Abstract
Abstract: :
Purpose: To study the pathogenesis of ocular hypotony in patients with ciliochoroidal detachments. Methods: Tonography, vasotonometry, reoophthalmography, photocalibrometry of episcleral vessels, registration of central retinal vein and central retinal artery pulsations together with electrocardiography, two-dimensional ultrasound Dopplerography, color Doppler imaging and ultrasonography of eyeball were used to assess ocular hemodynamics in normal eyes and in ciliochoroidal detachment. Ocular hemodynamics of patients with ciliochoroidal detachment was compared with ocular hemodynamics of healthy volunteers. Results: We have ascertained pulsating flow in vortex veins ampules inversely to the arterial pulsation. We suggest the following explanation of this process. The ampules of the vortex veins collapse between choroid and sclera during the cardiac systole when intraocular arterial vessels are expanded by the pulse wave. At this moment venous blood flow stops in vortex veins. During the cardiac diastole the lumens of vortex veins ampules are open, and venous outflow is resumed. Pulsative regimen of the blood flow in the vortex veins provides relatively high transmural pressure in capillaries of the ciliary processes, maintaining normal level of aqueous production. In all cases of ciliochoroidal detachment we did not observe vortex veins pulsation. Conclusions: In ciliochoroidal detachment the systaltic blood flow in the vortex veins is destroyed, and venous blood leaves the eyeball continuously. As a result, transmural capillary pressure in ciliary processes decreases and aqueous production weakens, causing ocular hypotony. Because of uninterrupted venous blood flow in the vortex veins episcleral venous hypertension develops. We believe, the main direction in the treatment of ciliochoroidal detachment should be manipulations to re-establish vortex vein ampules pressing between choroid and sclera during cardiac cycle.
Keywords: aqueous • inflow/ciliary body • choroid