Ben J. Janson, MD and Ian C. Han, MD

• Loss Of Fluid Mac Os X
• Loss Of Fluid Mac Os Download

Plus, theres no loss of image quality. System Requirements: – Power PC G4/G5 or Intel Processor – Mac OS X Tiger v10.4.11, Leopard v10.5.8, Snow Leopard v10.6.2 or later – XGA (1024×768) 24-bit (millions of colors) display – 512Mb RAM (1Gb or more recommended) – 250Mb of available hard-disk space. Fluid Mask 3 as a Photoshop plug-in. After a certain amount of time a Mac will typically go into hibernate mode. Note how effective this is depends on the hardware: The MacBook Air and Retina MacBook Pros are supposed to have 30 days on standby, whereas the older machines that have CD/DVD drives get less time.

posted November 22, 2017

INITIAL PRESENTATION

Chief Complaint

'My vision is blurry and distorted.'

• Fluid for Mac turns your favorite Web sites into Mac apps that you can run as standalone OS X desktop apps. If running Web apps like Facebook, Pandora, or Gmail in a separate tab of your Web.
• Mac OS X Snow Leopard (version 10.6) is the seventh major release of macOS, Apple's desktop and server operating system for Macintosh computers. Snow Leopard was publicly unveiled on June 8, 2009 at Apple’s Worldwide Developers Conference.On August 28, 2009, it was released worldwide, and was made available for purchase from Apple's website and retail stores at the price of US$29 for a.

History of Present Illness

The patient is a 68-year-old female with a history of non-exudative macular degeneration referred for vision changes. She began to notice increased difficulty reading due to blurry vision and distortion of vision in the right eye (OD) about 6 months prior to presentation. The left eye (OS) was unchanged. She had no previous history of exudative macular degeneration.

Past Ocular History

Non-exudative macular degeneration of both eyes (OU), nuclear sclerosis cataracts OU

Past Medical History

Hypertension, gastroesophageal reflux disease (GERD), hemifacial spasm with facial nerve release, carpel tunnel syndrome, bilateral knee replacements

Loss Of Fluid Mac Os X

Medications

AREDS vitamins, hydrochlorothiazide, propranolol, ranitidine

Allergies

Non-steroidal anti-inflammatory drugs (NSAIDs)

Family History

Non-contributory

Social History

Non-contributory

Review of Systems

Negative except for what is detailed in the history of present illness

OCULAR EXAMINATION

Visual Acuity with correction by Snellen chart

• OD: 20/80-1 eccentrically (pinhole no improvement)
• OS: 20/20-2 (pinhole no improvement)

Ocular Motility/Alignment

Full ocular motility OU, orthophoria in primary gaze

Intraocular Pressure (by Tonopen)

• OD: 17 mmHg
• OS: 17 mmHg

Pupils

• OD: 4 mm in dark, 3 mm in light, no relative afferent pupillary defect (RAPD)
• OS: 4 mm in dark, 3 mm in light, no RAPD

External

Normal

Slit lamp exam

• Lids/lashes: Normal OU
• Conjunctiva/sclera: Clear and quiet OU
• Cornea: Clear OU
• Anterior chamber: Deep and quiet OU
• Iris: Normal architecture OU
• Lens: 2+ nuclear sclerosis OU

Dilated fundus examination (DFE)

• Vitreous: No posterior vitreous detachment (PVD) OU
• Disc: Normal OU
• Cup-to-disc ratio: 0.2 OU
• Macula: 400 micron full-thickness macular hole OD. Pigment mottling and fine drusen OS.
• Vessels: Normal OU
• Periphery: Reticular pigment change OU

Additional Testing

Figure 1: Spectralis ocular coherence tomography (OCT) of the macula OD on initial presentation demonstrating the presence of a full-thickness macular hole with interstitial and subretinal fluid.

