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TURBAN TUMOUR
It is a descriptive term wherein entire scalp looks like a turban
because of multiple scalp swellings. It can be due to multiple
cylindroma; multiple hidradenomas; subcutaneous neurofibromas; nodular multiple basal cell carcinoma.
Multiple cylindroma is usually considered disease under
this term. Cylindroma is a variant of eccrine spiradenoma
(skin adnexal tumor). Multiple firm pinkish nodules in the
scalp are the presentation in multiple cylindroma. They are
rare, often locally malignant, grows slowly over the span
SRB’s Manual of Surgery
of many years to cover entire scalp with reddish lobulated
lesion.
Hidradenoma is a rare benign sweat gland tumour. Multiple
tumours commonly look like a turban in the scalp. They are
painless, disfiguring, cosmetically problematic, soft, boggy,
non-fluctuant, non-compressible cutaneous swellings;
commonly observed in middle age group.
Multiple sebaceous cysts over the scalp mimic the same.
Management is initial biopsy to find out the cause; then wide
excision with skin grafting.
1. Hairy mole is a mole with a hair growing on its surface.
Fig. 1.528: Hairy naevus.
2. Nonhairy mole.
3. Blue naevus. It is seen in children. It is located deep in
the dermis, hence appears blue. It is common in buttock
(Mongolian spot), hand, feet.
4. Junctional naevus. It lies centred in the junctional layer
(basal layer) of the epidermis as clusters. It is immature,
unstable and premalignant. Micro
proliferation of melanocytes at the epidermal junction.
Features of malignant transfor
size, colour, bleeding, ulceration, crusting, satellite spots.
sco pically there is
mation are—change in the
NAEVI (MOLES)
It is excessive proliferation of melanocytes. It is hamartoma of
melanocytes due to excessive stimulation. The risk in a small
or medium-sized mole turning into melanoma is under 1%. It
may present during birth or appear later.
Types
Fig. 1.527: Different types of naevi.
Fig. 1.529: Junctional naevus.
5. Compound naevus. It is combination of intradermal and
junctional naevus. Intradermal part is inactive but junctional
part is potentially malignant.
Fig. 1.530: Compound naevus.
6. Juvenile melanoma (Spitz naevus) (It is a misnomer). It
appears as junctional like mole before puberty. It is seen
in children on face. They present as brownish red nodular
lesion which needs always excision.
7. Hutchinson’s freckle. It is seen in elderly with large area of
dark pigmentation. In the macular stage it is smooth and
brown. In the tumour stage it is dark and irregular. It can
turn into melanoma commonly.
8. Halo naevus: Halo of depigmentation around the pigmented
naevus. This halo is due to antibody response to melano-
cytes. Halo naevus is often seen along with vitiligo. Similar
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halo may develop around a malignant melanoma lesion.
9. Intradermal naevus: Cluster of dermal melanocytes is seen
without junctional component. Common in face.
Fig. 1.531: Intradermal naevus.
10. Spindle cell naevus: It is dense, black pigmented lesion
containing spindle cells and atypical melanocytes at dermoepidermal junction; seen in females on high with malignant
potential.
11. Naevus spilus: It is hyperpigmented speckles throughout,
also called as speckled lentiginous naevus. Malignant
potential is rare.
12. Naevus of Ota is dermal melanocytic hamartoma seen in
distribution area of trigeminal nerve (ophthalmic /maxillary).
It is seen in oriental and African race adolescent females
(thigh) with a hormonal influence.
13. Naevus of Ito is similar lesion occurring in shoulder region.
14. Dysplastic naevus is proliferation of atypical melanocytes
from epidermal basal layer having variegated irregular look;
it is usually >5 mm in size; can be familial; 10% cases may
turn into superficial spreading melanoma.
15. Congenital naevus: It is present since birth.
Fig. 1.533: Giant congenital naevus (Courtesy: Dr MuraliKeshav,
MD, Pediatrician, KMC Mangaluru).
Treatment
Excision. Always should be sent for histopathology.
