Retinopathy is diagnosed by an ophthalmologist or an optometrist during eye examination. Stereoscopic fundus photography is the gold standard for the diagnosis of retinopathy. Dilated fundoscopy, or direct visualization of the fundus, has been shown to be effective as well.

Imaging studies such as ultrasonography (US), Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) can aid diagnosis. On ultrasound, Coats' disease appears as a hyperechoic mass in the posterior vitreous without posterior acoustic shadowing; vitreous and subretinal hemorrhage may often be observed.

On CT, the globe appears hyperdense compared to normal vitreous due to the proteinaceous exudate, which may obliterate the vitreous space in advanced disease. The anterior margin of the subretinal exudate enhances with contrast. Since the retina is fixed posteriorly at the optic disc, this enhancement has a V-shaped configuration.

On MRI, the subretinal exudate shows high signal intensity on both T1- and T2-weighted images. The exudate may appear heterogeneous if hemorrhage or fibrosis is present. The subretinal space does not enhance with gadolinium contrast. Mild to moderate linear enhancement may be seen between the exudate and the remaining vitreous. The exudate shows a large peak at 1-1.6 ppm on proton MR spectroscopy.

Grossly, retinal detachment and yellowish subretinal exudate containing cholesterol crystals are commonly seen.

Microscopically, the wall of retinal vessels may be thickened in some cases, while in other cases the wall may be thinned with irregular dilatation of the lumen. The subretinal exudate consists of cholesterol crystals, macrophages laden with cholesterol and pigment, erythrocytes, and hemosiderin. A granulomatous reaction, induced by the exudate, may be seen with the retina. Portions of the retina may develop gliosis as a response to injury.

Generally speaking, people diagnosed with photic retinopathy recover visual acuity completely within two months, though more severe cases may take longer, or not see complete recovery at all.

Although there has been extensive research in the past decades on this disease, there is still no evidence based therapies for this condition. This condition is often diagnosed at an early age; usually as a teenager or young adult.

To make a specific diagnosis, intraocular fluid samples may be taken and sent for analysis. In some cases, blood or cerebrospinal fluid (CSF) are also tested. Imaging may be done to help make the diagnosis.

Photic retinopathy generally goes away on its own over time, but there is no specific treatment known to be reliable for speeding recovery. One path sometimes attempted, which has unclear results, is to treat the initial macular edema with corticosteroids.

There are two types of retinitis: Retinitis pigmentosa (RP) and cytomegalovirus (CMV) retinitis. Both conditions result in the swelling and damage to the retinitis. However, the key difference in both these conditions is that Retinitis pigmentosa is a genetic eye disease that you inherit from one or both of your parents. On the other hand, CMV retinitis develops from a viral infection in the retina. Although there is no cure for this disease, there are steps you can take to protect your eyes from worsening. Supplements can slow the progression of the disease and alleviate symptoms temporarily. Research also shows that vitamin A, lutein, and omega-3 fatty acids also help alleviate symptoms.

Patients with optic disc drusen should be monitored periodically for ophthalmoscopy, Snellen acuity, contrast sensitivity, color vision, intraocular pressure and threshold visual fields. For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer thickness. Associated conditions such as angioid streaks and retinitis pigmentosa should be screened for. Both the severity of optic disc drusen and the degree of intraocular pressure elevation have been associated with visual field loss. There is no widely accepted treatment for ODD, although some clinicians will prescribe eye drops designed to decrease the intra-ocular pressure and theoretically relieve mechanical stress on fibers of the optic disc. Rarely choroidal neovascular membranes may develop adjacent to the optic disc threatening bleeding and retinal scarring. Laser treatment or photodynamic therapy or other evolving therapies may prevent this complication.

Telemedicine programs are available that allow primary care clinics to take images using specially designed retinal imaging equipment which can then be shared electronically with specialists at other locations for review. In 2009, Community Health Center, Inc. implemented a telemedicine retinal screening program for low-income patients with diabetes as part of those patients annual visits at the Federally Qualified Health Center.

