Eyes Disorder

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Retinitis Pigmentosa Retinitis pigmentosa (RP) is a group of genetic eye conditions. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their life. Others go completely blind from RP, in some cases as early as childhood. Progression of RP is different in each case. RP is a type of hereditary retinal dystrophy, a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by reduction of the peripheral visual field (known as tunnel vision) and, sometimes, loss of central vision late in the course of the disease.

Normal vision. Courtesy NIH National Eye Institute

Signs Mottling of the retinal pigment epithelium with black bone-spicule pigmentation is typically indicative (or pathognomonic) of retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuation (thinning) of the retinal vessels, cellophane maculopathy, cystic macular edema and posterior subcapsular cataract.

The same view with tunnel vision from retinitis pigmentosa. The blackness surrounding the central image does not indicate darkness, but rather a lack of perceived visual information.

Diagnosis The diagnosis of retinitis pigmentosa relies upon documentation of progressive loss in photoreceptor function by electroretinography (ERG) and visual field testing. The mode of inheritance of RP is determined by family history. At least 35 different genes or loci are known to cause "nonsyndromic RP" (RP that is not the result of another disease or part of a wider syndrome).

Treatment There is currently no medical treatment that can completely cure retinitis pigmentosa, although the progression of the disease can be reduced by the daily intake of 15000 IU of vitamin A palmitate.[12] Recent studies have shown that proper vitamin A supplementation can postpone blindness by up to 10 years. Scientists continue to investigate possible treatments. Future treatments may involve retinal transplants, artificial retinal implants, gene therapy, stem cells, nutritional supplements, and/or drug therapies. Scientists at the Osaka Bioscience Institute have identified a protein, named Pikachurin, which they believe could lead to a treatment for retinitis pigmentosa.[15][16]

Amblyopia Amblyopia, otherwise known as lazy eye,[1] is a disorder of the visual system that is characterized by poor or indistinct vision in an eye that is otherwise physically normal, or out of proportion to associated structural abnormalities. It has been estimated to affect 1– 5% of the population.[2] The problem is caused by either no transmission or poor transmission of the visual image to the brain for a sustained period of dysfunction or during early childhood. Amblyopia normally only affects one eye, but it is possible to be amblyopic in both eyes if both are similarly deprived of a good, clear visual image. Detecting the condition in early childhood increases the chance of successful treatment. While the colloquialism "lazy eye" is frequently used to refer to amblyopia, the term is inaccurate because there is no "laziness" of either the eye or the amblyope involved in the condition. This term is imprecise because "lazy eye" is also a layman's term for strabismus, particularly exotropia

Symptoms Many people with amblyopia, especially those who are only mildly so, are not even aware they have the condition until tested at older ages, since the vision in their stronger eye is normal. However, people who have severe amblyopia may experience associated visual disorders, most notably poor depth perception. Amblyopes may suffer from poor spatial acuity, low sensitivity to contrast and some "higher-level" deficits to vision such as reduced sensitivity to motion.[5] These deficits are usually specific to the amblyopic eye. Amblyopes also suffer from problems of binocular vision such as limited stereoscopic depth perception and usually have difficulty seeing the three-dimensional images in hidden stereoscopic displays such as autostereograms.[6] However perception of depth from monocular cues such as size, perspective, and motion parallax is normal.

Types Amblyopia can be caused by deprivation of vision early in life by vision-obstructing disorders such as congenital cataracts, by strabismus (misaligned eyes), or by anisometropia (different degrees of myopia or hyperopia in each eye). Ambylopia can also occur physiologically after tobacco or alcohol consumption.

