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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Venous, arterial, neuropathic and malignant ulcers

Dermatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Threatened limb, spreading infection or haemorrhage

Sudden severe pain, pallor, pulselessness, paraesthesia, paralysis or coldness indicates acute limb ischaemia; rapidly spreading infection, crepitus, systemic toxicity, wet gangrene, uncontrolled tumour bleeding or a hot swollen diabetic foot can destroy tissue or life quickly.

Action: Arrange immediate vascular, surgical or diabetic-foot admission as appropriate, keep an ischaemic limb dependent and uncompressed, begin sepsis and antimicrobial care when indicated, and control bleeding with non-adherent pressure while urgent cancer or interventional support is mobilised.

Overview

Classify a chronic ulcer by perfusion, venous pressure, sensation and malignant features, choose stepwise vascular and tissue investigations, and route compression, revascularisation, offloading, infection or cancer care safely.

A chronic ulcer is an endpoint shared by venous hypertension, inadequate arterial inflow, loss of protective sensation, pressure, inflammation, infection and neoplasia. Mixed mechanisms are common: a patient can have venous oedema and peripheral arterial disease, or neuropathy plus ischaemia and infection. Begin with pain at rest and on walking, swelling, previous thrombosis or varicose treatment, diabetes and kidney disease, smoking, footwear, trauma, immune disease and duration. Remove dressings gently, clean enough to see the base, and examine both limbs from groin to toes.

Morphology helps but does not grant treatment permission. A broad shallow medial-gaiter wound with stasis change supports venous disease; a neat distal punched-out defect and dependent rest pain supports arterial disease; a plantar callus crater with absent monofilament sensation supports neuropathic pressure. Yet palpable pulses do not

Practice

Two practice questions

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DermatologyOriginal SBA

Gaiter ulcer with poor inflow

A patient has a shallow medial-gaiter ulcer with oedema and haemosiderin, but also nocturnal forefoot pain, cool toes and an ABPI of 0.45. What is the safest next step?

Choose one answer, then submit
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Sources and review status6 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

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.

  • NICE CG147 peripheral arterial diseasePAD recognition, Doppler assessment, diabetic limitations, vascular referral and risk treatment.
  • NICE NG19 diabetic foot problemsUrgency, multidisciplinary foot care, infection, offloading, Charcot and osteomyelitis pathways.
  • NICE NG152 leg ulcer infectionClinical infection criteria, antibiotic choices, review timing and microbiology.
  • NICE CG168 varicose veinsVenous-ulcer referral, duplex and intervention for superficial reflux.
  • NICE NG12 suspected cancer referralUrgent specialist assessment and biopsy context for suspicious skin malignancy.
  • NHS leg ulcerAccessible venous-ulcer assessment, compression, healing and recurrence prevention.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draft
rule out diabetic PAD and an ulcer can become infected whatever its origin. Measure dimensions, depth, undermining, exudate, exposed tendon or bone, surrounding heat and oedema and the condition of the opposite foot. Photograph with consent and a scale.

Cancer enters whenever behaviour is discordant. Squamous carcinoma can arise within a longstanding scar, burn or ulcer, while primary skin cancer and metastatic or haematological disease may ulcerate de novo. Induration, everted edge, exuberant granulation, contact bleeding, focal pain, nodal enlargement or failure of an evidence-based wound plan warrants representative biopsy. Infection and malignancy can coexist, so a positive swab must not close the diagnostic pathway.

