VOLUME 1 • ISSUE 4 • MARCH 2007 The Aging Retinafocus-ed.net/Retinal Diseases_AR v1n4.pdftype of retinal diseases. The Aging Retina is a 4-part series that was designed to educate

Featured in this Issue:

DISEASES OF THE RETINA

Introduction ..................................................................2

Age-related Macular Degeneration ................................2

Diabetic Retinopathy ....................................................5

Diabetic Macular Edema ...............................................6

Retinal Detachment ......................................................8

Retinal Vascular Disease ............................................. 10

Macular Hole .............................................................. 10

Conclusion .................................................................. 11

Departments:

CE POSTTEST ..............................................14

uPCOMINg EVENTS .....................................16

Supported by an unrestricted educational grant from

VOLUME 1 • ISSUE 4 • MARCH 2007

A Continuing Education activity for nurses, ophthalmic technicians & assistants, and ophthalmic photographers

A supplement to the journal Insight - the Journal of the American Society of Ophthalmic Registered Nurses

The Aging

Retina

The Aging Retina

PAGE 2

DISEASES OF THE RETINA

IntroductionAs an allied healthcare provider in the field of ophthalmology, you may encounter patients with any type of retinal diseases. The Aging Retina is a 4-part series that was designed to educate the reader on retinal diseases commonly observed in a mature retina—their causes, symptoms, and treatment options—so that the reader, in turn, could educate patients and their families on their disease. Each issue focused on specific aspects of retinal diseases, and these are summarized below:

Issue 1, The Science behind the Aging Retina, concentrated on the etiology of retinal disease, particularly diabetic retinopathy, retinal detachment, macular hole, and age-related macular degeneration (AMD). The diagnosis and risk factors of each of these were discussed in detail, and therapies also were presented, especially recently developed anti-angiogenic and anti–vascular endothelial growth factor (VEGF) agents.

Issue 2, Clinical Management of Retinal Disease, expanded on treatment options for AMD, especially wet AMD. Current and investigational therapies were discussed, with a focus on anti-VEGF agents including Lucentis® (ranibizumab) and Macugen® (pegaptanib sodium). This issue also presented information on complications associated with intravitreal injections and recommended procedures to prevent the risk of

infection following injection. The issue contained helpful tips about reducing your patient’s anxiety about the injection procedure and improving patient compliance and comprehension. Supportive resources also were provided for you to recommend to your patients with low vision and their family members to assist them with your patient’s needs.

Issue 3, Age-Related Macular Degeneration, focused entirely on AMD, the leading cause of irreversible vision loss among persons over 65 years of age and one of the most common causes of blindness in the Untied States.1 This issue presented detailed information on the symptoms of and the risk factors for developing the disease. The diagnosis and classification of AMD also were featured, along with a discussion of approved and investigational therapies for both dry and wet AMD was included.

This fourth issue, Diseases of the Retina, will provide an exploration of diseases of the aging retina, namely AMD, diabetic retinopathy, retinal detachment, retinal vascular occlusion, and macular holes. Moreover, an in-depth review of the staging and screening of AMD also will be covered. At the conclusion of this issue, you will have completed a comprehensive overview of diseases of the aging retina and their risk factors, symptoms, and treatment options. You should be able to help your patients to better understand their disease so they can manage their low vision and maintain or improve their quality of life. If you missed any of the previously mentioned issues, you can request them and the continuing education posttest that was provided by contacting The American Society of Registered Ophthalmic Nurses (ASORN) or Focus-ed (see page 15 for contact information).

Age-Related Macular Degeneration

The incidence of AMD correlates with increasing age, from 18% in those aged 70 to 74 years to 47% among people aged 85 years and older.2 About 7.3 million people in the Untied States have the early stages of AMD, and 1.75 million people have advanced

Proliferative retinopathy, an advanced form of diabetic retinopathy, occurs when abnormal new blood vessels and scar tissue form on the surface of the retina. © National Eye Institute, National Institutes of Health

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Volume 1 • Issue 4 • MARCH 2007

AMD, defined by neovascular (“wet”) AMD or central geographic atrophy in at least one eye.3 AMD causes the loss of light-sensing photoreceptor cells in the macula, the center of the retina that is responsible for sharp visual acuity and color vision. Damaged retinal cells can no longer send normal signals through the optic nerve to the brain, thus impairing central vision.2 In the early stages of AMD, patients have trouble reading fine print and seeing in dim light, but in the advanced stage, the disease destroys the macula, leading to severe vision loss and legal blindness. Patients with advanced AMD

are unable to read, drive a car, recognize faces, or perform daily tasks that require hand-eye coordination; thus, these patients experience a significant decrease in mobility, independence, and quality of life.

AMD can progress so slowly that the patient notices little change in vision; or progresses rapidly and leads to noticeable vision loss in one or both eyes. Changes leading to AMD occur in the outer retina, which is adjacent to the choroid and includes the photoreceptors (rods and cones), the retinal pigment epithelium (RPE), and Bruch’s membrane.4 The choriocapillaris (the capillary layer of the choroid) is adjacent to the outer retina and is the vascular system that provides it with oxygen and nutrients. The RPE is central in the pathogenesis of AMD and is involved with various functions such as the regeneration of rhodopsin, a visual pigment that absorbs light and creates a visual signal that, in turn, results in the reconstitution of dark-adapted visual pigment. RPE cells also are responsible for the phagocytosis (engulfing and ingesting foreign bodies) of the tips of the photoreceptors that are naturally shed from their outer segments in the RPE. This process is important to the renewal of photoreceptors. As the tips are shed, membranes are formed at the base of the outer segments of the rods and nucleic acids, proteins and lipids are replaced throughout the cones. The shed debris fuses with lysosomes (special cellular compartments filled with enzymes involved with phagocytosis) and is ingested in the RPE. The residue of this ingestion, called lipofuscin, remains in the RPE and accumulates over time.

This accumulation of lipofuscin becomes an increasing burden on RPE cells and eventually overcomes the phagocytotic process.5 High concentrations of lipofuscin have been associated with the presence of early-stage AMD, and tools such as autofluorescence imaging have been used to evaluate patients with AMD (see callout box to the left for more information).

Dry AMD occurs with the deterioration of the RPE19 and is characterized by the appearance of drusen, which are yellow lesions that appear in the photoreceptor cells (light-sensing cells) in the retina. The accumulation of drusen can result in the failure of the exchange of nutrients between the RPE cells and the choroidal blood vessels. Thus, the RPE cells may die, which leads to the death of the photoreceptors that receive their nutritional support from the choroid through RPE cells (detailed information on drusen is available in Vo. 1, No. 3).

