Uveitis Explained

12/18/14

Uveitis is defined as inflammation of the uveal tissue. The uvea includes the iris, ciliary body, and the choroid of the eye. The iris is located in the anterior compartment of the eye and acts like the aperture of the camera, precisely filtering the amount of light entering the eye. The ciliary body, which is attached posteriorly to the iris, is involved in both the production of the aqueous fluid in the eye as well as the accommodation of the lens apparatus. The choroid is a dense layer of blood vessels that sits underneath the retina on the back wall of the eye, helping to nourish and remove metabolic waste products from the retina. Inflammation of any of these structures will consequently cause disruption of the visual pathway and over the long term can cause permanent visual loss. In fact, uveitis is the third most common cause of preventable blindness in the developed world.

Symptoms of uveitis include blurry vision, ocular pain, photophobia, redness, and floaters. These can be acute in nature, lasting a few days to weeks, and in some cases can be chronic, lasting weeks or months. Anyone with any of these symptoms should see their eye care provider as soon as possible, as faster treatment of uveitis has shown to result in better long term visual outcomes.

Uveitis can affect virtually any part of the eye, from front to back. Anterior uveitis or iridocyclitis is confined to the iris, ciliary body, anterior chamber, and cornea. Inflammation affecting the vitreous is termed intermediate uveitis, or pars planitis, and any inflammation affecting only the retina or choroid is termed posterior uveitis. The term panuveitis may be used when multiple layers of the eye are affected.

There are many possible causes of uveitis, including infection, inflammatory diseases, autoimmune diseases, and trauma. However, the majority of cases of uveitis, approximately half, are considered idiopathic, where no etiology is ever found. Trauma is the next most common cause of intraocular inflammation, accounting for approximately 20% of all cases. The remaining cases are secondary to a systemic disorder or localized ocular condition. Systemic etiologies can include inflammatory disorders such as sarcoidosis, infections such as tuberculosis and syphilis, as well as autoimmune diseases such as rheumatoid arthritis and lupus.

Treatment of uveitis is aimed at both blunting the intraocular inflammation as well as addressing any underlying systemic etiology. The most common treatment is the use of corticosteroids. These can be taken orally, or used topically as eye drops. In some cases, corticosteroids can be injected in or near the eye as well. If the uveitis is caused by an infection, such as tuberculosis or syphilis, the patient is also given antibiotics. Systemic corticosteroids can have major side effects when taken chronically, such as weight gain, hair loss, osteoporosis, hypertension, secondary diabetes, psychosis, and reduced growth in children. Because of these potential problems, the chronic use of systemic corticosteroids is not recommended. In cases of chronic uveitis that require long term treatment, immunosuppressive agents with less known side effects such as methotrexate, cyclosporine, and mycophenolate mofetil (Cellcept) are more commonly used. However, these biologic agents have their own set of potential side effects and therefore, it is recommended that a rheumatologist should also be involved in the care of the patient when using these agents. Topical and intraocular steroids localized to the eye can cause elevated intraocular pressure as well as cataracts. In most cases, elevated intraocular pressure can be controlled with topical glaucoma drops, but in some cases surgical intervention is required to prevent severe glaucomatous damage.

The most common type of uveitis is acute anterior uveitis or iridocyclitis. Many cases of anterior uveitis are idiopathic though almost half of all cases are associated with the HLA- B27 haplotype. Systemic diseases associated with HLA-B27 include psoriatic arthritis, ankylosing spondylitis, reactive arthritis, and inflammatory bowel syndrome. Signs of anterior uveitis include redness of the eye, sometimes termed ciliary flush. The conjunctiva can become extremely red, and when associated with ocular pain and photophobia, is a strong indicator of anterior uveitis. Inflammatory cells found in the anterior chamber are the hallmark of anterior uveitis, sometimes deposited on the corneal endothelium (keratic precipitates) or iris (Bussaca nodules). Patients with anterior uveitis are typically treated with topical corticosteroid and cycloplegic eye drops. A laboratory workup for systemic etiologies is usually not necessary unless the patient experiences a recurrent episode.

Inflammation affecting primarily the vitreous cavity is known as intermediate uveitis or pars planitis. Inflammatory cells in the vitreous, known as vitritis, are typically bilateral, and when severe, can be found clumped in the vitreous cavity (snowballs) or deposited on the inferior pars plana (snowbanking). Intermediate uveitis is typically idiopathic though sarcoidosis, multiple sclerosis, and Lyme disease are also possible causes. Certain malignancies such as lymphoma can also ‘masquerade’ as intermediate uveitis, and when seen in older patients, should be suspected and ruled out.

Posterior uveitis involves the retina, choroid, and/or the retinal vasculature, and usually is more difficult to treat than anterior uveitis.

Uveitis Explained — This patient with Cat-scratch disease, caused by infection with Bartonella henselae, is an example of posterior uveitis. Note the characteristic star-like pattern of exudate in the macula along with optic nerve swelling.

