Skin Ulcers

Last updated 1 Jun 2026 · Dermatology / Vascular

📋 Key Information Summary

📋

Skin ulcers are defined as full-thickness epithelial defects failing to heal within 4–6 weeks; chronic wounds affect ~450,000 Australians annually, costing the health system > billion per year.
The four major categories are venous (40–60%), arterial (10–20%), neuropathic/diabetic (15–25%), and inflammatory/mixed aetiology (<5%).
Venous ulcers classically occur in the gaiter area (between ankle and mid-calf), are shallow with irregular borders, and produce moderate-to-heavy exudate; they are associated with oedema, haemosiderin staining, and lipodermatosclerosis.
Arterial ulcers are painful, punched-out, and located on toes, heels, or bony prominences; they feature pale/grey base, absent pulses, and prolonged capillary refill (>3 seconds).
Always measure the Ankle-Brachial Pressure Index (ABPI) before initiating compression therapy; an ABPI <0.5 indicates critical limb ischaemia and contraindicates standard compression.
ABPI ≥0.8 permits multilayer compression (25–35 mmHg); ABPI 0.5–0.8 allows reduced compression (15–25 mmHg) under specialist supervision.
Pyoderma gangrenosum is a neutrophilic dermatosis that presents with rapidly enlarging, painful ulcers with violaceous undermined borders; it is a diagnosis of exclusion and biopsy risks pathergy.
First-line therapy for pyoderma gangrenosum is systemic corticosteroids (prednisolone 0.5–1 mg/kg/day); steroid-sparing agents include ciclosporin, dapsone, and biologics.
All wound management should follow the TIME framework: Tissue, Infection/Inflammation, Moisture balance, and Edge advancement.
Diabetic/neuropathic ulcers require offloading (total contact casting or irremovable knee-high walkers), glycaemic optimisation, and podiatry involvement.
Peripheral arterial disease evaluation, smoking cessation, and risk-factor modification (statins, antiplatelets, BP control) are essential for all chronic ulcer patients.
Referral to a vascular surgeon is indicated for ABPI <0.5, critical limb ischaemia, non-healing ulcers despite 12 weeks of optimal care, or suspected malignancy (Marjolin ulcer).
Aboriginal and Torres Strait Islander Australians experience chronic wounds at 3–5 times the rate of non-Indigenous Australians, with delayed presentation, limited specialist access, and higher amputation rates in remote communities.

Introduction & Australian Epidemiology

A skin ulcer is a localised area of full-thickness epidermal and dermal loss that fails to progress through the normal stages of wound healing within an expected timeframe. When a wound has not achieved at least 50% reduction in area by 4 weeks, it is classified as chronic and warrants systematic evaluation for underlying aetiology. Skin ulcers are a significant cause of morbidity, reduced quality of life, and healthcare expenditure in Australia.

The Australian and New Zealand Clinical Practice Guideline for Prevention and Management of Venous Leg Ulcers (2022) estimates that approximately 450,000 Australians are living with a chronic wound at any given time, with prevalence increasing sharply with age. Venous leg ulcers account for the majority (40–60%) of all lower-limb ulcers, followed by arterial ulcers (10–20%) and diabetic/neuropathic ulcers (15–25%). Inflammatory, malignant, and mixed-aetiology ulcers are less common but frequently pose diagnostic challenges.

The total annual cost of chronic wound management in Australia exceeds billion, with inpatient admissions for wound-related complications consuming a substantial share. General practitioners manage the majority of skin ulcers in the community, while specialist referral to vascular surgery, dermatology, or multidisciplinary wound clinics is required for complex or non-healing wounds.

Key risk factors for chronic skin ulceration in the Australian population include increasing age, obesity, immobility, peripheral vascular disease, diabetes mellitus, venous insufficiency, peripheral neuropathy, smoking, and chronic corticosteroid use. Early identification of the ulcer aetiology, measurement of ABPI, and initiation of evidence-based management are essential to reduce healing times and prevent complications such as infection, osteomyelitis, and amputation.

⚠️

Never apply compression bandaging without first measuring ABPI. Compression in the setting of undiagnosed peripheral arterial disease can precipitate critical limb ischaemia, tissue necrosis, and limb loss.

Types & Causes of Skin Ulcers

Accurate classification of skin ulcers by aetiology is the cornerstone of effective management. A systematic approach involves history (onset, duration, risk factors, medications, comorbidities), examination (site, size, depth, margins, base, exudate, surrounding skin, pulses), and targeted investigations.

