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COMMON SKIN CANCERS Recognition and Management

Marlyn J. Storch-Escott

RN, BSN, MSN, ANP

Objectives

• List the most common types of skin cancers.

• Identify 2-3 clinical manifestations of each common skin cancer.

• Explain the difference between shave biopsy, punch biopsy, and excisional biopsy.

• Describe the treatment modalities for the common types of skin cancer.

Structure of the Skin

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Epidermis

• Outermost layer of the skin

• Composition

– Stratum basalis (separates dermis from epidermis)

– Stratum spinosum (spiny cell layer)

– Stratum granulosum (granular cell layer)

– Stratum corneum (cornified layer)

Dermis

• Two layers

• Adventitial layer

– Reticular

• Functions

– Temperature control

– Mechanical

– Cutaneous sensation

Subcutaneous

• Composition

– Distinct flat lobules

– Blood vessels, nerves, and lymphatics

• Functions

– Heat insulator

– Shock absorber

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Ancillary Skin Structures

• Glands

– Sebaceous (sebum: antifungal properties)

– Eccrine (sweat)

– Apocrine (produce scent in axilla and perineum)

• Hair

• Nails

General Functions of the Skin

• Sensation

• Protection

»Thermoregulation

• Secretion

• Flexibility

Sunlight and the Skin

Photobiology

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• Photobiologic skin reactions and diseases

• Caused by ultraviolet light

From the sun in the form of

Solar radiation

Solar Radiation

• Continuous spectrum of wave lengths of electromagnetic energy over 290 nm (nm = unit for measuring the wavelength of light = nanometer)

Ultraviolet light

• Divided into:

– UVA (320 -400 nm)

• Constant throughout the day

• Penetrates window glass

• Interacts with topical and systemic chemicals and medications

• Produces immediate and delayed tanning – Results in Photoaging

• Can reach dermis and subcutaneous fat (longer wavelenths)

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– UVB (290 -320 nm)

• Most intense between 10 AM and 4 PM

• Absorbed by window glass

• Prior exposure to UVA enhances sunburn reaction of UVB

• Primarily responsible for sunburn, suntan, and skin cancers

• Delivers high amount of energy to stratum corneum and superficial layers of the epidermis

– UVC (100 – 290 nm)

• Absorbed by the ozone layer

• Only transmitted artificially in germicidal lamps and mercury arc lamps

Effects of Sun Damaged Skin

• Photoaging – Solar elastosis

– Course, deep wrinkling

– Skin thickens

– Persistent pigmentation

– Telangiectasia

– Maturation of keratinocytes

• Sun tan and sun burn

• Skin cancers

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Tolerance to Sunlight

• Dependent on individual’s skin type

– Estimated on response to first 30 minutes of exposure to summer sun

Skin Types

• Type 1: always burns easily; never tans, very sensitive

• Type 2: usually burns easily; tans minimally, very sensitive

• Type 3: Burns moderately; tans gradually and uniformly, sensitive

• Type 4: burns minimally; always tans well, moderately sensitive

• Type 5: Rarely burns; tans profusely, minimally sensitive

• Type 6: Never burns: deeply pigmented, insensitive

Types of skin lesions due to

Solar radiation and/or tanning beds

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Actinic Keratosis (AK)

• Appears as a poorly circumscribed, pink, red or tan papule that feels or looks scaly, crusty, or crumbly, generally rough and dry

– May itch or present with burning or pricking sensation

– Can bleed, but rarely

– May present as cutaneous horn

– Actinic cheilitis on lips

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• Located on sun-exposed areas of the skin

– Face, head, neck, arms, hands, and legs

• Mainly on skin types 1 -3

– Possibility on 4 and 5

• May be visualized but mainly located by feel

AKs considered pre-malignant lesions

• Regarded as precursor to SCC or BCC

– Mainly progress to SCC

– Estimates of transformation range from 0.025% to 20% per year

• 44% - 97% SCCs

• 36% BCCs

– Dictates need to treat these lesions

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AKs

• Seen more frequently in males

• Increase in numbers with age

• Skin types 1 – 3 mainly

• History of excessive sun exposure without protection

– Produce atypical squamous cells in the epidermis

• Penetration of the epidermis/dermis junction indicates development of SCC

Diagnosis of AKs

• History of extreme frequent sun exposure

• Clinical picture

– Felt and/or visualized

• Biopsy (shave biopsy)

