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Lecture 1: Introduction, Anatomy and Diagnostics
- 1. I N T R O D U C T I O N , ANATOMY REVIEW AND DIAGNOSTICS P O S T E R I O R S E G M E N T
- 2. WELCOME
- 3. S Y L L A B U S 8072 Ocular Disease IV • P O S T E D O N B L A C K B O A R D A N D W E B S I T E : M A Y C H A N G E • C O U R S E W E B S I T E H T T P : / / W W W . Y O U N G E Y E S . I N F O • P A P E R S A N D C A S E R E P O R T S C A N B E U P D A T E D W E E K L Y • P O P Q U I Z • G U E S T L E C T U R E R S • C O N T A C T I N F O R M A T I O N • G R A D I N G
- 4. N O R M A L H E A L T H / D I S E A S E / T R A U M A N B E O P A R T 2
- 5. L E A R N I N G O B J E C T I V E S • Recognize normal anatomical structures discussed in the lecture and their physiological variations. • Recognize the location, depth and extent of pathological lesions. • Identify and interpret the findings of diagnostic tests discussed in the course. • List indications, contraindications and side effects of Diagnostic tests
- 6. V I T R E O U S A N A T O M Y Ultrastructure of posterior vitreous cortex in humans. Scanning electron microscopy demonstrates the dense packing of collagen fibrils in the vitreous cortex. To some extent this arrangement is exaggerated by the dehydration that occurs during specimen preparation for scanning electron microscopy (bar = 10 [a 5]mm). (Sebag J: The Vitreous--Structure, Function and Pathobiology. New York, Springer-Verlag, 1989)
- 7. V I T R E O U S A N A T O M Y Eye (2008) 22, 1214–1222; doi:10.1038/eye.2008.21; published online 29 February 2008 Adult vitreous structure and postnatal changes M M Le Goff1 and P N Bishop1 Eye (2008) 22, 1214–1222; doi:10.1038/eye.2008.21; published online 29 February 2008 Adult vitreous structure and postnatal changes M M Le Goff1 and P N Bishop1
- 8. V I T R E O U S A N A T O M Y Lens Attachment of vitreous
- 11. V I T R E O U S B A S E A N A T O M Y Dissection of Human Vitreous Body Elements for Proteomic Analysis Jessica M. Skeie1, Vinit B. Mahajan1 Department of Ophthalmology and Visual Sciences, Omics Laboratory, University of Iowa
- 12. V I T R E O U S B A S E A N A T O M Y
- 13. P R O M I N E N T V I T R E O U S B A S E A N A T O M Y
- 14. V I T R E O U S A T T A C H M E N T S A N A T O M Y Major Blood Vessels premacular bursa, or precortical vitreous pocket (Area of Martegiani) (ciliobursal canal) Annular Gap (Space of Garnier)
- 15. N E U R O S E N S O R Y R E T I N A A N A T O M Y F a = umbo; b = foveola; c = fovea; d = parafovea; e = perifovea
- 16. B E Y O N D P O S T E R I O R P O L E A N A T O M Y www.oculist.net
- 17. O R A S E R R A T A A N A T O M Y Meridional folds possible site for break Dentate Processes Oral bay
- 18. C R O S S - S E C T I O N R E T I N A A N A T O M Y MLM=middle limiting membrane inner/outer segment junction
- 20. C R O S S - S E C T I O N R E T I N A A N A T O M Y
- 21. C R O S S - S E C T I O N R E T I N A A N A T O M Y
- 22. P H O T O R E C E P T O R M O S A I C A N A T O M Y
- 23. C I R C U L A T I O N
- 24. C I L I O R E T I N A L A R T E R Y A N A T O M Y
- 25. 4 L A Y E R S O F C A P I L L A R I E S 1. Radial Peripapillary network: NFL 2. Superficial capillary plexus 3. Deep capillary plexus: either side of the INL. 4. Choriocapillaris: supplied by the short posterior ciliary arteries: outer retina
- 27. R P E C E L L S • Monolayer pigmented hexagonal, cuboidal cells approx 16 μm in diameter: taller and denser in macula • Continuous with the pigment epithelium of the ciliary body and iris. • Apical portion envelop the outer segments of the photoreceptor cells with villous processes
- 28. R P E C E L L S F U N C T I O N • Absorbs light (Melanosomes) • Phagocytoses rod and cone outer segments/ Discs • Participates in retinal and polyunsaturated fatty acid metabolism • Forms the outer blood–ocular barrier • Maintains the subretinal space • Heals and forms scar tissue
