All newborns should have screening eye examinations, including an evaluation of the red reflexes.

- The red reflex test is best performed in a darkened room and involves shining a bright direct ophthalmoscope into both eyes simultaneously from a distance of 1– 2 ft. This test can be used for routine ocular screening by nurses, pediatricians, family practitioners, and optometrists.

- Retinoscopy through the child's undilated pupil is helpful for assessing the potential visual significance of an axial lens opacity in a pre-verbal child. Any central opacity or surrounding cortical distortion greater than 3 mm can be assumed to be visually significant.

- Laboratory Tests : In contrast to unilateral cataracts, bilateral congenital cataracts may be associated with many systemic and metabolic diseases. A basic laboratory evaluation for bilateral cataracts of unknown cause in apparently healthy children includes:

Retinal detachment can be examined by fundus photography or ophthalmoscopy. Fundus photography generally needs a considerably larger instrument than the ophthalmoscope, but has the advantage of availing the image to be examined by a specialist at another location and/or time, as well as providing photo documentation for future reference. Modern fundus photographs generally recreate considerably larger areas of the fundus than what can be seen at any one time with handheld ophthalmoscopes.

Ultrasound has diagnostic accuracy similar to that of examination by an ophthalmologist. The recent meta-analysis shows the diagnostic accuracy of emergency department (ED) ocular ultrasonography is high. The sensitivity and specificity ranged from 97% to 100% and 83% to 100%. The typical feature of retinal detachment when viewed on ultrasound is "flying angel sign". It shows the detached retina moving with a fixed point under the B mode, linear probe 10 MHz.

A minority of retinal detachments result from trauma, including blunt blows to the orbit, penetrating trauma, and concussions to the head. A retrospective Indian study of more than 500 cases of rhegmatogenous detachments found that 11% were due to trauma, and that gradual onset was the norm, with over 50% presenting more than one month after the inciting injury.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

Serious complications of cataract surgery include retinal detachment and endophthalmitis. In both cases, patients notice a sudden decrease in vision. In endophthalmitis, patients often describe pain. Retinal detachment frequently presents with unilateral visual field defects, blurring of vision, flashes of light, or floating spots.

The risk of retinal detachment was estimated as about 0.4% within 5.5 years, corresponding to a 2.3-fold risk increase compared to naturally expected incidence, with older studies reporting a substantially higher risk. The incidence is increasing over time in a somewhat linear manner, and the risk increase lasts for at least 20 years after the procedure. Particular risk factors are younger age, male sex, longer axial length, and complications during surgery. In the highest risk group of patients, the incidence of pseudophakic retinal detachment may be as high as 20%.

The risk of endophthalmitis occurring after surgery is less than one in 1000.

Corneal edema and cystoid macular edema are less serious but more common, and occur because of persistent swelling at the front of the eye in corneal edema or back of the eye in cystoid macular edema. They are normally the result of excessive inflammation following surgery, and in both cases, patients may notice blurred, foggy vision. They normally improve with time and with application of anti-inflammatory drops. The risk of either occurring is around one in 100. It is unclear whether NSAIDs or corticosteroids are superior at reducing postoperative inflammation.

Posterior capsular opacification, also known as after-cataract, is a condition in which months or years after successful cataract surgery, vision deteriorates or problems with glare and light scattering recur, usually due to thickening of the back or posterior capsule surrounding the implanted lens, so-called 'posterior lens capsule opacification'. Growth of natural lens cells remaining after the natural lens was removed may be the cause, and the younger the patient, the greater the chance of this occurring. Management involves cutting a small, circular area in the posterior capsule with targeted beams of energy from a laser, called capsulotomy, after the type of laser used. The laser can be aimed very accurately, and the small part of the capsule which is cut falls harmlessly to the bottom of the inside of the eye. This procedure leaves sufficient capsule to hold the lens in place, but removes enough to allow light to pass directly through to the retina. Serious side effects are rare. Posterior capsular opacification is common and occurs following up to one in four operations, but these rates are decreasing following the introduction of modern intraocular lenses together with a better understanding of the causes.

