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Time-Based Pain Descriptors

Last updated 1 Jun 2026 · Pain & analgesia

📋 Key Information Summary

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  • Pain is classified by duration and temporal pattern into acute, recurrent, chronic, and flare categories, each carrying distinct diagnostic and therapeutic implications.
  • Acute pain (duration <3 months) serves a protective nociceptive function, typically resolves with tissue healing, and responds well to multimodal analgesia including paracetamol, NSAIDs, and short-course opioids when indicated.
  • Recurrent pain consists of discrete episodes with pain-free intervals and often signals an underlying episodic condition (e.g. migraine, endometriosis, gout) requiring both acute treatment and preventive strategies.
  • Chronic pain (≥3 months or beyond expected healing) is now recognised as a disease entity in its own right under ICD-11, involving maladaptive neuroplasticity and requiring a biopsychosocial, multidisciplinary approach.
  • Pain flares are transient exacerbations superimposed on baseline chronic or recurrent pain, often triggered by activity, stress, illness, or treatment gaps, and require pre-planned action plans.
  • Temporal descriptors help identify red flags: rapidly escalating acute pain may indicate visceral catastrophe; new-onset chronic pain in the elderly demands malignancy screening.
  • Australian data (ABS National Health Survey 2022) estimates 3.4 million Australians live with chronic pain, with higher prevalence in Aboriginal and Torres Strait Islander communities and rural/remote populations.
  • The WHO Analgesic Ladder remains relevant for acute and cancer pain but is less applicable to chronic non-cancer pain, where functional restoration and psychological therapies are central.
  • Opioid prescribing for chronic non-cancer pain in Australia is declining under real-time prescription monitoring (SafeScript, SafeScript NSW), yet acute pain remains undertreated in some settings.
  • Multimodal analgesia — combining paracetamol, NSAIDs (where safe), neuropathic agents, and non-pharmacological strategies — reduces opioid reliance across all pain durations.
  • All patients with recurrent or chronic pain should have an individualised written pain management plan, ideally documented via the GP Management Plan (GPMP) and Team Care Arrangements (TCA) items (MBS 721, 723).
  • Pain flares should be anticipated and managed with pre-agreed rescue strategies rather than reactive opioid dose escalation.

Introduction & Australian Epidemiology

Pain classification by duration and temporal pattern is a cornerstone of clinical assessment. The International Association for the Study of Pain (IASP, 2020 revised definition) describes pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage." Importantly, the IASP now acknowledges that pain can exist without identifiable nociception and that persistent pain may be a primary disease state rather than a symptom.

Time-based descriptors — acute, recurrent, chronic, and flare — provide a shared language between clinicians and patients that guides investigation urgency, analgesic selection, escalation pathways, and the balance between pharmacological and non-pharmacological interventions. In Australian primary care, pain is the most common presenting complaint, accounting for approximately 20% of all general practice encounters (Britt et al., 2023).

Australian Burden of Pain

  • Approximately 3.4 million Australians (16.1% of the population) live with chronic pain; this is projected to reach 5.2 million by 2050 due to population ageing (Painaustralia, 2019).
  • Chronic pain costs the Australian economy an estimated 9.3 billion annually, including healthcare expenditure, lost productivity, and carer costs.
  • Acute pain presentations to Australian emergency departments exceed 4.5 million per year, with musculoskeletal, abdominal, and headache the leading causes (AIHW, 2023).
  • Aboriginal and Torres Strait Islander Australians experience chronic pain at 1.5–2 times the rate of non-Indigenous Australians, compounded by reduced access to multidisciplinary pain services.
  • Rural and remote Australians have 40% fewer pain specialists per capita and are more likely to receive opioids as monotherapy rather than multidisciplinary care.
  • Common recurrent pain conditions — migraine (affecting ~4.9 million Australians), endometriosis (~1 in 9 women), and gout (~3% of adults) — contribute significantly to primary care workload and pharmaceutical expenditure.
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Temporal pattern recognition is not merely descriptive — it is a diagnostic tool. Acute-onset severe pain ("thunderclap" quality) may indicate subarachnoid haemorrhage, aortic dissection, or mesenteric ischaemia. Failure to distinguish a chronic pain flare from a new acute pathology can result in missed diagnoses.

Acute Pain

Acute pain is defined as pain of recent onset (typically <3 months) that is directly related to tissue injury or a specific disease process. It serves a vital biological protective function, usually resolves as the underlying cause heals, and is associated with identifiable nociceptive and inflammatory mechanisms. Acute pain can be somatic (musculoskeletal), visceral (organ-derived), or neuropathic (nerve injury, e.g. acute herpes zoster).

