Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups 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.

Opaque specks may occur in the lens in glaucoma, known as glaukomflecken.

A rhegmatogenous retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

- flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision

- a sudden dramatic increase in the number of floaters

- a ring of floaters or hairs just to the temporal (skull) side of the central vision

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

- a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision

- the impression that a veil or curtain was drawn over the field of vision

- straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)

- central visual loss

In the event of an appearance of sudden flashes of light or floaters, an eye doctor needs to be consulted immediately. A shower of floaters or any loss of vision, too, is a medical emergency.

Secondary glaucoma (H40.3-H40.6)

- Inflammatory glaucoma

- Phacogenic glaucoma

- Glaucoma secondary to intraocular hemorrhage

- Traumatic glaucoma

- Neovascular glaucoma (see below for more details)

- Drug-induced glaucoma

- Glaucoma of miscellaneous origin

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 the 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.

Toxic glaucoma is open angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach . 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 phacoemulsification 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.

Seeing rainbows around lights, especially at night, usually indicates swelling of the cornea. This may occur from a variety of causes which are discussed under Corneal Edema. Cataract can sometimes cause this also.

Colour vision is perceived mainly by the macula, which is the central vision portion of the retina. Thus any disorder affecting the macula may cause a disturbance in color vision. However, about 8% of males and 0.5% of females have some version of "colour blindness" from birth. Usually this is a genetically inherited trait, and is of the "red-green confusion" variety. The reds, browns, olives, and gold may be confused. Purple may be confused with blue, and pastel pinks, oranges, yellows, and greens look similar. Usually both eyes are affected equally.

There are many obscure macular retinal disorders that can lead to a loss of colour vision, and many of these syndromes are inherited as well. There may also be a problem with a generalized loss of vision with these problems as well. Other retinal problems can lead to a temporary disturbance of colour vision, such as Central serous chorioretinopathy, Macular Edema of different causes, and Macular Degeneration.

Certain types of cataract can gradually affect the colour vision, but this is usually not noticed until one cataract is removed. The cataract seems to filter out the colour blue, and everything seems more blue after cataract extraction. Optic nerve disorders such as Optic Neuritis can greatly affect colour vision, with colours seeming washed out during or after an episode.

Eye floaters and loss of accommodation are among the earliest symptoms. The disease may progress to severe uveitis with pain and photophobia. Commonly the eye remains relatively painless while the inflammatory disease spreads through the uvea, where characteristic focal infiltrates in the choroid named Dalén-Fuchs nodules can be seen. The retina, however, usually remains uninvolved, although perivascular cuffing of the retinal vessels with inflammatory cells may occur. Papilledema, secondary glaucoma, vitiligo, and poliosis of the eyelashes may accompany SO.

Migraine headaches may be preceded by a visual "aura", lasting for 20 to 30 minutes, and then proceeding to the headache. Some people, however, experience the aura but do not have a headache. This visual aura can be very dramatic. Classically, a small blind spot appears in the central vision with a shimmering, zig-zag light inside of it. This enlarges, and moves to one side or the other of the vision, over a 20 to 30 minute period. When it is large, this crescent shaped blind spot containing this brightly flashing light can be difficult to ignore, and some people fear that they are having a stroke. In reality, it is generally a harmless phenomenon, except in people who subsequently get the headache of migraine. Since migraine originates in the brain, the visual effect typically involves the same side of vision in each eye, although it may seem more prominent in one eye or the other.

Some people get different variations of this phenomenon, with the central vision being involved, or with the visual effect similar to "heat rising off of a car". Some people describe a "kaleidoscope" effect, with pieces of the vision being missing. All of these variations are consistent with ophthalmic migraine.

Retinal detachment is a disorder of the eye in which the retina separates from the layer underneath. Symptoms include an increase in the number of floaters, flashes of light, and worsening of the outer part of the visual field. This may be described as a curtain over part of the field of vision. In about 7% of cases both eyes are affected. Without treatment permanent loss of vision may occur.

