Pathologists happy with new deal but it’s ‘another blow for GPs’

GPs have expressed concerns over the Coalition’s announcement that it will cap rent on pathology collection centres.

The deal would take place under a returned Turnbull Coalition Government and will help reduce regulatory cost pressures on pathology providers to help them provide affordable services and maintain current bulk billing rates.

It’s a move that is supported by the Royal College of Pathologists of Australasia:

“The Coalition’s new proposed plans will see a delay in the changes to the bulk billing incentive, as well as a solution to the high cost of rents being paid for pathology collection centres. In addition there will be a moratorium for the next 3 years on any further changes to Pathology Services Table without agreement from the profession. The RCPA believes this will result in the profession maintaining the current billing practices and high quality services and efficiencies offered,” Dr Michael Harrison, President of the RCPA said.

However the Royal Australian College of General Practitioners says the changes are another blow to GPs, on top of the ongoing Medical Benefits Freeze.

“The RACGP has always supported universal access to healthcare services and therefore welcomes the announcement of continued bulk-billing arrangements for pathology services,” RACGP President Dr Frank Jones said.

“However, the proposed changes effectively create an anti-competitive environment, where multi-national corporations who make hundreds of millions of profit each year are propped up, while GPs running small businesses lose funding.”

AMA President Professor Brian Owler said the deal “doesn’t guarantee anything”.

“The cut to bulk billing incentives for pathology has merely been deferred. The cuts are still there, they’re still taking $650 million out of health over the next four years,” Professor Owler said.

He also said there is no guarantee that the pathologists will not abandon bulk billing.

When he spoke to Pathology Australia, they admitted they don’t have the ability to make that guarantee.

“It will be up to the individual pathology companies to actually make that decision over time,” he said.

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E-cigarettes most popular with young people

The use of e-cigarettes in New South Wales is highest in young people, however they are mostly using them less than weekly.

Research published in the Medical Journal of Australia found that 16% of respondents age 18-29 were currently using e-cigarettes.

Unlike older e-cigarette users, these respondents weren’t using the products to help them quit smoking. Instead they said it was because e-cigarettes tasted better and they could smoke them in places where cigarettes were banned.

The study found adults over the age of 55 were the most frequent users of e-cigarettes and those over 30 were more likely to use the products to help them quit tobacco.

Related: E-cigs: a help or a harm?

However researchers expressed concerns about this, saying many users in the sample were smoking both conventional and e-cigarettes.

“For avoiding the risks of smoking-related premature death, however, reducing cigarette numbers is much less effective than quitting, and future research should investigate whether tobacco smokers using e-cigarettes to cut down are doing so as part of a cessation strategy or in the hope of reducing smoking-related harm,” the authors wrote.

According to an accompanying editorial in MJA, there is a lack of evidence that e-cigarettes were any more effective than other unassisted cessation or conventional nicotine replacement therapies.

“A Cochrane review reported the evidence as being of ‘low/very low quality’, and a recent metaanalysis concluded that they, in fact, reduced the probability of quitting,” they wrote.

Recent statistics released by HealthStats NSW certainly seem to back up that evidence. According to new data, the 45-54 year old age bracket has seen tobacco smoking rates jump more than 2% in the last year.

While smoking rates overall have fallen in the last year from 15.6% to 13.5%, the results haven’t been seen in the older age groups.

Anita Dessaix, manager of Cancer Prevention at the Cancer Institute NSW told Fairfax media that older people would find it harder to quit as most took up smoking as teenagers.

“The message particularly for old people is not to despair and keep trying and that there is hope and support and that they can quit smoking,” Ms Dessaix said.

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How can we ensure that people with lung cancer living in rural and remote areas are treated surgically when appropriate?

We have the will to improve cancer services for patients outside major cities but, thus far, not the way

In 2012, 30% of the Australians newly diagnosed with cancers other than non-melanoma skin cancer lived in rural and remote areas. Some rural locations have visiting cancer specialists or outreach services, others have telemedicine available to assist local clinicians, but many subspecialty surgical services are located only in major cities. Therefore, to have their cancers adequately staged and, if suitable, to have potentially curative surgery, most rural and remote cancer patients will have to travel to see an appropriately specialised surgeon. It is necessary to centralise cancer care to make it possible to give patients access to the full range of clinical expertise and to provide the surgical services needed to achieve the best outcomes.1,2 This desired level of centralisation is rarely available except in major cities.

Using linked New South Wales cancer registry and admitted patients’ data and death records for the years 2000–2008, with geocoded residential and institutional addresses, we showed that patients with potentially curable non-small-cell lung cancer (NSCLC) who lived farthest from the nearest accessible hospital with a thoracic surgical service were the most likely to be admitted to a general rather than to a specialist hospital and, as a result, the least likely to have potentially curative surgery.3 Similar findings have been reported in other regions, for example, the East Anglian region of England. Moreover, in NSW, lack of surgical treatment fully explained the lower rate of survival from lung cancer observed in patients living farthest from an accessible thoracic surgical service.4 Thus, distance from specialised surgical services puts NSCLC patients at a significant disadvantage.

There is policy-level awareness of the disadvantage experienced by rural and remote cancer patients. Australia’s “National Strategic Framework for Rural and Remote Health” states that the goal of cancer care is to ensure that rural patients have increased access to diagnostic testing, coordinated care, multidisciplinary team review, patient accommodation, and appropriate medical oncology and radiotherapy services locally. To achieve this goal, the federal government has dedicated $1.3 billion in its budget not only to building two comprehensive cancer centres in Melbourne and Sydney but also to enhancing or building ten regional cancer centres. These developments should greatly improve cancer diagnosis in rural and remote areas and some aspects of cancer treatment, but they will not remove the need for some patients to travel for specialised surgical assessment and surgery.

In recognition of this need as it relates to lung cancer, the National Health Pathways initiative5 has, since 2013, included a detailed lung cancer referral pathway that provides general practitioners with up-to-date advice on the closest specialist cancer services so that rural patients are referred early and to the right place. While welcome, it will require much more than just publishing and promoting information to ensure reliable rapid referral of patients with NSCLC to specialist assessment and care. The NSW Ministry of Health’s planning for surgical services in greater Sydney6 and Rural Surgery Futures7 recommend that surgery be collocated with other specialist cancer services. While action on these recommendations may improve access to multidisciplinary care in general, it is unlikely to make highly specialised surgical care, such as thoracic surgery for lung cancer, more readily available in rural and regional areas, because of the large populations required to sustain such services.

There are guidelines and programs aimed at increasing early and appropriate surgical referral for cancer patients and some evidence that they work. For example, guidelines for recognition of and referral for suspected lung cancer of the United Kingdom’s National Institute for Health and Care Excellence (updated in 2015) recommend immediate referral if a chest x-ray suggests cancer or if someone aged 40 years or older has unexplained haemoptysis; and urgent chest x-ray if a person has two or more of, or has smoked and has one of, cough, fatigue, shortness of breath, chest pain or weight loss.8 Potentially more discriminating algorithms for urgent chest x-ray than these are being developed and evaluated.9 Recent evaluations of urgent referral initiatives in the UK suggest that they increase cancer detection rates, reduce delays in diagnosis and reduce the risk of death from cancer.10,11

In summary, available evidence suggests that people living remotely in Australia have poorer outcomes from NSCLC because they are often not referred to specialist thoracic surgical centres where their disease will be adequately staged and, if appropriate, they will be offered potentially curative surgery.

Australian health policy supports rapid referral of patients with suspected lung cancer for expert assessment. However, at present, there is a substantial lack of well organised processes to ensure that such patients are referred and assessed appropriately. This must change.

5th case of Legionnaires identified in Sydney

Two more people have been diagnosed with the potentially deadly Legionnaires’ disease after another outbreak was announced last week.

The men in their 40s and 50s were in the CBD at the same time as the other three patients identified.

