how often the patient takes the hypnotic/anxiolytic, as some patients stockpile these
medicines and never take them, some only take them occasionally, whereas others may give
them to someone else. The anxiolytic/hypnotic can be stopped in these patients.
• If the patient agrees to participate in the scheme, agree on a treatment regime and arrange a
follow-up appointment.
• Record the agreed plan in the patient-held record sheet. Provide the patient with information
leaflets regarding non-drug alternatives to reduce anxiety and sleep problems.
• Following the consultation, document the outcome on the patient’s electronic record and in the
paper notes. Print out a prescription if one is required (leave the prescription for the GP to sign
with the clinical summary sheet).
• In the patient’s clinical summary sheet, complete the outcome box and pass it to the responsible GP.
Once the GP has read it, they should initial it and pass it to the receptionist for filing in the patient’s
notes.
• Explain the intervention to local pharmacies to ensure a consistent message is conveyed to patients.
• Ensure the patient fully understands how prescriptions will be issued and that all practice staff are
briefed on this.
• Offer patients general support if they call the practice for advice. If the patient wishes, arrange for
an appointment to explain the program.
• If the patient is not suitable for withdrawal, consider whether no action should be taken, or to refer
to the substance misuse services or psychiatric services.
• Classify your patient on your computer system in order to make identification easier. Everyone
withdrawing from hypnotics/anxiolytics should have this added to their record.
Reduction protocols to support the withdrawal from hypnotics

Different withdrawal plans are given for guidance only. The rate of withdrawal should be individualised
according to the drug, dose and duration of treatment. Patient factors such as personality, lifestyle,
previous experiences and specific vulnerabilities should also be taken into account.
• Throughout the process, it is important to provide advice on good sleep hygiene and basic
measures to reduce anxiety.
• At each stage, enquire about general progress and withdrawal symptoms.

• If patients experience difficulties with a dose reduction, encourage them to persevere and suggest
delaying the next step down. Do not revert to a higher dose.
• Offer information leaflets to help with the withdrawal program.
• Reassure patients that if they are experiencing any difficulties with the withdrawal schedule, they
can contact the practice for advice.
• A copy of the protocol should be given to the patient and the patient’s pharmacy. A copy should
be also kept in the practice’s records.
Benzodiazepines
Examples of hypnotic withdrawal schedules

To be adapted and adjusted according to individual patient needs.
Nitrazepam
Start from the most relevant point of the schedule based on the patient’s current dose.
Note that the dosage reduction withdrawal schedule is flexible and should be tailored to individual
patients.
Table D.2.1. Sample nitrazepam withdrawal schedule

Number of 5 mg Number of 5 mg
Dose of nitrazepam
tablets/day tablets/week
Starting dose 20 mg 4 28
Stage 1 (1-2 weeks) 15 mg 3 21
Stage 2 (1-2 weeks) 12.5 mg 2% 18
Stage 4 (1-2 weeks) 7.5 mg 1% 11
Stage 6 (1-2 weeks) 2.5 mg % 4
Stage 7 (1-2 weeks) 2.5 mg alternate nights % 2
Stage 8 Stop nitrazepam
Temazepam
Note that the dosage reduction withdrawal schedule is flexible and should be tailored to each individual
patient.
Table D.2.2. Sample temazepam withdrawal schedule

Dose of temazepam
Stage 1 (1-2 weeks) 25 mg 2% 18
Stage 3 (1-2 weeks) 15 mg 1% 11
Stage 5 (1-2 weeks) 5 mg % 4
Stage 6 (1-2 weeks) 5 mg alternate nights % 2
Stage 7 Stop temazepam
Benzodiazepines
Zopiclone
patient.
Table D.2.3. Sample zopiclone withdrawal schedule

Number of tablets/ Number of tablets/
Dose of zopiclone
day week
Starting dose 15 mg 2 x 7.5 mg 14 x 7.5 mg
Stage 1 (1-2 weeks) 11.25 mg 1 x 7.5 mg 7 x 7.5 mg
1 x 3.75 mg 7 x 3.75 mg
Stage 4 (1-2 weeks) 3.75 mg alternate nights 1 x 3.75 mg 4 x 3.75 mg
Stage 5 Stop zopiclone
Zolpidem
patient.
Table D.2.4. Sample zolpidem withdrawal schedule

Dose of zolpidem
Stage 1 (1-2 weeks) 7.5 mg 1% 11
Stage 3 (1-2 weeks) 2.5 mg % 4
Stage 4 (1-2 weeks) 2.5 mg alternate nights % 2
Stage 5 Stop zolpidem
Benzodiazepines
Reduction protocols for anxiolytics

Different withdrawal plans are given for guidance only. The rate of withdrawal should be individualised
according to the drug, dose and duration of treatment. Patient factors such as personality, lifestyle,
previous experiences and specific vulnerabilities should also be taken into account.
• Throughout the process, it is important to provide advice on good sleep hygiene and basic
measures to reduce anxiety.
• At each stage, enquire about general progress and withdrawal symptoms.

• If patients experience difficulties with a dose reduction, encourage them to persevere and suggest
delaying the next step down. Do not revert to a higher dosage.
• Offer information leaflets to help with the withdrawal program.
• Reassure patients that if they are experiencing any difficulties with the withdrawal schedule, they
can contact the practice for advice.
• Give the patient and the patient’s pharmacy a copy of the protocol. Keep a copy in the practice’s
records.
• If a patient has complex needs, refer to appropriate specialist services for further advice.
• Lorazepam and oxazepam have short half-lives making withdrawal effects more pronounced.
Patients treated with these drugs may need to be converted to diazepam during the withdrawal
process. Initial dose reductions should be made using their current medication, followed by
conversion to diazepam, and subsequent reduction of the diazepam dose according to the
following schedules.
Note: Some patients will prefer to remain on the original drug for the duration of the withdrawal.
Table D.2.5. Diazepam equivalent doses

Approximate equivalent doses to diazepam 5 mg
Lorazepam 0.5 mg
Oxazepam 15 mg
Clonazepam 0.25 mg
Resource D.2B is adapted with permission from Educational pack - Material to support appropriate prescribing of
hypnotics and anxiolytics across Wales - Welsh Medicines Partnership, April 2011. For more information visit: http://
awttc.org/about_wmp.html
Benzodiazepines
D.3 Stopping benzodiazepines (benzodiazepine withdrawal)

fact sheet for patients
How would I benefit by stopping benzodiazepines?
People who have been on long-term benzodiazepines often feel like they need to stay on them. This
may be because of fears about returning symptoms of anxiety or sleeplessness, or due to withdrawal
symptoms or needing the medication to feel normal.
While you might feel ‘normal’ when you take benzodiazepines, studies have found people who stopped
taking them have:
• improved memory and reaction times
• increased levels of alertness

• improved quality of life (more vitality, better ability to function).
Stopping benzodiazepines also reduces your risk of falls, accidents, fractures and other injuries.
How should I stop taking benzodiazepines?

The best place to start is by talking to your general practitioner (GP). Some people can stop quickly
and easily; others need a more gradual approach with additional support. Your GP can advise you
on the rate at which you should reduce the dose and help you to consider other ways of dealing with
your worries or sleeping problems. Sometimes your GP will change your prescription to a different
benzodiazepine before withdrawing.
If you are taking other addictive medicines, in addition to benzodiazepines, you may need specialist help
to come off the various medicines. Your GP will be able to advise you or refer you to local services that
can help.
Some tips for withdrawing from benzodiazepines:
• Choose when to start reducing - If you have been taking benzodiazepines to help you cope
with a personal crisis, it may be advisable to wait until things settle down before starting to reduce
the dose. Consider starting while on holiday, when you have less pressure from work, fewer family
commitments or less stress.
• Do not try to stop suddenly - Unless your GP has advised you to do so. You should reduce your
medication in a slow, gradual process, as this often gives a better chance of long-term success. You
can go as slowly as you need to.
• Do not increase the dose - It is common to have a bad patch at some time during the withdrawal.
You might be tempted to go back to the higher dose, but it is best to stick with the current dose.
Don’t consider a further reduction until you feel ready; this may take several weeks.
• Get help and support - Consider asking family or friends for encouragement and support, or
consider joining a self-help group. Advice and support from other people in similar circumstances, or
those who have come off a benzodiazepine, can be very encouraging.
• Keep a record - Keeping a diary can help as it records your progress and achievements. This in itself
will give you more confidence and encouragement to carry on.
Benzodiazepines
How do I cope with withdrawal symptoms?

Not everyone experiences the same degree or type of symptoms when withdrawing from
benzodiazepines. The best way to cope is to go slowly to minimise the withdrawal symptoms. It can
also help to know what to expect and know that these will pass.
• Panic attacks commonly occur due to the effects of adrenaline and rapid, shallow breathing
(hyperventilation). When this happens, you may experience palpitations, sweating, unsteady legs and
trembling. Regaining control of your breathing can help to alleviate the symptoms.
• Anxiety is also common upon withdrawal, especially if dose reduction is not gradual enough.
• Agoraphobia can present in a range of forms from a reluctance to go out in public to feeling
completely unable to do so. However agoraphobic feelings usually lessen as withdrawal continues.
• Aches and pains are very common during withdrawal.
• Problems with sleeping can occur during withdrawal. Strategies such as ensuring enough exercise
during the day, resolving concerns before bedtime and not trying to force sleep can help.
• Stomach and bowel problems such as diarrhoea and irritable bowel syndrome are very common
during withdrawal and can be very distressing. Your GP may be able to recommend a diet and
indigestion remedies that can improve these symptoms, which usually disappear after withdrawal is
complete.
• Hot flushes and shivering are also common.
• Sinus problems are experienced by many people as they withdraw.
• Vivid dreams and nightmares are another common occurrence during withdrawal. However this may
in fact be a good sign, as it can indicate your sleep and your body are re-adjusting to normal.
Where can I get some more information and help?

Reconnexion, www.reconnexion.org.au, an Australian not-for-profit organisation that offers programs,
counselling, telephone information and support for people with anxiety, stress, depression and
benzodiazepine dependence and related conditions.
* Kenny T, Harding M. Stopping Benzodiazepines and Z Drugs [Internet]. London: patient.co.uk; 2014 [updated October
2014]. Available at www.patient.co.uk/health/stopping-benzodiazepines-and-z-drugs [Accessed 11 June 2015].
Welsh Medicines Partnership. Educational pack - Material to support appropriate prescribing of hypnotics and anxiolytics
across Wales. Wales: Welsh Medicines Partnership; 2011. Available at www.awmsg.org/docs/awmsg/medman/
Educational%20Resource%20Pack%20-%20Material%20to%20support%20appropriate%20prescribing%20of%20
hypnotics%20and%20anxiolytics%20across%20Wales.pdf [Accessed 12 June 2015].
Benzodiazepines
D.4 Sleep hygiene and stimulus control fact sheet for patients
Sleep hygiene
Good sleep hygiene refers to actions you can take to improve and maintain good sleep. These actions
include:
• Sleep as long as necessary to feel rested (usually 7-8 hours for adults), then get out of bed.
• Maintain a regular sleep schedule.
• Try not to force sleep.
• Avoid caffeinated beverages after lunch.
• Avoid alcohol near bedtime (late afternoon and evening).
• Avoid smoking or other nicotine intake, particularly during the evening.

• Adjust the bedroom environment as needed to decrease stimuli (eg reduce ambient light, turn off the
television or radio).
• Resolve concerns or worries before bedtime.
• Exercise regularly for at least 20 minutes, preferably more than 4-5 hours prior to bedtime.
• Avoid daytime naps, especially if they are longer than 20-30 minutes or occur late in the day.
• Avoid going to bed until you are drowsy and ready to sleep.
• If you are not asleep within 15-20 minutes, get out of bed and return only when drowsy.
Stimulus control
People with insomnia may associate their bed and bedroom with the stress of not sleeping, rather than
the more pleasurable anticipation of sleep. The longer you stay in bed trying to sleep, the stronger the
association becomes. This perpetuates the difficulty of falling asleep.
Stimulus control therapy is designed is to disrupt this association by enhancing the likelihood of sleep. Your
sleep may not improve immediately. However, sticking with this should improve your ability to get to sleep.
Stimulus control instructions

• Go to bed only when sleepy.
• Get out of bed if unable to sleep after 15-20 minutes, leave the bedroom and do something relaxing
(eg reading or listening to soothing music). Avoid stimulating activities such as eating or watching TV.
Return to bed only when sleepy. (Repeat as necessary.)
• Use the bed/bedroom only for sleep (not reading, watching TV or worrying).
• Arise at the same time each day (including weekends).
• Do not take naps during the day.

Benzodiazepines
Sleep restriction therapy

Some people with insomnia stay in bed longer to try to make up for lost sleep. This causes a shift in
your day/night cycle. It makes sleep onset the following night more difficult and results in the need to
stay in bed even longer.
Sleep restriction therapy limits the total time allowed in bed, including naps and other sleep periods
outside of bed, in order to increase your drive to sleep and improve the efficiency of your sleep.
Sleep restriction therapy begins by decreasing the time you spend in bed to the same amount of time
that you actually sleep (usually this is determined from a sleep diaries or logs), but not less than 5 hours
per night.
On a daily basis, you record the amount of sleep obtained the previous night and the amount of time
spent in bed. Once you are spending more than 85% of the time in bed asleep, you increase the time
spent in bed (by 15-30 minutes).
You repeat this process until you achieve improved sleep without residual daytime sleepiness.
Naps are not permitted.
Relaxation
You may implement relaxation therapy before going to sleep. There are two common techniques for
relaxation therapy:
• Progressive relaxation is based upon the theory that you can learn to relax one muscle at a time
until the entire body is relaxed. Beginning with the muscles in your face, you contract the muscles
gently for 1-2 seconds and then relax. You repeat this several times. Use the same technique for
other muscle groups, usually in the following sequence: jaw and neck, upper arms, lower arms,
fingers, chest, abdomen, buttocks, thighs, calves and then feet. Repeat this cycle for approximately
45 minutes, if necessary.
The relaxation response begins by lying or sitting comfortably. Close your eyes and allow relaxation
to spread throughout your body. Use relaxed, abdominal breathing and redirect your thoughts away
from everyday worries and toward a something like a peaceful word or image.108
Benzodiazepines
Resource E. Practice policies and forms
E.1 Practice policy example for repeat prescriptions

Purpose
To inform patients about practice policies regarding repeat prescriptions for benzodiazepines.
Example policy
Date effective:
Review date:
REQUESTS FOR REPEAT DRUG OF DEPENDENCE PRESCRIPTIONS - BENZODIAZEPINES

Patients should be aware of their responsibilities in requesting prescriptions for drugs of dependence, including
benzodiazepines.
Patients should note the following:
• All requests for repeat scripts for drugs of dependence will go to your usual doctor.
• All requests require a clinical review by your doctor. If it appears to your doctor that there is no improvement in your
daily function or quality of life from the controlled substance, your medication may be discontinued.
• As a patient, you agree to and understand that your usual doctor reserves the right to perform random or
unannounced urine drug testing. This is a safety issue.
• Patients are responsible for their prescriptions. Lost prescriptions will not be replaced.
• Repeat prescriptions are generally written for a maximum of 1 month supply and will be filled at the same
pharmacy.
• Patients have the responsibility to schedule appointments for the next benzodiazepine prescription before leaving
the clinic or within 3 days of the last clinic visit.
• Patients have the responsibility for keeping medications in a safe and secure place, such as a locked cabinet or
safe. If medications are lost, misplaced or stolen your doctor may choose not to replace the medications or to taper
and discontinue the medications.
• Patients have the responsibility for taking medications as directed and understand that increasing the dose without
the close supervision of your doctor could lead to cessation of prescribing. Early requests for repeat scripts will not
be performed.
• Patients have the responsibility to set appointments to review ongoing therapy. This should be monthly and made
at the last clinic appointment. No walk-in appointments for medication refills will be granted.
Benzodiazepines
E.2 Prescription plan/agreement for a trial of longer term

treatment
Purpose
To inform patients of their responsibilities and expected behaviours regarding benzodiazepines.
Example agreement
This example is based on the Blaustein Pain Treatment Center - Johns Hopkins Medicine therapy agreement and
should be modified by the practice to suit local circumstances.
Date effective:
Review date:
PATIENT AGREEMENT FOR BENZODIAZEPINE THERAPY

Benzodiazepines are drugs of dependence. People who take them long term can risk adverse effects including
becoming dependent (addicted). Therefore, benzodiazepine prescription is highly regulated. These drugs also have a
high potential for misuse and are therefore closely controlled by the local, state and Federal government.
Generally, benzodiazepines are used in the short term for reduction of distressing symptoms (eg anxiety and insomnia).
A trial of long-term benzodiazepine therapy may be considered for severe or resistant mental illness.
The purpose of this agreement is to give you information about the benzodiazepine medications prescribed at this
practice, and to assure that you and your general practitioner (GP) comply with all relevant regulations.
Your GP’s goal is for you to have the best quality of life possible given the reality of your clinical condition. The success
of treatment depends on the mutual trust and honesty in the doctor-patient relationship, and full agreement and
understanding of the risks and benefits of using potentially addictive drugs to manage your condition.
In signing this agreement, you have agreed to a trial of long-term use of potentially addictive medications as part of
your treatment. Because your doctor is prescribing such medication to help manage your condition, it is considered
good practice to agree to the conditions outlined below.
My responsibilities as a patient
• I agree to see one doctor at one practice for all my health needs and prescriptions.
• I will have all my medications dispensed at one pharmacy.
• I agree that this medication is prescribed as a trial. If it appears to my doctor that there is no improvement in my
daily function or quality of life from the controlled substance, my medication may be discontinued. I will gradually
taper my medication as prescribed by my doctor.
• I will inform my doctor of all medications I am taking, including herbal remedies and illicit medication. Medications
can interact with drugs of dependence and produce serious side effects.
• I will fully communicate with my doctor to the best of my ability at the initial and all follow-up visits my pain level and
functional activity along with any side effects of the medications. This information allows my doctor to adjust my
treatment plan accordingly.
• I will not request or accept drugs of dependence from any other doctor or individual while I am receiving such
medication from my doctor at the [insert practice name].
• I understand the use of alcohol together with benzodiazepines is contraindicated.
• I will not use any illicit substances (eg cocaine, amphetamines or marijuana) while taking these medications. Use of
these substances may result in a change to my treatment plan, including safe discontinuation of my benzodiazepine
medications when applicable or complete termination of the doctor-patient relationship.
• If I have a history of alcohol or drug misuse/addiction, I must notify my doctor of such history since treatment with
benzodiazepines may increase the possibility of relapse.
... Continues on page 69

Benzodiazepines
... Continued from page 68
• I agree and understand that my doctor reserves the right to perform random or unannounced urine drug testing. If
requested to provide a urine sample, I agree to cooperate. If I decide not to provide a urine sample, I understand
that my doctor may change my treatment plan, including safe discontinuation of my benzodiazepine medications
when applicable or complete termination of the doctor-patient relationship. The presence of a non-prescribed
drug(s) or illicit drug(s) in the urine can be grounds for termination of the doctor-patient relationship. Urine drug
testing is not forensic testing, but is done for my benefit as a diagnostic tool and in accordance with certain legal
and regulatory materials on the use of controlled substances to treat pain.
• I agree to allow my doctor/healthcare provider to contact any healthcare professional, family member, pharmacy,
legal authority or regulatory agency to obtain or provide information about my care or actions, if my doctor feels it is
necessary.
• I understand my capacity to drive may be affected and I may be asked to cease driving.
My prescriptions
• I am responsible for my prescriptions. I understand that lost prescriptions will not be replaced.
• I understand that benzodiazepine prescriptions will not be mailed if I am unable to obtain my prescriptions monthly.
• Repeat prescriptions can be written for a maximum of 1 month supply and will be filled at the same pharmacy.
Pharmacy: ___________________________ Phone number: __________________________
• It is my responsibility to schedule appointments for the next benzodiazepine prescription before I leave the clinic or
within 3 days of the last clinic visit.
Taking my medications
• I understand that the medication is strictly for my own use. My medication should never be given or sold to others
because it may endanger that person’s health and is against the law.
• I am responsible for keeping my medication in a safe and secure place, such as a locked cabinet or safe. I am
expected to protect my medications from loss or theft. If my medication is stolen, I will report this to my local police
department and obtain a stolen item report. I will then report the stolen medication to my doctor. If my medications
are lost, misplaced or stolen my doctor may choose not to replace the medications or to taper and discontinue the
medications.
• I am responsible for taking my medications as directed. I agree to take the medication only as prescribed.
• I understand increasing my dose without the close supervision of my doctor could lead to drug overdose, causing
severe sedation and respiratory depression and death.
• I understand that decreasing or stopping my medication without the close supervision of my doctor can lead to
withdrawal. Withdrawal symptoms can include yawning, sweating, watery eyes, runny nose, anxiety, tremors,
aching muscles, hot and cold flashes, ‘goose flesh’, abdominal cramps and diarrhoea. These symptoms can occur
24-48 hours after the last dose and can last up to 3 weeks.
• Any evidence of drug hoarding, acquisition of any benzodiazepine medication or additional drugs of dependence
from other doctors (which includes emergency rooms), uncontrolled dose escalation or reduction, loss of
prescriptions, or failure to follow the agreement may result in termination of the doctor-patient relationship.
Monitoring effects of treatment
• I accept that drug of dependence therapy is only part of my care, and that I must be fully compliant with additional
care interventions deemed appropriate for my health.
• I accept that set appointments must be made to review ongoing therapy. This should be monthly and made at the
last clinic appointment. No walk-in appointments for medication refills will be granted.
• If an appointment is missed, another appointment will be made as soon as possible. Immediate or emergency
appointments will not be granted.
• I will be seen on a regular basis and given prescriptions for enough medication to last from appointment to
appointment, and sometimes 2-3 days extra if the prescription ends on a weekend or holiday. This extra
medication is not to be used without the explicit permission of the prescribing doctor unless an emergency requires
your appointment to be deferred 1 or 2 days.
... Continues on page 70

Benzodiazepines
... Continued from page 69
• It is my responsibility to notify my doctor of any side effects that continue or are severe (eg sedation, confusion). I
am also responsible for notifying my doctor immediately if I need to visit another healthcare provider or need to visit
an emergency room, or if I become pregnant.
• I understand that during the time that my dose is being adjusted, I will be expected to return to the clinic as
instructed by my clinic doctor. After I have been placed on a stable dose, I may receive longer-term therapy from
my doctor, but will return to the medical centre for a medical evaluation at least once every 3 months.
• I understand that a reduction of medication will occur if I have deterioration at home or work, or reduction of social
activities because of medication, or due to medication side effects.
• I understand that while physical dependence is to be expected after the long-term use of benzodiazepines, any
signs of addiction, abuse or misuse shall prompt the need for substance dependence treatment as well as weaning
and detoxification from the benzodiazepines.
My behaviour
I understand that cessation of the medication trial, or cessation of the doctor-patient relationship may occur if I display
any of the following behaviours:
• presenting to the clinic intoxicated, as assessed by clinical staff
• making any physical threat to any member of staff or other patients
• aggressively complaining about a need for medication
• persistently requesting to have my medication dose increased despite clinical advice
• taking a few extra, unauthorised doses on occasion
• visiting multiple doctors for controlled substances (doctor shopping)
• hoarding medication
• using my medication for non-medical purposes (ie in any other way than prescribed)
• starting frequent unscheduled clinic visits for early refills
• using consistently disruptive behaviour when arriving at the clinic
• obtaining drugs of dependence from family members (including stealing from older relatives)
• having a pattern of lost or stolen prescriptions
• displaying anger or irritability when questioned closely about my symptoms
• being unwilling to consider other medications or non-pharmacologic treatments
• escalating my dose without authorisation
• testing positive for a non-prescribed drug(s) or illicit drug(s) in my urine
• injecting an oral formulation
• forging prescriptions
• selling medications
• refusing diagnostic workup or investigation
• obtaining controlled substance analgesics from illicit sources.
I understand that non-compliance with the above conditions may result in a re-evaluation of my treatment plan and
discontinuation of benzodiazepine therapy. I may be gradually taken off these medications, or even discharged from
the clinic.
I ____________________________________________ have read the above information or it has been read to me and
all my questions regarding treatment with benzodiazepines have been answered to my satisfaction. I hereby give my
consent to participate in trial benzodiazepine therapy and acknowledge receipt of this document.
Patient’s signature Date
Doctor’s signature Date

Benzodiazepines
Resource F. Drug and alcohol assessment tool
Alcohol Use Disorders Identification Test

AUDIT questionnaire: Screen for alcohol misuse
The Alcohol Use Disorders Identification Test (AUDIT) was developed by the World Health Organization as a
questionnaire to identify persons whose alcohol consumption has become hazardous or harmful to their health.
The AUDIT tool and its Guidelines for use in primary care are available at www.who.int/substance_abuse/
activities/sbi/en
The Department of Veterans Affairs has an easy-to-use AUDIT tool that can be printed to work through with
your patients. It is available at http://at-ease.dva.gov.au/therightmix/resources/for-health-professionals
The AUDIT-C tool is a modified version of the 10-question AUDIT instrument. It is printed below and is available
at www.racgp.org.au/your-practice/guidelines/redbook/appendices/appendix-3-audit-c
Each AUDIT-C question has a choice of five answers. It is scored on a scale of 0-12.
In men, a score of 4 or more, and in women, a score of 3 or more, is considered positive, optimal for identifying
hazardous drinking or active alcohol use disorders. However, when the points are all from Question 1 alone
(questions 2 and 3 are zero), it can be assumed that the patient is drinking below recommended limits and it is
suggested the provider review the patient’s alcohol intake over recent months to confirm accuracy. * Generally,
the higher the score, the more likely it is that the patient’s drinking is affecting their safety.
* Bradley 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 Intern Med 2003;163(7):821-9.
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. 5 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
a = 0 points; b = 1 point; c = 2 points; d = 3 points; e = 4 points
AUDIT-C is based on The Alcohol Use Disorders Identification Test. Reproduced, with the permission of the publisher, from
The Alcohol Use Disorders Identification Test: guidelines for use in primary care, AUDIT, second edition. Geneva: World Health
Organization; 2000. P 17. Available at http://whqlibdoc.who.int/hq/2001/WHO_MSD_MSB_01.6a.pdf [Accessed 22 January 2015].
Benzodiazepines
Resource G. GP guide to behavioural therapy for

insomnia
Behavioural therapy for insomnia - Information for GPs

Behavioural therapies for insomnia include sleep hygiene education, stimulus control, relaxation and sleep
restriction therapy.108
Sleep hygiene
Sleep hygiene refers to actions that tend to improve and maintain good sleep.108,195,196
• Sleep as long as necessary to feel rested (usually 7-8 hours for adults), then get out of bed.
• Maintain a regular sleep schedule.
• Try not to force sleep.
• Avoid caffeinated beverages after lunch.
• Avoid alcohol near bedtime (late afternoon and evening).
• Avoid smoking or other nicotine intake, particularly during the evening.
• Adjust the bedroom environment as needed to decrease stimuli (eg reduce ambient light, turn off the
television or radio).
• Resolve concerns or worries before bedtime
• Exercise regularly for at least 20 minutes, preferably more than 4-5 hours prior to bedtime.
• Avoid daytime naps, especially if they are longer than 20-30 minutes or occur late in the day.
• Avoid going to bed until you are drowsy and ready to sleep.
• If you are not asleep within 15-20 minutes, get out of bed and return only when drowsy.
Stimulus control
Patients with insomnia may associate their bed and bedroom with the fear of not sleeping or other arousing
events, rather than the more pleasurable anticipation of sleep. The longer you stay in bed trying to sleep,
the stronger the association becomes. This perpetuates the difficulty of falling asleep.108
Stimulus control therapy is designed is to disrupt this association by enhancing the likelihood of sleep.197
Patients should not go to bed until they are sleepy and should use the bed primarily for sleep (and not
for reading, watching television, eating or worrying). They should not spend more than 20 minutes in bed
awake. If they are awake after 20 minutes, they should leave the bedroom and engage in a relaxing activity,
such as reading or listening to soothing music. Patients should not engage in activities that stimulate them
or reward them for being awake in the middle of the night, such as eating or watching television. In addition,
they should not return to bed until they are tired and feel ready to sleep. If they return to bed and still cannot
sleep within 20 minutes, the process should be repeated. An alarm clock should be set to wake the patient
at the same time every morning, including weekends. Daytime naps are not allowed. Patients may not
improve immediately. However, accumulating sleepiness will facilitate sleep during successive nights.108
Stimulus control instructions

• Go to bed only when sleepy.
• Get out of bed if unable to sleep after 15-20 minutes, leave the bedroom and do something relaxing (eg
reading or listening to soothing music). Avoid stimulating activities such as eating or watching TV. Return
to bed only when sleepy. (Repeat as necessary.)
• Use the bed/bedroom only for sleep (not reading, watching TV or worrying).
• Arise at the same time each day (including weekends).
• Do not take naps during the day.108
Benzodiazepines
Sleep restriction therapy

Some patients with insomnia stay in bed longer to try to make up for lost sleep. This causes a circadian
shift and a reduction in the homeostatic drive that makes sleep onset the following night more difficult and
results in the need to stay in bed even longer.108
Sleep restriction therapy counteracts this tendency by limiting the total time allowed in bed, including naps
and other sleep periods outside of bed, in order to increase the drive to sleep.198 This consolidates sleep
and improves sleep efficiency (the percentage of time in bed that the patient is asleep).108
Sleep restriction therapy begins by decreasing the time spent in bed to the same amount of time that the
patient reports sleeping (usually determined from sleep diaries or logs completed by the patient), but not
less than 5 hours per night. On a daily basis, the patient reports the amount of sleep obtained the previous
night and the amount of time spent in bed. The clinician then computes the sleep efficiency, which is the
reported time asleep divided by the time in bed. The time in bed is increased by 15-30 minutes once the
sleep efficiency exceeds 85%. This process is repeated until the patient reports improved sleep without
residual daytime sleepiness.108
Naps are not permitted.
To improve compliance, the rationale for the therapy needs to be carefully explained to patients. Some care
needs to be used to determine and schedule the time in bed in a manner that maximises the ability to sleep
that is acceptable to the patient. Older patients tend to have more difficulty maintaining sleep even when
restricted; therefore, they are given more lenient criteria.108
Relaxation
Relaxation therapy may be implemented before each sleep period. There are two common techniques for
relaxation therapy: progressive muscle relaxation and the relaxation response.108
Progressive relaxation is based on the theory that an individual can learn to relax one muscle at a time until
the entire body is relaxed. Beginning with the muscles in the face, the patient contracts the muscles gently for
1-2 seconds and then relaxes. This is repeated several times. The same technique is used for other muscle
groups, usually in the following sequence: jaw and neck, upper arms, lower arms, fingers, chest, abdomen,
buttocks, thighs, calves and then feet. This cycle is repeated for approximately 45 minutes, if necessary.108
The relaxation response begins by lying or sitting comfortably. The eyes are closed and relaxation is allowed to
spread throughout the body. A relaxed, abdominal breathing pattern is established. Thoughts are redirected
away from everyday thoughts and toward a neutral mental focusing device, such as a peaceful word or image.108
Cognitive therapies
Patients who are awake at night commonly become concerned that they will perform poorly the next day
if they do not obtain adequate sleep. This worry can exacerbate their difficulty falling asleep, creating a
vicious cycle of wakefulness and concern. A person may begin to blame all negative events in their life on
poor sleep. During cognitive therapy, a person works with a therapist to deal with anxiety and catastrophic
thinking, while establishing realistic expectations related to insomnia and the need for sleep.108
Cognitive behavioural therapy (CBT) is a strategy that combines several of the previously described
approaches over several weeks.199 A sample, 8-session CBT program may include an introductory sleep
education session, followed by two sessions that focus on stimulus control and sleep restriction. These may
be followed by two sessions that focus on cognitive therapy and then a session on sleep hygiene. Finally,
there may be a session that reviews and integrates the previous session and a session that addresses
future problems, such as stress and relapse.200
Patients are encouraged to complete sleep logs as they learn and apply the various strategies. This allows
improvement to be measured. The advantage of the educational nature of CBT is that it provides patients
with the tools to apply it in the future. Disadvantages of CBT include the duration of therapy, and the
relatively few clinicians who are skilled at all of its components.108
The benefit of CBT may be reduced when it is administered by less experienced clinicians.108,201
Benzodiazepines
Appendix A. Key terms and definitions
A.1 Drugs of addiction and drugs of dependence

Legal definitions of drugs of dependence and drugs of addiction vary between states/territories. Refer to
RACGP’s Prescribing drugs of dependence in general practice, Part A - Clinical governance framework.
This guide uses the following definitions:
Drugs of addiction refer to all Schedule 8 (S8) drugs. These have strict legislative controls regarding
their manufacture, supply, distribution, possession and use to reduce abuse, misuse, and physical and
psychological dependence. Examples of S8 drugs include morphine, oxycodone, dexamphetamine,
flunitrazepam (Rohypnol) and, as of February 2014, alprazolam.
*
Drugs of dependence describe all S8 drugs plus specified Schedule 4 (S4) drugs that are subject to
misuse, abuse and trafficking. All S4 drugs are restricted substances, but only some (eg benzodiazepines)
can form dependence (these are called S4D drugs in New South Wales). Some others drugs, like anabolic
steroids and amphetamines, are restricted and can only be prescribed by authority.
Each state and territory has its own legislative requirements. Refer to RACGP’s Prescribing drugs of
dependence in general practice, Part A - Clinical governance framework.
*Xanax (Pfizer) has been withdrawn from the Australian market, however generic alprazolam is still currently available.
A.2 Tolerance, dependence, substance use

disorder and withdrawal
The two commonly used classification systems for data collection are the International Statistical
Classification of Diseases and Related Health Problems, 10th revision, (ICD-10) and the Diagnostic and
Statistical Manual of Mental Disorders, 5th edition, (DSM-5). Some of the terminology adapts poorly to the
situation where prescription drugs are used to treat conditions, such as chronic non-malignant pain.
Tolerance is a decrease in response to a drug dose. It occurs with all chronically used drugs of
dependence, including opioids and benzodiazepines. Increased doses are required to achieve the effects
originally produced by lower doses.31
Dependence, in strict pharmacological terms, is a state that develops during chronic drug treatment in
which drug cessation elicits an abstinence reaction (withdrawal).
Dependence can be associated associated with a whole range of psychoactive drugs or chemicals (eg
caffeine, alcohol, opioid, cannabis or stimulant dependence). As awareness of problematic drug use grew,
the definition of dependence changed to include addiction and abuse. Various definitions of dependence
evolved with DSM-4, ICD-10, World Health Organization (WHO) and leading authors describing it as a
cluster of behavioural, cognitive and physiological phenomena that may develop after repeated substance
use. Now people link dependence with ‘addiction’ when in fact dependence can be a normal body
response to a substance. While drug dependence can be part of addiction, is not the same thing.
To reduce confusion, the new DSM-5 (2013) criteria has replaced drug dependence with DSM-5 substance
use disorder measured on a continuum from mild to severe. Refer to Appendix A.3 Misuse, non-medical
use and abuse.
Note: There are legal implications involving the term dependence (eg restrictions around prescribing to
drug-dependent persons). Characteristics of person who is drug dependent include having a history of
substance misuse and being identified as a ‘doctor shopper’ or ‘prescription shopper’.202 Refer to Appendix
A.4, Drug-seeking behaviour.
Benzodiazepines
Substance use disorder has been introduced in DSM-540 to replace dependence (or dependence
syndrome) as used to refer to complex symptoms beyond tolerance and withdrawal. The essential feature
of SUD is a cluster of cognitive, behavioral and physiological symptoms indicating the individual continues
using the substance despite significant substance-related problems.40 Diagnosis of SUD requires the
presence of at least two of 11 criteria, across four categories: impaired control, social impairment, risky use
and pharmacology.
Note: In DSM-5, substance dependence and substance abuse have been combined into a single
category of SUDs (eg ‘benzodiazepines dependence’ would be included within sedative, hypnotic, or
anxiolytic use disorder).40 Each SUD is divided into mild, moderate and severe subtypes, with the number
of criteria present determining the severity. (Refer to Table 3 for DSM-5 criteria and Table A.1 for ICD-10
criteria.)
Withdrawal or withdrawal syndrome is a group of symptoms of variable clustering and degree of severity
which occur on cessation or reduction of use of a psychoactive substance that has been taken repeatedly,
usually for a prolonged period and/or in high doses. Signs of physiological disturbance may accompany the
syndrome. A withdrawal syndrome is one of the indicators of a dependence syndrome.31
Table A.1. ICD-10 criteria for diagnosing benzodiazepine dependence

*
Drug related criteria • Compulsion/craving to take benzodiazepine
• Difficulties in controlling benzodiazepine use
Consequences of use criteria • Progressive neglect of alternative pleasures/interests due to

benzodiazepine use
• Persistent benzodiazepine use despite harmful consequences
Physiological criteria • Characteristic benzodiazepine withdrawal state

• Evidence of tolerance to benzodiazepines
Notes: A diagnosis of dependence is made if three of six criteria listed above have been met in the last 12 months.
* World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders - ICD-10 criteria for diagnosing benzodiazepine
dependence. Geneva: WHO; 2010. Available at http://www.who.int/substance_abuse/terminology/icd_10/en/ [Accessed 12 June 2015].
A.3 Misuse, non-medical use and abuse

Misuse refers to use of a substance for a purpose that is not consistent with legal or medical guidelines,
and includes the non-medical use of prescription medication. Patients may inadvertently misuse
prescription medication by taking them as prescribed but in response to inappropriate prescribing practices.
Patients may deliberately misuse medication for non-medical purposes.31
Non-medical use describes use of a prescription drug, whether obtained by prescription or otherwise, for
any purposes other than in the manner or for the time period prescribed, or by a person for whom the drug
was not prescribed (ie diversion). Non-medical use occurs for a variety of reasons such as enjoyment of
effects (especially when binge dosed), to enhance the effects of other drugs (eg benzodiazepines taken with
opiates), to decrease withdrawal symptoms, to enhance confidence, to feel normal and to facilitate sexual
assault (eg flunitrazepam used as ‘date rape’ drug).31
Abuse is a commonly used term with a variety of meanings. It is sometimes used disapprovingly to refer
to any use at all, particularly of illicit drugs, while in other contexts abuse has referred to non-medical or
unsanctioned patterns of use, irrespective of consequences.31
Problematic drug use may be a wider, yet clearer, more descriptive and less judgemental term than
misuse or abuse.31
Benzodiazepines
A.4 Drug-seeking behaviour

Drug-seeking behaviour is a poorly defined term that describes a range of activities directed towards
attainment of sought after medications. The most common medications sought are opioids and
benzodiazepines. Behaviours include attending multiple practitioners (prescription or doctor shopping) and
employing manipulating tactics.203
A comprehensive list of tactics and behaviours used to obtain medication is available in RACGP’s
Prescribing drugs of dependence in general practice, Part A - Clinical governance framework.
Prescription or doctor shopping is when patients unknowingly or deliberately obtain more medicines
than is medically needed. This is often done by visiting many doctors, without telling them about their
other consultations.204 The Medicare Australia Prescription Shopping Information Service (PSIS) defines
prescription shoppers as anyone, within any 3-month period, that has been supplied with PBS items
prescribed by six or more different prescribers (including nurse practitioners and midwives, but excluding
specialists and consultant physicians), and/or a total of 25 or more target PBS items, and/or a total of 50 or
more items.204 Target items are analgesics, anti-epileptics, anti-parkinson medicine, psycholeptics (including
antidepressants), and all other nervous system medicine.
A.5 Prescriber behaviour

Appropriate prescriber behaviour refers to prescription decisions based on evidence at the time of
assessment and taking into account the patient’s perspective. This is related to the term accountable
prescribing.
Accountable prescribing is defined as a commitment to evidence-based practice, the use of medicines
with proven effectiveness and the avoidance of medicines when they do not help or cause harm.205
Inappropriate prescriber behaviour refers to persistent prescribing of drugs of dependence despite

absence of sustained improvement in function, deterioration of function and/or the development of
unacceptable side effects.206
A.6 Staged supply

Staged supply is the process by which pharmacists supply medicine to a patient in periodic instalments
of less than the originally prescribed quantity, at agreed time intervals. The balance of the medicine is
held by the pharmacy to fulfil subsequent instalments. This service can be initiated by the pharmacist, the
prescriber, the patient (or their carer) or another health professional involved in the patient’s care.207
Benzodiazepines
Appendix B. Recommendations
and grading
B.1 Evidence-based statements and

recommendations - Insomnia
Number Recommendations Grading and source of grade
Rec 1 Cognitive behavioural Grade A recommendation
therapy based treatment Source:
packages for chronic
Wilson SJ, Nutt DJ, Alford C, et al. British Association for Psychopharmacology
insomnia including sleep consensus statement on evidence-based treatment of insomnia, parasomnias and
restriction and stimulus circadian rhythm disorders. J Psychopharmacol 2010;24(11):1577-601.
control are effective and
*
Supported by:
should therefore be offered
Bloom HG, Ahmed I, Alessi CA, et al. Evidence-based recommendations for the
to patients as a first-line
assessment and management of sleep disorders in older persons. J Am Geriat Soc
treatment 2009;57(5):761-89.
Bonnet MH, Arand DL. Treatment of insomnia. In UpToDate, Benca R (ed). UpToDate,
Waltham, MA 2014. Available at www.uptodate.com/contents/treatment-of-insomnia
[Accessed October 2014].
Guideline Development Group for the management of patients with insomnia in
primary care. Clinical Practice Guidelines for the management of patients with
Insomnia in Primary Care. UETS No 2007/5-1. Madrid: Ministry of Health and Social
Policy; 2009.
Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M. Clinical guideline for
the evaluation and management of chronic insomnia in adults. J Clin Sleep Med
2008;4(5):487-504.
RACGP Handbook of non-drug interventions (HANDI). Brief behavioural therapy:
Insomnia in adults. Available at www.racgp.org.au/your-practice/guidelines/handi/
interventions/mental-health/brief-behavioural-therapy-for-insomnia-in-adults
[Accessed October 2014].
Riemann D, Perlis ML. The treatments of chronic insomnia: a review of
benzodiazepine receptor agonists and psychological and behavioral therapies. Sleep
Med Rev 2009;13(3):205-14.
Rec 2 Z drugs and short-acting Grade A recommendation

benzodiazepines are Source:
efficacious for insomnia
Wilson SJ, Nutt DJ, et al. British Association for Psychopharmacology consensus
statement on evidence-based treatment of insomnia, parasomnias and circadian
rhythm disorders. J Psychopharmacol 2010;24(11):1577-601.
*
Supported by:
Guideline Development Group for the management of patients with insomnia in primary
care. Clinical Practice Guidelines for the management of patients with Insomnia in
Primary Care. UETS No 2007/5-1. Madrid: Ministry of Health and Social Policy; 2009.
benzodiazepine receptor agonists and psychological and behavioral therapies. Sleep
Med Rev 2009;13(3):205-14.
Rec 3 Prescription of zolpidem and Grade A recommendation

zopiclone should be treated Source:
with the same cautions as
Ministry of Health Singapore. Prescribing of Benzodiazepines: MOH Clinical Practice
benzodiazepines Guidelines 2/2008. Singapore: MOH; 2008.
*
Supported by:
benzodiazepine receptor agonists and psychological and behavioural therapies. Sleep
Med Rev 2009;13(3):205-14.
Benzodiazepines

Rec 4 Intermittent dosing may Grade B recommendation
further reduce the risk of
Source:
tolerance and dependence
Wilson SJ, Nutt DJ, Alford C, et al. British Association for Psychopharmacology
consensus statement on evidence-based treatment of insomnia, parasomnias and
circadian rhythm disorders. J Psychopharmacol 2010;24(11):1577-601
Rec 5 If hypnotics are to be used Grade B recommendation

for treating insomnia, it
Source:
is recommended that
Guideline Development Group for the management of patients with insomnia in
treatment is short term (ie primary care. Clinical Practice Guidelines for the management of patients with
not more than 4 weeks) and Insomnia in Primary Care. UETS No 2007/5-1. Madrid: Ministry of Health and Social
at the lowest possible dose Policy; 2009.
*Recommendation supported, however gradings (where given) may be different from source.

recommendations - Anxiety
Rec 6 Cognitive behavioural Grade A recommendation
therapy is recommended Source: Guideline Working Group for the Treatment of Patients with
as one of the treatments Anxiety Disorders in Primary Care. Clinical Practice Guideline for
of choice for generalised Treatment of Patients with Anxiety Disorders in Primary Care. UETS no
anxiety disorder, panic 2006/10 ed. Madrid: Ministry of Health and Social Policy; 2008.
disorder, and panic
attacks due to its Supported by:
*
effectiveness at reducing Agency for Healthcare Research and Quality (AHRQ). Guideline Summary NGC - 7124:
Practice guideline for the treatment of patients with panic disorder. Derived from:
the symptoms of anxiety
American Psychiatric Association (APA). Practice guideline for the treatment of patients
in the short and long with panic disorder. 2nd ed. Washington, DC: APA; 2009.
term, although patient
Agency for Healthcare Research and Quality (AHRQ). Guideline Summary NGC -8660:
preference must be taken Generalised anxiety disorder and Panic Disorder (with or without agorophobia) in adults.
into consideration Management in primary, secondary and community care.208 Derived from: National
Collaborating Centre for Mental Health, National Collaborating Centre for Primary Care.
Generalised anxiety disorder and panic disorder (with or without agorophobia) in adults.
Management in primary, secondary and community care (Clinical guide no 113). London:
National Institute for Health and Clinical Excellence (NICE); 2011.
Rec 7 Consider an selective Grade A recommendation

serotonin reuptake Source: Baldwin DS, Anderson IM, Nutt DJ, et al. Evidence-based
inhibitor (SSRI) for first- pharmacological treatment of anxiety disorders, post-traumatic stress
line treatment, as SSRI disorder and obsessive-compulsive disorder: A revision of the 2005
are effective across guidelines from the British Association for Psychopharmacology. J
the anxiety and related Psychopharmacol 2014;28(5):403-39.
disorders, in both the
short term and long term, Supported by:
*
and are generally well Agency for Healthcare Research and Quality (AHRQ). Guideline Summary NGC - 7124:
tolerated
with panic disorder. 2nd ed. Washington, DC: APA; 2009.
Agency for Healthcare Research and Quality (AHRQ). Guideline Summary NGC -8660:
Generalised anxiety disorder and Panic Disorder (with or without agorophobia) in
adults. Management in primary, secondary and community care. Derived from: National
Collaborating Centre for Mental Health, National Collaborating Centre for Primary Care.
Generalised anxiety disorder and panic disorder (with or without agorophobia) in adults.
Management in primary, secondary and community care (Clinical guide no 113). London:
National Institute for Health and Clinical Excellence (NICE); 2011.
Guideline Working Group for the Treatment of Patients with Anxiety Disorders in Primary
Care. Clinical Practice Guideline for Treatment of Patients with Anxiety Disorders in
Primary Care. UETS no 2006/10 ed. Madrid: Ministry of Health and Social Policy; 2008.
Benzodiazepines

Rec 8 Benzodiazepines have Grade A/B recommendation
evidence of benefit in Source: Bandelow B, Sher L, Bunevicius R, et al. Guidelines for the
generalised anxiety pharmacological treatment of anxiety disorders, obsessive-compulsive
disorder, social anxiety disorder and posttraumatic stress disorder in primary care. Int J
disorder and panic Psychiatry Clin Pract 2012;16(2):77-84.
disorder, but not
obsessive compulsive *
Supported by:
disorder or post-traumatic Agency for Healthcare Research and Quality (AHRQ). Guideline Summary NGC - 7124:
stress disorder
with panic disorder. 2nd ed. Washington, DC: APA; 2009.
Baldwin DS, Anderson IM, Nutt DJ, et al. Evidence-based pharmacological treatment of
anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder: A
revision of the 2005 guidelines from the British Association for Psychopharmacology. J
Psychopharmacol 2014;28(5):403-39.
Bandelow B, Boerner JR, Kasper S, Linden M, Wittchen HU, Moller HJ. The diagnosis
and treatment of generalized anxiety disorder. Dtsch Arztebl Int 2013;110(17):300-9.
Bandelow B, Zohar J, Hollander E, Kasper S, Moller HJ, WFSBP Task Force on
Treatment Guidelines for Anxiety Obsessive-Compulsive Post-Traumatic Stress
Disorders. World Federation of Societies of Biological Psychiatry (WFSBP) guidelines
for the pharmacological treatment of anxiety, obsessive-compulsive and post-traumatic
stress disorders - first revision. World J Biol Psychiatry 2008;9(4):248-312.
Canadian Agency for Drugs and Technologies in Health (CADTH). Short- and Long-Term
Use of Benzodiazepines in Patients with Generalized Anxiety Disorder: A Review of
Guidelines. Ottawa: CADTH; 2014.
Davidson JR, Feltner DE, Dugar A. Management of generalized anxiety disorder in
primary care: identifying the challenges and unmet needs. Prim Care Companion J Clin
Psychiatry 2010;12(2).
Dell’osso B, Lader M. Do benzodiazepines still deserve a major role in the treatment
of psychiatric disorders? A critical reappraisal. European psychiatry: J Assoc Europ
Psychiat 2013;28(1):7-20.
Guideline Working Group for the Treatment of Patients with Anxiety Disorders in Primary
Care. Clinical Practice Guideline for Treatment of Patients with Anxiety Disorders in
Primary Care. UETS no 2006/10 ed. Madrid: Ministry of Health and Social Policy; 2008.
Katzman MA, Bleau P Blier P et al. Canadian clinical practice guidelines for the
management of anxiety, posttraumatic stress and obsessive-compulsive disorders. BMC
Psychiatry 2014;14 Suppl 1:S1
*Recommendation supported, however gradings (where given) may be different from source.

recommendations - Alcohol withdrawal
Number Recommendations Grade and source of grading
Rec 9 Benzodiazepines (eg diazepam, oxazepam) Grade A recommendation
are the drugs of choice for treatment of acute Source: Scottish Intercollegiate Guideline
alcohol withdrawal (including alcohol withdrawal Network. The Management of Harmful
delirium), but for a maximum of 7 days Drinking and Alcohol Dependence in
Primary Care. Guideline No 74. Edinburgh:
SIGN; 2004
Benzodiazepines
Appendix C. Process of development

This guide was developed in response to calls for a resource for GPs and general practice teams to
manage benzodiazepine prescribing. It represents a synthesis of current scientific knowledge and rational
clinical practice regarding treatment with benzodiazepines. The content broadly conforms to the highest
evidence-based standards according to the principles underlying the Appraisal of Guidelines Research and
Evaluation (AGREE) Instrument. It strives to be as free as possible of bias toward any theoretical approach
to treatment.
The RACGP convened a GP-led advisory group, comprising GP members with expertise and experience
in drugs of dependence and guideline development. A literature search was conducted and key resources
were identified.
A limited literature search was conducted, using key resources including PubMed, The Cochrane Library,
University of York Centre for Reviews and Dissemination (CRD) databases, international health technology
agencies, in addition to a focused Internet search. Filters were applied to limit retrieval to articles in English,
health technology assessments, systematic reviews, meta-analyses and guidelines. In the first level of
screening, titles and abstracts were reviewed and potentially relevant articles were retrieved based on:
• national and international benzodiazepine prescribing guidelines

• national and international guidelines of specific disease state management (eg insomnia, anxiety)
• high-quality systematic reviews on benzodiazepine prescribing
• high-quality publications that address key issues with benzodiazepine pharmacology, dependence,
tolerance and adverse effects.
An in-depth critical analysis of the publications was not undertaken.
This guide provides recommendations based on current evidence-based guidelines, including the Scottish
Intercollegiate Guidelines Network (SIGN), the British Association of Psychopharmacology, and the Health
Technology Assessment Unit of the Spanish Ministry of Health and Social Policy.
In cases where guideline recommendations specific to the indication were not available, other sources, such
as systematic reviews, have been used to inform the recommendations.
The advisory group did not attempt to re-evaluate the evidence behind these recommendations or
convert the recommendation grades to the Australian National Health and Medical Research Council
(NHMRC) grading levels. Therefore, the recommendations tables include the reference and sources of
recommendations, the recommendation grade and links to further information on the evidence grade where
available (refer to Appendix B). For some recommendations, an evidence grade was not available; therefore,
these recommendations should be treated as expert opinion
Benzodiazepines
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& RACGP
Healthy Profession.
Healthy Australia.
PROFESSIONAL
GP supervisors assessing GP
registrars - theory and practice
Susan Wearne
James Brown
Why assess?
Background
General practice supervisors are increasingly being expected to assess their Patient safety and registrars
registrars. at risk
Objective Early assessment1,2 helps supervisors gauge how
In this article we explore the issues this raises for supervisors, and discuss the much direct clinical oversight registrars need.3 The
literature, which suggests that global assessments are the most accurate and privacy of general practice consulting rooms can
feasible. delay supervisors’ realisations that new registrars
are struggling.4 Relying on registrars’ insight to know
Discussion
We suggest the following guidelines for supervisors: inform registrars at the when to ask questions can be flawed, particularly
beginning of the term about how and when they will be assessed; be clear that for poor performers5 who tend to overestimate their
the aim is to decide if the registrars’ practice is safe for patients and appropriate ability.6,7
for their stage of training; observe registrars at work; make an initial judgement
of registrars’ performance; test the initial judgement on performance applying Assessment facilitates early
qualitative research methods to improve trustworthiness and reduce potential educational intervention
biases; use the working diagnosis of registrar performance to guide the level Educational organisations, such as regional training
of support and clinical oversight needed and flag registrars who require further
providers, rely on supervisors to assess registrars’
assessment by educational organisations for remediation decisions.
progress through training. A minority of registrars need
Keywords extra educational support. Early identification of these
education, medical; general practice; assessment doctors facilitates early intervention,2 which may lead
to successful remediation. Very rarely, registrars may
need to be removed from the training program and
counselled to consider an alternative career.
Introduction Supervisors facilitating learning
General practice supervisors are There is a strong case that supervisors’ tasks of
increasingly being expected to assess facilitating registrars’ learning will be augmented by
their registrars. The Australian College supervisors undertaking an assessment of registrars’
of Rural and Remote Medicine (ACRRM) performance.
describe supervisors’ assessments as It is recognised that assessment drives learning.8
a means of giving registrars feedback, Assessment informs feedback, which registrars expect
developing their self-evaluation skills and supervisors to be skilled in giving.9,10 Supervisors’
informing their learning plans.1 The Royal feedback is valued by registrars11 and has credibility
Australian College of General Practitioners because of their currency in the same job,12 and their
(RACGP) 2013 Vocational Standards, longitudinal observations of registrars at work.13
to be implemented nationally in 2015,
require supervisors to ‘assess registrars’
Challenges for supervisors as
competence and tailor supervision to that
assessors
competence’ (Table 1).2 This emphasis on Supervisors who assess registrars may find it harder
assessment raises some questions and to also support them, and registrars’ willingness to
challenges for supervisors. be open about their vulnerabilities14 may be reduced.
REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 43, NO. 12, DECEMBER 2014 887
PROFESSIONAL GP supervisors assessing GP registrars - theory and practice
Table 1. General practice colleges standards for supervisors

Australian College of Rural and Remote Medicine1 Plan assessment
Clarify roles and assessment
7.2.7 The supervisor must conduct formative assessment of the registrar, in accordance
methods
with their stage of training. In the first 12 months of training, the supervisor agrees
to undertake regular reviews (at least once every 4 months) of registrar patient Clarify purpose: decide on
consultations. This may be achieved by sitting in on patient consultations or supervision level needed and
through reviewing videotaped/audio-taped consultations supplied by the registrar. progress through training
The supervisor will use this exercise to provide the registrar with feedback on their
performance and to guide the registrar in self-evaluation. I \
Note: registrars are required to submit six consultations assessed using the miniCEX Gather data: observe
7.3.2 The supervisor must be skilled in assessing and providing feedback on consultations
performance, including establishing and reviewing learning plans. It is very important
that positive and negative feedback are given appropriately and in a timely fashion.
I [
Feedback is best when it is based on first hand observation and when it is constructive Intuitive assessment of
in nature. It should be given as soon as possible when the opportunity occurs in a performance
learning situation. Waiting until mid-term or end of placement to give feedback about
deficiencies is potentially dangerous for patients and provides the registrar with little I \
opportunity to improve. Test and revise intuitive
Royal Australian College of General Practitioners2 assessment
Reflection: consider biases
Standard 1.1 - Supervision is matched to the individual registrar’s level of
competence and learning needs in the context of their training post. Triangulation: practice team
feedback, review notes & referrals
Criterion 1.1.1.1 The registrar’s competence is assessed prior to entry to the post and
monitored throughout the term and training.
Standard 1.2 - A model of supervision is developed that in the context of the training
I \
post ensures quality training for the registrar and safety for patients. Feedback to registrar
There is a documented process by which the supervisor conducts and records the • Modify learning plan
assessment activities and other means of determining a registrar’s competencies Feedback to practice team
during their time in the placement. The process is approved by the training provider • Review supervision plan
and regular reporting and feedback between training provider and supervisor is Document assessment
established. P6
Feedback to external
^Reproduced with permission from the Australian College of Remote and Rural organisations
Medicine, from Primary rural and remote training: standards for supervisors and • Satisfaction with registrar
teaching posts. Brisbane: ACRRM, 2013. performance - continue
^Reproduced with permission from the Royal Australian College of General standard training
Practitioners, from Vocational Training Standards. East Melbourne: RACGR 2013 • Uncertain about registrar
performance - seek external
review
Assessment of registrars by their supervisors can mainstream general practice. It can be difficult • Serious concerns about
exaggerate the power imbalance between them. to distinguish between performance that will registrar performance - urgent
This is particularly an issue when supervisors are improve once registrars have adjusted to new review of placement needed
also registrars’ employers, and/or visa sponsors, or contexts, and performance that indicates
when registrars provide valuable workforce to the educational problems that are unlikely to resolve Figure 1. Framework for in-practice
assessment of registrars
practice. Time taken assessing registrars can also with experience. Supervisors have requested
be costly. training in assessment,16 which the following
Supervisors may doubt the accuracy of guide based on practical experience and research
their assessment and opinion15 and may evidence aims to provide (Figure 1). assessment role can create clarity.18 Ideally,
avoid expressing concerns about registrars’ registrars should be advised at the beginning of
performance, hoping that they will improve over Guide for supervisors in their term how and when they will be assessed.
time. This is particularly relevant if registrars assessing registrars
Clarify purpose
have switched to practise in a different context,
given the heterogeneity of general practices in
1. Plan assessments Traditionally, the purpose of assessment has been
Australia. For example, the content and culture Clarify roles considered formative or summative. Formative
of medical practice varies between Aboriginal General practice supervisors have multiple assessment aims to improve teaching and learning,
Community Controlled Health Services and roles.17 A brief explanation to registrars of their and summative assessment determines learners’
888 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 43, NO. 12, DECEMBER 2014
GP supervisors assessing GP registrars - theory and practice PROFESSIONAL
progress and and can be used for certification judgments.27 Although such intuitive judgments lead to being granted the privilege of independent
of this progress. Recently, this divide has been are often more accurate,28 they are inherently practice.30
bridged by the notion that all assessment should subject to a range of biases29 and may overlook Qualitative researchers face similar challenges
promote learning.19 The two main considerations key data,27 resulting in judgment error. This can be in assessing the trustworthiness of their assertions
for supervisors are whether registrars are problematic for ranking registrars on the basis of and have tools that can be applied to these
performing safely in the context of their current supervisors assessments21 or for assessments that qualitative, intuitive, work-based assessments.25
level of supervision and whether registrars are
performing at the expected level of their training.
Table 2. Qualitative research tools applied to registrar assessment
Clarify assessment methods and
their limitations Tool Description Parallel in registrar assessment
Prolonged Engagement of researchers Assessment of registrars over an
The choice of assessment method depends on engagement over an extended period of extended period
what is being assessed and the purpose of the time with the phenomenon of
assessment, as all methods have advantages interest
and disadvantages.20 Miller differentiated the Triangulation Collecting data from multiple Using several methods
assessment of clinical skills into competency sources of assessing registrars’
assessment and performance assessment.21 performance
Competency assessment evaluates what doctors Reflexivity Critiquing the impact of the Supervisors examine their own
investigator on the data and biases and impact on registrars’
do in controlled representations of professional
the conclusions made performance and assessment
practice and performance assessment evaluates
Peer debriefing Discussion of the data and Discussion of registrars
what they actually do in practice.
its interpretation with other assessment with other members
Competency assessment has its basis in researchers of the practice team
behaviourism22 and works successfully in the
Negative case Seeking disconfirming Actively seeking evidence
vocational education and training sector.23 Each analysis evidence that refutes the assessment of
skill is broken down into its components and registrars
checklists are created for assessors to complete Member checks Checking the data and Checking with registrars the
when learners demonstrate competence in each conclusions with the subjects supervisors’ observations
component. However, competency at individual of the investigation and conclusions on their
performance
aspects of practice does not prove that doctors
are able to perform skilfully at work. Good doctors
Audit trail Documenting the data Documenting the means of
collection, the methodology, assessing registrars, and
are more than a sum of individual competencies,
decisions and rationale. the ways of validating the
and focus on competency alone risks missing assessment
more important but less quantifiable elements of
practice such as wisdom and clinical judgment.22
The Australian Medical Council proposed that ‘the
coarse-grained concept of competent professional Expert Qualitative
practice, where observed performance is assessment
more than the sum of the set of competencies
used, should be retained’.23 As yet there is no
dependable set of competency-based assessment
tools for clinical practice.24
Professional performance is most
appropriately judged by work-based assessment.25
For registrars this means observing their work in
clinical practice (Figure 2). However, implementing
work-based assessment has proved challenging
and has been criticised for being unpredictable,
Quantitative
unstandardised and biased.21,26 This is in part
Novice assessment
because experienced practitioners tend to
make automatic intuitive judgments rather Figure 2. Choosing methods to assess clinical practice21,22,25,34
than engaging in analytic processes to reach
PROFESSIONAL GP supervisors assessing GP registrars - theory and practice
These tools are prolonged engagement, remainder of the performance highly; the converse future learning and supervisors can modify the
triangulation, negative case analysis, reflexivity, can also occur. Using a structured form, such practice supervision plan if needed.
peer debriefing, member-checking and audit trails as the mini-CEX, can ensure all domains and
(Table 2). The sources of error in work-based aspects of the consultation are considered. Social
6. Action - feedback to
assessments can be addressed as below29 by and cultural biases are important to recognise,
external organisations
applying these tools of analytical rigour31,32 to as registrars towards whom supervisors have The external organisation responsible for
reconsider initial, intuitive judgments. a natural affinity are more likely to be regarded overseeing the whole of registrars’ training needs
positively. to know the outcome of supervisors’ assessments.
2. Collect the data - observe Adequate performance permits progress through
consultations Triangulation training and continuation of current supervision
Most information comes from observing Triangulation of the data can be achieved by levels. For a minority of registrars, supervisors will
registrars consult directly or via video recordings. using multiple methods of observing registrars’ judge their performance as below expectations.
Other options are random case note reviews,33 performance (see 2 above). This can also be These judgments require adjustment to
audits of investigation ordering4 and arranging against non-work-based competency assessments supervision levels to ensure patient safety and
consultations where registrars present their such as knowledge tests and role playing. the educational organisation to arrange further
diagnosis and management to supervisors before registrar assessments and determine what, if
then concluding consultations. Watching for the
Prolonged engagement any, remedial action is indicated.30 If assessment
red flags of registrars who are unconsciously Programmatic assessment enacts prolonged reveals consistent problems and patient safety is
incompetent, such as issues of punctuality, engagement by using a combination of threatened, supervisors may need to seek further
poor communication, defensive justifications assessment instruments, each of which is used external assessors, significantly reduce, or rarely,
and inability to change behaviour in the light of to assess multiple facets of learning at intervals even remove registrars’ rights to practise.
feedback is also recommended.4 during training.36 This is more commonly arranged
by educational organisations than by individual Summary
3. Make an initial judgment on supervisors or their practices. General practice supervisors have roles in registrar
performance assessment both to promote patient safety and
Negative case analysis
Next, supervisors need to make working registrar learning. Work-based assessment of
diagnoses of registrars’ performances. This is an Negative case analysis is a deliberate effort performance seems to be the most accurate and
intuitive, overall assessment of the standard of to reveal key evidence that refutes the initial feasible way to assess registrars’ day-to-day work,
registrars’ clinical practice. judgment, which may have been overlooked. For but is prone to error. An assessment framework,
example, is a registrar whose practice was good with explicit processes that aim to minimise bias
4. Test the initial judgment on observation over-investigating or not getting and errors, is recommended. General practice
using qualitative research
methods repeat bookings from patients? supervisors’ assessments can produce working
diagnoses of registrars’ performances, which guide
Peer debriefing
Using reflexivity to reduce bias the level of support and clinical oversight needed,
For supervisors, this means first reflecting on how Peer debriefing would normally be achieved by and flag registrars that require further assessment
current stresses and personal biases are likely discussing the assessment of the registrar with by educational organisations for remediation
to affect their judgments and whether the initial other practice or supervisory team members. decisions.
judgment should be revised.
A range of sources of bias can contribute to
Audit trail Acknowledgements
We would like to thank Dr Hamshi Singh, Registrar
erroneous intuitive judgments.34 Some assessors Documenting assessments creates an audit trail Research and Development Officer at General
are naturally stringent (hawks) or lenient (doves). for supervisors, registrars or educators to review Practice Education and Training for her insightful
Case-related bias (the hobby-horse effect) arises decisions if needed. This is usually in writing comments on earlier drafts of this article, and
when the subject of the assessment activity is but a brief voice memo made immediately after Dr Tim Clements and Dr Patrick Kinsella from
Southern GP Training, who collaborated with us
a supervisor’s specific interest, which results in observing registrars may be quicker, and can be
at workshops that started our discussions about
their having higher expectations of performance. transcribed later. supervisors as assessors.
Recent ‘near-miss’ experiences by supervisors
may similarly alter their performance expectations
5. Action - feedback to the Authors
for particular presentations. Subject-related
registrar and practice team Susan Wearne BM MMedSc FRACGP FACRRM
DCH DRCOG DFFP GCTEd, Supervisor Research and
bias (the halo effect)35 occurs when learners Supervisors then give feedback to registrars
Development Adviser, General Practice Education
perform one aspect of a consultation particularly about their perceived strengths and weaknesses. and Training, Canberra, ACT. susan.wearne@gpet.
well, which leads the supervisor to assess the Registrars can use this information to plan their com.au
890 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 43, NO. 12, DECEMBER 2014
GP supervisors assessing GP registrars - theory and practice PROFESSIONAL
James Brown FRACGP, FACRRM, DRANZCOG, 13. Smith VC, Wiener-Ogilvie S. Describing the learning 33. Morgan S, Ingham G. Random case analysis - a new
MFM (Clin), Director of Training, Southern GP climate of general practice training: the learner’s framework for Australian general practice training.
perspective. Educ Prim Care 2009;20:435-40. Aust Fam Physician 2013;42:69-73.
Training, Churchill, VIC
14. Clandinin DJ, Cave M-T. Creating pedagogical 34. Crossley J. Validity and truth in assessment. Med
spaces for developing doctor professional identity. Educ 2013;47:1152-4.
Competing interests:
Med Educ 2008;42:765-70. 35. Nisbett RE, Wilson TD. The halo effect: Evidence
Southern GP Training paid Susan Wearne to assist 15. Kogan JR, Conforti LN, Bernabeo EC, Durning SJ, for unconscious alteration of judgments. J Pers Soc
with a workshop for supervisors on this topic. Hauer KE, Holmboe ES. Faculty staff perceptions Psychol 1977;35:250-56.
36. Schuwirth LW, Van der Vleuten CP. Programmatic
The views expressed in this article are those of of feedback to residents after direct observation of
clinical skills. Med Educ 2012;46:201-15. assessment: From assessment of learning to assess
the authors and not necessarily those of their
16. Thomson J, Haesler E, Anderson K, Barnard A. What ment for learning. Med Teach 2011;33:478-85.
respective employers. Southern GP Training is
motivates general practitioners to teach. Clin Teach
undertaking a research project ‘Ad hoc supervisory 2014;11:124-30.
encounters between GP-supervisors and 17. Wearne S, Dornan T, Teunissen PW, Skinner T.
GP-registrars: Enhancing quality and effectiveness.’ General practitioners as supervisors in postgraduate
This was funded by a GPET Education Integration clinical education: an integrative review. Med Educ
research grant. 2012;46:1161-73.
18. Reitz R, Simmons PD, Runyan C, Hodgson J, Carter
Provenance and peer review: Not commissioned, Henry S. Multiple role relationships in healthcare
externally peer reviewed. education. Fam Syst Health 2013;31:96-107.
19. Schuwirth LW, van der Vleuten CP. General overview
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tence lead to inflated self-assessments. J Pers Soc Health Sci Educ theory Pract 2014;19:43-51.
Psychol 1999;77:1121-34. 28. Regehr G, MacRae H, Reznick RK, Szalay D.
8. Newble DI, Jaeger K. The effect of assessments and Comparing the psychometric properties of checklists
examinations on the learning of medical students. and global rating scales for assessing performance
Med Educ 1983;17:165-71. on an OSCE-format examination. Acad Med
9. Munro N, Hornung R, McAleer S. What are the key 1998;73:993-97.
attributes of a good general practice trainer: a Delphi 29. Hall KH. Reviewing intuitive decision-making and
study. Educ Gen Pract 1998;9:263-70. uncertainty: the implications for medical education.
10. Boendermaker PM, Conradi MH, Schuling J, Med Educ 2002;36:216-24.
Meyboom-de Jong B, Zwierstra RP, Metz JC. Core 30. Rethans JJ, Norcini JJ, Baron-Maldonado M, et
characteristics of the competent general practice al. The relationship between competence and
trainer, a Delphi study. Adv Health Sci Educ Theory performance: implications for assessing practice
Pract 2003;8:111-16. performance. Med Educ 2002;36:901-09.
11. Wearne S, Giles S, Hope A. Barriers and enablers 31. Stolper E, van de Wiel M, van Royen P, van
for implementing general practice training. Aust Fam Bokhoven M, van der Wiejden T, Dinant G. Gut
Physician 2004;33:182-84. feelings as a third track in general practition
12. Watling C, Driessen E, van der Vleuten CPM, Lingard ers’ diagnostic reasoning. J Gen Intern Med
L. Learning from clinical work: the roles of learn 2011;26:197-203.
ing cues and credibility judgements. Med Educ 32. Dhaliwal G. Going with your gut. J Gen Intern Med
2012;46:192-200. 2011;26:107-09. correspondence afp@racgp.org.au
PROFESSIONAL
Guidelines and systematic reviews:

Sizing up guidelines in general practice
Mieke L van Driel, Geoffrey Spurling
This article is the second in a series on general practice research in Australia. The series explores strategies to strengthen general practice
research and further develop the evidence base for primary care.
Case Guideline development Conflict of interest

Anne, 39 years of age, presents with The first step in assessing the quality Transparency of the development process
signs and symptoms of moderately severe of a guideline is to understand how it is is not the only factor that determines how
depression. Her depression has been developed. Increasingly, guidelines include confident we can be about guidelines.
building on the background of difficulties information on their development process. One of the most important threats to
at work, a poor relationship with her In Australia, the National Health and Medical the reliability of evidence is conflict
daughter, and the deteriorating health of Research Council (NHMRC) has published of interest. Much of the evidence we
her parents. She has not been treated for guidance for developing, implementing rely on, especially in the therapeutic
depression in the past, and is not keen and evaluating the effectiveness of clinical domain, is generated by pharmaceutical
on seeing a counsellor. Anne’s friend practice guidelines.6 The international companies who develop and test their
suggested she asks for an antidepressant. ‘Appraisal of Guidelines for Research products. Pharmaceutical companies
In order to ensure you are up to date and Evaluation’ (AGREE) instrument is used recover the investments for discovery
with the latest guidance, you turn to to ‘score’ how individual guidelines adhere to and development by selling successful
evidence-based sources at hand. a transparent process (www.agreetrust.org). products. Therefore, demonstrating
These organisations emphasise that success and strong relationships with their
Guidelines are an inseparable part of recommendations should be based on customers (ie prescribers) are essential.
the general practitioner (GP) toolkit and systematic searches of the literature and
in Australia we have several to choose rigorous assessment of the quality of
from. For example, The Royal Australian evidence. Levels of evidence and an indicator
College of General Practitioners’ (RACGP’s) of the strength of recommendations tell
Guidelines for preventive activities in clinicians how robust the evidence is. The
general practice (Red Book) provides levels of evidence refer to a ‘hierarchy’ (Figure
guidance on preventive care and how to 1), where reasoning based on mechanism of
screen for conditions, including depression.1 action or case reports are the least reliable,
Therapeutic Guidelines advises on the and systematic reviews of rigorous studies
best evidence-based treatments.2 These are the most reliable evidence.7
sources of guidance are based on the Turning evidence from clinical studies
best available evidence, translated into into recommendations for clinical practice
practical recommendations.1-3 The number is based on the judgement of the guideline
of Australian clinical practice guidelines has developers. The guideline developers may
skyrocketed over the past three decades. assign a strength to recommendations on the
Buchan et al4 identified nine times more basis of the Grading of Recommendations
guidelines in 2010 than in a 1993 review.5 Assessment, Development and Evaluation
Figure 1. Hierarchy of levels of evidence
Many clinical resources are also available (GRADE) standard (www.gradeworkinggroup .
Adapted from Murad MH, Asi N, Alsawas M,
electronically for subscribers (eg UpToDate, org). GRADE provides an overall assessment Alahdab F. New Evidence pyramid, BMJ Blogs, with
DynaMed, BestBETS), but how can you tell of the quality of the evidence and how it permission from BMJ Publishing Group Ltd
which guidance is reliable and relevant? compares to current best practice (Table 1).
438 reprinted from afp vol.46, no.6, june 2017

GUIDELINES AND SYSTEMATIC REVIEWS PROFESSIONAL
There is ample evidence that the investigating the same question to reach to women at risk of delivering prematurely.
relationship between clinicians and the opposing conclusions. Authors may have Before the results were combined in a
pharmaceutical industry changes doctors’ preconceived ideas of the outcome, which meta-analysis, individual studies found
prescribing,8,9 and may not be in the best may influence their decisions.18 Likewise, inconsistent results, throwing doubt on the
interest of public health and safety.10,11 guideline developers use their expertise to intervention. Unfortunately, many years
Transparency about the provenance of weigh evidence and interpret the findings. passed before this new knowledge became
research findings and authors’ industry They decide what and how to include the routine practice.
links has improved over the past decade. available evidence. Guidelines developed Since the 1990s, systematic reviews
Most journals and conference organisers by different teams may therefore produce have established their position as the
now require authors to disclose any different recommendations.19 highest level of evidence and central role in
potential or perceived conflicts of interest, clinical practice guidelines. The most recent
including links with the pharmaceutical Systematic reviews meta-analysis of antidepressant medication
industry. Similarly, the independence of The ‘evidence hierarchy’ illustrates the found no significant difference in efficacy
guideline developers has been scrutinised.12 importance of systematic reviews in between antidepressants.21 If you decide to
However, reporting of guideline authors’ guideline development. Systematic reviews offer Anne an antidepressant, therapeutic
conflicts of interest is still poor.13,14 In collate all empirical evidence that fits guidelines recommend choosing one on the
the current climate of diminishing public pre-specified eligibility criteria to answer a basis of the adverse effects profile.
funding for independent research, the issue specific question.20 The key elements are a
of entanglement of conflicts is likely to systematic approach, and transparent and Relevance to primary care
become even more prominent. reproducible methods. The ‘ecology’ of general practice is unique,
The Cochrane Library includes more than with a low prevalence of serious illness,
Bias 7000 systematic reviews (www.cochrane. high prevalence of multimorbidity, and
‘Publication bias’, the preference to org/about-us) that are mostly focused on multiple interactions with social and
publish studies with a ‘positive’ result in the effectiveness of interventions, but environmental factors. The evidence
favour of a new product over ‘negative’ diagnostic reviews and evaluations of supporting best practice, therefore, should
trials that show no difference, is another healthcare interventions are being added. reflect this complexity. Is that the case?
risk to evidence. Publication bias is Cochrane was founded following Archie A review of 45 UK guidelines found
common and its potential harms are Cochrane’s call for the more efficient use that many of these recommendations
well documented. For example, thinking of evidence that was not used because were based on studies with little or no
about Anne, publication bias has been a studies were not visible or too small to relevance to primary care.22 Reliance on
particular issue for antidepressants. One reach statistical significance. Pooling smaller research from secondary care may also
analysis of 74 registered antidepressant studies into a meta-analysis (the numerical ignore interventions and approaches used
studies found that 31% of these studies outcome of a systematic review) overcomes successfully in primary care. For instance,
were not published. Moreover, 91% of the issue of statistical power. One of the in an analysis of depression guidelines,
the published studies showed positive first examples of how systematic reviews associated social risk factors were often
results for antidepressant efficacy when can influence clinical practice is embodied not mentioned, with limited attention to
compared with 51% of the unpublished in the Cochrane logo, demonstrating the psychological treatments.23 Problems of
studies.15 Perhaps the published evidence benefit to neonates of giving corticosteroids guideline relevance for GPs are exacerbated
is not the best guide to antidepressant
efficacy (www.alltrials.net). A recent
Cochrane review found that studies Table 1. The GRADE domains of quality assessment
funded by pharmaceutical companies were
Quality level Definition
more likely to report a result favouring
High We are very confident that the true effect lies close to the estimate of the effect
the company’s product than research not
funded by pharmaceutical companies.16 We are moderately confident in the effect estimate; it is possible that the true
Moderate
Publication bias is also a limitation effect is substantially different
of systematic reviews that underpin Our confidence in the effect estimate is limited; the true effect may be
Low
recommendations in guidelines. One substantially different
would hope that authors of reviews We have very little confidence in the effect estimate; the true effect is likely to be
Very low
present and interpret their findings as substantially different
objectively as possible.17 However, it
Reproduced with permission from Schunemann H, Brozek J, Guyatt G, Oxman A. GRADE handbook 2013.
is not uncommon for different reviews
reprinted from afp vol.46, no.6, june 2017 439

PROFESSIONAL GUIDELINES AND SYSTEMATIC REVIEWS
9. Wazana A. Physicians and the pharmaceutical

Box 1. Tips for guideline users: How reliable and relevant is this guideline? industry: Is a gift ever just a gift? JAMA
2000;283(3):373-80.
Reliability
10. Every-Palmer S, Howick J. How evidence
• Who published the guideline? based medicine is failing due to biased trials
and selective publication. J Eval Clin Pract
• Is the development process transparent?
2014;20(6):908-14.
• What do we know about the publisher’s and authors’ conflicts of interest? 11. Spurling GK, Mansfield PR, Montgomery BD,
et al. Information from pharmaceutical companies
• Has an evidence grading system been used?
and the quality, quantity, and cost of physicians’
Relevance for general practice prescribing: A systematic review. PLoS Medicine
2010;7(10):e1000352.
• Have general practitioners been involved in development of the guideline? 12. Scott IA, Guyatt GH. Clinical practice guidelines:
• Has evidence from general practice been incorporated? the need for greater transparency in formulating
recommendations. Med J Aust 2011;195(1):29-33.
• Is applicability to general practice discussed?
13. Norris SL, Holmer HK, Ogden LA, Burda BU.
Conflict of interest in clinical practice guideline
development: A systematic review. PloS One
2011;6(10):e25153.
by the lack of sufficient research conducted in summarising and synthesising evidence
14. Williams MJ, Kevat DA, Loff B. Conflict of interest
in general practice. Although Australian to ensure better relevance of guidelines and guidelines for clinical guidelines. Med J Aust
general practice research has grown better outcomes for patients. 2011;195(8):442-45.
15. Turner EH, Matthews AM, Linardatos E, Tell
significantly over the past two decades,
RA, Rosenthal R. Selective publication of
recent defunding of programs supporting Authors
antidepressant trials and its influence on apparent
Mieke L van Driel, MD, DipTropMed, MSc, PhD, efficacy. N Engl J Med 2008;358(3):252-60.
primary-care based research is feared to
FRACGP, Professor of General Practice and 16. Lundh A, Lexchin J, Mintzes B, Schroll
reduce research productivity.24 Head Primary Care Clinical Unit and Discipline JB, Bero L. Industry sponsorship and research
of General Practice, Primary Care Clinical Unit, outcome. Cochrane Database Syst Rev
Faculty of Medicine, University of Queensland, Qld.
Guideline implementation m.vandriel@uq.edu.au
2017;2:MR000033.
17. PRISMA Transparent Reporting of Systematic
Australian GPs have access to guidelines Geoffrey Spurling, MBBS, MPH, FRACGP, Senior Reviews and Meta-Analyses. Website. Oxford:
Lecturer, Primary Care Clinical Unit, Faculty of PRISMA, 2016. Available at www.prisma-
that build recommendations on the best
Medicine, University of Queensland, Qld. statement.org [Accessed 31 January 2017].
available evidence, while acknowledging 18. Goodyear-Smith FA, van Driel ML, Arroll B, Del
their shortcomings. Guidelines have Mar C. Analysis of decisions made in meta
Provenance and peer review: Commissioned,
analyses of depression screening and the risk of
improved patient care,25 but there is room externally peer reviewed.
confirmation bias: A case study. BMC Med Res
for improvement. Addressing the issues of Methodol 2012;12:76.
transparency, conflict entanglement and References 19. Matthys J, De Meyere M, van Driel ML, De Sutter
1. The Royal Australian College of General A. Differences among international pharyngitis
relevance of research to general practice is guidelines: Not just academic. Ann Fam Med
Practitioners. Guidelines for preventive activities
imperative. in general practice. 9th edn. East Melbourne, Vic: 2007;5(5):436-43.
What this means for guideline users is that RACGP, 2016. 20. Higgins JPT, Green S. Cochrane handbook for
2. Therapeutic Guidelines. How therapeutic guidelines systematic reviews of interventions. London: The
a critical attitude, and high levels of scrutiny are produced. Melbourne: Therapeutic Guidelines, Cochrane Collaboration, 2011. Available at http://
of the evidence and our own preconceptions 2016. Available at www.tg.org.au/how-therapeutic- handbook.cochrane.org [Accessed 31 January 2017].
guidelines-are-produced [Accessed 31 January 21. Gartlehner G, Hansen RA, Morgan LC, et al.
remain crucial. Creating a ‘repository’ of
2017]. Comparative benefits and harms of second-
reliable and relevant resources, such as the 3. Harris MF, Bailey L, Snowdon T, et al. Developing generation antidepressants for treating major
National Guideline Clearinghouse in the US the guidelines for preventive care -Two depressive disorder: An updated meta-analysis.
decades of experience. Aust Fam Physician Ann Intern Med 2011;155(11):772-85.
(www.guideline.gov), will make it easier 2010;39(1-2):63-65. 22. Steel N, Abdelhamid A, Stokes T, et al. A review of
to access guidelines. Transparency of the 4. Buchan HA, Currie KC, Lourey EJ, Duggan GR. clinical practice guidelines found that they were
Australian clinical practice guidelines - A national often based on evidence of uncertain relevance
provenance of guidelines can help protect
study. Med J Aust 2010;192(9):490-94. to primary care patients. J Clin Epidemiol
us and our patients from harm driven by 5. Ward JE, Grieco V. Why we need guidelines for 2014;67(11):1251-57.
commercial interests (Box 1). Improving the guidelines: A study of the quality of clinical practice 23. Hegarty K, Gunn J, Blashki G, Griffiths F, Dowell
guidelines in Australia. Med J Aust 1996;165:574-76. T, Kendrick T. How could depression guidelines be
relevance of evidence for GPs requires a made more relevant and applicable to primary care?
6. National Health and Medical Research Council. A
concerted effort to increase the number of guide to the development, implementation and A quantitative and qualitative review of national
evaluation of clinical practice guidelines. Canberra: guidelines. Br J Gen Pract 2009;59(562):e149-56.
studies conducted in primary care.24
NHMRC, 1999. 24. Winzenberg TM, Gill GF. Prioritising general
We need evidence about all aspects of 7. Oxford Levels of Evidence Working Group. Levels of practice research. Med J Aust 2016;205(11):529.
healthcare, including prevention, diagnosis, evidence. Oxford: Oxford Centre for Evidence-Based 25. Lugtenberg M, Burgers JS, Westert GP. Effects
Medicine, 2011. Available at www.cebm.net/wp- of evidence-based clinical practice guidelines on
treatment, health services delivery
content/uploads/2014/06/CEBM-Levels-of-Evidence- quality of care: A systematic review. Qual Saf
and policies. All stakeholders, including 2.1.pdf [Accessed 31 January 2017]. Health Care 2009;18(5):385-92.
patients, clinicians, administrators and 8. Lieb K, Scheurich A. Contact between doctors and
the pharmaceutical industry, their perceptions,
policymakers, must be part of this process. and the effects on prescribing habits. PLoS One
In addition, more GPs need to be involved 2014;9(10):e110130. correspondence afp@racgp.org.au

RESEARCH
Growing and retaining general practice

research leaders in Australia: How can
we do better?
Mieke van Driel, Laura Deckx, Georga Cooke, Marie Pirotta, Gerard F Gill, Tania Winzenberg
Background and objective eneral practitioners (GPs) provide the vast majority of
The aim of this study was to explore the experiences of

Australian general practitioners (GPs) with a Doctor of
Philosophy (PhD) about their choice to abandon or pursue
G medical care,1 yet the majority of medical research is based
in hospitals. Evidence generated in the hospital setting
is often not directly applicable to primary care because patients
seen in hospitals usually present with more advanced and ‘pre
an academic career.
selected’ conditions.2 As a result, treatment benefits may not
be transferable to low-risk populations in primary care.3 Dealing
Method
with primary care populations requires a different approach and
A qualitative study of 18 GPs (PhD obtained between 2006 and an evidence base that takes into account the uncertainty of a
2016) was conducted. Semi-structured telephone interviews low-risk environment and the complexity of comorbidity and
were transcribed and analysed using concurrent thematic polypharmacy.
analysis. Therefore, evidence generated in general practice is
important; GPs’ research expertise is as contextually critical
Results to primary care research as an academic oncologist is to
cancer research.4 Unfortunately, building a general practice
General practice researchers faced insecure career pathways.
research workforce has been a challenge internationally as
They often work in isolation, there is a lack of critical mass, and
well as in Australia.5-9 This situation has been exacerbated by
research was often described as a hobby (ie unfunded, done
from home). Solutions included expanding academic general the recent defunding of several Australian general practice
practice registrar positions to include advanced research research capacity-building initiatives.3 The aim of this study
training, building professional networks, mentoring, and better was to describe the research career experiences of GPs within
marketing of general practice research. 10 years of achieving their Doctor of Philosophy (PhD) to address
the question of how we can grow and retain general practice
Discussion research leaders in an increasingly tight funding climate.
Focused investment in developing clear and sustainable career Methods

pathways is essential to nurture and retain general practice
This qualitative study used semi-structured interviews with GPs
researchers and research leaders. The research culture and
who obtained a PhD between 2006 and 2016. Semi-structured
professional standing of general practice researchers also need
interviews were chosen because this method is well suited
to improve. Support from professional bodies and colleagues,
and enabling research collaborations, are key. for an exploratory study focused on elucidating participants’
experiences and points of view.10
A list of potential participants was created by one author
(GFG) using publicly available data.11,12 Additional participants
were identified through a snowballing technique (ie participants
were asked if they knew any other GP researchers who would
be eligible to participate).13
© The Royal Australian College of General Practitioners 2017 reprinted from afp vol.46, no.10, october 2017 757
RESEARCH GROWING AND RETAINING GENERAL PRACTICE RESEARCH LEADERS
An invitation to participate was sent (14/18). Three participants were full-time intellectually) was seen as a barrier to
by email to a purposefully selected GPs and their involvement in research was continuing a research career. The difficulty
subsample. We selected a diverse sample unpaid. One participant was a full-time of maintaining a good work-life balance
of GPs with different levels of involvement academic who was not clinically active. was also a recurrent theme (subtheme E).
in academia and academic positions, The level of experience was diverse;
aiming to include participants who had participants included research fellows Theme 2. Specific challenges
ceased and those who had continued (2/18), (senior) lecturers (6/18), associate specific for general practice
research activity. We also strove to include professors (2/18), professors (6/18), and research
equal numbers of men and women, honorary research fellows (2/18). Three Challenges specific to general practice
and participants from all states and main themes were identified from the research related to such research being
territories. Participants were interviewed interviews: conducted on a small scale, unfunded
by telephone or face to face. A single 1. General challenges of research as a and informal - somewhat like a ‘cottage
researcher (LD) conducted the interviews, career path industry’ (Table 1 - Theme 2). Academic
following a semi-structured interview 2. Specific challenges of general practice general practice departments are generally
guide (Appendix 1; available online only).14 research small, and general practice encompasses
Interviews were digitally recorded 3. Facilitators of career progression. many fields. As a result, the overlap in
and transcribed verbatim. Interview data Subthemes falling under these major research interests between department
were analysed using inductive thematic themes and supporting quotes are staff is limited, so general practice
analysis.15,16Two researchers (LD, GC) provided in Table 1 (Theme 1 - subthemes researchers often work alone (subtheme
independently coded all interviews line A-F); Theme 2 - subthemes G-O) and G). This lack of a critical mass was thought
by line. They compared, discussed and Table 2 (Theme 3 - subthemes A-G). to be a barrier to collaborations with
adjusted the themes that emerged from other researchers, limiting the ability to
the first six interviews. The remaining Theme 1. General challenges of build and maintain a team of experienced
interviews were separately coded against research as a career path researchers.
the agreed set of themes and adjusted Overall, most participants were passionate Participants perceived much research
if necessary. Subsequently, LD and GC about research, as they found it rewarding to be more of a ‘hobby’, unfunded
discussed all themes until consensus was and valued the flexibility of an academic and done from home (subtheme H).
reached. The final thematic framework job. However, not all participants would Participants also pointed to the lack
was verified by all authors. Interviews recommend a research career to a of a long-established research culture
continued until data saturation was younger colleague. Some participants in general practice (subtheme I). They
achieved, which we considered to be perceived that they could have advanced note that general practice research has
when no new major themes emerged more quickly in their academic career less ‘standing’ in universities and the
from additional interviews.17 if they had done things differently professional community (subthemes J
The Human Research Ethics Committee (subtheme A) - for example, by being and K).
of the University of Queensland more ambitious, moving to another GPs often start their research career later
approved this study (reference number: institution, prioritising research over clinical in life, limiting the time they have to build
2015001131). Participation was voluntary work and family (Table 1 - Theme 1). a track record and become competitive
and each participant signed an informed Job insecurity (subtheme B) was an as academics (subtheme F). The issue
consent form. important impediment to an academic of track record is further complicated by
career. Even senior general practice the focus of universities on citations and
Results academics did not have tenure and journal impact factors as a determinant
Of 74 GPs who completed a PhD, 35 were would have to leave academia if grant for career progression. General practice
invited to participate. Eighteen GPs agreed funds were no longer available. Similarly, journals do not have high impact factors
to participate and were interviewed the amount of time spent on teaching and, therefore, general practice research
between April and May 2016 (two face-to- and administration was considered seems - in academia - not prestigious.
face interviews; 16 telephone interviews; demotivating as it left little room for In addition, general practice researchers
mean duration: 26 minutes). The mean research (subtheme C). aim to publish in highly regarded,
age of the participants was 50 years For many participants, the first few often international, journals. As these
(standard deviation [SD] = 8.23) and eight years after finishing a PhD, when the journals may not be read by Australian
were women. The majority of participants transition to academia occurred, were GPs, the general practice community
had official (paid) academic roles (15/18), challenging (Subtheme D). Lack of support in Australia may not be aware of the
and combined academic and clinical work for early career researchers (ie financially, research produced by their colleagues.
758 reprinted from afp vol.46, no.10, october 2017 © The Royal Australian College of General Practitioners 2017
GROWING AND RETAINING GENERAL PRACTICE RESEARCH LEADERS RESEARCH
Table 1. Challenges to a career in general practice research

Theme Quotes
Theme 1. General challenges of research as a career path
A. Moving GP6: ‘So the question is, are you prepared to move ... because the smaller regional universities are going to have a number of
institutions vacancies coming up soon and so you have to ask yourself, is that where I want to be and so you need to see if your family is
prepared to accept that or not.’
GP9: ‘I think I could have done it faster if I was prepared to shift institutions. There’s this difficulty with staying within one place
that people, I think, take a little bit for granted and it makes it a little difficult to progress a bit more rapidly.’
B. Job insecurity GP9: ‘I do not have a permanent position although I am so highly qualified and experienced ... and yet I cannot get a real job, it
is frustrating. I think one of the wasteful things is that people invest millions of dollars into training someone like myself ... and for
the sake of you know one year of funding. In three years’ time, I might leave the profession and that is crazy.’
C. Administrative GP8: ‘While I was doing my PhD, I recognised that the bulk of their job was not remotely attractive to me ... a lot of it was
burden teaching and I like teaching students, I really enjoy that, but I do not aspire to be someone who has to do all the bureaucratic
stuff around teaching.’
D. Transition to GP7: ‘I think it is because I am still very junior ... it is hard to get your name on a grant because you are not famous enough in
academia your area ... for an early-career person to be competing with professors of general practice who have already been published in
the BMJ.’
E. Work-life balance GP14: ‘I am not really keen to work all day, all night. The full-time academics that I see in senior positions do not get a lot of sleep.’
F. Stage of life GP14: ‘I think I may be more interested in academic work when the kids are a bit older.’
Theme 2. Specific challenges of general practice research
G. Working in GP17: ‘I’m not very well supported in the kind of project that I’m trying to do, so I kind of feel like I’m doing it all on my own .
isolation I thought I was going to have people working with me, it was going to be a team kind of thing . it has not worked out like that
and that has also been very off-putting for me and very frustrating.’
H. Research as a GP14: ‘If I’m going to have a research career over the next fve years, a lot of that is just going to be on my own time, at my own
hobby expense. I will be sitting writing papers in my days off . rather than actually funded in the position.’
I. No GP research GP7: ‘When I went into general practice training, I did not really know it was an option. We do not have [research] culture around
culture general practice . in broadsheet GP newspapers like Australian Doctor . where instead of actually embracing research, a lot
of people put it down, so I think that there is some work to be done on the culture of our profession.’
J. No professional GP9: ‘The fact that general practice journals do not rate highly in terms of stature compared to the other specialty journals. So
standing in when we come to look at our track record . we often have to mount an argument that our journals are aimed at clinicians, not at
research other researchers. Clinicians do not cite our work very often, we have to deliver impact in other ways, not through journal citations.’
community GP 6: 'The universities are not that interested in us because we don’t produce Nobel Prizes, we don’t produce patented drugs
or diagnostic testing and we are not seen as being that important, but intriguingly ... about 70% of the years of health-adjusted
life expectancy gained from the decline in cardiovascular disease, has been driven by the care provided in general practice.'
K. No professional GP17: ‘Other GPs . There is that tendency to see people who work in academia as being separate ... and lacking hands-on
standing in GP experience ... They did not see the kind of things I would have learnt in my academic work as being of any value to my clinical
community work ... it was more seen as a potential hindrance.’
L. No added value GP13: ‘There is no advantage to you by and large for a career in general practice in having a research qualifcation ... whereas, if
of doing a PhD I was a cardiologist or a neurologist or a surgeon, then a PhD or a MD or a string of publications would be extremely useful to me
for GP because that would increase my chances of being employed at a prestigious hospital or having a position in a teaching hospital.’
M. Juggling multiple GP5: ‘Many of the opportunities for primary care researchers actually require some ongoing clinical connection. It would be
careers very easy to lose touch with what is happening in clinical practice.’
GP8: ‘I think the two should go hand in hand. I should not really be telling other GPs how to live and work unless I am doing
it myself.’
GP17: 'I think it is less likely now [pursuing an academic career]. I am really interested in research, but it is really hard for
me to balance the clinical work and the academic work.'
N. Funding GP9: ‘You might have a general practice musculoskeletal project that goes to a panel [that] is 50% diabetes researchers and
50% rheumatologists, and they do not get the more pragmatic nature of a lot of GP research compared to conventional RCTs
and so forth.’
O. Remuneration GP7: ‘The money does matter at the end of the day.’
GP5: ‘The payment for research is at a much lower rate than the earning rate of a GP working in practice, so if you get
accustomed to one income level ... you have to accept a much lower income level if you are going to be involved in research.’
Table 2. Theme 3: Facilitators of career progression
Theme Quotes
A. Mentorship GP14: ‘In fact, probably the only reason I’ve continued this far has been through mentorship from senior academics.’
GP7: ‘I am lucky that people in my department are actively looking for opportunities for me ... they want to help me to
succeed and I think that is very important as well.’
B. Alliances and GP7: ‘Keep on developing collaborations with key people in the area so that I could maximise the chances of getting
collaborations funding for the areas that I really want to work in.’
GP3: ‘I have been lucky to work with good people and have good collaborators and to have good collaborators is
usually important.’
C. Leadership training GP11: ‘Apart from being [in] the Brisbane Initiative, which is meant to have a leadership element, I’ve never really sought
and support out leadership development courses or mentoring or it’s not been my sort of personality I suppose ... I can see that if you
were more proactive, you’d end up being more productive. I can see that people around me who pursue leadership skills
and strategies and they are more proactive in really trying to lead a group and build collaborations and they are sort of more
energetic on that front where I’m a bit more, you know let things grow naturally. I can see that if you were the former, the
outcomes in terms of building the group would be stronger but it is not my style, I don’t regret it. I am who I am.’
GP2: ‘The College [RACGP] can certainly do a lot of things to make sure that academic GPs are leaders of GPs in Australia
. it’s time that GPs and general practice as a profession start creating our own knowledge base [that] is not just derived
from what specialists think we ought to do but which is derived from our own research, our own data, our own experience
and that needs to be led by clinician GPs and I think the College of GPs really needs to take that into account and lead that.’
D. Better marketing GP5: ‘The best way to achieve that might be to showcase the GP-led research from around the country.’
of GP-led research GP7: ‘I don’t think there is enough to actively encourage people. You just can’t say everything is bad all the time. You have to
give some people a bit of hope otherwise why would they put themselves through all of that.’
GP9: ‘The RACGP Conference has lost a bit of its appeal for researchers to present there and, I mean, part of that might
be the competition from the Primary Health Care Conference and part I know was a conscious decision to ensure the key
membership, the grass roots GPs are engaged in that important activity, but you know if we can’t reach our GP clinical
colleagues through the RACGP’s Conference, it’s very hard for researchers to reach those people and link with those people.’
E. Combined GP13: ‘Seeing how a combined fellowship research qualification could be gained during that period of time [GP training] and
fellowship that is something that really, I think, is probably crucial to maintaining a critical mass of GP researchers . I like the idea of
trying to incorporate research training into your fellowship training and somehow combining that.’
F. Academic general GP8: ‘I know in Canada for example, there are ... academic general practices, they do research in the practices, they teach
practices in the practices and they see patients. I like the idea of working in a practice where I could be combining all of those things.’
GP2: ‘There is a new concept I think we need to come up with and that’s basically an academic health centre type concept,
so that’s where you combine clinical practice and research and teaching in one job, done in the same centre.’
G. Funding support GP8: ‘In the UK . GPs get paid the same basically to be a GP or to be an academic and that makes [being an] academic
far more realistic and attractive.’
GP6: ‘What we need is to give people early in their careers some financial support because otherwise you have to earn it in
general practice.’
This negatively affects the professional clinical work. However, most participants related to remuneration (subtheme O).
standing of general practice researchers mentioned that they try to combine clinical Most GPs acknowledged that they could
within the community. Importantly, and academic work so they do not lose earn more money as a full-time clinician
participants mentioned that there is little touch with clinical practice. than as an academic.
value for a GP in completing a PhD as Funding was universally mentioned
it does not benefit their clinical career by the participants as a major barrier Theme 3. Facilitators of career
progression (subtheme L). (subtheme N). Funding sources are often progression
Participants also mentioned having to disease-focused and favour biomedical The main two facilitators in pursuing a
juggle three different careers: clinician, research. Participants felt that grant research career were support from a good
researcher and teacher (subtheme M). For assessors did not seem to understand mentor or supervisor (subtheme A), and
some, this meant completely giving up general practice research well. Another collaborations with other researchers
their academic career; for others, giving up barrier to pursuing an academic career (subtheme B). Specific advice on how to
GROWING AND RETAINING GENERAL PRACTICE RESEARCH LEADERS RESEARCH
foster collaboration with other researchers on research output, further hampering targeted at building on successes from
included joining professional organisations career progression in academia. Positive previous capacity-building efforts. A small
and attending conferences. previous experiences and role models beginning to this was the recent call for an
Several solutions were offered to were important enablers for pursuing an ‘NHMRC Centre of Research Excellence in
improve the general practice research academic career. Primary Health Care’, but a much greater,
culture and professional standing What we have learned from the systematic commitment is needed.
(subthemes D and E). These included participants in this study is consistent Nonetheless, given the current
positions combining research and with previous research in the broader financial climate, how can we do better
general practice training, more advanced international and Australian primary in growing and retaining Australian
research training in the vocational training healthcare research setting.8,18,19 For general practice researchers? Our study
program (eg through combined PhD example, perceptions of a lack of suggests that feasible options should
and Fellowship), and better marketing of clear research career pathways was focus on mentorship, positive role
general practice research (eg increase demonstrated in a recent Australian models and improving the visibility of
the visibility of GP-led research through survey among primary healthcare general practice research. This is in line
relevant journals and organisations). researchers (including but not limited with recommendations from the UK,
With respect to university remuneration, to GPs). This survey showed that which suggest that the sustainability of
participants mentioned that GPs can the predominant reasons for primary primary healthcare researchers could be
apply for a clinical loading, which helps healthcare researchers leaving research enhanced by good mentorship, positive
to cover some of the drop in income were a lack of funding and positions, organisational cultures5 and exposure to
that GPs experience when they take and the requirements of a teaching or charismatic role models.7
up a research job. Others suggested clinical role limiting time for research.19 The Oxford Primary Care Research
the re-establishment of more financially Other surveys have found that lack of Leadership Program (‘Brisbane Initiative’)
attractive funding programs, or ensuring clear career paths and uncertainty in is an example of how leadership training,
remuneration is similar for university and employment were barriers to sustainable networking and mentoring can connect
clinical practice. research careers in primary care.8,18 primary care researchers worldwide and
Balancing different careers could be For academic GPs to gain protected advance individual careers,20 but that is
achieved by integrating clinical practice, research time that is not impinged upon not enough. There is a role for professional
research and teaching. International by teaching and administrative duties, the bodies such as The Royal Australian
examples of ‘academic general practices’ creation of academic career paths with College of General Practitioners (RACGP)
would be a welcome option in Australia a stronger research focus, supported and Australasian Association for Academic
(subtheme F). Support for writing grant by government investment, is required. Primary Care (AAAPC) to improve the
applications and making funds available Research funds appear maldistributed in visibility of general practice research. As
for pilot work were also mentioned as major research funding schemes (eg the the peak professional body of general
important enablers (subtheme G). National Health and Medical Research practice, the RACGP in particular must
Council [NHMRC]). Support for general continue to champion the importance of
Discussion practice researchers is very poor in these general practice research.
General practice researchers face many schemes in terms of project funds and This begins at the earliest career
challenges on their career paths. In this salary support. This is especially crucial stage through the RACGP’s Oath of
study, some identified barriers are universal given the importance of general practice Fellowship, in which new fellows commit
to research careers (eg job uncertainty). to the healthcare system, and potential for to ‘contribute, wherever possible, to the
However, some challenges were specific efficiencies in healthcare service delivery science of general practice’, and through
to general practice research. Examples that can be achieved through primary care RACGP publications and advocacy. In
include the lack of a research culture in research-driven innovation.3 addition, expanding and further integrating
general practice, low profile of primary care Active intervention is essential to research training into general practice
research and low impact factors of general prioritise investment into capacity building vocational training would generate a
practice journals. Research experience in general practice research - for example, more research-savvy and enabled clinical
seems to have no added value for career through a sustained commitment to workforce. Enhancing the evidence base
progression as a GP, and academic GPs funding research fellowships at all career of general practice requires engagement
earn significantly less than those in clinical levels, and replacing the withdrawn at all levels, from users of research to
practice. Combining a clinical commitment funding from the ‘Primary Health Care research leaders.21 Creating a combined
with academic work, even if there is a Research, Evaluation and Development’ GP-PhD and fellowship pathway could
shared part-time workload, has an impact (PHCRED) program with new activities be a strategy to expand the general
Georga Cooke MD, MSc, FRACGP, Honorary 9. Magin P, Pirotta M, Farrell E, Van Driel M.
practice research workforce. This has been
Research Fellow, Primary Care Clinical Unit, General practice research - Training and capacity
particularly successful in The Netherlands Faculty of Medicine, University of Queensland, building. Aust Fam Physician 2010;39(5):265-66.
and the UK. Not surprisingly, these Brisbane, Qld 10. Hansen E. Successful qualitative health
Marie Pirotta MD, MSc, PhD, FRACGP, Associate research: A practical introduction. Crows Nest,
countries are among the best performers NSW: Allen & Unwin, 2006.
Professor, Department of General Practice,
in primary care research output.22 University of Melbourne, Melbourne, Vic 11. Gill GF. Australian general practitioner doctorates
This study has some limitations. We Gerard F Gill RFD, PhD, FRACGP, FARGP, Clinical and doctoral candidates, 2005-2009. Med J Aust
Professor in General Practice, School of Medicine, 2012;196(3):173.
interviewed a small sample of GPs with 12. Gill GF. Successful Australian GP doctorate
Deakin University, Geelong, Vic
a PhD, and not all of those who were Tania Winzenberg MBBS, FRACGP, MMedSc
candidates 2010-2014. GP15; Melbourne, 2015.
invited participated in the study. However, (ClinEpi), PhD, Professor of Chronic Disease 13. Lewis-Beck M, Bryman A, Futing Liao T. The
Management, Menzies Institute for Medical SAGE encyclopedia of social science research
our purposive sampling approach across methods. Thousand Oaks, Calif: SAGE, 2004.
Research and Faculty of Health, University of
a wide range of GPs means that we are Tasmania, Hobart, Tas 14. Kelly S. Qualitative interviewing techniques and
styles. In: The SAGE handbook of qualitative
likely to have captured a range of different Competing interests: Mieke van Driel, Georga
methods in health research. London: SAGE,
Cooke, Marie Pirotta, Gerard F Gill and Tania
experiences. Further supporting the 2010; p. 307-26.
Winzenberg have been members of the RACGP
validity of our results is the observation National Standing Committee - Research. Marie 15. Braun V, Clarke V. Using thematic analysis in
Pirotta was chair of the committee from 2008 psychology. Qual Res Psychol 2006;3(2):77-101.
that the same themes were recurring, 16. Thomas DR. A general inductive approach for
to 2014. Tania Winzenberg is the current chair
and that our findings are in line with other of the RACGP Expert Committee - Research analyzing qualitative evaluation data. Am J Eval
(previously known as National Standing Committee 2006;27(2):237-46.
studies in primary healthcare research.8,18,19
- Research). Gerard F Gill has been a member 17. Fusch PI, Ness LR. Are we there yet? Data
Unfortunately, the views of those not of the RACGP Council (2002) and the Australian saturation in qualitative research. Qual Rep
currently involved in research are not Medical Association Council of General Practice 2015;20(9):1408-16.
(1991). All authors are members of the Australasian 18. Calitri R, Adams A, Atherton H, Reeve J, Hill NR.
represented, despite actively attempting
Association for Academic Primary Care. Tania Investigating the sustainability of careers in
to recruit such participants. Therefore, the Winzenberg has at various points in her career academic primary care: A UK survey. BMC Fam
reasons for GPs completely abandoning been supported by the PHCRED program. Pract 2014;15:205.
Provenance and peer review: Not commissioned, 19. Oliver-Baxter J, Brown L, McIntyre E. Surviving
research activity remain unknown. GPs or thriving in the primary health care research
externally peer reviewed.
were interviewed immediately after the workforce: The Australian experience. Aust J
Acknowledgements Prim Health 2016;23(2):183-88.
announcement of the official defunding
20. Magin PJ, Furler JS, van Driel ML. The Brisbane
of the Bettering the Evaluation and Care The researchers gratefully acknowledge the RACGP
International Initiative: Fostering leadership
Foundation for its support of this project. While
of Health (BEACH) program.23 The impact and international collaboration in primary care
the researchers received a grant from the RACGP
research. Med J Aust 2008;189(2):100-02.
of this could have influenced participants’ Foundation, the researchers had complete authority
over the design, execution and interpretation of the 21. Del Mar C. Publishing research in Australian
interview responses. Our qualitative study. The authors would also like to thank all GPs Family Physician. Aust Fam Physician
findings point to a broad range of issues who participated in this study. 2001;30(11):1094-95.
22. Glanville J, Kendrick T, McNally R, Campbell J,
and their importance could be further Hobbs FD. Research output on primary care in
References
explored in subsequent studies. Australia, Canada, Germany, the Netherlands,
1. Australian Institute of Health and Welfare. the United Kingdom, and the United States:
Australia's health 2016. Canberra: AIHW, 2016. Bibliometric analysis. BMJ 2011;342:d1028.
Implications for general Available at www.aihw.gov.au/WorkArea/
23. Primary Health Care Research & Information
practice DownloadAsset.aspx?id=60129555788
Service. Closure of BEACH program after
[Accessed 3 September 2017].
18 years. NSW: Family Medicine Research
To nurture and retain general practice 2. Rosser WW. Application of evidence from Centre, University of Sydney, 14 April 2016.
researchers and research leaders, focused randomised controlled trials to general practice. Available at www.phcris.org.au/news/in-the-
Lancet 1999;353(9153):661-64. media/item.php?id=16984&spindex=5&
investment in developing clear and 3. Winzenberg TM, Gill GF. Prioritising general promoid=833&mid=39&stype= twiphc&linkid=
sustainable career pathways is essential. practice research. Med J Aust 2016;205(2):55-57 516984 [Accessed 10 August 2017].
4. Hobbs FR, Taylor CJ. Academic primary
In addition, the research culture of general
care: At a tipping point? Br J Gen Pract
practice and the professional standing 2014;64(622):214-15.
of general practice researchers need 5. Adams A, Lester H, Reeve J, Roberts J,
Wilson A. Investigating the sustainability
improvement. Support from professional
of careers in academic primary care in the
bodies and colleagues and efforts to United Kingdom. Prim Health Care Res Dev
2014;15(3):331-35.
enable research collaborations are key.
6. Gray DP. Academic general practice: A viewpoint
on achievements and challenges. Br J Gen Pract
Authors 2015;65(640):e786-88.
Mieke van Driel MD, MSc, PhD, FRACGP, Professor 7. Campbell J, Hobbs FD, Irish B, et al. UK
and Head, Primary Care Clinical Unit, Faculty of academic general practice and primary care.
Medicine, University of Queensland, Brisbane, Qld. BMJ 2015;351:h4164.
m.vandriel@uq.edu.au 8. Barton C, Reeve J, Adams A, McIntyre E.
Laura Deckx MSc, PhD, Postdoctoral Research Australian academic primary health-care
Fellow, Primary Care Clinical Unit, Faculty of careers: A scoping survey. Aust J Prim Health
Medicine, University of Queensland, Brisbane, Qld 2016;22(2):167-73. correspondence afp@racgp.org.au
CLINICAL
Early detection of eating disorders in

general practice
Elizabeth Rowe
Background ating disorders are complex, these modifications broaden the criteria
General practitioners (GPs) are often

the first health professional consulted
in regard to eating disorders and
their varied presentations. Given the
E potentially life-threatening conditions
characterised by significant
disturbances in eating behaviour that
result in serious medical, psychiatric
for specific eating disorders such as
anorexia nervosa and bulimia nervosa,
but also more precisely categorise the
previous diagnostic category of EDNOS.
and psychosocial consequences. Eating Patients who lose significant amounts
prognostic significance of early detection
disorders are formally classified on the of weight and meet the other diagnostic
of, and intervention for, such conditions,
basis of the Diagnostic and statistical criteria for anorexia nervosa, but who are
it is important that GPs feel confident to
manual of mental disorders, 5th edition not underweight, will now be diagnosed
do so.
(DSM-5) criteria (Table 1).1 with atypical anorexia nervosa.4
Objective DSM-5 classification and Magnitude of the problem
The aim of this article was to criteria The prevalence of eating disorders in
heighten awareness of the role of early The diagnostic criteria for anorexia nervosa Australia is conservatively estimated to
identification and diagnosis of eating and bulimia nervosa were updated in the be 9% of the adult population, and this
disorders, especially anorexia nervosa
DSM-5. Other eating disorders, including figure continues to increase.5 In fact,
and bulimia nervosa, in the primary
binge-eating disorder (BED), pica, a 2015 study of older adolescents and
care setting. The focus will be on their
rumination and avoidant/restrictive food adults found a point prevalence as high as
presentations and diagnosis, including
intake disorder (ARFID), have also been 16.3%, where BED accounted for 6.3%
changes to the Diagnostic and statistical
added in the DSM-5. In addition, atypical and subthreshold BED 7%. By contrast,
manual of mental disorders, 5th edition
presentations are now included under the anorexia nervosa and bulimia nervosa
(DSM-5), with a brief overview of
management recommendations and newly named categories of other specified each occurred in less than 1% of the
admission criteria. feeding or eating disorder (OSFED), and population.6
unspecified feeding or eating disorder In spite of the seemingly low prevalence
Discussion (UFED); these replace eating disorder not rate in the general population, anorexia
otherwise specified (EDNOS). nervosa and bulimia nervosa are of great
Eating disorders are complex, potentially Some of the significant revisions significance because of their incidence
life-threatening illnesses with significant are the removal of amenorrhoea as a in adolescent female patients and their
medical and psychosocial consequences.
diagnostic criterion for anorexia nervosa mortality rate.7 These conditions represent
Early detection and intervention can
in female patients, and reduction of binge the third most common chronic illness
significantly contribute to better outcomes,
frequency to an average of once per week (after asthma and obesity) in adolescent
and GPs are ideally placed to effect this.
for bulimia nervosa.2 The modifications female patients.7 In addition, anorexia
were anticipated to better represent the nervosa has the highest mortality rate of
symptoms and behaviours of patients all psychiatric disorders;8 long-term studies
dealing with these conditions, and enable report mortality rates of approximately
more specific eating disorder diagnoses, 20%.9 It has been noted that ‘compared
thereby facilitating initiation of appropriate with their peers without the illness, the
and timely management.2-4 In theory, risk of premature death is approximately
© The Royal Australian College of General Practitioners 2017 reprinted from afp vol.46, no.11, november 2017 833
CLINICAL EARLY DETECTION OF EATING DISORDERS
Table 1. Summary of DSM-5 diagnostic criteria for eating disorders
Anorexia nervosa Bulimia nervosa
a. Restriction of energy intake resulting in a significantly low body a. Recurrent episodes of binge eating (this involves eating an excessive
weight; or a less than minimally expected weight (based on age, sex amount of food in a discrete period of time AND a sense of lack of
or developed trajectory) control)
b. Intense fear of gaining weight; or persistent behaviour that interferes b. Recurrent inappropriate compensatory behaviours to prevent weight
with weight gain, despite low weight gain, such as vomiting, laxatives, diuretics, fasting or excessive
c. Disturbance in body image; or persistent lack of recognition of the exercise
seriousness of the current low body weight c. Frequency of at least once per week for three months
Subtypes: Restricting type, binge-eating/purging type d. Self-evaluation unduly influenced by body shape and weight
e. Absence of anorexia nervosa
Binge eating disorder Other specified feeding or eating disorder (OSFED)
a. Recurrent episodes of binge eating Eating disorders causing significant distress but not meeting criteria for
b. Associated with symptoms such as eating more rapidly, feeling other diagnostic categories
uncomfortably full, not feeling hungry, eating alone due to Examples:
embarrassment and/or feelings of self-disgust • Atypical anorexia nervosa - ‘normal weight anorexia nervosa’
c. Marked distress regarding binge eating • Bulimia nervosa (of low frequency and/or limited duration)
d. Frequency of at least once per week for three months • Subthreshold binge-eating disorder
e. Absence of compensatory behaviours, anorexia nervosa and bulimia • Purging disorder
nervosa • Night eating syndrome
Avoidant/restrictive food intake disorder (ARFID) Unspecified feeding or eating disorder (UFED)
a. Eating or feeding disturbance with persistent failure to meet nutritional Presentations in which clinically significant symptoms occur but do not
needs associated with either significant weight loss (or growth failure), meet full criteria for other eating disorders. Includes situations where the
significant nutritional deficiency, dependence on enteral/supplemental clinician chooses not to specify the reason criteria are not met or where
feeding or marked interference with psychosocial functioning this may be unknown (eg emergency room setting)
b. Not explained by lack of available food or culturally sanctioned
practice
c. Absence of anorexia nervosa, bulimia nervosa or body image
disturbance
d. No intercurrent medical illness
tenfold higher in a person with anorexia of most presentations. Given that early the adolescent brought in by a parent
nervosa’.10 intervention may limit the progression and who is concerned about their child’s
In addition, these illnesses represent improve outcomes of eating disorders, nutritional intake, behaviours surrounding
a significant socioeconomic cost to the early recognition is imperative.12-15 Hence, food and/or weight, should alert the GP
community. In 2012, Deloitte Access it is appropriate to commence medical to the possibility of an eating disorder
Economics estimated the figure to be management before a patient fulfils all with a more directed history and
$69.7 billion. Of this amount, the direct of the diagnostic criteria of a particular examination protocol.
healthcare cost is $99.9 million and the eating disorder,14 thereby limiting or However, far more challenging from
remainder is due to productivity loss reversing symptom progression and a detection and therefore diagnostic
and loss of healthy years of life.11 optimising prognosis. standpoint is a patient who presents with
seemingly ‘unrelated complaints’.15 These
Importance of early General practice complaints include psychological issues
identification consultation such as stress, depression or anxiety;
To limit the impact of these disorders GPs face a number of challenges in the physical complaints such as fatigue,
in terms of physical, psychiatric and early identification of patients with an dizziness, gastrointestinal problems
economic outcomes, it is essential that eating disorder;15,16 this is particularly (especially constipation and bloating)
general practitioners (GPs) are able to the case when the presentation does and, for female patients, menstrual
identify and initiate management in such not relate to dietary intake or weight. irregularities; chronic health problems
patients, as primary care is the context Conversely, the classic presentation of such as osteoporosis; and socioeconomic
834 reprinted from afp vol.46, no.11, november 2017 © The Royal Australian College of General Practitioners 2017
EARLY DETECTION OF EATING DISORDERS CLINICAL
consequences such as financial behaviours.14,19 However, other signs can empathic and non-judgemental manner,
insecurity due to inability to sustain be readily observed in the consultation it provides an ideal opportunity for
employment.17-19 or described by family members. The engagement with patients and a greater
Of course, the other impediment warning signs include psychological likelihood that they will accept the
to early identification is delayed manifestations, commonly anxiety; medical care they require.14,18 There are
presentation. Patient factors contributing behaviours such as avoiding meals; and only a few other medical conditions
to this include:15,20 physical issues that include menstrual where the therapeutic alliance between
• ambivalence about recovery irregularity or cessation in female patients. doctor and patient is so critical.19
• stigma and shame A detailed list of these features is shown A thorough history will also eliminate
• denial of, and failure to, perceive the in Table 2. many of the other potential differential
severity of the illness Hence, a detailed history is paramount diagnoses of weight loss or symptoms
• low motivation to change in the assessment process. When a (eg amenorrhoea in female patients). GPs’
• negative attitudes towards seeking help detailed history is performed in an failure to identify that certain symptoms
• lack of knowledge about available
resources
• practical issues (eg distance, cost). Table 2. Eating disorder warning signs1,2,7,14,18,24
There are a number of screening tools that Behavioural
can be used in the primary care setting
• Avoiding eating in public • Excessive use of the toilet
to assist in the detection and diagnosis
• Fussy eater/banned foods • Body checking
of eating disorders. The best known of
• Cooking for others yet not eating • Constant focus on food, diet and exercise
these is the SCOFF questionnaire, which
• Frequent weighing • Has different meals to rest of family
consists of five questions:21
• Excessive exercise • Social isolation
1. Do you make yourself Sick • Stressed when unable to exercise • Calorie counting
because you feel uncomfortably • Trains through injury • Use of diet pills, laxatives, supplements
full? • Restricted/rigid diet • Throws away food
2. Do you worry you have lost • Wears baggy clothing • Denies problem
Control over how much you eat? • Avoiding meals • Slow eating/picking at food
• Raiding the refrigerator • Developing ‘allergies’ to food
3. Have you recently lost more than
• Eating low-calorie foods • Eating in secret
One stone (6.35 kg) in a 3 month
period? Psychological
4. Do you believe yourself to be Fat
• Anxiety, especially in regards to food/ • Poor concentration
when others say you are too thin? eating • Perfectionism
5. Would you say that Food • Depression • Low self-esteem
dominates your life? • Social phobia/withdrawal • Guilt, especially around food
• Distorted body image • Obsessiveness
Each ‘yes’ answer scores one point and
• Negative body image • Subtle cognitive changes
a score of >2 indicates a likely diagnosis
• Feelings of lack of control • Hopelessness
of anorexia nervosa or bulimia nervosa.21
• Suicidality
However, the most poignant comment
on diagnosis is conveyed in this quote Physical
from the National Institute for Health and • Sensitivity to the cold • Dry hair or skin
Clinical Excellence (NICE) guidelines: • Brittle nails • Lanugo
‘The most effective screening device • Dorsal finger callouses • Feeling faint, cold or tired
probably remains the general practitioner • Stress fractures • Bone pain
thinking about the possibility of an eating • Muscle cramps • Injuries due to over-exercising
disorder’.19 • Dental caries • Gingivitis
In addition to screening tools, there are • Parotid enlargement • Self harm
a number of ‘warning signs’ that can aid • Irregular or cessation of menstruation • Abdominal pain/distension
in the detection of eating disorders. Some • Gastrointestinal symptoms - bloating, • Early satiety
nausea • Hypercarotenaemia
of these warning signs can be difficult to
• Anaemia • Halitosis
detect because of the patient’s secrecy,
• Insomnia
deception or shame surrounding their
and signs may represent an eating A multidisciplinary team approach is

Table 3. Assessment of the
disorder may preclude early detection. often required to manage the physical patient with a suspected eating
NICE guidelines note that ‘diagnosis is and psychosocial consequences of the disorder7,14,18,19,22-25
often delayed when doctors inadvertently condition. The team could include a
collude by over-investigating and referring psychiatrist, psychologist, paediatrician, The initial physical assessment should
to other specialties rather than confronting dietitian, social worker, psychiatric include:
the possibility of an eating disorder’.19 nurse, community support organisations • Height, weight, body mass index (BMI;
adults), BMI percentile for age (children)
Physical examination and investigation and other medical specialists (eg
are the next steps in assessment, but endocrinologist, gastroenterologist).18 The • Pulse and blood pressure, with postural
measurements
there may not be any abnormal physical role of the GP includes:14,18,22,23
findings and, often, laboratory results are • assessment and initial diagnosis • Temperature
normal.7 Table 3 summarises a relevant (including urgent referral to the • Assessment of breathing and breath (eg
ketosis)
assessment for a patient with a suspected emergency department, if indicated)
eating disorder. • treatment of medical complications (eg • Examination of periphery for circulation
and oedema
iron deficiency)
Management • nutritional/weight assessment • Assessment of skin colour (eg anaemia,
hypercarotenaemia, cyanosis)
The first priority in the management of a • referral to appropriate health
• Hydration state (eg moisture of mucosal
patient with an eating disorder is securing professionals
membranes, tissue turgor)
medical and psychiatric safety.2,18 It is • involvement of community or hospital
• Examination of head and neck (eg
prudent to remember that a patient’s based mental health services
parotid swelling, dental enamel erosion,
visible habitus is not a reliable indicator • education for the patient and their gingivitis, conjunctival injection)
of their medical risk. For example, a family
• Examination of skin, hair and nails (eg
patient can have a normal body mass • provision of regular ongoing medical dry skin, brittle nails, lanugo, dorsal
index (BMI) but also have a potassium monitoring. finger callouses [Russell’s sign])
level of 2.5 mmol/L due to their purging The more detailed aspects of • Sit-up or squat test (ie a test of muscle
behaviours. In addition, BMI may be management are beyond the scope power)
normal, but the patient might be at of this article, but are provided in the
risk because of rapid weight loss or, in list of resources supplied. Certainly, in Useful laboratory investigations include:
children, there may be failure to gain the scenario of early presentation and • Full blood count
weight.7,18,22 The criteria for admission to diagnosis (or prior to the patient fulfilling • Urea and electrolytes, creatinine
hospital are listed in Table 4.22 diagnostic criteria), education and regular • Liver function tests
For most patients who will not need monitoring in the primary care setting
• Blood glucose
immediate hospitalisation, treatment may be all that is required to prevent
• Urinalysis
should be individualised and take place symptom progression.
• Electrocardiography
initially in an outpatient community
setting, if possible.14 Decisions Conclusion • Iron studies
surrounding management options are Eating disorders are serious, • B12, folate
dependent on:2 life-threatening conditions with significant • Calcium, magnesium, phosphate

• age of the patient physical, psychiatric, psychosocial • Hormonal testing - thyroid function
• symptom severity and financial outcomes. The impact of tests, follicle stimulating hormone,
• course of illness these consequences can be minimised luteinising hormone, oestradiol, prolactin
• medical stability or avoided by early identification and • Plain X-rays - useful for identification of
bone age in cases of delayed growth
• patient motivation management in the general practice
• psychosocial or family support setting. This article outlines an approach • Bone densitometry - relevant after
9-12 months of the disease or of
• regional availability of specialised to assessment in the primary care
amenorrhoea and as a baseline in
inpatient/outpatient programs setting with an emphasis on early adolescents. The recommendation is
• associated psychiatric comorbidity. detection. Ideally, this is achieved by a for two-yearly scans thereafter while the
Other significant factors that influence thorough history, a trusting therapeutic DEXA scans are abnormal.
the necessary treatment interventions relationship between doctor and patient,
Other investigations may be indicated in certain
are whether identification or presentation and intervention before a patient fulfils
clinical presentations to exclude other differential
occurs early, and the competence of the all of the diagnostic criteria of a particular diagnoses (eg coeliac autoantibodies).
GP in the field of eating disorders.16 eating disorder.
EARLY DETECTION OF EATING DISORDERS CLINICAL
Table 4. RANZCP clinical practice guidelines for the treatment of eating disorders 2014
Psychiatric admission indicated* Medical admission indicated*
Weight Body mass index (BMI) <14 kg/m2 BMI <12 kg/m2
Rapid weight loss 1 kg per week over several weeks or grossly inadequate
nutritional intake (<100 kcal daily) or continued weight
loss despite community treatment
Systolic blood pressure <90 mmHg <80 mmHg
Postural blood pressure >10 mmHg drop with standing >20 mmHg drop with standing
Heart rate <40 bpm or >120 bpm or postural tachycardia >20 bpm
Temperature <35.5°C or cold/blue extremities <35°C or cold/blue extremities
12-lead Any arrhythmia including QTc prolongation, non-specific ST

electrocardiogram or T-wave changes including inversion or biphasic waves
Blood sugar Below normal range* <2.5 mmol/L
Sodium <130 mmol/L* <125 mmol/L
Potassium Below normal range* <3.0 mmol/L
Magnesium Below normal range*
Phosphate Below normal range*
Estimated glomerular <60 ml/min/1.73m2 or rapidly dropping (25% drop within

filtration rate a week)
Albumin Below normal range <30 g/L
Liver enzymes Mildly elevated Markedly elevated (AST and ALT >500)*
Neutrophils <1.5 x 109/L <1.0 x 109/L
Risk assessment Suicidal ideation

Active self-harm
Moderate to high agitation and distress
*Patients who are not as unwell as indicated above may still require admission to a psychiatric or other inpatient facility. ¿Medical admission refers to admission to a
medical ward, short-stay medical assessment unit or similar. ¿Please note, any biochemical abnormality that has not responded to adequate replacement within the first
24 hours of admission should be reviewed by a medical registrar urgently.
ALT, alanine aminotransferase; AST, aspartate aminotransferase
Admission criteria for children
Indicators for admission

* and specialist consultation
Medical status Heart rate: <50 bpm QTc: >450 msec

Cardiac arrhythmia Temperature: <35.5oC
Postural tachycardia: >20/min Hypokalaemia
Blood pressure: <80/50 mm Neutropaenia
Postural hypotension: >20 mm
Weight Children <75% of expected body weight or rapid weight loss
Note: These are a guide only and do not replace the need for individual clinical judgement
*For children, admission would generally be to a medical ward. ¿People may also require admission for:
• uncontrolled eating disorder behaviour
• failure to respond to outpatient treatment
• severe psychiatric comorbidity
Reproduced with permission from the Royal Australian and New Zealand College of Psychiatrists. Clinical practice guidelines for the treatment of eating disorders.
Melbourne: RANZCP, 2014.
Resources for GPs 9. Touyz S. What kind of illness is anorexia 25. Brown C, Mehler PS. Medical complications
nervosa? A clinical update. Melbourne: of anorexia nervosa and their treatments: An
• The Royal Australian and New Zealand Australian Psychology Society, 2011. update on some critical aspects. Eat Weight
College of Psychiatrists’ eating disorder 10. Button EJ, Chadalavada B, Palmer RL. Mortality Disord 2015;20(4):419-25.
and predictors of death in a cohort of patients
guidelines, www.ranzcp.org presenting to an eating disorders service. Int J
• Australian and New Zealand Academy Eat Disord 2010;43(5):387-92.
for Eating Disorders (ANZAED), 11. Butterfly Foundation. Paying the price: The
economic and social impact of eating disorders.
www.anzaed.org.au Melbourne: Butterfly Foundation, 2012. Available
• National Eating Disorders Collaboration, at www.thebutterflyfoundation.org.au/about-us/
information-and-resources/paying-the-price
www.nedc.com.au
[Accessed 1 August 2017].
• NICE eating disorder guidelines, 12. Schmidt U, Brown A, McClelland J, Glennon D,
www.nice.org.uk Mountford VA. Will a comprehensive, person
centered, team-based early intervention
• Victorian Centre of Excellence in Eating approach to first episode illness improve
Disorders (CEED), www.ceed.org.au outcomes in eating disorders? Int J Eat Disord
2016;49(4):374-77.
• Eating Disorders Victoria (EDV),
13. Franko D, Keshaviah A, Eddy K, et al. Do
www.eatingdisorders.org.au mortality rates in eating disorders change
• The Butterfly Foundation, over time? A longitudinal look at anorexia
nervosa and bulimia nervosa. Am J Psychiatry
www.butterflyfoundation.org.au 2013;170(8):917-25.
• Eating Disorders Association Inc 14. Redston S, Tiller J, Schweitzer I, et al. ‘Help us,
Queensland, www.eda.org.au she’s fading away’: How to manage the patient
with anorexia nervosa. Aust Fam Physician
2014;43(8):531-36.
Author 15. Surgenor L, Maguire S. Assessment of anorexia
Elizabeth Rowe MBBS, FRACGP, General nervosa: An overview of universal issues and
Practitioner, Airlie Women’s Clinic, Malvern, Vic. contextual challenges. J Eat Disord 2013;1:29.
drlibby.rowe@gmail.com 16. Bj0rnelv S. Eating disorders in general practice.
Competing interests: None. Tidsskr Nor Laegeforen 2014;134(21):2020-21.
17. Gatt L, Jan S, Mondraty N, et al. The household
Provenance and peer review: Not commissioned,
economic burden of eating disorders and
adherence to treatment in Australia. BMC
Psychiatry 2014;14:338.
References 18. National Eating Disorders Collaboration. Eating
1. American Psychiatric Association. Diagnostic disorders: A professional resource for general
and statistical manual of mental disorders. practitioners - Fact sheets. Crows Nest, NSW:
5th edn. Arlington, TX: American Psychiatric National Eating Disorders Collaboration, 2014.
Association, 2013. Available at www.nedc.com.au/files/Resources//
2. Harrington BC, Jimerson M, Haxton C, GPs%20Resource.pdf [Accessed 1 August 2017].
Jimerson DC. Initial evaluation, diagnosis, and 19. National Institute for Health and Care Excellence.
treatment of anorexia nervosa and bulimia Eating disorder guidelines. London: NICE, 2017.
nervosa. Am Fam Physician 2015;91(1):46-52. Available at www.nice.org.uk/guidance/ng69
3. Fairweather-Schmidt AK, Wade TD. DSM-5 eating [Accessed 1 August 2017].
disorders and other specified eating and feeding 20. Ali K, Farrer L, Fassnacht DB, Gulliver A,
disorders: Is there a meaningful differentiation? Bauer S, Griffiths KM. Perceived barriers and
Int J Eat Disord 2014;47(5):524-33. facilitators towards help-seeking for eating
4. Golden N, Katzman D, Sawyer SM, et al. Update disorders: A systematic review. Int J Eat Disord
on the medical management of eating disorders in 2017;50(1):9-21.
adolescents. J Adolesc Health 2015;56(4):370-75. 21. Morgan JF, Reid F, Lacey JH. The SCOFF
5. The Butterfly Foundation. Submission to Mental questionnaire: Assessment of a new
Health Commission. Crows Nest, NSW: Butterfly screening tool for eating disorders. BMJ
Foundation for Eating Disorders, 2012. Available 1999;319(7223):1467-68.
at https://nswmentalhealthcommission.com . 22. Hay P, Chinn D, Forbes D, et al. Royal Australian
au/sites/default/files/TheButterflyFoundation_ and New Zealand College of Psychiatrists
SubmissionMentalHealthCommissionNSW.pdf clinical practice guidelines for the treatment
[Accessed 1 August 2017]. of eating disorders. Aust N Z J Psychiatry
6. Hay P, Girosi F, Mond J. Prevalence and 2014;48(11):977-1008.
sociodemographic correlates of DSM-5 eating 23. Royal Colleges of Psychiatrists, Physicians and
disorders in the Australian population. J Eat Pathologists. MARSIPAN: Management of really
Disord 2015;3:19. sick patients with anorexia nervosa. 2nd edn.
7 Yeo M, Hughes E. Eating disorders - Early London: RCPPP, 2014. Available at www.rcpsych.
identification in general practice. Aust Fam ac.uk/files/pdfversion/CR189.pdf [Accessed
Physician 2011;40(3):108-11. 1 August 2017].
8. Harris EC, Barraclough B. Excess mortality of 24. Cooke R, Sawyer SM. Eating disorders in
mental disorder. Br J Psychiatry 1998;173:11-53. adolescence. An approach to diagnosis
and management. Aust Fam Physician
2004;33(1-2):27-31.
FOCUS
Pulmonary embolism: An update

Steven Doherty
Biffi ©>
Background ulmonary embolism, first described by Virchow in the
Pulmonary embolism is a common condition and can be the

source of significant morbidity and mortality.
Objective
P 1800s, was often a terminal event. A 1960 trial on the
efficacy of heparin in pulmonary embolism found a
mortality rate of 17%,1 and noted that ‘pulmonary embolism
was rarely diagnosed before death’. The Therapeutic Guidelines2
introduces pulmonary embolism as ‘frequently underdiagnosed’,
This article reviews the approach to the diagnostic assessment with ‘a high mortality if untreated; continued suspicion of and
and management of patients with suspected pulmonary embolism. urgent therapy for pulmonary embolism is therefore required’.
Assertions such as this have led to a hyper-vigilance about the
Discussion diagnosis of pulmonary embolism.
The Centers for Disease Control and Prevention estimate
Various clinical decision rules and algorithms are available to
there are 60,000-100,000 deaths per annum from pulmonary
assist in the diagnosis of pulmonary embolism, and the Wells
embolism in the US.3 Mortality data in Australia and the UK do not
score and Pulmonary Embolism Rule-out Criteria rule are
support such figures. In 2015, there were 340 deaths (0.2% of all
presented in this article. The utility of D-dimer testing and the role
deaths) from pulmonary embolism in Australia.4 In the UK, there
of imaging to confirm the diagnosis are also discussed. Treatment
were 2300 deaths from pulmonary embolism in 2012,5 which
options once pulmonary embolism is confirmed are presented.
accounted for 0.4% of all deaths.6
Pulmonary emboli large enough to cause haemodynamic
compromise are a major source of morbidity and mortality.
However, modern tests, especially multidetector row computed
tomography pulmonary angiography (CTPA), have changed the
nature of pulmonary embolism as a clinical entity. From 1998 to
2006, the rate of pulmonary embolism detection in the US nearly
doubled without any change in mortality.7
There is a growing realisation that although the presence
of a large pulmonary embolus is a serious and potentially
fatal event, we are now, with better technology, able to
detect pulmonary emboli that were previously missed but not
necessarily clinically relevant.7,8
The challenge with cases of potential pulmonary embolism
is to weigh up the relevance of diagnosis and the benefits of
treatment against the harms of not only the treatment but also
the investigation.
Acute onset of dyspnoea and chest pain, especially pleuritic in
nature, generally leads to consideration of pulmonary embolism
as a possible diagnosis. Other symptoms, such as cough and
haemoptysis, concurrent symptoms of deep venous thrombosis
PULMONARY EMBOLISM FOCUS
(DVT), and signs of tachypnoea, tachycardia and hypoxia, The current solution to this problem is to risk-stratify patients
may also be present. However, chest pain and dyspnoea with suspected pulmonary embolism, and to use validated risk
are common symptoms in general practice and emergency stratification tools to guide investigation. There are numerous
departments, and the vast majority of these patients will not clinical decision rules, including the Wells score (Table 1), modified
have pulmonary embolism. Wells score, simplified Wells score, revised Geneva score,
Charlotte rule and Pulmonary Embolism Rule-out Criteria (PERC)
Risk stratification rule. The Wells score and PERC rule are the most validated tools of
these studies,9 are simple to use, and can be incorporated into the
History assessment of patients with suspected pulmonary embolism.
There are numerous risk factors for pulmonary embolism, some Rules such as the Wells score incorporate clinical impression,
of which are included in Box 1. These, along with other features on to a degree, into their scoring system. A 2011 systematic review
presentation, help determine the clinical impression or gestalt of found that clinical decision rules such as Wells score were more
the presence or absence of pulmonary embolism. specific and just as sensitive as clinical impression.10
Historically, pulmonary embolism had high morbidity and The greater the specificity of a test, the better it is at ruling the
mortality rates. However, the modern ability to detect even the condition in (a positive result is likely to be a true positive); the
smallest pulmonary emboli means we are currently detecting greater the sensitivity, the better the test is at ruling the disease
‘disease’ that used to be considered part of the normal function out (a negative result is likely to be a true negative). This allows
of the lung - to filter small clots. The mortality of otherwise more rational use of investigations, and the benefits of this are
healthy individuals, in the outpatient setting, with proven a reduction in exposure to ionising radiation (especially breast
pulmonary embolism and normal physiology approaches 0%.8 tissue in women of child-bearing age), decreased risk of reactions
This is lower than the mortality associated with diagnosing and to intravenous contrast, and a reduction in healthcare costs to the
treating pulmonary embolism in this subgroup. Numerous studies patient and society.
suggest that small pulmonary emboli are transient and normal,8 Wells score comprises a set of mostly objective criteria
and that the diagnosis of pulmonary embolism in the modern era designed to determine a pre-test probability for pulmonary
should not ‘chill the marrow of clinicians’.8 embolism. Calculators for Wells criteria and the PERC rule are
Without question, pulmonary embolism can be a devastating available online (www.mdcalc.com). Wells score can only be
and fatal diagnosis; however, the ability to detect pulmonary applied if symptoms have been present for <30 days, and is not
emboli of all sizes leaves clinicians with a conundrum. If we seek validated for use if:9
to diagnose every pulmonary embolus, even ones that evidence • upper limb DVT is suspected as a source of pulmonary
suggests are ‘normal’, then at some point along the spectrum, we embolism
will start to cause more harm than good. The difficulty is knowing • the patient has been on anticoagulants for >72 hours
where that point is. • the patient has been asymptomatic for 72 hours prior to
presentation
• the patient is pregnant.
Box 1. Risk factors for pulmonary embolism If clinical signs and symptoms of DVT are the clinical features that
make the Wells or simplified Wells score sufficiently positive to
Surgery - major joint surgery, lower limb surgery, abdominal or pelvic warrant imaging then, intuitively, a negative venous ultrasound
surgery for cancer, major gastrointestinal tract surgery, multi-trauma, scan could make the patient low risk and potentially reduce the
spinal cord injury with paresis
need for CTPA or ventilation/perfusion (V/Q) scanning. There is
Acute and chronic medical illness - chronic heart failure, myocardial no specific evidence in the literature for this approach, but one
infarction, inflammatory bowel disease, active rheumatic disease, recent study that combined lung and venous ultrasound scanning
nephrotic syndrome, acute respiratory failure, chronic lung disease with Wells criteria led to a 23% reduction in CTPA ordering.11
A Wells score <4 makes pulmonary embolism unlikely, but
Malignancy-related factors - active malignancy, myeloproliferative
neoplasms, cancer treatment does not fully exclude it. Tests such as D-dimer can add greater
certainty to excluding pulmonary embolism as a diagnosis. In
Hormonal-related factors - pregnancy or early postpartum, oral low-risk patients, a positive D-dimer is more likely to be a false
contraceptive pill, hormone replacement therapy
positive than a true positive.9 Observations such as this led to the
Known thrombophilia development and validation of the PERC rule.12,13 If the PTP is low
using the Wells score then the PERC rule (Box 2) can be applied.
Other - body mass index >30 kg/m2, venous stasis/varicose veins, past If the answer to all of the criteria in Box 1 is ‘Yes’, then the PERC
history of deep venous thrombosis or pulmonary embolism, prolonged
rule is negative. No further testing is required and pulmonary
immobilisation/travel
embolism is safely excluded.
FOCUS PULMONARY EMBOLISM
hypotension, tachycardia or hypoxia.9 If deemed less urgent, or

Table 1. Wells criteria
if access to imaging is limited (eg remote location, weekends),
Clinical feature Wells score it is reasonable to commence low-molecular weight heparin
Clinical signs and symptoms of DVT 3 (LMWH) and arrange imaging for the next available day.14
Chest X-ray remains useful in determining alternative
Pulmonary embolism most likely diagnosis 3
diagnoses (eg pneumothorax, pneumonia) in appropriate clinical
Heart rate >100 beats per minute 1.5 cases. Definitive diagnosis will require CTPA or V/Q scanning.
Immobilisation at least three days or surgery CTPA is the most commonly used modality, but V/Q scanning
1.5
within past four weeks should be considered the modality of choice in pregnancy if the
Previous DVT or pulmonary embolism 1.5 scanning device is readily available.9
For severely compromised patients, bedside echocardiography
Haemoptysis 1
findings of right ventricular dilation, right ventricular hypokinesis
Malignancy treatment within six months or 1 and high right atrial pressures may confirm the presence of
palliative massive pulmonary emboli.
DVT, deep venous thrombosis
A Well’s score >4 warrants imaging Imaging considerations in pregnancy
Radiation risk in pregnancy relates to maternal and fetal risk.
The radiation dose to the breast is much higher with CTPA
Box 2. PERC rule than with V/Q scanning, and CTPA has a significantly higher
maternal risk.9 Radiation risk to the fetus is low and comparable
Aged <50 years
with both CTPA and V/Q scanning.9 Patients who are pregnant
Pulse <100 beats per minute
are generally younger and have fewer comorbidities than non
SaO2 >95%
pregnant patients with suspected pulmonary embolism. V/Q
No haemoptysis
scanning, especially in the presence of a normal chest X-ray,
No oestrogen use
is a more reliable test in pregnancy than in the non-pregnant
No surgery or trauma requiring hospitalisation within four weeks
population.15 Low-dose perfusion-only scanning minimises the
No prior venous thromboembolism
No unilateral leg swelling radiation dose to the fetus and is safe; however, if concerns
persist, exposure to radiation can be further reduced by using
a urinary catheter, which removes isotope from the bladder
The PERC rule validation study13 included patients who more quickly.16
presented with a primary complaint of shortness of breath
or chest pain, and it is reasonable to use it for either of these Treatment
symptoms. The PERC rule has not been validated for people with: Anticoagulation is the mainstay of treatment for pulmonary
• active cancer, thrombophilia or a strong family history of embolism. Massive pulmonary embolism may warrant
thrombophilia thrombolytic therapy. One controversy is the benefit or otherwise
• transient tachycardia or beta-blocker use that may mask of treating subsegmental pulmonary embolism (SSPE).
tachycardia
• leg amputations Thrombolysis
• morbid obesity (leg swelling not easily determined) For severely compromised patients, the American College of
• baseline hypoxaemia when oximetry reading <95% is Chest Physicians (ACCP) recommend systemic thrombolysis
longstanding. if systolic blood pressure is <90 mmHg.17 The American Heart
If the patient’s PERC score is >0, then an enzyme-linked Association18 also states that ‘fibrinolysis is reasonable for
immunosorbent assay (ELISA)-type D-dimer is recommended. patients with massive acute pulmonary embolism and acceptable
If this is negative, pulmonary embolism is ruled out and no risk of bleeding complications’. This includes patients with a
further investigation is required; if positive, then imaging is systolic blood pressure <90 mmHg or bradycardia <40 beats/
recommended. The approach to the investigation above is minute, and that ‘fibrinolysis may be considered for ... submassive
summarised in Figure 1. acute pulmonary embolism (with) ... hemodynamic instability,
worsening respiratory insufficiency, severe right ventricular
Imaging dysfunction, or major myocardial necrosis and low risk of bleeding
If imaging is required, this should be performed as soon as complications’. Patients with massive pulmonary embolism will
possible and urgently (via the emergency department) if there generally be managed in the hospital setting, and the Therapeutic
are significant cardiac or respiratory signs, such as tachypnoea, Guidelines recommend heparin infusion and alteplase.2
PULMONARY EMBOLISM FOCUS
Figure 1. Approach to investigation of pulmonary embolism

PERC, Pulmonary Embolism Rule-out Criteria
Anticoagulation as an alternative to LMWH and warfarin in the treatment of

LMWH reduces complications and thrombus size, compared pulmonary embolism.20,21 High-risk patients, such as those with
with unfractionated heparin, for the initial treatment of VTE antiphospholipid syndrome and recurrent unprovoked pulmonary
without altering mortality.19 The Therapeutic Guidelines2 embolism, were excluded from the clinical trials.20The dose of
recommendations for the treatment of acute pulmonary rivaroxaban is 15 mg twice daily for three weeks, then 20 mg
embolism are dalteparin 200 U/kg, up to 18,000 U daily or 100 daily. Treatment duration is six months, but may be three months
U/kg, up to 9000 U twice daily; or enoxaparin 1.5 mg/kg daily or in the presence of a transient major risk factor, or indefinite
1 mg/kg twice daily.Twice-daily dosing is preferred if the risk of if there are ongoing major risk factors (eg cancer, recurrent
bleeding or thrombus extension is high (eg older age, obesity, unprovoked pulmonary embolism).
malignancy). If creatinine clearance is <30 mL/min, dose
adjustment is required. Subsegmental pulmonary embolism
Warfarin should be commenced and the INR maintained The ACCP17 recommends that clinical surveillance is preferred
at 2-3. Rivaroxaban is currently approved and subsidised for to anticoagulation for patients with SSPE (no involvement of
use in pulmonary embolism in Australia, and can be used proximal pulmonary arteries) and no proximal DVT with low risk
FOCUS PULMONARY EMBOLISM
14. British Thoracic Society Standards of Care Committee Pulmonary Embolism

for recurrent VTE. The ACCP adds that ultrasound scanning of the
Guideline Development Group. British Thoracic Society guidelines for
deep veins in both legs should be performed to exclude proximal the management of suspected acute pulmonary embolism. Thorax
DVT, and that clinical surveillance may be supplemented by serial 2CC3;58(6):47C-83.
15. Chan WS, Ray JG, Murray S, Coady GE, Coates G, Ginsberg JS. Suspected
ultrasound scanning. pulmonary embolism in pregnancy: Clinical presentation, results of lung
In a retrospective review, Donato et al22 found that patients scanning, and subsequent maternal and pediatric outcomes. Arch Intern Med
2002:162(10):117C-75.
with SSPE had favourable outcomes at three months without
16. American Academy of Emergency Medicine. My patient is pregnant and I
anticoagulation, and may do better without treatment, although suspect PE/appendicitis. Milwaukee, WI: AAEM, 2CC9. Available at www.heti.
there were only 22 patients in the no-treatment group, none of nsw.gov.au/Global/HETI-Resources/emergency/clinical-updates/2CC9/Clinical-
update-142-23-July-2CC9-imaging-for-appx-PE-in-pregn.pdf [Accessed 5 July
whom had recurrent pulmonary embolism. 2C17].
Recommendations to not treat SSPE are weak as there are 17. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease:
no randomised trials on the safety of anticoagulation versus no CHEST guideline and expert panel report. Chest 2C16;149(2):315-52.
18. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and
treatment in this subgroup;23 GPs may want to seek advice from submassive pulmonary embolism, iliofemoral deep vein thrombosis, and
specialist colleagues for this group. chronic thromboembolic pulmonary hypertension: A scientific statement from
the American Heart Association. Circulation 2C11;123(16):1788-83C.
Author 19. Robertson L, Jones LE. Fixed dose subcutaneous low molecular weight
Steven Doherty PhD, MBBS, FACEM, Critical Care VMO Tamworth and heparins versus adjusted dose unfractionated heparin for the initial treatment
Armidale Rural Referral Hospitals, Adjunct Professor University of New England, of venous thromboembolism. Cochrane Database Syst Rev 2C17;2:CDCC11CC.
Armidale, NSW. steven.doherty@hnehealth.nsw.gov.au 2C. Einstein-PE Investigators, Büller HR, Prins MH, et al. Oral rivaroxaban
Competing interests: Dr Doherty reports personal fees from Pfizer India outside for the treatment of symptomatic pulmonary embolism. N Engl J Med
the submitted work. 2C12;366(14):1287-97.
21. Brieger D. Anticoagulation: A GP primer on the new oral anticoagulants. Aust
Provenance and peer review: Commissioned, externally peer reviewed.
Fam Physician 2C14;43(5):254-59.
22. Donato AA, Khoche S, Santora J, Wagner B. Clinical outcomes in patients
References
with isolated subsegmental pulmonary emboli diagnosed by multidetector CT
1. Barritt DW, Jordan SC. Anticoagulant drugs in the treatment of pulmonary pulmonary angiography. Thromb Res 2C1C;126(4):e266-7C.
embolism. A controlled trial. Lancet 1960;1(7138):1309-12. 23. Yoo HH, Queluz TH, El Dib R. Anticoagulant treatment for subsegmental
2. Cardiovascular Working Group. Treatment of deep vein thrombosis pulmonary embolism. Cochrane Database Syst Rev 2C16;(1):CDC1C222.
and pulmonary embolism. Melbourne: Therapeutic Guidelines
Limited, 2017. Available at https://tgldcdp.tg.org.au.acs.hcn.com.au/
viewTopic?topicfile=deep-vein-thromobosis-and-pulmonary-embolism-treatm
ent&guidelineName=Cardiovascular#toc_d1e374 [Accessed 2 May 2017].
3. Centers for Disease Control and Prevention. Venous thromboembolism (blood
clots). Atlanta: CDC, 2015. Available at www.cdc.gov/ncbddd/dvt/data.html
[Accessed 2 May 2017].
4. Australian Bureau of Statistics. Causes of death, Australia, 2015.
Canberra: ABS, 2016. Available at www.abs.gov.au/AUSSTATS/abs@.nsf/
DetailsPage/3303.02015?OpenDocument [Accessed 2 May 2017].
5. British Lung Foundation. Pulmonary embolism statistics. London: British Lung
Foundation, 2015. Available at https://statistics.blf.org.uk/pulmonary-embolism
[Accessed 26 April 2017].
6. Office for National Statistics. Deaths registered in England and Wales: 2012.
London: Office for National Statistics, 2013. Available at www.ons.gov.uk/
peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/bulletins/
deathsregistrationsummarytables/2013-07-10 [Accessed 26 April 2017].
7. Long B. Controversies in pulmonary embolism imaging and treatment of
subsegmental thromboembolic disease. emDocs, 2016. Available at www.
emdocs.net/controversies-in-pe-diagnosis-and-treatment [Accessed 5 July 2017].
8. Newman DH, Schriger DL. Rethinking testing for pulmonary embolism: Less
is more. Ann Emerg Med 2011;57(6):622-27
9. Goergen S, Tran H, Jong I, Zallman M. Suspected pulmonary embolism.
Sydney: The Royal Australian and New Zealand College of Radiologists, 2015.
10. Lucassen W, Geersing GJ, Erkens PM, et al. Clinical decision rules
for excluding pulmonary embolism: A meta-analysis. Ann Intern Med
2011;155(7):448-60.
11. Nazerian P, Volpicelli G, Gigli C, et al. Diagnostic performance of Wells score
combined with point-of-care lung and venous ultrasound in suspected
pulmonary embolism. Acad Emerg Med 2017;24(3):270-80.
12. Kline JA, Nelson RD, Jackson RE, Courtney DM. Criteria for the safe use
of D-dimer testing in emergency department patients with suspected
pulmonary embolism: A multicenter US study. Ann Emerg Med
2002;39(2):144-52.
13. Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter
evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost
2008;6(5):772-80. correspondence afp@racgp.org.au
FOCUS
Bariatric-metabolic surgery: A guide

for the primary care physician
Phong Ching Lee, John Dixon
Bsa ©
Background ver the past decade, bariatric-metabolic surgery has

Bariatric-metabolic surgery has emerged as an attractive option
that offers significant and durable weight loss in the treatment
of clinically severe obesity. Given the high prevalence of obesity,
and growing numbers of bariatric-metabolic surgeries performed,
O emerged as an attractive, evidence-based option that
offers significant and durable weight loss and improved
health outcomes for those with clinically severe obesity. Given
the exponential increase in the number of Australians with
primary care physicians increasingly encounter patients who clinically severe obesity over recent decades, and the growing
have had, or are considering, bariatric-metabolic surgery. numbers of bariatric-metabolic surgeries performed, primary care
physicians increasingly encounter patients who have had, or are
Objectives considering, bariatric-metabolic surgery. The aim of this article is
The aim of this article is to provide guidance on common to provide guidance on:
issues pertaining to bariatric-metabolic surgery that general • evidence for the use of bariatric-metabolic surgery
practitioners (GPs) face, including patient selection, pre-operative • selection of appropriate patients for bariatric-metabolic surgery
work-up, acute and long-term complications following the • pre-operative work-up prior to surgery
surgery, and long-term lifestyle and nutritional support. • acute and long-term complications after surgery
• long-term lifestyle, nutritional and comorbidity follow-up.
Discussion
In properly selected patients with clinically severe obesity,
Types of surgery
there is clear net benefit in terms of improved health outcomes The three most commonly performed operations for the treatment
and reduced mortality following bariatric-metabolic surgery. of obesity in Australia and worldwide are sleeve gastrectomy (SG),
Similarly to other chronic conditions, GPs play a crucial role in adjustable gastric band (AGB) and Roux-en-Y gastric bypass
the management of obesity, and in the multidisciplinary, long (RYGB; Figure 1). A brief description of these procedures and their
term postoperative support and monitoring that is important for key characteristics are summarised in Table 1.
optimal outcomes after surgery.
Figure 1. Common bariatric-metabolic

procedures3
A. Adjustable gastric band
B. Sleeve gastrectomy
C. Roux-en-Y gastric bypass
© The Royal Australian College of General Practitioners 2017 reprinted from afp vol.46, no.7, july 2017 465
FOCUS BARIATRIC-METABOLIC SURGERY
Evidence for the use of bariatric-metabolic Improved diabetes control and diabetes remission
surgery Type 2 diabetes mellitus (T2DM), a global epidemic that mirrors the
rise in obesity rates, has recently been a major focus of bariatric-
Weight loss metabolic surgery. Marked weight loss from bariatric-metabolic
A landmark prospective study on bariatric-metabolic surgery, surgery leads to substantial improvement in T2DM, even to the
the Swedish Obese Subjects study, has indicated that maximal point of remission. Randomised controlled trials have found that
weight loss of 20-32% was achieved at one to two years after treatment of obesity and T2DM with bariatric-metabolic surgery
surgery.1 Weight loss was sustained at 18% even after 20 is superior to medical therapy in controlling hyperglycaemia and
years.2 In general, RYGB offers the largest mean percentage cardiovascular risk factors over the medium term.7,8
weight loss (25-35%), followed by SG (20-30%) and AGB
(17-20%).3 Weight loss seen after AGB is slow and gradual, Improvement in other obesity-related complications
whereas rapid weight loss can be expected with SG and RYGB. Apart from better glycaemic control, sustained weight loss
With all three procedures, the weight loss achieved translates following bariatric-metabolic surgery also results in significant
to numerous health benefits, including reduced mortality, improvement in other obesity-related complications, and some of
especially from cardiovascular disease and cancer; improvement the key complications are shown in Table 2.
in obesity-related diseases; and improved physical functioning
and emotional wellbeing.4 Health-related quality of life
It has been estimated that obesity has a greater negative impact
Mortality on quality of life than 20 years of ageing, an impact that persists
Large meta-analyses have found that cardiovascular and cancer even after accounting for demographics, health habits, medical
mortality were approximately halved after bariatric-metabolic conditions and depression.9 Numerous studies have consistently
surgery when compared with the matched non-surgical cohort5,6 found substantial improvement in health-related quality of life
in studies of up to 14 years’ duration. following weight loss from bariatric-metabolic surgery.7,9
Table 1. Summary of characteristics of current bariatric-metabolic procedures3,25
Adjustable gastric band Sleeve gastrectomy Roux-en-Y gastric bypass
Description Adjustable silicone band placed Greater portion of the fundus and Combination procedure:
just below the gastroesophageal body of the stomach is removed. 1. Small stomach pouch created,
junction, applying gentle pressure Gastric volume is reduced by thereby reducing gastric volume
that suppresses hunger. Level about 80% 2. The pouch is joined to the
of restriction can be adjusted by jejunum, hence, diverting
varying the amount of fluid placed nutrients from lower stomach,
in the band duodenum and proximal jejunum
Mean total body weight loss 17-20% 20-30% 25-35%
Mortality rate (at 30 days)20,21 0.03-0.1% 0.3-0.5% 0.1-0.4%
Morbidity at one year 4.6% 10.8% 14.9%
Nutritional concerns Low (deficiencies in iron, vitamin Moderate (deficiencies in iron, Moderate (deficiencies in iron,
B12, folate, thiamine) vitamin B12, folate, calcium, vitamin B12, folate, calcium,
vitamin D, thiamine, copper, zinc) vitamin D, thiamine, copper, zinc)
Advantages Effective, with good long-term Very effective with good mid-term Largest amount of weight loss
weight maintenance weight maintenance with good long-term weight
Degree of restriction adjustable maintenance
Reversible Highest rate of diabetes remission
Lowest morbidity and mortality rate (for patients with pre-existing type
2 diabetes mellitus)
Disadvantages and Highest long-term re-operation rate Staple line leak, gastroesophageal Staple line leak, dumping, stomal
key complications Gastric pouch dilatation, erosion of reflux disease, dilatation of the ulcer, intestinal obstruction,
band into the stomach, leaks to the gastric remnant, weight regain gallstones, nutritional deficiency,
adjustable gastric band system, Limited long-term data altered alcohol metabolism, weight
weight regain regain
466 reprinted from afp vol.46, no.7, july 2017 © The Royal Australian College of General Practitioners 2017
BARIATRIC-METABOLIC SURGERY FOCUS
Patients who could benefit from surgery In addition, bariatric-metabolic surgery may be considered
The pre-operative assessment starts with a detailed history and in those with a BMI of 30-35 kg/m2 and with uncontrolled
physical examination (Box 1). Eligibility criteria for surgery are hyperglycaemia, despite optimal medical therapy.11,12 However,
primarily based on body mass index (BMI) and the presence of the number of studies in this population is limited, and there is a
obesity-related complications,10,11 including: lack of long-term data demonstrating net benefit.
• individuals with BMI >40 kg/m2 Absolute contraindications in bariatric-metabolic surgery
• individuals with BMI >35 kg/m2 with one or more are few and include contraindications to general anaesthesia,
obesity-related complications. serious blood or autoimmune disorders, active drug or alcohol
In a recent statement by major international diabetes abuse, and severe, untreated psychiatric illness. Patients with
organisations, which was endorsed by the Australian Diabetes limited life expectancy due to cardiopulmonary or other end
Society, bariatric-metabolic surgery was proposed to be an organ failure or metastatic/inoperable malignancy are also not
established treatment option in the algorithm to manage T2DM.12 suitable for surgery.
Bariatric-metabolic surgery is recommended for: Throughout the pre-operative workup process, new information
• all individuals with T2DM and BMI >40 kg/m2 will be obtained, and the risk-benefit profile changes. As with any
• individuals with BMI 35-40 kg/m2 with inadequate glycaemic operation, the potential benefits of surgery must outweigh the
control despite lifestyle and optimal medical therapy. peri-operative and long-term risks of surgery.
As a general rule, bariatric-metabolic surgery is strongly
recommended and should be prioritised for individuals with super
Box 1. Pre-operative assessment for bariatric-metabolic obesity (BMI >50 kg/m2) or class III obesity (BMI >40 kg/m2) with
surgery serious complications that are sensitive to weight loss. Surgery
History is also suitable for younger patients who are likely to develop
Weight history (eg age of onset of obesity, minimum and maximum complications of obesity and subsequent reduced quality of life
weight), previous weight loss attempts (including diets, medications, over time without active intervention. On the other hand, increasing
previous weight-loss surgery), triggers for weight gain/regain age is a risk factor for postoperative complications and mortality.13,14
Presence of obesity-related comorbidities, family history, medication The risks of overweight and obesity attenuate with age and the role
history
of intentional weight loss becomes less clear.15 Caution is advised if
Assessment of current lifestyle: dietary behaviour and physical activity
levels; work and home environment, psychosocial support
the patient is older than 65 years of age.
Physical examination A large observational study found that bariatric-metabolic
Weight or body mass index, neck circumference, waist circumference, surgery was associated with reduced risks of gestational
blood pressure diabetes and excessive fetal growth, but with increased risk of
Signs of specific causes of obesity (eg hypothyroidism, Cushing’s pre-term birth and small-for-gestational-age infants.16 All women
syndrome) of childbearing potential should be counselled on contraceptive
Investigations choices and the need to avoid pregnancy pre-operatively and 12-18
Routine laboratory screen: fasting lipids, full blood count, urea and
months postoperatively. There is concern that rapid weight loss
electrolytes, liver function tests, coagulation screen, urinalysis; fasting
during the early postoperative period may be detrimental to the
glucose and glycated haemoglobin (HbA1c) to screen for diabetes
In pre-existing T2DM: C-peptide level to predict diabetes remission
developing fetus. Patients who become pregnant after bariatric-
Nutritional screen: iron studies, vitamin B12, folate, 25-OH vitamin D metabolic surgery should be monitored closely for appropriate
Gastrointestinal evaluations such as abdominal ultrasound and weight gain, nutritional supplementation and fetal wellbeing.
endoscopy may be required Most importantly, patients must be able, willing and motivated
Electrocardiogram: referral to cardiologist for echocardiogram or stress to adhere to the postoperative lifestyle changes, nutritional
testing may be required supplementation and follow-ups that are necessary to ensure
Polysomnography if moderate or severe obstructive sleep apnoea
safety and success.
suspected
Psychological evaluation Pre-operative assessment
Assess commitment, motivation, understanding and expectations of
surgery Once a decision has been made for bariatric-metabolic surgery, a
Psychiatry referral if known or suspected psychiatric illness or series of detailed assessments would be organised (summarised
substance abuse in Box 1).
Management
Cigarette smokers should stop smoking, preferably at least six weeks Nutritional assessment
prior to surgery A state of high-energy malnutrition is often observed in clinically
Pre-operative very low energy diet at least two weeks prior to surgery
severe obesity, which is masked by ample energy excess. Up to
to induce weight loss and reduce complications
80% of bariatric-metabolic surgery candidates have micronutrient
Table 2. Pre-operative optimisation of obesity-related complications4,26

Obesity-related complication Pre-operative screening and optimisation Improvement after weight loss post-surgery
Type 2 diabetes mellitus Glycated haemoglobin (HbA1c) and fasting glucose to Better glycaemic control and a reduced medication
screen for diabetes burden
Aim for good glycaemic control (HbA1c <7%) prior to Diabetes remission in some cases
surgery
Cardiovascular disease Electrocardiogram (ECG) and cardiac risk assessment Reduction of cardiovascular morbidity of >50%
Referral to cardiology if high cardiovascular risk, (compared to body mass index [BMI] and age
presence of cardiac symptoms or abnormal ECG matched controls)
Non-alcoholic fatty liver disease Liver function tests Improved liver histological appearance
Consider abdominal ultrasound scan if liver function Potential regression of established liver disease
test increased, specifically to detect fibrotic liver disease
Obstructive sleep apnoea Screening questionnaire (eg STOP-BANG) to identify Significant improvement in apnoea-hypopnoea index
(OSA) and asthma those at risk for OSA Remission of OSA in some cases
Refer to sleep specialist if STOP-BANG score >327
deficiencies pre-operatively, and appropriate nutritional meal replacements that provide <3350 kJ/day (<800 kcal/day).
assessment allows deficiencies to be corrected prior to surgery.17 VLED is started at least two weeks prior to surgery. During a
VLED, patients with T2DM should self-monitor their capillary
Identifying and optimising complications prior to blood glucose regularly, especially if they are on insulin or insulin
surgery secretagogues. Reductions in insulin doses are often necessary
Pre-operative assessment also includes identification and while on a VLED to prevent hypoglycaemia.
optimisation of obesity-related complications, with the aim to Smoking is associated with adverse postoperative outcomes,
improve peri-operative safety and outcomes after surgery. Key including poor wound healing, anastomotic ulceration and
complications are shown in Table 2. pneumonia. All patients who smoke should be advised to stop
smoking, preferably six weeks before surgery. Following RYGB,
Psychosocial assessment alcohol metabolism is impaired and high-risk groups should
Prior to surgery, thorough assessment of the patient’s behaviour, abstain from alcohol consumption to reduce the risk of alcohol-use
home and work environments, family dynamics, and their disorder postoperatively.
ability to incorporate nutritional and lifestyle changes should
be conducted. Incorrect beliefs and unrealistic expectations on Procedure selection
what the procedure can achieve must be rectified. Depression, The choice of surgical procedure is guided by the individual’s
anxiety and other psychiatric disorders are prevalent in individuals characteristics, aims of therapy and available surgical expertise.
considering bariatric-metabolic surgery; referral to a psychologist RYGB produces the greatest amount of weight loss and may
or psychiatrist should be considered if psychiatric illness is be appropriate for individuals with a very high BMI. AGB has
suspected. lower peri-operative risk, compared with RYGB, but higher rate
of re-operation for inadequate weight loss19 and thus may be
Anatomical assessment suitable for older individuals or those at lower BMI ranges. RYGB
As part of the pre-operative assessment, evaluation of the upper provides the greatest rate of diabetes remission, a consideration
gastrointestinal anatomy may be performed, depending on factors for patients with T2DM. RYGB is also the treatment of choice in
such as the presence of gastrointestinal symptoms or type of patients with gastro-oesophageal reflux disease (GORD); SG and
surgery being considered. AGB may exacerbate GORD, whereas GORD frequently improves
after RYGB. Finally, good-quality, postoperative care is crucial to
Pre-operative preparation the success of the AGB. The decision for AGB should take into
Weight loss prior to bariatric-metabolic surgery can reduce liver account the availability of an appropriate after-care program.
volume and visceral adiposity, which may ease technical aspects
of the surgery and lead to improved short-term outcomes.18 Acute and chronic complications
In T2DM, pre-operative weight loss with medical nutrition Bariatric-metabolic surgery is generally regarded as safe, with low
therapy can also improve glycaemic control. This can reasonably morbidity and mortality that is comparable to elective laparoscopic
be achieved using very low energy diets (VLEDs) consisting of cholecystectomy.20,21 Procedure-specific complications are shown
in Table 1, and the presence of abdominal pain, nausea or vomiting by a multidisciplinary team involving the bariatric physician,
should alert consideration of these key complications as possible bariatric surgeon, general practitioner, nurse, dietitian, exercise
differential diagnoses. Presentation of common and important physiologist and psychologist.
acute and long-term complications after bariatric-metabolic Detailed information on postoperative diet and nutritional
surgery are summarised in Table 3. These features should prompt recommendations have previously been reviewed elsewhere,4,17
referral back to surgical or nutritional team. and recommended nutritional supplementation and monitoring
are shown in Box 2.
Postoperative follow-up Maintenance of physical activity after bariatric-metabolic surgery
aids in maintaining muscle strength, enhanced fitness and greater
Lifestyle changes after surgery
weight loss. Moderate-intensity physical activity of at least 150
Recommended postoperative lifestyle changes and follow-up minutes per week and a target of 300 minutes per week including
care are summarised in Box 2. This care is best delivered strength training two to three times per week is recommended.11
Table 3. Specific adverse events following bariatric-metabolic surgery and management plan |
Adverse events Presentation Management
Acute complications
Surgical complications Abdominal pain, tachycardia, breathlessness, drop Usually detected during immediate postoperative period
(eg leaks, perforations, obstruction, in haemoglobin and managed by the surgical team
infection, haemorrhage) Presence of these symptoms should prompt urgent
referral back to the surgical team
Hypoglycaemia (usually in patients Sweating, dizziness, headaches, palpitations Fairly common, especially in patients on insulin
with pre-existing diabetes) Low capillary blood glucose on testing or insulin secretagogues
Stop sulphonylureas, and stop insulin or decrease dose
Close self-monitoring of capillary blood glucose
Dumping syndrome Abdominal pain, diarrhoea, nausea, flushing, Dietary modification, with small regular meals containing
palpitations, sweating, agitation, and syncope after protein and complex carbohydrates
meals rich in simple carbohydrates Acarbose may be helpful in some refractory cases
Long-term complications
Iron-deficiency anaemia Microcytic, hypochromic anaemia, lethargy, Oral iron supplements, consider intravenous
anorexia, pallor, hair loss, muscle fatigue iron for severe deficiency
Vitamin C to increase iron absorption
Rule out bleeding ulcers, neoplastic disease
or diverticular disease
B12 deficiency Macrocytic anaemia, leukopenia, glossitis, Vitamin B12 repletion (oral or intramuscular)
thrombocytopenia, peripheral neuropathy Prevention - B12 containing multivitamin
supplementation
Annual serum B12 level evaluation
Thiamine deficiency Neurological symptoms, Wernicke’s Appropriate postoperative diet, with regular dietitian
encephalopathy in severe cases follow-up
Screen for other nutritional deficiencies
Thiamine supplementation
Over-restricted gastric band (for Maladaptive eating, gastro-oesophageal reflux Reduce amount of fluid in gastric band
patients with adjustable gastric band) disorder, vomiting, regurgitation, chronic cough, or Consider referral to bariatric surgeon for assessment of
recurrent aspiration pneumonia band position and function
Weight regain Maximal weight loss usually achieved at one to For patients with laparoscopic adjustable gastric band -
two years after surgery, with some weight regain evaluation of band, adjust as required
thereafter Consider adjuncts (eg very low energy diet,
pharmacotherapy)
Consider referral back to weight management clinic
Adjustment of chronic medications Box 2. Postoperative follow-up checklist

In patients with T2DM, adjustments to the antidiabetes
Monitor weight loss progress and complications at each visit
agents are frequently necessary in the early postoperative
Monitor adherence to appropriate diet and physical activity levels
period to prevent hypoglycaemia. Insulin secretagogues (ie
Medication review -
sulphonylureas, metiglinides) should be discontinued and
• Avoid nonsteroidal anti-inflammatory drugs
insulin doses reduced as appropriate. Metformin should be
• Adjust antihypertensives, lipid medications as appropriate. These
continued postoperatively and withdrawal considered if stable medications should not be discontinued empirically
non-diabetic glycaemia (ie glycated haemoglobin in the normal • Adjust diabetes medications. Requirement for anti-diabetes
range for at least six months) is demonstrated. Screening for medications often decreases, and in many cases, diabetes remission
diabetes complications should continue even with diabetes is achieved. Preference for use of agents with favourable weight profile
remission, at least for the first five years.12 Nutritional supplements -
The effect of weight loss on lipids, especially low-density • Adult multivitamin and multimineral - containing iron, folic acid,
thiamine, vitamin B12. Doses: two daily for sleeve gastrectomy or
lipoprotein, is variable and generally modest. Therefore, lipid
Roux-en-Y gastric bypass; one daily for adjustable gastric band
lowering medications should not be discontinued unless • Citrated calcium - elemental calcium 1200-1500 mg/day
clearly indicated. Although blood pressure often improves • Vitamin D - titrate to 25-OH vitamin D levels >30 ng/mL. Typical
with weight loss, the effect is variable and incomplete, and dose required 3000 IU/day
occasionally transient. Therefore, antihypertensives should • Additional iron and vitamin B12 supplementation as required, based
be actively titrated on follow-up. Medications with a narrow on lab results
therapeutic index (eg warfarin, digoxin, lithium, antiepileptic Laboratory assessment -
medications) also require close monitoring and titration • Full blood count, urea and electrolytes, liver function tests, uric acid,
glucose, lipids (every 6-12 months)
because of altered oral drug bioavailability following bariatric-
• 25-OH vitamin D, iPTH, calcium, albumin, phosphate, B12, folate,
metabolic surgery. iron studies (annually, more frequently if deficiencies identified)
Cost-effectiveness and access to care

