DPCA2-1

Diabetes 

& Primary Care Australia 

Vol 2 No 1 2017 

The primary care diabetes journal for healthcare professionals in Australia 

Clinical vascular 

screening of the foot: 

For life and limb 

Build a personalised 

record of all your PCDSA 

e-learning. Access a suite 

of FREE modules, reflect 

on your practice and 

gain CPD certificates at 

www.pcdsa.com.au/cpd 

Page 16 

IN THIS ISSUE 

Diabetes education 

Editorial and article on the 

current situation of diabetes 

education in Australia. 

Pages 5 and 10 

Fenofibrate 

What primary care clinicians 

should know about using 

fenofibrate for people with 

diabetes. Page 30 

GLP-1 receptor analogues 

A practical guide to the 

initiation of GLP-1 receptor 

agonists for people with 

type 2 diabetes. Page 35 

WEBSITE 

Journal content online at 

www.pcdsa.com.au/journal

The PCDSA is a multidisciplinary society with the aim 

of supporting primary health care professionals to deliver 

high quality, clinically effective care in order to improve 

the lives of people with diabetes. 

The PCDSA will 

Share best practice in delivering quality diabetes care. 

Provide high-quality education tailored to health professional needs. 

Promote and participate in high quality research in diabetes. 

Disseminate up-to-date, evidence-based information to health 

professionals. 

Form partnerships and collaborate with other diabetes related, 

high level professional organisations committed to the care of 

people with diabetes. 

Promote co-ordinated and timely interdisciplinary care. 

Membership of the PCDSA is free and members get access to a quarterly 

online journal and continuing professional development activities. Our first 

annual conference will feature internationally and nationally regarded experts 

in the field of diabetes. 

To register, visit our website: 

www.pcdsa.com.au

Contents 

Diabetes 

& Primary Care Australia 

Volume 2 No 1 2017 

Website: www.pcdsa.com.au/journal 

Editorial 

Diabetes education 5 

Rajna Ogrin reflects on the importance of diabetes education in Australia. 

From the desktop 

Patient and practitioner: Flash glucose monitoring 7 

Gary Kilov gives a first-hand perspective on using flash glucose monitoring. 

CPD module 

Clinical vascular screening of the foot: For life and limb 16 

Sylvia McAra, Robert Trevethan, Lexin Wang and Paul Tinley provide guidance to support early detection of peripheral arterial disease 

using evidence-based clinical tests. 

Articles 

Diabetes education: Essential but underfunded in Australia 10 

Mark Kennedy and Trisha Dunning explain why more is required to improve and provide diabetes education. 

Antimicrobial management of diabetic foot infection 25 

Roy Rasalam, Caroline McIntosh and Aonghus O’Loughlin provides an overview of the current evidence for diagnosis and 

management of diabetic foot infections in practice. 

What primary care clinicians should know about fenofibrate for people with diabetes 30 

Alicia J Jenkins, Andrzej S Januszewski, Emma S Scott and Anthony C Keech review fenofibrate's mechanisms of action, 

proven clinical benefits in type 2 diabetes and practical aspects of its prescription. 

GLP-1 receptor analogues – a practical guide to initiation 35 

Ralph Audehm and Laura Dean provide a practical guide to initiating glucagon-like peptide 1 analogues in people with type 2 diabetes. 

Editor-in-Chief 

Rajna Ogrin 

Senior Research Fellow, RDNS Institute, St Kilda, Vic 

Associate Editor 

Gary Kilov 

Practice Principal, The Seaport Practice, and Senior 

Lecturer, University of Tasmania, Launceston, Tas 

Editorial Board 

Ralph Audehm 

GP Director, Dianella Community Health, and 

Associate Professor, University of Melbourne, 

Melbourne, Vic 

Werner Bischof 

Periodontist, and Associate Professor, LaTrobe 

University, Bendigo, Vic 

Laura Dean 

Course Director of the Graduate Certificate in 

Pharmacy Practice, Monash University, Vic 

Nicholas Forgione 

Principal, Trigg Health Care Centre, Perth, WA 

John Furler 

Principal Research Fellow and Associate Professor, 

University of Melbourne, Vic 

Mark Kennedy 

Medical Director, Northern Bay Health, Geelong, and 

Honorary Clinical Associate Professor, University of 

Melbourne, Melbourne, Vic 

Peter Lazzarini 

Senior Research Fellow, Queensland University of 

Technology, Brisbane, Qld 

Roy Rasalam 

Head of Clinical Skills and Medical Director, 

James Cook University, and Clinical Researcher, 

Townsville Hospital, Townsville, Qld 

Suzane Ryan 

Practice Principal, Newcastle Family Practice, 

Newcastle, NSW 

Editor 

Olivia Tamburello 

Editorial Manager 

Richard Owen 

Publisher 

Simon Breed 

© OmniaMed SB and the Primary Care 

Diabetes Society of Australia 

Published by OmniaMed SB, 

1–2 Hatfields, London 

SE1 9PG, UK 

All rights reserved. No part of this 

journal may be reproduced or transmitted 

in any form, by any means, electronic 

or mechanic, including photocopying, 

recording or any information retrieval 

system, without the publisher’s 

permission. 

ISSN 2397-2254 

Diabetes & Primary Care Australia Vol 2 No 1 2017 3

Call for papers 

Would you like to write an article 

for Diabetes & Primary Care Australia? 

The new journal from the Primary Care Diabetes Society of Australia 

To submit an article or if you have any queries, please contact: gary.kilov@pcdsa.com.au. 

Title page 

Please include the article title, the full names of the authors 

and their institutional affiliations, as well as full details of 

each author’s current appointment. This page should also have 

the name, address and contact telephone number(s) of the 

corresponding author. 

Article points and key words 

Four or five sentences of 15–20 words that summarise the major 

themes of the article. Please also provide four or five key words 

that highlight the content of the article. 

Abstract 

Approximately 150 words briefly introducing your article, 

outlining the discussion points and main conclusions. 

Introduction 

In 60–120 words, this should aim to draw the reader into the 

article as well as broadly stating what the article is about. 

Main body 

Use sub-headings liberally and apply formatting to differentiate 

between heading levels (you may have up to three heading levels). 

The article must have a conclusion, which should be succinct and 

logically ordered, ideally identifying gaps in present knowledge and 

implications for practice, as well as suggesting future initiatives. 

Tables and illustrations 

Tables and figures – particularly photographs – are encouraged 

wherever appropriate. Figures and tables should be numbered 

consecutively in the order of their first citation in the text. Present 

tables at the end of the articles; supply figures as logically labelled 

separate files. If a figure or table has been published previously, 

acknowledge the original source and submit written permission 

from the copyright holder to reproduce the material. 

References 

In the text 

Use the name and year (Harvard) system for references in the 

text, as exemplified by the following: 

● As Smith and Jones (2013) have shown … 

● As already reported (Smith and Jones, 2013) … 

For three or more authors, give the first author’s surname 

followed by et al: 

● As Robson et al (2015) have shown … 

Simultaneous references should be ordered chronologically first, 

and then alphabetically: 

● (Smith and Jones, 2013; Young, 2013; Black, 2014). 

Statements based on a personal communication should be 

indicated as such, with the name of the person and the year. 

In the reference list 

The total number of references should not exceed 30 without prior 

discussion with the Editor. Arrange references alphabetically first, 

and then chronologically. Give the surnames and initials of all 

authors for references with four or fewer authors; for five or more, 

give the first three and add “et al”. Papers accepted but not yet 

published may be included in the reference list as being “[In press]”. 

Journal article example: Robson R, Seed J, Khan E et al (2015) 

Diabetes in childhood. Diabetes Journal 9: 119–23 

Whole book example: White F, Moore B (2014) Childhood 

Diabetes. Academic Press, Melbourne 

Book chapter example: Fisher M (2012) The role of age. In: Merson 

A, Kriek U (eds). Diabetes in Children. 2nd edn. Academic Press, 

Melbourne: 15–32 

Document on website example: Department of Health (2009) 

Australian type 2 diabetes risk assessment tool (AUSDRISK). 

Australian Government, Canberra. Available at: http://www. 

health.gov.au/preventionoftype2diabetes (accessed 22.07.15) 

Article types 

Articles may fall into the categories below. All articles should be 

1700–2300 words in length and written with consideration of 

the journal’s readership (general practitioners, practice nurses, 

prescribing advisers and other healthcare professionals with an 

interest in primary care diabetes). 

Clinical reviews should present a balanced consideration of a 

particular clinical area, covering the evidence that exists. The 

relevance to practice should be highlighted where appropriate. 

Original research articles should be presented with sections 

for the background, aims, methods, results, discussion and 

conclusion. The discussion should consider the implications 

for practice. 

Clinical guideline articles should appraise newly published 

clinical guidelines and assess how they will sit alongside 

existing guidelines and impact on the management of diabetes. 

Organisational articles could provide information on newly 

published organisational guidelines or explain how a particular 

local service has been organised to benefit people with diabetes. 

— Diabetes & Primary Care Australia —

Editorial 


We are all aware that diabetes 

mellitus prevalence is rising, 

affecting around half a billion 

people worldwide (International Diabetes 

Federation, 2015) and approximately 5% 

of Australians (917 000 people; Australian 

Institute of Health and Welfare, 2012). 

Unfortunately, almost half of people with 

type 2 diabetes have glycaemic levels out 

of target range (Si et al, 2010), leading to 

increased rates of macro- and microvascular 

complications and early mortality (Holman 

et al, 2008), as well as increasing healthcare 

costs (Lee et al, 2013). 

Diabetes education is pivotal in supporting 

effective diabetes self-management, and 

structured diabetes education supports selfmanagement, 

having been shown to improve 

blood glucose levels, blood pressure, weight 

and lipid levels, as well as having a positive 

effect on blood glucose self-monitoring 

(Norris et al, 2001; 2002; Ellis et al, 2004; 

Minet et al, 2010). Despite the advantages of 

structured education, over 40% of Australians 

with diabetes do not have access to such 

programs (Deloittes Access Economics, 2014). 

To provide an independent analysis of 

the cost effectiveness of diabetes education, 

the Australian Diabetes Educator Association 

(ADEA) commissioned Deloittes Access 

Economics (2014) to produce the report 

Benefits of Credentialled Diabetes Educators to 

people with diabetes and Australia. The report 

identified that for every $173 investment in 

diabetes education, there would be a return 

of $2827 per patient, per annum in healthcare 

cost savings. These cost savings were due 

to a reduction in frequency of hospital 

admission, emergency presentation, GP 

visits and treatment of related comorbidities. 

If diabetes education was made available 

to all Australians with diabetes, the total 

healthcare cost savings in 2014 would have 

been $3.9 billion and the lives of thousands 

of people with diabetes would have been 

improved. 

Unfortunately, many private health 

insurance companies do not fund diabetes 

education services, and current Medicare 

funding includes diabetes education as part 

of the five annual team care arrangement 

visits, alongside podiatry, dietetics and other 

associated healthcare providers. This means 

that many Australians with diabetes either 

have to pay for sessions with a diabetes 

educator themselves or miss out entirely. Outof-pocket 

costs for people with diabetes is 

one of the main barriers to accessing diabetes 

education (Deloittes Access Economics, 

2014). 

More is needed to support all Australians 

with diabetes accessing diabetes education. 

One way to do this is through private 

health insurers funding diabetes education. 

This would be feasible given that diabetes 

education is a relatively inexpensive cost 

compared to the healthcare costs incurred 

later on from sub-optimally managed diabetes 

(Deloittes Access Economics, 2014), such as 

the management of blindness, amputation, 

kidney failure and early mortality. Some 

therapies, which have less evidence for 

effectiveness compared to diabetes education, 

are currently reimbursed by private health 

insurance companies. Effective support of 

optimal diabetes management would lead 

to significant gains in the health of many 

people, as well as reduced health costs. Of 

course, private health insurance-funded 

diabetes education will only increase access 

to those who have private health insurance. 

Many people with the poorest diabetes 

outcomes are those of low socio-economic 

status and marginalised groups who are likely 

to not have private health insurance. In this 

issue, Mark Kennedy and Trisha Dunning 

provide the evidence for structured education 

and helpful guidance to encourage uptake 

(page 10). They highlight the importance of 

diabetes education in supporting people with 

diabetes to achieve optimal management of 

their diabetes while also highlighting the 

Rajna Ogrin 

Editor of Diabetes & Primary Care 

Australia, and Senior Research 

Fellow, RDNS Institute, St Kilda, 

Vic. 


Editorial 

“Many people 

with the poorest 

diabetes outcomes 

are those of low 

socio-economic status 

and marginalised 

groups who are likely 

to not have private 

health insurance.” 

funding constraints that limit access for some 

people. 

Also in this issue 

This issue also includes a CPD module 

on peripheral arterial disease screening. 

Read the article on page 16 and then go 

to www.pcdsa.com.au/cpd to complete the 

10-question module. After completing the 

module you will receive a certificate that 

can go towards your continued professional 

development. There is an additional article 

on page 25 on antimicrobial infection of 

foot ulcers in people with diabetes by Roy 

Rasalam, Caroline McIntosh and Aonghus 

O’Loughlin. 

Ralph Audehm and Laura Dean provide 

a practical guidance on using and initiating 

glucagon-like peptide-1 analogues in people 

with type 2 diabetes (page 35), and there is 

an interesting, practical article on the role of a 

readily available, but under-used medication, 

fenofibrate, a cholesterol-lowering drug. This 

issue’s From the Desktop is by Gary Kilov, 

who provides the practitioner, and patient, 

perspective on flash glucose monitoring on 

page 7. 

n 

Australian Institute of Health and Welfare (2012) Diabetes. 

Australian Government, Canberra, ACT. Available at: http:// 

www.aihw.gov.au/diabetes/prevalence/ (accessed 10.08.12) 

Deloittes Access Economics (2014) Benefits of Credentialled 

Diabetes Educators (CDEs) to people with diabetes in Australia. 

