The United States Preventive Services Task Force as of 2013 states there is insufficient evidence to recommend for or against screening for glaucoma. Therefore, there is no national screening program in the US. Screening, however, is recommended starting at age 40 by the American Academy of Ophthalmology.

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.

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, 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).

Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with pachymetry to measure the 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.

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

Glaucoma has been classified into specific types:

PEX is usually diagnosed by an eye doctor who examines the eye using a microscope. The method is termed slit lamp examination and it is done with an "85% sensitivity rate and a 100% specificity rate." Since the symptom of increased pressure within the eye is generally painless until the condition becomes rather advanced, it is possible for people afflicted with glaucoma to be in danger yet not be aware of it. As a result, it is recommended that persons have regular eye examinations to have their levels of intraocular pressure measured, so that treatments can be prescribed before there is any serious damage to the optic nerve and subsequent loss of vision.

Diagnosis is made by an ophthalmologist or optometrist based on the clinical presentation. One indication can be the Amsler sign, which is the presence of blood (hyphema) in the aspirated vitreous fluid, in paracentesis of the anterior chamber. This is caused due to iris atrophy usually seen in FHI and exposure of the fragile iris vasculature to the vitreous fluid. The sudden change of pressure in the anterior chamber upon suction induced by the paracentesis, or during a cataract surgery, causes bursting of the fragile superficial iris capillaries resultsing in micro-bleeding. This is one clinical diagnostic sign of FHI slit lamp examination shows stringy keratic precipitates

The diagnosis of childhood blindness is done via methods to ascertain the degree of visual impairment in the affected child doing so via "dilating eye drops" and the proceeding eye exam.

Intraocular pressure should be measured as part of the routine eye examination.

It is usually only elevated by iridocyclitis or acute-closure glaucoma, but not by relatively benign conditions.

In iritis and traumatic perforating ocular injuries, the intraocular pressure is usually low.

It is important that people be examined by someone specializing in low vision care prior to other rehabilitation training to rule out potential medical or surgical correction for the problem and to establish a careful baseline refraction and prescription of both normal and low vision glasses and optical aids. Only a doctor is qualified to evaluate visual functioning of a compromised visual system effectively. The American Medical Association provides an approach to evaluating visual loss as it affects an individual's ability to perform activities of daily living.

Screening adults who have no symptoms is of uncertain benefit.

Braille is a universal way to learn how to read and write, for the blind. A refreshable braille display is an assistive learning device that can help such children in school. Schools for the blind are a form of management, however the limitations of using studies done in such schools has been recognized. Children that are enrolled presently, usually, had developed blindness 5 or more years prior to enrollment, consequently not reflecting current possible causes. About 66% of children with visual impairment also have one other disability (comorbidity), be it, intellectual disabilities, cerebral palsy, or hearing loss. Eye care/screening for children within primary health care is important as catching ocular disease issues can lead to better outcomes.

In an eye with iridocyclitis, (inflammation of both the iris and ciliary body), the involved pupil will be smaller than the uninvolved, due to reflex muscle spasm of the sphincter muscle of the iris.

Generally, conjunctivitis does not affect the pupils.

With acute angle-closure glaucoma, the pupil is generally fixed in mid-position, oval, and responds sluggishly to light, if at all.

Shallow anterior chamber depth may indicate a predisposition to one form of glaucoma (narrow angle) but requires slit-lamp examination or other special techniques to determine it.

In the presence of a "red eye", a shallow anterior chamber may indicate acute glaucoma, which requires immediate attention.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.

The diagnosis is clinical. The intraocular pressure (IOP) can be measured in the office in a conscious swaddled infant using a Tonopen or hand-held Goldmann tonometer. Usually, the IOP in normal infants is in the range of 11-14 mmHg. Buphthalmos and Haab's striae can often be seen in case of congenital glaucoma.

Imaging studies such as ultrasonography (US), Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) can aid diagnosis. On ultrasound, Coats' disease appears as a hyperechoic mass in the posterior vitreous without posterior acoustic shadowing; vitreous and subretinal hemorrhage may often be observed.

