Diseases

Diseases 2018-12-06T21:20:45+00:00
MACULAR DEGENERATION
BRANCH VEIN OCCLUSION
CENTRAL RETINAL VEIN OCCLUSION
DETACHED AND TORN RETINA
CENTRAL SEROUS CHOROIDOPATHY
DIABETIC RETINOPATHY
EPIRETINAL MEMBRANE (Macular Pucker)
LATTICE DEGENERATION OF THE RETINA *
MACULAR HOLE
PERIPHERAL UVEITIS
RETINAL TEAR AND VITREOUS HEMORRHAGE
TOXOPLASMOSIS
VITREOUS COLLAPSE
WHAT IS A SCLERAL BUCKLE

MACULAR DEGENERATION

The retina is the light sensitive tissue at the back of the eye that is connected to the optic nerve. Light hits the retina sending a signal through the optic nerve to the brain. Age Related Macular Degeneration (AMO} is a term that describes deterioration of the retinal cellular structure in the center of the retina, the macula. The macula is responsible for fine detail and reading vision. Damage to the macula results in loss of central vision and is usually gradual in the case of macular degeneration. Peripheral vision remains healthy in this condition. The central retina is dense with cone receptors. Peripheral vision does not have the retinal cones that permit fine detail but does allow the ability to navigate around and to see objects moving from the side and to distinguish large objects. It is recommended for patients to monitor changes that may occur in their vision and a good way to do that is by using an Amsler Grid twice weekly. With early diagnosis and proper treatment, the progression of AMO can often be delayed. The earlier AMO is detected, the better you chances are of keeping your vision.

There are two types of macular degeneration. The “dry” type and the “wet” type. The dry type generally causes a slow progressive loss of central visual acuity. It affects both eyes and may eventually cause a significant visual disability to read or to recognize faces and colors. There are currently no medications available to treat dry macular degeneration but certain lifestyle changes and vitamin therapies may be helpful to slow the progression of the disease. A clinical trial sponsored by the National Eye Institute studied the effect of nutritional therapy, along with higher quantities of certain vitamins and minerals and found that they may increase healthy pigments and support cell structure of the macula. No prescription is necessary. Dr. Srouji can discuss the use of antioxidant vitamins with you.

In the “wet” type there is a hemorrhage or fluid leakage in the retina area. Abnormal blood vessels develop underneath the retina to compensate for the loss of normal function but these new vessels are fragile and may leak causing permanent damage to the retinal tissue. This can occur in both eyes but usually happens in only one eye at a time.

In the past, laser was the only treatment. The problem with laser is that while it destroys the abnormal vessels it does destroy a portion of the retina so vision is lost. In the past few years, a new class of medicines have been developed in the form of an injection into the eye. A class of drugs known as anti-VEGF is the most recent and most commonly utilized treatment for the wet type of AMO. These medicines block a substance known as vascular endothelial growth factor or VEGF. By blocking or inhibiting this growth factor in the eye, the abnormal vessels will often stop leaking.

You do not have to receive treatment for your condition, although without treatment, wet macular degeneration and macular edema (swelling) may lead to further vision loss and sometimes very quickly.

At present, the FDA approved treatments for neovascular macular degeneration are: Photodynamic therapy with a drug called Visudyne and injections into the eye of the drugs Macugen, Lucentis, and Eylea. Although Visudyne and Macugen have been proven to slow down the rate of visual loss, most people do not get back better vision. Lucentis and Eylea have been compared and found to have equivalent efficacy and safety. In 2006, Ophthalmologists started using another anti-VEGF drug called Avastin to treat macular deneration and macular edema showing good results. The use of Avastin is “off label”. Avastin was not initially developed to treat eye conditions. Avastin is FDA approved for the treatment of colon cancer. Lucentis was designed by the same company that makes Avastin. Lucentis molecule is very similar to Avastin molecule. Clinical treals to date have shown that the two drugs have equal efficacy and no significant safety differences between the two. Eylea is relatively new and is FDA approved for the eye. It has been shown to produce similar results as Lucentis. The most commonly used medicines are Avastin and Eylea. The medication is injected into the eye at regular intervals every 4-8 weeks, often for several months until the leakage stops. In some patients the abnormal vessels will not come back but may return several months after the injections are stopped. As good as these treatments are, close follow up and often retreatment is necessary. The treatment plan is customized for each patient. Dr. Srouji will discuss with you the benefits and risks associated with these choices of treatment.

