Chronic Pain

Last updated 1 Jun 2026 · General Practice / Pain Medicine

📋 Key Information Summary

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Chronic pain is defined as pain persisting or recurring for ≥3 months, affecting approximately 3.4 million Australians and representing one of the most common reasons for primary care consultation.
Pain categories include acute (nociceptive, tissue-injury related, self-limiting), chronic (persistent, often maladaptive neuroplastic changes), and cancer-related (may be nociceptive, neuropactic, or mixed).
The transition from acute to chronic pain involves peripheral and central sensitisation, neuroplastic remodelling, psychosocial amplification, and loss of descending inhibitory modulation — early intervention can interrupt this cascade.
Use validated assessment tools: Numeric Rating Scale (NRS 0–10), Brief Pain Inventory (BPI), and body charts to localise pain; assess function, mood, sleep, and quality of life simultaneously.
Adopt a biopsychosocial model — multidimensional assessment incorporating physical, psychological, social, and occupational domains is essential for effective management.
Non-pharmacological therapies are first-line: education, graded exercise, cognitive-behavioural therapy (CBT), physiotherapy, sleep hygiene, and mindfulness-based stress reduction.
Pharmacotherapy should be adjunctive: paracetamol and NSAIDs for nociceptive pain; amitriptyline, duloxetine, or pregabalin/gabapentin for neuropathic pain; opioids only for short-term or cancer-related pain under strict criteria.
Opioid prescribing requires careful risk–benefit analysis, informed consent, regular review, and adherence to RACGP Prescribing Drugs of Dependence guidelines; avoid dose escalation beyond 50 mg morphine equivalent daily (MED) without specialist review.
Multidisciplinary pain management programs (MMPs) combining physical, psychological, and pharmacological interventions produce the best long-term outcomes; refer to specialist pain services when primary care management is insufficient.
Aboriginal and Torres Strait Islander Australians experience chronic pain at 1.4× the rate of non-Indigenous Australians; culturally safe, trauma-informed care and community-based models are essential.
Regularly reassess treatment goals — focus on functional improvement and quality of life rather than numerical pain scores alone; set SMART goals with patients.
Document pain management plans, reassess at defined intervals, and use real-time prescription monitoring (RTPM) systems such as SafeScript or ScriptCheck when prescribing Schedule 8 medicines.

Introduction & Australian Epidemiology

Chronic pain is a major public health challenge in Australia and globally. The International Association for the Study of Pain (IASP) revised its definition in 2020 to describe chronic pain as "pain that persists or recurs for longer than 3 months," distinguishing it from acute pain, which serves as a physiological warning signal of tissue damage.

In Australia, the 2020 National Study of Mental Health and Wellbeing and AIHW data estimate that approximately 3.4 million Australians (16% of the population) live with chronic pain. Prevalence increases sharply with age — affecting over 30% of adults aged 65 years and older. Chronic pain is the leading cause of early retirement, disability pension, and reduced workforce participation, costing the Australian economy an estimated 9.3 billion annually in direct healthcare costs, lost productivity, and carer burden (PainAustralia, 2019).

In general practice, chronic pain accounts for approximately 1 in 5 consultations. Despite this, evidence consistently demonstrates gaps in pain education — many Australian GP trainees report inadequate undergraduate and vocational training in pain science. The RACGP and the Faculty of Pain Medicine (FPM) of the Australian and New Zealand College of Anaesthetists (ANZCA) have published frameworks to support evidence-based, patient-centred chronic pain management at the primary care level.

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Key principle: Chronic pain is a condition in its own right, not merely a symptom of unresolved pathology. It requires a biopsychosocial approach and may persist even when the original tissue injury has healed.

The burden falls disproportionately on certain populations: Aboriginal and Torres Strait Islander Australians, people from low socioeconomic backgrounds, those in rural and remote areas with limited access to multidisciplinary services, older adults, and individuals with comorbid mental health conditions. Inequities in access to specialist pain services remain a significant concern, particularly in regional and remote Australia where wait times of 12–18 months are common.

Categories of Pain

Understanding pain mechanisms is fundamental to appropriate classification, investigation, and treatment. Pain is classified by duration (acute vs chronic), mechanism (nociceptive, neuropathic, nociplastic), and aetiology (cancer vs non-cancer). These categories overlap, and many patients present with mixed pain phenotypes.

Acute Pain

Acute pain is a normal physiological response to tissue injury or potential tissue damage. It is typically self-limiting, proportional to the stimulus, and resolves with healing (usually within 1–3 months). Examples include post-operative pain, acute musculoskeletal injury, renal colic, and acute infection.

Pathophysiology: Activation of peripheral nociceptors (Aδ and C fibres) by mechanical, thermal, or chemical stimuli. Transduction → transmission → modulation → perception. Peripheral sensitisation lowers nociceptor thresholds at the injury site (primary hyperalgesia).

Management principle: Treat the underlying cause; provide effective, timely analgesia to prevent central sensitisation; use multimodal analgesia; avoid unnecessary opioid prescribing.

Chronic Pain

Chronic pain persists beyond normal tissue healing time (≥3 months) and is often disproportionate to identifiable pathology. It may arise from persistent nociceptive input, neuropathic damage, or maladaptive neuroplastic changes in the absence of ongoing tissue injury.

