Eye Care In The News

Cataracts

Cataracts are an inevitability of aging. Proteins that make up the lens break down and clump together, and as the damage builds, the lens grows cloudier. All people, by the time they reach their 60's or 70's, have some translucence in their lenses, although some aren't bothered by it right away- or ever.

 

People who live near the equator or spend a lot of time outdoors, with more exposure to direct sunlight, are more susceptible to cataracts, as are smokers and people with diabetes. "A cataract is like a dirty window", says Ralph Levinson, an eye surgeon at the Jules Stein Eye Institute at the University of California, Los Angeles. "At some point, you're not going to be able to see through it.”  The only long term solution is surgery to replace the cloudy natural lens with a clear artificial one.

Contact Lenses

Whether you already wear contact lenses or are considering them, this section serves as a primer. Facts and statistics about contact lens wearers, pointers for safe and successful use of contact lenses, and contact lenses and cosmetics are just a few of the topics covered here.

Getting started right with your contact lenses involves going to a doctor who provides full-service care. This includes a thorough eye examination, an evaluation of your suitability for contact lens wear, the lenses, necessary lens care kits, individual instructions for wear and care and unlimited follow-up visits over a specified time.

Recommendations for Contact Lens Wearers from the American Optometric Association

  1. Always wash your hands before handling contact lenses.

  2. Carefully and regularly clean contact lenses, as directed by your optometrist. Rub the contact lenses with fingers and rinse thoroughly before soaking lenses overnight in sufficient multi-purpose solution to completely cover the lens.

  3. Store lenses in the proper lens storage case and replace the case at a minimum of every three months. Clean the case after each use, and keep it open and dry between cleanings.

  4. Use only products recommended by your optometrist to clean and disinfect your lenses. Saline solution and rewetting drops are not designed to disinfect lenses.

  5. Only fresh solution should be used to clean and store contact lenses. Never re-use old solution. Contact lens solution must be changed according to the manufacturer's recommendations, even if the lenses are not used daily.

  6. Always follow the recommended contact lens replacement schedule prescribed by your optometrist.

  7. Remove contact lenses before swimming or entering a hot tub.

  8. See your optometrist for your regularly scheduled contact lens and eye examination.
Cornea

The cornea is the transparent front part of the eye that covers the iris, pupil, and anterior chamber. Together with the lens, the cornea refracts light, accounting for approximately two-thirds of the eye's total optical power.[1][2] In humans, the refractive power of the cornea is approximately 43 dioptres.[3] While the cornea contributes most of the eye's focusing power, its focus is fixed. The curvature of the lens, on the other hand, can be adjusted to "tune" the focus depending upon the object's distance. Medical terms related to the cornea often start with the prefix "kerat-" from the Greek word κέρας, horn.

Contents

Structure

The cornea has unmyelinated nerve endings sensitive to touch, temperature and chemicals; a touch of the cornea causes an involuntary reflex to close the eyelid. Because transparency is of prime importance the cornea does not have blood vessels; it receives nutrients via diffusion from the tear fluid at the outside and the aqueous humour at the inside and also from neurotrophins supplied by nerve fibres that innervate it. In humans, the cornea has a diameter of about 11.5 mm and a thickness of 0.5–0.6 mm in the center and 0.6–0.8 mm at the periphery. Transparency, avascularity, the presence of immature resident immune cells, and immunologic privilege makes the cornea a very special tissue. The cornea has no blood supply; it gets oxygen directly through the air.

It borders with the sclera by the corneal limbus.

Layers

The human cornea, like those of other primates, has five layers; the corneas of cats, dogs, and other carnivores only have four.[4] From the anterior to posterior the five layers of the human cornea are:

  1. Corneal epithelium: a thin epithelial multicellular tissue layer (stratified squamous epithelium) of fast-growing and easily-regenerated cells, kept moist with tears. Irregularity or edema of the corneal epithelium disrupts the smoothness of the air-tear film interface, the most significant component of the total refractive power of the eye, thereby reducing visual acuity. It is continuous with the conjunctival epithelium is composed of about 6 layers of cells which are shed constantly on the exposed layer and are regenerated in the basal layer.
  2. Bowman's layer (also erroneously known as the anterior limiting membrane, when in fact it is not a membrane but a condensed layer of collagen): a tough layer that protects the corneal stroma, consisting of a similar irregularly-arranged collagen fibers, essentially a type of stroma. It is eight to 14 micrometres thick.[5] This layer is absent in carnivores.[4]
  3. Corneal stroma (also substantia propria): a thick, transparent middle layer, consisting of regularly-arranged collagen fibers along with sparsely distributed interconnected keratocytes. The corneal stroma consists of approximately 200 layers of type I collagen fibrils. 90% of the corneal thickness is composed of stroma. There are 2 theories of how transparency in the cornea comes about:
    1. The lattice arrangements of the collagen fibrils in the stroma. The light scatter by individual fibrils is cancelled by destructive interference from the scattered light from other individual fibrils.(Maurice)
    2. The spacing of the neighbouring collagen fibrils in the stroma must be < 200 nm for there to be transparency. (Goldman and Benedek)
  4. Descemet's membrane (also posterior limiting membrane): a thin acellular layer that serves as the modified basement membrane of the corneal endothelium, from which the cells are derived (but in a different collagen structure. It is 5-10 microns thick
  5. Corneal endothelium: a simple squamous or low cuboidal monolayer of mitochondria-rich cells responsible for regulating fluid and solute transport between the aqueous and corneal stromal compartments. (The term endothelium is a misnomer here. The corneal endothelium is bathed by aqueous humour, not by blood or lymph, and has a very different origin, function, and appearance from vascular endothelia.) Unlike the corneal epithelium the cells of the endothelium do not regenerate. Instead, they stretch to compensate for dead cells which reduces the overall cell density of the endothelium and has an impact on fluid regulation. If the endothelium can no longer maintain a proper fluid balance, stromal swelling due to excess fluids and subsequent loss of transparency will occur.

The mnemonic "EBSDEin", read as "Ebstein" can be used to remember the layers in sequence.[6]

Keeping the cornea transparent

Upon death or removal of an eye the cornea absorbs the aqueous humor, thickens, and becomes hazy. Transparency can be restored by putting it in a warm, well-ventilated chamber at 31 °C (88 °F, the normal temperature), allowing the fluid to leave the cornea and become transparent. The cornea takes in fluid from the aqueous humor and the small blood vessels of the limbus, but a pump ejects the fluid immediately upon entry. When energy is deficient the pump may fail, or works too slowly to compensate, causing swelling. This could arise at death, but a dead eye can be placed in a warm chamber and the reservoirs of sugar and glycogen can keep the cornea transparent for at least one day. The endothelium controls this pumping action, and as discussed above, damage thereof is more serious, and is a cause of opaqueness and swelling. When damage to the cornea occurs, such as in a viral infection, the collagen used to repair the process is not regularly arranged, leading to an opaque patch (leukoma).[7]

Innervation

The cornea is one of the most sensitive tissues of the body, it is densely innervated with sensory nerve fibres via the ophthalmic division of the trigeminal nerve by way of 70 - 80 long ciliary nerves; and short ciliary nerves derived from the oculomotor nerve.

The nerves enter the cornea via three levels, scleral, episcleral and conjunctival. Most of the bundles give rise by subdivision to a network in the stroma, from which fibres supply the different regions. The three networks are midstromal, subepithelial/Bowman's layer, and epithelium. The receptive fields of each nerve ending are very large, and may overlap.

Corneal nerves of the subepithelial layer converge and terminate near the apex of the cornea in a logarithmic spiral pattern.[8]

Refractive nature

The optical component is concerned with producing a reduced inverted image on the retina. The eye's optical system consists of not only two but four surfaces - two on the cornea, two on the lens. Rays are refracted toward the midline. Distant rays, due to their parallel nature, converge to a point on the retina. The cornea admits light at the greatest angle. The aqueous and vitreous humors have a refractive index of 1.336, and that of the cornea is minutely different, i.e., 1.3376. Therefore, its passage from the cornea to the aqueous humor is negligible.[9]

Dry Eyes

Dry eye is a condition in which there are insufficient tears to lubricate and nourish the eye. Tears are necessary for maintaining the health of the front surface of the eye and for providing clear vision. People with dry eyes either do not produce enough tears or have a poor quality of tears. Dry eye is a common and often chronic problem, particularly in older adults.

With each blink of the eyelids, tears are spread across the front surface of the eye, known as the cornea. Tears provide lubrication, reduce the risk of eye infection, wash away foreign matter in the eye, and keep the surface of the eyes smooth and clear. Excess tears in the eyes flow into small drainage ducts, in the inner corners of the eyelids, which drain in the back of the nose.

