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The retina (The nervous inner coat of the eye ball)Lecture-1
The nervous coat, or retina, is the internal layer of the eyeball. Is a thin, transparent membrane   purplish-red in color . Its thickness varies from O.6 mm near the optic disc to 0.1 mm at the ora serrata. It is thinnest at the center of the fovea. It is continuous with the optic nerve posteriorly,   it extends forward to become the epithelium of the ciliary body and the iris. The outer surface of the retina in contactwith the choroid;the inner surface in contact with the vitreous body. The retina consists of an outer pigmented layer and an inner neurosensory layer.
At thecenter of theposterior part of the retina is an oval, yellowish area, the macula lutea, which is the area for the most distinct vision. It has a central depression, the fovea centralis. The optic nerve leaves the retina 3 mm  medial to the macula lutea at the optic disc. The optic disc is slightly depressed at its center, where it is pierced by the central retinal artery and vein.
Pigmented Layer of the Retina (RPE) consists of a single layer of cells. Functions of the RPE:The pigment cells have numerous functions, including the absorption of light, participation in the turnover of the outer segments of the photoreceptors, and the formation of rhodopsin and iodopsin by storing and releasing vitamin A, which is a precursor of the photosensitive pigments. These cells may also have a secretoryfunction. Blood-Retinal Barrier:The pigment epithelial cells are joined to each other by tight junctions that completely encircle the cells. This arrangement forms a barrier that limits the flow of ions and prevents diffusion of large toxic molecules from the choroid capillaries to the photoreceptors of the neural retina.
Neural Retina The photoreceptors are similar to sensory receptors elsewhere in the body. The bipolar cells are similar to the neurons in the posterior root ganglia and form the first-order neuron. The ganglion cells are similar to the relay neurons found in the spinal cord and brain stem and form the second-order neurons. The axons of the ganglion cells become myelinated after they have passed through the lamina cribrosaand entered the substanceof the optic nerve.
Photoreceptors There are two types of photoreceptors, the rods and the cones. The rods are mainly responsible for vision indim light and produce images consisting of varyingshades of black and white, while the cones are adapted to bright light and can resolve fine details and color vision. The total number of the rods in the retina has been estimated to be about 110 to 125 million and of the cones. 6.3 to 6.8 million. The density of the rods and cones varies in different parts of the retina. The rods are absent at the fovea, rising rapidly in numbers toward the periphery and then slowly diminishing at the extreme periphery of the retina.
Bipolar CellsThe bipolar cells have a radial orientation. One or more dendrites of the bipolar cells pass outward to synapse with the photoreceptor cell terminals. Ganglion CellsThe ganglion cells are so named because they resemble cells found in nervous ganglia. They are situated in the inner part of the retina. The ganglion cells are the second neurons in the visual pathway. 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 epithelium2. The rods and cones3. The external limiting membrane 4. The outer nuclear layer5. The outer plexiform layer6. The inner nuclear layer 7. The inner plexiform layer8. The ganglion cells9. The nerve fiber layer10.The internal limiting membrane
12
Optic Disc The optic disc lies about 3 mm medially to the macula lutea. It is pale pink or almost white in color and much paler than the surrounding retina, it measures about 1.5 mm in diameter. The edge of the disc is slightly raised, while the central part has a slight depression. It is in this depression thatthe central retinal vessels enter and leave the eye. It is at the optic disc that the optic nerve fibers exit the eye by piercing the sclera. This area of the sclera is known as the lamina cribrosa. It is a relatively weak area and can be made to bulge out by a rise in pressure inside the eyeball. A rise in cerebrospinal fluid pressure in the meningeal sheath that surrounds the optic nerve may cause the optic disc to bulge into the eyeball.
 It is believed that the external pressure on the optic nerve impedes the axon flow of its fibers and this causes the optic disc to swell (papilloedema).  OraSerrata: is the scalloped anterior margin of the retina. Here the nervoustissues of the retina end. Blood Supply of the Retina The blood supply of the retina is from two sources. (1) The outer laminae, including the rods and cones and outer nuclear layer, 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 central artery and vein. The retinal arteries are anatomic end arteries, and there are no artieriovenous anastomoses. It should be emphasized that the integrity of the retina depends on both of these circulations, neither of which alone is sufficient.
17
19 Visual Function Testing: The normal human retina has about 130 million photoreceptors; the rods outnumber the cones by about 13 to 1.  Patients with normal cone function and absent rod function would be expected to 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.
