Lecture: Masses and Bumps of the Eyelids: Practical Approaches to Diagnosis and Management

[Robert] Good morning. My name is Dr. Robert Fante, I’m in Denver, Colorado. And I’m going to be talking today about masses and bumps of the eyelids, strategies for diagnosis and management. Hopefully we’ll be able to cover lots of things today. I have no relevant financial disclosures, although I do have a private practice and I was formally the president of ASOPRS.

Today we’re going to be talking about a variety of different masses as you can see from these two pictures, some of them might be a little more severe than others. And most of them we’re going to be able to make at least an attempt at making a visual diagnosis.

Today we’re going to build a common language and a strategy for evaluation. We’re going to review the characteristics of common eyelid and adnexal bumps and masses that are routinely seen in clinical ophthalmology. And I’m going to push you to apply the terminology and use the tactics that we’ll discuss so that you can apply your resources appropriately wherever you are.

One of the interesting questions is about this idea of making a visual diagnosis. A study done about 30 years ago showed that untrained medical students and experienced professors had similar accuracy rates in guessing a diagnosis based on just photographs. It was fair. Other studies have shown that non-analytic pattern recognition training results in some large gains in diagnostic accuracy. We’re going to be using both pattern recognition and careful observation and description tactics, using also the patient’s history, chronicity, and other symptoms to help us decide. Ultimately a biopsy is going to be our gold standard and we’ll always be thinking that that’s going to be our backup plan.

We’re going to think about several different ways of differential diagnosis categorization. Congenital versus acquired turns out to not be very helpful for this particular group. We’ll think instead about inflammatory, developmental error, degeneration and disease, and neoplastic disease.

From an inflammatory point of view, there’s tissue reaction and damage from an immune response to either a microorganism, a foreign body, allergen or autoimmune process, or abnormal cells such as cancer. inflammation can be the entire problem or just one component of the problem.

Developmental error, trauma, metaplasia, means that normal cells are in abnormal places. That’s the key idea. Cysts, hamartomas, variations, and metaplasia all fall into this category.

Degenerations and disease is abnormal but not neoplastic cells in normal places. Age-related tissue senescence, intracellular and extracellular dispositions such as amyloid, and aberrant healing patterns from minor or major trauma all fall into this category.

Finally, there’s neoplasia, where we have new, non-normal cells. These can be, as you know, benign or malignant. We have microscopic histopathology as a way to understand this, also macroscopic, local externally observable changes, and of course, growth control is the key issue. That these grow without control ultimately causing tissue destruction and possibly metastasis depending on the tumor.

I’ll go over this slide more than once during this talk. But I want to remind you that the signs for potential malignancy include the ulceration that can’t be explained any other way, irregular edges or pigmentation, destruction of the eye lashes or eyelid architecture, firm or heaped up pearly margins, tortuous blood vessels or fine telangiectasia. Inflammation without tenderness and then persistent growth.

History helps a great deal here. Here’s a mass that’s been present for years, has been recently growing, which changes our mind considerably from something that’s been present for years and hasn’t changed in all those years, as these two masses are.

I’m going to remind you a little bit of the skin anatomy, we’re going to be talking about the epidermis, the outer layers, the dermis, pilosebaceous units which are the oil glands and hair follicles together, and then sweat glands.

I’ll also remind you of the eyelid margin anatomy which I know we all know well, but the glands of Zeis that provide oil for the eyelashes, the glands of Moll that provide sweat, Meibomian glands that provide oil for the tears, and then this idea of the mucocutaneous junction where the skin and mucous membrane meet at essentially the gray line for the normal eyelid.

An important part of this talk is going to be understanding this vocabulary and whatever your first language is, you’ll have similar words. But in English, I’m going to go over these. These first few are the most important ones. A papule is a small less than five millimeter solid circumscribed elevation. A nodule is a larger solid circumscribed elevation. A pustule has pus inside it, a vesicle, also known as a blister, where there’s fluid separating the layers of the epidermis. A macule is a small flat spot, neither elevated nor depressed, you can’t feel it with your finger. Instead, a plaque has a superficial minimally elevated, flat lesion that you can feel with your finger.

A cyst is a fluid-filled or semisolid filled cavity that’s lined by epithelium. A scale would be flaky dead cells. An erosion is a focal loss of part of the epidermis. An ulcer is a focal loss through the epidermis into the dermis. Erythema, of course, is another word for redness. Hyperkeratosis is superficial epidermal thickening.

Madarosis is a word meaning the loss of eyelashes. Telangiectasia is a dilated superficial blood vessel. As I mentioned, the pilosebaceous unit is the hair follicle with its associated sebaceous glands. A comedone is a plug of sebaceous material and dead skin stuck in the opening of a hair follicle. These are pimples in the American vernacular, also known as blackheads or whiteheads. An umbilication is a superficial cavity in a mass, often loosely filled with tissue.

Finally, there’s verrucous which means warty, multilobulated. Papillomatous which means fingerlike projections of epidermis, circumscribed which is the same as well-demarcated which is the same as discrete versus diffuse which is more ill-defined. And then we think in terms of superficial versus subcutaneous versus deep. And then we can describe the growth patterns as either exophytic, working its way outward or endophytic, working its way inward.

If you want to learn more about these dermatological ideas, these are some great books that have lots of pictures and will help you understand some of these common skin-related masses. You can also look at the ASOPRSeducation.org, online education center which is freely available to anyone, anywhere and has the in-depth articles about most of the things we’ll talk about today.

I also want to mention the concept of fast versus slow thinking. You may have read this book by Daniel Kahneman, “Thinking Fast and Slow.” He won a Nobel Prize. But the idea that there’s two systems of human thinking and they’re a fast, instinctive, and emotional one and then a slow, deliberate, logical one. Malcolm Gladwell and the book “Blink” also describes these two ideas. It turns out that both could be refined with practice and experience and ideally we want to use both.

We’ll talk about pattern recognition and standard terminology. Careful examination and use of these terminology will help clarify the alternatives for the differential diagnosis using slow analytic thinking. But a lot of common lesions that clinically present with typical appearance, practice and repetition will help to develop our diagnostic judgment using fast intuitive thinking. I’m going to show you multiple examples of most of the things we’ll see today, trying to help work toward that one. Doesn’t always work, so again, everything that I’m going to show you was biopsied so that I can tell you for sure that what I’m telling it is is what it was.

Here’s a picture of Colorado, where I live.

