Hypertensive retinopathy uAcute systemic hypertension causes constriction of the retinal arterioles and clinically focal narrowing. uProlonged acute systemic hypertension may cause disruption of the blood-retinal barrier. uClinically, flame or splinter hemorrhages, macular exudate (star) and cotton-wool spots are observed. uMalignant hypertension may result in swelling of the optic nerve head. u u Hypertensive retinopathy uProlonged systemic hypertension results in thickening of the walls of the retinal arterioles and the ophthalmoscopic signs of retinal arteriolar sclerosis. u uClinically, the thickened arterioles have a broader and brighter light reflex, in the place where arteries cross veins thickening of the artery causes compression of the vein. Diabetic retinopathy uDiabetic retinopathy is one of the most frequent causes of new blindness in Europe and USA. u25% of the diabetic population has some form of diabetic retinopathy. uThe prevalence of all types of retinopathy in the diabetic population increases with the duration of diabetes and patient age. u Diabetic retinopathy uDiabetic retinopathy is microangiopathy. uEarly in the course of diabetic retinopathy certain physiologic abnormalities have been identified- impaired autoregulation of the retinal vasculature, alterations in retinal blood flow, and breakdown of the blood- retinal barrier, u Diabetic retinopathy uLater in the course of diabetic retinopathy we observe capillary closure. uCapillary closure is believed to result in retinal ischemia. uRetinal ischemia causes the release of a vasoproliferative factor stimulating neovascularization. Diabetic retinopathy uFor clinical use diabetic retinopathy may be classified into two stages: u u1. Nonproliferative retinopathy u2. Proliferative retinopathy Nonproliferative diabetic retinopathy uMicroaneurysms uIntraretinal hemorrhages uFocal and diffuse edema uHard exsudates uCotton-wool spots synkova color 1 synkova FAg 2 synkova FAg 4 kolarik color 1 kolarik FAg 2 kolarik FAg 4 Nonproliferative diabetic retinopathy uDiabetic maculopathy may present as focal or diffuse retinal thickening with or without deposits of intraretinal lipid-protein exudates. uThe visual prognosis is poorer for the diffuse edema pattern then for the focal pattern. color 1 foto Chre Proliferative diabetic retinopathy uThe extraretinal fibrovascular proliferation is viewed as a response to widespread intraretinal capillary obliteration and ischemia. u The neovascularization can cause haemophthalmus, traction retinal detachment, secondary glaucoma. Nov Nov Diabetic retinopathy uPhotocoagulation is currently used to treat eyes with non-proliferative retinopathy with macular edema, and eyes with proliferative disease. Clinically significant macular edema uThickening of the retina at or within 500 microns of the center of the macula uHard exsudate at or within 500 microns of the center of the macula associated with thickening of adjacent retina uA zone(s) of retinal thickening one disc area or larger any part of which is within one disc diameter of the center of the macula. Diabetic retinopathy uThe technique of photocoagulation for clinically significant macular edema includes focal therapy directed to the leaking mikroaneurysms in the posterior retina or grid photocoagulation for diffuse leakage of all capillaries of the posterior retina. color 1 FAg 1 FAg 4 color 3 color 4 foto Chre Foto Chre foto po DK Chre OD Diabetic retinopathy uFor proliferative retinopathy we perform panretinal photocoagulation uThe goal of panretinal photocoagulation is to cause regression of neovascularizations and to prevent new vessel formation in the future. vetr vetr Retinopathy of prematurity uRetinopathy of prematurity is a proliferative retinopathy of premature and low birth weight infants. uIt is recommended to perform examination of all high-risk infants= less than 36 weeks gestation or birth weight less than 2000 grams. Retinopathy of prematurity uNormal retinal vascularization proceeds from the optic disc to the periphery and is complete in the nasal quadrants at approximately 36 weeks of gestation and on the temporal side at 40 weeks. Retinopathy of prematurity u Pathogenesis: uBy the premature children, exposure to oxygen and possibly