Keratoconus Eye Doctors Treatments Today

August 1, 2010 By admin 2 Comments

Keratoconus | Eye Doctors Contact Lenses And New Options For Treatment

Eye Doctors find rapid increases in nearsightedness and astigmatism are common with frequent changes in your eyeglass prescription. Scarring of the cornea can also occur in some cases resulting in significant vision loss.

Fort Collins Keratoconus Cases Probably Effect At Least 200-400 Individuals |Tell Your Eye Doctor If You Notice These Symptoms:

The appearance of long light streaks in your eyesight at night
Visual Glare and halos around lights, especially car headlights and taillights at night
Double Vision
Distorted Vision
Blurry Vision making it difficult to read
Ghost like images of white light surrounding objects you are viewing
Eye sensitivity to light

Eye Doctors Agree Keratoconus usually shows up most commonly between the teenage years of 16 up to age 30

Optometrist And Eye Research Institutes Know Surprisingly Little About Keratoconus But Knowledge Is Starting To Grow

It is hard for eye doctors to pin down the exact rate of this eye disease because it can be very mild and remain undiagnosed, especially when it burns out early (form fruste), or stops progressing after several years. Corneal Keratoconus creates irregular astigmatism, causing curvatures on the cornea tissue that are not nice smooth curves. Instead the eye curvature resembles the surface of a potato with dips and valleys on a very irregular shape. This type of shape makes it very difficult for your optometrist to provide a prescription for eyeglasses that results in clear vision. The lenses would have to be made in very strange shapes to result in clear vision. Even lenses that have been designed in this manner are rendered ineffective the moment your eyes look off the center of the lens. Irregular astigmatism also occurs without keratoconus, but it does not tend to progress and result in the characteristic steepening of the cornea resembling a cone shaped area. Usually keratoconus presents in one eye and over time well over half of the eye patients will have both eyes involved.

In the past, much speculation centered around eye rubbing and ocular allergies. Some eye physicians have speculated that Keratoconus is triggered by eye rubbing that starts an inflammatory cascade in the cornea. Frequent eye rubbing also could cause mechanical tissue breakdown in areas of the cornea that are already compromised. Research by eye doctors has shown between 6-8% of patients with keratoconus have a family history, indicating there can be strong genetic components in a small percentage of families. Over 90% of the time if you have Keratoconus it is unlikly to be passed on to your children. Several areas of chromosomes have been identified as potential genetic markers and are being investigated further.

Also, certain eye diseases such as retinitis pigmentosa, retinopathy of prematurely (damage to the retina tissue in the back of the eye from premature birth), Leber’s congenital amaurosis (a degenerative disease of the optic nerve), and vernal keratoconjunctivitis (a type of allergic eye disease) appear to occur more frequently in conjunction with Keratonus.

Some disease of the body also have a degree of co-occurrence with Kerataconus- Ehlers-Danlos syndrome, Down syndrome, osteogenesis imperfecta, pseuodoxanthoma elasticum), mitral valve prolapse in the heart, Laurence-Moon-Biedl syndrome, Rieger’s syndrome and neurofibromatosis. Several of these diseases interfere with normal collagen development and may precipitate kerataconus by disrupting collagen development in the cornea.

The changes to the cornea from Kerataconus are mostly unknown. The cornea consists of 5 layers and is about 1/2 mm thick (550 microns or about the width of 5 human hairs). The epithelium layer is the surface layers of cells. Underneath the eyes epithelium layers is a thin basement membrane sitting on the anterior limiting membrane, also know as bowman’s membrane. The bulk of the corneal thickness is in the stromal layer, where the collagen protein fibers run across the cornea, adding the tensile strength. Tensile strength is the degree a material can be stressed and still return to it’s original state and shape. Collagen is the memory material of the cornea. The structure of collagen changes in the center area of the cornea with shorter fibers, that cross more, run at different angles, run though each other, form connections to Bowmans membrane, and also form connections originating from Bowman’s membrane. It has been suggested from research by Jan P.G. Bergmanson, OD, PhD, PhD h.c, DSc, & Jessica H. Mathew, OD that this alteration in structure near the central cornea may help explain the nature of Keratoconus in the future, With shorter fibers running in differing directions with various connections the central cornea would seem to be more prone to breakdown of the normal collagen structure. Optometrists have found the bulging cone area characteristic of Keratoconus cones usually form close to the central cornea, slightly inferior, which seems to substantiate the altered central corneal tissues may play a part in the eye condition. Early changes may occur in the surface epithelial cells disrupting the basement membrane. When keratoconus begins, whatever the cause may be, protein damaging enzymes called proteases increase and start damaging the epithelial basement membrane. This is the membrane formed underneath the lowest level of epithelial cells. Subsequent breaks in the corneal anterior limiting membrane occur and the cornea starts to thin centrally, probably due to the susceptibility of the different surface anatomy of the collagen fibers under lying Bowman’s membrane. As these breaks occur the surface epithelial cells can contact the stromal level of the cornea where most of the structural framework of this eye tissue is located. Small proteins called cytokines are released and alter the fluids around the cells, leading to scarring of the cornea. Stromal fibers may move through the anterior limiting membrane. Whatever the cause, a disruption of the normal collagen structure causes the memory shape to lose its capacity and irregular shaped corneas to subsequently develop. There are indications of changes in the different enzymes that degrade proteins and induce changes in the collagen and the spaces surrounding the cells in the cornea. Cathepsins are one type of protein that increase as kerataconus starts to occur. These could lead to destruction of the so called extra cellular matrix, the substances surrounding the cells and lead to degenerative effects in the cornea.
They may also indirectly cause a reduction in the antioxidants and increase oxidative damage to the cornea, another theory that has been proposed. Matrix metalloproteinase-2 is also activated and changes the extra cellular matrix surrounding the corneal cells. Keratocytes are numerous cells in the cornea that produce the collagen for the fibers and the extracellular matrix components, turning mostly dormant by birth. In Kerataconus they have been observed to have increased apoptosis (increased programmed cellular death). There is a reduction in the number of collagen fiber and they also reduce in diameter. While there is little indication of dry eye causing Keratoconus, at our Dry Eye Institute of Northern Colorado, we do seem to see a possible correlation. Dry Eye Syndrome increases inflammatory compounds in the tear film that do cause cellular damage in the epithelium layers. It is possible this could start the cycle of damage that helps initiate damage to the eye that optometry eye exams have found over the years. While this has not been suggested yet, there is a reasonably high level of floppy eyelid syndrome associated with obstructive sleep apnea and Keratoconus. Eye researchers Cintia S De Paiva, Lindsey D Harris, and Stephen C Pflugfelder have demonstrated it is possible that eyes exposed at night by staying partially open can create Keratoconus like change in the cornea. Most likely, keratoconus will be found to be several different disease processes and also multifactoral. Multifactoral eye diseases have multiple factors that combine to create the eye condition. For instance, the different collagen structure in the central cornea makes the eye susceptible, changes in enzymes may alter the tissues and start causing minor breakdowns in the epithelial surface cells, enzyme changes may lead to increased oxidative stress further weakening the eye tissue, and constant rubbing of the eyes may push the eyes over the edge by inducing mechanical damage to the eye tissues that could only occur with a compromised cornea. A genetic alteration of the cornea could make the cornea of the eye more susceptible to the entire chain of events.

Your eye doctor will initially treat Kerataconus with contact lenses. Treatment of Kerataconus usually begins with a rigid gas permeable contact lens when vision can no longer be maintained clearly with spectacle lenses. Sometimes, a gas permeable lens will be fit over the top of a soft contact lens in a piggyback contact lens fitting, with a soft contact lens and a rigid gas permeable contact lens on top of it. While used years ago, piggyback contact lens fittings fell out of favor due to the complications from reduced oxygen flow with older soft contact lenses. With the new super oxygen permeable silicone hydrogel soft contact lenses, it is enjoying a small resurgence. It is primarily used to increase eye comfort for the keratoconic eye patient. There are also combination contact lenses available today, such as the SynergEyes contact lens that is a rigid contact lens with a soft skirt attached surrounding the lens. The primary issue with Kerataconic contact lens fittings is matching the steeply curved cone with the surrounding flatter eye tissue, while dealing with the irregularities of curvature that are present. While custom mapping technology is highly touted as the way to achieve the required fit, the truth is observation of contact lenses on a keratoconic eye by an optometrist and adjustments based on how dyes accumulate under the contact lenses is still the most accurate method to achieve an excellent final fit. Due to the drastic changes in curvature the contact lenses require multiple different curves as you move toward the edge of the lens. While many different lenses have been developed with special names as the ultimate Keratoconus contact lens, they are all variations on the basic concept of a steep contact lens center and a gradient of changing curvatures to the edge. Rigid contact lenses work because the light bending capacity of the tears is very close to the light bending capacity of the cornea. The tears fill in between the irregular eye surface and the smooth surface on the back of the lens. This essentially removes the irregular astigmatism and nearsightedness by utilizing the back contact lens surface as a new regular surface where light is altered, and often restores the corrected eyesight close to 20/20. Eye glasses may only achieve 20/40 vision or much worse because the irregular surface remains. Occasionally Scleral rigid gas permeable lenses are used. These are gas permeable lenses larger than normal that extend out onto the white part of the eye. All contact lenses today are gas permeable, or designed to let air pass through to keep the cornea healthy. Soft contact lenses are usually not referred to as gas permeable because of historical changes. Hard lenses were the first contact lenses and they were made of a material that passed no oxygen through the lens. When changes were made to the polymers used to make hard contact lenses that allowed them to breathe or pass needed air to the underlying cornea, they were renamed rigid gas permeable contact lenses. Rigid because they are still a hard material with only 1-2% water, and gas permeable because unlike the older hard contact lenses they now transmitted air to the eyes. Soon they became called by the acronym of RGP’s to save a few words (even prior to the texting era). With time they also came to be referred to as gas perms, in spite of the fact that all soft contact lenses are also gas permeable. Soft contact lenses are never rigid however, as they normally are composed of about 50% water. This softness comes at the price of increased flexibility and they drape across the eye, imitating the irregularities of a Keratoconic cornea and do not correct the vision back to optimum levels. Once your eye doctor has achieved an excellent fit and optimized your contact lens prescription, there may be frequent changes in your contact lens prescription as the Keratoconus goes through progressive changes.

