Glaucoma

Glaucoma

Acute angle closure glaucoma of the right eye. Note the mid-sized pupil, which was nonreactive to light, and redness of the conjunctiva.
Classification and external resources
Specialty Ophthalmology
ICD-10 H40-H42
ICD-9-CM 365
DiseasesDB 5226
MedlinePlus 001620
eMedicine oph/578
MeSH D005901

Glaucoma is a group of eye diseases which result in damage to the optic nerve and vision loss. A major risk factor is increased pressure in the eye.[1] The disorders can be roughly divided into two main categories: "open-angle" and "closed-angle" (or "angle closure") glaucoma. Open-angle chronic glaucoma is painless, tends to develop slowly over time and often has no symptoms until the disease has progressed significantly. Closed angle glaucoma is usually chronic and asymptomatic but can present all of a sudden as well. This involves sudden eye pain, blurred vision, mid-dilated pupil, redness, nausea and vomiting, resulting from a sudden spike in intraocular pressure from iridotrabecular contact. Glaucoma can permanently damage vision in the affected eye, first by decreasing peripheral vision (reducing the visual field), and then potentially leading to blindness if left untreated.[2]

The many subtypes of glaucoma can all be considered to be a type of optic neuropathy. The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. Raised intraocular pressure (above 21 mmHg or 2.8 kPa) is the most important and only modifiable risk factor for glaucoma. Some may have high eye pressure for years and never develop damage, a condition known as "ocular hypertension". Conversely, the term 'low tension' or 'normal tension' glaucoma is used for those with optic nerve damage and associated visual field loss, but normal or low intraocular pressure.[3] Closed-angle glaucoma also involves damage to the optic nerve, however, is characterized by closure of part of the filtration angle as a result of iris apposition to the trabecular meshwork(iridotrabecular contact).

If the condition is detected early enough, it is possible to arrest the development or slow the progression with medical and surgical means. Open angle chronic glaucoma is treated with either glaucoma medication to lower the pressure, or with various pressure-reducing glaucoma surgeries. Treatment of closed angle glaucoma involves medication to bring the intraocular pressure down and laser surgery to the iris to open the drainage angle and hence reduce the eye pressure.

Glaucoma has been called the "silent thief of sight" because the loss of vision often occurs gradually over a long period, and symptoms only occur when the disease is quite advanced.[4] Worldwide, glaucoma is the second-leading cause of blindness after cataracts.[5][6] It is also the leading cause of blindness among African Americans.[7] Although the term "glaucoma" has a history relating to disorders of the eye going back to ancient Greece, in English the word was not commonly used until after 1850, when the development of the ophthalmoscope permitted visualization of the optic nerve damage caused by glaucoma.[8]

Types

Glaucoma is an umbrella term for eye conditions which damage the optic nerve, and which can lead to a loss of vision.[9] The main cause of damage to the optic nerve is intraocular pressure (IOP), excessive fluid pressure within the eye, which can be due to various reasons including blockage of drainage ducts, and narrowing or closure of the angle between the iris and cornea.

The primary division in categorizing different types of glaucoma is open-angle and closed angle (or angle-closure) glaucoma. The open angle refers to the angle where the iris meets the cornea being as wide and open as it should be, allowing the fluid from inside the eye to drain, thus relieving the internal pressure. Where this angle is narrowed or closed, pressure can build up, and eventually damage the optic nerve leading to loss of vision.

Primary open-angle glaucoma (also, primary glaucoma, chronic glaucoma) refers to slow clogging of the drainage canals resulting in increased eye pressure which causes progressive optic nerve damage. This manifests as a gradual loss of the visual field, starting with a loss of peripheral vision, but eventually the entire vision will be lost if not treated.[10] This is the most common type of glaucoma, accounting for 90% of cases in the United States, but fewer in Asian countries. Onset is slow and painless, and loss of vision is gradual and irreversible.

Narrow angle glaucoma (also closed angle glaucoma) the iris bows forward, narrowing the angle that drains the eye, increasing pressure within the eye. If untreated, it can lead to the medical emergency of angle closure glaucoma.

In angle closure glaucoma (also closed angle glaucoma, primary angle closure glaucoma, acute glaucoma) the iris bows forward and causes physical contact between the iris and trabecular meshwork, which in turn blocks outflow of the aqueous humor from within the eye. This contact may gradually damage the draining function of the meshwork until it fails to keep pace with aqueous production, and the intraocular pressure rises. Onset of symptoms is sudden, and causes pain and other symptoms that are noticeable, and is treated as a medical emergency. Unlike open-angle glaucoma, angle-closure glaucoma is a result of the angle between the iris and cornea closing. Tends to occur in the far-sighted, who have smaller than normal anterior chambers, making the physical contact more likely.

