Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Differentiate venous from arterial ulceration, assess perfusion before compression and coordinate wound, vascular and infection treatment.
A leg ulcer is a break in the skin below the knee that fails to heal as expected. Venous hypertension is the commonest cause, but PAD, diabetes/neuropathy, pressure, vasculitis, malignancy and inflammatory disease may coexist or mimic it.
The early management bundle is cause, perfusion, infection, oedema and pressure assessment—not selection of an expensive dressing. Compression heals venous ulceration when arterial supply is adequate; revascularisation is the central disease-modifying treatment for arterial ulceration.
Pain out of proportion, atypical site/edge, undermining, purpura, rapidly enlarging necrosis or failure despite correct therapy should prompt specialist review and possible biopsy rather than repeated empirical treatment.
Superficial or deep venous reflux, previous thrombosis, obstruction or calf-pump failure sustains high ambulatory venous pressure, particularly in people with varicosities, oedema or limited mobility.
Atherosclerotic narrowing reduces distal perfusion. Smoking, diabetes, hypertension, dyslipidaemia and kidney disease increase arterial risk and impair the tissue reserve needed for wound healing.
Diabetes or another neuropathy removes protective sensation, while deformity concentrates pressure at the foot. Repeated unnoticed trauma then causes ulceration, often with coexisting arterial disease.
Vasculitis, pyoderma gangrenosum and skin malignancy can ulcerate through vascular inflammation, neutrophilic injury or tumour invasion, particularly when the site, edge or progression is atypical.
Venous valve failure or obstruction impairs the normal pressure reduction during walking, transmitting sustained venous hypertension into the superficial veins and dermal microcirculation.
Capillary leakage and chronic inflammation cause oedema, haemosiderin deposition, eczema and fibrosis. Vulnerable gaiter skin may then break down into a shallow exudative ulcer.
Arterial stenoses lower perfusion pressure and oxygen delivery to distal tissues, especially toes and pressure points, producing cool skin and poor tolerance of minor injury.
When demand from pressure or trauma exceeds the limited blood supply, tissue may die and form an often painful, punched-out ulcer with a pale or necrotic base.
Oedema, repeated pressure, infection, neuropathy or combined arterial and venous disease can perpetuate inflammation and delay or prevent granulation, re-epithelialisation and durable wound closure.
Shallow irregular ulcer in the medial/lateral gaiter area, often wet or granulating, with oedema, haemosiderin pigmentation, eczema, lipodermatosclerosis and varicosities.
Distal toe/foot, pressure-point or lateral malleolar lesion with a punched-out pale/necrotic base, cool shiny skin, delayed refill and reduced pulses; often painful and worse with elevation.
Venous skin changes plus reduced perfusion; strong compression may be unsafe and requires vascular/tissue-viability planning.
Pressure-site callus, altered sensation and deformity; infection and ischaemia may be painless and require the NICE diabetic-foot pathway.
Spreading erythema/swelling beyond the ulcer, warmth, increased pain, purulent discharge or fever; wet gangrene, systemic illness or deep infection is an emergency.
Raised/everted edge, violaceous undermining, livedo/purpura, rapid progression or non-healing despite correct care suggests malignancy, vasculitis, pyoderma gangrenosum or another diagnosis.
A plantar pressure-site lesion surrounded by callus, with sensory loss and foot deformity, favours neuropathy; infection or ischaemia may be advanced despite little pain.
Prolonged immobility can produce tissue injury over a bony prominence through pressure and shear. Location and the immobility or pressure history are more characteristic than gaiter-region venous skin change.
Painful ulcers accompanied by palpable purpura, livedo or systemic inflammatory features suggest vessel-wall inflammation and require targeted laboratory, dermatological and sometimes histological assessment.
Rapid expansion, severe pain and an undermined violaceous edge suggest neutrophilic disease. Trauma or debridement may worsen it, so specialist review should precede further tissue injury.
A raised, everted or irregular edge, abnormal tissue growth or failure despite correct vascular care warrants biopsy to exclude squamous or another cutaneous malignancy.
A breached skin barrier permits invasive bacterial infection, causing spreading erythema, warmth, pain and systemic illness. Bacterial colonisation alone does not establish invasive tissue infection.
Infection may track into fascia, tendon, joint or bone, particularly in deep diabetic or ischaemic wounds, substantially prolonging treatment and threatening limb viability.
Severe unrevascularised ischaemia can progress from ulcer necrosis to dry or infected gangrene. Tissue loss and uncontrolled infection may ultimately make limb preservation impossible.
A healed venous ulcer commonly recurs when reflux, oedema or calf-pump dysfunction persists, while ongoing arterial risk can produce new distal tissue loss.
Chronic wound pain and treatment burden can reduce walking, weakening the calf pump and worsening venous oedema, frailty and social isolation.
It needs a cause assessment, arterial check, correct product, trained application and monitoring—not simply a bandage order.
Bacteria on a chronic wound do not predict benefit from antibiotics without clinical infection.
An ABPI above 1.3 often reflects calcification; use toe pressures/waveforms before compression decisions.
Compression can begin while vascular referral proceeds; superficial venous intervention addresses the cause and can reduce recurrence.
Severe pain, rapid necrosis or an unusual border/site should trigger vascular/dermatology review rather than stronger dressings or repeated antibiotics.
Starting 40 mmHg compression before arterial assessment.
Calling a high ABPI normal in a diabetic patient with calcified vessels.
Swabbing every ulcer and treating the culture rather than clinical infection.
Using dressings alone for an arterial ulcer without urgent vascular referral.
Failing to refer an active venous ulcer after 2 weeks or a healed ulcer for venous assessment.
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A gaiter-region ulcer has typical venous features and ABPI is 0.92. There are no infection or acute ischaemia signs. What is the core treatment?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Do not use for colonisation alone. Check true penicillin allergy, liver history and interactions; 1 g four times daily is off-label but included in NICE dosing.
Avoid in pregnancy; counsel on photosensitivity, oesophageal irritation and separation from antacids/iron/calcium.
Check combination medicines and reassess unexpectedly severe pain for ischaemia or deep infection.