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254
Manipal Manual of Surgery
Key Box 31.3
CO2 Laser in Basal Cell Carcinoma
Useful in superficial BCC that are confined to
epidermis and papillary dermis.
At least 4 mm surrounding healthy skin should be
removed.
Patients with multiple tumours or in hereditary Gorlin’s
syndrome—laser is very useful.
Acts by superficial vaporisation.
Pathological margins cannot be examined.
Indication in high risk BCC—large (>2 cm), located
near eye, nose, ear.
Precancerous/low grade BCC.
Flaps and Reconstruction following Tumour Excision
1. Healing by secondary intention:
Simplest method: Suitable only if the defect is <1 cm,
superficial, and located in a cosmetically inconspicuous site.
Disadvantage: Not always cosmetically acceptable;
may result in contour irregularity, distortion of
surrounding structure, and unstable coverage.
2. Primary closure: In the majority of cases, this is
possible. Simple, but the defect needs to be small.
Possible only if excessive tension and distortion can
be avoided.
3. Skin graft:
• A skin graft does not look like normal skin, but
provides a good skin cover.
• Cannot be used across a joint. Cosmetically accept-
able, but does not give colour and contour match.
Preferred if the patient has a high risk of local
recurrence, such as in malignant melanoma. Two
types of skin garft : Split and full thickness grafts.
• Skin grafts will not take on in following situations:
Cortical bone without periosteum, Cartilage
without perichondrium, tendon without paratenon
and in irradiated tissues.
4. Commonly used skin flaps:
• Rotation flap: It is a semicircular flap of skin and
subcutaneous tissues which rotate about a pivot
point into the defect to be closed. A small triangle
of skin may be removed to facilitate rotation.
• Advancement flap: The defect is closed by stretch-
ing the skin. It may be a single, double, or V-Y
advancement flap. V-Y flap is an example: Good
for defects on the medial cheek and ala of the nose.
V-shaped incision is made and then advanced to
cover the defect, which is later sutured in a ‘Y’
shape.
• Transposition flap: Bilobed and rhomboid flaps are
Section II • General Surgery
a few examples. A rectangular piece of skin and
subcutaneous tissue is rotated. Types of
transposition flap are: 1. Banner flap: Provides
excellent contour and a reasonable colour match.
It can only be used for small defects. 2. Bilobed
flap: Banner flap uses a single lobe. In this flap,
however, two lobes are created and then rotated.
It is used when the defect is too large enough to be
closed with a banner flap, especially useful in the
area around the nose. It produces a conspicuous
scar and is less desirable than a banner flap.
3. Rhomboid flap: Geometric modification of the
banner flap. It may be used for medium-sized defects.
5. Complex flaps: Pectoralis major myocutaneous flaps
and radial artery free flaps are the complex flaps used
for reconstruction.
RECONSTRUCTION OPTIONS FOR LIPS
The most important factor that dictates reconstruction
is the amount of remaining lip vermilion.
Primary closure for small defects
A.
B. Vermilion advancement flap
C. Abbe flap: Mainly used for the upper lip. It is
harvested based on the labial artery. It provides a
good cosmetic effect. It causes minimal loss of
function in the lower lip. Modification of the Abbe
flap, like reverse Abbe flap, may also be used for
lower lip defects.
D. Estlander flap: It is a type of rotational flap from
upper lip to lower lip. It produces a round commissure and loss of the normal taper of vermilion.
E. Webster-Bernard flap: It is a medial advancement
of cheek tissue to create a new lower lip. It gives a
good result. Disadvantage: Results in significant
facial scarring.
F. Very large lower lip defects may also be closed with
‘double central severe Abbe’s flap’ or bilateral
Karapandzic flap (see page 364).
SQUAMOUS CELL CARCINOMA (SCC)/EPITHELIOMA
It is the second most common malignant skin tumour,
after basal cell carcinoma. It arises from the prickle cell
layer of the Malpighian layer of the skin. It usually
affects elderly males. All the premalignant conditions
listed earlier apply to this condition as well. It may also
occur de novo. Basosquamous carcinoma is the term
applied to squamous cell carcinoma arising in a preexisting basal cell carcinoma. It is interesting to note
that a variety of names have been given to squamous
cell carcinoma, based on its site (Table 31.2).
Also
Table 31.3 summarizes the typical sites of SCC, in terms
of skin, mucous membrane, and junction involvement.
