Lid Lesions PDF - OPT 539 Ocular Disease I F24

Summary

This document provides a presentation on eyelid lesions, including benign and malignant tumors. It covers terminology, clinical presentation, evaluation, and management strategies, with images and supplementary information. The key topics discussed are crucial for understanding ocular health in patients.

Full Transcript

Lid Lesions OPT 539: Ocular Disease I Scott D. Klemens, O.D., F.A.A.O. November 12, 2024 Objective Introduce and review benign tumors of the eyelid Introduce and review malignant neoplasms of the eyelid Dermatology Terminology Tumors a...

Lid Lesions OPT 539: Ocular Disease I Scott D. Klemens, O.D., F.A.A.O. November 12, 2024 Objective Introduce and review benign tumors of the eyelid Introduce and review malignant neoplasms of the eyelid Dermatology Terminology Tumors are often divided into benign vs malignant Benign: Non-cancerous Composed of cells that will not invade other tissues or organs of the body May continue to grow in size abnormally, may have secondary complications Malignant Cancerous Cells invade the basement membrane and can invade or spread to other parts of the body Occurs by direct extension to neighboring organs/tissue or by metastasizing (vascular system, lymphatic system, seeding/implantation) Derm Terms Abnormal Cell Growth Neoplasia (neo=new, plasia=tissue or cells), serves no useful function Hyperplasia: abnormal increase in the number of cells, which are in normal component of that tissue Hypertrophy: abnormal increase size of each cell Metaplasia: replacement of one mature cell type with another mature cell type Dysplasia: replacement of one mature cell type with a less mature cell type *Hyperplasia, metaplasia, and dysplasia are reversible because they are results of a stimulus. Neoplasia is irreversible because it is autonomous. Derm Terms Tumors usually end in “oma” Ex: Benign glandular tumor “adenoma”, malignant “adenocarcinoma” Ex: Benign bone tumor “osteoma”, malignant “osteosarcoma” Carcinoma: Epithelial tissue Sarcoma: Bones, soft tissue including fat, muscles, lymph, blood vessels Hemangioma: Tumor comprised of blood vessels/vasculature Lymphoma: Tumor of lymphatic system (leukemia) Melanoma: Tumor of pigmented cells Hamartoma: Benign tumor made up of the same cells found in surrounding tissue Blastoma: Tumor derived from embryonic cells (retinoblastoma) It’s Not a Tumor! Derm Terms Primary Descriptors Macule: Circumscribed, flat discoloration , 1cm Papule: Circumscribed, elevated superficial solid lesions, < 1cm Plaque: Circumscribed, elevated superficial solid lesions, > 1cm Nodule: Solid lesions with depth above, level or below surface, < 1cm Tumor: Solid lesions with depth, above, level or below surface, > 1cm Vesicle: Circumscribed elevations containing serous fluid, < 1cm Bulla: Circumscribed elevations containing serous fluid, > 1cm Petechia: Circumscribed deposits of blood or blood products, < 4mm Purpura: Circumscribed deposits of blood or blood products, 4- 10mm Ecchymoses: Purpura spots > 1cm Derm Terms Secondary Descriptors Sessile: A lesion fixed to the skin on a broad base Pedunculated: A lesion on a stalk Papillomatous: A lesion exhibiting a surface resembling a cauliflower or artichoke Scales: Shedding, dead epidermal cells, dry or greasy Umbilicated: The lesion exhibits a central crater like an umbilicus or belly button Crusts: Dried masses of skin exudates Ulcer: Irregularly sized and shaped excavations extending into the dermis Benign Eyelid Lesions Squamous Papilloma aka acrochordon or skin tag Most common benign non-infectious eyelid lesion Overgrowth of squamous epithelium Often occurs in areas where skin layers rub against each other Eyelids, groin armpits, neck Usually slow growing Clinical Presentation Can present as sessile (flattened) Usually pedunculated on a stalk Can vary in color either be same as skin or pigmented Cauliflower floret! Patient’s usually asymptomatic Papilloma Evaluation Rule-out neoplastic growth Look for rapid growth, color change Bleeding is highly unlikely unless it is traumatized Vascularization – not present on surface of papilloma Surface may be roughened, but usually not eroded or ulcerated Management Generally no treatment indicated, patient educated and reassurance of benign lesion Cosmetic treatment only if desired (excision) Can produce lash misdirection (trichiasis) may need epilation Can be easily excised if pedunculated on a stalk Refer to dermatologist or oculo-plastics if