Vitreous touch syndrome is a possible complication of intracapsular cataract extraction.

In general, the younger the child, the greater the urgency in removing the cataract, because of the risk of amblyopia. For optimal visual development in newborns and young infants, a visually significant unilateral congenital cataract should be detected and removed before age 6 weeks, and visually significant bilateral congenital cataracts should be removed before age 10 weeks.

Some congenital cataracts are too small to affect vision, therefore no surgery or treatment will be done. If they are superficial and small, an ophthalmologist will continue to monitor them throughout a patient's life. Commonly, a patient with small congenital cataracts that do not affect vision will eventually be affected later in life; generally this will take decades to occur.

On photographs taken using a flash, instead of the familiar red-eye effect, leukocoria can cause a bright white reflection in an affected eye. Leukocoria may appear also in low indirect light, similar to eyeshine.

Leukocoria can be detected by a routine eye exam (see Ophthalmoscopy). For screening purposes, the red reflex test is used. In this test, when a light is shone briefly through the pupil, an orange red reflection is normal. A white reflection is leukocoria.

Floaters are often readily observed by an ophthalmologist or an optometrist with the use of an ophthalmoscope or slit lamp. However, if the floater is near the retina, it may not be visible to the observer even if it appears large to the patient.

Increasing background illumination or using a pinhole to effectively decrease pupil diameter may allow a person to obtain a better view of his or her own floaters. The head may be tilted in such a way that one of the floaters drifts towards the central axis of the eye. In the sharpened image the fibrous elements are more conspicuous.

The presence of retinal tears with new onset of floaters was surprisingly high (14%; 95% confidence interval, 12–16%) as reported in a meta-analysis published as part of the Rational Clinical Examination Series in the Journal of the American Medical Association. Patients with new onset flashes and/or floaters, especially when associated with visual loss or restriction in the visual field, should seek more urgent ophthalmologic evaluation.

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

In general, strabismus can be approached and treated with a variety of procedures. Depending on the individual case, treatment options include:

- Correction of refractive errors by glasses

- Prism therapy (if tolerated, to manage diplopia)

- Patching (mainly to manage amblyopia in children and diplopia in adults)

- Botulinum toxin injection

- Surgical correction

Surgical correction of the hypertropia is desired to achieve binocularity, manage diplopia and/or correct the cosmetic defect. Steps to achieve the same depend on mechanism of the hypertropia and identification of the offending muscles causing the misalignment. Various surgical procedures have been described and should be offered after careful examination of eyes, including a detailed orthoptic examination focussing on the disturbances in ocular motility and visual status. Specialty fellowship trained pediatric ophthalmologists and strabismus surgeons are best equipped to deal with these complex procedures.

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

Molecular (DNA) testing for PAX6 gene mutations (by sequencing of the entire coding region and deletion/duplication analysis) is available for isolated aniridia and the Gillespie syndrome. For the WAGR syndrome, high-resolution cytogenetic analysis and fluorescence in situ hybridization (FISH) can be utilized to identify deletions within chromosome band 11p13, where both the PAX6 and WT1 genes are located.

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.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

Treatment is done by changing the optical magnification properties of the auxiliary optics (corrective lenses). The optical magnification properties of spectacle lenses can be adjusted by changing parameters like the base curve, vertex distance, and center thickness. Contact lenses may also provide a better optical magnification to reduce the difference in image size. The difference in magnification can also be eliminated by a combination of contact lenses and glasses (creating a weak telescope system). The optimum design solution will depend on different parameters like cost, cosmetic implications, and if the patient can tolerate wearing a contact lens.

Note however that before the optics can be designed, first the aniseikonia should be known=measured. When the image disparity is astigmatic (cylindrical) and not uniform, images can appear wider, taller, or diagonally different. When the disparity appears to vary across the visual field (field-dependent aniseikonia), as may be the case with an epiretinal membrane or retinal detachment, the aniseikonia cannot fully be corrected with traditional optical techniques like standard corrective lenses. However, partial correction often improves the patient's vision comfort significantly. Little is known yet about the possibilities of using surgical intervention to correct aniseikonia.