Normal tension glaucoma (also NTG, low tension glaucoma, normal pressure glaucoma) is a condition where the optic nerve is damaged although intraocular pressure (IOP) is in normal range (12-22mm Hg). At higher risk are those with family history of NTG, those of Japanese ancestry, and those with history of systemic heart disease. The cause of NTG is unknown.

Secondary glaucoma refers to any case in which another disease, trauma, drug or procedure causes increased eye pressure, resulting in optic nerve damage and vision loss, and may be mild or severe. It can be due to eye injury, inflammation, a tumor, or advanced cases of cataracts or diabetes. It can also be caused by certain drugs such as steroids. Treatment depends on whether it is open-angle or angle-closure glaucoma.

In pseudoexfoliation glaucoma (also, PEX, exfoliation glaucoma) the pressure is due to the accumulation of microscopic granular protein fibers, which can block normal drainage of the aqueous humor. PEX is prevalent in Scandinavia, primarily in those over 70, and more in women.

Pigmentary glaucoma (also, pigmentary dispersion syndrome) is caused by pigment cells sloughing off from the back of the iris and floating around in the aqueous humor. Over time, these pigment cells can accumulate in the anterior chamber in such a way that it can begin to clog the trabecular meshwork. A rare condition, it occurs mostly among Caucasians, mostly males in their mid 20s to 40s, most nearsighted.

Primary juvenile glaucoma is a neonate or juvenile abnormality where ocular hypertension is evident at birth or shortly thereafter and is caused by abnormalities in the anterior chamber angle development that blocks outflow of the aqueous humor.

Uveitic Glaucoma is due to uveitis, the swelling and inflammation of the uvea, the middle layer of the eye. The uvea provides most of the blood supply to the retina. Increased eye pressure in uveitis can result from the inflammation itself or from the steroids used to treat it.

Signs and symptoms

Photo showing conjunctival vessels dilated at the corneal edge (ciliary flush, circumcorneal flush) and hazy cornea characteristic of acute angle closure glaucoma

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye checkups important. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).

About 10% of people with closed-angles present with acute angle closure characterized by sudden ocular pain, seeing halos around 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

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 open-angle glaucoma actually have elevated ocular pressure.[11]

Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. 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).

Dietary

No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma.[12] Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect normal individuals.[13]

Ethnicity

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.[14] Higher rates of glaucoma have also been reported for Eskimo populations, compared to white populations, in Canada and Greenland.[15]

Genetics

Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle glaucoma (POAG) is increased about two- to four-fold for individuals who have a sibling with glaucoma.[16] Glaucoma, particularly primary open-angle glaucoma, is associated with mutations in several genes (including MYOC, ASB10, WDR36, NTF4, and TBK1 genes),[17] 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).[18]

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,[19][20][21] and has been modelled in mice.[22]

Other

Other factors can cause glaucoma, known as "secondary glaucoma", 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).

Pathophysiology

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. 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.[23]

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.[24]

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 increased intraocular pressure 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.[25][26][27][28][29][30][31][32][33][34][35][36]

Diagnosis

Screening for glaucoma is usually performed as part of a standard eye examination performed by optometrists and ophthalmologists. Testing for glaucoma should include measurements of the intraocular pressure via tonometry,[37] 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 (Heidelberg retinal tomogram).[38][39][40]

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 perimeter.[41]

Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug use, refraction, inheritance and family history.[38]

Glaucoma tests[42][43][44]
What test examines How it 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.

Glaucoma has been classified into specific types:[45]

Primary glaucoma and its variants

Primary glaucoma (H40.1-H40.2)

  • High-tension glaucoma
  • Low-tension glaucoma
  • Acute angle closure glaucoma (aka AACG)[46]
  • Chronic angle closure glaucoma
  • Intermittent angle closure glaucoma
  • Superimposed on chronic open-angle closure glaucoma ("combined mechanism" – uncommon)

Variants of primary glaucoma

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 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, 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.[10] 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.

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 (Q15.0)

Secondary glaucoma

Secondary glaucoma (H40.3-H40.6)

  • Uveitis of all types
  • Fuchs heterochromic iridocyclitis
  • Angle-closure glaucoma with mature cataract
  • Phacoanaphylactic glaucoma secondary to rupture of lens capsule
  • Phacolytic glaucoma due to phacotoxic meshwork blockage
  • Subluxation of lens
  • Hyphema
  • Hemolytic glaucoma, also known as erythroclastic glaucoma
  • Angle recession glaucoma: Traumatic recession on anterior chamber angle
  • Postsurgical glaucoma
  • Aphakic pupillary block
  • Ciliary block glaucoma
  • Corticosteroid induced glaucoma
  • Alpha-chymotrypsin glaucoma. Postoperative ocular hypertension from use of alpha chymotrypsin.
  • 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 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 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. Currently there are no high quality controlled trials demonstrating a beneficial effect of anti-VEGF treatments in lowering IOP in people with neovascular glaucoma.[47]

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 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.[48]

Absolute glaucoma

Absolute glaucoma (H44.5) 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.

