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.

The development of accurate and reliable non-invasive ICP measurement methods for VIIP has the potential to benefit many patients on earth who need screening and/or diagnostic ICP measurements, including those with hydrocephalus, intracranial hypertension, intracranial hypotension, and patients with cerebrospinal fluid shunts. Current ICP measurement techniques are invasive and require either a lumbar puncture, insertion of a temporary spinal catheter, insertion of a cranial ICP monitor, or insertion of a needle into a shunt reservoir.

Macular telangiectasia type 1 must be differentiated from secondary telangiectasis caused by retinal vascular diseases such as retinal venous occlusions, diabetic retinopathy, radiation retinopathy, sickle cell maculopathy, inflammatory retinopathy/Irvine–Gass syndrome, ocular ischemic syndrome/carotid artery obstruction, hypertensive retinopathy, polycythemia vera retinopathy, and localized retinal capillary hemangioma. In addition, Macular telangiectasia type 1 should be clearly differentiated from dilated perifoveal capillaries with evidence of vitreous cellular infiltration secondary to acquired inflammatory disease or tapetoretinal dystrophy. Less commonly, macular telangiectasis has been described in association with fascioscapulohumeral muscular dystrophy, incontinentia pigmenti, and familial exudative vitreoretinopathy with posterior pole involvement.

Macular telangiectasia type 2 is commonly under-diagnosed. The findings may appear very similar to diabetic retinopathy, and many cases ave been incorrectly ascribed to diabetic retinopathy or age-related macular degeneration. Recognition of this condition can save an affected patient from unnecessarily undergoing extensive medical testing and/or treatment. MacTel should be considered in cases of mild paramacular dot and blot hemorrhages and in cases of macular and paramacular RPE hyperplasia where no other cause can be identified.

Although MacTel is uncommon, its prevalence is probably higher than most physicians believe. The early findings are subtle, so the diagnosis is likely often missed by optometrists and general ophthalmologists. MacTel was detected in 0.1% of subjects in the Beaver Dam study population over age 45 years, but this is probably an underestimate because identification was made based only on color photographs.

No major new biomicroscopic features of MacTel have been identified since the early work of Gass and colleagues.

The advent of optical coherence tomography (OCT) has allowed better characterization of the nature of the inner and outer lamellar cavities. Loss of central masking seen on autofluorescence studies, apparently due to loss of luteal pigment, is now recognized as probably the earliest and most sensitive and specific MacTel abnormality.

The key fundus findings in macular telangiectasia type 2 involve retinal crystalline—fine, refractile deposits in the superficial retinal layers—may be seen within the affected area.a focal area of diminished retinal transparency (i.e. "greying") and/or small retinal hemorrhages just temporal to the fovea. Dilated capillaries may also be noted within this area, and while this is often difficult to visualize ophthalmoscopically, the abnormal capillary pattern is readily identifiable with fluorescein angiography.

Areas of focal RPE hyperplasia, i.e.pigment plaques, often develop in the paramacular region as a response to these abnormal vessels. Other signs of macular telangiectasia type 2 include right angle venules, representing an unusual alteration of the vasculature in the paramacular area, with vessels taking an abrupt turn toward the macula as if being dragged.

Diagnosis of MacTel type 2 may be aided by the use of advanced imaging techniques such as fluorescein angiography, fundus autofluorescence, and OCT. These can help to identify the abnormal vessels, pigment plaques, retinal crystals, foveal atrophy and intraretinal cavities associated with this disorder.

Fluorescein angiography (FA) is helpful in identifying the anomalous vasculature, particularly in the early stages of Type 2 disease. Formerly, FA was essential in making a definitive diagnosis. However, the diagnosis can be established with less invasive imaging techniques such as OCT and fundus autofluorescence. Some clinicians argue that FA testing may be unnecessary when a diagnosis is apparent via less invasive means.

The natural history of macular telangiectasia suggests a slowly progressive disorder. A retrospective series of 20 patients over 10 to 21 years showed deterioration of vision in more than 84% of eyes, either due to intra-retinal edema and serous retinal detachment (Type 1) or pigmented RPE scar formation or neovascularisation (Type 2).

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.

In general, BRVO has a good prognosis: after 1 year 50–60% of eyes have been reported to have a final VA of 20/40 or better even without any treatment. With time the dramatic picture of an acute BRVO becomes more subtle, hemorrhages fade so that the retina can look almost normal. Collateral vessels develop to help drain the affected area.

Risk factors and underlying mechanisms based on anatomy, physiology, genetics and epigenetics need to be researched further.

The following actions have been recommended to assist in the research of vision impairment and increased intracranial pressure associated with long-duration space flight:

In the UK, screening for diabetic retinopathy is part of the standard of care for people with diabetes. After one normal screening in people with diabetes, further screening is recommended every two years. Teleophthalmology has been employed in these programs.

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.

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.

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.

Diabetic retinopathy is diagnosed entirely by recognizing abnormalities on retinal images taken by fundoscopy. Color fundus photography is mainly used for staging the disease. Fluorescein angiography is used to assess the extent of retinopathy that aids in treatment plan development. Optical coherence tomography (OCT) is used to determine the severity of edema and treatment response.