Australian Diabetes Educators Association, Canberra, Australia 

Ellis SE, Speroff T, Dittus RS et al (2004) Diabetes patient 

education: a meta-analysis and meta-regression. Patient Educ 

Couns 52: 97–105 

Holman RR, Paul SK, Bethel MA et al (2008) 10-Year follow-up of 

intensive glucose control in type 2 diabetes. New Engl J Med 

359: 1577–89 

IDF (2015) IDF Diabetes Atlas (7 th edition). International Diabetes 

Federation, Brussels, Belgium 

Lee CMY, Colagiuri R, Magliano DJ et al (2013) The cost of diabetes 

in adults in Australia. Diabetes Res Clin Pract 99: 385–90 

Minet L, Maller S, Vach W et al (2010) Mediating the effect of 

self-care management intervention in type 2 diabetes: A metaanalysis 

of 47 randomised controlled trials. Patient Educ Couns 

80: 24–41 

Norris SL, Engelgau MM, Narayan KMV (2001) Effectiveness of selfmanagement 

training in type 2 diabetes: a systematic review of 

randomized controlled trials. Diabetes Care 24: 561–87 

Norris SL, Lau J, Smith SJ et al (2002) Self-management education 

for adults with type 2 diabetes: a meta-analysis of the effect on 

glycemic control. Diabetes Care 25: 1159–71 

Si D, Bailie R, Wang Z, Weeramanthri T (2010) Comparison 

of diabetes management in five countries for general and 

indigenous populations: an internet-based review. BMC Health 

Services Research 10: 169 

6 Diabetes & Primary Care Australia Vol 2 No 1 2017



Patient and practitioner: 

Flash glucose monitoring 

Gary Kilov 

I 

have been caring for people with diabetes 

for about three decades, which is similar to 

the length of time that I have been living 

with type 1 diabetes. It would, therefore, come 

as no surprise that I have a vested interest in 

keeping abreast of the latest developments and 

innovations as they pertain to the management 

of diabetes – specifically, any progress that 

improves quality of life and eases the burden 

of living with diabetes. When I am fortunate 

enough to be offered the opportunity to try 

out some of the more innovative new products, 

I jump at the opportunity, and such was the 

case with the FreeStyle Libre Flash Glucose 

Monitoring System (Abbott Diabetes Care, 

Alameda, California, USA). 

Among the most significant advances in 

diabetes management in recent decades has 

been the progress in glucose sensing. For over 

2000 years, urine tasters were trained to detect 

glycosuria (Kirchoff et al, 2008); that is, until the 

the first half of the 20 th century, when chemical 

reagents took the place of taste buds to detect 

glucose in urine. Since then, the pace of change 

has been rapid, progressing from testing urine 

with tablets or strips to measuring glucose in 

blood. Regular, frequent blood glucose level 

(BGL) testing is essential for patients on multiple 

doses of insulin to guide dosing and optimise 

glycaemic management whilst mitigating 

hypoglycaemia. Until recently, the gold standard 

for BGL sensing for most of our patients has 

been self-blood glucose monitoring using fingerprick 

testing. Despite significant improvements 

in this technology, several limitations remain. 

Finger-prick testing is inconvenient, painful and 

gives only a momentary snapshot in time, falling 

short of providing a comprehensive profile of 

dynamically changing BGLs. Ideally, continuous 

monitoring of BGLs should be more widely 

available for people with diabetes as emerging 

data supports its effectiveness in maintaining 

glycaemic control, and international professional 

organisations endorse it as the gold standard for 

those with type 1 diabetes (Endocrine Society, 

2016). 

Since the turn of this century, access to 

continuous glucose monitoring (CGM) has been 

steadily increasing but significant limitations and 

barriers remain. It is more costly than traditional 

blood glucose monitoring and is, therefore, 

limited to a small cohort of patients, usually 

those with type 1 diabetes using insulin pumps 

and to whom the cost has not been a barrier. 

Over time, the affordability of CGM devices 

has improved and the entry of new players into 

the space has resulted in gradual, but steadily 

increasing access. 

However, it is only with the release 

of the FreeStyle Libre that we have seen a 

democratisation of this space with the device 

promoted to healthcare providers, but firmly 

marketed directly to consumers who have driven 

the demand. As clichéd as this may sound, this 

has been a game changer. The FreeStyle Libre 

provides greater accessibility for consumers and, 

not surprisingly, has proven very popular. The 

system has been available in the UK and Europe 

for almost 3 years, while in Australia it has been 

available for several months. By all accounts so 

far, it has proven to be just as popular here as in 

the northern hemisphere. 

So what does it do? The FreeStyle Libre offers 

flash glucose sensing. What this entails is the 

application of a sensor (which lasts for 2 weeks 

before requiring a replacement) to the upper arm 

Citation: Kilov G (2017) Patient 

and practitioner: Flash glucose 

monitoring. Diabetes & Primary Care 

Australia 2: 7–9 

About this series 

The aim of the “From the desktop” 

series is to provide practical 

expert opinion and comment 

from the clinic. In this issue, Gary 

Kilov gives a first-hand patient and 

practitioner perspective on using 

flash glucose monitoring. 

Author 

Gary Kilov is Associate Editor of 

Diabetes & Primary Care Australia, 

and Director at Seaport Diabetes, 

Launceston Area, Tas, and Senior 

Lecturer at University of Tasmania, 

Launceston, Tas. 



“On the infrequent 

occasion that I have to 

do a finger-prick test, 

it reminds me how 

much I don’t miss it.” 

Figure 1. The FreeStyle Libre Flash Glucose Monitoring System (Abbott, Diabetes Care, Alameda, California, USA), 

and the sensor and reader in use. 

and a reader that, when waved over the sensor, 

connects wirelessly and downloads and displays 

the BGL readings. As long as the reader is waved 

over the sensor at least once every 8 hours, up to 

8 hours of stored information will be transferred 

to the reader and will be instantly displayed. 

This includes the current BGL and a graph of 

the day’s glucose readings, as well as a display 

of trend arrows indicating whether the BGL 

is rising or falling. The angle of the depicted 

arrows indicates whether the BGL is trending 

higher or lower, rapidly or gradually, or is in 

fact steady. 

Whilst this information is available with 

CGM, flash glucose monitoring is different in 

that no calibration is required using finger-prick 

testing. This feature is particularly attractive to 

me, and dare I say, to all my patients using this 

device. On the infrequent occasion that I have 

to do a finger-prick test, it reminds me how 

much I don’t miss it. There are times when it 

is wise to confirm BGL reading with a fingerprick 

test and this is detailed in the product 

information and borne out by real-world 

experience. When BGLs are trending rapidly, 

the lag in interstitial fluid glucose means that 

the accuracy of the result is compromised. 

This has been particularly important when my 

BGLs are trending down. I am also prompted 

occasionally to do a finger-prick test when I 

am experiencing symptoms that are discordant 

with the readings, irrespective of what the 

BGL readings or trend arrows might indicate. 

So, in general, how accurate do I find the 

FreeStyle Libre? I can say that, by and large, I 

have discontinued finger-prick testing and use 

it only occasionally as detailed above, as flash 

monitoring has proven to be very reliable. 

Another attraction of this system for me 

has been the deeper understanding that I have 

gained. The FreeStyle Libre has afforded me 

a greater degree of finesse in managing my 

diabetes. Whilst this may be a honeymoon 

phase with my new-found love, the Libre, my 

HbA 1c 

has dropped by 0.5% (5.5 mmol/mol), 

from already low levels, without an increase 

in hypoglycaemia. I’ve also developed some 

insights into what happens to my BGLs in 

certain situations that would have previously 

been difficult to discern. A case in point is 

real-time BGL monitoring during exercise. This 

has allowed me to manage my glycaemia more 

confidently by understanding my blood glucose 

patterns in response to certain stimuli and, 

therefore, anticipate my BGL trajectory and the 

appropriate proactive interventions to take. For 

example, as readers would know, BGLs tend to 

rise with exercise followed by the potential risk 

for delayed hypoglycaemia, as muscles replenish 

their spent stores of glycogen, and increased postexercise 

insulin sensitivity. What I discovered 

by careful experimentation was that by giving 

myself just one unit of rapid-acting insulin 

15 minutes before I exercise (something I would 

never have been comfortable doing prior to 

having the FreeStyle Libre) I have been able to 

mitigate the exercise-induced hyperglycaemia. 

By simply removing that one unit from the next 



dose, I have also been able to reduce the rate of 

post-exercise hypoglycaemia. 

And what of patient experience? For users 

of flash monitoring, this has generally been 

very positive. Sensor failure or a sensor failing 

to adhere occurred rarely in the early days. 

This has been easily corrected by improving 

the application technique of the sensor, and 

there have been no subsequent sensor failures 

or loss of sensors reported. I now make a point 

of inviting patients to see me or the practice’s 

diabetes educator for the initial application of 

the sensor in a bid to obviate potential errors 

with the system. The FreeStyle Libre can also 

be a boon for “significant others” who may fear 

undetected nocturnal hypos. My wife need only 

“flash” my sensor for a quick check of my BGLs 

and decide, with confidence, whether to wake 

me to treat a hypo or allow me to slumber on. A 

win–win situation. 

However, sadly, nothing is perfect. So 

what are the downsides? Whilst the system 

is a great improvement on self-monitoring of 

BGLs, it is not without room for improvement. 

Cost remains prohibitive for some. At $100 

per fortnight on an ongoing basis, this is 

unaffordable for many. One compromise is to 

use the FreeStyle Libre much as we currently use 

CGM – using a sensor intermittently to provide 

insights and make adjustments as necessary. 

When a sensor is not in use, the reader can 

be used as a standalone BGL meter that will 

measure both BGLs and ketones using the same 

strips used in the FreeStyle Optium Neo. 

One of the great strengths of the system 

is the enormous amount of information that 

it provides. Paradoxically, for some, this is 

a disadvantage. Having lots of data at one’s 

disposal is one thing, what to do with it is 

another. It can also be quite difficult for some 

patients, particularly those who like to micromanage, 

to curtail the urge to react to every 

trend or nuanced change highlighted by the 

Libre. Additionally, there is no low glucose 

alarm on the Libre, a feature present in CGMs. 

Even though low BGLs may be recorded by the 

Libre sensor, no alerts are sounded until the 

sensor is scanned. 

What’s on the wish list for glucose monitoring? 

It has recently been announced that there will 

be CGM subsidies for children and young 

people with type 1 diabetes, and it is on my 

wish list for subsidies to be available for adults, 

as well as for flash glucose monitoring to be 

covered in addition to CGM. If CGM or flash 

glucose monitoring were more affordable, it 

would unquestionably be the system of choice 

for both individuals with type 1 diabetes and 

those with type 2 diabetes on complex insulin 

regimens. 

Overall, the FreeStyle Libre has been a boon 

for me and many other people with diabetes 

who have used flash glucose monitoring. It has 

improved our quality of life as well as improved 

our ability to manage our diabetes, and I 

am looking forward to the next innovation. 

Perhaps I could give the bionic pancreas a 

test drive…? 

n 

Declaration 

Selected healthcare professionals, especially 

endocrinologists, diabetes educators, and 

GPs specialising in diabetes management, 

were offered the opportunity to participate in 

the FreeStyle Libre Healthcare Professional 

Experience Program. A FreeStyle Libre Reader 

and two FreeStyle Libre Sensors were provided, 

free of charge to Gary Kilov, as part of the 

FreeStyle Libre HCP Experience Program. All 

subsequent sensors used by Gary Kilov have been 

purchased from the Australian Freestyle Libre 

website as per all consumers. No inducements, 

honoraria or support was provided to write 

this comment, which is an independent and 

personal reflection on the Flash Libre and its 

utility. 

Endocrine Society (2016) Experts recommend continuous 

glucose monitors for adults with type 1 diabetes. 

Endocrine Society, Washington DC, USA. Available at: 

http://bit.ly/2i4MKeT (accessed 30.11.16) 

Kirchhof M, Popat N, Malowany J (2008) A Historical Perspective 

of the Diagnosis of Diabetes. UWOMJ 70: 7–11 

“If continuous 

glucose monitoring 

or flash glucose 

monitoring were more 

affordable, it would 

unquestionably be 

the system of choice 

for both individuals 

with type 1 diabetes 

and those with type 2 

diabetes on complex 

insulin regimens.” 


Article 

Diabetes education: Essential but 

underfunded in Australia 

Citation: Kennedy M, Dunning T 

(2017) Diabetes education: Essential 

but underfunded in Australia. 

Diabetes & Primary Care Australia 

2: 10–4 

Article points 

1. More work is needed to 

support improved access for 

Australians with diabetes to 

education, and thereby achieve 

optimal glycaemic levels and 

reduce early mortality and 

complication development. 

2. Despite a multitude of new 

treatments for lowering 

cardiovascular risk factors, 

many people with diabetes 

remain far above target levels. 

3. Structured diabetes education 

has beneficial effects 

on blood glucose, lipids 

and blood pressure and 

specialist attendance rates. 

4. Structured diabetes education 

remains underfunded by 

Government and private 

health insurers, and this 

restricts access for people 

with diabetes contributing to 

sub-optimal health outcomes. 

Key words 

– Access to education 

– Diabetes educator 

– Health funding 

Authors 

Mark Kennedy is Honorary 

Clinical Associate Professor, 

Department of General Practice, 

University of Melbourne, and a 

GP, Geelong, Vic. Trisha Dunning 

is Chair in Nursing and Director 

for the Centre for Nursing and 

Allied Health Research, Deakin 

University and Barwon Health, 

Melbourne, Vic. 

Mark Kennedy, Trisha Dunning 

Many people with diabetes develop comorbidities during their lives. These include 

diabetes-related complications, such as cardiovascular disease, neuropathy and chronic 

kidney disease, and other medical problems such as arthritis, heart failure and depression. 

