Here is the full list of pages on eye-ailments.phoolish.org

Here is the full list of pages on eye-ailments.phoolish.org



47. Worm Removed From Eye
46. Guy's Eye Pops Out
45. All About Macular degeneration
44. All About Retinopathy of prematurity
43. All About Retinopathy
42. All About Diabetic retinopathy
41. All About Hypertensive retinopathy
40. All About Retinoschisis
39. All About Retinal detachment
38. All About Cataracts
37. All About Uveitis
36. All About Iritis
35. All About Keratoconjunctivitis sicca
34. All About Keratoconus
33. All About Fuchs' dystrophy
32. All About Corneal neovascularization
31. All About Thygeson's superficial punctate keratopathy
30. All About Arc eye
29. All About Snow blindness
28. All About Corneal abrasions
27. All About Corneal ulcers
26. All About Scleritis
25. Eye Ailments Caused by the Acanthamoeba
24. All About Subconjunctival hemorrhage
23. All About Pterygium
22. All About Keratitis
21. All About Keratoconjunctivitis
20. All About Conjunctivitis - Pink Eye
19. All About Exophthalmos
18. All About Epiphora
17. Ocular Herpes
16. All About Phthiriasis
15. All About Onchocerciasis - River Blindness
14. All About Loa loa filariasis
13. All About Leishmaniasis
12. All About Xanthelasma
11. All About Ptosis of the eyelid
10. All About Blepharochalasis
09. All About Lagophthalmos
08. All About Ectropion
07. All About Trichiasis
06. All About Entropion
05. All About Blepharitis
04. All About Chalazion
03. All About Styes - Hordeolum
02. All About Diseases of the eye and adnexa - a List
01. All About the Eyes

Worm Removed From Eye

stay away from 3rd world countries, unless you enjoy insects IN YOUR EYE!

Guy's Eye Pops Out

watch the guy on the far right, at 11 seconds into the video. and prepare to be disgusted.

All About Macular degeneration

Macular degeneration is a medical condition in which the light sensing cells in the macula malfunction and, over time, cease to work. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for those over the age of fifty years. Although some macular dystrophies that affect younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD).

Age related macular degeneration

Age-related macular degeneration begins with characteristic yellow deposits in the macula (central area of the retina) called drusen. Most people with these early changes have good vision. People with drusen can go on to develop advanced AMD. The risk is considerably higher when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula.

Advanced AMD, which is responsible for profound vision loss, has two forms: dry and wet. Central geographic atrophy, the dry form of advanced AMD, causes vision loss through loss of photoreceptors and cells supporting the photoreceptors in the central part of the eye. Currently, no treatment is available for this condition. Neovascular or exudative AMD, the wet form of advanced AMD, causes vision loss due to abnormal blood vessel growth under the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and supporting cells, if left untreated. New, effective treatments for the neovascular form of AMD are now available.

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.[citation needed]
* Smoking: The only environmental exposure clearly associated with macular degeneration is tobacco smoking.[1] Exposure to cigarette smoke more than doubles the risk of macular degeneration.
* Family history: The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration vs. 12% for people who do not have relatives with macular degeneration, i.e. a four fold higher risk.[citation needed]
* Macular degeneration gene: The genes for the complement system proteins factor H (CFH) and factor B (CFB) 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 active complex 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 . But the mutation in CFH(Tyr402His) reduces the affinity of CFH for CRP and probably also alters the ability of factor H to recognise specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialised membrane at the back of the eye and leads to increased inflammatory response within the macula. In two 2006 studies at Yale Department of Epidemiology and Public Health and the Department of Ophthalmology and Visual Sciences, Moran Eye Center at the University of Utah School of Medicine, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified. [2][3]
* Hypertension: Also known as high blood pressure.
* Cardiovascular status - high cholesterol, obesity.
* High fat intake is associated with an increased risk of macular degeneration in both women and men. Fat provides about 42% of the food energy in the average American diet. A diet that derives closer to 20-25% of total food energy from fat is probably healthier. Reducing fat intake to this level means cutting down greatly on consumption of red meats and dairy products such as milk, cheese, and butter. Eating more cold-water fish (at least twice weekly), rather than red meats and eating any type of nuts may help macular degeneration patients.[4]
* Oxidative stress: It has been proposed that age related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation - a classic sign associated with macular degeneration.[5]
* Race Macular degeneration is more likely to be found in whites than in blacks.[6][7]
* Exposure to sunlight especially blue light. There is conflicting evidence as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study in the British Journal of Ophthalmology on 446 subjects found that it does not.[8] High energy visible light (HEV) has been implicated as a cause of age-related macular degeneration.[9][10]