The original cases included two women and an elderly man. A woman in her 30s is still in a critical condition in hospital.

According to the director of the NSW Health Communicable Diseases Branch, Dr Vicky Sheppeard, five cooling towers have tested positive to legionella however it’s possible that the actual source of the outbreak won’t be found as they may have already cleaned the building prior to authorities gaining access.

Related: Legionnaires strikes Sydney again

“We’ve already taken regulatory action against those five towers and ordered cleaning and disinfection,” Dr Sheppeard said. “We don’t believe there is an ongoing risk in the city of Sydney.”

The five people all spent time in the area of the city bordered by Market, George, King and Kent streets since Anzac Day.

Legionnaires is an infection of the lungs (pneumonia) that is caused by bacteria of the Legionella family which is caused by when a person breathes in the affected bacteria. Legionnaires disease most often affects middle-aged and older people, those who are heavy smokers or who have a chronic lung disease. People with suppressed immunity are also more at risk.

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Call yourself a cosmetic surgeon? New guidelines fix only half the problem

The dangers associated with cosmetic surgery, detailed in a report by the Health Care Complaints Commission in 1999, are well known and still present. The new cosmetic guidelines for doctors, published this week by the Medical Board of Australia, are welcome, but tackle only half the problem.

The guidelines for registered medical practitioners who perform cosmetic medical and surgical procedures cover all phases from patient assessment through to aftercare. They will be a valuable tool for cosmetic surgeons. But two areas of public concern – the use of the title cosmetic surgeon and the facility in which the surgery is performed – remain untouched.

Who is a cosmetic surgeon?

The public can be forgiven for thinking a person who calls themselves a cosmetic surgeon has surgical qualifications. But this is not the case. Any registered medical practitioner can use the title, even those without any specialist training.

The 1999 cosmetic surgery report recommended any medical practitioner performing invasive cosmetic surgical procedures should have adequate surgical training equivalent to that required for fellows of the Royal Australasian College of Surgeons.

It is unthinkable today that any registered doctor could start performing non-cosmetic surgical operations without qualifications from an accredited training body. But this remains permissible for surgery that is “cosmetic”, although cosmetic surgery is as complicated and risky as other forms of surgery.

The guidelines tackle this problem by recommending procedures should be provided only if the medical practitioner has the appropriate training, expertise and experience to perform the procedure and to deal with all routine aspects of care and any likely complications.

This guideline is steering doctors towards having appropriate qualifications and training. However, it stops short of mandating a minimum qualification. The decision as to the level of expertise or experience is left to the doctor.

The effect of not requiring a minimum surgical qualification or accreditation is that when doctors provide surgery without the required knowledge, expertise and experience, it will primarily leave patients responsible for bringing them to the medical board’s attention using the complaint system.

We know qualified surgeons also harm patients and generate complaints. But the fact that the public, in the case of qualified surgeons, can trust the level of training and supervision involved is some reassurance a minimum level of skill has been obtained.

The guidelines would have had more force, and offer more protection to the public, if the requirement was for any person who performs major cosmetic medical or surgical procedures to have a minimum qualification of general surgery awarded by an accredited training body.

Where is cosmetic surgery performed?

Doctors performing cosmetic surgery such as breast augmentations in their rooms, outside of a licensed hospital or day surgery centre, are prohibited from administering a general anaesthetic. They may only use conscious sedation – where medications to help patients relax and to block pain during a medical procedure are given. The patient stays awake but can’t usually speak.

This is because the real risks associated with general anaesthesia and unconscious patients require a properly equipped theatre and trained staff.

Cosmetic surgeons have been able to bypass this requirement and perform surgical procedures in unlicensed facilities because they use local anaesthetic agents and sedatives. Risks such as seizures, cardiac arrest and rapid heartbeat are associated with overdosing of local anaesthetic agents and sedatives.

Patients need to be still during any procedure. So, if a patient is moving about or agitated, additional local anaesthetic may be administered. But this could lead to an overdose, which is potentially fatal. Local anaesthetic overdose is a preventable adverse event, which can be avoided if the surgery is in a licensed facility with the equipment to manage an emergency.

Since March 2015, the Health Care Complaints Commission has identified 33 patients who had breast augmentation surgery where the level of sedation was of concern. Six had an adverse event associated with sedative drug combinations consistent with deep sedation – some even at the level of general anaesthesia.

The new guidelines require doctors to perform surgery in a facility that is appropriate for the level of risk involved in the procedure. Facilities should be appropriately staffed and equipped to manage possible complications and emergencies. The judgement as to risk and equipment is left to the doctor to decide.

Cosmetic surgeons have a significant conflict of interest – putting patient interest ahead of profits. The guidelines make clear cosmetic surgeons must place the safety of their patients first. But the Medical Board of Australia has no jurisdiction over facilities and cannot mandate the level of facility for major cosmetic medical and surgical procedures. Only the state and territory governments can do this.

The new guidelines present for the first time an opportunity to bring the cosmetic “industry” back into medicine – where ethical obligations to patients override profits. This is an important first step, but it cannot be the last.

Merrilyn Walton, Professor of Medical Education (Patient Safety), University of Sydney

This article was originally published on The Conversation. Read the original article.

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Probiotics – do they benefit healthy people?

A systematic review has found that probiotics have little effect on the gut microbiota of healthy people.

The study was undertaken by researchers at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen and published in Genome Medicine.

It involved a review of seven randomised controlled trials to investigate the effect of probiotics on the faecal microbiota of healthy adults. The probiotics products administered were biscuits, milk-based drinks, sachets, or capsules for periods of 21 to 42 days.

The researchers looked at reported effects on the overall structure of faecal microbiota including the number of species present, the evenness and whether the healthy people taking probiotics had different changes of bacteria living in their guts compared to the placebo groups.

Related: Patrick Charles: Power of poo

The researchers investigated the trials for reported effects of probiotics on the overall structure of the fecal microbiota of healthy adults, including the number of species present, the evenness (distribution of species within the populations) and whether the probiotics groups of study participants as a result of the intervention had different changes in bacteria living in their gut than the placebo groups.

“According to our systematic review, no convincing evidence exists for consistent effects of examined probiotics on fecal microbiota composition in healthy adults, despite probiotic products being consumed to a large extent by the general population,” PhD student and junior author Nadja Buus Kristensen said.

Of the seven original trials, only one found observed changes in the bacterial composition of faecal microbiota.

Related: John Dwyer: Promoting wellness

The authors note that various limitations include small sample size, use of different probiotic strains, variations of diet and variation in susceptibility of probiotics between individuals could mask the true impact of probiotic intake.

Oluf Pedersen, professor at the University of Copenhagen and senior author of the paper said: “While there is some evidence from previous reviews that probiotic interventions may benefit those with disease-associated imbalances of the gut microbiota, there is little evidence of an effect in healthy individuals. To explore the potential of probiotics to contribute to disease prevention in healthy people there is a major need for much larger, carefully designed and carefully conducted clinical trials. These should include ideal composition and dosage of known and newly developed probiotics combined with specified dietary advice, optimal trial duration and relevant monitoring of host health status.”

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New cosmetic surgery guidelines encourage cooling off periods

The Medical Board of Australia has introduced a range of new guidelines in a bid to crackdown on the cosmetic surgery industry.

The guidelines aim to inform medical professionals and the community about the expectations the Board has for doctors who perform cosmetic surgery procedures.

According to Board Chair, Dr Joanna Flynn, “The guidelines will help keep patients safe, without imposing an unreasonable regulatory burden on practitioners.”

Related: Delay implants, women advised

The 6 page guidelines were developed after draft guidelines were circulated in March 2015.

“The Board listened to stakeholder feedback, and responded with a new set of guidelines that will best keep patients safe,” Dr Flynn said.