Screening

The United States Preventive Services Task Force as of 2013 states there is insufficient evidence to recommend for or against screening for glaucoma.[49] Therefore, there is no national screening program in the US; however, there is a glaucoma screening program in the UK. Those at risk are advised to have a dilated eye examination at least once a year.[50]

Treatment

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.[51][52] This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although intraocular pressure is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment.

Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial.

Medication

Main article: Glaucoma medication

Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several 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.[53]

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.[54] 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.[12][55][56][57]

Surgery

Conventional surgery to treat glaucoma makes a new opening in the meshwork, which 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.[58] Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma.

Canaloplasty

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. Long-term results are not available.[59][60]

Laser surgery

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.[38]

Trabeculectomy

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 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[61][62][63][64] 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

Main article: Glaucoma valve

Professor Anthony Molteno developed the first glaucoma drainage implant, in Cape Town in 1966.[65] Since then, several 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 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,[70][71] 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.[72][73] And for glaucomatous painful blind eye and some cases of glaucoma, cyclocryotherapy for ciliary body ablation could be considered to be performed.[74]

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 (longer than a year) in a pilot study in medically refractory dogs with advanced glaucoma.[75]

Laser-assisted nonpenetrating deep sclerectomy

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. However, NPDS is performed manually and requires higher level of skills that may be assisted with instruments. 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,[76] ologen Collagen Matrix,[77][78][79] or Xenoplast glaucoma implant.[80]

Laser-assisted NPDS is performed 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 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.

Prognosis

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.[81] The intraocular pressure can also have an effect, with higher pressures reducing the time until blindness.[82]

Epidemiology

Disability-adjusted life year for glaucoma per 100,000 inhabitants in 2004[83]
  no data
  fewer 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

As of 2010, there were 44.7 million people in the world with open angle glaucoma.[84] The same year, there were 2.8 million people in the United States with open angle glaucoma.[84] By 2020, the prevalence is projected to increase to 58.6 million worldwide and 3.4 million the United States.[84]

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.[85] Bilateral vision loss can negatively affect mobility and interfere with driving.[86]

A meta-analysis published in 2009 found that people with primary open angle glaucoma do not have increased mortality rates, or increased risk of cardiovascular death.[87]

Etymology

The word "glaucoma" comes from the Greek γλαύκωμα, a derivative of γλαυκóς, which commonly described the color of eyes which were not dark (i.e. blue, green, light gray). Eyes described as γλαυκóς due to disease might have had a gray cataract in the Hippocratic era, or, in the early Common Era, the greenish pupillary hue sometimes seen in angle-closure glaucoma.[88][89]

Research

scientists track eye movements in glaucoma patients to check vision impairment while driving

Neuroprotective agents

A 2013 Cochrane Systematic Review compared the effect of brimonidine and timolol in slowing the progression of open angle glaucoma in adult participants.[91] The results showed that participants assigned to brimonidine showed less visual field progression that those assigned to timolol, though the results were not significant, given the heavy loss-to-followup and limited evidence.[91] The mean intraocular pressure for both groups were similar. Participants in the brimonidine group had a higher occurrence of side effects caused by medication than participants in the timolol group.[91]

Alternative medicine

Natural compounds of research interest in glaucoma prevention or treatment include: fish oil and omega-3 fatty acids, alpha lipoic acid,[92] 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. However, most of these compounds have not demonstrated effectiveness in clinical trials.[55][56][57]

Cannabis

Studies in the 1970s reported that the use of cannabis may lower intraocular pressure.[93][94][95] 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 stating that cannabis was not more effective than prescription medications. Furthermore, no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of cannabis use to treat glaucoma compared with the wide variety of pharmaceutical agents now available.[95][96]

In 2012 the American Glaucoma Society published a position paper discrediting the use of cannabis as a legitimate treatment for elevated intraocular pressure, for reasons including short duration of action and side effects that limit many activities of daily living.[97]

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.[98][99]

