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Leg Ulcers — Systematic Primary Care Assessment 9-step pathway · venous, arterial, neuropathic and malignant ulceration · arterial assessment before strong compression · UK GP / RCGP SCA preparation
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Snapshot: decision tree. The whole pathway on one page: start at the top, act on any red flag, then follow the arrows. The Steps tab holds the detail.

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1
Safety

Red Flags — Limb-threatening ischaemia, infection and malignancy

Scope: adults with an ulcer below the knee — venous, arterial, mixed, neuropathic/diabetic, pressure, inflammatory and malignant. Local tissue-viability, vascular and diabetic-foot pathways take precedence. Many ulcers are venous, but none is "manageable in primary care" until arterial disease, diabetes, infection, atypical disease and malignancy have been assessed. Escalate the groups below before any wound care decision is made.

Limb-threatening ischaemia Ischaemic rest pain (worse at night, eased by hanging the leg out of bed), gangrene or tissue loss with a cold, pale or pulseless foot, rapidly worsening ulceration, suspected acute-on-chronic ischaemia → same-day vascular assessment. Acute limb ischaemia (sudden pain, pallor, pulselessness, coldness, paraesthesia or paralysis), rapidly progressive tissue loss, or gangrene with spreading infection or sepsis → 999 / emergency admission. Remove any compression; keep the limb warm, dependent and protected — do not elevate an ischaemic leg.
Diabetic foot ulcer An active diabetic foot problem → refer within 1 working day to the local foot-protection / MDT diabetic foot service, for triage within 1 further working day (NICE NG19). Immediate hospital referral if fever or sepsis, limb ischaemia, gangrene, suspected deep soft-tissue or bone infection, severe or rapidly progressive infection, or suspected acute Charcot with an ulcer or systemic concern.
Necrotising fasciitis Pain out of proportion, rapidly progressive swelling or erythema, crepitus, bullae, dusky skin, systemic toxicity or shock → 999
Sepsis from cellulitis or osteomyelitis Fever, rigors, tachycardia, NEWS2 elevated → same-day admission for IV antibiotics; 999 if new confusion or altered consciousness, or haemodynamic compromise
Exposed or palpable bone Suspected osteomyelitis (a positive probe-to-bone test increases suspicion but is not diagnostic) → same-day orthopaedic or diabetic foot assessment; imaging (X-ray may be normal early; MRI generally preferred) and specialist evaluation
Rolled or everted edge, friable or exuberant granulation, bleeding, rapid change Possible SCC, including Marjolin's ulcer → Suspected skin cancer / biopsy per the local/NICE NG12 pathway. Non-healing at 12 weeks alone → reassess and escalate (not an NG12 criterion by itself)
Rapidly enlarging painful ulcer with a violaceous undermined edge Pyoderma gangrenosum → urgent dermatology; debridement makes it worse (pathergy)
Purpura, livedo, systemic symptoms, multiple ulcers Vasculitis or cryoglobulinaemia → urgent rheumatology; urinalysis and ANCA
Acute painful ulcer with a black eschar in a hypertensive diabetic Consider calciphylaxis or Martorell's hypertensive ulcer → urgent specialist input
Uncontrolled bleeding, or rapidly progressive ulceration with severe systemic illness Bleeding from varicose veins or ulceration → 999 / emergency admission
The diabetic foot ulcer deserves to be treated as a distinct emergency rather than a subtype of leg ulcer. NICE NG19 asks for referral of an active diabetic foot problem within 1 working day to the multidisciplinary foot care or foot-protection service, with immediate hospital referral for limb- or life-threatening disease, because the combination of neuropathy, ischaemia and impaired immunity means an apparently trivial ulcer can progress to osteomyelitis and amputation within days — and the patient cannot feel it deteriorating. Most diabetes-related amputations are preceded by a foot ulcer, and delayed referral is a modifiable factor. Pyoderma gangrenosum is included because the reflex response to a necrotic ulcer edge — debridement — actively worsens it through pathergy, so recognising it prevents harm. Marjolin's ulcer is rare but it is why non-healing ulcers are reassessed at 12 weeks: any chronic wound can undergo malignant transformation, and the tumour is often mistaken for exuberant granulation tissue for months.
2
Diagnose

