Age-Related Macular Degeneration
Age-related macular degeneration (ARMD or AMD) affects the part of the retina called the macula. The macula is the part of the retina responsible for your central vision, the vision you use to see things with fine detail, the eye chart in the eye doctor’s office, for example. It is the leading cause of blindness for patients aged 55 and older in the U.S.
The effect on vision can be mild, as with the dry-type of degeneration, or more severe, with some cases of dry degeneration and many cases of wet degeneration. Dry AMD accounts for 90% of AMD cases and wet AMD is responsible for 10%.
Again, the macula is a part of the retina, which is the inner lining of the back of the eyeball. The retina functions much like the film in a camera. Think of the eye as a hollow ball. Light comes through the front of the eye, is focused by the cornea and lens onto the retina. The retina has many layers. The outermost retinal layer is the RPE or the retinal pigment epithelium. Deep to the retina are other layers including Bruch’s membrane and choroid. The fovea is the focal point of the macula, located in the middle of the macula. This is where the vision is sharpest.
In dry AMD, yellowish deposits called drusen can be found in the macula. These are found deep to the retina. They can be small or large, very well-outlined or have fuzzier edges, and there can be just a few or many of them. When the drusen are well-outlined or discrete, they are called hard drusen. When the drusen have softer or fuzzier edges, they are called soft drusen. The retina has a normal background color which comes from the pigmentation of a layer called the RPE. In dry AMD, there can be a disturbance in the RPE, such that the retina can have spots or splotches of less pigmentation called atrophy, and spots and splotches of more pigmentation called hyperpigmentation. Large areas of atrophy are called geographic atrophy.
In wet AMD, all the findings of dry AMD can be seen, but in addition, there can be signs of bleeding and leakage. The primary difference between dry and wet AMD is that there are abnormal blood vessels with the wet form of AMD. These abnormal blood vessels are referred to as CNV (choroidal neovascularization). These abnormal blood vessels can bleed (hemorrhage), leak protein and fat, cause swelling of the retina, and result in scarring. It is felt that the abnormal blood vessels grow from the choroids, into the retina through weak spots or ruptures in the Bruch’s membrane.
In order to look at the macula carefully, he or she will usually hold a special focusing lens in front of a dilated eye, or place a special contact lens onto the eye (if a contact lens is used, anesthetic eyedrops are put into the eye, which makes this painless). Your doctor will look for all those things mentioned above. In addition, a fluoroscein angiogram (or FA) may be done to better evaluate the retina. With fluoroscein angiography, a special yellow dye is injected into an arm vein, and pictures of the retina are taken with a camera. The dye circulates throughout the body and travels into the blood vessels of the retina and a deeper layer, the choroid.
On photographs, the dye will light up where there is atrophy, will be hidden where there is hyperpigmentation, and actively leak when there are abnormal blood vessels as can be seen with wet AMD. For wet macular degeneration, the pattern of the fluoroscein angiogram can be used to determine whether laser treatment would be beneficial. Another type of angiogram is called indocyanine green angiography (ICG). This uses a different kind of dye. It can be helpful in identifying hard-to-detect (occult) abnormal blood vessels in wet AMD. An advanced imaging instrument called OCT can be used to obtain more detailed images of the retina than possible with lenses.
There is no single gene that is responsible for AMD. Age-related macular degeneration can run in families, so there is a higher chance for unaffected members of a family to develop AMD. The families of patients with AMD have a two- to fourfold higher risk of AMD compared to families with no history of AMD. Having a positive family history does not mean a person is destined to develop AMD.
At present, there is no known way of preventing the development of AMD in patients with no signs of degeneration, whether there is a family history or not. Yearly eye exams are suggested.
Blurry central vision (not peripheral) or distorted vision are the usual symptoms. However, a patient may not be aware of a problem, and have no complaints with early dry AMD. The vision in dry AMD may slowly worsen or stay the same. Dry AMD can change (but not always) into the wet type of AMD, and when it does, the vision usually worsens much more quickly. The vision becomes more blurry and distorted. It is very important for AMD patients to pay very careful attention to changes in their vision. Any change should be reason to see an ophthalmologist immediately.
Patients who have AMD are instructed to use an Amsler grid, to monitor their vision. This card has a grid pattern of lines. Patients are instructed to look at a central point, and use their peripheral or side vision to see the lines of the grid. If a patient notices a change in the grid, this may indicate a change in the AMD, perhaps transformation of dry into wet AMD. Such a change would be reason to see an ophthalmologist quickly.
