Central serous chorioretinopathy is a pathology of the visual organ characterized by serous detachment of the neuroepithelial layer of the retina in combination with or without detachment of the pigment epithelium. It is clinically manifested by a decrease in visual acuity, the appearance of “spots” in front of the eyes, macro- or microphotopsias, metamorphopsias, less often photophobia. Diagnosis of central serous chorioretinopathy includes fluorescence angiography, visometry, ophthalmoscopy, biomicroscopy, perimetry, OCT. Drug treatment is reduced to dehydration and vasoconstrictive therapy. In the absence of an effect, laser coagulation of the retina is indicated.
ICD 10
H35.7 Splitting of retinal layers
General information
Central serous chorioretinopathy is a disease in ophthalmology, manifested by the splitting of retinal layers due to increased permeability of the Bruch membrane and plasma leakage from the choroid capillaries through the retinal pigment epithelium. The pathology was first described by the German ophthalmologist Albert von Grefe in 1866.
Men get sick 8 times more often than women. As a rule, pathology occurs in people of young and middle age groups. With age, the number of binocular lesions of the visual organ increases. According to statistics, 52% of patients develop the disease after the use of exogenous steroids. Central serous chorioretinopathy is more common among residents of Spain and Asia, rarely observed in African Americans.
Causes
The risk group for the development of central serous chorioretinopathy includes people with arterial hypertension, hormonal imbalance in the anamnesis, because the mechanism of blood circulation in the choroid is regulated by the level of cortisol and adrenaline. The role of an etiological factor is often a change in the hormonal background during pregnancy.
The condition of the vessels is influenced by the tone of the autonomic nervous system. Persons with increased activity of the sympathetic department are at greater risk of disease than people with a predominance of the tone of the parasympathetic nervous system. Predisposes to the development of central serous chorioretinopathy burdened allergic history, the presence of atopy in close relatives.
In some cases, the disease develops against the background of systemic pathologies (Cushing’s syndrome, systemic lupus erythematosus). An increase in the permeability of the capillaries of the vascular membrane of the eye is provoked by the uncontrolled administration of steroids, taking drugs containing sildenafil citrate, or psychotropic drugs. Less often, the occurrence of pathology is caused by a complication after organ transplantation. In most cases, idiopathic central serous chorioretinopathy is diagnosed, since it is not possible to establish the etiology of the disease.
Pathogenesis
Central serous chorioretinopathy occurs due to an increase in the permeability of the capillaries of the eyeball’s own vascular membrane. Plasma release into the surrounding tissues leads to serous detachment of the sensorineural layer of the inner shell of the eye. As a rule, the areas of exfoliation correspond to places of increased exudation. The development of this process is caused by a violation of the transport of sodium and potassium ions through the pigment layer. Also, the trigger of the disease is the pathology of the vascular wall (choroidal vasculopathy). Local violation of microcirculation in the area of its own vascular membrane is the cause of secondary dysfunction of the pigment epithelium.
Symptoms
From a clinical point of view, there are acute, subacute and chronic course of central serous chorioretinopathy. The acute course is characterized by sudden absorption of serous fluid in an average of 1-6 months. At the same time, visual acuity is restored to reference values. With a subacute course, spontaneous resolution occurs within one year. The preservation of the clinical picture for more than 1 year indicates the chronization of the process.
Patients complain of soreness in the eye socket, the appearance of translucent spots in front of the eyes. The decrease in visual acuity is slowly progressing. Patients are more likely to notice a violation of visual functions in the morning. Secondary transient hypermetropia develops.
A specific symptom of this pathology is an increase or decrease in the size of the object under consideration, which indicates the development of macro- or microphotopsias. At the same time, the shape of the objects themselves can be distorted (metamorphopsies). A high degree of microphotopsies with a unilateral lesion leads to a violation of binocular vision. Violation of color perception or photophobia occurs extremely rarely, but patients consider the average illumination of the room to be the most comfortable. The progression of the disease leads to the appearance of central cattle. Patients may indicate the frequency of symptoms in the acute course of central serous chorioretinopathy.
Diagnostics
Diagnosis of central serous chorioretinopathy is based on fluorescence angiography, visometry, ophthalmoscopy, biomicroscopy, perimetry, optical coherence tomography (OCT):
- Fluorescent retinal angiography. In the acute course of the disease, one or more exudation sites through the pigment epithelium are visualized using angiography. Often, with a chronic course, diffuse seepage is detected, which is indicated by an increase in fluorescence.
- Visometry. Diagnoses a decrease in visual acuity within 0.2-0.3 diopters. In this case, the refraction is hypermetropic.
- Ophthalmoscopy. Ophthalmoscopically, serous detachment of the neuroepithelial layer, violation of the integrity of the pigment layer, subretinal accumulation of fibrin masses and lipofuscin are detected.
- Biomicroscopy. A more detailed examination can be carried out by biomicroscopy of the eye using special lenses (60, 78 dptr) or a Goldman three-mirror contact lens. In this case, the zone of serous detachment is determined, which has the form of a penetrating focus with a fuzzy contour. The shape of the affected area is rounded, limited by an arcuate reflex. In the area of chorioretinopathy, Baer precipitates are detected.
- Perimetry. During perimetry, central scotomas are determined. On OCT, the accumulation of fluid between the neuroepithelial and pigment layers is visualized.
Differential diagnosis of central serous chorioretinopathy is performed with choroidal neovascularization, chorioretinitis, choroid tumors.
Treatment
Conservative therapy
Conservative treatment of central serous chorioretinopathy is reduced to dehydration and vasoconstrictive therapy. In order to reduce the swelling of the inner shell of the eye, parabulbar injections of glucocorticosteroids are indicated. Also, this group of drugs has an anti-allergic effect. The appointment of diuretics is recommended for dehydration. In order to normalize tissue metabolism during the days of taking diuretics, it is advisable to use potassium and magnesium preparations. Strengthening of the vascular wall is achieved with the use of angioprotectors, multivitamin complexes. In case of positive dynamics during subsequent visits to the ophthalmologist (10th, 30th days), repeated parabulbar injections of glucocorticosteroids are necessary.
Surgical treatment
In the absence of the effect of drug treatment or frequent relapses of the disease, laser coagulation of the retina is indicated. Focal coagulation is carried out in the area of the lesion of the pigment epithelium. If the defect is located in the area of the papillomacular bundle or at a distance of less than 500 microns from the foveola, a macular barrage is recommended. After laser coagulation, instillations of nonsteroidal anti-inflammatory drugs in the form of drops are carried out for 3-7 days. The criterion for the effectiveness of treatment is an improvement in visual acuity by 0.1 dpt or more, a decrease in the severity of central cattle by 5-10 ° and a decrease in macular edema by 5-10%.
Prognosis and prevention
Specific preventive measures for the development of central serous chorioretinopathy have not been developed. Non-specific prevention is reduced to the use of steroids in minimally effective dosages, limiting psychoemotional overstrain, controlling blood pressure levels. Patients who are at risk or have a history of this disease should be examined by an ophthalmologist 2 times a year with mandatory measurement of intraocular pressure, ophthalmoscopy and visometry.
The prognosis for central serous chorioretinopathy is relatively favorable for life and working capacity, since the pathology is prone to frequent recurrence, and the restoration of visual acuity does not eliminate other clinical manifestations of the disease.