Autofluorescence imaging is a quick, noninvasive, and inexpensive method of assessing AMD progression that is based on the stimulated emission of light from molecules in the RPE—notably, lipofuscin.6-13 Lipofuscin results from the oxidative breakdown of various molecules, including polyunsaturated fatty acids, retinoids, and proteins.6 In addition, components of lipofuscin (ie, the retinoid A2E) react to light.5,6,14-16 The intensity of fundus autofluorescence correlates with the amount and distribution of lipofuscin; thus, the amount of autofluorescence reveals previous and possibly future oxidative damage.6

With autofluorescence imaging, any disease affecting the RPE can be evaluated. Current research is focused on the use of this tool in the diagnosis and management of AMD.17 Thus far, autofluorescence appears to be the best method to examine and grade geographic atrophy. In autofluorescence imaging, established geographic atrophy appears as clearly defined dark areas, and increased autofluorescence is often present in adjacent areas. Results of a study showed these areas were nearly atrophic during follow-up.18 In this scenario, autofluorescence imaging is best used with optical coherence tomography (OCT) and fluorescein angiography (FA); autofluorescence imaging provides the functional information to the anatomic information shown by OCT and FA. This integrated approach reflects the possible future trend of ocular examinations; instead of using only one evaluating tool to assess any eye disease, multiple tests may be used to get a more comprehensive picture of how that disease affects the eye.

AutofluoREsEnCE IMAGInG

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Based on results of AREDS 1, researchers developed 2 AMD severity scales that can be used to assess a patient’s 5-year risk of progression of the disease.17 The simplified scale is easy to use in office or clinical settings and provides patients with a quick and easy assessment of future AMD risk. The detailed scale is more practical for use in clinical trials. At the National Eye Institute both scales will be used in AREDS 2 studies; the simplified scale will be used to determine study eligibility, whereas the detailed scale will be used to assess disease progression.

The Simplified Severity Scale

The simplified scale quantifies the 5-year risk of progression to advanced AMD in patients who do not have advanced disease at baseline.17,28 It also can be used to quantify risk in the fellow eye of subjects with unilateral advanced AMD at baseline.

Maximum drusen size and the presence or absence of any pigmentary abnormality in one or both eyes are the principle baseline characteristics used to define risk factors in this scale.17 Large drusen are defined as being at least 125 µm in size. These characteristics were chosen because they can be assessed easily in an office or clinic via slit lamp or ophthalmoscopy that examines the retina and vitreous.

In patients who have advanced AMD in one eye, the 5-year rate of advanced AMD in the fellow eye can be predicted. Each abnormality counts as one factor. Patients with 4 risk factors have a 50% chance of developing advanced AMD in the eye within 5 years; 3 risk factors result in a 25% chance; and 2 risk factors present a 12% chance. With only one or no risk factors present, patients can be assured their risk for developing advanced AMD is very low (0.5 – 3%).

The Detailed Severity Scale

The detailed severity scale is based on a large study of more than 3,000 participants with a median age of 68 years at baseline. Good quality stereoscopic photographs were examined by trained graders utilizing a detailed protocol and measuring grids. Size, area, and location of abnormalities were assessed in photographs taken at baseline, at the 2-year follow-up visit, and years 3, 4, and 5.24

There are 9 steps in the detailed severity scale including a 6 step drusen area scale and a 5 step pigmentary abnormality scale. With each move up the 9-step scale, the 5-year risk of developing advanced AMD also increases, from less than 1% at Step 1 to 50% at Step 9. Defining risk factors for progression to advanced AMD were defined as large drusen size, extensive drusen area, soft indistinct drusen, and pigmentary abnormalities (ie, depigmentation, hyperpigmentation, or geographic atrophy).17

Investigators observed drusen area may be a stronger and more consistent predictor of progression than was drusen size, although both were closely associated with progression.17 Moreover, pigment abnormalities appeared to double the risk of progression when they occurred along with increasing drusen area. Finally, although depigmentation occurred less often than hyperpigmentation, it was a strong predictor of disease progression if it involved a moderate area or had progressed to noncentral geographic atrophy.

AMD sEVERIty sCAlEs

Right EyeLarge Drusen

No = 0

No = 0Yes = 1 1

1

1

1

Yes = 1

Yes = 1

Yes = 1

No = 0

No = 0

Large Drusen

PigmentAbnormalities

PigmentAbnormalities

Large Drusen and Pigment Abnormalities Patient Severity Score = 4 Risk Factors

Left Eye


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The regression of drusen can lead to geographic atrophy, which is defined as a confluent area (≥175 µm minimum in diameter) of RPE cell death accompanied by overlying photoreceptor atrophy.19,20 Geographic atrophy causes 20% of the legal blindness due to AMD.21 Dry AMD usually affects both eyes, but sometimes, the damage may be worse in one eye than in the other. For example, if the central vision is lost in one eye, but the fellow eye has good vision, the patient can maintain a high level of visual function, as tasks such as reading, driving, and other central visual tasks can be completed with the better-seeing eye.

Dry AMD usually develops slowly, often over years; with disease progression, patients may notice a blurring of central vision, which affects their ability to read fine print or see image detail.22 Eventually, patients may have difficulty recognizing faces or may need more light for reading or other tasks. As the disease progresses, central vision may be lost, and in 10% of cases, choroidal neovascularization (CNV) may develop, resulting in wet AMD.21

Investigators from the first Age-Related Eye Disease Study (AREDS 1) reported that high daily doses of specific vitamin supplements can help slow the progression of intermediate AMD to advanced AMD.21,23 The AREDS 1 report recommends the following preventive supplement therapy:

n 500 mg Vitamin Cn 400 IU of Vitamin En 15 mg Vitamin A (beta-carotene)n 80 mg of zinc (zinc oxide)n 2 mg copper (cupric oxide)

Patients who smoke cigarettes or are exposed to second-hand smoke should not take beta-carotene because of a possible association between high-dose beta-carotene and increased risk for lung cancer. AREDS 1 showed a benefit in patients with either bilateral intermediate disease or unilateral advanced disease. No significant benefit was demonstrated in those with early disease.23

In addition to the supplements promoted by the AREDS investigators, other dietary recommendations for lowering the risk of developing AMD have been identified, such as diets rich in omega-3 fatty acids (found in fish),24 fruits, and vegetables (especially leafy green vegetables), and those with a stable intake of lutein and zeaxanthin (natural ingredients of green, yellow, and

orange fruits and vegetables).25 A second study now underway (AREDS 2) is evaluating the effect of macular xanthophylls (lutein and zeaxanthin) with and without long-chain omega-3 fatty acids [(docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)] on AMD.27 Diets such as those described above may help prevent the development of AMD or delay the progression of the disease.

For additional information regarding the pathophysiology, symptoms, and treatment of wet AMD, please refer to The Aging Retina, Vol. 1, No. 1-3.

