Skin

SURGERY November 8, 2010

Dr. Penserga

Course Outline Review of anatomy and Physilogy Common surgical entities

o Traumatic injurieso Radiation exposure injurieso Inflammatory conditions

Pyoderma gangrenosum Staph scald skin syndrome Others

Neoplasmso Benign

Cyst: epidermal, dermoid, trichlemmal Nevi: acquired, congenital Soft tissue tumors: acrochordons,

dermatofibromatosis, lipomao Malignant

Predisposing factors leading to malignancy

Precancerous lesions Common cutaneous malignancy

BCC SCC Malignant Melanoma

Other malignant lesions

OBJECTIVES of this topic

To know the common skin and subcutaneous lesions amenable to surgical treatments

To know the pathophysiologic basis of the dieases and clinical manifestations

To know the management principles of the skin and subcutaneous lesions

ANATOMY and PHYSIOLOGY Skin is a complex organ with a complex of functions

like:o Protective barrier – main functiono Impermeability – protection against chemicalso Skin pigmentation – protection against sun

radiationo Immune function – protection against bacteriao Durability – against impact forceso Thermoregulation – sweat glandso Sensory functionso Customized functions

Thick palm and soles for weight bearing Nerve ending packed fingertips

o Hairo Skin lines and stretchability

Accommodate range of motionso Beauty – least maybe

The EPIDERMISo Horny Layer – keratinocytes mature, losses inter

connections, shed offo Granular Layer – keratinocytes gain keratohyalin

granules

o Spinous Layer – migrating keratinocytes losses mitosis

o Basal Layer – keratinocytes, mitotic, some migrate upwards

From basal layer exit to shedding, keratinocyte transit time approximates 40-60 days

Internal skeleton of keratinocytes (keratin) allows skin to resist stress

Other cells in the epidermiso Melanocytes:

From neural crest precursors Protection from radiation Produce melanin packed in the

melanosome Transported via dendrites Taken up by keratinocytes (apocopation) rate of production, transfer, and

degradation determines pigmentation other influences of pigmentation:

genetics Uv radiations Hormones

(estrogen, ACTH, msh) Despite the differences in skin tone, the

density of melanocytes is constant among individuals. It is the rate of melanin production, transfer to keratinocytes, and melanosome degradation that determine the degree of skin pigmentation

o Langerhans From bone marrow “skin’s macrophage” Has antigen presenting capability Acts against viruses Also involved in skin allograft rejection

The DERMISo Collagen

Makes up the 70% dermis The tensile strength of the skin

o Elastic Fibers Allows stretching twice the original length and

return to normalo Fibroblast

Responsible for protein matrix production Healing and organogenesis

o Basement membrane zone of the epidermis-dermis junction

Anchors the epidermis Pathology at this layer may cause separation

of the epidermis

Other dermal structureso Blood vessels

Thermoregulations Vertical channels – connect directly into

subcutaneous and skin vessels Glomus – AV shunts, allows more blood and

heat dissipationo Nerve endings

For temperature, vibration, and touch pressure

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o Adnexal structures: Eccrine glands – for sweating in entire body

but more on palms, soles, and forehead Apocrine glands – for sweating in the axilla,

and anorectalregions that produces scent hormones (pheromones)

INJURIES to the SKIN Violations of skin continuity Causes:

o Traumatic injuries – penetrating or blunt wounds, shear forces, bites, degloving

o Sharp lacerations, bullet wounds, road rash (injury from scraping against road pavement)

o Burns – thermal, caustic substanceso Prolonged pressure – bed or pressure soreso Radiations

WOUNDS Avulsion, lacerations, bites, degloving Varying degree of skin destructions Treated by gentle cleansing, debridement of all foreign

debris and necrotic tissue, and application of proper dressing

Dirty or Infected Wounds: left open to heal by secondary intention or delayed primary closure

Clean lacerations may be closed primarily Tangential abrasions and road rash injuries – should be

approached similarly to 2nd degree burns Degloving injuries – considered 3rd degree or full

thickness burns Degloved skin may be partially salvaged by placing it back

on the wound like a skin graft Bite wound:

o Whether from human or animal, is a contaminated wound and should not be closed primarily

o Except on selected facial wounds, that may be closed primarily after very thorough cleansing and initiation of antibiotic therapy

o Clenched fist injury: most serious human bite; occurs when the closed fist hits a person’s teeth (fight bite)