History — Risk factors that identify the ulcer type

Duration and course
How long present, how it started (spontaneous, minor trauma, insect bite, scratch), healing and breakdown cycles, previous ulcers on either leg and how they were treated
Infection symptoms
Fever, rigors, new erythema, purulence or malodour
Pain and what changes it
Venous: aching, heavy, worse standing, better on elevation. Arterial: severe, worse at night and worse on elevation, relieved by dangling the leg. Neuropathic: painless. Pain out of proportion or a sudden increase in pain → reassess for infection, ischaemia, pyoderma gangrenosum or another atypical diagnosis.
Venous risk factors
Previous DVT, varicose veins or vein surgery, leg fracture, pregnancy, obesity, occupations involving prolonged standing, family history, previous ulceration
Arterial risk factors
Smoking, diabetes, hypertension, hyperlipidaemia, known coronary or cerebrovascular disease, intermittent claudication and its distance, rest pain, previous revascularisation
Diabetes
Duration, control (HbA1c), known neuropathy or retinopathy, previous ulcer or amputation, footwear, whether the patient can see and reach their own feet
Mobility and oedema
Immobility, ankle range of movement, chair-bound (dependency oedema), heart failure, renal or hepatic disease, lymphoedema, calcium channel blocker use
Atypical clues
Inflammatory bowel disease or rheumatoid arthritis (pyoderma gangrenosum, vasculitis), vasculitis or connective-tissue disease, renal failure or dialysis (calciphylaxis risk), sickle cell disease, tropical travel, immunosuppression, injecting drug use, previous radiotherapy, long-standing scar or burn
Drugs
Steroids and immunosuppressants (impaired healing), hydroxycarbamide (ulceration), nicorandil (a well-recognised cause of painful ulceration — perianal, oral and cutaneous), anticoagulants, calcium-channel blockers (oedema)
Impact and capability
Pain at night, sleep, mobility, ability to wash and dress, exudate and odour, social isolation, who does the dressings, ability to tolerate compression and to apply hosiery
The relationship between pain and leg position is the most discriminating question in the history and costs nothing. Venous hypertension is relieved by elevation, so a venous ulcer feels better with the leg up; arterial perfusion depends on gravity, so an ischaemic leg hurts more when elevated and patients characteristically sleep in a chair or hang the leg out of bed. A patient who sleeps sitting up because of leg pain has arterial disease until proven otherwise. Nicorandil-induced ulceration is worth knowing specifically because it is drug-induced, often severe and non-healing, frequently misdiagnosed for months, and resolves completely on withdrawal of the drug — but only if someone thinks to look at the repeat prescription. Asking who actually does the dressings and whether the patient can reach their own feet changes the management plan more than any investigation.
3
Diagnose

