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OPHTHALMOLOGY

GLAUCOMA

 

Glaucoma is sometimes called the silent thief, slowly stealing the sight before the patient realizes anything’s wrong. The most common form of glaucoma develops gradually, giving no warning signs. Many people aren’t even aware they have an eye prob- lem until their vision is extensively damaged. Glaucoma is the second most common cause of vision loss in the United States. It affects approximately 3 million Americans.

Glaucoma is not just one disease but is a group of them. The common feature of these diseases is that abnormally high pres- sure inside the eyeball damages the optic nerve. The optic nerve is a bundle of more than a million nerve fibers at the back of the eye. It’s like a big electric cable made up of thousands of individual wires carrying the images the person sees from the retina to the brain. Blind spots develop in the visual field when the optic nerve deteriorates, starting with the peripheral (side) vision. If left untreated glaucoma may lead to blindness in both eyes.

Fortunately, only a small percentage of people with the disease lose their sight. Recent medical advances have made it easier to diagnose and treat glaucoma. And if detected and treated early, glaucoma need not cause even moderate vision loss. But it does require regular monitoring and treatment for the rest of the life.

 

SIGNS AND SYMPTOMS

 

Glaucoma occurs in several types. The differences have to do with what’s causing the pressure in the eye, which can lead to dam- age of the optic nerve. Signs and symptoms vary depending on the type of glaucoma.

 

Primary open-angle glaucoma progresses with few or no symptoms until the condition reaches an advanced stage. As increased

 

eye pressure continues to damage the optic nerve, the patient loses more and more of the peripheral vision. Open-angle glau- coma usually affects both eyes, although at first the patient may complain of symptoms in just one eye. Other symptoms include:

  • Sensitivity to light and glare
  • Trouble differentiating between varying shades of light and dark
  • Trouble with night vision

 

Acute angle-closure glaucoma develops suddenly in response to a rapid rise in eye pressure. Permanent vision loss can occur within hours of the attack, so it requires immediate medical attention. An attack often happens in the evening when the light is dim and the pupils are dilated. The symptoms may be severe. Signs and symptoms include:

  • Blurred vision
  • Halos around lights
  • Reddening of the eye
  • Headache
  • Severe eye pain
  • Nausea and vomiting
  • Hardness of the affected eye

 

Both open-angle and angle-closure glaucoma can be primary or secondary conditions. They’re called primary when the cause of the condition is unknown. They’re called secondary when the condition can be traced to a known cause, such as an injury or an eye disease. Signs and symptoms of secondary glaucoma vary and depend on what’s causing the glaucoma.

 

CAUSES

 

Internal pressure in the eye, called intraocular pressure, allows it to hold its shape and function properly. Intraocular pressure is like air in a balloon — too much pressure inside the balloon affects its shape and may even cause it to pop. In the case of the human eye, too much pressure can damage the optic nerve.

Fluids inside the eye help maintain the intraocular pressure. These fluids are the vitreous, which fills the vitreous cavity, at the back of the eye, and the aqueous humor, which fills the anterior chamber, at the front of the eye. Aqueous humor is continuously pro- duced and circulated through the anterior chamber before draining out of the eye. This continuous flow of fluid nourishes the lens and the cornea and removes unwanted debris. A healthy eye produces aqueous humor at the same rate that it drains fluid, thus maintaining a normal pressure.

Aqueous humor exits the eye through a drainage system located at the angle formed where the iris and the cornea meet. Here it passes through a sieve-like system of spongy tissue called the trabecular meshwork and drains into a channel called Schlemm’s canal. The fluid then merges into the bloodstream.

When the drainage system doesn’t function properly — for example, if the trabecular meshwork becomes clogged — the aque- ous humor can’t flow at its normal rate and pressure builds within the eye. For reasons that are not completely understood, the increased eye pressure gradually damages the nerve fibers that make up the optic nerve.

 

TYPES OF GLAUCOMA

 

Glaucoma occurs in several types. The differences have to do with what’s causing the fluid blockage that builds pressure in the eye.

  • Primary open-angle. Primary open-angle glaucoma, also called chronic open-angle glaucoma, accounts for most cases of the disease. Although the drainage angle formed by the cornea and the iris remains open, the aqueous humor drains too slowly. This leads to fluid backup and a gradual buildup of pressure within the eye. Damage to the optic nerve is so slow and painless that a large portion of the vision can be lost before even the patient is aware of a problem.

The cause of primary open-angle glaucoma remains unknown. It may be that the aqueous humor drains or is absorbed less effi- ciently with age, but not all older adults get this form of glaucoma.

  • Angle-closure. Angle-closure glaucoma, also called closed-angle glaucoma, is a less common form of the disease. It occurs when the drainage angle formed by the cornea and the iris closes or becomes blocked. The aqueous humor can’t exit through the trabecular meshwork, resulting in an increase in eye pressure. Angle-closure glaucoma can be chronic (progressing gradually) or acute (coming on suddenly).

