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Home  /  ACRRM FACRRM  /  Study notes  /  Chronic wound management — tropical ulcer, pressure areas, CARPA protocols

Chronic wound management — tropical ulcer, pressure areas, CARPA protocols

ACRRM FACRRM LO 2.7LO 6.3LO 8.5LO 1.10 3,074 words
Free preview. This study note covers 4 learning objectives (2.7, 6.3, 8.5, 1.10) from the ACRRM FACRRM curriculum. Inside Primex you get AI-graded SAQ practice on this topic, voice viva with the AI examiner, MCQs across the full syllabus, and a curriculum tracker that ticks off every learning objective.

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

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


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:

Management of Acute Tropical Ulcer

Wound care:

Antibiotic therapy:

Debridement:

Chronic/non-healing phase:


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

Management

Applicable to all stages:

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:

Post-healing:


Venous Leg Ulcers


Diabetic Foot Ulcers


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

Paediatric Considerations

Aged Care

Wound Malignancy Surveillance


Sources

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A small sample of the deck for this topic. Tap a question to reveal the answer. The full deck and spaced-repetition scheduler live inside Primex.

What is the most common aetiology of leg ulcers in Australia?

Approximately 80% of leg ulcers are vascular in origin, caused by venous hypertension, arterial insufficiency, or a combination of both (mixed ulcers).

What organism causes Buruli ulcer, and by what other names is this condition known in Australia?

Buruli ulcer is caused by Mycobacterium ulcerans. In Australia it is also called Bairnsdale ulcer or Daintree ulcer.

What are the two main geographic locations in Australia where Buruli (Bairnsdale/Daintree) ulcer is endemic?

Coastal Victoria and Far North Queensland are the two main endemic areas in Australia.

What is the classic clinical feature of a Buruli ulcer edge?

An undermined edge is the classic feature of a Buruli ulcer.

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