SKIN

DR. C.T. KARTHIKEYAN, ASSOCIATE PROFESSOR,

DEPT. OF GENERAL SURGERY.
FUNCTIONAL ANATOMY AND
PHYSIOLOGY OF SKIN
• Skin can be divided into two layers: the outer epidermis
and the inner dermis.
• Deep to the dermis lies subcutaneous fat and remnants
of the panniculus carnosus.

• Epidermis:
The epidermis is 5% of the skin and is composed of five
layers of keratinised, stratified squamous epithelium.
o Stratum basalis (deep)
o S. spinosum
o S. granulosum
o S. lucidum
o S. corneum (superficial).
• Dermis:
Dermis comprises 95% of skin and is structurally
divided into
o Superficial papillary layer- composed of delicate
collagen and elastin fibres in ground substance,
into which a capillary and lymphatic network
ramifies.
o Deeper reticular layer- composed of course
branching collagen.

• The epidermis and dermis meet at the dermo-

epidermal junction in a three-dimensional wave-
like arrangement.
• Skin adnexa
o Hair follicles
o Sebaceous and sweat glands
o Strips of smooth muscle (Arrector pili) are
inserted into the wall of the hair follicle
MALIGNANT SKIN TUMOURS
• BASAL CELL CARCINOMA
• SQUAMOUS CELL CARCINOMA
• MALIGNANT MELANOMA
I. BASAL CELL CARCINOMA
• This is usually a slow-growing, locally-invasive,
malignant tumour of pluripotential epithelial
cells arising from basal epidermis and hair
follicles, hence, it affects the pilo-sebaceous skin.
EPIDEMIOLOGY AND PREDISPOSING FACTORS
• It occurs in the elderly or the middle-aged after
excessive sun exposure, with 95% occurring
between the ages of 40 and 80 years.
• The strongest predisposing factor to BCC is
UVR.
• Exposure to arsenical compounds, coal tar,
aromatic hydrocarbons, ionizing radiation
• Genetic skin cancer syndromes.
• White-skinned people are almost exclusively
affected.
• BCC is more common in men than women.
PATHOGENESIS
• The most likely model of pathogenesis for BCCs involves
mesodermal factors as intrinsic promoters coupled with
an initiation step.
• BCCs metastasise extremely rarely.

MACROSCOPIC
• BCC can be divided into
o Localised
(nodular; nodulocystic; cystic; pigmented and naevoid).
90% of BCC are nodular and nodulocystic variants.
o Generalised
(superficial: multifocal and superficial spreading;
or infiltrative: morphoeic, ice pick and cicatrizing).
A nodulocystic basal carcinoma. An ulcerating BCC on the lower eyelid.

A recurrent morphoeic BCC.

MICROSCOPIC
• Twenty-six histological subtypes.
• The characteristic finding is of ovoid cells in nests with a
single ‘palisading’ layer.
• It is only the outer layer of cells that actively divide,
explaining why tumour growth rates are slower than their cell
cycle speed would suggest, and why incompletely excised
lesions are more aggressive.

PROGNOSIS
• There are ‘high-risk’ and ‘low-risk’ BCCs.
• High-risk BCCs are
o Large (>2 cm); located at sites where direct invasion gives
access to the cranium (near the eye, nose and ear)
o Recurrent tumours
o Tumours forming in the presence of immunosuppression
o Micronodular or infiltrating histological subtypes.
MANAGEMENT
• Treatment can be surgical or non-surgical.
• Tumour and surrounding surgical margins should
always be assessed and marked under loupe
magnification.
• Where margins are ill-defined, a two-stage
surgical approach with subsequent
reconstruction after confirmation of clear
margins.
• Mohs’ micrographic surgery.
• In the elderly or infirm patients- radiotherapy.
• Superficial tumours- topical treatments (5-
fluorouracil, imquimod).
MOH’S MICROGRAPHIC SURGERY
• A surgical procedure to remove a visible lesion on
the skin in several steps.

• First, a thin layer of cancerous tissue is removed.

• Then, a second thin layer of tissue is removed and

viewed under a microscope to check for cancer cells.

• More layers are removed one at a time until the

tissue viewed under a microscope shows no
remaining cancer.

• This type of surgery is used to remove as little

normal tissue as possible.
II. SQUAMOUS CELL CARCINOMA
• Cutaneous squamous cell carcinoma is a malignant
tumour of keratinising cells of the epidermis or its
appendages.
• It arises from the stratum basalis of the epidermis and
expresses cytokeratins 1 and 10.

