Venous vs arterial vs neurogenic (neuropathic) ulcers

Venous ulcer

• Diagnosis: Duplex ultrasound maps reflux and obstruction. Check the ABI before compression, because 15-30% of "venous" ulcers have coexisting arterial disease.
• Treatment: Multilayer graduated compression (4-layer, about 40 mmHg at the ankle) is the mainstay once arterial disease is excluded. Treat superficial reflux with endovenous ablation, which reduces recurrence. Add leg elevation and exercise.

Arterial ulcer

• Presentation: A red, painful plaque breaks down into a painful ulcer with surrounding purpuric erythema. Granulation is minimal and there is often little infection. A dry, inactive eschar may form (Andrews').
• Signs of arterial cause:
  • skin thinning and hair loss
  • reduced or absent pulses
  • pallor on elevation
  • a cool limb
  • dependent rubor
  • claudication
  • night pain relieved by hanging the foot down
• Cholesterol emboli: Suspect these if there is sudden onset, eosinophilia, renal insufficiency and palpable pulses.
• ABI: Below 0.75 indicates arterial insufficiency and below 0.5 indicates severe insufficiency (Andrews'). Falsely high values occur in calcified vessels, as in diabetes or renal failure, so use toe pressures or TcPO2 there.
• Treatment:
  • Revascularisation (endovascular or bypass) is the key step.
  • Do not apply compression to a limb with significant arterial disease.
  • Control risk factors and stop smoking.
  • Protect the area from injury and cold.
  • An ischaemic ulcer marks a limb at increased risk of loss.

Neuropathic ulcer

• Mechanism: Loss of protective sensation, with motor neuropathy causing deformity and high focal pressure. Autonomic neuropathy causes dry, fissured skin. The foot is warm with bounding pulses (Schwartz's).
• Treatment: Offloading is the primary principle (Andrews'). Total contact cast or removable walker are options, and shoes or padded boots can offload different areas.
  • Debride necrotic tissue back to bleeding viable tissue. This is usually painless because the foot is insensate.
  • Treat clinical infection, but colonisation alone usually does not need treatment.
  • Osteomyelitis is best treated by removing the infected bone.
  • After healing, use appropriately fitting depth and width shoes, inspect the feet regularly for hot spots, and debride dystrophic nails to prevent recurrence.
• Neuroischaemic foot: Diabetic feet often have both neuropathy and PAD. Always check perfusion.

Practical points

1. Check pulses and the ABI in every leg ulcer, and add duplex if venous disease is suspected.
2. Painless plantar ulcer with callus and good pulses points to neuropathic. Painful toe or ankle ulcer with absent pulses points to arterial. Gaiter-area ulcer with pigmentation and varicosities points to venous.
3. Biopsy any non-healing or atypical ulcer to exclude malignancy such as squamous cell carcinoma (Marjolin ulcer). Also consider vasculitis and pyoderma gangrenosum.

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History taking: digital pitting in Raynaud's

• characterise the Raynaud's
• characterise the pitting and any ulcers
• look for an underlying connective tissue disease (CTD) or other cause

1. Presenting complaint and Raynaud's characterisation

• Did the fingers go white, then blue, then red? Raynaud's is clinically a triphasic attack: painful pallor or ischaemia, then cyanosis in some, then reactive hyperaemia on rewarming (Fitzpatrick's Dermatology, p. 1119).
• Is the change sharply demarcated? Which digits are involved? Does it spare the thumbs?
• Pallor alone, or colour change in the toes, ears, nose or lips, also matters.

• Are attacks provoked by cold or by emotional stress?
• What is the frequency, duration and severity of attacks? Do they happen in summer?
• When did the first attack occur?

• Primary Raynaud's typically starts before age 30.
• Onset after age 30-40, rapid worsening, or attacks that are asymmetric, severe or painful point to a secondary cause.