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 on one of the valves of the heart in cases of subacute bacterial endocarditis or from a blood-clot in the left atrium. In this condition the left eye is more commonly affected. 3. Degenerative changes within the arterial wall, e.g. arteriosclerosis or atherosclerosis, leading to fibrino-platelet, cholesterol or calcific emboli originating from atheromatous plaques. 4. Inflammation of the vessel wall,e.g. giant-cell arteritis.
OCCLUSION OF THE CENTRALRETINAL ARTERY Symptoms  Complete occlusion: of the central retinal artery 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. A significant number of patients with carotid artery disease may also have systemic hypertension. Signs ofArterial OcclusionThe characteristic signs include: Fundus picture of central retinal artery occlusion, 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.").
Treatment Arterial retinal occlusion is an ophthalmic emergency and prompt treatment is essential. 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, and blindness always occurs if the obstruction has lasted for 24 hours. Therefore, the treatment is effective only if given within the first few minutes of such an occlusion.
THROMBOSIS OF THE CENTRAL RETINAL VEIN Etiology 1. Arteriosclerosis and hypertension in elderly people.  2. Abnormal states of blood leading to increased viscosity,  polycythaemia. 3. Diabetic retinopathy causing phlebosclerosis and a general sluggishness of the capillary and venous circulations due to the disturbed metabolism. 4. Infective phlebitis. 5. The thrombosis may be due to 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 cellulitismay damp the venous return from the eye. 8. Pressure of a sclerosed artery on the vein at an arterio-venous crossing is a common cause of a branch occlusion.
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, 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. This is because the occlusion often takes place during sleep when the circulation becomes sluggish, the general blood pressure is lowered and the intra-ocular pressure is slightly increased.
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. The arterioles are slightly narrowed and may be concealed by oedema and haemorrhages. Patches of white exudate may appear among the haemorrhages. Fundus picture of central retinal vein thrombosis, showing the fundus splashed with haemorrhages radiating from the optic disc, veins grossly distended and tortuous, and patches of white exudates.
Venous Occlusion Stagnation Increased extravascular pressure Hypoxia Oedema and haemorrhage
Complications 1. Secondary Neovascular Glaucoma.  2. Vitreous Haemorrhage.  3. Tractional Retinal Detachment. 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, 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 rubeosis iridis.

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Ophthalmology 5th year, 5th lecture (Dr. Bakhtyar)

  • 1. The retina (The nervous inner coat of the eye ball)Lecture-1
  • 2. The nervous coat, or retina, is the internal layer of the eyeball. Is a thin, transparent membrane purplish-red in color . Its thickness varies from O.6 mm near the optic disc to 0.1 mm at the ora serrata. It is thinnest at the center of the fovea. It is continuous with the optic nerve posteriorly, it extends forward to become the epithelium of the ciliary body and the iris. The outer surface of the retina in contactwith the choroid;the inner surface in contact with the vitreous body. The retina consists of an outer pigmented layer and an inner neurosensory layer.
  • 3.
  • 4. At thecenter of theposterior part of the retina is an oval, yellowish area, the macula lutea, which is the area for the most distinct vision. It has a central depression, the fovea centralis. The optic nerve leaves the retina 3 mm medial to the macula lutea at the optic disc. The optic disc is slightly depressed at its center, where it is pierced by the central retinal artery and vein.
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  • 7. Pigmented Layer of the Retina (RPE) consists of a single layer of cells. Functions of the RPE:The pigment cells have numerous functions, including the absorption of light, participation in the turnover of the outer segments of the photoreceptors, and the formation of rhodopsin and iodopsin by storing and releasing vitamin A, which is a precursor of the photosensitive pigments. These cells may also have a secretoryfunction. Blood-Retinal Barrier:The pigment epithelial cells are joined to each other by tight junctions that completely encircle the cells. This arrangement forms a barrier that limits the flow of ions and prevents diffusion of large toxic molecules from the choroid capillaries to the photoreceptors of the neural retina.
  • 8. Neural Retina The photoreceptors are similar to sensory receptors elsewhere in the body. The bipolar cells are similar to the neurons in the posterior root ganglia and form the first-order neuron. The ganglion cells are similar to the relay neurons found in the spinal cord and brain stem and form the second-order neurons. The axons of the ganglion cells become myelinated after they have passed through the lamina cribrosaand entered the substanceof the optic nerve.
  • 9. Photoreceptors There are two types of photoreceptors, the rods and the cones. The rods are mainly responsible for vision indim light and produce images consisting of varyingshades of black and white, while the cones are adapted to bright light and can resolve fine details and color vision. The total number of the rods in the retina has been estimated to be about 110 to 125 million and of the cones. 6.3 to 6.8 million. The density of the rods and cones varies in different parts of the retina. The rods are absent at the fovea, rising rapidly in numbers toward the periphery and then slowly diminishing at the extreme periphery of the retina.
