Eye Ailments

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

2008-07-18T20:38:00.001-07:00

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

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

Worm Removed From Eye

2007-06-02T23:23:00.000-07:00

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

Guy's Eye Pops Out

2007-06-02T17:19:00.000-07:00

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

All About Macular degeneration

2007-04-03T14:45:00.004-07:00

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

2007-04-03T14:45:00.003-07:00

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

2007-04-03T14:45:00.002-07:00

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

2007-04-03T14:45:00.001-07:00

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

2007-04-03T14:45:00.000-07:00

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

2007-04-03T04:25:00.005-07:00

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

2007-04-03T04:25:00.004-07:00

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

2007-04-03T04:25:00.003-07:00

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

2007-04-03T04:25:00.002-07:00

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

2007-04-03T04:25:00.001-07:00

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

2007-04-03T04:25:00.000-07:00

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 MiljanoviÄ‡ 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

All About Keratoconus

2007-04-02T23:50:00.032-07:00

Keratoconus (from Greek: kerato- horn, cornea; and konos cone), is a degenerative non-inflammatory disorder of the eye in which structural changes within the cornea cause it to thin and change to a more conical shape than its normal gradual curve. Keratoconus can cause substantial distortion of vision, with multiple images, streaking and sensitivity to light all often reported by the patient. Keratoconus is the most common dystrophy of the cornea, affecting around one person in a thousand, and it seems to occur in all ethnic groups worldwide, although for some groups the prevalence of keratoconus is greater than others. It is typically diagnosed in the patient's adolescent years and attains its most severe state in the twenties and thirties.

Keratoconus is a little-understood disease with an uncertain cause, and its progression following diagnosis is unpredictable. If afflicting both eyes, the deterioration in vision can affect the patient's ability to drive a car or read normal print. It does not however lead to blindness, and in most cases, corrective lenses are effective enough to allow the patient to continue to drive legally and likewise function normally. Further progression of the disease may lead to a need for surgery. Despite its uncertainties, keratoconus can be successfully managed with a variety of clinical and surgical techniques, and often with little or no impairment to the patient's quality of life.

In a 1748 doctoral dissertation, the German oculist Burchard Mauchart provided an early description of a case of keratoconus, which he called staphyloma diaphanum. However, it was not until 1854 that British physician John Nottingham clearly described keratoconus and distinguished it from other ectasias of the cornea.[1] Nottingham reported the cases of "conical cornea" that had come to his attention, and described several classic features of the disease, including polyopia, weakness of the cornea, and difficulty matching corrective lenses to the patient's vision. In 1859 British surgeon William Bowman used an ophthalmoscope (recently invented by German physician and physicist Hermann von Helmholtz) to diagnose keratoconus, and described how to angle the instrument's mirror so as to best see the conical shape of the cornea.[2] Bowman also attempted to restore the vision by pulling on the iris with a fine hook inserted through the cornea and stretching the pupil into a vertical stenopeic slit like that of a cat. He reported that he had had a measure of success with the technique, restoring vision to an 18-year old woman who had previously been unable to count fingers at a distance of 8 inches (20 cm). By 1869, when the pioneering Swiss ophthalmologist Johann Horner wrote a thesis entitled On the treatment of keratoconus,[3] the disorder had acquired its current name. The treatment at that time, endorsed by the leading German ophthalmologist Albrecht von Gräfe, was an attempt to physically reshape the cornea by chemical cauterization with a silver nitrate solution and application of a miosis-causing agent with a pressure dressing. In 1888 the treatment of keratoconus became one of the first practical applications of the then newly-invented contact lens, when the French physician Eugène Kalt manufactured a glass scleral shell which improved vision by compressing the cornea into a more regular shape.[4] Since the start of the twentieth century, research on keratoconus has both improved understanding of the disease and greatly expanded the range of treatment options.

Features

Symptoms
A simulation of the multiple images seen by a person with keratoconus. "... a candle, when looked at, appears like a number of lights, confusedly running into one another" — Nottingham
A simulation of the multiple images seen by a person with keratoconus.
"... a candle, when looked at, appears like a number of lights, confusedly running into one another" — Nottingham[1]

People with early keratoconus typically notice a minor blurring of their vision and come to their clinician seeking corrective lenses for reading or driving. At early stages, the symptoms of keratoconus may be no different from those of any other refractive defect of the eye. As the disease progresses, vision deteriorates, sometimes rapidly. Visual acuity becomes impaired at all distances, and night vision is often quite poor. Some individuals have vision in one eye that is markedly worse than that in the other eye. Some develop photophobia (sensitivity to bright light), eye strain from squinting in order to read, or itching in the eye. There is usually little or no sensation of pain.

The classic symptom of keratoconus is the perception of multiple 'ghost' images, known as monocular polyopia. This effect is most clearly seen with a high contrast field, such as a point of light on a dark background. Instead of seeing just one point, a person with keratoconus sees many images of the point, spread out in a chaotic pattern. This pattern does not typically change from day to day, but over time it often takes on new forms. Patients also commonly notice streaking and flaring distortion around light sources. Some even notice the images moving relative to one another in time with their heart beat.

Signs and diagnosis

Prior to any physical examination, the diagnosis of keratoconus frequently begins with an ophthalmologist's or optometrist's assessment of the patient's medical history, particularly the chief complaint and other visual symptoms, the presence of any history of ocular disease or injury which might affect vision, and the presence of any family history of ocular disease. An eye chart, such as a standard Snellen chart of progressively smaller letters, is then used to determine the patient's visual acuity. The eye examination may proceed to measurement of the localised curvature of the cornea with a manual keratometer,[5] with detection of irregular astigmatism suggesting a possibility of keratoconus. Severe cases can exceed the instrument's measuring ability. A further indication can be provided by retinoscopy, in which a light beam is focused on the patient's retina and the reflection, or reflex, observed as the examiner tilts the light source back and forth. Keratoconus is amongst the ophthalmic conditions that exhibit a scissor reflex action of two bands moving toward and away from each other like the blades of a pair of scissors.[6]

If keratoconus is suspected, the ophthalmologist or optometrist will search for other characteristic findings of the disease by means of slit lamp examination of the cornea. An advanced case is usually readily apparent to the examiner, and can provide for an unambiguous diagnosis prior to more specialised testing. Under close examination, a ring of yellow-brown to olive-green pigmentation known as a Fleischer ring can be observed in around half of keratoconic eyes.[7] The Fleischer ring, caused by deposition of the iron oxide hemosiderin within the corneal epithelium, is subtle and may not be readily detectable in all cases, but becomes more evident when viewed under a cobalt blue filter. Similarly, around 50% of subjects exhibit Vogt's striae, fine stress lines within the cornea caused by stretching and thinning.[7] The striae temporarily disappear while slight pressure is applied to the eyeball. A highly pronounced cone can create a V-shaped indentation in the lower eyelid when the patient's gaze is directed downwards, known as Munson's sign. Other clinical signs of keratoconus will normally have presented themselves long before Munson's sign becomes apparent,[8] and so this finding, though a classic sign of the disease, tends not to be of primary diagnostic importance.

Corneal topogram of a keratoconic eye

A handheld keratoscope, sometimes known as Placido's disk, can provide a simple non-invasive visualization of the surface of the cornea by projecting a series of concentric rings of light onto the cornea. A more definitive diagnosis can be obtained using corneal topography, in which an automated instrument projects the illuminated pattern onto the cornea and determines its topology from analysis of the digital image. The topographical map indicates any distortions or scarring in the cornea, with keratoconus revealed by a characteristic steepening of curvature which is usually below the centreline of the eye. The technique can record a snapshot of the degree and extent of the deformation as a benchmark for assessing its rate of progression. It is of particular value in detecting the disorder in its early stages when other signs have not yet presented.[9]

Once keratoconus has been diagnosed, its degree may be classified by several metrics:[10][11]

* The steepness of greatest curvature from mild (< 45 D), advanced (up to 52 D) or severe (> 52 D);
* The morphology of the cone: nipple (small: 5 mm and near-central), oval (larger, below-center and often sagging), or globus (more than 75% of cornea affected);
* The corneal thickness from mild (> 506 μm) to advanced (< 446 μm).

Increasing use of corneal topography has led to a decline in use of these terms.[11]

Epidemiology

The National Eye Institute reports that keratoconus is the most common corneal dystrophy in the United States, affecting approximately 1 in 2,000 Americans,[12][13] but some reports place the figure as high as 1 in 500.[14] The inconsistency may be due to variations in diagnostic criteria, with some cases of severe astigmatism interpreted as those of keratoconus, and vice versa.[8] A long-term study found a mean incidence rate of 2.0 new cases per 100,000 population per year.[13] It is suggested that males and females, and all ethnicities appear equally susceptible, though some recent studies have cast doubt upon this,[15] suggesting a higher prevalence amongst females; the literature however varying as to its extent. Also, a study carried out in the UK[16] suggests that people of an Asian heritage are 4.4 times as likely to suffer from keratoconus as Caucasians, and are also more likely to be affected with the condition earlier.

Keratoconus is normally bilateral[13] (affecting both eyes) although the distortion is usually asymmetric and is rarely completely identical in both corneas. Unilateral cases tend to be uncommon, and may in fact be very rare if a very mild condition in the better eye is simply below the limit of clinical detection.[8] It is common for keratoconus to be diagnosed first in one eye and not until later in the other. As the condition then progresses in both eyes, the vision in the earlier-diagnosed eye will often persist to be poorer than that in its fellow.

Prognosis

Patients with keratoconus typically present initially with mild astigmatism, commonly at the onset of puberty, and are diagnosed as having the disease by the late teenage years or early 20s. In rare cases keratoconus can occur in children or not present until later adulthood. A diagnosis of the disease at an early age may indicate a greater risk of severity in later life.[17] Patients' vision will seem to fluctuate over a period of months, driving them to change lens prescriptions frequently but as the condition worsens, contact lenses become required in the majority of cases. The course of the disorder can be quite variable, with some patients remaining stable for years or indefinitely, while others progress rapidly or experience occasional exacerbations over a long and otherwise steady course. Most commonly, keratoconus progresses for a period of ten to twenty years[8] before the course of the disease generally ceases.
Corneal hydrops

In advanced cases, bulging of the cornea can result in a localized rupture of Descemet's membrane, an inner layer of the cornea. Aqueous humor from the eye's anterior chamber seeps into the cornea before Descemet's membrane reseals. The patient experiences pain and a sudden severe clouding of vision, with the cornea taking on a translucent milky-white appearance known as a corneal hydrops.[18] Although disconcerting to the patient, the effect is normally temporary and after a period of six to eight weeks the cornea usually returns to its former transparency. The recovery can be aided non-surgically by bandaging with an osmotic saline solution. Although a hydrops usually causes increased scarring of the cornea, occasionally it will benefit a patient by creating a flatter cone, aiding the fitting of contact lenses.[18] Very occasionally, in extreme cases, the cornea thins to the point that a partial rupture occurs, resulting in a small, bead-like swelling on the cornea that has been filled with fluid. When this occurs, a corneal transplant can become urgently necessary to avoid complete rupture and resulting loss of the eye.[18]

Pathophysiology and cause

Despite considerable research, the etiology of keratoconus remains somewhat of a mystery. According to the United States National Keratoconus Foundation,[19] it is likely that keratoconus can arise from a number of different factors: genetic, environmental or cellular, any of which may form the trigger for the onset of the disease. Once initiated, the disease normally develops by progressive dissolution of Bowman's layer, the membrane lying between the corneal epithelium and stroma. As the two come into contact, cellular and structural changes in the cornea adversely affect its integrity and lead to the bulging and scarring that are characteristic of the disorder. Within any individual keratoconic cornea, there may be found regions of degenerative thinning coexisting with regions undergoing wound healing.

The visual distortion experienced by the patient comes from two sources, one being the irregular deformation of the surface of the cornea; the other being scarring that occurs on its exposed highpoints. These factors act to form regions on the cornea that map an image to different locations on the retina and give rise to the symptom of monocular polyopia. The effect can worsen in low light conditions as the dark-adapted pupil dilates to expose more of the irregular surface of the cornea. Scarring appears to be an aspect of the corneal degradation; however, a recent, large, multi-center study suggests that abrasion by contact lenses may increase the likelihood of this finding by a factor of over two.[20]

A number of studies have indicated that keratoconic corneas show signs of increased activity by proteases, a class of enzymes that break some of the collagen cross-linkages in the corneal stroma, with a simultaneous reduced expression of protease inhibitors.[21] Other studies have suggested that reduced activity by the enzyme aldehyde dehydrogenase may be responsible for a build-up of free radicals and oxidising species in the cornea.[22] It seems likely that, whatever the pathogenetical process, the damage caused by activity within the cornea results in a reduction in its thickness and biomechanical strength.

A genetic predisposition to keratoconus has been observed,[23] with the disease running in certain families,[24] and incidences reported of concordance in identical twins. The frequency of occurrence in close family members is not clearly defined, though it is known to be considerably higher than that in the general population, and studies have obtained estimates ranging between 6% and 19%.[25] A responsible gene has not been identified: two studies involving isolated, largely homogenetic communities have contrarily mapped putative gene locations to chromosomes 16q and 20q.[25] However, most genetic studies agree on an autosomal dominant model of inheritance. Keratoconus is also diagnosed more often in people with Down syndrome, though the reasons for this link have not yet been determined.[26] Keratoconus has been associated with atopic diseases, which include asthma, allergies, and eczema, and it is not uncommon for several or all of these diseases to affect one person. A number of studies suggest that vigorous eye rubbing may contribute to the progression of keratoconus, and that patients should be discouraged from the practice.[27][28][29][30][31]

Treatment

Contact lenses

Main article: Contact lens

In early stages of keratoconus, spectacles can suffice to correct for the mild astigmatism. As the condition progresses, spectacles may no longer provide the patient with a satisfactory degree of visual acuity, and most clinical practitioners will move to managing the condition with contact lenses.
Rigid gas permeable lens for keratoconus

In keratoconic patients, contact lenses improve vision by means of tear fluid filling the gap between the irregular corneal surface and the smooth regular inner surface of the lens, thereby creating the effect of a smoother cornea. Many specialized types of contact lenses have been developed for keratoconus, and affected people may seek out both doctors specialized in conditions of the cornea, and contact-lens fitters who have experience managing patients with keratoconus. The irregular cone presents a challenge and the fitter will endeavour to produce a lens with the optimal contact, stability and steepness. Some trial-and-error fitting may prove necessary.[8]

Traditionally, contact lenses for keratoconus have been the 'hard' or rigid gas-permeable variety, although manufacturers have also produced specialized 'soft' or hydrophilic lenses. A soft lens has a tendency to conform to the conical shape of the cornea, thus diminishing its effect. To counter this, hybrid lenses have been developed which are hard in the centre and encompassed by a soft skirt. Soft or hybrid lenses do not however prove effective for every patient.[32]

Some patients also find good vision correction and comfort with a "piggyback" lens combination, in which gas permeable rigid lenses are worn over soft lenses, both providing a degree of vision correction.[33] One form of piggyback lens makes use of a soft lens with a countersunk central area to accept the rigid lens. Fitting a piggyback lens combination requires experience on the part of the lens fitter, and tolerance on the part of the keratoconic patient.

Scleral lenses are sometimes prescribed for cases of advanced or very irregular keratoconus; these lenses cover a greater proportion of the surface of the eye and hence can offer improved stability.[34] The larger size of the lenses may make them unappealing or uncomfortable to some, however their easier handling can find favour with patients with reduced dexterity, such as the elderly.

Surgical options

Corneal transplant

Main article: Cornea transplant

Corneal transplant for keratoconus, approximately 1 week after surgery. Multiple light reflections indicate folds in the cornea which later resolved.
Corneal transplant for keratoconus, approximately 1 week after surgery. Multiple light reflections indicate folds in the cornea which later resolved.

Between 10% and 25% of cases of keratoconus[19][35][36] will progress to a point where vision correction is no longer possible, thinning of the cornea becomes excessive, or scarring as a result of contact lens wear causes problems of its own, and a corneal transplantation or penetrating keratoplasty becomes required. Keratoconus is the most common grounds for conducting a penetrating keratoplasty, generally accounting for around a quarter of such procedures.[37] The corneal transplant surgeon trephines a lenticule of corneal tissue and then grafts the donor cornea to the existing eye tissue, usually using a combination of running and individual sutures. The cornea does not have a direct blood supply, and so donor tissue is not required to be blood type matched. Eye banks check the donor corneas for any disease or cellular irregularities.

The acute recovery period can take four to six weeks and full post-operative vision stabilization often takes a year or more but most transplants are very stable in the long term.[36] The National Keratoconus Foundation reports that penetrating keratoplasty has the most successful outcome of all transplant procedures, and when performed for keratoconus in an otherwise healthy eye, its success rate can be 95% or greater.[19] The sutures used usually dissolve over a period of three to five years but individual sutures can be removed during the healing process if they are causing irritation to the patient.

In the USA, corneal transplants (also known as corneal grafts) for keratoconus are usually performed under sedation as outpatient surgery. In other countries, such as Australia and the UK, the operation is commonly performed with the patient undergoing a general anaesthetic. All cases a require careful follow-up with an eye surgeon (ophthalmologist) for a number of years. Frequently, vision is greatly improved after the surgery, but even if the actual visual acuity does not improve, because the cornea is a more normal shape after the healing is completed, patients can more easily be fitted with corrective lenses. Complications of corneal transplants are mostly related to vascularization of the corneal tissue and rejection of the donor cornea. Vision loss is very rare, though difficult-to-correct vision is possible. When rejection is severe, repeat transplants are often attempted, and are frequently successful.[38] Keratoconus will not normally reoccur in the transplanted cornea; incidences of this have been observed, but are usually attributed to incomplete excision of the original cornea or inadequate screening of the donor tissue.[39] The long-term outlook for corneal transplants performed for keratoconus is usually favorable once the initial healing period is completed and a few years have elapsed without problems.

DALK transplants

One way of reducing the risk of rejection is to use a newer technique called a Deep Anterior Lamellar Keratoplasty, referred to as DALK. In a DALK graft, only the outermost epithelium and the main bulk of the cornea, the stroma, are replaced; the patient's rearmost endothelium layer is retained, giving some additional structural integrity to the post-graft cornea. Because a graft rejection usually begins in the endothelium, the chance of a rejection episode is greatly reduced.

Furthermore, it is possible to transplant tissue from a donor which has been freeze-dried. The freeze-drying process ensures that this tissue is dead, so there is no chance at all of a rejection.

Some surgeons prefer to remove the donor epithelium, others leave the donor's cells in place. Removing it can cause a slight improvement in overall vision, but a corresponding increase in visual recovery time.

Epikeratophakia

Rarely, a non-penetrating keratoplasty known as an epikeratophakia (or epikeratoplasty) may be performed in cases of keratoconus. The corneal epithelium is removed and a lenticule of donor cornea grafted on top of it. The procedure requires a greater level of skill on the part of the surgeon, and is less frequently performed than a penetrating keratoplasty as the outcome is generally less favorable. It may however be seen as an option in a number of cases, particularly for young patients.[40]

Corneal ring segment inserts

Main article: Intrastromal corneal ring segments

A pair of Intacs inserts.

A recent surgical alternative to corneal transplant is the insertion of intrastromal corneal ring segments. A small incision is made in the periphery of the cornea and two thin arcs of polymethyl methacrylate are slid between the layers of the corneal stroma on either side of the pupil, the incision then being closed. The segments push out against the curvature of the cornea, flattening the peak of the cone and returning it to a more natural shape. The procedure, carried out on an outpatient basis under local anaesthesia, offers the benefit of being reversible and even potentially exchangeable as it involves no removal of eye tissue.

The two principal types of intrastromal rings available are known by the trade names of Intacs and Ferrara rings. Intacs are flatter and less centrally placed than the prismatic Ferrara rings. Intacs were first approved by the Food and Drug Administration (FDA) in the United States in 1999 for myopia; this was extended to the treatment of keratoconus in July 2004.[41] Ferrara rings await FDA approval for keratoconus. A development on the concept involves the injection of a transparent synthetic gel into a channel bored through the stroma. As the gel polymerises, it stiffens and takes on similar properties to the pre-formed rings.[42]

Clinical studies on the effectiveness of intrastromal rings on keratoconus are in their early stages, and results have so far been generally encouraging,[43][44] though they have yet to enter into wide acceptance with all refractive surgeons. In common with a penetrating keratoplasty, the requirement for some vision correction in the form of hydrophilic (soft) contact lenses or spectacles may remain subsequent to the operation. Potential complications of intrastromal rings include accidental penetration through to the anterior chamber when forming the channel, post-operative infection of the cornea, and migration or extrusion of the segments.[44] The rings offer a good chance of vision improvement even in otherwise hard to manage eyes, but it is not guaranteed and in a few cases may worsen.

Radial keratotomy

Main article: Radial keratotomy

Radial keratotomy is a refractive surgery procedure where the surgeon makes a spoke-like pattern of incisions into the cornea to modify its shape. This early surgical option for myopia has been largely superseded by LASIK and other similar procedures. LASIK itself is absolutely contraindicated in keratoconus and other corneal thinning conditions – it cannot be used for people with keratoconus because removal of corneal stromal tissue will further damage their already thin and weak corneas.[45]

For similar reasons, radial keratotomy has also generally not been used for keratoconic patients.[46][47] However, an Italian clinic has reported some success with a modified asymmetric radial keratotomy procedure,[48] in which the incisions are confined to one sector of the eye. The corneal thickness is first measured using a pachymeter, then the surgeon makes cuts to a depth of 70-80% of the measured thickness. The patient may initially experience photophobia and fluctuation of vision after radial keratotomy, just as with other forms of refractive surgery.[48]

Corneal Collagen Crosslinking with Riboflavin (C3-R)

A new treatment which has shown success but which has not yet been approved in all countries is Corneal Collagen Crosslinking with Riboflavin (C3-R), a one-time application of riboflavin eye drops to the eye.[21][49] The riboflavin, when activated by approximately 30 minutes illumination with UV-A light, augments the collagen cross-links within the stroma and so recovers some of the cornea's mechanical strength. C3-R, developed at the Technische Universität Dresden, has been shown to slow or arrest the progression of keratoconus, and in some cases even reverse it, particularly when applied in combination with intracorneal ring segments. Clinical trials are continuing, and to date relatively few procedures have been performed but the technique is showing promise in treating early cases of the disease.[50] Corrective lenses may still be required after the treatment but it is hoped that it could limit further deterioration in the patient's vision and reduce the case for keratoplasty.