1. Venous Ulcers

Venous leg ulcers (VLUs) arise from chronic venous insufficiency (CVI), where incompetent valves in the superficial or deep venous systems produce sustained venous hypertension. Blood pools in the lower limbs, leading to oedema, tissue hypoxia, fibrin cuff formation, and impaired microcirculation. Risk factors include deep vein thrombosis (DVT), varicose veins, prolonged standing, obesity, and family history.

2. Arterial Ulcers

Arterial ulcers result from inadequate arterial perfusion due to peripheral arterial disease (PAD). Atherosclerosis is the most common cause, with risk factors including smoking, diabetes, hyperlipidaemia, hypertension, and age >65 years. Tissue ischaemia leads to necrosis, typically at distal pressure points with limited collateral circulation.

3. Diabetic / Neuropathic Ulcers

Diabetic foot ulcers develop from the combination of peripheral neuropathy (loss of protective sensation), peripheral arterial disease, and biomechanical deformity. Repetitive trauma to insensate skin over bony prominences (metatarsal heads, heel, toes) goes unnoticed, leading to callus formation, tissue breakdown, and ulceration. Diabetes is present in approximately 30% of Australians aged ≥65, making diabetic foot disease a major primary care concern.

4. Pressure Injuries (Ulcers)

Pressure injuries (decubitus ulcers) result from sustained pressure and/or shear forces on skin overlying bony prominences, most commonly the sacrum, heels, ischial tuberosities, and greater trochanters. They are staged I–IV per the National Pressure Injury Advisory Panel (NPIAP) classification. Immobility, malnutrition, incontinence, and sensory deficits are key risk factors.

5. Inflammatory / Autoimmune Ulcers

Pyoderma gangrenosum, vasculitis (ANCA-associated, cryoglobulinaemic, livedoid vasculopathy), and connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis) can produce chronic skin ulcers through immune-mediated tissue destruction. These are discussed in detail in the Pyoderma Gangrenosum section below.

6. Malignant Ulcers

Marjolin ulcer is a squamous cell carcinoma arising in a chronic wound, scar, or burn. Any ulcer that fails to heal after 3 months, has irregular/everted edges, or develops a friable/nodular base warrants biopsy to exclude malignancy. Other malignancies presenting as ulcers include basal cell carcinoma, melanoma, and cutaneous T-cell lymphoma.

7. Infectious Ulcers

Tropical ulcer (polymicrobial, common in northern Queensland and remote communities), Buruli ulcer (Mycobacterium ulcerans, endemic in parts of Victoria — Bellarine and Mornington Peninsulas), leishmaniasis, cutaneous tuberculosis, and deep fungal infections can all produce chronic ulcers. Travel history and geographic exposure are essential in the Australian context.

ℹ️

Buruli ulcer (Mycobacterium ulcerans) is a notifiable disease in Australia. Cases have been increasing in the Geelong and Mornington Peninsula regions of Victoria and more recently in metropolitan Melbourne. Any non-healing ulcer in an endemic area should prompt consideration of this diagnosis.

Venous vs Arterial Ulcers — Clinical Comparison

Differentiating venous from arterial ulcers is a critical clinical skill in primary care. The two conditions require fundamentally different management — venous ulcers benefit from compression therapy, while arterial ulcers require revascularisation. Misdiagnosis can result in significant harm.

Feature	Venous Ulcer	Arterial Ulcer
Location	Gaiter area (above medial malleolus to mid-calf); medial aspect predominant	Distal — toes, heels, lateral foot, metatarsal heads; tips of toes
Shape & borders	Irregular, shallow, sloping edges	Punched-out, well-demarcated, deep
Ulcer base	Red granulation tissue or yellow slough	Pale, grey, or necrotic (black eschar)
Exudate	Moderate to heavy serous	Minimal to none
Pain	Mild to moderate; relieved by elevation	Severe, worse at rest, worse with elevation; relieved by dependency
Surrounding skin	Oedema, haemosiderin staining (brown), lipodermatosclerosis, eczema, atrophie blanche	Pale, thin, shiny, hair loss; cool to touch
Pulses	Usually present	Absent or diminished (dorsalis pedis, posterior tibial)
Capillary refill	Normal (<3 seconds)	Prolonged (>3 seconds)
ABPI	Usually ≥0.8	Often <0.8; <0.5 = critical ischaemia
Oedema	Prominent; pitting	Absent; limb may be wasted
Key treatment	Multilayer compression (25–35 mmHg) + wound care	Revascularisation (angioplasty / bypass) + wound care; NO compression

🚨

Safety critical: Compression bandaging on an ischaemic limb (ABPI <0.8) can cause tissue necrosis and limb loss. Always confirm arterial sufficiency before applying compression.