Common infectious organisms found with human bites include Viridians strep., S. Aureus, Eikenella corrodens, H. Influenza and beta lactamase producing bacteria

Management: drainage, copious irrigation, antibiotic therapy, extremity immobilization and elevation

o Dog bites: most common animal bite wound Crushing type injury Most common organisms include:

Pasteurella multocida, Staphylococcus, alpha haemolytic streptococci, Eikenella corrodens, Actinomycetes, Fusobacterium

Management: copious irrigation, debridement of devitalized tissue and antibiotic therapy

PROLONGED PRESSURE Bed sores (pressure sores) As pressure is applied to overlying tissues, cutaneous

vascular flow is decreased, rendering local tissues functionally ischemic

Varying depth of skin-subcutaneous tissue destructions Patients unable to sense pain or shift their body weight,

such as paraplegics or bedridden individuals, may

develop prolonged elevated tissue pressures and local necrosis

Pressure Ulcers (Decubitus Ulcerans) Caused by excessive, unrelieved pressure 60mmHg or pressure applied to the skin for 1 hour

produces histologically identifiable injuries such as venous thrombosis, muscle degeneration, tissue necrosis

Normal arteriole, capillary, venous pressures (32, 20 and 12mmHg respectively)

300mmHg – pressure on ischial tuberosities while a person is eated

100-150mmHg – sacral pressure while a person lies on standard hospital mattress

Muscle tissue more sensitive to ischemia than overlying skin

Necrotic area usually wider and deeper than it appears on first inspection

TREATMENT: relief of pressure with special cushions and beds and nutritional support to promote healing

o Removal of necrotic tissueo Shallow ulcers: may close by secondary

intention but deeper wounds with involvement of the underlying bone require surgical debridement and coverage

o Stable coverage should be obtained with local musculocutaneous or fasciocutanoeus flaps

PREVENTION: close attention to susceptible area and frequent repositioning of paralyzed patients

Exposure to caustic substances May be categorized as resulting from either acidic or

alkali If ACID:

o Hydrofluoric acid: colourless, fuming fluid that is corrosive to the skin

Cause extensive liquefaction necrosis and severe pain

Deep tissue injury may result, damaging nerves, blood vessels, tendons and bone

initial treatment includes copious skin irrigation for at least 30 minutes with either saline or water

Second aspect of treatment: inactivate free fluoride ions by promoting formation of insoluble fluoride salts

Topical Calcium Carbonate Gel: detoxify the fluoride ion and relieve pain

Treatment: massage 2.5% calcium carbonate for at least 30 minutes 6x/day for 4 days

o Sulfuric Acid Cause full-thickness tissue necrosis Treatment: immediate copious

irrigation; dilutes and removes sulphuric acid while returning skin to normal pH

o IVF extravasation Leakage of injectable fluids out of the

vein into the interstitial space Most common substances that

extravasate: cationic solutions (ex.

Poptassium ions, calcium ions, bicarbonate)

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osmotically active chemicals (ex. Total parenteral nutrition or hypertonic solutions)

antib iotics cytotoxic drugs

Commonly infused drugs that extravasate: Doxorubicin and Paclitaxel

Most common site of extravasation in adult: dorsum of hand (result in exposed extensor tendons and loss of function)

Cause tissue necrosis from chemical toxicity, osmotic toxicity or from the effects of pressure in a closed environment

Treatment options: varies from early debridement to observation

Surgery- limited to patients with necrotic tissue damage, pain or damage of underlying structures such as tendons or nerves

If ALKALI:o Penetrates skin, cause saponification of fat,

allows for deeper penetration and increased tissue damage

o Management: immediate irrigation of the affected area with continuous water flow should be maintained for at least 2 hours, or until symptomatic relief is achieved

o Management should be rapid as the tissue damage produced is progressive once penetration is achieved

o Large wounds: require additional reconstructive surgery

o Neutralization of alkaline wounds demonstrated a more rapid return to physiologic pH, less severe tissue damage and improved wound healing

TEMPERATURE

Hyperthermic injuryo Cause varying degrees of tissue injury,

depending on temperature and length of exposure

o Tissue is damaged from heat coagulation, becomes necrotic tissue

o Surrounding zone of coagulation is the zone of stasis, which has a marginal tissue perfusion and questionable viability

o Zone of hyperaemia is closest to the normal tissue and represents the tissue’s response to injury with an increase in blood flow