Here’s a list of some of the things we’ll talk about today in the inflammatory category. As you can see, all of these are relatively common, with perhaps the exception of discoid lupus.

I’m going to start off by showing you a picture like this and asking you to take a minute to think about how you would describe that using the scientific terms that we just discussed. I’m going to show you then how I’m describing it. My answer is not necessarily the only one or the right one, but it’s just a way of trying to carefully describe this to help us decide what it could be.

I called this an elevated, exophytic, warty, discrete mass with hyperkeratosis but no erythema. You all probably know that that’s a papilloma. We see a hyperkeratosis with a papillary growth pattern. These can be single or multiple, often involving the lid margin. Most commonly associated with human papilloma virus and the treatment is excisional biopsy or these can be observed.

Here’s another example of a papilloma. Here’s another example of a papilloma on the eyelid margin there on the patient’s right upper lid. Here’s another example of a papilloma at the lower lid margin. Here’s another example of a papilloma at the lid margin. You’re starting to get the idea here. Again, discrete, warty, no associated inflammation and no tissue destruction. Here’s another papilloma.

Instead, here’s another one. But take a moment to think about how you would describe this group of lesions. I describe this as dome-shaped, waxy papules and nodules with central umbilication but again, no erythema.

This is molluscum contagiosum which, as you know, is a poxvirus epidermal infection. It can cause a secondary follicular conjunctivitis. One of the classic highlights is central umbilication from necrotic cells that are filled with viral inclusions. This is self-limited in immune competent individuals usually resolves within a year. But it can be treated with cryosurgery, curettage, laser, and TCA.

Here’s another one. Think about how you would describe this. I described it as an erythematous scaly macule.

This is an inflammatory dermatitis. We see atopic dermatitis with skin hypersensitivity associated with asthma, rhinitis, and elevated levels of IgE. It can be contact dermatitis where it’s an irritant or allergy induced erythema. Cosmetics, nail polish, lots of ophthalmic medications, airborne irritants, sunscreen, can all cause this. Can also have an exfoliative dermatitis which is much more rare. The treatment is to avoid the offending agent, you can use topical steroids, sometimes a dermatologist could be helpful in identifying what’s the causative factor.

Here’s an example of contact dermatitis of the eyelids, especially with eyelid ointment. Again, itching, diffuse erythema, superficial edema, these are the hallmarks of a contact dermatitis.

How about this one? Take a few seconds and see what you see here. Showing both a facial picture and an eyelid picture. I’m calling this telangiectasia of the nose, cheeks, and glabella, and the eyelids with posterior blepharitis.

All of you know this is acne rosacea. Telangiectasia of the central facial skin in middle age and older adults, associated with immune dysregulation and often colonization with Demodex folliculorum mites. We see sebaceous gland hyperplasia with papules and pustules, rhinophyma, and meibomitis. And we treat this with topical metronidazole, systemic doxycycline or azithromycin, laser, IPL to the eyelids, et cetera.

How about this one? How would you describe this eyelid? Take a few seconds. I describe this as diffuse erythema, telangiectasia, and localized madarosis. It’s important to notice that the lashes are missing in the outer part of this lower eyelid.

This is discoid lupus erythematosus which has commonly asymmetric eyelid madarosis, erythema and scaling. The diagnosis is made with the full-thickness skin biopsy, you can get serum ANA and lupus-band test immunofluorescence. The treatment is topical steroid ointment or intralesional steroid together possibly with oral hydroxychloroquine.

Another example of discoid lupus erythematosus with more scattered eyelash loss rather than just in one focal area. But you can see the classic eyelid margin erythema.

This one should be immediately evident to most of you. As you know this could be described as crusting papules and vesicles with erythema in a dermatomal distribution. And this is herpes zoster or shingles. As you know this is caused by reactivation of a latent varicella-zoster virus from nerve root ganglion affecting one dermatome typically. Most patients are over 50. There is vaccination available that provides excellent prophylaxis. We worry a lot in older patients about postherpetic neuralgia. And we’ll screen for keratitis, uveitis, and neurotrophic keratitis in patients where the eye is involved. Treatment for this, at least here, is best coordinated with their primary care doctor, including systemic antivirals, topical antivirals, and sometimes systemic steroids.

We’ll next move to the next category: tissue development, growth or degeneration. Here’s the list of some of the things we’ll talk about.

Here’s our first picture and I’ll ask you to describe what you see at this patient’s left upper eyelid. Take a few seconds and think about what that might be. I’m going to describe that as a well-circumscribed, fluid-filled yellow-white mass without erythema.

This is an epidermal inclusion cyst, also known as a sebaceous cyst. The epidermal cells can get lodged in the dermis, producing keratin and fill up a cystic cavity. If it’s at the lid margin, it’s often the Glands of Zeis. It is sometimes associated with mild inflammation. Some of them will slowly grow but the treatment is excisional biopsy or these can be simply left alone.

Here’s another example of an epidermal inclusion cyst of the lateral canthus. Here’s another example of an epidermal inclusion cyst of the medial canthus. Here’s another example of an epidermal inclusion cyst, this time causing mechanical ptosis. Here’s another example of an epidermal inclusion cyst where the patient’s picked at it a little bit.

Finally, let’s talk about this one. Another category all together. How would you describe this mass seen at the medial canthus in this patient’s left eye? I’m going to describe this as a well demarcated clear fluid-filled cystic mass, again without erythema.

Most of you probably know this is a sudoriferous cyst also known as a hidrocystoma. This is a cyst of a single or multiple sweat glands that are filled with clear or milky fluid. If it’s at the lid margin, it’s from the gland of Moll. Typically no inflammation with this. These can be safely observed or an excisional biopsy is helpful.

Here’s another example of a hidrocystoma. Another example of a hidrocystoma, this time with a little bit of blood in it.

How about this one? How would you describe this mass at the right upper eyelid for this patient? I’m describing it as an elevated scaly nodule without erythema or variable pigmentation.

This is an acrochordon, also known as a skin tag. There’s a familial tendency for these, they certainly occur in areas of friction like the axilla, sometimes parts of the face. Again the treatment is observation, they can be safely left alone or excisional biopsy.

How about this one? I guess I have that up first, it’s the multiple small, white/yellow dome-shaped nodules. Hopefully that’s similar to what you might have said.

These are milia. These are transient dermal keratin cysts derived from any epithelial structure. Differential diagnosis includes things like sebaceous hyperplasia, syringoma, acne, and calcinosis. These can be observed safely or evacuated or treated with topical retinoids, Differin, or electrodessication.