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.
x Melanoblast: Primitive cell derived from the neural crest.
x Melanocyte: The cell which synthesises melanin is located in the
basal layer (melanocyte : basal cell : : 1 : 10).
x Melanophores are pigment melanin carriers through dendrites
into the epidermis.
x Melanophages are macrophages having melanin pigment.
x Melanoblasts and melanocytes contain DOPA oxidase enzyme and
synthesise melanin. They show +ve DOPA reaction.
x Melanophores and melanophages show –ve DOPA reaction.
x Melanin synthesis is controlled by melanocyte stimulating
hormone, ACTH and sex hormones.
x Dopa is 3,4-dioxyphenylalanine.
DOPA reaction:
Tyrosine
DOPA Melanin
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CHAPTER 1R General Surgery: Skin Tumours
Fig. 1.532: Congenital naevus.
Note:
• Giant naevus is naevus more than 1% of body surface area or more than
20 cm in size. Giant congenital pigmented naevus (GCPN) often shows
dermatomal distribution. Pigment cells spread from epidermis to fat and
muscle often. It may turn into melanoma (5% risk). Such melanomas
are usually axial; is usually associated with retroperitoneal / intracranial
melanosis. Curettage, dermabrasion, laser, excision and SSG are the
treatment options.
• Mongolian spot is a blue brown/grey pigmented macular area which is
seen in sacral region during birth and after initial intense pigmentation
regresses fully in 7 years.
• Normal number of melanocytes releasing abnormally higher number of
melanin granules is called as freckle/ephilis.
Tyrosinase Oxidase
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
SITES OF MELANOMA
B
x Head and neck—25%
x Trunk—25%
x Other sites—14%
Don’t sit back and take what comes; go after what you want.
x Lower limb—25%
x Upper limb—11%
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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.
Other sites:
Eyes (iris, ciliary body, choroids), muco
cutaneous junction (anorectal region, genitalia), head and neck (meninges,
oropharynx, nasopharynx, paranasal sinuses).
Patients who are on immunosuppressive drugs or after renal
transplantation or NHL (RR - 30).
MALIGNANCIES WHICH SPREAD FROM MOTHER TO
B
FOETUS
x Melanoma x Lymphosarcoma
Risk Factors
Exposure to sunlight (exposure to UV light; more common
in white-skinned—20 times).
SRB’s Manual of Surgery
Ethnic factors, socioeconomic status (high society), lifestyle,
climate.
Albinism.
Xeroderma pigmentosa—RR is 1000 (by Kaposi in 1874): It
is an autosomal recessive (Ch 9q) disease with defect in DNA
excision repair mechanism causing formation of aberrant
Classications
Breslow’s classification (1970): Based on thickness of invasion
measured by optical micrometer—most important prognostic indicator until nodal spread
I: Less than 0.75 mm II: Between 0.76 to 1.5 mm
III: 1.51 mm to 4 mm IV: More than 4 mm
Relation of Tumour Thickness to Nodal Spread—Based
on AJCC
Classication
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.
Lesion Tumour thickness Nodal spread
<1 mm <10%
Thin
Intermediate
Thick
1–4 mm 20–25%
>4 mm 60%
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.
CLARK’S LEVELS (1969)
B
Level 1: Only in epidermis
Level 2: Extension into papillary dermis
Level 3: Filling of papillary dermis completely
Level 4: Extension into reticular dermis
Level 5: Extension into subcutaneous tissue
Fig. 1.534: Xeroderma pigmentosa with BCC in the nose. Such patients
are prone for other skin malignancy like melanoma also. There is
defective DNA excision repair.
Junctional naevus.
Familial dysplastic naevus syndrome.
Sporadic dysplastic naevi. 10% risk.
Large congenital naevi (larger than 20 cm).
Family history of melanoma (10% through chromosomes
1p, 6q, 7 and 9). They often present with multiple primary
melanomas; associated with dysplastic naevus.
History of earlier skin cancers other than melanoma.
Fig. 1.535: Clark’s level.
Differential Diagnosis (Other Pigmented Lesions
of the Skin)
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
A
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B
Figs. 1.536A and B: (A) Pigmented lesion could be naevus or
melanoma or BCC. (B) Multiple pigmented lesions.
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.
Fig. 1.538: Nodular malignant melanoma.
3. Lentigo maligna melanoma:
¾
7–15%. Less common, least malignant. Occurs in
old age and common in face (Hutchinson’s melanotic
freckle). It is slow growing, variegated, brown macule/
lentigo; common in face/neck/hands; common in elderly
women. Lentigo maligna is in situ type.