Dry eyes can result from an improper balance of tear production and drainage.

  • Inadequate amount of tears – Tears are produced by several glands in and around the eyelids. Tear production tends to diminish with age, with various medical conditions, or as a side effect of certain medicines. Environmental conditions such as wind and dry climates can also affect tear volume by increasing tear evaporation. When the normal amount of tear production decreases or tears evaporate too quickly from the eyes, symptoms of dry eye can develop.

  • Layers of tearsPoor quality of tears – Tears are made up of three layers: oil, water, and mucus. Each component serves a function in protecting and nourishing the front surface of the eye. A smooth oil layer helps to prevent evaporation of the water layer, while the mucin layer functions in spreading the tears evenly over the surface of the eye. If the tears evaporate too quickly or do not spread evenly over the cornea due to deficiencies with any of the three tear layers, dry eye symptoms can develop.

The most common form of dry eyes is due to an inadequate amount of the water layer of tears. This condition, called keratoconjunctivitis sicca (KCS), is also referred to as dry eye syndrome.

People with dry eyes may experience symptoms of irritated, gritty, scratchy, or burning eyes, a feeling of something in their eyes, excess watering, and blurred vision. Advanced dry eyes may damage the front surface of the eye and impair vision.

Treatments for dry eyes aim to restore or maintain the normal amount of tears in the eye to minimize dryness and related discomfort and to maintain eye health

Eyelids

Blepharitis is an inflammation of the eyelids causing red, irritated, itchy eyelids and the formation of dandruff-like scales on eyelashes. It is a common eye disorder caused by either bacterial or a skin condition such as dandruff of the scalp or acne rosacea. It affects people of all ages. Although uncomfortable, blepharitis is not contagious and generally does not cause any permanent damage to eyesight.

Blepharitis is classified into two types:

  1. Anterior blepharitis occurs at the outside front edge of the eyelid where the eyelashes are attached.

  2. Posterior blepharitis affects the inner edge of the eyelid that comes in contact with the eyeball.

Individuals with blepharitis may experience a gritty or burning sensation in their eyes, excessive tearing, itching, red and swollen eyelids, dry eyes, or crusting of the eyelids. For some people, blepharitis causes only minor irritation and itching. However, it can lead to more severe signs and symptoms such as blurring of vision, missing or misdirected eyelashes, and inflammation of other eye tissue, particularly the cornea.

In many cases, good eyelid hygiene and a regular cleaning routine can control blepharitis. This includes frequent scalp and face washing, using warm compresses to soak the eyelids, and doing eyelid scrubs. In cases where a bacterial infection is the cause, various antibiotics and other medications may be prescribed along with eyelid hygiene.

Glaucoma

Glaucoma is a disease, rather than an inevitability of aging, that causes damage to the optic nerve and progressively impairs peripheral vision, sometimes narrowing the field of vision to the point of blindness.  It tends to run in families and is especially prevalent among people of African descent. Glaucoma is initially asymptomatic.

 

The most common form of glaucoma is caused by improper drainage of the fluid in front of the lens, which leads to a build up of pressure that harms the optic nerve.  The nerve damage is irreversible, but doctors can prescribe medications that reduce pressure either by reducing the amount of fluid made, increasing the drainage of the fluid or a combination of both.  This can stall the progression of the disease.  Surgery can also be used in advanced cases to improve fluid drainage.

Low Vision

Few people are totally without sight. Most individuals today classified as "blind" actually have remaining sight and, thanks to developments in the field of low vision rehabilitation, can be helped to make good use of it, improving their quality of life.

Anyone with noncorrectable reduced vision is visually impaired, and can have a wide range of problems. The World Health Organization uses the following classifications of visual impairment. When the vision in the better eye with best possible glasses correction is:

  • 20/30 to 20/60 is considered mild vision loss, or near-normal vision
  • 20/70 to 20/160 is considered moderate visual impairment, or moderate low vision
  • 20/200 to 20/400 is considered severe visual impairment, or severe low vision
  • 20/500 to 20/1,000 is considered profound visual impairment, or profound low vision
  • less than 20/1,000 is considered near-total visual impairment, or near total blindness
  • no light perception is considered total visual impairment, or total blindness

There are also levels of visual impairment based on visual field loss (loss of peripheral vision).