Differential Diagnosis

• Full-thickness macular hole (primary or secondary)
• Lamellar macular hole
• Pseudohole

DIAGNOSIS

Full-thickness macular hole (FTMH) OD

CLINICAL COURSE

The patient underwent 23-gauge pars plana vitrectomy, epiretinal membrane (ERM) peel, fluid-air exchange, 25% sulfur hexafluoride (SF6) OD. At the one-month post-operative visit, the patient's vision with correction had improved from 20/80-1 eccentrically to 20/60-2 eccentrically. On OCT images there was interval closure of the macular hole (Image Set 2). Vision ultimately returned to 20/30 over six months and was stable five years later.

Figure 2: Spectralis OCT of the macula OD at the one-month post-operative visit demonstrating interval closure of the macular hole.

DISCUSSION

Etiology/Epidemiology

FTMHs are a relatively uncommon problem of the retina with a reported prevalence of 0.2 per 1000 persons in the Blue Mountains Study and to up to 3.3 per 1000 persons in the Baltimore Eye Study.(1) Incidence is 8 per 100,000 persons per year.(2) There is bilateral involvement in 5-20% of cases, but FTMHs rarely present simultaneously.(1-3) FTMHs occur most in the 6th and 7th decades of life and have a female:male incidence of 2:1.(2, 3) It is unknown why females are more likely to have a FTMH in this age-related, idiopathic disease.

Pathophysiology

FTMHs were first described in 1869 by Knapp.(1) Initially, the pathophysiology was believed to be degenerative, and hence the early name by Kuhnt was 'retinitis atrophicans sive rarificans centralis.'(4) The understanding of the pathophysiology has expanded as examination techniques improved and with the advent of OCT.(1) FTMHs are currently divided into primary and secondary macular holes based on etiology.(1)

Vitreomacular traction plays a major role in the formation of primary FTMHs.(1, 4, 5) Gass, in his descriptions of the stages of macular holes, hypothesized that the shrinking of prefoveal vitreous cortex leads to anterior traction on the retina.(5) As the vitreous continues to detach, tangential traction from the prefoveal vitreous forms the hole within the fovea.(5) OCT has helped further our understanding of the vitreoretinal interface, showing that the process of PVD tends to begins perifoveally, leading to persistent adherence at the fovea.(4) This detachment of the vitreous can begin early in life.(1)

The following points further illustrate the role of the vitreous detachment in the pathophysiology of FTMH. In patients with a FTMH, if the fellow eye has already undergone PVD, there is a very low risk of FTMH in the fellow eye.(4, 5) In a study by Niwa, the fellow eyes of 201 patients with FTMHs were observed for two years. Of the fellow eyes of 201 patients, 58 still had vitreofoveal attachments. Of those 58 patients with vitreofoveal attachments, three patients developed a FTMH in the fellow eye, 24 had PVD over the fovea without macular hole, and 31 eyes did not have any changes in the vitreofoveal relationship over the two years.(6) Notably, macular holes developed only in those patients with changes in the vitreofoveal relationship.(6) In a series by Johnson, 96% of 26 eyes with Stage 1 or 2 idiopathic macular holes had a shallow, localized perifoveal vitreous detachment.(7) The vitreous often separates from the fovea last because of firm adherence to the areas of thinnest internal limiting membrane (ILM), including the 500 microns of the fovea. It is hypothesized that vitreous motion due to eye movement may exert localized forces on the fovea at the points of adherence.(7)

While the role of the vitreous is important in the pathophysiology of primary macular holes, retinal degeneration may also play a role. For example, some patients have developed macular holes after extended periods following vitrectomy, where vitreous has been previously removed.(8) Retinal thinning and degeneration may cause small holes to develop, which may close spontaneously via glial proliferation, and this hypothesis would explain the predominance of glial cells and Muller cells in the operculum.(8) Vitreous that is present may prevent closure due to the traction and chemical inhibition of cell migration.(8) It is likely that both degenerative and vitreous traction mechanisms are contributing to the pathophysiology.

