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:

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.

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.

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

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

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.

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.

If the diagnostic workup reveals a systemic disease process, directed therapies to treat that underlying cause should be initiated. If the amaurosis fugax is caused by an atherosclerotic lesion, aspirin is indicated, and a carotid endarterectomy considered based on the location and grade of the stenosis. Generally, if the carotid artery is still patent, the greater the stenosis, the greater the indication for endarterectomy. "Amaurosis fugax appears to be a particularly favorable indication for carotid endarterectomy. Left untreated, this event carries a high risk of stroke; after carotid endarterectomy, which has a low operative risk, there is a very low postoperative stroke rate." However, the rate of subsequent stroke after amaurosis is significantly less than after a hemispheric TIA, therefore there remains debate as to the precise indications for which a carotid endarterectomy should be performed. If the full diagnostic workup is completely normal, patient observation is recommended.

Despite the temporary nature of the vision loss, those experiencing amaurosis fugax are usually advised to consult a physician immediately as it is a symptom that may herald serious vascular events, including stroke. Restated, “because of the brief interval between the transient event and a stroke or blindness from temporal arteritis, the workup for transient monocular blindness should be undertaken without delay.” If the patient has no history of giant cell arteritis, the probability of vision preservation is high; however, the chance of a stroke reaches that for a hemispheric TIA. Therefore, investigation of cardiac disease is justified.

A diagnostic evaluation should begin with the patient's history, followed by a physical exam, with particular importance being paid to the ophthalmic examination with regards to signs of ocular ischemia. When investigating amaurosis fugax, an ophthalmologic consult is absolutely warranted if available. Several concomitant laboratory tests should also be ordered to investigate some of the more common, systemic causes listed above, including a complete blood count, erythrocyte sedimentation rate, lipid panel, and blood glucose level. If a particular cause is suspected based on the history and physical, additional relevant labs should be ordered.

If laboratory tests are abnormal, a systemic disease process is likely, and, if the ophthalmologic examination is abnormal, ocular disease is likely. However, in the event that both of these routes of investigation yield normal findings or an inadequate explanation, noninvasive duplex ultrasound studies are recommended to identify carotid artery disease. Most episodes of amaurosis fugax are the result of stenosis of the ipsilateral carotid artery. With that being the case, researchers investigated how best to evaluate these episodes of vision loss, and concluded that for patients ranging from 36–74 years old, "...carotid artery duplex scanning should be performed...as this investigation is more likely to provide useful information than an extensive cardiac screening (ECG, Holter 24-hour monitoring, and precordial echocardiography)." Additionally, concomitant head CT or MRI imaging is also recommended to investigate the presence of a “clinically silent cerebral embolism.”

If the results of the ultrasound and intracranial imaging are normal, “renewed diagnostic efforts may be made,” during which fluorescein angiography is an appropriate consideration. However, carotid angiography is not advisable in the presence of a normal ultrasound and CT.

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.

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.

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.

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.

A hypopyon should not be drained, because it offers protection against the invading pathogen due to the presence of white blood cells, although long-standing hypopyon can cause close-angle glaucoma and anterior synechiae.

Photophobia may also affect patients' socioeconomic status by limiting their career choices, since many workplaces require bright lights for safety or to accommodate the work being done. Sufferers may be shut out of a wide range of both skilled and unskilled jobs, such as in warehouses, offices, workshops, classrooms, supermarkets and storage spaces. Some photophobes are only able to work night shifts, which reduces their prospects for finding work.

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.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.

The center of the cornea shows normal thickness, with an intact central epithelium, but the inferior cornea exhibits a peripheral band of thinning, to about 1–2 mm. The portion of the cornea that is immediately adjacent to the limbus is spared, usually a strip of about 1–2 mm. In PMD we can see high against the rule astigmatism along with horizontal bow ties. The inferior peripheral thinning is seen between the 4 o'clock and 8 o'clock positions.

PMD lacks apical corneal scarring, Rizutti's phenomenon, Munson's sign, and the central corneal thickness is usually normal.