These complications and comorbidities can adversely affect mental health and self-care, 

and contribute to premature decline in functional status, morbidity, mortality and a 

significant reduction in quality of life. Despite better understanding of the natural history 

of diabetes and a multitude of new treatments for lowering the risk factors of the disease, 

many people with diabetes remain far above target levels. Structured diabetes education 

has beneficial effects on blood glucose, lipids and blood pressure and specialist attendance 

rates. Structured diabetes education remains underfunded by the Australian Government 

and private health insurers. Given the growing rates of diabetes and earlier diagnosis of 

the disease, without increased access to diabetes education for Australians with diabetes, 

suboptimal health outcomes will continue. Australia needs to do more to make diabetes 

education accessible to all people with type 2 diabetes. 

Diabetes mellitus is a complex, chronic 

and progressive disease affecting 

multiple body organs and systems. The 

prevalence in Australia in 2015 was estimated 

to be 6.3% of adults, representing more than 

1 million adults, with almost another 500 000 

thought to meet criteria for a diagnosis of 

diabetes but who are still undiagnosed 

(International Diabetes Federation [IDF] 

Diabetes Atlas Committee, 2015). It has also 

been estimated that the mean annual diabetesrelated 

expenditure per person with diabetes 

in Australia was more than $7600 in 2015, 

and that there were more than 6300 diabetesrelated 

deaths in Australia in the same year 

(IDF Diabetes Atlas Committee, 2015). The 

prevalence of diabetes has been rising across the 

world for many years and, in recent decades, 

there has been a fall in the average age of onset, 

so the number of cases on type 2 diabetes in 

the young has been rising (Alberti et al, 2004). 

With earlier onset type 2 diabetes, the increased 

lifetime exposure to hyperglycaemia is associated 

with a higher complication rate over time 

(Constantino et al, 2013). Many of these people 

have or will develop comorbidities during their 

lives, including diabetes-related complications 

and conditions, such as cardiovascular disease, 

neuropathy and chronic kidney disease, and 

other medical problems such as arthritis, heart 

failure and depression (Haas et al, 2013). 

These complications and comorbidities can 

adversely affect mental health and self-care, and 

contribute to premature decline in functional 

status, morbidity, mortality and significantly 

reduce quality of life (UK Prospective Diabetes 

Study Group, 1999; Skovlund and Peyrot, 

2005; Huxley et al, 2006; Seshasai et al, 2011). 

Self-care is often made more difficult by the 

emotional toll associated with the diagnosis of 

diabetes, the progressive nature of the condition 

and the emotional toll from the need for 

constant attention and care (Peyrot et al, 2009). 

In recent years, there have been significant 


Diabetes education: Essential but underfunded in Australia 

developments in the understanding and 

management of diabetes, and in the many 

ways in which complications of diabetes can 

be delayed or prevented. However, suboptimal 

management of many of the contributing 

factors to these complications, such as 

unhealthy lifestyle and elevated blood glucose, 

blood lipids and blood pressure, remains a 

significant problem for people with diabetes 

and the health care system. In all these areas, 

the most important person to address and 

optimally manage these factors is the person 

with diabetes. The person with diabetes needs 

timely and appropriate diabetes education to 

enable them to manage their diabetes. 


One of the goals of diabetes education 

is to assist people with diabetes to better 

understand their diabetes in order to enable 

them to make informed choices about selfmanagement, 

to improve their quality of 

life and to reduce the risk of complications 

(Australian Diabetes Educators Association, 

2016). This also increases the confidence of 

people with diabetes to manage their condition 

and assists them to undertake the practical 

aspects of monitoring and managing therapy 


2016). Diabetes education also helps people 

with diabetes and their families to deal with 

the daily physical and emotional demands 

of the condition in the context of their 

social, cultural and economic circumstances 


2016). 

Optimal diabetes management involves 

co-ordinated multidisciplinary care in the 

hospital setting and in the community, 

with the person with diabetes having the 

central role (Haas et al, 2013). Initial and 

ongoing education about diabetes is a critical 

process provided by all those involved in the 

multidisciplinary care of people with diabetes. 

This article focuses on the roles provided by 

diabetes educators and credentialled diabetes 

educators in Australia, and on the evidence 

supporting those roles, and highlights issues 

with access to these health professionals. 

Evidence for the importance and effectiveness 

of structured diabetes education 

There is randomised controlled trial evidence that 

structured diabetes education improves blood 

glucose levels, blood pressure, weight and lipid 

levels, as well as blood glucose self-monitoring 

(Norris et al, 2001; 2002; Ellis et al, 2004; 

Minet et al, 2010). There is also evidence that 

diabetes education can increase use of glucose, 

lipid and blood pressure-lowering medications, 

and consultation rates with optometrists or 

ophthalmologists (Murray and Shah, 2016). 

An Australian study showed that a structured 

education and treatment program can result in 

reduced mortality and reduced use of hospital 

services by people with type 2 diabetes (Lowe et 

al, 2009). 

While more recent local data is not available, 

the American Diabetes Association (ADA, 2013) 

estimated that in 2012 the average number 

of workdays lost per patient per year from 

diabetes was 1.1 days, with another 5.1 days 

characterised by reduced work performance 

and 5.8 days of reduced participation in the 

labour force. In 2002, it was estimated that 

the average income lost by patients and carers 

in Australia from type 2 diabetes was $35 per 

person per year, while income loss was higher 

when complications were present. However, the 

study population had a mean age of 65 years, 

so employment rates reflected that older age 

demographic, and the analysis did not include 

people with type 1 diabetes (Colagiuri, 2003). 

These analyses highlight the links between 

diabetes and reduced productivity, but studies 

connecting the provision of structured diabetes 

education to improvements in productivity have 

not yet been done. 

While the benefits of structured diabetes 

education are now well-established, there can be 

considerable variability in the amount and type 

of education provided. Comparison of studies 

examining effectiveness of diabetes education are 

often complicated by the variation in number 

of sessions provided, how they are delivered and 

the period of follow-up after study completion. 

Studies also vary in the methodology utilised for 

comparisons and in how rates of people dropping 

out of the study are managed. A recent meta- 

Page points 

1. One of the goals of diabetes 

education is to assist people 

with diabetes to better 

understand their diabetes in 

order to enable them to make 

informed choices about selfmanagement, 

to improve their 

quality of life and to reduce the 

risk of complications. 

2. An Australian study showed 

that a structured education and 

treatment program can result in 

reduced mortality and reduced 

use of hospital services by 

people with type 2 diabetes. 

3. While the benefits of structured 

diabetes education are now 

well-established, there is 

considerable variability in the 

amount and type of education 

provided. 



Page points 

1. A diabetes education 

assessment encompasses a 

detailed medical history, health 

beliefs and attitudes, baseline 

diabetes knowledge, cultural 

context, self-management skills, 

readiness to learn, general and 

health literacy, family and social 

support, and financial status. 

2. Effective diabetes education 

needs to be an ongoing process, 

involving ongoing support and 

reinforcement by the diabetes 

educator and other members of 

the multidisciplinary team. 

analysis showed that for every 1 hour of diabetes 

education provided, HbA 1c 

fell by an additional 

0.04% up to 28 hours of education, an amount 

that can be equal to the benefit provided by 

some glucose-lowering medications (Norris et 

al, 2002). 

Effective diabetes education requires teaching 

and assessment skills and the ability to 

personalise the information to the needs of the 

individual with diabetes (Australian Diabetes 

Educators Association, 2016). The increased 

benefits of individualised diabetes education 

are well-established and provide the basis of the 

initial assessment of a person with diabetes by a 

diabetes educator (Davis et al, 1981; Gilden et 

al, 1989; Davis et al, 1990; Glasgow et al, 1992; 

Brown, 1999). A diabetes education assessment 

encompasses a detailed medical history, 

health beliefs and attitudes, baseline diabetes 

knowledge, cultural context, self-management 

skills, readiness to learn, general and health 

literacy, family and social support, and financial 

status (Haas et al, 2013). An appropriate 

structured diabetes education program can be 

developed with and for the person with diabetes 

based on this assessment and using the various 

components of a diabetes educator’s role (See 

Table 1). 

Initial improvements in metabolic outcomes 

and other parameters after diabetes education 

often diminish over time, even after only 6 months 

(Norris et al, 2002). Effective diabetes education, 

therefore, needs to be an ongoing process 

involving ongoing support and reinforcement 

by the diabetes educator and other members 

of the multidisciplinary team. How often, 

and how intensive, the support and education 

is required will vary among individuals and 

Table 1. Core components of the diabetes educator role.* 

Role component Clinical input Competency 

Research 

Clinical practice 


• Translate research into practice and evaluate 

outcomes, and undertake audits and evaluate 

their practice. 

• Educate and support clinical staff to 

understand and use research. 

• Collaborate in or lead research. 

• Comprehensive clinical and educational 

assessment as part of the annual cycle of care. 

• Plan relevant care (personalised) and 

education with the individual with diabetes 

and often their families. 

• Deliver clinical care, such as foot care and 

wound care. 

• Provide diabetes education to individuals, 

groups and sometimes in public forums. 

• Provide diabetes education to care facility 

staff in undergraduate and postgraduate health 

professional education (e.g. nurses, allied 

health and medical students). 

• Supervise clinical placements. 

• Be able to read and analyse research reports 

and make decisions about the relevance to 

practice. 

• Understand glucose homeostasis and the 

impact of diabetes and related conditions. 

• Have an understanding of teaching and learning 

process. 

Management 

• Manage issues, such as referrals, product 

supply and clinical governance. 

• Facilitate complex communication pathways 

involving those with diabetes, their families, 

the other members of the multidisciplinary 

team, and one or more institutions involved in 

provision of care. 

• Staff management. 

• Collaborate with the interdisciplinary heath 

care team. 

• Help people with diabetes navigate transitions 

among services. 

• Have a solid understanding of good governance 

and service delivery systems. 

*The time spent in each component of the role depends on where the diabetes educator works and their position description. 



throughout their life course with diabetes. The 

effectiveness of diabetes education is enhanced 

when communication between multidisciplinary 

team members facilitates reinforcement of shared 

advice and when team members have agreed 

priorities with the people with diabetes they 

manage (Haas et al, 2013). 

Accessibility of diabetes education in Australia 

Despite the evidence supporting structured 

diabetes education, over 40% of Australians with 

diabetes do not have access to diabetes education 

programs (Deloittes Access Economics, 2014). 

Medicare funding through chronic disease 

management funding is often inadequate for the 

amount of initial and ongoing education required 

(Deloittes Access Economics, 2014), where a 

maximum of five individual sessions across all 

allied health staff per year is funded. The need for 

more education may be greater for those newly 

diagnosed or those transitioning onto injectable 

therapies and when functional status changes or 

complications develop. Many Australian private 

health insurance companies provide little or no 

coverage for diabetes education. 

Recently, the Australian Diabetes Educators 

Association commissioned Deloittes Access 

Economics to determine the cost-effectiveness 

of diabetes education in Australia. The report 

indicated that over $16 can be saved in health 

system costs for every dollar spent on diabetes 

education (Deloittes Access Economics, 

2014). The reduced spending results from a 

combination of fewer hospital admissions, 

emergency department attendances and physician 

consultations and the reduced costs from 

delayed or avoided secondary complications, 

such as retinopathy, chronic kidney disease, 

amputations, coronary heart disease and stroke. 

As the burden of diabetes on Australian 

families, our health care system and our 

economy continues to increase, providing 

adequate funding to train the additional required 

diabetes educator workforce and to ensure that 

all Australians with diabetes are able to access 

adequate structured diabetes education alongside 

their other multidisciplinary care must be a 

priority. Government and private health insurers 

must work together to address this underfunding 

of a vital component of diabetes care in this 

country. 

Conclusion 

Diabetes education is central to effective diabetes 

self-care to improve the ability of people with 

diabetes to self-manage, and has significant cost 

benefits and other benefits for the health system 

and individuals with diabetes. However the 

current funding for five allied health visits, which 

includes visits to diabetes education, is inadequate 

to meet those needs and is not consistent with 

the changes in information needs people with 

diabetes encounter over their life journey with 

diabetes. The lack of private health insurance 

funding of diabetes education contributes to the 

limited ability of people with diabetes to improve 

glycaemic self-management. More work is 

needed to support improved access of Australians 

with diabetes to diabetes education, and thereby 

achieve optimal glycaemic levels and reduce early 

mortality and complication development. n 

 

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1. Despite the evidence 

supporting structured diabetes 

education, over 40% of 

Australians with diabetes do 

not have access to diabetes 

education programs. 

2. Providing adequate funding 

to train the additional 

required diabetes educator 

workforce and to ensure that 

all Australians with diabetes 

are able to access adequate 

structured diabetes education 

must be a priority. 

3. Diabetes education is central 

to effective diabetes self-care 

in order to improve the ability 

of people with diabetes to 

self-manage, and has significant 

cost benefits and other benefits 

for the health system and 

individuals with diabetes. 



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self-care management intervention in type 2 diabetes: A metaanalysis 

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Save the date: 

The 2 nd PCDSA 

National Conference 

29 th April 2017 

Melbourne, VIC 

The 2017 PCDSA conference will be held on 29 th April 2017 in 

Melbourne, VIC. 

The conference has been specifically designed for all primary care 

clinicians working in diabetes care, with the aims of: 

l Advancing education and learning in the field of diabetes 

healthcare. 

l Promoting best practice standards and clinically effective care in 

the management of diabetes. 

l Facilitating collaboration between health professionals to improve 

the quality of diabetes primary care across Australia. 

Program 

The 2017 PCDSA National Conference program will combine cutting-edge 

scientific content with practical clinical sessions, basing the education on 

much more that just knowing the guidelines. The distinguished panel of 

speakers will share their specialised experience in an environment conducive 

to optimal learning. Ample question time and the opportunity for audience 

participation will feature on the agenda. 