– Only if indurated lesion

• Would indicate SCC

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Differential Diagnoses

• Seborrheic keratosis

• Bowen’s disease

• BCC

• SCC

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Treatment of AKs

Cryotherapy

• Use of liquid nitrogen to freeze the lesions – Boiling point of liquid nitrogen is – 196 C

– Freezes lesions to about -50 C

• Administered by direct spray or contact swab – 10 to 15 second exposure

• Margin beyond lesion of 1 -3 mm

• Allow slow thawing 20 -40 seconds

• Pain is moderate to severe during freezing

• May produce dyspigmentation

Cryotherapy after effects

• Erythema

• Edema (localized)

• Blister formation (7 -10 days for formation)

• May experience fluid drainage

• Dry crust forms

• 99% cure rate fro treated lesions

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Electrodesication and Curettage (ED&C)

• Requires local anesthesia (Lidocaine with epinephrine) • Equipment required:

– Electricator, Hyfrecator, Bantam Bovie, Ritter coagulator – Sharp dermal curets (1 7 mm)

• Using a small size curet, held like a pencil, skin around the lesion is held taut with fingers of free hand

• Use smooth, firm strokes with curet until firm tissue base is acquired and resistance occurs

• Then dessication is achieved by inserting needle of electrosurgical unit into the tissue – Char produced result in hemostasis

Care of ED&C site

• Heals by secondary intention

• Wound should be cleansed daily with soap and water

• Antibiotic ointment may be applied

• Light dressing in place until dry

• Follow-up visit in 7 -10 days

• Patient should be instructed in signs of infection

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Photodynamic Therapy (PDT)

• Light therapy for treatment of lesions

• Requires

– Photosensitizing drug and light source – 20% 5-aminolevulinic acid (hydrochloride salt) and a vehicle

– Light of proper wave length and power

» Blue light (BLU-U)

• Provides uniform blue light distribution for 1000 sec

• Power density fixed at 10mW/cm2

– Tissue oxygen

PDT

• Functions by light activating the drug in the tissue which creates a singlet oxygen which is highly cytotoxic, results in tissue destruction

• Safety precautions

– Protective eye goggles for both patient and provider

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Patient discomfort with PDT

• Stinging and burning occurs most severely in the initial stages; plateaus at approximately 6 minutes

• Symptoms diminish at completion of treatment

• Within 24 hours discomfort should abate entirely

PDT Discomfort Relief Measures

• NSAIDs prior to or after procedure

– May also use acetaminophen, diazepam, dipherhydramine HCl, hydrocodone

• Use of topical lidocaine 4% or ELA-Max

• Ice packs

• Cold compresses

• Post treatment topical steroid cream

Common local responses to PDT

• Crusting

• Pruritus

• Scaling

• Rarely, vesicle or blister formation

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TOPICAL MEDICATIONS for

Actinic Keratosis

5-FU 5%, 1%, 0.5% cream

• Applied QD or BID for 3 -5 weeks

• Inhibits thymidylate synthetase thus preventing cell proliferation and causing selective cell death

• Produces inflammation, erythema, and edema initially

• Continued until erosion, necrosis, and ulceration of lesions occurs

• Complete healing in 1 -2 months after cessation of medication

• Adverse reactions are local: burning, crusting, and allergic contact dermatitis

• May use weekly pulse dosing

– Apply BID two consecutive days a week

– F/U in 3 – 4 weeks

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IMIQUIMOD Cream 5%

• Applied 3x / week at HS for 4 – 6 weeks

• Left on 8 hours and then washed off

• Produces interferon which destroys precancerous and cancer cells, is an immune response modifier

• More readily accepted by patient – Lesser number of applications

– Skin response less intense than 5-FU

– Similar results to 5-FU

Diclofenac Sodium Gel 3%

• Applied BID for 60 – 90 days

• Inhibits cyclooxygenase and acts through induction of apoptosis, inhibition of angiogenesis and up-regulation of arachidonic acid pathway

• Adverse reactions: contact dermatitis, dry skin, edema, exfoliation, pain, paresthesia, pruritis, rash

