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.

All About Hypertensive retinopathy

Hypertensive retinopathy is damage to the retina due to high blood pressure (i.e. hypertension).

Pathophysiology

The retina is one of the "target organs" that are damaged by sustained hypertension. Subjected to excessively high blood pressure over prolonged time, the small blood vessels that involve the eye are damaged, thickening, bulging and leaking.

Early signs of retinopathy correlate less well with mortality and morbidity than used to be thought, but signs of accelerated or "malignant" hypertension indicate severe illness.

Symptoms

Most patients with hypertensive retinopathy present without visual symptoms, however, some may report decreased vision or headaches.

Signs

Signs of damage to the retina caused by hypertension include:

* Arteriosclerotic changes
o Arteriolar narrowing that is almost always bilateral
+ Grade I - 3/4 normal caliber
+ Grade II - 1/2 normal caliber
+ Grade III - 1/3 normal caliber
+ Grade IV - thread-like or invisible
o Arterio-venous crossing changes (aka "AV nicking) with venous constriction and banking
o Arteriolar color changes
+ Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width.
+ Silver wire arterioles are those in which the central light reflex occupies all of the width of the arteriole.
o Vessel sclerosis
* Ischemic changes (e.g. "cotton wool spots")
* Hemorrhages, often flame shaped.
* Edema
o Ring of exudates around the retina called a "macular star"
* Papilledema, or optic disc edema, in patients with malignant hypertension
* Visual acuity loss, typically due to macular involvement

Diagnosis

* Fluorescein angiography
* Ophthalmoscopy
* Sphygmomanometry

Treatment and management

A major aim of treatment is to prevent, limit, or reverse such target organ damage by lowering the patient's high blood pressure. The eye is an organ where damage is easily visible at an early stage, so regular eye examinations are important.

See also

* Hypertensive crisis
* List of eye diseases and disorders
* List of systemic diseases with ocular manifestations
* Ophthalmology
* Optometry

References

* The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease, J.B. Lippincott, 1994.
* Hypertensive retinopathy

All About Retinoschisis

Retinoschisis is an uncommon eye disease characterized by the abnormal splitting of the retina's sensory layers, usually in the outer plexiform layer, with resulting loss of visual function.[1] The retina, which consists of multiple layers of interconnected nerve and pigment cells, separates into separate layers resulting in a loss of vision in the corresponding visual field.

It is estimated that retinoschisis affects one in 5,000 to 25,000 individuals, primarily young males. "Schisis" is derived from the Greek word meaning "splitting," describing the splitting of the retinal layers from each other. If the retinoschisis involves the macula, then the high-resolution central area of vision used to view detail is lost, and this one form of macular degeneration. Treatment is often aimed at restricting any worsening of the separation so that it does not encroach on the macula.

Retinoschisis can be caused by an X-linked genetic defect, affecting the vision of men who inherit the disease from their unaffected carrier mothers. The genetic form of this disease usually starts during childhood and is called Juvenile X-linked Retinoschisis. Affected males are usually identified in grade school, but occasionally are identified as young infants. Senile retinoschisis, on the other hand, is the splitting of the retina as a result of aging. It can affect both men and women and is not a genetic condition.

Very few affected individuals go completely blind from retinoschisis, but some sufferers have very limited reading vision and are "legally blind". Visual acuity can be reduced to less than 20/200 in both eyes.

Retinoschisis causes acuity loss in the center of the visual field through the formation of tiny cysts in the retina, often forming a "spoke-wheel" pattern that can be very subtle. The cysts are usually only detectable by a trained clinician. Vision cannot be improved by glasses, as the nerve tissue itself is damaged by these cysts. Furthermore, peripheral vision can be lost due to the splitting of the inner layer of nerve cells from the outer layer of cells.

If the anchoring of the outer layer of the retina to the eye wall is impaired, retinal detachments can occur. Retinal detachments can be treated surgically when detected early, but the root cause - the splitting of the retina - cannot be corrected by current medications or surgeries. Since retinoschisis can be confused with other eye diseases such as lazy eye, it is important that a thorough exam be done by an ophthalmologist to ensure that retinal detachment is not overlooked.

[edit] References

1. ^ Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.

* http://www.kellogg.umich.edu/patientcare/conditions/retinoschisis.html
* http://www.mrcophth.com/retinacases/retinoschisis.html

All About Retinal detachment

Retinal detachment is a disorder of the eye in which the retina peels away from its underlying layer of support tissue. Initial detachment may be localized, but without rapid treatment the entire retina may detach, leading to vision loss and blindness. It is a medical emergency. [1]

The retina is a thin disc-shaped layer of light-sensitive tissue on the back wall of the eye. Its job is to translate what we see into neural impulses and send them to the brain via the optic nerve. Occasionally, injury or trauma to the eye or head may cause a small tear in the retina, which allows fluid to seep through, and peel it away like a bubble in wallpaper.

Types

* Rhegmatogenous retinal detachment - A rhegmatogenous retinal detachment occurs due to a hole, tear, or break in the retina that allows fluid to pass into the subretinal space between the sensory retina and the retinal pigment epithelium.
* Exudative, serous, or secondary retinal detachment - An exudative retinal detachment occurs due to inflammation, injury or vascular abnormalities that results in fluid accumulating underneath the retina without the presence of a hole, tear, or break.
* Tractional retinal detachment - A tractional retinal detachment occurs when fibrovascular tissue, caused by an injury, inflammation or neovascularization, pulls the sensory retina from the retinal pigment epithelium.

Prevalence

The risk of retinal detachment in otherwise normal eyes is around 5 in 100,000 per year.[2] Detachment is more frequent in the middle-aged or elderly population with rates of around 20 in 100,000 per year [1]. The lifetime risk in normal eyes is about 1 in 300 [2].

* Retinal detachment is more common in those with severe or extreme myopia (above 5-6 diopters), as their eyes are longer and the retina is stretched thin. The lifetime risk increases to 1 in 20 [3]. Myopia is associated with 67% of retinal detachment cases. Patients suffering from a detachment related to myopia tend to be younger than non-myopic detachment patients.

