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Optic fundus in clinical medicine

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Optic fundus in clinical medicine

  1. 1. 26/02/2008
  2. 2.  Only place in the body where blood vessels can be visualized directly Mirror the status of the systemic circulation Continuity of nerve fibers and meninges Reflects specific changes in systemic diseases Contribute to diagnosis
  3. 3.  Direct ophthalmoscopy Indirect opthalmoscopy Sterioscopical view possible
  4. 4.  Ideally fundus should be examined in a darkened room Patient should be asked to fix their gaze on a distant object Examine with corresponding eyes The ideal line of approach should bring the optic disc straight in to view If only blood vessels on a pink background are seen they should be followed , the disk will eventually come in to view
  5. 5.  Media- hazy, clear Disc- size, shape, colour, margin, physiological cup, neuroretinal rim Blood vessels- caliber, tortousity, irregularities, changes in the vessel wall, aneurism, neovascularisation Exudates Haemorrhage
  6. 6.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  7. 7.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  8. 8.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  9. 9.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  10. 10.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  11. 11.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  12. 12.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  13. 13.  Uniform red to pink Disc-pale pink 1.5 mm in diameter Nasal margin slightly blurred Vessels emanate from optic cup Consist of central cup and peripheral neuroretinal rim Macula temporally Fovea 2.5mm-diameter, darker
  14. 14.  Tygroid fundus Deeply pigmented choroid Choroidal vessels are seen Polygonal pigmented areas in between
  15. 15.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  16. 16.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  17. 17.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  18. 18.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  19. 19.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  20. 20.  Dot haemorrhages  Deep within the retina  Leakage of capillaries, venules  Common in diabetes Flame haemorrhages  Superficial nerve fibre layer  Leakage of capillaries, venules that are ischemic or, in the case of veins, under high pressure Boat haemorrhages (pre-retinal)  Interface between retina & vitreous Sub macular h‟ge, Preretinal h‟ge, Retinal h‟ge
  21. 21.  Hard exudate  Deep yellow with sharp margins  Often circinate  Leakage from pre-capillary arterioles  DM, HTN, VHL disease, radiation  „Macular star‟ Soft exudate(cotton wool spot)  Fluffygray-white, near optic disc  Retinal nerve fiber layer microinfarction  HTN, DM, connective tissue disease,HIV
  22. 22.  Hard exudate  Deep yellow with sharp margins  Often circinate  Leakage from pre-capillary arterioles  DM, HTN, VHL disease, radiation  „Macular star‟ Soft exudate(cotton wool spot)  Fluffygray-white, near optic disc  Retinal nerve fiber layer microinfarction  HTN, DM, connective tissue disease,HIV
  23. 23.  Hard exudate  Deep yellow with sharp margins  Often circinate  Leakage from pre-capillary arterioles  DM, HTN, VHL disease, radiation  „Macular fan‟ Soft exudate(cotton wool spot)  Fluffygray-white, near optic disc  Retinal nerve fiber layer microinfarction  HTN, DM, connective tissue disease,HIV
  24. 24.  White centered retinal haemorrhages CWS surrounded by h‟mage CWS- ischaemic axons H‟maghe- precapillary arterioles Sub acute bacterial endocarditis Leukaemia Diabetes
  25. 25.  Deposition in ganglion cell layer Thickening & loss of transparency of retina Foveola-ganglion cells absent, thin, so contrast Sphingolipidoses Central retinal artery occlusion Berlins edema
  26. 26.  Crack like dehiscence in brusch‟ membrane Degenerative process combined with calcium deposition Linear reddish brown lesion Lies beneath normal blood vessels “Pseu d‟orange” Salmon spots, optic nerve drusen Pseudoxanthoma elasticum, EDS Paget‟s, Hemoglobinopathies
  27. 27.  Papillopheblitis (optic disc vasculitis)  Affects healthyindividuals <50  Disc edema, cotton wool spots  Venous dilatation and tortousity  Retinal haemorrhages Retinal vasculitis  Occurs in sarcoidosis, Behcet‟s disease, Multiple sclerosis, idiopathic  Extremely rare in lupus  Perivenous lymphocytic infiltration (sheathing)