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CHEMICAL PEEL for

Actinic Keratosis

• Alpha hydroxy acids topically cause epidermolysis and elimination or keratosis

• Includes – 30 – 70% Glycolic acid

– Trichloroacetic acid 35 %

– Jessner’s solution

• 5-FU often used for 5 – 7 days prior to peel to “light up” the lesions

• Acid is applied to the lesions with cotton swab and left on for 5 – 10 minutes

• Then removed with alcohol – Produces a controlled, partial thickness exfoliation of

epidermis and outer dermis

Local complications of chemical peel

• Pigmentation changes

• Scarring

• Milia

• Ectropion

• Infection

• Activation of herpes simplex

• Toxic shock syndrome

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Chemical facial exfoliation can be:

• DEEP

– Phenol in Baker’s formula is used

– Burn extends 2 – 3 mm

– May cause cardiac arrhythmias

– Full epithelialization occurs in 6 – 7 days

– Provides substantial improvement in rhytidosis and actinic damage

• MEDIUM – DEPTH

– Trichloroacetic acid 35% - 50%

– Lightens pigmentation and improves rhytides

– Minimal systemic toxicity

– Local complications: scarring and pigmentation problems.

• SUPERFICIAL

– Trichloroacetic acid 10% - 25% or

– Glycolic acid 50% - 70%

– Depth of penetration titrated by timed duration of acid placement

• Left on 3 – 7 minutes

• Repeated 3 - 4 times

– Removes AKs, fine wrinkles, lentigines, melasma, and seborrheic keratoses

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BASAL CELL CARCINOMA (BCC)

• Most common form of skin cancer

• Locally invasive, aggressive, and destructive

– Extremely rare metastasis

• Persistently bleeding and scabbing, non-healing papule is most common presentation

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Risk Factors for BCC

• Fair skin (mainly types 1 -3)

• Degree of sun exposure

• Men have higher incidence than women

• Tanning beds ( emit both UVA and UVB radiation)

• Over 40 years of age

Location of BCCs

• Head and neck: most commonly

– 25 – 30% on the nose

• Shoulders

• Back

• Upper chest

• Arms and legs

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Pathophysiology of BCC

• Arises from basal keratinocytes of the epidermis and adnexal structures (hair follicles and eccrine sweat ducts)

Histologic Types

• Nodular (21%)

• Superficial (17%)

• Micronodular (15%)

• Infiltrative (7%)

• Morpheaform (1%)

– Mixed pattern can be present in 38.5% if the lesions of BCC

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Morphology of BCC

• Papule or nodule with rolled border

• Translucent or “pearly” with possible crust

• Round or ovoid with depressed center

• Erythematous (red to pink)

• Telangiectasia present

• May be pigmented brown, black, or blue

• Generally firm or hard

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Diagnosis of BCC

• Visual exam – Good lighting, hand magnifier, palpation

• Biopsy – Shave biopsy

• Removal of small piece of suspect lesion

– Excisional biopsy • Removal of entire suspect lesion

– Punch biopsy • Removal of entire suspect lesion down to subcutaneous

level

• All biopsies require local anesthesia – Generally Lidocaine with epinephrine

• A scalpel blade or a punch instrument if punch biopsy being performed

• Medication for hemostasis – 25% - 30% aluminum chloride

– Silver nitrate sticks

• Sutures if punch biopsy or excisional biopsy performed

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Differential diagnoses for BCCs

• Sebaceous hyperplasia

• Seborrheic keratosis

• Bowen’s disease

• Granuloma annulare

• Actinic keratosis

• Nevus

• Melanoma

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Treatment Modalities for BCC

• Excisional surgery

• Moh’s Micrographic surgery

• ED&C (can be combined with cryotherapy or topical medications)

• Cryotherapy (can be combined with topical medications)

• Photodynamic Therapy (PDT)

• Topical medications (5-FU or Imiquimod)

• Rarely radiation or laser surgery

Variant of BCC Gorlin’s syndrome

• Basal cell nevoid syndrome – Rare inherited disease

– Autosomal dominant • Gene located on chromosome 9q22.3q31

• Characterized by – Multiple nevoid BCCs

– Pits in palms of hands and soles of feet

– Multiple jaw cysts

– Facial structure changes

– Skeletal abnormalities

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SQUAMOUS CELL CARCINOMA (scc)

