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Retinopathies

Retinopathies

Definition

Retinopathy is a noninflammatory disease of the retina. There are many causes and types of retinopathy.

Description

The retina is the thin membrane that lines the back of the eye and contains light-sensitive cells (photoreceptors). Light enters the eye and is focused onto the retina. The photoreceptors send a message to the brain via the optic nerve. The brain then "interprets" the electrical message sent to it, resulting in vision. The macula is a specific area of the retina responsible for central vision. The fovea is about 1.5 mm in size and located in the macula. The fovea is responsible for sharp vision. When looking at something, the fovea should be directed at the object.

Retinopathy, or damage to the retina, has various causes. A hardening or thickening of the retinal arteries is called arteriosclerotic retinopathy. High blood pressure in the arteries of the body can damage the retinal arteries and is called hypertensive retinopathy. The spreading of a syphilis infection to the retinal blood vessels cases syphilitic retinopathy, and diabetes damages the retinal vessels resulting in a condition called diabetic retinopathy. Sickle cell anemia also affects the blood vessels in the eyes. Exposure to the sun (or looking at the sun during an eclipse) can cause damage (solar retinopathy), as well as certain drugs (for example, chloroquine, thioridazine, and large doses of tamoxifen). The arteries and veins can become blocked, thus resulting in a retinal artery or vein occlusion. These are just some of the causes of the various retinopathies.

Retinopathies are divided into two broad categories, simple or nonproliferative retinopathies and proliferative retinopathies. The simple retinopathies include the defects identified by bulging of the vessel walls, by bleeding into the eye, by small clumps of dead retinal cells called cotton wool exudates, and by closed vessels. This form of retinopathy is considered mild. The proliferative, or severe, forms of retinopathies include the defects identified by newly grown blood vessels, by scar tissue formed within the eye, by closed-off blood vessels that are badly damaged, and by the retina breaking away from the mesh of blood vessels that nourish it (retinal detachment ).

While each disease has its own specific effect on the retina, a general scenario for many of the retinopathies is as follows (note: not all retinopathies necessarily affect the blood vessels). Blood flow to the retina is disrupted, either by blockage or breakdown of the various vessels. This can lead to bleeding (hemorrhage) and fluids, cells, and proteins leaking into the area (exudates). There can be a lack of oxygen to surrounding tissues (hypoxia) or decreased blood flow (ischemia ). Chemicals produced by the body then can cause new blood vessels to grow (neovascularization), however, these new vessels generally leak and cause more problems. Neovascularization even can grow on the colored part of the eye (iris). The retina can swell and vision will be affected.

Diabetic retinopathy is the leading cause of blindness in people ages 20 to 74. Diabetic retinopathy will occur in 90% of persons with type 1 diabetes (insulin-dependent, or insulin requiring) and 65% of persons with type II diabetes (non-insulin-dependent, or not requiring insulin) by about 10 years after the beginning of diabetes. In the United States, new cases of blindness most often are caused by diabetic retinopathy. Among these new cases of blindness, 12% are people between the ages of 20 to 44 years, and 19% are people between the ages of 45 to 64 years.

Causes and symptoms

There are many causes of retinopathy. Some of the more common ones are listed below.

Diabetic retinopathy

Diabetes is a complex disorder characterized by an inability of the body to properly regulate the levels of sugar and insulin (a hormone made by the pancreas) in the blood. As diabetes progresses, the blood vessels that feed the retina become damaged in different ways. The damaged vessels can have bulges in their walls (aneurysms); they can leak blood into the surrounding jelly-like material (vitreous) that fills the inside of the eyeball; they can become completely closed; or new vessels can begin to grow where there would not normally be blood vessels. However, although these new blood vessels are growing in the eye, they cannot nourish the retina and they bleed easily, releasing blood into the inner region of the eyeball, which can cause dark spots and cloudy vision.

Diabetic retinopathy begins prior to any outward signs of disease being noticed. Once symptoms are noticed, they include poorer than normal vision, fluctuating or distorted vision, cloudy vision, dark spots, episodes of temporary blindness, or permanent blindness.

Hypertensive retinopathy

High blood pressure can affect the vessels in the eyes. Some blood vessels can narrow. The blood vessels can thicken and harden (arteriosclerosis). There will be flame-shaped hemorrhages and macular swelling (edema ). This edema may cause distorted or decreased vision.

Sickle cell retinopathy

Sickle cell anemia occurs mostly in blacks and is a hereditary disease that affects the red blood cells. The sickle-shaped blood cell reduces blood flow. People will not have visual symptoms early in the disease. However, patients need to be followed closely in case neovascularization occurs.

