LECTURE No. 18. Choroiditis

Choroiditis is an inflammation of the choroid itself.

Etiology and pathogenesis. The cause of the inflammatory process of the choroid is an infection (tuberculous, streptococcal, staphylococcal, viral, syphilitic, brucellosis). The structure and functions of the choroid are such that they contribute to the retention of bacteria, viruses, protozoa, helminths and other pathogens brought in with the blood or lymph flow.

The mechanism of development of choroiditis is based on immune reactions. The changes that determine the clinical picture of choroiditis are the result of antigens and immune complexes entering the eye. Extraocular foci of infection serve as sources of antigens. The occurrence of choroiditis can provoke hypothermia, acute and chronic infectious diseases, eye injury. Of particular importance is microbial allergy, manifested by hyperergic inflammation (hyperergy, increased reactivity). In this case, microbes can play the role of a trigger, and the inflammatory reaction develops as an autoimmune process.

Choroiditis can be endogenous and exogenous. Endogenous are caused by tubercle bacillus, viruses, the causative agent of toxoplasmosis, streptococcus, brucellosis infection, etc. The occurrence of exogenous choroiditis occurs as a result of involvement in the inflammatory process of the choroid in traumatic iridocyclitis and diseases of the cornea. Choroiditis is divided into focal and diffuse. In the case of focal choroiditis, foci of inflammation can be single (isolated) and multiple (with scattered, disseminated choroiditis). Depending on the localization of the inflammatory formation, choroiditis is divided into central (with a focus in the central region of the fundus), peripapillary (with a focus around the optic nerve head), equatorial (with a focus in the equatorial zone of the eye) and peripheral, in which the inflammatory formation is localized in the peripheral regions. fundus near the dentate line.

Pathological anatomy. With focal choroiditis, a limited infiltrate (a focus of inflammation with an increased volume and increased density) from lymphoid elements located around the dilated vessels throughout its entire thickness is found in the choroid.

In diffuse choroiditis, the components of the infiltrate are lymphocytes, epithelioid and sometimes giant cells. The infiltrate compresses blood vessels and disrupts the blood supply to tissues. Inflammation of the choroid causes changes in the retina due to the destruction of the pigment epithelium layer, as well as the development of edema and hemorrhage.

In the course of treatment, the infiltrate in the choroid can resolve. Then the cellular elements of the infiltrate are replaced by connective tissue, forming a scar. The retinal pigment epithelium grows along the periphery of the scar. With tuberculous choroiditis, cellular changes depend on the stage of development of the tuberculous process. In primary tuberculosis, inflammation in the choroid proceeds according to the exudative type. Diffuse infiltration includes epithelioid cells and Pirogov-Langhans giant cells. In secondary tuberculosis, granulomas are formed with caseous (curdled) necrosis and subsequent formation of tuberculomas.

clinical picture. Patients with choroiditis do not have eye pain and visual disturbances. Therefore, it is detected only with ophthalmoscopy. When involved in the process of adjacent parts of the retina (chorioretinitis), visual impairment occurs. When the chorioretinal focus is located in the central parts of the fundus, there is a sharp decrease in vision and distortion of the objects in question, and the patient notes a sensation of flashes and flicker (photopsia). With damage to the peripheral parts of the fundus, twilight vision decreases, sometimes "flying flies" are observed before the eyes. Limited defects are revealed in the field of view of the scotoma, corresponding to the location of the foci. With inflammation in the fundus, grayish or yellowish foci with fuzzy contours are visible, protruding into the vitreous body; retinal vessels are located above them, without interruption. During this period, hemorrhages in the choroid, retina and vitreous body are possible. The progression of the disease leads to clouding of the retina in the focus area.

