Pathology of Retina and Vitreous
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This lecture is part of the yearly Basic Course Lectures in Ophthalmology given by the Dept of Ophthalmology and Visual Sciences at the Philippine General Hospital. Originally given by Dr Pearl Tamesis-Villalon, it is a 1:30:00 hour lecture on the pathologic lesions seen in the vitreous, retina and choroid. It is meant for the general physician and the beginning ophthalmology resident who is interested in the basics of retinal pathology. It includes pathologic changes seen in hypertension, diabetes, vaso occlusive disease, vitreous, membranes, choroid, retinal pigment epithelium, retinal detachments, etc. Lesions such as hemorrhages, cotton wool spots, hard exudates and their location in the retinal layers are explained. Fluorescein angiogram and OCT images are also incorporated. Some images were grabbed from the internet, apologies for not making the necessary acknowledgements.
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Pathology of Retina and Vitreous
- 1. PATHOLOGY OF THE RETINA & VITREOUS 1 OCTOBER 2019 BASIC COURSE LECTURES IN OPHTHALMOLOGY DARBY E SANTIAGO, MD RETINA CLINICAL ASSOCIATE PROFESSOR University of the Philippines Manila Doctors Hospital De la Salle Health Sciences Institute Notre Dame de Chartres Hospital Baguio General Hospital
- 2. PATHOLOGY OF THE RETINA AND THE VITREOUS Pearl M. Tamesis-Villalon MD Chair, DOVS UP-PGH (2011-13) Chief of Service, Retina & Vitreous Surgery (1991-2011) Founding Chair, Retinopathy of Prematurity Working Group Past President, Asia-Pacific Academy of Ophthalmology (1998-1999) Past President, Philippine Academy of Ophthalmology Past President & Founding VP, VitreoRetina Society of the Philippines
- 3. OBJECTIVES To familiarize the beginning ophthalmologist with common retinal lesions that will be encountered in the clinics. To discuss the pathologic processes of common retinal, vitreous and choroidal diseases. To discuss the consequent clinical manifestations of these pathologic processes in the retina, vitreous and choroid.
- 6. Pathologic Responses of the Retina Edema Ischemia Hemorrhages Neovascularization Deposition of Material Fluid Accumulation Membrane Formation & Traction
- 7. Pathologic Responses of the Retina • Tissue loss • New Growth / Tumors • Splitting of Layers • Pigment Hyperplasia • Atrophy & Thinning • Vessel Inflammation, Congestion, Tortuosity
- 8. OUTLINE • EDEMA • HEMORRHAGES • MEMBRANES • ANGIOGENESIS • HYPERTENSION • VITREOUS DETACHMENT • RETINAL DETACHMENT
- 9. EDEMA ETIOLOGY PATHOPHYSIOLOGY APPEARANCE IN THE ANGIOGRAM & OCULAR COMPUTED TOMOGRAPHY
- 10. Retinal Edema • Due to breakdown in the inner blood-retinal barrier. • Accumulation of fluid within retinal tissue. • Appearance: lighter in color, soggy and thick, cystic spaces at macula if chronic/ presence hard exudates.
- 11. Retinal Edema • Symptoms: • Blurring of vision if macula is involved • Possibly none if extrafoveal in location
- 12. Diabetic Retinopathy Capillary damage and breakdown of inner blood retinal barrier is due to: 1. Pericyte loss from oxidative stress 2. Increased transcellular endocytosis 3. Increased Vascular Endothelial Growth Factor 4. Protein Kinase C PATHOPHYSIOLOGY OF MACULAR EDEMA IN DIABETES
- 13. Pathophysiology of Macular Edema: VASCULAR LEAKAGE in DIABETIC RETINOPATHY Lipids also exit the vessels into the retinal interstitia continuously. The fluid is resorbed continuously by the RPE cells. Leaving the large lipids molecules to aggregate and form HARD EXUDATES
- 14. Normal Angiogram
- 15. Non-Proliferative DM Retinopathy Severe Clinically Significant Macular Edema, OS
- 16. Non Cystoid Macular Edema : Diffuse Retinal Thickening
- 17. PATHOPHYSIOLOGY OF MACULAR EDEMA in UVEITIS Anterior segment surgery/ Uveitis Active transport of PGs from the ciliary body Transvitreal travel of PGs to the retina Increased permeability of retinal vascular endothelium Development of Cystoid Macular Edema
- 18. Pathophysiology of Macular Edema: VASCULAR LEAKAGE in INFLAMMATION
- 19. Cystoid Macular Edema • The Macula and Fiber Layer of Henlé (in the outer plexiform layer) are particularly susceptible to accumulation of fluid and lipids from surrounding leaky vessels.