 

Most people with this type of glaucoma have a very narrow drainage angle, which may be an abnormality from birth. Angle- closure glaucoma is more common among farsighted people, who tend to have smaller eyes that can narrow the angle. Normal aging also may cause angle blockage. As the patient gets older, the lens becomes larger, pushing the iris forward and narrowing the space between the iris and the cornea.

If the patient has a narrow drainage angle and his/her pupils become widely dilated, the angle may close and cause a sudden increase in eye pressure. This attack of acute angle-closure glaucoma requires immediate treatment. Although an acute attack often affects only one eye, the other eye is at risk of an attack as well.

Several factors can cause the pupils to dilate, including darkness or dim light, stress or excitement, and certain medications. These medications include antihistamines, tricyclic antidepressants and eyedrops used to dilate the pupils, which may not cause the angle to close until several hours after the drops have been instilled.

 

Acute angle-closure glaucoma is a medical emergency that can cause vision loss within hours of its onset. Without treatment the eye can become blind in as little as 1 or 2 days.

 

  • Secondary. Both open-angle and angle-closure glaucoma can be primary or secondary conditions. They’re called primary when the cause of the condition is unknown. They’re called secondary when the condition can be traced to a known cause, such as an injury or an eye disease. Secondary glaucoma may be caused by a variety of medical conditions, medications, physical injuries, and eye abnormalities or deformities. Infrequently eye surgery can cause secondary glaucoma.

 

  • Low-tension. Low-tension glaucoma is an unusual and poorly understood form of the disease. In this form, eye pressure remains within a normal range but the optic nerve is damaged nevertheless. Why this happens is unknown, although some experts believe that people with low-tension glaucoma may have an abnormally fragile optic nerve or a reduced blood supply to the optic nerve, caused by a condition such as closed arteries (atherosclerosis). Under these circumstances even normal pressure on the optic nerve is enough to cause damage.

 

Doctors don’t completely understand the underlying causes of glaucoma. Open-angle glaucoma may have a genetic link. That is, a defect in one or more genes may cause the disease. People with a family history of glaucoma are more likely to develop it them- selves. However, the exact genetic defects responsible for its occurrence haven’t been identified.

Other factors appear to contribute to the disease, but doctors don’t know for sure what these factors are and the relationships among them. Although glaucoma is normally associated with increased eye pressure, people with normal or low eye pressure can experience vision loss. And people with higher-than-normal eye pressure may never experience optic nerve damage.

Doctors have debated for many years about how damage to the optic nerve occurs. One theory holds that the pressure of backed up aqueous humor causes structural damage and ultimately death to the nerve fibers. Another theory suggests that nerve fibers die when small blood vessels that feed the optic nerve become blocked or when the blood supply is disrupted.

 

The cause of decreased drainage through the trabecular meshwork also presents a puzzle. The changes that slow drainage may be a result of normal aging, yet not all older adults develop glaucoma.

 

RISK FACTORS

 

If the intraocular pressure is higher than what’s considered normal, the patient is at increased risk of developing glaucoma. Yet most people with slightly elevated intraocular pressure don’t develop the disease. This makes it difficult to predict who will get glaucoma.

 

Certain other factors increase the risk. Because chronic forms of glaucoma can destroy vision before any symptoms are apparent, the following factors should be watched:

  • Age. Open-angle glaucoma is rare before age 40. The risk of developing glaucoma nearly doubles every 10 years after age 50. Approximately 14 percent of people in the United States who are at least age 80 have the disease. Primary open-angle glaucoma is most common in older adult women.
  • Race. In the United States, blacks are three to four times more likely to get glaucoma than are whites, and they are six times more likely to suffer permanent blindness as a result. The reasons for these differences aren’t known, but blacks may be more susceptible to damage to the optic nerve, or they may not respond to current treatments as well as whites do. Asian-Americans, particularly people of Vietnamese descent, also are at higher risk. Japanese-Americans are more prone to develop low-tension glaucoma.
  • Family history of glaucoma. If one of the parents has glaucoma, the patient has about a 20 percent chance of developing the disease. If there is a sibling with the disease, the chance of getting it is about 50 percent.
  • Medical conditions. If the patient is diabetic, his risk of developing glaucoma is about three times greater than that of people who don’t have diabetes. A history of high blood pressure or heart disease also can increase the risk. Other risk factors include retinal detachment, eye tumors and eye inflammations such as chronic uveitis and iritis. Previous eye surgery may trigger second- ary glaucoma.
  • Physical injuries. Severe trauma, such as being hit in the eye, can result in increased eye pressure. Injury can also dislocate the lens, closing the drainage angle.
  • Nearsightedness. Severe nearsightedness increases the risk of developing glaucoma. An extensive study of eye health found that nearsighted people had a two to three times higher risk of developing glaucoma than did people who were not nearsighted.
  • Prolonged corticosteroid use. Using corticosteroids for prolonged periods of time increase the risk of getting secondary glau- coma.
  • Eye abnormalities. Structural abnormalities of the eye can lead to secondary glaucoma. For example, pigmentary glaucoma is a form of secondary glaucoma caused by pigment granules being released from the back of the iris. These granules can block the trabecular meshwork.