“The changes prioritise patient safety and reduce some of the regulatory requirements proposed in the previous draft guidelines, when either there was no evidence of improved safety or the costs significantly outweighed the benefits of a proposal,” she said.

9 key points from the guidelines include:

There should be a 7 day cooling off period for all adults before any major procedure (anything that involves cutting beneath the skin);
Adult patients should be referred to a psychologist, psychiatrist or general practitioner if there are any indications of underlying psychological problems;
There should be a 3 month cooling off period for all under 18s before major procedures and a mandatory evaluation from a registered psychiatrist, psychologist or general practitioner;
There should be a 7 day cooling off period for all under 18s before minor procedures (cosmetic medical procedures that do not involve cutting beneath the skin but may involve piercing the skin);
The treating medical practitioner must take responsibility for any post-operative care;
The treating medical practitioner must make sure there are emergency facilities when using sedation, anaesthesia or analgesia;
There needs to be a mandatory consultation (either by person or by video conference) before medical practitioner prescribes schedule 4 cosmetic injectables;
Medical practioners need to provide detailed, written information to the patient to ensure they are making informed consent. Information should include the range of possible outcomes, complications and recovery times associated with the procedure and the qualifications and experience of the medical practioner;
Medical practitioners need to provide patients with detailed written information about costs including any costs for follow-up care or any potential revision surgery or treatment.

The new guidelines will take effect on 1 October 2016. Read the Cosmetic Surgery Guidelines.

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Tick a box – For the good of whom?

As a new intern, I am an infant in medicine and Indigenous medicine. I chose to study medicine because I wanted to work in the area of Indigenous social justice, with a particular interest in research and mental health. Seeing the medical world from a professional perspective has informally and formally educated me about Indigenous health, but also highlighted the ways that the health system can disempower and discriminate against Indigenous people. Although I currently have limited clinical experience in Indigenous health, I have a breadth of personal experience that I would like to share.

I identify with two Aboriginal communities from the north of Western Australia. On my father’s side the Palku people and on my mother’s side the Yindjibarndi people, who are both situated in the Pilbara region of Western Australia. Although I identify with both these communities, I have never lived in them, and grew up in Perth until high school when I moved to Sydney. I have always been proud of my heritage, keen to learn about it and tell others about it. Growing up in a Perth suburb where you and your brother are the only Indigenous students in your primary school however means I have always felt somewhat different. Despite this, being judged for being Indigenous and being a victim of racism has been a relatively uncommon experience in my life. This has been due to the fact that I do not fit the stereotype. I don’t look, speak and act as people expect of an Indigenous person. I have never thought of myself as, nor have been, disadvantaged: I went to a great school, my parents and family are all successful in their chosen careers and I have never gone without. Throughout my life I have found that many in Australian society equate being Indigenous with poverty and disadvantage, and therefore I do not fit the common stereotype of Aboriginality. Not being perceived as Aboriginal has been a challenge in medicine and my personal life because it means that people speak freely about Indigenous people in front of me, and say things they probably would not, if they knew I was Indigenous. I feel like a spy: secretly gathering racial intelligence in the medical world. This is equally true for my experience of seeing how doctors treat their Indigenous patients and my own experiences as an Indigenous patient.

Three years ago I took my nine-month-old daughter to the emergency department with a broken arm after she fell from a trampoline. It was one of those injuries every parent has a story about – one second of lapsed supervision leading to disaster. While in the waiting room I filled out the generic admission form and ticked the ‘Yes Aboriginal’ box. I did not hesitate. After all, why should it matter? There are posters everywhere about how knowing this information helps the hospital to treat you better and helps the health system by contributing to public health data. And I am proud to be Aboriginal. There is no reason to be ashamed. However during our admission my partner and I were interrogated multiple times about the circumstances of the injury, my GP to whom I had first presented was called to ask what kind of people we were and we were reported to the Department of Family and Community Services with a concern of child abuse. I felt my morals and parenting were judged. I felt that all my interactions with my daughter thereafter were being scrutinised. There was no single moment or comment that made me think the way we were treated was related to our Indigenous status but somehow I felt like it contributed. She had to have a cast which meant a lot of sleepless nights with a very annoyed child, but she recovered well. As for the report I assume it has been filed in a database, as we never had any other contact regarding the situation. I do not blame the doctor who was managing us. I know they were doing their job and in matters of child abuse nobody wants to miss something by under-calling a situation. But I did feel as if my, and my daughter’s Aboriginality, rather than our individual clinical picture, played too much into the decision to take that pathway, and I can’t help but wonder if things may have turned out differently if I hadn’t ticked that box.

Other members of my family and friends have had similar experiences: where they have felt their identification as Aboriginal impacted negatively on the perceptions of the professionals treating them or their children. Where parenting integrity has been called into question or our children are seen to be automatically disadvantaged because of their heritage. Where we are guilty until proven innocent. The overwhelming experience is one where we are left feeling either degraded and judged or pitied and patronised. This encounter made me reluctant to take my children to the emergency department for any reason after that, despite the fact that I have a positive view of the healthcare system. So I can easily see how someone who has been disenfranchised or experienced racism in other areas of their life, could easily become distrusting of health care institutions. In addition, when someone is encountering a system they do not know particularly well, it would be easy to attribute how you have been treated to your race, rather than thinking that this is just how everyone is treated in a similar situation.

National health guideline recommendations clearly encourage the use of standardised identification of Aboriginal and Torres Strait Islander clients in order to maximise the ability to collect reliable data about service delivery, service effectiveness and inform policies on healthcare strategy (Australian Institute of Health and Welfare, 2010). Nowhere in the recommendations is it suggested that a client’s identification as Indigenous should have a bearing on the treatment they are given and more specifically

‘the collection of Indigenous status as a routine administrative procedure does not in itself contravene a service’s commitment to equitable service provision’.

Additionally, failure to ask about Indigenous status has been identified as a barrier in the uptake and application of Indigenous specific services. Knowing if someone is Indigenous can improve management by allowing them to maximise the in-hospital and community services that might be available. It allows us as providers to think holistically about our patient and what we as a service can offer to benefit them moving forward. However, it is not the asking of the question that is the issue. Tick box systems and asking patients outright should be standard practice. However it is the response to the answer that becomes a more important outcome of the interaction due to the potential for discrimination or scrutiny based on Indigenous status alone.

Presuming Aboriginality is associated with poverty and disadvantage is a flawed and disempowering stereotype. Although, disappointingly Aboriginality and poverty are often interconnected, they are not interchangeable. It seems there is a pervading discourse within the health care system, structures and policies that frame Indigenous people with the assumption of deficit and inferiority.

We are taught to approach each patient with an aim to understand their current complaint in the context of the multitude of factors that individually contribute to that person’s health, including their past medical, familial, social and racial characteristics. Viewing every Aboriginal patient as a representation of statistics that are drawn from national data means that patient centered care is erroneously replaced with pattern centered care.

The key to understanding Aboriginal patients, I believe, is not presuming to know them; by not presuming in either a good or bad way to know their story, their history or their health concerns. Be open-minded. If we believe we know, then we stop trying to learn. I never claim to know medicine despite having a wealth of information at the end of a grueling medical degree. Because if I think I know medicine I will stop trying to learn it. Not knowing medicine is what makes it exciting and challenging and it is why, for the rest of my working life, I will have the privilege of being a student. The medical profession has a lot more learning to do about the best way to manage Indigenous health care needs and delivery of effective services. In addition, it is important to change the discourse surrounding Indigenous people to one where patients can feel empowered by their Indigenous status rather than inadequate. Research into Indigenous health is a great place to begin, but allowing Indigenous patients to tell their stories and feel safe doing so is something that each clinician should strive for.