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CHAPTER 1R General Surgery: Skin Tumours
TYPES
B
x Cutaneous melanoma
x Extracutaneous—10% (ocular is common site)
x Occult (Unknown primary)—2–7%
Clinical Types
1. Superficial spreading:
¾
Most common. 70%. Occurs in any part of the body with
variegated irregular look. It has more radial growth and
better prognosis. It commonly arises from a pre-existing
naevus. In men, common in back; in women in leg.
Fig. 1.539: Lentigo maligna melanoma.
4. Acral lentiginous melanoma:
¾
5%. Occurs in palms, soles and subungual region. It has
got a poor prognosis. It is least common. Usually attains
large size; nodular type with more vertical growth phase.
It is common in Africa and Asia. It is less common in
whites. It is often flat, irregular macule. It mimics fungal
infection/pyogenic granuloma.
Fig. 1.537: Superficial spreading melanoma (70%).
2. Nodular melanoma: 12–25%.
¾
More aggressive. It is common in younger age group,
occurring in any part of the body. It has more vertical
growth. Common in mucosa and mucocutaneous junction;
Fig. 1.540: Melanoma in the sole. Often such
pigmentation may be unnoticed.
Note:
• Amelanotic melanoma:
- This is the worst type. Because of the undifferentiation, tumour cells
loose their capacity to synthesise melanin. It presents as rapidly
progressive pinkish fleshy tumour. It may mimic soft tissue sarcoma.
It needs markers like S100, HMB45 for diagnosis.
In time of test, family is best.
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Fig. 1.541: Amelanotic melanoma; often mimics soft tissue sarcoma.
• Desmoplastic melanoma has high affinity for perineural invasion;
SRB’s Manual of Surgery
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.
•
Subungual melanoma which was earlier thought of acral lentiginous type
is now considered as superficial spreading type. It is involvement of nail
fold matrix (not nail plate). Triangular, macular, progressively widening
pigmentation of nail fold with nail dystrophy is typical—Hutchinson’s
sign. It should be differentiated from benign racial melanonychia which
are dark streaks under the nail. Biopsy of nail matrix should be done here.
• Ocular melanoma: It is the commonest malignancy arising in eye. It may
arise from retina, iris, ciliary body, choroid. It rarely metastasize or only
at late stage as it is devoid of lymphatics. Ocular melanoma commonly
shows its distant spread to liver. Massive hepatomegaly is typical and
is often seen many years after the treatment of primary ocular lesion.
Condition is treated with enucleation, radiation, photocoagulation.
• Clark’s concept—Two phases of growth: Initial radial growth phase
occurs horizon tally, later vertical growth phase occurs with invasion.
• Major signs: Change in size (diameter more than 6 mm), shape and
colour
• Other changes:
–
Inflammation, crusting, bleeding, itching
–
Nodularity, ulceration, halo around a mole
–
Satellite lesions
–
Doppler positive pigmented lesions using hand held Doppler
(> 1 mm thick lesion)
ABCDE OF MELANOMA (UGLY DUCKLING RULE)
B
x Asymmetry
x Border irregularity – coast of Marine sign
x Colour variation
x Diameter > 6 mm
x Evolving (changing progressively)
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.
BLOOD SPREAD IN MELANOMA
B
x Brain—convulsions, localising features and raised intracranial
pressure
x Lung—cannon ball secondaries, pleural effusion-haemoptysis,
chest pain and cough
x Liver (massive liver), ascites
x Skin—cutaneous nodules often pigmented
x Bones—bone pain, pathological fracture. Paraplegia/neurological
deficits in spine metastasis
Extensive visceral involvement causes melanuria
Fig. 1.542: Aggressive melanoma in the axilla; could be
desmoplastic type.
Clinical Features
It can stat in a pre-existing naevus (commonly junctional
naevus)—50–60% or as de novo in a normal skin—40-50%.
Melanoma is unknown before puberty.
Induration is not seen in melanoma.
Pigmentation with irregular surface and margin with rapid
growth.
Ulceration, bleeding, itching, change in the colour.
Note:
When a mole turns malignant, following changes should be observed
(Glasgow criteria):
Melanoma in choroid has got better prognosis, because as
there are no lymphatics, spread is delayed.
Sometimes primary is very small and un noticed (in anus,
subungual region). They present with features of secondaries
only.