Diabetic Retinopathy More than 4 million people with diabetes in the United States have diabetic retinopathy (DR).2 Diabetes is a life-long condition in which patients ultimately need to maintain strict blood sugar control. The endocrinologist and nephrologist become a part of the healthcare team. Diabetic retinopathy is defined as progressive damage to the retina resulting from long-term diabetes.29 It usually affects both eyes and can ultimately lead to blindness. DR is classified into 4 stages:

n Mild nonproliferative diabetic retinopathy is the earliest stage of the disease. During this stage, microaneurysms and intraretinal hemorrhages occur and appear as small areas of balloon-like swelling in the retina’s blood vessels and dot- or flame-shaped collections of blood in the retina.

n Moderate nonproliferative retinopathy is characterized by more extensive microaneurysms and intraretinal hemorrhages and is due to decreased blood flow that nourishes the retina.

n Severe nonproliferative retinopathy includes even more microaneurysms and intraretinal hemorrhages, abnormal blood vessels within the retina, and dilation of retinal veins. It occurs from progressive loss of retinal capillaries, depriving more areas of the retina from their blood supply. As a result, these areas send signals to grow new blood vessels (angiogenesis) for nourishment.

n Proliferative retinopathy is the advanced stage of DR that occurs when the growth of new blood vessels (neovascularization) is triggered by lack of nourishment in the retina. These abnormal new blood vessels are fragile and grow on the surface

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treatment In general, no treatment is needed for the first 3 stages of DR, unless DME is diagnosed (see Focal laser treatment section for more information). To prevent disease progression, patients with diabetes should control their blood sugar, blood pressure, and blood cholesterol.29 However, patients with advanced disease require treatment, often with scatter laser treatment.

scatter laser treatmentIn this procedure, 1000 to 2000 laser burns are applied to the areas of the retina that are away from the macula to reduce the neovascularization. Since this therapy involves so many burns, multiple visits are often necessary to complete treatment. Scatter laser treatment is most effective before the neovascularization hemorrhages, but it still may be used in the presence of vitreous hemorrhage, if the amount of blood is not too severe. This scatter laser treatment is also known as panretinal photocoagulation.

Adverse effects associated with scatter laser treatment include loss of side vision (peripheral vision) and a slight loss in color vision and night vision. Patients receiving scatter laser treatment may feel a stinging sensation during the procedure. They will not be able to take themselves home after surgery, since their pupils will remain dilated and their vision will be blurry for the rest of the day.

In patients with a large amount of bleeding in the center of the eye (vitreous), a vitrectomy with panretinal laser may help to restore vision if the hemorrhage does not clear on its own in a reasonable amount of time. If both eyes require a vitrectomy, the procedures are done several weeks apart.29 A vitrectomy with panretinal laser can be performed under local or general anesthesia. A small incision is made in the eye, and the vitreous gel that is clouded with blood is removed and replaced with balanced salt solution. Although most patients undergoing vitrectomy go home after the procedure, some stay in the hospital overnight. Postoperatively, the treated eye is red and sensitive, and patients wear an eye patch/shield to protect the eye as it heals. Antibiotic and corticosteroid eye drops are usually prescribed to help prevent infection and inflammation.

Both scatter laser treatment and vitrectomy are effective in reducing vision loss, but neither can cure diabetic retinopathy. Since patients with proliferative retinopathy

of the retina. Alone, these new blood vessels do not cause vision loss, but if they leak blood or cause tractional retinal detachment, severe vision loss and blindness can result.

All individuals with type 1 or type 2 diabetes are at risk for developing DR. Estimates show about 40% to 45% of Americans with diabetes also have some stage of DR. It is recommended that everyone with diabetes has a comprehensive dilated eye exam at least once a year.29 Finally, pregnant women with diabetes should have a comprehensive dilated eye exam as soon as possible, with additional eye exams during pregnancy if necessary, to prevent any complications resulting from DR.

Vision may be affected at any stage of diabetic retinopathy and may be due to macular edema, vitreous hemorrhage, retinal detachment, or ischemia. Macular edema is the accumulation of fluid within the retina and may cause vision loss if the fovea is affected. In proliferative retinopathy with leaking or bleeding (hemorrhaging) vessels, patients may initially see a few “floating” specks of blood or spots.29 Although the spots may clear without treatment, the patient should seek medical attention to prevent more serious bleeding from occurring. Retinal detachments can be caused by traction from neovascularization and can reduce vision if the macula is involved. Macular ischemia results from progressive capillary drop-out and resultant photoreceptor degeneration.

Diabetic macular edema

About 50% of patients with proliferative retinopathy also have DME. Fluid leaking from the fragile, abnormal blood vessels into the macula (the part of the eye responsible for sharp, straight-ahead vision) can cause the macula to swell, resulting in blurred vision.

DME can occur at any stage of DR, although it is more likely to occur as the disease progresses.

Both DR and DME are diagnosed during a dilated retinal examination, which may include fluorescein angiography and optical coherence tomography to help evaluate capillary drop-out, neovascularization, and macular edema. The earlier the patient receives treatment, the more effective it is likely to be.


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are at risk for recurrent bleeding, retreatment may be necessary to preserve vision.

focal laser treatmentIn patients with DME threatening the central part of vision, focal laser treatment is used to slow the leakage of fluid and reduce the amount of fluid in the retina.29 This procedure involves the application of dozens to over one hundred small laser burns in the areas of retinal leakage surrounding the center of the macula and can be completed in only one session. The burns are made closer to the macula than those in scatter laser treatment. Retreatment may be needed to control leakage. If both eyes require laser surgery, one eye is treated at a time, with one to several weeks between sessions. Focal laser treatment stabilizes vision and reduces the risk of vision loss by 50%.

Anti-VEGf therapyStudies evaluating the off-label use of certain anti-VEGF agents in the treatment of DME have been conducted because of the hypothesis that vascular endothelial growth factor (VEGF) may participate in the development of DME. The agents discussed in this section have demonstrated efficacy in AMD, but none have been approved for use in DME.