Again, patients who don’t have AMD (even with a family history of the disease) should have a yearly check-up. At the present time, there is no therapy to prevent the initial development of AMD (see Smoking below)
For patients who already have AMD, there are steps that can be taken, to try to prevent it and vision from getting worse. The Age-Related Eye Disease Study (AREDS) showed that taking vitamin and mineral supplements can decrease the risk of AMD getting worse. Patients who have intermediate AMD in one or both eyes, or who have advanced AMD in one eye, but not the other eye, should take the supplements recommended by the AREDS study. The supplements used in AREDS include the following (to be taken daily):
- Vitamin C 500 mg
- Vitamin E 400 IU (International Units)
- Beta-carotene 15 mg
- Zinc 80 mg, as zinc oxide
- Copper 2 mg, as cupric oxide (copper is necessary because high-dose zinc can cause a copper deficiency)
Results from a follow-up study to the original AREDS, called AREDS 2, showed that eliminating beta-carotene and reducing the zinc to 25 mg did not affect the benefits of the the formulation. It also found that patients who had poor dietary intake of lutein and zeaxanthin, benefited from taking 10mg of lutein and 2 mg of zeaxanthin. Lutein and zeaxanthin, what are called antioxidant carotenoids, found in spinach and other green leafy vegetables. Adding omega-3 fatty acids to the original formulation did not provide any additional benefit.
Based on AREDS2, the National Eye Institute researchers recommend taking the following (to be taken daily):
- Vitamin C 500mg
- Vitamin E 400 IU
- Lutein 10mg
- Zeaxanthin 2mg
- Zinc 80 mg, as zinc oxide
- Copper 2 mg, as cupric oxide
There are a number of supplements which are commercially available, including Ocuvite PreserVision and I-Caps AREDS formula. Both contain the vitamins and minerals in doses used in the AREDS study. There are many other brands containing the AREDS formula. It is expected that manufacturers of these supplements will change the formulations of their products to reflect the results of the AREDS 2 study. Until that time, we recommend that patients take the currently available smokers-version of the original formulation (which excludes beta-carotene) and consider taking 10mg of lutein and 2 mg of zeaxanthin.
As with any over-the-counter medication, patients should discuss the use of this with their primary care doctor. Patients who are smokers or who have smoked within the last 5 years, should not take supplements containing beta-carotene, as it may increase the risk of lung cancer. Therefore, smokers should not use formulations containing beta-carotene (as noted above, there are commercially available formulations of AREDS which omit the beta-carotene).
It is permissible to take a daily multivitamin, in addition to the AREDS supplement. A daily multivitamin by itself, however, does not provide the protection of the AREDS formulation.
Remember, the AREDS-type formula does not prevent the initial development of AMD, and it provides no significant benefit for patients who only have minimal AMD. Smoking is a major risk factor for AMD. People who smoke have three times the risk of developing macular degeneration, and once they develop it, with continued smoking, they have three times the risk of losing vision from it. People who smoke more and smoke longer, have more risk. When smoking is stopped, the risk decreases but never goes to zero.
Exposure to certain types of light may play some role in AMD, but this has not been proven. In particular, blue light is especially damaging to the retina. The natural human lens becomes more yellow in color, as it turns into a cataract. A yellow colored lens filters out blue light, so that a cataract, in a rather strange way, can protect the retina. Natural sunlight is a mixture of many colors, including blue light. For the time being, the use of visors, hats, and sunglasses is a reasonable step for protection.
Currently, treatment is available only for wet AMD. There are several treatment methods. The first effective treatment developed years ago is the standard laser photocoagulation. This laser technique is painless. The laser is aimed at the abnormal blood vessels of wet AMD, and the resulting heat essentially cauterizes the leaking blood vessels or CNV. The problem with this technique is that the heat not only destroys the bad blood vessels, but destroys the retina and healthy tissue as well. Since the retina is responsible for vision, laser treatment of the CNV can cause damage to vision by itself (though the patient may ultimately end up with better vision than had he or she left the CNV untreated).
PDP or photodynamic therapy is another treatment method that tries to minimize this “collateral” damage to healthy retina. PDT was developed to selectively destroy the abnormal blood vessels but leave the retina undamaged. With PDT, a special drug called Visudyne is injected into an arm vein. Visudyne preferentially binds to the abnormal blood vessels. Once the drug circulates and travels to the retina, the retina is exposed to a laser light of a certain wavelength or color. The light activates the drug which then destroys the CNV. Unlike standard laser photocoagulation, the laser used in PDT is “cold”. The strength or “fluence” of the laser can be reduced to improve the selectivity of PDT, what is referred to as (RF)PDT. Photodynamic therapy usually needs to be repeated, as often as every 3 months, since the CNV can come back or recur. Both standard laser photocoagulation and PDT are imperfect. Both can only be used under certain circumstances, and both sometimes only provide temporary benefit–CNV often comes back. Many patients continue to lose vision despite treatment.
There are now a whole class of drugs designed to attack a special protein called VEGF. VEGF stands for vascular endothelial growth factor. It is normally found in the body, but in wet AMD, it is responsible for stimulating the growth of the abnormal blood vessels. Currently, there are three drugs that work by binding or attaching to VEGF, preventing VEGF from causing its bad effects in macular degeneration; these are Macugen, Lucentis, and Avastin. These medications are administered by direct injection in the vitreous gel, which is located in the back of the eyeball. Despite what you might think, the injection is not painful. Multiple injections, as often as one every month, may be necessary to maintain any improvement. Macugen has been shown to slow the rate of vision loss but does not improve vision in a majority of patients. On the other hand, Lucentis has been shown to stabilize vision and, unlike Macugen, is capable of actually improving vision when vision has been damaged. Avastin is a drug related to Lucentis (it comes from the same parent molecule as Lucentis, and is made by the same drug company) and it appears to be as effective as Lucentis. Avastin is FDA-approved only for the treatment of colon and other cancers, so when it’s used to treat AMD, its use in this fashion is considered off-label.
