1. Glaucoma
From Wikipedia, the free encyclopedia
Glaucoma
Classification and external resources
Acute angle closure glaucoma of the right eye. Note the mid sized pupil,
which was nonreactive to light, and injection (nonuniform redness) of the
conjunctiva.
ICD-10
H40-H42
ICD-9
365
DiseasesDB
5226
MedlinePlus
001620
eMedicine
oph/578
MeSH
D005901
Glaucoma is a term describing a group of ocular disorders with multi-factorial etiology united by a clinically
characteristic intraocular pressure-associated optic neuropathy.[1] This can permanently damage vision in
the affected eye(s) and lead to blindness if left untreated. It is normally associated with increased fluid
pressure in the eye (aqueous humour).[2] The term "ocular hypertension" is used for people with
consistently raised intraocular pressure (IOP) without any associated optic nerve damage. Conversely, the
term 'normal tension' or 'low tension' glaucoma is used for those with optic nerve damage and associated
visual field loss, but normal or low IOP.
The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. The many different
subtypes of glaucoma can all be considered to be a type of optic neuropathy. Raised intraocular pressure
(above 21 mmHg or 2.8 kPa) is the most important and only modifiable risk factor for glaucoma. However,

2. some may have high eye pressure for years and never develop damage, while others can develop nerve
damage at a relatively low pressure. Untreated glaucoma can lead to permanent damage of the optic
nerve and resultantvisual field loss, which over time can progress to blindness.
Glaucoma can be roughly divided into two main categories, "open-angle" and "closed-angle" (or "angle
closure") glaucoma. The angle refers to the area between the iris and cornea, through which fluid must flow
to escape via the trabecular meshwork. 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 patients
may not notice they have lost vision until the disease has progressed significantly.
When the scleral venous sinus is blocked to where aqueous humor is not reabsorbed at a faster rate than it
is being secreted, elevated pressure within the eye occurs. Pressure in the anterior and posterior chambers
pushes the lens back and puts pressure on the vitreous body. The vitreous body presses the retina against
the choroid and compresses the blood vessels that feed the retina. Without a sufficient blood supply, retinal
cells will die and the optic nerve may atrophy, causing blindness.[3] Typically, the nerves furthest from the
focal point fail first because of their distance from the central blood supply to the eye; thus, vision loss due
to glaucoma tends to start at the edges with the peripheral visual field, leading to progressively
worse tunnel vision.[4]
Glaucoma has been called the "silent thief of sight" because the loss of vision often occurs gradually over a
long period of time, and symptoms only occur when the disease is quite advanced. Once lost, vision cannot
normally be recovered, so treatment is aimed at preventing further loss. Worldwide, glaucoma is the
second-leading cause of blindness aftercataracts.[5][6] It is also the leading cause of blindness among
African Americans.[7] Glaucoma affects one in 200 people aged 50 and younger, and one 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". (Cataracts and
glaucoma were not distinguished until circa 1705).[8]
Contents
[hide]
1 Signs and symptoms
2 Causes
o
2.1 Dietary
o
2.2 Ethnicity and sex
o
2.3 Genetics
o
2.4 Other
3 Pathophysiology

3. 4 Diagnosis
5 Screening
6 Management
o
6.1 Balance and postural control
o
6.2 Medication
o
6.3 Surgery
7 Epidemiology
8 Research
o
8.1 Implanted sensor
o
8.2 ES cell
9 Classification
o
9.1 Primary glaucoma and its variants (H40.1-H40.2)
o
9.2 Developmental glaucoma (Q15.0)
o
9.3 Secondary glaucoma (H40.3-H40.6)
o
9.4 Absolute glaucoma (H44.5)
10 Prognosis
11 References
12 External links
Signs and symptoms[edit]
Photo showing conjunctival vessels dilated at the corneal edge (ciliary flush, circumcorneal flush) and hazy cornea
characteristic of acute angle closure glaucoma
The two main types of glaucoma are open-angle glaucoma and closed-angle glaucoma (also called angle
closure 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 many
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

4. lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, suddenly decreased
vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle
closure is an emergency.
Causes[edit]
A normal range of vision
The same view with advanced vision loss from glaucoma
Of the several causes for glaucoma, ocular hypertension (increased pressure within the eye) is the most
important risk factor in most glaucomas, but in some populations, only 50% of people with primary openangle glaucoma actually have elevated ocular pressure.[9]
Dietary[edit]
No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral
vitamin supplementation is not a recommended treatment for glaucoma.[10] Caffeine increases intraocular
pressure in those with glaucoma, but does not appear to affect normal individuals.[11]
Ethnicity and sex[edit]
Many people of East Asian descent are prone to developing angle closure glaucoma due to shallower
anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form
of angle closure.[12] Inuit also have a 20 to 40 times higher risk 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. People of African descent are three times more likely to develop primary
open angle glaucoma.

5. Genetics[edit]
Positive family history is a risk factor for glaucoma. The relative risk of having primary open angle
glaucoma (POAG) is increased approximately 2–4 fold for individuals who have a sibling with
glaucoma.[13] Glaucoma, particularly primary open angle glaucoma, is associated with mutations in several
different genes (including MYOC, ASB10, WDR36, NTF4, TBK1 genes),[14] although most cases of
glaucoma do not involve these genetic mutations. Normal tension glaucoma, which comprises one-third of
POAG, is also associated with genetic mutations (including OPA1 and OPTN genes).[15]
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,[16][17][18] and modelled in mice.[19]
Other[edit]
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). In a large study in the UK, glaucoma patients had a
29% increased incidence of systemic hypertension compared to age- and sex-matched controls.[20]
Pathophysiology[edit]
This section includes a list of references, but its sources remain unclear because
it has insufficient inline citations.Please help to improve this article
by introducing more precise citations. (June 2012)
Human eye cross-sectional view
The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology.
However, the major risk factor for most glaucomas, and the focus of treatment, is increased intraocular
pressure, i.e. ocular hypertension. Intraocular pressure is a function of production of liquid aqueous
humor by the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous
humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and
the zonules of Zinn, and anteriorly by the iris. It then flows through the pupil of the iris into the anterior

6. chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here, the trabecular meshwork
drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation.[21]
In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the degeneration
and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss
of aqueous humor absorption leads to increased resistance and thus a chronic, painless buildup of
pressure in the eye.[22] In close/narrow-angle, the iridocorneal angle is completely closed because of
forward displacement of the final roll and root of the iris against the cornea, resulting in the inability of the
aqueous fluid to flow from the posterior to the anterior chamber and then out of the trabecular network. This
accumulation of aqueous humor causes an acute increase of pressure and pain.
The inconsistent relationship of glaucomatous optic neuropathy with ocular hypertension has provoked
hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve
blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon degeneration, glial support
cell, immune system, aging mechanisms of neuron loss, and severing of the nerve fibers at the scleral
edge.[23][24][25][26][27][28][29][30][31][32][33][34]
Diagnosis[edit]
Screening for glaucoma is usually performed as part of a standard eye examination performed
by optometrists, orthoptists and ophthalmologists. 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, scanning laser polarimetry, and/or scanning laser ophthalmoscopy.[35][36]
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 thickerthan-average cornea can result in a pressure reading higher than the 'true' pressure, whereas a thinnerthan-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 perimeter.[37]
Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug
use, refraction, inheritance and family history.[35]
Glaucoma Tests[38][39][40]

