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SURGICAL SHORT CASES
1.LIPOMA
2. SEBAECEOUS CYST
3.DERMOID CYST
4. KELOID
5.BCC
BY
DR.A.SASIDHARAN MBBS
Introduction
 Commonest tumor of s/c
tissue.
 Benign
 Arising from yellow fat
 Universal tumor
 Karyotype 12q change
 Hibernoma
Types
Encapsulated s/c lipoma
Diffuse variety
Multiple lipomas- Dercum’s
d/s
Histological types
Fibrolipoma
Neurolipom
a
Naevolipom
a
location presentation d.d. Significance
s/c Mobile, lobular,
edge slips under
palp.fingers
Neurofibrom
a
Most common
variety
subfascial Diff. to appreciate
edge & lobulation
Implantation
dermoid ,
Tbtenosynovitis
In scalp- erodes
bone
Subsynovial,
intra-articular
Knee/elbow
sweling
Bursa,
Baker’s cyst
Intra-articular is
rare
Intermuscular Swelling Fibrosarcoma
Hematoma
More chance of
devpg
liposarcoma
Parosteal Feels hard Bony tumor Very, very rare
Contd..
location presentation d.d. Significance
Submucus Asymptomatic/
stridor
Intestinal/laryngea
l tumor
Intussusception
Subserosal Retroperitoneal
swelling
Hydronephrosis,
retroperitoneal
cyst
Liposarcoma
Extradural Very rare - -
Intraglandula
r
Breast, pancreas Cystic lesions Very rare
Clinical features
 Localized, lobular, non-
tender
 Semi-fluctuant
 Mobile
 Slip sign
 Skin free
 Pedunculated +/-
Complications
 Myxomatous degeneration
 Saponification
 Calcification
 Infection
 Ulceration
 Intussusception & intestinal
obstruction
Liposarcoma
 Common in retroperitoneum, thigh &
back
 Rapid growth
 Warm & vascular
 Dilated veins
 Restriction of mobility
 Skin fixation & fungation
 Hematogenous spread to lungs
Treatment
 Excision
 Liposarcoma- wide
excision, reconstruction, adjuvant chemo-
& radiotherapy
DISEASES OF SEBACEOUS GLANDS
sebaceous gland: Holocaine glands in the skin that secrete
sebum
usually through the hair follicles.
• Sebaceous hyperplasia
• Adenoma sebaceum (Sebaceous adenoma)
• Sebaceous cyst (Epidermoid cyst)
4 Acne
5 Sebaceous gland carcinoma
SEBACEOUS CYST (EPIDERMOID CYST)
• Epidermoid cyst originates in the epidermis and a pilar cyst originates
from hair follicles, but neither type of cyst is strictly a sebaceous cyst
• The fatty, white, semi-solid material in both cysts is not sebum, but
keratin,
and under the microscope neither entity contains sebaceous glands.
• "True" sebaceous cysts are known as steatocystomas or, if multiple, as
steatocystoma multiplex.
Steatocystoma multiplex Epidermoid cyst
Pathogenesis: formation of acne
1 Increased activity of sebaceous glands with production of
excess sebum plays an important role
2 Occlusion of the pilo sebaceous orifices plays an
important
role
1 Hormones : Increased activity of sebaceous glands and
occlusion of the cornfied hypertrophic pilosebaceous
follicles lead to retention of sebum into the follicles, which
dilate and rupture by time.