 

WHEN TO SEEK MEDICAL ADVICE

 

Primary open-angle glaucoma gives few warning signs until permanent damage has already occurred. That’s why regular eye exams are the key to detecting glaucoma early enough for successful treatment. It’s best to have routine eye checkups every 2 to 4 years after age 40 and every 1 to 2 years after age 65. Symptoms of any kind should not be allowed to occur. If the patient has one or more risk factors for glaucoma, he should be advised to talk to his doctor about scheduling regular eye exams. Some tests can be performed by the doctor, but others need to be done by an eye care specialist.

In addition, the patient should be alert for signs of an acute angle-closure glaucoma attack, such as a severe headache or pain in the eye or eyebrow, nausea, blurred vision or rainbow halos around lights. If any of these symptoms is experienced , the patient should seek immediate care at his local hospital emergency room.

If glaucoma is diagnosed, a regular schedule of examinations should be established with his doctor to be sure treatment is helping maintain a safe pressure of fluid in his eyes.

 

SCREENING AND DIAGNOSIS

 

If glaucoma is suspected, the patient may perform a series of tests to detect any signs of damage. Tests include:

  • Tonometry. Tonometry is a simple, painless procedure that measures the intraocular pressure. It is usually the initial screening test for glaucoma. Two common techniques are air-puff tonometry and applanation tonometry. Air-puff tonometry uses a puff of air to measure the amount of force needed to indent the cornea. An applanation tonometer is a sophisticated device that’s usu-

 

ally fitted to a slit lamp. Slit lamps use an intense line of light — a slit — providing illumination of the cornea, iris, lens and anterior chamber, and allowing the doctor a good view of these structures. In tonometry, the doctor numbs the patient’s eyes with drops and has him/her sit at the slit lamp, where a small flat-tipped cone pushes lightly against the eyeball. The force required to flatten (applanate) a small area of the cornea translates into a measure of the intraocular pressure.

Normal eye pressure ranges from 10 to 22 mm Hg. Doctors consider anyone with eye pressure over 23 mm Hg to be at risk of developing glaucoma and in need of careful monitoring for early signs of glaucoma. People with intraocular pressure greater than 30 mm Hg are at high risk.

  • Test for optic nerve damage. To check the fibers in the optic nerve, the ophthalmologist uses an instrument called an ophthal- moscope, which enables him or her to look directly through the pupil to the back of the patient’s eye. The doctor may also use laser light and computers to create a three-dimensional image of the optic nerve. This can reveal slight changes that may indicate the beginnings of glaucoma.
  • Visual field test. To check how the visual field has been affected by glaucoma, the ophthalmologist uses a perimetry test. One method, known as tangent screen perimetry, requires looking at a screen with a target in the center. The ophthalmologist manipu- lates a small object on a wand at different locations in the visual field. The patient indicates whenever he sees the object come into view. By repeating this process over and over again, the ophthalmologist can map the entire visual field.
  • Other tests. To distinguish between open-angle glaucoma and angle-closure glaucoma, the ophthalmologist may use a tech- nique called gonioscopy, in which a special lens is placed on the eye to inspect the drainage angle. Another test, tonography, can measure how fast fluid drains through the trabecular meshwork.

To receive a diagnosis of glaucoma, the patient must exhibit several factors. These include elevated intraocular pressure, areas of vision loss and damage to the optic nerve. In glaucoma, the optic disk shows visible signs of damage. The optic disk is the area where all of the nerve fibers come together at the back of the eye before exiting the eyeball. An optic disk that has been affected by glaucoma appears indented, or excavated, as if someone scooped out part of the center of the disk. This condition is known as cupping. The normal contour and color of the disk may be affected by the loss of nerve fibers.

 

TREATMENT

 

If the ophthalmologist diagnosis elevated intraocular pressure, an excavated optic disk and loss of visual field, the patient will likely be treated for glaucoma. If the patient has only slightly elevated eye pressure, an undamaged optic nerve and no visual field loss, he may not need treatment, but the ophthalmologist may advise more frequent examinations to detect any future changes. If the patient has signs of optic nerve damage and visual field loss, even if the eye pressure is in the normal range, treatment may be needed to lower eye pressure further, which may help slow the progression of glaucoma.

Glaucoma can’t be cured, and damage caused by the disease can’t be reversed. But with treatment, glaucoma can be controlled. Eyedrops, oral medications and surgical procedures can prevent or slow further damage.

 

Having glaucoma means treatment needs to be continued for the rest of the life. Because the disease can progress or change without the patient being aware of it, the treatment may need to be changed over time. Regular checkups and adherence to a treatment plan may seem burdensome, but they’re essential to prevent vision loss.