I cannot know with certainty how ticking the box that day in the ED impacted my treatment. But I still regret it. I felt for the rest of my time in that emergency department I was treated, not with less care, but differently. If a patient has a pre-conception of how they will be treated, our actions can be misinterpreted as racially driven, rather than standard practice. Nevertheless, there are innumerable encounters between health professionals and Indigenous and non-Indigenous people everyday. If every encounter became an opportunity to educate, reassure, or reassess our own perspectives the medical community would become a force for change for the better.

This blog was first published for onthewards on 12 March 2016 and can be read at its original location at Tick a box – For the good of whom?. onthewards.org is a free open access medical education website and not for profit organisation that aims to improve the availability of resources for medical students and junior doctors. If you work in healthcare and have a blog topic you would like to write for doctorportal, please get in touch.

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Photo: Oliver Tacke

Acute pain management: scientific evidence, fourth edition, 2015

In 1999, the first edition of Acute pain management: scientific evidence was written by a multidisciplinary committee under the guidance of Michael Cousins and published by the National Health and Medical Research Council (NHMRC).1 As there has been a substantial increase in the quantity and quality of publications about acute pain management, the Australian and New Zealand College of Anaesthetists (ANZCA) and its Faculty of Pain Medicine (FPMANZCA) have taken responsibility for revising and updating the available evidence every 5 years.2,3 The fourth edition, which became publicly available in December 2015,4 will be available in hardcopy soon, but can already be downloaded for free in pdf format from http://www.anzca.edu.au/resources/college-publications.

Development and methods

As with the first three editions, the document aimed to combine a review of the best available evidence on acute pain management with current clinical and expert practice, rather than to formulate specific recommendations for clinical practice. Accordingly, the document summarises the evidence currently available on the management of acute pain from over 8000 references, and presents it in a concise and easily readable form to aid practising clinicians. The document was prepared by following the methods established over the preceding three editions. All evidence is documented according to NHMRC levels of evidence, from Level I (systematic reviews of randomised controlled trials [RCTs]) to Level IV (case series).5 However, for the first time, this fourth edition scores systematic reviews and RCTs for quality, and reports the numbers of studies included and patients randomised, to allow readers to assess the relevance of the evidence presented. As in previous editions, the document is preceded by a summary list of all key messages (now totalling 669). These key messages provide concise statements on each topic, showing the highest level of evidence, and clinical practice points based on clinical experience or expert opinion. The document also shows the status of each key message in comparison with the previous edition (eg, new, unchanged, strengthened, qualified, or reversed).

The document addresses all aspects of acute pain management. There are sections on:

the physiology, psychology and the assessment of acute pain;
analgesic medicines and routes and techniques of their administration (eg, regional techniques, patient-controlled analgesia [PCA]); and
non-pharmacological techniques (eg, physical therapies, acupuncture and psychological techniques).

Furthermore, specific clinical situations, such as post-operative pain and acute medical and cancer pain, are addressed, as well as acute pain in specific settings (eg, burns units, intensive care units, emergency departments). Pain in children is dealt with for the first time in a detailed section presenting evidence-based management for this complex and challenging group. Other groups covered in detail are pregnant women, older patients, and patients with opioid tolerance or with an addiction. Culturally responsive care for culturally and linguistically diverse patients, with an emphasis on Aboriginal, Torres Strait Islander and Maori peoples, is also addressed.

Post-operative pain management

This brief overview cannot cover all the evidence provided in the document, but focuses on that related to post-operative pain, one of the most common manifestations of acute pain. However, many of the issues related to post-operative pain are translatable to other acute pain scenarios, in particular pain after trauma. Most of the following statements are summaries or direct quotations of the key messages in the fourth edition.4

Multimodal analgesia

The overall concept underlying post-operative (and other) acute pain relief is multimodal or “balanced” analgesia, that is, the use of combinations of analgesics or analgesic techniques with different modes or sites of action. Such an approach (eg, combining a non-opioid with an opioid or a regional analgesia technique with a systemic analgesic) improves pain control compared with mainly opioid-based analgesia, and reduces opioid consumption (ie, is “opioid-sparing”) and thereby reduces adverse effects.

Opioid-sparing analgesic approaches permit earlier mobilisation and earlier enteral feeding after surgery and so may contribute to early recovery overall. However, providing appropriate analgesia is only one of several elements of “enhanced recovery after surgery (ERAS)” protocols aiming to reduce hospital stays and complication rates. Furthermore, different surgical procedures cause different pain states (eg, musculoskeletal versus visceral) of different severity in different locations.

Procedure-specific post-operative pain management

As the efficacy of analgesics can be different in different surgical settings, pooling of data from various post-operative pain states may ignore the specific effects of a specific analgesic or technique in a specific post-operative setting. Therefore, post-operative pain requires a procedure-specific approach to analgesia. The recognition of this need has led to the development of the Prospect (PROcedure-SPECific post-operative pain managemenT) initiative (http://www.postoppain.org), which provides procedure-specific evidence-based recommendations for the treatment of pain after a wide range of operations.6,7

Acute neuropathic pain

In assessing acute pain after surgery and trauma, acute neuropathic pain is often overlooked or its severity underestimated. This has important consequences, as neuropathic pain does not respond to many common analgesics, and requires specific therapeutic approaches. Ketamine, opioids (including tramadol or tapentadol) and α₂δ ligands (gabapentin or pregabalin) are the preferred systemic treatment options for acute neuropathic pain, as a rapid onset of effect is needed in this setting. Early recognition of neuropathic pain in an acute setting is also relevant, as chronic post-surgical pain and post-traumatic pain often have a neuropathic component. Risk factors that predispose to the development of such pain include the severity of pre-surgical chronic pain and post-surgical acute pain, and intraoperative nerve injury. Chronic pain after surgery and trauma is more common than generally thought, and can lead to significant disability. Diagnosis and subsequent appropriate treatment of acute neuropathic pain might prevent the development of chronic pain.

Preventive analgesia

Some analgesic interventions have an effect on post-operative pain and/or analgesic consumption that exceeds the expected duration of action of the medicine. Such interventions are defined as preventive analgesia. Ketamine and local anaesthetics have such a preventive effect. There are now also data that show that ketamine, certain regional analgesic techniques and possibly calcium channel α₂δ subunit ligands (gabapentin and pregabalin) prevent the development of chronic post-surgical pain. There are significant associations between psychosocial factors such as anxiety, pain catastrophising, depression, psychological vulnerability and stress and the subsequent development of chronic post-surgical pain.

Regional analgesia and continuous peripheral nerve blocks

There is increasing evidence for the role of regional anaesthesia techniques in providing effective post-operative pain relief. Such techniques are not only preventive as outlined above, but provide overall excellent analgesia with minimal systemic adverse effects and can thereby improve and accelerate recovery. The evidence remains strong for continuous epidural analgesia, in particular after major thoracic and abdominal surgery with improved return of bowel function and overall reduced morbidity and possibly even mortality. However, this technique is underutilised in some parts of the world due to the fear of serious complications, in particular in conjunction with use of anticoagulants, and to the perceived increased workload in managing patients with thoracic epidural analgesia. This has led to increased use of continuous peripheral nerve blocks in the post-operative setting, which, compared with single-injection peripheral nerve blocks, result in improved pain control, decreased need for opioid analgesics, reduced nausea and improved patient satisfaction.

Compared with opioid analgesia, continuous peripheral nerve blocks (regardless of catheter location) provide better post-operative analgesia and reductions in opioid use as well as decreased nausea, vomiting, pruritus and sedation. The use of ultrasound guidance to perform blocks increases block success rates, reduces block performance time and the risk of local anaesthetic toxicity and results in faster onset and longer duration of analgesia compared with localisation using a peripheral nerve stimulator.

Techniques for which there is particularly good evidence include continuous thoracic paravertebral analgesia (for unilateral thoracotomies and after rib fractures) and transversus abdominis plane blocks (after abdominal surgery), as well as a broad range of peripheral nerve blocks of the upper and lower limb (after orthopaedic surgery). After total knee joint replacement, femoral nerve blocks are a proven approach, but there is also increasing evidence to support local infiltration analgesia.