Intraocular Kenalog® (triamcinolone acetonide)Recent data has shown intravitreal administration Kenalog to be efficacious in treating retinal diseases including DME. Kenalog is a corticosteroid, a drug class that has anti-inflammatory properties and that has been demonstrated to inhibit the expression of the VEGF gene.30,31 For DME, it is generally administered intravitreally at a dose of 4 mg in a volume of 0.1 mL.30,32

One off-label study was conducted in 16 eyes with macular edema due to DR; none of the 16 eyes had responded to prior treatment with multiple sessions of laser photocoagulation.32 Kenalog 4 mg (0.1 mL) was administered intravitreally through the inferior pars plana; treatment response was monitored functionally by visual acuity assessment and anatomically by optical coherence tomography (OCT). Results show mean central retinal thickness decreased from 540 µg preinjection (baseline) to 242 µg postinjection. Visual acuity improved by 2.4, 2.4, and 1.3 lines compared with baselines values at the 1-, 3-, and 6-month follow-up intervals, respectively. In another study in DME, intravitreal Kenalog use resulted in a mean visual acuity

improvement of 20/165 at baseline to 20/105 at follow-up (mean, 6.6 months).33

Avastin® (bevacizumab)Avastin is approved for treatment of metastatic colorectal cancer and non-small cell lung cancer; however, it has been studied in the off-label use of retinal diseases such as wet AMD and DME. Results from a study conducted by Haritoglou and colleagues34 show that intravitreal injection of Avastin 1.25 mg (0.05 mL) administered to subjects who failed other prior treatments for DME is associated with improvements in visual acuity and central retinal thickness. Mean central retinal thickness by OCT was 501 ± 163 µm (range, 252-1,031 µm) at baseline and 425 ± 180 µm at 2 weeks, 416 ± 180 µm at 6 weeks; and 377 ± 117 µm at 12 weeks. Mean visual acuity increased at 6 weeks postinjection, with some regression of Snellen letters after 12 weeks. Changes in ETDRS letters were not significant throughout follow-up. Based on these results, the investigators believe that Avastin may be a viable treatment option for DME in the future; however, larger studies are needed to explore this possibility.

MacugenOff-label investigational studies have been conducted evaluating the efficacy of intravitreal injection with Macugen in patients with DME. Macugen is not approved for the treatment of DME or diabetic retinopathy. In one study, 172 patients with DME received Macugen (0.3 mg, 1 mg, or 3 mg) or sham at study entry, Week 6, and Week 12, with additional injections and/or photocoagulation as needed for another 18 weeks;

Fundus photo showing focal laser surgery for diabetic retinopathy. © National Eye Institute, National Institutes of Health

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with no ocular or systemic adverse events. The results of this and the study described above indicate that more studies may help to explore the role of Lucentis therapy in the treatment of DME.

Retinal Tears and Detachment

Although they most commonly happen spontaneously, blunt trauma can cause injury to the retina, including retinal edema (swelling) and breaks (holes or tears) in the retina and retinal edema (swelling).40 Whether spontaneous or traumatic, retinal breaks can result in retinal detachment (see below) because fluid can leak through these breaks to the space behind the retina and lift the retina from its normal position.

Retinal DetachmentA retinal detachment or retinal tear occurs when the retina is lifted or pulled from its normal position. The incidence of retinal detachment in the United States is 1 in 15,000 people, with a prevalence of 0.3%.2 If it is not treated promptly, it can cause permanent vision loss. Retinal detachment is classified into 3 categories41:

n Rhegmatogenous – This is the most common type of retinal detachment. It occurs when fluid seeps through the retinal tear and goes under the retina, separating it from the retinal pigment epithelium (RPE). It is most commonly treated surgically.

n Tractional – This is a less common type that occurs when scar tissue on the surface of the retina contracts and causes the retina to separate from the RPE. It usually occurs in proliferative retinopathies, most commonly PDR or proliferative vitreoretinopathy (PVR). The treatment of tractional retinal detachment depends on the extent of the detachment and whether the macula is in danger.

n Exudative – This type often results from retinal diseases, including inflammatory disorders and injury or trauma to the eye. It is caused when fluid leaks into the area underneath the retina, but there are no breaks or tears in the retina. Retinal detachments of this type are managed by treating the underlying cause.

Retinal detachment is more common in people older than age 40, but it can occur at any age.41 Men have a

final patient evaluations were conducted at Week 36.35 Patients who received Macugen 0.3 mg had a better median visual acuity than those who received sham, and compared to the sham group, a larger proportion of those on Macugen 0.3-mg dose gained ≥10 letters (approximately 2 lines; 10% vs 34%, respectively, P = 0.003) and ≥15 letters (7% vs 18%, respectively, P = 0.12). Mean central retinal thickness decreases were greater in the Macugen groups than in the sham group, and photocoagulation was used in fewer patients in the Macugen groups compared to those in the sham group. Macugen was well tolerated in all treatment groups, and endopthalmitis was reported in 1 of 652 injections. In a subset of 16 patients who had retinal neovascularization at baseline, those receiving Macugen showed a regression or absence of leakage from neovascularization at 36 Weeks. Among those with regression following Macugen therapy (37%), neovascularization recurred at Week 52 after the last injection at Week 30.36 Thus, current results indicate that the experimental use of Macugen in patients with DME may be an alternative therapy for this population.

LucentisSimilarly, Lucentis also has been evaluated in off-label studies in patients with DME. Lucentis is not approved by the FDA in the treatment of DME. One study showed Lucentis was well tolerated and efficacious in patients with DME.37 Ten eyes of 10 patients received 3 intravitreal injections of Lucentis 0.3 mg or 0.5 mg at Day 0, Month 1, and Month 2 and were observed until Month 24. At Month 3, 4 patients gained at least 15 letters or more, 5 gained at least 10 letters, and 8 gained at least 1 letter, and mean central retinal thickness decreased 45 microns in the low-dose group and 198 microns in the high-dose group. Five occurrences of mild-to-moderate ocular inflammation were reported. Results of this study confirmed the hypothesis that Lucentis’ ability to interfere with VEGF signaling can reduce DME.38.

Results were published recently from another small study examining this off-label use of Lucentis in DME; in this trial, 10 patients with chronic DME received intraocular injections of Lucentis 0.5 mg at baseline, Month 1, Month 2, Month 4, and Month 6.39 Investigators reported a decrease in the foveal thickness and a reduction in the macular volume in the treated eyes of these patients, and an improvement in visual acuity (gain of 12.3 letters from baseline). In addition, Lucentis was well tolerated


PAGE �

higher incidence than women. Other risk factors include having:

n Myopia (nearsighted)n A retinal detachment in the other eyen A family history of retinal detachmentn A history of cataract surgeryn A history of certain other ocular disease or disorders

(eg, retinoschisis, uveitis, degenerative myopia, or lattice degeneration)

n A history of an eye injury

Symptoms of a retinal detachment can include a sudden or gradual increase in the number of floaters in the field of vision; a sudden or gradual increase of flashes in one eye or both eyes; a shadow in the peripheral vision; and/or a sudden onset of blurred vision.41 People who experience any of these symptoms should seek immediate medical attention.

treatment of Retinal DetachmentThe objective of retinal detachment surgery is to re-attach the sensory layer of the retina to the pigmented retinal layer, thus preserving or restoring vision. The appropriate treatment for retinal detachment depends on the severity and extent of the detachment.41 Diagnostic examination includes indirect ophthalmoscopy with scleral depression and possibly ultrasonography if the vitreous gel is opaque. When the macula remains attached, the procedure is emergent in nature to preserve the central vision. Small holes or tears in the attached retina can be treated with laser retinopexy or cryopexy. Cryopexy is a freezing treatment that is applied with an external probe to the sclera to create a chorioretinal

scar. Pneumatic retinopexy is considered in certain retinal detachments and involves the cryopexy and/or laser treatment to the detached area. A gas is injected into the vitreous. The gases used are perfluoropropane (C3F8) or sulfur hexafluoride (SF6). These expand and act as a tamponade to gently hold the retina in place. The gas bubble is injected into the vitreous cavity, and the patient is positioned so the gas pushes the retina around the retinal break or tear against the outside of the eye until the chorioretinal adhesion forms in 1 to 2 weeks. These treatment options can be performed in the office or clinics. Surgical therapies can be performed on an outpatient basis or may require the patient to stay in the hospital. These include scleral buckling, vitrectomy, or pneumatic retinopexy.