Strabismic amblyopia Strabismus, sometimes erroneously also called lazy eye, is a condition in which the eyes are misaligned. Strabismus usually results in normal vision in the preferred sighting (or "fellow") eye, but may cause abnormal vision in the deviating or strabismic A child wearing an adhesive eye due to the discrepancy between the images [7] projecting to the brain from the two eyes. Adult-onset eyepatch to correct amblyopia strabismus usually causes double vision (diplopia), since the two eyes are not fixated on the same object. Children's brains, however, are more neuroplastic, and therefore can more easily adapt by suppressing images from one of the eyes, eliminating the double vision. This plastic response of the brain, however, interrupts the brain's normal development, resulting in the amblyopia. Strabismic amblyopia is treated by clarifying the visual image with glasses,

and/or encouraging use of the amblyopic eye with an eyepatch over the dominant eye or pharmacologic penalization of it. Penalization usually consists of applying atropine drops to temporarily dilate the pupil, which leads to blurring of vision in the good eye. This helps to prevent the bullying and teasing associated with wearing a patch, although application of the eyedrops is more challenging. The ocular alignment itself may be treated with surgical or non-surgical methods, depending on the type and severity of the strabismus.[8]

Refractive or anisometropic amblyopia Refractive amblyopia may result from anisometropia (unequal refractive error between the two eyes). Anisometropia exists when there is a difference in the refraction between the two eyes. The eye which provides the brain with a clearer image (closer to 20/20) typically becomes the dominant eye. The image in the other eye is blurred, which results in abnormal development of one half of the visual system. Refractive amblyopia is usually less severe than strabismic amblyopia and is commonly missed by primary care physicians because of its less dramatic appearance and lack of obvious physical manifestation, such as with strabismus.[9] Frequently, amblyopia is associated with a combination of anisometropia and strabismus. Pure refractive amblyopia is treated by correcting the refractive error early with prescription lenses and patching or penalizing the good eye. Meridional amblyopia is a mild condition in which lines are seen less clearly at some orientations than others after full refractive correction. An individual who had an astigmatism at a young age that was not corrected by glasses will later have astigmatism that cannot be optically corrected

Form-deprivation and occlusion amblyopia Form-deprivation amblyopia (Amblyopia ex anopsia) results when the ocular media become opaque, such as is the case with cataracts or corneal scarring from forceps injuries during birth.[10] These opacities prevent adequate visual input from reaching the eye, and therefore disrupt development. If not treated in a timely fashion, amblyopia may persist even after the cause of the opacity is removed. Sometimes, drooping of the eyelid (ptosis) A man with minor amblyopia or some other problem causes the upper eyelid to physically occlude a child's vision, which may cause amblyopia quickly. Occlusion amblyopia may be a complication of a hemangioma that blocks some or all of the eye.

Treatments Treatment of strabismic or anisometropic amblyopia consists of correcting the optical deficit and forcing use of the amblyopic eye, either by patching the good eye, or by instilling topical atropine in the eye with better vision. One should also be wary of over-patching or over-penalizing the good eye when treating for amblyopia, as this can create so-called "reverse amblyopia" in the other eye.[8][11] Form deprivation amblyopia is treated by removing the opacity as soon as possible followed by patching or penalizing the good eye to encourage use of the amblyopic eye.[

Macular Degeneration Macular degeneration is a medical condition usually of older adults which results in a loss of vision in the center of the visual field (the macula) because of damage to the retina. It occurs in “dry” and “wet” forms. It is a major cause of blindness in the elderly (>50 years)[citation needed]. Macular degeneration can make it difficult or impossible to read or recognize faces, although enough peripheral vision remains to allow other activities of daily life. The inner layer of the eye is the retina, which contains nerves that communicate sight, and behind the retina is the choroid, which contains the blood supply to the retina. In the dry (nonexudative) form, cellular debris called drusen accumulate between the retina and the choroid, and the retina can become detached. In the wet (exudative) form, which is more severe, blood vessels grow up from the choroid behind the retina, and the retina can also become detached. It can be treated with laser coagulation, and with medication that stops and sometimes reverses the growth of blood vessels.[1][2] Although some macular dystrophies affecting younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration).

Normal vision (B&W). Courtesy NIH National Eye Institute

The same view with age-related macular degeneration (B&W).