A
Figs. 1.543A and B: Primary melanoma with lymph node secondaries
in two different individuals. Note the pigmented ulcerated secondaries
in one.
B
BA
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Figs. 1.544A and B: (A) ‘In-transit’ nodules in melanoma. They are
secondary depositions in dermal lymphatics; (B) Satellite nodule in
melanoma occurs within 2 cm of primary. Note the primary in the heel
and satellite nodule adjacent to it.
Note:
• Satellite nodule occurs within 2 cm of the primary melanoma whereas in
– transit nodules occur in between primary and lymph node secondaries.
• Infiltration into deep fascia by melanoma is rare in initial stages as deep
fascia acts as a strong barrier.
• Melanoma can also occur in places other than skin like tongue, mucous
membrane or genitalia.
OCCULT MELANOMAS (PRIMARY UNKNOWN) ARE
B
COMMON IN
x Anus
x Genitalia
x Scalp
x Eye
MELANOMA
B
x 5% of all skin cancers—incidence
x 20 times more common in whites than blacks
x Mucosal melanoma has got poor prognosis
x Can spread from mother to foetus
x Multiple melanomas are 1% common
x Melanoma in choroid will not cause lymph node involvement, as
x External auditory canal
x Adrenal medulla
x Nail bed
it has no lymphatic drainage. But late massive liver secondaries
even after 10-20 years is known to occur
x 10% of melanomas are familial—in whites
x Satellite nodules are secondary skin nodules within 2 cm of
primary
x In transit’ nodules are secondary skin nodules beyond 2 cm of
primary any where up to lymph node region
x Melanoma may present as secondary (in liver, lungs, bone,
brain) with occult primary when primary is situated in anus,
genitalia, eye, external auditory canal, adrenal gland, nail bed
and scalp—7%
x Pigmentation is not mandatory to diagnose melanoma even
though it is commonly present
x Melanoma also can occur in fishes, dogs and horses
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CHAPTER 1R General Surgery: Skin Tumours
Fig. 1.545: Melanoma in tongue.
A
B
Figs. 1.546A and B: Melanoma in vagina—in mucocutaneous
junction. On table and excised specimen of melanoma.
Investigations
No incision biopsy. It can cause early blood spread. Only in
large lesions or already metastatic lesions incision biopsy
is advocated.
Excision biopsy of primary. It is done with 2 mm margin with
deeper fatty tissue. One should avoid using cautery and avoid
crushing the tissues as much as possible. Instead of excision
biopsy, punch biopsy is done in case of large primary tumour
very close to pinna, eye, nose. Punch biopsy assesses the
depth/thickness of the lesion. Punch should be done at the
most elevated part of the lesion to get proper depth.
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).
Tumour markers—LDH; Melan – A; S 100; tyrosinase; HMB
45 are the tumour markers used. Human melanoma black 45
(HMB 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.
In time of test, family is best.
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TNM STAGING (AJCC, 8TH EDITION, 2018)
B
T (Tumour)
T0 - No evidence of primary tumor; Primary site of tumor is unknown
Tis- in situ carcinoma (thickness, ulceration not applicable)
T1: < 1 mm; T1a - < 0.8 mm without ulceration; T1b - < 0.8 mm with ulceration or > 0.8 to 1 mm with or without ulceration.
T2: 1-2 mm; T2a without ulceration; T2b is with ulceration.
T3: 2-4 mm; T3a is without ulceration; T3b is with ulceration.
T4 > 4 mm; T4a is without ulceration; T4b is with ulceration.
N – Nodes
N0: No regional nods involved.
N1: N1a – Clinically occult One node detected by SLNB: N1b – Clinically detected one node; N1c – No nodes but presence of in transit, satellite
or microsatellite metastasis.
SRB’s Manual of Surgery
N2: N2a – 2 or 3 clinically occult nodes; N2b – 2 or 3 nodes with at least one clinically detectable node; N2c – One clinically occult or detectable node with in transit, satellite or microsatellite metastasis.
N3: N3a – 4 or more clinically occult nodes; N3b – 4 or more nodes with at least one clinically detectable nodes; N3c – 2 or more clinically
occult or detectable nodes with in transit, satellite or microsatellite metastasis.