Your Eye Doctor May Be Able to Avoid Corneal Transplants

While only 10-20% of eyes will undergo ongoing serious changes, they do present challenges to fitting contact lenses on eyes with Kerataconus. At some point, scarring of the cornea can start to occur and patients become intolerant to contact lenses. In years past, the only remaining option was a corneal transplant. While corneal transplants enjoy a relatively high success rate, there are still risks and problems. Recently there have been some new exciting options starting to evolve.

Permanent Contact Lenses-Intacs

Intacs are small rigid half rings similar to portions of a gas permeable contact lens that are implanted in the cornea. They were originally developed to reverse nearsightedness, but did not prove as effective as originally thought and were replaced by LASIK eye correction procedures. A few years ago they found a new use in stabilizing Kerataconus. They are not a cure for Kerataconus, but can restore some more regularity and allow some patients to continue contact lens wear while avoiding a corneal transplant. They also appear to have some effect in decreasing the rate of change in Kerataconus. While they are promoted as being completely removable and reversible if patients have problems, this is not entirely true. About 10-15% of Intacs cause some complications and issues that cannot be resolved if they are removed. Still, it is often a better option than jumping straight to a corneal transplant.

Kerataconus Corneal collagen cross-linking therapy

Corneal collagen cross-linking therapy (CXL) is intended to stabilize the tissue by forming more bonds between the existing collagen fibers and also increasing the size of the fibers, making the cornea much firmer and less likely to continue deforming. It involves pretreatment the cornea with riboflavin (Vitamin B2) for 30 minutes then using radiation from the ultraviolet A band light spectrum (normally around 370 nanometers) to increase the cross links over about a 30 minute period. While it has been more extensively in Europe, it is starting to enter the U.S. market. The riboflavin acts to keep the UVA from completely passing through the cornea so the UV can act to create more cross links. Riboflavin also may have a photo reactive effect that further increases cross linking of the collagen bands. Questions still surround this treatment. It is not an FDA approved treatment in the United States but is undergoing clinical trials, and currently is used off label as a treatment for Keratoconus. The FDA (Food and Drug Administration) regulates drugs and medical devices but not eye doctors. Any procedure that uses drugs or medical devices can be performed by an eye doctor if you are properly informed, share in the decision, and it has an acceptable possibility of helping. The riboflavin still allows a significant amount of UVA to pass through the cornea. This could potentially increase future risks for cataract development. UVA with riboflavin is cytotoxic (damaging to cells) and can damage the endothelial cells that line the back of the cornea and are vital for its long term health. Corneal thickness needs to be factored in to keep this type of damage far enough away from the endothelium cells of the cornea. A minimum corneal thickness of 400 microns has been suggested but a better choice would be 450 to 500 microns. Cellular damage to the keratocytes, changes to the matrix of the cornea, and changes to the epithelium do occur in the cornea after the procedure. Normally they regenerate over the next 6 months. Riboflavin has poor penetration into the cornea so the surface layers of epithelium cells need to be removed. It is unknown if the effect of increased rigidity created by this treatment will last indefinitely, or if there are any other long term problems from increasing the cross linking and rigidity of the cornea. Some cases of persistent haze, infections, and increased eye pressure reading have been noted. The increased eye pressures may be partially due to an artifact since we know thicker (more firm) corneas read artificially high with most current glaucoma instruments. With careful consideration about the stage of Keratoconus and treatment of the eye at the appropriate stage, cross linking of collagen fibers in the cornea appears to be a great addition to eye doctors armetarium in treating keratoconus. While it may improve the condition mildly in many patients, it should always be considered as a stabilizing treatment and not a curative treatment.

New treatments for Keratoconus and other eye diseases are improving at a rapid rate. If you are a family members have concerns about Keratoconus, feel free to contact Dr David Kisling in Fort Collins, Colorado at (970) 225-0959.

Filed Under: Contact Lenses, Corneal Transplants, double vision, Eye Surgery, Eye Symptoms, Keratitis, Uncategorized Tagged With: astigmatism, collagen cross linking eyes, collagen cross linking for keratoconus, Colorado, contact lens fittings, contact lens prescription, Contact Lenses, corneal tissue, Corneal Transplants, distorted vision, doctor, double vision, Dr David Kisling, Dr David Kisling Keratoconus Treatment, Dr. Kisling, dry eye, eye, eye doctors, eye research, Fort Collins, Fort Collins Keratoconus, Ft Collins Optometrist Keratoconus, halos around lights, irregular astigmatism, irregular astigmatism fort collins, irregular shape, Kerataconic, kerataconus, Keratocytes, light, light streaks, Northern Colorado, Optometrist, optometry, piggyback, rapidly changing astigmatism, synergeyes, treatment

Eye Doctors Study Projects Vision Loss Problems By 2020

July 21, 2010 By admin Leave a Comment

Fort Collins Eye Doctors-Dr Kisling | Your Eye Health Is Our Number One Concern

Eye Doctors Report Macular Degeneration And Other Eye Disease Are Rapidly Increasing

Macular Degneration | National Eye Institute

According to the National Eye Insitute, a study that was conducted by the Eye Disease Prevalence Research Group found the graying of America is asssociated with vision loss becoming a major public health issue in the next 10 years. The number of people over the age of 40 who suffer vision loss or blindness is expected to be as follows:

Macular Degeneration: Currently 1.8 million people, by 2020 2.9 million (62% Increase)
Glaucoma: Currently: 2.2 million people, by 2020 3.3 million (66% Increase)
Vision Loss From Diabetes: Currently 4.1 million people, by 2020 7.2 million (56% Increase)

In Fort Collins Optometry Finds The Same Problems Seen Nationally- But At A Lower Rate Due To Our Younger Eye Demographics

Eye Doctors Reported Some Further Vision Loss Statistics:

Nationally, people 80 or more years old comprise 8% of the total population but have such a higher incidence of serious eye disease that their age bracket contains almost 70% of the cases of blindness
Over 10% of eyesight cases have significant vision loss from macular degeneration
Eye researchers found the prevalence of glaucoma is about three times higher in African Americans, and is also the leading cause of blindness in Hispanics
About 8% of people with diabetes over the age of 40 have some eye condition that puts them at substancial risk for sight loss.

Fort Collins Eye Doctors Find A Higher Risk For Vision Loss And Macular Degeneration Due To Our Increased UV Exposure From The Mountain Altitudes In Northern Colorado

Practicing Optometry n Fort Collins I see an increase in the number of patients with macular degeneration every year. There is less filtering of ultraviolet radiation when people with active lifestyles spend time in the mountains of Northern Colorado. Optomerist reccomendations include quality sunwear, hats with brows, and spending more time outdoors before 11:00 AM and after 3:00 PM to avoid the intense UV of the midday.

Schedule Your Optometrist Visit Today-Annual Eye Exams Become More Important With Age

This research highlights the fact that many cases of sight loss can be prevented by early detecion and treatment. Nutritional supplements and new injectable drugs can often slow the progerssion of vision loss from macular degeneration. Glaucoma is more treatable than ever before, with stepped choices of multiple medication, laser surgery, and filtering surgery to drain fluid slowly from the eyes. A large number of cases of diabetes eye problems can be prevented by early lifestyle interventions, and well regulated blood sugar can delay the onset of eye problems. After 40, annual eye exams should become routine, and by age 65 seeing your eye doctor annually is essential to insure you have healthy eyes and good vision for a lifetime.