In contrast to primary macular holes, FTMH can also be secondary, for example after trauma and sudden axial compression.(1) This leads to retinal rupture of the fovea in addition to other traumatic injuries including sclopetaria, peripheral retinal breaks, and commotio retinae. One major distinguishing feature of secondary macular holes is that the vitreous may not be detached and is a far less common etiology of macular holes than primary macular holes.(1)

Symptoms/Signs

Patients with macular holes may present with painless decreased central vision with a central scotoma and/or metamorphopsia.(3) In some cases, patients may not notice vision loss unless the other eye is occluded, especially for Stage 1 macular holes.(3) Visual acuity is not only decreased due to the central retinal tissue defect but also worsened by the surrounding retinal detachment and cystic changes that can be present.(3)

The clinical signs of macular holes depend on the stages as first defined by Gass.(5) Clinically, these stages were revised by Gass in 1995 and represented in Figure 1.(9) In Stage 1 macular holes, there is cystic foveal change that appears clinically as a yellow spot (Stage 1a) or a yellow foveal ring (Stage 1b). Stage 2 is a full-thickness retinal defect that has a pseudo-operculum and appears as an eccentric oval or crescent shaped defect on a yellow ring. Stage 2 often has an irreversible progression to Stage 3, which is a >400 micron full-thickness retinal defect with a persistent hyaloid attachment, often with a small ring of subretinal fluid. The presence of a Weiss ring suggesting the presence of a complete PVD qualifies as a Stage 4, and yellow deposits are often visible in the defect. The Watzke-Allen test is a useful clinical test for confirming a FTMH. In the Watzke-Allen test, a thin slit beam is projected over the suspected hole, and patients are asked to report if they see a break in the light beam, which confirms a full-thickness retinal defect.

Figure 3: This figure demonstrates the stages of macular holes based on the 1995 paper by J. Donald M. Gass.(9) This figure shows the range of pathology between cystic changes (Stage 1) to full thickness defects with a complete posterior vitreous detachment (Stage 4)

Testing

Optical coherence tomography (OCT) is very useful in diagnosing a FTMH and distinguishing it from other similar-appearing diagnoses. Lamellar macular holes have missing inner retinal tissue, but the RPE and photoreceptor layers are intact on OCT and often have a tri- or bilobulated appearance on fundus exam/photos.(1) Lamellar macular holes often lack the thickening, subretinal fluid, or cystic changes common to FTMHs.(3) Pseudoholes are due to centripetal contraction of an ERM resulting in the appearance of a hole on clinical examination, but pseudoholes do not have loss of retinal tissue on OCT.(1, 3) OCT can also help distinguish FTMHs from other similar-appearing conditions such as solar retinopathy, central serous chorioretinopathy, macular druse, pattern dystrophy, and pseudo-operculum.(3, 4) Macular holes can be sized on OCT and are classified as small <250 microns, medium 250-400 microns, or large >400 microns.(2) These are sized based on using the narrowest point in the mid retina in a plane parallel to the retina.(1)

Treatment/Management/Guidelines

Treatment of FTMHs was initially proposed by Kelly and Wendel in 1991, and in their early series of 52 patients, pars plana vitrectomy with vitreous cortex detachment and fluid-gas exchange was successful in closing 58% of macular holes.(10) In those who had closure, 73% had improvement in visual acuity by two lines or better.(10) The proposed mechanism in which this procedure closes holes is the release of vitreomacular traction, then gas to dehydrate the hole edges, occlude fluid, and allow glial cells to proliferate and close the hole.(1) With modern surgical techniques, the successful anatomical closure rates approach 100%.(1) Complications of the surgery include iatrogenic retinal tears (10%), ocular hypertension, endophthalmitis, cataract (50% at two-year follow up) and visual field loss.(1-3) The addition of ILM peeling has the additional complications of ganglion cell layer loss and dissociation of the nerve fiber layer.(1)
The treatment and prognosis is often dependent on the stage. Stage 1 holes will spontaneously resolve in about 50% of eyes.(2) If they do progress, it is usually early and the Vitrectomy for Prevention of Macular Hole Study Group reported that 40% of eyes with Stage 1 holes progressed over 4.1 months.(4) Once the hole is Stage 2 or more, the spontaneous closure rate is low (2-4%), and surgery is indicated to close the hole and restore vision.(3) The size of the hole is important, as holes <250 microns have a 98% surgical closure rate, while holes >400 microns have a lower closure rate at about 90%.(1) By 2-4 weeks after surgery, the successful closure is apparent on OCT with reapproximation of the retinal tissue.(3) Final vision after treatment is quite good, with 2/3 of patients 20/50 or better.(3)