Steering committee 

• Clinical A/Prof Ralph Audehm 

• Dr Nicholas Forgione 

• Clinical A/Prof Mark Kennedy 

• Dr Gary Kilov 

• Dr Jo-Anne Manski-Nankervis 

• Dr Rajna Ogrin 

• Dr Suzane Ryan

CPD module 

Clinical vascular screening of the foot: 

For life and limb 

Sylvia McAra, Robert Trevethan, Lexin Wang, Paul Tinley 

Citation: McAra S, Trevethan R, 

Wang L, Tinley P (2017) Clinical 

vascular screening of the foot: 

For life and limb. Diabetes & 

Primary Care Australia 2: 16–24 


1. This article presents evidence 

to inform clinical pedal vascular 

assessment with an update 

of concepts and practices. 

2. Peripheral arterial disease 

(PAD) is prevalent but 

underrecognised due to 

difficulties with effective 

clinical screening, particularly 

in at-risk groups. 

3. Enhanced awareness of PAD 

and the implementation 

of the most sensitive 

tests address barriers to 

clinical PAD screening. 

4. Peripheral vascular status 

is important as a marker 

of cardiovascular risk and 

predictor of mortality. 

5. Opportunities for preventing 

cardiovascular mortality 

exist by identifying 

asymptomatic PAD. 

Key words 

– Ankle and toe pressures 

– Cardiovascular risk 

– Doppler ultrasound 

– Peripheral arterial disease 

– Vascular assessment 

Authors 

See page 23 for author details. 

Peripheral arterial disease (PAD) is asymptomatic in 50–75% of cases and tends to be 

underdiagnosed due to the inherent difficulties in screening. Accurate peripheral vascular 

testing is particularly important for those at highest risk of PAD, including older people 

and people with diabetes, renal disease or a history of smoking. Unfortunately, commonly 

used tests for PAD have limited sensitivity in these most at-risk populations. This article 

provides guidance to support early detection of PAD using evidence-based clinical tests. It 

also contains a flowchart as a clinical guide and a set of recommendations concerning the 

measurement of toe pressures. More targeted screening can reduce morbidity and mortality 

rates in people with PAD who are at high risk of cardiovascular events and who often remain 

undiagnosed. 

Peripheral arterial disease (PAD) is a 

degenerative condition involving 

changes of the arterial walls and 

endothelial responses. Large epidemiological 

studies confirm the importance of PAD as an 

indicator for generalised atherosclerosis (Caro 

et al, 2005; Diehm et al, 2009). Low peripheral 

perfusion indicates the presence of widespread 

atheromatous disease (Greenland et al, 2001). 

Distal perfusion predicts the risk of pedal 

wounds and their healing potential (Sonter et 

al, 2014), but, of greater significance, strong 

links exist between PAD and cardiovascular 

disease (CVD; Hooi et al, 2004; Caro et al, 

2005). Advanced age, male gender, diabetes, 

renal disease and smoking are also associated 

with a higher prevalence and severity of PAD 

(Caro et al, 2005). The presence of PAD carries 

the same mortality risk as a previous myocardial 

infarction or stroke (Caro et al, 2005). 

Historically, symptoms and visual signs 

have been used as indicators to generate the 

index of suspicion for further clinical testing. 

However, this approach is flawed because PAD 

is asymptomatic in 50–75% of cases (Diehm 

et al, 2009) and most visual signs of vascular 

insufficiency are low in sensitivity for PAD 

screening (McGee and Boyko, 1998; Williams 

et al, 2005). The ankle–brachial index (ABI) has 

value in screening general populations, but loses 

sensitivity in proportion to an increasing degree 

of vessel stenosis, a primary pathophysiological 

manifestation of PAD (Xu et al, 2010). Absolute 

toe pressures and toe–brachial indices (TBIs) 

are now being recommended and are attracting 

research attention as adjuncts to improve the 

quality of PAD screening. 

Why screen for PAD? 

PAD is prevalent and often invisible, and it is 

underdiagnosed and commonly undertreated 

(Lange et al, 2004) due to barriers to screening 

(Haigh et al, 2013) and difficulties of 

recognition (Hirsch et al, 2001; Menz, 2010). 

A high proportion of cases of sudden cardiac 

death (25%) have no previously identified 

symptoms or appreciable risk factors of CVD 

(Greenland et al, 2001). There is, therefore, a 

need for tests and markers to assist clinicians in 

identifying people at risk (Aboyans and Criqui, 


Clinical vascular screening of the foot 

2006; Aboyans et al, 2008; World Health 

Organization, 2013; Brownrigg et al, 2016), 

particularly when risks can be modified with 

interventions (Hinchcliffe et al, 2015). 

Prevalence, identification and 

classification of PAD 

Estimates of the prevalence of PAD vary 

widely from 4–57%, depending on how the 

disease is identified and on age and risk factor 

distributions in specific populations (Caro et 

al, 2005). In a summary statement about 

prevalence, Høyer et al (2013) cite evidence 

that more than 50% of people with PAD are 

asymptomatic. 

PAD is best known for ischaemic pain 

associated with intermittent claudication. 

However, in a large study, only 11% of people 

with PAD had intermittent claudication (Hirsch 

et al, 2001). The prevalence of pathology 

is similar in symptomatic and asymptomatic 

PAD (Diehm et al, 2009), but significant 

impairment of the vascular tree often exists 

before and without any symptoms or signs. 

Previously, the severity of PAD has been 

described and stratified using the symptoms 

of claudication and rest pain, then tissue 

death, as in the Rutherford and Fontaine 

classification systems (Mills et al, 2014). Due to 

a growing appreciation of both the prevalence 

and pathological significance of asymptomatic 

PAD, new international guidelines for vascular 

surgery contain recommendations that pedal 

risk stratification be based, instead of on 

symptoms, on an algorithm including foot 

wound status, ischaemia and infection (Mills 

et al, 2014). 

Standard CVD risk scores, such as the 

Framingham risk score, have low-, middleand 

high-risk stratification categories. The 

diagnostic utility of these indicators may be 

improved by adding non-invasive clinical pedal 

vascular assessment to identify asymptomatic 

PAD in the intermediate risk group (Greenland 

et al, 2001). 

Limitations in screening for PAD 

A major limitation associated with screening 

for PAD is that there is currently no agreement 

concerning the use of any single test or 

combination of tests to detect PAD in primary 

healthcare settings. People’s medical history, as 

well as their pulses, pedal Doppler waveforms, 

ABIs and TBIs, are quoted in guidelines as 

being strongly recommended, but there is little 

evidence to support their use (Hinchcliffe et 

al, 2015). Most clinical tests used for PAD 

screening have low sensitivity and therefore fail 

to identify a large proportion of people who have 

the disease (Williams et al, 2005; Brownrigg et 

al, 2016). Many people with PAD have no 

obvious visual signs, and visual signs such as 

skin colour, lack of hair growth, nail changes 

and skin atrophy are low in sensitivity for PAD 

detection (Williams et al, 2005; Menz, 2010). 

In addition to visual screening, standard clinical 

tests include assessment of pulses, impressions 

of skin temperature, capillary refilling time and 

possibly ABIs. These screening processes may 

underestimate PAD by up to 60% (Williams 

et al, 2005; Høyer et al, 2013). Pulse palpation, 

although a useful clinical skill, is not adequate 

as a primary screening tool for PAD due to its 

variable sensitivity, which declines as vascular 

disease states advance (McGee and Boyko, 

1998; Williams et al, 2005). 

The ABI has been the cornerstone of peripheral 

vascular assessment in primary care for PAD and 

associated CVD risk, and it is supported by four 

decades of evidence (Caruana et al, 2005; Rooke 

et al, 2011). However, when Australian GPs were 

surveyed for the barriers they experienced in 

performing vascular assessment, 58% indicated 

that they did not use ABIs to perform vascular 

assessments, with time constraints stated as the 

greatest barrier, followed by lack of equipment 

and skills (Haigh et al, 2013). This is despite 

Medicare rebates currently applying for both 

toe- and ankle-pressure studies (See Table 1). 

The ABI is useful for identifying CVD 

risk in the general population (Caruana et al, 

2005; Guo et al, 2008). However, its sensitivity 

is reduced in proportion to the degree of 

atherosclerosis and vascular stenosis, both of 

which are common in people of advanced age 

and those who have complications of diabetes, 

especially neuropathy (Aboyans et al, 2008; Xu 

et al, 2010; Craike et al, 2013; Formosa et al, 

Page points 

1. Estimates of the prevalence 

of peripheral arterial disease 

(PAD) vary widely from 4–57%, 

depending on how the disease 

is identified and on age and risk 

factor distributions in specific 

populations. 

2. A major limitation associated 

with screening for PAD is that 

there is currently no agreement 

concerning the use of any 

single test or combination of 

tests to detect PAD in primary 

healthcare settings. 



Table 1. Medicare fees and benefits for vascular testing (Australian Government Department of Health, 2016). 

Test 

Ankle– or toe–brachial index and arterial waveform study 

Measurement of ankle:brachial indices and arterial waveform analysis 

Measurement of posterior tibial and dorsalis pedis (or toe) and brachial arterial pressures bilaterally using Doppler or 

plethysmographic techniques, the calculation of ankle (or toe)–brachial systolic pressure indices and assessment of arterial 

waveforms for the evaluation of lower extremity arterial disease, examination, hard copy trace and report. 

Ankle– or toe–brachial index-exercise study 

Exercise study for the evaluation of lower extremity arterial disease 

Measurement of posterior tibial and dorsalis pedis (or toe) and brachial arterial pressures bilaterally using Doppler or 

plethysmographic techniques, the calculation of ankle (or toe) brachial systolic pressure indices for the evaluation of lower 

extremity arterial disease at rest and following exercise using a treadmill or bicycle ergometer or other such equipment 

where the exercise workload is quantifiably documented, examination and report. 

Item 

number 

11610 

11612 

Fees and Medicare 

benefits 

Fee: $63.75 

Benefit: 75% = $47.85 

85% = $54.20 

Fee: $112.40 

Benefit: 75% = $84.30 

85% = $95.55 

2013; Hyun et al, 2014). 

Medial arterial calcification is prevalent in 

renal disease (An et al, 2010) and in longterm 

type 1 diabetes (Ix et al, 2012). It places 

limitations on the sensitivity of vascular 

pressure measurements due to the associated 

non-compressibility of vessels. 

Sensitive clinical screening methods 

Buerger’s sign demonstrates the pathophysiology 

of endothelial-driven maximal vasodilation of 

vessels in the presence of tissue ischaemia, 

resulting in pallor on elevation from rapid and 

extensive draining, and rubor on dependency 

with gravity-assisted refill of dilated vessels 

(Figure 1). Buerger’s sign has high sensitivity, 

up to 100% in severe arterial disease (McGee 

and Boyko, 1998). It, therefore, holds an 

important place in the PAD screening armoury. 

A degree of sensitive clinical screening can 

also be achieved by assessing pedal arteries 

by means of handheld Doppler ultrasound 

a. b. 

Figure 1. Buerger’s sign: pallor in elevation (a), rubor in dependency (b). Colour change is notable within 10 seconds of position change. Buerger’s sign 

is the only visual sign that is highly sensitive for peripheral arterial disease screening. See also http://bit.ly/2gUqGzS (Kang and Chung, 2007 [accessed 

05.12.16]). 



and waveform analysis ([Figure 2] as distinct 

from laboratory Doppler ultrasound colour 

imaging). Sound and waveform analysis is a 

good indicator of pathology and has prognostic 

relevance, and it also maintains sensitivity 

in the presence of neuropathy (Williams 

et al, 2005; Alavi et al, 2015). Although 

some ambiguity is associated with biphasic 

and triphasic Doppler signals (both can be 

confounded by a variety of influences including 

flow turbulence and valvular incompetence), 

monophasic Doppler signals are highly sensitive 

indicators of significant vascular pathology. 

Doppler analysis can be performed in the same 

brief time period needed for other auscultation 

techniques. Investigations of the sensitivity 

of the ABI versus Doppler ultrasound and 

waveforms in PAD screening endorse Doppler 

and document the limitations of the reliability 

of the ABI alone (Formosa et al, 2013; Alavi 

et al, 2015). 

Additional prospects for effective screening 

are offered by TBIs. In a recent systematic 

review based on seven studies, Tehan et al 

(2016) found that the sensitivity of TBIs for 

detecting PAD ranged from 45% to 100%, 

with TBIs being most sensitive in samples 

known to be at risk of PAD and among people 

who experienced intermittent claudication. 

The small number of studies reviewed were 

of varying quality and comprised disparate 

samples, indicating the need for more extensive, 

systematic and rigorous investigation regarding 

the effectiveness of TBIs for detecting PAD. 

Nevertheless, use of the TBI in place of the 

ABI is recommended because of the TBI’s 

superior sensitivity among people who have 

known vascular disease risk – specifically 

people with diabetes and renal disease and of 

advanced age (Williams et al, 2005; Aboyans 

et al, 2008; Hyun et al, 2014). An alternative 

assessment algorithm incorporating Doppler 

ultrasound waveform analysis and TBIs for 

people with diabetes has been found to increase 

the sensitivity for PAD detection from 33% to 

50% (Craike and Chuter, 2015). 

When vascular disease is widespread and 

other comorbidities (such as cardiac output 

disorders, respiratory disease and diabetes) 

Figure 2. The presence of a monophasic signal in a pedal artery from handheld Doppler 

ultrasound is a highly sensitive indicator of peripheral arterial disease. Tibialis posterior, dorsalis 

pedis and tibialis anterior arteries are useful for auscultation and the test can be performed in 

less than a minute. 

complicate systemic pressure measurements, 

absolute toe pressures are probably more 

valuable than are indices such as ABIs and 

TBIs (Caruana et al, 2005; Potier et al, 2011; 

Okada et al, 2015; McAra and Trevethan, 

2016). 

