duelling with pain - Faculty of pain medicine - Australian and New ...

2009 SPRING MEETING 

FACULTY OF PAIN MEDICINE, ANZCA 

ACUTE PAIN SPECIAL INTEREST GROUP OF ANZCA, ASA AND NZSA 

‘DUELLING 

WITH PAIN’

Major Sponsor 

Exhibitors

2009 SPRING MEETING 

FACULTY OF PAIN MEDICINE, ANZCA 

ACUTE PAIN SPECIAL INTEREST GROUP OF ANZCA, ASA AND NZSA 

‘DUELLING 

WITH PAIN’ 

Contents 

Welcome message 2 

Invited speakers 4 

Scientific program 6–8 

Abstracts 

Opioids, Pain and Addiction – Facts vs Fiction 10 

Intrathecal Analgesia – Duelling with Efficiency and Safety 12 

Non Neuronal Opioid Actions 14 

Novel Approaches to Cancer Pain 15 

Spinal Cord Magic Bullets – 

Current and Future Analgesic Developments 15 

Opioids in Dyspnoea and Sleep Apnoea 16 

Contemporary Approaches to Opioid Addiction 16 

Methadone Pharmacology 17 

Methadone Re-visited in Cancer Pain 18 

Methadone in Chronic Pain 20 

Managing Placebo and Nocebo Effects – 

Mechanisms and Implications for Clinical Practice 21 

Pain and Addiction – Treatment Strategies 22 

Predictors of Persistent Pain after Trauma 24 

Procedural Pain Analgesia 25 

Psychological Adjuncts for Pain Occurring with 

Dressing Changes in Burns Patients 26 

Australia’s Worst Bushfire Disaster: 

The Medical Response to Victoria’s Black Saturday 27 

PBLD and Topical Session outlines 28–39

Welcome 

Welcome message from the Dean 

As a Faculty, it is my pleasure to 

welcome you to the 2009 Spring 

Meeting ‘Duelling with Pain’ being 

held at the Sofitel Hotel, Melbourne. 

Acute, Chronic and Cancer Pain 

Specialists need to work closely 

together for the good of our patients 

and to promote “Pain Medicine” to 

our colleagues. 

The concept of bringing acute, chronic 

and cancer pain expertise together 

follows on from the goodwill generated 

at the 2008 Spring Meeting in Uluru. 

Dr Carolyn Arnold as Convener with 

support from Dr Jane Trinca, Chair 

of the Acute Pain SIG, and a regional 

organising committee have put together 

an innovative program over three days. 

Dr Roman D. Jovey from Canada and 

Dr Suellen Walker, currently residing in 

the UK, are our international speakers. 

There is a focus on opioid use in chronic 

pain and addiction and new knowledge 

about analgesic medications from the 

laboratory. The program is also rich with 

clinically-based topics for small-group 

discussion. 

Spring time in Melbourne is beautiful, 

so come and enjoy good medicine, 

good food and catch up with friends 

and colleagues. 

Dr Penelope Briscoe 

Dean, Faculty of Pain Medicine 

2 

2009 SPRING MEETING • FACULTY OF PAIN MEDICINE, ANZCA • ACUTE PAIN SPECIAL INTEREST GROUP OF ANZCA, ASA AND NZSA

Welcome message from the Convenors 

It is with great pleasure that the Faculty 

of Pain Medicine, in association with the 

Acute Pain Special Interest Group of ANZCA, 

ASA and NZSA welcomes you to the third 

Spring Meeting. 

The theme of the meeting is “Duelling with Pain”. 

This stimulating and practical programme is presented 

by a faculty of international and national speakers 

who will highlight the challenges we face in managing 

the spectrum of complex acute and chronic pain 

problems. In particular there will be an emphasis on the 

growing knowledge base surrounding pain medicine 

and addiction medicine. The program will encompass 

discussion about dealing with difficult patients, advances 

in management of acutely painful procedures and new 

advances in intrathecal analgesia. 

This multidisciplinary faculty will show how input from 

anaesthetists’ acute and chronic pain clinicians, nurses, 

general practitioners, psychiatrists, surgeons and 

addiction medicine specialists may lead to better patient 

outcomes. The program will challenge participants to 

expand their horizons to better manage pain in a broad 

spectrum of patients and settings. 

Melbourne is a wonderful city to visit in spring, with the 

racing carnival, wonderful theatre, restaurants, shopping 

precincts and parks. Our social programme will give you 

the chance to experience an insider’s view of Melbourne. 

Our thanks are extended to our sponsors and exhibitors 

for their generous support of the meeting. 

Dr Carolyn Arnold 

Convenor 

Dr Jane Trinca 

Co-Convener, Chair of The Acute Pain SIG 

3

International keynote speakers 

Dr Roman D. Jovey 

Dr. Jovey, a graduate of the University of Toronto, 

was a general practitioner and emergency physician 

for almost 20 years. In 1999, he closed his family 

practice to focus exclusively on outpatient chronic pain 

management and addiction medicine. Dr. Jovey has 

had a career-long interest in addiction medicine. He 

has been the Physician Director of the Credit Valley 

Hospital, Addictions and Concurrent Disorders Centre, 

in Mississauga, since 1991. 

Since 1991, Dr. Jovey has been treating patients with 

chronic non-cancer pain using pharmacotherapy - with 

a special interest in the use of long-term opioid therapy. 

He has presented workshops and seminars on this topic 

to over 9000 health care professionals in Canada 

and abroad. 

He is the Program Medical Director at CPM Centres 

for Pain Management, an outpatient chronic pain 

management company. He is the Past-President of the 

Canadian Pain Society and a medico-legal expert for 

the Canadian Medical Protective Association. 

Dr Suellen Walker 

Dr Suellen Walker is a Clinical Senior Lecturer and 

Consultant in Paediatric Anaesthesia and Pain Medicine 

at University College London Institute of Child Health 

and Great Ormond Street Hospital for Children, London. 

Her recent research has investigated longterm effects 

of pain and surgery in clinical and laboratory studies. 

She has also developed a model for investigating toxicity 

of spinally administered analgesics during postnatal 

development in collaboration with Tony Yaksh at UCSD. 

She has been a major contributor to national documents 

including “Acute Pain Management: Scientific Evidence” 

(ANZCA/ FPM) and “Good Practice in Procedural 

and Postoperative Pain” ( Association of Paediatric 

Anaesthetists of Great Britain and Ireland). 

Travel for Dr Roman D. Jovey is 

generously sponsored by Mundipharma. 

4 


Australian invited speakers 

Mr Damien Finniss 

Damien Finniss is a Clinician at the University of Sydney 

Pain Management and Research Institute at Royal North 

Shore Hospital and a Clinical Lecturer at the University 

of Sydney Faculty of Medicine. Damien is currently the 

Chairman of the International Association for the Study 

of Pain (IASP) group on Placebo and has published 

multiple papers in International Peer Reviewed Journals 

and book chapters on the topic area. 

Professor Andrew A. Somogyi 

Andrew Somogyi is Professor in Clinical and 

Experimental Pharmacology and Associate Dean 

(Research) in the Faculty of Health Sciences at the 

University of Adelaide. His major research interests 

are in the clinical pharmacology of the opioid class 

of drugs with specific reference to examining the genetic, 

biological and environmental factors that contribute 

to efficacy and toxicity in pain and addiction therapies. 

He has NHMRC project grant funding, serves 

on several journal editorial boards and has established 

a pharmacogenetics service at the Royal 

Adelaide Hospital. 

National Invited Speakers and Facilitators 

Dr Charles Brooker 

Royal North Shore Hospital, 

NSW 

Dr Robert Brzozek 

Health Services Group of 

TAC and Worksafe, VIC 

Dr Chui Chong 

Royal Perth Hospital, WA 

Professor Jon Currie 

St Vincent’s Hospital, VIC 

Dr Bronwen Evans 

Western Health Service, VIC 

Professor Julia Fleming 

Royal Brisbane Hospital, 

QLD 

Professor Colin Goodchild 

Monash University, VIC 

Dr Chris Hayes 

Hunter Integrated Pain 

Service, NSW 

Dr Malcolm Hogg 

Royal Melbourne Hospital, 

VIC 

Dr Alex Holmes 

Royal Melbourne Hospital, 

VIC 

Dr Winnie Hong 

Concord Repatriation 

General Hospital, NSW 

Assoc Professor Kate 

Jackson 

Southern Health and 


Dr Charles Kim 

St Vincent Hospital and 

Melbourne Health, VIC 

Dr Alex Konstantatos 

Alfred Hospital, VIC 

Ms Dale Long 

Peter MacCallum Cancer 

Centre, VIC 

Assoc Professor Pam 

Macintyre 

Royal Adelaide Hospital, SA 

Assoc Professor Christine 

McDonald 

Austin Health, VIC 

Dr Mike McDonough 

Western Health, VIC 

Dr John Moloney 


Dr Tobie Sacks 


Ms Cathy Senserrick 


Mr Andrew Shelton 


Dr Lisa Sherry 

Health Services Group of 

TAC and Worksafe, VIC 

Dr Odette Spruyt 

Peter MacCallum Cancer 

Center, VIC 

Dr Helen Sweeting 


Dr Joel Symons 


Dr Brett Todhunter 

Wodonga Regional Health 

Service, VIC 


Austin Health and St 

Vincent’s Hospital, VIC 

Ms Jill Woods 


Professor Barbara 

Workman 

Monash University, 

Southern Healthcare 

Network, VIC 

5

Program 

FRIDAY 16 OCTOBER 

0900–1000 REGISTRATION 

1005–1015 Opening Welcome 

Dr Penny Briscoe 

1015–1230 PLENARY LECTURES – Arthur Streeton Auditorium 

Chair: Dr Carolyn Arnold 


Opiods, Pain and Addiction – Facts vs Fiction 


Intrathecal Analgesia – Duelling with Efficiency and Safety 


Non Neuronal Opioid Actions 

1200–1230 Lunch 

1330–1500 PBLD and Topical Discussion Sessions 

PBLD 01 – Victoria Suite 1 

Facilitator – Dr Malcolm Hogg 

Implementing a Preventative Strategy in Acute Pain 

Topical Session 01 – Arthur Streeton Auditorium 

Facilitator – Dr Penny Briscoe 

Presenter – Dr Roman D. Jovey 

Office Based Pain Management – Optimising Outcome, Reducing Risk 


Facilitator – Dr Chris Hayes 

Cessation of Established Intrathecal Analgesia in Persistent Non-Cancer Pain 

Topical Session 02 – Victoria Suite 2 

Facilitator – Assoc Professor Kate Jackson 

Presenters – Ms Dale Long & Dr Brett Todhunter 

Community Management of Intrathecal Infusions for Cancer 

1500–1530 Afternoon Tea 

1530–1730 LECTURES – Arthur Streeton Auditorium 

Chair – Dr David Jones 

Dr Julia Fleming 

Novel Approaches to Cancer Pain 


Spinal Cord Magic Bullets – Current and Future Analgesic Developments 

Assoc Professor Christine McDonald 

Opioids in Dyspnoea and Sleep Apnoea 

1730–1930 Welcome Cocktail Reception 

6 


Saturday 17 October 

0830–0900 Registration 


Chair – Dr Jane Trinca 


Contemporary Approaches to Opioid Addiction 


Methadone Pharmacology 

Assoc Professor Kate Jackson 

Methadone Re-visited in Cancer Pain 


Methadone in Chronic Pain 

1100–1130 Morning Tea 



Facilitator – Dr Bronwen Evans 

Management of Ischaemic Limb Pain 

Topical Session 03 – Arthur Streeton Auditorium 

Facilitator – Assoc Professor Kate Jackson 

Presenters – Dr Chui Chong, Professor Colin Goodchild, Assoc Professor Kate Jackson, 

Dr Odette Spruyt, Ms Jill Woods 

Incident/Procedural Pain Management Without an IV 


Facilitator – Dr Winnie Hong 

A Case of Recurrent Acute on Chronic Visceral Pain - Here Pancreatitis - 

How to Balance Analgesia with Concerns about Appropriate Opioid Usage 

Topical Session 04 – Victoria Suite 2 

Facilitator – Dr Clayton Thomas 

Presenters – Dr Robert Brzozek, Dr Tobie Sacks, Dr Lisa Sherry, Dr Helen Sweeting 

Getting to Opioid Detoxification, Part 1. Preparing the Patient: 3 Approaches 

1300–1400 Lunch 


Chair – Dr Chris Hayes 


Managing Placebo and Nocebo Effects – Mechanisms and Implications for Clinical Practice 