References

  1. ↑ Casson, Robert J; Chidlow, Glyn; Wood, John PM; Crowston, Jonathan G; Goldberg, Ivan (2012). "Definition of glaucoma: Clinical and experimental concepts". Clinical & Experimental Ophthalmology 40 (4): 341–9. doi:10.1111/j.1442-9071.2012.02773.x. PMID 22356435.
  2. ↑ Rhee, Douglas J. (August 2013). Porter, Robert S.; Kaplan, Justin L., eds. "Glaucoma". The Merck Manual Home Health Handbook. Retrieved December 12, 2013.
  3. ↑ Mi, Xue-Song; Yuan, Ti-Fei; So, Kwok-Fai (16 September 2014). "The current research status of normal tension glaucoma". Clinical Interventions in Aging 9: 1563–71. doi:10.2147/CIA.S67263. PMID 25258525.
  4. ↑ "Glaucoma: The 'silent thief' begins to tell its secrets" (Press release). National Eye Institute. 21 January 2014.
  5. ↑ Kingman, Sharon (2004). "Glaucoma is second leading cause of blindness globally". Bulletin of the World Health Organization 82 (11): 887–8. doi:10.1590/S0042-96862004001100019 (inactive 2015-01-01). PMC 2623060. PMID 15640929.
  6. ↑ Resnikoff, Serge; Pascolini, Donatella; Etya'Ale, Daniel; Kocur, Ivo; Pararajasegaram, Ramachandra; Pokharel, Gopal P.; Mariotti, Silvio P. (2004). "Global data on visual impairment in the year 2002". Bulletin of the World Health Organization 82 (11): 844–51. doi:10.1590/S0042-96862004001100009 (inactive 2015-01-01). PMC 2623053. PMID 15640920.
  7. ↑ "Glaucoma and Marijuana use". National Eye Institute. June 21, 2005.
  8. ↑ Leffler CT, Schwartz SG, Stackhouse R, Davenport B, Spetzler K (2013). "Evolution and impact of eye and vision terms in written English". JAMA Ophthalmol 131 (12): 1625–31. doi:10.1001/jamaophthalmol.2013.917. PMID 24337558.
  9. ↑ Arthur J. Sit, MD (April 23, 2006). "Many types of glaucoma, one kind of damage to optic nerve". Chicago Tribune. Archived from the original on 2012-10-06. Retrieved 2015-08-18. Glaucoma is a broad term for a number of different conditions that damage the optic nerve, the 'cable' that carries visual information from the eye to the brain, thereby causing changes in vision.
  10. 1 2 "Primary Open-Angle Glaucoma: Glaucoma: Merck Manual Professional". Merck.com. Retrieved 2011-01-24.
  11. ↑ Sommer A, Tielsch JM, Katz J, et al. (August 1991). "Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey". Arch Ophthalmol. 109 (8): 1090–5. doi:10.1001/archopht.1991.01080080050026. PMID 1867550.
  12. 1 2 Rhee DJ, Katz LJ, Spaeth GL, Myers JS (2001). "Complementary and alternative medicine for glaucoma". Surv Ophthalmol 46 (1): 43–55. doi:10.1016/S0039-6257(01)00233-8. PMID 11525790.
  13. ↑ Li, M; Wang, M; Guo, W; Wang, J; Sun, X (March 2011). "The effect of caffeine on intraocular pressure: a systematic review and meta-analysis". Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv für klinische und experimentelle Ophthalmologie 249 (3): 435–42. doi:10.1007/s00417-010-1455-1. PMID 20706731.
  14. ↑ Wang N, Wu H, Fan Z (November 2002). "Primary angle closure glaucoma in Chinese and Western populations". Chin Med J. 115 (11): 1706–15. PMID 12609093.
  15. ↑ Friedman D, Vedula SS (2006). "Lens extraction for chronic angle-closure glaucoma". Cochrane Database Syst Rev 3: CD005555. doi:10.1002/14651858.CD005555.pub2. PMID 16856103.
  16. ↑ Myron Yanoff, Jay S. Duker (2009). Ophthalmology (3rd ed.). Mosby Elsevier. p. 1096. ISBN 9780323043328.
  17. ↑ Online 'Mendelian Inheritance in Man' (OMIM) GLAUCOMA, PRIMARY OPEN ANGLE; POAG -137760
  18. ↑ Online 'Mendelian Inheritance in Man' (OMIM) GLAUCOMA, NORMAL TENSION, SUSCEPTIBILITY TO -606657
  19. ↑ Pardianto G, et al. (2005). "Aqueous Flow and the Glaucoma". Mimbar Ilmiah Oftalmologi Indonesia 2: 12–5.
  20. ↑ Chaum E, et al. "A 5-year-old girl who failed her school vision screening. Case presentation of Persistent fetal vasculature (PFV), also called persistent hyperplastic primary vitreous (PHPV)". Digital Journal of Ophthalmology.