Key points

  • Most leg ulcers are not diagnosed from the wound bed alone: location, edge, surrounding skin, pulses, capillary refill, oedema, sensation, footwear and walking history define mechanism.
  • Venous ulcers are usually shallow, irregular and exudative in the gaiter area with oedema, varicosities, haemosiderin, eczema or lipodermatosclerosis.
  • Arterial ulcers favour toes, heel or lateral malleolus and are punched out, painful and cool with weak pulses, delayed refill, dependent rubor or gangrene.
  • Neuropathic ulcers occur at repetitive pressure points beneath callus and may be painless despite depth; a warm pulseless or pulse-present diabetic foot can still have infection, ischaemia or Charcot disease.
  • Malignant ulceration is suggested by an enlarging indurated, rolled or everted edge, exuberant tissue, unexpected bleeding, pain, odour or failure to improve after the presumed cause is treated.
  • First-line vascular testing is pulse examination plus Doppler pressure assessment; ABPI can be falsely high in diabetes or CKD, so toe pressure, waveforms or vascular imaging may be required.
  • First-line venous-ulcer treatment is therapeutic compression only after arterial sufficiency is established; significant ischaemia needs vascular review rather than stronger bandaging.
  • First-line neuropathic management is pressure removal with multidisciplinary diabetic-foot assessment, not repeated dressings while the patient continues loading the same site.
  • Biopsy a suspicious viable edge and base with enough depth and communicate anticoagulation, vascular status and tumour concern; never repeatedly cauterise unexplained granulation.

Aetiology

01

Venous hypertension

Valve reflux, obstruction and calf-pump failure maintain high ambulatory venous pressure, driving oedema, inflammation, skin fibrosis and eventual gaiter breakdown.

02

Arterial inflow failure

Atherosclerotic narrowing, embolism or small-vessel disease reduces oxygen delivery, particularly at distal pressure sites, and impairs every phase of repair.

03

Neuropathy and mechanical load

Loss of protective pain, motor deformity and dry fissured skin permit repetitive plantar stress to build callus, haemorrhage and a deep crater.

04

Neoplastic tissue destruction

Primary skin cancer, metastatic or haematological disease and malignant transformation within chronic scars can outgrow blood supply and ulcerate.

Pathophysiology

  1. 1
    Venous fluid escapes

    Sustained capillary pressure leaks fluid, proteins and erythrocytes into tissue, causing oedema, haemosiderin, leukocyte activation and lipodermatosclerosis.

  2. 2
    Ischaemia starves repair

    Low macrovascular and microvascular flow limits oxygen, immune-cell delivery, collagen synthesis and epithelial migration and increases necrosis after trauma or compression.

  3. 3
    Unfelt pressure repeats injury

    Neuropathy removes protective feedback, so every step reloads a callused bony prominence and drives damage from surface haemorrhage towards deep tissue and bone.

  4. 4
    Tumour replaces normal tissue

    Invasive malignant cells disrupt epidermis, dermis, vessels and lymphatics, creating indurated growth, friability, bleeding, necrosis and a non-healing edge.

  5. 5
    Biofilm complicates all mechanisms

    Microbial communities colonise chronic surfaces and can delay repair, but invasive infection occurs only when organisms provoke surrounding tissue or systemic response.

Clinical features and red flags

Venous gaiter ulcer

A shallow irregular moist wound near the medial lower leg sits among oedema, visible veins, brown haemosiderin, eczema and indurated lipodermatosclerosis.

Arterial distal ulcerRed flag

A sharply punched-out toe, heel or malleolar defect with cool shiny skin, delayed refill, weak pulses and rest pain indicates poor inflow.

Neuropathic pressure crater

A plantar or bony-prominence ulcer beneath callus may be unexpectedly painless, with lost monofilament sensation and deformity driving repetitive load.

Infected diabetic footRed flag

New warmth, swelling, pain despite neuropathy, purulence, spreading erythema, systemic illness or metabolic deterioration suggests infection and may mask deep bone involvement.

Malignant edge

Firm everted or rolled tissue, irregular fungation, spontaneous bleeding and expansion despite appropriate care makes neoplasia a biopsy priority.

Mixed ulcer clues

Gaiter oedema and pigmentation can coexist with weak pulses, nocturnal rest pain or low toe pressure, preventing full-strength routine compression.

