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By- DR. PRIYANKA RAJ
 The eyelid is composed of two lamellae
 Anteror lamella skin, orbicularis oculi
 Posterior lamella tarsus and palpebral conjunctiva
 Eyelid margin
 hair follicles + associated glands
 Meibomian glands
 Transitional conjunctiva
TUMORS OF THE
EYELID
BENIGN PRE-MALIGNANT MALIGNANT
CYSTIC TUMORS 1. Eccrine hidrocystoma
2. Apocrine hidrocystoma
3. Sebaceous cyst
4. Epidermal inclusion cyst
EPIDERMAL
TUMORS
1. Squamous papilloma
2. Seborrhoeic keratitis
3. Inverted follicular keratitis
4. Keratoacanthoma
1. Actinic keratosis
2. Xeroderma
pigmentosum
3. Sebaceous naevus
1. Squamous cell
carcinoma
2. Basal cell carcinoma
SEBACEOUS
GLAND TUMORS
1. Sebaceous adenoma 1. Sebaceous carcinoma
SWEAT GLAND
TUMORS
1. Syringoma
2. Eccrine hidradenoma
1. Sweat gland
adenocarcinoma
HAIR FOLLICLE
TUMOURS
1. Trichoepithelioma
2. Trichofolliculoma
3. Trichoadenoma
4. tricholemmoma
1. Trichilemmal
carcinoma
TUMORS OF THE
EYELID
BENIGN PRE-MALIGNANT MALIGNANT
MELANOCYTIC
TUMOURS
1. Melanocytic nevus
2. Oculodermal
melanocytosis
1. Lentigo maligna 1. Malignant melanoma
NEURAL TUMOURS 1. Neurofibroma
2. Schwannoma
1. Merkel cell carcinoma
VASCULAR TUMOURS 1. Congenital capillary
hemangioma
2. Acquired capillary
hemangioma
3. Varix
4. Hemangioma
1. Kaposi’s sarcoma
2. Angiosarcoma
3. Glomus tumour
HISTIOCYTIC AND
FIBROUS TUMOURS
1. Xanthelasma and
xanthema
2. Xanthogranuloma
3. Angiofibroma
LYMPHOID TUMOURS 1. Eccrine hidradenoma 1. Lymphoma
ECCRINE HIDROCYSTOMA
 Retention cyst of the eccrine sweat glands
 Clear cyst
 Near the eyelid margin
 Multiple
APOCRINE HIDROCYSTOMA
 Retention cyst of the apocrine sweat glands
 Bluish in colour
 Near the lid margin
 From glands of Moll
 solitary
SEBACEOUS CYST
 Retention cyst of sebaceous glands
 (Meibomian or zeis)
 Yellow opaque lesion
 Near the lid margin
EPIDERMOID CYST
 Retention cyst caused by obstruction of
pilosebaceous glands
 Clinically resembles a sebaceous cyst
 Contains desquamated keratin
OBSERVATION SURGICAL EXCISION
CO2 laser assisted
Or
Radiofrequency
assisted
vapourization
 Benign hyperplasia of squamous epithelium
 Most common eyelid lesion
 No strong association with HPV
 Seen in Elderly
 Sessile/pedunculated
 solitary/multiple
 smooth/convoluted surface
 Management
 Observation
 Shave excision
 CO2 laser assisted or Radiofrequency assisted
vapourization
 It recently was reclassified as a low-grade
form of squamous carcinoma.
 104/100,000 in the white population
 rapidly grow over a period of 2–6 months
 elderly age
 dome-shaped tumors with distinct borders
and a central keratin core.
 Management:
1. Observation
2. Cryoapplication
3. Surgical resection
 There have been some reports of
spontaneous regression.