With regard to complications, post-operative neurological dysfunction is often related to patient and surgical factors, and the incidence of neuropathy directly related to regional anaesthesia is rare. Continuous peripheral and regional nerve blocks carry a risk of infection; skin preparation with alcohol-based chlorhexidine and full barrier precautions (including face masks) are recommended for insertion of peri-neural catheters.

Patient-controlled analgesia

Opioids remain an important component of systemic analgesia for the relief of severe pain despite the multiple opioid-sparing approaches. In the early post-operative setting, intravenous opioids delivered via PCA provide better analgesia than conventional parenteral opioid regimens and result in greater patient satisfaction. Adding a background infusion to morphine delivered intravenously via PCA in opioid-naive patients increases the incidence of respiratory depression and does not improve pain relief or sleep, or reduce the number of PCA demands. There is little evidence that any particular opioid delivered via PCA is superior to another in regard to analgesic or adverse effects in general, but individual patients may tolerate one opioid better than another. The safety of PCA use can be significantly improved by hospital-wide safety initiatives (“smart pumps”, equipment, guidelines, education, monitoring).

Non-opioid analgesics

There is good evidence to support the use of non-opioid analgesics to complement opioid analgesics for multimodal analgesia; non-steroidal anti-inflammatory drugs (NSAIDs) are superior to paracetamol (and combining both increases efficacy) and COX-2 inhibitors (coxibs) offer safety advantages over non-selective NSAIDs, in particular with regard to platelet dysfunction leading to blood loss. The risk of adverse renal effects of non-selective NSAIDs and coxibs is increased in the presence of factors such as pre-existing renal impairment, hypovolaemia, hypotension and the use of other nephrotoxic agents including angiotensin-converting enzyme inhibitors. Other analgesic options include peri-operative intravenous lignocaine, which has been shown to reduce pain and opioid requirements after abdominal surgery and to decrease nausea, vomiting, duration of ileus and length of hospital stay. Peri-operative intravenous ketamine reduces opioid consumption, time to first analgesic request and post-operative nausea and vomiting compared with placebo. It is particularly helpful in opioid-tolerant patients. Peri-operative administration of α₂δ ligands reduce post-operative pain and opioid requirements and reduce the incidence of vomiting, pruritus and urinary retention, but increase the risk of sedation. The peri-operative use of systemic α₂-receptor agonists (clonidine and dexmedetomidine) reduces post-operative pain intensity, opioid consumption and nausea without prolonging recovery times, but the frequency and severity of adverse effects (bradycardia and hypotension) sometimes limit their clinical usefulness. Dexamethasone reduces post-operative pain and opioid requirements to a limited extent, but also reduces nausea and vomiting, fatigue, and improves the quality of recovery compared with placebo. Current evidence does not support the use of cannabinoids in acute pain management.

Non-pharmacological strategies

There is some evidence to support non-pharmacological techniques for providing post-operative analgesia. Transcutaneous electrical nerve stimulation (TENS) compared with sham TENS reduces acute pain (procedural and non-procedural), including pain after thoracic surgery. Acupuncture (specifically, auricular acupuncture) reduces post-operative pain and opioid requirements, as well as opioid-related adverse effects compared with a variety of controls. Beneficial effects of acupuncture on post-operative pain have been confirmed in particular after back surgery and ambulatory knee surgery and total knee joint replacement. Psychological (including distraction [music, books, video] and hypnosis), physical (including holding, warming, non-nutritive sucking) and use of sweet solution (sucrose) interventions are particularly beneficial in painful procedures in children and are being used peri-operatively.

Conclusion

The increase in evidence in the area of acute pain management over the past 15 years is impressive. Based on the evidence available, which is summarised in the fourth edition of Acute pain management: scientific evidence,4 physicians can make evidence-based decisions in most acute pain scenarios. Such an approach improves the safety and effectiveness of treatment of patients in acute pain, thereby reducing pain and suffering. These guidelines are even relevant to primary care physicians, who may influence outcomes in these patient populations.

However, a significant gap remains between evidence and practice in the area of acute pain management. It is the challenge for all health care professionals to reduce this gap to benefit our patients.

Absolute risk of cardiovascular disease events, and blood pressure- and lipid-lowering therapy in Australia

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality internationally.1,2 A large proportion of CVD events are preventable by appropriate population-level interventions and individual management of risk. The potential for benefit, the balance of benefits and harms, and the cost-effectiveness of treatments to reduce CVD events are more closely related to an individual’s absolute CVD risk — the absolute probability that they will experience a CVD event in a given time period — than to isolated individual risk factors or relative risks.3,4

Accurate assessment of absolute CVD risk applies quantitative data on multiple factors that influence risk, including smoking status, blood pressure (BP), blood lipid levels, and diabetes status, to a person’s age- and sex-specific background level of absolute risk.3 Assessment that is based only on individual risk factors (eg, considering cholesterol levels alone) and does not use tools that allow quantification of overall absolute CVD risk leads to substantial misclassification, a general underestimation of risk, and under- and overtreatment.5 Quantitative absolute risk models that assess risk and guide management are central to the primary prevention of CVD, nationally and internationally.6–9

Population-level data on absolute CVD risk have the potential to inform programs, policy and planning, including those associated with implementing large scale treatment strategies according to absolute CVD risk.10 However, population-level data on absolute CVD risk are not available for most countries, including Australia.

Our investigation aimed to quantify absolute CVD risk in the Australian adult population, as well as treatment with BP- and lipid-lowering medications, using data from a representative health survey. It focused on individuals aged 45–74 years, the age group for which most risk calculators have been validated, and with the greatest population burden of premature CVD.

Methods

Study population

The study population comprised 9564 participants from the Australian Bureau of Statistics (ABS) Australian Health Survey11 aged 18 years or over who provided biomedical data for the National Health Measures Survey (NHMS) between March 2011 and September 2012. Details of the Australian Health Survey and NHMS are provided in the Appendix. Of the 30 329 respondents eligible to participate in the NHMS (ie, Australian Health Survey participants aged 5 years and over), 11 246 (37.1%) did so (46.5% of those aged 45–74 years).

Data and variables

Data on sociodemographic and health-related factors, including prior CVD, medical history and health behaviours, were provided by self-report at the home-based interview for the Australian Health Survey. Height, weight, waist circumference, and systolic and diastolic BP were measured directly, fasting blood samples taken and assayed, and a medications review conducted, using standard methods. Details of these methods and the derived variables (eg, diabetes status) are included in the Appendix, in reference and in Box 1.

Absolute risk of a primary CVD event

The absolute risk of a primary CVD event over the next 5 years for a participant without prior CVD was estimated by applying the Australian National Vascular Disease Prevention Alliance (NVDPA) risk assessment and risk management algorithm, which includes the Framingham CVD risk equation;7,11–13 see the Appendix for details. The absolute risk of a primary CVD event over the next 5 years was categorised using the cut-points: low (< 10%); moderate (10–15%); high (> 15%).7

Statistical methods

All analyses were conducted by staff at the ABS, in collaboration with the authors and using ABS statistical programs, in accordance with the Australian Census and Statistics Act 1905 (Cth), supplemented by calculations by the authors, based on these analyses.

The proportions of people with and without prior CVD were calculated for the entire population aged 18 years or more, as well as by sex and age group. Among those without prior CVD, the distributions of the risk factors contributing to the CVD risk algorithm were estimated for those aged 45 years or more.

The proportions of those aged 18 years or more with low, moderate and high absolute CVD risk were calculated for those without prior CVD and presented according to age group and sex. In those aged 45–74 years, the proportions of those with selected health characteristics and risk factors and the proportions receiving BP- and/or lipid-lowering medications were estimated according to prior CVD and absolute primary CVD risk.