Retinal vein and artery occlusion

Retinal vein occlusion generally occurs in the elderly. There is usually a history of other systemic disease, such as diabetes or high blood pressure. The central retinal vein (CRV), or the retinal veins branching off of the CRV, can become compressed, thus stopping the drainage of blood from the retina. This may occur if the central retinal artery hardens.

Symptoms of retinal vein occlusion include a sudden, painless loss of vision or field of vision in one eye. There may be a sudden onset of floating spots (floaters) or flashing lights. Vision may be unchanged or decrease dramatically.

Retinal artery occlusion generally is the result of an embolism that dislodges from somewhere else in the body and travels to the eye. Transient loss of vision may precede an occlusion. Symptoms of a central retinal artery or branch occlusion include a sudden, painless loss of vision or decrease in visual field. Ten percent of the cases of a retinal artery occlusion occur because of giant cell arteritis (a chronic vascular disease).

Solar retinopathy

Looking directly at the sun or watching an eclipse can cause damage. There may be a loss of the central visual field or decreased vision. The symptoms can occur hours to days after the incident.

Drug-related retinopathies

Certain medications can affect different areas of the retina. Doses of 20-40 mg a day of tamoxifen usually do not cause a problem, but much higher doses may cause irreversible damage.

Patients taking chloroquine for lupus, rheumatoid arthritis, or other disorders may notice a decrease in vision. If so, discontinuing medication will stop, but not reverse, any damage. However, patients should never discontinue medication without the advice of their physician.

Patients taking thioridazine may notice a decrease in vision or color vision.

These drug-related retinopathies generally only affect patients taking large doses. However, patients need to be aware if any medication they are taking will affect the eyes. Patients should inform their doctors of any visual effects.

Diagnosis

The damaged retinal blood vessels and other retinal changes are visible to an eye doctor when an examination of the retina (fundus exam) is done. This can be done using a hand-held instrument called an ophthalmoscope or another instrument called a binocular indirect ophthalmoscope. This allows the doctor to see the back of the eye. Certain retinopathies have classic signs (for example, vascular "sea fans" in sickle cell, dot and blot hemorrhages in diabetes, flame-shaped hemorrhages in high blood pressure). Patients then may be referred for other tests to confirm the underlying cause of the retinopathy. These tests include blood tests and measurement of blood pressure.

Fluorescein angiography, where a dye is injected into the patient and the back of the eyes are viewed and photographed, helps to locate leaky vessels. Sometimes patients may become nauseated from the dye.

A newer diagnostic method called digital retinal photography can be used to screen those at high risk for retinopathies, in particular, diabetics. Some researchers say the technique could lead to more cost-effective screening for people with diabetic retinopathy.

Treatment

Retinal specialists are ophthalmologists who specialize in retinal disorders. Retinopathy is a disorder of the retina that can result from different underlying systemic causes, so general physicians should be consulted as well. For drug-related retinopathies, the treatment generally is discontinuation of the drug (only under the care of a physician).

Surgery with lasers can help to prevent blindness or lessen any losses in vision. The high-energy light from a laser is aimed at the weakened blood vessels in the eye, destroying them. Scars will remain where the laser treatment was performed. For that reason, laser treatment cannot be performed everywhere. For example, laser photocoagulation at the fovea would destroy the area for sharp vision. Panretinal photocoagulation may be performed. This is a larger area of treatment in the periphery of the retina; hopefully it will decrease neovascularization. Prompt treatment of proliferative retinopathy may reduce the risk of severe vision loss by 50%.

Patients with retinal artery occlusion should be referred to a cardiologist. Patients with retinal vein occlusion need to be referred to a physician, as they may have an underlying systemic disorder, such as high blood pressure.

Prognosis

Nonproliferative retinopathy has a better prognosis than proliferative retinopathy. Prognosis depends on the extent of the retinopathy, the cause, and promptness of treatment.

Prevention

Complete eye examinations done regularly can help detect early signs of retinopathy. Patients on certain medications should have more frequent eye exams. They also should have a baseline eye exam when starting the drug. People with diabetes must take extra care to have thorough, periodic eye exams, especially if early signs of visual impairment are noticed. A 2003 report recommended re-screening eye exams every two years for diabetics whose blood sugar had remained in control, and more frequent exams if visual symptoms appear. Anyone experiencing a sudden loss of vision, decrease in vision or visual field, flashes of light, or floating spots should contact their eye doctor right away.