Hypothermiao Defined as core body temperature less than

35 degrees Celsiuso Frostbite : acute freezing of tissues

Severity related to duration of exposure and to the temperature gradient at the skin surface

Tensile strength of a healing wound decreased by 20% in cold (12 degrees Celsius)

Severe hypothermia: primarily affects the vasculature as the blood vessels become severely injured by a combination of direct

cellular injury or microvascular thrombosis

Treatment: rapid rewarming, close observation, elevation and splinting, daily hydrotherapy, serial debridements

RADIATION Medical Radiation

Acute radiation changeso Basal epithelial cell deatho Dry squamationo Moist desquamationo Cellular repairo Permanent hyper pigmentation

Chronic radiation changeso Loss of capillarieso Hypovascularityo Ulceration

Solar radiation – most common form of radiation exposure

UVA – spectrum 400-315 nm UVB – spectrum 315-290 nm

o Causes sunburn, chronic skin damage leading to malignancy

o Only less than 5% of UV gets thru the skin UVC – spectrum 290-200 nm

o Filtered by ozone layer

Inflammatory reactions of the skin (immunologic)

TOXIC EPIDERMAL NECROLYSIS (TEN) SSSS and TEN creates a similar clinical picture

including skin ertythema, bullae formation, and wide areas of tissue loss

Immunologic reaction to drugs like sulfonamides, phenytoin, barbiturates, and tetracycline

If epidermal detachements is <10% it is called “steven-Johnson’s syndrome”

Whereas if more than 30% of total body surface area involvement are classified as TEN

TEN has similar damaged as 2nd degree burns Diagnosis is made via skin biopsy Skin biopsy differentiates TEN from SSSS

o TEN – cleavage in dermoepidermal junctiono SSSS – cleavage in granular layer of epidermiso Management is fluids, electrolytes and proper

wound care like in burns

Viral infectionsHUMAN PAPILLOMA VIRUSWarts: epidermal growths resulting from the human papillomavirus infection

1. Common warts (verruca vulgaris) found in the fingers and toes and is rough and bulbous

2. Plantar warts (verruca plantaris) occur in the soles and palms and may resemble common callus

3. Flat warts (verruca plana) are slightly raised and flat appearing on face, legs and hands

4. Venereal warts (condyloma acuminate) from HPV types 6 and 11, grow in moist area around vulva, anus and scrotum

Characteristic of WartsHyperkeratosis (hypertrophy of horny layer)Acanthosis (hypertrophy of spinous layer)Papillmoatosis

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TREATMENT: removal via application of chemicals (formalin, podophyllum, phenol-nitric acid)Curettage with electrodessicationSurgical excision under general anesthesiaRecurrences are common; repeated excisions often are necessary to eliminate lesionsAdjuvant tx: interferon, isotretinoin, or autologous tumor vaccine decreases recurrence rates

HUMAN IMMUNODEFICIENCY VIRUS Develop chronic wounds: because of wound healing

deficiencies Risk of surgical wound complications increases with

the progression of the disease Delayed wound healing is thought to be secondary

to a decreasing Tcell CD4 count, presence of an opportunistic infection, low serum albumin, and poor nutrition

Wounds of the HIV patients have a lower resilience, toughness, and maximum extension

o Resilience: ability of tissue to endure loads without inducing a tension exceeding the elastic limit

o Toughness: property of tissue enabling it to endure loads

o Maximum extension: displacement of tissue at the point of wound rupture

Bacterial InfectionsSTAPHYLOCOCCAL SCALD SKIN SYNDROME

Erythema, bulla, wide areas of skin loss SSSS – is caused by an exotoxin produced during

staphylococcal infection of the nasopharynx or middle ear

Clinical picture is similar to 2nd degree burns Caused by exotoxin produced during a staphylococcal

infection of the nasopharynx or middle ear in the pediatric population

PYODERMA GANGRENOSUM Relatively uncommon Associated with underlying systemic disease like

o IBD, hematologic malignancy, monoclonal IgA gammopathy

Management:o Treat underlying causeo Local wound careo Skin graft if necessary

Inflammatory reactions of the skin (infection)FOLLICULITIS

Infection of the hair follicle Causative organism is usually Staph, but gram (-) may

also cause as well Folliculitis furuncle (boil) fluctuant nodule

abscess rupture resolves

CARBUNCLE Deep-seated infection of the skin and underlying tissue

that typically forms in closely placed hair follicles Result in multiple draining cutaneous sinuses More difficult to treat: requires incision and drainage

or wide excision of the infected tissue and sinuses TREATMENT: warm soaks + antibiotics