 Periocular region of older individuals
 Minially tan-brown plaque
 Solitary, slow growing
 SIGN OF LESER-TRELAT sudden
appearance of multiple lesions indicate the
presence of an internal malignancy
(specifically- GI adenocarcinomas)
 Treatment
 Observation
 Shave excision
 CO2 laser assisted or Radiofrequency assisted
vapourization
 Autosomal recessive disorder
 Defect in DNA-repairing enzymes
 Patients are extrememly sensitive to UV radiation
from sun
 Clinical presentation-
 Variegted pigmentation
 Scaling
 Telangectasia
 Multiple tumors develop by the end of 1st decade
 SCC
 BCC
 Malignant melanoma
 sarcomas
 Management:
1. Protection from sunlight
2. Topical sunscreen
3. Protective clothing
4. UV blocking spectacles
5. Surgical ecision of small pre-malignant and malignant lesions
SEBACEOUS NAEVUS
 Can be an isolated lesion in eyelid
 Or a part of systemic syndrome
 ORGANOID NAEVUS SYNDROME-
 Primalrily neurological manifestations
 Arachnoid cysts+ cerebral atrophy seizures and
mental retardation
 Ocular findings
 large pigmented patch (tan-brown) on scalp, eyelids,
face retroauricular area and conjunctival choristoma
 Cutaneous lesions give rise to BCC (20% patients)
 Management:
 Small lesions excised
 Extensive lesions observed
 If tumors arising complete excision
 5-10% periocular cutaneous tumors
 Second most common cancer of eyelids
 arise denovo
precursor lesions
(actinic keratitis, Bowen’s disease,
xeroderma pigmentos, albinism)
 Patients with XP younger, have multiple &
recurrent lesions (eyelids and other parts of
body)
 More common in lower eyelid
 Features:
 Sessile/elevated, erythematous with
indurated borders, scaly surface
 Ulcerate and become friable
 Bleed on touch
 Central part of necrotic lesion may develop
secondary infection
 Shows neurotropism and regional lymph
node metastasis
 Histopatologically:
 Nests of squamous epithelial cells arising
from epidermis and extending into dermis
 Cells are eosinophilic & contain keratin
pearls
 Prognosis:
 Aggressive tumor
 Prognosis depends upon recurrence and metastasis
 Management:
1. excision biopsy in conjunction with histological monitoring of tumor margins
2. Radiation: as an adjunctive therapy, specially in cases with perineural invasion
3. Cryotherapy
4. Intralesional chemotherapy
5. Intralesiional interferon
 Most common malignant tumor of
periocular skin
 Lower lid (65%)> medial
canthus(15%)=upper eyelid (15%)
 Risk fator- UV exposre
 Associated with genetic syndromes
 Gorlin-Goltz syndrome
 Xeroderma pigmentosa
 Clinical features:
 well circumscribes
 Pearly
 waxy/translucent
 telangiectasia visible near the border of the
lesion
 Types:
 Nodular
 Nodulo-ulcerative
 Ulcerative
 Pigmented
 Cystic
 Superficila
 Morpheaform
 Histopathologically- tumor cells consist of nests of well-differentiated basal cells in
a palisade pattern
 Natural history
 gradual course, low incidence of metastasis
 Advanced BCC- invade orbit, nasal cavity, sinuses
common
 MANAGEMENT
 Early lesions-complete surgical excision
 Small lesions- cryotherapy, immunomodulators (topical 5%Imiquimod)
 Advanced lesions- radiotherapy (orbital, intranasal, intracranial extension)
 Locally advanced BCC- VISMODEGIB (FDA approved- 150mg OD)
 Arise from- Meibomian glans, Zeis glands of cilia,
glands of eyebrows, caruncle, glands of hair
follicles
 Periocular region= 75% of tumors
 Incidence
 2-7% of eyelid malignancies in west
 30% in India, Japan, China (2nd most common after
BCC)
 Syndromes- Muir-Torre syndrome
 Neoplasm of sebaceous glands and visceral
malignancies
 Due to mutation of DNA mismatch repair genes
propagation of genetic defects within replicating
cells tumor formation
 Histopathologically
 Malignant proliferation ofsebaceouos cells with
vacuolated cytoplasm due to presence of lipid
 Clinical features
 Solitary nodule/ diffuse thickening (misinterpreted as chronic blephritis)
 Distortion of posterior lid margin
 Meibomina gland orifice obstruction
 Loss of cilia with surrounding telangectasia
 Ulceration in advanced cases
 Management
 Wide local excision with frozen section or Mohs microsurgery
 Conjunctival spread- small map biopsies followed by excision
 Anterior orbital spread- extentration
 Locoregional metastasis- radical neck dissection
 Alternatives- cryotherapy, topical, systemic chemotherapy (neoadjuvant), radiotherapy,
topical Mitomycin C
 Comprises of melanocytes derived from