Despite the relatively high success rate of repair, many controversies in macular hole surgery remain. This includes the utility of adjuvant therapies including TGF-b, autologous serum, whole blood, and autologous concentrated platelets to aid in the closure of chronic or large holes. Another controversy is the benefit of ILM removal for improved closure rates versus posterior hyaloid removal and/or ERM removal alone.(1) In one study of FTMHs >400 microns, the closure rate was 73.3% without peel and 100% with ILM peel.(1) In FTMHs <400 microns, the closure rates were 100% for both groups (with and without ILM peel), arguing against the need for ILM peel in small FTMHs.(1)

Post-operative face down positioning has been recommended since the invention of the surgery, but its necessity is becoming less clear. Often, face down positioning for one week is recommended to provide maximum gas tamponade.(2) More recent studies have found comparable success rates with no face-down positioning after surgery, or assuming a less-strict 'reading' position.(3) This is especially true if enough gas is present to isolate the hole from the vitreous over the 3-7 days required for closure.(1) Additionally, the role of gas tamponade itself is unclear. Vitreous release without gas has successfully closed some holes.(8) The release of vitreomacular traction may be the most important factor in allowing the hole to close and reparative gliosis to occur.(8)

Pharmacologic therapy has been developed, and intravitreal ocriplasmin is FDA-approved for the treatment of macular holes. There remains controversy about the utility of ocriplasmin, and success rates are best in the treatment of small holes with persistent vitreomacular traction.(1) In phase 3 clinical trials, small holes <250 microns had a closure rate of 58.3%.(2)

EPIDEMIOLOGY OR ETIOLOGY Bilateral involvement in 5-20% 6th and 7th decades of life Female to male incidence of 2:1	SIGNS Gass Stages: Stage 1 - cystic foveal change Stage 2 - 100-300 micron full-thickness retinal defect with pseudo-operculum Stage 3 - 250-600 micron full-thickness retinal defect with a persistent hyaloid attachment Stage 4 - stage 3 with complete PVD
SYMPTOMS Central scotoma Painless central vision loss Metamorphopsia Central blurred vision	TREATMENT/MANAGEMENT Observation of Stage 1 holes often is appropriate Pars plana vitrectomy with vitreous cortex detachment, epiretinal/internal limiting membrane peel, and fluid-gas exchange Intravitreal ocriplasmin in select cases

>

References

1. Guadric, A and Tadayoni, R. Macular Hole. Ryan's Retina. Atlanta: Elsevier; 2018; p. 2213-2232.
2. McCannel, CA. Diseases of the vitreous and vitreoretinal interface. Section 12: Retina and Vitreous. San Francisco: American Academy of Ophthalmology; 2016-2017; Chapter 16, p. 294-297.
3. Moshfeghi, AA and Duker, JS. Macular hole. Ophthalmology. Edinburgh: Mosby/Elsevier; 2009; Chapter 6.31, p. 610-613.
4. Gottlieb, JL. Idiopathic macular hole. Albert & Jakobiec's Principles and Practice of Ophthalmology. Atlanta: Elsevier; 2008; p. 2029-2037.
5. Gass, JD. Idiopathic senile macular hole. Its early stages and pathogenesis. Arch Ophthalmol 1988;106(5):629-39.
6. Niwa, H, Terasaki, H, Ito, Y and Miyake, Y. Macular hole development in fellow eyes of patients with unilateral macular hole. Am J Ophthalmol 2005;140(3):370-5.
7. Johnson, MW, Van Newkirk, MR and Meyer, KA. Perifoveal vitreous detachment is the primary pathogenic event in idiopathic macular hole formation. Arch Ophthalmol 2001;119(2):215-22.
8. Smiddy, WE and Flynn, HW, Jr. Pathogenesis of macular holes and therapeutic implications. Am J Ophthalmol 2004;137(3):525-37.
9. Gass, JD. Reappraisal of biomicroscopic classification of stages of development of a macular hole. Am J Ophthalmol 1995;119(6):752-9.
10. Kelly, NE and Wendel, RT. Vitreous surgery for idiopathic macular holes. Results of a pilot study. Arch Ophthalmol 1991;109(5):654-9.