Proper medical treatment for any of the systemic diseases known to cause retinal damage will help prevent retinopathy. For diabetics, maintaining proper blood sugar and blood pressure levels is important as well; however, some form of retinopathy usually will occur in diabetics, given enough time. A proper diet, particularly for those persons with diabetes, and stopping smoking also will help delay retinopathy.

Frequent, thorough eye exams and control of systemic disorders are the best prevention.

Resources

PERIODICALS

Selby, Joe, Lynn Ackerson, and Talmadge Cooper. "Three-year Incidence of Treatable Diabetic Eye Disease After Negative Funduscopic Examination." Diabetes June 2003: A60.

Usher, David, et al. "Automated Detection of Diabetic Retinopathy in Digital Retinal Images." Diabetes June 2003: A204.

ORGANIZATIONS

American Academy of Ophthalmology. 655 Beach Street, P.O. Box 7424, San Francisco, CA 94120-7424. http://www.eyenet.org.

American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 342-2383. http://www.diabetes.org.

American Optometric Association. 243 North Lindbergh Blvd., St. Louis, MO 63141. (314) 991-4100. http://www.aoanet.org.

Foundation Fighting Blindness. Executive Plaza I, Suite 800, 11350 McCormick Road, Hunt Valley, MD 21031-1014. (888) 394-3937. http://www.blindness.org.

Prevent Blindness America. 500 East Remington Road, Schaumburg, IL 60173. (800) 331-2020. http://www.preventblindness.org.

KEY TERMS

Exudate Cells, protein, fluid, or other material that passes through blood vessel walls to accumulate in the surrounding tissue.

Neovascularization New blood vessel formation-usually leaky vessels.

Nonproliferative retinopathy Retinopathy without the growth of new blood vessels.

Proliferative retinopathy Retinopathy with the growth of new blood vessels (neovascularization).

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Retinal Artery Occlusion

Retinal Artery Occlusion

Definition

Retinal artery occlusion refers to the closure of the central retinal artery and usually results in complete loss of vision in one eye. Occlusion of its branches causes loss of vision in only a portion of the field of vision.

Description

Retinal artery occlusion (RAO) occurs when the central retinal artery, the main source of blood supply to the retina, or one of its branches becomes blocked.

Causes and symptoms

The main causes of RAO are the following:

  • embolism (the sudden obstruction of a blood vessel by a blood clot)
  • atherosclerotic disease that results in the progressive narrowing of the arteries over time
  • endarteritis (the chronic inflammation of the inner layer of arteries)
  • angiospasm (a spasmodic contraction of a blood vessel with increase in blood pressure)

The most common symptom of RAO is an acute, painless loss of vision in one eye. The degree of loss depends on the location of the occlusion. If the occlusion occurs in the central artery of the retina, damage usually results in complete loss of vision in the affected eye. If occlusion occurs in a branch artery, vision loss will be partial and may even go unnoticed if only a section of the peripheral vision is affected.

People affected by RAO typically have high blood pressure, heart disease, or diabetes as an underlying condition. Other conditions that may increase the risk of RAO include high cholesterol and glaucoma. Incidence is slightly more common in men and in people age 60 or older.

Diagnosis

RAO is diagnosed by examination of the retina with an ophtalmoscope.

Treatment

Central retinal artery occlusion (CRAO) is an emergency. If treatment begins within an hour, the patient has the highest possibility of regaining vision in the affected eye, although complete restoration is unlikely.

A common treatment is inhalation of carbon dioxide so as to dilate the retinal vessels and move the occlusion from the central retinal artery to a branch artery. This movement reduces the area of the retina affected and may restore a certain amount of vision. Eyeball massage may also be performed, also in an effort to remove the occlusion. The physician may also consider puncturing the eyeball.

Drug therapy includes the use of carbonic anhydrase inhibitors to reduce the internal eye pressure and enhance movement of the occlusion. Both of the treatments would be used within the first 24 hours of noticeable vision loss.

Alternative treatment

Hyperbaric oxygen therapy may be beneficial if started within 90 minutes of the onset of symptoms. Some studies indicate a 40% improvement of visual acuity using this method.

Prognosis

The prognosis for central retinal visual acuity is poor with only about one-third of patients recovering useful vision. The longest delay in getting treatment that has been associated with significant visual recovery was approximately 72 hours.

Branch retinal artery occlusions (BRAO) have a recovery rate of 80% where vision is restored to 20/40 or better.

Prevention

Individuals affected by underlying conditions such as high blood pressure, heart disease, diabetes, glaucoma, and elevated cholesterol should treat their conditions appropriately to minimize the possibility of a retinal artery occlusion.