In many cases, patients with posterior uveitis will exhibit characteristic exam findings that help narrow the differential diagnosis. For instance, an area of active retinitis next to an old pigmented chorioretinal scar is highly suggestive of toxoplasmosis. The most common symptom in patients with posterior uveitis is blurred vision. One of the more typical findings in posterior uveitis is macular edema, which is usually treated with periocular or intraocular corticosteroids.

In summary, uveitis is a visually threatening inflammatory condition that should be diagnosed and treated immediately. It is important to determine as best as possible the etiology of the uveitis and treat appropriately. In general, most patients with uveitis have good visual recovery with the proper management. However, in some cases, severe damage can occur, either due to the inflammation itself (usually chronic) or as a side effect of therapy (corticosteroids).

Richard H. Roe, MD, MHS
Retina-Vitreous Associates Medical Group

Drugs to Treat Dry AMD and Inflammation

12/2/14

Below is an article from the monthly Macular Degeneration Partnership E-Update on potential drugs to treat dry AMD and inflamation. To learn more about dry AMD, including stem cell treatments, go to AMD.org. You can also subscribe and have the monthly newsletter delivered to your inbox.

There are many causes of age-related macular degeneration and any of them may prove a good target for treatment for dry AMD. A long list of these was discussed at the recent Academy of Ophthalmology meeting. They were divided into the types of drugs being studied. We’ll look first at inflammation and the complement factor system, which is part of the immune system.

Inflammation is known to be associated with macular degeneration. The target may be the inflammation itself, or the cause of the inflammation.

Lampalizumab (or anti-Factor D) is a drug that is injected into the eye. In earlier Phase II trials, it was shown to reduce the area of the geographic atrophy by 20%. A Phase III clinical trial is now underway for individuals with geographic atrophy from dry AMD. Several research sites are actively recruiting now and many others will start recruiting in the near future. For more information and a list of participating centers, visit Clinical Trials.

LFG316 is also an antibody and an injection. This Phase 2 study is a randomized clinical trial of a drug that targets the C5 complement pathway (part of our immune system). It is designed to test the safety and efficacy of different doses of LFG316. There are three arms in the study: one group receiving a higher dose of the drug; one group receiving a lower dose of the drug; one group receiving a sham injection (no drug). These are successive monthly injections for people with geographic atrophy (GA). It is taking place in multiple locations throughout the U.S. and is sponsored by Novartis. For more information and a list of participating centers, visit Clinical Trials.

Oracea is a pill for dry macular degeneration, now in Phase II/III clinical trials around the U.S.. The pill contains doxycyline, which suppresses inflammation. Participants will be randomly assigned to either receive the drug or a placebo. More information at Clinical Trials.

Zimura by Ophthotech has been tested as a drug for wet AMD, but also seems to affect the drusen of dry AMD. Zimura targets the complement pathway plays a significant role in dry AMD. A Phase 2/3 clinical trial investigating ZimuraTM for treatment of geographic atrophy, is in the planning stages.

Eculizumab was also presented. This intravenous treatment for dry AMD did not show the desired effect in clinical trial, so no further development is planned at this time.

POT-4 is another drug that targets the complement factor system involved in inflammation. It is delivered through injection into the eye. The Phase I trial is completed and a Phase II clinical will be announced soon.

Iluvien is a drug delivery system that has been used in patients with diabetic retinopathy. A Phase II clinical trial for dry AMD is underway, though it is no longer recruiting patients. This is an implant inside the eye that releases fluocinolone acetonide. For more information, see Clinical Trials.

Judith Delgado
Executive Director
Macular Degeneration Partnership
A Program of the Discovery Eye Foundation

Diabetes And The Potential For Diabetic Retinopathy

11/20/14

Defining Diabetes

Diabetes mellitus is a group of metabolic disorders in which a person has high blood sugar levels. It occurs either because the pancreas does not produce enough insulin, or because the body does not respond appropriately to the insulin that is produced. Insulin is the hormone that converts sugar into energy for the body. There are several forms of diabetes.

Type 1 diabetes occurs when the pancreas does not produce adequate levels of insulin. It usually develops during childhood or adolescence; however, it can also occur in adults. Those with type 1 diabetes must take insulin injections. About 10 percent of those with diabetes have type 1.

Type 2 diabetes is the most common type of diabetes, affecting about 90 percent of those with diabetes. It is caused by the combination of the body’s resistance to insulin (not using its own insulin efficiently) and the pancreas not producing enough insulin. As a result, there is an increase in the level of sugar, or glucose, in the blood.

Gestational diabetes occurs in pregnant woman who have not previously had diabetes but whose blood sugars become elevated during pregnancy. In many patients, their blood sugars will return to normal after the pregnancy is over. Placental hormones make the mother resistant to insulin, causing a buildup of blood sugars. These women are at high risk for type 2 diabetes later on in their lives.

Diabetic Retinopathy: An Overview

Anyone with uncontrolled diabetes is at risk for developing diabetic retinopathy. According to the National Eye Institute, between 40 to 45 percent of Americans with diabetes have some form of diabetic retinopathy, the most common eye condition associated with diabetes.