2 Anaerobes such as Corynebacterium (Propionibacterium)
acne, Pityrosporon ovale and Staphylococci cause split of
the sebum into fatty acids and triglycerides which act as
an important irritating factors & → to the formation of the
different clinical types of acne which varies from
papules, pustules ,cysts and comedones
RX : SURGICAL
EXCISION OF THE CYST
SEBACEOUS CYST
DERMOID CYST
 Cyst lined by squamous epithelium
containing desquamated cells
 CONTENTS
mixture of sweat, sebum,
desquamated epithelial cells, hair
CLINICAL
TYPES
 CONGENITAL / SEQUESTRATION
DERMOID
SITE: along lines of embryonic fusion
(midline of body or face)
FORMATION: dermal cells sequestrated in
subcutaneous plane > proliferate & liquify
> cyst > grows & indents
mesoderm(future bone) > bony defects
 MEDIAL NASAL DERMOID CYST
(root of nose at fusion lines of frontal
process)
 EXTERNAL AND INTERNAL
ANGULAR DERMOID ( fusion line of
frontonasal and maxillary processes)
 SUBLINGUAL DERMOID
 PRE –AURICULAR DERMOID
 POST AURICULAR DERMOID
CLINICAL
FEATURES Manifests in childhood or adolescence
 Typically a painless slow growing
swelling
 Soft, cystic, fluctuant, yield to pressure of
finger and will not slip away
 Transillumination negative
 Putty in consistency
 No impulse on coughing
 Underlying bony defect – clue to
diagnosis
OTHER
TYPES
 IMPLANTATION DERMOID
> in women, tailors, agriculturists who
sustain repeated minor injuries
> sharp injury- epidermal cells implanted
in subcutaneous plane- dermoid cyst
> fingers, palm, sole of foot
> hard in consistency ( skin is thick)
 TERATOMATOUS DERMOID
> arise from totipotent cells
> ectodermal, mesodermal, endodermal
elements
> ovary, testis,retroperitoneum, mediastinum
 TUBULO-EMBRYONIC DERMOID
> from ectodermal tubes
> thyroglossal cyst, post- anal
dermoid
INVESTIGATIO
NS
 BLOOD – TC, DC,Hb,ESR
 URINE Examination
 FNAC-
 X ray- subjacent bone eroded by
dermoid
 Ultrasonography- mass cystic/ solid
 CT scan- size , shape , local spread
TREATME
NT Excision of the
cyst
Mass shown ( implantation
dermoid)
Incision
marked
Incision started ( cyst contents
leaking)
cyst being
removed
KELOID
History
A 23 year old female was referred by
plastic surgeons for radiotherapy to th
posterior ear lobe, following the
development of a Keloid Scar, three
years after an ear piercing
No family history of keloids
e
Pathology
Keloid is a unique huma
fibroproliferative disorde
inflammation, surgery,a
Commonly causes of kel
folliculitis, chicken pox,
(such as, earlobe piercin
wounds).
It is a benign growth, we
fibrous tissue overgrowt
original defect
n dermal
r that occurs after injury,
nd burn.
oids include acne,
accinations and trauma
g, lacerations, or surgical
ll-demarcated area of
h that extends beyond
the
v
Baron Jean-Louis Alibert
(1768-1837)
Described appearance
Crab-claw-like  Cheloid  Keloid
Effects of keloids
Compromise aesthetic Impairment of function
Itchy
Pain
Pruruti
c
How best can they be treated?
Treatment Options
Surgery
Intralesional Steroids
Radiation
Laser
Cryotherapy
Pressure
Multimodality
Therapy
Still Trying
Surgery Drawbac
ks
Painful
Difficult reconstruction with large keloids
Utilizes normal surrounding tissue – limiting later
reconstructive options
Low long term success as monotherapy
Steroids
 Triamcinolone
 Hydrocortisone
 Dexamethasone
 Methylprednisone
Laser
1980s in vogue
Proposed Mechanism
No knife  Less tissue
trauma
Cryotherapy- cold treatment
Di
us
 <10
minishes size and induration (HTS >Keloid) when
ed as monotherapy
% Recurrence when combined with surgery
Photos Courtesy of Dr.
Pressure Therapy
Radiation
Basal cell carcinoma (BCC) is a slow
progressing nonmelanocytic skin cancer
that arises from basal cells (ie, small,
round cells found in the lower layer of
the epidermis).
