Keep the postoperative bandage in place until showering the next morning. Before showering, remove and discard the bandage. Cleanse your incision with soap and water (not hydrogen peroxide, not alcohol) to remove any drainage and crusting. Pat the wound dry and apply a generous layer of Vaseline, Bacitracin, Bactroban ointment to the incision. Cover the Vaseline, Bacitracin, Bactroban with a non-adherent Telfa dressing. Tape the Telfa dressing in place with paper tape. Continue this wound care once daily until you return for suture removal.

Prescription Medications

Continue your regular medications as you normally would. If you take doctor-prescribed aspirin, Coumadin or Plavix, please continue your prescribed dosage. Unless doctor prescribed, do not take aspirin or aspirin containing medications (Alka-Seltzer, Anacin, Excedrin, Aleve, Bufferin, Emprin Compound, Ecotin, multiple “cold remedies”) and/or Motrin, Advil, Nuprin, Ibuprofen, high dose vitamin E within the first 24 hours following surgery. Tylenol or acetaminophen is acceptable to take during this period for any procedure-related discomfort.

Activity Level Following Surgery

The recommended activity level following the surgery will depend on the location of the skin cancer, the type of post-operative repair and underlying medical status of the patient.

If possible, please spend the first day following surgery relaxing. Surgery performed on scalp and/or face (forehead, nose, cheeks, and eyelids) may result in swelling and bruising around the eyes (black eyes). Swelling and bruising may increase progressively during the initial 48 hrs post-operatively and resolve over the subsequent 7 to 10 days. To decrease the likelihood of postoperative side effects:

• Keep your head elevated during the first few evenings with extra pillows if surgery was performed on the scalp and/or face.
• Apply ice packs (10 minutes of ice application every hour) to the surgically treated area during the first 48 hours to minimize bruising and swelling.
• Heavy lifting and exercise should be limited until after the sutures have been removed.
• Showering can be started the morning after surgery. Bathing is allowed if the incision site is not soaked. Pat the wound dry after leaving the shower and reapply the Vaseline and bandage. Swimming should be postponed until after the sutures have been removed.

Sun spots, also known as “solar lentigines,” present as tan to brown spots on sun exposed areas such as the face, neck, chest, upper back and arms. Solar lentigines are caused by an increase in the production of pigment (melanin) and melanocytes (pigment producing cells) as a response to UV radiation. Unlike moles where the melanocytes are clustered together, melanocytes in lentigines are evenly dispersed along the epidermis. Lentigines are benign but can be a reflection of sun damage. Patients with solar lentigines should take preventive measures to protect their skin from further UV exposure. Treatment consists of aggressive sun protection along with other options:

• Hydroquinone cream: Bleaching cream which helps reduce the production of pigment (melanin) by melanocytes.
• Tretinoin cream: Increases the turnover of cells and helps resurface the skin. Tretinoin often works best when combined with a bleaching product such as hydroquinone.
• Sunscreen: Protection from the sun and liberal use of sunscreens is equally important in the treatment of solar lentigines as prescription medications. Despite proper treatment, lentigines can return with exposure to sun light and UV radiation.
• Azelaic acid: Has also been shown to decrease the activity of melanocytes, although less effective than hydroquinone.

In office treatment options for sun spots include:

CHEMICAL PEELS

SkinCeuticals Gel Peel, Jessner’s, Mesoestetic Cosmelan Pack

• Customized for your skin type to target hyperpigmentation, uneven texture, loss of elasticity, lines and wrinkles

GLOBAL SKIN REJUVENATION

Aerolase, GentleMAX

• ND-Yag lasering technology gently and effectively targets a variety of skin concerns, giving the skin a luminous glow with no downtime

IPL (INTENSE PULSED LIGHT)

• Light-based therapy that rejuvenates while improving the overall appearance of the skin for a clear, radiant, even-toned complexion
• Repairs the look of photoaging freckling, age spots, blotchiness, irregular pigmentation and broken capillaries
• Improves redness, sensitivity and flushing of the face, neck, and/or chest.