Risk factors •









Aging: Approximately 10% of patients 66 to 74 years of age will have findings of macular degeneration. The prevalence increases to 30% in patients 75 to 85 years of age.[4] Family history: The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration, versus 12% for people who do not have relatives with macular degeneration, a fourfold higher risk.[ Macular degeneration gene: The genes for the complement system proteins factor H (CFH) and factor B (CFB) and factor 3 (C3) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the inflammatory response mediated via C3b (and the Alternative Pathway of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the activecomplex that forms between C3b and factor B. C-reactive protein and polyanionic surface markers such as glycosaminoglycans normally enhance the ability of factor H to inhibit complement Mutation of the ATP synthase gene: Retinitis Pigmentosa (RP) is a genetically linked dysfunction of the retina and is related to mutation of the Adenosine TriPhosphate (ATP) Synthase Gene 615.1617 Hypertension: Also known as high blood pressure.

• •

Cardiovascular status — high cholesterol, obesity. Race Macular degeneration is more likely to be found in Caucasians than in people of African descent.[13][14] Exposure to sunlight especially blue light. There is conflicting evidence as to whether exposure to sunlight contributes to the development of macular degeneration

Signs • • • • •

Drusen Pigmentary alterations Exudative changes: hemorrhages in the eye, hard exudates, subretinal/subRPE/intraretinal fluid Atrophy: incipient and geographic Visual acuity drastically decreasing ((two levels or more) ex: 20/20 to 20/80)

Symptoms •

• •

• • •

Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss. Central scotomas (shadows or missing areas of vision) Distorted vision (i.e. metamorphopsia) - A grid of straight lines appears wavy and parts of the grid may appear blank. Patients often first notice this when looking at mini-blinds in their home. Trouble discerning colors; specifically dark ones from dark ones and light ones from light ones. Slow recovery of visual function after exposure to bright light A loss in contrast sensitivity.

Diagnosis Fluorescein angiography allows for the identification and localization of abnormal vascular processes. Optical coherence tomography is now used by most ophthalmologists in the diagnosis and the followup evaluation of the response to treatment by using either Avastin or Lucentis which are injected into the vitreous of the eye at various intervals.

Prevention The Age-Related Eye Disease Study showed that a combination of high-dose betacarotene, vitamin C, vitamin E, and zinc can reduce the risk of progressing from early to advanced AMD by about 25 percent.[21] A followup study, Age-Related Eye Disease Study 2, to study the potential benefits of lutein, zeaxanthine, and fish oil, is underway.[22] Studies are underway at Harvard, with the goal of reducing lipofuscin accumulation. [12] In 2007, a study at the National Eye Institute, Maryland found that Lutein and zeaxanthin (nutrients in eggs and green vegetables) protect against macular degeneration. [23] Studies found that antioxidants disrupt the link of two processes that cause macular degeneration and extend the lifetime of irreplaceable photoreceptors and other retinal cells

Cataract A cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in degree from slight to complete opacity and obstructing the passage of light. Early in the development of age-related cataract the power of the lens may be increased, causing near-sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially blinding if untreated. The condition usually affects both the eyes, but almost always one eye is affected earlier than the other.[1] A senile cataract, occurring in the aged, is characterized by an initial opacity in the lens, subsequent swelling of the lens and final shrinkage with complete loss of transparency.[2] Moreover, with time the cataract cortex liquefies to form a milky white fluid in a Morgagnian cataract, which can cause severe inflammation if the lens capsule ruptures and leaks. Untreated, the cataract can cause phacomorphic glaucoma. Very advanced cataracts with weak zonules are liable to dislocation anteriorly or posteriorly. Such spontaneous posterior dislocations (akin to the historical surgical procedure of couching) in ancient times were regarded as a blessing from the heavens, because some perception of light was restored in the cataractous patients. Cataract derives from the Latin cataracta meaning "waterfall" and the Greek kataraktes and katarrhaktes, from katarassein meaning "to dash down" (kata-, "down"; arassein, "to strike, dash"[3]). As rapidly running water turns white, the term may later have been used metaphorically to describe the similar appearance of mature ocular opacities. In Latin, cataracta had the alternate meaning "portcullis",[4] so it is also possible that the name came about through the sense of "obstruction". Early Persian physicians called the term nazul-i-ah, or 'descent of the water' - vulgarised into waterfall disease or cataract believing such blindness to be caused by an outpouring of corrupt humour into the eye.[5] In dialect English a cataract is called a pearl, as in "pearl eye" and "pearl-eyed"