Pain and Addiction – Treatment Strategies 

7

1530–1600 Afternoon Tea 



Facilitator – Dr Helen Sweeting 

Issues to Consider with Conversion to Use of Buprenorphine 

Topical Session 05 – room to be confirmed 

Facilitator – Dr Carolyn Arnold 

Presenters – Assoc Professor Pam Macintyre & Professor Barbara Workman 

Prescribing for Pain in the Elderly 


Facilitator – Dr Jane Trinca 

Presenters – Dr Charles Kim, Ms Cathy Senserrick, Mr Andrew Shelton, Dr Jane Trinca 

Acute Pain Management for Orthopaedics. Managing the Pain and Fast Tracking Rehab 


Facilitator – Dr Dilip Kapur 

Presenters – Dr Charles Brooker, Professor Jon Currie, Dr Mike McDonough 

Detoxification Part 2. How to do it: 3 Approaches 

1900–2300 Conference Dinner – The Italian Restaurant, 101 Collins Street, Melbourne 

Sunday 18 October 


Chair – Dr Clayton Thomas 


Predictors of Persistent Pain after Trauma 


Procedural Pain Analgesia 


Psychological Adjuncts for Pain Occurring with Dressing Changes in Burns Patients 

1100–1130 Morning Tea 


Chair – Dr Terry Lim 


Australia’s Worst Bushfire Disaster: The Medical Response to Victoria’s Black Saturday 

1235 Close 

Dr Chris Hayes presents the 2010 Spring Meeting 

8 


Summary of PBLDs and Topical Sessions 

PBLD 01 

Friday 16 October 

1330–1500 

Facilitator: Dr Malcolm Hogg 

Implementing a Preventative 

Strategy in Acute Pain 

Identifying patients at risk 

of persistent post operative 

pain and implementing a 

preventative strategy 

Topical Session 01 


1330–1500 

Facilitator: Dr Penny Briscoe 

Office Based Pain 

Management – Optimising 

Outcome, Reducing Risk 

This session incorporates 

the essentials of a chronic 

pain assessment, including 

screening and risk 

stratification, examples of 

a low risk patient managed 

with OA and discussion of 

NSAIDS risks, and in contrast 

a high risk patient with back 

pain requiring screening for 

opioid risk. The concept of 

Universal Precautions in pain 

management to reduce risks 

will be discussed, and essential 

outcome documentation. 

PBLD 02 


1330–1500 

Facilitator: Dr Chris Hayes 

Cessation of Established 

Intrathecal Analgesia in 

Persistent Non-Cancer Pain 

A 47 year old man has been 

on established intrathecal 

therapy with hydromorphone 

and clonidine for 5 years. This 

is directed at the management 

of persistent low back pain 

previously unresponsive to 

3 spinal surgical procedures 

and oral opioids. Some 

modest benefits had been 

reported with initiation of 

intrathecal therapy. However 

these benefits had not been 

sustained. He had undertaken 

a group pain management 

program but had not effectively 

engaged with the process. 

Where to next? 



1330–1500 

Facilitator: A/Prof Kate Jackson 

Community Management 

of Intrathecal Infusions for 

Cancer 

This session will address 

indications, methods and drug 

combinations for intrathecal 

infusions for refractory cancer 

pain, plus the “nitty gritty” of 

day to day management of 

these infusions by domiciliary 

palliative care services. 

PBLD 03 


1130–1300 

Facilitator: Dr Bronwen Evans 

Management of Ischaemic 

Limb Pain 

John is a 55 year old man 

with Berger’s disease who 

is experiencing severe pain 

in his foot in association 

with ischaemic ulcers and 

is begging for more pain 

relief; when you meet him he 

is rocking to and fro whilst 

rubbing his painful foot. 

What challenges await in the 

management of this man’s 

pain and how might one 

proceed? 



1130–1300 

Facilitator: A/Prof Kate Jackson 

Incident/Procedural Pain 

Management Without an IV 

This session will discuss 

the extent of this problem, 

and a number of different 

management techniques, 

including Intranasal 

Sufentanil, OTFC lozenges, 

methoxyflurane and ketamine 

lozenges. 

PBLD 04 


1130–1300 

Facilitator: Dr Winnie Hong 

A Case of Recurrent Acute on 

Chronic Visceral Pain- Here 

Pancreatitis- How to Balance 

Analgesia with Concerns about 

Opioid Usage 

You are asked to manage a 42 

year old woman with a history 

of chronic pancreatitis who 

presents with an exacerbation 

of abdominal pain, and 

normal amylase. She has been 

admitted and treated with 

parenteral opioid over the 

weekend, and is demanding 

better analgesia. 



1130–1300 

Facilitator: Dr Clayton Thomas 

Getting to Opioid 

Detoxification, Part 1. 

Preparing the Patient: 3 

Approaches 

You have identified a patient 

with opioid dependence 

and chronic pain for whom 

medication reduction or 

even withdrawal is being 

considered. How will you 

work with the patient to 

help them consider this 

option? Three experts discuss 

their approaches covering 

psychological and behavioral 

approaches, considerations 

of social factors including 

compensation and pain 

management. 

PBLD 05 


1600–1730 

Facilitator: Dr Helen Sweeting 

Issues to Consider with 

Conversion to Buprenorphine 

You are asked to see a young 

heroin injecting male, who is 

currently receiving parenteral 

opioids for pain associated 

with spinal osteomyelitis, 

and who requires ongoing 

analgesia. 



1600–1730 

Facilitator: Dr Carolyn Arnold 

Prescribing for Pain in 

the Elderly 

Participants will learn how 

pain processing differs in 

older patients and appropriate 

selection and dosing of 

medication. Strategies for safe 

and effective treatment of pain 

in the elderly will be discussed. 



1600–1730 

Facilitator: Dr Jane Trinca 

Acute Pain Management for 

Orthopaedics. 

Managing the Pain and Fast 

Tracking the Rehabilitation of 

patients undergoing Knee or 

Hip Replacement 

Developing approaches to 

management of pain, which 

involves input from the nurse, 

physiotherapist, surgeon and 

others may have important 

benefits for the patient and 

healthcare system. This 

session aims to bring these 

disciplines together to develop 

best practice. 



1600–1730 

Facilitator: Dr Dilip Kapur 

Detoxification Part 2. How to 

do it: 3 Approaches 

Having reached agreement 

with your patient to reduce 

or withdraw the opioid for 

chronic pain, how will you do 

it? Three experts present their 

approaches ranging from rapid 

detox, detox over 1 to 2 weeks, 

or slower reduction. 

Continuing Medical Education Approvals 

Australian and New Zealand College of Anaesthetists • Lecture sessions: Category 1/Level 1: 1 Credit per hour 

Topical sessions: Category 1/Level 2: 2 Credits per hour • PBLDs: Category 3/Level 1:2 Credits per hour • The approval number is 1440 

This Active Learning Module has been approved by the RACGP QA&CPD Program in the 2008 – 2010 triennium. 

TOTAL POINTS: 40 (Category 1) 

9

Opioids, Pain and Addiction – 

Facts vs Fiction 


Credit Valley Hospital, Ontario, Canada and 

CPM Centres for Pain Management, Mississauga, Ontario, Canada 

EDUCATIONAL OBJECTIVES 

1. Update knowledge on the prevalence and neurobiology 

of addiction and the potential overlap with chronic pain; 

2. Review the appropriate definitions of addiction in 

patients with pain on opioid therapy; 

3. Describe the concepts of ‘Universal Precautions’ for 

optimizing the prescribing of opioids for chronic pain, 

including screening strategies, written agreements and 

urine drug screening; 

4. Summarize current knowledge on potential “new” 

adverse effects of long-term opioid therapy. 

summary 

Chronic non-cancer pain (CNCP) remains a common 

problem affecting an estimated 20% of the adult 

population, with a huge burden of illness to the 

individual, the health care system and the economy. 

In spite of this impact, resources devoted to research, 

education and treatment of pain remain meagre 

compared to other chronic conditions. 

The use of long-term opioid (LTO) therapy for the 

treatment of CNCP has gradually become accepted 

internationally as an evidence-based component of 

multi-modal pain management by a majority of pain 

clinicians, pain and addiction organizations and medical 

regulators. This does not mean the current practice 

is without ongoing controversy. 

The increased prescribing of opioids for pain, has 

coincided with an increase in misuse, addiction and 

diversion of prescribed opioids. To reduce this risk, 

existing guidelines recommend that clinicians screen 

for addiction risk and structure treatment accordingly. 

As a result, there is a growing need for pain clinicians 

to understand some of the essentials of addiction 

medicine – much as there is a need for addiction 

specialists to understand something about 

pain medicine. 

Substance use disorders affect approximately 10% of 

the general population. Patients with chronic pain either 

have the same or somewhat higher risk of concurrent 

substance abuse or addiction. The development of 

addiction requires not only repeated exposure to a 

potentially addicting substance or behaviour, but an 

individual with a particular biopsychogenetic vulnerability 

living in a particular social milieu. Without the presence 

of these risk factors, it is unlikely that a physician can 

“create” an addict de novo from an opioid-naïve patient 

by the prescription of opioids for pain. On the other 

hand, physicians can certainly enable the ‘rekindling’ 

of a previous addictive disorder by failing to screen 

patients for risk factors or by ignoring the early 

symptoms and signs of a developing addiction to 

prescribed opioids. 

There is an overlap between the neural circuitry of 

addiction and that of chronic pain. However it is 

important to properly use the labels ‘misuse’, ‘abuse’ 

‘tolerance’ and ‘addiction’ when referring to patients 

with pain on opioids. 

Gourlay et al published the concept of ‘Universal 

Precautions in pain medicine’, to help manage all 

patients in pain with a standardized approach in order 

to optimize benefit and reduce risks. This includes 

screening and risk stratification and the use of opioid 

prescribing agreements and urine drug screening in 

higher risk patients. 

Finally, our recent clinical experience with the use of LTO 

for chronic pain has raised the issue of some ‘new’ longterm 

side effects of opioids, namely opioid hyperalgesia, 

sex hormone disturbances, worsening sleep apnea and 

potential immune effects. Other than opioid-induced 

hypogonadism, the current published data is not robust 

enough to allow for firm conclusions regarding these 

other adverse effects. 

10 


In the absence of other alternatives, opioids will continue 

to be a valuable treatment option for pain management. 

Genetically and psychosocially vulnerable people will 

continue to misuse substances for psychic effect. 

By incorporating some fundamental concepts from 

addiction medicine into a structured approach to patient 

assessment and treatment, the clinician can optimize 

the benefits and reduce the risks of chronic pain 

management. 

REFERENCES 

1. Adinoff B. Neurobiologic processes in drug reward and addiction. 

Harv Rev Psychiatry. 2004 Nov-Dec;12(6):305-20. Review. 

2. Chou R, Ballantyne JC, Fanciullo GJ, Fine PG, Miaskowski C. Research 

gaps on use of opioids for chronic noncancer pain: findings from 

a review of the evidence for an American Pain Society and American 

Academy of Pain Medicine clinical practice guideline. J Pain. 2009 

Feb;10(2):147-59. Review. 

3. Chou R, Fanciullo GJ, Fine PG, Miaskowski C, Passik SD, Portenoy RK. 

Opioids for chronic noncancer pain: prediction and identification of 

aberrant drug-related behaviors: a review of the evidence for 

an American Pain Society and American Academy of Pain Medicine 

clinical practice guideline. J Pain. 2009 Feb;10(2):131-46. Review. 

4. Fishbain DA, Cole B, Lewis JE, Gao J, Rosomoff RS. Do Opioids Induce 

hyperalgesia in humans? An Evidence-Based Structured Review. 

Pain Med. 2009 Jul 6. [Epub ahead of print] 

5. Fishbain DA, Cole B, Lewis J, Rosomoff HL, Rosomoff RS. What 

percentage of chronic nonmalignant pain patients exposed to chronic 

opioid analgesic therapy develop abuse/addiction and/or aberrant 

drug-related behaviors? A structured evidence-based review. Pain Med. 

2008 May-Jun;9(4):444-59. Review. 

6. Gourlay DL, Heit HA, Almahrezi A. Universal precautions in pain 

medicine: a rational approach to the treatment of chronic pain. 

Pain Med 2005;6:107-112. 

7. Heit HA, Gourlay DL. Urine drug testing in pain medicine. 

J Pain Symptom Manage 2004;27:260-267. 

8. Jovey RD. Pain and Addiction: Prevalence, Neurobiology and 

Definitions. In: Castro-Lopes J. (Ed). Pain 2008 An Updated Review 

(Refresher Course Syllabus) IASP Press, Seattle, 2008: 359-364. 

9. Koob GF. The neurobiology of addiction: a neuroadaptational review 

relevant for diagnosis. Addiction 2006; 101 (Suppl 1): 23-30. 

10. Savage SR. Assessment for addiction in pain-treatment settings. 

Clin J Pain 2002;18:S28-S38. 