Classification — Ulcer type by site, appearance and pulses

Venous
Medial gaiter area (above the malleolus); shallow, irregular sloping edge, granulating base, heavy exudate; surrounded by oedema, varicose eczema, haemosiderin staining, lipodermatosclerosis, atrophie blanche; pulses may be present; ABPI usually 0.8–1.3
Arterial
Lateral malleolus, shin, toes, pressure points; deep, punched-out, sharply demarcated, pale or necrotic dry base; cold shiny hairless skin, absent pulses, delayed capillary refill, dependent rubor; ABPI <0.8
Mixed arteriovenous
Features of both venous and arterial disease (ABPI often 0.5–0.8). Requires vascular/tissue-viability assessment before deciding compression — mild compression may be considered under the local pathway, never on GP initiative
Neuropathic / diabetic foot
Plantar surface, metatarsal heads, heel, under callus; painless, punched-out with surrounding hyperkeratosis; warm foot, palpable pulses, absent sensation to 10 g monofilament; Charcot deformity. Refer to the foot service within 1 working day (NICE NG19).
Pressure ulcer
Heel, malleolus, sacrum; in immobile patients; graded 1–4. Requires pressure redistribution, repositioning, appropriate support surfaces and the local pressure-ulcer pathway; do not apply venous-ulcer compression automatically; consider safeguarding if care was inadequate
Malignant
SCC (including Marjolin's in chronic ulceration), BCC, melanoma, cutaneous lymphoma. Rolled or everted edge, exuberant friable granulation, bleeding, atypical site, failure to progress despite appropriate treatment → biopsy / urgent skin-cancer assessment
Inflammatory / vasculitic
Pyoderma gangrenosum (violaceous undermined edge, IBD/RA association, pathergy), vasculitis, rheumatoid ulcers, necrobiosis lipoidica, calciphylaxis in renal failure
Infective
Cellulitis complicating any ulcer; necrotising infection; rarely tuberculosis, syphilis, deep fungal or tropical infection (Buruli, leishmaniasis) — consider with relevant travel
Caution
No single appearance reliably establishes the diagnosis; mixed aetiology is common.
Other
Sickle cell ulceration, hydroxycarbamide- or nicorandil-induced, factitious, trauma or burn, lymphoedema-related, Martorell's hypertensive ischaemic ulcer
Site and pain together identify the type in the great majority of cases before any equipment is involved: medial and better up is venous, lateral or toes and worse up is arterial, plantar and painless is neuropathic. The important subtlety is mixed disease, which is common in older patients and in diabetes and is where harm occurs — a leg can look convincingly venous, with oedema and staining, while the ABPI is 0.6. This is precisely why arterial assessment is required before strong compression rather than being a formality: the clinical appearance of a venous ulcer does not exclude significant arterial disease. In diabetes, the ABPI can additionally be falsely elevated above 1.3 by medial arterial calcification, so a high reading is also a referral trigger rather than reassurance, and toe-brachial pressures or duplex are needed instead.
4
Diagnose

Examination & ABPI — The measurement the pathway turns on

Both legs, both feet, shoes and socks off
Compare sides. Examine between the toes and under any callus. Ulcers are frequently bilateral and a second ulcer changes the diagnosis.
Ulcer characterisation
Site, size (measure two dimensions or trace), depth, edge, base tissue type (granulation, slough, necrosis, exposed tendon or bone), exudate volume and type, odour
Surrounding skin
Oedema (pitting or non-pitting), varicose eczema, haemosiderin staining, lipodermatosclerosis, atrophie blanche, cellulitis, maceration, contact dermatitis from dressings
Pulses
Temperature, colour and capillary refill. Palpate posterior tibial and dorsalis pedis in both feet, plus popliteal and femoral. Absent pulses mandate Doppler; palpable pulses do not exclude arterial disease.
ABPI — required before strong compression
Handheld Doppler by a trained, competent practitioner, both legs, patient rested supine; highest brachial systolic as the denominator and the highest ankle systolic (dorsalis pedis or posterior tibial); document value, date and method. Practical thresholds, not absolute: 0.8–1.3 → strong compression may be appropriate if the clinical assessment supports venous disease, applied by a trained practitioner. 0.5–0.8 → mixed disease likely; vascular/tissue-viability advice, mild compression only under the local pathway. <0.5 → severe arterial disease; discuss with vascular the same day, particularly with tissue loss or rest pain (chronic limb-threatening ischaemia is a clinical diagnosis). >1.3 → likely incompressible vessels, ABPI unreliable — toe pressure, Doppler waveform or vascular assessment. In diabetes, CKD and older age a falsely reassuring ABPI is possible; consider toe-brachial index or vascular referral if results conflict with clinical findings.
Neurological assessment
10 g monofilament at 10 sites, vibration (128 Hz tuning fork), ankle reflexes, proprioception. Loss of protective sensation defines the at-risk foot
Foot assessment in diabetes
Deformity, callus, nail disease, interdigital fungal infection, footwear fit and foreign bodies inside the shoe, temperature asymmetry (Charcot)
General
BMI, mobility, ankle range of movement and calf-pump function, pressure points (heel, malleoli, sacrum), evidence of heart failure, BP, lymphadenopathy, general skin survey for other lesions
Photograph and document
Dated photograph with a scale (where local information-governance arrangements permit), plus measured dimensions, at baseline and at each review. This is how non-healing at 12 weeks is actually recognised rather than assumed.
The ABPI is the fulcrum of this entire pathway. Full-strength compression applied to a leg with an ABPI below 0.5 can cause pressure necrosis and has led to amputations; it is one of the clearest examples in community practice of a well-intentioned treatment causing catastrophic harm when a five-minute measurement is skipped. The technique details matter: the patient must be supine and rested, because standing or recent exertion distorts the reading, and the highest of the two brachial pressures is used as the denominator. A falsely high ABPI above 1.3 is a particular trap in diabetes and chronic kidney disease, where medial calcification makes the vessel incompressible — this reading must never be interpreted as good perfusion. Serial measurement and photography are equally important: the 12-week non-healing review which triggers reassessment and escalation can only be applied if the baseline size was recorded, and in practice the absence of a baseline measurement is why chronic ulcers drift for years.
5
Diagnose

