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Retina 1 Clinical anatomy and retinal Micro-circulation 2 Characteristics of Normal Fundus, Optic Disc, Dr Mahmood Fauzi MBBS MS FCLI ASSIST PROF OPHTHALMOLOGY AL MAAREFA COLLEGE Objectives Explain the clinical anatomy of retina and retinal microcirculation Enumerate retinal diagnostic procedures -Retinal examination Describe patho-physiology and clinical presentation and management of retinal vascular disorders ie(a) Periphlebitis (b) Central retinal artery/ vein occlusion (c)Retinopathy-diabetic and hypertensive • Other retinal conditions (Macular Degeneration, Retinitis Pigmentosa, Retinal Detachment, Retinal Dystrophy,Retinoblastoma) DEVELOPMENT OF THE RETINA During the fourth week of gestation the optic vesicle is converted into a doublelayered optic cup The conversion of the optic vesicle to the optic cup is due to the differential growth of the walls of the vesicle. The retina develops from the two parts of the optic cup i. the retinal pigment epithelium develops from the outer layer of the optic cup, ii. the neurosensory retina develops from the inner layer of the optic cup. Blood supply: The central retinal artery(branch of opthalmic artery) enters the globe from the center of the optic nerve, immediately adjacent and parallel to the exiting central retinal vein. Inner layer→ central retinal vascular system Outer layer→ choroid(ciliary vascular system) Macula lutea→ choriocapillaries Inner barrier(blood–retina barrier) Dense connection of retinal capillary endothelium Outer barrier(choroid-retinabarrier) zonula occludens between the RPE RPE- Bruch’s membrane +choriocapillaries complex Clinical Anatomy of Retina Retina Contain photoreceptors-Rods and Cones. Rods and cones converts light rays into electrical impulses Optic Nerve sends electrical impulses towards brain. Retina is 0.56 mm thick near optic disc, 0.1 mm at ora serrata Thinnest at center of fovea Rods contain photo chemical called Rhodopsin mainly responsible for black and white/dark vision. Cones: contain light sensitive photochemical (color pigment) responsible for color vision Macula- yellow spot near the center of the retina, Diameter around 5 mm. Fovea centralis is present at the center of macula , Highest visual resolution is seen in fovea and is also responsible for sharp central vision. Optic Disc: (Blind Spot) area where retinal nerve fibres join to form optic nerve, no rods and cones present here. Optic nerve starts from optic disc and extends up to Optic chiasma Functions of retina Form sense Color vision Dark adaptation DISCRIPTION OF FUNDUS 1 Size, Shape and Borders of the Optic Disc. Optic disc size is about 1.92 millimeters vertically by 1.76 millimeters horizontally.. Shape of optic disc is a vertically oval normally a sharply defined, yellowish- orange structure and forms head of optic nerve. Edge of optic disc is known as peripapillary area which may be hyperpigmented or scalloped pale Temporal creasent is seen in myopia 2 Cup to Disc Ratio---1:3 or 0.3:1 central depression at optic disc known as the optic or physiologic cup 3 Relative size of the Arteries(smaller) and Veins(darker)--- 2:3 (veins are 1.5 times wider than arteries) 4 Texture of the Retina-- retina is normally completely transparent without any intrinsic color 5 Color of the Retina---Orangeish color is from vasculature of the choroid. 6 Trace the vascular structure to the equator of the retina. 