“Off-label” does not necessarily mean that this is unsafe, only that the FDA has not examined data regarding safety or effectiveness of the drug for this alternate use. The FDA is not in the business of telling doctors how to practice medicine. This is why, for example, some prescription medications are routinely used for reasons other than the original indications. The Comparison of Age-Related Macular Degeneration Treatment Trials (CATT), sponsored by the National Eye Institute, showed that Lucentis and Avastin were comparable in effectiveness. The CATT study showed that monthly administration of either drug resulted in slightly better visual results than when they were used on “as-needed” basis. There are now other drugs in development, which work by interfering with different steps in the VEGF “pathway” (there are a number of steps leading up to the production of VEGF, and additional steps after VEGF is produced, which ultimately cause the new blood vessel growth at the heart of the problem and wet AMD).
There are also other drugs in development which are designed to work in ways that have nothing to do with VEGF. Finally, the future of treatment may involve combinations of the available drugs or lasers.
Astigmatism
In simplistic terms, if there is no astigmatism, the cornea of the eye is shaped like a baseball cut in half. The curvature or steepness of the half-dome is the same all the way around. Compare this to a cornea which is similar to a football cut in half lengthwise (in the long direction, through both pointy ends). The curvature of the cornea in the long direction (along the seams) is not as steep as along the short direction. Such a cornea focuses light, not at a single point, but at 2 points. Someone who has uncorrected astigmatism may see images that are fuzzy and doubled. A cornea shaped like a football, cut lengthwise, has astigmatism.
In these diagrams of an eye with astigmatism, the rays of light from the object are being brought into sharp focus at two different points, one on the retina and the other, behind the retina. This is an eye with a cornea that has astigmatism, a non-uniform curvature like the football cut lengthwise. The two different curvatures results in two different focal points.
There are several different combinations of astigmatism, depending on where the focal points are located.
- Simple myopic astigmatism:One point in front of retina, other on the retina
- Compound myopic astigmatism: Both points of focus in front of the retina
- Simple hyperopic astigmatism: One point behind the retina, other on the retina
- Compound hyperopic astigmatism: Both points of focus behind the retina
- Mixed astigmatism: One point in front of the retina, the other behind the retina
Cataracts and Cataract Surgery
A cataract is defined as any opacity or cloudiness in the lens of the eye. The lens of the eye is a normally clear structure located behind the pupil and iris. The pupil is the round opening in the middle of the iris or colored part of the eye. The pupil usually constricts or becomes smaller when exposed to light, and tends to dilate or become larger under low lighting or dark conditions. The human lens can be thought of as being similar in shape to a magnifying lens. This lens is held in place by many tiny fibers (zonules) which stretch from the innermost layer of the wall of the eyeball, to attach to the edge of the lens all the way around. The normal human lens is elastic; it can stretch when it is pulled by the attaching fibers. Many people think that a cataract is a film that grows over the front of the eye, but in fact, it is a cloudiness of the lens which is located inside the front of the eye.
Cataracts can develop as a result of the aging process, but they can also be present at birth (congenital). A congenital cataract in an baby can be a medical emergency. If it is visually significant, it can cause permanent poor vision, unless it is quickly removed with surgery. Anything that affects the quality of vision, whether it be a corneal scar or cataract, can interrupt normal visual development, resulting in a poorly seeing or amblyopic (“lazy”) eye. Once normal vision has fully developed, usually by 6-7 years of age, for all purposes, a cataract will rarely cause irreversible loss of vision.
A cataract can be classified or named in many ways. One way is based on where the cloudiness is located. A normal lens has a inner core or nucleus, and an outer layer called the cortex. The entire lens is wrapped in a clear outer coating called the capsule. The capsule can be thought of a kind of shrink wrap, the elastic wrap that’s used to package loose vegetables in the grocery store. One type of cataract is a nuclear sclerotic cataract, when the nucleus is cloudy. In a cortical cataract, the outer cortex layer is cloudy. When the cloudiness is located just underneath the capsule, you have a subcapsular cataract. A subcapsular cataract can be further named by its location; if it is at the back of the lens, it is posterior (back) subcapsular; if it is in the front of the lens, it is an anterior (front) subcapsular cataract. A person can have cloudiness that only affects one layer of the lens, or any combination of two or more layers. As an example, a person can have both a nuclear sclerotic and cortical cataract.