Weights were applied to all prevalence estimates to account for the sampling strategy and non-response (see Appendix). The numbers of individuals in Australia with different CVD risk factors, absolute risk levels, and treatment profiles were estimated by applying the weighted proportions to Australian general population data.11 Standard errors were calculated, taking into account variability due to sampling and to random adjustment, as were 95% confidence intervals (CIs).

Ethics approval

Ethics approval for NHMS data collection was provided by the Australian Government Department of Health Human Research Ethics Committee (reference 2/2011). Additional approval was granted by the Australian National University Human Research Ethics Committee (reference 2014/208).

Results

Respondents for whom data were missing about previous CVD or any components of the risk assessment algorithm, including factors in the Framingham CVD risk equation, were excluded from the analyses; 1059 participants were excluded by these criteria. We therefore analysed the data for 8505 participants aged 18 years or more (3828 men and 4677 women), of whom 4844 were aged 45–74 years (2210 men, 2634 women). The Appendix includes the separate results for men and women.

Prior CVD and absolute risk of a primary CVD event

Overall, 6.2% of those aged 18 years or more (corresponding to an estimated 1 071 000 adults in Australia), including 8.7% (95% CI, 7.8–9.6%) of those aged 45–74 years (an estimated 634 000 adults), were classified as having prior CVD (Box 2).

A total of 8.2% of those aged 18 years or more (an estimated 1 412 000 adults) were at high absolute risk of a primary CVD event (Box 2). The proportion at high primary risk was 1.9% in those aged 18–44 years, and increased with age (Box 2, Box 3). Major risk factors were often present in those aged 45–74 years without prior CVD (Box 1, Appendix).

Among those aged 45–74 years, 71.5% (95% CI, 70.1–72.9%; an estimated 5 209 000 people) were at low risk of a primary CVD event, 8.6% (95% CI, 7.4–9.8%; an estimated 625 000 people) were at moderate primary risk, and 11.2% (95% CI, 10.2–12.2%; an estimated 811 000 people) were at high primary risk (Box 2).

Combining those with prior CVD and those at high risk of a primary event, an estimated 19.9% (95% CI, 18.5–21.3%) of people in Australia aged 45–74 years had a high 5-year risk of a CVD event (an estimated 1 445 000 people), including 25.8% (95% CI, 23.4–28.2%) of men (an estimated 925 000 people) and 14.2% (95% CI, 12.6–15.8%) of women (an estimated 522 000 people) in this age bracket (Box 2, Appendix). As would be expected, risk was related to major CVD risk factors (Appendix, Table S2).

BP- and lipid-lowering medications

Use of BP- and lipid-lowering medications was substantially more common in those with prior CVD and in those at higher primary risk than in those at lower risk (Box 4, Box 5; Appendix, Table S3). In those aged 45–74 years with prior CVD, 44.2% were receiving both BP- and lipid-lowering medications (an estimated 280 000 people), 35.4% were receiving only one of these medication types (an estimated 225 000 people), and 20.4% were receiving neither (an estimated 129 000 people) (Box 4).

Among people aged 45–74 years who did not have prior CVD and were at high absolute risk of a primary event, 24.3% were receiving both BP- and lipid-lowering medications (an estimated 197 000 people), 28.7% were receiving only one of these medication types (an estimated 233 000 people), and 47.1% were receiving neither (an estimated 382 000 people) (Box 4). Corresponding figures for those at moderate primary CVD risk were 13.2% (an estimated 82 000 people); 29.5% (an estimated 185 000 people); and 57.3% (an estimated 358 000 people). Of those at low primary CVD risk, 6.6% were receiving both BP- and lipid-lowering medications (an estimated 346 000 people), 18.6% were receiving only one of these medication types (an estimated 966 000 people), and 74.8% were receiving neither (an estimated 3 896 000 people) (Box 4).

Discussion

An estimated one-fifth of the Australian population aged 45–74 years, or about 1.4 million people, had a greater than 15% absolute risk of a CVD event in the next 5 years. This was made up of 11% of individuals aged 45–74 years (about 800 000 people) with a greater than 15% probability of a primary CVD event in the next 5 years, and 9% (about 630 000 people) with existing CVD. Although the risk assessment tools used have not generally been validated outside this age range, our data also suggest that around 2.6% of the population aged 18–44 years (about 230 000 people) and 60.6% of those aged 75 years or more (about 850 000 people) were at high absolute risk of a future CVD event. Levels of absolute CVD risk were higher for men than for women; risk also increased markedly with age.

The Australian NVDPA algorithm uses global CVD (which encompasses coronary heart disease, cerebrovascular disease, peripheral vascular disease and heart failure) as its predicted outcome.14 For more than a decade, Australian national guidelines have recommended lipid-lowering therapies for those at high absolute CVD risk, and consideration of absolute CVD risk in the management of hypertension.15,16 The 2012 NVDPA guidelines recommend combination treatment with BP- and lipid-lowering medications unless contraindicated or clinically inappropriate, together with lifestyle advice, for those with a 5-year primary CVD risk of more than 15%; it advises considering combination treatment for those at moderate risk (5-year primary CVD risk of 10–15%) if 3 to 6 months of lifestyle intervention does not reduce risk sufficiently, or if certain risk factors are present, such as a family history of premature CVD.7 Recently, United Kingdom and United States guidelines have changed from recommending lipid-lowering treatment for those with a 10-year CVD risk of 20% or greater (roughly equivalent to the Australian moderate and high risk categories) to recommending it for individuals with 10-year CVD risks of 10% (UK)9 or 7.5% (US)8 or greater.

We were unable to identify any previous studies that had profiled absolute global CVD risk for a national population, integrating representative information on the absolute risk of primary and secondary CVD events, and treatment with BP- and lipid-lowering medications. A recent article reported that 15.5% of the US population aged 20–79 years was at high absolute risk of a future coronary heart disease event (rather than global CVD event) within 10 years according to the US Adult Treatment Panel (ATP) III guidelines.17 Although CVD absolute risk is likely to vary by population and over time, these US results on coronary heart disease are comparable with our findings that 6.2% of those aged 18 years or more have prior CVD of any kind, and that 13.0% have at least a 10% primary risk of global CVD over the next 5 years.17,18

About half of those with prior CVD aged 45–74 years and one-quarter of those with a 5-year primary CVD risk above 15% were receiving both BP- and lipid-lowering medications, compared with one in 15 of those at low primary risk. This indicates that these medications were, to some extent, being targeted. At the same time, large opportunities for improvement in treatment are apparent, especially in the younger age group: 76% of individuals aged 45–74 years and 88% of individuals aged 45–59 years with a 5-year primary CVD risk greater than 15% were not receiving combination BP- and lipid-lowering treatment.

Applying our estimates to the general population in 2011–12, an estimated 510 000 individuals aged 45–74 years in Australia were at high risk of primary CVD or had prior CVD and were receiving neither BP-lowering nor lipid-lowering medications; a further 460 000 in these groups were receiving only one of the two medication types. This suggests that up to 970 000 people, or 13% of the Australian population aged 45–74 years, have a 5-year risk of a CVD event greater than 15% and are not receiving currently recommended combination BP- and lipid-lowering therapies. A further 620 000 people are at moderate absolute risk of CVD, with about 540 000 not receiving combination BP- and lipid-lowering therapies.

BP- and lipid-lowering treatments were the focus of our analyses because they are the main treatments for preventing CVD events, and are indicated in both primary and secondary prevention. Additional medications, including anti-platelet agents, are recommended for individuals with existing CVD. The treatment gaps we have identified are therefore likely to be underestimates.

