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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 precedestunnel 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 progressivevisual loss. Affected individuals first experiencedefective 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.

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.

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]

 Normal vision. Courtesy  NIH  National

Eye Institute

The same view with tunnel vision fromretinitis pigmentosa. The blackness

surrounding the central image does not

indicate darkness, but rather a lack of 

 perceived visual information.

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AmblyopiaAmblyopia, 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 imageto 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 earlyin 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 aremisaligned. Strabismus usually results in normal vision

in the preferred sighting (or "fellow") eye, but may

cause abnormal vision in the deviating or strabismiceye due to the discrepancy between the images

 projecting to the brain from the two eyes.[7] Adult-onset

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 theamblyopia. Strabismic amblyopia is treated by clarifying the visual image with glasses,

A child wearing an adhesive

eyepatch to correct amblyopia

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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 thestrabismus.[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 acombination 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 someorientations 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 astigmatismthat cannot be optically corrected

Form-deprivation and occlusion amblyopia

Form-deprivation amblyopia ( Amblyopia exanopsia) 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)

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.[

A man with minor amblyopia

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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 andthe 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 The same view with age-related

 NIH National Eye Institute 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 theAlternative 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 geneticallylinked dysfunction of the retina and is related to mutation of the Adenosine Tri-

Phosphate (ATP) Synthase Gene 615.1617

• Hypertension: Also known as high blood pressure.

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• 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/sub-

RPE/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 atmini-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 beta-

carotene, 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

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CataractA cataract is a clouding that develops in the crystalline lens 

of the eye or in its envelope, varying in degree from slight tocomplete 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 perceptionof 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 usedmetaphorically 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, hypertensionand 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 peoplewith 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.

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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).

 SymptomsAs 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 animportant 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

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ConjunctivitisConjunctivitis (commonly called "pink eye" or "Madras

eye"[1]) is an inflammation of the conjunctiva (the outermostlayer 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

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.

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]

An eye with viral conjunctivitis.

Eyes with conjunctivitis

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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 andsometimes 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 punctatekeratitis.

Pyogenic bacterial conjunctivitis shows anopaque 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 bedifficult 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 witha 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 maynot 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.

An eye red due to acute conjunctivitis.

An eye with bacterial conjunctivitis.

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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 viralcause, 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 managementConjunctivitis 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.

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Diabetic RetinopathyDiabetic retinopathy is retinopathy (damage to the retina) caused by

complications of diabetes mellitus, which caneventually 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 earlywarning 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 somecases, the vision will get better or worse during

the day.

As new blood vessels form at the back of the

eye as a part of  proliferative diabetic

retinopathy (PDR), they can bleed

(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 dot-

 blot 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 

 Normal vision. Courtesy NIH  NationalEye Institute

The same view with diabetic retinopathy.

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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. Notethat hand-held ophthalmoscopy is insufficient to rule out significant and treatablediabetic 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 atleast 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 Programmefor 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.

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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 thesclera, 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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