Classification of Acute Pain by Origin

Category Examples Key Features
Somatic Fracture, laceration, surgical wound, osteoarthritis flare Well-localised, sharp or aching
Visceral Appendicitis, renal colic, myocardial infarction, pancreatitis Poorly localised, cramping or pressure-like, may refer
Neuropathic Acute disc prolapse with radiculopathy, herpes zoster, nerve injury Burning, shooting, electric; dermatomal distribution
Inflammatory Acute gout, cellulitis, post-operative inflammation Swelling, warmth, erythema; worse with movement
Procedural Needle procedures, wound dressings, physiotherapy Anticipatory; manageable with pre-emptive analgesia

Red Flags in Acute Pain

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Seek immediate specialist assessment if acute pain is accompanied by:
  • Haemodynamic instability (tachycardia, hypotension, diaphoresis)
  • Thunderclap onset (peak intensity within seconds) — subarachnoid haemorrhage, aortic dissection
  • Abdominal rigidity or peritonism
  • Neurological deficit (weakness, saddle anaesthesia, bowel/bladder dysfunction)
  • Fever with focal pain suggesting abscess or septic arthritis
  • Acute pain in immunocompromised patients (opportunistic infection, neutropenic enterocolitis)

Management of Acute Pain — Multimodal Approach

Australian guidelines (eTG, RACGP) recommend a stepped multimodal strategy for acute pain, beginning with non-opioid agents and escalating only when necessary.

1
Non-Pharmacological
Ice/heat, elevation, immobilisation, patient education, reassurance. First-line for mild acute musculoskeletal pain.
2
Simple Analgesics
Paracetamol (1 g PO/IV QID) ± NSAIDs (e.g. ibuprofen 400 mg PO TDS). Scheduled dosing preferred over PRN for the first 48–72 hours.
3
Weak Opioids ± Adjuvants
Tramadol 50–100 mg PO Q4–6H (max 400 mg/day) or codeine 30–60 mg PO Q4–6H. Add neuropathic agents if indicated (e.g. gabapentin for radiculopathy).
4
Strong Opioids
Oxycodone 5–10 mg PO Q4–6H or morphine 2.5–5 mg SC Q4H (for severe acute pain). Use lowest effective dose for shortest duration. Prescribe naloxone if ≥50 mg morphine equivalents/day.

Acute Pain Pharmacotherapy — Key Agents

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Paracetamol
Panadol®, Panamax®, Dymadon® · Analgesic/antipyretic
Adult dose 500 mg–1 g PO/PR Q4–6H (max 4 g/day); IV 1 g Q6H
Paediatric dose 15 mg/kg PO/PR Q4–6H (max 60 mg/kg/day); IV 15 mg/kg Q6H
Renal adjustment eGFR 10–50: max 500 mg Q6H; eGFR <10: max 500 mg Q8H
Hepatic adjustment Severe hepatic impairment or active alcoholism: max 2 g/day; consult hepatologist
PBS status ✔ PBS General Benefit
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Ibuprofen
Nurofen®, Brufen® · NSAID
Adult dose 200–400 mg PO TDS (max 1.2 g/day for OTC; 2.4 g/day prescription)
Paediatric dose 5–10 mg/kg PO TDS (max 30 mg/kg/day)
Renal adjustment eGFR <30: avoid if possible; otherwise short course with monitoring
Key safety Avoid in GI bleeding, severe cardiac failure, third-trimester pregnancy. Use with PPI if GI risk.
PBS status ✔ PBS General Benefit
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Oxycodone (immediate-release)
OxyNorm®, Endone® · Strong opioid
Adult dose 5–10 mg PO Q4–6H (opioid-naïve); titrate to effect
Paediatric dose 0.1–0.2 mg/kg PO Q4–6H (specialist guidance recommended)
Renal adjustment eGFR 10–50: reduce dose by 25–50%, extend interval; eGFR <10: avoid or use morphine with caution
Key safety Shortest duration possible; prescribe naloxone if ≥50 mg OME/day; real-time monitoring via SafeScript
PBS status ⚠ PBS Authority Required
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Ketamine (sub-dissociative IV)
Ketalar® · NMDA antagonist / adjuvant
Adult dose 0.1–0.3 mg/kg IV bolus for refractory acute pain (ED/anaesthesia settings)
Paediatric dose Procedural: 1–2 mg/kg IV; analgesic: 0.1–0.2 mg/kg IV (specialist only)
Key safety Avoid in uncontrolled hypertension, raised ICP, psychosis; monitor for emergence phenomena
PBS status ✖ Not PBS (hospital use)

Duration of Acute Pain Treatment

Most acute pain resolves within days to weeks. Opioid prescriptions for acute pain should be limited to 3–5 days for most conditions (e.g. dental pain, minor musculoskeletal injury) and rarely exceed 7 days unless post-surgical or trauma-related (RACGP, 2022). Patients whose acute pain persists beyond 4–6 weeks should be reassessed for evolving chronicity or missed diagnosis.

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Transition to chronic pain: Approximately 10–15% of patients with acute musculoskeletal pain develop chronic pain. Risk factors for chronification include high initial pain severity, psychological distress, catastrophising, poor sleep, and avoidance behaviours. Early identification allows targeted biopsychosocial intervention.