The mechanism most commonly involves a break in the retina that then allows the fluid in the eye to get behind the retina. A break in the retina can occur from a posterior vitreous detachment, injury to the eye, or inflammation of the eye. Other risk factors include being short sighted and previous cataract surgery. Retinal detachments also rarely occur due to a choroidal tumor. Diagnosis is by either looking at the back of the eye with an ophthalmoscope or by ultrasound.

In those with a retinal tear, efforts to prevent it becoming a detachment include cryotherapy using a cold probe or photocoagulation using a laser. Treatment of retinal detachment should be carried out in a timely manner. This may include scleral buckling where silicone is sutured to the outside of the eye, pneumatic retinopexy where gas is injected into the eye, or vitrectomy where the vitreous is partly removed and replaced with either gas or oil.

Retinal detachments affect between 0.6 and 1.8 people per 10,000 per year. About 0.3% of people are affected at some point in their life. It is most common in people who are in their 60s or 70s. Males are more often affected than females. The long term outcomes depend on the duration of the detachment and whether the macula was detached. If treated before the macula detaches outcomes are generally good.

The typical infant who has congenital glaucoma usually is initially referred to an ophthalmologist because of apparent corneal edema. The commonly described triad of epiphora (excessive tearing), blepharospasm and photophobia may be missed until the corneal edema becomes apparent.

Sympathetic ophthalmia (SO) or Sympathetic uveitis is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

A reduction in visual acuity in a 'red eye' is indicative of serious ocular disease, such as keratitis, iridocyclitis, and glaucoma, and never occurs in simple conjunctivitis without accompanying corneal involvement.

Of the many causes, conjunctivitis is the most common. Others include:

"Usually nonurgent"

- blepharitis - a usually chronic inflammation of the eyelids with scaling, sometimes resolving spontaneously

- subconjunctival hemorrhage - a sometimes dramatic, but usually harmless, bleeding underneath the conjunctiva most often from spontaneous rupture of the small, fragile blood vessels, commonly from a cough or sneeze

- inflamed pterygium - a benign, triangular, horizontal growth of the conjunctiva, arising from the inner side, at the level of contact of the upper and lower eyelids, associated with exposure to sunlight, low humidity and dust. It may be more common in occupations such as farming and welding.

- inflamed pinguecula - a yellow-white deposit close to the junction between the cornea and sclera, on the conjunctiva. It is most prevalent in tropical climates with much UV exposure. Although harmless, it can occasionally become inflamed.

- dry eye syndrome - caused by either decreased tear production or increased tear film evaporation which may lead to irritation and redness

- airborne contaminants or irritants

- tiredness

- drug use including cannabis

"Usually urgent"

- acute angle closure glaucoma - implies injury to the optic nerve with the potential for irreversible vision loss which may be permanent unless treated quickly, as a result of increased pressure within the eyeball. Not all forms of glaucoma are acute, and not all are associated with increased 'intra-ocular' pressure.

- injury

- keratitis - a potentially serious inflammation or injury to the cornea (window), often associated with significant pain, light intolerance, and deterioration in vision. Numerous causes include virus infection. Injury from contact lenses can lead to keratitis.

- iritis - together with the ciliary body and choroid, the iris makes up the uvea, part of the middle, pigmented, structures of the eye. Inflammation of this layer (uveitis) requires urgent control and is estimated to be responsible for 10% of blindness in the United States.

- scleritis - a serious inflammatory condition, often painful, that can result in permanent vision loss, and without an identifiable cause in half of those presenting with it. About 30-40% have an underlying systemic autoimmune condition.

- episcleritis - most often a mild, inflammatory disorder of the 'white' of the eye unassociated with eye complications in contrast to scleritis, and responding to topical medications such as anti-inflammatory drops.

- tick borne illnesses like Rocky Mountain spotted fever - the eye is not primarily involved, but the presence of conjunctivitis, along with fever and rash, may help with the diagnosis in appropriate circumstances.

