Retinal Detachment

What is a retinal detachment?

A retinal detachment is a separation of the retina from its attachments to its underlying tissue within the eye. Most retinal detachments are a result of a retinal break, hole, or tear. These retinal breaks may occur when the vitreous gel pulls loose or separates from its attachment to the retina, usually in the peripheral parts of the retina. The vitreous is a clear gel that fills 2/3 of the inside of the eye and occupies the space in front of the retina. As the vitreous gel pulls loose, it will sometimes exert traction on the retina, and if the retina is weak, the retina will tear. Most retinal breaks are not a result of injury. Retinal tears are sometimes accompanied by bleeding if a retinal blood vessel is included in the tear.

Once the retina has torn, liquid from the vitreous gel can then pass through the tear and accumulate behind the retina. The build-up of fluid behind the retina is what separates (detaches) the retina from the back of the eye. As more of the liquid vitreous collects behind the retina, the extent of the retinal detachment can progress and involve the entire retina, leading to a total retinal detachment. A retinal detachment almost always affects only one eye. The second eye, however, must be checked thoroughly for any signs of predisposing factors that may lead to detachment in the future.

What are the signs and symptoms of a retinal detachment?

Flashing lights and floaters may be the initial symptoms of a retinal detachment or of a retinal tear that precedes the detachment itself. Anyone who is beginning to experience these symptoms should see an eye doctor (ophthalmologist) for a retinal exam. In the exam, drops are used to dilate the patient's pupils to make a more detailed exam easier. The symptoms of flashing lights and floaters may often be unassociated with a tear or detachment and can merely result from a separation of the vitreous gel from the retina. This condition is called a posterior vitreous detachment (PVD). Although a PVD occurs commonly, there are no tears associated with the condition most of the time.

The flashing lights are caused by the vitreous gel pulling on the retina or a looseness of the vitreous, which allows the vitreous gel to bump against the retina. The lights are often described as resembling brief lightning streaks in the outside edges (periphery) of the eye. The floaters are caused by condensations (small solidifications) in the vitreous gel and frequently are described by patients as spots, strands, or little flies. There is no safe treatment to make the floaters disappear. Floaters are usually not associated with tears of the retina.

If the patient experiences a shadow or curtain that affects any part of the vision, this can indicate that a retinal tear has progressed to a detached retina. In this situation, one should immediately consult an eye doctor since time can be critical. The goal for the ophthalmologist is to make the diagnosis and treat the retinal tear or detachment before the central macular area of the retina detaches.

What are the risk factors for developing a retinal detachment?

Studies have shown that the incidence of retinal detachments caused by tears in the retina is fairly low, affecting approximately one in 10,000 people each year. Many retinal tears do not progress to retinal detachment. Nevertheless, many risk factors for developing retinal detachments are recognized, including certain diseases of the eyes (discussed below), cataract surgery, and trauma to the eye. Retinal detachments can occur at any age. They occur most commonly in younger adults (25 to 50 years of age) who are highly nearsighted (myopic) and in older people following cataract surgery.

Which diseases of the eyes predispose to the development of a retinal detachment?

Lattice degeneration of the retina is a type of thinning of the outside edges of the retina, which occurs in 6%-8% of the general population. The lattice degeneration, so-called because the thinned retina resembles the crisscross pattern of a lattice, often contains small holes. Lattice degeneration is more common in patients with nearsightedness (myopia). This tendency to lattice degeneration occurs because myopic eyes are larger than normal eyes and, therefore, the peripheral retina is stretched more thinly. Fortunately, only about 1% of patients with lattice degeneration go on to develop a retinal detachment.

High myopia (greater than 5 or 6 diopters of nearsightedness) increases the risk of a retinal detachment. In fact, the risk increases to 2.4% as compared to a 0.06% risk for a normal eye at age 60. (Diopters are units of measurement that indicate the power of the lens to focus rays of light.) Cataract surgery or other operations of the eye can further increase this risk in patients with high myopia.

Patients taking certain eye drops have an increased risk of developing a retinal detachment. Pilocarpine (Polocarp 2 or 4%), which for many years has been a mainstay of therapy for glaucoma, has long been associated with retinal detachment. Moreover, by constricting the pupil, pilocarpine makes the diagnostic exam of the peripheral retina more difficult, possibly leading to a delay in the diagnosis.

