Overview
Chronic wounds represent a significant burden in rural and remote Australian practice, particularly in Aboriginal and Torres Strait Islander communities where diabetes, malnutrition, vascular disease, scabies, and limited specialist access compound outcomes. The rural generalist must assess, classify, and manage the full spectrum, tropical ulcers in Far North Queensland and the Northern Territory, pressure injuries in aged care and remote facilities, and complex diabetic and vascular ulcers.
Fundamental principle: accurate diagnosis precedes management. Missing a Marjolin ulcer (SCC developing in a chronic scar or ulcer, burns, venous ulcers, tropical ulcers), amelanotic melanoma, or pyoderma gangrenosum can be fatal.
Classification of Chronic Wounds Relevant to Remote Australian Practice
| Category | Examples | Key Features |
|---|---|---|
| Vascular | Venous leg ulcer, arterial/ischaemic, mixed venous/arterial | Medial gaiter area (venous); distal, painful (arterial); ~80% of leg ulcers are vascular |
| Pressure injury | Sacral, heel, hip, elbow ulcers | Over bony prominences in immobile patients (decubitus) |
| Tropical/infective | Tropical (phagedenic) ulcer, Buruli ulcer, yaws, cutaneous diphtheria, cutaneous TB, leishmaniasis | Endemic in tropical and remote regions |
| Diabetic/neuropathic | Diabetic foot ulcer, neuropathic, ischaemic, or neuroischaemic | Plantar surface, callus, sensory neuropathy; pressure damage |
| Malignant | SCC (Marjolin ulcer), BCC (rodent ulcer), amelanotic melanoma, ulcerating metastases | Non-healing, atypical edge, failure to respond to treatment |
| Inflammatory/autoimmune | Pyoderma gangrenosum, vasculitic ulcer (RA, SLE, scleroderma) | Very painful; resistant to antibiotics; require immunosuppressants |
| Haematological | Sickle cell anaemia, spherocytosis, polycythaemia | Ankle ulcers; relevant in some ATSI and Pacific Islander populations |
| Miscellaneous | Artefactual, drug-induced (hydroxyurea, nicorandil, nicotine), Martorell hypertensive ulcer, insect/spider bites | Drug history essential |
Presentation and Assessment
History
- Duration and trajectory, non-healing wounds >3 months require biopsy consideration
- Mechanism: trauma (barefoot walking over vegetation), pressure, or spontaneous onset
- Geographic and travel history, tropical regions (FNQ, NT, parts of WA), coastal Victoria and Far North Queensland (Buruli ulcer), Pacific Islands and West Africa (yaws)
- Comorbidities: diabetes, peripheral vascular disease, renal disease, RA, SLE, IBD, myeloproliferative disease
- Medications that impair healing or cause ulcers: corticosteroids, NSAIDs, beta-blockers, ergotamine (compromise arterial circulation), nifedipine (aggravates ankle oedema), calcium channel blockers (oedema), hydroxyurea (direct ulcerogenic)
- Nutritional status, malnutrition profoundly impairs healing and is prevalent in remote communities
- DVT or PE history, intermittent claudication, ischaemic rest pain
- Social circumstances: housing quality, overcrowding, capacity for wound care
Wound Examination
| Parameter | Assessment Points |
|---|---|
| Site | Medial gaiter (venous); distal/dorsal (arterial); plantar (neuropathic); bony prominence (pressure); lower leg (tropical) |
| Size | Length × width × depth (cm), photograph and measure at each visit |
| Edge | Rolled/everted (malignant SCC); undermined (Buruli, tropical ulcer); punched-out (arterial, syphilitic); sloping (healing venous) |
| Base/floor | Slough (yellow), necrotic (black/brown), granulating (red/pink), epithelialising (pale pink) |
| Depth | Superficial; full-thickness; exposed tendon/bone/joint |
| Exudate | Volume, colour, odour, malodour suggests anaerobes |
| Surrounding skin | Erythema, induration, lipodermatosclerosis, haemosiderin staining, lymphoedema, varicose eczema |
| Regional lymph nodes | Lymphadenopathy suggests infection or malignancy |
| Perfusion | Capillary refill, peripheral pulses; ABI if pulses absent or arterial disease suspected |
| Sensation | 10-g monofilament testing, essential in all diabetic patients |
Ankle-Brachial Index (ABI)
$$\text{ABI} = \frac{\text{Systolic BP (ankle)}}{\text{Systolic BP (brachial)}}$$
| ABI | Interpretation | Compression |
|---|---|---|
| >0.9 | Normal | Safe to compress |
| 0.8-0.9 | Mild arterial disease | Compression with caution |
| 0.5-0.8 | Moderate arterial disease | Avoid compression; vascular assessment |
| <0.5 | Severe ischaemia | No compression; urgent vascular referral |
Duplex Doppler ultrasound is the key investigation for both venous and arterial disease (requires regional/tertiary referral).