* Retinal detachment can occur more frequently after surgery for cataracts. The estimate of risk of retinal detachment after cataract surgery is 5 to 16 per 1000 cataract operations.[4]. The risk may be much higher in those who are highly myopic, with a frequency of 7% reported in one study [5]. Young age at cataract removal further increased risk in this study.

* Tractional retinal detachments can also occur in patients with proliferative diabetic retinopathy [6]or those with proliferative retinopathy of sickle cell disease [7]. In proliferative retinopathy, abnormal blood vessels (neovascularization) grow within the retina and extend into the vitreous. In advanced disease, the vessels can pull the retina away from the back wall of the eye causing a traction retinal detachment.

Although retinal detachment usually occurs in one eye, there is a 15% chance of developing it in the other eye, and this risk increases to 25-30% in patients who had cataracts extracted from both eyes [8].

Symptoms

A retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

* flashes of light (photopsia) - very brief in the extreme temporal (outside away from the nose) part of vision
* a sudden dramatic increase in the number of floaters
* a ring of floaters or hairs just to the temporal side of the central vision
* a slight feeling of heaviness in the eye

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

* a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision
* the impression that a veil or curtain was drawn over the field of vision
* straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)
* central visual loss

Treatment

There are several methods of treating a detached retina which all depend on finding and closing the holes (tears) which have formed in the retina.

* Cryopexy and Laser Photocoagulation

Cryotherapy (freezing) and laser photocoagulation are treatments used to create a scar/adhesion around the retinal hole to prevent fluid from entering the hole and accumulating behind the retina and excacerbating the retinal detachment. Cryopexy and photocoagulation are generally interchangeable. However, cryopexy is generally used in instances where there is a lot of fluid behind the hole;laser retinopexy will not take.

* Scleral buckle surgery

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (bands , tyres) to the outside of the eyeball. The bands push the wall of the eye inward against the retinal hole, closing the hole and allowing the retina to re-attach. The bands do not usually have to be removed. The most common side effect of a scleral operation is myopic shift. The operated eye generally will be 3-5 diopters more near sighted after the scleral buckle operation.

* Pneumatic retinopexy

This operation is generally performed in the doctor's office under local anesthesia. It is another method of repairing a retinal detachment in which a gas bubble ( SF6 or C3F8 gas ) is injected into the eye after laser or freezing treatment is applied to surround the retinal hole. The patient's head is then positioned so that the bubble rests against the retinal hole. Patients may have to keep their heads tilted for several days to keep the gas bubble in contact with the retinal hole. The surface tension of the air/water interface seals the hole in the retina, and allows the retinal pigment epithelium to pump the subretinal space dry and pull the retina back into place. This strict positioning requirement makes the treatment of the retinal holes and detachments that occurs in the lower part of the eyeball impractical.

* Vitrectomy

Vitrectomy is an increasingly widely used treatment for retinal detachment in countries with modern healthcare systems. It involves the removal of the vitreous gel and is usually combined with filling the eye with a gas bubble (SF6 or C3F8 gas). Advantages of this operation is that there is no myopic shift after the operation. A disadvantage is that a vitrectomy always leads to more rapid progression of a cataract in the operated eye. Another major disadvantage of the operation is that , should a vitrectomy operation fail to work, the recurrent retinal detachment is much harder to repair. As such, except for special instances, the vitrectomy operation is not usually used as the initial operation to attempt to repair a rhegmatogenous retinal detachment.

* Ignipuncture

Ignipuncture is an outdated procedure that involves cauterization of the retina with a very hot pointed instrument.[3] It was pioneered and named by Jules Gonin in the early 1900s.[3]

After treatment, patients gradually regain their vision over a period of a few weeks, although the visual acuity may not be as good as it was prior to the detachment, particularly if the macula was involved in the area of the detachment. However, if left untreated, total blindness can occur in a matter of days.

Prevention

Retinal detachment can be prevented in some. The most effective way of preventing retinal detachment is educating people to seek ophthalmic medical attention if they suffer symptoms suggestive of a posterior vitreous detachment [9]. Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20.

There are some known risk factors for retinal detachment. There are also many activities which at one time or another have been forbidden to those at risk of retinal detachment, with varying degrees of evidence supporting the restrictions.

Cataract surgery is a major cause, and can result in detachment even a long time after the operation. The risk is increased if there are complications during cataract surgery, but remains even in apparently uncomplicated surgery. The increasing rates of cataract surgery, and decreasing age at cataract surgery, will inevitably lead to an increased incidence of retinal detachment.

Trauma is a less frequent cause. Activities which cause direct trauma to the eye (boxing, kick-boxing, karate and others) can cause a particular type of retinal tear called a retinal dialysis. This type of tear can be detected and treated before it develops into a retinal detachment. For this reason governing bodies in some of these sports require regular ophthalmic examination.

Individuals prone to retinal detachment due to a high level of myopia are encouraged to avoid activities where there is a risk of shock to the head or eyes, although without direct trauma to the eye the evidence base for this may not be convincing [4]. Some doctors recommend avoiding activities that increase pressure in the eye, including diving, skydiving, again with little supporting evidence. Retinal detachment does not happen as a result of straining your eyes, bending or heavy lifting.[5] Therefore, heavy weightlifting is fine.

Activities that involve sudden acceleration or deceleration also increase eye pressure and are discouraged by some doctors. These include bungee jumping,[4] but may also include rollercoaster rides.