M – Metastases
M0 – No distant spread
M1: M1a – Skin, soft tissue, non regional node spread without (M1a (0)) or with LDH elevation (M1a (1)). M1b – Distant spread to lungs with
or without M1a without raise in LDH (M1b (0)) or with raised LDH (M1b (1)). M1c – Distant spread to Non CNS viscera with or without M1a
or M1b without raise in LDH (M1c (0)) or with raise in LDH (M1c (1)). M1d – Distant spread to CNS with or without M1a,b,c without raise in
LDH (M1c (0)) or with raise in LDH (M1c (1)).
Staging
Stage 0: Tis, N0, M0.
IA: T1a, T1b, N0 M0. Stage IB: T2a, N0 M0.
Stage
Stage
IIA: T2b, T3a, N0, M0. Stage IIB: T3b, T4a, N0, M0. Stage IIC: T4b, N0, M0.
Stage IIIA: T1a/b, T2a; N1a or N2a; M0. Stage IIIB: T1a/b, T2a; N1 b/c, N2b; M0. T2b, T3a, N1a, N2b, M0; T0, N1b/c, M0. Stage IIIC: T1a
to T3a, N2c or N3a/b/c, M0; T3b/ T4a, any N ≥ N1, M0; T4b, N1a to N2c, M0; T0, N2b, N2c, N3b / N3c, M0. Stage
Stage IV: Any T, Any N, M1.
IIID: T4b, N3a/b/c, M0.
TUMOUR MARKERS FOR MELANOMA
B
x MELAN-A
x HMB 45 (Human Melanoma
Black 45)
x S 100
x LDH
Treatment
Surgery is the main treatment.
For Primary:
a. Handley’s wide local excision (WLE) is wide excision with
clearance of margin as well as depth. Clearance margin used
in olden days is 3–5 cm.
Tumour thickness in mm Wide Local Excision (WLE)
clearance margin in cm
In situ and <1 mm 0.5 to 1 cm
1 to 2 mm 1.0 to 2.0 cm
2 to 4 mm 2.0 cm
>4 mm 2.0 cm
Present recommendation is—in situ melanoma needs
0.5 cm clearance; melanoma < 1 mm thickness needs 1.0 cm
clearance; 1–2 mm thickness needs 1–2 (1.5) cm clearance;
2 cm/3 cm clearance is sufficient for >2.0 mm thickness.
Procedure can be done under regional or local anaesthesia.
Evidence says that more than 2 cm clearance will not show
any additional advantage in treating primary tumour.
Primary closure or SSG or local flaps are used to cover the
defect.
b. If primary area is wide and deep, then amputation with one
joint above is done.
c. In fingers and toes, disarticulation is required.
d.
Melanoma in anal canal may require abdominoperineal resec-
tion.
e. Enucleation in case of melanoma in eye.
f. Melanoma in pregnancy is treated with termination of preg-
nancy and specific therapy for melanoma. Pregnancy should
be postponed for 2 years.
For lymph node secondaries:
1. 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%.
2. In a fixed lymph node, only chemotherapy is the treatment
because it is inoperable.
3. Lymphatic mapping and sentinel node biopsy (Dr Donald
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CHAPTER 1R General Surgery: Skin Tumours
A B
Figs. 1.547A and B: Widely excised melanoma specimen from heel.
Cut section of widely excised specimen of melanoma from heel shows
the depth of the tumour.
A
Figs. 1.548A and B: Wide excision and skin grafting done for melanoma;
(B) Disarticulation of lateral two toes for interdigital melanoma.
B
A B
Figs. 1.550A and B: Melanoma secondaries in groin nodes after
block dissection. Black lesions are observed in cut section.
Figs. 1.551: Secondaries in inguinal lymph nodes from primary
melanoma sole-on table finding. Pigmented nodes are observed.
Fig. 1.549: Wide excision of melanoma from the heel. Note the
clearance margin and depth of dissection.
Everytime something good happens to you, make something good happen to someone else.
Morton, 1970): Radioactive colloid is injected around primary
site and lymphoscintigraphy is done using hand held gamma
camera to visualise the mi rometastasis in the nodal field. If
there are micrometastasis, then regional block dissection
(therapeutic LND) is done.