large, flat, or high level of suspicion Suspicious new lesions photo-document and follow-up in a month vs old follow annually Excision Ellman Unit Uses radiofrequency to cut tissue The probe is not hot unlike electrocautery Reacts to water molecules in cells Less bleeding than traditional methods Verrucae aka verruca vulgaris, viral wart Viral papilloma usually caused by human papilloma virus More prevalent in children or younger adults Can be transmitted by direct or indirect contact and autoinoculation Clinical Presentation Two forms: Filiform or digitate: project in finger- like nature from their base Plana: flat Usually start as small papules and are slightly lighter than surrounding skin Tend to darken and become hyperkeratotic (thicken) with time Tx/Mx Lesions can spontaneously regress! Reassure patient and monitor Can also consider excision if needed Chemical cautery (dichloroacetic acid) Cryotherapy can also be used and recommended to accompany excision Molluscum Contagiosum Associated with DNA poxvirus Four main types (I-IV), Type I: 95% of infections, Type II: 60% of HIV infections, Type III and IV: very rare More common in children and immunocompromised patients Contagious (skin-skin) Can cause follicular conjunctivitis Clinical Presentation Small (1-2mm) flesh-colored papules often with an umbilicated center Elevated, round, waxy, pearly Multiple will present Management If quiet, leave alone, may spontaneously regress (months) 1/3 of patients may get recurrence If large number of lesions (100+) r/o HIV Adolescents/Adults: sexual transmission common Patient Education: Hand wash, cover if possible, avoid scratching, avoid physical contact and sharing towels/clothes Treatment Topical Treatments: Podophyllotoxin cream (0.5%) Fetus toxicity; avoid with pregnancy Iodine Salicylic acid (ASA, Aspirin) Potassium hydroxide Tretinoin cream Cantharidin (blistering agent) Imiquimod (T cell modifier) not recommended for children due to possible adverse events and not effective in children Oral Treatment: Cimetidine Seborrheic Keratosis “barnacles of old age” Hyperkeratinized plaques Most common benign epidermal tumor in the middle age/elderly Common on trunk and head Can occur on eyebrow and lids Not pre-malignant (actinic keratosis is) Clinical Presentation Sharply defined, slightly elevated, brown, plastered on lesion – like a “brown plaque” on the skin Looks like it is tacked on or stuck onto surface of skin, little invasion into epidermis and none in dermis Waxy, greasy or scaly Tx/Mx Monitor no treatment needed Refer to Derm and or oculoplastics Excision and or removal for cosmetic reasons Dermoid Choriostoms: not neoplasms, arise during development, tumor-like growth with normal tissue If dermoid is observed look for other congenital anomalies Goldenhar’s syndrome: dermoids on surface of globe often accompanied by lid coloboma and appendages on ears Clinical Presentation Tend to be cystic in nature – “dermoid cyst” Usually superior temporal in location; usually adherent to periosteum of orbit Skin slides over surface easily Anterior lesions: Painless fullness of upper eyelid, most commonly at lateral orbital rim Deep lesions: Painless, progressive proptosis, diplopia. Tx/Mx Rule-out other possible differentials? May need to consider imaging depending on location/size Small, asymptomatic cyst do not require surgery, may stabilize or decrease in size Surgeons will excise early to reduce risk of spontaneous rupture Xanthelasma Cholesterol plaques on eyelids Common slowly progressive Usually develops in 4th and 5th decade Can be associated with hyperlipidemia, diabetes, thyroid dysfunction 50% of adult patients have abnormal lipid levels May also be present in younger patients with history of inherited dyslipidemia (hypercholesteremia, hyperapobetalipoproteinemia) Lipid Disorders Primary Lipid Disorders Secondary Lipid Disorders Type IIa and IIb phenotype hyperlipidemias Primary biliary cholangitis (PBC) characterized by the buildup of elevated Type IV phenotype hyperlipidemia levels of lipoprotein X, a carrier of Low levels of high-density lipoprotein substantial cholesterol in the bloodstream (HDL) Acquired hyperlipoproteinemia resulting from systemic illnesses such as diabetes, hypothyroidism, and nephrotic syndrome Treatment with retinoids and estrogens Sarcoidosis Clinical Presentation Elevated yellowish discoloration of skin Often observed bilaterally on medial aspect of upper lid Plaque-like, with a slightly granulated surface Patients