neural crest cells that migrate to skin
during embryonic development
 Congenital/ acquired
 Types
 Junctional (childhood)
 Compund
 Intradermal
 Can vary in size, location, pigmentation
 Variant of congenital naevus= kissing
naevus
 Management- surgical excision
 Bluis-black pigmentation of periocular skin,
uveal tract, ipsilateral orbital soft tissues,
pinna, meninges, hard palate
 Congenital
 Eyelid pigmentation- NEAVUS OF OTA
 Follows distribution of 1st & 2nd divisions of
trigeminal nerves
 Bilateral in 10%
 Malignant transformation = rare
 Uveal tract uveal melanoma
 Histopathologically- increased number of
scaterred dendritic melanocytes in dermis
 Management- close observation
 Aka MELANOCYIC FRECKLE OF HUTCHINSON
 Acquired pigmentation of sun-exposed areas
 Rarely involve eyelids, rare in darly pigmented individuals
 Clinically-
 Small localized,well-demarcated, flat, tan-brown pigmentation
 Progresses slowly over the years
 Precursor of lentigo maligna elanoma
Management- wide surgical resection
 Rare (<1% of eyelid malignancies)
 Primary lesion/ local extension of conjunctival
melanoma/ metastasis from a distant primary
lesion
 Age- 6th-7th decade
 Types-
 Lentigo maligna melanoma most common
 Superficial melanoma
 Nodular melanoma
 Lower lid> upper lid, lateral canthus, medial
canthus
 Histopathologically-
 Malignant cells are of3 types spindle cells,
epitheloid cells, naevus-like cells
 Lentigo and superficial melanoma
limited to epidermis in early stages
subepidermal invasion
 Nodular melanoma- early subepidermal
invasion
 Clinically- sudden change in appearance
of a pre-exsisting naevus
(size/pigmentation/elevation/tenderness/ul
ceration)
 Management
 Treatment of choice- wide local excision
 Advanced cases- orbital extentration
 Congenital (infantile capillary
hemangiomas/ strawberry hemangiomas)
or acquired
 Acquired
 very tiny, red-blue
 seen in elderly
 Do not require treatment
 Congenital
 Placental origin
 At birth/ within 1st year of life
 Superficial/ deep/ both
 Superficial hemangiomas maybe limited to
subcutaneous tissues (with no involvement
of epidermis)
 Capillary hemangiomas developing few
months after birth- enlarge over 6-12
months (proliferative phase) regress
within 8 years (involutional phase)
 Associated with- Kasabach-Merritt
syndrome
 Large visceral hemangiomas, platelet
entrapment, thrombocytopenia
 Overlying skin has bluish hue and lesion
becomes more apparent during crying
 Complications (>1cm)
 Amblyopia (60%) pupil obstruction/
refractive error from globe compression
 Strabismus secondary to compressions of
recti or amblyopia
 Management
 Observation mostly
 Amblyopia refraction and occlusive patching
 Oral/ local corticosteroids
 Oral prednisolone x 2-4 weeks
 Intralesional triamcinolone (1ml) + dexamethasone (1ml)
 Vision threatening hemangiomas- Subcutaneous INFα2a daily
 Oral propranolol 2-3mg/kg/day
 Surgical treatment- rare
 Endothelial malignancy
 Immunocompromised individuals
 Associated with AIDS
 Clinically
 Red/purple/blue flat subcutanoes well-
circumscribed nodule
 (maybe diffuse and large)
 Composed of proliferating groups of
endothelial cells containing blood filled spaces
 Management- palliative
 Small- low-dose radiotherapy
 diffuse- chemotherapy
 Xanthalesma- benign, common,
subcutaneous, minimally elevated
 Xantoma- nodular xanthalesma
 Mostly Bilateral and symmetrical
 More common in- elderly, females
 50%- primary or secondary
hyperlipidaemic
 Clinically- yellow, placoid lesion at medial
aspect of the eyelids
 Microscopically- foamy histiocytes
infilterating dermis
 Management
 Surgical excision (cosmetic blemish)
 Topical 35%trichloroacetic scid
 CO2 laser assisted/ radiofrequency-assisted vapourization
 Idiopathic granulomatous inflammation
 Affects Older children
 Clincally-
 Orange nodule which regresses on its own
 Histopathologically-
 Comprised of histiocytes, lymphocytes,
mononuclear cells, eosinophils, Touton giant
cells
 Management-
 observation
 Systemic/ intralesionalcorticosteroids
 Surgical excision- if steroids fail
 Exremely rare
 Mostly B-cell types, (rarely- cutaneous T-
cell lymphoma in immunocompromised
individuals)
 Clinically-
 Painless suncutaneous mass
 Eczema/ulceration
 Subcutaenous inflammation with
induration
 Solitary/multiple
 Management
 Radiation
 Systemic chemotherapy

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Eyelid tumors

  • 2.