- 29. B R U C H M E M B R A N E http://www.eophtha.com/eophtha/Anatomy/Uvea/Bruch's.PNG
- 30. C H O R O I D • Max thickness 0.22mm posterior to 0.1mm anterior http://www.intechopen.com/source/html/37889/media/image1.jpeg http://www.iovs.org/content/49/7/2812/F4.large.jpg posterior ciliary artery low pressure by Endarterioles Looks like lobules in center Irregular and more radial periphery
- 31. Date of download: 7/23/2014 Copyright © 2014 McGraw-Hill Education. All rights reserved. From: Chapter 1. Anatomy & Embryology of the Eye Vaughan & Asbury's General Ophthalmology, 18e, 2011 E M B R Y O L O G Y • RPE: outer layer of the optic cup: remains single layer. Pigmentation begins at 5 weeks. • Secretion of the inner layer of Bruch's membrane occurs by 6 weeks. • Other 9 layers: inner layer of the optic cup slowly throughout gestation. • 7th month, outer nuclear layer of the rods and cones is present with bipolar, amacrine, and ganglion cells and nerve fibers. • Macular region thicker than the rest of the retina until the 8 month, when the macular depression develop. • Macular development is not complete in anatomic terms until 6 months after birth.
- 32. S T A G E S O F V I T R E O U S • First Stage/Primary vitreous: 3–6 weeks: Fibrils from Cells and fibroblasts derived from mesenchyme at the rim of the optic cup or associated with the hyaloid vascular system, together with minor contributions from the embryonic lens and the inner layer of the optic vesicle: Ultimately, the primary vitreous comes to lie just behind the posterior pole of the lens in association with remnants of the hyaloid vessels (Cloquet's canal). http://www.oculist.net/downaton502/prof/ebook/duanes/graphics/figures/v7/0020/036f.gif
- 33. S T A G E S O F V I T R E O U S • Second Stage/ Secondary vitreous: 6–10 weeks: Fibrils and cells (hyalocytes) originate from the vascular primary vitreous. Anterior: firm attachment to the internal limiting membrane of the retina constitutes the early stages of formation of the vitreous base. The hyaloid system develops a set of vitreous vessels as well as vessels on the lens capsule surface (tunica vasculosa lentis). The hyaloid system is at its height at 2 months and then atrophies from posterior to anterior. http://www.oculist.net/downaton502/prof/ebook/duanes/graphics/figures/v7/0020/036f.gif
- 34. S T A G E S O F V I T R E O U S • Third Stage/Tertiary vitreous: 10 weeks on: During the third month, the marginal bundle of Drualt is forming. This consists of vitreous fibrillar condensations extending from the future ciliary epithelium of the optic cup to the equator of the lens. Condensations then form the suspensory ligament of the lens, which is well developed by 4 months. The hyaloid system atrophies complete during this stage. http://www.oculist.net/downaton502/prof/ebook/duanes/graphics/figures/v7/0020/036f.gif
- 35. D I A G N O S T I C S
- 36. C O L O R P H O T O S
- 37. C O L O R P H O T O S
- 38. C O L O R P H O T O S
- 39. F I L T E R S
- 40. F I L T E R S
- 41. F I L T E R S Blue-green 490 nm NFL, ILM, EMR retinal folds & cysts Media Opacities limit
- 42. F I L T E R S Green 540 nm Retinal vasculature, & common findings such as hemorrhages, drusen and exudates Green filter = "red-free" baseline before FA
- 43. F I L T E R S Red 630 nm Pigmentary disturbances, Choroidal ruptures, Choroidal nevi Choroidal melanomas
- 44. F L U O R E S C E I N A N G I O G R A P H Y D I A G N O S T I C S
- 45. F L U O R E S C E I N A N G I O G R A P H Y D I A G N O S T I C S
- 46. F L U O R E S C E I N A N G I O G R A P H Y D I A G N O S T I C S Light from camera flash Pass through blue filter excites Fluorescein in blood vessels Emits yellow green light Excitatory Pass through yellow green filter 520–530 nm465-490 nm
- 47. F L U O R E S C E I N A N G I O G R A P H Y D I A G N O S T I C S
- 48. E A R L Y P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation 1. Choroidal flush. Transit phase:10s range 10-15s
