Eye injury and head trauma may also coincide with a black eye. Some common signs of a more serious injury may include:

- Double vision

- Loss of sight and/or fuzzy vision could occur

- Loss of consciousness

- Inability to move the eye or large swelling around the eye

- Blood or clear fluid from the nose or the ears

- Blood on the surface of the eye itself or cuts on the eye itself

- Persistent headache or migraine

Blast-related ocular trauma comprises a specialized group of penetrating and blunt force injuries to the eye and its structure caused by the detonation of explosive materials. The incidence of ocular trauma due to blast forces has increased dramatically with the introduction of new explosives technology into modern warfare. The availability of these volatile materials, coupled with the tactics of contemporary terrorism, has caused a rise in the number of homemade bombs capable of extreme physical harm.

Physical or chemical injuries of the eye can be a serious threat to vision if not treated appropriately and in a timely fashion. The most obvious presentation of ocular (eye) injuries is redness and pain of the affected eyes. This is not, however, universally true, as tiny metallic projectiles may cause neither symptom. Tiny metallic projectiles should be suspected when a patient reports "metal on metal" contact, such as with hammering a metal surface. Intraocular foreign bodies do not cause pain because of the lack of nerve endings in the vitreous humour and retina that can transmit pain sensations. As such, general or emergency room doctors should refer cases involving the posterior segment of the eye or intraocular foreign bodies to an ophthalmologist. Ideally, ointment would not be used when referring to an ophthalmologist, since it diminishes the ability to carry out a thorough eye examination.

Flicking sand, flying pieces of wood, metal, glass, stone and other material are notorious for causing much of the eye trauma. Sporting balls such as cricket ball, lawn tennis ball, squash ball, shuttlecock, and other high speed flying objects can strike the eye. The eye is also susceptible to blunt trauma in a fistfight. The games of young children such as bow-and-arrows, bb guns and firecrackers can lead to eye trauma. Road traffic accidents (RTAs) with head and facial trauma may also have an eye injury - these are usually severe in nature with multiple lacerations, shards of glasses embedded in tissues, orbital fractures, severe hematoma and penetrating open-globe injuries with prolapse of eye contents. Other causes of intraocular trauma may arise from workplace tools or even common household implements.

About 5.3 million cases of foreign bodies in the eyes occurred in 2013.

A black eye, periorbital hematoma, or shiner, is bruising around the eye commonly due to an injury to the face rather than to the eye. The name is given due to the color of bruising. The so-called black eye is caused by bleeding beneath the skin and around the eye. Sometimes a black eye could get worse if not referring to a doctor after a few months, indicating a more extensive injury, even a skull fracture, particularly if the area around both eyes is bruised (raccoon eyes), or if there has been a prior head injury.

Although most black eye injuries are not serious, bleeding within the eye, called a hyphema, is serious and can reduce vision and damage the cornea. In some cases, abnormally high pressure inside the eyeball (ocular hypertension) can also result.

Signs and symptoms of corneal abrasion include pain, trouble with bright lights, a foreign-body sensation, excessive squinting, and reflex production of tears. Signs include epithelial defects and edema, and often redness of the eye. The vision may be blurred, both from any swelling of the cornea and from excess tears. Crusty buildup from excess tears may also be present.

Multiple complications are known to occur following eye injury: corneal scarring, hyphema, iridodialysis, post-traumatic glaucoma, uveitis cataract, vitreous hemorrhage and retinal detachment. The complications risk is high with retinal tears, penetrating injuries and severe blunt trauma.

A person with photic retinopathy may notice an impairment in their vision, for example a spot that does not go away after a reasonable recovery time, or blurring. They may also have eye pain or headaches. Vision impairment is usually in both eyes, but "can" be in just one. Impairment of a person with 20/20 vision usually ends up being about 20/40 or 20/60, but can be better or far worse.

A doctor examining an eye with retinopathy may be able to see no signs at all, or a slight macular edema, which is a sort of blister on or under the macula, an oval colored spot normally visible to an eye doctor on each person's retina.

But while even that edema goes away, within a few days the patient will generally develop a discoloration of the retina at the injured point, often yellow or white, turning red over the next few weeks.

If the vitreous is firmly attached to the retina when it pulls away, it can tear the retina and create a macular hole. Also, once the vitreous has pulled away from the surface of the retina, some of the fibers can remain on the retinal surface and can contract. This increases tension on the retina and can lead to a macular hole. In either case, the fluid that has replaced the shrunken vitreous can then seep through the hole onto the macula, blurring and distorting central vision.

A macular hole is a small break in the macula, located in the center of the eye's light-sensitive tissue called the retina.