  • 3.  The eyelid is composed of two lamellae  Anteror lamella skin, orbicularis oculi  Posterior lamella tarsus and palpebral conjunctiva  Eyelid margin  hair follicles + associated glands  Meibomian glands  Transitional conjunctiva
  • 4. TUMORS OF THE EYELID BENIGN PRE-MALIGNANT MALIGNANT CYSTIC TUMORS 1. Eccrine hidrocystoma 2. Apocrine hidrocystoma 3. Sebaceous cyst 4. Epidermal inclusion cyst EPIDERMAL TUMORS 1. Squamous papilloma 2. Seborrhoeic keratitis 3. Inverted follicular keratitis 4. Keratoacanthoma 1. Actinic keratosis 2. Xeroderma pigmentosum 3. Sebaceous naevus 1. Squamous cell carcinoma 2. Basal cell carcinoma SEBACEOUS GLAND TUMORS 1. Sebaceous adenoma 1. Sebaceous carcinoma SWEAT GLAND TUMORS 1. Syringoma 2. Eccrine hidradenoma 1. Sweat gland adenocarcinoma HAIR FOLLICLE TUMOURS 1. Trichoepithelioma 2. Trichofolliculoma 3. Trichoadenoma 4. tricholemmoma 1. Trichilemmal carcinoma
  • 5. TUMORS OF THE EYELID BENIGN PRE-MALIGNANT MALIGNANT MELANOCYTIC TUMOURS 1. Melanocytic nevus 2. Oculodermal melanocytosis 1. Lentigo maligna 1. Malignant melanoma NEURAL TUMOURS 1. Neurofibroma 2. Schwannoma 1. Merkel cell carcinoma VASCULAR TUMOURS 1. Congenital capillary hemangioma 2. Acquired capillary hemangioma 3. Varix 4. Hemangioma 1. Kaposi’s sarcoma 2. Angiosarcoma 3. Glomus tumour HISTIOCYTIC AND FIBROUS TUMOURS 1. Xanthelasma and xanthema 2. Xanthogranuloma 3. Angiofibroma LYMPHOID TUMOURS 1. Eccrine hidradenoma 1. Lymphoma
  • 6.
  • 7. ECCRINE HIDROCYSTOMA  Retention cyst of the eccrine sweat glands  Clear cyst  Near the eyelid margin  Multiple APOCRINE HIDROCYSTOMA  Retention cyst of the apocrine sweat glands  Bluish in colour  Near the lid margin  From glands of Moll  solitary
  • 8. SEBACEOUS CYST  Retention cyst of sebaceous glands  (Meibomian or zeis)  Yellow opaque lesion  Near the lid margin EPIDERMOID CYST  Retention cyst caused by obstruction of pilosebaceous glands  Clinically resembles a sebaceous cyst  Contains desquamated keratin
  • 9. OBSERVATION SURGICAL EXCISION CO2 laser assisted Or Radiofrequency assisted vapourization
  • 10.
  • 11.  Benign hyperplasia of squamous epithelium  Most common eyelid lesion  No strong association with HPV  Seen in Elderly  Sessile/pedunculated  solitary/multiple  smooth/convoluted surface  Management  Observation  Shave excision  CO2 laser assisted or Radiofrequency assisted vapourization
  • 12.  It recently was reclassified as a low-grade form of squamous carcinoma.  104/100,000 in the white population  rapidly grow over a period of 2–6 months  elderly age  dome-shaped tumors with distinct borders and a central keratin core.  Management: 1. Observation 2. Cryoapplication 3. Surgical resection  There have been some reports of spontaneous regression.
