A detailed presentation on the clinical features, predisposing factors and treatment of skin cancers especially Squamous Cell Carcinoma. Pre - malignant conditions like Actinic keratosis, Bowen disease, Porokeratosis are also discussed. Also the presentation provides a detail of the various differential diagnoses of the skin cancers. Useful for medical students, post graduate trainees and nursing staff. Role of sunlight is also discussed.
6. ACTINIC KERATOSIS
UV-induced precancerous skin lesion that may progress to
skin cancer on chronically sun exposed areas affecting
elderly males & females
More common in white population & those with red hair &
blue eyes.
Relapsing-remitting lesions.
7. Initially: small lesion
(macules or papules)
with rough surface
→ coarse sandpaper-
like texture
Usually asymptomatic
Better appreciated by
palpation
May pass unnoticed by
patient
8. Later: lesions grow and
become erythematous and
adherent hyperkeratotic
scale -removed with difficulty
and pain , revealing punctate
bleeding points
Presence of tenderness,
induration , or a raised
shoulder beyond
disorganized scaling-
malignant transformation.
11. HIGH RISK CLINICAL FEATURES OF AK --EARLY
INVASIVE SCC
Multiple thick Aks
Past history of NMSC
Extensive actinic damage
Immunocompromised state
Tenderness, induration & enlarging lesion
17. CUTANEOUS HORN
• Benign curved, hard, yellow-to-
brown outgrowths composed
of keratin - resembles a horn & may
develop from preexisting actinic
and seborrheic keratosis or warts
• UVR-induced on light exposed areas
• May progress to squamous cell
carcinoma (SCC) ~ 40%
18. Keratotic lesion with a height of at least half the widest
diameter of its base
Dysplastic epidermal changes similar to AK
Inflammation, induration & pain at the base suggests
malignant transformation
clinically – wide base or low height-to-weight ratio
H/P – budding from basal layers in long established lesions
22. ARSENICAL KERATOSIS
A corn like punctate keratosis caused
by arsenic / a few years after
exposure, mainly affecting the palms &
soles.
Hyperpigmentation –raindrop pattern ,
accompanied by hypopigmenated
areas, and progression to generalized
thickness of palms and soles .
Smoking , nutritional deficiencies
(retinol, Ca, iron, folate ,vitamin
A,E,C)
23. H/P – epithelial dysplasia or hyperplasia. No typical
microscopic feature.
May progress to BCC, SCC or Bowen’s disease – induration ,
inflammation and ulceration become apparent.
DIFFERNTIAL DIAGNOSIS
Disseminated puntate keratoderma
Darier’s disease
Lichen planus
Planter warts
24. MANAGEMENT
Reduce arsenic exposure
Well balanced diet
1st line
Solitary / few lesions – cryotherapy ,cautery or curettage.
Multiple keratosis – oral retinoid in combination with
keratolytics
2nd line
Imiquimod cream 5% OD for 6weeks or OD 3-5times per
week
26. BOWEN’S DISEASE
Squamous cell carcinoma in situ
(SCCIS) of the skin.
UVR-induced damage in sun-exposed
areas & non exposed areas, often
associated with HPV
Single, large, persistently non-elevated,
well demarcated, erythematous plaque,
with white-to-yellow scale – moist ,
reddened, granular surface on
detachment with no bleeding point.
27. ~10-20% multiple lesions , either
widely spread or sometimes close
together.
Slower growth rate and spontaneous
partial regression at times.
Can occur on perianal skin,
subungal region, palms & soles -
higher risk of invasion & recurrence.
May progress to invasive squamous
cell carcinoma. ~3-5% risk
29. Histopathology
Full thickness epidermal dysplasia
& disordered differentiation with
loss of epithelial polarity.
Parakeratosis & acanthosis.
Large hyperchromatic nuclei
Atypical mitosis and gaint cells.
35. POST –IONIZING RADIATION
KERATOSIS
An area of scarring following accidental exposure to radiation
or after therapeutic radiotherapy or excessive fluoroscopy
Relatively uncommon –after months to years following
exposure
On limbs mostly or covered body sites.
Changes similar to AK, telangiectasia, vasculitis, radiation
ulcers, hemangiomas, subcutaneous sclerosis of connective
tissue.
36. D/D – Actinic Keratosis
H/P – epidermal changes similar to
AK.
Dermis – much extensive
replacement of collagen by scar and
elastotic material
MANAGEMENT
Skin biopsy to confirm the
diagnosis
Immediate reduction to exposure
Cryotherapy for individual lesions.
38. DISSEMINATED SUPERFICIAL
ACTINIC POROKERATOSIS
Multiple enlarging rough hyperkeratotic
papules surrounded by a thread like
elevated border , on distal extermeties
– usually around a follicle
Skin within the ring is atrophic ,
erythematous or hyperpigmented.
Hypopigmented ring just inside the
ridge.
39. Prominent in summer &
improve in winter.
Very low chances of
malignant transformation.
H/P
-cornoid lamella at the
margins.
- narrow column of altered
keratin
- dyskeratotic & vacuolated
epidermal cells
41. DIFFERENTIAL DIAGNOSIS
Actinic keratosis
– esp if on face , but present on other sun exposed sites as
well
Bowen’s disease
– on legs
Superficial BCC
42. MANAGEMENT
Good use of emollient & high factor broad spectrum sunscreen
Cryotherapy with liquid nitrogen
Topical diclofenac gel , vit D3 analogues, 5% 5-FU cream, 5%
imiquimod cream
Photodynamic therapy
Erbium , CO2, Q-switch ruby laser, Nd:YAG –under successful
trials.