Fort Collins Eye Doctors-Dr Kisling | Your Eye Health Is Our Number One Concern

Filed Under: Eye Diseases, glaucoma, Macular Degeneration Tagged With: age and blindness, aging eyes, blindness, diabetes vision loss, Eye Doctor, eye health, Eye Symptoms, eyesight, Fort Collins, Fort Collins Eye Doctor, Fort Collins Eye Doctors, Fort Collins Optometrist, Ft Collins, ft Collins eye exams, glaucoma, increase in blindness, Macular Degeneration, NOCO optometrist, Northern Colorado, Optometrist, vision loss

Treating Eye Problems from Adult Diabetes | The Accord Study

June 29, 2010 By admin Leave a Comment

Treatments For Eye Problems In Type 2 Adult Diabetes Shown To Be Effective In New Study

Three therapies were compared for people with type 2 diabetes in a recent study. The study, known as the Action to Control Cardiovascular Risk in Diabetes or (ACCORD) Eye Study published results today. Very intensive blood sugar control reduced the progression of diabetic retinopathy compared with standard blood sugar control, and the combination of two drugs used to treat high cholesterol and lipid imbalances both lowered eye complications from small blood vessels in the eye by about 30%. The drugs used were a fibrate and statin, (fenofibrate and simvastatin). Intensive blood sugar control is shifting towards normalizing blood sugar to the levels in the general healthy population.

Controlling Blood Pressure Did Not Correlate With Decreased Cardiovascular Disease

Surprisingly, blood pressure control had no correlation with slowing diabetic eye complication.

There Was No Decrease in Deaths Due to Cardiovascular Disease

Actually the overall risk of death increased with tight control, possibly because the near normal blood sugar levels had less cushioning room to fall and makes severe hypoglycemia a much higher risk. Patients in the intensive blood sugar group had a 22 percent higher risk of death (5.0 percent versus 4.0 percent) and a three times higher risk of seriously low blood sugar (10.5 percent versus 3.5 percent) compared with participants in the standard blood sugar control group. People with diabetes should have an annual dilated exam of the inside and back of their eyes to make sure no changes. If there are any changes or complications, they should be addressed immediately.

Filed Under: Eye Diseases Tagged With: adult diabetes, blood pressure control, blood sugar control, blood sugar levels, blood vessels in the eye, cardiovascular risk, diabetic retinopathy, eye complication, eye complications, Eye Doctor, fenofibrate, fibrate, Fort Collins Eye Doctors, ft collins optometrist, high cholesterol, normal blood sugar, Optometrist, risk patients, type 2 diabetes

Eye Growth & Bumps Often Pinguecula

June 26, 2010 By admin Leave a Comment

Optometrists Find High Incidence of Eye Growths and Bumps on White of Eyes in Northern Colorado are Benign & Often Pinguecula

A large number of people in the Fort Collins show up at the optometrists office with benign growths on the white part of their eye referred to as pingueculas. Actually they develop on the conjunctiva, the clear tissue that covers the white part of the eye (the sclera). Often they appear as mildly elevated yellowish bumps, visible to the patient or a family member with a urgent rush to the eye doctor. Often people are reluctant to discuss their concerns hoping it will be found during an eye exam. You should not hesitate to mention this at the beginning of you visit to the optometrists office. Because they are so common, you eye doctor may not mention the presence of a pinguecula on your eye unless you ask. While most optometrists find pingueculas developing in patients eyes who are over the age of 40, it is becoming more common to see them by the mid twenties. They are presumed to be caused by a UV radiation from the sun and low level irritants like dust and small particles in the wind. The incidence increases closer to the equator. Fort Collins East of I-25 they are extremely common due to the farming industry with people spending larger amounts of time outdoors and in dusty environments. People who spend their leisure time on motorcycles are also more at risk due to the ultraviolet exposure and particles from the blowing wind.

What Causes Eye Growths of Pingucula

Just as skin loses is capacity to stretch with age, so does the conjunctival tissue when it is exposed to sunlight and irritation over a cumulative period of years. In Northern Colorado people frequently visit doctors for skin changes that are essentially occurring from the the same as the eye conjuntival changes.

Eye Doctors have found the elastosis, or the capacity of the tissue to smoothly stretch and return to normal is compromised from changes to the conjunctival tissue. Collagen forms the framework, but elastin protein fibers around the collagen fibers provide the stretching capacity. The UV radiation in Fort Collins is higher due to the altitude, reflections from snow, and the amount of time we spend outdoors. With close to 300 days a year of sunshine the UV exposure is higher than most areas at a similar latitude. Altitude increases the UV dosage by 4-5% /1000 feet of elevation gain. Compared to sea level this adds approximately 25% above sea level exposures.

First there is an accumulation of abnormal cells that are altered elastin and / or collagen. Eventually the area starts to lose cells and becomes more of a deposit of protein materials often referred to as hyaline deposits. Calcification can occur over time also. Several theories have been proposed by eye research clinics for the changes seen in the tissues that form the pinguecula. This UV radiation and low level chronic irritation causes changes that may be:

An increase in the production of elastin fibers by the fibroblast cells and changes to the elastin nature into a more twisted form as they replace some of the collagen fibers. This may induce degenerative changes to the collagen fibers.
A interference with the natural cycle of cell programmed cell death of elastin resulting in an overproduction that takes on the abnormalities.
A degradation of the collagen fibers into a compromised form resembling elastin.
A combination of the above

Other factors may make the conjunctival tissue more susceptible to forming pinguecula.

Since the conjunctiva tissue does not have the tough keratin layer like the skin it is damaged faster by UV radiation.
The clear conjunctiva tissue is also transparent and the solar radiation that is not absorbed passes through to the sclera. We know from science that color of the surface being irradiated has a large bearing on the amount of back reflected radiation including UV.[1] It is a very thin tissue, and the white scleral tissue underneath it with it’s white coloration should have an albedo in the range of 80-90% similar to the reflectance of snow. Measured animal studies of conjunctival tissue reflectivity across the 440 to 1000+nm range shows a steady reflectance of above 40%. Somewhere between 40 to 80 percent of the UV radiation is being added to the initial dose as it passes through. This extra back reflection of UV into the conjunctiva tissue also increases the exposure and ages the tissue faster than skin.
Eye conditions that increase the size of the fissure, or how wide your eye stays open, also will increase the incidence of pinguecula. Thyroid eye disease and eyes that are not as deeply recessed (the beady eyed individual with a protruding eyebrow to shadow the eye) or more likely to develop pinguecula. Studies have shown an increase in pinguecula in patients with Thyroid Orbitopathy (hyperthyroid or an overactive thyroid gland that effects the eye) that is only significant with the widened eye fissure or amount of the eye normally exposed when open). Increased dry eyes was not correlated further suggesting UV exposure as a causative factor. [5]
The nose acts to reflect more light onto the eye somewhat like a dull mirror, and pinguecula are more commonly found on the white side closest to the eyes, but they are also found on the temporal side.
The deeper, or basal layers of the superior nasal conjunctival tissue contain more dendritic cells. Dendritic cells are a type of antigen-presenting cell (APC). Antigens are molecules or molecular fragments that bind to a site on on the surface of cells, and except for autoimmune diseases they are the molecules from outside the body. Dendritic cells present them to the T helper cells that increase the immune response and that cause an increase in inflammatory cells. The tears flow towards the nose by slight eyelid horizontal movements that accompany each blink. This ensures a continuous flushing of debris and antigens from the tear film, Since the tears flow in this direction logically their would be more dendritic cells to help remove the excess antigens. Due to the density of the dendritic cells and the propensity to create more inflammation, it has been postulated this may increase the overall likelihood of pinguecula forming in the nasal region.
Psoralen plus ultraviolet A (PUVA) treatment has been used widely in the past for various dermatoligic conditions. It has seen a reduction in use due to other methods. PUVA uses a photosensitizing agent (8-methoxypsoralen, Oxsoralen®) taken orally or applied to the effected area before exposure to ultraviolet A light (320-400 nm). At least one case of pinguecula associated with PUVA has been reported. (the patient was in poor in compliance with eye protection)

Pinguecula Are Always Benign Growths

Once a Pingueclua has been properly diagnosed by your optometrist you can rest assured. Pinguecula are always benign growths and never develop into any form of eye cancer. They can start to grow across the clear cornea tissue on the front of the eye at which point they are referred to as pterygium. Pterygium need to be followed as they need to be removed by an eye surgeon if they approach to close to the line of sight. While the surgical removal is fairly simple, they tend to recur and leave a scar. That leaves a wait and follow choice by your eye doctor. Because they are so slow to develop it is fairly easy to manage. New technology is reducing the recurrence, but remember, the majority of pingueculas don’t develop into pterygiums. In our Fort Collins Eye Clinic we occasionally see patients with symptoms related to pinguecula.