The general findings that BP- and lipid-lowering treatment was more common among those at high risk than in those at low risk, and that there were considerable gaps in treatment, are broadly consistent with findings from earlier clinical and non-representative studies, despite the generally higher levels of CVD risk in these samples.19,20 These studies found that 40–75% of patients with existing CVD were receiving both BP- and lipid-lowering therapies,21–23 consistent with the 44% combined treatment rate we found. Also consistent are primary care data from Australia and New Zealand which indicate that about one-quarter of those with a 5-year primary risk of 15% or more are taking combination BP- and lipid-lowering treatments.19,20,22

Our findings concern the general population, a substantial proportion of whom are receiving treatment likely to influence their CVD risk and risk factors. The Framingham Risk Equation is aimed at treatment-naive individuals and will tend to underestimate risk in those receiving treatment. Ideally, absolute CVD risk should be assessed before commencing treatment; however, this is not practical for a population-based sample of this type. It is not possible to reliably ascertain the underlying prior absolute CVD risk status of those who are being treated with BP- and/or lipid-lowering medications and who are assessed as being at low or moderate absolute CVD risk, as they may have moved to a lower risk category because of changes in BP and/or blood lipid profiles. Further, treatment with BP- and lipid-lowering medication is still recommended in some contexts for individuals with abnormalities in single risk factors. Consequently, while lipid-lowering treatments are not recommended for those at low CVD risk, data from our study are relatively uninformative with regard to potential overtreatment in this group.

The gap between current guideline-recommended treatment and the use of BP- and lipid-lowering medications we describe is likely to be related to a number of factors, including the extent of absolute risk-based CVD assessment, appropriate prescribing and uptake, and continuation of treatment. In Australia, CVD risk assessment is recommended from age 45 for the general population and from age 35 for people of Aboriginal and/or Torres Strait Islander background.7 The fact that more than 97% of individuals aged 18–44 years in our study were estimated to be at low primary CVD risk supports the current age cut-off for assessment. It is not known what proportion of the general population undergoes guideline-based absolute CVD risk assessment. Recent evidence indicates that less than half of the eligible individuals attending primary care have had a documented quantitative CVD risk assessment.20,22,23 Although BP- and lipid-lowering medications are generally well tolerated and relatively safe, it is likely that their not being used is, in some cases, the result of contraindications, adverse drug events, a lack of prescription, cost, or their being declined by the patient. Further, international summary estimates of continuation with BP-lowering medications are 42–61% and 62–79% for primary and secondary prevention of coronary heart disease respectively; corresponding figures for statins are 57% and 76%.24

The NHMS assessed CVD risk and medication using inclusive home interview-based sampling and high quality methods. Despite its large size, particularly in comparison with other representative surveys, numbers were limited and confidence intervals were wide in some subgroups. There were insufficient numbers of Aboriginal and Torres Strait Islander participants to quantify risk in this group; relevant analyses would be beneficial when appropriate data become available. The study response rate was 46.5% in the target population (those aged 45–74 years) and the study methods produced estimates representative of the general non-institutionalised Australian population. The NHMS used validated data collection tools that have inherent limitations, including a range of measures based on self-report (such as smoking status, alcohol consumption, and previous CVD). Data were lacking for some measures incorporated into the NVDPA algorithm, including familial hypercholesterolaemia and persistent proteinuria. These limitations and the under-inclusion of institutionalised participants (who are more likely to be older and to have a greater illness burden) mean that absolute CVD risk may have been underestimated, particularly in those over 74 years of age.

Implications

Our results highlight the ongoing efforts and the major opportunities for reducing the frequency of CVD events. Implementation of large scale CVD risk assessment and treatment based on absolute risk is considered to be one of the most cost-effective interventions.25 We estimate that about 870 000 individuals aged 45–74 years at moderate to high absolute risk of CVD are receiving neither BP- nor lipid-lowering therapies. Broadly speaking, lowering systolic BP by around 8 mmHg in this group would prevent an estimated 20 to 37 cardiovascular events per 1000 treated;4 an estimated 31 to 61 events would be prevented for each 1 mmol/L reduction in low-density lipoprotein cholesterol levels.26 While detailed modelling is required for accurate quantification, these findings indicate that more extensive treatment of this single risk group alone could prevent tens of thousands of CVD events in Australia.

Box 1 –
Estimated distribution of cardiovascular disease (CVD) risk factors included in the National Vascular Disease Prevention Alliance algorithm for the Australian-population without prior CVD, by age group

Characteristic	Age group (years)
Characteristic	45–54	55–64	65–74	≥ 75	Total (≥ 45)

Total number
Smoking status
Never smoked	48.1%	48.7%	49.6%	48.9%	48.7%
Ex-smoker	37.8%	38.6%	43.4%	48.4%	40.4%
Current smoker	14.1%	12.7%	7.0%	2.6%	11.0%
Systolic blood pressure
< 120 mmHg	49.3%	33.3%	21.1%	16.6%	35.3%
120–139 mmHg	35.9%	40.1%	40.9%	40.0%	38.6%
140–179 mmHg	14.5%	25.6%	35.8%	37.6%	24.6%
≥ 180 mmHg	0.2%	1.0%	2.2%	5.7%	1.5%
Diastolic blood pressure
< 90 mmHg	83.0%	84.3%	86.8%	91.3%	85.1%
90–109 mmHg	16.7%	15.3%	12.5%	8.0%	14.5%
≥ 110 mmHg	0.3%	0.4%	0.7%	0.7%	0.4%
Low density lipoprotein cholesterol
< 2.0 mmol/L	2.0%	4.0%	9.1%	12.4%	5.2%
2.0–3.5 mmol/L	52.5%	47.6%	51.7%	59.8%	51.6%
> 3.5 mmol/L	45.4%	48.4%	39.2%	27.8%	43.2%
High density lipoprotein cholesterol
≥ 1.0 mmol/L	88.7%	89.8%	89.7%	91.5%	89.6%
< 1.0 mmol/L	11.3%	10.2%	10.3%	8.5%	10.4%
Total cholesterol
< 4.0 mmol/L	4.7%	6.2%	10.8%	15.3%	7.6%
4.0–7.5 mmol/L	92.8%	91.5%	87.0%	83.3%	90.2%
> 7.5 mmol/L	2.5%	2.3%	2.2%	1.5%	2.2%
Total cholesterol:high density lipoprotein cholesterol ratio
< 4.5	62.3%	67.8%	73.7%	79.7%	68.2%
4.5–5.9	28.3%	24.1%	20.1%	16.5%	24.0%
≥ 6	9.4%	8.2%	6.2%	3.7%	7.7%
Diabetes	4.7%	8.1%	14.5%	11.2%	8.4%
Diabetes with microalbuminuria	0.8%	1.4%	4.5%	4.0%	2.1%
Moderate to severe chronic kidney disease	0.1%	0.4%	1.7%	6.8%	1.3%

Box 2 –
Estimated proportions and numbers of individuals in the Australian population with prior cardiovascular disease (CVD), and among those without prior CVD with low, moderate or high absolute 5-year risk of a primary CVD event, by age group and sex

Age group and sex

No prior CVD

Prior CVD

Absolute CVD risk category

Low (< 10%)

Moderate (10–15%)

High (> 15%)

% [95% CI]

Total population

18–34 years

97.8 [96.6–99.0]

5271

0.0 [0.0–0.0]

1.8 [0.8–2.8]

0.4 [0.0–0.8]

35–44 years

96.3 [95.2–97.4]

3042

0.3 [0.0–0.6]

2.1 [1.3–2.9]

1.3 [0.5–2.1]

45–54 years

88.4 [86.5–90.3]

2685

3.0 [1.7–4.3]

4.0 [2.7–5.3]

121

4.6 [3.3–5.9]

139

55–64 years

70.3 [67.7–72.9]

1800

11.0 [8.9–13.1]

281

10.2 [8.3–12.1]

263

8.5 [6.7–10.3]

218

65–74 years

43.1 [39.7–46.5]

724

15.1 [12.7–17.5]

254

25.4 [22.5–28.3]

427

16.4 [13.9–18.9]