PHOTODYNAMIC THERAPY

• FDA-approved treatment for pre-cancerous skin lesions, including actinic keratosis and early skin cancers including superficial basal cell carcinomas and squamous cell carcinomas
• Evens out skin texture and minimizes imperfections. Normalizes sun damaged, acne and rosacea-prone skin

RESURFACING LASER TREATMENTS

Clear & Brilliant Non-Ablative Resurfacing, Fraxel DUAL Non-Ablative Resurfacing, Coolpeel CO2 Resurfacing, Lumenis UltraPulse CO2 Ablative Resurfacing

• Stimulates new collagen synthesis for a radiantly smooth complexion
• Promotes skin repair and regeneration
• Minimizes the appearance of pores, discolorations, fine lines and wrinkles
• Reduces pore congestion to eliminate acne and prevent it from forming

Unlike melasma, solar lentigines are not influenced by hormonal fluctuations. Lesions that are changing or growing should be evaluated by a dermatologist to rule out potentially concerning growths. A biopsy may be performed on atypical lesions to rule out lentigo maligna melanoma, a type of melanoma that results from excessive sun damage.

Squamous cell carcinoma (SCC) is the second most common form of skin cancer and frequently arises on the sun-exposed skin of middle-aged individuals. Estimated annual incidence of squamous cell carcinoma in the United States is 107 cases per 100,000 people.  People who have fair skin, light hair, and blue, green, or gray eyes are at highest risk of developing the disease.

Squamous cell carcinomas may occur on all areas of the body including the mucous membranes and genitals, but are most common in areas frequently exposed to the sun, such as the rim of the ear, lower lip, face, bald scalp, neck, hands, arms and legs.

Squamous cell carcinoma can occur either de novo i.e. in the absence of a precursor lesion or from sun-induced precancerous lesions known as actinic keratoses (AKs).  Patients with multiple AKs are at increased risk of developing squamous cell carcinoma.  Other precancerous conditions include actinic cheilitis, Bowen’s disease, leukoplakia and others.

Risk Factors

General risk factors associated with the development of squamous cell carcinomas are as follows:

• Age older than 50 years
• Male sex
• Fair skin (i.e., burns easily, never or rarely tans)
• Geography (closer to the equator)
• History of prior non-melanoma (squamous cell  or basal cell) skin cancer
• Exposure to UV light (high cumulative dose) including tanning beds
• Exposure to chemical carcinogens (eg., arsenic, tar)
• Exposure to ionizing radiation
• Chronic immunosuppression
• Chronic scarring condition
• Human papilloma virus (HPV) infection (specific subtypes)

Clinical Presentations

Several clinical presentations of squamous cell carcinomas are possible:

•  A new and/or scaly enlarging patch.  Most SCCs grow slowly, some subtypes may enlarge rapidly.
• A persistent, scaly red patch with irregular borders that sometimes crusts or bleeds.
• An elevated growth with a central depression that occasionally bleeds. A growth of this type may rapidly increase in size.
• An open sore that bleeds and crusts and persists for weeks.
• A wart-like growth that crusts and occasionally bleeds.

Although most squamous cell carcinomas are asymptomatic, symptoms such as bleeding, weeping, pain or tenderness may occur.  Numbness, tingling, or muscle weakness though rare may reflect underlying perineural involvement.

If readily and properly treated most squamous cell carcinomas produce few sequelae.  Untreated squamous cell carcinomas may cause extensive destruction of tissue, and its delayed removal may entail substantial cosmetic deformity.

MANAGEMENT OPTIONS

The choice of treatment is based on the type, size, location, and depth of penetration of the tumor, as well as the patient’s age and general health.

Treatment can almost always be performed on an outpatient basis in a physician’s office or at a clinic. A local anesthetic is used during most surgical procedures.