Causes Cataracts develop from a variety of reasons, including long-term exposure to ultraviolet light, exposure to radiation, secondary effects of diseases such as diabetes, hypertension and advanced age, or trauma (possibly much earlier); they are usually a result of denaturation of lens protein. Genetic factors are often a cause of congenital cataracts and positive family history may also play a role in predisposing someone to cataracts at an earlier age, a phenomenon of "anticipation" in pre-senile cataracts. Cataracts may also be produced by eye injury or physical trauma. A study among Icelandair pilots showed commercial airline pilots are three times more likely to develop cataracts than people with non-flying jobs. This is thought to be caused by excessive exposure to radiation coming from outer space.[7] Cataracts are also unusually common in persons exposed to infrared radiation, such as glassblowers who suffer from "exfoliation syndrome". Exposure to microwave radiation can cause cataracts. Atopic or allergic conditions are also known to quicken the progression of cataracts, especially in children.[8] Cataracts may be partial or complete, stationary or progressive, hard or soft. Some drugs can induce cataract development, such as corticosteroids[9] and Ezetimibeand Seroquel.

There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also classified by their location, e.g. posterior (classically due to steroid use) and anterior (common (senile) cataract related to aging).

Symptoms As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted. Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare can be a problem as light is scattered by the cataract into the eye. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is demonstrated an eye specialist consultation is recommended. In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon appears to be confined to one eye only.

Epidemiology Age-related cataract is responsible for 48% of world blindness, which represents about 18 million people, according to the World Health Organization (WHO).[11] In many countries surgical services are inadequate, and cataracts remain the leading cause of blindness. As populations age, the number of people with cataracts is growing. Cataracts are also an important cause of low vision in both developed and developing countries. Even where surgical services are available, low vision associated with cataracts may still be prevalent, as a result of long waits for operations and barriers to surgical uptake, such as cost, lack of information and transportation problems. In the United States, age-related lenticular changes have been reported in 42% of those between the ages of 52 to 64,[12] 60% of those between the ages 65 and 74,[13] and 91% of those between the ages of 75 and 85

Conjunctivitis Conjunctivitis (commonly called "pink eye" or "Madras eye"[1]) is an inflammation of the conjunctiva (the outermost layer of the eye and the inner surface of the eyelids), most commonly due to an allergic reaction or an infection (usually viral, but sometimes bacterial

Symptoms

An eye with viral conjunctivitis.

Redness (Hyperaemia), irritation (Chemosis) and watering (Epiphora) of the eyes are symptoms common to all forms of conjunctivitis. Acute allergic conjunctivitis is typically itchy, sometimes distressingly so, and often involves some lid swelling. Chronic allergy often causes just itch or irritation.

Eyes with conjunctivitis

Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, and/or a sore throat. Its symptoms include watery discharge and variable itch. The infection usually begins with one eye, but may spread easily to the other. Bacterial conjunctivitis due to the common pyogenic (pus-producing) bacteria causes marked grittiness/irritation and a stringy, opaque, grey or yellowish mucopurulent discharge (gowl, goop, "gunk", "eye crust", or other regional names, officially known as 'gound') that may cause the lids to stick together (matting), especially after sleeping. Another symptom that could be caused by bacterial conjunctivitis is severe crusting of the infected eye and the surrounding skin. However discharge is not essential to the diagnosis, contrary to popular belief. Bacteria such as Chlamydia trachomatis or Moraxella can cause a non-exudative but persistent conjunctivitis without much redness. The gritty and/or scratchy feeling is sometimes localised enough for patients to insist they must have a foreign body in the eye. The more acute pyogenic infections can be painful. Like viral conjunctivitis, it usually affects only one eye but may spread easily to the other eye. However, it is dormant in the eye for three days before the patient shows signs of symptoms. Irritant or toxic conjunctivitis is irritable or painful when the infected eye is pointed far down or far up. Discharge and itch are usually absent. This is the only group in which severe pain may occur. Inclusion conjunctivitis of the newborn (ICN) is a conjunctivitis that may be caused by the bacteria Chlamydia trachomatis, and may lead to acute, purulent conjunctivitis.[4] However, it is usually self-healing.[4]