Subtypes by mechanism:

Nociceptive: Ongoing activation of nociceptors by tissue damage or inflammation (e.g., osteoarthritis, chronic inflammatory arthritis, endometriosis). Responsive to NSAIDs and simple analgesics.
Neuropathic: Caused by a lesion or disease of the somatosensory nervous system. Descriptors include burning, shooting, electric-shock-like, tingling, and numbness. Affects approximately 17–26% of chronic pain patients. Common causes: diabetic peripheral neuropathy, post-herpetic neuralgia, radiculopathy, chemotherapy-induced peripheral neuropathy, spinal cord injury. Responds to specific agents (amitriptyline, duloxetine, pregabalin, gabapentin).
Nociplastic (central sensitisation): Pain arising from altered nociception without clear evidence of tissue damage or somatosensory lesion. Conditions include fibromyalgia, irritable bowel syndrome (IBS), chronic tension-type headache, non-specific chronic low back pain. Characterised by widespread hyperalgesia, allodynia, and disproportionate pain. Responds poorly to opioids; best managed with exercise, CBT, and centrally-acting agents.

Feature	Nociceptive	Neuropathic	Nociplastic
Source	Tissue damage/inflammation	Nerve lesion/disease	Altered CNS processing
Character	Aching, throbbing, sharp	Burning, shooting, electric	Diffuse, deep aching, pressure
Distribution	Localised, dermatomal/myotomal	Dermatomal or peripheral nerve	Widespread, variable
Neuro signs	None	Sensory loss, allodynia, hyperalgesia	Tenderness, widespread allodynia
Responsive to	NSAIDs, paracetamol, opioids	TCAs, SNRIs, gabapentinoids	Exercise, CBT, duloxetine, low-dose amitriptyline

Cancer Pain

Cancer pain is a distinct category with unique considerations. It may be caused by the tumour itself (compression, infiltration of nerves/bone/viscera, obstruction), cancer treatment (chemotherapy-induced peripheral neuropathy, radiation fibrosis, post-surgical pain), or comorbid conditions. Approximately 55–70% of patients with advanced cancer experience significant pain.

Unlike non-cancer chronic pain, cancer pain generally has identifiable ongoing nociceptive pathology and often requires opioid analgesia titrated to effect. The WHO Analgesic Ladder (1986) remains a useful framework — adapted to modern practice with adjuvant agents used at all steps, not just Step 3.

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WHO Analgesic Ladder (adapted):
Step 1 — Mild pain (NRS 1–3): Paracetamol ± NSAID + adjuvants
Step 2 — Moderate pain (NRS 4–6): Low-dose opioid (codeine 30–60 mg or tramadol 50–100 mg) + paracetamol ± NSAID + adjuvants
Step 3 — Severe pain (NRS 7–10): Strong opioid (morphine, oxycodone, fentanyl) + paracetamol ± NSAID + adjuvants

Cancer survivors may also develop chronic pain syndromes after treatment completion, including aromatase inhibitor-associated musculoskeletal syndrome (AIMSS), chemotherapy-induced peripheral neuropathy (CIPN), post-mastectomy pain syndrome, and radiation-induced brachial plexopathy. These require ongoing management in primary care with specialist oncology input as needed.

Transition from Acute to Chronic Pain

The progression from acute to chronic pain is not simply a matter of duration — it involves fundamental changes in neural processing, psychological state, and social functioning. Understanding this transition is critical for early identification and prevention.

Neurobiological Mechanisms

Peripheral sensitisation: Inflammatory mediators (prostaglandins, bradykinin, substance P, NGF) lower nociceptor activation thresholds at the injury site. This is reversible and normally resolves with tissue healing.
Central sensitisation: Persistent nociceptive input leads to increased excitability of dorsal horn neurons via NMDA receptor activation, wind-up phenomenon, and expansion of receptive fields. Results in hyperalgesia and allodynia in areas beyond the original injury. This is the hallmark of the transition to chronic pain.
Neuroplastic remodelling: Chronic nociceptive input reorganises cortical maps (somatosensory cortex, anterior cingulate cortex, prefrontal cortex), leading to altered pain perception and emotional processing.
Loss of descending inhibition: Descending inhibitory pathways from the periaqueductal grey (PAG) and rostral ventromedial medulla (RVM) become dysfunctional, reducing endogenous analgesia (conditioned pain modulation failure).
Neuroimmune interactions: Microglial activation in the spinal cord and brain release pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), perpetuating central sensitisation.

Psychosocial Risk Factors (Yellow Flags)

Psychosocial factors are stronger predictors of chronic pain development than biomedical findings. Australian guidelines identify "yellow flags" that increase the risk of chronification:

Yellow Flag Domain	Examples
Beliefs & attitudes	Catastrophising ("I'll never get better"), fear-avoidance beliefs, belief that pain = damage
Emotional state	Depression, anxiety, anger, helplessness
Behaviour	Withdrawal from activity, excessive rest, over-reliance on passive treatments
Workplace	Job dissatisfaction, lack of modified duties, compensation/disputes
Social	Social isolation, unsupportive family, secondary gain

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Screen early: The STarT Back Screening Tool and the Örebro Musculoskeletal Pain Questionnaire are validated tools for identifying patients at high risk of developing chronic pain after acute presentations. Early identification enables targeted biopsychosocial intervention.

