DR. PARAMESWARA RAO(PROFESSOR)   DR.SIVA KUMAR( PG)
<ul><li>AT BIRTH </li></ul><ul><li>Fovea contains many layers </li></ul><ul><li>Ora serrata is less developed </li></ul><u...
<ul><li>WITH AGE </li></ul><ul><li>1. RPE ---Melanin granules lose oval contour—become rounded--- basement membrane thicke...
<ul><li>WITH AGE Contd… </li></ul><ul><li>2.Vacuoles appear in the inner nuclear and  </li></ul><ul><li>outer plexiform la...
 
 
 
 
Retinal vasculature at the age of 81/2 months…. 80 % of retina is perfused….  Peripheral retina especially the temporal si...
<ul><li>Premature infants, bilateral </li></ul><ul><li>After birth if high oxygen is given to these infants---transient(10...
<ul><li>This reaction is peculiar only to incompletely vascularised retina. </li></ul><ul><li>A fully vascularised retina ...
 
<ul><li>COLOBOMA   </li></ul><ul><li>Due to abnormal closure of fetal fissure mostly inferonasal </li></ul><ul><li>The RPE...
 
 
<ul><li>ALBINISM   </li></ul><ul><li>Gross absence of macula / hypoplasia of  </li></ul><ul><li>macula  </li></ul><ul><li>...
 
 
<ul><li>Pre retinal hemorrage   </li></ul><ul><li>Seen in  proliferative retinopthy , trauma, subarachnoid hemorrhage, val...
 
<ul><li>Superficial hemorrages   </li></ul><ul><li>Seen in CRVO ,HTN retinopathy, background dr,  </li></ul><ul><li>Periph...
 
<ul><li>ROTH SPOTS </li></ul><ul><li>Haemorrhages with white centres </li></ul><ul><li>Seen in anaemias , leukemias, HIV  ...
<ul><li>Deep hemorrhages </li></ul><ul><li>Also called dot and blot haemorrhages. </li></ul><ul><li>Mainly diabetic retino...
<ul><li>Seen between layer of rods and cones and RPE </li></ul><ul><li>Large bright red indistinct outline </li></ul><ul><...
<ul><li>Between RPE and bruch’s membrane </li></ul><ul><li>Choroidal neovascularisation is the common cause. </li></ul>
<ul><li>Yellowish waxy plaques with relatively distinct margins seen in the  inner nuclear layer of retina . </li></ul><ul...
<ul><li>Cotton wool spots. </li></ul><ul><li>Seen in the NFL layer </li></ul><ul><li>Cottony appearance with frayed edges ...
<ul><li>Seen in HTN retinopathy , CRVO, HIV, Scleroderma, Pre proliferative DR, systemic vasculitis </li></ul>
<ul><li>Pathogenesis </li></ul><ul><li>Arterial occlusion---the vascularity of the involved retina is decreased---cloudy s...
<ul><li>CHERRY RED SPOT(DD) </li></ul><ul><li>The mechanism by which a cherry red spotis  </li></ul><ul><li>formed in niem...
 
Central Retinal Artery Occlusion Branch Retinal Artery Occlusion Afferent Pupillary Defect Cherry Red Spot Retinal Edema
<ul><li>Pathogenesis: </li></ul><ul><li>Venous occlusions---marked congestion of capillaries---marked edema of affected ti...
Central Retinal Vein Occlusion Branch Retinal Vein Occlusion
 
<ul><li>Fibrino platelet </li></ul><ul><li>Cholesterol(hollen horst) </li></ul><ul><li>Calcific </li></ul>
 
 
 
 
 
 
<ul><li>Normally the vessels are seen as columns of pigmented RBC’s filling the lumina </li></ul><ul><li>Retinal arteriola...
<ul><li>Normally at the AV crossing T.adventitia forms a common sheath for artery and vein AND the vein passes under the a...
<ul><li>Long standing HTN- Tributary venous occlusions – usually temporal vein is occluded because of more arterial crossi...
<ul><li>Grade I   : It consists of mild generalized arteriolar attenuation, particularly of small branches, with broadenin...
HTN  RETINOPATHY
<ul><li>SOFT EXUDATES </li></ul>
 
<ul><li>MALIGNANT HTN: </li></ul><ul><li>Edematous fluid diffuses through all layers --- collects in pools in the fibre la...
<ul><li>Rarely focal choroidal infarction with patchy proliferation of RPE is evident clinically as elschnig spots and sie...
 