  28. 28.  Diffuse retinal dystrophy(rods) Classic clinical triad  Arteriolarattenuation  Retinal bone-spicule pigmentation  Waxy disc pallor Starts at mid periphery Maculopathy Associations  Bassen-Kornzwieg syndrome, Refsum‟s disease, Kearn-sayre syndrome , Usher‟s syndrome Muchopolysaccharidoses, Lauren‟s moon biedel syndrome, Friederisch ataxia
  29. 29.  Attempt at vascularising ischaemic tissue Lacks bifurcating pattern Bleed spontaneously Diabetic retinopathy Retinal vein occlusion Radiation Sickle cell retinopathy Retinopathy of prematurity
  30. 30.  Separation of sensory retina from pigment epithelium Rhegmatogenous RD Non-rhegmatogenous RD  Tractional- PDR, ROP, sickle cell retinopathy, penetrating posterior segment trauma  Exudative- choroidal tumours, exophytic retinoblastoma, harada disease, posterior scleritis, subretinal neovascularisation, severe hypertension Elevated sheath of retinal tissue with folds
  31. 31.  Separation of sensory retina from pigment epithelium Rhegmatogenous RD Non-rhegmatogenous RD  Tractional- PDR, ROP, sickle cell retinopathy, penetrating posterior segment trauma  Exudative- choroidal tumours, exophytic retinoblastoma, harada disease, posterior scleritis, subretinal neovascularisation, severe hypertension Elevated sheath of retinal tissue with folds
  32. 32.  Atherosclerosis, embolism Retina appears white Attenuation of arteries and veins Cherry red spot Investigate for Valvular heart disease, endocarditis, mural thrombi, Carotid artery disease, systemic vasculitis, hematological disorders
  33. 33. Cholesterol Fibrinoplatelet Calcific(Hollenhorst plaques)
  34. 34.  Atherosclerosis, embolism Retina appears white Attenuation of arteries and veins Cherry red spot Investigate for Valvular heart disease, endocarditis, mural thrombi, Carotid artery disease, systemic vasculitis, hematological disorders
  35. 35.  Atherosclerosis, embolism Cattle-trucking Retina appears white Attenuation of arteries and veins Cherry red spot Investigate for Valvular heart disease, endocarditis, mural thrombi, Carotid artery disease, systemic vasculitis, hematological disorders
  36. 36.  Embolism, periarteritis Retinal cloudiness corresponding to the areas of ischemia Narrowing of arteries and veins One or more emboli may be present
  37. 37.  Present in 20% of population It may be isolated, combined CRVO, combined AION Localised cloudiness- macula and papillomacular bundle
  38. 38.  Occlusion of short posterior ciliary arteries Disc is pale Diffuse or sectoral edema Splinter shaped h‟mages „Pseudo-Foster kennedy syndrome‟
  39. 39.  Giant cell arteritis Cotton wool spots are uncommon Cilioretinal artery occlusion Central artery occlusion
  40. 40.  Etiology Arteriosclerosis Increasing age Hypertension Diabetes mellitus Blood dyscrasiasis Periphlebitis Raised intraocular tension
  41. 41.  Dilatation & tortousity of all branches of CRV Retinal h‟age- superficial & deep throughout “Blood and thunder” Cotton wool spots Optic disc edema Macular edema
  42. 42.  Venous dilatation and tortousity peripheral to the site of occlusion Hemorrhages Retinal edema Cotton wool spots Neovascularisation
  43. 43.  Most common cause of legal blindness in 20-65 yrs Type 1>Type 2 (40% , 20%) Risk factors  Duration of diabetes  Poor metabolic control  Pregnancy  Hypertension  Nephropathy  Smocking  Obesity  Hyperlipidaemia
  44. 44.  Micro vascular occlusion  Microvascular leakage
  45. 45. Eva kohner‟s classification Non-proliferative diabetic retinopathy Pre-proliferative diabetic retinopathy Proliferative diabetic retinopathy
  46. 46.  Micro aneurysms (earliest lesion) Hard exudates Retinal edema Haemorrhages
  47. 47.  Cotton wool spots Intra retinal micro vascular abnormalities(IRMA) Venous changes  Dilatation,looping  Beading, segmentation Arterial changes  Narrowing, occlusion  Silver wiring Dark blot haemorrhages
  48. 48.  Involvement of fovea Perifoveal hard exudates Dark blot hemorrhages
  49. 49. Neovascularisation Venous looping NVD Venous beading NVE
  50. 50. NVD NVE
  51. 51.  Primary response to HTN- vasoconstriction Narrowing depend on pre-existing sclerosis Narrowing seen in its pure form only in young individuals Sustained HTN-inner BRB disrupted Increased vascular permeability Narrowing and sclerosis suggests duration of hypertension