Mixed (Venous-Arterial) Ulcers

Many patients, particularly the elderly and those with diabetes, have coexistent venous and arterial disease. In these cases, modified (reduced) compression at 15–25 mmHg may be used under specialist guidance when ABPI is 0.5–0.8. A vascular surgery or wound clinic assessment should be obtained before commencing any compression in patients with mixed disease.

Ankle-Brachial Pressure Index (ABPI)

The Ankle-Brachial Pressure Index (ABPI) is a simple, non-invasive bedside test used to assess lower-limb arterial perfusion. It is an essential investigation in the initial assessment of all patients presenting with lower-limb skin ulcers, and is mandatory before any compression therapy is commenced.

How to Measure ABPI

A handheld continuous-wave Doppler ultrasound probe (8–10 MHz) and a blood pressure cuff are used. The patient should rest supine for at least 10 minutes prior to measurement.

Measure the systolic blood pressure in both brachial arteries using the Doppler probe at the antecubital fossa.
Measure the systolic blood pressure in both dorsalis pedis and posterior tibial arteries using the Doppler probe at the ankle.
Calculate ABPI for each leg: ABPI = Highest ankle systolic pressure ÷ Highest brachial systolic pressure.

Interpreting ABPI Results

Normal / Mild

ABPI 0.91–1.3

No significant arterial disease. Full multilayer compression (25–35 mmHg) can be safely applied for venous ulcers.

Setting: Primary care — standard compression

Moderate PAD

ABPI 0.5–0.8

Significant peripheral arterial disease. Reduced compression (15–25 mmHg) may be used under specialist supervision. Vascular assessment recommended.

Setting: Specialist-supervised modified compression

Critical Ischaemia

ABPI <0.5

Severe peripheral arterial disease / critical limb ischaemia. Compression is CONTRAINDICATED. Urgent vascular surgical referral for revascularisation assessment.

Setting: Vascular surgery — urgent referral

⚠️

ABPI >1.3 may indicate calcified, non-compressible arteries (common in diabetes and end-stage renal disease). In this situation, ABPI is unreliable and toe pressures or transcutaneous oxygen pressure (TcPO₂) measurements should be obtained. Do NOT assume normal perfusion with an ABPI >1.3 in a diabetic or renal patient.

When to Measure ABPI

All patients presenting with a new lower-limb ulcer
Before initiating or renewing compression therapy (minimum every 6–12 months)
If there is clinical suspicion of peripheral arterial disease (cool limb, absent pulses, rest pain, claudication history)
If a previously healing venous ulcer deteriorates or stops healing
Prior to referral for duplex ultrasound or vascular intervention

MBS (Medicare Benefits Schedule) Considerations

ABPI measurement using handheld Doppler is a clinical skill performed in general practice and does not attract a specific MBS item number as a standalone test. However, it is included in comprehensive vascular assessments performed in specialist vascular laboratories (MBS items 11300–11312 for duplex ultrasound of peripheral arteries). Point-of-care ABPI in general practice is covered under standard consultation items.

Pyoderma Gangrenosum & Other Inflammatory Ulcers

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterised by rapidly progressive, painful skin ulcers. It accounts for approximately 1–5% of chronic leg ulcers but is frequently misdiagnosed, leading to inappropriate wound management and delayed treatment. PG must be considered in any ulcer that is disproportionately painful, rapidly enlarging, or failing to respond to standard wound care.

Pathophysiology

PG is driven by dysregulated innate immunity with excessive neutrophilic infiltration of the dermis. It is associated with systemic diseases in approximately 50–70% of cases, most commonly inflammatory bowel disease (ulcerative colitis > Crohn disease), rheumatoid arthritis, haematological malignancies (especially myelodysplastic syndrome), and monoclonal gammopathies.

Clinical Features

Pathergy: New lesions may develop at sites of trauma, including surgical wounds, biopsy sites, and IV access — a hallmark feature.
Borders: Violaceous (purple-blue), undermined, and erythematous with a raised, advancing edge.
Base: Necrotic with purulent or haemorrhagic exudate; cribriform (sieve-like) scarring is characteristic during healing.
Pain: Often severe and disproportionate to the apparent size of the wound.
Site: Most commonly the lower limbs (shins), but can occur anywhere — including the abdomen (especially around stomas), upper limbs, and genitals.
Systemic symptoms: Fever, malaise, and arthralgia may be present, especially in association with underlying systemic disease.