How about this one? I would describe these lesions that affect both eyes as well-circumscribed, mildly elevated, yellow plaques. And probably most of you can identify those as xanthelasma. This is caused by hyperlipidemia types II or III in about 30% of patients. Although most of them don’t have that disease. They are histologically histiocytes with foamy lipid-laden cytoplasm within the reticular dermis. And the treatment is normalization of hyperlipidemia if it’s present. These can be safely observed or these can be excised for biopsy or even ablated with a laser.

This is a picture of Auckland, New Zealand which I had an opportunity to visit not long ago.

How about this? Here we’ve got a young child looking at the right upper lid and eyebrow area. I would describe this as a rubbery, deep mass at the lateral upper lid and eyebrow without erythema or ulceration.

This is a dermoid cyst which, as you know, is a hamartoma of skin elements caught in the deep facial tissues during embryonic development. They can contain teeth and hair. They’re most commonly seen at the lateral but sometimes at the medial orbital rim and upper eyelid. If there’s accidental rupture it causes marked inflammation. Although these can be observed for a while, most parents want these removed, at least in the United States, excisional biopsy will solve the problem.

Here’s an example of a dermoid cyst again. Here’s another example of a dermoid cyst, this time more medially. Here’s an example of a dermoid cyst that can be seen on eversion of the upper lid because it’s dropped down a bit. Here’s an example of one that you can see at the lateral left upper lid. And here it is being removed through a lid crease incision.

Let’s talk next about some benign neoplasia. As we keep moving through this, we’ll talk about this group here and eventually we’ll get to the malignant ones.

We’ll start with this. How would you describe this group of masses that you can see at the right lower lid of this patient. I’m describing this as a group of shiny small papules without erythema.

This is syringoma. These typically are dermal papules less than three millimeters, translucent to yellow-white and they occur in groups. This is a benign tumor of the sweat gland ducts. The benign cells grow in tubules, it’s common in younger women. The lower lids, forehead, and cheeks are most commonly involved. These can be treated by excisional biopsy or laser ablation, or just observed safely.

Syringoma are similar to milia so I thought it might be helpful to look at this at least from the outside. They actually have some substantial differences. The syringoma are deeper to the epidermis, where the milia are very superficial. The milia can be scraped away without too much difficulty, they’re easy to remove. Whereas the syringoma are not easy to remove. The syringoma tend to be more confluent and the milia tend to be less confluent.

Here’s another example of a more rare thing called a syringocystadenoma.

How about this mass? How would you describe this at the patient’s right lower lid? I describe this as an elevated, waxy, warty, well-demarcated, variable pigmented nodule. In English we use the term stuck on, it looks like someone just stuck it there.

Seborrheic keratosis is the diagnosis. This is a benign proliferation of immature keratinocytes with hyperkeratosis, acanthosis, and papillomatosis. Scaly, flatly elevated, stuck on, waxy, warty, well-demarcated, variably pigmented. Very common in the elderly population, they can be post-inflammatory. There is also an autosomal dominant inherited version of this. There’s a thing called the Leser-Trelat sign: where sudden onset of these indicates a systemic malignancy, usually in the gastrointestinal system. The treatment for this is excisional biopsy or observation.

Other examples of seborrheic keratosis. Another seborrheic keratosis. The entropion is unrelated. Seborrheic keratosis. And here we see in a child this is not actually not a seborrheic keratosis although it looks a lot the same, this is called hyperkeratosis.

How about this mass? You see the patient at the left upper lid you can see this mass. How would you describe it using that terminology? I would describe it as indiscrete, this time, subcutaneous grayish papule with some associated erythema. It does have mild erythema here.

This is a hair follicle tumor. The category here of pilomatrixoma and trichilemmoma include benign and solitary or multiple masses. These tend to be flesh-colored or gray, they typically don’t have hair, even though they’re hair follicle tumors. There’s a syndrome associated with multiple of these with a higher risk of GI cancers called Cowden’s syndrome. The treatment is excisional biopsy or observation.

Here’s another example of a trichilemmoma, this one pink. Here’s another example of a pilomatrixoma this time, lifting up his eyebrow you can see a little, though it looked like it was a bit pink because of the lighting it actually isn’t.

How about this mass at this patient’s left lower lid, upper cheek area. Describing this as a purple-red circumscribed superficial papule. And this is hemangioma. These are benign vascular tumors derived from local blood vessels. More than 50% of these occur on the head and neck. In English they’re also known as strawberry or cherry nevus. They tend to be stationary or very slowly growing. They can be observed, cauterized, or biopsied.

Here’s another example of larger hemangioma.

An example of, and this a slightly version in a child, how would you describe this in this child? I’m going to describe this as a purple fluctuant diffuse deep mass. These can have rapid growth with a high risk of amblyopia. This is infantile hemangioma, used to be known as capillary hemangioma. This is a little more dangerous than the other ones because of the risk of damage to the visual system. Most common periocular tumor of childhood. It’s usually deep in the eyelid when it’s congenital. The acquired adult type tends to be more superficial and smaller. These typically grow rapidly over the first year and then spontaneously regress but not always completely.

Treatment options include oral propranolol, topical timolol gel, pulsed dye laser, and intralesional steroid injections.

Here’s an example of a patient I saw who was treated with systemic propranolol. You see the first presentation, after a few months of propranolol you see it getting smaller and diluting over the course of the first year or two of this patient’s life. Clearly a big advance in our treatment of this.

How about this? This is a pretty shocking person to see as you walk into your exam room. How would you describe what he has? I described this as multiple exophytic nodules without ulceration or erythema. You probably can guess given the widespread involvement that this is neurofibromatosis. This is infiltrative benign tumors of the peripheral nerves associated with multiple facial and ocular anomalies, as we all know. Treated with observation unless particular lesions cause symptoms such as mechanical ptosis. Surgical excision can be difficult. These tend to bleed quite a bit and the carbon dioxide laser is helpful if you have access to that. A Colorado needle or similar electrocautery can also be utilized.

Another example of a neurofibroma. This time causing ptosis.

How about this one? How would you describe this? Here we have a mass of the medial canthus. I’m describing this as a purple discrete papule at the caruncle.

This is called an oncocytoma. Benign, slightly more uncommon neoplasm. It’s usually found at the caruncle. It’s associated with apocrine cells with extra mitochondria. These can be difficult to completely excise, but fortunately they only rarely have malignant degeneration. And the treatment typically is excisional biopsy because we want to know for sure what this is.