Recurrent Pain

Recurrent pain is characterised by discrete episodes of pain separated by pain-free intervals. The pain-free intervals may last days, weeks, or months. Recurrent pain is a temporal pattern rather than a diagnosis — it signals an underlying episodic condition that warrants identification and targeted management of both the acute episodes and the predisposing condition.

Common Conditions Presenting as Recurrent Pain

Condition Pain Pattern Frequency Key Features
Migraine 4–72 hr episodes, often unilateral, pulsating 1–15+ episodes/month ± aura, photophobia, phonophobia, nausea; may evolve to chronic migraine (≥15 days/month)
Endometriosis Cyclical pelvic pain, dysmenorrhoea, dyspareunia With each menstrual cycle ~1 in 9 Australian women; diagnostic delay avg. 6.5 years
Gout Acute monoarthritis (1st MTP classic), self-limiting 7–14 days Variable — months to years if untreated Flares may become polyarticular; tophi with chronicity
Trigeminal neuralgia Brief (seconds–2 min), lancinating facial pain Multiple attacks daily in clusters V2/V3 distribution; triggered by touch, wind, chewing
Sickle cell crises Acute severe bony/abdominal pain lasting days Highly variable (0–>6/year) Predominantly in migrant communities; requires coordinated care
Irritable bowel syndrome Recurrent abdominal pain ≥1 day/week (Rome IV) Chronic/recurrent overlap Associated with altered bowel habit; pain-free intervals common
Renal colic Acute severe flank pain, waves, 20–60 min ~50% recurrence within 5 years Haematuria; CT KUB gold standard
Cluster headache Severe unilateral orbital pain, 15–180 min 1–8 attacks/day during cluster (weeks–months) Restlessness, lacrimation, rhinorrhoea; male predominance

Dual Management Strategy

Recurrent pain requires a two-pronged approach: treatment of acute episodes and prevention/modification of the underlying condition to reduce frequency and severity.

Acute Episode Management
  • Condition-specific abortive therapy (e.g. triptans for migraine, colchicine/NSAIDs for gout)
  • Symptomatic relief: paracetamol, NSAIDs, anti-emetics
  • Written action plan for self-management at home
  • Criteria for emergency presentation (e.g. status migrainosus >72 hr, suspected septic joint)
Preventive Strategy
  • Prophylactic medications (e.g. topiramate/propranolol for migraine, allopurinol for gout)
  • Trigger identification and avoidance (e.g. dietary triggers in gout, hormonal cycle in endometriosis)
  • Lifestyle modification (weight, alcohol, sleep hygiene, stress management)
  • Specialist referral when episodes are frequent (≥4 migraine days/month, recurrent gout despite ULT)

When Recurrent Pain Becomes Chronic

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Frequency escalation: When episodic conditions increase in frequency (e.g. migraine evolving from 4 to ≥15 headache days/month, termed "chronic migraine"), the management approach must shift from episodic treatment toward chronic pain strategies including preventives, neuromodulation, and psychological interventions. Medication-overuse headache (MOH) must be excluded — regular use of simple analgesia ≥15 days/month or triptans/opioids ≥10 days/month may perpetuate the cycle.

Recording Recurrent Pain Patterns

Patients should be encouraged to keep a pain diary documenting frequency, duration, severity (0–10 NRS), triggers, associated features, and response to treatment. Digital tools (e.g. ManagePain app, Headache Diary apps) facilitate data collection and support PBS authority applications for preventive medications. Pain diary data also supports GPMP/TCA (MBS items 721, 723, 732) review and chronic disease management planning.

Chronic Pain

Chronic pain is defined as pain that persists or recurs for ≥3 months, or beyond the expected time for tissue healing. The IASP (2020) and ICD-11 recognise chronic pain as a disease entity in its own right, not merely a symptom. Chronic pain involves maladaptive neuroplastic changes in both the peripheral and central nervous systems, including central sensitisation, descending inhibitory pathway dysfunction, and altered cortical representation.

ICD-11 Classification of Chronic Pain

ICD-11 Category Examples Prevalence in Australia
Chronic primary pain Fibromyalgia, chronic widespread pain, chronic primary headache, irritable bowel syndrome, chronic pelvic pain ~5–8% of adults
Chronic cancer pain Tumour-related, treatment-related (chemotherapy neuropathy, radiation fibrosis), survivorship pain ~35–40% during treatment; ~5–10% of survivors
Chronic post-surgical/post-traumatic Post-mastectomy pain, chronic post-herniorrhaphy pain, phantom limb pain ~10–50% depending on surgery type
Chronic neuropathic Diabetic peripheral neuropathy, post-herpetic neuralgia, spinal cord injury pain ~7–8% of adults
Chronic secondary headache/orofacial Medication-overuse headache, chronic tension-type headache, trigeminal neuropathic pain ~3–4% of adults
Chronic secondary visceral Chronic pancreatitis pain, endometriosis-related, interstitial cystitis Variable by condition
Chronic secondary musculoskeletal Chronic low back pain (non-specific), osteoarthritis, rheumatoid arthritis, ankylosing spondylitis ~15–20% of adults

Central Sensitisation

In chronic pain, sustained nociceptive input drives central sensitisation — increased excitability of central neurons resulting in: pain hypersensitivity (allodynia, hyperalgesia), expansion of receptive fields, and continued pain in the absence of ongoing tissue damage. This concept is critical because it explains why purely peripherally-targeted treatments (e.g. repeated opioids, surgery) may fail in chronic pain, and why centrally-acting agents and non-pharmacological approaches are often more effective.