Diagnosis

🚨

PG is a diagnosis of exclusion. There is no pathognomonic test. Biopsy is helpful to exclude other causes (vasculitis, malignancy, infection) but the histopathology of PG is non-specific (dense neutrophilic infiltrate without vasculitis). Importantly, biopsy may worsen PG through pathergy. Punch biopsy from the wound edge (not the centre) is recommended, and a full set of investigations to exclude differential diagnoses must be performed.

Diagnostic Criteria (Modified Su Criteria)

Diagnosis requires at least one major and four minor criteria:

Major: Rapid (days to weeks) progression of a painful, necrolytic ulcer with an irregular, violaceous, undermined border.
Minor criteria: (1) History of pathergy or PG-associated disease (IBD, arthritis, haematological malignancy); (2) Exclusion of other causes of ulceration (infection, vasculitis, malignancy, coagulopathy); (3) Histopathology showing neutrophilic infiltrate without vasculitis; (4) Rapid response to systemic corticosteroids.

Differential Diagnosis

Infectious causes (including mycobacterial, deep fungal, and bacterial), vasculitis (ANCA-associated, cryoglobulinaemic, livedoid vasculopathy), calciphylaxis, malignancy (squamous cell carcinoma, lymphoma), antiphospholipid syndrome, arterial insufficiency, and factitious disorder must all be excluded.

Management of Pyoderma Gangrenosum

First-Line — Systemic Corticosteroids

💊

Prednisolone

Various generics · Corticosteroid

Adult dose 0.5–1 mg/kg/day PO (typically 40–60 mg/day) for 1–2 weeks, then taper over 3–6 months

Paediatric dose 1–2 mg/kg/day PO, taper as per specialist advice

Renal adjustment None required

Hepatic adjustment Use with caution in severe hepatic impairment

PBS status ✔ PBS General Benefit

ℹ️

For severe or rapidly progressive PG, intravenous pulse methylprednisolone (500–1000 mg/day for 3–5 days) may be used in a hospital setting before transitioning to oral prednisolone.

Steroid-Sparing Agents

💊

Ciclosporin (Cyclosporine)

Neoral® · Generic · Calcineurin inhibitor

Adult dose 3–5 mg/kg/day PO in 2 divided doses

Renal adjustment Avoid in eGFR <30 mL/min; monitor creatinine closely

PBS status ⚠ Authority Required

💊

Dapsone

Dapsone · Sulfone antibiotic / anti-inflammatory

Adult dose 50–100 mg PO daily

Key caution Check G6PD status before commencing; risk of haemolytic anaemia

PBS status ✔ PBS General Benefit

💊

Adalimumab

Humira® · TNF-α inhibitor

Adult dose 160 mg SC week 0, then 80 mg week 2, then 40 mg every 2 weeks (as per PG-specific dosing in IBD protocols)

Key caution Screen for latent TB (IGRA/TST), hepatitis B, and heart failure before initiation

PBS status ✖ Authority Required (Specialist only)

Other Inflammatory Ulcers

Vasculitis-Associated Ulcers

Cutaneous vasculitis (small-vessel, medium-vessel, or mixed) can produce ulceration. ANCA-associated vasculitis (granulomatosis with polyangiitis, microscopic polyangiitis), cryoglobulinaemic vasculitis (hepatitis C–associated in Australia), and livedoid vasculopathy should be considered. Management involves treatment of the underlying vasculitis (immunosuppression) plus wound care. A biopsy demonstrating true leukocytoclastic vasculitis distinguishes these from PG.

Calciphylaxis

Calciphylaxis (calcific uraemic arteriolopathy) occurs predominantly in patients with end-stage kidney disease on dialysis. It presents as painful, reticulate violaceous patches progressing to necrotic ulcers with black eschar, predominantly on the thighs and abdomen. Mortality is high (60–80%). Management requires urgent nephrology input, wound care, sodium thiosulfate (off-label), and optimisation of calcium-phosphate metabolism.

Investigations

Investigations for skin ulcers should be guided by the suspected aetiology. The following represents a structured approach.