Pinguecula Symptoms and Signs

The elevation may disrupt the normal tear resurfacing on the eye and create an area of dryness and discomfort. It can also result in the edges of soft contact lenses settling poorly on the eye and leaving a gap between the soft contact lens and the conjunctiva. This often results in the lens drying out and the peripheral contact lens edge curling away from the conjunctiva. Contact lens patients will blink and subsequently the eyelid movement can eject the contact lens. Rigid gas permeable lenses may leave a gap over the conjunctiva and edges of the cornea that dies out and damages the peripheral cornea epithelium surface cells and the conjunctival cells. The edge of the gas permeable lens may also irritate the pinguecula and result in a chronic red eye when contact lenses are worn. This can often be resolved by changing the diameter or size of the gas permeable contact lens. A test used in research facilities called “tear ferning” evaluates the mucous layer of tears by allowing a sample to dry on a slide and crystallize. This is often abnormal around pinguecula indicating a mucous irregularity inducing dry eyes. Occasionally pinguecula become inflamed and need prescription eyedrops to restore comfort. The incidence of problems is low and treatable so eye doctors almost never remove a pinguecula.

Optometrists Prevetative Steps For Pinguecula

UV prescription eyeglasses (or non prescription quality sunwear) is the most important preventive step you can take. Not only will it help prevent pinguecula, but also a number of other eye diseases associated with sunlight exposure. Do a favor for your children and teenagers eye health, start them in prescription sunglasses (transition lenses that lighten and darken also offer UV protection). When you think of sunscreen think of sunscreen for the eyes. The more time you spend in the sun, the more you should think of sunwear that wraps around your face and protects the sides. Up to 40% of the UV exposure can still enter from the unprotected side of a normal pair of eye glasses. Special motorcycle eyeglass frames have become very popular in our Ft Collins Eye Care Center due to the side protection from UV and wind & dust. Wearing a hat with a brow helps reduce UV exposure. Limiting midday sun exposure is very useful when possible. The morning and afternoon sun is lower on the horizon and has a much longer path to travel through the atmosphere which filters out more UV. Don’t avoid the sun totally. While there is much controversy at this point, it does appear that some sun exposure is good for your health, reducing some forms of cancer and possibly decreasing the incidence of multiple sclerosis. While vitamin D may be the protective factor some studies indicate their may be other factors and biochemical involved. Keep your eyes posted for more eye updates as we learn more about the fascinating world of vision!

References

[1] http://geography.about.com/od/physicalgeography/a/solarradiation.htm

[2} http://www3.interscience.wiley.com/journal/112130369/abstract?CRETRY=1&SRETRY=0

[3] Hoang-Xuan,Thanh; Baudouin, Christophe Inflammatory Diseases of the Conjunctiva, Catherine Creuzot-Garcher

[4] Journal of the American Academy of Dermatology
Volume 57, Issue 1, Pages 177-178 (July 2007)
Pinguecula following psoralen and ultraviolet A therapy
Amit Garg, Michael Loosemore, BAb

[5] Cornea:
June 2010 – Volume 29 – Issue 6 – pp 659-663
doi: 10.1097/ICO.0b013e3181c296ab
Clinical Science
Prevalence of Pinguecula and Pterygium in Patients With Thyroid Orbitopathy
Ozer, Pnar Altiaylik MD; Altiparmak, Ugur E MD; Yalniz, Zuleyha MD; Kasim, Remzi MD; Duman, Sunay MD

Filed Under: Contact Lens Problems, Dry Eyes, Eye Diseases Tagged With: altitude, Benign, benign growths, bump on eye, Bumps, collagen fibers, conjunctiva, conjunctival, Contact Lens Problems, contact lenses bump on eye, contact lenses falling out, contact lenses growth on eye, Dry Eyes, dryness, dusty environments, elastin protein, eye changes, Eye Doctor, eye doctor fort collins, eye doctors, eye exam, eye growths, eyebrow, Fort Collins, growth on eye, Growths, hard contact lenses contact lens irritation, hyaline, irritation, Northern Colorado, Optometrist, optometrist fort collins, Optometrists, Pingucula, Pingueclua, pinguecula, prescription, red eye, red eye on white of eye contact lenses, red eye when wear contact lenses, rigid gas permeable contact lenses, sclera, sight, skin changes, soft contact lenses, soft contact lenses keep falling out of eye, Thyroid, Ultraviolet

Macular Degeneration Genetic Causes Found

June 15, 2010 By admin Leave a Comment

Northern Colorado Fort Collins Region Sees Rise In Macular Degeneration

March 10, 2005

Recent studies by four groups of investigators have uncovered a gene that seems to have a strong association with macular degeneration. Age related macular degeneration is very important in Northern Colorado due to the aging of the population and the high amount of outdoors activities we play at. Unfortunately, these activities increase our exposure to UV radiation from the sun which is a contributing factor in macular degeneration. Better understanding the genetic contributions to age related macualar degeneration by optometrists in Fort Collins and similar environments may lead to preventative treatments in the future. Investigators have identified a gene that is “strongly associated” with a person’s risk for developing age-related macular degeneration (AMD). The finding was made by four independent teams, which include researchers with the National Eye Institute (NEI) and the National Cancer Institute, components of the National Institutes of Health (NIH), and other leading research centers. Detecting an AMD-associated gene may lead to early detection and new strategies for prevention and treatment for the debilitating eye disease. Papers from three independent teams appear in the April 15 issue of the journal Science, with a fourth paper published in the May 3 issue of the Proceedings of the National Academy of Sciences (PNAS).

AMD is a disease well known by Doctors of Optometry, and it blurs or destroys sharp, central vision and is the leading cause of blindness in people over age 60. There is no known cure for AMD but routine eye exams by your eye doctor may help intervention for early treatment. Most scientists think the cause lies in a complex interplay of hereditary and environmental factors. Family history of AMD is a risk factor for the disease. In recent years, researchers have been applying several genome-derived experimental approaches to find AMD-associated genes. The new studies provide the strongest evidence yet of a role for common genetic variants in the development of AMD.

“The four studies are a significant step in AMD research. They confirm a strong genetic component of AMD, which may allow scientists to develop tests for the disease before symptoms begin to appear and when therapies might help slow its progress,” said Paul A. Sieving, M.D., Ph.D., director of the National Eye Institute.

Our Fort Collins Optometry Office Provides You WIth The Following Actions You Can Take Now To Lesson Your Risk From Macualr Degeneration:

Consider fully protective UV sunglasses as a necessity for being outdoors-lenses should also protect into the blue visible light range which means avoid blue lenses.
Sunglasses from the gas station may allow the eye pupils to dilate without providing UV protection-rely on optical quality sunwear
In ou Ft Collins Eye Doctors Office we often recommend transitions lenses that lighten inside and darken outside. They have inherent UV protection. Since transition lenses don’t fully activate behind a car window shield, adding a magnetic clip on provides great relief and safe vision for driving home or to work facing the sun. The morning sun reflecting off snow or bodies of water in Northern Colorado can be blinding and dangerous without this added protection. On a good note, the transitions lenses don’t fully activate behind a car window shield because a significant of UV radiation is stopped by a regular automobile window, it’s the glare and eyestrain that overwhelms your capacity to see at dawn and dusk.
Sunglasses that wrap around the side of the face can lower the UV exposure by another 30-40%
Hats worn outside will make a marked reduction in the amount of UV and blue visible light that can reach the eyes
Talk to your optometrist about nutritional supplements for macular degeneration. Science supports using certain supplements at certain points in the disease stage to slow down changes and loss of vision. As someone who spends lots of time outdoors, and as an optometrist in Fort Collins, I frequently use supplements in a different manner to try and prevent or delay the onset of macular degeneration. The jury is out on the effects, but it was not too long ago that the same could be said of the accepted uses and type of supplements being prescribed by eye doctors today that have been found to be effective.
If you are fair skinned and have blue eyes, double your precautions. Blue eyes have very little pigment and allow much more UV to pas through to potentially damage the retina.
Stop Smoking. Probably the best preventive measure you can take.
Eat a healthy diet and exercise well. A healthy cardiovascular system is essential in preventing macular degeneration.

When Eye Doctors fully understand the genetics dehind macualar degeneration, interventions combined with healthy lifestlye choices may make ARMD Blindness a thing of the past!

Make Sure Your Eyes See as Well as They Can and Stay Healthy! Contact Fort Collins Eye Doctors-Dr Kisling For A Complete Eye Health Wellness Exam!

Call Dr Kisling at:(970) 226-0959

Filed Under: Eye Diseases, Macular Degeneration Tagged With: age related macular degeneration, age related macular degeneration optometrist ft collins, aging, AMD-associated, degeneration, eye, eye doctor macular degeneration ft collins, eye supplements macular degeneration prevention, Eyestrain, Fort Collins, fort collins eye doctors.eye doctors, Fort Collins Optometrist, ft collins optometrist macular degeneration, gene, genetic contributions, glare, Hats, intervention, light, Macualr, macular, Macular Degeneration, national eye institute, national institutes of health nih, northern coloado, Northern Colorado, northern colorado macular degeneration, Optometrist, optometry, preventative treatments, protection, Research, routine eye exams, science, snow, sun, sunglasses, sunglasses protection macular degeneration, sunwear, transition, transitions sus lenses macular degeneration, treatment, Vision

Kerataconus New Treatments

May 16, 2010 By admin Leave a Comment

Keratoconus | Eye Doctors Contact Lenses and New Options for Treatment

Keratoconus Courtesy of Indiana University Department of Ophthalmology

Keratoconus is an eye disease that causes vision to gradually worsen over time, as the transparent corneal tissue that covers the front of the eye thins and bulges forward, forming the cone shape that keratoconus is named for. Rapid increases in nearsightedness and astigmatism are common with frequent changes in your eyeglass prescription. Scarring of the cornea can also occur resulting in significant vision loss.