A systematic review of numerous studies has demonstrated
John Dixon MBBS, PhD, FRACGP, FRCP (Edin), NHMRC Senior Research
that bariatric-metabolic surgery is clinically effective and Fellow; Head of Clinical Obesity Research, Baker Heart and Diabetes Institute;
cost-effective for moderate-to-severe obesity, compared with Adjunct Professor, Primary Care Research Unit, Monash University, Vic. john.
dixon@bakeridi.edu.au
non-surgical treatment.22 However, access to surgery remains
Competing interests: John Dixon has provided consultancy services to Apollo
an issue in the Australian public healthcare system. The Endosurgery, Covidien, Nestle Health Science, Bariatric Advantage, I-Nova and
majority of procedures are still performed in private hospitals, Novo-Nordisk. Phong Ching Lee has no competing interests to declare.
Acknowledgement: John Dixon acknowledges the support of the National Health
and for those who can afford private health insurance and
and Medical Research Council (NHMRC) through a senior research fellowship.
the associated out-of-pocket costs.23 Meanwhile, obesity Provenance and peer review: Commissioned, externally peer reviewed.
and its complications disproportionately affect those at lower
socioeconomic status.24 Improving accessibility of surgery to References
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J Intern Med 2013;273(3):219-34.
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3. Dixon JB, Straznicky NE, Lambert EA, Schlaich MP, Lambert GW. Surgical
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4. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for the
In properly selected patients with clinically severe obesity,
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there is clear net benefit in terms of improved health surgery patient - 2013 update: Cosponsored by American Association of
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Int J Cardiol 2014;173(1):20-28.
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Authors 8. Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric-metabolic surgery
Phong Ching Lee MBChB, MRCP (UK), Consultant Endocrinologist, versus conventional medical treatment in obese patients with type 2
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algorithm for type 2 diabetes: A joint statement by International Diabetes
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13. Finks JF, Kole KL, Yenumula PR, et al. Predicting risk for serious complications
with bariatric surgery: Results from the Michigan Bariatric Surgery
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FOCUS
Clare Bayram, Lisa Valenti, Helena Britt
en’s health is often described in terms of male-specific 45-64 years and 65 years or older were compared. Data about
M (sexual and reproductive health) problems, but it is their

broader health behaviours and use of health services
that contribute to their overall health. Australian men have a
shorter life expectancy than women,1 and seven of the 10 most
patients’ regular general practice were gathered from June to
September 2013 from a SAND sub-study.7 The average use of
GP services in the population was calculated using Medicare
claims data (supplied by Australian Government Department
common risk factors that contribute to burden of disease are of Health) and Australian Bureau of Statistics (ABS) population
more common in men than women.2 These differences are data.8
driven by a combination of gender and biological influences.3
Men see general practitioners (GPs) less frequently than Results
women.4 A report describing GP consultations with male patients Use of GP services
using Bettering the Evaluation and Care of Health (BEACH) data In 2013-14, males in the Australian population were less likely
from 1999-2000 found that patterns of attendance and health to see a GP at least once (80% of males in the population)
problems managed differed across age groups. Younger men than females (88%; Figure 1). Males also had a lower average
(aged <40 years) were less likely than women to visit a GP, annual number of GP consultations per head of population (4.6)
and when they did attend, they tended to have acute illnesses, than females (6.1; Figure 2). While attendance patterns were
injuries and psychological problems managed. In middle age similar for male and female children, there were differences in
(40-64 years) chronic conditions began to emerge, particularly the older age groups, particularly in the 15-44 year age group,
musculoskeletal morbidities. For older men (>65 years), chronic where only 71% of men attended at least once (Figure 1) and
conditions were predominant.5 visited an average 3.1 times per head of population that year
In this study, we investigated men’s use of GP services by age (Figure 2).
(compared with women) to see whether patterns identified in
the previous study on their use of GP services and the types of Regular general practice
problems managed in different age groups have changed. Of the 7799 patients sampled in the SAND sub-study, 94.8% of
all males and 96.8% of all females had a general practice they
Method considered their regular practice. Men aged 15-44 years were
We analysed GP-patient encounters with male patients from significantly less likely to have a regular practice (87.3%; 95%
data collected in the BEACH program from April 2014 to March confidence interval [CI]: 84.4-90.3) than women of the same
2015. The methods of the BEACH program and supplementary age (94.3%; 95% CI: 92.9-95.7). For all other age groups, there
analysis of nominated data (SAND) sub-studies are described was no difference in the proportion of males and females who
in detail elsewhere.6 Encounters with men aged 15-44 years, had a regular practice.
© The Royal Australian College of General Practitioners 2016 afp vol.45, no.4, april 2016 171
FOCUS GENERAL PRACTICE ENCOUNTERS WITH MEN
Encounters with male patients (14.2%) problems. Depression and anxiety were the most common
In 2014-15, 42.9% of all encounters were with male patients. individual psychological problems managed, and back complaint and
Compared with those in older age groups (5.2% aged 45-64 years sprain/strain were the most common musculoskeletal problems.
and 2.3% aged 65+ years), male patients aged 15-44 years were Men aged 45-64 years most commonly had musculoskeletal
significantly more likely to be new to the practice (12.2%). These (14.0%), circulatory (12.7%), and general and unspecified (such
young men had high rates of new problems managed at encounters as check-ups; 12.4%) problems managed. The chronic conditions
(64.9 per 100 encounters) and this decreased significantly in each hypertension, diabetes, lipid disorders and depression were the
subsequent age group. By contrast, the number of problems and most common individual problems managed, together accounting
chronic problems managed per encounter increased with age. The for 17.7% of problems in this age group.
distribution of problems managed by body system is shown in Men aged 65 years and older had circulatory (20.2%), skin
Table 1. (12.0%), and general and unspecified (11.9%) problems commonly
Overall, respiratory, psychological and musculoskeletal problems managed. Hypertension (9%), diabetes (5%), osteoarthritis (3%) and
were more commonly managed in young men, whereas circulatory lipid disorders (3%) were the most common individual problems.
and endocrine/metabolic problems were more common among Male-specific problems (those classified as related to the genital
older men. system) accounted for a small proportion of all problems managed
Respiratory problems (in particular upper respiratory tract infection in men. These problems were more common at encounters with
[URTI], asthma and acute bronchitis) were the most common older men (3.3% of problems) than at those with men aged 45-64
types of problem managed in men aged 15-44 years (15.1% of years (2.9%) and 15-44 years (2.4%).
problems), followed by psychological (14.8%) and musculoskeletal
Discussion
Sex-specific changes in GP service use occur during adolescence.
While the majority of young women continue to have regular
contact with GPs, the same cannot be said for young men. For
women, this is likely to be due to the need for ongoing contact for
cervical cancer screening, contraception and reproductive issues.
Men in the 15-44 year age group are the least likely of all age-sex
groups in the Australian population to have seen a GP at least once
in a year, and have the lowest number of attendances per head of
population.
Lower attendance patterns do not necessarily indicate that young
men have a problem with access to GPs or that there is an unmet
need for services. It would be expected that younger men would
Age group (years) be healthy and have less need for GP services. However, our study
demonstrates that they are the least likely to have a regular general
Figure 1. Proportion of the population who saw a GP at least once by sex
practice and to have visited a GP. This picture is consistent with
and age groups, 2013-14
previous studies.4,5 Young men are also more likely than other age
sex groups to engage in risky behaviours, such as at risky alcohol
consumption and tobacco smoking.7,9 GPs should be mindful that
young men may not have established an ongoing relationship with
a GP or practice. Encouraging such a relationship is thought to
support continuity of care, disclosure of sensitive information and
optimal health outcomes.10,11
The types of problems GPs managed at encounters with
male patients changed with increasing patient age. The patterns
identified were similar to the results from the 1999-2000 study.5 In
the younger age group, acute conditions, injury and psychological
problems were common. From the age of 45 years onward, chronic
diseases start to emerge among the most common problems. For
older men, chronic diseases are the predominant types of problem
managed.
Figure 2. Average number of GP visits per head of population by sex and
age groups, 2013-14 Traditionally, discussion about men’s health focuses on male
specific problems. Men are encouraged to talk to their doctor
172 afp vol.45, no.4, april 2016 © The Royal Australian College of General Practitioners 2016
GENERAL PRACTICE ENCOUNTERS WITH MEN FOCUS
about their ‘tackle - those bits below the belt’.12 We applaud this, particularly in young men who are less frequent users of GP
but our study highlights that such problems account for a small services and may miss out on the benefits (such as prevention,
proportion of all problems dealt with in men in general practice. continuity of care and early diagnosis of disease) associated with
A holistic approach to men’s health would be beneficial, a having a regular practice.
Table 1. Encounters with male patients aged 15-44 years, 45--64 years and 65+ years, 2014-15
15-44 years 45-64 years 65+ years

(n = 10,958) (n = 11,629) (n = 13,195)
New to practice, per cent of patients 12.2 5.2 2.3

(95% CI) (11.1-13.2) (4.4-5.9) (1.9-2.7)
Problems managed, rate per 100 encounters 135.3 160.2 175.1

(95% CI) (132.8-137.8) (157.4-162.9) (171.9-178.3)
New problems, rate per 100 encounters 64.9 54.0 47.9

(95% CI) (62.6-67.2) (52.0-56.1) (46.1-49.8)
Chronic problems, rate per 100 encounters 35.8 69.3 87.8

(95% CI) (34.0-37.6) (66.7-71.8) (84.4-91.2)
Type of problem managed

*, per cent of problems managed (95% CI)
Respiratory 15.1 9.0 8.3

(14.1-16.1) (8.4-9.6) (7.8-8.8)
Psychological 14.8 9.9 4.9

(13.5-16.1) (9.2-10.6) (4.5-5.3)
Musculoskeletal 14.2 14.0 10.9

(13.4-15.0) (13.3-14.7) (10.3-11.4)
General & unspecified 13.1 12.4 11.9

(12.3-13.9) (11.6-13.2) (11.1-12.7)
Skin 13.1 10.7 12.0

(12.4-13.8) (10.0-11.4) (11.3-12.6)
Digestive 8.9 7.8 6.9

(8.3-9.5) (7.4-8.3) (6.5-7.3)
Endocrine & metabolic 5.4 11.7 10.8

(4.9-6.0) (11.0-12.3) (10.2-11.4)
Circulatory 3.9 12.7 20.2

(3.5-4.3) (12.1-13.4) (19.5-21.0)
Neurological 2.7 2.7 2.4

(2.4-3.0) (2.4-3.0) (2.2-2.7)
Ear 2.4 1.9 2.0

(2.1-2.7) (1.7-2.2) (1.8-2.2)
Male genital system 2.4 2.9 3.3

(2.1-2.7) (2.6-3.3) (3.1-3.6)
Eye 1.4 1.2 1.8

(1.1-1.6) (1.0-1.4) (1.6-1.9)
Urology 1.1 1.5 2.7

(0.9-1.3) (1.3-1.7) (2.4-2.9)
Blood 0.8 0.9 1.6

(0.6-1.0) (0.7-1.2) (1.3-1.9)
Social 0.6 0.6 0.3

(0.4-0.8) (0.4-0.7) (0.2-0.4)
*Types of problems are classified according to the International Classification of Primary Care, version 2 (ICPC-2)
© The Royal Australian College of General Practitioners 2016 afp vol.45, no.4, april 2016 173
FOCUS GENERAL PRACTICE ENCOUNTERS WITH MEN
Authors
Clare Bayram BAppSc (HIM) (Hons), PhD, Research Fellow and Project Manager,
BEACH program, Family Medicine Research Centre, Sydney School of Public
Health, Sydney Medical School, University of Sydney, Parramatta, NSW. clare.
bayram@sydney.edu.au
Lisa Valenti BEc, MMedStat, Senior Research Analyst, Family Medicine
Research Centre, Sydney School of Public Health, Sydney Medical School,
University of Sydney, Parramatta, NSW
Helena Britt BA, PhD, Professor of Primary Care Research, Director, Family
Medicine Research Centre, Sydney School of Public Health, Sydney Medical
School, University of Sydney, Parramatta, NSW
Acknowledgements
We wish to thank the general practitioners who participated for their generosity.
During the data collection period of this study, the BEACH program was
funded by the Australian Government Department of Health, AstraZeneca Pty
Ltd (Australia), Novartis Pharmaceuticals Australia Pty Ltd, bioCSL (Australia)
Pty Ltd, AbbVie Pty Ltd, Merck Sharp & Dohme (Australia) Pty Ltd, and the
Australian Government Department of Veterans’ Affairs. Funding organisations
had no editorial control over any aspect of this article.
References
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174 afp vol.45, no.4, april 2016 © The Royal Australian College of General Practitioners 2016
RESEARCH
Improving blood pressure control in

general practice: A pilot study of the
ImPress intervention
Nicholas Zwar, Oshana Hermiz, Elizabeth Halcomb, Patricia Davidson, Thomas Bodenheimer
Background and objectives ontrol of blood pressure has been shown to delay or
Patients with hypertension and at high absolute cardiovascular

disease risk are a priority group for improved blood pressure
control. This study examined the impact of an intervention,
C improve the outcome of a range of cardiovascular diseases
(CVDs).1 People at high absolute CVD risk, which includes
those who have already experienced a CVD event, have the
most to gain from improved blood pressure control.2 A large,
primarily delivered by the general practice nurse, to identify,
individual patient data meta-analysis concluded that lowering
recall and manage patients with uncontrolled hypertension who
blood pressure provides progressively greater absolute CVD risk
are at high risk of cardiovascular disease.
reduction as baseline risk increases,3 while the recently published
SPRINT study4 has further shown the benefits of blood pressure
Methods
control in people at high CVD risk.
A before-and-after pilot study with a six-month follow-up period In Australia, general practice is the key setting for interventions
was conducted in eight general practices in Sydney, Australia. to improve the management of hypertension, as this is
the context where hypertension is diagnosed and treated.
Results Hypertension is the most common problem managed at general
practice consultations, occurring at a rate of 9.1 problems per
From 507 patients identified, 82 (16.2%) attended an
100 encounters.5 However, blood pressure control, even in
assessment visit, were eligible and provided baseline data.
Of these, 55 (67.1%) completed the six-month follow-up. The people at high absolute CVD risk, is often not optimal and many
mean decrease in blood pressure was 14.5 mmHg systolic and people with hypertension have behavioural risk factors for CVD.
7 mmHg diastolic. Significant decreases were also found in The AusDiab survey found that the prevalence of hypertension
mean weight (1.3 kg), body mass index (0.5 kg/m2) and waist in the Australian population was 28.6%, with 13.4% treated with
circumference (1.9 cm). Adherence to blood pressure treatment, antihypertensive medicines.6 Of those on treatments, 60% had
as measured by the Hill-Bone scale, significantly improved a blood pressure >140/90 mmHg, 20% were obese, 31% had
(P = 0.01) diabetes, 29% had hyperlipidaemia, 27% were smoking, 23%
had excessive alcohol intake and 28% had insufficient physical
Discussion activity.6
The ImPress intervention is a systematic, population approach
The results of this study justify further investigation in a
tailored to primary care. It is geared to identifying, recalling,
randomised trial. If effective, the approach could alter the way
assessing and treating patients with known hypertension who
hypertension care is organised and delivered in Australian
general practice. are at high absolute CVD risk and whose blood pressure is
not treated to target. This intervention is novel as it targets
nurse-led care to those with the most to gain from improved
blood pressure and control of other CVD risk factors. This
complex intervention is based on the elements of the chronic
care model,7 with a focus on clinical information systems,
306 reprinted from afp vol.46, no.5, may 2017 © The Royal Australian College of General Practitioners 2017
IMPROVING BLOOD PRESSURE CONTROL RESEARCH
self-management support and delivery Potentially eligible patients were pressure (office measurement according
system design.8,9 ImPress is primarily identified and invited to an assessment to guidelines);1 body mass index (BMI),
delivered by the general practice nurse visit with the GPN via a search of practice waist circumference, and waist-to-hip ratio.
(GPN) in collaboration with the patient and desktop software using the Penn CS Treatment compliance measures were
the general practitioner (GP). The Australian Clinical Audit Tool. Criteria for invitation the Hill-Bone compliance to high blood
GPN workforce has grown exponentially, were: aged 45-74 years; active patients pressure therapy scale12 and the Morisky
with most general practices now employing according to The Royal Australian College medication adherence scale (MMAS-8).13
at least one registered nurse.10 The role of General Practitioners (RACGP) definition The Hill-Bone compliance to high blood
of the GPN is well suited to guideline (ie attended three or more times in pressure therapy scale assesses three
implementation, self-management support past two years); have a diagnosis of behavioural domains of high blood pressure
and supporting behaviour change.11 This hypertension recorded; are at high risk of treatment: reduced sodium intake;
pilot study examined the impact of the a CVD event (defined as five year absolute appointment keeping; and medication
ImPress intervention on blood pressure, risk >15% or the presence of CVD); and taking. This scale comprises 14 items in
anthropometric measures, treatment have uncontrolled hypertension. three subscales and is rated on a four-point
adherence and lifestyle behaviours. Uncontrolled hypertension was Likert-type scale. The eight-item MMAS-8
Qualitative feedback from GPNs, GPs and defined using criteria from the National has been used in hypertension and in a
patients involved in the study is being Heart Foundation (NHF) of Australia’s range of chronic illnesses. The first seven
reported separately. hypertension guidelines1 as patients items are Yes/No responses, and the last
without an associated condition(s) or item is a five-point Likert response. The
Methods end-organ damage where their most additional items focus on medication-taking
A before-and-after pilot study was recent manual office blood pressure behaviours, especially related to underuse.
conducted in general practices in measurement was >140/90 mmHg or, Smoking, nutrition, alcohol and physical
metropolitan Sydney. Practices were for those with an associated condition(s) activity (SNAP)14 health behaviour measures
selected for invitation to participate from or end-organ damage, the most recent were: self-reported smoking and alcohol
the membership of the University of New blood pressure measurement was use (based on questions from the New
South Wales (UNSW) practice-based >130/80 mmHg. Letters of invitation were South Wales Health Adult Health Survey
research network (PHReNet-GP). Practices sent to these patients; non-responders had 2002 and Australian Bureau of Statistics
were eligible to participate if they used one follow-up phone call from the GPN. National Health Survey 2001); dietary
Best Practice or Medical Director software, Outcome measures were collected assessment (fruit and vegetable; cereal and
employed a registered nurse, and both the by the GPN at baseline and follow-up cooked cereal; processed meat, hot and
nurse and GP were willing to participate in at six months. Physiological outcome crisp chips; cereal and cooked cereal; type
the study. measures were systolic and diastolic blood of milk consumed);15 and physical activity.16
Action plan preparation - two weeks Action plan implementation - five months
GPN visit GPN visit GPN visit GPN contacts (3) and GP visit(s)
Education in use of CAT Mentoring and intervention monitoring calls to practices.
Figure 1. Impress intervention based on 5As framework

GP, general practitioner; GPN, general practice nurse
© The Royal Australian College of General Practitioners 2017 reprinted from afp vol.46, no.5, may 2017 307
RESEARCH IMPROVING BLOOD PRESSURE CONTROL
Intervention
A one-day educational workshop was
held for GPNs. This workshop covered
the study rationale, study procedures,
blood pressure measurement, use of
study tools and collaborative care for
hypertension management. GPNs were
provided a template for a hypertension
management action plan, which covered
key issues in medicines adherence and
lifestyle modification. Templates were
also provided for the GPN assessment
visit, each of the GPN face-to-face and
telephone contacts and GP visits, as well
as a tool for tracking patient progress
throughout the intervention. All these
were made available in an automatically
pre-populating electronic format for use in
both Best Practice and Medical Director
software. The GPNs were also provided
a stepped algorithm for treatment
intensification from the NHF hypertension
guide.1
Two weeks after the GPN workshop,
a webinar was held with the nurses and
participating GPs to explain the aims of the
project to GPs, encourage commitment
to participation, agree on roles and
responsibilities, and discuss how progress
of the intervention would be monitored
in the practice. The intervention involved
an assessment visit, development of
the action plan and a series of contacts
with the GPN and GP for implementation
(Figure 1). The number of contacts was
tailored to individual patients’ needs.
Following the education workshops, the
nurses were contacted by one of the
investigators (EH) by telephone to provide
mentoring and monitor implementation of
the intervention.
Results
Practice recruitment for the study was
rapid, with 13 practices, of 32 approached,
responding; however, three practices
withdrew before patient identification
and invitation, and two further practices
withdrew at a later stage, leaving eight
practices that completed the project
(Figure 2, flowchart for recruitment Figure 2. Practice and patient recruitment flowchart
information and reasons for losses to
follow-up). Thirteen GPNs (mean age 43 most recent blood pressure measurement) uncontrolled hypertension. Of these, 82
years) and 14 GPs (mean age 52 years) was 125. From the patients identified, patients consented to be involved and
participated in the study. a random sample of 507 patients was provided baseline data. The mean age
The mean number of patients identified invited to attend the GPN assessment of participating patients was 62.5 ± 19.2
per practice with high CVD risk and visit. Of these, 118 (23%) attended and years and 62.2% were male. Details
uncontrolled blood pressure (based on the 85 (72.0%) were confirmed as having of participating patients’ demographic
characteristics are shown in Table 1.
Fifty-five patients (67.1%) provided
Tablel. Patient demographics (n = 82) follow-up data at six months. The mean
Patient characteristic Questions decrease in systolic blood pressure was
14.5 mmHg (95% confidence intervals
Age Mean (SD) 62.5 (19.2)
[CI]: -10.7, -18.2 mmHg) and diastolic
Sex Male - n (%) 51 (62.2)
7 mmHg (95% CI: -4.3, -10.7 mmHg).
Female - n (%) 31 (37.8) Significant decreases were also found in
Married or de facto Yes - n (%) 64 (78.0) mean weight (1.3 kg), waist circumference
No - n (%) 18 (22.0) (1.9 cm) and BMI (0.6 kg/m2). Adherence
to blood pressure treatment, as measured
Country of birth Australia - n (%) 40 (48.8)
by the Hill-Bone scale, significantly
Other - n (%) 42 (51.2)
improved (P = 0.01) and there was no
Language spoken at home English - n (%) 58 (70.7) significant change in medicines adherence
Other - n (%) 24 (29/3) as measured by the MMAS-8 (Table 2).
Aboriginal or Torres Strait Islander
* Yes - n (%) 2 (2.4) No significant change was found in SNAP
lifestyle behaviours, although there was a
No - n (%) 50 (61.0)
trend towards increased physical activity at
Completed high school or higher Yes - n (%) 57 (69.5)
follow-up (Table 3).
No - n (%) 25 (30.5)
In paid employment Yes - n (%) 26 (31.7) Discussion

No - n (%) 56 (68.3) The study found a substantial (14.5 mmHg,
*Missing n (%) = 30 (36.6)
95% CI: -10.7, -18.2 mmHg) reduction
in mean systolic blood pressure from
baseline to follow-up. This is larger than
Table 2. Physiological and treatment adherence outcomes reported in a meta-analysis that found
n = 55 unless otherwise stated that nurse-led interventions, including a
stepped treatment algorithm, reduced
P value for
Variable difference in systolic blood pressure by a weighted
Mean value Baseline Six months means
* mean difference of -8.2 mm Hg (95% CI:
Systolic blood pressure (mmHg) 149.2 134.7 <0.001 -11.5, -4.9).17 Our results are similar to the
findings of a study conducted in Australian
Diastolic blood pressure (mmHg) 88.1 80.6 <0.001
general practice, which examined the
Weight (kg) 88.5 87.1 0.001
impact of a program of management with
BMI (kg/m2)+ 31.2 30.7 0.002 four GP visits and use of a stepwise drug
Waist circumference (cm)* 106.0 104.2 0.034 titration algorithm.18 However, none of
Hip circumference (cm)§ 109.8 108.5 0.131 these studies was targeted to patients
at high CVD risk, which is a novel aspect
Waist-to-hip ratio| 0.96 0.96 0.636
of our approach. Our results suggest
Morisky Medication Adherence Score (SD)# 2.02 1.75 0.240
that the likely mechanism of the effect is
(1.78) (1.47) increased adherence to blood pressure
treatment. This interpretation is supported
Hill-Bone compliance scale (SD)** 19.8 18.9 0.01
by the improvement in adherence to
(3.10) (3.11) blood pressure treatment as measured
*Paired sample t-test only includes cases that have values at both follow-up points by the Hill-Bone scale. There was also
n = 47; sd, standard deviation
tn = 50; tn = 54; §n = 51; n = 51; #n = 53; **
a non-significant improvement in the
RESEARCH IMPROVING BLOOD PRESSURE CONTROL
MMAS-8. However, there could be a range recent measurement and may have emphasis on primary care and population
of other explanations for the change in identified some patients whose mean health approaches, the ImPress model of
blood pressure, including weight loss.1 blood pressure was within the target intervention shows promise.
It is also possible that a non-specific range.
Authors
(Hawthorne) effect related to receiving an The response to the invitation was
Nicholas Zwar MBBS, MPH, PhD, FRACGP,
intervention and/or regression to the mean 23% and there is a potential bias towards Professor of General Practice, School of Public
could account for some or all of the fall in participation by more motivated patients. Health and Community Medicine, UNSW; School
of Medicine, University of Wollongong, NSW.
blood pressure observed. How the weight It should be noted that a response rate n.zwar@unsw.edu.au
loss and decreased waist circumference of approximately 20% is similar to that Oshana Hermiz MBBS, Project Office, Centre for
were achieved is not clear from our found in a previous study of a mailed Primary Health Care and Equity, UNSW, NSW
Elizabeth Halcomb RN, BN (Hons), PhD, FRCNA,
results as there was no significant change invitation for a GPN intervention.19 Further
School of Nursing, University of Wollongong
observed in dietary behaviours or in the research is needed to identify strategies Patricia Davidson RN, BA, Med, PhD, Dean, School
level of physical activity. to increase uptake of proactive care in of Nursing, Johns Hopkins University, Baltimore,
USA
general practice. There is also a risk of bias
Limitations in the results due to loss of practices and,
Thomas Bodenheimer MD, Professor, Department
of Family and Community Medicine, University of
The major limitation of the study is the therefore, patients to follow-up. California, San Francisco, USA
uncontrolled before-and-after design. The Competing interests: None.
lack of a control group means we cannot Implications for general practice Provenance and peer review: Not commissioned,
be sure that the observed effects are The promising findings from this pilot
due to the ImPress intervention rather study of the ImPress intervention, Acknowledgements
than some other factor(s). There are also together with the positive feedback from We thank the patients, nurses and GPs who took
part in this project. Funding was from a National
questions about generalisability, given that GPs, GPNs and patients (authors’ own), Heart Foundation of Australia Vanguard Grant
it was a small sample of research-active justify further research in the form of a (award number 100246).
practices that may be more enthusiastic to randomised trial. If effective, the approach
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CLINICAL
Traumatic nasal injuries

in general practice
Joo H Koh, Osama Bhatti, Abbas Mahmood, Nicholas Agar
Background he nose is the most prominent and external carotid arteries. Venous
Traumatic nasal injuries are common

in all age groups of the community.
Significant nasal trauma can cause nasal
T feature projecting from the face and
is prone to injury arising from facial
trauma. Injury can occur in all age groups
and from a variety of causes, which may
drainage occurs anteriorly via the facial
vein and posteriorly via the pharyngeal
and pterygoid plexus. These pathways
lack internal valves, creating the risk of
fractures and a range of complicating
be either blunt or penetrating. The majority retrograde intracranial infection.1
injuries.
of injuries result in either bruising alone
or a simple nasal fracture. Nasal fractures Uncomplicated nasal
Objectives injuries
should be referred to ear, nose and throat
This article provides general (ENT) or maxillofacial services for prompt Nasal bones are the most commonly
practitioners (GPs) with a succinct reduction (ideally one to two weeks from fractured facial bones.2The mainstay of
overview of pathology arising from injury). assessment is a thorough history and
nasal trauma, and a framework on Complicated injuries include suspected physical examination. Important aspects
the assessment and management of facial fractures, full thickness lacerations, of history include injury mechanism, if
common nasal injuries. septal haematoma, septal abscess and there was immediate deformity (prior to
cerebrospinal fluid (CSF) leak. It is critical soft tissue swelling), and new-onset nasal
Discussion that these are recognised early and obstruction. It is also important to note
During assessment of traumatic nasal managed appropriately in primary care. any previous nasal injury or pre-existing
injuries, it is essential to exclude a deformity.
septal haematoma, which requires Anatomy Physical examination involves assessing
urgent drainage. Undisplaced nasal The nose can be subdivided into thirds. the degree of bony deformity by
fractures without functional symptoms The upper third is made up of the paired inspection and palpation, and excluding
can be managed conservatively. nasal bones, which are attached to
Displaced fractures should be referred the frontal bones superiorly, forming
for reduction. There is a window of two a pyramid-shaped bony vault. The
weeks before the displaced nasal bones perpendicular plate of the ethmoid fuses
start uniting. Investigations are rarely with the nasal bones on the inner aspect,
indicated for traumatic nasal injuries. providing additional support. The middle
Blood tests, including full blood count
third is composed of the quadrilateral
and coagulation screening, may be
cartilage of the septum in the midline and
indicated in severe epistaxis. X-rays
the upper lateral cartilages laterally. The
are not helpful for the assessment of
lower third contains fibrofatty soft tissues
traumatic nasal injuries. Computed
of the nasal tip, supported by the lower
tomography (CT) scans are only
lateral (alar) cartilages (Figure 1).
indicated if there is a suspected orbital,
maxillary, frontal or zygomatic fractures. The nerve supply is from the
ophthalmic and maxillary divisions of the
Figure 1. Anatomical illustration of nasal bones
trigeminal nerve. Blood supply to the and cartilages
nose has contributions from the internal
650 afp vol.45, no.9, september 2016 © The Royal Australian College of General Practitioners 2016
TRAUMATIC NASAL INJURIES CLINICAL
features of a complicated nasal injury.2 time frame for reduction is three to five persistent bleeding may have associated
Soft tissue oedema arises within hours days after the injury, and early referral nasoethmoid orbital fracture. In these
of injury and may significantly affect to an ENT service is needed.6 In very circumstances, proper technique prevents
assessment. frail patients, or patients with advanced intracranial placement of a nasal pack.
Plain X-ray investigations are frequently dementia who have nasal fractures with To facilitate nasal packing, there is a
inaccurate and generally do not contribute only minor cosmetic change, it is prudent range of commercial products available,
to the assessment of nasal injuries. False to discuss the option of leaving the fracture with Merocel and Rapid Rhinos commonly
positive results can occur from previous to unite, albeit with slight deformity used in Australia. Merocel (Medtronic,
injuries, prominent vascular markings or remaining. This is often more appropriate to Minneapolis) is a nasal tampon that
suture lines, whereas cartilaginous injuries avoid further discomfort and potential harm expands with saline and is efficient for
can cause a false negative result.3 from anaesthetic agents. anterior packing.10 Rapid Rhino (AthroCare,
Austin) is a balloon device available in
Cartilage deformity Complications of nasal sizes suitable for anterior and posterior
If the nasal bones are midline but a injury packing.10 Rapid Rhinos are soaked in
cartilaginous septal deformity exists, Lacerations sterile water before insertion into the
these injuries are non-reducible acutely as Traumatic lacerations of the nose are nasal cavity. Once inserted, the attached
the tissues spring back to their deformed common. Debride and irrigate the wound balloon can be inflated with air to increase
state. It is appropriate to exclude a septal well before closure.7 Most skin lacerations the volume and pressure of packing. Rapid
haematoma. If there is persisting nasal without involvement of cartilage or Rhinos are found to be more comfortable
obstruction after one month of the injury, mucosa can be repaired with 6-0 non than Merocel.10
patients can be referred to ENT outpatient absorbable monofilament sutures. Place If commercial nasal packing is not
services for consideration of elective sutures with small bites as nasal skin has available, anterior nasal packing can still be
septoplasty. little redundancy and poor flexibility.8 Refer achieved with layered insertion of ribbon
deeper lacerations involving cartilage or gauze soaked in petroleum jelly (Vaseline).
Uncomplicated nasal fracture mucosa to ENT or plastics services on Alternatively, intranasal insertion of cotton
Nasal fractures are generally managed the same day. Selected lacerations that pledgets soaked in tranexamic acid has
with closed reduction under local or are clean and have well-opposed edges been shown to be effective treatment for
general anaesthesia. The choice of may be closed with tissue adhesives, anterior epistaxis.11 In suspected posterior
anaesthesia does not affect the success particularly in children.7 Determine and epistaxis, a Foley catheter is advanced into
rate.4 Whenever possible, patients update tetanus immunisation status. the posterior oropharynx, then inflated.
with suspected nasal fractures should The anterior nasal cavity can then be
be referred to an ENT service. Closed Epistaxis packed with Vaseline gauze. This packing
reduction should be performed once Epistaxis is common with nasal injuries method can be secured in place with a
oedema resolves, ideally within 10-14 days caused by trauma to the nasal mucosa and clamp over the gauze.10
of the injury. vessels. To administer first aid, the nose All patients with nasal packing
In remote areas that do not have timely should be held firmly with the thumb and should be placed on oral antibiotics
access to ENT services, appropriately forefinger, closing the nostrils. The head is (eg amoxicillin, cephalexin) to prevent
skilled general practitioners (GPs) may tilted forwards and the patient instructed toxic shock syndrome.10 These patients
perform closed reduction under local to spit rather than swallow the blood. should be referred promptly to ENT
anaesthesia in a compliant adult patient. A Continue pressure for 10-20 minutes.9 services for admission as there is a risk
local anaesthetic, such as lignocaine with If available, vasoconstrictors such as of inadvertently dislodging the nasal pack
adrenaline, is effective when administered cophenlycaine may slow or stop bleeding. into the oropharynx. The nasal packs are
into the root of the nose and lateral aspect Patients with haemodynamic instability or left in situ for three to five days to facilitate
of the bones.4 Severe injuries with gross persistent bleeding (particularly patients mucosal healing.10
external deformities or compound nasal taking anticoagulant agents) should be
fractures require early surgical intervention referred to the emergency department. Septal haematoma and abscess
and should be referred to the emergency Nasal packing may be required to Nasal septal haematomas occur as a
department immediately.2 stabilise a patient for transfer. It is significant complication of nasal trauma
Paediatric patients have incomplete essential to ensure these are placed in 2% of nasal injuries.12 Blood vessels
ossification of nasal bones and a greater horizontally along the floor of the in the overlying mucoperichondrium
proportion of nasal cartilage; hence, they nose. Nasal packing should not be supply the septal cartilage, which can be
are prone to greenstick injuries.5 The ideal directed superiorly as patients with injured resulting in formation of septal
© The Royal Australian College of General Practitioners 2016 afp vol.45, no.9, september 2016 651
CLINICAL TRAUMATIC NASAL INJURIES
haematoma. If left undrained, a septal Septal abscesses are a delayed

haematoma can develop into a septal complication of nasal trauma. It is
abscess or lead to ischaemic necrosis of common to have progressive worsening
the septal cartilage in a delayed manner bilateral nasal obstruction with increasing
and subsequent saddle nose deformity.12,13 pain, headache and malaise. There may
Septal abscesses can result in meningitis, be fevers and purulent nasal discharge.
intracranial abscesses and cavernous Examination findings are similar to septal
sinus thrombosis because of the valveless haematomas. Assessment should include
venous drainage pathways creating an vital signs and neurological examination.13
intracranial entry point.13 Nasal septal haematomas and abscesses
Figure 2. Clinical photograph showing septal
On examination, nasal septal require intravenous (IV) antibiotics and haematoma in a paediatric patient
haematomas show bilateral septal urgent drainage, and the patient should be
swelling obstructing the nasal airway, referred to the emergency department.
which is boggy on palpation with a blunt
Cerebrospinal fluid rhinorrhoea
instrument (Figure 2). This is in contrast to can result from fracture and associated
a cartilaginous deformity (convex in one The presence of thin, clear rhinorrhoea dural tear of the cribriform plate in the
nostril, concave in other) with a firmness after nasal trauma should be considered anterior skull base.9 The time frame for
to palpation. CSF leak until proven otherwise. This presentation can range from two days to
Table 1. Clinical features and assessment of facial fractures associated with traumatic nasal injuries15,16
Fracture type Assessment essentials Key assessment findings Key points/management
Mandibular fracture • Palpate mandible • Trismus • Second most frequent fractured facial bone
• Inspect mandible dentition • Malocclusion • Angle and body most common fracture site
• Assess mouth occlusion • Chin numbness (mental • Refer for CT facial bones and maxillofacial
nerve injury) services (within 24 hours)
Zygomaticomaxillary • Palpate zygoma and maxilla • Mid-face numbness • Fractures may involve lateral orbital wall,
complex fracture • Intraoral and intranasal examination • Malar depression zygomatic arch, anterior or lateral maxillary sinus
wall, or orbital floor
• Visual acuity and range of eye • Enopthalmus
movement • Trismus • Refer for CT facial bones and maxillofacial
• Mid-face sensation services (within 24 hours)
• Malocclusion
• Ophthalmology review for visual symptoms or
orbital injury
Frontal fracture • Palpate frontal bar • Forehead lacerations • Prone to injury due to anatomic position
• Assess forehead sensation • Forehead numbness • CT facial bones and sinuses
• Visual acuity • Epistaxis • Be wary of intracranial complications
• Assess for CSF leak • Rhinorrhoea • Delayed complications include CSF leak and
frontal sinusitis
Orbital fracture • Palpate orbital rims • Visual changes • Essential to document visual acuity and range of
• Examine eyelids and globe position • Forehead/mid-face eye movements
• Visual acuity and range of eye numbness • CT facial bones and sinuses
movement • Enophthalmos • Ophthalmology review for visual symptoms or
• Forehead sensation • Chemosis orbital injury (within 24 hours)
• Sub-conjunctival
haemorrhage
Nasoethmoid orbital • Palpate nasal bones • Posterior displacement of • Prone to injury in high-velocity mid-facial trauma
fracture • Visual acuity nasal pyramid • Nasoethmoid orbital fractures can be minimally
• Examine eyelids and globe position • Telecanthus displaced
• Palpate and exert pressure on • Enophthalmos • Mobility or crepitus on palpation is abnormal
medial orbital rim • Epiphora • Refer for CT facial bones and maxillofacial
services (within 24 hours)
CSF, cerebrospinal fluid; CT, computed tomography
652 afp vol.45, no.9, september 2016 © The Royal Australian College of General Practitioners 2016
TRAUMATIC NASAL INJURIES CLINICAL
three months post-injury.14 Typically, there Training Supervisor - Southern GP Training, Corio 14. Gonen L, Monteiro E, Klironomos G, et al.
Bay Medical Centre, Corio, Vic Endoscopic endonasal repair of spontaneous and
is a positional element to the rhinorrhoea,
Nicholas Agar MBBS, FRACS (OHNS), ENT Surgery traumatic cerebrospinal fluid rhinorrhea: A review
occurring when patients lower their head Consultant, Barwon Health, Geelong, Vic and local experience. Neurosurg Clin N Am
forwards. 2015;26(3):333-48.
15. Chi JJ, Alam DS. Facial trauma: Evaluation
If CSF rhinorrhoea is suspected, a few Provenance and peer review: Not commissioned, and management. In: Cameron J, Cameron A,
drops of the fluid should be collected and editors. Current surgical therapy. 11th edn.
Philadelphia: Elsevier Saunders, 2014; p. 1070-81.
sent for beta-2-transferrin assay, which is References 16. Sargent LA. Nasoethmoid orbital fractures:
specific for CSF.14 These patients should 1. Stevens MR, Emam HA. Applied surgical Diagnosis and treatment. Plast Reconstr Surg
be transferred immediately to a hospital anatomy of the nose. Oral Maxillofacial Surg Clin 2007;120(7 Suppl 2):16-31S.
N Am 2012;24(1):25-38.
with ENT and neurosurgery support for
2. Mondin V, Rinaldo A, Ferlito A. Management
further management. of nasal bone fractures. Am J Otolaryngol
2005;26(3):181-85.
Nasal injury with 3. Oluwasanmi AF, Pinto AL. Management of nasal
trauma - Widespread misuse of radiographs.
facial fracture British J of Clin Gov 2000;5(2):83-85.
Traumatic nasal injuries with high 4. Atighechi S, Baradaranfar MH, Akbari SA.
Reduction of nasal bone fractures: A comparative
force trauma should be suspected for study of general, local and topical anesthesia
concomitant facial fractures. Computed techniques. J Craniofac Surg 2009;20(2):382-84.
5. Renner GJ. Management of nasal fractures.
tomography (CT) imaging should be
Otolaryngol Clin North Am 1991;24(1):195-213.
ordered and these patients referred 6. Desrosiers AE, Thaller SR. Pediatric nasal
to plastics or maxillofacial services for fractures: Evaluation and management. J
Craniofac Surg 2011;22(4):1327-29.
assessment if indicated. Table 1 provides a
7. Lawton B, Hadj A. Laceration repair in children.
summary of associated facial fractures. Aust Fam Physician 2014;43(9):600-02.
8. Trott A. Wounds and lacerations. 4th edn.
Conclusion Philadelphia: Saunders, 2012; p. 137-60.
9. Weller MD, Drake-Lee AB. A review of nasal
Traumatic nasal injuries encompass a trauma. Trauma 2006;8(1):21-28.
wide range of potential complications, 10. Kasperek Z, Pollock G. Epistaxis: An overview.
Emerg Med Clin North Am 2013;31(2):443-54.
where prompt recognition and timely
11. Zahed R, Moharamzadeh P, Alizadeharasi S,
management are key to good functional Ghasemi A, Saeedi M. A new and rapid
and aesthetic outcomes. method for epistaxis treatment using
injectable form of tranexamic acid topically: A
randomized controlled trial. Am J Emerg Med
Authors
2013;31(9):1389-92.
Joo H Koh MBBS, DipSurg. Anatomy, ENT 12. Elcock M. Nasal septal haematomas: A case
Service Registrar, Barwon Health, Geelong, Vic. series and literature review. Emerg Med
joohoekoh@gmail.com 1999;11(1):41-44.
Osama Bhatti MBBS, General Practice Registrar, 13. Alshaikh N, Lo S. Nasal septal abscess in
Southern GP Training, Corio Bay Medical Centre, children: From diagnosis to management and
Corio, Vic prevention. Int J Pediatr Otorhinolaryngol
Abbas Mahmood MBBS, FRACGP, GP Consultant, 2011;75(6):737-44. correspondence afp@racgp.org.au
© The Royal Australian College of General Practitioners 2016 afp vol.45, no.9, september 2016 653
The Royal Australian The RACGP Healthy Profession
College of General National Faculty of Aboriginal
and Tones Strait Islander Health Healthy Australia.
Practitioners
Working Together
An introduction to Aboriginal
and Torres Strait Islander
health cultural protocols and
perspectives
An introduction to Aboriginal and Torres Strait Islander health
cultural protocols and perspectives
Disclaimer
The information set out in this publication is current at the date of first
publication and is intended for use as a guide of a general nature only and
may or may not be relevant to particular patients or circumstances. Nor
is this publication exhaustive of the subject matter. Persons implementing
any recommendations contained in this publication must exercise their
own independent skill or judgement or seek appropriate professional
advice relevant to their own particular circumstances when so doing.
Compliance with any recommendations cannot of itself guarantee
discharge of the duty of care owed to patients and others coming into
contact with the health professional and the premises from which the
health professional operates.
While the text is directed to health professionals possessing appropriate

qualifications and skills in ascertaining and discharging their professional
(including legal) duties, it is not to be regarded as clinical advice and,
in particular, is no substitute for a full examination and consideration of
medical history in reaching a diagnosis and treatment based on accepted
clinical practices.
Accordingly The Royal Australian College of General Practitioners

and its employees and agents shall have no liability (including without
limitation liability by reason of negligence) to any users of the information
contained in this publication for any loss or damage (consequential
or otherwise), cost or expense incurred or arising by reason of any
person using or relying on the information contained in this publication
and whether caused by reason of any error, negligent act, omission or
misrepresentation in the information.
Published by:
College House
1 Palmerston Crescent
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Australia
Tel 03 8699 0414
Fax 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-332-3
Published May 2012
© The Royal Australian College of General Practitioners 2012. All rights reserved.
The Royal Australian TheRACGP
National Faculty of Aboriginal
College of General
and Torres Strait Islander Health
Practitioners Working Together
An introduction to Aboriginal
and Torres Strait Islander
health cultural protocols and
perspectives
Healthy Profession. The RACGP
Healthy Australia. An introduction to Aboriginal and Torres Strait Islander health cultural protocols and perspectives
Acknowledgements
The National Faculty of Aboriginal and Torres Strait Islander Health would
like to thank the many people who provided advice and feedback during
the development of this publication. In particular, we would like to thank:
• Dr Elizabeth Hindmarsh, past Board member, National Faculty of
Aboriginal and Torres Strait Islander Health
• Mr Alan Brown, Board member, National Faculty of Aboriginal and Torres
Strait Islander Health
• Associate Professor Dennis McDermott, Flinders University
• Professor Jenny Reath, Deputy Chair, National Faculty of Aboriginal and
Torres Strait Islander Health
• Dr John Scopel, Board member, National Faculty of Aboriginal and
Torres Strait Islander Health
• Dr Keith Gleeson, member, Australian Indigenous Doctors Association
• Ms Marianne Gleeson
• Des Martin and Sharon Busby, Aboriginal Health Council of Western
Australia (AHCWA).
We also drew from resources that are made available free of charge by
several organisations, and acknowledge the contribution of:
• The NSW Department of Community Services, for its publication Working
with Aboriginal people and communities, available at www.health.nsw.
gov.au/pubs/2004/pdf/aboriginal_terms.pdf
• Community Cultural Development NSW, whose report Respect,
acknowledge, listen (2004) is available on the Australian Indigenous
health InfoNet website at www.healthinfonet.ecu.edu.au/key-resources/
promotion-resources?lid=4119
• The Queensland Government, for the report Protocols for consultation
and negotiation with Aboriginal people, available at www.atsip.qld.gov.au/
everybodys-business/protocols-aboriginal.
The publication was developed by Jill Dixon, National Advisor, and Lauren
Cordwell, Manager, of the RACGP National Faculty of Aboriginal and Torres
Strait Islander Health.
The RACGP Healthy Profession.
An introduction to Aboriginal and Torres Strait Islander health cultural protocols and perspectives Healthy Australia.
Contents
Introduction 1
Background 1
Purpose 2
Torres Strait Islander peoples 2
Overview 2
How to use this resource 3
Related documents 3
Definitions 4
Aboriginal and Torres Strait Islander history, and why it matters 6
Aboriginal Australia map 7
Before colonisation 8
Colonisation 9
Protectionism 12
Assimilation 14
The referendum 15
Self determination 15
Native title 16
Northern Territory intervention 16
Close the Gap 18
The national apology 19
Core principles for working with Aboriginal and Torres Strait

Islander people 20
Understanding culture 20
Core principles 22
Protocols for culturally respectful engagement with Aboriginal

and Torres Strait Islander people 25
Describing Aboriginal and Torres StraitIslander people 25
Deceased people 25
A death in a community 25
Permission: for what, whom and how long 26
Depictions of people who have died 26
Smoking ceremony 27
‘Avoidance’ behaviour 27
Culturally appropriate communication 28

The importance of culturally appropriate, nondiscriminatory and
accurate language 28
Healthy Profession. The RACGP
Nonverbal communication 28
Verbal communication 29
Terms used to describe Aboriginal andTorresStrait Islander people 31
Terms describing communities 35
Consulting with Aboriginal and Torres StraitIslander communities 38

Five levels of engagement 38
Respectful consultation 39
Conducting meetings with Aboriginal and Torres Strait Islander

organisations and groups 42
Preparation and groundwork 42
Planning the meeting 43
Conducting the meeting 43
After the meeting 44
The Aboriginal community controlledhealthsector 44
Use of Aboriginal and Torres Strait Islander intellectual and

cultural property 48
Recognition and protection under the law 48
Respecting Aboriginal and Torres Strait Islander intellectual and
cultural property 48
Representations of Aboriginal and Torres Strait Islander people
and stereotyping 49
Event planning: Observation of Aboriginal and Torres Strait

Islander cultural protocols 51
Minimum requirements 51
Welcome to Country 52
Acknowledgement of Country 53
The Aboriginal and Torres Strait Islander flags 54
Use of the flags 55
Purchase of corporate gifts 55
Undertaking projects and research 56

‘Nothing about us, without us’ 56
Resources 59
Additional reading 59
Useful websites 60
References 61
Healthy Profession.
Healthy Australia.
The RACGP
An introduction to Aboriginal and Torres Strait Islander health cultural protocols and perspectives 1
Introduction
Background
In its 2010 position statement on Aboriginal and Torres Strait Islander health,1
the Royal Australian College of General Practitioners (RACGP) acknowledges
that improving the health of Aboriginal and Torres Strait Islander people is
one of Australia’s highest health priorities. The RACGP encourages all general
practitioners (GPs) to develop an understanding of Aboriginal and Torres Strait
Islander culture, history and health, and to incorporate this into their professional
practice, through a holistic, comprehensive, primary healthcare team-based
approach. The RACGP also calls on Australian GPs to challenge racism,
especially in the context of general practice.
Building strong working relationships with Aboriginal and Torres Strait Islander
individuals, communities and organisations is fundamental to your ability to work
effectively to improve Aboriginal and Torres Strait Islander health. Not only do
you enhance your awareness of health and culture, you can also learn about the
issues faced by the local community, the skills and experiences they possess
and the services they provide to the Aboriginal and Torres Strait Islander
community.
Many Aboriginal and Torres Strait Islander groups and organisations are eager
to form relationships with non-Indigenous counterparts or stakeholders and
many of these relationships can lead to fruitful partnerships to enhance health
outcomes for the whole community.
To build these relationships, RACGP staff and members need to have a sound
understanding of Aboriginal and Torres Strait Islander culture, history and
health, so that they can act with sensitivity and respect when dealing with the
variety of issues that affect the health outcomes of Aboriginal and Torres Strait
Islander Australians.
A strong culture is central to strong health and wellbeing among Aboriginal
and Torres Strait Islander people. Policies and procedures within the RACGP
need to reflect an understanding of this culture as a first step towards building
an environment that is supportive of staff and members acting in a culturally
sensitive manner. The adoption of cultural safety as a policy tenet by an
organisation builds the overall capability of that organisation to positively
affect health outcomes. It harnesses self reflection on one’s own cultural
underpinnings and awareness of the power relationships inherent in health
profession settings, enabling development, over time, of greater competence
and ease in working with Aboriginal and Torres Strait Islander people. It
supports RACGP staff and members to act in culturally appropriate ways.
Working towards such an environment will make the RACGP’s work more
effective, and thus have an indirect, but important, impact on health services
for Aboriginal and Torres Strait Islander people. All staff will be better placed
to support RACGP members to enhance their cultural awareness and develop
culturally safe practice or service environments for Aboriginal and Torres Strait
2 The RACGP
An introduction to Aboriginal and Torres Strait Islander health cultural protocols and perspectives
Healthy Profession.
Healthy Australia.
Islander people. It will also assist Aboriginal and Torres Strait Islander people to
feel confident in working with, and within, the RACGP, thus allowing the RACGP
to directly incorporate Aboriginal and Torres Strait Islander perspectives within
its policies and activities, as well as reflect upon the proportion of Indigenous
Australians within its workforce.
Purpose
This document provides a guide to appropriate and respectful behaviour with
Aboriginal and Torres Strait Islander people. It is intended to give RACGP
members and staff background information and guidance on Aboriginal and
Torres Strait Islander perspectives, along with an understanding of important
protocols and other relevant cultural issues. It can be used to guide the
RACGP’s overall engagement with Aboriginal and Torres Strait Islander people,
communities and organisations in the improvement of their health and wellbeing.
Because Aboriginal and Torres Strait Islander beliefs and practices differ
according to variables such as location and culture, the guidelines and protocols
cannot apply to every community or to every situation. Members and staff are
therefore strongly encouraged to seek additional information regarding specific
local communities. Where a staff member or GP has considerable dealings with
Aboriginal and Torres Strait Islander people and their health issues, the RACGP
strongly recommends that appropriately recognised cultural safety training is
undertaken.
This document is the start of the journey, not the end. It can be used as an
adjunct to other cultural awareness raising or cultural safety training activities,
including supporting staff undertaking related education and training.
Torres Strait Islander peoples

These protocols and guidelines are inclusive of Torres Strait Islander people
living in integrated communities on mainland Australia. They do not cover
protocols for visiting the 18 communities in the Torres Strait Islands and the two
Torres Strait communities on the Northern Peninsula of Australia (northern tip of
Cape York), Bamaga and Seisia.
Protocols for visiting these communities are different from those described in
this document and can be accessed on the Torres Strait Regional Authority
website at www.tsra.gov.au/publications/tsra-cultural-policy.aspx.
Overview
The RACGP National Faculty of Aboriginal and Torres Strait Islander Health
Introduction to Aboriginal and Torres Strait Islander health cultural protocols and
perspectives is intended to provide for RACGP staff and members:
• a historical, political and cultural context for working with Aboriginal and
Torres Strait Islander people
• core principles to guide behaviour and communication
Healthy Profession.
Healthy Australia.
The RACGP
• cultural protocols that may impact on RACGP business processes and

that can better inform the RACGP’s position on Aboriginal and Torres Strait
Islander health
• guidelines for consulting, meeting with and conducting research involving
Aboriginal and Torres Strait Islander people, including the use of intellectual
and cultural property.
How to use this resource

This document starts with the general and moves to the particular. Readers
are strongly urged to read sections 1-6, which provide an overview of
Aboriginal and Torres Strait Islander history, outline core RACGP principles
and protocols for engaging with Aboriginal and Torres Strait Islander people
and/or organisations, and present basic guidelines for verbal and nonverbal
communications.
The next sections address specific forms of engagement, listed below. RACGP
staff or members who are planning any of these forms of engagement should
first familiarise themselves with the introductory sections 1-6 before moving to
the sections covering the specific action they wish to take.
• Consulting with Aboriginal and Torres Strait Islander communities
• Conducting meetings with Aboriginal and Torres Strait Islander organisations
• Using Aboriginal and Torres Strait Islander intellectual or cultural property
• Observing cultural protocols when planning events
• Undertaking research into Aboriginal and Torres Strait Islander health
Related documents
The RACGP recommends that this document be read in conjunction with other
RACGP publications that reflect official RACGP policy. They include:
• RACGP Cultural safety policy
• RACGP Welcome to country policy and Acknowledgement of country policy
These policies are available on the website of the National Faculty of Aboriginal
and Torres Strait Islander Health at www.racgp.org.au/aboriginalhealth.
Consult the Resources section at the end of this document for more resources.
4 The RACGP
Healthy Profession.
Healthy Australia.
Definitions
Aboriginal and Torres Strait Islander health workers: Employed in many

health services working with Aboriginal and Torres Strait Islander communities.
They provide clinical or primary healthcare for individuals, families and
community groups; deal with patients and visitors at hospitals and health clinics;
and assist in arranging, coordinating and providing healthcare in Aboriginal and
Torres Strait Islander community health clinics. Very often they are the key link
between non-Indigenous health professionals and the local community, and
provide considerable cultural education to practice staff.
Assimilation Policy: The 1961 Native Welfare Conference noted: ‘The policy of
assimilation means in the view of all Australian governments that all aborigines
and part-aborigines are expected eventually to attain the same manner of living
as other Australians and to live as members of a single Australian community
enjoying the same rights and privileges, accepting the same responsibilities,
observing the same customs and influenced by the same beliefs, hopes and
loyalties as other Australians. Thus, any special measures taken for aborigines
and part-aborigines are regarded as temporary measures not based on colour
but intended to meet their need for special care and assistance to protect them
from any ill effects of sudden change and to assist them to make the transition
from one stage to another in such a way as will be favourable to their future
social, economic and political advancement’.2
Colonisation: ‘To settle among and establish control over (the Indigenous
people of) an area’.3
Culture: ‘Accepted and traditionally patterned ways of behaving ... a common
understanding shared by the members of a group or community. It includes
land, beliefs and spirituality, language, ways of living and working, artistic
expression, relationships and identity.’4
Cultural safety: ‘The outcome of education that enables safe services to
be defined by those who receive the service.’5 Unsafe cultural practice is ‘any
action which diminishes, demeans or disempowers the cultural identity and
wellbeing of an individual’.6
Lore: ‘Knowledge gained through tradition or anecdote.’7
Native title: The official recognition under federal Australian law of the
traditional rights and interests of Aboriginal and Torres Strait Islander people in
relation to land and water.8
Protectionism: A range of practices and beliefs about how Indigenous people
should be ‘managed’ by governments and their institutions, which were in place
from the 1850s to the mid-1900s. Different state and territory laws established
protection boards and native affairs departments that managed the protection/
segregation of a considerable number of Indigenous people.9
Self determination: The right of all peoples to ‘freely determine their political
status and freely pursue their economic, social and cultural development’.10
Healthy Profession.
Healthy Australia.
The RACGP
Sorry business: Walpiri English term for the rituals performed when a death
has occurred.11
Stolen Generations: Coined by the Canberra-based historian Peter Read,
who became aware of the large number of Indigenous children removed from
their families and communities through much of the 20th century, many in ways
which could only be described as stealing or kidnapping. Upon the release
of the National Inquiry (or ‘Bringing them home’) report the media coined the
term to describe the Indigenous people and others who told their stories to the
Inquiry.12
Terra nullius: A Latin term meaning ‘not inhabited’ or ‘empty land’.13
6 The RACGP
Healthy Profession.
Healthy Australia.
Aboriginal and Torres Strait Islander history,

and why it matters
Learning about Aboriginal and Torres Strait Islander history has not been a
priority in many Australian schools and what has been taught about this period
has often been from the European settler or explorer perspective, starting with
Captain Cook. More recent historical accounts of the experiences of Aboriginal
and Torres Strait Islander people after colonisation have often been derided as
the ‘black armband’ view of history.
It is important to become aware of this history, because it has had a significant
impact on previous and current generations of Aboriginal and Torres Strait
Islander people. It is equally important to understand government policies
in relation to Aboriginal and Torres Strait Islander people. From shortly
after colonisation until the present day, many policies covering Aboriginal
and Torres Strait Islander people have been enacted by state and federal
governments. These policies have often had significant and long lasting adverse
consequences for Aboriginal and Torres Strait Islander communities and can
continue to influence perceptions, behaviours and health outcomes to this day.
It is only with this understanding that we can appropriately engage with current
generations of Aboriginal and Torres Strait Islander people.
The history of abuse of Aboriginal and Torres Strait Islander people’s
human rights by government authorities and those who participated in the
implementation of government policies described below has given rise to
ongoing fear and mistrust of government by Aboriginal and Torres Strait Islander
people. Consequently they may be fearful and suspicious of people from certain
occupational groups (such as police, welfare workers, doctors and teachers),
whose intentions may now be quite different.
The events and policies described in this section caused great intergenerational
trauma - trauma that reverberates not only across communities but across the
generations - and led to disadvantage in people and communities today. The
long term effects of such traumatic events such as separation and removal from
family (described later) are complex, and are experienced differently by different
people. However, we know that the effects of such removal were ‘multiple,
continuing and profoundly disabling’,14 and left several generations of Aboriginal
people traumatised for life.
Many Aboriginal and Torres Strait Islander people alive today experienced this
trauma, either directly (eg. by being a member of the Stolen Generations) or
indirectly (eg. by being a child, parent, sibling or other relation to a member
of the Stolen Generations, or a descendant of a community that suffered
massacres at the hand of colonists).
Many people in the Northern Territory feel that the current ‘Northern
Territory intervention’ (Northern Territory Emergency Response) has severely
disadvantaged their community. The NTER has generated strong and varied
reactions among Aboriginal people and in that respect has had a very divisive
effect.
Healthy Profession.
Healthy Australia.
The RACGP
This section briefly discusses key periods in history, government policies, and
their meaning for Aboriginal and Torres Strait Islander people, and implications
for engaging with Aboriginal and Torres Strait Islander Australians.
Aboriginal Australia map

The ‘Aboriginal Australia’ map (Figure 1) indicates the general location
of groupings of Aboriginal and Torres Strait Islander people in Australia
and demonstrates the diversity of the communities that make up the First
Australians. The red lines show regional boundaries. The different colours show
different language groups. These often cross over state and territory borders.
David R Horton, creator. © Aboriginal Studies Press, AIATSIS and Auslig/Sinclair, Knight, Merz,
1996. Reproduced with permission.
This map is just one representation of many other map sources that are available for Aboriginal
Australia. Using published resources available between 1988-1994, this map attempts to
represent all the language or tribal or nation groups of the Indigenous people of Australia.
It indicates only the general location of larger groupings of people which may include smaller
groups such as clans, dialects or individual languages in a group. Boundaries are not intended
to be exact. This map is not suitable for use in native title and other land claims.
8 The RACGP
Healthy Profession.
Healthy Australia.
Before colonisation
Australia was traditionally inhabited by two Indigenous populations that were,
and are, ethnically and culturally very different: Aboriginal people and Torres
Strait Islander people.
Aboriginal people comprised diverse Aboriginal nations, each with its own
language and traditions. They historically lived on mainland Australia, Tasmania
and many of the continent’s offshore islands.
Torres Strait Islander people come from the islands of the Torres Strait, between
the tip of Cape York in Queensland and Papua New Guinea.
These diverse communities, over many thousands of years, adapted
successfully to their physical environment and developed ways of ensuring their
physical survival as well as social, cultural and spiritual ways of living.
While some Aboriginal communities were transient, this practice was usually
conducted in order to find supplies of food and water and was seasonally
determined. Thus nomadic communities were more prevalent in the desert than
in the rainforest, where food and water supplies were more plentiful and reliable.
In Aboriginal culture, the land was created by the journeys of the spirit
ancestors. Through stories, art and dance (corroboree), and later poetry and
drama, stories were (and are) told of how the spirit ancestors (each symbolised
by an animal that is the totem of the clan) gave life to the land and rules for
human behaviour. Spirituality and culture explain the origin of the universe,
the workings of nature and humanity, and life cycles. It shapes and structures
Aboriginal life and the relations between the sexes, and prescribes a network of
obligations to people, land and spirits.
To Aboriginal people, the land is life. They are connected spiritually to the land,
water, flora, fauna, air, soil, rocks, trees, salt and fresh water. They have creation
stories, which indicate how the land was formed. An important part of cultural
practice is to respect connection to the land through the creation stories.
According to these, Aboriginal people did not own the land in the European
sense, but, rather, belonged, or perhaps more accurately, were ‘beholden’, to
the land, in that their role is to be custodians of the land.
The rules of the law as passed on by the creation stories were absolute
throughout all aspects of Aboriginal life and were guarded by Elders: select
men and women who possessed great knowledge of the law. Elders made
important decisions; gave inspiration and advice; arranged marriages; organised
learning, initiations and ceremonies; arbitrated and settled disputes; and fixed
punishments if laws were broken.
Like Aboriginal communities, pre-contact Torres Strait Islanders were fishermen,
hunters and agriculturalists. There are now 19 communities living on 17 islands
and the northern peninsula area of the mainland. Then and now, Torres Strait
Islanders associate themselves with the land, the sea and the sky, interwoven
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Healthy Australia.
The RACGP
through spiritual beliefs, stories, songs and dances. Torres Strait Islander people
maintain close cultural, social, spiritual and economic connections with their ‘sea
country’. The Torres Strait culture is traditionally an oral culture, with languages,
songs, dances and beliefs passed down verbally through generations.
‘Pre and post contact’ is preferred when referring to the period before and
after European arrival. Using the terminology ‘pre-history/post-history’ is not
acceptable as it implies that history did not begin until the landing of the First
Fleet and the subsequent European domination.
Colonisation
Colonisation of mainland Australia began with the landing of the First Fleet in
1788. Although there were between 300,000 and 1 million Aboriginal people
living on the mainland at that time, the European people claimed the land for
their own purposes, with devastating impact on Aboriginal people and culture.
What followed was a period of episodic brutality and sustained attack on every
aspect of traditional Aboriginal life, leading to enduring disadvantage.
Following colonial arrival, settlement spread piecemeal across the country.
This was accompanied by a drastic decline in the Aboriginal population as
colonisation brought with it diseases to which Aboriginal people had no
immunity. The traditional ways were destroyed as hunting grounds were taken
over for grazing and agriculture, causing Aboriginal people to be treated as
trespassers on their own land under European law.
In addition, the European settlers brought with them their own, very different,
beliefs and systems for preservation of their line, and social, cultural and
religious ways of living. Because the colonists saw local communities through
their own cultural ‘filters’, and because of their innate sense of cultural
superiority, colonial society was generally intolerant of all others. This led to a
culture clash, where the Aboriginal people were, by and large, seen not just
as ‘different’ or ‘other’, but as ‘primitive’, ‘backward’, ‘savage’ and worse. It
was inevitable, because of the colonists’ greater power and numbers, deadly
weaponry and a belief in their right to occupy the land, that the traditional
owners of the country were subjugated.
Europeans brought with them the concept of social class, having come from
a culture with distinct divisions between upper, middle and lower classes, with
further sub-classes. Aboriginal people were identified as belonging to the lower
class. Bottom social positioning was reinforced through policy development and
such measures as the implementation of protection boards (discussed later).
Material goals were (and, of course, still are) highly valued. Attitudes towards
land were driven by the desire to control it in order to produce crops and stock
of value to the colony. Overall, the Australian model of settler superiority led to
a system of dominance and control over Indigenous lives, which was followed
by a more recent period of denial of the extent of the social and economic
exclusion involved.
10 The RACGP Healthy Profession.
European settlers did not recognise Aboriginal culture, and the close connection
between Aboriginal people and the land was not recognised under British law.
Because Aboriginal land was deemed unoccupied it was declared terra nullius
- belonging to no-one - and was taken away without negotiations or treaties.
The relationship between Aboriginal people and their land was ignored by most
settlers, although Robinson recognised the concept of ownership as follows:
‘The Aborigines have ideas of property in land. Every tribe has its own
distinct boundaries [which] are well known and defended. All the wild ducks
are considered as much the property of the tribe’s inhabitants or ranging on
its whole extent as the flocks of sheep and herds of cattle that have been
introduced into the country by adventurous Europeans.’
George Augustus Robinson, undated jotting
Many clans suffered such depopulation, through varying combinations of newly
introduced disease and lack of access to usual food and water supplies, that
neither the traditional means of living nor further resistance to the invader could
be sustained.
The insidious impact of agricultural practices such as grazing had long term
and disastrous effects on local Aboriginal populations. For example, Sir Thomas
Livingstone Mitchell, an explorer and surveyor, was so enchanted by his 1835
travel to the southwest part of Victoria that he called it ‘Australia Felix’ (meaning
‘fortunate’ or ‘happy’). Reporting on what he found on his return to Sydney, the
rapid occupation of Australia Felix followed. Already settlers from Van Diemen’s
Land were crossing Bass Strait and soon others were driving their flocks south
west along the tracks that had been created by Mitchell’s heavy wagons.
What followed was a dramatic rise in pastoralism in one of the richest regions
of Australia. The devastation of the local Aboriginal population, distressingly,
was virtually unacknowledged. A local pastoralist, James Dawson, was moved
to record life during this period, and it is richly detailed in the book: Australian
aborigines: the languages and customs of several tribes of aborigines in the
western district of Victoria, Australia.15
The remnants of Aboriginal clans were forced to relocate, sometimes hundreds
of kilometres away from traditional lands, onto reserves or missions where they
were forbidden to speak traditional languages or practise cultural traditions.
Many Aboriginal communities were forced to live alongside, and intermingle
with, different communities, with little consideration of the effect on the culture
of both communities.16
During this period, many Aboriginal peoples resisted British settlement in
various ways, ranging from skirmishes to wars. For example, in south western
Victoria, in an episode known as the Eumerella wars of resistance, Gunditjmara
traditional owners led a widespread attack on pastoralists in the region:
damaging crops; attacking stations, farm labourers and their stock; killing
European settlers; ambushing travelling parties; and petitioning government
Healthy Profession. The RACGP 11
for the return of their land. Other strategies used by Aboriginal peoples to fight
against takeover of land and other injustices included dialogue with settlers,
disruption of farming practices, and verbal and physical confrontation. To this
extent, these sites are battlefields like any other.
Similarly, settlers would engage in killings, punitive expeditions and massacres
throughout the colonies, sometimes with the approval of governments, and
often without charges laid. Deaths from these killings were many and added to
the destruction of Aboriginal communities and ongoing trauma.
After reports of an extended period of massacres of Aboriginal peoples in
Tasmania, known as the Black War, George Augustus Robinson, an English
settler, was called upon by the Colonial Office in Great Britain to mount a
‘friendly mission’ to find the 300 remaining Aboriginal people in Tasmania and
resettle them on Flinders Island. By 1835, nearly all Tasmanian Aboriginal people
had been relocated to the new settlement, which subsequently deteriorated into
something more like a prison camp, where many of its residents died of ill-health
and homesickness.
Robinson later became Chief Protector of Aborigines in Victoria. His diaries
provide a rich source of observations about attitudes towards Aboriginal
peoples at this time, such as the following:
‘The natives should be treated [as] men, they work as men and they should
be treated same as men, a fair day’s wage for a fair day’s labor but this is
never accorded them. It is thought that if they get food it is enough for blacks.
The natives have a feeling that they are men and they evince that [they are]
higher beings. The settlers all abuse them, men great scoundrels &c.’
George Augustus Robinson, Journal, 28 January 1850
It wasn’t until the 1838 Myall Creek Massacre near Inverell (New South Wales),
when 28 Aboriginal people, mainly women and children, were killed, that seven
stockmen were hanged for the murder. They were the first people to be charged
and punished for a massacre of Aboriginal people.
One of the last documented massacres, the Coniston Massacre, took place
in central Australia in 1928, when police went on a vengeful rampage, killing
dozens of Aboriginal people in retribution for the death of a white hunter.
Historians estimate that at least 60 Aboriginal people were killed, although many
claim the numbers were far greater. No-one was ever charged or convicted over
their deaths.
An extraordinary Victorian book, Scars in the landscape: a register of massacre
sites in Western Victoria 1803-1859,1 categorises the many massacres in this
area, many from non-Indigenous recording and references, and most virtually
unacknowledged.
A similar, though less brutal, experience of European settlement was suffered
by Torres Strait Islander peoples. Although explorers, including Torres (a
Spanish captain), Cook, Bligh and Flinders, sailed through the strait from late
1600, it was only in 1863 that the first European settlement was established, on
Albany Island, just off Cape York. The discovery of large amounts of pearl shell
attracted thousands of foreign seamen from 1870 onwards.
In 1871 the first Christian missionary teachers were placed on Erub (now Darney
Island), in the Torres Strait Islands, by the London Missionary Society, which
saw Torres Strait as a ‘stepping stone’ to evangelising New Guinea.
Ostensibly, Christian missionaries were expected to attend to the spiritual and
material welfare needs of Aboriginal and Torres Strait Islander peoples. In reality,
these missions were largely about ‘Christianising’ people and teaching them
what were considered ‘habits of order, industry and subordination, to which
they were before entire strangers’.18
In 1879 all Torres Strait Islands were annexed to Queensland. Although this
brought protection from the abuses of fishermen and pearlers, it also introduced
colonialism, alienation of land and increasing control by outsiders.
In 1904, the Torres Strait Islands, being part of Queensland, became subject to
the Queensland Aboriginal Protection Act.
In 1912 the first Torres Strait Islands ‘reserves’ were gazetted; the last were
gazetted in 1926. Superintendent teachers were appointed to all the permanently
settled islands to supervise daily activities. Islanders now had to ask permission
of the local superintendent to travel. Their wages were controlled by the Protector
and permission was required if Islanders wished to withdraw their own money.
In 1936 resentment against the Protector and local superintendent teachers
resulted in a strike by workers of the private trading company, Pacific Industries
Ltd. The following year, Torres Strait Islander councillors gathered together
for a historic meeting at Masig (Yorke Island), demanding concessions from
the Queensland government, including improved services, an end to some
regulations and a power transfer from superintendent teachers to local councils.
Two years later, the Queensland Government repealed its previous ‘protection’
legislation and passed the Torres Strait Islanders Act, which recognised Torres
Strait Islanders as a separate people.
Protectionism
In the late 1880s, many places where Aboriginal and Torres Strait Islander
peoples had settled were taken over by the colonial government through a
policy of ‘protection’. They were run as stations or reserves and controlled by
‘protection boards’ in all Australian states.
Protection boards throughout Australia oversaw the removal of thousands
of Aboriginal children (known as the Stolen Generations) from their parents.
Nationally, for the period 1910-1970, there were likely to have been between
20 000 and 30 000 removals.
The remnants of Aboriginal clans were forced to relocate, sometimes hundreds

of kilometres away from traditional lands, onto reserves or missions, where they
were forbidden to speak traditional languages or practise cultural traditions.
Many Aboriginal communities were forced to live alongside, and intermingle
with, different communities, with little consideration of the effect on the culture
of both communities.19
Aboriginal and Torres Strait Islander peoples were again forced to leave their
traditional lands or country to live on reserves or missions, which was extremely
restrictive to their traditional way of life as hunters and gatherers. Relocation to
lands away from their traditional area also resulted in the destruction of families,
culture and lore, and sometimes led to animosity between the various traditional
groups struggling to survive.
Life on the missions was harsh and there was little respect for human rights.
Aboriginal peoples were treated as incapable of managing their own lives and
were subject to arbitrary rule by mission managers and police. Many Aboriginal
people alive today were brought up on a mission, and this experience, and the
memory of it, has been hugely formative in their lives.
Mission life had disastrous effects on the health of Aboriginal and Torres Strait
Islander peoples as they were forced to give up traditional foods for a diet made
up almost exclusively of flour and tea, and, for some, reduced rations. While
inactivity was the norm in some missions, other Aboriginal communities were
expected to run market gardens and produce stock - although if they were too
successful at this, their efforts were often undermined.
Reserve or mission managers controlled and regimented every aspect of
Aboriginal and Torres Strait Islander people’s lives. They had the right to search
people, their dwellings and belongings at any time, confiscate their property,
read their mail and order medical inspections. They could also order children to
sleep in dormitories, expel people to other reserves and break up families.
Members from one community were often placed with members of a
community that was a traditional enemy, thus creating conditions for
longstanding conflict. Wadeye, an Aboriginal community in the Northern
Territory, is an example of the legacy of this policy. It is located in an area that
includes the traditional lands of about 20 Aboriginal communities. The founding
of a Catholic mission in Wadeye in 1935 saw many of these communities
moving into the region. These people were always considered by the traditional
owners of Wadeye, the Kardu Diminin, as visitors with none of the rights that go
with the ownership of Wadeye land.
Christianity had a powerful impact on traditional religious and political life.
Most importantly, Aboriginal peoples were prohibited from sharing, learning
and enjoying traditional culture, language and family associations. They were
forbidden from speaking traditional languages and practising their culture in
the form of ceremonies, rites of passage and corroborees. Breaking these
rules attracted serious penalties, including the expulsion of individuals from

the mission.
Added to the grief, dislocation, loss and trauma associated with the direct
effects of removal - on both the individual person and their extended family/
community - was the suppression of Aboriginal identity and widespread
physical and/or sexual abuse. The personal and communal desolation resulting
from the removal of Aboriginal children from their families was recognised
at the 1996 hearings of the National Inquiry into the Separation of Aboriginal
and Torres Strait Islander Children from Their Families, which gave rise to the
Bringing them home report of May 1997 (available at www.hreoc.gov.au/social_
justice/bth_report/index.html).
While the trauma arising from these policies and its associated effects has
caused significant disadvantage for Aboriginal and Torres Strait Islander
people alive today, many have chosen jobs, roles or professions to address
some of these disadvantages. Associate Professor Noel Hayman, Director of
Inala Indigenous Health Service in Brisbane and Queensland 2011 Australian
of the Year, has this to say about his grandparents’ experience of the Stolen
Generation period:
‘My background is actually from the Stolen Generation. My grandfather was
Roy Smith, a Wakka Wakka, and my grandmother Daisy Smith, a Kalkadoon.
When grandfather was about 12 years old he was put on Purga mission
in the south east of Queensland. When my grandfather got an exemption
certificate he left the mission and then went to live at Eidsvold. At that time
they used to do spot checks to see how Aboriginal people were living and
compile a report on the Aboriginals they conducted spot checks on. So if you
didn’t have a good report you were actually put back in the mission’.20,21
Assimilation
In 1937 the Commonwealth Government convened a conference with the
states, where it was officially agreed that the aim for those Aboriginal and Torres
Strait Islander peoples not of ‘full blood’ should be their ultimate absorption
into the wider population. This policy, referred to as ‘assimilation’, was designed
to solve the ‘Aboriginal problem’ by ensuring that Aboriginal and Torres Strait
Islander people would lose their identity and culture within the wider community.
Under the Commonwealth’s assimilation policy, thousands of Aboriginal and
Torres Strait Islander children were removed from their parents. Often, these
children were sent to ‘training homes’ where they were trained as domestic
servants or farm labourers, or fostered out to non-Indigenous families away
from their community of origin.
The human rights abuses and active attempts to destroy Aboriginal and Torres
Strait Islander culture had deep and long term effects that continue to be felt
today.
It is important to be aware of the sensitive issues that have arisen in these

communities as a result of forced removal from traditional lands onto missions
and reserves, and of the history of grief, loss and trauma experienced by
Aboriginal and Torres Strait Islander peoples. The policies that led to the Stolen
Generations had immense impacts on Aboriginal and Torres Strait Islander
culture, community and relationships. These impacts are ongoing and range
from psychological harm to loss of native title entitlements, increased risk of
incarceration, poverty, poor health and early death.
The referendum
From the late 1950s, Aboriginal and non-Aboriginal activists came together to
campaign for equal civil rights for Indigenous Australians.
In 1967, after a decade-long campaign including several petitions and hundreds
of public meetings, an overwhelming 90% of voting Australians returned a
‘Yes’ vote to the referendum to allow the counting of Aboriginal and Torres
Strait Islander peoples in the census and to open the way for much greater
Commonwealth Government involvement in Aboriginal affairs. Australians
have in most instances voted ‘No’ to referendum questions: only 8 out of 44
referendums since 1906 have been carried. This marked the start of the political
movement.
While the referendum was much less far reaching than many people believe, it
set in motion other changes, including, later, the ability of the Labor government
under prime minister Gough Whitlam to override state laws that allowed racial
discrimination against Aboriginal and Torres Strait Islander peoples. On reserves
in Queensland, for example, Aboriginal peoples were forbidden to gamble,
use foul language, undertake traditional cultural practices or drink alcohol.
The overturning of this legislation provided sudden access to alcohol that had
previously been denied.
While wage equality was the result of an unrelated process, in 1968 the
Commonwealth Conciliation and Arbitration Commission found that Aboriginal
people employed on Northern Territory cattle stations would be covered by the
Cattle Station Industry (Northern Territory) Award and would be paid the same
rates as non-Aboriginal workers.
These constitutional changes, coupled with escalating calls for action, led
eventually to the Commonwealth granting Aboriginal and Torres Strait Islander
land rights in 1975.
Self determination
The Australian Government’s policy of assimilation was not officially abandoned
until the federal election in 1972, when, as a direct result of growing Aboriginal
and Torres Strait Islander activism, it was officially replaced with a policy of
self determination - defined as the right of all peoples to ‘freely determine
their political status and freely pursue their economic, social and cultural
development’ (see Article 1 of the International Covenant on Civil and Political
Rights at the Australian Human Rights Commission: www.hreoc.gov.au/racial_
discrimination/face_facts_05/atsi.html).
Despite these changes, social indicators for Aboriginal and Torres Strait Islander
peoples, including health indicators, remain the lowest of all Australian groups.22
Although the impact of European colonisation on Aboriginal and Torres Strait
Islander ways of life is immense and longstanding, Aboriginal and Torres Strait
Islander peoples have survived and the culture is alive and strong. In line with
the concept of self determination, the active involvement of Aboriginal and
Torres Strait Islander peoples in all decision making relating to health matters is
fundamental.
Native title
Native title is the official recognition under Commonwealth Australian law of the
traditional rights and interests of Aboriginal and Torres Strait Islander peoples in
relation to land and water.
Aboriginal and Torres Strait Islander peoples have fought long and hard for
their rights and several important landmark decisions have marked modern
Aboriginal and Torres Strait Islander history.
In the historic 1992 Mabo judgement, the High Court of Australia reversed the
concept of terra nullius by holding that a ‘native title’ to land had survived the
colonisation of Australia, thus enshrining Aboriginal and Torres Strait Islander
land rights in Australia’s common law.
To Aboriginal and Torres Strait Islander communities, land is not only about
hunting and gathering, it is also the basis of spiritual life. The Mabo finding
asserted that sovereign power resided in the state has compromised the
development of native title in two significant ways:
• by erasing Indigenous sovereignty (the political, social and economic systems
that unite and distinguish Indigenous people as a people) from native title
• by retaining the state’s supreme power to extinguish native title.23
Understanding the impact of past injustice and striving to eliminate
discriminatory practices are important factors in improving social outcomes for
Northern Territory intervention

The Northern Territory National Emergency Response (NTER or NT intervention)
was a package of changes to welfare provision, law enforcement, land tenure
and other measures, introduced by the Commonwealth Government in 2007.
At the time, the changes were said to be introduced by the Commonwealth
in response to the Northern Territory government’s publication of the Little
children are sacred report, which documented widespread child sexual abuse
and neglect across the Northern Territory.24 However, these actions were taken
without prior consultation and were only loosely based on the report findings.
There has been widespread criticism of the NTER from both professional
groups and Aboriginal communities. The Australian Indigenous Doctors
Association (AIDA) formally put forward a position statement, part of which
includes the following:
‘AIDA believes that any Indigenous health intervention or program should be
guided by the following principles:
• Land, culture and connectedness are important for Indigenous health;
• Take a strengths-based, healing approach, which incorporates kinship care
and builds on the resilience of Aboriginal and Torres Strait Islander people;
• Genuine partnership with Indigenous people;
• Learn from existing good practice in Indigenous health;
• Value existing Indigenous health expertise and engage Indigenous health
workforce.’
AIDA Submission to the Northern Territory Emergency Response Review Board,
2008, www.aida.org.au/pdf/submissions/Submission_8.pdf
Australians for Native Title and Reconciliation (ANTaR) publish the following
statement on their website, www.antar.org.au/abetterway:
‘ANTaR considers that Australian governments have a responsibility to intervene
to protect children in danger from violence, neglect and abuse. However,
ANTaR is concerned that the changes introduced by the Federal Government
failed to adopt the approach recommended by the Little Children are Sacred
report to positively engage Aboriginal communities and to provide the additional
services and capacities necessary to establish the conditions for safe and
strong communities. We therefore welcome the support given by both the
Australian and NT governments for the recommendations of the recent Growing
them strong, together report on child protection in the NT that highlights the
need for increased Aboriginal engagement and community controlled service
delivery in relation to family support and child protection.
Meanwhile, ANTaR has consistently maintained that breaching the Racial
Discrimination Act was not necessary to protect children. In particular, we
have expressed our concerns that this led to mistrust, division and increased
intolerance towards Aboriginal people that are barriers to empowering
Aboriginal communities and keeping children safe. Whilst ANTaR welcomed the
recent partial reinstatement of the Racial Discrimination Act, we are concerned
that this does not go far enough in protecting the human rights of Aboriginal
people in the Northern Territory. We will continue to call for the full reinstatement
of the Act.’
Although heavily criticised, the intervention received bipartisan parliamentary
support, and continues to be implemented by succeeding Labor governments.

Opinions were and still are split about the efficacy, equity, need for and
outcomes of the intervention, including among GPs. These reflect many of the
underlying assumptions and attitudes that continue to limit equitable access to
primary care by Aboriginal and Torres Strait Islander peoples.
Close the Gap

In 2005 the Aboriginal and Torres Strait Islander social justice commissioner,
Tom Calma, presented the annual social justice report to the federal attorney
general. In it he argued that it was unacceptable for a rich country to tolerate the
gross health inequality that continued to exist between Aboriginal and Torres
Strait Islander and non-Indigenous Australians. He called for action, and made
recommendations to bring the inequality to an end as soon as possible.
Shortly after, with strong championing by the Aboriginal health services
sector, a group of Aboriginal and Torres Strait Islander organisations and other
government and non-government organisations led a national Indigenous health
equality campaign, better known as the Close the Gap Campaign. A steering
committee was formed to guide the development of the campaign and worked
with a coalition of 40 or so organisations, all committed to bringing Indigenous
health inequality to an end.
The campaign was formally launched in April 2007 and culminated in the
National Indigenous Health Equality Summit held in Canberra in March
2008, where, among other actions, the Commonwealth Government and
the Opposition committed to achieving Indigenous health equality within a
generation through signing the Close the Gap Statement of Intent. The then
president of the RACGP, Dr Vasantha Preetham, was one of the signatories, a
clear statement of commitment by the College to work towards closing the gap.
Later in 2008 the Coalition of Australian Governments (COAG) lndigenous
Reform Agreement, known as Close the Gap, was signed. Close the Gap is
‘a commitment by all Australian governments to work towards a better future
for Aboriginal and Torres Strait Islander peoples. It aims to close the gap of
Aboriginal and Torres Strait Islander disadvantage in areas such as health,
housing, education and employment’.
The Close the Gap report is available at www.hreoc.gov.au/social_justice/
health/statement_intent.html.
The RACGP National Standing Committee - Aboriginal Health, and its
successor, the National Faculty of Aboriginal and Torres Strait Islander Health,
were established to improve health outcomes for Aboriginal and Torres Strait
Islander peoples and to support the work of GPs and other health workers
involved in delivering healthcare to Indigenous Australians. Through enhanced
understanding of the cultural context and via a range of initiatives to support
GPs working in Aboriginal and Torres Strait Islander health in all primary
healthcare settings, the RACGP hopes to contribute to the growth of culturally

appropriate health delivery systems that will improve health outcomes for
Aboriginal and Torres Strait Islander Australians.
The national apology

On 13th February 2008, more than 10 years after the Bringing them home
report was tabled in Federal Parliament, prime minister Kevin Rudd tabled a
motion apologising to Australia’s Aboriginal and Torres Strait Islander peoples,
particularly the Stolen Generations and their families and communities, for laws
and policies that had ‘inflicted profound grief, suffering and loss on these our
fellow Australians’ (available at www.aph.gov.au/house/Rudd_Speech.pdf ).
The momentum for the apology had intensified from 2000, when the prime
minister of the time refused calls for the Commonwealth Government to
apologise for past government policies. During the period 1997-2001, all state
and territory governments had already issued formal apologies.
On the same day as the apology was tabled in Federal Parliament, the Church
of the Torres Strait conducted a ‘Coming of Light to Boigu’ re-enactment to
apologise to the people of the Torres Strait for actions taken by members of the
London Missionary Society when they landed there 137 years ago.
Core principles for working with Aboriginal

and Torres Strait Islander people
Understanding culture
Lack of knowledge about the longstanding consequences of the impact of
European settlement and the differences between Aboriginal and Torres Strait
Islander and non-Indigenous culture can create a breakdown in respect and
can lead to offensive misrepresentation of Aboriginal and Torres Strait Islander
peoples.
Understanding and respecting cultures that are not familiar or may appear to
reflect different beliefs is sometimes difficult when viewed through your own
cultural lens. For example, it may be hard to understand the importance of
land if this concept is simply viewed for its utilitarian purposes rather than for
its spiritual significance. People’s relationships to family and community differ
widely and may or may not embrace the principles of kinship and belonging,
which have different expectations and obligations. Spirituality and culture may
seem like superstition to people whose cultures do not incorporate the spiritual
and supernatural beliefs and traditions that may have been present in past
generations.
For Aboriginal and Torres Strait Islander peoples, family, kinship, community,
connections to the land and spirituality are fundamental and complex.
Differences between many urban and remote communities add a further
dimension, and, like all cultures, Aboriginal and Torres Strait Islander cultures
have evolved over time. Urban-dwelling Aboriginal and Torres Strait Islander
peoples are more likely to live nontraditional lifestyles than those in remote
communities. However, they may retain some values, practices and obligations
that are distinct from mainstream norms, for example, shared care of relatives’
children and significant obligations to extended family members.
Aboriginal and Torres Strait Islander cultures and their language groups were,
and are still, many and varied; there is no homogeneous Aboriginal or Torres
Strait Islander culture. It has been estimated that, before colonisation, there
were about 600 Aboriginal language groups, while now the number is thought
to be about 200.
Every community, while sharing some common beliefs and practices, is unique.
It may help to think about the use of the word ‘nation’ in this context. People
may see Germany and The Netherlands or Australia and New Zealand as similar
nations. While this may be true, there are also important cultural differences.
This is similar for Aboriginal nations - there may be significant cultural
differences between them. For example, talking about ‘Aboriginal health’ would
be like talking about ‘European health’.
Consequently, when engaging with Aboriginal and Torres Strait Islander
communities, it is important to keep learning about local Aboriginal and Torres
Strait Islander culture. Ways to do this include participating in local Aboriginal
and/or Torres Strait Islander community events and inviting members of the
Aboriginal and Torres Strait Islander community to participate in College
activities. Such events and activities may include launches, conferences,

workshops and major events such as the annual Reconciliation Week (from 27
May to 3 June each year) and NAIDOC (National Aboriginal and Islander Day
Observance Committee) Week (held in the first full week of July). An event close
to the hearts of people working in Aboriginal and Torres Strait Islander health is
the national Close the Gap day.25
The RACGP also recommends that members and staff participate in formal and
informal ways of learning about Aboriginal and Torres Strait Islander cultures.
These can include developing an understanding of and appreciation for the
artistic and cultural works produced by Aboriginal and Torres Strait Islander
writers, artists, film makers, dancers, musicians, and for the history of your own
area. This form of cultural ‘immersion’ is likely to not only enhance your own
cultural sensibility and awareness, but will also help support the burgeoning
Indigenous artistic and cultural communities across Australia.
There are important general protocols to be aware of when interacting with
The RACGP position statement on Aboriginal and Torres Strait Islander health
states:
‘How Australia treats Aboriginal and Torres Strait Islander people is a mark
of us as a nation. How we as health professionals work to improve the health
of Aboriginal and Torres Strait Islander people will inform all of our work in
health’.26
As this statement suggests, following these principles (described below) can
open up opportunities to broaden your understanding and delivery of healthcare
generally. These opportunities include greater understanding of yourself and
your own cultural perspectives, expansion of world views, greater awareness of
cultural and interpersonal influences in healthcare provision, and an enhanced
understanding of social and emotional determinants of health leading to a
holistic view of health.
Many of the principles described below are fundamental to the development of
authentic and trusting relationships generally. For Aboriginal and Torres Strait
Islander people, having a trusting relationship with a health service provider or
professional organisation is an essential precondition to the delivery of good
service. The following statement by Associate Professor Dennis McDermott, an
Aboriginal psychologist from Flinders University, explains one reason for this:
‘I’m trying to get professionals to look at introducing, if you like, the non
professional you, a little bit, to the person or organisation you are working
with. There’s a very good reason for that. It’s not about taking over and letting
your needs dominate the situation. It’s very much about being a known
quantity because in Indigenous parlance whether you’re a Koori here from
this part of Australia or a Murri from Queensland, or a Nyungah from Western
Australia it’s very much about who you are, where you’re from, who’s your
mob. And the reason we ask these questions is we want to situate a person,
we want to find out where you fit in a universe, and once we’ve situated you
we can deal with you.
And I’d suggest for non-Indigenous people in dealing with Indigenous
patients, it’s incredibly important because of mistrust. There’s a huge historic
mistrust. It might be very simple though, it might just be about letting people
know casually that you have a couple of kids, or you’re actually from, like I
am, from Tamworth.’27
In addition to sharing information about the ‘nonprofessional you’ with Aboriginal
or Torres Strait Islander people, it can be useful to ask more general questions
too. For example at the first encounter, appropriate questions might be asked
about family or local events. Later, when the relationship is better established, it
may be appropriate to use a ‘placing question’, by enquiring as to ‘skin name’,
place of origin or language group. This often helps to engender openness and
trust, especially in remote communities.
Core principles
Respect for culture
Aboriginal and Torres Strait Islander world views, languages, lifestyles and
customary laws are respected in all settings. The diversity and richness of
Indigenous cultures is acknowledged and respected.
Respect for community
The importance to Aboriginal and Torres Strait Islander people of immediate and
extended family, kinship structures and community is respected.
Consultation, communication and consent

Aboriginal and Torres Strait Islander people are consulted on the way in which
they and their history, community, lives and families are represented and used,
in all aspects of College and general practice business.
Involvement and engagement

Initiatives involving Aboriginal and Torres Strait Islander communities are based
on genuine engagement and partnership, based on the concept of ‘with, not for’.
As Conrad Ratara, an Arrente Elder from Hermannsburg, says:
‘It’s a long road we have come and it’s a long road we can go. We have to
walk together and talk together. If you never listen to me, I will never listen to
you. If you walk in front of me, I will not follow you. Walk side by side and let’s
get there.’28
Recognising the social, emotional and environmental determinants of health

Effectively working to improve the health of Aboriginal and Torres Strait Islander
people requires ‘an understanding of the social and emotional factors that
influence health and wellbeing. In Aboriginal and Torres Strait Islander cultures
these include the connection to land, culture, spirituality, ancestry, family and
community. They also include issues arising from unresolved grief and loss,
trauma and abuse, removal from family, substance misuse, family breakdown,
cultural dislocation, racism and discrimination, and social disadvantage’.29
Holistic view of health
An understanding and appreciation of a holistic view of health is essential in
order for health professionals to work with Aboriginal and Torres Strait Islander
individuals and communities on health and health-related matters.
The National Aboriginal Community Controlled Health Organisation (NACCHO)
definition of Aboriginal and Torres Strait Islander health is:
‘“Aboriginal health” means not just the physical wellbeing of an individual but
refers to the social, emotional and cultural wellbeing of the whole Community
in which each individual is able to achieve their full potential as a human being
thereby bringing about the total wellbeing of their Community. It is a whole of
life view and includes the cyclical concept of life-death-life.’30
Self determination and community control

Aboriginal and Torres Strait Islander peoples have the right to self determination
in their cultural and health affairs. Self determination is expressed most strongly
in Aboriginal Community Controlled Health Services, where:
‘Community Control is a process which allows the local Aboriginal
community to be involved in its affairs in accordance with whatever protocols
or procedures are determined by the Community.’31
Aboriginal and Torres Strait Islander people are consulted concerning the
integrity and authenticity of the ways in which history, community, interviews,
lives and families are represented, and are consulted concerning the integrity
and authenticity of the representation of their cultural and intellectual property.
Acceptance of complexity
While the medical knowledge required to work in Aboriginal and Torres Strait
Islander health is not necessarily complicated, the factors contributing to poor
health outcomes are often multiple, complex and interconnected. Keeping an
open mind, being self reflective, understanding the context for current health
circumstances and having a desire to learn and understand are important
qualities for people working in every area of Aboriginal and Torres Strait
Islander health.
As Dr Justin Coleman, Senior VMO at Inala Indigenous Health Service, says:
‘The medical knowledge is easy; its delivery is the complex part. The doctors
I know who have mastered the art of Indigenous health have combined
excellent communication skills with a drive to engage their patients. Doctor
patient trust is the key, and nowhere else in medicine does it open more
doors. I believe Aboriginal and Torres Strait Islanders have a particularly
keen sense when it comes to detecting lack of respect, perhaps honed by

two centuries of frequent practice. But, if you are prepared to listen and
learn, and to make genuine efforts at communication, the work becomes
immensely satisfying.’32
The culture and belief systems of local communities are also complex, and
understanding their implications for the development of culturally sensitive
behaviours and processes takes time. While participating in cultural awareness
education and locally delivered cultural safety training is vital, continued
engagement with, and learning from, local communities and individuals is
essential. A ‘cultural mistake’ made by a non-Indigenous person may be easily
tolerated by Aboriginal and Torres Strait Islander people, provided goodwill and
the desire to keep learning is evident.
Protocols for culturally respectful engagement with

Aboriginal and Torres Strait Islander people
In the context of engagement with Aboriginal and Torres Strait Islander people,
protocol means ‘following the customs and lores of the people or community
you are working with and communicating in a way that is relevant to them’.33
The following protocols outline basic guidelines for culturally appropriate
behaviour when RACGP staff and members engage with, or represent,
Aboriginal and Torres Strait Islander people and communities. They cover
some of the key cultural issues of which staff and members should be aware,
and provide guidance in terms of the behaviours required. Keep in mind that
different communities have different practices, so it is important to check with
them if you are unsure.
Describing Aboriginal and Torres Strait Islander people

Aboriginal and Torres Strait Islander people are sometimes described in ways
that ignore their occupation or position in the community. For example, the
word ‘activist’ has often been used to describe Aboriginal and Torres Strait
Islander people who campaigned or advocated for improvement. This and
other similar generic terms fails to credit people with their achievements.
Generally, Aboriginal and Torres Strait Islander people, like other people, wish
to be identified in terms of their occupation or their position in the community,
for example as a spokesperson, media liaison officer or Elder. Correct names,
spelling and titles of Aboriginal and Torres Strait Islander contributors and their
materials are important.
Accurate representation protects the integrity of the Aboriginal or Torres Strait
Islander person’s contribution and the authenticity and integrity of the work.
It may be important to consult with the community to ensure the authentic
identification of both the work and its contributor.
Deceased people
Where they exist, it is important to follow Aboriginal or Torres Strait Islander
protocols for the avoidance of naming deceased people. Protocols differ
across the country. Where necessary, consult the local community for correct
procedures, avoidance names, time periods for avoidance and the use of
images and naming of deceased people.
A death in a community
The question on how to deal with members of a community who have passed
away can be a significant issue. Death and ‘sorry business’ is a continuous
cycle that impacts greatly on communities. Culturally, it is difficult for some
family members to mention the deceased person by name. It is best to contact
the local Aboriginal health service or land council to liaise with a family member,
rather than go to family members directly while they are grieving.
In some Aboriginal or Torres Strait Islander communities, the entire community
will shut down for sorry business following the death of a member. As a result,
it is advisable to contact communities before leaving for a scheduled meeting

to make sure that they are able to conduct formal business. Many communities
have a mourning period where that person’s name and image cannot be used.
The time of mourning is different between communities. It can be for a week, a
year or an indefinite period of time, during which you will not be able to use the
name, image, voice or video of the deceased.
Permission: for what, whom and how long

If you have been granted explicit permission to use a person’s name, image,
voice or video, this should be clearly stated.34 It is highly recommended that you
establish whether or not the permission is a blanket rule for perpetuity. It should
be made clear whether permission is restricted to the specific segment, state or
town and whether it includes later segmentation.
To minimise potential problems, staff and College members are strongly
encouraged to obtain explicit permission when using such images. Ensure that
consent to use includes discussion about the way in which the material will be
used, for what parties, and the length of time over which the image will be used
(eg. for a specific period or for perpetuity). For example, the National Faculty of
Aboriginal and Torres Strait Islander Health sought written permission to use
the Aboriginal and Torres Strait Islander flags and a photograph of Dr Lowitja
O’Donoghue in its online activity: Introduction to Aboriginal and Torres Strait
Islander cultural awareness in general practice. Where possible, it is helpful
to document the consent. If written permission is difficult to obtain, it will be
important to consult with the community to determine alternative permission
strategies.
This issue can be important when dealing with visual images, which may
be stored for some time and used following the death of a person. Each
community deals with the death of an individual differently and therefore you
should contact someone from the community to ask for written permission
if you wish to use the name, image, voice or video of that person. Written
permission should include the date in which the mourning period ends to assist
with archiving and the use of archives. In some cases images will need to be
removed from documents, records and websites.
Depictions of people who have died

To many Aboriginal and/or Torres Strait Islander communities it is distressful
and offensive to depict persons who have died. The RACGP uses the following
warning on the National Faculty of Aboriginal and Torres Strait Islander Health
website; it could be used in the introduction to other materials:
Warning
Please be aware that this website may contain the names or images of
Aboriginal and/or Torres Strait Islander people who may now be deceased.
Smoking ceremony
Smoking ceremonies are conducted by Aboriginal people with specialised
cultural knowledge. The ceremony aims to cleanse people and the space in
which the ceremony takes place. Given the significant nature of the ceremony,
smoking ceremonies are usually only performed for significant spiritual events.
‘Avoidance’ behaviour
‘Avoidance’ behaviour reflects the responsibility to be respectful of cultural
beliefs and customs that constrain some interactions between Aboriginal
people. This can include the use of certain language and the right to be in the
presence of certain people or groups.
Avoidance behaviour can include respecting the restriction of access to, or
discussion of, knowledge that is specific to gender (commonly called ‘women’s
business’ or ‘men’s business’).
Avoidance issues may arise specifically in the context of ceremonies and clinical
settings, the latter with respect to genitourinary or reproductive issues.
In Aboriginal and Torres Strait Islander communities, some members of families
are unable to address one another and may refer to each other differently. For
example, in some cases a son-in-law is unable to be in the presence of a father
in-law, or a brother is not able to use his sister-in-law’s name.
In some cases, members of the Aboriginal community will advise outsiders of
intrusive behaviour and/or whether they are not permitted to discuss protocol
or ceremony for reasons of age, gender, or status or because the visitor does
not belong to their clan or tribal group. In other cases, Aboriginal people will
avoid the interaction that they believe would be disrespectful. This can lead
to unexplained silences or absences. As a result, it can be helpful to be both
transparent about who will be present, and sensitive to the possibility that
circumstances may change the capacity of people to be present and remain
respectful of the position of others in the community.
Culturally appropriate communication
For protocols for communicating with Torres Strait Islander communities in

the Torres Strait region, refer to the Torres Strait Regional Authority cultural
protocols on its website at www.tsra.gov.au/publications/tsra-cultural-policy.
aspx.
The importance of culturally appropriate, nondiscriminatory and

accurate language
Following European colonisation, Aboriginal and Torres Strait Islander peoples
were often forbidden from speaking traditional languages. Many languages
suffered enormous erosion as a result. English was used to describe and
communicate with Aboriginal and Torres Strait Islander peoples and led to
the use of inappropriate and often discriminatory language. Massacres also
contributed to the decline of many languages.
Generally, language can be seen as a direct reflection of a particular culture and
the beliefs that have given rise to it. The English language is not fully capable
of embodying the cultural imperatives, values and contexts associated with
Aboriginal and Torres Strait Islander languages.
Because European colonists did not understand, considered themselves
superior to, and were largely prejudiced against, Aboriginal and Torres Strait
Islander ways of life, the language they used to address and describe Aboriginal
peoples was often discriminatory and offensive.
Today, as attitudes towards Aboriginal and Torres Strait Islander culture are
changing, terms to describe Aboriginal and Torres Strait Islander peoples
are continually evolving. Understanding distinctions between words, and to
whom they apply, can pose a challenge for health professionals. However,
using appropriate and accurate language is fundamental to ensuring the use
of nondiscriminatory language and developing positive relationships between
Aboriginal and Torres Strait Islander people and communities and people in
general practice.
This section explores the use of the most appropriate terminology to describe
Aboriginal and Torres Strait Islander people, communities and organisations.
Note that the many and varied names of individual Aboriginal and Torres Strait
Islander language groups are not covered here.
Nonverbal communication
As with all communication, it is important to be sensitive to the use of nonverbal
cues, such as body position, eye contact, silence, voice tone and facial
expression. Like all cultures, these are a natural part of Aboriginal and Torres
Strait Islander communication patterns. They may differ from those with which
you are familiar, and Aboriginal and Torres Strait Islander people may be so
familiar with them as not to be conscious of using them or of the impact they
have unless a problem arises.
Differences in nonverbal communication will be found between non-Indigenous

and Aboriginal and Torres Strait Islander communities and also within cultures.
Patterns of nonverbal communication experienced in one community may not
apply in another, or if similar patterns are encountered elsewhere, they may have
a different meaning.
It is important to remember that, just as you may be aware of and
(even unconsciously) derive meaning from another person’s nonverbal
communication, so, too, will your own body language be attended to and
interpreted. If you feel distrustful, annoyed or judgemental, these feelings are
likely to ‘leak through’ in your body language.
If your encounter with an Aboriginal and/or Torres Strait Islander person is
conducted on the basis of goodwill and eagerness to understand, this will be
demonstrated in your body language. As Ena Chong (2010) says:
‘We take our cues from the other person. If someone, like, we have a medical
student here at the moment, who is keen to learn so that he can deal better
with the Murrie people he meets. He was a bit concerned because he’s never
met an Aboriginal person before. That doesn’t matter, he’ll have no worries,
‘cos he’s responsive and very caring.’35
While specific guidelines for nonverbal communication are not recommended,
the following rules of thumb may be useful.
• Be as willing to listen as you are to speak.
• Be aware of your feelings before and during the encounter.
• ‘Listen’ with your eyes as well as your ears; tune in to nonverbal as well as
verbal cues and reflect on what you’re seeing and hearing.
• Silence does not mean people of Aboriginal and Torres Strait Islander
communities do not understand; they may be listening, remaining
noncommittal or waiting for family or community support.
It is also important to be aware of what is appropriate behaviour between sexes.
In some places there is very clearly delineated ‘men’s business’ and ‘women’s
business’.
Verbal communication
Aboriginal and Torres Strait Islander peoples are a diverse lot; it is impossible to
know, with any certainty, the first-language status, the educational experience
or the urban/rural/remote origin of the person in front of you. Cultural safety and
cultural humility precepts guide us here: it’s best not to assume. Rather, tune
in to the person and the setting and let them guide. Where a person’s usual
language is not standard Australian English, or where their education or hearing
has been compromised, it is important to speak plainly, though without use of
offensive, ‘kiddie’ English.
English is often a second, and sometimes, a third, fourth or even fifth language
for people of many remote Aboriginal and Torres Strait Islander communities.
Wherever possible, and with permission, RACGP staff or members should work
with an Aboriginal or Torres Strait Islander health worker or other appropriate
member of the community to make sure that the communication is heard in the
correct language and in a culturally appropriate way.
It is useful to keep technical words or jargon to a minimum. Aboriginal and
Torres Strait Islander communities may use different constructs for the way
things work, and different ideas about how health and wellbeing are created
and maintained may underpin discussions. Thus it can be useful to consider
whether underlying ideas and concepts are shared when having discussions.
If it is necessary to explain a term, it might also be necessary to explain its
(cultural) background as well.
It is not appropriate to mimic Aboriginal or Torres Strait Islander speech patterns.
The complexities of intercultural communication are widely documented, and it
is well accepted that the influence of cultural perspectives on communication
is pervasive. Less well documented are the additional complexities of
communications between Aboriginal and Torres Strait Islander patients and
non-Indigenous staff in a primary healthcare environment.36
Some issues to consider are:
• The majority of healthcare settings are not designed to accommodate the
cultural and linguistic needs of Aboriginal and Torres Strait Islander, providers
and patients.
• There is generally a power imbalance between client and service provider,
often exacerbated when the client is of Aboriginal or Torres Strait Islander
origin.
• Communications tend to be biased towards a Western biomedical model,
and Aboriginal and Torres Strait Islander health literacy levels in that
‘language’ may be low.
• Different ideas or opinions tend to be dealt with differently in Aboriginal and
other Australian cultures. It is appropriate for non-Indigenous people to
express disagreement, while many Aboriginal people prefer to avoid direct
verbal confrontation and to respect personal privacy. To preserve consensus,
they may avoid assertiveness and direct argument, and defer discussing
topics that may produce disharmony.
• While each patient may be seen as an individual in the eye of most GPs,
nurses or reception staff, Aboriginal and Torres Strait Islander cultures are
collectivist in nature. Staff are far more likely to engage effectively with their
Aboriginal or Torres Strait Islander patients if they treat the individual as if they
were working with the family and/or the community of that patient as well. In
Aboriginal and Torres Strait Islander cultures, when an individual suffers, the
family and community suffer, too. Also, one patient’s experience with a health
service can influence the decisions of their family and community on whether
they will attend or avoid that health service.
• It is possible for both staff and patients to overestimate the effectiveness of
intercultural communication, with both parties relying on false assumptions
or interpretations. Some researchers conclude that medical efficacy is
compromised as a result.
The importance of good general communication skills such as listening,
attending to nonverbal signals and verbally checking for understanding is
reinforced in situations where risks of miscommunication are high.
It is wise to avoid direct questions, which may threaten the privacy of the
thoughts and feelings of an Aboriginal person. Direct questioning can, at times,
lead to ‘gratuitous concurrence’, or agreement with the questioner regardless
of whether the agreement is truly felt. This can most frequently occur when
the questioner is in a position of authority, but it can also signal feelings of
hopelessness or resignation.
A more useful communication strategy is to present information for confirmation
or denial, allowing sufficient time for a response. While this approach can create
problems with matters of choice, these can be managed by clearly presenting
options and possible outcomes of each. Using diagrams is also a useful means
of identifying issues and presenting options.
Strategies have been developed to improve intercultural communication
in primary healthcare (see, for example, the American Academy of Family
Physicians advice: Five communication strategies to promote self management
of chronic illness at www.aafp.org/fpm/2009/0900/p12.html).
It may be useful to learn words of the local language. This will be a positive
step in improving your relationship with the community. The words will have
a ‘surface’ meaning and, like all languages, a ‘deep’ meaning that conveys
nuances. Pronunciation should be checked for accuracy.
It is important to use a language within its home community. It might be
inappropriate to use the language of one community in another community.
It might lead to the language being misinterpreted, which might mean being
excluded from the community.
Terms used to describe Aboriginal and Torres Strait Islander

people
The RACGP acknowledges that the definition of an Aboriginal and/or Torres Strait
Islander person that is accepted by NACCHO requires three kinds of evidence:
• Evidence of Aboriginal or Torres Strait Islander descent:
- birth records or genealogies verified by a suitable authority as applicable; or
- a letter signed by the chairperson of an Aboriginal and/or Torres Strait
Islander incorporated organisation (if records are not available).
• Evidence of self identification as an Aboriginal or Torres Strait Islander:

- a signed affirmation that the applicant identifies as an Australian Aboriginal
or Torres Strait Islander.
• Evidence of community recognition:
- confirmation in writing by the chairperson of an Aboriginal or Torres Strait
Islander incorporated organisation in a community in which the applicant
lives or has previously lived.
However the RACGP believes that every individual has the right to determine
their own identity and can do so by being asked: ‘Are you of Aboriginal or
Torres Strait Islander origin?’ This approach is in line with Schedule F of the
COAG National Indigenous Reform Agreement and the Australian Institute of
Health and Welfare 2010 report National best practice guidelines for collecting
Indigenous status in health data sets.37 Keep in mind that some Australians are
of both Aboriginal and Torres Strait Islander origin.
Acceptable terms
The following terms to describe Aboriginal and/or Torres Strait Islander people
are acceptable:
• Aboriginal person
• Torres Strait Islander person
• First Australian
It is also acceptable to refer to local groups or traditional nations.
Some terms (such as half caste) were widely used by non-Indigenous people in
the past but are now considered racist and discriminatory. However, some of
these are still in use today, even if only sporadically, and require explanation as
to why they are offensive.
Terms such as full or half blood, half caste or part-Aboriginal are offensive.
Not only do they imply inferiority, they hark back to the assimilation period,
when clear notions of European superiority abounded. Also, the description
raises questions of identity. Some commentators have questioned a person’s
‘Aboriginality’ on the basis that they have a European name, skin or hair colour,
or that they have obtained benefits not available to non-Indigenous people by
claiming to be Aboriginal.
People who identify as Aboriginal and Torres Strait Islander are describing identity,
and usually one that is accepted with pride. It is important to remember, too, that
many Aboriginal and Torres Strait Islander people, like many other Australians,
have a mixed race background and may not ‘look Aboriginal’. It is important not
to decide whether a person is Aboriginal or Torres Strait Islander based on their
physical appearance, including skin tone, hair colour and eye colour.
Use of words or phrases like ‘them’ or ‘those people’ imply ‘otherness’ or a ‘them’
and ‘us’ mentality. Also, never assume that someone who is part of the ‘us’ (ie.
like ourselves) is not themselves of Aboriginal or Torres Strait Islander origin.
Always capitalise the ‘A’ in ‘Aboriginal’ as you would other designations like
‘Australian’, ‘Arabic’ or ‘Nordic’. The word ‘aboriginal’ with a lowercase ‘a’
refers to an indigenous person from any part of the world. As such, it does not
necessarily refer to the Aboriginal people of Australia.
Be aware that the term ‘Aboriginal’ is not generally inclusive of Torres Strait
Islander people, and reference to both Aboriginal and Torres Strait Islander
people should made where necessary.
Do not use ‘Aboriginal’ as a noun - it should only be used as an adjective. For
example:
• It is incorrect to write: ‘The RACGP will support self determination in health
matters by Aboriginals.’
• It is correct to write: ‘The RACGP will support self determination in health
matters by Aboriginal people.’
Never abbreviate the word ‘Aboriginal’, as this is offensive.
Remember that when preparing speech notes or documents that refer to ‘our
history’, ensure that the use of the word ‘Australian(s)’ includes Aboriginal and
Torres Strait Islander people(s). For example:
• It is incorrect to write: ‘Most Australians continue to see Aboriginal and
Torres Strait Islander people ...’ This implies that Aboriginal and Torres Strait
Islander people are not Australian.
• It is correct to write: ‘Most non-Indigenous Australians continue to see
Aboriginal and Torres Strait Islander people .’
Aboriginal and Torres Strait Islander people(s)

It is appropriate to use the term ‘Aboriginal people’ or ‘Aboriginal community’ if
you know that the group to which you refer consists only of Aboriginal people.
It is inappropriate to use only the word ‘Aboriginal’ if you are referring to Torres
Strait Islander people as well.
‘Aboriginal people’ is a collective name for the original people of mainland
Australia and their descendants, and does not emphasise the diversity of
languages, cultural practices and spiritual beliefs. Adding an ‘s’ (i.e. ‘Aboriginal
peoples’) emphasises this diversity.
‘Aboriginal people’ can also be used to refer to more than one Aboriginal person.
Both ‘Aboriginal people’ and ‘Aboriginal peoples’ are acceptable, depending on
the context. For example:
• ‘At the time of British colonisation, there were between 300 000 and 1
million Aboriginal peoples.’ Here ‘peoples’ is used to describe the groups of
Aboriginal people, each with their own language, cultural practices and beliefs.
• ‘At the time of British colonisation, there were between 300 000 and 1 million
Aboriginal people living in mainland Australia’. In this instance, ‘people’ refers
to more than one person.
If you wish to emphasise the fact that Aboriginal and Torres Strait Islander
people are Australians, consider the use of ‘Aboriginal and Torres Strait Islander
Australians’ instead of ‘Aboriginal and Torres Strait Islander people’.
First people/first Australians
‘First people’ or ‘First Australians’ are collective names for the original people of
Australia and their descendants, and are used to emphasise that Aboriginal and
Torres Strait Islander people lived on this continent before European domination.
Both ‘First people’ and ‘First Australians’ are acceptable. Use these terms
to emphasise that Aboriginal and Torres Strait Islander people lived on this
continent before European arrival.
Indigenous people(s)
The Macquarie Dictionary defines ‘indigenous’ as ‘originating in and
characterising a particular region or country’.38 Based on this definition, an
indigenous person is a person who originates from and characterises a
particular region or country.
If using the term ‘Indigenous’, always capitalise ‘I’ when referring to Australian
Aboriginal and Torres Strait Islander peoples. The word ‘indigenous’, with a
lowercase ‘i’ is only used when referring to people originating in more than one
region or country such as the Pacific region, Asiatic region, Canada or New
Zealand. Because ‘Indigenous’ is not specific, some Aboriginal and Torres
Strait Islander people feel that the term diminishes their identity and should be
avoided.
The RACGP recommends using the term ‘Aboriginal and Torres Strait Islander’
in preference to ‘Indigenous’. If in doubt and before using the term ‘Indigenous’,
always consult with the local Aboriginal and Torres Strait Islander community.
It is acceptable to use the term ‘non-Indigenous’ when referring to people who
are not of Aboriginal and/or Torres Strait Islander origin.
If using the term ‘Indigenous people’, define what you mean by ‘Indigenous’ -
that is, if you are referring to Aboriginal and Torres Strait Islander people, it is
better to say so.
Torres Strait Islander person

A Torres Strait Islander person is a person/descendant from the Torres Strait
Islands, which are located off mainland Australia. Torres Strait Islander people
comprise around 10% of all Indigenous Australians and 0.3% of the total
Australian population. Always capitalise ‘Torres Strait Islander’.
Aboriginal and/or Torres Strait Islander people

About 38% of all Torres Strait Islander people are estimated to be of both
Aboriginal and Torres Strait Islander origin.39 Generally, the term ‘Aboriginal
and Torres Strait Islander’ is understood to include people who are of both
Aboriginal and Torres Strait Islander origin. However, the term ‘Aboriginal and/
or Torres Strait Islander’ may be necessary when you want to make it clear that
you are describing all three groups.
Goori, Murri, Nunga and other such terms

These terms are directly derived from Aboriginal languages and are the names
used by Aboriginal and Torres Strait Islander communities in specific areas
when referring to themselves. Examples - and acceptable terms - are:
• Murri (in northwest New South Wales and Queensland)
• Noongar (in southwest Western Australia)
• Nunga (in South Australia)
• Yolngu (in northeast Arnhem Land, Northern Territory).
Always check with the local community about using this type of terminology.
There are many Aboriginal and Torres Strait language groups within the above
mentioned geographic areas and the use of such terms can be restrictive. Also,
many community members may be from other parts of Australia, and wish to be
known by their place or origin. Some may wish to be known by their clan group.
Torres Strait Islanders may wish to be identified by their clan or island name.
Terms describing communities

The following terms used to describe Aboriginal and Torres Strait Islander
groups or communities, or positions within them, are acceptable:
• Clan
• Community
• Country
• Elder
• Mob
• Nation
• Traditional owner
• Tribe
Clan
The ‘clan’ is a local descent group, larger than a family but based on family links
through a common ancestry. A ‘clan’ is a subset of a nation, so nations may
have several clans within it.
The term ‘clan’ has a specific meaning that is derived from European and other
societies, and therefore may not necessarily be applicable to Aboriginal and
Torres Strait Islander cultures. Some Aboriginal and Torres Strait Islander people
use the term and such usage should be respected. If unsure, ask the local
community for guidance.
Community
There are many different perspectives on what a ‘community’ is. Non-
Indigenous people often use ‘community’ to refer to a particular geographic
locality. For example, the use of the expression ‘Warrnambool Aboriginal
community’ refers to all the Aboriginal people living in and around Warrnambool.
However, because Aboriginal and Torres Strait Islander people were forcibly
removed from their ancestral lands to live elsewhere, a community may
comprise people from many areas of Australia. Therefore, what non-Indigenous
people see as one Aboriginal and Torres Strait Islander community is in fact not
necessarily seen as such by its people.
Note too that an Aboriginal and/or Torres Strait Islander person may belong
to more than one community, identified by where they come from, where their
family is and where they live or work. The important thing to remember is that in
Aboriginal and Torres Strait Islander cultures a community is first and foremost
about country, (extended) family ties and shared experience. Community is
about interrelatedness and belonging and is central to identity.
It is generally acceptable to use the term ‘community’ to refer to Aboriginal
and Torres Strait Islander people living within a particular geographic location.
However, keep in mind the diversity of Aboriginal people within that ‘community’.
If you wish to emphasise the diversity of communities within the one geographic
location, use ‘communities’ in the plural form.
Country
‘Country’ is a term used to describe a culturally defined area of land associated
with a particular, culturally distinct group of people or nation. Use ‘country’ to
refer to a particular, culturally defined area of land, such as ‘Wiradjuri country’ or
‘Dunghutti country’.
Elder
The traditional meaning of an Aboriginal or Torres Strait Islander Elder is
someone who has gained recognition within their community as a custodian of
knowledge and lore, and who has permission to disclose cultural knowledge
and beliefs. Recognised Elders are highly respected people within Aboriginal
and Torres Strait Islander communities.
In some instances, Aboriginal people above a certain age will refer to
themselves as Elders. However, it is important to understand that in traditional
Aboriginal and Torres Strait Islander culture, age alone does not necessarily
mean that one is a recognised Elder. The use of the word Elder (uppercase)
is generally acceptable, but it is important to be aware of the differences
in the meaning outlined above. Also, keep in mind that, due to large scale
displacement during the protection and assimilation period, an Elder in a local
community may not be the traditional owner of the land.
Mob
‘Mob’ is a term identifying a group of Aboriginal or Torres Strait Islander people
associated with a particular place or country. It is a term that is extremely
important to Aboriginal and Torres Strait Islander people because it is used to
identify who they are and where they are from. ‘Mob’ is generally used by, and
between, Aboriginal and Torres Strait Islander people. While it may not always
be appropriate for other people to use this term, generally it is acceptable to
ask: ‘Who is your mob?’.
Nation/s
‘Nation’ refers to a culturally distinct group of people associated with a
particular, culturally defined area of land or country. Each nation has boundaries
that are strongly fought over and occasionally changed, and language is tied to
that nation and its country.
‘Nation’ can be used to refer to a culturally distinct Aboriginal and Torres Strait
Islander group and its associated country. Be aware that the boundaries of
some Aboriginal and Torres Strait Islander nations cross over state and territory
boundaries. This has important implications for service delivery and provision,
as well as negotiation processes.
The RACGP strongly recommends that staff and members identify the nation(s)
and clans in their local area, and those in areas visited regularly. This can be
done by contacting the local Aboriginal community controlled health service in
the first instance. If no such service exists in your region, contact the local land
council or other Aboriginal or Torres Strait Islander representative organisation,
or the state or territory NACCHO affiliate.
Traditional owner or custodian

The term ‘traditional owner(s)’ describes an Aboriginal or Torres Strait Islander
person or group of people directly descended from the original Aboriginal and
Torres Strait Islander inhabitants of a culturally defined area of land or country.
Traditional owners have a cultural association with this area of land or country,
deriving from the traditions, observances, customs, beliefs or history of the
original Aboriginal and Torres Strait Islander inhabitants of the area.
Despite this accepted usage, the term ‘owner’ reflects European views of
property so, in the above context, some prefer the term ‘custodian’, which
reflects a different association with the land.
Tribe
Like ‘nation’, a ‘tribe’ refers to a culturally distinct group of people associated
with a particular, culturally defined area of land or country. Be aware that
‘tribe’ has a specific meaning derived from European and other societies, and
therefore might not necessarily be applicable to Aboriginal and Torres Strait
Islander culture. Some Aboriginal and Torres Strait Islander people use the term
and such usage should be respected. If unsure ask the local community for
guidance.
Consulting with Aboriginal and Torres Strait

Islander communities
For protocols for visiting and consulting with Torres Strait Islander communities
in the Torres Strait region, refer to the Torres Strait Regional Authority cultural
aspx.
Consultation with Aboriginal and Torres Strait Islander groups and communities
is commonly used to seek information, advice, opinion or approval for a
proposed action or process. The strong oral tradition in Aboriginal and Torres
Strait Islander cultures should be honoured through face-to-face consultation.
Five levels of engagement

The Department of Families, Housing, Community Services and Indigenous
Affairs website describes five levels of engagement with Aboriginal and Torres
Strait Islander groups.40 While these may not be fully representative of the
perspective of Aboriginal and Torres Strait Islander people and may be overly
simplistic, they are worth considering. This is because there may be many
instances where consultation alone is an insufficient and even disrespectful form
of engagement.
The different levels are outlined below, with general practice examples identified.
Inform: Provide welcoming information for Aboriginal and Torres Strait Islander
peoples, information on how the practice will identify Aboriginal and Torres Strait
Islander people, and information on the Indigenous Health Incentive and the
PBS Co-payment measures.
Consult: The practice might ask patients identified as Aboriginal or Torres Strait
Islander what they think of the service provided by the practice in a survey, or by
contacting a local representative organisation.
Involve: The practice might conduct a focus group of Aboriginal people or
local Elders to determine how to improve programs for local Aboriginal and
Torres Strait Islander peoples. This process involves a longer term relationship
than consulting, but the practice is responsible for implementing any changes
it sees fit.
Collaborate: The practice has an ongoing discussion about a program, moving
some responsibility for implementation from the practice to the community.
This could be a project to provide cultural safety training to practice staff, or to
enhance referrals to an Aboriginal and Torres Strait Islander community health
service.
Empower: The Aboriginal or Torres Strait Islander community has control over
the planning, implementation and evaluation of an initiative (consistent with the
principle of self determination) and the practice provides advice and services
into this initiative. An example of this might be an audit of the practice’s activities
in the area of Aboriginal health or a community preventive health program.
Respectful consultation
It is stressed that each community has individual and unique customs and
beliefs and staff and members should therefore approach each community
individually. At the same time, there are some important characteristics common
to many Aboriginal and Torres Strait Islander groups and communities that
should be kept in mind.
Many Aboriginal and Torres Strait Islander communities and organisations
are consulted frequently and sometimes excessively, and have found that the
outcomes had no or little benefit for them. Being respectful includes respecting
the consultation time that may be required of the community and ensuring
that meaningful and positive outcomes ensue for both parties. It also involves
seeking genuine, not tokenistic, consultation.
Effective consultation should start early and throughout the decision making
process. Clarity about the purpose of the consultation and the amount of
influence the group will have is essential. This will help the people with whom
you wish to meet determine the most appropriate person to participate, and to
understand what is being asked of them.
It is important to respect the communal nature of Aboriginal and Torres Strait
Islander social structures in the process of consultation, communication and
consent. Most often decisions are not made by one individual. It is generally
necessary to consult with a series of people, families or clan representatives to
inform, consult and seek consent. Or a representative group of the community
or organisation will make the decision. Because decision making is collective
and by consensus, rather than hierarchical, time needs to be allowed for
decisions to be made.
Keep in mind, too, that ‘word of mouth’ is a powerful force in Aboriginal and
Torres Strait Islander cultures, and an individual encounter can engage or
alienate a community.
The complex relationships and obligations found in extended families
of Aboriginal and Torres Strait Islander Australians means that added
responsibilities not normally expected of non-Indigenous families are imposed
on Aboriginal and Torres Strait Islander group members. This can affect the
ways agreements might be achieved.
Aboriginal and Torres Strait Islander people may take some time to consider
an issue. Decision making processes may require further consultation, further
thought and discussion or further information. A group may have to wait until
everyone can be present, or meetings may need to be scheduled around
cultural obligations or travel considerations, especially in remote areas where
weather can determine travel.
Time delays (sometimes lengthy) before communities impart requested
information, or a less direct communication style, are common with Aboriginal
and Torres Strait Islander communities. This may reflect a number of important
factors including:
• the strength of the relationship that you have with the community
• the relative importance of the issue for the community
• the need for discussion within the community
• the need for the community to gain confidence in your long term commitment
to the welfare of the community.
As a result, Aboriginal and Torres Strait Islander timeframes may differ from
those expected, and it may be important to keep in mind and plan for this when
consulting with Aboriginal and Torres Strait Islander people.
To be direct may be seen as confrontational. During discussions, some
Aboriginal and Torres Strait Islander people may delay expressing a firm opinion
even though they may hold one. Instead, they may listen to others before
offering their own view. If their view conflicts with others they may understate it.
Aboriginal and Torres Strait Islander people may choose to remain silent, rather
than be seen to be disrespectful of the views of others.
The willingness of Aboriginal and Torres Strait Islander people to discuss issues
may also depend on their role in the community. It may not be appropriate
for some people to express views, even personal views, on issues that are
considered to be the responsibility of other people in the community.
The question ‘why?’ is virtually absent from the language of remote Aboriginal
and Torres Strait communities. Instead, observation is used as a learning
device.
When negotiating with Aboriginal and Torres Strait Islander communities, ensure
that opportunities for input by recognised Elders are made available. This may
occur indirectly. For example, an Aboriginal community controlled peak body
such as the state or territory NACCHO affiliate or the local Aboriginal community
controlled health service may be willing to negotiate with Elders on your behalf.
Be aware that although negotiation with recognised Elders is important,
it should not replace negotiation with Aboriginal community organisations
such as an ACCHS. Consultations with an Aboriginal or Torres Strait
Islander organisation or professional body should be conducted in a way
that acknowledges, includes and respects the specific knowledge, role and
experience of representatives of that organisation so that they can contribute in
a meaningful way to the process.
The Department of Families Housing Community Services and Indigenous
Affairs website: What is good engagement? has some useful information,
accessible at www.fahcsia.gov.au/sa/indigenous/progserv/engagement/
engagement/Pages/default.aspx.
On several occasions the RACGP National Faculty of Aboriginal and Torres

Strait Islander Health has sought feedback from key Aboriginal and Torres Strait
Islander health peak bodies - the National Aboriginal Community Controlled
Health Organisation (NACCHO) and the Australian Indigenous Doctors
Association (AIDA) - on policy documents or education programs. On these
occasions, a formal letter was sent by the President of the RACGP Council to
the President or Chair of the NACCHO and AIDA Boards. In each case, and
after consulting with the staff and members of these peak bodies, a formal letter
was sent to the RACGP President with a separate attachment detailing the
feedback.
Conducting meetings with Aboriginal and Torres

Strait Islander organisations and groups
For protocols regarding engagement with Torres Strait Islander communities
in the Torres Strait region, refer to the Torres Strait Regional Authority cultural
aspx.
Face-to-face meetings are the preferred way to engage and communicate with
a group of Aboriginal or Torres Strait Islander people. The general procedures,
protocols and simple behavioural courtesies relevant to all meetings, such as
not interrupting, taking turns and being respectful even if you disagree, hold true
in this context. However, there are some additional processes and actions that
are important to get right.
Preparation and groundwork

Because trust is so fundamental to developing a good working relationship with
an Aboriginal and Torres Strait Islander organisation, it is important to get to
know the people who are part of the professional community within which you
work, and who may be likely to be involved in a future meeting. This helps you to
become known to the community, and for its members to form an impression of
you. It can also provide a means by which you can better understand some of
the contextual and political issues related to the subject of the meeting, and to
learn who some of the key players may be.
You can do this by participating in local Aboriginal and/or Torres Strait Islander
community events, becoming active in professional membership networks,
contacting the local Aboriginal community controlled health service or land
council, or tapping into informal networks that have been established by
organisations known to you.
It is likely that through networks such as these, you will find individuals or
groups who will be willing to advise you on the way forward and help you build
understanding about the processes and practices of the local Aboriginal and
Torres Strait Islander community, including which people you should contact
initially. You will also have the opportunity to learn about the issues that are
considered important and the influential people advocating particular perspectives.
Keep in mind that these opportunities will only be of value if you keep an open
mind and learn from the people or groups with whom you are interacting. Stay
aware of your own cultural perspectives and expectations about the way things
should be done, because they may limit your ability to listen and learn about
alternative perspectives and customs. It is always possible to develop a way
forward that encompasses different cultural perspectives and processes; the
key is to be open and flexible, and to avoid imposing non-Indigenous values on
Aboriginal and/or Torres Strait Islander people.
The RACGP’s National Faculty of Aboriginal and Torres Strait Islander Health
was established in 2010, and so could have been considered the ‘new kid on
the block’ by the many organisations that have been working in Aboriginal and
Torres Strait Islander health for a considerable time. The Faculty indicated its
interest in meeting with the senior leadership of a number of these key national
organisations, but for some time was content to meet with their staff individually,
driven by common work interests or projects. Over time, a sense of the role
and purpose of each organisation was developed, and key milestones on
shared projects were reached. The Faculty believes that this has led to a greater
sense of trust, leading to opportunities to now develop more formal working
relationships at the senior level.
If you don’t know the people with whom you wish to meet, introduce yourself
before setting up the meeting. This can be by telephone, letter or email. If you
wish to meet with staff from a single organisation, it is best to make first contact
with the most senior person (usually via their personal assistant), and be guided
by their advice as to who you should approach.
Also be guided by advice as to the nature and logistics of the meeting -
whether it should be formal or informal, who should be invited and where it
should be located. If you invite the Aboriginal or Torres Strait Islander person or
organisation to choose the time and location of the meeting they are likely to feel
more comfortable attending. If your Aboriginal or Torres Strait Islander adviser
will be attending the meeting too, allow them to take the lead role. That person
will be relying on, or establishing, their credibility with this organisation, so they
must be allowed to do this without impediment.
Planning the meeting

Activities leading towards the arrangement of meetings should include:
• a clear and agreed statement of the purpose and possible longer term
outcomes of the meeting
• an agenda, agreed by both parties
• a good understanding by both parties of who will attend
• clarity about roles and expectations (if necessary)
• awareness of other ground rules, such as whether there is a need for
confidentiality, or whether the media will be involved - and if so, who should
speak to them
• consideration of resources needed - human, financial, physical and time -
and who will cover these.
Conducting the meeting

As indicated earlier, the usual protocols and courtesies of meeting behaviour
should be followed. In addition:
• Be aware of verbal and nonverbal messages being communicated by
Aboriginal or Torres Strait Islander participants, and use them as cues for
your own behaviour.
• Be clear in your own communications, both verbal and nonverbal.

• Remember that the ‘business’ of the meeting cannot proceed without the
development of a trustful and respectful relationship, and ensure that this is
your first priority, even if it takes time.
• Don’t be afraid of silence.
• Be wary of dominating the meeting; being seen to take over or apply
pressure will reduce the possibility of a positive outcome.
• Recognise that meeting participants have skills, knowledge and experience
of which you may be unaware, and involve them as much as possible.
• If additional issues emerge during the meeting, allow time to discuss them;
they may be relevant or important in ways that you do not understand.
• Don’t make promises that you cannot deliver on or encourage unrealistic
expectations.
• In particular, avoid trying to please an unhappy person or group if you can’t
follow through.
• Take notes, especially of any commitments you make.
After the meeting

Again, the commonly used postmeeting protocols apply to most of what needs
to be done after the meeting has concluded. Important tasks are:
• sending minutes or a summary of the meeting and what was agreed to
meeting participants for their approval and confirmation
• incorporating key points made or advice given into your thinking and planning
about the way forward, if you wish to work with the organisation over a
sustained period
• ensuring that you do whatever you promised.
The Aboriginal community controlled health sector41

The 2008 COAG ‘Closing the Gap’ initiative includes a number of measures
to improve health outcomes for Aboriginal and Torres Strait Islander people
in primary healthcare settings. One such measure, the Practice Incentives
Program Indigenous Health Incentive, aims to support general practices and
Indigenous health services to provide better healthcare for Aboriginal and
Torres Strait Islander patients, including best practice management of chronic
disease.42
The general practices or other health services that have registered for the
Indigenous Health Incentive will begin to identify their existing Aboriginal and
Torres Strait Islander patients and perhaps take on new patients as word of
mouth spreads. Over time, these practices and services may find that they
wish to make contact with their local Aboriginal and Torres Strait Islander
health service.
The RACGP is in the process of developing national and state/territory

relationships with the peak bodies for the Aboriginal community controlled
health services, in part to prepare the way for the development of such
contacts.
Already the RACGP’s National Faculty of Aboriginal and Torres Strait Islander
Health works with the National Aboriginal Community Controlled Health
Organisation (NACCHO) in number of ways.
State Faculties of the RACGP are meeting with state and territory NACCHO
affiliates to develop engagement principles and processes. These state/territory
relationships will be vital in overseeing engagement processes between local
Aboriginal community controlled health services and general practices.
The provision of primary healthcare services specifically for Aboriginal and
Torres Strait Islander communities across Australia is managed by various
providers, including state and territory governments (Northern Territory and
Queensland), private general practices, Aboriginal community controlled health
services and church groups.
In every state and territory in Australia, Aboriginal and/or Torres Strait islander
communities have developed and now manage their own primary healthcare
services. These services are called Aboriginal community controlled health
services. NACCHO is the national peak body for Aboriginal community
controlled health services, supported by state and territory peak bodies or
‘affiliates’.
The information in this section is partly drawn from the NACCHO website, www.
naccho.org.au/aboutus/aboutus.html.
Aboriginal community controlled health services are largely funded by the
Office of Aboriginal and Torres Strait Islander Health, operated by the local
Aboriginal and/or Torres Strait Islander community, and governed by a locally
elected board of management according to the principle of self determination.
The role of Aboriginal community controlled health services is to deliver holistic,
comprehensive and culturally appropriate healthcare to their community.
The first Aboriginal community controlled health service was established by the
local Aboriginal community in Redfern, Sydney, in July 1971. Since then, over
150 urban, regional, rural and remote Aboriginal community controlled health
services have been established across Australia. While many of these services
are found in urban or regional areas, over one third operate in remote or very
remote areas, where mainstream general practices are unlikely to be found.
Urban Aboriginal community controlled health services tend to be fewer in
number but larger in scope than their rural/remote counterparts, delivering more
episodes of care.
The differences between Aboriginal community controlled health services
and private general practices and many government-run health services can
be profound, but, if multiple service types operate in the same community, it

is important that they work together. A trusting and constructive relationship
between a general practice and an Aboriginal community controlled service can
lead to far better health outcomes for the Aboriginal and Torres Strait Islander
community than if the two services work in isolation.
Apart from the characteristics mentioned above, Aboriginal community controlled
health services may possess any or all of the following characteristics:
• focus on population health, of the whole community rather than the individual
• engagement in a number of preventive health activities, such as patient
education, nutrition classes
• focus on social and emotional wellbeing of the individual, family, community
• actions to address the social and emotional determinants of health
• provision of team based multidisciplinary care
• provision of other services such as dentistry, social work and counselling
• provision of services usually provided by outside agencies, such as financial
and housing assistance
• community-based health promotion, education and development activities
• recognition of the role of traditional culture
• mobile outreach services delivered to where people live
• strong professional networks via partnerships, written agreements and
collaborations
• strong and systematic continuous improvement focus
• presence of a community board of management.
Many Aboriginal community controlled health services are structured and
managed in a similar fashion to any other organisation, with a board of
management, a senior leadership team, program managers and service
delivery teams, including GPs. Regular meetings are held, staff training and
development conducted, and monitoring and reporting processes undertaken.
The largest Aboriginal community controlled health services would be urban,
and would have a workforce of well over 100 people.
Other, smaller and mainly remote, Aboriginal community controlled health
services may have no full time medical officers and rely on visiting GP and
specialist services. Instead day-to-day services would be delivered by practice
nurses and Aboriginal and Torres Strait Islander health workers.
Whether urban, regional, rural or remote, few Aboriginal community controlled
health services are staffed exclusively by Aboriginal and Torres Strait Islander
people. It is common to find highly committed, internationally or locally trained
health professionals working alongside their Aboriginal and/or Torres Strait
Islander colleagues.
The recommended processes for arranging a meeting with your local Aboriginal
community controlled health service are similar to those outlined in the earlier
part of this section. However, there are several important issues to keep in mind:
• Depending on your purpose, a meeting with the state or territory affiliate may
be more appropriate. For example, if you wish to conduct a research project
in partnership with an Aboriginal community controlled health service, it is
best to approach the affiliate.
• Every Aboriginal community controlled health service is very busy and deals
with constant requests for meetings, consultation, research opportunities
and so on. Be respectful of this and make the most of your meeting time
with them. Also, make sure that a relationship between your organisation and
theirs provides value to both parties and to their community.
A list of the national and state and territory peak bodies representing the
Aboriginal community controlled health services sector appears in the
Resources section at the end of this document. All websites contain details
of their member Aboriginal community controlled health services, some with
their own websites. Take some time to explore the culturally rich and diverse
communities they service and to learn about the services they provide.
Use ofAboriginal and Torres Strait Islander

intellectual and cultural property
Recognition and protection under the law
For many years, up to the present day, there have been countless instances
of the misappropriation and exploitation by non-Indigenous people of the
(traditional and contemporary) knowledge and creative expressions of Aboriginal
and Torres Strait Islander people. The application of intellectual property and
copyright law has more recently assisted to protect Aboriginal and Torres Strait
Islander intellectual property, but cultural property is less well covered under
these laws.
The RACGP acknowledges that Aboriginal and Torres Strait Islander people
have the right to control exploitation of their cultural and intellectual property,
and respects and protects the rights of Aboriginal and Torres Strait Islander
people to their cultural and intellectual property. The issue of copyright
ownership of stories, images, music, contributions and artwork should be
discussed prior to any modification or use of materials.
It is important to be aware of legislation relevant to the intellectual or cultural
property you wish to use or reproduce, and vital to request permission from the
appropriate authority representing the Aboriginal or Torres Strait Islander people
who own the information. Behaving ethically and with respect, and recognising
the moral rights of the owners or custodians of the work in question, is an
essential starting point.
The Australian Institute of Aboriginal and Islander Studies website has a section
with links to information and protocols regarding different areas of intellectual
and cultural property rights, at www1.aiatsis.gov.au/atsilirn/protocols.atsilirn.asn.
au/indexbebd.html.
Respecting Aboriginal and Torres Strait Islander intellectual and

cultural property
Secrecy and confidentiality
The right of Aboriginal and Torres Strait Islander people to keep secret and
sacred their cultural knowledge should be respected. Sacred and secret
material refers to information that is restricted under customary law. For
instance, some information may only be learned or viewed by men or women, or
only after initiation.
Aboriginal and Torres Strait Islander people have the right to maintain
confidentiality about their personal and cultural affairs.
Attribution
Aboriginal and Torres Strait Islander people should be given proper credit for,
and appropriate acknowledgement of, their achievements, contributions and
roles in the development of stories, and for the use of cultural material. In all
cases, permission to reproduce materials should be sought and copyright law
followed.
Continuing cultures
Aboriginal and Torres Strait Islander people have responsibility to ensure that
the practice and transmission of Indigenous cultural expression is continued for
the benefit of future generations. This responsibility is respected and supported
by the RACGP and should be incorporated in any dealings with material on
Aboriginal and Torres Strait Islander people.
Sharing of benefits
Aboriginal and Torres Strait Islander people have the right to be paid for the
use of cultural and intellectual property and to share in the benefits from any
commercialisation of cultural material.
In providing cultural services such as Welcome to Country, performances
and ceremonies, Aboriginal and Torres Strait Islander people are using their
intellectual property. As such, providers of these services should be appropriately
remunerated. Appropriate remuneration and/or assistance should be negotiated
between the cultural service provider and the agency, Aboriginal controlled
community health service or land council considering the travel required to and
from an event and the public profile of the event. Usually the land council will
work to ensure these opportunities are shared among those able to perform
them and frequently the community receives a portion of the payment.
Representations of Aboriginal and Torres Strait Islander people

and stereotyping
Representation of Aboriginal and Torres Strait Islander people in the health
professions needs to be handled with care. Some issues of concern are
discussed below.
Published materials
Aboriginal and Torres Strait Islander people’s obligation to continue their culture
includes observation of responsibility for material that is published with their
participation. Aboriginal and Torres Strait Islander people need an opportunity
to check that work they have participated in has not breached any cultural
norms or customary laws. This includes the use of images within the work.
Images should be related to the story. For example, it is inappropriate to place
an image of Torres Strait dancers next to a story about New South Wales South
Coast dancers.
Perpetuation of racist stereotypes

Perpetuation of racist stereotypes is one means through which Aboriginal and
Torres Strait Islander people are misrepresented. In particular, it is important to
ensure that educational and assessment resources and materials do not make
use of stereotyped case studies.
The perpetuation of racist stereotypes occurs, for instance, through presenting
homeless or alcohol dependent people as the subjects for case studies, rather
than, for instance, an Aboriginal man who has initiated a health maintenance
behaviour program, such as screening for diabetes.
It occurs through visual depictions of unwell Aboriginal and Torres Strait Islander
people in the absence of a clinical rationale for the image. There is value in using
a picture or case study of an Aboriginal child who is unwell when it illustrates
the illness being discussed. However, the same value does not exist when the
image is used to discuss Aboriginal and Torres Strait Islander health generally.
In this context, it is far preferable to use case studies and images of Aboriginal
and Torres Strait Islander people who seek and enjoy good wellbeing, unless
there is a specific educational purpose for the use of other images. This does
not deny the usefulness of discussing issues such as strategies for addressing
substance abuse (such as harm minimisation) in Aboriginal or Torres Strait
Islander communities, without stereotyping.
The purpose of this is not to ‘whitewash’ the very significant inequity in the
health of Aboriginal and Torres Strait Islander people, but rather to promote
wellbeing and reinforce positive messages.
Event planning: Observation ofAboriginal

and Torres Strait Islander cultural protocols
An increasing number of organisations and levels of government now incorporate
Aboriginal and Torres Strait Islander cultural practices or ceremonies into their
official events. This practice is often one of many that are part of the organisation’s
Reconciliation Action Plan, intended to help build mutually respectful relationships
between Aboriginal and Torres Strait Islander and other Australians.
By observing Aboriginal and Torres Strait Islander cultural protocols in RACGP
official and unofficial events, we are able to:
• recognise and pay respect to Aboriginal and Torres Strait Islander peoples,
cultures and heritage
• communicate Aboriginal and Torres Strait Islander cultural practices to the
broader community to promote respect and understanding
• demonstrate that Aboriginal and Torres Strait Islander cultures are living
through maintenance and practice of ceremonies and protocols
• demonstrate the recognition of Aboriginal and Torres Strait Islander people’s
unique position, which can assist in building relationships and partnerships.
If using an external venue, the RACGP recommends sourcing a venue and
catering owned and/or operated by Aboriginal and/or Torres Strait Islander
people where possible. This, too, demonstrates your acknowledgement of and
support for Aboriginal and Torres Strait Islander enterprises and cultures.
It is important to note that ceremonies and practices differ from place to place.
The planning timetable of official events should allow time for negotiations
with Aboriginal and Torres Strait Islander communities, and for discussion and
decision making within those communities.
The type of ceremony undertaken at an official event should be appropriate
to the nature and size of the event in accordance with the procedures set out
below and negotiations with local Aboriginal and Torres Strait Islander Elders and
organisations.
It is essential that these observances are meaningful and not done simply for
the sake of ritual.
Minimum requirements
When planning an official event, staff should consult with the RACGP National
Faculty of Aboriginal and Torres Strait Islander Health, or have a pre-agreed
approach that has been oversighted by the Faculty.
There may be instances when staff or members need to consult with the
local Aboriginal community controlled health service, local land council or an
appropriate agency for Torres Strait Islander people.
As a minimum requirement, an Acknowledgement of Country ceremony should
occur.
Protocol for the ceremony is provided on the following pages.
Welcome to Country
All major official events should include a Welcome to Country, which should
always occur in the opening ceremony of an event, preferably as the first item.
Major events include:
• provision of awards (including Fellowship of the RACGP)
• investitures
• conferences
• events where members of the public, representatives of governments and/or
the media are present.
If there is uncertainty as to whether an ‘acknowledgement’ or a ‘welcome’
is appropriate, advice may be sought from the RACGP’s National Faculty of
Aboriginal and Torres Strait Islander Health, or from the local community or land
council.
The Welcome to Country is conducted by a representative or representatives
of the local Aboriginal or Torres Strait Islander custodians, who welcome the
delegates and all in attendance.
A Welcome to Country may consist of a single speech by the representative
of the local Aboriginal or Torres Strait Islander community, or it may also
include a performance of some description. Performances may include a
traditional welcoming song, a traditional dance, a didgeridoo performance or
a combination of any of the above. In most communities, there are performing
artists who are regularly available for such occasions.
Staff and members of the RACGP are encouraged to be innovative in
recognising Aboriginal and Torres Strait Islander heritage. Other ceremonies or
practices may also be undertaken as considered appropriate by Aboriginal and
Torres Strait Islander people, including dances and performances. However,
all such decisions need to be made in consultation with the appropriate
community members.
Steps should be taken to ensure that the appropriate representative is invited
to perform the Welcome to Country, because it is a significant recognition
and a formal process. Some regions have two local Aboriginal or Torres Strait
Islander communities, in which case it may be appropriate to invite Elders from
both communities to perform Welcome to Country. Again, check with the local
communities or land council, to determine the correct protocol.
Protocols in relation to the performance of a Welcome to Country ceremony
are well established in most Aboriginal and Torres Strait Islander communities.
Where a Welcome to Country cannot be undertaken by Elders, a locally
recognised Aboriginal or Torres Strait Islander community spokesperson or a
locally recognised cultural service provider may be suitable to the community on
whose land the event is occurring.
There is no exact wording for the Welcome to Country. As such, the content
of the ceremony should be negotiated between the agency and the provider
with reference to the nature of the event and community practices. This is
best accomplished by preparing a written brief about the nature and purpose
of the event, so that the agency is able to meet your requirements. Generally,
providers offer participants local Aboriginal and Torres Strait Islander history and
cultural information and will go on to welcome the delegates to the country.
It is important that the Aboriginal and Torres Strait Islander representative (or
representatives) be contacted by telephone to be asked personally, and then
through a formal letter of invitation. The local Aboriginal community controlled
health service should be contacted in the first instance, or the land council
if there is no Aboriginal community controlled health service in your area.
All arrangements thereafter for the Welcome to Country should be mutually
negotiated. It is very important that the Aboriginal and Torres Strait Islander
representative has been involved in, and is comfortable with, the arrangements.
This may include the format of the ceremony: Who should be invited? Who
should perform the Welcome to Country? How will that person be recognised
for their time and commitment?
Keep in mind that the health status of many Aboriginal and Torres Strait Islander
Elders reflects that of their community, and they often have chronic illnesses. As
a result, it is respectful to ascertain whether they have particular needs for being
accompanied or seated for the ceremony.
It can also be useful to remember that people from other cultures (eg. Maori and
other indigenous cultures) may need to respond to the welcome and will require
time and/or space for this to occur.
Acknowledgement of Country
An Acknowledgement of Country would be used at minor functions such as
lectures, in house training, workshops, seminars and meetings. It demonstrates
respect for Aboriginal and Torres Strait Islander heritage and the ongoing
relationship of traditional custodians with the land.
On such occasions, the chair or speaker of the occasion may begin by
acknowledging that the meeting is taking place in the country of the traditional
custodians, for example:
I would like to acknowledge the Wiradjuri people who are the traditional
custodians of the land. I would also like to pay respect to the Elders both
past and present of the Wiradjuri Nation and extend that respect to other
Indigenous Australians who are present.
On occasion, there may be disputes about who the traditional custodians are.
Those who acknowledge the country can acknowledge ‘all’ the traditional
custodians of the land or can acknowledge the traditional custodians of ‘this’
land without naming those people. Acknowledging country in this way will
not cause offence where there is some potential or actual dispute around
ownership.
Typical Acknowledgement of Country statements can include the following:
‘I would like to acknowledge that this meeting is being held on the traditional
lands of the (appropriate group) people.’
‘I would like to acknowledge that this meeting is being held on Aboriginal land
and recognise the strength, resilience and capacity of Aboriginal people in
this land’.
Some Aboriginal and Torres Strait Islander communities would make less
distinction between past, current and future generations than do many
Europeans - in this context Aboriginal and Torres Strait Islander communities
may prefer that ancestors and descendants, as well as living Aboriginal and
Torres Strait Islander people, be acknowledged.
It is essential that the choice of words be meaningful to the person making them.
The Aboriginal and Torres Strait Islander flags

The Aboriginal flag
The Aboriginal flag is red, black and yellow: the top half is black, the bottom half
is red and a yellow sun is represented in the middle.
The flag is a symbol of Aboriginal pride, identity and struggle. Harold Thomas
is recognised as having created the flag in 1970. In 1995 the artistic work was
proclaimed officially as the Aboriginal flag. No permission was sought from the
copyright owner. In Thomas v Brown and Another, the court confirmed Thomas
as the copyright owner.
The symbolic meaning of the flag colours (as stated by Mr Harold Thomas) are:
• Black: Represents the Aboriginal people of Australia
• Red: Represents the red earth, the red ochre and a spiritual relation to the
land
• Yellow: Represents the Sun, the giver of life and protector.
The Torres Strait Islander flag
The green, black and blue flag incorporates a white Dar (headdress) and the
white five pointed star beneath it symbolises the five major island groups and
the navigational importance of stars to Torres Strait Islanders. The green stripes
represent the land, the black stripes represent the people and the blue, the sea.
According to the Torres Strait Regional Authority, the flag is a symbol of unity for
all Torres Strait Islanders.
The Torres Strait Islander flag was created by Bernard Namok of Thursday
Island (now deceased).
Use of the flags

There are some important considerations that need to be observed when using
Aboriginal and Torres Strait Islander flags:
• It is important to use the correct flag in stories relating to Aboriginal and
Torres Strait Islander people.
• For any Aboriginal and Torres Strait Islander events, the preferred protocol is
to use both flags.
• It is critical to make sure both flags are reproduced, hung and depicted the
correct way. The Australian flag should always be flown on the far left of a
person facing the flags, with the Aboriginal flag and Torres Strait Islander flag
flown next. The Aboriginal flag should be displayed with the black at the top
and the red at the bottom.
Special permission is needed to reproduce the Aboriginal flag and the Torres
Strait Islander flag. Contact the Commonwealth Flag Officer at the Department
of Prime Minister and Cabinet.
Purchase of corporate gifts

If the purchase of a corporate gift is required, the RACGP recommends that
preference is given to artefacts created by Aboriginal and Torres Strait Islander
peoples where possible. This approach has merit, in that it can bring attention
to these communities, while at the same time providing a vehicle to recognise
their talents.
Where gifts with Indigenous imagery or form are purchased, the college needs
to ensure that the intellectual property of Indigenous people has been respected
(eg. that the motifs have been used with permission), and, preferably, that the
source of the gift is an Indigenous-owned body that is respected within the
relevant community.
Undertaking projects and research
For protocols for conducting research in a Torres Strait Islander community in

the Torres Strait region, refer to the TSRA cultural protocols on the Torres Strait
Regional Authority website at www.tsra.gov.au/publications/tsra-cultural-policy.
aspx.
‘Nothing about us, without us’

Much research on indigenous people worldwide has been undertaken by
non-indigenous people, who imposed their worldviews on the subject, failed to
take a collaborative approach and tended to take ownership of the results. As
Angeline Hurley, in her paper ‘Respect, acknowledge, listen’, says:
‘Indigenous communities have been extensively researched, written about
and consulted with in the past, and as a result of negative experiences may
be sceptical 43
More recently, researchers have been encouraged to take a much more inclusive
approach to research into Aboriginal and Torres Strait Islander issues, and major
health research centres have adopted policies to reflect this. For example, one of
the principles of the charter of the Lowitja Institute, Australia’s National Institute
for Aboriginal and Torres Strait Islander Health Research, states:
‘Aboriginal and Torres Strait Islander individuals and organisations
must be fully involved - not just consulted - in the initiation, design and
implementation of the research the Institute undertakes. The point of
research must always be questioned. Whose interests does it serve? Who will
benefit? Who is asking the research questions?’44
The RACGP encourages GPs to participate in research, believing that being
part of the research community provides enhanced access to the latest
evidence, opportunities to collaborate with or be mentored by other GP
researchers, and enhanced research writing skills.45
The RACGP offers an individual general practice research module and a clinical
audit as part of its QI&CPD program. If you are a member, you can find a case
study in Aboriginal and Torres Strait Islander health at http://qicpd.racgp.org.au/
gps/activities/cat1/gp-research.
For a further example of general practice research in Aboriginal and Torres Strait
Islander health, see: Participatory action research in Indigenous health, which
recounts the experiences of Danila Dilba Health Service in working with staff
and patients on a participatory action research project at www.racgp.org.au/
afp/200806/200806esler.pdf.
It is vital that any proposal to conduct research involving Aboriginal and/or
Torres Strait Islander people or organisations has a clear statement regarding
the potential benefits for them - and especially for their community - and that
the proposal is approved before being progressed. Be prepared to accept
suggestions for changing the proposal, or even a ‘No’.
In line with the core principles outlined earlier, it is important for RACGP staff
and members to ensure that Aboriginal and Torres Strait Islander people have
meaningful involvement in the decisions about which projects and research to
do (priority setting), how they are done (design and implementation), and how
they are evaluated.
Any agreement should be clearly documented and signed by both parties.
Particular issues regarding end user and other relevant stakeholder issues
should be clarified in this agreement. Use of permissions, including ownership of
the data collected in the process of the research project, is an issue that needs
to be addressed in the development of an agreement between the two parties.
This should include a clear statement about what the information will be used
for and any further use that will be made of it. Don’t assume that permission to
use the data for a specific purpose represents a global permission. NACCHO or
the relevant state or territory affiliate is a good resource if you are unsure.
All institutions that conduct or sponsor research (including the RACGP) have a
human research ethics policy and processes governing all research conducted
under their auspices. The RACGP National Research and Evaluation Ethics
Committee follows the 2007 National statement on ethical conduct in human
research, developed by the National Health and Medical Research Council, and
available at www.nhmrc.gov.au/publications/synopses/e72syn.htm.
Rather than provide internal protocols that are specific to Aboriginal and Torres
Strait Islander health, the RACGP recommends that staff and members follow
both the National Health and Medical Research Council statement and one of two
national research ethics guidelines specifically developed for conducting research
into Aboriginal and Torres Strait Islander health. The two key guidelines are:
• The Australian Institute of Aboriginal and Islander Studies Guidelines for
ethical research in Australian Indigenous studies, available at www.aiatsis.gov.
au/research/ethical.html.
• The National Health and Medical Research Council Values and ethics:
Guidelines for ethical conduct in Aboriginal and Torres Strait Islander health
research, which provides guidance for ethical health research concerning
Aboriginal and Torres Strait Islander peoples, based on a framework of
Aboriginal and Torres Strait Islander values and principles. It is available at www.
nhmrc.gov.au/_files_nhmrc/file/health_ethics/human/conduct/guidelines/e52.
pdf.
Terri Janke, a Sydney-based intellectual property lawyer with family connections
to both the Torres Strait Islands (Meriam) and Cape York Peninsula (Wuthathi)
has written a paper: Writing up Indigenous research: authorship, copyright and
Indigenous knowledge systems, which is available at www.terrijanke.com.au/
documents/WritingupIndigenousresearch_14Sep09.pdf.
Principles applying to staff and member research in Aboriginal and Torres Strait
Islander health may also be extended to decisions about external stakeholders
who participate in the College’s conference and faculty based workshops. It is

important to be aware of the risk that Indigenous ownership will be downplayed
or overlooked by some external individuals or organisations, and of the need
to be vigilant in ensuring that all elements of the College’s activities, including
presentations by external stakeholders sponsored by the RACGP, adhere to
these key principles.
Meaningful involvement of people in projects and research can be expensive
in both time and other resources (eg. travel); it is important to plan project and
research budgets with this in mind.
Resources
Additional reading
• Horton D (Ed). Encyclopaedia of Aboriginal Australia. Canberra: Australian
Institute of Aboriginal and Torres Strait Islander Studies, 1994.
• Human Rights and Equal Opportunity Commission. Bringing them home:
National Inquiry into the Separation of Aboriginal and Torres Strait Islander
Children from Their Families. Sydney: HREOC, 1997. Available at www.hreoc.
gov.au/pdf/social_justice/bringing_them_home_report.pdf.
• The Australian Institute of Aboriginal and Torres Strait Islander Studies is the
world’s premier institution for information and research about the cultures
and lifestyles of Aboriginal and Torres Strait Islander peoples, past and
present. Visit its website at www.aiatsis.gov.au/index.html.
• The Australian Museum website has a section called ‘Stories of the
Dreaming’, which shares some stories of the history and culture of Australia’s
Indigenous people, handed down since the beginning of time at www.
dreamtime.net.au/Indigenous.
• The National Health and Medical Research Council’s publication: Keeping
research on track: A guide for Aboriginal and Torres Strait Islander peoples
about health research ethics, is available at www.nhmrc.gov.au/_files_nhmrc/
file/publications/synopses/e65.pdf.
• The Nursing Council of New Zealand website has Guidelines for cultural
safety, the Treaty of Waitangi, and Maori health in nursing education and
practice (2009) at www.nursingcouncil.org.nz/download/97/cultural-safety09.
pdf.
• The Koori History website of Aboriginal activist/academic Gary Foley is part
of a major historic archive collected over the past 45 years. It contains a huge
online collection of digital indigenous education materials. Available at www.
kooriweb.org/foley/indexb.html.
Protocols for using Aboriginal and Torres Strait Islander intellectual and
cultural property
Visual arts: Protocols for producing Indigenous Australian visual arts, Australia
Council, 2008
www.australiacouncil.gov.au/resources/reports_and_publications/artforms/
visual_arts/visual_arts_protocols_for_producing_indigenous_australian_visual_
arts
Performing arts: Protocols for producing Indigenous Australian performing arts,
Australia Council, 2008
dance/performing_arts_protocols_for_producing_indigenous_australian_
performing_arts
Media arts: Protocols for producing Indigenous Australian media arts,

Australia Council, 2008
indigenous_arts/media_arts_protocols_for_producing_indigenous_australian
media_arts
Music: Protocols for producing Indigenous Australian music, Australia
Council, 2008
music/music_protocols_for_producing_indigenous_australian_music
Writing: Protocols for producing Indigenous Australian writing, Australia
Council, 2008
literature/writing_protocols_for_producing_indigenous_australian_writing
Useful websites
• National: National Aboriginal Community Controlled Health Organisation
www.naccho.org.au
• ACT: Winnunga Nimmityjah Aboriginal Health Service
www.winnunga.org.au
• NSW: Aboriginal Health and Research Council of NSW
www.ahmrc.org.au/index.htm
• NT: Aboriginal Medical Services Alliance Northern Territory
www.amsant.org.au
• QLD: Queensland Aboriginal and Islander Health Council
www.qaihc.com.au
• SA: Aboriginal Health Council of South Australia
www.ahcsa.org.au
• Tasmanian Aboriginal Centre: no website available; contact TAC Health
Service, Hobart at: (03) 6234 0700
• Torres Strait Islands: Queensland Aboriginal and Islander Health Council
www.qaihc.com.au
• VIC: Victorian Aboriginal Community Controlled Organisation
www.vaccho.org.au
• WA: Aboriginal Health Council of Western Australia
www.ahcwa.org.au
References
1. RACGP. Position statement: Aboriginal and Torres Strait Islander health. South Melbourne
(Australia): RACGP; 2010 [cited 2012 Jan 16]. Available at www.racgp.org.au/scriptcontent/
policy/policydocs/Aboriginal_Health_policy.pdf.
2. Australian Institute of Aboriginal and Torres Strait Islander Studies. (AIATSIS) website at
http://archive.aiatsis.gov.au/referendum/20782.pdf
3. Oxford Dictionaries [Internet]. Definition of ‘colonize’. Oxford [UK]: Oxford Dictionaries; 2011
[cited 2011 Sept 13]. Available at http://oxforddictionaries.com/definition/colonize.
4. NSW Health. Communicating positively: A guide to appropriate Aboriginal terminology.
Sydney: NSW Health; 2004 p. 22 [cited 2010 June 1]. Available at www.health.nsw.gov.au.
5. Nursing Council of New Zealand. Guidelines for cultural safety in nursing and midwifery.
Wellington: NCNZ; 2002 p.9.
6. Nursing Council of New Zealand 2002. Guidelines for cultural safety in nursing and midwifery.
Wellington: NCNZ; 2002.
7. Webster’s Online Dictionary. Definition of ‘lore’. Webster’s Dictionary; 2011 [cited 2011
Sept 13]. Available at www.websters-online-dictionary.org/definitions/lore?cx=partner-pub-
0939450753529744%3Av0qd01-tdlq&cof=FORID%3A9&ie=UTF-8&q=lore&sa=Search#906.
8. Department of Foreign Affairs and Trade. Indigenous land rights and native title. Canberra: DFAT;
2011 [cited 2011 Sept 13]. Available at www.dfat.gov.au/facts/indigenous_land_rights.html.
9 . Australian Human Rights Commission. Bringing them home education module. Sydney:
AHRC; 2011 [cited 2011 Sept 13]. Available at www.humanrights.gov.au/education/bth/
glossary.html.
10. United Nations. Article 1 of the United Nations International Covenant on Civil and Political
Rights. Geneva: UN; 1994 [cited 2011 Sept 11]. Available at www.hrweb.org/legal/cpr.html.
11. Reconciliation Australia [cited 2011 Sept 13]. Available at www.reconciliation.org.au.
12. Australian Human Rights Commission. Bringing them home education module glossary.
Sydney: AHRC; 2010 [cited 2011 Sept 11]. Available at www.humanrights.gov.au/education/
bth/glossary.html.
13. Ibid.
14. Australian Human Rights Commission. Bringing them home: The stolen generation report.
Sydney: AHRC; 1997 [cited 2012 Jan 16]. Available at www.humanrights.gov.au/Social_
Justice/native_title/nt_issues/children.html.
15. Dawson, J (1881). Australian aborigines: The languages and customs of several tribes of
aborigines in the western district of Victoria, Australia. Cambridge: Cambridge University
Press, 2009.
16. Deverall M, MacFarlane I. ‘My heart is breaking’: A joint guide to records about Aboriginal
people in the Public Record Office of Victoria and the Australian Archives, Victorian Regional
Office. Canberra: Australian Government Publishing Service, 1993. Provides factual and very
moving records of pleas from Aboriginal people who were victims of this policy of separation.
17. Clark ID. Scars in the landscape: A register of massacre sites in Western Victoria 1803-1859.
Canberra: Aboriginal Studies Press for the Australian Institute of Aboriginal and Torres Strait
Islander Studies, 1995.
18. Bernard T, Society for Bettering the Condition of the Poor. Of the education of the poor.
London: W Bulmer & Co, 1809.
19. Deverall M, MacFarlane I. ‘My heart is breaking’: A joint guide to records about Aboriginal
people in the Public Record Office of Victoria and the Australian Archives, Victorian Regional
Office. Canberra: Australian Government Publishing Service, 1993.
20. Cilento Oration 2011. Indigenous health care: Managing emerging challenges. The RACMA
Quarterly. Aug 2011.
21. The Aboriginals Protection and the Restriction of the Sale of Opium Act 1897 (Qld) can be
viewed on the AIATSIS website at http://asset0.aiatsis.gov.au/webclient/StreamGate?folder_
id=0&dvs=1316052583786~449.
22. See, for instance, the Australian Institute of Health and Welfare May 2011 report, The health
and welfare of Australia’s Aboriginal and Torres Strait Islander people: An overview 2011.
Available at www.aihw.gov.au/publication-detail/?id=10737418989&tab=2.
23. To read further about the implications of the Mabo judgment, read Gary Foley’s essays
on the Koori Heritage website, including ‘Nativetitle is not land rights’. Available at www.
kooriweb.org/foley/essays/essay_2.html.
24. Northern Territory Board of Inquiry into the Protection of Aboriginal Children from Sexual
Abuse. Report of the Board of Inquiry into the Protection of Aboriginal Children from Sexual
Abuse. Northern Territory Government, 2007. Available at www.inquirysaac.nt.gov.au/pdf/
bipacsa_final_report.pdf.
25. Find out more on the Oxfam website at www.oxfam.org.au/explore/indigenous-australia/
close-the-gap/national-close-the-gap-day-2011.
26. RACGP. Position statement: Aboriginal and Torres Strait Islander health. South Melbourne
(Australia): RACGP; 2010 [cited 2012 Jan 16]. Available at www.racgp.org.au/scriptcontent/
policy/policydocs/Aboriginal_Health_policy.pdf.
27. Deep listening: Working with Indigenous mental distress. All in the Mind, ABC Radio National,
2007 [cited 2011 June 6]. Available at www.abc.net.au/rn/allinthemind/stories/2007/1967830.
htm.
28. Gordon M. Emotions run high as elders accept PM’s land hand-back deal. The Age
2011;June 8 [cited 2012 Jan 19]. Available at www.theage.com.au/national/emotions-run-
high-as-elders-accept-pms-land-handback-20110607-1fr3z.html#ixzz1OdmN0ula.
29. Social Health Reference Group. National strategic framework for Aboriginal and Torres Strait
Islander peoples’ mental health and social and emotional wellbeing 2004-2009. National
Aboriginal and Torres Strait Islander Health Council and National Mental Health Working
Group, 2004, p.9.
30. National Aboriginal Community Controlled Health organisation. ‘Aboriginal health’ definition.
Braddon ACT: NACCHO, 2011 [cited 2011 Sept 1]. Available at www.naccho.org.au/
definitions/abhealth.html.
31. National Aboriginal Community Controlled Health Organisation. ‘Community control’
definition. Braddon ACT: NACCHO, 2011 [cited 2011 June 6]. Available at www.naccho.org.
au/definitions/communitycont.html.
32. Coleman J. Confessions of an ordinary doctor in a Centre of Excellence. Good Practice
2011;5.
33. Huggins J. Protocols for consultation and negotiation with Aboriginal people. Brisbane:
Queensland Government, 1999.
34. Staff should refer to the talent release form on the RACGP Intranet for this purpose.
35. Eckermann A, Dowd T, Chong E, et al. Binan Goonj: Bridging cultures in Aboriginal health.
Elsevier, 2010 p.119.
36. For more discussion on these issues, visit Sharing the True Stories: Improving
Communication in Indigenous Health Care at www.cdu.edu.au/centres/stts/home.html.
37. This approach is further explained in the RACGP position statement: Identification of
Aboriginal and Torres Strait Islander people in Australian general practice, available on the
College website at www.racgp.org.au/aboriginalhealth/identificationpositionpaper.pdf .
38. The Macquarie Dictionary. Second edn. Sydney: The Macquarie Library 1992, p. 896.
39. Australian Bureau of Statistics. 4704.0 The health and welfare of Australia’s Aboriginal and
Torres Strait Islander peoples. Canberra: ABS 2008. Available at www.abs.gov.au/ausstats/
abs@.nsf/mf/4704.0.
40. Department of Families, Housing, Community Services and Indigenous Affairs. The
engagement spectrum. Canberra: FAHCSIA, 2010 [cited 2011 June 20]. Available at www.
fahcsia.gov.au/sa/indigenous/progserv/engagement/engagement/Pages/engagement_
spectrum.aspx.
41. This term is endorsed by NACCHO members and includes services in relation to Torres Strait
Islander communities.
42. Find out more on the Medicare Australia website at www.medicareaustralia.gov.au/provider/
incentives/pip/files/indigenous-health-incentive-guidelines.pdf.
43. Hurley A. Respect, acknowledge, listen: Practical protocols for working with the Indigenous
communities of Western Sydney. Indigenous Program of Cultural Community Development
NSW, 2003.
44. The Lowitja Institute. Home page. Available AT www.lowitja.org.au/about-lowitja-institute.
45. RACGP. QI&CPD website http://qicpd.racgp.org.au/gps/activities/cat1/gp-research.
A’ RACGP
Curriculum for Australian
General Practice 2016
CS16 Core skills unit

Healthy Australia.
Curriculum for Australian General Practice 2016 - CS16 Core skills unit
Disclaimer
The Royal Australian College of General Practitioners. Curriculum for Australian General Practice 2016 -
CS16 Core skills unit. East Melbourne, Vic: RACGP, 2016.