Signs

* Drusen
* Pigmentary alterations
* Exudative changes: hemorrhages, 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

Image courtesy AgingEye Times

* Blurred vision: Those with nonexudative macular degeneration may by 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

The Amsler Grid Test is one of the simplest and most effective methods for patients to monitor the health of the macula. The Amsler Grid is essentially a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing.

'Vision loss' or 'blindness' in macular degeneration refers to the loss of 'central vision' only. The peripheral vision is preserved. Blindness in macular degeneration does not mean 'inability to see light' and even with far advanced macular degeneration, the peripheral retina allows for useful vision.

The loss of central vision profoundly affects visual functioning. It is not possible, for example, to read without central vision. Pictures which attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters 6 inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this surprisingly difficult to do.

Similar symptoms with a very different etiology and different treatment can be caused by Epiretinal membrane or macular pucker.

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.

Treatment

Most of the treatments that are available now and and currently being studied are aimed at stopping the neovascular (or wet) form of AMD.

In June 2006, the drug ranibizumab (Lucentis) has been approved by the FDA for use in the treatment of AMD.[11] Ranibizumab has been shown to halt the progression of the disease in most patients receiving the treatment. Unlike previous treatments, a significant majority (70%) receiving ranibizumab had an improvement in vision of at least 1 letter. Up to 40% of patients had a significant vision increase of 3 lines or more. In addition, up to 50% had a vision of 20/40 or better after 12 months of treatment. This is significant as 20/40 is commonly seen as the vision at which a person can still drive a car. Ranibizumab was the first therapy to show a statistically significant improvement in patient reported outcomes.[12][13] Ranibizumab is given as an injection into the eye. The initial studies required an injection every 4 weeks for 2 years.

Bevacizumab (Avastin), a drug approved for use in colon cancer, has been used by ophthalmologists in the treatment of wet macular degeneration. Bevacizumab and ranibizumab were developed for the same monoclonal antibody parent. However, ranibizumab has been affinity matured 140x and is a much smaller molecule than bevazicumab. Being smaller allows ranibizumab to penetrate all layers of the retina and also to clear faster systemically from the eye. Doubts about whether bevacizumab can penetrate the layers of the retina led to the development of ranibizumab. There are also concerns about the safety of bevacizumab as it known to have significant systemic effects. Before Lucentis was available, bevacizumab was widely used by ophthalmologists who treat macular degeneration. Some of their experiences with large numbers of patients with relatively short follow-up times were recently published. No randomized controlled clinical trial with systematic safety data collection has been performed to validate its efficacy and safety with same certainty as ranibizumab. Bevacizumab, when administered at the usual cancer treatment doses, has been shown to cause systemic adverse effects. The most common adverse effect was hypertension. There is a continued interest as the bevacizumab for use in the eye can be obtained for about 30-50 dollars per dose, compared to 2,000 dollars per dose for ranibizumab. One concern is that bevacizumab is aliquotted out by compounding pharmacies from a single use vial of bevacizumab. This may lead to degradation and impurities within the product. Following the recommended protocol for ranibizumab costs about $50,000 per eye over two years. The National Eye Institute is planning a head-to-head ranibizumab vs. bevacizumab, randomized, controlled clinical trial for treatment of macular degeneration. Currently more than 50% of retinal specialists use bevacizumab as the first line drug (ACRS Practice Patterns Survey).

