Chorioiditis

The term "choroiditis" unites a large group of diseases of inflammatory genesis, developing in the choroid itself. Isolated choroiditis is observed rarely, since the retina and optic nerve are usually involved in the pathological process early, resulting in chorioretinitis, neuroretinochoroiditis or neurouveitis.

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Causes choroiditis

The occurrence of inflammatory diseases of the choroid is caused by 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 infections that cause the development of choroiditis are toxoplasmosis, tuberculosis, histoplasmosis, toxocariasis, candidiasis, syphilis, as well as viral infections (mainly the herpes group), which can cause a clinical picture of acute neuroretinochoroiditis or cause severe widespread chorioretinitis in conditions of immunosuppression (in AIDS, organ transplantation, etc.). The anatomical structure of the choroid creates favorable conditions for the development of the inflammatory process, since the vascular network of the choroid is the site of passage and deposition of a large number of infectious agents, toxic products and antigens.

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Risk factors

Risk factors for the development of choroiditis include trauma, hypothermia, weakening of the body, etc.

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Pathogenesis

To date, the significance of the infectious factor in the pathogenesis of choroiditis has not been finally determined and is a subject for discussion in the literature, although its role in viral infections and in patients with suppressed immunity is obvious. Great importance is attached to genetic factors (genetic control of the immune response) and local cellular reactions. One of the main links in the pathogenesis of choroiditis is autoimmune reactions to various antigens, including their own (retinal S-antigen), arising in connection with damage to eye tissue, for example, with the persistence of a virus or the deposition of immune complexes.

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Symptoms choroiditis

Complaints of flashes, flickering and flying "flies" before the eyes, fogging and decreased vision, floating opacities, distortion of objects, decreased twilight vision occur when the process is localized in the posterior part of the eye, involving the retina and vitreous body in the pathological process. When the inflammation focus is peripherally located, complaints are often absent, and therefore the disease is detected accidentally during ophthalmoscopy.

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Forms

Choroiditis can be endogenous, i.e. caused by viruses, bacteria or protozoa and parasites circulating in the blood, and exogenous, occurring with traumatic iridocyclitis and corneal diseases.

Based on the localization of the process, choroiditis is divided into central (the infiltrate is located in the macular region), peripapillary (the focus of inflammation is localized near or around the optic nerve head), equatorial (in the equatorial zone) and peripheral (on the periphery of the fundus near the dentate line).

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

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Complications and consequences

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

In the focal process, a limited infiltrate consisting of lymphoid elements is found around the dilated vessels in all layers of the choroid proper. In diffuse choroiditis, the inflammatory infiltrate consists of lymphocytes, epithelioid and giant cells compressing the vascular plexus. When the retina is involved in the pathological process, destruction of the pigment epithelium layer, edema and hemorrhage are observed. 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. The remnants of altered large choroidal vessels are preserved in the newly formed scar, and proliferation of the retinal pigment epithelium is observed along the periphery of the scar.

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Diagnostics choroiditis

The diagnosis is established based on the results of direct and reverse ophthalmoscopy, FAG, immunological and biochemical studies, ERG and EOG recording, etc. In 30% of cases, the etiology cannot be determined.

Ophthalmoscopy reveals chorioretinal infiltrates, paravascular exudates, which correspond to scotomas in the visual field. With active inflammation, grayish or yellowish foci with fuzzy edges protruding into the vitreous body are visible on the fundus; the retinal vessels pass over them without interruption. The foci of inflammation may vary in size and shape, most often round, their size is equal to 0.5-1.5 times the diameter of the optic nerve disc. Smaller or very large foci are rarely observed. During this period, hemorrhages into the choroid, retina and vitreous body are possible. As the process progresses, retinal clouding is observed 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 body due to its infiltration by cellular elements and the formation of membranes. Under the influence of treatment, the chorioretinal focus flattens, becomes transparent, and acquires clearer edges. When the inflammatory process subsides, pigmentation in the form of small dots appears at the border of the lesion. Small and medium vessels of the choroid disappear at the site of the lesion, the choroid becomes thinner, and the sclera shines through. Ophthalmoscopy shows a white lesion or lesion with large vessels of the choroid and pigment lumps. Clear boundaries and pigmentation of the lesion indicate the transition of inflammation to the stage of atrophy of the choroid and retinal pigment epithelium.

When the inflammation is located near the optic nerve disc, the inflammatory process may spread to the optic nerve. In such cases, a characteristic scotoma appears in the visual field, merging with the physiological one. Ophthalmoscopy reveals blurred borders of the optic nerve. Peripapillary chorioretinitis develops, called periapillary neuroretinitis, Jensen's juxtapapillary retinochoroiditis, or circumpapillary retinitis.

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Differential diagnosis

Differential diagnostics are performed with external exudative retinitis, nevus and choroidal melanoma at an early stage. Unlike choroiditis, exudative retinitis is characterized by vascular changes in the retina, micro- and macroaneurysms, arterial shunts detected by ophthalmoscopy and FAG. Choroidal nevus is defined by ophthalmoscopy as a flat slate-colored or gray-slate-colored area with clear boundaries, the retina above it is unchanged, visual acuity is not reduced. Choroidal melanoma has characteristic clinical and functional symptoms. The diagnosis is clarified using electrophysiological (ERG, EOG registration), ultrasound and radioisotope studies.