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Retinal Conditions

Diabetic Retinopathy

Diabetes mellitus is a disorder that is caused by a deficiency in insulin (Type 1) or an inability of existing insulin (Type 2 ) to keep blood sugars under control. Over time patients with diabetes, especially those with poorly controlled blood sugar may develop eye, kidney, heart, nerve and skin problems. In the eye, diabetes mainly affects the retina and causes diabetic retinopathy. Diabetes affects small blood vessels all over the body and makes them abnormally leaky. In the retina, capillaries (the tiniest of blood vessels) that supply nutrients and remove waste products become leaky and allow contents of blood (serum, lipids, and blood cells) to leak into the retina, causing the retina to swell (edema). This stage of retinopathy is called non-proliferative or background retinopathy. When swelling occurs in the macula (the part of the retina responsible for color and fine vision), vision becomes blurred and permanent damage can occur to the retina. Your retina specialist will examine your eye to determine if there is swelling in the macula that requires treatment (clinically significant macular edema). Treatment can be performed with laser in the office and may be repeated one or more times over the course of the lifetime of the patient. In some cases injections of steroid into the eye may be performed to help reduce swelling. In severe cases, vitrectomy surgery (removal of the vitreous gel) may be necessary, especially if laser and steroids have failed.

In more severe cases of diabetic retinopathy, leaky capillaries may become permanently damaged and may not work at all. This capillary damage results in lack of blood flow to sections of the retina (ischemia). Ischemia results in the production of chemical messengers in the retina that lead to development of abnormal new blood vessels (retinal neovascularization) that can grow out of the retina and into the vitreous (the jelly like substance that fills the eye). This stage of retinopathy is called proliferative diabetic retinopathy. These blood vessels use the vitreous gel as scaffolding and grow along its back surface (posterior hyaloid). Since the gel is in motion when the eye moves and these blood vessels are pulled on by the gel and in turn pull on the retina, they can lead to vitreous hemorrhage. Vitreous hemorrhage causes string like floaters that worsen and result in severe haze. The hemorrhage can become severe enough to cause severe vision loss and blindness. The pulling on the retina also can cause retinal detachment and result in severe visual loss and blindness. Your retina specialist will examine your eye for neovascularization. It is best to detect and treat neovascularization early with scatter laser treatment. (Yes, you can have 20/20 vision and still have abnormal retinal vessels!) This type of laser treatment destroys the damaged retina that is making the chemicals that cause these abnormal blood vessels to grow. After laser treatment, abnormal blood vessels shrink and are less likely to result in vitreous hemorrhage and retinal detachment. If vitreous hemorrhage or retinal detachment is severe or sight threatening, vitrectomy surgery may be necessary to restore vision and stabilize the retinopathy.

The most important way to prevent visual loss in diabetes to keep blood sugars and blood pressures under good control. Keeping the Hemoglobin A1C (long term measure of sugar control) under 7.0 is extremely important. Tight blood sugar control reduces the risk of developing diabetic retinopathy. Even if retinopathy develops, patients with tight control tend to have mild and non-sight threatening retinopathy. Annual check-ups by your eye doctor or retina specialist after the diagnosis of diabetes and every 6 month follow-up evaluation once diabetic retinopathy develops is important. Women who have diabetes and become pregnant may need very close monitoring during pregnancy.

Flashes and Floaters

The eye is like a complex hollow ball. The back 2/3rds of this hollow ball are filled with a gel like tissue called the vitreous. The vitreous has the consistency of solid gelatin at birth and is important for the normal maturation and development of the eye. After age 4 or 5, the eye matures to its adult size and the vitreous begins a long process of degeneration (liquefaction) and becomes more jelly like in consistency. Small pockets of liquefaction occur in the central vitreous and, between age 50-70, these pockets combine together and form one large pocket of liquefied gel. The peripheral gel is still solid and attached firmly to the retina and optic disc but there is no support from the central liquefied vitreous. The peripheral gel eventually and suddenly collapses and pulls away from the retina. This event is called a Posterior Vitreous Detachment (PVD). The tugging of the vitreous on the retina causes streaks of flashing lights in the peripheral visual field. The collapse of the vitreous results in one or more large floaters. When the PVD occurs, the vitreous may tug hard enough on the peripheral retina to tear it. A tear in the retina may be associated with hundreds or thousands of tiny, dot-like floaters. A tear the retina should be treated prompted with laser or cryotherapy (freezing treatment) to decrease the risk of retinal detachment.

Retinal Detachment

A retinal detachment occurs when a tear or hole in the retina allows the liquid vitreous to get under the retina and accumulate. The retina separates from the back wall of the eye. This detachment causes symptoms of a gradually enlarging veil or dark shadow in the peripheral visual field. When the detachment extends into the central part of the retina (macula) the central vision is lost. Retinal detachments should generally be fixed or complete loss of vision will result. Ideally the retinal detachment should be repaired prior to the involvement of the macula. If the macula becomes detached, the vision is unlikely to be as good as it was prior to the retinal detachment even with successful surgical re-attachment.

