Choroiditis

The term "choroiditis" unites a large group of inflammatory diseases, developing in the actual choroid of the eye. Isolated choroiditis is rarely observed, as the retina and the optic nerve are usually involved early in the pathological process, as a result of which chorioretinitis, neurooretiochoroiditis, or neuroneitis develops.

[1], [2], [3], [4], [5], [6]

Causes of the choroiditis

The occurrence of inflammatory diseases of the choroid are responsible for bacterial, viral, parasitic, fungal, toxic, radiation, allergic agents. Choroiditis can be a manifestation of a number of systemic diseases, as well as some immunopathological conditions. The most common development of choroiditis is caused by infections such as toxoplasmosis, tuberculosis, histoplasmosis, toxocariasis, candidiasis, syphilis, as well as viral infections (mainly herpes groups) that can cause a clinical picture of acute neuroretochoroiditis or cause severe common chorioretinitis under immunosuppression (in AIDS, transplantation of organs, etc.). The anatomical structure of the choroid creates favorable conditions for the development of the inflammatory process, since the choroidal vasculature is the place of passage and deposition of a large number of infectious agents, toxic products and antigens.

[7], [8]

Risk factors

The risk factors for choroiditis include trauma, hypothermia, weakening of the body, etc.

[9], [10], [11], [12], [13],

Pathogenesis

Until now, the importance of the infectious factor in the pathogenesis of choroiditis has not been fully determined and is subject to debate in the literature, although its role in viral infection and in patients with suppressed immunity is obvious. Great importance is attached to genetic factors (genetic control of the immune response) and local cellular responses. One of the main links in the pathogenesis of choroiditis are autoimmune reactions to various antigens, including the own (retinal S-antigen) arising from damage to the eye tissues, for example, during the persistence of the virus or the deposition of immune complexes.

[14], [15], [16], [17], [18], [19], [20], [21], [22],

Symptoms of the choroiditis

Complaints about outbreaks, flickering and flying "flies" before the eyes, fogging and loss of vision, floating opacities, distortion of objects, reduction of twilight vision occur when the process is localized in the back of the eye, involving the pathological process of the retina and vitreous. With the peripheral location of the inflammation focus, complaints are often absent, which is why the disease is detected accidentally with ophthalmoscopy.

[23], [24], [25], [26],

Forms

Choroiditis can be endogenous, that is, caused by viruses, bacteria or protozoa and parasites circulating in the blood, and exogenous, arising from traumatic iridocyclitis and corneal diseases.

By localization of the process, the choroiditis is divided into the central ones (the infiltrate is located in the macular area), peripapillary (the focus of inflammation is localized near or around the optic nerve disc), equatorial (in the equatorial zone) and peripheral (on the periphery of the eye bottom near the dentate line).

Depending on the prevalence of the process, the choroiditis can be focal (focal), multifocal disseminated (multifocal) and diffuse.

[27], [28], [29]

Complications and consequences

Choroiditis can be complicated by secondary dystrophy and exudative retinal detachment, neuritis with the transition to secondary optic atrophy, extensive haemorrhage into the vitreous with subsequent mooring. Hemorrhages in the choroid and retina can lead to the formation of coarse connective tissue scars and the formation of neovascular membranes, which is accompanied by a significant decrease in visual acuity.

In the focal process, a limited infiltrate around the dilated vessels, consisting of lymphoid elements, is found in all layers of the vascular envelope itself. In diffuse choroiditis, the inflammatory infiltrate consists of lymphocytes, epithelioid and giant cells that compress the vascular plexus. When involved in the pathological process of the retina, destruction of the layer of pigment epithelium, edema and hemorrhage are noted. As the process develops, the cellular elements of the infiltrate are replaced by fibroblasts and connective tissue fibers, resulting in the formation of scar tissue. In the newly formed rumen, the remains of the altered large vessels of the choroid remain, and on the periphery of the scar there is a proliferation of retinal pigment epithelium.

[30], [31], [32], [33], [34], [35],

Diagnostics of the choroiditis

Diagnosis is established on the basis of the results of direct and reverse ophthalmoscopy, PHAG, immunological and biochemical studies, registration of ERG and EOG, etc. In 30% of cases, etiology can not be determined.

Ophthalmoscopy reveals chorioretinal infiltrates, paravascular exudates, which correspond to scotoma in the field of vision. With active inflammation on the fundus there are grayish or yellowish foci with indistinct contours, penetrating into the vitreous, the retinal vessels pass over them without interruption. The centers of an inflammation can be various in size and the form, more often round, their size is equal 0,5-1,5 diameter of a disk of an optic nerve. Rarely small or very large foci are observed. During this period, hemorrhages in the choroid, retina and vitreous are possible. When the process progresses, the retina becomes clouded over the choroidal focus, small retinal vessels in the edema zone become invisible. In some cases, clouding develops in the posterior parts of the vitreous humor due to infiltration of its cellular elements and the formation of membranes. Under the influence of treatment, the chorioretinal focus is flattened. Becomes transparent, acquires more precise contours. When the inflammatory process subsides, pigmentation in the form of small dots appears on the border of the focus. In the place of the focus, the small and medium vessels of the choroid disappear, which is thinned, and through it the sclera shines. With ophthalmoscopy, a white foci or foci with large choroid vessels and pigmented lumps are seen. Clear boundaries and pigmentation of the focus indicate the transition of inflammation to the stage of atrophy of the choroid and retinal pigment epithelium.

When the focus of inflammation is located near the optic nerve disk, the inflammatory process can spread to the optic nerve. In such cases, a characteristic scotoma appears in the field of vision, merging with the physiological scotoma. When ophthalmoscopy is defined stsenicity of the boundaries of the optic nerve. Peripapillary chorioretinitis, called peri-papillary neuroretinitis, Jensen's juxtapapillary retinochoroiditis, or circumpapillary retinitis develops.

[36], [37], [38], [39], [40]

Differential diagnosis

Differential diagnosis is performed with external exudative retinitis, nevus and melanoma of the choroid in the initial stage. For exudative retinitis, in contrast to choroiditis, vascular changes in the retina, micro- and macroaneurysms, arterial shunts detected in ophthalmoscopy and FAH are characteristic. The nevi of the choroid in ophthalmoscopy is defined as a flat segment of aspid or gray-aspid color with clear boundaries, the retina above it is not changed, visual acuity is not reduced. Melanoma of the choroid has a characteristic clinical and functional symptomatology. The diagnosis is refined with the help of electrophysiological (registration of ERG, EOG), ultrasound and radioisotope studies.