Resources

ORGANIZATIONS

American Academy of Ophthalmology. P.O. Box 7424, San Francisco, CA 94120-7424. (415) 561-8500. Fax: (415) 561-8533. http://www.eyenet.org/.

American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) DIABETES. http://www.diabetes.org/.

American Heart Association National Center. 7272 Greenville Avenue, Dallas, Texas 75231. (877) 242-4277. http://www.americanheart.org/.

CliniWeb International. http://www.ohsu.edu/cliniweb/C11/C11.768.html.

KEY TERMS

Angiospasm Spasmodic contraction of a blood vessel with increase in blood pressure.

Arterioles Small blood vessels that carry arterial (oxygenated) blood.

Atherosclerotic disease The progressive narrowing and hardening of the arteries over time.

Central retinal artery A branch of the ophthalmic artery that supplies blood to the retina and branches to form the arterioles of the retina.

Embolism The sudden obstruction of a blood vessel by a blood clot.

Endarteritis Chronic inflammation of the inner layer of arteries.

Hyperbaric oxygenation Administration of oxygen in a compression chamber at an ambient pressure greater than 1 atmosphere, in order to increase the amount of oxygen in organs and tissues.

Occlusion Momentary complete closure of some area or channel of the body.

Ophthalmic artery The artery supplying the eye and adjacent structures with blood.

Ophthalmoscope An instrument used for viewing the inside of the eye that consists of a concave mirror with a hole in the middle through which the physician examines the eye, and a light source that is reflected into the eye by the mirror.

Retina Light sensitive layer of the eye, that consists of four major layers: the outer neural layer, containing nerve cells and blood vessels, the photoreceptor layer, a single layer that contains the light sensing rods and cones, the pigmented retinal epithelium (PRE) and the choroid, consisting of connective tissue and capillaries.

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Retinal Vein Occlusion

Retinal Vein Occlusion

Definition

Retinal vein occlusion refers to the closure of the central retinal vein that drains the retina or to that of one of its branches.

Description

Retinal vein occlusion (RVO) occurs when the central retinal vein, the blood vessel that drains the retina, or one of its branches becomes blocked. RVO may be categorized by the anatomy of the occluded vein and the degree of ischemia produced. The two major RVO types are central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). CRVO has been diagnosed in patients as young as nine months to patients of 90 years. The age of affected individuals is usually low to mid 60s. Approximately 90% of patients are over 50 at the time of diagnosis, with 57% of them being male and 43% being female. BRVO accounts for some 30% of all vein occlusions.

Causes and symptoms

CRVO is a painless loss of vision that can be caused by a swollen optic disk, the small area in the retina where the optic nerve enters the eye, by dilated retinal veins, and by retinal hemorrhages. CRVO is also called venous stasis retinopathy, or hemorrhagic retinopathy.

In BRVO, the superotemporal branch vein is the most often affected vessel. Retinal hemorrhages follows, often occurring at the crossing of two vessels near the optic disk. Initially the hemorrhage may be extensive and underlie the fovea.

The exact cause of RVO is not yet identified, but the following mechanisms been proposed:

  • external compression between the central connective strand and the cribriform plate
  • venous disease
  • blood clot formation

Conditions associated with RVO risk include:

  • hypertension
  • hyperlipidemia
  • diabetes mellitus
  • hyperviscosity
  • hypercoagulability
  • glaucoma
  • trauma

Diagnosis

A complete physical evaluation is recommended for CRVO and BRVO, including complete blood tests, and glucose tolerance test (for non-diabetics). In the case of a head injury when bleeding around the optic nerve is a possibility, an MRI may be performed.

Treatment

Following a patient with RVO is vital. Patients should be seen at least monthly for the first three months to monitor for signs of other complications, such as the abnormal formation of blood vessels (neovascularization) in the iris of the eye or glaucoma.

The treatment for retinal vein occlusion varies for each case and should be given based on the doctor's best recommendation. Although treatments for occlusion itself are limited, surgical treatment of the occlusion provides an option.

Treatments may include anticoagulants with heparin, bishydroxycoumarin, and streptokinase. When the blood is highly viscous, dilution of the blood may be useful. Ideally, an alternate pathway is needed to allow venous drainage. Recent reports published in 1999 suggest that use of a laser to create a retinal choroidal hole may be useful to treat CRVO. Laser therapy depends on the type of occlusion. The management of laser therapy should be controlled by an ophthalmologist.

Alternative treatment

There are no documented alternative treatment methods.

Prognosis

The outlook for people with RVO is fairly good whether it is treated early or not. With no treatment at all, approximately 60% of all patients recover 20/40 vision or better within a year.