Related disorders

Several other non-inflammatory eye disorders, generally rarer than keratoconus, also cause thinning of the cornea:[8]

Keratoglobus
Keratoglobus is a very rare condition that may be genetically related to keratoconus. It causes corneal thinning, primarily at the margins, resulting in a spherical, slightly enlarged eye.
Pellucid marginal degeneration
Pellucid marginal degeneration causes thinning of a narrow (1-2 mm) band of the cornea, usually along the inferior corneal margin. It causes an irregular astigmatism that can often be corrected by spectacles.
Posterior keratoconus
Keratoconus and posterior keratoconus are distinct disorders, despite their similar names. Posterior keratoconus is a rare abnormality, usually congenital, which causes a non-progressive thinning of the inner surface of the cornea. Posterior keratoconus generally affects only a single eye.

See also

* List of eye diseases and disorders
* Ophthalmology

References

* Arffa R (1997). Grayson's Diseases of the Cornea. Chap. 17. Mosby. ISBN 0-8151-3654-4.
* Brown D. Research Overview. National Keratoconus Foundation. Retrieved on 2006-03-12.
* Burger D, Shovlin J, Zadnik K (2003). Keratoconus: Diagnosis & Management. Pacific University College of Optometry. Retrieved on 2006-03-12.
* Caroline P, Andre M, Kinoshita B, and Choo, J. Etiology, Diagnosis, and Management of Keratoconus: New Thoughts and New Understandings. Pacific University College of Optometry. Retrieved on 2006-03-12.
* Epstein A (2000). Keratoconus and related disorders (PDF). North Shore Contact Lens. Retrieved on 2006-03-12.
* Feder R, Kshettry P (2005). "Chap 78: Non-inflammatory Ectactic Disorders", in Edited: Krachmer J: Cornea. Mosby. ISBN 0-323-02315-0.
* Heverly V, Lowther G. Keratoconus. School of Optometry, Indiana University. Retrieved on 2006-03-12.
* Rabonitz Y (2004). "Ectatic Disorders of the Cornea", in Edited: Foster C et al.: The Cornea, 4th Ed.. ISBN 0-7817-4206-4.
* Yanoff M, Duker J (2004). Ophthalmology, 2nd Ed., Mosby. ISBN 0-323-01634-0.
* Zadnik K, Barr J (1999). Diagnosis, Contact Lens Prescribing, and Care of the Keratoconus Patient. Butterworth Heinemann. ISBN 0-7506-9676-1.

Notes

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46. ^ Colin J, Velou S. Current surgical options for keratoconus., J Cataract Refract Surg. 2003 Feb;29(2):379-86. PMID 12648653
47. ^ Bergmanson JP, Farmer EJ. A return to primitive practice? Radial keratotomy revisited. Cont Lens Anterior Eye. 1999;22(1):2-10. PMID 16303397
48. ^ a b Lombardi M, Abbondanza M Asymmetric radial keratotomy for the correction of keratoconus. J Refract Surg. 1997 May-Jun;13(3):302-7. PMID 9183763
49. ^ Spoerl E, Wollensak G, Dittert DD, Seiler T. Thermomechanical behavior of collagen-cross-linked porcine cornea. Ophthalmologica. 2004 Mar-Apr;218(2):136-40. PMID 15004504
50. ^ Guttman, C. "Early keratoconus responds to corneal cross-linking: Italian study shows significant improvement in UCVA, BSCVA", Ophthalmology Times, Nov 1, 2005.

All About Fuchs' dystrophy

2007-04-02T23:50:00.031-07:00

Fuchs' dystrophy, also known as Fuchs' endothelial dystrophy, is a slowly progressing corneal disease that usually affects both eyes and is slightly more common in women than in men. Although doctors can often see early signs of Fuchs' dystrophy in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

The condition was first described by Austrian Ernst Fuchs (1851-1930), for whom it is named.

Etiology

In Fuchs' dystrophy endothelial cells gradually deteriorate without any apparent reason (other than aging). Progressive endothelial cell loss causes relative influx of aqueous humor into the cornea, leading to swelling (corneal stromal edema), with resultant distorted vision. Eventually, the epithelium also becomes edematous, resulting more severe visual impairment. Focal areas or blisters of epithelial edema ("bullae") may be particularly painful.

Endothelial cell loss may be aggravated or accelerated by intraocular trauma or surgery. A common scenario involves excessive corneal edema following cataract surgery.

Signs and symptoms

At first, a person with Fuchs' dystrophy will awaken with blurred vision that will gradually clear during the day. This occurs because the cornea is normally thicker in the morning; it retains fluids during sleep that evaporate in the tear film while we are awake. As the disease worsens, this swelling will remain constant and reduce vision throughout the day.

Treatment

When treating the disease, doctors will try first to reduce the swelling with drops, ointments, or soft contact lenses. They also may instruct a person to use a hair dryer, held at arm's length or directed across the face, to dry out the epithelial blisters. This can be done two or three times a day.

When the disease interferes with daily activities, a person may need to consider having a corneal transplant to restore sight. The short-term success rate of corneal transplantation is quite good for people with Fuchs' dystrophy.

References

This article was originally based on content from the National Eye Institute web page Facts About The Cornea and Corneal Disease. The National Eye Institute (NEI) is one of the United States federal government's National Institutes of Health.

All About Corneal neovascularization

2007-04-02T23:50:00.030-07:00

Corneal neovascularization is the excessive ingrowth of blood vessels from the limbal vascular plexus into the cornea. One of the most common causes is contact lens wear.

Reduction of neovascularization has been achieved in rats by chemical cauterization.[1]

All About Thygeson's superficial punctate keratopathy

2007-04-02T23:50:00.029-07:00

Thygeson's superficial punctate keratopathy (TSPK) is a disease of the eyes. The causes of TSPK are not currently known, but details of the disease were first published in the Journal of the American Medical Association in 1950 by Phillips Thygeson - after whom it is named.

Symptoms

A patient with TSPK may complain of blurred vision, watery eyes, a sensation of having a foreign body stuck in the eye and sensitivity to bright light. On inspection with a slit lamp, tiny lumps can be found on the cornea of the eye. These lumps can be more easily seen after applying fluorescein or rose bengal dye eye-drops. The lumps appear to be randomly positioned on the cornea and they may appear and disappear over a period of time (with or without treatment).

TSPK may affect one or both eyes. When both eyes are affected, the tiny lumps found on the cornea may differ in number between eyes. The severity of the symptoms often vary during the course of the disease. The disease may appear to go into remission, only to later reappear after months or years.

Causes

The causes of TSPK are not currently known.

Treatment

There are a number of different treatments to deal with TSPK. Symptoms may disappear without treatment, but treatment may help increase time to and success of remission.

* Artificial tear eye-drops or ointments may be a suitable treatment for mild cases.
* Low-dosage steroidal eye-drops, such as prednisone, fluorometholone or rimexolone. Steroidal drops should be used with caution and the eye pressure should be regularly checked during treatment.
* Soft contact lenses.
* Cyclosporine is an experimental treatment for TSPK. It is usually used during transplants as it reduces the immune system response.
* Laser eye treatment.

Reference

* Thygeson P. Superficial punctate keratitis. J Am Med Assoc 1950;144:1544-9. PMID 14794375.

See also

* List of eye diseases and disorders

All About Arc eye

2007-04-02T23:50:00.028-07:00

Arc eye, also known as arc flash, welder's flash, corneal flash burns, or flash burns, is a painful ocular condition sometimes experienced by welders who have failed to use adequate eye protection. It can also occur due to light from tanning beds, light reflected from snow (known as snow blindness), water or sand. The intense ultraviolet light emitted by the arc causes a superficial and painful keratitis.

Symptoms tend to occur a number of hours after exposure and typically resolve spontaneously within 36 hours. The sensation has been described as having sand poured into the eyes.

This phenomenon results from intense levels of illumination, greater than that of more common over-illumination found in many factories and offices.

Standards

Four principal standards govern arc flash hazards :

* OSHA Standards 29-CFR, Part 1910. Occupational Safety and Health Standards. 1910 sub part S (electrical) Standard number 1910.333 specifically addresses Standards for Work Practices and references NFPA 70E.
* The National Fire Protection Association (NFPA) Standard 70 - 2002 “The National Electrical Code” (NEC) contains requirements for warning labels.
* NFPA 70E 2000 provides guidance on implementing appropriate work practices that are required to safeguard workers from injury while working on or near exposed electrical conductors or circuit parts that could become energized.
* The Institute of Electronics and Electrical Engineers (IEEE) 1584 – 2002 Guide to Performing Arc-Flash Hazard Calculations.

Arc flash hazard software exists that allow businesses to comply with the myriad of government regulations while providing their workforce with an optimally safe environment. Many software companies now offer arc flash hazard solutions.

Signs

* Intense lacrimation
* Blepharospasm
* Photophobia [1]
* Fluorescein dye staining will reveal corneal ulcers under blue light
* Constricted pupils note: this symptom may last as long as 96 to 128 hours in some cases.

Management

* Instill topical anaesthesia
* Inspect the cornea for any foreign body
* Patch the worse of the two eyes and prescribe analgesia
* Topical antibiotics in the form of eye drops or eye ointment or both should be prescribed for prophylaxis against infection

All About Snow blindness

2007-04-02T23:50:00.027-07:00

Snow blindness is a painful condition, typically a keratitis, caused by exposure of unprotected eyes to the ultraviolet (UV) rays in bright sunlight reflected from snow or ice. This is especially a problem in polar regions and at high altitudes, as with every thousand feet increase in elevation, the intensity of UV rays goes up five percent.

The problem is also related to the condition arc eye sometimes experienced by welders.

Snow blindness is akin to a sunburn of the cornea and conjunctiva, and may not be noticed for several hours from exposure. Symptoms can run the gamut from eyes being bloodshot and teary to increased pain, feeling gritty and swelling shut. Snow blindness only causes permanent vision loss in very severe cases.

The Inuit carved goggles from caribou antler to help prevent snow blindness. The goggles were curved to fit the user's face and had a large groove cut in the back to allow for the nose. A long thin slit was cut through the goggles to allow in a small amount of light. The goggles were held to the head by a cord made of caribou sinew.

Prevention

When trekking, mountaineering or skiing, sunglasses that offer the following are frequently recommended:

* 99-100% UV absorption
* Polycarbonate or CR-39 lens (lighter, more comfortable than glass)
* 5-10% visible light transmittance
* Large lenses that fit close to the face
* Wraparound, side-shielded, or dark-lensed 'glacier' glasses to prevent incidental light exposure
* Wear even when the sky is overcast, as UV rays can still filter through clouds
* In the event of lost or damaged sunglasses, fashion emergency goggles by cutting slits in dark fabric or tape folded back onto itself

Treatment

Following these guidelines will allow the pain and symptoms of snow blindness to disappear as the cornea heals:

* Avoid rubbing eyes and remove contact lenses
* Administer an oral pain medication such as ibuprofen
* Cover eyes with soft thick cloth pads or gauze bandages to prevent irritation from eyelid movement and protect from light; rest in a dark room if possible
* Apply cold wet compresses to ease burning sensations
* Check injury at half-day intervals; remove dressing when eyes can remain open comfortably
* Wear sunglasses outside until symptoms completely disappear

See also

* Glare (vision)
* Over-illumination
* Winter sport
* Sunglasses

All About Corneal abrasions

2007-04-02T23:50:00.026-07:00

Corneal abrasion is a medical condition involving the loss of the surface epithelial layer of the eye's cornea.

Etiology

It is generally caused by trauma, of which there are any number of possible causes, including from a finger 'poked' into an eye or from walking into the branch of a tree. A foreign body getting to the eye may also cause a scratch as the eye is rubbed. It can also be caused by "Hard" or RGP conctact lenses that have been left in too long,this usually does not happen when the lenses are still in contact with the eyes but rather when the lenses are removed and scratch the cornea.

Symptoms and signs

Symptoms of corneal abrasion include pain, photophobia, a foreign-body sensation, and a reflex production of tears. Signs include epithelial defects and edema, and often conjunctival injection, swollen eyelids, and a mild anterior-chamber reaction. The vision may be blurred, both from any swelling of the cornea and the excess tears.

Diagnosis

Although corneal abrasions may be seen with ophthalmoscopes, slit lamp microscopes provide higher magnification which allow for a more thorough evaluation. To aid in viewing, a fluorescein stain that fills in the corneal defect and glows with a cobalt blue-light is generally instilled first.

A careful search should be made for any foreign body, in particular looking under the eyelids. Injury following use of hammers or power-tools should aways raise the possibility of a penetrating foreign body into the eye, for which urgent ophthalmology opinion should be sought.

Treatment

Although small abrasions may require no specific treatment, larger abrasions are typically treated for a few days with a topical antibiotic to prevent infection and a topical cycloplegic to reduce pain and improve comfort. The cycloplegic will also reduce a secondary inflammation of the iris know as an iritis. Eye pads used in "pressure patching" may also improve comfort and promote healing by preventing repeated eyelid blinking that may cause further physical distruption to the cornea, but they are generally not applied in contact lens wearers or when the abrasion is caused by vegetative material, such as a tree branch, or a finger nail. These conditions may pose the threat of a fungal infection and the warm, moist environment provided by pressure patching increases this possibility.

Due to the introduction of newer contact lens materials, mainly silicon hydrogels, pressure patch treatment is being phased out and replaced by "bandage contact lenses". These newer materials provide much more oxygen to the cornea and can be fit tightly (providing minimal movement) with a low risk of corneal hypoxia and edema. These lenses greatly decrease the patients pain and allow the patient to administer drops.

For recurrent corneal erosions, treatment may be had with a laser surgery called phototherapeutic keratectomy.

Complications

Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body is identified and removed, especially if containing iron as rusting will occur.

Occasionally the healed epithelium may be poorly adherent to the underlying basement membrane in which case it may detach at intervals giving rise to recurrent corneal erosions.
Retrieved from "http://en.wikipedia.org/wiki/Corneal_abrasion"

Category: Ophthalmology

All About Corneal ulcers

2007-04-02T23:50:00.025-07:00

A corneal ulcer, or ulcerative keratitis, is an inflammatory or more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, as well as in Florida, corneal ulcer is frequently the cause of great morbidity as well as economic loss to the person and family. Children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong, causing tremendous & avoidable loss to the person and the society.

Corneal anatomy of the humans

The cornea is a transparent structure that is part of the outer layer of the eye. It refracts light and protects the contents of the eye. The corneal thickness ranges from 450 - 610 microns and on an average 550 μm. thick in caucasian eyes. In Indian eyes, the average thickness is slightly less at 510 μm. The trigeminal nerve supplies the cornea via the long ciliary nerves. There are pain receptors in the outer layers and pressure receptors are deeper.

Transparency is achieved through a lack of blood vessels, pigmentation, and keratin, and through tight layered organization of the collagen fibers. The collagen fibers cross the full diameter of the cornea in a strictly parallel fashion and allow 99 percent of the light to pass through without scattering.

There are five layers in the human cornea, from outer to inner:

* Epithelium
* Bowman's membrane
* Stroma
* Descemet's membrane
* Endothelium

The outer layer is the epithelium, which is 25 to 40 μm micrometers and five to seven cell layers thick. The epithelium holds the tear film in place and also prevents water from invading the cornea and disrupting the collagen fibers. This prevents corneal edema, which gives it a cloudy appearance. It is also a barrier to infectious agents. The epithelium sticks to the basement membrane, which also separates the epithelium from the stroma. The corneal stroma comprises 90 percent of the thickness of the cornea. It contains the collagen fibers organized into lamellae. The lamellae are in sheets which separate easily. Posterior to the stroma is Descemet's membrane, which is a basement membrane for the corneal endothelium. The endothelium is a single cell layer that separates the cornea from the aqueous humor.

Corneal healing

An ulcer of the cornea heals by two methods: migration of surrounding epithelial cells followed by mitosis (dividing) of the cells, and introduction of blood vessels from the conjunctiva. Superficial small ulcers heal rapidly by the first method. However, larger or deeper ulcers often require the presence of blood vessels to supply inflammatory cells. White blood cells and fibroblasts produce granulation tissue and then scar tissue, effectively healing the cornea.

Superficial and deep corneal ulcers

Corneal ulcers are a common eye disease of the humans. They are caused by trauma, particularly with vegetable matter, as also chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiae, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa and chlamydia. Bacterial keratitis is caused by Staphylococcus aureus, Staph. viridans, E. coli, enterococci, Pseudomonas, Nocardia and many other bacteria.

Fungal keratitis causes deep and severe corneal ulcer. It is caused by Aspergillus sp., Fusarium sp., Candida sp., as also Rhizopus, Mucor and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes Zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can be recur and relapse over the lifetime of an individual. Protozoa infection like Acanthamoeba keratitis is characterized by severe pain and is associated with contact lens users swimming in pools. Chlamydia trachomatis can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and distichiasis (inturning of eye lashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

Symptoms

Corneal ulcers are painful due to nerve exposure, and can cause tearing, squinting, and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation — stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine.

Diagnosis

Diagnosis is through direct observation under magnified view of slit lamp revealing the ulcer. The use of fluorescein stain, which is taken up by exposed corneal stroma and appears green, helps in defining the margins of the corneal ulcer, and can reveal additional details of the surrounding epithelium. With descemetoceles, Descemet's membrane will bulge forward and after staining will appear as a dark circle with a green boundary, because it does not absorb the stain. Other tests that may be necessary include a Schirmer's test for keratoconjunctivitis sicca and an analysis of facial nerve function for facial nerve paralysis.

Treatment

Proper diagnosis is essential for optimal treatment. Bacterial corneal ulcer require intensive fortified antibiotic therapy to treat the infection. Fungal corneal ulcers require intensive application of topical anti-fungal agents. Viral corneal ulceration caused by herpes virus may antivirals like topical acyclovir oint instilled at least five times a day. Alongside, supportive therapy like pain medications are given, including topical cycloplegics like atropine or homatropine to dilate the pupil and thereby stop spasms of the ciliary muscle. Superficial ulcers may heal in less than a week. Deep ulcers and descemetoceles may require conjunctival grafts or conjunctival flaps, soft contact lenses, or corneal transplant. Proper nutrition, including protein intake and Vitamin C are usually advised. In cases of Keratomalacia, where the corneal ulceration is due to a deficiency of Vitamin A, supplementation of the Vitamin A by oral or intramuscular route is given. Drugs that are usually contraindicated in corneal ulcer are topical corticosteroids and anesthetics - these should not be used on any type of corneal ulcer because they prevent healing, may lead to superinfection with fungi and other bacteria and will often make the condition much worse.

Refractory corneal ulcers

(See also: Recurrent corneal erosion) Refractory corneal ulcers are superficial ulcers that heal poorly and tend to recur. They are also known as indolent ulcers or Boxer ulcers. They are believed to be caused by a defect in the basement membrane and a lack of hemidesmosomal attachments. They are recognized by undermined epithelium that surrounds the ulcer and easily peels back. Refractory corneal ulcers are most commonly seen in diabetics and often occur in the other eye later. They are similar to Cogan's cystic dystrophy.

Treatment

Topical fortified antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye drops are applied to give rest to the eye.Pain medications are given as needed. Loose epithelium and ulcer base can be scraped off and sent for culture sensitiviy studies to find out the pathogenic organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about few weeks to few months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-healing ulcers, surgical intervention in the form of corneal transplantation may be required to save the eye. This procedure is performed after due evaluation, consent and by a qualified Ophthalmologist, preferably with training in cornea. In all corneal ulcers it is important to rule out predisposing factors like Diabetes Mellitus and Immunodeficiency.

Melting ulcers

Melting ulcers are a type of corneal ulcer involving progressive loss of stroma in a dissolving fashion. This is most commonly seen in Pseudomonas infection, but it can be caused by other types of bacteria or fungi. These infectious agents produce proteases and collagenases which break down the corneal stroma. Complete loss of the stroma can occur within 24 hours. Treatment includes antibiotics and collagenase inhibitors such as acetylcysteine. Surgery in the form of corneal transplantation (penetrating keratoplasty) is usually necessary to save the eye.

See also

* Corneal abrasion
* Keratitis

All About Scleritis

2007-04-02T23:50:00.024-07:00

Scleritis is a serious inflammatory disease that affects the white outer coating of the eye, known as the sclera. The disease is often contracted through association with other diseases of the body, such as Wegener's granulomatosis or rheumatoid arthritis; it can also be attained through disorders of menstruation. For this reason, scleritis occurs frequently among young women. There are three types of scleritis: diffuse scleritis (the most common), nodular scleritis, and necrotizing scleritis (the most severe).

The term "Episcleritis" refers to inflammation of the episclera.

Signs and symptoms

Symptoms of the disease include:

* Redness of the sclera and conjunctiva, sometimes changing to a purple hue
* Severe ocular pain (not present in episcleritis)
* Increased light sensitivity and tearing
* Loss of vision

Diagnosis

Scleritis can be detected through visual acuity testing, as well as through CT scans, MRIs, and ultrasonographies.