• Second most common form of skin cancer

• Lesion is metastatic – 5 year survival rate 14 – 39%

– Matastasizes to regional lymph nodes

– Then to liver, lungs, bone, and brain

• Most common in sun-exposed areas – Scalp, dorsal hands, and pinna

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Risk Factors of SCC

• Sun exposure, especially UVB radiation

• Immunosuppression

• Other lesions: AKs, Bowen’s disease, keratoacanthomas, lichen sclerosis et atrophicus (vulva), leukoplakia

• Chemical exposure: arsenic and therapeutic tar

• Sites of chronic infections: sinus tracks and bone

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Location of SCC

• Most commonly: rim of ear and lips

• Face and neck

• Bald scalp

• Shoulders, arms, hands

• Back

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Pathophysiology of SCC

• Originates in epidermis from keratinocytes

• Proliferates indefinitely

• Penetrated the epidermal basement membrane

• Proliferates into the dermis

Histologic Types of SCC

• Highly differentiated SCC

– Firm or hard on palpation

• Poorly differentiated SCC

– Fleshy, granulomatous, and soft on palpation

Morphology of SCC

• Indurated papule, plaque, or nodule

• May have thick keratotic scale or hyperkeratosis

• Firm, hard, often freely moveable or soft and, fleshy

• Erythematous base, yellowish skin color

• Polygonal, oval, round or umbilicated

• Telangiectasia

• Freckling

• Dry, scaly atrophic skin

• Regional lymphadenopathy

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Diagnosis of SCC

• Visual examination

• Palpate lymph nodes

• Biopsy

– Shave

– Excisional

– Punch

Differential Diagnosis of SCC

• Keratoacanthoma

• Wart

• Seborrheic keratosis

• Nummular eczema

• Psoriasis

• Paget’s disease

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Treatment Modalities for SCC

• Excisional surgery

• Mohs micrographic surgery

• Radiation

• ED&C

• Photodynamic therapy (PDT)

• Topical medication: 5-FU or Imiquimod

• Laser surgery

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Variables for Recurrence and Metastasis of SCC

• Size: <2cm or >2cm • Depth: <4mm/Clark level I to II or >4mm/Clark level of

IV or V • Differentiation: well differentiated or poorly

differentiated (greater risk with poorly) • Site: Ear (greater for recurrence) or lip (greater for

metastasis) • Scar carcinoma (metastasis) • Previous treatment • Perineural involvement • Immunosuppression (metastasis)

Variants of SCC

• Bowen’s disease (SC in situ)

• Erythroplasia (Queyrat)

• Marjolin’s ulcer

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MALIGNANT MELANOMA

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• One of the most dangerous tumors

• Ability to metastasize to any organ

• Can present anywhere on the body

• May arise from a newly developed lesion or a pre-existing lesion

• Only common cancer in the US whose incidence is increasing

• Most common cancer in adults aged 25 – 29 and second most common in ages 15 - 29

Risk Factors for Melanoma

• High levels of sun exposure • TANNING BEDS • Experiencing sunburns (more than 3 in lifetime) • Having numerous nevi (moles) • White race • History of melanoma in first degree relative • Immunosuppression • Previous cutaneous melanoma • Sun sensitivity

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Location of melanoma

• ANYWHERE on the body

– Be especially vigilant with feet, between toes, perineal area, gluteal fold, and mouth

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Pathophysiology of Melanoma

• Originates in melanocytes

– Primarily found in basal layer of skin

– Also located in GI tract, eyes, ears, and oral and genital mucosa

• Melanocyte degenerates and becomes neoplastic

– Then can move into any area

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Histologic Types

• Type I: Superficial spreading (70%)

– Most common in middle age

– Occurs anywhere on the body

• Upper back, both sexes

• Women’s legs

– Bizarre lesion shapes, especially over time

– Multiple colors, including dull red

• Type II: Lentigo maligna (10%)

– Most common in 60 or 70 year olds

– Mainly on the facial area

– Mainly radial growth

– Mainly brown or black in color

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• Type III: Acral lentiginous melanoma (2 -8%)

– Seen in 29% to 72% in black and Asian patients

– Found on palms, soles, terminal phalanges, and mucous membranes

– Sudden appearance of Hutchinson’s sign

• Pigmented band in proximal nail fold

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• Type IV: Nodular melanoma (10 – 15%)

– Multiple colors: Blue-black, purple, red-brown, flesh-colored

– Raised above the skin

– May be ulcerated, crusty, and frequently bleeds

– More frequent in males

– Dome-shaped, polyploidy, pedunculated

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Morphology of Melanoma

• ABCDs of melanoma – A: asymmetry – B: border – C: color – D: diameter – E: elevation and enlargement