References

1. ^ Retinal detachment. MedlinePlus Medical Encyclopedia. National Institutes of Health (2005). Retrieved on 2006-07-18.
2. ^ Ivanisevic M, Bojic L, Eterovic D. "Epidemiological study of nontraumatic phakic rhegmatogenous retinal detachment." Ophthalmic Res. 2000 Sep-Oct;32(5):237-9. PMID 10971186.
3. ^ a b Wolfensberger TJ. "Jules Gonin. Pioneer of retinal detachment surgery." Indian J Ophthalmol. 2003 Dec;51(4):303-8. PMID 14750617.
4. ^ a b http://www.emedicine.com/emerg/topic504.htm
5. ^ http://www.rnib.org.uk/xpedio/groups/public/documents/PublicWebsite/public_rnib003661.hcsp

See also

* Lattice degeneration
* Retinoschisis

All About Cataracts

A cataract is an opacity that develops in the crystalline lens of the eye or in its envelope. Early on in the development of senile cataract the power of the crystaline lens may be increased, causing 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.[1] Moreover, with time the cataract cortex liquefies to form a milky white fluid in a Morgagnian Cataract, and 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 earliest surgical procedure of couching) in ancient times were regarded as a blessing from the heavens, because it restored some perception of light in the bilaterally affected 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"[2]). 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"[3], so it is also possible that the name came about through the sense of "obstruction".

Causes
Normal vision. Courtesy National Institutes of Health, USA (NIH).
Normal vision. Courtesy National Institutes of Health, USA (NIH).
Hazy view as seen by a person with a cataract, Courtesy NIH
Hazy view as seen by a person with a cataract, Courtesy NIH

Cataracts develop from a variety of reasons, including long-term ultraviolet exposure, secondary effects of diseases such as diabetes, or simply due to advanced age; they are usually a result of denaturation of lens proteins. 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 can also be produced by eye injury or physical trauma. A study among Icelandair pilots showed commercial airline pilots as 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.[4] 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.

Cataracts may be partial or complete, stationary or progressive, hard or soft.

Some drugs can induce cataract development:

* Corticosteroids[5]
* Ezetimibe

There are various types of cataracts, e.g. nuclear, cortical, mature, hypermature. Cataracts are also classified by their location, e.g. posterior (classically due to steroid use[5][6]) and anterior (common (senile) cataract related to aging).

Epidemiology

Cataracts are the leading cause of blindness in the world.[7]

In the United States, age-related lenticular changes have been reported in 42% of those between the ages of 52 to 64[8], 60% of those between the ages 65 and 74[9], and 91% of those between the ages of 75 and 85[8].

Cataract surgery

Main article: Cataract surgery

Cataract surgery, using a temporal approach phacoemulsification probe (in right hand) and "chopper"(in left hand) being done under operating microscope at a Navy medical center


The most effective and common treatment is to surgically remove the cloudy lens. There are two types of surgery that can be used to remove cataracts, extra-capsular (extracapsular cataract extraction, or ECCE) and intra-capsular surgery (intracapsular cataract extraction, or ICCE). Extra-capsular surgery consists of removing the lens but leaving the majority of the lens capsule intact. High frequency sound waves (phacoemulsification) are sometimes used to break up the lens before extraction. Intra-capsular surgery involves removing the entire lens of the eye, including the lens capsule, but it is rarely performed in modern practice. In either extra-capsular surgery or intra-capsular surgery, the cataractous lens is removed and replaced with a plastic lens (an intraocular lens implant) which stays in the eye permanently.

Cataract operations are usually performed using a local anaesthetic and the patient will be allowed to go home the same day. Recent improvements in intraocular technology now allow cataract patients to choose a multifocal lens to create a visual environment where they are less dependent on glasses. Traditional intraocular lenses were monofocal. Medicare has allowed physicians, for the first time, to bill patients for this advanced lens design.

Complications after cataract surgery, including posterior capsular opacification and retinal detachment, are possible.

In ICCE there is the issue of the Jack in the box Phenomenon where the patient has to wear aphakic glasses...alternatives include contact lenses but these can prove to be high maintainance in dusty areas, which can lead to the complications of contact lenses.

Prevention

Although cataracts have no scientifically proven prevention, it is sometimes said that wearing ultraviolet-protecting sunglasses may slow the development of cataracts.[citation needed] Regular intake of antioxidants (such as vitamin C and E) is theoretically helpful, but this is also not proven.

Recent research

Although statins are known for their ability to lower lipids, they are also believed to have antioxidant qualities. It is believed that oxidative stress plays a role in the development of nuclear cataracts, which are the most common type of age-related cataract. To explore the relationship between nuclear cataracts and statin use, a group of researchers took a group of 1299 patients who were at risk of developing nuclear cataracts and gave some of them statins. Their results suggest that statin use in a general population may be associated with a lower risk of developing nuclear cataract. [10]

Types of cataracts
Bilateral cataracts in an infant due to Congenital rubella syndrome, courtesy CDC


The following is a classification of the various types of cataracts. This is not comprehensive and other unusual types may be noted.

* Classified by etiology

* Age-related cataract

* Immature Senile Cataract (IMSC) - partially opaque lens, disc view hazy
* Mature Senile Cataract (MSC) - Completely opaque lens, no disc view
* Hypermature Senile Cataract (HMSC) - Liquefied cortical matter: Morgagnian Cataract

* Congenital cataract

* Sutural cataract
* Lamellar cataract
* Zonular cataract
* Total cataract

* Secondary cataract

Slit lamp photo of Anterior capsular opacification visible few months after implantation of Intraocular lens in eye, magnified view
Slit lamp photo of Anterior capsular opacification visible few months after implantation of Intraocular lens in eye, magnified view

* Drug-induced cataract (e.g. Corticosteroids)

* Traumatic cataract

* Blunt trauma (capsule usually intact)
* Penetrating trauma (capsular rupture & leakage of lens material - calls for an emergency surgery for extraction of lens and leaked material to minimise further damage)

* Classified by location of opacity within lens structure (However, mixed morphology is quite commonly seen, e.g. PSC with nuclear changes & cortical spokes of cataract)

* Anterior cortical cataract
* Anterior polar cataract
* Anterior subcapsular cataract