Skin Tumours
Table 31.2 Sites of squamous cell carcinoma
Site Name Reason/explanation
Skin of the abdomen or back of thigh Kangri cancer Kangri is the name given to the pot containing
in Kashmiri patients hot charcoal which is applied to the abdominal
wall because of excessive cold in Kashmir (India)
Buttocks, heels, elbows Kang cancer Tibetans sleep on the oven bed due to excess
cold
Scrotum Chimney sweep cancer Seen in chimney sweepers due to prolonged
irritation by chemicals such as tar
Abdominal wall Saree cancer and Dhothi cancer Due to chronic irritation caused by wearing dhothi
or saree too tight
Lower lip Countryman’s lip Carcinoma lower lip is common in agriculturists
(outdoor occupation)
Table 31.3 Typical sites of squamous cell carcinoma
Skin Junction Mucous membrane
• Dorsum of hand • Between skin and mucous membrane • Lined by stratified squamous epithelium as in oral
• Limbs • Lip cavity and oesophagus
• Face • Penis • Lined by columnar epithelium, wherein squamous
• Abdominal wall • Vulva metaplasia occurs, such as gallbladder, bronchus
• Lined by transitional cell epithelium with metaplasia
as in urinary bladder
255
Pathological Types
• Ulcerative variety—most common
• Proliferative growth—cauliflower like
• Ulcero-proliferative
Clinical Features (Figs 31.21–31.27)
• Most lesions are preceded by actinic keratosis. Such
lesions grow slowly and are locally invasive without
metastasis. If not from keratosis, the lesion is
aggressive and metastatic.
• Typically, it is an ulcerative or cauliflower-like lesion
(Fig. 31.21).
• The edge is everted and the base is indurated and it
may be subcutaneous tissue, muscle or bone. The
floor contains cancerous tissue which looks like
granulation tissue. It is pale, friable, and bleeds easily
on touch (Figs 31.22–31.23).
• The surrounding area is also indurated.
• Mobility is usually restricted, due to infiltration of
the underlying structures. In very early cases, the
ulcer can be moved along with skin over the underlying structures.
• Regional lymph nodes, such as inguinal lymph nodes
(both vertical and horizontal groups), may get
Fig. 31.21: Squamous cell carcinoma affecting
dorsum of the hand—ulceroproliferative lesion
Fig. 31.22: Squamous cell carcinoma—
bleeds on touch
Fig. 31.23: Epithelioma
scalp—large ulcerating
bleeding lesion
Section II • General Surgery
256
Manipal Manual of Surgery
Fig. 31.24: Squamous cell
carcinoma arising in leprosy
scar
Fig. 31.25: Squamous cell carcinoma of
the sole
enlarged when squamous cell carcinoma affects the
lower limb or abdominal wall. Hard lymph nodes
are suggestive of secondaries.
Spread
. Local spread occurs by infiltration into the surround-
1
ing tissues. Depending on the site, various structures
may be involved. Some examples are:
• Tendon involvement in the dorsum of the hand.
• Muscle involvement in the abdominal wall.
• Bone involvement (e.g. tibia is involved in carci-
noma developing in a varicose ulcer or mandible
in carcinoma cheek).
2. Lymphatic spread is the chief mode of spread, though
it occurs relatively late. Regional nodes are involved
first.
• Nodes which are soft to firm and tender are due to
secondary infection.
• Nodes which are hard, nontender, with or without
fixity are due to secondary deposits.
• In untreated cases, nodes start ulcerating through
the skin and result in bleeding and pain.
• As already stated, nodes are not involved in
Marjolin ulcer.
3. Blood spread is rare and late.
Differential Diagnoses
Various benign skin lesions may look like squamous
cell carcinoma in early cases
(Key Box 31.4).
Investigations
• A wedge biopsy from the edge of the ulcer/growth
is taken. Main reason being edge is the most proliferative area in malignancies. However, in proliferative
Section II • General Surgery
lesions, punch biopsy may also be taken.
Fig. 31.26: A large epithelioma
of the scalp—biopsy proved
squamous cell carcinoma
Epithelial pearls are absent in poorly differentiated carcinomas.