Tel 03 8699 0510

Fax 03 9696 7511
www.racgp.org.au
ISBN: 978-0-86906-446-7
Published May 2016

Curriculum for Australian General Practice 2016
Contents
Introduction 1
High level problem solving in general practice consultations 2
Core skills - the star of general practice 3
CS16 Core skills unit 4

Domain 1. Communication and the patient-doctor relationship 4
Context and application: Domain 1 7
Domain 2. Applied professional knowledge and skills 22
Domain 3. Population health and the context of general practice 55
Domain 4. Professional and ethical role 64
Domain 5. Organisational and legal dimensions 76

1
Introduction
The core skills that form the centrepiece of the Curriculum for Australian General Practice clearly state, in
measurable terms, the knowledge and skills required for each stage of general practice training. The unit was
developed by identifying the unifying elements in each of the former curriculum statements that collectively defined
the core skills and the unique nature of the Australian general practitioner (GP).
The development of this unit has been an organic process. It evolved throughout the Curriculum review process as
a result of subject matter experts, stakeholders, medical writers and editors recognising that there was significant
repetition in the existing curriculum, which could be addressed by the identification and articulation of the core skills.
The Core skills unit, in combination with specific units in Rural health and Aboriginal and Torres Strait Islander
health, now constitutes the Curriculum for Australian General Practice, replacing the 36 statements that made up
the 2011 Curriculum. The broad variety of groups of important conditions and unique populations that constituted
the former curriculum statements in the 2011 Curriculum for Australian General Practice are maintained as
curriculum support materials. These population, presentation and process contextual unit statements are made
up of a rationale for the importance of inclusion of this subject area in the skills framework and contain regularly
updated references. By separating the core skills from the populations and presentations to which they can
be applied, the opportunity has opened up to develop more resource materials for additional populations and
presentations as the need arises.
An important change to the format of the Curriculum for Australian General Practice is the reduction of the four
learning pathways to three. They have been divided into ‘Pre-general practice’ (refers to medical students and
doctors who have not entered into any of the formal general practice training pathways), ‘General practice under
supervision’ (eg pre-Fellow GPs enrolled in a training pathway) and ‘General practice - lifelong learning’ (eg
GPs who hold Fellowship of the RACGP [FRACGP] or Fellowship of the Australian College of Rural and Remote
Medicine [FACRRM], or who are vocationally registered).
The Core skills unit is designed to assist the RACGP, regional training organisations (RTOs), Quality Improvement
and Continuing Professional Development (QI&CPD) providers, specific interest groups, general practice
supervisors and other users of the Curriculum to design learning programs, courses, and assessments to meet
the stated outcomes and criteria. In conjunction with the Competency Profile of the Australian General Practitioner,
the Core skills unit will also provide guidance for those who assess overseas doctors on alternate pathways and
doctors wishing to be recognised as eligible for the FRACGP.
The nature of competency-based education means that the outcomes and criteria outlined in the Curriculum are
broad. This in turn enables training providers to develop the processes that enable the outcomes and criteria to be met
within the context of where, when, how and to whom the training is delivered. The ‘range statement’ provides further
detail of the terminology used, providing examples of how the outcomes and criteria can be brought to life in a variety
of ways. This curriculum is not a syllabus nor an exhaustive list of all of the knowledge and skills required to work as a
GP, but should rather be viewed as the foundations upon which more detailed learning programs are developed.
2 Core skills unit CS16
High level problem solving in general practice consultations
CONTEXT OF GENERAL PRACTICE

Broad range of patients presenting with broad range of conditions across the lifespan.
High incidence of transient and undifferentiated illness. High prevalence of chronic,

complex and multisystem illness. High incidence of psychological illness and
psychological factors contributing to presentations.
1. Communication and the patient-doctor relationship
2. Applied professional knowledge and skills
3. Population health and the context of general practice
4. Professional and ethical role
5. Organisational and legal dimension

3
Core skills - the star of general practice

Domain 1-----------------------
Communication and the
patient-doctor relationship
CS1.1 General practitioners communicate
effectively and appropriately to provide quality
care.
CS1.2 Through effective health education,

general practitioners promote health and
wellbeing to empower patients.
Domain 5--------------- P Domain 2

Organisational and legal Applied professional
dimension knowledge and skills
CS5.1 General practitioners use CS2.1 General practitioners provide the
quality and effective practice primary contact for holistic and patient
management processes and systems centred care.
to optimise safety.
CS2.2 General practitioners diagnose
CS5.2 General practitioners work and manage the full range of health
within statutory and regulatory conditions in a diverse range of
requirements and guidelines. patients, across the lifespan through a
CS2.3 General practitioners are

informed and innovative.
CS2.4 General practitioners collaborate

and coordinate care.
Domain 4 Domain 3 —1
Professional and ethical role Population health and the
context of general practice
CS4.1 General practitioners are ethical and
professional.
CS3.1 General practitioners make rational
decisions based on the current and future health
CS4.2 General practitioners are self-aware.
needs of the community and the Australian
healthcare system.
CS4.3 General practitioners mentor and teach to
improve quality care.
CS3.2 General practitioners effectively lead to
address the unique health needs of the
community.
Domain 1. Communication and the patient

doctor relationship
‘It is more important to know what sort of person has the disease than to know what sort of disease the person
has’ - Hippocrates
Criteria for stage of training

Core Competency
skills outcomes Pre-general General practice General practice - lifelong
practice under supervision learning
CS1.1 GPs CS1.1.1 CS1.1.1.1a CS1.1.1.1b Use effective CS1.1.1.1c Reflect on
communicate Communication Communicate communication skills with communication style to
effectively is clear, effectively with a a broad range of patients identify areas for improvement
and respectful, range of patients in the general practice
appropriately empathic and setting
to provide appropriate to
quality care the person and CS1.1.1.2a Empathy CS1.1.1.2b Identify CS1.1.1.2c Develop cultural
their sociocultura and sensitivity and manage barriers to competence with a broad
are consistently effective communication range of patients
context
demonstrated
CS1.1.1.3a Identify CS1.1.1.3b Develop CS1.1.1.3c Provide

factors that may strategies for cultural mentoring for junior
impact effective safety, to explore and colleagues regarding effective
communication integrate sociocultural communication
context into consultations
CS1.1.1.4a Describe CS1.1.1.4b Identify CS1.1.1.4c Review practice

strategies to situations where effective processes to improve the
overcome barriers to use of empathy and quality of communication for
communication sensitivity could improve patients in the practice
outcomes
CS1.1.1.5a CS1.1.1.5b Effectively CS1.1.1.5c Review and

Identify the factors utilise professional enhance the use of empathy
to optimise interpreter services and sensitivity in consultations
communication
when professional
interpreters are used
CS1.1.1.6c Review
practice use of professional
interpreters
CS1.1.2 Effective CS1.1.2.1a Outline CS1.1.2.1b Formulate CS1.1.2.1c Review and

communication the key factors strategies to assist in implement strategies to
is used in to consider when breaking bad news optimise safety of staff from
challenging breaking bad news aggressive patients
situations
CS1.1.2.2a Identify CS1.1.2.2b Assess and
and effectively effectively manage an
manage patients who agitated patient or family
are distressed or member
agitated
5

Core Competency
CS1.1.2.3a Identify CS1.1.2.3b Sensitively
patients who may discuss prognosis and
be experiencing end-of-life decisions
consequences of
trauma
CS1.1.2.4b Identify
and sensitively manage
patients experiencing
current or consequences
of trauma
CS1.1.3 CS1.1.3.1a Identify CS1.1.3.1b Identify CS1.1.3.1c Implement

Communication patients whose care and manage potential strategies to mentor and
with family, may be enhanced difficulties regarding support colleagues regarding
carers and by communication involvement of family ethical and effective
others involved with carers or family members and/or carers communication with family
in the care of members members and/or carers
the patient is
appropriate and
clear CS1.1.3.2a Identify CS1.1.3.2b CS1.1.3.2c Develop practice
situations where the Communicate guidelines for the involvement
involvement of family appropriately and of and disclosure to family
or carers may be ethically with family members and carers
detrimental to the members to obtain
care of the patient corroborating medical
history
CS1.1.3.3a Utilise CS1.1.3.3b Appropriately

ethical strategies engage and
to manage communicate with care
confidentiality and givers in management
to obtain informed plan discussions
consent prior to
communication with
family members and/
or carers and/or
others.
CS1.1.3.4a Develop CS1.1.3.4b Identify

communication and manage impacts of
strategies to assist in burden of care on carers
breaking bad news
to carers and family
members
CS1.1.3.5b Effectively
break bad news to family
members and carers
CS1.1.4 CS1.1.4.1a Identify CS1.1.4.1b Utilise CS1.1.4.1c Support and

Complaints cues that suggest effective problem-solving mentor colleagues for whom
and concerns a patient may have approaches to address patient complaints have
are managed concerns or issues patient complaints arisen
effectively regarding their care

Core
voi e Competency ____________________________
CS1.1.4.2a Analyse CS1.1.4.2b Appraise CS1.1.4.2c Enhance
and propose and review management problem-solving skills to
management of patient complaints optimise resolution of patient
strategies in clinical to determine if future and staff complaints
scenarios where improvements could be
issues have arisen made
CS1.1.4.3b Formulate CS1.1.4.3c Provide support

strategies to reduce risk for staff involved in complaint
of issues or complaints management
arising in the future
CS1.1.4.4b Facilitate CS1.1.4.4c Review practice

access to external structures for managing
resources if outcome complaints effectively
of concerns is
unsatisfactory
CS1.2 GPs CS1.2.1 Ways in CS1.2.1.1a Identify CS1.2.1.1b Identify CS1.2.1.1c Review health
use effective which health can patients who would opportunities to effect education resources and
health be optimised and benefit from health positive change through ensure that they are relevant
education maintained are promotion education health education and and up to date
to promote communicated to optimise health promotion
health and to patients, family outcomes
wellbeing members and
CS1.2.1.2a Describe CS1.2.1.2b Provide CS1.2.1.2c Use a variety of
to empower carers
patients possible barriers to opportunistic, effective strategies with individuals with
patients implementing counselling about normal different health belief systems,
important health life stages to optimise to explain the biomedical
promotion and self wellbeing model treatment approaches
care activities
CS1.2.1.3a Identify CS1.2.1.3b Identify

patients who and address barriers to
would benefit from patients implementing
opportunistic life health promotion and
stage counselling and self-care activities into
health education daily life
CS1.2.1.4b Identify and

address gaps in health
education resources
CS1.2.1.5b Utilise
appropriate strategies
to motivate and assist
patients in maintaining
healthy behaviours
7
Context and application: Domain 1

CS1.1 Communicate effectively and appropriately to provide quality care - includes the use of
socioculturally appropriate (eg age, developmental stage and gender-specific communication to relate effectively),
and non-judgemental verbal and non-verbal cues to communicate sensitively but efficiently to obtain and share
important information. Effective communication is an essential component of quality general practice to enable
effective history taking, facilitate physical examination, discuss investigations, diagnosis and management, and
ultimately to encourage improved health outcomes through collaborative continuity of care.
Through ongoing continuity of care, GPs often develop a comprehensive understanding of their patients and are
thus uniquely situated to identify patient verbal and non-verbal cues (which may identify important issues such
as exposure to violence and abuse). This knowledge and establishment of trust, gained through continuity of
care, is the basis of an effective therapeutic relationship. The development of a respectful therapeutic relationship
usually involves empathy and sensitivity where the GP makes an effort to see things from the perspective of the
patient, validates that perspective to enable patient-centred quality diagnosis and management to be initiated,
and effective collaboration through provision of appropriate health education and consequent shared, informed
decision making.
Effective communication is the culmination of a number of important skills and attitudes, including:
• being respectful, empathic and sensitive

• utilising attentive listening (active and reflective)
• humility
• effective use of silence and open questions

• acknowledgement of the patient’s level of health literacy and modification of language to match
• other non-verbal communication, such as body language, eye contact and appropriate touch.
Utilisation of other strategies, such as reflection, regularly ‘checking back’ with patients, summarising issues
discussed, management plans and provision of appropriate health information, are all important.
Evaluation of an individual’s level of health literacy and acknowledgement of the existence of any power
imbalance in the therapeutic relationship is an important step to enable rapport and trust to be established prior
to the provision of health information through verbal, electronic or paper-based means. This will more readily
enable effective health education, communication of risks and consequent utilisation of motivational and/or
supportive counselling to encourage behavioural change with the aim of optimising health outcomes.
Another aspect of effective communication is being mindful that patients of Aboriginal and Torres Strait
Islander and other culturally and linguistically diverse (CALD) backgrounds, individuals with cognitive or sensory
impairments or with limited health literacy and other vulnerabilities (such as mental illness, history of trauma,
substance use issues, etc) have the same rights to quality healthcare as everyone else, and the right to the same
respect and courtesy. This attitude can be demonstrated by maintaining a person-centred approach through
techniques such as the development of cultural awareness and competency, effective use of interpreters where
appropriate, speaking directly to the person (even when an interpreter is being utilised), using an age-appropriate
tone of voice, appropriate scheduling of long appointments, etc.
Appropriate communication with family, carers, health professionals and others takes into account duty of care
responsibilities, particularly in regards to confidentiality and respect for patient autonomy, as well as the provision
of concise and meaningful information to optimise collaborative care and thus clinical outcomes.
Useful resource
• Warnecke E. The art of communication. Aust Fam Physician 2014;43(3):156-58, www.racgp.org.au/afp/2014/march/art-of-
communication
CS1.1.1 Sociocultural context - has a broad range of meanings, but generally refers to an individual’s ‘way of life’.
This context may be described as the influences which can impact an individual’s behaviour, perspective, choices,
health and spiritual beliefs (including use of traditional medicines), values and risk classification to varying degrees.
Factors to consider when assessing an individual’s sociocultural context include:
• determination of Aboriginal and Torres Strait Islander status
• race/ethnicity
• gender identity
• sexuality
• religious beliefs (may have relevance to choice of medical procedures and acceptable managements)
• socioeconomic status
• family connections and traditions
• peer groups
• occupation
• age.
It is important not to make assumptions about an individual’s sociocultural context based on their appearance.
The most reliable way to determine the potential influences on an individual’s health beliefs and values is through
sensitive, open and respectful questioning. Health beliefs may arise from traditional healing systems that may utilise
a number of modalities, such as mind-body medicine, dietary advice, acupuncture and herbal medicines, to address
health problems (eg Ayurvedic Indian medicine, traditional Chinese medicine and traditional healing systems used
by the Aboriginal and Torres Strait Islander peoples gathered from thousands of years of empirical knowledge and
clinical experience).
CS1.1.1.1a Range of patients - refers to the broad range of individuals who may present to general practice.
This includes:
• age ranges and life stages of development
• different levels of physical, emotional and intellectual ability
• acute, chronic and preventive health presentations and impairments affecting any body system or combination
of systems (to comply with the RACGP definition of general practice and the requirements for completion of the
training program)
• gender
• socioeconomic and health literacy backgrounds
• culturally and linguistically diverse backgrounds
• diversity of religion, sexuality and occupation.
CS1.1.1.2a Empathy and sensitivity - may be expressed verbally and/or non-verbally to indicate a GP’s
understanding of the patient’s feelings through an open and non-judgemental approach. Empathy and sensitivity may
be defined as demonstrating the ability to sense what other people are experiencing emotionally and/or spiritually,
combined with the ability to imagine what the individual may be thinking or feeling based on understanding of their
personality, previous experiences, sociocultural context and belief systems. Empathy may be demonstrated by a GP
through the use of active listening, considering influences of personality, sociocultural context, previous experience
and level of health literacy, as well as acknowledging and, if appropriate, validating the patient’s belief systems.
9
CS1.1.1.3a Factors that may impact effective communication - includes:
• patients who speak English as a second language and the importance of recognition of the need to engage
professional interpreters (either onsite or by phone)
• inadequate provision of time for consultation with individuals of culturally and linguistically diverse backgrounds
and/or low health literacy
• failure to recognise impacts of cognitive and/or sensory impairments on ability to communicate and process
information
• recognition of different health beliefs stemming from cultural, spiritual or religious backgrounds (eg the need for
gender-concordant care)
• failure of the GP to recognise and manage their own cultural bias and cultural lens, which can have potentially
negative impacts on the quality of communication and, thus, on the future ability to work collaboratively with
individuals
• recognition that individuals with sensory or cognitive impairment may require different communication styles and
strategies.
Useful resources
• Britt H, Valenti L, Miller G. Determinants of consultation length in Australian general practice. Med J Aust 2005;183(2):68-71,
www.mja.com.au/journal/2005/183/2/determinants-consultation-length-australian-general-practice
• Harrison C, Britt H, Charles J. Sex of the GP - 20 years on. Med J Aust 2011;195(4):192-96, www.mja.com.au/journal/2011/195/4/
sex-gp-20-year
CS1.1.1.4a Strategies to overcome barriers to communication - includes non-judgemental acknowledgement

of gender, cultural and sexual diversity, which is an essential component of effectively incorporating sociocultural
context into consultations. Assessment of an individual’s health literacy is another important consideration within
sociocultural context which will assist the GP in presenting information in a way which will be readily understood
to enable effective engagement and a collaborative approach to care. Acknowledgement of own cultural lens
and cultural bias, utilising empathy and sensitivity to deliver person-centred care which is culturally safe, are all
important strategies to incorporate into routine care.
Undertaking a ‘cultural assessment’ is a valuable way to establish any important cultural influences on an
individual’s health beliefs and consequent decision making. The basic premise of cultural assessments is that
patients have a right to their cultural beliefs, values and practices, and these factors should be understood,
respected, and considered when giving culturally competent care. A comprehensive cultural assessment allows the
practitioner to gain an understanding of how embedded the individual is in their culture and its belief system, which
may be gained through asking about migration history and whether this was involuntary or voluntary, whether they
live in an area with many people of the same culture, which traditions they follow (ie accessing traditional healers
and therapies), learning about the meaning of the illness in terms of the patient’s cultural lens (eg what they think
has caused their illness and their expectations of treatment and care), etc.
CS1.1.1.2b Manage barriers to effective communication - barriers may include social, language and cultural
barriers that can be exacerbated by a GP displaying ignorance, cultural incompetence or disrespect. This can
lead to the GP failing to recognise the impact of social and/or language differences on the therapeutic relationship,
patient fear and mistrust of mainstream health services due to previous experiences, low levels of health literacy,
provision of inadequate time for complex consultations, and cultural factors which may impact on communication
and an individual’s ability to engage with health services.
Other barriers may include individual perceptions of power imbalances, failing to acknowledge financial concerns,
other responsibilities or transport issues which may impede health service access, and demonstrations of lack of
person-centred care through labelling an individual as being non-compliant rather than seeking to understand the
reasons behind them either choosing to be non-compliant or struggling to comply with suggested treatments,
which may be related to many bio-psycho-socio-cultural factors.
Language barriers may be minimised by use of professional interpreters (including Translating and Interpreting
Services [TIS] and Auslan interpreters). There should be consideration of the potential impact of communication
difficulties on capacity to provide informed consent. When using professional interpreters, a number of factors
need to be considered (outlined in CS1.1.1.5b). Multilingual patient resources may include use of culturally
appropriate pictures and diagrams, health promotion posters in languages common in the local community, written
information and reliable online resources, etc.1
Other barriers to communication may include:
• sensory impairment (acute or chronic hearing and/or visual or neurological impairment)
• chronic cognitive impairment
• acute medical conditions and injuries which may impair a conscious state related to head injury, hypoxia,
cerebrovascular event, hypotension secondary to blood loss, delirium secondary to substance use, metabolic
condition (eg ketoacidosis), renal or hepatic failure
• perceptual disturbance related to mental illness (eg acute psychosis)
• changed or challenging behaviours in individuals with intellectual disability or cognitive impairment, etc.
For individuals with sensory or chronic cognitive impairments, barriers can be managed by a combination of
strategies such as respectfully asking individuals and/or carers about communication preferences, styles and
techniques, using visual cues, written and pictorial materials, assistive technology and using ‘check back’
strategies to ensure that you are communicating effectively. Acknowledgement and minimisation of the impacts
of clinic environmental factors on effectiveness of communication (eg interruptions, background noise) with
individuals with sensory and/or cognitive impairment is important wherever possible.
It is also important to consider capacity to accommodate individuals who require gender-concordant care, skills
to negotiate time alone with children and adolescents presenting with an adult guardian, (eg to discuss sexual
health issues such as flagging a need for contraception), understanding of sexual consent, and ability to recognise
unwanted sexual experiences.
Conditions to which stigma is attached (which may be related to sociocultural context) with consequent reticence
to disclose, such as mental health or other sensitive issues (eg intimate partner or family violence, sexual assault,
female genital mutilation, sexuality and gender issues, ie gender dysphoria), need to be handled sensitively and
empathically. Patients are more likely to disclose sensitive or intimate issues when they have established trust in
their therapeutic relationship. GPs need to have the capacity to recognise cues from their patients and ensure that
they approach concerns about these experiences sensitively (refer to CS1.1.2.3).
Patients who present in an emotionally charged state may impact the effectiveness of communication. De
escalation skills are important to learn to improve confidence in managing such individuals (refer to CS1.1.1.5a).
Use of technology during consultations can act as a barrier to communication. Computerised medical software is
commonly used and GPs need to be mindful about using good communication skills to ensure that the computer
does not hold the focus of the consultation. As a balance to this, comprehensive and well-structured clinical notes
are important for continuity of care and communication with other health professionals.
Useful resource
• Victorian Refugee Health Network. Promoting Refugee Health: A guide for doctors, nurses and other health care providers caring for
people of refugee backgrounds. 3rd edn. Melbourne: Victorian Foundation for Survivors of Torture, 2012, http://refugeehealthnetwork.
org.au/learn/guides
CS1.1.1.3b Strategies to explore and integrate sociocultural context into consultations - may include routine
incorporation of cultural assessment into consultations (refer to CS1.1.1.3a), and a focus on cultural safety and
development of cultural competence combined with awareness and management of an individual’s cultural bias
and cultural lens (refer to CS1.1.1.2c).
11
CS1.1.1.4b Consultation where effective use of empathy and sensitivity could improve outcomes - includes
consultations where the GP has delivered patient-centred care through efforts to see things from the perspective of
the patient, validation of that perspective, and utilising techniques such as active listening, reflection and summarising,
asking questions to clarify, paying close attention to verbal and non-verbal cues, effective use of silence, etc. Patients
experiencing chronic pain is an example of a common clinical situation where effective use of empathy is paramount -
GPs who acknowledge that perceptions of pain are individual and often inherently linked with social, cultural, spiritual
and psychological factors and comorbidities, and who sensitively incorporate relevant factors into management plans
and communicate non-judgementally, will typically optimise outcomes for their patients.
Useful resource
• Warnecke E. The art of communication. Aust Fam Physician 2014;43(3):156-58, www.racgp.org.au/afp/2014/march/art-of-
communication
CS1.1.1.5b Professional interpreter services - includes consultations with patients who speak no or limited
English, or who may appear fluent but are more comfortable with their primary language when discussing complex
health issues. It is important for GPs to recognise that language difficulties can negatively impact upon the care
received by those from a culturally and linguistically diverse background. While an interpreter can assist in bridging
the language gap, the cultural meaning embedded within language adds further complexity to cross-cultural
consultations. Different cultures attach different meanings to parts of the body and types of illness, and this can
impact upon the presentation of the illness or compliance with treatment. Linguistic difference can also reduce
access to health education materials and impacts patients’ knowledge about available health services.
Australian GPs are fortunate to have access to an Australian Government funded interpreter service (the Translating
Interpreting Service Doctors Priority Line). Practices need to obtain a TIS client code to enable access by staff at
the clinic. Effective use of professional phone or onsite interpreters is of paramount importance and is therefore a
vital skill to learn. This service is free to the medical practice and the patient. It should be noted that general practice
clinic staff, pharmacists and specialists in private practice also have access to free interpreting via TIS.
It can be argued that failure to use a professional interpreter in consultations with people from linguistically diverse
backgrounds may be considered to be a breach in duty of care in many cases. Given the importance of effective
communication in healthcare, interpreter use is an important risk management strategy. There are significant
ethical concerns about using untrained individuals to interpret (such as family or friend), including the fact that there
is no certainty of the accuracy of the information being conveyed, concerns about confidentiality and imposing
unreasonable responsibility and stress on these individuals, particularly children and youth.
Key points to consider when using professional interpreters include:
• Use promotional material, which is readily visible in the waiting room, to make patients aware that the clinic uses
onsite or telephone interpreters when needed.
• Early identification of the need for an interpreter, including noting this in the individual’s clinical file, in order
to enable an interpreter to be booked and an appropriate length of time for the consultation. Be aware that
individuals may have preferences regarding preferred language, gender, ethnicity and, for individuals from small
communities, even the location of the interpreter (interstate professionals may be preferred).
• Be clear on the language required. For example there are many variations/accents/dialects of Arabic, including
Egyptian, Sudanese, Iraqi, Syrian, and more. This needs to be clear when booking an interpreter; however, the
preferred dialect may not always be available.
• Be aware of whether the patient demonstrates signs of discomfort or suspicion regarding the interpreter, and
address any problems as required (this can occur in the case of individuals who, for example, have migrated
from areas of conflict where professionals may have participated in torture or informed on individuals to the
government or armed forces).
• Inform patients that confidentiality is implicit in the role of interpreters.
• Discuss the process of the consultation with the interpreter and the patient in order to ensure each person is
aware that they can clarify anything that does not make sense during the consultation.
• Speak to and (if culturally appropriate) maintain eye contact with the patient rather than the interpreter. Use the
second person, eg ‘Do you ... ’, not ‘Does he/she ...’
• Speak in short, readily interpretable segments and avoid medical jargon. Do not speak to the interpreter while
excluding the patient; everything said in the consultation should be interpreted (this also applies to what the
patient says).
Useful resources
• Victorian Refugee Health Network. Caring for refugee patients in general practice: A desktop guide. 4th edn. Melbourne: Victorian
Foundation for Survivors of Torture, 2012, http://refugeehealthnetwork.org.au/?s=desktop+guide&silverghyll_tpicker=s=desktop+guide
• Huang Y, Phillips C. Telephone interpreters in general practice. Bridging the barriers to their use. Aust Fam Physician 2009;38(6):443-46.
• Victorian Refugee Health Network. Promoting Refugee Health: A guide for doctors, nurses and other health care providers caring for
people of refugee backgrounds. 3rd edn. Melbourne: Victorian Foundation for Survivors of Torture, 2012, http://refugeehealthnetwork.
org.au/learn/guides
C1.1.1.2c Cultural competence - may be viewed as a continuum and defined as the development of awareness
and respect for differences in social structure and culture, and acknowledgement of the impacts of these on health
and wellness beliefs and ability to engage with Australian health services. Culturally competent GPs have the ability
to manage these differences respectfully.
Cultural competence has been defined as:
‘A set of congruent behaviours, attitudes, and policies that come together in a system, agency, or amongst
professionals and enables that system, agency, or those professionals to work effectively in cross-cultural
situations. The word culture is used because it implies the integrated patterns of human behaviour that includes
thoughts, communications, actions, customs, beliefs, values, and institutions of a racial, ethnic, religious, or
social group. The word competence is used because it implies having the capacity to function effectively. A
culturally competent system of care acknowledges and incorporates - at all levels - the importance of culture,
the assessment of cross-cultural relations, vigilance towards the dynamics that result from cultural differences,
the expansion of cultural knowledge, and the adaptation of services to meet culturally-unique needs’.1
Skills in cultural competence may be attained through routine use of cultural assessments (refer to CS1.1.1.3a) and
ongoing acknowledgement and management of a professional’s own cultural bias and cultural lens.
Cultural safety is an important part of the spectrum of cultural competency. The emphasis for cultural safety is
on reflective practice and professional empathy rather than awareness of culturally specific beliefs or practices.
Cultural safety involves the development of awareness of power imbalance in therapeutic relationships which can
negatively impact quality of care and development of strategies to minimise this.2
The ‘cultural lens’ refers to the GP’s own unique personal worldview influenced by the cultures that nurtured them.
This ‘lens’ may influence the way a health professional judges and makes assumptions about patients from a different
background, and recognising this cultural bias is a necessary step for clinical effectiveness. A patient’s cultural lens
shapes beliefs about illness causation, the nature of a particular illness, and the appropriate treatment and expected
outcome and thus it is important for health professionals to factor this into developing a collaborative therapeutic
relationship. Cultural bias may be defined as interpreting and judging phenomena by standards inherent to one’s own
culture which in healthcare can contribute to misunderstandings impacting diagnosis and consequent management,
power imbalances in the doctor-patient relationship, as well as bring up issues of class in some cultures.
Useful resources
• Kleinman A, Benson P.Anthropology in the clinic: The problem of cultural competency and how to fix it. PLoS Medicine 2006;3(10):1673-76.
• Klein HA. Cognition in natural settings: The cultural lens model. Cultural Ergonomics: Advances in Human Performance and Cognitive
Engineering Research, Vol 4. Emerald Group Publishing Ltd, 2004; p 249-80.
• NACCHO Cultural Safety Training Standards: A background paper, www.naccho.org.au/download/cultural_safety/
CSTStandardsBackgroundPaper.pdf
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CS1.1.1.4c Practice processes to improve the quality of communication for patients in the practice - may
include ensuring patients are aware that feedback is welcomed (this can occur through provision of practice
information brochures or posters) and that contact details of the state or territory provider of oversight of health
service delivery (ie health services commissioner or ombudsman) are displayed in a prominent position. It is also
important to consider systems that ensure appropriate feedback and support is provided if complaints are raised
about communication skills and that follow-up occurs to ensure improvements have been made as a result,
guaranteeing that systems are in place to routinely organise interpreters for patients who require this service,
multilingual patient information is provided to the relevant patient population, and appropriate information is
available according to the various levels of health literacy of patients at the practice.
CS1.1.2.1a Factors to consider when breaking bad news - may include informing a patient or family member
that they or a relative has a condition which may seriously impact their future. This often is thought to relate to
informing a patient about a potentially terminal diagnosis; however, whether a diagnosis is perceived as being ‘bad
news’ is most impacted by the context and expectations of the patient. Such diagnoses may include cancer, type
1 diabetes, psoriasis, alopecia, multiple sclerosis, dementia, a significant injury which may impact a sportsperson’s
ability to compete long-term, and informing a pregnant couple that their baby has a chromosomal abnormality or
congenital abnormality, etc.
It can be difficult to estimate the impact the bad news will have on the recipient until the GP has determined the
expectations that the individual has of the consultation and their understanding of the possible diagnoses and/
or outcomes. There are a number of different frameworks to assist with developing skills in this area, including
the widely used SPIKES (Setting, Perception, Invitation/Information, Knowledge, Empathy, Summarise/Strategise)
model,3 which is explained in detail at CS1.1.1.4b.
CS1.1.2.2a Effectively manage patients who are distressed or agitated - may include individuals who:
• are emotionally distressed after receiving bad news
• have unmet expectations during or after a consultation (eg drug-seeking patients whose requests have been
declined)
• are agitated due to experiencing delirium or psychosis related to medical or psychiatric conditions
• are frustrated because of long wait times
• are substance-affected.
There is a broad range of presentations of distress and/or agitation and, at the more extreme end, this can result
in threats to the wellbeing of the GP, practice staff and members of the public in the vicinity. Early identification
cues of distress or agitation can include aggressive body language, expressing dissatisfaction in the waiting room,
appearing to be responding to auditory or visual hallucinations, smelling of alcohol, or demonstrating signs of
being substance-affected, etc.
Attempting to understand the reason for the agitation or distress can be important in managing such individuals;
however, a tentative diagnosis is often all that is possible in emergency situations if there is no prior knowledge
or experience with the patient. Ensuring personal safety and the safety of others in the vicinity, including practice
staff and other patients, is of paramount importance. This can be improved by physical and experiential practice
structures such as the availability of duress alarms, avoidance of extremes in sound, wall colour and temperature to
minimise sensory overstimulation, adequate exits to ensure that staff have access to safe exits if others are blocked,
and the availability of regular staff training in managing behavioural emergencies and identifying early signs of
agitation.
De-escalation techniques are important skills to develop. These may include paying attention to respect
for personal space, avoidance of provocative language or physicality, establishing clear and concise verbal
communication, identifying wants and feelings of the individual, trying to avoid judgement and clearly stating
whether you agree or disagree with them, setting clear and non-threatening limits, providing individuals with
choices and optimism, and ensuring all staff members have access to debriefing following the incident.
Useful resources
• Richmond JS, Berlin JS, Fishkind AB, et al. Verbal de-escalation of the agitated patient: Consensus Statement of the American
Association for Emergency Psychiatry Project BETA De-escalation Workgroup. West J Emerg Med 2012;13(1):17-25, www.ncbi.nlm.
nih.gov/pmc/articles/PMC3298202
• Fishkind AB. Calming agitation with words not drugs: 10 commandments for safety. Current Psych 2002;1(4), www.currentpsychiatry.
com/index.php?id=22661&tx_ttnews[tt_news]=181234
CS1.1.2.3a Patients who may be experiencing consequences of trauma - may include patients who have had
a history of exposure to family violence in childhood and may then develop complex post-traumatic stress disorder
(PTSD) (formerly known as borderline personality disorder), and women who have been exposed to intimate partner
violence and may present with anxiety disorders or substance abuse disorders. These histories are often hidden
and the signs of possible previous exposure therefore need to be keenly sought out.
Individuals who have migrated to Australia under a humanitarian program or as asylum seekers often have histories
of exposure to torture and trauma, which can be compounded by issues following their arrival in Australia (eg time in
detention).
Military and emergency service personnel are commonly exposed to trauma which can present soon after a
particular event or many years later. PTSD is a common consequence of such circumstances and needs to be
identified and managed to optimise outcomes. Vicarious trauma is another possibility to be considered in individuals
who provide support and/or counselling to groups who have experienced traumatic events. Peer support through
regular debriefing and/or professional counselling can be beneficial for these people.
Useful resources
• The Royal Australian College of General Practitioners. Abuse and violence: Working with our patients in general practice (White book).
Melbourne: RACGP, 2014, www.racgp.org.au/your-practice/guidelines/whitebook
• Adults Surviving Child Abuse. Practice guidelines for treatment of complex trauma and trauma informed care and service delivery.
ASCA, 2012, www.asca.org.au/Portals/2/Practice%20Guidelines/ASCA%20Guidelines%202014_WEB_Final.pdf
CS1.1.2.1.b Strategies to assist in breaking bad news (also refer to CS1.1.1.4a) - may include:
• ensuring that you have adequate time available to ensure that the patient does not feel rushed and is able to
express what they need to, and to enable the GP to respond to the patient’s emotional reactions
• involving the patient in decision-making
• dealing with the stress created by the patient’s expectations for cure
• the involvement of multiple family members
• the dilemma of how to give hope when the situation is bleak.
The complexity of the interaction can sometimes create serious miscommunications, such as patient
misunderstanding about the prognosis of the illness or purpose of care. Poor communication may also thwart the
goal of understanding patient expectations of treatment or involving the patient in treatment planning. The SPIKES
model is a useful framework to assist in delivering bad news:
• Set up interview - sit down, ensure privacy, minimise interruptions, involve significant others, ensure the patient
has a safe way to get home.
• Perception assessment - ‘What have you been told so far?’
• Obtaining the patient’s Invitation to proceed; Invite patient to determine how consultation will go - ‘How would
you like me to give you this information?’
• Giving Knowledge and information - ‘I’m so sorry, I’m afraid I have bad news’.
• Emotional assessment and Empathy - sit with the patient, provide them time to express what they need to, use
appropriate physical contact.
• Strategy and Summary - ask the patient whether they are ready to talk about a plan from this point.3
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CS1.1.2.2b .Assess and effectively manage an agitated patient or family member - may include the need
to assess the person in order to evaluate the cause of their agitation, including emotional distress related to a
bad prognosis, anger at perceptions of being treated unfairly or inappropriately (refer to CS1.3.4) , having unmet
expectations regarding treatment (particularly relevant to drug-seeking patients ), experiencing a delirium related
to substance use or a health condition such as a metabolic imbalance, a head injury or a psychotic disorder, etc.
Effective management involves optimising safety of the GP, practice staff and members of the public in the vicinity
(including family members and carers of the agitated individual).
CS1.1.2.3b Prognosis and end-of-life decisions - refers to ensuring that the patient and/or carer understands
the likely outcome of the diagnosed condition with consequent impacts on quality of life indicators, and
requirements for care and management plans. This is relevant for a broad range of conditions and, as per
CS1.1.1.4a, can include:
• sports injuries for athletes
• chronic dermatological conditions with cosmetic consequences and subsequent impacts on self-image and
self-esteem
• chronic diseases requiring intervention and ongoing management (eg chronic obstructive pulmonary disease
[COPD], diabetes, congestive cardiac failure, epilepsy)
• diseases with a course that is likely to involve ongoing deterioration, such as primary progressive multiple
sclerosis or amyotrophic lateral sclerosis).
It is often the role of the GP to facilitate advanced care planning and directives in patients nearing the end of their
lives. This will enable future health and wellbeing care which is person-centred and based on the principles of self
determination, dignity and the avoidance of suffering. The purpose is to incorporate the individual’s values, beliefs
and preferences to guide decision making if and when the individual is unable to communicate their wishes.
Useful resource
• Bird S. Advance care planning. Aust Fam Physician 2014;43(8):526-28, www.racgp.org.au/afp/2014/august/advance-care-planning
CS1.1.2.4b Consequences of trauma - may include individuals who have been traumatised as a result of
exposure to a single incident or cumulative exposure, and those experiencing an acute stress reaction or more
chronic effects (PTSD and complex PTSD). Individuals who have experienced the effects of trauma are common
in general practice (65% of men and 50% of women are exposed to a potentially traumatic event in their lifetime4)
and are often unrecognised. It is thus important for GPs to recognise the many ways in which trauma can present.
Examples of traumatic exposures include:
• involvement in war
• experiencing natural disasters
• survivors of torture
• survivors of childhood emotional, physical or sexual abuse (may present as complex PTSD in adults, previously
known as borderline personality disorder)
• adult survivors of family violence
• survivors of violent crime or accidents
• individuals who have experienced medical trauma, which can result from medical procedures that are
considered successful but experienced as traumatic by the individual (eg complicated labour, involuntary
admission to a psychiatric unit).5
The experience of trauma stems from the overwhelming of coping capacity in light of precipitating event(s) and, if
not resolved, has a range of negative impacts on physical and psychological health. The consequences of trauma
can impact on how individuals engage with health professionals and services, and their ability to undertake medical
care such as routine screening (eg Pap smears in women who have experienced childhood or adult sexual abuse).
Individuals who have experienced trauma can appear with a wide variety of presentations, including eating
disorders, substance-use issues, anxiety, self-harming and undifferentiated illness (such as complex pain
syndromes), etc. Not all individuals with these health issues have experienced trauma; however, it may be useful for
GPs to assume that every patient in practice may have been exposed to a form of trauma in the past. GPs need
to communicate sensitively and empathically when caring for individuals who may have experienced trauma, and
utilise communication techniques such as active listening and validation of patient experience.
Assessing safety levels for individuals who are in situations in which they are continuing to experience trauma
is imperative, by utilising techniques such as ‘psychological first aid’ (which may include monitoring of mental
state, provision of emotional support, education and encouragement of active use of social support and self-care
strategies), consideration of trauma-focused cognitive behavioural therapy (CBT) or dialectical behaviour therapy
(DBT) for complex PTSD and eye movement desensitisation and reprocessing (EMDR), etc.
Useful resources
• Adults Surviving Child Abuse. Practice guidelines for treatment of complex trauma and trauma informed care and service delivery.
ASCA, 2012, www.asca.org.au/Portals/2/Practice%20Guidelines/ASCA%20Guidelines%202014_WEB_Final.pdf
• Centers for Disease Control and Prevention. Adverse Childhood Experiences Study 1997, www.cdc.gov/violenceprevention/acestudy
• Forbes D, Creamer MC, Phelps AJ, et al. Treating adults with acute stress disorder and post-traumatic stress disorder in general
practice: a clinical update. Med J Aust 2007;187(2):120-23.
CS1.1.2.1c Optimise safety of staff - may include:

• regular training in identification of early signs which may lead to aggressive behaviour (eg individuals who are
noticeably affected by substances such as alcohol or methamphetamine)
• identifying individuals in the waiting room who are pacing or visibly irritable
• training in management of aggressive individuals, including simple de-escalation techniques and confidence to
implement safety net strategies if these are not effective
• ensuring there is an escape route if confronted
• ensuring there are at least two staff members in the facility at all times
• ensuring there are duress alarms in place and that emergency service contact numbers are visible.
CS1.1.3 Family, carers and others - may include any individual who participates in a care role for a patient,
including staff in residential aged care facilities and interpreters.
CS1.1.3.3a Ethical strategies to manage confidentiality and to obtain informed consent - acknowledges that
confidentiality is central to an effective therapeutic relationship and that assessment of capacity to provide consent
is an integral part of ensuring ethical practice (refer to CS5.2.1 and CS5.2.2). Strategies may include ensuring that
GPs have specific informed consent from their patients to discuss particular health issues with family and/or carers,
advising family members of the importance of confidentiality, and not providing confidential patient information
without consent. Complexities may arise in regards to individuals where their capacity to provide consent is not
clear to the GP and/or the family and/or carers. Examples of this may include adolescents who may have a legal
right to provide informed consent to medical procedures/management without parental consent according to
the GP but the parents do not agree, or individuals with cognitive impairment who have a legal medical power of
attorney or guardian but disagree with a decision made by this person.
CS1.1.3.3b Management plan discussions - may include discussions regarding end-of-life care, eg palliation,
in regards to advanced care planning in collaboration with patients, patients with cognitive decline or intellectual
disability, etc.
CS1.1.3.4b Impacts of burden of care - may include:
• examples of identifying signs of stress in carers (particularly individuals with chronic mental health issues, older
patients with intensive needs, individuals with sensory, physical or intellectual disabilities, individuals who are
receiving palliation for end-of-life care, etc)
17
• discussing and organising respite as required
• identifying grief reactions, distress and fatigue
• identifying signs that carers are not coping with their workload and providing support and advice regarding
management
• assisting with bereavement, etc.
CS1.1.4 Complaints and concerns - may include complaints about yourself, a colleague within your clinic
or a practitioner to whom you have referred a patient. Complaints may be made by patients, family members,
health professionals or other staff within or external to the clinic. Broad categories of complaints include patient
perceptions of poor communication and interpersonal skills, inappropriate or inadequate treatment, inadequate
quality of care such as incorrect or missed diagnoses, inappropriate referrals for diagnostic or management
procedures, issues raised by family members or carers regarding quality of care provided and concerns about
waiting times, etc. Effective management strategies may include those outlined in 1.1.4.1b.
Useful resource
• Walton M, Smith-Merry J, Healy J, McDonald F. Health complaint commissions in Australia: Time for a national approach to data
collection. Australian Review of Public Affairs 2012;11(1):1-18, www.australianreview.net/journal/v11/n1/walton_etal.pdf
CS1.1.4.1b Effective problem-solving approaches to address patient complaints - may include:
• acknowledging and, if appropriate, validating the complaint or concern and its impact on the individual (issues
that may appear trivial to you may be emotionally distressing for the patient)
• offering an apology to the complainant if appropriate, while recognising that this is not admission of guilt (eg ‘I
am sorry that this has happened’ or ‘I am sorry that you are upset about this’)
• developing an understanding of the needs of the person making the complaint and addressing these in a logical
and clear fashion
• using an empathic approach to relate to the perspective of the individual
• ensuring that you do not ignore complaints and make a concerted effort to manage complaints made about
you. This may consist of acknowledging the complaint in person or over the phone, and either dealing with it at
the time or discussing the plan as to how this is going to be addressed with the individual.
• organising a follow-up time to discuss the outcome of the complaint investigation.
It is important to try to maintain the therapeutic relationship; however, if this is not possible ensure that you hand
over care to another health professional. It may also be important to contact your medical defence organisation to
notify them of the complaint. Managing complaints can be extremely stressful, so ensure that you are looking after
yourself and that you have support and space to debrief if required. When the complaint has been resolved, ensure
that you reflect back on what has occurred and review practices and processes to minimise risk of this happening
again in the future.
CS1.1.4.4b External resources - may include providing patients with contact details of the state-based
or territory-based complaint management mechanisms, such as the health services commissioner, health
ombudsman or Australian Health Practitioner Regulation Agency (AHPRA).
CS1.1.4.4c Practice structures for managing complaints effectively - may include:
• designation of roles within the practice for complaint management (ie a senior administrative staff member to
manage complaints related to reception staff and a senior clinical staff member to manage complaints related to
clinical staff or management)
• ensuring that patients are aware of mechanisms available for managing complaints
• ensuring that review strategies are in place when complaints are made
• improving practice systems and processes to minimise future risk
• ensuring that staff are adequately supported during the usually stressful complaint process, etc.
CS1.2 Effective health education - encapsulates the provision of accurate and timely, evidence-based, quality
health information and decision aids to patients by means most appropriate to their individual context (taking
into account sociocultural factors and level of health literacy). Mechanisms may include through socioculturally
appropriate verbal and written information on diagnoses and/or management options, including health promotion
activities via electronic or paper-based resources to educate, empower and assist in developing rapport with
patients. The use of psychological techniques such as motivational counselling, CBT and/or mindfulness to
encourage and sustain behavioural change to optimise health are also important educational tools to address
barriers to optimising care and maintaining compliance with treatment. Empowerment through education and
provision of ongoing support to maintain self-care strategies to optimise health outcomes is another important
aspect of effective health education.
Health education provided by GPs covers a broad range of issues to suit the diverse range of patients and health
conditions seen in general practice, eg information on reproductive health (such as safe sex), optimising fertility
and options for effective contraception, information on prevention regarding healthy lifestyle, nutrition and exercise,
smoking cessation, stress minimisation, sexuality, mental health awareness, etc.
CS1.2 Promote health and wellbeing - the World Health Organization (WHO) defines health as ‘A state of
complete physical, mental and social wellbeing and not merely the absence of disease or infirmity’.6
Health may be promoted in general practice through provision of advice that caters to the bio-psychosocial needs
of the individual. This may include ways to prevent illness through:
• optimising nutrition and exercise
• minimising and managing stress
• education and promotion of early return-to-work after work-related injuries or illness
• provision of education on safe sex and other strategies to maintain or improve sexual and reproductive health
(eg effective contraception, education around consent and identification of individuals at risk of intimate partner
violence)
• identification of need for harm minimisation strategies regarding substance use
• identification of signs of substance dependence and addiction (eg alcohol, cigarettes, marijuana,
methamphetamine, gambling, etc)
• identification of opportunities to prevent injury and disease in at-risk individuals (eg due to participation in certain
sports, hobbies or occupations)
• identifying and managing safety risks for older patients, etc.
CS1.2 To empower patients - describes the process of supporting and increasing the capacity of individuals or
groups to make informed choices and to transform those choices into desired actions and health and wellbeing
outcomes. Shared decision making and effective provision of health education appropriate to the individual’s level of
health literacy and needs are important factors to assist in achieving this. An example of empowerment may include
providing information which enables individuals to self-care and to recognise when they need to seek advice.
CS1.2.1.1a Identify patients who would benefit from health promotion education - highlights the need to
identify individuals or groups who are at risk of disease or injury and thus require education and/or intervention
to minimise this risk through provision of preventive care. It would be difficult to find a patient attending a general
practice who wouldn’t benefit from targeted health promotion education. Some examples include:
• older patients - may be at risk of falls, so enrolment in a falls prevention program, as well as education of the
individual and family members about the importance of enhancing safety structures at home (eg avoiding clutter
on the floor, use of safety rails) may be useful
19
• women or couples who are contemplating conceiving or are in the early stages of pregnancy - may need
information regarding reducing risk factors for adverse pregnancy outcomes, such as smoking, alcohol intake,
illicit substance use, and consideration of opportunistic vaccination and screening for those at risk of inherited
conditions such as thalassaemia
• gay, lesbian, bisexual, transgender or intersex individuals - may require non-judgemental support in regards to
gender identify or sexual identity issues, may benefit from education about maintaining sexual health through
risk reduction and/or regular access to screening, and adolescents may benefit from education about safe sex,
support and normalisation of sexual and gender identity beliefs
• patients recognised to be overweight - may benefit from an empathic provision of support and advice around
nutrition and exercise
• new parents - may benefit from opportunistic provision of advice on vaccination of relatives of new babies
• individuals at risk of genetically inherited conditions - may consider genetic testing, screening or review of
themselves or family members as appropriate. Inherited conditions may include hereditary nonpolyposis
colorectal cancer (HNPCC), breast cancer if two or more family members diagnosed under 50 years or one male
family member has bilateral disease diagnosed, haemochromatosis, hypertrophic obstructive cardiomyopathy
(HOCM) and coeliac disease.
CS1.2.1.1b Opportunities to effect positive change through health education and promotion - the WHO
defines effective health promotion as ‘the process of enabling people to increase control over and improve their
health’. The principles and efforts of health promotion are utilised in social systems, diseases, risk factors and
population groups and may occur through provision of quality information and education which is appropriate to
the individual and to their sociocultural context.7
GPs are often in a prime position to offer preventive health advice and thus health promotion. Examples may
include:
• provision of advice on lifestyle modification in regards to maintaining a nutritious, balanced diet, healthy exercise
regime, smoking cessation, minimising alcohol intake and stress management
• timely discussions around return-to-work, including the health benefits of work, early in the experience of a
physical or mental illness and framing expectations regarding early return-to-work and effective rehabilitation to
reduce risk of chronicity, recurrence and/or re-injury
• effective pre-conception and antenatal counselling regarding genetic screening of women and couples at risk of
inherited conditions through family history of inherited conditions or other risk factors for genetic abnormalities,
such as parental age. Effective counselling includes discussion of risks such as financial costs and potential
benefits of screening
• provision of information in travel medicine consultations to reduce risk of injury or illness during travel
• harm minimisation discussions with patients with substance addictions.
The use of electronic technologies such as videoconferencing and mobile phone health applications to
communicate information can be valuable in effecting positive changes which optimise health outcomes.
CS1.2.1.2a Barriers to patients implementing important health promotion and self-care activities - may
include individuals who:
• are struggling to manage social stressors and work commitments and who are unable to make time for their
own health
• have a severe health condition which impacts their ability to recognise other health conditions or access care
• have language or cultural barriers impacting access to information and care (eg refugees or asylum seekers)
• have problems with addiction or substance dependence (eg dependent on alcohol, marijuana,
methamphetamine, gambling, etc) and are unable to prioritise their own health due to the consequences of their
addictions
• are carers for people with high-level needs (eg cognitive and/or physical disabilities, terminal conditions, etc)
• are experiencing severe mental health issues which impact their ability to prioritise other health needs (eg
psychotic conditions, complex PTSD, severe depression, etc).
CS1.2.1.3a Opportunistic life-stage counselling - describes the important role that GPs play in recognising
when an individual may benefit from the provision of information to improve their health and wellbeing, when they
may have presented with an unrelated issue. This strategy is often key to the provision of preventive healthcare.
Examples may include counselling:
• parents of young children regarding developmental screening
• women in the child-bearing years regarding pre-conception care and screening
• adolescents regarding safe sex, mental health awareness and gender or sexual identity issues
• middle-aged women regarding common issues experienced at this time related to menopause
• older individuals regarding falls prevention, consideration of advanced care plans, etc.
CS1.2.1.2b Opportunistic effective counselling about normal life stages - refers to the importance of
developing skills to identify and explain normal physiology and psychology, and the pathological deviations from
this. Examples include recognition of:
• functional and dysfunctional personality traits, and consequent behaviours and impacts on health
• normal and complicated grief and stress reactions
• the role of hormonal change around menarche, pregnancy, fertility and menopause on physical and
psychological functioning and sexuality
• prostatic hypertrophy, and the impacts of hormonal changes on physical and psychological functioning and
sexuality throughout the lifecycle of men
• methods to optimise fertility using lifestyle modification and education regarding fertility awareness-based
methods (FABM) of contraception, such as the Billings ovulation method.
CS1.2.1.3b Address barriers to patients implementing health promotion and self-care activities - involves
recognising how behaviour, sociocultural values and attitudes impact health, and the utilisation of strategies to
address these. Examples include:
• harnessing specific individual traits and behaviours to promote greater self-care and access to healthcare (eg
using individually appropriate analogies for some male patients, such as prioritising regular health checks,
similarly to regular car services)
• utilising technology such as smart phone apps, and web-based or paper-based resources to track - and thus
improve - insight into symptoms or behaviours to motivate change (eg for weight loss, diabetes management, etc)
• organising regular review and follow-up for individuals who have low levels of motivation and/or insight into
health risks in order to provide support and education to assist them in moving through the ‘stages of change’
more efficiently.
CS1.2.1.4b Gaps in health education resources - relates to the need to identify that the available health
education resources do not meet the needs of the local community. This includes recognising the need for
multilingual health education resources for patients from CALD backgrounds, audio tools for patients who
are vision-impaired, diverse and appropriate resources for patients who identify as gay, lesbian, bisexual or
transgender.
CS1.2.1.5b Appropriate strategies to motivate - may include identifying the stage of the change model8 at which
an individual is currently sitting, assessing their level of health literacy, gaining insight into their health risks, and
acknowledging any sociocultural factors which may be promoters or barriers to sustaining healthy behaviour change.
Provision of education about risks to the individual of not changing behaviour is an important part of this process.
21
The SNAP (smoking, nutrition, alcohol and physical activity) model9 can be a useful framework to identify unhealthy
behaviours which, when combined with the development of an effective therapeutic relationship with regular review,
follow-up and/or referral, can assist in establishing and maintaining positive change. Other strategies to consider
include education, provision of web-based or paper based-resources and tools (such as sleep diaries, activity
logs or food diaries), and use of motivational interviewing, CBT, interpersonal skills training, anger management,
structured problem solving and family therapy.
CS1.2.1.2c Different health belief systems - it is broadly accepted that health behaviour is determined by
personal beliefs or perceptions about a disease and the strategies available to decrease its occurrence. Personal
perception is influenced by a broad range of sociocultural factors, particularly education and health literacy,
previous experiences, cultural factors, religion, peer group and family beliefs. The health belief model is made up
of four perceptual constructs which can be used individually, or in combination, to explain health behaviour. These
perceptual constructs are: perceived seriousness of disease, perceived susceptibility to disease, perceived benefits
of changing behaviour at reducing risk to disease, and barriers to changes in behaviour.10
Other important modifying influences which impact health behaviour include cues to action or motivating factors (eg
illness in a family member or friend, media reports, health warnings) and sense of self-efficacy (ie a belief in one’s own
ability to do something). Beliefs of Aboriginal and Torres Strait Islander peoples, traditional Chinese medicine, the
Catholic church and contraception, Jehovah’s witnesses and blood transfusions are examples of well-established
health belief systems which need to be acknowledged and understood in consultations, as they vary from the Western
biomedical model and thus may impact whether individuals are likely to engage with and accept health services.
CS1.2.1.2c Biomedical model - describes a conceptual framework for objectively explaining disease that
includes only biological factors such as pathology, biochemistry and physiology, and does not take social,
psychological or individual subjective influences into account.
References
1. Cross TL, Bazron BJ, Dennis KW, Isaacs MR. Towards a culturally competent system of care. Washington, DC: CASSP Technical
Assistance Center, Georgetown University Child Development Center, 1989.
2. Australian Institute of Health and Welfare. Cultural competency in the delivery of health services for Indigenous people. AIHW, 2015.
Available at www.aihw.gov.au/uploadedFiles/ClosingTheGap/Content/Our_publications/2015/ctgc-ip13.pdf
3. Buckman RA. Breaking bad news: The S-P-I-K-E-S strategy. Available at www.acssurgerynews.com/view-pdf.html?file=co/journal/
articles/0202138 [Accessed 9 December 2015].
4. Forbes D, Creamer MC, Phelps AJ, et al. Treating adults with acute stress disorder and post-traumatic stress disorder in general
practice: a clinical update. Med J Aust 2007;187(2):120-23.
5. Levine PA. In an unspoken voice: How the body releases trauma and restores goodness. Berkeley California: North Atlantic
Books, 2010.
6. World Health Organization. Preamble to the Constitution of the World Health Organization as adopted by the International Health
Conference, New York, 19-22 June, 1946; signed on 22 July 1946 by the representatives of 61 States (Official Records of the
World Health Organization, no. 2, p. 100) and entered into force on 7 April 1948. Available at www.who.int/about/definition/en/print.
7. World Health Organization. Health promotion definition. Available at www.who.int/topics/health_promotion/en [Accessed 9
December 2015].
8. Prochaska JO, DiClemente CC. Stages and processes of self-change of smoking: Toward an integrative model of change. J
Consult Clin Psychol 1983;51(3):390-95.
9. The Royal Australian College of General Practitioners. Smoking, nutrition, alcohol, physical activity (SNAP): A population health
guide to behavioural risk factors in general practice. 2nd edn. Melbourne: RACGP, 2015. Available at www.racgp.org.au/download/
Documents/Guidelines/snap.pdf [Accessed 9 December 2015].
10. Rosenstock IM, Strecher VJ, Becker MH. Social learning theory and the Health Belief Model. Health Educ Q 1988;15(2):175-83.
Domain 2. Applied professional knowledge and skills

‘Cure sometimes, treat often and comfort always’ - Hippocrates.

Competency
Core skills General practice under General practice - lifelong
outcomes Pre-general practice
supervision learning
CS2.1 GPs CS2.1.1 The CS2.1.1.1a Define holistic CS2.1.1.1b Incorporate CS2.1.1.1c Evaluate the
provide the conduct of the and patient-centred care patient treatment and provision of holistic and
primary consultation is management preferences patient-centred care in the
contact for appropriate to when appropriate practice
holistic and the needs of the
patient- patient and the CS2.1.1.2a Utilise CS2.1.1.2b Incorporate CS2.1.1.2c Implement
strategies to identify the the impact of diagnoses strategies to mentor and
centred care sociocultural
needs, expectations and and management on other support colleagues to provide
context
sociocultural context of family members and/or holistic and patient-centred
patients carers into care planning care
CS2.1.1.3a Explain the CS2.1.1.3b Identify and

benefits and difficulties manage situations where
of individualising there are challenges to
consultations to delivering a patient-centred
incorporate needs, approach
expectations and
sociocultural context
CS2.1.1.4a Describe CS2.1.1.4b Implement

strategies to identify and effective strategies to
manage unreasonable manage patient needs and
patient or carer expectations that cannot
expectations be met
CS2.1.2 CS2.1.2.1a Identify the CS2.1.2.1b Identify and CS2.1.2.1c Identify

Continuity of care key factors that support manage factors that are consequences of missed
promotes quality and contribute to quality barriers to, and those that opportunities for continuity
and safety continuity of care promote, continuity of care of care and review practice
structures to reduce future
risk and to optimise care
CS2.1.2.2a Outline the CS2.1.2.2c Implement quality

risks of not providing improvements that support
adequate continuity of continuity of care for patients
care
CS2.1.3 CS2.1.3.1a Utilise and CS2.1.3.1b Formulate a CS2.1.3.1c Develop

Comprehensive contribute to event and collaborative approach systems to support effective
and holistic shared health summaries to management plan management planning to
management development optimise outcomes
plans are
developed CS2.1.3.2a Identify CS2.1.3.2b Develop
individuals who would strategies to maintain
collaboratively
benefit from having a management plans that are
management plan in relevant to patient needs
place
CS2.1.3.3a Outline
the key features of
an effective, holistic
management plan
23

Competency
CS2.2 GPs CS2.2.1 A CS2.2.1.1a Describe CS2.2.1.1b Identify CS2.2.1.1c Appraise
diagnose comprehensive, the key features of priorities and negotiate an and revise as appropriate
and manage clearly a comprehensive agenda for the consultation biopsychosocial history taking
the full range documented biopsychosocial history to maintain quality of care
of health biopsychosocial
conditions in a history is taken CS2.2.1.2a Demonstrate CS2.2.1.2b Identify
effective history taking and sensitively address
diverse range from the patient
and documentation using psychological factors
of patients
across the the biopsychosocial contributing to or
lifespan model consequences of physical
symptoms
through a
therapeutic CS2.2.1.3a Identify CS2.2.1.3b Appropriately
relationship the key signs to be utilise and interpret
determined on physical assessment tools to
examination during history optimise history taking
taking
CS2.2.1.4a Identify
potentia impacts of
sociocultural factors on
presentation, engagement
and compliance
CS2.2.2 An CS2.2.2.1a Obtain CS2.2.2.1b Use strategies CS2.1.2.1c Identify and

appropriate informed consent prior that ensure patient address any skill gaps for
and respectful to undertaking a physica comfort when undertaking effective physical examination
physical examination respectful physical
examination of examination
the patient is
undertaken CS2.2.2.2a Demonstrate CS2.2.2.2b Effectively CS2.1.2.2c Support
appropriate and respectful utilise appropriate and mentor colleagues
physical examination clinical tools to optimise in maintaining physical
technique examination examination skills
CS2.2.2.3a Identify and CS2.2.2.3b Effectively CS2.1.2.3c Mentor

manage situations where summarise key colleagues in sensitive
there may be barriers to examination findings for management of
physical examination the patient inconsistencies between
physical examination findings
and history
CS2.2.2.4a Acquire CS2.2.2.4b Identify,

positive and relevant negotiate and manage
negative signs to assist barriers to effective
with diagnosis physical examination to
avoid compromising quality
of care
CS2.2.2.5a Identify CS2.2.2.5b Effectively

situations where physical manage situations where
examination findings are the physica examination
inconsistent with history findings are not consistent
with history provided

Competency
CS2.2.3 CS2.2.3.1a Outline the CS2.2.3.1b Establish a CS2.2.3.1c Undertake
A significantly key symptoms and signs diagnosis and manage regular reviews of emergency
ill patient is to identify a significantly ill clinical presentations of management skills to ensure
identified and patient across the lifespan acute serious illness and relevance and currency is
managed trauma efficiently and maintained
appropriately appropriately
CS2.2.3.2a Explain the CS2.2.3.2b Evaluate CS2.2.3.2c Support and

criteria used to determine emergency management debrief colleagues as required
when acute resuscitation skills to identify areas following management of a
should be instituted requiring improvement and significantly ill patient
support
CS2.2.3.3a Devise an CS2.1.3.3b Outline

efficient treatment plan to criteria for and maintain
optimise outcomes competence in basic and
advanced life support
CS2.2.3.4a Demonstrate
contemporary practice of
basic life support
CS2.2.4 CS2.2.4.1a Differentiate CS2.2.4.1b Effectively CS2.2.4.1c Review quality of

A rational list variations of normal counsel patients documentation of differential
of differential physiology and regarding variations of diagnoses
diagnoses is psychology from normal physiology and
formulated pathological ones management
CS2.2.4.2a Describe CS2.2.4.2b Routinely CS2.2.4.2c Assist

the principles and document and stratify risk colleagues in identification
criteria used to develop of differential diagnoses and management of non
differential diagnoses when assessing patients accidental injury
CS2.2.4.3a Formulate CS2.2.4.3b Formulate,

concise differential defend and prioritise
diagnoses for common differential diagnoses to
presentations by assist with clinical decision
integrating information making
gained from effective
history taking and
examination

manage non-accidental
injury
CS2.2.5 CS2.2.5.1a Identify CS2.2.5.1b Choose the CS2.2.5.1c Review

Appropriate individuals who may appropriate procedure procedural skills and undergo
procedures benefit from procedural based on the patient's further training as appropriate
are undertaken intervention need and context to maintain quality care
after receiving
CS2.2.5.2a Outline the CS2.2.5.2b Perform and CS2.2.5.2c Support and
informed consent
key features of quality document appropriate mentor colleagues in
informed consent for medical procedures and performing appropriate
procedures aftercare with informed procedures
consent
25

Competency
CS2.2.5.3a Describe CS2.2.5.3b Identify
factors that influence procedural skill limitations
which procedures may and refer appropriately
be undertaken safely in
general practice
CS.2.5.4a Undertake
procedures under
appropriate supervision
CS2.2.6 Rational CS2.2.6.1a Identify CS2.2.6.1b Outline CS2.2.6.1c Review and

options for individuals who require and justify referrals for compare investigation referral
investigations are further investigation to investigations in the patterns with peers to ensure
offered obtain a diagnosis or to individual’s context quality provision of care
clarify a management plan
CS2.2.6.2a Outline CS2.2.6.2b Effectively

the factors to consider communicate regarding
when choosing the most the limitations, risks and
appropriate investigations benefits of proposed
investigations to enable
informed consent
CS2.2.7 The CS2.2.7.1a Identify CS2.2.7.1b Develop CS2.2.7.1c Assist

results of clinical situations where strategies to ensure that colleagues in interpreting and
investigations are normal (or abnormal) results are reviewed and communicating complex or
interpreted in the results are not considered interpreted difficult results
context of the normal (or abnormal) for
patient the individual
CS2.2.7.2a Effectively CS2.2.7.2b Demonstrate CS2.2.7.2c Develop

communicate relevant effective communication of robust and efficient
results, integrating the both normal and abnormal systems to ensure that
context of the individual results to patients results are interpreted and
communicated to patients
CS2.2.8 CS2.2.8.1a Identify CS2.2.8.1b Demonstrate CS2.2.8.1c Validate treatment

Diagnosis and approaches to effective counselling recommendations against
management is communicating evidence regarding management quality evidence-based
evidence-based effectively to patients options resources
and relevant to
CS2.2.8.2a Routinely CS2.2.8.2b Formulate CS2.2.8.2c Implement or
the needs of the
patient summarise holistic safe strategies to provide review processes to maintain
treatment options when care for patients who currency of evidence-based
seeing patients decline evidence-based knowledge to provide quality
management options care
CS2.2.8.2b Formulate CS2.2.8.3b Identify

safe strategies to provide and address modifiable
care for patients who primary, secondary and
decline evidence-based tertiary prognostic factors
management options for common conditions
CS2.2.9 Rational CS2.2.9.1a identify the CS2.2.9.1b Identify and CS2.2.9.1c Review and revise
prescribing key factors to consider utilise quality and unbiased patterns of prescribing to
and medication when selecting the most resources to assist in improve quality and safety
monitoring is appropriate medication appropriate prescribing of
undertaken treatments

Competency
CS2.2.9.2a Identify CS2.2.9.2b Identify the CS2.2.9.2c Review and
useful evidence-based role of off-label prescribing address issues with practice
guidelines to assist in and implement risk policies regarding storage and
prescribing appropriately minimisation strategies use of medications
CS2.2.9.3a Effectively CS2.2.9.3b Utilise robust CS2.2.9.3c Maintain and

counsel patients strategies to monitor disseminate up-to-date
regarding medication and manage medication prescribing knowledge and
safety and compliance side effects and risks of strategies
polypharmacy
CS2.2.9.4a Outline CS2.2.9.4b Report CS2.2.9.4c Meet patient

common prescription and medication side effects needs through specialised
over-the-counter drug appropriately prescribing
interactions
CS2.2.9.5a Describe CS2.2.9.5b Identify and

principles of effectively address barriers
pharmacotherapy to medication compliance
withdrawal
CS2.2.9.6b Devise
strategies to provide
quality care to patients
who decline recommended
medications
CS2.2.9.7b Develop
strategies to identify and
manage medication misuse
and withdrawal
CS2.2.9.8b Safely
prescribe restricted
medications using
appropriate permits

manage any conflicts
of interest in prescribed
treatments
CS2.2.10 The CS2.2.10.1a Outline CS2.2.10.1b Develop CS2.2.10.1c Evaluate

uncertainty areas of risk in management plans how diagnostic uncertainty
of ongoing managing patients that support the early impacts referral and
undifferentiated with undifferentiated identification of evolving management practices in
conditions is conditions conditions patients with undifferentiated
managed conditions
CS2.2.10.2a Evaluate CS2.2.10.2b Identify and CS2.2.10.2c Appraise

the potential for delayed manage the key mental management strategies of
or incorrect diagnosis in health diagnoses that may common undifferentiated
cases of undifferentiated present as, or compound, conditions
conditions undifferentiated condition
presentations
27

Competency
CS2.2.10.3b Identify CS2.2.10.3c Outline
and manage the key strategies and obstacles
sociocultural factors to implementing an
that may present evidence-based approach
as, or compound, to management of common
undifferentiated condition undifferentiated conditions
presentations
CS2.2.10.4b Assess
impacts of diagnostic
uncertainty on clinical
decision making, balancing
benefits against risks
CS2.3 GPs are CS2.3.1 Quality CS2.3.1.1a Define and CS2.3.1.1b Critically CS.2.3.1.1c Review and
informed and evidence-based critique evidence-based analyse research relevant revise utilisation of evidence
innovative resources are medicine as an approach to common clinical based resources and skills in
critically analysed to care presentations critical analysis
and utilised
CS2.3.2 CS2.3.1.2a Identify useful CS2.3.1.2b Identify CS2.3.1.2c Support

Innovative and relevant resources to commonly used resources colleagues in utilising and
approach to refer to when assessing and their evidence basis critically interpreting evidence
care of patients patients based resources relevant to
with multisystem practice
and/or complex
health issues is CS2.3.1.3a Describe and CS2.3.1.3b Differentiate
taken develop skills in critical between the various levels
appraisal of resources of evidence for common
therapies
CS2.3.1.4a Outline the CS2.3.1.4b Identify factors

challenges in applying important in determining
research evidence to validity and relevance of
individual patients research to an individual
patient
CS2.3.2.1a Identify the CS2.3.2.1b Devise CS2.3.2.1c Facilitate

role of, and opportunities strategies to manage appropriate research in clinical
for, innovation in general clinical scenarios where practice to improve health
practice evidence is lacking outcomes
CS2.3.2.2a Identify CS2.3.2.2b Practise

opportunities to innovation to address
implement harm obstacles in delivering
minimisation and quality of care in the
therapeutic intervention community
programs
CS2.4 GPs CS2.4.1 CS2.4.1.1a Identify the CS2.4.1.1b Distinguish CS2.4.1.1c Review
collaborate Appropriate variety of models of patients for whom care effectiveness of care
and coordinate mode of care care provided in general versus cure management coordination in the practice
care delivery to suit practice is appropriate
the needs of the
patient

Competency
CS2.4.2 CS2.4.1.2a Assess the CS2.4.1.2b Identify and CS2.4.1.2c Evaluate and
Fragmentation of role of general practice maintain skills in required revise models of care delivery
care is minimised in coordination of quality care delivery models to optimise outcomes
patient care
CS2.4.2.1a Identify CS2.4.2.1b Evaluate the CS2.4.2.1c Develop efficient

the roles of health criteria used to determine if systems to promote effective
professionals involved in a a referral is appropriate for communication with other
care team the individual patient health professionals
CS2.4.2.2a Describe CS2.4.2.2b Implement CS2.4.2.2c Develop and

efficient strategies for efficient strategies to maintain effective referral
effective communication communicate with key networks of individuals and
in the care team health professionals groups within the community
involved in collaborative
care
CS2.4.2.3a Identify CS2.4.2.3b Utilise the CS2.4.2.3c Support and

patients with chronic and/ most effective mode of mentor colleagues in
or complex health issues handover to minimise risks establishing and maintaining
who would benefit from networks of quality health
multidisciplinary care resource providers
CS2.4.2.4a Outline the CS2.4.2.4b Identify and CS2.4.2.4c Effectively

key factors to consider address potential barriers manage conflict within a care
prior to making a referral to effective communication team
with other health
professionals
CS2.4.2.5a Identify CS2.4.2.5b Identify

key local and national strategies to prevent
organisations or fragmentation and
individuals who may facilitate delivery of quality
provide resources to collaborative care
assist in quality patient
care
CS2.4.2.6a Provide timely CS2.4.2.6b Establish and

and high-quality referral use referral networks of
letters appropriate individuals and
organisations that support
health
CS2.4.2.7a Document CS2.4.2.7b Identify

and implement differences in care
appropriate follow-up providers’ opinions and
and handover plans negotiate agreement on
that minimise risk and management plans to
optimise health outcomes optimise care
CS2.4.3 CS2.4.3.1a Identify CS2.4.3.1b Identify and CS2.4.3.1c Support and

Demonstrate factors that contribute manage potential risks to mentor colleagues to provide
leadership in to effective teamwork in the safety of others in an leadership in emergency
emergency emergency situations emergency situation situations
situations
29

Competency
CS2.4.3.2a Identify CS2.4.3.2b Address
criteria by which to impacts on, and concerns
assess appropriate time of, family members and
to withdraw treatment in carers in emergency
emergency situations situations
CS2.4.3.3b Communicate
effectively with emergency
and specialist services to
optimise outcomes

CS2.1 Holistic and patient-centred care - describes the ability to relate the diagnostic and management process
to the available scientific evidence and the patient’s:
• sociocultural context
• level of health literacy
• needs, values, goals and expectations
• any existing comorbidities
• health beliefs.
A holistic approach takes into account the patient’s physical, psychological, cultural, social and existential
dimensions when problem-solving, and seeks to develop and sustain patient collaboration wherever possible
through empowerment by education, health promotion and goal-setting.
Respect for patient autonomy is a core ethical principle in the practice of medicine. It is the moral right of individuals
to make their own clinical decisions if they have the capacity to do so and if not, be provided with support to
identify a guardian who holds their best interests at the centre of any decision making.
CS2.1.1 Needs of the patient - health needs and expectations can vary significantly between individuals and if
not recognised and addressed, can have a major impact on consequent satisfaction with healthcare delivery and
clinical outcomes. It is therefore important to avoid making assumptions and to clarify individuals’ specific needs
and expectations in regards to factors such as style of communication and rapport with their GP, quality of care,
discretion and confidentiality, knowledge base, ability to relieve symptoms and to provide continuity of care, etc.
It is also important to identify factors such as the greater social roles and responsibilities of individuals, eg an elite
athlete is more likely to be adversely impacted by an ankle sprain than an office worker.
Health needs also often expand to include family members and/or carers. GPs need to recognise when family
members should be made aware of certain diagnoses, particularly areas such as reproductive health needs and
genetic conditions for which screening is required or diagnoses which may impact the care needs of individuals
who require support from a carer.
CS2.1.1.4a Manage unreasonable patient or carer expectations - it is important to identify when a patient,
family member or carer has unrealistic or unreasonable expectations which may controvert the GP’s professional
and ethical responsibilities, including doctor-patient therapeutic boundaries, duty of care, confidentiality, or
legislative responsibilities such as legalities regarding prescribing drugs of dependence. Strategies to manage these
expectations may include:
• consistent management of drug-seeking behaviour (eg not prescribing at all or not without contacting other
health professionals involved in care of the individual)
• applying for a permit and asking the individual to commit to an ongoing management plan (including referral to
pain management services, etc)
• in the case of inappropriate behaviour toward the GP or practice staff, advising the individual that they are no
longer welcome to attend the practice (after arranging follow-up care elsewhere)
• negotiating a code of conduct (to be signed by the patient) which, if breached, will lead to them not being able
to attend the practice in the future
• informing family members about the importance of avoiding breaches of confidentiality, etc.
CS2.1.1.3b Challenges to delivering a patient-centred approach - may include:
• management of patients with complex PTSD, where attempted ‘splitting’ of health professionals in the team is
common
• situations where the wishes of the patient are not well understood (eg individuals with severe cognitive
impairment or intellectual disability, or who are floridly psychotic)
31
• patients who present seeking analgesics but are unwilling to be properly assessed - address other factors which
may be contributing to their physical and/or psychological pain, or consider other therapeutic options.
CS2.1.2 Continuity of care - may be described as the quality provision of care over time. This should be viewed
from the perspective of the patient, as a continuous caring therapeutic relationship with a provider they trust with
whom they can communicate effectively, and the perspective of a GP, whereby there is a seamless transition
through multidimensional models and types of care within the practice and externally with other health services.
This care typically provides an integrated, coordinated framework which delivers quality care and optimises
outcomes for the individual. Whichever form it takes, an integral part of continuity of care is to ensure that acute,
undifferentiated and chronic conditions and abnormal results are followed up in a timely fashion to minimise risks
and improve health outcomes, and that preventive care is delivered opportunistically.
CS2.1.2.1a Factors that support and contribute to quality continuity of care - may include the maintenance
of respectful, effective communication and holistic patient-centred care over time. The maintenance of reliable and
effective communication with other health providers involved in the care of the patients (refer to CS2.4.2.1) is an
important factor which can contribute to this quality care. This can be facilitated by the effective use of eHealth
processes and tools to maintain current and relevant medical records.
In addition, effective use of the personally controlled electronic health record (PCEHR)as a piece of public eHealth
infrastructure that enhances the ability of clinicians to provide patient-centred care and which is a tool that
connects GPs with other healthcare providers and health consumers, is also an important factor. The PCEHR
allows GPs to create key pieces of health information with their patients, which then may be widely used and
viewed by patients and other healthcare providers with important implications for patient safety and the provision of
high-quality care.
CS2.1.2.2a Risks of not providing adequate continuity of care - principally refers to the risks of loss to follow-up
in that individuals with abnormal results and/or serious diagnoses are not identified or managed effectively, leading to
adverse health outcomes. Lack of continuity of care also misses opportunities for provision of health education, health
promotion and screening, which can prevent or identify disease early and help to improve outcomes.
CS 2.1.2.3a Event and shared health summaries - refers to hospital discharge summaries, summaries
within PCEHR tools and provision of documented information updates of changes in an individual’s condition or
management to relevant individuals within the health team, all of which improve quality of care.
CS2.1.2.1b Barriers to, and those that promote, continuity of care - professional barriers may include:
• the use of judgemental communication
• not using interpreters where necessary
• lack of cultural competence
• failure to acknowledge an individual’s cultural bias or cultural lens
• failure to identify and address the health needs of an individual
• practice facilities which impair access (eg not appropriate for individuals from particular sociocultural groups,
with disabilities, or who are employed full-time).
Patient barriers may include:
• issues which can impair the level of insight or capacity to engage with health services in a meaningful way (eg
substance use or addictive disorder)
• drug-seeking patients who are unwilling to work collaboratively with their GP
• patients with delusional disorders, which impact their ability to participate in a therapeutic relationship.
CS2.1.3 Holistic management plans - involves engaging the individual, carers and family members in a
therapeutic relationship where appropriate. This includes health education and promotion, preventive screening (for
diagnosed disease complications or other diseases with common risk factors) and management to improve quality
of life, clinical outcomes, enhanced work participation and reduce the risk of disease complications.
An effective management plan should include all relevant bio-psycho-socio-cultural risk factors that contribute to
disease processes. This will help to define patient and health professional team goals and priorities, and facilitate
access to appropriate community resources that are available from a physical and financial perspective. Enhanced
primary care chronic disease management plans are available to assist individuals in accessing health services that
would otherwise likely be unavailable due to financial concerns.
Advanced care directives are an important consideration in management planning for individuals with health
conditions which are likely to deteriorate in the near future, enabling such individuals to clearly define their wishes
to optimise the possibility of patient-centred care being delivered when the individual is no longer able to provide
consent. When discussing the development of management plans, it is important to acknowledge holistic
contributing factors to health (eg the benefits of meaningful work for individuals with physical and mental health
problems), as well as review of contributing factors to illness or injury (eg biomechanics, ergonomics, recognition of
modifiable risk factors and genetic factors to enable family screening).
CS2.1.3.2a Individuals who would benefit from having a management plan - incorporates most patients
who attend general practices (although this does not solely refer to enhanced primary care management plans).
This includes individuals with acute, severe, chronic and/or undifferentiated conditions that require intervention,
follow-up, referral to other health providers or services, and/or establishment of criteria for review. These conditions
include individuals with:
• depression
• schizophrenia
• anxiety
• PTSD and complex PTSD
• diabetes
• cardiac failure
• ischaemic heart disease
• epilepsy
• psoriasis
• chronic fatigue syndrome
• cancer
• children with recurrent otitis media
• asthma
• eczema, etc.
CS2.1.3.1b Collaborative approach to management plan development - this includes:
• acknowledging the sociocultural context and level of health literacy of the individual
• engaging in discussion and negotiation around available management options
• agreement on strategies attempted in the case of recurrence or relapse, including advice on when to seek
medical help
• provision of adequate information to enable informed choice (eg obstetric delivery options, relapse prevention
plans for patients with substance use or mental health issues, plans to manage potentially stressful future life
events and stigma associated with the condition, return-to-work and activity plans based on knowledge of
workplace systems and management)
• integrating pharmacological and non-pharmacological approaches for chronic pain management (eg rational
prescribing of complex regimens of pain medication, comprehensive graded exercise programs, muscle
strengthening).
33
Discussion around prioritisation of issues is an important part of collaborative plans (eg quality of life over prolongation
of life), as is assessment, assistance and management of the functional impact of health condition on the individual.
CS2.1.3.2b Management plans that are relevant to patient needs - may include ensuring, where appropriate,
that management plans are ‘living documents’ that are regularly updated when new diagnoses are made or changes
occur, that plans are collaborative, and that individuals feel they are useful in order to help improve their health
outcomes and reduce risk.
CS2.2 Full range of health conditions - includes multisystem disease and the broad range of acute and chronic
physical and mental health issues, comorbidities and complications which present throughout the lifespan and affect
all body systems. Some disabilities are often associated with comorbid conditions - bodily impairments that may
occur simultaneously, such as cerebral palsy and epilepsy, and the conditions may be related to one another or
distinct in their aetiology. A person with a disability is also exposed to secondary conditions, which are resultant from
the primary disability (eg pressure sores in the immobile).
GPs should be skilled in assessment and identification of common acute (including emergency presentations),
undifferentiated/well defined, and chronic conditions, and be confident in managing common conditions. Some
individuals with ongoing undifferentiated conditions, complex common conditions or rarer conditions may require
referral. This is viewed as a valid part of general practice management and the time at which this occurs varies
depending on the context, and the skills and confidence of the GP.
CS2.2 Across the lifespan - refers to the full range of ages and life stages within which individuals present to
general practice.
CS2.2 Therapeutic relationship - may be described as a helping partnership based on mutual respect and
collaboration, where doctors and patients have a number of rights and responsibilities, particularly to contribute to
shared decision making. Doctors have a duty of care to their patients, which includes a foundation of confidentiality,
professionalism and ethics. Patients are encouraged to actively participate in their own healthcare, make informed
decisions, and undertake recommended treatments, tests, referrals, and follow-up appointments.
Some important components of these relationships include consensus on treatment goals, commitment to
activities of the therapeutic journey, and development of mutual confidence in one another. An effective therapeutic
relationship is built over various encounters, actions and interactions and includes the use of quality communication
with clear provision of information to enable the individual to make informed choices. Also important is the provision
of a patient-centred approach in which the GP acknowledges the sociocultural context, needs and expectations of
the individual and provides ongoing support throughout the investigation, diagnosis and management process. If an
individual decides not to pursue a particular investigation or management option, the provision of ongoing support,
follow-up and appropriate screening to minimise risks are important therapeutic considerations.
CS2.2.1 Comprehensive biopsychosocial history - may be used to describe a comprehensive approach to history
taking which can assist in ascertaining the possible contributing factors to a clinical presentation and, therefore, the
development of a meaningful management plan. This process acknowledges the impact of psychological factors (eg
personality type, beliefs, past experiences, resilience, comorbidities) and environmental factors (eg concomitant social
stressors, substance use, financial stress impeding access to functional housing, good nutrition and health services) on
the patient’s frame of reference, physical symptoms and biological disease states.
Comprehensive biological, psychological and social history includes current symptoms. For example, when
assessing injuries it is important to consider taking a history of the mechanism of injury (evaluation of this utilises
applied anatomy and physiology), obtaining a detailed description of experience of pain (which may assist in
distinguishing pain mechanism) as well as past medical history, use of medications (including over-the-counter, and
herbal and nutritional supplements), history of allergies, and occupational, relational and family history.
Family history includes documentation of a three-generation family tree, where appropriate, to identify modes of
inheritance for conditions such as:
• haemochromatosis
• coeliac disease
• Down syndrome
• familial hypercholesterolaemia
• Factor V Leiden
• haemophilia
• polycystic kidney disease
• thalassaemia.
It is important to ensure sensitivity is used when exploring family relationships, including issues of adoption,
paternity and consanguinity. Effective history taking should also include consideration of sensitive questioning
about mental health issues and past or current exposure to trauma.
CS2.2.1.2a Effective history taking documentation using the bio-psychosocial model - refers to the
importance of accurate, concise and structured recording of information conveyed in consultations. This will
help other health professionals to easily understand what took place and assist in quality continuity of care. It is
important to document factors such as:
• presenting symptoms
• possible associated risk factors
• family history
• allergies
• current medications
• relevant social history (eg smoking and alcohol intake)
• previous experiences which may adversely impact consultations (eg medical trauma).
CS2.2.1.4a Identify potential impacts of sociocultural factors on presentation, engagement and

compliance - this includes consideration of potential factors which may affect how an individual presents with
illness or in health, and their consequent ability to engage with the health service. These factors can include key
gender differences (ie tendency for men to describe physical and externalising symptoms of depression more
than emotional1 and sexuality and gender issues in cultural minority groups.
CS2.2.1.1b Identify priorities and negotiate an agenda - achieved through respectful, effective
communication with an individual, such as requesting a list of problems at the beginning of a consultation in
order to enable both the patient and GP to identify key priorities. Reprioritisation of issues may be required if
significant issues arise during the consultation, but this typically needs to be negotiated and timely, appropriate
follow-up organised.
CC2.2.1.2b Sensitively address psychological factors contributing to, or consequences of, physical
symptoms - may include recognising:
• somatic dysfunction, such as chronic pain and irritable bowel syndrome, which may or may not have an
identified biological or physiological basis
• autoimmune conditions, such as rheumatoid arthritis, ulcerative colitis, psoriasis, eczema and hypertension,
which are potentially associated with, or exacerbated by, psychosocial yellow flags like stress related to work,
bereavement and exposure to family violence or previous trauma
• complex PTSD with its associated recurrent self-harming
• Munchausen syndrome or Munchausen by proxy,
• trichotillomania
• compulsive skin-picking causing unusual rashes
• weight changes related to eating disorders (these are predominantly psychological conditions which can
primarily present with physical symptoms).
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Identification of these conditions and the factors contributing to them is imperative, and evaluation of these
possibilities in a non-judgemental and empathic way is important in order to ascertain the patient’ perspective and
insight to assist in the development of a meaningful management plan.
CS2.2.1.3b Assessment tools - those relevant to a GPs may include:
• mini-mental status examination
• suicide risk assessment (eg SAFE-T - Suicide Assessment Five-step Evaluation and Triage)
• Health of the Nation Outcome Scales Child and Adolescent Mental Health (HoNOSCA)
• Strengths and Difficulties Questionnaire (SDQ)
• Kessler Psychological Distress Scale (K10)
• Depression Anxiety Stress Scales (DASS)
• Edinburgh Postnatal Depression Scale (EPDS)
• psychosocial assessment tools for young people (eg HEADSS [Home and Environment, Education and
Employment, Eating, Peer Related Activities, Drugs, Sexuality, Suicidality/Depression])
• developmental screening for infants and children (Australian developmental screening test)
• visual analogue pain scales and functional assessment charts to contribute to pain history
• pain scales for use in residential aged care facilities (eg Abbey Pain Scale, Pain Assessment in Advanced
Dementia Scale [PAINAD], Non-Communicative Patient’s Pain Assessment Instrument [NOPPAIN], Pain
Assessment Checklist for Seniors with Limited Ability to Communicate [PACSLAC])
• GP Assessment Scale for Cognition (GP COG).

GPs need to have an understanding of the sensitivity, specificity and validity in the individual on which the tools
are being used. This requires evaluation of the level of health literacy and other sociocultural factors, such as
language and cultural background.
CS2.2.2 Appropriate and respectful physical examination - may be defined as undertaking an examination
which is appropriate to the presenting complaint, age and gender of the patient, in a comprehensive way that
preserves the dignity and maximises comfort, involvement and safety of the patient (eg use of privacy screens
and sheets for women when undertaking, breast, genital and/or pelvic examinations). It is important to ensure the
examination occurs following clear explanations which allow informed provision of consent.
The use of tools to aid physical examination may vary depending on the remoteness and context of clinical
setting, but may include visual acuity charts, (pan) ophthalmoscopes, auroscopes, hearing tests, slit lamps,
biomechanical assessment testing, Rinne and Weber tests, ultrasounds and dermatoscopes, etc.
CS2.2.2.1a Informed consent prior to undertaking a physical examination - requirements for informed
consent vary based on a number of factors, such as the history of the therapeutic relationship, type of
examination, sociocultural factors (eg need for a gender-concordant health professional), and history of the patient
(areas like sexual abuse or medical trauma).
Obtaining consent does not necessarily mean a prolonged discussion is required before every physical
examination. Consent is often implied in the case of patients with whom the GP has established a therapeutic
relationship and can be checked by simple requests such as, ‘Is it okay if I examine you now?’ However, a more
detailed explanation is often advisable in the case of patients who require more intimate examination (eg genital
or breast). This helps to explain the reasons why such an examination needs to be undertaken, and to check
whether the patient has any objections or requirements (eg the presence of a chaperone).
CS2.2.2.3a Barriers to physical examination - may include individual requests for gender-concordant care,
individuals with body dysmorphia declining physical examination due to embarrassment or anxiety, and individuals
who have experienced sexual assault or abuse who fear having PTSD triggered. There are many complex reasons
and beliefs as to why individuals may decline examination and it is important for the GP to be empathic and non
judgemental and use sensitive questioning to develop an understanding of the reason(s) for concern.
Once the basis of the individual’s concerns are understood, a plan as to how their health needs can be met
can then be negotiated. This may include referral to another gender-concordant GP, presence of a chaperone,
counselling regarding fears and anxieties, etc.
CS2.2.2.4a Acquire positive and relevant negative signs to assist in diagnosis - it is important GP establish
a list of differential diagnoses based on history and knowledge of the patient prior to undertaking a physical
examination, and be mindful of the relevant positive and negative signs to seek out which will assist in clarifying the
most likely diagnosis.
CS2.2.2.5a Situations where physical examination findings are inconsistent with history - important
conditions to consider include:
• causes of non-accidental injury (including concerns about intimate partner or family violence)
• individuals at risk of intentional self-harm (eg misuse of medication, disordered eating, cutting, etc) such as
occurs in complex PTSD or recurrent somatic complaints which remain undifferentiated, despite investigation
where there is a suspicion that there may be a psychological basis
• stress related to being a carer, recent bereavement, work/career, finances, potential for secondary gain
• Munchausen syndrome or Munchausen by proxy.
CS2.2.2.1b Strategies that ensure patient comfort - may include:
• clear communication about the purpose of the examination
• obtaining informed consent
• ensuring that privacy and dignity are paramount
• regular checking back with the patient during examination to ensure that they are comfortable
• optimising sense of empowerment of the patient by ensuring that they feel comfortable to stop the examination
at any point if they are uncomfortable, etc.
CS2.2.3 Significantly ill - a term which may be used to describe an individual at any life stage who is at risk of
actual or acute potentially life-threatening health problems. Early identification of significant illness managed in line
with accepted guidelines can often improve outcomes.
Important critical illnesses can be grouped in a variety of ways, including:
• by age or life stage, such as paediatric presentations (eg epiglottitis, bronchiolitis, croup), obstetric (eg
antepartum haemorrhage, preeclampsia, ectopic pregnancy) or end-of-life emergencies
• system or body region affected (eg orbital cellulitis, acute glaucoma, ocular trauma)
• chest pain (eg acute coronary syndromes, pulmonary embolism, aortic dissection)
• acute cerebrovascular events (eg cerebrovascular ischaemia, intracerebral haemorrhage, assessment of

collapsed patient)
• mental health emergencies (eg acute psychosis, high-risk suicidality)
• acute abdominal pain (eg bowel obstruction, appendicitis, abdominal aortic aneurysm)
• respiratory compromise (eg severe asthma, COPD, pulmonary embolism, pneumonia)
• metabolic problems (eg ketoacidosis, Addisonian crisis, acute renal failure)
• dermatological problems (eg Stevens-Johnson syndrome, pustular psoriasis)
• urologic problems (eg priapism, acute urinary obstruction)
• causative factors or mechanism (eg anaphylaxis)
• infections (eg meningococcal meningitis, septic shock, eczema herpeticum, necrotising fasciitis)
37
• major trauma (eg head, face, chest, traumatic pneumothorax, abdomen, visceral rupture, pelvis, spine)
• illicit or prescription drug overdose or serious adverse effect (eg heroin overdose, serotonin syndrome,
oculogyric crisis)
• envenomation or poisoning (eg snake and spider bites)
• oncological emergencies (eg spinal cord compression, superior vena cava syndrome, hypercalcaemia, bowel
obstruction, tumour lysis syndrome, bone marrow suppression).
CS2.2.3.1a Identify a significantly ill patient across the lifespan - includes the key features which, on initial
assessment, flag that there is a risk of further deterioration. Infants can deteriorate very quickly and thus require
careful assessment. Symptoms and signs include reduced feeding and looking ‘floppy’ when unwell, as well as
signs of dehydration. In addition, increased respiratory effort and decompensation are very important to elicit in
children under 12 months of age (eg cool peripheries, greater respiratory rate with increased work of breathing,
poor skin turgor, sunken fontanelle).
Toddlers tend to not be interested in playing or engaging with surroundings when unwell, and tachycardia is
usually the first physical sign of decompensation. Fit young adults often maintain blood pressure until condition
deteriorates and very severe tachycardia can occur for hours before clinical hypotension. Older people or those
with chronic conditions, can experience hypotension early on and tachycardia may be masked by pre-existing
conditions (eg heart block) or use of medications (eg calcium channel or beta blockers).
CS2.2.3.2a Criteria used to determine when acute resuscitation should be instituted - includes:
• absence of danger to attendees

• identification of loss of consciousness
• lack of normal breathing and/or loss of palpable pulses
• absence of a not-for-resuscitation order (eg advanced care directive documenting patient’s wish to not be
resuscitated).
CS2.2.3.3a An efficient treatment plan to optimise outcomes - may include rapidly prioritising issues to
manage, including the DRSABCD action plan (Danger, Response, Send for help, Breathing, CPR, Defibrillation),
in line with Australian Resuscitation Council (ARC) guidelines, remembering to prioritise health of yourself and
others assisting before starting CPR and engaging help from a senior colleague or emergency services early on in
resuscitation.2
CS2.2.3.4a Contemporary practice of basic life support - refers to developing skills and confidence in utilising
basic life support protocols according to the most current version of the ARC guidelines.
CS2.2.3.1b Manage clinical presentations of acute serious illness and trauma efficiently and appropriately
- the range of emergency presentations that may occur in general practice is broad (refer to CS2.2.3 for example)
and the skills required in management are directly related to the context of the general practice setting. GPs
should maintain confidence in their level of emergency management skills and be cognisant of the need to access
assistance when required. Appropriate management of emergency presentations includes utilising evidence-based
guidelines (eg ARC guidelines).
CS2.2.3.2b Emergency management skills - refers to the need to maintain skills which are appropriate to the
general practice environment and access to specialised emergency services.
CS2.2.3.3b Maintain competence in basic and advanced life support - assessed by participating and
obtaining a certificate of competence in ARC-approved training on a three-yearly basis.
CS2.2.3.2c Debrief colleagues as required following management of a significantly ill patient - it is common
for health professionals to experience stress reactions following involvement in a critical incident. These can range
from uncomplicated stress reactions to more complex PTSD responses. The response of health professionals
and their ability to seek out psychological support can be negatively impacted by feelings of guilt, fear of litigation
or disciplinary action. This means that having structures by which all individuals involved in a stressful event are
invited to group or individual debriefing can be very useful in exploring emotional responses and providing support,
as well as assessing whether there is anything to be learned from the experience. It is important to recognise that
experienced practitioners are not immune to the need for debriefing following stressful events.
CS2.2.4 Rational list of differential diagnoses - may be used to describe the process of developing a list of
conditions which are most likely in a given clinical scenario after acknowledging the individual’s background and
context and undertaking history and examination. In order to minimise risk, this should highlight the possible
spectrum of disease, prioritising the most important conditions to exclude due to their potential severity, through to
those which are least likely and therefore at least risk of causing harm to the individual. This process should then
support the practitioner in creating a rational investigation and management plan.
CS2.2.4.1a Variations of normal physiology and psychology from pathological ones - may include:
• distinguishing ‘normal’ psychological responses to stress and grief from ‘abnormal’ responses and variations
which may occur between sociocultural groups
• identifying functional from dysfunctional personality traits
• acknowledging variability in physical and psychological effects of various life stages and ageing on different
individuals
• variations in signs like normal range of movement of joints during musculoskeletal examinations (eg ability to
identify hypermobility syndrome)
• identifying variations of normal skin (eg ephiles) from pathological ones
• normal trajectories of decline in older people compared to the degree of decline related to disease processes.
Some examples of ‘normal’ life stages which need to be distinguished from pathological processes include:
• puberty (need to identify precocious puberty)
• menarche and early menses (need to identify endometriosis)
• menopause (distinguish from premature menopause and identify perimenopausal symptoms which are
negatively impacting quality of life and thus may require intervention)
• differentiation of andropause from normal ageing in men
• pregnancy/fertility (distinguish from subfertility or infertility)

• developmental milestones (significant deviations from these in childhood and adolescence).
CS2.2.4.2a Principles and criteria used to develop differential diagnoses - may include utilisation of clinical
flags as a structure to assist in prioritisation of issues. Clinical flags include:
• red (possibility of serious pathology)
• yellow (psychosocial pointers which may indicate risk of progression to long-term distress, disability and/or
pain)
• orange (psychological equivalent of red flags, suggest need for mental health review)
• blue (perceptions about the relationship between work and health which may inhibit recovery)
• black (systemic or contextual obstacles related to particular people, systems or policies).
Consideration of all of the relevant factors to the individual assist in recognising the multidimensional aspects of
conditions, particularly pain, and assist in risk stratification and the development of a meaningful management plan.
CS2.2.4.2b Stratify risk of differential diagnoses - involves the assessment of the individual’s risk of having a
disease state based on the information available. This information includes knowledge of the individual’s clinical
flags and other risk factors, particularly family history and mode of inheritance of the condition, as well as lifestyle
factors, concomitant disease and medication history.
39
CS2.2.4.4b Identify and manage non-accidental injury - includes identifying patients who present with physical
signs and symptoms which are inconsistent with the history provided and who may be at risk of family violence,
child abuse, elder abuse, sexual abuse or intentional self-harm. Once a possibility of non-accidental injury has been
raised, it is important to sensitively and empathically discuss this with the individual in order to ascertain whether
they are currently safe and, if child protection concerns are raised, to discuss the need for mandatory notification.
Engage in non-judgemental discussion with active listening, debriefing and/or counselling, and provide support and
information which will enable the individual to return for review when needed or to access other support services to
enable them to minimise future risk.
CS2.2.5 Appropriate procedures - may be used to describe those procedures which are likely to be most
beneficial to the individual’s health and wellbeing from a diagnostic and/or management perspective. Assessment
of the appropriate nature of procedures is inherently related to the practice setting (ie urban versus rural and
remote), individual sociocultural context and consequent availability of access to more specialised services.
Recommendations for such procedures should consider the potential benefits, taking into account the evidence
basis and the possible risks and costs in the context of any relevant sociocultural beliefs of the individual.
Decision-making and processes around procedures include:
• choosing the appropriate procedure
• communicating clearly with the patient
• obtaining and documenting informed consent
• safely performing the procedure using strict infection control standards
• accurately documenting what took place.
The range of procedures which may be deemed appropriate for general practice includes:
• eye procedures (eg the use of ocular cycloplegics, topical anaesthetics and/or fluoroscein to assist in eye
examination, removal of a corneal foreign body, eyelid eversion)
• removal of foreign bodies in ears and nose
• nasal cautery/packing for epistaxis
• guided and unguided musculoskeletal injections (eg trigger point, joint, bursal, intra-articular, carpal tunnel,
nerve blocks)
• acupuncture or dry needling
• patient blood management (eg intravenous iron infusion and venesection for haemochromatosis)
• dermatological procedures (eg biopsy, shave, punch, excisional biopsy cryotherapy, electrocautery, diathermy,
skin and nail scrapings for fungal disease, skin swabs for bacterial or viral disease, injection of keloid scar,
drainage of abscess)
• ingrown toenail surgery
• suturing
• application of plaster for fractured limbs.
CS2.2.5.2a Quality informed consent regarding procedures - based on a clear appreciation and understanding
of the facts, implications and consequences of undergoing a procedure. The ability to educate and inform patients
of the risks and benefits of each procedure, and to ensure that informed consent is obtained, is part of procedural
skills competency. This includes discussing any discomfort or pain and how these will be managed. The patient must
demonstrate adequate reasoning faculties and be in possession of all relevant facts at the time consent is given.
Factors which may influence the patient’s ability to provide informed consent may include impaired cognitive
function, language barriers, low level of health literacy, etc (refer to CS5.2.2).
CS2.2.5.3a Factors that influence which procedures may be undertaken safely in general practice - it is
imperative to ensure the development and maintenance of procedural skill competencies are in line with medical
registration criteria. This includes skills in management of complications, which helps to minimise potential medico
legal consequences as well as any potential harm to patients. Continuing surveillance for trends in procedural risk
complications in reports from medical boards, and alerts and bulletins from medical defence organisations and
surveillance authorities provides an important opportunity to identify and minimise adverse risk associated with
medical procedures. Education on the potential hazards to the health of the clinician performing the procedure and
their assistant(s) is critical for the prevention and management of procedural-related harm.
Clinicians and workplace managers need to be aware of their roles and responsibilities in maintaining a safe
work environment during procedural tasks or procedural complications in accordance with workplace standards.
This is particularly important in the case of infection control standards relating to the safe handling of body fluids
and substances, the clinician’s responsibilities regarding blood-borne virus transmission, and the avoidance and
management of needlestick injuries. Use of simulation-based teaching techniques to acquire and practise skills is
highly recommended.
Clinicians must also recognise that psychomotor impairment or medical conditions may affect the ability to
successfully and safely perform technical tasks, and must act appropriately in each particular circumstance. This
may require limiting their procedural participation to those tasks for which they can demonstrate competence. GPs
with a special interest area, or who are undertaking additional procedures, must ensure their skill levels meet the
recognised standards/curriculum requirements for procedural skill competency acquisition and maintenance (eg
special training for Implanon insertion, advanced rural skills training such as the RACGP Fellowship in Advanced
Rural General Practice (FARGP), RACGP Joint Consultative Committees and jurisdictional requirements/standards).
CS2.2.5.1b Appropriate procedure based on patient’s need and context - includes being aware of the
procedure options and undertaking the most potentially beneficial to treat the condition, with minimal risk, after
appropriate counselling and obtaining informed consent from the patient.
CS2.2.5.2.b Appropriate medical procedures and aftercare with informed consent - refers to the importance
of clear documentation, which may include:
• which procedure was undertaken
• whether informed consent was obtained
• the indications for the procedure
• any adverse events
• what information was provided to the patient regarding aftercare
• whether a review appointment was organised.
CS2.2.6 Rational options for investigations - may be defined as the diagnostic tests which are likely to be most
beneficial to the health and wellbeing of the individual. Recommendations for such referrals should be evidence
based (eg magnetic resonance imaging [MRI] and prostate specific antigen [PSA] referral guidelines) and consider
the balance between potential benefits, considering the evidence basis and available resources and guidelines
(including from a societal health economic perspective) against the possible risks and costs. The decision-making
should occur within the context of the sociocultural beliefs of the individual after provision of adequate information
to enable informed consent.
CS2.2.6.2a Factors to consider when choosing the most appropriate investigations - considerations may include:
• being aware of the purpose of referral for investigation and whether a positive or negative result will alter the
management plan (eg a tissue diagnosis is usually essential to guide management in patients with suspected
cancer)
• the evidence basis of the different investigation options

• evaluation of the validity, sensitivity and specificity of investigations
• the cost and risks of investigations (both to the patient and to society through Medicare funding), etc.
41
CS2.2.6.2b Limitations, risks and benefits - need to be based on the best available and current evidence and
include information about the potential harm caused by some investigations, such as multiple CT scans, or the
sensitivity and specificity of some tests (eg PSA), including information on false positives and false negatives, where
further investigation and treatment may pose risks, and pre-test counselling for blood-borne viruses in an individual
who is at risk of possible exposure to ensure that the concept of the window period and need for follow-up is
understood.
Risks, costs of investigations, and possible treatment options in the event the investigations are suggestive of
disease should be discussed prior to the investigation being undertaken. These discussions may include financial
costs of the investigation and potential for increased insurance costs if a suspected diagnosis is confirmed (eg
Factor V Leiden heterozygote).
Effective counselling should be provided regarding the possible implications of predictive predisposition testing
for later onset disorders to assist in gaining informed consent. This is particularly true in situations where there are
few treatment or risk-mitigation strategies available (eg Huntington’s disease), the options for treatment involve
risks, the development of the condition is not a certainty (eg option of radical mastectomy and/or oophorectomy
for women with BRCA1 and BRCA2 genes compared to ongoing surveillance screening). These issues need to be
discussed prior to the genetic testing being undertaken.3
CS2.2.6.1c Review and compare investigation referral patterns with peers - this is done to ensure that referral
patterns are reasonable and rational. If significant variations are found, ensure that referral patterns are in keeping
with current guidelines (if available) and that you are able to justify the variations in regards to potential benefits and
minimisation of risks and costs.
CS2.2.7 Results of investigations are interpreted in the context of the patient - refers to the skill set required
to identify the significance of abnormal or, in some cases, normal investigation results for the individual in the
context of their relevant past and family history, current symptoms and medications. An understanding of the
physiological impacts of ageing and disease processes is an important aspect of result interpretation, such as:
• understanding the significance of low normal platelets and low-level elevation of transaminases in individuals
with hepatitis B
• ideal ferritin targets for individuals with haemochromatosis
• HbA1C targets for individuals with type 1 and type 2 diabetes
• acceptable creatinine levels in an individual with chronic renal impairment
• mildly elevated bilirubin in patients with Gilbert’s syndrome.
CS2.2.7.2a Effectively communicate relevant results, integrating the context of the individual - refers to the
need to incorporate your knowledge of the patient, including level of health literacy, expectations, and previous
experience with health services, past history and family history, to communicate with them in a clear and rational
way. This may include discussion around abnormalities which do not necessarily correlate with symptoms (eg disc
prolapses on CT scan in patients without back pain or neurological symptoms).
CS2.2.7.1b Strategies to ensure that results are reviewed and interpreted - refers to the importance of
individual GP and practice structures to ensure that results are checked and appropriate actions are taken as a
result. There should be clear handover processes within a practice when leave is taken, as well as routines for
ensuring that results are checked (eg abnormal Pap smears and mammograms). Patients should be informed of
their responsibilities and the practice processes of being informed of their results.
CS2.2.8 Diagnosis and management is evidence-based - includes identifying modifiable risk factors and early
recognition of physical and psychological conditions in order to provide effective health education, promotion and
appropriate management. Management may include the broad range of therapeutic options, including no active
intervention to lifestyle modification (including changes to diet, stress modification and exercise regimens), medical
therapies (eg pharmaceuticals and/or herbal and nutritional supplements), physical therapies (eg physiotherapy,
osteopathy, hand therapy, etc), psychological approaches (eg meditation, psychological and trauma counselling),
surgical procedures, and return-to-work planning.
The decision to pursue one or multiple treatment options is made following provision of education and advice
related to options in order to enable informed consent and after consideration of the:
• presentation
• existing evidence and guidelines

• risks and benefits of the various options
• values, beliefs and sociocultural context of the individual

• ability to access treatment from a financial or physical point of view.
This approach optimises health outcomes and reduces risk of complications and progression in acute and chronic
conditions.
CS2.2.8.1a Approaches to communicating evidence effectively to patients - may include exploration and
acknowledgement of the level of health literacy, values, preferences and health belief system of the individual, and
tailoring the way in which the information is conveyed in order to assist in collaboration and achieve patient-centred
care. Typically, the GP and patient view health through very different lenses:
• Doctors approach health from a Western biomedical model and may think in terms of probabilities applicable to
populations, rather than individual patients.
• Patient perspectives may be based on a combination of personal experience, interpretation of scientific
evidence through mass media, and ‘common sense’ understandings of health and illness.
These differences mean it is important for both parties to be prepared to respect the other’s frame of reference and
clearly articulate their own perspective and preferences.
CS2.2.8.2a Treatment options - includes physical, social and psychological therapeutic modalities which are
likely to be of most benefit to the health and wellbeing of the individual, taking into account sociocultural beliefs and
balancing the risk of side effects, interactions and costs. These may include:
• advice on exercise regimens, dietary improvements and sleep routine
• adequate sun exposure
• involvement in community activities
• stress management techniques
• communication strategies
• conflict resolution with significant others
• avoidance or minimisation of exposure to risk factors like smoking, alcohol, illicit substances, environmental
pollutants, etc
• pharmaceuticals
• herbal or nutritional supplements
• referrals for physical or psychological therapy, or to other specialists for different forms of intervention or
management
• addressing social determinants of health.
CS2.2.8.1b Effective counselling regarding management options - includes discussion of possible outcomes
and uncertainties of treatment options. This includes balanced communication regarding risks versus benefits in
language appropriate to the individual and their sociocultural context to enable informed consent. For example,
non-judgemental, non-directive counselling about care options for unintended pregnancy, including medical
termination if appropriate, oncology treatments, chemotherapy, radiotherapy, and integrative and palliative care
treatments and procedures.
43
CS2.2.8.2b Formulate safe strategies to provide care for patients who decline evidence-based management
options - may include individuals who opt to access non-evidence-based treatment as an alternative to, or in
combination with, no treatment rather than evidence-based options. It is often important for GPs to take a non
judgemental approach and offer of ongoing support for monitoring, review, education and health promotion. It is
also important that GPs be adequately informed about alternative options for management and ensure that they are
aware of potential interactions and contraindications. Maintaining an open dialogue with patients helps to facilitate
discussion about other therapies they may be accessing and assists in optimising safety and the provision of quality,
collaborative care.
CS2.2.8.3b Primary, secondary and tertiary prognostic factors - prognostic factors may differ from risk or
predictive factors: risk factors are associated with causing a condition, whereas prognostic factors are those which
in people with the condition influence the outcome. There is some crossover with prognostic and predictive factors.
For example, in the case of women with breast cancer, primary prognostic factors such as tumour size, presence of
axillary lymph node involvement and hormone receptor positivity all determine the treatment recommended regimen,
and secondary prognostic factors such as level of exercise and diet are thought to contribute to risk of recurrence.
CS2.2.9 Rational prescribing and medication monitoring - refers to evidence-based prescribing, utilising
accepted guidelines combined with consideration of individual factors regarding contraindications or warnings,
particularly any issues regarding individual capacity, to safely metabolise medication (eg patients with renal or hepatic
impairment, or who are pregnant or breastfeeding).
Age is also an important factor. This is partly related to metabolism and decisions regarding dosing, but also to
effectiveness of medication, including those used for prevention, such as statins, which are unlikely to be of benefit in
older people. Other factors include capacity for compliance and concomitant medications (eg other pharmaceuticals,
and herbal and nutritional supplements) with risk of interactions.
‘Medications’ refers to appropriate topical ocular and aural agents, dermatological agents, rational use of antibiotics,
sedatives, analgesics (including those used for acute and chronic pain management). It is important to consider
regular clinical audits of analgesic, antibiotic and/or sedative prescribing in order to ensure this occurs within
recommended guidelines and legislative frameworks.
CS2.2.9.1a Key factors to consider when selecting the most appropriate medication - may include considering
the age, concomitant medications and comorbidities of the patient and, thus, their physiological ability to metabolise
the medication and tolerate potential side effects. It is very important to balance the potential benefits of the
medication with potential risks, consider the possibility of placebo response, consider the cognitive capacity of the
individual to manage potentially complex medication dosing, recognise potential side effects, and consider financial
cost.
Individuals should be provided with adequate information about the potential risks and benefits, need for review
and therapeutic monitoring, and potential interactions with other medications (eg St John’s Wort) or particular
foods (eg those that contain vitamin K and warfarin) in order to enable informed consent. The occupation and other
responsibilities of the person is another factor to assess, particularly in regards to potentially sedative medication or
for individuals who are elite athletes.
‘Medication’ includes pharmaceutical medications (prescribed and over-the-counter), as well as herbal and nutritional
supplements. It is important to consider certain factors specific to particular groups of medications, such as the
need for regular monitoring (eg regular INRs with warfarin and being confident that the individual is able to comply),
need for titration of dosing, opioid equivalents of different analgesic medications, and where relevant, ‘wash out’
period of medications to ensure that changeover to an alternative occurs safely (eg with antidepressants).
CS2.2.9.2a Useful evidence-based guidelines to assist in prescribing appropriately - include:
• unbiased resources to assist with rational antimicrobial prescribing (eg antibiotic guidelines)
• appropriate and judicious use of chemical (and physical) restraints in patients with impaired cognition as a last
resort (eg psychotropic guidelines)
• appropriate analgesic prescribing (eg analgesic guidelines)

• the Australian Medicines Handbook4

• Pharmaceutical Benefits Scheme (PBS)
• other therapeutic guidelines.
Other important resources to consider are those which detail evidence-based integrative therapies and interactions
with conventional treatments, and drugs in sport guidelines regarding banned substances, etc.
CS2.2.9.3a Safety and compliance - may include providing adequate verbal and/or written information about the
medication prescribed. This information should take the sociocultural context of the patient into account and can
include a list of common side effects, any important drug and/or food interactions, and explanation of the need for
therapeutic monitoring or screening (eg pelvic ultrasound with tamoxifen use) in order to enable informed consent,
etc.
CS2.2.9.4a Common prescription and over-the-counter drug interactions - include:
• St John’s Wort and selective serotonin reuptake inhibitor (SSRI) antidepressants
• warfarin and aspirin
• phenytoin and alcohol
• combined oral contraceptive pill and certain antibiotics.
CS2.2.9.5a Principles of pharmacotherapy withdrawal - relevant to a number of groups of medications,

including benzodiazepines, antidepressants (particularly venlafaxine) and opioids. There are guidelines to assist in
recognising and assisting in management of withdrawal symptoms to optimise safety for patients, including:
• Therapeutic Guidelines: Psychotropic version 7
• National guidelines for medication-assisted treatment of opioid dependence
• Alcohol and other drug withdrawal: Practice guidelines
• Graylands Hospital drug bulletin: Antidepressant switching strategies.
CS2.2.9.2b Identify role of off-label prescribing and implement risk minimisation strategies - off-label
prescribing refers to a medication for an indication or patient group that is not included in the approved product
information. This does not mean that the Therapeutic Goods Administration (TGA) has rejected the medication for
use in this indication or group, but is often due to a lack of evidence in this group, which may be due to the group
being small and thus providing little motivation for the drug company to register for this purpose.
Off-label prescribing needs to be approached rationally and from an-evidence based perspective. If the prescriber believes
that there is adequate evidence for the use and safety profile for the individual, then it may be reasonable to prescribe
it. However, it is important that the patient is aware that the medication is being prescribed off-label and that there
consequently may be different review or follow-up processes required to ensure that adverse effects are detected early.
CS2.2.9.3b Robust strategies to monitor for medication side effects and risks of polypharmacy - includes
planned medication reviews to enable monitoring for acute and chronic side effects. This allows dosage or
medication changes, appropriate referrals for home medicines review for patients prescribed multiple medications
or where there are concerns about compliance or safety, etc.
CS2.2.9.4b Report medication side effects appropriately - relevant authorities include the TGA’s Database of
Adverse Events Notification (DAEN), within which notifications regarding conventional and integrative medications
can be made, and the National Centre for Immunisation Research and Surveillance.
CS 2.2.9.5b Address barriers to medication compliance - may include:
• effective communication with patients about the role of medications
• discussion about patient concerns or reticence
• ensuring patients are aware how and when to contact you if they have concerns about a medication or side
effects
45
• organising regular review to ensure that medication is being tolerated and is effectively treating the condition for
which it is prescribed
• use of the ‘Webster-pak’ to assist with compliance for patients who are taking multiple medications or who may
have cognitive impairment which impacts their memory
• referral to district nursing service or enlisting family help to assist with medication management
• ensuring maintenance of current medication records
• ensuring utilisation of home medication reviews with a local pharmacist
• ensuring patients have access to quality information to assist in compliance.
CS2.2.9.6b Quality care to patients who decline recommended medications - refers to individuals who, due to
personal experience, health, or religious or cultural beliefs, do not believe that a particular medication is suitable for
them. It is imperative to ensure that individuals are provided with quality information which is appropriate to their level
of health literacy to ensure that they are able to provide fully informed consent. These patients need to fully understand
the likely consequences of their choice and be made aware of all of the management options available to them.
Maintaining an effective therapeutic relationship in this situation can be challenging, but should be provided every
opportunity to develop through non-judgemental and open communication. The GP should seek to understand
the beliefs, perspectives and values of the individual in order to continue to support them. Other strategies may
include attempting to organise regular review and monitoring for progression of the condition for which the
medication was recommended, as well as ongoing support and education about possible alternative options.
CS2.2.9.7b Medication misuse and withdrawal - may include recognising the most commonly misused and/or
abused medications which are sought out by individuals who want to them for non-medically indicated reasons,
such as injecting oral medications, overusing prescribed amounts or selling medications on the street (eg opioids,
benzodiazepines, sedating antipsychotics). Identifying possible signs of inappropriate use of drugs of dependency
can include patients who:
• present close to the practice’s closing time without an appointment

• request a specific drug and refuse all other suggestions (may also display considerable knowledge of drugs)
• typically request short-acting or injectable forms of drugs

• present with inconsistent symptoms (eg does not appear to suffer significant pain)
• decline referrals for therapy
• report a recent move into the area from somewhere beyond the vicinity of the practice, making direct validation
of prescribed drug supply with the previous practitioner difficult (any supporting letters apparently from previous
practitioners should be checked when possible)
• are awaiting admission to hospital
• demonstrate scars, or present old X-ray or investigation reports (may not be authentic)
• state that they have lost their last script
• admit to injecting oral formulation
• admit concurrent abuse of alcohol or illicit substances
• have a history of multiple non-sanctioned dose escalations
• report psychic effects of using medication not intended by a prescribing clinician.
Careful observation of patients may be useful in identifying them as drug users. Look for signs of drug use,
intoxication and withdrawal:
• Benzodiazepine intoxication is characterised by sedation, poor coordination and balance, impaired memory
and general impairment of cognitive function.
• Benzodiazepine withdrawal is characterised by anxiety, irritability, palpitations and tremor.

• Opioid intoxication patients may present with pupillary constriction, itching nose and skin, difficulty
concentrating, dry mouth, and visible injection-site marks.
• Opioid withdrawal is characterised by dilated pupils, increased heart rate and blood pressure, diarrhoea, muscle
cramps, aches and pains, frequent yawning, rhinorrhoea and lacrimation.
It is important to note that opioid-dependent patients may seek benzodiazepines, particularly if they are
experiencing withdrawal and want these drugs to alleviate some of the symptoms.
It is helpful to have a good understanding of their pharmacological and pathophysiological effects in order to manage
what appear to be inappropriate requests for these medications. Reasons for misuse of medications are broad and
varied. An important part of recognising and managing misuse is seeking to understand the motivations and/or needs
of the individual (eg recognition of concomitant mental health or illicit substance-use issues for which the individual
may be self-medicating). Once the motivations and needs are understood, a management plan can be established to
address the medication use and develop strategies to minimise the risks and impacts. Strategies may include:
• regular review
• referral to appropriate support or specialist services (eg pain management clinics or mental health services)
• utilisation of opiate substitution and pharmacotherapy
• application for appropriate jurisdictional health department permits for prescribing drugs of dependency to a
drug-dependant person (refer to CS2.2.9.8)
• development of an agreement between the GP and patient as to acceptable behaviour and actions in the event
particular situations arise
• contacting the Department of Health Prescription Shopping Information Service (PSIS).5
CS2.2.9.8b Restricted medications using appropriate permits - examples of Schedule 4 and Schedule 8
medications (common drugs of dependence) include:
• benzodiazepines (particularly alprazolam and flunitrazepam)
• codeine (when not combined with any other medicine)
• buprenorphine
• fentanyl
• hydromorphone
• morphine
• oxycodone
• pethidine
• methadone
• dexamphetamine
• methylphenidate.
Legislative requirements vary between states and territories. It is important for GPs to be aware of the legislation
within the jurisdiction in which they practice, to take all reasonable steps to confirm the identity of the patient, and
to ensure that a therapeutic need exists.
Safe prescribing includes:
• avoidance of injectable opioids
• clear and accurate records regarding rationale for prescribing
• date and quantity of scripts provided to ensure that higher than prescribed doses are not being used
47
• pain management plans for patients prescribed opioids being in place; ensuring that patients are referred to pain
management specialists if more than the maximum recommended dose is prescribed.
CS2.2.9.9b Conflicts of interest - refers to the importance of acknowledging and addressing any biases an
individual may have which may impact prescribing habits that are not in line with evidence-based guidelines (eg the
GP having a pecuniary interest in a particular treatment being prescribed, or being incentivised through other means
to prescribe a particular treatment).
CS2.2.9.3c Up-to-date prescribing knowledge - refers to the importance of maintaining currency with changes
to prescribing practices. This can be done through staying up-to-date with guidelines and legislative changes and
undertaking training in general practice-specialised medication prescribing if suitable for your patient population
(refer to CS2.2.9.5c).
GPs can also benefit from maintaining awareness of the development of new technologies to personalise
pharmaceuticals through pharmacogenomics, which utilises information about an individual’s genetic make-up to
assist in effective pharmaceutical prescribing. Current examples include prescribing;
• abacavir (anti-retroviral drug) - doctors now routinely test HIV-positive patients for a genetic variant that makes
them more likely to have an adverse reaction to the drug
• trastuzumab (breast cancer drug) - this therapy works only for women whose tumours have a particular genetic
profile that leads to overproduction of the HER2 protein.
CS2.2.9.4c Specialised prescribing - may include undergoing specialised training, supervision and gaining clinical
experience in s100 prescribing for conditions such as tuberculosis, HIV, hepatitis B.
CS2.2.10 Ongoing undifferentiated conditions - can cause considerable anxiety in both GPs and patients,
and highlights the need for a structured approach which is evidence-based and minimises risk from health and
economic perspectives. The range of common ongoing undifferentiated conditions in general practice includes such
presentations as:
• fatigue
• insomnia
• cough
• dizziness
• anorexia
• nausea
• sexual difficulty
• weight and appetite loss
• chronic pain (including headache, chest, back, pelvic and abdominal pain, which have been explored clinically
and investigated, where appropriate, with no precise diagnosis being made).
In these clinical situations, a management plan typically needs to be formulated in the absence of a diagnosis. A
management plan may be framed in terms of dichotomous decisions: treatment versus non-treatment; referral
versus non-referral; and serious versus non-serious. For example, back pain may be successfully treated empirically
in the absence of ‘red flags’, without an expectation of ever investigating further or confirming a diagnosis.
Understanding the role of the passage of time, effective communication skills, and knowledge of the natural history
of these conditions are key in managing undifferentiated conditions.
CS2.2.10.1a Areas of risk in managing patients with undifferentiated conditions - undifferentiated conditions
are commonly associated with clinical uncertainty and ambiguity, which presents management challenges for the
clinician, including how to communicate these uncertainties to patients. Clinical decision-making around choices
of investigations and management need to be rational and balance the potential risks (of both under and over
investigating and management) against the benefits in the context of the individual.
The role of uncertainty in clinical outcomes remains unclear. Uncertainty in clinical decision-making has been linked
to potential and actual adverse outcomes in patient care in the prevocational setting. Clinical strategies for managing
undifferentiated conditions need to adopt a fail-safe approach, including regular review of the presentation, while
recognising that some symptoms and presentations may never be attributed to specific conditions.
The potential for diagnostic uncertainty is compounded by somatisation, when psychological conditions present
as physical symptoms. Clinicians need to remain alert to this potential and develop clear strategies for delineating
physical and psychological components of the presenting conditions. Effective and appropriate management of
somatisation may also require a multidisciplinary approach and professional support to ensure that diagnoses are
not being missed. Being clear about decisions and referring to evidence during the history taking, examination and
investigations helps to maximise diagnostic effectiveness and patient safety, and minimise over-investigation. This
includes familiarity with serious conditions that must not be missed, conditions commonly missed, and conditions
that may present with unusual or elusive symptoms. Evidence-based approaches to assessment and management
can help to clarify and strengthen decision-making.
Communication skills are critical to characterising undifferentiated conditions and to communicating management
outcomes to patients. Patients with limited capacity to give complete histories (eg children, patients with dementia,
and patients with disabilities) may need family, friends and carers to be consulted for further clarification. Clinicians
need to observe confidentiality and the legal status of carers or guardians, as well as the potential for carers
or guardians to abuse or misuse the position by deliberately providing incorrect and misleading information
concerning the patient.
Uncertainty can be a source of considerable anxiety for patients and learning to manage this is a key skill of general
practice. Communication skills are the key to successful outcomes in managing undifferentiated conditions of a
psychogenic origin.
CS2.2.10.1b Management plans that support the early identification of evolving conditions - may include
ensuring that differential diagnoses are stratified in regards to risk. This can mean creating a list of differential
diagnoses and prioritising them in order of conditions which are most likely and most important to exclude due
to their potential severity, down to those which are least likely and at least risk of causing harm to the individual.
Creating such a list will ideally support the practitioner in creating a safe management plan.
Creation of this list should be followed by consideration of referral for appropriate tests and procedures or specialist
opinion, which are those that are likely to be of the most benefit to the health and wellbeing of the individual.
Recommendations for such referrals should consider the balance between potential benefits, taking into account
the evidence basis, the possible risks and costs, and the sociocultural beliefs of the individual.
CS2.2.10.2b Key mental health diagnoses that may present as, or compound, undifferentiated condition
presentations - may include anxiety (generalised anxiety and obsessive compulsive disorders) and depressive
symptoms, somatoform disorders, psychotic disorders, complex PTSD, substance-use disorders etc. Other
psychological contributing factors may include fear related to past experiences of the individual or close family or
friends, obsessional thinking or anxiety related to concomitant mental health diagnosis, thinking pertinent to the
individual’s personality type or disorder, etc.
CS2.2.10.3b Key sociocultural factors that may present as, or compound, undifferentiated conditions
presentations - influences that can impact an individual’s behaviour, perspective and choices. These influences
can include:
• personality type
• mental health diagnoses (eg anxiety and depressive symptoms)
• race
• ethnicity
• gender
• religion
• social class
49
• family traditions
• peer groups
• age.
CS2.3.1 Evidence-based resources - may include easy access to, and utilisation, of current paper-based or
web-based guidelines, as well as other resources regarding diagnosis, management or social determinants that
impact health. Please refer to the Population, presentation and process contextual units for detailed information
regarding resource and guidelines for specific population groups, presentations and general practice processes.
CS2.3.1.1a Evidence-based medicine - may be described as a process of lifelong learning in which caring for
patients creates a need for ‘the integration of best research evidence with clinical expertise and patient values’.
CS2.3.1.2a Useful and relevant resources to refer to when assessing patients - evidence-based resources,
listed in order of quality of evidence (from least to most significant), include:
• research papers (such as randomised controlled trials, qualitative studies and cohort studies)
• evidence-based guidelines
• evidence summaries
• abstracts, systematic reviews and meta-analyses (eg those found on the Cochrane database) which support
practitioners to make clinical decisions when this information is integrated with clinical expertise and individual context.
CS2.3.1.3a Skills in critical appraisal of resources - refers to the systematic process by which practitioners
assess the relevance and validity of research to a particular individual or condition. Practitioners should take a
number of factors into account, including:
• the design and type of research or analysis, and thus the levels of evidence for the findings
• whether the study design addressed potential sources of bias, confounding factors and/or conflicts of interest
• whether the data analyses were correct

• whether the data justified the conclusions drawn.
Prior to applying the conclusions of the research to clinical practice, the similarities and differences of the patient
population studied need to be compared with the individuals to whom the practitioner wishes to apply the findings.
CS2.3.1.4a Research evidence to individual patients - may include interactions with patients who have health
beliefs which are not based in a Western biomedical context, or who have a low level of health literacy due to
sociocultural factors.
CS2.3.1.3b Various levels of evidence -refers to each study design being assessed according to its place in the
research hierarchy. The hierarchy reflects the potential of each study design to adequately answer a particular research
question, based on the probability that its design has minimised the impact of bias on the results. For example, a
common hierarchy used by the National Health and Medical Research Council (NHMRC) may be Level 1 systematic
reviews of Level 2 studies; Level 2 randomised controlled trials; Level 3 non-randomised experimental trials, cohort
studies, case-control studies; Level 3 comparative studies without concurrent controls; Level 4 case series.
Clinical guidelines are often the most applicable and useful to GPs, provided that they are current and have been
developed through a rigorous process (eg such as those by the NHMRC).6
CS2.3.1.5b Factors important in determining validity and relevance of research to an individual patient -
includes assessing:
• whether the relevant research was done in a comparable population group to the patient
• age
• ethnicity
• presence of comorbidities or complications (eg renal or hepatic impairment)

• cognitive impairment (which may increase risk of side effects if medication is not taken correctly)
• concomitant use of other medications with risk of interactions.
CS2.3.2 Innovative approach to care of patients with multisystem and/or complex health issues - examples
of such health issues include:
• endocrine conditions such as type 2 diabetes with vascular or neurological complications,
• rheumatological conditions such as rheumatoid arthritis and systemic lupus erythematosus,
• immunosuppressive conditions such as HIV
• older patients with multimorbidity such as mental health comorbidities in the context of physical illness
• patients with complex PTSD.
Other complexities include the approach to vulnerable individuals for whom negative social determinants of health
(such as poor access to employment and education opportunities, adequate and safe housing), may complicate
identification, ability to prioritise and management of chronic health problems (eg individuals who are homeless,
refugees and asylum seekers, individuals with disabilities, individuals with addiction issues or who have been
exposed to family violence).
Innovative approaches may include the development and maintenance of knowledge of eHealth developments
(eg utilisation of the PCEHR to improve continuity of care and communication with other health professionals, and
therapeutic mental health tools to optimise outcomes for patients), involvement in or awareness of clinical research
which may be relevant to patients, ability to be flexible to accommodate patient needs and belief systems when
managing patients with multisystem and/or complex medical and/or social conditions.
CS2.3.2.1a Opportunities for innovation in general practice - may include:
• participation in general practice research
• eHealth tools (eg health tracking tools to monitor weight, steps, dietary intake, blood glucose readings)
• utilisation of and contribution to the PCEHR

• collaboration with community health resources to deliver more efficient and better quality care
• considering different models of care to suit the needs of vulnerable groups in the local community (eg outreach
adolescent health clinics in rural and remote communities, mobile screening and/or vaccination clinics in
workplaces).
CS2.3.2.2a Harm minimisation and therapeutic intervention programs - may include identifying patients who
demonstrate signs of drug addiction and utilising brief intervention techniques through effective communication
and motivational counselling to establish a collaborative therapeutic relationship and minimise risk of harm to the
individual. Initial acknowledgement that drug addiction is a treatable disease is an important step and attempting to
gain an understanding of the psycho-sociocultural contributing factors to the addiction. Throughout this process,
it is important to identify mutual goals to minimise the risk of harm from use of these substances and develop a
management plan (eg providing education around safe injecting techniques for patients who use intravenous drugs).
Therapeutic intervention programs include behavioural treatments and/or prescribing medications to enable
cessation or reduction in use of addictive substances (eg prescribing methadone, naltrexone or buprenorphine
for opiate addiction); use of naltrexone, acamprosate and disulfirim in individuals who are alcohol-dependant;
benzodiazepine withdrawal regimens using diazepam, etc.
CS2.3.2.1b Strategies to manage clinical scenarios where evidence is lacking - may include the use of
off-label prescribing (refer to CS2.2.9.2b), or situations such as being advised by a patient that they are using
a complementary therapy for which the GP has little information in combination with a conventional therapy. In
this scenario, it is important to be non-judgemental, listen to the reasons why the individual is choosing to use
this therapy, and seek out reliable resources (refer to Integrative medicine contextual unit IM16) in order to obtain
evidence for use and risk of potential interactions or side effects. This will enable adequate counselling and
informed consent by the individual to continue or to cease therapy. In counselling patients about use of integrative
51
or conventional therapies for which there is little evidence, it is important to balance the potential benefits and risks
in a non-judgemental and empathic way, which will enable them to make an informed choice while maintaining
the therapeutic relationship. Utilising effective communication is imperative to optimise chances of the individual
returning to continue care (refer to CS2.2.9.6b).
CS2.3.2.2b Innovation to address obstacles to delivering quality care in the community - may include
addressing time pressures of practice by delivering group education or therapy to individuals with similar health
concerns, and addressing vulnerable groups’ obstacles in accessing to care by offering screening in the community
(eg workplaces, community centres, sporting facilities, etc).
CS2.4.1.1a Variety of models of care - includes:
• care
• cure
• rehabilitation
• palliation
• health promotion and prevention
• delivery of care to vulnerable communities (eg Aboriginal and Torres Strait Islander peoples, refugees and asylum
seekers, groups in custodial settings, homeless people)
• specialised general practice (eg sports medicine, military medicine, sexual health)
• options for models of care in regards to specific populations (eg obstetric care and delivery, including birth
centres versus labour wards and GP versus specialist care).
CS2.4.1.1b Care versus cure management - includes situations where an option for palliation versus active
treatment may be chosen by patients with, for example, advanced cancer; severe ischaemic heart disease (eg
elderly patient with significant other comorbidities who may opt to decline surgical intervention); an incurable
chronic condition (eg COPD, Alzheimer’s disease); and schizophrenia.
These patients may utilise therapies and lifestyle interventions which may improve quality of life, reduce risk of
complications and prolong life.
CS2.4.1.2a Role of general practice in coordination of quality patient care - acknowledges the important
role that the GP can play in being the professional who takes responsibility for the quality of care provided to an
individual. This can be achieved by:
• making appropriate referrals
• following up to ensure the individual attended specialist or allied health appointments and that they understand
the diagnosis, investigations or management recommended
• assisting with extra education and support to improve compliance and health outcomes
• utilising recalls to ensure the individual is up-to-date with screening and every aspect of their health needs is being met.
CS2.4.2 Fragmentation of care is minimised - acknowledges the importance of providing holistic patient-
centred care to efficiently identify and manage acute and chronic conditions, and to deliver preventive care and
provide health education. This care is often best delivered by a GP who has a good therapeutic relationship with an
individual, including an in-depth understanding of their psychosocial context. The capacity to organise appropriate
referrals for allied health and specialist care is an important role for GPs; however, this needs to be done efficiently
utilising quality communication to minimise the risk of unnecessary repetition of investigations or therapies which
can be burdensome to patients and the broader community.
CS 2.4.2.1a Roles of health professionals involved in a care team - clarification of roles is an important way to
minimise fragmentation and reduce risks, as well as unnecessary duplication of care. A care team typically consists
of professionals from different disciplines within healthcare who bring different skills and expertise to optimise
patient outcomes. The types of professionals required in a care team for a particular patient depends on the
individual’s acute and chronic health needs and risk factors, as well as their social context. Important and common
members of a care team may include a practice nurse, allied health professionals (eg physiotherapists, dentists,
podiatrists, optometrists, exercise physiologists, psychologists, etc), social workers, residential healthcare staff,
audiologists and specialists (eg endocrinologists, renal physicians, opthalmologists, oncologists, surgeons, etc).
CS2.4.2.2a Efficient strategies for effective communication - may include ensuring the care team is kept up-to-
date with relevant information regarding an individual’s health status and therapies, and is cognisant of the patient’s
needs and wishes. This is central to the delivery of quality collaborative care through the provision of concise and
relevant patient information, whether written (ie quality referral letters) or verbally (ie during case conferences).
Effective communication can also be achieved via the use of eHealth strategies, such as:
• video conferencing
• internet telephone services (eg Skype)
• email
• SMS
• web services and e-care planning tools
• electronic referrals systems (with use of appropriate encryption)
• electronic prescribing
• electronic patient health records (including PCEHR)
• electronic communication with Medicare, pathology and medical imaging providers
• electronic or tele-based recall systems.
CS2.4.2.3a Beneft from multidisciplinary care - includes recognition of the GP’s skill set and the
complementary skills that other clinic staff (particularly practice nurses), specialists and allied health professionals
may provide to optimise quality of care and improve outcomes. This is particularly important for individuals
with complex, chronic health conditions who have psychosocial risk factors such as unstable accommodation,
addiction issues, problems with medication compliance, etc.
CS2.4.2.4a Key factors to consider prior to making a referral - include being clear as to the purpose of the
referral (eg opinion on diagnosis or management, request for therapy), whether the professional to whom the
patient is being referred has appropriate skills to meet the individual’s needs, whether there are other patient
needs to consider (eg a request for gender-concordant care), and consideration of cost to the individual, as well
as timeliness of appointment, to ensure there is minimal risk of deterioration due to long wait times. Requesting
feedback, or involvement in case conferencing or a care plan, can also encourage quality collaborative care.
It is also for important for GPs to understand that they may have an important role to play in providing health
information to individuals who request referrals. This can ensure these patients have a good understanding of the
potential risks posed by undergoing procedures prior to their specialist appointment which, in turn helps to enable
informed consent. A good example of this situation is providing appropriate information prior to the provision of
referrals for women requesting cosmetic procedures, particularly genital cosmetic surgery, where the potential risks
may not have been made clear by the specialist to whom you have referred (as they may have a pecuniary interest
in the individual proceeding with surgery even if this is not clinically indicated).7
CS2.4.2.5a Key local and national organisations or individuals - may include health professionals and
organisations to whom individuals are referred for specialised investigation and management, individuals and
organisations (private and government-funded) who provide support and act as resources regarding public health
matters or a particular diagnosis or vulnerable group.
CS2.4.2.6a Timely and high-quality referral letters - identifies the important role GPs play in facilitation of access
to optimal specialist and allied health care at an appropriate level and in a timely and cost-effective fashion with
an aim to optimise health outcomes. This acknowledges the context of the economic impacts of unnecessary or
inappropriate use of government-funded services which do not positively affect health outcomes. Referral letters
53
should contain adequate information to accurately identify the patient, including a National E-Health Transition
Authority (NEHTA) unique patient identifier if available, and sufficient information to assist the allied health or
specialist professional to provide quality care (eg clear reason for the referral, current and relevant past history, family
history, medication list, allergies, vaccination status, need for an interpreter, etc). It is also important to maintain
confidentiality and not disclose sensitive information which is not relevant to the referral. Referrals sent electronically
must be encrypted and the practice must comply with standards for secure transmission of health information.
CS2.4.2.7a Appropriate follow-up and handover plans - may include ensuring patients at risk of deterioration,
and who require follow-up of investigations or progress with management, are appropriately handed over if their
primary GP is going to be away from the clinic. Utilisation of recall systems to remind GPs when patients are
due for review or screening can be useful. The development of strategies to ensure that investigation results and
specialist letters are regularly reviewed and appropriately acted upon is a key area in provision of quality care.
CS2.4.2.1b Criteria used to determine if a referral is appropriate - may include:
• being clear on the purpose of the referral
• ensuring the professional to whom the individual is being referred has the appropriate skills and meets the needs
of the patient (particularly regarding gender-concordant care, if requested)
• ensuring the individual is aware of potential costs and wait times
• ensuring an appropriate work-up has been completed and the results are included in the referral letter where
appropriate (eg recent liver function tests and other screening results for an individual with hepatitis B being
referred to a liver clinic).
It is also important that the GP provides the patient with information about elective procedures where there may be
risks associated, and to ensure the patient understands this information, in order to enable informed consent. This
is particularly pertinent for cosmetic procedures.7
CS2.4.2.3b Most effective mode of handover - may include verbal or written.

CS2.4.2.4b Barriers to effective communication with other health professionals - may include difficulties
communicating during consulting hours, delays in creating and handing over documentation (eg referral letters and
discharge summaries), incomplete or difficult-to-read documentation as a result of time pressures or inadequate
medical record systems, etc.
CS2.4.2.4c Conflict within a care team - may include conflicting opinions about management of an individual,
personality conflicts or bullying. Such conflicts can have adverse effects on morale and productivity.
An effective strategy to minimise conflict includes recognising and addressing signs that there are dysfunctional
interactions within a team, avoiding judgement or blame and behaving empathically to all members of the team.
Identifying situations where individuals may be breaching their professional code of ethics in how they interact with
others is an important part of this process. In some situations, an external mediator may be required to facilitate an
individual to take responsibility for their behaviour, to resolve the source of conflict and to implement strategies to
minimise risks in the future.8
CS2.4.3 Leadership in emergency situations - includes coordination of emergency situations (eg an individual
with a life-threatening illness such as a cardiac arrest, anaphylaxis, collapse or airway obstruction, or a mass
casualty event such as a multi-person road trauma, bushfire, chemical spill, etc) whereby tasks are delegated to
appropriately skilled individuals (eg the practice nurse or other GPs), effective triaging occurs, safety of healthcare
providers and bystanders is made paramount, and effective communication with emergency and other specialised
services occurs, etc. An effective response in emergency situations may be enhanced in settings where these
occur frequently, with the running of regular practice drills so staff are familiar with where emergency equipment is
situated, which staff member is allocated to which role in the team, etc.
CS2.4.3.1a Teamwork in emergency situations - refers to the importance of having the most appropriately
skilled individual responsible for coordinating the event (may be a GP or the practice nurse), and delegating
appropriate tasks to individuals who carry these out and work effectively with other members of the team to
optimise outcomes for the affected individual(s). Effective communication is paramount in such situations.
CS2.4.3.2a Appropriate time to withdraw treatment - these vary significantly between patients and the reasons
for their critical condition. If an individual has a detailed advanced care plan, this can help by providing clear criteria
for discontinuation of treatment in the case of a critical event. In a situation where there is evidence that persisting
with life support measures is futile, there are established decision-making principles regarding discontinuing life
support measures. These generally include acknowledgement that all decisions must be based on respect for
life and the patient’s right to choose (or the patient’s next of kin if this is not possible and not documented in an
advanced care plan), and must meet the standards of good professional and ethical practice. All efforts, with
transparency and accountability for all decision-making, must be made to obtain the appropriate consent.
Criteria to establish irreversible loss of function of the individual’s brain include the presence of a Glasgow Coma
Scale score of three, combined with absence of brainstem reflexes, and no spontaneous respirations in the
absence of hypothermia, or other situations such as the use of anaesthetic agents.9,10
CS2.4.3.1b Potential risks to the safety of others in an emergency situation - refer to hazards such as those
found at the site of road traumas (eg fuel leakage with the risk of fire, fallen power lines, risk of contamination
from blood and body fluids requiring use of appropriate precautions, risks from natural hazards such as bushfires,
chemical spills, etc).
References
1. Wide J, Mok H, McKenna M, Ogrodniczuk JS. Effect of gender socialization on the presentation of depression among men: A pilot
study. Can Fam Physician 2011;57(2):e74-78.
2. Australian Resuscitation Council. The ARC Guidelines. Available at http://resus.org.au/guidelines [Accessed 9 December 2015].
3. Skinner S. Radiation safety. Aust Fam Physician 2013;42(6):387-89.
4. Australian Medicines Handbook. Available at https://shop.amh.net.au/products/books/2016 [Accessed 9 December 2015].
5. Australian Government Department of Human Services. Prescription Shopping Programme. Available at www.humanservices.gov.
au/health-professionals/services/prescription-shopping-information-service [Accessed 9 December 2015].
6. National Health and Medical Research Council. How NHMRC develops its guidelines. Available at www.nhmrc.gov.au/guidelines-
publications/how-nhmrc-develops-its-guidelines [Accessed 9 December 2015].
7. The Royal Australian College of General Practitioners. Female genital cosmetic surgery - A resource for general practitioners and
other health professionals. Melbourne: RACGP, 2015. Available at www.racgp.org.au/your-practice/guidelines/female-genital-
cosmetic-surgery [Accessed 9 December 2015].
8. Ramsay M. Conflict in the healthcare workplace. Proc (Bayl Univ Med Cent) 2001;14(2):138-39. Available at www.ncbi.nlm.nih.gov/
pmc/articles/PMC1291328.
9. Queensland Government. Queensland Health. End-of-life care: Decision-making for withholding and withdrawing life-sustaining
measures from adult patients. Part 1. Legal Framework and Clinical Considerations. Available at https://www.health.qld.gov.au/
qhpolicy/docs/gdl/qh-gdl-005-1-1.pdf.
10. NSW Government. NSW Health. End-of-Life Care and Decision-Making Guidelines 2005. Available at www0.health.nsw.gov.au/
policies/gl/2005/pdf/GL2005_057.pdf [Accessed 9 December 2015].
55
Domain 3. Population health and the context of

general practice
‘I believe that the basic attribute of mankind is to look after each other’ - Fred Hollows

Competency
Core skills General practice under General practice -
supervision lifelong learning
CS3.1 GPs CS3.1.1 The CS3.1.1.1a Undertake CS3.1.1.1b Implement CS3.1.1.1c Analyse
make rational patterns and early identification of screening and prevention effectiveness of
decisions prevalence of modifiable risk factors strategies to improve vulnerable population
based on the disease are through screening of outcomes for individuals at based screening and
current and incorporated into individuals and their risk of common causes of preventive strategies
future health screening and relatives at risk of morbidity and mortality among the local
needs of the management common diseases population
community practices
CS3.1.1.2a Identify the CS3.1.1.2b Incorporate
and the
Australian risk factors that define national population
healthcare groups vulnerable to based screening
common causes of recommendations into
system
national morbidity and individual care
mortality
CS3.1.1.3a Identify CS3.1.1.3b Utilise

environmental influences motivational counselling
on health and individuals to address modifiable
at risk risk factors in vulnerable
groups
CS3.1.1.4b Identify
and manage individuals
vulnerable to environmental
risk factors
CS3.1.2 The CS3.1.2.1a Identify CS3.1.2.1b Evaluate the CS3.1.2.1c Analyse

impacts of sociocultural factors that impact of systemic and impacts of systemic,
the social can negatively impact on societal dysfunction on societal and familial
determinants health individuals and propose dysfunction on the
of health are management plans to local population
identified and reduce risks
addressed
CS3.1.2.2a Evaluate CS3.1.2.2b Identify CS3.1.2.2c Advocate

the role, benefits and and address cause for change to improve
difficulties of public health and impacts of familial health
epidemiology in provision dysfunction on individuals
of care to individuals
CS3.1.3 CS3.1.3.1a Outline public CS3.1.3.1b Integrate CS3.1.3.1c Mentor

Current and health roles relevant to important public health and support
emerging public general practice considerations into clinical colleagues to
health risks practice consider public health
are effectively perspectives and
managed responsibilities in
clinical practice
CS3.1.3.2a Describe CS3.1.3.2b Describe CS3.1.3.2c Initiate

public health risks and criteria for appropriate use public health
issues that are addressed of medical isolation programs and
by GPs activities in the
community
Criteria for stage of trainin'g

Competency
CS3.1.3.3b Utilise CS3.1.3.3c Provide
resources to assist community education
in management of related to culturally
communicable disease specific practices that
outbreaks may impact health
CS3.1.3.4b Notify public

health risks and concerns
according to relevant
legislation and regulations
CS3.1.3.5b Participate in
public health initiatives in
the community
CS3.2 GPs CS3.2.1 Barriers CS3.2.1.1a Identify CS3.2.1.1b Develop CS3.2.1.1c

effectively lead to equitable vulnerable groups within strategies to improve Assess practice
to address the access to the local community and access to general and demographics to
unique health quality care are barriers they may have to preventive care for determine whether
needs of the addressed healthcare access vulnerable groups the needs of
community vulnerable groups are
being met
CS3.2.1.2a Detail CS3.2.1.2c Maintain

community sociocultural up-to-date practice
factors that may impact information on
on health presentations Medicare benefits to
and outcomes inform colleagues and
patients
CS3.2.2 The CS3.2.2.1a Outline the CS3.2.2.1b Appraise and

health needs of roles of the Medicare review Medicare billings to
individuals are Benefits Schedule (MBS) ensure compliance with
balanced with and PBS guidelines
the health needs
CS3.2.2.2b Review use
of the community
of the PBS to ensure
through effective
utilisation of compliance
resources CS3.2.2.3b Appropriately
access Australian
Government funded
programs for vulnerable
groups
CS3.2.3 Effective CS3.2.3.1a Define types CS3.2.3.1b Identify CS3.2.3.1c Mentor

leadership of general practice opportunities and colleagues to take on
improves leadership obstacles to effective leadership roles
outcomes for leadership in general
patients practice
CS3.2.3.2a Define the CS3.2.3.2b Advocate

qualities of effective for vulnerable individuals
leadership in general or groups within the
practice community
57

CS3.1 Australian healthcare system - may be described as a complex network of public and private services
constructed to promote, restore and maintain the health of the population through provision of cost-effective,
quality healthcare. The components of the system include:
• primary healthcare, which is provided by Aboriginal and community controlled health services; GPs and
nurses, dentists and allied health professionals in private or community health centres, the PBS which enables
subsidised access to some medications, and the MBS which enables subsidised access to some primary,
secondary and tertiary care services, investigations and procedures
• secondary care, which is provided by specialists or facilities after referrals have been made by a GP
• tertiary care , which incorporates public and private hospitals and their emergency departments.
Behind this network is a structure of governance and support mechanisms, including the MBS and PBS, the
Australian Commission on Safety and Quality in Health Care (ACSQHC), the TGA, and state and territory health
and insurance ombudsmen.1
CS3.1.1 Patterns and prevalence of disease - prevalence refers to the number of cases of a disease, and
contributing factors, in a particular population at a particular time. Identifying patterns of disease assists in
clarifying risk factors, which may include:
• stage of the lifecycle
• geography
• lifestyle (eg smoking, inactivity, nutritional status)
• environment (eg climate change and its consequences, such as extreme weather events and forced migration)
• socioeconomic status
• gender
• race
• genetics
• occupational.
Identification of risk factors assists in appropriately targeting screening to enable early diagnosis and
management of particular conditions to improve health outcomes, and to plan for adequate health service
provision.
Diseases of population health concern in Australia (priority diseases) include the major causes of morbidity and
mortality which affect subgroups of the population with specific risk factors (eg obesity, obstructive sleep apnoea,
cerebrovascular and ischaemic heart disease, breast and prostate cancer, osteoarthritis, COPD, asthma,
noninsulin-dependent diabetes mellitus [NIDDM], dementia, mental health, etc), as well as those for which the
entire population is at risk (eg notifiable communicable diseases, including varicella, measles, meningococcal
meningitis, severe acute respiratory syndrome [SARS], etc).
It is also important to identify other trends that impact health, such as substance use (eg methamphetamines,
alcohol, marijuana, heroin, e-cigarettes), fertility and unintended pregnancy rates.
CS3.1.1 Screening and management practices - population-based preventive health strategies are determined
largely by disease prevalence and recognition of existent risk factors and vulnerabilities in the local population. For
example:
• provision of opportunistic immunisation
• engagement in age-appropriate and risk-appropriate screening (eg well child checks, Pap smears,
mammograms, fasting lipids and glucose, blood pressure checks, etc)
• management of lifestyle risk factors (particularly smoking, nutrition, alcohol and physical activity)
• comprehensive travel health consultations
• stress management interventions, etc.
CS3.1.1.1a Individuals and their relatives at risk of common diseases - includes:
• identifying individuals at risk due to lifestyle factors
• being of an ethnicity or race which is at risk of certain diseases (eg breast cancer and Ashkenazi Jewish
descent, oesophageal cancer in southern Chinese) and genetic predisposition
• recognising families in which genetic transmission of particular disease states is likely (eg haemachromatosis,
coeliac disease, Down’s syndrome, familial hypercholesterolaemia, Factor V Leiden, haemophilia, polycystic
kidney disease, etc).
Identification of individuals at risk also includes screening those at risk of substance use and addiction-related
issues, and educating those at risk of occupational injuries regarding the need for immunisation, workplace
ergonomic modification, prevention of musculoskeletal and stress-related injuries, etc.
CS3.1.1.1a Modifiable risk factors - exposures which increase risk of disease that can be changed through
lifestyle modification or commencement of treatment for elevated blood pressure, lipids, to assist with smoking or
alcohol cessation, etc. GPs are often well placed to provide advice on lifestyle modification, including:
• exercise regimens
• dietary improvements
• sleep routine
• adequate sun exposure
• involvement in community activities
• stress management techniques

• communication strategies and conflict resolution with significant others
• avoidance of chemicals, pollutants, alcohol, smoking and other addictive substances.
CS3.1.1.3a and 4b Environmental influences on health - may include consequences of climate change (eg
extreme weather events with heat and cold impacting older patients and infants), impacts of forced migration,
increased temperatures leading to introduction of new vector-borne diseases (eg dengue fever, malaria, Ross
River fever in historically cooler areas), etc. Geographical position of practice is important in regards to areas at risk
of natural disasters (eg flooding, cyclones and bushfires), whereby it is important for GPs in these areas to have
disaster management plans in place.
Other influences include impacts of airborne allergens, pollution and occupational exposures (eg asbestos, lead,
dust, chemicals, radiation, flammable liquids, gases, etc).
CS3.1.1.1b Screening and prevention strategies - includes utilising recall system and flags in patient records
for reminders regarding vaccinations, screening, and where appropriate, prophylactic treatment for those at risk,
as well as opportunistic screening when risk factors are identified based on established guidelines.
Targeted vaccinations may include pneumococcal vaccine and flu vaccination for individuals aged older than 65,
Aboriginal and Torres Strait Islander individuals aged six months to five years and who are older than 15 years, and
individuals with chronic diseases that place them at increased risk; hepatitis B vaccination for family members of
individuals diagnosed with hepatitis B; and screening of at-risk groups for prevalent diseases.
Targeted screening using evidence-based tools may include:
• the geriatric depression scale and mini-mental state examination (MMSE) in older individuals
• offering women chlamydia polymerase chain reaction (PCR) with Pap smears
• referring for screening for glaucoma or macular degeneration in individuals with a family history
59
• mental health and substance use screening questions for any individual experiencing stressors.
Utilisation of preventive strategies may include adequate counselling for travellers regarding antimalarials if
travelling to high-risk areas, and education regarding avoidance of mosquito bites and traveller’s diarrhoea.
CS3.1.1.3b Modifiable risk factors in vulnerable groups - vulnerability may be defined by a number of
parameters, including ethnic or sociocultural factors which make individuals prone to particular conditions and impact
their access to healthcare, and physical vulnerabilities due to illness or life stage. Vulnerable groups may include:
• Aboriginal and Torres Strait Islander peoples
• individuals from CALD communities, particularly refugees and asylum seekers
• lesbian, gay, transgender, bisexual, intersex and queer (LGTBIQ) individuals
• people with low health literacy
• individuals in rural and remote areas
• individuals with severe mental health problems which impact their ability to prioritise their own health (eg
schizophrenia, severe depression, complex PTSD)
• war veterans
• emergency service personnel and other occupations at risk of physical and/or psychological injuries related to
hazards of their employment
• socially disadvantaged individuals (eg unemployed, homeless, etc)
• individuals with physical and/or intellectual disabilities or impairments
• antepartum, antenatal and postnatal women
• individuals who are using illicit substances (eg individuals who inject and are at risk of blood-borne viruses and
bacterial infections)
• adolescents
• individuals detained in correctional facilities or immigration detention.
CS3.1.2 Social determinants of health - may be described as, ‘the conditions into which people are born, grow,
work, live and age and the wider set of forces and systems shaping the conditions of daily life’ which impact health
equity.2 Examples include:
• social inclusion
• connectedness
• meaningful participation (measure of the degree to which individuals or groups are able to access opportunities
and resources available to others)
• employment
• functional housing
• access to quality education and early childhood developmental opportunities
• adequate nutrition.
CS3.1.2.2a Public health epidemiology in provision of care to individuals - public health epidemiology may
be defined as the science of patterns, causes and effects of health and disease conditions in defined populations.
This is important knowledge for GPs to maintain in order to enable targeted screening and early management of
disease states to improve outcomes. Useful epidemiological skills and concepts include gaining an
understanding of:
incidence and prevalence of common and serious conditions within the Australian population and vulnerable
subgroups
• transmission rates
• mortality and morbidity rates
• pandemic versus epidemic versus endemic
• number needed to treat
• odds ratio, relative risk reduction
• relative risk.
It is important to acknowledge knowledge of the priority diseases as the most common contributors to mortality
and morbidity, and thus the justification that these are the focus for population-based preventive health strategies.
As of 2012, the Australian Institute of Health and Welfare (AIHW) has defined cardiovascular disease, cancer,
mental health, diabetes, asthma, dementia, injury, obesity, and arthritis and musculoskeletal conditions as the key
national health priorities.3.
When delivering patient-centred care, integration of population health knowledge to individuals can add another
layer of complexity and time to consultations, and social determinants of health may impact the individual’s ability
to access screening and preventive care. The GP plays an important role in assisting individuals to negotiate
obstacles to access the care they need.
CS3.1.2.1.b Systemic and societal dysfunction - refers to the importance of identifying social factors which
increase the risk of particular diseases to assess whether they can be modified to reduce risks in the future (eg
the impacts of poverty in some residential areas, consequent homelessness, crime, illicit substance use, etc).
CS3.1.2.2b Familial dysfunction - may include situations of family violence, child abuse, substance use, and
consequences of poverty and addiction (eg substance and behavioural addiction). Impacts may include physical
and psychological trauma (particularly complex PTSD), substance use, involvement in crime, etc.
CS3.1.3 Public health risks - may include:

• notifiable communicable diseases (eg hepatitis A, giardia, rotavirus, salmonella, etc)
• sexually transmitted infections (eg chlamydia, gonorrhoea, syphilis, human papillomavirus [HPV], etc)
• vector-borne diseases (eg malaria, dengue fever, etc)

• airborne viruses (influenza, tuberculosis, etc)
• vaccine-preventable diseases (eg hepatitis B, measles, mumps, varicella, tetanus, polio, meningococcus,
haemophilus, etc)
• blood-borne viruses (eg HIV, hepatitis C, etc)
• infections spread by contact (eg chlamydial eye infections)
• potential environmental hazards (eg water quality, respiratory effects of pollution, etc)
• occupational-related hazards (eg asbestos exposure).
CS3.1.3.1a Public health roles relevant to general practice - may include:

• making notifications to the state or territory Department of Health and assisting with contact-tracing once
informed consent has been provided regarding sexually transmitted infections
• communicable diseases (eg active pulmonary tuberculosis)
• implementing vaccination programs with appropriate education (and typically in a team with practice nurse/s)
• identifying health concerns in the local community (eg related to occupational or environmental risk factors)
and managing these through advocacy and professional support
• staying informed of disease trends and guidelines regarding screening and prevention to assist in identifying
vulnerable groups, and detecting or preventing disease to improve health outcomes.
61
CS3.1.3.2b Criteria for appropriate use of medical isolation - may include suspicion of an individual
demonstrating signs of infection due to an airborne or droplet-spread pathogen which is a communicable
notifiable condition (eg measles, varicella, influenza, etc) whose presence in a public area of the clinic may pose
risks to others. This is particularly relevant in the case of individuals who may be immunocompromised (eg young
children, pregnant women, older individuals or those taking immunosuppressants). Efficient identification and
management of individuals with readily communicable diseases requires a team approach, particularly involving
the practice nurse(s) to assist with efficient triage and empowerment of reception staff to ask simple questions
of patients when they attend (assisted with appropriate use of signage) in the setting of disease outbreaks (eg
influenza, Ebola, etc).
CS3.1.3.3b Resources to assist in management of communicable disease outbreaks - may include:
• effective triaging of febrile patients
• robust use of infection control procedures
• appropriate use of medical isolation
• vaccination of vulnerable members of the population

• use of communicable disease notification framework
• contact-tracing after diagnosis
• effective transmission-minimisation education for patients, family members and/or carers

• efficient communication with hospitals prior to patient transfer.
CS3.1.3.4b Relevant health legislation and regulations - refers to the importance of GPs understanding their
state or territory requirements for reporting of notifiable conditions and the time limits in which this should occur.
CS3.1.3.5b Public health initiatives - may include participation in health education and promotion campaigns,
implementation of vaccination programs, advocacy regarding issues of public health concern, etc.
CS3.1.3.3c Culturally-specific practice which may impact health - may include female genital mutilation,
circumcision, forced marriage, etc.
CS3.2 Effectively lead - relates to the important role of the GP in addressing stigma and advocating for the
rights of patients within the community, with health organisations and institutions, with the government and, if
appropriate, in the media. Examples of issues that may require leadership include improving public awareness
and reducing stigma about mental health issues, advocating for vulnerable individuals or groups (eg cultural
minority groups), improving health literacy, etc.
CS3.2 Address the unique health needs of the community - refers to the importance of identifying the factors
such as age, gender, socioeconomic status, cultural differences, demography of the area, remoteness, and
costs of healthcare in prioritisation of health issues and consequent access. An example of a way to address
the needs of the community is attention to youth, sexual and gender-diversity-friendly structures (these include
physical environment, and attitudes and knowledge of doctors, nurses and other staff members) and consequent
strategies to make a practice welcoming to all people.
CS3.2.1 Barriers to equitable access to quality care - health services must be available, affordable, physically
accessible, acceptable and in adequate supply. Barriers may include low socioeconomic indicators, lack of health
literacy, lack of resources or supply, beliefs and social attitudes, language and lengthy waiting times.
CS3.2.2 Utilisation of resources - may include:
• the importance of mindfulness of the economic costs of each consultation to the state or territory
• a referral made and prescription written as a check to ensure these are provided based on evidence and equity
• the need for compliance with MBS and PBS requirements

• utilisation of telehealth resources (eg tele-dermatology to access specialist services efficiently), etc.
CS3.2.2.1a MBS and PBS - provide Australian Government funds to fully or partially subsidise access to primary,
allied and specialist healthcare, and to the range of medications which are listed in the schedule. The availability of
these benefits contributes to improving equitable access to care and treatment for the Australian population.
CS3.2.2.3b Australian Government-funded programs - examples include:
• chronic disease management plans for individuals on low incomes to enable access to allied health services
• Aboriginal and Torres Strait Islander health assessments
• mental health plans for individuals on low incomes to enable access to clinical psychologists or counsellors
(DoH Better Access initiatives)
• health assessments for individuals aged 75 and older
• refugee health assessments
• utilisation of TIS
• mental health nurse incentive program.
CS3.2.3.1a Types of general practice leadership - Effective general practice leadership can take a number
of forms. Many GPs struggle to define themselves as leaders; however, a GP who takes a central role in the
coordination of patient care with external health professionals in the community, using a holistic, patient-centred
approach, effective communication, vision-setting and a strategic approach to advocate for individual patients
when there are issues with equitable access, can be said to be demonstrating a form of leadership. Other forms of
leadership include:
• medical educators who enhance quality of care through inspiring and setting the vision for future GPs
• practice owners who provide inspiration, a clear vision and direction for their staff to create a collegiate,
functional and innovative service - an important part of this is creating a team, which is not hierarchial, which
uses respectful communication and acknowledgement of the skills and experience of each of its members to
optimise care and a healthy work environment
• clinical leaders who create better patient outcomes by improving healthcare provision through quality and safety
developments, at both the macro and micro levels
• GPs who participate in advocacy regarding issues pertinent to the health of the population and/or vulnerable
groups within the community, identifying a need and demonstrating skills in increasing awareness and initiating
change in relation to those needs
• academic GPs who drive research into important areas, impacting health or general practice service provision.
CS3.2.3.2a Qualities of effective leadership in general practice - involves a combination of skills, which may include:
• knowledge about a particular issue, organisation, value or goal

• demonstrating confidence and a capacity for self-reflection of strengths and weaknesses, and creating a team
which complements these abilities, to achieve a common goal
• use of clear, motivational and respectful communication which facilitates a supportive and collegiate environment
and inspires action
• vision and goal-setting, as well as the ability to clearly communicate these ideas
• ability to take measured risks
• being perceptive and respectful of team members’ feedback

• ability to demonstrate empathy and flexibility when obstacles are faced
• having integrity.
CS3.2.3.1b Opportunities and obstacles to effective leadership - having a broad base of knowledge and
professional networks, the experienced GP is well suited to taking on leadership roles. Involvement in committees
63
and advisory groups can be a valuable way to gain experience to further interests in advocacy and other forms of
leadership in the future. Obstacles may be overcome by strategies such as accessing mentoring to enable individuals
to have the confidence and develop the skills to fulfil these roles adequately, accessing support with media training,
and seeking further education in areas of interest (eg medical administration, small business management, etc).
References
1. Australian Institute of Health and Welfare. Australia’s Health System 2014. Available at www.aihw.gov.au/australias-health/2014/
health-system [Accessed 9 December 2015].
2. World Health Organization. Social determinants of health. Available at www.who.int/social_determinants/en [Accessed 9 December
2015].
3. Australian Institute of Health and Welfare. National health priority areas. Available at www.aihw.gov.au/national-health-priority-areas
[Accessed 9 December 2015].
Domain 4. Professional and ethical role

‘It takes less time to do things right than to explain why you did it wrong’ - Henry Wadsworth Longfellow

Competency
CS4.1 GPs are CS4.1.1 CS4.1.1.1a Identify key CS4.1.1.1b Identify ethical CS4.1.1.1c
ethical and Adherence to features of professional dilemmas in practice Regularly reflect on
professional relevant codes codes of ethics and situations professionalism and
and standards conduct relevant to ethical conduct
of ethical and clinical practice
professional
behaviour CS4.1.1.2a Distinguish CS4.1.1.2b Access CS4.1.1.2c
the impact of the professional resources to Implement changes
power differential in the obtain support for ethical and quality
therapeutic relationship dilemmas improvements based
on reflections
CS4.1.1.3b Evaluate CS4.1.1.3c Mentor

and review professional and support
behaviour against colleagues to access
appropriate codes of and adhere to
conduct professional codes of
conduct

manage areas of disparity
between behaviour and
codes of conduct
CS4.1.2 Duty CS4.1.2.1a Define duty CS4.1.2.1b Identify and CS4.1.2.1c Facilitate
of care is of care manage clinical situations and support
maintained where there are obstacles colleagues in
to provision of duty of care adhering to duty of
care responsibilities
CS4.1.2.2a Identify CS4.1.2.2b Record and CS4.1.2.2c Review

potential obstacles to report any instances where and revise policies
duty of care duty of care may have and procedures
been compromised relating to duty of
care in the practice
CS4.1.2.3a Identify duty

of care responsibilities in
different clinical scenarios
CS4.1.4 Critical CS4.1.4.1a Identify CS4.1.4.1b Implement CS4.1.4.1c

incidents and potential and actual strategies to review Facilitate debriefing
potential critical critical incidents and potential and actual critical and support for
incidents are propose strategies to incidents to manage colleagues following
identified and review and improve consequences and reduce critical incidents
managed quality of care as a result future risk
CS4.1.4.2a Identify the CS4.1.4.2c

need to debrief and Document critical
obtain support after incidents to use
critical incidents for further quality
improvement and
reporting
65

Competency
CS4.2 GPs are CS4.2.1 CS4.2.1.1a Identify CS4.2.1.1b Formulate CS4.2.1.1c Identify
self-aware Professional knowledge and strategies to identify and and address learning
knowledge skills gaps, and plan address learning needs and skill development
and skills are meaningful learning to needs through
reviewed and address them ongoing professional
developed development
CS4.2.1.2a Implement CS4.2.1.2b Appraise CS4.2.1.2c Actively

and review planned and review response to engage with
learning constructive feedback professional bodies in
special interest areas
CS4.2.1.3b Identify
and utilise professional
resources that may assist
in quality care provision
CS4.2.1.4b Outline factors

that create an effective
learning environment
CS4.2.2 CS4.2.2.1a Identify CS4.2.2.1b Implement CS4.2.2.1c Mentor

Reflection and personal factors that strategies to recognise and and support
self-appraisal may impact therapeutic manage personal factors colleagues to
are undertaken relationships and delivery if they impact on quality of implement reflective
regularly of care care or personal wellbeing practice and self
appraisal
CS4.2.2.2b Reflect on CS4.2.2.2c Engage

and review personal and in reflective practice
professional performance
with supervisors and other
professionals
CS4.2.2.3c Identify
and address potential
conflict that may
occur if a variety of
professional roles are
held
CS4.2.3 CS4.2.3.1a Evaluate CS4.2.3.1b Identify and CS4.2.3.1c Identify

Personal health personal wellbeing manage personal health and address barriers
and wellbeing regularly and identify issues by accessing to maintaining health
is evaluated, health issues that create professional support as and wellbeing
maintained and risk and may impact needed
developed quality of care

Competency
CS4.2.3.2a Distinguish CS4.2.3.2b Identify need CS4.2.3.2c Develop
importance of medical and access support an occupational
professionals accessing for emotiona reactions environment that
healthcare when needed to confronting clinical promotes personal
situations and professional
wellbeing
CS4.2.3.3a Devise CS4.2.3.3b Identify and CS4.2.3.3c Mentor

structures to support manage occupationa and develop skills in
personal health and health risks of GPs debriefing colleagues
wellbeing after distressing
experiences
CS4.2.3.4b Identify
mentors to support
personal and professional
development
CS4.3 GPs CS4.3.1 CS4.3.1.1a Identify and CS4.3.1.1b Develop CS4.3.1.1c Maintain
mentor, teach Professional respond to the personal strategies to share appropriate role
and research knowledge learning needs of others recently acquired skills and boundaries, and
to improve and skills are knowledge with peers manage time
quality care effectively shared constraints to
with others mentor and support
colleagues to improve
knowledge and skills
CS4.3.1.2a Encourage CS4.3.1.2b Assist peers CS4.3.1.2c

and support peer and colleagues to identify Teach effectively
discussion and clinical and prioritise areas of and accountably
questioning clinical knowledge and by utilising
skill that are in need of communication and
development leadership skills
CS4.3.1.3a Describe CS4.3.1.3b Identify CS4.3.1.3c Identify

resources accessed to strategies to create an safety net strategies
assist with knowledge inclusive team-based to enable clinical
and skill development approach to teaching and exposure and
of peers and junior leadership minimise risks
colleagues to patients from
inexperienced
colleagues
CS4.3.1.4a Identify CS4.3.1.4b Contribute to CS4.3.1.4c Optimise

clinical knowledge gaps and utilise best practice teaching skills
that would be suitable for guidelines in general through networking
general practice research practice research and ongoing
development
CS4.3.1.5c
Implement
procedures to ensure
research complies
with relevant
guidelines
67

Competency
CS4.3.1.6c Lead or
participate in general
practice research
CS4.3.2 Identify CS4.3.2.1a Identify CS4.3.2.1b Identify, CS4.3.2.1c Develop

and support professional resources support and appropriately and disseminate
colleagues that are available to assist refer colleagues who are in procedures and
who may be in health professionals who difficulty information relating
difficulty are in difficulty to doctors or other
health professionals
in difficulty
CS4.3.2.2b Formulate CS4.3.2.2c Identify

strategies to maintain and support
duty of care if a colleague colleagues who may
displays limited insight be vulnerable
into reduced capacity to
practice

CS4.1.1 Relevant codes and standards of ethical and professional behaviour - includes resources which
can assist health professionals by defining acceptable conduct and practice in relation to their peers, in working
with professional values and ethics primarily by making the care of the patient the primary concern, and in
practising medicine safely. Examples of professional codes and standards include:
• Medical Board of Australia’s Good medical practice: A code of conduct for doctors in Australia1
• RACGP’s Standards for general practices2, clinical3 and practice management policies4
• Australian Medical Association’s (AMA) Code of ethics5
• Medicines Australia’s Code of Conduct6
• NHMRC’s National statement on ethical conduct in human research7
CS4.1.1.2a Impact of power differential in the therapeutic relationship - it is important to recognise that
there exists a power differential between the GP and the patient in many consultations. This difference can be
minimised through the development of an effective, respectful therapeutic relationship and good communication;
however, it often still exists. This difference arises as a consequence of many factors, including:
• sociocultural backgrounds and cultural lens
• previous experiences
• personality types of patient and doctor
• health beliefs
• the perceived degree of patient dependence on the GP to receive the type of care they require.
This power difference is particularly pertinent when patients are asked about participation in research and quality
improvement activities. In this situation, it is important to acknowledge this difference and its potential effects
on the patient’s capacity to provide informed consent and feel comfortable in declining the invitation without
concerns about their care being impacted as a result.
CS4.1.1.1b Ethical dilemmas - may arise when there are apparent contradictions between the elements of a
GP’s ethical code and that of the patient broader society. Some examples include:
• in the context of care of people with disabilities, where dilemmas may arise around complex instances (eg
potential conflict between competent medical care, patient autonomy, inherent concepts of ‘social worth’ and
universal human dignity, etc)
• in the realm of antenatal screening and/or the decision to continue or to terminate pregnancies for genetic
abnormalities or bodily impairments
• in more routine provision of individual care (eg sexual wellbeing, definition of ‘troublesome behaviours’,
decisions regarding degree of carer and family involvement for individuals who have questions over their
capacity to provide consent, in the disparity between public and private health policies and access to care,
etc)
• where a patient refuses to inform family members who are at risk when a diagnosis is made (eg a
communicable disease) which causes duty of care issues to predominate.
It is important to consider the significance of ensuring that each professional is aware of their own values
and belief systems, and how these may have an impact on patient care when dealing with examples such as
those outlined above. If a conflict is recognised, the GP has a duty of care to identify and assess the situation,
reflect on their own role, and consider multiple perspectives and options available to facilitate a decision.
Resolutions need to be timely for patient care and in line with professional codes of conduct, and individuals are
encouraged to seek formal or informal guidance and document their decision-making. Referring patients to other
professionals who are able to provide the care they require may be the appropriate course of action in some
situations.
69
CS4.1.2 Duty of care - refers to the professional’s responsibility for the optimal care of patients. Important criteria
which assist in defining this responsibility include:
• acting on patient cues
• respecting patient-doctor boundaries

• maintaining confidentiality
• recognising professional limitations in one’s self and in colleagues
• ensuring appropriate reporting and follow-up
• undertaking advocacy as appropriate.
• respecting a patient’s culture and values, and maintaining an awareness of how these have an impact on the
therapeutic relationship
• understanding patients’ rights of to access competent, compassionate care, be fully informed, and self
determination.
CS4.1.2.2a Obstacles to duty of care - may arise in more complex situations where the GP has duty of care to a
number of parties involved in a situation (including to the general community) in which there is perceived or actual
conflict between these responsibilities. Examples may include:
• situations where contact-tracing is required for communicable diseases, particularly STIs where the patient of
the GPs wishes to remain anonymous due to concerns regarding consequences
• identifying and managing expectations of workplace stakeholders, particularly considerations regarding whether
to modify patient management to suit employer culture for individuals with occupational injuries (this is especially
relevant for elite athletes who are under pressure from coaches and/or sporting organisations to compete
despite injuries or illness)
• mandatory reporting to the Department of Human Services’ Child Protection, where the alleged perpetrator and
child are both patients of the GP (the GP’s duty of care to the minor should always take precedence in such a
situation)
• situations where an individual may have impaired capacity to provide consent and their carer is also a patient of
the GP and there is a conflict in decision-making regarding management
• during reviews for fitness to drive, where the GP is aware that the patient is demonstrating diminished capacity
to drive, but would be severely impacted by having their licence revoked
• utilisation of involuntary admission certification for individuals who are putting themselves or others at risk due to
experiencing severe mental health issues.
CS4.1.2.2b Instances where duty of care may have been compromised - refers to situations such as those
outlined in CS4.1.2.2a, where a GP believes the decisions around duty of care responsibilities may have been
flawed or have been consequently challenged by another party. In situations where there are questions over duty
of care, it is important for the reasons for decisions made to be documented, to consider notifying the appropriate
medical defence organisation, and to debrief with trusted senior colleagues.
CS4.1.3 Patient-doctor boundaries - refers to maintaining a separation of personal and professional

relationships, particularly where there is a possible imbalance of power in the relationship (eg when a patient’s
judgement may be impaired), in order to enable maintenance of a therapeutic relationship. Recognition of
transference and countertransference is very important to ensure that appropriate boundaries are maintained.
Transference refers to the phenomenon by which individuals ‘unconsciously transfer feelings and attitudes from a
person or situation in the past on to a person or situation in the present. The process is at least partly inappropriate
to the present.’ This process is unconscious and can occur in either direction in the patient-doctor relationship.
Risk factors for transference include vulnerable (eg complex PTSD, severe depression or anxiety), perceptions of
dependence, associated anxiety about physical or psychological safety, and frequency of contact (inside or outside
of the clinic).
Countertransference refers to the response elicited in the GP by the patient’s transference communications. It
is important for GPs to recognise when this is occurring and to address it empathically and respectfully, and to
agree with the patient on some clear therapeutic boundaries.
CS4.1.3.2a Potential consequences of unclear boundaries - includes the development of unreasonable

patient expectations which are unable to be met, and may put the patient at risk or raise the possibility of legal
action.
CS4.1.3.1b Patient interactions where there is a blurring of therapeutic boundaries - red flags for the risk of
inappropriate interactions need to be firstly recognised by the GP and managed (as outlined in CS4.1.3) in order
to minimise risks. Examples of such red flags include:
• the GP feeling uncomfortable about seeing a particular patient
• requests from patients for dishonest or unethical behaviour by the GP (eg supplying medications that are not
clinically indicated, providing incorrect information on legal documentation, taking part in an intimate relationship,
etc)
• situations where the GP may be providing a level of care that is outside of their normal practice.
Patients with complex PTSD are often particularly vulnerable to developing transference with their health
providers. While this behaviour is subconscious, it needs to be acknowledged and appropriately managed.
CS4.1.3.2b Terminating therapeutic relationships where boundaries are not maintained - in this situation
it is important for GPs to consider that they have a duty of care to refer the individual to another GP in order to
enable continuity of care. While strategies used to achieve this referral vary according to the situation, it needs to
be effectively communicated with empathy and respect.
CS4.1.4 Critical incidents and potential critical incidents - to situations which are not necessarily dramatic
events, but which carry significance for the health professional and/or the patient. Critical incidents may raise
questions about individual or organisational beliefs, behaviours, values or attitudes that create space for reflection,
and may prompt change in thinking, policy or behaviour. Critical incidents may be caused by issues related to
knowledge, culture, beliefs, emotions, relationships or communication.
Examples of critical incidents may include:
• a missed diagnosis leading to poor clinical outcome

• a communication problem or difficult interaction between a health professional and a patient or family member
• situations which cause individuals to feel inadequate, unsupported or confronted, etc.
CS4.1.4.1b Critical incidents to manage consequences and reduce future risk - may include assignment of
a senior clinical professional in the practice as the individual who organises debriefing after a potential or actual
clinical incident, and educating new staff about how critical incidents are managed.
CS4.1.4.1c Debriefing and support for colleagues following critical incidents - may include establishment
of formal or informal support for professional peers, development of education in recognising when colleagues
are struggling with a specific issue or generally, and provision of information on strategies to assist peers with
specific or general issues and options for more intensive assistance. Avoiding blame is an integral part of effective
debriefing.
CS4.2 Self-aware - may be used in this context to describe a professional’s ability to be reflective and develop
a clear perception of their own personality, communication style, knowledge base, thoughts, beliefs, possible
biases, motivation, values and emotions. This enables insight into how the professional may be perceived by
others and how to minimise risks of problems with communication or professional and therapeutic relationship.
CS4.2.1.1a Plan meaningful learning - incorporates a normative curriculum that identifies what students should
learn, as well as student-centred learning intent (ie what they want to learn, which may be determined through
reflective practice), collaboratively developing learning needs, objectives and a plan by which to address them. It is
also helpful to plan for regular evaluation and feedback, collection of evidence of learning, and periodic revision of
the learning plan prior to submission.
71
CS4.2.1.1b Formulate strategies - reflective practice is a core aspect of learning need identification. This
includes developing the capacity to reflect on clinical skills and knowledge in order to engage in a process
of continuous learning. As well as paying attention to whether clinical practice is evidence-based and if not,
determining whether it is in line with peers, there is justification and rationale behind clinical choices, effective
communication is being used, and practice is ethical and professional.
Appropriate supervision of junior medical staff, and regular evaluation of that supervision, takes into account the
knowledge and skills of the individual, as well as their capacity for insight into their learning needs. This provides
knowledge as to whether the individual is able to identify when supervision is required or whether the supervisor
needs to be prescriptive as to the types of consultations and procedures which require supervisor input (eg
prescribing of Schedule 8 medications, minor procedures, etc). Safety of the patient must be paramount in this
consideration.
Strategies to stimulate learning and encourage reflection may include use of role plays, observation of consultations
through sitting in or recording, case presentations of complex cases at practice meetings, critical case discussions,
etc.
CS4.2.1.3b Professional resources that may assist in quality care provision - easy access to evidence-based
resources to assist in provision of quality care is an important aspect of general practice in the context of the broad
range of populations and conditions that present for care. A good level of self-awareness and utilisation of reflective
practice can assist in recognising when additional resources are required to deliver high-quality care and improved
outcomes for patients. Utilisation of critical appraisal skills in determining whether the resources are applicable
to a particular patient are another essential skill. Professional resources may include diagnostic and prescribing
guidelines, position statements of key national and local health organisations, and other resources outlined in
CS2.4.2.5, CS 2.3.1 and CS2.3.1.2.
CS4.2.1.4b Learning environment - may include factors such as:
• being accessible as a supervisor and mentor both physically onsite and through a non-judgemental, non-critical
and respectful approach to mentoring and teaching - this enables junior staff members to be comfortable in
requesting assistance when required
• provision of therapeutic and management guidelines to assist junior staff members
• creating structures to allow time for education opportunities as they arise
• creating structures to enable honest and fair provision of feedback regarding teaching and mentoring in order to
maintain quality improvement
• recognising any difficulties which arise for junior staff and providing support, either personally or by
recommendation of other external resources externally.
CS4.2.1.1c Ongoing professional development - may take many forms and it is important for GPs to identify
types of learning from which they benefit most readily. This is partly related to the learning style of the individual and
specific learning needs identified. Professional development may include:
• the use of small group learning and journal clubs
• Balint groups
• clinical audit and e-audit tools
• participation in external data extraction/research projects
• active learning modules (ALMs)
• cultural awareness training
• peer reviewing journal articles
• graduate certificate or diploma courses, master’s degree.