Inflammatory discordance

Violaceous undermining, pathergy, palpable purpura or retiform necrosis suggests pyoderma, vasculitis or occlusion rather than a purely haemodynamic ulcer.

Red flags requiring action

  • Rest pain, tissue coldness, absent pulses, gangrene, rapidly spreading erythema, systemic illness, crepitus, exposed bone, suspected Charcot change, major bleeding, everted induration, exuberant growth or a changing scar ulcer requires expedited specialist assessment.

Investigations

  1. 01
    Complete limb and wound assessmentFirst step
    Why
    Classify urgency, mechanism and baseline healing trajectory.
    Interpretation and limitations
    Record pulses, refill, temperature, oedema, skin change, sensation, deformity, footwear, wound site, edge, base, dimensions, depth, exudate and nodes; compare the opposite limb.
  2. 02
    Handheld Doppler and ABPI
    Why
    Estimate arterial supply before compression and identify peripheral arterial disease.
    Interpretation and limitations
    A reduced ratio supports PAD, but a normal or high value can be falsely reassuring with calcified incompressible vessels in diabetes or CKD; waveform quality and symptoms remain important.
  3. 03
    Toe pressure, TBI and vascular imaging
    Why
    Clarify perfusion when ABPI is unreliable or tissue threat is present and plan revascularisation.
    Interpretation and limitations
    Toe vessels are often less calcified; low pressure or abnormal waveforms support impaired healing, while duplex, CT or MR angiography maps anatomy for vascular intervention.
  4. 04
    Venous duplex ultrasound
    Why
    Confirm superficial or deep reflux and obstruction and identify treatable venous hypertension.
    Interpretation and limitations
    Duplex guides ablation or other intervention; reflux does not remove the need to assess arterial inflow, oedema causes and compression tolerance.
  5. 05
    Neuropathy and diabetic-foot assessment
    Why
    Demonstrate loss of protective sensation, deformity, pressure and acute Charcot or infection risk.
    Interpretation and limitations
    Use 10-g monofilament with another modality, inspect footwear and callus and assess temperature asymmetry; neuropathy cannot explain an absent pulse or systemic illness.
  6. 06
    Infection and osteomyelitis tests
    Why
    Distinguish colonisation from tissue infection and define deep extension.
    Interpretation and limitations
    Culture a cleaned deep specimen when worsening or not improving; probe-to-bone, plain radiograph and MRI inform osteomyelitis, but negative early imaging does not overrule a high-risk diabetic foot.
  7. 07
    Representative ulcer biopsy
    Why
    Diagnose malignancy, vasculitis, neutrophilic disease, atypical infection or another non-healing process.
    Interpretation and limitations
    Sample viable edge and involved base deeply enough and consider multiple sites in a heterogeneous lesion; alert pathology to scar, cancer, organisms and pathergy concern.
  8. 08
    Systemic healing screen
    Why
    Identify anaemia, diabetes, renal disease, malnutrition and inflammatory or clonal contributors.
    Interpretation and limitations
    Use FBC, HbA1c, renal and liver profiles, CRP and nutrition assessment selectively; correcting a laboratory value cannot substitute for perfusion and pressure correction.

Differential diagnosis

01

Pyoderma gangrenosum

Extreme pain, rapid pathergic expansion and an undermined violaceous border contrasts with stable haemodynamic wounds and can worsen after sharp debridement.

02

Vasculitis or occlusion

Palpable purpura, livedo, angular infarction and systemic renal or neurological signs indicate inflammatory or thrombotic vascular injury requiring tissue and systemic tests.

03

Pressure injury

Ulceration over a bony prominence after immobility or device pressure follows load and shear rather than primary venous, arterial or tumour behaviour.

04

Atypical infection

Deep fungal, mycobacterial, leishmanial and ecthyma lesions require exposure history and tissue culture when ordinary wound treatment repeatedly fails.

05

Factitial or traumatic ulcer

Geometric accessible lesions, inconsistent evolution or repeated injury needs compassionate safeguarding and psychological assessment while organic disease is still excluded.

