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بسم الله الرحمن الرحيم. THE RETINA. Dr.Bakhtiar Qadr Jaf. OBJECTIVES. 1-SHORTLY DISCUSS THE ANATOMY & PHYSIOLOGY OF THE RETINA. SHORTLY DISCUSS COMMON VISION THREATENING RETINAL DISEASES. Introduction. the retina is a thin, transparent purplish-red membrane.

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  1. بسم الله الرحمن الرحيم THE RETINA Dr.BakhtiarQadrJaf


  3. Introduction • the retina is a thin, transparent purplish-red membrane. • It ‘s thickness varies from 0.1 mm at the oraserrata to O.6 mm near the optic disc. It is thinnest at the center of the fovea. • The retina is continuous with the optic nerve posteriorly, and it extends for ward to become the epithelium of the ciliary body.

  4. Anatomy • The retina consists of an outer pigmented layer called retinal pigment epithelium (RPE) and an inner neurosensory layer. Both are from neuroectoderm. • At the center of the posterior part of the retina is an oval, yellowish area, the maculalutea, which is the retinal area for the most distinct vision. It has a central depression, the fovea centralis. • OraSerrata: is the most anterior part of the retina in which the nervus tissue ends.

  5. Photoreceptors • The photoreceptors are similar to sensory receptors elsewhere in the body. They are two types: the rods and the cones. • The rods are mainly responsible for vision indim light , producing images of varyingshades of black and white. • The totalnumber of the rods in the retina has been estimated to be about 120 million, they are absent at the fovea, rising rapidly in numbers toward the periphery and then slowly diminishingat the extreme periphery of the retina.

  6. Rod & Cone

  7. Retinal cells • The bipolar cells are first-order neurons similar to the neurons in the posterior root ganglia. They have a radial orientation. dendrites of the bipolar cells pass outward to synapse with the photoreceptor cell terminals. • The ganglion cells are so named because they resemble cells found in nervous ganglia and form the second-order neurons similar to the relay neurons found in the spinal cord and brain stem . The axons of these cells become myelinated after they passe the lamina cribrosaand enterethe optic nerve.

  8. Visual Function Testing: Rods & cones • Patients with normal cone function and absent rod function have a visual acuity of 6/6 and have normal color vision. • Patients with normal rod function and absent cone function would be expected to have visual acuity of 6/60 and have absent color vision. • Patients can read fine newspaper print with either their cones or their rods, although patients with only rod function usually require magnification to read. • while the cones are adapted to bright light and can resolve fine details and color vision.

  9. Layers of the Retina Traditionally, based on light microscopic finding: the whole retina was said to be composed of ten layers. These from outside inward, as follows: 1.The pigment epithelium RPE2. The rods and cones3. The external limiting membrane ELM 4. The outer nuclear layer ONL5. The outer plexiform layer OPL6. The inner nuclear layer INL 7. The inner plexiformlayer IPL8. The ganglion cells9. The nerve fiber layer NFL10.The internal limiting membrane ILM

  10. Optic Disc • measured 1.5 mm in diameter, it lies 3 mm medial to the macula lutea. It is pale pink in color, much paler than the surrounding retina. • The disc margin is slightly raised, while the central part has a slight depression, in which the central retinal vessels enter and leave the eye. • The optic nerve fibers exit the eye by piercing the sclera, through the lamina cribrosa, it is a weak area, a rise in cerebrospinal fluid pressure in the meningeal sheath of the optic nerve may cause the optic disc to swell by impending the axon flow of the optic nerve fibers (papilloedema).

  11. Blood Supply of the Retina It is from two sources. (1) The outer laminae, including the rods and cones and ONL, are supplied by the choroidal capillaries; the vessels do not enter these laminae, but tissue fluid exudes between these cells. (2) The inner laminae are supplied by the CRA, CRV. The retinal arteries are anatomic end arteries, and there are no artieriovenousanastomoses. It should be emphasized that the integrity of the retina depends on both of these circulations, neither of which alone is sufficient.