Common symptoms of vitreous hemorrhage include:

- Blurry vision

- Floaters- faint cobweb-like apparitions floating through the field of vision

- Reddish tint to vision

- Photopsia – brief flashes of light in the peripheral vision

Small vitreous hemorrhage often manifests itself as "floaters". A moderate case will often result in dark streaks in the vision, while dense vitreous hemorrhage can significantly inhibit vision.

Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify cause. Some common tests include:

- Examination of the eye with a microscope

- Pupil dilation and examination

- An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye

- Blood tests to check for specific causes such as diabetes

- A CT scan to check for injury around the eye

- Referral to a retinal specialist

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.

Patients may have no specific symptoms. In some cases, patients may complain of lessened visual acuity or changes in their perceived visual field, and such changes may be secondary to or different from symptoms normally associated with cataracts or glaucoma.

PEX is characterized by tiny microscopic white or grey granular flakes which are clumps of proteins within the eye which look somewhat like dandruff when seen through a microscope and which are released by cells. The abnormal flakes, sometimes compared to amyloid-like material, are visible during an examination of the lens of an eye by an ophthalmologist or optometrist, which is the usual diagnosis. The white fluffy material is seen in many tissues both ocular and extraocular, such as in the anterior chamber structures, trabecular meshwork, central disc, zonular fibres, anterior hyaloid membrane, pupillary and anterior iris, trabecula, and occasionally the cornea. The flakes are widespread. One report suggested that the granular flakes were from abnormalities of the basement membrane in epithelial cells, and that they were distributed widely throughout the body and not just within structures of the eye. There is some research suggesting that the material may be produced in the iris pigment epithelium, ciliary epithelium, or the peripheral anterior lens epithelium. A similar report suggests that the proteins come from the lens, iris, and other parts of the eye. A report in 2010 found indications of an abnormal ocular surface in PEX patients, discovered by an eye staining method known as rose bengal.

PEX can become problematic when the flakes become enmeshed in a "spongy area" known as the trabecular meshwork and block its normal functioning, and may interact with degenerative changes in the Schlemm's canal and the juxtacanalicular area. The blockage leads to greater-than-normal elevated intraocular pressure which, in turn, can damage the optic nerve. The eye produces a clear fluid called the aqueous humor which subsequently drains such that there is a constant level of safe pressure within the eye, but glaucoma can result if this normal outflow of fluid is blocked. Glaucoma is an umbrella term indicating ailments which damage the neural cable from the eye to the brain called the optic nerve, and which can lead to a loss of vision. In most cases of glaucoma, typically called "primary open-angle glaucoma", the outflow does not happen normally but doctors can not see what is causing the blockage; with PEX, however, the flakes are believed to be a cause of the blockage. PEX flakes by themselves do not directly "cause" glaucoma, but can cause glaucoma indirectly by blocking the outflow of aqueous humor, which leads to higher intraocular pressure, and this can cause glaucoma. PEX has been known to cause a weakening of structures within the eye which help hold the eye's lens in place, called lens zonules.

With anterior lens luxation, the lens pushes into the iris or actually enters the anterior chamber of the eye. This can cause glaucoma, uveitis, or damage to the cornea. Uveitis (inflammation of the eye) causes the pupil to constrict (miosis) and trap the lens in the anterior chamber, leading to an obstruction of outflow of aqueous humour and subsequent increase in ocular pressure (glaucoma). Better prognosis is valued in lens replacement surgery (retained vision and normal intraocular pressure) when it is performed before the onset of secondary glaucoma. Glaucoma secondary to anterior lens luxation is less common in cats than dogs due to their naturally deeper anterior chamber and the liquification of the vitreous humour secondary to chronic inflammation. Anterior lens luxation is considered to be an ophthalmological emergency.

Childhood blindness is an important cause contributing to the burden of blindness. Blindness in children can be defined as a visual acuity of <3/60 in the eye with better vision of a child under 16 years of age. This generally means that the child cannot see something three feet (about one meter) away, that another child could see if it was 60 feet (about 20 meters) away.