When this magnification difference becomes excessive the effect can cause diplopia, suppression, disorientation, eyestrain, headache, and dizziness and balance disorders.

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

The diagnosis of BRVO is made clinically by finding retinal hemorrhages in the distribution of an obstructed retinal vein.

- Fluorescein angiography is a helpful adjunct. Findings include delayed venous filling, hypofluorescence caused by hemorrhage and capillary nonperfusion, dilation and tortuosity of veins, leakage due to neovascularization and macular edema.

- Optical coherence tomography is an adjunctive test in BRVO. Macular edema is commonly seen in BRVO in OCT exams. Serial OCT is used as a rapid and noninvasive way of monitoring the macular edema.

Distorted vision is a symptom with several different possible causes.

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.

Leukocoria (also leukokoria or white pupillary reflex) is an abnormal white reflection from the retina of the eye. Leukocoria resembles eyeshine, but leukocoria can occur in humans and other animals that lack eyeshine because their retina lacks a "tapetum lucidum".

Leukocoria is a medical sign for a number of conditions, including Coats disease, congenital cataract, corneal scarring, melanoma of the ciliary body, Norrie disease, ocular toxocariasis, persistence of the tunica vasculosa lentis (PFV/PHPV), retinoblastoma, and retrolental fibroplasia.

Because of the potentially life-threatening nature of retinoblastoma, a cancer, that condition is usually considered in the evaluation of leukocoria. In some rare cases (1%) the leukocoria is caused by Coats' disease (leaking retinal vessels).

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

Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. Prophylactic use of Nonsteroidal anti-inflammatory drugs has been reported to reduce the risk of macular edema to some extent.

In 2010 the US FDA approved the use of Lucentis intravitreal injections for macular edema.

Iluvien, a sustained release intravitreal implant developed by Alimera Sciences, has been approved in Austria, Portugal and the U.K. for the treatment of vision impairment associated with chronic diabetic macular edema (DME) considered insufficiently responsive to available therapies. Additional EU country approvals are anticipated.

In 2013 Lucentis by intravitreal injection was approved by the National Institute for Health and Care Excellence in the UK for the treatment of macular edema caused by diabetes and/or retinal vein occlusion.

On July 29, 2014, Eylea (aflibercept), an intravitreal injection produced by Regeneron Pharmaceuticals Inc., was approved to treat DME in the United States.

In 2005, steroids were investigated for the treatment of macular edema due to retinal blood vessel blockage such as CRVO and BRVO.

Non-surgical treatments of FCED may be used to treat symptoms of early disease. Medical management includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. Hypertonic saline draws water out of the cornea through osmosis. When using a hairdryer, the patient is instructed to hold it at an arm's length or directed across the face on a cold setting, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation. The most common types of surgery for FCED are Descemet's stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK), which account for over half of corneal transplants in the United States.

More speculative future directions in the treatment of FED include in-vitro expansion of human corneal endothelial cells for transplantation, artificial corneas (keratoprosthesis) and genetic modification. Surgery where the central diseased endothelium is stripped off but not replaced with donor tissue, with subsequent Rho-Associated Kinase (ROCK) inhibition of endothelial cell division may offer a viable medical treatment.

A greater understanding of FED pathophysiology may assist in the future with the development of treatments to prevent progression of disease. Although much progress has been made in the research and treatment of FED, many questions remain to be answered. The exact causes of illness, the prediction of disease progression and delivery of an accurate prognosis, methods of prevention and effective nonsurgical treatment are all the subject of inquiries that necessitate an answer.

Increased attention must be given to research that can address the most basic questions of how the disease develops: what are the biomolecular pathways implicated in disease, and what genetic or environmental factors contribute to its progression? In addition to shaping our understanding of FED, identification of these factors would be essential for the prevention and management of this condition.