Signs Injection (redness) of the conjunctiva on one or both eyes should be apparent, but may be quite mild. Except in obvious pyogenic or toxic/chemical conjunctivitis, a slit lamp (biomicroscope) is needed to have any confidence in the diagnosis. Examination of the tarsal conjunctiva is usually more diagnostic than the bulbar conjunctiva. Allergic conjunctivitis shows pale watery swelling or edema of the conjunctiva and sometimes the whole eyelid, often with a ropy, non-purulent mucoid discharge. There is variable redness. Viral conjunctivitis, commonly known as "pink eye", shows a fine diffuse pinkness of the conjunctiva which is easily mistaken for the 'ciliary injection' of iritis, but there are usually corroborative signs on bio microscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a punctate keratitis.

An eye red due to acute conjunctivitis.

An eye with bacterial conjunctivitis.

Pyogenic bacterial conjunctivitis shows an opaque purulent discharge, a very red eye, and on bio microscopy there are numerous white cells and desquamated epithelial cells seen in the 'tear gutter' along the lid margin. The tarsal conjunctiva is a velvety red and not particularly follicular. Non-pyogenic infections can show just mild infection and be difficult to diagnose. Scarring of the tarsal conjunctiva is occasionally seen in chronic infections, especially in trachoma. Irritant or toxic conjunctivitis show primarily marked redness. If due to splash injury, it is often present only in the lower conjunctival sac. With some chemicals—above all with caustic alkalis such as sodium hydroxide—there may be necrosis of the conjunctiva with a deceptively white eye due to vascular closure, followed by sloughing of the dead epithelium. This is likely to be associated with slit-lamp evidence of anterior uveitis.

Causes The leading cause of a red, inflamed eye is a bacterial infection. A number of different bacteria can be responsible for the infection. Bacterial symptoms are usually associated with more of a discharge that is green or yellow in color. Often, bacterial "cold-like" symptoms, such as sinus congestion and runny nose, are also present. The eyelids may be swollen. Sometimes looking at bright lights is painful. While bacterial conjunctivitis may not require an antibiotic, those affected should see a doctor, as occasionally this form of conjunctivitis can be associated with infection of the cornea (the clear portion of the front of the eyeball). This infection must be correctly detected and treated. Bacterial conjunctivitis is highly contagious and airborne, but usually resolves in seven to 10 days after symptoms appear.

Differential diagnosis Formally known as the Ian Wood Virus, Conjunctivitis symptoms and signs are relatively non-specific. Even after bio microscopy, laboratory tests are often necessary if proof of etiology is needed. A purulent discharge (a whitish-yellow, yellow or yellow-brown substance more commonly known as pus) strongly suggests bacterial cause, unless there is known exposure to toxins. Pink eye can also be caused by bacteria from feces, pet hair, or smoke or other fumes. Infection with Neisseria gonorrhoeae should be suspected if the discharge is particularly thick and copious. Itching (rubbing eyes) is the hallmark symptom of allergic conjunctivitis. Other symptoms include past history of eczema, or asthma. A diffuse, less "injected" conjunctivitis (looking pink rather than red) suggests a viral cause, especially if numerous follicles are present on the lower tarsal conjunctiva on bio microscopy. Scarring of the tarsal conjunctiva suggests trachoma, especially if seen in endemic areas, if the scarring is linear (von Arlt's line), or if there is also corneal vascularisation. Clinical tests for lagophthalmos, dry eye (Schirmer test) and unstable tear film may help distinguish the various types of pink eye. Other symptoms including pain, blurring of vision and photophobia should not be prominent in conjunctivitis. Fluctuating blurring is common, due to tearing and mucoid discharge. Mild photophobia is common. However, if any of these symptoms are prominent, it is important to exclude other diseases such as glaucoma, uveitis, keratitis and even meningitis or caroticocavernous fistula. Many people who have conjunctivitis have trouble opening their eyes in the morning because of the dried mucus on their eyelids. There is often excess mucus over the eye after sleeping for an extended period.