Squamous cell carcinoma treatment modalities and associated cure rates are listed below.

1. Mohs Micrographic surgery (LINK)

• • For SCC less than 2 cm cure rate is 98%
  • For SCC greater than 2 cm cure rate is 75%
  • Poorly differentiated (by histological assessment) cure rate is 67%

2. Excision

• • Best for SCC less than 2cm

3. Non-surgical modalities (cryotherapy- spraying with liquid nitrogen, electrodessication and currettage)

• • For well-differentiated SCC (determined by tumor histology) 81% cure rate
  • For SCC less than 2 cm cure rate is 58%
  • For poorly differentiated SCC (determined by tumor histology) cure rate is 46%

4. Radiation

• • Recommended for nerve involvement and regional metastatic disease

5. Photodynamic therapy (PDT)

• • PDT treatment is not yet FDA-approved for squamous cell carcinoma, and while it may be effective with early, noninvasive tumors, overall recurrence rates vary considerably (from 0 to 52 percent), so the technique is not currently recommended for invasive squamous cell carcinoma.

6. Topical medications including 5-fluorouracil (5-FU, Carac, Efudex) and imiquimod (Aldara, Zyclara). Both medications are FDA-approved for treatment of actinic keratoses and superficial basal cell carcinomas, are also being tested for the treatment of some superficial squamous cell carcinomas. Successful treatment of Bowen’s disease, a noninvasive squamous cell carcinoma, has been reported. However, invasive squamous cell carcinoma should not be treated with 5-FU.

Risk of Metastasis

The overall risk of metastasis for SCC is in the range of 0.3-16%; however, this rate may be as high as 47% for certain high-risk tumor subtypes.  When metastasis occurs, squamous cell carcinomas frequently can be life-threatening. About 2,500 deaths result each year in the U.S.

Risk of metastasis is increased with:

• Size greater than 2 cm
• Location (lips, ears, eyelids, genitals)
• Depth of invasion
• Presence of neural (skin nerve) involvement
• Immunosuppression
• Recurrence

Most common metastasis site is lymph nodes followed by the lung.

10-year survival for regional metastasis is 20% and for distant metastasis is 10%

Prevention and Recurrence

A person who has had one squamous cell cancer is at an increased risk of developing another, especially in the same skin area or nearby. That is usually due to the face that the skin has already suffered irreversible sun damage.

Thus, it is crucial to pay particular attention to any previously treated site, and any changes noted should be shown immediately to a physician.  Squamous cell carcinomas on the nose, ears, and lips are especially prone to recurrence. Even if no suspicious signs are noticed, regularly scheduled follow-up visits including total-body skin exams are an essential part of post-treatment care.

Subtypes of SCC

• SCC in situ (SCCIS): SCCIS defined histologically by atypia involving the full thickness of the epidermis (top layer of skin) but without invasion into the dermis.
• Actinically derived SCC: The most common type of SCC is the sun-induced type.
• Invasive SCC: The invasive SCC is a raised, firm, pink-to-flesh–colored keratotic papule or plaque arising on sun-exposed skin. Approximately 70% of all SCCs occur on the head and neck, with an additional 15% found on the upper extremities. Surface changes may include scaling, ulceration, crusting, or the presence of a cutaneous horn. Less commonly, SCC may manifest as a pink cutaneous nodule without overlying surface changes. A background of severely sun-damaged skin, including solar elastosis, mottled dyspigmentation, telangiectasia, and multiple AKs, is often noted.
• Periungual SCC: Periungual SCC typically mimics a verruca (wart).
• Marjolin ulcer: This subtype of SCC appears as a new area of induration, elevation, or ulceration at the site of a preexisting scar or ulcer.
• Perioral SCC: SCC of the lip usually arises on the vermillion border of the lower lip, close to the midline. The precursor lesion is actinic cheilitis, which manifests as xerosis, fissuring, atrophy, and dyspigmentation and which is analogous to AK of the skin.
• Verrucous carcinoma (VC): VC is a subtype of SCC that can be locally destructive but rarely metastasizes. Lesions appear as exophytic, fungating, verrucous nodules or plaques, which may be described as “cauliflower-like”.
• Anogenital SCC: SCC in the anogenital region. Associated symptoms include pain, pruritus, and intermittent bleeding.
• HPV-associated SCC: Virally induced SCC most commonly manifests as a new or enlarging warty growth on the penis, vulva, perianal area, or periungual region.