Scleral buckling involves the attachment of a tiny synthetic band to the outside of the eyeball to gently push the wall of the eye against the detached retina.41 The breaks or tears are localized using indirect ophthalmoscopy and scleral depression. These areas are treated with retinal cryotherapy. The detachment is then repaired by externally fixing an exoplant (buckle) onto the sclera indenting the area over the detachment. Silicone is the most frequently used material to make the buckling components or exoplants. Vitrectomy also is an option, as well as combined procedures, which include vitrectomy with endophotocoagulation and gas, vitrectomy with scleral buckling and membrane stripping, and endophotocoagulation and fluid gas exchange. A pars plana vitrectomy is the surgical removal of the vitreous from the posterior segment of the eye. To provide access to the posterior segment, 3 sclerotomies are made into the eye; one is used as an infusion port to maintain pressure and volume in the globe. The other 2 sclerotomies are working ports for illumination and instrumentation. Cautery or laser may also be used through these ports. During the procedure, the removed vitreous gel is most often replaced with a balanced salt solution or with air or gas. Over time, after removing the vitreous humor (vitrectomy) the balanced salt solution, air, or gas is absorbed by the eye and is slowly replaced with aqueous humor. Vitreous fluid does not regenerate because it is an embryonic structure, and the genetic coding for production is not available.

Silicone oil is placed into the vitreous cavity when alternative therapies have been exhausted. It is typically used for giant retinal tears, proliferative vitreoretinopathy

Slit lamp photograph showing retinal detachment in Von Hippel-Lindau disease. © National Eye Institute, National Institutes of Health

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(PVR), CMV retinitis, choroidal hemorrhage, and for patients who are unable to maintain facedown positioning necessary if gas is injected. It remains in the eye and needs to be removed surgically when healing is completed. It also is removed when complications occur, including corneal decompensation, elevated intraocular pressure, and emulsification of the oil.

About 90% of retinal detachments are successfully treated with one procedure, but retreatment may be required.41 Visual results are best if the retinal detachment is repaired before the macula detaches. The final visual result may not be known for up to several months following surgery. In some cases, despite ideal circumstances and multiple attempts at repair, treatment may fail, and vision may eventually be lost.

Retinal Vascular Disease

Retinal blood vessel occlusion is a blockage of the blood supply to the retina, which occurs when retinal arteries or veins become blocked by an embolus or by a thrombus (build up of substances such as fat or plaque in the blood vessels).42 This is often caused by an underlying disorder such as glaucoma, hypertension, diabetes, coagulation disorders, atherosclerosis, or hyperlipidemia. Symptoms for retinal blood vessel occlusion include sudden blurring or loss of vision in all or part of one eye.

Individuals with retinal artery occlusion are at risk for stroke since the source of the emboli affecting the eye could also send emboli to the brain. Treatment depends on whether the occlusion occurred in a vein or artery. Patients with either retinal arterial blockage or retinal vein occlusion may have a poor prognosis for visual recovery, depending on the location and severity of the blockage.

Retinal vein occlusionThe incidence of vision loss after retinal vein occlusion varies, depending on the extent of intraretinal hemorrhage (bleeding), retinal edema, and macular ischemia. A complication that may also occur is neovascular glaucoma. There are 2 main types of retinal vein occlusion: central retinal vein occlusion (CRVO), which involves a blockage in the central retinal vein through which blood leaves the retina, and branch retinal vein occlusion (BRVO), in which the blockage occurs in one

of the tributaries of the central vein of the retina.

Treatment options for retinal vein occlusion include aspirin and laser therapy.42 In patients younger than 40, blood tests should be done to check for a clotting problem. The blockage should be closely monitored for several months, since many harmful effects take 3 or more months to develop. Another option for patients with this disease will be studied in a 1-year clinical trial of Lucentis to treat macular edema.

Retinal artery occlusionRetinal artery occlusion often results in considerable vision loss, and the degree of this vision loss is partly related to the location of the occlusion.43 Treatments for retinal artery occlusion include inhaling a carbon dioxide/oxygen mixture or digital massage of the globe. These therapies are thought to widen the retinal arteries, which may allow the embolus to move further down the artery to reduce the size of the affected area. In addition, in retinal artery occlusion, the cause of the blockage should be investigated, as the blockage may reflect a life-threatening medical situation. Patients with retinal artery occlusion should be screened for hypertension, valvular heart disease, or carotid artery blockage.

Macular Hole

A macular hole is a small break in the center of the macula.44 Macular holes are most common among people aged 60 years or older. The overall prevalence in the United States is 3.3 cases in 1000 people older

Diabetic macular edema. © National Eye Institute, National Institutes of Health


PAGE 11

than 55 years. With age, the vitreous slowly contracts (shrinks) and pulls away from the retinal surface. Natural fluid fills the space where the vitreous has contracted as a normal part of the process. However, if the vitreous is firmly attached to the retina as it contracts, it can tear the retina, resulting in a macular hole. Central vision can be blurred and distorted by the anatomic disruption of the retina, surrounding macular edema, or accumulation of fluid near the edge of the hole. Macular holes also can result from high myopia, macular pucker, rhegmatogenous retinal detachment, DR, and trauma to the eye.

Macular holes often begin gradually. There are 4 stages to a macular hole44:

n Stage I – Foveal detachment. If left untreated, roughly 50% of Stage I macular holes will progress.

n Stage II – Small, full-thickness holes. Without treatment, about 70% of Stage II macular holes will progress.

n Stage III – Full-thickness holes (>400 microns). At this stage, damage is severe, and most central and detailed vision can be lost.

n Stage IV – Full-thickness hole with complete separation of the vitreous gel from the surface of the retina.

In the early stages of a macular hole, people may notice a slight distortion or blurriness in their central vision; straight lines or objects may begin to look bent or wavy, and reading and other routine tasks may become difficult.44 The size of the hole and its location on the retina determine how the person’s vision is affected. Without treatment, a macular hole can lead to permanently reduced vision and in some cases, a detached retina (see the previous section for more information on retinal detachment). Finally, if one eye has a macular hole, there is a 10% to 15% risk of developing a macular hole in the other eye.