Keratoconus Symptoms Your Optometrist may discuss

The appearance of long linear light streaks in your eyesight at night

Visual Glare and halos around lights, especially car headlights and taillights at night

Double Vision

Distorted Vision

Blurry Vision making it difficult to read

Ghost like eye images of white light surrounding objects you are viewing, sometimes noticed as multiple dots when viewing on small light image-can be seen with one eye

Eye Sensitivity to light

Eye Doctors Agree Keratoconus usually show up most commonly between the teenage years of 16 up to age 30

When this corneal eye disease manifests at earlier ages optometrists often find a more aggressive form with ongoing, frequent changes in your eyeglass or contact lens prescription. The best guess is the occurrence rate is about 1 in 2000 people. It is hard for eye doctors to pin down the exact rate of this eye disease because it can be very mild and remain undiagnosed, especially when it burns out early (form fruste), or stops progressing after several years. Corneal Keratoconus creates irregular astigmatism, causing curvatures on the cornea tissue that are not nice smooth curves. Instead the eye curvature resembles the surface of a potato with dips and valleys on a very irregular shape. This type of shape makes it very difficult for your optometrist to prescribe an eye prescription for eyeglasses that results in clear vision. The lenses would have to be made in very strange shapes to result in clear vision. Even lenses that have been designed in this manner are rendered ineffective the moment your eyes look off the center of the lens. Irregular astigmatism also occurs without kerataconus, but it does not tend to progress and result in the characteristic steepening of the cornea resembling a cone shaped area. Usually kerataconus presents in one eye and over time well over half of the eye patients will have both eyes involved.

The cause of Kerataconus and the changes in the cornea are surprisingly not well known by the optometric research clinics at this time. In the past, much speculation centered around eye rubbing and ocular allergies. Some eye physicians have speculated that Keratoconus is triggered by eye rubbing that starts an inflammatory cascade in the cornea. Frequent eye rubbing also could cause mechanical tissue breakdown in areas of the cornea that are already compromised. Research by eye doctors has shown between 6-8% of patients with kerataconus have a family history, indicating there is a genetic component in some cases. Several areas of chromosomes have been identified as potential genetic markers and are being investigated further. Also, certain eye diseases such as retinitis pigmentosa, retinopathy of prematurely (damage to the retina tissue in the back of the eye from premature birth), Leber’s congenital amaurosis (a degenerative disease of the optic nerve), and vernal keratoconjunctivitis (a type of allergic eye disease which creates itchy eyes and frequent) appear to have some correlation. Some disease of the body also have a degree of co-occurrence with Keratoconus- Ehlers-Danlos syndrome, Down syndrome, osteogenesis imperfecta, pseuodoxanthoma elasticum), mitral valve prolapse in the heart, Laurence-Moon-Biedl syndrome, Rieger’s syndrome and neurofibromatosis. Several of these diseases interfere with normal collagen development and may precipitate kerataconus by disrupting collagen development in the cornea.

The changes to the cornea from Keratoconus are mostly unknown. The cornea consists of 5 layers and is about 1/2 mm thick (550 microns or about the width of 5 human hairs). The epithelium layer is the surface layers of cells. Underneath the eyes epithelium layers is a thin basement membrane sitting on the anterior limiting membrane, also know as bowman’s membrane. The bulk of the corneal thickness is in the stromal layer, where the collagen protein fibers run across the cornea, adding the tensile strength. Tensile strength is the degree a material can be stressed and still return to it’s original state and shape. Collagen is the memory material of the cornea. The structure of collagen changes in the center area of the cornea with shorter fibers, that cross more, run at different angles, run though each other, form connections to Bowmans membrane, and also form connections originating from Bowman’s membrane. It has been suggested from research by Jan P.G. Bergmanson, OD, PhD, PhD h.c, DSc, & Jessica H. Mathew, OD that this alteration in structure near the central cornea may help explain the nature of Keratoconus in the future, With shorter fibers running in differing directions with various connections the central cornea would seem to be more prone to breakdown of the normal collagen structure. Optometrists have found the bulging cone area characteristic of Keratoconus cones usually form close to the central cornea, slightly inferior, which seems to substantiate the altered central corneal tissues may play a part in the eye condition. Early changes may occur in the surface epithelial cells disrupting the basement membrane. When keratoconus begins, whatever the cause may be, enzymes increase and start damaging the epithelial basement membrane. This is the membrane formed underneath the lowest level of epithelial cells. Subsequent breaks in the corneal anterior limiting membrane occur and the cornea starts to thin centrally, probably due to the susceptibility of the different surface anatomy of the collagen fibers under lying Bowman’s membrane. As these breaks occur the surface epithelial cells can contact the stromal level of the cornea where most of the structural framework of this eye tissue is located. Small proteins called cytokines are released and alter the fluids around the cells, leading to scarring of the cornea. Stromal fibers may move through the anterior limiting membrane. Whatever the cause, a disruption of the normal collagen structure causes the memory shape to lose its capacity and irregular shaped corneas to subsequently develop. There are indications of changes in the different enzymes that degrade proteins and induce changes in the collagen and the spaces surrounding the cells in the cornea. Cathepsins are one type of protein that increase as kerataconus starts to occur. These could lead to destruction of the so called extra cellular matrix, the substances surrounding the cells and lead to degenerative effects in the cornea.
They may also indirectly cause a reduction in the antioxidants and increase oxidative damage to the cornea, another theory that has been proposed. Matrix metalloproteinase-2 is also activated and changes the extra cellular matrix surrounding the corneal cells. Keratocytes are numerous cells in the cornea that produce the collagen for the fibers and the extracllular matrix components, turning mostly dormant by birth. In Keratoconus they have been observed to have increased apoptosis (increased programmed cellular death). There us a reduction in the number of collagen fiber and they also reduce in diameter. Most likely, keratoconus will be found to be several different disease processes and also multifactoral. Multifactoral eye diseases have multiple factors that combine to create the eye condition. For instance, the different collagen structure in the central cornea makes the eye susceptible, changes in enzymes may alter the tissues and start causing minor breakdowns in the epithelial surface cells, enzyme changes may lead to increased oxidative stress further weakening the eye tissue, and constant rubbing of the eyes may push the eyes over the edge by inducing mechanical damage to the eye tissues that could only occur with a compromised cornea. A genetic alteration of the cornea could make the cornea of the eye more susceptible to the entire chain of events.

Your eye doctor will initially treat Keratoconus with contact lenses

Treatment of Keratoconus usually begins with a rigid gas permeable contact lens when vision can no longer be maintained clearly with spectacle lenses. Sometimes, a gas permeable lens will be fit over the top of a soft contact lens in a piggyback contact lens fitting, with a soft contact lens and a rigid gas permeable contact lens on top of it. While used years ago, piggyback contact lens fittings fell out of favor due to the complications from reduced oxygen flow with older soft contact lenses. With the new super oxygen permeable silicone hydrogel soft contact lenses, it is enjoying a small resurgence. It is primarily used to increase eye comfort for the keratoconic eye patient. There are also combination contact lenses available today, such as the SynergEyes contact lens that is a rigid contact lens with a soft skirt attached surrounding the lens. The primary issue with Keratoconic contact lens fittings is matching the steeply curved cone with the surrounding flatter eye tissue, while dealing with the irregularities of curvature that are present. While custom mapping technology is highly touted as the way to achieve the required fit, the truth is observation of contact lenses on a keratoconic eye by an optometrist and adjustments based on how dyes accumulate under the contact lenses is still the most accurate method to achieve an excellent final fit. Due to the drastic changes in curvature the contact lenses require multiple different curves as you move toward the edge of the lens. While many different lenses have been developed with special names as the ultimate Keratoconus contact lens, they are all variations on the basic concept of a steep contact lens center and a gradient of changing curvatures to the edge. Rigid contact lenses work because the light bending capacity of the tears is very close to the light bending capacity of the cornea. The tears fill in between the irregular eye surface and the smooth surface on the back of the lens. This essentially removes the irregular astigmatism and nearsightedness by utilizing the back contact lens surface as a new regular surface where light is altered, and often restores the corrected eyesight close to 20/20. Eye glasses may only achieve 20/40 vision or much worse because the irregular surface remains. Occasionally Scleral rigid gas permeable lenses are used. These are gas permeable lenses larger than normal that extend out onto the white part of the eye. All contact lenses today are gas permeable, or designed to let air pass through to keep the cornea healthy. Soft contact lenses are usually not referred to as gas permeable because of historical changes. Hard lenses were the first contact lenses and they were made of a material that passed no oxygen through the lens. When changes were made to the polymers used to make hard contact lenses that allowed them to breathe or pass needed air to the underlying cornea, they were renamed rigid gas permeable contact lenses. Rigid because they are still a hard material with only 1-2% water, and gas permeable because unlike the older hard contact lenses they now transmitted air to the eyes. Soon they became called by the acronym of RGP’s to save a few words (even prior to the texting era). With time they also came to be referred to as gas perms, in spite of the fact that all soft contact lenses are also gas permeable. Soft contact lenses are never rigid however, as they normally are composed of about 50% water. This softness comes at the price of increased flexibility and they drape across the eye, imitating the irregularities of a Keratoconic cornea and do not correct the vision back to optimum levels. Once your eye doctor has achieved an excellent fit and optimized your contact lens prescription, there may be frequent changes in your contact lens prescription as the Keratoconus goes through progressive changes.