In the United States, the Centers for Disease Control and Prevention reports between 12,000 and 24,000 new cases of blindness each year due to diabetic retinopathy, making it the leading cause of vision loss among American adults, ages twenty to seventy-four. The Center also projects that by 2050, the number of Americans age forty and older with diabetic retinopathy will grow from a current 5 million individuals to about 16 million. Although these statistics are alarming, you can prevent or delay damage to your vision by controlling your diabetes, along with obtaining regular eye evaluations and treatment.

Defining Diabetic Retinopathy
Diabetic retinopathy is a disease affecting the retina, caused by elevated blood sugar levels. It usually affects both eyes and occurs when uncontrolled blood sugar levels damage the small vessels of the retina, the light-sensitive tissue in the back of your eye. The retina is responsible for processing images that make vision possible. To produce clear, distortion-free vision, the retina must lie completely flat. If the delicate retinal tissue is damaged, images that you see may be blurred or distorted.

Diabetic retinopathy is a progressive disease, and thus worsens over time. Although some effects, such as blurriness and distortions, may be mild or subtle, the long-term consequences can cause severe vision loss.

Symptoms of Diabetic Retinopathy

Because diabetic retinopathy rarely causes pain, symptoms are not always apparent in the earliest stages. In fact, damage to your retina could be occurring long before you have noticeable signs. When symptoms do occur, they’re often caused by retinopathy affecting the macula, the area at the center of the retina. Symptoms may include the following:

• blurred vision

• seeing dark spots or “floaters” (small specs in your field of vision)

• decreased night vision

• vision loss

• problems seeing colors

It’s important that you see your eye specialist immediately if you have any such symptoms. Diabetic retinopathy cannot be cured, but with careful monitoring, it can be diagnosed and treated, before your vision is impaired. The treatment is typically less invasive and more effective when diagnosed at an earlier stage, before permanent damage has occurred.

How the Retina Works

The retina is made up of specialized nerve tissue that contain microscopic receptors (called cones and rods) and other nerve cells that line the back of the eyeball.

These cells carry signals (images that we see) along the optic nerve to a special area of the brain, where they’re interpreted into what we perceive as sight. You might compare the retina to film in a camera—the film delivers the photo image that the camera captures.

There are two main areas of the retina that can be damaged by diabetic retinopathy:

• The macula, the center of the retina. The macula allows you to read and see fine details and recognize colors. At the very center of the macula is a dimple known as the fovea. It is the most sensitive portion of the macula and makes sharp vision possible.

• The peripheral retina, which is the portion of the retina that is outside the macula. It’s responsible for your side vision and also makes night vision possible.

The retina lies on a nutrient-rich flat “carpet” of vessels that nourish it with necessary oxygen and nutrients. To reach the retina, however, nutrients must pass through two buffers—a thin membrane called Bruch’s membrane and a single layer of specialized cells called the retinal pigment epithelium. Waste products are also transported away from the retina through these two membranes. Diabetic retinopathy can interfere with this constant import of necessary nutrients and export of waste products.

Risk Factors for Diabetic Retinopathy

There are many factors that can raise your risk for diabetic retinopathy. However, you’ll note that many of these risk factors can be controlled.

Duration of Diabetes and Glucose Control

The longer you’ve had poorly controlled blood glucose levels, the higher your risk for diabetic retinopathy. Most diabetic individuals develop eye problems overtime, making duration of their diabetes one of the strongest predictors that they will develop this eye disease. Research has shown that nearly all type 1 diabetics and 60 percent of type 2 diabetics develop the condition within the first two decades of their diabetes diagnosis.

The American Diabetes Association (ADA) recommends fasting glucose levels between 70 and 120 mg/dL and less than 180 mg/dL two hours after meals. They also recommend a hemoglobin A1c of 7 percent of less. Hemoglobin A1c is a protein in red blood cells that bonds with blood sugars. Since red blood cells can live from 90 to 120 days, the hemoglobin A1c stays in the blood for that length of time. Accordingly, it is effective in measuring the average blood sugars over a period of time. This test tells doctors how well your treatment plan is working. You should always know what your hemoglobin A1c values are, as they may affect the interval between your retinal examinations.

Obesity

The more fatty tissue you have, the more resistant your cells are to insulin. Obesity increases your risk for diabetes as well as other serious conditions such as heart disease. Estimates suggest that 65 percent of Americans may be overweight. Being overweight aggravates high blood pressure and cholesterol. Achieving a healthy weight is important in controlling blood sugars and diabetes related complications.

Lifestyle Choices

A sedentary lifestyle, especially if you are overweight, contributes to many diseases, including diabetes, heart disease, high blood pressure, and high cholesterol levels. On the other hand, physical exercise improves circulation, lowers blood sugars, and improves your body’s use of insulin. This results in improved blood sugar levels. This benefit of increased sensitivity to insulin continues for hours after you stop exercising.

Exercise also promotes weight loss. A sedentary lifestyle contributes to insulin resistance, and makes it more difficult to keep weight off. Even light or moderate physical activity can help lower blood sugars.