Bedside / Point-of-Care

Essential ABPI — handheld Doppler All lower-limb ulcers; before compression. Available in most GP practices and all wound clinics. No specific MBS item (included in consultation).

Available Wound swab (superficial) Only if clinical signs of infection (increasing pain, erythema, warmth, purulent exudate, systemic signs). Use Levine technique (swab after cleansing, rotate over 1 cm² of granulation tissue for 5 seconds with firm pressure). MBS item 69350 (microscopy & culture).

Available Blood glucose / HbA1c All patients — screen for diabetes. MBS item 66551 (HbA1c).

Laboratory — General

Essential FBC, CRP, ESR Assess for infection, inflammation, and haematological causes. MBS items 65070, 65090.

Available UEC, LFT, Albumin Nutritional status, renal function (important for drug dosing and calciphylaxis assessment). MBS items 66512, 66515.

Available Iron studies, B12, folate, zinc, vitamin D Nutritional deficiencies impair wound healing. MBS items 66816, 66824.

Available Wound tissue biopsy (punch or incisional) Indicated for suspected malignancy (Marjolin ulcer), vasculitis, atypical ulcers, or PG (from wound edge). Send for histopathology and microbiology (including mycobacterial culture if Buruli suspected). MBS item 30071.

Laboratory — Suspected Pyoderma Gangrenosum / Inflammatory Ulcers

Specialist ANCA, ANA, ENA, complement (C3, C4), cryoglobulins Vasculitis screen. Request in conjunction with dermatology or rheumatology.

Specialist Serum protein electrophoresis, urine Bence Jones Screen for monoclonal gammopathy (associated with PG).

Available Faecal calprotectin Screen for inflammatory bowel disease if PG suspected. MBS item 69280.

Imaging

Available Lower-limb venous duplex ultrasound Assess for venous incompetence in suspected venous ulcers. MBS item 55060.

Referral CT angiography / digital subtraction angiography Assessment of peripheral arterial disease for revascularisation planning. Vascular surgery referral.

Available Plain X-ray of foot / affected area Assess for osteomyelitis (deep ulcer, probe-to-bone positive). MBS item 58100.

Referral MRI of foot / affected area Gold standard for osteomyelitis diagnosis when X-ray is inconclusive. MBS item 63001.

Management — General Principles

All chronic skin ulcers benefit from a structured, holistic management approach that addresses the underlying aetiology, optimises wound healing, manages infection, and treats modifiable risk factors.

The TIME Framework (Wound Bed Preparation)

Tissue

Remove non-viable tissue (necrotic, slough) through sharp debridement, autolytic debridement (hydrogels), or enzymatic debridement. Maintain a healthy wound bed.

Infection / Inflammation

Clinical infection requires treatment (topical or systemic antibiotics). Chronic biofilm may need regular debridement + antiseptic dressings. Do not treat colonisation.

Moisture Balance

Maintain optimal wound moisture. High exudate → foam/alginate dressings. Dry wound → hydrogel. Avoid desiccation and maceration.

Edge Advancement

Assess whether the wound edge is advancing (healing). Non-advancing edges after 4 weeks of optimal care require reassessment of aetiology, infection, and systemic factors.

Venous Ulcer — Compression Therapy

Multilayer high-compression bandaging systems (e.g., Profore™, Coban™ 2) delivering 30–40 mmHg at the ankle are the cornerstone of VLU treatment. Alternatives include short-stretch bandages, Velcro™ wraps (e.g., CircAid™), and compression hosiery (Class II, 23–32 mmHg) for maintenance after healing. The Australian Wound Management Association recommends 4-layer systems as first-line. Healing rates: ~70% of venous ulcers heal at 12 weeks with optimal compression.

ℹ️

Elevation: Patients should elevate the affected limb above heart level for 30 minutes, 3–4 times daily, in addition to compression. Walking and ankle exercises promote calf-muscle pump function.

Arterial Ulcer — Revascularisation & Risk-Factor Modification

Urgent vascular surgery referral for patients with critical limb ischaemia (rest pain, tissue loss, ABPI <0.5).
Endovascular (angioplasty ± stenting) or open surgical bypass (e.g., femoro-popliteal, femoro-distal) as determined by vascular anatomy.
Antiplatelet therapy: aspirin 100 mg PO daily OR clopidogrel 75 mg PO daily. ✔ PBS General Benefit
Statin therapy: atorvastatin 40–80 mg PO daily. ✔ PBS General Benefit
Smoking cessation — offer NRT, varenicline, or bupropion; refer to Quitline (13 7848).
BP target <130/80 mmHg (ACE inhibitor or ARB preferred).
Glycaemic optimisation in patients with diabetes (HbA1c target ≤53 mmol/mol or as individualised).