Another picture of my part of the world here.

Here, looking at this lady we can see several things. If you look at her right upper lid as seen in the close up photograph. This is a brown, well circumscribed maculopapule without erythema.

Here we have the same diagnosis but just showing another way that it can present. In this fellow I’m describing this as pale, pink papules and nodules without erythema.

These are all nevi or nevus. This is a benign collection of specialized melanocytes which are round instead of dendritic with growth into the adjacent structures. These can be described as junctional at the junction of the dermis and epidermis, intradermal that are in the superficial dermis, or compound. They sometimes can be amelanotic which is important. They evolve with age but are usually benign when they arrive prior to adulthood. Malignant transformation potential is generally quite low.

Here’s an example of intradermal nevus, here’s an example of a junctional nevus. Here’s an example of a junctional nevus at the eyelid margin.

This is slightly different. How would you describe what this young girl has? I’m describing this as a variably pigmented circumscribed maculopapular lesion involving the eyelids and conjunctiva.

This is a giant congenital nevus. Relatively rare, 1 in 20,000 births. Arises from neural crest cells and they often have dermatomal distribution, sometimes involving the deeper tissues. Tend to be light brown at birth but darken with time, developing coarse, dark hair and rougher textures. The melanoma risk is substantially higher than the general population and so the treatment typically will involve multistage excision and reconstruction. Although these can be observed in the short term.

This is actually in New Zealand again.

How about this one? If you look at this patient here, you can see initially when you first walk in, this mass at the eyelid. When the eyelid is pulled down you see these other masses on the inside. How might you describe this? I’m describing it as a brown, elevated, irregular, variably pigmented nodule with satellite lesions.

Most of you now can tell, we’re moving into a more dangerous category of the malignant neoplasia. Including melanoma, lymphoma, metastasis, microcystic adnexal carcinoma, sebaceous cell carcinoma, squamous cell carcinoma, basal cell carcinoma.

We’ll start off with melanoma. As you know this has a relatively high fatality rate. It’s only 1% of all skin tumors but 60% of all skin cancer deaths. It can cause widespread metastasis, the prognosis is related to the depth of the original lesion and so a more complete biopsy is appropriate rather than just a shave. As you can see the survival rate changes substantially if it’s deeper. As a consequence we do need to include the deep margin when we biopsy these.

Here’s a patient with progressively worsening ptosis from eyelid melanoma. Again you can see on eyelid eversion there’s involvement in superior fornix. Another example of melanoma. You can see this looks different from a nevus. It has this multilobulated, it’s variegated in pigmentation, it’s not quite as discrete. Another example of a recurrent melanoma this time.

How about this patient? How would you describe what you see here? Closer up view of it. You can see in the medial canthus in the upper lid there is some disturbance. I described this as lumpy, fibrous, indistinct, mildly tender, which you wouldn’t know from looking at it, but mildly ulcerating, subcutaneous mass. Here it is after excision.

This is microcystic adnexal carcinoma. This is the malignant form of syringoma where we talked about those as benign masses that we see all the time in young women. In this case the tubules grow and infiltrate the soft tissues, particularly following nerves. This can be locally aggressive but fortunately it rarely metastasizes. And the treatment is with wide local excision using Mohs technique or frozen sections and subsequent adjuvant external beam radiation.

Picture of Colorado.

Here we have a different lesion all together. How would you describe this? I’m going to call this a fleshy, salmon-colored, elevated subconjunctival discrete mass without erythema. You see the surrounding conjunctiva’s not injected.

Biopsy of this was MALT lymphoma. Noted mucosa associated lymphoid tissue in this classification system here. This is 10% of all non-Hodgkin’s lymphomas but it’s 60% of ocular adnexal lymphomas. An indolent B cell malignancy, it responds to radiation, sometimes it can be observed even without treatment. In some places it’s associated with Chlamydia psittaci and can respond to doxycycline. We do see this associated with Sjogren’s syndrome and it can occur in the gastrointestinal system as well.

Ocular adnexal lymphoma is the most common subconjunctival and orbital malignancy, it’s usually painless and indolent. Requires systemic oncology workup and biopsy. With these other categories of follicular, mantle cell, and Hodgkin’s disease, the MALT ones at least we can treat locally.

In this case you can see this boy has ocular adnexal lymphoma, a different type of mass than we’re seeing in the patients with MALT lymphoma with a larger area of involvement.

This person has something different, I showed this picture at the very beginning. And I’ll ask you to describe what you see here. I’m calling this inflamed, edematous, multinodular diffuse mass in both the upper and lower eyelids. In this case, this happened to be a metastatic breast disease. But this is a metastatic malignancy. You can also see a similar picture in multiple myeloma, which, I’m sorry, is the previous one, leukemia. And typically the treatment for this will follow the primary disease. But ophthalmologists can be helpful in making the diagnosis or in confirming it in somebody who has involvement from previous malignancy.

Now we’re going to talk about the more common eyelid cancers: sebaceous cell carcinoma, squamous cell carcinoma, and basal cell carcinoma. Again, I’m going to remind you of the signs of potential malignancy to look for: ulceration, irregular edges or pigmentation, destruction of lashes and lid architecture, firmed or heaped up pearly margins, tortuous blood vessels or fine telangiectasia, inflammation without tenderness, or persistent growth.

How would you describe this mass? I’m calling this an ulcerated nodule with associated erythema.

This is sebaceous carcinoma, more commonly seen in the upper than lower eyelids. People tend to be elderly. Can start off in the Meibomian glands, the Zeis glands, or the caruncle. Characteristic staining with Sudan black or Oil Red O can be performed prior to processing. Pagetoid spread can be seen with dissemination of clusters of cells in the epidermis or the conjunctiva. We need to do complete excision for this with preoperative mapping.

This is also known as the masquerade syndrome because it can look like a chronic chalazion, the last patient did not. But it can cause madarosis and lid margin inflammation similar to chronic blepharitis. We have to have a high index of suspicion with recurrent chalazia or unresolved blepharitis in the elderly and biopsy these.

Here we can see sebaceous cell carcinoma following excision and reconstruction. And both the before and then the after of treatment for this particular patient. Fortunately the upper eyelid skin hides the scar pretty well.

This is the town in Italy that my family comes from.

Let’s talk about squamous cell neoplasia. And I saved some of these for here because it’s important to understand how this all fits together with both the squamous cell neoplasia that are not malignant moving into squamous cell carcinoma. We think about squamous papilloma of the conjunctiva, ocular surface squamous neoplasia, actinic keratosis, and then squamous cell carcinoma.