The use of X-ray should be considered as a 

novel and important part of PAD screening 

because both toe and ankle vessels may 

become calcified, and, as a result, pressure 

measurement can be spuriously inflated due to 

vessel non-compressibility. By identifying the 

presence of calcification, X-rays provide a more 

informed context within which to interpret 

toe and ankle pressures. In a study of people 

with type 1 diabetes, the incidence of medial 

arterial calcification was 57% on plain X-ray, 

but only 8% of these people had ABIs >1.30 (Ix 

et al, 2012), demonstrating not only the value 

of X-ray, but also, as the researchers concluded, 

that the ABI should not to be relied on for 

identifying PAD due to its underdiagnosis of 

the disease. 

More research is needed about the prevalence 

of toe calcification to sharpen understanding of 

the utility of toe pressures in groups at highest 

risk of PAD. However, it is already known that 



toes are affected by calcification later than are 

ankles and only in cases of the most severe and 

long-standing disease. 

There is consensus that larger-scale studies are 

needed to consolidate normal and pathological 

TBI ranges and recommendations for TBI and 

toe pressure test procedures (Høyer et al, 2013; 

Sonter et al, 2014; McAra and Trevethan, 2016; 

Tehan et al, 2016). However, there is evidence 

that the most sensitive screening procedures 

parallel the most accurate prognostic indicators. 

Toe pressures and TBIs have been linked to 

amputation prognosis by a systematic review 

of the literature, which indicated that there is a 

3.25 times greater risk of non-healing when toe 

pressures are 10 mmHg 

Abnormal result 

Repeat measurement + 

medical referral + 

reassessments including 

X-ray and vascular 

imaging 

Borderline result 

Repeat measurements + 

document + 

routine reassessments 

Normal result 

Routine reassessment: 

Annual vascular review 

if over 65 or over 50 

with other risk factors 

Figure 3. Pedal vascular assessment guide. ABI=ankle–brachial index; PAD=Peripheral arterial disease; 

TBI=toe–brachial index. 



Measurement of vascular pressures 

Brachial pressures: Why check for inter-arm 

differences? 

Brachial blood pressures should ideally be 

taken in both arms, particularly in people at 

risk of PAD, as inter-arm differences in brachial 

blood pressure can predict mortality. In a 

recent meta-analysis (Clark et al, 2012), interarm 

differences >10 mmHg were shown to be a 

marker of cardiovascular mortality. Beyond an 

initial 10 mmHg inter-arm difference, every 

additional 1 mmHg difference accounted for 

a 5% greater hazard ratio when the CVD risk 

score was >20%. Obtaining brachial blood 

pressures provides an opportunity for health 

professionals involved in vascular screening 

to identify and assess people for appropriate 

medical management, including investigation 

and targeting of CVD risk factors. 

Lower limb pressure measurement 

considerations 

Lower limb vascular pressure measurements are 

known to be variable and subject to influence 

by numerous factors, including ambient and 

skin temperatures, length of any rest period 

before measurement, respiratory and cardiac 

outputs, the comfort of the person being 

tested, medications and cuff sizes (Påhlsson 

et al, 2004; Welch Allyn Inc, 2010; Sadler 

et al, 2014; Sonter et al, 2014; McAra and 

Trevethan, 2016). Some recommendations 

regarding measurement of blood pressure in 

toes are summarised in Box 1. 

One of the most important test conditions, 

and most pertinent to lower limb testing, 

is the relative position of the test segment. 

Lying with heart and foot at the same level 

is the ideal measurement position (Figure 4). 

Any elevation of the limb relative to the heart 

markedly decreases pressures (Welch Allyn 

Inc, 2010) and the reduction is in proportion 

to vascular impairment (Wiger and Styf, 

1998). This physiological principle, which is 

magnified in PAD and evident in Buerger’s 

sign, has an immediate influence on pressure 

“Lower limb vascular 

pressure measurements 

are known to be 

variable and subject 

to influence by 

numerous factors.” 

Box 1. Recommendations for toe pressure measurement. 

l Assess toe pressures in an ambient temperature between 21 and 24°C (Bonham, 2011). 

l Be aware that elevated blood pressure readings are likely if people being tested have a full bladder or have eaten, consumed 

caffeinated or alcoholic beverages, smoked, or engaged in vigorous physical activity within an hour of testing (Pickering et al, 

2005). 

l Place the person in a supine position with the heart, arms and feet at the same level (Bonham, 2011). Consider elevating the head 

only with one or two pillows for comfort. If taking a brachial pressure, place the arm on a pillow to bring it up to the same level as 

the heart (Pickering et al, 2005). 

l Provide an initial 10 minutes’ rest period of sitting or lying (Sadler et al, 2014), preferably lying. 

l Ensure skin temperature is at least 19°C (Cloete et al, 2009). Use some form of warming if necessary. 

l Avoid perturbations such as the subject’s talking, moving, coughing or sneezing (McAra and Trevethan, 2016). 

l Use photoplethysmography (PPG) as the sensing method, preferably using an automated device (Pérez Martin et al, 2010). 

l Use an occlusion cuff of 2.5 cm if possible; if smaller cuffs are used, allow for the possibility of inflated readings (Påhlsson et al, 

2004). 

l If measuring toe–brachial indices (TBIs), for each limb, take two readings of brachial systolic pressures and toe systolic pressures 

and, for each limb, average the readings if they are similar to each other. However, if they differ noticeably, take three or 

more readings and make a judicious decision about which ones should be averaged. Obtain brachial and pedal readings as 

simultaneously as possible (McAra and Trevethan, 2016). 

l Raise a high index of suspicion of peripheral arterial disease with a TBI reading of


a. b. 

Figure 4. Positioning for vascular pressure measurement requires the heart and the sites to be measured on the same horizontal plane. Flat lying is ideal (a). 

Note the pillows for the head and the brachium (Pickering et al, 2005). The angled chair allows for correct alignment when flat lying is not practical due to 

the person’s conditions (b). 

“Attention to test 

conditions and 

awareness of 

pathophysiology 

associated with 

peripheral arterial 

disease can lead 

to more effective 

screening.” 

readings as formalised with the pole test 

(Menz, 2010). As well as segment positioning 

being an important principle affecting accurate 

measurement, it extends to management: 

positioning of the foot in relative dependency 

may boost supply and thereby assist in arterial 

wound healing and the relief of rest pain. 

The issue of cuff size for toe pressures is 

important and has been underappreciated in 

the literature to date. Smaller cuff sizes have 

been demonstrated to produce higher blood 

pressure values (Påhlsson et al, 2004), and 

this can present problems, particularly as 

automated twin-cuff devices frequently require 

the use of a smaller occlusion cuff to fit the 

toe (McAra and Trevethan, 2016). As a result 

of commonly found fluctuations in vascular 

pressures, particularly brachial pressures in 

diabetes, repeat and serial testing of pedal 

pressures and indices is recommended (Sonter 

et al, 2014; McAra and Trevethan 2016). 

Conclusions 

l Effective PAD identification in primary 

clinical contact settings can improve 

disease identification and monitoring, and, 

importantly, CVD-risk modification. 

l Reliance on tests with low sensitivity has 

pervaded understanding and practice in the 

identification of PAD. This has contributed 

to a substantial proportion of missed 

diagnoses. 

l The ABI has fulfilled a valuable role in 

screening for PAD and CVD in the general 

population. However, ABI sensitivity 

declines substantially in populations at the 

highest risk of PAD and CVD when vessel 

stenosis becomes prevalent. 

l The most sensitive clinical options for 

PAD screening in at-risk populations 

are Buerger’s sign, Doppler ultrasound 

waveforms and, more recently, toe 

pressures (including TBIs). X-rays can 

assist in identifying vessel calcification, 

thus providing important information for 

interpreting vascular pressure values. 

l Time saved by avoiding less sensitive clinical 

assessments could be used to conduct more 

sensitive screening procedures. 

l Attention to test conditions and awareness 

of pathophysiology associated with PAD can 

lead to more effective screening. n 

Competing interests 

No competing interests to declare. 

Acknowledgements 

Richard Barkas, Martin Forbes, Rajna Ogrin, Barry 

Pitman and Caroline Robinson provided helpful 

suggestions, comments and advice concerning 

earlier drafts of this manuscript. 



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Authors 

Sylvia McAra, Adjunct Lecturer, 

Podiatry, School of Community 

Health, Charles Sturt University, 

Thurgoona, NSW; Robert 

Trevethan, Independent academic 

researcher and author, Albury, 

NSW; Lexin Wang, Professor of 

Clincial Pharmacology, School 

of Biomedical Sciences, Charles 

Sturt University, Wagga Wagga, 

NSW; Paul Tinley Associate 

Professor, Course Coordinator, 

Podiatry, School of Community 

Health, Charles Sturt University, 

Thurgoona, NSW. 



Online CPD activity 

Visit www.pcdsa.com.au/cpd to record your answers and gain a certificate of participation 

Participants should read the preceding article before answering the multiple choice questions below. There is ONE correct answer to each question. 

After submitting your answers online, you will be immediately notified of your score. A pass mark of 70% is required to obtain a certificate of 

successful participation; however, it is possible to take the test a maximum of three times. A short explanation of the correct answer is provided. 

Before accessing your certificate, you will be given the opportunity to evaluate the activity and reflect on the module, stating how you will use what 

you have learnt in practice. The CPD centre keeps a record of your CPD activities and provides the option to add items to an action plan, which will 

help you to collate evidence for your annual appraisal. 

1. In what percentage of sudden cardiac 

deaths are there no previously determined 

cardiovascular risk factors? Select ONE 

option only. 

A. 1% 

B. 10% 

C. 25% 

D. 50% 

2. The risk of mortality with peripheral 

arterial disease (PAD) is similar to the risk 

of mortality in which of the following 

groups of people? Select ONE option only. 

A. People who smoke cigarettes 

B. People who have diabetes 

C. People with a history of a previous 

cardiovascular or cerebrovascular event 

D. People with renal disease 

3. According to Caro et al (2005), what is 

the estimated range of prevalence of PAD? 

Select ONE option only. 

5. Of the visual signs of PAD, which of the 

following has the highest sensitivity? 

Select ONE option only. 

A. Colour 

B. Pallor 

C. Skin atrophy 

D. Buerger’s sign 

6. The ankle–brachial index (ABI) is useful 

for identifying cardiovascular disease risk 

in the general population; however, it has 

reduced sensitivity in proportion to the 

degree of vascular stenosis present in an 

individual. Which of the following factors 

reduces the sensitivity of the ABI for PAD 

screening? Select ONE option only. 

A. Diabetes 

B. Neuropathy 

C. Renal disease 

D. Advanced age 

E. All of the above 

8. In a recent meta-analysis of inter-arm 

differences in brachial systolic blood 

pressures (Clarke et al, 2012), what was 

the threshold shown to be a marker of 

cardiovascular mortality in the presence 

of a CVD risk score of >20%? Select ONE 

option only. 

A. A 45 mmHg difference 

B. A 25 mmHg difference 

C. A 10 mmHg difference 

D. A 5 mmHg difference 

9. Using a handheld Doppler ultrasound, the 

result of a monophasic signal (sound or 

waveform) is indicative of the following 

diagnosis? Select ONE option only. 

A. A normal result 

B. PAD is highly likely 

C. An ambiguous outcome with regard 

to PAD 

D. PAD is very unlikely 

A.

Article 

Antimicrobial management of 

diabetic foot infection 

Roy Rasalam, Caroline McIntosh, Aonghus O’Loughlin 

Diabetic foot infections (DFIs) are a frequent and costly complication associated 

with diabetes mellitus. Osteomyelitis is present in 44–68% of patients admitted to 

hospital and DFIs account for 60% of lower extremity amputations in developed 

countries. Diagnosis of DFIs should be based upon the presence of local and 

systemic signs and symptoms, and the management and outcomes of DFIs are 

superior through the involvement of a multidisciplinary team. This article presents 

an overview of the current evidence for diagnosis and management of DFIs in 

practice. 

The prevalence of diabetes mellitus has 

increased dramatically in recent decades, 

as have the complications associated 

with the condition (Lipsky et al, 2016). It 

is estimated there are currently 415 million, 

or one in 11, people with diabetes globally 

(International Diabetes Federation, 2015). 

Chronic hyperglycaemia associated with diabetes 

mellitus is known to have a detrimental effect on 

human immune function; specifically, cellular 

immunity and polymorphonuclear leukocytes 

are affected, and phagocytosis is impaired (Akkus 

et al, 2016). Thus, people with diabetes are at 

increased risk of diabetic foot infections (DFIs). 

According to Peters (2016), the incidence of foot 

infections in people with diabetes ranges from an 

overall lifetime risk of 4% to a yearly risk of 7%. 

Additionally, approximately 60% of diabetic 

foot ulcers (DFUs) are infected on presentation 

(Markakis et al, 2016). DFIs usually occur when 

pathogens enter the foot through a break in 

the skin’s integrity, such as a neuropathic or 

neuroischaemic foot ulceration (Peters, 2016). 

DFIs are associated with significant morbidity 

and mortality, as infection can spread rapidly in 

the diabetic foot. If infection spreads to deeper 

structures, including the underlying bone, diabetic 

foot osteomyelitis (DFO) develops. DFIs are 

the most frequent diabetes-related complication 

requiring hospitalisation, and DFO is present in 

44–68% of cases admitted to hospital (Lipsky 

et al, 2016; Peters, 2016). If not managed 

appropriately, DFI can trigger a cascade that 

results in lower extremity amputation, especially in 

people with peripheral arterial disease (Markakis 

et al, 2016). DFIs account for 60% of lower 

extremity amputations in developed countries 

(Peters, 2016). Prompt identification, rapid 

diagnosis, timely referral for specialist review 

and appropriate management strategies are all 

vital steps in the quest to minimise the adverse 

outcomes associated with DFIs. 

