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Title: El papel de los rayos UV en la enfermedad ocular
Author: Infolentes
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Visualizacion optima 1600x900 pixel Comenta.esta.publicación or Paul Karpecki, OD, FAAO OBJETIVO DECLARACIÓN: Optometristas han sab...
Visualizacion optima 1600x900 pixel Comenta.esta.publicación
or Paul Karpecki, OD, FAAO


OBJETIVO DECLARACIÓN:

Optometristas han sabido por mucho tiempo el impacto de la radiación ultravioleta (UV) la luz que puede resultar en el desarrollo de catarata relacionada con la edad degeneración macular e incluso pterigión o pinguecula. Este curso se ve en la última comprensión de la exposición UV y algunos de los más comunes, así como las enfermedades raras que optometristas enfrentan cuando se trata a los rayos UV.

FACULTY/EDITORIAL BOARD:

Paul Karpecki, OD, FAAO

CREDIT STATEMENT:

This course is COPE approved for 2 hours of CE credit. COPE ID 35694-SD. Check with your local state licensing board to see if this counts toward your CE requirements for relicensure.

JOINT-SPONSORSHIP STATEMENT:

This continuing education course is joint-sponsored by the University of Alabama School of Optometry and Essilor.

DISCLOSURE STATEMENT:

The author is a consultant for AMO, Alcon, Bausch + Lomb, Focus Labs and OcuSoft and is a stock shareholder of TearLab.
Dr. Karpecki is also on the Essilor Advisory Board, but has no financial interest in any products.

Optometrists have long known the impact of ultraviolet (UV) light radiation that can result in cataract development, age-related macular degeneration and even pterygia or pingueculae.
But these conditions continue to increase in prevalence even though many contact lenses, IOLs and spectacles have UV protection coatings. This paper looks at the latest understanding of UV exposure and some of the more common as well as rare diseases that optometrists face when it comes to UV damage.

UV EXPOSURE AND OCULAR HEALTH

There are three forms of ultraviolet light—UVA, UVB and UVC.
UVA has a wavelength of 315nm to 380nm and penetrates deeply into the skin. This is often associated with tanning, but also is linked to skin aging.
UVB has a wavelength that is even smaller, between 280nm to 315nm. UVB does not penetrate into the skin as deeply as UVA because the epidermis mostly absorbs it. Thus, it can be a more damaging form of ultraviolet light that can cause erythema or sunburn, blistering of the skin, and potentially various skin cancers.
UVC ranges from 100nm to 280nm in wavelength and is the most harmful to the skin, also resulting in skin cancer. Fortunately, most of it is absorbed by the ozone layer and does not reach the Earth's surface.

Figure 1: A patient diagnosed with a conjunctival malignant melanoma.

The sunlight that does reach the Earth is comprised of approximately 95% UVA light and 5% UVB/UVC.
UVB and especially UVC are directly absorbed by DNA molecules, so this is why experts believe that these have the greatest impact on altering skin tissue and are associated with skin cancers.1
UVC is also the form that plays a key role in cataract genesis, as well as macular degeneration.2 UVC can actually form free radicals that directly affect the DNA. This has the ability to disrupt structures such as collagen, which are prevalent in the cornea and conjunctiva, as well as glycans such as hyaluronic acid.
On the other hand, some sun exposure is critically important to vitality, as it delivers vitamin D. In fact, many experts believe a vitamin D deficiency exists in the United States, which results in significant morbidity.3
Fortunately only 1% of all UV light from the atmosphere reaches the retina.4 Most is absorbed at the cornea and the lens, which essentially work as filters to prevent its penetration.
Furthermore, transmission of UV light through the lens decreases greatly with age.5 For example, a 10-year-old has a 75% or greater lens transmission rate. By age 25, the transmission drops to 10%. It is remarkable that this change happens within such a short span of years, and the amount of UV light transmission only decreases as age increases. Specifically, 80% of all the damage patients experience may well happen before age 18.