11. Savage SR, Joranson DE, Covington EC, Schnoll SH, Heit HA, Gilson 

AM. Definitions related to the medical use of opioids: evolution 

towards universal agreement. J Pain Symptom Manage. 2003 

Jul;26(1):655-67. 

12. Sacerdote P. Opioid-induced immunosuppression. Curr Opin Support 

Palliat Care. 2008 Mar;2(1):14-8. 

13. Substance Abuse and Mental Health Services Administration. (2007). 

Results from the 2006 National Survey on Drug Use and Health: 

National Findings (Office of Applied Studies, NSDUH Series H-32, 

DHHS Publication No. SMA 07-4293). Rockville, MD. Available from: 

http://www.samhsa.gov Accessed Feb 1, 2003. 

14. Walker JM, Farney RJ. Are opioids associated with sleep apnea? A 

review of the evidence. Curr Pain Headache Rep. 2009 Apr;13(2):120-6. 

15. Webster LR, Webster RM. Predicting aberrant behaviors in opioidtreated 

patients: preliminary validation of the Opioid Risk Tool. 

Pain Med 2005;6:432-442. 

11

Intrathecal Analgesia – Duelling 

with Efficacy and Safety 


University College London and Great Ormond St Hospital, London, United Kingdom 

Adequate control of perioperative pain has been 

recognised for many years to improve acute 

postoperative outcomes in neonates and infants 1 and 

may also have an impact on long-term sensory 

function 2, 3 . Regional anaesthesia and analgesia has an 

established role in postoperative pain management 

for children of all ages 4 . Opioid and non-opioid spinal 

analgesics are frequently added to local anaesthetics 

for single dose injection or infusion, and can improve 

analgesic efficacy, reduce local anaesthetic requirements, 

and/or prolong analgesia. However, a large range 

of drugs and preparations have been administered 

spinally 5 and there is insufficient evidence regarding the 

comparative efficacy, side-effect profile, and potential 

for spinal toxicity to inform the clinical choice between 

different agents. Reports of neurological impairment 

following epidural and caudal analgesia in children are 

rare 6, 7 , but it has also been argued that a single case of 

serious neurological sequelae following injection of an 

inadequately tested drug could bring the technique into 

disrepute and deny many children the benefit of regional 

analgesia 8 . 

The requirements for preclinical evaluation of the 

toxicity of spinal analgesics have been established in 

adult models, and encompass effects on both function 

and spinal cord morphology 9 . However, there are 

additional factors that require consideration in early 

life. Developmental age has a significant impact on 

nociceptive processing 10 and on analgesic efficacy 

following both systemic 11 and spinal 12,13 administration. 

In addition, reductions in neural activity at critical 

developmental periods may precipitate programmed 

cell death or neuronal apoptosis. In laboratory models, 

general anaesthetics with NMDA antagonist or GABA 

agonist activity, particularly when given in combination, 

have been associated with acute apoptosis and longterm 

deficits in learning and memory 14 . A large clinical 

cohort study has also shown an association between the 

duration and number of anaesthetic exposures in early 

life and an increased risk of learning difficulties during 

childhood 15 . While clinical studies suggest an association 

but cannot confirm causation (as there will be multiple 

confounding factors and effects of intercurrent illness, 

drugs, surgical factors etc.), increased utilization of 

neuraxial techniques has been suggested as a means to 

reduce the potential risks related to exposure to general 

anaesthetic drugs 16 . Prolonged general anaesthesia 

has been associated with increased apoptosis in 

the spinal cord 17 , but the FDA has recognised that 

effects of spinally administered analgesics also require 

specific evaluation (www.fda.gov/ohrms/dockets/ 

ac/07/minutes/2007-4285m1-Final.pdf). We have 

developed a preclinical model for evaluation of toxicity 

in neonatal rats that includes behavioural testing, acute 

histopathological examination of the cord, evaluation 

of the impact of postnatal age and intrathecal drugs on 

apoptosis in the spinal cord, and longterm functional 

outcomes 18 . As drug doses in laboratory models are 

not directly comparable to “clinically relevant” doses, 

we determined the analgesic dose and then evaluated 

toxicity at increasing doses to determine a therapeutic 

index (ratio of toxic dose to analgesic dose), which 

allows comparison of the relative toxicity 

of different drugs at different ages. 

Due to advances in neonatal and paediatric care, 

neonates are surviving at earlier gestational ages and 

increasingly complex surgical procedures are being 

performed at earlier stages of development. Paediatric 

pain management requires a balance between multiple 

‘duelling’ factors. The primary requirement is to 

provide adequate anaesthesia and analgesia to ensure 

patient comfort, maintain cardiorespiratory stability, 

and improve postoperative outcomes. However, it is 

increasingly recognised that the effects of pain, injury, 

anaesthesia and analgesia on the developing nervous 

system may differ from those seen at older ages and 

may produce long-term changes in structure and 

function. In relation to spinal therapies, there is an 

ongoing ‘duel’ between efficacy and safety for patients 

of all ages. Preclinical spinal toxicity studies provide 

essential information for the evaluation of comparative 

risks and age-related changes in susceptibility, 

and can help to inform the clinical choice between 

different agents. Determining the most effective and 

developmentally appropriate analgesic interventions to 

improve both acute and long-term outcomes is a major 

ongoing challenge for researchers. In clinical practice, 

the emphasis remains on providing adequate and safe 

analgesia based on currently available best evidence 

and an analysis of the relative benefits and risks for 

each individual patient. 

12 


REFERENCES 

1. Anand KJ, Hickey PR. Halothane-morphine compared with high-dose 

sufentanil for anesthesia and postoperative analgesia in neonatal 

cardiac surgery. N Engl J Med. 1992 Jan 2;326(1):1-9. 

2. Walker SM, Franck LS, Fitzgerald M, Myles J, Stocks J, Marlow N. 

Long-term impact of neonatal intensive care and surgery on 

somatosensory perception in children born extremely preterm. 

Pain. 2009 Jan;141(1-2):79-87. 

3. Walker SM, Tochiki KK, Fitzgerald M. Hindpaw incision in early life 

increases the hyperalgesic response to repeat surgical injury: critical 

period and dependence on initial afferent activity. (submitted). 

4. Howard RF, Carter B, Curry J, Morton N, Rivett K, Rose M, et al. 

Association of Paediatric Anaesthetists: Good Practice in Postoperative 

and Procedural Pain. Pediatric Anesthesia. 2008;18 (Suppl. 1):1-81. 

5. Williams DG, Howard RF. Epidural analgesia in children. A survey of 

current opinions and practices amongst UK paediatric anaesthetists. 

Paediatr Anaesth. 2003 Nov;13(9):769-76. 

6. Llewellyn N, Moriarty A. The national pediatric epidural audit. 

Paediatr Anaesth. 2007 Jun;17(6):520-33. 

7. Royal College of Anaesthetists. Major Complications of Central Neural 

Blockade in the United Kingdom. 2009 Available from: 

www.rcoa.ac.uk/index.asp?PageID=717. 

8. Lonnqvist PA. Adjuncts to caudal block in children--Quo vadis? 

Br J Anaesth. 2005 Oct;95(4):431-3. 

9. Yaksh TL RM, Provencher JC. . Preclinical safety evaluation for spinal 

drugs. . In: Yaksh TL, editor. Spinal Drug Delivery. Amsterdam: 

Elsevier Science B.V.; 1999. p. 417-37. 

10. Fitzgerald M, Walker SM. Infant pain management: a developmental 

neurobiological approach. Nat Clin Pract Neurol. 2009 Jan;5(1):35-50. 

11. Nandi R, Beacham D, Middleton J, Koltzenburg M, Howard RF, 

Fitzgerald M. The functional expression of mu opioid receptors on 

sensory neurons is developmentally regulated; morphine analgesia 

is less selective in the neonate. Pain. 2004 Sep;111(1-2):38-50. 

12. Walker SM, Howard RF, Keay KA, Fitzgerald M. Developmental age 

influences the effect of epidural dexmedetomidine on inflammatory 

hyperalgesia in rat pups. Anesthesiology. 2005 Jun;102(6):1226-34. 

13. Walker SM, Fitzgerald M. Characterization of spinal alpha-adrenergic 

modulation of nociceptive transmission and hyperalgesia throughout 

postnatal development in rats. 

Br J Pharmacol. 2007 Aug;151(8):1334-42. 

14. Loepke AW, Soriano SG. An assessment of the effects of general 

anesthetics on developing brain structure and neurocognitive function. 

Anesth Analg. 2008 Jun;106(6):1681-707. 

15. Wilder RT, Flick RP, Sprung J, Katusic SK, Barbaresi WJ, Mickelson C, 

et al. Early exposure to anesthesia and learning disabilities 

in a population-based birth cohort. 

Anesthesiology. 2009 Apr;110(4):796-804. 

16. McGowan FX, Jr., Davis PJ. Anesthetic-related neurotoxicity in the 

developing infant: of mice, rats, monkeys and, possibly, humans. 

Anesth Analg. 2008 Jun;106(6):1599-602. 

17. Sanders RD, Xu J, Shu Y, Fidalgo A, Ma D, Maze M. General 

anesthetics induce apoptotic neurodegeneration in the neonatal rat 

spinal cord. Anesth Analg. 2008 Jun;106(6):1708-11. 

18. Westin BD, Walker SM, Grafe M, Yaksh TL. Intrathecal morphine in 

the neonatal rat: analgesic efficacy and preclinical evaluation of safety. 

Anesth Analg 2009;108:S235. 

13

Non Neuronal Opioid Actions 


University of Adelaide, SA 

Mark R Hutchinson 


More than 30 opioids are marketed worldwide for the 

treatment of acute and persistent moderate to severe 

pain. The traditional view regarding the mechanism of 

action of the opioids is that they bind to the G-protein 

coupled mu opioid receptor on pre- and post synaptic 

neurons causing the closing of voltage gated Ca++ 

channels (presynaptic) and opening of K+ channels 

(postsynaptic). This results in a reduction in transmitter 

release and hyperpolarisation and the beneficial clinical 

effects of analgesia. It is generally accepted that the 

same mechanisms are responsible for the adverse 

effects of opioids, such as respiratory depression, 

tolerance, dependence and neurotoxicity. However recent 

in vitro and animal findings indicate a role for opioidinduced 

glial activation. Glia are immune-like cells in the 

brain and spinal cord and express the innate immune 

receptor toll-like receptor 4 (TLR4) through which 

opioids cause signaling activation. Importantly, the rank 

order of effect at TLR4 by opioids is completely different 

compared to the classical neuronal mu receptor. For 

example, the non-opioid receptor active morphine 

metabolite, morphine-3-glucuronide, possesses 

significant TLR4 activity, whilst the potent morphine 

metabolite, morphine-6-glucuronide, has minimal 

activity. Opioids also target TLR4 in a nonstereoselective 

manner (in contrast to binding at the mu receptor); 

for example, the non-opioid S-methadone is as active at 

TLR4 as the opioid active R-methadone. Thus, opioids 

possess TLR4 signaling activation activity resulting in 

pro-inflammatory glial activation. This causes the release 

of neuroexcitatory pro-inflammatory cytokines such as 

IL-1 that can act on pre- and post-synaptic neurons to 

enhance pain, decrease analgesia and increase tolerance 

and dependence. Moreover, glial activation has also been 

linked to elevated morphine-induced dopamine release 

within the nucleus accumbens, suggesting an important 

role in modifying opioid reward. Chronic administration 

of opioids causes enhanced cytokine release from glia. 

Suppressing opioid-induced glial activation by targeting 

TLR4 or generally attenuating glial activation potentiates 

acute opioid analgesia, reduces the development 

of tolerance, opioid-induced hyperalgesia, reward, 

dependence and withdrawal, and reduces respiratory 

depression. Thus the beneficial and detrimental effects 

of opioids might be able to be separated by targeting 

and inhibiting opioid-induced glial activation. 

In animal studies, the antibiotic minocycline is an 

effective attenuator of opioid-induced glial activation. 

Whilst acutely potentiating morphine analgesia, 

it suppresses opioid dependence and respiratory 

depression. TLR4 signaling inhibitors such as the mu 

opioid inactive isomers of naloxone and naltrexone 

behave similarly and result in the separation of the 

wanted and unwanted actions of opioids. 

In conclusion, a new paradigm shift in our 

understanding of the mechanisms of action of the 

opioids is evolving. Consideration now needs to be 

given to the potentially important contribution of 

immune signalling in the central nervous system to the 

efficacy and toxicity of the opioids. Translation of these 

promising preclinical results into the clinical setting is 

required but contingent upon the development of newer 

and more selective TLR4 opioid binding site inhibitors. 