<ul><li>Basic pathology : thickening of the basement membrane and ischaema </li></ul><ul><li>Loss of pericytes ( normal en...
 
<ul><li>IRMA  : Increased  aggregation and stickiness of platelets leads to--extensive closure of capillary – capillary no...
 
 
<ul><li>Venous engorgement --- release of angiogenic factors--- NVD/NVE/ Rete mirabile ---vitreous haemorrhage---fibrovasc...
 
 
 
 
 
 
 
 
<ul><li>BLOW OVER THE EYE--- immediate changes in the retinal cells and vessels---vasoparalysis ---leakage of fluid into t...
 
 
<ul><li>ACUTE </li></ul><ul><li>CHRONIC- granulomatous </li></ul><ul><li>non granulomatous </li></ul>
<ul><li>Any inflammation--- vascular dilatation---increased fluid leakage from the vessel wall--- pressure by the fluid le...
 
<ul><li>The progress and the severity of the inflammation depends on the element causing it. </li></ul><ul><li>Tuberculosi...
<ul><li>LOSS OF RODS starts at the equator----subsequent degeneration of other photo receptor cells--- RPE proliferates an...
 
<ul><li>Massive opacification of RPE-  due to massive accumulation of yellowish brown pigment in the cytoplasm of RPE cell...
 
<ul><li>Lipofucsin deposition in the RPE </li></ul><ul><li>INITIAL EGG YOLK APPEARANCE </li></ul><ul><li>Egg SCRAMBLING---...
 
<ul><li>Separation of photoreceptor layer from RPE </li></ul><ul><li>Inflammatory– exudative—either localised /diffuse </l...
 
 
 
<ul><li>Seperation of OPL and INL </li></ul><ul><li>Two types </li></ul><ul><li>typical- split at OPL </li></ul><ul><li>re...
 
<ul><li>Typical is an exaggerated form of cystoid degeneration </li></ul><ul><li>Reticular form split at the NFL—if there ...
<ul><li>Discontinuity in the Bruchs mem---thickened and calcified at the level of elastic layer---calcification increases ...
<ul><li>Lamellar or full thickness </li></ul>
 
<ul><li>Age related sclerosis of choriocapillaries </li></ul><ul><li>Degeneration of the RPE—photo receptor layer degenera...
 
Bruch ’ s Membrane Drusen
Choroidal Neovascularization
<ul><li>Lattice like pattern of criss crossing sclerotic vessels </li></ul><ul><li>Focal areas of retinal thinning --- atr...
 
 
 
 
 
 
 
 
 
MALIGNANT MELANOMA CHOROID
 
 
 
 
 
 
 
 
<ul><li>Posterior neovascularisation </li></ul><ul><li>Peripheral neovascularisation </li></ul><ul><li>Arterial macroaneur...
 
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Retinal lesions Pathophysiology

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Retinal lesions Pathophysiology