SLN (Sentinel lymph node) can be identified in 95% or
more of groin and axillary nodes and in 85% cases of head
and neck melanomas. Often both blue dye and technetium
sulfur colloid is used together to identify the SLN. SLNB
is useful for melanoma with thickness more than 1 mm
depth. Less than 1 mm thickness is considered as low-risk
for metastases; between 1-4 mm thickness is considered
as intermediate-risk for metastases mainly of nodal spread;
more than 4 mm thickness will be considered as high-risk
for both nodal as well as blood spread. SLNB is the inves-
tigation of choice for staging in intermediate thickness
melanoma.
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TECHNIQUE OF SLNB
B
Preoperative lymphoscintigraphy is done on the day of surgery
for primary tumour. 0.5 mCi
injected into the normal dermis within 0.5 cm from the margin
of melanoma. Dynamic and static images are taken to identify
lymphatic channels, sentinel node (s), interval node (like popliteal
node in lower and epitrochlear node in upper limb). After that
under general anaesthesia, just before wide local excision (WLE)
of the melanoma, 1-5 ml of isosufan blue dye is injected into the
dermis similarly. By this, senile lymph node is identified in 99%
of patients.
SLN is defined as a node which indicates a direct lymphatic drainage
SRB’s Manual of Surgery
pathway from primary; it is the most radioactive node in nodal basin;
shows radioactive count 10% more than other nodes; takes blue
dye adequately; on table this node will be palpably suspicious of
tumour. In melanoma nodal basin usually 2 SLNs are identified (as
first echelon nodes in nodal basin).
Axillary and inguinal SLNs are easier to identify than head and neck
SLNs which are usually located adjacent to spinal accessory nerve.
Entire SLN (s) should be removed and sent for histology, immunohistochemistry—S-100 and HMB-45.
Interval lymph nodes like popliteal or epitrochlear when involved
should be cleared surgically.
SENTINEL NODE BIOPSY
B
a. Carcinoma breast b. Melanoma
Carcinoma penis
c.
Technetium 99 sulphur colloid is
4. 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.
5. 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 Loco Regional Recurrent Melanoma:
Local recurrence is one which recurs within 5 cm radius of
the primary tumour in skin or subcutaneous tissues. Risk
of local recurrence is 0.2% if primary tumour is less than
0.75 mm; 2% if it is between 0.75–1.5 mm; 6% if it is 1.5–4
mm; 12% if it is more than 4 mm.
¾
Isolated limb perfusion (ILP) (Creech et al, New Orleans,
1958) 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 10 mg/l perfusion
solution in leg (13 mg/l in arm).
With transverse incision, extremity vessels (artery and
vein like femorals) are exposed for 3 cm; secure tourniquet is applied; major artery and vein are cannulated or
arteriotomy and venotomy done transversely; Melphalan
(phenylalanime mustard, 1 mg/kg) and Actinomycin D
(0.5 gram) is injected at high temperature of 42°C with a
pump and oxygenator through cannulas in femoral artery
and vein (with a proximal tourniquet in situ). Drugs are
administered as single bolus through the pump along
the extracorporeal circuit. Patient is heparinised initially
later reversed using protamine after vascular suturing.
One hour pump run wash out is given. Hyperthermia and
oxygenation increase the metabolic activity of tumour
cells to make it more vulnerable to melphalan. Procedure
controls the local disease well with preserving the functioning limb. It is used in local recurrence or ‘In-transit’
deposits. It shows 80% response rate with 15% complete
response; but only of short period. Complications like
DVT, bleeding, sepsis can occur.
¾
Isolated limb infusion (ILI) (Thompson, 1993): Vascular
catheters are passed and placed across femoral artery
and vein through opposite femoral vessels or through
arm vessels. The limb is warmed; patient is anaesthetised 2 hours later and also heparinised; papaverine is
injected into arterial catheter and tourniquet is applied
in the thigh/arm. Melphalan 7.5 mg/l, actinomycin D
75 µg/l in 400 ml saline (10 mg and 100 µg/l in 300 ml
NS in upper limb) is infused into the isolated limb for 6
minutes which is pumped around the limb repeatedly for
30 minutes with a hypoxia in limb; drugs are washed out
using a Hartmann’s solution; tourniquet is removed and
normal circulation is regained with removal of vascular
catheters. Protamine is given to reverse heparin action.