CELLULITIS A superficial, spreading infection of the skin and

subcutaneous tissue Erythema, warmth, tenderness and edema Most common organisms associated are:

o Group A streptococcio Staph. Aureus

NECROTIZING SOFT TISSUE NECROSIS Necrotizing infections – denoting rapid spread

associated with septic shock Fournier’s Gangrene: abrupt, rapidly progressive

gangrenous infection of the external genitalia, perineum or abdominal wall

Meleney’s Gangrene: lethal and rapidly progressive soft tissue infection caused by microaerophilic streptococcus

Synergistic Gangrene: characterized by a symbiosis or anaerobic strep and staph

Basis of Classification:o The tissue plane affected and extent of

invasiono Anatomic siteo Causative pathogens

DEEP SOFT TISSUE INFECTIONS Necrotizing fasciitis: rapid, extensive infection of the

fascia deep to the adipose tissue Necrotizing Myositis: less common, involves muscles

and spreads to adjacent soft tissueso Most common organisms : Gram +

organisms, group A strep, etc.o Necrotizing soft tissue infections require

early recognition and intervention Treatment: broad- spectrum antibiotics, aggressive

surgical debridement, ICU Aggressive fluid replacement to offset acute renal

failure from ongoing sepsis and shock Debridement should be extensive, including all skin,

subcutaneous tissue and muscle until there is no further evidence of infected tissue, return to OR for debridement as necessary

HIDRADENITIS SUPPURATIVA Is a defect of the terminal follicular epithelium Apocrine gland blockage with obstructed infection

leads to abscess formation Arises most commonly on apocrine gland bearing

skin(axilla, inguinal and perianal regions) Treatment of acute infections includes application of

warm compress, antibiotics, and open drainage In cases of chronic hidradenitis, wide excision is

required and closure may be achieved via skin graft or local flap placement

PILONIDAL DISEASE Infected pilonidal cysts of the sacrococcygeal region Jeep driver’s disease is associated with a higher

incidence of pilonidal disease Acute pilonidal abscesses should be incised and

drained Treatment of chronic sinus tract: tract curettage.

Local excision and closure, wide excision and marsupialisation, wide excision and flap closure

ACTINOMYCOSIS Granulomatous suppurative bacterial disease caused

by Actinomyces Occur in craniofacial skeleton and mandible Usually caused by tooth extraction, odontogenic

infection or trauma MYcetomas : deep cutaneous infections that present

as nodules and spread to form draining tracts to the skin and surrounding soft tissue

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Most common site for infection is the foot : Madura foot

Treatment: penicillin and sulphonamides

LYMPOGRANULOMA VENERAUM Causative Agent: Chlamydia trachomatis Inconspicuous ulcer appears on penis or labia Nodes become very large and painful (buboes) and

are occasionally confused with an incarcerated inguinal hernia

Treatment: active infection: doxycycline for 1 week Azithromycin: in one dose for uncomplicated disease

and 14 days of treatment with doxycycline for complicated disease

ATYPICAL MYCOBACTERIUM Mycobacteria causing cutaneous disease: M.

fortuitum, MAC, M. ulcerans, M. Marinum (acquired through handling of fish tanks)

Lesions often associated with immunosuppression Burull’s Ulcer – skin ulcer due to Mycobacterium

BENIGN NEOPLASMS of the skin CYST – epidermal, dermoid, trichilemmal

DERMOID CYST May be noted at birth Commonly ignored until they become infected Location:

o Common in midline areas, nose, forehead, also in lateral eyebrow

o Rationale: epithelium trapped during midline closure

The cyst wall orientationo Epidermis is towards the inner side of the cysto Desquamated cells accumulate in the centero Creamy substance

Treatment:o Non-infected cyst – excisiono Infected cyst – incision and drainage is controlled

and antibiotics

EPIDERMAL INCLUSION CYST (EIC) Most common type of cutaneous cyst

TRICHILEMMAL CYST Second most common cutaneous cyst Usually in scalp More common in women Emits foul odor when ruptured