  1. 1. DR. PARAMESWARA RAO(PROFESSOR) DR.SIVA KUMAR( PG)
  2. 2. <ul><li>AT BIRTH </li></ul><ul><li>Fovea contains many layers </li></ul><ul><li>Ora serrata is less developed </li></ul><ul><li>There is a fold of redundant retina called </li></ul><ul><li>Lange’s fold. </li></ul><ul><li>Thicker retina </li></ul><ul><li>Peripheral retina circulation develops </li></ul><ul><li>only in the last trimester of gestation. </li></ul>
  3. 3. <ul><li>WITH AGE </li></ul><ul><li>1. RPE ---Melanin granules lose oval contour—become rounded--- basement membrane thickens----focal mould like refractile excrescences known as Drusen </li></ul><ul><li>(mucopolysaccharides and dystrophic </li></ul><ul><li>calcification) develop in that part of bruchs </li></ul><ul><li>membrane </li></ul>
  4. 4. <ul><li>WITH AGE Contd… </li></ul><ul><li>2.Vacuoles appear in the inner nuclear and </li></ul><ul><li>outer plexiform layer in the temporal aspect of ora serrata----coalesce to form cysts- </li></ul><ul><li>called BLESSING IWANOFF CYSTS . </li></ul><ul><li>3. Degenerative changes prominent in the periphery and macula as any decrease in the blood flow of large arteries the distal arterioles are first affected. </li></ul>
  5. 9. Retinal vasculature at the age of 81/2 months…. 80 % of retina is perfused…. Peripheral retina especially the temporal side of disc is less perfused…
  6. 10. <ul><li>Premature infants, bilateral </li></ul><ul><li>After birth if high oxygen is given to these infants---transient(10min) obliteration of terminal arterioles---dilatation of the vessels---delayed reversible obliteration---delayed irreversible vaso obliteration---vasoproliferative changes---angiogenesis---invade ILM---into vitreous---haemorrages, exudates, gliosis --- preretinal membranes---retrolental mass (DD-leucocoria) ---RD </li></ul>
  7. 11. <ul><li>This reaction is peculiar only to incompletely vascularised retina. </li></ul><ul><li>A fully vascularised retina does not react to hyperoxygenation in this way </li></ul>
  8. 13. <ul><li>COLOBOMA </li></ul><ul><li>Due to abnormal closure of fetal fissure mostly inferonasal </li></ul><ul><li>The RPE is totally absent in the coloboma </li></ul><ul><li>region or merely represented. </li></ul><ul><li>MEDULLATED NERVE FIBRES </li></ul><ul><li>Normal medullation stops at the lamina </li></ul><ul><li>cribrosa at birth. Rarely MNF’s appear near </li></ul><ul><li>the disc or elsewhere. Usually presence of such a </li></ul><ul><li>sheath does not interfere with the function of </li></ul><ul><li>affected fibres but reduces transparency of retina </li></ul><ul><li>producing a scotoma </li></ul>
  9. 16. <ul><li>ALBINISM </li></ul><ul><li>Gross absence of macula / hypoplasia of </li></ul><ul><li>macula </li></ul><ul><li>OGUCHI’S DISEASE </li></ul><ul><li>Total absence of Rods. Abnormal no of </li></ul><ul><li>cones present. Retardation of dark </li></ul><ul><li>adaptation. </li></ul><ul><li>RETINAL DYSPLASIA </li></ul><ul><li>Dev. Aberration(proliferation and infolding of </li></ul><ul><li>outer layers of retina) which is present at </li></ul><ul><li>birth. </li></ul>
  10. 19. <ul><li>Pre retinal hemorrage </li></ul><ul><li>Seen in proliferative retinopthy , trauma, subarachnoid hemorrhage, valsalva retinopathy, shaken baby syndrome etc.. </li></ul><ul><li>Round or boat </li></ul><ul><li>shaped </li></ul>
  11. 21. <ul><li>Superficial hemorrages </li></ul><ul><li>Seen in CRVO ,HTN retinopathy, background dr, </li></ul><ul><li>Periphlebitis etc </li></ul><ul><li>Flame shaped…seen in the nerve fibre layer </li></ul><ul><li>Mechanism : </li></ul><ul><li>Marked congestion of capillaries --- marked edema </li></ul><ul><li>of affected tissues ----capillaries of the NFL </li></ul><ul><li>rupture--- flame shaped haemorrages in the NFL </li></ul>
  12. 23. <ul><li>ROTH SPOTS </li></ul><ul><li>Haemorrhages with white centres </li></ul><ul><li>Seen in anaemias , leukemias, HIV </li></ul><ul><li>retinopathy, SABE etc </li></ul>