Here’s a squamous papilloma, not malignant. Another example then, instead of squamous cell carcinoma, you can see the leash vessels, the invasion of the conjunctiva and the obvious area of ulceration and erythema.

This is also squamous cell carcinoma. And this is ocular surface squamous neoplasia.

I’m going to ask you to describe this for a second now. Looking at this patient’s head, I’m describing these as pink, scaly, ulcerated macules with indistinct margins and some hyperkeratosis.

This is actinic keratosis, a common facial and eyelid precancerous lesion. The conversion rate to squamous cell carcinoma is approximately 1 in 20 over 10 years. Treatment varies by the number and size of the lesions. We sometimes will use excisional biopsy, cryotherapy, tropical chemotherapy such as 5-fluorouracil or Imiquimod. Levulinic acid and phototherapy, and even topical diclofenac gel.

Other examples of actinic keratosis. Some of them can be pigmented as you can see on your right.

This area here of the medial canthus of this woman, red, ulcerated macule with indistinct margins and hyperkeratosis.

Squamous cell carcinoma. More common on the conjunctiva and the cornea than on the eyelid. The lower lids are more common than the upper. Eyelid squamous cell carcinoma has a higher malignant potential than basal cell carcinoma. We do sometimes see vigorous local extension, occasionally even metastasis to regional lymph nodes. Fortunately it’s only 3% when it arises in a prior actinic keratosis. We have to follow these patients closely for late local deep extension.

Treatment for this. For me it would be to refer the corneal and conjunctival lesions. For many of you, you might treat those. Excision with margin control with Mohs or frozen section for the skin and eyelid lesions. When orbital extension is seen, especially in the medial canthus, will sometimes require a deeper work and pretreatment with cetuximab can be helpful. Exenteration is rarely used these days, but once and a while it’s our only way of controlling this. Close follow up with late deep extension is necessary.

You can see an example of a squamous cell carcinoma of the eyelid. Madarosis from squamous cell carcinoma, you see the central upper lid on this patient where the eyelashes are missing compared to the other eye.

Lid margin destruction from squamous cell carcinoma. Another area of lid margin destruction from squamous cell carcinoma. Here’s a patient with neglected squamous cell carcinoma. He kept hoping that this would just go away on its own. Here you can see an area of recurrent squamous cell carcinoma again with an indolent area of ulceration involving the eyebrow skin. This can go pretty bad. Here’s another patient with previous treatment involving a giant flap to his forehead who still has squamous cell carcinoma at the margins here, causing this type of destruction. Further example of the same patient later on.

The end result for this can be complete destruction of many of the orbital and cheek tissues. Here’s a patient following both maxillectomy and orbital exenteration. Another patient who had squamous cell carcinoma that involved the entire orbit. Here we see after initial forehead flap reconstruction following the exenteration and ultimately treatment using an orbital prosthesis. She doesn’t look too bad.

This is a picture taken from when I was a fellow at the University of Michigan, looking out the windows into the Michigan spring time.

How about this mass here seen at the medial canthus of the patient? I’m calling this pearly, elevated, pink nodule with madarosis and central ulcer here at the right lower lid.

This is basal cell carcinoma. It’s the most common eyelid malignancy, encompassing 90% of malignancies that we’ll see on the eyelid related to sun exposure and skin pigmentation. The typical signs are pearly, elevated edges, destruction of local architecture such as the lashes, and ulceration. We see it more commonly on the lower lid than the upper. The subtypes include nodular, cystic, and morpheaform basal cell carcinoma. This is locally invasive but fortunately it has a minimal potential for metastasis.

Here we see, usually it grows slowly, but here in this patient six weeks later, it certainly has grown. So occasionally there are ones that are more aggressive than others.

And it’s important to understand that the usual treatment is local excision with either Mohs or frozen section and subsequent reconstruction. If we look at the numerical breakdown of this, at least here in North America, the lower eyelid encompasses close to half of the basal cell carcinomas that we see at 44%. 16% in the upper lid, 19% in the medial canthus, unfortunately. 4% in the lateral canthus and 17% in the eyebrow.

Here’s an example of a nodular basal cell carcinoma. Example of morpheaform basal cell carcinoma. You can see this sort of rat eaten or moth eaten area of ulceration involving a larger area.

Here’s a basal cell carcinoma that was ignored for years. You can see the destruction to the medial canthus and upper and lower eyelids and the side of the nose. Here’s an example of a nodular basal cell carcinoma with destruction of the eyelid margin and loss of eyelashes. Another example of a nodular basal cell carcinoma with the eyebrow upper lid area. An example of a nodular basal cell carcinoma.

An example of a morpheaform basal cell carcinoma where you see more destruction of the local tissues. I certainly might have considered this to be a squamous cell carcinoma based on the type of pattern here. Obviously biopsy is important to understand what you’re actually dealing with. Another example of morpheaform basal cell carcinoma that’s gone further. Lots of destruction here. Morpheaform basal cell carcinoma of the medial canthus.

A cystic basal cell carcinoma. This one you might mistake for a benign lesion. You don’t see as much destruction, it seems like it’s less inflamed, more discrete. It highlights the reasons why biopsy is helpful. An example of a nodular basal cell carcinoma again. You might not be as worried about this one except for that small area of ulceration.

This is perhaps the youngest patient I’ve taken care of with morpheaform basal cell carcinoma involving the medial canthus there. Another example of morpheaform basal cell carcinoma with lots of erythema, local ulceration, destruction of the lid margin.

An example of cystic basal cell carcinoma where it looks more like a nevus. And here, the lashes don’t appear to be destroyed. Again highlighting the need for a biopsy.

Here we see another nodular basal cell carcinoma. And yet another nodular basal cell carcinoma. I’m hoping that seeing all of these in close proximity will help cement the ideas of what it might look like in our mind. Another example of a nodular basal cell carcinoma.

As you probably remember there’s a thing called basal cell nevus syndrome, also known as Gorlin-Goltz syndrome. This is an autosomal dominant syndrome of multiple basal cell carcinomas that arise in early adulthood. Also seen in palmar pits and odontogenic cysts. Nowadays this is treated with vismodegib or Erivedge.

Here you can see the palmar pits and odontogenic cysts in a patient with severe basal cell nevus syndrome. Prior to vismodegib, this man had multiple operations, you can see how destructive this disease could be. Fortunately we now have this systemic treatment.