Suggested Citation Format

Janson BJ, Han IC. Full-Thickness Macular Hole (FTMH). EyeRounds.org. November 22, 2017. Available from http://EyeRounds.org/cases/261-FTMH.htm

What is macular edema?

Macular edema is the build-up of fluid in the macula, an area in the center of the retina. The retina is the light-sensitive tissue at the back of the eye and the macula is the part of the retina responsible for sharp, straight-ahead vision. Fluid buildup causes the macula to swell and thicken, which distorts vision.

What are the symptoms of macular edema?

The primary symptom of macular edema is blurry or wavy vision near or in the center of your field of vision. Colors might also appear washed out or faded. Most people with macular edema will have symptoms that range from slightly blurry vision to noticeable vision loss. If only one eye is affected, you may not notice your vision is blurry until the condition is well-advanced.

What causes macular edema?

Macular edema occurs when there is abnormal leakage and accumulation of fluid in the macula from damaged blood vessels in the nearby retina. A common cause of macular edema is diabetic retinopathy, a disease that can happen to people with diabetes. Macular edema can also occur after eye surgery, in association with age-related macular degeneration, or as a consequence of inflammatory diseases that affect the eye. Any disease that damages blood vessels in the retina can cause macular edema.

Diabetic macular edema (DME)

Diabetic macular edema (DME) is caused by a complication of diabetes called diabetic retinopathy. Diabetic retinopathy is the most common diabetic eye disease and the leading cause of irreversible blindness in working age Americans. Diabetic retinopathy usually affects both eyes.

Diabetic retinopathy is caused by ongoing damage to the small blood vessels of the retina. The leakage of fluid into the retina may lead to swelling of the surrounding tissue, including the macula.

DME is the most common cause of vision loss in people with diabetic retinopathy. Poor blood sugar control and additional medical conditions, such as high blood pressure, increase the risk of blindness for people with DME. DME can occur at any stage of diabetic retinopathy, although it is more likely to occur later as the disease goes on.

Experts estimate that approximately 7.7 million Americans have diabetic retinopathy and of those, about 750,000 also have DME. A recent study suggests that non-Hispanic African Americans are three times more likely to develop DME than non-Hispanic whites, most likely due to the higher incidence of diabetes in the African American population.

Eye surgery

Macular edema may develop after any type of surgery that is performed inside the eye, including surgery for cataract, glaucoma, or retinal disease. A small number of people who have cataract surgery (experts estimate only 1-3 percent) may develop macular edema within a few weeks after surgery. If one eye is affected, there is a 50 percent chance that the other eye will also be affected. Macular edema after eye surgery is usually mild, short-lasting, and responds well to eye drops that treat inflammation.

Age-related macular degeneration

Age-related macular degeneration (AMD) is a disease characterized by deterioration or breakdown of the macula, which is responsible for sharp, central vision. In neovascular AMD, also called “wet” AMD, blood vessels begin to grow up from the choroid (the bed of blood vessels below the retina) and into the retina. These new and abnormal blood vessels leak fluid into the macula and cause macular edema.

Blockage of retinal blood vessels

When retinal veins are blocked (retinal vein occlusion), blood does not drain properly and it leaks into the retina. If it leaks into the macula, this produces macular edema. Leakage is worsened by the severity of the blockage, how many veins are involved, and the pressure inside them. Retinal vein occlusion is most often associated with age-related atherosclerosis, diabetes, high blood pressure, and eye conditions such as glaucoma or inflammation.