The diagnosis of CMV retinitis can be done via the following:

- Ophthalmic screening frequency is based on CD4 count,(CD4 < 50 cells/mL, 0- 35% possibility of CMV retinitis)

- BUN

- CD8+ T-lymphocyte count

- CMV DNA capture ( polymerase chain reaction (PCR) test)

- DNA PCR ( ocular fluids)

- Viral load

- Complete blood count

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.

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.

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

In most patients, optic disc drusen are an incidental finding. It is important to differentiate them from other conditions that present with optic disc elevation, especially papilledema, which could imply raised intracranial pressure or tumors. True papilledema may present with exudates or cotton-wool spots, unlike ODD. The optic disc margins are characteristically irregular in ODD but not blurred as there is no swelling of the retinal nerve fibers. Spontaneous venous pulsations are present in about 80 percent of patients with ODD, but absent in cases of true disc edema. Other causes of disc elevation clinicians must exclude may be: hyaloid traction, epipapillary glial tissue, myelinated nerve fibres, scleral infiltration, vitreopapillary traction and high hyperopia. Disorders associated with disc elevation include: Alagille syndrome, Down syndrome, Kenny-Caffey syndrome, Leber Hereditary Optic Neuropathy and linear nevus sebaceous syndrome.

The incidence and prevalence of PMD are unknown, and no studies have yet investigated its prevalence or incidence. However, it is generally agreed that PMD is a very rare condition. Some uncertainty regarding the incidence of PMD may be attributed to its confusion with keratoconus. PMD is not linked to race or age, although most cases present early in life, between 20 and 40 years of age. While PMD is usually considered to affect men and women equally, some studies suggest that it may affect men more frequently.

Several diseases have been observed in patients with PMD. However, no causal relationships have been established between any of the associated diseases and the pathogenesis of PMD. Such diseases include: chronic open-angle glaucoma, retinitis pigmentosa, retinal lattice degeneration, scleroderma, kerato-conjunctivitis, eczema, and hyperthyroidism.

Progressive vision loss in any dog in the absence of canine glaucoma or cataracts can be an indication of PRA. It usually starts with decreased vision at night, or nyctalopia. Other symptoms include dilated pupils and decreased pupillary light reflex. Fundoscopy to examine the retina will show shrinking of the blood vessels, decreased pigmentation of the nontapetal fundus, increased reflection from the tapetum due to thinning of the retina, and later in the disease a darkened, atrophied optic disc. Secondary cataract formation in the posterior portion of the lens can occur late in the disease. In these cases diagnosis of PRA may require electroretinography (ERG). For many breeds there are specific genetic tests of blood or buccal mucosa for PRA.

Absent a genetic test, animals of breeds susceptible to PRA can be cleared of the disease only by the passage of time—that is, by living past the age at which PRA symptoms are typically apparent in their breed. Breeds in which the PRA gene is recessive may still be carriers of the gene and pass it on to their offspring, however, even if they lack symptoms, and it is also possible for onset of the disease to be later than expected, making this an imperfect test at best.

An accurate diagnosis of retinitis pigmentosa relies on the documentation of the progressive loss photoreceptor cell function, confirmed by a combination of visual field and visual acuity tests, fundus and optical coherence imagery, and electroretinography (ERG),

Visual field and acuity tests measure and compare the size of the patient's field of vision and the clarity of their visual perception with the standard visual measurements associated with healthy 20/20 vision. Clinical diagnostic features indicative of retinitis pigmentosa include a substantially small and progressively decreasing visual area in the visual field test, and compromised levels of clarity measured during the visual acuity test. Additionally, optical tomography such as fundus and retinal (optical coherence) imagery provide further diagnostic tools when determining an RP diagnosis. Photographing the back of the dilated eye allows the confirmation of bone spicule accumulation in the fundus, which presents during the later stages of RP retinal degeneration. Combined with cross-sectional imagery of optical coherence tomography, which provides clues into photoreceptor thickness, retinal layer morphology, and retinal pigment epithelium physiology, fundus imagery can help determine the state of RP progression.

