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A cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in
degree from slight to complete opacity and obstructing the passage of light. Early in the development of
age-related cataract the power of the 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. The condition
usually affects both the eyes, but almost always one eye is affected earlier than the other.[1]
A senile cataract, occurring in the elderly, is characterized by an initial opacity in the lens, subsequent
swelling of the lens and final shrinkage with complete loss of transparency.[2] Moreover, with time the
cataract cortex liquefies to form a milky white fluid in a Morgagnian cataract, which 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 historical surgical procedure of couching) in ancient
times were regarded as a blessing from the heavens, because some perception of light was restored in the
cataractous 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").[3] 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",[4] so it is also possible that the name came about through the sense of "obstruction". Early
Persian physicians called the term nazul-i-ah, or "descent of the water"—vulgarised into waterfall disease
or cataract—believing such blindness to be caused by an outpouring of corrupt humour into the eye.[5] In
dialect English a cataract is called a pearl, as in "pearl eye" and "pearl-eyed".
Epidemiology
Age-related cataract is responsible for 48% of world blindness, which represents about 18 million people,
according to the World Health Organization (WHO).[8] In many countries surgical services are
inadequate, and cataracts remain the leading cause of blindness. As populations age, the number of people
with cataracts is growing. Cataracts are also an important cause of low vision in both developed and
developing countries. Even where surgical services are available, low vision associated with cataracts
may still be prevalent, as a result of long waits for operations and barriers to surgical uptake, such as cost,
lack of information and transportation problems
Classification
The following is a classification of the various types of cataracts. This is not comprehensive and other
unusual types may be noted.
 Classified by etiology
 Age-related cataract
 Cortical Senile Cataract
 Immature senile cataract (IMSC): partially opaque lens, disc view hazy
 Mature senile cataract (MSC): Completely opaque lens, no disc view
 Hypermature senile cataract (HMSC): Liquefied cortical matter: Morgagnian cataract
 Senile Nuclear Cataract
 Cataracta brunescens
 cataracta nigra
 cataracta rubra
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Congenital cataract
Sutural cataract
Lamellar cataract
Zonular cataract
Total cataract
Secondary cataract
Drug-induced cataract (e.g. corticosteroids)
Traumatic cataract
Blunt trauma (capsule usually intact)
Penetrating trauma (capsular rupture & leakage of lens material—calls for an
emergency surgery for extraction of lens and leaked material to minimize further
damage)
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Classified by opacities, cataract can be classified by using Lens Opacities Classification System III
(LOCS III: Nuclear NC1-5, Cortical C1-5 and Posterior P1-5. By application planning in procedures
of phacoemulsification, LCOS III can be converted in newer cataract grading system. Gede
Pardianto (2009) introduced Optical Biometry Based Cataract Grading System (OBBCGS) that so
helpful in cataract grading due to phacoemulsification planning. LOCS III's NC0, C0 and P0 acan
be converted as OBBCGS' No cataract (NC), LOCS III's NC1-3, C1-3, P1-4 can be converted to
OBBCGS' Optical Biometry Examined Cataract (OBEC) and LOCS III's NC4-5, C4-5, P4-5 can be
converted to OBBCGS's Optical Biometry Un-examined Cataract (OBUC); that need examination
by Applanation Ultrasound Biometry.[19]
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Classified by location of opacity within lens structure (However, mixed morphology is quite
commonly seen, e.g. PSC with nuclear changes & cortical spokes of cataract)
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Anterior cortical cataract
Anterior polar cataract
Anterior subcapsular cataract
Nuclear cataract—Grading correlates with hardness & difficulty of surgical removal
 1: Grey
 2: Yellow
 3: Amber
 4: Brown/Black (Note: "black cataract" translated in some languages (like Hindi) refers
to glaucoma, not the color of the lens nucleus)
 Posterior cortical cataract
 Posterior polar cataract (importance lies in higher risk of complication—posterior
capsular tears during surgery)
 Posterior subcapsular cataract (PSC) (clinically common)
 After-cataract: posterior capsular opacification (PCO) subsequent to a successful
extracapsular cataract surgery (usually within three months to two years) with or
without IOL implantation. Requires a quick & painless office procedure with Nd:YAG
laser capsulotomy to restore optical clarity.