Patients with chronic inflammation of the eye (uveitis) are at increased risk of developing retinal detachment.

How does cataract surgery lead to a retinal detachment?
Cataract surgery, especially if the operation has complications, increases the risk of a retinal detachment.

What other factors are associated with a retinal detachment?

Blunt trauma, as from a tennis ball or fist, or a penetrating injury by a sharp object to the eye can lead to a retinal detachment.
A family history of a detached retina that is non-traumatic in nature seems to indicate a genetic (inherited) tendency for developing retinal detachments.

In as many as 5% of patients with a non-traumatic retinal detachment of one eye, a detachment subsequently occurs in the other eye. Accordingly, the second eye of a patient with a retinal detachment must be examined thoroughly and followed closely, both by the patient and the ophthalmologist.

Diabetes can lead to a type of retinal detachment that is caused by pulling on the retina (traction) alone, without a tear. Because of abnormal blood vessels and scar tissue on the retinal surface in some patients with diabetes, the retina can be lifted off (detached) from the back of the eye. In addition, the blood vessels may bleed into the vitreous gel. This detachment may involve either the periphery or central area of the retina.

Why is it mandatory to treat a retinal detachment?

A tear or hole of the retina that leads to a peripheral retinal detachment causes the loss of side (peripheral) vision. Almost all of these patients will progress to a full retinal detachment and loss of all vision if the problem is not repaired. The dark shadow or curtain obscuring a portion of the vision, either from the side, above, or below, almost invariably will advance to the loss of all useful vision. Spontaneous reattachment of the retina is rare.

Early diagnosis and repair are urgent since visual improvement is much greater when the retina is repaired before the macula or central area is detached. The surgical repair of a retinal detachment is usually successful in reattaching the retina, although more than one procedure may be necessary. Once the retina is reattached, vision usually improves and then stabilizes. Successful reattachment does not always result in normal vision. The ability to read after successful surgery will depend on whether or not the macula (central part of the retina) was detached and the extent of time that it was detached.

How are detached retinas repaired?

Retinal holes or tears can be treated with laser therapy or cryotherapy (freezing) to prevent their progression to a full-scale detachment. Many factors determine which holes or tears need to be treated. These factors include the type and location of the defects, whether pulling on the retina (traction) or bleeding is involved, and the presence of any of the other risk factors discussed above. Three types of eye surgery are done for actual retinal detachment: scleral buckling, pneumatic retinopexy, and vitrectomy.

Scleral buckling

A scleral buckle, which is made of silicone, plastic, or sponge, is then sewn to the outer wall of the eye (the sclera). The buckle is like a tight cinch or belt around the eye. This application compresses the eye so that the hole or tear in the retina is pushed against the outer scleral wall of the eye, which has been indented by the buckle. The buckle may be left in place permanently. It usually is not visible because the buckle is located half way around the back of the eye (posteriorly) and is covered by the conjunctiva (the clear outer covering of the eye), which is carefully sewn (sutured) over it. Compressing the eye with the buckle also reduces any possible later pulling (traction) by the vitreous on the retina.

A small slit in the sclera allows the surgeon to drain some of the fluid that has passed through and behind the retina. Removal of this fluid allows the retina to flatten in place against the back wall of the eye. A gas or air bubble may be placed into the vitreous cavity to help keep the hole or tear in proper position against the scleral buckle until the scarring has taken place. This procedure may require special positioning of the patient's head (such as looking down) so that the bubble can rise and better seal the break in the retina. The patient may have to walk, eat, and sleep with the head facing down for two to four weeks to achieve the desired result.


Pneumatic retinopexy

Laser or cryotherapy is used to seal the hole or tear. The surgeon then injects a gas bubble directly inside the vitreous cavity of the eye to push the detached retina against the back outer wall of the eye (sclera). The gas bubble initially expands and then disappears over two to six weeks. Proper positioning of the head in the postoperative time period is crucial for success. Although this treatment is inappropriate for the repair of many retinal detachments, it is simpler and much less costly than scleral buckling. Furthermore, if pneumatic retinopexy is unsuccessful, scleral buckling still can be performed.