• Is there pain between attacks or at rest?
• Have you had fingertip ulcers, sores or gangrene?
• Any digital pulp loss or tightening?

2. The pitting and digital ulcers

• When and where: When was the pitting first noticed? Which fingers? Is it on the fingertip pulp only, or also over the extensor surfaces of the joints? Extensor ulcers over contractures are typical of diffuse SSc (Rheumatology, 2022).
• Ulcer history: Have there been ulcers before the pitting, and how many in total? How long did they take to heal? Have any recurred or become chronic? Chronic or recurrent DU carry the greatest risk and burden (Rheumatology, 2022).
• Complications:
  • infection, discharge or antibiotic courses
  • bone infection or hospital admission
  • gangrene, autoamputation or surgery
  • sudden severe persistent ischaemia with abrupt onset, which is a medical emergency (Rheumatology, 2022)
• Pain and function: How severe is the pain? Is there trouble with grip, buttons, writing or work?
• Trauma: Was there any injury or pressure at the site?

3. Screening for an underlying CTD (systems review)

• Puffy fingers or tight, thick skin? Where does the tightness extend (fingers only, forearm, face, trunk)? Have rings stopped fitting?
• Calcium lumps (calcinosis) or small red spots (telangiectasia)?
• Mouth tightness or reduced mouth opening?
• Rash, photosensitivity or hair loss (lupus)? Heliotrope or Gottron-type rash (dermatomyositis)?

• Joint pain or swelling, morning stiffness, proximal muscle weakness (overlap or mixed CTD)?

• Heartburn, dysphagia, early satiety, bloating, constipation or diarrhoea?

• Breathlessness, dry cough, exertional symptoms or syncope, which suggest interstitial lung disease or pulmonary hypertension?
• Chest pain, palpitations or oedema?

• New severe headache, visual change or hypertension, which may signal scleroderma renal crisis?

• Dry eyes or dry mouth?
• Recurrent oral or nasal ulcers? Pleuritic pain?

4. Other causes of Raynaud's and digital ischaemia

• Beta-blockers
• Ergotamine and triptans
• Stimulants (ADHD medication, amphetamines, cocaine)
• Chemotherapy (bleomycin, cisplatin)
• Interferon
• Nicotine

• Vibrating tools (vibration white finger)
• Vinyl chloride
• Repetitive hand trauma (hypothenar hammer syndrome)
• Cold exposure

• Cervical rib or thoracic outlet symptoms
• Atrial fibrillation
• Antiphospholipid syndrome (clots, miscarriages)
• Cryoglobulins or cold agglutinins (cold-induced purpura, hepatitis C)
• Malignancy
• Paraproteinaemia

• Heavy smoking with a young male patient points to Buerger disease. Arterial causes of digital ulceration are suggested by arm claudication, rest pain and tissue loss (Current Surgical Therapy 14e).

5. Other history

• Past medical history: Atherosclerotic risk factors, diabetes and previous vascular disease.
• Family history: CTD, Raynaud's, thyroid disease.
• Smoking: This worsens vasospasm and impairs ulcer healing, so ask about it directly.
• Medicines: Include over-the-counter products. Ask about any vasodilators or antiplatelets already used and whether they worked.
• Pregnancy plans: Relevant for drug choice, particularly endothelin antagonists, which are contraindicated in pregnancy.
• Social: Occupation, hobbies and impact on daily life.

Red flags to escalate

• Abrupt, severe, persistent ischaemia with threatened tissue (critical digital ischaemia)
• Signs of infection (spreading erythema, discharge, fever)
• New breathlessness or hypertension with headache
• Rapidly progressive skin tightening

Likely next steps

• Examination of hands, skin, nailfolds, pulses and blood pressure
• Nailfold capillaroscopy
• ANA with ENA panel, including centromere, Scl-70 and RNAP III antibodies
• Baseline FBC, renal function and urine dipstick
• Echocardiogram and lung function tests as directed by symptoms

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