[edit] Signs and symptoms
As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted.
Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare
can be a problem as light is scattered by the cataract into the eye. The affected eye will have an absent red
reflex. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is demonstrated
an eye specialist consultation is recommended.
In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek
medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon appears
to be confined to one eye only.
The symptoms of cataracts are very similar to the symptoms of ocular citrosis.
[edit] Causes
Cataracts develop for a variety of reasons, including long-term exposure to ultraviolet light, exposure to
radiation, secondary effects of diseases such as diabetes, hypertension and advanced age, or trauma
(possibly much earlier); they are usually a result of denaturation of lens protein. 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 are 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.[20] 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. Atopic or allergic conditions are also
known to quicken the progression of cataracts, especially in children.[21] Cataracts can also be caused by
iodine deficiency[22]
Cataracts may be partial or complete, stationary or progressive, hard or soft.
Some drugs can induce cataract development, such as corticosteroids[23] and Seroquel.
There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also
classified by their location, e.g. posterior (classically due to steroid use[23][24]) and anterior (common
(senile) cataract related to ageing).
[edit] Associations with systemic conditions
 Chromosomal disorders
 1q21.1 deletion syndrome
 Alport's syndrome
 Cri-du-chat syndrome
 Conradi's syndrome
 Myotonic dystrophy
 Patau's syndrome
 Schmid-Fraccaro syndrome
 Trisomy 18 (Edward's syndrome)
 Turner's syndrome
 Disease of the skin and mucous membranes
 Atopic dermatitis
 Basal-cell nevus syndrome
 Ichthyosis
 Pemphigus
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Metabolic and nutrition diseases
 Aminoaciduria (Lowe's syndrome)
 Diabetes mellitus
 Fabry's disease
 Galactosemia / galactosemic cataract
 Homocystinuria
 Hyperparathyroidism
 Hypervitaminosis D
 Hypothyroidism
 Mucopolysaccharidoses
 Wilson's disease
Infectious diseases
 Congenital
 Congenital herpes simplex
 Congenital syphilis
 Cytomegalic inclusion disease
 Rubella
 Others
 Cysticercosis
 Leprosy
 Onchocerciasis
 Toxoplasmosis
Toxic substances introduced systemically
 Corticosteroids
 Haloperidol
 Miotics
 Triparanol
Prevention
Although cataracts have no scientifically proven prevention, it is sometimes said that wearing ultravioletprotecting sunglasses may slow the development of cataracts.[25][26] Regular intake of antioxidants (such
as vitamin A, C and E) is theoretically helpful, but taking them as a supplement has been shown to have
no benefit.[27] The less well known antioxidant N-acetylcarnosine has been shown in randomized
controlled clinical trials to treat cataracts, and can be expected to prevent their formation by similar
mechanisms.[28] N-acetylcarnosine is a proposed treatment for other ocular disorders that are instigated, or
exacerbated by oxidative stress including glaucoma, retinal degeneration, corneal disordes, and ocular
inflammation.[29]
[edit] Treatment
When a cataract is sufficiently developed to be removed by surgery, the most effective and common
treatment is to make an incision (capsulotomy) into the capsule of the cloudy lens in order to surgically
remove the lens. There are two types of eye 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 are possible after cataract surgery, including endophthalmitis, posterior capsular
opacification and retinal detachment.
Glaucoma is a disease in which the optic nerve is damaged, leading to progressive, irreversible loss of
vision. It is often, but not always, associated with increased pressure of the fluid in the eye.[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 first 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.
Signs and symptoms
There 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.
[edit] Pathophysiology
The major risk factor for most glaucomas and focus of treatment is increased intraocular pressure.
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 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.[4] In open angle glaucoma there is reduced flow
through the trabecular meshwork;[5] in angle closure glaucoma, the iris is apposed to the lens resulting in
the inability of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the
trebecular network.
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, and aging mechanisms of neuron loss.[6][7][8][9][10][11][12][13][14][15][16]
The major types of glaucoma are discussed below.
[edit] Causes and risk factors
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.[18]
Those of African descent are three times more likely to develop primary open angle glaucoma.
Elder 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.