NEVUS Maybe acquired or congenital

ACQUIRED NEVUS Junctional, compound, dermal – varying stages in

maturation Accumulate in epidermis (junctional) Migrate into dermis (compound) Rest completely in dermis (dermal)

CONGENITAL NEVUS Uncommon among neonates (<1%) Large with hair 1-5% chance of malignancy Management: excision

HEMANGIOMA Benign vascular neoplasms that arise soon after birth Undergo rapid cellular proliferation and slowly

involute through early childhood

Enlarge during first year of life, and more than 90% of them involute over time

Allowing lesions to regress spontaneously usually gives optimal cosmetic results

CAPILLARY HEMANGIOMAS Soft, compressible popular lesions with sharp

borders located mostly on the shoulders, face and scalp

Composed of endothelial cells seen primarily in fetal veins

CAVERNOUS HEMANGIOMA Bright red or purple and have a spongy consistency Lesions contain large, blood filled spaces lined by

normal appearing endothelial cells

TREATMENT: limited to lesions that interfere with bodily function

Prednisone Interferon alpha-2a treatment Hemangiomas that remain after early

adolescence will not generally involute, therefore surgical excision is recommended

BENIGN NEOPLASMS/ Soft tissue tumorsACROCHORDON (skin tags)

Fleshy masses at axilla, neck, trunk, eyelids with a stalk (pedunculated)

DERMATOFIBROMA Often solitary 1-2 cm in diameter Can be found at any age Round to oval, firm nodules Deep component is attached to overlying skin a few

millimeters to several centimeters away Not encapsulated and vascularity is variable Pink to brown, darker in the center Commonly in legs, thighs, arms, and sides of trunks Etiology:

o Possibly a scar-like reaction to insect bites Behavior is slow growing Management is excision

LIPOMA Most common subcutaneous neoplasm Commonly seen in the trunk Managements:

o Excision – tumor is lobulated containing fat tissues

CAPILLARY HEMANGIOMAS 50% occurs in the head and face 3:1 ratio of females to males Present in 1-2% of neonates Grossly evident and frequently observed 90-100% of lesions is evident by 6-8 months Spontaneous involution is the rule

o 40% completely involutes by age 4o 80% completely involutes by age 8

Red or purple elevated, subcutaneous soft mass that blanch with pressure

May have both cutaneous and subcutaneous portions of the lesion

Management:o Intralesional steroid injection – with a mix of

long and short acting steroids (ex. 40mg/ml of triamcinolone and 6mg/ml of betamethasone mixed

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o Oral prednisolone – treatment is usually for months with slow taper (ex. 1-2mg/kg/day given)

o Surgical excision (for debulking) – lesion is not encapsulated and there is a risk of recurrence. Anticipate and control bleeding

o Other treatments: Topical steroids, radiation, and a variety

of lasers considered somewhat controversial and not used routinely

NEURILEMOMAS Solitary tumors found along peripheral nerves of the

head and extremities Discrete nodules that may be locally painful or

radiate along the distribution of the nerve

GRANULAR CELL TUMORS Solitary lesions of the skin or more commonly the

tongue Granular cells derived from Schwann cells that often

infiltrate the surrounding striated muscle

VASCULAR MALFORMATIONS Benign lesions that are present at birth Do not have the rapid growth cycle followed by

involution or regression of hemangioma They continue to grow slowly as the child grows

throughout life Vascular malformations include: port wine stain,

sturge-weber syndrome and klippel-trenaunay syndrome

Port Wine Stains Usually sporadic, occasionally autosomal dominant

inheritance Initially pink or red and grow in proportion to infant

growth Lighten in the first few months, later generally darkens

Sturge-Weber syndrome PWS forehead (V1 area of the trigeminal nerve) Eye abnormalities (choroidal vascular abnormalities,

glaucoma) Leptomeningeal and brain abnormalities (vascular

malformations, calcification, or cerebral atrophy)