Management

01First classification sequenceCheck blood flow before choosing a dressing pathwayFirst stepAny lower-limb or foot ulcer is newly assessed or has stopped healing.+
  1. 1Identify acute ischaemia, wet gangrene, sepsis, hot swollen diabetic foot and uncontrolled bleeding first and activate the corresponding emergency route.
  2. 2Examine pulses, refill, temperature, oedema, venous change, sensation and deformity and document a cleaned wound's site, edge, base and depth.
  3. 3Obtain Doppler waveforms and pressure assessment, using toe tests or vascular imaging when ABPI is unreliable or symptoms and the number disagree.
02First-line venous routeCompress only an adequately perfused limbFirst lineGaiter ulceration and venous hypertension predominate without limb-threatening arterial disease.+
  1. 1Use a trained clinician to apply evidence-based therapeutic compression after arterial assessment, matching system and strength to perfusion, limb shape, exudate, dexterity and tolerance.
  2. 2Treat venous eczema with emollient and a short site-appropriate topical corticosteroid and use a simple non-adherent absorbent dressing rather than an expensive product without a specific purpose.
  3. 3Refer for venous duplex and treatment of superficial reflux and address mobility, calf pump, weight and recurrence prevention with long-term compression after healing.
03Arterial and mixed routeRestore inflow before aggressive wound treatmentRest pain, distal necrosis, low pressures or mixed venous and arterial features are present.+
  1. 1Refer urgently for threatened tissue and promptly for chronic limb-threatening ischaemia, provide analgesia and protect the foot from pressure, cold and trauma.
  2. 2Avoid high compression and extensive debridement until vascular specialists define safe inflow and whether endovascular or surgical revascularisation is possible.
  3. 3Coordinate smoking cessation, lipid and antiplatelet treatment, diabetes and blood-pressure care through the PAD pathway while continuing cautious wound protection.
04First-line neuropathic routeRemove the force that created the craterFirst lineLoss of protective sensation and plantar or deformity-related loading dominates.+
  1. 1Arrange multidisciplinary diabetic-foot care, offload using the safest effective device and address callus, footwear and gait through trained podiatry rather than patient self-paring.
  2. 2EscalationAssess perfusion and infection at every visit and escalate a hot swollen foot for Charcot immobilisation and imaging even when the ulcer itself is small.
  3. 3Use glucose and renal management to support healing but measure success by pressure reduction, wound closure and prevention on both feet.
05Malignancy routeBiopsy behaviour that defies the labelThe edge is indurated, everted, rolled, fungating or bleeding, or the ulcer fails a correctly delivered plan.+
  1. 1Examine regional nodes and the whole skin, document growth and bleeding and arrange urgent dermatology or cancer-pathway review without waiting for repeated swab courses.
  2. 2Take representative deep edge and base tissue, using multiple samples for a large heterogeneous or scar-associated lesion and coordinating haemostasis and anticoagulants.
  3. 3After diagnosis, combine oncological surgery, radiotherapy or systemic treatment with exudate, odour, pain, bleeding and psychosocial support when cure is not immediately possible.
06Clinical infection routeTreat spreading tissue infection, not colonisationRedness or swelling extends beyond the ulcer, local warmth and pain increase or fever and systemic illness develop.+
  1. 1Assess sepsis and deep infection, clean the wound and start guideline-directed antibiotic promptly when clinical infection is present, using admission and intravenous therapy for severe disease.
  2. 2Review within two to three days and send a cleaned deep sample if worsening, severe or not improving, then narrow or change treatment using microbiology and clinical response.
  3. 3Reopen perfusion, osteomyelitis, abscess, malignancy and inflammatory-ulcer assessment when antibiotics do not produce the expected trajectory.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
NICE first-choice oral therapy for likely staphylococcal or streptococcal infection around a leg ulcer, not for an uninfected colonised wound.