Biopsychosocial Assessment

Chronic pain requires assessment beyond the biomedical model. The Australian National Pain Strategy (2010) and Painaustralia guidelines recommend systematic identification of:

  • Biological: Nociceptive source, neuropathic component (DN4 score ≥4), comorbidities, medication effects
  • Psychological: Depression (PHQ-9), anxiety (GAD-7), catastrophising (PCS), fear-avoidance beliefs, post-traumatic stress
  • Social: Employment impact, financial stress, relationship strain, social isolation, cultural beliefs about pain
  • Functional: Disability (Brief Pain Inventory Interference scale), sleep disturbance (PSQI), physical deconditioning

Management of Chronic Pain — Multidisciplinary Approach

1
Education & Self-Management
Pain neuroscience education (PNE), understanding central sensitisation, active coping strategies. Painaustralia's "My Pain Toolkit" is a free Australian resource.
2
Physical Therapies
Graded exercise therapy, physiotherapy, hydrotherapy, yoga, tai chi. Evidence strongest for chronic low back pain and fibromyalgia.
3
Psychological Therapies
Cognitive behavioural therapy (CBT), acceptance and commitment therapy (ACT), mindfulness-based stress reduction (MBSR). Accessible via Focussed Psychological Strategies (FPS) MBS items 80000–80015, 80100–80115, 80125–80140, 80150.
4
Pharmacotherapy (Adjunctive)
See drug cards below. Agents targeting specific pain mechanisms: antidepressants for neuropathic/central pain, anticonvulsants, topical agents. Opioids are generally NOT recommended long-term for chronic non-cancer pain.
5
Interventional / Specialist
Nerve blocks, spinal cord stimulation, intrathecal drug delivery, radiofrequency ablation. Access via specialist pain medicine physician. Medicare rebates under relevant MBS items (e.g. 39106, 39107, 18260).

Pharmacotherapy for Chronic Pain

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Amitriptyline
Endep®, Tryptanol® · TCA / neuropathic pain
Adult dose 10–25 mg PO nocte, titrate to 50–75 mg (max 150 mg)
Renal adjustment No specific adjustment; use with caution
Key safety Anticholinergic effects; avoid in significant cardiac conduction disease; counsel re: sedation, weight gain, dry mouth
PBS status ✔ PBS General Benefit
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Duloxetine
Cymbalta® · SNRI / neuropathic pain, fibromyalgia
Adult dose 30 mg PO daily for 1 week, then 60 mg PO daily (max 120 mg)
Renal adjustment eGFR <30: avoid
Key safety Avoid in severe hepatic impairment; monitor BP; serotonin syndrome risk with concurrent serotonergic agents
PBS status ⚠ PBS Authority Required (neuropathic pain)
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Pregabalin
Lyrica® · Gabapentinoid / neuropathic pain, fibromyalgia
Adult dose 75 mg PO BD, titrate to 150–300 mg BD (max 600 mg/day)
Renal adjustment eGFR 30–60: max 150 mg BD; eGFR 15–30: max 75 mg BD; eGFR <15: 25 mg daily
Key safety Risk of misuse/diversion (Schedule 4); taper on cessation; dizziness, weight gain, peripheral oedema
PBS status ⚠ PBS Authority Required (neuropathic pain)
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Tapentadol
Palexia® · Opioid + NRI / chronic non-cancer pain
Adult dose 50 mg PO BD, titrate by 50 mg BD every 3–7 days (max 500 mg/day)
Renal adjustment eGFR 30–60: max 100 mg BD; eGFR <30: avoid
Key safety Serotonin syndrome risk with SSRIs/SNRIs; lower abuse potential than traditional opioids but still Schedule 8
PBS status ⚠ PBS Authority Required
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Lidocaine 5% medicated plasters
Versatis® · Topical anaesthetic / post-herpetic neuralgia
Adult dose Up to 3 plasters applied to painful area for 12 hours on / 12 hours off
Renal/hepatic No adjustment (minimal systemic absorption)
PBS status ⚠ PBS Authority Required (post-herpetic neuralgia)
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Opioids in chronic non-cancer pain: Current Australian evidence and guidelines (RACGP 2022, eTG, Faculty of Pain Medicine ANZCA) recommend against long-term opioid therapy as first-line for chronic non-cancer pain. Benefits are modest and risks (dependence, hyperalgesia, cognitive effects, falls, respiratory depression) increase with dose and duration. If trialled, a time-limited trial with clear functional goals and regular review (<20 mg morphine equivalents/day preferred) is recommended. Naloxone should be co-prescribed if ≥50 mg OME/day.