KEY TERMS

Anticoagultants Drugs that act by lowering the capacity of the blood to coagulate, thus facilitating removal of blood clots.

Central retinal vein Central blood vessel and its branches that drains the retina.

Cribriform plate The horizontal bone plate perforated with several holes for the passage of olfactory nerve filaments from the nasal cavity.

Fovea A small area of the retina responsible for acute vision.

Glaucoma A group of eye diseases characterized by an increase in eyeball pressure.

Hyperlipidemia A general term for elevated concentrations of any or all of the lipids in the plasma.

Iris The contractile diaphragm located in the fluid in front of the lens of the eye and is perforated by the eye pupil.

Ischemia A state of low oxygen in a tissue usually due to organ dysfunction.

Neovascularization Abnormal or excessive formation of blood vessels as in some retinal disorders.

Occlusion Momentary complete closure of some area or channel of the body.

Optic disk The small area in the retina where the optic nerve enters the eye that is not sensitive to light. Also called the blind spot.

Retina Light sensitive layer of the eye, that consists of four major layers: the outer neural layer, containing nerve cells and blood vessels, the photoreceptor layer, a single layer that contains the light sensing rods and cones, the pigmented retinal epithelium (PRE) and the choroid, consisting of connective tissue and capillaries.

Prevention

Retinal vein occlusion is difficult to prevent because the exact cause is still uncertain. Ethnic factors may play a role since in the UK the disease is rare in Asians and West Indians.

Resources

BOOKS

Spaide, Richard F., MD. Diseases of the Retina and Vitreous. New York: W.B. Saunders Co., 1999.

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retinal artery occlusion

retinal artery occlusion n. blockage of an artery supplying blood to the retina, usually as a result of thrombosis or embolism. branch r. a. o. blockage of one of the branches of the central retinal artery, which results in visual field loss in the area of the retina supplied by the occluded vessel. central r. a. o. blockage of the central retinal artery, which enters the eye at the optic disc, usually resulting in sudden painless loss of vision.

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retinal vein occlusion

retinal vein occlusion n. blockage of a vein carrying blood from the retina. branch r. v. o. blockage of one of the small branches of the central retinal vein, resulting in painless reduction of vision in the affected area. central r. v. o. blockage of the central retinal vein, which leaves the eye at the optic disc, usually resulting in sudden painless reduction of vision.

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Retinopathies

Retinopathies

Definition

The retinopathies are a group of retinal diseases that cause vascular and neurological changes in the retina of the eye. They are reflective of ongoing systemic diseases, such as diabetes, arteriosclerosis, hypertension, and sickle cell anemia.

Description

The retina is an outward extension of the central nervous system that lines the inside of the eye. It has 10 layers and is comprised of the photoreceptor rods and cones and support cells, such as Mueller cells. The retinal pigment epithelium (RPE) is a single cell layer located behind the retina, which services the photoreceptors. Bruch's membrane is a basement membrane found between the RPE and the choriod, a highly vascular layer that includes the choriocapillaris, which supplies nutrients to the RPE and to the photoreceptors. The central retinal artery and its branches supply blood to the rest of the retina. The cilio-retinal artery that emerges from the optic nerve supplies the macula. The macula is located temporal to the optic nerve and is the part of the retina that contains the highest concentration of photoreceptors, especially cones. The part of the macula with the highest concentration of cones is the fovea. The vitreous humor is a gelatinous body that is located between the retina and the lens of the eye. The optic nerve is a large nerve in the posterior part of the eye through which the central artery and vein pass. It is actually formed from the axons of cells in the retina. It is through the optic nerve that visual stimuli leave the eye for the occipital lobe of the brain, where vision is processed. Hemoglobin is a molecule in red blood cells responsible for the transport of oxygen.

The presentation and pathogenesis of each of these retinal diseases are unique; and the signs can be seen by an ophthalmologist or an optometrist on dilation of the eye. All of these retinopathies can lead to blindness.

Causes and symptoms

Diabetic retinopathy

Diabetic retinopathy is the leading cause of blindness in the United States for people between 20 and 74 years of age. Risk factors for diabetic retinopathy include hypertension, elevated HgA1C (a hemoglobin test ), a history of smoking, and number of years as a diabetic. Within 10 years of diagnosis, over 70% of type I diabetics will have some retinopathy, and within 16 years of diagnosis, 60% of type II diabetics will have retinopathy. A diabetic may have normal vision, yet still have severe retinopathy.