Speaking for a second about the Hedgehog pathway inhibitors, there’s now more than one but associated for basal cell nevus syndrome and also for advantage or inoperable basal cell carcinoma. It’s a uniform dose of 100 milligrams given daily. This could be given for months or years to control or eradicate the tumor. Muscle spasm, dysgeusia, alopecia, nausea and diarrhea tend to be the side effects that limit it. Patients can go on a short holiday if those side effects become too problematic. Our main problem is it’s quite expensive but it also may have a role in some other cancers that we can see.

Here we see an example of basal cell carcinoma after complete excision. And then subsequent reconstruction just to give the idea of what happens there. This is not a talk about the surgery for this but we can answer questions.

Here you can see another version of a flap reconstruction involving what’s known here as a semicircular Tenzel flap.

I’m going to have now a quick challenge for you as we finish up. To test yourself on the terminology and check your fast and slow thinking, I’m not trying to stump you but these are all again biopsied cases.

Here’s the first one. Looking at this patient, how would you describe what you see here? Take a few seconds. And in case you’re wondering whether your focus is wrong, this patient does not have entropion or ectropion and there are no lashes there. I would describe this as a pearly, pale, sessile, ill-defined lesion with madarosis and destruction of the local architecture.

Here is the patient. Both eyes now to make it a little easier on you, you can see how many more lashes are visible on the patient’s left eye, on your right. And this, of course, is basal cell carcinoma. Here he is following a Hughes flap reconstruction with the final result.

How about this one? Here you can see at this patient’s left eye, how would you describe that? I’m going to call this elevated hyperkeratotic scaly mass with mild inflammation. And this is a papilloma, one of the first things we saw in this lecture. Hopefully that was memorable to you.

How about this one? Here at this patient’s right upper lid, how would you describe what you see there? I would describe that as an elevated, pale nodule with minimal inflammation. There’s quite a list of things that could be described like that that we saw. You might be surprised to know that this particular one turned out to be a neurofibroma without the associated disease, just an isolated neurofibroma. Just shows how interesting some of these things are sometimes.

How about this mass? How would you describe this? Here you can see if you pull the lower lid away from the eye, so you can see it from the inside as well. I’m describing this as a sessile, elevated mass without inflammation. And this is an amelanotic nevus.

How about this? The story on this patient is that he once worked at the Los Alamos Nuclear Laboratories. He comes in with this area of chronic irritation at the medial canthus of his left eye. I’m describing this as an ulcerated, ill-defined area of scaly inflammation. Here he is after excision of this mass. And that was squamous cell carcinoma. I’m sorry, I guess I missed that one.

Finally we got an area here on this patient’s cheek. You can see that the lower lid and cheek area. I can tell you that it feels lumpy and then the additional description that I would apply to this is that it’s a diffuse subcutaneous mass with mild inflammation. We saw something like this in the upper lid of the patient during the lecture. And here that is after complete excision because this turned out to be something bad. And this is microcystic adnexal carcinoma. As you remember, this is the sweat gland-associated microtubules turning into a malignant mass. And following his reconstruction.

Again, coming to this slide which I showed at the beginning. We know that it’s hard sometimes to make a diagnosis based on photographs, even for experienced professors. However, trying to use this non-analytic pattern recognition can gain diagnostic accuracy. Hopefully this lecture helped begin that process for you and in the course of your training if you’re paying attention and trying to use descriptive terminology throughout the course of seeing patients, you’ll gradually start to see patterns that will help you do some of that fast thinking.

History and chronicity, other symptoms, of course, are going to be helpful in deciding what to do for an individual patient. But I would advise you to obtain a biopsy for anything that seems suspicious to you.

I hope that this lecture’s been helpful for you. Thank you very much, I look forward to answering any questions.

I see someone wrote how urgent would referral for satellite lesions be? The answer to that, I think, is pretty urgent. I would be very concerned in that case, especially if it started off with a melanotic mass. Of course it could potentially be amelanotic as well, there’s a version of melanoma that’s that way. But I think satellite lesions would be helpful in thinking about malignant melanoma. Also helpful for thinking about sebaceous cell carcinoma, sebaceous carcinoma. I think referring either biopsing it yourself or referring it for biopsy and treatment is something that should be done sooner rather than later. It doesn’t have to be done in hours, not even probably days, but certainly within a week it would be ideally the standard.

The next question here is conjunctival nevus presented with sudden itching and pain but no increase in size. Does this indicate any emergency, what is the best treatment for this condition? I think if it’s known for sure to be a conjunctival nevus, that of course changes it a little bit. Our worry is the possibility that it’s something other than a nevus. Ideally, we would want to consider biopsy for that to make sure that is what it is. If it is a nevus, there isn’t really any other treatment other than removal. Obviously you can treat the associated itching with topical steroids, et cetera. But I would be at least concerned and a biopsy is such a simple thing to do for most of us, these aren’t complicated, assuming you have the right tools and local anesthesia.

I see, how can dermatochalasis be treated in a young patient? Is there any requirement in further investigations to rule out a systemic cause? I would say if the dermatochalasis is not associated with frequent recurrent swelling, which we would then call a blepharochalasis and can be associated with a different disease process altogether. But is a static, slow increase in the loose skin around a young patient, I don’t think there’s further investigation necessary. I think it would be unlikely that you’d find any systemic cause and that could be either treated locally with blepharoplasty type surgery or observed if the symptoms are mild.

Next question was what can be the reason of xanthelasma in a patient having cholesterol levels and blood sugar that are normal? Most of the patients who have xanthelasma do not have hyperlipidemia. We worry about it more in younger patients in particular but the truth is that we see these commonly in patients who have no systemic hyperlipidemia or certainly no problem with their blood sugar either. And so the reason for this is we don’t know. Just like we don’t know why many of these things occur in any one person. But fortunately they’re not dangerous and they can be treated locally if they’re bothersome to the patient.

Next question. How effective are tetracyclines in treating and reducing chalasia? I think the answer to this comes down to how far they’ve gotten. As we all know, the systemic use of tetracyclines and doxycycline and some of its cousins is helpful in dealing with post what we now call Meibomian gland disease, or used to be called posterior blepharitis. And clearing out some of the obstruction in the Meibomian glands when used with topical massage and topical medications.