In some cases, macular holes can seal themselves and require no treatment. However, in most cases, surgery is needed to help improve vision. During vitrectomy, the vitreous gel is removed to prevent it from pulling on the retina, and vitreous gel is replaced with a mixture of air and gas. This bubble acts as an internal, temporary “bandage” that holds the edge of the macular hole in place as it heals. This procedure can be performed

under local anesthesia and on an outpatient basis. The patient must remain in a face-down position, usually for 1 week, but sometimes for as long as 2 to 3 weeks. This position allows the bubble to press against the macula and be absorbed by the eye, sealing the hole. During this process, the vitreous space refills with natural eye fluids.

Without remaining in the face-down position, vision recovery may not be successful. Patients who cannot remain this position for long periods are not good candidates for this procedure; however, there are several positioning devices that can assist patients to facilitate the healing process.

Vision improvement varies from patient to patient, and those who have had a macular hole for less than 6 months have a better chance of recovering vision that those who have had one for longer.44 Complications of macular hole surgery include an increase in the rate of cataract development, infection, and retinal detachment.

Without remaining in the face-down position, vision recovery may not be successful. Patients who cannot remain this position for long periods are not good candidates for this procedure; however, there are several positioning devices that can assist patients to facilitate the healing process.

ConclusionAs a healthcare professional in the field of ophthalmology, you will most likely encounter patients with some type of retinal disease. Although most of these diseases affect primarily older people (AMD and macular holes), others can affect younger patients (retinal detachment and DR). It has been the goal of The Aging Retina series to provide you with a comprehensive overview of retinal diseases so that you may help your patients and their families better understand the underlying etiology and treatment options that may be available to them. Your role is critical in helping them to maintain their sight and cope with their vision loss. We hope you have found The Aging Retina series to be helpful to your work in this very important field.

The Aging Retina

PAGE 12

References1. Age-Related Eye Disease Study Research Group. Potential public

health impact of age-related eye disease study results. AREDS Report No. 11. Arch Ophthalmol 2003;121(11):1621-4.

2. National Institutes of Health, National Eye Institute. Progress in Eye and Vision Research 1999-2000. US Department of Health and Human Services; Bethesda, MD. 2005.

3. Desai MPL, Lentzner H, Robinson KN. Trends in vision and hearing among older Americans: aging trends. Hyattsville, MD: National Center for Health Statistics; 2001.

4. National Institutes of Health, National Eye Institute. Age-Related Macular Degeneration: What You Should Know. US Department of Health and Human Services; Bethesda, MD. NIH Publication No. 03-2294.

5. De Jong, PTVM. Age-related macular degeneration. N Engl J Med 2006;355(14):1474-85.

6. Spaide RF. Fundus autofluorescence and age-related macular degeneration. Ophthalmology 2003;110(2):392-9.

7. Kitagawa K, Nishida S, Ogura Y. In vivo quantitation of autofluorence in human retinal pigment epithelium. Ophthalmologica 1989;199(2-3):116-21.

8. Delori FC, Dorey CK, Staurenghi G, Arend O, Goger DG. Weiter JJ. In vivo fluorescence of the ocular fundus exhibits retinal pigment epithelium lipofuscin characteristics. Invest Ophthalmol Vis Sci 1995;36(3):718-29.

9. von Ruckmann A, Fitzke FW, Bird AC. Distribution of fundus autofluorescence with scanning laser ophthalmoscope. Br J Ophthalmol 1995;79(5):407-12.

10. von Ruckmann A, Fitzke FW, Bird AC. Fundus autofluorescence in age-related macular disease imaged with a laser scanning ophthalmoscope. Invest Ophthalmol Vis Sci 1997;38(2):478-86.

11. Solbach U, Keilhauer C, Knabben H, Wolf S. Imaging of retinal autofluorescence in patients with age-related macular degeneration. Retina 1997;17(5):385-9.

12. Delori FC, Fleckner MR, Goger DG, Weiter JJ, Dorey CK. Autofluorescence distribution associated with drusen in age-related macular degeneration. Invest Ophthalmol Vis Sci 2000;41(2):496-504.

13. Delori FC; Goger DG, Dorey CK. Age-related accumulation and spatial distribution of lipofuscin in RPE of normal subjects. Invest Ophthalmol Vis Sci 2001;42(8):1855-66.

14. Wihlmark U, Wrigstad A, Roberg A, Nilsson SE, Brunk UT. Lipofuscin accumulation in cultured retinal pigment epithelial cells causes enhanced sensitivity to blue light irradiation. Free Radic Biol Med 1997;22(7):1229-34.

15. Schutt F, Davies S, Kopitz J, Holz FG, Boulton ME. Photodamage to human RPE cells by A2-E, a retinoid component of lipofuscin. Invest Ophthalmol Vis Sci 2000;41(8):2303-8.

16. Gaillard ER, Atherton SJ, Eldred G, Dillon J. Photophysical studies on human retinal lipofuscin. Photochem Photobiol 1995;61(5):448-53.

17. Age-Related Macular Degeneration: Staging and Screening. EyeNet Extra. American Academy of Ophthalmology; San Francisco, CA. 2006.

18. Holz FG, Bellman C, Staudt S, Schütt F, Völcker HE. FundusFundus

autofluorescence and development of geographic atrophy in age-related macular degeneration. Invest Ophthalmol Vis Sci 2001;42(5):1051-6.

19. Ambati J, Ambati B, Yoo SH, Ianichev S, Adamis AP. Age-related macular degeneration: etiology, pathenogenesis, and therapeutic strategies. Surv Ophthalmol 2003;48(3):257-93.

20. Green WR, Key SN, III. Senile macular degeneration: a histopathologic study. Trans Am Ophthalmol Soc 1977;75:180-94.

21. Ferris FL, III, Fine SL, Hyman L. Age-related macular degeneration and blindness due to neovascular maculopathy. Arch Ophthalmol 1984;102(11):1640-2.

22. The Foundation of the American Academy of Ophthalmology Web site. Dry AMD and wet AMD. Available at: http://www.faao.org/what/AMD/DryWet.cfm. Accessed September 12, 2006.

23. Age-Related Disease Study Group. A randomized, placebo controlled, clinical trial of high-dose supplementation with vitamins C and E, beta-carotene, and zinc for age-related macular degeneration and vision loss. Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.

24. Davis MD, Gagnon RE, Lee LY, Hubbard LD, Klein BE, Klein R, et al. The Age-Related Eye Disease Study severity scale for age-related macular degeneration: AREDS Report No. 17. Arch Ophthalmol 2005;123(11):1484-98.