REFERENCES 

1. Hutchinson MR et al. Opioid-induced glial activation: mechanisms 

of activation and implications for opioid analgesia, dependence and 

reward. Sci World J 7: 98-111, 2007 

2. Hutchinson MR et al. Minocycline suppresses morphine-induced 

respiratory depression, suppresses morphine-induced withdrawal and 

enhances systemic morphine-induced analgesia. Brain Behav Immun 

22: 1248-56, 2008 

3. Milligan ED, Watkins LR. Pathological and protective roles of glia in 

chronic pain. Nature Rev Neurosci 10: 23-36, 2009. 

14 


Novel Approaches to Cancer Pain 

Professor Julia Fleming 

Royal Brisbane Hospital, QLD 

Not available at time of printing 

Spinal Cord Magic Bullets – 

Current and Future Analgesic Developments 



The holy grail of modern medicine is to find treatments 

that eradicate disease with no other effect on the host. 

Paul Ehrlich used the expression ‘magic bullet’ for the 

first time in 1908 in his Harben Lectures 1 . Ehrlich’s first 

magic bullet was Salvarsan, discovered in 1909, which 

provided the first cure for syphilis. The rational approach 

to modern therapeutics handed down by Ehrlich is 

first to identify a disease-specific target and then find a 

therapy selective for that compared with the rest of the 

host organism. This is not easy in pain medicine. 

The first target hailed as the ‘pain transmitter’ was 

Substance P 2,3 . This compound fulfilled the Dale criteria 

in being present at the correct site (C fibres), released 

physiologically during nociception, and exogenous 

Substance P caused pain behaviours in animals when 

administered intrathecally. A target was identified 

(NK1 receptors) and highly selective magic bullets were 

synthesised. Glutamate acting at NMDA receptors and 

subsequent NMDA antagonist development followed 

the same pattern 4 . NK1 and NMDA antagonists showed 

efficacy in animal pain models but were abysmal failures 

in the treatment of human clinical pain states. This 

was not the fault of the selectivity of the magic bullets 

but of our limited understanding of the physiology of 

pain. Valuable lessons were learned with respect to 

proper careful use of animal models and an awareness 

of the complex nature of the nervous system. Pain 

perception is the result of a complex process of multiple 

parallel pathways with changing inter-relationships 

(plasticity). Receptor targets are rarely, if at all, confined 

to nociception and pain, so a magic bullet for one 

such target is likely to cause harm to the organism by 

interactions, albeit selective, with the same receptor 

involved with systems other than pain and nociception. 

A more sensible approach is to administer two or more 

such compounds interfering with complementary 

pathways involved with pain and nociception – 

multimodal analgesia. 

There are many current targets that are the focus for 

drug development because they have been identified as 

being involved with peripheral nerves and spinal cord 

handling of nociceptive information. These include 

ligand-gated receptors, transporter mechanisms and 

voltage-gated calcium, potassium and sodium channels. 

Examples of some of these will be discussed. It remains 

to be seen which of the systems will lead to a true magic 

bullet unimodal therapy, and which will be useful as part 

of a multimodal approach. 

REFERENCES 

1. Royal Institute of Public Health (London: Lewis, 1908). Experimental 

Researches on Specific Therapy. On Immunity with special Reference 

to the Relationship between Distribution and Action of Antigens. 107 

2. Brain peptides: is substance P a transmitter of pain signals? Marx JL. 

Science. 1979, 205(4409):886-9. 

3. Pharmacology of pain and analgesia. Wilson PR, Yaksh TL. 

Anaesth Intensive Care. 1980 (3):248-56 

4. Spinal pharmacology of thermal hyperesthesia induced by constriction 

injury of sciatic nerve. Excitatory amino acid antagonists.Yamamoto T, 

Yaksh TL. Pain. 1992 Apr;49(1):121-8. 

15

Opioids in Dyspnoea and Sleep 

Apnoea 

Assoc Professor Christine McDonald 


Breathlessness is a common symptom in patients with 

a variety of advanced diseases. Opioids are frequently 

used to treat severe breathlessness and the efficacy of 

both oral and parenteral opioids has been confirmed 1 . 

Chronic obstructive pulmonary disease guidelines 

support the use of opioids in treating intractable 

breathlessness if disease specific therapy has been 

maximised but their use is limited, probably because 

of concerns about respiratory depression, hypercapnia 

and other adverse effects. Opioids are an effective tool 

in the management of severe, acute pain and pain 

associated with malignancy. They have also become 

increasingly used long-term for treating patients with 

chronic non-malignant pain. Although the potential for 

adverse respiratory effects is well-known, there are only 

relatively few studies examining sleep and breathing in 

patients receiving long-term opioid therapy. Methadone 

administration has been demonstrated to increase the 

risk for both obstructive and central sleep apnoea in 

patients receiving methadone either for chronic pain 

or as part of management for drug dependency. In a 

cohort of such patients receiving methadone through 

a maintenance program the presence of central sleep 

apnoea did not correlate with symptoms of excessive 

daytime somnolence 2 . Prospective studies before and 

after chronic opioid administration are needed to allow 

definitive conclusions to be drawn about the aetiological 

relationship between opioids and sleep apnoea 3 . It is 

estimated that a large proportion of people with sleep 

disordered breathing remain undiagnosed. Patients 

with undiagnosed obstructive sleep may be at risk of 

increased perioperative complications. The perioperative 

risk of patients with obstructive sleep apnoea may be 

reduced by appropriate screening to detect undiagnosed 

obstructive sleep apnoea. 

REFERENCES 

1. Jennings Al, Davies AN, Higgins JP, et al. (2002). A systematic review 

of the use of opioids in the management of dyspnoea. 

Thorax 57, 939-44 

2. Wang D, Teichtahl H, Goodman C et al. (2008) 

J Clin Sleep Med 15, 557-62 

3. Walker JM, Farney RJ. (2009) Are opioids associated with sleep apnea? 

A review of the evidence. Curr Pain Headache Rep13,120-126 

Contemporary Approaches to 

Opioid Addiction 



Dramatic advances in the neurosciences over the past 

two decades have revolutionised our understanding of 

drug abuse and addiction, with clear evidence emerging 

that drug addiction is a chronic relapsing brain disease. 

However, as Alan Leshner, former Director of the 

National Institute on Drug Abuse, wrote in a seminal 

article entitled ‘Addiction is a Brain Disease – and it 

Matters!’ (Science 1997; 278:45-47), despite this scientific 

knowledge, the concept of addiction as a chronic 

relapsing brain disease remains totally new for most of 

the general public, for many policy makers and sadly, for 

many health care professionals as well. Unfortunately 

little has changed in the subsequent 12 years. 

This presentation will explore some of the implications 

and opportunities that the neurobiological revolution 

now provides for the modern treatment and prevention 

of drug addiction in general, and for opioid dependence 

in particular. 

16 


Methadone Pharmacology 

Dr Andrew A. Somogyi 


INTRODUCTION 

Developed over 60 years ago, the use of methadone 

for severe persistent pain has steadily increased over 

the past 10 years. However it remains a difficult opioid 

to use because of concerns regarding toxicity due to 

excessive accumulation, cardiac rhythm disturbances 

and the diversity in reported dosage conversion ratios. 

BASIC PHARMACOLOGY 

Methadone is administered as a racemic mixture of 

2 enantiomers, the opioid-active R-methadone which 

has a much higher affinity for the mu opioid receptor 

than the ‘inactive’ S-methadone. Although methadone 

does not bind to the other opioid receptors, it does 

have very weak serotonin reuptake transporter blocking 

effects and is a noncompetitive NMDA antagonist; 

the clinical effects of such antagonism, if they occur 

at all, are unlikely to be important. Both enantiomers 

have immune suppressant and pro-inflammatory glial 

activation effects through TLR4 signaling activation and, 

prolong the QT interval by binding to the cardiac 

hERG potassium channel; in both cases, S-methadone 

is more active than R-methadone. 

CLINICAL PHARMACOLOGY 

Methadone has a high oral bioavailability and 

is mainly eliminated by metabolism via CYP3A4 

(nonstereoselective and subject to environmental 

influences) and CYP2B6 (stereoselective and subject 

also to genetic influences). Uptake into the brain is 

opposed by the efflux transporter p-glycoprotein which 

is influenced by genetic and environmental factors. 

Methadone has the longest half life of all the opioids, 

typically ranging from 15 to 90 hours with R-methadone 

being 60% longer than the S-enantiomer. A 6-fold 

difference in half life between patients results in a 

6-fold difference in accumulation on chronic dosing. 

In addition, it also means that steady-state for the 

opioid active R-methadone is not reached until about 

10 days and, the long half life calls into question 

dosing more frequently than twice daily. Its very steep 

dose- and plasma concentration–response relationship 

necessitates that monitoring is required in the two 

weeks following initiation of dosing to avoid and 

attend to any excessive accumulation as evidenced by 

sedation-respiratory depression. The cardiac effects of 

methadone have been somewhat over emphasized as 

long as dosage rates are kept to the minimum required 

for pain relief (usually < 50 mg/day) and the patient does 

not have any clinical or genetic factors that predispose 

to torsades de pointes. Many drugs may inhibit the 

metabolism of methadone mainly via CYP3A4 inhibition 

leading to toxicity and specific drug metabolism 

inducers may cause reduced analgesia. Since it has 

no active metabolites, methadone has advantages 

over some other opioids especially for the patient with 

renal impairment. The clinical effects of genetic factors 

in the metabolism (CYP2B6), brain efflux transport 

(ABCB1) and mu opioid receptor (OPRM1) binding of 

methadone are unclear but may be important in certain 

individuals. Whereas the single dose analgesia potency 

ratio of methadone to morphine IV is about unity, on 

chronic oral dosing the ratio is about 10 due to greater 

accumulation and incomplete cross tolerance. 

CONCLUSION 

Methadone is now regarded as an important and 

inexpensive back-up opioid for severe persistent pain 

especially that due to malignancies. Dosing guidelines 

have been promulgated to allow for supposedly “easier” 

transition from morphine and other commonly used 

opioids to oral methadone. An understanding of 

methadone’s ‘different’ pharmacological properties 

together with clinical and genetic factors that might 

contribute to toxicity should allow for greater confidence 

by pain physicians in adding methadone to their 

pharmaceutical armamentarium. 

REFERENCES 

1. Auret K et al. Pharmacokinetics and pharmacodynamics of methadone 

enantiomers in hospice patients with cancer pain. Ther Drug Monit 28: 

359-66, 2006 

2. Coller JK, Christrup LL, Somogyi AA. Role of active metabolites in the 

use of opioids. Eur J Clin Pharmacol 65: 121-39, 2009 

3. Eap CB et al. Stereoselective block of hERG channel by (S)-methadone 

and QT interval prolongation in CYP2B6 slow metabolisers. 

Clin Pharmacol Ther 81: 719-28, 2007 

4. Leppert W. The role of methadone in cancer pain treatment – a review. 

Int J Clin Prac 63: 1095-1109, 2009 

17

Methadone Re-visited in 

Cancer Pain 


Southern Health and Monash University, VIC 

INTRODUCTION 

Methadone has been around for more than 50 years, 

but until recently, in Australia and many other countries, 

it has been stigmatised by both the medical profession 

and the lay public as ‘the heroin addicts drug’. However 

due to a number of significant differences to other 

opioids its use is being revisited for both cancer and 

non cancer pain. 1 This has been bolstered by the better 

understanding of methadone’s pharmacokinetics, and 

the development of a number of newer and perceived 

safer dosing guidelines. 

We elected to audit McCulloch House’s (a level III 

inpatient hospice unit) methadone conversions for 2 

years using the Royal Perth Hospital’s protocol. 2 This 

protocol acknowledges the apparent paradox whereby 

the equi-analgesic dose of methadone is much lower 

in patients currently on high doses of morphine or 

other opioids. 

AIMS 

To prospectively audit all conversions over a 

2 year period 2005/2006, from another opioid to 

methadone for: 

• Indication for conversion 

• Efficacy and safety of the RPH conversion protocol 

• Pain control outcome 

• Retrospective cost comparison. 

METHODS 

All conversions were converted during an inpatient 

admission and used the RPH conversion protocol. 2 

This involves the calculation of the predicted daily 

methadone dose by determining the approximate daily 

oral morphine dose equivalent and using a conversion 

ratio in the table below: 

Daily Oral Morphine 

< 100 mg 3:1 

101 – 300 mg 5:1 

301 – 600 mg 10:1 

601 – 800 mg 12:1 

801 – 1000 mg 15:1 

RESULTS 

• From January 2005 to November 2006 24 pts of which 

23/24 had cancer related pain. 

• Age 40-78 yrs: mean 56, median 61. 