The underlying pathogenesis of diabetic retinopathy is hypoxia, a decreased oxygen supply that is caused by elevated blood sugar or hyperglycemia. Glucose is needed in the cells of the body for energy, and oxygen and insulin are required for entry of the glucose molecules. The diabetic, because of insufficient insulin or because of cellular resistance to insulin, cannot absorb glucose into the cell effectively. The pathologic response of the retina to a decreased oxygen supply is first a thickening of, and then a break-down of the retinal capillary basement membrane. Pericytes, cells that surround the capillaries and produce an inhibitor for angiogenesis, also degenerate. In the absence of this inhibitor, retinal neovascularization, or new vessel formation, is stimulated by vascular endothelial growth factor (VEGF). The new vessels that form are very fragile and can easily rupture, causing bleeding in the vitreous and subsequently leading to vitreous traction. Degeneration of retinal neural cells precedes the vascular changes of diabetic retinopathy.

Diabetic retinopathy is a condition that initially affects only the posterior pole of the retina. The peripheral retina is affected only in the extreme cases. Diabetic retinopathy is divided into two phases: nonproliferative and proliferative. In the nonproliferative phase the retina has microaneurysms, dot and blot hemorrhages, hard lipid exudates, a beading pattern of some of the venules, areas of local ischemia where there is little or no oxygen perfusion (called cotton-wool spots), or macular edema. The macular edema is called clinically significant macula (CSME) when there are hard exudates and macular thickening or edema, close to the fovea. In the proliferative phase of diabetic retinopathy, neovascularization of the retina and of the optic nerve can be observed. A fibrous substance that materializes when the new retinal vessels form adheres to the vitreous, causing retinal traction and retinal detachments. The newly formed blood vessels can invade the anterior part of the eye, causing neovascular glaucoma. Vitreous hemorrhaging occurs when the blood vessels attach to the vitreous. Venous and arterial occlusions are also seen in diabetic retinopathy.

Arteriosclerotic retinopathy

Arteriosclerotic retinopathy is the ocular manifestation of arteriosclerosis, a systemic condition in which the arterial walls thicken and harden. The risk factors for arteriosclerotic retinopathy include heart disease and elevated serum cholesterol. Arteriosclerotic retinopathy can be involved in hypertensive retinopathy. One of the first ophthalmoscopic signs of arterio-sclerotic retinopathy is an increased arterial reflex due to thickening of the retinal arterial walls. As the arteriosclerosis progresses, the vessels undergo color changes to a copper-wire and then to a silver-wire appearance. Arteriovenous or A-V crossing defects are also synonymous with arteriosclerotic retinopathy. In advanced arteriosclerosis, banking—a type of A-V crossing that completely cuts off distal venous circulation, forming a large dilated vein—occurs.

Arterial occlusion can occur as a result of arterio-sclerotic retinopathy. An embolus from the carotid artery or from the aortic arch of the heart can travel to the retina, occluding either the central retinal artery (CRAO) or one of its branches (BRAO). An embolus from the carotid artery usually is a cholesterol plaque; and that from the heart is usually fibrotic in appearance. Immediately after a CRAO, the retina becomes ischemic and then edematous. Due to the surrounding ischemia, the fovea takes on a characteristic cherry-red appearance. A pupil abnormality, called an afferent pupillary defect (APD), may be noted. The vision loss in a CRAO is severe, sudden, and painless, although the patient may have a history of amaurosis fugax. After resolution of the CRAO the retina takes on a normal appearance, but the retinal blood vessels are narrowed and the optic nerve shows pallor. Macular function will be intact if there is cilioretinal circulation. Patients with a BRAO may be asymptomatic if there is no macular involvement, but usually there is field loss in the affected quadrant as well as decreased visual acuity.

Hypertensive retinopathy

Hypertensive retinopathy is an ocular presentation of the effects of systemic hypertension, defined as systolic pressure over 140 mm/Hg and diastolic pressure over 90 mm/Hg. This type of retinopathy is usually bilateral. There is narrowing of retinal arterioles in systemic hypertension. Constriction of vessels in older hypertensive patients may not be observed because of involutional sclerosis of the arteries, which occurs during aging. When the integrity of the retinal vessels is compromised because of long-term hypertension, leakage of blood occurs, and flame-shaped hemorrhages that are characteristic of hypertensive retinopathy can be observed in the retina. Also, a star-shaped pattern of exudation appears in the macula. In the advanced stages of hypertensive retinopathy there will be cotton wool spots close to the optic nerve. In malignant hypertension the optic nerve will become swollen and the patient will often experience blurred vision, and, if the blood pressure is extremely elevated, encephalopathy can develop.

