CYSTOID MACULAR EDEMA

PRESENTATION

DIABETIC CMEM

Diabetic macular edema develops as a consequence of ischemia, leakage of fluid from retinal blood vessels, and tractional retinal changes. Chronic untreated macular edema, or thickening of the retina, can eventually lead to the collection or pooling of the fluid into cysts. When these cysts develop, it leads to cystoid macular degeneration changes associated with diabetic macular edema. This form of diabetic cystoid macular changes is generally resistant to traditional laser management and can also be seen in patients who have unresolved hypertension and protein urea (kidney failure) systemic problems.

POST-CATARACT SURGERY CME

In the post-operative period, patients may respond to the surgical intervention techniques by developing inflammation, a common consequence of all surgical procedures. However, in some patients, inflammation inside of the eye can lead to the development of cyst formations in the central macular area, or cystoid macular edema (CME). While common in the early post-operative period following cataract surgery, the majority of cysts resolve within four to six weeks post-operatively. However, some patients will develop chronic post-cystoid macular edema, which when left untreated, can lead to further visual loss and permanent deterioration of sight.

EPIRETINAL MEMBRANCE CME

An epiretinal membrane formation is the development of scar tissue on the pre-retinal surface. These chronic traction changes that develop from the retina membrane pulling on the retina can lead to the development of tractional associated edema. When chronic, this edema can eventually coalesce into frank cyst formation developing epiretinal cystoid macular degeneration changes. Traditionally, patients who develop CMD formation with their epiretinal membranes should be referred for surgical intervention since the risk for further progression of their disease and chronic deterioration of sight is quite high.

MYOPIC CME

In patients who have high myopia, the actual nature of the myopia (enlarged eyeball) is generally associated with the tissues on the inside lining of the eye being under considerable tension. This chronic tension inevitably leads to the formation of intra-retinal edema and thickness due to the abnormal interactions between the vitreous and the retina. These areas of localized retinal thickening eventually coalesce to form a full thickness cyst. Eventually these cysts may rupture, leading to myopic macular holes.

PREVENTION

CONTROL BLOOD PRESSURE

Diabetic patients with uncontrolled hypertension and renal failure problems may go on to develop more aggressive diabetic macular edema, in particular the type of diabetic macular edema associated with cystoid changes. Accordingly, in patients who have uncontrolled hypertension and diabetic nephropathy with diabetic cystoid macular degeneration formations in the retina, it is important that systemic management of these other problems be achieved if there is to be an attempt to resolve the intra-retinal cyst associated with their diabetic edema.

DIABETIC EARLY LASER

In diabetic patients with macular edema, untreated chronic macular edema will inevitably lead to retinal cyst formation. This can be aggravated in those patients who have underlying ischemia, nephropathy, and hypertension. Diabetic laser treatment in the early stages of macular edema are advocated by the Retina Team at OCC Eyecare. These early diabetic laser treatments are administered to prevent a critical mass of diabetic edema which, left untreated, could lead to the formation of a retinal cyst which could then lead to substantial loss of sight.

CATARCT SURGERY

Cystoid macular degeneration is one of the complications associated with cataract surgery. Pre-treating patients with anti-inflammatory medications can reduce the formation of post-cataract cystoid macular edema. Those patients at particular risk of developing CMD include those who have had previous central macular edema with uncomplicated cataract formation in their other eye. Accordingly, topical anti-inflammatories pre- and post-operatively can be quite helpful in preventing post-cataract associated cystoid macular degeneration.

TREATMENT

EYE DROPS

In cases of cystoid macular degeneration associated with inflammation, the use of topical anti-inflammatory medications may be warranted. The most common example of this is in post-cataract cystoid macular edema/degeneration cases. In these patients, the use of an anti-inflammatory, in the form of a non-steroidal anti-inflammatory medication and a topical steroid, can resolve the intra-retinal cystoid changes. Once the cystoid changes have been resolved, a large number of these patients will see improvements in their vision. However, in those patients in whom the cystoid changes have been longstanding, or in those cases where the cystoid changes have been quite severe, there may be no further improvement of sight despite resolution of the cystoid changes.