radical oxygen inhibits further vascularization, leaving a variable amount of anterior neurosensory retina without inner blood supply. uOther factors such as low birth weight, intercurrent illness, short gestational period and pCO2 may contribute to the development of retinopathy. Retinopathy of prematurity uClinically we can see the border between vascularized and nonvascularized retina. uStage 1: presence of a demarcation line between vascularized and nonvascularized retina. uStage 2:at the border zone is a mesenchymal arteriovenous shunt developed. Retinopathy of prematurity uStage 3: a demarcation ridge with extraretinal fibrovascular proliferation uStage 4: subtotal retinal detachment uStage 5: total retinal detachment Retinopathy of prematurity uTreatment: uStage 3= cryotherapy uStage 4= scleral buckle uStage 5= pars plana vitrectomy. Branch retinal vein occlusion uThe site of occlusion is almost invariably at an arteriovenous crossing point. uThe superotemporal quadrant is most commonly affected (63%), and nasal occlusions are rarely detected clinically. Branch retinal vein occlusion u Pathogenesis: uHistologic studies suggest that the common adventitia at these points binds the artery and vein together and that thickening of the arterial wall compresses the vein resulting in turbulence of flow, endothelial cell damage, and thrombotic occlusion. u Branch retinal vein occlusion uPredispose to BRVO: u- Systemic hypertension u- Diabetes u- Arteriosclerosis u- Hyperopia Branch retinal vein occlusion uThe oftalmoscopic findings include: u- superficial hemorrhages u- retinal edema u- cotton-wool spots u- the obstructed vein is dilated and turtuous -the corresponding artery may become narrowed - uThe area and location of involved retina depend on the site of the venous obstruction - - BRVO 1 BRVO 2 Branch retinal vein occlusion uThe visual prognosis is related to the extent of capillary damage and retinal ischemia. u uSometimes capillary compensation and collateral formation may permit restitution of flow with resolution of the edema and improvement in visual function. u Branch retinal vein occlusion uThe visual prognosis is related to the extent of capillary damage and retinal ischemia. u uExtensive retinal ischemia frequently results in cystoid macular edema, pigmentary macular disturbance, macular edema with hard lipid exudates, subretinal fibrosis, epiretinal membrane formation, and neovascularization u Branch retinal vein occlusion uPhotocoagulation therapy in BRVO is considered for two major complications: u -Chronic macular edema u u- Neovascularization Branch retinal vein occlusion uPhotocoagulation therapy: u uFor persistent macular edema, photocoagulation lesions are placed in the paramacular retina drained by the obstructed vein. The leaking microvascular abnormalities and areas of capillary nonperfusion are treated directly. BRVO 1 BRVO 3 Branch retinal vein occlusion uPhotocoagulation therapy: u uFor eyes with neovascularization, panretinal photocoagulation is effective in causing regression of the new vessels. Branch retinal vein occlusion u Drugs: uMedications that reduce platelet adhesiveness (Aspirin) uPeripheral vasodilators (Agapurin) uVasoprotectives, capillary stabilizing agents (Ascorutin) Central retinal vein occlusion uHistologic studies suggest that all forms of CRVO have a common mechanism, which is thrombosis of the central retinal vein at the level of the lamina cribrosa. u uTwo forms of the disease are recognized: uA milder form called non-ischemic uA severe form called ischemic Central retinal vein occlusion uNon-ischemic CRVO u- Mild optic disc swelling u- Mild dilatation and turtuosity of all branches of the central retinal vein u- Dot and flame hemorrhages in all quadrants of the retina u- Macular edema may or may not be present u- Capillary leakage, minimal areas of nonperfusion CRVO 1 CRVO FAg 1 CRVO FAg 2 Central retinal vein occlusion uIschemic CRVO u- Extensive four quadrant retinal edema and hemorrhage u- Marked venous dilatation u- Cotton-wool spots u- Fluorescein angiography demonstrates widespread capillary nonperfusion u- Later we observe neovascularization u CRVO 2 CRVO FAg 3 CRVO FAg 4 Central retinal vein occlusion u Therapy: -We use anti-thrombotic agents (Warfarin) -Panretinal photocoagulation is effective therapy for neovascularization Branch retinal artery occlusion uOcclusion is due to embolization or thrombosis of the affected vessel. u uThree types of emboli are recognized: u- Cholesterol emboli arising in the carotid arteries u- Platelet-fibrin emboli associated with large vessel arteriosclerosis u- Calcific emboli arising from diseased cardiac valves Branch retinal artery occlusion uAcute BRAO causes an edematous, white retina in the distribution of the affected vessel. Branch retinal artery occlusion uTherapy: Pressure on the globe may dislodge the embolus from a central large vessel and result in obstruction of a smaller more peripheral vessel. u Central retinal artery occlusion uCRAO is usually due to arteriosclerosis- related thrombosis, occuring at the level of the lamina cribrosa uEmbolization may be important in some cases. Central retinal artery occlusion uSudden, severe, and painless loss of vision. uThe retina becomes opaque and edematous. uThis permits an orange reflex, from the intact choroidal vasculature beneath the intact foveola, to stand out in contrast to the surrounding opaque retina, producing the „cherry red spot“. Central retinal artery occlusion uThe reduction in intraocular pressure by paracentesis, ocular massage and drugs. Central serous retinopathy uIs characterized by the development of a serous detachment of the sensory retina. u- Sudden onset of blurred and dim vision u- Micropsia u- Metamorphopsia u- Decreased color vision CSCHR color 1 Central serous retinopathy uThe most common fluorescein angiographic presentation is a small focal hyperfluorescent leak from the RPE that appears early in the angiogram and increases in size and intensity with time. u u CSCHR FAg 1 kan CSCHR FAg 2 kan CSCHR FAg 3 kan Central serous retinopathy uOccasionally, rapid leakage of fluorescein produces a pattern of subretinal pooling of dye referred to as a „smokestack“. fag 1 fag 2 fag 3 fag 4 Central serous retinopathy uMost eyes with central serous choroidopathy undergo spontaneous resorption of subretinal fluid within one to six months of the onset of symptoms. Central serous retinopathy uConsider laser photocoagulation u in the following instances: -Persistence of serous detachment beyond four months. -Recurrences in eyes with visual deficit from previous episodes. -Permanent visual deficit from previous episodes in opposite eye. -Occupational or other patient needs requiring prompt restoration of vision. Age-related macular degeneration uARMD is the leading cause of new blindness in the Europe and USA. u uDry form of ARMD uWet form of ARMD Age-related macular degeneration uDry form of ARMD: uChanges in the macula, affecting the outer retinal layer: u- Retinal pigment epithelium (loss of pigment granules) u- Bruch‘s membrane (drusen) u- Choriocapillaris (atrophy of capillaries) u ARMD 1 Age-related macular degeneration uWet form of ARMD ARMD 2 ARMD FAg 1 ARMD FAg 2 ARMD FAg 3 ARMD FAg 4 Age-related macular degeneration uChoroidal neovascularization (CNV) u u- Extrafoveal u- Juxtafoveal u- Subfoveal u ARMD FAg 2 ARMD FAg 7 ARMD FAg 5 ARMD FAg 6 Age-related macular degeneration uTherapy: uThere is no known effective medical treatment for the dry form of ARMD. u uWet form of ARMD: u- Argon laser u- Photodynamic therapy u- Anti-VEGF drugs ARMD 3 ARMD FAg 5 ARMD FAg 6 ARMD laser ARMD laser 2 Retinal detachment uRetinal detachment is a separation of the neuroepithelium from the retinal pigment epithelium. Retinal detachment uRhegmatogenous retinal detachment u (Greek rhegma, meaning break) u uNonrhegmatogenous retinal detachment u- Exudative retinal detachment u- Traction retinal detachment u Rhegmatogenous retinal detachment u uA retinal break can be found u50% of patient have photopsias or entopsias (floaters). uThe intraocular pressure is ussually lower in the affected eye then in the fellow eye. Rhegmatogenous retinal detachment uSmall clumps of pigmented cells in the vitreous. uThe detachment is convex toward the front of the eye. uThe detached retina has a corrugated appearance and undulates with eye movements. Rhegmatogenous retinal detachment uThe principles of retinal detachment surgery are first to find all breaks, and second to