Differential Diagnosis of Erosions and Ulcers

Introduction

Erosions and ulcers represent loss of skin integrity. An erosion is a superficial loss affecting only the epidermis (heals without scarring), while an ulcer extends into the dermis or deeper (heals with scarring). The approach to ulcers requires assessment of location, appearance (edge, base, depth), associated symptoms, and underlying systemic disease.

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41.1 Lower Leg Ulcers: Major Categories

Lower limb ulcers are the most common ulcer type in dermatology. The etiology determines treatment.

41.1.1 Venous Ulcers (Stasis Ulcers) - Most Common (~70%)

• Pathogenesis: Chronic venous insufficiency → Venous hypertension → Capillary leak → Fibrin cuff deposition → Tissue hypoxia → Ulceration.
• Location: Medial malleolus ("gaiter area"). Rarely lateral.
• Appearance:
  • Shallow, irregular borders.
  • Granulating base (red, moist).
  • Surrounding skin: Lipodermatosclerosis (induration, hyperpigmentation from hemosiderin, "inverted champagne bottle" leg), Varicose eczema, Edema.
• Symptoms: Dull aching, worse with standing, relieved by elevation.
• Management: Compression therapy (mainstay), Wound care, Treat infection, Venous surgery if indicated.

41.1.2 Arterial Ulcers (~10%)

• Pathogenesis: Peripheral arterial disease → Tissue ischemia → Necrosis.
• Location: Distal locations: Toes, dorsum of foot, heel, lateral malleolus.
• Appearance:
  • "Punched-out" with well-defined borders.
  • Pale or necrotic base (yellow slough or black eschar).
  • Surrounding skin: Shiny, atrophic, hairless, cool. Pale on elevation, dependent rubor.
• Symptoms: Severe pain, especially at night or when legs elevated. Claudication history.
• Examination: Absent or weak pedal pulses. ABI (Ankle-Brachial Index) < 0.9 confirms PAD.
• Management: Vascular surgery referral (revascularization). NO compression (worsens ischemia). Risk factor modification.

41.1.3 Neuropathic Ulcers (Diabetic Foot Ulcers)

• Pathogenesis: Peripheral neuropathy → Loss of protective sensation → Unnoticed trauma → Ulceration. Often combined with arterial disease.
• Location: Pressure points: Plantar surface (under metatarsal heads), Heel, Tips of toes.
• Appearance:
  • Surrounded by callus (hyperkeratosis).
  • Deep, may extend to bone (osteomyelitis risk).
  • Base may appear healthy or sloughy.
• Symptoms: Painless (due to neuropathy). Patient may be unaware.
• Examination: Reduced sensation (monofilament test), Absent ankle reflexes, Charcot foot deformity.
• Management: Offloading (pressure relief), Debridement, Wound care, Glucose control, Vascular assessment.

41.1.4 Mixed Arteriovenous Ulcers

• Combination of venous and arterial insufficiency.
• Require careful assessment before compression (reduced ABI indicates arterial component).

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41.2 Non-Healing Ulcers: Think Malignancy

[!CAUTION] Any chronic ulcer that fails to heal after 3 months of appropriate treatment warrants biopsy to exclude malignancy.

Marjolin's Ulcer

• Definition: Squamous cell carcinoma (SCC) arising in chronic wounds, scars, or ulcers.
• Risk Sites: Burn scars, Chronic venous ulcers, Osteomyelitis sinuses.
• Features: Raised, everted edges. Increased pain. Change in appearance.

Primary Cutaneous Malignancy

• SCC: Indurated, everted edges.
• BCC: Rolled, pearly edges with central ulceration ("rodent ulcer").
• Melanoma (Amelanotic): May present as non-pigmented ulcer.

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41.3 Inflammatory and Autoimmune Ulcers

41.3.1 Pyoderma Gangrenosum (PG)

[!IMPORTANT] Diagnosis of Exclusion

• Pathogenesis: Neutrophilic dermatosis. NOT infection.
• Clinical Features:
  • Starts as pustule or inflammatory nodule → rapidly expands → Irregularly shaped ulcer with violaceous, undermined borders.
  • Pathergy: Worsens with trauma (avoid debridement).
  • Cribriform scarring on healing.
• Associations: Inflammatory bowel disease (Crohn's, UC), Rheumatoid arthritis, Hematologic malignancy, PAPA syndrome.
• Diagnosis: Clinical. Biopsy shows neutrophilic infiltrate (non-specific). Must exclude infection.
• Treatment: Immunosuppression (steroids, Cyclosporine, Infliximab). Wound care. Avoid aggressive surgical debridement.

41.3.2 Vasculitic Ulcers

• Cause: Small or medium vessel vasculitis (Leukocytoclastic vasculitis, PAN, Rheumatoid vasculitis, SLE).
• Features: Palpable purpura preceding ulcer. Multiple, "punched-out" ulcers. Often on lower legs.
• Diagnosis: Biopsy (vasculitis histology), Autoimmune workup.

41.3.3 Calciphylaxis (Covered in Ch. 21)

• ESRD patients. Livedo + Painful necrotic ulcers. High mortality.

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41.4 Infectious Ulcers

41.4.1 Tropical Ulcers

• Buruli Ulcer: Mycobacterium ulcerans. Undermined edges, painless. West Africa, Australia.
• Cutaneous Leishmaniasis: Papule → nodule → ulcer with raised borders. Travel history.
• Tropical Phagedenic Ulcer: Polymicrobial. Painful, rapidly progressive.

41.4.2 Mycobacterial Infections

• Tuberculosis (Lupus Vulgaris, Scrofuloderma).
• Atypical Mycobacteria: M. marinum (aquarium exposure), M. fortuitum (post-procedure).

41.4.3 Ecthyma

• Deep form of impetigo. S. aureus or GAS.
• Punched-out ulcer with adherent crust.

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41.5 Drug-Induced and Factitial Ulcers

Drug-Induced

• Hydroxyurea: Leg ulcers, especially around ankles. Important cause.
• Methotrexate, Nicorandil.

Factitial (Self-Inflicted)

• Clues: Geometric shapes, Locations accessible to patient, Inconsistent history.
• Requires psychiatric evaluation.

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41.6 Diagnostic Algorithm

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41.7 Summary Comparison Table

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41.8 Clinical Pearls

1. Medial malleolus ulcer + Hemosiderin staining + Varicose veins → Venous ulcer. Compression is key.
2. Distal ulcer + Absent pulses + Severe pain → Arterial ulcer. NO compression. Revascularize.
3. Plantar ulcer + Callus + Diabetes → Neuropathic. Offload pressure points.
4. Violaceous undermined edges + Pathergy → Pyoderma Gangrenosum. Don't debride aggressively. Immunosuppress.
5. Chronic non-healing ulcer >3 months → Biopsy to exclude SCC (Marjolin's ulcer).
6. Hydroxyurea: Important cause of leg ulcers. Check drug history.