Diabetic / Neuropathic Ulcer — Offloading

Offloading is the single most important intervention for diabetic foot ulcers. The gold standard is a non-removable total contact cast (TCC) or irremovable knee-high walker (iTCC). Removable walkers are significantly less effective due to poor compliance. Podiatry input is essential, and all diabetic foot ulcers should be managed through a multidisciplinary diabetic foot team where available.

Infection Management

Most chronic wounds are colonised and do not require antibiotics. Indicators of clinical infection include: increasing pain, expanding erythema, warmth, swelling, purulent exudate, delayed healing, and systemic signs (fever, malaise).

💊

Flucloxacillin

Staphlex® · Generic · Penicillinase-resistant penicillin

Adult dose 500 mg PO QDS for 7–14 days (for suspected staphylococcal/streptococcal infection)

Renal adjustment Reduce dose in severe renal impairment (eGFR <10)

PBS status ✔ PBS General Benefit

💊

Amoxicillin + Clavulanate

Augmentin® · Generic · Broad-spectrum penicillin

Adult dose 875/125 mg PO BD for 7–14 days (for polymicrobial or limb-threatening infection)

Renal adjustment eGFR 10–30: 500/125 mg BD; eGFR <10: 500/125 mg OD

PBS status ✔ PBS General Benefit

💊

Metronidazole

Flagyl® · Generic · Nitroimidazole (anaerobes)

Adult dose 400 mg PO TDS for 7–14 days (for anaerobic/malodorous wounds, often in combination)

Renal adjustment None required for oral dosing

PBS status ✔ PBS General Benefit

⚠️

For suspected CA-MRSA (community-associated methicillin-resistant Staphylococcus aureus), which is increasingly common in Australian remote communities, use trimethoprim + sulfamethoxazole (TMP-SMX) 160/800 mg PO BD or doxycycline 100 mg PO BD. Send a wound swab for culture and sensitivity to guide therapy. ✔ PBS General Benefit

Monitoring

Regular monitoring is essential to track healing progress, identify complications, and modify treatment. All patients with chronic ulcers should be reviewed by their treating GP or wound care nurse at defined intervals.

Monitoring Schedule

Week 0

Initial assessment: wound measurements (length × width × depth), photograph, wound swab if infected, ABPI. Establish aetiology and management plan. Refer to specialist if indicated.

Week 2

First review: assess tolerance of compression (if venous), check for adverse effects of systemic therapy (if PG/inflammatory). Reassess pain and exudate.

Week 4

Critical decision point: the wound should show ≥20–30% reduction in area at 4 weeks. If no progress, reassess aetiology, rule out infection, consider biopsy, and review systemic factors (nutrition, diabetes, vascular status).

Week 8–12

Expected healing for most venous ulcers with compression. If >50% area reduction at week 4, healing is likely by week 12. If not, consider specialist referral (vascular, dermatology, plastic surgery).

Week 12+

Non-healing ulcers (>12 weeks of optimal management) require multidisciplinary reassessment. Consider malignancy biopsy, advanced therapies (NPWT, skin grafts, bioengineered skin substitutes), and specialist wound clinic referral.

What to Document at Each Review

Wound dimensions (length × width in cm, depth in mm)
Percentage of wound bed by tissue type (granulation, slough, necrotic, epithelialising)
Wound edge (advancing, rolled, undermined, violaceous)
Exudate volume and character (serous, serosanguinous, purulent)
Peri-wound skin condition (erythema, maceration, eczema, lipodermatosclerosis)
Pain score (numeric rating scale 0–10)
Current dressing regimen and compression status
Photograph (with ruler for scale, standardised positioning)

Indicators for Referral

⚠️

No improvement at 4 weeks of optimal care
ABPI <0.5 or suspected critical limb ischaemia
Suspected pyoderma gangrenosum or vasculitis
Suspected malignancy (Marjolin ulcer)
Recurrent or extensive cellulitis
Suspected osteomyelitis (probe-to-bone positive, deep ulcer)
Complex wounds requiring negative-pressure wound therapy or skin grafting
Diagnostic uncertainty despite initial workup

Special Populations

🤰

Pregnancy

Venous disease is common in pregnancy; graduated compression stockings (Class I–II) are safe and recommended.
Avoid ciclosporin, dapsone, and most biologics for PG in pregnancy. Systemic corticosteroids may be used under specialist supervision.
Ensure tetanus immunisation status is up to date.
Wound care products with silver should be used with caution (limited safety data).