7. What Test
Examines
How Examination is Accomplished
Tonometry
Inner eye pressure
The eye is numbed via eye drops. The examiner then uses a
tonometer to measure the inner pressure of the eye through
pressure applied by a puff of warm air or a tiny tool.
Ophthalmoscopy(dilated
eye exam)
Shape and color of
the optic nerve
The pupil is dilated via the application of eye drops. Using a
small magnification device with a light on the end, the
examiner can examine the magnified optic nerve.
Perimetry (visual field test)
Complete field of
vision
The patient looks straight ahead and is asked to indicate
when light passes the patient's peripheral field of vision.
This allows the examiner to map the patient’s field of vision.
Gonioscopy
Angle in the eye
where the iris meets
the cornea
Eye drops are used to numb the eye. A hand-held contact
lens with a mirror is placed gently on the eye to allow the
examiner to see the angle between the cornea and the iris.
Pachymetry
Thickness of the
cornea
The examiner places a pachymeter gently on the front of the
eye to measure its thickness.
Nerve fiber analysis
Thickness of the
nerve fiber layer
Using one of several techniques, the nerve fibers are
examined.
Screening[edit]
The United States Preventive Services Task Force as of 2013 states there is insufficient evidence to
recommend for or against screening for glaucoma.[41] There is thus no national screening programs in the
US. There is in the UK. Those at risk are advised to have a dilated eye examination at least once a year.[42]
Management[edit]
The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and
preserve visual field and total quality of life for patients, with minimal side effects. [43][44] 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.

8. Balance and postural control[edit]
Because of the important role of the visual system in balance and maintaining posture in human beings,
glaucoma patients should consider themselves at greater risk of falls, and would be advised to take the
necessary precautions to help prevent any accidents. In addition, since the peripheral visual system has
such a high contribution to this intrinsic balancing mechanism, the severity of glaucoma and degree of
visual field obstruction should also be considered.[45] Because of the relationship of glaucoma with age,
other associated factors affecting balance (i.e. impaired proprioception) may also be present, further
increasing the risk of falls. Of interesting note, one cohort of open-angle glaucoma patients had their ability
to maintain posture measured (via measurements of sway) in binocular (two-eyed) and monocular (oneeyed, using both affected and unaffected eyes) conditions, as well as with their eyes closed. These patients
had increased sway (worse balance) in their one-eyed conditions compared to the two-eyed conditions,
and reduced sway (better balance) when using one eye than when their eyes were closed, but there were
no significant differences between the two monocular conditions, with the unaffected eye having only
slightly (but not significantly) reduced sway than when using their affected eyes. All patients in each
condition displayed increased sway compared to their age-matched controls.[46]
Medication[edit]
Main article: Glaucoma medication
Intraocular pressure can be lowered with medication, usually eye drops. Several different classes of
medications are used 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 them, 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.[47]
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 half failed to fill their prescriptions the first time, and
one-fourth failed to refill their prescriptions a second time.[48] 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.[10][49][50][51]
Prostaglandin analogs, such
as latanoprost (Xalatan), bimatoprost (Lumigan)
and travoprost (Travatan), increase uveoscleral outflow of aqueous
humor. Bimatoprost also increases trabecular outflow.

9. 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)
and apraclonidine, work by a dual mechanism, decreasing aqueous
humor production and increasing uveoscleral outflow.
Less-selective alpha agonists, such as epinephrine, decrease aqueous
humor production through vasoconstriction of ciliary body blood
vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic
effect, however, renders it unsuitable for closed-angle glaucoma due to
further narrowing of the uveoscleral outflow (i.e. further closure of
trabecular meshwork, which is responsible for absorption of aqueous
humor).
Miotic agents (parasympathomimetics), such as pilocarpine, work by
contraction of the ciliary muscle, opening the trabecular meshwork and
allowing increased outflow of the aqueous humour. Echothiophate, an
acetylcholinesterase inhibitor, is used in chronic glaucoma.
Carbonic anhydrase inhibitors, such
as dorzolamide (Trusopt), brinzolamide (Azopt),
and acetazolamide (Diamox), lower secretion of aqueous humor by
inhibiting carbonic anhydrase in the ciliary body.
Physostigmine is also used to treat glaucoma.
Marijuana was found, in the early 1970s, to reduce pressure in the
eyes, though how the cannabinoids in marijuana produce this effect
remains unknown.
Surgery[edit]
Conventional surgery to treat glaucoma makes a new opening in the meshwork, which helps fluid to leave the eye and
lowers intraocular pressure.