• Major pain mechanism/s: 

– Neuropathic + incident (vertebral mets) - 17 

– Neuropathic - 6 

– Digital Ischaemia (and renal failure) - 1 

• Indications: 

– Step down after response to “burst” ketamine in 

patients with refractory cancer pain 3 -15 

– Opioid rotation ie. for inefficacy (poor pain control) - 6 

– Opioid substitution ie. for opioid adverse effects - 3 

• Prior opioid – a wide range of different opioids/ 

formulations at relatively high doses (converted to oral 

morphine equivalents): 

– Range 150–1320 mg/24 hrs: mean 540mg/24 hrs, 

median 360mg/24 hrs 

CONCLUSIONS 

• Apparent support for the use of methadone: 

– For neuropathic and incident pain 

– As a step down from “burst” ketamine 

• Support for the RPH conversion protocol 

• Methadone demonstrated a significant cost advantage 

REFERENCES 

1. Bruera E and Sweeney C, Methadone Use in Cancer Patients with Pain: 

A review. Journal of Palliative Medicine 2002; 5(1): 127-138. 

2. Ayonrinde OT, Bridge TD. The rediscovery of methadone for cancer 

pain management. MJA 2000: 173; 536-540. 

3. Jackson K, Ashby M, Martin P, Pisasale M, Brumley D and Hayes B. 

‘Burst’ ketamine for refractory cancer pain: An open-label audit of 39 

patients. JPSM 2001; 22(4): 834-842. 

OUTCOMES 

• 22/24 good pain control. 

• 2 pts adequate analgesia not attained: 

– Further RT and lignocaine CSCI 

– Spinal decompression and internal fixation 

• Minimal Adverse Effects: 

– 2 pts drowsy and methadone reduced 

• 5 pts methadone increased after 3/7 due to inadequate 

analgesia 

• 3 pts repeated “burst” ketamine on subsequent 

admissions with 1 pt 3 “bursts” over 8/12 

19

Methadone in Chronic Pain 



Methadone is a synthetic opioid with potent analgesic 

effects. Although commonly associated with the 

treatment of opioid addiction, it is, as a result of its 

unique pharmacokinetics and pharmacodynamics, 

a valuable option in the treatment of Chronic Nonmalignant 

Pain: 

A highly lipophilic molecule with >80% bioavailability, 

it is rapidly absorbed from the stomach and distributed 

to the liver and other tissues that then act as a natural 

peripheral reservoir. Consequently, its extended 

elimination half-life, while variable between patients, 

generally provides stable analgesia with daily or twice 

daily dosing – reducing the salience of drug use. 

Methadone is a mu-opioid agonist with receptor 

affinity similar to morphine but, with repeated dosing, 

its efficacy is greater than that of morphine. It is also 

a NMDA receptor antagonist, potentially decreasing 

tolerance and craving for opioids and modulating 

the development of central sensitization. Although 

methadone also inhibits reuptake of monoamines 

(e.g., serotonin, noradrenaline), potentially augmenting 

the effects of antidepressants, its weak euphorigenic 

effects reduce the risk of it being abused 

Other potential benefits include low cost – and with 

regard to risk of diversion into the blackmarket, low 

street value compared to other prescribed opioids. 

Methadone does, however, have a number of 

disadvantages: Like other opioids, it is often associated 

with constipation and other GI symptoms, and in high 

doses, sleep-disordered breathing and arrhythmias. 

Its interactions with other medications, particularly 

benzodiazepines and antidepressant drugs, initiation 

and maintenance dosage regimens will also be 

discussed. 

20 


Managing Placebo 

and Nocebo Effects – 

Mechanisms and 

Implications for Clinical Practice 


University of Sydney, NSW 

The placebo effect is a term that has been widely used 

in health literature and its nature has been the focus of 

increasing research in recent years. A key conclusion 

of recent research is that there is not one placebo 

effect, but many, and that these effects are mediated by 

different psychological and neurobiological mechanisms. 

Less research has been devoted to the nocebo effect, 

a phenomenon that is opposite to the placebo effect, 

and despite the limited amount of research, several 

important mechanisms of nocebo effects have been 

identified. 

In the case of placebo analgesia, several effects 

have been identified and it is argued that by better 

understanding how they work, it might be possible for 

clinicians to ethically augment treatment effects, even 

when a placebo is not given. Several effects have also 

been identified in the case of nocebo hyperalgesia, and 

a better understanding of these effects may lead to 

managing them in routine care. 

This presentation will review placebo effects and nocebo 

effects at a conceptual level with a view to promoting a 

reconceptualisation of these phenomenons. A synthesis 

of the mechanistic literature will be provided both from 

psychological and neurobiological viewpoints. The 

implications for clinical practice will be presented based 

on analysis of mechanistic trials, clinical trials and review 

papers with a view to presenting some conclusions 

on how these effects may be managed to improve 

clinical care. 

references 

1. Benedetti, F., M. Lanotte, et al. (2007). “When words are painful: 

unravelling the mechanisms of the nocebo effect.” Neuroscience 

147(2): 260-71. 

2. Finniss, D. G. and F. Benedetti (2005). “Mechanisms of the placebo 

response and their impact on clinical trials and clinical practice.” 

Pain 114: 3-6. 

3. Kaptchuk, T. J., W. B. Stason, et al. (2006). “Sham device v inert pill: 

randomised controlled trial of two placebo treatments.” 

BMJ 332(7538): 391-7. 

4. Kaptchuk, T. J., J. M. Kelley, et al. (2008). “Components of placebo 

effect: randomised controlled trial in patients with irritable bowel 

syndrome.” BMJ 336(7651): 999-1003. 

5. Price, D. D., D. G. Finniss, et al. (2008). “A comprehensive review 

of the placebo effect: recent advances and current thought.” 

Annual Review of Psychology 59: 565-90. 

21

Pain and Addiction – 

Treatment Strategies 





1. Review the prevalence of chronic pain in patients with 

addiction and the prevalence of addiction in patients 

with chronic pain 

2. Operationalize and illustrate the concepts of Universal 

Precautions in the management of high risk patients 

with pain 

3. Describe an approach to managing acute pain in the 

patient on Opioid Agonist Treatment (OAT) for addiction 

SUMMARY 

The needs of patients with both pain and addiction are 

not well served in most countries. Pain clinicians are 

reluctant to prescribe opioids to high risk patients due 

to concerns regarding misuse and diversion. Addiction 

professionals are reluctant to manage pain due to 

regulatory limitations and lack of knowledge. There is a 

growing need for pain clinicians to understand essential 

prinicples of addiction medicine – much as there is a 

need for addiction specialists to understand something 

about pain medicine. 

It is important to properly use the labels ‘misuse’, 

‘abuse,’ ‘tolerance,’ ‘dependence,’ and ‘addiction’ when 

referring to patients with pain on opioids. Some patients 

are mislabelled and referred to detox facilities or OAT 

programs when they are simply physically dependent 

on opioid analgesics. In some regions, the only place 

that patients can access opioid therapy for pain is in 

an OAT program. Some patients in pain programs are 

benefitting from opioids but have difficulty managing 

their dosage due to inadequate pain relief or tolerance 

development. 

The concept of ‘Universal Precautions’ presents a 

standardized approach to assessment and treatment in 

order to optimize benefits and reduce risks, but may be 

difficult to implement due to limited local availability of 

multi-modal treatment resources. Some clinicians have 

successfully demonstrated these principles in novel 

approaches to managing patients with aberrant drugrelated 

behaviours. 

Brief screening tools for risk stratification have 

been published but have limited evidence due to 

methodological limitations of the research. Written 

opioid prescribing agreements are universally 

recommended but not all clinicians agree with their use 

and most published examples are written in language 

that is too high a reading level for a number of patients. 

Likewise, periodic urine drug testing is recommended as 

a monitoring technique, but urine is not the ideal testing 

substance due to technical lab issues and the increased 

susceptibility to tampering. 

Patients on OAT for addiction will periodically develop 

acutely painful conditions which require treatment. 

Undertreated acute pain is a stressor which can trigger 

a return to substance misuse behaviour. On the other 

hand, patients in good recovery from addiction may 

be fearful of exposure to opioids for pain. A careful 

approach to assessment and treatment along with good 

communication can provide humane treatment for pain 

along with reduced risk for relapse. 

By incorporating fundamental concepts from addiction 

medicine into a structured approach to patient 

assessment and treatment, the clinician can optimize 

the benefits and reduce the risks of chronic pain 

management, even in high risk individuals. 

22 


REFERENCES 

1. Arnold RM, Han PK, Seltzer D. Opioid contracts in chronic 

nonmalignant pain management: objectives and uncertainties. Am J 

Med. 2006 Apr;119(4):292-6. 

2. Blinderman CD, Sekine R, Zhang B, Nillson M, Shaiova L. Methadone 

as an analgesic for patients with chronic pain in methadone 

maintenance treatment programs (MMTPs). J Opioid Manag. 2009 

Mar-Apr;5(2):107-14. 

3. Chou R, Fanciullo GJ, Fine PG, Miaskowski C, Passik SD, Portenoy 

RK. Opioids for chronic noncancer pain: prediction and identification 

of aberrant drug-related behaviors: a review of the evidence for an 

American Pain Society and American Academy of Pain Medicine 

clinical practice guideline. J Pain. 2009 Feb;10(2):131-46. Review. 



Pain Med 2005;6:107-112. 

5. Jovey RD. Managing acute pain in the opioid-dependent patient. 

Proceedings of the 11th World Congress on Pain, edited by Herta Flor, 

Eija Kalso, and Jonathan O. Dostrovsy, IASP Press, Seattle, 2006 

6. Meghani SH, Wiedemer NL, Becker WC, Gracely EJ, Gallagher RM. 

Predictors of Resolution of Aberrant Drug Behavior in Chronic Pain 

Patients Treated in a Structured Opioid Risk Management Program. 

Pain Med. 2009 Jun 11. [Epub ahead of print] 

7. Manchikanti L, Atluri S, Trescot AM, Giordano J. Monitoring opioid 

adherence in chronic pain patients: tools, techniques, and utility. Pain 

Physician. 2008 Mar;11(2 Suppl):S155-80. 

8. Nafziger AN, Bertino JS Jr. Utility and application of urine drug 

testing in chronic pain management with opioids. Clin J Pain. 2009 

Jan;25(1):73-9. 

9. Passik SD. Issues in long-term opioid therapy: unmet needs, risks, and 

solutions. Mayo Clin Proc. 2009 Jul;84(7):593-601. 

10. Rosenblum A, Joseph H, Fong C, Kipnis S, Cleland C, Portenoy RK. 

Prevalence and characteristics of chronic pain among chemically 

dependent patients in methadone maintenance and residential 

treatment facilities. JAMA. 2003 May 14;289(18):2370-8. 

11. Roskos SE, Keenum AJ, Newman LM, Wallace LS. Literacy demands 

and formatting characteristics of opioid contracts in chronic 

nonmalignant pain management. J Pain. 2007 Oct;8(10):753-8. 

12. Savage SR, Joranson DE, Covington EC, Schnoll SH, Heit HA, Gilson 

AM. Definitions related to the medical use of opioids: evolution 

towards universal agreement. 

J Pain Symptom Manage. 2003 Jul;26(1):655-67. 

13. Savage SR, Kirsh KL, Passik SD. Challenges in using opioids to treat 

pain in persons with substance use disorders. Addict Sci Clin Pract 

June 2008 pp 4-25. 

14. Wallace LS, Keenum AJ, Roskos SE, McDaniel KS. Development and 

validation of a low-literacy opioid contract. J Pain. 2007 Oct;8(10):759- 

66. Epub 2007 Jun 13. 

15. Wiedemer NL, Harden PS, Arndt IO, Gallagher RM. The opioid 

renewal clinic: a primary care, managed approach to opioid therapy 

in chronic pain patients at risk for substance abuse. Pain Med. 2007 

Oct-Nov;8(7):573-84. 

23

Predictors of Persistent Pain 

after Trauma 


Royal Melbourne Hospital, VIC 

The emergence of persistent pain after serious injury 

provides an opportunity for the triage of high risk 

patients to early intervention programs in order to 

improve long term outcomes. In order for triage to 

occur, a method is required for identifying high risk 

patients using measures available at or around the time 

of injury. To date, although range possible risk factors 

for persistent pain have been identified, no prospective 

studies have tested these factors concurrently. In order 

to determine the degree to which persistent pain can 

be predicted at the time of injury and to identify the 

individual risk factors a 12 month prospective cohort 

study of patients following serious injury was conducted. 

METHOD 

The study recruited patients admitted to RMH and Alfred 

Hospitals with injury between Oct 2006 and March 

2008. Eligible patients underwent a comprehensive 

physical and psychological assessment and were 

followed up at 3 and 12 months. 