Seborrheic Dermatitis is a common inflammatory condition that can cause redness, scaling, and flaking of the skin. It has a predilection for the scalp, face, and chest, and can affect up to 5% of the population. It commonly presents as redness and scaling on the scalp and central face (usually around the brows and nose). Patients may also experience irritation and itching of the skin. While the exact cause of seborrheic dermatitis is unknown, it may be due to a combination of environmental and genetic factors with overproduction of oil (sebum) in the skin and subsequent inflammation. Some studies suggest that it may involve an inflammatory reaction to a type of yeast that grows on oily skin, although this has not been proven. Seborrheic dermatitis can also be aggravated by illness, emotional stress, changes in weather, and certain medications.

While there are a variety of treatment options for seborrheic dermatitis, it tends to have a chronic and recurring course with periodic flares. Treatment options include:

• Medicated Shampoos: Over-the-counter shampoos containing coal tar, salicylic acid, zinc pyrithione, and selenium sulfide have proved to be effective in reducing inflammation and flaking associated with seborrheic dermatitis. Certain anti-fungal shampoos such as ketoconazole have also shown to be effective.
• Topical Corticosteroids: Steroid creams and ointments are effective in reducing inflammation and itching of the skin. When using topical steroids, it’s best to take periodic breaks to reduce the risk of steroid atrophy (thinning skin) and to prevent the body from getting used to the medicine.
• Non-steroidal Creams: Protopic and Elidel are non-steroidal anti-inflammatory creams which help reduce the symptoms of seborrheic dermatitis without the risks of topical steroids.
• Topical Antifungal Creams: Certain antifungal creams and shampoos have been shown to help by reducing the overgrowth of yeast on oily skin.

A combination of these medications and shampoos can be very effective in controlling the symptoms of seborrheic dermatitis.

Melanoma is a malignant tumor of melanocytes cells which produce the pigment melanin. Although most melanomas arise in the skin, they may also arise from mucosal surfaces (oral and genital) in the eyes, ears, gastrointestinal tract and brain (leptomeninges). Melanoma occurs predominantly in adults, and more than 50% of cases arise in apparently normal areas of the skin. Melanoma accounts for only 4% of all skin cancers; however, it causes the greatest number of skin cancer–related deaths worldwide. Early detection of thin cutaneous melanoma is the best means of reducing mortality.

ABCDE of Melanoma

Early signs that would suggest malignant change include:

• Asymmetry: Half the lesion does not match the other half.
• Border irregularity: The edges are ragged, notched, or blurred.
• Color variegation: Pigmentation is not uniform and may display shades of tan, brown, or black; white, reddish, or blue discoloration.
• Diameter: A diameter greater than 6 mm (greater than pencil eraser) is characteristic, although some melanomas may have smaller diameters; any growth in an existing nevus warrants an evaluation.
• Evolving: Changes in the lesion over time; changes include an increase in size, itching, or the development of satellites. Ulceration and/or bleeding are later signs.