It is the most common skin cancer (80%)
Estimated 3.3 million cases are diagnosed per
year(US) and incidence doubles every 25 years
The incidence high in areas of ↑UV radiation
(Australia,South africa)
estimated lifetime risk of 33-39% for men
and 23-28% for women
Men >Women
It increases with age (50-80 yrs )
 Rare in <40 yrs (5-15%)
Sun damage
Repeated prior episodes of
sunburn
Fair skin, blue eyes and blond or
red hair ( also affect darker skin
types)
Previous cutaneous injury,
thermal burn, disease
(eg cutaneous lupus, sebaceous
naevus)
Inherited syndromes: BCC is a particular problem
for families with basal cell naevus syndrome
(Gorlin syndrome), Bazex syndrome, Rombo
syndrome and xeroderma pigmentosum
,albinism
Other risk factors include ionising radiation,
exposure to arsenic, coal tar, smoking tanning
bed and immune suppression due
to disease or medicines
The cause of BCC is multifactorial.
DNA mutations in the patched
(PTCH) tumour suppressor gene, part of hedgehog
signalling pathway (SHH)
triggered by exposure to ultraviolet radiation
Various spontaneous and inherited gene defects
predispose to BCC
BCC is a locally invasive skin tumour and
rarely
metastatize(< 0.01%)
The main characteristics are:
Slow growing: 0.5 cm in 1-2 years
Varies in size from a few millimetres to several
centimetres in diameter
Skin coloured, pink or pigmented
Spontaneous bleeding or ulceration
Waxy papules with central depression
Pearly appearance
Oozing or crusted areas: In large
BCCs
Rolled (raised) border
Translucency
Telangiectases over the surface
Black-blue or brown areas
BCC distrubution
:
Head and neck
60%
Nose 14%
Trunk 30%
Extremities 10%
There are several distinct clinical types
of BCC, and over 20 histological growth
patterns of BCC
Nodular
Superficial
Morphoeic
Basisquamous
Fibroepithelial tumour of Pinkus
Most common type of facial BCC
Shiny or pearly nodule with a smooth
surface with telangiectases
May have central depression or ulceration,
so its edges appear rolled
Cystic variant is soft, with jelly-like
contents
Micronodular, microcystic and infiltrative
types are potentially aggressive subtypes
Most common type in younger adults
Most common type on upper trunk
and shoulders
Slightly scaly, irregular plaque
Thin, translucent rolled border
Multiple microerosions
Also known as morphoeiform or
sclerosing
BCC
Usually found in mid-facial sites
Waxy, scar-like plaque with indistinct
borders
Flat or slightly depressed, fibrotic, and
firm
Wide and deep subclinical extension
Mixed basal cell carcinoma (BCC)
and squamous cell carcinoma (SCC)
Infiltrative growth pattern
Potentially more aggressive than other forms of
BCC
Warty plaque
Usually on
trunk
Characteristics of recurrent BCC
often
include:
Incomplete excision or narrow margins
at
primary excision
Morphoeic, micronodular, and
infiltrative subtypes
Location on head and neck
Advanced BCC
Advanced BCCs are large, often neglected tumours.
They may be several centimetres in diameter
They may be deeply infiltrating into tissues below
the
skin
They are difficult or impossible to treat surgically
Nevi malignant
melanoma
Keratoacanthoma
Seborrheic keratosis
Bowen disease
Actinic keratosis
Squamous cell carcinoma
 Skin biopsy
 To confirm and diagnose bcc and
its subtype Shave biopsy
Punch biospy
 Cytology
 Histologic findings
 Laser doppler (eyelids tumor
margins)
Treatment depends on size ,location and type
of
BCC
Curretage and electrosessication
Mohs micrographic surgery
Excisional surgery
Radiation
Cryosurgery
Photodynamic theray
Laser surgery
Topical medications
Curretage and electricdesiccation : The growth is
scraped off with a curette, an instrument with a
sharp, ring-shaped tip), then the tumor site is
desiccated (burned) with an electrocautery needle.
Small lesions
Leaves round whiitish scar
Not suitable for advanced bcc, in high risk sites.
Excision means the lesion is cut out and the skin
stitched up.