  21. ↑ Hunt A, Rowe N, Lam A, Martin F (July 2005). "Outcomes in persistent hyperplastic primary vitreous". Br J Ophthalmol 89 (7): 859–63. doi:10.1136/bjo.2004.053595. PMC 1772745. PMID 15965167.
  22. ↑ Chang B, Smith RS, Peters M, et al. (2001). "Haploinsufficient Bmp4 ocular phenotypes include anterior segment dysgenesis with elevated intraocular pressure". BMC Genet. 2: 18. doi:10.1186/1471-2156-2-18. PMC 59999. PMID 11722794.
  23. ↑ Alguire P (1990). "The Eye Chapter 118 Tonometry>Basic Science". In Walker HK, Hall WD, Hurst JW. Clinical methods: the history, physical, and laboratory examinations (3rd ed.). London: Butterworths. ISBN 0-409-90077-X.
  24. ↑ Mozaffarieh M, Grieshaber MC, Flammer J (2008). "Oxygen and blood flow: players in the pathogenesis of glaucoma". Mol Vis. 14: 224–33. PMC 2267728. PMID 18334938.
  25. ↑ Hasnain, Syed S (2006). "Scleral edge, not optic disc or retina is the primary site of injury in chronic glaucoma". Medical Hypotheses 67 (6): 1320–1325. doi:10.1016/j.mehy.2006.05.030. PMID 16824694.
  26. ↑ Osborne NN, Wood JP, Chidlow G, Bae JH, Melena J, Nash MS (August 1999). "Ganglion cell death in glaucoma: what do we really know?". Br J Ophthalmol 83 (8): 980–6. doi:10.1136/bjo.83.8.980. PMC 1723166. PMID 10413706.
  27. ↑ Levin LA, Peeples P (February 2008). "History of neuroprotection and rationale as a therapy for glaucoma". Am J Manag Care 14 (1 Suppl): S11–4. PMID 18284310.
  28. ↑ Varma R, Peeples P, Walt JG, Bramley TJ (February 2008). "Disease progression and the need for neuroprotection in glaucoma management". Am J Manag Care 14 (1 Suppl): S15–9. PMID 18284311.
  29. ↑ Hernández M, Urcola JH, Vecino E (May 2008). "Retinal ganglion cell neuroprotection in a rat model of glaucoma following brimonidine, latanoprost or combined treatments". Exp Eye Res. 86 (5): 798–806. doi:10.1016/j.exer.2008.02.008. PMID 18394603.
  30. ↑ Cantor LB (December 2006). "Brimonidine in the treatment of glaucoma and ocular hypertension". Ther Clin Risk Manag 2 (4): 337–46. doi:10.2147/tcrm.2006.2.4.337. PMC 1936355. PMID 18360646.
  31. ↑ Schwartz M (June 2007). "Modulating the immune system: a vaccine for glaucoma?". Can J Ophthalmol. 42 (3): 439–41. doi:10.3129/I07-050. PMID 17508041.
  32. ↑ Morrison JC (2006). "INTEGRINS IN THE OPTIC NERVE HEAD: POTENTIAL ROLES IN GLAUCOMATOUS OPTIC NEUROPATHY (AN AMERICAN OPHTHALMOLOGICAL SOCIETY THESIS)". Trans Am Ophthalmol Soc 104: 453–77. PMC 1809896. PMID 17471356.
  33. ↑ Knox DL, Eagle RC, Green WR (March 2007). "Optic nerve hydropic axonal degeneration and blocked retrograde axoplasmic transport: histopathologic features in human high-pressure secondary glaucoma". Arch Ophthalmol. 125 (3): 347–53. doi:10.1001/archopht.125.3.347. PMID 17353405.
  34. ↑ Tezel G, Luo C, Yang X (March 2007). "Accelerated Aging in Glaucoma: Immunohistochemical Assessment of Advanced Glycation End Products in the Human Retina and Optic Nerve Head". Invest. Ophthalmol. Vis. Sci. 48 (3): 1201–11. doi:10.1167/iovs.06-0737. PMC 2492883. PMID 17325164.
  35. ↑ Berry FB, Mirzayans F, Walter MA (April 2006). "Regulation of FOXC1 stability and transcriptional activity by an epidermal growth factor-activated mitogen-activated protein kinase signaling cascade". J Biol Chem. 281 (15): 10098–104. doi:10.1074/jbc.M513629200. PMID 16492674.
  36. ↑ "Issue on neuroprotection". Can J Ophthalmol. 42 (3). June 2007. ISSN 1715-3360.
  37. ↑ Farandos, NM; Yetisen, AK; Monteiro, MJ; Lowe, CR; Yun, SH (November 2014). "Contact Lens Sensors in Ocular Diagnostics". Advanced Healthcare Materials. doi:10.1002/adhm.201400504.
  38. 1 2 3 Pardianto G et al. Some difficulties on Glaucoma. Mimbar Ilmiah Oftalmologi Indonesia.2006;3: 49–52.
  39. ↑ Thomas R, Parikh RS (September 2006). "How to assess a patient for glaucoma". Community Eye Health 19 (59): 36–7. PMC 1705629. PMID 17491713.