Cataracts that develop as part of the aging process typically will start after the ages of 30-40, and are progressive (worsen with time). Cataracts can also be caused by trauma, diabetes and other systemic metabolic diseases, radiation, and some drugs and chemicals. One drug which can cause cataract formation, usually posterior subcapsular, is prednisone, a steroid medication. A cataract can also be the result of other eye diseases, such as iritis, an inflammatory condition of the eye. Long-term use of glaucoma medications may contribute to cataract formation. A strong link between cigarette smoking and nuclear sclerotic cataracts has been demonstrated.
There are some types of age-related cataracts (cortical) for which genetics or heredity account play a significant role.
Regardless of the type of cataract, or the cause, the problem it can cause is decreased vision. If a cataract is primarily nuclear sclerotic, there may be more of an effect on distance vision. Some patients with nuclear sclerotic cataracts will develop “second sight”, being able to read without glasses, though the distance vision will be blurry. For some of these patients, a change of glasses prescription may allow for improved distance vision. Other patients may have more problems with their near or reading vision, as can occur with the posterior subcapsular type of cataract. Other symptoms of cataract include glare when it’s sunny outdoors, or at nighttime with the headlights of oncoming cars. Halos or rings around lights, and double and multiple images can also be caused by cataracts.
The rate at which a cataract grows can be unpredictable. Nuclear cataracts tend to be slow growing, while subcapsular cataracts can progress or grow quickly, but these are generalizations. One method of grading the severity of a cataract uses a numbering system from 0 to 4+, with 0 being no cataract and 4+ being the most severe.
One of the most frequently asked questions is when cataract surgery should be performed (see Cataract surgery below). In general, surgery is reasonable when the best-corrected vision in an eye is unsatisfactory to the patient. Best-corrected vision is the vision a person gets with the most up-to-date glasses or contacts. A person may decide to get surgery because he or she has problems seeing road signs, recognizing faces of people, trouble reading or reading for long periods of time, glare on sunny or bright days, glare with headlights when driving at night, and double or multiple vision. Color vision may also be changed.
People have different visual needs. Some people don’t require sharp vision to enjoy good quality of life. Others need crystal-clear vision to perform job duties or hobbies. There was a time when patients were advised to wait until their cataracts became “ripe” or “mature”. This is an out-of-date concept. Obviously, a cataract needs to be present, but more importantly, a patient needs to feel he or she is not enjoying good quality of life because of visual difficulty. There are patients who have 4+ nuclear sclerotic cataracts and are content with their vision because they can watch televison comfortably. Other patients have 2+ cataracts and are miserable because they can’t read clearly.
The decision to have cataract surgery is made on a case-by-case basis. It is a joint decision made by both patient and doctor. A patient should not feel pressured to have surgery; waiting is nearly always an option. Cataract surgery is nearly always elective; it is the rare instance when cataract surgery needs to be done right away. The bottom-line is that if a patient does not feel he or she is having visual difficulty, surgery is usually not required. A few exceptions to this rule include the following: 1) your eye doctor has difficulty looking at the back of the eye to follow the progress of a disease such as diabetic retinopathy or age-related macular degeneration; 2) the cataract is pushing the iris forward as it grows, compromising the angle of the eye to cause narrow angle glaucoma (see Glaucoma); and 3) the cataract becomes hypermature, with leakage of lens material through the capsule, causing inflammation and a type of glaucoma. Not meeting state standards of safe driving vision may also prompt the need for cataract surgery.
Cataract surgery is one of the most commonly performed surgeries in the United States. It is an outpatient-type of surgery where staying overnight in a hospital is almost never required. It is done under local anesthesia, so the patient is awake. Generally, an intravenous line is started in an arm vein, so that sedatives can be given to relax the patient. After surgery, the patient is taken to a recovery room before being sent home. The one thing patients are most concerned about, is whether there is any pain. I tell my patients that cataract surgery is painless; it is the rare patient who feels anything at all. Anesthetic or numbing eyedrops are instilled into the eye having surgery, and additional anesthetic is used to bathe the inside of the eye. Patients are sometimes worried they may move or be unable to keep their eyes open during surgery. This is almost never a problem. Through a combination of reassurance, sedation, and instrumentation, the eye surgeon can safely guide a patient through surgery.
Cataract surgery involves two major steps, removal of the cloudy lensand replacement with an artificial lens implant. The implant takes over the job of focusing that the old lens used to do. In the early days of cataract surgery, lens implants were not available, hence, patients used to wear unsightly thick cataract glasses. This is no longer an acceptable means of restoring vision. Successful cataract surgery requires use of an implant.