- 20. Cystoid Macular Edema (After cataract extraction) “PETALOID PATTERN”
- 21. Retinal Edema: Causes • Retinal Vascular Disease : – DM Retinopathy – CRVO, BRVO, ROP – Radiation Retinopathy – Collagen Disease Retinopathy – Hypertensive Retinopathy – Ecclampsia – Ocular Ischemic Syndrome • Trauma: Blunt and Perforating Injuries • Posterior Uveitis – Vogt-Koyanagi-Harada – Sympathetic Ophthalmia
- 22. Retinal Edema: Causes • Toxic retinopathy • Infectious: – endophthalmitis – intraocular larvae – TB choroiditis – HIV retinopathy • Macular Disease: – CME – Solar Retinopathy – Photic maculopathy • Cataract Surgery
- 24. Retinal Hemorrhages Color: • brighter red: inner layers (towards vitreous) • darker red: outer layers (towards sclera) – covered by pigment as in hemorrhagic PED Shape : • Flame shaped / Splinter – nerve fiber layer – usually found within the posterior pole • Dot and Blot – inner nuclear and outer plexiform layers – NLF if in the thinner peripheral retina
- 26. Preretinal Hemorrhage: Subhyaloid Hemorrhage Subinternal Limiting Membrane Hemorrhage
- 29. Non Proliferative Diabetic Retinopathy (NPDR) INTRARETINAL Blot Hge (arrowheads)
- 30. Deeper Red Very dark red SUBRETINAL Blood comes from choroidal new vessels growing under the retina. Seen in diseases like: Age-Related Macular Degeneration (AMD) Idiopathic Polypoidal Choroidal Vasculopathy (IPCV)
- 31. Deeper Red SUBPIGMENT EPITHELIUM hemorrhage due to RPE-choroidal disruptions in TRAUMA
- 33. Suprachoroidal Hemorrhage Due to: Trauma CNVM bleed Sudden decompression in a hypertensive patient
- 34. MEMBRANES ETIOLOGY I. EPIRETINAL MEMBRANES II. PROLIFERATIVE VITREO RETINOPATHY (PVR) III. FIBROPROLIFERATIVE / DIABETIC MEMBRANES
- 35. Etiology of Retinal Membranes Preretinal Membranes • Reactive to various causes: retinal ischemia, vascular leakage, posterior uveitis, trauma, laser tx, Cryo tx • Idiopathic membranes • Part of retinal pathology Proliferative VitreoRetinopathy in Retinal Detachment cases Diabetic Retinopathy Subretinal Membranes •In chronic RD
- 36. RISK FACTORS EPIRETINAL MEMBRANE MYOPIA INCREASING AGE NARROWER RETINAL ARTERIAL DIAMETER PREVIOUS CATARACT SURGERY DIABETIC RETINOPATHY HYPERCHOLESTEROLEMIA ??? STROKE BODY MASS INDEX SMOKING HIGHER EDUCATION GENDER
- 37. I. Epiretinal or Pre-Retinal Membranes Associated with Age Related Posterior Vitreous Detachment (PVD) Theorised Pathophysiology Physical disruption of ILM Glial cells spread over the retinal surface, proliferate, and leave fibrin molecules Contraction of the fibrin molecules, leading to traction and distortion of retinal surface
- 40. Proliferative Vitreoretinopathy (PVR) Most common cause of Redetachment after Retinal Detachment Surgery Glial cells, RPE cells, fibroblasts form membrane on surface and under retina Fixed retinal folds are formed Old breaks re-open Anterior loop traction Subretinal membranes New breaks form Complicated retinal detachment
- 41. Proliferative VitreoRetinopathy (PVR) formation in Chronic Retinal Detachment or Post-RD Surgery After RPE cells are liberated and enter the vitreous chamber, they settle on the retinal surface, TRANSFORM to fibroblast cells, and lay down FIBRIN. The fibrin will later contract to form PVR.