Most appropriate treatment for nodular,
infiltrative and morphoeic BCCs
Should include 3 to 5 mm margin of normal skin
around the tumour
Very large lesions may require flap or skin graft to
repair the defect
Further surgery is recommended for lesions that
are
incompletely excised
Cryotherapy is the treatment of a superficial
skin lesion by freezing it, usually with liquid nitrogen.
Suitable for small superficial BCCs on covered areas
of trunk and limbs
Results in a blister that crusts over and heals within
several weeks.
Leaves permanent white mark
Photodynamic therapy (PDT) refers to a technique in
which BCC is treated with a photosensitising
chemical, and exposed to light several hours later.
Topical photosensitisers include aminolevulinic acid
lotion and methyl aminolevulinate cream
Suitable for low-risk small, superficial BCCs
Results in inflammatory reaction, maximal 3–4 days
after procedure
Treatment repeated 7 days after initial treatment
Excellent cosmetic results
Radiotherapy or X-ray treatment can be used to treat
primary BCCs or as adjunctive treatment if margins are
incomplete.
Mainly used if surgery is not suitable
Best avoided in young patients and in genetic conditions
predisposing to skin cancer
Best cosmetic results achieved using multiple fractions
Typically, patient attends once-weekly for several weeks
Causes inflammatory reaction followed by scar
Risk of radiodermatitis, late recurrence, and new
tumours
Imiquimod cream
Imiquimod is an immune response modifier.
Best used for superficial BCCs less than 2 cm diameter
Applied three to five times each week, for 6–16 weeks
Fluorouracil cream
5-Fluorouracil cream is a topical cytotoxic agent.
Used to treat small superficial basal cell carcinomas
Requires prolonged course, eg twice daily for 6–12
weeks
Causes inflammatory reaction
Has high recurrence rates
SURGERY
TARGET THERAPY (SHH PATHWAY
INHIBITORS)
Vismodegib Erivedge™ȋ Ȍ
Sonidegib (Odomzo®)
Protect skin from sun exposure daily, year-round
and
lifelong.
Stay indoors or under the shade in the middle of the
day
Wear covering clothing
Apply high protection factor SPF50+ broad-
spectrum sunscreens generously to exposed skin if
outdoors
Avoid indoor tanning (sun beds, solaria)

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SURGERY SHORT CASES

  • 1. SURGICAL SHORT CASES 1.LIPOMA 2. SEBAECEOUS CYST 3.DERMOID CYST 4. KELOID 5.BCC BY DR.A.SASIDHARAN MBBS
  • 2.
  • 3. Introduction  Commonest tumor of s/c tissue.  Benign  Arising from yellow fat  Universal tumor  Karyotype 12q change  Hibernoma
  • 4. Types Encapsulated s/c lipoma Diffuse variety Multiple lipomas- Dercum’s d/s
  • 5.
  • 7. location presentation d.d. Significance s/c Mobile, lobular, edge slips under palp.fingers Neurofibrom a Most common variety subfascial Diff. to appreciate edge & lobulation Implantation dermoid , Tbtenosynovitis In scalp- erodes bone Subsynovial, intra-articular Knee/elbow sweling Bursa, Baker’s cyst Intra-articular is rare Intermuscular Swelling Fibrosarcoma Hematoma More chance of devpg liposarcoma Parosteal Feels hard Bony tumor Very, very rare
  • 8. Contd.. location presentation d.d. Significance Submucus Asymptomatic/ stridor Intestinal/laryngea l tumor Intussusception Subserosal Retroperitoneal swelling Hydronephrosis, retroperitoneal cyst Liposarcoma Extradural Very rare - - Intraglandula r Breast, pancreas Cystic lesions Very rare
  • 9. Clinical features  Localized, lobular, non- tender  Semi-fluctuant  Mobile  Slip sign  Skin free  Pedunculated +/-
  • 10.