Prevention Strategies

Preventing chronification requires a proactive approach in the acute pain phase:

Adequate, multimodal acute pain control to minimise peripheral and central sensitisation
Patient education — explain that pain does not equal harm; encourage graded return to activity
Address yellow flags early — refer for psychological support if catastrophising or fear-avoidance present
Avoid unnecessary investigations (imaging without clinical indication reinforces the "damage" narrative)
Maintain function as a primary goal, not pain elimination
Limit opioid prescribing for acute pain — use time-limited prescriptions with clear cessation plans
Schedule follow-up to monitor trajectory — pain not improving at 4–6 weeks warrants reassessment

Assessing & Measuring Pain

Pain assessment in chronic pain must go beyond the question "How bad is your pain?" A comprehensive, multidimensional assessment is the foundation of effective management. The Australian Pain Society and RACGP recommend structured assessment covering intensity, quality, location, functional impact, and psychosocial factors.

Unidimensional Pain Intensity Tools

Useful for initial screening and monitoring response to treatment over time:

Numeric Rating Scale (NRS 0–10): Most widely used in Australian primary care. Patient rates pain from 0 (no pain) to 10 (worst imaginable pain). Mild (1–3), moderate (4–6), severe (7–10). Quick, validated, easy to track.
Visual Analogue Scale (VAS): 100 mm horizontal line from "no pain" to "worst pain." More sensitive to change but less practical in some settings.
Verbal Rating Scale (VRS): Categorical (none, mild, moderate, severe). Useful for patients with cognitive impairment or language barriers.
Wong-Baker FACES® Pain Scale: Preferred for paediatric patients (≥3 years), older adults with cognitive impairment, and patients with limited English proficiency.

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Practice tip: Do not rely solely on a pain intensity score. A patient reporting NRS 7/10 who remains fully functional has different management needs from a patient at NRS 7/10 who is bed-bound and depressed. Always assess alongside functional impact.

Multidimensional Pain Assessment Tools

Tool	Domains Assessed	Setting	Time
Brief Pain Inventory (BPI)	Pain intensity, interference with function (7 domains), pain location, treatments	Primary care, pain clinics	5–10 min
Douleur Neuropathique 4 (DN4)	Screening for neuropathic pain (interview + physical exam items)	Any setting	2–5 min
PainDETECT	Self-report neuropathic pain screening	Primary care	5 min
Örebro Musculoskeletal Pain Questionnaire	Risk of chronification (yellow flags, function, beliefs)	Primary care, physiotherapy	5–10 min
STarT Back Screening Tool	Low back pain prognosis (psychosocial risk stratification)	GP, physiotherapy	2–5 min
EQ-5D-5L	Quality of life (mobility, self-care, usual activities, pain/discomfort, anxiety/depression)	Research, health economics	5 min

Body Charts

Body charts (pain body diagrams) are a simple, highly effective clinical tool for pain assessment. The patient marks the location, distribution, and character of their pain on an anatomical diagram. Body charts help:

Localise and differentiate pain patterns (dermatomal vs diffuse vs regional)
Identify neuropathic distributions (e.g., L5 radiculopathy vs lateral thigh meralgia paraesthetica)
Monitor changes over time (comparison at follow-up visits)
Detect widespread pain patterns suggestive of central sensitisation/fibromyalgia (≥4 of 5 body regions)
Facilitate communication between the patient and multidisciplinary team members

Neuropathic Pain Screening

The DN4 questionnaire (Douleur Neuropathique 4 items) is the preferred screening tool recommended by the Neuropathic Pain Special Interest Group (NeuPSIG). A score ≥4/10 suggests neuropathic pain. Components include:

Interview: burning, painful cold, electric shocks, tingling, pins and needles, numbness, itching
Examination: hypoesthesia to touch, hypoesthesia to pinprick, allodynia (brushing)

The PainDETECT questionnaire is an alternative self-report tool (score ≥19 suggests neuropathic pain; ≤12 suggests nociceptive pain; 13–18 is ambiguous).

Comprehensive Pain Assessment Framework

Australian guidelines recommend a structured biopsychosocial assessment at the initial chronic pain consultation:

Biological: Pain character, onset, duration, aggravating/relieving factors, prior investigations/treatments, comorbidities, sleep quality, medication history (including over-the-counter and complementary), substance use
Psychological: Mood (PHQ-9 for depression, GAD-7 for anxiety), catastrophising (Pain Catastrophising Scale), self-efficacy, beliefs about pain, coping strategies, history of trauma/PTSD
Social: Impact on work/education, relationship quality, financial stress, social support, cultural factors, compensation/litigation status
Functional: Activities of daily living, exercise capacity, occupational demands, goals for recovery

Non-Pharmacological Management

Non-pharmacological therapies are the cornerstone of chronic pain management. International and Australian guidelines consistently recommend them as first-line or foundational interventions, with pharmacotherapy used as adjunctive support. The evidence base for physical, psychological, and self-management strategies has grown substantially.

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First-line approach: Patient education + graded physical activity + psychological support should form the foundation of every chronic pain management plan before considering pharmacological escalation.

Pain Education

Pain neuroscience education (PNE) — also known as pain neuroscience education or explanatory pain neuroscience — involves teaching patients about the neurobiology of pain, including the distinction between tissue damage and pain perception, the role of central sensitisation, and the modifiability of pain. Systematic reviews demonstrate that PNE reduces pain catastrophising, improves function, and enhances engagement with active rehabilitation.