Primary risk factors and clinical warning signs for melanoma include:

• • Changing mole (most important clinical warning sign)
  • Clinical atypical (dysplastic) nevi (particularly if more than 5-10)
  • Large numbers of common nevi (over 100)
  • Large (giant) congenital nevi (over 20 cm diameter in an adult)
  • History of previous melanoma
  • Sun sensitivity, history of excessive sun exposure including blistering sunburns in childhood and adolescence
  • Melanoma in first-degree relative(s)
  • Prior non-melanoma skin cancer (basal cell (BCC) and squamous cell carcinoma (SCC))
  • Male gender
  • Over 50 years of age
  • Presence of xeroderma pigmentosum or familial atypical mole melanoma syndrome
  • A fair-skin phenotype (blue/green eyes, blond or red hair, light complexion, sun sensitivity)

Melanoma in women occurs more commonly on the extremities and in men on the trunk or head and neck, but it can arise from any site on the skin surface.

Overall prognosis is affected by clinical and histological factors and by anatomic location of the lesion. Thickness and/or level of invasion of the melanoma, mitotic index, presence of tumor infiltrating lymphocytes, number of regional lymph nodes involved, and ulceration or bleeding at the primary site affect the prognosis.

Favorable prognostic factors include:

• Younger age
• Female gender
• Location of melanoma on the extremities

Clinical subtypes of malignant melanoma are:

• Superficial spreading
• Nodular
• Lentigo maligna
• Acral lentiginous (palmar/plantar and subungual)
• Miscellaneous unusual types:
  • Mucosal lentiginous (oral and genital)
  • Verrucous

Individual subtypes do not have independent prognostic or therapeutic significance.

Melanoma Staging (AJCC 2002 Revised)

Clinical staging of melanoma is based on whether the tumor has spread to regional lymph nodes or distant sites. In cases where disease is clinically confined to the primary site, the greater the thickness and depth of local invasion of the melanoma, the higher the chance of lymph node or systemic metastases and the worse the prognosis.

Melanoma can spread by local extension (through lymphatics) and/or by hematogenous routes to distant sites. Any organ may be involved by metastases, but lungs and liver are common sites. The risk of relapse decreases substantially over time, though late relapses are not uncommon.

*Met = metastasis.

The seventh edition of the AJCC Cancer Staging manual (published in 2009) has recommended no major changes for TNM categories and stage groupings, with the exception of removing Clark level and instead incorporating mitotic rate of greater than or equal to 1/mm² to upstage T1a to T1b melanomas.

TREATMENT

Thin melanomas which have not spread beyond the site at which they developed are highly curable. The treatment of localized melanoma is surgical excision with margins proportional to the microscopic stage of the primary lesion.  For most lesions 2 mm or less in Breslow thickness 1-2 cm radial, re-excision margins is recommended.

Melanomas with a Breslow thickness of 2 mm or more are still curable in a significant proportion of patients, but the risk of lymph node and/or systemic metastasis increases with increasing thickness.  The local treatment for these melanomas is surgical excision with margins based on Breslow thickness and anatomic location.  For most melanomas 2 mm to 4 mm in thickness 2 cm to 3 cm radial excision margins are recommended and sentinel lymph node (SLN) biopsy may be required.   Sentinel node biopsy should be performed prior to wide excision of the primary melanoma to ensure accurate lymphatic mapping.

Patients with melanomas that have a Breslow thickness more than 4 mm should be considered for adjuvant therapy with high-dose interferon.

Some melanomas that have spread to regional lymph nodes may be curable with wide local excision of the primary tumor and removal of the involved regional lymph nodes.  Adjuvant high-dose interferon was shown to increase relapse-free survival but not overall survival when compared to observation

Melanoma that has spread to distant sites is rarely curable with standard therapy, though high-dose interleukin-2 (IL-2) has been reported to produce durable responses in a small number of patients.  In patients with systemic metastasis confined to one anatomic site, long-term survival is occasionally achieved by complete resection of all metastatic disease.  All patients with distant metastasis are appropriately considered candidates for clinical trials exploring new forms of treatment, including a combination of chemotherapy, biological response modifiers (such as specific monoclonal antibodies, interferons, IL-2, or tumor necrosis factor-alpha), vaccine immunotherapy, or biochemotherapy (chemoimmunotherapy).