Slit lamp photo of Posterior capsular opacification visible few months after implantation of Intraocular lens in eye, seen on retroillumination
Slit lamp photo of Posterior capsular opacification visible few months after implantation of Intraocular lens in eye, seen on retroillumination

* Nuclear cataract - Grading correlates with hardness & difficulty of surgical removal

* 1 - Grey
* 2 - Yellow
* 3 - Amber
* 4 - Brown/Black (Note: "Black cataract" translated in some languages (like Hindi) refers to Glaucoma, not the color of the lens nucleus)

* Posterior cortical cataract
* Posterior polar cataract (importance lies in higher risk of complication - posterior capuslar tears during surgery)
* Posterior subcapsular cataract (PSC) (clinically common)

* After-cataract - posterior capsular opacification subsequent to a successful extracapsular cataract surgery (usually within 3 months - 2 years) with or without IOL implantation. Requires a quick & painless office procedure with Nd:YAG laser capsulotomy to restore optical clarity.

Associations with systemic conditions

* Chromosomal disorders

* Alport's syndrome
* Cri-du-chat syndrome
* Conradi's syndrome
* Myotonia dystrophica
* Patau's syndrome
* Schmid-Fraccaro syndrome
* Trisomy 18 (Edward's syndrome)
* Turner's syndrome

* Disease of the skin and mucous membranes

* Atopic dermatitis
* Basal-cell nevus syndrome
* Ichthyosis
* Pemphigus

* Metabolic and nutrition diseases

* Aminoaciduria (Lowe's syndrome)
* Diabetes mellitus
* Fabry's disease
* Galactosemia
* Homocystinuria
* Hypervitaminosis D
* Hyperparathyroidism
* Hypothyroidism
* Mucopolysaccharidoses
* Wilson's disease

* Infectious diseases

* Congenital

* Congential herpes simplex
* Congenital syphilis
* Cytomegalic inclusion disease
* Rubella

* Others

* Cysticercosis
* Leprosy
* Onchocerciasis
* Toxoplasmosis

* Toxic substances introduced systemically

* Corticosteroids
* Haloperidol
* Miotics
* Triparanol

References

1. ^ http://www.aafp.org/afp/990700ap/99.html
2. ^ http://dictionary.reference.com/wordoftheday/archive/2003/10/29.html]
3. ^ http://www.etymonline.com/index.php?term=cataract
4. ^ Rafnsson, V; Olafsdottir E, Hrafnkelsson J, Sasaki H, Arnarsson A, Jonasson F. "Cosmic radiation increases the risk of nuclear cataract in airline pilots: a population-based case-control study". Arch Ophthalmol 123: 1102-1105.
5. ^ a b SPENCER R, ANDELMAN S. "STEROID CATARACTS. POSTERIOR SUBCAPSULAR CATARACT FORMATION IN RHEUMATOID ARTHRITIS PATIENTS ON LONG TERM STEROID THERAPY". Arch Ophthalmol 74: 38-41. PMID 14303339.
6. ^ Greiner J, Chylack L (1979). "Posterior subcapsular cataracts: histopathologic study of steroid-associated cataracts". Arch Ophthalmol 97 (1): 135-44. PMID 758890.
7. ^ https://web.emmes.com/study/areds/mopfiles/chp2_mop.pdf
8. ^ a b Sperduto RD, Seigel D. Sperduto RD, Seigel D. "Senile lens and senile macular changes in a population-based sample." Am J Ophthalmol. 1980 Jul;90(1):86-91. PMID 7395962.
9. ^ Kahn HA, Leibowitz HM, Ganley JP, Kini MM, Colton T, Nickerson RS, Dawber TR. "The Framingham Eye Study. I. Outline and major prevalence findings." Am J Epidemiol. 1977 Jul;106(1):17-32. PMID 879158.
10. ^ Klein, Barbara; Ronald Klein, Kristine Lee, and Lisa Grady. "Statin Use and Incident Nuclear Cataract". Journal of the American Medical Association 295 (23): 2752-2758.

* Pavan-Langston, Deborah (1990). Manual of Ocular Diagnosis and Therapy. Little, Brown and Company.

See also

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

All About Uveitis

Uveitis specifically refers to inflammation of the middle layer of the eye, termed the "uvea" but in common usage may refer to any inflammatory process involving the interior of the eye.

Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States.[citation needed] Uveitis requires an urgent referral and thorough examination by an optometrist or an ophthalmologist, along with urgent treatment to control the inflammation.

Types

Uveitis is usually categorized anatomically into anterior, intermediate, posterior and panuveitic forms.

* Anywhere from two-thirds to 90% of uveitis cases are anterior in location (anterior uveitis), frequently termed iritis - or inflammation of the iris and anterior chamber. This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature. Symptoms include red eye, injected conjunctiva, pain and decreased vision. Signs include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates ("KP") on the posterior surface of the cornea.
* Intermediate uveitis consists of vitritis - inflammatory cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana.
* Posterior uveitis is the inflammation of the retina and choroid.
* Pan-uveitis is the inflammation of all the layers of the uvea.

Causes

A myriad of conditions can lead to the development of uveitis, including systemic diseases as well as syndromes confined to the eye. In anterior uveitis, no specific diagnosis is made in approximately one-half of cases. However, anterior uveitis is often one of the syndromes associated with HLA-B27.

Systemic disorders causing uveitis

Systemic disorders that can cause uveitis include: White G. "Uveitis." AllAboutVision.com. Retrieved August 20, 2006.