Your Eye Doctor May Be Able to Avoid Corneal Transplants

While only 10-20% of eyes will undergo ongoing serious changes, they do present challenges to fitting contact lenses on eyes with Keratoconus. At some point, scarring of the cornea can start to occur and patients become intolerant to contact lenses. In years past, the only remaining option was a corneal transplant. While corneal transplants enjoy a relatively high success rate, there are still risks and problems. Recently there have been some new exciting options starting to evolve.

Permanent Contact Lenses-Intacs

Intacs are small rigid half rings similar to portions of a gas permeable contact lens that are implanted in the cornea. They were originally developed to reverse nearsightedness, but did not prove as effective as originally thought and were replaced by LASIK eye correction procedures. A few years ago they found a new use in stabilizing Kerataconus. They are not a cure for Keratoconus, but can restore some more regularity and allow some patients to continue contact lens wear while avoiding a corneal transplant. They also appear to have some effect in decreasing the rate of change in Keratoconus. While they are promoted as being completely removable and reversible if patients have problems, this is not entirely true. About 10-15% of Intacs cause some complications and issues that cannot be resolved if they are removed. Still, it is a better option than jumping straight to a corneal transplant.

Keratoconus Corneal collagen cross-linking therapy

Corneal collagen cross-linking therapy (CXL) is intended to stabilize the tissue by forming more bonds between the existing collagen fibers and also increasing the size of the fibers, making the cornea much firmer and less likely to continue deforming. It involves pretreatment the cornea with riboflavin (Vitamin B2) for 30 minutes then using radiation from the ultraviolet A band light spectrum (normally around 370 nanometers) to increase the cross links over about a 30 minute period. While it has been more extensively in Europe, it is starting to enter the U.S. market. The riboflavin acts to keep the UVA from completely passing through the cornea so the UV can act to create more cross links. Riboflavin also may have a photo reactive effect that further increases cross linking of the collagen bands. Questions still surround this treatment. It is not an FDA approved treatment in the United States but is undergoing clinical trials, and currently is used off label as a treatment for Keratoconus. The FDA (Food and Drug Administration) regulates drugs and medical devices but not doctors. Any procedure that uses drugs or medical devices can be performed by a doctor if you are properly informed, share in the decision, and it has an acceptable possibility of helping. The riboflavin still allows a significant amount of UVA to pass through the cornea. This could potentially increase future risks for cataract development. UVA with riboflavin is cytotoxic (damaging to cells) and can damage the endothelial cells that line the back of the cornea and are vital for its long term health. Corneal thickness needs to be factored to keep this type of damage far enough away from the endothelium cells of the cornea. A minimum corneal thickness of 400 microns has been suggested but a better choice would be 450 to 500 microns. Cellular damage to the keratocytes, changes to the matrix of the cornea, and changes to the epithelium do occur in the cornea after the procedure. Normally they regenerate over the next 6 months. Riboflavin has poor penetration into the cornea so the surface layers of epithelium cells need to be removed. It is unknown if the effect of increased rigidity created by this treatment will last indefinitely, or if there are any other long term problems from increasing the cross linking and rigidity of the cornea. Some cases of persistent haze, infections, and increased eye pressure reading have been noted. The increased eye pressures are presumably an artifact since we know thicker (more firm) corneas read artificially high with most current glaucoma instruments. With careful consideration about the stage of Keratoconus and treatment of the eye at the appropriate stage, cross linking of collagen fibers in the cornea appears to be a great addition to eye doctors armetarium in treating keratoconus. While it may improve the condition mildly in many patients, it should always be considered as a stabilizing treatment and not a curative treatment.

Future therapies will evolve. Cross linking collagen therapy is still in its infancy. Stem cell and genetic treatments may be seen at some time. Someday we will no longer be treating Keratoconus but acting to prevent it from ever distorting peoples vision and lives.

Filed Under: Contact Lenses, double vision, Eye Diseases, Kerataconus, Vision Service Plan -VSP Tagged With: astigmatism, car headlights, Cathepsins, collagen, cone shape, contact, contact lens fittings for keratoconus, contact lens prescription, corneal tissue, cross linked collagen therapy kerataconus, curvatures, damage, disease, distorted vision, doctor, eye, eye doctors, eye images, eyeglass prescription, eyesight, Fort Collins, fort collins contact lenses, Fort Collins Eye Doctors, Fort Collins Keratoconus, Fort Collins Optometrist, halos around lights, hydrogel, Intacs Keratoconus, irregular astigmatism, irregular shape, keratoconus, keratoconus contact len fittings, keratoconus contact lenses, Keratocytes, light, light image, light streaks, metalloproteinase, Northern Colorado, Optometrist, piggyback contact lens, Scleral, silicone, Soft, spectacle, stromal, synergeyes, treatment

Northern Colorado Macular Degeneration

April 21, 2010 By admin Leave a Comment

Macular Degeneration In Northern Colorado

Age-related macular degeneration (AMD) is a disease associated with aging that gradually destroys sharp, central vision. Central vision is needed for seeing objects clearly and for common daily tasks such as reading and driving. Due to the higher altitude a high numbers of sunny days in Fort Collins, there is more UV exposure which is a risk factor for macular degeneration.

AMD affects the macula, the part of the eye that allows you to see fine detail. AMD causes no pain. In some cases, AMD advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision in both eyes. AMD is a leading cause of vision loss in Americans 60 years of age and older. AMD occurs in two forms: wet and dry.

Where is the macula?

The macula is located in the center of the retina, the light-sensitive tissue at the back of the eye. The retina instantly converts light, or an image, into electrical impulses. The retina then sends these impulses, or nerve signals to the visual cortex region of the brain.

Wet AMD occurs when abnormal blood vessels behind the retina start to grow under the macula. These new blood vessels tend to be very fragile and often leak blood and fluid. The blood and fluid raise the macula from its normal place at the back of the eye. Damage to the macula occurs rapidly.

With wet AMD, loss of central vision can occur quickly. Wet AMD is also known as advanced AMD. It does not have stages like dry AMD.

An early symptom of wet AMD is that straight lines appear wavy. If you notice this condition or other changes to your vision, contact your eye care professional at once. You need a comprehensive dilated eye exam.

Dry AMD occurs when the light-sensitive cells in the macula slowly break down, gradually blurring central vision in the affected eye. As dry AMD gets worse, you may see a blurred spot in the center of your vision. Over time, as less of the macula functions, central vision is gradually lost in the affected eye.

The most common symptom of dry AMD is slightly blurred vision. You may have difficulty recognizing faces. You may need more light for reading and other tasks. Dry AMD generally affects both eyes, but vision can be lost in one eye while the other eye seems unaffected.

One of the most common early signs of dry AMD is drusen

Drusen are yellow deposits under the retina. They often are found in people over age 60. Your eye care professional can detect drusen during a comprehensive dilated eye exam. Drusen alone do not usually cause vision loss. In fact, scientists are unclear about the connection between drusen and AMD. They do know that an increase in the size or number of drusen raises a person’s risk of developing either advanced dry AMD or wet AMD. These changes can cause serious vision loss.

Dry AMD has three stages, all of which may occur in one or both eyes:

Early AMD. People with early AMD have either several small drusen or a few medium-sized drusen. At this stage, there are no symptoms and no vision loss.
Intermediate AMD. People with intermediate AMD have either many medium-sized drusen or one or more large drusen. Some people see a blurred spot in the center of their vision. More light may be needed for reading and other tasks.
Advanced Dry AMD. In addition to drusen, people with advanced dry AMD have a breakdown of light-sensitive cells and supporting tissue in the central retinal area. This breakdown can cause a blurred spot in the center of your vision. Over time, the blurred spot may get bigger and darker, taking more of your central vision. You may have difficulty reading or recognizing faces until they are very close to you.

If you have vision loss from dry AMD in one eye only, you may not notice any changes in your overall vision. With the other eye seeing clearly, you still can drive, read, and see fine details. You may notice changes in your vision only if AMD affects both eyes. If blurriness occurs in your vision, see an eye care professional for a comprehensive dilated eye exam.

Ninety percent of all people with AMD have this type. Scientists are still not sure what causes dry AMD.

Frequently Asked Questions about wet and dry macular degeneration

Which is more common-the dry form or the wet form?

