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    Malignant Melaoma - PreFinal

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    Sukumaran S 130

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    Malignant Melaoma - PreFinal

    Uploaded by

    Sukumaran S 130
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    malignant Melaoma - PreFinal

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    5 views36 pages

    Malignant Melaoma - PreFinal

    Uploaded by

    Sukumaran S 130

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 36

    MALIGNANT

    MELANOMA
    MELANOMA

     It is a malignant tumour arising from epidermal melanocyte which is


    most aggressive cutaneous malignant tumour.
     It is of neural crest (ectodermal) origin.
     It is 20 times more commonly seen in whites than blacks.
     Its incidence is equal in both sexes.
     Its incidence is increasing over the years.
     Five per cent of skin cancers are melanomas.
     It is most common in Queensland, Australia. Auckland, New Zealand.
    Sites of Melanoma

     Head and neck-25%


     Trunk-25%
     Lower limb-25%
     Upper limb-11%
     Other sites-14%
     In females, leg is the commonest site.
     In males, the front or back of the trunk.
     In the Bantu tribe, sole is the commonest site
    Risk factors
     Exposure to sunlight (exposure to UV light; more common in white-skinned-20 times).
     Ethnic factors, socioeconomic status (high society), lifestyle, climate.
     Albinism.
     Xeroderma pigmentosa
     Junctional naevus.
     Familial dysplastic naevus syndrome.
     Sporadic dysplastic naevi.
     Large congenital naevi (larger than 20 cm).
     Family history of melanoma
     History of earlier skin cancers other than melanoma.
     Patients who are on immunosuppressive drugs or after renal transplantation or NHL
    Xeroderma pigmentosa

     RR is 1000
     It is an autosomal recessive (Ch 9q) disease with defect in DNA excision repair
    mechanism causing formation of aberrant nucleotide
     causing ‘ultraviolet rays’ intolerance, erythema, pigmentation, photophobia,
    premature skin ageing, severe sunburn, painful sun sensitive eyes with
    corneal ulcers, freckling and blistering of skin, dry, scaly, irregular skin,
    multiple malignancies with 60% mortality at the age of 20.
     Incidence is one in 1,00,000 people;
     more common in Japan.
     DNA repair assessment of skin and blood, amniocentesis or chorionic villous
    sampling in fetus can confirm it.
    Classifications
    Classifications
    Classifications
    Differntial diagnosis – other
    pigmented lesions

     Seborrhoeic keratosis, dermatofibroma


     Pigmented BCC, pigmented SCC
     Naevus, sebaceous epidermal naevus
     Kaposi’s sarcoma, mycosis fungoides
     Cutaneous haemangioma
     Certain skin adnexal tumours
     Solar keratosis
     Pyogenic granuloma
     Cutaneous angiosarcoma
    Types
    Clinical types
    1. Superficial spreading
     Most common. 70%.
     Occurs in any part of the body with variegated
    irregular look.
     has more radial growth and better prognosis.
     commonly arises from a pre-existing naevus.
     In men, common in back; in women in leg
    2. Nodular Melanoma 12-25%
     More aggressive.
     It is common in younger age group, occurring in any part
    of the body.
     has more vertical growth.
     Common in mucosa and mucocutaneous junction
     Uniform; nodular; more vertical growth
     nodal spread is common
     has got poor prognosis.
     It usually appears as de novo.
     Common in men; common in trunk, head and neck.
    3.Lentigo maligna melanoma
     7-15%.
     Less common, least malignant.
     Occurs in old age and common in face (Hutchinson’s
    melanotic freckle). I
     t is slow growing, variegated, brown macule/ lentigo;
     common in face/neck/hands;
     common in elderly women.
     Lentigo maligna is in situ type.
     4.Acral lentiginous melanoma:
     5%.
     Occurs in palms, soles and subungual region. It has got a
    poor prognosis.
     least common.
     Usually attains large size; nodular type with more vertical
    growth phase.
     common in Africa and Asia.
     less common in whites.
     often flat, irregular macule.
     mimics fungal infection/pyogenic granuloma
     Desmoplastic melanoma has high affinity for perineural invasion; is
    common in head and neck with higher recurrence rate. It is often
    amelanotic melanoma with thicker lesion carrying poor prognosis due
    to neural invasion.
    Spread

