COMMON SKIN CANCERS Recognition and Management. Objectives. Structure of the Skin 2/3/2014. Marlyn J. Storch-Escott RN, BSN, MSN, ANP

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1 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 1

2 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 2

3 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 3

4 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 ( 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) 4

5 UVB ( 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 ( 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 5

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7 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 7

rough and dry May itch or present with burning or pricking sensation

8 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 8

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

9 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 9

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

10 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 10

11 Differential Diagnoses Seborrheic keratosis Bowen s disease BCC SCC 11

12 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 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 12

Electrodesication and Curettage (ED&C) Requires local anesthesia (Lidocaine with epinephrine) Equipment required: Electricator, Hyfrecator, Bantam Bovie, Ritter coagulator Sharp dermal curets

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

13 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 13

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

14 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 14

15 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 15

16 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 16

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18 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 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 18

19 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 19

20 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 20

21 BASAL CELL CARCINOMA (BCC) Most common form of skin cancer Locally invasive, aggressive, and destructive Extremely rare metastasis Persistently bleeding and scabbing, nonhealing papule is most common presentation 21

22 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 22

Pathophysiology of BCC Arises from basal keratinocytes of the epidermis and adnexal structures (hair follicles and eccrine sweat ducts) Nodular (21%)

23 Pathophysiology of BCC Arises from basal keratinocytes of the epidermis and adnexal structures (hair follicles and eccrine sweat ducts) Nodular (21%) Superficial (17%) Micronodular (15%) Infiltrative (7%) Morpheaform (1%) Histologic Types Mixed pattern can be present in 38.5% if the lesions of BCC 23

depressed center Erythematous (red to pink) Telangiectasia

24 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 24

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

25 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 25

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27 Differential diagnoses for BCCs Sebaceous hyperplasia Seborrheic keratosis Bowen s disease Granuloma annulare Actinic keratosis Nevus Melanoma 27

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)

28 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 28

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30 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 30

keratoacanthomas, lichen sclerosis et atrophicus (vulva), leukoplakia

31 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 31

32 Location of SCC Most commonly: rim of ear and lips Face and neck Bald scalp Shoulders, arms, hands Back 32

33 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 33

34 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 34

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36 Treatment Modalities for SCC Excisional surgery Mohs micrographic surgery Radiation ED&C Photodynamic therapy (PDT) Topical medication: 5-FU or Imiquimod Laser surgery 36

37 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 37

38 MALIGNANT MELANOMA 38

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

39 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 and second most common in ages 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 39

40 Location of melanoma ANYWHERE on the body Be especially vigilant with feet, between toes, perineal area, gluteal fold, and mouth 40

41 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 41

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

42 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 42

terminal phalanges, and mucous membranes Sudden appearance

43 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 43

44 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 44

45 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 45

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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

47 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 47

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50 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 % 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) 50

51 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 51

52 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 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 52

53 Physical Blockers Zinc oxide Titanium dioxide Iron oxide Kaolin Veterinary petrolatum Thank You for Your Attention ANY QUESTIONS? 53

Clinical characteristics

Skin Cancer Fernando Vega, MD Seattle Healing Arts Clinical characteristics Precancerous lesions Common skin cancers ACTINIC KERATOSIS Precancerous skin lesions Actinic keratoses Dysplastic melanocytic