Investigations — Confirm the type and find the treatable comorbidity

Bedside
ABPI (both legs) · Capillary glucose / HbA1c · Urinalysis (glucose, protein, blood — vasculitis) · 10 g monofilament · BP and BMI
Bloods (targeted)
HbA1c / glucose FBC U&Es LFTs Lipids (cardiovascular-risk assessment) · CRP if infection or inflammatory disease suspected · Ferritin / albumin if nutritional deficiency or anaemia suspected. Do not routinely request ANCA, ANA, rheumatoid factor, cryoglobulins without compatible clinical features
Wound swab
Do not swab routinely at initial presentation, even when infection is suspected (NICE NG152). Consider a wound sample after cleaning if infection is worsening or has not improved as expected. All chronic ulcers are colonised; colonisation, exudate or odour alone is not an indication for antibiotics.
Venous duplex ultrasound
Generally arranged by the vascular service rather than directly by the GP. NICE CG168: refer people with a venous leg ulcer or a healed venous leg ulcer to a vascular service for assessment and consideration of intervention — duplex is part of that assessment.
Arterial imaging
Arterial duplex, CT or MR angiography — vascular-led, where ABPI or symptoms indicate significant disease and revascularisation is being considered
Biopsy
Urgent dermatology / skin-cancer assessment (local pathway) Rolled or everted edges, friable or exuberant granulation, unexplained bleeding, rapid enlargement or change, atypical site, failure to progress despite appropriate treatment, or a chronic ulcer with diagnostic uncertainty (a lesion that raises suspicion of SCC → consider an NG12 suspected cancer pathway referral). A 12-week non-healing ulcer is an escalation point, not by itself an NG12 criterion. Biopsy the active edge and adjacent skin, per local dermatology/pathology guidance. Do not biopsy suspected pyoderma gangrenosum without specialist advice (pathergy).
Imaging for osteomyelitis
Consider with exposed or palpable bone, a deep or chronic diabetic foot ulcer, recurrent infection, failure to heal despite appropriate care, or persistent inflammatory features. Plain X-ray may be an initial test but can be normal early; MRI is generally preferred if osteomyelitis remains suspected. A positive probe-to-bone test increases suspicion but is not diagnostic. In diabetic foot disease classify with SINBAD or University of Texas — NICE NG19 advises against Wagner.
Patch testing
Consider in persistent surrounding eczema — contact allergy to dressings, adhesives, lanolin, topical antibiotics and rubber accelerators is common in this group
Do not do
Do not routinely swab; do not start antibiotics for odour or exudate alone; do not use antimicrobial dressings prophylactically; do not start strong compression before arterial assessment
Two investigative habits cause most of the avoidable harm in leg ulcer care, and both involve doing more rather than less. Routine wound swabbing generates positive cultures from colonising flora in almost every chronic ulcer, which in turn generates repeated antibiotic courses that do not improve healing and do drive resistance and C. difficile. Infection in an ulcer is a clinical diagnosis — increasing pain, spreading erythema, purulence, systemic upset — and swabs are not taken routinely at presentation — a sample after cleaning is considered only if infection worsens or fails to improve (NICE NG152). The second habit is antimicrobial and advanced dressings in place of compression: the evidence consistently shows that dressing choice has a marginal effect on healing while compression has a large one, so a simple non-adherent dressing under proper compression outperforms an expensive dressing without it. Biopsy technique also matters: the diagnostic tissue in a malignant ulcer is at the raised edge, and a biopsy taken from the necrotic centre is commonly non-diagnostic.
6
Refer