Modern cataract surgery is done using phacoemulsification. This technique uses an instrument that vibrates at ultrasonic frequency, to emulsify or break up and remove the cataract. Most surgeons make a tiny incision, usually 2.75 millimeters or less in length, through which the cataract is removed. This incision is made in such a way that it is self-sealing or closing, so that stitches are rarely required. Prior to actual surgery, a patient’s eye is dilated, that is, the pupil is made larger with eyedrops. The surgeon makes the incision in the cornea (clear dome that arches over the colored part of the eye), where it meets the sclera, the white part of the eye. This incision is so tiny, it cannot be seen with the naked eye. Through this small incision, the surgeon makes an round opening in the capsule, the shrink-wrap that is wrapped around the cloudy lens. The phacoemulsification instrument which is held like a pencil, is placed through the incision, and the inner portions of the cloudy lens is removed through the opening in the capsule. What is left, is a clear, empty sack or capsular bag, with the opening in the front. The surgeon then slides an intraocular lens implant into the eye, and places it inside the capsular bag. To take advantage of the tiny incision, most surgeons use a foldable implant, an implant that can be folded like a taco shell. This folded implant can be inserted through the small incision (without making it larger). Once the implant is inside the capsular bag, it unfolds and opens up to its full size. The implant looks like a miniature magnifying lens which has tiny “feet” or haptics that spread open inside the bag to hold the lens in place. After the position of the implant has been checked, the surgeon makes sure the incision does not leak (water-tight). Antibiotic and anti-inflammatory eyedrops are usually instilled into the eye. A protective eye shield is taped over the eye, before the patient is taken to the recovery room. Surgery usually takes less than half an hour.
There is a relatively new technique called femto-laser assisted cataract surgery. Essentially, this is what the lay press would term “Bladeless Cataract Surgery”. At present, there is no scientific proof that it is more effective or safer than the traditional technique of cataract surgery. This laser technology should not be confused with the Yag laser (Yag Capsulotomy) which is used to remove “secondary cataracts“. The back part of the capsular bag, in which the intraocular lens implant is placed, can become cloudy, months to years after the cataract surgery. This cloudy membrane can be removed in an office-setting with the Yag laser.
Cataract surgery is one of the safest surgeries being done today. Like all surgeries, however, there is some risk of which patients need to be aware. Your surgeon can minimize risk by fully evaluating your eyes, and taking steps to tailor surgery for your circumstances. Some patients require special steps or instrumentation which can be planned in advance.
Many surgeons start patients on antibiotic eyedrops before the actual surgery, to hopefully decrease the risk of infection. The benefit of starting these antibiotics before surgery has not been proven beyond a shadow of a doubt, but it seems reasonable. The risk of a serious eye infection is about one in a thousand cases. Besides infection, there is risk of retinal detachment, perhaps one percent or less in the Medicare population. Any discussion of risk should balance the benefit of surgery with the risk. It is presumed that you are having enough difficulty with your quality of life (because of visual difficulty), to warrant the risks of surgery. Patients differ in what they feel is acceptable vision, and the amount of risk they will tolerate. Your surgeon should help you make sense of the relative risks and benefits.
All surgeons, no matter how skilled, have complications. The most skilled surgeons have fewer complications and may be better able to deal with those complications. Most complications can be handled with a satisfactory outcome. If your surgeon tells you there is no risk, or he or she has never had a complication, you should seek a second opinion.
One question that is frequently asked, is whether cataract surgery can worsen age-related macular degeneration. Thus far, study results are mixed. Macular degeneration can spontaneously progress or worsen even when cataract surgery is not performed. At present, there is no overriding evidence to suggest that cataract surgery aggravates macular degeneration. Remember, the vast majority of patients have excellent outcomes with cataract surgery.
Avoid smoking and take steps to protect your eyes from sunlight exposure. If you are diabetic, be sure to maintain strict control of your blood sugar. Be careful using steroid medications; these types of medications are undeniably beneficial for certain medical conditions, but they can contribute to cataract formation.
Outside the United States, eyedrops are available that are supposed to slow or stop the development of cataracts. These drops contain antioxidants. As of yet, there are no good scientific studies which show these are effective.
Dry Eye
Dry eye refers to a group of conditions in which the tear film of the eye (the tear layer coating the front of your eye) is abnormal, either because of decreased tear formation or excessive tear evaporation, and that is associated with symptoms of eye discomfort. There may be damage to the surface of the eye. In the majority of patients, it is not vision-threatening. It is a chronic disease which can be treated but usually not cured.
Patients will often describe their eyes feeling “dry”. Other symptoms include burning, foreign body sensation, stinging, grittiness, fatigue, and light sensitivity. Dry eye is a major cause of blurry vision. Typically, dry eye symptoms are worse later in the day. Symptoms can also fluctuate in severity over time. Certain circumstances can make symptoms worse.
For example the relative dryness of an airplane during travel, sitting near an air conditioner vent, extensive reading (because the rate of blinking decreases; more time for tears to evaporate), exposure to wind, and the drying effect of many medications, both prescription and over-the-counter drugs (diuretics, anti-histamines, drugs for depression and anxiety, and Accutane, as examples). Patients who have dry eye may not be able to comfortably wear contact lenses.
Signs of dry eye include redness, increased frequency of blinking, and mucous discharge.