- 49. E A R L Y P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation 2. Arterial phase 12s
- 50. E A R L Y P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation 3. Arteriovenous phase
- 51. E A R L Y P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation 4. Venous Phase 30s
- 52. M I D P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation Recirculation Phase 2-4 min
- 53. L A T E P H A S E F L U O R E S C E I N A N G I O G R A P H Y http://www.opsweb.org/?page=FAinterpretation 7 to 15 min
- 54. F L U O R E S C E I N A N G I O G R A P H Y I N T E R P R E T A T I O N Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.892p
- 55. Hypofluorescence TWO MAIN CAUSES 1. Vascular filling defect 2. Blocked fluorescencee
- 56. B L O C K F R O M P R E R E T I N A L H E M E H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.894p
- 57. B L O C K F R O M I N T R A R E T I N A L H E M E H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896
- 58. B L O C K F R O M S U B R E T I N A L H E M E H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 59. B L O C K F R O M R P E H Y P E R T R O P H Y H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 60. B L O C K F R O M N E V U S H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 61. F I L L I N G D E F E C T H Y P O F L U O R E S C E N C E Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.898p
- 62. Filling defect: Choroideremia H Y P O F L U O R E S C E N C E http://imagebank.asrs.org/file/5375/choroideremia
- 63. Filling defect: Choroideremia H Y P O F L U O R E S C E N C E http://imagebank.asrs.org/file/5373/choroideremia
- 64. F I L L I N G D E F E C T : O P T I C N E R V E P I T H Y P O F L U O R E S C E N C E http://imagebank.asrs.org/file/544/optic-nerve-pit
- 65. F I L L I N G D E F E C T : O P T I C N E R V E P I T H Y P O F L U O R E S C E N C E http://imagebank.asrs.org/file/545/optic-nerve-pit
- 66. F L U O R E S C E I N A N G I O G R A P H Y I N T E R P R E T A T I O N Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.892p
- 67. Auto-fluorescence: Optic Nerve Drusen H Y P E R - F L U O R E S C E N C E : P R E I N J E C T I O N
- 68. Auto-fluorescence: Optic Nerve Drusen H Y P E R - F L U O R E S C E N C E : P R E I N J E C T I O N
- 69. Auto-fluorescence: Optic Nerve Hemartoma http://www.aao.org/publications/eyenet/200410/blink.cfm?RenderForPrint=1&# (C) AAO 2014 H Y P E R - F L U O R E S C E N C E : P R E I N J E C T I O N
- 70. H Y P E R - F L U O R E S C E N C E : P R E - I N J E C T I O N Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 71. True Hyper-fluorescence • Leakage • Staining • Pooling • Transmission • Window defect
- 72. TRUE HYPER-FLUORESCENCE • Leakage: seepage of Fluorescein, increase in intensity and margins blur in late phase • Staining: Fluorescein enters tissue that retains it: inten sity increase during transit but then stay same later, ma rgins are distinct. • Pooling: accumulation of fluorescein in a fluid-filled sp ace, so fluid space from invisible become visible. • Transmission or Window defect: increased normal cho roidal fluorescence through RPE defects.
- 73. Vascular:Neovascularization H Y P E R - F L U O R E S C E N C E : E A R L Y : V A S C U L A R This image was originally published in the ASRS Retina Image Bank. Author: Roy Schwartz, MD, Title:Proliferative Diabetic Retinopathy With Neovascularization - FA Retina Image Bank. Year 2014 Image Number: 133326. © the American Society of Retina Specialists.
- 74. Vascular: Microaneurysms H Y P E R - F L U O R E S C E N C E : E A R L Y : V A S C U L A R This image was originally published in the ASRS Retina Image Bank. Author: James B. Soque, CRA, COA , Title: Diabetic Macular Edema, Proliferative Diabetic Retinopathy, Neovascularization Elsewhere, DME, PDR, NVE Retina Image Bank. Year 2013 Image Number: 5480.© the American Society of Retina Specialists.