Because fundoscopic images are the main sources for diagnosis of diabetic retinopathy, manually analyzing those images can be time-consuming and unreliable, as the ability of detecting abnormalities varies by years of experience. Therefore, scientists have explored developing computer-aided diagnosis approaches to automate the process, which involves extracting information about the blood vessels and any abnormal patterns from the rest of the fundoscopic image and analyzing them.

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

Penetrating karatoplasty and endothelial keratoplasty can be used as treatments for severe cases of ICE [2,8]. Because glaucoma and elevated intraocular pressure are often present in ICE patients, long term follow up may be needed to ensure adequate intraocular pressures are maintained [2,7]

The disease is chronic and often progresses slowly. Prognosis is generally poor when associated with glaucoma [1,2].

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.

Fuchs' dystrophy, also referred to as Fuchs' corneal endothelial dystrophy (FCED) and Fuchs' endothelial dystrophy (FED), is a slowly progressing corneal dystrophy that usually affects both eyes and is slightly more common in women than in men. Although early signs of Fuchs' dystrophy are sometimes seen in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

The condition was first described by Austrian ophthalmologist Ernst Fuchs (1851–1930), after whom it is named. In 1910, Fuchs first reported 13 cases of central corneal clouding, loss of corneal sensation and the formation of epithelial bullae, or blisters, which he labeled 'dystrophia epithelialis corneae'. It was characterized by late onset, slow progression, decreased visual acuity in the morning, lack of inflammation, diffuse corneal opacity, intense centrally, and roughened epithelium with vesicle-like features.

A shift to the understanding of FCED as primarily a disease of the corneal endothelium resulted after a number of observations in the 1920s. Crystal-like features of the endothelium were noted by Kraupa in 1920, who suggested that the epithelial changes were dependent on the endothelium. Using a slit lamp, Vogt described the excrescences associated with FCD as drop-like in appearance in 1921. In 1924, Graves then provided an extremely detailed explanation of the endothelial elevations visible with slit-lamp biomicroscopy. A patient with unilateral epithelial dystrophy and bilateral endothelial changes was described by the Friedenwalds in 1925; subsequent involvement of the second eye led them to emphasize that endothelial changes preceded epithelial changes. As only a subset of patients with endothelial changes proceeded to epithelial involvement, Graves stated on 19 October 1925 to the New York Academy of Medicine that "Fuchs' epithelial dystrophy may be a very late sequel to severer cases of the deeper affection".

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

Many studies of the mechanical properties of brain edema were conducted in the 2010, most of them based on finite element analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used the finite element method to study changes in intracranial pressure during craniotomy operations. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.

The diagnosis is typically made clinically with magnetic resonance imaging of the brain often revealing hyperintensities on "T"-weighed imaging. Three patterns have been described: superior frontal sulcus, dominant parieto-occipital, and holohemispheric watershed.

Treatment approaches can include osmotherapy using mannitol, diuretics to decrease fluid volume, corticosteroids to suppress the immune system, hypertonic saline, and surgical decompression to allow the brain tissue room to swell without compressive injury.

Clinical signs of cerebral edema, such as focal neurological deficits, papilledema and decreased level of consciousness, if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes.

MRI of the head has been used in research to better understand DDS.

Reinke's edema is often diagnosed by an Ear, Nose & Throat (ENT) specialist or an Otolaryngologist by examination of the vocal cords. First, the doctor will review the patient's medical history and symptoms, such as hoarseness, dysphonia, and reduced vocal range. There is no familial or hereditary link to Reinke's edema. Because Reinke's edema is linked heavily to smoking, the doctor will need to know if the patient is a habitual smoker. Once the patient's history is reviewed, the vocal cords will be visualized using laryngoscopy, a technique in which a tube with a camera (endoscope) is passed through the nose and down the larynx. Laryngoscopes can be rigid or flexible. Flexible laryngoscopes, such as fiber laryngoscopes, allow the patient to produce sound as the tube is placed, and therefore allows the doctor to visualize movement of the vocal cord.

Based on the results of the laryngoscopy, Reinke's edema can be classified using a standardized system set in place by Yonekawa. This system characterizes the disease based disease .

Yonekawa Classification:

- Grade I – Lesions contact the anterior third of the vocal fold

- Grade II – Lesions contact the anterior two-thirds of the vocal fold

- Grade III – Lesions contact the entirety of the vocal fold

If further evaluation is needed, stroboscopy is used to examine mucosal waves of the vocal cords. Mucosal waves describe the waves produced by vibration of the vocal cords during speech. Stroboscopes produce flashes of light that are timed to the patient's vocal frequency. Every time the light is flashed, it will create a still frame image of the vocal cords at that particular moment in time. These are combined to produce an image of the wave. In the case of Reinke's edema, structural changes to the vocal cords will result in abnormal wave patterns.

The diagnosis of protein losing enteropathy is made by excluding other causes of protein loss. Endoscopy can be used to localize the cause of the protein loss in the bowel. Different methods include faecal excretion of alpha 1-antitrypsin which is a marker of protein losing enteropathy, as well as, viral serologies which may be useful to detect PLE.