RESULTS 

Two hundred ninety patients were recruited and 233 

patients followed up at twelve months. At 12 months 

the majority of patients (71.2%) reported some pain, 

and 14.6% reported moderate or severe pain. Five 

independent factors predicted the presence of moderate 

or severe pain at 12 months: 

• Not working at time of injury 

• Pain at initial assessment 

• Injury severity - AIS total 

• Initial pain control cognitions 

• Compensable injury. 

These factors combined to be able to predict of most 

(80%) of patients with moderate or severe pain with 

a specificity of 70%. 

CONCLUSIONS 

Injury leading to admission to a trauma hospital is 

associated with significant pain at 12 months. The 

presence of moderate or severe pain at 12 months can 

be predicated by 5 factors. The application of these 

factors allows for the division of injured patients into 

a low risk group and a high risk groups. A third of the 

high risk group will go on to develop persistent pain. 

The identification of a high risk group provides the 

opportunity of targeted early intervention to reduce 

chronic pain. 

24 


Procedural Pain Analgesia 



INTRODUCTION 

Procedural pain may be difficult to manage, especially 

in burns patients where there is a period of an 

intensely painful stimulus over and above the patient’s 

background pain. This period may also continue into 

the post-procedure period. Adequate and effective 

management of analgesia in this period is essential in 

order to prevent wind up and the psychological stress 

that may accompany poorly managed analgesia. 

SCOPE OF PRESENTATION 

This presentation will focus mainly on the treatment 

of procedural pain related to burns patients. Most of the 

content will deal with our experience from managing 

burns patients from the Black Saturday fires in 

February 2009. 

Procedural pain is often undertreated with a large 

percentage of burns patients reporting severe pain 

during the procedure 1 . Effective analgesia is required 

to facilitate burns dressings changes, staple removal, 

physiotherapy and occupational therapy as well as 

to reduce anxiety during the procedure. This should 

be achieved without producing excessive respiratory 

depression. Analgesia should be administered by 

a practitioner who is skilled in dealing with the 

consequences which can occur (eg airway obstruction) 

after administration of these drugs. 

Analgesia should also cover the post procedure period. 

Maintaining continuity of a successful procedural 

analgesic plan amongst anaesthetists and nursing staff 

is essential. 

In our institution, analgesia for burns dressings changes 

is administered either by nursing staff (in ICU or 

on the burns ward), or by an anaesthetist when the 

analgesic requirement requires much larger doses 

of analgesics to be administered. When analgesia is 

administered by nursing staff, a prior analgesic plan is 

drawn up in consultation with the Acute Pain Service. 

Our pain service has well established protocols 

for management of procedural analgesia for burns 

patients. Patients are administered a loading dose of 

intravenous morphine or oral oxycodone fifteen or 

thirty minutes respectively prior to the commencement 

of the procedure. This dose is based on the patient’s 

background analgesic requirements. 

During the procedure, intravenous opioid therapy 

administered by anaesthetic or nursing staff remains 

the mainstay of analgesia 2 . This is supplemented with 

a ketamine/midazolam combination and propofol 

in order to minimize opioid requirements and to 

provide sedation 3 . When the abovementioned regime 

is suboptimal, we have found that an intravenous 

lignocaine infusion 4 commenced 1 hour prior to the 

procedure and continued for 4 hours post procedure 

has been effective despite a Cochrane review suggesting 

that more trials are required to determine the efficacy 

of this drug 5 and a recent trial possibly refuting its use 

for this purpose 6 . 

Breakthrough analgesia after the procedure is provided 

with morphine boluses and ketamine when required. 

Patients who have dressings changes as outpatients 

are often administered inhaled Penthrane (Penthrox ® ) 

by nursing staff. 

The evidence for the use of the above agents as 

well as alternative methods of administration (PCA, 

intranasal, topical routes), will be reviewed. The use of 

other agents such as nitrous oxide, dexmedetomidine, 

hydromorphone, ketamine lozenges and regional 

anaesthesia will also be covered. 

CONCLUSIONS 

Effective management of procedural pain analgesia 

requires a multimodal and multidisciplinary approach 

in order to obtain the best patient outcomes. 

REFERENCES 

1. Ashburn MA (1995) Burn pain: the management of procedure-related 

pain. J Burn care Rehabil 16(3 pt 2):365-71 

2. Linneman PK et al (2000) The efficacy and safety of fentanyl for the 

management of severe procedural pain in patients with burn injuries. 

J Burn Care Rehabil 21(6):519-22 

3. Gregoretti C et al. (2008) Analgo-sedation of patients with burns 

outside the operating room. Drugs 68(17):2427-43 

4. Jonsson A et al. (1991) Inhibition of burn pain by intravenous 

lignocaine infusion. Lancet 338 (8760):151-2 

5. Wasiak J et al. (2007) Lidocaine for pain relief in burn injured patients. 

Cochrane Database Syst Rev (3):CD005622 

6. Wasiak J (2009). Personal communication 

25

Psychological Adjuncts for Pain 

Occurring with Dressing Changes 

in Burns Patients 



Burns injuries have wide ranging ramifications, which 

include the potential for severe and persistent pain and 

psychological sequelae. 

The prospect of multiple burns dressings changes can 

heighten pain through repeated stimulation of pain 

pathways and add to existing anxiety. Post traumatic 

stress disorder is a common accompaniment to burns 

injury with a prevalence of 11-50% 1 . 

Adjunctive psychological therapies are a logical 

accompaniment to analgesic therapies in the setting 

of burns dressings changes. Such therapies include 

pharmacological management with benzodiazepines 

or reliance on the sedating effects of opioids or a 

range of nonpharmacological therapies. These include 

cognitive techniques to provide distraction or redirect 

patient attention to more relaxing themes, behavioural 

techniques modelled on principles of conditioning or 

autonomic feedback, detailed education to help patients 

anticipate potentially stressful moments, alternative 

medicine and hypnosis 2 . Recent developments 

have made it possible for virtual reality technology 

to incorporate themes of relaxation, hypnosis and 

distraction allowing for potent visual and auditory 

cues to guide therapies. 

Current research examining the role for psychological 

interventions is currently dominated by case reports 

attesting to improved pain scores 3,4,5,6,7,8 . Larger studies 

which include some randomized controlled trials have 

provided more conflicting results 9,10 . 

Clearly the potential for psychological therapies to 

improve patient outcome is not questioned, but the ideal 

indications and best timimg still need to be resolved 

and confirmed scientifically. 

REFERENCES 

1. Bauer KM, Hardy PE, Van Dorsten B. Posttraumatic stress disorder in 

burn populations. A critical review of the literature. J Burn Care Rehabil 

19: 230-240, 1998 

2. Summer GJ, Puntillo KA, Miaskowski C, Green PG, Levine JD. 

Burn injury pain: The continuing challenge. J Pain 8(7): 533-548, 2007. 

3. Edwin DM. Emergency room hypnosis for the burned patient. 

Am J Clin Hypn 29(1): 7-12, 1986. 

4. Edwin DM. Emergency room hypnosis for the burned patient. 

Am J Clin Hypn. 26(1); 5-8, 1983 

5. Hammond DC, Keye WR, Grnat CWJr. Hypnotic analgesia with burns: 

an initial study. Am J Clin Hypn 26(1): 9-15, 1983. 

6. Margolis CG, Domangue BB, Ehleben C, Shrier L. Hypnosis in the 

early treatment of burns: a pilot study. Am J Clin Hypn 26(1): 9-15. 

7. Patterson DR, Everett JJ, Burns GL, Marvin JA. Hypnosis for the 

treatment of burn pain. J Consult Clin Psychol 60(5): 713-717, 1992. 

8. Wright BR, Drummond PD, Rapid induction analgesia for the 

alleviation of procedural pain during burn care. 

Burns 26: 275-282, 2000. 

9. Frenay M, Faymonville M, Devlieger S, Albert A, Vanderkelen A. 

Psychological approaches during dressings changes of burned 

patients: a prospective randomized study comparing hypnosis against 

stress reducing strategy. Burns 27(8): 793-799, 2001. 

10. Konstantatos AH, Angliss M, Costello V, Cleland H, Stafrace S. 

Predicting the effectiveness of Virtual Reality relaxation on pain 

and anxiety when added to PCA Morphine in patients having burns 

dressings Changes. Burns (35) 491-499, 2009 

26 


Australia’s Worst Bushfire Disaster: 

The Medical Response 

to Victoria’s Black Saturday 



“The rich plains, denied their beneficent rains, lay bare 

and baking; and the forests, from the foothills to the alpine 

heights, were tinder. The soft carpet of the forest floor was 

gone; the bone-dry litter crackled underfoot; dry heat and 

hot dry winds worked upon a land already dry, to suck 

from it the last, least drop of moisture.” 

After years of drought, south-eastern Australia suffered 

under days of record heat during January, 2009. A day 

of unprecedented weather was predicted for February 

7th. The premier was warning of the ‘worst day in 

Victoria’s history’. 

The worst bushfires in Australia’s history took place 

that day – Black Saturday. 172 people were killed, and 

a firefighter was fatally injured in the subsequent weeks. 

The extreme weather conditions played havoc with 

‘normal’ aeromedical work. With ambulance planes 

and helicopters unable to fly, critically ill patients were 

unable to be readily evacuated to Melbourne’s intensive 

care units. As fires threatened and then closed major 

highways to the North and East, road transport was 

removed as an option. Then a major regional hospital 

had fires only 2km away. 

With the evening approaching, it was becoming clear 

that not only were major parts of the state ablaze, 

but that many of these were in areas with significant 

populations. Small townships on the urban fringe were 

under threat, or had in fact already been attacked. The 

Coordinator for the Field Emergency Medical Officer 

Program, part of the State Health Emergency Response 

Plan, was activated, subsequently arranging for disaster 

medicine specialists to be in the field the night of 

Black Saturday. These doctors worked with ambulance 

paramedics, first aid organisations and other volunteers. 

The flow of information was chaotic, hindered by the 

speed with which events were unfolding and the loss 

of communications infrastructure. 

The Alfred houses Victoria’s Adult Burns Unit, and is 

one of two adult major trauma centers. The Alfred didn’t 

have any information on potentially how many burns 

patients there would be, so the plan was to basically 

take all patients with more than 30 percent burns and 

anything that wasn’t quite so severe went to one of the 

other major hospitals. Another procedure that was put 

in place was for the Alfred to only receive burns patients 

and the Royal Melbourne Hospital to receive all other 

trauma patients. Other adult hospitals in Melbourne 

were planned to receive everything else. 

The Alfred staff coped fairly well with the burns crisis. 

One intensivist said it was actually easier than some 

Saturday nights. The Alfred put 10 patients through 

ICU and about another 10 into wards, and yet still had 

ICU bed capacity by Monday morning. Within 36 hours, 

despite the influx of major burns, they had created 

ICU capacity. 

Extra staff were called in and The Alfred basically ran 

two burns theatres all day Sunday, Monday and Tuesday 

and then ran one burns theatre for the rest of the week. 

Normally there would have burns theatres running for 

only three half days a week. 

The Burns Unit had the experience of dealing with 

some of the survivors of the Bali Bombings. They paced 

themselves a bit more, so they didn’t run themselves 

into the ground. The great thing was that everyone was 

willing to help. Every department went out of its way to 

work extraordinarily well together and show good will. 

As the initial response moved from the field to hospitals, 

and although the bushfires had subsided, it was thought 

people from isolated areas would start presenting with 

injuries. A medical presence was needed. 

Some aspects of the extended response weren’t as 

considered. If there was a need, it was met, but some of 

it wasn’t explicitly planned for. To have so many people 

affected and the destruction of infrastructure over 

such a large area was unimaginable. The general practice 

in Marysville was burnt out and the whole town was 

basically inaccessible. The pharmacist in Yea was busy 

defending his house and in Alexandra, one of the GPs 

was defending his house while another was missing for 

a period of time. So instead of having four GPs they were 

down to one. Medical teams supported communities 

including Kinglake, Alexandra, Eildon, Flowerdale, Buxton 

and Narbethong. This was facilitated by DHS, RWAV and 

RDNS, and also included medical and nursing staff from 

many metropolitan and regional hospitals. 

Black Saturday wasn’t specifically a burns response but 

a mass casualty incident with multiple victims that 

needed people with expertise and experience in dealing 

with multiple patients at the same time. 

“These dreadful expectations were matched by the 

calamity that resulted on 7 February.” 

REFERENCES 

1. Interim Report, 2009 Victorian Bushfires Royal Commission 

2. Judge Stretton, 1939 Royal Commission 

27

PBLD 01 

Implementing a Preventative Strategy 

in Acute Pain 


Royal Melbourne Hospital, VIC 

CASE PRESENTATION 

30 yr female with persistent wrist and hand pain 

presents for carpel tunnel release and removal of 

hardware. She describes a history of a MVA with open 

radial fracture, requiring an ORIF one year previously. 

