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Peripheral uveitis: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 23.04.2024
 
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Peripheral uveitis isolated in a separate nosological group in 1967.

The primary inflammatory focus is localized in the flat part of the vitreous humor and the peripheral part of the choroid in the form of a perivasculitis of the retina. As a result of inflammation, a pre-retinal cyclic membrane is formed, which can cause a rupture and detachment of the retina.

It is an inflammatory disease with a vascular factor. Most often, the first symptom is a decrease in vision due to opacity of the vitreous, as well as edema and macular degeneration. It is more common in young people, after the flu, ARI and other infections. The first symptom of this disease is a decrease in vision. When capturing the process of the ciliary body, there may be an opacification of the anterior chamber. If the exudate settles on the trabeculae, there may be a secondary uveitis.

If vascular phenomena predominate (periphlebitis, perivasculitis), bleeding can occur in the retina and vitreous humor, the iris is usually not clinically altered, and posterior synechiae are not formed. Changes in the anterior vitreous layers first have the form of small powdered opacities, which through different periods (from 6 months to 2 children) accumulate in the region of the flat part of the cilpum body and at the extreme periphery of the retina in the form of snow-like opacities or exudative masses. Peripheral exudate is the most significant and permanent sign of parsplanitis. It is white or grayish-white in color, dense, well-bound, localized near the dentate line, extending into the region of the ciliary body. Snow-like foci of peripheral exudate can be single or multiple. Determine their presence in the region of the flat part of the ciliary body when examining a three-mirror Goldman lens and scleral depression. The most frequent localization of such changes in the zone between 3 and 9 hours in the lower part of the anterior segment of the eye. By their nature, snowy masses lying on the flat part of the ciliary body, refer to inflammatory, exudative changes or to condensed areas of the vitreous. Their preferential localization in the lower zone of the flat part of the ciliary body is possibly related to the attraction of the vitreous humor to the inflammatory altered base or the fact that the largest number of vitreous cells is located in the lower ocular part.

In some cases, especially in young patients, there is a posterior detachment of the vitreous humor. The inflammation of the vitreous body caused by inflammation leads to tractive retinal tension, and sometimes to ruptures of the internal border membrane. There is also a development of a complex cataract starting at the back pole. Sometimes gradually, and sometimes quite quickly, it becomes complete. Often the process is complicated by the development of secondary glaucoma.

Cystic edema of the macular area and small edema of the optic nerve are typical symptoms accompanying parsplanitis. Sometimes there are changes in the vessels of the retina such as vasculitis or perivasculitis. After a partial resolution of the exudate in the atrophy zone, pigmentation, characteristic of hornroid disease, appears. The percentage correlation of complications of peripheral uveitis to the submitted literature is as follows: cataract - 60.7%, maculopathy - 42.8%, edema of the optic nerve - 17.8%.

To less frequent complications include retinal detachment, reticular hemorrhages. Thus, with peripheral uveitis, three stages of the process are noted;

  1. early stage - reduced visual acuity, external accommodation, cellular reaction in the anterior chamber and small corneal precipitates, appearance of cells in the vitreous body;
  2. an intermediate stage characterized by further deterioration of vision and the appearance of strabismus simultaneously with the increase in inflammatory phenomena in the vascular tract, expressed in photophobia, pain and the formation of exudate in the vitreous body;
  3. late stage, which is characterized by a sharp loss of vision due to cystic degeneration of the macula, the formation of posterior subcapsular cataracts and sometimes atrophy of the eyeball.

In the clinical manifestation of parsplatypia, forms of diffuse and focal inflammation are distinguished. Diffuse form corresponds to the described picture of the disease. With focal inflammation, granulomatous foci appear along the entire circumference of the flat part of the ciliary body without localization in any meridian. In the beginning, the granulomas are grayish, unclear. After their resolution, atrophic pigmented scars remain. In acute inflammatory processes in the stage of recovery, infiltration in the lower part of the base of the vitreous body disappears.

Chronic inflammatory processes, existing for a long time, lead to secondary changes in the form of scarring. Primarily affecting the vitreous cortex and internal layers of the retina, they cause fibrotic degeneration of the vitreous base and diffuse thickening of the periphery of the retina. Scarring can be common with the formation of cysts. Sometimes there are newly formed vessels and ruptures of the retina, leading to its detachment. An important feature that distinguishes the disease of parsplanitis is noted: scarring occurs only in the lower zone of the periphery of the retina, without affecting the flat part of the ciliary body. Sources of peripheral deposits of exudate are all inflammatory processes that capture the vitreous bark. Such deposits can quickly develop with focal chorioretinitis. In patients with disseminated peripheral chorioretinitis, exudate can cover the entire periphery of the retina, simulating the posterior cyclite pattern. However, the flat part of the ciliary body remains free of exudative deposits.

Analysis of clinical signs allows us to distinguish three criteria for differentiation of anterior and posterior uveitis with parsplanitis:

  • exudate is on the lower periphery;
  • he is always intravitreal;
  • the flat part of the ciliary body has no signs of inflammation in the initial phase of the disease, when certain morphological changes have not yet been formed.

The etiology of the disease is not established. Perhaps the involvement of the herpes virus and immunological factors.

trusted-source[1], [2], [3], [4], [5]

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