Vitreous hemorrhage is a polyethological disease of the organ of vision, which develops due to rupture of blood vessels and hemorrhage into the vitreous body. It is clinically manifested by the presence of shadows, “fog”, floating opacity of black or red color in front of the eyes, decreased visual acuity and the development of photopsia. Ophthalmoscopy, visometry, biomicroscopy, tonometry, ultrasound are recommended for diagnosis. Treatment tactics depend on the extent of the lesion. With partial vitreous hemorrhage, treatment is not indicated. Subtotal hemorrhages require laser coagulation and drug therapy, total hemorrhages require vitrgemectomy.
Vitreous hemorrhage is an urgent condition in ophthalmology in which the vitreous cavity is filled with blood or blood clots. The prevalence of vitreous hemorrhage is 7:100,000. The risk group includes people with diabetes mellitus and hypertension in the decompensation stage, myocardial infarction or a history of stroke. The relationship between this pathology and elevated blood cholesterol levels has been established. The disease most often develops in people over 40 years of age. In children, vitreous hemorrhage can occur with infant shaking syndrome. Women are more prone to this disease than men. The total form in 95% of cases leads to complete loss of vision and disability of the patient.
A common cause of vitreous hemorrhage is proliferative diabetic retinopathy, which develops mainly in patients with type 1 diabetes mellitus. Insulin insufficiency is accompanied by a violation of the blood supply to the posterior segment of the eye. This, in turn, stimulates the synthesis of angiogenic factors. The most intense vascular neoplasm is observed in the vitreoretinal fusion zone. As a consequence, vitreous detachment or eye movements lead to vascular rupture with further hemorrhage. Somewhat less often, pathology occurs against the background of occlusion of the central retinal vein (CRV) or its branches.
Inflammatory or degenerative changes in the vascular wall are predictors of retinal tears or regmatogenic retinal detachment. These pathological conditions are found among patients with vasculitis, sickle cell anemia and Ilsa disease. In some cases, the etiological factor of vitreous hemorrhage is blunt trauma or penetrating injury of the eye, which are similar to manifestations of subarachnoid hemorrhage (Terson syndrome) in ophthalmology. With false Terson syndrome, neovascularization of the retina after parsplanitis is observed.
Arterial microaneurysms lead to the fact that in a certain area the vessel loses its elastic properties, and its wall becomes thinner. An increase in intraocular pressure, arterial hypertension or a change in the rheological properties of blood provokes a rupture in the aneurysm zone. Clinical manifestations of intravitreal hemorrhage are characteristic of posterior detachment of the scleral body, which may be accompanied by retinal rupture. It has been proven that autoimmune processes that develop in systemic lupus erythematosus can also affect the vascular wall. At the same time, increased vascular permeability leads to the accumulation of hemorrhagic exudate in the vitreous body. This mechanism is also characteristic of the exudative form of age-related macular degeneration, which can also be the cause of vitreous hemorrhage.
The progression of malignant choroidal melanoma or Norrie’s disease (congenital bilateral pseudoglyoma of the retina) leads to a violation of the structure of the microcirculatory bed, which in the later stages is manifested by frequent retinal tears and bleeding. Most oncological diseases lead to neovascularization, but the vessels that provide the trophism of the tumor are poorly differentiated. A low degree of differentiation causes frequent ruptures and hemorrhage in the vitreous.
Clinical manifestations of intravitreal hemorrhage depend on the volume of blood, its rheological properties and the stage of development. At the stage of bleeding, which lasts from a few seconds to 24 hours, patients note the appearance of a “fog” in front of their eyes, which gradually changes to oblakoid or cobweb shadows. Turbidity develops suddenly, against the background of complete well-being. A distinctive symptom of vitreous hemorrhage is the black or red color of the shadows that have appeared. The degree of visual acuity reduction directly depends on the volume of blood in the vitreous cavity. With massive hemorrhages, patients do not respond to light. With small hematomas, visual acuity decreases slightly. Involvement of ganglion cells in the pathological process with posterior retinal detachment leads to the development of photopsias. Pain syndrome occurs only with vitreous hemorrhage due to traumatic injury or iatrogenism.