OCULAR DISEASES ASSOCIATED WITH UV EXPOSURE

* Photokeratitis: Photokeratitis— more commonly known as "snow blindness"—is essentially an inflammation of the cornea secondary to UV exposure. The condition is much more likely to be found by practitioners who live in ski resort areas (such as in Colorado or Utah), as well as those who live near beaches (such as in California and Florida).
Photokeratitis is directly attributed to environmental UV radiation exposure and generally occurs eight to 24 hours after being in the sun. It is more typical in individuals who have not used sun protection, such as sunglasses or hats, or were exposed to significant UV radiation for long periods.


Figure 2: Conjunctival intraepithelial neoplasm.

The primary symptoms are similar to a welder's burn and include significant photophobia and pain. Patients may even have blepharospasm due to the level of photophobia. The cornea often shows signs of ocular surface disease damage, very similar to what you might see with an advanced dry eye disease patient. It is not uncommon to see filamentary keratitis, conjunctival injection and even significant superficial punctate keratopathy.
Patients are typically treated with a combination steroid/antibiotic agent, ample lubrication with preservative-free artificial tears, and are instructed to remain indoors with cool compresses.
* Climatic Droplet Keratopathy: Another very rare corneal disease due directly to UV exposure is a condition called climatic droplet keratopathy. This degeneration affects the stromal layer of the cornea. Due to the significant UV effects, particularly from UVB and UVC, an accumulation of droplet-like deposits occurs in the cornea. Further research shows that these are actually altered proteins, but they have an appearance that mimic that of droplets.6
Similar to photokeratitis, climatic droplet keratopathy tends to be a binocular condition. Unfortunately, this can also be sight threatening, as it can lead to scarring and opaci-fication of the cornea.
Treatment is very similar to that of photokeratitis and involves a combination of corticosteroids, cool compresses and artificial tears. The patient should also be monitored for the potential of neovascularization and, in rare cases, eventual conjunctivalization (i.e., invasion of conjunctival epithelial cells onto the corneal surface).
* Pinguecula: A more common condition due to UV exposure is pinguecula. This raised nodule appears on the conjunctiva, particularly around the limbal area, and is nasal or temporal in location. Pingueculae can become inflamed due to dryness or sun exposure. In fact, research shows that pingueculae are much more likely to be found in individuals who live in areas of greater sun exposure or dry air environments.7
This combination suggests that this condition may be related to sun, but could also be related to dry eyes with irritation. Pingueculae are much more common in individuals who work or spend significant amounts of time outdoors.
Most commonly, patients with this condition have a cosmetic issue and at times may even get inflammation resulting in a pingue-culitis. Furthermore, patients with a pinguecula may have difficulty with contact lens wear, depending on the nodule's location.
* Pterygium: Another similar condition is that of a pterygium. In this example, the patient has a raised, wedge-shaped area of growth over the temporal aspect of the cornea with a lipid line suggesting an aggressive condition. The pterygium is differentiated tissue that is migrating into the corneal space. However, very similar to a pinguecula, these tend to be found in arid conditions or where significant UV exposure is noted, such as near the equator.7

The significance of a pterygium is that it continues to migrate into the visual axis of the cornea, resulting in topographical changes or even scarring of the visual axis if it progresses. For this reason, once the initial changes are noted or it appears to be progressing rapidly, a conjunctival resection is required.
Unfortunately, most resections have a high recurrence rate, and newer techniques—such as the use of a Gunderson flap, mitomycin C application or even amniotic membrane transfer—often have to be utilized to prevent recurrence and scarring.

Figure 3: Early nuclear sclerotic cataract in a 58-year-old patient who admitted to excessive sun exposure over many years.

Figure 4: A 43-year-old patient with a sebaceous cell carcinoma.