 

Preventing further damage to the optic nerve and continued loss of visual field may be accomplished by keeping the eye pres- sure under control. The ophthalmologist may focus on lowering the intraocular pressure to a level that’s unlikely to cause further optic nerve damage. This level is often referred to as the target pressure and will probably be a range rather than a single num- ber. Target pressure differs for each person, depending on the extent of the damage and other factors. The target pressure may change over the course of the lifetime.

 

Medications are the most common early treatment for glaucoma. Standard practice has been to move on to surgery if medications are ineffective. However, surgery is an option as a safe and effective initial treatment.

 

Eyedrops

 

Glaucoma treatment often starts with medicated eyedrops. There are several types of drops, and they must be used exactly as prescribed to control the intraocular pressure. Skipping even a few doses can cause damage to the optic nerve to worsen. Some drops need to be applied several times each day, and others must be used just once a day. The doctor should be informed of all other medications taken, to avoid any undesirable drug interactions.

Because some of the eyedrops are absorbed into the bloodstream, side effects unrelated to the eyes may be experienced. To minimize this absorption, the eyes should be closed for 1 to 2 minutes after instilling the drops. The patient is taught to press lightly at the corner of the eye near the nose to close the tear duct, and wipe off any unused drops from the eyelid. More than one type of eyedrop may be prescribed, and they should be used with 5 to 10 minutes intervals between applications.

 

The types of eyedrops that doctors most commonly prescribe include:

  • Beta blockers. These reduce the production of aqueous humor. Examples include levobunolol, timolol , carteolol, betaxolol and metipranolol. Possible side effects include difficulty breathing, slowed pulse, hair loss, decreased blood pressure, impotence, fatigue, weakness, depression and memory loss. If the patient suffers from asthma, bronchitis or emphysema, or if he has diabe- tes and uses insulin, beta blockers shouldn’t be used unless no alternative is possible, and then only with great care.
  • Alpha-adrenergic agents. These reduce the production of aqueous humor. Examples include apraclonidine and brimonidine. Possible side effects include increased blood pressure, tremors, headache, anxiety, red and itchy eyes, dry mouth and allergic reactions.
  • Carbonic anhydrase inhibitors. These medications, which include dorzolamide, reduce the amount of aqueous humor. Possible side effects include a bad taste in the mouth. Frequent urination and a tingling sensation in the fingers and the toes are common when a carbonic anhydrase inhibitor is taken orally but rare when it is taken as drops. If the patient is allergic to sulfa drugs, this type of medication shouldn’t be used unless no alternative is possible, and then only with great care.
  • Prostaglandin analogues. These eyedrops increase the outflow of aqueous humor. These hormone-like substances, which include latanoprost, may be used in conjunction with a drug that reduces production of aqueous humor. Possible side effects

 

include mild reddening and stinging of the eyes and darkening of the iris and the eyelid skin.

  • Prostamides. These include bimatoprost. They increase the outflow of aqueous humor. Possible side effects include mild to moderate reddening of the eyes and eyelash growth.

 

Other eyedrops that are rarely used include:

  • Miotics. These increase the outflow of aqueous humor. Examples include pilocarpine. Possible side effects include pain around or inside the eyes, brow ache, blurred or dim vision, nearsightedness, allergic reactions, a stuffy nose, sweating, increased saliva- tion and occasional digestive problems.
  • Epinephrine compounds. These increase the outflow of aqueous humor. Examples include epinephrine. Possible side effects include red eyes, allergic reactions, palpitations, high blood pressure, headache and anxiety.

 

Oral medications

 

If eyedrops alone don’t bring the eye pressure down to the desired level, the doctor may also prescribe oral medication. The most common oral medications for glaucoma are carbonic anhydrase inhibitors. These include acetazolamide, dichlorphenamide and methazolamide. The pills should be taken with meals to reduce side effects. Potassium loss that these medications cause can be minimized by adding bananas and apple juice to the diet.

When these oral medications are started, The patient may experience a frequent need to urinate and a tingling sensation in the fingers and the toes. These symptoms often disappear after a few days. Other possible side effects of carbonic anhydrase inhibi- tors include rashes, depression, fatigue, lethargy, stomach upset, a metallic taste in carbonated beverages, impotence and weight loss. Kidney stones also can occur.

 

Surgery

 

Surgery may be need surgery to treat glaucoma if medications are not tolerated or they’re ineffective. Doctors use several types of surgery to treat glaucoma:

  • Laser surgery. In the last couple of decades, a procedure called trabeculoplasty has been used increasingly in the treatment of open-angle glaucoma. The doctor uses a high-energy laser beam to shrink part of the trabecular meshwork, which causes other parts of the meshwork to stretch and open up. This helps aqueous humor drain more easily from the eye.

This type of laser surgery is an office procedure that takes 10 to 20 minutes. The patient is given anesthetic eyedrop, seated at a slit lamp and fitted with a special lens on the eye. The doctor aims the laser through the lens at the trabecular meshwork and applies burns to it. the patient will see bright flashes of light.