At the stage of fresh hematoma (up to 2-3 days), the first manifestations of phagocytosis are observed. During this period, the patient notes the migration of shadows in his field of vision, which is associated with the formation of blood clots. From day 3 to 10, hemolysis of erythrocytes occurs. Hemoglobin and its decay products spread to other structures of the eyeball. Visual acuity is progressively decreasing. The release of toxins can lead to hemodynamic instability, headache and general weakness. Starting from day 10, irreversible hemosiderotic dystrophy of the vitreous, retina and lens develops. In turn, the hematoma is replaced by connective tissue, which is accompanied by increased synthesis of melanocytes of the pigment epithelium and proliferation of retinal neuroglia. Within six months of the onset of the first symptoms of vitreous hemorrhage, total vision loss occurs. After six months, intraocular fibrosis develops, which is accompanied by intravitreal mooring, retinal hemosiderosis with further detachment and phthisis. The final stage of massive vitreous hemorrhage is atrophy of the eyeball.
Instrumental diagnostics is based on indirect binocular ophthalmoscopy with scleral suppression, visometry, biomicroscopy, tonometry, ultrasound B-scanning.
The method of indirect binocular ophthalmoscopy with scleral perforation makes it possible to inspect the peripheral parts of the retina and verify the retinal rupture in which melanocytes are visualized. For greater reliability, ophthalmoscopy with a Goldman three-mirror lens is recommended. With the help of visometry, it is possible to measure visual acuity, which in patients with vitreous hemorrhage varies from a slight decrease to a complete absence of light perception. The method of biomicroscopy reveals melanocytes in the anterior parts of the vitreous body, condensation and hemorrhage foci.
An indication for an ultrasound of the eyeball is a decrease in the transparency of the optical system of the eye caused by corneal opacity or cataract. This technique allows you to visualize ruptures or a foreign body of the eye in the traumatic genesis of vitreous hemorrhage and assess the degree of fit of the retina and vitreous detachment. In the B-scan mode, in addition to the above changes, intraocular melanoma, foci of neovascularization can be detected and the condition of the posterior vitreous can be studied. Ultrasound examination should be performed serially for early diagnosis of retinal detachment. It is repeated until the moment of enlightenment of the vitreous hemorrhage.
All patients are recommended to conduct laboratory tests: a blood test, a coagulogram and a study of blood glucose levels. Suspicion of occlusion of CVS is an indication for conducting an analysis of rovi, in which an increase in ESR is detected. The coagulogram may indicate the phenomenon of blood thickening. In patients with diabetic retinopathy, an increase in glucose levels is determined.
Treatment of vitreous hemorrhage
If you suspect the development of vitreous hemorrhage, you need to consult an ophthalmologist. Treatment tactics depend on the etiology of the disease. If a small hemorrhage is detected, specific treatment is not required. In case of relapse, vitreous lavage is recommended. Conservative therapy consists in oral administration of tissue plasminogen activators (alteplase). From day 3 to 28, it is advisable to take prourokinase. Subtotal and total vitreous hemorrhage require surgical treatment (vitrgemectomy). Proliferative retinopathy, accompanied by retinal rupture, is corrected by laser coagulation. With obvious opacity of the vitreous body against the background of conservative therapy, vitrectomy is indicated.
For patients in the late postoperative period, with a recurrence of vitreous hemorrhage at home, oral administration of 10% CaCl solution, applying a compress with ice to the eye area and urgent seeking help from a specialist is recommended.
Prognosis and prevention
Specific measures for the prevention of vitreous hemorrhage have not been developed. Patients are recommended to monitor the level of blood pressure, after 40 years to measure intraocular pressure once a year. Patients with diabetes mellitus should monitor blood glucose levels, follow basic treatment and undergo a preventive examination by an ophthalmologist twice a year, which should include ophthalmoscopy, tonometry and visometry.
The prognosis depends on the volume of hemorrhage. Early diagnosis and timely treatment make it possible to fully restore the functions of the eye. If the vitreous body is filled with blood by 1/8, the prognosis is favorable; by 1/8 – 1/4, there is a high risk of retinal detachment; by 1/4 – 3/4, the prognosis for the restoration of visual functions is doubtful. With total vitreous hemorrhage, it is not possible to restore vision. 95% of patients have atrophy of the eyeball, which leads to complete blindness and further disability.