CS4.2.1.2c Professional bodies in special interest areas - may include groups and organisations such as:
• RACGP Aboriginal and Torres Strait Islander Health, RACGP Specific Interests, RACGP Rural
• Australasian Society for HIV Medicine
• International Society of Travel Medicine
• Public Health Association of Australia
• Refugee Health Network of Australia
• Australian Medical Acupuncture College
• Australasian Integrative Medicine Association
• Australian Association of Musculoskeletal Medicine
• Australasian Faculty of Musculoskeletal Medicine
• Sports Medicine Australia
• Sports Doctors Australia
• Australian College Physical Medicine.
CS4.2.2 Reflection and self-appraisal - reflective practice is a term that may be used to describe the recognition
and evaluation of multiple perspectives in healthcare interactions, including an emphasis on self-awareness and
insight. Reflective practice comprises the critical examination of one’s self (acknowledging factors such as cultural
bias, personal values and beliefs), interpersonal relationships and the health system. Reflective learning is an active
learning style grounded in an ethical framework that enables real-time self-appraisal as a basis for learning and
development, even in complex situations
CS4.2.2.1a Personal factors - may include cultural bias, personal values and beliefs, motivations, style of
communication, and gender differences in provision of care (eg female GPs typically provide longer consultations
and more reasons for encounter per consultation than males.8,9 Refer to CS4.1.3 regarding therapeutic boundaries.
CS4.2.2.1b Strategies to recognise and manage personal factors - may include use of regular self-reflection
and maintenance of self-awareness to recognise if personal factors are impacting on the quality of care being
delivered. If this is identified, the GP needs to consider if they are able to continue providing care to the patient or
whether a referral to another provider is warranted.
CS4.2.2.3c Address potential conflict that may occur if a variety of professional roles are held - this issue is
pertinent to a number of consultation types and special interest areas of general practice. Examples include:
• patients who are family members, professional colleagues or close friends of the GP
• patients who have another type of professional relationship with their GP (eg accountant, lawyer, etc)
• rural GPs who carry out multiple roles within their community (eg involvement in local sporting clubs, council, etc).
One of the key factors to consider in addressing these potential conflicts is recognition of the importance of
maintaining therapeutic boundaries in order to avoid power imbalances (in regards to the GP or to the patient
being the holder of most significant power), which may then impact how the other party behaves (eg GPs
feeling pressured into prescribing medications outside of guidelines or writing inappropriate sickness or disability
certificates). Refer to CS4.1.3.
CS4.2.3 Personal health and wellbeing - refers to physical, psychological, social, spiritual and cultural wellbeing.
The applications of this principle are important to acknowledge for each individual GP. General practice is a very
rewarding and fulfilling, but sometimes can be very stressful and personally challenging profession. The health of
GPs can be adversely impacted in many ways as a consequence of the type of work they do and it is important
that they have insight into their own health needs and are able to prioritise them when required. It is important to
recognise potentially risky situations or therapeutic relationships early and to minimise risk by engaging support
from colleagues, other health professionals or organisations, and implement protective strategies.
73
Optimising physical safety at work is important to minimise risk of patient-initiated violence. It is vital to ensure
that duress alarms are in place, develop and maintaining skills in de-escalation techniques, and confirm that all
staff members are aware of the action plan if a situation that puts the staff or other patients at risk arises (refer to
CS1.1.2.1c and CS1.1.2.2a).
Listening to their own advice as a GP is important; however, every healthcare professional should have their
own GP to assist in implementing preventive strategies to ensure that they develop and maintain physical and
psychological wellness, and are thus are able to deliver quality care. Fatigue management is an important aspect
of self-care, particularly for doctors who work in rural and remote areas with onerous on-call responsibilities.
Identifying any blurring of boundaries in therapeutic relationships is another important area of risk (refer to
CS4.1.3 and CS4.1.3.1b).
In the event of a physical or psychological impairment which may impact the GP’s wellbeing or ability to manage
their professional responsibilities, a robust management plan may need to be developed, working collaboratively
with other health professionals as appropriate.
CS4.2.3.2b Support for emotional reactions to confronting clinical situations - identifying the need to
access support may be the biggest obstacle for GP. As health professionals, GPs can be confronted with very
traumatic and emotional situations. They often expect themselves to put their own emotional responses aside
in order for them to appropriately deal with the situation at hand. It is important for GPs to recognise symptoms
of stress and anxiety in response to traumatic or confronting situations and to access support, whether through
formal or informal debriefing with colleagues.
CS4.2.3.3b Occupational health risks - may include impacts of stress and fatigue from working with vulnerable
communities (eg Aboriginal and Torres Strait Islander peoples, homeless people, etc), working in remote and
regional areas, and being placed in in emotionally challenging clinical situations (eg palliative care), etc. Risk
minimisation strategies may include installation of duress alarms, awareness of safety issues in the workplace,
ensuring safety during visits outside the practice, and routine debriefing after critical or potentially critical incidents,
etc.
CS4.2.3.3c Skills in debriefing colleagues - there are a number of ways to approach debriefing colleagues
after a critical or near critical incident. It is important to recognise that many professionals experience critical
incident stress following an event. There is a broad spectrum of responses to such situations, which vary due
to factors such as previous experiences, personality, feelings of responsibility, values, and beliefs of individuals
involved.
It is recognised that clinical critical incidents may be under-reported due to health professionals’ medico-legal
concerns (particularly in regards to individuals being concerned about being blamed and/or disciplined as a
result) and that debriefing is an important part of stress management to assist individuals to cope and reduce
the risk of long-term effects. Some people find a peer-driven, therapist-mediated group approach is a useful
debriefing structure. This may consist of an immediate response whereby the affected professional is provided
support. This is followed by a second phase that consists of identifying what can be learned from the incident,
rather than placing blame on any one individual, which many believe to be more useful if done as a group. The
‘Mitchell model’ to debriefing is one approach which may be useful.10
CS4.3.1.3b Inclusive team-based approach to teaching and leadership - may include identifying strengths
and areas for improvement of the individuals within the team. It is helpful to focus on delegating responsibilities to
match these skills, including teaching junior colleagues and providing clinical or other types of leadership (refer to
CS3.2.3.1a).
CS4.3.1.4b Best practice guidelines in general practice research - doctors contribute to expanding the
knowledge base of general practice through designing, coordinating and/or contributing to research in order to
enable them to make informed, evidence-based decisions about patient care. Much of this evidence can only be
obtained from research undertaken in the general practice setting. Contributions may be as simple as facilitating
patient recruitment or access to patient data, but there are opportunities to play a more active role in research
design and implementation. Participating in design or research depends on the research being performed to
appropriate ethics and best practice standards.
Best practice guidelines in general practice research has ethical and clinical practice guidelines to which
researchers need to adhere when running or participating in research (eg the NHMRC’s National statement on
ethical conduct in human research and Good clinical practice in Australia). Following such ethical and clinical
practice guidelines is the responsibility of the researchers. GPs need to be aware that such guidelines exist and
ensure that any research in which they participate has been approved by a human research ethics committee.
CS4.3.1.1c Appropriate role boundaries - the variety of professional roles may include teacher, clinician,
supervisor, clinical leader, mentor, etc. Maintaining appropriate boundaries with junior colleagues is as important
as therapeutic relationship boundaries with patients.
CS4.3.1.2c Teach effectively and accountably - effective teaching and mentoring includes:
• the use of effective communication skills (eg the importance of recognising the learning needs of peers and
junior colleagues)
• development of rapport with learner/mentee

• reflection and provision of respectful feedback (positive before negative), which challenges individuals to self
reflect and develop knowledge and skills
• clear explanations as to reasoning behind use of clinical strategies
• formulating appropriate questions to encourage learners to develop problem-solving skills.
Extended teaching skills for learners who are more advanced in their training may include assisting learners to
use reflective practice to encourage them to ‘learn’, rather than the GP ‘teaching’, facilitating development of
skills by teaching in a way that caters to their individual learning style, and facilitating learning at an appropriate
level of autonomy for the individual.
Demonstrating accountability for teaching identifies the important role which a teacher/mentor of junior
colleagues plays when assisting in the development of clinical skills and knowledge. Exposure to patients is an
important part of this process; however, the senior staff member needs to remain accountable for the outcomes
when this occurs. The senior staff member should thus be mindful of the level of supervision required after
assessment of the potential risks, taking into account the junior colleague’s experience and knowledge.
Ensuring that an evaluation process is in place includes requests for provision of formal/informal and structured/
unstructured feedback on quality of leadership, quality and content of education and mentoring, and
development of effective ways to manage this information, and any subsequent communication and changes to
the way in which team-based learning is carried out in the future.
CS4.3.1.3c Safety net strategies - may include developing triggered supervision for specific clinical issues or
procedures (eg before prescribing Schedule 8 medications, suturing, corneal foreign-body removal, etc). This
will depend on the skills and clinical experience of the individual, use of regular observation of consultations, and
review of clinical notes in order to identify issues before they pose a potential risk.
CS4.3.1.5c Procedures to ensure that research complies with relevant guidelines - the NHMRC’s
Australian code for the responsible conduct of research and National statement on ethical conduct in human
research are useful references. If designing or coordinating a research project, it is imperative to develop a robust
research protocol that outlines key information for research assistants in regards to running the project. This
ensures that participants are not put at risk and are adequately informed, etc.. It is also important to consult the
relevant ethics committee for potentially high-risk projects (eg those which involve participation from vulnerable
groups) and gain its approval before research is undertaken.
CS4.3.2 Colleagues who may be in difficulty - includes individuals who may be experiencing problems
related to mental health (eg depression, anxiety, PTSD), bullying, personality (eg narcissistic personality disorder),
substance use, and physical health. Identification and support of colleagues in difficulty is important; however,
it is also imperative that GPs are aware of their mandatory reporting responsibilities if a colleague is conducting
themselves in a way that meets the notification guidelines (eg practising while intoxicated, engaging in sexual
misconduct, placing patients at risk due to an impairment, practising in a way which is a significant departure
from professional standards, etc).11
75
CS4.3.2.1a Professional resources that are available to assist health professionals who are in difficulty
- there are a number of resources available to assist GPs who may be experiencing difficulties. Encouraging
individuals to have their own regular GP is very important. The Australasian Doctors Health Network is a helpful
resource that contains a useful list of resources and contacts in the event immediate assistance is needed. Other
important support structures include offering professional debriefng after a critical incident (refer to CS4.2.33c),
professional counselling (refer to CS4.2.3.2b), and encouraging colleagues to contact their medical defence
organisation in the event of a clinical incident which has potential legal consequences.
Individuals may sometimes demonstrate a lack of insight into the impact their physical or psychological health
issues, or personality traits has on their ability to practice safely. If this occurs, and the GP is resistant to accessing
help, the GP colleague has a duty of care to consider making a notifcation to AHPRA. This can be done
anonymously.
References
1. Medical Board of Australia. Good medical practice: a code of conduct for doctors in Australia. Available at www.medicalboard.
gov.au/Codes-Guidelines-Policies.aspx [Accessed 9 December 2015].
2. The Royal Australian College of General Practitioners. Standards for general practices. 4th edn. Melbourne: RACGP, 2010.
Available at www.racgp.org.au/your-practice/standards/standards4thedition [Accessed 9 December 2015].
3. The Royal Australian College of General Practitioners. Clinical guidelines. Available at www.racgp.org.au/your-practice/guidelines
4. The Royal Australian College of General Practitioners. Your practice. Available at www.racgp.org.au/your-practice [Accessed 9
December 2015].
5. Australian Medical Association. AMA Code of Ethics 2006. Available at https://ama.com.au/position-statement/ama-code-ethics-
2004-editorially-revised-2006 [Accessed 9 December 2015].
6. Medicines Australia. Code of Conduct 2015. Edition 18. Available at https://medicinesaustralia.com.au/code-of-conduct/code-of-
conduct-current-edition [Accessed 9 December 2015].
7. National Health and Medical Research Council. National Statement on Ethical Conduct in Human Research 2015 . Available at
www.nhmrc.gov.au/guidelines-publications/e72 [Accessed 9 December 2015].
8. Britt HC, Valenti L, Miller GC. Determinants of consultation length in Australian general practice. Med J Aust 2005;183(2):68-71.
9. Harrison CM, Britt HC, Charles J. Sex of the GP - 20 years on. Med J Aust 2011;195(4):192-96.
10. Mitchell JT, Everly GS. Critical incident stress debriefng: An operations manual for CISD, defusing and other group crisis
intervention services. 3rd edn. Chevron Pub Corp, 2001.
11. Medical Board of Australia. Guidelines for mandatory notifcations. Available at www.medicalboard.gov.au/Codes-Guidelines-
Policies/Guidelines-for-mandatory-notifcations.aspx
Domain 5. Organisational and legal dimensions

‘Make a habit of two things: to help; or at least to do no harm’ - Hippocrates

Competency
CS5.1 GPs CS5.1.1 CS5.1.1.1a Describe and CS5.1.1.1b Identify the CS5.1.1.1c Appraise
use quality Infection control demonstrate strategies role of RACGP practice and maintain
and effective and relevant for infection prevention standards and integrate compliance with
practice clinical practice and control them into clinical care RACGP practice
management standards are standards
processes maintained
and systems CS5.1.1.2b Implement
to optimise best practice guidelines for
infection control measures
safety
CS5.1.1.3b Identify
the role and relevance
of clinical indicators in
improving quality of care
CS5.1.2 Effective CS5.1.2.1a Identify CS5.1.2.1b Identify CS5.1.2.1c Drive

clinical leadership examples of clinical opportunities to lead an improvements in
is demonstrated leadership improvement in quality care quality of care within
practice setting
CS5.1.2.2a Evaluate the CS5.1.2.2b Support peers CS5.1.2.2c Identify

key characteristics of, and to step into leadership roles and manage
obstacles to, effective obstacles to
clinical leadership demonstrating
leadership in the
practice setting
CS5.1.3 Relevant CS5.1.3.1a Identify key CS5.1.3.1b Formulate CS5.1.3.1c Review

data is clearly patient information that strategies to maintain and revise data
documented, needs to be collected and medical record data quality collection and storage
securely stored stored to meet legislative
and appropriately requirements
shared for quality
improvement
CS5.1.3.2a Maintain CS5.1.3.2b Utilise CS5.1.3.2c Maintain

comprehensive and strategies to maintain ethical standards
accurate clinical notes accurate medication when using patient
records data for research or
quality improvement
activities
CS5.1.3.3a Describe key

aspects of secure storage
of data
CS5.1.3.4a Describe the

legislative requirements
relevant to the use of
patient information
for research or quality
improvement purposes
77

Competency
CS5.1.4 Quality CS5.1.4.1a Identify CS5.1.4.1b Utilise best CS5.1.4.1c Review
and safety the key principles of practice guidelines for and address clinical
is enhanced appropriate use of health appropriate use of health issues that arise as a
through the information systems information systems result of inadequacies
effective use in health information
of information systems
systems
CS5.1.4.2a Describe CS5.1.4.2b Demonstrate CS5.1.4.2c Appraise
the benefits and risks efficient use of recall and effectively utilise
associated with health systems to optimise health eHealth systems to
information systems outcomes optimise care
CS5.1.4.3c Appraise
effectiveness of recall
systems to maximise
quality of care
CS5.1.5 Effective CS5.1.5.1a Outline the CS5.1.5.1b Formulate CS5.1.5.1c

triaging and time principles of medical strategies to maintain Support and mentor
management triage effective time management colleagues in
structures are in effective triaging and
place to allow development of time
timely provision management skills
of care
CS5.1.5.2b Address
barriers to, and implement
criteria for, effective triage
CS5.1.5.3b Prioritise
patient consultation times
according to severity of
presenting illness in order
to optimise care
CS5.1.6 Ethical CS5.1.6.1a Identify CS5.1.6.1.c

business any perceived unethical Recognise and
processes business practices in address any potential
and practices, place of work or actual breaches
and effective of ethical business
governance practices
structures are
CS5.1.6.2a Access CS5.1.6.2a Identify ethical
implemented
support to address business principles in
concerns regarding place of work and address
unethical processes, any practices that do not
structures or practices comply
CS5.2 GPs CS5.2.1 Patient CS5.2.1.1a Define the CS5.2.1.1b Identify and CS5.2.1.1c Review
work within confidentiality key responsibilities for manage situations where any breaches of
statutory and is managed medical professionals in duty of care responsibilities confidentiality and
regulatory appropriately regards to confidentiality are not compliant with review processes to
requirements confidentiality requirements reduce future risk
and guidelines
CS5.2.1.2a Explain CS5.2.1.2b Identify and
confidentiality demonstrate sensitive
requirements to patients management of mandatory
as appropriate and voluntary reporting
responsibilities

Competency
CS5.2.2 Shared CS5.2.2.1a Outline the CS5.2.2.1b Demonstrate CS5.2.2.1c Review
decision making principles of patient appropriate utilisation of and revise existing
and informed autonomy, shared shared decision making policies and
consent are decision making and and informed consent procedures that relate
explained and informed consent to informed consent
obtained and shared decision
making
CS5.2.2.2a Identify CS5.2.2.2b Determine

barriers to provision of patient competency to
informed consent and provide informed consent
shared decision making
CS5.2.2.3c Integrate
legislative requirements
into care of individuals
who are unable to provide
consent
CS5.2.3 CS5.2.3.1a Identify the CS5.2.3.1b Accurately CS5.2.3.1c

Medico-legal legal documents and complete legal Review and revise
requirements reports that form as part documentation appropriate documentation
are integrated of the professional life of to the situation to reflect current
into accurate a doctor legal and legislative
documentation requirements
CS5.2.3.2a Describe CS5.2.3.2b Seek support

criteria for reportable from other professionals
deaths and accurately to complete complex or
complete death unclear documentation
certificates
79

CS5.1.1 Infection control and relevant clinical practice standards - refers to the standards developed as a
template to assist in improving quality and safety of general practice service provision in Australia (eg the RACGP’s
Standards for general practices1 and Infection prevention and control standards,2 and the NHMRC’s Australian
Guidelines for the prevention and control of infection in healthcare3). The aim of clinical standards is to manage risk
and to deliver better health outcomes for patients.
CS5.1.1.1a Infection prevention and control - includes:
• hand hygiene
• environmental hygiene
• body fluid spills management
• sterilisation
• immunisation of self and staff
• standard and transmission-based precautions (eg outbreak control, including identifying individuals who may
have communicable diseases and implementing appropriate procedures to minimise risk of spread)
• healthcare-associated infection surveillance, including notifiable diseases.
CS5.1.1.3b Clinical indicators - these are markers of quality care and can help to assist in development of
quality improvement strategies. Clinical indicators may include:
• patient experience surveys

• proportion of clinical files with health summaries and up-to-date adverse drug reaction warnings
• provision of care that adheres with clinical guidelines
• use of interpreter service for patients of linguistically diverse backgrounds
• quality of referral letters
• currency of medication lists
• evidence of timely review of test results
• maintenance of infection control standards

• proportion of files with appropriate recalls.
CS5.1.2 Clinical leadership - may be demonstrated by improving clinical outcomes through quality and safety
developments in healthcare provision, at both micro and macro levels. Strong clinical leadership is essential for
robust clinical governance. Clinical leadership responsibilities include:
• determining priorities for allocation or resources to support quality patient care
• contributing to the development of a workplace culture of trust and honesty in order to encourage open
discussion about adverse events without blaming individuals
• developing systems to flag and respond to concerns about patient care
• monitoring clinical performance indicators.
CS5.1.3 Relevant data - a term which may be used to describe any information related to patient demographics,
or which is collected in regards to health, such as diagnoses, measurable parameters, referrals, management,
therapeutics.
CS5.1.3 Shared appropriately refers primarily to the need for the patient’s informed consent prior to information
being shared with external parties. The exceptions to this are situations where mandatory reporting legislation
takes precedence (refer to CS5.2.1.2b).
CS5.1.3.1a Key patient information that needs to be collected and stored - information from a legible health
record containing all relevant health information, which includes:
• patient demographics (name, date of birth, gender, contact details, next of kin details, Medicare number)
• cultural status, including migration history (to assist with risk assessment and advice)
• preferred language (whether an interpreter is required)
• medical information (allergies, up-to-date list of health problems)
• medication (up-to-date list)
• family history (particularly inheritable conditions relevant to the individual)

• social and occupational history (relationship status, sexuality, gender identification, education level, type of
occupation)
• lifestyle risk factors (smoking, alcohol intake, illicit drug use, etc)
• health screening (whether up-to-date with developmental screening, blood pressure, mammograms, Pap
smears, annual diabetes assessments, etc).
CS5.1.3.2a Comprehensive and accurate - refers to the importance of ensuring that all of the relevant
information for an individual is incorporated into the clinical notes (as outlined CS 5.1.3.1a). Accuracy of clinical
notes is always important, but it is especially vital in regards to consultations where mandatory reporting may be
necessary, legal documentation is being completed (refer to CS5.2.3), or where there is a forensic component in
which clinical notes may be used as evidence in court.
CS5.1.3.3a Key aspects of secure storage - may include the use of unique healthcare identifiers, ensuring that
electronic health information is transferred securely, ensuring that clinical information is password-protected and
regularly backed-up to a secure server, etc.
CS5.1.3.4a Legislative requirements relevant to the use of patient information - outlined in the Australian
Government’s Privacy Act 1988. Health information is rightly denoted to be ‘sensitive information’ and it is
imperative that it is securely stored and confidentiality is maintained. The primary exceptions to these requirements
arise when mandatory reporting legislation takes precedence.
The Privacy Act 1988 includes additional requirements in rare situations where maintaining confidentiality may
place someone else at significant risk (eg an individual who has had a genetic test that demonstrates a risk of a
serious health condition who then refuses to provide consent to inform relatives who may also be affected).4
CS5.1.3.1b Medical record data quality - includes creating structures within consultations to ensure that
important information, such as demographic information, current medical conditions and current medications and
allergies, are up-to-date. Use of the PCEHR can help to reduce patient harm and adverse events, and enhance
communication between health service providers. Regular clinical audits of medical records to evaluate the
appropriateness of care, or how much it aligns with recommendations, can be a useful tool.
Useful resource
• Quality health records in Australian primary healthcare: A guide, www.racgp.org.au/yourpractice/business/tools/support/
qualityhealthrecords
CS5.1.4 Information systems - may include:
• computerised or hand-written documentation
• the use of effective recall systems to optimise follow-up and continuity of care
• professional handover regarding high-risk individuals
• clear and concise documentation of diagnosis

81
• management and follow-up plans
• utilisation of PCEHR.
Effective health information systems are cost-effective, context-relevant, secure, user-friendly and reliable in
assisting assist with care delivery and health outcomes. General practice information systems can refer to
computers with adequate internet access, security systems, video-conferencing equipment, etc.
Useful resource
• National E-Health Transition Authority publication e-Health Clinician’s Desktop User Guide - GP Version). Section 3.2.1.
CS5.1.4.1a Key principles of appropriate use of health information systems - to uphold patient privacy and
confidentiality, and optimise quality continuity of care and communication by utilising health information systems (eg
password-protected medical software, ensuring only clinical staff have access to clinical files, ensuring any patient
information sent by email is only done through encrypted software, etc).
CS5.1.4.2b Efficient use of recall systems - describes the information systems used to identify and notify
individuals in need of follow-up, including further investigation or specialist referral, after routine screening or
abnormal. The GP’s consequent concise and comprehensive handover provided verbally or through documentation
enables continuity of care and reduces clinical risks. Information technology (IT) is important when considering
recall options for individuals with visual or hearing impairment, who have problems with literacy, or who have no
fixed address or move frequently.
CS5.1.4.2c eHealth systems - may include use of:
• clinical software
• verbal communication with specialised organisations and clinics
• telehealth facilities in remote and rural areas
• PCEHR
• encrypted email to transfer patient information
• a knowledge of useful health tools and applications available for professionals and patients (eg e-mental health
interventions).
Useful resources
• RACGP Standards for general practices offering video consultations, www.racgp.org.au/download/Documents/Standards/2011standa
rdsforvideoconsultations.pdf
• RACGP position statement: Personally Controlled Electronic Health Record (PCEHR) www.racgp.org.au/yourracgp/news/
reports/20120412pcehr
CS5.1.5 Triaging and time management structures - triaging structures refers to the frameworks which assist in
appropriately prioritising patients to be assessed, including:
• current symptoms and severity
• amount of time symptoms have been present
• whether the individual recently travelled to a high-risk area for particular communicable diseases
• existing vulnerabilities and thus a risk of acute deterioration (eg age and existence of concomitant illness).
Time management structures may include:

• flexible appointment scheduling that allows for urgent walk-in appointments
• scheduling regular breaks to allow for consultations that run over time
• routinely booking long appointments for individuals with complex health problems or communication issues
• allotting time for completion of care plans, home visits, etc.
CS5.1.5.1a Medical triage - refers to the process by which individuals are prioritised for care based on their
clinical urgency. This refers to the severity of their symptoms and signs and thus their requirement for timely
assessment and management.
CS5.1.5.1b Strategies to maintain effective time management - may include provision of ‘on the day’
appointments, long appointments for counselling, acceptance of walk-in patients in certain circumstances, and
long appointments as a default for patients with known complex needs, etc.
CS5.1.6 Business processes, practices and effective governance structures - includes processes related to:
• management of patient and staff feedback
• practice quality improvement activities achieved through clinical audits
• structures related to security of health information
• robust processes related to staff induction and clinical risk management structures
• anti-discrimination and gender-balance practices.

GPs should also consider the importance of ensuring that any potential conflicts of interest regarding financial
remuneration and patient care are recognised, declared and managed. This helps to make sure such conflicts
of interest do not impact the provision of informed consent, professional contracts are fair and within codes of
ethics, and business processes do not reduce quality of care and thus risk poor health outcomes, etc.
CS5.1.6.2a Access support to address concerns - may be from peers, senior colleagues or medical indemnity
providers.
CS5.2.1 Patient confidentiality - refers to legal management which is in the context of the situation and the
patient and can be described as one of the core duties of health professionals. This situation refers to the
professional obligation to respect patient privacy by keeping any information which is identifiable to an individual
private, emphasising that it is the professional’s responsibility to ensure that this privacy is maintained. There are,
however, exceptions to this obligation, including the need to release records if a legal subpoena is received; or in
situations where duty of care is the predominant factor, wherein the professional believes the individual’s capacity
for consent is impaired and they pose a risk to themselves or to others if information pertaining to their current risk
is not shared with individuals or organisations with the capacity to provide protection from that risk.
CS5.2.1.1b Situations where duty-of-care responsibilities are not compliant with confidentiality
requirements - refers to clinical situations where the need for patient privacy is overridden by the need to protect
the general public or the individual in question. Examples include:
• mandatory reporting of communicable diseases (full details of the individual are not required for some
notifications )
• recommendation for involuntary admission under the relevant mental health jurisdictional laws
• mandatory reporting of suspected child abuse
• mandatory reporting of suspected impairment of professional colleagues
• individuals who have guardians who hold medical power of attorney
• individuals with occupational injuries being managed under WorkCover.
CS5.2.1.2b Sensitive management of mandatory and voluntary reporting responsibilities - these reporting
responsibilities are developed under law to provide a framework for the health service delivery process, and to
address health service provision and public health issues. They are developed to provide clear and consistent
direction to achieve quality health outcomes and define professional accountability. Examples include:
83
• communicable diseases notification requirements
• drugs and poisons requirements (particularly Schedule 8 medications)
• the recommendation for involuntary admission under the relevant mental health jurisdictional laws (particularly
involuntary admission)
• mandatory reporting of professional colleagues who demonstrate impairments in their capacity to practise, etc.
The issues which may lead to these reports are broad and varied. Most necessitate careful, diplomatic management
through the use of clear communication by the GP to the affected person(s), where the rationale for the report, as
well as for what the information in the report will be used and the likely next steps for the individual, is explained.
CS5.2.2 Shared decision making and informed consent - are based upon provision of accurate and
comprehensive information, tailored to the individual’s sociocultural context (particularly the level of health literacy),
the options available, and the risks and benefits of these options to the individual. In determining capacity to
provide consent, the individual needs to demonstrate to the GP a clear appreciation and understanding of the facts,
implications and consequences of an action. The individual must also show they have adequate reasoning faculties
and are in possession of all relevant facts at the time consent is given.
‘Capacity to provide consent’ is a legal term with a variety of definitions. Capacity is dependent on the decision being
made and is specific to each decision in healthcare settings (incapacity to one area may not mean incapacity for
all decisions). It is prudent for GPs to assume the existence of capacity and seek to overcome any communication
barriers that may be present. Most people can be supported in making their own decisions, including whether to
involve a spouse, family members, friends or carers in the process. In the uncommon situations where an individual’s
capacity is thought to be impaired, assistance can be obtained from the relevant office of the public advocate or
public guardian. Requirements for consent do not only relate to management plans for individuals, but Include
consent to have a third party in the room for educational purposes (eg a supervisor or external clinical teaching visit
assessor).
Useful resource
• Bird S. Consent to medical treatment: the mature minor. Aust Fam Physician 2011:40(3):159-60, www.racgp.org.au/download/
documents/AFP/2011/March/201103bird.pdf
CS5.2.2.1a Patient autonomy - refers to the individual’s right to make decisions about their medical care, whereby
the GP provides health education and information appropriate to the individual to enable an informed decision.
CS5.2.2.2a Provision of informed consent and shared decision making - includes factors which impact
capacity to provide informed consent (refer to CS5.2.2.2b).
CS5.2.2.2b Patient competency to provide informed consent - when considering competency to provide
consent, individuals from these following groups, or who are involved in the following clinical scenarios, may warrant
more detailed assessment and consideration:
• older patients
• young people (younger than 19 years of age)
• individuals with cognitive impairment
• individuals who have involuntary treatment orders
• use of restraint
• involuntary admissions.
It should be recognised that capacity is a concept that may vary between consultations for individuals who have
an unstable mental or physical health condition and thus may need to regularly be assessed if significant decisions
need to be made.
Useful resource
• Office of the Public Advocate. Medical consent, www.publicadvocate.vic.gov.au/medical-consent (Includes useful flow chart for health
professional decision making around capacity for consent.)
CS5.2.2.3c Legislative requirements into care of individuals who are unable to provide consent - includes
temporary and ongoing medical power of attorney, understanding of guardianship arrangements and advanced
care directives.
Useful resources
• www.australia.gov.au/content/powers-of-attorney
• www.racgp.org.au/your-practice/business/tools/support/acp
CS5.2.3 Medico-legal requirements are integrated into accurate documentation - includes:

• knowledge of criteria for certifiable and reportable deaths
• effective and accurate completion of work capacity or fitness certificates (eg Centrelink, WorkCover, sick
certificates), focusing on capacities the patient has rather than those they don’t, and acknowledging that they
strongest predictive factors for a return-to-work concern an individual’s expectations, number of sick leave days
taken in the past, and presence of somatic disorders
• understanding of criteria and resources to assist, to deem an individual fit to drive
• medical reports for criminal proceedings (eg documentation of injuries resulting from alleged family violence,
child abuse or other types of violence)
• recommendation for involuntary admission under the relevant mental health jurisdictional laws
• completion of advanced care directives and assessment of capacity to provide informed consent/testamentary
capacity
• mandatory reporting of suspected child abuse, understanding of occupational health and safety (OH&S)
legislative requirements.
Most states and territories now use the same OH&S legislation (eg needle-stick injuries, handling of bodily fluids,
infection guidelines), carer allowance applications, will preparation, etc.
References
1. The Royal Australian College of General Practitioners. Standards for general practices. 4th edn. Melbourne: RACGP, 2010.
Available at www.racgp.org.au/your-practice/standards/standards4thedition [Accessed 9 December 2015].
2. The Royal Australian College of General Practitioners. Infection prevention and control standards. 5th edn. Melbourne RACGP,
2014 Available at www.racgp.org.au/download/Documents/Standards/infectionpreventionandcontrolstandards.pdf [Accessed 9
December 2015].
3. National Health and Medical Research Council. Australian Guidelines for the Prevention and Control of Infection in Healthcare 2010.
Available at www.nhmrc.gov.au/guidelines-publications/cd33 [Accessed 9 December 2015].
4. Australian Government. Office of the Australian Information Commissioner. Business resource: Key health privacy concepts.
Available at www.oaic.gov.au/engage-with-us/consultations/health-privacy-guidance/business-resource-key-health-privacy-
concepts [Accessed 9 December 2015].
Useful resource
• www.rch.org.au/clinicalguide/guideline_index/Child_Abuse_Guideline
85
Requirements for competence

Required knowledge Required attitudes
• Holistic approaches and perspectives • Empathy
• Knowledge of own scope of safe practice • Ability to deal with uncertainty and ambiguity
• Australian healthcare system • Collegiality
• Preventive health, health promotion theory and practice • Self-awareness
• Community and patient resources • Curiosity
• Duty of care theory and practice • Professionalism
• Critical evaluation of demographic data and health • Commitment to learning and development
information • Commitment to contribute to improving the evidence
• Access and equity in the context of the patient and the base for general practice research
setting • Respect for patient autonomy
• Human body and disease • Commitment to self/family care
• Ethical principles in medicine
• Legislation relevant to general practice
• Safe management of common and important
presentations in general practice
• Professional resources and guidelines
Required skills Methods of assessment

• High-level problem solving • Small-group projects
• Critical thinking • Literature review
• Cultural safety • Essays
• High-level communication skills (verbal and non-verbal • Observations
including de-escalation skills) • Simulations
• Negotiation • Role-play
• Identifying relevant evidence • Third-party reports
• Integrating evidence into decisions and actions • Written and verbal questioning
• Assessment of opportunities to participate in general • Reflective practice reports
practice research • Participation in face-to-face and online assessment
• Comprehensive history taking social, cultural and activities
medical
• Competent physical examinations
• Patient advocacy
• Developing management plans with patients, their
family/carers and other providers
• Essential and relevant procedural skills
• Comprehensive diagnostic skills
• Patient-centred and safe clinical decision making
• Safe and appropriate prescribing
• Networking
• Multidisciplinary teamwork
• Setting and up working with practice systems
• Reflective practice
JgRACGP
Healthy Profession.
Healthy Australia.
HANDI
Making non-drug
interventions easier
to find and use
îiimhtt
DASH (Dietary Approaches to Stop Hypertension)
diet to prevent and control hypertension
Intervention A change in overall diet pattern that emphasises fruits, vegetables and low-fat dairy
products, and which includes whole grains, fish, poultry and nuts but limits saturated
fat, red meat, sweets and sugar-containing beverages.
The dietary changes result in a reduced consumption of sodium and an increased
consumption of potassium, calcium and magnesium compared with a typical
Australian diet.
There are strong similarities between the DASH diet and the Mediterranean diet.
However, the DASH diet does not emphasise olive oil and fish and does not include
wine: http://www.racgp.org.au/your-practice/guidelines/handi/interventions/nutrition/
the-mediterranean-diet-for-reducing-cardiovascular-disease-risk/
Indication Reduction of blood pressure. The DASH diet has been shown to reduce
blood pressure within 2 to 4 weeks (by 6 mmHg systolic and 3 mmHg diastolic).
The DASH diet has been After this initial reduction the blood pressure is maintained rather than reduced further.
rated the best diet for overall Effects are more pronounced in people who are hypertensive rather than normotensive.
health and wellness for the
The DASH diet may further reduce cardiovascular disease (CVD) risk through reduction
past 5 years in a row.
in total cholesterol, low density lipoproteins (LDLs) and body mass index (BMI).
Changes achieved with the DASH diet predict a reduction of CVD of approximately
13% using the 10-year Framingham risk score.
Availability The DASH diet consists of foods that are readily available in Australia.
Description The DASH diet plan includes the following:
Type of food Servings Serving size

Fruits 4-5 a day 1 medium fruit
1/4 cup dried fruit
1/2 cup fresh, frozen,
or canned fruit
Vegetables 4-5 a day 1 cup raw leafy vegetable

1/2 cup cooked vegetable
Low-fat or non-fat dairy 2-4 a day 250 mL milk

foods 1 cup yogurt
50 g cheese
Grains and grain products 6-8 a day 1 slice bread

(include at least 3 whole 1 cup cereal
grain foods each day) 1/2 cup cooked rice
or pasta
Lean meats, poultry and 2 or fewer a day 90 g cooked lean meat,

fish skinless poultry or fish
www.racgp.org.au/handi RACGP
First published: October 2015 Reprinted with permission from The Royal Australian College of General Practitioners.
iLJII >
* HW. ■ ■ Making non-drug
__.■____ .
to find and use
.iinuhtt
Description Nuts, seeds and legumes 4-5 per week 1/3 cup nuts
(continued) 1 tablespoon seeds 1/2
cup cooked dry beans
Fats and oils 2-3 a day 1 teaspoon margarine

1 tablespoon low-fat
mayonnaise
2 tablespoons light
salad dressing
1 teaspoon vegetable oil
Sweets 5 or fewer per week 1 tablespoon sugar

1 tablespoon jam
15 g jelly beans
250 mL lemonade
Tips and Challenges Referral to a dietitian is recommended for tailored advice and ongoing follow-up.
Refer to Dietitians Association of Australia.
Grading NHMRC Level 2 evidence.
References Salehi-Abargouei A, Maghsoudi Z, Shirani F. Effects of Dietary Approaches to

Stop Hypertension (DASH)-style diet on fatal or nonfatal cardiovascular diseases -
incidence: a systematic review and meta-analysis on observational prospective studies.
Nutrition 2013; 29:611-618.
Siervo M, Lara J, Chowdhury S et al. Effects of the Dietary Approach to Stop

Hypertension (DASH) diet on cardiovascular risk factors: a systematic review
and meta-analysis. British Journal of Nutrition 2015;113: 1-15.
Consumer Resources There are numerous books about the DASH diet (e.g. The DASH diet, The DASH
diet for beginners, The DASH diet action plan The DASH diet for weight loss).
Most consumer resources for the DASH diet have been developed in the United
States (US). The National Heart, Lung and Blood Institute (part of the US Department
of Health and Human Services) promotes the DASH diet as a well-balanced diet
for the general public as well as those with hypertension. Some call it the American
version of the Mediterranean diet.
• The US Department of Health and Human Services has produced a brief guide
to lowering blood pressure with the DASH diet http://www.nhlbi.nih.gov/files/
docs/public/heart/dash_brief.pdf and a more general guide to lowering blood
pressure http://www.nhlbi.nih.gov/files/docs/public/heart/hbp_low.pdf
• WebMD offers some tips to starting and staying on the DASH diet:
http://www. webmd.com/hypertension-high-blood-pressure/guide/dash-diet
It also has an action set for using the DASH diet: http://www.webmd.com/
hypertension-high-blood-pressure/tips-for-following-the-dietary-approaches-
to-stop-hypertension-dash-diet
• DASH Diet Oregon provides some useful information and resources about the
DASH diet. While this is a free site, it is paid for by the Oregon Dairy Council.
www.dashdietoregon
• A US-based paid site offers online DASH diet programs (including education,
support, meal plans, tracking tools and recipes). http://www.dashforhealth.com
First published: October 2015 Reprinted with permission from The Royal Australian College of General Practitioners.
Diagnostic Imaging Pathways - Homepage
Printed from Diagnostic Imaging Pathways
www.imagingpathways.health.wa.gov.au
© Government of Western Australia
What's New Initiatives What's In The News
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Disclaimer
The information set out in this publication is current at
the date of first publication. It is intended for use as a
general guide only and may or may not be relevant to
particular patients or circumstances. This publication is
not exhaustive of the subject matter. People implementing
any recommendations contained in this publication must
exercise their own independent skill or judgement, or
seek appropriate professional advice relevant to their
own 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.
The text is directed to health professionals possessing

appropriate qualifications and skills in ascertaining and
discharging their professional (including legal) duties.
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.
RACGP e-health
Practice, Policy and Innovation unit
Effective solutions for e-waste in your practice
Contents
Introduction 1
What is e-waste? 1
Why is e-waste a problem? 1
What is the Australian government
doing about e-waste? 2
What happens to e-waste? 2
What can I do to be part of the solution? 3
How to securely remove data before disposing of e-waste 4
How to recycle storage devices 5
Develop an e-waste recycling policy for your practice 6
E-waste policy template 6
Recycling resources 7
References 9
1 Effective solutions for e-waste in your practice
Introduction
Technology is constantly being upgraded and Australians are continually renewing their electronic equipment
and gadgets. The discarded and obsolete electronic equipment is known as e-waste, and it is becoming a
worldwide problem.
Disposing of e-waste safely and securely is important for general practices, as it is for individuals and business.
The Royal Australian College of General Practitioners has compiled this resource to explain what e-waste is,
and to advise on ways to minimise it and dispose of it safely.
What is e-waste?
E-waste is the term given to discarded electrical and electronic technologies; it includes, but is not limited to:
• computers, laptops and tablets

• televisions
• mobile phones
• digital cameras
• printers and photocopiers
• fax machines
• USBs.
Such equipment may or may not be in working order. With technology constantly being upgraded, disposal
of outdated electronic equipment is occurring frequently. E-waste has accumulated at such a rapid rate that
it has become the fastest growing form of waste in Australia.
A total of 106 000 tonnes of e-waste had been dumped into landfill across Australia by 2008. By 2028 this
figure is expected to rise to 181 000 tonnes.1 Until recently, e-waste has not been disposed of in the most
efficient and environmentally sound manner.
Why is e-waste a problem?

Australians are among the highest users of new technology, and e-waste from obsolete electronic goods
is one of the fastest growing types of waste.2 E-waste now makes up 5% of all municipal solid waste
worldwide, nearly the same amount as all plastic packaging, but it is more hazardous.
E-waste has a negative impact on our environment and is putting pressure on limited landfill capacity in
Australia and around the world.
Electronic technology includes toxic and harmful materials that to date have not been disposed of efficiently
or safely. Treating e-waste correctly will help minimise pollution, protect our environment and reduce our
carbon footprint.
Many of the materials that make up electronic technology can be recycled for other uses. For example, 90%
of the materials in a mobile phone handset can be recovered and reused. Sixty per cent to 90% of future
greenhouse gas emissions can be avoided by using these recycled materials.3
Fact: Recycling 50 000 mobile phone handsets can remove the need to mine 110 tonnes of gold
ore, 213 tonnes of silver-bearing ore or 11 tonnes of copper sulphide ore.4
Effective solutions for e-waste in your practice 2
What is the Australian government

doing about e-waste?
In response to the accumulating waste across the nation, the Australian government, with input from
industry, business and the community, has developed the National Waste Policy.5 This policy is a nationwide
waste management plan within which the National Television and Computer Recycling Scheme has been
developed. This scheme began in 2011 and is steadily being rolled out nationally. This national e-waste
recycling scheme has signed up service providers to administer free collection and recycling services for
computers, printers, televisions and other electronics from households and businesses. The scheme is
supported by legislation that ensures all manufacturers and importers of televisions and computers are
taking responsibility for their electronic products. As part of the scheme, companies that produce and/or
import computers and televisions into Australia will be required to pay for and arrange the collection and
end-of-life recycling of their products.
An Australian standard for e-waste recycling will be established and implemented within the National Waste
Policy.
The National Television and Computer Recycling Scheme is already available as well as other sustainable
e-waste recycling options.
The e-waste recycling scheme supports free pick-up of electronics from households and businesses, and
ideally will help increase television and computer recycling rates from only 17% in 2010 to 80% by 2021.
What happens to e-waste?

Electronic waste contains many components that can be recycled and reused. These resources, such as
plastics and glass, can be recovered to manufacture new products. Once hazardous materials like bromine,
lead, mercury and zinc are removed, the remaining components, such as cables, metals and circuit boards,
can be recycled.
Unfortunately, e-waste is not always disposed of in an environmentally friendly way and at times has been
dumped as hazardous waste. A staggering amount of e-waste from developed countries is being exported
and dumped in developing countries such as Ghana. This is an illegal trade that is being investigated by the
Australian government, and the national Hazardous Waste Act is under review to ensure that everything is
being done to cease this trade. It is important to know what is happening to your e-waste and ensure it is
being recycled by a reputable organisation.
The National Television and Computer Recycling Scheme also aims to improve the recycling of these
materials, minimising the solid and hazardous waste that ends up in landfill. This helps reduce the need to
use raw materials and essentially assists in saving our natural resources.
Before you discard your old computer, consider whether it is still in good working order. Perhaps, instead of
being disposed of, it could be donated to a local community group or charity.
What can I do to be part of the solution?

There are several ways that general practices can be mindful of the current situation, and begin to discard
electronic waste in a responsible way. It is no longer acceptable to leave electronic hardware on the nature
strip for garbage collection. Recycling companies can be contacted to collect various types of e-waste that
need to be removed and recycled, and there are organisations where you can drop off your e-waste without
charge.
To find e-waste recycling service locations near your general practice, visit the Recycling Near You or
Cleanup.org.au websites.
Initial steps include:
• avoid purchasing new electronic products that cannot be reused and recycled by the manufacturer
• reduce your consumption of electronic devices, and repair broken equipment before purchasing new
items
• reuse your electronic devices by donating items to charity, friends or family
• recycle your electronic devices instead of sending them to landfill.
Computers and televisions

While the National Television and Computer Recycling Scheme is being rolled out and more collection and
recycle drop-off points are announced, here are some suggestions for what you can do with computers and
televisions that you no longer need:
• if they are still in good working order, ask a charity, school or secondhand store if they will take them
• pass them on to friends or family
• contact your local council for more information on their recycling services
• store electronic equipment out of the weather until access to the scheme is available in your area
• approach a company that will refurbish your old computer equipment for use by those who cannot afford
new items.
The Australian government has produced a fact sheet that provides householders and small businesses with
essential information about the National Television and Computer Recycling Scheme.
Mobile phones
Mobile phones are constructed out of numerous non-renewable materials such as plastics, metals, ceramics
and glass, and the contents vary from model to model. As mobile phone technology continuously advances,
the materials can change; there is no exact formula or single list of the substances used for mobile phones.
However, around 90% of these non-renewable materials can be recycled and reused. The official recycling
program of the mobile phone industry is run by MobileMuster. It is a voluntary recycling program that collects
and recycles mobile phone handsets, batteries, chargers and accessories. There are drop-off points across
Australia located at mobile phone retailers, local councils, government agents and business.
MobileMuster ensures that all components of the mobile phones are recycled to the highest environmental
standards and that none is refurbished or resold in developing countries.
Clean Up Australia also runs a campaign to assist in recycling your old mobile phone. You can request a
Clean Up Mobile Phones Recycling Satchel for your device or organise a larger collection.
Many mobile phone parts can be recycled and reused:
• batteries include nickel, cobalt and cadmium, which can be used to make stainless steel and new batteries
• circuit boards include small amounts of gold and silver that can be used in jewellery and other applications
• handset casings include plastics that can be reused to make fence posts and pallets
• plastics and metals found in mobile phone accessories can be shredded, sorted and used to make new
plastic or metal products.
But remember, prior to handing in your mobile device for recycling, ensure that all sensitive data have been
removed!
Mobile phones contain highly toxic elements, including cadmium, arsenic, lead and mercury. It is important
that our old mobile phones do not end up in landfill.
Fact: There are over 22 million unwanted mobile phones hidden away in drawers, cupboards
and garages across Australia, the equivalent of 2200 tonnes of metal, minerals, plastic and glass.
These are all materials that could be recycled and reused!6
Printers, photocopiers and fax machines

Large electronic office equipment, such as printers and photocopiers, can be collected or dropped off
at recycling plants. Some recycling companies will come and pick up equipment for a fee. They will then
remove and recycle ferrous and non-ferrous materials, which diverts them away from landfill sites.
• Use Cartridges 4 Planet Ark, a national program, such as to recycle your printer cartridges. Don’t throw
them in the garbage bin!
• Visit the electrical equipment pages on the website Business Recycling for information about recycling
e-waste and to search for local recycling options.
How to securely remove data before disposing of e-waste

Before any of your electronic equipment can be recycled or donated from general practice, it is important to
remove all data from the device. Data can be related to personal details of patients or information about the
business of your practice.
Failure to remove data from these electronic devices, particularly sensitive information, breaches patient
information privacy and security.
If electronic media such as hard drives, USB flash drives, CDs and DVDs are not properly erased, patient
data and general business data may be used for many purposes, such as appropriating and creating bank
accounts and loans, or purchasing medicines and medical insurance.7 Patient-identifiable information can be
a prime target for identify theft.
Sold and donated computers have been found in secondary markets, such as auctions, still containing
personal information.8 This data can be more valuable than the electronic equipment it is stored on. Further,
it can be relatively easy for those who are technically capable to recover such information from any electronic
media.
Don’t just delete files

It is not sufficient to delete files and documents on your computer, or to drag and drop files into the recycle
bin. The data after deletion still reside on the hard drive even though you cannot access them directly. It is
very important to take further measures to ensure this data are securely erased.
Implement effective security

As a first step, it is important for your practice to put effective computer and information security measures
in place. The RACGP Computer and information security standards and accompanying workbook provide
essential guidance on establishing good information security practices and help to ‘future proof’ your
practice’s computer and information systems.
Link to information on the standards and computer and information security at www.racgp.org.au/your-
practice/standards/ciss
Securely erase data or destroy equipment

Higher levels of sanitisation include wiping the disk, using a secure erase tool or destroying the equipment.
A secure erase tool overwrites the data multiple times so that they cannot be accessed forensically. There
are numerous free secure erase tools available on the internet. Since such tools and software are constantly
being updated and new products released, we recommend you seek advice from your computer supplier or
an IT professional regarding the most suitable secure erase software for your electronic device.
The secure erasing of data should extend to any back-up media, such as tapes, and any media that are
used to store or transfer practice data, including hard drives.
How to recycle storage devices

Before these items are sent to be recycled, ensure all sensitive data are removed to maintain data security.
Data can easily be deleted from CDs and DVDs; these data are non-recoverable.
CDs, DVDs, USB flash drives and external hard drives are all used as data storage devices. Disks are often
discarded into bins when the data are no longer required; however, it is important to remember that CDs
and DVDs are non-biodegradable products that contain toxic chemicals and metals. These toxins can
contaminate the environment if they end up in landfill.
CDs and DVDs can be recycled to reuse up to 98% of the original disk, including the polycarbonate
(plastic) materials and aluminium found within these items. More information can be found at
http://businessrecycling.com.au/recycle/cd-dvd
Remove data from mobile phones

Before recycling your mobile phone, make sure any sensitive information saved onto the phone memory is
erased. While the subscriber identification module (SIM) card can be transferred from your old to your new
updated mobile phone, information stored on these cards can also be simply deleted if no longer required.
Information on how to remove data from your mobile phone can be found on the handset manufacturer’s
website.
Develop an e-waste recycling policy for your practice

Your policy is a reference document for the decisions your practice has made about what constitutes
reasonable e-waste recycling requirements and how these are to be managed.
Your policy should include your practice’s objective, specific areas of responsibility and the consequences of
policy violations.
You need to document your e-waste recycling policy and associated procedure. This should include the
method by which e-waste will be recycled and the measures by which data will be safely and securely
erased from electronic devices that hold sensitive information.
Remember, before discarding equipment, consider whether the item contains a hard drive or has additional
memory capacity.
Why not encourage your practice staff to bring in their old mobile phones, laptops and tablets for recycling
or reuse? This will give them another recycling avenue and reinforce the need to recycle more in the practice.
The National Television and Computer Recycling Scheme details proposed changes to recycling and the
responsibilities that different parties have through the lifecycle of electronic products. It is a great initiative to
encourage change in the workplace and its introduction marks a good time to make these changes when
implementing an e-waste policy.
E-waste policy template

[PRACTICE NAME] is committed to providing continuing, comprehensive and coordinated whole-person
healthcare to individuals and families in our community. [PRACTICE NAME] is committed to the protection
of health and the environment and is determined to minimise any adverse impacts from its activities.
[PRACTICE NAME] is committed to addressing the following issues.
Promote awareness
We will inform and motivate all our staff and encourage them to play an active role in [PRACTICE NAME]’s
commitment to its e-waste disposal/environmental policy.
Secure erasure
Prior to discarding electronic equipment, we will securely erase all confidential material from any devices that
store data. We will use [name of secure program/method] to complete the sanitisation procedure.
Reuse
We will donate any redundant electronic equipment to [ORGANISATION/NAME].
Recycling
If electronic equipment is beyond repair, we will utilise the services of [COMPANY] to recycle these e-waste
items. We will favour suppliers and contractors that are reputable and adopt best environmental practices.
Waste management
We will continue to promote, develop and implement waste prevention, reduction, reuse and recycling
onsite in a systematic and cost-effective manner. We will use appropriately regulated waste management
contractors to ensure safe management of hazardous and non-hazardous waste sent offsite in accordance
with best environmental practice.
Recycling resources
Locate your nearest recycling and waste service

Recycling Near You
http://recyclingnearyou.com.au
Planet Ark
http://planetark.org
Byteback
www.bytebackaustralia.com.au
Recycling organisations and companies
National
1800ewaste
www.ewaste.com.au
Planet Green Recycling

www.planetgreenrecycling.net.au
MRI Recycling
www.mri.com.au
Sims Recycling Solutions

http://apac.simsrecycling.com
Veolia Environmental Services

www.veoliaes.com.au/commercial-services/waste-collection-and-recycling/electronic-waste-recycling
Australian Capital Territory

Department of Sustainability, Environment, Water, Population and Communities
www.environment.gov.au/index.html
New South Wales

City of Sydney - Zero Waste
www.cityofsydney.nsw.gov.au/zerowaste
Northern Territory
Northern Territory Government Waste Minimisation in the Northern Territory
www.nretas.nt.gov.au/__data/assets/pdf_file/0013/14026/fs_recycling.pdf
Queensland
ACT Logistics
www.actlogistics.com.au
Buyequip
www.buyequip.com.au
Charity Computers
www.charitycomputersbrisbane.com
ComputerBank Queensland
www.cbq.org.au
Greenbox
www.greenbox.com.au
GreenICT
http://greenict.com.au/index.php
SiMS GROUP e-Recycling

www.simsmm.com/au
Brisbane City Council - Electronic Waste

www.brisbane.qld.gov.au/environment-waste/rubbish-tips-and-bins/electronic-waste/index.htm
South Australia
Government of South Australia - Zero Waste
www.zerowaste.sa.gov.au
E-cycle Recovery Pty. Ltd

www.ecyclerecovery.com.au
Tasmania
E-waste Tasmania
www.ewastetas.com.au
Victoria
Byteback Australia
www.bytebackaustralia.com.au
Victorian Government - Zero Waste

www.sustainability.vic.gov.au/www/html/1344-towards-zero-waste.asp
Western Australia
The Government of Western Australia - Waste Authority
www.zerowaste.wa.gov.au/
References
1. Planet Ark. National E-waste recycling scheme launched, set to lift recycling from 10% to 80%.
Broadway, NSW: Greenpages, 2011. Available at www.thegreenpages.com.au/news/national-ewaste-
recycling-scheme-launched-set-to-lift-recycling-from-10-to-80/ [Accessed 28 May 2012].
2. Australian Bureau of Statistics. Waste generated per person. In: 1370.0 Measures of Australia’s
progress, 2010. Canberra: ABS, 2010. Available at www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20
Subject/1370.0~2010~Chapter~Waste%20per%20person%20(6.6.3) [accessed 28 May 2012].
3. MobileMuster. Why recycling matters. North Sydney, NSW: MobileMuster. Available at www.
mobilemuster.com.au/learn-about-recycling/why-recycling-matters [Accessed 28 May 2012].
4. ibid.
5. Department of the Environment, Water, Heritage and the Arts. National Waste Policy: less waste, more
resources. Adelaide, South Australia: Environment Protection and Heritage Council, 2010. Available at: www.
ephc.gov.au/sites/default/files/WasteMgt__National_Waste_Policy_Implementation_Plan_Final_201007.pdf
6. MobileMuster, op cit.
7. Medlin B, Cazier J. A study of hard drive forensic on consumers’ PCs: data recovery and exploitation.
Journal of Management Policy and Practice 2011;12(1):27.
8. Jones A, Valli C, Dardick G, et al. The 2009 analysis of information remaining on disks offered for sale
on the second hand market. Proceedings of the 8th Australian Digital Forensics Conference. Perth,
Western Australia: Edith Cowan University, 2010:92-105.
The Royal Australian Healthy Profession.
College of General
Practitioners Healthy Australia.
RACGP Female genital
cosmetic surgery
A resource for general practitioners
and other health professionals

Healthy Australia.
Female genital cosmetic surgery - A resource for general practitioners and
other health professionals
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.
Accordingly, The Royal Australian College of General Practitioners (RACGP) 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.
Female genital cosmetic surgery - A resource for general practitioners and other health professionals.
Melbourne: The Royal Australian College of General Practitioners, 2015.
Published by
Tel 03 8699 0510

Fax 03 9696 7511
www.racgp.org.au
ISBN 987-0-86906-431-3
Published July 2015

Female genital cosmetic surgery
A resource for general practitioners and other health professionals
Contents
Preface iii
Acknowledgements iv
Introduction 1
1. Information on FGCS 2
1.1 Genital diversity 2
1.2 Female genital cosmetic procedures 2
1.3 Who performs FGCS? 2
1.4 Range of surgical procedures 2
1.5 Risks and complications 3
2. Factors influencing increased demand for FGCS 5
2.1 Perception of ‘normal’ versus ‘desirable’ 5
2.2 Digital communication, digitally modified images and pornography 5
2.3 Lack of anatomy education throughout life 6
2.4 A woman’s genital area is usually hidden 6
2.5 ‘Brazilian’ waxing, grooming and fashion trends 6
3. Recommendations for management of patients requesting FGCS or expressing concern
about their genitalia 7
3.1 Listen to the patient and explore the reasons for concern or request for FGCS 7
3.2 Take a medical, gynaecological and psychosexual history 8
3.3 Mental health and relationship or sexual abuse issues should be considered and referred accordingly 8
3.4 Examine the patient confidently and respectfully 8
3.5 Use diagrams to educate the patient at the time of examination and during the consultation 9
3.6 Reassure the patient 9
3.7 Address all symptoms and concerns 9
3.8 Refer the patient 10
3.9 Explain what the FGCS procedures entail, including risks and potential complications 10
3.10 Referral pathway for patients who state that their surgery has ‘gone wrong’ 10
4. How female genital mutilation/cutting legislation applies to FGCS 11
5. Adolescents and FGCS requests 12
6. Summary of recommendations for GPs and other health professionals 13
7. Appendices 14
Appendix 1 - Australian media code of conduct on body image 14
Appendix 2 - Taking a psychosexual history 15
Appendix 3 - Guidelines for gynaecological examinations and procedures 16
Appendix 4 - How FGM legislation applies to cosmetic procedures 17
Appendix 5 - Statements from peak bodies 20
Appendix 6 - Good medical practice code of conduct 26
References 27
iii
Preface
The subject of female genital cosmetic surgery (FGCS) has only recently been investigated in Australia.
International medical research is also limited, with the few published articles that deal with the primary care
physician’s role available from a search of journal databases such as Medline and PubMed, having been
published in the UK. Timeframe restrictions were not applied in these journal searches and saturation of
material was achieved in early 2015, when no new papers were discovered in either database. Overall, the
search showed there was a lack of evidence-based research in the literature.
References and publications used by key authors were analysed. The works of the most commonly cited
and published researchers are from the UK, Canada and the US. Their material was searched by hand. The
ethical discussion papers from various countries’ colleges of obstetrics and gynaecology have also been
very informative.
The range of information acquired was from sources as diverse as mainstream media, documentary
programs, ethical and feminist publications, case studies and surveys by plastic surgeons, public
discussion forums and web-based platforms. Exploration of online marketing of FGCS, available surgical
procedures and discussions in women’s magazines were also considered. FGCS raises many issues for the
general practitioner (GP) and other health professionals, as well as the broader community.
Some compare FGCS procedures to female genital mutilation/cutting (FGM/C). The World Health
Organization (WHO) defines FGM/C as ‘all procedures involving partial or total removal of the external
female genitalia or other injury to the female genital organs whether for cultural, religious or non-therapeutic
reasons’.
Given the paucity of quality evidence in the area of FGCS, all recommendations in this document should be
considered at National Health and Medical Research Council (NHMRC) practice-point level. However, the
rising demand for this procedure means there is an urgent need to provide the profession with guidance.
There are similarities in the rate of increase for FGCS in the UK, the US and Western Europe between
2000-14. Continuing research will serve to expand and broaden our understanding of the issues raised.
iv Female genital cosmetic surgery
Acknowledgements
Author
Dr Magdalena Simonis
Reviewers and contributors

The Royal Australian College of General Practitioners National Standing Committee - Quality Care
(NSC-QC)
The Royal Australian College of General Practitioners Women in General Practice (WIGP) Committee
Dr Lih-Mei Liao, Consultant Clinical Psychologist Women’s Health Division, University College London
Hospitals, UK
Professor Susan Bewley, Professor of Complex Obstetrics, Women’s Health Academic Centre
Dr Paul Wood, Chair, British Society for Paediatric and Adolescent Gynaecology
Dr Chris Bayly, Senior Clinical Adviser - Women’s Health, Royal Women’s Hospital, Melbourne
General Practice and Primary Health Care Academic Centre, University of Melbourne
Victorian Primary Care Practice-Based Research Network (VicReN), University of Melbourne
Royal Australasian College of Physicians
Royal Australian and New Zealand College of Obstetricians and Gynaecologists

1
Introduction
Female Genital Cosmetic Surgery (FGCS) refers to non-medically indicated cosmetic surgical procedures
that change the structure and appearance of the healthy external genitalia of women, or internally in
the case of vaginal tightening. This definition includes the most common procedure, labiaplasty, as well
as others, such as hymenoplasty and vaginoplasty, also known as vaginal reconstruction and vaginal
rejuvenation.1,2
According to figures from Medicare, the number of women undergoing medicare-billed vulvoplasty or
labiaplasty in Australia has increased from 640 in 2001 to more than 1500 in 2013, an increase of 140%.3
The highest number of claims was equally distributed between three age groups: 15-24, 25-34 and 35-44.
However, these numbers do not reflect the whole picture as many may seek FGCS through the private
health system without necessarily claiming a rebate or may not meet the criteria for this item number.4
There has been no concomitant rise in the incidence of congenital or acquired disease conditions that
warrant this surgery.4 Rather, it appears that in response to changing cultural norms, this surgery is
increasingly being sought by women who want to either feel ‘normal’ or look ‘desirable’.2 As a result,
general practitioners (GPs) are increasingly managing patients who present seeking surgery due to
concerns about the appearance of their genitalia.5
Labiaplasty is the most common form of FGCS requested and performed, accounting for around 50% of
the procedures performed.4,5 The terms labiaplasty and FGCS will be used interchangeably throughout this
document unless otherwise specified.
This guide aims to help inform GPs and health professionals about FGCS, including the factors influencing
demand, and provide a set of recommendations on how to manage women requesting referral for FGCS or
expressing concern regarding their genitalia.
2 Female genital cosmetic surgery
1. Information on FGCS
1.1 Genital diversity

Exactly what constitutes ‘normal’ female genitalia is an area of medicine in which very few studies
have been published. The handful of articles that do outline the measurements of female genitalia
vary in their definition of hypertrophy and normal.4,6-10 There are currently no criteria that measure
and describe normal female genital anatomy and medical textbooks also lack detail regarding
range of diversity and measurements.
FGCS has been described as aiming to ‘improve the appearance of the external female genitalia’
and cure labial hypertrophy,9 yet it relies on little evidence of what exactly constitutes labial
hypertrophy and, by extension, a normal labia which can include size, colour and shape.11
1.2 Female genital cosmetic procedures

FGCS is also referred to in the public domain as ‘designer vagina’, ‘vulvovaginal aesthetic
surgery’,2 ‘barbiplasty’ and ‘vaginal rejuvenation’. Documentation describes the labiaplasty
procedure as being performed as early as 1976.9
1.3 Who performs FGCS?

FGCS can be performed by anyone with a medical degree, including cosmetic surgeons (usually
a GP or dermatologist who performs cosmetic procedures), gynaecologists, plastic surgeons and
urologists.3,5,9,12
No formal training is required and there are currently no evidence-based guidelines that support
the cosmetic procedures. For all specialties, guidelines need to be established from reputable
long-term studies in order to support surgical procedures, but these have not yet been
developed.4
1.4 Range of surgical procedures

Labiaplasty - the most commonly performed FGCS procedure, this involves removal of tissue
from labia minora that extends beyond the labia majora and/or removal or increase tissue from the
labia majora in order to achieve symmetry.
The procedure falls into two broad categories:
• Amputation technique, or labial trim, where the edge of the labium is cut out and the edges
sewn over.10
• Removal of a section of the labia to preserve the natural contour, such as wedge resection4,5
and de-epithelialisation techniques.12,13
A resource for general practitioners and other health professionals 3
Clitoral hood reduction - exposes clitoris and aims to increase sensitivity. This is sometimes
combined with a labiaplasty procedure.
Perineoplasty - undertaken to strengthen the pelvic floor and, in the FGCS setting, aimed at
establishing penile pressure with coital thrust.14 This procedure is technically similar to perineal
reconstruction, in which the perineal length is restored following childbirth trauma or previous
surgery. It is commonly performed as part of vaginal prolapse surgery. However, even in this
setting there is no evidence that this procedure improves sexual function and, in fact, it may cause
dyspareunia.
Vaginoplasty - the purpose of this procedure is vaginal creation in gender reassignment but, in
the FGCS setting, it refers to tightening the vagina, which can be surgical or non-surgical - as in
‘laser vaginal rejuvenation’ or ‘designer laser vaginoplasty’.
Hymenoplasty - also called ‘revirgination’ and is designed to restore the hymen. It is often
advertised as a ‘gift’ to one’s partner.14 This procedure is occasionally requested by women
of certain cultural backgrounds in which premarital sex is forbidden and an intact hymen is
considered evidence of virginity.12
Vulval lipoplasty - removal of fat from mons pubis or augmentation of the vulva.
G-spot augmentation - involves autologous fat or collagen transfer via injection into the pre-de
termined G-spot location. There is no existing scientific literature describing this procedure. Similar
procedures include G-spot amplification and G-shot collagen injection into the region.15
Orgasm shot (O-shot) - often described as a sexual and cosmetic rejuvenation procedure for the
vagina using the preparation and injection of blood-derived growth factors into the G-spot, clitoris
and labia.12,14
Terms such as ‘vaginal rejuvenation’, ‘designer laser vaginoplasty’, ‘revirgination’ and ‘G-shot’ are
commercial in nature. The consumers at whom they are targeted can then mistakenly believe such
official-sounding terms refer to medically-recognised procedures.17,18
Cosmetic surgery redefines the patient as a ‘consumer’, and uses advertising to promote
the ‘product’. Advertising for female genital cosmetic surgery tends to reflect and reinforce
sociocultural messages about the vulva and vagina, potentially creating dissatisfaction among
women who do not meet the narrow ideal of normality. Advertising suggests that FGCS
procedures are simple, and offer high levels of satisfaction. It normalises surgical procedures and is
likely to create demand among those women who experience genital dissatisfaction.14,15
1.5 Risks and complications

The potential risks associated with FGCS include:
• bleeding4
• wound dehiscence4
• infection4
• scarring, resulting in lumpy irregular margins of tissue or eversion of inner lining of labia, resulting
in an unnatural appearance4,12
• sensorineural complications secondary to poor healing or scarring
• dyspareunia4,19
• removal of too much tissue, resulting in pain with and without intercourse - for example, clitoral
hood reductions where too much clitoral tissue remains exposed and rubs onto undergarments
and causes pain and discomfort3
• tearing of scar tissue during childbirth following previous FGCS procedures4
• psychological distress4
• reduced lubrication.4
The long-term outcomes of FGCS have not yet been researched.10 Trends change and the
aesthetic ideal that is promoted now might alter with time.8
No controlled evaluation of short- and long-term clinical effectiveness of cosmetic procedures

can be identified in published literature.4,16,20 According to Professor Helen O’Connell, urological
surgeon at the Royal Melbourne Hospital, tissue that is excised in labiaplasty may appear to be
‘just skin’, but the labia minora are derived from the primordial phallus and its excision is likely to
interfere with sexual pleasure.19
In the past, cosmetic genitoplasty has been criticised and debated because it can result in
impaired sexual function.21-23 The nerve density, epithelial qualities and vascular compartments
of the labia minora that contribute to sexual arousal and orgasm are poorly defined. Surgical
procedure development and counselling about surgical risks related to labiaplasty may be based
on inadequate information.24
2. Factors influencing increased demand

for FGCS
2.1 Perception of ‘normal’ versus ‘desirable’

The sociocultural norms that are believed to influence women’s perceptions of ‘normal’ are
considered to be significant in driving the climb in this group of procedures.1,25-27
Not only does modern culture classify the minimalist vulva, where the labia minora do not extend
beyond the margin of the labia majora, as ‘good’, but also the protruding labia as ‘bad’.27, 28-31
Currently available research indicates that perceptions of ‘normal’ versus ‘desirable’ may be
skewed and disparate, resulting in a narrow definition of normal.29-31 Labiaplasty has also been
intensively marketed as an unproblematic lifestyle choice for women.1,14,18,20,27,32
2.2 Digital communication, digitally modified images

and pornography
There is little doubt that today’s digital age is changing the way we acquire information and
communicate. As a result, people are influenced by information and digitally-modified images
found on the internet. Despite access to these images and the plethora of internet-based
pornography, there is little firm knowledge regarding female genital structure, function and
vocabulary within the community.33 Pornography mostly depicts digitally-modified images that
portray women’s genitals with no labia minora protrusion, thus potentially skewing young women’s
(and men’s) perceptions of what is considered normal.32,34,35,36
Australian censorship laws prohibit the publication of illustrations of the labia minora and the
clitoris.32,35 Vulvas are invariably made to resemble that of prepubescent girls, with pubic hair
removed and a single crease placed between the labia majora,29-32 which contributes to the
general lack of knowledge and understanding about female genital diversity.
A recent study from South Australia’s Flinders University revealed that women who had greater
exposure to images of female genitals were more likely to consider labiaplasty. Of the 351 women
aged 18-69 who were surveyed as part of the study, 17% were interested in having labiaplasty.27
Most women who are contemplating any form of FGCS are likely to seek information from provider
websites. These sites often describe aesthetically pleasing or desirable genitalia as the neat
single slit. The quality and quantity of clinical information in FGCS provider sites is poor, providing
erroneous information in some instances.14,28,29,34
Health professionals are influenced by similar sociocultural forces that skew preferences for
desirable versus normal.10,37,38 It is important to be mindful of this when addressing women
who present requesting FGCS or have concerns regarding their own appearance (also refer to
Appendix 1 for information on the Australian media code of conduct on body image).
2.3 Lack of anatomy education throughout life

People have limited formal education in the areas of female genital anatomy and its variations10,33
and, to date, there is no evidence-based research that outlines what its normal spectrum is
considered to be.
The most common complaint is protrusion of the labia minora beyond the labia majora.10,11,37 Given
the paucity of textbook images that provide measurements and ranges of anatomical diversity,
GPs who do not perform regular gynaecological examinations as a part of their routine practice
may not feel comfortable stating that something is considered normal.
General practice and other medical training curricula do not currently include education in the area
of genital anatomy and its diversity. With the absence of formal training, it is not surprising that
GPs, surgeons and other health professionals are influenced by the same kind of sociocultural
forces that skew preferences for normal versus desirable.10,34
2.4 A woman’s genital area is usually hidden

Women have few opportunities to see other women’s genitals throughout their life due to the
fact the region is concealed, for the most part, behind pubic hair and there is little opportunity
along the educational lifespan of women (and men) to become better informed. The inherent lack
of understanding of the diverse normal platform that exists in the community is, therefore, quite
understandable.
Recent studies have shown that women have limited knowledge regarding the names and function
of genital parts and the diversity of appearance.11,23,24,31
2.5 ‘Brazilian’ waxing, grooming and fashion trends

Grooming and fashion trends are believed to influence women’s attitudes to their genital region.
Practices such as ‘Brazilian’ waxing involve removal of most or all pubic hair, exposing sensitive
genital tissue and areas that could not be seen prior to hair removal.11,24 This practice is now
extending to permanent hair removal via laser treatments.
Tight-fitting clothing and sportswear tend to give definition to the genital area, and poorly-fitting
undergarments, such as G-strings, cover a minimal portion of the mons pubis. These factors can
create the feeling that women’s genital size should be small and discrete.
Fashion that depicts genital contour has resulted in the evolution of new terms like ‘camel toe’ and
‘outie’, which appear in popular media. While women often comment that wearing these items can
feel uncomfortable, they remain popular fashion items.
Few will dispute that the request for Brazilian waxing and genital hair removal has gradually
become commonplace over the past 20 years. The results from a phone review of the course
work undertaken by Australian beauty therapists during their training indicate they receive little
formal training regarding all aspects of genital anatomy.39 Given women are more likely to visit their
beauty therapists than their GP, supporting this frontline group through the provision of information
regarding genital anatomy and teaching them how to talk with women who might express concern
at their appearance could also be a useful way of addressing women’s lack of knowledge and
provide reassurance.
7
3. Recommendations for management of

patients requesting FGCS or expressing
concern about their genitalia
3.1 Listen to the patient and explore the reasons for

concern or request for FGCS
GPs should deal with a patient’s concerns in a sensitive and appropriate manner, asking what
influences have played a role in this desire for surgery. It is also important to address the issues,
such as lack of knowledge of diversity, clothing, exposure to digital images, partner criticism, family
or peer comments, or the result of pubic hair removal.
Discuss factors influencing patient’s concern:
• Clothing, including G-string underwear, tight jeans and body-hugging sportswear that outlines
genital detail.
• Images found on the internet, especially pornography. These images are often required to be
airbrushed due to classification rules which deem explicit depictions of female genitalia to be
inappropriate.4,35
• Physical symptoms may relate to concerns regarding maintaining hygiene, such as during
menstruation and with toileting. Pain or discomfort either when wearing tight clothing or
during sporting activities such as walking, horse riding, cycling may also be described. Other
symptoms may be related to painful intercourse such as with invagination of the labia minora
at the time of penetration. Some women may be concerned regarding vaginal laxity, especially
following vaginal childbirth. Assess the degree to which these issues impact the woman’s life
and wellbeing both physically and psychologically.
• Lack of knowledge of genital diversity due to limited education in genital appearance.
• Comments made by others, directed at them or otherwise, and why this path has been
considered. Offer counselling where coercion from a partner, friend or relative is suspected. This
is an opportunity for the GP to enquire about intimate partner abuse, a history of sexual abuse
or other domestic or family violence. Appropriate counselling should be provided in these cases.
Refer to section 3.3.
• Grooming habits, such as waxing, depilation, shaving and lasering of pubic hair expose more
genital skin, while some women develop recurrent skin irritations from procedures such as
folliculitis, ingrown hairs and chafing. Draw the distinction between the grooming practices and
the complications that can result from them, emphasising the fact surgery will not diminish the
likelihood of these complications.
3.2 Take a medical, gynaecological and psychosexual history

Documentation of psychosexual history as a baseline, along with a full gynaecological and medical
history, is very important when discussing FGCS with a patient. The psychosocial context of the
patient’s request should be an integral part of the discussion, thereby ensuring the patient’s decision
making is as well informed as possible.
Key aspects of a psychosexual history that will assist the GP:
• Assess the degree of anxiety/concern.
• Ask the patient how her concern affects her.

• Ask if the patient’s concern is affecting her intimate relationships, self-esteem, confidence and
ability to function happily.
• Ask the patient if there is physical discomfort with or without sex.
• Acknowledge how she feels about the issue.
Refer to Appendix 2 for more information about how to take a psychosexual history.
3.3 Mental health and relationship or sexual abuse issues

should be considered and referred accordingly
When a woman presents to her GP with dissatisfaction regarding the appearance of her genitalia,
it is important to consider the fact that body image concerns could be linked with psychological or
relationship issues that have not been identified or managed. If a mental health diagnosis is made or
the request is related to a relationship issue, a referral for counselling should be given.
The spectrum of anxiety can range from women feeling embarrassed about the appearance of
their genitalia to thinking they are abnormal. This level of concern can be resolved by provision of
information that counters this belief through education in the consultation room and the display of
images that depict the diverse range of appearances. At the other end of the spectrum there is a
pervasive, unrelenting belief that they are ugly and abnormal to the degree that it affects their quality
of life and relationships. For some, this can present as clinical depression, social anxiety, an eating
disorder or body dysmorphic disorder.
A referral to a psychologist or psychiatrist, rather than a direct referral for surgery, would be
recommended.5,29 A referral for counselling should be offered when the patient already has a history
of mental health issues.
3.4 Examine the patient confidently and respectfully

In cases where the GP lacks specific skill in women’s health, or is not granted permission to conduct
a physical examination, referral to a women’s health GP, sexual health clinic or a gynaecologist
is recommended. Dutch guidelines recommend patients be offered a mirror to assist their
understanding of the anatomy and what constitutes normal at the time of a physical examination.40
If a referral to another medical practitioner is made, it should clearly state that it is for patient
reassurance and examination, not for surgery.
Some patients do not outwardly state that they wish to modify their genital anatomy. However, the
GP may take the opportunity to explore any such concerns at the time of a routine Pap smear or
gynaecological check-up if and when a woman expresses embarrassment or even apologises for her
appearance. Look for dermatological conditions that require appropriate management.
Refer to Appendix 3 for more information on how to examine the patient.41

3.5 Use diagrams to educate the patient at the time of

examination and during the consultation (refer to Figure 1)
Refer patients to appropriate online resources, such as the Labia Library42 or other publications,
including 101 vagina43 and Femalia44, in which there has been no digital enhancement.
When discussing female anatomy, it is important to focus on the sensorineural and functional
aspects, and to clarify the differences in terminology.
Figure 1. Anatomy of female genitalia
Pubic hair
Vulva
Clitoris
Urethra
Labia minora
Vagina
Labia majora
Anus
Reproduced with permission from Women’s Health Victoria.
3.6 Reassure the patient

Upon examining the genital region, use non-judgemental language to reassure the patient of their
normality (provided there is no medical basis for the concern).
Care should be taken not to ‘medicalise’ cosmetic concerns and minor physical symptoms, such
as chafing and discomfort from grooming procedures and clothing.
3.7 Address all symptoms and concerns

Physical symptoms, if any, need to be discussed with the patient. Identify whether these
symptoms are related to the dimensions of her anatomy or due to other factors, such as recurrent
infections, tight or poorly-fitted clothing, and skin irritations that are a result of chemical irritants or
over-washing.
The medical conditions that constitute reasonable cause for the surgery to be performed have
been changed as of November 2014, following the Australian Attorney-General’s investigation
into reasons why labiaplasty and other forms of FGCS were being performed and claimed under
Medicare. Currently, Medicare item 35533 is intended for the surgical repair of female genital
mutilation/cutting (FGM/C) and major congenital anomalies of the uro-gynaecological tract not
covered by existing item numbers. It is valid only for inpatient services and will not be paid for
outpatient procedures.
A new Medicare item number, 35534, is for ‘localised gigantism which causes significant functional
impairment and where non-surgical treatments have failed’. This item number now requires a
specific application to the Department of Human Services, which will then be reviewed by the
Medicare Claims Review Panel, to determine if there is enough evidence to qualify for the item
number. Medicare benefits can no longer be claimed for non-therapeutic cosmetic genital surgery.
In summary, the clinically relevant indications for vulvoplasty include non-inflammatory disorders of
the vulva and perineum, congenital disorders and to repair or reconstruct normal female anatomy
following trauma, harmful traditional practices or pathologic processes4 (refer to Appendix 4 and
Appendix 5.3 for more information).
3.8 Refer the patient

Refer the patient for a second opinion. A gynaecologist is likely to provide education and resources
regarding the range of normal diversity of the anatomy.33 It is important to clearly state that the
referral is for opinion and not surgery, unless it is medically indicated.
Referral of adolescents (younger than 18 years of age) for genital cosmetic surgery is not advised
unless it is to a specialist adolescent gynaecologist. Full genital development is not normally
achieved before 18 years of age, therefore FGCS should not be carried out on adolescent girls27,46
(refer to section 5 for further information).
3.9 Explain what the FGCS procedures entail, including

risks and potential complications (refer to Section 1.5)
If the patient is still considering undergoing FGCS, encourage them to describe exactly what they
wish to have removed. Discuss the lack of long-term data on outcomes and satisfaction, as the
potential for injury or complications.
Patients should be warned that the benefits of FGCS are not proven and they are not approved
medical procedures. Genital cutaneous sensitivity, erotic sensitivity and orgasmic capacity, which
can all be effected by FGCS, have important implications for women’s quality of life.19,24
Providing the patient with a list of current, publicly-available position statements and
recommendations from peak bodies around the world may be helpful (refer to Appendix 5).
Where appropriate, referral to appropriate colleagues (gynaecologists, women’s health GPs, plastic
surgeons, etc) can be made. The Medical Board of Australia’s Good medical practice: A code of
conduct for doctors in Australia should also be considered (refer to Appendix 6).
3.10 Referral pathway for patients who state that their

surgery has ‘gone wrong’
Given FGCS is classified as a set of procedures conducted for cosmetic reasons that have no
set guidelines and can be performed by a range of practitioners as diverse as GPs, urologists,
cosmetic doctors, gynaecologists and plastic surgeons, patients should be aware that outcomes
might not be as expected. When a patient presents with postoperative complaints, it may be
helpful to refer them to the psychosexual or gynaecological service at the women’s and children’s
hospital in their state or territory.
11
4. How female genital mutilation/cutting

legislation applies to FGCS
The World Health Organization (WHO) defines FGM/C as ‘all procedures involving partial or total removal
of the external female genitalia or other injury to the female genital organs for non-medical reasons’. It is
generally performed on children or adolescents who are not able to provide informed consent. There are no
known health benefits and it is known to be harmful to girls and women in many ways.47
All Australian states and territories have enacted legislation banning FGM/C and a variety of health and
educational activities are in place to promote health and support cultural change required to eliminate
its practice. Some people from countries that have traditionally practised FGM/C regard the selective
application of the legislation to FGM/C but not FGCS, both of which could be considered to be culturally
determined, to be discriminatory and unfair.48
There is some debate about whether FGCS is covered by legal definitions of FGM/C and, therefore, illegal
under existing regulations. The adequacy of outcome data considered is central to informed consent for
FGCS, as for all medical procedures.49
According to medical defence organisation, Avant:
‘purely cosmetic procedures may not trigger the exceptions under each Act, particularly in NSW and
VIC where the procedure must be necessary for the health of the person. However Acts do not define
the words ‘necessary’ and ‘health’. Legal concern is heightened given the fact that the patient’s consent
is not a defence.’49,50
The Australian Government’s Review of Australia’s Female Genital Mutilation legal framework - Final report
is a valuable source of further information and is available at www.ag.gov.au/Publications/Pages/ReviewofA
ustraliasFemaleGenitalMutilationlegalframework-FinalReportPublicationandforms.aspx
5. Adolescents and FGCS requests

According to the British Society for Paediatric and Adolescent Gynaecology (BritSPAG) position statement
on adolescents and FGCS requests issued in 2013:46
There is no evidence that the incidence of labial pathology has changed. The increase in activities cannot
be accounted for in medical terms. Labiaplasty does not tackle the cultural and economic factors that
are giving rise to vulval appearance distress. There is no scientific evidence to support the practice of
labiaplasty and, for girls under the age of 18 years, the risk of harm is even more significant.
Frontline and specialist clinicians should improve their skills and confidence in educating and supporting the
girls and, where appropriate, their parents. Further development of age-appropriate resources for girls and
their parents should be a priority for clinicians. Information on the following should be presented sensitively
and clearly with opportunities for discussion:
• labial anatomy and its development
• diversity in vulval appearance
• the distortions in popular culture
• the unknowns about labiaplasty
• the measures for managing labial discomfort and

• where distress is significant, the importance of a psychological assessment.
Reproduced with permission from British Society of Paediatric and Adolescent Gynaecology (BritsPAG). Position statement:
Labial reduction surgery (labiaplasty) on adolescents. London: BritsPAG; 2013.
6. Summary of recommendations for GPs

and other health professionals
FGCS incidence is climbing. Informed GPs can reduce unnecessary anxiety

regarding vulval/genital anatomy, thereby deflecting a climb in FGCS.
Patient examination should be performed by the GP or referred to a doctor experienced in women’s

health. This is an opportunity to educate female patients about genital anatomy.
It is important to consider mental health and relationship abuse issues and refer accordingly.
Educate patients about genital diversity, using tools such as the online resource Labia Library
and the publication Femalia, and possible complications of surgery.
It is recommended GPs initially refer patients for a gynaecological assessment.
If the patient is younger than 18, they should be referred to a specialist adolescent gynaecologist.
7. Appendices
Appendix 1 - Australian media code of conduct on body image

Australia’s Voluntary media code of conduct on body image was designed to encourage the fashion, media
and advertising industries to place greater emphasis on diversity, positive body images and a focus on
health rather than body shape. In doing so, it aims to reduce young people’s susceptibility to feelings of low
self-esteem, eating disorders and negative body image that are associated with exposure to idealised and
unrealistic images seen in the media and advertising.4,35,51
The code of conduct:
• discourages the use of digitally enhanced or altered pictures and suggests these digitally pictures be
identified as such
• encourages the use of images that represent the diversity of body shapes
• encourages the considered placement of advertising on dieting, cosmetic surgery, etc
• discourages the ‘glamourisation’ of models and celebrities who are particularly underweight and instead
encourages a focus on models with a healthy body shape.
Appendix 2 - Taking a psychosexual history

When taking a psychosexual history, it is important to offer a chaperone and ask the patient about:
*
• Personal history:
- At what age did you reach puberty/menarche?
- What was your parent’s attitude toward sexual matters?
- How did you attain sexual information?

- What is your sexual orientation?
• Relationships and marital history:

- At what age did you have your first sexual relationship?
- How long was your longest relationship? What were some of the reasons for break ups? Any
extramarital affairs?
- Do you practice safe sex? Has that always been the case? Have you had any sexually transmitted
infections?
- Are you currently in a relationship? Any problems? Is there any inconsistency between your partner’s
and your sexual desire? How does that affect you? Are you and your partner committed to each
other? How would you describe the communication in your relationship?
- Do you have children? Have you had any abortions? Are you in contact with your children?
- Do you have any sexual difficulties? Have you noticed a change in desire? Do you know how to
achieve orgasm? Can you achieve orgasm and do you enjoy having sexual relations with your
partner?
- Do you have any problems with penetration (vaginismus) and pain during intercourse?
- Do you use any street drugs?
- Are you on any regular medications?

- Have you ever been hurt in any way? Any violence in any of your relationships?
- Do you have a history of depression, anxiety or other mental health concerns, including eating
disorders?
*Adapted with permission from the Royal College of Psychiatrists (UK) for use in the primary care setting.
Appendix 3 - Guidelines for gynaecological examinations

and procedures
The gynaecological examination of women is a formal process and potentially intimidating to women, some
of whom may have suffered various degrees of physical or sexual abuse during their lives.
Doctors should consider the information provided by women, listen and respond sensitively to their
questions and concerns.
According to the Royal Australian and New Zealand College of Obstetricians and Gynaecologists
(RANZCOG) Guidelines for Gynaecological Examinations and Procedures C-Gyn 30:41
Awareness of cultural or religious factors is essential when discussing and offering gynaecological
examination.
Where examination is indicated, doctors should ensure that:
• an adequate explanation is provided about the nature of an examination and the information that it will
provide
• the patient has the opportunity to decline examination
• permission is obtained, especially for breast and/or pelvic examination
• privacy is provided for disrobing
• suitable cover is provided during examination, for example, gown or cover sheet
• a chaperone is available to attend any patient undergoing physical examination when requested,
irrespective of the gender of the doctor.
• the patient must be made aware in advance of the presence of medical students and the right to decline
their attendance at any examination
• it may be appropriate to delay examination until a follow-up appointment.
With respect to examination of young women and children, see the Royal Australasian College of Physicians
(RACP) policy Genital Examinations in Girls and Young Women: A Clinical Practice Guideline, available at
https://www.racp.edu.au/docs/default-source/advocacy-library/genital-examinations-in-girls-and-young-
women-a-clinical-practice-guideline.pdf
In addition to these RANZCOG guidelines, it is recommended that patients watch the examination with a
mirror to assist their understanding of the anatomy and what constitutes normal.40
The doctor should refrain from using language that is judgemental, expresses surprise or can be construed
as derogatory when performing the examination.
Reproduced with permission from the Royal Australian and New Zealand College of Obstetricians and
Gynaecologists (RANZCOG) College Statement C-Gyn 30. Melbourne: RANZCOG; 2004.
17
Appendix 4 - How FGM legislation applies to cosmetic

procedures
RACGP fact sheet

UAvant mutual group------ '
Female genital cosmetic surgery and the law
Currently, each state and territory has provisions in their respective criminal law
statutes which make the practice of female genital mutilation (FGM)1 illegal.
These laws apply extraterritorially in all jurisdictions, which means people who
are involved in FGM overseas or in another state or territory can be charged
under these laws. In all states except NSW, it is also an offence to remove
someone from the jurisdiction with the intention of having FGM performed on that
person. The penalties range from seven years to 21 years’ imprisonment.
All jurisdictions define FGM. These definitions are broadly consistent with each
other and cover the same conduct for FGM as defined by the World Health
Organisation (WHO). Under the legislation in each state and territory, having the
consent of the person who is to be the subject of FGM, or their parent or
guardian, is not a defence for the practice of FGM.
The legal definitions
The various statutes define FGM as the excision, infibulation or any other
mutilation of the whole or any part of the female genitalia2. The definitions would
arguably apply to some procedures such as labiaplasty. However, the Acts state
that it is not an offence if a procedure is performed for a “genuine therapeutic
purpose”3; a “proper medical purpose”4; or is “necessary for the health”5 of the
patient.
In a report released in March 2013, the Commonwealth Attorney-General’s

Department raised concerns about how the law and policy apply to female genital
cosmetic surgery (FGCS). The report stated that anecdotal evidence suggests the
incidence of FGCS has increased significantly since 1998, when the Model Laws
(on which the legislation in each state and territory is based) were drafted.
Statistics from the Australian Institute of Health and Welfare (AIHW) show the
number of labiaplasty procedures performed annually has been steady for the last
10 years, at about 1,500 procedures per year.
It was contemplated in the Attorney-General’s report that the legislation, and how
it may apply to FGCS, would be reviewed and clarified. The report’s
recommendations were considered by the Standing Council on Law and Justice6 in
April 2013 and agreed to by the Standing Council, but there have been no further
developments as at the date of release of the toolkit. Therefore some legal
uncertainty remains.
In the interim, the Royal Australian and New Zealand College of Obstetricians and
Gynaecologists (RANZCOG) released an updated statement in relation to FGCS in
March 20157.
Concerns and recommendations
It is arguable that the legislative exceptions for medical treatment would apply to
a cosmetic procedure where consent had been provided and the procedure is
performed by an appropriately qualified medical practitioner.
However, if a procedure is purely cosmetic, for example because a patient has

anxiety about the appearance of their labia, it may not trigger the exceptions
under each State and Territory Act. This applies particularly in NSW and Victoria,
where the respective Acts state the procedure must be “necessary for the health
UAvant
of the person on whom it is performed” but without defining the words
mutual group------ '
“necessary” and “health”. This concern is heightened given the patient’s consent
is not a defence8.
The absence of greater legal clarity does not mean that FGCS needs to be
avoided altogether. Rather, it means that medical practitioners should be mindful
of this when discussing FGCS with patients and documenting those discussions in
their clinical records.
This uncertainty is likely to have a greater impact on the surgeons performing the
procedures in question, rather than on general practitioners or other health
professionals whose involvement will largely be limited to referrals. However, in
the course of providing such referrals to patients, there is likely to be some
discussion about the patient’s reason for requesting the referral and you may find
yourself giving them some information or advice about various options in general
terms.
Given the legal uncertainty, it is even more important that doctors make sure
their clinical records include notes addressing:
• The patient’s presenting problem and concerns;
• Any options for treatment discussed with the patient;
• The nature and details of the referral provided;
• Any other matters discussed with the patient regarding the procedure or
their concerns.
Avant will continue to monitor this issue and how it affects members. If in doubt,
please contact Avant on 1800 128 268.
1 See sections 73 to 77 inclusive of the Crimes Act 1900 (ACT); sections 15, 32 to
34A inclusive of the Crimes Act 1958 (Vic); section 45 of the Crimes Act 1900
(NSW); sections 323A and 323B of the Criminal Code 1899 (Qld); sections 186A,
186B, 186C and 186D of the Criminal Code Act 1983 (NT); sections 33, 33A and
33B of the Criminal Law Consolidation Act 1935 (SA); sections 178A, 178B, 178C
and Schedule 1 of the Criminal Code Act 1924 (Tas); section 306 of the Criminal
Code Act Compilation Act 1913 (WA).
2 This includes the labia majora, labia minor or clitoris, as specified in some of the
state and territory legislative definitions.
3 In the ACT, Northern Territory, Queensland, South Australia and Tasmania.
4 In Western Australia.
5 In New South Wales and Victoria.
6 Now called the Law, Crime and Community Safety Council (LCCSC).
7 “Vaginal ‘rejuvenation’ and cosmetic vaginal procedures” statement, C-Gyn 24,
RANZCOG, reviewed and released in March 2015.
8 To date, there have been no successful prosecutions under the various Acts in
the states and territories. As far as we are aware, there have only been two cases
where charges have been brought in NSW and one case in WA. The charge in the
first NSW case was against a medical practitioner but was not upheld by the jury
because of the “medical necessity” defence (charges were subsequently brought
and upheld under a different section of the Crimes Act). The WA case (against
parents of the victim) and the second NSW case (against eight people including a
retired nurse) have not yet been concluded.
Reproduced with permission from Avant: RACGP fact sheet: Female genital cosmetic surgery and the law. Sydney: Avant; 2015.
■
MDA National
Support Protect Promote
Female Genital Mutilation and Female Genital

Cosmetic Surgery - Legal Issues
Female Genital Mutilation (FGM) is currently a criminal The incidence of FGCS in Australia is increasing3 and
offence in Australia.1 The penalties for FGM range from a number of clinics advertise various procedures.
7 to 21 years imprisonment. Whilst there is some There are currently no Australian clinical practice
variation in each state and territory, the legislation guidelines for FGCS. It is arguable that some of the
is broadly consistent in defining FGM as including: FGCS procedures fall within the definition of FGM and
ajaclitoridectomyor some of these procedures may be contrary to the FGM
legislation, if the exceptions under the FGM legislation
b) excision of any other part of the female
do not apply.
genital organs; or
c) infibulation or any other similar procedure; or Conclusion
d) any other mutilation of the female genital organs. It is essential that medical practitioners who are
involved in FGCS ensure they are familiarwith the
Depending on the state or territory, the FGM legislation FGM legislation intheirstateorterritory. The absence
provides exceptions relating to medical procedures: of comprehensive clinical guidelines for FGCS
• for genuine therapeutic purposes, or increases the risk that practitioners who perform
• if necessary for the health of the person, or these procedures may be prosecuted.
• performed on a person in labourer who has just
given birth, and for medical purposes connected
1. Crimes Act 1900 (ACT) $73-77; Crimes Act 1900 (NSW) s45;
with that labour or birth, or Criminal Code Act (NT) S186A-186D; Criminal Code 1899 (Qld)
• for sexual reassignment procedures. S323A-323B; Criminal Law Consolidation Act 1935 (SA) s33-33B;
Crimes Act 1958 (Vic) S32-34A; Criminal Code Act 1924 (Tas)
S178A, 178B, s389; The Criminal Code (WA) s306
Cultural, religious or other social custom is not to be
regarded as a genuine therapeutic purpose. 2. Australian Governments Review of Australia’s Female Genital
Mutilation Legal Framework Final Report, issued March 2013.
It is not a defence to a charge of FGM that the person Available at http://www.ag.gov.au/publications/documents/
revi e wofa ustra 11 a sfema I eg e n ita I m ut 11 ati o n I eg a If ra mewo rk/
on whom the procedure was performed, or their review%20of%20australias%20female%20genital%20
parent, consented to the procedure. mutilation%20legal%20framework.pdf
3. Australian Government Department of Health MBS

A 2013 review by the Attorney General's Department Reviews Vulvoplasty Report, issued April 2014. Available
notes the broad definition of FGM and the removal at:http://www.health.gov.au/lnternet/maln/publlshlng.nsf/
of consent as a defence and that this raises issues Content/0C64684BA76544CCCA257BF0001E0243/$File/
Vulvoplasty_Review_Report.pdf
in relation to female genital cosmetic surgery (FGCS)
which may involve procedures that are technically
very similar to those defined in the FGM legislation.
The review further notes that the status of these
procedures under existing laws is untested and that
this is a complex issue.2
Youfiro n & mdanational.com.au Freecall: 1800 011 255

The MDA National Croup Is made up of MDA National Limited ABN 67 055 001771 and MDA National Insurance Rty Ltd ABN 56 05B 271417 AFS Licence No. 230079. 7161.1
Reproduced with permission from MDA National. Female genital mutilation and female genital cosmetic surgery - Legal issues.
Sydney: MDA National; 2015.
Appendix 5 - Statements from peak bodies

5.1 Royal College of Obstetricians and Gynaecologists and BritSPAG
According to the joint Royal College of Obstetricians and Gynaecologists (RCOG)-BritSPAG release, Issues
surrounding women and girls undergoing female genital cosmetic surgery explored, the RCOG ethical
opinion paper, Ethical considerations in relation to female genital cosmetic surgery (FGCS), has been
produced by the College’s Ethics Committee and focuses on women of all ages undergoing FGCS.
FGCS refers to non-medically indicated cosmetic surgical procedures which change the structure and
appearance of the healthy external genitalia of women, or internally in the case of vaginal tightening. This
definition includes the most common procedure, labiaplasty, as well as others, such as hymenoplasty and
vaginoplasty, also known as vaginal reconstruction and vaginal rejuvenation.
A number of recommendations are made in the paper, including:
• Women should be provided with accurate information about the normal variations in female genitalia and
offered counselling and other psychological treatments for problems such as body image distress.
• Women must be informed about the risks of the procedure and the lack of reliable evidence concerning
its positive effects.
• As full genital development is not normally achieved before 18 years of age, FGCS should not normally
be carried out on girls under this age.
• Surgeons who undertake FGCS should keep written records of the physical and mental health reasons
why the procedure was carried out.
• Advertising of FGCS should not mislead people on what is deemed to be normal or what is possible with
surgery.
• In general, FGCS should not be undertaken within the National Health Service (NHS) unless it is medically
indicated.
The paper offers clinicians recommendations for best practice, including:
• A genital examination should be offered and conducted sensitively.

• Information about normal variations should be offered.
• Surgical reduction before the completion of pubertal development may lead to long term problems and
this should be communicated to the girl and her guardian where appropriate.
• Simple measures to relieve labial discomfort should be suggested.

• In case of significant psychological distress, the girl and family should be offered a referral to a paediatric
clinical psychologist.
Reproduced with permission from the Royal College of Obstetricians and Gynaecologists. Female genital cosmetic surgery.
Ethical opinion paper. London: RCOG; 2013.
21
5.2 Society of Obstetricians and Gynaecologists of Canada

According to the article ‘Female genital cosmetic surgery’, published in Journal of Obstetrics and
Gynaecology Canada:52
Recommendations
1. The obstetrician and gynaecologist should play an important role in helping women to
understand their anatomy and to respect individual variations. (III-A)
2. For women who present with requests for vaginal cosmetic procedures, a complete medical,
sexual, and gynaecologic history should be obtained and the absence of any major sexual or
psychological dysfunction should be ascertained. Any possibility of coercion or exploitation
should be ruled out. (III-B)
3. Counselling should be a priority for women requesting FGCS. Topics should include normal
variation and physiological changes over the lifespan, as well as the possibility of unintended
consequences of cosmetic surgery to the genital area. The lack of evidence regarding
outcomes and the lack of data on the impact of subsequent changes during pregnancy or
menopause should also be discussed and considered part of the informed consent process.
(III-L)
4. There is little evidence to support any of the FGCSs in terms of improvement to sexual
satisfaction or self-image. Physicians choosing to proceed with these cosmetic procedures
should not promote these surgeries for the enhancement of sexual function and advertising of
female genital cosmetic surgical procedures should be avoided. (III-L)
5. Physicians who see adolescents requesting FGCS require additional expertise in counselling
adolescents. Such procedures should not be offered until complete maturity including genital
maturity, and parental consent is not required at that time. (III-L)
6. Non-medical terms, including but not restricted to vaginal rejuvenation, clitoral resurfacing, and
G-spot enhancement, should be recognized as marketing terms only, with no medical origin;
therefore they cannot be scientifically evaluated. (III-L)
Key to evidence statements and grading of recommendations, using the ranking of the Canadian
Task Force on Preventive Health Care.
Quality of evidence assessment

I: Evidence obtained from at least one properly randomized controlled trial.
II-1: Evidence from well-designed controlled trials without randomization.
II-2: Evidence from well-designed cohort (prospective or retrospective) or case-control studies,

preferably from more than one centre or research group.
II-3: Evidence obtained from comparisons between times or places with or without the
intervention. Dramatic results in uncontrolled experiments (such as the results of treatment with
penicillin in the 1940s) could also be included in this category.
III: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports
of expert committees.
Classification of recommendations
A. There is good evidence to recommend the clinical preventive action.
B. There is fair evidence to recommend the clinical preventive action.

C. The existing evidence is conflicting and does not allow to make a recommendation for
or against use of the clinical preventive action; however, other factors may influence
decision-making.
D. There is fair evidence to recommend against the clinical preventive action.
E. There is good evidence to recommend against the clinical preventive action.

L. There is insufficient evidence (in quantity or quality) to make a recommendation; however,
other factors may influence decision-making.
Reproduced with permission from Shaw D, Lefebvre G, Bouchard C, et al. Female genital cosmetic surgery.
J Obstet Gynaecol Can 2013:35(12);1108-14.
23
5.3 The Royal Australian and New Zealand College of Obstetricians

and Gynaecologists
The Royal Australian

and New Zealand
College of
Obstetricians and
Gynaecologists
Vaginal ‘rejuvenation’ and cosmetic

vaginal procedures
Background: This statement was first developed by
This statement has been developed and reviewed by
Women’s Health Committee in July 2008 and most
the Women’s Health Committee and approved by
recently reviewed in March 2015.
the RANZCOG Board and Council.
Funding: The development and review of this

A list of Women’s Health Committee Members can
statement was funded by RANZCOG.
be found in Appendix A.
Disclosure statements have been received from all

members of this committee.
DisclaimerlThis information is intended to provide

general advice to practitioners. This information
should not be relied on as a substitute for proper
assessment with respect to the particular
circumstances of each case and the needs of any
patient. This document reflects emerging clinical
and scientific advances as of the date issued and is
subject to change. The document has been
prepared having regard to general circumstances.
First endorsed by RANZCOG: July 2008

Current: March 2015
Review due: March 2018
Surgical or laser techniques available which claim to improve the appearance of the female genitial tract
and enhance sexual function such as “vaginal rejuvenation”, “revirgination”, “designer vaginoplasty”, “G
spot amplification” are poorly understood and what is involved in these procedures is often unclear since
recognised clinical nomenclature is not being used.
The American College of Obstetricians and Gynecologists (ACOG) Committee on Gynecologic Practice
and the Society of Obstetricians and Gynaecologists of Canada have produced documents discouraging the
practice of female genital cosmetic surgeries which do not include medically-indicated reconstructions. 1, 2
Gynaecological conditions that merit surgery include genital prolapse, reconstructive surgery following
female genital mutilation and labioplasties with clinical indications. Medical practitioners performing any
vaginal surgery should be appropriately trained.
Recommendations by these bodies include that the obstetrician and gynaecologist should have a role in
educating women that there is a large number of variations in the appearance of normal female external
genitalia and that there are normal physiological changes over time, especially following childbirth and
menopause. Patients requesting procedures other than for gynaecological conditions should be assessed
thoroughly and the reasons for such a request assessed carefully. Sexual counselling is also recommended
for patients requesting surgery that is purported to enhance gratification. The College is particularly
concerned that such surgery may exploit vulnerable women. Doctors who perform these procedures should
not promote or advertise that these surgeries enhance sexual function.
The College strongly discourages the performance of any surgical or laser procedure that lacks current peer
reviewed scientific evidence other than in the context of an appropriately constructed clinical trial. At present,
there is little high quality evidence, that these procedures are effective, enhance sexual function or improve
self-image. The risks of potential complications such as scarring, adhesions, permanent disfigurement,
infection, dyspareunia and altered sexual sensations should be discussed in detail with women seeking such
treatments.3
References
1. Vaginal “rejuvenation” and cosmetic vaginal procedures, ACOG Committee Opinion No. 376.
American College of Obstetricians and Gynecologists. Obstet Gynecol 2007; 110: 737-738.
2. Shaw D, Lefebvre G, Bouchard C etal. Female genital cosmetic surgery. J Obstet Gynaecol Can.
2013;35:1108-14
3. Singh A, Swift S, Khullar V, Digesu A. Laser vaginal rejuvenation: not ready for prime time. Int
Urogynecol J. 2015;26:163-164.
Reproduced with permission from the Royal Australian and New Zealand College of Obstetricians and Gynaecologists
Vaginal ‘rejuvenation’ and cosmetic vaginal procedures C-Gyn 24. Melbourne: RANZCOG; 2008.
25
5.4 Medical Women’s International Association

According to resolutions passed at the Medical Women’s International Association (MWIA) 29th
International Congress in Seoul, 2013:
MWIA recognises the autonomy of women and upholds the right of adult women to choose to
undergo lawful medical and surgical treatments. MWIA advocates for the provision of informed
consent for all patients undergoing medical and surgical procedures.
MWIA opposes the advertising of regulated health services (eg those usually provided by a
healthcare practitioner) in a way that directly or indirectly encourages their indiscriminate or
unnecessary use.
MWIA opposes the promotion of and use of surgical products and techniques that make
unproven claims of enhancing female sexual satisfaction and/or attractiveness. MWIA believes that
promoting and performing such surgery carries significant risks of physical and psychological harm
to women and girls.
MWIA supports the use of gynaecological and plastic surgical techniques where the primary aim
is to repair or reconstruct normal female anatomy following trauma, harmful traditional practices,
pathologic processes or congenital anomalies.
MWIA opposes media depictions that directly or indirectly promote a prepubescent appearance
of female genitalia as sexually desirable. MWIA opposes media images that directly or indirectly
promote abnormal perceptions of the appearance of normal female adult genitalia.
Refer to: http://mwia.net/wp-content/uploads/2013/09/MWIA_update_september_2013.pdf
5.5 The American College of Obstetricians and Gynaecologists

The American College of Obstetricians and Gynaecologists released a committee opinion in 2007
titled Vaginal ‘Rejuvenation’ and Cosmetic Vaginal Procedures, available at www.acog.org/
Resources-And-Publications/Committee-Opinions/Committee-on-Gynecologic-Practice/Vaginal-
Rejuvenation-and-Cosmetic-Vaginal-Procedures
5.6 The Royal Australasian College of Physicians

The Royal Australasian College of Physicians have released a clinical practice guideline in 2009,
titled Genital examinations in girls and young women: a clinical practice guideline, available at
www.racp.edu.au/docs/default-source/advocacy-library/genital-examinations-in-girls-and-young-
women-a-clinical-practice-guideline.pdf
Appendix 6 - Good medical practice code of conduct

Under a set of draft guidelines released by the Medical Board of Australia in March 2015, GPs have a
central role to play in advising patients considering cosmetic surgery.
According to a committee of the Australian Health Workforce Ministerial Council, the guidelines will be
added as a supplement to the Medical Board of Australia’s Good medical practice: A code of conduct for
doctors in Australia, available at www.amc.org.au/about/good-medical-practice
27
References
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lease: Issues surrounding women and girls undergoing female genital cosmetic surgery explored. Available at www.rcog.org.uk/en/news/ joint-
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2. Bramwell R, Morland C, Garden A. Expectations and experience of labial reduction: a qualitative study. Br J Obstet Gynaecol
2007;114(12):1493-9.
3. Australian Government Department of Human Services. Medicare Item Reports. Available at http://medicarestatistics.humanservices.gov.au/
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lishing.nsf/Content/0C64684BA76544CCCA257BF0001E0243/$File/Vulvoplasty_Review_Report.pdf [Accessed January 2015].
5. Liao LM, Creighton SM. Female genital cosmetic surgery: a new dilemma for GPs. Br J Gen Pract 2011;61(582):7-8.
6. Iglesia CB, Yurteri-Kaplan L, Alinsod R. Female genital cosmetic surgery: a review of techniques and outcomes. Int Urogynacol J
2013;24(12):1997-2009.
7. Lloyd J, Crouch N, Minto C, Liao LM, Creighton S. Female genital appearance: “normality” unfolds. BJOG 2004;112(5):643-6.
8. Basaran M, Kosif R, Bayar U, Civelek B. Characteristics of external genitalia in pre- and postmenopausal women. Climacteric
2008;11(5):416-21.
9. Davison SP, Baker C, West J. Labiaplasty and labia minora reduction. Medscape 2014. Available at http://reference.medscape.com/
article/1372175-overview [Accessed May 2015].
10. Andrikopoulou M, Michala L, Creighton SM, Liao LM. The normal vulva in medical textbooks. J Obst Gynaecol 2013;33(7):648-50.
11. McDougall LJ. Towards a clean slit: how medicine and notions of normality are shaping female genital aesthetics. Cult Health Sex
2013;15(7):774-87.
12. Alter GJ. Labia minora reconstruction using clitoral hood flaps, wedge excisions, and YV advancement flaps. Plast Reconstr Surg
2011;127(6):2356-63.
13. Pardo J, Sola V, Ricci P, Guilloff E. Laser labioplasty of labia minora. Int J Gynaecol Obstet 2006;93(1):38-43.
14. Rouzier R, Louis-Sylvestre C, Paniel BJ, Haddad B. Hypertrophy of labia minora: experience with 163 reductions. Am J Obstet Gynaecol
2000;182:35-40.
15. Liao LM, Taghinejadi N, Creighton SM. An analysis of the content and clinical implications of online advertisements for female genital cosmetic
surgery. BMJ Open 2012;2(6):DOI:10.1136/ bmjopen-2012-001908.
16. Choi HY, Kim KT. A new method for aesthetic reduction of labia minora (the deepithelialized reduction of labioplasty). Plast Reconstr Surg
2000;105(1):419-22.
17. Balmforth J, Cardozo L. Designer vaginas. Journal of the Association of Chartered Physiotherapists in Women’s Health 2006;99:72-7.
18. O’Connor M. Reconstructing the hymen: mutilation or restoration? J Law Med 2008;16(1):161-75.
19. O’Connell HE, Eizenberg N, Rahman M, Cleeve J. The anatomy of the distal vagina: towards unity. J Sex Med 2008;5(8):1883-91.
20. Tiefer L. Female genital cosmetic surgery: freakish or inevitable? Analysis from medical marketing, bioethics, and feminist theory. Fem Psychol
2008;18:466-72.
21. Chase C. Re: measurement of pudendal evoked potentials during feminizing genitoplasty: technique and applications. J Urol
1996;156(3):1139-40.
22. Diamond M, Sigmundson HK. Sex reassignment at birth: long-term review and clinical implications. Arch Pediatr Adolesc Med
1997;150:298-304.
23. Schober JM, Meyer-Bahlburg HF, Ransley PG. Self-assessment of genital anatomy, sexual sensitivity and function in women: implications for
genitoplasty. BJU Int 2004; 94(4):589-94.
24. Schober JM, Alguacil NM, Cooper RS, Pfaff DW, Meyer-Bahlburg FL. Self-assessment of anatomy, sexual sensitivity, and function of the labia
and vagina. Clin Anat 2015;28:355-62.
25. Ostrzenski A. Cosmetic gynecology in the view of evidence-based medicine and ACOG recommendations: a review. Arch Gynecol Obstet
2011;284(3):617-30.
26. Goodman MP. Female cosmetic genital surgery. Obstet Gynecol 2009;113(1):154-9.
27. Sharp G, Tiggemann M, Mattiske J. Predictors of consideration of labiaplasty: an extension of the tripartite influence model of beauty ideals.
Psychology of Women Quarterly 2014;DOI: 10.1177/0361684314549949.
28. Fatah, F. Should all advertising of cosmetic surgery be banned? Yes. BMJ 2012;345:DOI: 10.1136/bmj.e7489.
29. Keil A, Greenhalgh, S. Genital anxiety and the quest for the perfect vulva: A feminist analysis of female genital cosmetic surgery. Women and
the Body 2010. Available at www.anthropology.uci.edu/files/docs/2010_benedict_keil.pdf [Accessed March 2014].
30. Howarth H, Sommer V, Jordan FM. Visual depictions of female genitalia differ depending on source. Med Humanit 2010;36(2):75-9.
31. Howarth C, Temple-Smith M, Simonis M, Hayes J. What are young women’s views on ‘normal’ and ‘desirable’ vulval anatomy? Melbourne:
General Practice and Primary Health Care Academic Centre, University of Melbourne; 2013/2014 (research pending publication).
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zine-stop-digitally-altering-images-to-change-appearances-realgirlscleo [Accessed March 2013].
33. Women’s Health Victoria. Women and genital cosmetic surgery. Available at http://whv.org.au/static/files/assets/ca7e9b2f/Women-and- geni-
tal-cosmetic-surgery-issues-paper.pdf [Accessed March 2013].
34. Cain JM, Iglesia CB, Dickens B, Montgomery O. Body enhancement through female genital cosmetic surgery creates ethical and rights dilem
mas. Int J Gynaecol Obstet 2013;122(2):169-72.
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Available at www.comlaw.gov.au/Series/F2005L01285 [Accessed October 2014].
36. Hungry Beast - Labiaplasty 2010, television program, Australian Broadcasting Corporation, Sydney.
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Gynaecologist 2012;14(3):203-6.
38. Reitsma W, Mourits MJ, Koning M, Pascal, van der Lei B. No (wo)man is an island - the influence of physician’s personal predisposition to
labia minora appearance on their clinical decision making: a cross-sectional study. J Sex Med 2011;8(8):2377-85.
39. Simonis M. Addressing young women’s desire for genital beauty. Australasian Sexual Health Conference, 2013.
40. Paarlberg KM, Weijenborg PT. Request for operative reduction of the labia minora; a proposal for a practical guideline for gynecologists. J
Psychosom Obstet Gynaecol 2008;29(4):230-4.
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C-Gyn 30. Available at www.ranzcog.edu.au/college-statements-guidelines.html [Accessed October 2014].
42. Women’s Health Victoria. Labia Library. Available at www.labialibrary.org.au.
43. Werner P. 101 vagina: One hundred and one women, one hundred and one stories. Melbourne; Philip Werner; 2013.
44. Blank J. Femalia. San Francisco: Last Gasp paperback; 2011.
45. Liao LM, Michala L, Creighton SM. Labial surgery for well women: a review of the literature. BJOG 2010;117(1):20-5.
46. British Society of Paediatric and Adolescent Gynaecology. Position statement: Labial reduction surgery (labiaplasty) on adolescents. Available
at www.britspag.org/sites/default/files/downloads/Labiaplasty%20%20final%20Position%20Statement.pdf [Accessed March 2014].
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tions/2008/9789241596442_eng.pdf?ua=1 [Accessed October 2014].
48. Vaughan C, White N, Keogh L, et al. Listening to North Yarra Communities about female genital cutting. Melbourne: The University of Mel
bourne; 2014.
49. Australian Government Attorney General’s Department. Review of Australia’s female genital mutilation legal framework: Final report. Avail
able at www.ag.gov.au/publications/documents/reviewofaustraliasfemalegenitalmutilationlegalframework/review%20of%20australias%20
female%20genital%20mutilation%20legal%20framework.pdf [Accessed October 2014].
50. Avant. How FGM legislation applies to cosmetic procedures. Available at www.avant.org.au/news/20130701-how-fmg-legislation-applies-to-
cosmetic-procedures [Accessed October 2014].
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ties; 2008
52. Shaw D, Lefebvre G, Bouchard C, et al. Female genital cosmetic surgery. J Obstet Gynaecol Can 2013;35(12):1108-14.
Marine envenomations
Ingrid Berling
Geoffrey Isbister
Background The majority of marine envenomings are minor and do

Marine stings are common but most are minor and do not not require medical intervention. Jellyfish stings are a
require medical intervention. Severe and systemic marine frequent reason for presentation to first aid and primary
envenoming is uncommon, but includes box jellyfish stings, healthcare providers. A knowledge of the variety of stings
Irukandji syndrome, major stingray trauma and blue-ringed and envenoming syndromes that occur in Australia,
octopus envenoming. Almost all marine injuries are caused
including those that are clinically significant, and available
by jellyfish stings, and penetrating injuries from spiny fish,
treatments, is necessary for practitioners, particularly those
stingrays or sea urchins.
working in coastal regions.
Objective
This article describes the presentation and management Marine envenoming can be considered in two broad categories:
of marine envenomations and injuries that may occur in jellyfish stings and penetrating venomous marine injuries. Jellyfish
Australia.
stings range from the life-threatening major box jellyfish (Chironex
Discussion fleckeri) to painful, but generally benign, bluebottle stings common
First aid for jellyfish includes tentacle removal, application to most southeastern Australian beaches (Figure 1). Penetrating
of vinegar for box jellyfish, and hot water immersion (45°C venomous marine injuries often occur when handling fish, but can
for 20 min) for bluebottle jellyfish stings. Basic life support occur to anyone involved in water activities, fresh water or marine.
is essential for severe marine envenomings that result in
They are typically more painful than just the trauma of the wound, and
cardiac collapse or paralysis. Irukandji syndrome causes
injury severity is related to the anatomical location. Deaths, although
severe generalised pain, autonomic excess and minimal local
rare, have occurred from penetrating thoracoabdominal injuries from
pain, which may require large amounts of analgesia, and,
stingrays.
uncommonly, myocardial depression and pulmonary oedema
occur. Penetrating marine injuries can cause significant
trauma depending on location of the injury. Large and unclean
wounds may have delayed healing and secondary infection if
not adequately irrigated, debrided and observed.
Keywords
bites and stings; emergencies; environmental medicine;
marine toxins; toxicology
Figure 1. Blue bottle (Physalia spp.) from eastern Australia
wgg o
Photo by Geoffrey Isbister
Jellyfish stings
Jellyfish cause stings when their tentacles contact skin. Contact
triggers the jellyfish to release venom from millions of tiny stinging
cells (nematocytes) covering the tentacles. The venom is released via
a harpoon-like mechanism that injects venom into the dermis.
28 REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 44, NO. 1-2, JANUARY-FEBRUARY 2015
Sting severity is related to: distinctive and can last hours to days (Figure 2A, B). Typically, the pain
• the number of stinging cells that fire, which depends on the amount resolves within 1-2 hours. Mild systemic symptoms such as nausea,
of tentacle contact with skin vomiting and malaise occur uncommonly. Rarely, there may be delayed
• the potency of injected venom, which depends on the species. reactions such as papular urticarial rashes along the sting sites
The most dangerous jellyfish, the major box jellyfish (C. fleckeri), has (C. fleckeri), bullous lesions or keloid scarring (usually in predisposed
a highly potent venom as well as multiple long tentacles. Deaths from individuals). Although the presentation of most C. fleckeri stings is
the major box jellyfish have occurred in Northern Australia, but remain similar to other stings, severe envenoming resulting in cardiovascular
rare. Bluebottles (Physalia species) are the most common cause of collapse and death can occur. These cases are characterised by
jellyfish stings worldwide and in Australia, although few people significant hypotension within 20-30 minutes, which leads to death
present to hospital. Stings occur at times when swarms of bluebottles without basic life support.
are in shallow coastal waters or along the shoreline. Irukandji-like Irukandji-like stings can often initially go unnoticed in divers in
stings occur in Northern Australia, most commonly due to Carukia deep water. Within 20-30 minutes they develop severe, excruciating
barnesi, but cases have occurred less commonly in other parts of generalised pain (abdominal, back and chest pain). There is rarely
Australia and from other jellyfish types. local pain and often there is only a minimal skin reaction. The patient
is often distressed and may have associated agitation, nausea,
Clinical manifestations vomiting and diaphoresis. Patients can develop tachycardia and
Patients stung by jellyfish present in one of two ways: hypertension, which may result in myocardial injury and pulmonary
• the majority present with an immediately painful, linear/tentacle- oedema. Animal studies have shown that C. barnesi envenoming
like sting is associated with the release of endogenous catecholamines,
• a minority present with delayed pain - Irukandji-like sting (Table 1). consistent with a sympathomimetic toxidrome.1 Electrocardiogram
Linear/tentacle stings usually result in local pain where the tentacles (ECG) ST segment and T wave changes, and elevated troponins due to
contact skin. There is a raised erythematous or urticarial lesion that is myocardial injury can occur.
Table 1. Summary of the clinical effects, first aid and treatment of the most common medically
important jellyfish
Jellyfish stings
Linear/tentacle-like stings Irukandji-like stings
Bluebottle and minor jellyfish Major box jellyfish Other box jellyfish
(Physalia spp, Pelagia, Cyanea, ( Chironex fleckeri) (Carukia barnesi, etc)
Aurelia, some Carybdidaee)
Clinical effects
Typically, these stings cause These stings cause severe local pain Irukandji syndrome is typically
immediate local intense pain for and associated erythematous eruptions delayed (20-30 mins) with generalised
1-2 hours, and associated linear along the lines of tentacle contact. In severe pain and systemic effects
erythematous eruptions large surface area contact exposures (tachycardia, agitation, hypertension)
cardiovascular collapse and death can and in a small proportion cardiac
occur injury/pulmonary oedema
First aid
• Wash sting site with seawater • Apply vinegar and remove tentacles • Apply vinegar and remove any
and remove tentacles • Commence immediate remaining tentacles
• Hot water immersion cardiopulmonary resuscitation on any
(45°C for 20 minutes
)* patient who is unconscious
• Avoid vinegar as it may
worsen the pain
Further medical management
Generally no further intervention is Transport to hospital for: Transport to hospital for:
necessary • Analgesia (oral and IV) • Analgesia (oral and intravenous)
• Consider antivenom in patients with • Investigation and treatment of
cardiovascular collapse not responsive cardiac effects (troponin, ECHO)
to standard advanced life support • Cardiac monitoring
*Evidence only for bluebottle stings but likely to work with other minor jellyfish stings2
REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 44, NO. 1-2, JANUARY-FEBRUARY 2015 29
FOCUS Marine envenomations
systemic envenoming and cardiac arrest should be treated according

to standard advanced cardiac life support protocols, including
initiation of cardiopulmonary resuscitation (CPR) at the scene.
Antivenom is available and intravenous administration should be
considered in severe cases where cardiac collapse occurs, although
immediate CPR is by far the most critical life-saving intervention.3
Irukandji-like stings
Patients presenting with Irukandji-like stings often require hospital
admission for large doses of titrated opioid analgesia. Additional
treatment with antiemetics and benzodiazepines may provide
symptomatic relief. Hypertension will almost always resolve with
good analgesia and benzodiazepines. Patients should have cardiac
monitoring, including careful evaluation for hypertensive emergencies
such as myocardial injury, pulmonary oedema and intracranial
haemorrhage. All patients should have an ECG and troponin, and if
these are abnormal then an echocardiogram should be obtained.
Penetrating venomous marine injury

Venomous fish and stingrays all have sheath-covered venomous
spines in their dorsum, ventral surface or tail. These spines can
penetrate human tissue. As the spine penetrates, the venom between
the sheath and spine is injected into the wound. The venom seems
to contribute to the severity of the pain, typically out of proportion
Figure 2. with the extent of the wound. Penetrating venomous marine wounds
A. Bluebottle sting on the back of a child 2 days after can present with delayed healing and secondary infection, again
the sting; B. Multiple linear stings following a major box
worsened by the dermonecrotic effects of the venom (Table 2). Larger
jellyfish (C. fleckeri) sting
Photos by Geoffrey Isbister penetrating injuries, usually from stingrays, and thoracoabdominal
penetrations in particular, can lead to major and life-threatening
trauma and should be treated as such. For this reason spines should
not be removed before admission to hospital.
Treatment
Clinical manifestations
Linear/tentacle stings
The site of injury is typically related to the type of encounter with
In all cases the tentacles should be carefully removed, either by venomous fish or stingrays. Stonefish and bullrout tend to cause
washing with seawater, or by hand. For bluebottles, the sting site injuries when trodden on (foot wounds), whereas catfish tend to
should be immersed in hot water for 20 minutes. This treatment sting fingers (Figure 3) and hands when handled. These wounds are
is supported by an open-labelled randomised controlled trial that typically very painful, with minimal bleeding, but can develop swelling
showed hot water immersion (45°C) for 20 minutes was effective, and oedema. Stingrays are most often trodden on, causing an injury
compared with ice packs.2 Immersion should be limited to 20 minutes to the ankle as the tail spine whips around behind the leg (Figure 4).
and the water should be tested to prevent burns. For other minor Serious trauma and death can occur when the spine enters major body
jellyfish stings, hot water can be used but there is less evidence to cavities, which can occur during diving.
support this.
C. fleckeri stings can be life-threatening so early resuscitation
Treatment
may be required. Recommended first aid is the liberal application First aid for venomous fish stings and stingray injuries is hot water
of vinegar after tentacles are removed to potentially prevent further immersion (45°C) for up to 90 minutes. This provides symptomatic
discharge of venom from nematocysts. The aim is to prevent relief while the limb is immersed, but pain often returns once
life-threatening envenoming. Vinegar is not a treatment for pain, removed. There is little evidence except experience and case reports
which should be treated with ice packs, oral analgesia and titrated to support hot water immersion. It is important to check the water
intravenous opioid analgesia, as required. The role of hot water temperature with an unaffected limb to prevent burns and it should
immersion in C. fleckeri stings remains unclear. Patients with severe not be used for more than 90 minutes. If hot water immersion and
Marine envenomations FOCUS
Table 2. Penetrating venomous marine injuries

Venomous fish Stingray Sea urchin Sponges
Clinical effects
Typically present as Injury more trauma than Pain generally not severe Local pain, itchiness,
puncture wounds with venom-induced. Local but multiple retained spines paraesthesia and numbness
localised pain. The pain is bleeding with swelling and Gradually occur over hours
dependent on how much oedema. Rare cases develop and can last for days
venom is injected necrosis with secondary
infection
First aid
Wash the wound site Wash out wound
Immerse in hot (45°C) water for up to 90 minutes
Further medical management
Due to the risk of a retained foreign body the wound(s) needs irrigation and debridement Simple analgesia
Consider local or regional analgesia to assist debridement
XR/US to exclude retained spine
Consider surgical referral for deep or truncal wounds, wounds involving joints/bones or
retained spines
Stonefish antivenom is Truncal injuries can cause These wounds may
available if simple measures severe haemorrhage require regular follow-up
do not control pain requiring urgent and review to ensure
resuscitation and theatre as all retained spines are
a major trauma removed and to prevent
infection
Although uncommon, observe for secondary infection for at least a week
Typical organisms are Vibrio spp. in marine injuries and Aeromonas spp. in freshwater
Commence antibiotics if any evidence of infection (once swabbed)
Figure 3. Catfish sting at the base of the index finger Figure 4. Sting ray injury to the back of the ankle
Photo by Geoffrey Isbister Photo by Geoffrey Isbister
oral analgesia are not sufficient then titrated intravenous opioids Secondary infection is the most important complication of
should be administered while arranging local anaesthesia at the penetrating marine injuries and is more likely to occur with unclean and
wound site or regional nerve block. These will also assist exploration larger wounds. Other complications are related to the site of the injury
and cleaning of the wound, but should not be used with hot water. (eg thoracoabdominal trauma). The use of prophylactic antibiotics is
All penetrating marine injuries require irrigation and cleaning. Larger controversial but is suggested for high-risk wounds. It is more important
wounds, those involving joints or containing debris, require surgical for the wounds to be irrigated and cleaned, and patients to be reviewed
review, exploration and debridement. every 1-2 days for the first week after discharge home.
REPRINTED FROM AUSTRALIAN FAMILY PHYSICIAN VOL. 44, NO. 1-2, JANUARY-FEBRUARY 2015 31
FOCUS Marine envenomations
Sea urchins
Sea urchins cause injury when they are trodden on or picked up. Sea
urchins cause a penetrating marine injury but rarely cause severe pain.
The major problem is multiple retained spines within the injury site,
which can cause persistent pain. Removal of the spines, especially
if deep, can be particularly problematic, and may require referral for
surgical management. Imaging of the wound site with X-ray and/or
ultrasonography is essential to locate any embedded spines and those
close to the surface should be removed.
Sponges
Sponge-related injuries are rare. Patients may present with local pain
or a tingling sensation that develops over hours, paraesthesia and/or
itch. In most cases symptoms persist for hours to 1 day. Patients injured
by fire sponges (Tedania spp.) can represent with erythema, swelling
and, sometimes, desquamation 2 weeks after the contact. First aid
includes ensuring the wound site is cleaned, simple analgesia and
antihistamines. There is no specific treatment.
Blue-ringed octopus
The blue-ringed octopus has tetrodotoxin in its saliva, which is injected
when it bites. In the majority of cases, the bite causes local pain, but
severe envenoming is similar to puffer fish poisoning, which causes
rapid-onset generalised paralysis requiring mechanical ventilation.
Most bites occur when the octopus is unwittingly picked up. First aid is
a pressure bandage with immobilisation and, if necessary, CPR.
Conclusion
Most marine envenomations are treated with simple first aid so
patients rarely seek medical assistance. Knowledge of the effective use
of hot-water immersion, appropriate use of vinegar and identification of
patients who require further referral to hospital or follow-up is vital for
GPs, particularly in coastal regions. Further expert toxicology advice can
be obtained from the Australian Poisons Information Centre on 13 11 26.
Authors
Ingrid Berling BMed, FACEM, Emergency Staff Specialist and Clinical
Toxicology Fellow, Clinical Toxicology and Pharmacology, Calvary Mater
Hospital, Newcastle, NSW. ingrid.berling@gmail.com
Geoffrey Isbister BSc, MBBS, FACEM, Professor, Clinical Toxicology
Reasearch Group, University of Newcastle, NSW
References
1. Winter KL, Isbister GK, Schneider JJ, Konstantakopoulos N, Seymour JE,
Hodgson WC. An examination of the cardiovascular effects of an ‘Irukandji’
jellyfish, Alatina nr mordens. Toxicol Lett 2008;179:118-23.
2. Loten C, Stokes B, Worsley D, Seymour JE, Jiang S, Isbister GK. A ran
domised controlled trial of hot water (45°C) immersion versus ice packs for
pain relief in bluebottle stings. Med J Aust 2006;184:329-33.
3. Currie BJ, Jacups SP. Prospective study of Chironex fleckeri and other box
jellyfish stings in the ‘Top End’ of Australia’s Northern Territory. Med J Aust
2005;183:631-36. correspondence afp@racgp.org.au
fi RACGP diabetes
Royal Australian College 0/General Practitioners d australia
General practice management

of type 2 diabetes
2016-18
racgp.org.au Healthy Profession.

Healthy Australia.
General practice management of type 2 diabetes: 2016-18
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.
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 (RACGP), Diabetes Australia
and their 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.
The Royal Australian College of General Practitioners. General practice management of type 2
diabetes: 2016-18. East Melbourne, Vic: RACGP, 2016.

Tel 03 8699 0414

Fax 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-453-5 (web)

ISBN 978-0-86906-454-2 (print)
Published September 2016.
The development of this handbook was principally funded by the RACGP with support from
Diabetes Australia.
© The Royal Australian College of General Practitioners and Diabetes Australia, 2016.
This work is subject to copyright. Unless permitted under the Copyright Act 1968, no part may be
reproduced in any way without The Royal Australian College of General Practitioners’ prior written
permission. Requests and enquiries should be sent to permissions@racgp.org.au
Supporting the education programs of Diabetes Australia
AstraZeneca SANOFI gÌhIÌotascular

Type 2 diabetes:
Goals for optimum
management
The table on the reverse

lists goals for optimum
management that all
people with type 2
diabetes should be
encouraged to reach.
This table has

been specifically
designed as a
card for you to
pull out and place
on your desk or
nearby for easy
reference.
diabetes
RACGP
Royal Australian College of General Practitioners d australia
Type 2 diabetes: Goals for optimum management
Encourage all people with type 2 diabetes to approach/reach these goals

Diet Advise eating according to Australian dietary guidelines, with attention to
quantity and type of food
If concerns are held regarding cardiovascular disease (CVD) risk, advise
individual dietary review
Body mass index (BMI) Therapeutic goal is 5-10% weight loss for people who are overweight or
obese with type 2 diabetes
Those with BMI >35 kg/m2and comorbidities, or BMI >40 kg/m2, greater
weight loss measures should be considered
Note that BMI is a difficult parameter to standardise between different
population groups
Physical activity At least 30 minutes of moderate physical activity on most if not all days
of the week (total >150 minutes/week)
Cigarette consumption 0 per day
Alcohol consumption Advise <2 standard drinks (20 g) per day for men and women
Blood glucose level (BGL) Advise 6-8 mmol/L fasting and 8-10 mmol/L postprandial
Ongoing self-monitoring of blood glucose is recommended for people
with diabetes using insulin, people using sulphonylureas or other medicines
that may cause hypoglycaemia, hyperglycaemia arising from illness, with
haemoglobinopathies, pregnancy or other conditions where data on
glycaemic patterns is required
Routine self-monitoring of blood glucose in low-risk patients who are
using oral glucose-lowering drugs (with the exception of sulphonylureas)
is not recommended
Glycated haemoglobin (HbA1c) Needs individualisation according to patient circumstances. Generally:
• <53 mmol/mol (48-58 mmol/mol)
• <7% (6.5-7.5%)
Allowing for normal variation in test accuracy, HbA1c results that range
between 6.5% and 7.5% (48 and 58 mmol/mol) would reflect this goal.
Total cholesterol <4.0 mmol/L Initiation of pharmacotherapy is dependent on the assessment of absolute
CVD risk (refer to the Australian absolute CVD risk calculator at www.
High-density lipoprotein
cvdcheck.org.au). This requires using multiple risk factors, which is
cholesterol (HDL-C) >1.0 mmol/L
considered more accurate than the use of individual parameters
Low-density lipoprotein Once therapy is initiated, the specified targets apply; however, these targets
cholesterol (LDL-C) <2.0 mmol/L should be used as a guide to treatment and not as a mandatory target
Non-HDL-C <2.5 mmol/L
Triglycerides <2.0 mmol/L
Blood pressure (BP) Lower BP targets may be considered for younger people and for secondary
<140/90 mmHg prevention in those at high risk of stroke, as long as treatment burden does
not increase risk
The target BP for people with diabetes and albuminuria/proteinuria remains
<130/80 mmHg. As always, treatment targets should be individualised and
monitored for side effects from medications used to lower BP
Urine albumin excretion Urine albumin-to-creatinine ratio (UACR):
• women: <3.5 mg/mmol
• men: <2.5 mg/mmol
Timed overnight collection: <20 mcg/min
Spot collection: <20 mg/L
Vaccination Consider immunisation against influenza and pneumococcal disease,

and the diphtheria-tetanus-acellular pertussis (dTpa) vaccine
General practice management
of type 2 diabetes
2016-18
General practice management of type 2 diabetes
2016-18
iii
Acknowledgements
The Royal Australian College of General Practitioners (RACGP) and Diabetes Australia
gratefully acknowledge the contributors listed below.
Clinical editors
Dr Gary Deed, Chair, RACGP Specific Interests Diabetes Network
Dr Evan Ackermann, Chair, RACGP Expert Committee - Quality Care
Contributors
Members of the RACGP Specific Interests Diabetes Network:
Dr Ian Arthur
Dr John Barlow
Dr Sugantha Jagadeesan
Dr Dev Kawol
Dr Gary Kilov
Dr Stephen Leow
Dr Jo-Anne Manski-Nankervis
Dr Roy Rasalam
Dr Ashraf Saleh
Dr Rosalie Schulz
Dr Anita Sharma
Diabetes Australia
Adjunct Professor Greg Johnson, Chief Executive Officer
Professor Sophia Zoungas

Professor Sophia Zoungas, President
iv 2016-18
Reviewers
Diabetes Australia Medical Education and Scientific Committee
Australian Diabetes Educators Association
Australasian Podiatry Council
Exercise and Sports Science Australia
Kidney Health Australia
NPS MedicineWise
Dr Ralph Audehm
2016-18
v
About the RACGP

The RACGP is Australia’s largest professional general practice organisation and
represents urban and rural general practitioners (GPs). We represent more than
33,000 members working in or towards a career in general practice and are proud that
more than 22,500 GPs in Australia have chosen to be a member of the RACGP.
The RACGP is responsible for defining the nature of the general practice discipline,
setting the standards and curriculum for education and training, maintaining the
standards for quality clinical practice, and supporting GPs in their pursuit of excellence
in patient care and community service. We offer our members access to a vast suite
of clinical resources, business support tools, education programs and are proud to
advocate for the general practice profession on behalf of all GPs.
The RACGP advocates and promotes high-quality diabetes management and care
through:
• regular articles in Australian Family Physician (AFP), the most widely read peer-
reviewed general practice journal in Australia, available at www.racgp.org.au/
publications/afp
• online general practice education provided by gplearning - the RACGP’s online
learning portal
• advocacy on key issues related to diabetes management
• partnership with Diabetes Australia in the production of this handbook
• giving members access to an extensive library collection, with many items available
electronically
• the flagship products Guidelines for preventive activities in general practice (Red
Book), Putting prevention into practice: Guidelines for the implementation of
prevention in the general practice setting (Green Book) and Smoking, nutrition,
alcohol, physical activity (SNAP): A population health guide to behavioural risk
factors in general practice, available at www.racgp.org.au/your-practice/guidelines
vi 2016-18
About Diabetes Australia

Diabetes Australia is the national body for people affected by all types of diabetes
and those at risk. We are committed to reducing the impact of diabetes.
Diabetes Australia combines the voice of consumers, health professionals

and researchers dedicated to diabetes.
Diabetes Australia has four key activities:
• National leadership - National policy and advocacy, and raising of awareness

of diabetes and its impact.
• Management of diabetes - Supporting and developing national self-management
programs, and promoting the best possible management of diabetes to help
prevent complications. These activities cover type 1, type 2 and gestational
diabetes.
• Prevention - Supporting and developing prevention policies and programs for both
the high-risk population (two million Australians at high risk) and the primary
prevention at a whole-of-population level.
• Research - Supporting, funding and promoting the best diabetes research.
Diabetes Australia is the Australian member of the International Diabetes Federation

(IDF), through which we work to reduce the impact of diabetes throughout the world,
particularly in the Western Pacific region.
Working with general practice

Diabetes Australia publishes the Diabetes Management Journal quarterly, to inform
GPs and health professionals in the field of diabetes management. This ensures
that the latest information on the optimum care for people with diabetes, and the
latest developments in diabetes management are delivered to frontline healthcare
providers. The Diabetes Management Journal is available through Diabetes Australia,
and professional membership of state and territory diabetes organisations at
www.diabetesaustralia.com.au
2016-18
National Diabetes Services Scheme

Diabetes Australia administers the National Diabetes Services Scheme (NDSS) in
conjunction with state and territory diabetes organisations. The NDSS is an Australian
Government initiative and has operated successfully for more than 28 years. The
NDSS provides universal access for all Australians with diabetes to subsidised
diabetes products, and education and support services. As at December 2015, there
were more than 1.2 million Australians registered with the NDSS.
Through the NDSS, people with diabetes can receive telephone support via the National
Helpline 1300 136 588, along with a range of diabetes information and educational
resources and programs targeted for type 1, type 2 and gestational diabetes.
Educational resources from Diabetes Australia

Membership of state and territory diabetes organisations provides access to a wide
range of educational resources and support for people with diabetes, their families
and carers. To find out more, visit www.diabetesaustralia.com.au and click on your
state or territory.
viii 2016-18
Acronyms
AACB Australasian Association of Clinical Biochemists
ABI ankle-brachial index
ACCORD Action to Control Cardiovascular Risk in Diabetes
ACE angiotensin converting enzyme
ACEI angiotensin converting enzyme inhibitor
ACR albumin-to-creatinine ratio
ADA American Diabetes Association
ADEA Australian Diabetes Educators Association
ADIPS Australian Diabetes in Pregnancy Society
ADS Australian Diabetes Society
ADVANCE Advance in Diabetes and Vascular Disease
AEP Accredited Exercise Physiologist
AHRQ Agency for Healthcare Research and Quality
AIHW Australian Institute of Health and Welfare
AN acanthosis nigricans
APD Accredited Practising Dietitian
ARA angiotensin-receptor antagonist
ARB angiotensin receptor blocker
AUSDRISK Australian type 2 diabetes risk assessment tool
BGL blood glucose level
BMI body mass index
BP blood pressure
CAD coronary artery disease
CCM Chronic Care Model
CDE Credentialled Diabetes Educator
CDM chronic disease management
CEITC Centre for Excellence in Indigenous Tobacco Control
CI confidence interval
CKD chronic kidney disease
COI conflict of interest
COPD chronic obstructive pulmonary disease
DBP diastolic blood pressure
DE diabetes educator
2016-18 IX
DKA diabetic ketoacidosis

DR dIabetIc retInopathy
DPP-4 dIpeptIdyl peptIdase-4
DPP-4i dIpeptIdyl peptIdase-4 InhIbItor
dTpa dIphtherIa-tetanus-acellular pertussIs
ECG electrocardIogram
eGFR estImated glomerular filtratIon rate
ELIXA EvaluatIon of LIxIsenatIde In Acute Coronary Syndrome
EMPA-REG EmpaglIflozIn, CardIovascular Outcomes, and MortalIty In
Type 2 DIabetes
EXAMINE ExamInatIon of CardIovascular Outcomes wIth AloglIptIn versus
Standard of Care
FBG fastIng blood glucose
FIELD Fenofibrate InterventIon and Event LowerIng In DIabetes
FRE FramIngham rIsk evaluatIon
GAD glutamIc acId decarboxylase
GDM gestatIonal dIabetes mellItus
GI glycaemIc Index
GIP glucose-dependent InsulInotropIc polypeptIde
GLP-1 glucagon-lIke peptIde-1
GLP-1 RA glucagon-lIke peptIde-1 receptor agonIst
GP general practItIoner
GPMP general practIce management plan
HAPO HyperglycaemIa and Adverse Pregnancy Outcome
HbA1c glycated haemoglobIn
HDL-C hIgh-densIty lIpoproteIn-cholesterol
HHS hyperosmolar hyperglycaemIc state
HOCM hypertrophIc obstructIve cardIomyopathy
HONC hyperosmolar nonketotIc coma
IA-2 InsulInoma antIgen-2
IADPSG InternatIonal AssocIatIon of the DIabetes and Pregnancy
Study Groups
IBD IrrItable bowel dIsease
IBS IrrItable bowel syndrome
IDF InternatIonal DIabetes FederatIon
IFG ImpaIred fastIng glucose
IGT ImpaIred glucose tolerance
x 2016-18
IMPROVE-IT Improved reduction of outcomes: Vytorin efficacy international trial

IUCD intrauterine contraceptive device
LADA latent autoimmune diabetes of adults
LDL-C low-density lipoprotein-cholesterol
LEADER Liraglutide Effect and Action in Diabetes: Evaluation
of Cardiovascular Outcome Results
MACE major adverse cardiovascular events
MI myocardial infarction
MODY maturity onset diabetes of the young
MR modified release
NDSS National Diabetes Services Scheme
NHMRC National Health and Medical Research Council
NICE National Institute for Health and Care Excellence
NICEQOF National Institute for Health and Clinical Excellence Quality
and Outcomes Framework
NIH National Institutes of Health
NPH Neutral Protamine Hagedorn
NPS National Prescribing Service
NSAID non-steroidal anti-inflammatory drug
NVDPA National Vascular Disease Prevention Alliance
OCP oral contraceptive pill
OGTT oral glucose tolerance test
OHA oral hypoglycaemic agent
OR odds ratio
ORIGIN Outcome Reduction with Initial Glargine Intervention
PAD peripheral arterial disease
PAID problem areas in diabetes
PBAC Pharmaceutical Benefits Advisory Committee
PBS Pharmaceutical Benefits Scheme
PCOS polycystic ovary syndrome
PHN Primary Health Network
PHQ-2 Patient health questionnaire-2
PHQ-9 Patient health questionnaire-9
PIP Practice Incentives Program
PROactive Prospective pioglitazone clinical trial in macrovascular events
2016-18
RACGP The Royal Australian College of General Practitioners

RANZCOG The Royal Australian and New Zealand College of Obstetricians
and Gynaecologists
RBG random blood glucose
RCPA The Royal College of Pathologists of Australasia
RR relative risk
RRR relative risk reduction
SAVOR-TIMI Saxagliptin Assessment of Vascular Outcomes Recorded in Patients
with Diabetes Mellitus Thrombolysis in Myocardial Infarction
SBP systolic blood pressure
SGLT2 sodium glucose co-transporter 2
SGLT2i sodium glucose co-transporter 2 inhibitor
SIGN Scottish Intercollegiate Guidelines Network
SIP Service Incentive Payments
SMBG Self-monitoring of blood glucose
SNAP Smoking, nutrition, alcohol, physical activity
SOE statement of evidence
STOP-NIDDM Study to Prevent Non-Insulin-Dependant Diabetes Mellitus
SU sulphonylureas
TBI toe-brachial index
TCA team care arrangement
TECOS Trial to Evaluate Cardiovascular Outcomes after Treatment
with Sitagliptin
TIA transient ischaemic attack
TZD thiazolidinedione
UACR Urine albumin-to-creatinine ratio
UKPDS UK Prospective Diabetes Study
2016-18
Contents
Acknowledgements iii
About the RACGP v
About Diabetes Australia vi
Working with general practice vi
National Diabetes Services Scheme (NDSS) vii
Educational resources from Diabetes Australia vii
Acronyms viii
Summary, explanation and source of recommendations xvi
Summary of recommendations xix
Updates in this edition xxxii
1. Introduction 1
1.1 Defining type 2 diabetes 2
1.2 A patient-centred approach 3
1.3 How to use these guidelines 3
2. Clinical governance - Sustaining and improving high standards of care 4
2.1 Applying a clinical governance framework to diabetes care 4
2.2 Models of high-quality healthcare 5
2.3 A quality improvement program relevant to diabetes care 9
3. Screening, risk assessment, case finding and diagnosis 11
3.1 Identifying risk of diabetes in asymptomatic patients 11
3.2 Case finding in patients with symptoms suggestive of diabetes 14
3.3 Impaired fasting glucose or impaired glucose tolerance 18
4. Preventing type 2 diabetes 21
5. Structured care and patient education 24
5.1 Patient-centred diabetes care 24
5.2 A structured diabetes care program consistent with the Chronic Care Model 26
5.3 Patient education and self management 28
6. Lifestyle modification 29
6.2 Diet 32
6.3 Weight 36
6.4 Smoking cessation 38
2016-18
6.5 Alcohol consumption 40

7. The person with diabetes - Assessment 41
7.1 Understanding the person - Initial assessment 41
7.2 What needs ongoing assessment? 44
7.3 What should be evaluated yearly? 46
8. Managing glycaemia 50
8.1 Glycaemic monitoring 50
8.2 Medication 55
8.2.1 General medication 55
8.2.2 Glucose-lowering agents 56
8.3 Insulin 64
9. Managing cardiovascular risk 72
10. Managing microvascular and other complications 79
10.1 Diabetic retinopathy 79
10.2 Other ophthalmological effects 81
10.3 Neuropathy 82
10.4 Nephropathy 85
10.5 Foot complications 89
11. Glycaemic emergencies 94
12. Diabetes, multimorbidity and medication complications 97
12.1 Multimorbidity 97
12.2 Medication complications 103
13. Diabetes and reproductive health 106
13.1 Polycystic ovary syndrome 106
13.2 Pregnancy with pre-existing diabetes 108
13.3 Gestational diabetes mellitus 112
13.4 Contraception 117
13.5 Sexual problems - Men 117
13.6 Sexual problems - Women 118
14. Management of other impacts of diabetes 119
14.1 Sick day management 119
14.2 Planned surgical procedures 122
14.3 Driving 123
14.4 Diving 125
14.5 Travel 125
2016-18
xv
15. Diabetes and end-of-life care 128

16. Issues under debate 131
Appendix A. Accessing government support for diabetes care in general practice 134
Appendix B. Structured patient-centred care plan - Example of a general practice
management plan and patient care plan 137
Appendix C. Problem areas in diabetes questionnaire 146
Appendix D. Patient health questionnaire-2 tool 149
Appendix E. Available glucose-lowering agents 150
Appendix F. Table of evidence and properties of glucose-lowering agents 156
Appendix G. Types of insulin available 161
Appendix H. Examples for insulin initiation and titration 162
Appendix I. Tools for assessing neuropathy, circulation and foot deformity 165
Appendix J. Detailed information on glycaemic emergencies 166
References 172
xvi 2016-18
Summary, explanation and source of

recommendations
The coding scheme for levels of evidence and grades of recommendation in this
publication are provided in this summary. Refer to Section 1.3. How to use these
guidelines for further explanation on how to use these recommendations.
National Health and Medical Research Council’s 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-RCT (ie 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 Opinions of respected authorities, based on clinical experience, descriptive studies
Point or reports of expert committees
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
2016-18
Scottish Intercollegiate Guidelines Network’s levels of

evidence and grades of recommendations (1999-2012)
Levels of evidence
Level Explanation
1++ High-quality meta-analyses, systematic reviews of randomised controlled trial (RCTs),
or RCTs with a very low risk of bias
1+ Well-conducted meta-analyses, systematic reviews or RCTs with a low risk of bias
1- Meta-analyses, systematic reviews of RCTs or RCTs with a high risk of bias
2++ High-quality systematic reviews of case control or cohort or studies
High-quality case control or cohort studies with a very low risk of confounding or bias
and a high probability that the relationship is causal
2+ Well-conducted case control or cohort studies with a low risk of confounding or bias
and a moderate probability that the relationship is causal
2- Case control or cohort studies with a high risk of confounding bias or chance
and significant risk that the relationship is not causal
3 Non-analytic studies (eg case reports, case series)
4 Expert opinion
A At least one meta-analysis, systematic review, or RCT rated as 1++, and directly
applicable to the target population; or
A body of evidence consisting principally of studies rated as 1+, directly applicable
to the target population, and demonstrating overall consistency of results
B A body of evidence including studies rated as 2++, directly applicable to the target
population, and demonstrating overall consistency of results; or
Extrapolated evidence from studies rated as 1++ or 1 +
C A body of evidence including studies rated as 2+, directly applicable to the target
population and demonstrating overall consistency of results; or
Extrapolated evidence from studies rated as 2++
D Evidence level 3 or 4; or
Extrapolated evidence from studies rated as 2+
Good Recommended best practice based on the clinical experience of the guideline
practice development group
points
xviii 2016-18
American Diabetes Association’s levels of evidence

Levels of
Explanation
evidence
A Clear evidence from well-conducted, generalisable randomised controlled trials (RCTs)
that are adequately powered, including:
• evidence from a well-conducted multicenter trial
• evidence from a meta-analysis that incorporated quality ratings in the analysis
Compelling non-experimental evidence (ie ‘all or none’ rule developed by the Centre
for Evidence-Based Medicine at the University of Oxford)
Supportive evidence from well-conducted RCTs that are adequately powered, including:
• evidence from a well-conducted trial at one or more institutions
• evidence from a meta-analysis that incorporated quality ratings in the analysis
B Supportive evidence from well-conducted cohort studies:
• evidence from a well-conducted prospective cohort study or registry
• evidence from a well-conducted meta-analysis of cohort studies
Supportive evidence from a well-conducted case-control study
C Supportive evidence from poorly controlled or uncontrolled studies:
• evidence from randomised clinical trials with one or more major or three or more
minor methodological flaws that could invalidate the results
• evidence from observational studies with high potential for bias (such as case
series with comparison with historical controls)
• evidence from case series or case reports
Conflicting evidence with the weight of evidence supporting the recommendation
E Expert consensus or clinical experience
2016-18
Summary of recommendations
Please note that the asterisk (*) that appears next to ‘Grade’ in the following
recommendations are explained in Summary, explanation and source of
recommendations.
3.1 Identifying risk of diabetes in asymptomatic

patients
Recommendations Reference Grade
*
Individuals should be screened for risk of diabetes every three 25 C
years from 40 years of age using AUSDRISK NHMRC, 2009
Individuals at high risk with any one of following risk factors: 25
- AUSDRISK score of 12 or more NHMRC, 2009
- all people with a history of a previous cardiovascular event
(acute myocardial infarction or stroke)
• should be screened with fasting blood glucose B

(or glycated haemoglobin [HbA1c])
• every three years
Individuals at high risk with impaired glucose tolerance test or 25 C
fasting glucose (not limited by age) should be screened: NHMRC, 2009
• with fasting blood glucose (or HbA1c) B
• every 12 months C
Risk assessment should begin from 18 years of age in Aboriginal 25 Practice
and Torres Strait Islander peoples NHMRC, 2009 Point
xx 2016-18
4. Preventing type 2 diabetes

*
Lifestyle modifications that focus on increased physical activity, 42 A
dietary change and weight loss should be offered to all individuals NHMRC, 2009
at high risk of developing type 2 diabetes
Structured diabetes prevention programs are available
Bariatric surgery can be considered in selected morbidly 42 C
obese individuals (based on weight alone or the presence of NHMRC, 2009
comorbidities) who are at high risk of type 2 diabetes
Individuals who are at high risk of diabetes should be identified 42 C
through the use of risk assessment tools NHMRC, 2009
5.1 Patient-centred diabetes care

*
A patient-centred communication style that incorporates patient 19 B
preferences, assesses literacy and numeracy, and addresses American
cultural barriers to care should be used Diabetes
Association, 2015
5.2 A structured diabetes care program consistent

with the Chronic Care Model
*
Care should be aligned with components of the Chronic Care 56 A
Model (CCM) to ensure productive interactions between a prepared American
proactive practice team and an informed activated patient Diabetes
Association, 2016
When feasible, care systems should support team-based care, 56 B
community involvement, patient registries and embedded American
decision-support tools to meet patient needs Diabetes
Association, 2016
Treatment decisions should be timely and based on evidence 56 B
based guidelines that are tailored to individual patient preferences, American
prognoses and comorbidities Diabetes
Association, 2016
2016-18
5.3 Patient education and self management

*
All people with type 2 diabetes should be referred for structured 42 A
diabetes patient education NHMRC, 2009
Diabetes education should be delivered in groups or individually 42 A
NHMRC, 2009
Diabetes education should be culturally sensitive and tailored 42 B
to the needs of socioeconomically disadvantaged populations NHMRC, 2009

*
People with type 2 diabetes of all ages benefit from accumulating 64 B
30 minutes or more of moderate physical activity on most if not all Briffa T et al,
days of the week 2006
Exercise and physical activity (involving aerobic and/or resistance 65 D
exercise) should be performed on a regular basis SIGN, 2014
6.2 Diet
*
Consumption of cereal foods (especially three serves a day of 71 B
wholegrains) is associated with reduced risk of type 2 diabetes NHMRC, 2013
Consumption of at least one and a half serves of dairy foods (eg 71 C
milk, yoghurt, cheese) per day is associated with reduced risk of NHMRC, 2013
type 2 diabetes
xxii 2016-18
6.3 Weight
*
Adults with impaired fasting glucose, impaired glucose tolerance 78 A
or diabetes can be strongly advised that the health benefits of NHMRC, 2013
5-10% weight loss include prevention, delayed progression or
improved control of type 2 diabetes
For adults with body mass index (BMI) >40 kg/m2, or adults with 78 A
BMI >35 kg/m2 and comorbidities that may improve with weight NHMRC, 2013
loss, bariatric surgery may be considered, taking into account the
individual situation
Use BMI to classify overweight or obesity in adults 78 B
NHMRC, 2013
For adults, use waist circumference, in addition to BMI, to refine 78 C
assessment of risk of obesity-related comorbidities NHMRC, 2013
6.4 Smoking cessation

*
Smoking cessation should be a major focus of the management 86 A
of people with smoking-related diseases RACGP, 2011
All smokers should be offered brief advice to quit smoking 86 A
RACGP 2011
6.5 Alcohol consumption

*
People with diabetes can take alcohol in moderation as part 65 B
of a healthy lifestyle, but should aim to keep within the target SIGN, 2014
consumption recommended for people without diabetes
2016-18
8.1 Glycaemic monitoring

*
Glycated haemoglobin (HbA1c) measurement should be used to 96 A
assess long-term blood glucose control NHMRC, 2009
Self-monitoring of blood glucose is recommended for patients 65 B
with type 2 diabetes who are using insulin, where patients have SIGN, 2014
been educated in appropriate alterations in insulin dose
(Refer to Self-monitoring of blood glucose under Section 8.2.
Medication for examples of instances when self-monitoring of
blood glucose may be considered)
Routine self-monitoring of blood glucose in people with type 2 65 B
diabetes who are using oral glucose-lowering drugs (with the SIGN, 2010
exception of sulphonylureas) is not recommended
In practice
*
Blood glucose control should be optimised because of its 96 A
beneficial effects on the development and progression of NHMRC, 2009
microvascular complications
The potential harmful effects of optimising blood glucose control 96 A
in people with type 2 diabetes should be considered when setting NHMRC, 2009
individual glycaemic targets
The general glycated haemoglobin (HbA1c) target in people with 96 A
type 2 diabetes is <53 mmol/mol (<7%). Adjustments to diabetes NHMRC, 2009
treatment should be considered when HbA1c is above this level
Targets for self-monitoring of blood glucose levels are 6-8 mmol/L for 96 C
fasting and preprandial, and 6-10 mmol/L for two hour postprandial NHMRC, 2009
2016-18
8.2.1 General medication

*
Care should be taken to address the potential harmful effects 96 A
of optimising blood glucose control when setting individual NHMRC, 2009
glycaemic targets
Interventions to achieve target glycated haemoglobin 96 A

(HbA1c) should begin with lifestyle modification followed by NHMRC, 2009
pharmacological options selected on the basis of individual clinical
circumstances, side effects and contraindications
Blood glucose control should be optimised because of its 96 A

beneficial effects on the development and progression of NHMRC, 2009
microvascular complications
9. Managing cardiovascular disease risk

*
Patients with pre-existing cardiovascular disease (CVD) are at 149 A
high risk NVDPA, 2012
All adults with type 2 diabetes and known prior CVD (except 150 A
haemorrhagic stroke) should receive the maximum tolerated dose Baker IDI, 2015
of a statin, irrespective of their lipid levels
Note: The maximum tolerated dose should not exceed the
maximum available dose (eg 80 mg atorvastatin, 40 mg
rosuvastatin)
Adults with any of the following conditions do not require absolute 149 D
CVD risk assessment using the Framingham Risk Equation NVDPA, 2012
because they are already known to be at clinically determined
high risk of CVD:
• Diabetes and aged >60 years
• Diabetes with microalbuminuria (>20 mcg/min or urine
albumin-to-creatinine ratio [UACR] >2.5 mg/mmol for men,
and >3.5 mg/mmol for women)
• Moderate or severe chronic kidney disease (CKD) (persistent
proteinuria or estimated glomerular filtration rate [eGFR]
<45 mL/min/1.73 m2)
• A previous diagnosis of familial hypercholesterolaemia
• Systolic blood pressure >180 mmHg or diastolic blood
pressure >110 mmHg
• Serum total cholesterol >7.5 mmol/L
2016-18
xxv
Calculate risk level using an evidence-based tool: 149 B

• National Vascular Disease Prevention Alliance charts, NVDPA, 2012
www.cvdcheck.org.au
• New Zealand Cardiovascular Risk charts,
www.health.govt.nz/publications
• Heart Foundation NZ, www.knowyournumbers.co.nz
Aboriginal and Torres Strait Islander peoples are generally 149 B
assumed to be at higher risk NVDPA, 2012
Antihypertensive medication to manage

cardiovascular risk
*
Blood pressure-lowering therapy in people with diabetes should 149 A
preferentially include an angiotensin converting enzyme inhibitor NVDPA, 2012
(ACEI) or angiotensin receptor blocker (ARB)
If monotherapy does not sufficiently reduce blood pressure, add
one of the following:
• Calcium channel blocker 149 B
NVDPA, 2012
• Low-dose thiazide or thiazide-like diuretic 149 C
NVDPA, 2012
Lipid medication to manage cardiovascular risk

*
Use statins as first-line therapy 149 A
NVDPA, 2012
xxvi 2016-18
Antithrombotic therapy
*
All adults with type 2 diabetes and known prior cardiovascular 150 A
disease should receive long-term antiplatelet therapy unless there Baker IDI, 2015
is a clear contraindication
All adults with type 2 diabetes and a history of ischaemic stroke 150
or transient ischaemic attack should receive: Baker IDI, 2015
• low-dose aspirin, or A
• clopidogrel, or A
• combination low-dose aspirin and extended-release B
dipyridamole
All adults with type 2 diabetes and recent acute coronary 150
syndrome and/or coronary stent should receive, for 12 months Baker IDI, 2015
after the event or procedure:
• combination low-dose aspirin and clopidogrel, or B
• combination low-dose aspirin and prasugrel, or B
• combination low-dose aspirin and ticagrelor C
All adults with type 2 diabetes and a history of coronary artery 150
disease, but no acute event in the past 12 months should receive: Baker IDI, 2015
• long-term low-dose aspirin, or A
• long-term clopidogrel if intolerant to aspirin B
In the presence of atrial fibrillation or other major risk factors for 150 Practice
thromboembolism, there should be consideration of anticoagulant Baker IDI, 2015 Point
therapy according to other relevant guidelines
2016-18
10.1 Diabetic retinopathy

*
Ensure that all people with diabetes have a dilated fundus 158 None
examination and visual acuity assessment at the diagnosis NHMRC, 2008 provided
of diabetes and at least every two years (Level I
evidence)
Examine higher risk patients (eg longer duration of diabetes, 158 None
or poor glycaemic control, blood pressure or blood lipid control) NHMRC, 2008 provided
without diabetic retinopathy at least annually (Level I
evidence)
Conduct annual screening for Aboriginal or Torres Strait Islander 158 None
peoples with diabetes NHMRC, 2008 provided
(Level IV
evidence)
10.3 Neuropathy
Diabetic peripheral neuropathy

*
All patients should be screened for distal symmetric 19 B
polyneuropathy starting at diagnosis of type 2 diabetes and American
at least annually thereafter, using simple clinical tests Diabetes
Association, 2015
Antidepressants, including tricyclics, duloxetine and venlafaxine 65 A
should be considered for the treatment of patients with painful SIGN, 2014
diabetic peripheral neuropathy
Anticonvulsants, including pregabalin and gabapentin, should 65 A
be considered for the treatment of patients with painful diabetic SIGN, 2014
peripheral neuropathy
xxviii 2016-18
10.4 Nephropathy
*
Assessment
Kidney status in people with type 2 diabetes should be assessed
by:
• annual screening for albuminuria (note that dipstick urine test 166 B
is not adequate to identify albuminuria) NHMRC, 2009
• annual estimated glomerular filtration rate (eGFR; in mL/ 166 B
min/1.73 m2) NHMRC, 2009
Management
Reducing the risk or slowing the progression of nephropathy can
be achieved by:
• blood glucose control should be optimised aiming 166 A
for a general glycated haemoglobin (HbA1c) target <7% NMHRC 2009
• optimising blood pressure control 166 A
NMHRC 2009
In people with type 2 diabetes and microalbuminuria or 166 A
macroalbuminuria, angiotensin receptor blocker (ARB) or NHMRC, 2009
angiotensin converting enzyme inhibitor (ACEI) antihypertensive
should be used to protect against progression of kidney disease
People with type 2 diabetes should be informed that smoking 166 B
increases the risk of chronic kidney disease NHMRC, 2009
People with diabetes and microalbuminuria are considered 149 D
at high cardiovascular disease risk, and should be treated NVDPA, 2012
with multifactorial interventions (refer to Chapter 9. Managing
cardiovascular risk)
2016-18 XXiX
10.5 Foot complications

*
Assess all people with diabetes and stratify their risk of developing 160 C
foot complications NHMRC, 2011
Assess risk stratification by inquiring about previous foot ulceration 160 C
and amputation plus falls risk, visually inspecting the feet for NHMRC, 2011
structural abnormalities and ulceration, assessing for neuropathy
using either the neuropathy disability score or a 10 g monofilament
and palpating foot
People assessed as having intermediate-risk or high-risk feet 160 C
should be offered a foot protection program. This includes foot NHMRC, 2011
care education, podiatry review and appropriate footwear
Pressure reduction, otherwise referred to as redistribution 160 B
of pressure or offloading, is required to optimise the healing NHMRC, 2011
of plantar foot ulcers
Offloading of the wound can be achieved with the use of a total 160 B
contact cast or other device rendered irremovable NHMRC, 2011
People with diabetes-related foot ulceration are best managed 160 C
by a multidisciplinary foot care team NHMRC, 2011
11. Glycaemic emergencies

*
in people with diabetes should be considered when setting NHMRC, 2009
Improving blood glucose control increases the risk 96 None
of hypoglycaemia NHMRC, 2009 provided
(Level I
evidence)
xxx 2016-18
13.2 Pregnancy with pre-existing diabetes

*
Pre-pregnancy glycaemic control should be maintained as close 65 C
to the non-diabetic range as possible, taking into account risk of SIGN, 2014
maternal hypoglycaemia
All women with diabetes should be prescribed *high-dose pre 65 B
pregnancy folate supplementation, continuing up to 12 weeks’ SIGN, 2014
gestation
All women with pre-gestational diabetes should be encouraged 65 D
to achieve excellent glycaemic control1" SIGN, 2014
Postprandial glucose monitoring should be carried out in pregnant 65 C
women with type 1 or 2 diabetes SIGN, 2014
Postprandial glucose monitoring should be carried out in pregnant
women with gestational diabetes and may be considered in
pregnant women with type 1 or 2 diabetes
Pre-pregnancy care provided by a multidisciplinary team 65 C
is strongly recommended for women with diabetes SIGN, 2014
*5 mg of folate
tGlycated haemoglobin (HbA1c) <48 mmol/mol (6.5%) and consider stabilisation using metformin
and/or insulin to achieve glycaemic targets. However, metformin has a category C rating in
pregnancy. Continuation or initiation of metformin therapy should be considered only following full
disclosure to the patient and under specialist supervision. Sulphonylureas may be associated with
adverse neonatal outcomes and are thus best avoided66,229-232
Management
*
Pregnant women with gestational diabetes mellitus should be 65 A
offered dietary advice and blood glucose monitoring, and be SIGN, 2014
treated with glucose-lowering therapy depending on target values
for fasting and postprandial targets
Follow-up of patients with a history

of gestational diabetes mellitus
*
Women with a history of gestational diabetes mellitus should 19 E
receive a postpartum oral glucose tolerance test at 6-12 weeks American
Diabetes
Association, 2015
2016-18 XXXi
14.1 Sick day management

*
Patients should be educated to develop a sick day management 261 None
plan after initial diagnosis. This plan should be reviewed at regular Australian provided
intervals Diabetes
Educators
Association,
2014
Assist in the development of a sick day care plan and preparation 261 None
of a home sick day management kit for patients to use during Australian provided
episodes of sickness Diabetes
Educators
Association,
2014
15. Diabetes and end-of-life care

*
To minimise the risks of hypoglycaemia and metabolic compensation, 265 None
a blood glucose range of 6-15 mmol/L is appropriate for most Diabetes UK, provided
palliative care patients
2013
Maintain glycated haemoglobin (HbA1c) at no lower than 58 mmol/mol 265 None
(7.5%) if on hypoglycaemic medication depending on the individual’s Diabetes UK, provided
life expectancy, as HbA1c will be less relevant in patients with months
2013
or days left to live
xxxii 2016-18
Updates in this edition

Chapter
Summary of recommendations This has been moved to the front of the handbook
4. Preventing type 2 diabetes This chapter references interventions in clinical trials
that may assist general practitioners (GPs) understand,
and consider implementing with, patients at high risk of
diabetes to prevent progress to type 2 diabetes
6. Lifestyle modification This chapter has been reviewed and includes some
practical updates for GPs to implement in patients
diagnosed with type 2 diabetes
7. The person with diabetes - Revision on practice guidelines on clinical assessment
Assessment is included
8. Managing glycaemia The new Australian blood glucose treatment algorithm
developed in collaboration with the Australian Diabetes
Society is now included (Figure 4)
A table to guide clinical considerations of glucose
lowering agents is also newly embedded (Table 6)
A revised insulin titration algorithm is included for
premixed insulins
9. Managing cardiovascular risk Updated information on antithrombotic therapy including
aspirin
10. Managing microvascular and other Expanded section on foot complications
complications
11. Glycaemic emergencies Expanded information on the management of diabetes
glycaemic emergencies - including Appendix J. Detailed
information on glycaemic emergencies
13. Diabetes and reproductive health Revision of advice with emerging evidence, both in
pregnancy with existing diabetes and gestational diabetes
16. Issues under debate Revision of blood pressure targets is discussed, based
upon new evidence particular to diabetes
Possible new criteria for screening for diabetes in at-risk
populations are discussed
Appendices Australian type 2 diabetes risk assessment tool
The following appendices from the (AUSDRISK)
2014-15 edition have been removed General outline of management of hyperosmolar
nonketotic coma from glycaemic emergencies
Potential drug interactions
2016-18
1
1. Introduction
Diabetes is a national health priority. The Australian National Diabetes Strategy 2016
2020 was released by the Australian Government in November 2013. The number
of people with type 2 diabetes is growing, most likely the result of rising overweight
and obesity rates, lifestyle and dietary changes, and an ageing population. Within 20
years, the number of people in Australia with type 2 diabetes may increase from an
estimated 870,000 in 2014, to more than 2.5 million.1 The most socially disadvantaged
Australians are twice as likely to develop diabetes.
If left undiagnosed or poorly managed, type 2 diabetes can lead to coronary artery
disease (CAD), stroke, kidney failure, limb amputations and blindness. The early
identification and optimal management of people with type 2 diabetes is therefore
critical. General practice has the central role in type 2 diabetes management across
the spectrum, from identifying those at risk right through to caring for patients at the
end of life. These guidelines give up-to-date, evidence-based information tailored for
general practice to support general practitioners (GPs) and their teams in providing
high-quality management.1
In the development of the 2016-18 edition of General practice management of type 2

diabetes, The Royal Australian College of General Practitioners (RACGP) has focused
on factors relevant to current Australian clinical practice. The RACGP has used the
skills and knowledge of your general practice peers who have an interest in diabetes
management and are members of the RACGP Specific Interests Diabetes Network.
This publication has been produced in accordance with the rules and processes
outlined in the RACGP’s conflict of interest (COI) policy. The RACGP’s COI policy is
available at www.racgp.org.au/support/policies/organisational
This edition represents 19 years of a successful relationship between the RACGP

and Diabetes Australia. We acknowledge the support of the RACGP Expert
Committee - Quality Care, the Medical Education and Scientific Committee of
Diabetes Australia, and RACGP staff in the development of these guidelines.
2 2016-18
1.1 Defining type 2 diabetes

Diabetes is a group of disorders and the 10th leading cause of deaths in Australia.
There are four clinical classes of diabetes:1
• Type 1 diabetes - Results from B-cell destruction due to an autoimmune process

usually leading to insulin deficiency
• Type 2 diabetes - Results from a progressive insulin secretory defect on the

background of insulin resistance
• Gestational diabetes mellitus (GDM) - Defined as glucose intolerance with
onset or first recognition during pregnancy
• Other specific types of diabetes (Section 3.3. Impaired fasting glucose or

impaired glucose tolerance) - Due to other causes such as genetic defects in
B-cell function, genetic defects in insulin action, diseases of the exocrine pancreas
(eg cystic fibrosis), and drug-induced or chemical-induced causes (eg treatment
of human immunodeficiency virus/acquired immune deficiency syndrome [HIV/
AIDS] or after organ transplantation)
Type 2 diabetes is a largely preventable, chronic and progressive medical condition

that results from two major metabolic dysfunctions: insulin resistance and then
pancreatic islet cell dysfunction causing a relative insulin deficiency. In an individual,
these occur due to modifiable lifestyle-related risk factors interacting with non-
modifiable and genetic risk factors.
The relative insulin deficiency leads to chronic hyperglycaemia and multiple

disturbances in carbohydrate, protein and fat metabolism including:
• B-islet cell dysfunction, failure of response to insulin signalling and increased islet
cell apoptosis
• a-cell dysfunction with elevated glucagon levels
• resultant disorders of hepatic gluconeogenesis and insulin resistance with elevated
glucose production
• muscle cell insulin resistance with decreased glucose uptake
• kidney adaptation with altered gluconeogenesis and increased glucose
reabsorption via increased sodium glucose transporter protein activity
• diminished incretin hormonal production or resistance
• maladaptive cerebral hormonal responses to insulin and appetite
• increased lipolysis with elevated free fatty acids.
2016-18
3
1.2 A patient-centred approach

Throughout these guidelines we refer to patient-centred care.
The concept of patient-centred care incorporates the patient’s experience of care and
patients as partners in their healthcare.2 In practice, this means providing care that is
‘respectful of and responsive to individual patient preferences, needs and values, and
ensures that patient values guide all clinical decisions’3 and supports self management.
Understanding a patient’s diabetes-related (and comorbidity) experiences can improve

practitioner-patient communication and help the GP understand their patient’s priorities
for education, resources and management. This is essential for building and adapting
diabetes management plans to be consistent with an individual patient’s needs.
1.3 How to use these guidelines

These guidelines have been designed to provide pragmatic, evidence
based recommendations for use in general practice, and adopt the most
recent recommendations from organisations including the National Health
and Medical Research Council (NHMRC), Scottish Intercollegiate Guidelines
Network (SIGN), American Diabetes Association (ADA) and other relevant
sources. The recommendations tables include the reference or source of each
recommendation, and the grade of recommendation. In cases where these are not
available or current, results of systematic reviews and primary research studies have
been considered to formulate the overall recommendation. References to support
these recommendations are included.
In each section, where possible, information is presented as:
• recommendations
• clinical context (or what you need to know)
• in practice (or what you can do).
Information specific to the Aboriginal and Torres Strait Islander population is
highlighted in boxed text. Recommendations in some areas are different for Aboriginal
and Torres Strait Islander patients. It is therefore important to identify, record and
report the Aboriginal and Torres Strait Islander status of patients.
The RACGP has a position paper outlining the processes of identification, available
at www.racgp.org.au/yourracgp/faculties/aboriginal
Refer to Summary, explanation and source of recommendations.

4 2016-18
2. Clinical governance - Sustaining

and improving high standards of care
The RACGP defines clinical governance as a framework through which clinicians
and health service managers are jointly responsible and accountable for patient safety
and quality care.4
Within this framework are embedded the principles of recognisably high standards
of care, transparent responsibility and accountability for maintaining those standards,
and a constant dynamic of quality improvement.5
2.1 Applying a clinical governance framework

to diabetes care
Achieving equitable, safe, effective and high-quality care for patients across the
spectrum of type 2 diabetes is no small task. It requires a coordinated interaction
between patients, healthcare providers and the healthcare system, with a focus on
improving the patient’s experience and outcomes throughout the continuum of care.
Each of these elements requires systems and support. For example, comprehensive
care for diabetes starts with prevention: through timely identification of at-risk
individuals, education and support, it is possible to prevent or delay the onset of type
2 diabetes. The key is implementing risk assessment strategies and subsequently
having the resources and communication strategies to effect change in patients’
lifestyles. These need to operate and be supported at local and national levels.
Effective leadership is essential. Owners of a general practice (and others involved

in its corporate governance) play an active role in developing these systems by
cultivating a culture focused on clinical quality and patient-centred care.
In practice
Applying a clinical governance approach to your general practice means focusing on:
• patients - providing high-quality, effective and ongoing care, and ensuring good
communication and support to enable patients to be informed and involved
• healthcare teams - ensuring adequate training and resources for the practice
team and developing working relationships with all potential members of a diabetes
team, including endocrinologists and Credentialled Diabetes Educators (CDEs)
2016-18
5
• quality improvement - managing risk, ensuring high standards of care, using

clinical audits, and creating and maintaining an environment that supports clinical
excellence
• information - ensuring high-quality information systems, management and sharing
that are the backbone to integrated care.
2.2 Models of high-quality healthcare
The medical home

Quality and safety in diabetes care start with coordinated, ongoing and comprehensive
primary healthcare. Primary care is the central component of care across the spectrum
of patients with diabetes: those dealing with a new diagnosis, managing (often
multiple) medications, with complications of diabetes and multimorbidity, through
to patients at the end of life.
A general practice chosen by a patient to provide ongoing, comprehensive, patient-

centred care is known as a ‘medical home’. The medical home is responsible for
the patient’s healthcare across their entire health journey, and this approach results
in better health outcomes for patients and their families.6 Australian general practice
encapsulates the medical home model.7
This model has measurable benefits, including improved continuity of patient care,8
and improved quality and cost effectiveness of care for patients with a chronic disease.9
Medical homes reduce disparities in access to quality care among traditionally difficult to
reach groups,10,11 which leads to improved overall population health12 and lower overall
healthcare spending.13-15 The RACGP’s Vision for general practice and a sustainable
healthcare system (www.racgp.org.au/vision) is based on the patient-centred medical
home model and is informed by RACGP’s definition of quality general practice.
A model for chronic disease management

For patients with type 2 diabetes across the spectrum, structured care programs that
are easy to implement, well supported and meet the needs of the individual are required.
These programs bring together healthcare teams, evidence-based guidelines, useful
support tools and good systems to support patients throughout their journey.
Refer to Chapter 5. Structured care and patient education for more information.
6 2016-18
The Chronic Care Model (CCM), developed by the MacColl Institute

(www.improvingchroniccare.org/index.php?p=The_Chronic_Care_Model&s=2)
identifies the fundamental elements of a healthcare system that supports high-quality
chronic disease care:
• health system (organisation and mechanisms)

• delivery system design
• decision support
• clinical information systems
• self-management support
• the community.
The CCM has been shown to be an effective framework for improving the quality
of diabetes care.16
In practice
Health system
GPs can help create a health system that facilitates easy and appropriate access
to care for people with diabetes by reducing barriers associated with accessing,
and maintaining healthcare across primary care and other health tiers.
General practices can access the Australian Government system level incentives to
support diabetes care. This support is provided through Medicare Benefits Schedule
(MBS) payments to GPs, nurses, allied health professionals and general practices.
These include the Chronic Disease Management (CDM) items (formerly known as
Enhanced Primary Care), which provide support for developing management plans
and organising team care.
Patients have experienced improvements in process and clinical outcomes with these
management plans and team care arrangements.17
ABORIGINAL AND TORRES STRAIT ISLANDER POINT

It is recommended that all practices identify patients of Aboriginal or Torres Strait
Islander descent. Registering patients also allows access to the Closing the
Gap Pharmaceutical Benefits Scheme (PBS) co-payment, earlier interventions
(as determined by PBS criteria) and access to specific MBS item numbers.
Refer to Appendix A. Accessing government support for diabetes care in general

practice.
2016-18
7
Delivery system design

Diabetes care requires a proactive preventive approach to keeping patients as healthy
as possible rather than episodic or reactive intervention when complications arise. An
effective system to achieve this will engage patients with a range of healthcare providers
using good communication and information technology.17
Collaborative multidisciplinary teams are best suited to provide diabetes care, facilitate
patient self management, identify those patients who require individualised support and
coordinated case management.18,19 Using multidisciplinary care and engaging the wider
team have been shown to improve outcomes for people with diabetes.20
A team approach provides flexible and comprehensive care to meet individual patient
needs. Roles within a general practice team are not mutually exclusive, and clear
guidance is required to identify the team member primarily responsible for key activities.
Teamwork success may be supported by workflow coordination and management of
structured care programs (care planning).
Decision support
Accessible guidelines for diabetes management and associated issues (eg management
and prevention guidelines for all types of diabetes; refer to Austroads and National
Transport Commission [www.austroads.com.au/drivers-vehicles/assessing-fitness-to-
drive] Therapeutic Guidelines Limited [TGL] antibiotic guidelines [https://tgldcdp.tg.org.
au/etgAccess]) are required for GPs to make decisions about diabetes care that is
consistent with evidence and meets regulations.
Having electronic records also facilitates decision to support this goal by ensuring
prescription error checking against medication allergy, and drug-drug and drug
disease interactions, creating diabetes clinical measures and databases, facilitating risk
assessment such as cardiovascular disease (CVD) risk scoring and thus providing a
basis for data collection linked to quality improvement processes.
Clinical information and recall and reminder systems

Structured diabetes care programs are based upon good information management
systems (eg registers, recalls and reminders) combined with risk factor, complication
assessment management and comorbidity strategies. Management plans are most
effective when they involve a team care arrangement and are reviewed regularly.17
8 2016-18
Structured recall systems ensure a patient receives formal reviews at regular intervals.
Several studies have shown that computerised recall systems, monitoring and
reminding patients and practice team members about appointments, investigations
and referrals, improve diabetes care.21-24 Computerised systems can also provide
automated reminders, generate mailing lists of those overdue for preventive activities
and help minimise repeat data entries.
Combining a reminder system with a practice register ensures that the reminder
system is systematic and targeted. This can prevent patients with diabetes missing
out on basic care such as screening for retinopathy and foot care. Depending on the
complexity of individual patient needs, structured recall may occur on a three-month to
12-month basis.
For example, during a consultation, the GP and patient make key management
decisions or team care changes dependent on care plan progress. A recall is added in
a time frame suited to the patient’s needs. This cycle then repeats. Another example is
where a structured recall may ensure that all necessary investigations are completed
before the next practice visit by the patient.
Self-management support
The aim of self-management support is to facilitate skills-based learning and patient
empowerment. Diabetes self-management, education and support programs improve
understanding of, and belief in, the importance of those factors that influence diabetes
(eg goals, complications, living with a chronic illness), and thus might be able to be
modified by patients’ behaviours and actions (eg self-monitoring of blood glucose
[SMBG], dietary choices and physical activity). Other factors, such as medication(s),
foot care, individual complication risk assessment and understanding of laboratory
results, may need engagement with a health professional team.
The community
Community resources and policies can be harnessed to improve the quality of the
practice service including:
• National Diabetes Services Scheme (NDSS)

• Diabetes Australia resources
• Primary Health Network (PHN) collaborations
• local endocrinology specialist services - private and tertiary-level care
• allied health support teams including CDEs, Accredited Practising Dietitians (APDs)
and Accredited Exercise Physiologists (AEPs)
• partnerships with universities or hospitals in providing diabetes care
2016-18
9
• medication advice at pharmacies

• diabetes support groups, diabetes support applications and online support groups
• community health centres.
Translated diabetes resources are available from the NDSS diabetes portal, which
includes resources from Diabetes Australia, Diabetes Australia state and territory
agents, and non-government organisations (http://multiculturalportal.ndss.com.au).