  12. CENTRALRETINAL ARTERY OCCLUSION CRAO Etiology: 1.Spasm of the arterial wall, generally hypertensive in origin. 2. Embolizationis the most common cause of obstruction to the retinal circulation, e.g. an embolus from a vegetation in subacute bacterial endocarditis or from a blood-clot in the left atrium.Degenerative changes within the arterial wall, e.g. arteriosclerosis or atherosclerosis, leading to fibrino-platelet, cholesterol or calcific emboli from atheromatous plaques. 3. Inflammation of the vessel wall,e.g. giant-cell arteritis.

  13. Clinical feature of CRAO Symptoms Complete occlusion: of the CRA usually results in sudden and complete blindness perception of light is generally lost. Branch occlusion: produces localized effects confined to the area of the retina supplied by this branch. Signs ofArterial OcclusionThe characteristic signs include: Fundus picture of CRA, showing milky-white appearance of the retina and cherry-red spot at the macula. The retinal arteries are attenuated and the veins are slightly filled with blood. The vision rapidly diminishes to just perception of light ("P.L.") or complete loss of vision ("N.P.L.").

  14. Treatment It is an ophthalmic emergency and prompt treatment is essential. The treatment is effective only if given within the first few minutes of such an occlusion.. Attempts should be made urgently to relieve any arterial spasm or to dislodge the causative embolus into a less important branch. No return of good central vision is expected if the obstruction has lasted for over 6 hours. Blindness always occurs if the obstruction has lasted for 24 hours.

  15. central retinal vein occlusion -Etiology • Arteriosclerosis and hypertension in elderly people. Pressure of a sclerosed artery on the vein at an arterio-venous crossing is a common cause of a branch occlusion. • Increased blood viscosity, as polycythaemia. 3. Diabetic retinopathy causing phlebosclerosis and a general sluggish capillary and venous circulations due to the disturbed metabolism. 4. Infective phlebitis. 5. The infiltration of the wall of the vein by leucocytes leading to narrowing of the lumen of the vein or to clot formation. 6. Pre-existing chronic simple glaucoma. 7. An orbital cellulitis may damp the venous return from the eye.

  16. Symptoms of Venous Occlusion The patient, usually middle-aged and arteriosclerotic, complains of sudden diminution of vision commonly down to the perception of hand movement HM, he notices dark irregular patches in the centre of his field of vision (i.e. positive central scotoma). The defective vision is often noticed by the patient when waking up in the morning, because the occlusion often takes place during sleep when the circulation becomes sluggish, the general blood pressure is lowered.

  17. Signs of Central Retinal Vein Thrombosis • There are no external signs except that the pupillary reaction to direct light may be a little sluggish. The ophthalmoscopic picture is very characteristic : • The fundus appears splashed with haemorrhages radiating from the disc in all directions. The retinal veins are grossly distended and tortuous. and patches of white exudates. • The arterioles are slightly narrowed and may be concealed by oedema and haemorrhages. Patches of white exudate may appear among the haemorrhages.

  18. Venous Occlusion Stagnation Increased extravascular pressure Hypoxia Oedema and haemorrhage

  19. Complications • Secondary Neovascular Glaucoma. • Vitreous Haemorrhage. • Tractional Retinal Detachment. •  The treatment • The primary systemic causative conditions should always receive appropriate attention. Unfortunately, there is no effective treatment once the blockage has become fully established. If the patient is seen within a few hours of the onset of symptoms,

  20. the administration of anticoagulants may be effective in maintaining the circulation and preventing the spread of the thrombotic process. This anticoagulant treatment must be controlled by prothrombin estimation.Anticoagulants should be employed with care in arteriosclerotic patients. However, there is no guarantee of improvement with the administration of anticoagulants or steroids.If fluorescein angiography reveals widespread capillary occlusion and retinal ischaemia, panretinal laser photocoagulation is of benefit in treating the retinal complications of the ischaemic response and aborting the development of neovascular glaucoma and rubeosisiridis.