43.
44.
45. SCC
Older males
Common type of Non Melanoma Skin Cancer
( NMSC )
It is derived from keratinocytes
May develop de novo or from precursor AK or SCC in situ
Mainly on sun exposed sites
(hairless scalp, upper part of face, lips (Lowerlip), ears
(helices), dorsa of hands, forearms, lower legs)
Size
few milimeters to centimeters in diameter.
51. ...cont
Viral Infections (HPV-16,-18) – viral warts,genital warts, many
mucosal SCCs.
B-type of HPV > excess risk of SCC.
Longstanding dermatosis
longstanding leg ulcer, fistula tracts, chronic injury site,
inflammation sec to Hidradenitis supparativa.Thermal scars –
Marjolin’s ulcer that occurs on chronic wound or scar including
scars from burn.
Immunosuppression ( ciclosposrin , azathioprine , organ
transplant recipients , haematological malignancies , HIV )
52.
53. 1st clinical sign – induration.
Firm , tender , erythematous nodule or plaque with keratotic
crust , verrucous, tumid
Eroded fungating mass – that shows easy bleeding
Lesions that fail to heal – develop ulcers
with everted edge , indurated base & necrotic floor
Outline – mostly irregular , sometimes rounded.
54.
55. Mobile structures like lip & Genitalia
show early fissuring or small erosions or ulcers that fail to
heal and bleeds recurrently.
May be associated with other features of photodamage or
premalignant lesions.
Parestheisa , anesthesia, tenderness, pain particularly in
perineural invasion
Regional LN enlargement (later –hard & fixed)
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69. Proliferation of Atypical
Keratinocytes
Typical SCC has nests of
squamous epithelial cells
arising from epidermis
and invading into dermis
70. Malignant cell – large,
abundant eosinophilic
cytoplasm & large
vesicular or
hyperchromatic
nucleus with
pleomorphism &
mitosis.
71. Variable keratinaization
squamous eddies ,
keratin pearls
(concentric layers of
squamous cells with
increasing keratinization
towards the center)
Inflammatory infiltrates –
varies considerably in
intensity
primarily lymphocytes &
plasma cells
72. Grading of SCC
Depends on how easy it is to recognize the characteristics
of squamous epithelium (e.g, intracellular bridges ,
keratinization ) , pleomorphism & mitotic activity
The greater the degree of keratinization – the better
differentiated tumor.
75. METASTATIC SCC
Upto 5% RISK OF METASTASIS
Invasive SCC rarely metastasize and prove fetal.
that refers to growth into deeper layers of skin , the
dermis.
More difficult to treat than the original skin lesions.
In 80% cases metastases develops from draining LN.
80. DIAGNOSIS DIFFERENTIATING POINTS
Keratoacanthoma (KA ) Faster growth rate, involute to leave a scar.
Classified as well differentiated SCC.
No precursor lesion unlike SCC.
Presents (initially) as firm, rounded flesh coloured papule
(like MC) , (later) if keratotic > like a viral wart.
More hyperkeratotic than AK
Spontaneous resolution ~ 3months
Actinic keratosis ( AK ) Sun exposed area. Multiple. Macules or papules with
rough scaly surface & lack of dermal component on
palpation. Asymptomatic. 10% chances of SCC
Bowen’s disease / carcinoma in situ Solitary, larger, persistently non elevated, erythematous
scaly plaque, with no bleeding on detachment. Slower
growth rate and spont partial regression at times.
Asymptoamtic
81. … cont
Cutaneous horns Curved , hard, yellow to brown keratotic outgro
circumferential ridges.Mostly single. Inflammati
induration & pain at the base suggests malignan
transformation. ~40%/usually SCC
Warty leasion ( viral warts , seborrheic keratosis) Multiple , not indurated.
SK have darker, raised & greasy warty surface.
Basal cell carcinoma ( BCC ) Single , less hyperkeratotic than AK, irregular
erythematous base.
Arsenical keratosis Corn like , punctate keratosis caused by arsenic
after exposure), mainly on palms and soles.
Presents as hyperpigmentation of skin ,accompa
hypopigmented areas.
Progress over time with increase in numbers. Hi
developing BCC, SCC/ bowen’s disease.
83. Skin biopsy - to confirm diagnosis
MRI (in case of head and neck tumors and higher chances of
mets)
CT scan(in case of nerve involvement )
USG combined with a guided fine needle aspiration or core
biopsy (in case of LN involvement )
High resolution micro oil MRI / SPECT / PET – role in future.
Reflectance confocal microscopy & high resolution optical
coherence tomography – under trials.
84.
85. Aim
Remove primary tumor & prevent recurrence
Rx
Depends on clinical (size, location, number) & pathological
features of tumor.
Long term prognosis for adequately treated SCC is excellent.
Larger / aggressive lesions need imaging before starting the
treatment.
86.
87. High Risk Clinical Features (HRCP)
- diameter >20mm
- immunosuppressive
- site: ear, lip, scalp,eyelid
- SCC arising in burns, scars, chronic
ulceration , radiation damage.
Bowen’s disease in non sun exposed
skin , inflammatory conditions.
High Risk Pathological Features (HRPF)
- depth >4mm & diameter >20mm
-poorly differentiated
- perineural invasion
-lymphovascular invasion
-subtypes: desmoplastic , spindle cell,
acantholytic, arising in Bowen’s
disease in non-sun-exposed skin