Smoking is another major risk factor for developing diabetic retinopathy. Smoking also causes diabetic retinopathy to progress faster. The nicotine in tobacco not only contributes to higher blood pressure and higher cholesterol levels, but it also impairs insulin activity. Even though quitting can be difficult, it is critical to heart health and diabetes control.
Unlike smoking, alcohol consumption doesn’t have a direct influence on diabetic retinopathy. Yet because it can affect diabetes control, drinking in excess can affect the health of your eyes. Your doctor can tell you what constitutes drinking in moderation for you.

High Cholesterol Levels

Diabetes puts you at risk for chronically high cholesterol or blood fats that promote the buildup of plaque in your arteries. Although the tiniest vessels of the retina are too small for such build-up, uncontrolled cholesterol can contribute to macular edema and the development of hard exudates, the small yellow spots or lipid deposits that may form in the macula. Both conditions are associated with a higher risk of vision loss.

Doctors advise keeping “bad” or low density cholesterol (LDLs) less than 70 mg/dL. Good cholesterol or high density lipoproteins (HDLs) should be greater than 40 mg/dL in men and 50 mg/dL in women. Both men and women should strive for triglycerides, another type of fat, at levels less than 150.

High Blood Pressure

If you have both diabetes and high blood pressure (also called hypertension), you may be at higher risk for a number of eye-related problems, including retinopathy, glaucoma and optic nerve damage. Seriously elevated blood pressure not only stresses your heart, it also raises the risk for eye problems, particularly macular edema and bleeding. Chronic hypertension combined with long-term diabetes also increases the chance that your retinopathy will be more destructive and progress more rapidly. Research has consistently shown that keeping your blood pressure below 130/80 mmHg is important in minimizing the risk of hypertension related complications.

Race/Ethnicity

Diabetic retinopathy is more common in some ethnic and racial groups than others. African Americans, Asian Americans, Hispanic/Latino Americans, American Indians and Alaskan Natives are at higher risk for type 2 diabetes than non-Hispanic whites.

African Americans and Mexicans are almost twice as likely as whites to have eye problems, according to the American Diabetes Association. Native Americans also have an increased for diabetic retinopathy. Researchers aren’t sure why some ethnic groups have higher rates of diabetes, which increase the risk for retinopathy and other problems.

Age and Gender

As mentioned earlier, the longer you have diabetes, the greater your risk for diabetic retinopathy. Not surprisingly, this complication is rare among children but common among older diabetic adults. A recent study by Prevent Blindness America and the National Eye Institute, demonstrated that older adult Americans are facing a bigger threat of all age-related eye diseases (diabetic retinopathy, age-related macular degeneration, cataracts and open angle glaucoma) today than at any other time.

Genetics

Our genetic make up has an important effect on our predisposition for many health issues such as diabetes. Scientists believe that many genes or combinations of genes either promote diabetes in certain individuals or protect them from developing it.

Scientists have yet to identify every gene involved in type 1 and type 2 diabetes, but they have shown that genetics are a factor. Research studies of identical twins, for instance, have demonstrated that if one twin has type 1 diabetes, the other twin has a 50 percent change of developing the disease. If one twin has type 2 diabetes, the other twin has a 75 percent chance of developing it.

Pregnancy

Gestational diabetes is a type of diabetes linked to pregnancy; however, diabetic retinopathy is usually not a complication in these women. However, if you’re already a diabetic and become pregnant, you are at an increased risk of developing diabetic retinopathy. This is a result of the hormonal and metabolic changes that occur during pregnancy, making the disease and its complications progress more rapidly. It is recommended that you see a retinal specialist for evaluation and monitoring.

In Summary

• Diabetic retinopathy is a serious complication of diabetes that results from high glucose levels damaging the retinal blood vessels. This can cause loss of vision.

• Between 40 and 45 percent of diabetic Americans have some form of diabetic retinopathy.

• The earliest form of the disease is called background diabetic retinopathy. With time it progresses to mild, moderate, or severe nonproliferative diabetic retinopathy.

• Without proper diagnosis and treatment of nonproliferative diabetic retinopathy, the condition can advance to proliferative diabetic retinopathy, which is a serious sight-threatening stage of the disease.

• Macular edema is due to build up of fluid and thickening of the macula and can occur with any type of diabetic retinopathy. It is the most common cause of vision loss in those with diabetes.

• The duration of your diabetes and how well blood glucose is controlled are major risk factors for the development and progression of diabetic retinopathy.

• Other risk factors that play a significant role in the development of retinopathy, include high blood pressure, high cholesterol, and smoking.

• As an individual with diabetes, you’re also at increased risk for other eye diseases, especially glaucoma, cataracts, retinal vein occlusion and optic nerve damage.

• Good blood sugar control, regular eye examination, and timely treatment are the key factors in reducing the damage to the eye and keeping your vision.

Pouya N. Dayani, MD
Retina-Vitreous Associates Medical Group

Diabetes Awareness Month & Diabetic Eye Disease

11/11/14

Even though people with diabetes are at a greater risk of developing blinding eye diseases, a recent study of Medicare beneficiaries show that very few of the people at risk have a preventative yearly eye exam.