7 Macula- color and size Differentiating arteries from veins & Identifying Optic disc, Macula, Fovea Arteries are lighter in color. Shinier due to light reflex. Narrower in caliber than veins. Optic disc is at the post. pole of eye ball. Oval in shape and pale in color. Optic disc aka Blind spot–area where optic nerve leaves eyeball. Arteries and veins radiate outwards from the disc in a tree like fashion. Identify disc-to-cup ratio The pink rim of disc contains nerve fibers. The white cup is a pit with no nerve fibers. Macula is less vascular zone ,temporally located,1.5DD away from disc.Central a-vascular zone is Fovea Structures of the retina Nasal Temporal Diagnostic Procedures Of Retina Fundus examination by Ophthalmoscopy (A) (B) Direct Ophthalmoscopy In-Direct Ophthalmoscopy Slit lamp examination with 70-9O D Digital Fundus Photography Fluorescein angiography Ultrasonography b-scan Optical coherence tomography(OCT) Retinal examination Direct Ophthalmoscopy In-Direct Ophthalmoscopy can visualize upto peripheral fundus Opthalmoscope Fundus Indirect slit-lamp biomicroscopy Fluorescein Angiography Used for examining circulation of retina, Bolus of 5 cc 10% sodium fluoresceine injected in arm Dye reaches retinal circulation approx 10 sec after inj. Normal circulatory filling times 0 seconds — injection of fluorescein 9.5 sec — posterior ciliary arteries 10 sec — choroidal flush (or "pre-arterial phase") 10-12 sec — retinal arterial stage 13 sec — capillary transition stage 14-15 sec — early venous stage (or "laminar stage", "arterial-venous stage") 16-17 sec — venous stage 18-20 sec — late venous stage 5 minutes — late staining Photos are taken approximately once every second for about 20 seconds, then less often. A delayed image is obtained at 5 and 10 minutes. Optical coherence tomography(OCT) Ocular ultrasound electrooculogram EOG electroretinogram ERG visual evoked potential VEP Retinal vascular disorders Periphlebitis retinae Inflammation of the wall of the retinal veins commonly due to 1. tuberculosis (Mycobacterium tuberculosis). 2. Sarcoidosis, 3. multiple sclerosis, 4. Eales Disease (“periphlebitis retinae). Cause hemorrhages in retina and vitreous Commonly effect adult(20-30 year) Cause sudden loss of vision due to vitreous hemorrhage Treatment Control the basic etiology Corticosteroid help to control inflammation Photocoagulation (laser) of leakage area Central retinal artery occlusion-CRAO It is obstruction of the circulation of the retina due to embolus and thrombosis. Caused by hypertension and arteriosclerosis. Commonly results in complete or permanent blindness. Due to Permanent damage to the ganglion cells caused by prolonged interruption of retinal arterial blood flow Months later, pale disc due to death of ganglion cells and their axons No optic disc swelling unless there is ophthalmic or carotid artery occlusion True ophthalmic emergency FFA in CRAO- complete absence in filling central retinal artery PATHOPHYSIOLOGY OF CRAO Embolism is common cause of CRAO Sourse of emboli Heart – mural thrombus in MI calcific emboli from mitral or aortic valve vegetation as in bacterial endocarditis cardiac myxoma rare case Internal carotid artery cholesterol emboli, calcific emboli fibrin–platelet emboli as in amaurosis fugax(Retinal TIA) Inflammatory diseases such as SLE, PAN,Wageners granulomatosis, Behcets disease,giant cell arteritis Symptoms Signs Sudden painless vision lose of one eye Direct light reflex disappear, indirect light reflex normal Retinal edema、cherry-red spot Retinal artery narrowing Retinal hemorrhages Treatment Ocular massage: To dislodge a small embolus in CRA and restore circulation Pressing firmly for 10 seconds and then releasing for 10 seconds over a period of ~ 5 minutes Vasodilator (acetylencholine) dilate the spasm artery acetylsalicylic acid(aspirin) to prevent clot formation Central retinal vein occlusion - CRVO Obstruction due to veins circulation thrombosis and embolus Caused by hypertension, Arteriosclerosis,Hyperviscosity and glaucoma Predisposing factor advancing age Causes unilateral sudden impairment of vision not sudden loss of vision In central retinal vein occlusion, the thrombus lies at the level of the lamina cribrosa; In branch retinal vein occlusion, it is frequently at an arteriovenous crossing. Long term risk for neovascular glaucoma, so periodic ophtho f/u Ischemic type CRVO Non-Ischemic type CRVO TYPES : Nonischemic CRVO is milder form of disease. May present with good vision, few retinal hemorrhages and cotton-wool spots, no relative afferent pupillary defect, and good perfusion to the