Erosions And Ulcers: Diagnosis, Treatment, Prevention

Some skin diseases are very prone to break down into sores. Surface sores are called

erosions

; these may start off as blisters or pustules. Full-thickness sores are

ulcers

.

What are Erosions and Ulcers?

Erosions represent partial-thickness loss of the epidermis, where the skin surface breaks down without penetrating deeper layers. They often heal without scarring as the epidermis regenerates quickly. Ulcers, in contrast, involve full-thickness skin loss, extending into the dermis or deeper, potentially exposing subcutaneous tissue, muscle, or bone, and commonly result in scarring.

These lesions arise from various dermatological conditions, trauma, infections, vascular issues, or pressure. Understanding their distinctions is crucial for accurate diagnosis and management, as erosions may evolve into ulcers if untreated.

Causes of Erosions and Ulcers

Skin erosions and ulcers stem from multiple etiologies, broadly categorized into infectious, traumatic, vascular, inflammatory, neoplastic, and other systemic causes. Infectious agents like bacteria (*Staphylococcus aureus*, *Streptococcus pyogenes*) cause superficial erosions in impetigo, progressing to deeper ulcers in ecthyma.

Vascular insufficiency leads to arterial ulcers from ischaemia due to atherosclerosis, often on lower legs and feet, presenting as punched-out lesions with pale bases. Pressure ulcers result from prolonged external pressure causing tissue ischaemia, particularly in immobile patients.

• Infectious causes: Bacterial (impetigo, ecthyma), viral (herpes simplex), fungal (candidiasis).
• Traumatic/pressure: Bedsores on bony prominences like sacrum, heels.
• Vascular: Arterial and venous insufficiency.
• Inflammatory/autoimmune: Lichen planus (erosive forms), aphthosis, pyoderma gangrenosum.
• Mucosal/genital: Vulval ulcers from STIs or aphthae.
• Neoplastic: Basal cell carcinoma, squamous cell carcinoma causing ulceration.

In the mouth, ulcers arise from trauma, infections, or aphthous stomatitis, presenting as painful erosions on oral mucosa.

Clinical Features

**Erosions** appear moist, superficial, red, and weepy, often from ruptured blisters. They lack depth and heal rapidly.

Ulcers

are deeper, with defined edges, variable bases (necrotic, sloughy, granulating), and surrounding skin changes like induration or hyperpigmentation.

Site-specific features include:

Type	Common Sites	Key Features
Pressure Ulcers	Coccyx, heels, elbows	Staged I-IV; non-blanchable erythema to full-thickness loss.
Arterial Ulcers	Lower legs, toes, feet	Punched-out, pale/gray base, minimal exudate, painful.
Vulval Ulcers	Vulva, perineum	Multiple shallow/painful or solitary deep; discharge possible.
Impetigo Erosions	Face, extremities	Honey-crusted, contagious.

Pressure ulcers use ‘BEST SHOT’ sites: Bones, Ears, Spine, Tailbone (sacrum), Shoulders/hips, Heels, Occiput, Toes. In darker skin types, stage 1 ulcers may lack visible erythema; assess warmth, firmness.

Diagnosis

Diagnosis combines history, examination, and investigations. History assesses risk factors: immobility, vascular disease, infections, medications.

Examination evaluates lesion depth, edges, base, exudate, pain, surrounding skin (varicose veins, pulses).

• Bedside tests: Ankle-brachial pressure index (ABPI) for arterial disease (<0.9 indicates insufficiency).
• Swabs/biopsy: For infection, malignancy.
• Imaging: Infrared thermography for early pressure ulcer detection (5-18 days prior).
• Serology/PCR: For STIs in genital ulcers.

Differential diagnoses include venous ulcers, diabetic foot ulcers, malignancies, vasculitis.

Treatment

Treatment targets underlying cause, wound bed preparation (TIME: Tissue debridement, Infection control, Moisture balance, Edge advancement).

• Pressure ulcers: Repositioning, pressure-relieving devices, nutrition.
• Arterial ulcers: Revascularization (angioplasty, bypass), debridement, no occlusive dressings.
• Infectious: Topical/systemic antibiotics (e.g., mupirocin for impetigo); avoid routine antiseptics.
• Inflammatory: Topical/intralesional steroids, immunosuppressants for lichen planus.
• Surgical: Grafting, flaps for non-healing ulcers.

Wound care: Cleanse with saline, appropriate dressings (foams, alginates). Multidisciplinary approach vital.

Prevention

Prevention focuses on risk reduction:

• Promote mobility, repositioning every 2-4 hours.
• Pressure redistribution mattresses.
• Nutrition: Protein, vitamins A/C.
• Moisture management, skin hygiene.
• Vascular risk control: Smoking cessation, blood pressure management.

Complications

Untreated lesions risk infection (cellulitis, osteomyelitis), sepsis, prolonged hospitalization, reduced quality of life, and mortality (pressure ulcers). Chronic ulcers may lead to squamous cell carcinoma (Marjolin ulcer).

Outcome

Prognosis varies: Superficial erosions heal in days-weeks; chronic ulcers (arterial/pressure) may persist months-years without intervention. Early detection improves outcomes.

Frequently Asked Questions (FAQs)

What is the difference between an erosion and an ulcer?

An

erosion

is superficial epidermal loss healing without scar; an

ulcer

is full-thickness, often scarring.

Who is at risk for pressure ulcers?

Immobile elderly, critically ill, spinal injury patients.

How are arterial ulcers diagnosed?

Clinical exam plus ABPI <0.9; Doppler ultrasound.

Can vulval ulcers be from non-STI causes?

Yes, aphthosis, autoimmune diseases common.

What prevents skin ulcers?

Repositioning, nutrition, pressure relief.