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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
The nerve damage involves loss of retinal ganglion cells in a
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
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. It is also the leading cause of
blindness among African Americans. 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
"opacity of the
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.
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
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
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. 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
Primary open angle glaucoma (POAG) has been found to be associated with
mutations in genes at several loci. Normal tension glaucoma, which
comprises one third of POAG, is associated with genetic mutations.
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.
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). 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.
Examination for glaucoma also could be assessed with more attention
given to sex, race, history of drug use, refraction, inheritance and
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. 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.
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.
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.
Patient education and communication must be ongoing to sustain
successful treatment plans for this lifelong disease with no early
The possible neuroprotective effects of various topical and systemic
medications are also being investigated.
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
Surgery is the primary therapy for those with congenital glaucoma.
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.
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
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.
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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