Establishing the diagnosis 

Peters (2016) stresses the importance of an 

initial diagnosis of DFI based on clinical signs 

and symptoms, as the reliance on bloods, 

microbiological and radiological studies could 

lead to a delay in diagnosis. However, he also 

acknowledges the challenges faced by clinicians 

when using clinical judgement. It is possible 

that the signs and symptoms of infection are less 

prevalent in people with diabetes. This may be 

due to the presence of foot ischaemia, neuropathy 

and immunopathy, which could, theoretically, 

reduce the inflammatory response and mask the 

classic signs of infection (Peters, 2016). Though as 

Peters (2016) highlights, this theory is not proven. 

Citation: Rasalam R, McIntosh C, 

O’Loughlin A (2017) Antimicrobial 

management of diabetic foot 

infection. Diabetes & Primary 

Care Australia 2: 25–9 


1. Diabetic foot infections 

(DFIs) are the most frequent 

diabetes-related complications 

requiring hospitalisation. 

2. Approximately 60% of 

diabetic foot ulcers are 

infected on presentation. 

3. Osteomyelitis is present in 

44–68% of patients admitted 

into hospital with DFIs. 

4. DFIs account for 60% of 

lower extremity amputations 

in developed countries. 

5. Diagnosis of DFIs should be 

based upon the presence 

of local and systemic 

signs and symptoms. 

6. The management and 

outcome for a DFI is superior 

if there is the involvement of 

a multidisciplinary team. 

Key words 

– Antimicrobials 

– Diabetic foot infections 

– Diagnosis 

– Management 

Authors 

Roy Rasalam is Head of Clinical 

Skills & Medical Director, 

College of Medicine, James 

Cook University, Townsville 

City, Qld, Australia; Caroline 

McIntosh is Professor of Podiatric 

Medicine, Discipline of Podiatric 

Medicine, National University 

of Ireland Galway, Galway, 

Ireland; Aonghus O’Loughlin is 

Consultant Physician, Diabetes 

Day Centre, Galway University 

Hospital, Galway, Ireland. 


Antimicrobial management of diabetic foot infection 

Table 1. Infectious Diseases Society of America (IDSA) and International 

Working Group on the Diabetic Foot classification of diabetic foot infection 

(adapted from Lipsky et al, 2012). 

Clinical manifestation 

of infection 

No symptoms or signs of 

infection 

Infection present (defined 

by the presence of two or 

more signs/symptoms): 

l Local swelling or 

induration 

l Erythema 

l Local tenderness or pain 

l Local warmth 

l Purulent discharge 

IDSA infection severity 

Not infected 

Mild 

Local infection involving only the skin and subcutaneous tissues. 

Moderate 

Local infection with erythema >2 cm or involving structures deeper 

than skin and subcutaneous tissues (e.g. abscess, osteomyelitis, septic 

arthritis, fasciitis), AND no systemic inflammatory response signs (as 

described below). 

Severe 

Local infection (as described above) with the signs of SIRS, as 

manifested by ≥2 of the following: 

l Temperature >38 o C or 90 bpm 

SIRS=Systemic inflammatory response syndrome. 

l Respiratory rate >20 breaths/min or PaCO 2 

12 000 or


Table 2. Suggested route, setting and duration of antibiotic therapy by severity of extent of infection (adapted from Lipsky et al, 

2016). 

Severity or extent of infection Route of administration Setting Duration of therapy 

Soft-tissue only 

Mild Topical or oral Outpatient 

1–2 weeks (may extend up to 4 weeks 

if slow to resolve) 

Moderate Oral (or initial parenteral) Outpatient/inpatient 1–3 weeks 

Severe 

Initial parenteral, switch to oral 

when possible 

Inpatient, then outpatient 

2–4 weeks 

Bone or joint 

No residual infected tissue (e.g. postamputation) 

Parenteral or oral 

Oral or initial parenteral administration 

depending on the clinical situation 

2–5 days 

Residual infected soft tissue but not bone Parenteral or oral Oral or initial parenteral administration 


1–3 weeks 

Residual infected (but viable) bone 

Initial parenteral, then consider oral 

switch 



4–6 weeks 

No surgery, or residual dead bone 

postoperatively 

Initial parenteral, then consider oral 

switch 



≥3 months 

2016). Furthermore, NICE (2016) recommends 

that the choice of antibiotic treatment may 

be influenced by the care setting, patient 

preferences, the clinical situation and the 

patient’s medical history. 

The IWGDF and NICE make specific 

recommendations with regards to antimicrobial 

therapy for DFIs dependent on severity (Table 2): 

l For mild infections, initially offer oral 

antibiotics with activity against Gram-positive 

organisms. 

l A 1–2-week course of antibiotic therapy is 

usually sufficient for mild infections. 

l For moderate and severe infections, administer 

antibiotics with activity against Gram-positive 

and Gram-negative organisms, including 

anaerobic bacteria. 

l For moderate infections, offer oral or initial 

parental administration depending on the 

clinical situation and choice of antibiotic. 

l For severe infections, administer parental 

therapy with a switch to oral therapy based 

on the clinical situation and response to 

treatment. 

l For DFO, offer 6 weeks of antibiotic therapy 

for patients who do not undergo surgical 

resection of the infected bone, according to 

local protocols. 

l For those who have had surgical intervention 

and all infected bone is resected, offer no more 

than 1 week of antibiotic therapy (Lipsky et al, 

2016; NICE, 2016). 

All open wounds are colonised with potential 

pathogens, but all may not be infected 

(Schaper et al, 2016). Lipsky et al (2012) do 

not recommend the prophylactic treatment of 

clinically uninfected wounds with antimicrobial 

therapy, and they advise against the selection of 

any specific type of dressing for DFIs with the 

aim of preventing an infection or improving its 

outcome. 

Outpatient or inpatient? 

Diabetic foot clinics typically operate through 

an outpatient system. The management and 

outcome for a DFI is superior if there is the 

involvement of a multidisciplinary team 

(MDT) that includes podiatrists, nurses, 

endocrinologists, infectious disease specialists 

and vascular and orthopaedic surgeons (Lipsky 

et al, 2012). In 2012, the IDSA published a 

clinical practice guideline for the diagnosis and 

treatment of DFIs (Lipsky et al, 2012) and, in 

2015, the IWGDF produced guidelines and a 

global evidence-based consensus document on 

the management of foot problems in diabetes 

(Bakker et al, 2016). Both documents provide 



Page points 

1. The considerations of distance 

of travel to outpatient clinics, 

family and caregiver support, 

adherence to antibiotic 

treatment and offloading 

regimens are important in the 

successful treatment of an 

infected diabetic foot ulcer and 

in the decision to manage an 

individual as an inpatient or 

outpatient. 

2. The optimum duration of 

antibiotic treatment is of 

significant clinical importance. 

3. Guidelines recommend a 

course of antibiotic therapy of 

1–2 weeks for most mild and 

moderate infections. 

the treating clinician with practical guidance 

on which specific patients require, and would 

benefit most from, hospitalisation. As acute 

hospitals are constantly under sustained pressure 

due to limited bed capacity, the question of 

continuing outpatient care or admission to 

hospital is of significant importance. 

The presence of a severe infection, as defined 

by IDSA criteria, requires emergency admission 

to hospital for parenteral antibiotics, assessment 

from a surgical specialist (possible need for 

surgical intervention to remove necrotic tissue, 

including infected bone, and to drain abscesses 

[Schaper et al, 2016]), and rapid access to the 

MDT. Imaging studies and diagnostic tests 

(e.g. MRI scanning) is readily accessible as 

an inpatient. Patients with moderate DFI 

with complicating features, such as severe 

peripheral arterial disease (which, if present, 

may need urgent revascularisation [Schaper et 

al, 2016]), or lack of home support or who are 

unable to comply with the required outpatient 

treatment regimen for psychological or social 

reasons should be hospitalised initially (Lipsky 

et al, 2012). Other factors that would result in 

hospitalisation include haemodynamic and 

metabolic stabilisation, the need for careful 

continuous observation, and the use of complex 

dressings. If intravenous therapy is required, 

but not available as an outpatient, or if surgical 

procedures (more than minor) are required, then 

inpatient care is optimal (Bakker et al, 2015). 

If an MDT is not available in the outpatient 

setting, people with moderate grade diabetic 

foot ulceration may benefit from an inpatient 

“short stay” of approximately 5 days to obtain 

diagnostic tests, and clinical consultations 

from the MDT. This approach addresses 

the complexities of the person with a DFI 

and allows a more complete evaluation and 

establishment of a treatment regimen. This 

clinical care pathway would allow parenteral 

antibiotics to be administered initially with 

a switch to oral agents when the patient 

is systemically well and culture results are 

available. Surgical intervention may be 

performed and glycaemic control would be 

optimised with an effective individualised 

discharge plan instituted. 

A significant factor is the social circumstances 

of a patient. The considerations of distance of 

travel to outpatient clinics, family and caregiver 

support, adherence to antibiotic treatment 

and offloading regimens are important in the 

successful treatment of an infected DFU and 

in the decision to manage an individual as an 

inpatient or outpatient. This highlights the need 

for, and the importance of, an individualised 

treatment plan. 

How long is long enough? 

The optimum duration of antibiotic treatment 

is of significant clinical importance, as 

under-treatment will lead to persistence of 

infection with inherent risk of amputation 

and systemic sepsis, while over-treatment 

may increase the risk of multi-drug-resistant 

organisms and antibiotic-associated infections 

(e.g. Clostridium difficile). The duration of 

antibiotic therapy for a DFI should be based 

on the severity of the infection, the presence or 

absence of bone infection, the likely or proven 

causative agents and the clinical response to 

therapy (Lipsky et al, 2012; Bakker et al, 2015). 

Antibiotics can usually be discontinued once the 

clinical signs and symptoms of infection have 

resolved. There is no evidence-base to support 

continuing antibiotic therapy until the wound 

is healed in order to either accelerate closure 

or prevent subsequent infection (Lipsky et al, 

2012). 

Guidelines recommend a course of antibiotic 

therapy of 1–2 weeks for most mild and 

moderate infections (Lipsky et al, 2012). 

Parenteral therapy should be administered 

initially for severe infections and some moderate 

infections, with a switch to oral therapy when 

the infection is responding (Bakker et al, 2015). 

The duration of antibiotics in moderate to severe 

diabetic foot infection is 1–4 weeks (Table 2). 

In non-healing diabetic foot ulceration 

(>4 weeks), the presence of underlying DFO 

and peripheral arterial disease should be 

assessed. If DFO is present, there are medical or 

surgical treatment approaches. Both treatment 

approaches have demonstrated efficacy in 

selected patients. Antibiotic treatment alone for 

DFO will likely succeed with smaller ulcers, 



with more extensive ulceration requiring 

surgery. Resection of infected bone will treat 

osteomyelitis but increases the risk of altered 

foot biomechanics and transfer ulceration. 

Surgical intervention should be considered in 

cases of osteomyelitis accompanied by: spreading 

soft tissue infection; destroyed soft tissue 

envelope; progressive bone destruction on X-ray; 

or bone protruding through the ulcer (Bakker 

et al, 2015). The decision to institute either a 

primary medical or surgical approach based on 

randomised clinical trial data is difficult, as the 

diagnosis of osteomyelitis in some trials was not 

based on bone culture and histology. 

The IWGDF guideline recommends 6 weeks 

of antibiotic therapy for patients who do not 

undergo resection of infected bone and no 

more than a week of antibiotic treatment if all 

infected bone is resected. Similar guidance 

is provided with the IDSA guidelines, which 

advise 4–6 weeks of antibiotics if there is 

residual infected, but viable, bone. However, 

the IDSA guidelines recommend greater than 

3 months, of antibiotic therapy if there is no 

surgery or residual dead bone postoperatively 

(Table 2 [Lipsky et al, 2012; Bakker et al, 

2015). There is variance in the recommendation 

between the two guidelines, and the decision 

to extend antibiotic treatment beyond 6 weeks 

to 3 months should be made in consultation 

with an infectious diseases or clinical 

microbiological specialist. 

The optimal treatment of DFI with DFO will 

be based on clinical severity, likely or proven 

causative agents and clinical progression. A 

consultation with an infectious diseases or 

clinical microbiological specialist and the wider 

MDT is recommended. 

Conclusion 

DFIs are a common and serious complication 

of diabetes (present in up to 60% of DFUs; 

Markakis et al, 2016). DFIs can spread rapidly 

to underlying tissues, including bone, and 

DFO is a frequent outcome. Early diagnosis 

of DFI and rapid initiation of antimicrobial 

therapy is vital to minimise the adverse patient 

outcomes associated with foot infections, such as 

amputation. The Australian guidelines, IDSA, 

IWGDF and NICE all offer clear guidance on 

appropriate antimicrobial therapy dependent on 

the severity of the infection, clinical situation 

and efficacy of the agents. 

n 

Acknowledgement 

This article has been modified from one 

previously published in The Diabetic Foot Journal 

(2016, 3: 132–7). 

Akkus G, Evran M, Gungor D et al (2016) Tinea pedis and 

onychomycosis frequency in diabetes mellitus patients and 

diabetic foot ulcers: A cross sectional-observational study. 

Pak J Med Sci 32: 891–5 

Baker IDI (2011) National Evidence-Based Guideline on 

Prevention, Identification and Management of Foot 

Complications in Diabetes (Part of the Guidelines on 

Management of Type 2 Diabetes) 2011. Australian 

Government National Health and Medical Research Council, 

Melbourne, Vic 

Bakker K, Apelqvist J, Lipsky BA et al (2016) The 2015 IWGDF 

guidance documents on prevention and management of foot 

problems in diabetes: development of an evidence-based 

global consensus. Diabetes Metab Res Rev 32(Suppl 1): 2–6 

Bravo-Molina A, Linares-Palomino JP, Lozano-Alonso S et 

al (2016) Influence of wound scores and microbiology on 

the outcome of the diabetic foot syndrome. J Diabetes 

Complications 30: 329–34 

International Diabetes Federation (2015) IDF Atlas (7 th edition). 