Vitrectomy

Certain complicated or severe retinal detachments may require a more complicated operation called a vitrectomy. These detachments include those that are caused by the growth of abnormal blood vessels on the retina or in the vitreous, as occurs in advanced diabetes. Vitrectomy also is used with giant retinal tears, vitreous hemorrhage (blood in the vitreous cavity that obscures the surgeon's view of the retina), extensive tractional retinal detachments (pulling from scar tissue), membranes (extra tissue) on the retina, or severe infections in the eye (endophthalmitis). Vitrectomy surgery is performed in the hospital under general or local anesthesia. Small openings are made through the sclera to allow positioning of a fiberoptic light, a cutting source (specialized scissors), and a delicate forceps. The vitreous gel of the eye is removed and replaced with a gas to refill the eye and reposition the retina. The gas eventually is absorbed and is replaced by the eye's own natural fluid. A scleral buckle is usually also performed with the vitrectomy.


What are the results of surgery for a retinal detachment?

The surgical repair of retinal detachments is successful in about 80% of patients with a single procedure. With additional surgery, over 90% of retinas are reattached successfully. Several months may pass, however, before vision returns to its final level. The final outcome for vision depends on several factors. For example, if the macula was detached, central vision rarely will return to normal. Even if the macula was not detached, some vision may still be lost, although most will be regained. New holes, tears, or pulling may develop, leading to new retinal detachments. If a gas or air bubble was inserted in the eye during surgery, maintaining proper positioning of the head is also important in determining the final outcome. Close follow-up by an ophthalmologist, therefore, is required. Long-term studies have shown that even after preventive treatment of a retinal hole or tear, 5% to 9% of patients may develop new breaks in the retina, which could lead to a retinal detachment. Overall, however, repair of retinal detachments has made great strides in the past 20 years with the restoration of useful vision to many thousands of patients

Who is at risk for AMD?

The greatest risk factor is age. Although AMD may occur during middle age, studies show that people over age 60 are clearly at greater risk than other age groups. For instance, a large study found that people in middle-age have about a 2 percent risk of getting AMD, but this risk increased to nearly 30 percent in those over age 75.

Other risk factors include :
Smoking. Smoking may increase the risk of AMD.
Obesity. Research studies suggest a link between obesity and the progression of early and intermediate stage AMD to advanced AMD.
Race. Whites are much more likely to lose vision from AMD than African Americans.
Family history. Those with immediate family members who have AMD are at a higher risk of developing the disease.
Gender. Women appear to be at greater risk than men.

Can my lifestyle make a difference?

Your lifestyle can play a role in reducing your risk of developing AMD.
Eat a healthy diet high in green leafy vegetables and fish.
Don't smoke.
Maintain normal blood pressure.
Watch your weight.
Exercise.

What are the symptoms?

Both dry and wet AMD cause no pain.
For dry AMD: the most common early sign is blurred vision. As fewer cells in the macula are able to function, people will see details less clearly in front of them, such as faces or words in a book. Often this blurred vision will go away in brighter light. If the loss of these light-sensing cells becomes great, people may see a small—but growing—blind spot in the middle of their field of vision.

For wet AMD: the classic early symptom is that straight lines appear crooked. This results when fluid from the leaking blood vessels gathers and lifts the macula, distorting vision. A small blind spot may also appear in wet AMD, resulting in loss of one's central vision.

How is AMD detected?

AMD is detected during a comprehensive eye exam that includes:

1. Visual acuity test. This eye chart test measures how well you see at various distances.

2. Dilated eye exam. Drops are placed in your eyes to widen, or dilate, the pupils. Your ophthalmologist uses a special magnifying lens to examine your retina and optic nerve for signs of AMD and other eye problems. After the exam, your close-up vision may remain blurred for several hours.

3. Tonometry. An instrument measures the pressure inside the eye. Numbing drops may be applied to your eye for this test.

4. Fluorescein angiogram. In this test, a special dye is injected into your arm. Pictures are taken as the dye passes through the blood vessels in your retina. The test allows your eye care professional to identify any leaking blood vessels and recommend treatment

5 Optical coherence tomography (OCT) A breakthrough technology to study swelling and distortion of anatomical layers in your retina. Provides invaluable information in managing AMD patients.