  13. 24. <ul><li>Deep hemorrhages </li></ul><ul><li>Also called dot and blot haemorrhages. </li></ul><ul><li>Mainly diabetic retinopathy. </li></ul><ul><li>Mechanism : </li></ul><ul><li>Degeneration of the deep capillary walls --- </li></ul><ul><li>lead to hemorrhages in the inner nuclear </li></ul><ul><li>layer----dot and blot hemorrhages </li></ul>
  14. 25. <ul><li>Seen between layer of rods and cones and RPE </li></ul><ul><li>Large bright red indistinct outline </li></ul><ul><li>Seen in choroidal neovascularisation ,COAT’ s dis, Sickle cell anaemia, blunt trauma </li></ul>
  15. 26. <ul><li>Between RPE and bruch’s membrane </li></ul><ul><li>Choroidal neovascularisation is the common cause. </li></ul>
  16. 27. <ul><li>Yellowish waxy plaques with relatively distinct margins seen in the inner nuclear layer of retina . </li></ul><ul><li>Mechanism: </li></ul><ul><li>Formed mainly due prolonged leakage from the capillaries. </li></ul><ul><li>Seen in rings/clumps : diabetis , old </li></ul><ul><li>BRVO ,radiation retinopathy, </li></ul><ul><li>telangiectasias </li></ul><ul><li>stellate : htn , papilledema, </li></ul><ul><li>neuroretinitis </li></ul><ul><li>sub retinal : CNVM, COAT’s, toxocara canis </li></ul>
  17. 28. <ul><li>Cotton wool spots. </li></ul><ul><li>Seen in the NFL layer </li></ul><ul><li>Cottony appearance with frayed edges central fibrin and peripheral mucopolysaccharide </li></ul><ul><li>Mechanism : </li></ul><ul><li>Decreased perfusion ---micro infarcts in the </li></ul><ul><li>NFL----blockage in the axoplasmic flow--- </li></ul><ul><li>cotton wool exudates are formed </li></ul>
  18. 29. <ul><li>Seen in HTN retinopathy , CRVO, HIV, Scleroderma, Pre proliferative DR, systemic vasculitis </li></ul>
  19. 30. <ul><li>Pathogenesis </li></ul><ul><li>Arterial occlusion---the vascularity of the involved retina is decreased---cloudy swelling of the affected retina---affected part becomes opaque---fovea retains its reddish hue as it is supplied by choricapillaries--- CHERRY RED SPOT </li></ul><ul><li>Because of the low perfusion --- inner retinal layers undergo coagulative necrosis---microglia remove the debris---small or large infarcts formed---formation of cotton wool spots in NFL due to blockage of axoplasmic flow. </li></ul>
  20. 31. <ul><li>CHERRY RED SPOT(DD) </li></ul><ul><li>The mechanism by which a cherry red spotis </li></ul><ul><li>formed in niemann-pick and tay-sachs is </li></ul><ul><li>different </li></ul><ul><li>Due to defective metabolism(lipoidal </li></ul><ul><li>degeneration) sphingolipids </li></ul><ul><li>get accumulated---ganglion cells are more </li></ul><ul><li>susceptible---retina becomes opaque in </li></ul><ul><li>areas where ganglion cells are more---as </li></ul><ul><li>ganglion cells are absent in macula it retains it </li></ul><ul><li>natural colour---appearance of cherry red spot </li></ul>
  21. 33. Central Retinal Artery Occlusion Branch Retinal Artery Occlusion Afferent Pupillary Defect Cherry Red Spot Retinal Edema
  22. 34. <ul><li>Pathogenesis: </li></ul><ul><li>Venous occlusions---marked congestion of capillaries---marked edema of affected tissues---hemorrhages and soft exudates in the NFL---large hemorrages in the entire thickness of retina---may erupt through ILM---pre retinal hemorrhage---edema may escape sub retinally to produce flat detachment of retina </li></ul><ul><li>Final outcome : organization of hemorrhages, formation of blood vessels on the inner retinal surface extending into vitreous. </li></ul>
  23. 35. Central Retinal Vein Occlusion Branch Retinal Vein Occlusion
  24. 37. <ul><li>Fibrino platelet </li></ul><ul><li>Cholesterol(hollen horst) </li></ul><ul><li>Calcific </li></ul>