- 75. Vascular: Telangiectasia H Y P E R - F L U O R E S C E N C E : E A R L Y : V A S C U L A R This image was originally published in the ASRS Retina Image Bank. Author: Avris Romario Diparaja Siahaan, Title: Macular Telangiectasia (FA Early Phase) Retina Image Bank. Year 2014 Image Number: 17957. © the American Society of Retina Specialists.
- 76. Vascular:Macular Pucker H Y P E R - F L U O R E S C E N C E : E A R L Y : V A S C U L A R This image was originally published in the ASRS Retina Image Bank. Author: David R. Chow, MD, FRCS(C) , Title: Pucker FA Late Retina Image Bank. Year 2012 Image Number: 1153. © the American Society of Retina Specialists.
- 77. CHOROIDAL:CNVM H Y P E R - F L U O R E S C E N C E : E A R L Y : C H O R O I D A L This image was originally published in the ASRS Retina Image Bank. Author: Neha Goel, MS DNB FRCS (Glasg) , Title: Angioid Streaks With CNVM FFA LE Retina Image Bank. Year 2014 Image Number: 18451. © the American Society of Retina Specialists.
- 78. WINDOW DEFECT: MACULAR HOLE H Y P E R - F L U O R E S C E N C E : E A R L Y : C H O R O I D A L Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 79. WINDOW DEFECT: MACULAR HOLE H Y P E R - F L U O R E S C E N C E : E A R L Y : C H O R O I D A L This image was originally published in the ASRS Retina Image Bank. Author: Jerald A. Bovino, MD Title: Macular hole. Retina Image Bank. Year 2013 Image Number: 5616. © the American Society of Retina Specialists.
- 80. WINDOW DEFECT:RPE LOSS H Y P E R - F L U O R E S C E N C E : E A R L Y C H O R O I D A L Ryan, Stephen J. Retina. 4th ed. by MD, Elsevier Mosby; c2005.896p
- 81. WINDOW DEFECT:RPE LOSS H Y P E R - F L U O R E S C E N C E : E A R L Y : C H O R O I D A L This image was originally published in the ASRS Retina Image Bank. Author: David Callanan, MD, Title: Cuticular Drusen. Retina Image Bank. Year 2014 Image Number: 18734. © the American Society of Retina Specialists.
- 82. WINDOW DEFECT:RPE LOSS H Y P E R - F L U O R E S C E N C E : E A R L Y : C H O R O I D A L This image was originally published in the ASRS Retina Image Bank. Author: David Callanan, MD, Title: Cuticular Drusen. Retina Image Bank. Year 2014 Image Number: 18738. © the American Society of Retina Specialists.
- 83. Choroidal: Staining H Y P E R - F L U O R E S C E N C E : L A T E : C H O R O I D A L This image was originally published in the ASRS Retina Image Bank. Author: Jason S. Calhoun,MD Title: CNVM Staining Retina Image Bank. Year 2014 Image Number: 7706. © the American Society of Retina Specialists.
- 84. Retinal: Cystoid edema (CME) H Y P E R - F L U O R E S C E N C E : L A T E : R E T I N A L This image was originally published in the ASRS Retina Image Bank. Author: David Callanan, MD Title: CME Retina Image Bank. Year 2014 Image Number: 15227 © the American Society of Retina Specialists.
- 85. Retinal: Non-Cystoid edema (CSR) H Y P E R - F L U O R E S C E N C E : L A T E : R E T I N A L This image was originally published in the ASRS Retina Image Bank. Author: Carl C. Awh, MD Title: CSR Retina Image Bank. Year 2014 Image Number: 5642 © the American Society of Retina Specialists.
- 86. A D V E R S E E F F E C T S • Temp. Yellowing skin and conjunctiva 6–12h Orange- yellow Urine: 24–36 hours • Nausea, vomiting, or vasovagal reactions: 10% More severe vasovagal reactions, including bradycardia, hypotension, shock, and syncope, are rare • Extravasation with subcutaneous granuloma, toxic neuritis, or local tissue necrosis—these are extremely rare • Urticarial/Anaphylactoid reactions about 1% of cases • Anaphylactic reactions (cardiovascular shock) less than 1 in 100,000 injections
- 87. A D V E R S E E F F E C T S • Prior urticarial reactions increase a patient’s risk of having a similar reaction: Premedicating with antihistamines, corticosteroids, or both. • Dye extravasate: Local pain: Ice-cold compresses 5– 10 minutes. Reassessed over hours or days until the edema, pain, and redness resolve. • Teratogenic effects not identified avoid in pregnant in the first trimester. Fluorescein is transmitted to breast milk • Lower doses of fluorescein should be used in patients with renal insufficiency.