After the surgery normal activities can be resumed immediately without discomfort. The doctor will check the eye pressure 1 to 2 hours after the procedure and several times in the following weeks. Anti-inflammatory eyedrops may be prescribed for a few days following trabeculoplasty. It may take a few weeks before the full effect of the surgery becomes apparent.

In almost all cases, laser surgery for glaucoma initially lowers intraocular pressure. However, its effects may wear off over time. Studies show that eye pressure rises in many people 2 to 5 years after they receive the laser treatment.

  • Conventional surgery. If eyedrops and laser surgery aren’t effective in controlling the eye pressure, a trabeculectomy may be needed. This procedure is done in a hospital or an outpatient surgery center. The patient will receive medication to help him/her relax and eyedrops and an injection of anesthetic to numb the eye. Using delicate instruments under an operating microscope, the surgeon creates an opening in the sclera — the white of the eye — and removes a small piece of the trabecular meshwork. The aqueous humor can now freely leave the eye through this hole. As a result the eye pressure will be lowered. The hole is covered by the conjunctiva, so there’s not an open hole in the eye.

The doctor will check the eye in several follow-up visits. Antibiotic and anti-inflammatory eyedrops will be used for some time after the operation to fight infection and scarring of the newly created drainage opening. Scarring is a particular problem for young adults, blacks and people who have had cataract surgery. This procedure works best if the patient hasn’t had any previous eye surgery.

Although glaucoma surgery may preserve current vision, it can’t restore already lost vision. Sometimes a single surgical procedure may not lower eye pressure enough, in which case the patient needs to continue using glaucoma drops or have another trab- eculectomy operation.

  • Drainage implants. Another type of operation, called drainage implant surgery, may be performed on people with secondary glaucoma or on children with glaucoma.

Like the trabeculectomy, drainage implant surgery is performed at a hospital or an outpatient clinic. The patient will be given medi- cation to help him/her relax and eyedrops and an anesthetic to numb the eye. Then the doctor inserts a small silicone tube in the eye to help drain aqueous humor.

After the surgery an eye patch will be worn for 24 hours and eyedrops will be used for several weeks to fight infection and scar- ring. The doctor will check the eyes several times in the weeks that follow.

Complications from glaucoma surgery may include infection, bleeding, eye pressure that remains too high or too low and, poten- tially, loss of vision. Having eye surgery may also speed up the development of cataracts. Most of these complications can be effectively treated.

 

TREATING ACUTE ANGLE-CLOSURE GLAUCOMA

 

Acute angle-closure glaucoma is a medical emergency. When this condition occurs, doctors may administer several medications to reduce eye pressure as quickly as possible. Once the eye pressure is under control, an operation called iridotomy is recom- mended. In this procedure the doctor uses a laser beam to create a small hole in the iris that allows aqueous humor to flow more freely into the anterior chamber. Many doctors recommend an iridotomy on the other eye at a later date because of the high risk that it too will have an attack within the next few years.

 

PREVENTION

 

There’s no known way to prevent glaucoma, but regular checkups can help detect the disease in its early stages before irrevers- ible damage has occurred. As a general rule, an eye exam is recommended every 2 to 4 years between the ages of 40 and 65, and every 1 to 2 years at > 65 years.

More frequent monitoring may be recommended if the patient is at increased risk of developing glaucoma. More frequent check- ups may also be needed if the patient has received a diagnosis of abnormally high intraocular pressure or has a history of serious eye injury.

 

SELFCARE

 

The most important thing can be done in case of glaucoma is taking the medications exactly as prescribed. Frequent eye exams will help the doctor monitor the eye pressure and keep the patient and the doctor aware of any changes in the vision.

Other self-care tips:

  • Maintain a healthy diet. Vitamins and minerals that are important for the eyes include vitamin A, vitamin C, vitamin E, zinc and copper. Drink fluids in small amounts over the course of a day. Drinking a quart or more of any liquid within a short time may increase eye pressure. Limit caffeine to low or moderate levels.
  • Exercise regularly. Studies show that people with open-angle glaucoma who exercise regularly — at least three times a week
  • can reduce their eye pressure by an average of 20 percent. However, angle-closure glaucoma isn’t affected by exercise, and people with pigmentary glaucoma, a form of secondary glaucoma, may experience increased eye pressure after exercise.
  • Steer clear of herbal remedies. A number of herbal supplements, such as bilberry, are advertised as glaucoma remedies. Bilberry is not effective in preventing or treating glaucoma. Be cautious about herbal supplements and discuss them with the doc- tor before trying them.
  • Find healthy ways to cope with stress. Stress can trigger an attack of acute angle-closure glaucoma. Relaxation techniques, such as meditation and progressive muscle relaxation, may be helpful in dealing with stress.
  • Wear sunglasses with full ultraviolet protection. Whenever you’re out in the sun, even if only for a few minutes, wear sun- glasses that block ultraviolet (UV) light.
  • Wear proper eye protection. Eye trauma can result in increased eye pressure. Use safety glasses or goggles when you play sports, use tools or machinery, or work with chemicals.