  25. 44. <ul><li>Normally the vessels are seen as columns of pigmented RBC’s filling the lumina </li></ul><ul><li>Retinal arteriolar sclerosis- obscures blood column- light reflex is widened and imparts an orange or coppery hue to the arterioles </li></ul><ul><li>Process prolonged- perivascular fibrosis may totally hide the blood column – silver wire appearance </li></ul>
  26. 45. <ul><li>Normally at the AV crossing T.adventitia forms a common sheath for artery and vein AND the vein passes under the artery at a rather acute angle </li></ul><ul><li>At AV crossings--- due to thickening and increased rigidity of of the arteriolar wall- venular wall is compressed (tapering gunn’s sign)-vein is dilated distal to the crossing(bonnet’s sign) –deflection of veins at obtuse angle (salu’s sign). </li></ul>
  27. 46. <ul><li>Long standing HTN- Tributary venous occlusions – usually temporal vein is occluded because of more arterial crossings </li></ul><ul><li>Necrosis of capillary walls- supericial haemorraghes </li></ul><ul><li>Microinfarcts in the NFL – SOFT EXUDATES </li></ul>
  28. 47. <ul><li>Grade I : It consists of mild generalized arteriolar attenuation, particularly of small branches, with broadening of the arteriolar light reflex and vein concealment. </li></ul><ul><li>Grade II : It comprises marked generalized narrowing and focal attenuation of arterioles associated with deflection of veins at arteriovenous crossings (Salus’ sign). </li></ul><ul><li>Grade III : This consists of Grade II changes plus copper-wiring of arterioles, banking of veins distal to arteriovenous crossings (Bonnet sign), tapering of veins on either side of the crossings (Gunn sign) and right-angle deflection of veins (Salu’s sign). Flame-shaped haemorrhages, cotton-wool spots and hard exudates are also present. </li></ul><ul><li>Grade IV : This consists of all changes of Grade III and silver wiring with papilloedema. </li></ul>
  29. 48. HTN RETINOPATHY
  30. 49. <ul><li>SOFT EXUDATES </li></ul>
  31. 51. <ul><li>MALIGNANT HTN: </li></ul><ul><li>Edematous fluid diffuses through all layers --- collects in pools in the fibre layers ---fluid contains fibrin, debris,lipids,proteins---visible as hard exudates at the jn of INL and OPL---macular region--- MACULAR STAR </li></ul>
  32. 52. <ul><li>Rarely focal choroidal infarction with patchy proliferation of RPE is evident clinically as elschnig spots and siegrist lines (increased pigmentation along a sclerotic vessel) </li></ul>
  33. 54. <ul><li>Basic pathology : thickening of the basement membrane and ischaema </li></ul><ul><li>Loss of pericytes ( normal endothelial to pericyte ratio is 1:1. Pericytes have contractile properties and inhibit endothelial proliferation) </li></ul><ul><li>As the capillaries become acellular and their contractile nature is lost --- microaneurysms are formed---leakage may produce hard exudates </li></ul><ul><li>Aneurysmal wall break down- dot and blot hemorrhages </li></ul>
  34. 56. <ul><li>IRMA : Increased aggregation and stickiness of platelets leads to--extensive closure of capillary – capillary non perfusion – ischemia of retina. Seen in mid retinal periphery – leads to opening up shunt vessels- run from arterioles to vennules. Often referred to – Intraretinal microvascular abnormalities (IRMA). </li></ul>
  35. 59. <ul><li>Venous engorgement --- release of angiogenic factors--- NVD/NVE/ Rete mirabile ---vitreous haemorrhage---fibrovascular proliferation --- RD </li></ul>
  36. 68. <ul><li>BLOW OVER THE EYE--- immediate changes in the retinal cells and vessels---vasoparalysis ---leakage of fluid into the tissuses--- edematous fluid accumulates more in the OPL--- hence in the macula (berlin’s)--- there will be RPE degeneration – small cystic spaces--- large spaces--- ILM breach macular hole formation ---- RD </li></ul>
  37. 71. <ul><li>ACUTE </li></ul><ul><li>CHRONIC- granulomatous </li></ul><ul><li>non granulomatous </li></ul>