Notes de l'éditeur
- Transparent gel composed of collagen fibrils filled with hyaluronan hydrated with water; it occupies 80% of the volume of the eye.
- Based on arrangement of collagen can be central and cortical
- Has circular tight attachment posterior to lens called Wieger Ligament
- The retrolental indentation of the anterior vitreous is called the patellar fossa
- The potential space between lens and anterior cortical gel bordered by the Wieger ligament is called the Berger space
- The vitreous base is a semi-transparent substructure of the vitreous body located along the ora serrata (white arrows), which is the dividing line separating the ciliary body and retina In the vitreous base
- the collagen fibers are especially dense; they insert firmly into a ringlike area that extends 2 mm anterior and 3 mm posterior to the ora serrata.
- Optos photo showing Vitreous Base
- Other areas of dense vitreous attachments: lens, fovea-parafoveal area, margin of the optic nerve head, and along major retinal blood vessels. There is no basement membrane separating lens from vitreous but is gap: annular separating aqueous from vitreous.
- F. Also called Foveal Avascular Zone and as we’ll discuss in Fluorescein Angiography it’s center is considered as center of macula
- Area of vertex veins is around equator then posterior to it 1.5-mm ring peripheral to the temporal major vascular arcades called the near periphery or mid periphery and area anterior to equator is far periphery till we hit Ora
- Ora Serrata: ora bay, dentate process. Meridional folds are pleats of redundant retina. Tears may occur at the posterior end of such folds.
- The mitochondria, cilia, and inner discs together form the IS/OS junction, which is apparent with optical coherence tomography (OCT) and provides evidence of the origin of the photoreceptor as a modified sensory cilium prone to the full range of ciliopathies.
- In the fovea, the inner cellular layers are laterally displaced, and there is an increased density of pigment in the retinal pigment epithelium (RPE). The incident light falls directly on the photoreceptor outer segments, reducing the potential for scattering of light by overlying tissue elements.
- Similar cross sections introducing as important for FA to be discussed later today
- Similar cross sections introducing as important for FA to be discussed later today
- Light must travel through the full thickness of the retina to reach the photoreceptors. The density and distribution of photoreceptors vary with topographic location. In the fovea, densely packed cones are predominantly red- and green-sensitive, with a density exceeding 140,000 cones/mm2. The fovea has no rods; it contains only cones and processes of Müller cells. The number of cone photoreceptors decreases rapidly away from the center, even though 90% of cones overall reside outside the foveal region. The rods have their greatest density in a zone lying approximately 20° from fixation, where they reach a peak density of about 160,000 rods/mm2. The density of rods also decreases toward the periphery.
- The central retinal artery (a branch of the ophthalmic artery) enters the eye and divides into 4 branches, each supplying blood to a quadrant of the retina. These branches are located in the inner retina.
- Occasionally cilioretinal artery, derived from the ciliary circulation, will supply a portion of the inner retina between the optic nerve and the center of the macula.
- The boundary between the retinal vascular supply and the diffusion from the choriocapillaris varies according to the topographic location, retinal thickness, and amount of light present. The retinal vasculature, including its capillaries, retains the blood–brain barrier with tight junctions between capillary endothelial cells. Blood collected from the capillaries accumulates within a branch retinal vein, which in turn forms the central retinal vein. The retinal vascular system is thought to supply about 5% of the oxygen used in the fundus; the choroid supplies the rest.
- This explains the correlation of appearance of retinal bleed to it’s source and location
- Lateral surfaces of adjacent cells are closely apposed and joined by tight junctional complexes (zonulae occludentes) near the apices, forming apical girdles and the outer blood–ocular barrier. The basal surface of the cells shows a rich infolding of the plasma membrane. The basement membrane does not follow these in foldings.