 

Additional Resources

  • National Association for Visually Handicapped
  • Glaucoma Foundation

© 1998-2003 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved.

 

                    RETINAL DETACHMENT  

 

Retinal detachment is a serious eye condition that almost always leads to blindness if not treated promptly. Each year the condi- tion affects about 30,000 people in the United States.

The retina is the light-sensitive tissue that lies smoothly against the inside back wall of the eye. Underneath the retina is the choroid, a thin layer of blood vessels that supplies oxygen and nutrients to the retina. Retinal detachment occurs when the retina separates from this underlying layer of blood vessels. Unless the detached retina is surgically reattached, the patient may perma- nently lose his/her vision in the affected eye.

The good news is that warning signs often appear before retinal detachment occurs, and early diagnosis and treatment by an ophthalmologist can save the vision.

 

SIGNS AND SYMPTOMS

 

Retinal detachment is painless, but visual symptoms almost always appear before it occurs. Warning signs of retinal detachment include:

  • The sudden appearance of many floaters — small bits of debris in the field of vision that look like spots, hairs or strings and that appear to float before the patient’s eyes
  • A sensation of flashing lights that usually occurs in one eye but can be present in both eyes at the same time
  • A shadow over a portion of the visual field
  • Blurred vision

Because most tears occur along the periphery of the retina, the patient may not initially notice blurring in his peripheral vision.

 

CAUSES

 

At the root of retinal detachment are changes to the jelly-like vitreous that fills the vitreous cavity of the patient’s eye. Over time the vitreous may change in consistency and partially liquefy. It may also begin to shrink. The partial liquefaction may progress to a point where the vitreous sags and separates from the surface of the retina. This is called posterior vitreous detachment (PVD), or vitreous collapse. It’s a common condition and occurs to some extent in most people’s eyes as they age.

 

PVD usually doesn’t cause serious problems. The shifting or sagging vitreous may cause the appearance of new or different float- ers in the field of vision. What look like spots, specks, hairs and strings are actually small clumps of gel, fibers and cells floating in the vitreous. And what the patient is seeing are the shadows that this material casts on the retina. Common floaters appear gradu- ally over time and, although they’re annoying, they are rarely a problem. They hardly ever require treatment.

 

If the vitreous pulls on the retina as it shifts and sags, the patient may see flashes of sparkling lights (photopsia) when his/her eyes are closed or when he/she is in a darkened room. The phenomenon lasts for only a few seconds.

 

However, floaters and flashes can signal a more serious eye problem, particularly if they appear suddenly and with great intensity. When the pull of a sagging vitreous is strong enough, the retina may tear, leaving what looks like a small, jagged flap in the retina. Most tears occur along the periphery of the retina. That’s where the vitreous is more firmly attached and can’t separate without tugging hard. Such tears can lead to retinal detachment.

 

Retinal detachment occurs when vitreous liquid starts to leak underneath the retina at places opened by the tears. Leakage can also occur at tiny holes where the retina has thinned due to aging or other retinal disorders. As liquid collects, the areas of the retina surrounding these defects may begin to peel away from the underlying layer, the choroid. Over time these detached areas may expand, like wallpaper that, once torn, slowly peels off a wall. The areas where the retina is detached lose their ability to see.

 

Not all tears and holes in the retina lead to retinal detachment. Sometimes the retina in the area of these defects remains relatively well attached to the choroid. But detachment that goes undetected and untreated can progress and eventually involve the entire retina with complete loss of vision.

 

RISK FACTORS

 

The risk of developing a detached retina generally increases with age simply because the vitreous changes as we grow older. There is also at greater risk if the patient has had a previous retinal detachment in one eye or a family history of retinal detachment or are:

  • Nearsighted (myopic)
  • Male
  • White

 

The following factors can cause the vitreous to pull at and tear the retina, so they also increase the risk of retinal detachment:

  • Previous eye surgery (for example, cataract removal)
  • Previous severe eye injury
  • Weak areas in the periphery of the retina

 

WHEN TO SEEK MEDICAL ADVICE

 

When the retina tears, small blood vessels may be broken, letting blood seep into the vitreous and causing hazy vision or specks that appear to float before the patient’s eyes. If the floaters appear suddenly as a cloud of spots or a spider web and are accom- panied by flashes of light, the ophthalmologist should be consulted immediately — because this may be the beginnings of a reti- nal detachment. Prompt medical attention is necessary to save vision.

The ophthalmologist can tell the patient about the various risks and benefits of all his treatment options. This will help the patient determine what treatment is appropriate for him.

 

SCREENING AND DIAGNOSIS

 

The ophthalmologist can determine if the patient has a retinal hole, tear or detachment by looking carefully at the retina with an ophthalmoscope, an instrument with a bright light and powerful lens that allows the doctor to view the inside of the eyes in great detail and in three dimensions.