Key Box 31.4
Fig. 31.27: Bowen’s
disease with squamous
cell carcinoma
Differential Diagnosis
Basal cell carcinoma : Typical sites
Keratoacanthoma : Benign self-limiting
Papilloma : Benign lesion
Pyogenic granuloma : Painful, short duration
Tuberculous ulcer : Uncommon
• Microscopic picture: 80% of these cancers are well-
differentiated (Key Box 31.5), characterised by a
central, structureless mass of keratin, surrounded by
normal looking squamous cells arranged in con-
centric manner like onion skin. This appearance is
known as an epithelial pearl or cell nest (Fig. 31.28).
In 20% of cases, cells are undifferentiated with
numerous mitoses and without keratinisation.
Key Box 31.5
Broder’s Classification
I. Well differentiated 75% keratin pearls
II. Moderately differentiated 50% keratin pearls
III. Poorly differentiated 25% keratin pearls
IV. Anaplastic <25% keratin pearls
Treatment
I. Treatment of the primary: Epithelioma is treated by
wide excision or radiotherapy.
A.Surgery (Figs 31.29 and 31.30): It is indicated when
lesion is small and superficial, lesion involving deeper
tissues, such as muscles, cartilage, or bone or in radiorecurrent cases. Excision involves removal of the
growth along with 1 cm of normal healthy tissue from
Skin Tumours
257
Fig. 31.28: Classical keratin pearls—well-differentiated
squamous cell carcinoma (Courtesy: Dr. Laxmi Rao, Head,
Department of Pathology, KMC, Manipal)
Fig. 31.29: Wide
excision of squamous
cell carcinoma
Fig. 31.30: Wide excision followed by
skin grafting on 3rd year follow-up
the palpable, indurated edge of the tumour in highrisk cases. In low-risk patients, lesions may be excised
with a 4–6 mm margin. After wide excision, the defect
may be closed with a split skin graft or with a flap to
reconstruct the part, depending on the extent of
resection. If the growth is fixed to the tibia, growth
can be removed with involved periosteum followed
by radiotherapy. One attempt should be aimed at
preserving the limb. If it recurs then below knee
amputation is performed.
B. Radiotherapy: Is indicted for the following reasons
Primary
1. Patients unable or unwilling to undergo surgical
treatment for the primary lesion
. Clear margins cannot be obtained by surgery
2
3. Adjuvant treatment
4. Histologically aggressive (e.g. perineural invasion)
5. High grade
6. Bone invasion (Fig. 31.31)
7. Lymph nodes—adjuvant or palliative intent
II. Treatment of the metastasis in the lymph nodes
• In about 20% patients, enlarged regional nodes are
due to secondary infection. In all such suspected
Fig. 31.31: Large penetrating baso-squamous cell carcinoma
with destruction of the left ear and infiltrating mastoid process
and external ear
cases, ultrasound guided FNAC is done. If found
negative, treat the primary. Once the primary is
treated and antibiotics are administered, lymph nodes
may regress. During follow-up ‘wait and watch policy’
is observed.
• If the lymph nodes are positive for malignancy, radical
block dissection is done.
Thus, squamous cell carci-
noma of the leg requires inguinal block dissection.
If lymph nodes are hard and fixed to the femoral
vessels, chemo-radiotherapy is given first. combinations of cisplatin with 5-fluorouracil (5-FU), doxorubicin,
or bleomycin have been used. Radiotherapy dose is
3000–4000 cGy units over 3–4 weeks, 200 units/day.
• Lymph nodes may regress following chemoradio-
therapy and block dissection is done.
• Even in advanced fungating lesions, the response rate
to radiotherapy is reasonably good. Dose: 3000 to
4000 cGy units over 3 to 4 weeks 200 units/day.
Structures Removed in Inguinal Block Dissection
(More details in page 270)
• The superficial group of nodes, consisting of a
horizontal chain which lies below inguinal ligament
and a vertical chain which lies along the upper 5–6 cm
of the long saphenous vein (these two groups of
nodes form the letter T).
• The deep glands, located along the proximal end of
the femoral vein and one lying within the femoral
canal.
• Fat, fascia, and lymphatics are cleared from 2 cm
above the inguinal ligament up to 2 cm below the
saphenofemoral junction. The medial clearance is
important up to the femoral canal. Around 8–10 cm
of the long saphenous vein near its termination is
removed to facilitate lymph node clearance.
• The saphenous vein may be preserved if nodal tissue
is removed from the vessel circumferentially; otherwise, it is sacrificed.