  21. HYPERTENSIVE RETINOPATHY • Essential hypertension is associated with thickening of the arteriolar wall as a result of hypertrophy of muscle fibres in the media and increase of fibrous tissue in the intima. • Sustained elevation of blood pressure leads to necrosis of the vascular smooth muscle and leakage of plasma into the unsupported vessel wall through a damaged endothelium which eventually results in secondary vascular occlusion. • The changes that occur in the retina in hypertension are primarily vascular due to the persistently elevated diastolic blood pressure. The retinal changes depend on the state of the retinal vessels prior to the development of hypertension and to some extent on any associated renal damage, as for example in malignant hypertension. • The primary response of healthy retinal arterioles to systemic hypertension is spasm leading to narrowing.

  22. Hypertensive retinopathy Arteriolar constriction Focal Generalized Arteriolosclerosis (A-V changes) Extravascular signs Disc oedema Cotton-wool spots and macular star Flame-shaped retinal haemorrhages

  23. Grading of arteriolosclerosis

  24. DIABETIC RETINOPATHY • Diabetic retinopathy is essentially a microangiopathy affecting the retinal precapillary arterioles, capillaries and venules. The retinopathy is the result of two mechanisms : • Microvascular Occlusion.—This is due to thickening of the capillary basement membrane, endothelial proliferation, deformation of the red blood corpuscles and increased stickness of the platelets. The microvascular occlusion leads to retinal capillary non-perfusion and retinal ischaemia which cause the formation of A/V shunts and neovascularisation. • Microvascular Leakage.—This is due to reduction in the number of mural cells of the capillary wall leading to microaneurisms as a result of local capillary distensions, diffuse retinal oedema due to extensive capillary leakage and/or localised retinal oedema due to focal leakage from microaneurysms.

  25. Adverse Risk Factors 1. Long duration of diabetes 2. Poor metabolic control 3. Pregnancy 4. Hypertension 5. Renal disease 6. Other • Obesity • Hyperlipidaemia • Smoking • Anaemia

  26. Pathogenesis of diabetic retinopathy

  27. Consequences of retinal ischaemia

  28. Consequences of chronic leakage

  29. Clinical Picture of Background Diabetic Retinopathy : Ophthalmoscopically, the earliest changes affect the smaller blood Vs: 1. Presence of Microaneurysms.—They are located in the inner nuclear layer of the retina and appear as small round dots, usually located temporal to the macula. 2. Venous Dilatations and Beading.— A common and early finding is dilatation of veins with marked irregularity in caliber that gives rise to beading and loop formation. 3. Retinal Hemorrhages. —The shape of the haemorrhages depend on their location within the retina : Dot and Blot haemorrhages denote hasmorrhage in mid retina. Flame-shaped haemorrhages denote haemorrhage in nerve fiber layer. iii) Red patch with fluid level • Hard Yellow Waxy Exudates. — They are composed of lipoprotein and lipid-laden macrophages. Theyare located between the IPL & INL of the retina. They appear as yellow-white refractile deposits, particularly in the region of the macula. • 5. Retinal oedema.—This is due to increased permeability of the retinal capillaries and is characterized by retinal thickening obscuring the underlying choroidal pattern.

  30. Location of lesions in background diabetic retinopathy

  31. Signs of background diabetic retinopathy Microaneurysmsusually temporal to fovea Intraretinal dot and blot haemorrhages Retinal oedemaseen as thickening on biomicroscopy Hard exudates frequently arranged in clumps or rings

  32. Preproliferative diabetic retinopathy Signs • Dark blot haemorrhages • Intraretinal microvascular • abnormalities (IRMA) • Cotton-wool spots • Venous irregularities Treatment - not required but watch for proliferative disease

  33. Preproliferative Diabetic Retinopathy.—This is characterised by the presence of: 1. Cotton-Wool Patches.—They are microinfarction of ganglion cells due to capillary occlusion in the nerve fiber layer. 2. Intraretinal Microvascular Abnormalities,resembling flat retinal revascularization. 3. Dilatation of Retinal Veinswith marked irregularity in caliber giving rise to beading and loop formation. 4. Arteriolar Narrowing. 5. Large Dark Blot Haemorrhage.