  52. 52.  GRADE 1  GRADE2 Generalised arteriolar  Exaggeration of light reflex narrowing  AV crossing changes (Salus sign)
  53. 53.  GRADE 1  GRADE2 Focal arteriolar  Exaggeration of light reflex narrowing  AV crossing changes (Salus sign)
  54. 54.  GRADE 3  GRADE 4 Prominent AV changes  Features of grade 3 (Bonnet, Gunn signs)  Papilloedema Retina edema, CWS Flame h‟mages
  55. 55. Grade 0Grade 4 Grade 1Grade 3 Grade 2
  56. 56.  Rare, occurs in hypertensive crisis „Elschnig spots‟ „Siegrist streaks‟ Exudative retinal detachment
  57. 57.  Creamy appearance of the vessels in the posterior pole and peripheral area Triglycerides >2500mg/dl
  58. 58.  Micro vascular occlusion and ischemia Severe head trauma, chest compression injury, Embolism, a/c pancreatitis, carcinoma, connective tissue diseases, Lymphoma, TTP, Bone marrow transplantation Multiple superficial white retinal patches Superficial pericapillary haemorrhages
  59. 59.  Sickle cell anaemia & Sickle cell thalassemia are associated severe ocular manifestations Proliferative changes Seafan neovascularisation Haemorrhages
  60. 60. STAGING5 1 1. Peripheral arteriolar occlusion 2. Peripheral AV anastomosis4 2 3. Sprouting new vessels 4. Vitreous haemorrhage 5. Retinal detachment 3
  61. 61.  Venous tortousity Silver wiring of arterioles „Salmon patches‟ „Black sunbursts‟ Macular depression sign Peripheral retinal holes Artery & vein occlusion Angioid streaks
  62. 62.  Venous tortousity Silver wiring of arterioles „Salmon patches‟ „Black sunbursts‟ Macular depression sign Peripheral retinal holes Artery & vein occlusion Angioid streaks
  63. 63.  Rarely diagnostic importance Duration &type don‟t influence Pale fundus Haemorrhages Cotton wool spots Roth spot Venous tortousity-related severity of anemia
  64. 64.  More common in a/c leukaemia Primary- infiltration Secondary- anemia, thrombocytopaenia, hyperviscosity, infection Superficial haemorrhages Roth spot Cotton wool spot
  65. 65.  Peripheral retinal vascularisation Pigment epitheliopathy- ‛leopard spot‟
  66. 66.  Venous dilatation Segmentation Venous tortousity Retinal haemorrhages
  67. 67.  Viral  CMV  HIV  Rubella Bacterial  Tuberculosis  Syphilis Parasitic  Toxoplasmosis Fungal
  68. 68.  Most common ocular infection in AIDS Indolent retinitis  Startsin the periphery  Mild granular opacification Fulminating retinitis  Dense white opacification  Vasculitis, mild vitritis  Hemorrhages  Extension along blood vessels  Involve optic nerve head
  69. 69.  60% of AIDS patients Retinal microangiopathy Multiple cotton wool spots Non infectious
  70. 70.  Salt & pepper retinopathy, most marked at macula Disc & vessels normal Pigmentery disturbance at posterior pole Optic neuritis
  71. 71.  Intractable chronic uveitis Focal/multi focal choroiditis Choroidal granuloma Periphlebits Panuveitis
  72. 72.  Quiscent  Bilateral/unilateral healed chorio retinal scars Reactivation retinochoroiditis  Adjacent to old scar (satellite lesion)  Vasculitis,  Severe vitritis (headlight in the fog‟ appearance) Papillitis (secondary to juxtapapillary retinitis) Atypical lesions
  73. 73.  Quiscent  Bilateral/unilateral healed chorio retinal scars Reactivation retinochoroiditis  Adjacent to old scar (satellite lesion)  Vasculitis,  Severe vitritis (headlight in the fog‟ appearance) Papillitis (secondary to juxtapapillary retinitis) Atypical lesions
  74. 74.  Quiscent  Bilateral/unilateral healed chorio retinal scars Reactivation retinochoroiditis  Adjacent to old scar (satellite lesion)  Vasculitis,  Severe vitritis (headlight in the fog‟ appearance) Papillitis (secondary to juxtapapillary retinitis) Atypical lesions
  75. 75.  Retinal periphlebitis „Candle wax drippings‟ Branch retinal vein occlusion Cotton ball vitreous opacities Haemorrhages, Granulomas Optic nerve edema and granuloma
  76. 76.  Optic disc granuloma  Retinal granuloma ‟Landers sign‟
  77. 77.  Optic disc granuloma  Retinal granuloma ‟Landers sign‟
  78. 78.  A/c recurrent Hypopyon uveitis Retinitis- superficial infiltrates Retinal vasculitis  Periphlebitis& periarteritis  Vascular occlusion Vascular leakage Optic disc edema Retinal exudation Vitritis