Pain Flares

Pain flares are transient episodes of increased pain severity that occur superimposed on a patient's baseline chronic or recurrent pain. They are extremely common — reported in 65–80% of patients with chronic pain conditions — and are a major source of distress, emergency presentations, and opioid dose escalation. Flares are distinct from disease progression and usually self-limit over hours to days.

Common Triggers of Pain Flares

Category Examples
Physical Overactivity, unfamiliar exercise, prolonged posture, physiotherapy session, intercurrent illness (UTI, respiratory infection)
Psychological Stress, anxiety, poor sleep, depressed mood, grief, work conflict
Environmental Weather changes (cold, humidity), travel, disrupted routine
Iatrogenic Medication dose reduction/cessation, missed doses, treatment gaps (e.g. pandemic-related service disruption)
Disease-specific New fracture in osteoporosis, gout flare superimposed on chronic tophaceous gout, cancer progression

Flare Action Plans

Every patient with chronic or recurrent pain should have a written flare management plan co-developed with their GP or pain specialist. This reduces anxiety during flares, prevents unnecessary ED presentations, and supports self-efficacy.

1
Recognise
Patient identifies the flare early. Agree on a severity threshold (e.g. pain ≥7/10 for >4 hours, or functional impact preventing essential activities).
2
Self-Manage (Mild Flares)
Heat/cold, gentle movement (not bed rest), pacing strategies, relaxation/breathing techniques, distraction, topical analgesics. Continue baseline medications.
3
Pharmacological Rescue (Moderate Flares)
Short course (3–5 days) of step-up analgesia: paracetamol 1 g QID, NSAID (if safe), or prescribed rescue medication (e.g. tramadol 50–100 mg PRN, low-dose oxycodone for cancer pain). Return to baseline regimen when flare settles.
4
Seek Help (Severe/Refractory Flares)
Contact GP, specialist pain service, or present to ED if: pain is atypical, associated with new neurological features, fever, haemodynamic changes, or unresponsive to rescue plan >48 hours.

Cancer Pain Flares — Breakthrough Pain

In cancer pain, flares are termed breakthrough pain (BTP) — a transient exacerbation of moderate-to-severe pain occurring on a background of otherwise controlled baseline pain. BTP may be incident-related (movement, procedures), spontaneous, or due to end-of-dose failure of regular analgesia.

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Fentanyl intranasal
Instanyl®, Pecfent® · Rapid-onset opioid
Adult dose 50–100 mcg intranasal PRN for breakthrough pain (onset ~5–10 min); titrate in 50 mcg increments
Key safety For opioid-tolerant patients only (≥60 mg OME/day baseline); risk of respiratory depression; monitor closely
PBS status ⚠ PBS Authority Required (cancer breakthrough pain)
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Morphine oral solution (immediate-release)
Ordine® · Strong opioid
Adult dose Breakthrough: 1/6th to 1/10th of total daily morphine equivalent dose, PO Q2–4H PRN
Renal adjustment eGFR 10–50: reduce dose 25–50%, extend interval; eGFR <10: avoid active metabolites — use fentanyl or hydromorphone
PBS status ⚠ PBS Authority Required
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Key principle: Pain flares are expected, not a treatment failure. Pre-planning reduces suffering. If flares become more frequent or severe, it may indicate disease progression, treatment tolerance, or psychosocial deterioration — not simply a reason to increase baseline opioids.

Pathophysiology of Pain Duration & Temporal Patterns

Understanding why pain persists, recurs, or flares requires knowledge of the neurobiological continuum from acute nociception to chronic pain states.

Acute Nociception

  • Tissue injury activates peripheral nociceptors (Aδ and C fibres) via bradykinin, prostaglandins, substance P, and H⁺ ions.
  • Signals travel to the dorsal horn of the spinal cord (laminae I, II, V) and ascend via the spinothalamic and spinoreticular tracts.
  • Inflammatory mediators cause peripheral sensitisation — lowered thresholds and increased responsiveness of nociceptors.
  • Descending modulatory pathways (periaqueductal grey → raphe nucleus) provide inhibitory tone via serotonin and noradrenaline.
  • Pain resolves with tissue healing and resolution of the inflammatory cascade.

Transition to Chronic Pain

  • Persistent nociceptive input triggers central sensitisation: NMDA receptor activation, wind-up phenomenon, loss of inhibitory interneurons (GABA/glycine depletion).
  • Neuroplastic changes include expansion of receptive fields, recruitment of Aβ fibres for pain transmission, and cortical reorganisation.
  • Glial cell activation (microglia, astrocytes) in the spinal cord sustains neuroinflammation independent of peripheral input.
  • Psychosocial factors (stress, catastrophising, fear-avoidance) amplify central sensitisation via top-down facilitation from the amygdala and anterior cingulate cortex.
  • The result is pain perception that is disproportionate to or independent of tissue damage — the hallmark of chronic pain.