  34. Proliferative diabetic retinopathy • Affects 5-10% of diabetics • IDD at increased risk (60% after 30 years) Neovascularization • Flat or elevated • Severity determined by comparing with area of disc Neovascularization of disc = NVD Neovascularization elsewhere = NVE

  35. Proliferative Diabetic Retinopathy.—This is characterised by the presence of : 1. Neovascularisation.— New vessels may proliferate on the optic nerve head and along the course of the major temporal arcade. The predilection for revascularization at the optic disc may be explained by the absence of internal limiting membrane over the optic nerve head. The new vessels start as endothelial proliferations arising from the veins and are enveloped in fibrovascular epiretinal membrane which has the potential to contract. 2. Fibrovascular Tissue Proliferation. —Fibrovascular networks become adherent to the posterior vitreous face and continue to proliferate with increased tendency to bleeding. 3. Recurrent Vitreous Haemorrhage. —This leads to shrinkage of the vitreous and promotion of tractional retinal detachment.

  36. Indications for treatment of proliferative diabetic retinopathy NVE > 1/2 disc in area + haemorrhage NVD > 1/3 disc in area Less extensive NVD + haemorrhage

  37. Treatment of Diabetic Retinopathy Medical Treatment.—Although there is no medical cure for diabetic retinopathy, the following therapeutic measures may be helpful in minimising complications : Control of Blood Sugar. Control of Systemic Blood Pressure. Decrease of Platelets Stickiness.—Acetyl salycilic acid may help in decreasing platelet stickiness. Treatment of Anaemia.—

  38. RETINAL DETACHMENT Retinal detachment, or more accurately retinal separation, is a condition in which the sensory retina is separated from the underlying pigment epithelium at the line of cleavage between the layer of visual receptors and the pigment epithelium, with an accumulation of fluid in the potential space between them. The fluid may accumulate between the sensory retina and the retinal pigment epithelium by any of the following mechanisms :

  39. HEREDITARY RETINAL DYSTROPHIESRETINITIS PIGMENTOSA 1- can be an isolated condition, inherited as an autosomal recessive, autosomal dominant, or X-linked recessive trait. 2- The changes of retinitis pigmentosa can also be seen in a number of ocular, central nervous system, and systemic conditions. Clinically In primary retinitis pigmentosa the manifestations are least severe in the autosomal dominant form and most severe in the X-linked form. • In all patients, an early symptom is decreased night vision. Gradually, the visual fields become more constricted. • The fundus shows the characteristic spicule arrangement of pigment, waxy pallor of the optic disc, and marked attenuation of the arterioles. • Female carriers of the X-linked form can have normal fundi or patchy involvement of the fundus with some visual reduction.


  41. Retinoblastoma. • a primary malignant intraocular neoplasm that arises from immature retinoblasts within the developing retina. • It is the most common primary intraocular malignancy of childhood, occurring in about 1 of 15,000 children • Most cases occur in children younger than 6 years of age. • The neoplasm has strong tendencies to invade the brain via the optic nerve and to metastasize widely • Approximately 60% to 70% of retinoblastoma cases are unilateral. • The most common presenting symptom of retinoblastoma is • 1-leukokoria,a white pupil, in the tumor-containing eye or eyes. • 2-strabismus(i.e., esotropia or exotropia) and symptomatic or asymptomatic visual impairment. • 3-Less common presenting symptoms include a red eye, a cloudy cornea, or a change in color of iris, and pain in or around the eye.

  42. Retinoblastoma.

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