Treatment

In very severe cases of necrotizing scleritis, eye surgery must be performed to repair damaged corneal tissue in the eye and preserve the patient's vision. For less severe cases, nonsteroidal anti-inflammatory drugs, such as ibuprofen, are prescribed for pain relief. Scleritis itself is treated with an oral medication containing corticosteroids and an eye solution. In some cases, antibiotics are prescribed. Simply using eye drops will not treat scleritis. If not treated, scleritis can cause blindness.

Eye Ailments Caused by the Acanthamoeba

2007-04-02T23:50:00.023-07:00

Acanthamoeba is a genus of amoebae, one of the most common protozoa in soil, and also frequently found in fresh water and other habitats. The cells are small, usually 15 to 35 μm in length and oval to triangular in shape when moving. The pseudopods form a clear hemispherical lobe at the anterior, and there are various short filose extensions from the margins of the body. These give it a spiny appearance, which is what the name Acanthamoeba refers to. Cysts are common. Most species are free-living bacterivores, but some are opportunists that can cause infections in humans and other animals.

Acanthamoeba as a human pathogen
Acanthamoeba encephalitis
Acanthamoeba encephalitis

Diseases caused by Acanthamoeba include amoebic keratitis and encephalitis[1]. The latter is caused by Acanthamoeba entering cuts and spreading to the central nervous system. The former is a rare disease where amoebae invade the cornea of the eye. It is nearly always associated with contact lens use, as Acanthamoeba can survive in the space between the lens and the eye.[2][3][4][5] For this reason, contact lenses should be washed with special saline solutions and should be removed when swimming or surfing. To detect Acanthamoeba on a contact lens in a laboratory, a sheep blood agar plate with a layer (a lawn) of E. coli is made. Part of the contact lens is placed on the agar plate. If Acanthamoeba are present, they will ingest the bacteria, leaving a clear patch on the plate around the area of the lens.

Acanthamoeba and MRSA

Methicillin-resistant Staphylococcus aureus (MRSA) is an important pathogen in the hospital setting due to its resistance to many antibiotics. Recent findings from the University of Bath demonstrate that MRSA can infect and replicate inside of Acanthamoeba polyphaga; this Acanthamoeba species is widespread throughout the environment. Since A. polyphaga can form cysts, cysts infected with MRSA can act as a mode of airborne dispersal for MRSA. Additionally, it is noted that "evidence with other pathogens suggests that pathogens that emerge from amoeba are more resistant to antibiotics and more virulent."[6] It has been observed that Acanthamoeba can increase MRSA numbers by 1000-fold.[7]

Importance of Acanthamoeba in soil ecology

A. castellanii can be found at high densities in various soil ecosystems. It preys on bacteria, but also fungi and other protozoa.

This species is able to lyse bacteria and produce a wide range of enzymes such as cellulases or chitinases[8] and probably contributes to the break down of organic matter in soil, contributing to the microbial loop.

Acanthamoeba species

Species of Acanthamoeba are distinguished mainly on the form of cysts, and include the following; those marked with an asterisk are known to cause infections.

A. astronyxis*
A. castellanii*
A. comandoni
A. culbertsoni*
A. divionensis
A. griffini
A. hatchetti*
A. healyi
A. jacobsi
A. lenticulata
A. lugdunensis*
A. mauritaniensis
A. palestinensis*
A. pearcei
A. polyphaga*
A. pustulosa
A. quina*
A. rhysodes*
A. royreba
A. terricola
A. triangularis
A. tubiashi

Endosymbiontes of Acanthamoeba

Acanthamoeba sp. contain diverse bacterial endosymbionts which are similar to human pathogens. Because of this they are considered to be potential emerging human pathogens.[9] The exact nature of these symbionts and the benefit they represent for the amoebal host still have to be clarified.

See also

* Legionella
* Momus (artist)

References

* Khan, N. A. (2006) Acanthamoeba: biology and increasing importance in human health. Fems Microbiology Reviews 30, 564-595.

1. ^ Di Gregorio, C; Rivasi F, Mongiardo N, De Rienzo B, Wallace S, Visvesvara GS (Dec 1992). "Acanthamoeba meningoencephalitis in a patient with acquired immunodeficiency syndrome". Archives of Pathology & Laboratory Medicine 116 (12): 1363-5. PMID 1456885. Retrieved on 2007-02-12.
2. ^ Auran, JD; Starr MB, Jakobiec FA (1987). "Acanthamoeba keratitis. A review of the literature". Cornea 6 (1): 2-26. PMID 3556011. Retrieved on 2007-02-12.
3. ^ JOHN D.T. (1993) Opportunistically pathogenic free-living amebae. In: J.P. Kreier and J.R. Baker (Eds.), Parasitic Protozoa. Vol. 3. Academic Press, New York, pp. 143–246.
4. ^ Badenoch, PR; Adams M, Coster DJ (Feb 1995). "Corneal virulence, cytopathic effect on human keratocytes and genetic characterization of Acanthamoeba". International journal for parasitology 25 (2): 229-39. PMID 7622330. Retrieved on 2007-02-12.
5. ^ Niederkorn, JY; Alizadeh H, Leher H, McCulley JP (May 1999). "The pathogenesis of Acanthamoeba keratitis". Microbes and Infection 1 (6): 437-43. PMID 10602676. Retrieved on 2007-02-12.
6. ^ University of Bath (2006-02-28). MRSA use amoeba to spread, sidestepping hospital protection measures, new research shows. Press release. Retrieved on 2007-02-12.
7. ^ Blackwell Publishing (2006-03-01). Single Cell Amoeba Increases MRSA Numbers One Thousand Fold. Press release. Retrieved on 2007-02-12.
8. ^ Anderson, I. J.; Watkins, R. F., Samuelson, J., Spencer, D. F., Majoros, W. H., Gray, M. W. and Loftus, B. J. (Aug 2005). "Gene Discovery in the Acanthamoeba castellanii Genome". Protist 156 (2): 203-14. PMID 16171187. Retrieved on 2007-02-12.
9. ^ Horn, M; Wagner, M (Sep-Oct 2004). "Bacterial Endosymbionts of Free-living Amoebae". Journal of Eukaryotic Microbiology 51 (5): 509-14. PMID 15537084. Retrieved on 2007-02-12.

All About Subconjunctival hemorrhage

2007-04-02T23:50:00.022-07:00

A subconjunctival hemorrhage (or subconjunctival haemorrhage) is bleeding underneath the conjunctiva. The conjunctiva contains many small, fragile blood vessels that are easily ruptured or broken. When this happens, blood is leaked into the space between the conjunctiva and sclera.

Whereas a bruise typically appears black or blue underneath the skin, a subconjunctival hemorrhage initially appears bright red underneath the transparent conjunctiva. Later the hemorrhage may spread and become green or yellow, like a bruise. Usually this disappears within 2 weeks. [1]

Although its appearance may be alarming, a subconjunctival hemorrhage is generally a painless and harmless condition; however, it may be associated with high blood pressure, or trauma to the eye.

Causes

* Minor eye trauma
* Spontaneously with increased venous pressure

* Streneuous Exercising
* Coughing
* Touching/widening eyes
* Sneezing
* Vomiting, particularly forced vomiting as seen in bulimia nervosa
* Straining
* Severe alcohol intoxication, leading to raised blood pressure

* Blood dyscrasia (rare)
* Severe hypertension
* LASIK
* Blood thinners, such as ginger, capsaicin, ginseng, garlic, aspirin, or Herba if taken in high doses or combined. These can also make the vessels in the eye more susceptible to the pressure causes listed above.

Subconjunctival hemorrhages in infants may be associated with scurvy (a vitamin C deficiency)[2],[3], abuse or traumatic asphyxia syndrome [4].

Treatment and management

A subconjunctival hemorrhage is typically a self-limiting condition that requires no treatment in the absence of infection or significant trauma. The elective use of aspirin and NSAIDs is typically discouraged.

A common symptom of a subconjunctival hemorrhage, itchy eyes, is often treated by appling eye drops or artificial tears to the affected eye(s).

All About Pterygium

2007-04-02T23:50:00.021-07:00

Pterygium usually refers to a benign growth of the conjunctiva. Alternately, it refers to any winglike triangular membrane occurring in the neck, eyelids, knees, elbows, ankles or digits (J Pediatr Orthop B 2004, 13:197-201). An example is popliteal pterygium syndrome, which affects the legs. The term comes from the Greek word pterygion meaning "wing".

When associated with the conjunctiva, a pterygium commonly grows from the nasal side of the sclera. It is associated with, and thought to be caused by ultraviolet-light exposure (e.g. sunshine), low humidity, and dust. It appears predominantly on the nasal side because the cornea acts as a lens for sunlight on the medial/nasal side but not on the lateral/temporal side, owing to the shadow cast by the nose.

Pathology

Pterygium in the conjunctiva is characterized by elastotic degeneration of collagen and fibrovascular proliferation. It has an advancing portion called the head of the pterygium, which is connected to the main body of the pterygium by the neck. Sometimes a line of iron deposition can be seen adjacent to the head of the pterygium called Stocker's line. The location of the line can give an indication of the pattern of growth. As it is a benign growth, it requires no treatment unless it grows to such an extent that it covers the pupil, obstructing vision. Some patients may also choose surgery if the growth becomes too unsightly. The exact cause is unknown. Wearing protective sunglasses with side shields and/or wide brimmed hats and using artificial tears throughout the day may help prevent their formation or stop further growth.

Occasionally it is found as an incidental finding in middle aged patients who spend a lot of time in the sun.

See also

* List of eye diseases and disorders
* Pinguecula

All About Keratitis

2007-04-02T23:50:00.020-07:00

Keratitis is a condition in which the eye's cornea is inflamed.

Types

Superficial keratitis involves the superficial layers of the cornea. After healing, this form of keratitis does not generally leave a scar.

Deep keratitis involves deeper layers of the cornea. Upon healing, a scar remains that impairs vision if on or near the visual axis.

Causes

Keratitis has a number of causes.

Pathogens

* Amoebic keratitis. Amoebic infection of the cornea is the most serious corneal infection, usually affecting soft contact lens wearers. It is usually caused by Acanthamoeba.
* Bacterial keratitis. Bacterial infection of the cornea can follow from an injury or from wearing contact lenses. The bacteriums usually involved are Staphylococcus aureas and for contact lens wearers it's Pseudomonas aeruginosa.
* Fungal keratitis (cf. Fusarium, causing recent incidences of keratitis through the possible vector of Bausch & Lomb ReNu with MoistureLoc contact lens solution)
* Viral keratitis

* Herpes simplex keratitis. Viral infection of the cornea is often caused by the herpes simplex virus which frequently leaves what is called a 'dendritic ulcer'.
* Herpes zoster keratitis

Other

* Exposure keratitis
* Photokeratitis - keratitis due to intense ultraviolet radiation exposure (e.g. snow blindness or welder's arc eye.)
* Ulcerative keratitis
* Contact lens acute red eye (CLARE) - a non-ulcerative sterile keratitis associated with colonization of Gram-negative bacteria on contact lenses
* Severe allergic response may lead to corneal inflammation and ulceration (i.e. vernal keratoconjunctivitis).[1]

Symptoms

The symptoms are often very similar to those of conjunctivitis, an inflammation of the conjunctiva. The eye turns very red and there may be sensitivity to light, and the eye may feel uncomfortable. In the later stages of more severe cases, there can be strong pain, loss of vision/blurriness, and pus may form.

Diagnosis

Effective diagnosis is important in detecting this condition and subsequent treatment as keratitis is sometimes mistaken for an allergic conjunctivitis.

Treatment

Treatment depends on the cause of the keratitis.

Infectious keratitis generally requires antibacterial, antifungal, or antiviral therapy is to treat the infection. This treatment can involve prescription eye drops, pills, or even intravenous therapy. Over-the-counter eye drops are typically not helpful in treating infections. In addition, contact lens wearers are typically advised to discontinue contact lens wear and discarding contaminated contact lenses and contact lens cases. Antibacterial solutions include Quixin (levofloxacin), Zymar (gatifloxacin), Vigamox (moxifloxacin), Ocuflox (ofloxacin — available generically). Steroid containing medications should not be used for bacterial infections, as they may exacerbate the disease and lead to severe corneal ulceration and corneal perforation. These include Maxitrol (neomycin+polymyxin+dexamethasone — available generically), as well as other steroid medications. One should consult a qualified Ophthalmologist for treatment of an eye condition.

Some infections may scar the cornea to limit vision. Others may result in perforation of the cornea, endophthalmitis (an infection inside the eye), or even loss of the eye. With proper medical attention, infections can usually be successfully treated without long-term visual loss.

References

See also

* List of eye diseases and disorders
* List of systemic diseases with ocular manifestations
* Thygeson's superficial punctate keratopathy

All About Keratoconjunctivitis

2007-04-02T23:50:00.019-07:00

Keratoconjunctivitis refers to an inflammation ("itis") of the cornea and conjunctiva.

When only the cornea is inflamed, it is called keratitis; when only the conjunctiva is inflamed, it is called conjunctivitis.

There several potential causes of the inflammation:

* Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.)
* The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.
* "Atopic keratoconjunctivitis" is one manifestation of atopy.
* "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.
* "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria Moraxella bovis.
* "Superior limbic keratoconjuctivitis" is thought to be caused by mechanical trauma.
* "Keratoconjunctivitis photoelectrica" (arc eye) means that the inflammation is caused by UV light. This can be caused, by example, by welding without wearing protective eye glass. The inflammation will only appear after about 6 to 12 hours. It can be treated by rest (it usually heals within 24 to 48 hours). Additionally, one can wear sunglasses. Antibiotics are not proven to be helpful, however oxybuprocaine may help.

All About Conjunctivitis - Pink Eye

2007-04-02T23:50:00.018-07:00

Conjunctivitis (commonly called "pinkeye" in the USA and "Madras Eye" in India) is an inflammation of the conjunctiva (the outermost layer of the eye and the inner surface of the eyelids), most commonly due to an allergic reaction or an infection (usually bacterial or viral).

Blepharoconjunctivitis is the combination of conjunctivitis with blepharitis (inflammation of the eyelids).

Keratoconjunctivitis is the combination of conjunctivitis and keratitis (corneal inflammation).

Epidemiology

There are three common varieties of conjunctivitis, viral, allergic, and bacterial.[1] Other causes of conjunctivitis include thermal and ultraviolet burns, chemicals, toxins, overuse of contact lenses, foreign bodies, vitamin deficiency, dry eye, dryness due to inadequate lid closure, exposure to chickens infected with Newcastle disease, epithelial dysplasia (pre-cancerous changes), and some conditions of unknown cause such as sarcoidosis.

Bacterial conjunctivitis
is most often caused by pyogenic bacteria such as Staphylococcus or Streptococcus from the patient's own skin or respiratory flora. Others are due to infection from the environment (e.g. insect-borne), from other people (usually by touch—especially in children), but occasionally via eye makeup or facial lotions. An example of this is conjunctivitis due to the bacteria Haemophilus influenzae biogroup aegyptius.

Viral conjunctivitis
is spread by aerosol or contact of a variety of contagious viruses, including many that cause the common cold, so that it is often associated with upper respiratory tract symptoms.
It may also be caused by adenoviruses which was first identified in Chennai (Madras), India, during early 20th Century, hence the name "Madras Eye".[2] This disease mostly appears during Rainy season and during winter months and spreads faster via air due to increased dampness and humidity.[3]
Clusters of cases have been due to transfer from inadequately-sterilised ophthalmic instruments that make contact with the eye (e.g., tonometers).

Allergic conjunctivitis
occurs more frequently among those with allergic conditions, with the symptoms having a seasonal correlation. It can also be caused by allergies to substances such as cosmetics, perfume, protein deposits on contact lenses, or drugs. It usually affects both eyes, and is accompanied by swollen eyelids.

Irritant, toxic, thermal and chemical conjunctivitis
are associated with exposure to the specific agents, such as flame burns, irritant plant saps, irritant gases (e.g., chlorine or hydrochloric acid ("pool acid") fumes), natural toxins (e.g., ricin picked up by handling castor oil bean necklaces), or splash injury from an enormous variety of industrial chemicals, the most dangerous being strongly alkaline materials.

Xerophthalmia
is a term that usually implies a destructive dryness of the conjunctival epithelium due to dietary vitamin A deficiency—a condition virtually forgotten in developed countries, but still causing much damage in developing countries. Other forms of dry eye are associated with aging, poor lid closure, scarring from previous injury, or autoimmune diseases such as rheumatoid arthritis, and these can all cause chronic conjunctivitis.

Diagnosis

Symptoms
Eyes with conjunctivitis.

Redness, irritation and watering of the eyes are symptoms common to all forms of conjunctivitis. Itch is variable.

Acute allergic conjunctivitis is typically itchy, sometimes distressingly so, and the patient often complains of some lid swelling. Chronic allergy often causes just itch or irritation, and often much frustration because the absence of redness or discharge can lead to accusations of hypochondria.

Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, or a sore throat. Its symptoms include watery discharge and variable itch. The infection usually begins with one eye, but may spread easily to the fellow eye.

Bacterial conjunctivitis due to the common pyogenic (pus-producing) bacteria causes marked grittiness/irritation and a stringy, opaque, grey or yellowish mucopurulent discharge (gowl, goop, sleep, or other regional names) that may cause the lids to stick together (matting), especially after sleeping. However discharge is not essential to the diagnosis, contrary to popular belief. Many other bacteria (e.g., Chlamydia, Moraxella) can cause a non-exudative but very persistent conjunctivitis without much redness. The gritty feeling is sometimes localised enough for patients to insist they must have a foreign body in the eye. The more acute pyogenic infections can be painful. Like viral conjunctivitis, it usually affects only one eye but may spread easily to the other eye.

Irritant or toxic conjunctivitis is irritable or painful. Discharge and itch are usually absent. This is the only group in which severe pain may occur.

Signs

Infection (redness) of the conjunctiva on one or both eyes should be apparent, but may be quite mild. Except in obvious pyogenic or toxic/chemical conjunctivitis, a slit lamp (biomicroscope) is needed to have any confidence in the diagnosis. Examination of the tarsal conjunctiva is usually more diagnostic than the bulbar conjunctiva.

Allergic conjunctivitis shows pale watery swelling or edema of the conjunctiva and sometimes the whole eyelid, often with a ropy, non-purulent mucoid discharge. There is variable redness.

Viral conjunctivitis, commonly known as "pink eye", shows a fine diffuse pinkness of the conjunctiva which is easily mistaken for the 'ciliary infection' of iritis, but there are usually corroborative signs on biomicroscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a punctate keratitis.

Pyogenic bacterial conjunctivitis shows an opaque purulent discharge, a very red eye, and on biomicroscopy there are numerous white cells and desquamated epithelial cells seen in the 'tear gutter' along the lid margin. The tarsal conjunctiva is a velvety red and not particularly follicular. Non-pyogenic infections can show just mild injection and be difficult to diagnose. Scarring of the tarsal conjunctiva is occasionally seen in chronic infections, especially in trachoma.

Irritant or toxic conjunctivitis show primarily marked redness. If due to splash injury, it is often present only in the lower conjunctival sac. With some chemicals—above all with caustic alkalis such as sodium hydroxide—there may be necrosis of the conjunctiva with a deceptively white eye due to vascular closure, followed by sloughing of the dead epithelium. This is likely to be associated with slit-lamp evidence of anterior uveitis.

Differential diagnosis

Conjunctivitis symptoms and signs are relatively non-specific. Even after biomicrosopy, laboratory tests are often necessary if proof of aetiology is needed.

A purulent discharge strongly suggests bacterial cause, unless there is known exposure to toxins. Infection with Neisseria gonorrhoeae should be suspected if the discharge is particularly thick and copious.

A diffuse, less "injected" conjunctivitis (looking pink rather than red) suggests a viral cause, especially if numerous follicles are present on the lower tarsal conjunctiva on biomicroscopy.

Scarring of the tarsal conjunctiva suggests trachoma, especially if seen in endemic areas, if the scarring is linear (von Arlt's line), or if there is also corneal vascularisation.

Clinical tests for lagophthalmos, dry eye (Schirmer test) and unstable tear film may help distinguish the various types of dry eye.

Other symptoms including pain, blurring of vision and photophobia should not be prominent in conjunctivitis. Fluctuating blurring is common, due to tearing and mucoid discharge. Mild photophobia is common. However, if any of these symptoms are prominent, it is important to exclude other diseases such as glaucoma, uveitis, keratitis and even meningitis or caroticocavernous fistula.

Investigations

These are done infrequently because most cases of conjunctivitis are treated empirically and (eventually) successfully, but often only after running the gamut of the common possibilities.

Swabs for bacterial culture are necessary if the history & signs suggest bacterial conjunctivitis, but there is no response to topical antibiotics. Research studies indicate that many bacteria implicated in low-grade conjunctivitis are not detected by the usual culture methods of medical microbiology labs, so negative results are common. Viral culture may be appropriate in epidemic case clusters. Conjunctival scrapes for cytology can be useful in detecting chlamydial and fungal infections, allergy and dysplasia, but are rarely done because of the cost and the general lack of laboratory staff experienced in handling ocular specimens. Conjunctival incisional biopsy is occasionally done when granulomatous diseases (e.g., sarcoidosis) or dysplasia are suspected.