Red Flags Requiring Urgent Review
- Rapid wound enlargement or deepening
- Cellulitis, lymphangitis, or systemic sepsis
- Exposed bone, tendon, or joint
- Failure to reduce in size after 4-6 weeks of appropriate management
- Atypical appearance suggesting malignancy
- Crepitus, gas, or deep tissue necrosis (gas gangrene, necrotising fasciitis, surgical emergency)
Tropical Ulcer
Pathophysiology and Epidemiology
Tropical (phagedenic) ulcer is a polymicrobial necrotising infection caused by synergistic action of anaerobes (Fusobacterium ulcerans) and Treponema vincentii. It occurs in hot, humid climates, predominantly among children, adolescents, and young men (e.g. farmers) in remote communities in the NT, FNQ, and Pacific Island nations. Repeated minor leg trauma from vegetation (acacia thorns) provides the entry portal.
A painful papule or vesicle develops and rapidly ulcerates, with necrosis, foul-smelling exudate, and surrounding erythema. After weeks, acute inflammation subsides and the ulcer may become chronic, persisting for years. Chronic tropical ulcers carry a significant risk of malignant transformation (Marjolin ulcer, SCC).
Differential Diagnosis of Tropical Ulcers
| Organism/Cause | Features |
|---|---|
| Tropical (phagedenic) ulcer | Painful, rapid onset, necrotic, polymicrobial; lower leg; children/young adults |
| Buruli ulcer (M. ulcerans) | Painless, undermined edge, patient systemically well; PCR diagnosis |
| Yaws (T. pallidum subsp. pertenue) | Children <15 years; papular then chronic ulcer; syphilis serology positive (cross-reactive) |
| Cutaneous leishmaniasis | Chronic, slowly enlarging ulcer ('oriental sore'); sandfly exposure |
| Cutaneous diphtheria | Painful ulcer with grey membrane; rarely seen |
| Pyoderma gangrenosum | Nodular pustules → large ulcer; worsened by trauma; associated with IBD, RA, myeloproliferative disease; not antibiotic-responsive |
| SCC/Marjolin ulcer | Everted edge, hypergranulation, non-healing >3 months; biopsy essential |
Buruli Ulcer (Bairnsdale/Daintree Ulcer)
Caused by Mycobacterium ulcerans, the third most common mycobacterial disease (after TB and leprosy) in HIV-negative individuals. It is the third commonest mycobacterial disease in HIV-negative individuals. Common in children; affects all ages. Endemic in coastal Victoria (2021 epidemic; possum reservoir implicated), Far North Queensland, and tropical Central and West Africa. M. ulcerans likely resides in muddy/swampy water.
Clinical features: painless papule or nodule → necrotic ulcer with classically undermined edges over weeks to months; extensive ulcers possible; secondary infection, sepsis, osteomyelitis, and contractures may complicate.
Diagnosis: PCR (may require repeat) and biopsy. Early referral to infectious diseases is recommended.