Key messages: "Pain is not always a reliable indicator of tissue damage," "The nervous system can become overprotective," "Your brain can learn to turn the pain volume down"
Resources: Explain Pain (Butler & Moseley), PainAustralia patient resources, Pain Health (WA Government)
MBS items: GP Management Plans (GPMP, MBS item 721) and Team Care Arrangements (TCA, MBS item 723) facilitate structured care coordination with allied health

Physical Activity & Exercise

Graded exercise therapy is one of the most evidence-supported interventions for chronic pain. Exercise reduces pain intensity, improves function, enhances mood, and addresses deconditioning. The key principle is graded exposure — starting at a tolerable level and progressively increasing activity.

Exercise Type	Evidence	Conditions
Aerobic (walking, swimming, cycling)	Strong evidence for pain reduction and mood improvement	Chronic low back pain, fibromyalgia, osteoarthritis, widespread pain
Resistance/strength training	Improves function and reduces pain in musculoskeletal conditions	Knee/hip OA, chronic low back pain
Yoga, Pilates, tai chi	Moderate evidence for chronic low back pain and fibromyalgia	Low back pain, fibromyalgia, general chronic pain
Aquatic/hydrotherapy	Good for patients unable to tolerate land-based exercise	Fibromyalgia, OA, chronic widespread pain

MBS items for exercise physiology services (MBS item 10952–10954) are accessible via GP Management Plans. Physiotherapy services are rebatable under private health insurance and under Medicare with TCA referrals (up to 5 allied health services per calendar year, MBS item 10950–10970).

Psychological Therapies

Psychological interventions address the cognitive, emotional, and behavioural dimensions of chronic pain:

Cognitive-Behavioural Therapy (CBT): Strongest evidence base. Addresses maladaptive thoughts (catastrophising, fear-avoidance), promotes activity pacing, graded exposure, and coping skills. Delivered by clinical psychologists. Medicare Better Access (MBS items 80100–80171) provides up to 10 sessions per calendar year (20 sessions under exceptional circumstances).
Acceptance and Commitment Therapy (ACT): Focuses on psychological flexibility, acceptance of pain, and engagement in valued activities despite pain. Growing evidence, particularly for conditions with central sensitisation.
Mindfulness-Based Stress Reduction (MBSR): 8-week group programme incorporating mindfulness meditation, body scanning, and gentle yoga. Moderate evidence for chronic pain reduction and improved quality of life.
Graded Motor Imagery (GMI) & Mirror Therapy: Particularly effective for complex regional pain syndrome (CRPS) and phantom limb pain. Involves laterality recognition, explicit motor imagery, and mirror therapy in sequence.

Physical Therapies

Physiotherapy: Manual therapy, exercise prescription, education, and pain neuroscience education. Evidence strongest when combined with active exercise programmes rather than passive treatments alone.
Occupational therapy: Functional assessment, workplace ergonomic modification, activity pacing, and adaptive equipment prescription.
Acupuncture: Moderate evidence for chronic low back pain, knee osteoarthritis, and headache. May be used as adjunct; available under some private health insurance extras cover.
Transcutaneous electrical nerve stimulation (TENS): Low-to-moderate evidence. Self-administered, low risk. May provide short-term symptom relief. Not PBS-listed; devices available for purchase or loan from some community health services.

Multidisciplinary Pain Management Programmes (MMPs)

MMPs combine physical, psychological, educational, and pharmacological interventions delivered by a coordinated team (typically including a pain medicine specialist, physiotherapist, psychologist, occupational therapist, and nurse). They represent the most effective intervention for complex chronic pain, with evidence demonstrating improvements in pain, function, mood, medication use, and healthcare utilisation. Available at public hospital pain clinics and some private pain management centres across Australia. Wait times in the public system can exceed 6–18 months.

Pharmacological Management

Pharmacotherapy in chronic pain should be adjunctive to non-pharmacological strategies, not a replacement. The goal is to reduce pain sufficiently to enable engagement in rehabilitation, improve function, and enhance quality of life — not necessarily to achieve a pain-free state. Medication selection should target the underlying pain mechanism, consider comorbidities, and follow a stepwise approach.

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Core principle: "Start low, go slow, aim for functional improvement." Every medication trial should have a defined therapeutic goal, a review timeframe (typically 4–8 weeks), and a clear plan for tapering if goals are not met.

Simple Analgesics

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Paracetamol

Panadol®, Panamax®, Dymadon® · Simple analgesic

Adult dose 500–1000 mg PO QID (max 4 g/day; ≤2 g/day if hepatic impairment or <50 kg)

Paediatric dose 15 mg/kg PO QID (max 60 mg/kg/day, max 4 g/day)

Route Oral, IV (Perfalgan®)

Renal adjustment eGFR 10–50: max 2 g/day; eGFR <10: avoid or use with caution

Key notes Minimal efficacy in chronic low back pain and OA (NNT ~15–17). Use for acute flares. Avoid regular scheduled dosing for chronic pain unless clear benefit demonstrated.

PBS status ✔ PBS General Benefit

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Ibuprofen

Nurofen®, Brufen® · NSAID (propionic acid derivative)

Adult dose 200–400 mg PO TDS-QID (max 2.4 g/day); lowest effective dose for shortest duration

Paediatric dose 5–10 mg/kg PO TDS (max 30 mg/kg/day, max 2.4 g/day)

Renal adjustment Avoid if eGFR <30; use with caution in CKD 3a

Key notes Use lowest dose, shortest duration. Co-prescribe PPI (omeprazole 20 mg daily) if GI risk factors. Avoid in cardiovascular disease, CKD, anticoagulant use. NNT ≈ 2.5–4 for OA pain.