Pegaptanib (Macugen) was approved in 2004 for treatment of neovascular AMD. It targets certain forms of VEGF molecules and is injected directly into the eye like ranibizumab or bevacizumab. Although this was shown to decrease the risk of vision loss significantly compared to no treatment, it is felt to be relatively ineffective compared to the newer treatments.

Photodynamic therapy (PDT) with verteporfin (Visudyne) had been the treatment of choice for neovascular AMD until recently. This was the first treatment shown to decrease the chance of severe vision loss in 2 years in patients with neovascular AMD without first causing immediate vision loss at the time of the treatment. A photosenstive dye with affinity for the abnormal blood vessels are first injected through the veins. A low-energy activating laser is then directed toward the abnormal blood vessels, causing selective damage to those blood vessels. This has also fallen out of favor as newer, more effective treatments became available.

Direct laser treatment for neovascular AMD was shown to decrease the chance of profound vision loss at 2 years in patients with neovascular AMD but it is seldom used as the treatment itself causes significant vision loss immediately. Infrequently, abnormal blood vessels outside of the center part of the macula are detected. Direct laser treatment can be an effective way to treat these patients with acceptable morbidity.

Other drugs that are currently under investigation include: anecortave (Retaane), squalamine (Evizon), VEGF TRAP-EYE (made by Regeneron), and siRNA. Second generation antisense oligonucleotides iCo-007 targeting the Raf-1 kinase are also under investigation as a target for broad inhibition of multiple pro-angiogenic signals. Radiation therapy (brachytherapy) and rheopheresis are also being evaluated for wet macular degeneration.[14]

None of the drugs or laser treatment can restore vision to patients that have already suffered permanent damage to the photoreceptors or retinal pigmented epithelial cells due to advanced forms of AMD. Stem cells are currently being studied as a potential solution to this problem.

OT-551 eyedrop is currently being evaluated in an National Eye Institute-sponsored trial as a treatment for the dry form of AMD (the drug is already under investigation as a treatment for cataracts).

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 developing advanced AMD by about 25 percent in those patients who have earlier but significant forms of the disease. This is the only proven intervention to decrease the risk of advanced AMD at this time. A follow up study, Age-Related Eye Disease Study 2 to study the potential benefits of lutein, zeaxanthine, and fish oil, is currently underway. Despite the reported benefits there is considerable debate about the formulation and use of these supplements. [15] [16]

Anecortave acetate, (Retanne), is an anti-angiogenic drug that is given as an injection behind the eye (avoiding an injection directly into the eye) that is currently being studied as a potential way of reducing the risk of neovascular (or wet) AMD in high-risk patients.

Recent studies suggest that statins, a family of drugs used for reducing cholesterol levels, may be effective in prevention of AMD, and in slowing its progression.[17]

Juvenile macular degeneration

Juvenile macular degeneration is not a term in standard usage at this time. The preferred term for conditions that affect the macula in younger individuals related to genetics is macular dystrophy. Examples of these include:

* Best's disease
* Doyne's honeycomb retinal dystrophy
* Sorsby's disease
* Stargardt's disease

Impact

Macular degeneration, in its advanced forms, can result in legal blindness, resulting in a loss of driving privileges and an inability to read all but very large type. Perhaps the most grievous loss is the inability to see faces clearly or at all.

Some of these losses can be offset by the use of adaptive devices. A closed-circuit television reader can make reading possible, and specialized screen-reading computer software, e.g., JAWS for Windows, can give the blind person access to word processing, spreadsheet, financial, and e-mail access.