* Acute posterior multifocal placoid pigment epitheliopathy
* Ankylosing spondylitis
* Behçet's disease
* Birdshot retinochoroidopathy
* Brucellosis
* Herpes simplex
* Herpes zoster
* Inflammatory bowel disease
* Juvenile rheumatoid arthritis
* Kawasaki's disease
* Leptospirosis
* Lyme disease
* Multiple sclerosis
* Presumed ocular histoplasmosis syndrome
* Psoriatic arthritis
* Reiter's syndrome
* Sarcoidosis
* Syphilis
* Systemic lupus erythematosus
* Toxocariasis
* Toxoplasmosis
* Tuberculosis
* Vogt-Koyanagi-Harada syndrome

Masquerade syndromes

Masquerade syndromes are ophthalmic disorders that clinically present as either an anterior or posterior uveitis, but are not primarily inflammatory. The following are some of the most common:

* Anterior segment

* Intraocular foreign body
* Juvenile xanthogranuloma
* Leukemia
* Malignant melanoma
* Retinoblastoma
* Retinal detachment

* Posterior segment

* Lymphoma
* Malignant melanoma
* Multiple sclerosis
* Reticulum cell sarcoma
* Retinitis pigmentosa
* Retinoblastoma

Symptoms

* Redness of the eye
* Blurred vision
* Sensitivity to light
* Dark, floating spots along the visual field
* Eye pain

Treatment

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication (including cataracts, glaucoma, band keratopathy, retinal edema and permanent vision loss) may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor in to the outlook.[1]

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (such as betamethasone, dexamethasone or prednisolone) or oral therapy with prednisolone tablets. In addition topical cycloplegics, such as atropine or homatropine, may be used.[1]

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatment with Infliximab infusions may prove helpful.

See also

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

Footnotes

1. ^ BNF 45 March 2003

All About Iritis

Iritis is a form of anterior uveitis and refers to the inflammation of the iris of the eye.

Types

There are two main types of iritis, which are called acute iritis and chronic iritis. Acute iritis is a type of iritis that can heal independantly within a few weeks. If treatment is provided, acute iritis improves quickly. Chronic iritis can exist for months or years before recovery occurs. Chronic iritis does not respond to treatment as well as acute iritis does. Chronic iritis is also accompanied by a higher risk of serious visual impairment.

Signs and symptoms

* Ocular and periorbital pain
* Photophobia
* Consensual photophobia (pain in affected eye when light is shone in unaffected eye)
* Blurred or cloudy vision
* White blood cells (leukocytes) (resulting in a grey or near-white haze) and protein (resulting in tiny white dots) in the anterior chamber, often called "cells and flare."
* Synechia or adhesion of iris to lens or cornea

Causes

People with ankylosing spondylitis and other HLA-B27 related disorders are prone to iritis, iridocyclitis, and other forms of uveal tract inflammation. Iritis is also found in those with rheumatoid arthritis, Behcet's disease, Crohn's disease, lupus, Reiter's disease, chronic psoriasis, psoriatic arthritis, sarcoidosis, scleroderma, and ulcerative colitis. Iritis is usually secondary to some other systemic condition, but can be the only apparent somatic symptom.

Complications

Complications of iritis may include the following: Cataract, glaucoma, corneal calcification, posterior uveitis, blindness, band keratopathy, and cystoid macular oedema.

Treatment

* Steroid anti-inflammatory eye drops (such as prednisolone acetate)
* Dilating eye drops (to help prevent synechia and reduce photophobia)
* Pressure-reducing eye drops (such as brimonidine tartrate)
* Oral steroids (such as prednisone)
* Subconjunctival steroid injections
* Steroid-sparing agents such as methotrexate (for prolonged, chronic iritis)

References

* Care of the Patient with Anterior Uveitis (CPG7) (PDF)
* Iritis Organization
* Assessment of the Red Eye - Iritis
* Medical Info on Iritis

All About Keratoconjunctivitis sicca

Keratoconjunctivitis sicca (KCS), also called keratitis sicca,[1] sicca syndrome,[1] xerophthalmia,[1] dry eye syndrome (DES),[1] or simply dry eyes,[1] is an eye disease caused by decreased tear production or increased tear film evaporation commonly found in humans and some animals[2]. Keratoconjunctivitis sicca is Latin and its literal translation is "dryness of the cornea and conjunctiva".

Symptoms

Typical symptoms of keratoconjunctivitis are dryness, burning[3] and a sandy-gritty eye irritation that gets worse as the day goes on.[1] Symptoms may also be described as itchy,[3] scratchy,[4] stingy[3] or tired[3] eyes. Other symptoms are pain,[5] redness,[5] a pulling sensation,[3] and pressure behind the eye[3]. There may be a feeling that something,[3] such as a speck of dirt,[5] is in the eye. The resultant damage to the eye surface increases discomfort and sensitivity to bright light.[3] Both eyes usually are affected.[6]

There may also be a stringy discharge from the eyes.[5] Although it may seem strange, dry eye can cause the eyes to water.[5] This can happen because the eyes are irritated.[5] One may experience excessive tearing in the same way as one would if something got into the eye.[5] These reflex tears will not necessarily make the eyes feel better.[5] This is because they are the watery type that are produced in response to injury, irritation, or emotion.[5] They do not have the lubricating qualities necessary to prevent dry eye.[5]

Because blinking coats the eye with tears,[5] symptoms are worsened by activities in which the rate of blinking is reduced due to prolonged use of the eyes[3]. These activities include prolonged reading,[1] computer usage,[1][5][3] driving,[3] or watching television[5][3]. Symptoms increase in windy,[5] dusty[5][3] or smoky (including cigarette smoke[5]) areas,[1][3] in dry environments[1][3], high altitudes including airplanes,[6] on days with low humidity,[3] and in areas where an air conditioner[5] (especially in a car[3]), fan,[3] heater,[3] or even a hair dryer[5] is being used. Symptoms reduce during cool, rainy, or foggy weather and in humid places, such as in the shower.[3]

Most people who have dry eyes experience mild irritation with no long-term effects.[5] However, if the condition is left untreated or becomes severe, it can produce complications that can cause eye damage,[5] resulting in impaired vision or (rarely[3]) in the loss of vision[5].

Symptom assessment is a key component of dry eye diagnosis - to the extent that many believe dry eye syndrome to be a symptom-based disease. Several questionnaires have been developed to determine a score that would allow for dry eye diagnosis. McMonnies & Ho dry eye questionnaire is the one that is often used in clinical studies of dry eyes. There are 14 questions that can give a score from 0 to 45. Scores above 14.5 are consistent with dry eye diagnosis.