retina. May resolve fully with good visual outcome or may progress to the ischemic type. Ischemic CRVO is severe form of the disease.May present initially as the ischemic type, or it may progress from nonischemic. Usually, presents with severe visual loss, extensive retinal hemorrhages and cotton-wool spots, presence of relative afferent pupillary defect, poor perfusion to retina, and presence of severe electroretinographic changes. In addition, patients may end up with neovascular glaucoma and a painful blind eye. NON ISCHEMIC CRVO –Diffuse flame shaped retinal hemorrhage Tortuosity and engorgement of retinal veins ISCHEMIC CRVO: diffuse capillary non perfusion—rubiosis iridis— neovascular glaucoma(NVG) Non-Ischemic CRVO Ischemic CRVO Causes Central retinal vein obstruction has been associated with various systemic pathological conditions, although the exact cause and effect relationship has not been proven. Some of the conditions in which CRVO has been associated include the following: Systemic vascular disease - Hypertension, diabetes mellitus, cardiovascular disease Blood dyscrasias - Polycythemia vera, lymphoma, leukemia Clotting disorders - Activated protein C resistance, lupus anticoagulant, anticardiolipin antibodies, protein C, protein S, antithrombin III Paraproteinemia and dysproteinemias - Multiple myeloma, cryoglobulinemia Vasculitis - Syphilis, sarcoidosis Autoimmune disease - Systemic lupus erythematosus Oral contraceptive use in women Obstructive sleep apnea - This affects more patients with retinal vein obstruction than other disorders; treatment of the sleep apnea may help prevent central vein obstruction.[11] Other rare associations - Closed-head trauma, optic disc drusen, arteriovenous malformations of retina Treatment exact pathogenesis of the CRVO is not known Identifying and treating any systemic medical problems to reduce further complications is important Advocated treatments are as follows: Aspirin Anti-inflammatory agents Isovolemic hemodilution Plasmapheresis Systemic anticoagulation with warfarin, heparin, and alteplase Fibrinolytic agents Systemic corticosteroids intravitreal injection of anti-angiogenic drugs like ranibizumab , aflibercept , triamcinolone , bevacizumab Dexamethasone intra vitreal implants Hypertensive retinopathy Fundus changes occurring in patient suffering from systemic hypertension due to vaso-construction and arteriosclerosis etc. High blood pressure can cause damage to blood vessels in the eyes. Cause headaches and visual disturbance. The changes seen in the fundus secondary to hypertension are representative of changes taking place in the arterioles throughout the body. Grading of hypertensive retinopathy : grade 0 -- no changes grade I, barely detectable arteriolar narrowing; grade II, generalized narrowing and focal constrictions; grade III, gr2+hemorrhage, and exudation; grade IV, gr 3 + papilloedema of the disc. Vaso-constrictive and early sclerotic changes in hypertensive retinopathy, including diffuse arteriolar narrowing, sinusoidal tortuosity, copper wire appearance, arteriovenous crossing changes, tapering of veins and increased arteriolar branching angles Thickening and sclerosis of arterioles light reflex width (copper silver wire) A-V nicking Diabetic retinopathy PATHO-PHYSIOLOGY OF DIABETIC RETINOPATHY 1 Diabetic retinopathy is a microangiopathy. This results in a thickening of the basement membrane of the vessels and loss of pericytes and vascular endothelial cells. 2 Hyperglycemia plays an important role at this early stage. Later, capillary closure occurs, resulting in retinal ischemia. The further course is triggered by hypoxia. 3 In the ischemic retina, angiogenic factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) are produced. 4 Ischemia and VEGF contribute to new vessel formation in the preretinal area and iris. 5 At any stage, a breakdown of the blood–retina barrier with increased vascular permeability can occur, leading to macular edema. 