On CT, the globe appears hyperdense compared to normal vitreous due to the proteinaceous exudate, which may obliterate the vitreous space in advanced disease. The anterior margin of the subretinal exudate enhances with contrast. Since the retina is fixed posteriorly at the optic disc, this enhancement has a V-shaped configuration.

On MRI, the subretinal exudate shows high signal intensity on both T1- and T2-weighted images. The exudate may appear heterogeneous if hemorrhage or fibrosis is present. The subretinal space does not enhance with gadolinium contrast. Mild to moderate linear enhancement may be seen between the exudate and the remaining vitreous. The exudate shows a large peak at 1-1.6 ppm on proton MR spectroscopy.

Grossly, retinal detachment and yellowish subretinal exudate containing cholesterol crystals are commonly seen.

Microscopically, the wall of retinal vessels may be thickened in some cases, while in other cases the wall may be thinned with irregular dilatation of the lumen. The subretinal exudate consists of cholesterol crystals, macrophages laden with cholesterol and pigment, erythrocytes, and hemosiderin. A granulomatous reaction, induced by the exudate, may be seen with the retina. Portions of the retina may develop gliosis as a response to injury.

The World Health Organization estimates that 80% of visual loss is either preventable or curable with treatment. This includes cataracts, onchocerciasis, trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness. The Center for Disease Control and Prevention estimates that half of blindness in the United States is preventable.

Ocular hypertension is treated with either medications or laser. Medications that lower intraocular pressure work by decreasing aqueous humor production and/or increasing aqueous humor outflow. Laser trabeculoplasty works by increasing outflow. The cannabinoids found in cannabis sativa and indica (marijuana) have been shown to reduce intraocular pressure, by up to 50% for approximately four to five hours. But due to the duration of effect, significant side-effect profile, and lack of research proving efficacy, the American Glaucoma Society issued a position statement in 2009 regarding the use of marijuana as a treatment for glaucoma.

The preferred treatment of congenital glaucoma is surgical not medical. The initial procedures of choice are goniotomy or trabeculotomy if the cornea is clear, and trabeculectomy ab externo if the cornea is hazy. The success rates are similar for both procedures in patients with clear corneas. Trabeculectomy and shunt procedures should be reserved for those cases in which goniotomy or trabeculotomy has failed. Cyclophotocoagulation is necessary in some intractable cases but should be avoided whenever possible because of its potential adverse

effects on the lens and the retina.

Mydriatic/cycloplegic agents, such as topical homatropine, which is similar in action to atropine, are useful in breaking and preventing the formation of posterior synechia by keeping the iris dilated and away from the crystalline lens. Dilation of the pupil in an eye with the synechia can cause the pupil to take an irregular, non-circular shape (Dyscoria) as shown in the photograph. If the pupil can be fully dilated during the treatment of iritis, the prognosis for recovery from synechia is good. This is a treatable status.

To subdue the inflammation, use topical corticosteroids. If the intra-ocular pressure is elevated then use a PGA such as Travatan Z.

While tonometry, the measuring of IOP and thus a classical instrument in the diagnosis of glaucoma, is not helpful, ophthalmoscopy leads to the diagnosis by showing typical glaucomatous damage, primarily at the optic nerve head, in the absence of elevated IOP. While the excavation of the optic nerve head and the thinning of its rim appear in all kinds of glaucoma (with high tension and with normal tension,in Primary open angle glaucoma (POAG) and in secondary glaucoma), small hemorrhages close to the optic disc have been identified as a characteristic clinical sign of normal tension glaucoma. Visual field is very important to detect NTG. It shows a defect that typically appear deeper, steeper and closer to fixation comparing to patients with POAG.

Since NTG is closely linked to vascular irregularities, a medical check-up by a general practitioner or a specialist in internal medicine is widely recommended in cases of newly diagnosed normal tension glaucoma. An examination that is considered to be of particular importance is a 24-hour monitoring of the blood pressure. NTG patients tend to suffer "dips", sudden and unnoticed drops in blood pressure during sleep.

Diagnosis includes dilated fundus examination to rule out posterior uveitis, which presents with white spots across the retina along with retinitis and vasculitis.