Referral Criteria — Same-day, suspected cancer and planned pathways

999
Suspected necrotising fasciitis (pain out of proportion, rapidly progressive swelling or erythema, crepitus, bullae, dusky skin, systemic toxicity or shock); sepsis with haemodynamic compromise or altered consciousness; acute limb ischaemia; chronic limb-threatening ischaemia with rapidly progressive tissue loss, or gangrene with spreading infection or sepsis; diabetic foot ulcer with sepsis, limb ischaemia, gangrene, deep abscess, necrotising infection or suspected extensive osteomyelitis; uncontrolled bleeding from varicose veins or ulceration; rapidly progressive ulceration with severe systemic illness
Same-day vascular
Ischaemic rest pain; gangrene or tissue loss with a cold, pale or pulseless foot; rapidly worsening ulceration; suspected acute-on-chronic limb ischaemia; ABPI <0.5 where reliable, especially with tissue loss or rest pain; mixed arterial/venous disease with worsening pain or deterioration. Do not interpret ABPI in isolation — a normal or high ABPI does not exclude clinically important arterial disease in diabetes or CKD. Acute limb ischaemia (the six Ps) is a surgical emergency
Diabetic foot service — within 1 working day
NICE NG19: a diabetic foot ulcer is an active diabetic foot problem — refer within 1 working day to the local foot-protection or multidisciplinary diabetic foot service, for triage within 1 further working day (community foot-protection services may provide some care). Immediate hospital referral for ulceration with fever or sepsis, limb ischaemia, gangrene, suspected deep soft-tissue or bone infection, severe or rapidly progressive infection, or suspected acute Charcot arthropathy with an ulcer or systemic concern
Suspected skin cancer
NICE NG12 (updated April 2026): a skin lesion that raises the suspicion of squamous cell carcinoma → consider a suspected cancer pathway referral. An ulcer with a rolled or everted edge, exuberant friable granulation, unexplained bleeding, rapid change or an atypical site raises that suspicion — consider referral or arrange biopsy for SCC, including Marjolin's ulcer in chronic ulceration. An ulcer that fails to heal after 12 weeks is an escalation point (SIGN 120) but not, by itself, an NG12 criterion. Pigmented or changing lesion → suspected melanoma pathway
Suspected cancer: sarcoma
NICE NG12 (updated April 2026): an associated unexplained soft-tissue lump that is increasing in size → consider an urgent direct-access ultrasound (in line with the local pathway) for suspected soft-tissue sarcoma; consider a suspected cancer pathway referral if the scan suggests sarcoma or is uncertain with persisting concern
Vascular — before compression
ABPI <0.8 or >1.3, or mixed arteriovenous features. Do not apply strong compression outside 0.8–1.3; mild compression only under vascular/tissue-viability direction or the local pathway
Vascular / venous service (routine)
NICE CG168: refer people with a venous leg ulcer or a healed venous leg ulcer to a vascular service for assessment and consideration of intervention (duplex arranged by the vascular service) — this can reduce recurrence
Dermatology
Suspected pyoderma gangrenosum (urgent), vasculitis, atypical or non-healing ulcer needing biopsy, persistent surrounding eczema for patch testing
Tissue viability / community nursing
Compression initiation and maintenance, complex exudate management, debridement, pressure redistribution, repositioning and support surfaces (local pressure-ulcer pathway), hosiery fitting and long-term prevention
Primary care manage
Uncomplicated venous ulcer with ABPI 0.8–1.3 — only after arterial disease, diabetes, infection, atypical disease and malignancy have been assessed — in partnership with community nursing and with vascular referral; cardiovascular risk modification; pain control; oedema and comorbidity optimisation
Two referrals are systematically under-made. The first is the vascular referral for venous intervention: NICE CG168 recommends referring people with a venous leg ulcer, or a healed venous leg ulcer, to a vascular service for assessment and consideration of intervention, because correcting the underlying venous incompetence can reduce recurrence — yet most ulcers are managed indefinitely with dressings alone and never reach a vascular clinic. The second is reassessment, biopsy or skin cancer referral for the atypical or non-progressing ulcer. The 12-week review matters because squamous cell carcinoma arising in chronic ulceration is typically diagnosed late, after months or years of dressing changes, and by then it may have metastasised; the tumour can look identical to exuberant granulation tissue. Applying both rules requires only that the ulcer's size was measured at the start and that someone reviews the whole plan at 12 weeks, which is a diary entry rather than a clinical skill.
7
Treat