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.[20] Normal tension glaucoma, which comprises one third of POAG, is associated with genetic
mutations.[21]
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 probably not useful in glaucoma treatment.[22]
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.[23][24][25] and modelled in mice [26].
[edit] Diagnosis
Screening 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).[27][28] 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.[29]
Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug
use, refraction, inheritance and family history.[27]
[edit] 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.[32]
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.[33] 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.
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Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost
(Travatan) increase uveoscleral outflow of aqueous humor. Bimatoprost also increases
trabecular outflow
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 trabecular outflow.
Less-selective sympathomimetics such as epinephrine decrease aqueous humor production
through vasoconstriction of ciliary body blood vessels.
Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary
muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous
humour. Ecothiopate is used in chronic glaucoma.
Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide
(Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
Physostigmine is also used to treat glaucoma and delayed gastric emptying.
Surgery
Canaloplasty, Laser surgery, Trabeculectomy, Glaucoma drainage implants
Veterinary implant, Laser assisted non-penetrating deep sclerectomy
Classification
Glaucoma has been classified into specific types:[48]
Primary glaucoma and its variants (H40.1-H40.2)
 Primary glaucoma
 Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrowangle 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
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Variants of primary glaucoma
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Pigmentary glaucoma
Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare
Primary angle-closure glaucoma – This 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 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 mid-dilated and unresponsive to light,
cornea edematous (cloudy), reduced vision, redness, 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 – Optic nerve damage resulting in progressive visual field loss[49]. 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 which is where
the aqueous humor in the eye drains out. Because the microscopic passage ways 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. 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
 Developmental glaucoma
 Primary congenital glaucoma
 Infantile glaucoma
 Glaucoma associated with hereditary of familial diseases
Secondary glaucoma
 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
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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 (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 is an uncommon type of glaucoma that is difficult or nearly impossible to treat.
This condition 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 lose their eyesight. Sometimes,
the disease appears very rapidly, specially after cataract surgery procedure. A new treatment for this
disease, as first reported by Kahook and colleagues, involves use of a novel group of medications known
as Anti-VEGF 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) reports on four patients who had toxic glaucoma. One of them
underwent phaecoemulsification with small 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.[50]
Absolute glaucoma
Absolute glaucoma is the end stage of all types of glaucoma. The eye has no vision, absence of PL and
PR, and has a stony hard in appearance. Severe pain is present in eye. The treatment of absolute
glaucoma is a destructive procedure like cyclocryo application, cyclophotocoagulation, or injection of
100% alcohol.
What are the different types of glaucoma?
There are many different types of glaucoma. Most, however, can be classified as either open-angle
glaucomas, which are usually conditions of long duration (chronic), or angle-closure (closed angle)
glaucomas, which include conditions occurring both suddenly (acute) and over a long period of time
(chronic). The glaucomas usually affect both eyes, but the disease can progress more rapidly in one eye
than in the other. Involvement of just one eye occurs only when the glaucoma is brought on by factors
such as a prior injury, inflammation, or the use of steroids only in that eye.
Open-angle glaucoma
Primary chronic open-angle glaucoma (COAG) is by far the most common type of glaucoma.
Moreover, its frequency increases greatly with age. This increase occurs because the drainage mechanism
gradually may become clogged with aging, even though the drainage angle is open. As a consequence, the
aqueous fluid does not drain from the eye properly. The pressure within the eye, therefore, builds up
painlessly and without symptoms. Furthermore, as mentioned previously, since the resulting loss of vision
starts on the side (peripherally), people are usually not aware of the problem until the loss encroaches on
their central visual area.
Normal tension (pressure) glaucoma or low tension glaucoma are variants of primary chronic openangle glaucoma that are being recognized more frequently than in the past. This type of glaucoma is
thought to be due to decreased blood flow to the optic nerve. This condition is characterized by
progressive optic-nerve damage and loss of peripheral vision (visual field) despite intraocular pressures in
the normal range or even below normal. This type of glaucoma can be diagnosed by repeated
examinations by the eye doctor to detect the nerve damage or the visual field loss.
