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.

Congenital cataracts refers to a lens opacity present at birth. Congenital cataracts cover a broad spectrum of severity: whereas some lens opacities do not progress and are visually insignificant, others can produce profound visual impairment.

Congenital cataracts may be unilateral or bilateral. They can be classified by morphology, presumed or defined genetic cause, presence of specific metabolic disorders, or associated ocular anomalies or systemic findings.

Signs and symptoms vary depending on the type of cataract, though considerable overlap occurs. People with nuclear sclerotic or brunescent cataracts often notice a reduction of vision. Those with posterior subcapsular cataracts usually complain of glare as their major symptom.

The severity of cataract formation, assuming no other eye disease is present, is judged primarily by a visual acuity test. The appropriateness of surgery depends on a patient's particular functional and visual needs and other risk factors, all of which may vary widely.

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.

Congenital cataracts occur in a variety of morphologic configurations, including lamellar, polar, sutural, coronary, cerulean, nuclear, capsular, complete, membranous.

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.

The effects a coloboma has on the vision can be mild or more severe depending on the size and location of the gap. If, for example, only a small part of the iris is missing, vision may be normal, whereas if a large part of the retina or optic nerve is missing, vision may be poor and a large part of the visual field may be missing. This is more likely to cause problems with mobility if the lower visual field is absent. Other conditions can be associated with a coloboma. Sometimes, the eye may be reduced in size, a condition called microphthalmia. Glaucoma, nystagmus, scotoma, or strabismus may also occur.

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.

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.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

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.

Other ocular malformations that include coloboma or are related to it:

- CHARGE syndrome, a term that came into use as an acronym for the set of unusual congenital features seen in a number of newborn children. The letters stand for: coloboma of the eye, heart defects, atresia of the nasal choanae, retardation of growth and/or development, genital and/or urinary abnormalities, and ear abnormalities and deafness. Although these features are no longer used in making a diagnosis, the name has remained.

- Cat eye syndrome, caused by the short arm (p) and a small section of the long arm (q) of human chromosome 22 being present three (trisomic) or four times (tetrasomic) instead of the usual two times. The term "cat eye" was coined because of the particular appearance of the vertical colobomas in the eyes of some patients.

- Patau syndrome (trisomy 13), a chromosomal abnormality that can cause a number of deformities, some of which include structural eye defects, including microphthalmia, Peters anomaly, cataract, iris and/or fundus coloboma, retinal dysplasia or retinal detachment, sensory nystagmus, cortical visual loss, and optic nerve hypoplasia.

- Treacher Collins syndrome, autosomal dominant syndrome caused by mutation of "TCOF1". Coloboma is part of a set of characteristic facies that features craniofacial malformations, such as downslanting eyes, ear anomalies, or hypoplasia of zygomatic bone and jaw (micrognathia).

Nearly every person who undergoes a vitrectomy—without ever having had cataract surgery—will experience progression of nuclear sclerosis after the operation. This may be because the native vitreous humor is different to the solutions used to replace the vitreous (vitreous substitutes), such as BSS Plus. This may also be because the native vitreous humour contains ascorbic acid which helps neutralize oxidative damage to the lens and because traditional vitreous substitutes do not contain ascorbic acid. As such, for phakic patients requiring a vitrectomy it is becoming increasingly common for ophthalmologists to offer the vitrectomy with a combined prophylactic cataract surgery procedure to prophylactically prevent cataract formation.

With posterior lens luxation, the lens falls back into the vitreous humour and lies on the floor of the eye. This type causes fewer problems than anterior lens luxation, although glaucoma or ocular inflammation may occur. Surgery is used to treat dogs with significant symptoms. Removal of the lens before it moves to the anterior chamber may prevent secondary glaucoma.

This condition is usually unilateral, and its symptoms vary from none to mild blurring and discomfort. Signs include diffuse iris atrophy and small white keratic precipitates (deposits on the inner surface of the cornea), cells presenting in the anterior chamber as well as the anterior vitreous. Glaucoma and cataract occur frequently.

Primary juvenile glaucoma is glaucoma that develops due to ocular hypertension and is evident either at birth or within the first few years of life. It is caused due to abnormalities in the anterior chamber angle development that obstruct aqueous outflow in the absence of systemic anomalies or other ocular malformation.

Aphakia is the absence of the lens of the eye, due to surgical removal, a perforating wound or ulcer, or congenital anomaly. It causes a loss of accommodation, far sightedness (hyperopia), and a deep anterior chamber. Complications include detachment of the vitreous or retina, and glaucoma.

Babies are rarely born with aphakia. Occurrence most often results from surgery to remove congenital cataract (clouding of the eye's lens, which can block light from entering the eye and focusing clearly). Congenital cataracts usually develop as a result of infection of the fetus or genetic reasons. It is often difficult to identify the exact cause of these cataracts, especially if only one eye is affected.

People with aphakia have relatively small pupils and their pupils dilate to a lesser degree.

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.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

There is another retinal disease in Briards known as hereditary retinal dysplasia. These dogs are night blind from birth, and day vision varies. Puppies affected often have nystagmus. It is also known as lipid retinopathy.

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.

Infantile glaucoma, which often produces the clinical sign of buphthalmos, can be caused when an abnormally narrow angle between the cornea and iris blocks the outflow of aqueous humor; this causes increased intraocular pressure and eventual enlargement of the globe (eyeball). Angle closure can be caused by developmental abnormalities of the eye as well as the presence of abnormal structures within the vitreous.

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.

Irvine–Gass syndrome, pseudophakic cystoid macular edema or postcataract CME is one of the most common causes of visual loss after cataract surgery. The syndrome is named in honor of S. Rodman Irvine and J. Donald M. Gass.

The incidence is more common in older types of cataract surgery, where postcataract CME could occur in 20–60% of patients, but with modern cataract surgery, incidence of Irvine–Gass syndrome have reduced significantly.

Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) this could occur as the surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. This is less common today with modern lens replacement techniques

Without the focusing power of the lens, the eye becomes very farsighted. This can be corrected by wearing glasses, contact lenses, or by implant of an artificial lens. Artificial lenses are described as "pseudophakic." Also, since the lens is responsible for adjusting the focus of vision to different lengths, patients with aphakia have a total loss of accommodation.

Some individuals have said that they perceive ultraviolet light, invisible to those with a lens, as whitish blue or whitish-violet.