Treatment:
- 8 weeks rifampicin + clarithromycin orally (preferred oral regimen); OR
- 8 weeks rifampicin + 4 weeks streptomycin (if injectable available) + 4 weeks clarithromycin
- Total course 8-12 weeks; specialist wound care concurrent
- Surgical debridement and skin grafting may be needed for extensive ulcers
- Severe contractures may require reconstructive surgery
Management of Acute Tropical Ulcer
Wound care:
- Thorough wound cleaning, remove pus, slough, and necrotic debris
- Saline-moistened dressings changed regularly (every 6 hours initially in heavily contaminated wounds); alternatively, 1-6% hydrogen peroxide or dilute sodium hypochlorite (0.5% available chlorine) at dressing changes
- Hydrocolloid dressings are not suitable in humid climates
- Non-adherent dressings preferred, adherent dressings cause pain, bleeding, and tear healing epithelium on removal
- Dressings impregnated with honey, coconut oil, or white soft paraffin keep wound moist and soften crusts
- Zinc oxide cream/paste to wound margins, prevents maceration of healthy peri-wound skin
- Elevation and rest of the affected limb; reduce pressure on the wound
- Nutritional support, address protein-energy malnutrition actively
Antibiotic therapy:
- Procaine benzylpenicillin 0.6-1.2 g IM daily for 3-7 days is first-line for acute tropical ulcer (CARPA-aligned)
- Adjust based on clinical response and culture where available
- Oral step-down (amoxicillin or metronidazole combinations) for less severe or improving presentations
Debridement:
- Remove necrotic tissue and slough, sharp debridement is well tolerated as dead tissue is insensate
- Local application of honey or aloe vera improves wound healing and is appropriate in resource-limited settings
- Avoid herbal remedies with unclear safety profiles
Chronic/non-healing phase:
- Biopsy to exclude SCC (Marjolin ulcer), hypergranulation not responding quickly to silver nitrate, hypertonic saline, and compression should be biopsied urgently
- Skin grafting (pinch or split-thickness) for large non-healing wounds, plan retrieval to surgical facility
Pressure Injuries
Staging (NPUAP/EPUAP International Classification)
| Stage | Description |
|---|---|
| Stage 1 | Non-blanchable erythema of intact skin |
| Stage 2 | Partial-thickness skin loss, shallow open ulcer, no slough; may present as intact or ruptured blister |
| Stage 3 | Full-thickness skin loss, subcutaneous fat visible; no bone, tendon, or muscle exposed |
| Stage 4 | Full-thickness tissue loss with exposed bone, muscle, or tendon |
| Unstageable | Base obscured by slough or eschar, cannot assess depth |
| Deep tissue injury (DTI) | Purple or maroon intact or non-intact skin; blood-filled blister; underlying tissue damage |
Common sites: sacrum, heels, ischial tuberosities, hips, medial malleoli, elbows, occiput.
Heel pressure injuries are particularly common and preventable, float heels with pillows placed longitudinally under the calves; sheepskin boots are also protective.
Risk Factors
Immobility, advanced age, incontinence, malnutrition, diabetes, sensory impairment (spinal cord injury, stroke), low body weight. In remote settings: elderly patients in aged care facilities, patients with end-stage renal disease or severe diabetes are particularly high risk.
Use validated risk assessment tools (e.g. Braden Scale or Waterlow Scale) to guide preventive intensity.
Prevention
- Reposition at minimum every 2 hours for bed-bound patients; maintain regular turning schedules
- Pressure-redistributing mattresses (foam, alternating air) and seat cushions
- Sheepskin boots or foam wedges for heel protection; avoid doughnut cushions (increase ischaemia at ulcer margins)
- Maintain skin hygiene; barrier creams for incontinence-associated moisture
- Keep sheets clean, dry, wrinkle-free, and free of food scraps
- Do not massage over bony prominences, increases shear injury
- Avoid hot water and soap directly on at-risk skin; use soap-free wash
- Optimise nutrition, protein, vitamin C, and zinc supplementation supports healing
- Bed cradle to keep bedclothes off pressure areas
- Early mobilisation where clinically possible
Management
Applicable to all stages:
- Relieve pressure completely, non-negotiable
- Clean with normal saline; avoid routine antiseptic solutions (impair healing)
- Moist wound environment, moist (not wet) conditions are physiologically optimal
- Avoid tight wound packing
Dressing selection by wound type:
| Wound Type | Preferred Dressing |
|---|---|
| Sloughy/necrotic | Hydrogel (e.g. IntraSite Gel) ± foam dressing cover; enzymatic debridement |
| Heavily exuding | Foam dressing (e.g. Mepilex), alginate |
| Granulating | Non-adherent (e.g. Mepitel, Melolin) |
| Infected | Silver-containing dressings; systemic antibiotics for clinical infection |