Facts About Diabetes

In the US there are 29.1 million that have diabetes, 21 million have been diagnosed and 8.1 million are undiagnosed. Unfortunately, if left undiagnosed or untreated, diabetes can lead to serious health problems such as high blood pressure, increased LDL cholesterol, heart disease, stroke, kidney disease and blindness.

Although African-Americans and Hispanics are more likely to have diabetes, less than a third are aware of diabetic eye disease. And for those that have been diagnosed with diabetes, where a yearly eye exam is considered essential, ¾ of them have not had an eye exam in five years.

Diabetic Eye Disease – 3 Ways Diabetes Affects Vision

Diabetic retinopathy affects 28.5% of people 40 and older that have been diagnosed with diabetes. It happens when the blood vessels in the retina are damaged by leaking or blocking blood flow to the retina (the source of your central vision for reading, driving, recognizing faces, etc.) and if untreated, it can lead to complete blindness. In the very early stages there are no symptoms. And while there are some treatments that may help slow the progression of the macular edema, there is no way to regain sight that is lost.

Cataracts occur when there is a clouding of the eye’s lens, making your vision blurry or cloudy. While it is a normal for this to happen as a person ages, someone with diabetes is more likely to develop them at an earlier age. While beginning cataracts can be treated with glasses, when they become more advanced, cataract surgery will be needed to replace the cloudy lens with an artificial lens.

glauccoma diabetic eye disease — Courtesy of National Eye Institute, National Institutes of Health

A person with diabetes is nearly twice as likely to get glaucoma as other adults. Glaucoma is an eye disease that damages the optic nerve. The damage occurs when the pressure in the eye increases, squeezing the optic nerve and restricting its visual transmissions to the brain. Like diabetic retinopathy, you rarely notice any changes in your vision in the early stages, but as it progresses you begin to lose your peripheral vision. It can be treated with eye drops or surgery, but left untreated it can result in blindness.

Controlling Diabetes

Diabetes can be controlled, and some cases prevented, with careful attention to diet, watching your weight and exercise. Also learn your family medical history. You are at a higher risk of diabetes if a mother, father, brother or sister has the disease. If you are diagnosed with diabetes, make sure you have a yearly comprehensive eye exam to avoid vision loss. To learn more about diabetes go to www.ndep.nih.gov.

Susan DeRemer, CFRE
Vice Pesident of Development
Discovery Eye Foundation

Posterior Vitreous Detachment

10/30/14

Have you ever noticed floaters in your vision? Perhaps they looked like a bunch of small dots or maybe a cobweb swaying back and forth in your visual field. Were the floaters associated with flashing lights that made you think there was a lightning storm coming your way? These are typical symptoms of a posterior vitreous detachment (PVD), and if you have had these symptoms you are far from alone.

PVD is a natural process that occurs in the majority of people usually over the age of 50. The vitreous is a jelly-like substance that occupies the back portion of the eye. The vitreous is comprised primarily of water, which accounts for 99% of its volume, and the remaining 1% includes proteinaceous substances such as collagen fibers as well as hyaluronic and ascorbic acids. The collagen fibers act as a scaffold to allow the vitreous to maintain a formed shape as well as provide a means for the vitreous to attach to the retina, which is the light-sensitive tissue that lines the inner back wall of the eye and is critical for vision. As we age, changes in these fibers cause the vitreous to lose its shape and eventually pull away from the retina. When the vitreous separates from the retina, this is called a PVD.

As we age, the collagen components of the vitreous can clump together and are free to float in the eye. When the vitreous separates from the retina during the development of a PVD, the floaters may become more noticeable or numerous. It is common for patients to describe floaters of different shapes and sizes, and patients may notice just one or in some cases many. In many people, a PVD develops slowly and there may be no symptoms or just a few annoying floaters. In others, a PVD may occur abruptly and cause more dramatic symptoms that can be very anxiety provoking.

Since the normal process of PVD development involves the vitreous tugging on the retina until it can fully separate, this tugging can result in flashing lights that can commonly appear in the peripheral, or side, vision. These flashing lights are sometimes described as lightning streaks, and patients may notice them more readily in settings with low ambient light. The flashes of light typically resolve once the vitreous has fully separated from the retina and the tugging has ceased.

The good news is that PVD is usually harmless in the vast majority of cases, and the annoying floaters will become less bothersome over time. In approximately 5-10% of cases, the vitreous can tug too hard on the retina as it tries to separate and it may pull a hole or tear in the retina. Tears in the retina can predispose to retinal detachment, which is a serious condition that can lead to permanent vision loss.
It is important to recognize that the typical symptoms of a regular PVD are often similar to a PVD with an associated tear. For this reason, it is recommended that all patients with the new onset of floaters or flashes have a dilated eye exam. If a retinal tear or detachment is discovered, early treatment can help prevent loss of vision.