Vision loss due to solar retinopathy is typically reversible, lasting for as short as one month to over one year. The fundus changes are variable and usually bilateral, mild cases often show no alteration and moderate to severe cases show a foveal yellow spot on the first days after exposure. After a few days it is replaced by a reddish dot often surrounded by pigment.

Permanent holes and lesions are possible; prognosis worsens with dilated pupils or prolonged exposure.

Visual outcomes for patients with ocular trauma due to blast injuries vary, and prognoses depend upon the type of injury sustained. The majority of poor visual outcomes arise from perforating injuries: only 21% of patients with perforating injuries with pre-operative light perception had a final best-corrected visual acuity (BCVA) better than 20/200. Collectively, patients who experienced choroidal hemorrhage, perforated or penetrated globes, retinal detachment, traumatic optic neuropathy, and subretinal macular hemorrhage carried the highest incidence rates of BCVAs worse than 20/200. Reports from Operation Iraqi Freedom (OIF) indicate that 42% of soldiers with globe injuries of any kind had a BCVA greater than or equal to 20/40 six months after injury, and soldiers with intraocular foreign bodies (IOFBs) retained 20/40 or better vision in 52% of studied cases.

Globe perforation, oculoplastic intervention, and neuro-ophthalmic injuries contribute significantly to reported poor visual outcomes. 21% of tertiary centers treating patients exposed to blast trauma reported traumatic optic neuropathy (TON) in their patients, although avulsion of the optic nerve and TON were reported in only 3% of combat injuries. In the event that a victim of globe penetrating trauma cannot perceive any light within two weeks of surgical intervention, the ophthalmologist may choose to enucleate as a preventative measure against sympathetic ophthalmia. However, this procedure is extremely rare, and current reports indicate that only one soldier in OIF has undergone enucleation in a tertiary care facility to prevent sympathetic ophthalmia.

Berlin's edema (commotio retinae) is a common condition caused by blunt injury to the eye. It is characterized by decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen along with "cherry red spot" in the foveal reigion.This whitening is indicative of cell damage, which occurs in the retinal pigment epithelium and outer segment layer of photoreceptors. Damage to the outer segment often results in photoreceptor death through uncertain mechanisms. Usually there is no leakage of fluid and therefore it is not considered a true edema. The choroidal fluorescence in fluorescent angiography is absent. Visual acuity ranges from 20/20 to 20/400.

The prognosis is excellent except in case of complications of choroidal rupture, hemorrhage or pigment epithelial damage, but damage to the macula will result in poorer recovery. The outcome can be worsened in the case of retinal detachment, atrophy or hyperplasia. Visual field defects can occur. In late cases cystoid macular edema sometimes develops which can further lead to macular destruction.

Commotio retinae is usually self limiting and there is no treatment as such. It usually resolves in 3–4 weeks without any complications and sequelae.

Typical symptoms of dry eye syndrome are dryness, burning and a sandy-gritty eye irritation that gets worse as the day goes on. Symptoms may also be described as itchy, scratchy, stinging or tired eyes. Other symptoms are pain, redness, a pulling sensation, and pressure behind the eye. There may be a feeling that something, such as a speck of dirt, is in the eye. The resultant damage to the eye surface increases discomfort and sensitivity to bright light. Both eyes usually are affected.

There may also be a stringy discharge from the eyes. Although it may seem strange, dry eye can cause the eyes to water. This can happen because the eyes are irritated. One may experience excessive tearing in the same way as one would if something got into the eye. These reflex tears will not necessarily make the eyes feel better. This is because they are the watery type that are produced in response to injury, irritation, or emotion. They do not have the lubricating qualities necessary to prevent dry eye.

Because blinking coats the eye with tears, symptoms are worsened by activities in which the rate of blinking is reduced due to prolonged use of the eyes. These activities include prolonged reading, computer usage, driving, or watching television. Symptoms increase in windy, dusty or smoky (including cigarette smoke) areas, in dry environments high altitudes including airplanes, on days with low humidity, and in areas where an air conditioner (especially in a car), fan, heater, or even a hair dryer is being used. Symptoms reduce during cool, rainy, or foggy weather and in humid places, such as in the shower.

Most people who have dry eyes experience mild irritation with no long-term effects. However, if the condition is left untreated or becomes severe, it can produce complications that can cause eye damage, resulting in impaired vision or (rarely) in the loss of vision.

Symptom assessment is a key component of dry eye diagnosis – to the extent that many believe dry eye syndrome to be a symptom-based disease. Several questionnaires have been developed to determine a score that would allow for dry eye diagnosis. The McMonnies & Ho dry eye questionnaire is often used in clinical studies of dry eyes.