Dry eye occurs more frequently in the elderly, but young people can have it as well. It has been estimated 14% of people 65 to 84 years old have symptoms of dry eye often or all the time. It is also more common in women than men, particularly after menopause. It is felt that the hormone imbalance of menopause promotes dry eye symptoms. Hormone replacement therapy can sometimes worsen dry eye, and estrogen-only hormone replacement seems to be worse than estrogen and progesterone combined therapy.
Sjogren’s syndrome is characterized by dry eyes and dry mouth. It is a systemic (whole body) disease in which there is an underlying problem with the immune system. There are two types of Sjogren’s syndrome, primary and secondary. Patients who have primary Sjogren’s syndrome do not have a specific, identifiable systemic disease, and have symptoms that may include aching joints, muscle pain, or fatigue. Secondary Sjogren’s has an underlying autoimmune disease process such as rheumatoid arthritis and lupus.
Rosacea is a condition of the skin and eye, characterized by abnormal functioning oil glands. The skin findings include redness, fine blood vessels, pustules, and thickening of the skin of the nose. The meibomian glands of the eyelids (these glands open up into pores located along the eyelid margin) do not function properly in many patients with rosacea.
Dry eye is a complex disease. By definition, it is either rooted in decreased tear production or excessive tear evaporation. On the production end, inflammation of the tear-producing glands seems to be a major problem. Increased numbers of inflammatory cells called T-lymphocytes are found in the glands. These inflammatory cells damage the glands, resulting in decreased tear formation. This is what occurs in Sjogren’s syndrome.
Increased tear loss through evaporation can create relative dryness. There are conditions which can affect the oily component of the tear film, which then leads to increased evaporation. The normal tear film has 3 components: the mucin layer at the bottom, the aqueous layer in the middle, and the sebaceous or oily layer at the top which protects the middle layer from evaporation. When the meibomian glands do not work properly, the top oily layer is deficient, which causes the aqueous layer to evaporate more quickly.
If the mucin layer is deficient, as can be caused by diseases which destroy the goblet cells of the mucous membrane covering the sclera or white part of the eye (the conjunctivae), the tear film may be of poor quality, resulting in dry eye syndrome.
Dry eye that is mild in severity may be difficult to diagnose with certainty. There are many eye diseases which produce symptoms similar to those found in dry eye. When an ophthalmologist feels dry eye is likely, based on symptoms alone (no signs), he or she may start the patient on a trial of medical therapy such as artificial tears. Patients who have more significant dry eye may be diagnosed with the help of office tests. There are three tests which can be used to aid in the diagnosis of dry eye: 1) Tear film break-up time; 2) Dye staining pattern; and 3) Schirmer or basic secretion test. These tests are quick and painless. Your doctor can explain how these tests are performed. There are other tests which can be of help, though they are not widely available.
Treatment usually consists of one or several of the following:
- As much as possible, reducing or stopping the use of medications which can interfere with tear production. These medications include diuretics used to treat high blood pressure, antihistamines used to treat allergies, sinus decongestants, anti-anxiety and antidepressants, and Accutane. There are many other such medications. You should not reduce or stop any of these medications without first talking to your primary medical doctor.There are some supplements which may help dry eye patients. These include formulations containing omega-3 fatty acids, such as Hydroeyes. Flax seed oil capsules have also been purported to help.
- Modify environmental factors. This means minimizing your direct exposure to heating and air-conditioning vents, both in your car and at work and home, humidifying the air if possible, protecting your eyes from direct wind exposure outdoors, and avoiding prolonged reading without taking breaks. All the above can affect dry eye by their effect on tear loss through evaporation.Patients can use spectacle side shields (plastic shields which clip onto the temples of glasses) and even special moisture retaining glasses to shield themselves from these environmental factors.
- Aqueous enhancement refers to the use of tear replacement therapy. The tear replacement products are available over-the-counter (no prescription necessary); these are drops or ointments that are put into the eyes. The different artificial tear preparations come in different forms. They may differ in how they are preserved and their thickness or viscosity. Many eye medications are preserved; the preservative maintains the sterility of the preparation. The fully preserved tear drops, if used frequently enough, can irritate the eyes because of the amount of preservative to which the eyes are exposed. Some of the available tear preparations are preserved, but the preservative disappears once the drop is put into the eye. The truly preservative-free tear preparations come in single-use dispensers; they are more expensive but may be of benefit to some dry eye patients who need to use drops very frequently. Some of the tear preparations come in a thicker form, which means they may provide longer-lasting relief; the trade-off may be some degree of blurry vision. The thickest type of tear preparation are the ointments which are usually put into the eyes at bedtime; they are usually not used during the waking hours because they can blur the vision substantially.
- Patients who have an underlying systemic disease such as rheumatoid arthritis, can be treated with anti-inflammatory medications which suppress the immune system. By treating the underlying problem, dry eye can be helped.
- There is a new medication called Restasis (Allergan) which is the first FDA-approved drug for the treatment of dry eye. Restasis is topical cyclosporine, an anti-inflammatory medication. (Cyclosporine taken orally is used by some patients to prevent kidney transplant rejection). The drop comes in single-use dispensers; it is used twice a day. The drug works by reducing the inflammation in the tear-producing glands of the eye, allowing the glands to function better. The effect is not immediate; it may take one month or even longer before any benefit is noticed. The worse the dry eye condition, the longer it may take for an effect to be felt. Side-effects are few, with the main one being a burning sensation after instillation.