In the United States, any person with vision that cannot be corrected to better than 20/200 in the best eye, or who has 20 degrees or less of visual field remaining, is considered legally blind.

Visual impairments take many forms and exist in varying degrees.  It is important to understand that visual acuity alone is not a good predictor of the degree of problems a person may have. Someone with relatively good acuity (e.g., 20/40) can have difficulty functioning, while someone with worse acuity (e.g., 20/200) might not be having any real problems.

Macular Degeneration
Emerging Treatment for Dry Macular Degeneration-  New treatments for wet macular degeneration, the less common but more devastating visually form of AMD, have been available for several years.  They are anti-VEGF compounds that prevent the growth of leaky retinal blood vessels that cause vision loss ( Lucentis and the off-label Avastin).  Now a multi-institutional study has uncovered the first link to Dry AMD the more common but less harmful form of AMD.  A compound that inhibits the mechanism that causes dry AMD will enter clinical trials this year.  Currently nutritional supplements containing antioxidant sources as well as zinc and copper (known as the AREDS formula) and lutein are used to slow the progression of dry AMD in some patients.
Nutrition

Adding powerful antioxidants to your diet
can improve your eye health.

There’s no substitute for the quality of life good vision offers.  Adding certain nutrients to your diet every day – either through foods or supplements – can help save your vision.  Researchers have linked eye-friendly nutrients such as lutein/zeaxanthin, vitamin C, vitamin E, and zinc to reducing the risk of certain eye diseases, including macular degeneration and cataract formation.

  • Lutein & Zeaxanthin

    Lutein and zeaxanthin are important nutrients found in green leafy vegetables, as well as other foods, such as eggs. Many studies have shown that lutein and zeaxanthin reduce the risk of chronic eye diseases, including age-related macular degeneration and cataracts.

  • Vitamin C

    Vitamin C (ascorbic acid) is an antioxidant found in fruits and vegetables. Scientific evidence suggests vitamin C lowers the risk of developing cataracts, and when taken in combination with other essential nutrients, can slow the progression of age-related macular degeneration and visual acuity loss.

  • Vitamin E

    Vitamin E in its most biologically active form is a powerful antioxidant found in nuts, fortified cereals and sweet potatoes. It is thought to protect cells of the eyes from damage caused by unstable molecules called free radicals which break down healthy tissue.

  • Essential Fatty Acids

    Fats are a necessary part of the human diet. They maintain the integrity of the nervous system, fuel cells and boost the immune system. Two omega-3 fatty acids have been shown to be important for proper visual development and retinal function.

  • Zinc

    Zinc is an essential trace mineral or ‘helper molecule.’ It plays a vital role in bringing vitamin A from the liver to the retina in order to produce melanin, a protective pigment in the eyes. Zinc is highly concentrated in the eye, mostly in the retina and choroid, the vascular tissue layer lying under the retina.

  • Emerging Research

    In the last 20 years, eye health research has linked diet and nutrition with a decreased risk of age-related macular degeneration (AMD).

Written in partnership with AOA members Stuart Richer, O.D., Ph.D., and Steven Newman, O.D.

Diabetic Retinopathy

Diabetic retinopathy is a condition occurring in persons with diabetes, which causes progressive damage to the retina, the light sensitive lining at the back of the eye. It is a serious sight-threatening complication of diabetes.

Diabetes is a disease that interferes with the body's ability to use and store sugar, which can cause many health problems. Too much sugar in the blood can cause damage throughout the body, including the eyes. Over time, diabetes affects the circulatory system of the retina.

Diabetic retinopathy is the result of damage to the tiny blood vessels that nourish the retina. They leak blood and other fluids that cause swelling of retinal tissue and clouding of vision. The condition usually affects both eyes. The longer a person has diabetes, the more likely they will develop diabetic retinopathy. If left untreated, diabetic retinopathy can cause blindness.

Symptoms of diabetic retinopathy include:

  • Seeing spots or floaters in your field of vision
  • Blurred vision
  • Having a dark or empty spot in the center of your vision
  • Difficulty seeing well at night

In patients with diabetes, prolonged periods of high blood sugar can lead to the accumulation of fluid in the lens inside the eye that controls eye focusing. This changes the curvature of the lens and results in the development of symptoms of blurred vision. The blurring of distance vision as a result of lens swelling will subside once the blood sugar levels are brought under control. Better control of blood sugar levels in patients with diabetes also slows the onset and progression of diabetic retinopathy.

