Sympathetic ophthalmia is a binocular lesion of the visual organ that develops after damage to the uveal tract, followed by involvement in the pathological process of the second intact eyeball. The most common symptoms are hyperemia, lacrimation, photophobia, “flies” in front of the eyes, decreased visual acuity. Diagnosis of sympathetic ophthalmia is reduced to the collection of anamnesis, external examination, biomicroscopy, visometry, tonometry, gonioscopy, ophthalmoscopy, ultrasound in In-mode, OCT. Depending on the severity of the disease, the course of treatment may include glucocorticosteroids for systemic and topical use, immunosuppressants, NSAIDs.
Sympathetic ophthalmia is a polyethological pathology of the organ of vision in ophthalmology, which proceeds according to the type of granulomatous uveitis. The term “sympathetic ophthalmia” was first proposed in 1835 by the Scottish ophthalmologist W. Mackenzie. According to statistics, in 0.2-0.4% of cases, the disease occurs against the background of penetrating wounds of the eyeball. In 0.01-0.06%, intraorbital surgical interventions are the cause of development. Sympathetic ophthalmia can be diagnosed at any age, but, as a rule, pathology is most often detected in 25-50 years. Men get sick more often than women, which is associated with a greater prevalence of visual organ injuries among males.
Often, sympathetic ophthalmia develops against the background of iridocyclitis caused by perforation of the visual organ, perforation of corneal ulcers, subconjunctival rupture of the sclera, intraorbital neoplasms. Less often, the trigger is iatrogenism. Autoimmune damage to the structures of the eyeball plays a key role in the pathogenesis of the disease. At the same time, antibodies to S-antigens of the retina, pigment epithelium and uveal tract are produced. It has been experimentally proved that the development of sympathetic ophthalmia can be caused by an immunogenetic relationship with HLA class II antigens. Immunomorphological features of the inflammatory process proceed according to the type of delayed hypersensitivity with the involvement of Th type 1 T-lymphocytes. This theory of pathogenesis is confirmed by the detection of sensitized T cells and specific antibodies to uveal tract antigens, as well as the positive dynamics of pathology regression when using immunosuppressants.
Etiological factors of the development of sympathetic ophthalmia may be endogenous endotoxins formed after apoptosis of uveal tract cells. Toxemia provokes the involvement of an intact eye in the pathological process. Also, enzymes such as trypsin and zimase can become triggers. Infection of the eyeball structures with the herpes virus can lead to the development of a clinical picture of sympathetic ophthalmia, which is replaced by a clinic of endophthalmitis.
As a rule, sympathetic ophthalmia develops 10-12 days after traumatic eye injury or surgery. Involvement in the pathological process of the second intact eye may occur 8-10 weeks after the appearance of clinical symptoms on the side of the primary lesion. The disease in most cases occurs in the form of anterior serous, plastic or generalized uveitis, less often – posterior uveitis or neuroretinitis. There are mild, moderate and severe degrees of severity of symptomatic ophthalmia. With the development of symptoms of anterior serous inflammation of the uveal tract, patients complain of photophobia, hyperemia of the eyes and lacrimation.
Plastic uveitis is characterized by a severe course. Patients note a decrease in visual acuity, the appearance of “flies” or “fog” in front of their eyes, headache, general weakness. A feature of generalized uveitis is a tendency to frequent relapses. This form of sympathetic ophthalmia is often complicated by exudative retinal detachment and optic neuritis. Patients complain of a rapidly progressive decrease in visual acuity. The development of posterior uveitis or neuroretinitis has a latent course for a long time and manifests itself in the form of a pronounced decrease in visual functions and the appearance of a “veil” in front of the eyes. The most common complications of sympathetic ophthalmia are secondary cataracts and ophthalmohypertension.
The diagnosis of sympathetic ophthalmia is based on anamnestic data, the results of external examination, biomicroscopy, visometry, tonometry, gonioscopy, ophthalmoscopy, ultrasound in In-mode, optical coherence tomography (OCT). Patients note the relationship between the development of the disease and injury to the eyeball or intraocular surgery. An external examination reveals a moderate injection of eye vessels.
In anterior serous uveitis, a small number of small precipitates are determined by biomicroscopy. Visual acuity and intraocular pressure (IOP) in this form of sympathetic ophthalmia are within the age norm. Biomicroscopy for plastic uveitis allows you to identify a large number of precipitates, pericorneal injection of vessels. The exudate in the anterior chamber of the eye is visualized by gonioscopy. Also, with this form of sympathetic ophthalmia, many posterior synechiae are formed. When conducting visiometry, there is a decrease in visual acuity. Ophthalmotonus corresponds to the norm.
In the generalized form of sympathetic ophthalmia, granulomatous foci of Dahlen-Fuchs are detected by gonioscopy in the anterior chamber. They can also be detected by ultrasound in B-mode in the anterior parts of the vitreous body. Ophthalmoscopy allows to confirm retinal edema, its exudative detachment, signs of optic neuritis. In this form of the disease, visual acuity is significantly reduced and varies from 0.01 to 0.02 dpt. Posterior uveitis and neuroretinitis can be diagnosed with OCT. There is a large number of posterior synechiae and pupil occlusion. Ultrasound of the eye in these forms of sympathetic ophthalmia indicates a violation of the transparency of the pupil due to the formation of a large number of precipitates.
The tactics of treatment of sympathetic ophthalmia depends on the form and severity of the disease. With anterior serous uveitis, local use of corticosteroids in the form of drops or parabulbar injections is indicated. The duration of the course of conservative therapy is 6 months. After carrying out therapeutic measures, relapses, as a rule, are not observed. The development of plastic uveitis is an indication for the appointment of a course of local and systemic glucocorticosteroid therapy. The duration of the use of glucocorticosteroids is 5-6 months. After their cancellation, nonsteroidal anti-inflammatory drugs (NSAIDs) should be taken for 3-4 weeks.
The development of a generalized form of sympathetic ophthalmia requires the systemic administration of pulse therapy with corticosteroids in high dosages for 3-4 days and immunosuppressants in a standard dose. Further, the dosages of the drugs gradually decrease. The indication for the cancellation of the course of treatment is a persistent remission of sympathetic ophthalmia. Surgical intervention is indicated in the development of secondary cataracts. At the same time, cataract phacoemulsification is performed, followed by implantation of an intraocular lens. It is possible to eliminate the clinical manifestations of ophthalmohypertension with pupil occlusion and involvement of the iris in the pathological process by laser membranotomy.
Prognosis and prevention
There is no specific prevention of sympathetic ophthalmia. Non-specific preventive measures are reduced to compliance with safety regulations (wearing protective glasses and helmets) at work, prevention of viral diseases, timely treatment of erosive damage to the organ of vision. Patients with sympathetic ophthalmia should be under the dynamic supervision of the attending ophthalmologist. Timely diagnosis and treatment ensure complete restoration of visual functions. Nevertheless, with a severe form of the disease with binocular lesion, there is a high risk of complete loss of vision and subsequent disability of the patient. The prognosis for life and ability to work depends on the severity of the course and the effectiveness of the therapy.