Treatment for PVD usually involves simple observation. With time, the flashes will go away, and the floaters will become less noticeable. More recently, few providers have claimed that floaters can be treated with a laser in order to make them less noticeable. I would caution that this is not mainstream therapy at the current time, and I do not advise my patients to pursue this option. Another treatment possibility is vitrectomy surgery, where the vitreous gel is removed as part of a surgical procedure. Due to safety advances in vitrectomy surgery, this is now a potential option for the rare patient who has floaters that are so numerous and bothersome that they are negatively impacting their activities of daily living. For the vast majority of patients this is not necessary.

When I see a patient with a PVD, I often recommend one follow-up visit in 4-6 weeks to make sure there are no retinal holes or tears that have developed in the interim. If the other eye has not had a PVD yet, I will counsel them that a PVD will most likely develop in that eye within the next few years, and when it does they need to be examined. I will also discuss the retinal detachment warning signs. Patients with retinal detachment will not only have symptoms similar to PVD, including flashes and floaters, but in addition they may also notice what looks like a black shade or curtain that starts in the peripheral vision and extends towards the central vision. My patients are taught that this symptom requires an immediate examination.

In conclusion, PVD is a natural process that the majority of people will experience in their lives. The symptoms can range from having no symptoms at all to many floaters with associated lightning flashes. In the majority of patients, there is no damage to the eye or threat to the vision. A dilated exam is recommended to look for possible holes or tears in the retina, and if these are uncovered, prompt treatment can prevent vision loss.

Daniel D. Esmaili, MD
Retina Vitreous Associates Medical Group

Night Blindness

10/28/14

As the number of daylight hours decrease and daylight savings time is about to end, many of us feel that the days are getting much shorter. If you suffer from night blindness, your days are shorter, because getting around or driving at night, are sometimes impossible.

Night blindness is a condition that makes it difficult for a person to see in low-light situations or at night. Some types are treatable, while others are not. You will need to consult your eye doctor to determine the underlying cause of your night blindness to determine what can or cannot be done.

There are several things that could cause night blindness:
•Cataracts
•Genetic eye disease
•Vitamin A deficiency
•Diabetes
•Aging eye
•Sunlight exposure

Here is a brief look at each.
Cataracts – This is when the lens of the eye becomes gradually becomes clouded, reducing vision. Besides reducing vision at night you may also experience halos around lights. This is a treatable condition requiring cataract surgery and replacing your clouded lens with a clear artificial lens. Your vision should improve considerably.

Genetic Eye Disease – Both retinitis pigmentosa or Usher syndrome are progressive genetic eye diseases where the rods that regulate light, and cones that control color perception and detail die. Progressive night blindness is one of the first visual symptoms of these two diseases. Currently there is no treatment for them as there is no way to treat or replace the dying rods.

Vitamin A Deficiency – While rare in the US, it can be a result of other diseases or conditions such as Crohn’s disease, celiac disease, cystic fibrosis or problems with the pancreas. Options to help with the deficiency include vitamin supplements suggested by your doctor, or increasing your intake of orange, yellow or green leafy vegetables.

Diabetes – People with diabetes are at higher risk for night vision problems because of the damage to the blood vessels and nerves in the resulting in diabetic retinopathy. Not only can it cause poor night vision, it may also take longer to see normally after coming indoors from bright light outside. There is no cure, but controlling blood sugar levels with medicine and diet can help prevent developing retinopathy or help slow the progression.

Aging Eye – As we age several things happen to our eyes. Our iris, which regulates the amount of light going into the eye, gets weaker and less responsive. This can make adapting from light to dark more difficult and slower. Our pupils shrink slightly allowing less light into the eye. The lens of the eye becomes cloudier, as explained above in cataracts, limiting the amount of light into the eye. We also have fewer rods for light perception. Aside from cataract surgery there is no treatment for age-related night blindness. However, eating a diet rich in fruits and vegetables and low in saturated fat is the best way to slow the progression. Here is more information on how the aging eye is affected.

Sunlight Exposure – If your night vision seems temporarily worse after a trip to the beach or a day on the ski slopes, it probably is. Sustained bright sunlight can impair your vision, especially if you fail to wear sunglasses or goggles.

Night blindness due to genetic conditions or aging cannot be prevented. However if you protect your eyes from extreme sunlight, eat a healthy diet, and monitor blood sugar levels if needed, you can reduce your chances for night blindness.

As we head into the holiday season, you should know that some great sources of vitamin A include sweet potatoes, butternut squash and … pumpkins!

Susan DeRemer, CFRE
Vice President of Development

15 Things Doctors Might Like Us To Know

10/16/14

The Doctor Patient Relationship

Doctors are human. Professional decorum may not let them speak their minds and for that reason, I have gathered comments heard from eye doctors with whom I have been privileged to associate as a so-called “expert patient”. These may not speak for all, but I do think they represent the majority. Here are 15 of the most important, which we might benefit from hearing.

1. Your eyes are growing older, and I can’t turn back the years in an aging retina. I can, however, help you try to maintain your current vision for as long as possible.

