skin tumours prof.k.s.ravishankar m.s,f.i.c.s shree balaji medical college
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SKIN TUMOURS
PROF.K.S.RAVISHANKAR M.S,F.I.C.S
SHREE BALAJI MEDICAL COLLEGE
ANATOMY OF SKIN
SKIN TUMOURS SITES
CLASSIFICATION OF SKIN TUMOURS
• BENIGN
EPIDERMAL• SEBORRHIC KERATOSIS• PAPILLOMA• TRICHILEMMAL TUMOUR• SEBACEOUS ADENOMA• SEBACEOUS EPITHELIOMA• HYDROCYSTOMA,SYRINGOMA,SPIRADENOMA
DERMAL -NEUROFIBROMA
– DERMATOFIBROMA
CLASSIFICATION OF SKIN TUMOURS
• MALIGNANT TUMOURS– SQUAMOUS CELL CARCINOMA– BASAL CELL CARCINOMA– MALIGNANT MELANOMA– MALIGNANT SKIN ADNEXAL
TUMOUR– SECONDARIES IN SKIN (eg.
sister joseph nodule)
SKIN ADNEXAL TUMOURS
• Tumours arising from accessory skin structures like sebaceous glands , sweat glands , hair follicles
•CLASSIFICATION– ECCRINE GLAND TUMOURS
•Syringoma , Hidradenoma,Syringo cystadenoma
– HAIR TUMOURS•Trichoepithelioma,Tricholemmoma
PRE MALIGNANT LESIONS• Actinic Keratosis- 5-20% will develop
Squamous/basal cell ca• Actinic Cheilitis• Paget’s disease of nipple• Xeroderma pigmentosa• Chronic Radiation Keratosis• Bowen’s Disease• Bowenoid Papulosis• Leukoplakia / Erythroplakia• Dysplastic Melanocytic Nevi (DMN)
BCC AND SCC
Risk factors:-• ACTINIC LIGHT:- 90% OF TUMORS
OCCURS IN SUN EXPOSED AREAS.
• ARSENIC:- EXPOSURE PREDISPOSE TO DEVELOPMENT OF BOWENS DISEASE,MULTIPLE SCC AND BCC.
• IRRADIATION:-FOR BENIGN CONDITIONS
• COAL TAR EXPOSURE• IMMUNOSUPPRESSION:-POST TRANSPLANT
• CHRONIC INFLAMMATION AND TRAUMA:-
CHRONIC OSTEOMYELITIS, FISTULAS,THERMAL OR ELECTRICAL BURNS.
• ATROPHIC SKIN LESIONS:-DISCOID LUPUS.
• VACCINATION SCARS.
HEREDITARY FACTORS• XERODERMA PIGMENTOSA:-AUTOSOMMAL RECESSIVE.• BASAL CELL NEVUS SYNDROME:AUTOSOMAL
DOMINANT.
INFECTIVE FACTOR;-• HUMAN PAPPILOMA VIRUS TYPES 5 AND 8:- VERRUCUS• SCC OF GENITALS:-HPV 16&18• PERIUNGUAL SCC.
Xeroderma pigmentosaActinic keratosis
Bowen’s disease of penisLeukoplakia
BASAL CELL CARCINOMA
• Most common skin cancer arising from the basal layer of epidermis and its appendages
• Low metastatic potiential• Locally invasive,
aggressive, and destructive to skin and bone.
ETIOLOGY OF BCC• Sun exposure is the most important environmental
cause of BCC.
• Ionizing radiation causes mutation of tumor suppressor genes
• UV B light: 280-320nm, UV A light 320-400nm
• Amount of UV B exposure during childhood and adolescence is directly proportional to risk for BCC
Clinical presentation
Distribution of BCC: 70% on face 25% on trunk 5% on penis, vulva, or perianal skin
Clinical subtypes (4) Nodular- most commonSuperficial- small buds of tumour massesPigmented- resembles naevus or melanomaMorpheaform- aggressive behavior, worst
prognosis
NODULAR PIGMENTED
SUPERFICIAL MORPHEA FORM
DIAGNOSIS
Initial evaluation involves
Assessment of location
Punch or excisional biopsy
Staging
SQUAMOUS CELL CA
SQUAMOUS CELL CA TYPES
• Bowen’s disease– SCCA in situ– Full thickness
dysplasia
• Bowenoid SCCA– Looks like bowen’s– Invades through BM
• Adenoid SCCA– Nodular ulcerative
lesion– Often periauricular
• Generic SCCA– Most common
– Highest rate of metastasis
• Verrucous SCCA– Verruciform lesions
– Invades by blunt, pseudopod-like growth
• Spindle SCCA– Indistinct clinically
CLINICAL FEATURES
• An ulcerative or ulceroproliferative lesion
• Raised and everted edge
• Indurated, bloody discharge from lesion +
• Regional lymph nodes commonly involved
• Variants- marjolin’s ulcer and verrucous carcinoma
Histology of SCC
• Malignant whorls of squamous cells with epithelial or keratin pearls are characteristic.