close all breaks. u- A careful preoperative examination u- A scleral buckling procedure -Pars plana vitrectomy u uIf all breaks are closed, the subretinal fluid will be absorbed. - Exudative retinal detachment uERD occurs when either retinal blood vessels or the RPE are demaged, allowing fluid to pass into the subretinal space. uNeoplasia and inflammatory diseases are the leading causes of such detachments. uWe have to treat the reason (neoplasia and inflammatory diseases). Traction retinal detachment uVitreous membranes pull the sensory retina away from the RPE, causing a traction retinal detachment. uThe retina has a smooth surface and is immobile. uThe detachment is concave toward the front of the eye. uTreatment=PPV Angiomatosis retinae (von Hippeľs disease) uIn angiomatosis retinae, capillary hemangiomas develop in the retina or optic nerve head. uCapillary hemangioma is a spherical orange-red tumor fed by a dilated turtuous retinal artery and drained by an engorged vein. Angiomatosis retinae (von Hippeľs disease) uMultiple angiomas may be found in the same eye. uBilateral involvement occurs in 50% of patients. u Angiomatosis retinae (von Hippeľs disease) uLeakage of plasma constituents from an angioma may result in serous detachment of the retina and/or accumulation of exudate in the macula resulting in reduction in visual acuity. uOccasionally vitreous hemorrhage may occur. Angiomatosis retinae (von Hippeľs disease) uAngiomatosis retinae has both a hereditary and sporadic form. uThe type of transmission is autosomal dominant, often with incomplete penetrance and delayed expression. uThe retinal angiomas may be associated with cerebral (hemangioblastomas of the cerebellum, medulla, pons, and spinal cord) and visceral lesions ( cysts of the kidney, pancreas, liver, epididymis, ovary). Angiomatosis retinae (von Hippeľs disease) uWhen angiomatosis retinae is associated with central nervous system and visual involvement, the name von Hippel-Lindau disease is used. uManagement includes treatment of identified angiomas if associated with leakage (photocoagulation, cryotherapy). Racemose hemangioma Wyburn-Mason syndrome uCongenital retinal arteriovenous communications are rare developmental anomalies. uThe abnormalities may range from a single arteriovenous communication to a complex anastomotic system. uIn many cases the lesions are unilateral, non-hereditary. Racemose hemangioma Wyburn-Mason syndrome uThe retinal lesions may be associated with similar ipsilateral vascular malformations in the brain, face , and orbit = Wyburn-Mason syndrome. uIf the lesions are large, however, they may have subretinal fluid and exudate. Retinal cavernous hemangioma uRetinal cavernous hemangioma is characterized by the formation of grape-like- clusters of thin-walled, angiomatous lesions in the inner retina or on the optic nerve head. uLeakage is characteristically absent. uOccasionally the angiomas may bleed into the vitreous but they usually remain asymptomatic. uTreatment (photocoagulation, cryotherapy) is usually not necessary. Retinoblastoma uRetinoblastoma is the most common intraocular malignancy of childhood. uThe tumor occurs bilaterally in 30% to 35% of cases. uAbout 90% of cases are diagnosed prior to age 3 years. Retinoblastoma u6% of retinoblastoma patients will have a family history of retinoblastoma. The condition is generally inherited through an autosomal dominant gene with high but incomplete penetrance. uWhen retinoblastoma is bilateral, it is caused by a germinal mutation. Retinoblastoma uThe most common presenting signs of retinoblastoma appear to be leukocoria and strabismus. uOther features, such as visual difficulties, red eye, discoloration of the iris, and spontaneous hyphema are uncommon. Retinoblastoma uSmall retinoblastoma lesions generally appear as white, vascular intraretinal tumors fed and drained by dilated, tortuous retinal vessels. uFar- advanced retinoblastoma commonly extends outside the eye and invades the optic nerve and orbit. Retinoblastoma uRetinoblastoma undergoes spontaneous regression in approximately 1% of tumors. uManagement options that are currently used in children with retinoblastoma include enucleation, radiation therapy, photocoagulation, cryotherapy, and chemotherapy.