Malignant melanoma has been reported to spontaneously regress; however, the incidence of spontaneous complete regressions is less than 1%.

SENTINEL LYMPH NODE BIOPSY/DISSECTION

Lymphatic mapping and sentinel lymph node biopsy (SLNB) may be recommended in patients with thicker melanomas (greater than 1 mm in depth) and in those of less than 1 mm depth but with specific histologic features (eg, ulceration, lymphovascular invasion, mitotic rate 1 mm²).

SLNB for cutaneous melanoma was developed in the early 1990s to allow a selective approach to identifying occult regional nodal metastasis through localization of the first-draining, or sentinel, node. The success of the technique is based on the concept that cutaneous lymphatic flow is well-delineated in melanoma and that the histology of the sentinel node is characteristic of the entire lymph node basin (ie, a negative sentinel node obviates the need for further lymph node dissection).

Pre-operative radiographic mapping (lymphoscintigraphy) and vital blue dye injection around the primary melanoma or biopsy scar (at the time of wide local excision/re-excision) is performed to identify and remove the initial draining regional node(s).

The sentinel node is examined for the presence of micrometastasis using both routine histology and immunohistochemistry; if present, a therapeutic or completion lymph node dissection (CLND) is performed. A negative sentinel node biopsy result prevents the morbidity associated with an unnecessary lymphadenectomy.

Sentinel node status (positive or negative) is the most important prognostic factor for recurrence and is the most powerful predictor of survival in melanoma patients. Current AJCC melanoma staging and National Comprehensive Cancer Network clinical practice guidelines advocate pathologic staging of the regional lymph nodes for cutaneous melanoma of greater than 1 mm depth along with microstaging of the primary melanoma as the most complete means of staging.  However, the impact of SLN assessment on overall survival has yet to be determined.

Dysplastic or atypical nevi/moles have a potential of progressing into melanoma.

Early signs that would suggest malignant change include:

• Asymmetry: Half the lesion does not match the other half.
• Border irregularity: The edges are ragged, notched, or blurred.
• Color variegation: Pigmentation is not uniform and may display shades of tan, brown, or black; white, reddish, or blue discoloration.
• Diameter: A diameter greater than 6 mm (greater than pencil eraser) is characteristic, although some melanomas may have smaller diameters; any growth in an existing nevus warrants an evaluation.
• Evolving: Changes in the lesion over time; changes include an increase in size, itching, or the development of satellites. Ulceration and/or bleeding are later signs.

Basal cell carcinoma (BCC) is the most common form of skin cancer; an estimated 2.8 million BCCs are diagnosed annually in the US.  In fact, it is the most common of all cancers.

The estimated lifetime risk of BCC in the Caucasian population is 33-39% in men and 23-28% in women.  BCC usually presents as a slow growing, skin colored or reddish, shinny, non-healing growth.  Mild trauma, such as face washing, shaving or drying with a towel, may cause bleeding.  Other presentations include a pink growth, reddish patch or scar-like area.

BCC typically occurs in areas of chronic sun exposure and is typically seen on the face, ears, scalp, neck, or upper trunk.  Chronic recreational or occupational sun exposure as well as intense sun exposure during childhood or young adulthood all contribute to the development of BCC.

Anyone with a history of sun exposure can develop BCC. However, people who are at highest risk have fair skin, blond or red hair, and blue, green, or grey eyes.

BCCs are rarely fatal, usually slow growing and rarely metastasize.  The treatment is, however, essential to prevent significant local destruction and potential disfigurement.  Prognosis is excellent with proper therapy.

To prevent development of BCC, avoidance of sun UV radiation is essential.

Individuals with one BCC have a 30% greater risk of having another BCC either in the same area or elsewhere on the body compared with the risk in the general population.  All previously treated sites must be monitored after therapy as incompletely treated BCCs may recur.

Treatment

The choice of therapy depends on the size and location of the tumor, its histological subtype, whether or not the tumor has been previously treated and the patient’s health condition and personal preferences.

