Premalignant Lesions: Actinic Keratosis & Actinic Cheilitis

Overview

• Focus of module: identification, diagnosis, treatment, and long-term management of premalignant skin lesions—principally actinic keratoses (AKs) and actinic cheilitis.
• Major goals:
  • Recognize subtle physical findings guiding therapeutic choice.
  • Understand anatomic-site–specific therapies (isolated vs. regional disease).
  • Formulate comprehensive plans for patients with advanced actinic damage.

Actinic Keratoses (AKs)

• Definition: Common precancerous epidermal growths caused by prolonged, repetitive ultraviolet (UV) exposure; potential precursor to squamous cell carcinoma (SCC).
• Progression risk: Impossible to predict lesion-by-lesion; hyperkeratotic or indurated plaques carry higher malignant potential.
• Epidemiology / Risk Factors
  • Fitzpatrick skin types $I \rightarrow III$.
  • Decades of cumulative sun exposure (occupational & recreational).
  • Residence at lower latitudes (closer to Equator).
  • Immunosuppression, especially solid-organ transplant recipients.
• Typical Distribution
  • Photo-exposed areas: scalp (balding), face, ears, neck, dorsal hands/forearms.
  • Women uniquely show lesions on lower legs, ankles, dorsal feet.
• Early Clinical Description
  • "Sandpaper" feel; easier to palpate than visualize.
  • Size $\approx$ $1–10\,\text{mm}$; discrete, rough adherent scale with faint peripheral erythema.
• Variants / Increasing Severity
  1. Thin AKs: $1–3\,\text{mm}$ rough macules or papules.
  2. Hypertrophic / hyperkeratotic AKs: $4–10\,\text{mm}$ thick plaques; may contain purulence after trauma.
  3. Superficial spreading AKs: >$1\,\text{cm}$ confluent plaques.
  4. Cutaneous horns: markedly hyperkeratotic projection; base often SCC.
• Physical-Exam Pearls (Image Examples Recapped)
  • Temple: 2 small “sandpaper” lesions $1–3\,\text{mm}$.
  • Volar–dorsal thumb junction: solitary $4–6\,\text{mm}$ keratotic plaque.
  • Bald scalp: multiple $6\,\text{mm}$ plaques, background erythema/scarring; farmers develop densely packed lesions.
  • Preauricular/sideburn: several $3–6\,\text{mm}$ plaques + additional ear lesions—necessity of full-area inspection.
  • Dorsum hand: dozens of $2–6\,\text{mm}$ plaques + pink erythematous halo (sites of prior LN2 treatment).
  • Nasal cutaneous horn w/ erythematous nodule → high SCC suspicion; smaller adjacent AK resembled its appearance initially (progression lesson).
  • Medial cheek: >$1\,\text{cm}$ superficial spreading plaque; numerous nasal lesions.
  • Advanced balding scalp series: central >$1\,\text{cm}$ AK, widespread scarring from earlier treatments, biopsy site marked.
  • Diffuse facial disease (patient w/ split-thickness graft): innumerable AKs across forehead, brow, cheek, ear rims, lateral neck.
  • Forehead + scalp ulcerated/crusted lesion = probable SCC amidst countless crusted AKs.
  • Barefoot patient: thick plaque on 2nd toe plus multiple $2–3\,\text{mm}$ AKs on toes/metatarsals.

Actinic Cheilitis

• Definition: Non-inflammatory, UV-induced epidermal neoplasia of lip vermilion; precursor to SCC of lip.
• Risk Factors mirror AKs: age, >$20$ yr UV exposure, fair skin, outdoor lifestyle, male sex, immunosuppression.
• Clinical Findings
  • Predominantly lower lip.
  • Early: whitish, scaly plaque, sandpaper texture, obscured vermilion border, diffusely dry/crusted lip.
  • Advanced: crusted, draining, friable, painful non-healing plaque → biopsy mandatory.
• Differential: eczematous/contact cheilitis (toothpaste/cosmetics), nutritional deficiencies, other inflammations.
• Treatment Algorithm
  1. Always consider biopsy of suspicious areas before therapy.
  2. Mild disease
  • Low-potency topical steroid $\times$ $2$ wk to reduce inflammation.
  • Focal cryotherapy (LN2) ± local anesthetic for multi-spot freeze.
  • 5-fluorouracil (5-FU) or imiquimod courses (see below); high discontinuation due to pain/cosmesis.
  • $20\%–30\%$ trichloroacetic acid peel to vermilion.
  1. Moderate–severe disease
  • CO$_2$ laser vermilionectomy: excellent healing/cosmesis; no histology; equipment & expertise required.
  • Scalpel vermilionectomy: provides specimen but $6–10\%$ risk of permanent lip shortening, food spillage, chronic discomfort.
  1. Combined diffuse AK + biopsy-proven SCC: treat with Mohs micrographic surgery or excision with frozen-section control.