  • 11. Complications  Myxomatous degeneration  Saponification  Calcification  Infection  Ulceration  Intussusception & intestinal obstruction
  • 12. Liposarcoma  Common in retroperitoneum, thigh & back  Rapid growth  Warm & vascular  Dilated veins  Restriction of mobility  Skin fixation & fungation  Hematogenous spread to lungs
  • 13. Treatment  Excision  Liposarcoma- wide excision, reconstruction, adjuvant chemo- & radiotherapy
  • 14.
  • 15. DISEASES OF SEBACEOUS GLANDS sebaceous gland: Holocaine glands in the skin that secrete sebum usually through the hair follicles. • Sebaceous hyperplasia • Adenoma sebaceum (Sebaceous adenoma) • Sebaceous cyst (Epidermoid cyst) 4 Acne 5 Sebaceous gland carcinoma
  • 16. SEBACEOUS CYST (EPIDERMOID CYST) • Epidermoid cyst originates in the epidermis and a pilar cyst originates from hair follicles, but neither type of cyst is strictly a sebaceous cyst • The fatty, white, semi-solid material in both cysts is not sebum, but keratin, and under the microscope neither entity contains sebaceous glands. • "True" sebaceous cysts are known as steatocystomas or, if multiple, as steatocystoma multiplex. Steatocystoma multiplex Epidermoid cyst
  • 17. Pathogenesis: formation of acne 1 Increased activity of sebaceous glands with production of excess sebum plays an important role 2 Occlusion of the pilo sebaceous orifices plays an important role 1 Hormones : Increased activity of sebaceous glands and occlusion of the cornfied hypertrophic pilosebaceous follicles lead to retention of sebum into the follicles, which dilate and rupture by time. 2 Anaerobes such as Corynebacterium (Propionibacterium) acne, Pityrosporon ovale and Staphylococci cause split of the sebum into fatty acids and triglycerides which act as an important irritating factors & → to the formation of the different clinical types of acne which varies from papules, pustules ,cysts and comedones
  • 18. RX : SURGICAL EXCISION OF THE CYST
  • 21.  Cyst lined by squamous epithelium containing desquamated cells  CONTENTS mixture of sweat, sebum, desquamated epithelial cells, hair
  • 22. CLINICAL TYPES  CONGENITAL / SEQUESTRATION DERMOID SITE: along lines of embryonic fusion (midline of body or face) FORMATION: dermal cells sequestrated in subcutaneous plane > proliferate & liquify > cyst > grows & indents mesoderm(future bone) > bony defects
  • 23.  MEDIAL NASAL DERMOID CYST (root of nose at fusion lines of frontal process)  EXTERNAL AND INTERNAL ANGULAR DERMOID ( fusion line of frontonasal and maxillary processes)  SUBLINGUAL DERMOID  PRE –AURICULAR DERMOID  POST AURICULAR DERMOID
  • 24.
  • 25. CLINICAL FEATURES Manifests in childhood or adolescence  Typically a painless slow growing swelling  Soft, cystic, fluctuant, yield to pressure of finger and will not slip away  Transillumination negative  Putty in consistency  No impulse on coughing  Underlying bony defect – clue to diagnosis
  • 26.
  • 27. OTHER TYPES  IMPLANTATION DERMOID > in women, tailors, agriculturists who sustain repeated minor injuries > sharp injury- epidermal cells implanted in subcutaneous plane- dermoid cyst > fingers, palm, sole of foot > hard in consistency ( skin is thick)
  • 28.  TERATOMATOUS DERMOID > arise from totipotent cells > ectodermal, mesodermal, endodermal elements > ovary, testis,retroperitoneum, mediastinum
  • 29.
  • 30.  TUBULO-EMBRYONIC DERMOID > from ectodermal tubes > thyroglossal cyst, post- anal dermoid
  • 31. INVESTIGATIO NS  BLOOD – TC, DC,Hb,ESR  URINE Examination  FNAC-  X ray- subjacent bone eroded by dermoid  Ultrasonography- mass cystic/ solid  CT scan- size , shape , local spread
  • 32. TREATME NT Excision of the cyst Mass shown ( implantation dermoid) Incision marked
  • 33. Incision started ( cyst contents leaking) cyst being removed
  • 34.