Both medical and surgical therapeutic options exist for BCCs and are easily treated in their early stages. The larger the tumor has grown, however, the more extensive the treatment needed.

Medical therapy includes chemotherapeutic (5-fluorouracil, 5-FU, Efudex, Carac), immune-modulating agents (imiquimod, Aldara, Zyclara) and photodynamic therapy (PDT) and is usually reserved for most superficial forms BCC.  Surgical treatment can almost always be performed on an outpatient basis in the physician’s office with a local anesthetic.

The common surgical treatment modalities include cryotherapy (freezing), curettage, excision with margin examination, Mohs micrographic surgery (LINK), and radiotherapy.

• For superficial or small (less than 1 cm) lesions of the trunk, cryosurgery, curettage and electrodesiccation (ED&C) provides an acceptable cure rate and good cosmetic outcome.  ED&C is not the preferred treatment for facial lesions, and is not recommended for large primary BCC, morpheaform or recurrent BCC.  Complications resulting from ED&C and cryosurgery include scarring and post-inflammatory pigmentary changes.
• Indications for Mohs micrographic surgery:
  • Facial lesions greater than 1 cm in diameter
  • Tumors greater than 2 cm in size on the body
  • Lesions located in the temple, eyelid, medial canthus, nose, and nasolabial fold that are more likely to recur
  • Recurrent BCCs
  • Lesions with clinically indistinct margins
  • Histopathology is morpheaform or micronodular pattern
  • Tumors that will require extensive reconstruction to repair the surgical defect

Actinic keratoses (AKs) are common cutaneous lesions that occur on sun-exposed areas particularly in blond or red-haired, fair-skinned individuals with green or blue eyes. They of course can occur in patients that do not possess these phenotypic features and relate most directly to cumulative sun exposure.  AKs represent the initial intraepidermal manifestation of abnormal proliferation of keratinocytes with the possibility of progression to squamous cell carcinoma in situ (SCC in situ) and invasive squamous cell carcinoma (SCC).

Clinically, AKs have three possible behavioral patterns: spontaneous regression, persistence, or progression into invasive SCC.   The risk of progression of AK to SCC has been calculated to be between 0.025 and 16% per year and the calculated lifetime risk of malignant transformation for a patient with AKs followed for a period of 10 years ranges from 6.1 to 10.2%.  The long-term risk of development of invasive SCC in patients with multiple AKs has been estimated to be as high as 10%.  Approximately 60-65% of SCCs arise from prior AKs.  Spontaneous regression has been reported in as high as 25.9% of AKs over a 12-month period, although a 15% recurrence rate was noted at follow-up.

Pathogenesis

Factors linked to pathogenesis of AKs include

• exposure to ultraviolet B (UVB) light; UVB causes mutations of the tumor suppressor gene (TSG) p53
• genetic DNA instability (i.e. xeroderma pigmentosum) or melanin deficiency (albinism)
• older age
• male gender
• anatomical location; over 80% of AKs are located on the head and neck, dorsal forearms and hands
• history of immunosuppression; solid organ transplant patients are at significantly increased risk.

Clinical Features

AKs are red, pink, or brown papules with a scaly (hyperkeratotic) surface.  They occur on sun-exposed areas and are especially common on the balding scalp, forehead, face, dorsal forearms and hands.   Subclinical (non-visible) AKs are estimated to occur up to 10 times more often than clinically visible AKs, particularly on sun-exposed skin.

Treatment

Prevention of disease is always superior and preferable to the need for treatment. Effective preventative measures include avoidance of excessive sun exposure (use of broad-brimmed hats, sun-protective clothing and sunscreen), patient education, and regular self-examinations to detect the earliest signs of malignant transformation.