Often there are no visual symptoms in the early stages of diabetic retinopathy. That is why the American Optometric Association recommends that everyone with diabetes have a comprehensive dilated eye examination once a year. Early detection and treatment can limit the potential for significant vision loss from diabetic retinopathy.

Treatment of diabetic retinopathy varies depending on the extent of the disease. It may require laser surgery to seal leaking blood vessels or to discourage new leaky blood vessels from forming. Injections of medications into the eye may be needed to decrease inflammation or stop the formation of new blood vessels. In more advanced cases, a surgical procedure to remove and replace the gel-like fluid in the back of the eye, called the vitreous, may be needed. A retinal detachment, defined as a separation of the light-receiving lining in the back of the eye, resulting from diabetic retinopathy, may also require surgical repair.

If you are a diabetic, you can help prevent or slow the development of diabetic retinopathy by taking your prescribed medication, sticking to your diet, exercising regularly, controlling high blood pressure and avoiding alcohol and smoking.

What causes diabetic retinopathy?

Non-proliferative diabetic retinopathy

Non-proliferative diabetic retinopathy (NPDR) is the early state of the disease in which symptoms will be mild or non-existent. In NPDR, the blood vessels in the retina are weakened causing tiny bulges called microanuerysms to protrude from their walls.



Proliferative diabetic retinopathy (PDR)

Proliferative diabetic retinopathy (PDR) is the more advanced form of the disease. At this stage, new fragile blood vessels can begin to grow in the retina and into the vitreous, the gel-like fluid that fills the back of the eye. The new blood vessel may leak blood into the vitreous, clouding vision.

Diabetic retinopathy is the result of damage caused by diabetes to the small blood vessels located in the retina. Blood vessels damaged from diabetic retinopathy can cause vision loss:

  • Fluid can leak into the macula, the area of the retina which is responsible for clear central vision. Although small, the macula is the part of the retina that allows us to see colors and fine detail. The fluid causes the macula to swell, resulting in blurred vision.

  • In an attempt to improve blood circulation in the retina, new blood vessels may form on its surface. These fragile, abnormal blood vessels can leak blood into the back of the eye and block vision.

Diabetic retinopathy is classified into two types:

  1. Non-proliferative diabetic retinopathy (NPDR) is the early state of the disease in which symptoms will be mild or non-existent. In NPDR, the blood vessels in the retina are weakened causing tiny bulges called microanuerysms to protrude from their walls. The microanuerysms may leak fluid into the retina, which may lead to swelling of the macula. 

  2. Proliferative diabetic retinopathy (PDR) is the more advanced form of the disease. At this stage, circulation problems cause the retina to become oxygen deprived. As a result new fragile blood vessels can begin to grow in the retina and into the vitreous, the gel-like fluid that fills the back of the eye. The new blood vessel may leak blood into the vitreous, clouding vision. Other complications of PDR include detachment of the retina due to scar tissue formation and the development of glaucoma. Glaucoma is an eye disease defined as progressive damage to the optic nerve. In cases of proliferative diabetic retinopathy, the cause of this nerve damage is due to extremely high pressure in the eye. If left untreated, proliferative diabetic retinopathy can cause severe vision loss and even blindness.

Risk factors for diabetic retinopathy include:

  • Diabetes — people with Type 1 or Type 2 diabetes are at risk for the development of diabetic retinopathy. The longer a person has diabetes, the more likely they are to develop diabetic retinopathy, particularly if the diabetes is poorly controlled.

  • Race — Hispanic and African Americans are at greater risk for developing diabetic retinopathy.

  • Medical conditions — persons with other medical conditions such as high blood pressure and high cholesterol are at greater risk.

  • Pregnancy — pregnant women face a higher risk for developing diabetes and diabetic retinopathy. If gestational diabetes develops, the patient is at much higher risk of developing diabetes as they age.

 

How is diabetic retinopathy diagnosed?

Comprehensive eye exam

Diabetic retinopathy can be diagnosed through a comprehensive eye examination.

Diabetic retinopathy can be diagnosed through a comprehensive eye examination. Testing, with special emphasis on evaluation of the retina and macula, may include:

  • Patient history to determine vision difficulties experienced by the patient, presence of diabetes, and other general health concerns that may be affecting vision

  • Visual acuity measurements to determine the extent to which central vision has been affected

  • Refraction to determine the need for changes in an eyeglass prescription

  • Evaluation of the ocular structures, including the evaluation of the retina through a dilated pupil

  • Measurement of the pressure within the eye

Supplemental testing may include:

  • Retinal photography or tomography to document current status of the retina

  • Fluorescein angiography to evaluate abnormal blood vessel growth

 

How is diabetic retinopathy treated?