Klippel-Trenaury syndrome With a capillary malformation and overgrowth of the

soft tissue and bone of the affected limb

NEURAL TUMORS Neurofibroma

Soft, dome-shaped, skin colored, asymptomatic Very common as a single or few scattered lesions Multiple lesions may be associated with

neurofibromatosis Closely resembles intradermal nevus clinically

Predisposing factors in cutaneous Malignancy UV exposure – predisposing factor to all 3 common

neoplasms Chemicals – tar, arsenic, and nitrogen mustard are

carcinogens Human Papilloma virus – oncogenesis of SCC Radiation therapy – results to chronis dermatitis that

increases incidence of BCC and SCC Chronic irritation of skin scar like in Marjolin’s ulcer in

burns Repeated sloughing of skin in bulla diseases Decubitus ulcers Immunodeficiency

Pre-cancerous Lesions Actinic keratosis Leukoplakia Paget’s disease Bowen’s disease Marjolin’s ulcer

KERATOSES Occur on chest, back and abdomen of older individuals Lesions are light brown or yellow and have a velvety,

greasy texture

SOLAR OR ACTINIC KERATOSES Arise in sun exposed areas of the body, such

as the face, the forearms and the back of the hands

Contain atypical appearing keratinocytes and evidence of solar damage in the dermis

May be premalignant lesions, squamous cell carcinoma may develop over time (20%)

TREATMENT: Liquid nitrogen cryotherapy Topical therapies: 5-FU (efudex),

imiquimod (aldara) Electrodessication and curettage for

hypertrophic lesionsLEUKOPLAKIA

Predisposing factors: (ex. Chewing of tobacco) Found on mucous membrane (mouth, vulva, rectum) Treatment:

o Cryotheraphyo Cessation of predisposing factors

BOWEN’s DISEASE (Squamous cell carcinoma in situ) Erythematous, sharp, irregular outline with crusting

center Multiple lesion often present Approximately 5% become invasive carcinoma Excision is most widely accepted treatment In penis, vulva, or oral cavity – Erythroplasia of Queyrat

MARJOLIN’s ULCER Aggressive ulcerating squamous cell carcinoma

presenting in an area of previously traumatized, chronically inflamed, or scarred skin

Commonly seen in patients with burns, venous ulcers, post radiotherapy scars, etc.

MALIGNANT NEOPLASMS

BASAL CELL CARCINOMA (BCC) Skin cancer that arises from the basal layer cells Most common among skin cancers (>90 percent of all

skin cancers) 4x more frequent than SCC Large, slow growing but highly locally destructive Seldom spreads to other parts of the body Death from metastasis is rare (<1% of cases) Generally is readily treatable 3 common types of BCC:

NODULO-CYSTIC or NODULO-ULCERATIVE typeo 70% of basal cell carcinomao Waxy appearance with rolled pearly borders

with central ulcero “Rodent ulcers” when largeo Chronic lesion that bleeds easily with pearly

bordero Surface telangiectasias

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o Common in the head, neck, trunk, and extremities

PIGEMENTED BASAL CELL CARCINOMAo Tan to dark coloro Must be differentiated from that of melanomao Similar to nodular but with black discolorationo Common in face, trunk, and scalp

SUPERFICIAL BASAL CELL CARCINOMAo Erythematous scaly plaqueo Slow growtho Asymptomatico Commonly in the trunk, face, extremities o Form a red scaling lesion that is difficult to

differentiate from Bowen’s disease

Less common types of BCC: BASO-SQUAMOUS BCC

o Rare type with elements of both???o Aggressive early metastasis treat

aggressively

MORPHEAFORM BCCo resembles a scaro asymptomatic and slow growingo ill-defined marginso marked subclinical extension

Management of Basal Cell Carcinoma (BCC) Small lesions (less than 2mm)

Electric dessication Laser vaporization – provides no tissue for biopsy

Larger lesions or lesions invading bones, or surrounding structures or the more aggressive type Excision with 2-4 mm margin of normal tissue

Characteristics of SQUAMOUS CELL CARCINOMA (SCC) Arises from the keratinocytes Less common but more aggressive and locally

destructive In situ lesions “Bowen’s Disease” In penis – “Eryhtroplasia of Queyrat”

Biologic Behavior of SQUAMOUS CELL CARCINOMA (SCC) Thickness of tumor correlates well with aggressiveness

o 4mm thick – locally destructiveo 10mm thick – likely with metastasis

Location of tumor correlates with aggressivenesso In burn wounds, chronic osteomyelitis, previous

injury early metastasiso In outer ear early lymph node involvement

and tends to recurrence

Management of SQUAMOUS CELL CARCINOMA (SCC) Excisions

o Lesions should be excised with 1cm margin to include invaded peripheral tissue

o Rationale: prevents or lowers recurrence Lymph node dissection

o Indicated when with palpable nodeso Indicated when without palpable nodes – if

lesions occur in chronic woundo Rationale: very aggressive behavior and cause

early metastasis Radiation

o For small and superficial lesionso Good cure rate; comparable to excision

Prognosis – metastatic lesion at 13% in 10 yearsMoh’s surgery for squamous and basal cell carcinoma

