Center for Retinal Diseases & Surgery, LLC

About Diabetic Retinopathy Diabetes mellitus causes a persistent elevation of blood sugar which eventually results in damage to the blood vessels within the retina. These damaging changes are known as diabetic retinopathy. Non-Proliferative Diabetic Retinopathy Non-Proliferative Diabetic Retinopathy or NPDR is an early stage of disease where tiny red spots appear in the retina. These spots may represent blood (hemorrhage) or abnormal pouching of the tiniest blood vessels or capillaries (microaneurysms). The lining of these blood vessels can become damaged enough to allow leakage of fluid (serum) and/or fatty material (exudates) into the retina to cause swelling (edema). This swelling, if it involves the central retina, is referred to as macular edema. Diabetic Retinopathy - hard exudates Such involvement of the macula can affect our high-resolution visual activities such as reading, driving, or threading a needle. As NPDR progresses, the smallest blood vessels (capillaries) can close leading to a loss of blood supply to the retina called ischemia. Proliferative Diabetic Retinopathy With more extensive loss of blood supply and because the retina is so oxygen-needy, abnormal new blood vessels (retinal neovascularization) will grow in an effort to supply blood to damaged retina. This more advanced stage of disease, called Proliferative Diabetic Retinopathy or PDR, can lead to severe vision loss if not recognized and left untreated. The abnormal new blood vessels typical of PDR do not resupply the retina and are extremely fragile unlike normal healthy retinal blood vessels. As the abnormal blood vessels grow along the surface of the retina, optic nerve, and into the vitreous cavity (the clear jelly-like sac which occupies the center of the eye), bleeding (vitreous hemorrhage) can occur. If the hemorrhage is small, the patient may only notice spots, floaters, or “cobwebs.” Larger hemorrhages can lead to severe loss of central and peripheral vision. With advancement of disease, scar tissue can grow with the abnormal new blood vessels. As the scar tissue contracts, it can pull on the retina resulting in traction retinal detachment. Limited involvement of the macula may result only in visual distortion, but larger areas of detachment can result in severe vision loss. Sometimes the retinal ischemia can be so extensive that abnormal blood vessels will grow over the iris which is the colored part of the eye. If this occurs, the new blood vessels can scar the front of the eye and block normal outflow of fluid resulting in a frequently painful and potentially blinding condition called neovascular glaucoma. Treatment Landmark clinical trials have established that careful and strict control of blood sugar will significantly reduce one’s risk of vision loss from diabetic retinopathy. Even in patients who have evidence of retinopathy, improving blood sugar control can lower the risk for long-term progression of disease. Laser. Laser treatment (specially focused light), has been the established standard-of-care for diabetic retinopathy for decades. A small focal or grid laser treatment can be applied to treat macular edema by reducing leakage from the damaged blood vessels near the macula. This treatment has been shown to limit worsening of edema and the risk of further vision loss. Panretinal Photocoagulation or scatter laser treatment is used to manage the abnormal new blood vessel growth from PDR. The peripheral damaged retinal tissue is treated so that the new blood vessels will shrink and limit or prevent additional scar tissue growth which could lead to vitreous hemorrhage and retinal detachment. It’s not uncommon for both types of laser treatment to be repeated as necessary to stabilize but not cure the disease. Intravitreal Injections During the past decade intravitreal steroids and bevacizumab (Avastin) have been used in an “off-label” fashion as additional treatments for diabetic retinopathy. These medicines, when injected into the eye, can control inflammation and Vascular Endothelial Growth Factor (VEGF) expression, both of which have been shown to cause retinopathy progression, in the eye. Ranibizumab (Lucentis) also targets VEGF and has very recently received approval for treatment of diabetic retinopathy. Aflibercept (Eylea) is another FDA-approved agent which is similarly effective to other anti-VEGF agents and in some patients with poor vision may represent a more advantageous treatment functionally. Ozurdex is an FDA-approved sustained-release intravitreal steroid implant that is very effective in treating diabetic macular edema (DME) and has the advantage of exerting a more durable treatment effect allowing a reduction in frequency of eye injections. As with other steroid preparations used in and around the eye, there is an increased risk of cataract progression and glaucoma.