This surgery was complicated by severe post 

operative pain and oedema, requiring POP split, and 

slow subsequent rehabilitation. Current medications 

included Oxycontin 40 mg BD and Gabapentin 

300 mg bd. 

REFERENCES 

1. Brill S et al. Perioperative management of chronic pain patients with 

opioid dependency. Current Opin Anaesth 2006; 19: 325 

2. Janig W & Baron R. Complex regional pain syndrome: mystery 

explained? The Lancet Neruology 2003; 2: 687 

3. Kehlet H, Jensen T & Woolf C. Persistent postsurgical pain: risk factors 

and prevention. The Lancet 2006; 367: 1618 

4. Tippana E et al. Do surgical patients benefit form perioperative 

gabapentin/Pregabalin? Anesth Analg 2007; 104: 1545 

5. White P. Multimodal analgesia: its role in preventing postoperative 

pain. Current Opin Investigational Drugs 2008; 9: 76 

OBJECTIVES 

At the conclusion of the PBLD, the participant should 

be able to: 

• Accurately identify and assess patients pre-operatively 

with regards to their potential to have poorly controlled 

post operative pain or persistent pain 

• Understand pertinent issues with regards to chronic 

opioid use 

• Design and implement a persistent pain “preventative” 

strategy 

• Have a clearer understanding of CRPS 

28 



Office Based Pain Management – 

Optimising Outcome, Reducing Risk 




TOPIC SUMMARY 

This topical session will review the practical aspects 

of an office-based chronic pain assessment, including 

screening and risk stratification, using standardized 

tools, to develop a risk-based treatment plan. The needs 

of a low risk older patient with osteoarthritis and a 

high risk patient with back pain will be compared and 

contrasted. The concepts of ‘Universal Precautions’ will 

be applied and time efficient strategies for essential 

outcome documentation illustrated. 


Using case vignettes, participants will discuss practical 

assessment and treatment issues in chronic pain 

management that: 

1. define a standardized approach to assessment using 

validated tools; 

2. optimize pain management outcomes; 

3. reduce pain management risk; 

4. ensure essential documentation 

REFERENCES 

1. Chou R, Fanciullo GJ, Fine PG, Adler JA, Ballantyne JC, et al. American 

Pain Society-American Academy of Pain Medicine Opioids Guidelines 

Panel. Clinical guidelines for the use of chronic opioid therapy in 

chronic noncancer pain. J Pain. 2009 Feb;10(2):113-30. 



Pain Med 2005;6:107-112. 

3. Smith HS, Kirsh KL. Documentation and potential tools in long-term 

opioid therapy for pain. Anesthesiol Clin. 2007 Dec;25(4):809-23, vii. 

4. The Royal Australasian of Physicians. Prescription Opioid Policy. 

Improving management of chronic non-malignant pain and prevention 

of problems associated with prescription opioid use. 

Sydney April 2009. 

29

PBLD 02 

Cessation of Established Intrathecal 

Analgesia in Persistent Non-Cancer Pain 

Dr Chris Hayes 

Hunter Integrated Pain Service, NSW 

OBJECTIVES 

1. To analyse the evidence in regard to effectiveness 

of intrathecal therapy in persistent non cancer pain. 

2. To weigh potential benefit and harm from 

intrathecal therapy. 

3. To discuss the feasibility of ceasing established 

intrathecal therapy. 

4. To formulate a broad based management plan 

appropriate to the care of a patient undergoing 

intrathecal cessation. 

BRIEF CASE OUTLINE 

A 47 year old man has been on established intrathecal 

therapy with hydromorphone and clonidine for 5 years. 

This is directed at the management of persistent low 

back pain previously unresponsive to 3 spinal surgical 

procedures and oral opioids. Some modest benefits 

had been reported with initiation of intrathecal therapy. 

However these benefits had not been sustained. 

He had undertaken a group pain management program 

but had not effectively engaged with the process. 

Where to next? At a team case discussion a number of 

options were debated including escalating the intrathecal 

dose or alternatively working toward cessation of 

intrathecal therapy altogether. What view would you 

express if you were in attendance at this meeting? 

QUESTIONS 

1. What benefit is to be expected from intrathecal therapy 

for persistent non cancer pain? 

2. What harm can occur from intrathecal therapy? What 

mechanisms are involved? 

3. Is cessation of intrathecal therapy feasible? How would 

you go about this process? 

4. Can intrathecal cessation be used to motivate greater 

engagement with active management? 

REFERENCES 

1. Turner JA, Sears JM, Loeser JD. Programmable intrathecal opioid 

delivery systems for chronic noncancer pain: a systematic review 

of effectiveness and complications. Clin J Pain 2007;23(2):180-194 

2. Molloy AR, Nicholas MK et al. Does a combination of intensive 

cognitive-behavioral pain management and a spinal implantable 

device confer any advantage? A preliminary examination. Pain Pract. 

2006;6(2):96-103 

3. Hutchinson MR, Watkins L et al. Opioid-induced glial activation: 

mechanisms of activation and implications for opioid analgesia, 

dependence, and reward. Scientific World Journal 2007;7:98-111 

30 



Community Management of Intrathecal 

Infusions for Cancer 

Ms Dale Long 

Peter MacCallum Cancer Centre, VIC 

Dr Brett Todhunter 

Wodonga Regional Health Service, VIC 

80-90% of cancer pain can be controlled without the 

need for an interventional technique. 

There are however a significant number of patients who 

require an interventional technique, the commonest 

of which is an intrathecal infusion. This technique should 

be considered before patients are escalated to industrial 

but ineffective doses of opioids and other medications 

and/or are showing obvious signs of drug toxicity. 

This session will discuss Intrathecal Infusions, 

in particular their management in the community. 

At the conclusion of what will be an interactive 

session, participants will: 

1. know when to consider intrathecal infusions. 

2. be aware of the indications/contraindications and 

risk vs benefit issues. 

3. be able to participate in the multidisciplinary 

(pain physician/neurosurgeon, domiciliary palliative 

care service, GP, patient and family) management 

of intrathecal infusions. 

4. Have a clear concept of the possible techniques, 

equipment and drugs used. 

5. Be able to identify any problems encountered in the 

community and their management including when 

to seek advise, and 

6. Be able to apply the knowledge learnt towards 

developing a comprehensive policy for the management 

of intrathecal infusions in the community. 

REFERENCES 

1. Peter S Staats. “Complications of Intrathecal Therapy”. Pain Medicine. 

Vol 9 Number S1. 2008 pp 102-107. 

2. D. Kedlaya, L. Reynolds, S. Waldman. “Epidural and Intrathecal 

Analgesia for Cancer Pain”. Best Practice and Research: Clinical 

Anaesthesiology and Pain Management State of the Art. 2002 Vol 16 

No. 4 pp 651-665. 

3. Neural Blockade in Clinical Anaesthesia and Management of Pain. 

2nd Edition. Cousins and Bridenbaugh. pp 1004-1015. 

4. Cousins K, Duggan G et al. Intrathecal catheters: developing 

consistency in filter use and dressings in Perth, Australia. International 

Journal of Palliative Nursing 2003, Vol 9, No 7. 

5. Gestin Y, Vainio A and Pegurier A M. Long term intrathecal infusion 

of morphine in the home care of patients with advanced cancer. 

Acta Anaesthesia Scand 1997; 41:12-17. 

31

PBLD 03 

Management of Ischaemic Limb Pain 


Western Health Service, VIC 

THE SCENARIO 

John is a 55 year old man with Berger’s disease who is 

experiencing severe pain in his foot in association with 

ischaemic ulcers and is begging for more pain relief; 

when you meet him he is rocking to and fro whilst 

rubbing his painful foot. What challenges await in the 

management of this man’s pain and how might one 

proceed? 

LEARNING OBJECTIVES 

The attendee will learn that the management of 

ischaemic limb pain is complex. Complications of 

polypharmacy and barriers to pain managment will be 

discussed as will possible solutions to these barriers. 

32 



Incident/Procedural Pain Management 

without an IV 

Dr Chui Chong 

Royal Perth Hospital, WA 




Southern Health and Monash University, VIC 

Dr Odette Spruyt 

Peter MacCallum Cancer Center, VIC 

Ms Jill Woods 


This workshop may well take staff used to the critical 

care environment outside their comfort zone. It aims 

to show how it is possible to provide rapid, onset, 

short duration but intensive analgesia for eg. bed sore 

dressings, positioning for radiotherapy and significant 

incident pain in patients with bony metastases in 

hospices or nursing homes. 

It will inform participants of needle free alternatives to 

the IV bolus dosing or IV PCAs used by anaesthetists 

in acute hospital wards or procedure rooms. 

The two techniques presented will be transmucosal drug 

administration and the use of methoxyflurane analgesia 

via a Penthrox inhaler. At the end of the workshop 

participants will: 

1. understand the analgesic as distinct from the 

anaesthetic use of drugs such as ketamine and 

methoxyflurane. 

2. understand the principles and practice of transmucosal 

drug delivery 

• the physiochemical properties needed for effective 

transmucosal delivery 

• drug selection 

• the different techniques 

• sublingual drugs 

• buccal lozenges 

• intranasal spray delivery 

3. the how/when/why of using a Penthrox inhaler 

4. be able to develop protocols using one or other of these 

techniques to improve the care of patients undergoing 

painful procedures or with severe incident pain thus 

improving the quality of life for patients in hospices, 

nursing homes and indeed at home. 

REFERENCES 

1. Zeppetella G, Ribeiro MD. Opioids for the management of 

breakthrough (episodic) pain in cancer patients. Cochrane Database 

Syst Rev 2006; (1): CD004311. 

2. Good P, Jackson K, Brumley D, Ashby M. Intranasal sufentanil 

for cancer associated breakthrough pain. 

Palliative Medicine 2009; 23:54-58. 

3. Carr D.B, Goudas L, Denman W et al. Safety and efficacy of intranasal 

ketamine for the treatment of breakthrough pain in patients with 

chronic pain: a randomized, double-blind, placebo-controlled, 

crossover study. Pain 2005; 108: 17-27. 

4. Chong C, Schug S, Page-Sharp M et al. Development of a sublingual/ 

oral formulation of ketamine for use in neuropathic pain. 

Clinical Drug Investigation 2009; 29(5): 317-324. 

5. Romagnoli A, Busque L, Power DJ. The “Analgizer ® ” in a general 

hospital: a preliminary report. Can Anaesth Soc J 1970;17(3):275-8 

6. Chin R, McCaskill M, Browne G, Lam L. A randomised control trial of 

inhaled methoxyflurane pain relief, in children with upper limb fracture. 

J Paediatr Child Health 2002;38(5):A13-A14 

33

PBLD 04 

A Case of Recurrent Acute on Chronic 

Visceral Pain – Here Pancreatitis – How 

to Balance Analgesia with Concerns about 

Opioid Usage 

Dr Winnie Hong 

Concord Repatriation General Hospital, NSW 

You are asked to manage a 42 year old woman with 

a history of chronic pancreatitis who presents with an 

exacerbation of abdominal pain and normal amylase. 

She has been admitted and treated with parenteral 

opioids over the weekend, and is demanding better 

analgesia. 


At the conclusion of this PBLD session, the participant 

should achieve the following: 

1. Differentiate between acute and chronic pain 

presentations, the different approaches utilized and 

the potential overlap of these 

2. Define specific pathophysiological processes relevant 

to treatment of pain in chronic pancreatitis 

3. Appreciate issues important in treating the opioid 

dependent patient with a painful condition 

4. Develop a strategy to treat opioid resistant pain 

5. Utilise a comprehensive multidisciplinary approach 

to treat chronic visceral pain 

SELECTED REFERENCES 

1. Perioperative management of acute pain in the opioid dependent 

patient. Mitra, Sinatra. Anesthesiology. Vol 101 (1) July 2004, 212-227. 

2. Chronic Pancreatitis:- the perspective of pain generation by immune 

interaction. Sebastiano et al. Gut. Vol 52 (6), June 2003, 907-911. 

3. Opioid –induced Hyperalgesia. Angst, Clark. Anesthesiology Vol 104 

(3) Mar. 2006, 570-587. 

4. Gabapentin prevents delayed and long lasting hyperalgesia induced by 

fentanyl in Rats. Van Elstraete et al. Anesthesiology Vol 108 (3), 

Mar 2008, 484-494. 

5. Oral methadone for chronic noncancer pain: A systematic literature 

review of reasons for administration, prescription patterns, 

effectiveness and side effects. The Clinical Journal of Pain. Sandoval 

et al. Vol 21 (6), Nov/Dec 2005, 503-512. 

34 



Getting to Opioid Detoxification, Part 1. 