- Melanosomes are spheroidal, with their melanin distributed on protein fibers. RPE cell is thought to phagocytose billions of outer segments over life time. Follows a daily (circadian) rhythm. Rods at dawn, and cones at dusk. Digested gradually through the action of enzymes within cytoplasmic organelles known as lysosomes. Visual pigments contain 11-cis-retinaldehyde that is converted to 11-trans-retinaldehyde. Most of the steps of regeneration of the 11-cis configuration occur in the RPE. A variety of pathologic changes may develop if this process of phagocytosis and renewal is impaired by genetic defects, drugs, dietary insufficiency (of vitamin A), or senescence. Barrier function of the RPE prevents diffusion of metabolites between the choroid and the subretinal space. Environment of the photoreceptors is largely regulated by the selective transport properties of the RPE. The RPE has a high capacity for water transport, so fluid does not accumulate in the subretinal space under normal circumstances. This RPE-mediated dehydration of the subretinal space also modulates the bonding properties of the interphotoreceptor matrix, which bridges between the RPE and photoreceptors and helps bond the neurosensory retina to the RPE. With deterioration or loss of the RPE, there is corresponding atrophy of the overlying photoreceptors and underlying choriocapillaris.
- Throughout life, lipids and oxidatively damaged materials build up within the Bruch membrane. Some disease states, such as pseudoxanthoma elasticum, are associated with increased fragility of the Bruch membrane, presumably caused by abnormalities within the membrane’s collagen or elastic portions.
- Second Stage/ Secondary vitreous: 6–10 weeks: Fibrils and cells (hyalocytes) originate from the vascular primary vitreous. Anteriorly, the firm attachment of the secondary vitreous to the internal limiting membrane of the retina constitutes the early stages of formation of the vitreous base. The hyaloid system develops a set of vitreous vessels as well as vessels on the lens capsule surface (tunica vasculosa lentis). The hyaloid system is at its height at 2 months and then atrophies from posterior to anterior. Third Stage/Tertiary vitreous: 10 weeks on: During the third month, the marginal bundle of Drualt is forming. This consists of vitreous fibrillar condensations extending from the future ciliary epithelium of the optic cup to the equator of the lens. Condensations then form the suspensory ligament of the lens, which is well developed by 4 months. The hyaloid system atrophies complete during this stage.
- Third Stage/Tertiary vitreous: 10 weeks on: During the third month, the marginal bundle of Drualt is forming. This consists of vitreous fibrillar condensations extending from the future ciliary epithelium of the optic cup to the equator of the lens. Condensations then form the suspensory ligament of the lens, which is well developed by 4 months. The hyaloid system atrophies complete during this stage.
- Red light has minimal scatter and more detail of landscape can be seen
- Similar here red light goes to more deeper details and blue light shows more superficial structures
- Blue light increases visibility of the anterior retinal layers, which normally are almost transparent in white light. Absorbed by retinal pigmentation and blood vessels, providing a dark background against which specular reflections and scattering in the anterior layers of the fundus is enhanced.
- Absorbed by blood, but is partially reflected by the retinal pigmentation in comparison to blue light. Less scatter than Blue Green light provides excellent contrast and the best overall view of the fundus.. For this reason,.
- Retinal pigmentation appears progressively lighter and more transparent in red light, revealing more of the choroidal pattern. Overall fundus contrast is greatly reduced with red illumination as many retinal structures are red in color. Retinal vessels look lighter and less obvious at longer wavelengths, with the oxygen-rich arterioles appearing very light in comparison to the venules. The optic nerve also appears very light and almost featureless.
- Fluorescein angiography (FA) allows study of the circulation of the retina and choroid in normal and diseased states. an orange-red crystalline hydrocarbon with a molecular weight of 376 Eliminated primarily through the liver and kidneys within 24–36 hours via the urine. 80% of the fluorescein is protein-bound, primarily to albumin, and not available for fluorescence; the remaining 20% is unbound and circulates in the vasculature and tissues of the retina and choroid, where it can be visualized.
- Excitatory filter ensures only light that is most “excitatory” for Fluorescein pass through Barrier filter ensures only the light of Fluorescence from where fluorescein is present pass thorough The images can be recorded in B-W digital or Analog camera and now a days even as video
- Normal person:10 seconds following injection. Major choroidal vessels are impermeable to fluorescein, but the choriocapillaris leaks fluorescein dye freely into the extravascular space. Usually little detail in the choroidal flush as the retinal pigment epithelium (RPE) acts as an irregular filter that partially obscures the view of the choroid. If a cilioretinal artery is present, this fills along with the choroidal flush as both are supplied by the short posterior ciliary arteries.