| Dry eschar (non-ischaemic) | Autolytic debridement; do not debride heel eschar in ischaemic limb without vascular assessment |
Infection management:
- Bacterial swabs of chronic wounds are diagnostically unhelpful, all chronic ulcers are colonised with Gram-positive and Gram-negative bacteria
- Infection is a clinical diagnosis: increasing pain, erythema, warmth, purulent discharge, wound breakdown, or systemic features
- If deep infection suspected: wound biopsy for microscopy and culture is preferred over surface swabs, clean wound surface with non-bacteriostatic cleanser before biopsy
- Antibiotic-impregnated dressings are not generally recommended
- Systemic antibiotics guided by clinical severity and local resistance patterns
- Osteomyelitis must be excluded in Stage 4 wounds, plain X-ray initially; MRI if available (requires retrieval to regional centre)
Post-healing:
- Encourage regular walking, good nutrition, no smoking, leg elevation when resting
- Great care to avoid re-injury (trauma is a common precipitant of recurrence)
- Vitamin C and zinc supplementation may promote healing
- Compression stockings (Jobst, Venosan, or Sigvaris grade) or Velcro wraps for venous/post-venous ulcer prevention
Venous Leg Ulcers
- ~80% of leg ulcers are vascular in origin; the majority are venous or mixed venous/arterial
- Located in the medial gaiter area, related to incompetent perforating veins
- Assess ABI before applying compression, compression is contraindicated if ABI <0.8
- High-stretch multilayer compression bandaging is most effective (superior to short-stretch or single-layer); elastic > non-elastic
- Short-stretch compression bandages are used primarily in lymphoedema
- Do not use crepe bandages or anti-embolic stockings, do not provide adequate therapeutic compression
- Clarify cause of oedema, calcium channel blockers are a reversible cause
- Consider oxpentifylline (pentoxifylline, Trental 400 mg) for chronic venous and occlusive arterial disease
- Venous surgery (foam sclerotherapy, laser, surgical stripping) may improve outcomes, arrange vascular referral
- Duplex Doppler is the gold standard investigation for venous and arterial disease
Diabetic Foot Ulcers
- May be neuropathic (pressure damage from sensory neuropathy, plantar, painless, surrounded by callus), ischaemic (peripheral arterial disease, distal, painful), or neuroischaemic (combined)
- Foot infections should be treated as medical emergencies ("foot attack")
- Clinical infection: purulent discharge, erythema, warmth, swelling; organisms on skin surface may not reflect deeper infecting organism
- Management: glycaemic optimisation, offloading (non-weight-bearing, special shoes/insoles, removable or non-removable casts), sharp debridement by podiatrist (callus distorts wound architecture), early broad-spectrum antibiotics adjusted on culture, drainage of collections, excision of infected bone if osteomyelitis unresponsive to antibiotics
- Regular X-rays to monitor progress; MRI for osteomyelitis where available
- Autoimmune diseases (RA, SLE, scleroderma) cause vasculitic ulcers, very painful, require immunosuppressants for healing
- Skin surface swab organisms may not represent deep infection organism, tissue biopsy preferred
Investigations
| Investigation | Purpose | Remote Availability |
|---|---|---|
| Wound biopsy | Exclude malignancy; confirm Buruli (PCR/histology); deep culture | Punch biopsy feasible; send-away pathology |
| Wound swab | Guide therapy in clinical infection only, not for colonisation | Available but limited diagnostic value |
| Blood glucose/HbA1c | Diabetes screening and monitoring | Point-of-care glucometer; send HbA1c |
| FBC, CRP, ESR | Systemic infection, haematological causes | Send-away |
| ABI | Assess arterial disease before compression | Handheld Doppler at most rural hospitals |
| Duplex Doppler | Gold standard for venous and arterial assessment | Regional/tertiary centre; telehealth review |
| Plain X-ray | Osteomyelitis, gas, foreign body | Most rural hospitals |
| MRI | Osteomyelitis confirmation | Tertiary centre; retrieval required |
| PCR for M. ulcerans | Confirm Buruli ulcer (repeat if initially negative) | Reference laboratory send-away |
| Syphilis serology | Treponematoses, yaws serology cross-reactive with syphilis tests | Send-away |
| Dark-ground microscopy | Yaws/treponematosis, identify organism from exudative lesions | Limited remote availability |
| Ferral angiography/CT angiography | Localise arterial occlusion for surgical/angioplasty planning | Tertiary centre |
Principles of Management, All Chronic Wounds
$$\text{Healing} \propto \text{Adequate perfusion} + \text{Moist environment} + \text{Infection control} + \text{Nutritional repletion} + \text{Pressure relief}$$
| Step | Action |
|---|---|