PBS status ✔ PBS General Benefit

Neuropathic Pain Agents

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Amitriptyline

Endep®, Tryptanol® · Tricyclic antidepressant (TCA)

Adult dose 10 mg nocte, titrate by 10 mg every 1–2 weeks; target 25–75 mg nocte (analgesic doses lower than antidepressant doses)

Renal adjustment No specific adjustment; use lower doses, monitor for sedation

Hepatic adjustment Reduce dose; avoid in severe hepatic impairment

Key notes First-line for neuropathic pain (NNT ≈ 3.5). Avoid in elderly (>65 years) — anticholinergic burden (sedation, constipation, urinary retention, falls risk, cardiac conduction). Avoid in cardiac disease (QT prolongation). Best for neuropathic pain with comorbid insomnia.

PBS status ✔ PBS General Benefit

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Duloxetine

Cymbalta®, Dulex® · Serotonin-noradrenaline reuptake inhibitor (SNRI)

Adult dose 30 mg PO daily for 1 week, then 60 mg PO daily (max 120 mg/day)

Renal adjustment Avoid if eGFR <30 mL/min

Hepatic adjustment Contraindicated in severe hepatic impairment

Key notes First-line for neuropathic pain (NNT ≈ 5–6). Dual benefit in comorbid depression/anxiety. Also evidence for fibromyalgia, chronic musculoskeletal pain, diabetic peripheral neuropathy. Lower anticholinergic burden than TCAs — preferred in elderly. Taper over ≥2 weeks to avoid discontinuation syndrome.

PBS status ⚠️ PBS Authority Required — neuropathic pain, major depressive disorder

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Pregabalin

Lyrica® · Gabapentinoid (α2δ ligand)

Adult dose 75 mg BD, titrate to 150–300 mg BD (max 600 mg/day) over 1–2 weeks

Renal adjustment eGFR 30–60: 75–300 mg/day in divided doses; eGFR 15–30: 25–150 mg/day; eGFR <15: 25–75 mg/day

Key notes First-line for neuropathic pain (NNT ≈ 7). Also evidence for fibromyalgia, generalised anxiety disorder. Advantages: rapid titration, well tolerated in elderly, no hepatic metabolism. Disadvantages: sedation, dizziness, weight gain, peripheral oedema, abuse potential (Schedule 4). Taper over ≥1 week to avoid rebound.

PBS status ⚠️ PBS Authority Required — neuropathic pain (inadequate response to trial of TCA or SNRI)

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Gabapentin

Neurontin®, Aclonium® · Gabapentinoid (α2δ ligand)

Adult dose 300 mg day 1, 300 mg BD day 2, 300 mg TDS day 3; titrate to 300–600 mg TDS (max 3.6 g/day)

Renal adjustment eGFR 30–60: 200–700 mg/day; eGFR 15–30: 100–300 mg/day; eGFR <15: 100–200 mg/day

Key notes Similar efficacy to pregabalin; slower titration required. Less expensive as generic. TID dosing may reduce adherence. Risk of misuse is lower than pregabalin but still present.

PBS status ✔ PBS General Benefit

Topical Agents

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Lidocaine 5% medicated plasters

Versatis® · Local anaesthetic (topical)

Adult dose Apply up to 3 plasters to painful area for up to 12 hours in 24 hours

Indication Post-herpetic neuralgia (first-line); localised neuropathic pain

Key notes Minimal systemic absorption. Apply only to intact skin. Avoid mucous membranes and eyes. Well tolerated in elderly and renally impaired patients.

PBS status ⚠️ PBS Authority Required — post-herpetic neuralgia

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Capsaicin 8% patch (Qutenza®)

Qutenza® · TRPV1 agonist (topical)

Adult dose Single application by trained healthcare professional for 30 minutes (peripheral neuropathic pain) or 60 minutes (feet in diabetic neuropathy). Repeat every 3 months if needed.

Indication Peripheral neuropathic pain (non-diabetic and diabetic)

Key notes Application-site burning/pain is common. Must be applied in a clinical setting. Defunctionalisation of TRPV1-expressing nociceptors. Only available at specialist pain clinics and some hospitals.

PBS status ✘ Not PBS-listed (cost ~0–500 per application)

Opioid Analgesics

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Opioids in non-cancer chronic pain: Current Australian and international evidence does not support long-term opioid therapy for chronic non-cancer pain. Systematic reviews demonstrate modest short-term benefit (NNT ≈ 7 for ≥50% pain relief) offset by significant harms: dependence, opioid-induced hyperalgesia, endocrine dysfunction, falls, and overdose. The RACGP recommends opioids be time-limited, used at the lowest effective dose, and combined with non-pharmacological strategies.

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Tramadol

Tramal® · Weak opioid + SNRI

Adult dose 50–100 mg PO QID PRN (max 400 mg/day); SR formulation 100–200 mg BD

Renal adjustment eGFR <30: max 200 mg/day; extend dosing interval

Key notes Use for short-term moderate pain or as step-down from stronger opioids. Risk of seizures (lower seizure threshold), serotonin syndrome with SSRIs/SNRIs/MAOIs. Avoid in epilepsy. Abuse potential — Schedule 4.