  79. 79.  Optic disc edema Multifocal detachments of the sensory retina Exudative retinal detachment Numerous, residual, small, atrophic scars (‛sunset glow‟ fundus)
  80. 80.  No typical features Retinopathy Haemorrhages Cotton wool spots Vascular occlusions
  81. 81.  Hyaline like calcific material within optic disc Often bilateral, 0.3% Buried drusen  Elevated disc, scalloped margin  No physiological cup  No hyperaemia  Vessels not obscured  Venous pulsation present Exposed drusen  Waxy pearl like irregularities
  82. 82.  Hyaline like calcific material within optic disc Often bilateral, 0.3% Buried drusen  Elevated disc, scalloped margin  No physiological cup  No hyperaemia  Vessels not obscured  Venous pulsation present Exposed drusen  Waxy pearl like irregularities
  83. 83.  Hyaline like calcific material within optic disc Often bilateral, 0.3% Buried drusen  Elevated disc, scalloped margin  No physiological cup  No hyperaemia  Vessels not obscured  Venous pulsation present Exposed drusen  Waxy pearl like irregularities
  84. 84.  Incomplete closure of the choroid fissure Discrete, focal, glistening, white, bowl shaped excavation Disc may enlarged Retinal vasculature normal Complication- RD Trisomy 13, 18, 22 CHARGE
  85. 85.  Visual acuity very poor Enlarged disc with funnel shaped excavation Central core -whitish glial tissue Spokes of wheel appearance Complication- RD Frontonasal dysplasia Neurofibromatosis type-2
  86. 86.  Myelination extend to retina Don‟t interfere with vision Larger & denser than CWS Always connected to optic disc No overlying vitreous haze
  87. 87. Normal vertical cup-disc ratio 0.3 or less
  88. 88.  Inflammatory, infective or demyelinating process Retrobulbar neuritis  Opticdisc normal  Most common type in adult, MS Papillitis  Hyperemia & edema of optic disc  Flame h‟mage Neuroretinitis  Papiiltiswith retinal nerve fibre layer inflammation  Macular star  Viral infection , cat scratch fever, syphilis
  89. 89.  Inflammatory, infective or demyelinating process Retrobulbar neuritis  Opticdisc normal  Most common type in adult, MS Papillitis  Hyperemia & edema of optic disc  Flame h‟mage Neuroretinitis  Papiiltiswith retinal nerve fibre layer inflammation  Macular star  Viral infection , cat scratch fever, syphilis
  90. 90.  Inflammatory, infective or demyelinating process Retrobulbar neuritis  Opticdisc normal  Most common type in adult, MS Papillitis  Hyperemia & edema of optic disc  Flame h‟mage Neuroretinitis  Papiiltiswith retinal nerve fibre layer inflammation  Macular star  Viral infection , cat scratch fever, syphilis
  91. 91.  Swelling of optic nerve head secondary to raised intracranial pressure Early papilloedema  Optic disc- hyperemia & mild elevation  Disk margins indistinct  Loss of spontaneous venous pulsation
  92. 92.  Established papilloedema  Hyperaemia of optic disc  Blurred, elevated margin  Obliterated cup  Venous engorgement  Flame shaped hemorrhages  Cotton wool spots  Hard exudates-‛macular fan‟
  93. 93.  Chronic papilloedema  Optic disc elevated and white ‛champagne cork appearance‟  Usual cause chronic elevated ICT  Corpora amylacea  Irreversible visual loss  Cotton wool spot & h‟mage absent
  94. 94.  Retro laminar portion of optic nerve to lateral geniculate body Lesion anterior to optic chiasma- unilateral RB neuritis, hereditary, compressive lesions, toxic& nutritional optic neuropathy Without antecedent swelling of optic disc Pale flat disc, clear margins Reduction in no. of small BV on the disc- „Kestenbaum sign‟ Atrophy may be diffuse/sectoral
  95. 95.  Retro laminar portion of optic nerve to lateral geniculate body RB neuritis, hereditary, compressive lesions, toxic& nutritional optic neuropathy Without antecedent swelling of optic disc Lesion anterior to optic chiasma- unilateral Pale flat disc, clear margins Reduction in no. of small BV on the disc- „Kestenbaum sign‟ Atrophy may be diffuse/sectoral
  96. 96.  Preceded by swelling Papilloedema, AION, Optic neuritis Dirty grey slightly raised disc Ill defined margins –gliosis Sheathed vessels Reduction in small vessels
  97. 97.  Clinical opthalmology- Jack J.Kanski 5th Ed. “The Eyes Have It”-University of Michigan Harrison‟s Principles of internal medicine 16th Ed. Parsons‟ Diseases of the Eye 20th Ed. New England Journal of Medicine

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