INTRAOCULAR KENALOG INJECTIONS

The use of Kenalog injections in patients who have cystoid macular degeneration may be warranted in inflammatory situations, as well as in patients who have tractional induced or systemic disease associated cystoid macular degeneration. For example, in post-cataract cystoid macular edema in patients who fail to respond to topical anti-inflammatories to resolve the CME formation, the use of an intraocular Kenalog injection can be quite helpful. Additionally, intraocular Kenalog injections are helpful for diabetic cystoid macular degeneration. With that said, it is important to remember that in diabetic patients with cystoid macular degeneration, there may also be underlying vitreo retinal tractional changes causing the cystoid macular degeneration. Epiretinal and myopic patients who develop cystoid macular degeneration tend not to be aided by intraocular Kenalog injections alone. However, the use of intraocular Kenalog injections at the time of vitrectomy surgery can hasten recovery and potentially lead to a better chance of overall improvement of sight following surgical intervention.

YAG VITREOLYSIS

In patients with significant vitreous extending into the anterior chamber, most commonly seen post- cataract surgery or post trauma, the use of a YAG laser to break the strands of vitreous in the anterior chamber may be warranted, especially if the amount of vitreous strands in the anterior chamber is of minimal significance. YAG Vitreolysis used to rupture these vitreous strands may resolve the intra-retinal cystoid changes. However, in those patients who have significant vitreous which is not treatable by YAG laser, a vitrectomy surgery may be indicated.

VITRECTOMY

In a variety of different diseases in which intra-retinal cystoid macular degeneration has occurred, vitrectomy surgery can be one of the few mechanisms by which recovery or reduction of the intra retinal cyst can occur, particularly in patients who have epiretinal membrane associated and myopic associated cystoid macular degeneration. In those patients who have diabetic cystoid macular degeneration, vitrectomy is generally reserved for those patients who have failed multiple laser treatments and injections.

PROGNOSIS

MYOPIC CUSTOID MACULAR EDEMA

In highly myopic, or nearsighted, patients who develop intra-retinal cystoid changes, the cyst may coalesce, eventually leading to full thickness macular hole formation. Patients with high myopia who start to develop cystoid or foveal schisis formation may show significant deterioration of sight.

EPIRETINAl MEMBRANCE & CYSTOID MACULAR EDEMA

In patients with epiretinal membrane formation and due cystoid macular changes, the development of cysts in the retina tends to indicate more progressive tractional changes on the retina which could lead to further deterioration of sight. At the stage where epiretinal membrane associated cystoid macular degeneration develops, there is an even further progression of sight deterioration. As the cyst coalesces, a partial thickness macular hole, or even full thickness macular hole, may form. Surgical intervention may be warranted when cystoid changes start to develop, depending on the visual acuity and other risk factors of the patient.

POST-CATARCT EXTRACTION CYSTOID MACULAR EDEMA

In some patients, cystoid changes, also known as cystoid macular edema, may develop in the central macula following cataract extraction surgery. These changes tend to be self limiting or can be treated with topical medications. In self-limiting cases in which the intra-retinal cyst resolves spontaneously, the chances for visual improvement are substantial. Additionally, for patients who are treated early with topical medications for persistent cystoid macular changes post-surgery, there is a good prognosis for recovery of sight. However, in those patients who have chronic cystoid macular edema, the chance for vision improvement is quite limited.

DIABETIC CYSTOID MACULAR EDEMA

In patients with diabetic cystoid macular degeneration or blister formation in the central portion of the macula, the prognosis for visual stabilization is quite guarded.

Cystoid macular degeneration is most commonly seen in diabetic patients who have severe ischemia of the central retina. Ischemia occurs when the very fine blood vessels which supply blood to the inner lining of the eye are damaged, generally by underlying an retinal disease or diabetes.

Unfortunately, there are currently no mechanisms for re-growth of these ischemic blood vessels. However, there are mechanisms which can be used to reduce diabetic cystoid macular degeneration. The mechanisms for treating diabetic cystoid macular degeneration include retinal lasers, intraocular surgical procedures, and injections.

The prognosis for patients with diabetic cystoid macular degeneration is guarded, at best, because it implies that there is severe retinal ischemia and the chance for visual loss is very high. The Retina team at OCC Eyecare offers the most advanced surgical and medical management for patients with diabetic cystoid macular degeneration and utilizes early surgical intervention techniques to help reduce the rate of progressive visual loss.