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.

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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

The main goals of treatment are to decrease the risk of rebleeding within the eye, corneal blood staining, and atrophy of the optic nerve. Small hyphemas can usually be treated on an outpatient basis. Most treatment plans consist of elevating the head at night, wearing a patch and shield, and controlling any increase in intraocular pressure. Surgery may be necessary for non-resolving hyphemas, or hyphaemas that are associated with high pressure that does not respond to medication. Surgery can be effective for cleaning out the anterior chamber and preventing corneal blood staining.

Elevation of the head of the bed by approximately 45 degrees (so that the hyphema can settle out inferiorly and avoid obstruction of vision, as well as to facilitate resolution). Bedrest may be considered, although evidence suggests that it does not improve outcomes. Wearing of an eye shield at night time (to prevent accidental rubbing of the eyes during sleep, which can precipitate a rebleed). An eye patch should be worn throughout the day to protect the injured eye.

If pain management is necessary, acetaminophen can be used. Aspirin and ibuprofen should be avoided, because they interfere with platelets' ability to form a clot and consequently increase the risk of additional bleeding. Sedation is not usually necessary for patients with hyphema. It is controversial amongst ophthalmologists whether a steroid medication or a dilating eye drop (mydriatic) should be used in treatment of hyphema. Steroids aim to reduce the amount of inflammation, but also cause side effects. Dilating drops aim to increase comfort from the traumatized iris as well as reduce bleeding, but can also cause the pupil to be fixed in a dilated state via posterior synechiae (adhesions).

Aminocaproic or tranexamic acids are often prescribed for hyphema. Although these medications actually cause hyphemas to take longer to clear, they reduce the risk of rebleeding and its associated complications. Tranexamic and aminocaproic acids inhibit the conversion of plasminogen to plasmin, plasmin being the agent of fibrin breakdown in blood clots. Keeping the clots intact allows time for the vessels to heal properly and avert a secondary bleed.

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.

Topical antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye drops are applied to give rest to the eye. Pain medications are given as needed. Loose epithelium and ulcer base can be scraped off and sent for culture sensitivity studies to find out the pathogenic organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about a few weeks to several months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-healing ulcers, surgical intervention by an ophthalmologist with corneal transplantation may be required to save the eye. In all corneal ulcers it is important to rule out predisposing factors like diabetes mellitus and immunodeficiency.