Some PHNs run chronic care coordination programs for Aboriginal and Torres
Strait Islander patients that can help access practical help in attending a range
of specialist and allied health appointments.
2.3 A quality improvement program relevant

to diabetes care
Accreditation against the RACGP’s Standards for general practices, 4th edn, requires
a commitment to quality improvement from a general practice. This can involve
examining practice structures, systems and clinical care. Using practice data to
identify areas in need of improvement is one way to achieve this.
Clinical audit software tools are widely available to assist practices to evaluate clinical
outcomes for patients with diabetes. Audit information can be used to improve
management of patients with diabetes on many levels. For example, patients can be
identified on the basis of:
• incomplete information such as no smoking status, no recent blood pressure (BP)

or glycated haemoglobin (HbA1c) reading
• Aboriginal and Torres Strait Islander status
• the presence of other risk factors such as HbA1c >75 mmol/mol (9%),
microalbuminuria or comorbidities
• outstanding diabetes cycle of care items
• recent hospitalisation
• existing complications or comorbidities.
To help practices start quality improvement activities, the RACGP is developing

a core set of clinical indicators to support care evaluation. This is supported with
the RACGP’s Practice guides and tools for clinical indicators, available at
www.racgp.org.au/your-practice/business/tools/support
101 General practice management of type 2 diabetes
2016-18
Four of these indicators are relevant to diabetes care:
Indicator Description
number
1 Practice infrastructure to support safety and quality of patient care
5 Assessment of absolute cardiovascular risk
12 Screening for retinopathy in patients with diabetes
13 Screening for nephropathy in high-risk patients (including diabetes)
Use of clinical indicators to assess care is advised but entirely voluntary.

2016-18
11
3. Screening, risk assessment, case finding

and diagnosis
3.1 Identifying risk of diabetes in asymptomatic

patients
*
Individuals should be screened for risk of diabetes every three 25 C
years from 40 years of age using AUSDRISK NHMRC, 2009
Individuals at high risk with any one of following risk factors: 25

- AUSDRISK score of 12 or more NHMRC, 2009
- all people with a history of a previous cardiovascular
event (acute myocardial infarction or stroke)
• should be screened with fasting blood glucose (or glycated B

haemoglobin [HbA1c])
• every three years C

Individuals at high risk with impaired glucose tolerance test 25
or fasting glucose (not limited by age) should be screened: NHMRC, 2009
• with fasting blood glucose (or HbA1c) B

• every 12 months C
Risk assessment should begin from 18 years of age in Aboriginal 25 Practice
and Torres Strait Islander peoples NHMRC, 2009 Point
*Refer to Summary, explanation and source of recommendations for an explanation of the level of
evidence and grade of evidence
12 2016-18
Clinical context
Type 2 diabetes is the most common form of diabetes in Australia, although many
cases remain undiagnosed. Additionally, almost one in six adults is affected by
impaired glucose tolerance (IGT) or impaired fasting glucose (IFG).1 Earlier detection
increases opportunities to reduce morbidity and mortality.
In practice
Patients should be screened for diabetes risk every three years from 40 years of age
using the Australian type 2 diabetes risk assessment tool (AUSDRISK; www.health.
gov.au/preventionoftype2diabetes). Aboriginal and Torres Strait Islander peoples
should be screened from 18 years of age. Those with a risk score of 12 or more
should have a blood examination for fasting blood glucose (FBG) or HbA1c.
Screen for undiagnosed diabetes in individuals at high risk25,26 (Box 1).
Box 1. People considered to be at high risk of type 2 diabetes

• People of any age with impaired glucose tolerance (IGT) or impaired fasting
*
glucose (IFG)
• All patients with a history of a cardiovascular event (eg acute myocardial
infarction, angina, peripheral vascular disease or stroke)
• People aged >35 years originating from the Pacific Islands, Indian
subcontinent or China
• People aged >40 years with body mass index (BMI) >30 kg/m2
or hypertension
• Women with a history of gestational diabetes mellitus (GDM)
• Women with polycystic ovary syndrome (PCOS)
• Patients taking antipsychotic medication
* Annual fasting blood glucose (FBG) or HbA1c is reserved for those people identified with
IGT test or IFG (not limited by age)
2016-18
13
Screening for risk of diabetes in specific or high-risk

populations
There is a higher prevalence of type 2 diabetes in lower socioeconomic than higher
socioeconomic Australians.27 Certain ethnic groups are more at risk.28 People with
Pacific Islander, Southern European or Asian backgrounds are twice as likely as other
Australians to have developed diabetes within five years.29
Aboriginal and Torres Strait Islander peoples are three times more likely to have
diabetes than non-Indigenous Australians, and type 2 diabetes is a direct or indirect
cause for 20% of Aboriginal and Torres Strait Islander peoples deaths.30
The AUSDRISK calculates the risk of developing diabetes over a five-year period.
Patients with scores of 12 or more are considered at high risk (Table 1).
Table 1. Diabetes risk
AUSDRISK score Risk of developing type 2 diabetes within five years

*
1 in 100 |
<5
1 in 50 |
6-8
1 in 30 |
9-11
1 in 14 |
12-15
16-19 1 in 7
>20 1 in 3
*The overall score may overestimate the risk of diabetes in those aged <25 years and underestimate
the risk in Aboriginal and Torres Strait Islander peoples
Practice points
• For Aboriginal and Torres Strait Islander peoples, AUSDRISK can be used from
18 years of age.
• Those considered at high risk (Box 1) should have an FBG or HbA1c test every
three years.
• People with low individual risk or who are from a community with low prevalence
(<5%) may be screened for risk with AUSDRISK every three years.25
Refer to Chapter 13. Diabetes and reproductive health for recommendations on
screening in pregnancy.
14 2016-18
3.2 Case finding in patients with symptoms

suggestive of diabetes
Clinical context
Clinical suspicion for type 2 diabetes needs to remain high, as type 2 diabetes is often
asymptomatic and developing in younger populations. Secondary causes of diabetes
should also be considered in the presence of symptoms suggestive of diabetes.31
Clinical symptoms suggestive of diabetes

Symptoms of diabetes include:
• lethargy, polyuria, polydipsia

• frequent fungal or bacterial infections
• blurred vision
• loss of sensation (ie touch, vibration, cold)
• poor wound healing
• weight loss.
Clinical signs of insulin resistance

Signs of insulin resistance may include the following:
• Acanthosis nigricans (AN) - Typically characterised by hyperpigmentation

(darkening of skin pigment) and usually accompanied by a velvety change in texture
of the affected skin. Common sites are the neck and axillae.32
• Skin tags - Benign (non-cancerous) skin growths on the body or face. They can be
smooth or wrinkled, skin-coloured or just slightly darker than skin colour and can
vary in size.
• Central obesity - Defined by a high waist-to-hip ratio, waist-to-thigh ratio and waist
circumference.
• Hirsutism - Excess facial and body hair, especially on women, which can indicate
insulin resistance.
Box 2 provides examples clarifying when insulin levels may be useful.
2016-18
15
Box 2. When are insulin levels helpful?

• There is no role for routinely testing insulin levels to assess insulin resistance
in impaired glucose tolerance (IGT), impaired fasting glucose (IFG) or in the
evaluation of type 2 diabetes
• Patients with signs of insulin resistance should be screened for diabetes with
fasting blood glucose (FBG) or glycated haemoglobin (HbA1c)
Tests to detect diabetes in symptomatic patients

In the presence of symptoms suggestive of hyperglycaemia or a clear clinical diagnosis
(eg a patient presenting with hyperglycaemic crisis, a single elevated FBG >7.0 mmol/L
or a random blood glucose >11.1 mmol/L), this is confirmatory of a diagnosis of
diabetes. A second laboratory test is not required to confirm the diagnosis.
Diagnosis of diabetes in asymptomatic patients

Testing those at high-risk or with a clinical suspicion for diabetes involves three types
of biochemical analyses (Box 3).
Box 3. Diagnostic criteria for type 2 diabetes

• Fasting blood glucose (FBG) >7.0 mmol/L or random blood glucose
>11.1 mmol/L confirmed by a second abnormal FBG on a separate day
• Oral glucose tolerance test (OGTT) before (fasting) and two hours after an oral
75 g glucose load is taken. Blood glucose is measured. Diabetes is diagnosed
as FBG >7.0 mmol/L or two-hour blood glucose is >11.1 mmol/L
• Glycated haemoglobin (HbA1c) >48 mmol/mol (6.5%; on two separate
occasions)
These are via venous sampling under laboratory methodology
Confirmatory testing for asymptomatic patients

A second laboratory result is required for confirmation of the diagnosis of diabetes in
asymptomatic patients. It is recommended that the same laboratory result be repeated
without delay using a new blood sample for confirmation because there will be a
greater likelihood of concurrence.
16 2016-18
Figure 1a. Screening and diagnosis algorithm - Fasting blood glucose
Fasting blood glucose
<5.5 mmol/L 5.5-6.9 mmol/L >7 mmol/L
Figure 1b. Screening and diagnosis algorithm - Glycated haemoglobin
Glycated haemoglobin (HbA1c)

Non-fasting - No preparation required. Interpret with care
for haemoglobinopathies or abnormal red cell lifespan
J
>48 mmol/mol (>6.5%)
Diabetes likely
Confirm with follow up

HbA1c test
* 8»
2016-18
17
Figure 1c. Screening and diagnosis algorithm - Oral glucose tolerance test
Oral glucose tolerance test (OGTT)
Practice Points for diagnosed diabetes

^ Monitor risk factors, and symptoms:
• Manage the individual patient by assessing modifiable risk factors and CVD risk
• Refer patients to a dietitian and a physical activity program
• Provide pre-conception advice to women in reproductive age with a history of gestational
diabetes
Provide access to diabetes health teams, and commence lifestyle modifications and/or medication.
^
Register with the NDSS and notify the RTA

§Medicare Benefits Schedule (MBS) item number 66841 allows for diagnostic use only once every
12 months. The request slip should be annotated as HbA1c for Service Incentive Payment (SIP)
and Practice Incentives Program (PIP) purposes. However, a confirmatory HbA1c test (MBS item
number 66551) should be ordered before treatment initiation37
| A value of <48 mmol/mol (6.5%) does not exclude diabetes diagnosed using plasma glucose testing in
symptomatic patients
NB: IGT and IFG cannot be diagnosed using HbA1c
18 2016-18
3.3 Impaired fasting glucose or impaired glucose

tolerance
The definition of diabetes is based on a collection of symptoms based on an agreed
glycaemic measure. On glucose challenge testing, patients with elevated glucose not
high enough to be diagnosed with type 2 diabetes, are considered to have either IFG
or IGT (Figure 1). To apply the diagnostic algorithm, refer to Table 2.
These states are not considered to be benign and reflect a risk of developing
diabetes in the future. In addition, as CVD risk is distributed across a continuum
of post-challenge glucose levels, any degree of post-challenge hyperglycaemia may
be associated with the development of premature CVD.33
Microvascular complications are commonly present at the time of diagnosis of type 2

diabetes in symptomatic and asymptomatic individuals.25
Table 2. Apply the diagnostic algorithm

Diagnostic Advantages/Disadvantages
method
Fasting blood Fasting (eight hours) Additionally may be
glucose (FBG) used to detect impaired
venous blood fasting glucose (IFG)
Glycated Non-fasting Not useful for
haemoglobin Note that HbA1c may lack accuracy (specificity and/or assessment of
(HbA1c) sensitivity) in: impaired glucose
>48 mmol/mol tolerance (IGT)
• acute onset glycaemic states such as post-traumatic
or >6.5% Threshold of
type 2 diabetes (eg pancreatitis), rapid onset of
glycaemia with sepsis and steroid use, etc 48 mmol/mol is
linked to escalating
• people with haemoglobinopathy or haemolysis, or
microvascular
advanced chronic kidney disease
disease, and HbA1c
• people with iron deficiency (artificially elevated). In
is a better predictor of
such cases, a fasting venous blood glucose or oral
macrovascular disease
glucose tolerance test (OGTT) may assist diagnosis
than FBG and two-
Abnormal HbA1c values generally should be repeated
hour post-glucose34,35
in asymptomatic patients and confirmed on a different
Lacks sensitivity with
day, unless two abnormal tests (eg FBG and HbA1c) are
acute glycaemic states
already available from the same day
OGTT Fasting (eight hours) Only standard method
75 g glucose administered orally used to detect IGT
May concurrently
Blood is collected from a fasting venous sample and
detect IFG
two-hour post-glucose challenge venous sample
2016-18
19
HbA1c as a diagnostic tool

HbA1c has recently been approved as a diagnostic test for diabetes under the Medicare
Benefits Schedule (MBS) and by the World Health Organization (WHO). The Australian
Diabetes Society (ADS), the Royal College of Pathologists of Australasia (RCPA), and
the Australasian Association of Clinical Biochemists (AACB) have reviewed the available
evidence and confirmed that HbA1c can be used to diagnose diabetes.38
Diagnostic dilemmas
Discordant testing
If diagnosing diabetes, due to the different physiological measures of glycaemia,
confirmatory tests at times may give discordant results especially if you do not repeat
the initial diagnostic test. For example, HbA1c levels may not be elevated in acute
glycaemic states in newly diagnosed diabetes, such that a value of <48 mmol/mol
(<6.5%) does not exclude diabetes in the presence of an elevated blood glucose
testing (>7 mmol/L fasting or >11.1 mmol/L random). When the results of more than
one test are discordant, the laboratory result that is above the diagnostic cut-off point
should be repeated to make the diagnosis.
Alternative diagnoses
Alternative diagnoses to type 2 diabetes include unusual presentations of:
Type 1 diabetes
Consider type 1 diabetes if there is the presence of:
• ketosis/ketonuria (which may be absent)

• polyuria, polydipsia
• weight loss or BMI <25 kg/m2
• <50 years of age
• personal and family history of autoimmune disease
• rapid onset of symptoms.
If suspicious of type 1 diabetes:
• Management of any hyperglycaemia should not be delayed and should include

immediate assessment for possible ketosis and metabolic disorders such as
hyperosmolar states. If blood ketone level is elevated seek help immediately.
Blood ketones >0.6 mmol/L are abnormal and require investigation in the presence
of hyperglycaemia.
20 2016-18
• Non-urgent confirmatory tests for glutamic acid decarboxylase (GAD) and/or

insulinoma antigen-2 (IA-2) antibodies. These will be present in 90% of patients with
type 1 diabetes. When measuring antibodies, higher rates of false negative results
occur early in the development of type 1 diabetes. However, false negative results
decrease when two different antibody tests are measured.
• Test for plasma C-peptide level.39 Levels <0.2 nmol/L on non-fasting sampling,
support the diagnosis of type 1 diabetes. This will determine those patients with
hyperglycaemia in the absence of or with minimal insulin production. This may not
be low in acute early onset type 1 diabetes.
Latent autoimmune diabetes of adults

Latent autoimmune diabetes of adults (LADA) is diabetes with B-islet cell antibodies
more commonly occurring in adulthood, with a more rapid course of B-cell destruction,
a poorer metabolic response to sulphonylurea therapy and a more rapid progression
to insulin requirement to control hyperglycaemia due to B-cell failure.40
Monogenic diabetes
Monogenic diabetes is a disorder with the following characteristics:
• onset before 25 years of age

• non-ketotic diabetes mellitus often with a stable lower level hyperglycaemia
• autosomal dominant inheritance
• primary defect in the function of the pancreatic B-cells.
Monogenic diabetes is genetically heterogeneous and all forms are dominantly
inherited. There is variance among the forms with two main types - neonatal diabetes
mellitus (rare) and maturity onset diabetes of the young (MODY). MODY subtypes
may vary in the severity of hyperglycaemia, need for insulin and risk for future
complications. Apart from MODY type 2, all other forms of monogenic diabetes are
due to transcription factor gene mutations. Not all forms of the MODY phenotype have
yet been defined. Suspected cases should be referred to a specialist endocrinologist,
and management options and possible genetic diagnosis should be considered.41
Gestational diabetes mellitus

Refer to Section 13.3. Gestational diabetes mellitus.
2016-18
21
4. Preventing type 2 diabetes

*
Lifestyle modifications that focus on increased physical activity, 42 A
dietary change and weight loss should be offered to all individuals nhmrc 2009
at high risk of developing type 2 diabetes
Structured diabetes prevention programs are available
Bariatric surgery can be considered in selected morbidly 42 C
obese individuals (based on weight alone or the presence NHMRC 2009
of comorbidities) who are at high risk of type 2 diabetes
Individuals who are at high risk of diabetes should be identified 42 C
through the use of risk assessment tools NHMRC, 2009
Clinical context
The dysglycaemic states (IFG, IGT) occur when blood glucose levels (BGLs) are
elevated above normal, but are not high enough to be diagnosed as diabetes.
Intervention is warranted to prevent or delay progression to type 2 diabetes,

and to reduce mortality associated with the metabolic condition itself.
Clinical trial evidence demonstrates that the metabolic progression to type 2 diabetes
can be slowed or stopped with effective diet and lifestyle modification, as well as
with some drug therapies. Studies demonstrating prevention of type 2 diabetes
development by structured lifestyle behaviour change programs have been conducted
in Finland, the US, China and India.43-46 These had intensive programs supporting
the intervention group, with the goals of intervention between 5% and 7% weight
reduction using a low-kilojoule and low-fat diet, and moderate intensity physical
activity (eg brisk walking) for at least 150 minutes/week.
In patients with dysglycaemic states, structured lifestyle interventions can achieve

a relative risk reduction (RRR) of up to 58% in the development of type 2 diabetes.
In the Indian study, the numbers needed to treat was 6.4, to prevent one incident
case of diabetes over three years using a lifestyle modification program. Longer term
follow-up has revealed a 43% reduction in the rate of diabetes at 20 years in the Da
Qing study, 43% reduction at seven years in the Finnish study, and 34% reduction
at 10 years in the US Diabetes Prevention program. Notably, in the US study, the
strongest determinant of reduced diabetes incidence was weight reduction, with each
1 kg loss leading to a RRR of 16%. Of the therapies, pharmacotherapy with metformin
22 2016-18
has been shown to achieve a RRR of 31%, particularly in obese individuals with BMI
>35 kg/m2. This is, however, still less effective than successful lifestyle change.47
Of the trials that evaluated mortality benefits from interventions, lifestyle has not
definitively shown clear benefits, except when mediated through diabetes prevention.
Pharmacological interventions have not shown reduced CVD mortality benefit.48
Note: At the time of publication, metformin does not have Therapeutic Goods
Administration (TGA) or Pharmaceutical Benefits Scheme (PBS) approval for this
indication within Australia.
In practice
In addition to providing comprehensive risk assessment, screening, diagnosis
and management for diabetes, GPs should consider systems for identifying and
managing patients with IGT or IFG who are at high risk of diabetes. They should
also include absolute CVD risk assessment, and chronic kidney disease risk
assessment and management in this group. Referral to government-supported type
2 diabetes and CVD prevention programs should be considered where these exist.
Programs and strategies for educating patients about diabetes to encourage lifestyle
modification should also be considered.
Lifestyle modification
Lifestyle modification programs (refer to Chapter 6. Lifestyle modification) should be
developed using a patient-centred approach. These should be individualised with
realistic goals based on what the patient can and wants to achieve. Each plan should:
focus on physical activity, dietary modification and weight control; be long term; and
involve partners and other family members.
The main element of the programs was an intensive lifestyle modification aimed at
helping participants achieve and maintain 7% weight loss and >150 minutes per week
of moderate-intensity physical activity. The US study included 75 minutes per week
of strength training, while the Finnish study provided strength training twice weekly.
All studies with success had individual goal setting, and provided individualised and
group counselling, predominantly on behavioural change and nutrition.49
Plans could involve other practice team members and may include referral to allied
health professionals such as, APDs, CDEs and AEPs, physiotherapists and clinical
psychologists. Consider structured goal-oriented programs and community resources.
2016-18
23
Diabetes prevention programs are supported by different state and local health
authorities. General practices may seek advice on local patient referral pathways
for those with IGT or IFG, or those identified by risk assessment tools such as
AUSDRISK by contacting their local Diabetes Australia state or territory organisation
on 1300 136 588 or at www.diabetesaustralia.com.au/prevention
24 2016-18
5. Structured care and patient education
5.1 Patient-centred diabetes care

*
A patient-centred communication style that incorporates 19 B
patient preferences, assesses literacy and numeracy, and American Diabetes
addresses cultural barriers to care should be used Association 2015
Clinical context
How well a patient can read and use numbers has a significant impact on their ability
to self-manage. Patients with diabetes and lower literacy or numeracy skills are at
greater risk for poor diabetes outcomes.50
Many factors influence a person’s literacy and numeracy (eg socioeconomic status,
cognitive function, culture). Health literacy is defined as an individual’s ability to read,
perform basic numeracy skills, and understand and use healthcare information
to make decisions and follow instructions for treatment.51 In 2006, the Australian
Bureau of Statistics (ABS) identified that half of healthcare clients lacked sufficient
health literacy to navigate the system.52 Importantly, this means that simply providing
brochures and written information is not health education, and is unlikely to change
health behaviour.
A patient’s health literacy typically improves through self-education and contact with
health providers.53
In practice
A patient-centred consultation involves assessing a patient’s clinical signs and
symptoms, as well as their thoughts, fears, preferences and expectations, and their
social context. This ensures a complete understanding of the individual who is living
with type 2 diabetes.
From a position of mutual understanding, management plans can then be developed

with the patient, and tailored to specifically meet their needs, values and choices.
Studies show that people with diabetes are more likely to engage actively in self
management and achieve optimal health outcomes if plans are person-centred.54
2016-18
25
Many of the assessments discussed in these guidelines are performed informally during
a routine consultation. However, systems should be developed within the practice to
allow appropriate assessment, review and management of individual patients.
Assess health literacy status

A patient’s literacy and numeracy skills affect their capacity for self management and
what resources they will need. Literacy and numeracy skills are not always obvious,
and GPs may worry that attempting to evaluate them will be uncomfortable for
patients. The evidence in the literature does not support this concern.55
Organisations such as Diabetes Australia provide self-management education and

support programs, peer support programs, mental health and diabetes programs,
culturally and linguistically appropriate education, and information in several languages.
They also have resources to help patients with low literacy skills.
Determine priorities for management

Discover what areas are affecting the patient’s quality of life in the context of
comorbidities and life expectancy. Determine the management priorities, focusing
on specific interventions (including those chosen by the patient) that have the most
impact on the individual and will form the basis of their continuing care.
Encourage enrolment in structured programs

Structured diabetes care programs and evidence-based structured self-management
training programs are available.
Refer to Appendix B. Structured patient-centred care plan - Examples of a General

practice management and Patient care plan for a template of a General practice
management plan (GPMP; structured patient-centred care plan).
26 2016-18
5.2 A structured diabetes care program consistent

with the Chronic Care Model
*
Care should be aligned with components of the chromic care 56 A
model (CCM) to ensure productive interactions between a American Diabetes
prepared proactive practice team and an informed activated Association, 2016
patient
When feasible, care systems should support team-based 56 B
care, community involvement, patient registries and American Diabetes
embedded decision-support tools to meet patient needs Association, 2016
Treatment decisions should be timely, and based on 56 B
evidence-based guidelines that are tailored to individual American Diabetes
patient preferences, prognoses and comorbidities Association, 2016
Clinical context
The goal of a structured care program is to increase the quality of life for people with
diabetes. Structured care means having all the necessary aspects of the required care
in place.
The structure of each diabetes care program will vary depending on the local
circumstances and the needs of the patient. There is good evidence to support patient
access to a variety of healthcare providers.17
Access to, and care delivery by, different healthcare providers allows the patient to
benefit from a broad perspective on their health and wellbeing. There are some team
roles that fit into most patients’ programs, but whatever the composition of the team,
care needs to be organised and delivered systematically.
Multidisciplinary care (Figure 2) also covers gaps in care that may be apparent to one
healthcare provider, but go unnoticed by another. For example, recognising a patient’s
social difficulties may be detected during an educator evaluation or by a practice nurse
rather than during a routine medical consultation.
2016-18
27
Figure 2. Potential members of the multidisciplinary diabetes care team
Registered and practice nurses within a general practice can provide an administrative
and a clinical role. Practice nurses often manage the diabetes register, structured
care-and-recall system, as well as provide a clinical assessment before the GP sees
the patient. Practice nurses have an important role in team-based care processes,
including motivational interviewing, education activities and support for lifestyle
modification. These can be facilitated and enabled upon GP assessment and
recommendation. This enables healthcare efficiency and allows the GP to focus on
any identified problems. Practice nurses can also act as practice liaison, and facilitate
rapid access to GP care in the event of a clinical problem.

Involvement of an Aboriginal health worker, or an Aboriginal liaison officer,
or Indigenous outreach worker or care coordinator is essential in the care
of Aboriginal and Torres Strait Islander peoples.
28 2016-18
5.3 Patient education and self management

*
All people with type 2 diabetes should be referred for structured 42 A
diabetes patient education NHMRC, 2009
Diabetes education should be delivered in groups or individually 42 A
NHMRC, 2009
Diabetes education should be culturally sensitive and tailored 42 B
to the needs of socioeconomically disadvantaged populations NHMRC, 2009
Education to support self management is an integral part of diabetes care. Patients

and their carers should be offered a structured, evidence-based education program
at the time of diagnosis, with an annual update and review.57
Educating people with diabetes about their condition and its treatment will assist in self
management.58-60
In addition to the team members mentioned in Figure 2, patients can obtain further
education and support through Diabetes Australia and the NDSS, and their state or
territory diabetes organisation. More information is available at www.diabetesaustralia.
com.au and www.ndss.com.au
Multiple online support and education programs may be available for patients who
are unable to access face-to-face group meetings. However, there are few studies
on the individual effectiveness of these programs. More information is available at
www.diabetesaustralia.com.au and www.adea.com.au/members/adea-website
Self management
Self management involves the person with diabetes working in partnership with their
carers and health professionals so they can:
• understand their condition and various treatment options

• contribute to, review and monitor a plan of care (eg care plan)
• engage in activities that protect and promote health
• monitor and manage the symptoms and signs of the condition
• manage the impact of the condition on physical functioning, emotions
and interpersonal relationships.
Identifying barriers to self management is important when developing a management
plan with the patient. Issues around cognition, physical disability, mental health, health
literacy, socioeconomic constraints, location and access to services can have an
impact on the ability of the person to self-manage their diabetes.61
2016-18
29
6. Lifestyle modification
Type 2 diabetes after initial diagnosis in some patients can usually be managed with
diet and exercise alone.62,63 Lifestyle modification continues to play an important role
in glycaemic control and managing CVD risk in more advanced stages of type 2
diabetes, and may be supported by allied health and specialist support services.

*
People with type 2 diabetes of all ages benefit from accumulating 64 B
30 minutes or more of moderate physical activity on most, if not Briffa T et al,
all, days of the week 2006
Exercise and physical activity (involving aerobic and/or resistance 65 D
exercise) should be performed on a regular basis SIGN, 2014
Clinical context
Exercise is regarded as one of the cornerstones for diabetes management, and
while generic physical activity can have a favourable impact on improving glycaemic
control, reducing CVD risk and reducing overall mortality,66, 67 more specialised and
individualised exercise prescription can achieve superior benefits.66 Aerobic exercise
has been shown to achieve a similar reduction on HbA1c as either metformin or a
sulphonylurea (ie a reduction of 0.73% with exercise and 0.9% with single medication).
Resistance training has a smaller effect. For more information on exercise and type 2
diabetes, visit www.racgp.org.au/your-practice/guidelines/handi/interventions/
cardiovascular/exercise-for-type-2-diabetes
Regular physical activity improves metabolic control, reduces CVD risks and can
reduce the risk of developing type 2 diabetes.68 Low-level aerobic exercise (eg brisk
walking for half an hour per day) and physical resistance training improves glucose
tolerance, energy expenditure, feeling of wellbeing and work capacity, and improves
BP, lipid profiles and mood.
30 2016-18
In practice
The goal is for patients to undertake aerobic training that brings the heart rate up to
55-69% of maximum (208 - 0.7 x age [years] = maximum beats per minute)69,70 for a
minimum of 30 minutes on most, if not all days of the week (>150 minutes/week). This
establishes and maintains fitness and aerobic capacity.
Evidence indicates that people with diabetes, IFG and/or IGT should aim for a
minimum of 210 minutes per week of moderate intensity exercise or 125 minutes per
week of vigorous intensity exercise, and no more than two consecutive days without
training. For more information on resistance training, visit www.racgp.org.au/your-
practice/guidelines/handi/interventions/cardiovascular/exercise-for-type-2-diabetes
Note that setting short-term, gradually increasing goals may assist the patient in
achieving goals. Evidence suggests that multidisciplinary and integrated care teams
are best practice in the management of type 2 diabetes, preventing and decreasing the
impact of complications and comorbidities, resulting in healthcare cost savings.67 Group-
based training that facilitates self management in people with type 2 diabetes is effective
in improving FBG levels, HbA1c and diabetes knowledge, and in reducing systolic blood
pressure (SBP) levels, body weight and the requirement for diabetes medication.66
People requiring insulin or those treated with sulphonylureas need to be aware

of potential delayed effects of physical activity on BGLs - in particular delayed
hypoglycaemia 6-12 hours after cessation of the activity.
People with diabetes need to be advised to moderate or cease their activity if they
develop cardiovascular symptoms or feel unwell. Patients with claudication need to
be encouraged to continue physical activity under appropriate clinical supervision.
When advising on physical activity, the GP should explain the:

• risks and benefits of physical activity for the individual
• importance of varying intensity of exercise levels
• importance of following the chest pain/discomfort and/or diabetes symptom
management plan.64
Clinical advice should be given to stop physical activity if the patient experiences
symptoms of hypoglycaemia and to discontinue further physical activity until reviewed
by their GP.
General physical activity safety advice for people with diabetes:
• Instruct patients to check their BGL before, during and after prolonged physical
activity if using insulin or sulphonylureas. Additional carbohydrate foods and
medications adjustments may be required depending on the patient’s BGLs.
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31
Advise patients that if their pre-exercise BGL is <5 mmol/L, they are at risk of a
hypoglycaemic episode during or after exercise, and to have access to additional
carbohydrates as per the advice of their CDE or APD. Delayed hypoglycaemia may
occur up to 24 hours post-exercise.
• Advise patients on how to recognise, prevent or manage hypoglycaemic events,
including potential post-exercise hypoglycaemia (ie need for carbohydrates or
medication adjustment).
• Advise patients to carry a rapid-acting glucose source at all times (eg jelly beans,
or glucose gel/drink).
• Advise patients to wear correct supportive footwear - especially if there is
neuropathy, vascular disease, abnormal foot structure or previous foot ulcer(s),
in which case the advice of a podiatrist with an interest in high-risk feet should be
sought. This advice would also include the appropriateness of ‘jolting’ exercises
such as running, skipping and jumping.
• Advise patients to check their feet daily and after physical activity for blisters, warm
areas or redness.
When prescribing a physical activity program, the GP should be aware of the following:
• A careful history should be taken.

• Special attention needs to be paid to exertion-induced symptoms, chest
or abdominal discomfort, claudication or syncope.
• People with type 2 diabetes frequently have silent macrovascular disease.
• For patients with hypertrophic obstructive cardiomyopathy (HOCM), heavy weight
lifting and high-intensity aerobic exercise are not recommended.
*
• For patients with long QT syndrome, exercise may trigger a cardiac arrhythmic
event.
*
• Vigorous exercise is contraindicated for those with proliferative retinopathy,
and for three months after laser retinal treatment.
*
• Exercise may be relatively contraindicated in patients with peripheral neuropathy,
a history of recurrent falls or uncontrolled hypertension.
*
• Recommendation for referral to an AEP should be considered.
*From The Royal Australian College of General Practitioners. HANDI interventions - Exercise: Type 2
diabetes. East Melbourne, Vic: RACGP, 2015. Available at www.racgp.org.au/your-practice/guidelines/
handi/interventions/cardiovascular/exercise-for-type-2-diabetes
Screening with a stress electrocardiogram (ECG) is not indicated in asymptomatic

individuals, but any symptoms suggestive of CVD need to be actively investigated.
32 2016-18

Many Aboriginal and Torres Strait Islander peoples are involved in physically
demanding sporting and cultural activities, although, overall, Aboriginal and
Torres Strait Islander peoples are not more physically active than non-Indigenous
Australians.
GPs should be aware of activities that are affordable, appropriate and accessible
for their Aboriginal and Torres Strait Islander patients, which may be run by local
community groups.
Aboriginal and Torres Strait Islander peoples may prefer exercise and physical
activities that are culturally, socially and economically meaningful. Such activities
or other cultural activities may not be described as ‘exercise’ or ‘physical
activity’, yet be of significant health and social benefit. A careful history in
the context of a trusting doctor-patient relationship may bring about better
understanding and opportunity.
6.2 Diet
*
Consumption of cereal foods (especially three serves a day of 71 B

wholegrains) is associated with reduced risk of type 2 diabetes NHMRC, 2013
Consumption of at least one and a half serves of dairy foods (eg 71 C
milk, yoghurt, cheese) per day is associated with reduced risk of NHMRC, 2013
type 2 diabetes
Clinical context
Most of the burden of disease due to poor nutrition in Australia is associated with
eating too much energy-dense and relatively nutrient-poor foods, and eating too few
micronutrient-dense foods, including vegetables, fruit and wholegrain cereals.
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33
Composition of a healthy diet

The Australian dietary guidelines promotes healthy eating patterns, emphasising a range
of nutrient-dense foods in appropriate portion sizes.71
• Enjoy a wide variety of nutritious foods from these core food groups every day:
- plenty of vegetables, including different types and colours, and legumes/beans
- fruit (consumption of fruit is not associated with risks of type 2 diabetes)
- grain (cereal) foods, mostly wholegrain and/or high cereal fibre varieties, such as
breads, cereals, rice, pasta, noodles, polenta, couscous, oats, quinoa and barley
- lean meats and poultry, fish, eggs, tofu, nuts and seeds, and legumes/beans
- milk, yoghurt, cheese and/or their alternatives, mostly reduced fat (reduced fat
milks are not suitable for children under two years of age).
• Drink plenty of water.
• Limit intake of foods containing saturated fat, added salt, added sugars and alcohol:
- Restrict foods high in saturated fat such as many biscuits, cakes, pastries, pies,
processed meats, commercial burgers, pizza, fried foods, potato chips, crisps and
other savoury snacks.
- Limit foods and drinks containing added salt.
- Avoid foods and drinks containing added sugars such as confectionary, sugar-
sweetened soft drinks and cordials, fruit drinks, vitamin waters, energy and sports
drinks.
- Alcohol intake should be as per the Australian dietary guidelines. For women who
are pregnant, planning a pregnancy or breastfeeding, not drinking alcohol is the
safest option.
Reproduced with permission from the National Health and Medical Research Council.
Australian dietary guidelines. Canberra: NHMRC, 2013. Available at www.nhmrc.gov.au/
guidelines-publications/n55 [Accessed 29 August 2016].
Two other key themes are eating for cardiovascular protection, and glycaemic
management and meal planning.
Eating for cardiovascular protection

Consultation with an APD will allow individualised advice on CVD risk reduction with
healthy food choices to be provided. A variety of eating patterns are acceptable for the
management of metabolic control. However, personal preferences for cultural, religious
and economic preferences should also be considered.72 One such dietary choice is the
Mediterranean diet, which is associated with a lowering of morbidity and mortality for some
chronic diseases, including CVD.73 In persons with high CVD risk, the Mediterranean diet
reduced CVD events when compared to a low-fat diet.74
34 2016-18
Glycaemic management and meal planning

Evaluation of current dietary intake and the eating patterns of an individual is an initial
critical step and should be recommended in all people to support the management
of type 2 diabetes. All patients should be offered and encouraged to seek advice on
medical nutrition therapy by referral to an APD. The APD can help support a person
living with diabetes to address the core themes around nutrition such as promoting
healthy eating patterns and, where appropriate, healthy body weight (loss) with
reduction in energy intake (portion control and type of food).
To influence the glycaemic response after eating, the amount and quality of the
carbohydrate eaten may be the most important factor. The amount of carbohydrate
eaten within a meal should therefore be considered when meal planning. Eating low-
glycaemic-load foods instead of higher glycaemic-load foods may modestly improve
glycaemic control.75 Low glycaemic index (GI) foods include dense wholegrain breads,
steel-cut oats, lower fat milk and yoghurt, minimally processed (eg wholegrain, low
GI) breakfast cereals, pasta, Doongara rice, legumes and most fruits. Intake of high
carbohydrate, low-nutrient-dense foods such as soft drinks, cakes and lollies should
be confined to infrequent, small amounts to reduce the risk of weight gain and a
worsening cardiometabolic profile.75 The total amount of carbohydrate consumed
(compared with other macronutrients or GI of the meal) may be the major dietary
factor contributing to high post-prandial BGLs.76
There is evidence that nutrition education may be particularly important for the
prevention of hypoglycaemia in people with type 2 diabetes on insulin or oral glucose
lowering medications that may cause hypoglycaemia (eg sulphonylureas). Consistency
in carbohydrate intake, and spacing and regularity of meal consumption may help
some patients manage BGL and weight. Inclusion of snacks as part of a person’s
meal plan should be individualised and should be balanced against the potential risk of
weight gain and/or hypoglycaemia.77
In practice
Dietary habit changes are often slow and incremental. There is no need for a ‘special’
diet for diabetes, just the requirement to follow a sensible, balanced eating plan.
Keep advice simple and educate patients about healthy food choices rather than on
unhealthy food choices or what they should not eat. All sugars do not need to be
eliminated. A small amount of sugar as part of a mixed meal or food (eg one teaspoon
of sugar/honey added to breakfast cereal) may not adversely affect the blood glucose
level. Small amounts of added sugar as part of a high-fibre, modified-fat meal plan
increases the choice of food available and may aid adherence. Foods naturally high
in sugars such as fruit and dairy do not need to be avoided.
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35
Consider recommending/referring to the Eat for Health website (www.eatforhealth.

gov.au), which is easy to access and its recommendations easy to implement.
Referral to an APD or a CDE will support implementation/reinforcement of these
recommendations. To find an APD, visit www.daa.asn.au
For basic dietary advice, visit www.diabetesaustralia.com.au/eating-well

There is evidence that Aboriginal and Torres Strait Islander communities in urban
and remote regions face significant access barriers to nutritious and affordable
food. Nutritious food tends to cost more, and requires refrigeration and
preparation, so lack of food security may affect the choice of glucose-lowering
medications. Food choices can be significantly altered when people have access
to appropriate foods and education about nutrition.
GPs should make themselves aware of local community initiatives for the supply
of fresh fruit and vegetables at affordable prices. In some areas, these include
arrangements with farmers’ markets or local community gardens. Information in
regards to Aboriginal and Torres Strait Islander peoples nutrition is available at:
• Australian Bureau of Statistics, www.abs.gov.au/ausstats/abs@.nsf/Lookup/

by%20Subject/4727.0.55.005~2012-13~Main%20Features~Key%20
Findings~1
• Australian Institute of Health and Welfare, www.aihw.gov.au/uploadedFiles/
ClosingTheGap/Content/Publications/2012/ctgc-rs09.pdf
• Department of Health, www.health.gov.au/internet/publications/publishing.
nsf/Content/oatsih-evidence-socialhealth-toc~nutrition
36 2016-18
6.3 Weight
*
Adults with impaired fasting glucose, impaired glucose tolerance 78 A
or diabetes can be strongly advised that the health benefits of NHMRC, 2013
5-10% weight loss include prevention, delayed progression or
improved control of type 2 diabetes
For adults with body mass index (BMI) >40 kg/m2, or BMI 78 A
>35 kg/m2 and comorbidities that may improve with weight loss, NHMRC, 2013
bariatric surgery may be considered, taking into account the
individual situation
Use BMI to classify overweight or obesity in adults 78 B
NHMRC, 2013
For adults, use waist circumference, in addition to BMI, to refine 78 C
assessment of risk of obesity-related comorbidities NHMRC, 2013
Clinical context
Excess weight in individuals usually results from a prolonged period of energy
imbalance. However, the causes of overweight and obesity are complex. Older people
with diabetes may also be at risk of malnutrition. Diet and physical activity are central
to the energy balance equation, but are directly and indirectly influenced by a wide
range of social, environmental, behavioural, genetic and physiological factors, the
relationships between which are not yet fully understood. Increasing physical activity
regardless of weight loss may reduce CVD risk factors, improve functional mobility
in older people and reduce HbA1c by ~0.6% in adults with type 2 diabetes.78 Table
4.4 in Clinical practice guidelines for the management of overweight and obesity
in adults, adolescents and children in Australia78 (www.nhmrc.gov.au/guidelines-
publications/n57) lists common medications associated with weight gain at 12 weeks
of commencement of a weight management diet.79
It is important to encourage some degree of healthy weight loss, except where there
are other associated risks (eg frail and elderly, or those with psychologically related
eating disorders). A healthy body weight is often not achievable and setting this as a
goal discourages patients from attempting any dietary change. Many studies suggest
that weight loss of 5-10% will improve glycaemic control.80, 81 Section 2.2.3 in the
above clinical practice guidelines discusses the importance of psychological issues
influencing weight management.78
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37
A recent multi-centre, randomised clinical trial (Action for Health in Diabetes [Look
AHEAD]) provided evidence that intensive lifestyle intervention focusing on weight loss
did not result in a significant reduction in cardiovascular events in overweight or obese
adults with established type 2 diabetes.82 This was despite greater reductions in
HbA1c and greater initial improvement in fitness and all CVD risk factors, except for
low-density lipoprotein cholesterol levels.
In practice
Weight assessment
Assessing weight is typically done using BMI. Note that BMI is a difficult parameter
to standardise between different population groups.
For those of European descent, a healthy BMI is 18.5-24.9 kg/m2, overweight is

25-29.9 kg/m2 and obese is >30 kg/m2.78 Different classification criteria may apply
to other population groups. Some groups may have equivalent levels of risk at a lower
BMI (eg people of Asian origin) or higher BMI (eg Torres Strait Islander and Maori
peoples).83
It is advisable to also assess waist circumference (in cm) as this is a good indicator
of total body fat and useful predictor of visceral fat. Waist circumference of >94 cm
in men and >80 cm in women conveys increased risk; >102 cm in males and >88
cm in females conveys high risk.84 As with BMI, these values may differ for other
population groups.78 Measuring waist circumference in patients with a BMI >35 kg/m2
may not add any further to predictive disease risk classification.85
Weight management
Modest weight loss (5-10%) may provide clinical benefits for those with type 2 diabetes,
especially early in the disease process.75 Loss of body weight often results in improved
glycaemic control, BP and lipid profiles. Sustained weight reduction of approximately
5 kg is associated with a reduction in HbA1c of approximately 0.5-1%.78 In adults with
BMI <35 kg/m2 with dysglycaemic states or hypertension, weight loss of at least 2-3 kg
achieved with lifestyle interventions may result in a clinically meaningful reduction in BP
(an average SBP of 4.5 mmHg and DBP of 3-3.5 mmHg).78
In overweight or obese people with diabetes, a nutritionally balanced, energy-reduced

diet should be recommended if a lower, healthier body weight is to be achieved and
maintained as part of a multicomponent lifestyle intervention (including healthy eating,
physical activity and support for behavioural change).
38 2016-18
Very low energy diets are a useful intensive medical therapy for supporting rapid weight
loss when used under medical supervision.78 This involves regular appointments with
appropriate health professionals aimed at supporting the progress of the individual.
These diets may be considered in adults with a BMI >30 kg/m2, or with BMI >27 kg/m2
and obesity-related comorbidities, taking into account each individual situation.
Pharmacotherapy is licensed by the TGA for weight management, including for

patients with diabetes, but is currently not PBS reimbursed. All agents are to be used
as adjuncts to dietary changes and physical activity improvement. Agents available
include phentermine (a sympathomimetic amine), orlistat (an inhibitor of intestinal
lipase) and liraglutide (a glucagon-like peptide-1 receptor agonist [GLP-1 RA]). Each
agent has the potential for significant clinical side effects and contraindications
associated with its use, and require careful clinical risk-benefit assessment when
applied in practice. Refer to the TGA website for more information (www.tga.gov.au).
Taking into account each individual situation, bariatric surgery may be considered for
people with a BMI >30 kg/m2 who have suboptimal blood glucose levels and are at
increased CVD risk and who are not achieving recommended targets with medical
therapy.78 GPs should assess the appropriateness of surgery for each individual
patient and provide information on the risks, benefits and appropriateness of the type
of procedure. Bariatric surgery performed in a high-volume specialist centre with an
experienced surgical team may have the lowest risks and GPs should liaise with a
specialised surgical team if there are concerns.78 Bariatric surgery, when indicated,
should be included as part of an overall clinical pathway for adult weight management
that is delivered by a multidisciplinary team (including surgeons, APDs, nurses,
psychologists and physicians), and includes planning for surgery, and continuing
follow-up.78
6.4 Smoking cessation

*
Smoking cessation should be a major focus of the management 86 A
of people with smoking-related diseases RACGP, 2011
All smokers should be offered brief advice to quit smoking 86 A
RACGP, 2011
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39
Clinical context
Smoking is associated with an increased risk of type 2 diabetes in men and women,87
and smoking negatively affects glycaemic control (eg smokers with type 2 diabetes
need larger doses of insulin to achieve control similar to that of those who do not
smoke).88
Patients with diabetes who smoke also further increase their risk of CVD, peripheral
vascular disease and neuropathy (and progression of neuropathy). Smoking also
increases the risk associated with hospitalisation for surgery.86
In practice
The importance of smoking cessation in those with or at risk of type 2 diabetes cannot
be overstated.
Guidelines for smoking cessation and a pharmacotherapy treatment algorithm are

available for download from the RACGP website (www.racgp.org.au) and in the
RACGP’s Supporting smoking cessation: A guide for health professionals.86

Resources and strategies for smoking cessation for Aboriginal and Torres
Strait Islander peoples are available at the Centre for Excellence in Indigenous
Tobacco Control (CEITC; www.ceitc.org.au). Specific support for Aboriginal and
Torres Strait Islander peoples is also provided by Quitline.
In the absence of contraindications, smokers who have evidence of nicotine

dependence should be offered pharmacotherapy if they are motivated to stop smoking.
The choice of pharmacotherapy is based on clinical suitability and patient choice.
There is a lack of safety data on the use of varenicline or bupropion in diabetes.

However, if diabetes is well controlled with insulin or oral glucose-lowering medication,
150 mg of bupropion once daily may be prescribed. If the diabetes is poorly
controlled, nicotine replacement therapy is considered preferable.86
40 2016-18
6.5 Alcohol consumption

*
People with diabetes can take alcohol in moderation as part 65 B
of a healthy lifestyle, but should aim to keep within the target SIGN, 2014
consumption recommended for people without diabetes
Clinical context
Alcohol affects the management of type 2 diabetes through its effects on diet and
control of BGLs. Alcohol interferes with the action of insulin, insulin secretagogues and
glucagon, thereby increasing the risk of hypoglycaemia in people with type 2 diabetes
who take these medications.71 Alcohol can lower BGLs and reduce awareness of
hypoglycaemia. Alcohol and hypoglycaemia have independent but additive adverse
effects on cognitive function.65
Reduction in energy intake, which may involve reducing alcohol intake, may be
important for managing weight in the overweight or obese person as part of diabetes
management.89
In practice
Patients should be educated on how to avoid hypoglycaemia when drinking alcohol.
The current Australian guidelines to reduce health risks from drinking alcohol (www.
nhmrc.gov.au/_files_nhmrc/publications/attachments/ds10-alcohol.pdf) recommends
<2 standard drinks (20 g) per day for men and women. Low-alcohol beers are a better
choice than ordinary or diet beers.89 The carbohydrate content of low-carbohydrate
beer is not significantly less than full-carbohydrate beers and the alcohol content is
often full strength.
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. Drinking
no more than four standard drinks on a single occasion reduces the risk of alcohol-
related injury arising from that occasion.89 It is recommended that people with diabetes
abstain from alcohol if they plan to drive.90
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7. The person with diabetes - Assessment
7.1 Understanding the person - Initial assessment

The aim of the initial assessment is to provide a whole-person evaluation, and
determine and understand which factors are affecting the patient’s health and quality
of life. Many people with diabetes are dealing with multiple medical conditions (not
necessarily related to diabetes) and family, work or financial stresses. Some are also
dealing with other factors including poor sleep, smoking, lack of exercise and pain that
affects their priorities for management.91 This can have an impact on the individualised
approach to diabetes management and outcomes.
A detailed assessment, including appraisal of CVD risk and end-organ damage,

should be made at first diagnosis.

In Aboriginal and Torres Strait Islander patients, the development of rapport
may take precedence over a detailed assessment in a single consultation.
An assessment could be done over several visits.92
Developing a doctor-patient (or patient-healthcare worker) relationship based

on trust and respect is the best way of overcoming cultural barriers and ensuring
effective care in the long term.
History
Ascertain symptoms supportive of a diagnosis of diabetes, including a history
regarding the onset of symptoms (including obstetric history).
Factors in a specific diabetes enquiry:
• Symptoms of hyperglycaemia: polyuria, polydipsia, polyphagia, weight loss, nocturia.

• Sequelae of hyperglycaemia and complications of diabetes: malaise/fatigue,
cardiovascular symptoms, neurological and autonomic symptoms, altered
vision, bladder and sexual function, foot and toe numbness and pain, and any
recurrent infections (especially urinary and skin with delayed wound healing) and
gastrointestinal dysfunction (such as gastroparesis and nausea). Include specific
enquiry about dental hygiene and gingivitis.
42 2016-18
Enquire about specific issues that may provide the aetiology or predisposition
to diabetes, including:
• age, family history, cultural group, overweight, physical inactivity, hypertension

• obstetric history of macrosomic babies or gestational diabetes
• medication causing hyperglycaemia (refer to Chapter 8. Managing glycaemia)
• personal or family history of haemochromatosis
• personal or family history of other autoimmune diseases (eg hypothyroidism
or hyperthyroidism)
• pancreatic disease, Cushing’s disease
• obstructive sleep apnoea.
Perform a general health enquiry for:
• presence of risk factors for diabetes complications or known comorbidities

(including personal or family history of CVD), smoking, hypertension, dyslipidaemia,
and also include a history of past or current mental health problems such as
depression
• health literacy and knowledge about diabetes and related complications
• emotional and mental health (use the Patient Health Questionnaire-2 [PHQ-2]
tool to assess depressive symptoms and problem areas in diabetes [PAID] tool to
assess diabetes-specific distress - refer to Appendix C. Problem areas in diabetes
questionnaire and Appendix D. Patient health questionnaire-2 tool)
• living situation (eg alone/with family, employment, financial worries).
It is important to confirm the patient’s immunisation currency. The following
vaccinations are recommended for patients with type 2 diabetes:
• Influenza - once per year
• Pneumococcal
- Non-Indigenous Australians: <65 years of age - single dose and revaccinate at
65 years of age or after 10 years, whichever is later; >65 years of age - single
dose and revaccinate after five years
- Aboriginal and Torres Strait Islander peoples: <50 years of age - single dose
and revaccinate at 50 years of age or after 10 years, whichever is later; >50
years of age - single dose and revaccinate after five years
• Tetanus - booster at 50 years of age (unless booster has been given within 10
years). Tetanus vaccination in adults is best given with a multivalent vaccine such
as dTpa.
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• Other vaccinations as required on an individual basis according to the Australian

immunisation handbook, 10th edn (www.immunise.health.gov.au/internet/
immunise/publishing.nsf/Content/Handbook10-home ).
Full physical assessment

This should be focused on determining current overall health status to provide
information that helps establish management strategies including treatment options.
Assess cardiovascular status and risks

Visceral fat accumulation and obesity increase the risks of developing diabetes,
and complications arising from diabetes and comorbidities such as hypertension,
dyslipidaemia and pancreatitis.
Hypertension is more common in diabetes, but autonomic neuropathy conversely may

arise and lead to postural hypotension. Macrovascular disease may be evident on
peripheral arterial examination including the presence of carotid bruits. Dysrhythmias
may indicate the presence of existing CVD.
Assess:
• weight: BMI = weight (kg) divided by height2 (m2)

• waist: waist circumference (cm)
• BP, central and peripheral vascular systems
• absolute CVD risk assessment (this may require calculation and investigations)
• for symptoms of ischaemic disease or dysrhythmia, in which case an ECG may
be considered.
Assess for the presence or absence of diabetes complications

Eyes: Visual acuity (with correction); screen for retinopathy (retinal photography
or examine with pupil dilation and ophthalmoscope) - it is prudent to assess for
retinopathy and maculopathy with diabetes, as they are the leading causes of
blindness and may occur asymptomatically.
Feet: Stratify the risk of developing foot complications (refer to Section 10.5. Foot
complications) - sensation and circulation, skin condition, pressure areas, interdigital
problems, abnormal bone architecture.
Peripheral nerves: Tendon reflexes, sensation - touch (eg 10 g monofilament)

and vibration (eg 128 Hz tuning fork) - existence of peripheral neuropathic changes
indicates the onset of microvascular diabetes complications.
44 2016-18
Urinalysis: Testing for albumin, ketones, nitrites and/or leucocytes. The presence of
proteinuria on clinic testing may necessitate further albumin-to-creatinine ratio (ACR)
investigation to exclude existing diabetes nephropathy.
• Microalbuminuria (http://patient.info/doctor/microalbuminuria) ACR >2.5 mg/mmol

(men) or >3.5 mg/mmol (women), or albumin concentration >20 mg/L.
• Proteinuria (http://patient.info/doctor/proteinuria-pro) ACR >25 mg/mmol (men)
or >35 mg/mmol (women; refer to Figure 5).
• Elevated leucocytes and nitrites may indicate genitourinary infection, which occurs
at a higher prevalence and severity in diabetes.
Investigations
To help determine CVD risks, and as clinically indicated, obtain levels of:
• urine microalbumin, calculated estimated glomerular filtration rate (eGFR)
• lipids - low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein
cholesterol (HDL-C), total cholesterol, triglycerides
• HbA1c (mmol/mol or %).
7.2 What needs ongoing assessment?

The purpose of ongoing structured evaluation is to determine the impact of care and
diabetes on the life of the person with diabetes. It is also to individually assess the
impact of clinical management by assessing the person’s diabetes goals and risk
factors. Review the use of medication every three or six months using the principles
of the ‘Stop rule’ (refer to What if medication is not working - The ‘Stop rule’ under
Section 8.2.2. Glucose-lowering agents).
History
Review the patient’s overall sense of wellbeing, ability to cope and self-manage with
the diagnosis of diabetes, and what effect this is having on the person’s life. Establish
their level of health literacy about their diabetes, and what to do in the event of
problems arising.
Review lifestyle interventions, particularly SNAP profiles: (S)moking persistence or
relapse, (N)utrition and diet, (A)lcohol intake and (P)hysical activity.
Enquire about possible diabetes complications as well as known comorbid conditions

including psychological stress and/or depression (refer to Appendix C. Problem areas
in diabetes questionnaire and Appendix D. Patient health questionnaire-2 tool).
Enquire about intercurrent illnesses (eg urinary tract infections, influenza, thyroid
disease) that may alter the degree of control. Urinary tract infections are common in
patients with diabetes, especially in females.
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Enquire about symptoms of hypoglycaemia if the patient is on insulin and/or oral agents
that can cause hypoglycaemia.
Enquire about the burdens of care/self management. Has the person been referred
or received structured diabetes self-management education?42 Does the person
experience any problems with medication taking, including side effects, forgetting or
sometimes intentionally not taking medications as recommended? Consider alternative
regimens or problem-solving with the patient if problems are significant.
Examination
To help re-evaluate therapeutic goals and assess for complications, check weight and
waist, height (children and adolescents), BP, feet examination (refer to Section 10.5.
Foot complications) if new symptoms or at risk (eg neuropathy ± peripheral vascular
disease). Assess a patient’s record of SMBG testing (if utilised). Individually assess the
need for further re-examination dependent on individual risk factors. For example, BP
may need re-evaluation in two months if elevated at systolic 140-159 mmHg/diastolic
90-99 mmHg, whereas BP at 160-179 mmHg systolic/100-109 mmHg diastolic may
need reassessment within one month.93
Routine investigations are best organised before the review appointment.
To determine measurable diabetes goals for the individual patient:
• Measure HbA1c as needed on an individual basis - this may be up to every third

month (maximum) in a newly diagnosed patient, patients undergoing therapeutic
changes or those outside of recommended ranges; stable patients at agreed targets
may need less-frequent interval testing.
• Base further investigations on re-evaluated clinical symptoms and history (eg a
urine assessment may be considered, or investigation of emotional issues including
depressive symptoms, diabetes-specific distress, or other diabetes-related issues
suspected or identified in earlier consultations).
Refining the management plan

Review the goals and individual targets with the patient to identify specific areas for
ongoing or interval therapeutic review.
Patient support - refer to structured self-management education (eg CDE). Does other
allied health intervention need to be considered (eg psychologist, APD)?
Medication/therapy choices - adjustment of agent, dose, combinations, enquire about

symptoms of hypoglycaemia. Review use of medication using the principles of the ‘Stop
rule’ every three or six months.
Complication management - specific intervention/support/referral when indicated.

46 2016-18
7.3 What should be evaluated yearly?

The annual review is a time for more detailed assessment, updating the problem
priority list, re-establishing goals and checking agreed arrangements for management.
As there is an increasing trend towards involving specialist allied health professionals,

the yearly visit is a good opportunity to coordinate follow-up.
Annual review
A full system review checking for vascular, renal, eye, nerve and podiatric problems
is required. An annual review or cycle of care may address the following:
History
• Review issues specific to diabetes:
- including symptoms of hyperglycaemia, hypoglycaemia and diabetes
complications.
• Preventive health issues:
- smoking
- nutrition (last contact with APD or CDE)
- alcohol intake
- physical activity.
• Adequacy of, or problems with, team care arrangements.
• Patients with diabetes can be assessed for perspectives on adequacy of treatment,
quality of life, medication burden, and concerns regarding diabetes such as mental
health issues, social isolation/networks and family or work stress. Daily diabetes
self care and management can place a considerable burden upon people with
diabetes. It is common for people with diabetes, at times, to feel overwhelmed,
frustrated, guilty, or to worry about their current and/or future diabetes management
and health outcomes.
• Immunisations.
Clinical examination
• Visual acuity. Retinal screening - every two years with no retinopathy, more
frequently if abnormal.
• Cardiovascular system, including postural BP, and central and peripheral vascular
systems. Calculate or re-evaluate absolute CVD risk assessment.
2016-18
• Weight, waist, height (children and adolescents).

• Feet examination without shoes - pulses, monofilament check, any foot discomfort.
• Consider assessment of diabetes distress through the use of the PAID94
questionnaire and depression with the PHQ-295 (refer to Appendix C. Problem areas
in diabetes questionnaire and Appendix D. Patient health questionnaire-2 tool).
Routine investigations
• Re-evaluate lipid parameters. If the patient has low CVD risk, these tests can be
performed every three years. More frequent testing can be justified if the clinical
situation varies or if therapeutic changes have been instituted. Some guidelines
suggest yearly testing of lipids when the patient is deemed to be at clinically high
risk.
• Re-evaluate urine microalbumin annually, unless existing pathology necessitates
more frequent testing.
• Based upon a clinical risk assessment, individually assess the need for further
investigations such as liver enzyme abnormalities for hepatic steatosis.
Evaluation and management

• Shared decision making - Identify specific clinical areas for focus within the
consultation and re-establish patient-specific goals for support and re-evaluation.
• Renew team care planning with identified specific interventions.
• Identify therapeutic management changes and additional education goals with
patient involvement.
• Organise appropriate referral where clinically necessary. Some patients may require
ongoing specialist or other allied health review. Others will have changed priorities;
hence, it is sometimes wise not to commit to referrals too early.
48 2016-18
Table 3. Suggested actions and health professionals providing treatment or

service
Suggested actions Team resource - Who?

Ask
Symptoms General practitioner (GP)
Goal setting supporting self management GP
Cardiovascular issues (eg blood pressure GP/practice nurse
[BP] measurement)
Glycaemic control GP/practice nurse/Credentialled Diabetes
Educator (CDE)/diabetes educator (DE)
Assess (inclusive within an annual cycle of care)

Risk factors for modification GP/practice nurse/CDE/DE
Weight, height GP/practice nurse
Cardiovascular disease risk assessment GP/practice nurse
Foot examination GP/podiatrist/practice nurse
Presence of other complications, especially GP/practice nurse/CDE/DE/
hypoglycaemia risk with insulin or sulphonylureas endocrinologist
Psychological status GP/psychologist
Eye examination GP/optometrist/ophthalmologist
Dental review GP/dentist
Consider other assessments where appropriate GP/endocrinologist/specialist (where
(eg cognitive impairment, obstructive sleep apnoea) indicated)
Advise
Review smoking, nutrition, alcohol, physical activity GP/registered nurse/CDE/DE
(SNAP) profiles, including specific issues
Nutrition GP/Accredited Practising Dietitian (APD)
Physical activity levels GP/Accredited Exercise Physiologist
(AEP)/physiotherapy
Driving GP/practice nurse/CDE
Immunisation GP/practice nurse
Sick day management GP/practice nurse/CDE
Medication issues GP/pharmacist/CDE/endocrinologist
Self-monitoring blood glucose GP/CDE/DE/practice nurse
Insulin/injectable management GP/CDE/registered nurse/accredited
nurse practitioner/endocrinologist
Psychological issues GP/practice nurse/CDE/DE/psychologist
2016-18
49
Assist
Register for National Diabetes Services Scheme (NDSS) GP/CDE/nurse practitioner
General practice management plan (GPMP) and GP/practice nurse
Chronic disease management plan
Cultural, psychosocial issues GP/Aboriginal health worker/social
worker/CDE/DE/psychologist
Arrange
Addition to the practice’s diabetes register and recall GP/practice nurse/practice staff
Organise reviews including pathology and annual GP/practice nurse
cycle of care
Driver’s licence assessment GP/practice nurse/endocrinologist
(when indicated)
50 2016-18
8. Managing glycaemia
The aim of glycaemic control is to assess each individual patient and balance the role
of prevention of glycaemic complications of diabetes while avoiding hyperglycaemia
and hypoglycaemia. Overall, managing CVD risk in each patient remains a higher
priority than strict glycaemic control.
Refer to Chapter 9. Managing cardiovascular risk.
8.1 Glycaemic monitoring

*
Glycated haemoglobin (HbA1c) measurement should be used to 96 A
assess long-term blood glucose control NHMRC, 2009
Self-monitoring of blood glucose is recommended for patients 65 B
with type 2 diabetes who are using insulin where patients have SIGN, 2014
been educated in appropriate alterations in insulin dose
(Refer to Self-monitoring of blood glucose under Section 8.2.
Medication for examples of instances when self-monitoring of
blood glucose may be considered)
Routine self-monitoring of blood glucose in people with type 2 65 B
diabetes who are using oral glucose-lowering drugs (with the SIGN, 2014
exception of sulphonylureas) is not recommended
Clinical context
Accuracy and limitations of the HbA1c test
Koenig first proposed the measurement of HbA1c in patients with diabetes as a
marker for evaluating long-term control of diabetes in 1976.97 Over time, this has
become a gold standard.
There are potential pitfalls of HbA1c as a measure of long-term diabetes management,

and all diabetes clinicians should be aware of natural test variations and conditions
that affect HbA1c results.
HbA1c measurement and natural test variation

HbA1c can be measured and reported using two different standards: the National
Glycohemoglobin Standardization Program method reported as a per cent of units
2016-18
51
(eg 7%) and the newer International Federation of Clinical Chemistry standardisation
reported as mmol/mol (eg 53 mmol/mol).
The variability of HbA1c values within Australia is now acceptably low. In a recent
Australian study, more than 90% of HbA1c results fell within 6% of the median. A true
level of 53 mmol/mol or 7.0% may be reported as anywhere between 49 mmol/mol or
6.6% and 57 mmol/mol or 7.4%.38
This variation needs to be considered when monitoring long-term glucose control.
Conditions affecting the HbA1c result

Any condition that shortens erythrocyte survival or decreases mean erythrocyte age
will falsely lower HbA1c test results regardless of the assay method used (Table 4).
The presence of abnormal haemoglobin variants can cause unusually high HbA1c
(eg HbF, HbE, HbD, HbJ Capetown, Hb Raleigh) or unusually low HbA1c readings
(eg HbS, HbC, HbJ, HbG, Hb Ramadan).
Table 4. Other causes of variances to HbA1c

Abnormally low glycated haemoglobin (HbA1c)
• Haemolytic anaemia: congenital (eg spherocytosis, elliptocytosis), haemoglobinopathies,
acquired haemolytic anaemias (eg drug-induced such as with dapsone, methyldopa)
• Recovery from acute blood loss
• Chronic blood loss
• Chronic renal failure (variable)
Abnormally high HbA1c

• Iron deficiency anaemia98
• Splenectomy
• Alcoholism
• Steroid therapy stress, surgery or illness in the past three months
Several situations may indicate the presence of a haemoglobinopathy, including when:
• results of SMBG have a low correlation with HbA1c results

• an HbA1c result is discordant with measured laboratory glycaemia
• an HbA1c result is more than 15%
• a patient’s HbA1c test result is radically different from a previous test result following
a change in laboratory HbA1c measurement methods.
If a haemoglobinopathy is suspected, then a haemoglobin electrophoresis is
suggested. Schnedl et al reported a prevalence of abnormal haemoglobin variants of
0.6% among 15,000 HbA1c estimations in a period of over six years.99
52 2016-18
Reliable HbA1c tests, in which haemoglobin variants do not cause interference, are
available. Otherwise, alternative forms of diabetes monitoring such as continual blood
glucose estimations, SMBG and fructosamine should be considered for these patients.
Self-monitoring of blood glucose

Self-monitoring in patients with type 2 diabetes is usually recommended:
• for patients on insulin and glucose lowering agents that can cause hypoglycaemia
• when monitoring hyperglycaemia arising from illness (Chapter 11. Glycaemic
emergencies and Appendix J. Detailed information on glycaemic emergencies)
• with pregnancy and pre-pregnancy planning
• when changes in treatment, lifestyle or other conditions requires data on glycaemic
patterns
• when HbA1c estimations are unreliable (eg haemoglobinopathies).
The method and frequency of monitoring need to reflect individual circumstances
and therapeutic aims, and where the person with diabetes and their healthcare
providers have the knowledge, skills and willingness to incorporate SMBG and therapy
adjustments into diabetes care plans.
A 2012 Cochrane review on the effect of SMBG in patients with type 2 diabetes
not using insulin found limited clinical benefit as measured by HbA1c from SMBG.
Therefore, routine SMBG for people with type 2 diabetes who are considered low risk
and using oral glucose lowering drugs (with the exception of sulphonylureas) is not
recommended.100-104
In practice
*
Blood glucose control should be optimised because of its beneficial 96 A
effects on the development and progression of microvascular NHMRC, 2009
complications
in people with type 2 diabetes should be considered when setting NHMRC, 2009
The general glycated haemoglobin (HbA1c) target in people with 96 A
type 2 diabetes is <53 mmol/mol (<7%). Adjustments to diabetes NHMRC, 2009
treatment should be considered when HbA1c is above this level
Targets for self-monitoring of blood glucose levels are 6-8 mmol/L for 96 C
fasting and preprandial, and 6-10 mmol/L for two hour postprandial NHMRC, 2009
2016-18
53
HbA1c targets and individualisation

The general HbA1c target in people with type 2 diabetes is HbA1c <53 mmol/mol (<7%).
Due to the natural variation of HbA1c test results, a target HbA1c of 53 mmol/mol would
be achieved by laboratory results being in a range of 48-58 mmol/mol (6.5-7.5%).
All patients with diabetes need to optimise their blood glucose control to improve short
term and long-term health outcomes. However, what is ‘optimal’ will vary depending on
the balance between benefits and risks, and the patient’s priorities (Figure 3).
Given the range of diabetes presentations to general practice, there is no single

glycaemic target that suits all patients. Targets need be individualised and balanced
against patient capabilities and the risk of severe hypoglycaemia, especially among
older people.
Control of diabetes symptoms (eg polydipsia, polyuria) can usually be achieved

around a HbA1c level of 64 mmol/mol (8%). This does not necessarily mean optimum
metabolic control.
More stringent HbA1c targets might be considered in selected patients (eg those with
short disease duration, long life expectancy, no significant CVD) if this can be easily and
safely achieved without significant hypoglycaemia or other adverse effects of treatment.
54 2016-18
Figure 3. Approach to management of hyperglycaemia
Patient/disease More stringent <—HbA1c —► Less stringent

features 7%
Risks potentially associated Low High

with hypoglycaemia, other
adverse events
Disease duration Newly diagnosed Longstanding
Life expectancy Long Short
Important comorbidities Absent Few/mild Severe
Established vascular Absent Few/mild Severe

complications
Patient attitude and Highly motivated, Less motivated, non-adherent,

expected treatment efforts adherent, excellent poor self-care capacities
self-care capacities
Resources, support system Readily available Limited
Usually not modifiable Potentially modifiable
Reproduced with permission from the American Diabetes Association from Inzucchi SE,
Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: A patient
centered approach: Position statement of the American Diabetes Association and the European
Association for the Study of Diabetes. Diabetes Care 2015;38(1):140-49.
2016-18
55
Not everyone benefits from long-term intensive glucose management.
Less stringent HbA1c goals (eg 58-64 mmol/mol [7.5-8.0%] or even slightly higher)
are appropriate for patients with a history of severe hypoglycaemia, limited life
expectancy, advanced complications, extensive comorbid conditions, and those for
whom the target is difficult to attain despite intensive self-management education,
repeated counselling, and effective doses of multiple glucose-lowering agents,
including insulin.105
Targets for self-monitored glycaemic control in type 2 diabetes are shown in Table 5.
Table 5. Targets for self-monitored glycaemic control in type 2 diabetes
Fasting blood Preprandial Postprandial Comment

glucose (FBG; blood glucose blood glucose
mmol/L) (mmol/L) (mmol/L)
6.0-8.0 6.0-8.0 6.0-10.0 NHMRC values96
8.2 Medication
8.2.1 General medication

*
Care should be taken to address the potential harmful effects of 96 A
optimising blood glucose control when setting individual glycaemic NHMRC,2009
targets
Interventions to achieve target glycated haemoglobin (HbA1c) 96 A
should begin with lifestyle modification followed by pharmacological NHMRC,2009
options selected on the basis of individual clinical circumstances,
side effects and contraindications
Blood glucose control should be optimised because of its beneficial 96 A
effects on the development and progression of microvascular NHMRC,2009
complications
56 2016-18
Clinical context
In addition to lifestyle modification, people with type 2 diabetes may require
pharmacotherapy to achieve long-term glycaemic control and to prevent
complications of diabetes. There may be a need to commence medication without
delay in patients who are symptomatic of hyperglycaemia or having accompanying
metabolic dysfunction (eg ketosis), while providing ongoing lifestyle support.
The benefits of management of hyperglycaemia for the prevention of microvascular
complications have been demonstrated in randomised clinical trials. BP and lipid
lowering therapy have also been demonstrated in clinical trials to show clear benefits
in preventing cardiovascular events and reducing premature mortality.
The choice, order and combination of medications used are based on evidence of
improved clinical outcomes, risk of side effects and patient choice/capacity.
In practice
Use of these therapies is associated with risks and other negative effects.
These should be taken into consideration when deciding the appropriateness of
implementing the treatment recommendations contained in these guidelines. These
therapies may be contraindicated in some situations and their use may result in
troublesome side effects.
8.2.2 Glucose-lowering agents
Clinical context
Multiple glucose-lowering pharmacotherapies are available (Appendix E. Available
glucose-lowering agents).
Algorithms have been designed to help navigate choice. However, applying the
principles of patient-centred care may mean that choices made by algorithm are
not always appropriate.
The Australian blood glucose treatment algorithm for type 2 diabetes (Figure 4) is
an evidence-based algorithm developed by the Australian Diabetes Society (ADS)
in consultation with all key stakeholders including the RACGP.
Additionally, when analysing combination therapies used in current suggested

algorithms for the management of hyperglycaemia, high-quality trials of clinical
outcomes may be lacking. The most studied agents include metformin and
sulphonylureas. However, randomised controlled trials (RCTs) investigating the safety
2016-18
57
of newer agents such as the incretins and sodium glucose co-transporter 2 (SGLT2)
inhibitors in patients with high CVD risk are now being reported.106-108
Prescribing algorithms suggest multiple ways of combining agents. Always consult the
PBS when combining therapy as restrictions and reimbursement may change. Table 6
provides a guide for clinical considerations when choosing diabetes medications.
Appendix F. Table of evidence and properties of glucose-lowering agents provides the

evidence and properties of glucose-lowering agents for this algorithm.
What if medication is not working - The ‘Stop rule’

At each visit, ask about the patient’s understanding of their diabetes and the role
of medication in management. Specific enquiry may help decisions on medication
efficacy and choices. Symptoms suggestive of hypoglycaemia or other side effects
of medication should trigger a clinical examination and review. Symptoms of
hyperglycaemia (eg polyuria, polydipsia), fatigue and visual changes may warn of
poor adherence to medication by the patient, or indicate that the medication(s) is/are
not effective in glycaemic management. Confirmation with an assessment of HbA1c
(usually every three months) in relation to the individual’s goals may be appropriate.
Consideration of the effect of comorbidities (refer Chapter 12. Diabetes multimorbidity
and medication complications) or other medication affecting glycaemic control may
need to be assessed and managed. Consideration of a home medicines review by
the treating pharmacist may also assist assessment of clinical reasons for problems of
persistence, side effects with medication or patient concerns.
Practice point
The ‘Stop rule’ emphasises that before advancing through additional glycaemic-
lowering combinations, after evaluating each patient’s HbA1c response after three
to six months, support the patient to engage in healthy lifestyle choices, assess for
comorbidities and complications (eg CVD risk or distress) and then evaluate the need
for additional or altered medication/combination therapy.
cn
co
Figure 4. Australian diabetes algorithm and clinical medication table

2016-18
First line: Metformin is the usual first-line therapy unless contraindicated or not tolerated
Dipeptidyl Sodium glucose

Sulphonylureas Thiazolidinedione
Metformin peptidase co-transporter 2 Insulin Acarbose (TZD)
(SU) inhibitor (DPP-4i) inhibitor (SGLT2i)
If glycated haemoglobin (HbA1c) target not achieved in three months:

• check and review current therapies, • review use of therapies
stop any that fail to improve glycaemic control . exclude other comorbidities/therapies impacting
• check patient's understanding and self-management on glycaemic control
Second line: If metformin was not used first line, add it now, if not contraindicated
SU are the usual initial agent to add to metformin. If SU are contraindicated or not tolerated, another agent may be
used
Glucagon-like
SU DPP-4Ì SGLT2Ì peptide-1 receptor *
Insulin Acarbose TZD
agonist (GLP-1RA)
If HbA1c target not achieved in three months:

stop any that fail to improve glycaemic control • exclude other comorbidities/therapies impacting
• check patient understanding and self-management on glycaemic control
Third line: Consider triple oral therapy or addition of GLP-1 RA or insulin
SU DPP-4Ì SGLT2Ì GLP-1 RA *

Insulin Acarbose TZD
If HbA1c target not achieved in three months:

stop any that fail to improve glycaemic control • exclude other comorbidities/therapies impacting
• check patient understanding and self-management on glycaemic control
If on triple oral therapy If on GLP-1 RA If on basal insulin

*

Switch >1 oral agent to Change to basal Add basal Add SGLT2 inhibitor or
GLP-1 RA or insulin
* or another or premixed or premixed GLP-1 RAor basal bolus
oral agenf insulin
* *
insulin or basal plus insulin
Australian blood glucose treatment algorithm for type 2 diabetes

Determine the individual’s HbA1c target - this will commonly be <53 mmol/mol (7%). If not at target, or if an HbA1c reduction of >0.5% is not
achieved after three months, move down the algorithm
Reproduced with permission from the Australian Diabetes Society.
2016-18
Dark blue boxes indicate usual therapeutic strategy (order is not meant to denote any specific preference) (usual refers to commonly available, evidence-based, cost-effective therapy). White boxes
indicate alternate approaches (order is not meant to denote any specific preference). Black outlines indicate the classes of glucose-lowering agent that include PBS-subsidised products
‘Unless metformin is contraindicated, or not tolerated, it is often therapeutically useful to continue it in combination with insulin in people with type 2 diabetes
fSwitching an oral agent is likely to have the smallest impact on glycaemia
60 2016-18
Table 6. Clinical considerations when choosing diabetes medications

Dipeptidyl
peptidase-4 inhibitor
Clinical outcome Metformin Sulphonylurea (SU) (DPP-4i)
Increase risk when SU compared

Patients with
to metformin monotherapy
established or high risk Neutral107,111-114
Neutral109 (excluding gliclazide), but neutral
cardiovascular disease Refer to Note A
when used in combination with
(CVD)
metformin110
Higher clinical risks as

monotherapy and combination
Patients with risk from Lower rates with other agents110 Lower rates
hypoglycaemia compared to SU110 Gliclazide - 50% fewer compared to SU110
hypoglycaemia episodes versus
glimepiride122
Patients at risk of
gastrointestinal
Known intolerance
conditions (eg irritable
as monotherapy or
bowel syndrome [IBS], Neutral effect Neutral effect
combination therapy
inflammatory bowel
- diarrhoea110,124
disease [IBD] and
gastroparesis)
Patients in whom Less weight gain

Neutral effect (gliclazide)125
stabilisation of body (when added to
Neutral effect Modest gain (other SUs) compared
mass index [BMI] or metformin versus
to metformin monotherapy110
weight loss is desired metformin and SU)110
Patients with renal Reduce dose eGFR

dysfunction (eg 30-60 Safe with dose
lowered estimated Hypoglycaemia risk increases reduction#
glomerular filtration Contraindication
Refer to Note D
rate [eGFR]) with eGFR <30124
Monotherapy or
combination with The Australian algorithm (refer to
Unique/class-specific Contraindication -
other agents (DPP- Figure 4) suggests they may be
pharmacological do not use with a
4i or SGLT2i) is used as monotherapy or combined
effects GLP-1 RA
available to reduce with other agents
‘pill burden’
2016-18
61
Sodium glucose Glucagon-like

Thiazolidinedione co-transporter 2 peptide-1 receptor
Acarbose (TZD) inhibitor (SGLT2i) agonist (GLP-1 RA) Insulin
Selective Selective
Contraindication if
Not yet benefit/not yet benefit/118,119 not yet
symptomatic heart Neutral109,120,121
known115 known117 known
*
failure 116
Refer to Note B Refer to Note C
Lower hypoglycaemia
when metformin is
Lower rates
Lower rates compared Lower rates added to basal versus
Neutral compared to
to SU110 compared to SU110 premixed insulin
SU110
(consider risks greater
with prandial insulin)123
Known Known intolerance

Intolerance - - nausea and
Neutral effect Neutral effect Neutral
bloating and vomiting, and
flatulence1 diarrhoea *110
Modest
Weight loss (in
weight loss (in
monotherapy, plus
monotherapy, plus
Modest gain in combination with
in combination Modest gain - risk
compared with other metformin versus
Neutral effect with metformin greater with prandial
dual combination metformin with
versus metformin insulin110,123
therapies110 alternate dual oral
with alternate
drug combinations)1
dual oral drug 110,126
combinations^ 110
Efficacy
Contraindica
decreases, thus
tion in severe Contraindication Hypoglycaemia risk
Neutral contraindication
renal eGFR<30* increases
with moderate
impairment
renal impairment11
Increased atypical Modest lowering

fractures relative risk of blood pressure
*
(RR) 1.57127 in women (BP)110
Once weekly
Rare - Pioglitazone Increased
formulations are
has been associated genitourinary Dose required to be
available*
with an overall 63% (especially titrated to glycaemic
females) Contraindication
increased risk of goals
- do not combine
bladder cancer, with Refer to Note E
with a DPP-4i
the risk increasing with Rare -
increasing duration of euglycaemic
use and dose128 ketoacidosis**
62 2016-18
DPP-4i, dipeptidyl peptidase-4 inhibitor; eGFR, estimated glomerular filtration rate; GLP-1 RA,
glucagon like peptide-1 receptor agonist; IBD, Inflammatory bowel disease; IBS, Irritable bowel
syndrome; insulin, basal, basal analogue, NPH and rapid-acting or prandial insulins including
mixed insulins; PI, product information; SGLT2i, sodium glucose co-transporter 2 inhibitor; SU,
sulphonylurea; TZD, thiazolidinedione
Important to note
Clinical considerations have been derived from the attached main references: Bennet W et al,127
Qaseem A et al129 and Bolen T et al110
Careful interpretation of results is recommended due to medication in combination studies having
variance from Australian prescribing algorithms
Due consideration to each individual patient, diabetes and metabolic goals, disease and complication
burden, medication side effects, and costs and psychosocial factors need to be incorporated in
decision making, not just the medication factors (Table 6)
Notes
SU: Statements of evidence (SOEs) strengths110 are related to the common forms available in the US -
but are not inclusive of gliclazide, the most commonly used SU agent in Australia
Note A. DPP-4i and heart failure: In the SAVOR-TIMI 53 trial107 - hospitalisations for heart failure (a
secondary outcome) increased with saxagliptin. Despite this, a recent meta-analysis found difficulty in
drawing firm negative conclusions on the comparative safety of this class of drugs in heart failure
Note B. SGLT2i: The EMPA-REG outcome trial117 found that patients with diabetes at high CVD risk
had reduced all-cause mortality and death from cardiovascular causes with empagliflozin. There have
been no reported clinical trials for other drugs in this class
Note C. GLP-1 RA - The LEADER trial, a prospective cardiovascular safety outcomes trial for
liraglutide, found a 13% reduction in major adverse cardiac events and a 22% reduction in
cardiovascular death in high-risk cardiovascular patients.130 This effect has not been replicated in
similar trials for lixisenatide and no trials on exenatide have yet been reported
Note D. DPP-4i: All except linagliptin (no dose reduction) as this is hepatically metabolised
Note E. All classes: The recent Agency for Healthcare Research and Quality (AHRQ) US review110
determined no moderate to high levels of evidence for the following adverse events (this does not
mean no risk):
• Lactic acidosis (metformin)
• Urinary tract infections/fractures/volume depletion (SGLT2i)
• pancreatitis (DPP-4i and GLP-1 RA)
• bladder cancer risks (pioglitazones)
• thyroid cancer (GLP-1 RA)
*Pioglitazone product information is available at www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/
pdf?0penAgent&id=CP-2015-PI-01220-1&d=2016060116114622483
tAcarbose product information is available at www.bayerresources.com.au/resources/uploads/PI/
file9350.pdf
Êxenatide product information is available at www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/

pdf?OpenAgent&id=CP-2013-PI-01780-1
§Dapagliflozin product information (-2.14 kg) as an add-on to metformin versus placebo at 104 weeks;
empagliflozin (-1.63 kg) and (-2.03 kg) at doses 10 mg and 25 mg respectively as an add-on to
metformin at 24 weeks
2016-18
63
“Exenatide -1 kg to 3.9 kg in comparative trials with combinations including metformin and SU and TZD
#All except linigliptin (no dose reduction)
"Exenatide (Bydureon) product information is available at www.ebs.tga.gov.au/ebs/picmi/

picmirepository.nsf/pdf?OpenAgent&id=CP-2013-PI-01764-1
t+ Dapagliflozin contraindicated of eGFR <60; empagliflozin/canagliflozin contraindicated of eGFR <45
^Safety advisory - risk of diabetic ketoacidosis available at www.tga.gov.au/alert/sodium-glucose-co-

transporter-2-inhibitors-used-treat-type-2-diabetes
In practice
Beginning glucose-lowering therapy
Healthy eating, physical activity and education remain the foundation of all type 2
diabetes treatment programs.
If lifestyle modification is not effective in controlling hyperglycaemia, metformin is the
first choice unless contraindicated or not tolerated.
Second-line agents (added to existing metformin) may be necessary and should be

chosen using an individualised approach, noting that agents work in different ways
and are chosen to work synergistically.
While these guidelines recommend a stepwise approach to the management of type

2 diabetes, glycaemic management has become more complex with an increasing
range of medications now available. There are a number of trials exploring the effects
of various therapies on major cardiovascular events such as myocardial infarction (MI)
and stroke. These trials include short-term trials of dipeptidyl peptidase-4 inhibitors
(DPP-4i; oral: saxagliptin, alogliptin and sitagliptin) and glucagon like peptide-1
receptor agonists (GLP-1 RA; injectables: lixisenatide and liraglutide) and a sodium
glucose co-transporter 2 inhibitor (SGLT2i; empagliflozin). However, there is a lack of
data regarding long-term outcomes as well as potentially serious adverse outcomes
associated with some of the newer agents. Unfortunately, a simple stepwise algorithm
cannot match all individual patient’s needs. The Australian Diabetes Society position
statement131 provides patient options based on consideration of efficacy, side effects,
and costs.
Start with the correct dose of each medication and review on an individual basis at least
every three to six months, keeping in mind the patient’s individual HbA1c target.132
64 2016-18
Safety
Each different class of glycaemic medications may have common and uncommon side
effects that impact quality of life and require careful clinical re-assessment. Examples
include some weight gain with sulphonylureas,110 or mycotic infections and the rare
euglycaemic diabetic ketoacidosis with SGLT2i.
Some patient groups (eg elderly and those with multiple comorbidities) may not be
represented in the published clinical outcome trials of newer diabetes agents, so
caution should be exercised when considering choice of agents for these patients.
When used as monotherapy, metformin, acarbose, glitazones, GLP-1 RA, DPP-4i

and SGLT2i should not cause hypoglycaemia.
Long-acting sulphonylureas (eg glimepiride) or sulphonylureas with renally excreted

active metabolites (eg glibenclamide) are more likely to cause hypoglycaemia than
shorter-acting sulphonylureas (eg gliclazide).133,134 Special care needs to be taken
with those at increased risk of hypoglycaemia, especially the elderly. People taking
sulphonylureas or insulin may need to notify motor vehicle licensing authorities as
these medications can affect driving performance, as well as increase the patient’s
burden by requiring glucose self monitoring, especially on initiation or dose titrations.
It is important that patients inform their insurance agents or companies (also refer to
Chapter 14. Management of other impacts of diabetes).
8.3 Insulin
Clinical context
The impact of insulin on microvascular and cardiovascular outcomes has been
partly evaluated in a comparative prospective outcome trial (eg the United Kingdom
Prospective Diabetes Study [UKPDS]).
In terms of glycaemic control in type 2 diabetes, rapid-acting insulin and long-acting

insulin analogues offer little benefit relative to conventional insulins.135 However,
a meta-analysis has demonstrated reduced hypoglycaemia with glargine insulin
when compared to isophane insulin.136 The Outcome Reduction with Initial Glargine
Intervention (ORIGIN) trial demonstrated no beneficial or detrimental effect of glargine
insulin on cardiovascular events.121
The use of insulin can improve glycaemic control in most people, but the increased risk
of hypoglycaemia and weight gain (especially prandial insulins) must be considered.
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65
Further long-term, high-quality prospective outcome studies of all glucose-lowering

agents including insulin analogues are required. Improvements in surrogate markers
such as HbA1c may not necessarily equate with longer term, clinically significant
benefits.
Side effects of insulin therapy

Rare adverse events associated with the use of insulin have been reported in
observational studies. Such events include congestive heart failure, oedema,
lipodystrophy, allergic reactions, reversible transaminitis, reversible nephrotic syndrome
and B-cell destruction.61
Common side effects include hypoglycaemia and weight gain.
Risk factors for hypoglycaemia include:
• inappropriate dose
• timing or type of insulin (refer to below)
• missing meals
• alcohol intake
• exercise
• weight loss
• treatment with agents potentiating hypoglycaemia (eg sulphonylureas)
• decreased insulin clearance (eg renal failure).
Strategies for preventing hypoglycaemia in patients involve educating them about
hypoglycaemic symptoms, structured SMBG, discussing and individualising glycaemic
goals, and continued team-based support.61
Weight gain is variable on initiation of insulin and may accompany initial titration such
that weight gain may eventually level off. Slower titration has been accompanied
by slower weight gain. Strategies to address weight include: referral to an APD,
management of any accompanying depression, a review of medications that may
contribute to weight gain and advice on increased physical activity.
66 2016-18
Early insulin intervention

Guidelines outlining the use of insulin in acute hyperglycaemic emergencies (including
ketosis inducing and hyperosmolar crises) are available.137-139 The use of insulin in
these cases may be life saving and re-assessment of long-term use can occur on
metabolic stabilisation.
Insulin types
Refer to Appendix G. Types of insulin available.
Insulin delivery options

A range of devices are available to deliver insulin, including insulin injectors (pens),
insulin syringes and insulin pumps. Choice will depend on patient preference and
capability. A CDE or a diabetes nurse practitioner can assist in the provision of patient
support.
Insulin injectors (pens) are the most common way of administering insulin as they
make multiple daily injection schedules much easier and allow people to be more
flexible in their self management. Some people may find the ‘InnoLet’ injector easier
to use because it is larger and has more visible markings; however, there are limited
forms of insulin available with this device.
Insulin pumps have traditionally only been used in the management of type 1 diabetes.
There is no evidence of the beneficial effects of using insulin pumps in people with
type 2 diabetes.
Single use of pen needles and syringes is recommended.
In practice
Insulin therapy can be well managed in general practice.
GPs should anticipate and proactively address the patient’s (and their own) reluctance
to starting insulin therapy. Many patient concerns can be easily alleviated.140
Insulin is still the most effective glucose-lowering agent for type 2 diabetes, and can
be titrated to suit the individual patient’s requirements. Commencement should not
be delayed if hyperglycaemia and symptoms cannot be adequately controlled by a
patient’s existing treatments. Insulin is not the end of the road for the person with
diabetes, nor does it represent therapeutic or patient failure. The potential need for
insulin should be broached early with patients.
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When should patients start insulin?

It is important to discuss with patients with diabetes that insulin may be used at some
point in their illness. Insulin should be initiated in patients with type 2 diabetes who
are taking maximal doses of oral glucose-lowering agents and who have suboptimal
glycaemic control (HbA1c or blood glucose above individualised target) whether they
are asymptomatic96,105,141,142 or symptomatic.96
Insulin therapy may remain an alternative for elderly or nursing home patients with
HbA1c >75 mmol/mol (9%), especially if control of symptomatic hyperglycaemia
is difficult.
Before starting insulin

Ensure that other possible causes of hyperglycaemia have been addressed (eg
lifestyle, non-adherence to oral glucose lowering agents, taking other medication
or medical conditions).141
Discuss with patients the benefits and costs of using insulin for better glycaemic
control (Box 4).
Insulin initiation requires planning for patients (or their carers) with a focus on self
management through education about dose adjustment, insulin delivery techniques,
and SMBG and sick day management. Referral is recommended to a CDE prior to
commencing insulin therapy. Insulin therapy requires initial education and skills training,
with regular structured follow-up on such topics as: dose adjustment, insulin needle
length and rotation techniques, hypoglycaemia management, exercise, illness and
travel considerations, sharps disposal, identification, roads and maritime services
notifications, and sick day management.
Box 4. Benefits and costs

Benefits: Costs:
• complications • weight
• quality of life • hypoglycaemic risk
• GP visits
Initiating insulin
All insulins work effectively140 and there is no wrong choice when commencing insulin.
At the same time as selecting the insulin preparation, consider which injecting device
is most suitable for the patient.
68 2016-18
Select one of two insulin schedules:
• Basal insulin (eg glargine, isophane) once daily (refer to Appendix H.1. Guide to
starting and adjusting basal insulin).
• Premixed (biphasic) insulin (eg lispro/lispro protamine or aspart/protamine insulin)
once daily before the largest meal of the day143 (refer to Appendix H.2. Guide to
starting and adjusting premixed insulin).
One way to commence insulin therapy is with basal insulin, which has a slightly lower
risk of nocturnal hypoglycaemia, especially if the fasting glucose is consistently above
target.105,141,143 Alternatively, premixed insulin may be more appropriate and simpler for
a patient where fasting and postprandial glucose are consistently elevated.
Dosage adjustment can be more complex with premixed insulins as both insulin
components are adjusted simultaneously, increasing the risk of hypoglycaemia and
weight gain compared with basal insulin.143-145
Oral glucose lowering medications (eg metformin, sulphonylureas) may be continued

as:141
• early cessation before blood glucose targets are achieved can result in significant
hyperglycaemia
• ongoing use can reduce weight gain
• ongoing use allows a smaller insulin dose and can reduce the risk of hypoglycaemia
or hyperglycaemia.
Titrating insulin
Set an individualised target (refer to Section 8.1. Glycaemic monitoring), then ‘start low
and go slow’ to gain patient confidence and reduce the risk of hypoglycaemia.141
If insulin is commenced early, HbA1c targets can often be achieved with a once-
daily insulin dose. Blood glucose control may be achieved before the HbA1c is at
target because HbA1c measures the BGL over the preceding three months. Careful
discussion of the impact of insulin on weight management needs to accompany dose
titration, as well as the effect of exercise, carbohydrate intake and timing of meals with
insulin dosing.
Check HbA1c (three months):
• Generally, if HbA1c is within target, then continue with the current schedule.132
• If HbA1c is outside the target, further action may be required (Box 5).
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Box 5. If HbA1c is outside target142

Look for hidden hyperglycaemia by checking BGL before and 2 hours after
lunch and dinner. Structured blood glucose monitoring may assist with this
If postprandial hyperglycaemia is identified, consider:141
• changing preceding meal size or composition
• increasing activity after meals
• adding an oral agent (eg acarbose, glucagon-like peptide-1 receptor agonist
[GLP-1 RA], sodium glucose co-transporter 2 inhibitor [SGLT2i] or dipeptidyl
peptidase-4 inhibitor [DPP-4i]) if the patient is not already taking one
• adding a prandial insulin dose (refer to ‘Insulin intensification’ below)
• switching to a premixed insulin (if on basal insulin alone).
Insulin intensification - Choosing a second-line

insulin schedule
If HbA1c is elevated despite achieving appropriate BGL, a second-line insulin schedule
(insulin intensification) should be implemented based on the individual patient’s needs
(Table 7).
70 2016-18
Table 7. Patient considerations with insulin intensification
Considerations when Lower target Higher

setting targets target
Willing to monitor blood glucose + —
level (BGL) several times per day
Support from family and general + —
practitioner (GP)
Physically and cognitively capable + —
Considerations when Basal plus/Basal + Basal Premixed

selecting a schedule glucagon-like-peptide-1 bolus
receptor agonist (GLP-
1 RA)/Basal + sodium
glucose co-transporter
2 (SGLT2) inhibitor/Basal
+ dipeptidyl peptidase-4
inhibitor (DPP-4i)
Patient preference for fewest + +
injections
Variable meal pattern + +
Variable daily routine + +
Better postprandial control + + ±

required
Limited capacity (eg dexterity) +
The preferred schedule is not the one with the most ‘+’, but one which best meets the
specific patient needs.146,147
There are newer insulin-intensification strategies146 that can be implemented.
Basal insulin may be intensified in the following ways:
• Commence with the addition of a GLP-1 RA (eg twice daily exenatide). This
strategy has the potential to improve HbA1c and postprandial BGL, while
controlling weight gain and not markedly increasing the risk of hypoglycaemia.148
Introduction of the GLP-1 RA requires instruction on injection technique - this is
usually slowly titrated from a starting dose over several weeks, to a stable twice
daily or once daily routine depending on the choice of agents. Only twice daily
exenatide is currently TGA and PBS listed for use in combination with insulin.
Liraglutide, an alternative GLP-1 RA, is currently TGA but not PBS approved. Long-
acting (weekly) exenatide is now PBS-approved for use in combination with oral
agents but not insulin.
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71
• Use with a single daily oral dose of an SGLT2i. If commenced - improved glycaemia
may require dose reduction of insulin at initiation by 10-20% of the total daily dose.
• Use with a daily dose of an oral DPP-4i - some agents have TGA approval and
Pharmaceutical Benefits Advisory Committee (PBAC) recommendations, and will
soon be PBS-approved, for this indication.
Complex regimes of additions to premixed insulin and basal bolus insulin may require
additional specialist endocrinology support and education because of insulin dose
adjustment complexity.
Insulin intensification regimes:

• Basal plus - where additional preprandial injection of short-acting insulin is added
to basal insulin (Appendix H.3. Guide to basal plus insulin intensification schedules).
• Premixed - where additional injections of premixed are added to meals - either two
or three times a day, or, alternatively, basal insulin is switched to premixed insulins
(Appendix H.2. Guide to starting and adjusting premixed insulin).
• Basal bolus - where short-acting insulin injections are used before each meal
in addition to basal insulin (Appendix H.3. Guide to basal plus insulin intensification
schedules).
As Basal bolus involves the most number of injections and monitoring, it is typically
the final strategy implemented.
When insulin intensification is initiated (eg multiple daily doses of insulin), metformin
should be continued, but any remaining insulin secretagogues may need to be
reviewed to minimise risk of hypoglycaemia.
Follow-up
The insulin schedule and dosing should be reviewed at each consultation. The insulin
dosage may need to be reduced if the person adopts a healthier lifestyle and/or loses
weight.
72 2016-18
9. Managing cardiovascular risk

*
Patients with pre-existing cardiovascular disease (CVD) are 149 A
at high risk NVDPA, 2012
All adults with type 2 diabetes and known prior CVD (except 150 A
haemorrhagic stroke) should receive the maximum tolerated dose Baker IDI, 2015
of a statin, irrespective of their lipid levels
Note: The maximum tolerated dose should not exceed the
maximum available dose (eg 80 mg atorvastatin, 40 mg rosuvastatin)
Adults with any of the following conditions do not require absolute 149 D
CVD risk assessment using the Framingham risk equation because NVDPA, 2012
they are already known to be at clinically determined high risk of
CVD:
• Diabetes and aged >60 years
• Diabetes with microalbuminuria (>20 mcg/min or urine albumin-
to-creatinine ratio [UACR] >2.5 mg/mmol for men and >3.5 mg/
mmol for women)
• Moderate or severe chronic kidney disease (persistent
proteinuria or estimated glomerular filtration rate [eGFR]
<45 mL/min/1.73 m2)
• A previous diagnosis of familial hypercholesterolaemia
• Systolic blood pressure >180 mmHg or diastolic blood
pressure >110 mmHg
• Serum total cholesterol >7.5 mmol/L
Calculate risk level using an evidence-based tool: 149 B
• National Vascular Disease Prevention Alliance charts, NVDPA, 2012
www.cvdcheck.org.au
• New Zealand Cardiovascular Risk charts,
www.health.govt.nz/publications
• Heart Foundation NZ, www.knowyournumbers.co.nz
Aboriginal and Torres Strait Islander peoples are generally assumed 149 B
to be at higher risk NVDPA, 2012
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73
Clinical context
CVD is the leading cause of death in people with diabetes, making assessment
of CVD risk a vital part of diabetes care.
Assessment of combined multiple risk factors (absolute CVD risk) is more accurate
than the use of individual risk factors.149
As with glycaemic targets, treatment targets in CVD need to be made on an

individual basis, balancing the benefits and risks of interventions. For example, the
CVD risk associated with lipid and BP levels is continuous; hence, specific targets
are somewhat arbitrary and should be used as a guide to treatment, and not as a
mandatory requirement. Table 8 can be used when developing a management plan
for patients.
The risks associated with the effort required to reach a particular target, as opposed to
achieving a near-target value, may outweigh any small absolute benefit. Any reduction
in risk factor values will be associated with some benefit.149
Recommendations are summarised from the Natural Vascular Disease Prevention

Alliance’s Guidelines for the management of absolute CVD risk.149
Table 8. Risk management summary
CVD risk Lifestyle Pharmacotherapy Targets Monitoring

High risk: Frequent and Treat simultaneously BP: Review response
Clinically sustained specific with lipid-lowering and • <140/90 mmHg 6-12 weekly
determined advice and support BP-lowering unless in general or peo- until sufficient
or calcu- regarding diet and contraindicated or ple with CKD improvement
lated using physical activity clinically inappropriate or maximum
• <130/80 mmHg
Framingham Appropriate advice, Aspirin not routinely tolerated dose
in all people with
risk evalu- support and recommended achieved
*
diabetes
ation (FRE) pharmacotherapy Consider withdrawal of Adjust medication
• <130/80 mmHg
as >15% for smoking therapy for people who as required
if microalbuminu-
absolute risk cessation make profound lifestyle Review of absolute
ria or macroalbu-
of cardiovas Advice given changes risk according to
minuria (UACR
cular disease simultaneously clinical context
>2.5 mg/mmol
events over with blood in men and
five years pressure (BP) and >3.5 mg/mmol
lipid-lowering drug in women)
treatment
2016-18
CVD risk Lifestyle Pharmacotherapy Targets Monitoring

Moderate Appropriate, Not routinely Lipids: Review response
risk: specific advice and recommended Total cholesterol 6-12 weekly
Calculated support regarding Consider BP-lowering <4.0 mmol/L; high- until sufficient
using FRE diet and physical and/or lipid-lowering density lipoprotein- improvement
as 10-15% activity in addition to lifestyle cholesterol >1.0 or maximum
absolute CVD Appropriate advice, advice if three to six mmol/L; low-density tolerated dose
risk events support and months of lifestyle lipoprotein- achieved
over five pharmacotherapy intervention does not cholesterol <2.0 Adjust medication
years for smoking reduce risk or: mmol/L; Non- as required
cessation • BP persistently HDL-C <2.5 Review absolute
Lifestyle advice >160/100 mmHg mmol/L; triglycerides risk every 6-12
given in preference <2.0 mmol/L. months
• Family history of
to drug therapy premature CVD Lifestyle:
• Specific population • Smoking
where the FRE cessation
underestimates risk (if smoker)
e.g. Aboriginal and • Consume diet
Torres Strait Islander, rich in vegetables
South Asian, Maori, and fruit, low in
Pacific Islander salt and saturated
and Middle Eastern and trans fats
peoples • At least 30 min
Consider withdrawal of physical activity
therapy for people who on most or
make profound lifestyle preferably every
changes day of the week
• Limit alcohol
intake
Low risk: Brief, general Not routinely Review response

Calculated lifestyle advice recommended 6-12 weekly
using FRE regarding diet and Consider BP-lowering until sufficient
as <10% physical activity therapy in addition to improvement
absolute CVD Appropriate advice, specific lifestyle advice or maximum
risk events support and if BP persistently tolerated dose
over five pharmacotherapy achieved
>160/100 mmHg.
years for smoking Adjust medication
Consider withdrawal of
cessation as required
therapy for people who
make profound lifestyle Review absolute
changes risk every two
years
Blood test results
within five years
can be used
Reproduced with permission from the National Vascular Disease Prevention Alliance from Guidelines for the
management of absolute CVD risk, 2012, an initiative of the National Vascular Disease Prevention Alliance
*Refer to the ‘Antihypertensive medication to manage cardiovascular risk’ section opposite for further discussion
of BP targets
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75
In practice
There are several interventions for managing CVD risk.
Lifestyle interventions to reduce CVD risk

Lifestyle changes in nutrition, physical activity and smoking status fundamentally
underpin a comprehensive approach to CVD risk minimisation. Lifestyle changes show
excellent cost-effectiveness in lowering the burden of disease and remain the basis for
the management of all CVD risk levels.151,152 However, the Look AHEAD study, showed
improved HbA1c and quality of life benefit, but no reduction in risk of cardiovascular
morbidity or mortality in people with type 2 diabetes who were obese (average BMI
36 kg/m2;82 refer to Chapter 6. Lifestyle modification).
Antihypertensive medication to manage cardiovascular risk

This section on antihypertensive interventions to reduce cardiovascular risk provides
further discussion of BP targets.

*
BP-lowering therapy in people with diabetes should preferentially 149 A
include an angiotensin converting enzyme inhibitor (ACEI) or NVDPA, 2012
angiotensin receptor blocker (ARB)
If monotherapy does not sufficiently reduce blood pressure (BP)
add one of the following:
• Calcium channel blocker 149 B
NVDPA, 2012
• Low-dose thiazide or thiazide-like diuretic 149 C
NVDPA, 2012
Lowering BP reduces cardiovascular events and all-cause mortality in people with type
2 diabetes in the same manner as for the general population.
While no difference is noted between different classes of BP-lowering therapy for CVD
outcomes, there is clear evidence that in people with type 2 diabetes, antihypertensive
therapy with an angiotensin receptor blocker (ARB) or angiotensin-converting enzyme
inhibitor (ACEI) decreases the rate of progression of albuminuria, promotes regression
to normoalbuminuria and may reduce the risk of decline in renal function. Combining
an ARB and an ACEI is not recommended.149
The target level for optimum BP is controversial.

76 2016-18
A number of international guidelines have changed their blood pressure targets to

<140/90 mmHg, while others remain at <130/80 mmHg. The target levels for BP
therapy have been based on little direct trial evidence. A number of meta-analyses
have demonstrated that the benefits of intensive BP control needs to be balanced
with the risks. One meta-analysis demonstrated that more intensive BP control (SBP
<130 mmHg) compared to usual (<140/90 mmHg) was associated with further
reduction in stroke but a 40% increase in serious adverse events.153 Two additional
meta-analyses have recently been published. The analysis by Emdin at al48 found
that risk reduction was attenuated below an SBP of 140mmHg. However, there did
appear to be a lower risk of stroke, retinopathy and albuminuria when blood pressure
was reduced to <130 mmHg. Another meta-analysis, however, found that treatment
of an SBP <140 mmHg was associated with increased CVD death.154 This may in
part be related to the selection of trials in this analysis which included patients with
comorbidites such as CKD, heart failure and CVD.155
In line with these findings, it would be reasonable for GPs to shift the BP target
to <140/90 mmHg for people with diabetes, with lower targets considered for
younger people and those at high risk of stroke (secondary prevention), as long
as the treatment burden is not high. The target BP for people with diabetes and
microalbuminuria or proteinuria remains <130/80 mmHg. As always, treatment targets
should be individualised and people with diabetes monitored for side effects from the
use of medications to achieve lower targets.
Lipid medication to manage cardiovascular risk

*
Use statins as first-line therapy 149 A
NVDPA, 2012
GPs should consider treatable secondary causes of raised blood lipids before
commencing drug therapy.
When commencing drug therapy, statins remain the clear first-line choice. The results
from several systematic reviews are consistent, and suggest that people with diabetes
gain at least similar benefits from statin therapy as people without diabetes. The
data clearly demonstrate that statin therapy results in a significant decrease in CAD
morbidity and mortality in type 2 diabetes for those at high CVD risk. This benefit is in
contrast to the contentious effects of improved glycaemic control in CVD.
Apart from statins, the evidence for other lipid-lowering therapy in decreasing the risk
of CAD is still accumulating. Ezetimibe has been studied in IMPROVE-IT (Improved
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77
reduction of outcomes: Vytorin efficacy international trial).156 Patients with existing

acute coronary syndrome and diabetes had a 14% reduction in death from CVD,
a major coronary event (eg nonfatal MI, documented unstable angina requiring
hospital admission, or coronary revascularisation occurring at least 30 days after
randomisation), or nonfatal stroke. Among the patients with diabetes, the rates of MI
and stroke were reduced by approximately 21% and 42% respectively.
Nicotinic acid, bile-acid resins, and fibrates (fenofibrate, gemfibrozil) have been
suggested as alternatives for people who cannot tolerate statins. Nicotinic acid has
been shown in one trial to reduce CVD outcomes, although the study was done in a
cohort of people without diabetes.157 More recent trials have not confirmed this initial
result. The use of nicotinic acid, in particular, as well as gemfibrozil and cholestyramine
is limited by a high rate of adverse effects.
The role of fibrates to decrease CVD is contentious. All large prospective randomised
clinical trials of fibric acids have failed to decrease the primary cardiovascular end
point. However, in all studies, predominantly post-hoc analyses, have shown that
sub-groups having a low HDL-C level <0.9 mmol/L together with a raised triglyceride
(generally >2.3 mmol/L) derive a significant benefit from fibrate therapy. Given these
results, it may be reasonable to consider the introduction of fenofibrate in high-risk
patients on statin therapy whose LDL-C is not at target and who have low HDL-C
and raised triglyceride levels. Newer injectable lipid lowering agents called PCSK9 i
(inactivate proprotein convertase subtilisin-kexin type 9 inhibitors) has TGA approval
for combination with other lipid lowering agents in select high-risk patients. Mortality or
morbidity outcomes are not yet established. Refer to the TGA website (www.ebs.tga.
gov.au) for more information.
2016-18
Antithrombotic therapy
*
All adults with type 2 diabetes and known prior cardiovascular disease 150 A
should receive long-term antiplatelet therapy unless there is a clear Baker IDI, 2015
contraindication
All adults with type 2 diabetes and a history of ischaemic stroke or 150
transient ischaemic attack should receive: Baker IDI, 2015
• low-dose aspirin or A
• clopidogrel or A
• combination low-dose aspirin and extended-release dipyridamole B
All adults with type 2 diabetes and recent acute coronary syndrome 150
and/or coronary stent should receive, for 12 months after the event or Baker IDI, 2015
procedure:
• combination low-dose aspirin and clopidogrel or B
• combination low-dose aspirin and prasugrel or B
• combination low-dose aspirin and ticagrelor C
All adults with type 2 diabetes and a history of coronary artery 150
disease, but no acute event in the past 12 months should receive Baker IDI, 2015
• long-term low-dose aspirin, or A
• long-term clopidogrel if intolerant to aspirin B
In the presence of atrial fibrillation or other major risk factors for 150 Practice
thromboembolism, there should be consideration of anticoagulant Baker IDI, 2015 Point
therapy according to other relevant guidelines
Prescription of antiplatelet therapy (eg aspirin, clopidogrel) is not usually recommended

in primary prevention, but for secondary prevention, the strong positive effects in the
following conditions need to be weighed against individual patient risks.
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79
10. Managing microvascular and other

complications
10.1 Diabetic retinopathy

*
Ensure that all people with diabetes have a dilated 158 None provided
fundus examination and visual acuity assessment NHMRC, 2008 (Level I evidence)
at the diagnosis of diabetes and at least every two
years
Examine higher risk patients (eg longer duration 158 None provided
of diabetes, or poor glycaemic control, blood NHMRC, 2008 (Level I evidence)
pressure or blood lipid control) without diabetic
retinopathy at least annually
Conduct annual screening for Aboriginal or Torres 158 None provided
Strait Islander peoples with diabetes NHMRC, 2008 (Level IV evidence)
Clinical context
Diabetic retinopathy (DR) occurs as a result of microvascular disease of the retina,
and causes visual impairment and blindness, and affects up to one in three people
with diabetes.
DR is categorised as either:
• non-proliferative DR
• proliferative DR.
Non-proliferative DR affects 19.3% of people with diabetes, while 2.1% may have
proliferative DR and 3.3% may suffer macular oedema.
Non-proliferative DR may be asymptomatic and is characterised by retinal

haemorrhages and exudates. Proliferative DR is characterised by new blood vessel
growth (neovascularisation), which may lead to severe complications and blindness.
Diabetes-related macular oedema is the leading cause of vision impairment with
diabetes and occurs when exudates impact the macula. Tight control of blood glucose
and blood pressure reduces the risk of onset and progression of diabetic eye disease
in type 2 diabetes.
80 2016-18
With good screening and care, visual impairment due to diabetes can be avoided for
the vast majority of patients.
Two studies have prospectively assessed the effect of fenofibrate on microvascular
disease, principally retinopathy. In both the Fenofibrate Intervention and Event
Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes
(ACCORD) studies, patients randomised to fenofibrate therapy had a significant
reduction in retinopathy and need for laser surgery.159 Additionally, in FIELD, there was
a reduction in peripheral neuropathy complications and an improvement in proteinuria,
suggesting a more generalised effect on microvascular disease. In Australia, the TGA
has approved the use of fenofibrate for the treatment of diabetic retinopathy. Its use
in patients with diabetes with evidence of retinopathy should now be considered. The
benefits on retinopathy were not dependent on the patient having dyslipidaemia.159
Retinal photography
Retinal photography is technically simple and now usually performed within the
Australian community by GPs, optometrists and ophthalmologists. Training is required
to ensure quality of image interpretation. Some isolated general practices and
Aboriginal health services are providing their own retinal photography services with
support through telemedicine.
People whose retinal images suggest they may be at increased risk of having,
or at some point developing, sight-threatening retinopathy should be referred for
ophthalmology.
NB: A new item on the MBS for retinal photography with a non-mydriatic retinal
camera will be available for general practice use from November 2016. The listing is
expected to benefit Aboriginal and Torres Strait Islander peoples and communities in
rural and remote locations where there is limited access to optometric and ophthalmic
services to diagnose DR.
In practice
Assess all patients with type 2 diabetes for risk factors (refer to Box 6).
Box 6. Risk factors for development and progression

of diabetic retinopathy
• Existing diabetic retinopathy • Microalbuminuria
• Poor glycaemic control • Dyslipidaemia
• Raised blood pressure • Anaemia
• Duration of diabetes >10 years • Pregnancy
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81
The aim is to prevent vision loss and this is best done with regular review of fundi,
early detection and optimisation of therapy.
GPs can monitor patients for diabetic eye disease if they are confident of their
technique and examine the eyes through dilated pupils or have their own retinal
camera. Where practitioners are not comfortable with fundoscopy and assessment
of the retina, referral to an ophthalmologist or optometrist is recommended.
Monitoring involves:
• visual acuity (with correction)
• cataracts (refer to Section 10.2. Other ophthalmological)
• retinopathy (examine with pupil dilation or retinal camera, or refer to an optometrist
or ophthalmologist).
Initial and then intermittent ongoing referral to an ophthalmologist or optometrist is

still recommended for DR or peripheral retinopathy, which can be treated with laser
photocoagulation therapy to prevent visual loss secondary to retinal haemorrhage.
Patients should be reviewed at least every two years and more frequently if problems
exist.
10.2 Other ophthalmological effects

Refractive errors
Refractive errors occur as the lens’ shape alters with changes in blood glucose
concentrations and result in blurred vision. Detection is done with pinhole test -
blurred vision due purely to refractive error corrects with the pinhole test.
Correction of refractive errors should be postponed until blood glucose levels are
stabilised.
Cataracts
Cataracts occur prematurely in people with diabetes. Patients present with blurred
vision and glare intolerance, and may find night vision a particular problem. Over time,
interpretation of colours becomes more difficult.
Clinically, the light reflex is reduced and fundus may be difficult to see.
Surgical treatment is recommended when reduced acuity is affecting lifestyle and

independence.
82 2016-18
Maculopathy
Maculopathy is difficult to see ophthalmoscopically, but is the most common cause
of visual loss in people with diabetes. Assessment is by direct ophthalmoscopy (with
dilated pupils), retinal photography and fluorescein angiography, depending on the
state of the patient’s fundi.
Intra-vitreous injectable ranibizumab and aflibercept have recently been approved
under the PBS as monotherapy or in combination with laser photocoagulation for
diabetic macular oedema under management by an ophthalmologist. Refer to the PBS
for further information at www.pbs.gov.au/pbs/home
Sudden blindness
Sudden loss of vision is an emergency and may be due to:
• central retinal artery occlusion

• retinal detachment
• vitreous haemorrhage.
These conditions can occur independently of diabetes. Urgent contact with
an ophthalmologist or timely assessment by a specialist team is indicated.
10.3 Neuropathy
Clinical context
Pain and paraesthesia are common peripheral neuropathic symptoms, and
if the autonomic nervous system is involved, gastrointestinal, bladder and sexual
problems arise.
Diabetic neuropathic complications increase the patient’s burden of self care and
overall management.
The clinical focus is on prevention via good glycaemic control, and early recognition
facilitated by good history and routine sensory testing. New modalities are arriving to
assist in the management of diabetic neuropathies.
Before any treatment is instigated, exclusion of non-diabetic causes of neuropathy is

suggested. This includes assessment for vitamin B12 deficiency, hypothyroidism, renal
disease and a review of neurotoxic drugs including excessive alcohol consumption.
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83
Autonomic neuropathy
Autonomic neuropathy may result in:
• orthostatic hypotension with >20 mmHg drop

• impaired and unpredictable gastric emptying (gastroparesis), which can cause a
person’s blood glucose levels to be erratic and difficult to control. Pro-kinetic agents
such as metoclopramide, domperidone or erythromycin may improve symptoms
• diarrhoea
• delayed/incomplete bladder emptying
• erectile dysfunction and retrograde ejaculation in males
• reduced vaginal lubrication with arousal in women
• loss of cardiac pain, ‘silent’ ischaemia or myocardial infarction
• sudden, unexpected cardiorespiratory arrest, especially under anaesthetic
or treatment with respiratory-depressant medications
• difficulty recognising hypoglycaemia (hypoglycaemic unawareness)
• unexplained ankle oedema.
Cardiovascular autonomic neuropathy should be suspected by resting tachycardia
(>100 bpm) or orthostatic reduction in BP (a fall in SBP >20 mmHg on standing
without an appropriate heart rate response). This applies to patients not currently
on antihypertensive agents that may cause variations in BP responsiveness such
as p—blockers. It is associated with increased cardiac event rates.
Diabetic peripheral neuropathy

*
All patients should be screened for distal symmetric 19 B
polyneuropathy starting at diagnosis of type 2 diabetes and at American Diabetes
least annually thereafter, using simple clinical tests Association, 2015
Antidepressants, including tricyclics, duloxetine and venlafaxine 65 A
should be considered for the treatment of patients with painful SIGN, 2014
diabetic peripheral neuropathy
Anticonvulsants, including pregabalin and gabapentin, should 65 A
be considered for the treatment of patients with painful diabetic SIGN, 2014
peripheral neuropathy
Diabetic neuropathies increase with age, duration of diabetes and level of control
of diabetes. They are heterogeneous with diverse clinical manifestations and may
be focal or diffuse.
84 2016-18
In practice
Early recognition and appropriate management is important. People with type 2
diabetes should have an annual check for diabetic peripheral neuropathy.
The appearance of peripheral neuropathy should prompt review and consideration

of improved glycaemic control.
The Diabetes Neuropathy Score may be used to confirm diagnosis and assess
severity (refer to Table 9).160,161
Table 9. Diabetic neuropathy symptom score162

1. Are you experiencing unsteadiness in walking (need for visual control, increase in the dark,
walk like a drunk man, lack of contact with floor)?
2. Do you have a burning, aching pain or tenderness at your legs or feet (occurring at rest
or at night, not related to exercise, excluding intermittent claudication)?
3. Do you have prickling sensations on your legs and feet (occurring at rest or at night,
distal>proximal, stocking glove distribution)?
4. Do you have places of numbness on your legs or feet (distal>proximal, stocking glove
distribution)?
Score:
• 1 point if a symptom occurred several times a week during the past two weeks
• No points if this does not occur
0 points, polyneuropathy absent; 1-4 points, polyneuropathy present
©Jan-Willem G (JWG) Meijer, MD PhD, Revant Rehabilitation Centers, Breda, The Netherlands,
jw.meijer@revant.nl
The pain of peripheral neuropathy can be difficult to manage, although there is evidence
that several agents can improve symptom control and quality of life. Tricyclic medications
should be used as a first-line treatment, although side effects are relatively uncommon.
Gabapentin provides pain relief of a high level in approximately one-third of people who
take this medication for painful neuropathic pain. Side effects are common (66%).163
Pregabalin at daily oral doses of 300-600 mg provides high levels of benefit for a minority
of patients experiencing neuropathic pain including painful diabetic neuropathy.164
Motor neuropathy sometimes occurs with muscle wasting, weakness and

abnormalities of gait. This can contribute to foot problems by altering the
biomechanics of the ankle and foot.
Combinations of more than one test have >87% sensitivity in detecting diabetic
peripheral neuropathy (refer to Box 7). Loss of 10 g monofilament perception and
reduced vibration perception predict foot ulcers.165
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85
Box 7. Tests to assess for peripheral neuropathy

• Pinprick sensation • 10 g monofilament pressure
• Vibration perception sensation at the distal plantar
(using a 128-hz tuning fork) aspect of both great toes and
metatarsal joints
• Assessment of ankle reflexes.
10.4 Nephropathy
*
Assessment
Kidney status in people with type 2 diabetes should be assessed by:
• annual screening for albuminuria (note that dipstick urine 166 B
test is not adequate to identify albuminuria) NHMRC, 2009
• annual estimated glomerular filtration rate (eGFR; in mL/ 166 B
min/1.73 m2) NHMRC, 2009
Management
Reducing the risk or slowing the progression of nephropathy can be achieved by:
• blood glucose control should be optimised aiming for a 166 A
general glycated haemoglobin (HbA1c) target <7% NMHRC 2009
• optimising blood pressure control 166 A
NMHRC 2009
In people with type 2 diabetes and microalbuminuria 166 A
or macroalbuminuria, angiotensin receptor blocker NHMRC, 2009
(ARB) or angiotensin converting enzyme inhibitor (ACEI)
antihypertensive should be used to protect against
progression of kidney disease
People with type 2 diabetes should be informed that smoking 166 B
increases the risk of chronic kidney disease NHMRC, 2009
People with diabetes and microalbuminuria are considered 149 D
at high cardiovascular disease risk, and should be treated NVDPA, 2012
with multifactorial interventions (refer to Chapter 9. Managing
cardiovascular risk)
*Refer to Summary, explanation and source of recommendations for an explanation of the level
of evidence and grade of evidence
86 2016-18
Clinical context
Diabetic nephropathy occurs in one in four women and one in five men with type 2
diabetes,167 and is the single leading cause of end-stage renal disease.
Diabetic nephropathy is more common in Aboriginal and Torres Strait Islander peoples.
Some non-European groups (eg South-East Asian, African American, Afro-Caribbean,
Maori peoples) have high rates of end-stage diabetic nephropathy, possibly, but not
entirely, due to later diagnosis and poorer care.30
There is strong evidence that treatment in the early stages of CKD reduces
progression of kidney damage, morbidity and mortality. Therefore, people with type
2 diabetes should be screened and retested regularly to detect early indications of
kidney damage and to monitor the effects of treatment.
SBP appears to be the best indicator of the risk of CKD in type 2 diabetes. However,
the optimum and safest lower limit of SBP has not been clearly defined. Refer to
general goals for diabetes (refer to Chapter 9. Managing cardiovascular risk) for
appropriate individual targets for BP.
In practice
Assessment
Screening for microalbuminuria can be performed by measurement of the urine
albumin-to-creatinine ratio (UACR) in a random spot collection (preferred method).
Any positive UACR needs to be confirmed with a repeated collection and also a
mid-stream urine to exclude urinary tract infection as a contributor to proteinuria.
The automatic calculation of eGFR on measurement of serum creatinine is now

implemented within Australia.
Review of possible nephrotoxic medication, investigations to exclude treatable

causes of kidney disease, and the assessment of a patient’s CVD risk form a baseline
approach to patients with confirmed kidney disease. Figure 5 provides an algorithm for
the initial detection of CKD.168
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87
Figure 5. Algorithm for initial detection of chronic kidney disease

Note: This algorithm does not allow for checks for people with glomerulonephritis, systemic lupus
erythematosus or people on nephrotoxic drugs.
Kidney eGFR (mL/ Normal Microalbuminuria Macroalbuminuria

function min/1.73 m2) (UACR; mg/mmol) (UACR; mg/mmol) (UACR; mg/mmol)
stage Male: <2.5 Male: 2.5-25 Male: >25
Female: <3.5 Female: 3.5-35 Female: >35
1 >90 Not CKD unless *
Yellow *
Red
haematuria, structural
2 60-89
or pathological *
Yellow *
Red
abnormalities present
3a 45-59 *
Yellow *
Orange *
Red
3b 30-44 *
Orange *
Orange *
Red
4 15-29 Red
* *
Red *
Red
5 <15 or on dialysis Red
* *
Red *
Red
Reproduced with permission from Kidney Health Australia. Chronic kidney disease management in general
practice. 3rd edn. Melbourne: Kidney Health Australia, 2015.
88 2016-18
Management
Due to potential reno-protective effects, the use of ACEIs or an ARB should be
considered for the small subgroup of people with normal BP who have type 2 diabetes
and microalbuminuria.169 It is not recommended that ACEIs and ARB medication be
used together.
ACEIs reduce the incidence of end-stage renal disease by 40%, and ARBs reduce
this progression by 22%. However, the absolute benefit was small (1.5% versus 0.8%
over approximately one year; number needed to treat = 160). Both drug classes
reduced the risk of disease-oriented renal outcomes such as doubling of creatinine
concentration and progression of micro-albuminuria to macro-albuminuria. Both
classes of medication also increased rates of regression from micro albuminuria- to
normoalbuminuria. There are no direct comparative trials of ACEIs and ARBs to
determine which is more effective. However, there is clear evidence of both classes
having benefits in comparison with placebo.170,171
A meta-analysis of RCTs demonstrated that ACEIs and ARBs differentially affect the
risk of all-cause mortality, cardiovascular deaths and cardiovascular events in patients
with diabetes.172 ACEIs reduce the risk of mortality, MI and heart failure, while ARBs
do not affect the risk of mortality and major cardiovascular events. No effect on stroke
was seen with either treatment.
Medication considerations:
• Metformin - should be used with caution (as risks of lactic acidosis increases),
and dose should be reduced when eGFR is 30-60 mL/min/1.73 m2. It is not
recommended and should be ceased when eGFR is <30 mL/min/1.73 m2.
• DPP-4i173 - reduction of dose of alogliptin, saxagliptin, sitagliptin and vildagliptin are
required with eGFR <60 mL/min/1.73 m2 due to pharmacologic accumulation without
toxicity. All except saxagliptin can be used in end-stage renal failure. Linagliptin has
no dose adjustment requirement in renal impairment due to hepatic metabolism.
• Sulphonylureas173 - as renal function declines, the half-life of sulphonylureas
increases, raising the risk of hypoglycaemia.
• SGLT2i - require renal function for glycaemic effect, dapagliflozin may be used if
the eGFR is >60 mL/min/1.73m2 and empagliflozin may be used if the eGFR is >45
mL/min/1.73 m2.
• Acarbose173 - avoid if eGFR < 25mL/min/1.73 m2.
• Glitazones - dose adjustment in patients with renal dysfunction is not
recommended. No information is available for patients on dialysis, therefore
pioglitazone should not be used in such patients.
• GLP-1 RA173 - exenatide and liraglutide use is not recommended below eGFR
<30 mL/min/1.73 m2.
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89
• Insulin - dose review with increasing renal impairment as risks of hypoglycaemia

increase
• any potentially nephrotoxic medications (eg non-steroidal anti-inflammatory drugs
[NSAIDs]) should be avoided.
Box 8 shows the criteria for referral to a renal specialist.
Box 8. Referral criteria for specialist renal care168

Referral criteria for specialist renal care may include:
• estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2

(Stage 4 or 5 chronic kidney disease [CKD] of any cause)
• persistent significant albuminuria (urine albumin-to-creatinine ratio [UACR]
>30 mg/mmol)
• a sustained decrease in eGFR of >25% OR a sustained decrease in eGFR
of 15 mL/min/1.73 m2 within 12 months
• CKD with hypertension that is hard to get to target despite at least three
antihypertensive agents
10.5 Foot complications

*
Assess all people with diabetes and stratify their risk of developing foot 160 C
complications NHMRC, 2011
Assess risk stratification by inquiring about previous foot ulceration 160 C
and amputation plus falls risk, visually inspecting the feet for structural NHMRC, 2011
abnormalities and ulceration, assessing for neuropathy using either the
neuropathy disability score or a 10 g monofilament and palpating foot
People assessed as having intermediate-risk or high-risk feet 160 C
should be offered a foot protection program. This includes foot care NHMRC, 2011
education, podiatry review and appropriate footwear
Pressure reduction, otherwise referred to as redistribution of pressure 160 B
or offloading, is required to optimise the healing of plantar foot ulcers NHMRC, 2011
Offloading of the wound can be achieved with the use of a total 160 B
contact cast or other device rendered irremovable NHMRC, 2011
People with diabetes-related foot ulceration are best managed 160 C
by a multidisciplinary foot care team NHMRC, 2011
90 2016-18
Clinical context
Foot ulceration and limb amputation are among the major drivers of disability and
healthcare costs in people with diabetes. Foot ulceration accounts for one in five of all
diabetes-related admissions to hospital.
Indications for immediate referral to a podiatrist include concerns about vascular

and/or neuropathic complications of diabetes. Predisposing structural problems often
exist, heightening complication risks. Improper footwear and tinea infection have been
associated with increased podiatry problems.
A care plan and foot protection program that includes prevention, patient education,
multidisciplinary care, and close monitoring and treatment of foot ulcers can
substantially reduce amputation rates.
Patients should understand the importance of appropriate footwear and foot care,
establish a regular self-monitoring schedule (including visual checks), and have an
action plan to respond to early problems (eg skin breakdown). Regular podiatric review
needs to be considered. Refer to Appendix I. Tools for assessing neuropathy circulation
and foot deformity for practice-based tools for assessing circulation and foot deformity.
In practice
Foot care education should be provided to all people with diabetes to assist with
prevention of foot complications. For people with intermediate and high risk, a podiatry
assessment is an important component of a foot protection program. However,
where this is not possible, a suitably trained healthcare worker may perform the foot
assessment.
A careful foot assessment should be performed to stratify the risk of developing foot
complications. Assessment is dependent on three risk factors:
• Peripheral arterial disease (PAD) - which can be assessed by dorsalis pedis and
tibialis anterior pulses or hand-held Doppler. If problems are suspected, consider
ankle-brachial index (ABI) testing, toe brachial index (TBI) testing or absolute toe
pressure.
• Neurological testing - which can be undertaken using a neuropathy disability score
or a 10 g monofilament assessment.
• Deformities and ulceration - these can be assessed by visual inspection.
Practitioners are advised to stratify foot risk according to the presence of risk factors
and history of ulceration and/or amputation. The intensity of monitoring and review
increases according to the level of risk. Table 10 shows risk categorisation for
complications and elements to consider during foot assessment.
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91
Table 10. Guidance on risk categorisation for complications and elements

to consider during foot assessment160
Stratification of foot ulceration and NHMRC Foot care and education

amputation risk in diabetes *grade tailored to foot risk status
Low risk No risk factors for foot C Offer basic foot care
ulceration or ulceration/ information and annual
amputation foot assessment
Intermediate One risk factor only (ie C Offer program that
risk neuropathy, peripheral includes foot care
arterial disease [PAD]) and education, podiatry review
no previous history of foot every six months and
ulceration or amputation footwear assessment
High risk Two or more risk factors C Offer program that
(ie neuropathy, PAD or includes foot care
foot deformity) and/or education, podiatry review
previous foot ulceration or and footwear assessment
amputation
High risk Aboriginal or Torres Strait Practice Offer program that
Islander peoples with Point includes foot care
diabetes education, podiatry review
and footwear assessment
Foot ulceration
A foot ulcer is a serious condition and needs to be managed immediately.
The University of Texas wound classification system is the most useful tool for grading
foot ulcers (refer to Table 11).174,175
If arterial insufficiency is suspected, assessment and management of the peripheral
vasculature is mandatory before removal of non-viable or necrotic tissue is considered.
Referral to a vascular surgeon, high-risk foot clinic and/or multidisciplinary team is

suggested in this situation.
The first priority of management of foot ulceration is to prepare the surface and edges
of a wound to facilitate healing. Local sharp debridement of non-ischaemic wounds
should be performed because it improves ulcer healing. Arterial supply needs to be
determined before beginning any treatment.
92 2016-18
Wound dressings need to be tailored to the specific characteristics of the wound.
In non-ischaemic ulcers, create a moist wound environment. Currently, there is

insufficient evidence to demonstrate the superiority of any one type of wound dressing
over another in the management of ulcers. Appropriate management of wound
exudate levels should be a guiding principle in dressing selection and the frequency of
dressing change. In ischaemic ulcers, maintain a dry wound environment using a dry,
non-adherent dressing until someone with experience in PAD has reviewed the wound.
Table 11: University of Texas wound grading system174,175
Grade/depth: ‘How deep is the wound?’

Stage/comorbidities: ‘ Is the wound infected, ischaemic or both? ’
Depth Grade
0 I II III
A Pre-ulcerative or Superficial wound Wound Wound
post-ulcerative not involving penetrating to penetrating to
lesion completely tendon, capsule tendon or capsule bone or joint
epithelialised or bone
B Pre-ulcerative or Superficial wound Wound Wound penetrating
post-ulcerative not involving penetrating to to bone or joint
lesion completely tendon, capsule or tendon or capsule with infection
epithelialised with bone with infection with infection
infection
C Pre-ulcerative or Superficial wound Wound Wound penetrating
post-ulcerative not involving penetrating to to bone or joint
lesion completely tendon, capsule tendon or capsule with ischaemia
epithelialised with or bone with with ischaemia
ischaemia ischaemia
D Pre-ulcerative or Superficial wound Wound Wound
post-ulcerative not involving penetrating to penetrating to
lesion completely tendon, capsule tendon or capsule bone or joint with
epithelialised with or bone with with infection and infection and
infection and infection and ischaemia ischaemia
ischaemia ischaemia
Reproduced with permission from Lavery LA, Armstrong DG, Harkless LB. Classification of diabetic
foot wounds. J Foot Ankle Surg 1996;35(6):528-31.
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93
Factors that favour referral to a multidisciplinary foot care team include:
• deep ulcers (eg probe to tendon, joint or bone)

• high-risk foot with active ulcer
• ulcers not reducing in size after four weeks despite appropriate treatment - if
in regional or remote areas, a telemedical review or telephone review would be
recommended
• the absence of foot pulses/ low ABI or TBI treading
• ascending cellulitis
• suspected Charcot neuroarthropathy (eg unilateral, red, hot, swollen, possibly
aching foot).
If access to a multidisciplinary foot care team is limited, foot ulceration or
complications other than those listed above may be managed by a GP together with
a podiatrist and/or wound care nurse.160
An important reason for failure of an ulcer to heal is continued trauma to the bed of the
wound. This generally occurs because the foot is insensate and the patient continues
to bear weight through the wound. A number of offloading devices are currently
available. These include total-contact casts and removable prefabricated devices (eg
controlled ankle-movement walkers, half-shoes, therapeutic shoes). Patient ability
to understand and undertake management should always be a factor in choosing
a treatment and in counselling the patient regarding the treatment plan.
Infection
The need for antibiotics should be determined on clinical grounds.
It is appropriate for cultures to be collected for identification of microbiological
organisms and antibiotic sensitivities. The most appropriate tissue samples for
microbiological evaluation are either deep tissue swabs after debridement or tissue/
bone biopsies.
Infected ulcers should be treated with antimicrobial therapy according

to published antibiotic guidelines (eg https://tgldcdp.tg.org.au/
guideLine?guidelinePage=Antibiotic&frompage=etgcomplete).
The duration of therapy may need to be for extended periods.
There is no need to culture clinically uninfected ulcers as colonising organisms will

always be detected.
94 2016-18
11. Glycaemic emergencies

Refer to Appendix J. Detailed information on glycaemic emergencies for more detailed
information.

*
The potential harmful effects of optimising blood 96 A
glucose control in people with diabetes should be NHMRC, 2009
considered when setting individual glycaemic targets
Improving blood glucose control increases the risk of 96 None provided
hypoglycaemia NHMRC, 2009 (Level I evidence)
Clinical context
In patients with type 2 diabetes, very high and low glucose states can occur. Both
have significant impacts and implications, and require patient knowledge and active
management planning.
Hypoglycaemia occurs in people with diabetes when their blood glucose level falls
below 4 mmol/L or is at a level that causes symptoms and signs. It is more common
in people taking insulin. However, it can also occur with sulphonylurea therapy either
alone or supplementing other oral therapies. Other causative factors are deficient
carbohydrate intake, renal impairment and excessive alcohol ingestion.
The frequency of hypoglycaemia must not be underestimated, particularly in patients

where the morbidity of hypoglycaemia poses particular problems and symptoms may
be unrecognised.
Higher risk patients include the elderly, and those with renal impairment and recent
hospitalisation or multiple medications.176 Impaired hypoglycaemia unawareness
is a clinical risk that increases with the duration of diabetes, and occurs where the
pathophysiologic symptoms that arise in response to mild or severe hypoglycaemia
(refer to below) are reduced or absent. In such cases, symptoms may be recognised
by other family members and carers before the patient. Such patients need referral to
an endocrinologist.
Emergency hyperglycaemic states include diabetic ketoacidosis (DKA) and

hyperosmolar hyperglycaemic states (HHS; formerly hyperosmolar known as non
ketotic coma [HONC]). These conditions occur due to very poor glycaemic control,
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95
implying diabetes management issues or underlying and/or precipitating causes

such as infection or MI and require emergency management. DKA is rare, but can
occur in type 2 diabetes. It is no longer a complication unique to type 1 diabetes.
Hyperglycaemic thresholds for notification and intervention may be considered in
management planning (eg SMBG >15mmol/L on two subsequent occasions, two
hours apart).
In practice
All patients with type 2 diabetes on insulin and/or sulphonylureas and their families
need to be informed about the risks, signs and symptoms, and actions to be taken.
If there has been severe hypoglycaemia, identification of a carer who may be trained
in glucagon administration may assist earlier intervention if recurrence is to be
avoided. The Australian Diabetes Educators Association (ADEA) sick day management
guidelines may be used to assist practical patient management. Visit www.adea.com.
au/about-us/our-publications
Recognising signs and symptoms

Symptoms of hypoglycaemia vary between persons. Common symptoms are:
• Adrenaline activation symptoms that include pale skin, sweating, shaking,

palpitations and a feeling of anxiety or dizziness.
• Neuroglycopenic symptoms that may include hunger, change in intellectual
processing, confusion and changes in behaviour (eg irritability), paraesthesiae,
then coma and seizures.
• Signs of hyperglycaemic states include severe dehydration, altered consciousness,
shock and ketotic breath in patients with DKA.
Intervention
Hypoglycaemia
Mild and moderate hypoglycaemia can be treated by following the ‘Rule of 15’
(refer to Appendix J. Detailed information on glycaemic emergencies). For severe
hypoglycaemia, the patient requires treatment by a carer or health professional.
Severe hypoglycaemia resulting in an hypoglycaemic coma (a person with diabetes

who presents unconscious, drowsy or unable to swallow) is an emergency.
Management is as follows:
• Commence appropriate resuscitation protocols.

96 2016-18
• Give an injection of glucagon 1 mg intramuscular or subcutaneous if available.

• If intravenous access is obtained, glucose 50% - 20 mL intravenous via a securely
positioned cannula (optimally the antecubital veins). Use 10% glucose in children,
as hyperosmolality has caused harm.
• Phone for an ambulance (dial 000) stating a ‘diabetic emergency’.
• Wait with the patient until the ambulance arrives.
• When the person regains full consciousness and can swallow, they can then
be orally given a source of carbohydrate.
• Review of medications, dietary intake, driving or licensing requirements
and hypoglycaemia management is mandatory.
Hyperglycaemic emergencies
A patient with a hyperglycaemic emergency requires the following:
• Correct extracellular fluid deficit and then slowly correct water depletion and
hyperglycaemia, monitoring sodium and potassium closely.
• Give subcutaneous rapid acting insulin 0.1 units/kg while awaiting transfer.
• Look for an underlying cause - sepsis, MI.
• Monitor blood glucose every one to two hours for the first four hours (then revert
to usual testing when BGL is <15 mmol/L).
• Transfer to a specialist unit as soon as possible.
• Review medications, dietary intake and hyperglycaemic and sick day management.
Refer to Appendix J. Detailed information on glycaemic emergencies for more
information.
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97
12. Diabetes, multimorbidity

and medication complications
12.1 Multimorbidity
Clinical context
Healthcare systems around the world face a growing challenge of managing
populations with multiple co-existent chronic conditions, including diabetes. On an
individual level, multimorbidity can have a profound effect on a patient’s ability to self
care and balance different treatment needs across multiple conditions.
The challenge for general practice is to optimise the care for these patients. Guidelines
are usually configured for individual diseases rather than multimorbidity. Guidelines can
only provide structured information and evidence-based recommendations. They are a
guide for decision making for individual patients and infrequently address the problems
of implementation in different patients with varying personal and clinical priorities.
High-quality management of diabetes cannot occur in isolation from other co

existing physical or mental health disorders, nor can management ignore age and
socioeconomic issues.177
Three out of four adults with diabetes have at least one comorbid chronic disease177
and up to 40% have at least three (refer to Figure 6).178,179 These comorbidities may or
may not be diabetes related, and awareness and treatment of comorbidities is related
to better glycaemic control.180
While many conditions have a concordant treatment focus (eg use of an ACEI
to reduce the risk of cardiovascular events), others, such as depression, chronic
obstructive pulmonary disease (COPD) and painful conditions may be discordant.181,182
For example, patients may require medications such as NSAIDs that may adversely
affect the management of diabetes and whose presence is a risk factor for poorer self
care, more frequent diabetes complications and death.183
Age and multimorbidity

Symptomatic conditions may receive priority from patients. Studies of symptomatic
burden have found that adults with type 2 diabetes aged >60 years report more
physical symptoms such as acute pain and dyspnoea, and are more likely to have
cognitive impairment and physical disability than those without diabetes.184
98 2016-18
Combined with obesity, these risks are approximately doubled. People aged <60
years report more psychosocial symptoms, such as depressed mood and insomnia.
Acute pain was prevalent (41.8%) and 39.7% reported chronic pain, 24.6% fatigue,
23.7% neuropathy, 23.5% depression, 24.2% insomnia and 15.6% physical/emotional
disability.184
Socioeconomic status and multimorbidity

Being part of the most socially disadvantaged groups in Australia doubles the risk of
developing diabetes. Within low socioeconomic groups, financial stressors may also
play a role in treatment choices. Hence, the management of diabetes should always
be considered as part of a comprehensive management plan, which addresses whole
patient priorities.
Figure 6. Many patients with diabetes have other medical conditions
Patients with this condition
Coronary heart disease 19 7 14 13 12 16 13 9 4

(most affluent)
Coronary heart disease 23 19 16 14 10 32 21

(most deprived)
Diabetes (most affluent)
Diabetes (most deprived)
COPD (most affluent)
COPD (most deprived)
Cancer (most affluent)
Cancer (most deprived)
Patients who also have this condition (%)
COPD; chronic obstructive pulmonary disease; TIA; transient ischaemic attack

Reproduced with permission from Elsevier from Barnett K, Mercer SW, Norbury M, et al. Epidemiology
of multimorbidity and implications for healthcare, research, and medical education: A cross-sectional
study. Lancet 2012;380(9836):37-43.
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99
Approach to multimorbidity
A number of comorbidities are commonly associated with diabetes (refer to Table
12). The best approach for a patient with multimorbidity is the subject of international
debate. Unfortunately, multimorbidity increases clinical complexity, which is unlikely to
be effectively addressed by more sophisticated guidelines181,185-187 or the Chronic Care
Model.188-191 Hence, a set of principles to guide an approach seems to offer a clinical
solution.
Table 12. Comorbidities associated with diabetes or arising

from complications of diabetes
Classification Common comorbidities

Psychological Chronic pain disorders
Depression and anxiety
Dementia
Macrovascular disease Hypertension
Coronary disease
Cerebrovascular disease
Peripheral vascular disease
High-risk foot issues
Microvascular disease Renal impairment and chronic kidney disease
Neuropathy - peripheral, autonomic
Retinopathy
Metabolic disorders Dyslipidaemia
Low testosterone in males
Hepatic steatosis
Joint issues (eg frozen shoulder)
Pancreatitis
Overweight and obesity-related Obstructive sleep apnoea
comorbidities Osteoarthritis
Other Bacterial, fungal and viral infections
Periodontal disease
In practice
Consider the following key principles in the approach to management of patients with
type 2 diabetes and co-existing morbidities.
Recognise clinical context and prognosis

Consider clinical management decisions within the context of risks, burdens, benefits,
and prognosis of a patient’s life (eg remaining life expectancy, functional status, quality
100 2016-18
of life).181,185,186 Treatment outcomes of glycaemia, hypertension, and hyperlipidaemia

all have multi-year time horizons required to provide benefit and these may not be
available in all clinical contexts.
Set treatment priorities with the patient

Focus on outcomes that matter most to the individual. Shared decision making with
patients is vital to ensure care is aligned with their values and preferences.185,192-195
Even though diabetes may be a clinically dominant condition, patients may prioritise
therapeutic interventions differently. For example, pain relief from low back pain or
respiratory relief from COPD may be considered above their diabetes needs, many
of which may not cause daily symptoms.
Recognise the limitations of the evidence base

Many of the patterns of multimorbidity have similar pathogenesis and therapeutic
management strategies (eg diabetes, hypertension, CAD).
Clinical guidance regarding discordant conditions such as steroid-dependent

conditions (which potentiate poor glycaemic control), mental health conditions, chronic
pain, cancer or conditions that alter medication pharmacokinetics (eg renal disease,
cardiac failure, liver disease, malabsorptive states) is often lacking or sparse. The
absolute harms and benefits of diabetic medications and burdens are not readily
known in these populations. Other unknowns are the realistic estimate of benefit to the
patient and treatment horizon (ie the length of time taken for the patient to benefit).185
A degree of clinical judgement and a ‘best care given the circumstances’ is required
in these situations.
Optimise therapies
Polypharmacy (taking >5 medications) is one consequence of following single-disease
guidelines in people with multimorbidity.185,196-198
Polypharmacy can be appropriate and has been said to be the price of success in
creating effective treatments. It is also associated with higher rates of adverse drug
events and hospitalisation, and is often particularly problematic in people who are
physically frail189 or have cognitive impairment.
Adherence to therapy can be much more difficult for patients taking numerous
medications for multiple conditions.199 Out-of-pocket costs for medication can be
significantly higher for patients with diabetes than for most other chronic conditions200
and the financial burden can lead to underuse of preventive services.201,202
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101
Consideration of a home medicine review may assist in some cases.

Use strategies for choosing therapies that optimise benefit, minimise harm
and enhance quality of life, particularly in older adults with multimorbidity.
Be aware of common comorbidities with diabetes

Macrovascular disease - includes CAD, hypertension, chronic heart failure,
hyperlipidaemia and cerebrovascular disease. CVD is the primary cause of death
for many persons with diabetes and is often found in patients with type 2 diabetes
(refer to Chapter 9. Managing cardiovascular risk).
Painful conditions (acute and chronic) - are common in patients with type 2
diabetes. Peripheral neuropathies and arthritis account for most causes of pain, as
well as tendinopathies.
Arthritis - is particularly problematic as it can reduce self-management capability

(eg hand arthritis causing medication administration issues). Arthritis and
tendinopathy (and any other cause of pain) can also affect the patient’s ability
to engage in physical activity.
Fractures - research has shown that overall fracture risks are significantly higher
for men and women with type 2 diabetes. The increased risk of hip fracture has been
observed despite patients having higher bone mineral density.
Obstructive sleep apnoea (OSA) - or sleep deprivation from any cause can
aggravate insulin resistance, hypertension and hyperglycaemia. OSA is especially
common in adults with diabetes (up to 17% of men).203 The usual approach to
obstructive sleep apnoea is diagnosis via a sleep study and management with
individualised interventions including continuous positive airway pressure. Driver’s
licence requirements, particularly in commercial drivers, are particularly relevant.
Cancer - is the second largest cause of death in type 2 diabetes. A growing body
of evidence suggests that diabetes and some antidiabetic treatments may increase
cancer risk. Patients with diabetes should undergo appropriate cancer screening as
recommended for all people in their age and sex. Patients should also try to reduce
modifiable cancer risk factors, including quitting smoking, losing weight and increasing
physical activity levels.204
Renal impairment - CKD affects approximately 40% of patients with diabetes.

It is both a complication of diabetes (http://outpatient.aace.com/type-2-diabetes/
management-of-common-comorbidities-of-diabetes) and an independent comorbidity
present before diabetes onset. The presence of kidney disease worsens CVD risk
and limits the number of glucose-lowering medication options available. Further,
the availability of over-the-counter nephrotoxic medications (eg NSAIDs) can easily
102 2016-18
exacerbate disease, and the ‘triple-whammy’ effect (ACEI/diuretic/NSAID) may

go unrecognised without specific questioning. The onset of renal disease can
be insidious.
Cognitive impairment - has been associated with type 2 diabetes205,206 as well as a

higher rates of dementia.207 Recurrent symptomatic and asymptomatic hypoglycaemia
have been suggested as possible causal links to this association.
Mental health issues - such as diabetes-related distress, depression and anxiety

are common. Rates of depression are increased by 15% in people with diabetes
compared with people without diabetes. An Australian study208 using the Patient health
questionaire-9 (PHQ-9) scale revealed moderate to severe depressive symptoms
in 23% of patients with non-insulin treated type 2 diabetes, rising to 35% in those
using insulin, with a proportion of these being undiagnosed. The odds ratio (OR) for
depression in patients with type 2 diabetes compared with people without diabetes is
higher in males (OR: 1.9; 95% confidence interval [CI]: 1.7-2.1) than females (OR: 1.3;
95% CI: 1.2-1.4).209 Anxiety issues also affect people living with diabetes, and, as with
depression, higher rates were seen in women.208
Mental health issues can adversely affect practitioner-patient communication,

and the patient’s ability to live and apply the principles of a diabetes management plan
and glycaemic control, as well as add to the burden of disease and reduce quality
of life. Depression and diabetes are also associated with a significantly increased all
cause and CVD-related mortality.
Some antipsychotic medications can increase the risk of developing diabetes.

Olanzapine and clozapine are associated with higher rates of diabetes compared with
other antipsychotic agents.
Dental problems - such as periodontitis (ie localised inflammation of the supporting
structures of the teeth due to a chronic bacterial infection) are more common
in patients with diabetes. Periodontitis can result in tooth loss and other dental
complications that can interfere with the diet. Additionally, there is a two-way
relationship between diabetes and periodontitis - the management of periodontitis
may lead to a modest reduction in HbA1c of approximately 0.4%.210-213 Inversely,
improving glycaemic control may also improve the severity and complications
associated with periodontitis.
Oral and periodontal health reviews should be incorporated into the systematic
individualised care of patients with diabetes. Early prevention and intervention may
prevent permanent dental loss and help aid in glycaemic control.
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103
12.2 Medication complications

Clinical context
People with type 2 diabetes often take many medications - a significant proportion
of patients take more than eight. There will always be a tension between multiple
drug therapy to achieve recommended goals on the one hand and health issues
from polypharmacy, drug-drug interactions and confusion (especially in the elderly)
on the other. Refer to the Australian Institute of Health and Welfare (AIHW) for more
information (www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=6442453548).
In 2007-08, 63% of people with diabetes reported using medications to help

manage their condition; 13% of people with type 2 diabetes reported using insulin;
and approximately 6% of people with diabetes reported using vitamin or mineral
supplements or herbal remedies, although this is likely to be underestimated.214
Additionally, approximately 50% of patients do not take their medication doses exactly
as prescribed by their healthcare professional.215 This may be a barrier to achieving
treatment targets and result in adverse outcomes.
It is important to understand the overall medication burden as it can lead to many

issues including non-adherence, increased risk of falls and hypoglycaemia.
Contributing factors to non-adherence may include cost, complex treatment

schedules and side effects.
In practice
GPs should be aware and assess for non-adherence, possible drug interactions and
side effects in every patient with type 2 diabetes. Patients on prescribed monotherapy
may be using complementary therapy or misusing their prescribed medication.
Medication use, both conventional and complementary, should be reviewed at least

once per year as part of the annual cycle of care.216,217
The RACGP’s Putting prevention into practice: Guidelines for the implementation
of prevention in the general practice setting218 provides some strategies to address
patient adherence on pages 24-26. The full reference for the guide is available at
www.racgp.org.au/your-practice/guidelines/greenbook
For information regarding drug interactions, consult publications such as the Australian
medicines handbook.
Pharmacists can be an invaluable resource as they have access to extensive

medications databases, can detect potential drug interactions, and provide useful
advice to the health professional and person with diabetes.219,220
104 2016-18
Important drug interactions and side effects

People with diabetes may be taking multiple glucose-lowering medications in
addition to other prescription and non-prescription agents. Some drug interactions
are dangerous and special care is required in older patients and patients with
comorbidities such as renal impairment and autonomic neuropathy. A full list of
potential drug interactions is beyond the scope of these guidelines. Use a home
medicines review and pharmacy support on an individualised basis in any patient
with diabetes.
Reporting of adverse events

Many medications are becoming available for the management of diabetes for which
long-term safety data is not yet available. Primary healthcare professionals have an
important role to play in identifying and reporting adverse events and possible drug
interactions. These should be reported to the TGA, either online or by completing the
Blue card (go to www.tga.gov.au/reporting-problems for further information).
Home medicines review

Multiple systematic reviews have concluded that there is a lack of evidence for
improved health outcomes for medication reviews. Benefit has been proposed where
pharmacists work in close liaison with primary care doctors.221
The review should include consideration of:
• the need for each medication

• issues around patient compliance and understanding of the medication
• enquiry regarding medication side effects, particularly falls and cognitive impairment
• the use of aids such as dosette boxes and Webster packaging.222
Complementary medicines
The use of complementary medicines is increasing in Australia. A survey of pharmacy
customers found that 72% of respondents had used complementary medicines within
the previous 12 months; 61% used prescription medicines daily and 43% had used
these concurrently. Multivitamins, fish oils, vitamin C, glucosamine and probiotics were
the five most popular complementary medicines.223
A substudy of the Fremantle Diabetes Study found that 23% of participants had
consumed at least one complementary medication in the last year. Of the medications
used, approximately 42% potentially necessitated additional patient monitoring or
could be considered inappropriate for patients with diabetes.216
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105
Predictable positive and negative interactions between complementary medicines and

prescribed diabetes medications may be variable as there is little formal assessment of
many of these products.
NPS MedicineWise has compiled a guide to medicines information resources relevant

to Australian health professionals. This list is available at www.nps.org.au/health-
professionals/guide-to-medicines-information-resources
Interactions can be checked by searching these resources, although NPS does not
guarantee their completeness or accuracy.
106 2016-18
13. Diabetes and reproductive health

13.1 Polycystic ovary syndrome
Clinical context
PCOS is a metabolic and endocrine disorder affecting about one in 15 women
worldwide.224 The endocrine disruptions consist of excessive androgen secretion or
activity, and a large proportion of women also have insulin resistance and metabolic
syndrome. The cause of PCOS is unknown, but studies suggest a strong genetic
component that is affected by gestational environment, lifestyle factors or both.
Clinical manifestations include menstrual dysfunction, infertility, hirsutism, acne, obesity

and glucose intolerance. Women with PCOS have an established increased risk of
developing type 2 diabetes and a 2.4-fold increased odds of GDM, independent of
age, race/ethnicity and multiple gestation.225 Refer to Section 3.1. Identifying risk of
diabetes in asymptomatic potients for identifying risk of diabetes in women with PCOS.
The diagnostic criteria of PCOS are hyperandrogenism, chronic anovulation and

polycystic ovaries, after exclusion of other conditions that cause these same
features (refer to Table 13).226,227 A consensus definition of the disorder based on the
importance of the three diagnostic criteria relative to each other remain controversial.
Table 13. Criteria for diagnosis of PCOS
The Rotterdam criteria are inclusive of National Institutes of Health (NIH)

criteria; however, the Rotterdam criteria may not meet NIH criteria
The Rotterdam diagnostic criteria requires two of:
• Oligo-ovulation or anovulation
• Clinical and/or biochemical signs of hyperandrogenism
• Polycystic ovaries
and exclusion of other aetiologies such as hyperthyroidism, hyperprolactinaemia, congenital adrenal
hyperplasia, androgen-secreting tumours and Cushing’s syndrome
The NIH diagnostic criteria requires:
• Oligo-ovulation or anovulation
• Clinical and/or biochemical signs of hyperandrogenism
and exclusion of other aetiologies such as congenital adrenal hyperplasia, androgen-secreting
tumours and Cushing’s syndrome
Reproduced with permission from Teede HJ, Misso ML, Deeks AA, et al. Assessment and
management of polycystic ovary syndrome: Summary of an evidence-based guideline. Med J Aust
2011;195 (6):65-112.
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107
In practice
Lifestyle modification is the foundation of management. The principles are similar to
those for diabetes prevention (ie weight control and ideally weight loss, support for
a balanced individual healthy eating plan, increased physical activity).
There are several targeted interventions for other manifestations of PCOS.
Oligomenorrhoea and amenorrhoea

Options include:
• an oral contraceptive pill (OCP; low oestrogen doses [eg 20 pg] may have less
impact on insulin resistance but also less impact on clinical hyperandrogenism)
• cyclic progestins (eg 10 mg medroxyprogesterone acetate, 10-14 days every two
to three months)
• metformin (improves ovulation and menstrual cycles - though it is not PBS
reimbursed for this option).228
Hirsutism
Choice of options depends on patient preference, impact on wellbeing, and access
to and affordability of professional cosmetic laser therapy. Eflornithine cream can be
added and may induce a more rapid response.
Pharmacological therapy is as follows:
• Primary therapy is the OCP.