EPIDEMIOLOGY
• Four BCCs occur for every SCC, which is the second most
common form of skin cancer.
• It is strongly-related to cumulative sun exposure and
damage, especially in white skinned individuals living
near the equator.
• It is more common in men than women.
PREDISPOSING FACTORS
• SCC is associated with chronic inflammation (chronic
sinus tracts, pre-existing scars, osteomyelitis, burns,
vaccination points) and immunosuppression.
• When a SCC appears in a scar it is known as a Marjolin’s
ulcer.
• IR
• Chemical carcinogens (arsenicals, tar)
• Infection with HPV 5 and 16.
• Current and previous tobacco use doubles the relative
risk of SCC.
• Actinic (solar) keratoses (AK), i.e. cutaneous horns and
keratoacanthomas, were also considered to be
premalignant lesions leading to SCC.
• Keratoacanthomas are rapidly-growing, nodular
tumours, considered as self-healing SCCs
A squamous cell carcinoma (SCC) on A recurrent SCC arising in a previously
the face. skin-grafted area of the scalp.

SCC arising on the dorsum of the hand in a renal

transplant recipient on immunosuppressive therapy.
SCC arising on the lip of a smoker who
worked outside on a farm.
Actinic keratoses
MACROSCOPIC
• The appearance of SCC may vary from smooth nodular,
verrucous, papillomatous to ulcerating lesions.
• All ulcerate eventually, as they grow.
• The ulcers have a characteristic everted edge and are
surrounded by inflamed, indurated skin.
• Differential diagnoses of SCC include:
AK, BCC, pyoderma gangrenosum, warts, and lichen
simplex chronicus

MICROSCOPIC
• Characteristic irregular masses of squamous epithelium
are noted to proliferate and invade the dermis from the
basal layer.
• SCC can be graded histologically according to Broder’s
grading, which describes the proportion of
dedifferentiated cells in the tumour.
PROGNOSIS
• There are several independent prognostic variables for
SCC:
• ● Depth: the deeper the lesion, the worse the prognosis.
• ● Surface size: lesions >2cm have a worse prognosis
• ● Histological grade: the higher the Broder’s grade, the
worse the prognosis.
• ● Microscopic invasion of lympho-vascular spaces or
nerve tissue.
• ● Site: SCCs on the lips and ears have higher local
recurrence rates than lesions elsewhere, and tumours at
the extremities fare worse than those on the trunk.
• ● Aetiology: SCCs that arise in burn scars, osteomyelitis
skin sinuses, chronic ulcers and areas of skin that have
been irradiated.
• ● Immunosuppression: SCCs will invade further in those
with impaired immune response.
• The overall rate of metastasis is 2% for SCC (usually to
regional nodes) with a local recurrence rate of 20%
MANAGEMENT
• Surgical excision.
A 4 mm clearance margin should be achieved if
the SCC measures 2 cm. 95% of local recurrence
and regional metastases occur within 5 years.
III. CUTANEOUS MALIGNANT MELANOMA
• Melanoma is a cancer of melanocytes and can,
therefore, arise in skin, mucosa, retina and the
leptomeninges.

EPIDEMIOLOGY
• Exposure to UVR.
• White skinned races, not suited to sun exposure.
• It is responsible for over 75% of skin malignancy-
related deaths.
• It is the commonest cancer in young adults (20–39
years) and the most likely cause of cancer-related
death.
PATHOPHYSIOLOGY
• Cumulative UV exposure favours the development of lentigo
maligna melanoma (LMM) and later onset of disease, whereas
‘flash fry’ exposure, typical of rapidly-acquired, holiday
tans, favours the other morphological variants and early onset
of disease.
• A small proportion of MM is genetically-mediated and
develops at an earlier age.

• People at most risk of developing MM include:

o Those with genetic syndromes
o Past history or family history of MM
o Those who have more than 30 sun-acquired naevi
o History of five significant sun-burns.
o Fair-skinned/ red-haired people living close to the equator
o Anyone with excessive UVR exposure (environmental or
salon-delivered)
o Anyone with immunosuppression (which increases MM
incidence 20–30-fold).
MACROSCOPIC