Therapeutic Modalities for AKs (Skin)

1 | Cryosurgery (Liquid Nitrogen – LN2)

• Often first-line for discrete lesions.
• Key technical pearls: rapid freeze, slow thaw; spray device for large fields vs. cotton-tip contact for focal spots.
• Performed in office; insured; no home compliance issues.
• Video demonstration & vendor list referenced in course.

2 | Topical Chemotherapy / Immunomodulators

General principles

• Best for multiple small lesions in a defined field (face, scalp, arm, etc.).
• Inflammation intensity ∝ actinic damage severity (erythema → edema → oozing/crust).
• Treat sequential body areas to avoid excessive reaction (“sip vs. fire-hose”).
• Avoid eyelids; wash hands after application; give WRITTEN calendars.

2a • 5-Fluorouracil (5-FU)

• Brands: Carac, Efudex, Fluoroplex.
• Forms: $1\%–5\%$ cream or solution.
• Mechanism: pyrimidine analog → toxic nucleotide metabolites in rapidly dividing cells.
• Regimen: $21–28$ consecutive daily applications.
• Clinical course
  • Days 1–7: erythema → edema.
  • Mid-course: oozing, crusting proportional to sun damage.
  • Day $\approx 26$ example: dried crusts, slight hyperpigmentation; eyelids spared; be sure to include ears.
• Misuse examples
  • Patient used daily for $3$ mo → lichenified, crusted plaque, severe pruritus/sting; management: discontinue, potent topical steroid $3–4$×/day, culture/treat infection.
  • Warning: On-again/off-again self-treatment of single lesions leads to chronic non-healing hypopigmented AKs hiding SCC/BCC underneath → delayed cancer diagnosis.

2b • Imiquimod

• Brands: Aldara, Zyclara.
• Immune-response modifier: binds toll-like receptors → cytokine cascade (IFN, TNF-α, ILs) → antitumor T-cell activity.
• Regimen (Zyclara example):
  • Apply $2–3$×/wk × $2$ wk → off $2$ wk → repeat $2$ wk (total $6$ wk) → rest $4$ wk → optional second $6$-wk cycle.
  • Leave on $8$ h, no occlusion; max $2$ pumps/24 h to prevent systemic flu-like reaction (fever, myalgia).
• Example image: patchy dried crusted plaques in treated zones corresponding to greatest AK burden.

2c • Diclofenac $3\%$ Gel

• NSAID; apply twice daily for $3$ mo.
• Patient adherence low; clinical efficacy modest in author’s experience.

3 | Photodynamic Therapy (PDT)

• Suited for regional field cancerization (face/scalp), including patients with prior non-melanoma skin cancer.
• Protocol steps
  1. Aggressive acetone scrub to degrease.
  2. Apply $5$-aminolevulinic acid (ALA) photosensitizer (Levulan® Kerastick) vigorously.
  3. Incubate $\approx 2$ h (longer for arms).
  4. Illuminate with blue-violet light $\lambda=405–420\,\text{nm}$.
  5. Reactive-oxygen species destroy dysplastic cells.
• Post-PDT Reactions
  • Severe edema, blistering, discomfort proportional to damage.
  • 24-h photo: confluent edema/erythema.
  • 72-h photo: marked periorbital swelling, crusted plaques.
• Photoprotection rules (first $48$ h)
  • Strict avoidance of sunlight (even <5 min triggers burning).
  • Physical sunblock with titanium dioxide (NOT chemical sunscreen).
  • Hat, sunglasses, long sleeves; photosensitizer is protein-bound and sheds after $\approx 48$ h.

4 | Mechanical Destruction (Non-Cryo)

• Indications: Thick (>$10\,\text{mm}$), recurrent, or cryo-resistant AKs—especially on scalp.
• Method: Local anesthesia → curettage ± electrode-desiccation; obtains specimen for histology.
• Biopsy Guidance
  • High-risk groups (transplant, prior NMSC): biopsy any indurated/thick lesion.
  • Convex facial sites—prefer punch biopsy (avoid deep scoop scars).
  • Consider dermatology referral for cosmetically sensitive areas.

Practical / Ethical / Patient-Care Considerations

• Always educate about sun protection: broad-spectrum $\geq$ SPF $30$, reapply $q2\,\text{h}$, protective clothing.
• Elderly/outdoor workers need counseling on UV avoidance and regular skin exams.
• Immunosuppressed patients require closer surveillance; faster AK → SCC progression.
• Provide clear written instructions for topical regimens; use calendars to track doses.
• Discuss potential cosmetic downtime and pain to align expectations and prevent premature discontinuation.
• Document lesions thoroughly (size, site, appearance) and photograph when possible to track response.

Connections & Broader Significance

• AKs and actinic cheilitis represent the visible tip of cumulative UV damage (“field cancerization”).
• Early detection and treatment reduce SCC burden, health-care costs, and morbidity (e.g., lip reconstruction, grafts).
• Modalities like PDT not only treat existing AKs but may reduce emergence of new NMSC—important preventive strategy.
• Treatment choice balances efficacy, cosmesis, patient adherence, cost, and access to technology (e.g., CO$_2$ laser, PDT equipment).