6 Hard Exudates representing lipid deposits in the retina Cotton-Wool spots and soft exudates representing nervefiber infarction RISK FACTORS OF DIABETIC RETINOPATHY 1 DURATION OF DIABETES IS MOST IMPORTAT RISK FACTOR 15% after 5 year 50% after 10 year 60% after 15 year 70% after 20 year 90% after 30 year 2 POOR METABOLIC CONTROL: RAISED HbA1c 3 PREGNANCY 4 HYPERTENSION Retinopathy effects the circulatory system of the retina Causing damage of blood vessels of eye Leakage of blood (hemorrhage) fluid leakage (oedema) Commonly cause blindness or loss of vision Cause darkening in image 1.Background retinopathy small red dots will appear on retina due to tiny swellings in the blood vessel walls 2.Pre-proliferative retinopathy retina swells and leaks blood reading small print may become particularly difficult. 3.Proliferative retinopathy It is third stage of retinopathy extensive neovascularization, usually causing a sudden loss of vision TREATMENT Background retinopathy Requires no treatment, but should have Regular eye Examinations by Ophthalmologist Pre-proliferative retinopathy also does not require treatment, Laser treatment can be an option if leakage begins Proliferative retinopathy Argon Laser is used to 'burn' the abnormal blood vessels to prevent further growth of new blood vessel Argon Laser cannot restore any lost vision, but to prevent further growth Diabetic maculopathy Involvement of fovea occur at any stage of retinopathy due to Macular edema Macular hemorrhages Macular detachment Other retinal disorders Macular Degeneration Also called age related macular degeneration It is a non hereditery most common cause of permanent irreversible central loss of vision Age related macular degeneration-AMRD Type Nonexudative(atrophic or dry) 90% most common type of ARMD Drusen (no neovascular membrane) RPE changes (atrophy,hyperplasia) Exudative(wet):10% cause of ARMD presence of fluid and hemorrhages it is more dangerous Choroidal Neovascularization Treatment Vit C & E, β-carotene, minerals(cupric oxide & zinc oxide) Omega-3 Antivascular endothelial growth factor-AVEGF(avastin) Photodynamic therapy(PDT) Retinal detachment Separation of neuro-sensory retina from pigmented epithelium is called retinal detachment Types Primary or simple or Rhegmatogenous: separation of retina in the form of hole or tear. This hole allows the vitreous to raise retina from its normal position Secondary or exudative : due to pathology and the accumulation of fluid to push retina from its normal position Tractional : due to fibrovascular proliferation as in proliferative diabetic retinopathy or trauma Treatment-Laser treatment Retinopexy use to reattach the detached retina. Rhegmatogenous Retinal Detachment Basis retinal degeneration liquefied vitreous retinal hole→RD Predisposing aging high myopia ocular trauma Night blindness Due to deficiency of vitamin- A V-A is present in cytoplasm of rods and pigmented layer of retina Without the V-A the amount of retinal and rhodopsin may severally depressed this condition is known as night blindness Color blindness As cones are responsible for color vision The missing of single group of cones from RGB the person unable to distinguish some color from other this condition is called color blindness If the red cone is missing this condition is called protonpe If green cone is missing this condition is called deutarnope Red-green color blindness is a genetic disorder inherited from mother And in rare cases blue cone missing Diagnosis- Ishihara Chart DRUGS CAUSING RETINAL TOXICITY – DIGITALIS ABNORMAL COLOUR VISION ETHOMBUTOL,QUININE– CHLOROQUINE PHENOTHIAZINE – TAMOXIFEN – OPTICNEUROPATHY BULLS EYE MACULOPATHY RETINAL DEGENERATION PIGMENTARY RETINOPATHY AND RETINAL EDEMA PIGMENTARY RETINOPATHY Resources http://www.mayoclinic.org/diseases-conditions/retinaldiseases/basics/definition/con-20036725 http://www.sciencedirect.com/science/journal/13509462 http://www.snec.com.sg/eye-conditions-andtreatments/common-eye-conditions-andprocedures/Pages/retinal-vascular-disorders.aspx http://www.academy.org.uk/lectures/barnard5.htm