Treatment and management

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

Bacterial conjunctivitis is usually treated with antibiotic eye drops or ointments that cover a broad range of bacteria (chloramphenicol or fusidic acid used in UK). However evidence suggests that this does not affect symptom severity and gains only modest reduction in duration from an average of 4.8 days (untreated controls) to 3.3 days for those given immediate antibiotics. Deferring antibiotics yields almost the same duration as those immediately starting treatment with 3.9 days duration, but with half the two-week clinic reattendance rate.[4]

Although there is no cure for viral conjunctivitis, symptomatic relief may be achieved with cool compresses and artificial tears. For the worst cases, topical steroid drops may be prescribed to reduce the discomfort from inflammation. Patients are often advised to avoid touching their eyes or sharing towels and washcloths. Viral conjunctivitis usually resolves within 3 weeks.[2]

Conjunctivitis due to burns, toxic and chemical require careful wash-out with saline, especially beneath the lids, and may require topical steroids. The more acute chemical injuries are medical emergencies, particularly alkali burns, which can lead to severe scarring, intraocular damage or even loss of the eye. Fortunately such injuries are uncommon.

In India, where the ancient medical system of Ayurveda is practiced, there are several remedies for most types of conjunctivitis; for example, goat milk is used in its purified form for certain cases and ointment made out of purified tender coconut water mixed with herbs. These are believed by Ayurvedic adherents to sooth the eyes and promote an environment in which organisms cannot thrive.

References

1. ^ http://www.mayoclinic.com/health/pink-eye/DS00258
2. ^ a b Dr Amar Agarwal. "Tips to manage Madras eye effectively", The Hindu, October 15, 2005. Retrieved on 2006-11-23.
3. ^ Staff Reporter. "Beware, `Madras eye' is here!", The Hindu, October 12, 2001. Retrieved on 2006-11-23.
4. ^ Hazel A Everitt, Paul S Little, Peter W F Smith (July 16 2006). "A randomised controlled trial of management strategies for acute infective conjunctivitis in general practice". BMJ. DOI::10.1136/bmj.38891.551088.7C.

All About Exophthalmos

2007-04-02T23:50:00.017-07:00

Exophthalmos is a bulging of the eye anteriorly out of the orbit. Exophthalmos can be either bilateral (as is often seen in Grave's Disease) or unilateral (as is often seen in an orbital tumor). Measurement of the degree of exophthalmos is performed using an exophthalmometer. Complete or partial dislocation from the orbit is also possible from trauma or swelling of surrounding tissue resulting from trauma.

In the case of Graves Disease, the displacement of the eye is due to abnormal connective tissue deposition in the orbit and extraocular muscles which can be visualized by CT or MRI.[1]

If left untreated, exophthalmos can causes the eye lids to fail to close during sleep leading to corneal damage. The process that is causing the displacement of the eye may also compress the optic nerve or ophthalmic artery leading to blindness.

Exophthalmos vs. proptosis

Some sources define "exophthalmos" as a protrusion of the globe greater than 18 mm and "proptosis" as a protusion equal to or less than 18 mm. (Epstein et al, 2003). Others define "exophthalmos" as protusion secondary to endocrine dysfunction and "proptosis" as any non-endocrine-mediated protusion [1].

Exophthalmos in dogs
Exophthalmos in a Pug
Exophthalmos in a Pug

Exophthalmos is commonly found in dogs. It is a normal condition in brachycephalic (short nosed) dog breeds because of the shallow orbit. However, it can lead to keratitis secondary to exposure of the cornea. Exophthalmos is commonly seen in the Pug, Boston Terrier, Pekingese, and Shih Tzu.

See also

* Boston's sign
* Enophthalmos
* Marty Feldman
* Von Graefe's sign

References

1. ^ Owen Epstein, David Perkin, John Cookson, David P de Bono (April 2003). Clinical examination, 3rd edition, St. Louis: Mosby. ISBN 0-7234-3229-5.

All About Epiphora

2007-04-02T23:50:00.016-07:00

Epiphora may mean:

* Epiphora, excessive tear production usually a result from an irritation of the eye. a clinical sign or condition that constitutes insufficient tear film drainage from the eyes in that tears will drain down the face rather than through the nasolacrimal system [1].

* Epiphora, a synonym for epistrophe.

Ocular Herpes

2007-04-02T23:50:00.015-07:00

Herpes simplex is a viral infection caused by one of two Herpes Simplex Viruses (HSV), members of the Herpesviridae family. Manifestations of herpes infections vary significantly between individuals. Most cases of genital herpes are caused by HSV-2. It is widespread, affecting an estimated 1 in 4 females and 1 in 5 males in the United States. Although certain therapies can prevent outbreaks or reduce the risk of transmission to partners, no cure is yet available.[1]

HSV disease

There are two types of Herpes Simplex Virus: HSV Type 1 and HSV Type 2. The ways in which herpes infections manifest themselves vary tremendously among individuals. The following are general descriptions of the courses outbreaks may take in the oral and genital regions.
Infectious fluid-filled blister on lower lip (herpes labialis)
Infectious fluid-filled blister on lower lip (herpes labialis)

Herpes is also formed on the tongue as bumps or white dots

Orofacial infection (generally HSV-1)

1. Prodromal symptoms
2. Skin appears irritated
3. Sore or cluster of fluid-filled blisters appear
4. Lesion begins to heal, usually without scarring

It is estimated that 50% of adults in the United Kingdom are carriers of the Herpes Simplex Virus,[2] many of which will never exibit any symptoms of infection. Similarly, 50% of Americans have HSV-1 antibodies in their blood by the time they're teenagers or young adults and 80-90% of Americans have HSV-1 antibodies by the time they are over age 50.[3] It is also possible for the virus to be transmitted across the skin in the absence of a coldsore. Oral herpes lesions typically occur on the lips, but can occur almost anywhere on the face. They can also occur on the fixed mucosa inside the mouth, including the hard palate (roof of the mouth), and gingiva (gums). Oral herpes and cold sores can sometimes be confused with canker sores. Only a medical physician can provide adequate diagnosis.

Genital infection (generally HSV-2)

1. Prodromal symptoms
2. Itching in affected area
3. Sore appears
4. Lesion begins to heal, usually without scarring

In males, the lesions may occur on the shaft of the penis, in the genital region, on the inner thigh, buttocks, or anus. In females, lesions may occur on or near the pubis, labia, clitoris, vulva, buttocks, or anus. This may require a very careful examination; for example, during delivery, examination by use of a flashlight may be necessary. Symptoms can be confused with that of chlamydia or gonorrhea, so careful observation by a doctor is important.

The appearance of herpes lesions and the experience of outbreaks in these areas varies tremendously among individuals. Herpes lesions on/near the genitals may look like cold sores. An outbreak may look like a paper cut, or chafing, or appear to be a yeast infection. Symptoms of a genital outbreak may include aches and pains in the area, discharge from the penis or vagina, and severe discomfort and burning when urinating.

Initial outbreaks are usually more severe than subsequent ones, and generally also involve flu-like symptoms and swollen glands for a week or so. Subsequent outbreaks tend to be periodic or episodic, typically occur four to five times a year, and can be triggered by stress, illness, fatigue, menstruation, and other changes. The virus sequesters in the nerve ganglia that serve the infected dermatome during non-eruptive periods, where it cannot be conventionally eliminated by the body's immune system.

[edit] Herpes simplex encephalitis (generally HSV-1)
Herpesviral encephalitis
Classification & external resources ICD-10 B00.4, G05.1
ICD-9 054.3

Herpes simplex encephalitis is a very serious disorder, thought to be caused by the retrograde transmission of the virus from a peripheral site to the central nervous system along a nerve axon. It is known that the virus lies dormant in the ganglion of the trigeminal or fifth cranial nerve. The reason for reactivation remains unclear. It has also been proposed that the olfactory nerve may be involved.[4] Without treatment, it results in rapid death in around 70% of cases. Even with the best modern treatment, it is fatal in around 20% of cases, and causes serious long-term neurological damage in over half the survivors. Again, for unknown reasons the virus seems to target the temporal lobes of the brain. A small population of survivors, perhaps 20%, show little long-term damage. It is most common in children and middle-aged adults. Although herpes simplex is by no means the most common cause of viral encephalitis (accounting for about 10% of cases in the US), because of the high risk associated with it if it is not treated as well as being one of the few encephalitis to which definitive treatment is available, patients presenting with encephalitis symptoms are likely to be treated against this disorder without waiting for a positive diagnosis. A positive diagnosis can be obtained by CSF PCR for herpes simplex DNA, CSF viral culture or a rising titre for antibodies. The fact that the Electroencephalogram is abnormal in >90% of the patients with Herpes Simplex Encephalitis further aids the diagnosis.

The virus usually infects through the mouth and enters the nucleus during the first 7 days, and will remain latent for 10 days to 100 years, and will then reactivate from common stress, fever, or a sunburn. The virus will soon be contagious through more cold sores, and the disease will start to attack the brain.

Neonatal herpes simplex
Congenital herpesviral (herpes simplex) infection
Classification & external resources ICD-10 P35.2
ICD-9 771.2
HSV at newborn child.
HSV at newborn child.

Neonatal HSV disease is a rare, but serious, consequence of vertical HSV transmission from mother to newborn child. Prospective active surveillance data indicate an incidence rate of 3.61 per 100,000 live births in Australia, with similar rates in the UK; but much lower than the USA. [5][6] Preliminary studies indicate the epidemiology in Canada is closer to Europe than to the United States. The mortality rate from neonatal HSV disease is high (up to 25%) despite current interventions with antiviral therapies. Death results from disseminated HSV disease and/or HSV encephalitis in the newborn children.

Ocular herpes

Ocular herpes (generally HSV-1) is a special case of herpes infection (herpes viral keratitis) that affects the nerves serving the cornea of the eye. It usually manifests as small white itchy lesions on the surface of the cornea, known as dendritic ulcers because they show a branching pattern. Additional symptoms include dull pain deep inside the eye, mild to acute dryness and sinusitis. Most first infections resolve spontaneously in a few weeks or with the use of oral and topical antivirals. However, the virus continues to inhabit the neurons of the eye and to multiply. Subsequent symptoms (with or without visible lesions) include chronic dry eye, low grade intermittent conjunctivitis or chronic unexplained sinusitis. When the patient is immunocompromised or the concentration of viral DNA reaches a critical limit, the presence of the virus can trigger a massive autoimmune response in the eye, resulting in the patient's own system destroying the corneal stroma. This usually results in loss of vision due to opacification of the cornea. Treatment with corneal transplants may be ineffective, as reinfection of the transplant is common; however, with concurrent use of antivirals the chance of graft acceptance is higher. Research is ongoing for a vaccine against ocular herpes.[citation needed]

Ocular herpes is the leading cause of infectious blindness in the developed world.[citation needed] As with orofacial or genital herpes, trauma to the eye increases the chance of a recurrence. Thus herpes viral keratitis can produce complications in the case of patients undergoing radial keratotomy by laser (lasik) to correct vision defects, and patients undergoing this procedure should be carefully screened.

A common cause of infection of the eye is the handling of contact lenses with hands infected by active sores at other sites, notably the mouth; thus the common practice of wetting lenses with saliva when no proprietary solution is available (such as for reinsertion after accidental dislodging) is extremely dangerous and should always be avoided.[citation needed]

Outbreak Triggers

Oral herpes

Physical or psychological stress can trigger an outbreak. Local injury to the face, lips, eyes or mouth, as through trauma, surgery, or sunburns are well established triggers of recurrent orolabial herpes due to herpes simplex virus type 1 (HSV-1). Similarly, intercurrent infections, such as upper respiratory viral infections or other febrile diseases, can cause outbreaks, hence the historic terms "cold sore" and "fever blister". Generalized psychological stress and anxiety are also triggers.

Genital herpes

Controversy exists about triggers of recurrent outbreaks of genital herpes, typically due to HSV-2. It is often stated that stress, menstruation, diet (such as foods high in arginine, like chocolate, peanuts and walnuts) or sexual activity may increase the chance and severity of outbreaks.[citation needed] However, no scientific studies have clearly documented such triggers, and the objective data available suggest that outbreaks are not influenced by stressful events, anxiety, depression, or similar influences. The clinical experience of most experts involved in clinical care is that attempts by infected persons to modify external triggers is virtually never effective in controlling symptomatic oubreaks of genital herpes. Similarly, neither objective data nor biololgical plausibility support the notion that excessive usage of antibiotics affect the immune system's ability to keep the disease within the nerve ganglia (particularly as antibiotics are useless against viruses of any type) or otherwise affect herpes recurrences, nor the occasional assertion that "chronic" genital herpes is in any way related to low-level food allergy.

Symptoms

Herpes infections, whether initial or recurring, are usually first felt as a tingling and/or itching sensation in the affected location. These initial feelings are usually followed, depending on how severe the infection is, by the emergence of a raised or swollen area on the skin. This swollen area then becomes painful in general, but acutely sore when touched, stretched or moved. Eventually the sore area will abscess, and emit a virus laden clear fluid for several days before scabbing over. Once scabbed over the lesion will usually heal completely within a period of a week to ten days. In immuno-compromised individuals this cycle can be significantly protracted.

From the onset of infection/outbreak, many patients experience headaches, fatigue (sometimes extreme), and peculiar twitching sensations in the nerves that lead to the area of the outbreak. The fatigue associated with herpes infections can concatenate with depression brought on by the cosmetic or sexually compromising nature of the infection, to yield a deeply gloomy overall mental state that some believe can contribute to increasing the length and severity of an infection.

Transmission

Herpes is contracted through direct skin contact (not necessarily in the genital area) with an infected person, and less frequently by indirect contact (for instance, by sharing lip balm or a virus infested shared towel). The virus travels through tiny breaks in the skin (or mucous membranes in the mouth and genital areas), so, healthy skin and mucous membranes are normally an effective barrier to infection. However, in the case of mucous membranes, even microscopic abrasions are sufficient to expose the nerve endings into which the virus splices itself. This is why most herpes transmission happens in mucous membranes, or in areas of the body where mucous membranes and normal skin merge (e.g., the corners of the mouth).

Symptoms may not appear for up to a month or more after infection.[citation needed]

Transmission was thought to be most common during an active outbreak; however, in the early 1980s, it was found that the virus can be shed from the skin, saliva and genital secretions in the absence of symptoms.

Recurrence

Herpes recurs only at a site of previous infection. The periodicity (frequency) and amplitude (severity) of recurrence varies greatly depending on the individual and various environmental factors including stress (both physical and mental). Often, for a given site, the infection will recur only two or three times, with severity attenuating (decreasing) each time. The mechanism by which the body seems to gain the upper-hand for a given recurrence site is poorly understood by the medical community.

Self Reinfection

Self reinfection, known medically as autoinoculation, is more likely during intensely virulent initial infection with either HSV-1 or HSV-2 in a given infection site. The most common manifestations are herpetic whitlow, a pustular lesion typically of a finger, and herpes of the eye (keratitis, keratoconjunctivitis).

General hygiene principles suggest that persons with recurrent oral or genital herpes should avoid direct contact with active lesions and should wash their hands immediately after using the toilet or touching the area of an oral lesion, to further limit the low risk of autoinoculation.

In cases where herpes is present in an area where the dermis is subject to high abrasive forces (such as the often irritated shaved beard region, or the surfaces of the penis and vagina during vigorous sexual activity), it is quite common to spread an initial lesion to other sites, which then become highly virulent initial infections, and so on. The medical community has failed to make this very obvious fact clear to patients and this has resulted in great amplification of their general misery, not to mention the much higher likelihood that a person infected in multiple sites (whether genital, or otherwise) will spread this disease to friends, family and sexual partners.

Asymptomatic Shedding

HSV asymptomatic shedding is believed to occur on 2.9% of days while on antiviral therapy, versus 10.8% of days without. Shedding is known to be more frequent within the first 12 months of acquiring HSV-2, and concurrent infection with HIV also increases the frequency and duration of asymptomatic shedding.[7] There are some indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified. Sex should always be avoided in the presence of symptomic lesions. Oral sex performed by someone with oral lesions or other symptoms should be avoided, to avoid transmission of HSV-1 to the partner's genitals. Even without symptoms it is possible for transmission to occur. Many people still believe Herpes cannot be transmitted through oral sex. This is a dangerous myth.

Women are more susceptible to acquiring genital HSV-2 than men; in the US, 11% of men and 23% of women carry HSV-2.[8] On an annual basis, without the use of antivirals or condoms, the transmission risk from infected male to female is approximately 8-10%. This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is approximately 4-5% annually. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios by about 50%, meaning the infected partner will be seropositive but symptom free. Condom use also reduces the transmission risk by 50%. Condom use is much more effective at preventing male to female transmission than vice-versa. [9] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk. These figures reflect experiences with subjects having frequently-recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.

Prevention

For genital herpes, condoms are a highly recommended way to limit transmission of herpes simplex infection, as demonstrated in research. [9][10] However, condoms are by no means completely effective. The effectiveness of this method is somewhat limited on a public health scale by the limited use of condoms in the community [11]; and on an individual scale because some blisters may not be covered by the condom, or free virus in female vaginal fluid may enable infection around the base of the penis or testicles not covered by the condom.

Condoms do not prevent the condom wearer from spreading the infection to new sites either on himself through abrasion (if he is already infected and suffering an outbreak), or on the female partner if she is suffering from an outbreak and the sexual activity spreads this infection from one site to another on her own body (see "Self Reinfection" above).

The use of condoms or dental dams can limit the transmission of Herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex.

When one partner has herpes simplex infection and the other does not, the use of valaciclovir, in conjunction with a condom, has been demonstrated to decrease further the chances of transmission to the uninfected partner, and the Food and Drug Administration (FDA) approved this as a new indication for the drug in August 2003.

Vaccines for HSV are currently undergoing trials. Once developed, they may be used to help with prevention or minimize initial infections as well as treatment for existing infections. [12]

Other measures that have been suggested include:

* Avoidance of cross-infecting new sites on the body if HSV blisters are present
* Gentle and well lubricated as opposed to vigorous, abrasive sex
* Thorough washing of the genitals after sex
* Not ejaculating inside a partner during sex (if herpes lesions have appeared inside the urethra)
* Management of stress
* Adequate sleep and nutrition
* Use of a lip protectant or lip gloss to avoid cracks and abrasions through which the virus may infect
* Treatment using ascorbate-Cu(II) [13]

Future vaccines

The National Institutes of Health (NIH) in the United States is currently in the midst of phase III trials of a vaccine against HSV-2. The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2. Assuming FDA approval, a commercial version of the vaccine is estimated to become available around 2008. During initial trials, the vaccine did not exhibit any evidence in preventing HSV-2 in males. Additionally, the vaccine only reduced the acquisition of HSV-2 and symptoms due to newly acquired HSV-2 among women who did not have HSV-1 infection at the time they got the vaccine. Because about 50% of persons in the United States have HSV-1 infection, this further reduces the population for whom this vaccine might be appropriate. The candidate vaccine is called Herpevac, and individuals who might be interested in learning about the study can easily find information at Herpevac Trial for Women

Treatment

Currently, there is no cure for herpes. There is no treatment that can eradicate herpes virus from the body at reactivations of the virus. Non-prescription analgesics can reduce pain and fever during initial outbreaks.

Anti-viral Medication

There are several prescription antiviral medications for controlling herpes outbreaks, including aciclovir (Zovirax), valaciclovir (Valtrex), famciclovir (Famvir), and penciclovir. Aciclovir was the original and prototypical member of this class and generic brands are now available at a greatly reduced cost. Some prescription drugs to treat herpes can cause diarrohea several times a day so patients are advised to take non prescribed diarrohea tablets as required in these cases along with the medication. It has been claimed that the evidence for the effectiveness of topically applied cream for recurrent labial outbreaks is weak.[14] Likewise oral therapy for episodes is inappropriate for most non-immunocompromised patients, whilst there is evidence for oral prophylactic role in preventing recurrences.[15]

Valaciclovir and famciclovir are prodrugs of aciclovir and penciclovir respectively, with improved oral bioavailability (55% vs 20% and 75% vs 5% respectively). These antiviral medications work by interfering with viral replication, effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral thymidine kinase to convert the drug to a monophosphate form and subsequently interfere with viral DNA replication. Penciclovir's primary advantage over aciclovir is that it has a far longer cellular half-life – 10 hours (HSV-1)/20 hours (HSV-2) for penciclovir versus 3 hours (HSV-1/2) for aciclovir.

Aciclovir is the recommended antiviral for suppressive therapy to prevent transmission of herpes simplex to the neonate. The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context. [16] There is evidence in mice that treatment with famciclovir, rather than aciclovir, during an initial outbreak can help lower the incidence of future outbreaks by reducing the amount of latent virus in the neural ganglia. This potential effect on latency over aciclovir drops to zero a few months post-infection. [17]

Other drugs exhibiting anti-viral activity

Docosanol (Abreva) is another treatment that may be effective. Docosanol works by preventing the virus from fusing to cell membranes, thus barring entry into the cell for the virus. This may keep an outbreak contained to a smaller area than would otherwise be observed.

Zilactin is an early relief cold sore/fever blister gel that works by applying the gel, which when dry forms a "shield" to prevent the sore from increasing in size and prevents spreading by breakage or oozing during the healing process.

Tromantadine is another antiviral drug effective against herpes.

Other drugs

Cimetidine, a common component of heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances, and offered some relief from herpes simplex [18] [19] [20] . This is an off-label use of the drug.

It and probenecid have been shown to reduce the renal clearance of aciclovir. [21] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.