277

≥ 75 years

25.6 [20.4–30.8]

359

13.8 [10.8–16.8]

194

32.4 [27.5–37.3]

456

28.2 [23.1–33.3]

396

Total

80.8 [80.0–81.6]

13 923

4.8 [4.3–5.3]

828

8.2 [7.5–8.9]

1412

6.2 [5.6–6.8]

1071

Men

18–34 years

98.5 [97.3–99.7]

2693

0.0 [0.0–0.0]

1.4 [0.3–2.5]

0.0 [0.0–0.0]

35–44 years

95.1 [93.2–97.0]

1492

0.4 [0.0–0.9]

3.1 [1.4–4.8]

1.4 [0.3–2.5]

45–54 years

85.0 [81.7–88.3]

1278

4.9 [2.5–7.3]

4.8 [2.6–7.0]

5.4 [3.1–7.7]

55–64 years

55.5 [51.1–59.9]

706

20.1 [16.0–24.2]

256

14.3 [11.4–17.2]

183

10.0 [7.1–12.9]

128

65–74 years

21.9 [17.6–26.2]

182

22.7 [18.8–26.6]

188

36.6 [31.4–41.8]

305

18.8 [14.7–22.9]

156

≥ 75 years

7.1 [3.0–11.2]

13.3 [9.3–17.3]

48.5 [41.5–55.5]

285

31.1 [24.6–37.6]

183

Total

74.8 [73.5–76.1]

6361

7.2 [6.2–8.2]

615

11.1 [10.1–12.1]

943

6.8 [5.9–7.7]

579

Women

18–34 years

97.1 [95.2–99.0]

2577

0.0 [0.0–0.0]

2.2 [0.5–3.9]

0.7 [0.0–1.5]

35–44 years

97.5 [96.2–98.8]

1552

0.2 [0.0–0.6]

1.2 [0.5–1.9]

1.2 [0.2–2.2]

45–54 years

91.8 [89.5–94.1]

1405

1.1 [0.2–2.0]

3.3 [1.8–4.8]

3.8 [2.3–5.3]

55–64 years

84.8 [81.6–88.0]

1093

1.9 [1.1–2.7]

6.2 [4.0–8.4]

7.0 [5.1–8.9]

65–74 years

64.0 [59.7–68.3]

544

7.5 [5.1–9.9]

14.4 [11.8–17.0]

122

14.1 [10.9–17.3]

120

≥ 75 years

41.6 [33.3–49.9]

340

14.3 [9.9–18.7]

117

18.5 [12.1–24.9]

151

25.6 [18.1–33.1]

210

Total

86.6 [85.6–87.6]

7570

2.4 [1.9–2.9]

210

5.3 [4.4–6.2]

466

5.6 [4.8–6.4]

490

* N = estimated number, in thousands, of persons in each category in Australia. Weighting and missing values mean that numbers do not always sum to totals.

Box 3 –
Estimated distribution of prior cardiovascular disease (CVD) and absolute risk of a primary CVD event over the next 5 years by age group, in the total Australian population aged 18 years or more (A) and for men (B) and women (C) separately

Box 4 –
Estimated proportions and numbers of individuals aged 45 or more in the Australian who were receiving blood pressure (BP)-lowering* and/or lipid-lowering^† medications, according to cardiovascular disease (CVD) risk

	No prior CVD						Prior CVD		Total
	Absolute primary CVD risk category
	Low (<10%)		Moderate (10-15%)		High (>15%)
	% [95% CI]	N^‡	% [95% CI]	N^‡	% [95% CI]	N^‡	% [95% CI]	N^‡	% [95% CI]	N^‡

Population aged 45–74 years
Lipid-lowering medication	13.7 [11.4–16.0]	714	20.1 [13.2–27.0]	126	32.5 [25.9–39.1]	265	55.7 [47.0–64.4]	354	19.8 [17.8–21.8]	1438
No lipid-lowering medication	86.3 [83.9–88.7]	4494	79.9 [73.0–86.8]	499	67.5 [60.9–74.1]	548	44.3 [35.5–53.1]	281	80.2 [78.2–82.2]	5842
BP-lowering medication	18.1 [15.9–20.3]	945	35.8 [27.1–44.5]	223	44.7 [37.7–51.7]	362	68.1 [60.5–75.7]	432	26.6 [24.3–28.9]	1940
No BP-lowering medication	81.9 [79.7–84.1]	4262	64.2 [55.5–72.9]	401	55.3 [48.3–62.3]	449	31.9 [24.3–39.5]	202	73.4 [71.1–75.7]	5340
BP- and lipid-lowering medication	6.6 [5.1–8.1]	346	13.2 [7.7–18.7]	82	24.3 [18.3–30.3]	197	44.2 [36.8–51.6]	280	12.2 [10.6–13.8]	889
Taking one medication only	18.6 [16.2–21.0]	966	29.5 [21.8–37.2]	185	28.7 [22.7–34.7]	233	35.4 [27.8–43.0]	225	22.0 [20.1–23.9]	1599
Taking neither medication	74.8 [72.2–77.4]	3896	57.3 [48.4–66.2]	358	47.1 [39.9–54.3]	382	20.4 [13.9–26.9]	129	65.8 [63.3–68.3]	4792
Population aged ≥ 75 years
Lipid-lowering medication	39.3 [25.5–53.1]	142	30.8 [16.7–44.9]	60	43.0 [30.8–55.2]	196	59.7 [45.9–73.5]	236	44.1 [36.6–51.6]	621
No lipid-lowering medication	60.7 [46.9–74.5]	219	69.2 [55.1–83.3]	134	57.0 [44.8–69.2]	259	40.3 [26.5–54.1]	160	55.9 [48.4–63.4]	785
BP-lowering medication	51.0 [35.3–66.7]	184	56.9 [38.9–74.9]	110	66.6 [58.6–74.6]	304	79.1 [69.5–88.7]	313	63.9 [58.0–69.8]	899
No BP-lowering medication	49.0 [33.3–64.7]	176	43.1 [25.2–61.0]	84	33.4 [25.3–41.5]	152	20.9 [11.3–30.5]	83	36.1 [30.2–42.0]	507
BP- and lipid-lowering medication	24.2 [12.9–35.5]	87	28.9 [14.5–43.3]	56	34.9 [24.2–45.6]	158	48.3 [35.0–61.6]	192	34.3 [27.8–40.8]	482
Taking one medication only	41.9 [28.8–55.0]	151	30.0 [15.9–44.1]	59	39.8 [28.4–51.2]	181	42.3 [29.6–55.0]	167	39.4 [32.2–46.6]	555
Taking neither medication	33.9 [19.7–48.1]	121	41.2 [23.6–58.8]	81	25.3 [16.2–34.4]	115	9.4 [2.9–15.9]	37	26.3 [19.7–32.9]	369

* Hypertension medications includes Anatomic Therapeutic Chemical Classification C02 (antihypertensives), C03 (diuretics), C07 (beta blocking agents), C08 (calcium channel blockers) and C09 (agents acting on the renin–angiotensin system). † Lipid-lowering medications include Anatomic Therapeutic Chemical Classification C10 (lipid modifying agents, plain and combinations. ‡ N = estimated number, in thousands, of persons in each category in Australia. Weighting and missing values mean that numbers do not always sum to totals.

Box 5 –
Estimated distribution of Australians receiving blood pressure (BP)-lowering* and/or lipid-lowering^† medications, by absolute risk of primary cardiovascular disease (CVD) event or prior CVD, by sex and age group

* Hypertension medications includes Anatomic Therapeutic Chemical Classification C02 (antihypertensives), C03 (diuretics), C07 (beta blocking agents), C08 (calcium channel blockers) and C09 (agents acting on the renin–angiotensin system). † Lipid-lowering medications include Anatomic Therapeutic Chemical Classification C10 (lipid modifying agents, plain and combinations.