• Changes in surface characteristics • Development of symptoms

– Itching (pruritus), tenderness, pain

•

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Diagnosis of Melanoma

• Visual examination – Using ABCDs of melanoma

• Use of dermatoscopy – Apply fluid to skin – Position dermatoscope over lesion – Three point checklist (novice)

• Asymmetry of color and structure • Atypical network of cells • Blue-white structure

– Pattern analysis

• Biopsy – Total excisional biopsy with narrow margins – Punch biopsy

Differential Diagnosis of Melanoma

• Congenital nevus

• Common acquired nevus

• Superficial spreading nevus

• Clark’s nevus

• Blue nevus

• Spitz nevus

• Pigmented BCC

• Pyogenic granuloma

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Treatment Modalities for Melanoma

• Depends upon staging of melanoma

– Looks at thickness, depth, and spread

• Diagnostic Indicators

– Clark’s level

• I: confined to the epidermis

• II: invasion of papillary dermis (upper)

• III: filling of the papillary dermis (lower)

• IV: extending into the reticular dermis

• V: invasion of the subcutaneous tissue

– Breslow Thickness

• Better melanoma stage diagnostic indicator

• Measure (in millimeters) of the vertical depth of tumor measured from the granular cell (very top) layer downward

• Breslow thickness and Survival rate – < 1mm: 5 year survival is 95 -100%

– 1 – 2mm: 5 year survival is 80 – 96%

– 2.1 – 4mm: 5 year survival is 60 – 75%

– > 4mm: 5 year survival is 37 – 50%

Staging of Tumor

• Process used to describe the extent of the disease

• Consider thickness, depth, and spread • Guides providers to appropriate treatment plan

and determines prognosis • Goes from 0 to 4 • Key information indicators

– T = tumor (thickness, number assigned, appearance of tumor [letter assigned]

– N = lymph nodes ( 0 – 3) – M = metastasis (spread of tumor)

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Types of Therapy for Melanoma

• Surgical excision – Simple excision – Mohs surgery – Wide local excision – Excision with sentinel lymph node biopsy

• Immunotherapy – Treats the whole body – Use of biologic agents that stimulated the immune system

• Include interferons and interleukins – Interferon alpha 2-b: Stage II and III – Interleukin – 2: Stage IV

» Requires hospitalization » Two cycles of high dose IV therapy drug » Must be closely monitored

• Chemotherapy – Decarbazine (DTIC)

– Taxanes (docetaxel and paclitaxes)

– Platinum agents • May be administered by isolated limb perfusion (ILP)

• Radiation therapy – Gamma knife

– Cyber knife

• Regional perfusion (ILP) – Melphalen: drug gold standard for ILP

• Clinical trials

Side Effects of Melanoma Treatment

• Pain

• Scarring

• Infection

• Lymphedema

• Fatigue

• GI discomfort

– Nausea, vomiting, diarrhea, constipation

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On-going Melanoma Monitoring

• Total body skin exams by dermatologist – Q 3 months – first year – Q 6 months – 2 – 5 years – Yearly – 6 years and on

• Lab Studies – CBC, electrolytes, renal function, liver function and

LDH levels

• Annual chest x-rays • Radiologic imaging

– Bone scan, CT scans, MRIs, PET scans

General Skin Cancer Prevention

• Avoid sun exposure during peak sun hours • Wear sun protectant clothes • Always wear wide-brimmed hat • Utilize sunscreen daily

– SPF (Sun protection factor) • Ratio of time required to produce erythema through a

sunscreen product to the time required to produce the same degree of erythema without the sunscreen

• SPF ranges from 15 – 65 or 70 • SPF 15 provides 50% protection • SPF 34 provided 97% protection

Agents for Protection Against Solar Radiation

• UVB protective agents – Para-aminobenzoic acid (PA

– PABA esters

– Cinnamates

– Salicylates

– Phenylbenzimidazole sulfonic acid

• UVA protectant agent – Benzophenes

– Dibenzolmethanes

– Avobenzones

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• Physical Blockers

– Zinc oxide

– Titanium dioxide

– Iron oxide

– Kaolin

– Veterinary petrolatum

Thank You for Your Attention

ANY QUESTIONS?