Photocoagulation

Laser treatment (photocoagulation) is used to stop the leakage of blood and fluid into the retina. A laser beam of light can be used to create small burns in areas of the retina with abnormal blood vessels to try to seal the leaks.

Treatment for diabetic retinopathy depends on the stage of the disease and is directed at trying to slow or stop the progression of the disease.

In the early stages of Non-proliferative Diabetic Retinopathy, treatment other than regular monitoring may not be required. Following your doctor's advice for diet and exercise and keeping blood sugar levels well-controlled can help control the progression of the disease.

If the disease advances, leakage of fluid from blood vessels can lead to macular edema. Laser treatment (photocoagulation) is used to stop the leakage of blood and fluid into the retina. A laser beam of light can be used to create small burns in areas of the retina with abnormal blood vessels to try to seal the leaks.

When blood vessel growth is more widespread throughout the retina, as in proliferative diabetic retinopathy, a pattern of scattered laser burns is created across the retina. This causes abnormal blood vessels to shrink and disappear. With this procedure, some side vision may be lost in order to safeguard central vision.

Some bleeding into the vitreous gel may clear up on its own. However, if significant amounts of blood leak into the vitreous fluid in the eye, it will cloud vision and can prevent laser photocoagulation from being used. A surgical procedure called a vitrectomy may be used to remove the blood-filled vitreous and replace it with a clearfluid to maintain the normal shape and health of the eye.

Persons with diabetic retinopathy can suffer significant vision loss. Special low vision devices such as telescopic and microscopic lenses, hand and stand magnifiers, and video magnification systems can be prescribed to make the most of remaining vision.

Refractive Surgery

Refractive eye surgery is any eye surgery used to improve the refractive state of the eye and decrease or eliminate dependency on glasses or contact lenses. This can include various methods of surgical remodeling of the cornea or cataract surgery. The most common methods today use excimer lasers to reshape curvature of the cornea. Successful refractive eye surgery can reduce or cure common vision disorders such as myopia, hyperopia and astigmatism.

According to surveys of members of the American Society of Cataract and Refractive Surgery, approximately 948,266 refractive surgery procedures were performed in the United States during 2004 and 928,737 in 2005.[1]

Contents

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History

The first experimental studies about refractive surgery were developed by Lendeer Jans Lans, an ophthalmology teacher in Holland, 1896 where he published a theoretic work proposing penetrating corneal cuts to correct astigmatism. In 1930 the Japanese ophthalmologist Tsutomu Sato made the first practical attempt to perform such surgery in military pilots. He practiced radial cuts in the cornea to correct effects by up to 6 diopters, but this procedure was soon rejected by the medical community because of the high rate of corneal degeneration. In 1963, in the Barraquer ophthalmologic clinic (Bogotá,Colombia) Ignacio Barraquer developed the first proficient technique to refractive surgery, called keratomileusis (from the Greek Kerato: cornea and Mileusis: to sculpt) meaning corneal reshaping. Keratomileusis allowed to correct not only myopia but also hyperopia. The early surgeries were made removing a corneal layer, freezing it so it could be manually sculpted in the required shape and finally reimplant the layer (Keratomileusis with freezing). In 1986 Dr Swinger improved the surgery (keratomileusis without freezing) but it was still a slightly imprecise technique. In 1958 Arthur Schawlow and Townes, from Bell Laboratories published their theory of stimulated emission of shorter length waves, included light, which gave place to the development of Laser. In 1975 experiments with laser using a mix of argon and fluor ended with the invention of the Excimer. This Laser was used with industrial purposes. In 1980, R. Srinivasan, a scientist of IBM who was using the Excimer to make microscopic circuits in microchips for informatics equipments, discovered that the Excimer could be used also to cut organic tissues with high accuracy without significant thermal damage. In 1983 Stephen Trokel, scientist of Columbia University in collaboration with Srinivasan performed the Photorefractive Keratectomy (PRK) or keratomileusis in situ (without separation of corneal layer) which was more technically exact, but the patients reported it to be very uncomfortable. Also a delay in the healing was observed. The first PRK was performed in Germany. The first patent for LASIK was granted by the US Patent Office to Gholam A. Peyman, MD on June 20, 1989, US Patent #4,840,175, "METHOD FOR MODIFYING CORNEAL CURVATURE", describing the surgical procedure in which a flap is cut in the cornea and pulled back to expose the corneal bed. This exposed surface is then ablated to the desired shape with an excimer laser, following which the flap is replaced. In 1991 the Creta University and the Vardinoyannion Eye coined the name "LASIK". However, there exists debate over the stability of the healing with the corneal flap. Current PRK procedures involve the removal of the corneal layer with an alcohol based solution for the corrective procedure, and then allowing the layer to regenerate. However, this is somewhat painful for the patient following the procedure and takes longer for visual acuity to stabilize.

