Venous and arterial leg ulcers

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

Key points

Venous ulcers are usually shallow, exudative and irregular in the gaiter region with oedema, pigmentation or eczema; arterial ulcers are often distal, punched out, painful and associated with a cool pulseless foot.
Assess both arterial perfusion and venous disease: ulcer appearance alone is not reliable, and mixed aetiology is common.
Measure Doppler ABPI before strong compression; in diabetes/CKD, add toe pressure or waveform assessment when vessels are calcified or ABPI is high/unreliable.
ABPI 0.8–1.3 generally permits full/strong venous compression; ABPI 0.5–0.79 needs reduced compression under specialist oversight; below 0.5 needs urgent vascular assessment and no routine compression.
For a venous ulcer with adequate arterial inflow, strong compression delivering about 40 mmHg at the ankle is the core healing treatment, applied by a trained clinician.
Arterial ulceration needs urgent vascular referral and revascularisation assessment; dressings and analgesia cannot restore perfusion.
Most leg ulcers are colonised: give antibiotics only for clinical infection such as spreading redness/swelling beyond the ulcer, local warmth, increasing pain or fever.
Refer a venous leg ulcer not healed within 2 weeks, and a healed venous ulcer, to a vascular service for duplex and treatment of superficial reflux.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Chronic venous hypertension

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.

Peripheral arterial disease

Atherosclerotic narrowing reduces distal perfusion. Smoking, diabetes, hypertension, dyslipidaemia and kidney disease increase arterial risk and impair the tissue reserve needed for wound healing.

Neuropathy and pressure

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.

Inflammatory or malignant 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.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Venous pressure transmission
Venous valve failure or obstruction impairs the normal pressure reduction during walking, transmitting sustained venous hypertension into the superficial veins and dermal microcirculation.
2
Venous tissue injury
Capillary leakage and chronic inflammation cause oedema, haemosiderin deposition, eczema and fibrosis. Vulnerable gaiter skin may then break down into a shallow exudative ulcer.
3
Arterial oxygen deficit
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.
4
Ischaemic necrosis
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.
5
Failure of repair
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.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Venous ulcer

Shallow irregular ulcer in the medial/lateral gaiter area, often wet or granulating, with oedema, haemosiderin pigmentation, eczema, lipodermatosclerosis and varicosities.

Arterial ulcerRed flag

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.

Mixed arterial–venous ulcer

Venous skin changes plus reduced perfusion; strong compression may be unsafe and requires vascular/tissue-viability planning.

Neuropathic/diabetic foot ulcerRed flag

Pressure-site callus, altered sensation and deformity; infection and ischaemia may be painless and require the NICE diabetic-foot pathway.

Clinical infectionRed flag

Spreading erythema/swelling beyond the ulcer, warmth, increased pain, purulent discharge or fever; wet gangrene, systemic illness or deep infection is an emergency.

Atypical ulcer

Raised/everted edge, violaceous undermining, livedo/purpura, rapid progression or non-healing despite correct care suggests malignancy, vasculitis, pyoderma gangrenosum or another diagnosis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Hand-held Doppler ABPIFirst step
Why
Measure arterial perfusion before therapeutic compression and support PAD diagnosis.
Interpretation and limitations
0.8–1.3 usually supports full compression; 0.5–0.79 indicates mixed disease requiring reduced/specialist compression; <0.5 suggests severe ischaemia and urgent vascular assessment; >1.3 may be incompressible.
02
Toe pressure/toe-brachial index and Doppler waveforms
Why
Clarify perfusion when ABPI is high, inconsistent or unreliable, especially in diabetes/CKD.
Interpretation and limitations
Low toe pressure or monophasic waveforms supports arterial compromise; use with clinical assessment and healing potential rather than an isolated cutoff.
03
Venous duplex ultrasound
Why
Identify superficial/deep reflux or obstruction and plan reflux treatment.
Interpretation and limitations
A qualifying active or healed venous ulcer should enter a vascular pathway even while compression and wound care continue.
04
Wound assessment and serial measurement
Why
Establish location, dimensions, depth, tissue, exudate, edge, surrounding skin and healing trajectory.
Interpretation and limitations
A meaningful reduction over 4 weeks supports the plan; stalled or worsening healing triggers reassessment of cause, compression, perfusion, pressure, infection and adherence.
05
Microbiology only when infection is worsening or not improving
Why
Guide antibiotics after initial empirical treatment fails.
Interpretation and limitations
Do not swab routinely at first presentation; if needed, clean the ulcer then sample because surface colonisers otherwise mislead.
06
Biopsy/targeted blood tests for atypical disease
Why
Investigate malignancy, vasculitis, inflammatory ulcer or nutritional/systemic modifiers.
Interpretation and limitations
Select the edge/depth and specialist pathway carefully; pathergy-prone pyoderma is a reason for dermatology advice before debridement.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Neuropathic diabetic ulcer

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.

Pressure ulcer

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.

Vasculitic ulcer

Painful ulcers accompanied by palpable purpura, livedo or systemic inflammatory features suggest vessel-wall inflammation and require targeted laboratory, dermatological and sometimes histological assessment.

Pyoderma gangrenosum

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.

Ulcerating skin malignancy

A raised, everted or irregular edge, abnormal tissue growth or failure despite correct vascular care warrants biopsy to exclude squamous or another cutaneous malignancy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01venousLikely venous ulcer with adequate perfusionFirst stepVenous phenotype and ABPI 0.8–1.3 with no acute arterial red flags.