are asymptomatic Eval/Tx/Mx Evaluation Tx/Mx R/o other evidence of hyperlipidemia Blood work-up (lipid panel, blood (corneal arcus, cholesterol emboli in glucose, CBC) retina) Referral for removal only for cosmetic R/o concomitant vascular disease (HTN, reasons DM) Surgery, electrocoagulation, chemical Careful review of Medical and Family cauterization History Pt. ed. Reassure patient on benign lesion, risk for underlying systemic disorder Vascular Lesions Capillary Hemangioma aka strawberry mark Congenital or present shortly after birth 1/3 present at birth Virtually all within 6mos Variable course can increase in size Usually spontaneously regress completely (most by age 5) Clinical Presentation Flat reddish or pink lobulated lesion Color can change with venous return – straining, crying, lifting (Valsalva maneuvers) can cause redder appearance Nevus Flammeus aka port-wine stain Congenital birthmark, capillary malformation, usually unilateral Can occur anywhere, but most commonly found on the face High correlation with Sturge Weber Syndrome Presence of PWS Leptomeningeal angiomas (abnormal blood vessels that form growths in brain) Seizures common Eye Conditions: Glaucoma Clinical Presentation Pink/red homogenous patch seen on face Variable size: increase in size proportionate to physical growth of child May darken, acquire purple hue with age Tx/Mx Slight pressure – easily blanches, r/o nevus or melanoma Look for other congenital anomalies Photodocumentation Capillary hemangiomas will likely spontaneously regress Laser therapy is effective for both Usually recommend referral after adolescence if concerned with cosmetic appearance Treat any associated glaucoma in PWS patients! Benign Melanotic Lesions Ephelis aka freckle Plural: ephelides Larger sized melanocytes (normal in number) Autosomal dominant inheritance pattern Intensified by sun exposure, may fade in winter Fair skinned, more prone Solar lentigines aka liver spots, sun spots, age spots Occur in response to sunlight Persist in the absence of sunlight Middle aged to older patients Expanding macules (flat patches) Normal number of melanocytes Nevus aka mole Plural: nevi Common benign neoplasms or melanocytes; overgrowth of melanin-containing cells in skin Congenital or early onset Occasional changes in size or pigmentation however change ALWAYS suggests malignancy Three main types, Dermal, Junctional, Compound Dermal Most common Located in dermis Raised, dome-shaped Brown or black, lighter with age Smooth or warty surface May have telangiectatic vessels on surface Exposed and prone to trauma from clothing Junctional Located at dermoepidermal junction (only in epidermis) FLAT or only slightly elevated Smooth surface Uniform light to medium brown Symmetrical borders Rarely become malignant Compound Transitional, both in dermoepidermal junction and dermis Somewhat elevated, more so with age Flesh colored or brown Smooth or warty surface Symmetric, uniformly round or oval Dysplastic Nevus Atypical nevus with “fried egg” appearance Pigmented or amelanotic Atypical nevi: diameter greater than 5mm, irregular margins, and lesional color variation Commonly found at lid margin, diameter less than 8-10mm Increased risk for melanoma if multiple and with +FHx of melanoma Treatment/Management R/o other pigmented lesions Careful history to document onset and progression Photodocumentation – Anterior segment photos Re-evaluate based on degree of suspicion: q3-6mos for suspicious lesions and q1year Any changes refer out for biopsy! Only biopsy can definitively r/o melanoma Nevus of Ota aka oculodermal melanosis Benign melanosis, primarily involves region of trigeminal nerve distribution (V1 and V2) Unilateral, Gray-blue hyperpigmentation due to entrapped melanocytes (increased) Increased risk of uveal melanoma and glaucoma with these patients Premalignant Lesions Actinic Keratosis aka solar keratosis Caused by UV exposure/damage to the skin Squamous cell dysplasia Can develop into squamous cell cancer Clinical Presentation Range from mm to 1cm in size Erythematous, scaly macules or papules Can have elevation, white flaky crust Tx/Mx R/o Neoplasia, keratoacanthoma, melanoma, seborrheic keratosis Dermatology consult Cryo, cutterage, topical anti-cancer cream (i.e. imiquidmod), PDT Educate on risk with sun exposure! Photodynamic Therapy Pros: Limits damage to healthy cells Does not cause scarring Cons: Can only pass up to 1cm so only superficial lesions can be treated Keratoacanthoma Pseudocarcinomatous