If it’s already progressed all the way to a chalazion, there isn’t really evidence that using the systemic drugs will change that. Whereas you know that chalazion, as I had in this lecture at one point and then I took it out because it seemed too common, is a lipogranuloma that’s not inside the eyelid itself that the tetracycline isn’t going to help us clear that. The patient’s immune system might deal with it on its own over the long run. Most commonly we find that at least here we’ll treat them with a steroid injection or local excision. But I probably wouldn’t use tetracycline as my first path in somebody that has a true chalazion.

How long would a patient be recommended to use topical steroids as a form of treatment in order to prevent it from affecting intraocular pressure? In general most of us start to worry after several weeks. I think a topical steroid drop that goes into the eye, I don’t think you should probably ever use that more or two or three weeks without checking the intraocular pressure to make sure that there isn’t a problem. Topical steroids used on the eyelids where there isn’t any entry into the eye itself, if it’s far away from the lid margin, probably you can go longer with that. I still would worry at some point if they’re on it more than, I would actually just worry that the disease we’re treating wasn’t really being treated appropriately if they still needed it more than a month or two after use of topical steroids on the eyelid where it didn’t actually get into the eye. But if it gets into the eye, we check intraocular pressure sooner rather than later.

Someone asked, the next question is what are the risk factor for these masses? I’m not sure what masses you’re talking about. In general, most of the ones that we saw, the only real risk factor we can identify, other than the possibility of hereditary disease, is sun exposure. As sun exposure, as you know, causes many of the degenerations that we discussed. But I’m not sure what else you could use as a risk factor for many of the other things that we see.

Next comment was not really a question. Thank you for the compliment.

What is the cause of nevus? I’m not sure I’m capable of answering that question. We see very commonly in children hereditary or congenital nevi that occur all over the patient’s body. We see it later in life, it’s probably like so many other neoplasia, it probably is a failure of the patient’s immune system that’s monitoring for neoplasia in general to identify that a neoplastic cell has begun to replicate. This, of course, is the failure of the immune system to recognize that these can lead to cancer as well. We’re lucky in the case of nevus that it typically is not cancer, but still they can be a failure to be identified.

What is the role of steroids in infantile hemangiomas, is the next question. Currently, if we can identify those patients early during their growth phase, we’re typically using the beta blockers instead. These come in both a topical form as topical timolol as a gel or a drop. And then more commonly, at least in the United States, it’s given systemically as propranolol usually supervised by a pediatrician so that the ophthalmologist doesn’t have to worry about the cardiac side effects.

Steroids still do have a role. We sometimes will give intralesional steroid injections. But it turns out, of course, that these are a little more dangerous, a little more difficult to do than putting the young child on a systemic medication. The systemic medication such as propranolol are quite inexpensive. Supervision by the patient’s pediatrician is certainly possible, it can be done by the ophthalmologist if they’re willing to watch out for the cardio-pulmonary effects.

Next question. What to do with treatment of recurrent chalazion in a child at four years old? That’s a patient that I would probably consider putting on systemic medications. Our problem with the cyclins, as you know, is that they can cause staining of the teeth and other problems with development. But I certainly would consider using topical steroids and probably topical use of, sorry, I’m blanking for a second here. But the azithromycin which could also be given systemically, which wouldn’t have the same negative effects for development assuming the patient isn’t allergic. This can be a problem for parents and children. Many children, as we know from treatment for amblyopia and other diseases, don’t cooperate with their parents who are trying hard to get this under control.

The good news for chalazion is that although it could potentially, if it’s bad enough, lead to something like amblyopia. It’s more of an annoyance than it is a danger, it’s not cancer, it’s unlikely to lead to loss of the eye. At the same time, I can understand why a parent would want to try to control this if they can. I would probably go in the direction of frequent warm compresses, topical steroids with close monitoring of the intraocular pressure, and then also use of azithromycin.

Anthony, sorry, I shouldn’t say who it is. With reconstruction after excision, I’m not sure what PX means, can PX have recurrence? I don’t know what that is, maybe the diagnosis? For anything that we excise, it’s possible to have recurrence. I guess I’ll answer it that way. Even with frozen section or Mohs treatment, the success rate’s not 100%. Most studies that use the various methods for excision of multiple using a tissue margin control after excision of a malignancy have a failure rate somewhere in the neighborhood of half a percent to 1% depending on where they’re treated. It’s certainly true of virtually of anything we do that there can be a recurrence. Wide local excisions, probably your best bet, especially if you don’t have availability pathologist. The eyelids, our problem is that the real estate’s expensive and difficult to replace. And so we try very hard not to excise any more than we have to because the reconstruction can be so complex. Nevertheless the possibility of recurrence always exists.

What is the treatment of recurrent papules on the eye of children? Again, I think when we have recurrent papules, we wonder a little bit about what’s the diagnosis? Is this something as simple as a milia, could it be something as simple as syringoma? Could it be these things that are slightly deformed, we don’t like the look of them, they’re slightly deforming but they’re not truly dangerous? I would certainly recommend biopsy at some point even in a child if you have a recurrent problem that you can’t control any other way. Once you have a diagnosis, oftentimes we then have a more specific treatment. Sometimes it will be possible to use laser ablation or various topical treatments or it can guide you into thinking when you might decide to go with a surgical excision following that.

What is the cause of recurrent dermoid cyst? Probably the most common situation there would be incomplete excision of the original dermoid cyst. As we talked about this is a case where normal tissue, sometimes involving skin elements, even teeth and hair, are caught underneath the epidermis and if they’re not completely excised then they certainly, the tissue can recur. If they are completely excised, there’d be no reason why it should recur in the exact same location.

There is, I didn’t show it, there is a possibility of having this abnormal tissue caught in between a cranial suture so that it’s possible that intracranial extension of a dermoid cyst. Those are pretty rare in my experience. But that’s another thing that I might worry about if you had a recurrence and you really thought you had completely excised it the first time. Then I would consider doing orbital imaging at that point to see if there’s intracranial extension.

Next question was how would you approach a suspicious lesion with no provision of frozen section? I think assuming that you can get pathology for the tissue that you excise, for the original biopsy, I still probably wouldn’t do anything too large. Unless you thought it a patient you weren’t going to be able to see again. Sometimes that will happen when we know the patient’s come from far away, or they’ve come from a place where it’s unlikely we’ll ever see them again. If you can remove something from wide, local excision knowing that you can close the wound that you create without causing too much harm. Say, for example, sometimes often in the lower lid and the cheek and the nose and the forehead, sometimes in the upper lid, we can close those incisions without causing major deformity for the patient, then wide local excision makes sense.