- 42. III. Extraretinal Fibro-Vascular Proliferation (Fibro-Proliferative Membranes or FPM) CAN BE SEEN IN THESE DISEASE ENTITIES: • Diabetic Retinopathy • Retinal Vein Occlusions (BRVO, CRVO) • Eales Disease • Retinal Vasculitis NOTE: All are ischemic retinal diseases
- 43. III. Extraretinal Fibro-Vascular Proliferation (Pathophysiology) Retinal Ischemia results in the massive expression Vascular Endothelial Growth Factor (VEGF) Resulting to massive growth of endothelial cells to form new vessels
- 44. VEGF is a Normal Molecule in the Eye Primary angiogenic molecule during embryonic development and in adult neovascular response • Main Sources: • RPE • Muller cells • Ganglion cells • Macrophages
- 45. PROPERTIES OF VEGF: 1. Angiogenic – new vessels 2. Inducer of Vascular Permeability – macular edema 3. Pro-Inflammatory – repair and edema 4. Neuroprotective
- 46. Growth factor production and release Bind to endothelial cell (EC) receptors EC activation EC proliferation and migration (ECM) Enzymes produced by ECs degrade basement membrane ECM remodeling Blood vessel tube formation Loop formation Vascular stabilization 1 2 3 4 5 6 7 8 9 VEGF Stimulates Angiogenesis
- 47. III. Extraretinal Fibro-Vascular Proliferation (Pathophysiology) Once new vessels from the retinal venules erupt from the ILM, growth into the vitreous ensues. Vascular tissue from intraretinal VENULES grows out thru ILM Proliferates within the vitreous gel as vascularized epiretinal membrane (flat new vessels) Membranes further grow into the gel resulting to strong VitreoRetinal adhesion Fibroblasts proliferate & collagen synthesis increases, which later contract Initial ILM striations, folds, then traction RD
- 49. VEGF in Eye Disease VEGF PLAYS A VERY SIGNIFICANT ROLE IN: ● Neovascular Age-Related Macular Degeneration ● Diabetic Retinopathy ● Retinal Vein Occlusion ● Retinopathy of Prematurity ● Corneal Neovascularization ● Iris Neovascularization
- 50. OUTLINE • EDEMA • HEMORRHAGES • MEMBRANES • ANGIOGENESIS • HYPERTENSION • RETINAL DETACHMENT • VITREOUS DETACHMENT
- 51. PATHOLOGIC RESPONSE TO HYPERTENSION SEVERE ACUTE BP ELEVATION CHRONIC BP ELEVATION CHOROID IN HYPERTENSION RETINAL ISCHEMIA TOXEMIA OF PREGNANCY
- 52. Pathologic Response to Systemic Hypertension arteriolar constriction due to autoregulation necrosis of smooth muscle in media due to ischemia vascular dilatation, leakage of plasma into vessel wall producing fibrinoid necrosis occlusion hemorrhage Acute BP Elevation Chronic BP elevation
- 53. Vessel Occlusion: Hemorrhage & Ischemia
- 54. Retinal Ischemia & Cotton-Wool Spots Peripapillary CW spots: Ischemia of Deep Retinal Layers Retinal CW Spots : • Occlusion of terminal arterioles • Axoplasmic flow interruption • Surrounded by dilated capillaries • Surrounded by microvascular remodeling
- 55. Pathologic Response to Systemic Hypertension vasoconstriction due to autoregulation arteriolar wall thickening, narrowing of lumen Chronic BP elevation & Effects on Arteries
- 56. The resistance of flow is equivalent to the fourth power of the diameter. Therefore, a 50% decrease in the lumen results in a 16-fold increase in the pressure.vasoconstriction due to autoregulation arteriolar wall thickening, narrowing of lumen mechanical problems in blood flow, AV crossing defects Chronic BP elevation
- 57. GUNN’s Sign - tapering of vein SALUS’ Sign - deflection of vein, S- shaped curving
- 58. BRANCH RETINAL VEIN OCCLUSION AV CROSSING CHANGES Venous compression by the artery due to sharing of common adventitia
- 59. Pathologic Response to Systemic Hypertension vasoconstriction due to autoregulation arteriolar wall thickening, narrowing of lumen Mechanical problems in blood flow AV crossing defects BRVO, arterial macroaneurysm form’n, Non Arteritic Ischemic Optic Neuropathy (NAION) MICROVASCULAR REMODELING: microaneurysms, dilated capillaries, focal areas of capillary non perfusion Chronic BP elevation
- 61. Microvascular Remodeling MICROVASCULAR REMODELING: microaneurysms capillary dilation capillary non- perfusion
- 62. Pathologic Response of CHOROID to Hypertension Fibrinoid necrosis of choriocapillaris Ischemia of RPE and outer retina Breakdown of outer blood retina barrier RPE Atrophy Exudative Retinal Detachment
- 64. Exudative Detachment in Severe Preeclampsia (taken lying down)
- 65. Exudative RD in Acute Hypertension Toxemia of Pregnancy ➢ Choroidal Ischemia ➢ Damage to RPE and outer Blood Retinal Barrier ➢ Exudative Retinal Detachment ➢ Late changes: RPE scars and atrophy
- 66. Exudative RD in Acute Hypertension Toxemia of Pregnancy
- 67. Exudative RD in Acute HPN Toxemia of Pregnancy ACUTE ELSCHNIG’S SPOT (white arrow)
- 68. Elschnig Spots (Latent) BLACK SPOTS surrounded by BRIGHT YELLOW or RED HALOs
- 69. SUMMARY: Pathologic Response to Hypertension • Retinal arteriolar narrowing (copper & silver wiring) • Cottonwool spots in peripapillary area • Retinal hemorrhages in NLF and inner nuclear layer • Intraretinal edema with waxy hard exudates • Microaneurysms • Telangiectasias • Diffuse macular edema • Macular star formation
- 71. Retinal Detachment Separation of Neurosensory Retina from RPE 1. Rhegmatogenous 2. Non-Rhegmatogenous Exudative Traction
- 72. Subretinal Space “Retinal Detachment” a misnomer because there never was any real attachment of the retina to the RPE.