Here extracorporeal circuit and oxygenator are not
required (unlike in limb perfusion). Procedure is also
used in extremity sarcomas.
Laser ablation of multiple small cutaneous lesions but with
doubtful benefits.
For Distant Spread
Brain, lung and liver are the most common sites; skin, bone,
GI are less common sites. But melanoma is one of the
commonest tumours to spread to intramural GIT to present
as intussusception.
Distant spread when found or suspected, CT scan of head,
chest, abdomen and pelvis are needed. PET scan and tumour
markers are very useful.
¾
Chemotherapy and immunotherapy is the main treatment.
¾
Isolated lung or liver metastasis can be resected.
¾
Radiotherapy is useful for bone and brain secondaries.
Stereotactic program using gamma knife is better for
brain secondaries.
Chemotherapy for Melanoma
Indications:
a. Secondaries in lungs, liver, bones.
b. After surgery for melanoma. Usually it is given intravenously.
Drugs are:
https://t.me/medicina_free
a.
DTIC: Diethyl triamine iminocarboxamide.
b.
Melphalan (Phenyl alanine mustard) (Melphalan for mela-
noma).
Carboplatin, vindesine.
c.
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.
Immunotherapy/Biological Therapy
It is done using specific tumour antibodies, BCG, levamisole,
Corynebacterium parvum, alpha interferon, interleukins and
tumour vaccines are tried with some success rate up to 40%
in advanced melanomas.
Biochemotherapy is combination of CVD with interferon α
and interleukin 2.
Interferon α is a cytokine which is antiangiogenic and stimulator
of natural killer NK cells. Dose is 20 mU/m
for 4 weeks then maintenance dose of 10 mU/m
2
IV 3 times a week
2
subcutaneously 3 times a week for one year. Severe myelodepression
and fulminant liver necrosis are the toxicity and so often dose
is reduced to 3 mU/m
Imiquimod is applied over the tumour as cream. Talimogene
2
three times weekly for 2 years.
laherparepvec (T-VEC), BCG, IL-2, IF alpha 2b, BCG are used
as liquid injected into the tumour.
GM2 ganglioside based vaccine (stimulates production of IgM
antibodies), Melacine (contains melanoma cell lysates) and
cancerVax are three vaccines under trial at present.
Ipilimumab is a monoclonal antibody that boosts the body’s
immune response against melanoma cells. Pembrolizumab
and nivolumab are two other drugs. They are PD 1 receptor
inhibitor (Programmed Death Receptor 1, seen in T cells)
drugs.
Endolymphatic Therapy
It can be done to control disease in the nodes using
radioactive I
or P32 with ultrafluid lipiodol along with
131
lymphangiography.
Targeted therapy
Fig. 1.5 52: Melanoma involving face extensively with destruction. Note
the maggots over the surface of tumour. Melanoma is most aggressive
cutaneous malignancy.
Prognosis for Melanoma
It is not good since it is a very aggressive tumour.
Old age has worse prognosis.
Females show better prognosis.
Extremity melanoma has better prognosis than head and
neck.
Prognostic factors—overall poor Staging as prognostic factor
•
Tumour thickness—very important factor
• Nodal spread—once regional
nodes are positive, 85% of
patients will have occult distant
spread. Number of positive
nodes is also important
• Ulceration—poor
Angiogenesis, vascular
•
invasion—poor
• In-transit nodules—poor
• Vertical growth—poor prog-
nosis
• Metastatic disease—poor
• Staging
Stage I: >90% prognosis
Stage II: 70%
Stage III: 35%
Stage IV: <2%
295
CHAPTER 1R General Surgery: Skin Tumours
Signal transduction inhibitor therapy using—(1) BRAF
inhibitors—Vemurafenib, dabrafenib; (2) MEK inhibitors—
Trametinib and cobemetinib; (3) C-Kit inhibitors—imatinib,
nilotinib are used. Usually combinations both groups are
used tablets (pill) to be swallowed. Other targeted therapies
are—oncolytic virus therapy; monoclonal antibody therapy.
Note:
• There is not much role for radiotherapy.
• Radiotherapy is beneficial only in secondaries in brain and bones.
Creativity begins with thinking different and progress with acting different, thus giving unique results.
Follow-up After Therapy in Melanoma
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 III disease, PET scan CT of head, chest and abdomen
are indicated.
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