  • 10. Bipolar CellsThe bipolar cells have a radial orientation. One or more dendrites of the bipolar cells pass outward to synapse with the photoreceptor cell terminals. Ganglion CellsThe ganglion cells are so named because they resemble cells found in nervous ganglia. They are situated in the inner part of the retina. The ganglion cells are the second neurons in the visual pathway. 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:
  • 11. 1. The pigment epithelium2. The rods and cones3. The external limiting membrane 4. The outer nuclear layer5. The outer plexiform layer6. The inner nuclear layer 7. The inner plexiform layer8. The ganglion cells9. The nerve fiber layer10.The internal limiting membrane
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  • 13.
  • 14. Optic Disc The optic disc lies about 3 mm medially to the macula lutea. It is pale pink or almost white in color and much paler than the surrounding retina, it measures about 1.5 mm in diameter. The edge of the disc is slightly raised, while the central part has a slight depression. It is in this depression thatthe central retinal vessels enter and leave the eye. It is at the optic disc that the optic nerve fibers exit the eye by piercing the sclera. This area of the sclera is known as the lamina cribrosa. It is a relatively weak area and can be made to bulge out by a rise in pressure inside the eyeball. A rise in cerebrospinal fluid pressure in the meningeal sheath that surrounds the optic nerve may cause the optic disc to bulge into the eyeball.
  • 15. It is believed that the external pressure on the optic nerve impedes the axon flow of its fibers and this causes the optic disc to swell (papilloedema). OraSerrata: is the scalloped anterior margin of the retina. Here the nervoustissues of the retina end. Blood Supply of the Retina The blood supply of the retina is from two sources. (1) The outer laminae, including the rods and cones and outer nuclear layer, 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 central artery and vein. The retinal arteries are anatomic end arteries, and there are no artieriovenous anastomoses. It should be emphasized that the integrity of the retina depends on both of these circulations, neither of which alone is sufficient.
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  • 19. 19 Visual Function Testing: The normal human retina has about 130 million photoreceptors; the rods outnumber the cones by about 13 to 1. Patients with normal cone function and absent rod function would be expected to 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.
  • 20. 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 on one of the valves of the heart in cases of subacute bacterial endocarditis or from a blood-clot in the left atrium. In this condition the left eye is more commonly affected. 3. Degenerative changes within the arterial wall, e.g. arteriosclerosis or atherosclerosis, leading to fibrino-platelet, cholesterol or calcific emboli originating from atheromatous plaques. 4. Inflammation of the vessel wall,e.g. giant-cell arteritis.
  • 21.
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  • 23.
  • 24. OCCLUSION OF THE CENTRALRETINAL ARTERY Symptoms Complete occlusion: of the central retinal artery 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. A significant number of patients with carotid artery disease may also have systemic hypertension. Signs ofArterial OcclusionThe characteristic signs include: Fundus picture of central retinal artery occlusion, 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.").
  • 25. Treatment Arterial retinal occlusion is an ophthalmic emergency and prompt treatment is essential. 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, and blindness always occurs if the obstruction has lasted for 24 hours. Therefore, the treatment is effective only if given within the first few minutes of such an occlusion.
  • 26. THROMBOSIS OF THE CENTRAL RETINAL VEIN Etiology 1. Arteriosclerosis and hypertension in elderly people. 2. Abnormal states of blood leading to increased viscosity, polycythaemia. 3. Diabetic retinopathy causing phlebosclerosis and a general sluggishness of the capillary and venous circulations due to the disturbed metabolism. 4. Infective phlebitis. 5. The thrombosis may be due to 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 cellulitismay damp the venous return from the eye. 8. Pressure of a sclerosed artery on the vein at an arterio-venous crossing is a common cause of a branch occlusion.
  • 27. 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, 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. This is because the occlusion often takes place during sleep when the circulation becomes sluggish, the general blood pressure is lowered and the intra-ocular pressure is slightly increased.
  • 28. 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. The arterioles are slightly narrowed and may be concealed by oedema and haemorrhages. Patches of white exudate may appear among the haemorrhages. Fundus picture of central retinal vein thrombosis, showing the fundus splashed with haemorrhages radiating from the optic disc, veins grossly distended and tortuous, and patches of white exudates.
  • 29.
  • 30. Venous Occlusion Stagnation Increased extravascular pressure Hypoxia Oedema and haemorrhage
  • 31. Complications 1. Secondary Neovascular Glaucoma. 2. Vitreous Haemorrhage. 3. Tractional Retinal Detachment. 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, 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.
  • 32. 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 rubeosis iridis.