• Anti-androgen monotherapy (eg spironolactone or cyproterone acetate) should
not be used without adequate contraception. Therapies should be trialled for >6
months before changing dose or medication.
• Combination therapy - if >6 months of OCP is ineffective, add anti-androgen to
OCP (twice daily spironolactone >50 mg or cyproterone acetate 25 mg/day, days
one to 10 of OCP).229
Infertility
Patients and their partner may need advice and appropriate referral for fertility
management.
108 2016-18
13.2 Pregnancy with pre-existing diabetes

*
Pre-pregnancy glycaemic control should be maintained as close to the 65 C
non-diabetic range as possible, taking into account risk of maternal SIGN, 2014
hypoglycaemia
All women with diabetes should be prescribed3 high-dose pre 65 B
pregnancy folate supplementation, continuing up to 12 weeks’ SIGN, 2014
gestation
All women with pre-gestational diabetes should be encouraged to 65 D
achieve excellent glycaemic control3 SIGN, 2014
Postprandial glucose monitoring should be carried out in pregnant 65 C
women with type 1 or 2 diabetes SIGN, 2014
Postprandial glucose monitoring should be carried out in pregnant
women with gestational diabetes and may be considered in pregnant
women with type 1 or 2 diabetes
Pre-pregnancy care provided by a multidisciplinary team is strongly 65 C
recommended for women with diabetes SIGN, 2014
5 mg of folate
+
3HbA1c <48 mmol/mol (<6.5%) and consider stabilisation using metformin and/or insulin to achieve
glycaemic targets. However, metformin has a category C rating in pregnancy. Continuation or
initiation of metformin therapy should be considered only following full disclosure to the patient and
under specialist supervision. Sulphonylureas may be associated with adverse neonatal outcomes
and are thus best avoided65,230-233
All pregnant women with diabetes should be encouraged to achieve optimal glycaemic
control.
Clinical context
GPs have a significant role in advising women of reproductive age with pre-gestational
diabetes to consider the benefits of contraception to prevent inadvertent pregnancy
before glycaemia can be optimised. Women should be advised of the need for advice,
education and support to achieve optimal glycaemic control before pregnancy.234
Women with type 2 diabetes and PCOS or irregular periods must be advised that
improved fertility may accompany use of metformin. Pre-pregnancy counselling should
include assessment of diabetes complication status, review of all medications and
commencement of folic acid (5 mg). Poor glycaemic control at conception and early
in pregnancy is associated with increased risk of congenital malformations and first
trimester miscarriages.
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109
Women with pre-gestational diabetes (types 1 and 2) are more prone to the
complications of pregnancy such as higher rates of pre-eclampsia prematurity and
caesarean section.235 In addition, pregnancy may accelerate maternal complications
of diabetes.236 Both maternal and fetal complications are increased by diabetes. Risk
is progressive with increasing glycaemia.234
Good glycaemic control can mitigate the risk of maternal and fetal complications and
the likelihood of birth trauma, and reduce the risk of early induction of labour and need
for caesarean section.
Refer to www.pregnancyanddiabetes.com.au for advice on pre-pregnancy blood

glucose targets
In practice
Pre-pregnancy
Where possible and practicable, formal pregnancy planning should occur prior
to pregnancy and be patient focused, support self management and involve a
multidisciplinary team on an individual basis. Deferring pregnancy should be a
recommendation until glycaemic control is optimal. Women should be reassured that
any reduction in HbA1c towards the individualised target is likely to reduce the risk of
congenital malformations. Medications should be reviewed and ceased or replaced
as appropriate.
It is important to do the following:
• Advise that optimisation with a balanced diet, physical activity and healthy weight
management may positively affect pregnancy outcomes.
• Advise that nausea and vomiting in pregnancy may affect blood glucose control.
• Advise that use of some form of contraception is recommended until glucose
control is optimised.
• Aim for glycaemic control to be as close to the normal (non-diabetic) range as
possible, ensuring risks of maternal hypoglycaemia are minimised. The risk of fetal
abnormalities increases with higher HbA1c levels at the time of conception and
during the first trimester.
• Review SMBG to determine if medication adjustment and/or commencement
of insulin is required and assess risk of hypoglycaemia.
• Recommend higher folate supplementation (5 mg) per day, starting one month
before pregnancy237 and continuing until 12 weeks of gestation to reduce the risk
of neural tube defects.
110 2016-18
• Be aware that women treated for hypothyroidism may require higher doses of
thyroid hormone replacement therapy.238 Based on re-assessment, a suggested
dose change is a 30% increase in dose (eg if on one tablet per day, to increase by
two tablets per week) may be needed.
• Advise examination of the retina prior to conception and during each trimester for
women with types 1 and 2 diabetes. More frequent assessment may be required
if retinopathy is present. Patients with active moderate to severe non-proliferative
retinopathy or with proliferative retinopathy who have not had an ophthalmological
assessment within the preceding six months should undergo testing prior to
pregnancy to see if the retinopathy is stable enough for pregnancy. Similarly, renal
function should be tested if this has not been done within the preceding three
months. Elevated creatinine or eGFR <45 mL/min/1.73 m2 or an ACR >30 mg/
mmol is an indication for pre-pregnancy nephrology review.239,240
• Counsel the patient that the risks associated with diabetes in pregnancy can be
reduced but not eliminated.
In pregnancy
Specialist endocrine and obstetric referral for multidisciplinary shared care is
considered best practice.
Safety and risks of medications before and during pregnancy

Consideration of the safety of current therapies should be undertaken ideally before
pregnancy is planned or urgently once pregnancy is confirmed. Consultation with
local specialist services is advised. Agents such as sulphonylureas, glitazones, SGLT2i
and incretin-based therapies will need to be reviewed or ceased, and insulin therapy
instituted.
Metformin
Metformin is not associated with an increase in congenital malformation or early
pregnancy loss, but remains a category C classified drug (refer to Table 14 for further
information).241,242 Some diabetes services believe that metformin may be used as an
adjunct or alternative to insulin in women with type 2 diabetes in the pre-conception
period and during pregnancy. Consult with your local specialist endocrine and
obstetric services.
Insulin
Rapid-acting insulin analogues aspart and lispro are safe to use during pregnancy.
There is insufficient evidence about the use of the long-acting insulin analogues (glargine
2016-18
111
- category B3). Detemir insulin (a long-acting insulin analogue) is now classified as

category A drug in pregnancy. Patients already stabilised on insulin glargine may have
this therapy continued in preference to switching to human insulin, but the B3 category
rating needs to be discussed with the woman. Isophane insulin (Neutral Protamine
Hagedorn [NPH] insulin) remains the most common long-acting insulin choice during
pregnancy for women with type 2 diabetes (refer to Table 14 for further information).
Antihypertensive medications
ACEIs and angiotensin-II receptor antagonists should be discontinued during the
pregnancy planning period or as soon as pregnancy is confirmed. Table 14 provides
advice on antihypertensive agents to be avoided before and during pregnancy.
Table 14. Antihypertensive agents to be reviewed pre-conception

and during pregnancy243
Antihypertensive agent Category in pregnancy

* Advice
Angiotensin-converting enzyme D Contraindicated
inhibitors
Angiotensin receptor blocker D Contraindicated
Calcium channel blocker C Avoid (except nifedipine)
ß blockers C Avoid (except labetalol
and oxprenolol)
Thiazide and loop diuretics C Seek advice
Methyldopa A Safe
Spironolactone B3 Seek advice
Moxonidine B3 Seek advice
*For definitions of the Australian categories for prescribing medicines in pregnancy, visit the
Therapeutic Goods Administration, Australian categorisation system for prescribing medicines in
pregnancy at www.tga.gov.au/australian-categorisation-system-prescribing-medicines-pregnancy
Statins
Statins should be discontinued during the pregnancy planning period or as soon
as pregnancy is confirmed.
Antenatal care
Intensive glycaemic control guided by SMBG results is required in the management of
diabetes in pregnancy. Insulin therapy will need regular review and titration to achieve
glycaemic goals.
112 2016-18
Close surveillance for new diabetes complications and monitoring of existing

complications should occur routinely.
Ultrasound screening at 10-13 weeks’ gestation (with biochemistry) for trisomies, and
at 18-20 weeks for congenital cardiac and other malformations, is advised. Pregnant
women with diabetes should be offered ultrasound monitoring of fetal growth and
amniotic fluid volume every four weeks from 28 to 36 weeks.240 Fetal growth and
wellbeing monitoring should occur under specialist supervision. Consult with your local
specialist endocrine and obstetric services.
Postpartum
The GP should maintain or re-establish contact with mother and child as early as
practicable to address any issues arising from the pregnancy, labour, surgery or
breastfeeding as well as review medications. Metformin may be continued while
breastfeeding with minimal effect on the baby.244 Glycaemic monitoring and medications
(especially insulin) need careful review during breastfeeding to minimise the risk of
hypoglycaemia. Re-establishing glycaemic management goals, re-assessment of
complications and timely contraceptive advice are also appropriate in the postnatal
period.
13.3 Gestational diabetes mellitus
Clinical context
Gestational diabetes, or GDM, is defined as glucose intolerance that begins or is first
diagnosed during pregnancy. It may appear earlier, particularly in women with a high
level of risk for GDM.
GDM generally develops and is diagnosed in the late second or early third trimester
of the pregnancy. GDM affects about 9.6-13.6% of pregnancies in Australia.245,246
The reported prevalence of GDM varies for a number of reasons. One reason is the
use of different screening and diagnostic criteria. The prevalence is also affected by
maternal factors such as history of previous gestational diabetes, ethnicity, advanced
maternal age, family history of diabetes, pre-pregnancy weight and high gestational
weight gain. Mothers of different ethnicity born in areas with high diabetes prevalence
such as Polynesia, Asia and the Middle East, are three times as likely to have GDM as
mothers born in Australia. Among Aboriginal and Torres Strait Islander mothers, GDM
is twice as common, and pre-gestational diabetes affecting pregnancy is three to four
times as common as in non-Indigenous mothers.245
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113
In pregnancy, there is a natural increase in levels of hormones including cortisol,

growth hormone, human placental lactogen, and progesterone and prolactin levels,
causing two to three fold increases in insulin resistance. The action of these hormones
is usually compensated by increased insulin release. In pregnant women with
abnormal glucose tolerance or impaired p-cell reserve, the pancreas is unable to
sufficiently increase insulin secretion in order to control BGLs.
Potential maternal complications during pregnancy and delivery include pre-eclampsia

and higher rates of caesarean delivery, maternal birth injury, postpartum haemorrhage.
For the neonate, complications can include macrosomia (large for gestational age)
growth restriction, birth injuries, respiratory distress, hypoglycaemia and jaundice.
The precise level of glucose intolerance characterising GDM has been controversial
due to differences in screening, diagnostic criteria and outcomes to which criteria
are applied. The NHMRC criteria25 were determined from glucose levels on antenatal
glucose tolerance tests that were associated with subsequent development of
diabetes in the mother. A recent Cochrane review247 determined that increased levels of
screening and management have not been clearly linked to improved health outcomes.
The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study was published
in 2008. This study reported a correlation between increasing maternal glucose levels
at 24-32 weeks’ gestation and a range of adverse maternal and fetal outcomes. The
study suggested that the relationship between increasing BGLs and adverse effects
was continuous, with no threshold or inflection point at which lower BGLs confer
protection.
In response to the HAPO study, the International Association of the Diabetes and
Pregnancy Study Groups (IADPSG) developed new consensus guidelines for the
testing and diagnosis of GDM. Although The Royal Australian and New Zealand
College of Obstetricians and Gynaecologists (RANZCOG) and the Australasian
Diabetes in Pregnancy Society (ADIPS)248 have recommended that these consensus
guidelines should be implemented, there has been controversy nationally and
internationally.249 Independent analysis of the HAPO data by the National Institute
for Health and Care Excellence (NICE) guideline groups has suggested alternative
diagnostic and management criteria that are not as low as IADPSG criteria,240 and the
UK has now developed its own diagnostic criteria.240
Ultimately, there is at present little evidence that clinical intervention is beneficial for the
additional women identified by the new screening criteria.250-253 As with any screening
intervention, the evidence must be clear that the benefits outweigh potential harms.
Until this evidence is forthcoming, the original NHMRC recommendations for screening
of GDM remain the preferred diagnostic criteria preferred by the RACGP.
114 2016-18
There is still a need for further studies to clearly outline the evidence of the benefits
and risks of altering diagnostic criteria, including the health economic costs of any
such consensus for change.
Acknowledging that in Australian general practice there are alternative diagnostic

criteria for GDM, the RACGP (preferred) and ADIPS (alternative) diagnostic criteria
are presented in Box 9 and in Chapter 16. Issues under debate. Furthermore, it
is important that each GP be aware of their obstetric service diagnostic criteria,
and support and manage patients in a manner confluent with their specialist team
guidelines to avoid conflict and patient confusion.
In practice
Screening for gestational diabetes mellitus
GDM is diagnosed by screening during pregnancy:
• All pregnant women should be screened between 26 and 28 weeks’ gestation with
a non-fasting glucose challenge.
• Women at high risk (refer to Box 3) should be screened at the first opportunity early
in pregnancy and repeat if negative screening at 24-28 weeks.
• Women whose levels are >7.8 mmol/L should have a formal (fasting) 75 g OGTT.
• The diagnosis of GDM is made on the basis of a 75 g OGTT (Box 9).
Box 9. Screening and diagnosis of gestational diabetes mellitus

The Royal Australian College of Australian Diabetes in Pregnancy
General Practitioners (RACGP; Society (ADIPS; alternative criteria)
preferred criteria)
Fasting plasma glucose >5.5 mmol/L, Fasting plasma glucose 5.1-6.9 mmol/L,
or or
two-hour plasma glucose or random one-hour post >10.0 mmol/L, or

glucose >8.0 mmol/L
two-hour 8.5-11.0 mmol/L
ADIPS (http://adips.org/information-for-health-care-providers-approved.asp) suggests

a universal single step 75 g OGTT at 24-28 weeks.
GPs should be aware of the differences in the diagnostic and management algorithms
of the RACGP (preferred) versus ADIPS (alternative) that are relevant to their local
referral pathways for patients with gestational diabetes services and pragmatically
manage patients within the context of these services.
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115
Management
*
Pregnant women with gestational diabetes mellitus should be offered 65 A
dietary advice and blood glucose monitoring, and be treated with SIGN, 2014
glucose-lowering therapy depending on target values for fasting and
postprandial targets
The basis for management for women with GDM includes nutritional therapy, weight
optimisation, physical activity, blood glucose monitoring and insulin therapy.
All women with GDM should be offered education, blood glucose monitoring and
dietary advice. Most GDM responds positively to lifestyle management.254 Referrals to
an APD and AEP are advised unless already provided by the obstetric services.
Limiting weight gain in pregnancy for obese or overweight women with GDM is
desirable. It is recognised that glycaemic targets in the treatment of GDM vary between
centres and clinicians around Australia. Targets suggested by ADIPS criteria have been
described within Australia as being aggressive. Care should be taken in approaching
these targets as most blood glucose monitors have a 5-10% margin of error and risks
of maternal hypoglycaemia need to be considered.
Given the lack of agreement for treatment targets and the accuracy of blood glucose
monitors, the RACGP suggests that readings between 4-6 mmol/L preprandially are
reasonable.
Metformin has been used internationally65 as initial glucose-lowering treatment in

women with GDM. However, it has not been approved for this use in Australia for this
indication. Lifestyle and insulin therapy remain the mainstay of therapy.
Close cooperation with the obstetric team is advised to monitor maternal and fetal
welfare.
Hypoglycaemia may have serious effects on placental function and the fetus in patients
with GDM. Thorough investigation is required in such patients.
Aim to achieve blood glucose levels:
• between 4 and 6 mmol/L preprandially

• <7 mmol/L two hours postprandially.
116 2016-18
Follow-up of patients with a history of gestational diabetes

mellitus
*
Women with a history of gestational diabetes mellitus should 19 American E
receive a postpartum oral glucose tolerance test at 6-12 weeks Diabetes
Association, 2015
Box 10 provides the RACGP (preferred criteria) and ADIPS (alternative criteria) for
follow up of patients with GDM history.
Box 10. Follow up of patients with gestational diabetes mellitus history

The Royal Australian College of Australian Diabetes in Pregnancy
General Practitioners (RACGP; Society (ADIPS; alternative
preferred criteria) criteria)
75 g two-hour oral glucose tolerance 75 g two-hour oral glucose tolerance
test at 6-12 weeks postpartum test, at 6-12 weeks postpartum
Thereafter, a fasting blood glucose
or glycated haemoglobin (HbA1c) test
every three years
The frequency and nature of this surveillance will depend on future pregnancy plans and the
perceived risk of converting to type 2 diabetes. Women contemplating another pregnancy should
have an oral glucose tolerance test annually
Although GDM usually resolves following birth, it is associated with increased risk for
developing maternal type 2 diabetes in later life. The lifetime risk of developing type 2
diabetes following a diagnosis of GDM is 60%.255
After delivery, it is recommended that advice be given on healthy diet and exercise,
which may include referral to a dietitian and physical activity program. Encourage
increasing physical activity (eg 30 minutes brisk walking five times a week) and/or weight
loss, which reduces risk of developing diabetes by 40-60% in those at high risk.256
Breastfeeding is encouraged for its many health advantages.
Women with normal glucose tolerance should be counselled regarding their risk
of developing GDM in subsequent pregnancies.
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13.4 Contraception
Contraception advice should follow guidelines that apply to women without diabetes.
However, the benefits of the use of an intrauterine contraceptive device (IUCD) versus
the less preferred, combined OCP, and any risks or contraindications caused by the
presence of diabetes complications, need to be discussed with each patient on an
individual basis. Smoking combined with diabetes and the use of the combined OCP
significantly elevates risks.
Progesterone-only oral contraceptives may then be used as an alternative. Other

contraceptive implants and intrauterine devices may also be an option on an
individual basis.
13.5 Sexual problems - Men

Clinical context
Erectile dysfunction is a common problem for men with diabetes.
Men with diabetes are four times more likely to develop erectile dysfunction than men
without diabetes. The prevalence in men aged >40 years with diabetes may be as
high as 50% and incidence increases by approximately 10% per annum. Men with
diabetes are also affected by erectile dysfunction at an earlier age, with occurrence
approximately a decade earlier.257,258
Erectile dysfunction may be acute or chronic during periods of high blood glucose.
Failure to achieve erection may be due to psychological causes, macrovascular
disease or pelvic autonomic neuropathy.
An organic cause is more likely when there are other macrovascular or microvascular
complications.
In addition, as a population/group/cohort, men with diabetes (types 1 and 2), have

been shown to have lower testosterone levels than men without diabetes. This may
contribute to reduced libido and aggravate or exacerbate erectile dysfunction.
In practice
It is important to enquire about erectile dysfunction in the annual review.
Differentiate organic and psychological erectile dysfunction by taking a detailed history

such as spontaneous early morning erections, anorgasmia and lack of libido.
Assessment of severity and management of psychological (anxiety and depression)

and physical symptoms.
118 2016-18
Psychological therapies such as supportive counselling for patients with organic erectile
dysfunction and behavioural therapy for psychogenic erectile dysfunction are useful.259
Phosphodiesterase inhibitors are useful and side effects are generally mild. Concomitant
use of vasodilating nitrates are contraindicated due to life-threatening hypotension.
The help of a urologist who specialises in erectile dysfunction should be sought for
those considering penile injection with vasoactive agents such as prostaglandin E1
(alprostadil), surgical treatments, vacuum devices, penile prostheses or implants
may help.
Potential CVD risk of engaging in and resuming sexual activity needs to be discussed.
13.6 Sexual problems - Women
Clinical context
The prevalence of sexual dysfunction among women appears to be lower than among
men (although studies have typically focused more on men than women), some
studies show that women may experience more psychological problems compared
with men, who have more physical symptoms.
Women with diabetes may also experience higher rates of sexual dysfunction than
women without diabetes.
Symptoms of sexual dysfunction in women include:
• decreased or total lack of interest in intimacy or sexual relations

• decreased or no sensation in the genital area
• a degree of anorgasmia
• dryness in the vaginal area (presumably due to pelvic autonomic neuropathy),
leading to dyspareunia.
Genital infections such as monilial vaginitis occur more frequently in women with
diabetes and may contribute to sexual dysfunction.
Rates of depression, anxiety and psychological distress are higher in people with
diabetes and may contribute to sexual dysfunction in men and women.95,260
In practice
It is important to enquire about sexual problems in the annual review and manage
physical and emotional aspects.
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14. Management of other impacts

of diabetes
14.1 Sick day management

*
Patients should be educated to develop a sick 261 None provided
day management plan after initial diagnosis. This Australian Diabetes
plan should be reviewed at regular intervals Educators Association, 2014
Assist in the development of a sick day care plan 261 None provided
and preparation of a home sick day management Australian Diabetes
kit for patients to use during episodes of sickness Educators Association, 2014
Clinical context
Patients with diabetes require careful individualised management during times of
illness (due to other causes) to prevent:
• hyperglycaemic and hypoglycaemic emergencies

• hyperosmolar hyperglycemic state
• DKA - uncommon (plus consider normoglycaemic DKA with SGLT2i medication).
A clear and specific action plan ensures that patients can either self-manage or have
access to their healthcare team for advice and early intervention, supervision and
support. General practices and GPs should consider routinely incorporating these
plans as part of a patient’s documented management plan.
The ADEA has developed clinical guiding principles for health professionals and a
consumer resource on sick day management.261,262 These are available at www.adea.
com.au/about-us/our-publications
Patient information is also available from state and territory diabetes organisations.
120 2016-18
In practice
Sick day management should be tailored to the individual patient and incorporate the
following actions:
• Identify the underlying cause and treat as appropriate. Underlying causes include:
- intercurrent illnesses, infections (eg skin, urinary tract and chest infections),
trauma, acute MI and stroke
- use of medications such as corticosteroids.
• An increase in SMBG may be required according to individual circumstances such

as those patients at risk of hypoglycaemia or using insulins.
• Ensure continuity of advice and accessibility - provide telephone access or after
hours support.
• Review medications - Refer to Table 15.
• A written action plan (refer to Table 15), which should be regularly updated (at least
once annually during the annual cycle of care) and provided to patient and carer.
Table 15. Action plan

Commence action plan • When feeling unwell
• Blood glucose >15 mmol/L on two consecutive readings
Frequent monitoring Two to four hourly monitoring, or more frequently if blood glucose is low
of blood glucose
Medication Insulin or diabetes medications should be continued but with assessment
on the use of metformin, sodium glucose co-transporter 2 (SGLT2)
inhibitors (dapagliflozin, canagliflozin and empagliflozin) and glucagon-like
peptide-1 receptor agonist (GLP-1 RA), which may require cessation if
vomiting or dehydration is a concern. Increased risks of hypoglycaemia
may occur if appropriate intake of meals are not able to be maintained.
Food and water intake • Patients should try to maintain their normal meal plans if possible
• Fluid intake (eg water) should be increased to prevent dehydration
• Advise about alternative easy-to-digest foods like soups if the patient
cannot tolerate a normal diet (some non-diet soft drinks may provide
essential carbohydrate in this situation)
• If blood glucose >15 mmol/L use non-glucose containing fluids
• If blood glucose <15 mmol/L use oral rehydration solutions (may
contain glucose) if needed
• If unable to tolerate oral fluids and blood glucose continues to drop -
inform patient to attend medical care
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Seek assistance Individuals and support people need to assess whether they are well
enough or able to follow the guidelines
If not, they should call for help or attend hospital
Practice points from ADEA - Clinical guiding principles for sick day management of adults with type
1 and type 2 diabetes - Technical document261
Special considerations
Different patient groups will need individualising of the sick day action plan
Managed with diet alone:

• Worsening control may require the introduction of medication and symptomatic
management of hyperglycaemia.
• Patients with type 2 diabetes may have impaired body immune mechanisms that
will make recovery slower.
• In addition, patients may become dehydrated because of the osmotic diuresis.
Managed with oral or non-insulin glucose lowering medication:

• Worsening control may require the urgent review by the GP or referral to a specialist
diabetes service or endocrinologist.
• Consideration of the use of insulin may be temporarily required for persistent
and resistant symptomatic hyperglycaemia (this may require hospital admission).
• In patients with nausea, vomiting and/or diarrhoea, consider stopping metformin
and GLP-1 mimetics temporarily as metformin may aggravate these symptoms
and GLP-1 mimetics may aggravate nausea/vomiting, and there may be a risk of
acute renal impairment due to dehydration. Cessation of any SGLT2 inhibitor should
be reviewed if gastrointestinal illnesses are present as they may further aggravate
dehydration and hypovolaemia.
Type 2 diabetes managed on insulin:

• All patients should be advised to seek the urgent review by their GP or health
professional when unwell or the blood glucose is consistently >15 mmol/L on two
consecutive SMBG readings as per the action plan. Blood glucose monitoring
should be increased to every two to four hours if unwell. Depending on these
levels, patients may need to increase their morning intermediate or long-acting
insulin dose by 10-20% if the glucose reading remains elevated and, depending
on further blood glucose levels, modify subsequent doses of short-acting insulin
during the day. Advice on the additional use of oral agents and GLP-1 RA is listed
122 2016-18
above. Additional blood ketone testing may be incorporated if there are symptoms
suggestive of ketosis (eg nausea, vomiting, shortness of breath or fruity odour,
abdominal pains, altered consciousness) or there is a past history of DKA, or if the
patient is using an SGLT2 inhibitor agent. This must be a documented strategy on
their sick day management plan. Note: many patients are only on basal insulin or a
premixed insulin. These patients require appropriate medical advice and access to
additional rapid-acting insulin to use as a supplemental insulin dose.262
• Patients with gastrointestinal upset who are not eating, but who feel well and
continue their usual activities, may need to reduce their insulin based upon their
SMBG readings (especially rapid-acting insulin) to avoid hypoglycaemia.
• A warning for the use of SGLT2 inhibitors: there have been rare reports of
euglycaemic DKA with all the SGLT2 inhibitors - symptoms of possible DKA need
to be incorporated in clinical management when considering use of these agents.
These agents are not indicated in type 1 diabetes.
14.2 Planned surgical procedures

People with diabetes should be seen several weeks before surgery for an assessment
of glycaemic control and anaesthetic suitability, including their CVD risks and any
treatment modifications instituted and stabilised before proceeding to surgery.
Attaining glycaemic control (ie an HbA1c approaching 53 mmol/mol or 7%) in the
preoperative period has been shown to result in fewer complications and shorter
hospital stays after surgery.169 A patient with a HbA1c of >75 mmol/mol (>9%) may
need to have their surgery delayed until glycaemic management is optimised.
Preoperative care is the same for minor and major surgery, but blood glucose levels
should be monitored intra-operatively (a prolonged procedure) and postoperatively
for several days. Insulin may be required postoperatively for some people with type 2
diabetes.
2016-18
123
In practice
Appropriate written instructions should be given to the patient beforehand.
Patients who are prescribed oral glucose-lowering medications (eg metformin,

sulphonylureas, acarbose, glitazones, SGLT2i, DPP-4i) as well as injectable GLP-1 RA
such as exenatide:
• can continue their diabetes medications on the day prior to surgery - be aware that
gastric emptying is affected by GLP-1 agonists
• on the advice of their anaesthetic team, may omit their oral glycaemic medications
on the morning of surgery, irrespective of whether they are on the morning or
afternoon list. Insulin requires individualised advice and is usually not completely
omitted. Proactively seek specialist endocrinology and anaesthetic advice before
planned procedures
• can generally recommence medications when they are able to eat meals -
specific advice is available in Australian Diabetes Society’s Peri-operative diabetes
management guidelines, available at https://diabetessociety.com.au/documents/
PerioperativeDiabetesManagementGuidelinesFINALCleanJuly2012.pdf
Metformin can generally be recommenced 24 hours after major surgery provided that
there has been no deterioration in serum creatinine.169 For patients pre-operatively
and post-operatively using metformin and SGLT2 inhibitors, maintenance of
hydration is important.
Patients with diabetes who are treated with insulin will usually require peri-operative
insulin and glucose infusions, and close blood glucose monitoring. Many hospitals
have a protocol or working plan that should be followed for the individual patient in
that service.
For colonoscopy preparation,263 colonlytely or glycoprep rather than fleet or
phosphoprep should be used in patients with renal impairment who may become
severely hyperphosphataemic with phosphate preparations. Modifications of
diet advised for colonoscopy preparation may alter glucose management and
hypoglycaemic risks, so instruction on appropriate SMBG testing may be required.
14.3 Driving
Diabetes is identified as one of the medical conditions that may impair driving ability.
Diabetes and diabetes medications may alter the capacity to drive safely.
Impairment can occur due to unexpected hypoglycaemia (main hazard) for drivers
with type 2 diabetes on glucose-lowering medications and/or sensory or end-organ
complications, particularly reduced vision and sensation in the feet. Other comorbidities
such as sleep apnoea and cardiovascular problems have substantial implications.
124 2016-18
Drivers with diabetes must meet specific national standards. Certain criteria must be
met to ensure that their health status does not increase the risk of a crash. Medical
assessment should include:
• therapeutic regimens (eg diabetes treated by any glucose-lowering agents

including insulin)
• commercial or private standards
• satisfactory control of diabetes
• hypoglycaemic unawareness
• recent severe hypoglycaemic event
• comorbidities and end-organ complications.
In practice
Evaluate patients with diabetes on their capacity to drive against national standards.
Medical standards for licensing and clinical management guidelines for commercial
and private vehicle drivers are contained in the Austroads and National Transport
Commission document Assessing fitness to drive for commercial and private vehicle
drivers, available at www.austroads.com.au/drivers-vehicles/assessing-fitness-to-
drive264 A flowchart to assist with the management of diabetes and driving can be
found on page 59 of the above document. The document is currently being updated
and the new version will be published on 1 October 2016.
As each state and territory has differing medical assessment instructions, check with
the relevant transport authority for requirements in respective states.
Specialist referral is usually required for commercial licences if the patient is on

oral glucose-lowering agents or insulin therapy. Licensing review periods are also
determined by therapeutic regimes. People with diabetes on commercial licences are
subject to yearly specialist review if they are on any form of glucose-lowering therapy,
unless they are on metformin alone, where ongoing fitness to drive may be assessed
by the treating GP by mutual agreement with the treating specialist. The initial
recommendation of a conditional licence must, however, be based on the opinion
of a specialist in diabetes.
An HbA1c level of >75 mmol/mol (>9.0%) should not be used administratively by

licensing authorities to deny eligibility for a licence in the absence of a medical review.
There is no strong evidence of high average blood glucose levels and driving risk. The
new national standards, which is due for publication later in 2016, will likely not include
an upper HbA1c threshold of concern regards driving requirements.
2016-18
125
These are national standards, so it is important to contact the driving authority in

individual states and territories as variations to the national standards do exist.
The Diabetes and driving: Above 5 to drive! consumer booklet (available at https://
static.diabetesaustralia.com.au/s/fileassets/diabetes-australia/bee30f0d-9b45-49f0-
9800-5d66ee1f49d9.pdf) provides a checklist and offers advice for people with
diabetes to ensure that they have safe blood glucose levels before they drive. The
importance of taking extra precautions to maximise road safety and reduce risks
of road accidents caused by hypoglycaemic incidents is highlighted and should be
actively promoted.
For example, drivers are required to perform a blood glucose check before they drive
and again during the journey if driving for more than two hours.
14.4 Diving
People with type 2 diabetes, including those who use medication (eg oral glucose
lowering agents, insulin), can participate in recreational scuba diving. They must
be otherwise qualified to dive and meet several criteria as outlined in consensus
guidelines for recreational diving with diabetes that was developed in 2005. For more
information, visit www.diversalertnetwork.org/medical/articles/DAN_and_UHMS_
Publish_Guidelines_for_Recreational_Diving_with_Diabetes
When evaluating persons with diabetes for medical fitness to dive, first ensure that
no other exclusionary conditions (eg epilepsy, pulmonary disease) exist.
The physiological demands of diving must then be considered. People with diabetes are
at higher risk than the general diving population of medical complications such as MI,
angina and hypoglycaemia.
14.5 Travel
People with diabetes can travel safely, provided a few extra precautions are taken
and the travel is planned.
Those not using insulin generally have few problems during travel. The stress of travel
may increase BGLs slightly. The decreased activity experienced in a long plane trip,
together with the amount of food given en route often results in increased BGLs. These
return to normal once a more usual lifestyle has been resumed at the destination.
Extra precautions before and during travel include:
• a medical consultation at least six weeks before the proposed travel to allow time
to assess control and alter management as required
126 2016-18
• checking of routine immunisation status and other medical conditions

• having a covering letter from their doctor and extra supplies of food, medication
and monitoring equipment
• getting advice about special insurance
• finding out about Australian air security guidelines.
Australian air authorities stipulate the following security guidelines. If the patient is
not using an Australian carrier, it is advisable for the patient to check with the chosen
airline for applicable security guidelines.
• All diabetes supplies including testing equipment, insulin and glucagon delivery
devices (eg syringes, pen needles, insulin pump consumables) carried on board must
be in the hand luggage of the person who has diabetes and whose name appears
on the airline ticket. It is not advisable to pack extra insulin in checked-in luggage as
insulin exposed to extreme temperatures of the aircraft holds will lose efficacy.
• The traveller’s name should appear on the insulin and/or glucagon prescription labels.
• It is advisable to carry legible prescriptions for all medications. The prescriptions
must include the traveller’s name, name and type of medication, and contact details
of attending medical practitioner.
• The NDSS card is accepted as primary proof that a person with insulin-treated
diabetes needs to carry with them their diabetes equipment such as insulin pen,
pump, syringes, needles and glucagon kit. Supplementary photographic proof of
identity such as a driver’s licence may also be requested.
• It is advisable to carry a letter from the attending medical practitioner that outlines
medical diagnoses, prescribed medications, if insulin is used and, if so, the delivery
device(s). The letter must stress the importance of the patient having to carry
medications with them and include the frequency of dosage. For those using an
insulin pump, the letter must stress the need for the pump to be worn at all times.
• Some international regulations set limits on fluid containers that may be personally
taken on board aircraft. People with diabetes who need to carry supplies of insulin
are exempt. They will be required to present the insulin at the security point and
carry proof of their condition and need for insulin.
• People wearing electronic devices to monitor blood glucose levels or to infuse
insulin should check with the airline as to whether these devices can be operated
during the flight.
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127
Rights of people with diabetes during security check

People with diabetes who use an insulin pump are not required to remove their pump
at the security point. If the security staff request this, the person with diabetes has the
right to request access to a private consultation room, which security staff are required
to provide. People with diabetes are also entitled to make this request if discussion
about their condition is required.
For more information about travel and diabetes, visit www.diabetesaustralia.com.au/

travel or http://travelsecure.infrastructure.gov.au and scroll down to ‘special needs’.
128 2016-18
15. Diabetes and end-of-life care

*
To minimise the risks of hypoglycaemia and metabolic 265 None
compensation, a blood glucose range of 6-15 mmol/L Diabetes UK, 2013 provided
is appropriate for most palliative care patients
Maintain at glycated haemoglobin (HbA1c) at no lower 265 None
than 58 mmol/mol (7.5%) if on hypoglycaemic medication Diabetes UK, 2013 provided
depending on the individual’s life expectancy, as HbA1c will
be less relevant in patients with months or days left to live
Clinical context
The aim of glycaemic control in patients at the end of life changes from preventing
and managing long-term complications of diabetes to preserving quality of life.
Terminally ill patients often have multiple factors affecting their glycaemic control
(refer to Box 11). Glucose-lowering therapy should be tailored to minimise the risks of
hypoglycaemia and hyperglycaemic states and symptoms.
Box 11. Factors affecting glycaemic control in patients with

type 2 diabetes at end of life
• Stress response to severe or • Poor appetite/smaller meals
sustained illness • Poor nutrition
• Organ failure • Cachexia
• Malignancy • Dehydration
• Chemotherapy • Difficulty taking medications (eg
• Use of steroids difficulty swallowing, nausea, stress)
• Frequent infections • Weight loss
Hyperglycaemia can worsen pain, confusion, thirst, cognition, confusion and

incontinence. Blood glucose levels >15 mmol/L may cause polyuria and increase risks
of infection.
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129
Hypoglycaemia can also cause discomfort, confusion and impaired cognitive function.
DKA can mimic terminal illness. If not recognised and treated, it can severely impair
quality and even duration of life.
Although there is little evidence about optimal blood glucose range, it is generally
agreed that a range of 6-15 mmol/L is appropriate for most palliative care patients to
optimise patient wellbeing and cognitive function.266,267
In practice
Aim to provide an appropriate level of intervention according to stage of illness,
symptom profile and respect for dignity. In most cases, tight glycaemic control to meet
general targets is no longer appropriate in patients nearing the end of life.
Ideally, discuss dying with patients and their families prior to the need for end-of-
life care so that the important considerations can be addressed in advance care
planning.268 Liaison with the palliative care team and community diabetes team is
recommended as part of a multidisciplinary approach to end-of-life diabetes care.269
Diabetes medications at end of life

Insulin alone is a simpler option for patients and their carers than combinations of
tablets and insulin. Consider switching patients from combinations to insulin alone,
once or twice daily. Patients on insulin with poor intake will need lower doses.
Avoid long-acting sulphonylurea preparations (eg glibenclamide, glimepiride) if small

meals are being taken.
Figure 7 shows an algorithm for an end-of-life diabetes care management strategy.265
Consider referral to specialist care for assistance with complex treatment decisions
such as frequent hypoglycaemia, use of insulin or managing the effects of steroids
on glycaemia.
130 2016-18
Figure 7. Algorithm for an end-of-life diabetes care management strategy
Discuss changing the approach to diabetes management with patient and/or family if not
already explored. If the patient remains on insulin, ensure the diabetes specialist nurses are
involved and agree with monitoring strategy
• Keep tests to a minimum. It may be necessary to perform some tests to ensure unpleasant
symptoms do not occur due to low or high blood glucose
• It is difficult to identify symptoms due to hypoglycaemia or hyperglycaemia in a dying patient
• If symptoms are observed, it could be due to abnormal blood glucose levels
• Test urine or blood for glucose if the patient is symptomatic
• Observe for symptoms in previously insulin-treated patient where insulin has been discontinued
*Byetta (Exenatide)/Victoza, (Liraglutide), Lyxumia (Lixisenatide)

Humalog/Novorapid/Apidra
+
Humulin I/Insulatard/Insuman Basal

^
Reproduced with permission from Diabetes UK from End of life diabetes care: A strategy document.
Clinical care recommendations. London: Diabetes UK, 2012. Available at www.diabetes.org.uk/About
us/What-we-say/Diagnosis-ongoing-management-monitoring/End-of-Life-Care/
2016-18
131
16. Issues under debate

Issue - Diagnostic criteria for GDM
ADIPS guidelines significantly lower diagnostic threshold
ADIPS guidelines are not accepted by the RACGP due to the need for high-quality evidence
and implications for resource utilisation270
Issue - Postnatal screening for type 2 diabetes mellitus

ADIPS guidelines have significantly increase screening frequency
ADIPS guidelines are not accepted by the RACGP due to the need for high-quality evidence
and implications for resource utilisation
Screening remains as in the RACGP’s Guidelines for preventive activities in general practice,
8th edition (Red Book) - fasting blood glucose every three years
Postpartum oral glucose tolerance test should be performed every three years
Comparison tables of RACGP (preferred) and ADIPS

(alternative) criteria
Screening and diagnosis of gestational diabetes mellitus
(on the basis of a 75 g oral glucose tolerance test)
The Royal Australian College of General Australian Diabetes in Pregnancy

Practitioners (RACGP; preferred criteria) Society (ADIPS; alternative criteria)
Fasting plasma glucose >5.5 mmol/L, or Fasting plasma glucose 5.1-6.9 mmol/L, or
two-hour plasma glucose or random glucose one-hour post >10.0 mmol/L, or
>8.0 mmol/L two-hour 8.5-11.0 mmol/L
Follow-up of patients with a history of gestational diabetes mellitus
The Royal Australian College of General Australian Diabetes in Pregnancy

Practitioners (RACGP; preferred criteria) Society (ADIPS; alternative criteria)
75 g two-hour oral glucose tolerance test at 6-12 75 g two-hour oral glucose tolerance test, at
weeks postpartum 6-12 weeks postpartum
Thereafter, a fasting blood glucose or glycated
haemoglobin (HbA1c) test every three years
The frequency and nature of this surveillance will depend on future pregnancy plans and the
perceived risk of converting to type 2 diabetes. Women contemplating another pregnancy should
have an oral glucose tolerance test annually
In patients with GDM, hypoglycaemia may have serious effects on placental function
and the fetus. Thorough investigation is required in such patients.
132 2016-18
Aim to achieve blood glucose levels:
• between 4 and 6 mmol/L preprandially

• <7 mmol/L two hours postprandially.
Issue - Blood pressure targets in diabetes management

Guidelines routinely advocate blood pressure (BP) target of systolic blood pressure (SBP) <130 mmHg
BP-lowering reduces cardiovascular events and mortality in people with type 2 diabetes. However,
the target levels for BP therapy have been based on little direct evidence. Meta-analyses
demonstrate that more intensive BP control (SBP <130 mmHg) was only associated with further
reduction in stroke. A 40% increase in serious adverse events was observed
The target level for optimum BP remains controversial
A number of international guidelines have changed their blood pressure targets to <140/90 mmHg,
while others remain at <130/80 mmHg. The target levels for BP therapy have been based on little
direct evidence. A number of meta-analyses have demonstrated that the benefits of intensive BP
control needs to be balanced with the risks. One meta-analysis demonstrated that more intensive
BP control (SBP <130 mmHg) compared with usual (<140/90 mmHg) was associated with further
reduction in stroke only, but there was a 40% increase in serious adverse events.153 Two additional
meta-analyses have recently been published. The analysis by Emdin at al48 found that risk reduction
was attenuated in SBP <140 mmHg. However, there did appear to be lower risk of stroke,
retinopathy and albuminuria when blood pressure was reduced to <130 mmHg. A more recent
meta-analysis, however, found that treatment of SBP <140 mmHg was associated with increased
cardiovascular disease (CVD) death.154 This may in part be related to the selection of trials in this
analysis, which included patients with comorbidites such as chronic kidney disease (CKD), heart
failure and CVD155
In line with these findings, it would be reasonable for GPs to shift the BP target to <140/90 mmHg
for people with diabetes, with lower targets considered for younger people and those at high risk of
stroke (secondary prevention) as long as treatment burden is not high. The target BP for people with
diabetes and microalbuminuria or proteinuria remains <130/80 mmHg. As always, treatment targets
should be individualised and people with diabetes monitored for side effects from use of medications
to achieve lower targets
Issue - Screening for adults aged 40-70 years who are overweight or obese
The US Preventive Services Task Force (USPSTF) has recently recommended screening for abnormal
blood glucose as part of cardiovascular disease (CVD) risk assessment in adults aged 40-70 years
who are overweight or obese. Clinicians should offer or refer patients with abnormal blood glucose
to intensive behavioural counselling interventions to promote a healthful diet and physical activity
(USPSTF Grade B recommendation)271
This recommendation applies to such adults seen in primary care settings who do not have
symptoms of diabetes. The target population includes persons who are most likely to have glucose
abnormalities that are associated with increased CVD risk and can be expected to benefit from
primary prevention of CVD through risk factor modification
2016-18
133
Issue - Target HbA1c levels

The National Institute for Health and Clinical Excellence Quality and Outcomes Framework
(NICEQOF) in the UK changed the glycated haemoglobin (HbA1c) target from 7.0% to 7.5% because
of the several large trials showing harm with a target that is too low. Because of the measurement
error, a range around that mean of, for example, 6.5-8% would be needed. This will allow for
measurement variation as well as some individualisation and negotiation with the patient, in a more
person-centred approach
Issue - Other
• Is an estimated glomerular filtration rate (eGFR) 45-60 mL/min/1.73 m2 of any clinical
consequence?
• Use of the Problem areas in diabetes (PAID)/Patient health questionnaire-2 (PHQ-2) tools to
detect depression and distress in diabetes and linkage to long-term improved outcomes and
complication reduction
• Are there possible benefits of low carbohydrate diets in diabetes management?272
• Reduction in carbohydrate intake has been shown to translate into lower glycaemic excursions
and lower overall glycaemic load273-275
- A recent study has highlighted the benefits of a very low carbohydrate, high unsaturated fat,
low saturated fat diet versus a high carbohydrate, low fat diet. The investigators evaluated
weight loss, glycaemic control and cardiovascular disease risk factors in patients with type 2
diabetes after 52 weeks. With the likely pathophysiological interaction between carbohydrate
and hyperglycaemia, this approach may be considered when more evidence is available.276
The definition of a low-carbohydrate diet varies across the spectrum of studies, causing
difficulty in generalising results
- Care may need to be exercised with patients on sodium glucose co-transporter 2 (SGLT2)
inhibitors due to risks of ketoacidosis277
134 2016-18
Appendix A. Accessing government support

for diabetes care in general practice
Support for developing management plans

and organising team care
The Australian government supports general practices that are taking a high-quality
and proactive approach to diabetes care through Medicare Benefits Schedule
(MBS) payments to general practitioners (GPs), nurses, allied health professionals
and general practices. These include the chronic disease management (CDM) items
(formerly enhanced primary care), Service Incentive Payments (SIPs) and the Practice
Incentives Program (PIP).
The CDM items provide support for developing management plans and organising
team care.
General practice management plan (GPMP, Medicare item number 721)
These are documented plans developed together by the GP and the patient. They
incorporate the patient’s needs and goals, how these are to be achieved, and
reference to any resources used. Templates are available via medical software
and various general practice networks and Primary Health Networks (PHNs).
Payments are made for development and for structured reviews of GPMPs.
Team care arrangement (TCA, Medicare item number 723)
These are expansions of the GPMP that detail allied healthcare professionals and
other members of the team who implement any part of the GPMP. This includes active
participation by at least two other providers who contribute to the GPMP or TCA and
the goals of management for the patient.
Both GPMPs and TCAs can have practice nurses or similar practice team members
involved in their development.
Payments are made for development and for structured reviews of the GPMP and
TCA under MBS item number 732.
There is evidence that GPMPs that are reviewed on a regular basis can result in
improvement in process and clinical outcomes.17 Medicare payments also support
the involvement of suitably qualified allied health members in providing care
as documented in the TCA. Up to five treatments per year are subsidised at the time
of publication.
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Medicare has strict eligibility criteria for claims for MBS items 721 and 723, and the
structured reviews under MBS item 732. Further information is available at www.
health.gov.au/internet/mbsonline/publishing.nsf/Content/Medicare-Benefits-Schedule-
MBS-1
Support for the annual cycle of care

The annual cycle of care is a method of incentivising quality diabetes care. However,
the scope of the annual cycle of care recommendations is less than the guidelines’
recommendations.
Completion of an annual cycle of care requires assessment of a number of parameters

(refer to Table A.1), and the professional attendance and appropriate documentation
by a GP, with any clinically relevant issues including:
• taking a patient history

• performing a clinical examination
• arranging any necessary investigation
• implementing a management plan
• providing appropriate preventive healthcare.
Patients and practitioners need to discuss desired outcomes and agree on goals
to achieve these. An example of a structured patient-centred care plan is provided
in Appendix B. Structured patient-centred care plan.
For practitioners - Support payments are provided for completing the annual cycle
of care. When a patient with diabetes completes their annual cycle of care, their GP
notifies Medicare and is paid a SIP.
For practices - When more than 50% of practice patients with diabetes have
completed their annual cycle of care, practices are automatically paid a quality
outcome payment. This is calculated by Medicare and is dependent on the number
of SIP payments claimed by GPs.
136 2016-18
Table A.1. Medicare Benefits Schedule item number 2517 - Minimum

requirements of care to complete an annual diabetes cycle of care for
patients with established diabetes mellitus
Minimum requirements Frequency

Weight and height plus body mass index (BMI) At least twice every cycle of care
Blood pressure index At least twice every cycle of care
Feet examination At least twice every cycle of care
Measure total cholesterol, triglycerides and high-density At least once every year
lipoprotein-cholesterol (HDL-C)
Glycated haemoglobin (HbA1c) At least once every year
Microalbuminuria At least once every year
Estimated glomerular filtration rate (eGFR) At least once every year
Self-care education, diet, physical activity, smoking evaluation At least once every year
Medication review At least once every year
Ensure that a comprehensive eye examination is carried out At least once a year if
at least once every two years complications are detected
NB: A new item on the Medicare Benefits Schedule (MBS) for retinal photography with a
non-mydriatic retinal camera will be available for general practice use from November 2016. The
listing is expected to benefit Aboriginal and Torres Strait Islander peoples and communities in rural
and remote locations, where there is limited access to optometric and ophthalmic services to
diagnose diabetic retinopathy
2016-18
137
Appendix B. Structured patient-centred

care plan - Example of a General practice
management plan and Patient care plan
[Insert practice letterhead]
General practice management plan (GPMP)

(MBS item number 721 - Diabetes)
Patient name: Date of birth:
[Full name] [Date of birth]
Contact: Medicare or private health insurance:
[Address] [Medicare number]
[Telephone] [Private health insurance number]
Date of last GPMP (if done): [Date]
This diabetes care plan was developed by staff at the [insert practice name]. While it specifically
relates to the management of your diabetes, your other health problems will also be considered.
This care plan uses the skills of many health professionals to help you to have the best of healthcare
and for you to manage your diabetes.
This plan focuses on proven therapies that, with support and care, may help prevent complications.
Diabetes is best treated early and some difficulties of management can occur when complications
arise. The management goals in this plan are set by national diabetes expert bodies. Your diabetes
will be monitored against these goals.
This plan encourages you to be actively involved in your care. It is important that you and your
healthcare team monitor your diabetes and report anything that is untoward.
We particularly urge you to report any chest pains, unexplained weakness, foot problems, visual
changes, or any symptom that concerns you. Report if you feel that you cannot cope or manage,
and if you feel distressed or sad by living with your illness.
Emergency contact at [insert practice name] for diabetes - [name] [contact number]
This document should be brought along with you to each visit to the dietitian, diabetes educator,
practice nurse, other health professional and to the doctor when your review is due.
138 2016-18
Management plan outcomes
Patient needs • To become educated regarding diabetes

• To understand the role of diabetes ‘goals’ - glucose management,
minimising heart risks and individually appropriate preventive activities
• To appropriately manage medication for diabetes and other supportive
therapies
• [Insert individual patient needs]
Management • To lead a happy, healthy lifestyle

goals • To progress toward/achieve recognised goals for diabetes care
• To prevent onset or progression of cadiovasular disease or its
complications
• To remain free of serious side effects from medication
• To minimise the burden of diabetes management and care
• To overcome barriers to self management including psychological
and social factors
Treatment • To participate in structured care system at the [insert practice name]

services • To involve other health service providers
• To provide holistic, person-centred care
• [Insert individualised patient treatment services] to assist in provision
of services
Patient actions • To undertake appropriate lifestyle measures if needed (eg quit smoking,
regular exercise, dietary changes)
• To participate in this management plan and be aware of the impact
of illness
• To become educated regarding diabetes
• [Insert individualised patient actions]
Monitoring • The first review will usually be at one to four weeks - to monitor impact
and review of any initial or ongoing therapy medication and other strategies
• Every three to six months a major review of the management plan goals
will occur
• Thereafter, reviews will depend on response to therapy and complexity
of all health issues
• A recall will be instituted at least every three months to monitor progress
Review date • [Insert review date]

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139
Past medical history

Family history
[Clinical details of family history]
Medications
[Clinical details - medication list]
Allergies
[Allergy details]
Social history
Alcohol intake
Cigarette smoking history
Patient name: [Full name]
GPMP (MBS Item 721, Diabetes)

Patient Required treatments Arrangements for
problems/ and services treatments/services
needs/relevant Goals - changes to be including patient (when, who, contact
conditions achieved actions details)
1. General
Patient’s Patient to have a clear Patient education GP/nurse/diabetes
understanding understanding of diabetes educator
of diabetes and their role in managing the
and self condition
management
Patient to understand the Patient education GP/nurse/
psychological and social diabetes educator/
impact of living with type 2 psychologist
diabetes
Patient to understand the role Patient education GP/nurse/diabetes
of self-monitoring of glucose educator
(SMBG) if this is required
140 2016-18

2. Lifestyle
Nutrition Eating according to Australian Patient education GP to monitor
dietary guidelines ( ww. OR Accredited Practising
nhmrc.gov.au/guidelines- Dietitian (APD)
As per Lifescripts
publications/n5 ) with
action plan
attention to quantity and type
of food
If concerns regarding
cardiovascular disease risk,
advise dietary review
Weight/body Your target: [insert patient Monitor Patient to monitor
mass index (BMI) target] kg/m2 Review six monthly GP/nurse to review
Therapeutic goal is 5-10% OR APD when
loss for people who are As per Lifescripts appropriate
overweight and obese with action plan BMI >35 kg/m2 -
type 2 diabetes consider specialist
With BMI >35 kg/m2 and referral and bariatric
comorbidities or BMI >40 options
kg/m2, greater weight
loss measures should be
considered
Physical activity Your target: [insert patient Patient exercise GP/Accredited
target] minutes/week routine OR Exercise Physiologist
At least 30 minutes of As per Lifescripts (AEP)
moderate physical activity on action plan Patient to implement
most if not all days of the week
(total >150 minutes/week)
Smoking Complete cessation Smoking cessation Patient to manage
strategy: GP to monitor
• Consider:
- quit
- medication
OR
As per Lifescripts
action plan
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Alcohol intake Your target: Reduce alcohol intake Patient to manage

<[insert patient target] Patient education GP to monitor
standard drinks/day OR As per Lifescripts
Healthy: action plan
<2 standard drinks/day (adults)

3. Biomedical
Cardiovascular
disease risk
calculation
Cholesterol/lipids Cholesterol level to accepted Initiation of GP
national target pharmacotherapy
is dependent on
Blood pressure BP to accepted national target GP/nurse
the assessment
(BP)
of absolute
cardiovascular disease
risk (Australian
absolute CVD risk
calculator)
This requires using
multiple risk factors,
which is considered to
be more accurate than
the use of individual
parameters
Once therapy is
initiated, the specified
targets apply;
however, these
targets are somewhat
arbitrary and should
be used as a guide
to treatment, and
not as a mandatory
requirement
Check every six
months
142 2016-18

Glycated Your target: <[insert patient Needs individualisation GP/nurse

haemoglobin target] mmol/mol according to patient
(HbA1c) Healthy: circumstances
<53 mmol/mol (range 48-58 Check every there

mmol/mol) to six months or as
advised by your GP
<7% (range 6.5-7.5%)
Blood glucose Advise 6-8 mmol/L fasting and Monitoring is Patient/GP/nurse
level 8-10 mmol/L postprandial dependent Diabetes educator
Ongoing self-monitoring of on individual when required
blood glucose is recommended circumstances
for people with diabetes
using insulin, people using
sulphonylureas or other
medicines that may cause
hypoglycaemia, hyperglycaemia
arising from illness, with
haemoglobinopathies,
pregnancy or other conditions
where data on glycaemic
patterns is required
Routine self-monitoring of
blood glucose in low-risk
patients who are using oral
glucose-lowering drugs
(with the exception of
sulphonylureas) is not
recommended
4. Medication
Medication Targeted and careful use of Patient education GP/Credentialled
review medications to maximise Review medications Diabetes Educator
benefit and minimise side (CDE) to review and
effects provide education
Pharmacist when
required/home
medicines review
Vaccinations Influenza Annually GP/nurse
Pneumococcal and diphtheria At appropriate
tetanus-acellular pertussis intervals
(dTpa) vaccine
5. Complications of diabetes
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Eye Early detection of any Eye check every two GP/optometrist/

complications problems years ophthalmologist
Retinal photography
or referral by GP
Foot Optimal foot care and Stratify the risk of GP/podiatrist/nurse
complications avoidance of ulceration and developing foot Patient
amputation by: complications: GP referral to
• patient education on foot • low/intermediate/ specialist foot clinic if
care and self-check high risk high risks detected
• professional check feet • the intensity of
every six months monitoring and
• early detection and review increases
management of according to level
complications of risk
Kidney damage Avoid kidney complications Test for GP

urine albumin-to-creatinine microalbuminuria
ratio (UACR): annually
<3.5 mg/mmol women
<2.5 mg/mmol men
Sexual Maintain sexual function To be discussed GP
dysfunction with patient where
applicable
6. Psychosocial/psychological
Mood and Minimise distress and GP/nurse
distress from depression Psychologist when
diabetes Minimise social isolation, required
support positive advocacy
against social stigma
Licence Maintain safe driving to road GP/nurse/
assessment authority standards endocrinologist/
specialist
7. Register with National Diabetes Services Scheme (NDSS)
Provide access to best Provision of self GP/nurse/ CDE
practice consumer resources management Diabetes Australia
to support self-management information and
consumer support
and advocacy
144 2016-18
Patient monitoring
Measurements Target Progress
Glycated haemoglobin (HbA1c): 48-58 mmol/mol or
This is a measure of how well your blood 6.5-7.5%
glucose has been controlled over the last Individualised, as low
three months as reasonably possible
without side effects
Cardiovascular disease (CVD) risk
assessment:
This is your risk of having a heart attack
or stroke in the next five years
Systolic blood pressure (SBP): <130- Initiation of
The highest reading in blood perssure (BP), 140 drug therapy
is more closely related to poor outcomes. depends on the
assessment of
Low-density lipoprotein-cholesterol (LDL-C):
<2.0 absolute CVD risk
This is the ‘bad’ cholesterol implicated in
Targets should be
causing CVD
used as a guide
High-density lipoprotein-cholesterol (HDL-C): >1.0 to treatment,
This is the ‘good’ cholesterol associated with and not as a
protection against CVD mandatory
requirement
Triglycerides <2.0
Renal function: eGFR
Estimated glomerular filtration rate (eGFR) Reduce albuminuria by
is an indicator of overall kidney function decreasing BP and blood
Microalbuminuria glucose levels
Microalbuminuria is a sign of kidney stress.

Identification at an early stage can prevent
kidney problems and/or progression to
kidney failure
Foot examination: Foot risk = low/
To identify potential and active foot problems intermediate/high
(eg presence of ulcers, infection, corns, Today’s examination
calluses, fissures)
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Vision: Visual care

This is to aid detection of early cataract Full eye review every
formation two years
Ophthalmology review - to detect small vessel
changes in your eyes
Copy of GPMP offered to patient? []
Copy/relevant parts of the GPMP supplied to other providers? []
GPMP added to the patient’s records? []
Date service completed: []
Proposed review date: []
I have explained the steps and costs involved, and the patient has agreed to proceed with the
service. [Steps and costs explained, patient agreed]
GP signature: Date:
146 2016-18
Appendix C. Problem areas in diabetes

questionnaire
The Problem areas in diabetes (PAID) questionnaire is a psychometrically sound tool
for detecting diabetes-related distress. The PAID questionnaire includes 20 items,
each of which focuses on a different commonly experienced problem with diabetes.
Patients indicate how much each issue affects them personally, on a scale of 0 (not
a problem) to 4 (serious problem). Individual items scored >3 (indicating a somewhat
serious or serious problem area) should be discussed with the patient.
Item scores can also be added and standardised to a score out of 100 (by multiplying
the total by 1.25). Higher scores indicate higher levels of diabetes-related distress.
Scores >40 indicate severe diabetes-related distress and warrant further exploration
and discussion with the patient.
Please read each question carefully. Put an X in the box that best describes
you for each question
Which of the following Not a Minor Moderate Somewhat Serious
diabetes issues are currently problem problem problem serious problem
a problem for you? problem
1. Not having clear and

concrete goals for your 0 1 2 3 4
diabetes care
2. Feeling discouraged with
your diabetes treatment 0 1 2 3 4
plan
3. Feeling scared when you
think about living with 0 1 2 3 4
diabetes
4. Uncomfortable social
situations related to your 0 1 2 3 4
diabetes care (eg people
telling you what to eat)
5. Feelings of deprivation
regarding food and meals 0 1 2 3 4
6. Feeling depressed when
you think about living with 0 1 2 3 4
diabetes
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147
7. Not knowing if your mood

or feelings are related to 01234
your diabetes
8. Feeling overwhelmed by
your diabetes 01234
9. Worrying about low blood
sugar reactions 01234
10. Feeling angry when you
think about living with 01234
diabetes
11. Feeling constantly
concerned about food 01234
and eating
12. Worrying about the
future and the possibility 01234
of serious diabetes
complications
13. Feelings of guilt or
anxiety when you get off 01234
track with your diabetes
management
14. Not ‘accepting’ your

diabetes
01234
15. Feeling unsatisfied with
your diabetes physician
01234
16. Feeling that diabetes is
taking up too much of
01234
your mental and physical
energy every day
17. Feeling alone with your

diabetes
01234
148 2016-18
18. Feeling that your

friends and family are 0 1 2 3 4
not supportive of your
diabetes management
efforts
19. Coping with

complications of diabetes 0 1 2 3 4
20. Feeling ‘burned out’
by the constant effort 0 1 2 3 4
needed to manage
diabetes
Investigation of specific concerns highlighted by the PAID questionnaire is useful for formulating and
adjusting treatment options for your patients. Severe and persistent diabetes-related distress may
warrant referral to a mental health specialist
Reproduced with permission from the Joslin Diabetes Center.
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149
Appendix D. Patient health

questionnaire-2 tool
The Patient health questionnaire-2 (PHQ-2) is a psychometrically sound tool for
detecting depression and anhedonia. The PHQ-2 is composed of the first two items
from the Patient health questionnaire-9 (PHQ-9; each describing a different problem/
symptom of depression), making it ideal for use in busy clinical settings.
Patients indicate how frequently they have been bothered by each problem (item) over
the past two weeks. The items are scored on a four-point Likert scale from 0 (not at
all) to 3 (nearly every day). Individual item scores are added together, resulting in a total
score from 0 to 6. Total scores >3 warrant further assessment for depression using
a diagnostic instrument or interview. Patients who are subsequently diagnosed with
depression should be provided with ongoing healthcare professional support for the
management and treatment of their depression and their ongoing diabetes care.
Note that as this tool has only two items, it may seem unnecessary to administer this
tool to patients using paper and pen. However, an advantage of doing so is that it
allows the patients to ‘grade’ their symptoms and allows the healthcare professional
to track their patient’s scores over time.
Over the past two weeks, how Not at Several More Nearly
often have you been bothered by all days than every
any of the following problems? half the day
days
1. Little interest or pleasure in doing things
2. Feeling down, depressed or hopeless
Developed by Spitzer RL, Williams JBW, Kroenke K, et al, with an educational grant from Pfizer Inc.
No permission required to reproduce, translate, display or distribute
150 2016-18
Appendix E. Available glucose-lowering

agents
When evaluating the clinical evidence of the following interventions, high-quality,
long-term prospective trials on clinical outcomes specific to type 2 diabetes and its
complications are useful. Of note, agents recently listed for glycaemic management have
short-term trials that have reported cardiovascular safety but no cardiovascular benefits.
Metformin
Prospective trials have demonstrated reduced progression (31%) from impaired fasting
glucose (IFG) or impaired glucose tolerance (IGT) to diabetes when metformin is used.
However, metformin is not currently Therapeutic Goods Administration (TGA) indicated
for this use.
In patients with type 2 diabetes, the UK Prospective Diabetes Study (UKPDS) has
demonstrated cardiovascular benefits with metformin use in overweight patients.
Metformin:
• is the medication of first choice for people with type 2 diabetes
• reduces hepatic glucose output and improves muscle cell insulin receptor resistance
• does not stimulate insulin release
• significantly reduces the risk of diabetes-related morbidity and mortality
in overweight patients
• should be used with caution in people with hepatic or cardiac disease, and those
with a heavy alcohol intake or dehydration (eg acute gastroenteritis) and renal
impairment due to risks of lactic acidosis.
Contraindication:
• Advanced renal impairment (estimated glomerular filtration rate [eGFR] <30 mL/
min/1.73 m2) is the only absolute contraindication to metformin. It should be used
with caution in people with an eGFR of 30-45 mL/min/1.73 m2 with dose reduction
is recommended.
Main side effects:278

• anorexia, nausea, vomiting
• diarrhoea, abdominal cramps, flatulence
• lactic acidosis (uncommon, but may occur with dehydration and co-existing renal,
liver or cardiovascular disease [CVD])
• possible vitamin B12 deficiency.
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Sulphonylureas
The UKPDS has demonstrated microvascular benefits with sulphonylurea use.
Cardiovascular benefts only emerged with long-term, post-trial follow-up of newly
diagnosed patients previously intensively treated with sulphonylureas and insulin. This
has been called the ‘legacy’ effect. Clear microvascular benefits have also been shown
in the Advance in Diabetes and Vascular Disease (ADVANCE) trial, which used the
more contemporary sulphonylurea agent gliclazide.
Sulphonylureas:
• act to increase insulin secretion in a non-glucose dependent fashion and rely

on some residual p-cell function
• can be considered after a trial of healthy lifestyle and used in combination with
agents such as metformin.
Main side effects:
• weight gain
• symptomatic hypoglycaemia
• anorexia, nausea, diarrhoea, skin rashes
• occasionally blood dyscrasias
• glibenclamide and glimepiride may cause high rates of hypoglycaemia (in older
patients and in patients with autonomic neuropathy or nephropathy).
Acarbose
One prospective trial Study to Prevent Non-Insulin-Dependant Diabetes Mellitus
(STOP-NIDDM) has shown reduced progression to diabetes in patients with IGT,
as well as macrovascular benefits.279 As yet, no prospective cardiovascular trials
have reported on acarbose use in type 2 diabetes.
Acarbose:
• can be used when blood glucose values remain high after meals despite dietary
modification
• inhibits the digestion of carbohydrate and thus slows the rate of glucose delivery
into the circulation
• needs to be taken at the time of starting the meal and introduced gradually to avoid
flatulence and abdominal discomfort.
If hypoglycaemia occurs (because of concurrent sulphonylurea or insulin treatment),

glucose rather than other carbohydrates is required. Care is necessary in those with
renal impairment or gastrointestinal disease, and liver enzymes need to be monitored.
152 2016-18
Main side effects:

• flatulence and abdominal bloating
• nonresponse to carbohydrates other than glucose if hypoglycaemic
• liver abnormalities (rare).
Glitazones (pioglitazone and rosiglitazone)

The Prospective pioglitazone clinical trial in macrovascular events (PROactive) trial
did not demonstrate benefit for the primary outcome of major adverse cardiovascular
events (MACE) but did report significantly increased risk of heart failure (11% versus
8% in placebo).116
Several meta-analyses have reported that glitazones (including rosiglitazone) increase

risk of hospitalisation with heart failure or heart failure death.
Glitazones:
• sensitise the liver and peripheral tissues to insulin and are effective in lowering blood
glucose by reducing insulin resistance
• can (pioglitazone and rosiglitazone) be used as combination therapy with
metformin, sulphonylureas or insulin.
Contraindications:280,281
• moderate to severe cardiac failure (pioglitazone and rosiglitazone)

• increased risk of bladder cancer.
Rosiglitazone is not recommended in patients with known ischaemic heart disease,

particularly in those taking nitrates.
Rosiglitazone is not listed on the Pharmaceutical Benefits Scheme (PBS) for triple
therapy with metformin and a sulphonylurea, or in combination with insulin.
Main side effects:

• increased subcutaneous fat and/or fluid
• decreased haemoglobin levels
• increased risk of peripheral fractures in women
• possible increased risk of myocardial infarction (rosiglitazone)
• increased LDL-C (rosiglitazone).
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Incretins
Two classes of incretin medications exist - dipeptidyl peptidase-4 inhibitor (DPP-4i)
and glucagon-like peptide-1 receptor agonist (GLP-1 RA).282
DPP-4i
DPP-4i includes sitagliptin, linagliptin, saxagliptin, vildagliptin and alogliptin.
Saxagliptin (Saxagliptin Assessment of Vascular Outcomes Recorded in Patients with

Diabetes Mellitus Thrombolysis in Myocardial Infarction [SAVOR-TIMI] trial) showed
secondary endpoint data: statistically significant increase in hospital admissions for
congestive heart failure. No demonstrated macrovascular benefits.
Alogliptin (Examination of Cardiovascular Outcomes with Alogliptin versus Standard of

Care [EXAMINE] trial) and sitagliptin (Trial to Evaluate Cardiovascular Outcomes after
Treatment with Sitagliptin [TECOS] trial) showed no increased cardiovascular risks, but
also did not demonstrate macrovascular benefits.
Other DPP-4i have no reported prospective cardiovascular trials demonstrating benefits.
DPP-4i:
• are oral agents and act by increasing levels of circulating incretins - glucagon-like
peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) - which
are released by intestinal cells in response to food
• block the enzyme dipeptidyl peptidase-4 (DPP-4), which is responsible for rapid
breakdown of GLP-1 and GIP
• cause elevated and prolonged action of physiologically released incretin hormones
• such as GLP-1 and GIP act on pancreatic cells to increase insulin levels and also
suppress a-cell secretion of glucagon (elevated in type 2 diabetes)
• are weight neutral and improve postprandial control
• rarely cause hypoglycaemia except in combination with agents such as
sulphonylureas and insulin
• dose reduction in renal impairment eGFR <60 mL/min/1.73 m2 for alogliptin,
saxagliptin, sitaglitpin, and vildagliptin; no dose adjustment required for hepatically
metabolised linagliptin; saxagplitin may not be used in end-stage renal failure stage
five of chronic kidney disease.283
Main side effects:
• nasopharyngitis
• headache
• upper respiratory tract symptoms.
154 2016-18
GLP-1 RA
GLP-1 RA includes exenatide, liraglutide and lixisenitide.
Lixisenatide (Evaluation of Lixisenatide in Acute Coronary Syndrome [ELIXA] trial)

showed no increased cardiovascular risks but also did not demonstrate macrovascular
benefits. A prospective cardiovascular safety outcomes trial (Liraglutide Effect and
Action in Diabetes: Evaluation of Cardiovascular Outcome Results [LEADER]) for
liraglutide, another GLP-1 RA in high risk patients, had a 13% reduction in major
adverse cardiac events and 22% reduction in cardiovascular death.130
GLP-1 RAs:
• are injectable medications that bind to the GLP-1 receptor (exenatide is currently
PBS subsidised; once weekly exenatide, liraglutide and lixisenitide are TGA
approved for use in Australia but are currently not PBS-listed)
• cause weight loss through actions on cerebral hormonal responses to insulin
and appetite
• may affect gastric emptying
• only cause hypoglycaemia in combination with other medications such
as sulphonylureas and insulin.
Main side effects:
• nausea, vomiting
• pancreatitis (rarely)
• weight loss.
Sodium glucose co-transporter 2 inhibitors

The EMPA-REG (Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2
Diabetes trial) OUTCOME trial (empagliflozin) showed reduced rates of death from
cardiovascular causes (38% relative risk reduction) and any cause (32% relative
reduction). In secondary endpoint analyses, a 35% reduction in hospitalisation for
heart failure was observed. The mechanism through which empagliflozin may mediate
these outcomes is still under investigation.
The other sodium glucose co-transporter 2 (SGLT2) inhibitors have no reported

prospective cardiovascular trials.
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155
SGLT2 inhibitors:
• are novel oral medications that selectively inhibit SGLT2, the main renal glucose
reabsorptive mechanism
• result in glycosuria with resultant lowering of glucose in a non-insulin dependent
manner and modest weight loss plus lowered BP
• rely on adequate renal function
• promote weight loss.
Side effects:
• weight loss
• increased urogenital mycotic and urinary tract infections
• aggravate dehydration
• euglycaemic diabetic ketoacidosis (DKA).
156 2016-18
Appendix F. Table of evidence and

properties of glucose-lowering agents
Refer to Figure 4 for more information.
Glucose-lowering Mechanism of action Outcome data Contraindications
class and drugs
Biguanide Reduces hepatic glucose UKPDS1 Renal impairment

• metformin output, lowers fasting (estimated glomerular
glucose levels filtration rate [eGFR] <30
• metformin XR
ml/min/1.73 m2)
Severe hepatic
impairment
Sulphonylureas Triggers insulin release in UKPDS2,3 Severe renal or hepatic

• glibenclamide a glucose-independent impairment
manner
• gliclazide
• gliclazide modified
release (MR)
• glimepiride
• glipizide
Dipeptidyl peptidase-4 Decreases inactivation of EXAMINE4,5 Pancreatitis9

inhibitors glucagon-like peptide 1 - Alogliptin
(DPP-4i) (GLP-1) thereby increasing
SAVOR-TIMI 536,7
its availability
• alogliptin - Saxagliptin
GLP-1 stimulates beta cell
• linagliptin TECOS8
insulin release and slows
• saxagliptin
gastric emptying - Sitaglipitn
• sitagliptin
• vildagliptin
Thiazolidinediones (TZD) Transcription factor PROACTIVE11

• pioglitazone peroxisome proliferator- - Pioglitazone
activated receptor PPARy
• rosiglitazon
agonists
Lowers glucose levels
through insulin sensitisation
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157
Precautions, side effects and administration Cost and accessibility
Precautions General schedule on Pharmaceutical Benefits

Suspend treatment during acute disease/conditions with the Scheme (PBS)
potential to cause tissue hypoxia or alter renal function.
Side effects
Gastrointestinal side effects, lactic acidosis, weight neutral
Administration
Oral administration
Start at low dose and up-titrate
Slow release preparations available
Precautions General schedule on PBS

Hypoglycaemia
Side effects
Weight gain
Administration
Oral administration
Start at low dose and up-titrate
Slow release preparation available
Precautions Alogliptin, linagliptin, saxagliptin, sitagliptin,

Nasopharyngitis - often subsides in 10-14 days vildagliptin:
Side effects • PBS-subsidised for use in combination with
Rash, pancreatitis, gastrointestinal disturbances, weight *
metformin and sulphonylureas or both
neutral • Linagliptin and sitagliptin will be listed on
Administration the PBS from October 2016 to be used in
Oral administration combination with insulin
Dosage adjustment in renal impairment (except Linagliptin)10
Precautions PBS-subsidised for use in combination with

Symptomatic heart failure metformin, sulphonylurea or both
Side effects Patient must have a contraindication or
Fluid retention, heart failure, increased risk of non-axial intolerance to metformin-sulphonylurea
fractures in women, increased risk of bladder cancer, combination
weight gain PBS-subsidised for use with insulin
Administration
Oral administration
158 2016-18
Table of evidence and properties of glucose-lowering agents - Continued
Glucose-lowering Mechanism of action Outcome data Contraindications

class and drugs
Alpha 1 glucosidase Slows intestinal Severe renal impairment

inhibitors carbohydrate absorption (creatinine clearance
• acarbose and reduces postprandial <25 mL/min/m2)
glucose levels
Sodium-glucose Inhibits a sodium-glucose EMPA-REG Diminished efficacy with

co-transporter-2 co-transporter to produce OUTCOME12 renal impairment (eGFR
(SGLT2) inhibitors urinary glucose loss and <60 ml/min/1.73 m2)
- Empagliflozin
decrease glucose levels
• canagliflozin
• dapagliflozin
• empagliflozin
Glucagon-like peptide-1 Stimulates beta-cell insulin ELIXA13,14 Avoid with history

receptor agonist (GLP-1 release and slows gastric - Lixisenatide of pancreatitis or
RA) emptying pancreatic malignancy
• exenatide
LEADER15
• exenatide ER
- Liraglutide
• liraglutide
• lixisenatide
Insulin Directly activates the insulin UKPDS2

receptor
*Saxagliptinand sitagliptin are currently PBS listed for triple oral therapy, linagliptin and vildagliptin have been recommended by
PBAC for triple oral therapy (date is not yet available)
Reproduced with permission from the Australian Diabetes Society.
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159
Precautions, side effects and administration Cost and accessibility

GI disorders associated with malabsorption
Side effects
Bloating and flatulence, weight neutral
Administration
Oral administration
Take with meals as tolerated
Precautions Dapagliflozin and empagliflozin:

Avoid use with loop diuretics • PBS-subsidised for use in combination with
Side effects metformin, sulphonylurea or both
Dehydration, dizziness, genitourinary infections (advise • PBS-subsidised for use with insulin
adequate fluid intake and meticulous toileting hygiene),
Not PBS-subsidised for use as monotherapy
ketoacidosis, weight loss
or in combination with a thiazolidinedione
Administration (glitazone), a dipeptidyl peptidase 4 inhibitor
Oral administration (gliptin) or a glucagon-like peptide-1
Canagliflozin: PBS-subsidisation withdrawn
Precautions Exenatide and exenatide ER:

Dosage adjustment in moderate-severe renal impairment • PBS-subsidised for use in combination with
Increased risk of pancreatitis metformin, sulphonylurea or both
Side effects • Exenatide

Nausea, vomiting, weight loss • PBS-subsidised for use with insulin
Administration Not PBS-subsidised for use as monotherapy
Subcutaneous injection or in combination with a dipeptidyl peptidase 4
inhibitor (gliptin), a thiazolidinedione (glitazone) or
an SGLT2 inhibitor
Liraglutide: not PBS-subsidised

Consider need for dosage adjustment in moderate-severe Levemir insulin: PBS-subsidisation restricted
renal disease to type 1 Diabetes
Side effects
Hypoglycaemia, weight gain
Administration
Subcutaneous injection
Considered early if blood glucose level (BGL) is very high
160 2016-18
References - Appendix F
1. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with
metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet
1998;352(9131):854-65.
2. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with
sulphonylureas or insulin compared with conventional treatment and risk of complications in
patients with type 2 diabetes (UKPDS 33). Lancet 1998;352(9131):837-53.
3. The ADVANCE Collaborative Group. Intensive blood glucose control and vascular outcomes in
patients with type 2 diabetes. N Engl J Med 2008;358:2560-72.
4. White WB, Cannon CP, Heller SR, et al. Alogliptin after acute coronary syndrome in patients with
type 2 diabetes. N Engl J Med 2013;369:1327-35.
5. Zannad F, Cannon CP, Cushman WC, et al. Heart failure and mortality outcomes in patients
with type 2 diabetes taking alogliptin versus placebo in EXAMINE: A multicentre, randomised,
double-blind trial. Lancet 2015;385(9982):2067-76.
6. Scirica BM, Bhatt DL, Braunwald E, et al. Saxagliptin and cardiovascular outcomes in patients
with type 2 diabetes mellitus. N Engl J Med 2013;369:1317-26.
7. Scirica BM, Braunwald E, Raz I, et al. Heart failure, saxagliptin, and diabetes mellitus:
Observations from the SAVOR-TIMI 53 randomized trial. Circulation 2014;130(18):1579-88.
8. Green JB, Bethel MA, Armstrong PW, et al. Effect of sitagliptin on cardiovascular outcomes in
type 2 diabetes. N Engl J Med 2015;373(3):232-42.
9. Meier JJ, Nauck MA. Risk of pancreatitis in patients treated with incretin-based therapies.
Diabetologia 2014;57(7):1320-24.
10. McGill JB, Sloan L, Newman J, et al. Long-term efficacy and safety of linagliptin in patients with
type 2 diabetes and severe renal impairment: A 1-year, randomized, double-blind, placebo-
controlled study. Diabetes Care 2013;36(2):237-44.
11. Dormandy JA, Charbonnel B, Eckland DJ, et al. Secondary prevention of macrovascular events
in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial
In macroVascular Events): A randomised controlled trial. Lancet 2005;366(9493):1279-89.
12. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in
13. Diaz R, McMurrayJJV, Lewis EF, et al. The evaluation of lixisenatide in acute coronary syndrome
- The results of ELIXA symposium. Boston, MA: 75th Scientific Sessions of the American
Diabetes Association, 2015.
14. Bentley-Lewis R, Aguilar D, Riddle MC, et al. Rationale, design, and baseline characteristics in
evaluation of lixisenatide in acute coronary syndrome, a long-term cardiovascular end point trial
of lixisenatide versus placebo. Am Heart J 2015;169(5):631-38.e7.
15. Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and cardiovascular outcomes in
2016-18
161
Appendix G. Types of insulin available

The pharmacokinetics of the different insulins is patient-dependent. Review product
information for each product before prescribing. An empirical approach to dosage
together with a ‘go slow’ policy will result in the smoothest fine tuning of management.
Some of these insulins are available as injection devices, pen injectors, disposable
insulin pens, cartridges and vials.
Type Brand name Manufacturer Nature

Rapid-acting (peak at one hour, last 3.5-4.5 hours)
Insulin lispro Humalog
* Lilly Analogue
Insulin aspart NovoRapid
* Novo Nordisk Analogue
Insulin glulisine Apidra
* Sanofi Analogue
Short-acting (peak at two to five hours, last six to eight hours)
Neutral Actrapid Novo Nordisk Human
Humulin R Lilly Human
Hypurin Neutral Aspen Bovine
Intermediate acting (12-24 hours)
Isophane Humulin NPH Lilly Human
Protaphane Novo Nordisk Human
Hypurin Aspen Bovine
Isophane
Long-acting (BASAL)
Insulin detemir Levemir Novo Nordisk Analogue
Insulin glargine Lantus Sanofi Analogue
Insulin glargine (U300) Toujeo Sanofi Analogue
Premixed insulins
Lispro 25%/lispro protamine 75% Humalog Mix25
* Lilly Analogue
Lispro 50%/lispro protamine 50% Humalog Mix Lilly Analogue
50
*
Insulin aspart 30%/insulin aspart NovoMix 30
* Novo Nordisk Analogue
protamine 70%
Neutral 30%/isophane 70% Humulin 30/70 Lilly Human
Mixtard 30/70 Novo Nordisk Human
Neutral 50%/isophane 50% Mixtard 50/50 Novo Nordisk Human
*Rapid-acting - should be given immediately before eating
162 2016-18
Appendix H. Examples for insulin

initiation and titration
H.1. Guide to starting and adjusting basal insulin141,284
Practitioner-led titration OR Patient-led titration
Adjust insulin
Mean FBG
dose twice
over previous t by 2 units every three days,
weekly until
two days until FBG target is achieved
FBG target is
*
(mmol/L)
achieved
10 1 by 4 units A. If FBG >6 mmol/L but <8 mmol/L
for three consecutive days, no change
8-9.9 1 by 2-4 units
7-7.9 No change or B. If FBG is 4-6 mmol/L on any day,
1 by 2 units J insulin dose by 2 units
6-6.9 No change
C. If FBG <4 mmol/L on any day,
4-5.9 J by 2 units
J insulin dose by 4 units
<4, or if severe J by 2-4 units
hypoglycaemic
episode *Do not increase the insulin dose if FBG is
<4 mmol/L at any time in the preceding week
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H.2. Guide to starting and adjusting premixed insulin

STEP 1. SELECT premixed insulin and injecting device
।
INSULIN-NAIVE patients
STEP 2. START premixed insulin 10 units immediately before or soon after the largest meal
(usually evening meal)
CONTINUE metformin if indicated, consider tapering sulphonylureas as glycaemic control improves
STEP 3. TITRATION
Adjust the evening premixed insulin dose once or twice a week according to the schedule below
to a fasting blood glucose (FBG)285
Lowest blood glucose level (BGL) reading Insulin dosage

(mmol/L) of the previous three days - fasting adjustment
or preprandial
>10 f by 4 units
8-10 f by 2 units
7-7.9 No change or f by 2 units
6-6.9 No change
4-5.9 J by 2 units
<4.0 or severe hypoglycaemic event
* J by 4 units
If a morning insulin dose is given, adjust the insulin dose according to evening preprandial BGL
according to the same titration recommendations
*Hypoglycaemia should prompt a review of other oral therapy. Which insulin is adjusted depends
on regimen and target glucose
STEP 4. INTENSIFICATION: Once daily insulin to twice daily premixed insulin

When?
• If the FBG is at target, if evening preprandial BGL > FBG or if evening preprandial BGL
is high, or
• after three months if glycated haemoglobin (HbA1c) > target despite FBG and evening
preprandial BGL at target
How?
1. Halve the current once daily insulin dose and give the total dose as a twice daily injection
(pre-breakfast and pre-dinner)
2. Monitor pre-dinner BGL and FBG versus targets
3. Once a week, adjust both insulin doses independently (according to protocol above in step 3);
pre-breakfast insulin is adjusted according to pre-dinner BGL and pre-dinner insulin is adjusted
according to FBG
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H.3. Guide to basal plus insulin intensification

schedules
STEP 1. SELECT rapid-acting (prandial) insulin and injecting device to be added in addition to
basal insulin
STEP 2. START rapid-acting insulin (4 units) to be given before the meal with the largest
carbohydrate content
CONTINUE basal insulin at the current dose
CONTINUE metformin, consider tapering sulphonylureas as glycaemic control improves
MONITOR two-hour postprandial blood glucose level (BGL)
STEP 3. TITRATION
Increase rapid acting (prandial) insulin dose by 2 units every three days to achieve target
Two-hour postprandial BGL (mmol/L) Rapid-acting (prandial)

insulin dosage
adjustment
>8 (for three consecutive days) No change or î by 2 units
6.0-7.9 No change
4.0-5.9 J by 2 units
<4.0 on any day J by 2-4 units
.....................................................................
4. Basal plus titration to basal bolus - intensification
When?
If HbA1c is not at target after three months, add a further prandial insulin dose to another meal
(eg basal plus 2 to basal bolus)
How?
1. Keep the current prandial and basal insulin doses unchanged
2. Add a new rapid-acting (prandial) insulin to the next largest meal of the day (starting at 10%
of the basal insulin dose or 4 units)
3. î new prandial insulin dose by 2 units every three days until postprandial target is achieved
as per step 3 above
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Appendix I. Tools for assessing

neuropathy, circulation and foot
deformity160
Neuropathy
10 g monofilament sensitivity
Vibration perception (tuning fork or biothesiometer)
Neuropathy disability score - ankle (Achilles) reflexes and the sensory modalities of pinprick, vibration
and temperature perception
Circulation
Palpation of peripheral pulses
Ankle-brachial pressure index
Toe-brachial pressure index
Foot deformity score

Six point scale (one point for each characteristic)
small muscle wasting
Charcot foot deformity
bony prominence
prominent metatarsal heads
hammer or claw toes
limited joint mobility
A score of >3 indicates foot deformity

166 2016-18
Appendix J. Detailed information on

glycaemic emergencies
J.1 Hypoglycaemia
Hypoglycaemia is a common complication of the management of type 1 diabetes.
But the frequency of hypoglycaemia in type 2 diabetes is underestimated. Its clinical
significance, especially in the elderly patient, is great. Hypoglycaemia can lead to
falls, fractures, injuries, arrhythmias and, in severe cases, death. Symptoms may go
unrecognised or may be mistaken for other conditions (eg transient ischaemic attack
[TIA], vasovagal episodes).
Patients at risk of hypoglycaemia (apart from the elderly) include people who have:
• longstanding type 2 diabetes with cardiovascular disease (CVD)

• renal impairment and chronic kidney disease (CKD)
• monotherapy or combination therapy with insulin or long-acting sulphonylureas
• excessive alcohol intake
• beta-blocker therapy (rare), in particular vasodilatory agents
(eg propranolol, atenolol)
• participated in unaccustomed or vigorous exercise.
The risk of hypoglycaemia with each sulphonylurea relates to the drugs’

pharmacokinetic properties. Long-acting preparations are associated with higher risks
of hypoglycaemia (eg glibenclamide [Daonil, Glimel]). Studies have shown significantly
lower rates of hypoglycaemia associated with the use of gliclazide (Diamicron)
compared with other sulphonylureas.
Although many newer therapies for type 2 diabetes do not cause hypoglycaemia
when used as monotherapy, their use in combination with insulin or sulphonylureas
increases the risk of hypoglycaemia. The use of insulin analogues may limit, but not
eradicate, the risk of hypoglycaemia.
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Symptoms of hypoglycaemia vary between persons. Patients often learn to

recognise their unique symptoms. The onset of symptoms usually occurs with a blood
glucose level (BGL) of <4.0 mmol/L. Common symptoms fall into two categories:
• Adrenergic symptoms - trembling or shaking, sweating, hunger, lightheadedness

and numbness around the lips and fingers
• Neuroglycopaenic symptoms - lack of concentration, weakness, behavioural
change, tearfulness/crying, irritability, headache and dizziness.
Severe hypoglycaemia occurs clinically when a patient develops a reduced
conscious state and requires assistance from another person to manage an episode
of hypoglycaemia. A BGL of <3.0 mmol/L puts the person at increased risk of severe
hypogylcaemia.
Asymptomatic hypoglycaemia (or biochemical hypoglycaemia) occurs when a BGL

is low (<3.9 mmol/L).
Impaired hypoglycaemia awareness is of particular concern and refers to the

clinical situation where a patient loses the ability to detect the early symptoms of
hypoglycaemia. This results from repeated episodes of mild hypoglycaemia or can
arise with long duration of diabetes due to loss of adrenergic and glucagon response,
with eventual loss of adrenergic and neuroglycopaenic symptoms. It can lead to
confusion and marked behavioural change, which is not recognised by the patient
and may progress to loss of consciousness.
The cause needs to be identified and the episode dealt with by reinforcing education,
counselling the patient and perhaps changing treatment.
Management of an episode of hypoglycaemia

If a patient with diabetes is showing signs of potential hypoglycaemia, first make sure
that the patient is safe (eg seated securely and not at risk of falling).
If possible, confirm that the symptoms are due to hypoglycaemia by performing
a finger prick BGL.
If the person is awake, alert and can swallow, hypoglycaemia may be managed
according to the ‘Rule of 15’.
If the patient is symptomatic, or if BGL is <4.0 mmol/L:
• provide 15 g of quick-acting carbohydrate that is easy to consume (eg half a can

of regular - non-diet - soft drink, half a glass of fruit juice, three teaspoons of sugar
or honey, six or seven jellybeans, three glucose tablets)
168 2016-18
• wait 15 minutes and repeat blood glucose check - if the level is not rising, suggest
eating another quick-acting carbohydrate from the above list
• provide some longer acting carbohydrate if the patient’s next meal is more than
15 minutes away (eg a sandwich; one glass of milk or soy milk; one piece of fruit;
two or three pieces of dried apricots, figs or other dried fruit; one tub of natural low-
fat yoghurt; six small dry biscuits and cheese)
• test glucose every one to two hours for the next four hours.
Patients and carers should be made aware of the use of an alternative ‘Rule of 15’.
If the patient is symptomatic, but the blood glucose or capillary glucose cannot be
performed to confirm that the episode is due to hypoglycaemia, treat the patient as if
they have hypoglycaemia by administering 15 g of quick-acting carbohydrate. If there
is no improvement after 15 minutes, the patient could have another cause for the
episode and further medical assistance may be necessary.
If the patient cannot safely swallow 15 g of carbohydrate due to their reduced

conscious state, consider the administration of 1 mg of glucagon intramuscularly
or subcutaneously into the thigh, buttock or upper arm, if available. If not, further
emergency medical assistance will be required.
If glucagon is administered, always review the monitored capillary glucose after 15

minutes to ensure effective management of the hypoglycaemia has occurred and the
blood glucose remains >4 mmol/L. Test again one hour after severe hypoglycaemia
to ensure stable glucose levels.
Post-hypoglycaemia - Re-assess the patient’s circumstances, medication dosages,

and dietary intake, as well as overall need for glucose monitoring after any severe
hypoglycaemic episode with the patient and/or with their immediate family or support
persons. Also ensure implications for driving competence (refer to Section 14.3 Driving
and www.austroads.com.au/drivers-vehicles/assessing-fitness-to-drive), operation of
machinery and other similar areas are discussed with the patient.
J.2 Hyperglycaemic emergencies

Severe hyperglycaemia has significant morbidity and mortality.
Hyperglycaemic emergencies should be preventable in people known to have

diabetes, and their occurrence in this group signifies a major breakdown in medical
management. Adequate early management of sick patients with diabetes will prevent
the development of hyperglycaemic emergencies.
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169
Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is a medical emergency requiring specialist care and
should generally be managed in hospital. Whatever the setting, it is important that
treatment commences as early as possible.
DKA, once thought to typify type 1 diabetes mellitus, can occur in patients with type
2 diabetes mellitus under stress (eg during surgery, trauma, infections, high dose
steroids). The very young, older people and pregnant patients are also at greater risk
of DKA. A type of ketoacidosis has now been identified (although rarely) with the use
of sodium glucose co-transporter 2 (SGLT2) inhibitors alone or in combination with
other glucose lowering medications. This type of diabetic ketosis is characterised by
the absence of extreme hyperglycaemia and may lead to overlooked diagnoses. Refer
to the Therapeutic Goods Administration (TGA) warning at www.tga.gov.au/alert/
sodium-glucose-co-transporter-2-inhibitors-used-treat-type-2-diabetes
Pathophysiology
DKA occurs when there is an absolute deficiency of insulin. For DKA to occur in type
2 diabetes, there needs to be significantly impaired insulin secretion as a result of
‘glucotoxicity’, or a long duration of diabetes together with severe insulin resistance,
typically as the result of severe infection or other stresses.
This results in:
• increasing hepatic glucose production causing hyperglycaemia

• increasing peripheral lipolysis releasing free fatty acids - these are converted
to ketoacids by the liver resulting in a metabolic acidosis
• hyperglycaemia-induced osmotic diuresis leading to sodium, potassium
and phosphate depletion
• dehydration causing pre-renal failure.
Assessment
The biochemical criteria for DKA are:

• hyperglycaemia, defined by a BGL >11 mmol/L
*
• venous pH <7.3 or bicarbonate <15 mmol/L
• presence of blood ketones or urinary ketones (abnormal ketones is >0.5 mmol/L,
severe ketosis is >3.0 mmol/L)
*Note the absence of hyperglycaemia may occur with ketosis with SGLT2 inhibitors
Blood ketone testing is preferred but urinalysis may be used for initial assessment if
blood ketone testing is not available. Blood ketone testing equipment should be made
available for medical practices and ‘at risk’ patient use.
170 2016-18
When treating adult patients with DKA, the following must be considered and closely
monitored:
• correction of fluid loss with intravenous fluids
• correction of hyperglycaemia and suppression of ketone production with insulin
• correction of electrolyte disturbances, particularly potassium loss
• resolution of acid-base balance
• treatment of concurrent infection/conditions (eg stroke, myocardial infarction,
deep vein thrombosis), if present.
The main aim in treating DKA is to progressively normalise the blood pH and clear
the body of excessive ketones - achieved by aggressive fluid replacement and insulin
therapy. This also improves the blood glucose concentration. The hyperglycaemia
corrects before the acidosis. Therefore, intravenous glucose is required to allow the
insulin infusion to continue to suppress ketone production while acidosis resolves.176
Wherever possible the patient should be managed in a specialist medical unit. In

rural and remote practice, this may not be possible. In this situation, it is advisable to
contact the most appropriate diabetes resource person for advice while commencing
treatment promptly.
Hyperosmolar hyperglycaemic state

Hyperosmolar hyperglycaemia usually occurs in type 2 diabetes most often in the
elderly, or in those with newly diagnosed type 2 diabetes. It is characterised by severe
hyperglycaemia (usually >25 mmol/L) , hyperosmolality, dehydration and a change
in mental state with little or no ketoacidosis. It may present as hypovolaemic shock
and coma in severe cases.176 This is usually a result of illness or infection; however,
it can also be due to poor patient compliance. Older patients are at higher risk of
hyperosmolar hyperglycaemic state (HHS).
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171
Pathophysiology
HHS develops because of relative rather than absolute insulin deficiency. Significant
insulin deficiency causes hyperglycaemia due to increased hepatic gluconeogenesis.
However, as absolute insulin deficiency is not present, peripheral lipolysis remains
suppressed and the release of free fatty acids is low. Little substrate is available for the
generation of ketoacids and a metabolic acidosis does not occur.
The hyperglycaemia results in an osmotic diuresis leading to pre-renal failure.

Eventually, severe intravascular volume depletion occurs resulting in a further
deterioration of renal function. Consequently, glomerular filtration diminishes,
preventing the further excretion of glucose. With ongoing increasing hepatic glucose
production, decreased peripheral glucose utilisation and reduced urinary glucose
losses, severe hyperglycaemia results.
The depletion of the total body water leads to the hyperosmolality of body
fluids reflected by the extreme hyperglycaemia and increased plasma sodium.
This hyperosmolar state affects consciousness and may cause coma.
General outline for the management of HHS

Wherever possible, the patient with HHS should be managed in a specialist medical
unit. It may present as hypovolaemic shock and coma in severe cases.176 It is
important to note that blood glucose meters do not register very high glucose levels,
so access to a laboratory is necessary to monitor the correction of hyperglycaemia as
well as to monitor sodium and potassium levels. Rapid correction of the hyperosmolar
state is dangerous.
In remote rural practice, this may not be possible. In this situation it is advisable to
contact the most appropriate diabetes resource person (specialist endocrinologist)
for advice while promptly commencing treatment.
172 2016-18
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noss
national diabetes services scheme
d
diabetes
australia
National
Diabetes
Services
Scheme
The NDSS supports your patients
with diabetes
If you have a patient with diabetes, make sure

you register them with the NDSS to provide
them with life-long access to diabetes education
and support services. Where they meet the
eligibility criteria, they will also have access
to subsidised products to help them manage
their diabetes.
Registration is free and only done once.
The reverse side of this page has information on

the NDSS and how to register your patients. You
can pull this card out of the booklet and place it
on your desk or nearby for easy reference.
The National Diabetes Services Scheme is an initiative of the Australian Government

administered with the assistance of Diabetes Australia.
The National Diabetes Services How to register
Scheme (NDSS) commenced in 1987, Registration is free and is as simple as
as an initiative of the Australian completing the NDSS registration form:
Government administered by » Fill in the NDSS registration form.
Diabetes Australia. » Ensure the form is signed by a medical
practitioner or credentialled diabetes
Why register? educator.
When you register your patients with
» Submit the completed registration
diabetes on the NDSS, they will have life-long
form to the NDSS via:
access to diabetes education and support.
- email ndss@diabetesaustralia.com.au
Subject to meeting NDSS eligibility criteria,
they will also have access to subsidised - fax 1300 536 953 or
products to help them manage their diabetes. - an NDSS Access Point.
On registration, your patient will receive There is a national network of NDSS

a ‘starter’ information pack, and a few community pharmacy Access Points.
months later they will receive a follow up To find the nearest Access Point phone
phone call about their self-management 1300 136 588 or visit osd.ndss.com.au
of their diabetes. You can order multiple copies of the
Your patients will also be able to access registration form by phoning your local
a range of free diabetes information and NDSS Agent on 1300 136 588 or you can
support services. Encourage your patients download it from the NDSS website
to contact their local NDSS Agent on the www.ndss.com.au
NDSS Helpline 1300 136 588 to find out
about the services they can take advantage National Gestational Diabetes Register
of to improve their knowledge and All women diagnosed with gestational
management of diabetes. diabetes and registered with the NDSS
are also registered on the NDSS National
Subject to eligibility, they will also be
Gestational Diabetes Register.
able to access:
» subsidised blood glucose and urine How registration will help your patients
testing strips with gestational diabetes
» free needles and syringes for people Your patients will receive:
with diabetes who require insulin or » regular reminders to have follow up
an approved non-insulin injectable diabetes screening after the birth
medication
» valuable information on how to
» subsidised insulin pump consumables maintain a healthy lifestyle and minimise
for people with type 1 diabetes and the risk of developing type 2 diabetes
gestational diabetes. in the future.
For a full list of products and prices, Your patients with gestational diabetes
download the order form at will receive these benefits when you
www.ndss.com.au register them with the NDSS.
Who can register? For more information

All Australians who hold a Medicare card Refer your patients to their local
and have been diagnosed with diabetes can NDSS Agent
receive the benefits of NDSS registration. P: 1300 136 588 W: www.ndss.com.au
npss diabetes 1300 136 588
d custralio ndss.com.au
The National Diabetes Services Scheme is an initiative of the Australian Government
administered with the assistance of Diabetes Australia.
Type 2 diabetes: Goals for optimum management
Encourage all people with type 2 diabetes to approach/reach these goals

Diet Advise eating according to Australian dietary guidelines, with attention to
quantity and type of food
If concerns are held regarding cardiovascular disease risk, advise individual
dietary review
Body mass index (BMI) Therapeutic goal is 5-10% weight loss for people who are overweight or
obese with type 2 diabetes
Those with BMI >35 kg/m2and comorbidities, or BMI >40 kg/m2, greater
weight loss measures should be considered
Note that BMI is a difficult parameter to standardise between different
population groups
Physical activity At least 30 minutes of moderate physical activity on most if not all days
of the week (total >150 minutes/week)
Cigarette consumption 0 per day
Alcohol consumption Advise <2 standard drinks (20 g) per day for men and women
Blood glucose level (BGL) Advise 6-8 mmol/L fasting and 8-10 mmol/L postprandial
Ongoing self-monitoring of blood glucose is recommended for people
with diabetes using insulin, people using sulphonylureas or other medicines
that may cause hypoglycaemia, hyperglycaemia arising from illness, with
haemoglobinopathies, pregnancy or other conditions where data on
glycaemic patterns is required
Routine self-monitoring of blood glucose in low-risk patients who are
using oral glucose-lowering drugs (with the exception of sulphonylureas)
is not recommended
Glycated haemoglobin (HbA1c) Needs individualisation according to patient circumstances. Generally:
• <53 mmol/mol (48-58 mmol/mol)
• <7% (6.5-7.5%)
Allowing for normal variation in test accuracy, HbA1c results that range
between 6.5% and 7.5% (48 and 58 mmol/mol) would reflect this goal.
Total cholesterol <4.0 mmol/L Initiation of pharmacotherapy is dependent on the assessment of absolute
cardiovascular disease (CVD) risk (refer to the Australian absolute CVD risk
High-density lipoprotein
calculator at www.cvdcheck.org.au). This requires using multiple risk factors,
cholesterol (HDL-C) >1.0 mmol/L
which is considered more accurate than the use of individual parameters
Low-density lipoprotein Once therapy is initiated, the specified targets apply; however, these targets
cholesterol (LDL-C) <2.0 mmol/L should be used as a guide to treatment and not as a mandatory target
Non-HDL-C <2.5 mmol/L
Triglycerides <2.0 mmol/L
Blood pressure (BP) Lower BP targets may be considered for younger people and for secondary
<140/90 mmHg prevention in those at high risk of stroke, as long as treatment burden does
not increase risk
The target BP for people with diabetes and albuminuria/proteinuria remains
<130/80 mmHg. As always, treatment targets should be individualised and
monitored for side effects from medications used to lower BP
Urine albumin excretion Urine albumin-to-creatinine ratio (UACR):
• women: <3.5 mg/mmol
• men: <2.5 mg/mmol.
Timed overnight collection: <20 mcg/min
Spot collection: <20 mg/L
Vaccination Consider immunisation against influenza and pneumococcal disease,

and the diphtheria-tetanus-acellular pertussis (dTpa) vaccine
Supporting the education programs of Diabetes Australia
AstraZeneca SANOFI CARDIWASCUIAR „5

B" RACGP
Genomics in general practice
racgp.org.au Healthy Profession.

Healthy Australia.
Genomics in general practice
Disclaimer
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 Ltd (RACGP) and its employees and
agents shall have no liability (including without limitation liability by reason of negligence) to any users of the
The Royal Australian College of General Practitioners. Genomics in general practice. East Melbourne, Vic:
RACGP, 2020.
The Royal Australian College of General Practitioners Ltd

East Melbourne, Victoria 3002
Tel 03 8699 0414

Fax 03 8699 0400
www.racgp.org.au
ABN: 34 000 223 807

ISBN: 978-0-86906-488-7
Published April 2018; updated November 2018, June 2019 (minor), September 2020 (minor)
© The Royal Australian College of General Practitioners 2020
This resource is provided under licence by the RACGP. Full terms are available at www.racgp.org.au/
usage/licence. In summary, you must not edit or adapt it or use it for any commercial purposes. You must
acknowledge the RACGP as the owner.
We acknowledge the Traditional Custodians of the lands and seas on which we work and live, and pay our
respects to Elders, past, present and future.
19775.22
RACGP Genomics in general practice
Acknowledgements
The Royal Australian College of General Practitioners (RACGP) gratefully acknowledges the contributions of the members of
the Advisory Group and the writer for their roles in developing the content for this resource.
The RACGP is also grateful to the many reviewers and representatives who reviewed and provided scholarly feedback on
draft material.
In 2015, the RACGP inherited the 2007 publication Genetics in family medicine: The Australian handbook for general
practitioners, which was produced under the auspices of the now defunct agency, Biotechnology Australia, with support
from the National Health and Medical Research Council (NHMRC). The RACGP is grateful to the authors of the original 2007
resource and its contributors for their work, which formed the foundation of Genomics in general practice.
Advisory Group
Professor Jon Emery, Co-Chair, Genomics in general practice Advisory Group; Herman Professor of Primary Care Cancer
Research, The University of Melbourne and Victorian Comprehensive Cancer Centre
Professor Sylvia Metcalfe, Co-Chair, Genomics in general practice Advisory Group; Group Leader, Genetics Education and
Health Research, Murdoch Children’s Research Institute; Professor in Medical Genetics, Department of Paediatrics, The
University of Melbourne
Associate Professor Grant Blashki, Nossal Institute for Global Health, The University of Melbourne
Professor John Christodoulou, Theme Director, Genetics Research; Head, Neurodevelopmental Genomics Research Group;
Chair, Genomic Medicine, Department of Paediatrics, Murdoch Childrens Research Institute
Ms Kate Dunlop, Director, The Centre for Genetics Education, NSW Health
Dr Simon Morgan, General Practitioner, Elermore Vale General Practice, New South Wales
Writer
Ms Taryn Charles, Senior Project Officer, Murdoch Children’s Research Institute
Conflicts of interest
This publication has been produced in accordance with the rules and processes outlined in the RACGP’s Conflict of interest
policy (www.racgp.org.au/support/policies/organisational).
Contents
Acknowledgements ii
Background 1
Aim of the resource 1
Development process 1
A note on the title of the resource 1
Format 2
Scope 2
Ethical principles 3
Genetic counselling 4
Genetics support groups and organisations 5
Health and life insurance issues 6
Misconceptions about genetics 7
Summary of genetic tests 8
Glossary 9
Acronyms 14
Alzheimer’s disease 15
Autism spectrum disorder 17
Cystic fibrosis 19
Developmental delay and intellectual disability 21
Diabetes 23
Fragile X syndrome and associated conditions 25
Familial breast and ovarian cancer 27
Familial colorectal cancer 30
Familial hypercholesterolaemia 32
Familial melanoma 34
Familial prostate cancer 36
Haemoglobinopathies 38
Hereditary haemochromatosis 41
Hereditary thrombophilia 43
Mental health conditions 45
Neurofibromatosis type 1 47
Neurological conditions 49
Sudden arrhythmic death syndrome 51
Chromosome microarray 53
Family history 55
MTHFR gene testing 58
Newborn screening 60
Personal genomic testing: Summary 62
Personal genomic testing: More information 64
Pharmacogenomics: Summary 67
Pharmacogenomics: More information 69
Prenatal testing 72
Reproductive carrier screening 76
1
Background
In 2015, The Royal Australian College of General Practitioners (RACGP) took ownership of Genetics in family medicine:
The Australian handbook for general practitioners, a 2007 resource produced by the now defunct Biotechnology Australia,
with support from the National Health and Medical Research Council (NHMRC). Developed in collaboration with a broad
range of national stakeholders, Genetics in family medicine: The Australian handbook for general practitioners provided
comprehensive and authoritative advice on a range of issues in genetic medicine for general practitioners (GPs) at a time of
burgeoning interest in this field.
In the 10 years since it was published, the field of genetics and genomics has developed rapidly. Advances in genetics
and genomics offer great potential for identifying patients at risk of disease and targeting treatment. GPs need up-to-date
knowledge and skills in this domain.
To determine how best to update the 2007 resource, ensuring the material remains relevant to general practice, the
RACGP convened a panel of experts (the Advisory Group), which comprised representatives from the original development
consortium and new members. The result is Genomics in general practice, a suite of concise summaries on various clinical
topics in genetics and genomics.
Aim of the resource

Genomics in general practice is intended to be used as a point-of-care reference for GPs. It is designed to assist in clinical
decision-making by presenting a snapshot view of the identification and diagnosis of a range of genetic conditions, and the use
of genetic testing and technologies encountered in general practice. It is hoped Genomics in general practice will assist GPs to
provide information on genetics and genomics to patients and their families, and refer to specialist services as required.
Development process
Genomics in general practice was developed in accordance with RACGP procedures.
Members of the Advisory Group reviewed Genetics in family medicine: The Australian handbook for general practitioners to
determine the scope and purpose of the new publication.
A literature search was conducted for each topic, and relevant research papers and grey literature were identified.
Successive drafts of the resource were produced by the writer under the direction of the Advisory Group. Subject matter
experts were consulted during this content-development phase. Where contention existed within the literature or among
subject matter experts, the Advisory Group determined how to address this within the resource by consensus.
A broad range of GP and non-GP stakeholders were invited to review and provide feedback on a draft. Comments were
considered by the Advisory Group and amendments made prior to publication.
A note on the title of the resource

The terms ‘genetic’ and ‘genomic’ are sometimes used interchangeably. The term genetic refers to the study of single genes,
whereas genomic refers to the study of multiple genes. Traditional genetic testing involves the examination of individual
genes that are known to cause or increase risk for a particular disease. The new field of genomic testing allows for the
testing of a number of different genes at once, even a person’s entire genetic makeup (genome). As such, genomic testing
can provide a wealth of information about a patient’s health, including predisposition to common conditions and response to
particular drugs. The title for this resource, Genomics in general practice, reflects the possibilities inherent to genomic testing
for the practice of medicine.
Format
Genomics in general practice consists of short, practical summaries with key information that a GP might need to manage
common genetic conditions and issues of testing in primary care.
For two of the topics where there have been significant developments in the past 10 years, ‘Pharmacogenomics’ and
‘Personal genomic testing’, more detailed information is presented alongside the summary.
This resource is intended as a ‘guide’ rather than a ‘guideline’ with weighted recommendations for clinical decision-making.
Where appropriate clinical guidelines exist (ie they are recent and applicable to an Australian general practice context), they
have been referenced in the text.
The most important information for GPs is listed at the beginning of each chapter under the heading ‘Practice point’.
The issues considered in each chapter vary, but many include discussion of relevant tests and when GPs should refer to
another health professional or genetics services. Where relevant, useful websites and other resources to access for further
information for GPs and patients are listed at the end of the chapter.
Scope
Genomics in general practice is primarily intended for use by GPs and other primary care staff. Although it has not been
designed for use by patients and consumers, this resource does contain some information for that audience.
The resource does not include a discussion of very rare genetic conditions that are unlikely to be encountered in general
practice, or give comprehensive information about genetics services or use of the Medicare Benefits Schedule for billing
purposes.
Genomics in general practice 3
Ethical principles
The ethical principles that guide all medical care apply in genomics. However, ethical dilemmas arise when there is tension or
conflict between the rights of different family members. Key ethical principles include:1
• Justice - Patients should be treated equally, and there should be equity of access to services regardless of place of
residence, ethnicity, gender, religion, age or disability.
• Respect for autonomy - The right of an individual to self-determination, including privacy and confidentiality.
• Beneficence - Taking positive action to do good.
• Non-maleficence - Do no harm.
There may be tension when these principles are considered with respect to the right of an individual to:
• know, or not to know, information relevant to their own health (autonomy)
• disclose, or not to disclose, personal information (privacy)
• make an informed decision regarding genetic testing.
Genetic counselling emphasises that an autonomous choice be made; that is, a choice that is informed and reflective of the
individual’s own values, and made freely (without coercion). However, ethical dilemmas may arise. For example:
• as a result of genetic testing, an individual’s result may disclose the genetic status of another family member (eg a
monozygotic [identical] twin)2 who has not had testing (and may not wish to)
• an individual refuses to disclose to other family members that they are at risk of particular diseases3
• parents request that their child (<18 years of age) be tested for an adult-onset condition where there is no health benefit
for the child, thus affecting the child’s future autonomy.4
In any of these situations, it is important to explore with the patient the potential harms and benefits, and the reasons for their
request. Referral to genetic services for counselling is strongly recommended.
References
1. Beauchamp TL. The ‘four principles’ approach to health care ethics. In: Ashcroft RE, Dawson A, Draper H, McMillan JR,
editors. Principles of health care ethics. 2nd edn. Chichester, UK: John Wiley & Sons, 2007.
2. Andorno R. The right not to know: An autonomy based approach. J Med Ethics 2004;30(5):435-39.
3. Weaver M. The double helix: Applying an ethic of care to the duty to warn genetic relatives of genetic information.
Bioethics 2016;30(3):181-87.
4. Human Genetics Society of Australasia. Policy: Pre-symptomatic and predictive testing for children and young adults.
Sydney: HGSA, 2014. Available at www.hgsa.org.au/documents/item/272 [Accessed 13 December 2017].
Resources for general practitioners

• Centre for Genetics Education, Fact sheet 19: Ethical issues in human genetics and genomics, www.genetics.edu.au/
publications-and-resources/facts-sheets/fact-sheet-19-ethical-issues-in-human-genetics-and-genomics/view
• Financial Services Council, FSC Standard no. 16: Family medical history policy, www.fsc.org.au/resources/standards/16s-
family-history.pdf
• National Health and Medical Research Council, Genetic discrimination, www.nhmrc.gov.au/_files_nhmrc/publications/
attachments/g001_genetic_discrimination_150622.pdf
Genetic counselling
Genetic counselling is a communication process that aims to provide information and supportive counselling to members of
families regarding problems in growth, development and health that may have a genetic basis.
Patients can be referred to genetic counsellors available at genetics services in each state or territory.
The process of professional genetic counselling involves assisting patients to:
• comprehend the medical facts regarding a genetic condition, including the diagnosis, probable course of condition and
available management
• appreciate the way heredity contributes to the condition and risk of occurrence in relatives
• understand the options for dealing with the risk of recurrence
• choose the course of action that seems appropriate in view of their situation, and risk and values, and act in accordance
with that decision
• make the best possible adjustment to the condition in an affected family member and/or to the risk of recurrence of that
condition.
During a genetic counselling consultation, the counsellor may discuss the following issues with the patient:
• Information about the condition
- key clinical features
- genetic contribution to the cause of the condition, including gene(s) involved, inheritance pattern, likelihood that a
person who inherits the genetic susceptibility will develop the condition
- interactions between genes and the interplay between genes and the environment.
• Information about genetic testing
- availability of testing
- advantages and disadvantages for deciding whether to undergo genetic testing
- understanding and using genetic test results.
• Implications for family members
- medical and psychological implications
- implications for future reproductive choices, employment and insurance
- issues concerning the privacy and confidentiality of genetic information.
Resource for patients

• New South Wales’s Centre for Genetics Education maintains a list of genetics services, www.genetics.edu.au/genetic-services
Genetics support groups and organisations

In addition to support from general practitioners, genetic services and professional counselling, patient referral to support
groups or organisations can be beneficial and, in some cases, necessary for the wellbeing of the patient and/or their family.
Support groups and organisations can be an important source of peer support and empowerment, and provide practical
information and advice about living with a genetic condition. Families can benefit from contact with other people in similar
situations, regardless of their level of coping or need for support.
Support groups and organisations can have state-based or territory-based, national or international memberships, allowing
families to appreciate that they are not alone in the challenges they may face living with a particular genetic condition.

• New South Wales’s Centre for Genetics Education maintains a list of genetics services, www.genetics.edu.au/genetic-
services
Health and life insurance issues
General practitioners (GPs) are well placed to advise patients to consider the implications around health and life insurance for
themselves and their families before embarking on genetic testing.
Private health insurance is community-rated (ie based on population risk), and does not take into account genetic
information, but will take into account any existing condition.
However, individuals applying for a new life insurance policy (eg cover for death, disability, income protection) are required by
law to disclose ‘every matter known to the applicant, or could reasonably be expected to be known, that is relevant to the
insurer’s decision’.1 This includes the results of any genetic tests.
While some insurance companies will ask for more specific details than others, applicants must disclose all known genetic
information about themselves that would be relevant to the assessment of their risk, over and above the questions asked.
This includes information about any health condition(s) that were diagnosed in first-degree relatives (ie parents, children,
brothers, sisters) and the age at which they were diagnosed. It does not include any other information, including their genetic
test result(s), if known to you, their name or date of birth.
This information may have a range of consequences, depending on the condition involved and whether the genetic test was
positive, uninformative or negative.
If an application for health and/or life insurance is held or taken out before a genetic condition is diagnosed, or before a risk
is identified through a predictive genetic test, the applicant does not have to disclose this new information. Life insurance
cover is guaranteed renewable and, so as long as the premiums are paid, that cover will apply.
The Financial Services Council has announced the implementation of a moratorium on the disclosure of genetic test results
in life insurance product applications at a level below $500,000 for death and total and permanent disability, $200,000 for
trauma, and $4000 a month for income protection. This is to commence in July 2019.
References
1. Commonwealth of Australia. Insurance Contracts Act 1984. Canberra: Commonwealth of Australia, 1984; Section 21.
Available at www.austlii.edu.au/au/legis/cth/consol_act/ica1984220/s21.html [Accessed 13 December 2017].

• Centre for Genetics Education, Fact sheet 20: Life insurance products and genetic testing in Australia, www.genetics.edu.
au/publications-and-resources/facts-sheets/fact-sheet-20-life-insurance-products-and-genetic-testing-in-australia/view
• National Health and Medical Research Council, Genetic discrimination, www.nhmrc.gov.au/_files_nhmrc/publications/
attachments/g001_genetic_discrimination_150622.pdf
Misconceptions about genetics
General practitioners (GPs) can use the information below to address common misconceptions about genetic issues during
discussion with patients.
Information for patients

Misconception Fact
If your father has a genetic condition, but you look more like An individual’s physical similarity to other relatives (or lack thereof)
your mother, you will not develop it does not affect their risk of developing a condition
You can only inherit a ‘female’ cancer like breast or ovarian Gene variants in BRCA1 and BRCA2 can be passed through the
cancer from your mother’s side paternal line (a person’s father and his relatives) and maternal line
(a person’s mother and her relatives)
If you have the gene for a particular disease, you will The presence of a pathogenetic variant does not always mean an
eventually get the disease individual will develop the condition. If the gene variant shows
variable penetrance (ie penetrance less than 100%), the risk of
disease can be uncertain
A ‘one-in-four’ chance of having a child with the variant A ‘one-in-four’ chance of having a child with the variant applies to
means that after you have one affected child, the next three each pregnancy (for autosomal recessive conditions)
children will be unaffected
Female carriers of X-linked conditions are never affected This is not always the case and is influenced by X-inactivation.
Carriers may have a mild phenotype and are manifesting
heterozygotes. For example, female carriers of Duchenne muscular
dystrophy may show mild symptoms of a cardiomyopathy; female
carriers of haemophilia may have a bleeding diathesis
If you have no family history of a genetic condition, you are There may be no family history for a variety of reasons. For example,
not at risk of developing one and neither are your children reduced or incomplete penetrance, recessive conditions, small family
size, and new mutations (eg de novo, sporadic)
Genetic conditions can ‘skip’ a generation In the case of autosomal recessive and X-linked conditions, affected
family members may be scattered across a generation, giving the
appearance of skipping generations
Summary of genetic tests
The following table provides information about genetic tests that may be encountered in general practice and the tests’ indications.
Genetic test Indications
G-banded (conventional microscopic) karyotype - Chromosomes Suspected chromosome rearrangement; investigate

are stained to reveal patterns of alternating light and dark bands multiple miscarriages
Fluorescent in situ hybridisation (FISH) - Using fluorescent Determine physical arrangement of chromosomal conditions or
dyes or tags specific to a chromosome, FISH can visualise correct number of chromosomes (eg rapid method of aneuploidy
chromosomes to identify abnormalities screening in prenatal setting)
Chromosomal microarray (CMA) or molecular karyotype (eg Unexplained intellectual disability or developmental delay;
single nucleotide polymorphism [SNP] microarray) - CMA uses a prenatal investigation of abnormality on ultrasound
microchip-based platform to perform a genome-wide assay that
looks for sub-microscopic copy number variants (CNVs). These
variants are extra (duplications) or missing (deletions) segments
of deoxyribonucleic acid (DNA). Many CNVs are common and
benign, while some are pathogenic
Sanger sequencing - The exact order of base pairs A, G, T Suspect condition with a known single-gene cause
and C in an individual‘s genetic makeup is known as the DNA (eg cystic fibrosis, thalassaemia)
sequence. Sanger sequencing is old, low through-put, but
reliable technology, and sequences just one gene at a time
Next generation sequencing (NGS) or massively parallel Genome sequencing: A comprehensive approach that
sequencing - NGS sequences millions of small DNA fragments, captures the entire genome
which are then mapped to a reference genome. NGS can Exome sequencing: A more cost-effective approach to
sequence the entire genome, just the exome (coding genes) capture and analyse all known disease-causing genes
or a panel of selected genes (eg rare childhood syndromes)
Panel sequencing: A more targeted approach focusing on a
large number of key genes related to a clinical indication
(eg cancer, cardiac conditions)
SNP genotyping or genomic profiling or scan - Testing that Determine ability to metabolise certain drugs (eg CYP2D6, codeine),
analyses single nucleotide variations in the genome paternity testing, personal genomic testing (direct to consumer)
Polymerase chain reaction (PCR) - A method for amplifying DNA Disorders caused by triplet repeat expansions (eg Fragile X
(ie making millions of copies of a particular sequence of DNA) syndrome, Huntington’s disease)
Multiplex ligation-dependent probe amplification (MLPA) - A PCR Suspect disorder caused by large deletions or duplications of
method of detecting copy number variants and SNPs specific genes (eg Duchenne muscular dystrophy)
DNA methylation studies of specific chromosome region Suspect disorder caused by abnormal gene methylation which
affects gene expression (eg Beckwith-Wiedemann syndrome)
Maternal serum screening

Combined first trimester screening - Biochemical screening First trimester: Screening at 11-13 weeks to estimate risk for
of maternal blood combined with ultrasound trisomy 21, trisomy 18, trisomy 13
Second trimester serum screening - Biochemical screening Second trimester: screening at 14-20 weeks to estimate risk for
of maternal blood trisomy 21, trisomy 18 and neural tube defects
Non-invasive prenatal testing (NIPT) - Analysis of cell-free fetal Pregnancy screening from 10 weeks to detect evidence of trisomy
DNA (cfDNA) in maternal plasma 21, 18 or 13 in fetus with higher sensitivity and specificity than
maternal serum screening
Adapted from Donoghue S, Downie L, Stutterd C. Advances in genomic testing. Aust Fam Physician 2017;46(4):200-05. Available at
www.racgp.org.au/afp/2017/april/advances-in-genomic-testing [Accessed 27 July 2017].
Glossary
Anticipation
Anticipation describes a situation where a genetic condition appears at an earlier age with successive generations. The
severity of the condition can also increase. This phenomenon is often seen in conditions caused by trinucleotide repeats,
such as Huntington’s disease, myotonic dystrophy and Fragile X syndrome. In these cases, the size of the trinucleotide
repeat increases when it is passed from parent to child, which can result in earlier onset and more severe disease.
For more information, refer to the Genetics Home Reference’s explanation ‘What do geneticists mean by anticipation?’
(https://ghr.nlm.nih.gov/primer/inheritance/anticipation) and ‘What are the different ways in which a genetic condition can be
inherited?’ (https://ghr.nlm.nih.gov/primer/inheritance/inheritancepatterns).
Autosomal dominant inheritance

When a condition follows an autosomal dominant pattern of inheritance, the family tree will usually reveal multiple affected
members on the same side of the family. Dominant conditions or traits are expressed when only a single gene variant is
inherited. They are usually inherited on one side of the family and can be seen in multiple generations.
Wide variability in clinical expression is common in many autosomal dominant conditions, even within the same family.
Early onset of conditions, such as cancer, can be indicative of autosomal dominant inheritance within a family.
Not all dominant conditions show 100% penetrance (eg BRCA1 gene mutations).
Autosomal recessive inheritance

Autosomal recessive conditions affect either sex, and often occur in the absence of any family history. Recessive conditions
or traits appear when an individual inherits two copies of the same gene variant (one from each parent).
Parents of a child with an autosomal recessive condition are usually asymptomatic carriers. The affected child will carry two
copies of the particular gene change.
The recurrence risk of autosomal recessive conditions is one in four for each pregnancy.
Wide variability in clinical expression is common in many autosomal recessive conditions, even within the same family.
Consanguinity is noted to occur more often among the parents of individuals with rare autosomal recessive conditions.
Balanced translocation
A balanced translocation is a rearrangement of the chromosome with no apparent loss or gain of chromosomal material.
Individuals with balanced translocations are not usually affected.
Carrier
Recessive genetic conditions such as cystic fibrosis (CF) occur when a person inherits a particular genetic variant from each
parent. A carrier is an individual who only has one copy of the gene variant and generally does not have symptoms, but can
pass the variant to their children.
Some conditions are linked to the X chromosome (X-linked recessive inheritance). Typically, these conditions affect more
males (who have the sex chromosomes XY) than females (who have the sex chromosomes XX). A woman who is a carrier of
an X-linked condition has the variation on one of her X chromosomes, which she can pass on to her children. However, if the
biological male partner is a carrier, he will not pass it to his sons, but will pass it to his daughters.
Carrier screening
Carrier screening is a test to determine whether an individual carries a genetic variant or chromosomal alteration that does not
generally affect that individual’s health, but increases his or her chance of having children with the condition in question. The
outcome of such testing can influence future reproductive decisions. Carrier screening is performed on individuals who are not
necessarily known to be at increased risk for a particular genetic condition. Screening tests can be conducted on individuals,
groups such as those from a common ethnic background and entire populations (eg newborn screening).
Cascade screening
Cascade screening involves testing the close biological relatives of an individual who has a genetic condition in order to
determine whether these relatives carry the genetic variant or chromosomal alternation (thereby increasing their chances of
developing the condition or having a child with the condition).
Compound heterozygote, compound heterozygous and compound

heterozygosity
A compound heterozygote is an individual with two different pathogenic alleles at a particular location in a pair of
chromosomes. For example, in hereditary haemochromatosis, compound heterozygotes have both a C282Y and an H63D
variant, and are less likely to develop iron overload than C282Y homozygotes. However, the impact will be assessed on a
case-by-case situation as it depends on the variant (allele) and its pathogenicity. Additionally, as one allele will have come
from the mother and the other from the father, there might be implications in terms of cascade testing within the family.
Consanguinity
Consanguinity describes a relationship between two people who are related to each other because of a common ancestor.
Consanguineous relationships occur in all population groups, but may occur more frequently in certain cultures. The most
common form of consanguineous relationships is between first cousins.
Individuals who are blood relatives share a greater proportion of their genes than unrelated people, thus, these individuals
potentially share pathogenic variants for recessive conditions. When individuals are first cousins and there is no family history
of a specific condition, or of other consanguineous relationships in previous generations, the risk of them having a child
with a genetic condition is approximately 5-6%, compared with 3-4% in the general population. This risk will increase in
communities where there is a multi-generational tradition of first-cousin marriages, rendering couples closer in genetic
relationship.
De novo
A de novo variant is a new genetic variation that arises in the fetal stage of development (ie was not present in either parent).
Exome
The exome is the part of the genome that contains protein-coding genes only. The exome represents less than 2% of the
genome, but contains about 85% of known disease-causing gene variants.
Gene variants
Gene variants are small deoxyribonucleic acid (DNA) sequence changes (ie additions, duplications, deletions, substitutions).
These variants can have a range of effects: some may cause disease (pathogenic variant), while others do not cause disease
but may modify an individual’s risk of disease (eg increase risk, provide a protective effect).
Genome
The genome is the entire set of genetic material, including all coding and non-coding genes.
11
Genotyping, genomic profiling and genomic scan

Genotyping (also known as genomic profiling or genomic scanning) is a test to determine an individual’s single nucleotide
polymorphism (SNP) profile. A SNP profile may be used to predict disease susceptibility, tailor treatment and provide non
health related information (eg paternity, ancestry).
Heterozygote, heterozygous and heterozygosity

Heterozygosity refers to the presence of two different alleles (form of a gene variant) at a given location on a pair of
chromosomes (eg carrier for a pathogenic gene variant).
Homozygous, homozygous and homozygosity

Homozygosity refers to the presence of two identical alleles (form of a gene variant) at a given location on a pair of
chromosomes.
Incomplete penetrance
Refer to ‘Penetrant and penetrance’.
Multifactorial inheritance and complex inheritance

Multifactorial inheritance, also called complex inheritance, can be attributed to a combination of genetic (ie single gene,
multiple genes), environmental and lifestyle factors.
The number of necessary factors, and the impact those factors have on the presence or severity of a condition, will vary for
different conditions and individuals.
Often, when there are multiple susceptibility genes involved, there is an additive effect on the outcome.
Early onset of conditions, such as cancer, cardiovascular disease or type 2 diabetes, may be indicative of multifactorial
inheritance within a family.
This type of inheritance does not follow a characteristic pedigree pattern, but may look like autosomal dominant inheritance
with incomplete penetrance.
Pathogenic variant and gene mutation

A pathogenic variant is a genetic variant that increases an individual’s susceptibility or predisposition to certain diseases.
Pathogenic variants are also known as mutations. Some are responsible for normal human variation, and these are known as
polymorphisms (eg height).
There are variations that affect the way we metabolise drugs. For some variants, their effects are unknown or uncertain, while
others have no effect.
Penetrant and penetrance

Penetrance refers to the proportion of people with a particular genetic variant who will go on to develop the condition.
It describes the extent to which disease or characteristics controlled by the gene, or variation within the gene, will be
expressed. For example, people carrying an autosomal dominant variant may not always develop the condition - this
is called ‘incomplete penetrance’. If a condition is 100% penetrant, an individual will definitely develop the condition. If
penetrance is 80%, most but not all individuals will develop the condition. Other genes and lifestyle factors, such as diet,
exercise and smoker status, may affect the onset of some conditions.
For more information, refer to Genetics Home Reference’s ‘What are reduced penetrance and variable expressivity?’
(https://ghr.nlm.nih.gov/primer/inheritance/penetranceexpressivity).
Predictive testing
Predictive testing aims to determine whether a person who has no signs or symptoms of a specific condition at the time
of testing has specific genetic variations that increase the likelihood they will later develop the condition. Predictive testing
is often performed in relation to genetic conditions that are not evident at birth, but have their onset during adulthood,
such as some cancers. Predictive genetic testing in conditions such as familial cancer can only be conducted when the
family-specific genetic variant is known. Hence, genetic testing must first be done on a family member affected with the
specific condition, as they are the most likely to carry the genetic variant.
Pre-implantation genetic diagnosis

Pre-implantation genetic diagnosis (PGD) is cytogenetic testing, with or without molecular testing, performed on embryos
used in assisted reproductive technology procedures. Prenatal testing of successful pregnancies may be recommended for
confirmation of the test result.
Pre-symptomatic testing
Pre-symptomatic testing aims to determine whether a person will develop a particular genetic condition (eg Huntington’s
disease) at some point in the future when symptoms of the condition have not yet manifested.
Sensitivity
Sensitivity is the true positive rate for a test. For example, if the person has the condition, how often will the test give a
positive result?
Single nucleotide polymorphism

A nucleotide is a single base pair unit of deoxyribonucleic acid (DNA). A single nucleotide polymorphism (SNP or ‘snip’) is a
polymorphism in a single nucleotide occurring at a particular site in the genome. For example, one individual may have a ‘G’
at a particular location and another individual a ‘T’. If two or more alternative DNA variants occur at a particular location at
a population frequency of >1%, it is defined as a SNP. SNPs are the most common type of genetic variation in the human
genome and account for approximately 0.02% of the genome.
Specificity
Specificity is the true negative rate for a test. For example, if the person does not have the condition, how often will the test
give a negative result?
Variable expressivity
Variable expressivity refers to the range of signs and symptoms that an individual with a particular genetic condition will
display.
Variable expressivity is a factor that influences the effect of particular genetic variants. While some genetic variants are
consistent in terms of the effect they have on a disease or characteristic, other have a more variable effect. For example,
Lynch syndrome (hereditary non-polyposis colorectal cancer [HNPCC]) shows variable expressivity. An individual’s
presentation of this disease is modified by their genetic, lifestyle and environment factors.
Variable expressivity is not the same as reduced penetrance.

For more information, refer to the Genetics Home Reference’s ‘What are reduced penetrance and variable expressivity?’
(https://ghr.nlm.nih.gov/primer/inheritance/penetranceexpressivity).
13
X-inactivation
Inactivation of most genes on the X chromosome in female somatic cells ensures that males and females have the same
number of X chromosome genes instructing the body to perform particular functions.
This is usually a random process; thus, females will have a mixture of cells with respect to the inactivated X chromosomes
being of maternal or paternal origin.
The usual random process of X-inactivation means that female carriers of the mutation will not usually show any signs of the
condition as there are enough cells with the correct copy of the gene to instruct the body to perform particular functions.
Rarely, some female carriers may be mildly symptomatic because of unequal or skewed inactivation of the X chromosomes.
X-linked recessive inheritance

Since a male inherits only one X chromosome (from his mother), in a family affected by a condition that follows a pattern
of X-linked recessive inheritance, there will be more affected males than affected females. Males are usually more severely
affected than females because of X-inactivation.
Since a male only passes his Y chromosome to his sons, there is no male-to-male transmission of X-linked conditions.
With each pregnancy, females who are carriers for a gene variant involved have a one-in-two chance of passing on the
variant. Sons who inherit the variant will be affected and daughters who inherit the variation will be carriers like their mothers.
Daughters of affected males can only inherit the variation from their father and are known as ‘obligate carriers’.
Acronyms
AD Alzheimer’s disease MCH mean corpuscular haemoglobin
AGHDR Australian Genetic Heart Disease Registry MCV mean corpuscular volume
ASD autism spectrum disorder MLPA multiplex ligation-dependent probe amplification
CA 125 cancer antigen 125 MODY maturity onset diabetes of the young
CBAVD congenital bilateral absence of the vas deferens NF1 neurofibromatosis type 1
CF cystic fibrosis NGS next generation sequencing
cfDNA cell-free fetal DNA NHMRC National Health and Medical Research Council
CFTS combined first trimester screening NIPS non-invasive prenatal screening
CMA chromosomal microarray NIPT non-invasive prenatal testing
CNV copy number variant NT nuchal translucency
COC combined oral contraceptive PAPP-A pregnancy-associated plasma protein A
CPTI carnitine palmitoyl transferase deficiency types I PCR polymerase chain reaction
and II PGD pre-implantation genetic diagnosis
CPVT catecholaminergic polymorphic ventricular PGT personal genomic testing
tachycardia
PKU phenylketonuria
CRC colorectal cancer
PPV positive predictive value
PSA prostate-specific antigen
CVS chorionic villus sampling
QF-PCR quantitative fluorescence polymerase chain
CYP cytochrome P450 enzyme reaction
DD developmental delay RACGP The Royal Australian College of General
DLCNC Dutch Lipid Clinic Network Criteria Practitioners
DNA deoxyribonucleic acid SADS sudden arrhythmic death syndrome
DTC direct-to-consumer SCAD short chain acyl-CoA dehydrogenase deficiency
FAP familial adenomatous polyposis SCHAD short chain hydroxy acyl-CoA dehydrogenase
FBE full blood examination deficiency
FH familial hypercholesterolaemia SNP single nucleotide polymorphism

FISH fluorescent in situ hybridisation B-hCG human chorionic gonadotrophin
FOBT faecal occult blood test SSRI selective serotonin reuptake inhibitor
FRA-BOC familial risk assessment - breast and ovarian TFP trifunctional protein deficiency
cancer VLCAD very long chain acyl-CoA dehydrogenase
FSH follicle-stimulating hormone deficiency
FXPOI Fragile X-associated primary ovarian insufficiency VOUS variant(s) of unknown significance
FXS Fragile X syndrome VTE venous thromboembolism

FXTAS Fragile X-associated tremor/ataxia syndrome
HbE haemoglobin E
HHC hereditary haemochromatosis
HNPCC hereditary non-polyposis colorectal cancer
ID intellectual disability
IVF in-vitro fertilisation
LCHAD 3-hydroxy long chain acyl-CoA dehydrogenase
deficiency
LDL-C low-density lipoprotein cholesterol
MADD multiple acyl-CoA dehydrogenase deficiency
MCAD medium chain acyl-CoA dehydrogenase deficiency
15
Alzheimer’s disease
@ Practice point-----------------------------------------------------------------------------------
Currently, genetic testing of APOE gene variants is considered to have limited clinical utility for diagnostic purposes,
and is not recommended in clinical practice.1,2
Genetic testing is also available for gene variants in three genes APP, PSEN1, PSEN2 that confer a very high risk
for early onset familial Alzheimer’s disease (AD). However, these gene variants are responsible for only a small
percentage of AD cases.2,3
What do I need to know?

The average lifetime risk of developing AD is estimated to be between 10 and 12% (until the age of 75-80 years).3-5 The e4 variant
of the APOE gene is associated with an increased risk of late-onset AD,5,6 but this risk is confounded by other factors. These
factors include those that cannot be modified (eg other genetic variants, gender, family history, possibly ethnicity) and modifiable
risk factors (eg diet, exercise, cardiovascular health, environment). The clinical utility of knowing e4 status is uncertain.35-7
Research suggests that heterozygous carriers of the s4 variant have an approximately threefold increase in risk of developing
AD, while homozygous carriers have an approximately 15-fold increase in risk. Having a first-degree relative with AD doubles
the risk of developing the disease.3,7,8
The s4 variant is neither necessary nor sufficient to cause AD, and risk estimates are problematic given the range of
confounding factors. Therefore, the clinical utility of genetic testing is uncertain.2,3
Genetic testing
While the association of the APO-e4 variant with AD is significant, genetic testing has limited sensitivity and specificity2 The
APO-e4 variant may be included in some commercial test panels (refer to ‘Personal genomic testing: Summary’). Given the
lack of predictive value of APO-e4 for AD, this information may cause unnecessary anxiety for some individuals, especially
given the lack of preventive or therapeutic interventions.3 There may be broader implications for the individual and family
members (ie ethical principles, health and life insurance issues).3
When should I refer?

Genetic testing may be appropriate for families with a history of early onset AD (>2 affected family members; age at onset
<65 years of age), and referral to genetics services is appropriate.2
References
1. Human Genetics Society of Australasia and Choosing Wisely Australia. Tests, treatments and procedures clinicians
and consumers should question. Sydney: NPS MedicineWise, 2016. Available at www.choosingwisely.org.au/
recommendations/hgsa [Accessed 14 December 2017].
2. Bird TD. Alzheimer disease overview. In: Pagon RA, Adam MP, Ardinger HH, et al, editors. GeneReviews. Seattle, WA:
University of Washington, 1998. Available at www.ncbi.nlm.nih.gov/books/NBK1161 [Accessed 14 December 2017].
3. Goldman JS, Hahn SE, Catania JW, et al. Genetic counseling and testing for Alzheimer disease: Joint practice
guidelines of the American College of Medical Genetics and the National Society of Genetic Counselors. Genet Med
2011;13(6):597-605.
4. Cummings JL, Cole G. Alzheimer disease. JAMA 2002;287(18):2335-38.
5. Seshadri S, Drachman DA, Lippa CF. Apolipoprotein E e4 allele and the lifetime risk of Alzheimer’s disease: What
physicians know, and what they should know. Arch Neurol 1995;52(11):1074-49.
6. Ashford JW. APOE genotype effects on Alzheimer’s disease onset and epidemiology. J Mol Neurosci 2004;23(3):157-65.
7. Van Cauwenberghe C, Van Broeckhoven C, Sleegers K. The genetic landscape of Alzheimer disease: Clinical implications
and perspectives. Genet Med 2016;18(5):421.
8. Guerreiro RJ, Gustafson DR, Hardy J. The genetic architecture of Alzheimer’s disease: Beyond APP, PSENs and APOE.
Neurobiol Aging 2012;33(3):437-56.
Resources for patients

Information
• National Library of Medicine (US), Alzheimer disease, https://ghr.nlm.nih.gov/condition/alzheimer-disease
• National Library of Medicine (US), APOE gene: Normal function, https://ghr.nlm.nih.gov/gene/APOE#normalfunction
• National Library of Medicine (US), APOE gene, https://ghr.nlm.nih.gov/gene/APOE
Support
• Alzheimer’s Australia, www.fightdementia.org.au
17
Autism spectrum disorder

© Practice point-----------------------------------------------------------------------------------
Referral to a paediatrician for a clinical genetics evaluation of children with autism spectrum disorder (ASD) can
provide a specific diagnosis in between 30 and 40% of cases.1 General practitioners (GPs) can order a chromosome
microarray (CMA) at the point of referral to a paediatrician in order to speed up this process.

ASD is an umbrella term for a collection of pervasive developmental disorders. This term replaces previously used diagnostic
terminology, including autistic disorder, Asperger syndrome, Rett syndrome, childhood disintegrative disorder and pervasive
developmental disorder - not otherwise specified.2
ASD is characterised by impaired social communication and interaction, limited interests, and repetitive behaviours. Markers of
ASD usually appear during the first two years of life, in particular, problems with language development and social relatedness.3
Some rare genetic conditions show clinical features that are characteristic of ASD. These include:
• tuberous sclerosis (TSC1 or TSC2 genes)
• Fragile X syndrome (FXS; FMR1 gene)
• chromosomal abnormalities (eg inversions, duplications)
• metabolic conditions
• Rett syndrome (MECP2 gene in many cases).
Genetic testing
CMA is now considered a first-line genetic test for the investigation of developmental delay (DD) and intellectual disability
(ID), ASD, and congenital abnormalities (CMA).4 A CMA does not detect gene variants causing FXS
(a single-gene cause of ASD), so an additional deoxyribonucleic acid (DNA) test must be ordered alongside.
While GPs are able to order CMAs, many choose not to, given the complex interpretation of the results. However, ordering
CMA and FXS tests in parallel with referral to a paediatrician can reduce wait times for patients. A Medicare Benefits
Schedule (MBS) rebate is available for CMA in situations where the patient has DD, ID, ASD or at least two congenital
abnormalities. DNA testing for FXS is available with an MBS rebate when the patient:5
• exhibits ID, ataxia, neurodegeneration or premature ovarian failure consistent with an FMR1 mutation
• has a relative with an FMR1 mutation.

Refer to:
• a paediatrician for assessment of autistic features
• genetics services if the individual is dysmorphic
• a neurologist if regression of psychomotor skills occurs.
Other considerations
If a diagnosis of ASD is made, referral to a genetic counsellor may be appropriate in terms of family planning. Research
estimates the recurrence risk for siblings of children affected with ASD at up to 7%. If there are multiple affected siblings, the
recurrence risk is higher (up to 50%).1
References
1. Schaefer GB, Mendelsohn NJ. Clinical genetics evaluation in identifying the etiology of autism spectrum disorders: 2013
guideline revisions. Genet Med 2013;15(5):399-407.
2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th edn. Washington, DC:
American Psychiatric Publishing, 2013.
3. Tonge B, Brereton A. Autism spectrum disorders. Aust Fam Physician 2011;40(9):672-77. Available at www.racgp.org.
au/download/documents/AFP/2011/September/201109tonge.pdf [Accessed 15 December 2017].
4. Miller DT, Adam MP, Aradhya S, et al. Consensus statement: Chromosomal microarray is a first-tier clinical diagnostic test
for individuals with developmental disabilities or congenital anomalies. Am J Hum Genet 2010;86(5):749-64.
5. Department of Health. Medicare Benefits Schedule (MBS) Online. Canberra: DoH, 2017. Available at www.mbsonline.
gov.au [Accessed 15 December 2017].

Information
• Autism Spectrum Australia (Aspect), What is autism?, www.autismspectrum.org.au/content/what-autism
• Centre for Genetics Education, Autism spectrum disorder, www.genetics.edu.au/publications-and-resources/facts-sheets/
fact-sheet-46-autism-spectrum-disorder/view
Support
• Amaze, www.amaze.org.au
• Autism Spectrum Australia (Aspect), www.autismspectrum.org.au
19
Cystic fibrosis
@ Practice point-----------------------------------------------------------------------------------
The commonly used newborn screening tests will identify 85-90% of individuals with cystic fibrosis (CF), but will not
identify individuals with rare (atypical) CF variants. 1 Such patients may present to the general practitioner (GP).

CF is the most common life threatening genetic condition in Australia. CF primarily affects the lungs and digestive system,
which become obstructed with excessive, thick mucus. It is a condition that follows an autosomal recessive inheritance
pattern, meaning both parents must carry a CF-causing gene variant to be at risk of having a child with the disease.
About one in 25 Australians of northern European ancestry are carriers of the CFTR gene variant. The most common
variant in the CFTR gene is the AF508 variant, which accounts for approximately 70% of all CFTR gene variant in those of
northern European ancestry. While there are more than 2000 variants in the CFTR gene, around 40 variants contribute to
approximately 90% of cases of CF in Australia.1,2
Genetic testing
Almost all babies in Australia are screened at birth for CF. There are some who may be lost to follow up or refuse to consent
for screening. Exact numbers in Australia are not available. Refer to ‘Newborn screening’ for more information.
Carrier screening for CF can be offered by GPs to all couples planning a pregnancy (or already pregnant), regardless of family
history or ethnicity. Refer to ‘Reproductive carrier screening’ for more information.
Carrier screening for CF is also available through some genetic screening programs for at-risk groups (eg people of
Ashkenazi Jewish ancestry) and through commercial carrier screening tests.1

Couples who are CF carriers should be referred for genetic counselling if they are planning a pregnancy or in the first
trimester of pregnancy.3
Children suspected of having CF (who have not been previously identified through newborn screening tests) should be
referred to a paediatrician for a sweat test. Symptoms may include recurrent cough, failure to thrive, lower respiratory tract
infection, bronchiectasis and/or rectal prolapse.
Males presenting with infertility due to congenital bilateral absence of the vas deferens (CBAVD) may have an atypical form of
CF. Refer the patient to a fertility specialist.4
Cascade screening should be offered following a diagnosis of CF in the family to identify other potential carriers.1
References
1. Delatycki MB, Burke J, Christie L, et al. Human Genetics Society of Australasia. Position statement: Population-based
carrier screening for cystic fibrosis. Twin Res Hum Genet 2014;17(6):578-83.
2. Cystic Fibrosis Foundation. The clinical and functional translation of CFTR (CFTR2). Baltimore, MD: Johns Hopkins
University, 2011. Available at http://cftr2.org [Accessed 15 December 2017].
3. The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 9th edn.
Melbourne: RACGP, 2016. Available at www.racgp.org.au/your-practice/guidelines/redbook [Accessed 15 December
2017].
4. Ong T, Marshall SG, Karczeski BA, et al. Cystic fibrosis and congenital absence of the vas deferens. GeneReviews.
Seattle, WA: University of Washington, 2001. Available at www.ncbi.nlm.nih.gov/books/NBK1250 [Accessed 15
December 2017].
Information
• National Library of Medicine, Cystic fibrosis, https://ghr.nlm.nih.gov/condition/cystic-fibrosis
• Better Health Channel, Cystic fibrosis, www.betterhealth.vic.gov.au/health/conditionsandtreatments/cystic-fibrosis-cf
• Centre for Genetics Education, Fact sheet 41: Cystic fibrosis, www.genetics.edu.au/publications-and-resources/facts-
sheets/fact-sheet-41-cystic-fibrosis.
Support
• Cystic Fibrosis Australia, www.cysticfibrosis.org.au
21
Developmental delay and intellectual disability

@ Practice point-------------------------------------------------------------------------------------
Children with features of developmental delay (DD) or intellectual disability (ID) should be referred to a paediatrician for
a clinical genetics evaluation.1

The causes of DD and ID can be genetic, non-genetic (eg fetal alcohol spectrum disorder, congenital infection) or unknown.
Knowledge that DD and ID are caused by an underlying genetic condition may inform:
• the ongoing management of the child’s condition
• parents of future reproductive risk.
There are several genetic causes of DD and ID:
• Chromosomal
- abnormalities of chromosome number (eg Down syndrome)
- loss (ie deletion) or gain (ie duplication) of part of a chromosome.
• Single-gene disorders
- de novo gene variants (occurring in the child but not inherited from a parent; eg Rett syndrome)
• Inherited causes
- conditions that follow an autosomal dominant inheritance pattern (eg tuberous sclerosis)
- conditions that follow an autosomal recessive inheritance pattern (eg phenylketonuria [PKU])
- conditions that follow an X-linked recessive inheritance pattern (eg Fragile X syndrome [FXS])
Genetic testing
Chromosome microarray (CMA) is now considered a first-line genetic test for the investigation of DD, ID, autism spectrum
disorder (ASD), and congenital abnormalities.2 CMA does not detect gene variants causing FXS (ie FMR1 gene), so an
additional deoxyribonucleic acid (DNA) test must be ordered alongside.
While general practitioners (GPs) are able to order CMAs, many choose not to, given the complex interpretation of the
results. However, ordering CMA and FXS tests in parallel with referral to a paediatrician can reduce waiting times for patients.
A Medicare Benefits Schedule (MBS) rebate is available for CMA in situations where the patient has DD, ID, ASD or at least
two congenital abnormalities. DNA testing for FXS is available with an MBS rebate when the patient:3
• exhibits ID, ataxia, neurodegeneration, or premature ovarian failure consistent with an FMR1 mutation

A genetic cause should be suspected in individuals with DD and any of the following:
• dysmorphic features
• autistic features
• epilepsy
• congenital anomalies (eg cleft palate, heart defects)
• a family history of autism, FXS or other developmental/learning disability.
Patients with these features should be referred to a paediatrician or genetics services.
Refer directly to a paediatric neurologist if there is regression of motor skills (eg suspected muscular dystrophy, spinal
muscular atrophy).
References
Melbourne: RACGP, 2016. Available at www.racgp.org.au/your-practice/guidelines/redbook [Accessed 24 July 2017].

• Raising Children Network, Developmental delay in babies, http://raisingchildren.net.au/articles/developmental_delay_video.html
23
Diabetes
@ Practice point-------------------------------------------------------------------------------------
Types 1 and 2 diabetes are multifactorial, and there are currently no indications for genetic testing.
Approximately 2% of people with diabetes have maturity onset diabetes of the young (MODY), which is caused by a
dominantly inherited variant in one of several known genes. It is important to identify these patients and family members,
as there are implications for clinical management, including choice of treatment, prognosis and reproduction.1

MODY typically presents in the second to fourth decade of life, and does not fit the clinical picture of either types 1 or 2
diabetes. Presentation is often subacute or incidental. Many cases are misdiagnosed as types 1 or 2 diabetes.2,3
MODY is the only type of diabetes caused by a single gene mutation. Mutations in 13 genes are known to cause MODY. The
most prevalent mutations are in the HNF1A, GCK and HNF4A genes. GCK-MODY constitutes 10-60% of all MODY cases.2
Testing for MODY should be considered in individuals with early onset diabetes with atypical features (ie not clearly type 1 or type 2):1
• atypical type 1 diabetes
• no history of diabetic ketoacidosis
• prandial plasma C-peptide >200 pmol/L and >5 years post-diagnosis of type 1 diabetes
• atypical type 2 diabetes
• <35 years of age
• absence of features of insulin resistance
• no obesity
• no dyslipidaemia
• no hypertension
• no polycystic ovary syndrome
• strong family history of diabetes.
If MODY is suspected, assess risk using the calculator available at www.diabetesgenes.org/content/mody-probability-calculator

Individuals with suspected MODY should be referred to an endocrinologist for assessment and consideration of genetic testing.
References
1. Carroll RW, Murphy R. Monogenic diabetes: A diagnostic algorithm for clinicians. Genes (Basel) 2013;4(4):522-35.
2. Bishay RH, Greenfield JR. A review of maturity onset diabetes of the young (MODY) and challenges in the management
of glucokinase-MODY. Med J Aust 2016;205(10):480-85.
3. Naylor R, Philipson LH. Who should have genetic testing for maturity-onset diabetes of the young? Clin Endocrinol (Oxf)
2011;75(4):422-26.
Resource for general practitioners

• McElduff A. Non-type 1, non-type 2 diabetes: What’s in a name?, www.nps.org.au/australian-prescriber/articles/non-type-
1-non-type-2-diabetes-what-s-in-a-name
24

• Centre for Genetics Education, Fact sheet 48: Diabetes types 1 and 2 and inherited predisposition, www.genetics.edu.au/
publications-and-resources/facts-sheets/fact-sheet-48-diabetes-type-1-and-2
25
Fragile X syndrome and associated conditions

@ Practice point-------------------------------------------------------------------------------
General practitioners (GPs) can order a test for Fragile X syndrome (FXS) for the following people:
• Individuals with intellectual disability (ID), developmental delay (DD) or autism spectrum disorder (ASD).
• Individuals seen for reproductive counselling who have a family history of FXS (or related conditions, such as
Fragile X-associated primary ovarian insufficiency [FXPOI]) or undiagnosed ID.
• Women with reproductive or fertility issues (associated with elevated follicle-stimulating hormone [FSH]).
• Older individuals (>50 years of age) with late-onset tremor or cerebellar ataxia of unknown origin.

FXS
FXS is the most common known inherited cause of ID, and the second most common cause of ID overall (after Down
syndrome). FXS affects approximately one in 3600 males and one in 6000 females.1
FXS presents clinically with a wide range of symptoms, including global DD; difficulties with learning, speech and language;
problems with coordination and sensory overload; and notably a range of emotional and behavioural difficulties.2,3
FXS follows an X-linked dominant inheritance pattern and is caused by an increase in length of the FMR1 gene on the X
chromosome. The length of the FMR1 gene is divided into four categories (Figure 1). The longer the gene, the more likely the
individual will have symptoms of FXS.2,3
Figure 1. Length of gene associated with FXS3
Normal Short
Grey zone Intermediate
Premutation carries Medium
Affected Long
Females who are premutation carriers of FXS can have a child affected with FXS. This is because the gene length can get
longer when passed from mother to child: this lengthening only occurs in women. Therefore, it is unlikely males who are
premutation carrier of FXS would have an affected child.4
Associated conditions
Females who are premutation carriers are at increased risk of FXPOI. Males (females to a lesser extent) are at increased risk
of Fragile X-associated tremor/ataxia syndrome (FXTAS) later in life.2,3,4
Genetic testing
Chromosome microarray (CMA) is now considered a first-line genetic test for the investigation of DD or congenital
abnormalities. CMA does not detect gene variants causing FXS, so an additional deoxyribonucleic acid (DNA) test for FXS
must be ordered alongside.5
While GPs are able to order CMAs, many choose not to, given the complex interpretation of the results. However, ordering
CMA and FXS tests in parallel with referral to a paediatrician can reduce waiting times for patients.
26
A Medicare Benefits Schedule (MBS) rebate is available for CMA in situations where the patient has DD, ID, ASD or at least
two congenital abnormalities. DNA testing for FXS is available with an MBS rebate when the patient:6
• exhibits ID, ataxia, neurodegeneration, or premature ovarian failure consistent with an FMR1 mutation
GPs should offer information on carrier screening for FXS to all couples planning a pregnancy (or who are already pregnant),
regardless of family history or ethnicity. Refer to Reproductive carrier screening for more information.

For symptomatic patients:
• A child with a test positive result should be referred to a paediatrician for further assessment.
• An adult with ataxic symptoms and a test positive result (ie premutation carrier) should be referred to a neurologist.
• A woman with FXPOI should be referred to an obstetrician and gynaecologist.2,3
Asymptomatic patients with a test positive result (eg received through pre-conception or prenatal carrier screening or
cascade testing) should be referred to genetics services.
References
1. Birch RC, Cohen J, Trollor JN. Fragile X-associated disorders: Don’t miss them. Aust Fam Physician 2017;46(7):487-91.
Available at www.racgp.org.au/afp/2017/july/fragile-x-associated-disorders-don%E2%80%99t-miss-them [Accessed 19
December 2017].
2. Finucane B, Abrams L, Cronister A, et al. Genetic counseling and testing for FMR1 gene mutations: Practice guidelines
of the National Society of Genetic Counselors. J Genet Couns 2012;21(6):752-60.
3. Metcalfe S, Jacques A, Archibald A, et al. A model for offering carrier screening for fragile X syndrome to nonpregnant
women: Results from a pilot study. Genet Med 2008;10(7):525-35.
4. Abrams L, Cronister A, Brown WT, et al. Newborn, carrier, and early childhood screening recommendations for fragile X.
Pediatrics 2012;130(6):1126-35.

Information
• National Library of Medicine (US), Fragile X syndrome, https://ghr.nlm.nih.gov/condition/fragile-x-syndrome
Support
• Fragile X Association of Australia, https://fragilex.org.au
27
Familial breast and ovarian cancer

@ Practice point-----------------------------------------------------------------------------------
To identify patients who may be at risk of familial breast and ovarian cancer, a comprehensive family history must be
taken and regularly updated.1,2
Refer individuals and families who meet high-risk criteria to a family cancer clinic.
Women who are at average or only slightly higher risk of familial breast and ovarian cancer do not require additional
surveillance beyond the National Breast Cancer Screening Program and National Cervical Screening Program nor
referral to a family cancer clinic.2

Highly penetrant gene variants in BRCA1 and BRCA2 genes are associated with increased risk of several cancers,
particularly breast and ovarian. These show autosomal dominant inheritance pattern.1,3 Pathogenic variants in BRCA1 and
BRCA2 are associated with increased risk of other cancers including prostate (for men specifically) and pancreatic.
The lifetime risk of breast cancer in Australian women is approximately one in eight.4 Inheriting pathogenic variants of the
BRCA1 and BRCA2 genes increase the chance of developing breast cancer to about 70% (cumulative risk to 80 years of
age). Despite this, BRCA1 and BRCA2 variants account for only about 5% of all breast cancer cases, because these variants
are relatively rare.3-6
Several other genes (low-to-moderate penetrant variants) predisposing to breast and/or ovarian cancer can now also be tested.7
Features within a family that are suggestive of increased risk of carrying a pathogenic BRCA1 or BRCA2 variant include:5
• multiple affected relatives on the same side of the family (maternal or paternal)
• breast and ovarian cancer in the same woman
• breast cancer diagnosed <40 years of age
• Ashkenazi Jewish ancestry (from central and eastern Europe)
• bilateral breast cancer
• male breast cancer.
A three-generation family history is key to identifying high-risk families who are most likely to benefit from genetic testing.
Such a history should include first-degree and second-degree relatives on both sides of the family, and ethnic background
(eg Ashkenazi Jewish). Note that sex-specific cancer can be inherited through maternal or paternal sides of the family
(eg BRCA variants can be passed from the paternal side). Type of cancer (including bilateral) and age of onset should be
recorded where available.4
Use existing risk criteria (eg www.racgp.org.au/your-practice/guidelines/redbook/9-early-detection-of-cancers/93-breast-
cancer) to identify families who are at increased risk of carrying a pathogenic BRCA1 or BRCA2 variant (high risk), or women
who may require additional screening or chemoprevention (moderately increased risk).2
Alternatively, the ‘Familial risk assessment - Breast and ovarian cancer’ (FRA-BOC) tool can be used to assess risk
(https://canceraustralia.gov.au/clinical-best-practice/gynaecological-cancers/familial-risk-assessment-fra-boc ).8
Genetic testing
Family cancer clinics can assess individual risk to determine the utility of genetic testing for BRCA1 and BRCA2 variants. As new
genetic variants predisposing to breast cancer are identified, these new variants may be offered as part of a panel of genetic
tests through the family cancer clinic. If a pathogenic variant is identified in an individual, testing will be offered to relatives.4
A rebate is available for BRCA1 and BRCA2 gene testing under the Medicare Benefits Schedule (MBS).9
There is currently no role in general practice for ordering a can cer-risk assessment based on a single nucleotide
polymorphism (SNP) profile (genotyping).
28

The recommended breast cancer screening strategy for women and different high-risk individuals is outlined in the Royal
Australian College of General Pracitioners (RACGP’s) 2016 Guidelines for preventive activities in general practice (Red Book;
available at www.racgp.org.au/your-practice/guidelines/redbook/9-early-detection-of-cancers/93-breast-cancer ).2
A cancer antigen 125 (CA 125) blood test and transvaginal ultrasound are not recommended as screening tests for ovarian
cancer, even in women who are at high risk.2
Women at increased risk for breast and ovarian cancer should be encouraged to:
• discuss their family history with all first-degree relatives
• advise family members to discuss their risk with their general practitioner (GP).
References
1. Dunlop K, Kirk J, Tucker K. In the wake of Angelina: Managing a family history of breast cancer. Aust Fam Physician
2014;43(1):76-78. Available at www.racgp.org.au/afp/2014/januaryfebruary/family-history-of-breast-cancer [Accessed 19
December 2017].
Melbourne, RACGP, 2016. Available at www.racgp.org.au/your-practice/guidelines/redbook [Accessed 19 December 2017].
3. National Cancer Institute (US). BRCA1 and BRCA2: Cancer risk and genetic testing. Bethesda, MD: National Institutes
of Health, 2015. Available at www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet [Accessed 19
December 2017].
4. Cancer Australia. Advice about familial aspects of breast cancer and epithelial ovarian cancer: A guide for health
professionals. Sydney: Cancer Australia, 2010. Available at https://canceraustralia.gov.au/sites/default/files/publications/
advice-about-familial-aspects-breast-cancer-and-epithelial-ovarian-cancer/pdf/2015_bog_familial_aspects_int.pdf
5. Kuchenbaecker KB, Hopper JL, Barnes DR, et al. Risks of breast, ovarian, and contralateral breast cancer for BRCA1
and BRCA2 mutation carriers. JAMA 2017;317(23):2402-16.
6. National Breast and Ovarian Cancer Centre. Breast cancer risk factors: A review of the evidence. Sydney: NBOCC,
2009. Available at https://canceraustralia.gov.au/system/tdf/publications/breast-cancer-risk-factors-review-evidence/pdf/
rfrw-breast-cancer-risk-factors-a-review-of-the-evidence_1.15.pdf?file=1&type=node&id=3074 [Accessed 19 December
2017].
7. Winship I, Southey MC. Gene panel testing for hereditary breast cancer. Med J Aust 2016;204(5):188-90.
8. Cancer Australia. Familial risk assessment FRA-BOC. Sydney: Cancer Australia, 2011. Available at https://
canceraustralia.gov.au/clinical-best-practice/gynaecological-cancers/familial-risk-assessment-fra-boc [Accessed 19
December 2017].
9. Department of Health. Medicare Benefits Schedule. Canberra: DoH, 2017. Available at www.mbsonline.gov.au/internet/
mbsonline/publishing.nsf/Content/Home [Accessed 22 January 2018].

• Cancer Institute NSW, eviQ, www.eviq.org.au

Information
• Better Health Channel, Breast cancer, www.betterhealth.vic.gov.au/health/conditionsandtreatments/breast-cancer
• Better Health Channel, Genetic testing for inherited cancer, www.betterhealth.vic.gov.au/health/conditionsandtreatments/
genetic-testing-for-inherited-cancer
• Centre for Genetics Education, Fact sheet 32: Breast and ovarian cancer and inherited predisposition, www.genetics.edu.
au/publications-and-resources/facts-sheets/fact-sheet-32-breast-and-ovarian-cancer-and-inherited-predisposition
Support
• Breast Cancer Network Australia, www.bcna.org.au
• Cancer Australia, https://canceraustralia.gov.au
• Cancer Council Australia, www.cancer.org.au
• Ovarian Cancer Australia, https://ovariancancer.net.au
• Pink Hope Australia, http://pinkhope.org.au
30
Familial colorectal cancer

@ Practice point------------------------------------------------------------------------------------
A comprehensive family history must be taken and regularly updated to identify patients who may be at risk of familial
colorectal cancer (CRC).1
Refer individuals and families who meet high-risk criteria to a family cancer clinic.
Individuals at average or only slightly higher risk do not require a colonoscopy, and should be encouraged to
participate in the National Bowel Cancer Screening Program (ie faecal occult blood test [FOBT]).1,2

Highly penetrant gene variants in several genes are associated with specific familial CRC syndromes:
• Lynch syndrome (associated with a range of cancers, including colorectal, endometrial, ovarian, gastric, renal pelvis,
ureter, small bowel, biliary tract, brain) is caused by dominantly inherited pathogenic variants in the MLH1, MSH2, MSH6
or PMS2 genes. Lynch syndrome accounts for up to 6% of all colorectal cancer.3
• Familial adenomatous polyposis (FAP), associated with multiple adenomas in the large bowel, is caused by dominantly
inherited pathogenic variants in the APC gene. FAP accounts for approximately 1% of colorectal cancer cases.3
• There are other rare inherited CRC syndromes that may be associated with specific polyp pathologies, phenotypic
features or other cancer types in a family.4,5
Features within a family that are suggestive of increased risk of carrying a pathogenic variant for Lynch syndrome or FAP include:1,5
• multiple affected relatives on the same side of the family
• multiple CRCs in the same person (ie metachronous)
• CRC diagnosed <50 years of age
• other Lynch-syndrome related cancers (as above)
• >20 adenomas in the large bowel
• adenomas diagnosed <30 years of age.
A three-generation family history is key to identifying high-risk families who are most likely to benefit from genetic testing.
Such a history should include first-degree and second-degree relatives on both sides of the family. Type of cancer (including
whether the cancer is metachronous) and age of onset should be recorded where available.1
Use existing risk criteria (eg www.racgp.org.au/your-practice/guidelines/redbook/9-early-detection-of-cancers/92-colorectal-
cancer) to identify families at increased risk of an inherited CRC syndrome (high risk), or individuals who may require
additional screening or chemoprevention (moderately increased risk).1
Genetic testing
Family cancer clinics will assess individual risk to determine the utility of genetic testing for Lynch syndrome or FAP. As new
genetic variants predisposing to CRC are identified, these new variants may be offered as part of a panel of genetic tests
through family cancer clinics.1
There is currently no role in general practice for ordering a cancer-risk assessment based on a single nucleotide

The recommended CRC screening strategy and different individual risk categories are outlined in The Royal Australian
College of General Practitioners’ (RACGP’s) 2016 Guidelines for preventive activities in general practice (Red Book;
www.racgp.org.au/your-practice/guidelines/redbook/9-early-detection-of-cancers/92-colorectal-cancer).1
31
Individuals at increased risk for CRC should be encouraged to:
• advise family members to discuss their risk with their general practitioners (GP).
References
1. The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 9th edn. East
2. The Royal Australian College of General Practitioners and Choosing Wisely Australia. Tests, treatments and procedures
clinicians and consumers should question. Sydney: NPS MedicineWise, 2016. Available at www.choosingwisely.org.au/
recommendations/racgp [Accessed 19 December 2017].
3. Win AK, Ouakrim, DA, Jenkins, MA. Risk profiling: Familial colorectal cancer. Cancer Forum (Cancer Council Australia)
2014;38(1):15.
4. Samadder NJ, Jasperson K, Burt RW. Hereditary and common familial colorectal cancer: Evidence for colorectal
screening. Dig Dis Sci 2015;60(3):734-47.
5. Rubenstein JH, Enns R, Heidelbaugh J, Barkun A. American Gastroenterological Association Institute guideline on the
diagnosis and management of Lynch syndrome. Gastroenterology 2015;149(3):777-82.

• Department of Health, National bowel cancer screening program, www.cancerscreening.gov.au/internet/screening/
publishing.nsf/Content/bowel-screening-1
• Cancer Council Victoria, Optimal care pathways, www.cancervic.org.au/for-health-professionals/optimal-care-pathways

Information
• Better Health Channel, Genetic testing for inherited cancer, www.betterhealth.vic.gov.au/health/conditionsandtreatments/
genetic-testing-for-inherited-cancer
• Centre for Genetics Education, Fact sheet 33: Bowel cancer and inherited predisposition, www.genetics.edu.au/
publications-and-resources/facts-sheets/fact-sheet-33-bowel-cancer-and-inherited-predisposition
Support
• Bowel Cancer Australia, www.bowelcanceraustralia.org
• Lynch Syndrome Australia, www.lynchsyndrome.org.au
32
Familial hypercholesterolaemia
@ Practice point------------------------------------------------------------------------------------
General practitioners (GPs) are well placed to undertake opportunistic screening for familial hypercholesterolaemia (FH).1
Family screening is critical when a diagnosis of FH is made in an individual.2,3

FH is a lipid disorder that leads to premature cardiovascular disease (CVD). FH follows an autosomal dominant inheritance
pattern. If FH is left untreated, males have a 50% chance of developing CVD before 50 years of age, and women have a
30% chance of developing CVD by 60 years of age. Early diagnosis and treatment of FH reduces the risk of CVD.1
The risk of FH can be assessed using the Dutch Lipid Clinic Network Criteria (DLCNC; www.racgp.org.au/your-practice/
guidelines/redbook/appendices/appendix-2b-dutch-lipid-clinic-network-criteria-for-making-a-diagnosis-of-familial-
hypercholestrolaemia-in-adults ).4
FH assessment should be conducted when an individual presents with:
• clinical features such as xanthomata
• low-density lipoprotein cholesterol (LDL-C) >4.0 mmol/L or total cholesterol >7.5 mmol/L
• premature CVD or a family history of such (CVD <55 years of age for males and <65 years of age for females).1,2,5
Genetic testing
While FH can be diagnosed clinically, a confirmatory deoxyribonucleic acid (DNA) test allows for cascade screening within the
family of an affected patient.5

Refer individuals with a DLCNC score of >3 (ie possible-to-definite FH) to a cardiologist or lipid clinic for confirmation of
diagnosis, including possible genetic testing.2,4
Those diagnosed with FH should be encouraged to:1
• inform family members that they may be at increased risk of FH
• direct family members to further information about FH
• advise family members to discuss their risk of FH with their GP.
References
1. Kirke A, Watts GF, Emery J. Detecting familial hypercholesterolaemia in general practice. Aust Fam Physician
2012;41(12):965-68. Available at www.racgp.org.au/afp/2012/december/familial-hypercholesterolaemia
Melbourne: RACGP, 2016. Available at www.racgp.org.au/your-practice/guidelines/redbook [Accessed 19 December 2017].
3. Bell DA, Watts GF. Progress in the care of familial hypercholesterolaemia: 2016. Med J Aust 2016;205(5):232-36.
4. Watts GF, Sullivan DR, Poplawski N, et al. Familial hypercholesterolaemia: A model of care for Australasia. Atherosclerosis
Supplements 2011;12(2):221-63.
5. Cardiac Society of Australia and New Zealand. Guidelines for the diagnosis and management of familial
hypercholesterolaemia. Sydney: CSANZ, 2013. Available at www.csanz.edu.au/wp-content/uploads/2014/12/Familial-
Hypercholesterolaemia_2013-November.pdf [Accessed 19 December 2017].
33

Information
• Better Health Channel, Genetic factors and cholesterol, www.betterhealth.vic.gov.au/health/conditionsandtreatments/
genetic-factors-and-cholesterol
• Centre for Genetics Education, Fact sheet 56: Familial hypercholesterolaemia, www.genetics.edu.au/publications-and-
resources/facts-sheets/fact-sheet-56-familial-hypercholesteraemia
Support
• FH Australasia Network, www.athero.org.au/fh
34
Familial melanoma
@ Practice point-------------------------------------------------------------------------------------
In order to identify patients who may be at risk of familial melanoma, a comprehensive family history must be taken
and regularly updated. Genetic testing for melanoma risk is not routine as it is does not alter the patient’s management
in most cases.1-3

Rare, highly penetrant variants in a small number of genes (CDKN2A and CDK4) are associated with familial melanoma.
These variants show an autosomal dominant inheritance pattern. Only 1-2% of melanomas are due to pathogenic variants.1,2
Having a first-degree relative with melanoma approximately doubles an individual’s risk of developing melanoma. Having
relatives who are affected with multiple melanomas or at a younger age further increases the risk of developing melanoma.3
Features within a family that are suggestive of increased risk of carrying a pathogenic variant for familial melanoma include
having three or more relatives affected by melanoma on the same side of the family.
Other features and red flags within a family are:1
• multiple melanomas in the same person

• melanoma diagnosed <40 years of age
• ocular melanoma
• pancreatic cancer
• astrocytoma.
Genetic testing
Genetic testing for CDKN2A gene variants has limited clinical utility in general practice. Testing should be restricted to
selected families with a strong history of melanoma.1,3 Assessment of individuals for genetic testing is performed by a family
cancer clinic.

Individuals with more than one family member with melanoma should be referred to a dermatologist for clinical risk
management.
Individuals with three or more relatives affected with melanoma and/or pancreatic cancer in the family should be referred to
a family cancer clinic for genetic risk assessment.3,4
Individuals with familial melanoma should be encouraged to advise family members to discuss their risk with their general
practitioner (GP).
35
References
1. Kefford R, Bishop JN, Tucker M, et al. Genetic testing for melanoma. Lancet Oncol. 2002;3(11):653-54.
2. National Cancer Institute (US). Genetics of skin cancer (PDQ) - Health professional version. Bethesda, MD: NIH, 2017.
Available at www.cancer.gov/types/skin/hp/skin-genetics-pdq [Accessed 19 December 2017].
3. Australian Cancer Network Melanoma Guidelines Revision Working Party. Clinical practice guidelines for the
management of melanoma in Australia and New Zealand. Sydney/Wellington: Cancer Council Australia/Australian Cancer
Network/Ministry of Health, New Zealand, 2008. Available at www.cancer.org.au/content/pdf/HealthProfessionals/
ClinicalGuidelines/ClinicalPracticeGuidelines-ManagementofMelanoma.pdf [Accessed 19 December 2017].
2017].


Information
• Centre for Genetics Education, Fact sheet 34: Genetics and melanoma, www.genetics.edu.au/publications-and-resources/
facts-sheets/fact-sheet-34-genetics-and-melanoma
Support
• Cancer Australia, canceraustralia.gov.au
• Melanoma Institute Australia, www.melanoma.org.au
36
Familial prostate cancer

@ Practice point-------------------------------------------------------------------------------------
A comprehensive family history must be taken and regularly updated to identify patients who may be at risk of familial
prostate cancer.1
Use existing risk criteria to identify individuals who are at increased risk of carrying a pathogenic variant of the BRCA1
or BRCA2 genes (high risk). These individuals should be referred to a family cancer clinic.
Men with family history of prostate cancer who decide to be tested should be offered prostate-specific antigen (PSA)
testing every two years from 40 or 45 years of age, with the starting age depending on the strength of their family history.2

Approximately 1-2% of prostate cancer is due to pathogenic variants in the BRCA1 and BRCA2 genes. These show an
autosomal dominant inheritance pattern.3
Multiple genetic and environmental factors are likely to influence the risk of prostate cancer. Genetic testing for gene variants
in men with multiple cases of prostate cancer only in their family is not widely available.
Features suggestive of increased risk of carrying a pathogenic BRCA1 or BRCA2 variant genes include two or more relatives
affected by breast or ovarian cancer on the same side of the family (maternal or paternal) plus an additional high-risk feature:4,5
• relatives with breast or ovarian cancer
• breast and ovarian cancer in the same woman
• breast cancer diagnosed <50 years of age
• Ashkenazi Jewish ancestry
• bilateral breast cancer
• male breast cancer.
A three-generation family history is key to identifying high-risk families who are most likely to benefit from genetic
assessment. Such a history should include first-degree and second-degree relatives on both sides of the family, and ethnic
background (eg Ashkenazi Jewish). Type of cancer (eg metachronous) and age of onset of affected relatives should be
recorded where available.
In men with a family history of prostate cancer, take a family history of other cancers to assess the risk of carrying a
pathogenic BRCA1 or BRCA2 variant genes. In the absence of a positive breast or ovarian cancer family history, BRCA1 and
BRCA2 testing is generally not warranted.
Genetic testing
Family cancer clinics will assess individual risk to determine the utility of genetic assessment for BRCA1 or BRCA2 gene
variants. As new genetic variants predisposing to prostate cancer are identified, these new variants may be offered as part of
a panel of genetic tests through the family cancer clinic.
There is currently no role in general practice for ordering a cancer-risk assessment based on a single nucleotide

Refer men to a family cancer clinic if they have:1,4
• a family history suggestive of a BRCA1 or BRCA2 pathogenic gene variant.
• three first-degree or second-degree relatives with prostate cancer
• two first-degree or second-degree relatives with prostate cancer, one of whom was diagnosed <50 years of age.
37
Individuals at increased risk of prostate cancer should be encouraged to:
Recommendations for PSA testing vary according to family history of prostate cancer:2
Number of relatives with prostate cancer Relative risk Testing recommendation

*
Father or one brother 2.5-3 PSA testing every two years for those aged 45-69 years
Father and two or more brothers 9-10 PSA testing every two years for those aged 40-69 years
*After discussion of benefits and harms of PSA testing.
References
2. Prostate Cancer Foundation of Australia and Cancer Council Australia PSA Testing Guidelines Expert Advisory Panel.
Clinical practice guidelines PSA testing and early management of test-detected prostate cancer. Sydney: Cancer Council
Australia, 2015. Available at http://wiki.cancer.org.au/australia/Guidelines:PSA_Testing [Accessed 19 December 2017].
3. Li D, Kumaraswamy E, Harlan-Williams LM, Jensen RA. The role of BRCA1 and BRCA2 in prostate cancer. Front Biosci
2013;18:1445-59.
4. National Cancer Institute (US). Genetics of prostate cancer (PDQ) - Health professional version. Bethesda, MD: National
Institutes of Health, 2017. Available at www.cancer.gov/types/prostate/hp/prostate-genetics-pdq [Accessed 19
December 2017].
5. National Cancer Institute (US). BRCA1 and BRCA2: Cancer risk and genetic testing. Bethesda, MD: National Institutes
of Health, 2017. Available at www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet [Accessed 19
December 2017].


Information
• Better Health Channel, Prostate cancer, www.betterhealth.vic.gov.au/health/conditionsandtreatments/prostate-cancer
• The Royal Australian College of General Practitioners, Patient information sheet - Should I have prostate cancer screening?,
www.racgp.org.au/your-practice/guidelines/prostate-cancer
Support
• Prostate Cancer Foundation of Australia, www.prostate.org.au
38
Haemoglobinopathies
@ Practice point-------------------------------------------------------------------------------------
General practitioners (GPs) play an important role in identifying potential carriers of haemoglobinopathy. They also play
an important role in identifying couples who are at risk of having a child with a haemoglobinopathy.
Carrier screening should be discussed with couples who are potential carriers of haemoglobinopathy because of their
ethnicity, and are planning pregnancy or in the first trimester of pregnancy.1
To enable timely reproductive choices during early pregnancy, carrier screening should be offered to couples at the
same time (ie both partners should be tested as early as possible).

The term ‘haemoglobinopathies’ covers a range of conditions with an autosomal recessive inheritance pattern that affect
haemoglobin, including a-thalassaemia and p-thalassaemia, sickle cell disease and other abnormal haemoglobins, such as
haemoglobin E (HbE).
Individuals with thalassaemia produce insufficient haemoglobin, while those with sickle cell disease produce structurally
abnormal haemoglobin. The clinical implications range from mild through to death in utero.
Collectively, haemoglobinopathies are the most common single gene disorders in humans, and around 7% of the world’s
population are carriers.1 Haemoglobinopathies are becoming more prevalent in Australia given immigration from endemic regions.2
While carriers are often asymptomatic, carrier status becomes clinically significant in women who are carriers and planning a
pregnancy, where the biological male partner is also a carrier.1 Screening for haemoglobinopathies is not part of the newborn
screening program in Australia.
Carrier screening should be discussed as part of pre-pregnancy and prenatal care in the following individuals:1-4
• Those with family history of anaemia or haemoglobinopathy.
• Those from the following ethnic backgrounds (have increased carrier frequency)
- southern European
- African
- Middle Eastern
- Chinese
- Indian subcontinent
- central and south-east Asian
- Pacific Islander
- New Zealand Maori
- South American
- Caribbean
- some northern Western Australian and Northern Territory Aboriginal and Torres Strait Islander communities.
• Those with a mean corpuscular volume (MCV) <80 fL or mean corpuscular haemoglobin (MCH) <27 pg.
• Biological male partners of known female carriers.
Genetic testing
Order a haemoglobinopathy screen to include:1,2,4
• full blood examination (FBE) for MCV and MCH
• ferritin to exclude iron deficiency
• haemoglobin electrophoresis
• deoxyribonucleic acid (DNA) testing if indicated (Table 1).
There is an urgency to test the biological male partner concurrently when an at-risk woman who is a carrier is pregnant.
DNA testing is required when a-thalassaemia cannot be excluded and the partner is a known carrier of two-gene deletion
a-thalassaemia (Table 1).
Table 1. Interpretation of haemoglobinopathy carrier testing results2

MCH (pg)/MCV (fL) Ferritin Haemoglobin electrophoresis Interpretation
MCH <27 and/or Normal HbA2 increased p-thalassaemia carrier

MCV <80
HbA2 normal a-thalassaemia carrier
HbH present
HbA2 normal Possible HbH a-thalassaemia

HbH high
HbA2 normal HbE carrier or homozygote

HbE present
Normal Possible a-thalassaemia carrier; DNA testing indicated
Low Normal Iron deficiency
Thalassaemia may co-exist (treat iron deficiency then retest)
If woman is pregnant, seek advice about further tests
MCH >27 and/or Normal Normal Thalassaemia unlikely but one-gene deletion a-thalassaemia
MCV >80 not excluded; DNA testing indicated only if partner is carrier of
a-thalassaemia
Normal HbS present Carrier for sickle cell disease
Low Normal Reduced iron stores or iron deficiency, thalassaemia unlikely

but one-gene deletion a-thalassaemia not excluded. Treat iron
deficiency then retest
HbA2, normal variant of haemoglobin with two a-globin and two p-globin chains; HbE, abnormal variant of haemoglobin, due to abnormal p-globin;
HbH, abnormal variant of haemoglobin, due to excess p-globin chains relative to p-globin chains, a type of a-thalassaemia; HbS, abnormal variant
of haemoglobin, due to abnormal p-globin; MCH, mean corpuscular haemoglobin; MCV, mean corpuscular volume
Adapted from Metcalfe SA, Barlow-Stewart K, Campbell J, Emery J. Genetics and blood - Haemoglobinopathies and clotting disorders. Aust Fam
Physician 2007;36(10):812-19.

Urgent referral should be made to genetics or haematology services when carrier couples are identified during pregnancy
in order to allow for timely reproductive decisions, or when a pregnant woman is identified as a carrier and of testing the
biological male partner has not been done.
Urgent referral should be made to haematology services if a pregnant woman is found to have abnormal variant of
haemoglobin (HbH) a-thalassaemia.
40
Do not assume low MCV or MCH is due to iron deficiency alone, especially in at-risk individuals.1 If the patient is not
pregnant, treat for the iron deficiency then retest. If MCV or MCH remain low, the individual is possibly a carrier of a
haemoglobinopathy. If the patient is pregnant, DNA testing for a-thalassaemia is indicated.1
A woman only needs to have haemoglobinopathy screening once - if MCV or MCH is low but was previously normal, it is
most likely due to iron deficiency.
References
1. Tan YL, Kidson-Gerber G. Antenatal haemoglobinopathy screening in Australia. Med J Aust 2016;204(6):226-30.
2. Metcalfe SA, Barlow-Stewart K, Campbell J, Emery J. Genetics and blood: Haemoglobinopathies and clotting disorders.
Aust Fam Physician 2007;36(10):812-19.
3. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists. Prenatal screening and diagnosis of
chromosomal and genetic conditions in the fetus in pregnancy (C-Obs 59). Sydney: RANZCOG, 2015. Available at www.
ranzcog.edu.au/Statements-Guidelines [Accessed 20 December 2017].
2017].

• Bender MA, Douthitt Seibel G, Sickle cell disease, www.ncbi.nlm.nih.gov/sites/books/NBK1377
• Origa R, Moi P, Alpha-thalassemia, www.ncbi.nlm.nih.gov/books/NBK1435
• Origa R, Beta-thalassemia, www.ncbi.nlm.nih.gov/books/NBK1426

• Centre for Genetics Education, Fact sheet 43: Thalassaemia, www.genetics.edu.au/publications-and-resources/facts-
sheets/fact-sheet-49-blood-clotting-conditions/view
• Centre for Genetics Education, Fact sheet 44: Sickle cell disease, www.genetics.edu.au/publications-and-resources/facts-
sheets/fact-sheet-44-sickle-cell-disease
• National Library of Medicine (US), Alpha thalassemia, https://ghr.nlm.nih.gov/condition/alpha-thalassemia
• National Library of Medicine (US), Beta thalassemia, https://ghr.nlm.nih.gov/condition/beta-thalassemia
• National Library of Medicine (US), Sickle cell disease, https://ghr.nlm.nih.gov/condition/sickle-cell-disease
41
Hereditary haemochromatosis
@ Practice point-------------------------------------------------------------------------------------
Hereditary haemochromatosis (HHC) is a common condition that affects an estimated one in 250 individuals of
northern European backgrounds. Genetic testing for HHC should be performed in patients with proven iron overload.
Cascade screening of relatives is also important when specific gene variants causing HHC are confirmed in the family.1
Screening for HHC in the general population is currently not recommended given its variable expressivity and
incomplete penetrance.2,3

HHC is a condition with an autosomal recessive inheritance pattern where excessive iron absorption leads to increased
blood iron stores. HHC is underdiagnosed as the symptoms are usually non-specific; however, early diagnosis and treatment
reduces serious complications and possible early death.
The most common genetic cause of HHC (up to 90%) is homozygosity of the C282Y gene variant in the HFE gene (HFE-
haemochromatosis). About one in 10 people are carriers of a C282Y variant, while one in every 200 carriers is homozygous
for the C282Y variant. Another common variant in the HFE gene is H63D. Not all individuals with a genetic predisposition to
HHC will develop iron overload (incomplete penetrance).2
The risk of iron overload varies according to genotype (Table 1).3-5
Table 1. Varying genotypes and risk of iron overload

Genotype Risk of iron overload with genotype Frequency of genotype
*
Heterozygous C282Y No increased risk 1 in 10
Homozygous C282Y Greatly increased risk - 40-60% for 1 in 200

females and 75-100% for males
Heterozygous H63D No increased risk 1 in 4
Homozygous H63D No increased risk 1 in 50
Compound heterozygous C282Y/H63D Small increase in risk - 1% 1 in 50

*Frequency data are approximate for those of northern European ancestry and ethnicity.
Genetic testing
Genetic testing for the risk of HHC is recommended in individuals with suspected iron overload (ie elevated serum ferritin
concentration >200 pg/L [(females)] or >300 pg/L [(males)], and a transferrin saturation >45% will identify almost all patients
with HFE-haemochromatosis).2,6-8
Cascade screening is warranted for all first-degree relatives of patients with HHC who are C282Y homozygous or C282Y/H63D
compound heterozygous.
A Medicare Benefits Schedule (MBS) rebate for the HFE gene test applies where the patient has an elevated transferrin
saturation or elevated serum ferritin on repeat testing or a first-degree relative with haemochromatosis or is homozygous for
the C282Y gene variant or a compound heterozygote.9
42
Asymptomatic individuals (identified through cascade screening) who are C282Y homozygous or C282Y/H63D compound
heterozygous should have their serum ferritin regularly monitored.2,6
Patients with HFE-haemochromatosis should be encouraged to:8
• inform all first-degree relatives of increased risk
• direct family to information about haemochromatosis (eg Haemochromatosis Australia)

References
2. European Association for the Study of the Liver. EASL clinical practice guidelines for HFE hemochromatosis. J Hepatol
2010;53(1):3-22.
3. US Preventive Services Task Force. Screening for hemochromatosis: Recommendation statement. Ann Intern Med
2006;145(3):204-08.
4. Allen KJ, Gurrin LC, Constantine CC, et al. Iron-overload-related disease in HFE hereditary hemochromatosis. N Engl J
Med 2008;358(3):221-30.
5. Goot K1, Hazeldine S, Bentley P, Olynyk J, Crawford D. Elevated serum ferritin: What should GPs know? Aust Fam
Physician 2012;41(12):945-49.
6. Allen K. Hereditary haemochromatosis: Diagnosis and management. Aust Fam Physician 2010;39(12):938.
7. St John AT, Stuart KA, Crawford DHG. Testing for HFE-related haemochromatosis. Aust Prescr 2011;34(3):73-76.
Available at www.nps.org.au/australian-prescriber/articles/testing-for-hfe-related-haemochromatosis [Accessed 20
December 2017].
8. Gastroenterological Society of Australia. Haemochromatosis. 3rd edn. Sydney: Digestive Health Foundation, 2007.

• Seckington R, Powell L. HFE-associated hereditary haemochromatosis. GeneReviews. Seattle, WA: University of
Washington, 2000, www.ncbi.nlm.nih.gov/books/NBK1440

Information
• Centre for Genetics Education, Fact sheet 47: Hereditary haemochromatosis, www.genetics.edu.au/publications-and-
resources/facts-sheets/fact-sheet-47-hereditary-haemochromatosis
• National Library of Medicine (US), Hereditary hemochromatosis, https://ghr.nlm.nih.gov/condition/hereditary-
hemochromatosis
Support
• Haemochromatosis Australia, https://haemochromatosis.org.au
43
Hereditary thrombophilia
@ Practice point---------------------------------------------------------------------------------
Individuals who may benefit from genetic testing for hereditary thrombophilia include:
• individuals with venous thromboembolism (VTE) <50 years of age without the following
- major transient risk factor (eg surgery, immobility, trauma)
- oestrogen provocation (eg pregnancy, prescribed oestrogens)
• individuals with VTE <50 years of age in an unusual site (eg central nervous system, abdominal veins, upper limb)1-3
• pregnant women who have had a previous episode of VTE or who have a strong family history of VTE (>2 family
members).1,4
Routine genetic testing for hereditary thrombophilia in individuals without any of the above features is not
recommended in general practice.1
What do I need to know? ©

Box 1. Major hereditary
Individuals with hereditary thrombophilia have an increased tendency to
develop blood clots. thrombophilia conditions6
There are a number of different types of hereditary thrombophilia Group 1 conditions - Due to
conditions (Box 1). At least half of thrombotic episodes in individuals with a defect or deficiency of an
hereditary thrombophilia occur during periods of increased risk, such as anticoagulant protein:
during pregnancy, immobilisation or surgery.5 • Antithrombin deficiency
The risk of VTE in women taking a low-dose combined oral contraceptive • Protein C deficiency
(COC; <35 ug ethinyl oestradiol) is increased two to three times,
compared with non-users. Despite this increase in risk, there is no • Protein S deficiency
indication for routine screening of women prior to prescribing a COC.5,7,8 Group 2 conditions - Due to
genetic mutations that result in
an increased tendency towards
Genetic testing
thrombosis:
Testing practices for hereditary thrombophilia are variable across
• Activated protein C resistance
Australia, in part due a to lack of local evidence-based guidelines.2
• Factor V Leiden
Factor V Leiden and prothrombin variant genetic testing is only available
on the Medicare Benefits Schedule (MBS) if the patient has a:9 • Prothrombin gene variant
• personal history of VTE • Elevated levels of factors VIII,
• family histroy of a diagnosed inherited thrombophilic condition. IX and XI
Other conditions:
When should I refer? • Hyperhomocysteinaemia
Refer women with hereditary thrombophilia who are pregnant or thinking The risk of thrombosis is higher for patients
about pregnancy. Management of hereditary thrombophilia in pregnancy with Group 1 conditions than Group 2
requires specialised risk assessment, and patients should be under the conditions. Group 2 conditions occur
approximately five times more frequently than
direction of a specialist haematologist, obstetric physician or obstetrician.4,5
Group 1 conditions.
Patients diagnosed with hereditary thrombophilia should be encouraged
to inform all first-degree relatives of increased risk; however, the benefit of cascade screening of relatives is uncertain.2,5,8,10
44
References
1. Baglin T, Gray E, Greaves M, et al. Clinical guidelines for testing for heritable thrombophilia. Br J Haematol
2010;149(2):209-20.
2. Ho WK, Hankey GJ, Eikelboom JW. Should adult patients be routinely tested for heritable thrombophilia after an episode
of venous thromboembolism? Med J Aust 2011;195(3):139-42.
3. Haematology Society of Australia and New Zealand and Choosing Wisely Australia. Tests, treatments and procedures
clinicians and consumers should question. Sydney: NPS MedicineWise, 2016. Available at www.choosingwisely.org.au/
recommendations/hsanz [Accessed 20 December 2017].
4. Gerhardt A, Scharf RE, Greer IA, Zotz RB. Hereditary risk factors for thrombophilia and probability of venous
thromboembolism during pregnancy and the puerperium. Blood 2016;128(19):2343-49.
5. Varga EA, Kujovich JL. Management of inherited thrombophilia: Guide for genetics professionals. Clin Genet 2012;81(1):7-
17.
6. Crowther MA, Kelton JG. Congenital thrombophilic states associated with venous thrombosis: A qualitative overview and
proposed classification system. Ann Intern Med 2003;138:128-34.
7. Bateson D, Butcher BE, Donovan C, et al. Risk of venous thromboembolism in women taking the combined oral
contraceptive: A systematic review and meta-analysis. Aust Fam Physician 2016;45(1-2):59.
8. Gialeraki A, Valsami S, Pittaras T, Panayiotakopoulos G, Politou M. Oral contraceptives and HRT risk of thrombosis. Clin
Appl Thromb Hemost 2016:1076029616683802.
9. Department of Health. Medicare benefits schedule book: Category 6. Canberra: DoH, 2017. Available at www.mbsonline.
gov.au/internet/mbsonline/publishing.nsf/Content/ED28842309B2CD13CA2580F7008294BE/$File/201705-Cat6.pdf
10. National Institute for Health and Care Excellence. Venous thromboembolic diseases: Diagnosis, management
and thrombophilia testing (CG144). London: NICE, 2012. Available at www.nice.org.uk/guidance/cg144/chapter/
recommendations [Accessed 20 December 2017].

• Centre for Genetics Education, Fact sheet 49: Blood clotting conditions (hereditary thrombophilias), www.genetics.edu.au/
publications-and-resources/facts-sheets/fact-sheet-49-blood-clotting-conditions/view
• NHS Choices (UK), Thrombophilia, www.nhs.uk/conditions/thrombophilia/Pages/Thrombophilia.aspx
• Varga E, The genetics of thrombophilia, www.stoptheclot.org/article143.htm
45
Mental health conditions

@ Practice point------------------------------------------------------------------------------------
There are currently no specific high-risk gene variants that are associated with mental health disorders that are useful
for predictive testing in clinical practice.1,2
Some companies that offer personal genomic testing may include variants that are associated with increased risk of
certain mental health conditions. The results are unlikely to have any clinical utility.

The causes of mental health conditions, such as schizophrenia, bipolar disorder and depression, are multifactorial, and
include environmental, social and genetic factors.
Table 1 outlines the empirical risk according to family history for schizophrenia and bipolar disorder.
Table 1. Empirical risk of schizophrenia according to family history3,4

Risk (%)
Affected relative Schizophrenia Bipolar disorder

No close relative (general population risk) 1 2-3
Sibling 9 13
Parent 13 15
Sibling and one parent 15 20
Both parents 40 50
Second-degree relative 3 5
Monozygotic twin 40 70
Dizygotic twin 10 20
Genetic testing
While some genetic variants have been shown to be associated with mental health conditions, there is no genetic test that
can predict mental illness with certainty.
Some commercial genetic tests available are used to tailor drug treatments to individuals with a mental health disorder
(Pharmacogenomics: Summary). There are currently no Australian clinical guidelines to support such use.1,5

There is no indication to refer patients with a family history of mental illness (eg couples considering pregnancy) to genetics services.
References
1. International Society of Psychiatric Genetics. Genetic testing and psychiatric disorders: A statement from the International
Society of Psychiatric Genetics. Brentwood, TN: ISPG, 2017. Available at https://ispg.net/genetic-testing-statement
2. State MW, Geschwind DH. Leveraging genetics and genomics to define the causes of mental illness. Biol Psychiatry
2015;77(1):3-5.
3. Harper PS. Practical genetic counselling. 7th edn. London: Hodder Arnold, 2010.
4. Slater E, Cowie V. The genetics of mental disorders. London: Oxford University Press, 1971.
5. Hamilton SP. The promise of psychiatric pharmacogenomics. Biol Psychiatry. 2015;77(1):29-35.

• Centre for Genetics Education, Fact sheet 59: Mental illness - Schizophrenia and bipolar disorder, www.genetics.edu.au/
publications-and-resources/facts-sheets/fact-sheet-59-mental-illness-disorders
• National Library of Medicine (US), Bipolar disorder, https://ghr.nlm.nih.gov/condition/bipolar-disorder
• National Library of Medicine (US), Schizophrenia, https://ghr.nlm.nih.gov/condition/schizophrenia
47
Neurofibromatosis type 1
@ Practice point-------------------------------------------------------------------------------------
The diagnosis of neurofibromatosis type 1 (NF1) is usually made on clinical grounds. While genetic testing is not needed to
confirm a diagnosis, confirmation of a gene variant can be useful information for family members and family planning.1,2

NF1 is a condition that follows an autosomal dominant inheritance pattern and affects nerve cell tissue, causing the growth
of small tumours throughout the nervous system.
Symptoms usually appear during childhood and may become more pronounced during puberty, pregnancy and when
hormonal changes take place. The severity of the condition can vary greatly, even within a family.
NF1 may be inherited, but up to 50% of cases are caused by a de novo mutation; therefore, family history may not be
present.2
The diagnosis of NF1 is made on the basis of presence of specific physical findings.
Characteristic features of NF1 include:

• multiple cafe-au-lait spots
• inguinal or axillary freckling
• multiple neurofibromas.
Additional features can include:1,2

• optic glioma
• Lisch nodules (iris hamartomas)
• osseous lesions (eg sphenoid dysplasia)
• increased risk of various cancers
• precocious puberty or delayed sexual development
• specific learning disabilities
• short stature
• macrocephaly
• scoliosis
• renal artery stenosis.
Genetic testing
While genetic testing is not needed to confirm a diagnosis, confirmation of a gene variant can provide useful information for
family members or family planning (ie prenatal diagnosis, pre-implantation genetic diagnosis).1

Patients with NF1 (or a relevant family history) should be referred to genetics, paediatrics or neurology services.
48
References
1. Ferner RE, Gutmann DH. Neurofibromatosis type 1 (NF1): Diagnosis and management. Handb Clin Neurol 2013;115:939-55.
2. Friedman JM. Neurofibromatosis 1. GeneReviews. Seattle, WA: University of Washington, 1998. Available at www.ncbi.
nlm.nih.gov/books/NBK1109 [Accessed 20 December 2017].