Treatment — Compression first, dressings second

Venous ulcer, ABPI 0.8–1.3
Strong compression 1st line
Graduated compression commonly targeting approximately 40 mmHg at the ankle, after adequate arterial assessment, applied by a trained practitioner per local competency and pathway — multilayer bandage, two-layer system or compression wrap. Monitor pain, colour, temperature, sensation and tolerance; reassess if pain increases or new numbness develops. This, not the dressing, is the principal treatment.
Wound bed
Simple non-adherent dressing
Simple low-adherent dressing chosen by exudate volume, maceration risk, pain at dressing change, patient preference and cost. Clean with tap water or saline. Debridement only by appropriately trained staff (not for suspected pyoderma gangrenosum). There is no reliable evidence that antimicrobial or "advanced" dressings improve healing when compression and underlying-cause treatment are inadequate; avoid routine antimicrobial dressings without clinical infection.
Clinically infected ulcer
Oral flucloxacillin (NG152/local)
First line per the current NICE NG152/local antimicrobial guideline (dose, duration and penicillin-allergy alternative as listed there). Only for clinical signs of infection — spreading erythema or swelling beyond the ulcer, local warmth, increasing pain, purulent discharge, fever or systemic illness. Review if worsening or not beginning to improve within 2–3 days; consider a wound sample after cleaning and specialist advice if treatment fails. Odour and exudate alone are not infection.
Arterial or mixed
No strong compression
Arrange vascular assessment and consider revascularisation; protect the wound with a simple dressing; address smoking, BP, lipids and cardiovascular risk (high-intensity statin, antiplatelet). Treat ischaemic rest pain urgently — not a routine wound-care problem. A small degree of compression may be used in selected oedematous mixed ulcers under vascular/tissue-viability supervision if there is no limb-threatening ischaemia — not started independently from this algorithm.
Surrounding varicose eczema
Moderate-potency topical steroid
Short course to the eczematous skin (not the ulcer bed) plus generous emollient. Avoid topical antibiotics and lanolin-containing products — sensitisation is common and perpetuates the problem. Compression after arterial assessment.
Stalled healing despite compression
Review — not a routine drug step
Review the diagnosis, arterial status and whether compression is therapeutic first — non-healing is more often wrong diagnosis, inadequate compression or unrecognised malignancy. Pentoxifylline is not a routine GP step: consider only after the diagnosis is confirmed, with adequate compression and specialist/local wound-service advice; it is not a substitute for compression or correction of arterial/venous disease.
PyodermaSuspect with a rapidly progressive, very painful ulcer with a violaceous undermined edge, particularly with IBD, rheumatoid arthritis or haematological disease. Avoid routine sharp debridement (pathergy); arrange urgent dermatology advice.
PainIndividualised analgesia — consider age, renal/GI/cardiovascular risk, anticoagulants and arterial disease before any NSAID; ischaemic rest pain often needs opioids and urgent vascular input. Neuropathic pain → amitriptyline, duloxetine, gabapentin or pregabalin (NICE CG173). Time analgesia to dressing changes; consider topical local anaesthetic before debridement.
OedemaElevate above hip level when sitting, avoid prolonged standing, ankle exercises hourly, treat heart failure, review calcium channel blockers and other oedema-causing drugs. Uncontrolled oedema defeats compression.
Cardiovascular riskWhere arterial disease is present, this is a coronary risk equivalent: high-intensity statin, antiplatelet, BP control, smoking cessation, supervised exercise programme. Treating the ulcer without treating the arteries treats the wrong problem.
DiabetesRefer within 1 working day to the local diabetic foot/foot-protection pathway (NICE NG19). Management usually requires offloading, assessment of perfusion, neuropathy and deformity assessment, debridement by appropriately trained staff, infection assessment and treatment, glycaemic optimisation, and appropriate footwear and pressure redistribution. Do not prescribe compression for a diabetic foot ulcer simply because the leg is oedematous.
NutritionScreen with MUST. Screen for and treat documented or clinically suspected deficiency (protein, vitamin C, zinc, iron) — do not routinely prescribe supplements without assessment; poor nutrition is a common and correctable reason for a wound that will not close, particularly in frail older patients.