Rubeosis iridis, also called neovascularization of the iris (NVI), is a medical condition of the iris of the eye in which new abnormal blood vessels (formed by neovascularization) are found on the surface of the iris.

In the anterior segment of the eye, involving the cornea and the nearby sclera. It is an ectasia of pseudocornea ( the scar formed from organised exudates and fibrous tissue covered with epithelium) which results after sloughing of cornea with iris plastered behind, it is known as anterior staphyloma.

Many cases are asymptomatic, however patients many have decreased vision, glare, monocular diplopia or polyopia, and noticeable iris changes [2,6]. On exam patients have normal to decreased visual acuity, and a “beaten metal appearance” of the corneal endothelium, corneal edema, increased intraocular pressure, peripheral anterior synechiae, and iris changes [1,2,6].

It is the name given to the localised bulge in limbal area, lined by the root of the iris. It results due to ectasia of weak scar tissue formed at the limbus, following healing of a perforating injury or a peripheral corneal ulcer. There may be associated secondary angle closure glaucoma, may cause progression of the bulge if not treated. Defective vision occurs due to marked corneal astigmatism. Treatment consists of localised staphylectomy under heavy doses of oral steroids.

The primary symptom is pupillary distortion (changing of the size or shape of the pupil). Distortion can occur in any segment of the iris. One part of the iris is pulled to a peak, and then returns to normal after the episode. Other symptoms may include blurred vision, abnormal periocular sensations (unusual feelings around the eyes), migraines, and feelings of a chilled face. Some patients who demonstrate tadpole pupil symptoms also experienced Horner’s syndrome or Adie’s tonic pupil

Tadpole pupil symptoms occur in episodes. Episodes are generally brief and less than 5 minutes, however, some episodes have been reported to last anywhere from 3 to 15 minutes. The episodes can occur multiple times a day for days, weeks, or months.

Studies show that a majority of those experiencing tadpole pupil are younger women from an age range of 24 to 48 years old, with no apparent health problems. Although women generally have the tadpole pupil, men are not unaffected by this disease and some have been reported to experience the symptoms.

Buphthalmos in itself is merely a clinical sign and does not generate symptoms. Patients with glaucoma often initially have no symptoms; later, they can exhibit excessive tearing (lacrimation) and extreme sensitivity to light (photophobia). On ophthalmologic exam, one can detect increased intraocular pressure, distortion of the optic disc, and corneal edema, which manifests as haziness.

Other symptoms include a prominent eyeball, Haab's striae in the Descemet's membrane of the cornea, an enlarged cornea, and myopia.

Refractive errors such as hyperopia and Anisometropia may be associated abnormalities found in patients with vertical strabismus.

The vertical miscoordination between the two eyes may lead to

- Strabismic amblyopia, (due to deprivation / suppression of the deviating eye)

- cosmetic defect (most noticed by parents of a young child and in photographs)

- Face turn, depending on presence of binocular vision in a particular gaze

- diplopia or double vision - more seen in adults (maturity / plasticity of neural pathways) and suppression mechanisms of the brain in sorting out the images from the two eyes.

- cyclotropia, a cyclotorsional deviation of the eyes (rotation around the visual axis), particularly when the root cause is an oblique muscle paresis causing the hypertropia.

Hypertropia is a condition of misalignment of the eyes (strabismus), whereby the visual axis of one eye is higher than the fellow fixating eye.

Hypotropia is the similar condition, focus being on the eye with the visual axis lower than the fellow fixating eye.

Dissociated Vertical Deviation is a special type of hypertropia leading to slow upward drift of one or rarely both eyes, usually when the patient is inattentive.

Ocular causes include:

- Iritis

- Keratitis

- Blepharitis

- Optic disc drusen

- Posterior vitreous detachment

- Closed-angle glaucoma

- Transient elevation of intraocular pressure

- Intraocular hemorrhage

- Coloboma

- Myopia

- Orbital hemangioma

- Orbital osteoma

- Keratoconjunctivitis sicca