The dry form is much more common. More than 85 percent of all people with intermediate and advanced AMD combined have the dry form.

However, if only advanced AMD is considered, about two-thirds of patients have the wet form. Because almost all vision loss comes from advanced AMD, the wet form leads to significantly more vision loss than the dry form.

Can the dry form turn into the wet form?

Yes. All people who have the wet form had the dry form first.

The dry form can advance and cause vision loss without turning into the wet form. The dry form also can suddenly turn into the wet form, even during early stage AMD. There is no way to tell if or when the dry form will turn into the wet form.

The dry form has early and intermediate stages. Does the wet form have similar stages?

No. The wet form is considered advanced AMD.

Can advanced AMD be either the dry form or the wet form?

Yes. Both the wet form and the advanced dry form are considered advanced AMD. Vision loss occurs with either form. In most cases, only advanced AMD can cause vision loss.

People who have advanced AMD in one eye are at especially high risk of developing advanced AMD in the other eye.

Causes and Risk Factors-Who is at risk for AMD?

The greatest risk factor is age. Although AMD may occur during middle age, studies show that people over age 60 are clearly at greater risk than other age groups. For instance, a large study found that people in middle-age have about a 2 percent risk of getting AMD, but this risk increased to nearly 30 percent in those over age 75.

Other risk factors include:

Smoking. Smoking may increase the risk of AMD.
Obesity. Research studies suggest a link between obesity and the progression of early and intermediate stage AMD to advanced AMD.
Race. Whites are much more likely to lose vision from AMD than African Americans.
Family history. Those with immediate family members who have AMD are at a higher risk of developing the disease.
Gender. Women appear to be at greater risk than men.

Can my lifestyle make a difference?

Your lifestyle can play a role in reducing your risk of developing AMD.

Eat a healthy diet high in green leafy vegetables and fish.
Don’t smoke.
Maintain normal blood pressure.
Watch your weight.
Exercise.

Symptoms and Detection

What are the symptoms?

Both dry and wet AMD cause no pain.

For dry AMD: the most common early sign is blurred vision. As fewer cells in the macula are able to function, people will see details less clearly in front of them, such as faces or words in a book. Often this blurred vision will go away in brighter light. If the loss of these light-sensing cells becomes great, people may see a small–but growing–blind spot in the middle of their field of vision.

For wet AMD: the classic early symptom is that straight lines appear crooked. This results when fluid from the leaking blood vessels gathers and lifts the macula, distorting vision. A small blind spot may also appear in wet AMD, resulting in loss of one’s central vision.

How is AMD detected?

Your eye care professional may suspect AMD if you are over age 60 and have had recent changes in your central vision. To look for signs of the disease, he or she will use eye drops to dilate, or enlarge, your pupils. Dilating the pupils allows your eye care professional to view the back of the eye better.

AMD is detected during a comprehensive eye exam that includes:

Visual acuity test. This eye chart test measures how well you see at various distances.
Dilated eye exam. Drops are placed in your eyes to widen, or dilate, the pupils. Your eye care professional uses a special magnifying lens to examine your retina and optic nerve for signs of AMD and other eye problems. After the exam, your close-up vision may remain blurred for several hours.
Tonometry. An instrument measures the pressure inside the eye. Numbing drops may be applied to your eye for this test.

Your eye care professional also may do other tests to learn more about the structure and health of your eye.

During an eye exam, you may be asked to look at an Amsler grid. The pattern of the grid resembles a checkerboard. You will cover one eye and stare at a black dot in the center of the grid. While staring at the dot, you may notice that the straight lines in the pattern appear wavy. You may notice that some of the lines are missing. These may be signs of AMD.

If your eye care professional believes you need treatment for wet AMD, he or she may suggest a fluorescein angiogram. In this test, a special dye is injected into your arm. Pictures are taken as the dye passes through the blood vessels in your retina. The test allows your eye care professional to identify any leaking blood vessels and recommend treatment.

How is wet AMD treated?

Wet AMD can be treated with laser surgery, photodynamic therapy, and injections into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.

Laser surgery. This procedure uses a laser to destroy the fragile, leaky blood vessels. A high energy beam of light is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. However, laser treatment may also destroy some surrounding healthy tissue and some vision. Only a small percentage of people with wet AMD can be treated with laser surgery. Laser surgery is more effective if the leaky blood vessels have developed away from the fovea, the central part of the macula. (See illustration at the beginning of this document.) Laser surgery is performed in a doctor’s office or eye clinic.The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.
Photodynamic therapy. A drug called verteporfin is injected into your arm. It travels throughout the body, including the new blood vessels in your eye. The drug tends to “stick” to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline. Unlike laser surgery, this drug does not destroy surrounding healthy tissue. Because the drug is activated by light, you must avoid exposing your skin or eyes to direct sunlight or bright indoor light for five days after treatment.Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor’s office.
Photodynamic therapy slows the rate of vision loss. It does not stop vision loss or restore vision in eyes already damaged by advanced AMD. Treatment results often are temporary. You may need to be treated again.
Injections. Wet AMD can now be treated with new drugs that are injected into the eye (anti-VEGF therapy). Abnormally high levels of a specific growth factor occur in eyes with wet AMD and promote the growth of abnormal new blood vessels. This drug treatment blocks the effects of the growth factor.You will need multiple injections that may be given as often as monthly. The eye is numbed before each injection. After the injection, you will remain in the doctor’s office for a while and your eye will be monitored. This drug treatment can help slow down vision loss from AMD and in some cases improve sight.

How is dry AMD treated?

Once dry AMD reaches the advanced stage, no form of treatment can prevent vision loss. However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage, in which vision loss occurs.

The National Eye Institute’s Age Related Eye Disease Study found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD’s progression from the intermediate stage to the advanced stage will save the vision of many people.

Age-Related Eye Disease Study (AREDS)

What is the dosage of the AREDS formulation?
The specific daily amounts of antioxidants and zinc used by the study researchers were 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene (often labeled as equivalent to 25,000 International Units of vitamin A), 80 milligrams of zinc as zinc oxide, and two milligrams of copper as cupric oxide. Copper was added to the AREDS formulation containing zinc to prevent copper deficiency anemia, a condition associated with high levels of zinc intake. New studies are underway to test refinements of the supplements being used, with omeag-3 oils being one of the possible future additions.

Who should take the AREDS formulation?

People who are at high risk for developing advanced AMD should consider taking the formulation. Vitamin A may be contra-indicted in smokers and an A free supplement form may be recommended by your optometrist. You are at high risk for developing advanced AMD if you have either:

1. Intermediate AMD in one or both eyes.

2. Advanced AMD (dry or wet) in one eye but not the other eye.

Your eye care professional can tell you if you have AMD, its stage, and your risk for developing the advanced form.

The AREDS formulation is not a cure for AMD. It will usually not restore vision already lost from the disease. However, it may delay the onset of advanced AMD. It may help people who are at high risk for developing advanced AMD keep their vision.

Can people with early stage AMD take the AREDS formulation to help prevent the disease from progressing to the intermediate stage?

There is no apparent need for those diagnosed with early stage AMD to take the AREDS formulation. However, you should discuss the possibilty with your optometrist. Some eye doctors are recommending supplementation if there is a strong family history present. The study did not find that the formulation provided a benefit to those with early stage AMD. If you have early stage AMD, a comprehensive dilated eye exam every year can help determine if the disease is progressing. You should discuss taking supplements at the early stage AMD and if it progresses to the intermediate stage.f antioxidants and zinc as the AREDS formulation?
No. The high levels of vitamins and minerals are difficult to achieve from diet alone. However, previous studies have suggested that people who have diets rich in green leafy vegetables have a lower risk of developing AMD.

Can a daily multivitamin alone provide the same high levels of antioxidants and zinc as the AREDS formulation?
No. The formulation’s levels of antioxidants and zinc are considerably higher than the amounts in any daily multivitamin.

If you are already taking daily multivitamins and your doctor suggests you take the high-dose AREDS formulation, be sure to review all your vitamin supplements with your doctor before you begin. Because multivitamins contain many important vitamins not found in the AREDS formulation, you may want to take a multivitamin along with the AREDS formulation. For example, people with osteoporosis need to be particularly concerned about taking vitamin D, which is not in the AREDS formulation.

How can I take care of my vision now that I have AMD?

Dry AMD. If you have dry AMD, you should have a comprehensive dilated eye exam at least once a year. Your eye care professional can monitor your condition and check for other eye diseases. Also, if you have intermediate AMD in one or both eyes, or advanced AMD in one eye only, your doctor may suggest that you take the AREDS formulation containing the high levels of antioxidants and zinc.

Because dry AMD can turn into wet AMD at any time, you should get an Amsler grid from your eye care professional. Use the grid every day to evaluate your vision for signs of wet AMD. This quick test works best for people who still have good central vision. Check each eye separately. Cover one eye and look at the grid. Then cover your other eye and look at the grid. If you detect any changes in the appearance of this grid or in your everyday vision while reading the newspaper or watching television, get a comprehensive dilated eye exam.