* Cataract: One of the most common ocular conditions associated with UV exposure is cataract development. A crystalline lens is made up of proteins. These proteins can be altered or denatured by exposure to UVB or UVC radiation. In fact, all three layers of the lens— nucleus, cortex and capsule—can have alterations in their protein structures.8
Depending on the location of the change, the type of cataract can range from nuclear sclerotic to cortical and others.
Once again, patients who live in high UV exposure areas, such as the equator, are more likely to have advanced cataract development. Although this is not too much of an issue in the United States, cataract is the leading cause of blindness in non-industrialized countries.
* AMD. Another condition highly associated with UV exposure is age-related macular degeneration (AMD). The worldwide prevalence rate of AMD resulting in impairment and blindness is 8.7%, making it one of the most common causes of blindness in patients over age 60. In the United States, for example, it is the number one cause of vision impairment in patients over age 50. Research suggests that AMD is the result of free radical damage.One of the more common reasons for free radical damage is exposure to ultraviolet radiation. Studies have shown that many individuals with macular degeneration have had greater UV exposure over their lifetime.10
* Solar Maculopathy: Solar maculopathy results in a burn to the foveal area due to excessive exposure to UV light. Reports show that even 20 seconds of sun gazing may be enough to burn the macula in certain patients.11 Of course, this can be an even shorter period of time if a person gazes at the sun during its zenith or uses binoculars or a telescope to watch a solar eclipse.
Damage associated with solar maculopathy is not reversible. It often mimics that of age-related macular degeneration, but of course it occurs in patients of any age who are not educated about the risks of solar gazing or staring at the sun. Unfortunately, most patients diagnosed with solar retinopathy or solar maculopathy tend to be those with mental disorders or patients with drug or alcohol abuse who do not have the understanding of the importance of not gazing directly at the sun.
The term solar retinopathy is sometimes interchangeable with solar maculopathy, but includes peripheral vision loss. It is indeed possible for patients to have peripheral retinopathy due to sun gazing or significant UV exposure. Because there are no pain receptors in the retina, patients may be unaware of any significant exposure until it is too late and the damage is done. In cases of short duration exposure, damage may be temporary and have some reversal; but if patients gaze at the sun for significant periods of time, it is more often a permanent vision loss.12
Patients with solar maculopathy present with a macula that typically shows retinal pigment epithelium (RPE) changes. There can also often be areas of hypopigmentation of the RPE at the fovea, which may show as hyperfluorescence on fluorescein angiography. Optical coherence tomography (OCT) will manifest an area of tissue loss or a punched-out lesion within an otherwise normal-thickness retina scan. This indicates the loss of the outer segments of the photoreceptors, as well as a loss of the inner portion of the hyperreflecting layer of the RPE.

Figure 5: A patient presenting with madarosis and a diagnosis of a basal cell carcinoma.

Research suggests that the pathophysiology of solar maculopathy involves fragmentation and vesiculation of the photoreceptors of the rod and cone outer segment lamella, as well as pyknosis of the receptor nuclei.13 However, because the cones are less likely to be affected, patients still may maintain relatively good vision. Even patients with significant solar maculopathy typically have vision of 20/50 to 20/70.13
The classic presentation of solar maculopathy is that of a brick red, well-defined lesion in the central fovea. In the very early stages of maculopathy, a small yellow-white spot, often surrounding a faint gray zone, is initially noted in the fovea. This may fade over one to two weeks, resulting in the classic, well-circumscribed brick red macular appearance.