A dilated eye exam with an office procedure called fluorescein angiography is used to detect leaking and hemorrhaging vessels. In this diagnostic test, the damaged blood vessels associated with macular degeneration are imaged by injecting a fluorescent dye into the vein of the arm and tracing its progression through the retinal blood vessels. We also may perform an OCT (scan showing the topography of the retina) of the retina layers to determine the degree of fluid that has leaked underneath and into the retina.

While age related macular degeneration is most commonly associated with the elderly, there are hereditary and juvenile forms of maculopathy. In addition, a

“secondary type” of maculopathy may develop as a result of a vascular or inflammatory disease. This type usually affects only one eye and may not progress after the primary cause has been removed.

There are risk factors of AMD which include the following:

  • Age – People over the age of 50 are at greater risk than any other age groups.
  • Genetics – Recent studies have shown that there is a strong genetic component causing AMD.
  • Race – Caucasians are much more likely to get AMD.
  • Family History- Those with a family history of AMD are more likely to develop AMD.
  • Smoking – Smoking and second hand smoke can drastically impact your chances of worsening AMD.

Here are some suggestions to help you see better:

Use a very bright light for reading as high as 300 watts may be necessary. Good quality high contrast print is the easiest to read. Low vision aids such as magnifiers and telescopic devices may be of value. When trying to read or watch TV, look slightly to one side rather than directly at it. Try up and down, right to left, until you find where you can see better.mes to improve the vision. Dr. Srouji will discuss with you the benefits and risks associated with these choices of treatment.


BRANCH VEIN OCCLUSION

An ocular condition called Branch Vein Occlusion occurs when the blood flow in one of the retinal veins becomes blocked. This occlusion is caused by hardening of the arteries which impedes the blood flow through the veins. This results in an increased pressure within the vein resulting in hemorrhaging and swelling within the retina. This bleeding and swelling in the retina reduces vision. Branch Vein Occlusions tend to happen in people often with some history of high blood pressure. Sometimes months or even years following a Branch Vein Occlusion new blood vessels form on the surface of the retina to try to replace damaged ones. These new blood vessels can easily rupture, causing further hemorrhage and damage to the inside of the eye.

Treatment of vein occlusions currently consist of cauterization by a light beam (laser photocoagulation) and of injections of medicine into the eye to reduce the amount of hemorrhage and swelling and to prevent the formation of the dangerous new blood vessels from forming within the eye. These treatments are used to try and improve the swelling in the retina to stabilize and sometimes to improve the vision. Dr. Srouji will discuss with you the benefits and risks associated with these choices of treatment.


CENTRAL RETINAL VEIN OCCLUSION

When there is a blockage of blood flow through the main retinal vein, a condition called Central Vein Occlusion occurs. This condition is usually associated with arteriosclerosis and hypertension (high blood pressure) and is found frequently in diabetic patients. The blockage of blood flow causes the pressure in the retinal veins to increase resulting in hemorrhage and swelling of the retina. Vision can be affected mildly or severely, especially if the central retina is involved.

Treatment may include laser and of injections of medicine into the eye to reduce the amount of hemorrhage and swelling. Lucentis (ranibizumab), Eylea (aflibercept), and Ozurdex (dexamethasone) are all FDA-approved for vein occlusions. Some ophthalmologists also use another anti-VEGF drug called Avastin (bevacizumab). This use of Avastin is “off label.” These anti-VEGF drugs are used to stop or slow down new vessel growth.

In some cases, new blood vessels are formed in the tissue that has been damaged. These new blood vessels (called neovascularization) are fragile and bleed easily, causing additional visual loss. Another late complication is Neovascular Glaucoma. In selected cases, laser and/or injection may be considered to prevent or control these secondary complications.

If the blockage is only partial, vision may not be lost but may be decreased and will fluctuate from time to time. In these cases, treatment is directed toward easing the blood flow within the eye by using medicines that thin the blood.


CENTRAL SEROUS CHOROIDOPATHY

Central serous choroidopathy (also known as idiopathic central serous retinopathy) is a spontaneously occurring condition causing reduction of central vision in healthy young adults. The patient, usually a male between the ages of 20 and 40, first notices blurring of central vision in one eye. He usually likens the condition to looking through a gray bubble” located in the central portion of his visual field. The patient may also notice that objects look smaller when viewed with the affected eye (micropsia).