Uses serial excision in small increments coupled with immediate microscopic analysis

Has the ability to remove a tumor with minimal sacrifice of uninvolved tissue

All specimen margins are evaluated

MELANOMA Arised from transformed melanocytes anywhere

that the cells have migrated during normal embryogenesis

Occur anywhere, 90% occur in skin Nevi (freckles) : benign melanocytic neoplasm found

on the skin of many people Increase risk of tumor development Once transformed into malignant phenotype, tumor

growth occurs radially in epidermal plane 4 Types:

o Superficial spreading: occurs anywhere except hands and feet; flat and measure 1-2cm

o Nodular type: darker coloration and often raised, noted for lack of radial growth, vertical growth phase at diagnosis

o Lentigo Maligna: most frequently on the neck, face and hands of elderly, tend to be quite large at diagnosis, best prognosis because invasive growth occurs late

o Arcal lentiginous melanoma: least common subtype, common on palms, soles and subungual regions, common on great toe or thum, subungual lesions appear as blue-black discolorations of posterial nail folds

Hutchinson’s sign: proximal/lateral nail folds

(+) tumor at regional lymph nodes: poor prognosis

ABCD of Melanomao Asymmetry : shape of one half does not match

the othero Border- The edges are often ragged, notched,

blurred, or irregular in outline, the pigment may spread into the surrounding skin

o Color- The color is uneven. Shades of black, brown, and tan may be present. Areas of white, grey, red, pink, or blue also may be seen.

o Diameter- There is a change in size, usually an increase. Melanomas are usually larger than than the eraser of a pensil (5mm or ¼ inch).

Diagnosis: Excisional/ incisional biopsy Treatment:o Surgery

1st line option Primary treatment Offers the only hope for cure

o Excision biopsy Most tumor are treated by excision with

1mm margin For all suspicious lesions excision biopsy Large lesions need to have incision biopsy

(+) malignancy excision Excision margins:

If lesion is 1mm or less = 1cm marginIf lesion is 1-4mm = 2cm marginIf fascia is involved remove

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o Prophylactic Dissection : for intermediate thickness tumors without clinical evidence of nodular/metastatic disease

o Elective LN dissection: for intermediate thickness melanomas

o Regional Nodal dissection: all microscopically/ clinically positive LN

What to do if nodes are clinically involved If clinically positive lymph node regional node

dissection Lower extremities inguinal node dissection Upper extremities axillary node dissection Scalp, face, ear parotidectomy and neck

dissection

What to do if nodes are NOT clinically involved If the lesion is <0.75mm thick (stage I, II) no

dissectiono Rationale: nodes unlikely to be involved

If the lesion is >4mm thick wait and observe o Rationale: high morbidity, does not improve

survivalo Most patients already have distant

metastases before lymph node becomes clinically involved

If the lesion is intermediate thickness with (-) nodal or metastasis prophylactic dissection may or may not be done (controversial)

The trend is do prophylactic dissectiono Rationale: evidence of improved survivalo 25-50% of cases have metastatic cell in the

non-palpable nodeso 20-25% of cases eventually developed

metastases

Sentinel Lymph Node Biopsy Recommended for MM with Breslow 1-4 mm Lymphadenectomy for positive sentinel nodes Useful prognostic tool for disseminated disease It does not affect survival of patients

What if there are already distant metastases? It means 7 months median survival is less than 5%

for 5 year …. Survival Surgical excision whenever possible should be done Rationale: provides or improved palliation

Non-surgical treatment of melanoma INTERFERON ALPHA

o Adjuvant therapy for stage IIb and IIIo Help improve relapse-free interval and over

all survival GANGLIOSIDE VACCINES

o Cho antigen in the surface of the melanoma

Immunotheraphy for melanoma Boost’s patients’ natural defense against cancer Effective in reducing risk of recurrence Improves relapse-free interval and over all survival Used in combination with surgery and/or

chemotherapy or as part of a clinical trial Most commonly used are interferon alpha-2b and

interleukin-2 adjuvant therapy for stage IIb and III

Chemotherapy for melanoma LOCALIZED chemotherapy

If melanoma has not spread beyond a limb (arm or leg)