If blood in the patient’s vitreous cavity prevents a clear view of the retina, the ophthalmologist might also use sound waves (ultra- sonography) to get a precise picture of the retina. Ultrasonography is a painless test that sends sound waves through the patient’s eye to bounce off the retina. The returning sound waves create an image on a monitor that allows the doctor to determine the condition of the retina and other structures inside the eye.

 

TREATMENT

 

Surgery is the only effective therapy for a retinal tear, hole or detachment. If a tear or a hole is treated before detachment develops or if a retinal detachment is treated before the central part of the retina (macula) detaches, the patient will probably retain much of his vision.

 

Surgery for retinal tears

When a retinal tear or hole hasn’t yet progressed to detachment, the eye surgeon may suggest one of two outpatient procedures: photocoagulation or cryopexy. Both methods can usually prevent the development of a retinal detachment. Healing typically takes 10 to 14 days. The vision may be blurred briefly following either procedure.

  • Photocoagulation. During photocoagulation the surgeon directs a laser beam through a special contact lens to make burns around the retinal tear. The burns cause scarring, which usually holds the retina to the underlying tissue. This procedure requires no surgical incision, and it causes less irritation to the eye than does cryopexy.
  • Cryopexy. With cryopexy the surgeon uses intense cold to freeze the retina around the retinal tear. After a local anesthetic numbs the eye, a freezing probe is applied to the outer surface of the eye directly over the retinal defect. This freezing produces an inflammation that leads to the formation of a scar — similar to that resulting from photocoagulation — which seals the hole and holds the retina to the underlying tissue. Cryopexy is used in instances where the tears are more difficult to reach with a laser, generally along the retinal periphery. The patient’s eye may be red and swollen for some time after cryopexy.

 

Surgery for retinal detachment

Three surgical procedures are commonly used to repair a retinal detachment: pneumatic retinopexy, scleral buckling and vitrec- tomy. Some of these procedures are done in conjunction with cryopexy. The purpose of these treatments is to close any retinal holes or tears and to reduce the tug on the retina from a shrinking vitreous. The patient’s particular condition will determine which procedure the eye surgeon recommends.

  • Pneumatic retinopexy. This surgical technique is used for an uncomplicated detachment when the tear is located in the upper

 

half of the retina. It’s done on an outpatient basis using local anesthesia. First, the surgeon performs cryopexy around the retinal tear. Then, to soften the eye, he or she withdraws a small amount of fluid from the space between the domed clear area at the front of your eye (cornea) and the colored part of the eye (iris). Next, the surgeon injects a bubble of expand- able gas into the vitreous cavity. Over the next several days, the gas bubble expands, sealing the retinal tear by pushing against it and the detached area that surrounds the tear. With no new fluid passing through the retinal tear, fluid that had previously collected under the retina is absorbed, and the retina is able to reattach itself to the back wall of the eye. Following surgery, the patient may have to hold his/her head in a cocked position for a few days, to make sure the gas bubble seals the retinal tear. It takes 2 to 6 weeks for the bubble to disappear. Until the gas is gone from the eye, the patient has to avoid lying or sleeping on his back. This keeps the bubble away from the lens and reduces the risk of cata- ract formation or a sudden pressure increase in the eye.

During this time the patient can’t travel by airplane or be at a high altitude because a sudden drop in pressure would cause the gas bubble to expand rapidly, resulting in dangerously high pressure in his eye. The surgeon should be con- sulted to find out when this danger has passed.

The success rate of pneumatic retinopexy isn’t as good as that of scleral buckling. However, it can avoid both a trip to the operating room and the need for incisional (cutting) surgery.

The complications of pneumatic retinopexy may include recurring retinal detachment, excessive scar tissue formation in the vitreous and retina, cataracts, increased pressure inside the eyeball (glaucoma), gas under the retina, and infec- tion. These complications are rare, but if they do occur and go untreated, they can cause severe loss of vision. A retinal detachment that has recurred can usually be repaired with scleral buckling or vitrectomy.

  • Scleral buckling. This is the most common surgery for repairing retinal detachment. It’s usually done in an operating room under local or general anesthesia. If the patient havs an uncomplicated retinal detachment, this surgery may be done on an outpatient basis.

First the surgeon treats the retinal tears or holes with cryopexy. Then he or she indents (buckles) the sclera over the affected area by pressing in with a piece of silicone. The silicone material is either in the form of a soft sponge or a solid piece. The buckle closes the tear and helps reduce the circumference of the eyeball, thereby preventing further vitreous pulling and separation. When ythere are several tears or holes or an extensive detachment, the surgeon may create an encircling scleral buckle around the entire circumference of the eye.