- 73. What are the Forces Keeping Retina Attached 1. Viscoelastic tamponade by the vitreous gel 2. Hydrostatic intraocular pressure *( transretinal fluid gradients) 3. Interphotoreceptor matrix 4. Suction forces of RPE 5. Osmotic pressure of choroid
- 74. Attachments of the Vitreous to the Retina 1. Disc 2. Fovea 3. Retinal Vessels 4. Pars Plana 5. Posterior Lens Capsule
- 75. Rhegmatogenous Retinal Detachment (Pathophysiology) • Break is a full thickness discontinuity in the neuroretina • Breaks may be : • tears: secondary to dynamic vitreoretinal traction • holes: secondary to localized retinal disintegration or atrophy
- 76. Rhegmatogenous Retinal Detachment: Tears Tears are U-shaped with a flap. • Found at the posterior edge of vitreous base • Vitreous pulls on the tip of the flap • The flap always points toward the disc
- 77. TEARS CLINICAL PEARLS Tugging of the vitreous on the retina give rise to “flashes” Tearing of the retina is frequently accompanied by hemorrhage giving rise to “floaters”
- 78. ATROPHIC HOLES • Atrophic holes carry low risk of RD • Not formed thru dynamic vitreous traction • Found in the retinal equator and usually within lattice degenerations
- 79. Formation of Retinal Detachment
- 80. Rhegmatogenous Retinal Detachment (Pathophysiology) • Steps in formation of RD • Syneresis - liquefaction of the vitreous core • Collapse of the vitreous centrally • Posterior vitreous detachment • Formation of tear in areas of strong attachments • Water enters the subretinal space as the vitreous tugs on the retinal break • Increasing detachment
- 81. CONFIGURATION of RETINAL DETACHMENT Gravitational forces play a major role in determining distribution of SUBRETINAL FLUID This diagram will be useful when you are looking for the location of the break using the indirect ophthalmoscope
- 82. Natural History of Retinal Death after Detachment • Neurosensory retina becomes edematous and less transparent. • Cystic spaces appear within the retinal layers • Photoreceptor outer segments are shed, nuclei degenerate. – Restoration of vision depends on reversal of edema and regeneration of receptor outer segments • After months of detachment, the retina thins out and becomes transparent again. • Release of RPE cells into the vitreous causes haze and proliferative vitreoretinopathy (PVR) Chronically Detached Retina
- 83. Natural History of RD Other changes in long standing RD : 1. RPE atrophies with reactive hyperplasia at stable margins, forming “demarcation or high water lines” in areas of subtotal RD 2. Anterior segment neovascularization 3. Subretinal fibrosis (white arrow) 4. Spontaneous reattachment is possible
- 84. OTHER FORMS OF NEUROSENSORY RETINAL DETACHMENTS
- 86. Vogt Koyanagi - Harada Syndrome
- 87. PATHOLOGIC RESPONSES OF THE VITREOUS
- 88. Pathologic Responses of the Vitreous 1. Vitreous Liquefaction 2. Posterior Vitreous Detachment 3. Vitreous Opacities – inflammatory material – hemorrhage – veils, membranes, bands – malignancies – metabolic products
- 89. A gel, not liquid 99% water, 1% solids ( hyaloronic acid molecules and collagen meshwork) Very few cells called hyalocytes No blood vessels Has a cortex that envelopes gel Attached to retina at certain points Plays a role in pathogenesis of many retinal problems The Vitreous Body
- 90. Posterior Vitreous Detachment • Occurs as part of the ageing process • Prevalence increases with AGE and AXIAL LENGTH – At age 60-69: 27% have PVD – At age 70: 63% have PVD
- 91. PVD
- 93. SYMPTOMS in Acute PVD 1. FLOATERS ➢ collagen fibers from meshworK ➢ epi-papillary glial tissue (Weiss ring) ➢ vitreous hemorrhage 2. FLASHES OR PHOTOPSIAS ➢ due to the stimulation of Vitreo-Retina interface attachments
- 94. • Acute Symptomatic PVD (with flashes or floater) • 8-15% will have a break • If with vitreous hemorrhage • 70% have retinal breaks Syptomatic PVD and Retinal Breaks UTZ photo shows: 1. Vitreous detachment 2. Vitreous hemorrhage 3. Fluid loculations
- 95. SUMMARY Common retinal lesions (edema, hemorrhages, membranes) encountered in the clinics were shown. Pathologic processes of angiogenesis, hypertension, retinal detachment and posterior vitreous detachment were discussed. Consequent clinical manifestations of these pathologic processes in the retina, vitreous and choroid were correlated.
