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Systemic hypertension affects not only the retinal vasculature but also choroidal and disc vessels. Of the three, the choroid is the most vulnerable to pressure elevation because of lack of autoregulation of its vessels. Acute hypertension will lead to necrosis of choroidal vessel endothelia seen as a tan fundus discoloration of choroidal lobular size, a so called Elschnig spot. The retinal vasculature responds to hypertensive insult with leakage of the precapillary arteriole as well as arteriolar narrowing, increased tortuosity and arterial venous nicking. Small vessel closure causes cotton wool spots and leakage of vessels causes intraretinal hemorrhage and lipid exudation of variable appearance depending on the level of accumulation location in the retina. Chronic hypertension results in intimal fibrosis, arteriolar sclerosis and predisposes to branch retinal vein occlusion, branch retinal artery occlusion, central retinal vein occlusion, microaneurysms, macroaneurysms, vitreous hemorrhage, epiretinal fibrosis as well as serous retinal detachments. The disc responds to hypertension with edema and hemorrhages, which is considered a sign of chronic hypertensive retinopathy age-related macular degeneration, hypertensive retinopathy, macular degeneration, maclar degeneration
Central retinal vein occlusion can occur in young healthy individuals but is most often associated with glaucoma, arteriolar sclerosis and hypertension. Compared to the subtotal visual loss of artery occlusions, the visual loss after central retinal vein occlusion is more variable, ranging from mild blurring of vision to light perception vision. On examination the retina shows multiple intraretinal hemorrhages (tomato-ketchup fundus) and may have many cotton wool spots (cheese-pizza fundus). Cotton wool spots and poor initial visual acuity indicate severe ischemia as opposed to non-ischemia of the retina. After vascular occlusion the retina accumulates intraretinal fluid, often involving fovea and/or optic disc. The ischemic type of vein occlusion is often
Central Retinal Artery Occlusion (CRAO)
Patients present with sudden, severe and painless loss of vision in one eye. The retina becomes opaque and edematous, particularly in the posterior pole where the nerve fiber and ganglion cell layers are the thickest. The retina is thin in the fovea, resulting in a translucent (cherry) red spot. The visual loss is usually severe with 66% of eyes having less vision than 20/400. Emboli are
Diabetic Retinopathy
Diabetic retinopathy affects the entire eye, ie, retina, choroid and optic nerve. The most prominent changes are in the retinal microvasculature i.e., capillaries which show selective loss of pericytes and formation of microaneurysms. The small vessels may occlude or they may leak. Occlusion appears as cotton wool spots - or after if bleeds into them - splinter hemorrhages. Leakage results in retinal edema and exudation of lipid or blood. An increase in areas of microvascular closure ("non perfusion"), microvascular abnormalities, accompanied by blood and lipid
AMD is a major cause of legal blindness in the elderly. It is probably related to cumulative light exposure of the neuroepithelia during life and to systemic vascular aging resulting in pigment epithelial atrophy, basement membrane like subepithelial material (drusen), thickening, splitting and calcification of Bruch's membrane, obliteration and thickening of the intercapillary spaces
Retinal Detachment Surgery
Retinal detachments are caused by retinal breaks allowing fluid to get underneath the retina. Symptoms are flashes, floaters, loss of peripheral and central vision. The principle of surgery is to find all breaks by ophthalmoscopy and then to close all breaks by applying cryopexy and buckles. A recently rediscovered technique is the treatment of retinal detachments by air or gas injection only (pneumatic retinopexy).
Vitreous Surgery
Vitreous surgery addresses the causes of vitreous traction on the retina. In some cases, if the retina is scarred, a previously immobile retina is mobilized and vitreous substitutes; hyaluronic acid, gas or oil are used to push the retina into a more normal position. The ultimate outcome will still be linked to finding and closing all retinal breaks permanently.
Uveal Melanoma
Uveal melanomas present as pigmented masses in iris, ciliary body or choroid (the uvea). They can reach a large size before detection. If the tumor involves the ciliary body, it may displace the lens and produce astigmatism or cataract. Often these tumors will be first noticed after cataract extraction. Melanomas may extend into the anterior chamber or through the sclera seen as an episcleral pigmented nodule. Prominent episcleral vessels (sentinel vessels) may be an important external indicator of an intraocular tumor. Posteriorly located choroidal melanomas appear as diffuse nodular or mushroom shaped masses. The mushroom shape is due to penetration of Bruch's membrane by the tumor and strangulation of the base of the tumor by this tough basement
Metastatic Tumors to the Uvea and Retina
Retinal metastases are rare, and if they occur, may present as occlusive vasculopathy and posterior uveitis. Most ocular metastases lodge in the posterior choroid. The lesions appear as tan-yellow masses that often produce a non-rhegmatogenous retinal detachment. The metastases are frequently bilateral and multifocal. Iris metastases appear as tan nodules, which can bleed into the anterior, chamber (hyphema). The most common primary tumor is breast cancer in women and lung cancer in men followed by prostate and GI primary sites. The treatment consists of observation, radiotherapy to