  • 36. History A 23 year old female was referred by plastic surgeons for radiotherapy to th posterior ear lobe, following the development of a Keloid Scar, three years after an ear piercing No family history of keloids e
  • 37. Pathology Keloid is a unique huma fibroproliferative disorde inflammation, surgery,a Commonly causes of kel folliculitis, chicken pox, (such as, earlobe piercin wounds). It is a benign growth, we fibrous tissue overgrowt original defect n dermal r that occurs after injury, nd burn. oids include acne, accinations and trauma g, lacerations, or surgical ll-demarcated area of h that extends beyond the v
  • 38. Baron Jean-Louis Alibert (1768-1837) Described appearance Crab-claw-like  Cheloid  Keloid
  • 39. Effects of keloids Compromise aesthetic Impairment of function
  • 41. How best can they be treated?
  • 44. Surgery Drawbac ks Painful Difficult reconstruction with large keloids Utilizes normal surrounding tissue – limiting later reconstructive options Low long term success as monotherapy
  • 45. Steroids  Triamcinolone  Hydrocortisone  Dexamethasone  Methylprednisone
  • 46.
  • 47. Laser 1980s in vogue Proposed Mechanism No knife  Less tissue trauma
  • 49. Di us  <10 minishes size and induration (HTS >Keloid) when ed as monotherapy % Recurrence when combined with surgery Photos Courtesy of Dr. Pressure Therapy
  • 51.
  • 52. Basal cell carcinoma (BCC) is a slow progressing nonmelanocytic skin cancer that arises from basal cells (ie, small, round cells found in the lower layer of the epidermis).
  • 53. It is the most common skin cancer (80%) Estimated 3.3 million cases are diagnosed per year(US) and incidence doubles every 25 years The incidence high in areas of ↑UV radiation (Australia,South africa) estimated lifetime risk of 33-39% for men and 23-28% for women Men >Women It increases with age (50-80 yrs )  Rare in <40 yrs (5-15%)
  • 54.
  • 55. Sun damage Repeated prior episodes of sunburn Fair skin, blue eyes and blond or red hair ( also affect darker skin types) Previous cutaneous injury, thermal burn, disease (eg cutaneous lupus, sebaceous naevus)
  • 56. Inherited syndromes: BCC is a particular problem for families with basal cell naevus syndrome (Gorlin syndrome), Bazex syndrome, Rombo syndrome and xeroderma pigmentosum ,albinism Other risk factors include ionising radiation, exposure to arsenic, coal tar, smoking tanning bed and immune suppression due to disease or medicines
  • 57. The cause of BCC is multifactorial. DNA mutations in the patched (PTCH) tumour suppressor gene, part of hedgehog signalling pathway (SHH) triggered by exposure to ultraviolet radiation Various spontaneous and inherited gene defects predispose to BCC
  • 58. BCC is a locally invasive skin tumour and rarely metastatize(< 0.01%) The main characteristics are: Slow growing: 0.5 cm in 1-2 years Varies in size from a few millimetres to several centimetres in diameter Skin coloured, pink or pigmented Spontaneous bleeding or ulceration Waxy papules with central depression Pearly appearance
  • 59. Oozing or crusted areas: In large BCCs Rolled (raised) border Translucency Telangiectases over the surface Black-blue or brown areas
  • 60. BCC distrubution : Head and neck 60% Nose 14% Trunk 30% Extremities 10%
  • 61. There are several distinct clinical types of BCC, and over 20 histological growth patterns of BCC Nodular Superficial Morphoeic Basisquamous Fibroepithelial tumour of Pinkus
  • 62. Most common type of facial BCC Shiny or pearly nodule with a smooth surface with telangiectases May have central depression or ulceration, so its edges appear rolled Cystic variant is soft, with jelly-like contents Micronodular, microcystic and infiltrative types are potentially aggressive subtypes
  • 63.