Section II • General Surgery
258
Manipal Manual of Surgery
• Cloquet’s node is sent as a separate specimen for
frozen section examination.
Fixity to muscle, veins, fascia and bones is not a contraindication for block dissection. Carotid and femoral artery infiltration
make it inoperable. Preoperative chemo-radiotherapy should
be given all such cases to downstage the disease. Reassessment
is done again. If operable, then radical block dissection is done.
Complications of Inguinal Block
Dissection and Treatment
• Wound infection → Broad-spectrum antibiotics
• Lymphorrhoea → Adequate drainage
• Haemorrhage → Perfect haemostasis
• Flap necrosis → Edges to be trimmed. At
surgery Avoid sharp corner
• Femoral blow-out → Dangerous complication.
Sartorius muscle slide to cover
femoral vessels at the end of
surgery should be done.
Summary of the Treatment of
Squamous Cell Carcinoma (Fig. 31.32)
Prognostic Factors (Key Box 31.6)
Key Box 31.6
Prognostic Factors of SCC
Invasion: Deeper the lesions or SCC less than 2 mm,
metastasis is unlikely. If it is greater than 6 mm—15%
SCC may have metastasised
Broder’s grade higher: Worse prognosis
Site: Lip and ear—high chances of recurrence
Immunosuppression: Poor prognosis
Perineural involvement: Worse prognosis
This patient with large epithelioma was examined by postgraduate student and he offered the correct diagnosis.
However, he did not examine the inguinal region. The
groin had 3–4 hard nodes (Figs 31.33 and 31.34). He
failed in the examination.
Fig. 31.32: Fixity to major vessels such as carotid and femoral
artery is a contraindication. After palliative radiotherapy—
Section II • General Surgery
reassessment should be done for the feasibility of surgery.
Fig. 31.33: Large epithelioma below
knee region
Fig. 31.34: Large lymph
nodes in the groin
MELANOCYTIC TUMOURS
Simple Melanocytic Tumours
• As the fetus develops, melanocytes migrate to different
parts of body, such as the skin, meninges, mucus
membrane, eyes, etc.
• Pigmented naevi are composed of modified melano-
cytes derived from the neural crest. All naevi have
excess melanin pigmentation which makes them tanbrown or black in colour. They are located in the basal
layer of the epidermis and are benign. They are of
following types:
1. Junctional naevus: Located within the epidermis at
the dermo-epidermal junction. They are common in
children. They appear as tan-brown to black macules.
They are smooth, flat, and hairless moles. As they
enlarge, they become slightly raised and may evolve
into an intradermal or a compound naevus. It has no
malignant potential.
Junctional naevi commonly occurs over the palm,
sole, digits, and genitalia.
Skin Tumours
259
2. Compound naevus: As the mole enlarges, naeval
cells also appear in the dermis along the intraepidermal cells. Such moles are described as compound
naevi. These are typically found in adolescents and
are usually benign.
3. Intradermal naevus: It is the most common mole in
adult. Because of its deep seated nature, it appears
blue (hence, the name blue naevus). It is seen over
the scalp and face. It contains hair and does not
become malignant.
4. Spitz naevus: Commonly occurs over the face and
legs. It grows rapidly initially, and then remains
static. It appears as a reddish-brown nodule, and is
occasionally deeply pigmented.
5. Spindle cell naevus: Occurs in women, commonly
over the thigh. It has malignant potential.
6. Congenital pigmented naevus: It is present at birth,
and has a greater potential for malignant change. It
may involve extensive areas of the skin (giant).
Giant congenital pigmented naevus (GCPN) or
giant hairy naevus (>20 cm size)
• It is an example of a hamartoma of naevomelano-
cytes. It involves extensive areas of the skin.
• Naevus cells are present not only in epidermis, but
also in the subdermal fat and muscle.
• The risk of malignant melanoma is about 10%.
• Malignant melanoma tends to be axial.
• Removal is performed for aesthetic and oncological
reasons.
7. Dysplastic naevi are different from acquired naevi
in the following ways:
• Malignant potential is more (Figs 31.35 and 31.36).
• Family members may have such lesions.
• Such syndrome is described as familial dysplastic
naevus syndrome.