| 1. Diagnose | Identify aetiology, treatment without diagnosis risks failure and harm |
| 2. Debride | Remove all necrotic tissue, slough, and foreign bodies; dead tissue is painless |
| 3. Moist environment | Select appropriate modern dressings; moist > wet or dry for healing |
| 4. Control infection | Systemic antibiotics for clinical infection only; colonisation does not require antibiotics |
| 5. Optimise host | Glycaemic control, smoking cessation, nutrition, offloading, compression where indicated |
| 6. Improve circulation | Reduce pressure, increase exercise, vascular intervention where appropriate |
| 7. Monitor | Photograph and measure at every visit; track trajectory |
| 8. Escalate early | Telehealth, RFDS coordination for non-responding or high-risk wounds |
| 9. Malignancy vigilance | Biopsy any chronic non-healing wound; hypergranulation not responding to treatment requires urgent biopsy |
Retrieval and Transfer Criteria
| Indication | Urgency |
|---|---|
| Systemic sepsis from wound source | Emergency, RFDS retrieval; stabilise with IV antibiotics/fluids before transfer |
| Suspected necrotising fasciitis or gas gangrene | Emergency, activate retrieval immediately; surgical debridement essential |
| Suspected Buruli ulcer requiring specialist management | Semi-urgent, telehealth first (infectious diseases/dermatology), then transfer |
| Suspected malignant transformation (SCC) | Urgent, biopsy in situ; arrange surgical transfer for excision |
| Exposed bone, tendon, or joint | Transfer for surgical assessment |
| Stage 3-4 pressure injury not responding to conservative care | Semi-urgent surgical review, debridement, grafting |
| Diabetic foot with osteomyelitis or deep-space infection | Semi-urgent, vascular surgery/infectious diseases |
| Wound requiring skin grafting | Elective/semi-elective transfer |
| Vascular assessment (duplex, angiography) for arterial/venous disease | Elective transfer to regional vascular service |
Pre-transfer management: IV access, systemic antibiotics if septic, wound covered with appropriate dressing, limb elevated, analgesia, RFDS base notification with full clinical summary and wound photographs.
Special Considerations
Aboriginal and Torres Strait Islander Cultural Safety
- Skin sores and tropical ulcers are endemic in many remote communities and are linked to overcrowding, scabies, impetigo, and skin trauma, community-level social determinant responses are required alongside clinical management
- Scabies and impetigo are the most common precursors to tropical ulcers in children, treat and prevent these conditions as primary prevention
- Post-streptococcal sequelae (acute rheumatic fever, post-streptococcal glomerulonephritis) are serious complications of wound infections in children, ensure complete treatment and appropriate antibiotic coverage
- Shame and stigma around wounds may delay presentation, non-judgmental engagement is essential
- Aboriginal Health Workers/Practitioners are central to wound management programs, include them in assessment, treatment, and education
- Consent for wound photographs (telehealth consultation, monitoring) requires explicit, culturally appropriate explanation
- Wound care should align with patient-directed goals; comfort-focused care may be appropriate for elders and those with terminal illness
- Involve family in wound care education, healing is a shared responsibility in many community contexts
- CARPA-aligned Skin Sore Programs in remote health centres emphasise standardised assessment, photographic monitoring, and antibiotic stewardship
Paediatric Considerations
- Tropical ulcers and phagedenic infections are disproportionately prevalent in children and adolescents in remote communities
- Procaine benzylpenicillin dosing should follow CARPA/eTG weight-based protocols
- Buruli ulcer affects all ages including children, a painless undermined ulcer in a child from an endemic area must prompt early infectious diseases referral
- Yaws predominantly affects children <15 years, consider in children with chronic ulcers who have lived in or visited endemic Pacific Island or West African regions
Aged Care
- Pressure injuries are the predominant chronic wound type in residential aged care in rural/remote Australia
- Regular telehealth review is essential for RFDS-serviced remote aged care facilities
- Goals of care discussions are critical, aggressive surgical intervention is not appropriate for all patients
- Regular repositioning schedules, nutrition plans, and skin integrity assessments must be embedded in all care plans
Wound Malignancy Surveillance
- All chronic non-healing ulcers of >3 months duration should be considered for biopsy
- Marjolin ulcer (SCC in chronic scar or ulcer, burns, venous ulcers, tropical ulcers) carries significant
Sources