25. Seddon JM, George S, Rosner C. Cigarette smoking, fish consumption, omega-3 fatty acid intake, and associations with age-related macular degeneration: the number of pack-years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularization. Br J Ophthalmol 2006;124:75-80.

26. Moeller SM, Parekh N, Tinker L, Ritenbaugh C, Blodi B, Wallace RB, et al. Associations between intermediate age-related macular degeneration and lutein and zeaxanthin in the Carotenoids in the Age-Related Eye Disease Study (CAREDS). Arch Ophthalmol 2006;124(8):1151-2.

27. National Institutes of Health. Age-Related Diseases Study 2 (AREDS 2). Available at: http://clinicaltrials.gov/ct/show/NCT00345176?order=2Accessed January 22, 2007.

28. Ferris FL, Davis MD, Clemons TE, Lee LY, Chew EY, Lindblad AS, et al. A simplified severity scale for age-related macular degeneration: AREDS Report No. 18. Arch Ophthalmol 2005;123(11):1570-4.

29. National Eye Institute. Diabetic Retinopathy: What You Should Know. Bethesda, MD. US Department of Health and Human Services, National Institutes of Health. Publication No. 03-2171.

30. Ip MS. Intravitreal injection of triamcinolone: an emerging treatment for diabetic macular edema. Diabetes Care 2004;27(7):1794-7.

31. Nauck M, Karakiulakis G, Perruchoud A, Papkonstantinou E, Roth M. Corticosteroids inhibit the expression of the vascular endothelial growth factor gene in human vascular smooth muscle cells. Euro J Pharmacol 1998;341:309-15.

32. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920-7.

33. Jonas J, Kreissig I, Sofker A, Degenring R. Intravitreal injection of triamcinolone for diffuse diabetic macular edema. Arch Ophthalmol 2003;121:51-61.


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34. Haritoglou C, Kook C, Neubauer A, et al. Intravitreal bevacizumabIntravitreal bevacizumab

(Avastin) therapy for persistent diffuse diabetic macular edema.

Retina 2006;26(9):999-1005.

35. Cunningham ET Jr., Adamis AP, Altaweel M, Aiello LP, Bressler

NM, D’Amico DJ, et al. A phase II randomized double-masked

trial of pegaptanib, an anti-vascular endothelial growth factor

apatamer, for diabetic macular edema. Ophthalmology

2005;112(10):1747-57.

36. Adamis AP, Altaweel M, Bressler NM, Cunningham ET Jr., Davis

MD, Goldbaum M, et al. Changes in retinal neovascularization

after pegaptanib (Macugen) therapy in diabetic individuals.

Ophthalmology 2006;113(1):23-8.

37. Chun DW, Heier JS, Topping TM, Duker JS, Bankert JM. A pilot

study of multiple intravitreal injections of ranibizumab in patients

with center-involving clinically significant diabetic macular edema.

Ophthalmology 2006;113(10):1706-12.

38. Ventura J. Drug treatment slows macular vision loss in diabetics.

The Gazette. December 18, 2006.

39. Nguyen QD, Tatlipinar S, Shah SM, Haller JA, Quinlan E, Sung J, et al. Vascular endothelial growth factor is a critical stimulus for diabetic macular edema. Am J Ophthalmol 2006;142(6):961-9. Epub 2006 Aug 2.

40. The National Retina Institute Web site. Types of eye injuries, part 2. Available from: http://www.bmgnri.com/eyehealth/ES02.htm. Accessed January 25, 2005.

41. National Eye Institute. Retinal detachment resource guide. 2005 [cited 2006 December 12]. Available from: http://www.nei.nih.gov/health/retinadetach/index.asp.

42. National Library of Medicine. Medical encyclopedia: retinal vessel occlusion. 2006 [cited 2006 December 7]. Available from: http://www.nlm.nih.gov/medlineplus/print/ency/article/001028.htm.

43. How are anti-VEGFs being used in AMD therapy? An expert interview with Dr. David Brown. Medscape Ophthalmology 2006;7(2). Available from: http://www.medscape.com/viewarticle/548665. Accessed December 12, 2006.

44. National Eye Institute. Macular hole resource guide. 2004 [cited 2006 December 12]. Available from: http://www.nei.nih.gov/health/macularhole/index.asp.

UNDERSTANDING NEW TREATMENT OPTIONSTO IMPROVE PATIENT OUTCOMES

www.AMD-Now.com

The Aging Retina

PAGE 14

POSTTEST INFORMATION

This activity is provided by ASORN, which is accredited as a provider of continuing education in nursing by the American Nurses Credentialing Center’s Commission on Accreditation and is provider approved by the California Board of Registered Nursing, provider number 11901. Approval is pending for JCAHPO CECs and OPS CECs. Please refer to www.asorn.org for updates on pending credit.To receive 1.5 nursing contact hours and/or 1.0 Group A JCAHPO CEC and 1.5 OPS CECs for this activity, read the article and complete the posttest and general evaluation form within three years of the publication date, and send it to:

ASORNPO Box 193030San Francisco, CA 94119Fax: 415-561-8531

No fee will be assessed for this complimentary continuing education activity. Successful completion is defined as a score of 80% or higher. Participants who do not achieve a minimum score of 80%

may retake the test within 30 days. Please allow a minimum of 3

weeks from date of receipt of posttest to receive your attendance

verification certificate. Requests for certificates less than 3 weeks

from date of receipt may be assessed a $10 fee. Please plan

ahead and submit your posttest well in advance of deadlines for

recertification and relicensure.

Contact ASORN at (415) 561-8513 for additional information.

Contact hours for these activities may be used for CRNO

recertification.

objectives1. Describe the severity of Age-related Macular Degeneration

2. Differentiate the stages of Diabetic Retinopathy

3. Discuss treatments for Diabetic Macular Edema

4. List classifications and treatments of Retinal Detachment

5. Differentiate Retinal Vascular Diseases

6. Explain Macular Holes

Diseases of the Retina

Registration Information and Evaluation Response form “Diseases of the Retina”

Name:

Address:

City: State: Zip:

Work Phone: Home Phone: Fax:

RN#: State of Licensure: Exp. Date:

Type of credit desired: ® Nursing Contact Hours ® JCAHPO CECs ® OPS CECs

test response: Circle the most appropriate response matching test question number and response number.