PBS status ✔ PBS General Benefit

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Morphine (immediate release)

Sevredol®, Kapanol® (SR) · Strong opioid

Adult dose IR: 5–10 mg PO QID PRN; SR: start 10–30 mg BD, titrate every 1–2 weeks

Renal adjustment eGFR 10–50: reduce dose by 25–50%, extend interval; eGFR <10: avoid or use with extreme caution (active metabolite accumulation)

Key notes First-line strong opioid for cancer pain and severe acute pain. For chronic non-cancer pain: only with defined goals, informed consent, regular review, and opioid agreement. Monitor for opioid-induced constipation (co-prescribe laxative). Avoid exceeding 50 mg MED/day without specialist review. Schedule 8 — requires state/territory authority for continued prescribing >2 months. Real-time prescription monitoring (SafeScript/ScriptCheck) mandatory.

PBS status ⚠️ PBS Authority Required — chronic non-cancer pain (≤12 months); PBS General Benefit for cancer pain

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Oxycodone

OxyNorm® (IR), Endone®, OxyContin® (SR) · Strong opioid

Adult dose IR: 5 mg PO QID PRN; SR: start 10 mg BD, titrate to effect

Renal adjustment eGFR <30: reduce dose by 50%, increase interval

Key notes Schedule 8. Same cautions as morphine. More predictable absorption than morphine. Oral:naloxone combination (Targin®) may reduce opioid-induced constipation. State/territory authority required for ongoing prescribing. RTPM monitoring required.

PBS status ⚠️ PBS Authority Required — chronic non-cancer pain; PBS General Benefit for cancer pain

Adjuvant Agents

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Low-dose naltrexone

Compounded · Opioid antagonist (off-label, low dose)

Adult dose 1.5–4.5 mg PO nocte (titrate from 0.5 mg); compounded formulation

Key notes Emerging evidence for fibromyalgia, CRPS, and other central sensitisation conditions. Proposed mechanism: modulation of microglial activation and Toll-like receptor 4 (TLR4). Not PBS-listed. Cost ~–60/month compounded. Use is off-label; discuss with patient and document informed consent.

PBS status ✘ Not PBS-listed (compounded)

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Cannabis-based medicines

Various (Sativex®, medicinal cannabis products) · Cannabinoid

Key notes Available via the Therapeutic Goods Administration (TGA) Special Access Scheme (SAS Category B) or Authorised Prescriber pathway for chronic non-cancer pain unresponsive to conventional therapies. Products include nabiximols (Sativex® — primarily for MS spasticity), oral THC:CBD oils, and purified CBD. Evidence for chronic pain is modest and heterogeneous. Not PBS-listed. Cost –300+/month. Driving restrictions apply — THC is detected in roadside drug testing in all Australian states/territories.

PBS status ✘ Not PBS-listed

Medications to Avoid or Use with Extreme Caution

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Benzodiazepines: No evidence for efficacy in chronic pain. Significant harms (dependence, falls, cognitive impairment, respiratory depression with opioids). Avoid for pain management. Taper if already prescribed.
Soma® (carisoprodol): Not available in Australia. Sedative with abuse potential. Not recommended.
Long-term opioids without review: All opioids for chronic non-cancer pain require regular review (minimum every 3 months), defined goals, and documented informed consent via an opioid management agreement.

Opioid Deprescribing

Patients on long-term opioids who have not achieved functional improvement, or who wish to reduce, should be supported with a structured tapering plan. Taper by 10% of the original dose every 2–4 weeks; slower tapers (5–10% per month) for patients on high doses or with long duration of use. Monitor for withdrawal symptoms, pain recurrence, and mood changes. Consider referral to a drug and alcohol service or specialist pain service for complex tapers.

Monitoring

Regular monitoring is essential in chronic pain management to evaluate treatment efficacy, detect adverse effects, and ensure treatment goals are being met. Monitoring should be proactive, structured, and patient-centred.

Monitoring Framework

Domain	Tool / Measure	Frequency
Pain intensity	NRS 0–10, BPI	Every visit; at least every 3 months
Function	BPI interference subscale, Patient-Specific Functional Scale	Every 1–3 months
Mood	PHQ-9 (depression), GAD-7 (anxiety)	Every 3–6 months; more often if mood instability
Sleep	Pittsburgh Sleep Quality Index (PSQI), single-item screening	Every 3 months
Quality of life	EQ-5D-5L	6–12 monthly
Medication safety	Medication review, renal/hepatic function, urine drug screen (if opioids)	Every 3–6 months
Opioid-specific	Morphine equivalent daily dose (MED), aberrant behaviour screening, naloxone co-prescription	Every prescription; minimum every 3 months

Treatment Goals

Goals should be SMART (Specific, Measurable, Achievable, Relevant, Time-bound) and agreed upon collaboratively with the patient. Examples:

"Walk for 20 minutes 3 days per week within 6 weeks"
"Return to part-time work within 3 months"
"Reduce pain-related catastrophising score by 30% within 8 weeks"
"Reduce opioid dose by 20% over 3 months while maintaining function"
"Improve sleep quality — sleeping ≥6 hours uninterrupted by 6 weeks"

When to Refer to Specialist Pain Services

Pain not responding to 3–6 months of primary care management
Suspected neuropathic pain requiring specialist confirmation or interventional approaches
Complex regional pain syndrome (CRPS)
Opioid dose escalation beyond 50 mg MED/day without functional improvement
Significant psychological comorbidity (PTSD, severe depression, suicidal ideation)
Need for multidisciplinary pain programme
Medicolegal or compensation-related complexity
Diagnostic uncertainty requiring advanced investigations (e.g., nerve conduction studies, MRI)

Real-Time Prescription Monitoring (RTPM)

All Australian states and territories have implemented or are implementing real-time prescription monitoring systems (SafeScript in Victoria, ScriptCheck in NSW/NT, QScript in Queensland, SCRIPTCheckWA in WA, Controlled Drugs Database in SA/Tasmania/ACT). These systems are mandatory to check before prescribing Schedule 8 medicines and are strongly recommended for Schedule 4 opioids and benzodiazepines. They help identify doctor/pharmacy shopping, polypharmacy risks, and potential overdose risk.

