Eye Condition Topics

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Glaucoma | Cataract | Diabetic Retinopathy | Macular Degeneration | Juvenile Macular Degeneration

Human Eye Cross-Sectional View

Courtesy of National Institutes of Health and National Eye Institute

What is Glaucoma?

Glaucoma is a group of diseases of the optic nerve involving loss of retinal ganglion cells in a characteristic pattern of optic neuropathy. Although raised intraocular pressure is a significant risk factor for developing glaucoma, there is no set threshold for intraocular pressure that causes glaucoma. One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

Glaucoma has been nicknamed "the silent sight thief". Worldwide, it is the second leading cause of blindness. Glaucoma affects one in two hundred people aged fifty and younger and one in ten over the age of eighty.

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- Risk Factors -

People with a family history of glaucoma have about a six percent chance of developing glaucoma. Diabetics and African Americans are three times more likely to develop primary open angle glaucoma. Asians are susceptible to angle-closure glaucoma, and Inuit have a twenty to forty times higher risk than caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers. Use of steroids can also cause glaucoma.

There is increasing evidence of ocular blood flow to be involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.

A number of studies also suggest that there is a correlation, not necessarily causal, between glaucoma and systemic hypertension (i.e. high blood pressure). In normal tension glaucoma, nocturnal hypotension may play a significant role. On the other hand there is no clear evidence that vitamin deficiencies cause glaucoma in humans, nor that oral vitamin supplementation is useful in glaucoma treatment.

Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.

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- Diagnosis -

Screening for glaucoma is usually performed as part of a standard eye examination performed by your optometrist. Testing for glaucoma should include measurements of the intraocular pressure via tonometry, changes in size or shape of the eye, and an examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio. If there is any suspicion of damage to the optic nerve, a formal visual field test should be performed. Scanning laser ophthalmoscopy may also be performed.

- Treatment -

Although intraocular pressure is only one major risk factors of glaucoma, lowering it via pharmaceuticals or surgery is currently the mainstay of glaucoma treatment. In Europe, Japan and Canada laser treatment is often the first line of therapy. In the U.S., adoption of early laser has lagged, even though prospective, multi-centered, peer-reviewed studies, since the early '90s, have shown laser to be at least as effective as topical medications in controlling intraocular pressure and preserving visual field.

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- Drugs -

Intraocular pressure can be lowered with medication, usually eye drops. There are several different classes of medications to treat glaucoma with several different medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or to communicate with the treating physician to improve the drug regimen.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigCommonly used medications

Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor.

Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.

Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing uveo-scleral outflow.

Less-selective sympathomimetics like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action.

Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour.

Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

- Surgery -

Conventional surgery to treat glaucoma makes a new opening in the meshwork. This new opening helps fluid to leave the eye and lowers intraocular pressure.

Surgery is the primary therapy for those with congenital glaucoma. Both laser and conventional surgeries are performed. Generally, these operations are a temporary solution, as there is no cure for glaucoma as of yet.

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- Canaloplasty -

Canaloplasty is an advanced, nonpenetrating procedure designed to enhance and restore the eye's natural drainage system to provide sustained reduction of IOP. Canaloplasty utilizes breakthrough microcatheter technology in a simple and minimally invasive procedure. To perform a canaloplasty, a doctor will create a tiny incision to gain access to a canal in the eye. A microcatheter will circumnavigate the canal around the iris, enlarging the main drainage channel and its smaller collector channels through the injection of a sterile, gel-like material called viscoelastic. The catheter is then removed and a suture is placed within the canal and tightened. By opening the canal, the pressure inside the eye will be relieved.

- Laser Surgery -

Laser trabeculoplasty may be used to treat open angle glaucoma. It is a temporary solution, not a cure. A 50 μm argon laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty utilizes a thermal argon laser. The procedure is called argon laser trabeculoplasty or ALT. A newer type of laser trabeculoplasty uses a "cold" (non-thermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure is call selective laser trabeculoplasty or SLT. Studies show that SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

Laser peripheral iridotomy may be used in patients susceptible to or affected by angle closure glaucoma. During laser iridotomy, laser energy is used to make a small full-thickness opening in the iris. This opening equalizes the pressure between the front and back of the iris, causing the iris to move backward. This uncovers the trabecular meshwork. In some cases of intermittent or short-term angle closure this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases it also reduces the risk of developing chronic angle closure or gradual adhesion of the iris to the trabecular meshwork.

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- Trabeculectomy -

The most common conventional surgery performed for glaucoma is the trabeculectomy. Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place. This allows fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the surface of the eye. Scarring can occur around or over the flap opening, causing it to become less effective or lose effectiveness altogether. One person can have multiple surgical procedures of the same or different types.

- Glaucoma Drainage Implants -

There are also several different glaucoma drainage implants. These include the original Molteno implant (1966), the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the eye and the plate is implanted underneath the conjunctiva to allow flow of aqueous fluid out of the eye into a chamber called a bleb.

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- Classification of Glaucoma -

Glaucoma has been classified into specific types:

Primary Glaucoma and its Variants

Primary Glaucoma

Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
Low-tension glaucoma
Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, iris-block glaucoma, acute congestive glaucoma
Acute angle-closure glaucoma
Chronic angle-closure glaucoma
Intermittent angle-closure glaucoma
Superimposed on chronic open-angle closure glaucoma (combined mechanism)

Variants of Primary Glaucoma

Pigmentary glaucoma
Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare

Developmental glaucoma

Developmental Glaucoma

Primary congenital glaucoma
Infantile glaucoma
Glaucoma associated with hereditary of familial diseases

Secondary Glaucoma

Inflammatory glaucoma
Uveitis of all types
Fuchs heterochromic iridocyclitis
Phacogenic glaucoma
Angle-closure glaucoma with mature cataract
Phacoanaphylactic glaucoma secondary to rupture of lens capsule
Phacolytic glaucoma due to phacotoxic meshwork blockage
Subluxation of lens
Glaucoma secondary to intraocular hemorrhage
Hyphema
Hemolytic glaucoma, also known as erythroclastic glaucoma
Traumatic glaucoma
Angle recession glaucoma: Traumatic recession on anterior chamber angle
Postsurgical glaucoma
Aphakic pupillary block
Ciliary block glaucoma
Neovascular glaucoma
Drug-induced glaucoma
Corticosteroid induced glaucoma
Alpha-chymotrypsin glaucoma. Postoperative ocular hypertension from use of alpha chymotrypsin.
Glaucoma of miscellaneous origin
Associated with intraocular tumors
Associated with retinal deatchments
Secondary to severe chemical burns of the eye
Associated with essential iris atrophy

What is Cataract?

A cataract is an opacity that develops in the crystalline lens of the eye or in its envelope. Early on in the development of age-related cataract the power of the crystalline lens may be increased, causing near-sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially blinding if untreated. 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"). 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", so it is also possible that the name came about through the senseof "obstruction".

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- Causes -

Cataracts develop from a variety of reasons, including long-term ultraviolet exposure, exposure to radiation, secondary effects of diseases such as diabetes, and 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 may 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. 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, such as Corticosteroids and 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) and anterior (common senile) cataract related to aging.

- Epidemiology -

Cataracts are the leading cause of blindness in the world.

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

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- 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 (intracapsular cataract extraction, or ICCE).

Extra-capsular (ECCE) 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 (ICCE) 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 is 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 in which they are less dependent on glasses. Under some medical systems multifocal lenses cost extra. Traditional intraocular lenses are monofocal.

Complications after cataract surgery, including endophthalmitis, 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 maintenance, particularly in dusty areas.

- 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][10] Regular intake of antioxidants (such as vitamin C and E) is theoretically helpful, but this has not been proven.

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- 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 disease.

Research is scant and mixed but weakly positive for the nutrients lutein and zeaxanthin. Bilberry extract shows promise in rat models and in clinical studies.

What is Diabetic Retinopathy?

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which could eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all diabetics who have had diabetes for 15 years or more[citation needed]. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes.

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- 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 -

Diabetic retinopathy is result of microvascular retinal changes. Hyperglycemia-induced pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damage change the formation of blood retinal barrier and also make retinal blood vessel become more permiable.

Small blood vessels – such as those in the eye – are especially vulnerable to poor blood glucose control. An overaccumulation of glucose and/or fructose 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 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 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.

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