hyperplasia – benign growth Usually develop on head/face Middle aged or older 50-70, more common in fair skin Grows rapidly 2-6wks Clinical Presentation Raised lesion initially – dome-shaped nodule with central core like molluscum Has central umbilicated apical region (composed of keratin) in a crater-like excavation Has elevated rolled borders. Mimics SCC and molluscum Grows rapidly to 1-2 cm with pore expanded to display keratin filled crater Growth stop, keratin plug is discharged leaving a pit Spontaneously regresses by involution Keratoacanthoma Tx/Mx R/o SCC Reassure patient Photograph and monitor closely Dermatology consult for evaluation and biopsy If lesion is excised and it returns most likely BCC or SCC Differentiating benign vs malignant “That lesion looks Sus” ABCDEs of Lesions Nevus to Melanoma Asymmetry: if any two halves of a lesion are not symmetric Borders: irregular borders or development of satellite pigmentation Color: uneven color or changes in color (especially white, gray, red or blue) Diameter: enlarging size or >6mm diameter Elevation or Evolving Other concerning changes including ulceration, scaling, discharge or bleeding Neoplastic Considerations Personal History Lesion is not common for patient’s age, sex, Other skin lesions elsewhere on the body race, demography Other neoplasias or systemic disease Older Patient Excessive UV skin exposure Fair-complexion Lesion does not act or respond as anticipated FHx of skin cancer (reoccurrence) Acute vs chronic onset and or duration Rapid or irregular growth patterns Pain or irritation associated with suspicious lesion Neoplastic Considerations Quality of the tissue looks irregular Bleeding or ulceration of lesion Changes in lesion not consistent or predictable Neovascular patterns around or within lesion Recurrent infections or inflammations at site Uncharacteristically large lumps or bumps Associated tearing or conjunctival hyperemia Erosion of the margins or surface of a lesion Neoplastic Considerations When in doubt refer out! If you are concerned about the suspicion of a lesion recommend referring out for evaluation/excision and biopsy If monitoring yourself Photodocument if possible Diagram/Measure/Document accurately If suspicious RTC q3mos vs annual Malignant Neoplasms of the Lid Basal Cell Carcinoma (BCC) Most common malignant neoplasm of the lids (~90%) Slowly growing lesion, takes months to double in size Usually in area of chronic UV exposure – lid is not as common as other areas of the exposed skin More common in older/Caucasian/males Higher incidence in areas of previous trauma, burns, physical trauma, or X- ray exposure Clinical Presentation Starts as small translucent, waxy, greyish-white nodule Classically the center slowly ulcerates with an increase in size – tends to have darkened, ulcerated center Borders tend to be smooth, pearly white with fine telangiectatic vessels Multiple subtypes Nodular (most common): shiny pink or flesh colored nodule Superficial: 2nd most common, pink, scaly, or erythematous patch or plaque on the skin Sclerosing: aka morpheaform look like white scars that change over time Clinical Presentation Lower lid most common (~ 60% of all BCC located on lids) Medical canthus; upper lid less common Symptoms: “lump or growth that doesn’t go away or does not heal.” Remember these lesion are slow growing, can be there for sometime, so length of time doesn’t indicate benign nature History: h/o previous damage to area h/o other growths Nodular BCC Superficial BCC Morpheaform BCC Other Considerations Does not usually metastasize (migration to different sites) If metastasis occurs will be the regional lymph nodes first – palpate preauricular and submandibular nodes for swelling and tenderness Look for other BCC’s If single BCC has occurred, 20% chance of a second within 1 year, after 2 BCC’s have occurred 40% chance of another ≤ 1 year On trunk or back BCC may appear as an erythematous plaque (superficial) Tx/Mx If in medial canthal region consider consultation ASAP, more aggressive Refer to Oculoplastics and or Dermatology Biopsy Surgery excision by Mohs Radiation, cryo, conventional surgery also effective Consider photos and make sure you document! Follow-up q3-6mos, recurrence rate 10% Carefully evaluate any patient with h/o BCC, long-term annual exams Mohs surgery aka Mohs micrographic surgery Visible tumor and thin layer of tissue surrounding tissue is removed. Tissue is checked for cancer cells. If cancer cells observed another thin layer