The visual acuity with the affected eye is usually reduced to the 20/40 – 20/80 range. The visual field examination usually reveals a dark spot in the center of the visual field (central scotoma). Examination with the ophthalmoscope shows a localized collection of fluid beneath the retina in the macular region. (The macular region is the specialized central portion of the retina that mediates fine visual discrimination.) Special photography of the retina following the injection of sterile fluorescein solution into a vein (fluorescein angiography) reveals the anatomical defect and confirms the diagnosis.

Although many cases of central serous choroidopathy resolve in time without specific medication or surgery, a certain percentage may require laser photocoagulation to bring about resolution of the condition.


DETACHED AND TORN RETINA

The retina is a nerve layer at the back of your eye that senses light and sends images to your brain. The eye is like a camera. Think of the retina as the film that lines the back of a camera. The lens in the front of the eye focuses light onto the retina.

A retinal detachment occurs when the retina is pulled away from its normal position. The retina does not work when it is detached. Vision is blurred, just as a photographic image would be blurry if the film were loose inside the camera. A retinal detachment is a very serious problem that almost always causes blindness unless it is treated.

A clear gel called vitreous fills the middle of the eye. As we get older, the vitreous may pull away from its attachment to the retina at the back of the eye.

Usually the vitreous separates from the retina without causing problems. But sometimes the vitreous pulls hard enough to tear the retina in one or more places. Fluid may pass through the retinal tear, lifting the retina off the back of the eye.

Conditions that increase the chance of having a retinal detachment include, nearsightedness, previous cataract surgery, glaucoma, severe injury or trauma, previous retinal detachment in your other eye or family history of retinal detachment

Certain symptoms may indicate the presence of a retinal detachment, however they do not always mean a retinal detachment is present. These include, flashing lights, new floaters, a shadow in the periphery of your field of vision, or a gray curtain moving across your field of vision.

Most retinal tears need to be treated with laser surgery or cryotherapy (freezing), which seals the retina to the back wall of the eye. These treatments cause little or no discomfort. Treatment usually prevents retinal detachment.

Almost all patients with retinal detachments require surgery to return the retina to its proper position. There are several ways to fix a retinal detachment. The characteristics of your detachment will determine the type of surgery to be performed and the form of anesthesia to be used.


DIABETIC RETINOPATHY

In diabetes the body does not use and store sugar properly. High blood sugar levels can damage blood vessels in the retina, the nerve layer at the back of the eye that senses light and helps to send images to the brain. The damage to retinal vessels is referred to as diabetic retinopathy.

There are two types of diabetic retinopathy: Nonproliferative Diabetic Retinopathy (NPDR), and Proliferative Diabetic Retinopathy (PDR).

NPDR is an early stage of diabetic retinopathy. In this stage, tiny blood vessels within the retina leak blood for fluid. The leaking fluid causes the retina to swell or to form deposits called exudates.

Many people with diabetes have mild NPDR, which usually does not affect their vision. When vision is affected it is the result of macular edema and/or macular ischemia.

Macular edema is swelling, or thickening, of the macula, a small area in the center of the retina that allows us to see fine details clearly. The swelling is caused by fluid leaking from retinal blood vessels. It is the most common cause of visual loss in diabetes. Vision loss may be mild to severe, but even in the worst cases, peripheral vision continues to function.

Macular ischemia occurs when small blood vessels (capillaries) close. Vision blurs because the macula no longer receives sufficient blood supply to work properly.

PDR is present when abnormal new vessels (neovascularization) begin growing on the surface of the retina or optic nerve. The main cause of PDR is widespread closure of retinal blood vessels, preventing adequate blood flow. The retina responds by growing new blood vessels in an attempt to supply blood to the area where the original vessels closed.

Unfortunately, the new, abnormal blood vessels do not resupply the retina with normal blood flow. The new vessels are often accompanied by scar tissue that may cause wrinkling or detachment of the retina. Macular wrinkling can cause visual distortion. More severe vision loss can occur if the macula or large areas of retina are detached.

The fragile new vessels may bleed into the vitreous, a clear, jelly-like substance that fills the center of the eye. If the vitreous hemorrhage is small, a person might see only a few new dark floaters. A very large hemorrhage might block out all vision.