  • 13.  Periocular region of older individuals  Minially tan-brown plaque  Solitary, slow growing  SIGN OF LESER-TRELAT sudden appearance of multiple lesions indicate the presence of an internal malignancy (specifically- GI adenocarcinomas)  Treatment  Observation  Shave excision  CO2 laser assisted or Radiofrequency assisted vapourization
  • 14.  Autosomal recessive disorder  Defect in DNA-repairing enzymes  Patients are extrememly sensitive to UV radiation from sun  Clinical presentation-  Variegted pigmentation  Scaling  Telangectasia  Multiple tumors develop by the end of 1st decade  SCC  BCC  Malignant melanoma  sarcomas
  • 15.  Management: 1. Protection from sunlight 2. Topical sunscreen 3. Protective clothing 4. UV blocking spectacles 5. Surgical ecision of small pre-malignant and malignant lesions
  • 16. SEBACEOUS NAEVUS  Can be an isolated lesion in eyelid  Or a part of systemic syndrome  ORGANOID NAEVUS SYNDROME-  Primalrily neurological manifestations  Arachnoid cysts+ cerebral atrophy seizures and mental retardation  Ocular findings  large pigmented patch (tan-brown) on scalp, eyelids, face retroauricular area and conjunctival choristoma  Cutaneous lesions give rise to BCC (20% patients)
  • 17.  Management:  Small lesions excised  Extensive lesions observed  If tumors arising complete excision
  • 18.  5-10% periocular cutaneous tumors  Second most common cancer of eyelids  arise denovo precursor lesions (actinic keratitis, Bowen’s disease, xeroderma pigmentos, albinism)  Patients with XP younger, have multiple & recurrent lesions (eyelids and other parts of body)  More common in lower eyelid
  • 19.  Features:  Sessile/elevated, erythematous with indurated borders, scaly surface  Ulcerate and become friable  Bleed on touch  Central part of necrotic lesion may develop secondary infection  Shows neurotropism and regional lymph node metastasis  Histopatologically:  Nests of squamous epithelial cells arising from epidermis and extending into dermis  Cells are eosinophilic & contain keratin pearls
  • 20.  Prognosis:  Aggressive tumor  Prognosis depends upon recurrence and metastasis  Management: 1. excision biopsy in conjunction with histological monitoring of tumor margins 2. Radiation: as an adjunctive therapy, specially in cases with perineural invasion 3. Cryotherapy 4. Intralesional chemotherapy 5. Intralesiional interferon
  • 21.  Most common malignant tumor of periocular skin  Lower lid (65%)> medial canthus(15%)=upper eyelid (15%)  Risk fator- UV exposre  Associated with genetic syndromes  Gorlin-Goltz syndrome  Xeroderma pigmentosa  Clinical features:  well circumscribes  Pearly  waxy/translucent  telangiectasia visible near the border of the lesion
  • 22.  Types:  Nodular  Nodulo-ulcerative  Ulcerative  Pigmented  Cystic  Superficila  Morpheaform  Histopathologically- tumor cells consist of nests of well-differentiated basal cells in a palisade pattern  Natural history  gradual course, low incidence of metastasis  Advanced BCC- invade orbit, nasal cavity, sinuses common
  • 23.  MANAGEMENT  Early lesions-complete surgical excision  Small lesions- cryotherapy, immunomodulators (topical 5%Imiquimod)  Advanced lesions- radiotherapy (orbital, intranasal, intracranial extension)  Locally advanced BCC- VISMODEGIB (FDA approved- 150mg OD)
  • 24.
  • 25.  Arise from- Meibomian glans, Zeis glands of cilia, glands of eyebrows, caruncle, glands of hair follicles  Periocular region= 75% of tumors  Incidence  2-7% of eyelid malignancies in west  30% in India, Japan, China (2nd most common after BCC)  Syndromes- Muir-Torre syndrome  Neoplasm of sebaceous glands and visceral malignancies  Due to mutation of DNA mismatch repair genes propagation of genetic defects within replicating cells tumor formation  Histopathologically  Malignant proliferation ofsebaceouos cells with vacuolated cytoplasm due to presence of lipid
  • 26.  Clinical features  Solitary nodule/ diffuse thickening (misinterpreted as chronic blephritis)  Distortion of posterior lid margin  Meibomina gland orifice obstruction  Loss of cilia with surrounding telangectasia  Ulceration in advanced cases  Management  Wide local excision with frozen section or Mohs microsurgery  Conjunctival spread- small map biopsies followed by excision  Anterior orbital spread- extentration  Locoregional metastasis- radical neck dissection  Alternatives- cryotherapy, topical, systemic chemotherapy (neoadjuvant), radiotherapy, topical Mitomycin C
  • 27.