IDF, Brussels, Belgium 

Lipsky BA, Berendt AR, Cornia PB et al (2012) Infectious 

Diseases Society of America Clinical Practice Guideline for 

the Diagnosis and Treatment of Diabetic Foot Infections. Clin 

Infect Dis 54: 132–73 

Lipsky BA, Aragon-Sanchez J, Diggle M et al (2016) IWGDF 

guidance on the diagnosis and management of foot 

infections in persons with diabetes. Diabetes Metab Res Rev 

32(Suppl 1): 45–74 

Markakis K, Bowling FL, Boulton AJ (2016) The diabetic foot 

in 2015: an overview. Diabetes Metab Res Rev 32(Suppl 1): 

169–78 

NICE (2016) Diabetes in Adults NICE Quality Standards (QS6). 

NICE, London, UK. Available at: https://www.nice.org.uk/ 

guidance/QS6 (accessed 20.08.2016) 

Peters EJ (2016) Pitfalls in diagnosing diabetic foot infections. 

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Schaper NC, Van Netten JJ, Apelqvist J et al (2016) Prevention 

and management of foot problems in diabetes: a Summary 

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7–15 

“Early diagnosis of 

diabetic foot infections 

and rapid initiation of 

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is vital to minimise 

the adverse patient 

outcomes associated 

with foot infections, 

such as amputation.” 


Article 

What primary care clinicians should know 

about fenofibrate for people with diabetes 

Alicia J Jenkins, Andrzej S Januszewski, Emma S Scott, Anthony C Keech 

Citation: Jenkins AJ, Januszewski AS, 

Scott ES, Keech AC (2017) What 

primary care clinicians should know 

about fenofibrate for people with 

diabetes. Diabetes & Primary Care 

Australia 2: 30–4 


1. Major clinical trials have 

demonstrated protective 

effects of oral fenofibrate 

against diabetic retinopathy 

(DR), nephropathy and some 

cardiovascular events in 

people with type 2 diabetes. 

2. There are multiple mechanisms 

by which fenofibrate may 

protect against the vascular 

and neurologic complications 

of diabetes, including 

molecular and cell-signalling 

effects, modulation of lipids, 

effects on growth factors 

and anti-inflammatory and 

anti-oxidant properties. 

3. Fenofibrate has been approved 

by the Therapeutic Goods 

Administration for the 

secondary prevention of DR 

in type 2 diabetes, but does 

not have a specific PBS-listing 

for this indication. However, 

most people with type 2 

diabetes qualify under current 

lipid/cardiovascular disease 

risk criteria, exactly the same 

as they qualify for statins. 

Key words 

– Cardiovascular disease 

– Fenofibrate 

– Risk factors 

Authors 

See page 34 for details. 

It has been proven that improving modifiable vascular risk factors of diabetes has a positive 

effect on clinical outcomes. Statins are commonly prescribed for people with type 1 and 

type 2 diabetes, and their use achieves similar LDL-cholesterol lowering and cardiovascular 

benefit as people without diabetes. The oral drug fenofibrate is less commonly used 

than statins, yet has been shown to have major protective effects for people with type 2 

diabetes, in particular for microvascular complications. In this article, the authors briefly 

review fenofibrate, its mechanisms of action, proven clinical benefits in type 2 diabetes and 

practical aspects of its prescription. 

Diabetes mellitus affects approximately 

8% of Australians and is associated with 

high rates of vascular complications, 

including diabetic retinopathy (DR), 

nephropathy, neuropathy and cardiovascular 

disease (CVD), which are associated with high 

personal burden and healthcare costs. Major 

risk factors for diabetic complications include 

long diabetes duration, poor glycaemic control, 

hypertension, smoking, renal dysfunction, 

dyslipidaemia and adiposity (Pedersen and 

Gaede, 2003; Jenkins et al, 2004). There are 

proven therapies relating to modifiable risk 

factors that improve diabetes outcomes, though 

unfortunately many individuals do not meet all 

recommended treatment targets. Lipid drugs, 

in particular “statins”, are commonly prescribed 

for people with type 1 and type 2 diabetes, and 

they gain similar LDL-cholesterol (LDL-C) 

lowering and CVD benefit as people without 

diabetes (Cholesterol Treatment Trialists’ 

[CTT] Collaborators, 2008). The triglyceride 

(TG)-lowering/HDL-C-elevating oral drug 

fenofibrate is less commonly used than statins, 

yet has been shown to have major protective 

effects for people with type 2 diabetes, in 

particular for microvascular complications. In 

this article, we briefly review fenofibrate, its 

mechanisms of action, proven clinical benefits 

in type 2 diabetes and practical aspects of its 

prescription. 

Fenofibrate 

Pharmacokinetics 

Fenofibrate, a peroxisome proliferator-activated 

receptor alpha (PPAR-alpha) agonist, is a oncedaily 

oral medication, which predominantly 

lowers TG and small dense LDL-C and 

increases HDL-C and apolipoprotein A1 levels, 

thus reversing a common (adverse) lipid profile 

in people with type 2 diabetes. The active 

form of fenofibrate is fenofibric acid, with 

activation occurring at the gut wall and by 

circulating esterases. Fenofibric acid’s half-life 

is approximately 20 hours and it is excreted 

predominantly renally, with approximately 

25% being excreted in faeces (Monthly Index 

of Medical Specialities [MIMS], 2015; Davis 

et al, 2011). Due to its predominant renal 

excretion, fenofibrate dosage is recommended 

to be reduced with significant renal impairment 

and is contraindicated if the estimated 

glomerular filtration rate (eGFR) is less than 

10 mL/min/1.73 m 2 (Australian Medicines 


What primary care clinicians should know about fenofibrate for people with diabetes 

Table 1. Recommended fenofibrate dose in 

Australia accordingly to eGFR (creatinine 

clearance; MIMS, 2015). 

eGFR (mL/min/1.73 m 2 ) 

Dose 

>60 145 mg once daily 

20–60 96 mg once daily 

10–20 48 mg once daily 


Table 2. Percentage reduction of vascular complications with fenofibrate 

relative to placebo in the FIELD and ACCORD Lipid studies. 

Outcomes FIELD ACCORD Lipid 

Primary outcomes* -11 (Keech et al, 2005) 

Secondary outcomes 

Silent myocardial infarction -16 (Burgess et al, 2010) Not available 

Death from cardiovascular 

cause † -4 (Burgess et al, 2010) 

Coronary revascularisation ‡ -21 (Keech et al, 2005) 

Stroke (fatal or non-fatal) -10 (Keech et al, 2005) 

Any amputation due to 

diabetes 

Microvascular outcomes 

-36 (Rajamani et al, 2009) Not available 

Retinopathy § -37 (Keech et al, 2007) 

Albuminuria || 

-14 (Keech et al, 2005; Davis 

et al, 2011) 

First minor (only) amputation -46 (Rajamani et al, 2009) Not available 

-8 (ACCORD Study Group, 

2010a) 


2010a) 


2010a) 

+5 (ACCORD Study Group, 

2010a) 


2010b) 


2010a) 

*FIELD: First myocardial infarction or coronary heart disease death; ACCORD Lipid: First non-fatal 

myocardial infraction or stroke or death from cardiovascular causes. 

† 

FIELD: Fatal myocardial infarction; ACCORD Lipid: Death from cardiovascular cause. 

‡ 

FIELD: Coronary revascularisation; ACCORD Lipid: Revascularisation or hospitalisation for congestive 

heart failure (together with primary outcome). 

§ 

FIELD: All events, laser treatment; ACCORD Lipid: Laser treatment and/or vitrectomy and/or 3-step 

Early Treatment Diabetic Retinopathy (ETDR) scale progression. 

|| 

FIELD: Progression (normo- to microalbuminuria or from micro- to macroalbuminuria) separately, 

FIELD study also reported a significant 18% increase in albuminuria regression (from macro- to 

microalbuminuria or from micro- to normoalbuminuria) in response to fenofibrate therapy versus 

placebo (Keech et al, 2005; Davis et al, 2011); ACCORD Lipid: microalbuminuria incidence (postrandomisation). 

 

P


with low rates (


“In two major 

randomised placebocontrolled 

trials, 

FIELD and ACCORD 

Lipid, oral fenofibrate 

has shown multiple 

protective effects in 

adults with type 2 

diabetes and to be very 

well tolerated.” 

retinopathy progression in type 2 diabetes. N Engl J Med 363: 

233–44 

Ansquer JC, Foucher C, Aubonnet P, Le Malicot K (2009) Fibrates 

and microvascular complications in diabetes–insight from the 

FIELD study. Curr Pharm Des 15: 537–52 

Australian Medicines Handbook (2015) Australian Medicines 

Handbook 2015. AMH Pty Ltd, Adelaide, SA. Available at: 

http://amhonline.amh.net.au/ (accessed 07.10.16) 

Burgess DC et al (2007) Abstract 3693: Effects of fenofibrate on 

silent myocardial infarction, hospitalization for acute coronary 

syndromes and amputation in type 2 diabetes: the Fenofibrate 

Intervention and Event Lowering in Diabetes (FIELD) study. 

Circulation 116(Suppl 16): II_838 

Monthly Index of Medical Specialities (2015) Fenofibrates. 

Haymarket Media Group Ltd, London, UK. Available at: 

http://www.mims.com.au (accessed 07.10.16) 

Noonan JE, Jenkins AJ, Ma JX et al (2013) An update on the 

molecular actions of fenofibrate and its clinical effects on 

diabetic retinopathy and other microvascular end points in 

patients with diabetes. Diabetes 62: 3968–75 

O’Callaghan CJ, Rong P, Goh MY (2014) National guidelines for the 

management of absolute cardiovascular disease risk. Med J Aust 

200: 454–6 

Papademetriou V, Lovato L, Doumas M et al (2015) Chronic kidney 

disease and intensive glycemic control increase cardiovascular 

risk in patients with type 2 diabetes. Kidney Int 87: 649–59 

Burgess DC, Hunt D, Li L et al (2010) Incidence and predictors of 

silent myocardial infarction in type 2 diabetes and the effect of 

fenofibrate: an analysis from the Fenofibrate Intervention and 

Event Lowering in Diabetes (FIELD) study. Eur Heart J 31: 92–9 

Pedersen O, Gaede P (2003) Intensified multifactorial intervention 

and cardiovascular outcome in type 2 diabetes: the Steno-2 

study. Metabolism 52(8 Suppl 1): 19–23 

Chen Y et al (2011) Mechanisms for the therapeutic effect of 

fenofibrate on diabetic retinopathy in type 1 diabetes models. 

Presented at: American Diabetes Association 71 st Scientific 

Sessions. San Diego, Ca, USA, June 24–28 

Rajamani K, Colman PG, Li LP et al (2009) Effect of fenofibrate 

on amputation events in people with type 2 diabetes mellitus 

(FIELD study): a prespecified analysis of a randomised 

controlled trial. Lancet 373: 1780–8 

Chen Y, Hu Y, Lin M et al (2013) Therapeutic effects of PPAR-alpha 

agonists on diabetic retinopathy in type 1 diabetes models. 

Diabetes 62: 261–72 

Rajamani K et al (2015) Abstract 18987: Fenofibrate reduces 

peripheral neuropathy in type 2 diabetes: the Fenofibrate 

Intervention and Event Lowering in Diabetes (FIELD) Study. 

Circulation 122(Suppl 21): A18987 

Cholesterol Treatment Trialists’ (CTT) Collaborators (2008) Efficacy 

of cholesterol-lowering therapy in 18,686 people with diabetes 

in 14 randomised trials of statins: a meta-analysis. Lancet 371: 

117–25 

Davis TM, Ting R, Best JD et al (2011) Effects of fenofibrate on 

renal function in patients with type 2 diabetes mellitus: the 

Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) 

Study. Diabetologia 54: 280–90 

Riddle MC (2010) Effects of intensive glucose lowering in the 

management of patients with type 2 diabetes mellitus in the 

Action to Control Cardiovascular Risk in Diabetes (ACCORD) 

trial. Circulation 122: 844–6 

Robins SJ, Collins D, Wittes JT et al (2001) Relation of gemfibrozil 

treatment and lipid levels with major coronary events: VA-HIT: a 

randomized controlled trial. JAMA 285: 1585–91 

Authors 

Professor Alicia Jenkins, 

Dr Andrzej Januszewski, Dr Emma 

Scott and Professor Anthony 

Keech are at the NHMRC Clinical 

Trials Centre, University of 

Sydney, Camperdown, NSW. 

Jenkins AJ, Rowley KG, Lyons TJ et al (2004) Lipoproteins and 

diabetic microvascular complications. Curr Pharm Des 10: 

3395–418 

Jones PH, Davidson MH (2005) Reporting rate of rhabdomyolysis 

with fenofibrate + statin versus gemfibrozil + any statin. 