References

1. ^ http://news.bbc.co.uk/2/hi/health/4217010.stm
2. ^ Yang Z, Camp NJ, Sun H, Tong Z, Gibbs D, Cameron DJ, Chen H, Zhao Y, Pearson E, Li X, Chien J, Dewan A, Harmon J, Bernstein PS, Shridhar V, Zabriskie NA, Hoh J, Howes K, Zhang K. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration." Science. 2006 Nov 10;314(5801):992-3. PMID 17053109.
3. ^ Dewan A, Liu M, Hartman S, Zhang SS, Liu DT, Zhao C, Tam PO, Chan WM, Lam DS, Snyder M, Barnstable C, Pang CP, Hoh J. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration". Science. 2006 Nov 10;314(5801):989-92. PMID 17053108
4. ^ Macular degeneration Types and Risk Factors
5. ^ "Melanin aggregation and polymerization: possible implications in age related macular degeneration." Ophthalmic Research, 2005; volume 37: pages 136-141.
6. ^ Age-Related Eye Disease Study Research Group. "Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3." Ophthalmology. 2000 Dec;107(12):2224-32. PMID 11097601.
7. ^ Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL 3rd; Age-Related Eye Disease Study Research Group. "Risk factors for the incidence of Advanced Age-Related Macular Degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report no. 19." Ophthalmology. 2005 Apr;112(4):533-9. PMID 15808240.
8. ^ Khan, JC; Shahid H, Thurlby DA, Bradley M, Clayton DG, Moore AT, Bird AC, Yates JR, Genetic Factors in AMD Study (Jan 2006). "Age related macular degeneration and sun exposure, iris colour, and skin sensitivity to sunlight". The British Journal of Ophthalmology 90 (1): 29-32. PMID 16361662. Retrieved on 2006-10-23.
9. ^ Glazer-Hockstein, C; Dunaief JL (Jan 2006). "Could blue light-blocking lenses decrease the risk of age-related macular degeneration?". Retina 26 (1): 1-4. PMID 16395131. Retrieved on 2006-10-23.
10. ^ Margrain, TH; Boulton M, Marshall J, Sliney DH (Sep 2004). "Do blue light filters confer protection against age-related macular degeneration?". Progress in Retinal and Eye Research 23 (5): 523-31. PMID 15302349. Retrieved on 2006-10-23.
11. ^ United States Food and Drug Administration (2006-06-30). FDA Approves New Biologic Treatment for Wet Age-Related Macular Degeneration. Press release. Retrieved on 2006-10-23.
12. ^ Brown, DM; Kaiser PK, Michels M, Soubrane G, Heier JS, Kim RY, Sy JP, Schneider S; ANCHOR Study Group (Oct 5 2006). "Ranibizumab versus verteporfin for neovascular age-related macular degeneration". New England Journal of Medicine 355 (14): 1432-44. PMID 17021319. Retrieved on 2006-10-23.
13. ^ Rosenfeld, PJ; Brown DM, Heier JS, Boyer DS, Kaiser PK, Chung CY, Kim RY; MARINA Study Group (Oct 5 2006). "Ranibizumab for neovascular age-related macular degeneration". New England Journal of Medicine 355 (14): 1419-31. PMID 17021318. Retrieved on 2006-10-23.
14. ^ http://www.agingeye.net/maculardegen/maculardegennewdevelopments.php
15. ^ http://www.biosyntrx.com/Article.php?ArticleID=462
16. ^ http://www.biosyntrx.com/Article.php?ArticleID=463
17. ^ http://bjo.bmjjournals.com/cgi/content/full/882/161

All About Retinopathy of prematurity

Retinopathy of prematurity (ROP), previously known as retrolental fibroplasia (RLF), is a disease of the eye that affects prematurely born babies. It is thought to be caused by disorganised growth of retinal blood vessels resulting in scarring and retinal detachment. ROP can be mild and may resolve spontaneously, but may lead to blindness in serious cases. Prematurity is a direct risk factor for ROP. As such, all preterm babies are at high risk for ROP, and very low birth weight is an additional risk factor. High oxygen concentration can contribute to the development of ROP.

Pathophysiology

Normally, maturation of the retina proceeds in-utero and at term, the mature infant has fully vascularised retina. However, in preterm infants, the retina is often not fully vascularised. ROP occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. The key disease element is fibrovascular proliferation. This is growth of abnormal new vessels that may regress, but frequently progresses. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Multiple factors can determine whether the disease progresses, including overall health, birth weight, the stage of ROP at initial diagnosis, and the presence or absence of "plus disease".

Patients with ROP are at greater risk for strabismus, glaucoma, cataracts and myopia later in life, and should be examined yearly to help prevent and treat these conditions.