While visual field and acuity test results combined with retinal imagery support the diagnosis of retinitis pigmentosa, additional testing is necessary to confirm other pathological features of this disease. Electroretinography (ERG) confirms the RP diagnosis by evaluating functional aspects associated with photoreceptor degeneration, and can detect physiological abnormalities before the initial manifestation of symptoms. An electrode lens is applied to the eye as photoreceptor response to varying degrees of quick light pulses is measured. Patients exhibiting the retinitis pigmentosa phenotype would show decreased or delayed electrical response in the rod photoreceptors, as well as possibly compromised cone photoreceptor cell response.

The patient's family history is also considered when determining a diagnosis due to the genetic mode of inheritance of retinitis pigmentosa. At least 35 different genes or loci are known to cause "nonsyndromic RP" (RP that is not the result of another disease or part of a wider syndrome). Indications of the RP mutation type can be determine through DNA testing, which is available on a clinical basis for:

- (autosomal recessive, Bothnia type RP)

- (autosomal dominant, RP1)

- (autosomal dominant, RP4)

- (autosomal dominant, RP7)

- (autosomal dominant, RP13)

- (autosomal dominant, RP18)

- CRB1 (autosomal recessive, RP12)

- (autosomal recessive, RP19)

- (autosomal recessive, RP20)

For all other genes (e.g. DHDDS), molecular genetic testing is available on a research basis only.

RP can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner. X-linked RP can be either recessive, affecting primarily only males, or dominant, affecting both males and females, although males are usually more mildly affected. Some digenic (controlled by two genes) and mitochondrial forms have also been described.

Genetic counseling depends on an accurate diagnosis, determination of the mode of inheritance in each family, and results of molecular genetic testing.

In terms of the treatment of cytomegalovirus retinitis, oral valganciclovir, intravenous ganciclovir, IV foscarnet, and IV cidofovir are all efficient in the treatment of this condition. Also intravitreal injections, an injection of medicine into the vitreous near the retina, of foscarnet in concomitance with oral valganciclovir can be used for treatment as well.

Often individuals with CMV retinitis will need surgery for either retinal detachment or intravitreal instillation of ganciclovir. Retinal detachment occurs in up to 29% of affected eyes, repair being most effective with endolaser and silicone oil endotamponade.Intravitreal ganciclovir implant has the benefit of less systemic toxicity. An adverse effect of this is retinal detachment (and vitreous hemorrhage), also there is no systemic beneficial effect for cytomegalovirus organ disease.

A diagnosis of choroideremia can be made based on family history, symptoms, and the characteristic appearance of the fundus. However, choroideremia shares several clinical features with retinitis pigmentosa, a similar but broader group of retinal degenerative diseases, making a specific diagnosis difficult without genetic testing. Because of this choroideremia is often initially misdiagnosed as retinitis pigmentosa. A variety of different genetic testing techniques can be used to make a differential diagnosis.

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

Distorted vision is a symptom with several different possible causes.

Diagnosis of ARN is outlined by the American Uveitis Society. Though most diagnosis's of ARN are made by clinical features, a physician may take a vitreous sample and have it tested for herpes markers. Common lab tests that are run on the sample include a viral culture, viral PCR, direct/indirect immunofluorescence, viral antibody measurement.

The American Uveitis Society has established the following guidelines for ARN diagnosis:

1. Retinal necrosis with one or more focus points borders in the peripheral retina

2. In the absence of antiviral treatment, the condition progresses rapidly

3. Spreading to the surroundings

4. Buildup of blood vessels

5. Inflammation of the vitreous.

Diagnosis includes dilated fundus examination to rule out posterior uveitis, which presents with white spots across the retina along with retinitis and vasculitis.

Laboratory testing is usually used to diagnose specific underlying diseases, including rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor, angiotensin converting enzyme inhibitor <-- error) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis).

Major histocompatibility antigen testing may be performed to investigate genetic susceptibility to uveitis. The most common antigens include HLA-B27, HLA-A29 (in birdshot chorioretinopathy) and HLA-B51 (in Behçet disease).

Radiology X-ray may be used to show coexisting arthritis and chest X-ray may be helpful in sarcoidosis.

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.

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication including cataracts, glaucoma, band keratopathy, macular edema and permanent vision loss may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor into the outlook.