  40. ↑ Michelessi M, Lucenteforte E, Oddone F, Brazzelli M, Parravano M, Franchi S, Ng SM, Virgili G (2015). "Optic nerve head and fibre layer imaging for diagnosing glaucoma". Cochrane Database Syst Rev 11: CD008803. doi:10.1002/14651858.CD008803.pub2. PMID 26618332.
  41. ↑ Johnson, Chris A. The use of a visual illusion to detect glaucoma. In Visual Perception: The Influence of H. W. Leibowitz, eds. Andre, J., Owens, D. A., and Harvey, Jr., L. O. (2003); 45–56. Washington, D.C.: The American Psychological Association.
  42. ↑ Foundation, G. R. (n.d.). "Five common Glaucoma Tests". Glaucoma.org. Retrieved 2014-02-20.
  43. ↑ Troy Bedinghaus, O (2010). "Six Tests for Glaucoma". Vision.about.com. Retrieved 2014-02-20.
  44. ↑ "Nerve Fiber Analysis". Glaucoma Associates of Texas. White Rabbit Communications, Inc. 2010. Retrieved 9 December 2012.
  45. ↑ Paton D, Craig JA; Craig (1976). "Glaucomas. Diagnosis and management". Clin Symp 28 (2): 1–47. PMID 1053095.
  46. ↑ Logan, Carolynn M.; Rice, M. Katherine (1987). Logan's Medical and Scientific Abbreviations. Philadelphia: J. B. Lippincott Company. p. 3. ISBN 0-397-54589-4.
  47. ↑ Simha A, Braganza A, Abraham L, Samuel P, Lindsley K (2013). "Anti-vascular endothelial growth factor for neovascular glaucoma". Cochrane Database Syst Rev 10: CD007920. doi:10.1002/14651858.CD007920.pub2. PMID 24089293.
  48. ↑ Pardianto G, Difficulties on glaucoma in Mimbar Ilmiah Oftalmologi Indonesia.2006;3: 48–9.
  49. ↑ Moyer, Virginia A. (9 July 2013). "Screening for Glaucoma: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. doi:10.7326/0003-4819-159-6-201309170-00685.
  50. ↑ "Glaucoma – National Institutes of Health". Nihseniorhealth.gov. Retrieved 2011-01-24.
  51. ↑ Noecker RJ (June 2006). "The management of glaucoma and intraocular hypertension: current approaches and recent advances". Ther Clin Risk Manag 2 (2): 193–206. doi:10.2147/tcrm.2006.2.2.193. PMC 1661659. PMID 18360593.
  52. ↑ Parikh RS, Parikh SR, Navin S, Arun E, Thomas R (1 May 2008). "Practical approach to medical management of glaucoma". Indian J Ophthalmol 56 (3): 223–30. doi:10.4103/0301-4738.40362. PMC 2636120. PMID 18417824.
  53. ↑ Leffler CT, Amini L (2007). "Interpretation of uniocular and binocular trials of glaucoma medications: an observational case series". BMC Ophthalmol 7: 17. doi:10.1186/1471-2415-7-17. PMC 2093925. PMID 17916260.
  54. ↑ Jaret, Peter. "A New Understanding of Glaucoma". NYTimes.com. Retrieved 2014-02-20.
  55. 1 2 Ritch R (June 2007). "Natural compounds: evidence for a protective role in eye disease". Can J Ophthalmol. 42 (3): 425–38. doi:10.3129/I07-044. PMID 17508040.
  56. 1 2 Tsai JC, Song BJ, Wu L, Forbes M (September 2007). "Erythropoietin: a candidate neuroprotective agent in the treatment of glaucoma". J Glaucoma 16 (6): 567–71. doi:10.1097/IJG.0b013e318156a556. PMID 17873720.
  57. 1 2 Mozaffarieh M, Flammer J (November 2007). "Is there more to glaucoma treatment than lowering IOP?". Surv Ophthalmol 52 (Suppl 2): S174–9. doi:10.1016/j.survophthal.2007.08.013. PMID 17998043.
  58. ↑ Online 'Mendelian Inheritance in Man' (OMIM) Glaucoma, Congenital: GLC3 Buphthalmos -231300
  59. ↑ Shingleton B, Tetz M, Korber N (March 2008). "Circumferential viscodilation and tensioning of Schlemm's canal (canaloplasty) with temporal clear corneal phacoemulsification cataract surgery for open-angle glaucoma and visually significant cataract: one-year results". J Cataract Refract Surg 34 (3): 433–40. doi:10.1016/j.jcrs.2007.11.029. PMID 18299068.
  60. ↑ Lewis RA, von Wolff K, Tetz M, et al. (July 2007). "Canaloplasty: circumferential viscodilation and tensioning of Schlemm's canal using a flexible microcatheter for the treatment of open-angle glaucoma in adults: interim clinical study analysis". J Cataract Refract Surg 33 (7): 1217–26. doi:10.1016/j.jcrs.2007.03.051. PMID 17586378.
