Frequently Asked Questions
RETINA: PAO SUBSPECIALTY SOCIETY: VITREO-RETINA SOCIETY OF THE PHILIPPINES
What are those little black spots and lines that I see especially in bright light? Are they dangerous? What are those lightning like flashes that I occasionally see in the sides of my visual field?
Those are called “floaters” by your eye doctor. Most of the cavity of the eye is filled with a gel-like substance called the vitreous gel. These floaters are clumps of vitreous collagen meshwork that have formed as a result of liquefaction of the vitreous gel, a physiologic process called “syneresis”. When we are young, the vitreous is a gel that has an invisible meshwork- like structure. When we age the gel liquefies. At age 50 years of age, 60% of us already have liquefaction of the vitreous, either partially or complete. When this happens the collagen meshwork collapses and forms little clumps that now become big enough to cast shadows on our retina. We see them as black or gray dots, patches, lines that move upwards and downwards, and left and right as if floating in our field of vision.
As a general rule these are not ominous signs as they occur as part of the aging process. In certain situations however, they can be dangerous. Occasionally people with vitreous floaters have retinal thinning called “lattice”, retinal breaks or tears and holes that must be treated right away with focal laser to prevent retinal detachment. Occasionally the floaters are actually red blood cells and clumps of vitreous hemorrhage. The hemorrhage is due to the avulsion of retinal blood vessels that are pulled by the collapse of the vitreous meshwork and separation of the posterior vitreous cortex from the retina.
Flashes are extremely bright lightning like streaks of light seen in the periphery of one’s visual field. They are caused by stimulation of the retina by pulling of the posterior vitreous cortex on the retina to which it is attached. They are actually similar to hallucinations since they are generated by the brain, as responses of the retina to the physical stimulation of pulling or traction.
Although usually harmless, it is best to see an Ophthalmologist (eyeMD) if you experience “floaters” or “flashes” just to make sure they are not signs of more serious conditions of the retina.
How does diabetes mellitus affect the eye? Will good blood sugar control reverse the bad effects of diabetes on my eye?
Diabetes is a potentially blinding disease. It causes diabetic retinopathy which happens as a result of poor blood circulation and therefore inadequate oxygen supply. Diabetic retinopathy is a retinal disease that results in retinal hemorrhages, ischemic patches and abnormalities in the retinal blood vessels. Abnormal vessel growth eventually leads to massive bleeding and/or traction membrane growth, and eventually traction retinal detachment. The major risk factors are the duration of diabetes, level of blood sugar control, concomitant hypertension and pregnancy. The longer the patient has diabetes, the more he is at risk of developing the disease. By the 15th year of diabetes mellitus, 80 % of diabetics have the lower stages of diabetic retinopathy and approximately 20% already have the blinding stages of the disease.
Good blood sugar control has been proven to reduce the chance of developing diabetic retinopathy or its progression by about 30%. If a patient already has diabetic retinopathy, control of blood sugar will neither reverse the process nor reduce the damage already done to the retina. Any treatments instituted, both to the eyes and the diabetes, including laser treatment to the eyes, blood sugar and blood pressure control are aimed at preventing progression to the higher stages of retinopathy.
The pregnant diabetic patient deserves special attention as progression of the disease can be aggravated by the pregnancy.
Diabetes can also cause affectation of the optic nerve, a condition called diabetic papillopathy. Eye muscle problems (deviation of the eyeball) can also be caused by diabetes mellitus as it can affect the nerve supply of the eye muscles. Cataracts can also be aggravated by diabetes mellitus.
If I eat plenty of carrots and yellow foods will my retina be stronger and more resistant to retinal disease?
The eye and the retina certainly need vitamins. While eating carrots and yellow veggies and foodstuffs rich in vitamin A can help one get this vitamin from natural sources, the eye and retina in particular need more than just vitamin A but also vitamin E and C, zinc and selenium as well. These are called antioxidants. Instead of taking vitamin A supplements alone, it would be better to take a vitamin preparation with A, C, E, selenium and zinc. These are marketed as “antioxidants”.
Antioxidants remove free radicals from our system and help “spare” retinal cells (and other body cells) from oxidative damage, and make metabolism more efficient. In this way they are good for not only for our eyes but for our entire body.
Taking these vitamins will not stop myopia and myopic degenerative disease of the retina. In the right amounts (the AREDS formula) antioxidants have been shown to be effective for Age Related Macular Degeneration. Your ophthalmologist can prescribe the anti-oxidant preparation for you.
Will a baby’s prematurity cause blindness? What can be done to prevent blindness from Retinopathy of Prematurity?
Not all prematurity results in blindness. A premature baby of a certain weight and birth age, defined as “high risk”, is open to the development of the disease during the first few weeks of life outside the womb. The definition of “high risk” is a birthweight of 1500 grams and below, and age at birth of 32 weeks and below. Only 15% of “high risk” babies actually develop some form//stage of the disease, but only 5-6% of these go into the severely visually debilitating stages. Fortunately only about 1% of all “high risk” premature babies actually develop blinding disease.
Prematurity is the greatest risk factor. The smaller the baby, and the more premature it is, the greater is the risk. Other risk factors are exposure to oxygen and the associated systemic problems after birth. Blood transfusions, infection, respiratory distress, etc, are definite negative factors that can increase risk and must be taken into consideration.
When a baby fits into the “high risk” criteria, the retina must be screened by an ophthalmologist who will perform a dilated fundus examination. This means that drops will be instilled onto the baby’s eyes to dilate the pupil temporarily to allow the ophthalmologist to examine the retina. Babies that are found to have some form of the disease will require serial examinations and/or actual management. When the fundus findings fit the description of “threshold” disease, treatment in the form of laser or cryopexy must be instituted. Sometimes “prethreshold” treatment may be justified. Higher stages called ROP 4 A & B and ROP 5 will need vitreoretinal surgery which is a more invasive and delicate procedure.
The visual prognosis for ROP 4 B is guarded, and is very bad for ROP 5.
Will I eventually become blind or poorly sighted later in life because of my nearsightedness?
Those who have “high myopia” or nearsightedness of 6 Diopters (“600” in common language) may have myopic retinal changes that have the potential to cause loss of vision of variable degrees. However, not everyone who is highly myopic has these problems. These myopic changes are collectively referred to as “myopic degeneration”. They come in the form of thinning of the peripheral retina (lattice degeneration), retinal tears and holes, staphylomatous changes (abnormal out-pouching) of the back of the eye, abnormal vessels under the macula (choroidal neovascular membranes), thinning of the retinal pigment epithelium.
When there are lattice lesions, retinal tears and holes, retinal detachment can occur, causing sudden drop in vision. A retinal detachment is a separation of retina from the underlying retinal pigment epithelium and accumulation of fluid in the space. Retinal detachment will need surgery to close this retinal tear or hole to reattach the detached retina. Visual prognosis is always guarded, and vison is almost always subnormal compared to fellow eye in spite of successful surgical reattachment.
Another cause of visial loss in high myopes is the growth of a submacular neovascular membrane. In this case there is a submacular hemorrhage and atrophy and scarring at the macula, the center of vision. When this happens the patient loses only central vision, not peripheral vision. These cases are managed with special pharmacologic and laser treatments. The eventual scar formation results in central visual loss of variable degrees.
Thinning of the layers of the retina at the posterior pole (back portion of the eye) causes loss of vision of varying degrees, depending on the tissue loss and scarring. There is no treatment for this problem.
Again, not everyone who is highly myopic will have these problems. And, patients who have myopic degenerative changes may have all of these at the same time, combinations of these, or perhaps only one.