10. Main article: Glaucoma surgery
Both laser and conventional surgeries are performed to treat glaucoma. Surgery is the primary therapy for
those with congenitalglaucoma.[52] Generally, these operations are a temporary solution, as there is not yet
a cure for glaucoma.
Canaloplasty[edit]
Canaloplasty is a nonpenetrating procedure using microcatheter technology. To perform a canaloplasty, an
incision is made into the eye to gain access to the 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. Longterm results are not available.[53][54]
Laser surgery[edit]
Argon laser trabeculoplasty (ALT) 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 uses a thermal argon laser in an argon laser trabeculoplasty procedure.
A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage in the
trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm,
frequency-doubled, Q-switched Nd:YAG laser, which selectively targets melanin pigment in the trabecular
meshwork cells. Studies show 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 to equalize the pressure between the front and back of the iris, thus
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.[35]
Trabeculectomy[edit]
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 is made under the flap to

11. remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place to allow
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. Traditionally, chemotherapeutic
adjuvants, such as mitomycin C (MMC, 0.5–0.2 mg/ml) or 5-fluorouracil (5-FU, 50 mg/ml), are applied with
soaked sponges on the wound bed to prevent filtering blebs from scarring by inhibiting fibroblast
proliferation. Contemporary alternatives include the sole or combinative implementation of
nonchemotherapeutic adjuvants, such as collagen matrix implant[55][56][57][58] or other biodegradable spacers,
to prevent super scarring by randomization and modulation of fibroblast proliferation in addition to the
mechanical prevention of wound contraction and adhesion.
Glaucoma drainage implants[edit]
Main article: Glaucoma valve
Professor Anthony Molteno developed the first glaucoma drainage implant, in Cape Town in 1966.[59] Since
then, several different types of implants have followed on from the original, 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.
The first-generation Molteno and other nonvalved implants sometimes
require the ligation of the tube until the bleb formed is mildly fibrosed
and water-tight.[60] This is done to reduce postoperative hypotony—
sudden drops in postoperative intraocular pressure.
Valved implants, such as the Ahmed glaucoma valve, attempt to
control postoperative hypotony by using a mechanical valve.
The ongoing scarring over the conjunctival dissipation segment of the shunt may become too thick for the
aqueous humor to filter through. This may require preventive measures using antifibrotic medications, such
as 5-fluorouracil or mitomycin-C (during the procedure), or other nonantifibrotic medication methods, such
as collagen matrix implant,[61][62] or biodegradable spacer, or later on create a necessity for revision surgery
with the sole or combinative use of donor patch grafts or collagen matrix implant.[63][64] And for
glaucomatous painful blind eye and some cases of glaucoma, cyclocryotherapy for ciliary body ablation
could be considered to be performed.[35]
Veterinary implant[edit]
TR BioSurgical has commercialized a new implant specifically for veterinary medicine, called TR-ClarifEYE.
The implant consists of a new biomaterial, the STAR BioMaterial, which consists of silicone with a very
precise homogenous pore size, a property which reduces fibrosis and improves tissue integration. The

12. implant contains no valves and is placed completely within the eye without sutures. To date, it has
demonstrated long-term success (longer than a year) in a pilot study in medically refractory dogs with
advanced glaucoma.[65]
Laser-assisted nonpenetrating deep sclerectomy[edit]
The most common surgical approach currently used for the treatment of glaucoma is trabeculectomy, in
which the sclera is punctured to alleviate intraocular pressure.
Nonpenetrating deep sclerectomy (NPDS) surgery is a similar, but modified, procedure, in which instead of
puncturing the scleral bed and trabecular meshwork under a scleral flap, a second deep scleral flap is
created, excised, with further procedures of deroofing the Schlemm's canal, upon which, percolation of
liquid from the inner eye is achieved and thus alleviating intraocular pressure, without penetrating the eye.
NPDS is demonstrated to cause significantly fewer side effects than trabeculectomy. [citation needed] However,
NPDS is performed manually and requires higher level of skills that may be assisted with instruments. [citation
needed]
In order to prevent wound adhesion after deep scleral excision and to maintain good filtering results,
NPDS as with other non-penetrating procedures is sometimes performed with a variety of biocompatible
spacer or devices, such as the Aquaflow collagen wick,[66] ologen Collagen Matrix,[67][68][69] or Xenoplast
glaucoma implant.[70]
Laser-assisted NPDS is performed with the use of a CO2 laser system. The laser-based system is selfterminating once the required scleral thickness and adequate drainage of the intraocular fluid have been
achieved. This self-regulation effect is achieved as the CO2 laser essentially stops ablating as soon as it
comes in contact with the intraocular percolated liquid, which occurs as soon as the laser reaches the
optimal residual intact layer thickness.
Epidemiology[edit]
Disability-adjusted life year for glaucoma per 100,000 inhabitants in 2004[71]
no data
fewer than 20
20–43
43–66
66–89
89–112
112–135
135–158
158–181