Mechanisms of Recurrence and Flares

  • Recurrence: Reflects reactivation of an underlying disease process (e.g. urate crystal deposition in gout, cortical spreading depression in migraine) during a quiescent interval.
  • Flares: In chronic pain, flares represent transient failure of descending inhibition, stress-mediated HPA axis activation increasing central sensitisation, or minor peripheral insults amplified by sensitised circuits.
  • In cancer pain, flares may reflect tumour growth through sensitive structures, procedural stimulation of nociceptors, or end-of-dose pharmacokinetic failure.
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Clinical relevance: The shift from peripheral to central mechanisms explains why chronic pain patients often report diffuse, migrating pain that doesn't follow dermatomal patterns, and why escalating peripheral-targeted treatments (more opioids, more injections) provide diminishing returns. This understanding supports the shift toward centrally-acting agents (antidepressants, anticonvulsants) and neuromodulatory therapies.

Investigations by Pain Temporal Pattern

Investigation strategy differs by temporal pattern. Acute pain demands urgent exclusion of serious pathology; chronic pain requires assessment of contributing factors rather than endless pursuit of a structural cause.

Essential FBC, CRP, ESR Baseline inflammatory markers; raise suspicion for infection, malignancy, or autoimmune disease in any temporal pattern. MBS item 65070/65073.
Essential U&E, eGFR, LFTs Renal function guides analgesic choice (NSAIDs, opioids, gabapentinoids); LFTs before hepatotoxic agents. MBS item 66500/66503.
Available Serum urate Diagnosis and monitoring of gout (recurrent acute arthritis). Perform 2+ weeks after acute flare for accuracy. MBS item 66549.
Available HbA1c, fasting glucose Screen for diabetes mellitus as a cause of peripheral neuropathic pain (chronic). MBS item 66545.
Available Calcium, vitamin D, PTH, bone profile For chronic pain in elderly — exclude osteomalacia, hyperparathyroidism, or occult fracture. MBS item 66516.
Available Thyroid function (TSH, fT4) Hypothyroidism and hyperthyroidism can contribute to musculoskeletal pain and myopathy. MBS item 66719.
Imaging Plain radiography Acute fracture assessment, osteoarthritis severity, gouty erosions. Available in most GP practices and all EDs. MBS item 58100–58122.
Imaging CT (non-contrast KUB, head, spine) Renal colic (CT KUB gold standard), acute headache (CT head for SAH exclusion), spinal pathology. Requires radiology referral. MBS items 56001–56806.
Imaging MRI Soft tissue, nerve root, spinal cord assessment. Requires specialist referral or radiology request. Long wait times in public sector. MBS items 63001–63564.
Specialist Nerve conduction studies / EMG Objective assessment of peripheral neuropathy, radiculopathy, and entrapment neuropathies. Requires neurologist or rehabilitation physician. MBS item 11005.
Specialist Diagnostic nerve blocks Identify pain generators for interventional management. Performed by pain specialist or proceduralist. MBS item 39106.
Available Validated screening tools DN4 (neuropathic pain screening), Brief Pain Inventory, PHQ-9, GAD-7, Pain Catastrophising Scale, Central Sensitisation Inventory. Free to use in clinical practice; no MBS item.
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Avoid "diagnostic odysseys": In chronic pain, repeated investigations in the absence of new clinical features are unlikely to change management and may worsen health anxiety. Normal MRI findings in chronic low back pain are common (disc bulges in ~30% of asymptomatic adults aged 30–50). Focus investigations on new, progressive, or red-flag symptoms.

Risk Stratification & Chronification Predictors

Identifying patients at risk of transitioning from acute to chronic pain enables early, targeted intervention. The following models and risk factors are endorsed by Australian pain guidelines.

Predictors of Pain Chronification

Low Risk
Acute Pain — Expected Resolution
Clear tissue injury, first episode, good coping, no psychosocial barriers, mild–moderate severity (<5/10 NRS), minimal functional impact.
Management: Standard acute pain pathway. GP follow-up in 2–4 weeks.
Moderate Risk
Acute Pain — Chronification Risk
High initial pain severity (≥7/10), multiple previous episodes, mild anxiety/depression, sedentary behaviour, poor sleep, occupational factors (heavy manual work, unsupportive employer).
Management: Address psychosocial factors early. Consider GPMP/TCA (MBS 721/723). Reassess at 4–6 weeks.
High Risk
Pain — Likely Chronicity
Significant psychological comorbidity (PTSD, severe depression, catastrophising PCS ≥30), prior chronic pain, poor social support, workers' compensation/litigation, opioid-naïve but prescribed opioids, avoidance behaviours, substance use history.
Management: Early multidisciplinary referral. Pain education at first presentation. Pain Management Plan within 6 weeks. Specialist pain service referral if not improving by 3 months.

The Keele STarT Back Screening Tool is a validated 9-item tool for low back pain stratification (low/medium/high risk of poor outcome), freely available and recommended by NICE and Australian physiotherapy guidelines.