About Macular Degeneration Macular degeneration, also known as age-related macular degeneration (AMD) is a common condition in older adults and the leading cause of vision loss in people over the age of 65. Macular degeneration affects the macula, the part of the retina responsible for sharp, detailed vision needed for reading or driving. As one ages, the retinal tissue responsible for central vision slowly begins to deteriorate, and this change can significantly affect a patient’s quality of life. Types Macular degeneration can be classified as either wet (neovascular) or dry (non-neovascular). Dry macular degeneration is the more common diagnosis, and is considered to be an early stage of the disease characterized by the development of aging deposits called macular drusen and the deposition of pigment under the retina. If the disease progresses, the retinal vision cells and their underlying supportive pigmented layer will degenerate, producing geographic atrophy, the disappearance of the retinal tissue. AMR - dry Only about 10% of patients see their condition progress to the more advanced and damaging wet macular degeneration. In wet macular degeneration, new blood vessels develop beneath the retina and cause leakage of blood and fluid under the retina. This leakage can lead to permanent damage of central vision and the creation of blind spots. Although it’s the less common form, wet macular degeneration, until recently, has been responsible for nearly 90% of the cases of severe vision loss caused by AMD. Symptoms Patients with dry macular degeneration may notice gradual changes in their vision, including shadowy areas in the central vision, or fuzzy and distorted vision. These areas grow larger as the disease progresses, and can eventually turn into blind spots if geographic atrophy develops. Patients may also have difficulty seeing color and fine details. If the disease advances to the wet form, patients more commonly may also see straight lines as wavy or new blurry spots. With wet macular degeneration, the central vision loss can occur rapidly, sometimes within a few days or weeks. Patients with a family history or diagnosis of AMD can monitor their vision at home using an Amsler grid test. Other home-based electronic systems, now commercially available, may be useful in patients with signs of disease which place patients at higher risk for vision loss. Diagnosis Your ophthalmologist can detect early signs of AMD, before the onset of symptoms, through a dilated retinal examination using special magnifying lenses, which provide a three-dimensional, stereoscopic view of the macula. Additional testing may involve high-resolution digital photography, a special type of retinal scan called Ocular Coherence Tomography (OCT), or Intravenous Fluorescein Angiography (IVFA) – a study which uses a contrast dye, injected into an arm vein, to outline the retinal blood supply for special photographs. Causes and Risk Factors Many factors have been recognized to increase one’s risk for AMD. These include age (typically over 50 years), smoking, high blood pressure, prolonged sun exposure, high-fat diet, and genetic factors. Variants of the gene which codes for complement factor H recently have been implicated in nearly half of the sight-damaging complications of AMD. Active research continues to reveal other genetic factors. Another chemical, Vascular Endothelial Growth Factor or VEGF, is a major cause of abnormal blood vessel growth typical of the wet form of AMD. It now represents a major target for treatment. Treatment While there is no cure for AMD, there are several treatment options available to help manage patients with this condition and preserve vision. The options for treatment depend on the type of AMD, its severity, and the patient’s vision potential. Anti-oxidant multivitamin therapy, as established by the Age Related Eye Disease Study (AREDS I) has been shown to slow progression of AMD by limiting the oxidative damage under the retina and, at this time, represents the only treatment for dry AMD. Additional information regarding adjustment in the dosing and types of multivitamins will be reported from the ongoing AREDS II trial in the near future. Intraocular injections of bevacizumab (Avastin), ranibizumab (Lucentis), and aflibercept (Eylea) are most commonly used to treat the wet form of AMD. These drugs target VEGF in varying degrees and allow control of abnormal blood vessel growth beneath the macula. Studies have shown that these medicines should be continually injected to achieve and maintain the best visual results since at this time there is no cure for the disease. It should be noted that the frequency and duration of injection treatments is highly variable. The treatment approach adopted must be customized to the each patient’s activity and severity of macular disease.