• BMJ Best Practice, Type 1 neurofibromatosis, http://bestpractice.bmj.com/best-practice/monograph/410/highlights/
summary.html

• Centre for Genetics Education, Fact sheet 45: Neurofibromatosis type 1, www.genetics.edu.au/publications-and-resources/
facts-sheets/fact-sheet-45-neurofibromatosis-type-1/at_download/file
• National Library of Medicine (US), Neurofibromatosis type 1, https://ghr.nlm.nih.gov/condition/neurofibromatosis-type-1
49
Neurological conditions
@ Practice point-------------------------------------------------------------------------------------
A small number of adult-onset neurological conditions are due primarily to a single gene mutation (eg Huntington’s
disease). There are some more common neurological and neuromuscular conditions that have subsets due to specific
gene variants (eg early-onset Alzheimer’s disease and early-onset Parkinson’s disease).1
Positive family history is important in diagnosing neurological conditions with a genetic cause (neurogenetic
conditions).2 Relevant history includes:
• two or more family members affected with the same condition
• a significantly earlier age of onset than average (ie <50 years old for Parkinson’s disease and <65 years old for
Alzheimer’s disease).

There are some neurological conditions that are caused by single gene variants that affect the normal function of muscles
and the nervous system (eg neuropathies, myopathies, ataxias). There are also a large number of complex neurological
conditions caused by an interplay of genetic and environmental factors.1,3
Many, but not all, paediatric neuromuscular disorders are genetic in nature. These disorders begin in childhood and affect
the peripheral nervous system at varying locations. Although paediatric neuromuscular disorders are rare, the more common
ones are:
• spinal muscular atrophy - incidence around 1 in 10,000 births4
• Duchenne muscular dystrophy - incidence around 1 in 5000 male births5
• Charcot-Marie-Tooth disease - incidence around 1 in 2500 births.6
Genetic studies continue to identify variants that contribute to complex neurological conditions; however, there is currently no
role for general practitioners (GPs) in ordering genetic testing for these conditions.
Genetic testing
Genetic testing (diagnostic testing and predictive testing) is available through specialist services4 for the following conditions:
• Creutzfeldt-Jakob disease and other prion diseases
• early onset Parkinson’s disease
• familial epilepsy
• familial motor neurone disease
• Friedreich ataxia
• hereditary peripheral neuropathies
(Charcot-Marie-Tooth disease)
• hereditary spastic paraparesis
• Huntington’s disease
• mitochondrial disorders
• muscular dystrophies
• myotonic dystrophy
• spinal muscular atrophy
• spinocerebellar ataxias.
50

Individuals with suspected neurological conditions should be referred to a neurologist for clinical diagnosis, which may
include genetic testing.
Referral to genetics services for predictive genetic testing of asymptomatic family members is appropriate in cases where:
• there is a proven (clinically or by genetic testing) family history of an inherited neurological or neuromuscular condition
• there is a suggestive family history as indicated by the presence of
- two or more family members affected with the same condition
- a significantly earlier age of onset than average.
References
1. Biskup S, Gasser T. Genetic testing in neurological diseases. J Neurol 2012;259(6):1249-54.
2. Bird TD. Approaches to the patient with neurogenetic disease. Clin Lab Med 2010;30(4):785-93.
3. Toft M. Advances in genetic diagnosis of neurological disorders. Acta Neurol Scand Suppl 2014(198):20-25.
4. Darras B. Spinal muscular atrophies. Pediatr Clin N Am 2015;62(3):743-66.
5. Stark AE. Determinants of the incidence of Duchenne muscular dystrophy. Ann Transl Med 2015;3(19):287.
doi: 10.3978/j.issn.2305-5839.2015.10.45.
6. Silva DL, Palheta Neto FX, Nunes CT, Matos AB, Matos LT, Pacheco A. Otorhinolaryngology clinical features of
Charcot-Marie-Tooth disease. Int Arch Otorhinolaryngol 2007;11(4):472-76.
7. The Royal College of Pathologists Australia (RCPA). Genetic tests and laboratories. Available at www.rcpa.edu.au/
Library/Practising-Pathology/RCPA-Genetic-Testing/RGTL/Home [Accessed 22 January 2018].

• Evans-Galea M, Delatycki M, Lockhart P. Explainer: What are neurogenetic diseases? Melbourne: The Conversation,
2014, http://theconversation.com/explainer-what-are-neurogenetic-diseases-22497

• The Royal Australian College of General Practitioners, Beware the Rare, education activity and other resources for GPs
about paediatric neuromuscular disorders and carrier screening, https://bewaretherare.com.au
Sudden arrhythmic death syndrome

@ Practice point
Genetic heart disorders are an important cause of sudden arrhythmic death syndrome (SADS) in people <40 years of age.1
In many cases, the death of a young person in the family can often be the first sign of a potential genetic heart disease
within that family.2 Identifying a genetic basis of sudden cardiac death is vital in being able to accurately manage families.3

SADS is an umbrella term to describe unexpected deaths in young people (usually <40 years of age), whose cause of death
following post mortem examination is ‘undetermined’ or ‘unascertained’.3
The most common SADS conditions include genetic arrhythmia syndromes such as long QT syndrome, catecholaminergic
polymorphic ventricular tachycardia (CPVT) and Brugada syndrome.
These conditions follow an autosomal dominant inheritance pattern. Therefore, first-degree relatives (ie parents, siblings,
children) of an individual who has a genetic arrhythmogenic disorder are at a 50% risk of also having a gene variant for
the condition, and thus, at risk of developing the condition. All these conditions show considerable clinical variability within
families and have incomplete penetrance.1,4,5
Of interest are individuals presenting with:3
• any first-degree relatives with unexplained sudden cardiac death <40 years of age
• episodes of unexplained syncope

• syncope or seizures during exercise, excitement or startle.
Collect a comprehensive family history (three generations), noting any relatives with the features above.3
Genetic testing
Genetic testing can be arranged through a genetics clinic if appropriate.6 There is currently no Medicare Benefits Schedule
(MBS) rebate for testing.

Refer those with relevant family history to cardiology for cardiac screening tests, and to a cardiac genetics clinic for risk assessment.2
Familial screening is vital when a genetic heart condition has been confirmed in an index case.
Emotional and psychological support is vital for families where sudden cardiac death has occurred and referrals for grief
counselling should be offered.2
52
References
1. Cardiac Society of Australia and New Zealand. Cardiac genetic investigation of young sudden unexplained death
and resuscitated out of hospital cardiac arrest. Sydney: CSANZ, 2011. Available at www.csanz.edu.au/wp-content/
uploads/2014/12/Young_SUD_and_Resuscitated_OHCA.pdf [Accessed 22 December 2017].
2. Ingles J, Semsarian C. Sudden cardiac death in the young: A clinical genetic approach. Intern Med J 2007;37(1):32-37.
3. Priori SG, Blomstrom-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with
ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with
Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Eur
Heart J 2015;36(41):2793-867.
4. Alders M, Christiaans I. Long QT syndrome. GeneReviews. Seattle, WA: University of Washington, 2003. Available at
www.ncbi.nlm.nih.gov/books/NBK1129 [Accessed 22 December 2017].
5. Brugada R, Campuzano O, Sarquella-Brugada G, et al. Brugada syndrome. GeneReviews. Seattle, WA: University of
Washington, 2005. Available at www.ncbi.nlm.nih.gov/books/NBK1517 [Accessed 22 December 2017].
6. Cardiac Society of Australia and New Zealand. Guidelines for genetic testing of inherited cardiac disorders. Sydney:
CSANZ, 2011. Available at www.csanz.edu.au/wp-content/uploads/2014/12/Genetic_testing_Inherited_Cardiac_
Disorders.pdf [Accessed 22 December 2017].

• Australian Genetic Heart Disease Registry (AGHDR), www.heartregistry.org.au

Information
• AGHDR information sheets, www.heartregistry.org.au/patients-families/genetic-heart-diseases
• Centre for Genetics Education, Fact sheet 58: Primary arrhythmogenic disorders, www.genetics.edu.au/publications-and-
resources/facts-sheets/fact-sheet-58-primary-arrhythmogenic-disorders
Support
• Sudden Arrhythmic Death Syndrome (SADS) Australia, www.sads.org.au
53
Chromosome microarray
What is it?
A chromosome microarray (CMA; also known as a chromosomal microarray or molecular karyotype) is a powerful diagnostic
tool that is used to identify genetic causes of illness and developmental problems. It is used to measure the expression of
multiple genes simultaneously. A CMA can identify small segments of missing or extra deoxyribonucleic acid (DNA), known
as copy number variants (CNVs).
Some CNVs have been linked with certain disabilities or conditions, while others represent normal human variations. There
are also some CNVs for which the clinical impact is unknown or uncertain.1
Why use it?

CMAs are commonly used in two clinical situations, as a:2
• prenatal diagnostic test
• first-line test for individuals presenting with developmental delay (DD), intellectual disability (ID), autism spectrum disorder
(ASD) or multiple congenital anomalies.
The use of CMAs has grown given they have much greater resolution than traditional karyotypes (ie can detect much smaller
variations and provide a greater diagnostic yield, compared with traditional karyotypes).
What does CMA test for?

CMA only tests for variations in DNA copy number. It can identify:1
• microdeletions and duplications
• most abnormalities of chromosome number (eg Down syndrome)
• unbalanced rearrangements of chromosome (eg complex insertions or deletions).
However, it does not identify:1
• single gene mutations
• cases of Fragile X syndrome (FXS)
• balanced rearrangements (translocations and inversions).
How does it work?

CMAs are performed using a blood sample, or in some cases, saliva. Testing uses a microchip platform, which allows the
analysis of many pieces of DNA at once. The microchip uses labels or probes that bind to certain chromosome regions.
Analysis compares the patient’s DNA sequence with a reference DNA sequence. Any differences are called ‘variations’.1
Should I order a CMA (or simply refer)?

In the prenatal setting, many women who undergo an invasive procedure (eg chorionic villus sampling [CVS], amniocentesis)
will have their sample analysed using a CMA (in addition to fluorescence in situ hybridisation [FISH] or quantitative
fluorescence polymerase chain reaction [QF-PCR]). General practitioners (GPs) working in this area may see the results from
CMAs; the section on interpretation of results below may be useful.
There are no clear guidelines about whether GPs should be ordering CMAs for investigating DD or ID in children. A CMA has
been identified as a first-line test for investigating non-syndromic DD and ID.2 A Medicare Benefits Schedule (MBS) rebate is
available for CMAs in the paediatric setting where a patient has DD, ID, ASD or at least two congenital abnormalities.
While GPs are able to order CMAs themselves, many choose not to given the complex interpretation of the results. However,
ordering a CMA (together with an FXS test) alongside a referral to a specialist can reduce waiting times for patients. It is
important to note that microarrays will not identify FXS; a separate DNA test is required.
What do the results mean?

In general, the results of a CMA are shown in Table 1.
Table 1. CMA results1

No clinically significant copy Pathogenic or likely CNVs of unknown or uncertain Secondary or unexpected
number variants (CNVs) pathogenic CNV significance findings
Normal result or known, Known copy number Copy number variant(s) of unknown Copy number VOUS identified.
benign changes detected variant identified significance (VOUS) identified. Clinical Usually a variant that is unrelated
impact is unknown or uncertain to the reason for testing
Laboratory report will suggest Laboratory report will suggest Laboratory report will suggest
next steps (eg referral to next steps (eg referral to genetics, next steps (eg referral to
genetics, family testing) family testing) genetics, family testing)
References
1. Palmer EE, Peters GB, Mowat D. Chromosome microarray in Australia: A guide for paediatricians. J Paediatr Child Health
2012;48(2):E59-67.

• Centre for Genetics Education, Fact sheet 16: Chromosome microarray (CMA) testing in children and adults, www.genetics.
edu.au/publications-and-resources/facts-sheets/fact-sheet-16-chromosome-microarray-cma-testing-in-children-and-adults
• Jackson Laboratory, What you need to know before ordering chromosomal microarray, www.jax.org/education-and-
learning/clinical-and-continuing-education/cancer-resources/deciding-to-test
55
Family history
@ Practice point------------------------------------------------------------------------------------
Ideally, a three-generation family history should be collected on all patients where possible, including first-degree
relatives (ie children, siblings, parents) and second-degree relatives (ie aunts, uncles, grandparents).1 The use of a
family history screening questionnaire1 (www.racgp.org.au/your-practice/guidelines/redbook/appendices/appendix-
2a-family-history-screening-questionnaire) can help identify individuals who may require a more detailed assessment
of their family history of cancer, heart disease or diabetes.

Family history is particularly useful for assessing the risk of autosomal dominant inheritance and multifactorial inheritance.
Conditions with an autosomal recessive inheritance or X-linked recessive inheritance pattern will often occur in the absence
of family history (eg cystic fibrosis [CF]).
General information to collect in a family history include:4

• age of patient
• age at diagnosis of conditions in the family
• ancestry and cultural background
• step-relationships and adoption
• children born to parents who are blood-related (consanguinity)
• known genetic conditions.4
Update the patient’s family history, including births, deaths and new diagnoses opportunistically.
Markers of possible genetically determined conditions in a family history include:1,3,4
• birth defects, multiple stillbirths and multiple miscarriages - consider referral to genetics services
• developmental delay (DD) - consider referral and ordering a chromosome microarray (CMA) and Fragile X syndrome (FXS)
testing (DD and intellectual disability [ID], FXS, autism spectrum disorder [ASD])
• neurodegenerative conditions, premature ischaemic heart disease, sudden death - consider referral to genetics services
• early onset of common cancers and/or unusual combinations of rare cancers - refer to eviQ online2 for further information
about familial cancer syndromes.
56
Pedigree
Drawing a pedigree can be helpful in identifying patterns of inheritance (Table 1).
Table 1. Common pedigree symbols

Male Female Sex unknown
Individual
b .192 5
o30 y
O
4 mo
o O
Affected individual
*
Affected individual with more

than one condition
*
K
® 4>
© <•>
Carrier •
Deceased individual
d . 35 y d. 4 mo
Stillbirth (SB) J/i 5^^
SB 28 wk SB 30 wk SB 34 wk
© <F>
Pregnancy (P)
P
S 28 wk SP 30 wk
*Use a key or legend to define the condition(s) denoted by t he sh ading in the pedigree.
Record the date on which the pedigree is drawn and update it as new information becomes available.
At each step, ask about the health of the family member being discussed.
It may not always be possible to complete the pedigree because of complexities such as adoption, a lack of reliable
information or family disruption. It is important to consider such issues in each family. Step-by-step instructions for drawing a
pedigree is shown in Table 2.
Table 2. Step-by-step instructions for drawing a pedigree3

Step 1 Draw the symbol for the family member being seen. Indicate this person with an
arrow and enter any pertinent details (eg name, age)
Step 2 If the individual has a child or is pregnant, draw a line directly across to a symbol for
the partner
Step 3 Ask about the number of pregnancies pertaining to the couple. Draw a reverse ‘T’
from the relationship line and add the symbol for each child and pregnancy
57
Step 4 Add a line from each child or pregnancy to the reverse ‘T’
Step 5 Ask about brothers and sisters for each partner. Add the relevant symbols alongside
the corresponding person
Step 6 Indicate the relationship between siblings by drawing a vertical line stemming from
each symbol and joining them together with a horizontal line
Step 7 Add a vertical line from this sibship line and add parents
Step 8 Indicate deceased family members by drawing a line through the symbol
Step 9 Repeat steps 5-8 for each parent of the family member you are seeing to include the aunts, uncles and grandparents
References
2. Cancer Institute NSW. eviQ. Sydney: Cancer Institute NSW, 2017 Available at www.eviq.org.au [Accessed 22 December 2017].
3. Bennett RL, French KS, Resta RG, Doyle DL. Standardized human pedigree nomenclature: Update and assessment of
the recommendations of the National Society of Genetic Counselors. J Genet Couns 2008;17(5):424-33.
4. Bennett RL. The family medical history as a tool in preconception consultation. J Community Genet 2012;3(3):175-83.

• National Genetics and Genomics Education Centre (UK), Taking and recording a family history, www.primarycaregenetics.org
• The Royal Australian College of General Practitioners, Family history screening questionnaire, www.racgp.org.au/your-
practice/guidelines/redbook/appendices/appendix-2a-family-history-screening-questionnaire
MTHFR gene testing

@ Practice point-----------------------------------------------------------------------------------
There is no substantial evidence to support the use of MTHFR gene testing in routine clinical practice. Knowledge of
MTHFR gene status is unlikely to change patient management.1-3

The MTHFR gene is involved in processing amino acids, specifically in relation to folate metabolism.
The MTHFR gene test identifies two gene variants associated with increased levels of homocysteine in the blood (C677T and
A1298C). These variants are common in the general population.3
MTHFR gene testing is promoted by some complementary and alternative practitioners to investigate infertility, recurrent
pregnancy loss and risk for particular diseases. However:1-3
• There is no significant evidence of a causal link between MTHFR gene variants and particular diseases.
• MTHFR status does not alter the recommendation that women who are planning a pregnancy or those in the first
trimester of pregnancy take folic acid supplements to reduce the risk of neural tube defects.
Patients can obtain MTHFR gene testing through private providers at their own expense.
There is no indication to refer the patient to genetics services. Given the lack of clinical utility, some genetics service providers
are no longer accepting patient referrals for consultations in relation to MTHFR.3
How can I manage MTHFR gene testing in general practice?

Advising patients who are considering MTHFR gene testing
The following points may be useful to raise in a discussion with patients who are interested in ordering a MTHFR gene test:
• MTHFR gene testing is not recommended when:
- many people have one or both MTHFR gene variants (C677T and/or A1298C)3
- there is a lack of strong scientific evidence to show that having one or both MTHFR gene variants causes particular
health problems1,3,4
- there are no evidence-based treatments that will improve the health of a patient with one or both of the MTHFR gene
variants.3
• There is an association between the presence of MTHFR gene variants and increased homocysteine levels; however
- while high homocysteine was once thought to increase risk of blood clots (thrombophilia), cardiovascular disease
(CVD) and recurrent pregnancy loss, recent studies have found that this is not the case1,4
- many other factors also increase homocysteine (ie diet, lifestyle, other gene variants). A person can reduce their risk
of disease by following a healthy, balanced diet and avoiding well-known risk factors such as smoking and being
overweight
- having a biochemical test for homocysteine levels may provide more useful information. This is less expensive than having
a MTHFR gene test, which in most cases is not covered under the Medicare Benefits Schedule (MBS).
59
Managing patients who have had MTHFR gene testing

The following points may be useful in a discussion with a patient who has had a MTHFR gene test and is concerned about
the results:
• The presence of one or both MTHFR gene variants (C677T and/or A1298C) is not associated with particular health problems
- Individuals who have the MTHFR gene variant(s) might have increased homocysteine levels. While this was once
thought to be associated with particular health problems (ie thrombophilia, CVD, recurrent pregnancy loss), recent
studies have found that this is not the case.1,4 Many other factors also increase homocysteine (ie diet, lifestyle, other
gene variants). A person can reduce their risk of disease by following a healthy, balanced diet and avoiding well-known
risk factors such as smoking and overweight.
- Women who have MTHFR gene variant(s) may have a slightly increased risk of having a baby with neural tube defects
(eg spina bifida). However, taking folic acid supplements before and during pregnancy decreases the risk, just as it
does in women who do not have MTHFR gene variant(s).
• Genetic services are unlikely to accept referrals for consultations about the results of MTHFR gene testing because the
presence of MTHFR gene variants is unlikely to significantly affect a patient’s health.
References
1. Hickie SE, Curry CJ, Toriello HV. ACMG Practice Guideline: Lack of evidence for MTHFR polymorphism testing. Genet Med
2013;15(2):153-56. Available at www.acmg.net/docs/mthfr_gim2012165a_feb2013.pdf [Accessed 22 December 2017].
2. Human Genetics Society of Australasia and Choosing Wisely Australia. 5 things clinicians and consumers should
question. Sydney: NPS MedicineWise, 2016. Available at www.choosingwisely.org.au/recommendations/hgsa [Accessed
22 December 2017].
3. Long S, Goldblatt J. MTHFR genetic testing: Controversy and clinical implications. Aust Fam Physician 2016;45(4):237-
40. Available at www.racgp.org.au/afp/2016/april/mthfr-genetic-testing-controversy-and-clinical-implications [Accessed
7 July 2017].
4. Levin BL, Varga E. MTHFR: Addressing genetic counseling dilemmas using evidence-based literature. J Genet Couns
2016;25(5):901-11.

• The Royal Australian College of General Practitioners, Position statement on responding to patient requests for tests not
considered clinically appropriate, www.racgp.org.au/your-practice/guidelines/position-statement-on-responding-to-patient-
requests-for-tests-not-considered-clinically-appropriate
• The Royal College of Pathologists of Australasia, Position statement: MTHFR genetic tests, www.rcpa.edu.au/
getattachment/7c454ef8-1dc2-4648-99a5-39d9354f55e3/MTHFR-Genetics-Tests.aspx
• The Royal Australian College of General Practitioners, Chapter 15, Screening tests of unproven benefit - Guidelines for
preventive activities in general practice, www.racgp.org.au/your-practice/guidelines/redbook/15-screening-tests-of-
unproven-benefit

• Centre for Genetics Education, Fact sheet 64: MTHFR gene test for patients, www.genetics.edu.au/health-professionals/
FS64-MTHFR-GENE-TESTING-FOR-PATIENTS.pdf/view
• The Royal Australian College of General Practitioners, Appropriate diagnostic testing: Patient information, www.racgp.org.
au/download/Documents/Policies/Clinical/Patient-information-on-appropriate-diagnostic-testing.pdf
60
Newborn screening
@ Practice point----------------------------------------------------------------------------------
Screening is available to all newborns in Australia free of charge, and almost all babies are screened. There are some
babies who may be lost to follow up or their parents may refuse consent for screening. Exact numbers in Australia are
not available. Depending on the condition, not all affected babies will be identified (eg only the most common variants
causing cystic fibrosis [CF] are included in the screening test). Therefore, any suggestive symptoms in a child warrant
further investigation by the general practitioner (GP).
Depending on the program, GPs may or may not be notified of a positive screening result. Follow-up is usually
handled by the screening program.

Screening can identify a number of rare but serious medical conditions, where early detection and intervention can save lives
or provide other benefits to the newborn.
Traditionally, conditions included in the program are based on the ability of clinicians to intervene early to avoid death,
disability or other harm. With the advancement of genetic technology, there is some interest in expanding newborn screening
panels to include a wider range of conditions.1-3
Newborn screening is optional in Australia,1 and research suggests participation is very high.4 Screening occurs two to
three days after birth, and is usually arranged by midwives. In general, parents are not contacted when screening results are
normal.
About 1-2% of babies tested require repeat or subsequent diagnostic testing. Screening programs in each state and territory
are usually responsible for following up cases that require further testing. About one per 1000 (0.1%) babies tested will be
diagnosed with a condition because of newborn screening.
Refer to Table 1 for a list of conditions currently included in newborn screening programs in Australasia.
Table 1. Conditions screened in newborn screening programs in Australasia1,3

Class Condition
Amino acids Argininaemia or arginase deficiency
Argininosuccinic aciduria
Citrullinaemia
Tyrosinaemia type 1
Homocystinuria
Maple syrup urine disease
Phenylketonuria
Pterin defects
Tyrosine aminotransferase deficiency
Organic acids Beta-ketothiolase deficiency
Cobalamin C defect
Glutaric acidaemia type I
Holocarboxylase synthetase deficiency
3-hydroxy-3-methylglutaryl-CoA lyase (HMGCoA lyase) deficiency
Isobutyryl-CoA dehydrogenase deficiency

61
Isovaleric acidaemia
Methylmalonic acidurias
Propionic acidaemia
3-methylcrotonyl-CoA carboxylase deficiency
2-methylbutyryl-CoA dehydrogenase deficiency
3-methylglutaconyl-CoA hydratase deficiency
Fatty acid oxidation Carnitine or acylcarnitine translocase deficiency
Carnitine transporter defect
Carnitine palmitoyl transferase deficiency types I and II (CPTI)
3-hydroxy long chain acyl-CoA dehydrogenase deficiency (LCHAD)
Medium chain acyl-CoA dehydrogenase deficiency (MCAD)
Multiple acyl-CoA dehydrogenase deficiency (MADD)
Short chain acyl-CoA dehydrogenase deficiency (SCAD)
Short chain hydroxy acyl-CoA dehydrogenase deficiency (SCHAD)
Trifunctional protein deficiency (TFP)
Very long chain acyl-CoA dehydrogenase deficiency (VLCAD)
Other Cystic fibrosis (CF)
Congenital hypothyroidism
Galactosaemia (not in Victoria)
In addition to the implications for a child diagnosed with an inherited condition, there are also implications for future pregnancies
in the family (ie carrier parents, siblings of the carrier parents). Information about carrier screening should be offered.
References
1. Human Genetics Society of Australasia. Policy: Newborn bloodspot testing. Sydney: HGSA, 2011. Available at www.hgsa.
org.au/documents/item/29 [Accessed 8 January 2018].
2. Howard HC, Knoppers BM, Cornel MC, et al. Whole-genome sequencing in newborn screening? A statement
on the continued importance of targeted approaches in newborn screening programmes. Eur J Hum Genet
2015;23(12):1593-600.
3. Wilcken B, Wiley V. Newborn screening. Pathology 2008;40(2):104-15.
4. Jacques AM, Collins VR, Pitt J, Halliday JL. Coverage of the Victorian newborn screening programme in 2003:
A retrospective population study. J Paed Child Health 2008;44(9):498-503.
62
Personal genomic testing: Summary

@ Practice point-------------------------------------------------------------------------------------
At this time, the clinical utility of personal genomic testing (PGT) is considered variable.1 If patients wish to pursue
testing, ensure they opt for a full-service provider that includes the need for referral by a general practitioner (GP), test
interpretation and genetic counselling support.

PGT refers to the analysis of some or all of a person’s genome. PGT is marketed for a variety of purposes, including:
• identification of susceptibility to a wide range of diseases
• carrier screening for autosomal recessive conditions

• pharmacogenomics
• nutrigenomics (ie diet, nutrition, wellness)
• fitness and sporting abilities
• ancestry
• relationship (eg paternity) testing.
PGT companies may or may not require a health professional to order the test. In situations where a referral is not required,
individuals can request a test kit online and provide a saliva or cheek swab sample to the PGT company via post. This is
referred to as ‘direct-to-consumer’ (DTC) or ‘at-home’ genetic testing.
PGT companies are mostly based overseas, but an increasing number are now based in Australia.
The cost of PGT varies according to the type of test (eg genotyping, exome sequencing, whole genome sequencing) and
how much information is provided with the results. PGT is not available under the Medicare Benefits Schedule (MBS), so
consumers incur the full cost (sometimes thousands of dollars).
PGT results may be provided with some clinical interpretation in the form of follow-up genetic counselling or a written report,
or as raw sequence data. In many situations, the consumer is left to interpret the results without clinical guidance. This can
prompt the individual to contact their GP for additional support. Referral of all such patients to public genetics services for
assistance is not practicable given the resource implications.1-3
How do I manage PGT in general practice?
Advising patients who want PGT

Patients may ask a GP to order PGT on their behalf. GPs asked to arrange PGT should consider the following:2,4
• How much does the patient understand about the test?
• What do they want to find out from the test and what will they do with that information?
• Has the patient thought about the possible impact of testing on life insurance? (Refer to ‘Ethical principles’)
• Will the company help interpret the results?
• Do you feel able to assist the patient in interpreting results?
63
Managing patients who have had PGT

Patients who have already had PGT might ask a GP for:
• help in interpreting the results
• further testing
• advice around treatment or management.
The majority of patients will have small variations in risks for a range of conditions, which will have limited clinical implications
(eg Alzheimer’s disease, MTHFR gene testing). In these circumstances, general preventive health advice is appropriate.
In a minority of patients, specific variants that put an individual at significantly increased risk of a condition (eg BRCA gene
mutations, HFE-haemochromatosis, macular degeneration) will be identified. In these situations, referral to genetics or
specialist services is appropriate.4
More information
Refer to ‘Personal genomic testing: More information’ for a detailed discussion of this topic.
References
1. Adams SD, Evans JP, Aylsworth AS. Direct-to-consumer genomic testing offers little clinical utility but appears to cause
minimal harm. NC Med J 2013;74(6):494-98.
2. Edelman E, Eng C. A practical guide to interpretation and clinical application of personal genomic screening. BMJ
2009;339:b4253.
3. Trent R. Direct-to-consumer DNA testing and the GP. Aust Fam Physician 2014;43(7):436-39. Available at
www.racgp.org.au/afp/2014/july/dna-testing [Accessed 8 January 2018].
4. Capriotti T, Kline M. What to know about home genetic-test kits. New York: Clinical Advisor, 2014. Available at
www.clinicaladvisor.com/features/what-to-know-about-home-genetic-test-kits/article/347156 [Accessed 8 January
2018].

• National Health and Medical Research Council, Direct-to-consumer (DTC) genetic testing: A statement from the National
Health and Medical Research Council, www.nhmrc.gov.au/guidelines-publications/g9
64
Personal genomic testing: More information

What is personal genomics?
With the advancement of gene sequencing technology, genetic testing is increasingly moving beyond the clinic and tertiary
medical centres, and into the community. This new form of testing is readily accessible via the internet, either through a
health practitioner or by patients themselves, and represents the new world of personal genomic testing (PGT).1
Clinical genetic testing has traditionally been used to gather information or confirm a diagnosis of a condition in an individual
showing symptoms. Testing has also been used to screen asymptomatic populations, such as carrier screening for recessive
conditions. Until recently, these genetic tests have been targeted, looking for particular gene variants (or mutations) in
specific genes. Clinical support, including genetic counselling, has generally been available to help individuals interpret and
manage genetic test results.
However, new technology (eg single nucleotide polymorphism [SNP] genotyping) can now examine thousands of gene
variants throughout a person’s genome. New sequencing technology also allows the entire sequencing of an individual
genome (whole genome sequencing) at a relatively low cost. The availability of such technology is challenging the traditional
model of genetic testing.2,3
Asymptomatic individuals now have the opportunity to access ‘direct-to-consumer’ (DTC) or ‘at-home’ testing through a
range of private providers.
Some DTC companies require a health practitioner to order a test on behalf of the consumer and take delivery of the test
results, while others do not. A test kit provided by the DTC company is used to collect a cheek swab or saliva sample and
mailed back for analysis. In some cases, results are returned to the consumer without comprehensive interpretation and/or
clinical support.
What is tested?
PGT can provide information that is health or non-health related.4 Non-health related information includes:
• physical traits (eg red hair, freckles)
• genetic relationship testing (eg paternity testing)
• ancestry.
Some tests offer information that have health-related implications to varying degrees. In some cases, the tests are the same
as those offered in regular clinical settings. Personal genomic tests might include genetic variants that:
• are strong predictors of risk for disease (eg BRCA1, familial breast and ovarian cancer)
• are limited predictors of disease (eg APO- s4, Alzheimer’s disease)
• identify carrier status for recessive conditions (eg cystic fibrosis [CF])
• can inform response to drugs (refer to ‘Pharmacogenomics: Summary’).

Some companies test for variants for other health-related information that are more uncertain, such as variants with low
penetrance, or with limited evidence to support associations with disease.3 These tests might include genetic variants that are:
• much more weakly associated with susceptibility to disease (eg complex conditions such as type 2 diabetes,
rheumatoid arthritis)
• marketed to predict sporting ability, including fitness and response to training regimens
• professed to provide information about response to diet and nutrition (nutritional genomics) or weight loss (eg MTHFR
gene testing). In Australia, these tests are advertised as ‘genomic wellness’ tests, and are increasingly available through
naturopaths and nutritionists.
How are results reported?

Companies may report estimates of risk from test results in a variety of ways, including odds ratios, percentages,
comparisons with average population risk (using a reference population) or lifetime risk. It is important to note that not all
companies use the same reference population and consumers may be a different ethnicity to the reference population.
Companies may also vary in the way they produce their estimate of risk (eg use of different algorithms). Consequently, test
results from one company may not match those from another company, even with the same deoxyribonucleic acid (DNA)
sample.
Customers are often able to download their ‘raw data’ (ie the actual variant or SNP data), which may provide health-related
information beyond what the original test results provide. This extra information often comes with no interpretation provided
to the consumer. Consumers can also upload their raw data to online databases (or to genetic testing companies) where a
further level of analysis is available. Again, this is often provided without appropriate clinical support.
Considerations with PGT
Questionable credibility
PGT companies use a combination of marketing rhetoric, and unsupported claims and research evidence to promote their
product. In many cases, there is no clinical support. The ability of these tests to accurately predict outcomes (clinical validity)
is variable. Consumers are faced with a difficult task of determining the credibility of these tests.
Regulatory landscape
The technology around PGT is changing rapidly, as is the variety of testing. Given the international reach of PGT, regulation
of the industry is challenging.
Empowered patients
There are many who support PGT as a means of empowering consumers to proactively manage their health (ie clinical and
personal utility). Others suggest individuals may be misled by information with poor clinical validity, leading to unnecessary
costs that are a burden to the consumer and health system.
Privacy and confidentiality

Information obtained by an individual can have implications for other family members, especially those who may not want to
know. Given the ease of testing, some people (eg children) may be tested without full consent.
The ownership of the data from testing is another complex issue. If a testing company changes ownership, so does the data.
Some consumers choose to share their genetic information or data (eg online) which can also allow for unintentional access
by others.
Personal utility
For many individuals, the concept of personal utility seems more relevant than the clinical utility of testing. Personal utility
includes the value of increased knowledge about oneself (where curiosity often motivates individuals wanting to be tested),
increased knowledge about the trait or condition tested, potential for anticipated coping, and altruism (eg helping research
as a motivation for testing, with opportunities for data sharing through not-for-profit websites or organisations).5,6
66
Implications for general practice

The uptake of PGT is likely to continue, and general practitioners (GPs) will increasingly encounter patients who are curious
about or have used PGT.
Some PGT companies recommend using specific practitioners (ie those they nominate who may have undertaken some
training) who will order the test on behalf of the consumer. Some of these companies may also provide genetic counsellors
who can discuss the results with the consumer.
Other companies state that the PGT reports are provided for information or educational purposes only. They may state that
the consumer should talk to their GP or other health practitioners about their results. However, practitioners themselves may
have a limited understanding of the nature of the test or its interpretation.
Involving health practitioners in the process, either in ordering tests and/or interpreting results, may have positive and
negative consequences. Some health practitioners, including GPs, may not feel confident in supporting patients to
understand their results.1,5
There is also the potential to overburden the healthcare system with subsequent inappropriate ordering of health services,
including referral to genetics services when it might not be warranted. Some genetic services no longer accept referral for
most people who have had the MTHFR gene testing, as its clinical validity and utility is questionable.
The National Health and Medical Research Council (NHMRC) has developed a PGT resource entitled ‘Understanding direct-
to-consumer (DTC) genetic DNA testing: An information resource for consumers’, available at www.nhmrc.gov.au/guidelines-
publications/g8. GPs can use this document to discuss PGT with patients who are interested in ordering a test.
Potential consumers of PGT testing should consider all aspects when they are thinking about having one of these tests and
GPs can play an important role in raising these issues with their patients.7
References
1. Brett GR, Metcalfe SA, Amor DJ, Halliday JL. An exploration of genetic health professionals’ experience with direct-to-
consumer genetic testing in their clinical practice. Eur J Hum Genet 2012;20:825-30.
2. Kalf RRJ, Mihaescu R, Kundu S, de Knijff P, Green RC, Janssens CJW. Variations in predicted risks in personal genomic
testing for common complex diseases. Genet Med 2014;16:85-91.
3. Bunnik EM, Schermer MH, Janssens AC. Personal genome testing: Test characteristics to clarify the discourse on
ethical, legal and societal issues. BMC Med Ethics 2011;12(1):11.
4. Felzmann H. ‘Just a bit of fun’: How recreational is direct-to-customer genetic testing? New Bioeth 2015;21(1):20-32.
5. Covolo L, Rubinelli S, Ceretti E, Gelatti U. Internet-based direct-to-consumer genetic testing: A systematic review. J Med
Internet Res 2015;17:e279.
6. Bunnik EM, Janssens AC, Schermer MH. Personal utility in genomic testing: Is there such a thing? J Med Ethics
2015;41(4):322-26.
7. ACMG Board of Directors. Direct-to-consumer genetic testing: A revised position statement of the American College of
Medical Genetics and Genomics. Genet Med 2016;18(2):207.
67
Pharmacogenomics: Summary
@ Practice point----------------------------------------------------------------------------------
While there are international guidelines about potential uses of pharmacogenomic testing, there is limited evidence
from randomised controlled trials of the clinical utility and cost effectiveness of using pharmacogenomics to tailor
prescribing, especially in primary care.1,2

The term ‘pharmacogenomics’ describes how common gene variants influence drug metabolism and response.
There are common variants in cytochrome P450 enzymes (CYPs) and drug receptors that influence the rate of metabolism
of many commonly prescribed drugs. Individuals are typically classified as ‘poor’, ‘intermediate’, ‘extensive’ or ‘ultrarapid’
metabolisers depending on their CYP variants. Poor and ultrarapid metabolisers may require different dosages, or be more
susceptible to adverse drug effects.3
Table 1 provides examples of drugs that may be affected by common gene variants.
Table 1. Examples of drugs affected by common gene variants1

Gene name Examples of drugs affected Clinical consequence
CYP2D6 (5-10% of Caucasians Codeine Poor metabolisers have no response to codeine; ultra-
are poor metabolisers; 1-2% metabolisers are at an increased risk of side effects
of Caucasians are ultrarapid
Selective serotonin reuptake inhibitors Ultrarapid metabolisers have no response to SSRI;
metabolisers)
(SSRIs; eg paroxetine, fluvoxamine) poor metabolisers may need 50% lower dose
CYP2C19 (poor metabolisers 2-15%) Clopidogrel Poor metabolisers may require alternative anti-platelet
VKORC1 and CYP2C9 Warfarin CYP2C9 and VKORC1 genotypes may be useful in
determining the optimal initial dose of warfarin
SLCO1B1 Simvastatin (not other statins) Low-function genotype associated with increased of
myopathy; consider alternative statin or lower dose
Genetic testing
Pharmacogenomic testing may be considered for patients with:
• significant side effects from drugs for where pharmacogenomic variation in response is known (refer to Table 1)
• poor therapeutic response to specific medications
• potential suitability for using doses outside the usual range.

Pharmacogenomic testing is not subsidised under the Medicare Benefits Schedule (MBS), but can be ordered by general
practitioners through a number of commercial providers.
More information
Refer to ‘Pharmacogenomics: More information’ for a detailed discussion of this topic.
References
1. Clinical Pharmacogenetics Implementation Consortium. CPIC guidelines. Stanford, CA: CPIC, 2014. Available at
https://cpicpgx.org [Accessed 8 January 2018].
2. Relling MV, Evans WE. Pharmacogenomics in the clinic. Nature 2015;526(7573):343.
3. Abbasi J. Getting pharmacogenomics into the clinic. JAMA 2016;316(15):1533-35.

• Centre for Genetics Education, Fact sheet 21: Pharmacogenetics/pharmacogenomics, www.genetics.edu.au/publications-
and-resources/facts-sheets/fact-sheet-21-pharmacogenomics-pharmacogenetics
• National Library of Medicine, What is pharmacogenetics?, https://ghr.nlm.nih.gov/primer/genomicresearch/
pharmacogenomics
69
Pharmacogenomics: More information

What is pharmacogenomics?
Genetic variations play a role in our ability to metabolise and respond to drugs, both in terms of efficacy and toxicity.
Pharmacogenomic testing assesses the type of response a patient may have to a particular drug. Testing before prescribing
medication can provide information about the likely effectiveness or risk of side effects for the patient.1,2
Pharmacogenetics versus pharmacogenomics

While pharmacogenetics examines the variability in response due to genetic variations in genes that metabolise drugs,
pharmacogenomics is a broader term that refers to the involvement of all genes in determining drug response. The two
terms are often used interchangeably.3-5
The ultimate goal of pharmacogenomics is the ability to target or ‘tailor’ drug therapy to individuals: being able to prescribe
the right drug at an appropriate dose to maximise efficacy and avoid adverse effects. This goal feeds into the wider concept
of personalised medicine, where an individual’s genetic profile is used to make decisions about all aspects of healthcare
(ie prevention, diagnosis, treatment).1,5
How genetic polymorphisms affect drug metabolism

Genetic variation can affect:5
• pharmacokinetics - how the drug metabolised by the body is affected by genetic variations in metabolising enzymes
• pharmacodynamics - what effect the drug has on the body is influenced by genetic variations in drug targets
(eg receptors).
Pharmacogenomics testing analyses genes involved in these two pathways.
One example is the cytochrome P450 genes, which produce enzymes involved in drug metabolism. P450 enzymes account
for 70-80% of enzymes involved in drug metabolism.5 Common variations in P450 genes can affect the function of the
enzymes produced, which in turn affects the metabolism of some drugs. For example, drugs may be metabolised too
quickly (ie higher dose needed for effect) or too slowly (ie lower dose needed for effect).
Genetic variations give rise to four different phenotypes in terms of drug response:1
• Poor metabolisers who have markedly reduced or absent enzyme activity.
• Intermediate metabolisers with reduced enzyme activity.
• Extensive (or normal) metabolisers.
• Ultrarapid metabolisers who have high enzyme activity.
Cytochrome P450 genes

Cytochorome P450 genes follow a certain naming system.6 For example, CYP2D6 is made up of the following codes:
• cytochrome P450 enzyme (CYP) - indicating it is part of the cytochrome gene family.
• 2 - a number associated with a specific group within the gene family.
• D - a letter which represents the gene subfamily.

• 6 - a number referring to the specific gene within the subfamily.
This gene can then have different forms or alleles. For example:6
• *CYP2D6
1 - allele 1 produces normal enzyme function
• *CYP2D6
4 - allele 4 produces enzyme with no activity
• 10
*CYP2D6 - allele 10 produces enzyme with decreased activity.
Codeine is a common analgesic metabolised by CYP2D6 enzymes (Figure 1).7
Codeine ^ CYP2D6 -^ morphine
70
Benefits of pharmacogenomics
The benefits of pharmacogenomic testing arise from the ability to tailor medication to the individual: specifically, to predict the
correct dose to avoid toxicity or adverse events, and to know whether a particular drug will be effective in any given patient.
The benefits of pharmacogenomics include:1,2
• achieving optimal drug doses quickly - the trial-and-error approach combined with repeated monitoring could be avoided
• minimising toxicity and adverse effects - knowledge of a patient’s genetic profile could reduce the likelihood of adverse
outcomes and help direct clinicians towards suitable alternatives
• efficacious medications - genetic variations can predict which patients are likely to respond to certain medications,
allowing clinicians to personalise treatment.
Limitations of pharmacogenomics
At present, there are several limitations of pharmacogenomic testing:1-4'9
• Cost - currently there is no Medicare Benefits Schedule (MBS) rebate for testing, therefore patients incur an
out-of-pocket cost.
• Testing turnaround time - some results can take between five and 10 working days to reach the clinician who ordered
the test. In some cases, the trial-and-error approach to dosage would be completed within this timeframe.
• Evolving science - our understanding of how genetics influences our response to drugs is incomplete. Confidence in the
clinical utility of pharmacogenomic testing is slowly growing, with some parts of the world further advanced than others.
• Lack of compelling evidence from clinical trials.
Current practice in Australia

While pharmacogenomics seem to offer the ability to improve patient care (and hence therapeutic outcomes), the clinical
adoption of pharmacogenomic interventions has been slow.
While many of the drugs commonly prescribed in general practice (eg warfarin, fluoxetine) are influenced by genetic variation,
there is currently no clear recommendation in Australia about the use of pharmacogenomic testing.
International guidelines exist about the potential use of pharmacogenomic testing;10 however, there is limited evidence from
randomised controlled trials of the clinical utility and cost effectiveness of using pharmacogenomics to tailor prescribing,
especially in primary care.1,9
71
References
1. Abbasi J. Getting pharmacogenomics into the clinic. JAMA 2016;316(15):1533-35.
2. Kapoor R, Tan-Koi WC, Teo YY. Role of pharmacogenetics in public health and clinical health care: A SWOT analysis.
Eur J Hum Genet 2016;24(12):1651-57.
3. Relling MV, Evans WE. Pharmacogenomics in the clinic. Nature 2015;526(7573):343.
4. Juli G, Juli L. Pharmacogenetics: Does a personal therapy exist? Psychiatria Danubina 2016;28(Suppl-1):141-44.
5. Trent RJ, Cheong PL, Chua EW, Kennedy MA. Progressing the utilisation of pharmacogenetics and pharmacogenomics
into clinical care. Pathology 2013;45(4):357-70.
6. Ingelman-Sundberg M (Webmaster). The Human Cytochrome P450 (CYP) Allele Nomenclature Database: Allele
nomenclature for cytochrome P450 enzymes. Undated. Available at www.PharmVar.org [Accessed 22 January 2018].
7. Kelly PA. Pharmacogenomics: Why standard codeine doses can have serious toxicities or no therapeutic effect. Oncol
Nurs Forum 2013;40(4):322.
8. PHG Foundation. Pharmacogenetics interactive tutorial. Pharmacogenomics. Cambridge, UK: PHG Foundation.
Available at www.phgfoundation.org/tutorials/pharmacogenomics [Accessed 8 January 2018].
9. Drew L. Pharmacogenetics: The right drug for you. Nature 2016;537(7619):S60-62.
10. Clinical Pharmacogenetics Implementation Consortium (CPIC). Guidelines. Stanford, CA: CPIC, undated. Available at
https://cpicpgx.org/guidelines [Accessed 8 January 2018].

• Centre for Genetics Education, Pharmacogenetics, www.genetics.edu.au/health-professionals/pharmacogenomics
• Centre for Genetics Education, Fact sheet 21: Pharmacogenetics/pharmacogenomics, www.genetics.edu.au/publications-
and-resources/facts-sheets/fact-sheet-21-pharmacogenomics-pharmacogenetics
• National Library of Medicine, What is pharmacogenetics?, https://ghr.nlm.nih.gov/primer/genomicresearch/
pharmacogenomics
Prenatal testing
@ Practice point
All pregnant women (ie regardless of age, ethnicity, family history) should be provided with information about prenatal
screening tests for chromosomal conditions such as Down syndrome. Screening options should be discussed in the
first trimester whenever possible.1,2
Prenatal screening tests should not be considered routine, but offered as a choice to women. General practitioners (GPs)
should support women and couples to make informed, independent decisions about the utility of prenatal testing and
reproductive options. Women who receive a high-risk screening result should be offered information about diagnostic testing.2
Those identified with a family history of inherited disorders should be made aware of the availability of carrier
screening for recessive conditions.1

Pre-pregnancy and pregnancy counselling that are relevant to genetics should include:1,2
• Any known genetic conditions among close family members (refer to ‘Family history’).
• History of intellectual disability (ID), multiple pregnancy loss, stillbirth, children with congenital abnormalities.
• Consanguinity (‘Is there any chance that a relative of yours might be related to someone in your partner’s family?’).
• Pre-pregnancy and pregnancy folic acid intake.
• Information about carrier screening (ideally pre-conception or early in first trimester).
All women should be provided information about prenatal screening for chromosomal conditions.1,2
While chromosomal conditions such as Down syndrome are more common in pregnancies of women who are older
(the chance of the baby having such a condition tends to increase with maternal age),3 younger women can also have
pregnancies with chromosomal conditions.
Prenatal screening information should include the following:
• Presenting the various screening options and their timing.
• An explanation of the meaning of results.
• A discussion of the potential implications of receiving a positive screening result (ie having to undergo an invasive
diagnostic test, thinking about the possibility of having a child with special needs or pregnancy termination).
Other important considerations:
• Screening tests can determine who is at increased risk of having a baby with a chromosomal condition. Women who
choose to undertake screening tests should be informed that they will be offered invasive diagnostic testing if they receive
a high-risk screening result. Individuals may choose not to proceed with diagnostic testing for a number of reasons
(eg concern about risk of miscarriage, not wishing to know prior to the birth, termination of pregnancy is not an option).
• Screening tests are non-invasive, so there is no increased risk of miscarriage from the procedure.
• Every screening test has a false positive rate: some women will receive an ‘increased risk’ result even though their baby
is unaffected.
• In the majority of pregnancies with an ‘increased risk’ screening result, the baby is unaffected. A common misconception
is that screening tests ‘show’ that the baby has Down syndrome.
• ‘Low-risk’ results do not exclude Down syndrome or other conditions.
• A second trimester ultrasound may detect some physical problems, but it is not recommended as a screening test for
Down syndrome.
• Neural tube defects and other physical conditions may also be detected with second trimester serum screening.
73
• Use of the term ‘risk’ in relation to the probability of a diagnosis of Down syndrome (or other disability) should be avoided
when discussing prenatal screening with patients because it implies a negative consequence, and can cause offense. The
recommended terminology is ‘chance’ or ‘probability’.
Genetic testing
Combined first trimester screening
Combined first trimester screening (CFTS) adds different measures together to provide a risk estimate for Down syndrome
(trisomy 21), Edwards syndrome (trisomy 18) and Patau syndrome (trisomy 13).
These measures are as follows:
• Maternal blood to measure pregnancy-associated plasma protein A (PAPP-A) and free 0-subunit of human chorionic
gonadotrophin (13-hCG). Levels of these proteins vary, but tend to be different in women carrying fetuses with Down
syndrome or trisomy 18. Increased free 0-hCG with decreased PAPP-A is suggestive of Down syndrome, while decreased
levels of both analytes is suggestive of trisomy 18.
• A nuchal translucency (NT) screening ultrasound.
• Maternal age, weight and gestation age.
• In some cases, an additional measurement called the nasal bone is included (presence or absence of nasal bone on ultrasound).
Approximately 5% of CFTS tests give an increased risk result. This figure varies depending on maternal age. Women with
an increased risk result should be offered a diagnostic test. The majority of increased risk results are not due to Down
syndrome, and most of these babies will be healthy.
There is a partial Medicare Benefits Schedule (MBS) rebate for the blood test component of CFTS; however, there are
out-of-pocket expenses for the ultrasound.7
Second trimester maternal serum screening

Second trimester maternal serum screening uses a blood test in conjunction with maternal age and weight, and gestational
age to calculate a risk estimate of the chance a pregnancy is affected by Down syndrome, Edwards syndrome or neural tube
defects (eg spina bifida).
Second trimester maternal serum screening is for women presenting late in pregnancy. The optimal time to have this test
performed is between 15 and 17 weeks, but it can be performed until 20 weeks.
In some cases, there is no out-of-pocket cost for second trimester screening (ie public patient in a public hospital).
Non-invasive prenatal testing or screening

Non-invasive prenatal testing (NIPT; also called non-invasive prenatal screening [NIPS], cell-free DNA [cfDNA] testing)
analyses cell-free fetal deoxyribonucleic acid (DNA) found circulating in maternal blood. Testing is usually available anytime
from 10 weeks’ gestation. This test analyses the relative proportion of DNA fragments from different chromosomes. If the
proportion of fragments from a specific chromosome is increased, then trisomy is suspected.
NIPT is the most accurate screening test available for detecting Down syndrome. Most available NIPT results will provide
a risk estimate for trisomies 21, 18 and 13, and sex chromosome aneuploidies (eg monosomy X). Some also provide
information about microdeletion syndromes, fetal sex and other autosomal trisomies.
While the accuracy of NIPT in identifying Down syndrome is very high, the accuracy is not as high for Edwards syndrome
and Patau syndrome. The accuracy of NIPT is also influenced by the age of the woman and prevalence of the particular
condition. For example, the positive predictive value (PPV) will be lower in younger women where the prevalence of
chromosome aneuploidies is lower.
NIPT does not screen for:
• all chromosome aneuploidies
• single-gene disorders
• neural tube defects.
It is crucial to perform a 12-week ultrasound alongside, as NIPT is not diagnostic. High-risk results should be confirmed
through diagnostic testing. False positive results are possible, and rates vary according to condition.
In some cases, NIPT can be performed as a second-tier screening test before progressing to chorionic villus sampling (CVS)
or amniocentesis. Given the higher test sensitivity, a negative NIPT result can reduce the need for CVS or amniocentesis.
Currently, NIPT is not available through the MBS or covered by private health insurance.
Figure 1. Summary of prenatal screening tests4

Screening tests *
Diagnostic procedures
Combined first trimester Second trimester Non-invasive prenatal Chorionic villus sampling
screening (CFTS) serum screening testing (NIPT) (CVS); amniocentesis
Type of test Blood test (maternal); ultrasound Blood test (maternal) Blood test (maternal) Needle aspirate of
placenta or amniotic fluid
Analytes Nuchal translucency, pregnancy- Estriol, Plasma cell-free DNA Fetal cells
associated plasma protein A beta-HCG,
(PAPP-A), B-subunit of human alphafetoprotein,
chorionic gonadotrophin (B-hCG) inhibin A
Timing of test Blood and ultrasound 11-13 15-20 weeks From 10 weeks CVS 11-13 weeks
(weeks) weeks Amniocentesis >15 weeks
Conditions Trisomies 21, 18, 13; structural Trisomies 21 and 18; Trisomies 21, 18, 13; sex Many chromosome and
detected anomalies neural tube defects chromosome conditions
* genetic conditions
Detection rate for 90% 75-80% 99% 99.9%

trisomy 21
False positive rate 3-5% 7-8% <1% <1%t

for trisomy 21
Test failure rate <1% <1% 1-5% <1%
Risk to pregnancy None None None Small risk of miscarriage

(<1%)
*Though not highly accurate and can be confounded by underlying maternal and fetal factors.1
+Diagnostic tests performed using fetal cells collected by diagnostic procedures include fluorescence in situ hybridisation (FISH), quantitative
fluorescence polymerase chain reaction (QF-PCR), karyotype, and chromosome microarray (CMA).
Adapted from Murdoch Childrens Research Institute. Your choice - Prenatal screening tests in pregnancy. Melbourne: Murdoch Childrens Research
Institute, 2017. Available at www.mcri.edu.au/prenatal-screening

The following people should be offered referral to specialist services (genetics or obstetrics):
• Couples who are known carriers of a genetic condition. Such couples could access pre-implantation genetic diagnosis
through in-vitro fertilisation (IVF) for future pregnancies.
• Women with an increased probability of a pregnancy with a chromosomal condition
- previous pregnancy with a chromosomal condition
- positive screening test or diagnostic test
- parent with chromosomal rearrangement (eg balanced translocation).
• Women with confirmed abnormality from diagnostic testing.
References
1. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists. Prenatal screening and diagnosis
of chromosomal and genetic conditions in the fetus in pregnancy (C-Obs 59).Melbourne: RANZCOG, 2015. Available at
www.ranzcog.edu.au/Statements-Guidelines [Accessed 8 January 2018].
Melbourne: RACGP, 2016. Available at www.racgp.org.au/your-practice/guidelines/redbook [Accessed 8 January 2018].
75
3. Loane M, Morris JK, Addor MC, et al. Twenty-year trends in the prevalence of Down syndrome and other trisomies in
Europe: Impact of maternal age and prenatal screening. Eur J Hum Genet 2013;21(1):27.
4. Murdoch Childrens Research Institute. Your choice - Prenatal screening tests in pregnancy. Melbourne: MCRI, 2017.
Available at www.mcri.edu.au/prenatal-screening [Accessed 8 January 2018].

• Centre for Genetics Education and The Royal Australian College of General Practitioners, First trimester screening in general
practice, www.genetics.edu.au/health-professionals/online-learning/first-trimester-learning-module

• Better Health Channel, Pregnancy - Prenatal tests, www.betterhealth.vic.gov.au/health/healthyliving/pregnancy-prenatal-tests
• Centre for Genetics Education, Fact sheet 24: Prenatal testing overview, www.genetics.edu.au/publications-and-resources/
facts-sheets/fact-sheet-24-prenatal-testing-overview
• Centre for Genetics Education, Fact sheet 25: Screening tests during pregnancy, www.genetics.edu.au/publications-and-
resources/facts-sheets/fact-sheet-25-screening-tests-during-pregnancy
• Centre for Genetics Education, Prenatal testing: Special tests for your baby during pregnancy - Includes NIPT,
www.genetics.edu.au/publications-and-resources/booklets-and-pamphlets/prenatal-testing-special-tests-for-your-baby-
during-pregnancy
76
Reproductive carrier screening

@ Practice point-------------------------------------------------------------------------------------
All women or couples planning a pregnancy, or who are already pregnant, should have a comprehensive family history
recorded.1
Women or couples who are known carriers of a genetic condition or have a relevant family history should be made
aware of the availability of carrier screening and offered referral to specialist services (ie genetics or obstetrics).1
Information on carrier screening for the more common genetic conditions that affect children (eg cystic fibrosis
[CF], spinal muscular atrophy [SMA], fragile X syndrome [FXS]) should be offered to low-risk women and couples (ie
regardless of family history and ethnicity).
The decision to have screening is a personal choice to be made by the individual or couple.

Reproductive carrier screening is used to identify carriers of genetic conditions with an autosomal recessive inheritance or
X-linked inheritance pattern.
Information about carrier screening should be offered to all women or couples during pre-conception and early in the
pregnancy (ie first trimester). Identifying carrier couples before pregnancy provides greater reproductive options. For example:
• in-vitro fertilisation (IVF) with pre-implantation genetic diagnosis

• use of donor gametes
• prenatal diagnostic testing.
Traditionally, reproductive carrier screening for inherited recessive conditions was offered on the basis of ethnicity. However,
this is known to lead to significant under-identification of carrier couples. Given the multicultural nature of society and
marriage between people of different ethnic backgrounds, ethnicity is poorly predictive of carrier frequency in Australia.
The decision to undertake carrier screening is a personal choice to be made by the individual or couple. Women or couples
should be informed of the benefits, limitations and cost of screening. Ideally, this information is provided pre-pregnancy.1
Genetic testing
A number of pathology services offer carrier screening, which can be ordered through general practice. However, carrier
screening is not available through the Medicare Benefits Schedule (MBS). Depending on the test provider:
• screening may look for a limited number of conditions (eg CF, Fragile X syndrome [FXS], spinal muscular atrophy) or
screen for an expanded range of conditions (ie >100)
• genetic counselling may or may not be available.
Note: Carriers of haemoglobinopathies may be initially identified through a routine full blood examination (FBE).
Mackenzie’s Mission, a national research project funded by the Federal Government, will commence in late 2019.
It aims to identify how reproductive carrier screening for an expanded range of conditions can best be made available
to Australian couples who want it.

Couples identified as carriers of a genetic condition should be offered referral to specialist services (ie genetics or obstetrics).
Carrier screening needs to occur in a timely manner to provide women or couples with reproductive options. The testing of
biological male partners of pregnant female carriers is of particular importance.
77
References
1. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists. Prenatal screening and diagnostic
testing for fetal chromosomal and genetic conditions (C-Obs 59). Melbourne: RANZCOG, 2018. Available at www.ranzcog.
edu.au/Statements-Guidelines [accessed November 2018].

• Henneman L, Borry P, Chokoshvili D, et al. Responsible implementation of expanded carrier screening. Eur J Hum Genet
2016;24(6):e1-e12.
• The Royal Australian College of General Practitioners, Guidelines for preventive activities in general practice, www.racgp.
org.au/your-practice/guidelines/redbook
• The Royal Australian College of General Practitioners, Beware the Rare, education activity and other resources for GPs
about paediatric neuromuscular disorders and carrier screening, https://bewaretherare.com.au
Information
• Cystic Fibrosis Community Care, Cystic fibrosis carrier screening, www.cysticfibrosis.org.au/vic/carrier-screening
Support
• Spinal Muscular Atrophy (SMA) Australia, https://smaaustralia.org.au
• The Fragile X Association of Australia, https://fragilex.org.au
Healthy Profession
Healthy Australia.
PROFESSIONAL
BEACH program update

Helena Britt, Graeme Miller
Background eneral practitioners (GPs) are the 10,300 individual GPs. The participating
The Bettering the Evaluation and Care of

Health (BEACH) program, a continuous
national study of general practice clinical
G gatekeepers to our healthcare
system and provide the majority
million residents in Australia.1 In 2013-14,

GPs receive audit points towards their
continuing professional development
of health services to the estimated 23.3 program and an individual can be selected
and approached only once in each program
activity, is now in its 18th year. In March government expenditure on general triennium.
2015 the database included details of
practice (including practice nurse) services The aims of the BEACH program are to:
almost 1.7 million encounters from 16,639
was $6.4 billion.2 • provide a reliable and valid data
participants, representing about 10,300
In April 2013 to March 2014 about collection process for general practice
individual general practitioners (GPs).
85% of the population had one or more that is responsive to the ever-changing
Medicare-paid GP service (personal needs of information users, and
Objectives
communication, Department of Health provides insight into the evolving
This paper summarises the BEACH [DoH], August 2014) and an average of character of GP-patient encounters in
methods, the uses to which the data 6.8 services each (5.8 GP visits per head Australia
supplied by participating GPs are put of population). Medicare paid rebates for • assess patient risk factors and health
and the many publications resulting from about 133.4 million GP service items3 - states, and the relationship between
the program, with an indication of how 2.57 million GP-patient encounters per these factors and health service
these can be accessed by readers. week. activity.4
Medicare statistics provide information
Discussion about frequency and cost of claimed Methods
BEACH is the only continuous nationally GP visits. The Pharmaceutical Benefits Detailed methods are published
representative study of general practice Scheme (PBS) provides information about elsewhere.4 In summary, each year
in the world that provides direct linkage government-subsidised prescriptions approximately 1000 randomly sampled,
of GP management actions to the filled, but not what problems the recognised GPs (including registrars)
problem being managed. This paper medications were prescribed for. By answer a questionnaire about themselves
provides the reference point for the contrast, the Bettering the Evaluation and their practice, and each records on
coming series of more specific articles and Care of Health (BEACH) program structured paper recording forms the
associated with the theme of each tells us about the content of GP-patient content of 100 consecutive GP-patient
edition of Australian Family Physician. consultations, the problems GPs managed encounters with consenting patients.
and the treatments they provide for each Details collected include encounter
problem. type, patient demographics and their
BEACH, a continuous, cross-sectional reason(s) for encounter (RFEs), problems
national study, began in April 1998 managed (up to 4) and, for each problem,
and is now in its 18th year. In March medications (prescribed, advised,
2015 the database included details of and supplied), clinical treatments and
almost 1.7 million encounters from procedures, pathology and imaging
16,639 participants, representing about ordered, and new referrals made.

PROFESSIONAL BEACH PROGRAM UPDATE
Data collection is evenly distributed across cluster. We use statistical procedures in being managed, a structure built into the
50 weeks, with 2 weeks closure over SAS version 9.47 to calculate and adjust recording form. Yet most EHRs lack a
Christmas. for the intracluster correlation created by problem-oriented structure that enforces
GPs eligible for random sampling from these similarities. this linkage. There are also no standards
Medicare claims data are those who for data field names and definitions,
claimed at least 375 GP Medicare items Confidentiality terminologies and classifications,8 so
of service in the previous quarter (to The privacy of both the GP and the drawing reliable data from multiple EHR
ensure recent active practice). Samples patient is ensured. Returned, completed systems is fraught with difficulties.9
are regularly drawn by the Australian research packs are only identified by a
Government Department of Health. Each GP participant number, and this identifier Dissemination of results
year about 33% of contactable GPs then remains throughout the program. BEACH allows us to measure changes
agree to participate, of whom about 80% We only link back to the GP name and over time. A recent publication10 showed
complete. address in order to send each GP an that, compared with 2004-05, in 2013-14:
We use statistical weights to adjust individual report of their results, which are • The average length of claimable
for any difference (no matter how small) compared with the national average and consultations was almost a minute
between the age-sex distribution of with results of nine other unidentified GPs longer so, nationally, GPs spent an extra
the final sample and that of all GPs in who participated at the same time. The 10 million hours in face-to-face clinical
the sample frame, and for the activity age group, sex, and rurality of the nine time.
level of each participant according to comparator GPs are provided to facilitate • The number of problems managed at
their number of Medicare claims in the comparison of results by the individual consultations had increased, so GPs
previous year. The age-sex distribution of GPs. Names of participants are never managed an additional 68 million health
patients at BEACH-sampled encounters released and data are always grouped in problems at encounters across the
for which a Medicare item was claimed is analysed reports. We have no identifying country.
repeatedly shown to accurately represent information for individual patients and • Management of these problems
the age-sex distribution of patients at all data are never released with birth dates or involved 10 million more procedures and
consultations claimed from Medicare.4 residential postcodes. 12 million more clinical treatments, such
All RFEs, problems managed, clinical as counselling and advice.
and procedural treatments, referrals and Ethics approval There have been 37 BEACH books
investigations are classified by trained The BEACH program and SAND sub published, all available for free electronic
coders according to the International studies are approved by the Human download or hard copy purchase.
Classification of Primary Care, Version 2 Research Ethics Committee of the Each year we publish two books, one
(ICPC-2).5 Pharmaceuticals are classified University of Sydney (ethics protocol Ref. describing GP clinical activity in the most
to the Anatomical Therapeutic Chemical No. 11428, valid until 31 March 2018). recent year,4 and another that identifies
(ATC) Classification (World Health changes over the previous decade in GPs,
Organization).6 Discussion their practices and their clinical work, and
Throughout the program, we conduct The reliability of BEACH is clearly provides comparative results for each
a series of Supplementary Analyses of demonstrated by the consistency of results year.11
Nominated Data (SAND) sub-studies. over time where no change is anticipated, There are also some special reports
In these patient-based studies, the GP and the measured change in practice found investigating differences in practice by
acts as an ‘expert interviewer’ to answer, where it is expected as a result of changes rurality12 and by state/territory,13 which
in discussion with the patient, specific in policy and guidelines, new evidence or a could well be repeated since they are
questions about aspects of the patient’s new pharmacological product. over a decade old, but the limited funding
health. Many GPs ask why we do not extract available for BEACH precludes preparation
these data from their electronic health of reports on many topics of interest,
Statistical methods records (EHRs). In 2013-14, BEACH including these. More recent special
BEACH has a single-stage cluster sample estimated 96% of practising GPs used reports include changes in practice after
study design, the GP being the sampling a computer for some clinical purpose, policy changes in national health priority
unit. The patients and encounters (the but many for selected purposes only areas14 and reports on pathology15 and
subject of interest) form a ‘cluster’ around (eg prescribing, pathology ordering). imaging ordering16 in comparison with
each participating GP. Each GP attracts a Further, the major advantage of BEACH guidelines.
particular patient mix, so there are always over other GP studies is the linkage of Reflecting the great breadth of general
some similarities within the sampled all management actions to the problem practice, we have published on a wide

BEACH PROGRAM UPDATE PROFESSIONAL
range of topics, (refer to ’Publications’ analyses to feed into PBS medication Prescribing Service Ltd (2005-09, 2012-13);
Novartis Pharmaceuticals Australia Pty Ltd (2009
on our website). Many readers will have reviews, quality use of pathology and
14); Pfizer Australia (2003-13); Roche Products Pty
seen the brief BEACH articles reflecting imaging programs, Medicare item Ltd(1998-2006); Sanofi-Aventis Australia Pty Ltd
the theme of each edition of Australian reviews and planning, Aboriginal and (2006-12); Wyeth Australia Pty Ltd (2008-2010).
Some financial support for the program was also
Family Physician since July 2003. Some Torres Strait Islander health reports and provided by: Aventis Pharma Pty Ltd (1998-2002);
current SAND sub-studies follow earlier many other areas. State governments Australian Government Department of Veterans’
Affairs (1998-2000, 2004-14); Bayer Australia
BEACH work, including prevalence of seek information on geographic areas of
Ltd (2010-11); National Occupational Health and
chronic diseases17,18 and multimorbidity,19,20 health concern. Safety Commission (1998-2000) and The Office of
and patient adverse drug events in the A limitation of BEACH is its cross the Australian Safety and Compensation Council;
Department of Employment and Workplace
previous 6 months.21,22 Other published sectional nature, which does not provide Relations (2004-06).
topics include (among many) future an understanding of the longitudinal
workforce needs,23 management of type 2 outcomes of patient care. However, it References
diabetes24 and low back pain,25 and patient 1. Australian Bureau of Statistics. Australian
remains the only continuous, randomised
demographic statistics: December quarter
home glucose monitoring.26 study of general practice activity in the 2013. Cat. no. 3101.0. Canberra: ABS, 2014.
We also use the BEACH data to world, and the only national program that Available at www.ausstats.abs.gov.au/Ausstats/
subscriber.nsf/0/E1FFDD84F70BC5C0CA257CF-
comment on policy matters. For example, provides direct linkage of all management B0014E932/$File/31010_dec%202013.pdf
when general practice was being actions to the problem. It fills many [Accessed 8 August 2014].
constantly referred to in the media as 2. Australian Government Department of Health.
people from other countries with envy
Annual Medicare Statistics - Financial Year
‘6-minute medicine’, we showed clearly because in Australia we can describe 2007-08 to 2013-14 (Table 1.1 BTOS Summary).
from BEACH that although consultations the activities of GPs, define their ever Canberra: Commonwealth of Australia, 2014.
of 6 minutes or less accounted for 10% Available at www.health.gov.au/internet/main/
changing contribution to healthcare, publishing.nsf/Content/34A89144DB4185ED-
of all timed consultations they only used draw attention to areas that could be CA257BF0001AFE29/$File/MBS%20Statis-
3.3% of GP face-to-face clinical time. tics%20Financial%20Year%202013-14%20ex-
improved and provide an understanding
ternal%2020140718.pdf [Accessed 17 October
Using BEACH data, we also recently of the health status and needs of the vast 2014].
contributed to the debate on the majority of the community who rely so 3. Australian Government Department of Health.
Medicare Benefits Schedule (MBS) freeze Quarterly Medicare Statistics - March Quarter
much on GPs’ care. 2007 to June Quarter 2014. Canberra: DoH,
and proposed patient co-payments.27 We 2014. Available at www.health.gov.au/internet/
estimated the likely additional patient Authors main/publishing.nsf/Content/Quarterly-Medi-
Helena Britt BA, PhD, Associate Professor and care-Statistics [Accessed 17 October 2014].
costs that co-payments would generate
Director, Family Medicine Research Centre, 4. Britt H, Miller GC, Henderson J, et al. General
and showed they would be higher University of Sydney, Parramatta, NSW. helena. practice activity in Australia 2013-14. General
than suggested in the media. We have britt@sydney.edu.au practice series no. 36. Sydney: Sydney Universi
Graeme Miller MBBS, PhD, FRACGP, Associate ty Press, 2014.
critiqued published papers describing
Professor and Medical Director, Family Medicine 5. Classification Committee of the World Organi
‘what GPs do’ based on analyses of Research Centre, University of Sydney, Parramatta, zation of Family Doctors. ICPC-2: International
Medicare or PBS claims data, and have NSW Classification of Primary Care. 2nd edn. Oxford:
Oxford University Press, 1998.
shown some published conclusions Competing interests: Helena Britt and Graeme
Miller have received a competitive grant from 6. World Health Organization Collaborating Centre
to be incorrect on the basis of what DoH and have research agreements with multiple for Drug Statistics Methodology. Anatomical
Therapeutic Chemical (ATC) classification index
BEACH tells us about the measured organisations, including AstraZeneca, the
Department of Veterans’ Affairs, bioCSL, Abbivie, with Defined Daily Doses (DDDs). January 1998
behaviour. These ‘Bytes from BEACH’, edn. Oslo: WHO, 1997.
Novartis and others. All research agreements
can be accessed at http://sydney.edu.au/ are at ‘arms length’, with no external control on 7. SAS proprietary software release 9.3. Cary: SAS
research Institute Inc, 2011.
medicine/fmrc/beach/bytes/index.php.
or publications. 8. Britt HC, Miller GC. The Bettering the Evaluation
Abstracts for all SAND sub-studies can and Care of Health (BEACH) program: where to
Provenance and peer review: Commissioned,
also be accessed online (http://sydney. from here? Med J Aust 2013;198:125-26.
9. Liaw ST, Taggart J, Yu H, de LS. Data extraction
edu.au/medicine/fmrc/publications/sand- from electronic health records - existing tools
abstracts/keyword-list.php). Acknowledgements may be unreliable and potentially unsafe. Aust
The authors thank the GP participants in the Fam Physician 2013;42:820-23.
We provide reports on specific
BEACH program and all members of the BEACH 10. Britt H, Harrison C, Bayram C, Miller G, Hender
topics in response to requests from team. Major financial contributors to BEACH son J, Gordon J. Medicare spending on general
professional bodies, pharmaceutical 1998-2014: practice is value for money. The Conversation,
Australian Government Department of Health 2014. Available at http://theconversation.com/
companies (particularly to inform their
(1998-2004, 2007-2014); Abbott Australasia Pty medicare-spending-on-general-practice-is-value-
applications for PBS listing), health Ltd (2006-2010); AstraZeneca Pty Ltd (Australia) for-money-33948 [Accessed 11 November 2014].
economists, educators, postgraduate (1998-2014); bioCSL (Australia) Pty Ltd (2010-14); 11. Britt H, Miller GC, Henderson J, et al. A decade
GlaxoSmithKline Australia Pty Ltd (2010-12); of Australian general practice activity 2004-05 to
research students and other researchers. Janssen-Cilag Pty Ltd (2000-10); Merck, Sharp and 2013-14. General practice series no. 37. Sydney:
Government committees request Dohme (Australia) Pty Ltd (2002-2013); National Sydney University Press, 2014.

PROFESSIONAL BEACH PROGRAM UPDATE
12. Knox S, Britt H, Pan Y, et al. Locality matters: 16. Britt H, Miller GC, Valenti L, et al. Evaluation 23. Harrison C, Britt H. General practice - workforce
The influence of geography on general practice of imaging ordering by general practitioners in gaps now and in 2020. Aust Fam Physician
activity in Australia 1998-2004. General Practice Australia 2002-03 to 2011-12. General practice 2011;40:12-15.
Series No. 17. AIHW Cat. no. GEP 17. Canberra: series no. 35. Sydney: The University of Sydney, 24. Britt H, Miller GC, Henderson J, et al. General
AIHW, 2005. 2014. practice activity in Australia 2012-13. General
13. Britt H, Miller GC, Knox S, et al. General 17. Knox SA, Harrison CM, Britt HC, Henderson JV. practice series no. 33. Sydney: Sydney Universi
practice activity in the states and territories of Estimating prevalence of common chronic mor ty Press, 2013.
Australia 1998-2003. General practice series no. bidities in Australia. Med J Aust 2008;189:66-70. 25. Williams CM, Maher CG, Hancock MJ, et al.
15. AIHW Cat. no. GEP 15. Canberra: AIHW, 18. Harrison C, Britt H, Miller G, Henderson J. Prev Low back pain and best practice care: A survey
2004. alence of chronic conditions in Australia. PLoS of general practice physicians. Arch Intern Med
14. Britt H, Miller GC, editors. General practice in One 2013;8:e67494. 2010;170:271-77.
Australia, health priorities and policies 1998 to 26. Henderson J, Valenti L, Bayram C, Miller GC.
19. Britt HC, Harrison CM, Miller GC, Knox SA.
2008. General practice series no. 24. AIHW Cat. Self-monitoring of blood glucose by patients
Prevalence and patterns of multimorbidity in
no. GEP 24. Canberra: AIHW, 2009. with non-insulin treated type 2 diabetes in
Australia. Med J Aust 2008;189:72-77.
15. Bayram C, Britt H, Miller G, Valenti L. Evi Australian general practice. Aust Fam Physician
20. Harrison C, Britt H, Miller G, Henderson J.
dence-practice gap in GP pathology test order 2013;42:646-50.
Examining different measures of multimorbid
ing: a comparison of BEACH pathology data and 27. Harrison C, Bayram C, Miller GC, Britt HC. The
ity, using a large prospective cross-sectional
recommended testing. Sydney: The University cost of freezing general practice. Med J Aust
study in Australian general practice. BMJ Open
of Sydney, 2009. Available at www.health.gov. 2015;202:313-16.
2014;4:e004694.
au/internet/publications/publishing.nsf/Content/
QUPP-integrated-analysis-of-quality-use-of-pa- 21. Miller GC, Valenti L, Britt H, Bayram C. Drugs
thology-program-final-reports-toc~Promot- causing adverse events in patients aged 45 or
ing-Evidence-Based-Practice~Evidence-Prac- older: a randomised survey of Australian general
tice-Gap-in-GP-Pathology-Test-Ordering-A-Com- practice patients. BMJ Open 2013;3:e003701.
parison-of-BEACH-Pathology-Data-and-Recom- 22. Miller GC, Britt HC, Valenti L. Adverse drug
mended-Testing-2009 [Accessed 17 October events in general practice patients in Australia.
2014]. Med J Aust 2006;184:321-24. correspondence afp@racgp.org.au

ÍRACGP
Emergency management
of hyperglycaemia in
Australian Diabetes Society primary care
RACGP and ADS joint clinical position statement
Working group members

The Royal Australian College of General Practitioners (RACGP)
Dr Gary Deed (Co-chair)
Dr Jo-Anne Manski-Nankervis
Dr John Barlow
Australian Diabetes Society (ADS)
Professor Sophia Zoungas (Co-chair)
Associate Professor Sof Andrikopoulos
Professor Liz Davis
Dr Sarah Price
Professor Jonathan Shaw
Professor Stephen Twigg

Position statement: Management of hyperglycaemic
emergencies
Hyperglycaemic emergencies require urgent assessment and management to reduce preventable morbidity and
mortality. Hyperglycaemic emergencies may occur as the first presentation of diabetes (undiagnosed), as well as
an acute metabolic decompensation in those already diagnosed with diabetes. Identification of at-risk patients,
together with access to point-of-care checking, can reduce delays to hospital presentation.
The objectives of this position statement are to:
• Raise clinical awareness of hyperglycaemic emergencies by identifying clinically important patient presentations
and risk factors.
• Ensure management of hyperglycaemic emergencies is optimised to prevent serious adverse outcomes.

• Provide action flow charts to inform management of hyperglycaemic emergencies before patients arrive
at hospital.
Context
This document should be read in conjunction with the relevant management flow charts (Figures 1 and 2), which
provide information for the management of hyperglycaemic emergencies in primary care.
This position statement should integrate with, but not replace, existing sick day, ambulance and hospital-based
management protocols.1-4 Clinicians should consult existing local/regional or health pathways/protocols for
inpatient management. For specific information for the management of diabetic ketoacidosis and hyperosmolar
hyperglycaemia, visit the National evidence-based clinical care guidelines for type 1 diabetes in children,
adolescents and adults or the Therapeutic Guidelines. This statement does not replace existing diagnostic
guidelines for routine (non-emergency) presentations, and should not be used for evaluating hyperglycaemia
associated with pregnancy where specialist advice on assessment and management must be sought.
Clinical presentations for hyperglycaemic emergencies

Recognition of hyperglycaemic emergencies in primary care is imperative to facilitate timely management.
• In people not known to have diabetes:
- Undiagnosed diabetes can lead to hyperglycaemic emergencies at all ages.
- Symptoms and signs, especially polyuria, polydipsia and/or weight loss (Boxes 1 and 2), particularly in
children and young adults, should prompt urgent point-of-care capillary blood glucose checking. Refer to the
management flow chart in Figure 1 for further action required.
• In people with an existing diagnosis of diabetes:
- Symptoms and signs described in Boxes 1 and 2 found in the patient with an acute illness and/or persistent
hyperglycaemia (defined as capillary blood glucose >15 mmol/L for greater than 8-12 hours, monitored every
two hours)4 should be considered a potential hyperglycaemic emergency (unless clinical discretion suggests
otherwise), and the management flow chart in Figure 2 should be referred to for further action.
- A high index of suspicion of a hyperglycaemic emergency is required in patients who are pregnant and in
those who use sodium glucose co-transporter 2 inhibitors (SGLT2i), as diabetic ketoacidosis (DKA) may occur
without hyperglycaemia.
Emergency management of hyperglycaemia in primary care 2

There are two main hyperglycaemic emergencies.
1. Diabetic ketoacidosis
• DKA is an acute, life-threatening emergency characterised by hyperglycaemia and acidosis that most commonly
occurs in people with type 1 diabetes. DKA can be the presenting feature of type 1 diabetes, especially in
younger children, but can also occur in type 2 diabetes.
People with DKA can deteriorate very quickly and develop an altered state of consciousness. Symptoms
suggestive of emerging metabolic crisis with DKA are shown in Box 1.
Suspected DKA is an emergency; transfer to an appropriate treating facility/hospital should not be delayed.
• Euglycaemic ketoacidosis refers to ketosis and acidosis in the presence of normal blood glucose levels (or
minor elevations of blood glucose levels) in symptomatic patients. This rare condition is more likely to occur in
patients with type 1 or type 2 diabetes who are pregnant, patients on a low-carbohydrate diet or using SGLT2i,
or patients who have just undergone surgery.
Box 1. Symptoms suggestive of emerging metabolic crisis associated with DKA2
Symptoms Signs
Polyuria/polydipsia/thirst Altered conscious state
Nausea/vomiting Kussmaul breathing, rapid respiratory rate
Abdominal pain Ketotic breath - smells like acetone
Weight loss *
Dehydration
*Clinical signs of dehydration include poor skin turgor, tachycardia, hypotension, dry mouth and tongue, oliguria or anuria. Atypical
symptoms (eg pain, fever) related to the aetiology, such as sepsis, may be present. Resources to assist in assessing dehydration in
children5 and adults6,7 are provided in the reference list.
2. Hyperosmolar hyperglycaemic states

Hyperosmolar hyperglycaemic states (HHS) refer to severe persistent hyperglycaemia, in the absence of
ketosis, and accompanied by profound dehydration. HHS is more common in type 2 diabetes in the presence
of acute sepsis (eg urinary tract infection, pneumonia), after a cardiovascular event (myocardial ischaemia or stroke)
or in people with renal dysfunction. HHS usually affects older people. Coma may develop in some patients and
neurological impairment is common.8 Mortality in HHS is higher than in DKA and relates to the precipitating cause.
Symptoms suggestive of emerging metabolic crisis with HHS are shown in Box 2. While metabolic acidosis present
in a person with HHS will usually be due to a lactic acidosis related to the precipitant and to any renal impairment,
HHS may sometimes occur with DKA in a mixed clinical picture of ketoacidosis and a hyperosmolar state.
Box 2. Symptoms suggestive of emerging metabolic crisis associated with HHS9
Symptoms Signs
May have atypical symptoms (eg pain, fever) Altered state of consciousness
associated with aetiology
Dry mouth/thirst/reduced urination Dehydration
* (may be extreme in HHS)
*Clinical signs of dehydration include decreased skin turgor, tachycardia, hypotension, oliguria or anuria. Resources to assist in assessing
dehydration in children5 and adults6,7 are provided in the reference list.

Comorbidities and conditions associated with an increased risk of hyperglycaemic emergencies are summarised
in Box 3. These include children and young people with known type 1 diabetes, users of insulin pumps and
medications including corticosteroids, atypical antipsychotics and SGLT2i medication.
Box 3. Factors associated with an increased risk of hyperglycaemic emergencies
• Children and young people with known type 1 diabetes
• Unstable glycaemic control
• Diabetes medication omission - especially insulin
• Use of an insulin pump - as only rapid-acting insulin is administered by pumps (no long-acting insulin is
used), any interruption to use of the pump can rapidly lead to hyperglycaemia and DKA
• Past DKA
• Acute infection and sepsis
• Pancreatitis
• Myocardial infarction/unstable angina
• Trauma, surgery or burns
• Medications - corticosteroids, atypical antipsychotics, immunosuppressive agents, SGLT2i
• Alcohol and recreational drugs
• In elderly people - signs of DKA may be subtle, mortality rates may be higher10 and type 1 diabetes can
present at any age
• Pregnancy
\__________________________________________________________________________ )
Clinical assessment
Clinical assessment of the patient should include temperature, blood pressure, heart rate, respiratory rate, Glasgow
Coma Scale and urgent point-of-care assessment.
Measurement of both blood glucose and blood ketone levels is critical in the assessment of potential
hyperglycaemic crises. It is the opinion of this working group that primary care practices should apply best
practice standards of care and ensure they have access to point-of-care capillary blood glucose and ketone
monitoring meters and strips. This access is particularly important because of the significant risks identified in the
management of these clinical presentations in primary care.
Preferred:
• Capillary (finger prick) blood glucose level (critical level >15 mmol/L)
• Capillary blood ketones (betahydroxybutyrate) (critical level >1.5 mmol/L)
Less preferred:
• Urine ketones (acetoacetate) (critical level 1+)
• Urine dipstick measurement may be used when blood ketone test strips are unavailable
• Urine ketone tests may be misleading when using SGLT2i agents, so blood ketone checking is
preferred11-13 (for a comparison between urine and capillary ketone measurement, refer to reference 13)
• Dehydration may preclude urine testing. If capillary blood glucose is >15 mmol/L and the person is
symptomatic as per information in Boxes 1 or 2, urgent consultation and/or transfer to hospital is
advised. Refer to the management flow charts (Figures 1 and 2) for further actions

Avoid delays
► Refer to the management flow charts (Figures 1 and 2) for further actions.
Delays in assessment and management may occur when clinical focus is diverted by non-urgent
investigations (such as glycated haemoglobin [HbA1c], C-peptide, islet cell antibodies or an oral glucose
tolerance test). Hyperglycaemic crises can be rapidly fatal, and whenever they are suspected, emergency
management must override any non-urgent investigation.
Management
► Refer to the management flow charts (Figures 1 and 2) for recommended actions.
Some people with known type 1 diabetes in particular may have a pre-existing sick day management plan (a written
document provided by their treating specialist, healthcare professional or team). If clinical conditions do not require
a rapid transfer to hospital, a pre-existing sick day plan may be put into place. This should include urgent contact
with the relevant specialist healthcare professional or team.

Figure 1. People not known to have diabetes
*
Polyuria/polydipsia or symptoms/signs of HHS or DKA
ACTION
BGL testing to be performed in clinic
Classical features HHS DKA Classical features HHS DKA
*Symptoms *Signs
Polyuria/polydipsia P P Altered conscious state P P
Nausea/vomiting P P Dehydration P P
Abdominal pain P P Kussmaul breathing P
Weight loss P Rapid respiratory rate P
Ketotic breath P
ÜRACGP ads Emergency management of hyperglycaemia in primary care 6

Figure 2. People known to have diabetes
Acute or critical illness/symptomatic

Manage precipitating illness
BGL <15 mmol/L BGL >15 mmol/L

BGL testing to be Waiting for non-urgent
Check ketones if performed in clinic Persistent/repeated investigations
pregnant or using hyperglycaemia (eg HbA1c, electrolytes)
SGLT2i
may delay critical
management
O TEST KETONES
*
(blood capillary ketones preferred)
© ASSESS VOLUME STATUS
<1.5 mmol/L
<1.5 mmol/L blood ketone >1.5 mmol/L blood ketone
blood ketone levels
levels or urine ketones levels or urine ketones
or urine ketones
negative/trace moderate/ heavy
negative/trace
MODERATE/SEVERE MILD/MODERATE
MINIMAL/MILD
DEHYDRATION DEHYDRATION
DEHYDRATION
*Elevated ketone
levels indicate possible
@ ACTION Sick day
HHS? DKA?
metabolic crisis that
management 1-2 needs urgent assessment
Re-evaluate BGL/ketones
in two hours
ACTION
Urgent transfer: further assessment and critical management
Classical features HHS DKA Classical features HHS DKA
Symptoms Signs
Polyuria/polydipsia P P Altered conscious state P P
Nausea/vomiting P P Dehydration P P
Abdominal pain P P Kussmaul breathing P
Weight loss P Rapid respiratory rate P
Ketotic breath P
References
1. Craig ME, Twigg SM, Donaghue KC, et al, for the Australian Type 1 Diabetes Guidelines Expert Advisory Group. National
evidence-based clinical care guidelines for type 1 diabetes in children, adolescents and adults. Canberra: Department of
Health and Ageing, 2011.
2. Australian Diabetes Educators Association. Clinical guiding principles for sick day management of adults with type 1 and
type 2 diabetes. Technical document. Canberra: ADEA, 2016.
ÜRACGP ads Emergency management of hyperglycaemia in primary care 7

References
1. Ambulance Victoria. Clinical practice guidelines for ambulance and MICA paramedics. Doncaster, Vic: Ambulance Victoria, 2016.
2. Craig ME, Twigg SM, Donaghue KC, et al, for the Australian Type 1 Diabetes Guidelines Expert Advisory Group. National evidence-based
clinical care guidelines for type 1 diabetes in children, adolescents and adults. Canberra: Department of Health and Ageing, 2011.
3. The Royal Australian College of General Practitioners. General practice management of type 2 diabetes 2016-18. East Melbourne, Vic:
RACGP, 2016.
4. Australian Diabetes Educators Association. Clinical guiding principles for sick day management of adults with type 1 and type 2
diabetes. Technical document. Canberra: ADEA, 2016.
5. Royal Children’s Hospital Melbourne. Diabetes mellitus. Parkville, Vic: RCH Melbourne, [no date]. Available at www.rch.org.au/
clinicalguide/guideline_index/Diabetes_mellitus [Accessed 15 September 2017].
6. Joint British Diabetes Societies Inpatient Care Group. The management of the hyperosmolar hyperglycaemic state (HHS) in adults with
diabetes. JBDS 06. UK: National Health Service, 2012.
7. Ambulance Victoria. Clinical practice guidelines for ambulance and MICA paramedics. Rev. edn. Version 1.2.1. Doncaster, Vic:
Ambulance Victoria, 2018. Available at https://s3-ap-southeast-2.amazonaws.com/prod.assets.ambulance.vic.gov.au/wp-content/
uploads/2018/03/latest-clinical-practice-guidelines.pdf [Accessed 26 April 2018].
8. Archival D, Blocher NC, with Hemphill RR. Hyperosmolar hyperglycemic state: Background, pathophysiology, etiology. Griffing GT, chief
editor. Medscape. 26 March 2016. Available at https://emedicine.medscape.com/article/1914705-overview [Accessed 20 April 2018].
9. Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician 2005;71(9):1723-30.
10. Nyenwe EA, Kitabchi AE. Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Res Clin Pract
2011;94(3):340-51.
11. Handelsman Y, Henry RR, Bloomgarden ZT, et al. American Association of Clinical Endocrinologists and American College of
Endocrinology position statement on the association of SGLT-2 inhibitors and diabetic ketoacidosis. Endocr Pract 2016;22(6):753-62.
12. Klocker AA, Phelan H, Twigg SM, Craig ME. Blood beta-hydroxybutyrate vs urine acetoacetate testing for the prevention and
management of ketoacidosis in Type 1 diabetes: A systematic review. Diabet Med 2013;30(7):818-24.
13. Brewster S, Curtis L, Poole R. Urine versus blood ketones. Practical Diabetes 2017;34(1):13-5.
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. The RACGP and its employees and agents have no liability
(including for negligence) to any users of the information contained in this publication.
© The Royal Australian College of General Practitioners 2018
This resource is provided under licence by the RACGP. Full terms are available at www.racgp.org.au/usage/licence
We acknowledge the Traditional Custodians of the lands and seas on which we work and live, and pay our respects to Elders, past, present and future.

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.
Accordingly, The Royal Australian College of General Practitioners (the

RACGP) 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.
Published by
College House, 100 Wellington Parade
East Melbourne VIC 3002 Australia
Tel 03 8699 0414

Fax 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-352-1
Published June 2013
© 2013 The Royal Australian College of General Practitioners

RACGP Managing emergencies
and pandemics in
general practice
A guide for preparation, response and recovery
Managing emergencies and pandemics in general practice Healthy Profession.
i A guide for preparation, response and recovery Healthy Australia.
Acknowledgements
Managing emergencies and pandemics in general practice: A guide for preparation, response and
recovery has been developed by The Royal Australian College of General Practitioners (RACGP)
under the guidance of the project’s steering committee.
The RACGP received project funding from the Department of Health and Ageing via the Office of
Health Protection to develop this resource.
The RACGP undertook an extensive consultation process to develop this resource and would like
to thank those who offered ideas and suggestions, provided feedback on drafts and attended the
national disaster management summit in 2012. The collective effort has resulted in the production
of a comprehensive resource that provides general practices with practical advice on how to better
prepare for, respond to and recover from the impact of emergencies and pandemics.
The RACGP would particularly like to thank:
• Dr Glynn Kelly (Chair, Project Steering Committee)
• Dr Penny Burns (Deputy Chair, Project Steering Committee)
• Professor Gerry Fitzgerald (Project Steering Committee)
• Dr Jenny Firman (Project Steering Committee)
• Mr Andy Wisheart (Northern Region Emergency Planning Manager, New Zealand)
• Members of the RACGP’s National Faculty of Specific Interests - Disaster Management Network
• Australian Psychological Society
• Australian Practice Nurses Association
• Australian Medicare Local Alliance
• All other GPs and practice staff who provided feedback during the consultation process.
Healthy Profession. Managing emergencies and pandemics in general practice
Healthy Australia. A guide for preparation, response and recovery iii
Foreword
The RACGP is committed to supporting GPs and practice teams in delivering quality care to
Australian patients. Recognising the vital role that general practitioners (GPs) and general practice
teams play in responding to emergencies and pandemics, the College has demonstrated its
commitment to supporting its Members by developing a range of resources relating to disaster,
emergency and pandemic planning and management.
The RACGP was actively involved in supporting GPs and practices adversely affected by the
floods in Queensland, Victoria and New South Wales in 2010, 2011 and 2013 and the Victorian and
Tasmanian bushfires in 2009 and 2013. Similarly, the College played an important role in developing
and disseminating crucial health information during the 2009 pandemic.
The aim of the guide is to assist general practices to better prepare for, respond to and recover
from the impacts of emergencies and pandemics. The guide has been designed as an educational
resource for general practice staff during emergency preparation and response efforts.
The RACGP continues working with GPs, other GP organisations, state and territory governments and
the Australian Government, and other stakeholders to coordinate the provision of clinically relevant
health information and emergency management resources to support GPs and their communities.
We would like to thank the people and organisations listed in the acknowledgements for their
dedication and support. We particularly would like to thank members of the project steering
committee and RACGP staff for their efforts in contributing to the development of this resource.
It is with great pride that we present Managing emergencies and pandemics in general practice:
A guide for preparation, response and recovery.
Dr Glynn Kelly Dr Liz Marles

Chair President
Disaster Management Network Royal Australian College of General Practitioners
iv A guide for preparation, response and recovery Healthy Australia.
Contents
1. Disasters and emergencies in Australia 1

2. General practice and emergencies 2
3. Emergency planning in general practice 3
3.1 The impact of emergencies in general practice 3
3.2 Why plan? 3
3.3 The emergency planning process 4
3.4 Important considerations during the planningprocess 7
4. Preparing the practice for an emergency 8
4.1 Practice layout 8
4.2 Emergency kit 8
4.3 Infrastructure and contents protection 9
5. Essential information and key contacts 10
5.1 Staff contact details 10
5.2 Contact for response agencies 10
5.3 Other health services 10
5.4 Practice information 10
6. Pandemic influenza 11
6.1 Background 11
6.2 Pandemic plans and key resources 13
6.3 Pandemic planning in general practice 15
6.4 Personal protective equipment 17
6.5 Pandemic management in general practice 21
7. A-Z of contingency planning and emergency response 24
7.1 Communicating during a disaster 24
7.2 Communication (telephones, internet and radio) 24
7.3 Establishing a temporary practice at an alternative location 25
7.4 Equipment and supplies 26
7.5 Initial response 26
7.6 Insurance 26
7.7 IT equipment and practice systems 27
7.8 Maintenance of vaccine refrigerators 28
7.9 Paper medical records 28
7.10 Power supply 29
7.11 Reduced staffing capacity in the practice 30
7.12 Re-entering the practice after a disaster 30
7.13 Water supply 30
8. Mental health in emergencies 31
8.1 Psychological preparation for a disaster 31
8.2 Psychosocial support and mental healthcare 32
8.3 Self-care for GPs and clinical staff 35
8.4 National Registration and Inquiry System 36
Appendix 1. Roles and responsibilities 37
Appendix 2. Useful websites 42
Appendix 3. Proposed pandemic stages 43
References 44
Healthy Australia. A guide for preparation, response and recovery 1
1. Disasters and emergencies in Australia
Disasters are unpredictable and destructive. They can cause significant damage, injury, illness,
loss, trauma and grief. Australia’s diverse landscape means that natural disasters such as
bushfires, floods, severe storms, heatwaves, earthquakes and tropical cyclones occur regularly
across the continent.
The Commonwealth of Australia defines a disaster as:
A serious disruption to community life which threatens or causes death or injury in that community
and/or damage to property which is beyond the day to day capacity of the prescribed statutory
authorities and which requires special mobilisation and organisation of resources other than those
normally available to those authorities.1
According to the United Nation’s Office for Disaster Reduction, approximately 517 775 Australians
are affected by a disaster each year.2 Between 1980 and 2010, there were 162 disasters in Australia,
resulting in the deaths of 959 people.2
While it is generally expected that bushfires occur seasonally in rural and remote areas, the
Tasmania (1967 and 2013) and Canberra (2003) bushfires demonstrated that urban metropolitan
areas are also at risk.3 The Tasmanian bushfires of 1967 consisted of 110 separate fires, causing
the homelessness of 7000 people, the injury of 900 people and the death of 62 people.3 The
Black Saturday Fires, which occurred in Victoria in February 2009, are considered to be the most
devastating fires in Australian history; they resulted in 173 fatalities and the destruction of more than
2100 homes.4
Disasters can have a profound impact on the population’s health and wellbeing, causing injury - both
short-term and long-term - and death. The degree to which people are affected will vary significantly
depending on the type and severity of the disaster. People affected by disasters can also have an
increased risk of mental health and social problems. However, the literature suggests that the majority
of people are resilient and have the courage and strength to overcome these setbacks. Psychological
first aid can provide basic support for the distressed immediately after an event.5
Disasters can also have long-term effects on the country’s economy. It is estimated that
disasters cause more than $1.14 billion damage to Australian businesses, homes and the nation’s
infrastructure each year.6 Insurance claims for the 2010 Queensland floods currently stand at
$2.38 billion (at May 2013), while claims for Queensland’s Cyclone Yasi, which occurred in 2011,
stand at $1.4 billion.7
Currently, scientific research indicates that the intensity and frequency of disasters is expected to
rise in the future.8 For this reason, thorough and comprehensive disaster planning and preparation
by all levels of government, statutory authorities, agencies, individuals, businesses and communities
is of paramount importance. Lessons learnt from past events highlight the importance of disaster
preparation in reducing the overall impact of a disaster.
Disaster planning should never be neglected or overlooked.
2 A guide for preparation, response and recovery Healthy Australia.
2. General practice and emergencies
The Royal Australian College of General Practitioners (RACGP) has developed Managing
emergencies and pandemics in general practice: A guide for preparation, response and recovery
with support from the Department of Health and Ageing.
The aim of the guide is to assist general practices to better prepare for, respond to and recover from
the impact of emergencies and pandemics. The guide has been designed to be an educational
resource for general practice staff during emergency preparations and response efforts.
While this guide has been specifically developed for the general practice setting, it is recognised
that other primary care settings might find it useful during their emergency preparations and we
encourage them to use it.
General practice is the linchpin of Australia’s health service infrastructure. GPs and practice teams
are at the forefront of medical care, providing Australians with access to quality healthcare on a daily
basis. It is estimated that GPs see approximately 88% of Australia’s population each year.9
In an emergency, it is generally expected that the demand for healthcare services will rise, especially
in the event of a pandemic.10 During previous emergency responses, GPs and practice teams have
consistently worked to provide individuals with the best care possible. They have demonstrated their
commitment to the communities they serve during emergencies and pandemics by ensuring that
individuals requiring urgent medical attention were seen and that people residing in disaster-affected
areas could continue to receive ongoing care.
This commitment reinforces the ongoing critical role that GPs and practice teams play in responding
to emergencies, from the immediate and acute phase to the long-term recovery phase. Evidence
surfacing since the outbreak of the H1N1 virus in 2009 suggests that the crucial role of general
practice in managing the pandemic was underestimated and not fully considered during pre
planning processes.10
It is crucial that general practices are able to continue providing essential services during
emergencies. To ensure that practices are able to continue providing these vital services, it is
imperative that they have an up-to-date emergency response plan so that they are prepared, well
stocked and ready to respond to any crisis.
Practices that are prepared for an emergency are more likely to have effective continuity of care
arrangements for their patients while ensuring that business operations continue to run as smoothly
as possible. Furthermore, practices that have a tested emergency response plan will ultimately be
better positioned to respond to the health needs of their communities.
While it is important for practices to be engaged in emergency planning processes at a practice
level, it is equally important for them to participate in emergency planning processes within the wider
community. The hospital sector is often represented on local emergency planning committees and
there is little or no representation from the primary care sector.
To remedy the lack of primary care representation on local disaster planning committees, GPs
and relevant practice staff are encouraged to engage with and/or participate in local disaster
planning committees. However, it is equally important that the primary care sector be supported by
governments so that they are well placed to continue providing vital services to their patients and
their communities, especially in their time of need.
3. Emergency planning in general practice
3.1 The impact of emergencies in general practice

Emergencies are unpredictable. They can strike any area at any time and can cause a
great deal of damage, injury, human suffering and loss of life. General practices can be
adversely affected by emergencies in a variety of ways.
In an emergency, general practices may experience:
• minor or significant damage to the practice’s infrastructure
• increased demand for services
• increased presentation of patients with injuries or highly infectious symptoms
• loss of critical equipment and supplies
• loss of access to key information
• loss of access to essential systems, networks and communication
• reduction in capacity and the loss of key staff
• practice closure
• loss of/disruption to power supply
• loss of/contamination of water supply.
To help reduce the overall impact of an emergency, it is essential that business owners
undertake appropriate emergency planning and preparation activities. While general
practices essentially operate as private businesses, they are unique in the sense that they
provide essential health services to individuals within the community.
Some practices may find fewer patients attend the practice during an emergency as a
result of damaged infrastructure and access issues. Conversely, other practices may see an
increase of patients attending due to injuries sustained during the event. So that practices are
well positioned to continue providing essential services to patients, it is extremely important
that they are appropriately prepared to manage the potential impact of an emergency.
3.2 Why plan?

Comprehensive planning can assist in reducing the overall impact of an emergency and
reduce liability and financial loss due to damages sustained during an event. Having
an emergency response plan will increase a practice’s capacity to continue to provide
essential services to patients during an emergency. The plan will identify contingency
measures that can be implemented to reduce the impact of an emergency and outline
appropriate actions to ensure that the practice can keep running (even if only in a
limited capacity) until the practice fully recovers and can return to normal functioning.
Furthermore, investing time and effort in developing a well-thought-out emergency
response plan will help to expedite the recovery process.
Engaging in simple emergency planning activities will help practice staff to feel confident
and prepared and will reduce any sense of panic in the event of an emergency. Through
the emergency planning process, practice staff would have anticipated what equipment
would be required and considered the key actions staff would undertake before an
emergency. Overall, practices that have an up-to-date emergency response plan will be
better positioned to respond to an emergency.
Potential loss of earnings for closure of a practice for 1 day
Major emergency events may affect a practice for many days or even weeks and can have devastating
effects on poorly prepared practices. If a practice is impacted by an emergency such as a flood or fire, the
practice may be forced to close until appropriate repairs are made. Closure of the practice will result in a
loss of earnings.
If a practice with four full-time equivalent (FTE) GPs were to close for a single day, the practice could
potentially lose $9600. This figure is based on the assumption that all four GPs work two full sessions
(approximately 3.5 hours each), seeing 20 patients, where the average fee is $60.
It is important to note that some overheads such as staffing costs will remain the same. However, there
may be a small reduction in other overhead costs such as consumables, electricity, gas and water bills,
etc.
3.3 The emergency planning process

Emergency planning is the process of identifying, reviewing and updating a series of
appropriate actions for managing an emergency. Practices should be aware that the
emergency planning process is fluid and ongoing; emergency response plans are of no
value if they contain out-of-date information.
To ensure that practices engage in emergency planning processes, it is recommended that
they undertake a range of emergency preparation activities.
3.3.1 Appoint an emergency management coordinator

Practices should have up-to-date knowledge of emergency planning and management
information. Therefore, it is recommended that practices appoint a staff member as their
‘emergency management coordinator’. Having one person in the practice responsible for
all things emergency related will ensure that emergency planning is placed at a preferential
level and not overlooked or neglected.
When deciding on an appropriate staff member, it is important to consider their role in the
practice, their level of experience, whether they have a broad understanding of the practice
and where they live.
Depending on the size of the practice, it may also be worth considering appointing a
deputy emergency management coordinator, in the event that the primary emergency
management coordinator is on extended leave or becomes ill during an emergency.
Role of the emergency management coordinator(s)

It is vital that the emergency management coordinator(s):
• ensure that they and all practice staff have up-to-date knowledge and skills relating to
emergency planning and management (which is specific to the location of the practice)
• draft and finalise an emergency response plan for the practice
• be responsible for training and educating the entire practice team about the plan
• be responsible for reviewing and updating the plan on a quarterly basis
• test or exercise the plan (or components of the plan) annually
• ensure practice staff can access the plan at any time
• make decisions as to whether/when the emergency response plan needs to be activated
• be responsible for building and maintaining relationships with other nearby practices and
Medicare Locals to discuss strategies of working together in the event of an emergency
• be responsible for connecting with local council and local emergency services.
3.3.2. Undertake local and other research

To start the planning process, it is recommended that the emergency management
coordinator(s) conduct preliminary research and obtain information regarding:
• the geographic location of the practice - to identify if the practice is located in a
disaster-prone area
• landscape and surroundings - to understand what additional steps need to be taken to
protect the practice’s infrastructure
• demographics of the patients - to identify vulnerable patient groups in the event of an
emergency or pandemic
• residential aged care facilities (RACFs) close to the practice - to ensure that patients
residing in RACFs are not overlooked and that they are able to access appropriate care
in the event of an emergency or pandemic
• support provided by the relevant Medicare Local - to ensure better integration of
services
• local emergency services - to ensure effective communication and emergency
management
• previous events that have affected the practice or community - to understand what can
be learnt from past events
• practice support facilities such as ambulance services, pharmacies and community
nurses - to identify what other services may be of assistance in an emergency.
It is envisaged that the information obtained, as detailed above, will assist in the planning
process and inform the overall development of the practice’s emergency response plan. An
important part of the emergency planning process is to understand how the practice might
be affected in the event of an emergency so that appropriate measures may be taken.
The emergency management coordinator will be able to access this important information
from local councils and local government emergency management committees.
3.3.3. Develop and document the emergency response plan

As discussed earlier, to ensure there is continuity in emergency planning processes, it is
recommended that the practice’s appointed emergency management coordinator be the
primary person responsible for developing and documenting the emergency response plan
(with the assistance of other team members as appropriate).
The emergency response plan includes important details regarding the appropriate actions
and steps to take in the event of an emergency. It is important the plan is documented
clearly, concisely and accurately and should be easy to read and understand.
The emergency management coordinator should ensure that the emergency response
plan is easily accessible by all practice staff. A copy of the plan should be kept at the
reception desk for easy access.
3.3.4. Provide staff education and training

Once the practice’s emergency response plan has been developed and documented, it
is recommended that the emergency management coordinator provide the practice team
with some basic education and training regarding the plan.
It is important that practice staff are aware that the practice has a plan in place and know
how and where to access the plan.
In addition to scheduled briefing sessions regarding the plan, it is recommended that the
/4k emergency management coordinator regularly discuss the plan at team meetings to ensure
that staff are reminded of the plan and that new staff are made aware of its existence.
3.3.5. Test components of the plan on an annual basis

Testing the emergency response plan or at least components of the plan is an important
component of the emergency planning process. Exercising the plan will give the
emergency management coordinator insight into the plan’s functionality and reinforce the
appropriate actions to take in an emergency.
3.3.6. Review and monitor the plan on a quarterly basis

Information sourced in the preliminary research will change regularly, so it is crucial that the
information in the plan remain current and up to date.
Emergency response plans should be fluid and revised when needed to reflect changes in
emergency management processes and incorporate learning from past events.
6
Review and
update the
plan on
1 Appoint the
emergency
management
quarterly basis coordinator
Test the plan (or

5 components of it)
on an annual basis 2
Undertake
local and other
research
Provide staff
4 education
and training
3 Develop and
document the
emergency
response plan
Figure 1. Summary of the initial planning process

3.4 Important considerations during the planning process

While undertaking research during the planning process, the emergency management
coordinator should consider if and how the practice has been affected by an emergency
previously and what practical steps can be taken to ensure that the practice is prepared to
effectively respond to an emergency.
This process will help inform the practice’s emergency response plan and will also help the
practice team (via the emergency management coordinator) feel that they are adequately
prepared to respond to an emergency.
The practice’s emergency management coordinator should take into account hazard
specific considerations.
Important considerations during the planning process
• If available, have the emergency management coordinator subscribe to text alert services (e.g. from
the local council, state governments, the State Emergency Service (SES), local fire agencies and public
health authorities) so that they can receive alerts in the event of a disaster affecting the area.
• Has the facility been damaged by flooding in the past?
• Is the practice located close to the waterfront, a low-lying river, stream, reservoir or any other body of water?
• What are the published flood levels for your area?
• What are the predicted flood levels for your area?
• Has information been obtained from the local council and emergency services regarding other flood/
disaster plans and relevant evacuation assembly points and routes?
• Does the emergency response plan outline the appropriate actions for the different predicted height levels?
• Is the practice located in a bushfire-prone area?
• Is the emergency management coordinator aware of the fire warning levels in the area (which are
determined by the local fire agency)?
• Has the practice been affected by cyclones previously?
• Is the practice emergency management coordinator aware of the Bureau of Meteorology’s cyclone
watch website, where notifications regarding imminent cyclones are issued?
• Has the practice been affected by earthquakes in the past?
4. Preparing the practice for an emergency
While developing the practice’s emergency response plan, it is important to consider the key
activities required to increase the practice’s capacity to effectively respond to an emergency. The
appointed emergency management coordinator and other practice staff can undertake a range of
activities that may reduce the overall impact of an emergency on the practice.
4.1 Practice layout

It is essential that staff are aware of the precise layout of the practice, where evacuation/
assembly points are located and where critical emergency supplies are stored so they are
well equiped to manage an emergency.
As part of the emergency planning process, the emergency management coordinator is
responsible for drawing up a comprehensive floor plan of the practice, highlighting the
specific location of:
• an evacuation route
• a safe assembly point
• fire extinguishers
• the main shut-off valves for water and gas
• heating/air conditioning equipment
• the electrical master switch
• hazardous material (e.g. chemicals)
• the emergency kit (as discussed in Section 4.2)
• first aid equipment
• outside water taps and hoses
• security and fire alarm systems
• underground or overhead power lines.
4.2 Emergency kit

In an emergency, some towns can expect to be isolated for days or weeks, depending on
road and other infrastructure damage. Practices should always have a generous amount
of critical supplies stored on site in the event of an emergency. Practices are advised to
gather and/or purchase appropriate resources and equipment to build an emergency kit
that can be utilised by practice staff in the event of an emergency.
Examples of some of the items to include in the emergency kit follow.
Emergency kit supplies
Disinfectant Battery-powered radio (including spare batteries)
Detergent Torches (including spare batteries)
Additional first aid kits Analogue or dial-up phone
Plastic and garbage bags Fire extinguisher with instructions
Bottles of clean water Additional doctors bags with extra medications
Non-perishable food items Small supply of office stationery
Medical certificate pad Prescription pad

4.3 Infrastructure and contents protection

There are also practical safeguards that staff can undertake to help protect the facility and
reduce the amount of damage caused to the practice’s infrastructure and contents. While
the advice provided below will not be relevant for all practices, it highlights some of the
key activities that practices should consider during the emergency planning process and
prepare for (as appropriate).
Preparing the practice for a bushfire
• Remove excess rubbish, leaves, litter and shrubs from around the practice.
• Remove any flammable materials such as paint from the premises.
• Clear guttering surrounding the practice regularly.
• Cut the grass and remove all trimmings regularly.
• Ensure there is a wide firebreak around the practice.
• Remove all tree branches so that the building is clear from overhanging branches.
• Install a sprinkler system around the practice.
Preparing the practice for a cyclone
• Check with your local council or a professional builder/architect that the practice has been built to meet
cyclone standards.
• Check that the practice’s infrastructure is in sound condition.
• Maintain the roof and eaves regularly.
• Fix all loose guttering around the practice.
• Remove or secure any dangerous debris outside the practice.
• Fit all windows with shutters or metal screens for added protection during high winds.
Preparing the practice for a flood
• Identify all indoor items that need to be raised off the floor in the event of a flood.
• If practical, consider alternatives to carpet such as tiles.
• Relocate all low power points well above previous flood levels (using a licensed electrician).
• Secure any objects in the practice that are likely to float.
• Install flood-proofing equipment (e.g. sandbags) if locking up the practice for an extended period of time.
Preparing the practice for an earthquake
• Remove heavy objects from shelves or store them on the lower shelves.
• Secure or fasten heavy equipment to a fixed surface or wall (e.g. television in waiting room).
• Secure all wall-mounted objects (e.g. whiteboards/clocks).
• Ensure all power boards are being used appropriately and not overloaded.
• Secure and fasten large expensive medical equipment to a fixed surface or wall.
• Ensure that medications and small medical equipment are stored in a safe place.
5. Essential information and key contacts
5.1 Staff contact details

In an emergency, the practice may need to contact practice staff urgently: to advise staff
not to attend the practice due to an imminent threat or to advise them the practice requires
extra support as a result of a recent emergency.
To ensure that staff have swift access to other staff contact details, it is recommended that a
list of all staff members’ phone numbers be created and regularly reviewed and updated. A
current copy of the staff contact list should be kept in a secure place at the reception desk for
easy access. An additional copy of this list should be stored in the practice’s emergency kit.
Practice staff can also keep a laminated, pocket-sized card with staff contact numbers
with them. Additionally, with the consent of practice staff, it is recommended that all staff
have up-to-date contact phone numbers stored in their mobile phones.
To ensure that staff can be informed of an imminent disaster swiftly, the practice should
establish a communication tree for practice staff. The communication tree can be initiated
by the emergency management coordinator: he or she calls another staff member and that
staff member calls another staff member, and so forth.
5.2 Contact for response agencies

During an emergency, staff may need to urgently seek assistance from an emergency
response agency. As discussed in Appendix 1 Roles and responsibilities, different
response agencies are responsible for different hazards. It is recommended that a list of
all relevant state and territory response agencies be created and that this list be kept in a
secure place at the reception desk for easy access during an emergency. A copy should
also be stored in the practice’s emergency kit.
The emergency management coordinator should have a laminated, pocket-sized list of all
relevant emergency agencies with them at all times.
5.3 Other health services

In the event of an emergency, practices may need to communicate with other health
services. They may need to access referral and discharge papers or they may need
to seek assistance from other practice staff due to capacity issues. To ensure that
communications can occur quickly, a list of close health services should be created
including details of local hospitals, nearby practices, other primary care facilities, state and
territory health departments and Medicare Locals.
5.4 Practice information

If the practice is adversely affected by an emergency, practice staff will need to
communicate with a range of service providers. To ensure that such communications can
occur easily and quickly, it is recommended that a list containing important information
regarding the practice’s accounts and service providers be created and regularly updated.
The list should include contact details and account and/or policy numbers of service
providers such as insurance, telephone, internet, utilities and disaster recovery specialists.
6. Pandemic influenza
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6.1 Background
6.1.1 What is seasonal influenza?
Every year, the influenza virus causes serious infection and even death worldwide, primarily
during the winter months. Influenza viruses evolve over time, changing slightly from year to
year, and various strains are continually spread throughout the world.
The influenza virus can lower the body’s ability to fight other bacterial infections and can
therefore often lead to other serious infections such as pneumonia. While the influenza virus XZ
can have serious complications, especially for the elderly and people with chronic medical __ .
conditions, generally most healthy people are able to fully recover from the virus.
6.1.2 What is pandemic influenza? a

The World Health Organization (WHO) describes a pandemic as the worldwide spread Z^\
of a new infectious disease. Pandemic influenza occurs when a new strain of the
influenza virus emerges that most people have not been exposed to and therefore have
no immunity. Pandemic influenza causes serious disease that is easily spread, infecting
large population groups across every continent, ultimately causing significant illness and zs.
death. Historically, viruses that have triggered pandemics have generally originated from
animal influenza viruses. v
Throughout the ages, the world has experienced pandemics of varying scales. More
recently, the world has endured outbreaks of infectious disease in 1918, 1957, 1968 and
2009.11 As a result of these pandemics, more than 800 million people lost their lives. While
significant advances in science and technology ensure that governments and health
professionals have a better understanding of how to manage an outbreak of infectious
disease, these statistics reinforce the need for medical practitioners and community
members to remain vigilant and be prepared for the next outbreak.
Unlike seasonal influenza, it is impossible to predict when and where the next pandemic
will start, what impact it will have on public health and how quickly it will spread.
Acknowledging the devastating impact that pandemic influenza can have on human
populations and the economy, governments around the world are increasingly taking
appropriate steps to prevent pandemic influenza from occurring.
6.1.3 Management of H1N1 in 2009

In a pandemic, GPs and practice teams play a significant role in supporting public health
goals in disease control. To reduce the overall impact and spread of pandemic influenza,
it is essential that the practice team have appropriate skills and knowledge regarding
infectious diseases so they are prepared to manage pandemic influenza in the general
practice setting.
Following the outbreak of the H1N1 virus in 2009, the evidence suggests that the role of
general practice in managing pandemics was underestimated and not fully considered during
planning. During the outbreak, general practice played a vital role in managing the virus in the
community, which was fortunate given that the hospital system was overstretched and did not
have the capacity to treat and manage high volumes of infected patients.10
61.4 Influenza versus the common cold

While both influenza and the common cold are viral respiratory infections (usually affecting
the nose, throat and lungs), it is important to note that the influenza virus is significantly
worse than the common cold.12
Table 1 outlines the primary differences in symptoms of the common cold and the
influenza virus.
Table 1. Symptoms of influenza and the common cold
Symptom Influenza Common cold
Fever Often high, lasting 3 to 4 days Rare
Headache Frequent Rare
Aches and pains Common; can be severe Slight
Cough Common; can become severe Sometimes; mild to moderate
Sneezing Sometimes Common
Runny nose Sometimes Common
Sore throat Sometimes Common
Shivering Common Rare
Physical capacity Frequently bedridden Normal
Energy levels May show moderate to extreme signs of weakness A littler lower than usual
Complications Pneumonia, kidney failure and heart failure Sinus or ear infection
Can be life-threatening
6.1.5 How is the influenza virus spread?

The influenza virus can be spread in a number of ways, including:
• a droplet - a large particle that can be propelled up to a metre while coughing or sneezing
• indirect contact, such as transmission to an object that is then touched by another person
• direct contact, such as person-to-person contact
• airborne - small particles that can remain suspended in the air and travel great distances.
6.1.6 Ways to protect against infection

The spread of infection can be reduced or minimised through a few simple techniques
including but not limited to:
• encouraging respiratory etiquette - covering the mouth or nose when coughing or
sneezing
• social distancing - maintaining at least 1 metre distance from other people
• hand hygiene - regularly washing hands or using alcohol-based rub
• correct use of personal protective equipment (PPE) - using PPE in accordance with
manufacturer’s instructions and evidence-based guidelines
• surface cleaning - regularly cleaning all surfaces.
See www.racgp.org.au/your-practice/standards/infectioncontrol for further information
regarding surface cleaning and PPE.
6.2 Pandemic plans and key resources

6.2.1 The Australian Health Management Plan for Pandemic Influenza
The Australian Health Management Plan for Pandemic Influenza (AHMPPI) 2009 is a
national health plan, based on international best practice and evidence for responding
to an influenza pandemic. The primary purpose of the AHMPPI is to provide information
regarding the required measures to healthcare providers so that they can effectively
manage an outbreak of infectious disease such as pandemic influenza.
It is recommended that general practices be familiar with the AHMPPI to ensure that they
are able to effectively respond in the event of a pandemic. It is important to note that the
AHMPPI is currently being revised (at May 2013) and a revised edition will be released in
late 2013 or early 2014.
Practices can download a current copy of the AHMPPI from the Department of Health and
Ageing (www.health.gov.au).
6.2.2 State and territory plans for pandemic influenza

While there is a single national plan for the management of pandemic influenza, states
and territories are responsible for emergency responses and are also required to have a
jurisdictional plan for the management of pandemic influenza. For continuity purposes, it is
expected that the jurisdictional plans are accurately aligned with the AHMPPI.
General practices are also advised to become familiar with their relevant state or territory
influenza pandemic plan to ensure that they are aware of its contents and are able to
effectively respond in the event of a pandemic (see Table 2).
Table 2. State/territory influenza pandemic plans
State/territory Pandemic plan Year Availability
Australian Capital Australian Capital Territory health 2007 www.health.act.gov.au

Territory management plan for pandemic influenza
New South Wales NSW health influenza pandemic plan 2010 www.health.nsw.gov.au
Northern Territory Special counter disaster plan - human 2009 www.health.nt.gov.au

pandemic influenza
Queensland Pandemic influenza plan 2009 www.health.qld.gov.au
South Australia Pandemic influenza - a summary of health’s 2012 www.health.sa.gov.au

operational plan
Tasmania Tasmanian action plan for pandemic influenza Under www.dhhs.tas.gov.au

review
Victoria Victorian action plan for human influenza 2012 www.health.vic.gov.au

pandemic
Western Australia Western Australian health management plan 2009 www.health.wa.gov.au

for pandemic influenza
6.2.3 WHO pandemic alert levels

WHO has identified six phases of pandemic alerts that are used to inform the world about an
outbreak of infectious disease and the need to employ intensive and appropriate measures.
The Department of Health and Ageing, via the Australian Health Protection Principal
Committee, has international systems in place so that it is alerted to pertinent information
regarding current and future pandemics.
See www.who.int/en for further information regarding the WHO pandemic alert levels.
6.2.4 Pandemic alert levels in Australia

Pandemic alert levels provide signals to governments to put their pandemic plans into
action. The WHO levels describe the pattern on a global level and differ from the Australian
alert levels. Australian general practices and health organisations need to follow the
Australian Government recommendations.
Further information regarding Australia’s pandemic alert levels can be accessed from the
Australian health management plan for pandemic influenza and the Department of Health
and Ageing website. A brief description of the alert levels is included in Table 3.
Table 3. Australia’s pandemic alert levels in summary
Australian phase Description
ALERT A novel virus with pandemic potential causes severe disease in humans who have
had contact with infected animals. There is no effective transmission between
humans. Novel virus has not arrived in Australia.
DELAY Effective transmission of novel virus detected overseas in:

- small cluster of cases in one country overseas
- large cluster(s) of cases in only one or two countries overseas
- large cluster(s) of cases in more than two countries overseas.
Novel virus not detected in Australia.
CONTAIN Pandemic virus has arrived in Australia causing A pandemic

a small number of cases and/or small number of virus, which is
clusters. mild in most but
severe in some
SUSTAIN Pandemic virus is established in Australia and PROTECT and moderate
spreading in the community. overall, is
established in
CONTROL Customised pandemic vaccine widely available and
Australia.
is beginning to bring the pandemic under control.
RECOVER Pandemic controlled in Australia but further waves may occur if the virus drifts and/or
is re-imported into Australia.
Source: Australian Government Department of Health and Ageing, Pandemic phases - 6 (last updated
January 2011)
As discussed in 6.2.1, the AHMPPI is currently being revised. It is expected that the
updated AHMPPI will also have new pandemic stages. The proposed pandemic stages
can be viewed in Appendix 3.
6.2.5 Disease surveillance

The Department of Health and Ageing has developed the National Notifiable Disease
Surveillance System, which monitors the incidence of an agreed list of communicable
diseases in Australia. It is crucial that all practice staff are aware that patients may
present with suspected or confirmed cases of infectious disease. In some cases,
clinical staff such as GPs and practice nurses will be required to notify the relevant state
or territory health authority when a patient presents to the practice with a suspected
or confirmed case of an infectious disease. Health authorities have contact tracing
systems that have been developed to trace people who have been in contact with
infectious patients.
See www.health.gov.au for further information regarding the National Notifiable Disease
Surveillance System.
GPs have access to important clinical information, beyond the level of data notified by
public health laboratories, which significantly contributes to surveillance systems and the
epidemiological investigation and control of communicable diseases in Australia.
6.3 Pandemic planning in general practice

Pandemic influenza can have a devastating impact on the population’s health and also the
country’s economy. General practice plays a unique and important role in managing and
preventing the spread of pandemic influenza. Appropriate preparation for future pandemics
will help lessen the overall impact of the pandemic.
Increasing the length of time the primary care sector can sustain increased patient
volumes is one of the most effective ways the health system can combat a pandemic. To
ensure this, there need to be strict protocols for the way that patients with influenza-like
symptoms are managed in the community. Additionally, there needs to be a significant
change in the way that general practices operate.
Given that general practice is the first point of health system contact for most Australians
experiencing influenza and other respiratory symptoms, it is essential that general
practices are adequately equipped and resourced to implement a timely response to the
next pandemic.
Despite the fact that services and staff in general practices are often overburdened and
overstretched, pandemic planning should never be neglected or overlooked. In order to
effectively manage the next pandemic, general practices need to understand the potential
impacts of pandemics so they can make appropriate arrangements.
6.31 Developing a pandemic plan

Developing a quality pandemic plan will ensure that the practice is well equipped to
manage the next outbreak of pandemic influenza. The plan explains how the practice
intends to operate before and during a pandemic.
The key components of an effective pandemic plan will include information regarding:
• the practice pandemic coordinator
• a list of pandemic resources and pandemic plans
• how the practice will run clinical sessions during a pandemic
• how the practice intends to triage patients in a pandemic
• the practice’s policies on infection control
• equipment (clinical and non-clinical) needed to manage pandemic influenza
• communication methodologies (with patients and other services)
• clinical management (including the use of antiviral medication)
• policies to manage multiple staff absenteeism.
6.3.2 Appointing a practice pandemic coordinator

As recommended in the RACGP’s Pandemic flu kit, it is advised that general practices
appoint a staff member with the appropriate experience and knowledge to act as the key
person to coordinate all practice activities relating to pandemic planning and management.
It is envisaged that the appointed practice pandemic coordinator will be responsible for
developing the practice’s pandemic plan (in liaison with key staff) and providing education
and training to other staff in the practice.
Key activities that the practice pandemic coordinator may undertake when preparing for
and responding to a pandemic include:
• undertaking appropriate education and training, such as review of the RACGP’s
Pandemic flu kit, national and state and territory plans and the RACGP’s Infection
control standards
• developing a plan for the management of pandemic influenza for the practice
• subscribing to appropriate communication networks regarding Australian pandemic
alert levels (e.g. the RACGP health alerts)
• regularly monitoring communication from the Department of Health and Ageing and the
RACGP regarding pandemics
• obtaining regular advice from state and territory governments regarding the
management of pandemics
• maintaining the practice’s stock of PPE
• scheduling regular team meetings for all practice staff and providing practice staff with
education and training regarding the plan
• providing the practice team with ongoing training regarding the plan so that new staff
are made aware of the plan.
6.3.3 Equipment required in a pandemic

Lessons learnt from past events indicate that during a pandemic there is an increased
demand for key supplies, often resulting in a shortage of essential equipment.
Where possible it is recommended that practices have appropriate stocks of clinical
(such as PPE) and non-clinical (such as cleaning products and alcohol rub) supplies to
ensure the practice can continue to run and provide patients with essential services in
the event of a pandemic.
6.3.3.1 Non-clinical equipment

• Rubbish bins: Areas with high human traffic such as waiting rooms and
reception areas will need to have additional waste bins to ensure that staff and
patients can dispose of used tissues easily. Bins should be lined with plastic bag
liners so that the contents are contained within the bin and easily disposed of
regularly. It is recommended that bins are emptied (double bagged) a couple of
times a day, especially in the peak of a pandemic. Staff disposing of rubbish bins
should wear gloves and appropriate PPE (see Section 6.4).
• Quality cleaning equipment and products: Practices will need to ensure a
well-stocked supply of cleaning products such as surface sprays, mops and
buckets. During peak traffic times, it is recommended that practice staff regularly
clean surface areas such as reception desks, waiting room tables and chairs
and entrance/exit areas or door handles.
• Tissues: During a pandemic there will be an increased demand for tissues in
the practice. It is essential that practices have a well-stocked supply of tissues
conveniently located around the practice. Areas with a high volume of traffic
such as waiting rooms, reception areas and bathrooms should have boxes of
tissues available for patients.
• Paper or linen covering for examination couches: Practices generally use
either paper or linen to cover examination couches located in consulting rooms.
During a pandemic it is advisable to either use paper towelling that is changed
after each patient or wipe down the examination couch with an approved
sanitiser between patients. Linen coverings are not recommended during a
pandemic.
• Alcohol-based hand sanitiser: Good infection control principles specify
the use of an alcohol-based hand sanitiser. In a pandemic, there will be an
increased need for alcohol hand rub. Practices need to have a well-stocked
supply of hand sanitiser and ensure that patients and staff can have easy access
to it throughout the different areas within the practice such as waiting rooms,
reception areas, consultation rooms and children’s play areas.
Hand Hygiene Australia has an online training module that practice staff can
undertake. See www.hha.org.au for further information.
6.3.3.2 Clinical equipment

• PPE: In the general practice setting, PPE is clothing and equipment designed to
protect employees and staff from risk of infection or illness. PPE can help prevent
contact with an infectious agent or bodily fluid that may contain an infectious agent
by creating a barrier between the staff member and the infectious material. This is
discussed in the next section.
6.4 Personal protective equipment

Given that general practice staff are at the front line of patient healthcare, there is an
increased risk of acquiring communicable disease(s) while interacting with and examining
patients. To eliminate/reduce the spread of pandemic influenza, the proper use of quality
PPE is imperative.
6.4.1 Availability and accessibility

While there is a national medical stockpile of PPE held by the Australian Government and
state and territory health departments, supplies are limited.
The Australian Health Protection Principal Committee has the authority to determine when
access to the national medical stockpile will be provided. Such determinations are usually
based on the risk of exposure and the availability of supply.
State and territory health departments will coordinate the distribution of PPE on the advice
of the Australian Health Protection Principal Committee. Jurisdictional pandemic plans also
provide further information regarding the arrangements for the distribution of PPE in the
event of a pandemic.
Given the above, it is important to note that individual practices are responsible for
sourcing and providing PPE for staff and patients within the practice. Practices are
therefore encouraged to maintain a small supply of PPE (for up to 4 weeks for all staff)
within the practice at all times.
Employers and practices should become familiar with occupational health and safety
legislation applicable to their state or territory to ensure that they are complying with all
legislative requirements in relation to the supply and use of PPE in the workplace.
6.4.2 Types of PPE

The types of PPE frequently utilised in general practice include:
• plastic aprons
• gowns
• surgical masks (P2 and N95)
• respirators
• goggles/glasses
• face shields
• gloves.
To ensure the effective utilisation of PPE in general practice, it is essential that:

• all PPE is used in accordance with the manufacturers’ instructions
• PPE is fitted and removed correctly
• regular education and training regarding the use of PPE is provided to appropriate staff
(including new staff members)
• a record of training in PPE is kept and updated regularly
• there is appropriate signage around the practice reminding staff how to don and remove
PPE.
6.4.3 Assessing risk

PPE should be used consistently by all practice staff involved in patient care or who may
have contact with respiratory secretions.
Additional precautions such as social distancing should be used when a patient is known
or suspected to be infected with micro-organisms. These precautions provide additional
barriers between practice staff and the infected patient.
Practices are required to assess the level of risk when determining which staff use PPE
(see Table 4). The level of risk is relative to exposure. The use of social distancing, hand
hygiene, cough etiquette, environmental controls and PPE will help reduce the exposure.
Table 4. Assessing risk to determine preventive measures
Extreme risk High risk Lower risk
Those highly likely to be exposed Those within a close proximity Those in an environment that has
to known or suspected sources to a patient with a cough. In this been modified, including social
of pandemic influenza during case the prevention measures distancing, vigilant cleaning
specific medical procedures, are distance and the patient protocols of contact surfaces
such as the taking of a throat wearing a mask. and prompt thorough waste
swab. Example: Patients sitting in the disposal.
In this case the prevention waiting room in close proximity Example: Reception staff do
measures are wearing a mask, to a patient with suspected not share pens with patients;
goggles, gown and gloves (PPE). pandemic influenza because patients perform hand hygiene
Example: GP or clinical staff reception staff have not been before presenting to reception,
taking a throat swab from a able to change the work reception staff are 1 metre away
patient with suspected pandemic environment allowing for at least from patients when they present
influenza. 1 metre between themselves and to reception.
the presenting patient. GPs, PNs
and other clinical staff treating
patients who have a cough but
are not wearing a mask. (Droplet
transmission).
6.4.4 Correct use of PPE

The correct use of PPE is essential in protecting the health of staff and limiting the spread
of influenza.
Recommended order of PPE application:
2. Put on your mask
3. Put on your goggles 4. Put on your gown
6. Treat your patient

Recommended order of PPE removal:
2. Clean your hands
5. Take off your goggles 6. Clean your hands

6.5 Pandemic management in general practice

The following practice and clinical management issues need to be carefully considered in
the event of a pandemic.
6.5.1 Management of the practice facility during a pandemic

During a pandemic, practices should implement a series of minor changes to the facility
which help reduce the spread of infection.
To help reduce the spread of infection, practices can:
• post signs requesting patients and family members to immediately report symptoms
of respiratory illness on arrival at the facility and use alcohol-based hand rubs when
entering the practice
• ask that patients use disposable tissues to cover the nose and mouth when coughing
• provide coughing patients with a mask as soon as they enter the practice
• provide conveniently located masks, tissues and alcohol-based hand rubs for waiting areas
• use an existing consulting room as a dedicated room for treating and managing
patients with suspected influenza symptoms
• request that patients with influenza-like symptoms wait in the car or outside
• ensure that staff are wearing appropriate PPE at the entrance so they can triage
patients into dedicated consulting rooms.
6.5.2 Infection control measures, principles and guides

General practices can reduce the risk or prevent the transmission of infectious diseases
by embedding effective infection control measures in everyday practice. GPs, clinical staff
and non-clinical staff should have a good understanding of infection control principles.
In summary, effective infection control measures in the practice can be employed by:
• having a policy that addresses how and how often the practice will be cleaned
• having a policy on how contaminated waste will be managed
• embedding quality triaging processes in everyday practice
• having a policy on practice staff hand hygiene
• encouraging respiratory etiquette and social distancing
• providing staff with information so they know how to order and store PPE and other
disposable consumables within the practice
• providing tissues and no-touch receptacles for used tissue disposal.
The application of quality infection control measures is key when treating patients with
infectious diseases.
Practices are advised to review the RACGP’s Infection control standards for office based
practices (4th edition) for detailed information regarding infection control (downloadable
from www.racgp.org.au/your-practice/standards/infectioncontrol). These Standards have
been developed specifically for the primary care setting. Practice staff are required to
comply with the Standards to ensure that the risk of cross-infection is minimised.
The Australian Commission on Safety and Quality Healthcare has developed the
Australian guidelines for the prevention and control of infection in healthcare (www.nhmrc.
gov.au/node/30290), which provide recommendations outlining the critical aspects of
infection prevention and control. It is important to note that these Guidelines are targeted
towards the acute hospital setting.
6.5.3 Practice staff

Practices will need to consider what measures they can take to ensure that the practice
can continue running smoothly. To help reduce absenteeism, it is recommended that all
practice staff be vaccinated. When considering the practice’s staffing needs, it is important
to also identify if any staff have underlying medical conditions or special needs that may
affect their ability to work in the practice during a pandemic.
Further information on managing staff absenteeism is discussed in Section 7.11.
6.5.4 Case definition

Case definitions for pandemic influenza viruses are communicated by public health
authorities. However, it is important to note that the case definitions may change at
different phases of a pandemic. The practice pandemic coordinator should therefore
maintain good communication pathways with state and territory health authorities so they
are aware of any changes made to case definition or clinical management.
6.5.5 Patient triage

Each practice needs to develop screening protocols so staff can effectively triage patients
with influenza-like symptoms. Screening protocols and triage algorithms guide practices
through the initial screening process and clinical assessment. Where practical to do so,
patients with influenza-like symptoms should be encouraged to contact the practice via
telephone first, rather than arriving at the practice unannounced.
There is also a need to educate patients about the importance of notifying reception staff
that they have a possible infectious disease when they present to the practice. Practices
are encouraged to display posters advising patients to notify reception staff if they have
influenza-like symptoms.
The RACGP’s Infection control standards state that it is vital that all staff are trained to
recognise symptoms and signs of potentially infectious disease so they can respond
appropriately.
As a general rule, there are three levels of questioning when trying to detect pandemic
influenza in patients:
• Routine questions - all patients asked.

- So that our GP can provide the best possible care, can you please give me a reason
for your visit?
• Additional questions - when a patient indicates signs and symptoms consistent with an
infectious disease.
- May I ask a few more questions relating to your health?
- Do you have a rash?
- Do you have a cough?
- Do you have diarrhoea?
• Further questions - when the practice suspects a local outbreak of an infectious
disease (such as measles or a suspected case of pandemic influenza). The case
definition will help in determining these types of targeted questions.
- Have you recently travelled overseas?
- Have you been exposed to anyone with a confirmed case of influenza?
6.5.6 Vaccination
The annual influenza immunisation does not always provide protection against new
viruses. Nevertheless, seasonal influenza vaccination is encouraged according to current
immunisation guidelines. Pneumonia can be a severe illness and a complication of
influenza infection. Pneumococcal vaccine is recommended to all at-risk groups, according
to recommendations in the National Health and Medical Research Council (NHMRC)
Immunisation handbook (10th edition).
See www.immunise.health.gov.au for further information regarding the NHMRC’s guidelines.
6.5.7 Advice regarding the use of antivirals

In the event of pandemic, antivirals may assist in preventing the development of infection
in people exposed to the influenza virus. In some cases, when antivirals are used as a
treatment, they can help to reduce the impact of the symptoms and the overall duration of
the illness.
Antiviral medications play a significant role in the treatment of pandemic influenza. To
ensure the effectiveness of antivirals, they must be administered either just before or
immediately after a person shows signs of influenza. It is important to note that influenza
viruses can mutate and become resistant to antivirals used to treat it.
In a pandemic, antiviral usage includes:
• treatment of pandemic influenza as clinically appropriate
• pre-exposure prophylaxis - for healthcare workers who have continuous frontline exposure to
infectious cases
• post-exposure prophylaxis - to help reduce the risk of infection for people who have had unprotected
contact with an infectious case.
During a pandemic, practices can obtain up-to-date information regarding new antiviral
medications from state and territory health departments, the Department of Health and
Ageing and the RACGP.
The Department of Health and Ageing’s Australian health management plan for pandemic
influenza (www.flupandemic.gov.au/internet/panflu/publishing.nsf) provides further details
regarding the government’s overall strategy for the use of antivirals during a pandemic.
7. A-Z of contingency planning and emergency response
In an emergency, irrespective of the hazard, practices may be affected in a number of ways. The
following section outlines contingency measures to be considered by the practice when developing
an emergency response plan and key steps to take when responding to an emergency.
The steps outlined in this section provide basic guidance to ensure the continuity of practice
operations during a disaster and during the recovery phase.
7.1 Communicating during a disaster

The majority of local councils now have well-developed text messaging services to notify
residents and individuals of potential and/or imminent disasters. It is recommended that the
emergency management coordinator register for this service via their local council or local
emergency service.
The emergency management coordinator should be responsible for activating the
communication tree as described earlier, which will ensure that all practice staff are
informed of the looming disaster.
In the event of an emergency, the coordinator should organise for phone calls to be diverted
to an analogue, non-powered phone (or mobile if still operational) with a recorded message
regarding the practice’s status and hours of operation, as well as relevant advice to patients.
If the practice has a website or uses social medial, information regarding its operation
should also be updated by the emergency management coordinator and/or relevant IT
support staff.
7.2 Communication (telephones, internet and radio)

Communication systems such as telephone lines and the internet can be affected during a
disaster. Disruptions to the practice’s communication channels can have a significant impact
on the practice’s overall business operations, including communication with patients, other
local practices, emergency services and insurance companies. Given this, a well-thought-
out contingency plan is key to the practice’s overall emergency response and should involve
as many different communication channels as possible.
7.2.1 Telephones
Emergencies will affect phone systems in different ways, so it is important to ensure that
there are multiple options available in the event of a disaster (e.g. a landline phone if mobile
towers are affected). Mobile phones can be overwhelmed during an emergency and should
not be solely relied upon.
In situations where mobile phone communication is down, it is recommended that analogue
phones be used by the practice.
Purchase, or reserve if available, an analogue phone (one that does not require a power
connection) and store the unit in the emergency kit to ensure easy access for all practice
staff. Training on how to divert phone calls, in the event of an emergency, should also be
provided to relevant practice staff.
In the event that communication lines (landlines) are affected, it is likely that mobile phones
will be utilised in an emergency. In this instance, the practice’s landline can be diverted to a
mobile number to ensure business continuity.
7.2.2 Internet
Communication via the internet may also be impacted during a disaster. Programs and
information such as pathology and radiology reports, patient discharge summaries and
personally controlled electronic health records (PCEHR) may be unavailable during this time.
By keeping a hard copy of important phone numbers such as pathology laboratories, practices
may be able to access urgent test results.
To ensure the continuation of services, practices may wish to keep hard copies of essential
information (e.g. patient appointments and other resources relating to the Medicare Benefits
Schedule such as the MBS Fee Summary, which can be accessed from: www.racgp.org.au/
your-practice/business/billing/mbs).
Practices may consider investing in alternative internet connection to ensure ongoing access to
the internet during a disaster. Alternative options include mobile data devices, dial-up modems
and satellite dishes. Practices need to also consider alternative ways for conducting business if
there is a loss of internet access, such as having cash transactions and manual swipe machines
(for credit card and Medicare cards) stored in the emergency kit.
Depending on the emergency, the practice should be able to employ a range of strategies (as
listed above, including both alternative electronic devices and manual hard copies) to continue
functioning in some capacity.
7.2.3 Radio
Where all other communication lines are down, a battery-powered radio can be used as a
reliable means of receiving important information regarding an emergency. Practices should
purchase a battery-powered radio, with a supply of batteries, and place it in the emergency
kit. Practice staff can tune it to ABC Radio for up-to-date information regarding emergencies
affecting their area.
7.3 Establishing a temporary practice at an alternative location

Disasters can cause significant damage to a building’s infrastructure, causing it to be
uninhabitable and unsafe. If a practice’s infrastructure is damaged as a result of a disaster, it
may be necessary for part or all of the operational activities of the practice to be shifted to a
temporary location.
Therefore, when preparing the practice for a disaster, it is worth considering how the practice
will continue providing essential services to the community if it is affected. If it is determined
that the practice will continue to provide services, then an appropriate and safe location for the
temporary practice will need to be identified.
To facilitate this process, practices are encouraged to enter discussions with other business
owners who could potentially allow a temporary clinic to be set up in their building. Other
possible venues might include community halls, schools or vacant shops. These discussions
will need to occur as part of the planning process and before an event. If an agreement is
made, it should be documented and communicated to both parties.
Practice staff need to be made aware of any arrangements, so that if the practice is affected
and the emergency response plan is activated, staff can begin to make the appropriate
arrangements to inform patients of the temporary location.
GPs are advised to clarify with Medicare Australia that they are able to use the same provider
number within the temporary practice or that a temporary provider number can be accessed.
It is also suggested that GPs operating from a temporary location/practice seek endorsement
from their relevant medical defence organisation to ensure that they are adequately covered.
While undertaking the preparations to set up a temporary practice, it is important to have a

printed copy of the practice’s emergency response plan including lists of key equipment and
supplies that are required to run a practice.
7.4 Equipment and supplies

General practices hold specialised equipment and medical supplies, such as diagnostic
equipment, pharmaceuticals and vaccines. Disasters can have devastating effects on the
practice’s infrastructure, including all of its contents.
As part of the emergency planning process, practices are advised to keep a log of all medical
equipment and supplies in the practice. In the event that some or all of the contents are
destroyed, practice staff can quickly assess what equipment and supplies have been lost or
damaged and what requires replacing. Both electronic and hard copies of this list should be
created and maintained.
7.5 Initial response

It is important to plan initial response processes. In preparation for an emergency, the
emergency management coordinator should:
• develop an initial response protocol, including first steps and identification of information
sources during an emergency, as discussed in Section 4
• develop, implement and communicate an emergency evacuation plan, including assembly
points.
At the first notification of a possible crisis, it is recommended that the emergency management
coordinator or delegate attend community briefings to assess risk to staff, the practice, patients
and the wider community.
The emergency management coordinator and other practice staff are advised to check the
relevant state or territory emergency service’s (SES) website to ascertain the anticipated degree
of impact. The SES will determine if there is a need to evacuate. If the risk is severe, it is advised
that practices keep checking the website for updates where possible.
Based on information provided by the SES, the emergency management coordinator will advise
whether practice staff will need to evacuate the premises. If an evacuation is required, the
emergency management coordinator will be responsible for communicating this to all staff via
the activation of the communication tree. The emergency management coordinator will also
need to provide practice staff with advice regarding safe evacuation and assembly points.
If it is determined that the practice does not need to be evacuated, then it is business as usual
unless determined otherwise by the practice owner or practice manager.
7.6 Insurance
Building, contents and business insurance are essential for any business, and general practices
are no exception.
During the disaster planning process, it is recommended that insurance policies for the practice
are reviewed regularly to ensure adequate coverage for the practice.
To ensure adequate coverage, it is important that the policy covers:
• all natural and man-made disasters
• extensive damage and total loss of the building
• the entire contents of the building, including loss and damage to medical equipment and supplies
• costs associated with interruption to the business (may include staff pay and loss of
revenue) - may trigger a higher premium
• costs associated with relocating to a temporary practice - may trigger a higher premium.
It is also recommended that a spreadsheet containing important information regarding the
insurance policies be created and maintained. Information such as name of insurer, policy
number, type of insurance, coverage and relevant claims telephone numbers should be
included. It is recommended that a copy be kept off site by the emergency management
coordinator and/or practice manager in the event of damage to the practice.
7.7 IT equipment and practice systems

Practices are becoming increasingly reliant on computer software and IT systems
specifically designed for the general practice setting. Practices affected by disasters
risk having computer hardware, software programs and IT systems damaged, including
practice management software.
7.7.1 Hardware
During the disaster planning process, it is important to take a stock of all hardware and
equipment. In the event that all of the hardware is destroyed or completely damaged, staff
will be able to access a comprehensive list of what needs to be replaced. This list can be
used as part of the practice’s asset register.
For those leasing computers and hardware, it is important to get in contact with the
leasing company as soon as practicable to discuss the damage and the process involved
in replacing items.
If equipment/computers in the practice have been damaged as a result of a disaster, first
determine the operational status of equipment (for safety purposes, practices may need to
seek advice from a professional) and then transfer any equipment and computers that have
not been damaged to a safe operational area within the practice so they are protected.
After an emergency, access to computers may be limited to those not damaged (if any).
However, if the server is damaged or corrupted, other desktop computers will not be able
to access information and/or programs from the network.
Practices should consider having at least one laptop with a long battery life with current
practice/patient data stored on it, or at least ensure access to the previous day’s back-up
(whether physical or on a secure cloud). With the correct connections, laptops can also be
charged from cars.
It is important that practices have suitable media reading devices to effectively restore data
when IT systems are affected.
7.7.2 Software and applications

Software and access codes should be stored in a safe place (such as a fireproof box
or secure online storage) so they can be easily accessed in the event they need to be
reinstalled. It is also recommended that a list of all software and access codes be created
and maintained, including software support phone numbers. This list can be used to
become part of the practice’s asset register.
If software and applications do not work due to server damage, the practice will need
to seek assistance from an experienced IT technician, who will need to reinstall them.
Software is generally stored on a disk or is downloadable from the vendor’s website. When
first purchased, software is either registered to the practice or to an individual working
within the practice.
7.7.3 Loss of data

In the general practice setting, data protection is key to effective business continuity. While
the majority of practices have back-up procedures in place to protect data in the event of
computer damage and data corruption, information management and information technology
should always be considered as a high priority in emergency planning.
Practice standards currently require storing critical and current information off site as part of
high-quality back-up systems for information technology. As a minimum, practices should be
performing daily back-ups of all data (including email, shared documents, network file and
databases and clinical and practice software). It is also important to ensure that the daily back
ups are verified. When a threat of a disaster is imminent, practices should keep a hard copy list
of appointments (patients seen) to enable records to be recreated.
Advanced planning of IT will make the recovery phase significantly easier and faster. Practices
are advised to test their restore procedures regularly. Practices should consider contacting
software vendors for product-specific recommendations regarding restoration processes and
checking data integrity.
Practices should also perform a recovery on a regular basis (dependant on the risk assessed
by the individual practice) to ensure that recovery methods are working and appropriate for the
practice. This can be coupled with a test plan to verify data integrity (e.g. searching for patient
X to confirm their history and demographics are correct as documented in the test plan).
When implementing data protection measures in the practice, consider the data stored on
desktop computers, as not all applications are connected to the server and therefore are not
necessarily backed up daily. It is important to conduct regular audits on desktop computers/
workstations to ascertain what data is being stored on local drives.
Further information regarding data security and loss of data can be accessed from the RACGP
Computer and information security standards (www.racgp.org.au/your-practice/standards/ciss).
7.8 Maintenance of vaccine refrigerators

During a heatwave or disruption to power supplies, it is essential that practices have
contingency plans in place for maintaining the temperature for vaccine fridges between +2°C
and +8°C. To ensure these temperatures are maintained, it is essential that vaccine fridges are
stored in a well-ventilated room with good circulation. Practice staff should regularly monitor
and record the temperatures at the start and end of the day.
Practices need to plan ahead for how vaccines will be managed if there is a disruption to
power. To reduce risk, practices may wish to enter into discussions with local pharmacies and
hospitals regarding the management of vaccines in the event of an emergency.
The Department of Health and Ageing National vaccine storage guidelines - strive for five
outlines the basic principles for safe vaccine management (see www.health.gov.au/internet/
immunise/publishing.nsf/Content/provider-store).
Practices are also advised to become familiar with relevant vaccine management guidelines for
their state or territory health department.
7.9 Paper medical records

While practices can undertake a range of activities to minimise the overall damage caused to
the practice in the event of an emergency, paper medical records can be damaged irrespective
of the protective measures employed.
During disaster planning and preparations, a list of disaster recovery specialists in the area
should be created, including their names, phone numbers and area of expertise.
If paper medical records are damaged by water or fire, practices will need to have systems in
place to assess whether the records can be recovered. Practices are advised to engage the
services of reputable disaster recovery specialists during the emergency planning process to
understand what services they provide.
Key steps to take when dealing with damaged paper records:
• assess the damage to the paper records and review the possible options for recovery
• separate the damaged records from the undamaged records
• where paper medical records have been damaged by water or fire, handle them as little as
possible. Even if the paper record is saturated, in most cases the majority of the writing will
remain legible if water-fast pens have been used
• for records only very slightly damaged by water, it may be appropriate to air or fan dry them
on site
• for records that have significant damage, it is recommended that practices contact an
appropriate disaster recovery specialist as a dehumidifier will be required to dry and restore
records.
7.10 Power supply

Power supplies to practices may be disrupted in the event of a disaster. Some practices may
even have a total loss of power for some time. Disruption to the power supply will affect many
of the practice’s appliances and systems. Consideration of how computer systems, telephone
systems, automatic doors, heating and cooling systems and lighting will be affected is key to
disaster planning.
7.10.1 Lighting
Battery-powered emergency lighting to highlight exit routes is a mandatory requirement for
facilities accessed by the public. However, this lighting will likely not be sufficient for all rooms
and parts of the practice if there is a disruption to the power supply. Therefore, for safety
purposes, ensure that practice staff have easy access to the emergency kit and additional
torches, including a well-stocked supply of batteries.
Practices may also wish to consider purchasing wind-up or solar dynamo torches that can also
be used to charge mobile phones.
7.10.2 Uninterrupted power supply

The majority of practices will have an uninterrupted power supply (UPS) installed, which is
designed to protect the computer server for a short period of time in the event of a power
outage. UPS are usually not intended to be used for long periods of operation. However, if this is
a significant concern, it may be worth considering increasing the capacity of the power supply
during emergency preparations. Refer to the use of power generators in Section 7.10.4.
7.10.3 Computer systems

If computers are not shut down properly during a power outage, they can incur significant
damage. Some practices may have a UPS, which should continue to deliver power to the
practice’s main server to allow extra time for computers to be shut down correctly and/or initiate
a forced shutdown of the system.
7.10.4 Power generators

Diesel or petrol generators can provide the practice with power if power supplies are disrupted.
Generators can be used for back-up lighting, vaccine refrigerators, computer systems and other
appliances in specific areas. Used in conjunction with a UPS, power generators can ensure that
clean power is delivered to sensitive equipment such as computers and medical equipment.
Practices may wish to consider the feasibility of hiring or purchasing back-up power
generators as part of the emergency planning process. Reserving a generator in the event
of an emergency may involve an annual reservation fee to ensure that the practice is given
priority during significant demand.
7.11 Reduced staffing capacity in the practice

In an emergency, many practices may find that they have a significant reduction in staffing
capacity and therefore cannot provide the same level of service to patients. In a pandemic,
there may be unexpected multiple staff absences: staff members may be sick, they may
have to care for sick family members, they may be pregnant or they may have regular
contact with someone who is terminally ill and cannot risk cross-infection. Staff affected by
other disasters may also be absent for similar reasons.
Practices are advised to consider how the practice will continue operating with a reduction
in key staff, especially in the event of a pandemic. One way to help alleviate staffing issues
in the event of a disaster is to provide staff with education and training in other roles (where
a similar level of expertise is required) within the practice.
If there are multiple staff absences as a result of an emergency or a pandemic, practice
staff with basic training and education in other roles can be cross-skilled and may be able
to perform other duties.
Practices may also wish to contact other practices nearby to ascertain if they have
capacity to provide some staff for a short period of time. Practices in close proximity may
wish to consider pooling staff and resources in an emergency. Practices can also contact
their Medicare Local to see if it can provide any advice or support.
7.12 Re-entering the practice after a disaster

As part of planning preparations, practice staff should be made aware that re-entering a
practice after a disaster can be extremely hazardous.
Before anyone re-enters the practice, the emergency management coordinator should
seek professional advice from either a building engineer or a responsible member of the
emergency response team about when it is safe to re-enter the building.
7.13 Water supply

In a disaster, practices may experience disruptions to their water supply. Disasters can
damage water pipes within the practice; affect local water supplies, which may become
contaminated; or even completely cut off water supply to the suburb/town.
It is crucial that staff know where the water mains is located and how to turn it off. The
location of the water mains should be highlighted on the practice map.
Practices should consider keeping a well-stocked supply of bottled water and alcohol
sanitiser in the event that the local water supply is contaminated. Bottled water can be
stored in the emergency kit. Arrangements for boiling and storing water for additional
supplies should also be considered during the disaster planning process.
If there is damage to the water pipes and flooding results, practice staff will need to shut
off the mains water supply to the practice.
8. Mental health in emergencies
Disasters affect individuals and communities in a range of ways and can cause major disruptions
to people’s lives, both physically and emotionally. Most individuals and communities draw on their
diverse strengths during disasters and are resilient: but, the impact of disasters can be felt by
individuals and their communities over a long period of time.
For individuals affected by emergencies, it may mean the loss of family or friends, their home, their
workplace, their school, their property, their community, their business, their health and their access
to services. Those affected by disasters may report feelings of grief, fear and anxiety, anger, guilt,
shame, numbness or depression. Some people’s belief systems are impacted and they experience
a sense of loss of control over their life and future.
People exposed to extreme stressors such as disasters may be at increased risk of physical, mental
and social health problems.13 There is evidence to suggest that those affected by disasters may be
at increased risk of developing anxiety, depression, increased substance use, acute stress disorder
(ASD), post-traumatic stress disorder (PTSD) and complicated grief.14 The majority of people recover
from disasters without long-term mental health sequelae but may benefit from some basic and
timely support during and/or immediately after a disaster.
Historically, governments and response agencies only invested their efforts in responding to the
physical needs of individuals and communities affected by disasters. There was little attention
given to the detrimental impact that a disaster could have on a person’s mental health and social
wellbeing. Emerging evidence regarding the psychological and social impacts of disasters has
sparked a significant shift in thinking; since the late 1970s it has become widely recognised that
emergencies can adversely impact a person’s mental health and wellbeing.15
Recognition that disasters can affect a person’s physical health, mental health and overall
wellbeing has led to the inclusion of mental health interventions in emergency planning and
management strategies.
Given that individuals affected by emergencies have an increased risk of developing social and
mental health issues, it is essential they receive appropriate services in a timely manner. It is
equally important that special consideration be given to the mental health and wellbeing of those
responding to disasters and emergencies.
As described earlier, state and territory governments have the primary responsibility for disaster
management and coordination. It is important to note that state and territory emergency
management plans also encompass arrangements for mental health services in the event of a
disaster or emergency. Given this, the provision of coordinated psychosocial support and adequate
mental healthcare is a critical component of disaster planning and response.
8.1 Psychological preparation for a disaster

While some disasters occur seasonally, such as floods and bushfires, other disasters, such
as earthquakes and pandemics, are less predictable. While governments and disaster
response agencies often start to prepare for disasters in anticipation of the disaster season,
less thought may be given to what people can do to psychologically prepare for a disaster.
Being both physically and psychologically prepared for a disaster is of paramount
importance. Understanding what people can do to psychologically prepare for a disaster
and what they can do to cope during and after a disaster can make a significant difference
to those adversely affected.
It is common and natural for people to experience stress and anxiety in a disaster.
However, having a good understanding of what to expect during and after a disaster can
assist in decreasing people’s anxiety levels. People who are psychologically prepared for a
<î> disaster are generally more confident and able to make effective decisions regarding their
emergency management plans.
Given this, it is good practice to also consider what activities practice staff can undertake
to ensure that that they are psychologically prepared for an emergency.
The Australian Red Cross, in collaboration with the Australian Psychological Society (APS),
has developed a model that outlines the appropriate steps people can take to ensure that
they are psychologically prepared for a disaster (see Table 5).
Table 5. Psychological preparation for a disaster

Anticipate Identify Manage
What you might need Matters needing attention Behaviours

What can you do to It is important to consider the Consider your behaviour during
psychologically and physically disaster planning process. a disaster.
prepare for a disaster? Neglecting disaster planning can Focus on practical tasks and
This will help you feel confident in make people feel anxious in the remember to focus on the
the event of a disaster. event there is a disaster warning. current situation.
Preparing may help alleviate
anxiety.
How you might feel Specific feelings Feelings

Think about the emotions you Identify specific feelings and Learn techniques for calming
might expect when faced with consider ways you might down anxious or distressed
environmental threats caused by manage them. feelings, like breathing exercises,
a disaster. Learn how to recognise the relaxation and calming
Will you feel anxious, scared? feeling of anxiety or stress in your techniques.
body.
Where in your body do you feel
stress or anxiety?
What you might be thinking Unhelpful thinking Thoughts

Anticipate what type of thoughts Identify and be wary of unhelpful Use helpful thoughts and
you might have. thinking such as: calming self-talk to help reduce
‘There is really not much you can anxiety and stay in control
do about a disaster’ or ‘Every ‘I have a good plan and I’m going
year we have cyclone warnings to work through it step by step’.
but they never result in anything
bad’.
Source: Adapted from Psychological preparedness for disasters 2012.
See www.psychology.org.au/publications/tip_sheets/disasters for further information

regarding how to psychologically prepare for a disaster.
8.2 Psychosocial support and mental healthcare

As a consequence of our increased understanding of needs both during and after
disasters, it has become routine procedure for government and non-government
organisations to provide and coordinate psychosocial support and mental health services
for affected populations.
Following the 2009 Victorian bushfires, a best-practice framework to guide provision
of support and mental healthcare to disaster-affected communities was developed by
a wide range of government and non-government stakeholders. The framework has
three levels of support, based on the level of distress experienced and the timing of the
intervention post disaster.
• Level 1 refers to early response information and support.

• Level 2 refers to simple psychological strategies that are helpful for people with more
persistent problems.
• Level 3 refers to formal mental health interventions for smaller numbers of people who
are at risk of developing significant mental health problems.
This framework and relevant programs have been successfully applied to the government
led natural disaster recovery plans that were implemented to assist communities affected
by the 2009 Victorian bushfires and the 2010-11 Queensland floods and cyclone disasters.
Training in all three levels was provided to appropriate people in disaster-affected
communities. The framework is referred to in the Attorney-General’s Disaster health
handbooks volumes 1 and 2.
A key component to this approach is that it is implemented in close collaboration with the
state and federal government departments responsible for community recovery, as well as all
the other professional mental health providers and key disaster agencies. This collaborative
approach maximises the possibility of creating an optimal recovery environment.
GPs are advised to familiarise themselves with these three levels and, when treating
patients in disaster-affected communities, determine what level of support is required.
Level 1 - Early response: information and support

Level 1 refers to information and simple practical and emotional support provided to
affected individuals and communities in the days or weeks following a disaster. Most
people will only require this level of support. It is the normal human response of caring,
kindness and support offered to a person who is suffering and in need. It is what GPs and
practice staff often do on a daily basis with their patients who are in distress. Psychological
first aid (PFA) for individuals is a well-known example of this, but it can also take the form
of support groups, community meetings, and other community development activities.
Level 1 support can often be provided by community members with basic training to assist
those experiencing distress and loss immediately following a disaster.
It is important to note that previously critical incident stress debriefings and single-session
psychological debriefing sessions were provided to individuals after a disaster or traumatic
event. However, the WHO’s Department of Mental Health and Substance Abuse has since
released a statement recommending that single session psychological debriefing not be used
as an early intervention after a disaster or trauma. Based on the available evidence, the WHO
suggests that this approach is ineffective and in some cases may even be detrimental.16
In the event of an emergency, it is recommended that PFA be employed when appropriate
to help people distressed by the impact of an emergency or a disaster.
PFA is an evidence-informed approach used to provide those affected by disaster with
basic support to help them in their immediate recovery after experiencing trauma: in the
initial hours, days and weeks post-disaster. Essentially, PFA provides people with a sense
of safety and helps them stay connected, calm, composed and optimistic. It also provides
people with access to physical, social and emotional support during their time of need.
It is important to note that PFA is not counselling or debriefing. While anyone with
appropriate PFA training can deliver it, it should be delivered by appropriate agencies as
part of state/territory and regional/local emergency management plans. The Australian
Red Cross has a list of training providers. However, those in the practice team who wish
to provide extra services to individuals and communities in disaster-affected areas are
encouraged to undertake training in psychological first aid.
Overall, this intervention aims to minimise stress and anxiety levels, meet immediate
needs, promote flexibility in coping mechanisms and encourage positive adjustment. This
intervention is a primary tool used in the immediate post-disaster period for people who
require assistance after experiencing a trauma.
The fundamental basis for this intervention is that people adversely affected by disasters will
naturally experience a range of emotional, behavioural, psychological and physical reactions
following a disaster that may hinder their ability to cope and recover from a disaster.
See www.psychology.org.au/Assets/Files/Red-Cross-Psychological-First-Aid-Book.pdf for
further information regarding PFA.
Note that PFA should not be confused with Mental Health First Aid, which aims to teach
people about mental health problems and disorders.
Figure 2. Core principles of psychological first aid
Source: Adapted from the Australian Guide to Psychological First Aid 2009
Level 2 - Simple psychological strategies

Disaster survivors and others affected by such events will experience a broad range
of reactions, and some of these reactions will cause enough distress to interfere with
adaptive coping and recovery.
While most mental health problems following disaster are of mild-moderate severity,
depending on the scale of the disaster, this may still mean that large numbers of people
with disaster or trauma-related mental health problems require low-intensity assistance to
help them cope better and recover, with the option of referral to mental health specialists
for higher-intensity interventions if required.
Level 2 support refers to simple, brief and practical psychological strategies that can
be taught to community members with more persistent mild-moderate mental health
problems.
Developed in the United States in the wake of Hurricane Katrina, ‘Skills for Psychological
Recovery’ is a skills-based approach that assists individuals to better recover from the
effects of disaster. Level 2 support can be provided by practitioners with basic counselling
skills working in general practice, primary care, mental healthcare providers and
community-based settings.
Level 3 - Formal mental health interventions

While PFA or other simple psychological strategies will be the only psychosocial support
needed for the majority of people to support their recovery from an emergency, some
people are more vulnerable and will be at greater risk for long-term mental health issues
such as anxiety, depression, increased substance use, ASD and PTSD. It is important that
GPs continue to monitor for and consider the possibility of long-term mental health effects
of disasters, which may not be evident for months or years. These individuals may require
referral for longer-term psychological interventions from mental health professionals such
as psychologists and psychiatrists.
Level 3 refers to formal evidence-based psychological and pharmacological interventions
for people with more persistent and severe distress, including those with diagnosable
mental health conditions, for example PTSD, depression, complicated grief and substance
use disorders. A relatively small number of people affected by disaster will require this level
of intervention. Level 3 interventions are typically provided by mental health specialists with
expertise in treating people with mental health conditions.
8.3 Self-care for GPs and clinical staff

By virtue of their profession, GPs are likely to want to assist individuals and communities
affected by disasters and emergencies. In a crisis situation, GPs, medical practitioners,
mental health nurses, nurses and other health professionals will generally band together to
provide essential medical services as best they can. However, it is important to recognise
that in a disaster GPs and other healthcare professionals can be both the victim and the
responder. Given this, special consideration of those responding is required.
GPs play a pivotal role in caring for and supporting those affected by natural disasters and
emergencies. With a large influx of patients requiring assistance within short timeframes,
front line responders tend to overlook their own personal needs for support and instead
focus on other people requiring medical attention.
This can put additional stress on already busy GPs, especially if their own practices,
family homes and communities have been affected. The effects of wide-scale disasters
and emergencies permeate both the professional and personal realms of GPs and their
practice teams’ lives. Although health professionals are vulnerable to the same emotional
and psychological responses as the public, if they are attentive to the challenge, they
can manage these stresses effectively and maintain exemplary standards of professional
treatment.
To be resilient, GPs and clinical staff in the practice team must acknowledge and
address their own psychological needs. The extraordinary demands on GPs during this
time intensify the need for self-monitoring with an eye to self-care strategies that can
help bolster professional resilience. GPs should be attuned to physical and emotional
vulnerabilities and attend to pre-existing stressors.
There are a few simple steps that GPs and their practice teams can take to ensure that
they are better supported during a crisis situation.
Practising self-care
• Ask yourself:
- How am I going?
- What do I need?
• Check on your family and friends in disaster-affected areas to ensure their safety: this will help to
alleviate potential anxiety and concern for loved ones.
• Limit your exposure to a tolerable level.
• Take regular breaks.
• Accept appropriate assistance offered to allow yourself time away from work.
• Monitor your own distress level.
• Notice where you embody stress and attend to your physical needs as much as possible.
• Maintain good general health with regular exercise, good nutrition and regular sleep habits.
• Use your personal and family support network.
• Maintain contact with friends and family, and talk to support people about your experiences and
feelings.
• Increase interaction with professional peers.
• Engage in activities that balance work and non-work life.
• Maintain connections with organisations or activities that are meaningful to you.
• Seek help if needed from:
- your GP
- colleagues
- the RACGP - members of the College have access to additional supports and psychology services
- other professional associations.
8.4 National Registration and Inquiry System

During a disaster, the Australian Red Cross launches its National Registration and Inquiry
System. People residing and working in disaster-affected areas are encouraged to register
their name and location details with the National Registration and Inquiry System. Once
people have registered with the system, friends and families will be able to locate those
living or working in disaster-affected areas.
By connecting people, this system aims to alleviate stress and anxiety levels of people
concerned for friends and families in disaster-affected areas.
The National Registration and Inquiry System can be accessed during a disaster by:
• visiting https://emergency.redcross.org.au
• calling 1800 727 077
• visiting an evacuation centre coordinated by the Red Cross.
Appendix 1. Roles and responsibilities
In Australia, the Australian Government Minister for Emergency Management is responsible for
national emergency management and disaster resilience. However, there are also a number of
government departments (national, state/territory and local levels), agencies, authorities and
organisations who engage in emergency planning and undertake emergency response activities.
Those working in emergency management must have a comprehensive understanding of
emergency planning processes and management strategies. To ensure this occurs, it is important to
firstly understand the roles and responsibilities that the different agencies and organisations play in
emergency planning and management.
This Appendix explains some roles and responsibilities of organisations involved in emergency
planning, response and coordination (which relate to the primary care sector).
National arrangements, organisations and committees

National health emergency response arrangements
In Australia, the primary responsibility for managing and coordinating emergency responses lies with
the state and territory governments. Under the Australian Constitution, the Australian Government
does not have the statutory authority to provide direction to the state and territory governments
on matters relating to emergency management. Therefore, an integrated, collaborative approach
between the state and territory governments is critical.
Arrangements for a national health emergency response have been developed by the Australian
Health Protection Principal Committee with assistance from the Department of Health and Ageing.
The National Health Emergency Response Arrangements 2011 (Nat Health Arrangements) outline
the strategic arrangements and mechanisms for coordinating Australian health sectors’ response to
national emergencies.
Australian Health Protection Principal Committee

The Australian Health Protection Principal Committee (AHPPC) is responsible for coordinating a
national response to a range of health emergencies, including a natural disaster, bombing, outbreak
of an infectious disease or a chemical, biological or radiological incident. The AHPPC comprises
representatives from all state and territory health authorities and Commonwealth defence and
emergency services agencies.
Office of Health Protection

The Office of Health Protection (OHP) is a division of the Department of Health and Ageing and was
established to protect the health of the Australian community through effective national leadership
and coordination. Additionally, it aims to build the appropriate capacity and capability to be able to
detect, prevent and respond to threats to public health and safety.
Pandemic Review Implementation Advisory Committee

The Pandemic Review Implementation Advisory Committee (PRIAC) was established to oversee the
implementation of the recommendations made in the Review of Australia’s health sector response to
pandemic (H1N1) 2009: lessons identified report.
PRIAC is chaired by the Chief Medical Officer and comprises stakeholders including Commonwealth,
jurisdictional and specialist representation. The recommendations made in the 2009 report should
inform the next review of the Australian Health Management Plan for Pandemic Influenza.

The Royal Australian College of General Practitioners (RACGP) is the key professional body representing
more than 21 500 GPs. It has a key role in advocating for and supporting the GP profession.
The College researches, lobbies and advocates on issues that influence GPs and general practice
teams. The RACGP also develops practice tools and guidelines to support GPs in their practice.
Key tasks and activities relating to emergency planning and management

undertaken by the Australian Government
Australian Government
• Engagement with all levels of government • Communication with all levels of government
• National crisis coordination • Provision of financial support and funding in

disaster management
• Development and maintenance of the National • Maintenance of the Australian Health Management
Health Emergency Response Arrangements Plan for Pandemic Influenza
State and territory arrangements, organisations and committees

As discussed earlier, the primary responsibility for managing and coordinating emergency
responses lies with the state and territory governments. Under the Constitution, each state and
territory government has the responsibility for preparing, reviewing, maintaining and exercising an
emergency plan for its jurisdiction.
State and territory health departments

Each state and territory has a health department responsible for:
• the health and wellbeing of people residing within the state or territory
• developing a jurisdictional plan for the management of pandemic influenza. It is essential that
such jurisdictional plans are accurately aligned with the Australian Government’s Australian Health
Management Plan for Pandemic Influenza and the Australian guidelines for the prevention and
control of infection in healthcare
• the coordination and distribution of personal protective equipment during an outbreak of an
infectious disease (upon the advice of the Office of Health Protection)
• providing a case definition of the influenza strain in the event of a pandemic, and providing advice
regarding the most appropriate treatment options for patients meeting the case definition.
State and territory authorities responsible for emergency response per hazard
The authorities responsible for planning and responding to disasters and emergencies differ
significantly across the jurisdictions.
The box below lists authorities responsible for disaster and emergency response in Australia’s states
and territories.
Victoria Tasmania
Bushfire - County Fire Authority Bushfire - Tasmania Fire Service / Department of

000 Primary Industries, Parks, Water and Environment
www.cfa.vic.gov.au 000
www.fire.tas.gov.au
Earthquake - SES Earthquake - Police

132 500 / 000 131 444 / 000
www.ses.vic.gov.au www.police.tas.gov.au
Floods - SES Floods - SES / Police

132 500 / 000 132 500 / 000
www.ses.vic.gov.au www.ses.tas.gov.au
Heatwave - Police Human disease - Department of Health and Human

131 444 / 000 Services
www.police.vic.gov.au 1800 671 738
www.dhhs.tas.gov.au
Human disease - Department of Health Storm - SES

1300 651 160 132 500 / 000
www.health.vic.gov.au www.ses.tas.gov.au
Storm - SES Tsunami - SES

132 500 / 000 132 500 / 000
www.ses.vic.gov.au www.ses.tas.gov.au
Tsunami - SES
132 500 / 000
www.ses.vic.gov.au
Australian Capital Territory South Australia
Bushfire - Emergency Services Agency (Fire and Bushfire - Country Fire Service
Rescue/Rural Fire Service) 000
000 www.ses.sa.gov.au
www.esa.act.gov.au
Floods - ACT Emergency Services Agency (SES) SES Earthquake - Police

132 500 / 000 131 444 / 000
www.esa.act.gov.au www.sapolice.sa.gov.au
Human disease - ACT Health Floods - SES

02 6205 1700 132 500 / 000
www.health.act.gov.au www.ses.sa.gov.au
Storm - ACT Emergency Services Agency (SES) Human disease - Department of Health
132 500 / 000 1300 232 272
www.esa.act.gov.au www.health.sa.gov.au
Storm - SES
132 500 / 000
www.ses.sa.gov.au
New South Wales Queensland
Bushfire - NSW Rural Fire Service (RFS) Bushfire - Queensland Fire and Rescue Service
NSW Fire Brigades 000
000 www.fire.qld.gov.au
www.rfs.nsw.gov.au
Earthquake - Police Cyclone - SES

131 444 / 000 132 500 / 000
www.police.nsw.gov.au www.emergency.qld.gov.au/ses
Floods - SES Earthquake - SES

132 500 / 000 000
www.ses.nsw.gov.au www.emergency.qld.gov.au/ses
Heatwave - Police Floods - SES

131 444 / 000 132 500 / 000
www.police.nsw.gov.au www.emergency.qld.gov.au/ses
Human disease - NSW Health Human disease - Queensland Health

1300 066 055 07 3328 9724
www.health.nsw.gov.au www.health.qld.gov.au
Storm - SES Storm - SES

132 500 / 000 132 500 / 000
www.ses.nsw.gov.au www.emergency.qld.gov.au/ses
Tsunami - Police
131 444 / 000
www.police.nsw.gov.au
Western Australia Northern Territory
Bushfire - Department of Fire and Emergency Bushfire - Bushfire NT

Services (DFES) / Department of Environment and 000
Conservation www.lrm.nt.gov.au/bushfires
000
www.dfes.wa.gov.au
Cyclone - DFES Cyclone - Police/Northern Territory Emergency

132 500 / 000 Service (NTES)
www.dfes.wa.gov.au 132 500 / 000
www.pfes.nt.gov.au
Earthquake - DFES Earthquake - Police / NTES

132 500 / 000 131 444 / 000
www.dfes.wa.gov.au www.pfes.nt.gov.au
Floods - DFES Floods - Police / NTES

132 500 / 000 132 500 / 000
Heatwave - State Health Coordinator Human disease - Department of Health

08 9222 4222 08 8922 8044
www.public.health.wa.gov.au www.pfes.nt.gov.au
Human disease - Department of Health Storm - Police / NTES

08 9388 4878 / A/H 08 9328 0553 132 500 / 000
www.public.health.wa.gov.au www.pfes.nt.gov.au
Storm - DFES / SES Tsunami - Police / NTES

132 500 / 000 131 444 / 000
Tsunami - DFES
132 500 / 000
www.dfes.wa.gov.au
Key tasks and activities relating to emergency planning

and management undertaken by state and territory governments
State and territory governments
• Maintenance of strong linkages with emergency • Development and maintenance of jurisdictional

services emergency plans
• Coordination and distribution of PPE • Management of public health
• Coordination of agency response (dependent on • Development and maintenance of pandemic plans

hazard)
Local arrangements, organisations and committees

General practices
General practice is a unique, important and essential component of health system infrastructure.
GPs play an ongoing critical role in emergency management and response, from the immediate/
acute phase to the long term recovery phase. GPs also play a key role in triage, coordinating care
for patients between other service providers, managing ongoing chronic illness, general health
issues and other illnesses arising both during and after an emergency.
During an emergency, GPs may need to look after patients with medical conditions that would
otherwise be referred to hospitals (e.g. heart attacks) as hospital services may be exhausted with
patients affected by the emergency.
Similarly, in the event of an outbreak of an infectious disease or an emergency, the profession also plays
a key role in educating community members and providing patients with quality health information.
Medicare Locals
Medicare Locals are locally governed and directed by local clinicians and other community health
leaders. Given that they are regional primary healthcare organisations, they are responsible for data
collection and identifying gaps in services and vulnerabilities in patient populations for their region.
As Medicare Locals have only been recently established, it is not entirely clear what role they will
play in emergency planning, response and coordination. However, it has been suggested that in
future it is likely that they will be tasked with providing primary healthcare facilities with support in
developing emergency response plans and business continuity plans including the coordination of
flu clinics in the event of a pandemic.
Key tasks and activities relating to emergency planning and management

undertaken by local governments
Local governments
• Maintenance of strong linkages with emergency • Development and maintenance of regional

services emergency plans
• Establishment and maintenance of strong linkages • Coordination of agency response (dependent on

with Medicare Locals and general practices hazard)
Appendix 2. Useful websites
National disaster/pandemic information and resources

• ABC Emergency - www.abc.net.au/news/emergency
• Australian Bureau of Meteorology (Tsunami Warning Centre) - www.bom.gov.au/index.shtml?ref=logo
• Australian Emergency Management Knowledge Hub - www.emknowledge.gov.au
• Australian Government - http://australia.gov.au/content/disaster-assistance
• Attorney-General’s Department - Australian Emergency Management - www.em.gov.au/Pages/
default.aspx
• Department of Health and Ageing - Pandemic Influenza - www.flupandemic.gov.au
• The Royal Australian College of General Practitioners - www.racgp.org.au/your-practice/
business/tools/disaster
Mental health and wellbeing

• Australian Centre for Grief and Bereavement - www.grief.org.au/grief
• Beyondblue - www.beyondblue.org.au
• Doctors’ Health Advisory Service - www.dhas.org.au
• Headspace - www.headspace.org.au
• Lifeline - www.lifeline.org.au
• Psychosocial Support in Disasters - www.psid.org.au
State/territory emergency contacts

• Australian Capital Territory Emergency Services Agency http://esa.act.gov.au/community-information
• New South Wales Ministry for Police and Emergency Services - www.emergency.nsw.gov.au/home.html
• Northern Territory Police, Fire and Emergency Services - www.pfes.nt.gov.au
• Queensland Disaster Management - http://disaster.qld.gov.au
• South Australian Fire and Emergency Services Commission - www.safecom.sa.gov.au/site/home.jsp
• Tasmanian Department of Police and Emergency Management - www.dpem.tas.gov.au
• Victorian State Emergency Service - www.ses.vic.gov.au
• Western Australia Department of Fire & Emergency Services - www.dfes.wa.gov.au/alerts/
Pages/default.aspx
State/territory health departments

• Australian Capital Territory - www.health.act.gov.au
• New South Wales - www.health.nsw.gov.au
• Northern Territory - www.health.nt.gov.au
• Queensland - www.health.qld.gov.au
• South Australia - www.health.sa.gov.au
• Tasmania - www.dhhs.tas.gov.au
• Victoria - www.health.vic.gov.au
• Western Australia - www.health.wa.gov.au
Appendix 3. Proposed pandemic stages
Australian phase Description
Preparedness • Establish arrangements and build and maintain capacities to ensure governments and the
health sector are able to respond effectively to seasonal influenza
• Monitor and investigate potential communicable disease threats
• Implement enhanced surveillance measures, if required
• Develop and exercise pandemic arrangements/plans ____
Standby • Prepare to commence enhanced arrangements

• Implement measures to raise awareness
• Continue enhanced surveillance measures
Response • Implement measures to minimise transmission, morbidity, mortality

• Response is divided into:
- Initial (when information about the disease is scarce); and
- Targeted
Standdown • Stand down enhanced arrangements

• Evaluation
Proposed pandemic stages provided by the Department of Health and Ageing
To reflect the differing focus of enhanced arrangements as the pandemic progresses, the AHMPPI is
divided into four stages. To ensure that flexibility is maintained, these stages are deliberately broad.
The activities associated with each stage may be implemented as determined by the needs of the
situation and may vary across jurisdictions.
References
1. Commonwealth of Australia. Attorney General’s Department. Disaster health - Handbook 1.