- For patients with dry eye caused by decreased tear production, a minor procedure done in the office-setting can provide relief. The tears which bathe the eye drain away from the eye through a drainage system. The beginning of the drainage system starts in the upper and lower eyelids in the inner corner of the eyes (toward the nose). Tears gain access to the drainage system through small openings called puncta. The tears then drain into the nose (this is why your nose gets congested if you cry; the excess tears go into your nose). Punctal plugs are very tiny devices which are inserted into the punctal openings. In essence, a punctal plug acts like a stopper in the drain of a sink; it prevents the tears your eye makes, or the artificial tears you put into your eye, from draining away too quickly.There are different types of punctal plugs, some are temporary, and others are “permanent”. The temporary plugs are sometimes used as a trial to see if occlusion of the puncta can help relieve dry eye symptoms. These plugs dissolve over the course of 5-7 days. The permanent plugs are usually made of either silicone (despite the bad reputation of silicone in breast implants, these punctal plugs are very safe) or acrylic. They are called permanent only because they do not dissolve; they can be easily removed if necessary. All plugs, temporary or permanent, are placed into the puncta without the need for anesthetic injections. It is, for all purposes, a painless procedure done in the office within a few minutes. These plugs are very tiny and barely visible, if at all, to the naked eye.
An alternative to the punctal plug, is cautery closure of the punctal openings. In this minor procedure, heat is used to close off the punctal openings. Laser treatment can be used as an alternative to cautery, though it is usually not as effective as cautery in achieving complete occlusion.
Emmetropia
In this diagram of an eye with perfect vision, the rays of light from the object are being brought into sharp focus on the retina. The eye has no prescription and is called “emmetropic”. This is what you want with laser or other vision correction procedures.
Glaucoma
A condition in which there is progressive (gets worse with time, if untreated) damage of the optic nerves of the eyes. The damage of the optic nerves causes vision loss, usually the peripheral or side vision at first, but the straight ahead or central vision can eventually be damaged.
There was a time when the glaucoma was defined by increased eye pressure (intraocular pressure, not blood pressure), so that anything over 21 mm Hg (the unit of measure of pressure is millimeters of mercury, mm Hg) was considered abnormal. While eye pressure is still an important measure of glaucoma (for diagnosis and treatment), it is not the only factor. There are a significant number of patients affected by glaucoma, who do not have high eye pressures; some patients, in fact, have a condition called normal pressure (tension) glaucoma. Pressure may still be important in these normal-pressure glaucoma patients, but pressure-independent (non-pressure) factors may be relatively more important in this group (see below). The cut-off value of 21 mm Hg is no longer valid.
Traditionally, the pressure-dependent (high eye pressure) mechanisms by which the optic nerves are damaged in glaucoma was either mechanical or vascular. The mechanical theory states that increased eye pressure directly puts pressure on the optic nerve head to cause damage. The vascular or ischemic theory states that the increased eye pressure decreases blood flow to the optic nerves, indirectly damaging the nerves.
To explain why there are glaucoma patients with normal levels of intraocular pressure (normal-pressure glaucoma), the pressure-independent mechanisms of damage have been proposed.
While it is not exactly clear what initiates the damage in high-pressure or normal-pressure glaucoma, there are theories of what ultimately causes the death of the retinal ganglion cells (RGC) that make up the human optic nerve. Some of these point to toxic amino acids such as glutamate, interruption of chemicals that help nourish the RGC (neurotrophin starvation), defects in protective mechanisms (heat shock proteins), autoimmunity (one’s body attacking itself), and nitric oxide (NO) pathways of damage.
Besides high-pressure and normal pressure glaucoma, the disease can also be classified as open or narrow angle(angle closure) glaucoma. The angle of the eye is the part of the eye located where the iris, the colored part of the eye, and the cornea, the clear dome of the eye, meet. It is in the angle that the trabecular meshwork is located; this is the sieve-like structure though which the aqueous fluid drains out of the eye.
The human eye produces a watery fluid called aqueous humor, which provides nourishment to the internal parts of the eye. The fluid circulates throughout the anterior or front chamber of the eye, only to drain out of the eye through the trabecular meshwork. For patients who have open-angle glaucoma, the aqueous has easy access to the trabecular meshwork, but cannot drain out quickly enough, resulting in a build-up of fluid and therefore, pressure. For all purposes, there is resistance to fluid moving out through the trabecular meshwork. For patients who have narrow-angle glaucoma, there is very little space where the iris and cornea meet; the aqueous may have trouble getting into the angle itself, unable to drain out through the trabecular meshwork.
There are patients who have narrow angles, but no glaucoma. The angles are narrow but not enough to cause a problem with fluid drainage under most circumstances. These patients need to be followed carefully for changes in their condition. Some may go on to develop some form of narrow angle glaucoma.