Next steps: see Varicose veins · Peripheral arterial disease · Atopic eczema · Cellulitis and erysipelas

Compression is one of the most effective interventions in community medicine and one of the most frequently under-dosed. The evidence for strong graduated compression is strong and consistent, while the comparative evidence between dressing types is weak — which means the expensive part of most ulcer care contributes least. Under-dosed compression is a common reversible cause of a non-healing venous ulcer, and tolerance often improves with good analgesia — but increasing pain or new numbness under compression must be reassessed the same day, not persisted with. Topical antibiotics deserve a specific warning: they achieve little, and neomycin and framycetin are potent sensitisers, so a proportion of patients with persistent peri-ulcer eczema have iatrogenic contact dermatitis. Where arterial disease is found, the ulcer is a marker of widespread atherosclerosis, and the statin and antiplatelet will do more for the patient's life expectancy than any dressing will.
8
Lifestyle

Non-Pharmacological — Prevention and self-management

Compression hosiery after healing Individualised and correctly fitted — selected according to arterial status, recurrence risk, limb shape, skin condition and the patient's ability to apply it, not a fixed class and replacement interval for everyone. Provide an applicator and check the patient can physically manage them.
Elevation and ankle exercises Elevation when seated for venous oedema; regular walking and ankle-pump exercises where safe to engage the calf muscle pump. Avoid prolonged standing and long periods with legs dependent.
Walking The calf pump is the mechanism that empties the deep veins — regular walking improves venous return, and in arterial disease supervised exercise improves claudication distance and collateral flow.
Skin care Daily emollient to the whole lower leg, wash with a soap substitute, dry carefully between the toes. Healthy skin is far less likely to break down after minor trauma.
Smoking cessation The most important single change in arterial ulceration — it improves healing, reduces amputation risk and reduces cardiovascular mortality. Refer to the stop-smoking service directly.
Weight and diet Obesity raises venous pressure and impairs mobility. Adequate nutrition, with assessment for malnutrition where clinically indicated.
Foot care in diabetes Daily inspection with a mirror, never walk barefoot, check inside shoes before wearing, professional nail and callus care, annual foot check (more often if at risk).
Protect from trauma Shin guards or long trousers, furniture padding, careful nail cutting, review sedating drugs and falls risk (NICE NG249: comprehensive falls assessment for older people meeting its criteria — medication review, vision, gait/balance and strength, home-hazard intervention) — many ulcers start as a minor knock.
Psychological and social support Chronic ulcers cause pain, odour, sleep loss, isolation and depression. Ask about mood and about who helps; leg clubs and group clinics improve both healing and quality of life.
Once a venous ulcer has healed, the clinical problem changes from healing to prevention, and compression hosiery is the intervention with the best evidence, and concordance is the main determinant of success. Concordance in turn depends on practical details that are easy to overlook: whether the patient can physically pull the stocking on (an applicator or a lower class worn consistently beats a higher class abandoned in a drawer), whether they have two pairs so one can be washed, and whether replacement is actually organised. Note that graduated compression stockings are not recommended for the prevention of post-thrombotic syndrome after DVT, which is a different indication — the evidence here is specifically about preventing ulcer recurrence. The psychosocial burden is also routinely under-addressed: pain, exudate and odour drive social withdrawal and depression, and community leg clubs improve healing rates partly through peer support and adherence.
9
Safety