Vitreous hemorrhage alone does not cause permanent vision loss. Sometimes the eye will reabsorb the blood on its own over a few weeks and vision will improve. If the eye does not clear the vitreous blood adequately within a reasonable time, vitrectomy surgery may be recommended. During this microsurgical procedure, which is performed in the operating room, the blood-filled vitreous is removed and replaced with a clear solution. Vitrectomy often prevents further bleeding by removing the abnormal vessels that caused the bleeding. If the retina is detached, it can be repaired during the vitrectomy surgery.

Occasionally, extensive retinal vessel closure will cause new, abnormal blood vessels to grow on the iris (colored part of the eye) and block the normal flow of fluid out of the eye. Pressure in the eye builds up resulting in neovascular glaucoma, a severe eye disease that causes damage to the optic nerve.

A medical eye examination is the only way to find changes inside your eye. An ophthalmologist can often diagnose and treat serious retinopathy before you are aware of any vision problems.

An office procedure called fluorescein angiography is used to detect hemorrhaging vessels. In the diagnostic test, the blood vessels are imaged by injecting a fluorescent dye into the vein of the arm and tracing its progression through the retinal blood vessels.

An OCT (scan showing topography of the retina) of the retinal layers is used to determine the amount of swelling.

The best treatment is to prevent the development of retinopathy as much as possible. Strict control of blood sugar will significantly reduce the long­term risk of vision loss from diabetic retinopathy. If high blood pressure and kidney problems are present, they need to be treated.

A combination of laser and/or injections into the eye is often recommended for macular edema or swelling. The laser is focused on the damaged retina near the macula to decrease the fluid leakage. The main goal of treatment is to prevent further loss of vision.

For PDR, the laser if focused on all parts of the retina except the macula. This PRP (panretinal photocoagulation) laser treatment causes abnormal new vessels to shrink and often prevent them from growing in the future. It also decreases the chance that vitreous bleeding or retinal distortion will occur. The goal of PRP laser is to decrease the risk of severe vision loss.

Multiple laser treatments over time are sometimes necessary. Laser treatment does not cure diabetic retinopathy and does not always prevent further loss of vision.

Vision loss is largely preventable. With improved methods of diagnosis and treatment, only a small percentage of people who develop retinopathy have serious vision problems. Early detection of diabetic retinopathy is the best protection against loss of vision.

Maintaining strict control of blood sugar and regular eye exams can significantly lower your risk of vision loss.

People with diabetes should schedule examinations at least once a year. More frequent medical eye examinations may be necessary after the diagnosis of diabetic retinopathy.

You should have your eyes checked promptly if you have visual changes that affect only one eye, last more than a few days, and that are not associated with a change in blood sugar.

When you are first diagnosed with diabetes, you should have your eyes checked within five years of the diagnosis if you are 30 years old or younger and within a few months of the diagnosis if you are older than 30 years.


EPIRETINAL MEMBRANE (Macular Pucker)

Scar tissue can grow on the surface of the retina, directly over the macula. This scar tissue can contract, and cause the retina to wrinkle. The scar tissue on the surface of the retina is called an “epiretinal membrane” or “macular pucker”. An epiretinal membrane can cause visual loss, as well as distorted or double vision.

Epiretinal membranes may be caused by a variety of eye problems. They may follow retinal detachment surgery, laser treatment or cryotherapy for retinal tears. They may be associated with retinal blood vessel problems. In most cases, the epiretinal membrane occurs in an otherwise healthy eye as a result of a posterior vitreous detachment.

Your ophthalmologist may perform a test called a fluorescein angiogram. This diagnostic procedure utilizes a specialized fundus camera to capture rapid-sequence photographs of the retinal vasculature following an intravenous injection of fluorescein sodium. Another diagnostic test called Optical Coherence Tomography (OCT) may be performed. This test has the ability to generate cross sectional images of the retina.

The only treatment of visual loss caused by an epiretinal membrane is surgery to remove the membrane. If the visual loss or distortion is significant, a vitrectomy may be performed to remove the membrane. This surgery is usually performed under local anesthesia, The membrane is picked up with a fine instrument and gently peeled off the surface of the retina.

Vision usually improves slowly after surgery, with most of the improvement coming within the first three months, though it may continue to improve for many months. In some cases, the vision may not improve at all. The chance that vision will improve following surgery is about 85%. On an average, patients regain approximately half of the vision that was lost because of the epiretinal membrane.