Pathophysiology

Having dry eyes for a while can lead to tiny abrasions on the surface of the eyes.[4] In advanced cases, the epithelium undergoes pathologic changes, namely squamous metaplasia and loss of goblet cells.[1] Some severe cases result in thickening of the corneal surface,[3] corneal erosion,[1] punctate keratopathy,[1] epithelial defects,[1] corneal ulceration (sterile and infected),[1] corneal neovascularization,[1] corneal scarring,[1][3] corneal thinning,[1] and even corneal perforation[1].

Causes

Any abnormality of any one of the three layers of tears produces an unstable tear film, resulting in symptoms of keratitis sicca.[1]

Deficient tear production

Keratoconjunctivitis sicca is usually due to inadequate tear production.[1][3] The aqueous tear layer is affected, resulting in aqueous tear deficiency (ATD) or lacrimal hyposecretion.[1] The lacrimal gland does not produce sufficient tears to keep the entire conjunctiva and cornea covered by a complete layer.[3] This usually occurs in people who are otherwise healthy. Increased age is associated with decreased tearing.[1] This is the most common type found in postmenopausal women.[3][7]

Causes include idiopathic, congenital alacrima, xerophthalmia, lacrimal gland ablation, and sensory denervation.[1] In rare cases, it may be a symptom of collagen vascular diseases, including rheumatoid arthritis[3], Wegener's granulomatosis, and systemic lupus erythematosus.[1] Sjögren's syndrome[3] and autoimmune diseases associated with Sjögren's syndrome are also conditions associated with aqueous tear deficiency.[1] Drugs such as isotretinoin,[3] sedatives,[3][6] diuretics,[3] tricyclic antidepressants,[6] antihypertensives,[3] oral contraceptives,[1][3] antihistamines,[1][5][3] nasal decongestants,[5] beta-blockers,[1] phenothiazines,[1] atropine,[1], and pain relieving opiates such as morphine[6] can cause or worsen this condition. Infiltration of the lacrimal glands by sarcoidosis or tumors, or postradiation fibrosis of the lacrimal glands can also cause this condition.[1]

Abnormal tear composition

Keratoconjunctivitis sicca can also be caused by abnormal tear composition resulting in rapid evaporation[3] or premature destruction of the tears.[1] When caused by rapid evaporation, it is termed evaporative dry eyes.[3] In this, although the tear gland produces a sufficient amount of tears, the rate of evaporation of the tears is too rapid.[3] There is a loss of water from the tears that results in tears that are too "salty" or hypertonic. As a result, the entire conjunctiva and cornea cannot be kept covered with a complete layer of tears during certain activities or in certain environments.[3]

Additional causes

Aging is one of the most common causes of dry eyes.[5] This is because tear production decreases with age.[5] It may be caused by thermal or chemical burns, or (in epidemic cases) by adenoviruses. A number of studies have found that diabetics are at increased risk for the disease.[8][9]

An eye injury or other problem with the eyes or eyelids, such as bulging eyes or a drooping eyelid can cause keratoconjunctivitis sicca.[4] Disorders of the eyelid can impair the complex blinking motion required to spread tears.[6]

About half of all people who wear contact lenses complain of dry eyes.[5] This is because soft contact lenses, which float on the tear film that covers the cornea, absorb the tears in the eyes.[5] Dry eyes also occurs or gets worse after LASIK and other refractive surgeries, in which the corneal nerves are cut during the creation of a corneal flap.[5] The corneal nerves stimulate tear secretion.[5] Dry eyes caused by these procedures usually resolves after several months.[6] Persons who are thinking about refractive surgery should consider this.[5]

Abnormalities of the lipid tear layer caused by blepharitis and rosacea, and abnormalities of the mucin tear layer caused by vitamin A deficiency, trachoma, diphtheric keratoconjunctivitis, mucocutaneous disorders and certain topical medications are causes of keratoconjunctivitis sicca.[1]

Persons with keratoconjunctivitis sicca have elevated levels of tear nerve growth factor (NGF).[1] It is possible that this ocular surface NGF plays an important role in ocular surface inflammation associated with dry eyes.[1]

Diagnosis

Dry eyes can usually be diagnosed by the symptoms alone.[3] Tests can determine both the quantity and the quality of the tears.[6] A slit lamp examination can be performed to diagnose dry eyes and to document any damage to the eye.[1][3]

A Schirmer's test can measure the amount of moisture bathing the eye.[3] This test is useful for determining the severity of the condition.[5] A five-minute Schirmer's test with and without anesthesia using a Whatman #41 filter paper 5 mm wide by 35 mm long is performed.[1] For this test, wetting under 5 mm with or without anesthesia is considered diagnostic for dry eyes.[1]

If the results for the Schirmer's test are abnormal, a Schirmer II test can be performed to measure reflex secretion.[1] In this test, the nasal mucosa is irritated with a cotton-tipped applicator, after which tear production is measured with a Whatman #41 filter paper.[1] For this test, wetting under 15 mm after five minutes is considered abnormal.[1]

A tear breakup time (TBUT) test measures the time it takes for tears to break up in the eye.[5] The tear breakup time can be determined after placing a drop of fluorescein in the cul-de-sac.[1]

A tear protein analysis test measures the lysozyme contained within tears.[1] In tears, lysozyme accounts for approximately 20 to 40 percent of total protein content.[1]

A lactoferrin analysis test provides good correlation with other tests.[1]

Recently it was described a molecule - Ap4A- which is intrinsic component of the tears. The presence of this molecule is abnormally high in different states of the ocular dryness. This molecule could quantifyied biochemically simply taking one tear sample with a plain Schirmer test. Utilizing this technique is possible to determine the concentrations of Ap4A in the tear of the patients and such way to diagnose in an objective way if the samples are corresponding to dry eye[10].

