Actinic Keratosis
Pre-malignant epidermal lesions caused by cumulative UV damage, commonly on sun-exposed skin of fair-skinned individuals. Approximately 5–10% may progress to squamous cell carcinoma over 10 years. Managed with cryotherapy, topical 5-FU, imiquimod, or photodynamic therapy per NICE CKS guidance.
Key Facts
Pre-malignant: ~5–10% progress to invasive SCC over 10 years UV-induced: cumulative UVB damage; most common on face, scalp (bald), dorsal hands Field cancerisation: widespread UV damage predisposes to multiple lesions Clinical features: rough, scaly, erythematous patches — better felt than seen Cryotherapy: first-line for isolated lesions — liquid nitrogen spray/freeze Topical 5-FU 5%: for field treatment — apply BD for 2–4 weeks Topical imiquimod 5%: alternative field treatment — 3 nights/week for 4 weeks Photodynamic therapy (PDT): for multiple/widespread AKs — good cosmetic outcome
Overview
Key Facts
Actinic keratoses (AKs) are the most common pre-malignant skin lesion. They are a marker of chronic UV damage and indicate increased risk of all skin cancers. Treatment is important to prevent progression and as part of skin cancer prevention.
Epidemiology
- Extremely common: affects ~15–25% of adults >40 in UK
- M > F (reflecting historical occupational UV exposure)
- Prevalence increases with age, fair skin, and geographic UV exposure
- Multiple AKs very common in organ transplant recipients
Aetiology
- Cumulative UV exposure (particularly UVB) — predominant cause
- Fair skin: Fitzpatrick types I–II
- Immunosuppression: transplant recipients — accelerated development and higher progression rate
- Occupational exposure: outdoor workers, farmers
- Field cancerisation: indicates widespread subclinical dysplasia in sun-damaged skin
Pathophysiology
- UV-induced mutations (p53, RAS) in epidermal keratinocytes → dysplasia confined to epidermis
- Represents a spectrum: AK → SCC in situ (Bowen's) → invasive SCC
- Histologically: disordered maturation of keratinocytes, parakeratosis, solar elastosis in dermis
Clinical Presentation
Typical Presentation
- Rough, scaly, erythematous papules or patches
- 'Sandpaper' texture — often better felt than seen
- Sun-exposed sites: face, ears, bald scalp, dorsal hands, forearms
- Usually multiple — indicates field damage
- May be skin-coloured, pink, or brown
- Typically <1 cm diameter
Variants
- Hypertrophic AK: thicker, keratotic — harder to distinguish from SCC clinically
- Cutaneous horn: conical keratin projection — AK at base (must biopsy to exclude SCC)
- Actinic cheilitis: AK of the lip — diffuse scaling/cracking of lower lip; higher progression risk
Red Flags
- Induration, rapid growth, or tenderness (suggests progression to SCC)
- Lesion >1 cm or increasing thickness
- Cutaneous horn (SCC at base in ~15–20%)
- Failure to respond to treatment
- Immunosuppressed patient — lower threshold for biopsy
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Bowen's disease (SCC in situ) | Well-demarcated erythematous plaque, larger | Biopsy |
| Invasive SCC | Indurated nodule, tender, ulcerated | Biopsy |
| Superficial BCC | Pearly border, telangiectasia | Biopsy, dermoscopy |
| Psoriasis | Silvery scale, Auspitz sign, extensor surfaces | Clinical, biopsy |
| Seborrhoeic keratosis | Stuck-on appearance, well-demarcated, waxy | Clinical, dermoscopy |
| Discoid eczema | Itchy, crusted, exudative | Clinical response to emollients/steroids |
Diagnosis / Investigation
Bedside
- Clinical examination: diagnosis is usually clinical; full skin survey for other lesions
- Dermoscopy: strawberry pattern (red pseudo-network with white/yellow scale)
Biopsy
- Not routinely required for typical AKs
- Biopsy indications: diagnostic uncertainty, hypertrophic lesion, suspected SCC, treatment failure, cutaneous horn
- Punch/shave biopsy: to exclude invasive SCC
Imaging
- Not required for AKs
Special Tests
- Reflectance confocal microscopy: emerging non-invasive technique for monitoring field cancerisation
Management
Non-Pharmacological
- Sun protection: SPF 30+, protective clothing, hat — lifelong; essential alongside treatment
- Patient education: self-monitoring, prompt reporting of changing lesions
- Observation: mild, few AKs in elderly — watchful waiting is acceptable with good sun protection
Pharmacological
- Cryotherapy (liquid nitrogen): first-line for isolated/few lesions — single freeze-thaw cycle; cure rate ~75–85%
- Topical 5-fluorouracil (Efudix) 5% cream: field treatment — apply BD for 2–4 weeks; expect marked inflammation; cure rate ~80%
- Topical imiquimod (Aldara) 5% cream: field treatment — 3 nights/week for 4 weeks; immune-mediated response
- Topical diclofenac 3% gel (Solaraze): apply BD for 60–90 days — better tolerated, lower efficacy (~50%)
- Topical tirbanibulin (Klisyri) 1% ointment: newer agent — apply OD for 5 days; NICE-approved
- Photodynamic therapy (PDT): methyl aminolaevulinate (MAL) or aminolaevulinic acid (ALA) + red/daylight activation — excellent for widespread AKs; good cosmetic result
Surgical
- Curettage: for hypertrophic AKs or where biopsy confirmation needed
Referral Criteria
- Dermatology referral: diagnostic uncertainty, treatment failure, immunosuppressed patients
- 2-week wait referral: if SCC suspected (NICE NG12)
Prognosis
- ~5–10% of individual AKs progress to invasive SCC over 10 years
- Spontaneous regression: ~15–25% of AKs may regress spontaneously
- Recurrence after treatment: common, especially with ongoing UV exposure
- Field cancerisation: ongoing risk of new lesions even after treatment
- Organ transplant recipients: higher progression rate — require more aggressive monitoring and treatment
- Patients with AKs are at increased risk of all skin cancers (BCC, SCC, melanoma)
Other Relevant Information
AK Treatment Comparison
| Treatment | Indication | Efficacy | Key Side Effect |
|---|---|---|---|
| Cryotherapy | Few, isolated AKs | 75–85% | Hypopigmentation, scarring |
| 5-FU 5% cream | Field treatment | ~80% | Marked inflammation, erosion |
| Imiquimod 5% | Field treatment | ~75% | Local inflammation, flu-like |
| PDT | Widespread AKs | ~75–85% | Pain during treatment |
| Diclofenac 3% gel | Mild, widespread | ~50% | Mild irritation |
| Tirbanibulin 1% | Field treatment | ~50–75% | Local irritation |
AK to SCC Progression Risk Factors
| Factor | Effect |
|---|---|
| Immunosuppression | Markedly increased risk |
| Hypertrophic AK | Higher progression rate |
| Actinic cheilitis (lip) | Higher progression rate |
| Multiple AKs (>10) | Higher cumulative risk |
| Ongoing UV exposure | Sustained risk |