Preparing the Patient: 3 Approaches 

Dr Robert Brzozek 

Health Services Group of TAC and Worksafe, VIC 



Dr Lisa Sherry 

Health Services Group of TAC and Worksafe, VIC 



The initial part of this will be looking at the use of opioid 

medication in compensable patients. This will be looking 

at it from the Transport Accident Commission and Work 

Safe Victoria perspective. The presentation will also look 

at the intersection between the monitoring roles and 

the Federal and State governments and the insurers in 

addition to providing in sighted in-house clinical panel 

approaches to the operation of injured workers. 

This presentation will be given by Dr Lisa Sherry and 

Dr Robert Brzozek, both of whom work as clinical 

advisers to the Health Services (TAC and WorkSafe 

Victoria). 

The second of this will be the presentation by Helen 

Sweeting. Her presentation is more clinically based 

looking at addressing issues arising when considering 

opioid withdrawal from patients. Her presentation will 

outline why opening the draw may be important, how it 

is negotiated and the potential difficulties with a service 

delivery for opioid withdrawal and expected outcomes 

from opioid withdrawal. 

The third part of the presentation will be Dr Tobie 

Sacks, Psychiatrist. Dr Sacks will outline his view as 

a psychiatrist and pain specialist in his approach to 

dealing with patients on complex opioid medication 

regimes and how he addresses the issue of drug 

detoxification. 

35

PBLD 05 

Issues to Consider with Conversion to 

Buprenorphine 



TITLES 

1. Buprenorphine as analgesia in comorbid chronic pain 

and opioid dependence. 

2. Conversion to buprenorphine in a hospital setting for 

a patient experiencing adverse effects of high dose 

methadone. 

3. Use of topical buprenorphine in a case of misuse 

of tramadol within the context of mild opioid 

neuroadaptation and chronic pain. 

OBJECTIVES 

At the end of the session the participant should be 

able to: 

1. Confidently initiate and titrate sublingual buprenorphine 

for managing chronic pain against a background of 

opioid dependence and mild neuroadaptation to opioids 

2. Confidently initiate and titrate sublingual buprenorphine 

in a hospital setting for managing chronic pain within 

the context of significant opioid neuroadaptation and 

comorbidity. 

3. Utilise acquired knowledge to use topical buprenorphine 

for managing dual chronic pain and opioid dependence 

REFERENCES 

1. Rolley et al (2005) Buprenorphine: Considerations for Pain 

Management , Journal of Pain and Symptom Management, 

Vol. 29 No. 3 pp 297 

2. Freye et al (2007) Opioid Rotation from High-Dose Morphine to 

Transdermal 

3. Buprenorphine (Transtec ® ) in Chronic Pain Patients, Pain Practice, 

Volume 7, (2) pp 123–129 

4. Malinoff et al, Sublingual Buprenorphine Is Effective in the Treatment 

of Chronic Pain Syndrome, American Journal of Therapeutics 12, 

pp 379–384 


Prescribing for Pain in the Elderly 

Assoc Professor Pam Macintyre 

Royal Adelaide Hospital, SA 

Professor Barbara Workman 

Monash University, Southern Healthcare Network, VIC 


At the conclusion of the topical session, the participant 

should be able to 

1. Describe the changes in pharmacokinetics and 

pharmacodynamics that occur as people age. 

2. Explain how these changes influence the prescribing 

of pain medications in the elderly. 

3. Apply new knowledge in pain assessment in the elderly. 

4. Describe some of the concepts in changed pain 

perception in the elderly. 

REFERENCES 

1. Macintyre PE & Upton R (2008) Acute pain management in the elderly 

patient. In: Clinical Pain Management: Acute Pain 2nd edn. Macintyre 

PE, Walker SM and Rowbotham DJ (eds). London, Hodder Arnold 

2. AGS Panel on Chronic Pain in Older Persons (1998) The Management 

of Chronic Pain in the Older Person, JAGS 46:635-651. 

3. Australian Pain Society (2005) Pain in residential care facilities. 

http://www.apsoc.org.au/news.php?scode=9e2c2n 

4. Australian and New Zealand College of Anaesthetists and Faculty of 

Pain Medicine (2005) Acute Pain Management: Scientific Evidence 3rd 

edition. http://www.anzca.edu.au/resources/books-and-publications/ 

(3rd edition in progress). Section 10.3 – Acute Pain in the Elderly. 

36 



Acute Pain Management for Orthopaedics. 

Managing the Pain and Fast Tracking the 

Rehabilitation of Patients Undergoing Knee 

or Hip Replacement 

Dr Charles Kim 

St Vincent’s Hospital and Melbourne Health, VIC 

Ms Cathy Senserrick 


Mr Andrew Shelton 



Austin Health and St Vincent’s Hospital, VIC 

Dr This workshop aims to address the many twists and 

turns involved in attempting to maximize post-operative 

analgesia and peri-operative care in order to improve 

the journey of patients requiring knee and hip 

replacements in Melbourne tertiary hospitals. This 

workshop has been developed by a team of health 

professionals with major input from Ms Anne Daly, 

Ms Narelle Peake and Ms Megan Yeomans with 

contribution from Professor Peter Choong. 

The speakers will describe: 

• The literature and evidence behind the analgesic choices 

to optimize rehabilitation 

• The gold standard physiotherapy required to optimize 

outcome and the available evidence available to support 

this and the barriers faced in achieving this 

• The analysis of nursing practice and care plans in order 

to improve the individual patient journey 

• How hospitals and government analyze outcome of joint 

replacements and the numerous variables involved in 

the interpretation of these figures 

There are many factors involved in determining the 

course of treatment for patients with severe knee and 

hip pathology referred for joint replacement. Whilst 

many analgesic techniques have been tried to aid the 

rehabilitation process such as epidural, continuous 

peripheral blockade, there is conflicting evidence as to 

whether such techniques alter the final outcome. Other 

factors that need to be considered are the status of the 

patient pre-operatively and whether physical therapy 

and education preparation is important. In addition 

ward culture may be of particular importance in 

determining how efficiently patients can be rehabilitated. 

It must not be forgotten that the surgeon can have a 

major influence on the overall journey of the patient. 

At the completion of the workshop, participants will: 

• Be able to describe the may factors influencing analgesic 

choice for knee and hip replacement, be cognisant of the 

evidence for use of these techniques and be confident to 

interpret this evidence 

• Appreciate that there are numerous non-analgesic 

factors influencing outcome 

• Be aware of interventions that health services are using 

to combat some of the barriers to efficient rehabilitation. 

• Be cognisant of the statistics that are kept by health care 

agencies and how these should be interpreted 

• Have an appreciation of surgical factors that may be 

of importance in improving outcome 

REFERENCES 

1. The Role of the Anesthesiologist in Fast-Track Surgery: From 

Multimodal Analgesia to Perioperative Medical Care; Paul F. White, 

, Henrik Kehlet, , Joseph M. Neal, Thomas Schricker, Daniel B. Carr, 

Franco Carli, MD, and the Fast-Track Surgery Study Group; Anesth 

Analg 2007;104:1380 –96 

2. PROSPECT: Providing evidence-based and procedure-specific 

recommendations and clinical decision support for the management 

of postoperative pain. www.postoppain.org 

3. The Effect of Single-Injection Femoral Nerve Block Versus Continuous 

Femoral Nerve Block After Total Knee Arthroplasty on Hospital Length 

of Stay and Long-Term Functional Recovery Within an Established 

Clinical Pathway; Francis V. Salinas, MD, Spencer S. Liu, MD, and 

Michael F. Mulroy, MD; (Anesth Analg 2006;102:1234 –9) 

4. Continuous Femoral Nerve Blockade or Epidural Analgesia After Total 

Knee Replacement: A Prospective RCT; Michael J. Barrington, David 

Olive, FANZCA, Keng Low,David A. Scott, ,Jennifer Brittain, and Peter 

Choong; (Anesth Analg 2005;101:1824 –9) 

5. Multimodal pain management after total hip and knee arthroplasty at 

the Ranawat Orthopaedic Center. Maheshwari AV, Blum YC, Shekhar L, 

Ranawat AS, Ranawat CS; Clin Orthop. 467(6):1418-23, 2009 June 

6. Continuous lumbar plexus block for postoperative pain control after 

total hip arthroplasty. A randomized controlled trial; Marino J, Russo 

J, Kenny M, Herenstein R, Livote E, Chelly JE Journal of Bone & Joint 

Surgery - American Volume. 91(1):29-37, 2009 Jan 

7. Multi-modal, pre-emptive analgesia decreases the length of hospital 

stay following total joint arthroplasty; Duellman Tj et al; Orthopedics. 

32(3):167, 2009 Mar 

37

8. Continuous lumbar plexus block provides improved analgesia 

with fewer side effects compared with systemic opioids after hip 

arthroplasty: a randomized controlled trial.Siddiqui ZI. Cepeda MS. 

Denman W. Schumann R. Carr DB. Regional Anesthesia & Pain 

Medicine. 32(5):393-8, 2007 Sep-Oct 

9. Effectiveness of accelerated peri-operative care and rehabilitation 

intervention compared to current intervention after hip and knee 

arthroplasty. A before-after trial of 247 patients with a 3-month followup; 

Kristian Larsen, Karen Elisabeth Hvass, Torben B Hansen, Per B 

Thomsen and Kjeld Søballe; BMC Musculoskeletal Disorders 2008, 9:59 

10. Pre-operative predictors of the length of hospital stay in total knee 

replacement; I. D. M. Smith,; R. Elton,; J. A. Ballantyne, and I. J. 

Brenkel, FRCSEd, J Bone Joint Surg Br 2008; 90-B: 1435-1440 

11. Targeted postoperative care improves discharge outcome after hip or 

knee arthroplasty,Leonie Oldmeadow et al 2004; Archives of Physical 

Medicine and Rehabilitation 85(9)1424-7 

12. Factors Influencing Early Rehabilitation After THA Systematic Review 

Vivek Sharma MD, Patrick M. Morgan MD, Edward Y. Cheng MD; Clin 

Orthop Relat Res (2009) 467:1400–1411 

13. Multidisciplinary rehabilitation programmes following joint 

replacement at the hip and knee in chronic arthropathy; Fary Khan, 

Louisa Ng, Senen Gonzalez, Tom Hale, Lynne Turner-Stokes Cochrane 

database of Systematic Reviews Year: 2008 

14. The effect of an educational program to improve health-related quality 

of life in patients with osteoarthritis on waiting list for total knee 

replacement: a randomized study. Nunez M, Nunez E, Segur JM, 

Macule F, Quinto L, Hernandez MV, Vilalta C: Osteoarthritis Cartilage 

2006, 14(3):279-285 

15. Effect of preoperative exercise on measures of functional status in 

men and women undergoing total hip and knee arthroplasty. Rooks 

DS, Huang J, Bierbaum BE, Bolus SA, Rubano J, Connolly CE, Alpert S, 

Iversen MD, Katz JN: Arthritis Rheum 2006, 55(5):700-708 

16. Pre-operative education for hip or knee replacement. McDonald S, 

Hetrick S, Green S 

17. Cochrane Database Syst Rev 2004, (1):CD003526 

38 



Detoxification Part 2 

How to do it: 3 Approaches 

Dr Charles Brooker 

Royal North Shore Hospital, NSW 



Dr Mike McDonough 


This session aims to examine the difficulties surrounding 

patients in whom inappropriate or unstable opioid use 

has developed. Cases will be presented highlighting 

successes and failures of detoxification approaches 

followed by a series of expert viewpoints of the 

appropriate detoxification techniques. 

Specific difficulties occur where opioid detoxification is 

viewed as an essential safety intervention in the ongoing 

management of the patient but the clinician’s view 

conflicts with the patient’s own desire to continue using 

opioids. Recent situations where this has been presented 

as a “human rights” issue will be discussed. 

Time will be allowed for an open forum discussion and 

participants can add to the quality of the discourse by 

understanding the legal and clinical obligations that may 

arise relating to their own specific practice. 

39

Notes 

40 


Organising Committee 

Dr Carolyn Arnold 



Dr Julia Fleming 



Dr Terry Lim 

Dr Clayton Thomas 

Convenor 

Co-Convenor 

Committee Member 






Conference Secretariat 

Christine Gill 

630 St Kilda Rd 

Melbourne VIC 3004 

Ph: +61 3 9510 6299 

Fax: +61 3 9510 6786 

Email: cgill@anzca.edu.au 

www.anzca.edu.au/fpm/events/2009springmeeting 

COMBINED CME SPRING MEETING • FACULTY OF PAIN MEDICINE, ANZCA • ACUTE PAIN SPECIAL INTEREST GROUP OF ANZCA, ASA AND NZSA 

• ACUTE PAIN SPECIAL INTEREST GROUP OF IASP

duelling with pain - Faculty of pain medicine - Australian and New ...

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