The scleral buckle is stitched to the outer surface of the sclera. Before tying the sutures that hold the buckle in place, the surgeon may make a small cut in the sclera and drain any fluid that has collected under the detached retina. The buckle remains in place for the rest of the patient’s life. Some surgeons may choose a temporary buckle for simple retinal detach- ments, using a small rubber balloon that’s inflated and later removed.

Repairing retinal detachment with scleral buckling works more than 80 percent of the time. But a reattached retina doesn’t guarantee normal vision. How well the patient sees following surgery depends in part on whether the macula was affected by the detachment before surgery, and if it was, for how long a period. The sight isn’t likely to return to normal if the macula was detached. Even if the macula wasn’t affected and scleral buckling successfully repairs the retina, there is a 10 percent chance of losing some vision due to wrinkling or puckering of the macula.

If the first operation fails, the doctor can usually try to reattach the retina with one or more additional operations. Additional surgery increases the rate of successful reattachment to more than 90 percent.

Although scleral buckling is generally successful, sometimes — in approximately 5 percent to 10 percent of the proce- dures — the retina fails to reattach to the choroid. This is often due to the formation of scar tissue on the retinal surface. Scar tissue present even before the operation can pull on the retina and prevent it from reattaching. The pull of scar tissue that forms after the operation can cause the retina to separate again after having been attached during surgery. This usu- ally happens 1 to 2 months following surgery.

This condition is treated by removing the scar tissue with a procedure called a vitrectomy and redoing the scleral buckling. In some complicated cases, the surgeon injects air, other gases or silicone oil into the vitreous cavity to push the retina back against the wall of the eye. Eventually the eye absorbs the air or gas and replaces it with fluid that the eye normally produces. Silicone, however, doesn’t get absorbed and has to be removed once the retina is reattached and healed com- pletely.

Complications occur infrequently in scleral buckling and can result in the need for more surgery, the loss of some or all vision in the involved eye, or in rare instances, the loss of that eye. Complications include: bleeding under the retina or into the vitreous cavity, glaucoma, and double vision (diplopia).

  • Vitrectomy. Occasionally, bleeding or inflammation clouds the vitreous and blocks the surgeon’s view of the detached retina. In other instances scar tissue makes it impossible to repair a retinal detachment with pneumatic retinopexy or scleral buckling alone. In these situations a procedure called vitrectomy can remove the clouded vitreous or scar tissue. The surgeon accomplishes this with a variety of delicate instruments passed into the eyeball through small openings in the sclera. These instruments include a light probe that illuminates the inside of the eye, a cutter to remove vitreous or scar tissue, and an infusion tube that replaces the volume of removed tissue with a balanced salt solution to maintain the nor- mal pressure and shape of the eye.

After completing the vitrectomy, the surgeon performs the scleral buckling procedure and may fill the inside of the eye with air, gas or silicone oil to help seal the retina against the wall of the eye.

Vitrectomy surgery typically lasts 1 to 2 hours but may take much longer in more complex cases. The complex cases are often done under general anesthesia, and shorter procedures are usually performed under local anesthesia.

Following surgery, the patient may experience some discomfort and a scratchy sensation in his/her eye. Severe pain is unlikely. If it occurs, the surgeon should know immediately. The eye can be expected to be red, swollen, watery and slight- ly sore for up to a month following any surgery for retinal detachment. Wearing an eye patch may provide some relief. The doctor may also prescribe antibacterial or dilating eyedrops to help the healing process. Strenuous activities during this time should be avoided. It’ll take about 8 to 10 weeks for the eye to heal fully. Then the eyes will be examined to assess postoperative vision and, if the patient wears eyeglasses, determine whether a new prescription is needed.

The vision may take many months to improve following surgery to repair a complicated retinal detachment. Some people don’t recover any lost vision.

The complications of vitrectomy are similar to those for other types of retinal detachment surgery. They include a retinal tear, re-detachment of the retina, a cataract or an infection. Any of these complications can lead to partial or complete loss of vision in the affected eye or, rarely, loss of the eye itself. How much vision the patient retains depends on the severity of the detachment.

 

COPING SKILLS

 

Unless the patient undergoes prompt surgery, retinal detachment will cause loss of vision in the portion of his/her field of vision that corresponds to the detached part of the retina. Losing part of vision can greatly change lifestyle — affecting the ability to drive, read and many other things the patient is accustomed to doing. Yet there are ways to cope with impaired vision. Below are a few suggestions:

  • Investigate vans and shuttles, volunteer driving networks, or rideshares available in your local area for people with impaired vision.
  • Optimize the vision you have with glasses that are specifically prescribed for the effects of retinal detachment and keep an extra pair in the car.
  • Have proper light in your home for reading and other activities.
  • Eliminate throw rugs and other tripping hazards within your home.
  • Tell friends and family members about your vision problems so that they can help you perform certain tasks and help you recog- nize people.
  • Take advantage of online networks, support groups and resources for people with impaired vision.
  • Ask your doctor about receiving professional help to make your home safer and more convenient for you to use.

 

By Mayo Clinic staff

© 1998-2004 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved.

 

 

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