Retinal vein occlusions

Retinal vein occlusions block the drainage of the retina. They can be either central (CRVO) or branched (BRVO). They are usually seen in older patients who have arteriosclerosis, hypertension or diabetes. Vein occlusions can also strike patients with sickle-cell anemia. Papillophlebitis is a form of retinal vein occlusion that is inflammatory in nature and seen in younger patients. A hemi-central vein occlusion is similar to a CRVO, but affects only one-half of the retina. A CRVO occurs when the central retinal artery compresses the central vein as it leaves the lamina cribosa. A BRVO occurs when there is constriction of a venule by a sclerotic artery that affects only one quadrant, usually the superior temporal one.

A CRVO can be either ischemic (characterized by decreased blood flow) or nonischemic. Approximately 80% of CRVO events are nonischemic. In the non-ischemic CRVO, hemorrhages are evident throughout the retina, but usually there are no cotton-wool spots. The optic nerve swelling is usually mild and macular edema is not always present. The visual acuity may be only mildly reduced. Months after such an occlusion, collateral blood vessels may appear on the optic nerve. Up to 20% of individuals with a nonischemic CRVO may progress to an ischemic event. The hallmark of ischemic CRVO is extensive capillary nonperfusion. Ophthalmoscopic examination following an ischemic event reveals extensive venous tortuosity and enlargement of the retinal veins. Edema of the macula and optic nerve are always present and cotton wool spots are common. Visual acuity is usually less than 20/200. Neovascularization of the iris and neovascular glaucoma are common complications of CRVO. There can be optic nerve neovascularization, bleeding into the vitreous, and vitreal traction, which increases the risk of a retinal detachment. The signs of a BRAO are similar, but present in just one quadrant.

Sickle-cell retinopathy

The underlying cause of sickle-cell retinopathy is different from that of the other retinopathies. Sickle-cell anemia is a genetically inherited condition seen primarily in persons of African descent. Close to 10% of African Americans carry one of the sickle-cell traits. Sickle-cell anemia is caused by mutant hemoglobin molecules that form either because of an amino acid substitution of valine for glutamic acid, causing a structural defect in the hemoglobin molecule, or because of a deficiency in the synthesis of one of the hemoglobin peptide chains. A normal red blood cell has a biconcave appearance and can easily pass through the capillary bed. A "sickle" cell does not have this biconcave shape, is less pliable than a normal red blood cell, and thus does not move well through the capillaries, triggering retinal microvascular occlusions and then ischemia.

Sickle-cell retinopathy can be nonproliferative or proliferative and affects primarily the peripheral retina. In the nonproliferative stage, the retinal vessel walls begin to deteriorate. The ophthalmoscopic signs of nonproliferative sickle-cell retinopathy include: venous tortuosity; intraretinal "salmon patch" hemorrhages, found near a vessel occlusion; "black sunburst" lesions, that develop when a vascular occlusion damages the RPE; silver-wired arterioles; and breaks in Bruch's membrane, called angioid streaks. Sickle-cell retinopathy becomes proliferative when neovascularization, in the form of arteriovenous anastomoses or connections between veins and arteries, appears in a sea-shaped formation. These vessels can adhere to the vitreous, but usually regress, forming a characteristic white tuft. Vitreous traction and retinal detachments are not common in sickle-cell retinopathy.

Diagnosis

The ophthalmologist or optometrist uses fluorescein angiography to determine the extent of vessel leakage and perfusion in the retinopathies. The fluorescein dye is injected into the body through a vein in the hand. Rarely does a patient have a reaction to the dye, but a localized redness at the injection site is occasionally observed. The fluorescein molecule binds to proteins in the blood and it excited by light of 490 nanometers (blue light). A retinal camera filters the light, such that only blue light enters the eye. Photos taken in rapid succession reveal the extent of perfusion, leakage, and ischemia in the retina. The results of this angiography help the doctor to determine if laser photocoagulation can benefit the patient.

Treatment

In laser treatment of retinopathy, the light energy of the laser is absorbed by certain cells in the retina, destroying them and thus reducing the oxygen demand of the area, while leaving the surrounding tissue intact. Pan-retinal photocoagulation (PRP) treats neovascularization following a BRAO or hemi-retinal arterial occlusion and the neovascularization of the optic nerve in diabetic retinopathy. The macular edema of arterial occlusions and diabetic retinopathy is treated by focal argon photocoagulation. Laser surgery is not performed close to the fovea. Often the edema that develops during an arterial occlusion will dissipate without treatment. Laser treatment is not usually beneficial in CRAO. Peripheral scatter photocoagulation treats the neovascularization of sickle-cell retinopathy.