UV LIGHT AND SKIN CANCER

In the last three decades, there have been more skin cancers diagnosed in the United States than all other cancers combined. In fact, 60% of all malignant melanomas are directly correlated to UV radiation, and 90% of squamous cell and basal cell carcinomas can be attributed to sun exposure.14 The direct cost to treat non-melanoma cancers is approximately $1.5 billion per year and continues to rise at a 4% per year increase.14
* Sebaceous Cell Carcinoma: The patient in Figure 4 was a 43-year-old white male who had noted a lesion return to the left upper eyelid for the third time in the exact location. Close examination shows that the raised area of tissue mimics a potential chalazion. However, there is significant madarosis (missing eyelashes) and tissue displacement.
Given the appearance of the lesion, this certainly could be a chalazion; however, certain skin cancers, such as a sebaceous cell carcinoma, can mimic a chalazion in presentation. Patients with this type of presentation should be asked about sun exposure; this gentleman worked outdoors approximately 12 hours a day. In his case, the lesion was removed, a biopsy was conducted, and the biopsy results were positive for sebaceous cell carcinoma.

Figure 6: A diagnosis of photokeratitis in a skiier.

Sebaceous cell carcinomas are relatively rare forms of skin cancer. However, optometrists can often be the ones to identify them because they usually originate in the meibomian glands. With time, they start to show alterations to skin tissue, typically madarosis.
This type of cancer can be highly malignant, significantly infiltrative and may metastasize. In fact, the mortality rate for sebaceous cell carcinomas reaches 30% in the United States.15 Surgical excision is the usual management; unfortunately, they are non-responsive to any further treatment.
* Basal Cell Carcinoma: A much more common type of cancer is basal cell carcinoma [Figure 5]; here, a different patient presents with madarosis. However, note that the lesion in this area is raised, with an umbilicated center and a glossy or pearly margin appearance. Also take note of the significantly large blood vessel, known as a feeder vessel, which is common in skin cancer presentations.

Figure 7: A young patient presenting with an advancing pterygium.

The most common complaints of patients with basal cell carcinoma are cosmetic changes and loss of lashes, as well as persistent scabbing or crusting, and bleeding. Optometry once again may be well positioned to make the diagnosis of basal cell carcinoma. This type of skin cancer is 10 times more common than any other form of skin cancer and is often found on the eyelid margins or even the caruncle region.16 Other common locations are the inner nose area as well as behind the ears.
* Malignant Melanoma: This is another form of skin cancer often observed by optometrists. Malignant melanomas can appear in the choroid, the iris or even the conjunctiva. Malignant means that the tumor has the potential to metastasize. Melanoma shows that it arises from the pigmented cells of the eye. Because the choroid has the highest blood flow of any structure in the body and is considered part of the uveal tract, which also includes the iris and sclera, these tumors can often be aggressive. In fact, malignant melanomas of the choroid are the most common intraocular malignancy present.17

Patients with a choroidal nevus are much more likely to develop a malignant melanoma. The difference between a benign choroidal nevus and a malignant melanoma is that nevi are typically smaller in size and flat (or non-elevated). A malignant melanoma, on the other hand, often has significant elevation, associated retinal detachment, and often presents in an overlying finding known as lipofuscin. It is also significantly larger and, depending on the location, may result in a change in refractive error or visual disturbance.
Malignant melanomas are life threatening because of their high predisposition to metastasis. They most commonly spread to the lungs, but also to the liver, GI tract and other areas of the skin. The diagnosis of malignant melanoma requires a prompt referral to a primary physician or an oncologist.
Malignant melanoma of the ocular surface also stems from the presence of melanin or pigment that is present on the conjunctiva. The presence of unilateral melanosis increases the malignancy potential. However, the incidence of melanonoma is only one in 400.18
Melanosis can range from congenital findings that may involve pigment flecks, usually near the limbus, or it can be significant, such as that of nevus of Ota. Melanosis typically does not change with time and tends to be relatively small. Large areas of pigment or melanin accumulation raise concern for a potential malignant melanoma.
Greater concern is warranted if it is found in the upper tarsal plate of the conjunctiva or the lower fornix.
Perhaps the most common area for malignant melanoma is on the skin tissue; many times this is found on other sun-exposed areas near the eye or even the forehead, and is brought up by patients. Follow the ABCDE rule to help determine if a lesion of the skin could be a malignant melanoma (See sidebar: Know Your ABCDEs).