I guess it depends on how suspicious it is too. If there’s a substantial damage to the lid margin, if there’s loss of eyelashes, if there’s an ulceration. If there’s things that really make us highly suspicious for malignancy, I would be more likely to do something larger if I didn’t have the opportunity to use frozen section and didn’t have availability of a pathologist to help me, I would use wide local excision and subsequent reconstruction. If it was going to be impossible or very difficult to repair the patient, such as needing to do a Hughes flap, sew the eye closed. I probably would push that patient to let us biopsy it and return once we knew for sure what it was.

Next question. What happens if dermoid cysts burst and contents into the eye? Well, usually it does not enter the eye but it can enter the eyelid tissues, which is probably what you meant. And I’ve certainly seen this happen. I think if you’re very careful about washing away the dermoid cyst contents from the local tissues, usually there is no problem, if that happens during excision. If the dermoid cyst bursts at another time, say the child has blunt trauma and it bursts underneath the skin before anyone’s had a chance to go after it, then we see much more inflammation. And then our problem is trying to clear that out, usually it involves putting the patient on systemic steroids first. Then doing a procedure to clear out as much as the contents as we possibly can find, and then continuing on with some systemic steroids. The tissue’s not dangerous in the sense of causing a major destruction, but it causes a lot of inflammation.

Do we perform cryo to all margins following wide margin excision biopsies? It depends on what it is, again. There’s certain lesions where cryo makes more sense than others. If we know that the lesion is squamous cell carcinoma, for example, it might make a little more sense to use cry where we’re worried more about local extension over the long run, then we would with, say, basal cell carcinoma, where we’re less worried. We know that we can control that more easily even if we had to with an additional excision. I think if we have a diagnosis it’s helpful.

If we don’t have a diagnosis I think it would be a reasonable thing to do if you’re trying to do it as the primary procedure before you’re going to know what it is, if you know you’re only going to see that patient one time, it’s reasonable to use cryo as a way to safeguard things. I don’t think there’s any evidence that that’s true but I don’t think it’s an unreasonable thing to do.

How can one differentiate pigmented lesions in dark skinned patients? Of course that can be difficult. I think we have to then use the other signs of malignancy that we talked about such as local tissue destruction, ulceration, change in local pigmentation, a loss of the discrete borders of a lesion so that it looks like it’s more infiltrated that no longer appears well-circumscribed and becomes more diffuse. And of course then, erythema or some evidence of local inflammation and other ways could be helpful. But it can be difficult. In many patients, as we all know, have multiple pigmented lesions on their bodies and it can be very difficult to know which one or two is suddenly turning into something bad or is newly arisen because they have so many they didn’t really notice which ones was which.

Next thing, how do we differentiate a caruncular nevus whether it’s benign or malignant? Feeder vessel? Yes. I think a caruncular nevus is something if it’s truly a pigmented area, even a pigmented one can be something like this oncocytoma that we showed. There is a version of that that is a malignant oncocytoma. There are also malignant, something like a malignant melanoma or a pigmented squamous cell or basal cell carcinoma can occur on the caruncle as well. I think in general we’re looking for those same signs we just discussed of inflammation, ulceration, loss of local discrete architecture and well-circumscribed appearance. In general I probably would be more liable to biopsy things. I know I live in a place where perhaps that’s easier to do than some of you. But I still think it makes sense when we’re worried. A feeder vessel could be helpful. I think in general looking for any sign of something being inflamed or destructive is a strong reason to biopsy it.

Another common benign lesion is orbital fat prolapse. For sure. Of course orbital fat prolapse is a degenerative problem where the orbital septum loses its integrity and we see the orbital fat either prolapse most commonly under the conjunctiva. Sometimes into other areas of the orbital tissue or upper lid. And I agree with you that that is something to identify. I do include that in lectures on orbital tumors, I didn’t think of it here, that’s a great addition. Thank you very much.

Does race play a role in the development of these masses? Eyelid masses are kind of rare in Africa, I rarely see these cases. I’m glad to hear that. I have been to South America many times, I have to do this sort of work. I haven’t done this in Africa, so I’m perhaps unaware of that. It makes sense that there might be some things that develop less commonly. Certainly most of the degenerative problems that we see are going to be more common in people with lighter skin when they’re related to sun damage. But I can’t comment beyond that.

Goldenhar syndrome. Does Goldenhar syndrome have eyelid masses? I don’t know that answer to that, so I’m going to pass on that one. I’ll ask you to look it up, I’m sorry.

What conditions are responsive to intralesional sclerotherapy? We think about those most commonly for vascular lesions where we’re going to be able to cut off the blood supply. At least here, intralesional sclerotherapy is more difficult to do than some of the other things that we have options to do. But I would be thinking about it for vascular lesions in general. As you probably know there are also intralesional approaches to some malignant conditions that have been described by colleagues in University of Miami and other places. My experience with use of sclerotherapy is relatively small so I’m going to pass on that question.

A detailed explanation with diagramatic representation which makes easy understanding, so this is a thank you. Thank you very much. I appreciate that.

When would we need conjunctival map biopsies? We think about these primarily with sebaceous carcinoma. That’s the one where we can have lesions that affect the conjunctiva that are not visible to the eye. Might be visible under slit lamp examination but most of us may not have time to do that kind of careful slit lamp examination. And so conjunctival map biopsy makes sense because the way that these spread.

Most commonly when we see satellite lesions from malignant, they’re easily identifiable because of the pigmentation, so I think the primary time where we’re thinking about conjunctival map biopsies is for sebaceous carcinoma.

Next question is what is the margin in millimeters that you’ll leave around any suspicious lesion during excisional biopsy of the lid margin? If I know that this is a patient that I’m not going to see again, it would depend a little bit on what the lesion appears to be. If I’m worried about malignancy, then I’ll probably want five millimeters of lid margin around the edges. If I think it’s more likely to be an epithelial malignancy such as a squamous or basal cell carcinoma, then I probably would cut that down to two.

If I believe that I’m going to have the opportunity to see the patient again, and treat them a second time after containing the biopsy, then I wouldn’t leave anything. I would just remove the lesion that I can see or even a chunk of lesion that I can see to get a diagnosis so that we can plan more definitive treatment. It depends a little bit on what I think the follow up will be and whether I’ll have a second chance at taking care of this patient.

Thank you very much for your attention. I hope that this was helpful and I apologize for not knowing the answers to some of those questions. In any case, good luck with all of your work and thank you for what you do for your own communities.