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.

Corneal abrasion is a scratch to the surface of the cornea of the eye. Symptoms include pain, redness, light sensitivity, and a feeling like a foreign body is in the eye. Most people recover completely within three days.

Most cases are due to minor trauma to the eye such as that which can occur with contact lens use or from fingernails. About 25% of cases occur at work. Diagnosis is often by slit lamp examination after fluorescein dye has been applied. More significant injuries like a corneal ulcer, globe rupture, recurrent erosion syndrome, and a foreign body within the eye should be ruled out.

Prevention includes the use of eye protection. Treatment is typically with antibiotic ointment. In those who wear contact lenses a fluoroquinolone antibiotic is often recommended. Paracetamol (acetaminophen), NSAIDs, and eye drops such as cyclopentolate that paralysis the pupil can help with pain. Evidence does not support the usefulness of eye patching for those with simple abrasions.

About 3 per 1,000 people are affected a year in the United States. Males are more often affected than females. The typical age group affected is those in their 20s and 30s. Complications can include bacterial keratitis, corneal ulcer, and iritis. Complications may occur in up to 8% of people.

Any abnormality of any one of the three layers of tears produces an unstable tear film, resulting in symptoms of dry eyes.

Vitreomacular adhesion (VMA) is a human medical condition where the vitreous gel (or simply vitreous) of the human eye adheres to the retina in an abnormally strong manner. As the eye ages, it is common for the vitreous to separate from the retina. But if this separation is not complete, i.e. there is still an adhesion, this can create pulling forces on the retina that may result in subsequent loss or distortion of vision. The adhesion in of itself is not dangerous, but the resulting pathological vitreomacular traction (VMT) can cause severe ocular damage.

The current standard of care for treating these adhesions is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye. A biological agent for non-invasive treatment of adhesions called ocriplasmin has been approved by the FDA on Oct 17 2012.

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.

Traction caused by VMA is the underlying pathology of an eye disease called symptomatic VMA. There is evidence that symptomatic VMA can contribute to the development of several well-known eye disorders, such as macular hole and macular pucker, that can cause visual impairment, including blindness. It may also be associated with age-related macular degeneration (AMD), diabetic macular edema (DME), retinal vein occlusion, and diabetic retinopathy (DR).

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.

The most common sign at presentation is leukocoria (abnormal white reflection of the retina). Symptoms typically begin as blurred vision, usually pronounced when one eye is closed (due to the unilateral nature of the disease). Often the unaffected eye will compensate for the loss of vision in the other eye; however, this results in some loss of depth perception and parallax. Deterioration of sight may begin in either the central or peripheral vision. Deterioration is likely to begin in the upper part of the vision field as this corresponds with the bottom of the eye where blood usually pools. Flashes of light, known as photopsia, and floaters are common symptoms. Persistent color patterns may also be perceived in the affected eye. Initially, these may be mistaken for psychological hallucinations, but are actually the result of both retinal detachment and foreign fluids mechanically interacting with the photoreceptors located on the retina.

One early warning sign of Coats' disease is yellow-eye in flash photography. Just as the red-eye effect is caused by a reflection off blood vessels in the back of a normal eye, an eye affected by Coats' will glow yellow in photographs as light reflects off cholesterol deposits. Children with yellow-eye in photographs are typically advised to immediately seek evaluation from an optometrist or ophthalmologist, who will assess and diagnose the condition and refer to a vitreo-retinal specialist.

Coats' disease itself is painless. Pain may occur if fluid is unable to drain from the eye properly, causing the internal pressure to swell, resulting in painful glaucoma.

In mechanical anisocoria, this is the result of damage to the iris dilator muscle, which may be caused by trauma, angle-closure glaucoma, surgery such as cataract removal, or uveitis (inflammation of the eye). Slit lamp examination is often used as a diagnostic aid: damage to the dilator muscle is indicated by anisocoria when light intensity is lowered.Anisocoria refers to a common eye condition in which the two pupils differ in size.

Neurological causes for photophobia include:

- Autism spectrum disorders

- Chiari malformation

- Occipital Neuralgia

- Dyslexia

- Encephalitis including Myalgic encephalomyelitis aka Chronic fatigue syndrome

- Meningitis

- Trigeminal disturbance causes central sensitization (hence, multiple other associated hypersensitivities. Causes can be bad bite, infected tooth, etc.

- Subarachnoid haemorrhage

- Tumor of the posterior cranial fossa

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.

Symptoms of entropion include:

- Redness and pain around the eye

- Sensitivity to light and wind

- Sagging skin around the eye

- Epiphora

- Decreased vision, especially if the cornea is damaged