Congenital (infantile) glaucoma is a relatively rare, inherited type of open-angle glaucoma. In this
condition, the drainage area is not properly developed before birth. This results in increased pressure in
the eye that can lead to the loss of vision from optic-nerve damage and also to an enlarged eye. The eye of
a young child enlarges in response to increased intraocular pressure because it is more pliable than the eye
of an adult. Early diagnosis and treatment with medicine and/or surgery are critical in these infants and
children to preserve their sight.
Secondary open-angle glaucoma is another type of open-angle glaucoma. It can result from an eye
(ocular) injury, even one that occurred many years ago. Other causes of secondary glaucoma are
inflammation in the iris of the eye (iritis), diabetes, cataracts, or in steroid-susceptible individuals, the use
of topical (drops) or systemic (oral or injected) steroids (cortisone). It can also be associated with a retinal
detachment or retinal vein occlusion or blockage. (The retina is the layer that lines the inside of the back
of the eye.) The treatments for the secondary open-angle glaucomas vary, depending on the cause.
Pigmentary glaucoma is a type of secondary glaucoma that is more common in younger men. In this
condition, for reasons not yet understood, granules of pigment detach from the iris, which is the colored
part of the eye. These granules then may block the trabecular meshwork, which, as noted above, is a key
element in the drainage system of the eye. Finally, the blocked drainage system leads to elevated
intraocular pressure, which results in damage to the optic nerve.
Exfoliative glaucoma (pseudoexfoliation) is another type of glaucoma that can occur with either open or
closed angles. This type of glaucoma is characterized by deposits of flaky material on the front surface of
the lens (anterior capsule) and in the angle of the eye. The accumulation of this material in the angle is
believed to block the drainage system of the eye and raise the eye pressure. While this type of glaucoma
can occur in any population, it is more prevalent in older people and people of Scandinavian descent. It is
recently been shown to often be associated with hearing loss in older people.
Angle-closure glaucoma
Angle-closure glaucoma is a less common form of glaucoma in the Western world but is extremely
common in Asia. Angle-closure glaucoma may be acute or chronic. The common element in both is that a
portion or all of the drainage angle becomes anatomically closed, so that the aqueous fluid within the eye
cannot even reach all or part of the trabecular meshwork. In acute angle-closure glaucoma, the patient's
intraocular pressure, which ordinarily is normal, can go up very suddenly (acutely). This sudden pressure
increase occurs because the drainage angle becomes closed and blocks off all the drainage channels. This
type of glaucoma can occur when the pupil dilates (widens or enlarges). As a result, the peripheral edge of
the iris can become bunched up against its corneal attachment, thereby causing the drainage angle to
close. Thus, the problem in angle-closure glaucoma is the difficulty with access of the eye fluid to the
drainage system (trabecular meshwork). In contrast, remember that the problem in open-angle glaucoma
is clogging within the drainage system itself. In chronic open-angle glaucoma, portions of the drainage
angle become closed over a long period of time. As more and more areas become closed, the pressure
within the eye rises, often over a period of months or years.
People with small eyes are predisposed to developing angle-closure glaucoma because they tend to have
narrow drainage angles. Small eyes are not obvious from their appearance, but they can be measured by
an eye doctor. Thus, individuals who are farsighted or of Asian descent may have small eyes, narrow
drainage angles, and an increased risk of developing angle-closure glaucoma. Furthermore, this condition
may be acutely triggered by medications that can dilate the pupils. These agents can be found in certain
eyedrops, cold remedies, citalopram (Celexa), topiramate (Topamax), or patches used to prevent
seasickness. This condition can also occur spontaneously in a darkened room or a movie theater, when the
pupil automatically dilates to let in more light. Sometimes, therefore, people with narrow angles are given
eyedrops to keep their pupils small. (See the section below on parasympathomimetic agents.)
An attack of acute angle-closure glaucoma may be associated with severe eye pain and headache, a red
(inflamed) eye, nausea, vomiting, and blurry vision. In addition, the high intraocular pressure leads to
corneal swelling (edema), which causes the patient to see haloes around lights. Sometimes, acute
glaucoma is treated with oral carbonic anhydrase inhibitors. (See the section below on these medications.)
An attack of acute glaucoma, however, is usually relieved by eye surgery. In this operation, the doctor
makes a small hole in the iris with a laser (laser iridotomy) to allow the fluid to resume draining into its
normal outflow channels.
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