Treatment and management Conjunctivitis sometimes requires medical attention. The appropriate treatment depends on the cause of the problem. For the allergic type, cool water poured over the face with the head inclined downward constricts capillaries, and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, non-steroidal anti-inflammatory medications and antihistamines may be prescribed. Some patients with persistent allergic conjunctivitis may also require topical steroid drops.

Diabetic Retinopathy Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more[1]. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes

Signs and symptoms Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.

Normal vision. Courtesy NIH National Eye Institute

As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed The same view with diabetic retinopathy. (hemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours. These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs vision. In extreme cases, a person will only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep. On fundoscopic exam, a doctor will see cotton wool spots, flame hemorrhages, and dotblot hemorrhages.

Diagnosis Diabetic retinopathy is detected during an eye examination that includes: • •

Visual acuity test: This test uses an eye chart to measure how well a person sees at various distances (i.e., visual acuity). Pupil dilation: The eye care professional places drops into the eye to widen the pupil. This allows him or her to see more of the retina and look for signs of









diabetic retinopathy. After the examination, close-up vision may remain blurred for several hours. Ophthalmoscopy: This is an examination of the retina in which the eye care professional: (1) looks through a device with a special magnifying lens that provides a narrow view of the retina, or (2) wearing a headset with a bright light, looks through a special magnifying glass and gains a wide view of the retina. Note that hand-held ophthalmoscopy is insufficient to rule out significant and treatable diabetic retinopathy. Optical coherence tomography (OCT): This is an optical imaging modality based upon interference, and analogous to ultrasound. It produces cross-sectional images of the retina (B-scans) which can be used to measure the thickness of the retina and to resolve its major layers, allowing the observation of swelling and or leakage. Digital Retinal Screening Programs: Systematic programs for the early detection of eye disease including diabetic retinopathy are becoming more common, such as in the UK, where all people with diabetes mellitus are offered retinal screening at least annually. This involves digital image capture and transmission of the images to a digital reading center for evaluation and treatment referral. See Vanderbilt Ophthalmic Imaging Center [1] and the English National Screening Programme for Diabetic Retinopathy [2] Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs for the early detection of diabetic retinopathy using slit-lamp biomicroscopy. These exist either as a standalone scheme or as part of the Digital program (above) where the digital photograph was considered to lack enough clarity for detection and/or diagnosis of any retinal abnormality.

Treatments Laser photocoagulation Laser photocoagulation can be used in two scenarios for the treatment of diabetic retinopathy.It is widely used for early stages of proliferative retinopathy.

Panretinal photocoagulation Panretinal photocoagulation, or PRP (also called scatter laser treatment), is used to treat proliferative diabetic retinopathy (PDR).The goal is to create 1,000 - 2,000 burns in the retina with the hope of reducing the retina's oxygen demand, and hence the possibility of ischemia. In treating advanced diabetic retinopathy, the burns are used to destroy the abnormal blood vessels that form in the retina. This has been shown to reduce the risk of severe vision loss for eyes at risk by 50%.

Intravitreal Triamcinolone acetonide Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it results in a decrease in the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, along with an increase in the visual acuity. The effect of triamcinolone is transient, lasting up to three months, and necessitating repeated injections for maintaining the beneficial effect. Complications of intravitreal injection of triamcinolone include cataract, steroid induced glaucoma and endophthalmitis.

Vitrectomy Instead of laser surgery, some people need an eye operation called a vitrectomy to restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous. It involves removing the cloudy vitreous and replacing it with a saline solution.

Studies show that people who have a vitrectomy soon after a large hemorrhage are more likely to protect their vision than someone who waits to have the operation. Early vitrectomy is especially effective in people with insulin-dependent diabetes, who may be at greater risk of blindness from a hemorrhage into the eye. Vitrectomy is often done under local anesthesia. The doctor makes a tiny incision in the sclera, or white of the eye. Next, a small instrument is placed into the eye to remove the vitreous and insert the saline solution into the eye. Patients may be able to return home soon after the vitrectomy, or may be asked to stay in the hospital overnight. After the operation, the eye will be red and sensitive, and patients usually need to wear an eyepatch for a few days or weeks to protect the eye. Medicated eye drops are also prescribed to protect against infection.

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