MALIGNANT MELANOMA (MELANOCARCINOMA)
It is a malignant tumour arising from pigment-forming
cells (melanoblasts) which are derived from the neural
crest. Melanoblasts and melanocytes convert dihydroxyphenylalanine (DOPA) into melanin. This is known as
a positive DOPA reaction (Key Box 31.7).
It is a potentially curable tumour in early stages. If it
is left untreated or is not treated properly, it disseminates
rapidly, showers the body with tumour emboli, and
offers a very painful death.
Some interesting ‘mosts’ about malignant melanoma
are listed in Key Box 31.8.
Key Box 31.7
Positive Dopa Reaction
TYROSINE
↓
DOPA
↓
MELANIN
Key Box 31.8
Interesting ‘Most’ for Malignant Melanoma
Most benign form of melanoma is lentigomaligna
melanoma.
Most common form of melanoma is superficial spread-
ing melanoma.
Most malignant type of melanoma is nodular melanoma.
Most reliable independent prognostic indicator in
malignant melanoma is tumour thickness based on
Breslow classification.
Most of them (majority) arise from pre-existing moles.
Most of the melanoma are pigmented. However, pig-
mentation is not mandatory for diagnosis of melanoma.
Fig. 31.35: Dysplastic naevi
over the face
1
Choroid has no lymphatics. Hence excellent prognosis.
Fig. 31.36: Dysplastic naevus
left parotid region
Common Sites of Malignant Melanoma
• Head and neck: 20–30%
• Lower extremity: 20–30%
• Trunk: 20–30%
• Remaining cases occur in the upper extremities,
1
genitalia, and choroid of the eye
.
Aetiopathogenesis (Fig. 31.37)
Risk factors for malignant melanoma are listed in
Key Box 31.9.
1. Ultraviolet rays: It is more common in white-skinned
people. There is a linear correlation between the
Section II • General Surgery
260
Fig. 31.37: Aetiopathogenesis
Key Box 31.9
Manipal Manual of Surgery
Risk Factors for Developing
Malignant Melanoma (MM)
Pigmentosa xeroderma
Immunocompromised—HIV, Hodgkin’s disease treated
with cyclosporin
Genetic—History of dysplastic naevus
Melanoma excised earlier
Early childhood burns and eyes blue, red hair
Naevus: GCPN and total number >20 naevi
Tendency to freckle
Remember as PIGMENT
intensity of exposure to sunlight and malignant
1
melanoma in white-skinned people
. White-skinned
people who live close to the equator have an increased
risk of developing malignant melanoma. The highest
incidence is found in Queensland (Australia). For the
same reason, malignant melanoma is common in the
United Kingdom, North America and Australia.
Ultraviolet A (UVA) rays have a long wavelength and
deep penetration, causing tanning and wrinkling.
2. Age and sex: Malignant melanoma is more common
in females. The higher incidence of the disease is
found during the reproductive age period. Even
though oestrogen and progesterone receptors are
found in malignant melanoma in some patients, their
true role is not yet established. The leg is the most
common site in females. The incidence of melanoma
is 1.7 times higher in women than men <39 years of
age. After 70 years of age, the incidence of melanoma
is 2.2-fold higher in men than women.
3. Genetic factors: Tumour suppressor gene mutation
9p21, Deletion or rearrangement of chromosomes
10 and 8p. Familial, atypical, multiple, mole, melanoma syndrome—previously known as familial,
dysplastic naevus syndrome . Multiple, large (> 5 cm),
atypical dysplastic nevus in areas covered by clothing
are characteristic. The disease is also common in
individuals of the Celtic race who give a family
history of malignant melanoma (3–5%).
4. Pre-existing mole: Approximately 2/3rd
of melanomas
arise in a pre-existing mole, and the remaining
1/3rd arise de novo. Malignant change occurs in the
junctional or compound naevus. Malignancy should
be suspected when certain changes occur in a mole
(Key Box 31.10). Patients with atypical mole, large
naevus in those with red hair, blue eyes, and
Fitzpatrick skin type are predisposed to malignant
melanoma.
5. Immunosuppression: Increased incidence of malig-
nant melanoma has been found in patients with renal
transplantation, leukaemia, and AIDS.
6. Xeroderma pigmentosum and albinism patients are
susceptible to melanomas.