During an eye exam, you may be asked to look at an Amsler grid. The pattern of the grid resembles a checkerboard. You will cover one eye and stare at a black dot in the center of the grid. While staring at the dot, you may notice that the straight lines in the pattern appear wavy. You may notice that some of the lines are missing. These may be signs of AMD.

How is wet AMD treated?

Wet AMD can be treated with laser surgery, photodynamic therapy, and injections into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.

1. Laser surgery. This procedure uses a laser to destroy the fragile, leaky blood vessels. A high energy beam of light is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. However, laser treatment may also destroy some surrounding healthy tissue and some vision. Only a small percentage of people with wet AMD can be treated with laser surgery. Laser surgery is more effective if the leaky blood vessels have developed away from the fovea, the central part of the macula. Laser surgery is performed in a doctor's office or eye clinic.
The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.

2. Photodynamic therapy. A drug called verteporfin is injected into your arm. It travels throughout the body, including the new blood vessels in your eye. The drug tends to "stick" to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline. Unlike laser surgery, this drug does not destroy surrounding healthy tissue. Because the drug is activated by light, you must avoid exposing your skin or eyes to direct sunlight or bright indoor light for five days after treatment.

Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor's office.
Photodynamic therapy slows the rate of vision loss. It does not stop vision loss or restore vision in eyes already damaged by advanced AMD. Treatment results often are temporary. You may need to be treated again.

3. Injections. Wet AMD can now be treated with new drugs (e.g. Avastin, Lucentis and Macugen) that are injected into the eye (anti-VEGF therapy). Abnormally high levels of a specific growth factor occur in eyes with wet AMD and promote the growth of abnormal new blood vessels. This drug treatment blocks the effects of the growth factor.

You will need multiple injections that may be given as often as monthly. The eye is numbed before each injection. After the injection, you will remain in the doctor's office for a while and your eye will be monitored. This drug treatment can help slow down vision loss from AMD and in some cases improve sight.

How is dry AMD treated?

Once dry AMD reaches the advanced stage, no form of treatment can prevent vision loss. However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage, in which vision loss occurs.
The National Eye Institute's Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD's progression from the intermediate stage to the advanced stage will save the vision of many people.

Age-related eye disease study (AREDS)

What is the dosage of the AREDS formulation?
The specific daily amounts of antioxidants and zinc used by the study researchers were 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene (often labeled as equivalent to 25,000 International Units of vitamin A), 80 milligrams of zinc as zin
xide, and two milligrams of copper as cupric oxide. Copper was added to the AREDS formulation containing zinc to prevent copper deficiency anemia, a condition associated with high levels of zinc intake.

Who should take the AREDS formulation?
People who are at high risk for developing advanced AMD should consider taking the formulation. You are at high risk for developing advanced AMD if you have either:
1. Intermediate AMD in one or both eyes.
OR
2. Advanced AMD (dry or wet) in one eye but not the other eye.

Your eye care professional can tell you if you have AMD, its stage, and your risk for developing the advanced form.
The AREDS formulation is not a cure for AMD. It will not restore vision already lost from the disease. However, it may delay the onset of advanced AMD. It may help people who are at high risk for developing advanced AMD keep their vision.

How can I take care of my vision now that I have AMD?

Dry AMD. If you have dry AMD, you should have a comprehensive dilated eye exam at least once a year. Your eye care professional can monitor your condition and check for other eye diseases. Also, if you have intermediate AMD in one or both eyes, or advanced AMD in one eye only, your doctor may suggest that you take the AREDS formulation containing the high levels of antioxidants and zinc.
Because dry AMD can turn into wet AMD at any time, you should get an Amsler grid from your eye care professional. Use the grid every day to evaluate your vision for signs of wet AMD. This quick test works best for people who still have good central vision. Check each eye separately. Cover one eye and look at the grid. Then cover your other eye and look at the grid. If you detect any changes in the appearance of this grid or in your everyday vision while reading the newspaper or watching television, get a comprehensive dilated eye exam.

Wet AMD. If you have wet AMD and your doctor advises treatment, do not wait. After laser surgery or photodynamic therapy, you will need frequent eye exams to detect any recurrence of leaking blood vessels. Studies show that people who smoke have a greater risk of recurrence than those who don't. In addition, check your vision at home with the Amsler grid. If you detect any changes, schedule an eye exam immediately.


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