Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or as oral therapy. Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluoresence dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis increases T-regulatory cells in the eye, which likely contributes to disease regression.

In some cases an injection of posterior subtenon triamcinolone acetate may also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatments with Infliximab or other anti-TNF infusions may prove helpful.

The anti-diabetic drug metformin is reported to inhibit the process that causes the inflammation in uveitis.

In the case of herpetic uveitis, anti-viral medications, such as valaciclovir or aciclovir, may be administered to treat the causative viral infection.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

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.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

In very severe cases of necrotizing scleritis, eye surgery must be performed to repair damaged corneal tissue in the eye and preserve the patient's vision. For less severe cases, nonsteroidal anti-inflammatory drugs, such as ibuprofen, are prescribed for pain relief. Scleritis itself is treated with an oral medication containing corticosteroids and an eye solution. In some cases, antibiotics are prescribed. Simply using eye drops will not treat scleritis. In more aggressive cases of scleritis, chemotherapy (such as systemic immunosuppressive therapy with such drugs as cyclophosphamide or azathioprine) may be used to treat the disease. If not treated, scleritis can cause blindness.

Currently treatment of ARN consists of antiviral therapy administered orally. Typical antiviral agents used include famciclovir, valganciclovir, and valacyclovir. While on these medications, a patient's kidney function should be watched. Some physician's also may administer the antiviral agents via intravitreal delivery. Though controversial, some physicians administer steroids (prednisone) and antithrombotic therapy (aspirin).

Some commonly admistered antiviral agents are as follows:

- Acyclovir

- Famciclovir

- Valacyclovir

- Gancicilovir

- Valganciclovir

While there is no prevention for ARN, exposing a patient to antiviral agents in the earlier phases of the outbreak tend to decrease the duration of the active phase of the disease. Taking antiviral agents after the issue is resolved seems to lessen the chance of it spreading to the other eye.

Often, treatment is not necessary, because episcleritis is a self-limiting condition. Artificial tears may be used to help with irritation and discomfort. More severe cases can be treated with either topical corticosteroids or oral non-steroidal anti-inflammatory drugs.

Ketorolac, a topical NSAID, may be used, but it is not more effective than artificial tears and it causes more side effects.

Horses that suffer from this disease can never be considered cured, although they can be managed by careful use of the therapy described above, and fast detection of new flare-ups. If the disease is not properly treated, it will eventually lead to blindness.

Birdshot chorioretinopathy may show resistance to treatment. Immunosuppressant therapy along with oral corticosteroid has been somewhat effective in slowing down the progressive inflammation associated with the disorder, preserving visual integrity as much as possible. Long-term use of such medications must be closely monitored, however, due to the discomforting and potentially debilitating and life-threatening side-effects.

Immunosuppressive drugs such as the therapeutic monoclonal antibody daclizumab, ciclosporin and methotrexate have proven to be effective treatment options for birdshot chorioretinopathy. Substantial reduction and even stabilization of both vitreous inflammation and retinal vasculitis have been evident via electroretinography, during daclizumab (IL-2 receptor blocker) therapy. This is also supported by the observation of elevated levels of IL-2 in the eyes of patients. Loss of visual acuity unrelated to the inflammation caused by the disorder, however, often remains unchanged despite usage of the drug. This is reflected by the lack of difference in visual acuity and the vision-related quality of life among various treatment categories in birdshot patients. Contraindications and adverse side-effects are always a factor, as well.

For the allergic type, cool water poured over the face with the head inclined downward constricts capillaries, and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, nonsteroidal anti-inflammatory medications and antihistamines may be prescribed. Persistent allergic conjunctivitis may also require topical steroid drops.

Viral conjunctivitis usually resolves on its own and does not require any specific treatment. Antihistamines (e.g., diphenhydramine) or mast cell stabilizers (e.g., cromolyn) may be used to help with the symptoms. Povidone iodine has been suggested as a treatment, but as of 2008 evidence to support it was poor.

Because SO is so rarely encountered following eye injury, even when the injured eye is retained, the first choice of treatment may not be enucleation or evisceration, especially if there is a chance that the injured eye may regain some function. Additionally, with current advanced surgical techniques, many eyes once considered nonviable now have a fair prognosis.

However, only if the injured eye has completely lost its vision and has no potential for any visual recovery, prevention of SO is done by enucleation of the injured eye preferably within the first 2 weeks of injury. Evisceration—the removal of the contents of the globe while leaving the sclera and extraocular muscles intact—is easier to perform, offers long-term orbital stability, and is more aesthetically pleasing, i.e., a greater measure of movement of the prosthesis and thus a more natural appearance. There is concern, however, that evisceration may lead to a higher incidence of SO compared to enucleation. Several retrospective studies involving over 3000 eviscerations, however, have failed to identify a single case of SO.

Once SO is developed, Immunosuppressive therapy is the mainstay of treatment. When initiated promptly following injury, it is effective in controlling the inflammation and improving the prognosis. Mild cases may be treated with local application of corticosteroids and pupillary dilators. More severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc.), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.

The acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. However, ocular complications may require an subtenon or intravitreous injection of corticosteroids or bevacizumab. In refractory situations, other immunosuppressives such as cyclosporine, or tacrolimus, antimetabolites (azathioprine, mycophenolate mofetil or methotrexate), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed.