  61. ↑ Cillino, S; Pace F Di; Cillino G; Casuccio A (Sep 2011). "Biodegradable collagen matrix implant vs mitomycin-C as an adjuvant in trabeculectomy: a 24-month, randomized clinical trial". Eye 25 (12): 1598–606. doi:10.1038/eye.2011.219. PMC 3234465. PMID 21921953.
  62. ↑ Papaconstantinou, Dimitris; Georgalas I; Karmiris E; Diagourtas A; Koutsandrea C; Ladas I; Apostolopoulos M; Georgopoulos G (Feb 2010). "Trabeculectomy with ologen versus trabeculectomy for the treatment of glaucoma: a pilot study". Acta Ophthalmol 88 (1): 80–85. doi:10.1111/j.1755-3768.2009.01753.x. PMID 19900209.
  63. ↑ Rosentreter, Andre; Schild AM; Jordan JF; Krieglstein GK; Dietlein TS (Sep 2010). "A prospective randomised trial of trabeculectomy using mitomycin C vs an ologen implant in open angle glaucoma". Eye 24 (9): 1449–57. doi:10.1038/eye.2010.106. PMID 20733558.
  64. ↑ Nilforushan, Naveed; Yadgari M; Falavarjani KG; Afshar AE (2010). "Evaluation of subconjunctival Oculusgen* implantation as an adjunct to trabeculectomy". Iranian J Ophthalmol 22 (2): 55–62. Retrieved 3 November 2011.
  65. ↑ "Eyelights Newsletter: About Glaucoma New Zealand" (PDF). Glaucoma.org. Retrieved 2014-02-20.
  66. ↑ Molteno AC, Polkinghorne PJ, Bowbyes JA (November 1986). "The vicryl tie technique for inserting a draining implant in the treatment of secondary glaucoma". Aust N Z J Ophthalmol 14 (4): 343–54. doi:10.1111/j.1442-9071.1986.tb00470.x. PMID 3814422.
  67. ↑ Lewis RA (Aug 2014). "Ab interno approach to the subconjunctival space using a collagen glaucoma stent.". J Cataract Refract Surg 40 (8): 1301–6. doi:10.1016/j.jcrs.2014.01.032. PMID 24943904. Retrieved 27 June 2015.
  68. ↑ "Xen Gel Stent". AqueSys. AqueSys. Retrieved 27 June 2015.
  69. ↑ "Advances in Glaucoma Filtration Surgery". Glaucoma Today. Retrieved 27 June 2015.
  70. ↑ Rosentreter, Andre; Andre M. Schild; Sven Dinslage; Thomas S. Dietlein (Jan 2011). "Biodegradable implant for tissue repair after glaucoma drainage device surgery". J Glaucoma 21 (2): 76–8. doi:10.1097/IJG.0b013e3182027ab0. PMID 21278584.
  71. ↑ Rosentreter, Andre; Anne C. Mellein; Walter W. Konen; Thomas S. Dietlein (Sep 2010). "Capsule excision and ologenTM implantation for revision after glaucoma drainage device surgery". Graefes Arch Clin Exp Ophthalmol 248 (9): 1319–24. doi:10.1007/s00417-010-1385-y. PMID 20405139.
  72. ↑ Rosentreter, A; Mellein AC; Konen WW; Dietlein TS (2010). "Capsule excision and ologenTM implantation for revision after glaucoma drainage device surgery". Graefes Arch Clin Exp Ophthalmol 248 (9): 1319–24. doi:10.1007/s00417-010-1385-y. PMID 20405139.
  73. ↑ Oana, Stirbu; Jorge Vila (Dec 2012). Shaarawy, Tarek, ed. "Tube Exposure Repair". Journal of Current Glaucoma Practice 6 (3): 139–142. doi:10.5005/jp-journals-10008-1121. Retrieved Dec 2012.
  74. ↑ Pardianto G, et al. (2006). "Some difficulties on Glaucoma". Mimbar Ilmiah Oftalmologi Indonesia 3: 49–50.
  75. ↑ Roberts S, Woods C. Effects of a novel porous implant in refractory glaucomatous Dogs. ACVO abstract 2008, Boston, MA.
  76. ↑ Iqbal "Ike" K. Ahmed (1 September 2005). "Making the Case for Nonpenetrating Surgery". Review of Ophthamology 12 (9). Archived from the original on 11 October 2007.
  77. ↑ Aptel, F; Dumas S; Denis P (2009). "Ultrasound biomicroscopy and optical coherence tomography imaging of filtering blebs after deep sclerectomy with new collagen implant". Eur J Ophthalmol 19 (2): 223–30. PMID 19253238.
  78. ↑ Tanuj, D; Amit S; Saptorshi M; Meenakshi G (May 2013). "Combined Subconjunctival and Subscleral Ologen Implant Insertion In Trabeculectomy". Eye. E-pub ahead of print; doi:10.1038/eye.2013.76 (7): 889. doi:10.1038/eye.2013.76. PMC 3709396. PMID 23640614.
  79. ↑ Matthew, SJ; Sarkisian S; Nathan B; James MR. "Initial experience using a collagen matrix implant (ologen) as a wound modulator with canaloplasty: 12 month results". 2012 ARVO Congress, Ft. Lauderdale. Retrieved May 2013.