Macular Hole A macular hole is exactly what it sounds like: a hole in the macula, the center of the retina responsible for central and reading vision. This hole or defect occurs in the fovea, the center of the macula, and the most sensitive part of the entire retina. Macular holes most commonly develop spontaneously during the natural aging process, when the vitreous (the gel that fills most of the eye) becomes more like a watery liquid and separates from the retina. Rather than separating cleanly, the vitreous may abnormally stick to and pull on the macula causing a hole to form. Less commonly, macular holes are caused by direct, blunt eye injury or can occur with intraocular inflammation, macular pucker, or retinal detachment. Most cases occur in people over the age of 60. At first, a macular hole may only cause a small blurry or distorted area in the center of vision. As the hole grows over several weeks or months, central vision progressively worsens. Peripheral vision usually is not affected, although in very rare instances such holes can cause retinal detachment. There are four stages of a macular hole: small foveal detachments with a partial-thickness defect (stage 1), small full-thickness holes (stage 2), larger full-thickness holes without vitreous separation from the retina (stage 3), and larger full-thickness holes with vitreous separation (stage 4). Each stage can progress to the next if not treated. Macular holes can be closed surgically and successfully treated in approximately 90-95% of cases. The level of vision improvement and final result depend on the size of the hole, duration of symptoms, and the level of vision loss before surgery is performed. Typically, smaller macular holes with a short duration of symptoms and limited vision loss have the best results with treatment. The surgery involves vitrectomy, or separation and removal of the vitreous gel from the eye with injection of a gas bubble within the eye. This procedure is performed in the outpatient setting under local anesthesia either in a surgery center or hospital. After surgery, patients must position themselves face down, as instructed by the surgeon, to allow the hole to heal completely. As the eye heals, the fluid in the eye is naturally replaced. A non-surgical alternative to treat macular holes is under development and investigation and awaits potential approval by the Food and Drug Administration (FDA). Ocriplasmin is a specially designed medicine injected in the eye which experimentally can dissolve the attachments of the vitreous gel to the retina. Recent studies have shown encouraging results and suggest that possibly 40% of holes may benefit without surgical treatment. Additional study is necessary to understand if this medicine will help the surgical treatment of macular holes. Macular Pucker An epiretinal membrane, also called macular pucker, is a thin layer or sheet of scar tissue that forms and grows over the macula, the area of the retina that gives us clear central and reading vision. Idiopathic or primary epiretinal membranes often develop on their own as a part of the natural aging process. These sheets of scar tissue most commonly grow after age-related vitreous separation. Less commonly with partial vitreous separation, tugging of the vitreous on the macula also can cause these membranes to form. p-macular-pucker Epiretinal membranes also may result from eye conditions or diseases such as diabetic retinopathy, retinal detachment, inflammation, eye trauma, or retinal vein blockage. These are called secondary epiretinal membranes. Many epiretinal membranes do not affect vision. Thicker membranes, however, can create a wrinkle or pucker of the macula as they grow over the surface of the retina. The retina can swell leading to macular edema. As this occurs, small blurry or distorted areas in the center of vision may develop. The growth of scar tissue can result in more visual distortion, blurring vision, and lead to severe central vision loss. Peripheral vision typically is not affected. While many epiretinal membranes don’t progress enough to require treatment, surgery is recommended for those patients who experience troublesome vision loss. Surgery involves vitrectomy to remove the vitreous gel and membrane stripping to delicately peel the sheet of scar tissue away from the macular surface using tiny, specially designed instruments. The surgery is performed as an outpatient procedure with local anesthesia. There is no non-surgical alternative to treat epiretinal membranes at this time. Please call our office at 301.571.2000 to learn more about macular hole / macular pucker or click here to schedule an appointment.