Flucloxacillin for infected leg ulcer

Take 500 mg to 1 g by mouth four times daily for 7 days when a leg ulcer has clinical bacterial infection and oral treatment is appropriate, following local antimicrobial guidance.

Check immediate and severe delayed penicillin allergy, liver disease, renal function and interactions and provide an alternative through the guideline when unsuitable. Review at two to three days; admit for sepsis, rapidly spreading disease or inability to take oral therapy.

Complications

01

Cellulitis and sepsis

Loss of barrier permits invasive infection, abscess, lymphangitis, bacteraemia and systemic collapse, especially with diabetes, ischaemia or immune compromise.

02

Osteomyelitis

Deep plantar, heel or malleolar wounds can seed adjacent bone, prolonging infection and increasing surgical and amputation risk.

03

Limb loss

Critical ischaemia, infected gangrene and uncontrolled diabetic-foot disease can progress to minor or major amputation and permanent mobility loss.

04

Cancer progression

Delayed biopsy allows local invasion, nodal or distant spread, bleeding, malodour and a larger reconstructive or palliative burden.

05

Recurrence and disability

Persistent venous pressure, neuropathic load or vascular risk causes repeated breakdown, pain, exudate, sleep loss, social isolation and reduced employment.

Monitoring and follow-up

  • Measure maximum length, perpendicular width, depth, undermining, exudate, edge and tissue type at a consistent interval and use photographs with consent.
  • Recheck pulses, Doppler findings and pain whenever a wound deteriorates or compression becomes painful; perfusion can change during a prolonged episode.
  • For compression, review slippage, pressure injury, toe colour, sensation, adherence and the patient's ability to apply and remove the selected system.
  • For a neuropathic foot, inspect both feet, footwear and offloading use frequently and act on new warmth, swelling, callus blood staining or metabolic deterioration.
  • During infection treatment reassess within two to three days and seek urgent care for fever, spreading erythema, confusion, hypotension, crepitus or wet gangrene.
  • If area does not reduce under a correctly delivered mechanism-specific plan, repeat the diagnosis, perfusion, pressure and malignancy assessment rather than merely changing dressings.
  • After healing, maintain prevention and rapid review of recurrence.

Special situations

Pulses do not end testing

Calcified diabetic or renal vessels and collateral flow can create palpable pulses or a misleading ABPI despite clinically important impaired tissue perfusion.

Callus records pressure

A rim of hyperkeratosis around a plantar crater identifies repeated mechanical load, and healing is unlikely until that force is redistributed.

Venous pigment is history

Haemosiderin and lipodermatosclerosis support long-standing venous hypertension but can coexist with new arterial disease or an unrelated malignant ulcer.

Swabs sample the ecosystem

Chronic wounds contain organisms routinely; clinical tissue inflammation and trajectory determine infection, while a cleaned deep specimen helps when treatment fails.

Cancer can colonise

A malignant ulcer may grow bacteria and smell, so temporary response to antibiotics cannot explain persistent induration, bleeding or exuberant tissue.

Common pitfalls

  1. 01

    Applying strong compression from visual venous features without Doppler and arterial assessment.

  2. 02

    Using a normal ABPI to dismiss symptomatic PAD in diabetes or CKD with incompressible calcified arteries.

  3. 03

    Treating a painless neuropathic ulcer as low risk while pressure, infection or osteomyelitis continues beneath callus.

  4. 04

    Prescribing antibiotics for every positive wound swab or malodour without clinical tissue infection.

  5. 05

    Repeatedly changing dressings while failing to correct venous pressure, arterial inflow or plantar load.

  6. 06

    Curetting exuberant tissue without biopsy when an ulcer has become indurated, everted or unexpectedly haemorrhagic.

  7. 07

    Aggressively debriding an ischaemic or pathergic ulcer before mechanism and perfusion are understood.

Clinical stateAwaiting review
JurisdictionUnited Kingdom