  80. ↑ Anisimova SY, Anisimova SI, Larionov EV. "Biological drainage – Xenoplast in glaucoma surgery (experimental and 10-year of clinical follow-up)" (PDF). 2012 EGS Congress, Copenhagen. Retrieved May 2013.
  81. ↑ Heijl, Anders; Bengtsson, Boel; Hyman, Leslie; Leske, M. Cristina (Dec 2009). "Natural History of Open-Angle Glaucoma". Ophthalmology 116 (12): 2271–2276. doi:10.1016/j.ophtha.2009.06.042. PMID 19854514.
  82. ↑ "Glaucoma". Coopereyecare.com. 2013-07-25. Retrieved 2014-02-20.
  83. ↑ "Death and DALY estimates for 2004 by cause for WHO Member States" (xls). World Health Organization. 2004.
  84. 1 2 3 Quigley, H A; Broman, AT (March 2006). "The number of people with glaucoma worldwide in 2010 and 2020". British Journal of Ophthalmology 90 (3): 262–267. doi:10.1136/bjo.2005.081224. PMC 1856963. PMID 16488940.
  85. ↑ Sommer, Alfred; Tielsch, James M.; Katz, Joanne; Quigley, Harry A.; Gottsch, John D.; Javitt, Jonathan C.; Martone, James F.; Royall, Richard M.; Witt, Kathe A.; Ezrine, Sandi (Nov 14, 1991). "Racial Differences in the Cause-Specific Prevalence of Blindness in East Baltimore". New England Journal of Medicine 325 (20): 1412–1417. doi:10.1056/NEJM199111143252004. PMID 1922252.
  86. ↑ Ramulu, Pradeep (March 2009). "Glaucoma and disability: which tasks are affected, and at what stage of disease?". Current opinion in ophthalmology 20 (2): 92–8. doi:10.1097/ICU.0b013e32832401a9. PMC 2692230. PMID 19240541.
  87. ↑ Akbari, M.; Akbari, S.; Pasquale, L. R. (February 2009). "The Association of Primary Open-angle Glaucoma With Mortality: A Meta-analysis of Observational Studies". Archives of Ophthalmology 127 (2): 204–210. doi:10.1001/archophthalmol.2008.571. PMID 19204241.
  88. ↑ Leffler CT, Schwartz SG, Hadi TM, Salman A, Vasuki V (2015). "The early history of glaucoma: the glaucous eye (800 BC to 1050 AD)". Clinical Ophthalmology 2015 (9): 207–15. doi:10.2147/OPTH.S77471. PMID 25673972.
  89. ↑ Leffler CT, Schwartz SG, Giliberti FM, Young MT, Bermudez D (2015). "What was glaucoma called before the 20th century?". Ophthalmology and Eye Diseases 2015 (7): 21–33. doi:10.4137/oed.s32004.
  90. ↑ Sean K Wang, Robert T Chang. "An emerging treatment option for glaucoma: Rho kinase inhibitors". Clin Ophthalmol. 2014 8: 883–89. doi:10.2147/OPTH.S41000. PMC 4025933. PMID 24872673.
  91. 1 2 3 Sena DF, Lindsley K; Ramchand; Lindsley (2013). "Neuroprotection for treatment of glaucoma in adults". Cochrane Database Syst Rev 2 (2): CD006539. doi:10.1002/14651858.CD006539.pub3. PMC 3478138. PMID 20166085.
  92. ↑ "Alpha-lipoic acid". University of Maryland Medical Center (UMMC). Retrieved 2011-04-09.
  93. ↑ "Marijuana and Medicine: Assessing the Science Base". Nap.edu. Retrieved 2014-02-20.
  94. ↑ "Marijuana and Medicine: Assessing the Science Base (1999), Institute of Medicine, National Academies Press". Nap.edu. Retrieved 2011-06-22.
  95. 1 2 "Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma". American Academy of Ophthalmology. Retrieved 2011-05-04.
  96. ↑ "Complementary Therapy Assessments : American Academy of Ophthalmology". One.aao.org. Retrieved 2011-01-24.
  97. ↑ Jampel, Henry (2010). "American Glaucoma Society Position Statement: Marijuana and the Treatment of Glaucoma". J Glaucoma 19 (2): 75.
  98. ↑ Sharif NA, Kelly CR, Crider JY, Davis TL; Kelly; Crider; Davis (December 2006). "Serotonin-2 (5-HT2) receptor-mediated signal transduction in human ciliary muscle cells: role in ocular hypotension". J Ocul Pharmacol Ther 22 (6): 389–401. doi:10.1089/jop.2006.22.389. PMID 17238805.
  99. ↑ Sharif NA, McLaughlin MA, Kelly CR; McLaughlin; Kelly (February 2007). "AL-34662: a potent, selective, and efficacious ocular hypotensive serotonin-2 receptor agonist". J Ocul Pharmacol Ther 23 (1): 1–13. doi:10.1089/jop.2006.0093. PMID 17341144.

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