Due to their low but real potential to develop into invasive SCC, AK therapy is generally recommended.  The management options for AKs should be chosen depending on whether a lesion-directed or a field-directed therapy is preferred.  Lesion-directed therapy, including ablative and surgical procedures, is reserved for selected cases where only a few clinically visible AKs are present.  Field-directed therapy, including ablative, non-ablative and topical treatments, offers the advantage of treating both clinically evident and subclinical lesions that may progress to visible AKs.

Lesion-directed treatment

Cryotherapy is the most commonly used lesion-directed treatment modality.  Clearance rates range from 39 to 98.8%.  In a large, multi-center Australian study evaluating the efficacy of cryotherapy for the treatment of AKs on the face and scalp, of the 89 patients and 421 lesions in the intended-to-treat population, there was an average of 67.2% lesion response rate per patient.  Cryotherapy treatment was associated with “good” and “excellent” cosmetic outcomes in 94% of the lesions.

Other lesion-directed treatment options include electrodessication and curettage (ED&C) and surgical excision.  Treatment with ED&C may require two or three cycles.  High cure rates and good cosmetic outcome have been reported.  C&D should be generally avoided in recurrent lesions, punch-biopsied lesions and hair bearing sites. 

Field-directed treatment

Field-directed treatment modalities include topical pharmacologic therapies including imiquimod, 5-FU and diclofenac, ablative and nonablative laser resurfacing, PDT, dermabrasion and deep and medium-depth chemical peels.

Retinoids

In a double-blind, randomized clinical trial 25 patients applied topical all-trans-retinoic acid (tretinoin) 0.05% cream twice daily for 16 weeks resulting in a 30.3% reduction in the number of AKs compared with baseline.

Imiquimod (Aldara, Zyclara)

The manufacturer-recommended standard imiquimod treatment protocol for AKs is twice weekly for sixteen weeks.  Other treatment protocols (three times a week for four weeks followed by a 4 week rest and an additional 4 weeks of treatment if remaining lesions are still present; two to three times a week for 16 weeks) have been reported.  Clearance rates with imiquimod range from 45 to 85%.  Reported recurrence rates are 10 and 16% within 1 year and 18 months of treatment respectively.

Common reported side effects of imiquimod therapy included site reactions (edema, erythema, vesicles and erosions/ulcerations), fatigue, headache, diarrhea, nausea and leucopenia.  No serious adverse events were reported.

5-FU (Efudex and Carac)

Manufacturer-recommended 5-FU treatment protocol for AKs is twice daily for 2-4 weeks.  Other protocols proposed in the literature include 5% 5-FU (Efudex) once to twice daily for 2-7 weeks; 5% 5-FU once daily, one day per week for 12 weeks; and 0.5% 5-FU (Carac) once or twice daily for 1-4 weeks.  The literature reported rates of AK resolution with 5-FU that reach 89% with twice weekly application for 16 weeks, albeit recurrence rates of up to 55% have been reported.  In addition, low compliance, due to adverse effects of medication, is associated with significant treatment failure rates.

Diclofenac

Efficacy of topically applied 3% diclofenac gel in 2.5% hyaluronic acid vehicle gel vs. vehicle was addressed in a multicenter, randomized, double-blind, placebo-controlled study of 195 patients.  Treatment with 3% diclofenac gel twice daily for 30-90 days resulted in an improvement of 59% compared with 31% with placebo.

Photodynamic Therapy (PDT) (LINK)

PDT with ALA (dALA or δ-ALA or 5ala or 5-aminolevulinic acid) activated by either blue or red light showed reported overall clearance values for AKs of 80% and 60%, respectively.   Response rates vary with duration of ALA incubation and thickness of AK lesions.  In a study of 243 patients with total of 1403 AKs on scalp and face, were treated with ALA (incubation time 1-18 hrs) and exposure to blue light.  At 8 weeks, 30% of patients with partial response were retreated.  At 12 weeks, 91% lesion clearance rate was reported.  Discomfort was the most commonly reported adverse event. Satisfaction with the cosmetic outcomes for PDT was 96%.