• Only 10–20% of MM form in pre-existing naevi,

with the remainder arising de novo in previously
normally pigmented skin.
• The most likely naevi to form MM are atypical
naevi, atypical junctional lenitiginous naevi
(usually facial) and giant pigmented congenital
naevi.
• Macroscopic features in a pre-existing naevus
that suggest malignant change .
 There are four common macroscopic variants of
MM and several other notable, but rarer forms:
1. Superficial spreading melanoma (SSM)
This is the most common presentation (70%),
usually arising in a pre-existent naevus after
several years of slow change, followed by rapid
growth in the preceding months before
presentation.
2. Nodular melanoma (NM)
• Nodular melanoma accounts for 15% of all MM and
tends to be more aggressive than SSM, with a shorter
clinical onset.
• These lesions often arise de novo in skin often presenting
in middle age and usually on the trunk, head or neck.
They typically appear as blue/black papules, 1–2cm in
diameter, and because they lack the horizontal growth
phase, they tend to be sharply demarcated.
3. Lentigo maligna melanoma
LMM was previously also known as Hutchinson’s
melanotic freckle.
• This variant presents as a slow-growing, variegated
brown macule on the face, neck or hands of the
elderly. They are positively correlated with
prolonged, intense sun exposure.
• LMM are thought to have less metastatic potential.
Nonetheless, when they have entered the vertical
growth phase their metastatic potential is the same
as any other melanoma.
4. Acral lentigious melanoma (ALM)
• ALM affects the soles of feet and palms of hands. It is
more common in the Afro-Caribbean, Hispanic and
Asian population.
• It usually presents as a flat, irregular macule in later life.
25% are amelanotic and may mimic a fungal infection or
pyogenic granuloma.
• For finger or toe nail lesions it is vital to biopsy the nail
matrix, rather than just the pigment on the nail plate.
A classical feature of a subungual melanoma is
Hutchinson’s sign: nail fold pigmentation that widens
progressively to produce a triangular pigmented macule
with associated nail dystrophy.
o Miscellaneous

● Amelanotic melanoma may present as a

flesh-coloured, skin lesion; as a metastasis from
an unknown skin primary; or, in the
gastrointestinal tract, with obstruction or
intussusception.

● Desmoplastic melanoma is mostly found on

the head and neck region. It has a propensity for
perineural infiltration and often recurs locally if
not widely excised. It may be amelanotic clinically.
MICROSCOPIC
• Malignant change occurs in the melanocytes in
the basal epidermis, while in situ, atypical
melanocytes are limited to the dermo-
epidermal junction and show no evidence of
dermal involvement.
• During the horizontal growth phase, cells spread
along the dermo-epidermal junction and
although they may breach the dermis, their
migration is predominantly radial.
• During the vertical growth phase, the dermis
maybe invaded. The greater the depth of
invasion, the greater is the metastatic potential
of the tumour.
MANAGEMENT
• History and clinical examination
• An excision biopsy with 2–3 mm margin of skin
• Incision biopsy is occasionally indicated
• Biopsy and pathological examination provide
the first step towards staging melanoma.
-The Breslow thickness of a melanoma (measured to
nearest 0.1 mm from granular layer to base of
tumour) is the most important prognostic indicator in
the absence of lymph node metastases.
-The American Joint Committee on Cancer (AJCC)
staging system then takes lymph node and distant
metastases into account.
INVESTIGATIONS

• Investigations should be directed towards detecting

occult disease, so as to upstage patients and treat
them accurately and appropriately, the only cure
for MM currently being appropriate surgery.

• Thus, offering sentinel node biopsy to patients

with T2a disease and greater is prudent and
investigations for T3a disease and greater should
be directed to individual clinical presentation.
LOCAL TREATMENT

• The treatment for melanoma is surgery.

• Lentigo maligna (melanoma in situ) should be
excised completely in most clinical situations
because of the risk of it entering the vertical
growth phase to become LMM.
• A complete excision requires no further
treatment.
• For in situ melanoma a wide excision of 5mm is
sufficient; for melanoma
REGIONAL LYMPH NODES

• The likelihood of metastatic spread to regional

lymph nodes is proportional to the Breslow
thickness of the melanoma.
• Sentinel node biopsy (SNB), an investigation
based on the fact that lymphatic metastases
proceed in an orderly fashion and can be
predicted by mapping the lymphatic drainage
from a primary tumor to the first or ‘sentinel’
node in the regional lymphatic basin.
ADJUVANT THERAPY
• Targeted therapy in stage IV melanoma using
Dabrafenib or Vemurafenib.

• Trametinib shows promising results in stage 4

disease.

• Ipilimumab or Nivolimumab demonstrate

benefit in metastatic or unresectable melanoma.
PROGNOSIS
• The Breslow thickness of the primary tumour
offers the best correlation with survival in stage I
disease.
• Mitotic index.
• Presence or absence of ulceration.
• Presence of lymph node metastasis.
• Extranodal extension.
• Once regional nodes are clinically involved, 70–
85% of patients will have occult distant
metastases.
Thank You