UV RADIATION AND SPECTACLE LENSES

Most patients and clinicians think that photochromic lenses, polarized lenses, sunglasses and tinted lenses block 100% of ultraviolet A and B radiation. Although that is typically true with direct transmission, it does not account for exposure due to reflected light. In other words, light that reflects off the back surface of a lens—including sunglasses, polarized and any spectacle lens—can still allow significant ultraviolet light to enter the eyes.
Furthermore, anti-reflective coatings, which are often applied to many of these types of lenses, may actually increase ultraviolet light radiation exposure to the eyes and skin around the eye area.
Dermatological exposure to UV light is highest between the peak times of 10 a.m. to 2 p.m. But, surprisingly, the most significant ocular exposure to UV light does not occur during this time frame. It actually occurs when the light hits at an angle, thus reflecting off the back surface of the lens and entering into the eye. These times are typically between 8 to 10 a.m. and between 2 to 4 p.m.19
Furthermore, these are times when patients are not typically wearing sunglasses. Research shows that 40% of the annual exposure occurs during these non-peak times into the eye.19 To add insult to injury, 23% of people never wear eye protection and only 6% of Americans know they need sun protection for their eyes.20

To make matters worse, the human skull and orbital configuration is designed to allow a large temporal field of vision. So, this large field of vision also allows for significant light from side exposure. This is known as peripheral light focusing radiation or the Coroneo effect.21 Light reaches the peripheral cornea or limbus as much as 20 times greater than other locations.
Furthermore, the limbus is associated with the uvea and is one of the most sensitive areas of the eye.
These zones of blue, blue-violet and UV light have been shown to be damaging to the ocular surface. So, depending on the geometry of the lens, the frame and environmental conditions, an average of 20% of this light (although the range is 10% to 50%) comes from the back and sides of the lens.22
Certain environmental conditions can have extreme UV exposure from the sides and back surface of the spectacle lenses. For example, snow reflectance transmits 94% of UVA light and 88% of UVB light.23
Clear lenses reflect 4% to 6% of UV radiation, while no-glare or an-tireflective lenses actually increase this reflectance to 25% of UV light radiation on average.22 Some types of lenses reflect up to 90% of the most damaging short wavelength lights, including UV and blue light transmission.22 So, although UV light protection is found on the front coatings of many lenses, it does not account for back surface reflection.
New technologies, such as Crizal lenses, can now eliminate backside UV radiation reflection and particularly focus on the shorter wavelength light, including UVB and UVC. Specifically, Crizal Sapphire UV and Crizal UV Avancé, which came out earlier this year, provide full-spectrum blocking technology on both the front and back surfaces.
Dr. Karpecki serves as corneal services and ocular disease research director at Koffl er Vision Group in Lexington, Ky., and heads its ocular surface disease clinic. 