Availability of non-generic prescriptions

* Valaciclovir (GlaxoSmithKline) is protected under U.S. Patent 4957924 protection expiring June 2009
* Famciclovir (Novartis) is protected under U.S. Patent 5246937 protection expiring Sept 2010
* Penciclovir (GlaxoSmithKline) is protected under U.S. Patent 5075445 protection expiring Sept 2010
* Docosanol (Avanir) is protected under U.S. Patent 4874794 protection expiring April 2014

Availability of generic prescriptions

* Acyclovir is no longer under US patent protection, available in generic form

Drugs in development

* BAY 57-1293, a helicase-primase inhibitor researched by Bayer AG scientist Gerald Kleymann's team in Wuppertal, Germany. [22][23]

* BILS 179 BS, BILS 45 BS, BILS 22 BS, also inhibitors of helicase-primase enzyme, researched in Ridgefield, Connecticut, by James Crute's team at Boehringer Ingelheim Pharmaceuticals. [24][25]

* Roscovitine is an inhibitor of cellular cyclin-dependent kinase and seems to prevent transcription of viral genomes. Roscovitine has entered clinical trials for HIV infection. [26][27][28]

Natural compounds

Lysine

Lysine supplementation has been proposed as a complementary therapy for the prophylaxis and treatment of herpes simplex. Lysine supplementation is highly dose-dependent, with beneficial effects apparent only at doses exceeding 1000 mg per day. A small randomised controlled trial indicated a decrease in recurrence rates in nonimmunocompromised patients at a dose of 1248 mg of lysine monohydrochloride, but no effect at 624 mg daily. This study did not show any evidence of shortening the healing time compared to placebo. [29] Another small randomised controlled trial indicated the benefit of 3000 mg lysine daily for the reduction of occurrence, severity and healing time for recurrent HSV infection. [30]

Tissue culture studies have shown the suppression of viral replication when the lysine to arginine ratio in vitro favours lysine. The therapeutic consequence of this finding is unclear, but dietary arginine may affect the effectiveness of lysine supplementation. [31]

Lysine intake may be supplemented by varying the diet. Dairy products offer the highest ratio of lysine to arginine amino-acid content. Contrarily, nuts (and peanuts, even though they aren't true nuts), deliver a large dose of arginine. To help forestall outbreaks, you might avoid nuts during stressful periods, and eat cheese any time you do eat nuts. During an outbreak, eating cheese may slow the spread of lesions, and reduce virus shedding and self-reinfection. Eating 100g (~4oz) of Parmesan cheese supplies 3.3g of lysine, vs. 1.3g of arginine. The same amount of almonds provides 0.7g of lysine, but 2.4g of arginine. (Cf. the Danish Food Composition Databank, http://www.foodcomp.dk/fcdb_alphlist.asp)

High doses of lysine (greater than 10 grams daily) are known to cause gastrointestinal adverse effects. Dyspepsia was reported in 3 of 114 subjects treated with L-lysine in one study. [30] Prolonged and/or very high lysine doses may also have adverse effects on renal function, indeed lysine is contraindicated in lysine hypersensitivity and kidney or liver disease. (Anon., 2005) One patient, with a history of risk factors for renal impairment, developed tubulointerstitial nephritis (Fanconi's Syndrome) after taking lysine 3000 mg daily for approximately 5 years. [32]

Polysaccharides

Carrageenans, linear sulphated polysaccharides extracted from red seaweeds, have been shown to have antiviral effects in HSV-infected cells.

* There are indications that a carrageenan based gel may offer some protection against HSV-2 transmission by binding to the receptors on the herpes virus thus preventing the virus from binding to cells. Researchers have shown that a carrageenan-based gel effectively prevented HSV-2 infection at a rate of 85% in a mouse model.[33] There is an ongoing large-scale trial of the efficacy of a similar formulation on humans results are expected to be published in 2007.
* The natural carrageenans 1T1, 1C1, 1C3 isolated from Gigartina skottsbergii seaweed inhibited the replication activity of HSV-1 and HSV-2 in infected mouse astrocyte nerve cells and vero cells.[34]

Lactoferrin

Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.[35] The concentration of lactoferrin which achieved 50% of maximum effectiveness observed (that is, the EC50) also acted in synergy with aciclovir; the concentration required to achieve EC50 for each substance was reduced "two- to seven-fold."

Resveratrol

Resveratrol, a compound in red wine, has been shown by researchers to prevent HSV replication in vitro by inhibiting a protein needed by the virus to replicate. Resveratrol alone was not considered potent enough by the researchers to be an effective treatment.[36] A more recent in vivo study in mice showed the efficacy of topical resveratrol cream in preventing cutaneous HSV lesion formation.[37] Research on a much more potent derivative of resveratol, named stil-5, is ongoing. There is no evidence that red wine consumption provides any similar benefits.

Unproven

Limited evidence suggests that low dose aspirin (125 mg daily) might be beneficial in patients with recurrent HSV infections. A small study of 21 volunteers with recurrent HSV indicated a significant reduction in duration of active HSV infections, milder symptoms, and longer symptom-free periods as compared to a control group. [38] A recent animal study found that aspirin inhibited thermal stress-induced ocular viral shedding of HSV-1, and a possible benefit in reducing recurrences. [39] Aspirin is not recommended in persons under 18 years of age with herpes simplex due to the increased risk of Reye's syndrome. Long term daily doses of aspirin have a side effect of reduced blood coagulation, facilitating bruising. A single 81 mg "daily dose" aspirin is a safer regimen given that there are no studies of the correlation between dosage and anti-viral effects of aspirin.

Other

The evidence for the effectiveness of zinc and Vitamin C supplementation is poor. [40] Other supplements with anecdotal evidence of benefits include monolaurin, vitamin A, vitamin B12, garlic, and echinacea. Daily multivitamin intake may be beneficial through maintenance of immune system health. High doses of vitamin A should not be taken in early pregnancy due to linkage with birth defects. In addition, some anecdotal reports indicate that placing ice in contact with an emerging cold sore for 5-10 minutes throughout the day can help shorten the duration of the outbreak, or prevent it from developing further.

Butylated Hydroxytoluene (BHT), commonly available as a food preservative, has been shown in in-vitro laboratory studies to inactivate the herpes virus.[41] In-vivo studies in animals confirmed the anti-viral activity of BHT against genital herpes.[42] However BHT has not been clinically tested and approved to treat herpes infections in humans.

Latent infection and biology

The herpes virus is a double-stranded DNA (dsDNA)-type virus. Herpes establishes a latent infection in cells of the nervous system. Double-stranded DNA is incorporated into the cell physiology by infection of the cell nucleus, where a loop of dsDNA is maintained. During inactive, or latent, periods of the infection, a subset of the Herpes genome termed LAT or Latency Associated Transcript is active and may be involved in maintenance of latency.

Long-term effects

The long-term effects of herpes are not well known, but the blisters may leave scars, and historically it was thought to contribute to the risk of cervical cancer in women. Subsequently, another virus, human papillomavirus (HPV), has been shown to be a primary cause of cervical cancer in women. Additionally, people with herpes are at a higher risk of HIV transmission because of open blisters. In newborns, however, herpes can cause serious damage: death, neurological damage, mental retardation, and blindness.

The immune system is able to destroy active herpes virus particles but the herpes virus has the ability to hide from the immune system in an inactive (or latent) state. Current research suggests that this ability to hide may be achieved via modification to cellular enzyme histone deacetylases (HDACs), namely HDAC1 and HDAC2. [43] Hypothetically, by interfering with the HDAC enzymes' effectiveness, it may be possible to block the virus's ability to hide from the immune system, leading to a complete elimination of the virus by the immune system. Studies on the impact of HDAC inhibitors on viral latency are ongoing in the HIV arena.

Obstetric / Neonatal risks

Recurrent genital herpes has very significant obstetrical/neonatal risks associated with it, and probably may merit treatment with acyclovir as an independent problem. [44]

Viral Meningitis

It is reasonably well-established in the last few years that herpes simplex virus 2 (HSV-2) is the most common cause of recurrent viral meningitis (Mollaret's meningitis). [45]

Psychological and social effects

Herpes can have a dramatic effect on an individual's mental well-being and sexual behaviour.

Quality of life issues

Upon diagnosis of genital herpes, people can experience a number of negative feelings related to the condition. Though these feelings lessen over time, they can include:[46]

* depression 81%
* fear of rejection 75%
* feeling of isolation 69%
* fear of being found out 55%
* self-destructive feelings 28%

The impact of genital herpes included:

* partial or complete cessation of sexual activity
* total or partial loss of interest in sex
* decreased sexual pleasure
* sex life more inhibited and less spontaneous
* anxiety related to sexual desirability
* increased depression

In order to improve the well-being of people with herpes, a number of support groups [47], communities [48] and dating sites [49][50] have formed a presence on the Internet.

Media portrayal

Media portrayals of genital herpes - which might help to destigmatise the condition - remain few and, when they occur, are often negative.[51]

Examples of such portrayals in the main types of media include:

* in the mainstream press, a 1982 article in Time magazine called “Herpes: Today’s Scarlet Letter”; [52]

* on television, a 1983 telefilm called “Intimate Agony”;[53]

* in music, a 1993 Marilyn Manson song called “Herpes”;[54]

* in the cinema, a 2005 film called “Merry Christmas… I Got You Herpes”;[55]

* in movies, a 2006 film called “John Tucker Must Die”

* in literature, a 2006 novel called “Stigma”;[56]

Disclosure to new partners

People with genital herpes are often hesitant to divulge to other people that they have the virus, including friends and family but especially new or potential sexual partners. People may be less likely to inform what they consider to be 'casual' partners.[57] In addition, the perception of the likely reaction is sometimes taken into account before making a decision about whether to inform new partners. An event such as a couple moving in together was found to be the point when some people disclosed their status. Reactions by sexual partners may not always be negative, and individuals often use various strategies to mitigate the impact of disclosure such as keeping the issue "low key," choosing a relaxed environment and suggesting the couple being tested jointly for a range of sexually transmitted infections.

Legal redress

Whether the law can help a person who catches herpes depends on the jurisdiction where it was contracted as legal jurisdictions define their own rules regarding the transmission of STIs such as herpes.[58] There can be both criminal and civil possibilities. For example, in the criminal case of R. v. Sullivan heard in England and Wales, a man was prosecuted for sexual assault after his partner experienced a primary outbreak of genital herpes, on the basis that he had failed to reveal the fact that he had herpes. Ultimately, the man was discharged due to an inability to prove prior knowledge. Civil claims for transmission of herpes are, for their part, usually based on negligence if transmission was accidental and battery if deliberate. The first successful case to allow such a claim in the United States was Kathleen K. v. Robert B., decided by the California Court of Appeals.

Myths

Some common misconceptions about herpes are:

* that it is fatal. Fact: This is only true for newborns, which is rare, but it is fatal in 25% of all such cases. It can also possibly kill an adult if it infects the brain causing encephalitis, or infects the meninges causing meningitis.
* that it only affects the genital areas. Fact: It can affect any part of the body. If you touch a genital herpes sore and then touch another part of your body, you can potentially spread the virus.
* that condoms are completely effective in preventing the spread of this disease. Fact: They do greatly improve protection but are imperfect only preventing transmission 50% of the time.
* that it is only transmittable in the presence of symptoms. Fact: There is more viral shedding during an outbreak but it's possible to transmit any time.
* that it can make you sterile Fact: Genital Herpes cannot make you sterile.
* that Pap smears detect herpes Fact PAP smears are not designed to detect herpes simplex virus infections. Type-specific serology tests and viral cultures are used to diagnose genital herpes and are not normally conducted during a woman's annual gynecological examination.
* that it can not be transmitted between the genitals and the mouth. Fact: Even the use of a condom will not prevent transmission between genital and oral regions.
* that only promiscuous people get it. Fact: It is so common that anyone can contract it. The more sexual partners an individual has, however, the more likely they are to contract the disease.[59]

There is a basis in fact that herpes could be transmitted via an inanimate object such as a toilet seat or wet towel but the conditions required for this kind of transmission (high heat, high moisture, and a vulnerable exposure site) make it extremely unlikely. Although there are no confirmed cases of this type of transmission, sharing a towel with somebody with active lesions should be avoided. Likewise, sharing lip or mouth products (toothbrushes, lipstick, lip balm, or similar) with somebody with active lesions should also be avoided.

Footnotes

1. ^ Center for Disease Control (CDC) - Herpes Fact Sheet Accessed February 7, 2007.
2. ^ U.K Herpes Viruses Association - [1] Accessed March 15, 2007.
3. ^ "Herpes Online: Exploring the "H" Community", American Social Health Association, 1996, pp. 1-4. Retrieved on 2007-03-29. (in English)
4. ^ Dinn J (1980). "Transolfactory spread of virus in herpes simplex encephalitis.". Br Med J 281 (6252): 1392. PMID 7437807.
5. ^ Elliott E, Rose D. (2003). "Australian Paediatric Surveillance Unit. Reporting of communicable disease conditions under surveillance by the APSU, 1 January to 30 September 2003". Commun. Dis. Intell. 28 (1): 90-91. PMID 15072162.
6. ^ Jones CA (2004). "Vaccines to prevent neonatal herpes simplex virus infection". Expert Rev. Vaccines 3 (4): 363-364. PMID 15270635.
7. ^ Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A (2006). "Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men.". J Infect Dis 194 (4): 420-7. PMID 16845624.
8. ^ Carla K. Johnson. "Percentage of people with herpes drops", Associated Press, Aug 23, 2006.
9. ^ a b Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L. (2001). "Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women". JAMA 285 (24): 3100-3106. PMID 11427138.
10. ^ Casper C, Wald A. (2002). "Condom use and the prevention of genital herpes acquisition.". Herpes 9 (1): 10-14. PMID 11916494.
11. ^ de Visser RO, Smith AM, Rissel CE, Richters J, Grulich AE. (2003). "Sex in Australia: safer sex and condom use among a representative sample of adults". Aust. N. Z. J. Public Health. 27 (2): 223-229. PMID 14696715.
12. ^ Seppa, Nathan. "One-Two Punch: Vaccine fights herpes with antibodies, T cells", Science News, 2005-01-05, pp. 5. Retrieved on 2007-03-29. (in English)
13. ^ Betanzos-, G; CabreraRamirez FJ, Munoz JL, Barron BL, Maldonado R. (2004-09-15). "Inactivation of HSV-2 by ascorbate-Cu(II) and its protecting evaluation in CF-1 mice against encephalitis.". Journal of virological methods 120 (2): 161-165. DOI:2004-09-15. 15288958. Retrieved on 2007-03-29.
14. ^ Graham Worrall (6 Jul 1996). "Evidence for efficacy of topical acyclovir in recurrent herpes labialis is weak". BMJ 313: 46. - Letter
15. ^ Graham Worrall (6 Jan 1996). "Acyclovir in recurrent herpes labialis". BMJ 312: 6. - Editorial
16. ^ Leung DT, Sacks SL. (2003). "Current treatment options to prevent perinatal transmission of herpes simplex virus". Expert Opin. Pharmacother. 4 (10): 1809-1819. PMID 14521490.
17. ^ Thackray AM, Field HJ. (1996). "Differential effects of famciclovir and valaciclovir on the pathogenesis of herpes simplex virus in a murine infection model including reactivation from latency". J. Infect. Dis. 173 (2): 291-299. PMID 8568288.
18. ^ Kapinska-Mrowiecka M, Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation.". Pol Tyg Lek. 51 (23-26): 338-339. PMID 9273526.
19. ^ Hayne ST, Mercer JB (1983). "Herpes zoster:treatment with cemetidine.". Can Med Assoc J 129 (12): 1284-1285. PMID 6652595.
20. ^ Komlos L, Notmann J, Arieli J, et.al. (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine.". Asian Pac J Allelrgy Immunol 12 (1): 51-58. PMID 7872992.
21. ^ De Bony F, Tod M, Bidault R, On NT, Posner J, Rolan P. (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir". Antimicrob. Agents Chemother. 46 (2): 458-463. PMID 11796358.
22. ^ Winstead ER.. Two new anti-herpes drugs tested. Genome News Network. Retrieved on 2006-03-20.
23. ^ Kleymann G, Fischer R, Betz UA, Hendrix M, Bender W, Schneider U, Handke G, Eckenberg P, Hewlett G, Pevzner V, Baumeister J, Weber O, Henninger K, Keldenich J, Jensen A, Kolb J, Bach U, Popp A, Maben J, Frappa I, Haebich D, Lockhoff O, Rubsamen-Waigmann H. (2002). "New helicase-primase inhibitors as drug candidates for the treatment of herpes simplex disease". Nat. Med. 8 (4): 392-398. PMID 11927946.
24. ^ Crute JJ, Grygon CA, Hargrave KD, Simoneau B, Faucher AM, Bolger G, Kibler P, Liuzzi M, Cordingley MG. (2002). "Herpes simplex virus helicase-primase inhibitors are active in animal models of human disease". Nat. Med. 8 (4): 386-391. PMID 11927945.
25. ^ Liuzzi M, Kibler P, Bousquet C, Harji F, Bolger G, Garneau M, Lapeyre N, McCollum RS, Faucher AM, Simoneau B, Cordingley MG. (2004). "Isolation and characterization of herpes simplex virus type 1 resistant to aminothiazolylphenyl-based inhibitors of the viral helicase-primase". Antiviral Res. 64 (3): 161-170. PMID 15550269.
26. ^ Schang LM, Coccaro E, Lacasse JJ. (2005). "Cdk inhibitory nucleoside analogs prevent transcription from viral genomes.". Nucleosides Nucleotides Nucleic Acids. 24 (5-7): 829-837. PMID 16248044.
27. ^ Diwan P, Lacasse JJ, Schang LM. (2004). "Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors". J. Virol. 78 (17): 9352-9365. PMID 15308730.
28. ^ Schang LM. (2005). "Advances on cyclin-dependent kinases (CDKs) as novel targets for antiviral drugs". Curr. Drug Targets Infect. Disord. 5 (1): 29-37. PMID 15777196.
29. ^ McCune MA, Perry HO, Muller SA, O'Fallon WM. (2005). "Treatment of recurrent herpes simplex infections with L-lysine monohydrochloride". Cutis. 34 (4): 366-373. PMID 6435961.
30. ^ a b Griffith RS, Walsh DE, Myrmel KH, Thompson RW, Behforooz A. (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183-190. PMID 3115841.
31. ^ Griffith RS, Norins AL, Kagan C. (1978). "A multicentered study of lysine therapy in Herpes simplex infection". Dermatologica. 156 (5): 257-267. PMID 640102.
32. ^ Lo JC, Chertow GM, Rennke H, Seifter JL. (1996). "Fanconi's syndrome and tubulointerstitial nephritis in association with L-lysine ingestion.". Am. J. Kidney Dis. 28 (4): 614-617. PMID 8840955.
33. ^ Zacharopoulos VR, Phillips DM. (1997). "Vaginal formulations of carrageenan protect mice from herpes simplex virus infection". Clin. Diagn. Lab. Immunol. 4 (4): 465-468. PMID 9220165.
34. ^ Carlucci MJ, Scolaro LA, Damonte EB. (1999). "Inhibitory action of natural carrageenans on Herpes simplex virus infection of mouse astrocytes". Chemotherapy 45 (6): 429-436. PMID 10567773.
35. ^ Andersen JH, Jenssen H, Gutteberg TJ. (2003). "Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir". Antiviral Res. 58 (3): 209-215. PMID 12767468.
36. ^ Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL. (1999). "Resveratrol inhibition of herpes simplex virus replication". Antiviral Res. 43 (3): 145-155. PMID 10551373.
37. ^ Docherty JJ, Smith JS, Fu MM, Stoner T, Booth T. (2004). "Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice". Antiviral Res. 61 (1): 19-26. PMID 14670590.
38. ^ Karadi I, Karpati S, Romics L. (1998). "Aspirin in the management of recurrent herpes simplex virus infection". Ann. Intern. Med. 128 (8): 696-697. PMID 9537952.
39. ^ Gebhardt BM, Varnell ED, Kaufman HE. (2004). "Acetylsalicylic acid reduces viral shedding induced by thermal stress". Curr. Eye Res. 29 (2-3): 119-125. PMID 15512958.
40. ^ Unknown (2005). "Herpes simplex virus oral", in Klasco RK (ed.): AltMedDex System. Greenwood Village, CO: Thomson Micromedex.
41. ^ Snipes W, Person S, Keith A, Cupp J. "Butylated hydroxytoluene inactivates lipid-containing viruses" Science. 1975;188(4183):64-6
42. ^ Richards JT, Katz ME, Kern ER. "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs" Antiviral Res 1985;5(5):281-90
43. ^ Poon AP, Liang Y, Roizman B. (2003). "Herpes simplex virus 1 gene expression is accelerated by inhibitors of histone deacetylases in rabbit skin cells infected with a mutant carrying a cDNA copy of the infected-cell protein no. 0". J. Virol. 77 (23): 12671-12678. PMID 14610189.
44. ^ Brocklehurst P, Kinghorn GA et al.. "randomised placebo controlled trial of suppressive acyclovir in late pregnancy in women with recurrent genital herpes infection" 105 (3): 275-80.
45. ^ Recurring viral meningitis & herpes II. Med Help International. Retrieved on 2006-11-21.
46. ^ Vezina C, Steben M. (2001). "Genital Herpes: Psychosexual Impacts and Counselling". The Canadian Journal of CME (June): 125-134.
47. ^ Herpes Support Groups & Clinics
48. ^ Herpes message forum with over 4000 members
49. ^ H-Date, a dating site for persons with either or both of HSV-1 or HSV-2
50. ^ MPwH - Meeting People with Herpes, a dating site with over 65000 members
51. ^ Webpage on social aspects of genital herpes
52. ^ Time Magazine archives
53. ^ Film Database description of Intimate Agony
54. ^ Wikipedia article including reference to the song Herpes
55. ^ Film Database description of Merry Christmas...
56. ^ Description of novel Stigma
57. ^ Green J, Ferrier S, Kocsis A, Shadrick J, Ukoumunne OC, Murphy S, Hetherton J. (2003). "Determinants of disclosure of genital herpes to partners.". Sex. Transm. Infect. 79 (1): 42-44. PMID 12576613.
58. ^ Webpage on social aspects of genital herpes
59. ^ Myths and Facts about Genital Herpes. Famciclovir (2007). Retrieved on 2007-01-31.