• Broder’s classification:– I-Well differentiated:75% keratin
pearls– II-Moderately differentiated: 50%
keratin pearls.– III- Poorly differentiated: 25%
keratin pearls– IV- < 25% keratin pearls
DIAGNOSIS• Although the diagnosis of SCC is often
strongly suspected based on clinical findings, a skin biopsy is required for definitive diagnosis.
• A shave biopsy, punch biopsy, incisional biopsy, or excisional biopsy, wedge biopsy may be used.
• All skin biopsy samples obtained to diagnose SCC must reach at least the depth of the mid dermis to allow for determination of the presence or absence of invasive disease.
STAGING• TX - Primary tumor cannot be assessed• T0 - No evidence of primary tumor• Tis - Carcinoma in situ• T1 - Tumor less than 2 cm in greatest
diameter• T2 - Tumor 2-5 cm in greatest diameter• T3 - Tumor greater than 5 cm in greatest
diameter• T4 - Tumor with deep invasion into
cartilage, muscle, or bone.
Regional lymph nodes[N]• NX Regional lymph nodes cannot be
assessed• NO No regional lymph node metastasis• N1 Regional lymph node metastasis,
DISTANT METASTASIS[M]• MX Presence of distant mets cannot
be assessed • M0 No distant metastasis• M1 Distant metastasis
MANAGEMENT• ACTINIC KERATOSIS:-LIQUID NITROGEN ,
ELECTRICAL CURETTAGE.
• BCC:-TRADITIONAL SURGICAL RESECTIONS, MOH’ S MICROGRAPHIC SURG
INDICATIONS FOR MOH’S SURG:-• LOCATED IN REGIONS WHERE HIGH RISK
FOR TUMOR RECURRENCE AREAS,• DIAMETER >1CM ON FACE,• PERINEURAL INVASION,• MORHEFORM,SCLEROTIC AND INFILTRATIVE
TYPE BCC.
• ELECTRO CURETTAGE, CRYOSURGERY, RADIOTHERAPHY,
EXTENSIVE RESCTION AND RECONSTRUCTION: -AMPUTATION IN CERTAIN CASES
• CHEMOTHERAPHY:- NO ADJUVANT ROLE,MAY BE OF USE N
METASTATIC SKIN LESIONS
SUPERFICIAL BRACHYTERAPY
MOH’S SURGERY
FOLLOW UP• Low-risk tumors are usually cured with
appropriate surgical therapy; recurrence may occur.
• Thus, patients with a history of SCC should be evaluated with a complete skin examination every 6-12 months.
• Patients with high-risk tumors require skin and lymph node examinations at 3- to 6-month intervals for at least 2 years after diagnosis.
Marjolin’s ulcerWell differentiated squamous cell ca that occurs in chronic scars like burn scar, scar of venous ulcer
No lymphatics in scar tissue hence no spread to regional lymph nodes.
Scar contains no nerves, hence painless.
Wide excision or amputation for larger lesions
Radiotherapy contraindicated for fear of transformation into poorly differentiated sq cell ca.
Verrucous cancer Dry, exophytic,warty growth
No lymph node spread
No blood spread
Surgery is the treatment of choice- wide excision
Examples:
1. Giant Condyloma Acuminatum (Buschke-Lowenstein tumour)- in genitalia
2. Carcinoma cuniculatum-( Verrucous ca of feet)
3. Oral florid verrucous ca
Melanoma - Outline
• General statistics and development• Risk factors and patient assessement• Pathology and prognosis• Work-up and staging• Surgical treatment• Lymph node controversy/sentinel
node • Adjuvant therapy
Melanoma - Statistics
• Mortality increase 2nd only to lung• 5th most prevalent, incidence 7%/year
increase• 5% skin cancer, 75% skin cancer death• Men common sites- front and back of
trunk• Women common sites- lower leg• Mostly arise from benign naevus or
adjacent area
Development of Nevi
• Junctional nevi– nests along dermal-epidermal junction
• Compound nevi– “invade” dermis, first as nests then cords and
single cells• Dermal nevi
– junctional component lost only in papillary and reticular dermis
Histologically, nevi are classified generally as having atypical cells, as in dysplastic nevi, or normal cytology, as in the common nevus.
Junctional Nevi
Compound Nevi
Dermal Nevi
Dysplastic Nevi
Types of Melanoma
• Acral lentiginous• Amelanotic melanoma• Superfical spreading melanoma• Lentigo maligna melanoma• Nodular melanoma
Superficial spreading
• Most common, 70% of all melanomas• 4th to 5th decade• Clinically variable
pigmentation,irregular borders, biphasic growth
• Histologically-asymmetry, poor circumscription and lack of maturation
Superficial spreading
Lentigo maligna
• 20% of cutaneous melanomas• Most benign form of melanoma• Longest radial growth phase >15
yrs• Occurs in Hutchinson’s freckle• Elderly sun exposed areas• Clinical dark, irregular ink spot
Lentigo maligna
Nodular melanoma
• 12% of all melanomas• Most malignant type• Aggressive vertical growth phase• Sun-exposed and nonexposed
areas• Usual presentation- darkly
pigmented raised nodule
Nodular melanoma
Acral lentiginous melanoma
• Occurs in palms,soles and subungual areas
• Worse prognosis than superficial spreading
• Pigment spread to the proximal or lateral nail folds is termed the Hutchinson sign, which is a hallmark for acral lentiginous melanoma.