About Retinal Tear & Detachment Retinal tear and retinal detachment are part of the same spectrum of disease requiring urgent, and frequently emergent, evaluation and treatment. In the young eye, the vitreous gel is in direct contact with the retina, the specialized, multilayered nerve tissue which lines the back of the eye. As the eye ages, the vitreous will shrink and separate from the retina. Most of the time the vitreous will separate cleanly without complication, but the patient may notice flashes and/or floaters. More rarely, the vitreous will remain attached to a part of the retina resulting in the development of one or more tears as the vitreous tries to pull away. If the retinal tear remains unrecognized and untreated, then fluid can rapidly accumulate through a defect (or multiple retinal defects). As the fluid builds up underneath the retina, retinal detachment, a blinding condition, can occur. These conditions tend to be more common in near-sighted individuals, especially those with higher refractive errors (who need stronger spectacles or contact lenses). Others are born with a tendency to develop peripheral patches of thinning called lattice degeneration. Within these patches of thinning, multiple holes may develop spontaneously allowing fluid to accumulate leading to retinal detachment. This mechanism, or cause, of retinal detachment can be seen especially in younger patients before the vitreous gel separates. The vitreous tends to be more stuck to the retina around patches of lattice degeneration making an individual more vulnerable to developing retinal tear or retinal detachment during or following recent vitreous separation. Symptoms The symptoms of vitreous separation, retinal tear, and retinal detachment are similar and sometimes can overlap. On occasion, the patient may notice the floaters and flashing lights (photopsia) more commonly associated with isolated vitreous separation. The ophthalmologist, optometrist, or primary care physician should be suspicious about a more serious problem if the above symptoms are of very recent or sudden onset and are accompanied by a shower of spots or “cobwebs.” Of even greater concern is the loss of peripheral vision which may present as a shadow moving toward the center of one’s field of vision. These symptoms should prompt urgent evaluation and treatment as clinically indicated. Diagnosis Retinal tear and retinal detachment can be recognized during ophthalmoscopy, an examination performed by using a specially designed scope and magnified condensing lens, which allows a clear, three-dimensional, panoramic view of the peripheral retina. Another technique, used during ophthalmoscopy, involves gentle indentation of the eye wall with a blunt instrument to enhance the view of the peripheral retina. This technique can bring all abnormalities, which may require treatment, into view. This latter technique is more commonly and typically performed by the treating retinal surgeon who has been trained specifically to evaluate and manage these disorders. Sometimes a magnifying contact lens will be used during ophthalmoscopy to bring other details, not easily seen with indentation, into view. In rarer circumstances, the view of the retina itself may be blocked by the presence of blood in the vitreous called vitreous hemorrhage. In this situation, an ultrasound of the eye may be necessary to create an image from sound waves in order to make the diagnosis of retinal tear or detachment. Treatment If performed in a timely fashion, treatment of a retinal tear can prevent progression to retinal detachment. This treatment is accomplished by delivering either laser or cryotherapy (freezing technique) and is highly successful. The application of either of these techniques creates a scar around the retinal defect preventing the extension of fluid which could lead to retinal detachment. Retinal detachment management depends on the degree of retinal involvement and symptoms the patient experiences. Many of these treatments can be performed in the office setting without the need for admission to a hospital or surgery center. Such treatment could involve laser (specially focused light) to block extension of a small, localized retinal detachment without any symptoms. Some retinal surgeons also use pneumatic retinopexy, which involves injecting a small gas bubble into the back of the eye. In a short period of time, this bubble can expand and close the retinal tear allowing the fluid under the retina to absorb. Following this treatment, the patient should be counseled to properly position his head in order to move the bubble over the tear. The tear can be treated either with laser or cryotherapy when the retina flattens.

About Low Vision In some cases, the macular or retinal disease may become so advanced that no further medical or surgical treatment can offer an opportunity for visual improvement. Such visual impairment may be mild, moderate or severe. Depending on the patient’s physical, cognitive, and emotional capacity, a low-vision evaluation may provide such impaired patients with strategies to manage and live with their permanent vision loss. An integrated team of specially-trained Low Vision Specialists/Optometrists and occupational therapists can work with the retina specialist to develop such strategies to aid with reading, driving, ambulation, and other domestic activities of daily living to optimize the patient’s quality of life.