Treatment

Purposefully blinking more often, and resting the eyes are basic steps one can take.[4] Rubbing one's eyes can irritate them further, so it should be avoided.[6] Persons with dry eyes caused by an eyelid disorder should undergo treatment for the underlying condition.[6]

Rehydration

For mild and moderate cases, supplemental lubrication is the most important part of treatment.[1]

Artificial tears

Main article: Artificial tears

Application of artificial tears every few hours[3] can provide temporary relief.

Additional options

Lubricating tear ointments can be used during the day, but they generally are used at bedtime due to poor vision after application.[1] They contain white petrolatum, mineral oil, and similar lubricants.[1] They serve as a lubricant and an emollient.[1] Application requires pulling down the eyelid and applying a small amount (0.25 in) inside.[1] Depending on the severity of the condition, it may be applied from every hour to just at bedtime.[1] It should not be used with contact lenses.[1]

Environmental control

Avoiding dry or drafty environments, or environments with smoke and dust may help.[3] This also includes avoiding environmental aggravation caused by hair dryers, heaters, air conditioners or fans, especially when directed toward the eyes.[6] Wearing wraparound glasses when outside can help reduce the drying effects of the wind.[6]

Using a humidifier,[3][4] especially in the winter,[4] adds moisture[6] to dry indoor air. Specially designed glasses that form a moisture chamber around the eye may be used to create additional humidity.[6]

Supplementation

Consumption of dietary omega-3 fatty acids is associated with a decreased incidence of dry eyes syndrome in women.[11] This finding is consistent with postulated biological mechanisms.[11]

Medication

Inflammation occurring in response to tears film hypertonicity can be suppressed by mild topical steroids or with topical immunosuppressants such as ciclosporin.[12][13] Elevated levels of tear NGF can be decreased with 0.1% prednisolone.[1]

Restasis

Topical ciclosporin A (tCSA) 0.05% ophthalmic emulsion, marketed in the United States by Allergan under the trade name Restasis[1], is the only prescription product for chronic dry eyes.[5] Approved by the U.S. Food and Drug Administration in 2002,[5] the drug decreases inflammation[6] on the eye surface. It increases healthy tear production,[6] which may be reduced because of inflammation on the eye surface.[5] In a clinical trial involving 1,200 individuals, Restasis increased tear production in 15 percent of patients, compared with 5 percent of patients in the placebo group.[5]

Usually, 1 gtt of Restasis is applied twice a day, 12 hours apart.[1] It should not be used when wearing contact lenses,[1] or by persons with eye infections[5] or hypersensitivity[5] to the ingredients. It has not been tested in people with herpes viral infections of the eye,[5] and it should not be used by anyone with a history[6] of such an infection. The most common side effect is a burning sensation.[5] Other side effects may be eye redness, discharge, watery eyes, eye pain, foreign body sensation, itching, stinging, and blurred vision.[1][5]

Generic alternatives

Cheaper generic alternatives to Restasis are available in some countries. In India, it is marketed as Cyclomune by Sun Pharma.[14]

Conserving tears

There are methods that allow both natural and artificial tears to stay longer.[6]

Blocking tear drainage

In each eye, there are two puncta[15] — little openings that drain tears into the tear ducts[5]. There are methods to partially or completely close the tear ducts.[6] This blocks the flow of tears into the nose, and thus more tears are available to the eyes.[3]

Punctal plugs

Punctal plugs are inserted into the puncta to block tear drainage.[5] For people who have not found dry eye relief with drugs, punctal plugs may help.[5] They are reserved for people with moderate or severe dry eye when other medical treatment has not been adequate.[5]

A temporary punctal occlusion can be inserted and tried first.[1][5] These are made of collagen and are dissolvable.[1][5] This is to ascertain that permanent ones will not cause excessive tearing.[5]

Permanent punctal plugs are usually made of silicone.[5] Some plugs are made of thermally reactive material.[5] Some of these are inserted into the punctum as a liquid and then they harden and conform to the individual's drainage system.[5] Others start out rigid and become soft and flexible, adapting to the individual's punctal size after they are inserted.[5]

Artificial tears are usually still required after punctal plug insertion.[5]

The risks of punctal plugs are fairly minimal.[5] There is a risk of eye irritation, excessive tearing, and, in rare cases, infection.[5]

Cauterization

If punctal plugs are effective, thermal[6] or electric[1] cauterization of puncti can be performed.

In thermal cauterization, a local anesthetic is used, and then a hot wire is applied.[6] This shrinks the drainage area tissues and causes scarring, which closes the tear duct.[6]

Customized contact lenses

Persons with severe dry eyes may benefit from the Boston Scleral Lens which is a customized contact lense.[6] Resting on the sclera, it creates a fluid filled layer over the cornea, thus preventing it from drying.[6]

Surgery

In severe cases of keratoconjunctivitis sicca, the eyelids may be partially sewn together to reduce tear evaporation.[3]

Prognosis

Keratoconjunctivitis sicca usually is a chronic problem.[6] Its prognosis shows considerable variance, depending upon the severity of the condition.[1] Most patients have mild-to-moderate cases, and can be treated symptomatically with lubricants.[1] This provides an adequate relief of symptoms.[1]

When dry eyes symptoms are severe, they can interfere with quality of life.[5] People sometimes feel their vision blurs with use,[3] or severe irritation[3] to the point that they have trouble keeping their eyes open[5] or they may not be able to work or drive[5].