13. 181–204
204–227
227–250
more than 250
As of 2010, there were 44.7 million people in the world with open angle glaucoma.[72] The same year, there
were 2.8 million people in the United States with open angle glaucoma.[72] By 2020, the prevalence is
projected to increase to 58.6 million worldwide and 3.4 million the United States.[72]
Internationally, glaucoma is the second-leading cause of blindness, after cataracts. Glaucoma is also the
leading cause of blindness in African Americans, who have higher rates of primary open angle
glaucoma.[73] Bilateral vision loss can negatively affect mobility and interfere with driving. [74]
A meta-analysis published in 2009 found that patients with primary open angle glaucoma do not have
increased mortality rates, or increased risk of cardiovascular death.[75]
Research[edit]
scientists track eye movements in glaucoma patients to check vision impairment while driving
The Advanced Glaucoma Intervention Study is a large American
National Eye Institute-sponsored study designed "to assess the longrange outcomes of sequences of interventions involving
trabeculectomy and argon laser trabeculoplasty in eyes that have failed
initial medical treatment for glaucoma". It recommends different
treatments based on race.
The Early Manifest Glaucoma Trial is another NEI study which found
immediate treatment of people who have early-stage glaucoma can
delay progression of the disease.
The Ocular Hypertension Treatment Study, also an NEI study, found
topical ocular hypotensive medication was effective in delaying or
preventing onset of primary open-angle glaucoma (POAG) in
individuals with elevated intraocular pressure (IOP). Although this does
not imply all patients with borderline or elevated IOP should receive
medication, clinicians should consider initiating treatment for individuals
with ocular hypertension who are at moderate or high risk for
developing POAG.
The Blue Mountains Eye Study was the first large, population-based
assessment of visual impairment and common eye diseases of a

14. representative older Australian community sample. Risk factors for
glaucoma and other eye disease were determined.
Natural compounds
Natural compounds of research interest in glaucoma prevention or treatment include: fish oil and omega-3
fatty acids, alpha lipoic acid,[76] bilberries, vitamin E, cannabinoids, carnitine, coenzyme
Q10, curcurmin, Salvia miltiorrhiza, dark chocolate, erythropoietin, folic acid, Ginkgo biloba, ginseng, Lglutathione, grape seed extract, green tea, magnesium, melatonin, methylcobalamin, N-acetyl-L
cysteine, pycnogenols, resveratrol, quercetin and salt. However, most of these compounds have not
demonstrated effectiveness in clinical trials.[49][50][51] Magnesium, ginkgo, salt and fludrocortisone, are
already used by some physicians. (Note: fludrocortisone is not a natural compound, but a steroid.)
Cannabis
Studies in the 1970s showed marijuana, when smoked or eaten, effectively lowers intraocular pressure by
about 25%, as much as standard medications.[77][78][79] In an effort to determine whether marijuana, or drugs
derived from it, might be effective as a glaucoma treatment, the US National Eye Institute supported
research studies from 1978 to 1984. These studies demonstrated some derivatives of marijuana lowered
intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied
to the eye.
In 2003, the American Academy of Ophthalmology released a position statement which said, "studies
demonstrated that some derivatives of marijuana did result in lowering of IOP when administered orally,
intravenously, or by smoking, but not when topically applied to the eye. The duration of the pressurelowering effect is reported to be in the range of 3 to 4 hours".[79][80]
However, the position paper qualified that statement by stating marijuana was not more effective than
prescription medications, and "no scientific evidence has been found that demonstrates increased benefits
and/or diminished risks of marijuana use to treat glaucoma compared with the wide variety of
pharmaceutical agents now available."
The first patient in the United States federal government's Compassionate Investigational New Drug
program, Robert Randall, was afflicted with glaucoma and had successfully fought charges of marijuana
cultivation because it was deemed a medical necessity (U.S. v. Randall) in 1976.[81]
5-HT2A agonists
Peripherally selective 5-HT2A agonists, such as the indazole derivative AL-34662, are currently under
development and show significant promise in the treatment of glaucoma.[82][83]
Implanted sensor[edit]
The world's smallest computer system, one millimeter square in size, has been developed by researchers
at the University of Michigan, and is designed to be implanted in a person's eye as a pressure monitor to
continuously track the progress of glaucoma. The processor consists of an ultra-low-power microprocessor,