The complications of surgery include retinal tears and detachment, cataract formation, infection, and regrowth of the membrane. These complications may result in mild to total loss of vision, although vision-losing complications are rare


LATTICE DEGENERATION OF THE RETINA *

There are several conditions that can affect the retina and cause weakness of the retina in certain places, thus making retinal detachment more likely. Among these so-called pre-detachment conditions, the most common is a degenerative condition of the retina called lattice degeneration. In this condition, thinning occurs in the periphery of the retina. In these thin areas, retinal holes or tears may form. Once a retinal hole or tear appears, an anatomical situation is created in which fluid from the inside of the eye (from the vitreous gel) can leak through the hole in the retina and accumulate behind the retina, displacing it forward and causing a retinal detachment.

Since the retina is the real seeing layer of the eye and lines the eyeball, when the retina detaches vision may become blurry and a dark shadow may appear before the affected eye.

Since lattice degeneration (especially when associated with nearsightedness and a family history of retinal detachment) increases an individual’s risk of retinal detachment, preventive therapy is often required.

Fortunately, technology has given us sophisticated methods to reinforce the adhesion of the retina to the other layers of the eye and thus decrease the risk of retinal detachment. The two most common forms of treatment used for lattice degeneration are cryopexy (freezing of the retinal tissues) and argon laser (using laser light). When laser is used, several dot-like spots are used to “spot-weld” the treated area. When cryopexy (freezing) is used, a wider area is treated by the brush-like effect of cold. Treatment can be done under local anesthesia if cryopexy is used, or just after the use of anesthetic drops if the laser is used. The type of treatment selected depends on the method that will bring the best results for each individual case. Cryopexy is the most common method chosen.

Periodic checkups will ensure good condition of the eyes and preventive treatment will greatly reduce the incidence of retinal detachment or its severity in patients with lattice degeneration.

* Name coined because of the resemblance to a white lattice fence.


MACULAR HOLE

What is a Macular Hole?

Think of the retina as a target with the center portion as the “bulls-eye”. This “bulls-eye” is the MACULA, the region of the retina that is used for reading and seeing fine detail. When a hole develops in the macula it is called a MACULAR HOLE.

What causes a Macular Hole?

A jelly-like substance or VITREOUS fills the eye ball. In a young person, the vitreous has the consistency of jello. As the person ages, the vitreous tends to become less like jello and more like liquid. Between the ages of 50 and 70 years, this vitreous often starts to separate from the retina and when that happens, the vitreous sticks to the macula, exerting traction and causing a MACULAR CYST. Eventually, this cyst ruptures, causing a macular hole. The body attempts to heal this hole but in doing so, develops scar tissue around the hole which causes it to open further. Think of the scarring process as a reversed “purse string” effect.

Treatment for Macular Holes:

Repair of macular holes is accomplished by surgery that involves an incision into the eye and removal of the diseased vitreous and scar tissue. Gas is injected into the eye to close up the hole. The gas acts as a band-aid, holding the hole closed while the eye grows a new membrane over the top of the hole to seal it.

Macular hole surgery has a 85% success rate, with success being defined as closure of the macular hole and improvement of near vision to 20/50 or better. There is a 50% chance of developing a cataract in the eye and a 1 % chance of a retinal tear or detachment.

Following the surgery, the patient must remain in a face down position to keep the gas bubble up against the macular hole while it is healing


PERIPHERAL UVEITIS

Peripheral uveitis (pars planitis or chronic cyclitis) is a disease entity that was described by Dr. Charles Schepens and Associates in the 1950’S. It is one of the most common types of ocular inflammation.

This inflammation has a predisposition for young adults. It is a widespread inflammation involving all parts of the eye including the vitreous, retina, optic nerve, and blood vessels. It may last for 10-15 years but usually it “burns itself out’ in the second or third decade of life. There is no preference for race or sex and it usually affects both eyes.

Peripheral uveitis is a chronic disease with a gradual onset and the symptoms are initially very mild, Blurry vision, floaters, and mild redness of the eyes are the most common symptoms. Peripheral uveitis is a chronic recurring inflammation which can cause secondary side effects such as cataract, scar tissue, and macular degeneration.

It is important therefore to control the inflammation in order to prevent or minimize these secondary complications.

There is no known cause for peripheral uveitis but the inflammation can be controlled by using anti-inflammatory agents. These can be administered in the form of pills, drops, or injections under the skin adjacent to the eye. In the more severe and persistent cases, cryotherapy (freezing) is used to control the inflammation.