The vitreous hemorrhaging of diabetes and sickle-cell retinopathy may require either a vitrectomy, which is a surgical removal of part or all of the vitreous, or cryopexy, the use of low-temperature probes to kill the blood vessels. Vitrectomy has been especially beneficial in restoring vision in diabetic patients in whom retinopathy has already affected visual acuity.

There is little that can be done to treat a CRAO. Massage of the globe to dislodge the embolus, the use of carbogen to increase blood carbon dioxide levels, and anterior chamber paracentesis have all been employed with limited success. Hyperbaric oxygen therapy has been successful in treatment of CRAO in one study.

In treatment of the patient with malignant hypertension it is important to slowly lower the blood pressure in order to reduce the risk of ischemic optic neuropathy.

The intraocular pressure must be lowered in the patient with a CRAO.

Nonmedical treatments may include changes in diet and exercise regimens.

Prognosis

Except when vitrectomy is performed (when indicated), and once the retinopathies have had an effect on vision, there is little that can be done to restore it. The goal of many of the treatments is to prevent further damage. If the proliferative phases of these retinopathies are treated early enough, normal vision is possible. The prognosis for patients with nonproliferative retinopathy is better than for patients with proliferative disease.

Health care team roles

The role of the allied health professional in diagnosis and treatment of retinopathy is to assist the ophthalmologist or optometrist in diagnosis. Ophthalmic technicians or nurses may instill the drops for dilation of the eye, inject the fluorescein dye used in angiography. The ophthalmic technician or a retinal photographer takes the photos needed for analysis of retinopathy. Dieticians assist diabetics, hypertensives, and those with heart disease.

Prevention

The first line in prevention of the retinopathies is an annual dilated eye exam performed by an ophthalmologist or an optometrist. Patients with systemic disease that can cause retinopathy must understand the ocular complications of their disease and the consequences if medical therapy is not followed as recommended by a physician.

Depending on the type of retinopathy, other preventive measures need to be taken. All patients with retinal emboli need a cardiac workup, including analysis of blood lipid levels. This is the case even in the absence of an occlusion. Older patients need testing for temporal arteritis once CRAO is detected. Over 65% of patients with temporal arteritis will have a CRAO in the fellow eye within days of the initial event. Since 70% of patients with BRAO have hypertension, all patients with such occlusions need to be evaluated for hypertension. Since sickle-cell anemia can cause a BRVO, African Americans need a Sickledex test. In the event of unilateral hypertensive retinopathy, a carotid artery obstruction should be suspected and a carotid workup is imperative. Finally, the best prevention of the retinopathies is management of the underlying systemic diseases.

KEY TERMS

Exudation— Leakage of cells, proteins, and fluids through the blood vessel wall into the surrounding tissue.

Ischemia— Lack of blood supply to a tissue or organ.

Neovascularization— Formation of new blood vessels.

Proliferative retinopathy— Retinopathy with neovascularization.

Resources

BOOKS

Muchnick, Bruce G. Clinical Medicine in Optometric Practice. St. Louis: Mosby-Yearbook, 1994.

Spalton, Roger J., et al. Atlas of Clinical Ophthalmology, 2nd ed. Wolfe Publishing, 1994.

PERIODICALS

Alexander, Larry J. "The Essentials of Managing Ocular Diabetes." Review of Optometry (Sept. 15, 1998): 108-123.

Arrigg, Paul G., and Jerry Cavallerano. "The Role of Vitrectomy for Diabetic Retinopathy." Journal of the American Optometric Association (Nov. 1998): 733-40.

Beaser, Richard S. "Managing Diabetes: Current Strategies." Journal of the American Optometric Association (Nov. 1998): 711-25

Brown, Gary. "Be Ready When Vascular Occlusion Strikes." Review of Ophthalmology (March 1998): 107-109.

Dunbar, Mark T. "What's New in Retinal Disease." Review of Optometry (May 15, 2001): 77-83.

Eisenberg, Jeffery S. "Raising Hopes of Preventing Diabetic Blindness." Review of Optometry 96-104.

Gurwood, Andrew S., et al. "Understanding Angioid Streaks." Journal of the American Optometric Association (May 1997): 309-324.

Marshall, Edwin C. "Hypertension and the Eye: Applications of the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure." Journal of the American Optometric Association (May 1998): 281-291.

Sowka, Joseph W., and Allan G. Kabat. "What the Eye Reveals About Vascular Disease." Review of Optometry (Feb. 15, 1998): 90-98.

Stokkermans, Thomas J. W. "Inside Hypertension: The Causes and Consequences of High Blood Pressure." Review of Optometry (Jan. 15, 1999): 78-99.

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