About Retinal Vascular Occlusive Disease The retina is a thin sheet of nerve tissue in the back of the eye where light rays are focused and transmitted to the brain. Tiny blood vessels supply the retina with oxygen and other nutrients. Arteries deliver the blood, and the retinal veins carry it out. Sometimes one of these arteries hardens and presses on a nearby vein. The vein can then become blocked, or occluded, making it difficult for blood to leave the eye. This is called a retinal vein occlusion (RVO). A milder, less advanced form of this condition is also known as venous stasis retinopathy. The blocked circulation can lead to swelling and bleeding within the retina, growth of abnormal retinal blood vessels, and partial or total vision loss. Retinal vein occlusions are the second most common cause of blood vessel-related vision loss (the first is diabetic retinopathy). The condition occurs most often in men and women over the age of 50, particularly those in their 60s and 70s. Risk factors include high blood pressure, high cholesterol, diabetes, smoking, glaucoma, and rarely, blood clotting and inflammatory conditions. Treatment depends on the severity of the blockage and the location of the blocked vein. If the large central vein leaving the eye is affected, the condition is known as a central retinal vein occlusion or CRVO; otherwise it is called a branch retinal vein occlusion, or BRVO. BRVOs often can occur with no pain or noticeable loss of vision. It is important to have routine eye exams to detect any developing problems early. Patients can monitor their vision between appointments by closing one eye at a time. Retinal vein occlusions are detected during a dilated retinal exam. A fluorescein angiogram may be performed to confirm the diagnosis and/or aid in treatment planning. Swelling of the macula, or macular edema, can be monitored using Ocular Coherence Tomography (OCT), a special type of retinal scan. Indications of an occlusion are bleeding in the eye, macular swelling or ischemia (loss of blood supply), and neovascularization – abnormal growth of new blood vessels. The retinal neovascularization can cause bleeding in the vitreous gel (vitreous hemorrhage) which can lead to severe vision loss if the blood does not clear on its own. While there is no cure for retinal vein occlusions, patients are counseled to control high blood pressure, high cholesterol, diabetes and other health conditions that increase the risk of vascular hardening, narrowing and blood clotting. Branch Retinal Vein Occlusions (BRVO) Macular swelling used to be commonly treated with a light focal or grid laser, but more recently, intraocular injections of steroid (Triamcinolone), bevacizumab (Avastin),or ranibizumab (Lucentis)are now effective and more commonly used to treat macular edema, especially when the center of the macula, or fovea, is involved. When more of the retinal blood supply is damaged, this ischemia can cause abnormal blood vessel growth leading to vitreous hemorrhage. BRVO Well-designed studies have shown that if this ischemic retinal damage is detected by careful examination and monitoring, scatter (or panretinal) laser treatment to the damaged area of retina can reduce or prevent vision loss. Even if new blood vessels are found before a serious bleed, such laser treatment is still helpful and may prevent the need for surgery to remove blood from the eye. If bleeding continues, a vitrectomy may be performed to remove the blood and its associated scar tissue if present. Scatter laser treatment also is performed at the time of surgery. Patients with a BRVO causing persistent visual problems may undergo a vitrectomy with an arteriovenous sheathotomy, a newer procedure in which the blocked vein is surgically separated from the artery compressing it. This procedure is not performed often since patients now can be stabilized or improved by the injection medicines introduced recently. Central Retinal Vein Occlusions (CRVO) Vision loss from CRVO most commonly is due to swelling of the central retina called macular edema. Unlike BRVO, grid laser treatment hasn’t been shown to stabilize or improve vision for CRVO. Recent studies have established that steroid or ranibizumab (Lucentis) injections in the eye can help patients with this disease. CRVO As with other retinal diseases, bevacizumab (Avastin) is commonly used by retinal surgeons with varying degrees of success depending on advancement of disease. Avastin, Lucentis, and Eylea target Vascular Endothelial Growth Factor or VEGF, and limit the leakage of fluid out of the damaged blood vessels causing macular edema while steroids treat inflammation which also causes more macular edema. Long-term follow-up and treatment may be required to maintain vision. Ozurdex, an intravitreal sustained-delivery dexamethasone(steroid) implant is also an effective treatment for selected patients.