Diagnosis

Following pupillary dilation using eye drops, the retina is examined using a special lighted instrument (an indirect ophthalmoscope). The peripheral portions of the retina are pushed into view using scleral depression. Examination of the retina of a premature infant is performed to determined how far the retinal blood vessels have grown (the zone), and whether or not the vessels are growing flat along the wall of the eye (the stage). Retinal vascularization is judged to be complete when vessels extend to the ora serrata. The stage of ROP refers to the character of the leading edge of growing retinal blood vessels (at the vascular-avascular border). The stages of ROP disease have been defined by the International Classification of Retinopathy of Prematurity (ICROP).

Retinal examination with scleral depression is generally recommended for patients born before 30-32 weeks gestation, with birthweight 1500 grams or less, or at the discretion of the treating neonatologist. The initial examination is usually performed at 4-6 weeks of life, and then repeat every 1-3 weeks until vascularization is complete (or until disease progression mandates treatment).

In older patients the appearance of the disease is less well described but includes the residua of the ICROP stages as well as secondary retinal responses.

Differential diagnosis

The most difficult aspect of the differential diagnosis may arise from the similarity of two other diseases:

* Familal Exudative Vitreoretinopathy which is a genetic disorder that also disrupts the retinal vascularization in full-term infants.
* Persistent Fetal Vascular Syndrome also known as Persistent Hyperplastic Primary Vitreous that can cause a traction retinal detachment difficult to differentiate but typically unilateral.

International Classification of Retinopathy of Prematurity (ICROP)

The system used for described the findings of active ROP is entitled The International Classification of Retinopathy of Prematurity (ICROP).[1] ICROP uses a number of parameters to describe the disease. They are location of the disease into zones (1, 2, and 3), the circumferential extent of the disease based on the clock hours (1-12), the severity of the disease (stage 1-5) and the presence or absence of "Plus Disease". Each aspect of the classification has a technical definition. This classification was used for the major clinical trials. It has been revised in 2005[2]
Zones of the retina in ROP


The zones are centered on the optic nerve. Zone 1 is the posterior zone of the retina, defined as the circle with a radius extending from the optic nerve to double the distance to the macula. Zone 2 is an annulus with the inner border defined by zone 1 and the outer border defined by the radius defined as the distance from the optic nerve to the nasal ora serrata. Zone 3 is the residual temporal crescent of the retina.

The circumferential extent of the disease is described in segments as if the top of the eye were 12 on the face of a clock. For example one might report that there is stage 1 disease for 3 clock hours from 4 to 7 o'clock. (The extent is a bit less important since the treatment indications from the Early Treatment for ROP[3])

The Stages describe the ophthalmoscopic findings at the junction between the vascularized and avascular retina.

* Stage 1 is a faint demarcation line.
* Stage 2 is an elevated ridge.
* Stage 3 is extraretinal fibrovascular tissue.
* Stage 4 is sub-total retinal detachment.
* Stage 5 is total retinal detachment.

In addition, Plus disease may be present at any stage. It describes a significant level of vascular dilation and tortuosity observed at the posterior retinal vessels. This reflects the increase of blood flow through the retina. [1]

Prognosis

Stages 1 and 2 do not lead to blindness. However, they can progress to the more severe stages. Threshold disease is defined as disease that has a 50% likelihood of progressing to retinal detachment. Threshold disease is considered to be present when stage 3 ROP is present in either zone I or zone II, with at least 5 continuous or 8 total clock hours of disease, and the presence of plus disease.[4] Progression to stage 4 (partial retinal detachment), or to stage 5 (total retinal detachment), will result in substantial or total loss of vision for the infant.

Monitoring

In order to allow timely intervention, a system of monitoring is undertaken for infants at risk of developing ROP. These monitoring protocols differ geographically because the definition of high-risk is not uniform or perfectly defined. In the USA the consensus statement of experts is informed by data derived by clinical trials and published in Pediatrics 2006. They included infants with birthweights under 1500 gms or under 28 (32 tentative till I reference the new guidelines) weeks gestation in most cases.

