Xalatan ®

manufactured by Pfizer

For teatment of Glucoma

Latanoprost (pronounced la-TA-noe-prost) ophthalmic solution is a topical medication used for controlling the progression of glaucoma or ocular hypertension by reducing intraocular pressure. It is a prostaglandin analogue that works by increasing the outflow of aqueous fluid from the eyes (through the uvealsclearal tract).[1]

It is also known by the brand name of Xalatan manufactured by Pfizer. Annual sales are approximately $1.6 billion. The patent for latanoprost expires in 2011.

Adverse reactions

Possible side effects:

•May cause reddening of the eyes (hyperemia)
•May cause blurred vision;
•May cause eyelid redness;
•May permanently darken eyelashes;
•May cause eye discomfort;
•May eventually cause permanent darkening of the iris to brown (heterochromia);
•May cause a temporary burning sensation during use.
•May cause thickening of the eyelashes.
•Rarely, herpes simplex keratitis.
•A single case report links latanoprost use to the progression of keratoconus.[2]


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 22 mmHg or 2.9 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 “sneak robber 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 exam).

Closed-angle Glaucoma Accounts for <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 ophthalmologic emergency.


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 pushed forward against the trabecular meshwork, blocking fluid from escaping.

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.


This article may require cleanup to meet Wikipedia’s quality standards. Please improve this article if you can. (April 2008)

A normal range of vision. Courtesy NIH National Eye Institute

The same view with advanced vision loss from glaucoma.

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.[17]

Those of African descent are three times more likely to develop primary open angle glaucoma. People who are older have thinner corneal thickness and often suffer from myopia. 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.[18] 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.[19] Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.[20]

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.[21]

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.[22][23][24] and modelled in mice [25].

Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.[26]


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]


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.[30][31] 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.[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.[21][34][35][36]

•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 like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action.
•Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour. 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.

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 and conventional surgeries are performed to treat glaucoma.

Surgery is the primary therapy for those with congenital glaucoma.[37]

Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma.


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.[38][39]

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.[27]


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

Glaucoma drainage implants

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

•The first-generation Molteno and other non-valved implants sometimes require the ligation of the tube until the bleb formed is mildly fibrosed and water-tight[40] This is done to reduce postoperative hypotony—sudden drops in postoperative intraocular pressure (IOP).
•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 anti-fibrotic medication like 5-fluorouracil (5-FU) or mitomycin-C (during the procedure), or additional surgery. And for Glaucomatous painful Blind Eye and some cases of Glaucoma, Cyclocryotherapy for ciliary body ablation could be considered to be performed.[27]

Veterinary implant

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 implant contains no valves and is placed completely within the eye without sutures. To date, it has demonstrated long term success (> 1yr) in a pilot study in medically refractory dogs with advanced glaucoma [41]

Laser assisted non-penetrating deep sclerectomy

The most common surgical approach currently used for the treatment of glaucoma, is trabeculectomy, in which the sclera is punctured to alleviate inner eye pressure (IOP). Non-penetrating deep sclerectomy (NPDS) surgery is a similar but modified procedure, in which instead of puncturing the scleral wall, a patch of the sclera is skimmed to a level, upon which, percolation of liquid from the inner eye is achieved and thus alleviating IOP, without penetrating the eye. NPDS is demonstrated to cause a significantly less side effects than trabeculectomy.[citation needed] However, NPDS is performed manually and requires great skill to achieve a lengthy learning curve.[citation needed]

Laser assisted NPDS is the performance of NPDS with the use of a CO2 laser system. The laser-based system is self-terminating once the required scleral thickness and adequate drainage of the intra ocular 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 intra-ocular percolated liquid, which occurs as soon as the laser reaches the optimal residual intact layer thickness.


Disability-adjusted life year for glaucoma per 100,000 inhabitants in 2004.[42]

no data less than 20 20-43 43-66 66-89 89-112 112-135 135-158 158-181 181-204 204-227 227-250 more than 250


•Advanced Glaucoma Intervention Study (AGIS) – large American National Eye Institute (NEI) sponsored study designed “to assess the long-range 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.
•Early Manifest Glaucoma Trial (EMGT) -Another NEI study found that immediately treating people who have early stage glaucoma can delay progression of the disease.
•Ocular Hypertension Treatment Study (OHTS) -NEI study findings: “…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 that 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.”
•Blue Mountains Eye Study “The Blue Mountains Eye Study was the first large population-based assessment of visual impairment and common eye diseases of a representative older Australian community sample.” Risk factors for glaucoma and other eye disease were determined.
Compounds in research

Natural compounds

Natural compounds of research interest in glaucoma prevention or treatment include: fish oil and omega 3 fatty acids, bilberries, vitamin E, cannabinoids, carnitine, coenzyme Q10, curcurmin, Salvia miltiorrhiza, dark chocolate, erythropoietin, folic acid, Ginkgo biloba, Ginseng, L-glutathione, grape seed extract, green tea, magnesium, melatonin, methylcobalamin, N-acetyl-L cysteine, pycnogenols, resveratrol, quercetin and salt.[34][35][36] Magnesium, ginkgo, salt and fludrocortisone, are already used by some physicians.


Studies in the 1970s showed that marijuana, when smoked, effectively lowers intraocular pressure.[43] In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated that 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 that “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 pressure-lowering effect is reported to be in the range of 3 to 4 hours”.[43][44]

However, the position paper qualified that by stating that marijuana was not more effective than prescription medications, stating that “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.[45]

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.[46][47]

Classification of glaucoma

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, 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 – 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 (Q15.0)

•Developmental glaucoma
· Primary congenital glaucoma

· Infantile glaucoma

· Glaucoma associated with hereditary of familial diseases

Secondary glaucoma (H40.3-H40.6)

•Secondary glaucoma
· Inflammatory glaucoma

· Uveitis of all types

· Fuchs heterochromic iridocyclitis

· Phacogenic glaucoma

· Angle-closure glaucoma with mature cataract

· Phacoanaphylactic glaucoma secondary to rupture of lens capsule

· Phacolytic glaucoma due to phacotoxic meshwork blockage

· Subluxation of lens

· Glaucoma secondary to intraocular hemorrhage

· Hyphema

· Hemolytic glaucoma, also known as erythroclastic glaucoma

· Traumatic glaucoma

· Angle recession glaucoma: Traumatic recession on anterior chamber angle

· Postsurgical glaucoma

· Aphakic pupillary block

· Ciliary block glaucoma

· Neovascular glaucoma (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.