The prognosis for maintaining good vision in most cases is good.


RETINAL TEAR AND VITREOUS HEMORRHAGE

There may be some areas where the vitreous is very strongly attached to the retina. If the vitreous pulls away from the retina in an area where the retina is weak, the retina may tear. One condition that weakens the retina is called lattice degeneration. When lattice degeneration is present, it indicates that the retina is thin and may be more susceptible to a tear of the retina than in an area without lattice degeneration. Imagine a piece of scotch tape attached to tissue paper. If you try to pull the scotch tape off the tissue paper, you will tear the paper. A tear of the retina works very much the same way. If the vitreous is firmly attached, it can tear the retina as it pulls away. If the retina tears across a retinal blood vessel, there will be bleeding into the vitreous. This is called vitreous hemorrhage.

When there is a little bleeding, red blood cells floating and moving in the vitreous create the sensation of walking through a swarm of flies. If even more bleeding occurs in the vitreous, it looks like a spider web or a swirling mass of black or red lines. If there is a great deal of bleeding into the vitreous cavity, vision may be reduced significantly, or even become very dark. When a retinal tear occurs, it is a potentially serious problem. If a vitreous hemorrhage also occurs, it is even more serious.

The retina can tear immediately following a posterior vitreous detachment (PVD), or weeks later. If no tear has developed within eight weeks after a PVD, the retina probably will not tear.

Any patient, who experiences sudden or new floaters, or flashing lights of any kind, should have a complete retinal examination immediately. These symptoms may indicate that a retinal tear has occurred. A retinal tear may result in a retinal detachment. Since retinal tears and retinal detachments begin in the peripheral retina, your doctor may suggest that you test your peripheral vision to be sure there are no changes.


TOXOPLASMOSIS

Few diseases are at once more widespread and more baffling than the parasitic infection called toxoplasmosis. It afflicts as many as 75 million Americans (along with an astonishing half a billion persons worldwide), and though the vast majority of victims never even know they have it (the symptoms in adults are similar to those of a mild case of the flu), the effects can be devastating when the disease is contracted by a pregnant woman and passed on to her unborn child.

The reason fetuses are susceptible while their mothers are not is because they do not develop the immunity that makes the affliction relatively harmless to adults. But in unborn children, toxoplasmosis can cause severe skull deformities, total blindness and hopeless brain damage. Even worse is the fact that in some of the 500 or more babies in the U.S. each year with toxoplasmosis, the disease has a delayed-action effect. The victims may appear perfectly normal until they reach their early 20’s, when the toxoplasma cysts which have been lying dormant burst open and release thousands of parasites that can attack and destroy the cells of the eye.

When the eye is affected, the macular area of the retina is often attacked, for this seems to be the preferred site for the parasite’s multiplication. There have even been a few rare cases, notably in patients already suffering from other diseases, in which toxoplasmosis has attacked the brain and other vital organs.

For two decades, doctors have known that a major source of toxoplasmosis is raw or undercooked meat containing the cysts. Although undercooked lamb or pork are the most common hosts for toxoplasma parasite, beef seems to be a major source of contamination, particularly because of the growing popularity in many areas of “steak tartare” (ingredients: raw chopped beef, a raw egg, chopped onions, capers, and freshly ground black pepper – a kind of uncooked spicy meatball). Eating ordinary hamburgers rare may also spread the disease.

Doctors, however, have been persistently puzzled by the fact that many cases were also diagnosed in persons who had never eaten meat of any kind. Now, simultaneous evidence from researchers in the U.S. and Scotland has finally pinpointed what seems to be another relay point in the transmission of toxoplasmosis. It is the common house cat.

The intestinal tract of the cat provides not only a potential host for the tiny organisms, but a virtual breeding ground as well. Inside the feline intestine, the one celled parasites do not merely divide and attack; rather they produce male and female cells which join together to form an egg called an oocyst, inside of which eight new toxoplasma parasites develop. The oocysts remain viable in the cat’s expelled feces for an indefinite period of time and can readily contaminate the hands of gardeners, children playing in sandboxes, and particularly cat owners changing their pet’s litter boxes.