👶

Paediatrics

Chronic skin ulcers in children are uncommon; consider underlying immunodeficiency, vasculitis, PG, factitious injury, and non-accidental injury.
Prednisolone dose for PG: 1–2 mg/kg/day (paediatric dosing); involve paediatric dermatology early.
Compression bandaging requires paediatric-sized products and careful application to avoid pressure injury.
Psychosocial assessment is important — chronic wounds impact school attendance and self-esteem.

👴

Elderly

Mixed aetiology ulcers (venous + arterial) are common in the elderly; always measure ABPI before treatment.
Oedema management: compression may need to be combined with diuretic therapy and limb elevation.
Malnutrition (low albumin, zinc deficiency) is common and impairs healing; nutritional assessment and supplementation are essential.
Polypharmacy: review medications — corticosteroids, NSAIDs, anticoagulants, and immunosuppressants may impair wound healing.
Pressure injury prevention: regular repositioning (minimum 2-hourly), pressure-redistributing surfaces, and skin inspection.

🫘

Renal Impairment

Patients on haemodialysis have significantly impaired wound healing and higher rates of PAD.
Calciphylaxis must be considered in any dialysis patient with painful, necrotic skin lesions.
ABPI may be unreliable due to arterial calcification (ABPI >1.3); use toe pressures or TcPO₂.
Drug adjustments: reduce ciclosporin dose and monitor levels; adjust antibiotic doses per eGFR; avoid nephrotoxic combinations.
Compression may cause hypotension in dialysis patients; coordinate with nephrology team.

🫁

Hepatic Impairment

Hepatic cirrhosis causes coagulopathy and hypoalbuminaemia, both of which impair wound healing.
Cryoglobulinaemic vasculitis (hepatitis C–associated) can cause lower-limb ulcers; HCV treatment with direct-acting antivirals (PBS-listed) may resolve the vasculitis.
Prednisolone may be used cautiously; ciclosporin is hepatotoxic and should be avoided or closely monitored.

🛡️

Immunocompromised

Immunosuppressed patients (transplant recipients, biologic therapy, chemotherapy, HIV) are at higher risk for atypical and opportunistic infections (non-tuberculous mycobacteria, deep fungal, CMV ulcers).
Wound swabs and tissue biopsies should be sent for extended microbiology (mycobacterial and fungal cultures) in addition to standard microscopy and culture.
TB screening is mandatory before initiating anti-TNF biologics for PG or vasculitis.
Wound healing is delayed; monitor closely and set realistic healing timelines.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of chronic skin ulcers compared with non-Indigenous Australians. The AIHW reports that chronic wounds affect Indigenous Australians at 3–5 times the non-Indigenous rate, driven by higher prevalence of diabetes (3–4 times), peripheral arterial disease, chronic kidney disease, and rheumatic heart disease. Diabetic foot ulcers and lower-limb amputations are particularly common in remote communities, with amputation rates up to 6 times higher than the non-Indigenous population in some jurisdictions.

Remote and rural access

Many Indigenous Australians live in remote and very remote communities where access to vascular surgery, podiatry, dermatology, and specialist wound care is extremely limited. Royal Flying Doctor Service (RFDS) retrieval and telehealth consultations are essential components of care. Health Promotion programs (e.g., DFMEA — Diabetic Foot Management Education in Aboriginal communities) aim to improve early detection.

Diabetes and chronic disease burden

Type 2 diabetes prevalence in Indigenous Australians is approximately 12–15% (compared with 5% in the non-Indigenous population), with onset occurring a decade earlier. Diabetic foot complications, including neuropathic and neuroischaemic ulcers, are a leading cause of hospitalisation and amputation. Regular foot checks (every 3–6 months for at-risk individuals) through Aboriginal Community Controlled Health Organisations (ACCHOs) are critical.

Trachoma and skin infections

Australia is the only high-income country where trachoma remains endemic, primarily in remote Indigenous communities. While trachoma itself does not cause ulcers, the environment of overcrowded housing and limited skin health resources contributes to skin breakdown and delayed wound healing. Scabies, impetigo, and tropical ulcer are common precursors to chronic wounds.