is removed Process is repeated until no cancer cells remain Attempts to remove as little tissue as possible Squamous Cell Carcinoma (SCC) Much less common than BCC, only accounts for 5-9% of malignancy on lids Much more rapid growth and can metastasize, spreads by local invasion and extension into regional nodes Elderly, fair skinned most susceptible Much exposure to UV Exposure to irritants, chemicals or trauma – radiation, sunlight, thermal burns, chronic heat and/or irritations, organic hydrocarbons Clinical Presentation No typical location, less on lids more on lips (~30%) Often arises from existing actinic keratosis or cutaneous horn Various appearance – none classic for SCC Can be raised nodule; flat crusty area; flat scaly area; ulcerated bleeding lesion, thickened margins Can be very keratotic with build up of keratin Hard to differentiate from benign growth (keratoacanthoma) DDx: BCC, Actinic keratosis, keratoacanthoma, seborrheic keratosis, sebaceous gland tumor SCC Tx/Mx If SCC suspected must refer for excisional biopsy only definitive way to make diagnosis Surgery if positive for SCC (Mohs technique) Recurrence rate is higher than BCC Patient Education: Always explain potential risk including blindness/death with cancer. Medicolegal aspects: If patient refuses referral Document your counseling and information given, make appointment yourself, send registered letter to patient Malignant Melanoma Most malignant skin tumor, derived from melanocytes Comprise ~ 3% of primary skin cancers but accounts for ~ 70% of deaths related to skin cancers High rate of metastasis, can metastasize in early stages Profile of susceptible patient is same as BCC/SCC Increasing numbers in middle-aged Clinical Presentation Asymmetric, pigmented lesion with irregular borders Variable coloration Variable diameter Types: Superficial spreading Melanoma Nodular melanoma Acral lentiginous melanoma Hutchison freckle/lentigo malignant melanoma Superficial Spreading Melanoma Most common of all melanomas ~ 70% of all melanomas Arises from pre-existing nevus Flat to slightly elevated Brown with black, blue, pink discoloration Usually greater than 6mm in diameter Irregular asymmetric borders Nodular Melanoma Account for about 15% of all melanomas in the U.S. Often from uninvolved area – no pre- existing lesion Elevated, dark colored, sharply demarcated Dark brown, red brown, red black Can be amelanotic Metastasizes early – poor prognosis Acral Lentiginous Melanoma Represents 8% of all melanomas Most common in dark-skinned people Represent up to 70% in Blacks and up to 46% in Asians Can occur on palms, soles, and nail beds Is extremely aggressive, with rapid progression Lentigo Malignant Melanoma Accounts for 5% of all melanoma Typically found in sun-exposed areas on adults Usually large > 3cm Dark brown-to-black, often elevated Least aggressive, local excision usually successful Stages of Melanoma Stage 0 (Melanoma in situ): Cancer is confined to the epidermis. No signs the cancer has spread to lymph nodes or other parts of the body Stage I: No more than 2mm thick and may/may not be ulcerated. No signs the cancer has spread to lymph nodes or other parts of the body Stage II: More than 1mm thick and be thicker than 4mm and may or may/may not be ulcerated. No signs the cancer has spread to lymph nodes or other parts of the body Stage III: Can be any thickness and may/may not be ulcerated. The cancer has spread to nearby lymph nodes and/or it has spread to very small areas of nearby skin or to lymphatic channels around the tumor. No signs the cancer has spread to other parts of the body. Stage IV: Can be any thickness and may/may not be ulcerated. May/may not have spread to lymph nodes. Has spread to distant parts of the body (lymph nodes, lungs, organs outside the CNS, CNS including brain, spinal cord and their coverings) Stages of Melanoma Survival Risk Tx/Mx Refer out for biopsy Surgery is the primary treatment Shave biopsies are not recommended, need to remove all layers of skin Careful evaluation of regional lymph nodes May consider removing lymph nodes in melanomas greater than 1mm depth Optometrist Role 1 in 5 Americans will develop skin cancer 1 in 3 Canadians will develop skin cancer Of the 15,000 new cases of skin cancer diagnosed every day, 10% are in the eye! Madarosis, lid notching, loss of meibomian gland orifices, surface telangiectasia, and ulceration classic signs of lid carcinoma. Moley! Questions?

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