Since the only effective drugs against toxoplasmosis are extremely dangerous to the fetus, precaution seems to be the one sure way to avoid the heartbreak of losing a child, having a deformed baby, or a child who may become blind at age 20. Every pregnant woman should at all costs avoid eating raw meat. And if there is a cat in the house, send it away for a nine-month vacation.

Scientists are currently testing the possibility of giving every pregnant woman a blood test for toxoplasmosis, which could be performed routinely in late adolescence or at the time that pregnancy is first suspected.

Preliminary work has also begun on the development of a vaccine. Further research is necessary, however, before either could be applied on a widespread basis.


VITREOUS COLLAPSE

The inside of the eye is filled with a clear, jelly-like substance called VITREOUS. Because it is clear, light rays are able to pass through it to reach the retina. However any change in the consistency, color, or structure of the vitreous can interfere with the transmission of light to the retina and thus can cause visual symptoms.

Vitreous undergoes certain changes which are associated with the normal aging process. In young people, the vitreous fills the entire inner cavity of the eye and has a solid, jelly-like consistency. With age, this consistency becomes less jelly-like and more liquid, and the vitreous begins gradually to pull away from the retina. This pulling away is called POSTERIOR VITREOUS COLLAPSE.

When the vitreous begins this “pulling away”, condensations within the jelly are formed and are called FLOATERS These can be seen as small dots that are “floating” in the field of vision. If these floaters are small and infrequent specks or threads, usually they are of no concern. However, if they are large or web-like and come in showers, they may indicate that a retinal tear has occurred or that there is bleeding within the eye. In this case, an ophthalmologist should be consulted.

Another symptom associated with posterior vitreous collapse is PHOTOPSIA. This term refers to flashes of light which appear in the side vision and which usually can be seen in a darkened room. Infrequent light flashes are associated generally with the normal aging process. A sudden onset of frequent light flashes, however, could indicate that the vitreous is putting traction on the retina, which could result in a retinal tear. How can the vitreous cause a retinal tear

In some areas, the vitreous may adhere stronger to the retina than in others. In these areas of what is called VITREORETINAL TRACTION, the bond between vitreous and retina may be so strong that instead of the vitreous collapsing away from the retina, the retina tears at the point of adherence. Pre-existing retinal problems also could make the retina more susceptible to tears. Some tears caused by vitreoretinal traction do not generate ocular symptoms.

However, the onset of constant floaters and frequent light flashes can be warning signs that a retinal tear has occurred.

Most retinal tears occur within the first three months after, but not necessarily immediately after, the onset of symptoms. As a precautionary measure, during this period of time it is wise to avoid strenuous physical activity, bending over, lifting heavy objects and active sports.

Posterior vitreous collapse occurs in most people between the ages of 50 and 70. It is part of the normal aging process and, in most people, causes no damage to the eye. Whereas 15% of the total population may develop symptoms that are associated with this condition – floaters and light flashes – only 1 % of these people develop retinal tears or holes. Can this condition be treated?

Treatment of retinal tears or holes is successful in most cases. To seal the affected area, the surgeon uses either argon laser photocoagulation or a freezing method called cryopexy. If the retina becomes detached, then a major surgical procedure is required.


WHAT IS A SCLERAL BUCKLE?

Retinal detachments are repaired by a surgical procedure called “scleral buckle”. Most retinal detachments are caused by breaks or tears in the peripheral retina which in turn are usually caused by traction or pulling of the vitreous (gelatin that fills the eye) on the peripheral retina. In order to close or seal the retinal tear, retinal surgeons must create an indentation or buckle on the eyeball. This buckling effect closes the retinal tear and also helps to prevent further retinal breaks caused by continuous vitreous traction.

The buckling material that is most commonly used is made of silicone. This is placed on the eye and held in place with sutures and a silicone belt to prevent it from slipping. The silicone creates the desired indentation on the globe, exactly where the tears which caused retinal detachment were located. The scleral buckle normally remains in place throughout the patient’s life since silicone is a material which is well tolerated. After the eye has recovered from surgery, the patient is not aware that anything is present.

Very rarely part of the scleral buckle either starts to extrude through the eyeball or may become infected or, in some cases, may start to erode or indent the eyeball too much. In this event, the scleral buckle is either removed or loosened. Sometimes scleral buckles will cause a slight muscle imbalance due to scar tissue forming around them and patients may occasionally have double vision for a few months following surgery. This double vision is usually temporary and is well tolerated by most patients.

The success rate of retinal detachment repair is very high with modern surgery.