Chorioretinitis is usually treated with a combination of corticosteroids and antibiotics. However, if there is an underlying cause such as HIV, specific therapy can be started as well.

A 2012 Cochrane Review found weak evidence suggesting that ivermectin could result in reduced chorioretinal lesions in patients with onchocercal eye disease. More research is needed to support this finding.

It is important to distinguish between treatment of the underlying inflammation (PIC) and the treatment of CNV.

2-pronged approach:

Treatment is not always necessary and observation may be appropriate for lesions if they are found in non-sight threatening areas (that is not centrally).

Active lesions of PIC can be treated with corticosteroids taken systemically (tablets) or regionally by injections around the eye (periorbital). It has been argued that treating lesions in this way may help minimise the development of CNV.

The treatment of CNV:

Early treatment is required for this complication. There are several possible treatment methods, but none of these treatments appears to be singly effective for the treatment of CNV.

1. Corticosteroids: systemic or intraocular

2. ‘Second line’ immunosuppressants: There is evidence that combined therapies of steroids and second line immunosuppressants may be important.

3. Surgical excision of the affected area in well selected cases.

4. Intravitreal anti-VEGF agents. Examples are bevacizumab (avastin) and ranibizumab. These relatively new drugs are injected into the eye.

5. Photodynamic therapy (PDT): A photosensitive drug is ‘activated’ by strong light. Consideration may be given to combined therapy of PDT and anti VEGF.

6. Laser photocoagulation: This is occasionally used unless the CNV is subfoveal (affecting the central or macular part of the vision). The laser treatment can damage the vision.

The use of the intravitreal anti VEGF agents namely bevacizumab and ranibizumab have been described recently. The current evidence supporting the use of anti-VEGF agents is based on retrospective case studies and could not be described as strong. However, further data from prospective controlled trials are needed before the therapeutic role of anti-VEGF therapy in the uveitis treatment regimen can be fully determined. The anti VEGF agents furthermore have not been shown to have an anti-inflammatory effect.

Thus, treatment of the underlying inflammatory disease should play a central role in the management of uveitic CNV. A two-pronged treatment that focuses on achieving control of inflammation through the use of corticosteroids and/or immunosuppressive agents, while treating

complications that arise despite adequate disease control with intravitreal anti-VEGF agents, may be useful.

Regular monitoring is essential to achieve a good outcome. This is because even if there is no active inflammation, there may still be occult CNV which requires treatment to avoid suffering vision loss.

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.

Owing to the self-limiting nature of the disease, treatment is generally not required. In cases where lesions appear to be interfering with the optic nerve, methyl prednisone is prescribed.

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

Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. Chronic eye effects such as cataracts, glaucoma, and optic atrophy can occur. Skin changes usually persist despite therapy.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

Clinical signs include redness of the eye, pain, blurring of vision, photophobia and floaters.

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

Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. The quality of the evidence for treating the oral ulcers associated with Behçet's disease, however, is poor.

High-dose corticosteroid therapy is often used for severe disease manifestations. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease. Another Anti-TNF agent, etanercept, may be useful in people with mainly skin and mucosal symptoms.

Interferon alpha-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers as well as ocular lesions. Azathioprine, when used in combination with interferon alpha-2b also shows promise, and colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis.

Thalidomide has also been used due to its immune-modifying effect. Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions.

Given its rarity, the optimal treatment for acute optic neuropathy in Behçet's disease has not been established. Early identification and treatment is essential. Response to ciclosporin, periocular triamcinolone, and IV methylprednisone followed by oral prednisone has been reported although relapses leading to irreversible visual loss may occur even with treatment. Immunosuppressants such as interferon alpha and tumour necrosis factor antagonists may improve though not completely reverse symptoms of ocular Behçet's disease, which may progress over time despite treatment. When symptoms are limited to the anterior chamber of the eye prognosis is improved. Posterior involvement, particularly optic nerve involvement, is a poor prognostic indicator. Secondary optic nerve atrophy is frequently irreversible. Lumbar puncture or surgical treatment may be required to prevent optic atrophy in cases of intracranial hypertension refractory to treatment with immunomodulators and steroids.

IVIG could be a treatment for severe or complicated cases.

Proper diagnosis is essential for optimal treatment. Bacterial corneal ulcer require intensive fortified antibiotic therapy to treat the infection. Fungal corneal ulcers require intensive application of topical anti-fungal agents. Viral corneal ulceration caused by herpes virus may respond to antivirals like topical acyclovir ointment instilled at least five times a day. Alongside, supportive therapy like pain medications are given, including topical cycloplegics like atropine or homatropine to dilate the pupil and thereby stop spasms of the ciliary muscle. Superficial ulcers may heal in less than a week. Deep ulcers and descemetoceles may require conjunctival grafts or conjunctival flaps, soft contact lenses, or corneal transplant. Proper nutrition, including protein intake and Vitamin C are usually advised. In cases of Keratomalacia, where the corneal ulceration is due to a deficiency of Vitamin A, supplementation of the Vitamin A by oral or intramuscular route is given. Drugs that are usually contraindicated in corneal ulcer are topical corticosteroids and anesthetics - these should not be used on any type of corneal ulcer because they prevent healing, may lead to superinfection with fungi and other bacteria and will often make the condition much worse.