Chronic Wounds

Chronic wounds fail to progress through the normal, orderly phases of healing within an expected timeframe, generally defined as persisting beyond four to six weeks without significant progress toward closure.

They encompass venous leg ulcers, arterial ulcers, diabetic foot ulcers, and pressure ulcers (decubitus ulcers). Venous disease accounts for the large majority of chronic lower limb ulceration.

Accurate identification of the underlying aetiology is required. Management approaches, particularly regarding compression therapy, differ fundamentally and potentially dangerously between venous and arterial causes.

Pathophysiology and classification

• Venous ulceration arises from chronic venous hypertension. This typically results from valvular incompetence within the deep or superficial venous system, frequently following prior deep vein thrombosis or from primary varicose vein disease.
• Sustained ambulatory venous hypertension drives capillary damage, fibrin deposition, and progressive skin and subcutaneous tissue changes. These culminate in ulceration, typically over the medial malleolus (the gaiter area).
• Arterial ulceration reflects inadequate tissue perfusion from significant peripheral arterial disease. It typically presents as a punched out, well demarcated ulcer, often over the distal foot or toes.
• Arterial ulcers are characteristically painful, in contrast to the frequently less painful venous ulcer. They are associated with other signs of critical limb ischaemia.
• Mixed arteriovenous ulceration reflects coexisting venous and arterial disease. It is common, particularly in older patients with multiple vascular risk factors.
• Carefully assess the relative contribution of each component, as this determines whether compression therapy can be applied safely.
• Less common causes of chronic lower limb ulceration include vasculitis, pyoderma gangrenosum, and malignant transformation.
• Pyoderma gangrenosum is a specific inflammatory, frequently rapidly progressive ulcerating condition associated with inflammatory bowel disease and other systemic inflammatory conditions. It is characterised by a violaceous, undermined border and requires immunosuppressive rather than standard wound care management.
• Consider malignant transformation in any chronic, non healing or atypical ulcer. Marjolin ulcer is squamous cell carcinoma arising within a longstanding chronic wound.

• Venous ulcers are typically located over the medial (and sometimes lateral) malleolus. They have irregular borders and a shallow, granulating wound bed.
• Surrounding skin changes include haemosiderin staining (brown pigmentation from extravasated red blood cell breakdown products), lipodermatosclerosis (fibrotic induration and champagne bottle shaped narrowing of the lower leg), and varicose eczema.
• In longstanding disease there is atrophie blanche (white, atrophic, scarred areas with surrounding telangiectasia).
• Arterial ulcers are typically located over the toes, heel, or other distal or pressure bearing areas. They have well defined, punched out edges and a pale, poorly granulating base.
• Associated features of significant peripheral arterial disease include absent pedal pulses, cool skin, hair loss, and pain that characteristically worsens with limb elevation and improves with dependency.
• This is in direct contrast to the typical pattern of venous disease, where leg elevation improves associated aching and swelling.
• Assess for signs of infection complicating a chronic wound at every review. Signs include increasing pain, spreading erythema, purulent discharge, malodour and delayed healing progress despite otherwise appropriate management.
• Any chronic wound with an atypical appearance should raise suspicion of malignant transformation and prompt biopsy. Atypical features are raised, everted or rolled edges, unusually rapid growth, bleeding, or failure to respond to appropriate standard treatment over a reasonable trial period.

• Ankle brachial pressure index measurement is an essential investigation in the assessment of any lower limb ulcer. It identifies significant arterial disease that would contraindicate standard compression therapy, and quantifies any arterial insufficiency.
• A value below 0.8 generally indicates significant arterial disease. It requires specific caution or full arterial assessment before considering compression.
• A value below 0.5 to 0.6 indicates severe disease warranting urgent vascular surgical referral.
• Duplex ultrasound of the venous system characterises the pattern and severity of venous reflux or obstruction where venous disease is suspected as a significant contributing factor. It informs decisions on potential venous intervention alongside standard compression based conservative management.
• Further arterial imaging (computed tomography angiography, or formal duplex arterial assessment) and vascular surgical referral are indicated where ankle brachial pressure index screening identifies significant arterial disease. This applies particularly with features suggesting critical limb ischaemia, given the potential need for revascularisation to achieve adequate perfusion for wound healing.
• Reserve wound swab culture for wounds with clinical evidence of infection rather than performing it routinely, given universal bacterial colonisation of chronic wounds.
• Biopsy is indicated for any atypical, non healing, or otherwise clinically concerning wound, to exclude malignancy or an alternative inflammatory cause such as pyoderma gangrenosum.
• Pyoderma gangrenosum also warrants broader systemic assessment, given its recognised association with underlying inflammatory bowel disease and other systemic conditions.
• Nutritional assessment completes the evaluation of a chronic, non healing wound. So does screening for relevant contributing systemic conditions, including diabetes and, where clinically suggested, an underlying connective tissue or vasculitic process.

• Compression therapy is the cornerstone of venous ulcer management. Apply multilayer compression bandaging or, once healed, compression hosiery for long term maintenance.
• Apply compression only after confirming adequate arterial supply by ankle brachial pressure index measurement. Compression carries a risk of precipitating critical ischaemia in the context of significant undiagnosed arterial disease.
• Leg elevation when resting, with regular ambulation and calf muscle pump exercise (encouraging active ankle movement to support venous return), is an important adjunctive measure alongside compression therapy for venous disease.
• Endovenous ablation (thermal or chemical) or surgical treatment of significant superficial venous reflux, where identified on duplex assessment, is increasingly used as an adjunct to standard compression therapy.
• Evidence supports improved healing rates and reduced recurrence when superficial venous incompetence is treated alongside conservative measures.
• Arterial ulceration requires vascular assessment. Where feasible and appropriate to the individual patient's overall clinical context, revascularisation (angioplasty or surgical bypass) restores adequate perfusion.
• Healing is generally not achievable without addressing the underlying inadequate blood supply. Compression therapy is contraindicated in significant arterial disease, given the risk of exacerbating ischaemia.
• Wound bed preparation includes debridement of any necrotic tissue or slough and selection of an appropriate moisture balancing dressing according to wound characteristics. It follows similar general principles to chronic wound care detailed under decubitus ulcer management.
• Adapt wound bed preparation to the specific aetiology and any relevant contraindications. An example is avoiding occlusive dressings in significant arterial insufficiency, where infection risk is heightened.
• Reserve antibiotic therapy for wounds with clear clinical evidence of infection rather than colonisation, following the same principles as detailed for other chronic wound types.
• Pyoderma gangrenosum requires systemic immunosuppression rather than standard wound care alone. Options are corticosteroids and, for more refractory disease, agents such as ciclosporin or biologic therapy targeting the underlying inflammatory process.
• Carefully avoid surgical debridement in pyoderma gangrenosum, as it can provoke pathergy and worsen the ulcer. This is an important and distinct consideration from the debridement based approach generally appropriate for other chronic wound types.
• Suspected malignant transformation within a chronic wound requires prompt biopsy. Where confirmed, refer for oncological management according to the histological diagnosis.
• Nutritional optimisation and management of any contributing systemic condition (diabetes, connective tissue disease) complete holistic management of this frequently chronic and recurrent condition.
• For venous disease particularly, educate patients on long term compression hosiery use to reduce recurrence risk after successful healing.