Key Box 31.10
Glasgow—Check List (Figs 31.38 and 31.39)
1. Change in size
2. Change in shape
3. Change in colour
4. Inflammation
5. Crusting, ulceration, bleeding
6. Sensory change
Ugly duckling sign: Patients
with multiple moles, which
are having similar characteristics and when malignancy
develops in one of the
moles, it deviates from the
normal. (It will be different).
7. Diameter >6 mm
Figs 31.38 and 31.39: Only complaint of this 28-year-old lady
was an increase in the size and oozing from the lesion
“Bronzed, blue-eyed, blond, body beautiful—high chances of
malignant melanoma”
3
Section II • General Surgery
Malignant melanoma is the killer of whites. Bronzed body beautiful concept should be discouraged.
Skin Tumours
261
Pathology (Fig. 31.40)
Microscopic picture: Anaplastic, pigment-laden
melanocytes confined to the epidermis. The cells which
have vacuolated cytoplasm (Paget’s cells resembling
those seen in Paget’s disease of the breast) are found.
Cells also invade the dermis. Along with pigment-laden
1
macrophages, dermal infiltration of lymphocytes
may
be present. Rarely, anaplastic melanocytes do not form
pigment (amelanotic melanoma).
All melanomas (except nodular) show radial growth
initially, in the form of intraepidermal growth.
However, nodular melanoma has a vertical growth
phase, which involves the dermis and results in nodule
formation. This has poor prognosis.
Pathological Grading of Malignant Melanoma
Breslow described staging depending on the maximum
thickness at the centre of the lesion.
Stage I: Thickness <0.75 mm
Stage II: 0.76–1.5 mm
Stage III: 1.51–3.0 mm
Stage IV: >3 mm
• <1 mm is regarded as thin melanoma.
Please note: Clarke’s level of invasion (it is no longer
followed).
Clinical Types (Table 31.4)
Clinical Features
• Malignant melanoma may present as changes in the
pre-existing mole (Key Box 31.11).
• The patient may present as a nonhealing ulcer of the
sole of the foot.
• It is a painless ulcer with irregular borders. Ulcer
bleeds easily on touch. Lesion is firm in consistency
and induration is absent. A halo may be present
around the ulcer.
• Ugly duckling sign: A lesion that stands out as
different from the patient’s own nevi
• Typically, the ulcer is pigmented (Fig. 31.41). In 10%
of patients, pigment is absent. They are called
amelanotic melanoma.
• The lesion moves with the skin and is usually not
fixed to underlying structures.
Key Box 31.11
ABCDE of Evaluating a Changing Mole
A Asymmetry: One half does not match the other
B Border irregular: Ragged or blurred
Fig. 31.40: Malignant melanoma with malignant cells showing
dark melanin pigment inside. Second picture is a close-up view
(Courtesy: Dr Laxmi Rao, Head, Department of Pathology, KMC,
Manipal)
Table 31.4 Clinical types of malignant melanoma (Figs 31.41 to 31.44)
Name Nature Behaviour
Lentigo malignant melanoma Arises from Hutchinson’s melanotic freckle Least common (5%)
Occurs in old people on face and temporal region Least malignant
Superficial spreading Any part, more in the trunk Most common (70%)
Nodular Any part, more in the leg, raised papular lesions Most malignant, invasive (15–30%)
Acral lentiginous Located on the palm, sole, digits Presents late, aggressive (4–8%)
Amelanotic Difficult to diagnose Rare, nonpigmented (5%)
Desmoplastic (neurotropic) Often involves nerve fibres Invasive melanoma
1
Presence of lymphocytes may be an indication of host response ‘Fight’ against cancer.
C Colour variation: Tan, black, brown
D Diameter: >6 mm
E Evolving (elevation): Change in a pre-existing lesion
Section II • General Surgery
262
Manipal Manual of Surgery
• Satellite nodules (within 5 cm of the primary) may
be found surrounding the lesion and are due to intradermal lymphatic spread (Fig. 31.42). Such patients
will have greatly enlarged, firm, nontender nodes.
• In-transit lesion—disease found in the dermis or
subcutaneous tissue >5 cm away from the primary
melanoma, but before the regional lymph node basin
(Figs 31.43–31.47).
• See Key Box 31.12 for the acral lentiginous variety.