Inflammatory diseases that affect the retina

Uveitis describes a group of inflammatory diseases that cause swelling in the eye and destroy eye tissues. The term “uveitis” is used because the diseases most often affect a part of the eye called the uvea. However, uveitis is not limited to the uvea. Uveitis can affect the cornea, iris, lens, vitreous, retina, optic nerve, and the white of the eye (sclera).

Inflammatory diseases and disorders of the immune system may also affect the eye and cause swelling and breakdown of tissue in the macula. These disorders include cytomegalovirus infection, retinal necrosis, sarcoidosis, Behçet’s syndrome, toxoplasmosis, Eales’ disease, and Vogt-Koyanagi-Harada syndrome.

How will my eye doctor check for macular edema?

To diagnose macular edema, your eye care professional will conduct a thorough eye exam and look for abnormalities in the retina. The following tests may be done to determine the location and extent of the disease:

Visual acuity test. A visual acuity test is a common way to identify vision loss and can help to diagnose vision loss as a result of macular edema. This test uses a standardized chart or card with rows of letters that decrease in size from top to bottom. Covering one eye, you will be asked to read out loud the smallest line of letters that you can see. When done, you will test the other eye.

Dilated eye exam. A dilated eye exam is used to more thoroughly examine the retina. It gives additional information about the condition of the macula and helps detect the presence of blood vessel leakage or cysts. Drops are placed in your eyes to widen, or dilate, your pupils. Your eye care professional then examines your retina for signs of damage or disease.

Fluorescein angiogram. If earlier tests indicate you could have macular edema, your eye care professional may perform a fluorescein angiogram. In this test, a special dye is injected into your arm and a camera takes photos of the retina as the dye travels through the blood vessels. This test helps your ophthalmologist identify the amount of damage to the macula.

Optical coherence tomography. This is a test that uses a special light and a camera for detailed views of the cell layers inside the retina. It detects the thickness of the retina and so it’s useful in determining the amount of swelling in the macula. Your eye care professional may also use optical coherence tomography after your treatment to track how well you are healing.

The Amsler Grid. The Amsler Grid provides an easy way to test whether or not your central vision has changed. It can recognize even small changes in your vision.

If you need reading glasses, wear them when you look at the Amsler grid. The grid should be at the same distance from your eyes as your usual reading material – about 14 inches. Test both eyes, one at a time, to see if any parts of the grid look distorted, missing, or dark. Mark the areas of the chart that you’re not seeing properly and bring it with you to your next eye exam.

What's the treatment for macular edema?

Treatment for macular edema is determined by the type of macular edema you have. The most effective treatment strategies first aim at the underlying cause of macular edema, such as diabetes or high blood pressure, and then directly treat the damage in the retina.

Treatments for diabetic macular edema and macular edema caused by other conditions are often the same. However, some cases of macular edema may need additional treatments to address associated conditions.

In the recent past, the standard treatment for macular edema was focal laser photocoagulation, which uses the heat from a laser to seal leaking blood vessels in the retina. However, recent clinical trials, many of them supported by NEI, have led doctors to move away from laser therapy to drug treatments injected directly into the eye.

Anti-VEGF injections

The current standard of care for macular edema is intravitreal injection. During this painless procedure, numbing drops are applied to the eye, and a short thin needle is used to inject medication into the vitreous gel (the fluid in the center of the eye). The drugs used in this treatment – Avastin, Eylea, and Lucentis – block the activity of a substance called vascular endothelial growth factor (VEGF). VEGF promotes blood vessel growth. In a healthy eye, this is not a problem. But in some conditions, the retina becomes starved for blood and VEGF becomes overactive. This causes the growth of fragile blood vessels which can rupture and leak blood into the retina and macula, causing macular edema. Anti-VEGF treatment blocks the activity of VEGF and slows the progress of macular edema.