Cultural safety and holistic care

Wound management must be culturally safe. In some communities, wound care may involve traditional healing practices alongside Western medicine — a collaborative, non-judgemental approach is essential. Gender considerations are important (same-sex health workers preferred for wound care in many communities). Address shame and stigma associated with chronic wounds, amputation, and body image. Involve family and community Elders in care planning where appropriate.

Social determinants

Overcrowded housing, limited access to clean water for wound hygiene, food insecurity (limited access to nutritious foods for healing in remote stores), limited refrigeration for medication storage, and transport barriers to attend follow-up appointments all significantly impact wound management outcomes. Engagement with ACCHOs and community health workers improves continuity of care.

Smoking and vascular disease

Smoking rates among Indigenous Australians are approximately 40% (vs 11% non-Indigenous), significantly contributing to PAD and impaired wound healing. Culturally appropriate smoking cessation programs (e.g., Tackling Indigenous Smoking) are available through ACCHOs and should be actively offered to all patients with vascular ulcers.

ℹ️

RHDAustralia (the Australian Rheumatic Heart Disease Register) recommends regular skin checks in communities with high rheumatic fever prevalence, as peripheral oedema from cardiac failure may contribute to venous ulceration. Echocardiography should be considered in young Indigenous Australians with unexplained lower-limb oedema and skin changes.

Quick Reference — Ulcer Type to Initial Management

Venous ulcer (ABPI ≥0.8)

Multilayer compression 30–40 mmHg + wound dressings (TIME)

12 weeks to assess healing

Elevate limb, walking exercises, leg oedema management

Mixed venous-arterial (ABPI 0.5–0.8)

Reduced compression 15–25 mmHg ± vascular referral

Specialist-supervised

Monitor closely for deterioration; vascular assessment mandatory

Arterial ulcer (ABPI <0.5)

Urgent vascular referral; aspirin + statin; smoking cessation

As determined by vascular team

NO compression; revascularisation if feasible

Diabetic / neuropathic foot ulcer

Offloading (TCC / iTCC) + wound care + podiatry + glycaemic optimisation

Weekly review until healed

Multidisciplinary diabetic foot team; antibiotics only if infection

Pyoderma gangrenosum

Prednisolone 0.5–1 mg/kg/day PO; ciclosporin or biologics for steroid-sparing

Taper over 3–6 months; dermatology co-management

Diagnosis of exclusion; avoid biopsy if possible; treat underlying disease

Pressure injury (stages I–IV)

Offloading, repositioning (2-hourly), pressure-redistributing surfaces, nutrition

Ongoing prevention + wound care

Prevention is key; NPIAP staging guides management

📚 References

1. Australian and New Zealand Clinical Practice Guideline for Prevention and Management of Venous Leg Ulcers. Melbourne: AWMA / NZWCS; 2022.
2. Australian Institute of Health and Welfare (AIHW). Chronic wounds in Australia. Cat. no. WEB 235. Canberra: AIHW; 2023.
3. Wounds Australia. Standards for Wound Prevention and Management. 3rd ed. Osborne Park, WA: Cambridge Media; 2016.
4. National Health and Medical Research Council (NHMRC). Australian Clinical Practice Guideline — Diabetic Foot Complications. Melbourne: NHMRC; 2024.
5. International Working Group on the Diabetic Foot (IWGDF). IWGDF Guidelines on the Prevention and Management of Diabetes-Related Foot Disease. Diabetes Metab Res Rev. 2023;39(S1):e3657.
6. Mihai MM, et al. Pyoderma gangrenosum: an updated literature review. An Bras Dermatol. 2022;97(3):313–325.
7. Su WPD, et al. Pyoderma gangrenosum: clinicopathologic correlation and proposed diagnostic criteria. Int J Dermatol. 2004;43(11):790–800.
8. National Pressure Injury Advisory Panel (NPIAP). Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline. 3rd ed. 2019.
9. Royal Australian College of General Practitioners (RACGP). Management of type 2 diabetes: A handbook for general practice. Melbourne: RACGP; 2020.
10. O'Donnell TF, et al. Management of venous leg ulcers: Clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2014;60(2 Suppl):3S–59S.
11. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023.
12. West M, et al. Mycobacterium ulcerans disease (Buruli ulcer) in Australia: an update. Med J Aust. 2023;218(8):369–374.
13. Schultz GS, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11(Suppl 1):S1–S28.
14. Westby MJ, et al. Compression bandages and stockings for venous leg ulcers. Cochrane Database Syst Rev. 2021;3(3):CD000265.

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).