2. Your appreciation means a lot. Don’t hesitate to compliment me if I have earned it.

3. I have quite a few patients who need my help and don’t want to be kept waiting. So I don’t have to keep repeating myself, please take notes, or bring someone with you who can refresh your memory later.

4. It is important that you comply with my instructions and show up for appointments if you want the best results.

5. My specialty is eye care. I will, however, try to provide you with resources for other ailments you may have.

6. Please be concise with your questions and stay on topic, so I’ll have time to treat other deserving patients.

7. Don’t believe everything you see in the media unless the source is reliable. If the information isn’t based on good evidence, my response to you may be disappointingly negative.

8. My services may seem expensive, but I have so many expenses and debts resulting from my profession that my bottom line may not be much different than yours.

9. An ethical physician will not choose a particular drug or treatment by how much of a profit he can make prescribing it.

10. I might not agree with everything you say, but rest assured that I will never let it affect the level of care I will provide.

11. Don’t expect me to keep all eye research in my head. I do know where to look it up, so allow me some time to get back to you on some questions.

12. Conferences I attend are sometimes in exotic places, but most of the time is spent going from one event to another, so it is really not a vacation.

13. Even if there is no current effective treatment for your eye disease, I still need to see you regularly to monitor your condition. Regular check-ups are important to your health and preventative care and treatment options are changing all the time.

14. I may not remember you personally, especially in the beginning or if I see you only see you once or twice a year, but your records contain everything I need to know to care for your vision.

15. I may not agree with your decision to try an alternative treatment, but I respect your right to do so. All I ask is that you seriously consider my opinion, and if you decide to go ahead with the treatment on your own, please keep me in the loop so I can monitor your condition.

We should try to understand that doctors are human beings who truly care about our welfare. Doing so could turn a top-down doctor-patient relationship into one of mutual respect and understanding. We might even get a few extra minutes of precious time in the chair, just because we’re a pleasure to have around.

Dan Roberts
“Expert Patient”

What Are A Macular Pucker and Macular Hole?

10/9/14

What is the macula?
The eye is very much like a camera, taking light from the outside world and converting it into picture information that our brains perceive as vision. The retina is the light sensitive layer in the back of the eye that is very much like the film in that camera. The central retina, also known as the macula, is essential for crisp, high definition vision. Conditions that damage or distort the macula can therefore result in blurred or distorted vision. Two common conditions that affect the macula are macular puckers and macular holes.

What is a macular pucker or macular hole?
A macular pucker is a thin layer of scar tissue that forms on top of the retina. The amount of scar tissue can range from mild to severe. Mild macular puckers may be barely noticeable during an eye exam and resemble a fine layer of cellophane resting on the macula. More severe macular puckers can cause wrinkling or distortion of the macula. In contrast to a macular pucker, a macular hole is a small gap that extends through the entire thickness of the macula.

What are the symptoms of a macular pucker or a macular hole?
At first, a macular pucker may lead to mild blurring of the central vision. Because the problem involves the back of the eye, glasses will not completely restore vision. More severe macular puckers may result in wavy or distorted vision. For instance, objects that normally appear straight, such as venetian blinds or a printed line of text, might appear to have a dip or bend in the center. Small macular holes can cause similar symptoms of blurring or distortion. Larger macular holes often result in a central blind spot. This can also result in straight lines appearing broken or having a piece missing in the middle. Patients with a macular pucker or hole do not normally experience difficulty with peripheral vision.

What can cause a macular pucker or macular hole?
Recall that a macular pucker is a scar tissue. Anything that causes scar tissue, such as trauma or inflammation in the eye, can result in scar tissue and hence a macular pucker. Certain diseases that affect the retinal blood vessels such as diabetes can also cause a macular pucker to form. However, one of the most common causes of macular pucker is simple aging of structures within the eye. As the eye ages, the clear jelly that fills it, called the vitreous gel, shrinks. When enough shrinkage occurs, the vitreous gel detaches from its normal position adjacent to the retina. This process of vitreous detachment can cause microscopic damage or inflammation leading to macular pucker formation. In some cases, the vitreous gel does not detach cleanly from the retina. Instead it can put traction on the macula, pulling its delicate structures apart in the center, resulting in a macular hole.

How are macular puckers and macular holes diagnosed?
A simple examination from an ophthalmologist or retina specialist is often enough to diagnose a macular pucker or hole. However, additional testing is often useful in diagnosing subtle cases or monitoring eyes for changes. An optical coherence tomography (OCT) scan is a specialized photograph that allows your physician to look for microscopic changes in the contour of the macula. The following figures show an OCT of a normal macula, a macular hole, and a macular pucker. Note that the normal macula has a central dip known as the fovea, shown in Figure 1. In Figure 2, the dip is replaced by a gap which is a macular hole. Finally, Figure 3 shows a macular pucker where the dip is no longer visible. This is because the macular pucker, seen as a thin white line is distorting the normal shape of the macula.