Prevention

There is no way to prevent keratoconjunctivitis sicca.[16] Complications can be prevented by use of wetting and lubricating drops and ointments.[16]

Epidemiology

Keratoconjunctivitis sicca is relatively common within the United States, especially so in older patients.[1] Specifically, the persons most likely to be affected by dry eyes are those aged 40 or older.[6]

While persons with autoimmune diseases have a have a high likelihood of having dry eyes, most persons with dry eyes do not have an autoimmune disease.[6] Instances of Sjögren syndrome and keratoconjunctivitis sicca associated with it are present much more commonly in women, with a ratio of 9:1.[1] In addition, milder forms of keratoconjunctivitis sicca also are more common in women.[1] This is partly because hormonal changes,[6] such as those that occur in pregnancy, menstruation, and menopause,[6] can decrease tear production.[5]

In areas of the world where malnutrition is common, vitamin A deficiency is a common cause.[16] This is rare in the United States.[16]

Racial predilections do not exist for this disease.[1]

Occurrence in animals

Among animals, keratoconjunctivitis sicca occurs in dogs, cats, and horses.[2]

Dogs

Keratoconjunctivitis sicca is common in dogs. Most cases are caused by a genetic predisposition, but chronic conjunctivitis, canine distemper, and drugs such as sulfasalazine and trimethoprim-sulfonamide also cause the disease.[17] Symptoms include eye redness, a yellow or greenish discharge, ulceration of the cornea, pigmented cornea, and blood vessels on the cornea. Diagnosis is made by measuring tear production with a Schirmer tear test. Less than 15 millimeters of tears produced in a minute is abnormal.[17]

Tear replacers are a mainstay of treatment, preferably containing methylcellulose or carboxymethyl cellulose.[17] Ciclosporin stimulates tear production and acts as a suppressant on the immune-mediated processes that cause the disease. Topical antibiotics and corticosteroids are sometimes used to treat secondary infections and inflammation. A surgery known as parotid duct transposition is used in some extreme cases where medical treatment has not helped. This redirects the duct from the parotid salivary gland to the eye. Saliva replaces the tears. Dogs suffering from cherry eye should have the condition corrected to help prevent this disease.

Commonly affected breeds include:

* Cavalier King Charles Spaniel
* English Bulldog
* Chinese Shar-Pei
* Lhasa Apso
* Shih Tzu
* West Highland White Terrier
* Pug
* Bloodhound
* Cocker Spaniel
* Pekingese
* Boston Terrier
* Miniature Schnauzer
* Samoyed[17]

Cats

Keratoconjunctivitis sicca is uncommon in cats. Most cases seem to be caused by chronic conjunctivitis, especially secondary to feline herpesvirus.[17] Diagnosis, symptoms, and treatment are similar to those for dogs.

See also

* Keratoconjunctivitis
* List of eye diseases and disorders

References

1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp Keratoconjunctivitis, Sicca. eMedicine. WebMD, Inc. (2006-04-21). Retrieved on 2006-11-12.
2. ^ a b Keratoconjunctivitis, Sicca. The Merck Veterinary Manual. Merck & Co., Inc.. Retrieved on 2006-11-18.
3. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av Keratoconjunctivitis Sicca. The Merck Manual, Home Edition. Merck & Co., Inc. (2003-02-01). Retrieved on 2006-11-12.
4. ^ a b c d e f Dry eyes. MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine (2006-10-04). Retrieved on 2006-11-16.
5. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg Meadows, Michelle (May-June 2005). Dealing with Dry Eye. FDA Consumer Magazine. U.S. Food and Drug Administration. Retrieved on 2006-11-16.
6. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac Dry eyes. Mayo Clinic. Mayo Foundation for Medical Education and Research (2006-06-14). Retrieved on 2006-11-17.
7. ^ Sendecka M, Baryluk A, Polz-Dacewicz M (2004). "Prevalence and risk factors of dry eye syndrome". Przegl Epidemiol 58 (1): 227-33. PMID 15218664.
8. ^ Kaiserman I, Kaiserman N, Nakar S, Vinker S (2005). "Dry eye in diabetic patients.". Am J Ophthalmol 139 (3): 498-503. PMID 15767060.
9. ^ Li H, Pang G, Xu Z (2004). "Tear film function of patients with type 2 diabetes". Zhongguo Yi Xue Ke Xue Yuan Xue Bao 26 (6): 682-6. PMID 15663232.
10. ^ A. Peral, G. Carracedo, M.C. Acosta, J. Gallar, J. Pintor."Increasing Levels of Diadenosine Polyphosphates in Dry Eye" (2006)Invest.Ophthalmol. Vis. Sci.47 (9):4053–4058 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed]
11. ^ a b Miljanović B, Trivedi K, Dana M, Gilbard J, Buring J, Schaumberg D (2005). "Relation between dietary n-3 and n-6 fatty acids and clinically diagnosed dry eye syndrome in women.". Am J Clin Nutr 82 (4): 887-93. PMID 16210721.
12. ^ Tatlipinar S, Akpek E (2005). "Topical ciclosporin in the treatment of ocular surface disorders.". Br J Ophthalmol 89 (10): 1363-7. PMID 16170133.
13. ^ Barber L, Pflugfelder S, Tauber J, Foulks G (2005). "Phase III safety evaluation of cyclosporine 0.1% ophthalmic emulsion administered twice daily to dry eye disease patients for up to 3 years.". Ophthalmology 112 (10): 1790-4. PMID 16102833.
14. ^ Sun Pharma Product List. Sun Pharma. Retrieved on 2006-11-27.
15. ^ Dry eye syndrome. Health encyclopaedia. NHS Direct (2006-04-10). Retrieved on 2007-02-26.
16. ^ a b c d Dry eyes syndrome. MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine (2006-10-04). Retrieved on 2006-11-16.
17. ^ a b c d e Gelatt, Kirk N. (ed.) (1999). Veterinary Ophthalmology, 3rd ed., Lippincott, Williams & Wilkins. ISBN 0-683-30076-8.

Further reading

* The Dry Eye: A Practical Approach, by Sudi Patel, Kenny Blades, 2003, Butterworth-Heinemann, ISBN 0-7506-4978-X
* Dry Eye Disease: The Clinician's Guide to Diagnosis And Treatment, by Penny A. Asbell, Michael A. Lemp, 2006, Thieme Medical Publishers, ISBN 1-58890-412-1