1. A B C D 4. A B C D 7. A B C D 10. A B C D



General Evaluation: Please use the scale below to evaluate this educational activity and objectives. Circle your response. As a result of completing this offering, I am able to: 4 3 2 1 Very Moderately fairly not at well well well all

1. Describe the severity of Age-related Macular Degeneration 4 3 2 1 2. Differentiate the stages of Diabetic Retinopathy 4 3 2 1 3. Discuss treatments for Diabetic Macular Edema 4 3 2 1 4. List classifications and treatments of Retinal Detachment 4 3 2 1 5. Differentiate Retinal Vascular Diseases 4 3 2 1 6. Explain Macular Holes 4 3 2 1 7. The content matches the objectives. 4 3 2 1 8. Independent study was an effective teaching method. 4 3 2 1 9. This course helped me achieve personal objectives. 4 3 2 110. The time required to complete this offering (in minutes) and take the test was: 60 75 90 >90

PAGE 1�


1) Proliferative Diabetic Retinopathy (PDR) is:

a) The first stage of DRb) The advanced stage of DR in whichThe advanced stage of DR in which

new blood vessels growc) The advanced stage of DR in whichThe advanced stage of DR in which

macular edema beginsd) Not affected by angiogenesisNot affected by angiogenesis

2) Which people with diabetes are at risk for developing DR?

a) All people with type I or type 2All people with type I or type 2 diabetes

b) Only those with type 1 diabetesc) Only those with type 1 diabetes for

more than 10 yearsd) Only those with type 2 diabetes

3) The goal of focal laser treatment for macular edema is to:

a) Sacrifice central vision slightly toSacrifice central vision slightly to preserve side vision

b) Destroy the leaking blood vesselsc) Transfer the leakage to another area

of the retinad) Slow the leakage of fluid in the retina

4) Retinal detachment risk factors include all of the following except:

a) MyopiaMyopia b) Hyperopiac) History of eye traumad) Previous cataract surgery

5) People with retinal vein occlusion are also at risk for:

a) Myocardial infarctionMyocardial infarctionb) Renal diseasec) Stroked) Increased intracranial pressure

6) It is recommended that everyone with diabetes have a dilated exam at least:

a) Every 6 monthsEvery 6 months b) Every year c) Every 2 years d) Every 9 months

7) The leading cause of blindness among persons over 65 years of age is:

a) Macular holesMacular holesb) Retinal detachmentc) AMDd) Ruptured globe

8) Geographic atrophy causes what percentage of legal blindness?

a) 5%5%b) 20 %c) 50%d) 100%

9) Which of the following is not a preventive supplement recommended by the AREDS 1 study? a) ZincZincb) Beta-carotenec) Vitamin Cd) Lutein

10) Early stage AMD has been associated with high concentrations of:

a) LipofuscinLipofuscin b) Lutein c) Glucose d) Hyoid

11) The intensity of fundus autofluorescence correlates with the amount and distribution of lipofuscin; thus, the amount of autofluorescence reveals previous and possibly:a) Future gene damageFuture gene damageb) Future ketone productionc) Interneuron impulsesd) Future oxidative damage

12) In Diabetic Retinopathy, when panretinal photogocgulartion is done, the patient is aware that his/her:

a) Peripheral or night vision may bePeripheral or night vision may be affected

b) Appetite will be affectedc) Sense of balance will be affectedd) Pupils will be pinpoint

CE POSTTEST VOLuME 1 • ISSuE 4 • MARCH 2007

The Aging Retina Volume 1 • Issue 4 • March 2007The Aging Retina, a supplement to the journal Insight - the Journal of the American Society of Ophthalmic Registered Nurses (ASORN), is published quarterly. Scheduled publication dates are June 2006, September 2006, December 2006, and March 2007. ASORN is located at 655 Beach Street, San Francisco, CA 94109, phone 415-561-8513. Periodicals Postage Paid at San Francisco, CA and at additional mailing offices. POSTMASTER: Send address changes to Insight the American Society of Ophthalmic Reg-istered Nurses, ASORN, PO Box 193030, San Francisco, CA 94119.

Educational ProviderASORN655 Beach StreetSan Francisco, CA 94109

The Aging Retina Editorial Board Members Joy M. Bankert, RN, BSNNancy King, RN, BSN, CRNOTheresa Libby, COABarbara Ann Harmer, RN, BSN, MHADal Chun, MD Suzanne Shaw, RN, CRNOSarah C. Smith, RN, MA, CRNO, COA

The Aging Retina is produced by focus-ed, LLC, located at 3110 Cherry Palm Drive, Suite 350, Tampa, FL 33619, phone 813-496-7573. © by focus-ed, LLC.

Educational Co-Provider

to request additional copies of The Aging Retinaor to offer ideas and opinions,Contact:focus-ed, LLC3110 Cherry Palm Drive, Suite 350Tampa, FL 33619Phone 813-496-7573Statements and opinions expressed in the articles and communications herein are those of the author(s) and not necessarily those of ASORN, ANCC, the editor(s), or the publisher, who disclaim any responsibility or liability for such material and do not guarantee, warrant, or endorse any product or service advertised in the publication, nor do they guarantee any claim made by the manufacturer of such product or service. It is the responsibility of the readers to determine efficacy and safety in clinical, research, and educational situations.

Diseases of the Retina

Don’t miss out on free CE credits from this half-day continuing education course for ophthalmic personnel. Expert speakers will cover state-of-the art techniques for understanding and managing

patients with Age-related Macular Degeneration (AMD). This seminar is provided at no cost to nurses, technicians, medical assistants and ophthalmic photographers who work with patients with AMD.

Do it today so you don’t miss out on a seminar coming soon to a city near you!

Supported by an unrestricted educational grant from

UNDERSTANDING NEW TREATMENT OPTIONSTO IMPROVE PATIENT OUTCOMES

March 3 Boston Park Plaza �4 Arlington Street Boston, MA 0211�

March 9 Marriott Coralville Hotel and Conference Center �00 E. �th St., Coralville, IA

March 10 Argonaut Hotel 4�� Jefferson Street at Hyde San Francisco, CA �410�

March 24 Crowne Plaza st. louis Downtown 200 North 4th Street St. Louis, MO ��102

March 24 Hyatt Regency Philadelphia at Penn’s landing 201 South Columbus Boulevard Philadelphia, PA 1�10�

March 31 Adams Mark Dallas, tower Royale 400 North Olive Dallas, TX 7�201

April 14 Chicago Chicago, IL

YOU & YOUR COLLEAGUES ARE INVITED TO ATTEND

Agenda7:30 AM Check-in & Complimentary Breakfast

8:30 AM Understanding AMD AMD Imaging AMD Treatments & Current Clinical Trials Treatment Logistics & Preparation Post-operative Side Effects & Patient

Follow-up Support for Patients with AMD

1:00 PM Meet the Faculty Roundtable Discussion & Complimentary Lunch

Additional information and Registration at www.AMD-Now.com or contact:

at (813) 496-7573 x250

VOLUME 1 • ISSUE 4 • MARCH 2007 The Aging Retinafocus-ed.net/Retinal Diseases_AR v1n4.pdftype of retinal diseases. The Aging Retina is a 4-part series that was designed to educate

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