     Through lymphatics it spreads to regional lymph nodes either by


    permeation or by embolisation.
     In-transit nodules are seen in the skin between the primary lesion and
    regional lymph node area, and is due to retrograde spread to dermal
    lymphatics.
     Through blood: To lungs, liver (huge liver), brain, skin, bones. Secondaries
    are typically black.
     Melanoma in choroid has got better prognosis, because as there are no
    lymphatics, spread is delayed.
     Sometimes primary is very small and unnoticed (in anus, subungual
    region). They present with features of secondaries only.
    Investigations
     No incision biopsy. It can cause early blood spread.
     Excision biopsy of primary
     FNAC of lymph node
     US abdomen to look for liver secondaries (usually huge hepatomegaly occurs).
     Chest X-ray to look for secondaries in lung (“cannon ball” appearance). HRCT of chest
    is ideal.
     Relevant other methods depending on site and spread, e.g. CT scan of head, chest,
    abdomen, pelvis.
     Urine for melanuria signifies advanced disease.
     Sentinel lymph node biopsy (SLNB).
    Investigations- contd
     Tumour markers-
     LDH
     Melan –A
     S 100
     tyrosinase
     HMB 45 (Human melanoma black 45 )is a monoclonal antibody against specific antigen (Pmel
    17) present in melanocytic tumours. HMB 45 has got 92% sensitivity.
     MRI of the area;
     PET scan to detect the spread-in seleted patients only. Desmoscopy in early cases.
    Treatment

     Surgery is the main treatment.


     For primary
    1. Handleys wide local excision
    Treatment

     For lymph node secondaries


     In a clinically palpable lymph node, FNAC of lymph node is done.
     In case of spread, then regional block dissection, i.e. ilioinguinal or
    axillary or neck is done.
     Once FNAC shows positive lymph node 5-year survival rate reduces to
    50%.
     In a fixed lymph node, only chemotherapy is the treatment because it
    is inoperable.
     Lymphatic mapping and sentinel node biopsy
     Prophylactic regional block dissection which was previously advocated
    is now controversial. But still used in many centres. Elective lymph
    node dissection (ELND) is done when tumour thickness is 1-4 mm.
     Management in unknown primary(2%) presenting as nodal secondaries
    is by nodal radical dissection at the region with adjuvant chemotherapy.
     They have better prognosis than with known primary. Patient should be
    monitored and evaluated to identify the primary site during every
    follow up. Once primary is identified it is treated accordingly depending
    on its location.
    For locoregional recurrent

    melanoma
    Local recurrence is one which recurs within 5 cm radius of the primary tumour in skin
    or subcutaneous tissues.
     Isolated limb perfusion (ILP) using cytotoxic agents like Melphalan (M for M),
    interleukin 2, tumour necrosis factor (TNF).
     Concentration used here is 15-25 times more than that is used for systemic therapy.
     Melphalan dose is 1 0 mg/I perfusion solution in leg (13 mg/I in arm).
     Isolated limb infusion {ILI)
    Distant spread

     Brain, lung and liver are the most common sites; skin, bone, GI are less
    common sites.
     Chemotherapy and immunotherapy is the main treatment. , Isolated
    lung or liver metastasis can be resected.
     Radiotherapy is useful for bone and brain secondaries.
     Stereotactic program using gamma knife is better for brain
    secondaries.
    Chemotherapy
     Indication
     Secondaries in lung liver , bones
     After surgery for melanoma
     Drugs are:
     a. DTIC: Diethyl triamine iminocarboxamide.
     B. Melphalan (Phenyl alanine mustard) (Melphalan for melanoma).
     C. Carboplatin, vindesine.
     D. CVD regime-is cisplatin, vinblastine and dacarbazine.
     E. Tamoxifen as a ceramide sensitizer rather than part of the chemotherapy regime
    (Dartmouth regimen-DTIC, BCNU, cisplatin and tamoxifen) may be beneficial.
    Prognosis
    Follow up

     In stage I and II disease after treatment, follow-up is done at 6 months


    interval for 3 years. It is done by clinical examination, LDH assay, USG
    abdomen and chest X-ray.
     In stage Ill disease, PET scan CT of head, chest and abdomen are
    indicated.
    THANK YOU

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