Am J Cardiol 95: 120–2 

Keech A, Simes RJ, Barter P et al (2005) Effects of long-term 

fenofibrate therapy on cardiovascular events in 9795 people 

with type 2 diabetes mellitus (the FIELD study): randomised 

controlled trial. Lancet 366: 1849–61 

Keech AC, Mitchell P, Summanen PA et al (2007) Effect of 

fenofibrate on the need for laser treatment for diabetic 

retinopathy (FIELD study): a randomised controlled trial. Lancet 

370: 1687–97 

Manninen V, Tenkanen L, Koskinen P et al (1992) Joint effects of 

serum triglyceride and LDL cholesterol and HDL cholesterol 

concentrations on coronary heart disease risk in the Helsinki 

Heart Study. Implications for treatment. Circulation 85: 37–45 

Scott R, O’Brien R, Fulcher G et al (2009) Effects of fenofibrate 

treatment on cardiovascular disease risk in 9,795 individuals 

with type 2 diabetes and various components of the metabolic 

syndrome: the Fenofibrate Intervention and Event Lowering in 

Diabetes (FIELD) study. Diabetes Care 32: 493–8 

Tenenbaum A, Motro M, Fisman EZ et al (2005) Bezafibrate for the 

secondary prevention of myocardial infarction in patients with 

metabolic syndrome. Arch Intern Med 165: 1154–60 

Ting RD, Keech AC, Drury PL et al (2012) Benefits and safety of 

long-term fenofibrate therapy in people with type 2 diabetes 

and renal impairment: the FIELD Study. Diabetes Care 35: 218– 

25 

Tziomalos K, Athyros VG (2006) Fenofibrate: a novel formulation 

(Triglide) in the treatment of lipid disorders: a review. Int J 

Nanomedicine 1: 129–47 

Vasudevan AR, Jones PH (2006) Effective use of combination lipid 

therapy. Curr Atheroscler Rep 8: 76–84 


Article 

Glucagon-like peptide-1 analogues – 

a practical guide to initiation 

Ralph Audehm and Laura Dean 

Glucagon-like peptide-1 (GLP-1) analogues are one of the more recent additions to the 

type 2 diabetes armamentarium and work by mimicking the incretin system to lower 

glucose and increase insulin. The drug class also exerts associated non-glycaemic 

advantages, such as weight loss. The first GLP-1 analogue was approved for use in Australia 

in 2007 and has been subsidised by the Pharmaceutical Benefits Scheme since 2008, yet its 

use remains relatively low. This article discusses the mode of action of GLP-1 analogues, 

their use in Australia and how to use and initiate GLP-1 analogues in people with type 2 

diabetes, using case studies. 

Glucagon-like peptide-1 (GLP-1) is a 

hormone released by the gut when 

sensory receptors in the small intestine 

detect dietary glucose and other nutrients. 

GLP-1 forms part of the “incretin effect” – the 

increased secretion of insulin when the same 

amount of glucose is ingested orally compared 

to when it is administered intravenously 

(Willard and Sloop, 2012). The incretin system 

potentiates glucose-induced insulin secretion 

and may be responsible for up to 70% of postprandial 

insulin secretion (Holst et al, 2009). 

GLP-1 is also known to be involved in the 

inhibition of glucagon release (thus decreasing 

hepatic production of glucose and fasting blood 

glucose levels), delayed gastric emptying (thus 

decreasing post-prandial blood glucose levels) 

and the suppression of appetite, which, in 

theory, leads to decreased calorie intake (Gupta, 

2013). The roles of GLP-1 make it an attractive 

target for drug development, especially for 

the management of type 2 diabetes where the 

incretin effect is severely reduced or absent 

in patients (Holst et al, 2009). In addition, 

the half-life of endogenous GLP-1 is less than 

2 minutes, so creating GLP-1 analogues that 

can be active for longer is of great benefit. 

Dipeptidyl peptidase-4 (DPP-4), an 

endogenous enzyme also involved in the 

incretin system, rapidly inactivates GLP- 

1, leading to its short half-life (Willard and 

Sloop, 2012). It is now possible to artificially 

prolong the half-life of GLP-1 and its effect 

by using DPP-4 inhibitors, or “gliptins”. The 

first DPP-4 inhibitor to be approved by the US 

Food and Drug Administration was saxagliptin 

in 2006. The drug class is well tolerated by 

users, is weight neutral and has a low risk of 

hypoglycaemia unless used in combination with 

medications with a risk of hypoglycaemia, such 

as sulfonylureas (Prasad-Reddy and Isaacs, 2015). 

They are administered in tablet form and are 

available in a combined tablet with metformin. 

Studies have shown they can reduce HbA 1c 

by 

4.4–7.7 mmol/mol (0.4–0.7%; Brunton, 2014). 

Around the same time, GLP-1 analogues were 

developed to be more resistant to the actions 

of DPP-4 inhibitors and with a longer halflife 

than endogenous GLP-1. The advantages 

and disadvantages of using GLP-1 analogues 

are presented in Table 1. GLP-1 analogues 

have been shown to reduce HbA 1c 

by around 

10.9 mmol/mol (1%; Kenkre et al, 2013) and 

they can be combined with insulin as GLP-1 

analogues are weight negative and insulin is 

weight positive (Cohen et al, 2013). Devices 

that contain both basal insulin and a GLP-1 

analogue in a single injection have been 

Citation: Audehm R, Dean L (2017) 

Glucagon-like peptide-1 analogues – 

a practical guide to initiation. 

Diabetes & Primary Care Australia 

2: 35–9 


1. The incretin system is used 

to develop pharmacological 

therapies for type 2 diabetes. 

2. The incretin mimetics, 

glucagon-like peptide-1 (GLP-1) 

analogues, represent a useful 

and effective tool in the 

management of type 2 diabetes 

3. GLP-1 analogues are an under 

utilised resource in the type 2 

diabetes armamentarium. 

Key words 

– Administration 

– Glucagon-like peptide-1 

analogues 

– Glucose-lowering medication 

– Incretin system 

Authors 

Ralph Audehm, Associate 

Professor, Department of General 

Practice, University of Melbourne, 

Vic, and Director, Primary Care 

Diabetes Society of Australia; 

Laura Dean, Course Director, 

Graduate Certificate in Pharmacy 

Practice, Faculty of Pharmacy and 

Pharmaceutical Sciences, Monash 

University, Vic. 


Glucagon-like peptide-1 analogues – a practical guide to initiation 

approved in Europe and USA (insulin degludec/ 

liraglutide; Greig and Scott, 2015). 

Table 2 gives an overview of GLP-1 analogues 

that are approved by the Therapeutic Goods 

Administration (TGA) for use in Australia: 

exenatide, exenatide-modified release, liraglutide 

Table 1. Advantages and disadvantages of glucagon-like peptide-1 (GLP-1) analogues. 

Advantages 

Significant weight loss: 3–4 kg on an intention to treat analysis (Robinson et al, 

2013). 

Decreased post-prandial excursions. 

Glucose-dependent manner: GLP-1 analogues do not cause hypoglycaemia 

unless used with other medications, such as sulfonylureas or insulin. 

Liraglutide has recently been shown to reduce mortality in people with type 2 

diabetes (Marso et al, 2016). 

Disadvantages 

Gastrointestinal effects (e.g. nausea and diarrhoea): 5–10% of people will stop a 

GLP-1 analogue due to nausea (Meier, 2012). 

Pancreatitis: There was an early signal suggesting that GLP-1 analogues may 

increase the risk of pancreatitis. Follow-up studies have shown that the risk for 

pancreatitis is no greater than the background incidence of pancreatitis in people 

with type 2 diabetes (Forsmark, 2016). 

Delivery of the dose: GLP-1 analogues must be injected. 

Renal insufficiency: GLP-1 analogues should not be used if eGFR 


and lixisenatide. Lixisenatide is not currently 

being supplied in Australia. 

How to initiate GLP-1 analogues 

Exenatide 

Exenatide (Byetta ® ) is available in two dose 

forms, 5 µg and 10 µg. Patients should initiate 

with 5 µg twice daily. The dose should be 

injected within the 60 minutes before their 

breakfast and evening meal. Exenatide can 

be administered before the lunch and evening 

meal, as long as the injections are at least 

6 hours apart. The dosage can be increased 

to 10 µg twice a day after 1 month at 5 µg if 

tolerated. 

Exenatide-modified release 

Exenatide-modified release (Bydureon ® ) is a 

long-acting form of exenatide. It is available 

in a 2 mg/mL dose and it is administered 

once a week on the same day. There is no dose 

titration required and it can be given at any 

time of the day without reference to meals. 

The formulation uses microspheres to provide 

the modified-release properties, which results 

in a delayed onset of action, such that it may 

take 2 weeks for the exenatide to begin being 

released, and up to 7 weeks for complete release 

(Cai et al, 2013). To manage expectations, 

people using once-weekly exenatide should be 

made aware of this delay. 

If a patient wishes to change the day on 

which they administer the injection, they 

may do so as long as there is more than one 

clear day between the injections. Similarly 

if a patient forgets to inject the exenatidemodified 

release, they may administer it as 

soon as they remember. However, if there are 

only one or two days until the next scheduled 

dose, they should wait until the scheduled 

day to take their dose (Eli Lilly Australia Pty, 

2013). 

It is important to be aware that the 

microspheres in long-acting exenatide can lead 

to an inflammatory reaction and “nodules” 

or subcutaneous lumps developing at the 

injection site, which are usually asymptomatic 

and resolve over 4–8 weeks (DeYoung et al, 

2011). 

Liraglutide 

Liraglutide (Victoza ® ) is available is a single 

pen device containing three different dosing 

options: 0.6 mg, 1.2 mg and 1.8 mg. The 

starting dose is 0.6 mg daily, which can be 

increased to 1.2 mg after at least 1 week and, 

if tolerated, can be increased to 1.8 mg to 

achieve maximum efficacy. The dose is given 

independently of meals but should be given 

around the same time each day. 

If patients are on insulin or a sulfonylurea, it 

is useful to ask them to monitor their glucose 

levels four times per day for the first 3–4 days to 

identify any risk of hypoglycaemia. If the HbA 1c 

for a patient is


“It is beneficial to 

warn all people using 

glucagon-like peptide-1 

analogues to expect 

nausea, especially in 

the first 2–3 days after 

initiation.” 

After discussing options for treatment 

intensification, he elected to trial exenatide. 

Exenatide 5 µg was commenced twice daily and 

increased to 10 µg after a month. He tolerated 

the injection very well and found the injections 

easy to administer. Six months later, Mr GL had 

achieved a weight loss of 4 kg and his HbA 1c 

was 

40 mmol/mol (5.8%). 

Case 2 

Ms PI is a 54-year-old lady with a HbA 1c 

88 mol/mol (10.2%). Her blood pressure 

(BP) is 140/85 mmHg and she has a BMI of 

31 kg/m 2 . She has no nephropathy and her 

estimated glomerular filtration rate (eGFR) is 

>90 mL/min/1.73 m 2 . She has retinopathy and 

has had laser therapy treatment in the past. She 

is currently on a combined tablet of metformin 

and DPP-4 inhibitor (metformin 1000 g/ 

linagliptin 2.5 mg) twice daily, but she has an 

erratic lifestyle and has difficulties remembering 

her medications. After discussing her options, 

including insulin, she elected to start exenatidemodified 

release, feeling that a weekly injection 

would be easier to manage. She understood 

that she would need insulin in the future but 

the GLP-1 analogue would help reduce the 

amount of weight she would gain with insulin. 

The metformin/DPP-4 inhibitor combination 

was stopped and the exenatide-modified release 

commenced with metformin XR 1000 mg twice 

daily. The initial injection was supervised with 

the practice nurse and Ms PI felt confident with 

the injections. 

At 3 weeks, she had lost 2.5 kg and her daily 

blood glucose levels were now in the low teens. 

Ms PI has had minimal side effects as a result of 

the change in drug regimen. She was happy with 

the weight loss she has achieved and improved 

blood glucose levels and is now more engaged 

with the practice and attending appointments 

more regularly, offering the opportunity for 

ongoing treatment intensification if required. 

Case 3 

RA is a 60-year-old male. He is on insulin 

glargine 48 units per day, metformin 

2000 mg daily and gliclazide MR 120 mg daily, 

as well as anti-hypertensives and a statin. His 

HbA 1c 

is 66 mmol/mol (8.2%). He has minimal 

non-proliferative retinopathy and a marginally 

elevated albumin–creatinine ratio (7 mg/mmol). 

His BP at his most recent appointment was 

138/70 mmHg and his BMI was 35 kg/m 2 . On 

discussion with the clinician, self-blood glucose 

monitoring results showed large post-prandial 

elevations: these were highest after dinner 

(around 12–13 mmol/L) but also high at lunch. 

His fasting blood glucose measurements were 

around 7 mmol/L. Exenatide was commenced 

at 5 µg bd, prior to breakfast and dinner. 

The device and the injection technique were 

demonstrated at an appointment later in the 

day so that he could then go home and have 

his evening meal. He was told to monitor his 

blood glucose levels four times a day and to 

carry jellybeans or another quick-acting glucose 

source with him at all times. 

At review 1 week later, his fasting blood 

glucose had dropped, and during the preceding 

week, were often below 5 mmol/L but not 

below 4 mmol/L. He was comfortable with 

adminstering the injections and elected to 

reduce his gliclazide to minimise his risk of 

hypoglycaemia. Another review was organised 

for a week’s time. If exentaide 5 µg dose 

continues to be well tolerated, after 1 month, 

the exenatide dose will be increased to 10 µg bd. 

How to manage the side effects of 

GLP-1 analogues 

The most common side effects reported by 

people using GLP-1 analogues are nausea 

and vomiting (Garber, 2011). Therefore, it is 

beneficial to warn all patients to expect nausea, 

especially in the first 2–3 days. The nausea will 

usually settle, but to diminish these effects 

you may suggest that they eat smaller meals or 

snacks in the interim. Anti-emetics can be used 

in the short term to help patients overcome this 

period of nausea. Exenatide-modified release 

and liraglutide have lower rates of nausea than 

exenatide (Garber, 2011). 

Summary 

The GLP-1 analogue drug class offers a drug 

regimen for people with type 2 diabetes that 

is well tolerated by users, weight neutral and 



with a low risk of hypoglycaemia. It is straightforward 

to initiate and titrate, but it is currently 

underutilised. In 2015, there were just over 

200 000 scripts for exenatide compared to more 

than 2 million scripts for a DPP-4 inhibitor 

(The Pharmaceutical Benefits Scheme, 2015). 

GLP-1 analogues are an excellent addition to 

our armamentarium. 

n 

Declaration 

Ralph Audehm has received monies from Sanofi, 

AstraZeneca, NovoNordisk, Novartis and Lilly 

for consultancy work. 

 

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