15. a pressure sensor, memory, a thin-film battery, a solar cell, and a wireless radio with an antenna that can
transmit data to an external reader device.[84]
ES cell[edit]
The survey team of Dr.Yoshiki Sasai,[85] working at the RIKEN of Center for Developmental Biology (CDB)
in Japan, succeeded in making a retina cell in three dimensions fromembryonic stem cells, as was reported
in Nature (7 April 2011).[86] It was the first such success in the world, and Dr. Sasai said the goal for putting
it to practical use in the retinas of human for clinical applications was within two years.
Classification[edit]
Glaucoma has been classified into specific types:[87]
Primary glaucoma and its variants (H40.1-H40.2)[edit]
Primary glaucoma
Primary angle closure glaucoma, also known as primary closed-angle
glaucoma, narrow-angle glaucoma, pupil-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" – uncommon)
Primary open-angle glaucoma, also known as chronic open-angle
glaucoma, chronic simple glaucoma, glaucoma simplex
High-tension glaucoma
Low-tension glaucoma
Variants of primary glaucoma
Pigmentary glaucoma
Exfoliation glaucoma, also known as pseudoexfoliative
glaucoma or glaucoma capsulare
Primary angle closure glaucoma is caused by contact between
the iris and trabecular meshwork, which in turn obstructs outflow of
the aqueous humor from the eye. This contact between iris and
trabecular meshwork (TM) may gradually damage the function of

16. the meshwork until it fails to keep pace with aqueous production,
and the pressure rises. In over half of all cases, prolonged contact
between iris and TM causes the formation of synechiae (effectively
"scars").
These cause permanent obstruction of aqueous outflow. In some
cases, pressure may rapidly build up in the eye, causing pain and
redness (symptomatic, or so called "acute" angle closure). In this
situation, the vision may become blurred, and halos may be seen
around bright lights. Accompanying symptoms may include
headache and vomiting.
Diagnosis is made from physical signs and symptoms: pupils middilated and unresponsive to light, cornea edematous (cloudy),
reduced vision, redness, and pain. However, the majority of cases
are asymptomatic. Prior to very severe loss of vision, these cases
can only be identified by examination, generally by an eye care
professional.
Once any symptoms have been controlled, the first line (and often
definitive) treatment is laser iridotomy. This may be performed
using either Nd:YAG or argon lasers, or in some cases by
conventional incisional surgery. The goal of treatment is to
reverse, and prevent, contact between iris and trabecular
meshwork. In early to moderately advanced cases, iridotomy is
successful in opening the angle in around 75% of cases. In the
other 25%, laser iridoplasty, medication (pilocarpine) or incisional
surgery may be required.
Primary open-angle glaucoma is when optic nerve damage
results in a progressive loss of the visual field.[88] This is
associated with increased pressure in the eye. Not all people with
primary open-angle glaucoma have eye pressure that is elevated
beyond normal, but decreasing the eye pressure further has been
shown to stop progression even in these cases.
The increased pressure is caused by trabecular blockage.
Because the microscopic passageways are blocked, the pressure
builds up in the eye and causes imperceptible very gradual vision
loss. Peripheral vision is affected first, but eventually the entire
vision will be lost if not treated.