Wet AMD. If you have wet AMD and your doctor advises treatment, do not wait. After laser surgery or photodynamic therapy, you will need frequent eye exams to detect any recurrence of leaking blood vessels. Studies show that people who smoke have a greater risk of recurrence than those who don’t. In addition, check your vision at home with the Amsler grid. If you detect any changes, schedule an eye exam immediately.

What can I do if I have already lost some vision from AMD?

If you have lost some sight from AMD, don’t be afraid to use your eyes for reading, watching TV, and other routine activities. Normal use of your eyes will not cause further damage to your vision.

If you have lost some sight from AMD, ask your eye care professional about low vision services and devices that may help you make the most of your remaining vision. Certain eyeglass lens tints have been benficial for some patients.

The National Eye Institute is conducting and supporting a number of studies to learn more about AMD. For example, scientists are:

Studying the possibility of transplanting healthy cells into a diseased retina.
Evaluating families with a history of AMD to understand genetic and hereditary factors that may cause the disease.
Looking at certain anti-inflammatory treatments for the wet form of AMD.

This research should provide better ways to detect, treat, and prevent vision loss in people with AMD.

Filed Under: Eye Diseases, Macular Degeneration Tagged With: age related macular degeneration, AMD, Amsler, angiogram, central vision, clinic, dilate, Dilated, Dilating, Drug, eye, eye damage, eye exam, Fort Collins, Fort Collins Eye Doctors, Fort Collins Optometrist, fovea, grid, laser, light, loss of vision, macula, Northern Colorado, Optometrist, Photodynamic, Retina, sunlight, Symptoms, therapy, uv exposure, VEGF, verteporfin, vision loss, visual cortex, wet amd

Macular Degeneration and Medical Marijuana

March 1, 2010 By admin 2 Comments

Optometrists are receiving more

calls and questions about

Marijuana and the treatment of

eye diseases

Medical Marijuana Fails full disclosure and eye doctors must work to provide clear education about what is known at this point.

Reports circulating the last few years indicate that there may be no increases risk of lung cancer associated with smoking marijuana. What they fail to mention is a rapid increase in chronic lung disease. Other studies have been quoted showing a decrease in VEGF (vascular endothelial growth factor) and supposed value in treating macular degeneration. VEGF stimulates new blood vessel growth. Decreasing VEGF would theoretically lower the conversion rate of dry macular degeneration to the more sight threatening wet form.

Unfortunately, the chronic lung disease and damage combined with the blood pressure lowering effect of marijuana will probably prove the reverse and show it accelerates the risk for macular degeneration. Decreased oxygen to the retinal tissues is a primer driver in the transformation of dry macular degeneration to wet macular degeneration.

Isolating the VEGF may someday prove useful in the treatment of macular degeneration by your optometrist, but for today it is still best to stay with the documented nutritional interventions and current VEGF treatments available, Avastin and Lucentis.

Don’t be timid in asking your optometrist for advice about medical marijuana and eye problems. The facts can potentially save your vision and prevent a lifetime of blindn

Glaucoma Treatment

ess.

Filed Under: Eye Diseases, Macular Degeneration Tagged With: avastin, blood vessel growth, chronic lung disease, dry macular degeneration, effect of marijuana, eye, Eye Clinic, Eye Diseases, Eye Doctor, eye doctors, eye problems, Fort Collins Eye Doctors, lucentis, lung cancer, Macular Degeneration, medical marijuana, nutritional interventions, Optometrist, pressure, Smoking, smoking marijuana, vascular endothelial growth factor, VEGF, Vision

Macular Degeneration Update

February 18, 2010 By admin Leave a Comment

Age Related Macular Degeneration

Several exciting new advances are going on in the treatment of macular degeneration. AREDS 2 is a refinement of the original age related eye disease study that showed a significant correlation between certain supplements and a decrease in progression of dry macular degeneration to the more sight threatening wet form.

Eye Doctors to Start New Age Related Eye Disease Study-AREDS-2

AREDS 2 will add and refine the supplements being tested. They will also be tested to see if there is a reduction in the development of cataracts. Omega 3 (fish oils) will be added to the supplements.

Omega-3 Fatty Acids Have Proven Effects on Dry Eye Treatment and are widely used by Optometrists Today. Now they may prove just as beneficial in Macular Degeneration Treatment.

Omega 3 oils contain docosahexaenoic acid (DHA) and decrease the production of inflammatory compounds like prostaglandins and Leukotrienes. They may possibly offer some form of neuroprotection to the cells of the retina and delay cellular death.

Lutein and zeaxanthin are the major phytopigments.

Phytopigments are pigments found in vegetables like broccoli, spinach, peas and a number of other foods. They are the major components of the pigment found in the macula, the area of retinal tissue effected by macular degeneration. They help prevent damage to the retinal cells from free radicals (oxidative damage) and may also offer some neuroprotective benefits. Beta-carotene, the precursor for vitamin A, may be tested to see if it has any impact on results. While included in the original studies, there have been questions raised about the possibility of beta-carotene increasing the risk of lung cancer in smokers. Smoking is one of the major risk factors that makes people susceptible to developing macular degeneration.

With about 4000 patients to be enrolled, this is an exciting move forward in studying the effects of nutrition and supplementation on eye diseases. The results of the original trial were as good as any major drug used in treating health problems, I expect this trial will only improve those outcomes.

Filed Under: Eye Nutrition, Macular Degeneration Tagged With: age related macular degeneration, AREDS, Beta-carotene, dha, dry eye treatment, dry macular degeneration, eye, eye disease, Eye Diseases, eye doctors, free radicals, Leukotrienes, lutein and zeaxanthin, macula, neuroprotection, nutrition, omega 3 fatty acids, omega 3 fish oils, omega 3 oils, Optometrists, Phytopigments, prostaglandins, retinal cells, supplementation

Marijuana for Glaucoma a Bad Choice

February 8, 2010 By admin Leave a Comment

Marijuana use has drastically increased recently in areas like Colorado that have passed amendments legalizing the medicinal use for certain chronic conditions. Glaucoma is listed as one of the main reasons for obtaining a registry identification card under Colorado‘s amendment 20, allowing the holder to use and retain limited quantities of marijuana. Cities like Fort Collins have had to react to the rapid proliferation of medical marijuana dispensaries and the lack of regulation and planning that has subsequently occurred. Federal law does not recognize the legality of state medical marijuana laws and the enforcement is still in question, even as the dispensaries proliferate.

The approval of marijuana for the treatment of glaucoma is lacking in justification and is not an FDA endorsed treatment. Glaucoma is a disease where the visual nerve cells degenerate and result in blindness over time if left untreated. Increased pressure inside the eye and impaired blood circulation to the optic nerve are part of the cycle that damages eyesight.

Research on the medical use of marijuana started to appear in the 1970′s. It does lower eye pressures in about 2/3 of the subjects by about 25-30%. This is an acceptable range for glaucoma drugs that are in use today. Unfortunately, the effect only lasts 3-4 hours and is probably not a steady state lowering over the time period. Effective treatment would require smoking marijuana every 2-3 hours. Eye pressure often spikes up at night and it would require use every few hours all night. Lowering eye pressure does not always treat glaucoma and there is currently little evidence to support that the eye pressure reduction from marijuana use has an effect on vision preservation. It has been postulated that the active ingredients of marijuana may increase the outflow of fluid from the eye through it’s drainage system to achieve the lowering effect. Unfortunately, there are also some effects on lowering blood pressure and episodes of systemic hypotension (sudden lowering of the blood pressure when standing). Since compromised blood flow to the optic nerve is a vital factor in glaucoma, there is the possibility it could worsen glaucoma even though the eye pressure has been lowered.

There are over 400 active components in marijuana with Delta9-tetrahydrocannabinol being the most studied component. Like any herbal medicine, the concentration of these components varies as does the effectively of the product provided by dispensaries. Inhalation is more effective than oral dosing and carries risks to the lungs and other body systems. Consuming adequate dosing by consumption every 2-3 hours would create a high health hazard to the body. Unfortunately, eye drop application of the active ingredients has not proven to be effective in lowering pressure. Eye side effects include a drastic increase in dry eyes, redness, and eye irritation. The inhalation properties may increase the risk of macular degeneration and cataracts.

The possibility of isolating the active ingredients and separating them from the euphoric effects do warrant further studies. The possibility of a topical preparation that is effective is being studied. Studies show a direct correlation between lower frequency of drug administration and patient compliance. Any medication that needs to be used more than four times per day is unlikely to be used correctly over a long period of time, and once or twice a day is today’s goal. Any viable preparation of a marijuana derivative treatment for glaucoma will need to meet these criteria. Until that day arrives, seek treatment from an eye doctor with traditional prescription eye medications and if desired, supplement that treatment with acceptable alternative medical care that will not cause damage and possibly end in blindness.

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Filed Under: Eye Diseases Tagged With: blood circulation, eye pressure, eye pressures, medical marijuana dispensaries, medical marijuana laws, medical use of marijuana, optic nerve, smoking marijuana, treatment of glaucoma, use of marijuana

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