Normal - Macular Pucker and Macular Hole — **Figure 1: Normal Macula**

Hole - Macular Pucker and Macular Hole — **Figure 2: Macular Hole**

Pucker - Macular Pucker and Macular Hole — **Figure 3: Macular Pucker**

What treatments are available for macular puckers and macular holes?
Macular puckers can be quite mild. For mild cases in patients with minimal symptoms, periodic monitoring may be all that is required. When blurred vision due to a macular pucker begins to affect activities such as driving or reading, treatment in the form of surgery can be considered. Surgery for a macular pucker is known as a vitrectomy. Vitrectomy surgery is usually done under local anesthesia and as an outpatient procedure. During the surgery, fine instruments are used to remove the scar tissue from the surface of the macula. After surgery, patients usually experience an improvement in the blurring and distortion as the eye recovers gradually over a period of months. Some residual waviness can be normal. Vitrectomy is generally very safe although there is a chance of increased cataract growth and a small risk of infection or retinal detachment.

For patients with small macular holes, close monitoring can also be an option since some macular holes can close on their own. For larger holes, there are two options. In select cases where the vitreous gel is actively pulling on the macula, an injection of medication into the eye may cause the gel to release cleanly, allowing the hole to close. In other cases, vitrectomy is recommended. During the surgery, any pulling on the macula is relieved and a gas bubble is placed in the eye to help the hole close. After surgery, patients are asked to look down for a several days to allow the bubble to float up against the hole. Once the body absorbs the bubble, vision is usually significantly improved.
In summary, both macular puckers and holes are common causes of blurry or distorted central vision. If treatment or surgery by a retina specialist is needed, the results are generally quite good and lead to significant restoration of vision.

David Liao, MD, PhD
Retina-Vitreous Medical Group

Our Thanks to Guest Bloggers Continues

10/7/14

More Amazing Guest Bloggers

Last week I took the opportunity to thank our very first guest bloggers for helping us launch the Discovery Eye Foundation Blog. We are pleased that so many people appreciate the wide range of eye-related information from eye care professionals, as well as the stories from people that live with eye disease on a daily basis.

Here is a round-up of guest bloggers since June 2014 that shared their time, experience and/or expertise to provide you with the best eye-related information.

Sumit “Sam“ Garg, MD – what you should know about cataracts

Randall V. Wong, MD – floaters, causes and treatments

Roy Kennedy – his personal experiences with the miniature telescope implant

Sandra Young, OD – the importance of getting vitamins and minerals from your food and not just supplements

Jeanette Hasseman – living with keratoconus

Greg Shane – theater for the blind

Caitlin Hernandez – blind actress and playwright

Jullia A. Rosdahl, MD, PhD – lasers for glaucoma and genetics and glaucoma

Maureen A. Duffy, CVRT – ways to reduce harmful effects of sun glare

Kooshay Malek – what is it like to lose your vision and being a blind therapist

Jeffrey J. Walline, OD PhD – children and contact lenses

Robert Mahoney – choosing a home care agency

Robert W. Lingua, MD – nystagmus in children

Buddy Russell, FCLSA, COMT – common pediatric eye diseases, treatment options for children and pediatric contact lenses

NIH (National Institute of Health) – telemedicine for ROP diagnosis

Harriet A. Hall, MD – evaluating online treatment claims

Patty Gadjewski – the life-changing effects of a telescopic implant

Michael A. Ward, MMSc, FAAO – proper contact lens care and wearing contacts and using cosmetics

Susan DeRemer, CFRE
Vice President of Development
Discovery Eye Foundation

Our First Three Months Of Eye Care

9/30/14

Discovery Eye Foundation Blog’s First Three Months

It is hard to believe, but this blog has been providing information and insights into eye disease, treatment options, personal experiences of living with vision loss, and other eye-related information for seven months.

All of this would not have been possible without the expertise of remarkable eye care professionals who took time out of their busy schedules to share information to help you cope with vision loss through a better understanding of your eye condition and practical tips. Since so much information was shared in the seven months, here is a look at the first three months, with the additional four months to be reviewed next Tuesday.

I am very thankful to these caring eye professionals and those with vision loss who were willing to share their stories:

Marjan Farid, MD – corneal transplants and new hope for corneal scarring

Bill Takeshita, OD, FAAO, FCOVD – proper lighting to get the most out of your vision and reduce eyestrain

Maureen A. Duffy, CVRT – low vision resources

M. Cristina Kenney, MD, PhD – the differences in the immune system of a person with age-related macular degeneration

Bezalel Schendowich, OD – blinking and dealing with eyestrain

Jason Marsack, PhD – using wavefront technology with custom contact lenses

S. Barry Eiden, OD, FAAO – contact lens fitting for keratoconus

Arthur B. Epstein, OD, FAAO – dry eye and tear dysfunction

Jeffrey Sonsino, OD, FAAO – using OCT to evaluate contact lenses

Lylas G. Mogk, MD – Charles Bonnet Syndrome

Dean Lloyd, Esq – living with the Argus II

Gil Johnson – employment for seniors with aging eyes

We would like to extend our thanks to these eye care professionals, and to you, the reader, for helping to make this blog a success. Please subscribe to the blog and share it with your family, friends and doctors.