  38. 72. <ul><li>Any inflammation--- vascular dilatation---increased fluid leakage from the vessel wall--- pressure by the fluid leads to degeneration of retinal elements---macrophages accumulate to remove the debris of the dead cells--- subsequent compensatory proliferation of the RPE along the periphery of the lesion( pigmented scar)---proliferation of glial tissue---fibro glial scar---distortion and folding of retina </li></ul>
  39. 74. <ul><li>The progress and the severity of the inflammation depends on the element causing it. </li></ul><ul><li>Tuberculosis </li></ul><ul><li>Sarcoidosis </li></ul><ul><li>Syphilis </li></ul><ul><li>Toxoplasmosis etc </li></ul>
  40. 75. <ul><li>LOSS OF RODS starts at the equator----subsequent degeneration of other photo receptor cells--- RPE proliferates and invades the atrophic retina along the blood vessels forming cuffs perivascular cuffs of intensely pigmented cells--- appear as bony spicules </li></ul><ul><li>Vascular walls are thickened and gliotic </li></ul><ul><li>Remaining outer retina adheres to the bruchs membrane </li></ul>
  41. 77. <ul><li>Massive opacification of RPE- due to massive accumulation of yellowish brown pigment in the cytoplasm of RPE cells---tall RPE cells with pigment give this characteristic appearance----form fish tail opacities in the periphery </li></ul><ul><li>Later RPE dysfunction and death of sub foveal RPE cells – photo receptor degeneration and atrophic macular degeneration </li></ul>
  42. 79. <ul><li>Lipofucsin deposition in the RPE </li></ul><ul><li>INITIAL EGG YOLK APPEARANCE </li></ul><ul><li>Egg SCRAMBLING---chorio retinal scarring develops </li></ul><ul><li>Impaired metabolism of the RPE </li></ul>
  43. 81. <ul><li>Separation of photoreceptor layer from RPE </li></ul><ul><li>Inflammatory– exudative—either localised /diffuse </li></ul><ul><li>Tractional – organisation of inflammatory exudates/ haemorrages /glial tissue </li></ul><ul><li>Rhegmatogenous- break in the retina </li></ul>
  44. 85. <ul><li>Seperation of OPL and INL </li></ul><ul><li>Two types </li></ul><ul><li>typical- split at OPL </li></ul><ul><li>reticular – split at NFL </li></ul>
  45. 87. <ul><li>Typical is an exaggerated form of cystoid degeneration </li></ul><ul><li>Reticular form split at the NFL—if there is an outer hole---may cause RD </li></ul>
  46. 88. <ul><li>Discontinuity in the Bruchs mem---thickened and calcified at the level of elastic layer---calcification increases brittleness of bruchs --- sub retinal neovascularisation </li></ul><ul><li>Seen in hemolytic anaemias , pagets, pseudoxanthoma elasticum </li></ul>
  47. 89. <ul><li>Lamellar or full thickness </li></ul>
  48. 91. <ul><li>Age related sclerosis of choriocapillaries </li></ul><ul><li>Degeneration of the RPE—photo receptor layer degeneration---retinal atrophy---the OLM lies almost in contact with the LAMINA VITREA </li></ul><ul><li>Hard drusen--- discrete round globular with overlying thinned RPE—beneath the BM of RPE—due to apoptosis of photoreceptors </li></ul><ul><li>Soft drusen – irregular, granular, in larger areas ---adhere loosely to the bruchs membrane </li></ul>
  49. 93. Bruch ’ s Membrane Drusen
  50. 94. Choroidal Neovascularization
  51. 95. <ul><li>Lattice like pattern of criss crossing sclerotic vessels </li></ul><ul><li>Focal areas of retinal thinning --- atrophic inner retinal layers--- ILM is absent---liquefied vitreous on the discontinuos membrane--- RPE hyperplasis---vitroretinal adhesions on the margins of atrophic retina---tractional retinal breaks and rhegmatogenous RD </li></ul>
  52. 105. MALIGNANT MELANOMA CHOROID
  53. 114. <ul><li>Posterior neovascularisation </li></ul><ul><li>Peripheral neovascularisation </li></ul><ul><li>Arterial macroaneurysm </li></ul><ul><li>PVD with retinal tear </li></ul><ul><li>Intra ocular tumour </li></ul><ul><li>Disciform degeneration </li></ul><ul><li>Ocular trauma </li></ul><ul><li>CRVO </li></ul>
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