All About Phthiriasis

2007-04-02T23:50:00.014-07:00

Phthiriasis is a common eyelid infestation, caused by Phthirus pubis (pubic lice, sometimes referred to as crab lice). Pediculosis is an eyelid infestation by either Pediculus humanus corporis(body) or Pediculus humanus capitus (head) lice.

Therapy

One of the following topical ocular therapy is recommended:

* Petroleum jelly or other bland ointments, TID
* Mercuric oxide 1%
* Ammoniated mercuric oxide 3%, twice a day
* Physostigmine (a Cholinesterase inhibitor)

All About Onchocerciasis - River Blindness

2007-04-02T23:50:00.013-07:00

Onchocerciasis (pronounced [ɒn.kəʊ.sɜːˈkaɪə.sɪs]) or river blindness is the world's second leading infectious cause of blindness. It is caused by Onchocerca volvulus, a parasitic worm that can live for up to fourteen years in the human body.

The life cycle of O. volvulus begins when a parasitised female Black fly of the genus Simulium takes a blood meal. Saliva containing stage three O. volvulus larvae passes into the blood of the host. From here the larvae migrate to the subcutaneous tissue where they form nodules and then mature into adult worms over a period of six to twelve months. After maturation, the smaller adult males migrate from nodules to subcutaneous tissue where they mate with the larger adult females, producing between 1000 and 3000 eggs per day. The normal adult worm lifespan is up to 15 years. The eggs mature internally to form stage one microfilariae, which are released from the female's body one at a time and remain in the subcutaneous tissue.

These stage one microfilariae are taken up by black flies upon a blood meal, in which they mature over the course of one to three weeks to stage three larvae, thereby completing the life cycle. Humans are the only definitive host for O. Volvulus. The normal microfilariae lifespan is 1-2 years.

Causes of morbidity

Adult worms remain in subcutaneous nodules, limiting access to the host's immune system. Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. Dying microfilariae have been recently discovered to release Wolbachia-derived antigens, triggering innate immune responses and producing the inflammation and its associated morbidity. Wolbachia species have been found to be endosymbionts of O. Volvulus adults and microfilariae and are thought to be the driving force behind most of O. Volvulus morbidity. Severity of illness is directly proportional to the number of microfilariae and the power of the resultant inflammatory response.

Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has developed to categorize the degree of skin involvement: Acute papular dermatitis - scattered pruritic papules; Chronic papular dermatitis - larger papules, resulting in hyperpigmentation; Lichenified dermatitis - hyperpigmented papules and plaques, with edema, lymphadenopathy, pruritus and common secondary bacterial infections; Skin atrophy - loss of elasticity, skin resembles tissue paper, 'lizard skin' appearance; Depigmentation - 'leopard skin' appearance, usually on anterior lower leg.

Ocular involvement provides the common name associated with onchocerciasis, river blindness. The surface of the cornea is another area to which the microfilariae migrate, where they are also attacked by the immune system. In the area that is damaged, punctate keratitis occurs, which clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time the entire cornea may become opaque, thus leading to blindness.

Treatment and control

The treatment for onchocerciasis is ivermectin (Mectizan); infected people can be treated once every twelve months. The drug paralyses the microfilariae and prevents them from causing itching. In addition, while the drug does not kill the adult worm, it does prevent them from producing additional offspring. The drug therefore prevents both morbidity and transmission.

Since 1988, ivermectin has been provided free of charge by Merck & Co. through the Mectizan Donation Program (MDP). The MDP works together with ministries of health and non-governmental development organisations such as the World Health Organization to provide free Mectizan to those who need it in endemic areas.

There are various control programs that aim to stop onchocerciasis from being a public health problem. The first was the Onchocerciasis Control Programme (OCP), which was launched in 1974 and at its peak covered 30 million people in eleven countries. Through the use of larvicide spraying of fast flowing rivers to control black fly populations and, from 1988 onwards, the use of ivermectin to treat infected people, the OCP eliminated onchocerciasis as a public health problem. The OCP, a joint effort of the World Health Organisation, the World Bank, the United Nations Development Programme and the UN Food and Agriculture Organization, was considered to be a success and came to an end in 2002. Continued monitoring ensures that onchocerciasis cannot reinvade the area of the OCP.

In 1992 the Onchocerciasis Elimination Programme for the Americas (OEPA) was launched. The OEPA also relies on ivermectin.

In 1995 the African Programme for Onchocerciasis Control (APOC) began covering another nineteen countries and mainly relying upon the use of ivermectin. Its goal is to set up a community-directed supply of ivermectin for those who are infected. In these ways, transmission has declined.

See also

* Carter Center River Blindness Program

CDC Parasites of Public Health Concern [1]

All About Loa loa filariasis

2007-04-02T23:50:00.012-07:00

Loa loa filariasis (also loiasis and African eyeworm) is a skin and eye disease caused by the nematode worm, loa loa filaria. Humans contract this disease through the bite of a horsefly, also known as mango fly. The deer fly is also a vector of Loa loa. The disease can cause red itchy swellings below the skin called "Calabar swellings". The disease is treated with the drug diethylcarbamazine (DEC).

Human loiasis geographical distribution is restricted to the rain forest and swamp forest areas of West Africa, being especially common in Cameroon and on the Ogowe River. Humans are the only known natural reservoir. It is estimated that 2-13 million humans are infected with the Loa loa larvae.

Life cycle
Loa loa life cycle. Source: CDC

The vector for Loa loa filariasis are flies from two hematophagous species of the genus Chrysops, C. silacea and C. dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. The larvae develop into adults that commonly reside in subcutaneous tissue. The female worms measure 40 to 70 mm in length and 0.5 mm in diameter, while the males measure 30 to 34 mm in length and 0.35 to 0.43 mm in diameter. Adults produce microfilariae measuring 250 to 300 μm by 6 to 8 μm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs. The fly ingests microfilariae during a blood meal. After ingestion, the microfilariae lose their sheaths and migrate from the fly's midgut through the hemocoel to the thoracic muscles of the arthropod. There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae. The third-stage infective larvae migrate to the fly's proboscis and can infect another human when the fly takes a blood meal.

Clinical features

Lymphatic filariasis such as loiasis most often consists of asymptomatic microfilaremia. Some patients develop lymphatic dysfunction causing lymphedema. Episodic angioedema (Calabar swellings) in the arms and legs, caused by immune reactions are common. When chronic, they can form cyst-like enlargements of the connective tissue around the sheaths of muscle tendons, becoming very painful when moved. The swellings may last for 1-3 days, and may be accompanied by localized urticaria (skin eruptions) and pruritus (itching). Subconjunctival migration of an adult worm to the eyes can also occur frequently, in this is the reason Loa loa is also called the "African eye worm." The passage over the eyeball can be sensed, but it usually takes less than 15 min. Gender incidence of eyeworms have approximately the same frequency, but it tends to increase with age. Eosinophilia is often prominent in filarial infections. Dead worms may cause chronic abscesses, which may lead to the formation of granulomatous reactions and fibrosis.

Laboratory diagnosis

Identification of microfilariae by microscopic examination is the most practical diagnostic procedure. Examination of blood samples will allow identification of microfilariae of Loa loa. It is important to time the blood collection with the known periodicity of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin (see staining (biology)). For increased sensitivity, concentration techniques can be used. These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore® membrane.

Antigen detection using an immunoassay for circulating filarial antigens constitutes a useful diagnostic approach, because microfilaremia can be low and variable. Identification of adult worms is possible from tissue samples collected during subcutaneous biopsies or worm removal from the eye. Antibody detection is of limited value. Substantial antigenic cross reactivity exists between filaria and other helminths, and a positive serologic test does not distinguish between past and current infection.

Source

* Loa Loa. Center for Disease Control and Prevention (CDC). US Government public domain text and images.

All About Leishmaniasis

2007-04-02T23:50:00.011-07:00

Leishmaniasis is a disease caused by protozoan parasites that belong to the genus Leishmania and is transmitted by the bite of certain species of sand fly, including flies in the genus Lutzomyia in the New World and Phlebotomus in the Old World. The disease was named in 1901 for the Scottish pathologist William Boog Leishman. This disease is also known as Leichmaniosis, Leishmaniose, leishmaniose, and formerly, Orient Boils, kala azar, black fever, sandfly disease, Dum-Dum fever or espundia.

Most forms of the disease are transmissible only from animals (zoonosis), but some can be spread between humans. Human infection is caused by about 21 of 30 species that infect mammals. These include the L. donovani complex with three species (L. donovani, L. infantum, and L. chagasi); the L. mexicana complex with 3 main species (L. mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Viannia with four main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L. (V.) peruviana). The different species are morphologically indistinguishable, but they can be differentiated by isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies.

Visceral leishmaniasis is a severe form in which the parasites have migrated to the vital organs.

Geography and epidemiology

Leishmaniasis can be transmitted in many tropical and sub-tropical countries, and is found in parts of about 88 countries. Approximately 350 million people live in these areas. The settings in which leishmaniasis is found range from rainforests in Central and South America to deserts in West Asia. More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.

Leishmaniasis is also found in Mexico, Central America, and South America—from northern Argentina to southern Texas (not in Uruguay, Chile, or Canada), southern Europe (leishmaniasis is not common in travelers to southern Europe), Asia (not Southeast Asia), the Middle East, and Africa (particularly East and North Africa, with some cases elsewhere). The disease is not found in Australia or Oceania.

Leishmaniasis is present in Iraq and was contracted by a number of the troops involved in the 2003 invasion of that country and the subsequent occupation. The soldiers nicknamed the disease the Baghdad boil. It has been reported by Agence France-Presse that more than 650 U.S. soldiers may have experienced the disease between the start of the invasion in March 2003 and late 2004. [1] [2]

During 2004, it is calculated that some 3,400 troops from the Colombian army, operating in the jungles near the south of the country (in particular around the Meta and Guaviare departments), were infected with Leishmaniasis. Apparently, a contributing factor was that many of the affected soldiers did not use the officially provided insect repellent, because of its allegedly disturbing odor. It is estimated that nearly 13,000 cases of the disease were recorded in all of Colombia throughout 2004, and about 360 new instances of the disease among soldiers had been reported in February 2005. [3] [4] [5]

In September 2005 the disease was contracted by at least four Dutch marines who were stationed in Mazari Sharif, Afghanistan and subsequently repatriated for treatment.

Life cycle
Life cycle of the Leishmaniasis parasite. Source: CDC
Life cycle of the Leishmaniasis parasite. Source: CDC

Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, metacyclic promastigotes, during blood meals (1). Metacyclic promastigotes that reach the puncture wound are phagocytized by macrophages (2) and transform into amastigotes (3). Amastigotes multiply in infected cells and affect different tissues, depending in part on which Leishmania species is involved (4). These differing tissue specificities cause the differing clinical manifestations of the various forms of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes (5,6). In the sandfly's midgut, the parasites differentiate into promastigotes (7), which multiply, differentiate into metacyclic promastigotes and migrate to the proboscis (8)

Signs and symptoms

The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person affected is bitten by sand flies. Other consequences, which can become manifest anywhere from a few months to years after infection, include fever, damage to the spleen and liver, and anaemia.

In the medical field, leishmaniasis is one of the famous causes of a markedly enlarged spleen, which may become larger even than the liver. There are four main forms of leishmaniasis:

* Visceral leishmaniasis - the most serious form and potentially fatal if untreated.
* Cutaneous leishmaniasis - the most common form which causes numerous sores on the body, which heal within a few months leaving unpleasant looking scars.
* Diffuse cutaneous leishmaniasis - this form produces widespread skin lesions which resemble leprosy and is particularly difficult to treat.
* Mucocutaneous leishmaniasis - commences with skin ulcers which spread causing tissue damage to (particularly) nose and mouth

Treatment

There are two common therapies containing antimony, meglumine antimoniate (Glucantim®) and sodium stibogluconate (Pentostam®). It is not completely understood how these drugs act against the parasite; they may disrupt its energy production or trypanothione metabolism. Unfortunately, in many parts of the world, the parasite has become resistant to antimony and for visceral or mucocutaneous leishmaniasis,[1] amphotericin is now the treatment of choice. Failure of AmBisome® to treat visceral leishmaniasis (Leishmania donovani) has been reported in Sudan,[2] but this failure may be related to host factors such as co-infection with HIV or tuberculosis rather than parasite resistance.

Miltefosine (Impavido®), is a new drug for visceral and cutaneous leishmaniasis. The cure rate of miltefosine in phase III clinical trials is 95%; Studies in Ethiopia show that is also effective in Africa. In HIV immunosuppressed people who are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment. Clinical trials in Colombia showed a high efficacy for cutaneous leishmaniasis. In mucocutaneous cases caused by L.brasiliensis it has shown to be more effective than other drugs. Miltefosine received approval by the Indian regulatory authorities in 2002 and in Germany in 2004. In 2005 it received the first approval for cutaneous leishmaniasis in Colombia. Miltefosine is also currently being investigated as treatment for mucocutaneous leishmaniasis caused by L. braziliensis in Colombia,[1] and preliminary results are very promising. It is now registered in many countries and is the first orally administered breakthrough therapy for visceral and cutaneous leishmaniasis.[3](More, et al, 2003). In October 2006 it received orphan drug status from the US Food and Drug administration. The drug is generally better tolerated than other drugs. Main side effects are gastrointetinal disturbance in the 1-2 days of treatment which does not affect the efficacy. Because it is available as an oral formulation, the expense and inconvenience of hospitalisation is avoided, which makes it an attractive alternative.

The Institute for OneWorld Health has developed paromomycin, results with which led to its approval as an orphan drug. The Drugs for Neglected Diseases Initiative is also actively facilitating the search for novel therapeutics.

Drug-resistant leishmaniasis may respond to immunotherapy (inoculation with parasite antigens plus an adjuvant) which aims to stimulate the body's own immune system to kill the parasite.[4]

Several potential vaccines are being developed, under pressure from the World Health Organization, but as of 2006 none is available. The team at the Laboratory for Organic Chemistry at the Swiss Federal Institute of Technology (ETH) in Zürich are trying to design a carbohydrate-based vaccine [6]. The genome of the parasite Leishmania major has been sequenced,[5] possibly allowing for identification of proteins that are used by the pathogen but not by humans; these proteins are potential targets for drug treatments.

Leishmaniosis as part of the CVBDs

CVBD stands for Canine Vector-borne diseases, which are diseases transmitted through Ectoparasites.

See also

* Visceral leishmaniasis (kala azar)

References

1. ^ a b Soto J, Toledo JT.. "Oral miltefosine to treat new world cutaneous leishmaniasis". Lancet Infect Dis 7 (1): 7.
2. ^ Mueller M, Ritmeijer K, Balasegaram M, Koummuki Y, Santana MR, Davidson R. (2007). "Unresponsiveness to AmBisome® in some Sudanese patients with kala-azar". Trans R Soc Trop Med Hyg 101 (1): 19–24. DOI:10.1016/j.trstmh.2006.02.005.
3. ^ Jha TK, Sundar S, Thakur CP et al. (1999). "Miltefosine, an oral agent, for the treatment of Indian visceral leishmaniasis". New Engl J Med 341: 1795–800.
4. ^ Badaro R, Lobo I, Munõs A, et al. (2006). "Immunotherapy for drug-refractory mucosal leishmaniasis". J Infect Dis 194: 1151–59.
5. ^ Ivens AC, et al. (2005). "The genome of the kinetoplastid parasite, Leishmania major". Science 309 (5733): 436–42. PMID 16020728.

All About Xanthelasma

2007-04-02T23:50:00.010-07:00

Xanthelasma (or xanthelasma palpebrarum) is a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids. Although not harmful or painful, these minor growths may be disfiguring and can be removed surgically. The plural is "xanthelasmata". They are common in people of Asian extraction and those from the Mediterranean region. Xanthelasmata can be removed surgically (scarring possible), or with laser or with cryotherapy, both of which can cause scarring and pigment changes. Because of the hereditary component, they may or may not indicate high blood levels of cholesterol. Where there is no family history of xanthelasmata they usually indicate high cholesterol and may correlate with a risk of atheromatous disease (cholesterol building up in arteries). The root of the word is from Greek xanthos, ξανθος, "yellow".

Associations

* high cholesterol levels (specifically familial hypercholesterolemia)
* primary biliary cirrhosis
* Menopause
* Diabetes

See also

* Xanthoma

All About Ptosis of the eyelid

2007-04-02T23:50:00.009-07:00

In ophthalmology, ptosis is an abnormally low position (drooping) of the upper eyelid which may grow more or less severe during the day. Ptosis occurs when the muscle that usually raises the eyelid is not strong enough to do so. It can affect one eye or both eyes and is more common in the elderly, as muscles in the eyelids may begin to deteriorate. One can, however, be born with ptosis, as it is hereditary. Ptosis may be caused by damage/trauma to the muscle which raises the eyelid, or damage to the nerve which controls this muscle. Such damage could be a sign or symptom of an underlying disease such as diabetes mellitus, a brain tumor, and diseases which may cause weakness in muscles or nerve damage, such as myasthenia gravis. Ptosis that is caused by a disease will improve if the disease is treated successfully.

Depending upon the cause it can be classified into:

* Neurogenic ptosis which includes IIIrd cranial nerve palsy, Horner's Syndrome, Marcus Gunn jaw winking syndrome, IIIrd cranial nerve misdirection.
* Myogenic ptosis which includes myasthenia gravis, myotonic dystrophy, ocular myopathy, simple congenital ptosis, blepharophimosis syndrome
* Aponeurotic ptosis which may be involutional or post-operative.
* Mechanical ptosis which occurs due to edema or tumors of the upper lid
* Neurotoxic ptosis which is a classic symptom of envenomation by elapids such as cobras and kraits etc. Neurotoxic ptosis is a precursor to respiratory failure and eventual suffocation. Urgent medical intervention is therefore required.

Treatment

Treatment depends on the type of ptosis.

Aponeurotic and congenital ptosis may require surgical correction if severe or if cosmesis is a concern. Surgical procedures include:

* Levator resection
* Frontalis sling operation

Non-surgical modalities like the use of "crutch" glasses to support the eyelid may also be used.

Well known persons with ptosis

* Forest Whitaker, Academy Award winning actor and director
* Thom Yorke, musician and singer for the rock band Radiohead

See also

* Dermatochalasis
* Horner's syndrome
* Iris sphincter muscle

All About Blepharochalasis

2007-04-02T23:50:00.008-07:00

Blepharochalasis is an inflammation of the eyelid that is characterized by exacerbations and remissions of eyelid edema, which results in a stretching and subsequent atrophy of the eyelid tissue. It typically affects only the upper eyelids, and may be unilateral as well as bilateral.

Pathophysiology

Blepharochalasis results from recurrent bouts of painless eyelid swelling, each lasting for several days. This is thought to be a form of localized angioedema, or rapid accumulation of fluid in the tissues. Recurrent episodes lead to thin and atrophic skin. Damage to the levator palpebrae superioris muscle causes ptosis, or drooping of the eyelid, when the muscle can no longer hold the eyelid up.

Causes

Blepharochalasis is idiopathic in most cases- the cause is unknown. Systemic conditions linked to blepharochalasis are renal agenesis, vertebral abnormalities, and congenital heart disease.

Epidemiology

It is encountered more commonly in younger rather than older individuals.

Complications

Complications of blepharochalasis may include conjunctival hyperemia (excessive blood flow through the moist tissues of the orbit), chemosis, entropion, ectropion, and ptosis.

Differential diagnosis

Dermatochalasis is sometimes confused with blepharochalasis, but these are two different conditions.

Treatment/Surgery

An oculoplastic surgeon is required to decide and perform the appropriate surgical procedure. Following procedures have been described for blepharochalasis:

* External levator aponeurosis tuck
* Blepharoplasty
* Lateral canthoplasty
* Dermis fat grafts

They are used to correct atrophic blepharochalasis after the syndrome had run its course.

All About Lagophthalmos

2007-04-02T23:50:00.007-07:00

Lagophthalmos is defined as the inability to close the eyelids completely.[1]

Blinking causes the eye to be being by a thin film of fluid (the tears). This is crucial to maintain lubrification and proper eye health. The tears also flush out foreign bodies and wash them away.

References

1. ^ Cline D; Hofstetter HW; Griffin JR. Dictionary of Visual Science. 4th ed. Butterworth-Heinemann, Boston 1997. ISBN 0-7506-9895-0

All About Ectropion

2007-04-02T23:50:00.006-07:00

Ectropion is a medical condition in which the lower eyelid turns outwards. The condition can be repaired surgically. Ectropion is also found in dogs as a genetic disorder in certain breeds.

Causes

* Congenital
* Aging
* Scarring
* Mechanical
* Allergic
* Facial nerve palsy

[edit] Ectropion in dogs
Ectropion in a Cocker Spaniel
Ectropion in a Cocker Spaniel

Ectropion in dogs usually involves the lower eyelid. Often the condition has no symptoms, but tearing and conjunctivitis may be seen. Breeds associated with ectropion include the Cocker Spaniel, the Saint Bernard, the Bloodhound, and the Basset Hound.[1] It can also result from trauma or nerve damage. Treatment (surgery) is only recommended if there is chronic conjunctivitis or if there is corneal damage. A small part of the affected lid is removed and then the lid is sewn back together.

References

1. ^ Gelatt, Kirk N. (ed.) (1999). Veterinary Ophthalmology, 3rd ed., Lippincott, Williams & Wilkins. ISBN 0-683-30076-8.

[edit] See also

* Entropion
* List of eye diseases and disorders

All About Trichiasis

2007-04-02T23:50:00.005-07:00

Trichiasis is a medical term for ingrown eyelashes. This can be caused by infection, inflammation, autoimmune conditions, and trauma such as burns or eyelid injury.