Techniques

Flap procedures

Excimer laser ablation is done under a partial-thickness lamellar corneal flap.

  • Automated lamellar keratoplasty (ALK): The surgeon uses an instrument called a microkeratome to cut a thin flap of the corneal tissue. The flap is lifted like a hinged door, targeted tissue is removed from the corneal stroma, again with the microkeratome, and then the flap is replaced.
  • Laser Assisted In-Situ Keratomileusis (LASIK): The surgeon uses a microkeratome to cut a flap of the corneal tissue (usually with a thickness of 100-180 micrometres). The flap is lifted like a hinged door, but in contrast to ALK, the targeted tissue is removed from the corneal stroma with an excimer laser. The flap is subsequently replaced. Another method of creating this flap is by using a procedure called IntraLasik, in which a femtosecond laser is used to create the flap. Proponents of this method tout its superiority over "traditional" LASIK, but there are no conclusive independent studies to prove that this is a true statement.

Surface procedures

The excimer laser is used to ablate the most anterior portion of the corneal stroma. These procedures do not require a partial thickness cut into the stroma. Surface ablation methods differ only in the way the epithelial layer is handled.

  • Photorefractive keratectomy (PRK) is an outpatient procedure generally performed with local anesthetic eye drops (as with LASIK/LASEK) . It is a type of refractive surgery which reshapes the cornea by removing microscopic amounts of tissue from the corneal stroma, using a computer-controlled beam of light (excimer laser). The difference from LASIK is that the top layer of the epithelium is removed (and a bandage contact lens is used), so no flap is created. Recovery time is longer with PRK than with LASIK, though the final outcome (after 3 months) is about the same (very good). More recently, customized ablation has been performed with LASIK, LASEK, and PRK.
  • Laser Assisted Sub-Epithelium Keratomileusis (LASEK) is a procedure that also changes the shape of the cornea using an excimer laser to ablate the tissue from the corneal stroma, under the corneal epithelium, which is kept mostly intact to act as a natural bandage. The surgeon uses an alcohol solution to loosen then lift a thin layer of the epithelium with a trephine blade (usually with a thickness of 50 micrometres). [2] During the weeks following LASEK, the epithelium heals, leaving no permanent flap in the cornea. This healing process can involve discomfort comparable to that with PRK.
  • EPI-LASIK is a new technique similar to LASEK that uses an epi-keratome (rather than a trephine blade and alcohol), to remove the top layer of the epithelium (usually with thickness of 50 micrometres), which is subsequently replaced. For some people it can provide better results than regular LASEK in that it avoids the possibility of negative effects from the alcohol, and recovery may involve less discomfort.

Corneal incision procedures

  • Radial keratotomy (RK) uses spoke-shaped incisions (usually made with a diamond knife) to alter the shape of the cornea and reduce myopia or astigmatism; this technique has now been largely replaced by the other methods (that use excimer laser).
  • Arcuate keratotomy (AK) is similar to radial keratotomy, but the incisions on the cornea are done at the periphery of the cornea. Arcuate keratotomy is used to correct astigmatism. Although most incisional procedures are replaced nowadays by Lasik, AK is still used in some special cases (correction of residual astigmatism after a keratoplasty procedure or during cataract surgery).
  • Limbal relaxing incisions (LRI) are incisions near the outer edge of the iris, used to correct minor astigmatism (typically less than 2 diopters). This is often performed in conjunction with an Intraocular Lens implantation.