There are many prescription and over-the-counter medications that may not be safe for patients who either have narrow angles or narrow angle glaucoma. Usually, these medications have labels that warn patients to ask their doctor if it’s safe to use these medications.
Hyperopia
The definition of farsightedness is a little more difficult to grasp. Someone who is farsighted may be able to see things in the distance clearly, and read without difficulty, if the amount of farsightedness is mild and the person is less than 40 years of age. Farsighted people can “self-correct” some or all of their farsightedness, without effort, when they are younger, but the ability to do this deteriorates as the 40s approach; first, near vision goes, and then even the distance gets fuzzy. Individuals who have a significant amount of farsightedness that cannot be “self-corrected” will complain of not being to see clearly up-close and even far away.
In this diagram of an eye with hyperopia or farsightedness, the rays of light from the object are being brought into sharp focus behind the retina, so the image on the retina is fuzzy. In essence, the cornea’s focusing power is too weak for the length of the eye.
Myopia
Very simply, without glasses or contacts, nearsighted people can see things up-close clearly, but things in the distance are fuzzy. The more nearsighted you are, the closer you have to hold things to see clearly.
In these diagrams of an eye with myopia or nearsightedness, the rays of light from the object are being brought into sharp focus in front of the retina, so the image on the retina is fuzzy. In essence, the cornea’s focusing power is too strong for the length of the eye.
Presbyopia
In patients under approximately 40 years of age, the natural crystalline lens retains the ability to flex in a process called accommodation. This allows an individual to generate the extra focusing power needed to read up close. After 40, the ability to accommodate diminishes more quickly, which results in a person needing bifocals or reading glasses. This normal, aging process by which accommodation diminishes, is called presbyopia. Nearsighted patients (who are affected by presbyopia like everyone else) may be able to read without glasses because by definition their focal point is up close, but if they wear glasses that correct for better distance vision, they will not be able to see up close without the addition of a bifocal segment or progressives.
Your Prescription
When my doctor measures my prescription (by what is called the “refraction”), what do the numbers on my glasses prescription mean?
If your eye is just nearsighted, there will be a single negative number. The minus sign indicates nearsightedness or myopia. The number that comes after the minus sign tells you the amount or “severity” of the nearsightedness.
Examples: -1.00 means one diopter of nearsightedness(a diopter is a unit of measure of focusing power, like an inch is a unit of measure of length) -5.25 means 5.25 or 5 and 1/4 diopters of near- sightedness. This is more nearsighted than -1.00, and so thicker glasses are needed.
If your eye is just farsighted, there will be a single positive number. The plus sign indicates farsightedness or hyperopia. The number that comes after the plus sign tells you the amount or “severity” of the farsightedness.
Examples: +1.00 means one diopter of farsightedness +5.75 means 5.75 or 5 and 3/4 diopters of farsightedness. This is more farsighted than +1.00, and so thicker glasses are needed.
If your eye has astigmatism, the numbers are harder to follow. There are actually 3 numbers in a prescription for an eye that has astigmatism. The general form is S x C x Axis.
Both S and C can be either positive or negative numbers. S refers to what is called the “sphere” or spherical portion of the prescription. The C refers to the amount of astigmatism. The Axis is a number anywhere between 0 and 180 degrees; this axis number tells where the difference in corneal curvature occurs or how the astigmatism is oriented or aligned. It is not enough to specify how much astigmatism there is, you have to know where the difference in curvature is taking place, by giving coordinates. So, if you see three numbers in your prescription, you have astigmatism of some kind and severity. The bigger the second number, C, the more the astigmatism you have. There are several categories of astigmatism, and by analyzing the 3-numbered prescription, you can tell the exact type of astigmatism you have.
Examples:
-2.00+1.50×180
-3.50+3.00×45
+4.00+1.00×89
-1.50+2.50×76
+1.00-2.50×66
Interestingly, the last 2 examples are identical, they are just in 2 different formats which depend on the signs of the first two numbers in each prescription. The signs are very important
Your Vision
When the doctor tells me what my vision is, what do the numbers mean?
First, the level of your vision is not the same as a glasses or contact lens prescription which can be taken to an optical shop to be filled. Vision is usually given in the Snellen format, for example, 20/40. If your vision is 20/40, it means an object you can see 20 feet away, can be seen from 40 feet away by someone who has perfect vision. Therefore, someone with 20/400 vision has even worse vision; the larger the denominator or the second number, the poorer the vision.
In the extreme, if the vision is even worse, such that a person cannot see the biggest letter on the eyechart, “E”, the number of fingers that can be counted is a way of measuring vision. If someone has “counting fingers at 3 feet”, it means the eye in question has worse than 20/400 vision, and can only identify the number of fingers held 3 feet away. The gold standard of perfect vision has been 20/20 vision, though there are patients capable of seeing better than “perfect”. While most patients use both eyes together, vision is tested in each eye separately, as is the measurement of a person’s prescription.