Treatment

* Peripheral Retinal Ablation is the mainstay of ROP treatment. The destruction of the avascular retina is performed with a solid state laser photocoagulation, as they are easily portable around the neonatal ICU. Cryotherapy used to be performed and has been evaluated in multi-center clinical trials as an effective modality for prevention and treatment of ROP. However, it is no longer preferred for routine retinal coagulation, due to tremendous amounts of inflammation and lid swelling accompanying cryotherapy in premature babies.

* Scleral buckling and/or Vitrectomy surgery may be considered for severe ROP (stage 4 and 5) for eyes that progress to retinal detachment. Few centers in the world specialize in this surgery, because of its attendant surgical risks and generally poor outcomes.

History

A significant time in the history of the disease was between 1941-1953, when a worldwide epidemic of ROP was seen. Over 12,000 babies worldwide were not only born with the disease but blinded by it - the musician Stevie Wonder is a famous victim of the disease. The first case of the epidemic was seen on St Valentine's Day in 1941, where a premature baby in Boston was diagnosed. Cases were then seen all over the world and the cause was, at that point, unknown. By 1951 a clear link between incidence and affluence became clear: many cases were seen in developed countries with organized and well-funded health care. Two British scientists suggested that it was oxygen toxicity that caused the disease. Babies born prematurely in such affluent areas were treated in incubators which had artificially high levels of oxygen. Studies on rats made this cause seem more likely, but the link was eventually confirmed by a controversial study undertaken by American pediatricians. The study involved two groups of babies. Some were given the usual oxygen concentrations in their incubators, while the other group had "curtailed" oxygen levels. The latter group was shown to have a lower incidence of the disease. As a result, oxygen levels in incubators were lowered and consequently the epidemic was halted.[5]

References

1. ^ Committee for the Classification of Retinopathy of Prematurity (1984 Aug). "An international classification of retinopathy of prematurity". Arch Ophthalmol. 102(8): 1130-1134.
2. ^ Committee for the Classification of Retinopathy of Prematurity (2005 Jul). "The International Classification of Retinopathy of Prematurity revisited". Arch Ophthalmol. 123(7): 991-999.
3. ^ Early Treatment for Retinopathy of Prematurity Cooperative Group (2003). "Revised indications for the treatment of retinopathy of prematurity: results of the early treatment for retinopathy of prematurity randomized trial". Arch Ophthalmol. 121: 1684-1696.
4. ^ Phelps, D.L. (2001). "Retinopathy of Prematurity: History, Classification, and Pathophysiology". NeoReviews 2(7): e153-e166.
5. ^ Silverman, William (1980). Retrolental Fibroplasia: A Modern Parable. Grune & Stratton, Inc..

All About Retinopathy

Retinopathy is a general term that refers to some form of non-inflammatory damage to the retina of the eye. Most commonly it is a problem with the blood supply that is the cause for this condition. Frequently, retinopathy is an ocular manifestation of systemic disease.

Main causes of retinopathy are :

* diabetes - diabetic retinopathy
* arterial hypertension - hypertensive retinopathy
* prematurity of the newborn - retinopathy of prematurity (ROP)
* sickle cell anemia
* direct sunlight exposure - solar retinopathy
* medicinal products - drug-related retinopathy
* retinal vein or artery occlusion

Many types of retinopathy are progressive and may result in blindness or severe vision loss or impairment, particularly if the macula becomes affected.

Retinopathy is diagnosed by an optometrist or an ophthalmologist during ophthalmoscopy. Treatment depends on the cause of the disease.

See also

* List of eye diseases and disorders
* List of systemic diseases with ocular manifestations

All About Diabetic retinopathy

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which could eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all diabetics who have had diabetes for 15 years or more[citation needed]. 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 and drive. In some cases, 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 (haemorrhage) 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.

Pathogenesis

Small blood vessels – such as those in the eye – are especially vulnerable to poor blood glucose control. An overaccumulation of glucose and/or fructose (Kawasaki et al 2004) damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any changes in their vision.

Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids (fat) onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.