Follow-Up & Safety-Netting

Every dressing change
Measure or trace the ulcer (dimensions and depth); record wound bed, exudate, surrounding skin and pain; record compression type, pressure system and tolerance; neurovascular findings where relevant; photograph per local governance
4 weeks
Expect clear progress. If none: review the diagnosis, confirm compression is therapeutic and correctly applied, recheck arterial status if symptoms have changed, assess infection, oedema, nutrition, diabetes and adherence, and consider vascular, tissue-viability or dermatology escalation.
12 weeks
Decision point. Not healed or not substantially progressed → reassess arterial and venous disease, review compression and adherence, and escalate to tissue viability, vascular or dermatology services; biopsy or suspected skin-cancer referral if atypical or clinically suspicious. This is a diary entry made at first presentation, not an afterthought
Ongoing review
Repeat ABPI when clinically indicated (deterioration, new ulceration or suspected progression) per local wound-service policy; review cardiovascular risk management; reassess venous intervention if not yet done; check hosiery fit and replacement
After healing
Individualised compression hosiery, selected after arterial assessment and a review of ability to apply it; periodic review of skin, arterial status and hosiery; prompt access for any new break in the skin
999
Pain far worse than the wound looks, crackling (crepitus), dusky or blistering skin, rapidly spreading redness, or fever with feeling very unwell, faint or confused (necrotising infection or sepsis); sudden pale, cold, painful, numb or weak foot, or loss of pulses (acute ischaemia); bleeding from the ulcer or a varicose vein that will not stop (press firmly and raise the leg while waiting)
Same-day GP or nurse
Increasing pain (particularly out of proportion) or new numbness or coldness under compression (remove the bandage), spreading erythema or warmth, purulent discharge with systemic symptoms, sudden ulcer enlargement, new gangrene or black areas, fever, new diabetic foot ulcer or suspected Charcot foot
Re-investigate if
Ulcer edge changes, becomes rolled or everted, bleeds or granulates exuberantly; ulcer enlarges despite compression; new ulcers at atypical sites; systemic symptoms develop
Documentation
Record ABPI value and date, ulcer measurements, compression system and who applies it, the 12-week review date, and the vascular referral decision. Photograph with a scale at baseline and at each review.
Remote / OOH
This assessment cannot be completed remotely: ABPI, pulses, monofilament testing and inspection of both feet (between the toes and inside the shoes) need a face-to-face review. Convert to face to face if the ulcer cannot be seen and measured; the patient has diabetes, is anticoagulated or is immunosuppressed; there is new pain under a bandage; or district nursing and timely review cannot be arranged. Under time pressure, choose the safer destination.
The four-week review is a useful prognostic point: wounds without clear progress in the first month are unlikely to heal on the current plan, and this is the moment to re-examine the diagnosis rather than to continue for another six months of dressings. Persistent or increasing pain under compression must always be treated as a warning rather than as expected discomfort — it is the presentation of pressure damage from bandaging on an under-recognised ischaemic limb, and the correct action is to remove the bandage and reassess the same day. Repeating the ABPI when the clinical picture changes matters because peripheral arterial disease progresses, and a leg that was safe to compress a year ago may no longer be. Finally, the 12-week review should be booked at the first appointment: the reason Marjolin's ulcers are diagnosed late is almost never a failure of knowledge, but the absence of a scheduled point at which someone steps back and asks why the wound is still there.
Educational use only. Pathway based on: NICE CG168 (Varicose veins in the legs, 2013), NICE NG19 (Diabetic foot problems, updated 2019), NICE NG12 (Suspected cancer: recognition and referral, updated April 2026), NICE NG152 (Leg ulcer infection: antimicrobial prescribing), NICE NG141 (Cellulitis antimicrobial prescribing), SIGN 120 (Chronic venous leg ulcers), National Wound Care Strategy Programme lower limb recommendations (2025), NICE HTG677 (ABPI measurement devices), NICE NG249 (Falls), and local tissue-viability, vascular and diabetic-foot pathways, which take precedence. Always adapt to individual patient context.