Laboratory testing is usually used to diagnose specific underlying diseases, including rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor, angiotensin converting enzyme inhibitor <-- error) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis).

Major histocompatibility antigen testing may be performed to investigate genetic susceptibility to uveitis. The most common antigens include HLA-B27, HLA-A29 (in birdshot chorioretinopathy) and HLA-B51 (in Behçet disease).

Radiology X-ray may be used to show coexisting arthritis and chest X-ray may be helpful in sarcoidosis.

Scientists are studying different populations and relationships to try to learn more about the disease. They have found associations with different groups but it is not yet clear what the underlying factors are and how they affect different peoples around the world.

- Glaucoma patients. While PEX and glaucoma are believed to be related, there are cases of persons with PEX without glaucoma, and persons with glaucoma without PEX. Generally, a person with PEX is considered as having a risk of developing glaucoma, and vice versa. One study suggested that the PEX was present in 12% of glaucoma patients. Another found that PEX was present in 6% of an "open-angle glaucoma" group. Pseudoexfoliation syndrome is considered to be the most common of identifiable causes of glaucoma. If PEX is diagnosed without glaucoma, there is a high risk of a patient subsequently developing glaucoma.

- Country and region. Prevalence of PEX varies by geography. In Europe, differing levels of PEX were found; 5% in England, 6% in Norway, 4% in Germany, 1% in Greece, and 6% in France. One contrary report suggested that levels of PEX were higher among Greek people. One study of a county in Minnesota found that the prevalence of PEX was 25.9 cases per 100,000 people. It is reportedly high in northern European countries such as Norway, Sweden and Finland, as well as among the Sami people of northern Europe, and high among Arabic populations, but relatively rare among African Americans and Eskimos. In southern Africa, prevalence was found to be 19% of patients in a glaucoma clinic attending to persons of the Bantu tribes.

- Race. It varies considerably according to race.

- Gender. It affects women more than men. One report was that women were three times more likely than men to develop PEX.

- Age. Older persons are more likely to develop PEX. And persons younger than 50 are highly unlikely to have PEX. A study in Norway found that the prevalence of PEX of persons aged 50–59 was 0.4% while it was 7.9% for persons aged 80–89 years. If a person is going to develop PEX, the average age in which this will happen is between 69 and 75 years, according to the Norwegian study. A second corroborating report suggested that it happens primarily to people 70 and older. While older people are more likely to develop PEX, it is not seen as a "normal" part of aging.

- Other diseases. Sometimes PEX is associated with the development of medical problems other than merely glaucoma. There are conflicting reports about whether PEX is associated with problems of the heart or brain; one study suggested no correlations while other studies found statistical links with Alzheimer's disease, senile dementia, cerebral atrophy, chronic cerebral ischemia, stroke, transient ischemic attacks, heart disease, and hearing loss.

In advanced stages, corneal neovascularization can threaten eyesight, which is why routine (annual) eye exams are recommended for contact lens patients.

Pigment dispersion syndrome (PDS) is an affliction of the eye that can lead to a form of glaucoma known as pigmentary glaucoma. It takes place when pigment cells slough off from the back of the iris and float 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 (the major site of aqueous humour drainage), which can in turn prevent the aqueous humour from draining and therefore increases the pressure inside the eye. With PDS, the intraocular pressure tends to spike at times and then can return to normal. Exercise has been shown to contribute to spikes in pressure as well. When the pressure is great enough to cause damage to the optic nerve, this is called pigmentary glaucoma. As with all types of glaucoma, when damage happens to the optic nerve fibers, the vision loss that occurs is irreversible and painless.

This condition is rare, but occurs most often in Caucasians, particularly men, and the age of onset is relatively low: mid 20s to 40s. As the crystalline lens hardens with age, the lens zonules pull away from the iris and the syndrome lessens and stops. Most sufferers are nearsighted.

There is no cure yet, but pigmentary glaucoma can be managed with eye drops or treated with simple surgeries. One of the surgeries is the YAG laser procedure in which a laser is used to break up the pigment clogs, and reduce pressure. If caught early and treated, chances of glaucoma are greatly reduced. Sufferers are often advised not to engage in high-impact sports such as long-distance running or martial arts, as strong impacts can cause more pigment cells to slough off.

