Uveitis

Uveitis is a general medical term for inflammation affecting the middle layer of the eye which is called the uvea. The uvea consists of 3 distinct structures: iris, ciliary body, and the choroid. The iris is the colored ring around the pupil of the eye; the choroid is a thin layer of blood vessels covering both the back and sides of the eye; and the ciliary body is a ring shaped structure between the iris and choroid that joins the iris with the retina, the inner layer of the eye. The ciliary body has two main functions: its muscles serve to focus the lens, and it also produces the aqueous humor, a nourishing liquid that bathes the front of the eye. Uveitis may affect any or all of these 3 parts of the eye.

The primary symptom of uveitis affecting the choroid, known as posterior uveitis, is a vague feeling of hazy or fading vision. Some people see black spots that seem to float before their eyes. Iritis, also known as anterior uveitis, is a type of uveitis that affects the iris, although the term is sometimes used for inflammation that includes the ciliary body as well. Iritis can cause redness, pain, blurred vision, an intolerance to light, and, sometimes, headaches.

Uveitis is often linked to an autoimmune disorder such as rheumatoid arthritis and other conditions which may have an autoimmune cause, but it can also be the result of infection. More often than not, there is no obvious cause. Uveitis can be a precursor of other eye problems, including glaucoma and detached retina. If you suspect you may have uveitis, then you should consult an ophthalmologist for a complete eye examination.

 


Signs, symptoms & indicators of Uveitis

Symptoms - Head - Eyes/Ocular  

Unilateral/bilateral eye pain



 

Vision disturbances



 

(High) sensitivity to bright light



 

Bloodshot eyes



Symptoms - Metabolic  

Current atypical recent headaches




Conditions that suggest Uveitis

Symptoms - Head - Eyes/Ocular  

Uveitis




Risk factors for Uveitis

Symptoms - Head - Eyes/Ocular  

History of uveitis



 

Past episodes of bloodshot eyes



Counter Indicators
Symptoms - Head - Eyes/Ocular  

Absence of uveitis




Uveitis suggests the following may be present

Autoimmune  



Recommendations for Uveitis

Drug  

Conventional Drugs / Information

Many uveitis specialists treat intermediate uveitis according to the method outlined by Kaplan. Patients whose visual acuity is better than 20/40 are generally not treated, unless they have CME, extensive neovascularization of the peripheral retina, extensive vasculitis, or if they complain of severe floaters. Patients whose visual acuity is 20/40 or worse usually are treated. As with most forms of uveitis, corticosteroids are the mainstay of therapy.

Topical therapy with prednisolone acetate 1% or prednisolone sodium phosphate 1% is only helpful in the treatment of the anterior segment inflammation. The intravitreal concentration of drugs administered topically is too low to be efficacious in the face of moderate-to-severe vitritis, especially in the phakic patient.

Periocular injections of corticosteroids are preferentially given in unilateral cases and occasionally in bilateral cases. Triamcinolone acetonide can be administered superotemporally into the sub-Tenon space or through the inferior eyelid into the retroseptal space. If the disease is not controlled after 2-3 injections given over an 8-week period, systemic prednisone should be considered. Some authorities advocate the use of a combination of betamethasone and depot methylprednisolone in an effort to achieve early onset and prolonged duration of action.

Oral prednisone may be the preferred treatment in patients with bilateral intermediate uveitis or in cases resistant to topical or periocular steroids. A purified protein derivative (PPD) test is imperative prior to starting any patient on systemic corticosteroids if there are any risk factors for TB. Once the inflammation stabilizes, the oral dose is tapered according to disease activity. An H2 blocker (Tagamet or Zantac) or a proton pump inhibitor (Prilosec or Prevacid) can be prescribed adjunctively to oral steroids.

Finally, intravitreal triamcinolone acetonide injections have been used to treat CME. In a small series by Androudi et al of 16 patients (20 eyes) with noninfectious uveitis and CME, of which 3 had intermediate uveitis, visual acuity improved in 11 eyes and improved but returned to baseline levels in another 5 eyes, respectively.

For recalcitrant cases with high corticosteroid requirements to control the inflammation, the surgical implantation of a device releasing fluocinolone acetonide in the vitreous can be considered (see Surgical Care).

In the event that corticosteroids cannot control the intermediate uveitis or in those whose disease invariably flares when steroids are discontinued, immunosuppressive therapy often is attempted. Immunosuppression or immune-modulation is also used as part of the concept of steroid-sparing therapy in an effort to reduce the patient’s requirement for systemic corticosteroids and, therefore, to diminish the adverse effects of systemic corticosteroid therapy.

Cyclosporine, tacrolimus, azathioprine, and methotrexate are the most commonly used agents with documented efficacy in many uveitic conditions. Chlorambucil can be considered for intractable cases. They can be used concurrently with corticosteroids as steroid sparing agents or alone.

Murphy et al prospectively evaluated the efficacy and the safety of cyclosporine and tacrolimus in patients with posterior and intermediate uveitis. The 2 agents did show a similar response rate (approximately 67%), but cyclosporine was associated with a higher incidence of adverse effects.

The use of infliximab, an anti-tumor necrosis factor (anti-TNF) monoclonal antibody, has been shown to be effective in improving macular thickness and visual acuity in patients with uveitic refractory CME due to intermediate uveitis or other noninfectious uveitis. Initial successful reports by Markomichelakis et al were duplicated by Rajaraman et al in a pediatric population in which infliximab achieved reduction in intraocular inflammation with concurrent elimination or decrease in steroid requirements.

More recently, daclizumab, an interleukin-2 receptor blocking antibody, has been shown to be effective in noninfectious uveitis in a multicenter nonrandomized interventional case series. It allowed control of ocular inflammation with stability in visual acuity with reduction of concomitant immunosuppression by at least 50%.

Finally, interferon-beta (INF-beta), which has an established value in the treatment of MS, appears to have a positive effect in terms of visual acuity, CME, and aqueous and vitreous inflammation in intermediate uveitis associated with MS. This information was taken from emedicine.com.



Key

Weak or unproven link
Strong or generally accepted link
Proven definite or direct link
Very strongly or absolutely counter-indicative
Highly recommended

Glossary

Ciliary

Often Ciliary activity: Activity of the eyelashes or any hairlike processes (cilia).

Retina

A 10-layered, frail nervous tissue membrane of the eye, parallel with the optic nerve. It receives images of outer objects and carries sight signals through the optic nerve to the brain.

Iritis

An inflammation of the iris of the eye.

Anterior

In the front or forward part of the organ or toward the head of the body.

Autoimmune Disease

One of a large group of diseases in which the immune system turns against the body's own cells, tissues and organs, leading to chronic and often deadly conditions. Examples include multiple sclerosis, rheumatoid arthritis, systemic lupus, Bright's disease and diabetes.

Rheumatoid Arthritis

A long-term, destructive connective tissue disease that results from the body rejecting its own tissue cells (autoimmune reaction).

Glaucoma

A disease of the eye characterized by vision loss due to an increase in the pressure of fluid within the eye. This rise in pressure results from a build-up of aqueous fluid and leads to progressive damage to the optic nerve that transmits visual signals to the brain. Over time, glaucoma can lead to a gradual loss in peripheral vision. There are usually no signs that you're developing glaucoma until vision loss occurs.

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