Standard treatment involves destruction of the affected eyelashes with electrology, specialized laser, or surgery.

Trichiasis in dogs is hair from the eyelid growing in the wrong direction and rubbing on the eye, causing irritation. It usually occurs at the lateral upper eyelid, especially in the English Cocker Spaniel.[1] Trichiasis also refers to hair from a nasal fold rubbing on the eye. This type of trichiasis can be flattened by rubbing petroleum jelly onto it, but surgery is sometimes necessary for permanent correction.

References

1. ^ Gelatt, Kirk N. (ed.) (1999). Veterinary Ophthalmology, 3rd ed., Lippincott, Williams & Wilkins. ISBN 0-683-30076-8.

All About Entropion

2007-04-02T23:50:00.004-07:00

Entropion is a medical condition in which the eyelids fold inward. It is very uncomfortable, as the eyelashes rub against the cornea constantly. Entropion is usually caused by genetic factors and may be congenital. Trachoma infection may cause scarring of the inner eyelid, which may cause entropion.

Symptoms of entropion include:

* Redness and pain around the eye
* Sensitivity to light and wind
* Sagging skin around the eye
* Excessive tearing
* Decreased vision, especially if the cornea is damaged

Treatment is a simple surgery in which excess skin of the outer lids is removed. Prognosis is excellent if surgery is performed before the cornea is damaged.

Causes

* Congenital
* Aging
* Scarring
* Spasm

Entropion in dogs

Entropion has been documented in most dog breeds, although there are some breeds (particularly purebreds) that are more commonly affected than others. These include the Chow Chow, Shar Pei, St. Bernard, Cocker Spaniel, Boxer, Springer Spaniel, Labrador Retriever, Cavalier King Charles Spaniel, Bull Mastiff, Great Dane, Irish Setter, and Poodle.[1] The condition is usually present by six months of age. Entropion can also occur secondary to pain in the eye, scarring of the eyelid, or nerve damage. The upper or lower eyelid can be involved, and one or both eyes may be affected. When entropion occurs in both eyes, this is known as "bilateral entropion."

Upper lid entropion involves the eyelashes rubbing on the eye, but the lower lid usually has no eyelashes, so hair rubs on the eye. Surgical correction is used in more severe cases. A strip of skin and orbicularis oculi muscle are removed parallel to the affected portion of the lid and then the skin is sutured. Shar Peis, who often are affected as young as two or three weeks old, respond well to temporary eyelid tacking. The entropion is often corrected after three to four weeks, and the sutures are removed.[1]

References

Humans

* http://www.kellogg.umich.edu/patientcare/conditions/entropion.html
* http://www.nlm.nih.gov/medlineplus/ency/article/001008.htm
* http://www.upei.ca/~cidd/Diseases/ocular%20disorders/entropion.htm

Dogs

1. ^ a b Gelatt, Kirk N. (ed.) (1999). Veterinary Ophthalmology, 3rd ed., Lippincott, Williams & Wilkins. ISBN 0-683-30076-8.

See also

* Ectropion
* List of eye diseases and disorders

All About Blepharitis

2007-04-02T23:50:00.003-07:00

Blepharitis is inflammation of the eyelids. It is characterized by flaky debris at the eyelash bases. Blepharitis usually causes redness of the eyes and itching and irritation of the eyelids in both eyes. Its appearance is often confused with conjunctivitis and due to its recurring nature it is the most common cause of "recurrent conjunctivitis" in older people. It is also often treated as 'dry eye' by patients due to the gritty sensation it may give the eyes - although lubricating drops do little to improve the condition.

There are two types:

1. Anterior blepharitis affects the front of the eyelids near the eyelashes. The causes are seborrheic dermatitis (similar to dandruff) and occasional infection by Staphylococcus bacteria.
2. Posterior blepharitis affects the back of the eyelids, the part that makes contact with the eyes. This is caused by the oil glands present in this region.

Staphylococcal blepharitis

Staphlycoccal blepharitis is a type of external eye inflammation. As with dandruff, it is usually asymptomatic until the disease progresses. As it progresses, the sufferer begins to notice a foreign body sensation, matting of the lashes, and burning. Usually, the primary care physician will prescribe topical antibiotics for staphylococcal blepharitis.

This ailment can sometimes lead to a stye, which is caused by the same bacterium.

Seborrheic blepharitis

Seborrheic blepharitis, the inherited most common type of blepharitis, is usually one part of the spectrum of seborrheic dermatitis seborrhea which involves the scalp, lashes, eyebrows, nasolabial folds and ears. Treatment is best accomplished by a dermatologist.

Treatment and management

Many forms of treatment will improve blepharitis, including both antibiotic or steroid eye drops, and certain oral antibiotics. Unfortunately it will usually recur when any treatment is ceased. Most doctors will therefore recommend a regime of daily eyelid cleaning which is both effective and can be continued safely long-term. Such a regime needs to be convenient enough to be continued lifelong, otherwise the cleaning will stop when symptoms subside. Therefore simply cleaning the eyelids with a face cloth during every bath or shower may be a good system for a sufferer to adopt. Using dilute baby shampoo with warm water to assist with this is often advised, although probably the most important factor is the mechanical clearance of discharge from the eyelid meibomian glands. Massaging the eyelids firmly during cleaning helps this.[1]

Dermatologists treat blepharitis similarly to seborrheic dermatitis by using safe topical anti-inflammatory medication like sulfacetamide or brief courses of a mild topical steroid. Although anti-fungals like ketoconazole (Nizoral) are commonly prescribed for seborrheic dermatitis, dermatologists and optometrists usually do not prescribe anti-fungals for seborrheic blepharitis. [2]

See also

* List of skin diseases
* List of eye diseases and disorders

References

1. ^ Moorfields eye hospital (UK) Patient information leaflet: Blepharitis - Lid Hygiene Advice For Patients
2. ^ Derbel M, Benzina Z, Ghorbel I, Abdelmoula S, Makni F, Ayadi A, Feki J (2005). "[Malassezia fungal blepharitis: a case report]". J Fr Ophtalmol 28 (8): 862-5. PMID 16249768.

All About Chalazion

2007-04-02T23:50:00.002-07:00

A chalazion, also known as a meibomian gland lipogranuloma, is a cyst in the eyelid that is caused by inflammation of the meibomian gland, usually on the upper eyelid. Chalazions differ from styes (hordeolums) in that they are usually painless apart from the tenderness caused when they swell up. A chalazion may eventually disappear on its own after a few months, though more often than not, some treatment is necessary.

Signs and symptoms

* Swelling on the eyelid
* Eyelid tenderness
* Sensitivity to light
* Increased tearing

Treatment

The primary treatment is application of warm compresses for 10 - 20 minutes at least 4 times a day. This may soften the hardened oils blocking the duct and promote drainage and healing.

Topical antibiotic eye drops or ointment (eg chloramphenicol or fusidic acid) are sometimes used for the initial acute infection, but are otherwise of little value in treating a chalazion. Chalazia will often disappear without further treatment within a few months and virtually all will resorb within two years.[1]

If they continue to enlarge or fail to settle within a few months, then smaller lessions may be injected with a corticosteroid or larger one may be surgically removed using local anesthesia.[2][3] This is usually done from underneath the eyelid to avoid a scar on the skin. Rarely chalazia may reoccur and these will be biopsied to help rule out tumors.

Complications

A large chalazion can cause astigmatism due to pressure on the cornea. This will resolve with resolution of the chalazion.

Complications including, but not limited to hypopigmentation may occur with corticosteroid injection.

The presence of recurring chalazion in the same area should lead to a consideration of sebaceous cell carcinoma.

Prevention

Proper cleansing of the eyelid may prevent recurrences in people prone to chalazia. Cleaning the eyelash area with diluted baby shampoo will help reduce clogging of the ducts.[4]

References

* (1994) in J.B. Lippincott: The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease.

Footnotes

1. ^ Chalazion GPnotebook 2080768019
2. ^ Khurana A, Ahluwalia B, Rajan C (1988). "Chalazion therapy. Intralesional steroids versus incision and curettage". Acta Ophthalmol (Copenh) 66 (3): 352-4. PMID 10994460.
3. ^ Jackson T, Beun L (2000). "A prospective study of cost, patient satisfaction, and outcome of treatment of chalazion by medical and nursing staff". Br J Ophthalmol 84 (7): 782-5. PMID 10873994. - in which of those cases attending a District General Hospital, approximately one third of selected chalazia resolved within 3 months with conservative treatment, and surgical treatment was successful for 72%.
4. ^ (UK) Moorfields Eye Hospital. Blepharitis - Lid Hygiene Advice For Patients (DOC). - Patient information leaflet

All About Styes - Hordeolum

2007-04-02T23:50:00.001-07:00

A stye (also spelled sty) or hordeolum is an infection of the sebaceous glands at the base of the eyelashes. While they produce no lasting damage, they can be quite painful.

Causes

Styes are generally caused by a Staphylococcus bacteria infection and are particularly common in infants, though people of any age may experience them. They are commonly associated with stress, probably because people under stress tend to get less sleep and therefore rub their eyes more often, thus transporting the bacteria into the eye.[citation needed]

A stye can be secondary, caused by blepharitis. A blocked oil gland near the eye, a chalazion, is often mistaken for a stye.[1]

Treatment

Most styes will drain on their own though this may be accelerated with a hot or warm compress. Styes typically resolve within 1 week with treatment. Since a stye is technically a pimple, it can be popped. However, doing so is not recommended without technical expertise.

Medical professionals will sometimes lance a particularly persistent or irritating stye with a needle, to accelerate its draining. A stye's spread or expansion can also be fought with the use of antibiotic ointment akin to Neosporin (e.g. Erythromycin ophthalmic ointment), a special version being available for styes, which can be applied in a ribbon along the lid, on either inside or out. Medical professionals may also prescribe Amoxicillin for over a period of a week.

Folk remedies

Various folk remedies call for holding a metal or wooden spoon against the stye[2],[3] or the rubbing of a gold ring over it.[4] A folk remedy known in East Asia is to pluck an eyelash from the infected area — while a common German folk remedy involves looking through a sieve. In the other countries, remedies vary even more, although most of them have something to do with rubbing or holding an object against the stye. In Costa Rica for example, it is believed that a stye will go away if rubbed against a cat's tail or a recently laid egg[citation needed]. In Colombia, it is believed that a stye can be cured by pouring warm wine on the affected eye. Also common in the Maori culture of New Zealand is to rub infant urine against the eye[citation needed]. Place a still warm, slightly drained steeped teabag (traditional tea) over the afflicted eyelid as a compress. The tannins in the tea will help to draw the stye to a head like a pimple. May take several applications. Once the stye bursts be careful to rinse the eye so as not to get infected[citation needed]

References

1. ^ Styes, AllAboutVision.com. Retrieved August 20, 2006.
2. ^ Eyelid lumps, Good Hope Hospital NHS Trust. Retrieved March 19, 2007
3. ^ Stye, Dr Lockie's homœopathic healthcare. Retrieved March 19, 2007
4. ^ Folk remedies, The Handbook of Texas Online, University of Texas at Austin. Retrieved March 19, 2007

See also

* Blepharitis
* Chalazion

All About Diseases of the eye and adnexa - a List

2007-04-02T23:50:00.000-07:00

H00-H06 Disorders of eyelid, lacrimal system and orbit

* (H00.0) Hordeolum ("stye" or "sty") — a bacterial infection of sebaceous glands of eyelashes
* (H00.1) Chalazion — a cyst in the eyelid (usually upper eyelid)
* (H01.0) Blepharitis — inflammation of eyelids and eyelashes; characterized by white flaky skin near the eyelashes
* (H02.0) Entropion and trichiasis
* (H02.1) Ectropion
* (H02.2) Lagophthalmos
* (H02.3) Blepharochalasis
* (H02.4) Ptosis
* (H02.6) Xanthelasma of eyelid
* (H03.0*) Parasitic infestation of eyelid in diseases classified elsewhere
o Dermatitis of eyelid due to Demodex species ( B88.0+ )
o Parasitic infestation of eyelid in:
+ leishmaniasis ( B55.-+ )
+ loiasis ( B74.3+ )
+ onchocerciasis ( B73+ )
+ phthiriasis ( B85.3+ )
* (H03.1*) Involvement of eyelid in other infectious diseases classified elsewhere
o Involvement of eyelid in:
+ herpesviral (herpes simplex) infection ( B00.5+ )
+ leprosy ( A30.-+ )
+ molluscum contagiosum ( B08.1+ )
+ tuberculosis ( A18.4+ )
+ yaws ( A66.-+ )
+ zoster ( B02.3+ )
* (H03.8*) Involvement of eyelid in other diseases classified elsewhere
o Involvement of eyelid in impetigo ( L01.0+ )
* (H04.0) Dacryoadenitis
* (H04.2) Epiphora
* (H06.2*) Dysthyroid exophthalmos

H10-H13 Disorders of conjunctiva

* (H10) Conjunctivitis — inflammation of the conjunctiva
* (H11.0) Pterygium — benign growth of the conjunctiva
* (H11.3) Subconjunctival hemorrhage — burst blood vessels on conjunctiva
* (H13.1*) Conjunctivitis in infectious and parasitic diseases classified elsewhere
o Conjunctivitis (due to):
+ Acanthamoeba B60.1+ )
+ adenoviral follicular (acute) ( B30.1+ )
+ chlamydial ( A74.0+ )
+ diphtheritic ( A36.8+ )
+ gonococcal ( A54.3+ )
+ haemorrhagic (acute)(epidemic) ( B30.3+ )
+ herpesviral [herpes simplex] ( B00.5+ )
+ meningococcal ( A39.8+ )
+ Newcastle ( B30.8+ )
+ zoster ( B02.3+ )

H15-H22 Disorders of sclera, cornea, iris and ciliary body

* (H15.0) Scleritis — a painful inflammation of the sclera
* (H16) Keratitis — inflammation of the cornea
* (H16.0) Corneal ulcer / Corneal abrasion — loss of the surface epithelial layer of the eye's cornea
* (H16.1) Snow blindness / Arc eye — a painful condition caused by exposure of unprotected eyes to bright light
* (H16.1) Thygeson's superficial punctate keratopathy
* (H16.4) Corneal neovascularization
* (H18.5) Fuchs' dystrophy — cloudy morning vision
* (H18.6) Keratoconus — the cornea thins and changes shape to be more like a cone than a parabola
* (H19.3) Keratoconjunctivitis sicca — dry eyes
* (H20.0) Iritis — inflammation of the iris
* (H20.0, H44.1) Uveitis — inflammatory process involving the interior of the eye

H25-H28 Disorders of lens

* (H25-H26) Cataract — the lens becomes opaque

H30-H36 Disorders of choroid and retina

* (H33) Retinal detachment — the retina detaches from the choroid, leading to blurred and distorted vision
* (H33.1) Retinoschisis — the retina separates into several layers and may detach
* (H35.0) Hypertensive retinopathy — burst blood vessels, due to long-term high blood pressure
o (H35.0/E10-E14) Diabetic retinopathy damage to the retina caused by complications of diabetes mellitus, which could eventually lead to blindness
* (H35.0-H35.2) Retinopathy — general term referring to non-inflammatory damage to the retina
* (H35.1) Retinopathy of prematurity — scarring and retinal detachment in premature babies
* (H35.3) Age-related macular degeneration — the photosensitive cells in the macula malfunction and over time cease to work
* (H35.3) Macular degeneration — loss of central vision, due to macular degeneration
* (H35.5) Retinitis pigmentosa — genetic disorder; tunnel vision preceded by night-blindness
* (H35.81) Macular edema — distorted central vision, due to a swollen macula

H40-H42 Glaucoma

* (H40-H42) Glaucoma — optic neuropathy

H43-H45 Disorders of vitreous body and globe

* (H43.9) Floaters — shadow-like shapes which appear singly or together with several others in the field of vision

H46-H48 Disorders of optic nerve and visual pathways

* (H47.2) Leber's hereditary optic neuropathy — genetic disorder; loss of central vision

H49-H52 Disorders of ocular muscles, binocular movement, accommodation and refraction

* (H49-H50) Strabismus (Crossed eye/Wandering eye/Walleye) — the eyes do not point in the same direction
o (H49.3-4) Ophthalmoparesis — the partial or total paralysis of the eye muscles
o (H49.4) Progressive external ophthalmoplegia — weakness of the external eye muscles
o (H50.0, H50.3) Esotropia — the tendency for eyes to become cross-eyed
o (H50.1, H50.3) Exotropia — the tendency for eyes to look outward
* H52 Disorders of refraction and accommodation
o (H52.0) Hyperopia (Farsightedness) — the inability to focus on near objects (and in extreme cases, any objects)
o (H52.1) Myopia (Nearsightedness) — distant objects appear blurred
o (H52.2) Astigmatism — the cornea or the lens of the eye is not perfectly spherical, resulting in different focal points in different planes
o (H52.3) Anisometropia — the lenses of the two eyes have different focal lengths
o (H52.4) Presbyopia — a condition that occurs with growing age and results in the inability to focus on close objects
o (H52.5) Disorders of accommodation
+ Internal ophthalmoplegia

H53-H54 Visual disturbances and blindness

* (H53.0) Amblyopia (lazy eye) — poor or blurry vision due to either no transmission or poor transmission of the visual image to the brain
* (H53.0) Leber's congenital amaurosis — genetic disorder; appears at birth, characterised by sluggish or no pupillary responses
* (H53.1, H53.4) Scotoma (blind spot) — an area impairment of vision surrounded by a field of relatively well-preserved vision
* (H53.5) Color blindness — the inability to perceive differences between some or all colors that other people can distinguish
o (H53.5) Achromatopsia / Maskun — a low cone count or lack of function in cone cells
* (H53.6) Nyctalopia (Nightblindness) — a condition making it difficult or impossible to see in the dark
* (H54) Blindness — the brain does not receive optical information, through various causes
o (H54/B73) River blindness — blindness caused by long-term infection by a parasetic worm (rare in western societies)

H55-H59 Other disorders of eye and adnexa

* (H57.9) Red eye — conjunctiva appears red typically due to illness or injury
* (H58.0) Argyll Robertson pupil — small, unequal, irregularly shaped pupils

Other codes

* (B36.1) Keratomycosis — fungal infection of the cornea
* (E50.6-E50.7) Xerophthalmia — dry eyes, caused by vitamin A deficiency
* (Q13.1) Aniridia — a rare congenital eye condition leading to underdevelopment or even absence of the iris of the eye

References

* World Health Organization's ICD-10 Codes

See also

* Corrective lenses
* List of common diseases
* List of diseases, for a complete alphabetical listing of diseases
* List of eye surgeries
* List of systemic diseases with ocular manifestations
* Ophthalmology

All About the Eyes

2007-04-02T23:21:00.000-07:00

An eye is an organ of vision that detects light. Different kinds of light-sensitive organs are found in a variety of organisms. The simplest eyes do nothing but detect whether the surroundings are light or dark, while more complex eyes can distinguish shapes and colors. Many animals, including some mammals, birds, reptiles and fish, have two eyes whose fields of vision largely overlap, to allow better depth perception (binocular vision), as in humans; and others are placed so as to minimize the overlap, such as in rabbits and chameleons.

In most vertebrates and some mollusks, the eye works by allowing light to enter it and project onto a light-sensitive panel of cells known as the retina at the rear of the eye, where the light is detected and converted into electrical signals. These are then transmitted to the brain via the optic nerve. Such eyes are typically roughly spherical, filled with a transparent gel-like substance called the vitreous humour, with a focusing lens and often an iris which regulates the intensity of the light that enters the eye. The eyes of cephalopods, fish, amphibians, and snakes usually have fixed lens shapes, and focusing vision is achieved by telescoping the lens—similar to how a camera focuses.

Compound eyes are found among the arthropods and are composed of many simple facets which give a pixelated image (not multiple images, as is often believed). Each sensor has its own lens and photosensitive cell(s). Some eyes have up to 28,000 such sensors, which are arranged hexagonally, and which can give a full 360 degree field of vision. Compound eyes are very sensitive to motion. Some arthropods, including many Strepsiptera, have compound eye composed of a few facets each, with a retina capable of creating an image, which does provide multiple-image vision. With each eye viewing a different angle, a fused image from all the eyes is produced in the brain, providing a very wide-angle, high-resolution image.
Compound eye of Antarctic krill.

Possessing detailed hyperspectral color vision, the Mantis shrimp has been reported to have the world's most complex color vision system.[1] Trilobites, which are now extinct, had unique compound eyes. They used clear calcite crystals to form the lenses of their eyes. In this, they differ from most other arthropods, which have soft eyes. The number of lenses in such an eye varied, however: some trilobites had only one, and some had thousands of lenses in one eye.

Some of the simplest eyes, called ocelli, can be found in animals like snails, who cannot actually "see" in the normal sense. They do have photosensitive cells, but no lens and no other means of projecting an image onto these cells. They can distinguish between light and dark, but no more. This enables snails to keep out of direct sunlight. Jumping spiders have simple eyes that are so large, supported by an array of other, smaller eyes, that they can get enough visual input to hunt and pounce on their prey. Some insect larvae, like caterpillars, have a different type of single eye (stemmata) which gives a rough image.

Evolution of eyes

Main article: Evolution of the eye

Diagram of major stages in the eye's evolution.

The common origin (monophyly) of all animal eyes is now widely accepted as fact based on shared anatomical and genetic features of all eyes; that is, all modern eyes, varied as they are, have their origins in a proto-eye evolved some 540 million years ago.[2][3][4] The majority of the advancements in early eyes are believed to have taken only a few million years to develop, as the first predator to gain true imaging would have touched off an "arms race".[5] Prey animals and competing predators alike would be forced to rapidly match or exceed any such capabilities to survive. Hence multiple eye types and subtypes developed in parallel.