A 2016 Cochrane Review sought to determine the effectiveness of YAG laser iridotomy versus no laser iridotomy for pigment dispersion syndrome and pigmentary glaucoma, in 195 participants, across five studies. No clear benefits in preventing loss of visual field were found for eyes treated with peripheral laser iridotomy. There was weak evidence suggesting that laser iridotomy could be more effective in lowering intraocular pressure in eyes versus no treatment.

Treatments for corneal neovascularization are predominately off-lab with a multitude of complications as a result. The desired results from medical therapy may not always occur, ergo an invasive procedure may be needed to prevent further decrease in corneal avascularity.

For contact lenses related hypoxia, ceasing the use of contact lenses is the first step until corneal neovascularization is addressed by a physician. Modern rigid gas permeable and silicon hydrogel contact lenses have a much higher level of oxygen transmissibility, making them effective alternatives to help prevent corneal neovascularization.

Topical administration of steroids and non-steroid anti-inflammatory drugs are first-line treatment for individuals with CNV. The administration of steroids can increase the risk of infection, glaucoma, cataracts, herpes simplex recurrence. The anti-inflammatory drugs, however, increase the risk of corneal ulceration and melting.

Since VEGF plays an important role in vasculogenesis and pathologic neovascularization associated with eye diseases, a potential treatment for CNV is to inhibit VEGF activity by competing the binding of VEGF with specific neutralizing anti-VEGF antibody. VEGF inhibitors include pegatanib sodium, ranibizumab, and off-label bevacizumab are currently used for treatment of various retinal disease. Anti-VEGF antibodies such as the application of ranibizumab or bevacizumab have has been shown to reduce corneal neovascularization. Both ranibizumab and bevacizumab uses the same mechanism and inhibits all iso-forms of VEGF. The significant reduction in invasion of in-growth blood vessels in terms of neovascular area and vessel caliber suggests that treatment with ranibizumab induces thinning of the blood vessels, however, there's no significant change of the blood vessel's length. Using anti-VEGF antibodies to treat CNV has some limitations such as it is not a cure and may require repeated treatments to maintain positive effects over time. Topical and/or subconjunctival administration of bevaicizumab or ranibizumab have demonstrated short-term safety and efficacy, however long term effects have not been documented. Anti-VEGF therapy is currently an experimental treatment.

If the cornea is inflamed via corneal neovascularization, the suppression of enzymes can block CNV by compromising with corneal structural integrity. Corneal neovascularization can be suppressed with a combination of orally administration of doxycycline and with topical corticosteroid.

Surgical Options

Invasive solutions for corneal neovascularization are reserved when the medical therapies do not provide the desired results.

Invading blood tissues and ablating tissues in the cornea can be obstructed by the use of laser treatments such as Argon and s. Irradiation and/or damages to adjacent tissues caused by the procedure can result in corneal hemorrhage and corneal thinning. Obstruction of the blood vessels can be unsuccessful due to the depth, size, and, high blood flow rate of the vessels. In conjunction, thermal damage from the lasers can trigger inflammatory response which can exaggerate the neovascularization.

An effective treatment is photodynamic therapy, however, this treatment has limited clinical acceptance due to high costs and many potential complications involved that are also related to laser ablation. Complications can include irradiation from previously injected photosensitive dye inducing apoptosis and necrosis of the endothelium and basement membrane.

Diathermy and cautery is a treatment where an electrolysis needle is inserted into the feeder vessels in the limbus. The vessels are obstructed by a coagulating current through the use of unipolar diathermy unit or by thermal cautery.

If caught early, the neovascularization can be reversed with prompt pan retinal photocoagulation (PRP), or injection of anti-VEGF medications with subsequent PRP. The injection blocks the direct effect of VEGF and acts more quickly but will wear off in about 6 weeks. PRP has a slower onset of action but can last permanently. Once the neovascularization has been longstanding, the new vessels recruit fibrous tissue, and as this forms and contracts, the angle can be permanently damaged, and will not respond to treatment. If this occurs, then surgical intervention is required to reduce the pressure (such as a glaucoma drainage implant)