REFERENCES

  1. Pfeifer GP, You YH, Besaratinia A. Mutations induced by ultraviolet light. Mutat Res. 2005 Apr 1;571(1-2):19-31. Epub 2005 Jan 20.
  2. Taylor HR, West S, Muñoz B, et al. The long-term effects of visible light on the eye. Arch Ophthalmol. 1992 Jan;110(1):99-104.
  3. Holick MF. The vitamin D epidemic and its health consequences. J Nutr. 2005 Nov;135(11):2739S-48S.
  4. Rosen ES. Filtration of non-ionizing radiation by the ocular media. In: Cronly-Dillon J, Rosen ES, Marshall J, eds. Hazards of Light: Myths and Realities of Eye and Skin. Oxford: Pergamon Press; 1986:145-152.
  5. Sample PA, Esterson FD, Weinreb RN, Boynton RM. The aging lens: in vivo assessment of light absorption in 84 human eyes. Invest Ophthalmol Vis Sci. 1988 Aug;29(8):1306-11.
  6. Menegay M, Lee D, Tabbara KF, et al. Proteomic analysis of climatic keratopathy droplets. Invest Ophthalmol Vis Sci. 2008 Jul;49(7):2829-37.
  7. Panchapakesan J, Hourihan F, Mitchell P. Prevalence of pterygium and pinguecula: the Blue Mountains Eye Study.
    Aust N Z J Ophthalmol. 1998 May;26 Suppl 1:S2-5.
  8. Bova LM, Sweeney MH, Jamie JF, Truscott RJ. Major changes in human ocular UV protection with age. Invest Ophthalmol Vis Sci. 2001 Jan;42(1):200-5.
  9. Chalam KV, Khetpal V, Rusovici R, Balaiya S. A review: role of ultraviolet radiation in age-related macular degeneration. Eye Contact Lens. 2011 Jul;37(4):225-32. Review.
  10. Taylor HR, West S, Muñoz B, et al. The long-term effects of visible light on the eye. Arch Ophthalmol. 1992 Jan;110(1):99-104.
  11. Mainster MA, Turner PL. Retinal injuries from light: mechanisms, hazards and prevention. In: Ryan SJ, Hinton DR, Schachat AP, et al, eds. Retina. Vol 2. London: Elsevier; 2006:1857-70.
  12. Symons RC, Mainster MA, Goldberg MF. Solar maculopathy in a young child. Br J Ophthalmol. 2010 Sep;94(9):1258-9, 1269.
  13. Hope-Ross MW, Mahon GJ, Gardiner TA, Archer DB. Ultrastructural findings in solar retinopathy. Eye (Lond). 1993;7 (Pt 1):29-33.
  14. Skin Cancer Facts. The Skin Cancer Foundation website. Available at: www.skincancer.org/skin-cancer-information/skin-cancer-facts. Accessed August 13, 2012.
  15. Shields JA, Demirci H, Marr BP, et al. Sebaceous car cinoma of the eyelids: personal experience with 60 cases. Ophthalmology. 2004 Dec;111(12):2151-7.
  16. Christenson LJ, Borrowman TA, Vachon CM, et al. Incidence of basal cell and squamous cell carcinomas in a population younger than 40 years. JAMA. 2005 Augoculo(dermal) melanocytosis. Ophthalmology. 1998 Jan;105(1):195-8.6. Menegay M, Lee D, Tabbara KF, et al. Proteomic analysis of climatic keratopathy droplets. Invest Ophthalmol Vis Sci. 2008 Jul;49(7):2829-37.
  17. Volpe NJ, Albert DM. Metastatic and secondary orbital tumours. In: Albert DM, Jackobeic FA, eds. Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders; 2000:3217-8.
  18. Singh AD, De Potter P, Fijal BA, et al. Lifetime prevalence of uveal melanoma in white patients with oculo(dermal) melanocytosis. Ophthalmology. 1998 Jan;105(1):195-8.
  19. Sasaki H, Sakamoto Y, Schnider C, et al. UV-B exposure to the eye depending on solar altitude. Eye Contact Lens. 2011 Jul;37(4):191-5.
  20. Glavas IP, Patel S, Donsoff I, Stenson S. Sunglasses-and photochromic lens-wearing patterns in spectacle and/ or contact lens-wearing individuals. Eye Contact Lens. 2004 Apr;30(2):81-4.
  21. Coroneo MT, Müller-Stolzenburg NW, Ho A. Peripheral light focusing by the anterior eye and the ophthalmohelio-ses. Ophthalmic Surg. 1991 Dec;22(12):705-11.
  22. Citek K. Anti-reflective coatings reflect ultraviolet radiation. Optometry. 2008 Mar;79(3):143-8.
  23. Sliney DH. Physical factors in cataractogenesis: ambient ultraviolet radiation and temperature. Invest Ophthalmol Vis Sci. 1986 May;27(5):781-90.



















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