AMELANOTIC MELANOMA
• Appear pink but close inspection reveals pigmentation
• Lack of pigmentation causes delay in diagnosis.
• Worst prognosis of all melanomas
Melanoma
• 70% of melanomas occur on a pre existing nevus.
• 30% of melanomas occur de-novo
When to suspect malignant transformation in a mole?
• Asymmetrical outline--- A• Border irregularity-------B• Colour change------------C• Diameter>6mm-----------D• Elevation------------------E
Diagnosis• Excision biopsy of suspected lesions
mainstay of diagnosis• Performed with 1-2mm margin and has to
be full thickness to ascertain the following:– Tumor thickness (Breslow depth)– Presence of ulceration– Anatomic level of invasion (Clark level)– Presence of mitoses– Presence of regression– Lymphatic/vessel invasion or vascular
involvement– Host response (tumor-infiltrating lymphocytes)
• LYMPHATIC SPREAD:-SINGLE REGIONAL LYMPHNODES[N1],
• MULTIPLE NODES{2-3 NODES}[N2A]
• SATELLITE NODULE AND INTRANSIT NODULES WITHOUT NODES
• MORE THAN FOUR NODES WITH INTRANSIT[N3].
DISTANT METASTASES:-METS TO SKIN SUBCUTANEOUS
TISSUE[DISTANT NODES]{M1A}{M1B} METS TO LUNG{M1C} ANY VISCERAL METS WITH RAISED LDH
SENTINEL LYMPH NODE BIOPSY
• Sentinel lymph node biopsy (SLNB) is indicated for pathologic staging of the regional nodal basin for primary tumors greater than or equal to 1 mm depth and when certain high-risk histologic features (eg, ulceration, extensive regression) are present in thinner melanomas < 1mm)
STAGING-CLARKE’S AND BRESLOW
Staging-Clark
• Level I - in situ at basement membrane
• Level II - through basement membrane into papillary dermis
• Level III - spread to papillary/reticular interface
• Level IV - spread to reticular dermis• Level V - sub-cutaneous invasion
Staging-Breslow
• <0.76 mm - thin• 0.76 - 1.49 - intermediate• 1.50 - 4.00 - intermediate• >4.00 mm - thick
Latest Breslow classification– <1mm- Thin melanomas– 1-4mm- Intermediate thickness
melanomas– >4mm- Thick melanomas
AJCC Staging
Work-up
• Labs and imaging– CXR , CT chest and LFT– H&N CT neck routine– If stage III(regional) or IV (distant) -
CT head, chest, abdomen, pelvis– Hpe: S-100 and homatropine
methylbromide (HMB45) stains are positive in melanoma.
Surgical Treatment
– Treatment of Primary (WLE)– Current recommendations for margins of
excision are as follows: •Lesions <1 mm in thickness - 1 cm
margin •Lesions 1-2 mm in thickness - 2 cm
margin •Lesions >2mm in thickness – 3 cm
margin• All depths to underlying muscle fascia
Management of lymph nodes
• SLN biopsy• Node dissection• Isolated limb perfusion
Adjuant chemotherapy• Cytotoxic drugs• Interferon• BCG
Metastatic disease• Bleomycin, Oncovin, Lomustin
Dacarbazin• Tamoxifen• interleukin
• Prognosis– anatomic site, ulceration, gender,
histologic type, nodal disease– head and neck, trunk and acral
regions worse prognosis– women better prognosis than men– Ulceration, angiogenesis and vascular
invasion-poor prognosis
PrognosisBreslow (thickness in millimeters) strongest predictor
Depth of tumor invasion
5 yr survival (%)
<0.5 mm 99
> 3 mm 30
Prognosis
Clark level less predictive, thin melanomas useful(<1mm)
Level
Tumor extent 5 yr Survival (%)
I Tumor is confined to epidermis (in situ) 100
II Tumor extends beyond basal lamina into papillary dermis
85
III Tumor extends into papillary dermis and abuts onto, but does not invade, the reticular dermis
65
IV Tumor extends into reticular dermis 50
V Tumor extends into subcutaneous fat 15
Prognosis• Survival according to regional
lymph node involvement
Node involvement
5 yr survival (%)
Negative nodes 75 (85% for negative SLN)
1 – 3 positive nodes 504 or more positive nodes
25
Prognosis• Survival according to metastatic spread
Stage
Extent 5 yr survival (%)
II Local recurrences within 3 cm of primary site
30
III Satellitosis <20
IV Distant metastases <10
ACANTHOSIS NIGRICANS
NECROLYTIC MIGRATORY ERYHTEMA
Thank You
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