  • 28.  Comprises of melanocytes derived from neural crest cells that migrate to skin during embryonic development  Congenital/ acquired  Types  Junctional (childhood)  Compund  Intradermal  Can vary in size, location, pigmentation  Variant of congenital naevus= kissing naevus  Management- surgical excision
  • 29.  Bluis-black pigmentation of periocular skin, uveal tract, ipsilateral orbital soft tissues, pinna, meninges, hard palate  Congenital  Eyelid pigmentation- NEAVUS OF OTA  Follows distribution of 1st & 2nd divisions of trigeminal nerves  Bilateral in 10%  Malignant transformation = rare  Uveal tract uveal melanoma  Histopathologically- increased number of scaterred dendritic melanocytes in dermis  Management- close observation
  • 30.  Aka MELANOCYIC FRECKLE OF HUTCHINSON  Acquired pigmentation of sun-exposed areas  Rarely involve eyelids, rare in darly pigmented individuals  Clinically-  Small localized,well-demarcated, flat, tan-brown pigmentation  Progresses slowly over the years  Precursor of lentigo maligna elanoma Management- wide surgical resection
  • 31.  Rare (<1% of eyelid malignancies)  Primary lesion/ local extension of conjunctival melanoma/ metastasis from a distant primary lesion  Age- 6th-7th decade  Types-  Lentigo maligna melanoma most common  Superficial melanoma  Nodular melanoma  Lower lid> upper lid, lateral canthus, medial canthus  Histopathologically-  Malignant cells are of3 types spindle cells, epitheloid cells, naevus-like cells
  • 32.  Lentigo and superficial melanoma limited to epidermis in early stages subepidermal invasion  Nodular melanoma- early subepidermal invasion  Clinically- sudden change in appearance of a pre-exsisting naevus (size/pigmentation/elevation/tenderness/ul ceration)  Management  Treatment of choice- wide local excision  Advanced cases- orbital extentration
  • 33.
  • 34.  Congenital (infantile capillary hemangiomas/ strawberry hemangiomas) or acquired  Acquired  very tiny, red-blue  seen in elderly  Do not require treatment  Congenital  Placental origin  At birth/ within 1st year of life  Superficial/ deep/ both  Superficial hemangiomas maybe limited to subcutaneous tissues (with no involvement of epidermis)
  • 35.  Capillary hemangiomas developing few months after birth- enlarge over 6-12 months (proliferative phase) regress within 8 years (involutional phase)  Associated with- Kasabach-Merritt syndrome  Large visceral hemangiomas, platelet entrapment, thrombocytopenia  Overlying skin has bluish hue and lesion becomes more apparent during crying  Complications (>1cm)  Amblyopia (60%) pupil obstruction/ refractive error from globe compression  Strabismus secondary to compressions of recti or amblyopia
  • 36.  Management  Observation mostly  Amblyopia refraction and occlusive patching  Oral/ local corticosteroids  Oral prednisolone x 2-4 weeks  Intralesional triamcinolone (1ml) + dexamethasone (1ml)  Vision threatening hemangiomas- Subcutaneous INFα2a daily  Oral propranolol 2-3mg/kg/day  Surgical treatment- rare
  • 37.  Endothelial malignancy  Immunocompromised individuals  Associated with AIDS  Clinically  Red/purple/blue flat subcutanoes well- circumscribed nodule  (maybe diffuse and large)  Composed of proliferating groups of endothelial cells containing blood filled spaces  Management- palliative  Small- low-dose radiotherapy  diffuse- chemotherapy
  • 38.
  • 39.  Xanthalesma- benign, common, subcutaneous, minimally elevated  Xantoma- nodular xanthalesma  Mostly Bilateral and symmetrical  More common in- elderly, females  50%- primary or secondary hyperlipidaemic  Clinically- yellow, placoid lesion at medial aspect of the eyelids  Microscopically- foamy histiocytes infilterating dermis
  • 40.  Management  Surgical excision (cosmetic blemish)  Topical 35%trichloroacetic scid  CO2 laser assisted/ radiofrequency-assisted vapourization
  • 41.  Idiopathic granulomatous inflammation  Affects Older children  Clincally-  Orange nodule which regresses on its own  Histopathologically-  Comprised of histiocytes, lymphocytes, mononuclear cells, eosinophils, Touton giant cells  Management-  observation  Systemic/ intralesionalcorticosteroids  Surgical excision- if steroids fail
  • 42.
  • 43.  Exremely rare  Mostly B-cell types, (rarely- cutaneous T- cell lymphoma in immunocompromised individuals)  Clinically-  Painless suncutaneous mass  Eczema/ulceration  Subcutaenous inflammation with induration  Solitary/multiple  Management  Radiation  Systemic chemotherapy