Other procedures

  • Thermal keratoplasty is used to correct hyperopia by putting a ring of 8 or 16 small burns surrounding the pupil, and steepen the cornea with a ring of collagen constriction. It can also be used to treat selected types of astigmatism.
  • Laser thermal keratoplasty (LTK) is a no-touch thermal keratoplasty performed with a Holmium laser, while conductive keratoplasty (CK) is thermal keratoplasty performed with a high-frequency electric probe. Thermal keratoplasty can also be used to improve presbyopia or reading vision after age 40.
  • Intrastromal corneal ring segments (Intacs) are approved by FDA for treatment of low degrees of myopia.
  • Lens implantation inside the eye can also be used to change refractive errors.

Expectations

The Council for Refractive Surgery Quality Assurance - an independent, nonprofit, patient/consumer health organization that provides information about refractive surgery and certifies LASIK surgeons - considers surgeons to have met the US national norms if 90% of their patients achieve 20/40 vision or better and 65% of their patients achieve 20/20 vision or better, with less than approximately 3% of their refractive surgery patients experiencing a surgery induced complication at six months after surgery, and less than 0.5% being serious complications requiring extensive maintenance or invasive treatment.[3]

Many people with myopia are able to read comfortably without eyeglasses. Myopes considering refractive surgery are advised that this may be a disadvantage after the age of 40 when the eyes become presbyopic and lose their ability to accommodate or change focus.

Risks

While refractive surgery is becoming more affordable and safe, it may not be recommended for everybody. Patients that have medical conditions such as glaucoma or diabetes, uncontrolled vascular disease, autoimmune disease, pregnant women or people with certain eye diseases involving the cornea or retina, are not good candidates for refractive surgery. Keratoconus, a progressive thinning of the cornea, is a common corneal disorder. It is believed that additional thinning of the cornea via refractive surgery may contribute to advancement of the disease,[4] that may lead to the need for a corneal transplant. Therefore, keratoconus is a contraindication to refractive surgery. Corneal topography, pachymetry and, more recently, Pentacam exams are used to screen for abnormal corneas. Furthermore, some people's eye shape may not permit effective refractive surgery without removing excessive amounts of corneal tissue. Those considering laser eye surgery should have a full eye examination.

Although the risk of complications is decreasing compared to the early days of refractive surgery,[5] there is still a small chance for serious problems. These include vision problems such as ghosting, halos, starbursts, double-vision, and dry-eye syndrome.[6] With procedures that create a permanent flap in the cornea (such as LASIK), there is also the possibility of accidental traumatic flap displacement years after the surgery,[7] with potentially disastrous results if not given prompt medical attention.[8]

References

  1. ^ http://www.aao.org/news/academy_express/20060405.cfm
  2. ^ LASIK VS LASEK - A Comparison Chart
  3. ^ The Odds You Will See 20/20 After Lasik, All-Laser Lasik, PRK, LASEK, Epi-Lasik, CK, P-IOL, RLE, etc
  4. ^ Research of corneal ectasia following laser in-situ keratomileusis in rabbits. Huang X, He X, Tan X.
  5. ^ USATODAY.com - LASIK risks understated
  6. ^ LASIK Risks and LASIK Complications - AllAboutVision.com
  7. ^ Late dislocation of LASIK flap following fingernail injury. Srinivasan M, Prasad S, Prajna NV, - Indian J Ophthalmol
  8. ^ Late Traumatic Flap Displacement after Laser In Situ Keratomileuisis | Military Medicine | Find Articles at BNET.com
Retina

The vertebrate retina is a light sensitive tissue lining the inner surface of the eye. The optics of the eye create an image of the visual world on the retina, which serves much the same function as the film in a camera. Light striking the retina initiates a cascade of chemical and electrical events that ultimately trigger nerve impulses. These are sent to various visual centers of the brain through the fibers of the optic nerve.

In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, so the retina is considered part of the central nervous system (CNS).[1]. It is the only part of the CNS that can be imaged non-invasively in the living organism.

The retina is a complex, layered structure with several layers of neurons interconnected by synapses. The only neurons that are directly sensitive to light are the photoreceptor cells. These are mainly of two types: the rods and cones. Rods function mainly in dim light and provide black-and-white vision, while cones support daytime vision and the perception of colour. A third, much rarer type of photoreceptor, the photosensitive ganglion cell, is important for reflexive responses to bright daylight.

Neural signals from the rods and cones undergo complex processing by other neurons of the retina. The output takes the form of action potentials in retinal ganglion cells whose axons form the optic nerve. Several important features of visual perception can be traced to the retinal encoding and processing of light.

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