17. Diagnosis is made by looking for cupping of the optic nerve.
Prostaglandin agonists work by opening uveoscleral
passageways. Beta blockers, such as timolol, work by decreasing
aqueous formation. Carbonic anhydrase inhibitors decrease
bicarbonate formation from ciliary processes in the eye, thus
decreasing formation of Aqueous humor. Parasympathetic
analogs are drugs that work on the trabecular outflow by opening
up the passageway and constricting the pupil. Alpha 2 agonists
(brimonidine, apraclonidine) both decrease fluid production (via.
inhibition of AC) and increase drainage.
Developmental glaucoma (Q15.0)[edit]
Developmental glaucoma
Primary congenital glaucoma
Infantile glaucoma
Glaucoma associated with hereditary of familial diseases
Secondary glaucoma (H40.3-H40.6)[edit]
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

18. Angle recession glaucoma: Traumatic recession on anterior
chamber angle
Postsurgical glaucoma
Aphakic pupillary block
Ciliary block glaucoma
Neovascular glaucoma (see below for more
details)
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 detachments
Secondary to severe chemical burns of the eye
Associated with essential iris atrophy
Toxic glaucoma
Neovascular glaucoma, an
uncommon type of glaucoma, is
difficult or nearly impossible to treat,
and is often caused by
proliferative diabetic retinopathy (PDR)
or central retinal vein
occlusion (CRVO). It may also be
triggered by other conditions that result
in ischemia of the retina or ciliary body.
Individuals with poor blood flow to the
eye are highly at risk for this condition.
Neovascular glaucoma results when
new, abnormal vessels begin
developing in the angle of the eye that
begin blocking the drainage. Patients
with such condition begin to rapidly

19. lose their eyesight. Sometimes, the
disease appears very rapidly,
especially after cataract surgery
procedures. A new treatment for this
disease, as first reported by Kahook
and colleagues, involves use of a novel
group of medications known as antiVEGF agents. These injectable
medications can lead to a dramatic
decrease in new vessel formation and,
if injected early enough in the disease
process, may lead to normalization of
intraocular pressure.
Toxic glaucoma is open angle
glaucoma with an unexplained
significant rise of intraocular
pressure following unknown
pathogenesis. Intraocular pressure can
sometimes reach 80 mmHg (11 kPa). It
characteristically manifests as ciliary
body inflammation and massive
trabecular oedema that sometimes
extends to Schlemm's canal. This
condition is differentiated from
malignant glaucoma by the presence
of a deep and clear anterior chamber
and a lack of aqueous misdirection.
Also, the corneal appearance is not as
hazy. A reduction in visual acuity can
occur followed neuroretinal breakdown.
Associated factors include
inflammation, drugs, trauma and
intraocular surgery, including cataract
surgery and vitrectomy procedures.
Gede Pardianto (2005) reported on
four patients who had toxic glaucoma.
One of them underwent
phaecoemulsification with small

20. particle nucleus drops. Some cases
can be resolved with some medication,
vitrectomy procedures or
trabeculectomy. Valving procedures
can give some relief, but further
research is required.[89]
Absolute glaucoma
(H44.5)[edit]
Absolute glaucoma is the end stage of
all types of glaucoma. The eye has no
vision, absence of pupillary light
reflex and pupillary response, and has
a stony appearance. Severe pain is
present in the eye. The treatment of
absolute glaucoma is a destructive
procedure like cyclocryoapplication,
cyclophotocoagulation, or injection of
99% alcohol.
Prognosis[edit]
In open-angle glaucoma, the typical
progression from normal vision to
complete blindness takes about 25
years to 70 years without treatment,
depending on the method of estimation
used.[90] The intraocular pressure can
also have an effect, with higher
pressures reducing the time until
blindness.[91]