1First: clean, choose a simple low-adherence absorbent dressing, moisturise surrounding skin and address pain/mobility.
2Next: apply strong multicomponent compression targeting about 40 mmHg at the ankle by a trained practitioner.
3Next: refer to a vascular service if unhealed at 2 weeks or previously healed, and use duplex to address superficial reflux.
4EscalationEscalation: reassess cause, compression delivery, perfusion and infection if the wound does not reduce substantially by about 4 weeks.

02mixedMixed arterial–venous ulcerVenous ulcer phenotype with ABPI 0.5–0.79 or other evidence of reduced arterial supply.

1First: prompt vascular/tissue-viability assessment and toe/waveform testing if ABPI reliability is uncertain.
2Next: use only reduced compression selected and monitored by clinicians competent in mixed disease.
3Next: assess for arterial revascularisation while continuing careful wound, oedema and risk-factor care.
4EscalationEscalation: stop compression and seek urgent review for increasing rest pain, pallor, coldness, numbness or tissue necrosis.

03arterialArterial ulcer or severe ischaemiaArterial phenotype, rest pain, gangrene, ABPI <0.5 or acute deterioration.

1First: urgent vascular referral; same-day acute assessment for wet gangrene, sepsis or acute limb-ischaemia signs.
2Next: protect from pressure/trauma, keep wounds appropriately dry/covered, provide analgesia and do not use routine strong compression.
3Next: obtain arterial imaging when revascularisation is considered and optimise antiplatelet/lipid/smoking/diabetes care.
4EscalationEscalation: coordinate drainage/debridement and antibiotics with revascularisation when infection is present.

04infectionInfected leg ulcerSpreading redness/swelling, warmth, increasing pain or fever attributable to the ulcer.

1First: assess severity, sepsis, arterial supply and risk of deep infection; refer to hospital for sepsis, necrotising infection or limb-threatening disease.
2Next: offer oral antibiotics when able to take them and severity does not require IV therapy; do not treat colonisation alone.
3Next: review if symptoms worsen at any time or do not begin to improve within 2–3 days; then clean and culture if needed.
4EscalationEscalation: seek specialist advice for resistant organisms, osteomyelitis, recurrent infection or severe vascular compromise.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

NICE first-choice oral antibiotic for a clinically infected leg ulcer.

Flucloxacillin

500 mg–1 g orally four times daily for 7 days.

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.

Alternative when flucloxacillin is unsuitable, including penicillin allergy.

Doxycycline

200 mg orally on day 1, then 100 mg once daily to complete 7 days (200 mg daily may be used for severe infection under NICE guidance).

Avoid in pregnancy; counsel on photosensitivity, oesophageal irritation and separation from antacids/iron/calcium.

Ulcer and compression-related pain control.

Paracetamol

500 mg–1 g orally every 4–6 hours as needed, maximum 4 g/24 h; lower the maximum in low body weight, frailty or liver risk.

Check combination medicines and reassess unexpectedly severe pain for ischaemia or deep infection.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cellulitis and sepsis

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.

Deep infection and osteomyelitis

Infection may track into fascia, tendon, joint or bone, particularly in deep diabetic or ischaemic wounds, substantially prolonging treatment and threatening limb viability.

Gangrene and amputation

Severe unrevascularised ischaemia can progress from ulcer necrosis to dry or infected gangrene. Tissue loss and uncontrolled infection may ultimately make limb preservation impossible.

Recurrence

A healed venous ulcer commonly recurs when reflux, oedema or calf-pump dysfunction persists, while ongoing arterial risk can produce new distal tissue loss.

Pain and immobility

Chronic wound pain and treatment burden can reduce walking, weakening the calf pump and worsening venous oedema, frailty and social isolation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure and photograph (with consent and governance) ulcer length, width, depth and tissue at consistent intervals.
Review compression pressure/fit, slippage, skin injury, pain and ability to self-manage at each change.
Repeat arterial assessment if pulses/symptoms change, healing stalls or the last ABPI is no longer clinically representative.
For infection, review within 2–3 days if not improving and immediately for systemic deterioration.
After healing, continue appropriate compression and venous reflux management to reduce recurrence; maintain arterial risk follow-up where relevant.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Compression is a prescription

It needs a cause assessment, arterial check, correct product, trained application and monitoring—not simply a bandage order.

Colonisation is expected

Bacteria on a chronic wound do not predict benefit from antibiotics without clinical infection.

High ABPI may be hazardous reassurance

An ABPI above 1.3 often reflects calcification; use toe pressures/waveforms before compression decisions.

Treat the reflux early

Compression can begin while vascular referral proceeds; superficial venous intervention addresses the cause and can reduce recurrence.

Atypical pain deserves a new diagnosis

Severe pain, rapid necrosis or an unusual border/site should trigger vascular/dermatology review rather than stronger dressings or repeated antibiotics.

11Common pitfallsFrequent interpretation and management errors.

01
Starting 40 mmHg compression before arterial assessment.
02
Calling a high ABPI normal in a diabetic patient with calcified vessels.
03
Swabbing every ulcer and treating the culture rather than clinical infection.
04
Using dressings alone for an arterial ulcer without urgent vascular referral.
05
Failing to refer an active venous ulcer after 2 weeks or a healed ulcer for venous assessment.