Special Populations

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Pregnancy

Paracetamol — Safe in all trimesters. Preferred simple analgesic.

NSAIDs — Avoid in 3rd trimester (premature ductus arteriosus closure, oligohydramnios). Avoid ibuprofen after 20 weeks if possible.

Opioids — Use at lowest dose, shortest duration. Risk of neonatal withdrawal syndrome with prolonged use. Codeine is now contraindicated in breastfeeding (ultra-rapid metaboliser risk — neonatal respiratory depression).

Amitriptyline/duloxetine — Use with caution; discuss risks/benefits with specialist. Duloxetine has limited pregnancy safety data.

Pregabalin — Limited data; avoid unless benefits outweigh risks. Category B3.

Prioritise non-pharmacological approaches. Physiotherapy and psychology are safe and recommended. Refer to obstetric medicine for complex cases.

👶

Paediatrics

Paracetamol — 15 mg/kg QID (max 60 mg/kg/day). First-line for all ages.

Ibuprofen — 5–10 mg/kg TDS. Avoid in dehydration, renal impairment.

Amitriptyline — Used off-label for neuropathic pain in paediatric chronic pain. Dose: 0.1–0.5 mg/kg nocte.

Gabapentin — Used off-label; paediatric dose: 5–10 mg/kg/day TDS, titrate to 15–30 mg/kg/day.

Chronic pain in children and adolescents requires family-centred, biopsychosocial management. School attendance and social participation are key functional goals. Refer to paediatric chronic pain services where available (e.g., The Children's Hospital at Westmead, RCH Melbourne). Pain neuroscience education is appropriate from age 8+.

👴

Older Adults (≥65 years)

Paracetamol — Preferred; reduce max dose to 2–3 g/day.

NSAIDs — Avoid or use with extreme caution. High risk of GI bleeding, renal impairment, cardiovascular events. If essential: short course, lowest dose, with PPI.

Amitriptyline — Avoid. Listed on the Beers Criteria (anticholinergic burden: sedation, falls, confusion, urinary retention, constipation, cardiac conduction disturbance).

Duloxetine — Preferred neuropathic agent in elderly. Start 30 mg, titrate to 60 mg. Monitor for hyponatraemia (SIADH).

Pregabalin/gabapentin — Use with caution; increased risk of dizziness, falls, peripheral oedema. Start at lowest dose and titrate slowly.

Opioids — Significant fall risk, cognitive impairment, constipation. If required, start very low (tramadol 25 mg, morphine 2.5 mg). Always co-prescribe laxatives.

Perform medication review using STOPP/START criteria. Assess polypharmacy. Falls risk assessment is mandatory. Cognitive function should be screened (MoCA/MMSE) before starting centrally-acting analgesics.

🫘

Renal Impairment

Paracetamol — Safe at reduced doses (≤2 g/day if eGFR <30).

NSAIDs — Avoid if eGFR <30. Nephrotoxic, cause fluid retention, hyperkalaemia, acute kidney injury.

Pregabalin — Significant renal clearance. Mandatory dose reduction in CKD.

Morphine — Active metabolite (M6G) accumulates in renal impairment — risk of respiratory depression. Use oxycodone or fentanyl (safer alternatives) with dose reduction.

Refer to renal medicine for complex pain management in CKD 4–5. Topical agents (lidocaine 5% plasters) are preferred where localised pain is present.

🫁

Hepatic Impairment

Paracetamol — Reduce to max 2 g/day (Child-Pugh A); avoid if possible in Child-Pugh B–C.

NSAIDs — Avoid. Risk of GI bleeding, hepatorenal syndrome.

Amitriptyline — Reduce dose; risk of hepatotoxicity.

Duloxetine — Contraindicated in severe hepatic impairment (Child-Pugh C).

Dose adjustments required for most hepatically metabolised agents. Pregabalin (not hepatically metabolised) may be preferred. Topical agents preferred where possible.

🛡️

Immunocompromised

Immunocompromised patients (HIV, transplant recipients, chemotherapy) may have unique pain aetiologies including infection-related neuropathy, treatment-induced pain (CIPN), and opportunistic infections.

Gabapentin/pregabalin — Useful for chemotherapy-induced peripheral neuropathy.

Duloxetine — Moderate evidence for CIPN.

Drug interactions with immunosuppressants must be considered (e.g., tramadol/serotonin syndrome risk with SSRIs used for immunosuppression-related depression). Refer to infectious disease or oncology for complex cases.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Chronic pain is a significant health burden for Aboriginal and Torres Strait Islander Australians. The 2018–19 National Aboriginal and Torres Strait Islander Health Survey found that approximately 28% of Indigenous Australians reported having chronic pain, compared to 16% of non-Indigenous Australians — a prevalence ratio of 1.4–1.8×. Chronic pain contributes to substantial disability, reduced workforce participation, psychological distress, and reduced life expectancy.