- Arterioles typically fill 1-2 seconds after the choroid; therefore, the normal "arm-to-retina” circulation time is approximately 12 seconds. A delay in the arm-to-retina time may reflect a problem with the fluorescein dye injection or circulatory problems with the patient including heart and peripheral vascular disease.
- Arteriovenous phase. Complete filling of the retinal capillary bed follows the arterial phase and the retinal veins begin to fill. In the early arteriovenous phase, thin columns of fluorescein are visualized along the walls of the larger veins (laminar flow). These columns become wider as the entire lumen fills with dye.
- 4. Venous phase. Complete filling of the veins occurs over the next ten seconds with maximum vessel fluorescence occurring approximately 30 seconds after injection. The perifoveal capillary network is best visualized in the peak venous phase of the angiogram.
- 2 to 4 minutes after injection. The veins and arteries remain roughly equal in brightness. The intensity of fluorescence diminishes slowly during this phase as much of the fluorescein is removed from the bloodstream on the first pass through the kidneys.
- Gradual elimination of dye from the retinal and choroidal vasculature. Photographs are typically captured 7 to 15 minutes after injection. Late staining of the optic disc is a normal finding. Any other areas of late hyperfluorescence suggest the presence of an abnormality.
- Vascular filling defects are those in which retinal or choroidal vessels cannot fill, as in nonperfusion of an artery, vein, or capillary in the retina or choroid. These defects show either a delay in or complete absence of filling of the involved vessels. Blocked fluorescence occurs when the stimulation or visualization of the fluorescein is blocked by fibrous tissue or another barrier, such as pigment or blood, obstructing normal retinal or choroidal fluorescence in the area.
- So Hypo not only from Block by heme here but also vascular filling defect and capillary non perfusion causing retina to be opaque so even choroidal fluorescence is not seen.
- A: Red-free photograph of left macula. pale C-shaped lesion dehemoglobinized blood: B fluorescein filters in place but before fluorescein injection: dehemoglobinized blood appears to fluoresce very faintly (arrows). C, Arteriovenous- phase fluorescein angiogram shows hypofluorescence caused by the large area of subretinal blood. D, Late-phase fluorescein angiogram shows hypofluorescence caused by the large patch of subretinal blood.The dehemoglobinized blood appears to fluoresce very faintly (arrows). COMMENT: pseudofluorescence – the light was not true fluorescence. The filters were thin and allowed reflected light through the filter system
- Leakage from seepage of fluorescein molecules through the pigment epithelium into the subretinal space or neurosensory retina, out of retinal blood vessels into the retinal interstitium, or from retinal neovascularization into the vitreous. When the only fluorescein dye remaining in the eye is extravascular. Leakage occurs, for example, in CNV, in diabetic macular edema (via microaneurysms or intraretinal microvascular abnormalities [IRMAs]), and in neovascularization of the disc. Staining refers to a pattern of hyperfluorescence in which the fluorescence gradually increases in intensity through transit views and persists in late views, but its borders remain fixed throughout the study. Staining results from fluorescein entry into a solid tissue or material that retains the fluorescein, such as a scar, drusen, optic nerve tissue, or sclera (see Fig 2-1B). Pooling refers to the accumulation of fluorescein in a fluid-filled space in the retina or choroid. At the beginning of the study, the fluid in the space contains no fluorescein and is invisible. As fluorescein leaks into the space, the margins of the space trap the fluorescein and appear distinct, as seen, for example, in an RPE detachment in central serous chorioretinopathy (Fig 2-2). As more fluorescein enters the space, the entire area fluoresces. A transmission defect, or window defect, refers to a view of the normal choroidal fluorescence through a defect in the pigment or loss of pigment in the RPE, such as shown in Figures 2-1A and 2-1B. In a transmission defect, the hyperfluorescence occurs early, corresponding to filling of the choroidal circulation, and reaches its greatest intensity with the peak of choroidal filling. The fluorescence does not increase in intensity or shape and usually fades in the late phases, as the choroidal fluorescence becomes diluted by blood that does not contain fluorescein. The fluorescein remains in the choroid and does not enter the retina.
- Here we have leaky new blood vessels
- With Macular pucker blood vessels are pulled in together and give appearance of Hyper
- With Macular pucker blood vessels are pulled in together and give appearance of Hyper
- With Macular pucker blood vessels are pulled in together and give appearance of Hyper