Retinal detachments may be fixed in the office in some selected cases by using a gas bubble and laser treatment called pneumatic retinopexy. More complex detachments commonly require sleral buckling or vitrectomy surgery in a hospital setting with anesthesia. In scleral buckling surgery, the retinal tear or tears (there may be several or many) are treated with cryotherapy (freezing treatment) and a band is sutured around the eyeball that indents the eye wall inward against the detached retina. This bump seals the retinal tears and the fluid under the retina is absorbed by the body. Thus, the retina becomes reattached to the back wall of the eye. A third way to fix retinal detachments is to perform vitrectomy surgery. The vitreous is removed using small needle like microinstruments. The tear is identified and treated with laser. The fluid under the retina removed with a straw like instrument. All of the fluid in the eye is then removed, and a gas bubble that usually lasts 2-6 weeks is placed in the eye. The bubble acts as an internal splint keeping the retina in place while the laser heals. The body absorbs the gas bubble slowly and the eye replaces the bubble with its own fluid. The vitreous does not grow back and is not necessary for the normal functioning of the eye. Remember that the collapsing vitreous gel actually caused the tear(s) that led to the detachment. Your retina surgeon will decide which of these three procedures is the best way to fix each retinal detachment.

Age-Related Macular Degeneration (ARMD)

ARMD is the leading cause of legal blindness in persons over the age of 55. Early symptoms include a reduction in reading speed, inability to read fine print, and skipping letters or lines when reading. Later symptoms can include distortion of straight lines or dark or missing areas in the central vision.

The macula is the central part of the retina and allows us to read fine print clearly and see colors vividly. It is this area of the retina that deteriorates in ARMD. There are 2 forms of ARMD. Everyone who has macular degeneration starts out with the dry type and 20% progress to the wet type over the course of a lifetime. Macular degeneration in its most severe forms almost never causes total blindness. Usually only central vision is lost. It is a disease that leaves older persons unable to read and drive. However, nearly all patients will still have enough vision to care for themselves.

Dry Macular degeneration:

Age Related Macular Degeneration (Dry)

As the macula ages, the retinal cells cannot remove their own waste products and begin to die. Deposits of these waste products, called drusen, build up under the retina. Drusen, when large in number and size, are the first signs of macular degeneration that an eye doctor sees on examination. Collections of drusen can crowd out other cells in the retina and can cause further damage to the retina and the pigmented cell layer underneath the retina called the retinal pigment epithelium. Eventually, clumping pigment and punched out areas of pigment loss called geographic atrophy are seen. These areas can cause blind spots in vision. These areas of atrophy progress slowly over years but can result in severe central vision loss. Currently there is no specific treatment for dry macular degeneration.

Wet Macular degeneration

20% of patients with dry degeneration will eventually develop abnormal blood vessels under the retina that can bleed and leak fluid. Patients often have abrupt vision loss with distortion of straight lines, or a stationary, dark or blurry spot in the central vision of one eye. The vision can worsen rapidly in a few days or weeks. Treatment can include traditional laser, injection of steroids into the eye, and/or ocular photodynamic therapy (cold laser). Each treatment has its risks and benefits and is individualized for the patient by the retina specialist. Multiple treatments may be necessary to control the disease. The treatments usually only slow down the disease and neither cure the disease nor commonly make the vision better.

Ocular Histoplasmosis Syndrome

Histoplasmosis is an infectious disease caused by Histoplasma capsulatum, a yeast like fungal organism that lives in the gastrointestinal tract of birds and is spread to humans by inhalation of dried and airborne dust containing spores. Almost everyone who lives or spends time in the Ohio and Mississippi River valleys has had systemic Histoplasmosis (almost 80 million people).

Amsler grid

Most of us get exposed to histoplasmosis and develop a flu-like illness and heal from it without problems. About 10% of persons who get this flu-like illness can develop scars in the back of the eye affecting the retina and a vascular layer under the retina called the choroid (Ocular Histoplasmosis). Sometimes these scars can occur around the optic nerve or near the macula. The scars themselves do not cause any visual problems. Many years later and generally in the prime of life (ages 20 to 55) these scars can be sites for the development of new blood vessels under the retina called choroidal neovascularization. Depending on where these blood vessels grow, they may or may not cause vision loss. The closer they are to the macula the more likely they are to cause vision loss. These new vessels are most often treated with laser, which can produce a blind spot at the site of treatment but will prevent further vision loss. Even with successful laser treatment, choroidal neovascularization may come back 25% of the time in the first five years in the treated eye. In some cases the abnormal blood vessels grow directly under the very center of the macula (fovea) and cannot be treated with laser because the resulting blind spot would be in the center of vision. In these cases, medical therapy with steroids (prednisone), cold laser treatment (ocular photodynamic therapy), or simply conservative observation may be recommended. In some very severe cases, surgical removal of blood vessels may be performed.

It is very important to monitor central vision in both eyes using an Amsler grid daily if you have ocular histoplasmosis and especially if the vision has been affected in one eye. Patients who develop choroidal neovascularization in one eye have a 25% chance of developing the same in the fellow eye within 3 years if they have histo scars close to the macula.

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