Special Populations

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Pregnancy

Paracetamol
First-line analgesic in pregnancy; considered safe at all gestations at standard doses (≤4 g/day).
NSAIDs
Avoid from 30 weeks' gestation (risk of premature closure of ductus arteriosus, oligohydramnios). Use with caution in the first trimester. Ibuprofen preferred over other NSAIDs when short-term use required before 30 weeks.
Opioids
Short-term use acceptable if needed (codeine, oxycodone). Neonatal withdrawal risk with prolonged use in third trimester. Codeine: CYP2D6 variability may cause excess morphine in breast milk — avoid in breastfeeding.
Gabapentinoids
Pregabalin Category B3; limited data. Avoid unless benefits outweigh risks; discuss with specialist. Gabapentin limited data — avoid if possible.
Chronic pelvic pain / endometriosis
Pregnancy often improves endometriosis symptoms; postpartum recurrence expected. Mirena® IUD can be inserted at Caesarean section for ongoing management.
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Paediatrics

Assessment
Use age-appropriate pain scales: FLACC (0–3 years), Wong-Baker FACES (3–7 years), NRS (≥8 years). Pain diaries suitable from school age.
Acute pain
Paracetamol 15 mg/kg Q4–6H (max 60 mg/kg/day); ibuprofen 5–10 mg/kg TDS. Codeine is CONTRAINDICATED in children <12 years and in 12–18-year-olds post-tonsillectomy (TGA, 2015).
Chronic pain
Paediatric chronic pain is common (25% of children report weekly pain). Biopsychosocial approach essential. Children's pain management programs (e.g. Royal Children's Hospital Melbourne, Westmead Children's Hospital) are the gold standard. Amitriptyline and gabapentin used off-label with specialist guidance.
Recurrent abdominal pain
Functional abdominal pain (Rome IV criteria) affects ~10–15% of school-age children. Exclude red flags (weight loss, rectal bleeding, fever, family IBD history). Management: reassurance, dietary advice, CBT.
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Elderly (≥65 years)

Polypharmacy risk
Review all medications for interactions. Paracetamol preferred first-line. NSAIDs: avoid chronic use (GI bleeding, renal decline, cardiovascular risk). Opioids: increased fall risk, cognitive impairment, constipation — use lowest effective dose.
Renal impairment
GFR declines ~1 mL/min/year after age 40. Adjust gabapentinoid doses (pregabalin: eGFR <15 → 25 mg daily). Avoid morphine (active metabolite M6G accumulates) — use fentanyl or hydromorphone if opioid needed in significant CKD.
Non-verbal pain assessment
In dementia, use PAINAD (Pain Assessment in Advanced Dementia) or Abbey Pain Scale. Observe for behavioural indicators: grimacing, guarding, agitation, withdrawal.
New-onset chronic pain
Always consider underlying malignancy, temporal arteritis, polymyalgia rheumatica, vertebral fracture, or Paget's disease. ESR/CRP mandatory.
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Renal Impairment

Paracetamol
Safe to eGFR 10; reduce dose below eGFR 10 (max 500 mg Q8H). First-line for all pain durations.
NSAIDs
Avoid in eGFR <30. Short courses only in eGFR 30–60 with monitoring. Risk of AKI, hyperkalaemia, fluid retention.
Opioids
Avoid morphine (M6G accumulation → toxicity). Preferred: fentanyl, hydromorphone, buprenorphine. Reduce doses 25–50% and extend intervals. HD patients: gabapentin 200–300 mg post-dialysis.
Gabapentin
Renally cleared — mandatory dose reduction. eGFR 30–59: max 300 mg BID; eGFR 15–29: max 300 mg daily; eGFR <15: 200–300 mg post-dialysis.
🫁

Hepatic Impairment

Paracetamol
In chronic liver disease or active alcoholism: max 2 g/day. Reduced glucuronidation increases NAPQI toxicity risk.
NSAIDs
Avoid in cirrhosis (portal hypertension, renal risk, coagulopathy). If essential, use lowest dose for shortest duration with PPI cover.
Opioids
Metabolism impaired → risk of hepatic encephalopathy and prolonged sedation. Reduce dose 50%, extend intervals. Avoid codeine and tramadol (CYP-dependent metabolism). Tramadol also lowers seizure threshold.
Duloxetine
Contraindicated in severe hepatic impairment. Amitriptyline: use with caution (hepatotoxicity rare but possible).
🛡️