  • 64. Most common type in younger adults Most common type on upper trunk and shoulders Slightly scaly, irregular plaque Thin, translucent rolled border Multiple microerosions
  • 65.
  • 66. Also known as morphoeiform or sclerosing BCC Usually found in mid-facial sites Waxy, scar-like plaque with indistinct borders Flat or slightly depressed, fibrotic, and firm Wide and deep subclinical extension
  • 67.
  • 68. Mixed basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) Infiltrative growth pattern Potentially more aggressive than other forms of BCC
  • 70. Characteristics of recurrent BCC often include: Incomplete excision or narrow margins at primary excision Morphoeic, micronodular, and infiltrative subtypes Location on head and neck
  • 71. Advanced BCC Advanced BCCs are large, often neglected tumours. They may be several centimetres in diameter They may be deeply infiltrating into tissues below the skin They are difficult or impossible to treat surgically
  • 72. Nevi malignant melanoma Keratoacanthoma Seborrheic keratosis Bowen disease Actinic keratosis Squamous cell carcinoma
  • 73.  Skin biopsy  To confirm and diagnose bcc and its subtype Shave biopsy Punch biospy  Cytology  Histologic findings  Laser doppler (eyelids tumor margins)
  • 74.
  • 75. Treatment depends on size ,location and type of BCC Curretage and electrosessication Mohs micrographic surgery Excisional surgery Radiation Cryosurgery Photodynamic theray Laser surgery Topical medications
  • 76. Curretage and electricdesiccation : The growth is scraped off with a curette, an instrument with a sharp, ring-shaped tip), then the tumor site is desiccated (burned) with an electrocautery needle. Small lesions Leaves round whiitish scar Not suitable for advanced bcc, in high risk sites.
  • 77. Excision means the lesion is cut out and the skin stitched up. Most appropriate treatment for nodular, infiltrative and morphoeic BCCs Should include 3 to 5 mm margin of normal skin around the tumour Very large lesions may require flap or skin graft to repair the defect Further surgery is recommended for lesions that are incompletely excised
  • 78.
  • 79. Cryotherapy is the treatment of a superficial skin lesion by freezing it, usually with liquid nitrogen. Suitable for small superficial BCCs on covered areas of trunk and limbs Results in a blister that crusts over and heals within several weeks. Leaves permanent white mark
  • 80. Photodynamic therapy (PDT) refers to a technique in which BCC is treated with a photosensitising chemical, and exposed to light several hours later. Topical photosensitisers include aminolevulinic acid lotion and methyl aminolevulinate cream Suitable for low-risk small, superficial BCCs Results in inflammatory reaction, maximal 3–4 days after procedure Treatment repeated 7 days after initial treatment Excellent cosmetic results
  • 81.
  • 82. Radiotherapy or X-ray treatment can be used to treat primary BCCs or as adjunctive treatment if margins are incomplete. Mainly used if surgery is not suitable Best avoided in young patients and in genetic conditions predisposing to skin cancer Best cosmetic results achieved using multiple fractions Typically, patient attends once-weekly for several weeks Causes inflammatory reaction followed by scar Risk of radiodermatitis, late recurrence, and new tumours
  • 83. Imiquimod cream Imiquimod is an immune response modifier. Best used for superficial BCCs less than 2 cm diameter Applied three to five times each week, for 6–16 weeks Fluorouracil cream 5-Fluorouracil cream is a topical cytotoxic agent. Used to treat small superficial basal cell carcinomas Requires prolonged course, eg twice daily for 6–12 weeks Causes inflammatory reaction Has high recurrence rates
  • 84.
  • 85. SURGERY TARGET THERAPY (SHH PATHWAY INHIBITORS) Vismodegib Erivedge™ȋ Ȍ Sonidegib (Odomzo®)
  • 86. Protect skin from sun exposure daily, year-round and lifelong. Stay indoors or under the shade in the middle of the day Wear covering clothing Apply high protection factor SPF50+ broad- spectrum sunscreens generously to exposed skin if outdoors Avoid indoor tanning (sun beds, solaria)