As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage. The lack of oxygen (ischemia) in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause Neovascular Glaucoma. Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative diabetic retinopathy (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.

Risk factors

All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset). The longer a person has diabetes, the higher the risk of developing some ocular problem.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes. It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.

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.
* Tonometry: A standard test that determines the fluid pressure (intraocular pressure) inside the eye. Elevated pressure is a possible sign of glaucoma, another common eye problem in people with diabetes.
* 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 UK National Screening Committee [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.

The eye care professional will look at the retina for early signs of the disease, such as: (1) leaking blood vessels, (2) retinal swelling, such as macular edema, (3) pale, fatty deposits on the retina (exudates) – signs of leaking blood vessels, (4) damaged nerve tissue (neuropathy), and (5) any changes in the blood vessels.

Should the doctor suspect macular edema, he or she may perform a test called fluorescein angiography. In this test, a special dye is injected into the arm. Pictures are then taken as the dye passes through the blood vessels in the retina. This test allows the doctor to find the leaking blood vessels.

Management

There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease. In fact, even people with advanced retinopathy have a 90 percent chance of keeping their vision when they get treatment before the retina is severely damaged. Still, the best way of addressing diabetic retinopathy is to monitor it vigilantly and ensure that it does not happen in the first place by careful blood glucose control and limitation of dietary fructose.

These three treatments are laser surgery, injection of triamcinolone into the eye and vitrectomy. It is important to note that although these treatments are very successful, they do not cure diabetic retinopathy. Caution should be exercised in treatment with laser surgery since it causes a loss of retinal tissue. It is often more prudent to inject triamcinolone. In some patients it results in a marked increase of vision, especially if there is an edema of the macula.

Laser surgery

A type of laser surgery called panretinal photocoagulation, or PRP, is used to treat severe macular edema and proliferative retinopathy. 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 at the back of the eye.

Before the surgery, the ophthalmologist dilates the pupil and applies anesthetic drops to numb the eye. In some cases, the doctor also may numb the area behind the eye to prevent any discomfort. The lights in the office are also dimmed to aid in dilating the pupil. The patient sits facing the laser machine while the doctor holds a special lens to the eye. During the procedure, the patient may see flashes of light. These flashes may eventually create an uncomfortable stinging sensation for the patient. After the laser treatment, patients should be advised not to drive for a few hours while the pupils are still dilated. Vision may remain a little blurry for the rest of the day, though there should not be much pain in the eye.

Scatter laser treatment

Rather than focus the light on a single spot, the eye care professional may make hundreds of small laser burns away from the center of the retina, a procedure called scatter laser treatment or panretinal photocoagulation. The treatment shrinks the abnormal blood vessels. Patients may lose some of their peripheral vision after this surgery, but the procedure saves the rest of the patient's sight. Laser surgery may also slightly reduce colour and night vision.

A person with proliferative retinopathy will always be at risk for new bleeding as well as glaucoma, a complication from the new blood vessels. This means that multiple treatments may be required to protect vision.

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 made up of salt and water. Because the vitreous is mostly water, there should be no change between the saline solution and the normal vitreous.

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.

References

* The original text of this document was taken from the public domain resource document "Facts About Diabetic Retinopathy", at http://www.nei.nih.gov/health/diabetic/retinopathy.asp See the copyright statement at http://www.nei.nih.gov/order/index.htm, which says "Our publications are not copyrighted and may be reproduced without permission. However, we do ask that credit be given to the National Eye Institute, National Institutes of Health."
* Basic ophthalmology for medical students and primary care residents, 7th edition
* Kawasaki T, Ogata N, Akanuma H, Sakai T, Watanabe H, Ichiyanagi K, Yamanouchi T. Postprandial plasma fructose level is associated with retinopathy in patients with type 2 diabetes. Metabolism 2004;53:583-8. Fulltext. PMID 15131761.
* Eye Care for Diabetics

Extras

The biggest threat to the eyesight is the Diabetic Retinopathy.Some people get eye treatments from lasers because the laser shrinks the abnormal blood vessels to stop leakage.