Fig. 31.41: Superficial spreading Fig. 31.42: Nodular
Key Box 31.12
Acral Lentiginous (Fig. 31.48)
Least common subtype
Popularly called hand and foot melanoma
Occurs in palms and soles
This subtype occurs in dark-skinned people (21–22%)
In subungual region—blue black discolouration of
posterior nail fold (most common on great toe or
thumb)
Pigmentation in proximal or lateral nail folds
(Hutchinson’s sign) due to radial spread
Fig. 31.43: Acral
lentiginous variety
with early changes—
never incise or c
terise such melanomas
A B
Fig. 31.45A: Observe the foot,
little toe has been amputated
five years back for malignant
melanoma
Section II • General Surgery
Fig. 31.44: The lesion resembles
squamous cell carcinoma. Punch
biopsy reported as amelanotic
au-
melanoma
Fig. 31.45B: Same patient
as in Fig. 31.45 A presented
to the hospital with in-transit
deposits
Fig. 31.46: Malignant melanoma operated—recurrence after
8 months with satellite nodule. It is important that the first surgery
should be the best surgery. Every attempt should be made to
do a three-dimensional excision
Fig. 31.47: Whole leg is studded with tumour. In-transit deposits
from malignant melanoma of the foot
AMELANOTIC MELANOMA (Fig. 31.47)
• Lesion appears pink.
• It has a poorer prognosis than nodular melanoma.
In all cases of suspected melanomatous skin lesions, examine
the axillae, scalp, soles, genitalia, oral cavity, and interdigital
webs also.
Skin Tumours
Fig. 31.48: Hutchinson’s sign—close-up view
Differential Diagnosis
• Pigmented basal cell carcinoma, histiocytoma
(sclerosing angioma)
• Naevus, Kaposi’s sarcoma, cavernous haeman-
gioma.
Spread
. Local spread occurs mainly by continuity and
1
contiguity. Satellite nodules are due to local and
lymphatic spread, situated within 5 cm of the primary
lesion. Malignant melanoma rarely infiltrates the
deep fascia unless and until a ‘blunder biopsy’ is
done. Inadequate local excision may result in local
recurrence later. Hence, initial surgery should
attempt at achieving cure.
2. Lymphatic spread is the principal mode of spread.
Regional nodes get involved very early, altering the
prognosis. Thus, nodes may get very enlarged even
when the lesion looks innocent. Spread occurs by both
permeation and embolisation. Permeation produces
satellite nodules and in-transit nodules which
develop between primary and secondaries. Embolisation occurs rapidly, producing massive regional
nodes early (Key Boxes 31.13 and 31.14).
In-transit metastases appear in the skin as intracutaneous metastases. They are thought to be due to
melanoma cells trapped within lymphatic vessels.
263
Key Box 31.13
Malignant Melanoma Sole
Inguinal nodes
↓
Iliac nodes
↓
Para-aortic nodes
↓
Mediastinal nodes
↓
Supraclavicular nodes
Key Box 31.14
Lymph Node Metastasis in Malignant Melanoma
It is the single-most important prognostic index and it
presents stage III disease.
Number of nodes is more important than size of nodes.
Poor survival in ulcerated malignant melanoma, even
if node-negative.
Extranodal extension has poor prognosis.
Lymph node metastasis proceeds as an orderly process.
Thus, evolved the concept of the first node to get
involved—sentinel node (SN).
Elective lymphadenectomy is not indicated in thin
melanoma (1 mm).
In thick melanoma, do a sentinel node biopsy. If
positive, proceed to complete lymphadenectomy
(block dissection).
3. Blood spread occurs relatively early and causes
secondaries in the liver, lung, brain, and bones,
producing miserable, pathetic situations (Table 31.5).
A 55-year-old lady presented to the hospital with enlarged
inguinal lymph nodes. Clinical examination revealed
nodules in the leg with firm to hard enlarged nodes in the
inguinal region. On careful observation, the little toe was
missing. On questioning, the patient admitted that the toe
had been amputated elsewhere five years back for a
painless, blackish lesion (Figs 31.45A, B).
Table 31.5 Spread of malignant melanoma
Spread Diagnosis Problems
Metastasis in lung Cannonball appearance, pleural effusion Respiratory failure
Metastasis in liver Massive hepatomegaly, ascites Abdominal discomfort
Metastasis in brain Raised intracranial tension Coma
Metastasis in bone Bony pains, pathological fractures Paraplegia, quadriplegia
Metastasis in bowel Bleeding Anaemia
Section II • General Surgery