Under the influence of the treatment process, the chorioretinal focus flattens, becomes transparent, acquires clearer contours, the choroid becomes thinner, and the sclera shines through it. With ophthalmoscopy, a white focus with large vessels of the choroid and pigment lumps is visible against the red background of the fundus, which indicates the onset of the stage of choroidal atrophy. When the chorioretinal focus is located near the optic nerve head, inflammation may spread to the optic nerve. A characteristic scotoma appears in the field of view, merging with the physiological one; with ophthalmoscopy, blurring of the boundaries of the optic nerve is determined. Peripapillary choreoretinitis develops, or Jensen's parapapillary neuroretinitis. With tuberculous lesions of the choroid, such clinical forms as miliary, disseminated, focal (with central and peripapillary localization of the focus) choroiditis, choroidal tuberculoma, and diffuse choroiditis are more common. The latter is more often observed at a young age against the background of chronically current primary tuberculosis. The inflammatory process in the choroid is accompanied by a pronounced reaction of the retina and vitreous body and ends with atrophy of the choroid. With toxoplasmosis, focal choroiditis develops, with congenital toxoplasmosis, central focal choroiditis. With acquired syphilis, diffuse choroiditis occurs. The course of choroiditis is often chronic, with relapses. Complications of choroiditis can be secondary retinal dystrophy, exudative retinal detachment, neuritis with transition to secondary optic nerve atrophy, extensive hemorrhages in the vitreous body with subsequent mooring. Hemorrhages in the choroid and retina can lead to the formation of rough connective tissue scars and the formation of a neovascular membrane, which is accompanied by a sharp decrease in visual functions.

Diagnosis and differential diagnosis. The diagnosis is made on the basis of the results of direct and reverse ophthalmoscopy, fluorescein angiography of the fundus. These methods allow you to establish the stage of the disease, which is of great importance for the treatment and outcome of the disease. In 1/3 of cases, the etiology remains unclear, which requires a comprehensive examination of the patient. Currently, immunological diagnostic methods are widely used, which include serological reactions, detection of sensitivity to various antigens, determination of immunoglobulins (antibodies) in blood serum, tears and intraocular fluid, detection of a focal reaction in the eye in response to the introduction of allergens.

Differential diagnosis is carried out with external exudative retinopathy, nevus (pigment tumor) and the initial stage of choroidal melanoma. Ultrasound and radioisotope research methods are necessary to clarify the diagnosis.

Treatment and prevention. Treatment is aimed at eliminating the underlying disease. The treatment complex includes pathogenetic, specific and non-specific hyposensitizing agents, physiotherapeutic and physical methods of influence (laser coagulation, cryocoagulation).

Specific hyposensitization is carried out in order to reduce the sensitivity of sensitized eye tissues in tuberculosis, toxoplasmosis, viral, staphylococcal and streptococcal choroiditis. The antigen is administered in small doses repeatedly. Specific hyposensitization is a promising method of treatment that excludes relapses. Nonspecific hyposensitization is indicated for chorioretinitis at all stages of treatment: during the period of active inflammation, with relapses, and also for the prevention of exacerbation. For this, antihistamines are used (diphenhydramine, suprastin, tavegil, pipolfen, diazolin, etc.).

An important role in the treatment of choroiditis is played by antibacterial therapy, which is used in accordance with the nature of the process and for the sanitation of foci of infection. With an unknown etiology (cause) of choroiditis, broad-spectrum antibiotics are used. Corticosteroids are prescribed along with other drugs, immunosuppressive drugs (mercaptopurine, imuran, metatrexate, fluorouracil, cyclophosphamide, etc.). Antibiotics, corticosteroids, cytostatics are administered intramuscularly, orally, retrobulbarno (behind the eyeball), suprachoroidally and by electrophoresis. The arsenal of therapeutic agents includes vitamins C, B1, B6, B12. For resorption of exudate and hemorrhages in the choroid, retina, vitreous body, enzymes are used (trypsin, fibrinolysin, lidase, papain, lecozyme, streptodecase), which are administered intramuscularly, retrobulbar and by electrophoresis.

Cryocoagulation of the choroid is indicated for secondary dystrophies after suffering choroiditis to prevent retinal detachment. For the same purposes, with hemorrhagic chorioretinitis, laser coagulation is used.

Prevention of choroiditis is reduced to the timely diagnosis and treatment of acute and chronic infectious diseases.

Author: Shilnikov L.V.

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>> Forward: Tumors of the choroid and anomalies of the vascular tract (Iris cysts. Ciliary body cysts. Choroidal angioma. Pigmented tumors. Neurofibromatosis. Vascular tract anomalies)

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