The gold standard diagnostic test for PMD is corneal topography. However, it may not as specific as corneal pachymetry, because corneal topography only evaluates the degree and distribution of surface irregularities on the cornea, not the thickness of the cornea. Corneal topography may show a "crab claw-like" appearance, a finding that is seen in both keratoconus and in pellucid marginal degeneration. Thus, if corneal topography is used for diagnosis, it should be in conjunction with clinical findings of peripheral, inferior corneal thinning.

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.

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)

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.

Hypopyon can be present in a corneal ulcer. Behcet's disease, endophthalmitis, panuveitis/panophthalmitis and adverse reactions to some drugs (such as rifabutin).

Hypopyon is also known as "sterile pus", as it occurs due to the release of toxins and not by the actual invasion of pathogens. The toxins secreted by the pathogens mediate the outpouring of leukocytes that settle in the anterior chamber of the eye. .

An inverse hypopyon is different from a standard hypopyon. Inverse hypopyon is seen after a pars plana vitrectomy with an insertion of silicone oil (as a replacement of the vitreous humour that has been removed in the operation; the silicone oil maintains internal tamponade). When the silicone oil emulsifies, it seeps into the anterior chamber and settles at the top of the anterior chamber. This is in contrast to hypopyon resulting from toxins where the leukocytes settle at the bottom of the anterior chamber. This is due to the effect of gravity, hence the name inverse hypopyon.

There are many causes of blurred vision:

- Use of atropine or other anticholinergics

- Presbyopia—Difficulty focusing on objects that are close. Common in the elderly. (Accommodation tends to decrease with age.)

- Cataracts—Cloudiness over the eye's lens, causing poor night-time vision, halos around lights, and sensitivity to glare. Daytime vision is eventually affected. Common in the elderly.

- Glaucoma—Increased pressure in the eye, causing poor night vision, blind spots, and loss of vision to either side. A major cause of blindness. Glaucoma can happen gradually or suddenly—if sudden, it is a medical emergency.

- Diabetes—Poorly controlled blood sugar can lead to temporary swelling of the lens of the eye, resulting in blurred vision. While it resolves if blood sugar control is reestablished, it is believed repeated occurrences promote the formation of cataracts (which are not temporary).

- Diabetic retinopathy—This complication of diabetes can lead to bleeding into the retina. Another common cause of blindness.

- Hypervitaminosis A—Excess consumption of vitamin A can cause blurred vision.

- Macular degeneration—Loss of central vision, blurred vision (especially while reading), distorted vision (like seeing wavy lines), and colors appearing faded. The most common cause of blindness in people over age 60.

- Eye infection, inflammation, or injury.

- Sjögren's syndrome, a chronic autoimmune inflammatory disease that destroys moisture producing glands, including lacrimal (tear)

- Floaters—Tiny particles drifting across the eye. Although often brief and harmless, they may be a sign of retinal detachment.

- Retinal detachment—Symptoms include floaters, flashes of light across your visual field, or a sensation of a shade or curtain hanging on one side of your visual field.

- Optic neuritis—Inflammation of the optic nerve from infection or multiple sclerosis. You may have pain when you move your eye or touch it through the eyelid.

- Stroke or transient ischemic attack

- Brain tumor

- Toxocara—A parasitic roundworm that can cause blurred vision

- Bleeding into the eye

- Temporal arteritis—Inflammation of an artery in the brain that supplies blood to the optic nerve.

- Migraine headaches—Spots of light, halos, or zigzag patterns are common symptoms prior to the start of the headache. A retinal migraine is when you have only visual symptoms without a headache.

- Myopia—Blurred vision may be a systemic sign of local anaesthetic toxicity

- Reduced blinking—Lid closure that occurs too infrequently often leads to irregularities of the tear film due to prolonged evaporation, thus resulting in disruptions in visual perception.

- Carbon monoxide poisoning—Reduced oxygen delivery can effect many areas of the body including vision. Other symptoms caused by CO include vertigo, hallucination and sensitivity to light.