Eyes in various animals show adaptation to their requirements. For example, birds of prey have much greater visual acuity than humans, and some can see ultraviolet light. The different forms of eyes in, for example, vertebrates and mollusks are often cited as examples of parallel evolution, despite their distant common ancestry.

The earliest eyes, called "eyespots", were simple patches of photoreceptor cells, physically similar to the receptor patches for taste and smell. These eyespots could only sense ambient brightness: they could distinguish light and dark, but not the direction of the lightsource.[6] This gradually changed as the eyespot depressed into a shallow "cup" shape, granting the ability to slightly discriminate directional brightness by using the angle at which the light hit certain cells to identify the source. The pit deepened over time, the opening diminished in size, and the number of photoreceptor cells increased, forming an effective pinhole camera that was capable of slightly distinguishing dim shapes.[7]

The thin overgrowth of transparent cells over the eye's aperture, originally formed to prevent damage to the eyespot, allowed the segregated contents of the eye chamber to specialize into a transparent humour that optimized color filtering, blocked harmful radiation, improved the eye's refractive index, and allowed functionality outside of water. The transparent protective cells eventually split into two layers, with circulatory fluid in between that allowed wider viewing angles and greater imaging resolution, and the thickness of the transparent layer gradually increased, in most species with the transparent crystallin protein.[8]

The gap between tissue layers naturally formed a bioconvex shape, an ideal structure for a normal refractive index. Independently, a transparent layer and a nontransparent layer split forward from the lens: the cornea and iris. Separation of the forward layer again forms a humour, the aqueous humour. This increases refractive power and again eases circulatory problems. Formation of a nontransparent ring allows more blood vessels, more circulation, and larger eye sizes.[8]

Anatomy of the mammalian eye

1:posterior chamber 2:ora serrata 3:ciliary muscle 4:ciliary zonules 5:canal of Schlemm 6:pupil 7:anterior chamber 8:cornea 9:iris 10:lens cortex 11:lens nucleus 12:ciliary process 13:conjuntiva 14:inferior oblique muscule 15:inferior rectus muscule 16:medial rectus muscle 17:retinal arteries and veins 18:optic disc 19:dura mater 20:central retinal artery 21:central retinal vein 22:optical nerve 23:vorticose vein 24:bulbar sheat 25:macula 26:fovea 27:sclera 28:choroid 29:superior rectus muscule 30:retina
1:posterior chamber 2:ora serrata 3:ciliary muscle 4:ciliary zonules 5:canal of Schlemm 6:pupil 7:anterior chamber 8:cornea 9:iris 10:lens cortex 11:lens nucleus 12:ciliary process 13:conjuntiva 14:inferior oblique muscule 15:inferior rectus muscule 16:medial rectus muscle 17:retinal arteries and veins 18:optic disc 19:dura mater 20:central retinal artery 21:central retinal vein 22:optical nerve 23:vorticose vein 24:bulbar sheat 25:macula 26:fovea 27:sclera 28:choroid 29:superior rectus muscule 30:retina

Three layers

The structure of the mammalian eye can be divided into three main layers or tunics whose names reflect their basic functions: the fibrous tunic, the vascular tunic, and the nervous tunic.[9][10][11]

* The fibrous tunic, also known as the tunica fibrosa oculi, is the outer layer of the eyeball consisting of the cornea and sclera.[12] The sclera gives the eye most of its white color. It consists of dense connective tissue filled with the protein collagen to both protect the inner components of the eye and maintain its shape.[13]
* The vascular tunic, also known as the tunica vasculosa oculi, is the middle vascularized layer which includes the iris, ciliary body, and choroid.[12][14][15] The choroid contains blood vessels that supply the retinal cells with necessary oxygen and remove the waste products of respiration. The choroid gives the inner eye a dark color, which prevents disruptive reflections within the eye.
* The nervous tunic, also known as the tunica nervosa oculi, is the inner sensory which includes the retina.[12][15] The retina contains the photosensitive rod and cone cells and associated neurons. To maximise vision and light absorption, the retina is a relatively smooth (but curved) layer. It does have two points at which it is different; the fovea and optic disc. The fovea is a dip in the retina directly opposite the lens, which is densely packed with cone cells. It is largely responsible for color vision in humans, and enables high acuity, such as is necessary in reading. The optic disc, sometimes referred to as the anatomical blind spot, is a point on the retina where the optic nerve pierces the retina to connect to the nerve cells on its inside. No photosensitive cells whatsoever exist at this point, it is thus "blind".

Anterior and posterior segments

The mammalian eye can also be divided into two main segments: the anterior segment and the posterior segment.[16]

Anterior segment

The anterior segment is the front third of the eye that includes the structures in front of the vitreous humour: the cornea, iris, ciliary body, and lens.[14][17] Within the anterior segment are two fluid-filled spaces: the anterior chamber and the posterior chamber. The anterior chamber is the space between the posterior surface of the cornea (i.e. the corneal endothelium) and the iris, whereas the posterior chamber is between the iris and the front face of the vitreous.[14]

The cornea and lens help to converge light rays to focus onto the retina. The lens, behind the iris, is a convex, springy disk which focuses light, through the second humour, onto the retina. It is attached to the ciliary body via a ring of suspensory ligaments known as the Zonule of Zinn. To clearly see an object far away, the ciliary muscle is relaxed, which stretches the fibers connecting it with the lens, flattening the lens. When the ciliary muscle contracts, the tension of the fibers decrease (imagine that the distance between the tip of a triangle to its base, is less than the tip of the triangle to the other two tips.) which lets the lens bounce back a more convex and round shape. Humans gradually lose this flexibility with age, resulting in the inability to focus on nearby objects, which is known as presbyopia. There are other refraction errors arising from the shape of the cornea and lens, and from the length of the eyeball. These include myopia, hyperopia, and astigmatism. The iris, between the lens and the first humour, is a pigmented ring of fibrovascular tissue and muscle fibres. Light must first pass though the centre of the iris, the pupil. The size of the pupil is actively adjusted by the circular and radial muscles to maintain a relatively constant level of light entering the eye. Too much light being let in could damage the retina; too little light makes sight difficult.

All of the individual components through which light travels within the eye before reaching the retina are transparent, minimising dimming of the light. Light enters the eye from an external medium such as air or water, passes through the cornea, and into the first of two humours, the aqueous humour. Most of the light refraction occurs at the cornea which has a fixed curvature. The first humour is a clear mass which connects the cornea with the lens of the eye, helps maintain the convex shape of the cornea (necessary to the convergence of light at the lens) and provides the corneal endothelium with nutrients.

Posterior segment
Diagram of a human eye. Note that not all eyes have the same anatomy as a human eye.
Diagram of a human eye. Note that not all eyes have the same anatomy as a human eye.

The posterior segment is the back two-thirds of the eye that includes the anterior hyaloid membrane and all structures behind it: the vitreous humor, retina, choroid, and optic nerve.[18] On the other side of the lens is the second humour, the vitreous humour, which is bounded on all sides: by the lens, ciliary body, suspensory ligaments and by the retina. It lets light through without refraction, helps maintain the shape of the eye and suspends the delicate lens. In some animals, the retina contains a reflective layer (the tapetum lucidum) which increases the amount of light each photosensitive cell perceives, allowing the animal to see better under low light conditions.
Light from a single point of a distant object and light from a single point of a near object being brought to a focus.

Extraocular anatomy

In many species, the eyes are inset in the portion of the skull known as the orbits or eyesockets. This placement of the eyes helps to protect them from injury.

In humans, the eyebrows redirect flowing substances (such as rainwater or sweat) away from the eye. Water in the eye can alter the refractive properties of the eye and blur vision. It can also wash away the tear fluid—along with it the protective lipid layer—and can alter corneal physiology, due to osmotic differences between tear fluid and freshwater. This is made apparent when swimming in freshwater pools, as the osmotic gradient draws "pool water" into the corneal tissue (the pool water is hypotonic), causing edema, and subsequently leaving the swimmer with "cloudy" or "misty" vision for a short period thereafter. It can be reversed by irrigating the eye with hypertonic saline which osmotically draws the excess water out of the eye.

In many animals, including humans, eyelids wipe the eye and prevent dehydration. They spread tears on the eyes, which contains substances which help fight bacterial infection as part of the immune system. Some aquatic animals have a second eyelid in each eye which refracts the light and helps them see clearly both above and below water. Most creatures will automatically react to a threat to its eyes (such as an object moving straight at the eye, or a bright light) by covering the eyes, and/or by turning the eyes away from the threat. Blinking the eyes is, of course, also a reflex.

In many animals, including humans, eyelashes prevent fine particles from entering the eye. Fine particles can be bacteria, but also simple dust which can cause irritation of the eye, and lead to tears and subsequent blurred vision.

Other articles regarding eye anatomy

Annulus of Zinn, Conjunctiva, Macula, Nictitating membrane, Schlemm's canal, Trabecular meshwork.

Cytology
This image clearly shows the pupil, iris, and blood vessels of the human eye.
This image clearly shows the pupil, iris, and blood vessels of the human eye.

The structure of the mammalian eye owes itself completely to the task of focusing light onto the retina. This light causes chemical changes in the photosensitive cells of the retina, the products of which trigger nerve impulses which travel to the brain.

The retina contains two forms of photosensitive cells important to vision—rods and cones. Though structurally and metabolically similar, their function is quite different. Rod cells are highly sensitive to light allowing them to respond in dim light and dark conditions, however, they cannot detect color. These are the cells which allow humans and other animals to see by moonlight, or with very little available light (as in a dark room). This is why the darker conditions become, the less color objects seem to have. Cone cells, conversely, need high light intensities to respond and have high visual acuity. Different cone cells respond to different wavelengths of light, which allows an organism to see color.

The differences are useful; apart from enabling sight in both dim and light conditions, humans have given them further application. The fovea, directly behind the lens, consists of mostly densely-packed cone cells. This gives humans a highly detailed central vision, allowing reading, bird watching, or any other task which primarily requires looking at things. Its requirement for high intensity light does cause problems for astronomers, as they cannot see dim stars, or other objects, using central vision because the light from these is not enough to stimulate cone cells. Because cone cells are all that exist directly in the fovea, astronomers have to look at stars through the "corner of their eyes" (averted vision) where rods also exist, and where the light is sufficient to stimulate cells, allowing the individual to observe distant stars.

Rods and cones are both photosensitive, but respond differently to different frequencies of light. They both contain different pigmented photoreceptor proteins. Rod cells contain the protein rhodopsin and cone cells contain different proteins for each color-range. The process through which these proteins go is quite similar—upon being subjected to electromagnetic radiation of a particular wavelength and intensity, the protein breaks down into two constituent products. Rhodopsin, of rods, breaks down into opsin and retinal; iodopsin of cones breaks down into photopsin and retinal. The opsin in both opens ion channels on the cell membrane which leads to hyperpolarization, this hyperpolarization of the cell leads to a release of transmitter molecules at the synapse.

This is the reason why cones and rods enable organisms to see in dark and light conditions—each of the photoreceptor proteins requires a different light intensity to break down into the constituent products. Further, synaptic convergence means that several rod cells are connected to a single bipolar cell, which then connects to a single ganglion cell by which information is relayed to the visual cortex. This is in direct contrast to the situation with cones, where each cone cell is connected to a single bipolar cell. This results in the high visual acuity, or the high ability to distinguish between detail, of cone cells and not rods. If a ray of light were to reach just one rod cell this may not be enough to hyperpolarize the connected bipolar cell. But because several "converge" onto a bipolar cell, enough transmitter molecules reach the synapse of the bipolar cell to hyperpolarize it.

Furthermore, color is distinguishable when breaking down the iodopsin of cone cells because there are three forms of this protein. One form is broken down by the particular EM wavelength that is red light, another green light, and lastly blue light. In simple terms, this allows human beings to see red, green and blue light. If all three forms of cones are stimulated equally, then white is seen. If none are stimulated, black is seen. Most of the time however, the three forms are stimulated to different extents—resulting in different colors being seen. If, for example, the red and green cones are stimulated to the same extent, and no blue cones are stimulated, yellow is seen. For this reason red, green and blue are called primary colors and the colors obtained by mixing two of them, secondary colors. The secondary colors can be further complimented with primary colors to see tertiary colors.

Acuity
Closeup of a hawk's eye.

Main article: Visual acuity

Visual acuity can be measured with several different metrics.

Cycles per degree (CPD) measures how much an eye can differentiate one object from another in terms of degree angles. It is essentially no different from angular resolution. To measure CPD, first draw a series of black and white lines of equal width on a grid (similar to a bar code). Next, place the observer at a distance such that the sides of the grid appear one degree apart. If the grid is 1 meter away, then the grid should be about 8.7 millimeters wide. Finally, increase the number of lines and decrease the width of each line until the grid appears as a solid grey block. In one degree, a human would not be able to distinguish more than about 12 lines without the lines blurring together. So a human can resolve distances of about 0.93 millimeters at a distance of one meter. A horse can resolve about 17 CPD (0.66 mm at 1 m) and a rat can resolve about 1 CPD (8.7 mm at 1 m).

A diopter is the unit of measure of optical power.

Dynamic range

The retina has a static contrast ratio of around 100:1 (about 6 1/2 stops). As soon as the eye moves (saccades) it re-adjusts its exposure both chemically and by adjusting the iris. Initial dark adaptation takes place in approximately four seconds of profound, uninterrupted darkness; full adaptation through adjustments in retinal chemistry (the Purkinje effect) are mostly complete in thirty minutes. Hence, a dynamic contrast ratio of about 1,000,000:1 (about 20 stops) is possible. The process is nonlinear and multifaceted, so an interruption by light nearly starts the adaptation process over again. Full adaptation is dependent on good blood flow; thus dark adaptation may be hampered by poor circulation, and vasoconstrictors like alcohol or tobacco.

Equivalent Resolution

Roger N. Clark estimates human vision resolution to be equivalent to 576 megapixels (24000 x 24000 pixels) for a 120 degree field of view. Extensive background, assumptions, and calculations are available at http://www.clarkvision.com/imagedetail/eye-resolution.html

However, it must be noted that the human eye itself has only a small spot of sharp vision in the middle of the retina, the fovea centralis, the rest of the field of view being blurry. The angle of the sharp vision being just few degrees in the middle of the view, the sharp area thus barely achieves even a single megapixel resolution. The experience of wide sharp human vision is in fact based on turning the eyes towards the current point of interest in the field of view, the brain thus preceiving an observation of a wide sharp field of view.

The narrow beam of sharp vision is easy to test by putting a fingertip on a newspaper and trying to read the text while staring at the finger tip—it is very difficult to read text that's just some centimeters away from the finger tip.

Eye movement
MRI scan of human eye.

Main article: Eye movements

Animals with compound eyes have a wide field of vision, allowing them to look in many directions. To see more, they have to move their entire head or even body.

The visual system in the brain is too slow to process that information if the images are slipping across the retina at more than a few degrees per second (Westheimer and McKee, 1954). Thus, for humans to be able to see while moving, the brain must compensate for the motion of the head by turning the eyes. Another complication for vision in frontal-eyed animals is the development of a small area of the retina with a very high visual acuity. This area is called the fovea, and covers about 2 degrees of visual angle in people. To get a clear view of the world, the brain must turn the eyes so that the image of the object of regard falls on the fovea. Eye movements are thus very important for visual perception, and any failure to make them correctly can lead to serious visual disabilities.

Having two eyes is an added complication, because the brain must point both of them accurately enough that the object of regard falls on corresponding points of the two retinas; otherwise, double vision would occur. The movements of different body parts are controlled by striated muscles acting around joints. The movements of the eye are no exception, but they have special advantages not shared by skeletal muscles and joints, and so are considerably different.

Extraocular muscles

Main article: Extraocular muscles

Each eye has six muscles that control its movements: the lateral rectus, the medial rectus, the inferior rectus, the superior rectus, the inferior oblique, and the superior oblique. When the muscles exert different tensions, a torque is exerted on the globe that causes it to turn. This is an almost pure rotation, with only about one millimeter of translation.[19] Thus, the eye can be considered as undergoing rotations about a single point in the center of the eye.

Rapid eye movement

Main article: Rapid eye movement

Rapid eye movement, or REM for short, typically refers to the stage during sleep during which the most vivid dreams occur. During this stage, the eyes move rapidly. It is not in itself a unique form of eye movement.

Saccades

Main article: Saccade

Saccades are quick, simultaneous movements of both eyes in the same direction controlled by the frontal lobe of the brain.

Microsaccades

Main article: Microsaccade

Even when looking intently at a single spot, the eyes drift around. This ensures that individual photosensitive cells are continually stimulated in different degrees. Without changing input, these cells would otherwise stop generating output. Microsaccades move the eye no more than a total of 0.2° in adult humans.

Vestibulo-ocular reflex

Main article: Vestibulo-ocular reflex

The vestibulo-ocular reflex is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa.

Smooth pursuit movement

Main article: Pursuit movement

The eyes can also follow a moving object around. This is less accurate than the vestibulo-ocular reflex as it requires the brain to process incoming visual information and supply feedback. Following an object moving at constant speed is relatively easy, though the eyes will often make saccadic jerks to keep up. The smooth pursuit movement can move the eye at up to 100°/s in adult humans.

While still, the eye can measure relative speed with high accuracy, however under movement relative speed is highly distorted. Take for example, when watching a plane while standing—the plane has normal visual speed. However, if an observer watches the plane while moving in the same direction as the plane's movement, the plane will appear as if it were standing still or moving very slowly.

When an observer views an object in motion moving away or towards himself, there is no eye movement occurring as in the examples above, however the ability to discern speed and speed difference is still present; although not as severe. The intensity of light (e.g. night vs. day) plays a major role in determining speed and speed difference. For example, no human can with reasonable accuracy, visually determine the speed of an approaching train in the evening as they could during the day. Similarly, while moving, the ability is further diminished unless there is another point of reference for determining speed; however the inaccuracy of speed or speed difference will always be present.

Optokinetic reflex

The optokinetic reflex is a combination of a saccade and smooth pursuit movement. When, for example, looking out of the window in a moving train, the eyes can focus on a 'moving' tree for a short moment (through smooth pursuit), until the tree moves out of the field of vision. At this point, the optokinetic reflex kicks in, and moves the eye back to the point where it first saw the tree (through a saccade).

Vergence movement

Main article: Vergence

The two eyes converge to point to the same object

When a creature with binocular vision looks at an object, the eyes must rotate around a vertical axis so that the projection of the image is in the centre of the retina in both eyes. To look at an object closer by, the eyes rotate 'towards each other' (convergence), while for an object farther away they rotate 'away from each other' (divergence). Exaggerated convergence is called cross eyed viewing (focussing on the nose for example) . When looking into the distance, or when 'staring into nothingness', the eyes neither converge nor diverge.

Vergence movements are closely connected to accommodation of the eye. Under normal conditions, changing the focus of the eyes to look at an object at a different distance will automatically cause vergence and accommodation.

Accommodation

Main article: Accommodation (eye)

To see clearly, the lens will be pulled flatter or allowed to regain its thicker form.

Diseases, disorders, and age-related changes

Main articles: List of eye diseases and disorders and List of systemic diseases with ocular manifestations

The stye is a common irritating inflammation of the eyelid.

There are many diseases, disorders, and age-related changes that may affect the eyes and surrounding structures.

As the eye ages certain changes occur that can be attributed solely to the aging process. Most of these anatomic and physiologic processes follow a gradual decline. With aging, the quality of vision worsens due to reasons independent of aging eye diseases. While there are many changes of significance in the nondiseased eye, the most functionally important changes seem to be a reduction in pupil size and the loss of accommodation or focusing capability (presbyopia). The area of the pupil governs the amount of light that can reach the retina. The extent to which the pupil dilates also decreases with age. Because of the smaller pupil size, older eyes receive much less light at the retina. In comparison to younger people, it is as though older persons wear medium-density sunglasses in bright light and extremely dark glasses in dim light. Therefore, for any detailed visually guided tasks on which performance varies with illumination, older persons require extra lighting. Certain Diseases can come from sexually transmitted diseases such as herpes and genital warts. If contact between eye and area of infection occurs, the STD will be transmitted to the eye. [20]

With aging a prominent white ring develops in the periphery of the cornea- called arcus senilis. Aging causes laxity and downward shift of eyelid tissues and atrophy of the orbital fat. These changes contribute to the etiology of several eyelid disorders such as ectropion, entropion, dermatochalasis, and ptosis. The vitreous gel undergoes liquefaction (posterior vitreous detachment or PVD) and its opacities—visible as floaters—gradually increase in number.

Various eye care professionals, including ophthalmologists, optometrists, and opticians, are involved in the treatment and management of ocular and vision disorders. A Snellen chart is one type of eye chart used to measure visual acuity. At the conclusion of an eye examination, an eye doctor may provide the patient with an eyeglass prescription for corrective lenses.

References
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2. ^ Halder, G., Callaerts, P. and Gehring, W.J. (1995). "New perspectives on eye evolution." Curr. Opin. Genet. Dev. 5 (pp. 602–609).
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13. ^ http://www.bartleby.com/107/225.html
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16. ^ http://www.e-sunbear.com/anatomy_02.html
17. ^ "Departments. Anterior segment." Cantabrian Institute of Ophthalmology.
18. ^ Posterior segment anatomy
19. ^ Roger H.S. Carpenter (1988); Movements of the Eyes (2nd ed.). Pion Ltd, London. ISBN 0-85086-109-8.
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* Anatomy. History of Ophthalmology. Retrieved on 23 April 2005.
* Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science, 4th ed. McGraw-Hill, New York (2000). ISBN 0-8385-7701-6

See also
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