Canberra: Australian Emergency Management Institute, 2011.
2. United Nations Office for Disaster Risk Reduction (UNISDR) - Prevention Web. Available at
http://www.preventionweb.net/english/countries/statistics/?cid=9 [accessed March 2013].
3. Bushfire Cooperative Research Centre. Black Tuesday 1967 Tasmania bushfires. East
Melbourne: Bushfire CRC, 2003-2013. Available at www.bushfirecrc.com/resources/product/
black-tuesday-1967-tasmania-bushfires [accessed February 2013].
4. Egan J. Perfect storm led to Black Saturday bushfires. Australian Geographic 2012;9 August.
Available at www.australiangeographic.com.au/journal/perfect-storm-of-weather-led-to-black-
saturday-bushfires.htm [accessed February 2013].
5. Australian Psychological Society & Australian Red Cross. Psychological first aid: An Australian
guide 2011. Available at www.psychology.org.au/Assets/Files/Red-Cross-Psychological-First-
Aid-Book.pdf [accessed March 2013].
6. Commonwealth of Australia Attorney General’s Department. Australian Emergency
Management Knowledge Hub, Mt Macedon, Victoria: Australian Emergency Management Unit,
2012. Available at www.emknowledge.gov.au/ [accessed February 2013].
7. Insurance Council of Australia. Disaster Statistics. Sydney: ICA, 2013. Available at - www.
insurancecouncil.com.au/statistics [accessed February 2013].
8. Natural Disasters in Australia: Reforming mitigation, relief and recovery arrangements. A report
to the Council of Australian Governments by a higher level officials’ group. Canberra: COAG,
2002.
9. Knox SA, Harrison CM, Brit HC, et al. Estimating prevalence of common chronic morbidities in
Australia. Medical Journal of Australia 2008;189(2):66-70.
10. Commonwealth of Australia Department of Health and Ageing. Review of Australia’s health
sector response to pandemic (H1N1) 2009: lessons identified. Canberra: Department of Health
and Ageing, 2011.
11. Commonwealth of Australia Department of Health and Ageing. History of pandemics: 2009,
2011. Canberra: Department of Health and Ageing, 2013. Available at www.flupandemic.gov.au/
internet/panflu/publishing.nsf/Content/history-1#2009 [accessed March 2013].
12. Centres for Disease Control and Prevention. 2009 H1N1 flu. Atlanta, Georgia: CDC, 2010.
Available at www.cdc.gov/flu/ [accessed February 2013].
13. NSW Health and University of Western Sydney. Disaster Mental Health Manual 2012. University
of Western Sydney: Disaster Response and Resilience Research Group, 2012. Available at:
www.health.nsw.gov.au/emergency_preparedness/mental/Documents/NSW%20Health%20
Disaster%20MH%20Manual%202012%20Final%20version%20Feb%202013.pdf [accessed
March 2013].
14. Neria Y, Galea S, Norris F. Mental health and disasters. New York: Cambridge University Press,
2009.
15. Norris FH, Friedman MJ, Watson PJ. 60,000 Disaster victims speak: Part II. Summary and
implications of the disaster mental health research. Psychiatry 2002;65(3):240-60.
16. Kessler RC, Galea S, Gruber MJ, Sampson NA, Ursano RJ, Wessely S. Trends in mental illness
and suicidality after Hurricane Katrina. Molecular Psychiatry 2008; 374-84.
jfjRACGP
Healthy Profession.
Healthy Australia.
CLINICAL
Premature ejaculation: A clinical review

for the general physician
Eric Chung, Brent Gilbert, Marlon Perera, Matthew J Roberts
Background remature ejaculation is one of the ejaculatory latency time (IELT). The
Premature ejaculation is one of the most

common sexual dysfunctions in men.
Recent epidemiological studies suggest
P most common sexual dysfunctions,
affecting up to 21-31% of the
Australian adult male population,
irrespective of their age, marital status or
IELT is defined as the time from vaginal
penetration to ejaculation. Lifelong
premature ejaculation is characterised
by an IELT of <1 minutes since first
its prevalence in Australia may range
ethnicity.1-5 This sexual condition is likely intercourse, whereas IELT of <3 minutes
from 21-31%.
to be under-reported and under-treated at any point in a man’s life is considered
because of the patients’ perceived shame to be acquired premature ejaculation.12
Objective
and low self-esteem. This is in addition to Premature ejaculation can be further
This article will discuss the current many physicians feeling uncomfortable divided into authority-based subtypes
definition of premature ejaculation from or uncertain about the management ‘variable’ and ‘subjective’ (Table 1),
a urological perspective. It will provide of premature ejaculation.6,7 The impact which describe individuals experiencing
an understanding of the pathogenesis of premature ejaculation is mostly felt significant distress and dissatisfaction
of premature ejaculation, as well as psychologically and in interpersonal with ejaculation.12
assessment and management options. relationships.8 Men with premature
ejaculation often experience significant Pathophysiology and
Discussion psychological distress, avoid physical and associations
Premature ejaculation can have a emotional intimacy, and become victims Psychological components often
significant adverse effect on the quality of false medical advertisings and unproven contribute to acquired premature
of life for the patient and his sexual medical management.8-11 ejaculation. However, it is likely
partner’s. It can potentially lead to The aim of this article is to provide that a complex interplay between
psychological distress, diminished self general practitioners (GPs) with an neurophysiological factors predominantly
esteem, anxiety, erectile dysfunction, overview to assess and manage patients influence premature ejaculation. In
reduced libido and poor interpersonal with premature ejaculation and other particular, genetic predisposition for
relationships. Most men feel reluctant associated sexual dysfunction. impairment of inhibitory serotonergic
to discuss premature ejaculation with pathways that regulate ejaculation,
their general practitioner despite its Definition and classification modulated by 5-HT2c , 5-HT1a, 5-HT1b
psychological, emotional and relational Premature ejaculation is defined as the receptors and synaptic serotonin
effects. Effective, evidence-based inability to control or delay ejaculation, transporters has been reported for
treatment options are available and
which results in dissatisfaction or distress lifelong premature ejaculation.13,14 Other
physicians should feel confident when
for the patient. Recently, the International conditions, such as chronic prostatitis and
exploring ways to improve the quality of
Society of Sexual Medicine (ISSM) hyperthyroidism, may also be associated
life for men with sexual dysfunction.
classified premature ejaculation as lifelong with acquired premature ejaculation.15,16
or acquired, and proposed inclusion of an Erectile dysfunction and premature
objective, quantifiable time to ejaculation, ejaculation frequently co-exist,5,17 as men
which is referred to as the intravaginal with erectile dysfunction might try to
© The Royal Australian College of General practitioners 2015 reprinted from afp vol.44, no.10, october 2015 737
CLINICAL PREMATURE EJACULATION
ejaculate early, before loss of erection.17,18 It is also important to explore the neurological, lower limb and genital
Thus, detection of comorbid erectile perceived degree of ejaculatory control, examinations are recommended. Although
dysfunction is crucial in guiding therapeutic estimated IELT (precise timing is not examination has a low diagnostic yield, it
implementation.19 necessary), previous attempts to correct facilitates important reassurance for the
premature ejaculation, and the impact patient that he is anatomically normal.
Assessment of premature on interpersonal relationships and quality There are no specific investigations to
ejaculation of life. Various screening questionnaires confirm or exclude premature ejaculation.
Patients with premature ejaculation may such as the Premature Ejaculation Any additional investigations should
present to general practice because Diagnostic Tool (PEDT), when combined investigate suspicion of contributory
of personal or partner-initiated reports with clinical assessment, are accurate factors identified during history and
of erectile or sexual dysfunction, and in diagnosing premature ejaculation if examination.
relationship difficulties. However, when the it is unclear.20-22 It is particularly crucial
physician is unsure of the context of the to ascertain whether the diagnosis is Management of premature
presenting complaint, or uncertain about lifelong or acquired, and be aware that ejaculation
what to ask, an open-ended question, such erectile dysfunction may exacerbate the Ideally, discussions about management
as ‘How are things at home?’, may evoke presentation. Simply inquiring about the should involve the patient and his regular
disclosure of relevant symptoms. A full loss of an erection before ejaculation can sexual partner. Treatment choice requires
evaluation of the patient’s medical, sexual, help to distinguish erectile dysfunction consideration of symptom severity,
psychological, social and drug history, from premature ejaculation. reversible causes, psychosocial impact,
along with his partner’s sexual history, is Physical examination of patients side effects and patient preferences.23
necessary to identify any factors that may who experience premature ejaculation In clinical practice, management is
be potentially reversible. is often unremarkable. Full abdominal, complex and requires a combination
Table 1. Summary of the four classifications of premature ejaculation
Lifelong (primary) Acquired (secondary) Variable Subjective
IELT criteria <1 minute4 <3 minutes4 Short or normal Normal or prolonged
Symptoms Ejaculation occurs too New onset of premature PE is inconsistent Subjective, self
early in nearly every ejaculation, usually the and occurs irregularly perception of rapid
sexual encounter result of an identifiable and not the result of ejaculation despite
source and patient has (psycho)pathology normal ejaculation
experienced normal time
ejaculations in the past
Onset Early, usually from first Can occur at any time in Can occur at any time Can occur at any time
sexual encounter a man’s life in a man’s life in a man’s life
Prevalence Low Low High High
Quality of Ejaculation remains Ability to delay Ability to delay Ability to delay

ejaculation rapid throughout ejaculation may be ejaculation may be ejaculation may be
control lifetime with no ability diminished or lacking diminished or lacking diminished or lacking
to control ejaculation
Aetiology • Genetic • Urological (erectile Normal variance of Psychological

• Neurobiological dysfunction, prostatitis) sexual performance preoccupation with
• Hormonal imagined rapid
(hyperthyroidism) ejaculation
• Psychological
• Relationship problems
Treatment • Pharmacotherapy • Medical management • Reassurance • Psychotherapy

• Psychotherapy +/- • Pharmacotherapy • Education • Reassurance
• Psychotherapy • Behavioural therapy • Education
• Education
ELT, intravaginal ejaculatory latency time
738 reprinted from afp vol.44, no.10, october 2015 © The Royal Australian College of General practitioners 2015
PREMATURE EJACULATION CLINICAL
of pharmacological, psychological and constraints, costs and requirement for related to sexual dysfunctional, or in
behavioural treatments (Figure 1). strong compliance from couples. combination with pharmacotherapy.12,27
Inconsistent, randomised evidence
Conservative management evaluating psychological therapy suggests Behavioural therapy
options its efficacy decreases over time24 and is Various behavioural changes have been
inferior to pharmacotherapy.25 However, suggested in the literature. For example,
Psychological therapy psychological therapy may be a suitable precoital masturbation is widely thought
Initially, psychological therapy was the first-line treatment for patients with to improve IELT, but there is a lack of
mainstay of treatment for premature subjective premature ejaculation, or when data to support this practice. Alternative
ejaculation. It is used less in current a clear psychological aetiology is present.26 behavioural therapy modalities attempt
clinical practice because of time This can also be used to manage distress to attenuate the sensory responses of
Patient/partner history
Figure 1. Premature ejaculation management algorithm4

Reproduced with permission from Althof SE, Abdo CH, Dean J, et al. International Society for Sexual Medicine’s guidelines for the diagnosis and treatment
of premature ejaculation. J Sex Med 2010;7:2947-69.
ejaculation by interrupting heightened The therapeutic efficacy of SSRIs for 30 minutes before sexual intercourse.
arousal. These include the ‘stop premature ejaculation is well supported Published studies found dapoxetine to be
start’ (ceased genital stimulation until by the literature.36 Daily SSRI use may equally effective in men with lifelong and
heightened arousal sensation subsides)28 improve ejaculation delay after a few days; acquired premature ejaculation. It was
and ‘squeeze’ (where the glans prepuce maximal delay is usually achieved after 1-2 also found to be well tolerated in men
is squeezed at heightened arousal)29 weeks. Paroxetine is the most effective with premature ejaculation and comorbid
techniques. These techniques are often SSRI. However, paroxetine is not suitable erectile dysfunction treated with
considered intrusive, mechanical and for on-demand use because it has a slow phosphodiesterase-5 type drugs.36,40
disruptive of the normal spontaneity of onset of action (5 hours) and long half-life
coitus, and of little benefit when used (1-3 days), and daily dosing is required to Phosphodiesterase-5 inhibitors
alone. Other behavioural techniques maintain efficacy.12 Daily SSRI dosing is
The precise beneficial mechanism
include the use of multiple condoms and more effective than on-demand treatment
of phosphodiesterase-5 inhibitors for
pelvic floor exercises. These techniques and is often favoured by patients because premature ejaculation is unclear and its
may improve premature ejaculation when spontaneity of sex is maintained; however, use as monotherapy is controversial.41,42
combined with pharmacotherapy, but compliance issues can occur with long It does not affect IELT but may improve
further efficacy studies are required.30 term use. premature ejaculation in patients
Doses of SSRI for premature ejaculation with comorbid erectile dysfunction
Complementary and alternative are significantly less than those used by providing a perception of greater
therapy for depression, but have a similar side control over ejaculation.41 In this
There is limited evidence supporting the effect profile. Common side effects are population, guidelines suggest treating
use of acupuncture for the treatment fatigue, nausea, diarrhoea, dry mouth erectile dysfunction and assessing the
of premature ejaculation.31 However, and decreased libido.37 There are also response on premature ejaculation
complementary and alternative medicine anecdotal accounts of infertility.38 symptomatology.12
is not a recommended form of treatment Serotonin syndrome may also pose a risk
Tramadol
for premature ejaculation.32 if the patient is on concomitant treatment
with drugs that elevate serotonin levels.37 Tramadol is an effective, on-demand
Medical management Despite evidence supporting the use treatment for premature ejaculation,
of clomipramine and traditional SSRIs (eg although the mechanism of action is
Topical anaesthetic agents paroxetine, sertraline and fluoxetine) for unknown. Doses of 25-62 mg were
Anaesthetic aerosols and creams the treatment of premature ejaculation, well tolerated, compared with placebo,
containing lignocaine, lignocaine/ they are not licenced for treatment of and were found to significantly increase
prilocaine or herbal-derived anaesthetic this condition. As such, use of these IELT, heighten sexual satisfaction and
agents can increase IELT and sexual agents for premature ejaculation would improve ejaculatory control.43,44 These
satisfaction. These agents are often be off-label and incur costs to the results were more pronounced in patients
recommended as treatments for patient, as they are not subsidised by the with severe premature ejaculation
premature ejaculation.12,33-35 They are Pharmaceutical Benefits Scheme (PBS) for (baseline IELT <1 minute). Tramadol has
applied to the glans penis well ahead of this indication.24 a number of drug interactions and should
sexual intercourse and should be used In 2010, the Therapeutic Goods be used with caution in combination
in conjunction with condoms to avoid Administration (TGA) approved dapoxetine with SSRIs because of the risk of
numbness in the partner’s genitals. for the use in premature ejaculation serotonin syndrome. It should only be
in Australia. However, this remains considered for monotherapy use in men
Serotonergic antidepressants unsubsidised by the PBS. Dapoxetine is with refractory premature ejaculation.12
Serotonin inhibits ejaculation and its a newly developed SSRI that is rapidly Ongoing studies are required to evaluate
effects are potentiated by tricyclic absorbed (1-3 hours) and provides drug interactions, opioid dependence
antidepressants (TCAs) and selective fast-acting treatment of premature issues and the underlining mechanism of
serotonin reuptake inhibitors (SSRIs). ejaculation.39 Similarly to other SSRIs, action.43
TCAs are effective, but infrequently dapoxetine should be used with caution
used because they have prominent side in patients with cardiac, hepatic or renal Surgical management
effects, including nausea, dry mouth, impairment. Dapoxetine has been shown Circumcision and surgical management
erectile dysfunction, hot flushes and to increase IELT by 2.5-3 minutes with options for premature ejaculation are
cardiotoxicity. Clomipramine is the only minimal adverse effects.36,40 Patients currently under investigation and not
TCA in routine use.12,35 should take 30 mg of dapoxetine at least recommended. Experimental surgical
Table 2. Summary of current medical agents for premature ejaculation
Recommended Half-life IELT fold

Agent dose (hours) increase Adverse effects Additional notes
Dapoxetine 30-60 mg, 1.5 2.5-3 Nausea, diarrhoea, • TGA approved, not
(SSRI) - short 1-3 hours before headache, currently on PBS
acting intercourse somnolence, dizziness • No significant drug-drug
interactions
• Effective treatment for both
acquired and lifelong PE
Paroxetine 10-40 mg/day 21 11.6 Insomnia, anxiety,

(SSRI) and nausea, loss of libido,
20 mg, 3-4 hours ED, anhidrosis
prior to
intercourse
Fluoxetine 20-40 mg/day 36 5 Insomnia, anxiety, • Used for lifelong and

(SSRI) nausea, loss of libido, acquired PE
ED, anhidrosis • Therapeutic effect
Sertraline 50-200 mg/day 26 5 Insomnia, anxiety, • May hinder sperm motility

(SSRI) and nausea, loss of libido, • May induce mania in
50 mg, 4-8 ED, anhidrosis bipolar patients
hours prior to • On-demand use not as
intercourse effective without daily
Clomipramine 12.5-50 mg/day 19-37 6 Nausea, dry mouth,

(TCA) and ED, hot flushes,
25 mg, 4-24 arrhythmias
hours prior to
intercourse
Tramadol 25-50 mg, 3-5 5-7 4-7.3 Nausea, dizziness, • Possible opioid addiction
hours prior to insomnia, dyspepsia, • TCAs and SSRIs are
intercourse seizures contraindicated with
Tramadol use
• Multiple drug interactions-
only indicated as
monotherapy in refractory
PE
Phosphodiester 25-100 mg, 3-6 Monotherapy Headache, flushing, • Used for concomitant ED
ase-5 inhibitors 30-50 minutes has no effect dyspepsia and PE
prior to on IELT • Improved efficacy when
intercourse combined with SSRI
therapy
• Not established
monotherapy for PE
Prilocaine- 2.5 g, applied 1-2 4-6 ED, loss of sensation • Condom use encouraged
lignocaine topical 20-30 minutes in penis and partner’s • Used with SSRIs
cream/aerosols prior to vagina, skin irritation • Off-label prescription
intercourse
ED, erectile dysfunction; SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressants; TGA, Therapeutic Goods Administration; PBS, Pharmaceutical
Benefits Scheme
therapies, such as dorsal penile nerve • Currently, no premature ejaculation 13. Jern P, Santtila P, Witting K, et al. Premature and
delayed ejaculation: Genetic and environmental
cryoablation, and neuromodulation and therapies are subsidised by the PBS.
effects in a population-based sample of Finnish
hyaluronic acid gel glans augmentation for twins. J Sex Med 2007;4:1739-49.
Authors
refractory lifelong premature ejaculation 14. Janssen PK, Bakker SC, Rethelyi J, et al.
Eric Chung MBBS, FRACS, Consultant Urological Serotonin transporter promoter region (5-HTTLPR)
have been reported to improve IELT.45-47 Surgeon, University of Queensland, Princess polymorphism is associated with the intravaginal
Botulinum toxin injections into ejaculatory Alexandra Hospital, Brisbane QLD; and ejaculation latency time in Dutch men with
AndroUrology Centre, Brisbane QLD. ericchg@ lifelong premature ejaculation. J Sex Med
muscles are currently being explored to hotmail.com 2009;6:276-84.
prevent premature ejaculation.48 Brent Gilbert MBBS, Urology Resident Medical 15. Maggi M, Buvat J, Corona G, Guay A, Torres LO.
Officer, Mackay Base Hospital, Mackay QLD Hormonal causes of male sexual dysfunctions
Follow-up and referral Marlon Perera MBBS, Urology Registrar, Mackay and their management (hyperprolactinemia,
Base Hospital, Mackay QLD thyroid disorders, GH disorders, and DHEA). J Sex
Follow-up is an essential part of premature Matthew J Roberts MBBS, PhD, Urology Registrar, Med 2013;10:661-77.
ejaculation management. lt facilitates Mackay Base Hospital, Mackay QLD, and The 16. Liang CZ, Zhang XJ, Hao ZY, Shi HQ, Wang KX.
University of Queensland, School of Medicine, Prevalence of sexual dysfunction in Chinese men
treatment optimisation, emphasis on key with chronic prostatitis. BJU Int 2004;93:568-70.
Brisbane QLD
features of premature ejaculation and Competing interests: Eric Chung has previously
17. Jannini EA, Lombardo F, Lenzi A. Correlation
between ejaculatory and erectile dysfunction. Int
enables additional information gathering.49 been paid for consultancy and/or lectures by Lilly,
J Androl 2005;28 Suppl 2:40-45.
GSK and Astellas.
ln complex or refractory cases, specialist 18. Rowland D, McMahon CG, Abdo C, et al.
Provenance and peer review: Not commissioned,
assistance may be sought from a sexual externally peer reviewed.
Disorders of orgasm and ejaculation in men.
J Sex Med 2010;7:1668-86.
health physician or urologist. lnput from
19. McMahon CG. Screening for erectile dysfunction
sex therapists or psychiatrists may also be References in men with lifelong premature ejaculation - Is the
beneficial. 1. Althof SE. Prevalence, characteristics and Sexual Health Inventory for Men (SHIM) reliable?
implications of premature ejaculation/rapid J Sex Med 2009;6:567-73.
ejaculation. J Urol 2006;175:842-48. 20. Althof S, Rosen R, Symonds T, Mundayat R, May
Conclusion 2. McMahon CG, Lee G, Park JK, Adaikan PG. K, Abraham L. Development and validation of a
Premature ejaculation is the most Premature ejaculation and erectile dysfunction new questionnaire to assess sexual satisfaction,
prevalence and attitudes in the Asia-Pacific region. control, and distress associated with premature
common cause of male sexual J Sex Med 2012;9:454-65. ejaculation. J Sex Med 2006;3:465-75.
dysfunction. Most patients who 3. Porst H, Montorsi F, Rosen RC, Gaynor L, Grupe S, 21. Symonds T, Perelman M, Althof S, et al. Further
Alexander J. The Premature Ejaculation Prevalence evidence of the reliability and validity of the
experience premature ejaculation are
and Attitudes (PEPA) survey: Prevalence, premature ejaculation diagnostic tool. Int J Impot
likely to require multi-modal management comorbidities, and professional help-seeking. Eur Res 2007;19:521-25.
strategies involving pharmacological, Urol 2007;51:816-23. 22. Kam SC, Han DH, Lee SW. The diagnostic value
4. Althof SE, Abdo CH, Dean J, et al. lnternational of the premature ejaculation diagnostic tool and
behavioural and psychological its association with intravaginal ejaculatory latency
Society for Sexual Medicine’s guidelines for the
components. Patients should be diagnosis and treatment of premature ejaculation. time. J Sex Med 2011;8:865-71.
monitored closely to ensure treatment and J Sex Med 2010;7:2947-69. 23. Porst H. An overview of pharmacotherapy in
5. Laumann EO, Paik A, Rosen RC. Sexual premature ejaculation. J Sex Med 2011;8 Suppl
sexual satisfaction. dysfunction in the United States: Prevalence and 4:335-41.
predictors. JAMA 1999;281:537-44. 24. Melnik T, Althof S, Atallah AN, Puga ME, Glina S,
Key points 6. Moreira ED Jr, Brock G, Glasser DB, et al. Help Riera R. Psychosocial interventions for premature
seeking behaviour for sexual problems: The global ejaculation. Cochrane Database Syst Rev
• Premature ejaculation is the most study of sexual attitudes and behaviors. lnt J Clin 2011:CD008195.
common cause of sexual dysfunction, Pract 2005;59:6-16. 25. Steggall MJ, Fowler CG, Pryce A. Combination
7. Aschka C, Himmel W, lttner E, Kochen MM. Sexual therapy for premature ejaculation: Results of a
especially in the younger age group.
problems of male patients in family practice. J Fam small scale study. Sex Relation Ther 2008;23:
• lt is estimated that premature Pract 2001;50:773-78. 365-76.
ejaculation affects up to 31% of 8. Symonds T, Roblin D, Hart K, Althof S. How does 26. Waldinger MD. Recent advances in the
premature ejaculation impact a man s life? J Sex classification, neurobiology and treatment of
Australian males. premature ejaculation. Adv Psychosom Med
Marital Ther 2003;29:361-70.
• Premature ejaculation causes 9. Althof S. The psychology of premature ejaculation: 2008;29:50-69.
significant psychological, emotional and Therapies and consequences. J Sex Med 2006;3 27. De Amicis LA, Goldberg DC, LoPiccolo J,
Suppl 4:324-31. Friedman J, Davies L. Clinical follow-up of couples
interpersonal distress for the patient treated for sexual dysfunction. Arch Sex Behavior
10. Rosen RC, Althof S. lmpact of premature
and his partner. ejaculation: The psychological, quality of life, and 1985;14:467-89.
sexual relationship consequences. J Sex Med 28. Semans JH. Premature ejaculation: A new
• Premature ejaculation can be lifelong
2008;5:1296-307. approach. South Med J 1956;49:353-58.
(primary) or acquired (secondary), and 11. Rowland D, Perelman M, Althof S, et al. Self 29. Masters WJV. Human sexual inadequacy. Boston:
this distinction guides management. reported premature ejaculation and aspects of Little Brown, 1970.
sexual functioning and satisfaction. J Sex Med 30. Hartmann UH. Words of wisdom. Re: Effects
• Management of premature ejaculation
2004;1:225-32. of a new functional-sexological treatment for
should involve the patient and his 12. Althof SE, McMahon CG, Waldinger MD, et al. premature ejaculation. Eur Urol 2007;52:1259-61.
partner, and is likely to require a multi An update of the lnternational Society of Sexual 31. Sunay D, Sunay M, Aydogmus Y, et al.
Medicine’s Guidelines for the Diagnosis and Acupuncture versus paroxetine for the treatment
modal approach with pharmacological, Treatment of Premature Ejaculation (PE). J Sex of premature ejaculation: A randomized, placebo-
behavioural and psychological therapies. Med 2014;2:60-90. controlled clinical trial. Eur Urol 2011;59:765-71.
32. Ho CC, Singam P, Hong GE, Zainuddin ZM. 39. Pryor JL, Althof SE, Steidle C, et al. Efficacy premature ejaculation: A double-blind, placebo-
Male sexual dysfunction in Asia. Asian J Androl and tolerability of dapoxetine in treatment of controlled, fixed-dose, randomized study. J Clin
2011;13:537-42. premature ejaculation: An integrated analysis of Psychopharmacol 2006;26:27-31.
33. Atan A, Basar MM, Tuncel A, Ferhat M, Agras K, two double-blind, randomised controlled trials. 45. Kwak TI, Jin MH, Kim JJ, Moon DG. Long-term
Tekdogan U. Comparison of efficacy of sildenafil- Lancet 2006;368:929-37. effects of glans penis augmentation using
only, sildenafil plus topical EMLA cream, and injectable hyaluronic acid gel for premature
40. Porst H, McMahon CG, Althof SE, et al. Baseline
topical EMLA-cream-only in treatment of ejaculation. Int J Impot Res 2008;20:425-28.
characteristics and treatment outcomes for men
premature ejaculation. Urol 2006;67:388-91. with acquired or lifelong premature ejaculation 46. Abdallah H, Abdelnasser T, Hosny H, Selim O,
34. Busato W, Galindo CC. Topical anaesthetic use with mild or no erectile dysfunction: Integrated Al-Ahwany A, Shamloul R. Treatment of premature
for treating premature ejaculation: A double analyses of two phase 3 dapoxetine trials. J Sex ejaculation by glans penis augmentation using
blind, randomized, placebo-controlled study. BJU Med 2010;7:2231-42. hyaluronic acid gel: A pilot study. Andrologia
Int 2004;93:1018-21. 2012;44 Suppl 1:650-53.
41. McMahon CG, McMahon CN, Leow
35. Hatzimouratidis K, Amar E, Eardley I, et al. LJ, Winestock CG. Efficacy of type-5 47. Namavar MR, Robati B. Removal of foreskin
Guidelines on male sexual dysfunction: Erectile phosphodiesterase inhibitors in the drug remnants in circumcised adults for treatment of
dysfunction and premature ejaculation. Eur Urol treatment of premature ejaculation: A systematic premature ejaculation. Urol Ann 2011;3:87-92.
2010;57:804-14. review. BJU Int 2006;98:259-72. 48. Serefoglu EC, Silay MS. Botulinum toxin-A injection
36. McMahon CG, Althof SE, Kaufman JM, et 42. Aversa A, Pili M, Francomano D, et al. Effects may be beneficial in the treatment of life-long
al. Efficacy and safety of dapoxetine for the of vardenafil administration on intravaginal premature ejaculation. Med Hypoth 2010;74:83-84.
treatment of premature ejaculation: Integrated ejaculatory latency time in men with lifelong 49. Moncada I. The importance of follow-up in patients
analysis of results from five phase 3 trials. J Sex premature ejaculation. Int J Impot Res with premature ejaculation. The J Sex Med 2011;8
Med 2011;8:524-39. 2009;21:221-27. Suppl 4:353-59.
37. Montague DK, Jarow J, Broderick GA, et al. AUA 43. Salem EA, Wilson SK, Bissada NK, Delk JR,
guideline on the pharmacologic management of Hellstrom WJ, Cleves MA. Tramadol HCL has
premature ejaculation. J Urol 2004;172:290-94. promise in on-demand use to treat premature
38. Tanrikut C, Feldman AS, Altemus M, Paduch DA, ejaculation. J Sex Med 2008;5:188-93.
Schlegel PN. Adverse effect of paroxetine on 44. Safarinejad MR, Hosseini SY. Safety and
sperm. Fert Ster 2010;94:1021-26. efficacy of tramadol in the treatment of correspondence afp@racgp.org.au
HANDI
Making non-drug
to find and use
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Physiotherapy: lateral epicondylitis
Intervention A physiotherapy program that includes exercise, elbow manipulation (manual therapy)
and self-manipulation.
Progressive exercise of the wrist extensor muscles may also be used alone, without
elbow manipulation.
Indication Lateral epicondylitis (LE), commonly known as ‘tennis elbow’, where pain persists for 6
weeks or more; however, earlier institution of exercise might also confer benefit.
Tennis elbow affects 1-3%
of the population; risk factors
include smoking, obesity, being LE is a chronic degenerative process stemming from microtrauma (rather than an acute
aged 45-54 and two or more inflammatory process). Hence, the term lateral epicondylalgia is also used.
hours of repetitive movement
per day.
In most cases, symptoms of LE are self-limiting and usually resolve within 12 months.
However, physiotherapy may reduce the time taken to improve pain (i.e. provide
short-term benefit) and reduce the recurrence and delayed recovery associated with
alternative interventions such as corticosteroid injection (i.e. provide improved long-term
outcomes).
When compared with a wait-and-see approach or corticosteroid injection, a

physiotherapy program involving exercise is associated with a greater reduction in
severity and greater success in both the short and long term.
Significant differences between study arms at six and 12 weeks: fcorticosteroid injection v wait and see;
^physiotherapy v wait and see; §corticosteroid injection v physiotherapy. *Significant differences between
groups (P<0.01)
Source: Bisset L, Beller E, Jull G et al. Mobilisation with movement and exercise, corticosteroid injection,
or wait and see for tennis elbow: randomised trial. BMJ. 2006;333(7575):939.
First published: January 2016 Reprinted with permission from The Royal Australian College of General Practitioners. Royal Australian College of General Practitioners
HANDI
Making non-drug
to find and use
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Availability A physiotherapy program will typically involve eight 30-minute sessions with a
physiotherapist. To find a physiotherapist, go to The Australian Physiotherapy
Association’s Find a Physio webpage.
A low-cost alternative is a home-based exercise program using rubber resistance

bands, which may be demonstrated in a general practice consultation.
Description A physiotherapy program will typically combine exercise and elbow manipulation
(manual therapy). Various techniques may be used, including those described here.
Exercise
Figures 1(a) and 1(b) below demonstrate a forearm muscle exercise for the wrist
extensor muscles. The exercise involves the application of load while the muscle
gradually contracts and moves the wrist from flexion to extension and back to flexion.
Figure 1(a). Starting and ending flexed position - do not go to end of range. Note elbow
is flexed and forearm is supported. The other end of the elastic band is fixed by the
patient’s foot or other hand.
iLJII >* HW. ■ ■ Making non-drug
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to find and use
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Description
(cont’d)
Figure 1(b). Extended position mid-point of exercise - the target. Note elbow is flexed
and forearm is supported on bench.
To perform the exercise: start with the wrist in a flexed position, then move through the
range of extension over 4 seconds and then return to a flexed position over 4 seconds.
Load is applied using a resistance band or small weight.
The exercise should be supervised f or the first 6-8 weeks to ensure the right load is
used and the correct movement/form is performed, and that the load and degree of
difficulty is progressed.
Exercise should not provoke pain beyond 2 out of 10 on a scale where 10 is the worst
pain imaginable and 0 is no pain. Where moving the wrist through flexion and extension
provokes pain, the patient can start with a static (or isometric) wrist extensor exercise
demonstrated in Figure 2. Here, without bending the wrist, the patient resists downward
pressure applied (by the other hand, physiotherapist or GP).
__.■____ .
to find and use
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Description
(cont’d)
Figure 2. Patient performing isometric exercise by using the other hand. Make sure to
have the wrist in some extension.
Duration, frequency and progression

In the first 2 weeks, the patient should exercise twice daily, doing 12-15 repetitions.
From 2 to 6 weeks, the patient should perform the exercise once daily, doing three sets
of 8-12 repetitions on both arms. From 6 weeks onward, the load can be progressed
and the patient performs three sets of 6-8 repetitions every other day (if the patient’s
strength is nearing 80% of the unaffected side).
Additional exercises
If the patient has time, other exercises can be used such as gripping exercise putty, or
supination and pronation exercises as shown in Figure 3 and Figure 4. Patients who
perform repetitive tasks in their day-to-day work should be specifically assessed for
individualised exercises for those tasks once their strength improves (to approximately
90% of the unaffected side).
iL-Jil >* HW ■ ■ Making non-drug
__.■_____ .
to find and use
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Description
(cont’d)
Figure 3(a). Resisted supination start position, moving to supination and then back to
this neutral position. A progression can be to start in a more pronated position.
Figure 3(b). Resisted supination exercise (at mid-position of supination), with forearm
supported on bench.
iL-Jil >* HW ■ ■ Making non-drug
__.■_____ .
to find and use
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Description
(cont’d)
Figure 4(a). Resisted pronation: starting in supination the patient pronates the forearm,
holding onto the elastic band with the other hand. Forearm is supported on bench.
Figure 4(b). Resisted pronation: target position of pronation is reached before slowly
returning to starting supinated position.
__.■____ .
to find and use
.iinuhtt
Description Elbow manipulation (manual therapy)
Two techniques used are the ulnar-humeral lateral glide (Figure 5) and radial head
(cont’d) posteroanterior glide (Figure 6).
Figure 5. Ulnar-humeral lateral glide: this involves lateral elbow mobilisation with
movement. While the patient performs (and relaxes) their painful action (e.g. gripping), a
lateral humero-ulnar accessory glide is applied and sustained. If significant improvement
in pain-free grip is observed, repeat the technique for a total 6 to 10 repetitions. A belt
may be used to assist with the glide.
__.■____ .
to find and use
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Description
(cont’d)
Figure 6. Radial head posteroanterior glide: while the patient performs (and relaxes) their
painful action (e.g. gripping), a posterior to anterior glide over the radial head is applied
and sustained. If significant improvement in pain-free grip is observed, repeat the
technique 6 to 10 times.
See Training for additional instructions.
Tips and challenges Patients with tennis elbow can be reassured that most cases will improve by adopting a
wait-and-see approach.
Wait-and-see approach
The symptoms of LE will usually resolve within 6-12 months if the patient follows simple
advice including:
• remain active and do not restrict arm or elbow movements
• do not perform movements and tasks that provoke pain greater than 3 out of 10
(where 10 is the worst pain imaginable)
• do not immobilise the elbow or upper limb
• do not lift an object with hands in the face-down position.
The wait-and-see approach typically results in a good outcome in the long term, but
many patients do seek active treatments. Where there has been no improvement after
6-12 weeks of waiting and seeing, physiotherapy may be beneficial.
HANDI
Making non-drug
to find and use
jinuhtt
Tips and challenges Other approaches
Corticosteroid injection may provide short-term pain relief (4-6 weeks) but long-term
(cont’d) outcomes will likely be worse than adopting a wait-and-see approach or physiotherapy.
(See Indication)
Most of the muscles in the upper limb (from the shoulder to the fingers) are weak in
patients with long-term LE, therefore patients should be advised to undertake general
strengthening exercises for the upper limb. These need to be done with care so to not
exacerbate elbow pain.
Grading NHMRC Level 1 evidence.
Training Vicenzino B. Lateral epicondylalgia: a musculoskeletal physiotherapy perspective. Man

Ther. 2003;8(2):66-79. (www.ncbi.nlm.nih.gov/pubmed/12890434)
Vicenzino B, Hing W, Rivett D, Hall T. Mobilisation with movement: the art and the
science. Churchill Livingstone; 2011.
References Sims S, Miller K, Elfar J, Hammert W. Non-surgical treatment of lateral epicondylitis: a

systematic review of randomized controlled trials. Hand. 2014;9:419-446.
Cullinane F, Boocock M, Trevelyan F. Is eccentric exercise an effective treatment for

lateral epicondylitis? A systematic review. Clin Rehab. 2014;28(1):3-19. (www.ncbi.nlm.
nih.gov/pubmed/25414603)
Olaussen M, Holmedal O, Lindeak M et al. Treating lateral epicondylitis with

corticosteroid injections or non-electrotherapeutical physiotherapy: a systematic review.
BMJ Open. 2013;3:e003564 doi:10.1136/bmjopen-2013-003564. (http://bmjopen.bmj.
com/content/3/10/e003564.abstract)
Consumer resources The Better Health Channel provides some basic information about elbow pain.
Patient.co.uk offers a brief decision aid for tennis elbow (http://patient.info/decision-

aids/tennis-elbow-decision) as well as general information (http://patient.info/blogs/
sarah-says/2013/07/getting-to-grips-with-tennis-elbow)
RACGP’s Patient Information sheet - Exercise for tennis elbow
Acknowledgement With thanks to Bill Vicenzino, Professor in Sports Physiotherapy at the University of
Queensland, for providing input and images.
The Royal Australian
College of General
Should I have prostate cancer
Practitioners
screening?
There is significant debate about prostate cancer
Who is this information for? screening. This is because many prostate cancers that
are detected are low risk (the slow growing type) and
This brief information sheet is designed to help you would never have caused harm to the man, but testing
have an informed discussion with your GP. It is for: for and treating these cancers can cause harm.
• healthy men with no signs or symptoms Because of these issues, population-based screening is
(known as asymptomatic) and with no close not recommended and there is no government organised
blood relative with the disease national population prostate cancer screening program like
there are for other cancers such as breast and bowel cancer.
• aged 50-69 years
• who are considering a prostate specific antigen
(PSA) blood test to screen for prostate cancer.
What are my options?
You can choose to have the prostate cancer screening or
If you have a family history or any symptoms,
decide not to have the test at this time. There is no right
such as difficulty passing urine, or other
or wrong answer.
concerns about your prostate you should
also speak to your GP. For men aged 50-69 (without a family history of prostate
cancer) the benefit/harm debate for prostate screening
using the PSA test is unclear and open to individual
interpretation. Hence Australian guidelines support
What is prostate cancer? informed decision-making about prostate cancer
Prostate cancer is a tumour (or growth of cell) that starts in screening based on personal circumstances. Since the
the prostate gland. The prostate gland sits just below the decision to have prostate cancer screening is a personal
bladder and is about the size of a golf ball. The prostate one, it is up to the individual to request testing from their GP.
produces most of the fluid that makes up semen and
Figure 1 is designed to assist you in seeing the numbers
nourishes the sperm.
of people affected by each option and help weigh up
There are different types of prostate cancer - most grow the benefits, harms and uncertainties of prostate cancer
slowly and never cause harm, while others spread to other screening.
parts of the body and cause serious harm, and even death.
What are the tests for prostate

What increases my risk of prostate
cancer?
cancer?
• Blood test for PSA. This test is controversial as a
Prostate cancer is more common as you get older. It is screening test because:
also more common if you have at least one close blood
relative with prostate cancer (ie father, brother or son - PSA levels may be elevated from causes other than
diagnosed under 65 years of age). prostate cancer
- there is debate about what constitutes a ‘normal’

and an ‘abnormal’ PSA level when screening.
Where can I get information if I have The test is often repeated if it is only mildly elevated
a family history of prostate cancer? - the PSA test does not discriminate between those
Information has been developed for men with a family cancers that will cause harm and those that will
history of prostate cancer and is available on the NSW not (see ‘What is prostate cancer?’ section above).
Health Department’s Centre for Genetic Education
• Digital rectal examination, where the doctor inserts
website at www.genetics.edu.au/Genetic-conditions- a finger into the anus to examine the prostate, is no
support-groups/prostate-cancer-screening
longer recommended in addition to PSA testing.
A prostate biopsy may be recommended if there is

What is prostate cancer screening? an elevated PSA or a rapid rise in PSA. A biopsy is
Cancer screening is testing to detect a disease early, a procedure in which samples of prostatic tissue are
removed. It is needed to confirm whether prostate
before any signs or symptoms of disease, in order to treat
the disease before it does any harm. The benefit of early cancer is present.
testing and detection has to outweigh any potential harm.
Healthy Profession.
Healthy Australia. www.racgp.org.au
Figure 1. Risks and benefits of PSA screening
Adapted with permission from Harding Center for Risk Literacy.
1000 men aged 55-69

WITHOUT annual PSA screening over 11 years WITH annual PSA screening over 11 years
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* 5 men die from prostate cancer * 4 men die from prostate cancer, * 1 man is possibly saved
through testing
fl 190 men die from other causes § 190 men die from other causes
* 55 men alive with symptomatic prostate cancer * 55 men alive with symptomatic prostate cancer
* 782 men alive with no prostate cancer * 715 men alive with no prostate cancer
* 87 men learned after biopsy their PSA result was a false
References positive
1. NHMRC PSA testing for Prostate Cancer in Asymptomatic men available at £ 28 men have side effects that require healthcare or
www.nhmrc.gov.au/
_files_nhmrc/publications/attachments/men4d_psa_testing_
hospitalisation after a biopsy
asymptomatic_men_140304.pdf 25 men will choose to have treatment due to uncertainty about
2. Schroder FH, Hugosson J, Roobol MJ, et al. NEJM 2012;366:981-90. which cancers need to be treated. Many of these men would
3. Harding Center for Risk Literacy. Available at do well without treatment (ie. they are over-treated)
www.harding-center.mpg.de/en/health-information/facts-boxes/psa
4. Schroder FH, Hugosson J, Roobol MJ, et al. Screening and prostate
* 37 men with an elevated PSA were found to have slow-growing
cancer mortality: results of the European Randomised Study of Screening cancers (ie harmless and therefore over-diagnosed)
for Prostate Cancer (ERSPC) at 13 years of follow-up. The Lancet 2014;
384(9959):2027-35. j 7-10 men who have treatment will experience impotence and/
5. Guidelines for preventive activities in general practice, 8th edn, Royal or urinary incontinence or bowel problems. 0.5 men could
Australian College of General Practitioners, 2012. have a heart attack due to treatment.
The Royal Australian College of General Practitioners, 100 Wellington Parade, East Melbourne Victoria 3002.
Tel 03 8699 0414 | Fax 03 8699 0400 | www.racgp.org.au
Acknowledgements
This fact sheet was developed by Professor Lyndal Trevena, University of Sydney; Professor Paul Glasziou, Bond University; Adjunct Associate
Professor Leanne Rowe, University of Sydney; and Dr Evan Ackermann, RACGP National Standing Committee - Quality Care.
Published August 2015. © The Royal Australian College of General Practitioners
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 general nature only and may or may not be
relevant to particular practices or circumstances. 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 doing so. 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 or any error, negligent act, omission or misrepresentation in the information.
JJracgp QI&CPD Program
Handbook for general

practitioners
2017
19
2017-19
www.racgp.org.au triennium
QI&CPD Program: 2017-19 triennium handbook for general practitioners
Disclaimer
The Royal Australian College of General Practitioners. QI&CPD Program: 2017-19 triennium handbook for
general practitioners. East Melbourne, Vic: RACGP, 2016.

Tel 03 8699 0510

Fax 03 9696 7511
www.racgp.org.au
ABN 34 000 223 807

978-0-86906-447-4 (web)
Published July 2016

2017
19
|RACGP QI&CPD Program
Handbook for general

practitioners
QI&CPD Program
2017-19 triennium handbook for general practitioners
iii
Acronyms
ACCHS Aboriginal community controlled health service
AHPRA Australian Health Practitioner Regulation Agency
ALM Active learning module
ALS Advanced life support
AQF Australian Qualifications Framework
ARC Australian Resuscitation Council
ARSP Advanced rural skills post
ASGC-RA Australian Standard Geographical Classification - Remoteness Area
CPD Continuing professional development
CPR Cardiopulmonary resuscitation
DRANZCOG Diploma of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists
EAR Education activity representative
EBMJC Evidence-based medicine journal club
FARGP Fellowship of Advanced Rural General Practice
FRACGP Fellowship of The Royal Australian College of General Practitioners
GP General practitioner
GPMHSC General Practice Mental Health Standards Collaboration
HREC Human Research Ethics Committee
NREEC National Research and Evaluation Ethics Committee
PDSA Plan, do, study, act
PLAN Planning learning and need
QI&CPD Quality improvement and continuing professional development
QI Quality improvement
RACGP Royal Australian College of General Practitioners
RPGP Rural Procedural Grants Program
RTO Regional training organisation
SCA Supervised clinical attachment
SGL Small group learning
QI&CPD Program
iv 2017-19 triennium handbook for general practitioners
Contents
Introduction 1
Educational underpinnings of theQI&CPD Program 2
QI&CPD Program requirements for the2017-19 triennium 3
QI&CPD Program activities 4
What is different in the 2017-19 QI&CPD requirements and why? 5
QI&CPD Program participation 6
Enhancing patient care through QI activities 7
Activity design components 8
Linking the curriculum and domains to the QI&CPD Program 9
Quality assurance assessment process 11
GPfeedback on education activities 11
Quality assurance of GP self-directed activities 12
Using myRACGP to navigate to myCPD 13
Category 1 activities 15
Planning learning and need (40 Category 1 points) 17
Small group learning (40 Category 1 points) 19
Supervised clinical attachment (40 Category 1 points) 21
The plan, do, study, act cycle (40 Category 1 points) 23
Clinical audit (40 Category 1 points) 25
Evidence-based medicine journal club (40 Category 1 points) 27
General practice research (40 Category 1 points) 29
Active learning module (40 Category 1 points) 31
Educator ALMs (40 Category 1 points) 33
Peer-reviewed journal article module (40 Category 1 points) 34
Higher education 35
Fellowship of the RACGP (150 Category 1 points) 36
Fellowship in Advanced Rural General Practice (150 Category 1 points) 36
QI&CPD Program
v
Category 2 activities 37
Provider accredited activities (Category 2 points) 39
Self-directed activities (Category 2 points) 40
Cardiopulmonary resuscitation (5 Category 2 points) 41
Quality improvement reflection 43
General information 45
How are points allocated to GPs’ credit point statement? 47
GPs with specific requirements 48
Rural Procedural Grants Program 49
Sponsorship guidance for all activities 50
Privacy and patient confidentiality 52
References 53
QI&CPD Program unit contact details 54
Appendix 1: RACGP QI&CPD Program activity standards 55
Appendix 2: Curriculum and domains matrix 56
QI&CPD Program
1
Introduction
The Royal Australian College of General Practitioners’ (RACGP) Quality Improvement and Continuing Professional
Development (QI&CPD) Program supports general practitioners (GPs) to provide the best possible care for
patients and their communities. The QI&CPD Program recognises the need for ongoing education to improve the
quality of everyday clinical practice by promoting the development and maintenance of general practice skills and
lifelong learning.
Continuing professional development and lifelong learning for Australian GPs

Continuing professional development (CPD) for medical practitioners includes a range of activities to meet individual
learning that is relevant to their scope of practice, in order to maintain, develop, update and enhance knowledge,
skills and performance to ensure that they deliver appropriate and safe care.1
As adult learners, Australian GPs take responsibility for:
• undertaking personal learning to support their CPD
• identifying CPD needs throughout lifelong learning
• planning how those identified CPD needs should be addressed
• continuously reflecting on their individual professional standards, scope of practice and competencies
• shaping learning assessments according to individual professional needs and the needs of the
communities which they serve.
In addition, a GP’s CPD needs to promote quality systems-based approaches in the workplace and the teams in
which they work.
GPs are also responsible for maintaining evidence that they are undertaking CPD.
QI&CPD Program objectives

The QI&CPD Program has been developed for the Australian general practice setting to:
• provide GPs with opportunities to improve patient safety and quality outcomes
• support continuous quality improvement within the general practice setting
• enable GPs to fulfil their individual and vocational CPD requirements.
The success of the RACGP’s internationally recognised QI&CPD Program is due to the central role of GPs in its
design, development and ongoing review. The RACGP supports a ‘Healthy Profession. Healthy Australia’ through
the delivery and ongoing enhancement of its QI&CPD Program.
The RACGP QI&CPD Program assists Australian GPs to maintain and improve the quality of care they provide
to patients, promotes care of the highest possible standard to the community and documents their learning
achievements for their own records and to meet the needs of regulatory and accrediting bodies.
QI&CPD Program
2 2017-19 triennium handbook for general practitioners
Educational underpinnings of
the QI&CPD Program
The RACGP QI&CPD Program recognises that CPD activities are more likely to result in improved personal and
patient outcomes if the learning:
• is self-directed
• is driven by the learner’s identified needs
• is integrated into an individual’s learning program
• encourages active participation
• considers the GP’s prior knowledge, skills, behaviours and attitudes
• involves reflection and evaluation of what has been learnt.
Accredited activities within the QI&CPD Program are based on adult learning principles that integrate the GPs’ prior
experience, promote high clinical, scientific and ethical standards, and extend knowledge and skills that impact
positively on the behaviour of GPs in relation to improved quality of patient care.
RACGP QI&CPD ensures that provider-led accredited activities are of a high quality and meet the needs of
Australian GPs through the adherence to QI&CPD activity standards.
These activity standards provide the framework for consistency and quality in the planning, development, delivery
and evaluation of QI&CPD accredited activities.
For more information on the QI&CPD Program activity standards, refer to Appendix 1.
Handbook overview
This handbook details the range of educational options offered by the RACGP QI&CPD Program for the 2017-19
triennium. All participants are required to undertake a range of different activities from across the domains and
the RACGP’s Curriculum for Australian General Practice 2016 (the Curriculum) to address their individual learning
needs.
GPs are encouraged to utilise the myRACGP web page to navigate to myCPD (www.racgp.org.au/education/
qicpd-program/cpd) to access self-directed activities, track progress in meeting requirements and find accredited
activities. GPs should contact their state QI&CPD unit for further advice and support regarding the program. Call
toll free 1800 472 247 or refer to contact details for offices in each state, located on page 54 of this handbook.
QI&CPD Program
2017-19 triennium handbook for general practitioners 3
QI&CPD Program requirements for

the 2017-19 triennium
A part of the RACGP’s commitment to continually evaluate and improve the QI&CPD Program, the 2017-19
triennium will include an increased focus on reflective learning practices.
To promote reflective learning practice in continuing professional education, the RACGP is introducing the planning
learning and need (PLAN) Category 1 quality improvement (QI) activity.
The PLAN activity enables GPs to self-identify priority areas of general practice learning needs in accordance with
their personal, patients and community needs. The PLAN activity is mandatory in the 2017-19 triennium and is
completed online through the myRACGP web page to navigate to myCPD.
A minimum of 130 QI&CPD points is required for the triennium, which must include:
• one PLAN QI activity
• one Category 1 activity
• a cardiopulmonary resuscitation (CPR) course.
The 2017-19 triennium commences 1 January 2017 and concludes 31 December 2019.
*NEW planning, learning and need (PLAN) activity

QI&CPD Program
QI&CPD Program activities

Activities available for GPs in the 2017-19 triennium
Category 1 activities Category 2 activities
QI activities (40 points) CPR (five points)
• Planning learning and need (PLAN)

*
• Clinical audit
Other Category 2 activities (two points
• Plan, do, study, act (PDSA) cycles
per hour, capped at 30 points)
• Small group learning (SGL)
• Evidence-based medical journal club (EBMJC) • Cultural awareness training
• Supervised clinical attachment (SCA) • Accredited activity provider activities
• General practice research
*Mandatory activity that can only be completed online as a
self-directed activity
Other Category 1 activities (40 points) Self-directed Category 2 activities
• GP self-directed active learning modules (ALMs) • Two points per hour, capped at 20
• Educator ALM points per triennium
• Accredited activity provider ALM
• Peer-review journal article
Higher education QI reflection (five Category 2 points)
• Graduate certificate courses (60 points) • Five points per reflection, capped at 15
• Graduate diploma courses (90 points) points per triennium
• Master’s degree (120 points)
• PhD (150 points)
These courses need to be relevant to general practice, and the
organisation and course must be accredited by the Tertiary Education
Quality Standards Agency (TEQSA) or equivalent
RACGP Fellowship (150 points)
• Fellowship of the RACGP (FRACGP)

• Fellowship of Advanced Rural General Practice (FARGP)
QI&CPD Program
What is different in the 2017-19

QI&CPD requirements and why?
The RACGP is increasing the focus on reflective learning practices in the 2017-19 QI&CPD Program for improved
learning and CPD accountability.
To support GPs to meet and document this requirement, the RACGP is introducing a mandatory reflective learning
activity - the planning learning and need (PLAN) QI activity.
The PLAN QI activity will further support GPs on their educational journey, providing improved capacity to structure
ongoing learning for their professional aspirations and the services required to meet the evolving needs of their
patients and the community.
Reflective learning practices promote effective learning and

better patient outcomes
Reflection in professional practice enables GPs to modify their learning according to their practical and professional
experience in an ongoing iterative process.
As learning from CPD becomes applied to practice, reflective learning enables GPs to test how relevant, useful and
appropriate their learning is to everyday practice, and accordingly, revise any learning needs.
Reflective learning practice requires ongoing observation and evaluation of professional skills and community needs
through a process of critical thinking and examination.
The deliberate process of reflective learning promotes deep and effective learning with the ultimate aim of
supporting high quality and safe practice tailored towards the GP’s scope of practice and community.
PLAN activity — Helping GPs to meet the needs of their

patients and community
The QI&CPD PLAN activity is an evidence-based approach to assist a GP to map out and document their learning
needs with respect to their practice presentation demographics, community needs and professional requirements
for work in general practice.
A PLAN activity may include, but is not confined to, clinical skills, practice management, research skills and/or
teaching skills by documenting:
• what the GP needs to learn and why
• evidence they have achieved their learning goals.
A PLAN activity recognises that GPs’ learning needs may change according to many factors, including the changing
and evolving nature of general practice and broader medical care, the GP’s career history, including clinical
experience (eg types of clinical medical practice), local practice demographics and significant life events, such as a
break in practice (eg parental leave) or a change in areas of practice.
As part of the 2017-19 QI&CPD Program, the PLAN activity provides a flexible online template that can assist GPs
in developing an analysis of skills and knowledge for the triennium.
QI&CPD Program participants are advised to complete the self-reflection section of the PLAN activity early in the
2017-19 triennium. The complete PLAN activity needs to be submitted by 31 December 2019.
To complete the PLAN activity, see the relevant section under Category 1 activities on page 17.
QI&CPD Program
QI&CPD Program participation

CPD is a professional obligation of all medical practitioners.
Full-time and part-time GPs have the same QI&CPD Program requirements for full-time or part-time participants, as
the required standard of practice is the same for all participants, regardless of the fraction of time worked as a GP.
CPD is a registration requirement of the Medical Board of Australia, including GPs taking a leave of absence from
clinical practice (refer to www.medicalboard.gov.au/Registration-Standards.aspx).
In addition, Australian GPs who are required to demonstrate participation in CPD include GPs requiring practice
accreditation and GPs seeking visiting medical officer credentials with local hospitals, particularly in rural areas.
GPs who are on the Medicare Vocational Register or Fellows list, or who are recognised as other medical practitioners,
are required to demonstrate participation in CPD in order to maintain their eligibility for A1 Medicare rebates.
Some GPs have specific requirements with other colleges or third party organisations for topics such as women’s
reproductive health, GP anaesthesia, general practice surgery, diagnostic radiology, mental health and medical
acupuncture. Those GPs are required to undertake mandatory or recommended CPD specific to that topic area
to maintain their relevant skills. This is part of, not in addition to, the overall QI&CPD requirements applicable to all
registered medical practitioners who are engaged in any form of medical practice under Medical Board of Australia
or Australian Health Practitioner Regulation Agency (AHPRA) standards.
Annual participation fees

The QI&CPD Program participation fee for each year reflects the costs of conducting a program for GPs across
Australia. The program’s administrative tasks are more complex and extensive than the collection of activity
attendance data related to the allocation and recording of CPD points for the production of GP credit point
statements. These tasks include:
• development of activity standards for education providers in order to ensure that GPs have access to high-
quality educational activities
• implementing quality assurance assessment processes to review educational providers regarding the best ways
to improve aspects of their educational activities, in order to ensure ongoing quality
• quality assurance and adjudication of individual activity submissions
• development and implementation of a range of quality learning tools and resources to assist GPs
• providing access to high-quality educational activities, both nationally and within state faculties
• addressing the diverse interests of Australian general practice and its GPs in order to ensure a wide choice of activities
• maintenance of an accurate and current database of participating GPs, including updating changes of status
and recording periods of inactivity, with respect to Medicare recognition status and providing CPD exemptions
for these periods
• provision of newsletters and information sessions
• updates to and ongoing maintenance of the QI&CPD website and myRACGP
• evaluation of the QI&CPD Program for continuous improvement.
All GPs who participate in the QI&CPD Program are required to pay the annual fee. RACGP members pay annual
subscription fees, which cover a range of benefits and services including QI&CPD Program participation. For more
information on RACGP membership options, call 1800 472 247.
QI&CPD Program
7
Enhancing patient care

through QI activities
The RACGP’s Standards for general practices (4th edition), describes a QI activity as an activity undertaken within
a general practice setting where the primary purpose is to monitor, evaluate or improve the quality of healthcare
delivered by the practice.2
The Standards for general practices encourages QI and enables practices to identify opportunities to make
changes that will improve patient safety and care.
The 2017-19 triennium focused on reflective learning practices with the aim to improve educational processes and
patient outcomes through the introduction of the compulsory PLAN activity (refer to page 17).
There are also other QI activities available that GPs are encouraged to complete, including the regular monitoring of
the practice’s structures, systems and clinical care.
Improvement needs to be based on the practice’s own information and data that can be collected in a number of
ways, including patient and staff feedback and audits of clinical data.
All practice staff members need to have the opportunity to contribute to the practice’s QI activities.
Activities that facilitate review and evaluation of GPs’ own practice include:
• PLAN (new compulsory requirement)
• SCA
• PDSA
• clinical audit
• general practice research
• EBMJC
• SGL
Systems-based approach to patient safety

The QI&CPD Program promoted patient safety through the implementation of appropriate systems as an integral
part of all accredited activities. A systems-based approach to patient safety considers factors within general
practice that may cause harm, such as the absence of processes and systems within a practice.3
The RACGP requires developers of accredited activities to identify effective risk management strategies4 within the
GP’s practice systems, to promote improvement of patient quality care and safety as they relate to the education
being provided. Accredited activity learning outcomes must include at least one outcome that focuses on a
systems-based approach to patient safety.
QI&CPD Program
Activity design components

The 2017-19 triennium specifies that all Category 1 and Category 2 accredited activities require the following
mandatory design components in order to meet the standards stated in Appendix 1:
• The primary outcome must be to improve the quality of patient care.
• Accredited activity content must be relevant to GPs and general practice.
• Planning and development of the accredited activity must involve GPs medically registered with AHPRA.
• Planning must include an evidence-based needs assessment to validate the education activity.
• The education activity must have learning outcomes that are informed by the evidence-based needs
assessment.
• All content (including reading material and references) must meet the highest ethical, clinical and educational
standards, as well as the objectives of the QI&CPD Program.
• All content (including reading material and references) must demonstrate critical appraisal of valid evidence and
be supported by accepted medical theory regarding techniques to improve patients’ health outcomes, including
a balanced appraisal of alternative treatment options for any condition.
• The use of interactive presentation and engagement modes must be appropriate for the content to be delivered.
• All content must account for prior knowledge, skills, attitude and behaviour of GP learners.
• All content must address a systems-based approach that can be applied within a GP’s practice to improve
patient safety.
• All content is mapped against one or more domains, competency outcomes and contextual units according to
the Curriculum.
• The learning environment must promote the fulfilment of stated learning outcomes.
• Relevant content must represent more than 50% of the activity in order to be eligible for a specific requirement.
• GPs who attend or participate are provided with an evaluation form at the end of the activity.
• The ‘QI&CPD GP feedback’ form is available to GPs at the time the activity is delivered.
• An activity report is submitted to the RACGP upon completion of the accredited activity.
QI&CPD Program
Linking the curriculum and domains to

the QI&CPD Program
The RACGP Curriculum details what vocational GPs need to learn throughout their general practice learning. It
details the knowledge, skills and attitudes that GPs require for:
• competent, unsupervised general practice
• meeting their community’s healthcare needs
• supporting current national health priorities and the future goals of the Australian healthcare system.
The Curriculum emphasises self-directed learning, the development of critical self-reflection and lifelong learning
skills, and the maintenance of professional practice standards.
The addition of the Core skills unit to the Curriculum is designed to assist the RACGP, regional training
organisations (RTOs), QI&CPD providers, specific interest groups, general practice supervisors and others in
designing learning programs, courses and assessments to meet the stated outcomes and criteria.
In conjunction with the RACGP’s Competency profile of the Australian general practitioner at the point of Fellowship
(www.racgp.org.au/education/competency), the Core skills unit provides guidance for those who assess overseas
doctors on alternate pathways and doctors wishing to be recognised as eligible for the FRACGP.
The five domains of general practice

The five domains of general practice represent the critical areas of knowledge, skills and attitudes necessary for
competent unsupervised general practice. They are relevant to every patient consultation.
The five domains have been expanded by the addition of the core skills that sit beneath them. The relationship
between the domains and core skills is quite clear.
Communication skills and the patient-doctor relationship (eg communication skills,

Domain 1
patient-centredness, health promotion, whole-person care)
Applied professional knowledge and skills (eg physical examination and procedural
. Domain 2
skills, medical conditions, decision making)
Population health and the context of general practice (eg epidemiology, public
Domain 3
health, prevention, family influence on health, resources)
Professional and ethical role (eg duty of care, standards, self-appraisal, teacher role,
Domain 4
research, self-care, networks)
Organisational and legal dimensions (eg information technology, records, reporting,

Domain 5
confidentiality, practice management)
The five domains of general practice provide a comprehensive and robust framework for ensuring the key skill
areas of general practice are included in education and RACGP.
All accredited activities must be mapped to the Curriculum. This process involves finding the appropriate domains
of general practice, selecting one competency outcome listed under that domain and selecting one or more
contextual areas that will be covered in the education. Refer to Appendix 2 for further information.
QI&CPD Program
Domain 1-----------------------
Communication and the
patient-doctor relationship
CS1.1 General practitioners communicate
effectively and appropriately to provide quality
care.
CS1.2 Through effective health education,

general practitioners promote health and
wellbeing to empower patients.
Domain 5--------------- P Domain 2

Organisational and legal Applied professional
dimension knowledge and skills
CS5.1 General practitioners use CS2.1 General practitioners provide the
quality and effective practice primary contact for holistic and patient
management processes and systems centred care.
to optimise safety.
CS2.2 General practitioners diagnose
CS5.2 General practitioners work and manage the full range of health
within statutory and regulatory conditions in a diverse range of
requirements and guidelines. patients, across the lifespan through a
CS2.3 General practitioners are

informed and innovative.
CS2.4 General practitioners collaborate

and coordinate care.
Domain 4 Domain 3—1

Professional and ethical role Population health and the
context of general practice
CS4.1 General practitioners are ethical and
professional.
CS3.1 General practitioners make rational
decisions based on the current and future health
CS4.2 General practitioners are self-aware.
needs of the community and the Australian
healthcare system.
CS4.3 General practitioners mentor and teach to
improve quality care.
CS3.2 General practitioners effectively lead to
address the unique health needs of the
community.
Figure 1. Core skills - the star of general practice, reproduced from the RACGP’s 2016 Curriculum for Australian General Practice
- Core skills unit
QI&CPD Program
11
Quality assurance assessment process

The primary purpose of all activities accredited by the RACGP QI&CPD Program is to improve the quality of care
provided to patients. The QI&CPD Program provides GPs with access to the highest quality education and utilises
a quality assurance process to maintain these high standards.
Continuing quality assurance assessment of accredited activities is integral to the RACGP QI&CPD Program.
Quality assurance of provider accredited activities

The quality assurance assessment process may be initiated:
• when the RACGP receives a complaint about an accredited activity
• as a result of a random audit made by the RACGP
• where at least 10% of all accredited activities will be selected for quality assurance assessment over the triennium
• when an activity contains previously appropriate content, including medical procedures and/or practices, that is
no longer regarded as safe or advisable
• when the content of an accredited activity may not be evidence-based or is controversial.
These examples do not represent an exhaustive list and the RACGP may undertake a quality assurance
assessment of an accredited activity at any time.
GP feedback on education activities

The RACGP encourages GP’s who participate in accredited activities to provide feedback of positive, high-quality
education experiences.
Alternatively, GPs who have concerns about the quality or conduct of a QI&CPD Program accredited activity are
encouraged to complete the ‘GP feedback form’ or report their concerns to their state QI&CPD unit.
Visit the RACGP website for more information on GP feedback and the quality assurance assessment process.
QI&CPD Program
Quality assurance of GP self-directed

activities
The RACGP provides GPs with access to myRACGP web page, where they can navigate to myCPD and submit a
record of their participation in CPD activities. Prior to submission of the form online, GPs must complete the following:
I declare to the RACGP:
I have completed this activity, and to the best of my knowledge it has been conducted and completed in accordance
with the relevant RACGP QI&CPD Program requirements, educational standards and criteria.
The information I have provided in this document is accurate and correct.
I understand and acknowledge that the RACGP reserves the right to withdraw recognition of the activity if in the opinion
of the RACGP the activity does not meet the QI&CPD Program requirements, educational standards and criteria.
The RACGP regularly conducts a quality assurance assessment of individual GPs’ self-directed activities.
QI&CPD Program
13
Using myRACGP to navigate to myCPD

www.racgp.org.au/education/qicpd-program/cpd
TRACK YOUR POINTS QUICK ACCESS VIEW YOUR STATEMENT

Your own personalised dashboard, Find education quickly and View your QI&CPD credit point
which allows you to track your access a diverse range of statement for the current and
ongoing progress. QI&CPD accredited activities. previous triennium.
Resources
My points
Login via ‘My Account’

View and on the RACGP homepage
print your
statement
£ KACGP
Submit a self-directed
activity
Visit www.racgp.org.au to login
Activities summary
Search
Healthy Profession.
www.racgp.org.au Healthy Australia.
Category 1 activities
QI&CPD Program
17
Planning learning and

need (40 Category 1 points)
Mandatory for the 2017-19 triennium, a planning learning and need (PLAN) activity is a means by which a GP can
map out and document their learning needs with respect to their professional work in general practice.
A PLAN activity may include, but is not confined to, clinical skills, practice management, research skills and/or
teaching skills.
A PLAN activity documents:
• what the GP needs to learn
• why they need to learn it
• how they are going to learn it
• evidence they have achieved their learning goals.
A PLAN activity recognises that GPs’ learning needs change according to many factors, including:
• the changing and evolving nature of general practice and broader medical care
• the GP’s career history, including clinical experience (eg types of clinical medical practice)
• local practice demographics
• significant life events, such as a break in practice (eg parental leave) or a change in areas of practice.
The RACGP QI&CPD Program provides a template that can assist GPs in developing an analysis of skills and
knowledge. It is recommended that GPs develop such an analysis at the beginning of a triennium. The PLAN
activity is available online and is mandatory for the 2017-19 triennium. Only one PLAN activity can be submitted
per triennium.
Criteria specific to PLAN activities

PLAN activities must:
• use the GP’s current practice as the basis of learning
• identify potential areas for skill improvement in meeting the general practice needs of the GP’s current practice
population
• assist the GP to make informed choices about their education needs
• assist the GP to integrate theory and practice into their work
• enhance the GP’s motivation to learn and to ask appropriate questions of themselves and others
• encourage the GP to regularly review their learning needs
• encourage the GP to share their learning experience with peers.
QI&CPD Program
NEW Mandatory Quality Improvement activity for 2017-19
Steps to complete the NEW online planning learning and need (PLAN) activity
□—
□ =- Step^l) Step ^2) Step (3) Step Step
Login to Complete practice Review the report Identify key areas Complete activities Reflect
myRACGP profile analysis generated from for improvement relevant to the and plan
select myCPD and self reflection step 1 from the report key areas ahead
select PLAN
NEW Mandatory Quality

feRACGP I QI&CPD Program Improvement activity for 2017-19
An example of the planning learning and need (PLAN) activity
[13 Login to myRACGP ^ select myCPD ^ select PLAN

QI&CPD Program
19
Small group learning

(40 Category 1 points)
Small groups are an ideal format in which GPs can share their knowledge and discuss daily practice with peers.
Small group learning (SGL) is designed to maximise the benefits of working and learning together in a small group
educational setting.
SGL utilises peer support, interaction and reflection to enhance participants’ clinical competence, knowledge,
skills, attitudes and performance. A skilled group facilitator can help people to stay focused and effectively deal with
group dynamics, and allow participants to take ownership of the process. This increases the likelihood of members
having a positive and rewarding learning experience.5
Evidence shows that motivation is high and more likely to result in changes in clinical practice when learners have
the opportunity to select topics relevant to their own practice and measure their practice against that of their peers.
The cycle may be completed over a short period, but may also span over the three years of the triennium,
depending on the needs of participants. This model may be conducted as a face-to-face meeting or by using
teleconferencing/videoconferencing for remote participants.
Criteria specific to SGL

SGL must:
• include a minimum of six hours of educational content (excluding planning meeting, review meeting, meal breaks
and other networking activities)
• include a minimum of two GP participants and a maximum of 12 total participants (SGL can include other health
professionals in addition to GPs)
• ensure the duration of each meeting is at least one hour
• have a facilitator
• convene and document a planning meeting and a review meeting
• include group QI reflection.
There must be evidence that the GP attended the planning meeting, the review meeting and at least six hours of
education activity in order for them to be eligible for the available 40 Category 1 points.
QI&CPD Program
Steps in developing an SGL

GPs must:
1. identify interested participants
2. identify a group facilitator and a person to organise the group (this can be the same person and the facilitator
role may be rotated within the group)
3. ensure each participant reflects on his/her personal learning needs and identifies them in relation to this group
prior to the planning meeting
4. ensure all participants attend the planning meeting, which should include review of the issues and options
for the group, and the development of a program of CPD activities (topics, dates) that reflects participants’
personal learning needs (consider the group QI reflection questions when planning)
5. undertake the program of activities, ensuring attendance records and a meeting summary are kept for each
meeting
6. ensure all participants attend the review meeting at the end of the cycle in order to reflect on the outcomes for
the group (it is important to determine a response to the group QI reflection questions)
7. ensure the facilitator/organiser arranges for completion and submission of the SGL application form.
Evidence
In addition to the online form, GPs must provide:
• attendance list for each meeting, including the planning meeting and the review meeting
• meeting agenda and minutes, showing duration, topics, presenters, etc.
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21
Supervised clinical attachment

Supervised clinical attachment (SCA) is a period of attachment with a health professional (supervisor) who is an
expert, or with someone with highly developed skills, in a specific field of healthcare (eg anaesthetics, women’s
health, surgery, obstetrics, etc). It is designed to provide an individualised and hands-on learning experience, where
the examples, scenarios and problems come in the form of real cases.
It is suitable for GPs who have identified a particular skill/knowledge they wish to upgrade or develop. SCA is an
opportunity for GPs to use the supervised environment to investigate, learn and increase knowledge and skill in a
manner that is unique to them.
The contact hours can be delivered face-to-face or in combination with other media, such as videoconferencing/
teleconferencing, case study discussions over the phone and email, or online discussion groups.
A supervisor with the relevant expertise, knowledge and skill must be appointed to conduct the SCA.
Criteria specific to SCA

SCA must include:
• a minimum of 10 hours of contact time
• the name and qualifications of the supervisor
• session summaries, including details of each session using only de-identified patient data
• completion of the QI reflection form.
Steps in developing an SCA

GPs must:
1. identify a particular skill or area to develop or upgrade, as well as an appropriate health professional willing to
act as a supervisor
2. discuss expectations with the supervisor, including:
a. opportunities to observe patient care and to practice specific skills (eg psychological treatment, specific
procedural skills)
b. an open and unbiased discussion of cases and treatments, which could take the form of end-of-session
debriefs or reviews
3. discuss and arrange attachment sessions (date, time and method/s) with the supervisor
4. identify specific learning outcomes/aims that support consistent application of skills and knowledge, and
provide a copy of the learning outcomes to the supervisor to aid planning and evaluation
5. complete a summary for each SCA session with the supervisor for up to at least 10 hours of attachments
6. complete the SCA application form via the myRACGP web page navigating to myCPD, upon completion of the
whole SCA - this must include relevant documentation (ie supervisor details and sessions summary).
QI&CPD Program
Evidence
In addition to the online form, GPs must document and retain:
• name, qualifications and contact details of the supervisor
• completed session summaries.
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23
The plan, do, study, act cycle

The plan, do, study, act (PDSA) cycle is a systematic series of steps for gaining valuable learning and knowledge
aimed at the continual improvement of a product or process. It is used in implementing a planned improvement
or change by breaking them down into small manageable parts and testing each change to make sure things are
improving and no efforts are wasted.
PDSA can be used to quickly and easily test suggestions for improvement, based on existing ideas and research or
through practical ideas that have been proven to work elsewhere. It is a cyclical model because the benefit is not
always achieved in one cycle, which means the process can be refined and the cycle repeated.6
PDSA cycles can be undertaken by an individual GP or practice/multidisciplinary team. Individual GPs can choose
to undertake PDSA cycles related to practice improvements or improvement of individual clinical knowledge and
skills. Practice or multidisciplinary PDSA cycles are those that focus on improving the capability of the practice to
deliver quality patient care, thus improving the quality, safety and performance of the practice (ie meeting RACGP
standards, improving systems and processes, etc).
A designated facilitator is recommended for practice or multidisciplinary team PDSA cycles.
PDSA cycles can be developed in a number of areas, such as:
• identifying patients with heart disease7
• providing smoking cessation advice to pregnant women
• recording patients’ allergy status
• reducing the number of demands for repeat prescriptions by telephone.
Criteria specific to PDSA

PDSA must include:
• completion of a minimum of two cycles
• completion of the QI reflection form.
QI&CPD Program
Steps in developing a PDSA cycle

GPs must:
1. select a leader/facilitator and identify the members of the group in practice or multidisciplinary team PDSAs
2. undertake a planning and development meeting, which may be conducted via face-to-face, videoconferencing/
teleconferencing or a combination of both. GPs should discuss the following questions and record the
responses:
a. What am I/are we trying to accomplish? (state the aims/expected learning outcomes)
b. How will I/we ensure privacy and confidentiality if patient records are involved?
3. carry out the first PDSA cycle (refer to Figure 2 as a guide)
4. develop the second and subsequent PDSA cycles as required
5. complete the QI&CPD PDSA application form via the myRACGP web page navigating to myCPD, including the
QI reflection form, and attach relevant supporting documentation (eg adherence to privacy and confidentiality
measures where patients’ records or information is required).
Plan
• Define aims/expected outcomes and
outline the steps to be taken
• Plan to answer who, what, where, when
and how in terms of data collection
Act
• Act on the results Do
• Adopt, reject or modify original plan as • Carry out the plan
required • Record observations and relevant data
• Plan the next cycle
Study
• Analyse and compare the data results to
expectations
• Summarise what was learned
Figure 2. PDSA model

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25
Clinical audit
A clinical audit is a planned medical education activity designed to help GPs systematically review aspects of their
own clinical performance against defined best practice guidelines, criteria or standards. Clinical audits improve the
quality of care provided by medical practitioners.8
A clinical audit has two main components:
• an evaluation of the care provided by an individual GP, a group of GPs or a multidisciplinary practice team
• a QI process.
Evidence-based medicine research supports that a clinical audit is more likely to result in changes in GPs’
behaviour and improvements in practice than didactic medical education methods.
Clinical audits can either be conducted over fixed time duration or based on patient numbers, depending on the
prevalence of the condition or audit topic. Collection and collation of data may be paper-based or done online, and
feedback mechanisms may be paper-based, face-to-face or online.
A clinical audit must consider ethical, privacy (PrivacyAct 1988) and confidentiality issues relating to patient
information, where applicable.
Refer to the Office of the Australian Information Commissioner (www.oaic.gov.au) for more detailed information on
privacy.
Criteria specific to a clinical audit

A clinical audit must include:
• completion of the five steps of the audit cycle
• completion of the QI reflection form
• Human Research Ethics Committee (HREC) approval if required
QI&CPD Program
Step 1:
Identification
of need -
preparation and
planning
Step 5:
Step 2:
Monitor
Identify
progress and
standards/
sustain
criteria
improvement
Step 4: Step 3:
Identifiy and Data
implement collection and
change analysis
Figure 3. Clinical audit cycle
Steps in completing a clinical audit

GPs must:
1. identify a particular topic that it is a priority for the practice or for everyone involved in the group, set the aims/
expected learning outcomes and discuss and develop a plan
2. identify the relevant standards/criteria or best practice guidelines against which to measure the audit
3. collect and analyse data
4. identify and implement change/improvement
5. monitor progress and sustain improvement
6. complete the clinical audit application form via the myRACGP web page navigating to myCPD,
upon completion of the five-step cycle, and attach relevant documentation, such as clinical audit
plan/information, including:
a. number of patients required and data collected
b. data collection and analysis method
c. relevant standards/criteria or best practice guidelines against which to measure the audit
d. changes or improvements implemented.
Evidence
In addition to the online form, GPs must document and retain a copy of HREC approval, if required.
QI&CPD Program
27
Evidence-based
medicine journal club
Evidence-based medicine journal clubs (EBMJCs) encourage GPs to take note of clinical questions that arise
in daily practice and to follow up by researching evidence, thereby assisting GPs to relate evidence directly to
clinical practice. It has been shown that EBMJCs are more successful in changing GP behaviour and improving
patient care than more traditional journal clubs, which discuss recent articles without directly focusing on clinical
relevance.9 When an EBMJC is based on individual patient cases, used as part of an evidence-gathering process
and discussed with colleagues, it offers an attractive quality improvement activity with variety, currency and
immediacy.
Criteria specific to EBMJC

An EBMJC must:
• include a minimum of six hours of educational content (excluding planning meeting, review meeting, meal breaks
and other social networking activities outside the education)
• include a minimum of two GP participants and a maximum of 12 total participants (EBMJCs can include other
health professionals in addition to GPs)
• have a meeting duration of at least one hour
• ensure each GP participant completes one literature review (from peer-reviewed journals) and presents the
results to the group
• have a facilitator
• convene and document a planning meeting and review meeting
• include group QI reflection.
Each EBMJC must record:
• the attendance of each meeting
• the clinical questions discussed
• reflections on aspects of practice systems that could be improved based on learning derived from journal articles
• a summary of the outcomes for each meeting.
In order to be eligible for 40 Category 1 points, there must be evidence that the GP attended the planning meeting
and review meeting, and at least six hours of education activity.
QI&CPD Program
Steps in developing an EBMJC module

GPs must:
1. identify interested participants
2. identify a group facilitator and organiser (this can be the same person)
3. ensure each GP participant maintains a log of potential questions that arise in their clinical practice and bring
their questions for discussion
4. ensure all participants attend the planning meeting, reviewing the proposed questions and developing a
program of activities (topics, dates, etc) - the group should agree on questions to be discussed and nominate
a member for each clinical question, and consider the group QI reflection questions in the planning stage
5. ensure each group member completes a literature search in order to answer their allocated clinical question
and presents findings at their scheduled meeting
6. ensure the nominated member distributes the relevant papers to the group at each meeting, explaining the
clinical background - the group must:
a. discuss results of the search and papers chosen for discussion
b. discuss and critically appraise each paper
c. determine how the results might enable change in clinical practice at either an individual or whole-of-
practice level
d. document the outcomes of the session (this cycle is repeated at each subsequent meeting until all GPs
have presented their session, leading to a minimum of six hours of meetings)
7. ensure all participants attend the review meeting at the end of the cycle in order to reflect on the outcomes for
the group, and determine a response to the group QI reflection questions
8. ensure the facilitator arranges for completion and submission of the EBMJC application form.
Evidence
• an attendance list for each meeting, including planning and review meeting
• a meeting agenda and minutes showing duration of meetings, topics, presenters, references, etc.
QI&CPD Program
29
General practice research

Research is a process of asking questions within the framework of existing knowledge and seeking answers following
a systematic approach, which includes:
• obtaining appropriate information in an ethical, transparent and reproducible manner
• appropriately analysing the information
• drawing conclusions on the basis of the validity and reliability of the information and meaning of the results, and
comparing these results to other studies
• disseminating the implications widely, including to those who may affect change.6
The spectrum of research activities is wide and can include evaluation studies, intervention studies, clinical audits,
large scale multicentre clinical trials, and patient satisfaction studies.9
General practice research aims to solve the problems that arise within the specific context of general practice. It
is important in identifying gaps in the evidence GPs need for making decisions and provision of the highest quality
patient care.6 It is important that research is undertaken in the Australian general practice setting, ensuring that
research is relevant, applicable and manageable within the average practice for Australian patients.
Participating in research offers many benefits for GPs, such as:
• access to the latest evidence
• opportunities to collaborate with or be mentored by other general practice researchers
• opportunity to refine research writing skills.
Research may be funded, seeking funding or unfunded and must have the necessary HREC approval where appropriate.
GPs can participate as either principal investigators or as participants in a group-based research. Both are eligible for
Category 1 points and the mandatory QI requirement in the QI&CPD Program.
Criteria specific to principal investigator

Principal investigators must:
• obtain HREC approval as required
• document the research proposal, report and dissemination
• complete the QI reflection form.
Steps specific to principal investigator

Principal investigators must:
1. define the research question
2. design the research study and/or write the research funding proposal, detailing GP participants as required
3. obtain ethics approval (as required) for the research study from an HREC constituted under National Health
and Medical Research Council (NHMRC) guidelines (eg RACGP National Research and Evaluation Ethics
Committee [NREEC])
QI&CPD Program
4. implement the research module for research participants

5. conduct the research within ethics parameters and be involved in, or supervise, the analysis of the collected data
6. provide a report of the findings from the research study to all GP research participants
7. disseminate the findings of the study by publication in a peer-reviewed journal or presentation at a conference
(workshop, oral or visual).
Criteria specific to GP participants

GP participants must:
• maintain a record of research enrolment/participation
• collect data and document analysis (comparison of own data to overall study results, and submitted final
research report to the principal investigator as required)
• complete a QI reflection form.
Steps specific to GP participants

GP participants:
1. enrol in the research activity
2. read all materials provided by the principal investigator
3. define own learning outcomes for participating in the research study
4. collect data as specified by the principal investigator, using data collection tools provided
5. conduct own analysis of the collected data and submit an individual report of findings to the principal
investigator within a given timeframe and ethics parameters
6. receive and review a report of findings from the principal investigator
7. compare own data to the overall study results and submit a brief final research report to the principal investigator.
Evidence
In addition to the online form, GPs must document and (where applicable) retain:
• HREC approval
• documentation for patients/participants outlining the research and their role and rights (where applicable)
• a research plan
• evaluation tool/s
• a research report
The principal investigator must retain evidence of dissemination of research findings. For example, an article
published in a peer-reviewed journal; a letter of acceptance from a peer-reviewed journal and a copy of the article;
a copy of the abstract and acceptance letter from a conference to present a workshop, visual or oral presentation;
documentation of submission of final grant report to the RACGP.
GP participants must retain documentation of research enrolment and completion of required data report and/or
research findings.
QI&CPD Program
31
Active learning module

Active learning modules (ALMs) are activities that result in demonstrable changes in GPs’ performance, knowledge,
skills, behaviours and attitudes, which lead to improvements in the quality of patient care.
The ALM must also consider improvement of practice systems that address patient safety.
Research shows that the most effective education methods involve participant interaction and varied educational
approaches.
ALMs can be developed by education providers or as self-directed activities.
The ALM takes the GP learner through a learning cycle involving these processes:
• self-reflection - what do I need?
• planning - how will I do it?
• action - carry out the plan
• review - did I meet my need? What changes or improvements resulted?
The structure of the ALM emulates this learning cycle, offering the GP learner a predisposing activity for self
reflection and planning, a structured learning activity to enable learning of new skills and knowledge, a reinforcing
activity to strengthen a new behaviour into their practice, and an opportunity to reflect on any unmet or further
learning needs.
Provider ALMs
Most GPs will complete ALMs that have been developed by an accredited activity provider. All provider ALMs have
been developed with a GP to ensure the content is relevant to GPs.
Providers offer ALMs on a range of topics to suit GPs - they may be delivered online, face-to-face or as a
combination of both.
All provider ALMs must include a predisposing activity and a reinforcing activity. GPs will be awarded 40 Category 1
QI&CPD points on completion of the full six hours of education and return of completed reinforcing activity to the
accredited activity provider within the required timeframe. The provider is responsible for uploading the QI&CPD
points upon completion of the activity requirements.
Criteria specific to ALMs

ALMs must:
• include a minimum of six hours of structured educational content (excluding registration time, meal breaks,
sponsor presentations)
• include at least two-thirds interactive or experiential content (may include skills practice, question and answers,
role plays, discussion, case studies)
• provide thematically-linked education content.
Provider ALMs must have predisposing and reinforcing activities.
QI&CPD Program
Individual ALMs for GPs

GPs can develop an individual ALM to suit their own learning needs. In recognition of the broad range of education
activities GPs complete to meet their personal learning needs, the RACGP has developed a flexible framework for
the development of individual ALMs.
Steps in developing an individual ALM

GPs must:
1. select an area of learning they wish to develop
2. set personal learning outcomes
3. complete a minimum of six hours of active learning on their chosen topic (a combination of different activities)
4. reflect on the learning and consider ways in which they can improve their practice
5. implement change in their clinical practice and/or practice systems that will reliably improve the quality of
patient care
6. complete and submit an individual ALM online application form.
Evidence
Individual ALMs
• a program or agenda as evidence of the minimum six hours education
• relevant supporting documentation, such as a certificate of attendance or completion.
Accredited activity provider ALMs

Accredited activity providers must issue the GP with a certificate of completion and upload the CPD points.
QI&CPD Program
33
Educator ALMs
Educator ALMs are for those GPs who teach medical students, and/or supervise registrars or other GPs. It focuses
on the development of teaching skills and the experience and learning outcomes for the educator.
General practice is well placed as a principal setting for medical student education. Clinical teaching practices can
positively influence the quality of the learning experience for medical students. However, individual general practice
educators can have gaps in skills and knowledge related to teaching that require extra personal study.
GPs occasionally undertake self-directed learning to address individual learning needs.
In line with the Curriculum, teaching and mentoring includes a degree of the educator sharing their clinical
expertise. This requires quality communication skills to ensure messages are heard. Receiving feedback from a
medical student, general practice registrar or other GPs is an important part of this learning process. Listening to
the learner’s needs ensures teaching occurs at the appropriate level and in the appropriate context. Reflection and
discussion are also important tools in order to improve teaching outcomes in the future.
Criteria specific to educator ALMs

Educator ALMs must:
• include a minimum of six hours of teaching and student engagement
• provide an education summary/learning program.
Steps in developing an educator ALM

GPs must:
1. outline the planning, teaching and evaluation process undertaken
2. include the learning program for the medical student, general practice registrar or other GP while they are at
the practice
3. reflect on their teaching practices and identify other areas of knowledge or skill in which they wish to improve
as an educator.
Evidence
In addition to completing the educator ALM online form, GPs can provide:
• a teaching schedule or timetable
• lesson plans
• a sample of a tutorial or face-to-face training
• confirmation from a hospital or practice confirming the teaching appointment.
QI&CPD Program
Peer-reviewed journal article module

A peer-reviewed (also known as ‘refereed’ or ‘scholarly’) journal article is written by experts or professionals in a
specific area and then reviewed by several other experts before the article is published in a journal, ensuring the
article’s quality and credibility. This process uses high-quality, evidence-based references, accepted theories,
best practice standards/guidelines, or is about scientifically valid processes or research results relevant to general
practice.
Criteria specific to a peer-reviewed journal

article module
A peer-reviewed journal article module must:
• be relevant to general practice
• use high-quality, evidence-based references, accepted theories, best practice standards/guidelines, or is about
scientifically valid processes or research results
• have undergone and passed an appropriate peer-review process for publication.
Steps in completing a peer-reviewed journal

article module
GPs must:
1. identify learning outcomes in writing an evidence-based article
2. write an article using high-quality, evidence-based references, accepted theory, best practice standards/
scientifically valid processes or research results relevant to general practice
3. submit the finished article to a peer-reviewed journal for publication
4. have the peer-reviewed article accepted for publication
5. complete the peer-reviewed journal article application form via the myRACGP web page navigating to myCPD
and attach a copy of the published article or letter of acceptance for publication.
Evidence
In addition to the online form, GPs must document and retain a copy of the published peer-review journal article or
a letter of acceptance for publication.
QI&CPD Program
35
Higher education
GPs may wish to complete postgraduate qualifications to advance their knowledge of topics relevant to general
practice.
Postgraduate courses from Australian providers recognised by the Tertiary Education Quality and Standards
Agency (TEQSA) will be eligible for Category 1 QI&CPD points, subject to the content of the course relating to
general practice. Details of eligible higher education providers can be found on the TEQSA website
(www.teqsa.gov.au).
Some courses from non-accredited and overseas providers may be eligible for QI&CPD points and will be
adjudicated on their own merits.
Category 1 points will be awarded upon successful completion of a:
• graduate certificate (60 points)
• graduate diploma (90 points)
• master’s degree (120 points)
• PhD (150 points).
Please note: completion of a higher education course does not exempt GPs from completing the QI&CPD
minimum requirements.
Criteria specific to higher education

Higher education courses must be:
• a postgraduate course
• relevant to general practice
• be administered by an education provider organisation recognised by TEQSA (or equivalent).
Evidence
GPs can apply for CPD points at the completion of the higher education course.
An academic transcript or certificate of completion from the university or course provider is required.
QI&CPD Program
Fellowship of the RACGP

Fellowship of the RACGP (FRACGP) is a practice-based postgraduate award designed to assist candidates to
increase competency and confidence to work unsupervised in general practice in Australia. Attaining FRACGP
qualifies the GP for 150 Category 1 points. There are various formats for completion of the FRACGP assessment
process. Eligibility and enrolment information is available via the RACGP website (www.racgp.org.au).
Points are allocated to GPs who successfully complete the FRACGP assessment process within the triennium,
and at the time the RACGP Council ratifies Fellowship, as this is considered to be the completion of the FRACGP
assessment process.
GPs who successfully complete the FRACGP assessment process during the triennium will satisfy their QI&CPD
Program requirements and will not need to complete additional Category 1 activities. Completion of a CPR course
within the triennium will need to be demonstrated.
Fellowship in Advanced Rural General

Practice (150 Category 1 points)
The Fellowship in Advanced Rural General Practice (FARGP) is a practice-based postgraduate award designed
to assist candidates to increase competency and confidence to work in rural and remote general practice. The
program is flexible and consists of core and optional educational activities which have a strong experiential focus.
The FARGP currently involves 720 hours of learning (normally over two to four years) consisting of:
• advanced rural skill posts (ARSPs)
• working in rural general practice module
• emergency medicine module
• self-identified learning activities.
This is a portfolio-based course undertaken via distance education in which evidence of learning and meeting
program requirements is necessary for final assessment at completion of study. GPs working toward vocational
FRACGP may work toward the FARGP at the same time.
Points are allocated at the time the RACGP Council ratifies FARGP, as this is considered to be the completion of
the assessment process.
GPs who successfully complete the FARGP assessment process during the triennium will satisfy their QI&CPD
Program requirements. Completion of a CPR course within the triennium will also need to be demonstrated.
QI&CPD Program
39
Provider accredited activities

(Category 2 points)
Category 2 activities developed and delivered by RACGP QI&CPD accredited activity provider organisations are
specifically relevant to GPs and general practice. Accredited activity providers are required to provide GPs with an
attendance certificate.
The QI&CPD Program accredits the following types of activities under the Category 2 framework:
• CPR courses (minimum one hour) that meet Australian Resuscitation Council (ARC) guidelines (five points).
• Cultural awareness activities.
Each Category 2 activity is allocated two points per hour and capped to a maximum of 30 points.
Criteria for Category 2 activities

Each Category 2 activity must ensure its:
• primary objective is to improve the quality of patient care
• content is relevant to GPs and general practice
• content observes the highest ethical standards
• content is of a high clinical standard which is evidence-based and supported by accepted medical theory
• specific requirements are identified and covered in the educational content.
Evidence
GPs must provide a certificate of attendance and a program outline.
QI&CPD Program
Self-directed activities
(Category 2 points)
The RACGP acknowledges the value of a diverse range of education activities based on GPs’ individual needs and,
as such, recognises education that is not accredited where the GP sees it as personally valuable and relevant.
Activities that would be recognised as Category 2 must be a minimum of one hour in duration and can include:
• conferences with diverse topics
• lecture-style seminars
• large group meetings
• unaccredited online modules
• professional reading and journals.
GPs can record an unlimited number of Category 2 self-directed activities at a rate of two points per hour; however,
QI&CPD points are capped at 20 points per triennium.
Evidence
The QI&CPD Program recommends that GPs retain details and evidence of participation for future reference,
including a certificate of attendance and a program outline.
QI&CPD Program
41
Cardiopulmonary resuscitation
According to the RACGP’s Standards for general practices (4th edition),GPs must be ‘suitably qualified and trained
and maintain the necessary knowledge and skills to provide good clinical care’.2 GPs have a duty to respond
to sudden cardiac arrest - they are expected to perform cardiopulmonary resuscitation (CPR) procedures in
accordance with current ARC guidelines and techniques, without the assistance of specialist emergency services or
equipment.
Evidence suggests the most important determinant of survival from sudden cardiac arrest is the presence of a
trained rescuer who is ready, willing, able and equipped to act.10 The RACGP recognises that CPR skills are used
infrequently and, thus, may diminish over time.2
Consistent with the RACGP’s Standards for general practices (4th edition), it is a requirement of the QI&CPD
Program that GPs maintain basic life support skills through the completion of a CPR course that meets the ARC
guidelines at least once per triennium.
Criteria specific to CPR

CPR requirements:
• GPs must complete a CPR course that meets the ARC guidelines.
• Courses must be a minimum of one hour.
• Courses can be either a Category 2 accredited activity or form part of a Category 1 accredited activity.
• Advanced life support (ALS) courses must meet the RACGP CPR requirements.
• Training courses are required to assess CPR competence - learners must be able to physically demonstrate
CPR on a mannequin on the floor upon completion of the course.
CPR and ALS requirements for candidates/registrars who are on a pathway

to Fellowship
Refer to the ‘CPR and ALS courses’ guidance document available at the education services policies page
(www.racgp.org.au/education/fellowship/fellowship-of-the-racgp/policies/guidance-documents/cardiopulmonary-
resuscitation-and-advanced-life-support-guidance-document) for details on the types of courses that meet the
requirements.
Evidence
GPs must provide a certificate of completion.
QI&CPD Program
The RACGP will recognise CPR certificates issued by:

• ARC council representative member organisations, including:
- ARC
- RACGP
- New Zealand Resuscitation Council
- Australian Red Cross
- St John Ambulance, Australia
- College of Emergency Nursing Australia
- Council of Ambulance Authorities
- Surf Life Saving Australia
- Australian College of Nursing
- Australasian College for Emergency Medicine
- Perinatal Society of Australia and New Zealand
- Paramedics Australia
- Royal Australasian College of Surgeons
- Australian and New Zealand Intensive Care Society
- Australian College of Critical Care Nurses
- Australian and New Zealand College of Anaesthetists
- Royal Life Saving Society Australia
- Australian Defence Force
- Cardiac Society of Australia and New Zealand
- Heart Foundation
• registered training organisations that provide:
- CPR
- first aid.
Exemptions
GPs who cannot physically perform CPR may apply for exemptions, which are valid for the current triennium only.
These GPs are required to:
• provide a medical certificate or declaration stating they have a disability or medical condition that prevents them
from being physically able to perform CPR
• inform the RACGP in writing about measures undertaken within their medical practice to ensure they are
prepared for a situation that requires CPR.
GPs with a current CPR/ALS instructor certificate are also exempt.
QI&CPD Program
43
Quality improvement reflection

The RACGP’s Standards for general practices (4th edition) recommend that practices engage in QI activities that
review structures, systems and processes to aid in the identification of required changes to increase the quality of
healthcare delivery and safety of patients.4
This process encourages self-reflection on completed Category 1 activities, in which QI is identified as either part
of, or the outcome of, the learning process, such as:
• review of specific cases or clinical outcomes
• implementation of new recall systems within a practice
• review and evaluation of practice resources and referrals list.
QI activities should be robust, systematic and relevant to a GP’s scope of practice.
They must include an element of action and evaluation and, where possible, demonstrate an outcome or change.
The QI reflection form is allocated five Category 2 points and capped at 15 points per triennium.
Criteria specific to QI reflection

QI reflection must:
• provide GPs with an opportunity to reflect on changes or improvements in knowledge, attitudes, behaviours,
skills and/or practice systems as a result of the learning
• be completed as an extension of a Category 1 accredited activity that occurred within the triennium.
Steps in QI reflection
GPs must:
1. identify a Category 1 activity they have completed
2. reflect on how they applied their learning, considering changes or improvements to knowledge, attitudes,
behaviours, skills and/or practice systems as an outcome of the Category 1 activity
3. complete a QI reflection form online via myRACGP web page navigating to myCPD. Alternatively GPs can
download and complete the form, then email it to their state QI&CPD unit.
General information
QI&CPD Program
47
How are points allocated to GPs’

credit point statement?
The 2017-19 triennium features a number of mechanisms for point allocation for education activities.
GP self-directed learning
GPs may complete an individual application for Category 1 activities. Applications may be submitted online via the
myRACGP web page on the RACGP website, or by sending a paper application to the relevant state faculty office.
Individual GP applications are subject to quality assurance assessments.
Category 2 self-directed activities

Individual GPs may record participation in educational activities that are not accredited by the QI&CPD Program
which they view as valuable in fulfilling their learning needs. Applications may be submitted online via the
myRACGP web page on the RACGP website, or by sending a paper application to the relevant state faculty office.
Provider activities
Providers will arrange for a GP’s points to be allocated to their QI&CPD credit points statement when they attend
an RACGP accredited activity. The provider should also forward a certificate of attendance to the GP upon
completion of the activity.
QI&CPD Program
GPs with specific requirements

Many GPs are required by other colleges or third parties to maintain recognition of particular skills or qualifications.
These requirements are often negotiated between the RACGP and other colleges, for example, recertification as
a Diplomate of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (DRANZCOG)
and reaccreditation as a rural GP anaesthetist.
Many of the specific requirements are overseen by joint consultative committees (JCC), which are tripartite groups
that include representation by the relevant specialist college, the RACGP and the Australian College of Rural and
Remote Medicine (ACRRM).
The actual requirements as set by the relevant groups are negotiated each triennium. They are communicated at
the start of each triennium through RACGP communications and are available by contacting your RACGP Faculty
Office or the relevant college or third party.
The QI&CPD Program records Category 1 CPD points for GP participation in the following areas of specific
requirement:
• diagnostic radiology
• mental health (Mental Health Skills Training [MHST] Primary Pathway, focused psychological strategies [FPS]
skills training)
• medical acupuncture
• women’s reproductive health
• GPs who provide anaesthesia
• GPs who provide surgical services.
Other topic areas are included on RACGP QI&CPD activity application forms and can be selected when
applications are submitted. They are not related to mandatory requirements and are currently only recorded for
CPD purposes. This includes cultural awareness training and cultural safety training.
Category 2 activities do not meet specific requirements criteria, with the exception of cultural awareness, mental
health clinical enhancement module (CEM), mental health core module (CM), and mental health CPD.
QI&CPD Program
49
Rural Procedural Grants Program

The Rural Procedural Grants Program (RPGP) provides financial support to maintain and enhance the clinical skills of
GPs and locums who deliver:
• unsupervised anaesthetics, obstetrics and/or surgery in Australian Standard Geographical Classification -
Remoteness Area (ASGC-RA) 1-5 locations (dependent on additional approval)
• unsupervised emergency medicine in 24-hour triaging accident and emergency facilities located in ASGC-RA
2-5 locations.
This financial support is offered in the form of a grant of $2000 per day for up to 10 days of training per financial
year for procedural GPs, and for up to three days of training per financial year for GPs providing hospital-based
emergency services.
GPs who deliver any of these services in a rural or remote location may be eligible to participate in the RPGP. GPs
must apply to register in the RPGP via either the RACGP or ACRRM prior to attending grant-approved training in
order to receive the grants.
In order to access this program, GPs need to complete an RPGP ‘Application to register’ form and provide
documentation indicating they are a current unsupervised provider of anaesthetic, obstetric, surgical and/or
emergency medicine in a hospital or other appropriately equipped facility. Eligibility for the program is determined
by the RACGP or ACRRM.
Visit www.racgp.org.au or call 1800 636 764 for further information.
QI&CPD Program
Sponsorship guidance for all activities

An ethical relationship with sponsoring organisations concerning the delivery of education to healthcare
professionals is essential. Education activities accredited by the RACGP QI&CPD Program must have a focus on
improving the quality of patient care as their primary purpose.
Interactions with sponsors, especially those dealing with therapeutic goods, are only appropriate if they do not
affect, breach, distort or influence the GP-patient relationship. Educational material covered within each accredited
activity should meet or exceed acceptable clinical and ethical standards. This applies to all sponsored accredited
activities.
The term ‘sponsorship’ in the context of the RACGP QI&CPD Program includes any benefit transfer for an event
in return for which various rights are given to the sponsoring party. Sponsorship may involve financial, ‘in-kind’ or
other support (such as free event promotion or hosting services). Sponsorship benefits may be received directly or
indirectly. Their receipt may be the dominant reason for the sponsor’s involvement, or merely an ancillary purpose.
The term ‘advertising’ in the context of the RACGP QI&CPD Program is any image or statement, or series of such
(including as part of a campaign), intended to promote the use or supply of particular goods or services, included
under the definition of sponsorship.
Sponsorship requirements
To obtain and retain accredited status, activities must comply with a number of rules:
• Education delivered to GPs must be developed completely independently of any sponsorship.
• The QI&CPD Program will not accredit educational activities with sponsor input into its design, development,
content or delivery. The RACGP considers such input a conflict of interest and a breach of the QI&CPD activity
standards.
• Facilitators and speakers delivering the material must have independence. They must not be briefed on, or
influenced, as to how they present or deliver the education.
• Facilitators and speakers must declare any conflicts regarding payment, or other benefits or inducements from a
sponsor to attending GPs prior to delivering the accredited activity.
• Speakers may be provided by a sponsor to present education where appropriately trained and professional.
However, the speaker will need to declare their conflict as a representative of the sponsor organisation prior to
any delivery.
• A sponsored accredited activity must declare how and by whom it is sponsored each time that activity is
promoted, advertised or delivered.
• All event administration concerning participants must be handled by the provider and not the sponsor.
This includes
- processing participants’ registration
- collection and collation of completed evaluation forms from participants.

• Sponsor banners, pop-ups, advertising, online resources or event flyers must include sufficient details of the
activity and the provider’s contact details. The sponsor’s contact details must not be included, but their logo
may be featured.
QI&CPD Program
51
• Accredited activities must not at any stage, either directly or indirectly, promote:
- products by use of their brand or trade names
- products or modes of treatment disproportionate to their normal contribution to quality patient care
- products or methods of treatment in areas of clinical practice where accepted management standards are
insufficient and a balanced rationale is not provided
- experimental treatments and methods that have not been fully evaluated by intervention research
- experimental treatments without the support of the medical profession by reason of inconclusive evidence of
therapeutic benefits
- theories and methods of treatment not supported by scientific evidence
- techniques not accepted by a significant proportion of the medical profession, or not supported by accepted
medical theory
- therapeutic goods not authorised by the Therapeutic Goods Administration (TGA) for use in Australia.
• When there is uncertainty about an accredited activity’s clinical, scientific or ethical standards, the RACGP
reserves the right to seek clarification on the program design and evidence-based methodology. The RACGP
may then decline (or withdraw, as appropriate) accreditation of the educational activity if it fails to meet the
activity standards.
QI&CPD Program
Privacy and patient confidentiality

GPs are reminded that their relationship with their patients is categorised by law as a relationship of trust and
confidence. Patients are entitled to claim privilege in relation to their treatment and to insist upon maintenance of its
confidentiality. It is not the right of a GP to use such information without the patient’s consent.
When a GP collects patient health information for QI or CPD activities, they may only transfer identified patient
health information to a third party once informed patient consent has been obtained.
When a GP is using de-identified patient health information for research purposes, there are some situations in
which they are required to obtain informed patient consent, as well as some situations in which informed patient
consent is not required. The requirement for consent when using de-identified data will be decided by an HREC.2
Ethics approval is not required for a QI activity undertaken within a general practice, where the primary purpose is
to monitor, evaluate or improve the quality of healthcare delivered by the practice.2
A practice’s QI or clinical audit activities for the purpose of seeking to improve the delivery of a particular treatment
or service would be considered a directly related secondary purpose for information use or disclosure. In other
words, the practice would likely not need to seek specific consent for this use of patients’ health information.2
In order to ensure patients understand and have reasonable expectations of QI activities, practices are encouraged
to include information about such activities and clinical audits in the practice policy on managing health information.
Systems should be implemented to ensure the patient consents to the use of information, and only in a format that
will not involve direct or indirect identification of the patient.2
Visit www.oaic.gov.au for more information.
QI&CPD Program
53
References
1. Medical Board of Australia. Continuing professional development registration standard. Canberra: Medical Board of Australia, 2016.
2. The Royal Australian College of General Practitioners. Standards for general practices. 4th edn. East Melbourne, Vic: RACGP, 2010.
3. Reason J. Beyond the organisational accident: The need for ‘error wisdom’ on the frontline. Qual Saf Health Care 2004;13 Suppl
2:ii28-33.
4. Vincent C. Patient safety. 2nd edn. London: Wiley-Blackwell, 2010.
5. McCalister P. Practice based small group learning. London: BMJ Careers, 2010. Available at http://careers.bmj.com/careers/
advice/view-article.html?id=20000765 [Accessed 28 April 2016].
6. Toussaint J, Gerard RA. On the Mend: Revolutionizing Healthcare to Save Lives and Transform the Industry. 1st edn. Cambridge,
MA: Lean Enterprise Institute, Inc, 2010.
7. The Royal Australian College of General Practitioners. Putting prevention into practice (Green book). 2nd edn. East Melbourne,
Vic: RACGP, 2006. Available at www.racgp.org.au/your-practice/guidelines/greenbook/prevention-in-general-practice/planning-for-
prevention/plan,-do,-study,-act-cycle/ [Accessed 17 September 2015].
8. Jamtvedt G, Young JM, Kristoffersen DT, O’Brien MA, Oxman AD. Audit and feedback: effects on professional practice and
healthcare outcomes. Cochrane Database Syst Rev 2006;(2):CD000259.
9. Phillips RS, Glasziou P What makes evidence-based journal clubs succeed? Evid Based Med 2004;9:36-37.
10. Australian Resuscitation Council Guidelines. East Melbourne, Vic: Australian Resuscitation Council, 2016. Available at
http://resus.org.au/guidelines/ [Accessed 28 April 2016].
QI&CPD Program
QI&CPD Program unit contact details

Toll free 1800 472 247
Victoria
100 Wellington Parade, East Melbourne VIC 3002
Phone: 03 8699 0483 Fax: 03 8699 0560 Email: vic.qicpd@racgp.org.au
South Australia and Northern Territory
15 Gover Street, North Adelaide SA 5006
Phone: 08 8267 8310 Fax: 08 8267 8319 Email: sant.qicpd@racgp.org.au
Queensland
PO Box 1616, Coorparoo DC QLD 4151
Phone: 07 3456 8944 Fax: 07 3391 7009 Email: qld.qicpd@racgp.org.au
Western Australia
PO Box 1065, West Leederville WA 6901
Phone: 08 9489 9555 Fax: 08 9489 9544 Email: wa.qicpd@racgp.org.au
New South Wales and Australian Capital Territory
PO Box 534, North Sydney NSW 2060
Phone: 02 9886 4700 Fax: 02 9886 4791 Email: nswact.qicpd@racgp.org.au
Tasmania
Level 1, ABC Centre, 1-7 Liverpool Street Hobart TAS 7000
Phone: 03 6234 2200 Fax: 03 6232 2344 Email: tas.qicpd@racgp.org.au
General Practice Mental Health Standards Collaboration (GPMHSC)
100 Wellington Parade, East Melbourne VIC 3002
Phone: 03 8699 0554 Fax: 03 8699 0570 Email: gpmhsc@racgp.org.au

QI&CPD Program
55
Appendix 1: RACGP QI&CPD

Program activity standards
Required outcomes are listed below each standard.
Standard 1 - Activities are planned and organised to lead to improvement in

quality patient care and safety
1.1 . Activity design/selection is based on current, relevant and evidence-based best practice for improving health.
1.2 . Outcomes and scope of activities are developed with GP input and reflect identified general practice learning
and development needs.
1.3 . Activity outcomes are linked to the Curriculum.
1.4 . Content, strategies and resources are professionally appropriate to the achievement of the stated activity
outcomes.
1.5 . Activity development and supporting materials are documented.
Standard 2 - Activities are relevant to GPs

2.1 Activities meet the aims and objectives of the RACGP QI&CPD Program.
2.2 Participation in the activity leads to the achievement of stated outcomes.
2.3 Activities provide opportunities for reflection.
2.4 Activities meet the highest ethical, clinical and educational standards.
Standard 3 - Activities are evaluated against relevance and achievement

of stated outcomes
3.1 Content and engagement are evaluated against the stated outcomes.
3.2 Evaluation processes measure the stated outcomes.
3.3 Evaluation is used for continuous improvement.
3.4 Evaluation examines how knowledge and skills gained through the activity can lead to improvement in
clinical practice.
Standard 4 - Quality assurance assessment processes focus on

continuous improvement
4.1 All documentation and reporting is submitted in accordance with RACGP requirements.
4.2 Providers participate in the RACGP QI&CPD Program quality assurance assessment processes.
4.3 Providers are compliant with RACGP QI&CPD conditions.
4.4 Quality assurance assessment leads to continuous improvement and corrective actions.
QI&CPD Program
Appendix 2: Curriculum and

domains matrix
Select the appropriate domains and competency outcomes
Domain 3.
Domain 1.
Population Domain 5.
Communication Domain 4.
Domain 2. Applied professional health and Organisational
skills and the Professional
knowledge and skills the context and legal
patient-doctor and ethical role
of general dimensions
relationship
practice
CS1.1.1 CS2.1.1 CS2.2.7 CS3.1.1 CS4.1.1 CS5.1.1

Communication The conduct of The results of The patterns Adherence to Infection control
is clear, the consultation investigations and prevalence relevant codes and relevant
respectful, is appropriate are interpreted of disease are and s tandards clinical practice
empathic and to the needs of in the context of incorporated of ethical and standards are
appropriate the patient and the patient into screening professional maintained
to the person the sociocultural and behaviour
and their context management
sociocultural practices
context
CS1.1.2 CS2.1.2 CS2.2.8 CS3.1.2 CS4.1.2 CS5.1.2

Effective Continuity of Diagnosis and The impacts Duty of care is Effective clinical
communication care promotes management is of the social maintained leadership is
is used in quality and evidence-based determinants demonstrated
challenging safety and relevant to of health are
situations the needs of the identified and
patient addressed
CS1.1.3 CS2.1.3 CS2.2.9 CS3.1.3 CS4.1.3 CS5.1.3

Communication Comprehensive Rational Current and Patient-doctor Relevant
with family, and holistic prescribing emerging public boundaries are data is clearly
carers and management and medication health risks identified and documented,
others involved plans are monitoring is are effectively maintained securely
in the care of developed undertaken managed stored and
the patient is collaboratively appropriately
appropriate and shared
clear for quality
improvement
CS1.1.4 CS2.2.1 CS2.2.10 CS3.2.1 CS4.1.4 CS5.1.4

Complaints A comprehensive, The uncertainty Barriers to Critical incidents Quality and
and concerns clearly of ongoing equitable access and potential safety is
are managed documented undifferentiated to quality care critical incidents enhanced
effectively biopsychosocial conditions is are addressed are identified through the
history is taken managed and managed effective use
from the patient of information
systems
QI&CPD Program
57
Curriculum and domains matrix (continued)
Select the appropriate domains and competency outcomes

Domain 3.
Domain 1.
Population Domain 5.
Communication Domain 4.
Domain 2. Applied professional health and Organisational
skills and the Professional
knowledge and skills the context and legal
patient-doctor and ethical role
of general dimensions
relationship
practice
CS1.2.1 CS2.2.2 CS2.3.1 CS3.2.2 CS4.2.1 CS5.1.5

Ways in which An appropriate Quality The health Professional Effective triaging
health can be and respectful evidence-based needs of knowledge and time
optimised and physical resources individuals and skills are management
maintained are examination of are critically are balanced reviewed and structures are in
communicated the patient is analysed and with the health developed place to allow
to patients, undertaken utilised needs of the timely provision
family members community of care
and carers through effective
utilisation of
resources
CS2.2.3 CS2.3.2 CS3.2.3 CS4.2.2 CS5.1.6

A significantly Innovative Effective Reflection and Ethical business
ill patient is approach to leadership self-appraisal processes
identified and care of patients improves are undertaken and practices,
managed with multisystem outcomes for regularly and effective
appropriately and/or complex patients governance
health issues is structures are
taken implemented
CS2.2.4 CS2.4.1 CS4.2.3 CS5.2.1

A rational list Appropriate Personal health Patient
of differential mode of care and wellbeing confidentiality
diagnoses is delivery to suit is evaluated, is managed
formulated the needs of the maintained and appropriately
patient developed
CS2.2.5 CS2.4.2 CS4.3.1 CS5.2.2

Appropriate Fragmentation Professional Shared decision
procedures of care is knowledge making and
are undertaken minimised and skills are informed
after receiving effectively consent are
informed shared with explained and
consent others obtained
CS2.2.6 CS2.4.3 CS4.3.2 CS5.2.3

Rational options Demonstrate Identify and Medico-legal
for investigations leadership in support requirements
are offered emergency colleagues are integrated
situations who may be in into accurate
difficulty documentation
QI&CPD Program
Curriculum and domains matrix (continued)
Curriculum contextual unit (tick at least one contextual unit covered in this activity)
Main units AM16 Addiction medicine
AH16 Aboriginal and Aboriginal Torres Strait

DE16 Dermatology
Islander health
RH16 Rural health DM16 Disaster management
Populations EN16 Ear and nose medicine
AD16 Adult health EY16 Eye medicine
CO16 Care of older people MS16 Musculoskeletal and sports medicine
CY16 Children and young people’s health OM16 Occupational medicine
CH16 Custodial health OP16 Oncology and palliative care
DH16 Doctors’ health OR16 Oral health
DB16 Individuals with disabilities PM16 Pain management
MH16 Men’s health PS16 Psychological health
MM16 Military medicine SH16 Sexual and reproductive health
PC16 Pregnancy care TM16 Travel medicine
RA16 Refugee and asylum seeker health Processes
RC16 Residential care GR16 General practice research
SG16 Sex, sexuality, gender diversity and health GT16 General practice teaching
WH16 Women’s health IM16 Integrative medicine
Presentations Other (please provide further information)
AV16 Abuse and violence
Visit http://curriculum.racgp.org.au for further information on the Curriculum and domains of general practice
130
points
including
PLAN* 1x 1x
Quality Category 1 CPR
Improvement activity
activity
*NEW planning, learning and need (PLAN) activity
A RACGP
Healthy Profession.
Healthy Australia.
Clinical guideline
for the diagnosis
and management
of juvenile
idiopathic arthritis
August 2009
Approved by NHMRC
on 12 june 2009
National Health and

Medical Research Council
NHMRC
The royal Australian

COLLEGE OF
General Practitioners
The Royal Australian College of General Practitioners, 1 Palmerston Crescent, South Melbourne, Vic 3205 Australia
ACN 000 223 807, ABN 34 000 223 807
Clinical guideline for the diagnosis and management of juvenile idiopathic arthritis
The National Health and Medical Research Council (NHMRC) is Australia’s leading funding body for health and
medical research. The NHMRC also provides the government, health professionals and the community with expert
and independent advice on a range of issues that directly affect the health and wellbeing of all Australians.
The NHMRC provided support to this project through the Guidelines Assessment Register (GAR) process. The GAR
consultant on this project was Karen Grimmer-Somers.
The guidelines were approved by the Chief Executive Officer of the NHMRC on 12 June 2009 under section 14A
of the National Health and Medical Research Council Act 1992. Approval for the guidelines by NHMRC is granted for
a period not exceeding 5 years, at which date the approval expires. The NHMRC expects that all guidelines will be
reviewed no less than once every 5 years.
This publication was supported by funding from the Australian Government. The publication reflects the views of
the authors and not necessarily reflects the views of the Australian Government.
Published by:
College House
1 Palmerston Crescent
South Melbourne, Victoria 3205
Australia
Tel 03 8699 0414
Fax 03 8699 0400
www.racgp.org.au
ISBN 978-0-86906-298-2
Published August 2009
© The Royal Australian College of General Practitioners. All rights reserved.

CONTENTS
INTRODUCTION 1
Expiry date for the recommendations 2
Commonly used abbreviations 2
BACKGROUND 3
Classification 3
Prognosis 3
Aim of the guideline 3
Scope and target population 4
Focus of the guideline 4
Methods 5
The guideline 6
Limitations of the guideline 7
ALGORITHMS 8
Diagnosis and early management of JIA 8
Management of JIA 9
SUMMARY OF RECOMMENDATIONS 10
RECOMMENDATIONS FOR PRIMARY CARE OF JIA 12

Diagnosis of JIA 12
Early diagnosis and referral 12
History and clinical examination 12
Diagnostic investigations 14
Management of JIA 15
General principles 15
Multidisciplinary care and care planning 15
Patient education and psychosocial support 16
Pharmacological interventions 17
Simple analgesics (eg. paracetamol) 17
Weak opioids (eg. codeine) 17
Traditional non-steroidal anti-inflammatory drugs (NSAIDs) 18
Topical NSAIDs 19
Disease modifying anti-rheumatic drugs (DMARDs) 19
Complementary/alternative medicines 20
Non-pharmacological interventions 20
Nutritional therapies - calcium supplementation 20
Land based exercises 21
Aquatic exercise 22
Orthotics management (splints ready made and custom made) 22
Orthotics management (foot orthotics) 22
Thermotherapy 23
Complementary/alternative physical therapies 23
Disease monitoring and comorbidities 24
Clinical guideline for the diagnosis and management of juvenile idiopathic arthritis August 2009
FURTHER INFORMATION 25
REFERENCES 26
APPENDIX A. PROCESS REPORT 28
APPENDIX B. RESOURCES 35
APPENDIX C. MEMBERSHIP AND TERMS OF REFERENCE OF THE RACGP

JIA WORKING GROUP 38
INTRODUCTION
In Australia, at least 5000 children are affected by juvenile idiopathic arthritis (JIA) at any one time.1,2
Disease prevalence in Australia is between one and four cases per 1000 children.3 Juvenile idiopathic
arthritis can have significant associated morbidity and mortality. Long term follow up studies have revealed
JIA carries the potential for longer term inflammatory activity and complications, leaving a lasting impact
on the patient’s function, growth and quality of life. Accurate and early diagnosis along with appropriate
management and referral are essential for maximising patient outcomes and quality of life.
General practice plays an important role within the Australian health care system in prevention, early
detection and chronic disease management (CDM). To manage chronic illness effectively requires well
coordinated, patient centred care that is continuous, comprehensive, and consistent. General practitioners
are well placed to provide this care and undertake this role in consultation with other medical specialists
as required.4-6 The role GPs play in CDM through multidisciplinary care coordination and long term care
planning is recognised within the national Medicare rebate framework. Children with arthritis are eligible
for broader funding arrangements under CDM items for GP Management Plans and associated reviews.6
As part of the Australian Federal Government’s Better Arthritis and Osteoporosis Care (BAOC) 2006-2007
budget initiative,7 guidelines for the management of osteoarthritis, rheumatoid arthritis, and juvenile idiopathic
arthritis have been developed to inform evidence based primary care of chronic disease in general practice.
It is important that children presenting with JIA are diagnosed early; have initial management commenced
by their GP; and are referred promptly to a paediatric rheumatologist. Because of the relatively low
prevalence of JIA in the general population, GPs often develop little experience with the diagnosis or
management of JIA. The Clinical guideline for the diagnosis and management ofjuvenile idiopathic arthritis has
been developed to fill that gap.
The guideline presents recommendations to assist GPs managing patients with JIA. It focuses on short
term care, long term care planning and management, and coordination of multidisciplinary care needs. The
guideline includes algorithms and resources to assist with the implementation of the recommendations.
The guideline has been endorsed by the National Health and Medical Research Council (NHMRC).
This project was supported by The Royal Australian College of General Practitioners (RACGP) and the
Australian Department of Health and Aging (DoHA). The following experts were involved in the development
of the guideline as part of the RACGP Juvenile Idiopathic Arthritis Working Group:
Dr Jane Munro (Chair), MBBS, MPH, FRACP
Dr Shane Brun, FFSEM(UK), FACRRM, FASMF, FARGP, MSpMed, DCH, GradDipRuralMed, GradDipEd,
BAppSc, FRACGP
Dr Morton Rawlin, BMed, MMedSci, DipPracDerm, DipFP, DipMedHyp, DipBusAdmin, FACRRM, FRACGP
Pam Webster (consumer representative), MCH, BA, DipT, AUA
Prof Karen Grimmer-Somers (NHMRC advisor), PhD, MMedSc, BPhty, LMusA, CertHlthEc
Amy Jasper, MBA, GDipHumServRes, BAppSci(AdvNsg)
Dr Jiri Rada, PhD, FRSH, MSc, BPHE, BA
Emily Haesler, BN, PGradDipAdvNsg
The following paediatric experts were involved as part of the Australian Paediatric Rheumatology
Expert Group:
Dr Roger Allen, MBBS, FRACP
Dr JD Akikusa, MBBS, FRACP
Dr Christina Boros, MBBS, PhD, FRACP
Dr Sue Piper, MBBS, FRACP
Dr Navid Adib, MBBS, PhD, FRACP
Dr Kevin Joseph Murray, MBBS, FRACP
Dr Jeff Chaitow, MMBCh, FRACP
NOTE: All website references were current at the time of publication.
Expiry date for the recommendations
This guideline presents a comprehensive review of pharmacological and non-pharmacological management
of JIA within the Australian health care context, based on the best available evidence up to January 2007.
Evidence published after this date has not been reviewed for the guideline.
The guideline was approved by the CEO of the NHMRC on 12 June 2009, under section 14A of the National
Health and Medical Research Council Act 1992. Approval for the guidelines by the NHMRC is granted for
a period not exceeding 5 years. It is expected that the guideline will be reviewed, and revised if necessary,
no less than once every 5 years. Review should be more frequent in areas where clinical practice or
research is known to be changing rapidly. Readers should check with the RACGP for any reviews or updates
of the guideline.
Commonly used abbreviations
ACR 30/50/70 American College of Rheumatology Paediatric 30/50/70 criteria

AE adverse event
ANA antinuclear antigen
BMC bone mineral content
BMD bone mineral density
CDM chronic disease management
CHAQ Childhood Health Assessment Questionnaire
CI confidence interval
COX-2 cyclo-oxygenase-2 selective inhibitors
CRP C-reactive protein
DMARDs disease modifying antirheumatic drugs
EPC enhanced primary care
ES effect size: 0.2 small effect, 0.5 moderate effect, 0.8 large effect
ESR erythrocyte sedimentation rate
FBC full blood count
GIT gastrointestinal
HRQOL Health related quality of life (usually measured on a self reported 10 cm VAS)
HLA human leukocyte antigen
JIA juvenile idiopathic arthritis
LFTs liver function tests
NS not statistically significant
NSAIDs non-steroidal anti-inflammatory drugs
RACGP [The] Royal Australian College of General Practitioners
RhF rheumatoid factor
ROM range of movement/motion
SR systematic review (also used in this report to describe meta-analysis)
TENS transcutaneous electrical nerve stimulation
VAS visual analogue scale
WMD weighted mean difference
2
BACKGROUND
Juvenile idiopathic arthritis is a chronic, autoimmune, inflammatory joint disease. It is the most common
rheumatic disease in children and adolescents. It is defined as ‘persistent arthritis of unknown aetiology
that begins before the age of 16 years and persists for at least 6 weeks’. It is diagnosed after excluding
other causes.8
The cause of JIA is unknown. It is suspected that environmental factors such as viral infections may trigger
the condition in genetically susceptible children.9 However, it is unusual for more than one child in a family
to have arthritis.
The aim of treatment is the induction of remission and control of the disease to minimise pain and function
loss, and maximise quality of life. There is currently no cure for JIA. Treatment has altered as a result of
recent research into the best practice approach to managing children. This guideline reflects the current
evidence based approach to managing children with JIA.
Classification
There are seven subtypes of JIA:8
1. Oligoarticular - affects four or less joints. This is the most common subtype
2. Polyarticular (RhF negative) - when five or more joints are affected. Rheumatoid factor (RhF)
antibody is not found on blood testing
3. Polyarticular (RhF positive) - when five or more joints are affected and RhF is found on blood
testing. This subtype may behave similarly to rheumatoid arthritis in adults
4. Systemic - a chronic arthritis associated with systemic features, including high spiking fever, transient
episodic erythematous rash, lymphadenopathy and hepatosplenomegaly (systemic features often precede
the arthritis)
5. Enthesitis related - (previously known as juvenile spondyloarthropathy). This is a chronic arthritis
associated with enthesitis (inflammation at insertion of tendons, ligaments or fascia to bone), or with
lower axial skeletal involvement. HLA B27 is present or there is a family history of a first degree relative
with a HLA B27 related disease. A significant proportion of patients will develop sacroiliitis as adults,
but back and sacroiliac joint involvement is uncommon during childhood
6. Psoriatic - chronic arthritis, usually with asymmetrical involvement of small and large joints, and either
the development of psoriasis or other evidence of a psoriatic diathesis (two of the following: family
history in a first degree relative, nail pits or onycholysis, or dactylitis).
7. Undifferentiated arthritis.
Prognosis
For many years it was believed that most children eventually outgrow JIA. Now it is known that half of children
with JIA will still have active arthritis 10 years after diagnosis unless treated appropriately. In moderate to
severe cases, JIA can produce serious joint and tissue damage and cause problems with bone development and
growth.10 In some cases, JIA symptoms are mild and do not cause progressive joint disease and deformities.
In the past, JIA has often been seen as a benign condition, which it is not. Children presenting with
JIA may be diagnosed inappropriately as having non-specific joint paints, ‘growing pains’ or recurrent
musculoskeletal ‘sprains’. As a result appropriate referral and treatment is delayed.
The outcomes for children with JIA are improved if managed by a multidisciplinary team with the input
of a paediatric rheumatologist.11,12
Aim of the guideline

This guideline seeks to provide recommendations for the early diagnosis and multidisciplinary management
of JIA in the primary care setting. The recommendations focus on the primary care practitioner’s role in:
• early identification of JIA
• early referral to a paediatric rheumatologist
• prevention of complications associated with JIA
• alleviation/minimisation of pain
• optimal management of acute exacerbations of JIA
• prevention and minimisation of joint damage
• maximisation of function
3
optimisation of normal growth and development
improved quality of life.
Scope and target population

This guideline is intended for use in the primary health care setting by health care professionals working
within a multidisciplinary team, including GPs and the following allied health professionals: physiotherapists;
occupational therapists; sports medicine personnel; podiatrists; dieticians; psychologists; pharmacists; nurses
and community health workers.
It is intended for patients under the age of 16 years presenting with arthritic symptoms, as well as those
diagnosed as having JIA. It does not cover patients over the age of 16 years, treatment of extra-articular
disease, or surgical interventions.
This guideline has been developed for use in primary care settings in metropolitan, regional, rural and
remote areas of Australia.
Focus of the guideline

The guideline focus is on JIA. It does not cover the management of other forms of arthritis, or complex
or unusual conditions. The following process model (Figure 1) identifies the stages in CDM and the focus
of the guideline.
Early diagnosis of juvenile idiopathic arthritis

• Early and accurate diagnosis
• Care and referral pathways
___________________________________ y___________________________________
Treatment and management in early stage of juvenile idiopathic arthritis
Best practice management
• Optimal use of medicines
• Non-pharmacological management
• Patient self management education
• Patient psychosocial support requirements
I
Treatment and management during acute episodes of juvenile idiopathic arthritis
Best practice management
Episode prevention
I
Long term management of juvenile idiopathic arthritis
Best practice management of chronic conditions
• Prevention of complications
• Optimise growth and development
Primary focus of guideline
Figure 1. Stages in CDM and the focus of the JIA guideline 4
Methods
The process used to develop the guideline is outlined in full detail in the Process Report (Appendix A). This
guideline is based on an evidence based literature review conducted to NHMRC requirements. The RACGP
JIA Working Group, who has overseen the development of the guideline and supporting documents,
comprised rheumatologists, GPs, consumer representatives, arthritis organisation representatives and
an NHMRC advisor. The evidence for the guideline is based on:
1. A review of the literature identified through a systematic search of evidence published from January 2000
to January 2007
2. A national guideline for JIA3 which was assessed using the AGREE instrument13 and identified as being
the most appropriate, recently published guideline to use as a primary reference
3. The Working Group’s expert opinion
4. Australian paediatric rheumatology expert opinion.
Literature review
The method used to conduct the evidence based literature review is outlined in full in the Process Report
(Appendix A). A search of MEDLINE, EMBASE, CINAHL and the Cochrane Library for English language
publications from January 2000 to January 2007 was performed. An additional manual search was used
to identify evidence for interventions not represented in the initial search or not covered by the primary
reference guidelines. Articles were also identified through review of reference lists of retrieved papers and
research known to RACGP Working Group members. Papers were initially selected for inclusion based
on reading the title and/or the abstract. Included literature was limited to Level 1 and Level 2 evidence
graded according to the NHMRC additional levels of evidence and grades for recommendations for developers of
guidelines (2005).14 For areas where randomised controlled trials (RCTs) or systematic reviews (SRs) were not
available, lesser levels of evidence and expert opinion were sourced. Papers that met the inclusion criteria
were critically appraised using checklists developed by SIGN and given an overall quality grade of high,
moderate or low. Findings from the literature were reported descriptively and in a tabulated format. The full
methods and findings are presented in Juvenile idiopathic arthritis: a literature review of recent evidence (www.
racgp.org.au/guidelines/juvenileidiopathicarthritis/literaturereview).
Recommendations
The method used to develop and grade recommendations is outlined in full in the Process Report (Appendix
A). Recommendations were based on the literature review and primary reference guideline. The RACGP
Working Group developed evidence statements from which each recommendation was developed, available
in Recommendations for the diagnosis and management ofjuvenile idiopathic arthritis (www.racgp.org.au/
guidelines/juvenileidiopathicarthritis/recommendations). Each recommendation statement is supported
by a grading that reflects the strength of the recommendation and implementability in terms of trust or
confidence practitioners can use in a clinical situation. The recommendation gradings used throughout the
guideline are based on NHMRC additional levels of evidence and grades for recommendations for developers of
guidelines14 presented in Table 1.
Table 1. Recommendation grades14

A Excellent evidence - body of evidence can be trusted to guide practice
B Good evidence - body of evidence can be trusted to guide practice in most situations
C Some evidence - body of evidence provides some support for recommendation(s) but care should
be taken in its application
D Weak evidence - body of evidence is weak and recommendation must be applied with caution
The overall grade of each recommendation is based on a summation of an appraisal of individual

components of the body of evidence on which the recommendation is based, including volume and
consistency of the evidence. Table 2 shows the body of evidence assessment matrix, listing all the
components that were considered when assessing the body of evidence, together with the grades used.14
The volume of evidence was defined to reflect the levels of evidence considered for this project. In reaching
an overall grade, recommendations did not receive a grading of A or B unless the volume and consistency
of evidence components were both graded either A or B. Overall grades were reached through consensus
consideration of the grading for each component listed below.
Table 2. Body of evidence assessment matrix14
Component A B C D
Excellent Good Satisfactory Poor
Volume of Several Level I or One or two Level Level III studies with Level IV studies or
evidence Level II studies II studies with low low risk of bias or Level I-III studies
with low risk of risk of bias or a SR Level II studies with with high risk of
bias of multiple Level III moderate risk of bias bias
studies with low risk
of bias
Consistency All studies Most studies Some inconsistency Evidence is
consistent consistent and reflecting genuine inconsistent
inconsistencies may uncertainty around
be explained clinical question
Clinical impact Very large Substantial Moderate Slight or restricted
Generalisability Population/s Population/s Population/s Population/s

studied in body studied in the body studied in the studied in the
of evidence of evidence are body of evidence body of evidence
are the same similar to the target different to the different to the
as the target population for the target population target population
population for guideline for the guideline for the guideline
the guideline but it is clinically and hard to
sensible to apply judge whether
this evidence to the it is sensible to
target population generalise to the
(eg. results in adults target population
that are clinically
sensible to apply
to children)
Applicability Directly Applicable to Probably applicable Not applicable to
applicable Australian health to Australian health Australian health
to Australian care context with care context with care context
health care few caveats some caveats
context
The guideline
The guideline has been designed to provide clear information to assist clinical decision making and support
optimal patient care. It is based on the best evidence available up to January 2007. Where appropriate,
the evidence has been interpreted with regard to the Australian context in which the guideline will be
implemented. It is intended that the guideline be considered according to the limitations outlined in
section 7 and used in conjunction with clinical judgment and patient preference. The guideline consists of:
Algorithms
The two algorithms summarise the main recommendations of the guideline and provide an accessible
desktop reference. The algorithms provide detailed flow charts for the diagnosis and the management of JIA.
Recommendations
The 21 recommendations contained in this guideline are limited to patients under the age of 16 years
presenting with arthritic symptoms, as well as those diagnosed as having JIA. They do not cover the
management of other forms of arthritis, complex or unusual conditions, or give detailed guidance on
pharmacological therapy in JIA. The recommendations have been developed on the basis of the best
evidence available up to January 2007.
Each recommendation has been graded according to the NHMRC additional levels of evidence and grades14
(from A to D).The grade reflects the degree of ‘trust’ that the clinician can place in the clinical application
of the recommendation. Each recommendation is supported by a summary of the evidence.
The RACGP Working Group supports all 21 recommendations and intends that they be used in
conjunction with clinical judgement and patient preferences. The full grading and evidence base for each
recommendation is available in Recommendations for the diagnosis and management ofjuvenile idiopathic
arthritis (www.racgp.org.au/guidelines/juvenileidiopathicarthritis/recommendations).
Good practice points

Where appropriate, recommendations are followed by good practice points. The good practice points
are essential tips on how to effectively implement the recommendations. These points are followed by
a summary of the evidence for each recommendation.
Resources
Useful references and supporting information are provided throughout the guideline. Appendix B contains
additional resources, as well as contact details for organisations providing services and support to both
patients with JIA and their carers.
The RACGP Working Group recommends consulting the National Prescribing Service
(www.nps.org.au), the Rheumatology Therapeutic Guidelines (www.tg.com.au), the Paediatric
Handbook (www.rch.org.au/paed_handbook) and the Australian Medicines Handbook
(amh.hcn.net.au) for detailed prescribing information including:
• indications
• drug dosage
• method and route of administration
• contraindications
• supervision and monitoring
• product characteristics.
Limitations of the guideline

Medication information
The literature search was not designed to retrieve safety trials for pharmacological interventions. The
guideline does not seek to provide full safety and usage information on pharmacological interventions.
The pharmacological interventions outlined in the guideline should not be applied without consideration
to the patient’s clinical profile and personal preferences. The Working Group recommends consulting
the sources listed above.
Search date
The guideline is based on the best evidence available up to January 2007. Evidence published after this date
has not been reviewed or considered for the guideline.
Interventions included
The initial search strategy was limited to include only papers graded as Level 1 or Level 2 evidence and
expanded to include lower levels of evidence for interventions where no high level evidence was found.
Interventions that have not been included in the recommendations may not have had readily identifiable
literature related to their use. The guideline is not intended to confirm or refute the effectiveness, nor provide
guidance on the use of interventions that have not been included, as the evidence has not been reviewed.
Lack of evidence
For some interventions included in the recommendations there was limited evidence from which to draw
conclusions on the intervention’s effectiveness. The Working Group acknowledges that lack of evidence
is not evidence of lack of effect, and has attempted to reflect this in the strength of the grading given to
recommendations on interventions that are not supported. In addition, some interventions were not supported
in the recommendations due to lack of evidence of effect. The Working Group acknowledges that this refers
to lack of evidence of effect over placebo, that is, patients may receive some beneficial outcomes from the
intervention, however these do not exceed beneficial effects that can be expected from a placebo therapy.
Cost effectiveness
As part of the brief, the evidence for this guideline does not include the cost effectiveness of the
recommended practice versus current/established practice. It also does not cover the economic feasibility
of the recommendations.
ALGORITHMS
Diagnosis and early management of JIA
Assessment and early management
Within 4 weeks of symptom onset
Management of JIA
Juvenile idiopathic arthritis

Management
The goals of treatment for JIA are to control inflammation, relieve pain, prevent or control joint damage,
0 -6 weeks
maximise functional abilities and manage complications
DIAGNOSIS
Confirm diagnosis, start initial treatment and organise paediatric rheumatology referral
(see Algorithm 1)
6-12 weeks
Psychosocial support and Ongoing monitoring of JIA (Grade C, Manage comorbidities

education (Grade C, page 16) page 24) (Grade C, page 24)
• Psychosocial support for patients, • Optimise multidisciplinary communication • Manage comorbidities
family members, and carers • Assess arthritis activity at least three times • Regular ophthalmological
• Ongoing education on disease per year and adjust therapy to maintain review for JIA related
management and medications swollen and tender joint count as low as diseases treated with long
• Refer patients to support possible term corticosteroids
organisations such as Arthritis • Monitor toxicity and medication side • Preventive medicine:
Australia effects immunisations, weight,
www.arthritisaustralia.com.au • Paediatric rheumatology review at least growth, nutrition, dental
and Carers Association twice per year • Monitor sleep, fatigue,
www.carersaustralia.com.au • Adjust medication in consultation with mood, school progress, peer
Ongoing
Tel 1800 242 636 paediatric rheumatologist and age appropriate activity
• Determine if persistent flare

• Manage short term flares symptomatically with analgesics +/- NSAIDs, heat, and relative rest
• Beware of infection if on immunosuppressive medication and evaluate for co-infection
• If persisting flare or other concerns, contact a paediatric rheumatologist or rheumatology team for advice
WARNING: Treatment may cause serious adverse effects. Physicians and patients/carers must monitor for signs
and symptoms of potential toxicity through regular clinical and laboratory review.
9
SUMMARY OF RECOMMENDATIONS
Note: There is one recommendation advising GPs not to use topical NSAIDs (highlighted in RED).
Recommendation 1 - Early diagnosis (Grade C)

General practitioners should aim to diagnose JIA as early as possible in order to optimise outcomes
for patients.
Recommendation 2 - Referral (Grade C)
Referral to a rheumatologist is advised for patients with confirmed or suspected JIA whose symptoms
persist beyond 4 weeks. Early referral enables aggressive intervention with disease modifying drugs,
which reduces long term joint damage and disability.
Recommendation 3 - Clinical examination (Grade C)
General practitioners should base diagnosis of JIA (and differential diagnosis) on history and clinical
examination in the first instance, with strong suspicion of JIA indicated by:
• pain and swelling of single or multiple joints
• persistent or worsening loss of function
• fever of at least 10 days with unknown cause, often associated with transient erythematous rash
• decreased range of motion (ROM)
• joint warmth
• effusion.
Recommendation 4 - Diagnostic investigations (Grade C)
In early assessment of patients presenting with painful and swollen joint(s), GPs should support clinical
examination with appropriate tests to assist in increasing diagnostic certainty, excluding differential
diagnoses, and predicting patients likely to progress to erosive disease. Base investigations usually
include:
• ESR or C-reactive protein (CRP)
• Full blood count (FBC).
Consider rheumatoid factor (RhF), antinuclear antigen (ANA), human leukocyte antigen (HLA) B27, and
plain radiographs. Depending on the clinical picture, additional investigations may be required.
Recommendation 5 - Multidisciplinary care (Grade D)
General practitioners should encourage and support a management approach based on individual patient
need and involving a multidisciplinary team of health professionals.
Recommendation 6 - Care plans (Grade D)
Involvement of the multidisciplinary team should be managed through the development of individual
care plans.
Recommendation 7 - Patient information (Grade C)
General practitioners should provide ongoing, tailored information to support their patients’
understanding of their disease, treatment options, possible outcomes and their role in self management,
and encourage patients and their carers to seek appropriate information and education opportunities
according to their individual needs.
Recommendation 8 - Patient support (Grade C)
General practitioners should provide ongoing psychosocial support and encourage patients and their
carers to seek support from appropriate sources according to their individual needs.
Recommendation 9 - Simple analgesics (Grade C)
General practitioners should consider using paracetamol in regular divided doses for treating moderate
pain in children and adolescents with JIA.
Recommendation 10 - Weak opioids (Grade D)
General practitioners could consider prescribing codeine in regular divided doses, in addition
to paracetamol, for treating moderate articular pain in children and adolescents with JIA.
10
Recommendation 11 - Traditional NSAIDs (Grade B)
General practitioners should prescribe NSAIDs as the initial drug of choice for reducing inflammation
and associated pain in the treatment of JIA.
Recommendation 12 - Topical NSAIDs (Grade D)
General practitioners should NOT prescribe topical NSAIDs to treat patients with JIA.
Recommendation 13 - Complementary/alternative medicines (Grade D)
General practitioners could inform patients and their families that, although there has been no research
in children with JIA, there is limited or no evidence of effectiveness above placebo of complementary/
alternative medicines in adult populations with arthritis.
Recommendation 14 - Nutritional therapy - calcium (Grade B)
General practitioners should monitor calcium intake in children with JIA, and provide advice on increasing
daily calcium intake. General practitioners could consider treating some patients with JIA with oral calcium
and vitamin D supplementation.
Recommendation 15 - Land based exercise (Grade C)
General practitioners should encourage patients with JIA to engage in regular physical activity compatible
with their general abilities and restrictions of their disease.
Recommendation 16 - Aquatic exercise (Grade C)
General practitioners could inform patients about aquatic exercise for children and adolescents, and its
limited effects.
Recommendation 17 - Splints (Grade D)
General practitioners could inform patients about use of splints and make individualised recommendations
in conjunction with appropriately trained multidisciplinary health professionals.
Recommendation 18 - Foot orthoses (Grade D)
General practitioners could inform patients with JIA in the lower limb about the role of comfortable,
supportive shoes. General practitioners could inform patients about the use of foot orthotics based on
an individualised assessment, safety, and personal preference, in conjunction with appropriately trained
multidisciplinary health professionals.
Recommendation 19 - Thermotherapy (Grade D)
General practitioners could consider recommending the use of heat and cold packs, warm baths and/or
ice massage for the symptomatic relief of JIA in children and adolescents.
Recommendation 20 - Complementary/alternative physical therapies (Grade D)
General practitioners could inform patients and their families who seek advice that there is no research
on complementary/alternative physical therapies in children with JIA.
Recommendation 21 - Disease monitoring (Grade C)
General practitioners should be involved in monitoring disease progression and managing comorbidities
in conjunction with the treating paediatric rheumatologist.
11
RECOMMENDATIONS FOR PRIMARY CARE OF JIA
Diagnosis of JIA
Early diagnosis and referral
Recommendation 1 - Early diagnosis (Grade C)
General practitioners should aim to diagnose JIA as early as possible in order to optimise outcomes
for patients.
Recommendation 2 - Referral (Grade C)
Referral to a rheumatologist is advised for patients with confirmed or suspected JIA whose symptoms
persist beyond 4 weeks. Early referral enables aggressive intervention with disease modifying drugs,
which reduces long term joint damage and disability.

• For advice about accessing a paediatric rheumatologist, either privately or through public clinics, contact
the Australian Rheumatology Association at www.rheumatology.org.au.
• When making a referral for a newly diagnosed or suspected case of JIA, make initial telephone contact
with a rheumatologist and mark the referral URGENT (recent onset JIA).
In JIA, persistent synovitis leads to joint deformity and destruction, and may occur less than 2 years
following onset of disease. Disruption of proper joint function predisposes children and young adults
to premature osteoarthritis and a potential of lifetime disability.15 An early, accurate diagnosis and disease
modifying therapy is essential in order to commence appropriate management aimed at promoting normal
growth and development, and to minimise disability and deformity.2
Early referral to a paediatric rheumatologist is recommended in the literature. With a large range of
differential diagnoses for possible JIA, assessment by a paediatric rheumatologist at an early stage should
be sought to confirm diagnosis.15
It is the consensus of the RACGP Working Group that patients with symptoms persisting
beyond 4 weeks and indicative of JIA be referred to a rheumatologist to enable early initiation
of therapy.
History and clinical examination

Recommendation 3 - Clinical examination (Grade C)
General practitioners should base a diagnosis of JIA (and differential diagnoses) on history and clinical
examination in the first instance, with strong suspicion of JIA indicated by:
• pain and swelling of single or multiple joints
• persistent or worsening loss of function
• fever of at least 10 days with unknown cause, often associated with transient erythematous rash
• decreased range of motion (ROM)
• joint warmth
• effusion.
The international literature15,16 and the Australian national JIA guideline3 recommends that diagnosis of JIA
should be based primarily on comprehensive history taking, complete clinical examination, and the ordering
appropriate diagnostic tests.
Patients commonly present with pain and stiffness in one or more joints. Juvenile idiopathic arthritis should
be particularly suspected in patients who present with persistent joint pain and swelling. In most patients,
symptoms emerge over weeks to months. Musculoskeletal symptoms and signs are common in children
and adolescents and may be the presenting feature of a broad spectrum of conditions. Clinical features and
laboratory findings may be relatively non-specific in rheumatological conditions, and it is important to look
for disease patterns when evaluating the presenting complaint and conducting a systems review.
Primary care physicians should particularly note that the absence of key symptoms, signs, or positive test
results, does not necessarily rule out a diagnosis of JIA. Thus, ongoing monitoring and early specialist
referral should be considered for patients with persistent symptoms.
12
It is the consensus of the RACGP Working Group and Australian paediatric rheumatology
experts that diagnosis of JIA should be based primarily on careful history taking and clinical
examination. Patients commonly present with pain and stiffness in one or more joints. Juvenile
idiopathic arthritis should be particularly suspected in patients who present with persistent
joint pain and swelling. In most patients, symptoms emerge over weeks to months.
The Working Group has developed the following history and clinical examination checklist (see also
Appendix B):
History
• Pain or swelling in one or more joints is present
• Check the nature of onset - is it acute or insidious? Previous episodes?
• Acute onset monoarticular arthritis associated with fever is septic until proven otherwise
• Check the timing of symptoms during the day - as a general guide:
• Early morning stiffness/stiffness after rest or sleep = inflammatory
• Post-activity pain = mechanical
• Check duration of illness - if >6 weeks it is less likely to be reactive/post-viral arthritis
• Are there any concurrent infections (respiratory, enteric or skin)? Post-viral infections are probably the
most common cause of transient arthritis
• Check constitutional features (eg. fever, rash, loss of weight)
• Has the child been taking any medications (eg. cefaclor)?
• What does the child, or parent consider to be the most symptomatic site - is it in the joint, muscle,
adjacent bone or a more diffuse area?
• Check for extra-articular symptoms - ensure a thorough systems review and keep the following
diagnoses in mind:
- septic arthritis
- post-infectious/reactive arthritis
- systemic lupus erythematosus (SLE)
- acute lymphoblastic leukaemia (ALL)
- trauma/non-accidental injury
- osteomyelitis
- bone tumour
- inflammatory bowel disease (IBD)
- Henoch-Schonlein purpura and other vasculitides
- rheumatic fever
• Assess whether normal activity levels or interests have been interrupted
• Assess the functional milieu of the patient (eg. school progress and attendance, sleep pattern, family
and peer relationships and stress experiences)
• Check the family history for other types of inflammatory arthritis, particularly the spondyloarthropathies,
autoimmune disorders and pain syndromes (eg. fibromyalgia or other models for pain behaviour).
Examination
Observe the patient as they move about the room looking for limitations or alterations in function and be
opportunistic when examining them.
• Examine all joints, not only the site of the presenting complaint. There may be inflammation without
symptoms in JIA
• Aim to localise the site of maximal discomfort (eg. is it the joint capsule, adjacent bone or muscle belly,
tendon or ligament attachments?)
• Examine for signs of systemic diseases with an articular component, extra-articular features of JIA,
or both. In particular examine the skin, eyes, abdomen, nails and lymph nodes.
A musculoskeletal assessment should include:
• Joints - signs of inflammation such as swelling or tenderness, the range of movement and deformity.
Joints affected by JIA are typically swollen, may be tender to touch and warm but are usually not
erythematous
13
• Entheses - bone attachment sites of ligaments/tendons (eg. Achilles tendon)
• Tendon sheaths of fingers and toes (eg. dactylitis in psoriasis)
• Gait - antalgic (pain) or limp, Trendelenburg sign
• Muscle tenderness, muscle wasting or weakness (eg. inability to toe or crouch walk)
• Patellar tracking pattern - does the patella move vertically on walking?
• Shoe sole and heel wearing pattern
• Leg length measurement
• Spinal flexion, including Schober test (the measurement of the lumbosacral range should increase in
distance by at least 6 cm on maximal flexion with knees straight; the starting range is a point 5 cm below
and 10 cm above the lumbosacral junction (use the Dimples of Venus as a guide)
• Assessment of growth parameters.
Juvenile idiopathic arthritis can resemble any disorder causing acute or chronic polyarthritis in children.
Elimination of other diseases is therefore a necessary step in the diagnosis of JIA.
Diagnostic investigations
Recommendation 4 - Diagnostic investigations (Grade C)
In early assessment of patients presenting with painful and swollen joint(s), GPs should support clinical
examination with appropriate tests to assist in increasing diagnostic certainty, excluding differential
diagnoses, and predicting patients likely to progress to erosive disease. Base investigations usually
include:
• ESR or CRP
• FBC.
Consider RhF, ANA, HLA B27, and plain radiographs. Depending on the clinical picture, additional
investigations may be required.

• Before JIA is diagnosed all other known conditions and causes of childhood arthritis must be excluded.
• Absence of any key symptoms, signs, or test results does not necessarily rule out a diagnosis of JIA.
There is no single test that accurately diagnoses JIA. A number of tests are useful in increasing diagnostic
certainty, excluding other forms of arthritis, predicting patients likely to progress to erosive disease, and
monitoring disease progression. Various tests also have a role in monitoring disease progression.
Given the level of distress and anxiety procedures may have for children, coordinating procedures and
optimising procedural pain management through appropriate preparation of child and parent, use of topical
local anaesthetic agents, and non-pharmacological techniques such as distraction and relaxation/breathing
should be implemented.
Erythrocyte sedimentation rate and CRP indicate an inflammatory process but have low specificity for
JIA. One of these tests is usually performed.8 These markers are usually elevated in JIA but may be normal.
The RhF test is not conclusive. RhF is positive in only a small percentage of JIA patients (unlike rheumatoid
arthritis). However, when present in combination with other factors, the level of RhF may indicate the
likelihood for aggressive disease progression and a poorer prognosis.17,18
A FBC is usually undertaken to provide general information relating to inflammation and anaemia.
(Working Group)
Plain X-rays have been key investigations in identifying erosions, and predicting disease; however, erosions
are not often apparent in disease of less than 3 months duration.7 Serial X-rays over years may show disease
progression and therefore indicate the need for a change in treatment strategy. Other imaging is unlikely to
be helpful at diagnosis and should be ordered only in discussion with a paediatric rheumatologist.
experts that GPs should support clinical examination with appropriate testing to support
diagnostic certainty, exclude differential diagnoses and to predict patients likely to develop
erosive disease.
14
Management of JIA
General principles
General practitioners should contribute to a management approach based on the following therapeutic goals:
• preservation of function and quality of life
• minimisation of pain and inflammation
• joint protection, and
• control of systemic complications.
Multidisciplinary care and care planning

Recommendation 5 - multidisciplinary care (Grade D)
General practitioners should encourage and support a management approach based on individual patient
need and involving a multidisciplinary team of health professionals.
Recommendation 6 - care plans (Grade D)
Involvement of the multidisciplinary team should be managed through the development of individual
care plans.

• GPs may utilise Enhanced Primary Care (EPC) items to facilitate access to appropriate services (see
Resources). Eligible services include, but are not limited to, those provided by physiotherapists,
osteopaths, occupational therapists, podiatrists, mental health workers, indigenous health workers,
chiropractors, chiropodists, audiologists and speech pathologists.
• GPs should refer carers to their state/territory Carers’ Association for information and support as part
of the ongoing management plan (see Resources).
• Include pain management and assessment of sleep quality in the treatment plan.
There is strong support for a multidisciplinary approach in the management of JIA to ensure all of the
child’s needs are met, including normal growth, social development and physical functioning.2,15,19,20 A wide
range of interventions implemented by multidisciplinary health care providers were reviewed for these
recommendations. In the vast majority of trials the intervention of interest was implemented by a health
care provider with specific training and qualifications. Seeking health advice and management from an
appropriately trained health care provider is considered to be a component of effective and safe therapy.
A wide range of multidisciplinary health care providers may be considered in the co-management of patients
with JIA, including but not limited to:
• physiotherapists
• occupational therapists
• mental health specialists
• ophthalmologists
• podiatrists or orthotists
• orthopaedic surgeons
• social workers
• pain management teams
• indigenous health workers
• community nursing teams.
The child’s family and school are also essential elements in ongoing management of the child. Family should
be involved in all aspects of care, and the psychosocial needs of carers should also be considered, as this
influences the ongoing management of the child patient.19 Liaison with the school (eg. principal, physical
education teacher, school liaison worker) is important, particularly if special arrangements are relevant
(eg. extra time for school work).2,15,20
It is the consensus of the RACGP Working Group that the GP, rheumatologist and
multidisciplinary team should aim to engage the patient in an individualised care plan,
agreeing on treatment goals that include an objective measure of disease.
15
Patient education and psychosocial support
Recommendation 7 - patient information (Grade C)
General practitioners should provide ongoing, tailored information to support patient understanding of
their disease, treatment options, possible outcomes and their role in self management, and encourage
patients and their carers to seek appropriate information and education opportunities according to their
individual needs.
Recommendation 8 - patient support (Grade C)
General practitioners should provide ongoing psychosocial support and encourage patients and their
carers to seek support from appropriate sources according to their individual needs.

• Joint protection, energy conservation, and problem solving skills training should be taught early on in the
disease course.
• GPs may access medication information for patients from the Australian Rheumatology Association (ARA)
or may refer patients and their carers (see Resources).
• Referral to Arthritis Australia is recommended for general disease and treatment information, as well as
support services (see Resources).
The evidence of the impact of patient education and psychosocial support remains limited, but most
literature agrees that while it is important to appropriately manage the medical aspects of arthritis in
children, it is equally important to provide psychosocial interventions such as:15
• patient/family education
• psychosocial interventions/support services
• community resources
• school based resources
• information and referral regarding insurance coverage and benefit coordination.
Education and behavioural interventions are important with specific interventions. For example, there is
strong evidence that a behavioural intervention involving group education sessions can have a positive
impact on increasing dietary calcium intake.21
Munro and Murray2 include education and support among the important aspects of effective JIA treatment.
Hashkes and Laxer18 agree that the treatment of JIA combines anti-inflammatory and immunomodulatory
medications with physical and occupational therapy, an occasional need for surgery, nutritional support,
and psychosocial and educational partnership with patients and parents.
It is the consensus of the RACGP Working Group that the above interventions represent
important aspects of the general management of JIA and should be encouraged among all
members of the multidisciplinary team. When in doubt, contact a paediatric rheumatologist.
The nearest paediatric rheumatologist contact is available from www.rheumatology.org.au.
16
Pharmacological interventions
The RACGP Working Group recommends consulting the National Prescribing Service
(www.nps.org.au), the Rheumatology Therapeutic Guidelines (www.tg.com.au), the Paediatric
Handbook (www.rch.org.au/paed_handbook) and the Australian Medicines Handbook
(amh.hcn.net.au/) for detailed prescribing information.
Simple analgesics (eg. paracetamol)

Recommendation 9 - simple analgesics (Grade C)
General practitioners should consider using paracetamol in regular divided doses for treating moderate
pain in children and adolescents with JIA.

• Use the correct dose for the child’s weight. In overweight children, the ideal body weight, rather than
actual weight, should be used to calculate dose.
• Chronic dosing should not exceed 48 hours without medical advice.
• Maximum daily dose is 90 mg/kg to a maximum of 4 g/day for treating persistent pain in children and
adolescents with JIA.
Cautions
• Paracetamol has few side effects, but dosing is limited by possible hepatotoxicity.
• Do not rely on dosing charts supplied by the manufacturer as these tend to underdose the child.
• Do not use slow release preparations in infants and children.
There is an accepted role for simple analgesics in managing pain in JIA, although the evidence supporting
effectiveness specifically in JIA is limited. Paracetamol remains the analgesic of choice for treating persistent
pain in children and adolescents.22
The recommended dose in children is 15 mg/kg orally, every 4 hours. Maximum daily dose is 90 mg/kg up to
a maximum of 4 g (60 mg/kg/day maximum for infants aged less than 6 months). A dose of 10 mg/kg is no
more effective than placebo for minor pain in children. General practitioners are reminded to use the correct
dose for the child’s weight.23,24
experts that paracetamol be used for treating persistent pain in children and adolescents with
JIA. Paediatric rheumatology experts recommend paracetamol should be used in the short
term and it is rarely needed in the long term in patients with JIA.
Weak opioids (eg. codeine)

Recommendation 10 - Weak opioids (Grade D)
General practitioners could consider prescribing codeine in regular divided doses in addition to
paracetamol for treating moderate articular pain in children and adolescents with JIA.

• Use the correct dose for the child’s weight. The oral dose for codeine in children is 0.5 to 1.0 mg/kg every
4-6 hours up to a maximum of 3 mg/kg/day.
• Chronic dosing should not exceed 48 hours without medical advice.
• In overweight children, the ideal body weight, rather than actual weight, should be used to calculate
dosage.
Cautions
• Adverse effects of codeine may occur in the absence of analgesia in poor metabolisers.
• Rapid metabolisers may experience excessive sedation.
• Be alert to paracetamol and codeine doses in combination preparations (eg. Painstop mixtures and
Panadeine tablets).
There are no SRs or RCTs of codeine for treating persistent pain in children and adolescents with JIA
published between January 2000 and January 2007.
Codeine is the weak opioid of choice for treating persistent pain in children and adolescents. The oral dose
for codeine in children is 0.5 to 1.0 mg/kg every 4-6 hours up to a maximum of 3 mg/kg/day.22
17
The cytochrome p450 enzyme responsible (CYP2D6) shows genetic polymorphism and age dependent
activity. The implications are that codeine is likely to be ineffective in poor metabolisers (9% English, 1%
Swedish, German and mainland Chinese, 30% Ethiopian and Hong Kong Chinese). Adverse effects of
codeine may occur in the absence of analgesia in poor metabolisers.23
experts that codeine be used for treating moderate articular pain in children and adolescents
with JIA in regular divided doses, in addition to paracetamol.
Traditional non-steroidal anti-inflammatory drugs (NSAIDs)

Recommendation 11 - traditional NSAIDs (Grade B)
General practitioners should prescribe NSAIDs as the initial drug of choice for reducing inflammation
and associated pain in the treatment of JIA.

• Prescribe only one NSAID or COX-2 inhibitor at a time.
• Long term use of NSAIDs or COX-2 inhibitors should be at the lowest effective dose.
• NSAIDs may be prescribed with methotrexate.
• Use NSAIDs in the liquid form for children unable to swallow tablets.
• Base the selection of NSAID on dosing requirements, availability, and patient preferences (eg. taste).
• Consider stopping NSAIDs and COX-2 inhibitors 7-10 days before any major surgical procedure,
particularly orthopaedic surgery. Discuss with the surgeon and make a decision on a case-by-case basis.
Cautions
• NSAIDs are generally well tolerated by children, but toxicity can occur. Caution should be applied in view
of the known side effects, although these tend to be less common or severe than in adults: increased
sleep disturbance and non-specific abdominal pain. A pseudoporphyria-like skin reaction occurs in about
5% of children taking naproxen. This latter complication is more common in fairer skinned children
living in sun exposed latitudes. The antiplatelet effect of the NSAIDs predisposes to excessive bruising
in particularly active children.25
• Most children with asthma can take NSAIDs safely. However, those with diagnosed or suspected aspirin
induced asthma - symptoms of asthma usually accompanied by facial flushing and rhinitis within 3 hours
of exposure to an NSAID - should avoid all NSAIDs.25
• Aspirin is not recommended in children because of the link with Reye syndrome.23
NSAIDs are the first line drug for the treatment of inflammation in children with JIA. They have well
established analgesic and anti-inflammatory effects; however, they do not influence progression of the
disease and do not prevent joint damage. Unlike adults, children tolerate NSAIDs very well, with few side
effects.23,26
Table 3. Recommended paediatric doses for oral NSAIDs for juvenile idiopathic arthritis22,26
Drug (Not in order of preference) Dose

Celecoxib 2-4 mg/kg twice daily
Diclofenac 1 mg/kg twice daily
Ibuprofen 10 mg/kg 3-4 times daily
Indomethacin 0.5-1.0 mg/kg 2-3 times daily
Meloxicam 0.15-0.30 mg/kg once daily
Naproxen 5-7.5 mg/kg twice daily
Piroxicam 0.2-0.4 mg/kg once daily
NSAIDs are valuable medications when used appropriately in carefully selected patients. Side effects are
well recognised and include gastrointestinal disturbance, rash, mood changes, and sleep disturbance.
No significant differences have been reported in the safety profiles of various NSAIDs.22,26
18
In both a good quality RCT27 and a low quality SR of 14 low quality studies,18 participants receiving all forms
and doses of NSAIDs achieved significant improvements in outcome measures, and no individual NSAID was
shown to have a clear advantage over others.
COX-2 inhibitors have not been studied extensively in children and potential adverse effects are not clear.
experts that NSAIDs are the initial drug of choice for reducing inflammation and associated
pain in the treatment of JIA.
Topical NSAIDs
Recommendation 12 - Topical NSAIDs (Grade D)
General practitioners should NOT prescribe topical NSAIDs to treat patients with JIA.
There are no studies of topical NSAIDs and JIA (2000-2007). Evidence from two literature reviews states
there is no evidence available on the use of topical NSAIDs for treating persistent pain in children and
adolescents with JIA.2,20
experts that using topical NSAIDs in children and adolescents with JIA is NOT recommended.
Disease modifying anti-rheumatic drugs (DMARDs)

In caring for children with arthritis, commencing and altering DMARD medication is seen as the role of the
specialist paediatric rheumatologist. Therefore, evidence on these drugs is not presented in this guideline.
General practitioners have an important role to play in monitoring adherence to DMARDs and their side
effects. For example, common side effects of methotrexate treatment include nausea, anticipatory nausea,
mouth ulcers, and abdominal discomfort; less commonly, altered liver function (increased transaminases),
infection, or haematologic toxicity.22,26
Other commonly used DMARDs include hydroxychloroquine, sulfasalazine, leflunomide and biological
DMARDs (bDMARDs).
Complementary/alternative medicines
Recommendation 13 - complementary/alternative medicines (Grade D)
General practitioners could inform patients and their families, that although there has been no research
in children with JIA, there is limited or no evidence of effectiveness above placebo of complementary/
alternative medicines in adult populations with arthritis.

• GPs should ask their patients about use of complementary medicines when prescribing treatment for JIA.
• GPs may consult a pharmacist if concerns arise regarding medication interactions related to
complementary medicines.
There are no RCTs or SRs (2000-2007) on the use of complementary/alternative medicines including herbal
and mineral supplements in children with JIA, nor is there commentary in relevant literature reviews.
Families/patients often seek complementary medicines for treatment of arthritis, particularly if they have had
insufficient results from conventional medication. Alternative therapies used for the treatment of arthritis
include herbs, vitamins and/or mineral supplements, aromatherapy, naturopathic and homeopathic products.
These products are widely available without prescription in Australia.28
A number of SRs on the use of a wide range of complementary medicines in the treatment of arthritis in
adult populations have not demonstrated any clinical benefits above placebo.29-31 Until further research is
conducted, these findings are likely to apply to paediatric populations with arthritis.
Although generally considered to have low risk of serious side effects, herbal and nutritional supplements
may have harmful effects, particularly through interaction with other medications.28
It is the consensus of the RACGP Working Group and Australian paediatric rheumatology experts
that GPs ask about complementary/alternative medicines when conducting medication reviews
for children and adolescents with JIA. General practitioners may inform patients and their
families that, although there has been no research in children, there is limited or no evidence of
effectiveness above placebo of complementary medicines in adult populations with arthritis.
19
Non-pharmacological interventions
Nutritional therapies - calcium supplementation
Recommendation 14 - nutritional therapy - calcium (Grade B)
General practitioners should monitor calcium intake in children with JIA, and provide advice on increasing
daily calcium intake. General practitioners could consider treating some patients with JIA with oral calcium
and vitamin D supplementation.

• Encourage appropriate caloric and calcium intake.
• Children with JIA on corticosteroid therapy are at increased risk of osteoporosis and osteopenia.22,25
Additional consideration should be given to calcium and vitamin D supplements when on corticosteroid
course.
Children with JIA have been reported to have low BMD early in the disease and independent of steroid use.
Additionally, 15-26% of JIA patients have pathologic fractures before adulthood.32
There is evidence from one good quality RCT that calcium supplementation can improve total BMD in
patients with JIA. Over 2 years, patients taking calcium supplements had net improvement in total body
bone mass density of 1% above those taking placebo. Some patients experienced nausea as a side effect.33
Evidence from a moderate quality RCT investigated achievement of daily calcium intake without dietary
supplement in children with JIA. Increase in calcium intake translated into statistically superior increases
at 6 and 12 months in some measures of BMD compared to those who received standard care. In the RCT,
families with younger children with JIA were more prepared to participate in the interventions. In this RCT,
a behavioral intervention had a positive impact on increasing dietary calcium intake. The improvement in
calcium intake was achieved without compromising dietary intake in other areas.21,32
In addition to risks associated with disease, treatment with corticosteroids results in bone loss in a range
of ways and increases the risk of osteoporosis. Steroids decrease absorption of calcium and increase urinary
calcium loss, leading to bone resorption. Preventive therapy with calcium and vitamin D supplementation
has been suggested for all patients taking corticosteroids.34
There are no SRs or RCTs conducted in children on the use of vitamin D in the protection against
osteoporosis (2000-2007). In a Cochrane review of five studies that investigated the role of vitamin D
supplements in adults receiving corticosteroid therapy, the meta-analysis showed that treatment with
calcium and vitamin D is more effective at preventing bone loss than placebo or calcium alone.34
experts that GPs monitor calcium intake in children with JIA and provide advice to families
on increasing daily calcium intake. In some patients, particularly those on corticosteroids,
consider calcium and vitamin D supplementation.
Land based exercises

Recommendation 15 - land based exercises (Grade C)
General practitioners should encourage patients with JIA to engage in regular physical activity compatible
with their general abilities and restrictions of their disease.

• GPs may utilise EPC items to facilitate access to appropriate services (see Resources). Eligible services
include, but are not limited to, those provided by physiotherapists, occupational therapists, and exercise
physiologists.
• GPs could refer patients to Arthritis Australia for information and services relating to exercise
(see Resources).
• Promote physical activity to decrease the risk of osteoporosis and osteopenia.
• Specific and individualised exercise therapy may be initiated with input from a paediatric trained
physiotherapist or occupational therapist (or other appropriately trained therapists).
• The choice of exercise may depend on the child’s specific needs and preferences.
One moderate quality RCT (80 children) evaluated the effects of exercise training on physical function
in children with JIA. Participation in a 12 week exercise program of both low and high intensity resulted in
improved physical function as measured by the self reported CHAQ, but not other self reported measures.
There was no differences achieved between low or high intensity exercise, but those in low intensity
programs were more likely to adhere to the regimen.35
A literature review summarised the findings from four low quality, small studies on land based exercise.
It suggested that participation in moderate physical activity for at least 6 weeks (1-3 exercise sessions/
week) can improve both muscle function and aerobic fitness in children with JIA. Additional points from
the reviewed literature suggest that:36
• children with JIA can participate in exercise without disease exacerbation
• participation in land based exercise at least twice a week for at least 6 weeks may help reduce disease
symptoms and improve endurance
• land based exercise may lead to greater improvements in muscle strength, performance on timed tasks,
and functional status than aquatic exercise
• weight bearing exercise is needed to develop optimal bone width and density during childhood
• individualised and supervised resistance exercise appears to be safe for children with JIA
• the choice of exercise may depend on the child’s specific needs and preferences
• with proper screening, children with mild disease should be able to participate in most sports. However,
highly competitive contact sports pose a potential risk for damage to the joint surface and growth plate,
and should be avoided during periods of active joint disease.
At least 1 yearly review by a specialised paediatric physiotherapist is recommended in the Australian
Paediatric Rheumatology standards of care.3
experts that regular physical activity compatible with the child’s general abilities and the
restrictions of their disease is recommended. Regular physical activity promotes normal
childhood development and may combat the adverse effects of disease on muscle strength,
endurance and aerobic capacity.
Aquatic exercise
Recommendation 16 - aquatic exercise (Grade C)
General practitioners could inform patients about aquatic exercise for children and adolescents, and its
limited effects.

• Not all children will have access to hydrotherapy.
• Aquatic exercises can be performed in a standard swimming pool.
There is evidence from one low quality RCT (54 patients with JIA) that aquatic exercise is safe, although it
has no significant impact on functional outcome measures. No statistically significant differences were found
on any outcome measures between the control group (standard care) and the intervention group (aquatic
training program consisted of aerobic exercises, and flexibility and intensity training in a heated pool in a
group setting by a physical therapist conducted for 1 hour per week) after 20 weeks of therapy. Participants
had water confidence before commencing the program.37
One literature review suggested that participation in an exercise program at least twice per week for at least
6 weeks may help to reduce disease symptoms and improve general exercise endurance.36
At least 1 yearly review by a specialised paediatric physiotherapist is recommended in the Australian
Paediatric Rheumatology standards of care.3
experts that hydrotherapy on an individualised basis is recommended for some patients with
JIA, and this is considered a safe form of exercise.
21
Clinical guideline for the diagnosis and management of juvenile idiopat

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■RAC GP Guidelines for preventive

Royal Australian College 0/General Practitioners

The Royal Australian College of General Practitioners

Tel 03 8699 0414

ISBN: 978-0-86906-451-1 (Print)

First edition published 1989

Cover image © istockphoto/skodonnell

Red Book Editorial Committee

Professor Jon Emery Associate Professor Jane Smith

Associate Professor John Furler Dr Christine Walker

Professor Jenny Doust Associate Professor Warrick Inder

Dr Jan Orman Clinical Associate Professor Liz Wylie

Professor Denis Spelman National Stroke Foundation

HDL high-density lipoprotein

HDL-C high-density lipoprotein-cholesterol OSA obstructive sleep apnoea

HHC hereditary haemochromatosis PBS Pharmaceutical Benefits Scheme

Hib haemophilus influenzae type b PCR polymerase chain reaction

HIV human immunodeficiency virus PEDS parents’ evaluation of developmental status

NMSC non-melanocytic skin cancer

NTD neural tube defect

II. Patient education and health literacy 8

III. Development of the Red Book 11

IV. How to use the Red Book 12

References - Chapters I-IV 14

V. What’s new in the 9th edition? 16

1. Preventive activities prior to pregnancy 18

2. Genetic counselling and testing 24

3. Preventive activities in children and young people 32

4. Preventive activities in middle age 42

5. Preventive activities in older age 45

7. Prevention of chronic disease 66

8. Prevention of vascular and metabolic disease 85

9. Early detection of cancers 104

10. Psychosocial 126

11. Oral health 134

12. Glaucoma 137

13. Urinary incontinence 138

14. Osteoporosis 141

15. Screening tests of unproven benefit 147

Lifecycle chart 158

Figure I.1. Leading risk factors contributing to the burden of disease3

Oral health •§ — •II •# — — —

The Red Book

These guidelines do not include:

The Australian experience

Figure I.2. Age-standardised death rates for potentially avoidable deaths,

Benefits and harms of preventive health activities

Prevention in the practice population

Figure I.3. The determinants of health and illness9

Individual physical and psychological make-up

Note: Bold highlights selected social determinants of health

Screening versus case finding

Opportunistic versus systematic prevention

II. Patient education and health literacy

Impact of patient education

Approaches to patient education

Supporting patient education and health literacy in

What can GPs do?

III. Development of the Red Book

The dimensions addressed are:

IV. How to use the Red Book

II Evidence obtained from a randomised controlled trial (RCT)

Evidence obtained from a comparative study with concurrent controls:

Evidence obtained from a comparative study without concurrent controls: