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Glaucoma



From Wikipedia, the free encyclopedia

Glaucoma is an eye disorder in which the optic nerve suffers damage, permanently impacting vision in the affected eye(s) and progressing to complete blindness if untreated. It is often, but not always, associated with increased pressure of the fluid in the eye (aqueous humour).[1]
The nerve damage involves loss of retinal ganglion cells in a characteristic pattern.
There are many different sub-types of glaucoma but they can all be considered a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg or 2.8 kPa). 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 can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.
Glaucoma has been nicknamed the "silent thief of sight" because the loss of vision normally occurs gradually over a long period of time and is often only recognized when the disease is quite advanced. Once lost, this damaged visual field cannot be recovered. Worldwide, it is the second leading cause of blindness.[2] It is also the leading cause of blindness among African Americans.[3] Glaucoma affects 1 in 200 people aged fifty and younger, and 1 in 10 over the age of eighty. If the condition is detected early enough it is possible to arrest the development or slow the progression with medical and surgical means.
The word glaucoma comes from the Greek γλαύκωμα, "opacity of the crystalline lens".[4]

Signs and symptomsThere are two main types of glaucoma: open-angle glaucoma and closed-angle glaucoma. Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. It is painless and does not have acute attacks. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).
Closed-angle glaucoma accounts for less than 10% of glaucoma cases in the United States, but as much as half of glaucoma cases in other nations (particularly Asian countries). About 10% of patients with closed angles present with acute angle closure crises characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, sudden decreased vision, and a fixed, mid-dilated pupil.
Acute angle closure is an ocular emergency. Causes and risk factors A normal range of vision The same view with advanced vision loss from glaucomaThere are several causes for glaucoma. Those at risk are advised to have a dilated eye examination at least once a year.[18]
Ocular hypertension (increased pressure within the eye) is the largest risk factor in most glaucomas, but in some populations only 50% of patients with primary open angle glaucoma actually have elevated ocular pressure.[19]
Those of African descent are three times more likely to develop primary open angle glaucoma.
Elderly people have thinner corneal thickness and often suffer from hypermetropia. They are also at higher risk for primary open angle glaucoma.
People with a family history of glaucoma have about six percent chance of developing glaucoma.
Many East Asian groups are prone to developing angle closure glaucoma due to their shallower anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure.[20] Inuit also 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.
Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes at several loci.[21] Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.[22]
There is increasing evidence that ocular blood flow is 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 a possible correlation between hypertension and the development of glaucoma. In normal tension glaucoma, nocturnal hypotension may play a significant role.
There is no clear evidence that vitamin deficiencies cause glaucoma in humans. It follows then that oral vitamin supplementation is not a recommended treatment for glaucoma.[23]
Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies and modelled in mice. DiagnosisScreening for glaucoma is usually performed as part of a standard eye examination performed by ophthalmologists, orthoptists and optometrists.
Testing for glaucoma should include measurements of the intraocular pressure via tonometry, changes in size or shape of the eye, anterior chamber angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio and also rim appearance and vascular change. A formal visual field test should be performed.
The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography (OCT), scanning laser polarimetry (GDx), and/or scanning laser ophthalmoscopy also known as Heidelberg Retina Tomography (HRT3).[28][29] Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with pachymetry to measure central corneal thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the 'true' pressure, whereas a thinner-than-average cornea can produce a pressure reading lower than the 'true' pressure.
Because pressure measurement error can be caused by more than just CCT (i.e., corneal hydration, elastic properties, etc.), it is impossible to 'adjust' pressure measurements based only on CCT measurements.
The Frequency Doubling Illusion can also be used to detect glaucoma with the use of a Frequency Doubling Technology (FDT) perimeter.[30] Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug use, refraction, inheritance and family history.[28]

Management The modern goals of glaucoma management are to avoid glaucomatous damage, nerve damage, preserve visual field and total quality of life for patients with minimal side effects.[31][32] This requires appropriate diagnostic techniques and follow up examinations and judicious selection of treatments for the individual patient. Although intraocular pressure is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies including nutritional compounds some of which may be regarded by clinicians as safe for use now, while others are on trial.

Medication
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. Initially, glaucoma drops may reasonably be started in either one or in both eyes.[33]
Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found that half failed to fill their prescription the first time and one in four failed to refill their prescriptions a second time.[34] 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 investigated.
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.Main article: Glaucoma surgery Both laser surgeries and conventional surgeries are performed to treat glaucoma.
Surgery is the primary therapy for those with congenital glaucoma.[38] Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma.

Canaloplasty Canaloplasty is a nonpenetrating procedure utilizing microcatheter technology. To perform a canaloplasty, an incision is made into the eye to gain access to Schlemm's canal in a similar fashion to a viscocanalostomy. 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 may be relieved, although the reason is unclear since the canal (of Schlemm) does not have any significant fluid resistance in glaucoma or healthy eyes.
Long-term results are not available.

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 exists that uses a "cold" (non-thermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure which uses a 532 nm frequency-doubled, Q-switched Nd:YAG laser which selectively targets melanin pigment in the trabecular meshwork cells, called 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.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. 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 correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover 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 of adhesions of the iris to the trabecular meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.[28] TrabeculectomyThe 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.

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