Immunocompromised

Acute pain
May represent opportunistic infection, immune reconstitution inflammatory syndrome (IRIS), or malignancy — maintain high index of suspicion. Low threshold for imaging and microbiological investigation.
Herpes zoster
Increased risk and severity in immunocompromised. Valaciclovir 1 g PO TDS for 7–10 days (longer than immunocompetent). IV aciclovir for disseminated disease. Shingrix® vaccine recommended (PBS-funded for ≥65 years).
Chemotherapy-induced peripheral neuropathy
Common with platinum agents, taxanes, vinca alkaloids, bortezomib. Duloxetine is recommended first-line (ASCO guidelines). Pregabalin/gabapentin second-line. Monitor and adjust as neuropathy evolves.
Aboriginal and Torres Strait Islander Health Considerations
Prevalence
Aboriginal and Torres Strait Islander Australians experience chronic pain at 1.5–2 times the rate of non-Indigenous Australians, with earlier onset and greater functional impact (AIHW, 2023). Musculoskeletal conditions are the leading cause of disability burden, and chronic pain prevalence in remote communities may exceed 30%.
Access to multidisciplinary care
Multidisciplinary pain services are concentrated in metropolitan tertiary centres. Indigenous Australians in regional and remote areas have limited access to pain specialists, psychologists, and physiotherapists. Aboriginal Community Controlled Health Organisations (ACCHOs) play a critical role in bridging this gap but are often under-resourced for chronic pain management. Telehealth (MBS items 91790, 91800, 91801) has improved access but requires reliable internet.
Cultural safety
Pain expression, beliefs, and help-seeking behaviours differ across Indigenous communities. Shame, stigma, and historical mistrust of the health system may delay presentation. Providers should use culturally safe communication, employ Aboriginal Health Workers/Practitioners (AHW/AHP) as care navigators, and validate patients' pain experience without minimising or over-pathologising.
Opioid prescribing
Indigenous Australians are disproportionately prescribed opioids for chronic pain, often as monotherapy rather than within a multidisciplinary framework. Real-time prescription monitoring (SafeScript Qld/NSW/Vic, NT SCRIPTS) may be less accessible in remote areas. Community pharmacy access is limited in some regions, leading to stockpiling and safety risks. Non-opioid alternatives and pain self-management programs should be prioritised.
Social determinants
Chronic pain intersects with broader social determinants of health — housing insecurity, food insecurity, intergenerational trauma, incarceration, and socioeconomic disadvantage. These factors amplify pain severity and impede recovery. Holistic, trauma-informed care that addresses these determinants is essential.
Specific considerations for time-based patterns
Acute: Delayed presentations are common — severe pathology may present late. Recurrent: Gout is highly prevalent (10–12% in some remote communities vs. 3% nationally) and undertreated with urate-lowering therapy. Chronic: "Yarning" and narrative-based approaches to pain education may be more effective than didactic education. Flares: Pre-agreed flare plans should consider geographic isolation and limited pharmacy access — stock rescue medications where possible.

📚 References

  1. 1. Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain. 2020;161(9):1976–1982.
  2. 2. International Association for the Study of Pain (IASP). ICD-11 chronic pain classification. Pain. 2019;160(12):2673–2677.
  3. 3. Australian Institute of Health and Welfare (AIHW). Chronic pain in Australia. Cat. no. PHE 267. Canberra: AIHW; 2023.
  4. 4. Painaustralia. The cost of pain in Australia. Canberra: Deloitte Access Economics for Painaustralia; 2019.
  5. 5. Britt H, Bayram C, Henderson J, et al. General practice activity in Australia 2022–23. Sydney: Sydney University Press; 2023.
  6. 6. Royal Australian College of General Practitioners (RACGP). Prescribing drugs of dependence in general practice: Part B — Opioids. Melbourne: RACGP; 2022.
  7. 7. Faculty of Pain Medicine, Australian and New Zealand College of Anaesthetists (FPM ANZCA). Position statement on the use of opioids in chronic non-cancer pain. Melbourne: ANZCA; 2023.
  8. 8. Nicholas M, Vlaeyen JWS, Rief W, et al. The IASP classification of chronic pain for ICD-11: chronic primary pain. Pain. 2019;160(1):28–37.
  9. 9. National Health and Medical Research Council (NHMRC). National Statement on Ethical Conduct in Human Research. Canberra: NHMRC; 2023 (updated). [Referenced for ethical frameworks in pain research.]
  10. 10. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.
  11. 11. Hill JC, Dunn KM, Lewis M, et al. A primary care back pain screening tool: identifying patient subgroups for initial treatment. Arthritis Care Res. 2008;59(5):632–641.
  12. 12. Crofford LJ. Chronic pain: where the body meets the brain. Trans Am Clin Climatol Assoc. 2015;126:167–183.
  13. 13. Australian Government Department of Health and Aged Care. MBS Online — Medicare Benefits Schedule. Canberra: Commonwealth of Australia; 2024. Available at: mbsonline.gov.au.
  14. 14. Jensen MP, Turk DC. Contributions of psychology to the understanding and treatment of people with chronic pain. Am Psychol. 2014;69(2):105–118.
  15. 15. Therapeutic Goods Administration (TGA). Codeine use in children — restricted in Australia. Australian Government Department of Health; 2015 (updated 2018).
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. 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. 2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
  3. 3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
  4. 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. 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. 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. 7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
  8. 8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
  9. 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. 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. 11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
  12. 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. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 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. 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. 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. 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. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 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. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 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. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 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. 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. 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
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. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 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. 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. 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. 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. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 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. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 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. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 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. 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. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).