- 96. DUANE’S FOUNDATIONS of clinical ophthalmology http://www.oculist.net/downaton502/prof/ebook/duanes/pages/contents.html FOUNDATIONS VOLUME 3 – Pathology of the Eye CHAPTER 7 – Pathologic Correlates in Ophthalmology CHAPTER 13 – Hypertension & the Eye CHAPTER 14 - Vitreous
- 97. ACKNOWLEDGEMENTS Dr. Mayos Pe-Yan, Basic Course Coordinator Dr. Milagros Herrera-Arroyo, Service Chief, UP-PGH Retina Service Dr. Pearl Tamesis-Villalon, former Chair of DOVS and Retina Service Chief
Editor's Notes
- Normal Retina Anatomy. Different Layers. Vascularity. Relationship with the choroid and RPE.
- The oblique orientation of the outer plexiform layer (connection of rods and cones to the bipolar layer) in the macula explains the appearance of several lesions. Cyst-like spaces may occur at the level of the OPL as the result of accumulation of fluid or hydropic swelling of Muller cells with subsequent distruption and formation of the spaces.
- These cyst-like spaces are not lined by epithelium and are therefore not designated as true cysts. Tso et al has shown that cystoid spaces can also form in the outer nuclear, inner plexiform and inner nuclear layers.
- The cysts are oriented along the plane of Henle’s layer and appear to originate from a central zone, like the petals of a flower: The Petaloid Pattern of CME in FA.
- The central dark red is an extension of the hemorrhage through the sensory retina into the sub-ILM layer.
- Does the abnormal rise in blood pressure logically lead to the bursting of vessel walls producing hemorrhage? Vessels with areas of Sclerosis lack muscle tone and tend to DILATE secondary to elevated intraluminal pressure. Non-Sclerotic vessels exhibit narrowing because of intact muscular walls and preserved autoregulatory response.
- The arteriole WALL is normally invisible, appearing only as an erythrocyte column with central light reflex. As the wall thickens, the light reflex becomes more diffuse and partially obscures the blood column, giving the once invisible WALL a yellowed or COPPER WIRE appearance. Progression of thickening and sclerotic changes eventually obscures the blood column completely producing a SILVER WIRE appearance. Advanced sclerosis of the retinal vasculature leads to increased optical density of the retinal blood vessel walls; this is visible on ophthalmoscopy as a phenomenon known as sheathing of the vessels. When the anterior surface becomes involved, the entire vessel appears opaque (pipe-stem sheathing). The patency of such vessels has been demonstrated by fluorescein angiography. When sheathing encircles the wall, it produces a silver-wire vessel
- According to Spencer, the normal light reflex of the retinal vasculature is formed by the reflection from the interface between the blood column and vessel wall. [1] Initially, the increased thickness of the vessel walls causes the reflex to be more diffuse and less bright. Progression of sclerosis and hyalinization causes the reflex to be more diffuse and the retinal arterioles to become red-brown. This is known as copper wiring.
- Hard exudates are edema residues (lipids and cholesterol). They seem to settle in a bathtub ring-like configuration. Assume patterns that reflect the 1. source of the leakage (i.e. circinate rings) and 2. the neural elements of the layer in which they are found (i.e. macular star). Extracellular Edema – increased transmural pressure lead to transudation of plasma Intracellular Edema – direct result of retinal ischemia