⚠️

Cultural safety is essential: Pain has cultural, spiritual, and social dimensions in many Aboriginal and Torres Strait Islander communities. Western biomedical models of pain may not align with Indigenous understandings of health and wellbeing. Always use a trauma-informed, culturally safe, and strengths-based approach. Use the AIATSIS Guidelines for Ethical Research and the Lowitja Institute frameworks for culturally responsive practice.

Higher prevalence

28% vs 16% in non-Indigenous Australians. Higher rates of musculoskeletal pain, headache, dental pain, and pain related to chronic conditions (diabetes, renal disease, cardiovascular disease). Pain is a leading cause of GP presentations in Aboriginal Medical Services (AMS).

Access barriers

Geographic remoteness limits access to specialist pain services, physiotherapy, psychology, and multidisciplinary programmes. Wait times for public pain clinics in regional/remote areas often exceed 12–18 months. Limited availability of allied health professionals in remote communities. Cultural and historical barriers to engaging with mainstream healthcare services due to experiences of racism and discrimination.

Pain expression & communication

Some Aboriginal and Torres Strait Islander people may underreport pain due to cultural norms, stoicism, or fear of being perceived as weak. Conversely, some may express pain differently. Standard pain scales may not be culturally appropriate — use culturally validated tools where available, and allow time for storytelling-based pain assessment. Interpreter services should be used when English is not the first language (particularly in remote NT, WA, and QLD communities).

Opioid prescribing concerns

Aboriginal and Torres Strait Islander Australians are disproportionately affected by opioid-related harms. Codeine-containing medicines and prescription opioids are prescribed at higher rates. Ensure adherence to RTPM systems. Consider community-level approaches to opioid safety including naloxone co-prescription and community education. The Aboriginal and Torres Strait Islander Pain Management Programme (AIHW) has highlighted the need for culturally appropriate opioid reduction strategies.

Culturally appropriate models of care

Aboriginal Community Controlled Health Organisations (ACCHOs/AMS) are the preferred setting for chronic pain management. Integrate pain management with existing chronic disease management programmes. Use of Aboriginal Health Practitioners and Aboriginal Health Workers for pain education, exercise programmes, and follow-up. Telehealth pain medicine consultations have expanded significantly and should be used to bridge geographic gaps. Community-based, group pain education programmes delivered by Indigenous health workers show promise.

Social determinants

Address the broader social determinants of health that contribute to chronic pain burden: housing, employment, education, food security, family violence, intergenerational trauma, and incarceration history. Pain management plans must be realistic within the patient's social context. Co-design of pain management approaches with communities is recommended (NHMRC guidelines).

Key resources for practitioners:

Lowitja Institute — Research and resources for Aboriginal and Torres Strait Islander health
NACCHO (National Aboriginal Community Controlled Health Organisation) — Clinical resources and health promotion
RACGP Specific Interests: Aboriginal and Torres Strait Islander Health — Practice guidance
PainAustralia — Fact Sheets — Including culturally relevant pain management information
Indigenous Allied Health Australia (IAHA) — Allied health workforce and culturally safe practice

📚 References

1. Australian Institute of Health and Welfare (AIHW). Chronic pain in Australia. Cat. no. PHE 267. Canberra: AIHW; 2020.
2. PainAustralia. The cost of pain in Australia. Sydney: PainAustralia; 2019.
3. Nicholas MK, Blyth FM. Are self-management strategies effective in chronic pain treatment? Pain Manag. 2016;6(1):75–88.
4. Royal Australian College of General Practitioners (RACGP). Prescribing drugs of dependence in general practice, Part B: Benzodiazepines. Melbourne: RACGP; 2015 (updated 2022).
5. Royal Australian College of General Practitioners (RACGP). Prescribing drugs of dependence in general practice, Part C1: Opioids. Melbourne: RACGP; 2022.
6. Faculty of Pain Medicine, Australian and New Zealand College of Anaesthetists (FPM ANZCA). Recommendations regarding the use of opioid analgesics in patients with chronic non-cancer pain. Melbourne: FPM ANZCA; 2022.
7. Finnerup NB, Attal N, Haroutounian S, et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14(2):162–173.
8. Dworkin RH, O'Connor AB, Kent J, et al. Interventional management of neuropathic pain: NeuPSIG recommendations. Pain. 2013;154(11):2249–2261.
9. Foster NE, Anema JR, Cherkin D, et al. Prevention and treatment of low back pain: evidence, challenges, and promising directions. Lancet. 2018;391(10137):2368–2383.
10. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.
11. National Health and Medical Research Council (NHMRC). National Statement on Ethical Conduct in Human Research. Canberra: NHMRC; 2023 (updated).
12. Kamper SJ, Apeldoorn AT, Chiarotto A, et al. Multidisciplinary biopsychosocial rehabilitation for chronic low back pain: Cochrane systematic review and meta-analysis. Cochrane Database Syst Rev. 2014;(9):CD000963.
13. de C Williams AC, Fisher E, Hearn L, Eccleston C. Psychological therapies for the management of chronic pain (excluding headache) in adults. Cochrane Database Syst Rev. 2020;(8):CD007407.
14. Geneen LJ, Moore RA, Clarke C, et al. Physical activity and exercise for chronic pain in adults: an overview of Cochrane Reviews. Cochrane Database Syst Rev. 2017;(1):CD011279.
15. Australian Bureau of Statistics (ABS). National Aboriginal and Torres Strait Islander Health Survey, 2018–19. Cat. no. 4715.0. Canberra: ABS; 2019.

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).