SYSTEMIC chemotherapy

Used when there is a high risk that the melanoma may spread or

To control advanced disease Combinations of medications are being tested in

clinical trials

Radiation therapy for melanoma Indications:

o To relieve symptoms caused by melanoma that has spread

o When surgery for a larger melanoma is limited by tumor location

o As adjuvant therapy for: After lymph node removal, or In combination with chemotherapy

Prognosis : Clark’s Staging (relates to level of invasion of tumor)

Stage Description DefinitionStage 0 “cancer in situ”

Non invasive CALesion contains CA cells only in outer layer of skin

Stage Ia Size is <1.0mm No ulcerationClark’s Level II/III

Stage Ib Size is <1.0mm (+) ulcerationsClark’s level IV/V invasion

ORSize is between 1.0mm -2.0mm(-) ulcerations

Stage IIc Size is larger than 4.0mm(+) ulceration

Stage III CA spread to nearby LN/ or there is in transit/ satellite involvement

Any tumor size(-) spread to other parts of the body

Stage IV Any tumor size(+) spread to other parts of the body beyond the LN

Breslow’s Staging (Modification of Clark’s staging) lesions thickness are measured from the granular layer

of the tumor or the base of the ulcer to the deepest part of the tumor (using ocular micrometer)

Tumor I 0.75mm or lessTumor II 0.76 -1.5mmTumor III 1.6- 4mmTumor IV >4mm

TNM system (AICC)

The T in Breslow is now incorporated to the TNM system by the AICC

considers not only the T (tumor), but also N (lymph nodes), M (metastasis)

Node involvement poor prognosis Automatically advances the stage to stage 3 Metastatic lesions- means median survival 2-7 months

Other factors affecting prognosis1) Location: Face poorer prognosis (68% 10-year survival

rate) than innExtremeties (82% 10-year survival rate

2) Ulceration: In stage 1, without ulceration has --78% 10 year SR

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With ulceration— 50% 10 year SR3) Gender:

In stage 1, Women has 80% 10 year Survival rate while men have 61 10 year survival rate

4) Histologic type:Lentigo maligna— better prognosisAcral lentiginous—worst prognosis

Who is at risk for skin cancer? Light skin color, hair color, eye color Family history of skin cancer Personal history of skin cancer Certain types and large number of moles Freckles, which indicate sun sensitivity and sun

damage Chronic exposure to the sun History of sunburns early in life

Other malignancies of the SkinMERKEL cell carcinoma

Primary neuroendocrine cancer of the skin that has neuroepithelial origin

Associated with synchronous or metachronous SCC in 25% of cases

Biologic Behavior:o Aggressive with tendency for metastases (in 1/3

of patients) Management:

o Wide (3cm margin) excisiono Prophylactic node biopsy and radiation theraphy

is recommended Prognosis:

o Worse than malignant melanomao Recurrences after treatment is high

KAPOSI’S SARCOMA Rubbery bluish nodules that occur in extremities Multifocal rather than metastatic Composed of capillaries lined by atypical endothelial

cells AIDS related Tx: radiation, surgery, chemotherapy

EXTRAMAMMARY PAGET’S DISEASE Pruritic red patch that doesn’t resolve Diagnosis: Biopsy

ANGIOSARCOMA Common in the:

o Scalp, face, or neck, or in post radiation area, chronic edematous area (post mastectomy arm) Stewart-Treves syndrome

Looks like bruise, bleeds easily Chemo and radiation provides better palliation Prognosis:

o Poor prognosis less than 20% 5 year survival

DERMATOFIBROSARCOMA PROTRUBERANS All soft tissue sarcomas in persons aged 20-50 Common in males: trunk, proximal extremities head

and neck Pink nodular lesion that may ulcerate and become

infected Tx: radiotherapy, chemotherapy

FIBROSARCOMA Hard irregular masses found in subcutaneous fat Marked anaplastic with disorganized growth

Tx: Excision

LIPOSARCOMA Arise in the deep muscle planes from subcutaneous

tissue Commonly on the thigh Tx: wide excision (treatment of choice)

o Radiation therapy for metastatic disease

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