The anti-VEGF drugs all work in similar ways to block vessel formation and prevent leakage in the retina. A recent NEI-supported clinical trial that directly compared the effectiveness of the three drugs for DME found that the drugs performed similarly for patients with mild vision problems. However, Eylea performed better for those with more serious vision loss (20/50 or worse). Your eye care professional will discuss which drug treatment is the best option for you.

DME, as viewed by optical coherence tomography (OCT). The two images were taken before (Top) and after anti-VEGF treatment (Bottom). The dip in the retina is the fovea, a region of the macula where vision is normally at its sharpest. Note the swelling of the macula and elevation of the fovea before treatment.

Anti-inflammatory treatments

Corticosteroid (steroid) treatments, which reduce inflammation, are the primary treatment for macular edema caused by inflammatory eye diseases. These anti-inflammatory drugs are usually administered via eye drops, pills, or injections of sustained-release corticosteroids into or around the eye. Clinicians now have the option of three FDA-approved sustained-release corticosteroid implants for more serious or longer-lasting conditions:

• Ozurdex is an implant that delivers an extended release dose of dexamethasone. It is approved for DME, macular edema following retinal vein occlusion, and [non-infectious] uveitis.
• Retisert is an implant that delivers an extended release dose of fluocinolone acetonide. It is approved for the treatment of uveitis, as well as DME that doesn’t respond to corticosteroids.
• Iluvien is an implant that releases small doses of fluocinolone acetonide over the course of several years. The U.S. Food and Drug Administration has approved it for treating DME.

Nonsteroidal anti-inflammatory drugs (NSAIDs), in the form of eye drops, are sometimes used either before or after cataract surgery to prevent the development of macular edema. Because they are chemically different from corticosteroids, NSAIDs may be used when the eye doesn’t respond to steroid treatment or to avoid the side-effects of steroid use in the eye.

Vitrectomy

Some cases of macular edema are caused when the vitreous (the gel that fills the area between the lens and the retina) pulls on the macula. Surgery to remove the vitreous gel, called a vitrectomy, relieves the pulling on the macula. Vitrectomy also may be required to remove blood that has collected in the vitreous or to correct vision when other treatments for macular edema are unsuccessful. Most vitrectomy surgeries are performed as outpatient surgery.

What's the latest research on macular edema?

NEI-supported researchers are working in laboratories and clinics across the country to better understand why people get macular edema and to develop treatments that are more effective and easier to administer. Ultimately, researchers hope to develop treatments that could reverse, or even prevent, the development of macular edema. For example:

Loss Of Fluid Mac Os Download

• The NEI-supported Studies of Comparative Treatments for Retinal Vein Occlusion (SCORE) is a Phase III clinical trial to compare treatment protocols for macular edema associated with central retinal vein occlusion. The trial will test two anti-VEGF treatments – Avastin and Eylea – to compare their effectiveness. Because there is a significant difference in cost per dose between the two drugs, it’s important for patients and doctors to have information about which drug might work best in specific cases.
• Anti-VEGF therapy has become the standard of care for DME, but not all patients respond to the treatment. In fact, close to half of those treated don’t improve. In addition to VEGF, a number of inflammatory factors also influence macular edema. NEI-supported researchers are looking at how growth factors like VEGF interact with inflammatory factors to contribute to macular edema. Their findings could lead to combined treatment approaches that would target both growth and inflammatory factors and be a more effective treatment for people with DME.
• Anti-VEGF drugs have additional limitations. Repeated injections are required and other cell types in the eye may be impacted. The drugs also don’t address other factors that may influence the development of macular edema, including inflammation. NEI-supported researchers are investigating a novel nanoparticle delivery platform that uses micro-RNAs, parts of the genome that influence gene expression, to determine if they can be used to shut down genes associated with the development of macular edema.
• NEI-supported researchers are investigating the potential to regenerate tissue that is destroyed or damaged in retinal diseases such as macular edema. The researchers are studying how cells in the retina respond when the retina is stressed from lack of blood. The goal is to understand how interactions between different cell types — including nerve cells and the cells that make blood vessels — can lead to abnormal blood vessel growth. This could potentially lead to the development of drugs to discourage abnormal vessel growth.