Retinal lesions Pathophysiology
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Retinal lesions Pathophysiology

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Retinal lesions Pathophysiology Presentation Transcript

  • 1. DR. PARAMESWARA RAO(PROFESSOR) DR.SIVA KUMAR( PG)
  • 2.
    • AT BIRTH
    • Fovea contains many layers
    • Ora serrata is less developed
    • There is a fold of redundant retina called
    • Lange’s fold.
    • Thicker retina
    • Peripheral retina circulation develops
    • only in the last trimester of gestation.
  • 3.
    • WITH AGE
    • 1. RPE ---Melanin granules lose oval contour—become rounded--- basement membrane thickens----focal mould like refractile excrescences known as Drusen
    • (mucopolysaccharides and dystrophic
    • calcification) develop in that part of bruchs
    • membrane
  • 4.
    • WITH AGE Contd…
    • 2.Vacuoles appear in the inner nuclear and
    • outer plexiform layer in the temporal aspect of ora serrata----coalesce to form cysts-
    • called BLESSING IWANOFF CYSTS .
    • 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.
  • 5.  
  • 6.  
  • 7.  
  • 8.  
  • 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…
  • 10.
    • Premature infants, bilateral
    • 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
  • 11.
    • This reaction is peculiar only to incompletely vascularised retina.
    • A fully vascularised retina does not react to hyperoxygenation in this way
  • 12.  
  • 13.
    • COLOBOMA
    • Due to abnormal closure of fetal fissure mostly inferonasal
    • The RPE is totally absent in the coloboma
    • region or merely represented.
    • MEDULLATED NERVE FIBRES
    • Normal medullation stops at the lamina
    • cribrosa at birth. Rarely MNF’s appear near
    • the disc or elsewhere. Usually presence of such a
    • sheath does not interfere with the function of
    • affected fibres but reduces transparency of retina
    • producing a scotoma
  • 14.  
  • 15.  
  • 16.
    • ALBINISM
    • Gross absence of macula / hypoplasia of
    • macula
    • OGUCHI’S DISEASE
    • Total absence of Rods. Abnormal no of
    • cones present. Retardation of dark
    • adaptation.
    • RETINAL DYSPLASIA
    • Dev. Aberration(proliferation and infolding of
    • outer layers of retina) which is present at
    • birth.
  • 17.  
  • 18.  
  • 19.
    • Pre retinal hemorrage
    • Seen in proliferative retinopthy , trauma, subarachnoid hemorrhage, valsalva retinopathy, shaken baby syndrome etc..
    • Round or boat
    • shaped
  • 20.  
  • 21.
    • Superficial hemorrages
    • Seen in CRVO ,HTN retinopathy, background dr,
    • Periphlebitis etc
    • Flame shaped…seen in the nerve fibre layer
    • Mechanism :
    • Marked congestion of capillaries --- marked edema
    • of affected tissues ----capillaries of the NFL
    • rupture--- flame shaped haemorrages in the NFL
  • 22.  
  • 23.
    • ROTH SPOTS
    • Haemorrhages with white centres
    • Seen in anaemias , leukemias, HIV
    • retinopathy, SABE etc
  • 24.
    • Deep hemorrhages
    • Also called dot and blot haemorrhages.
    • Mainly diabetic retinopathy.
    • Mechanism :
    • Degeneration of the deep capillary walls ---
    • lead to hemorrhages in the inner nuclear
    • layer----dot and blot hemorrhages
  • 25.
    • Seen between layer of rods and cones and RPE
    • Large bright red indistinct outline
    • Seen in choroidal neovascularisation ,COAT’ s dis, Sickle cell anaemia, blunt trauma
  • 26.
    • Between RPE and bruch’s membrane
    • Choroidal neovascularisation is the common cause.
  • 27.
    • Yellowish waxy plaques with relatively distinct margins seen in the inner nuclear layer of retina .
    • Mechanism:
    • Formed mainly due prolonged leakage from the capillaries.
    • Seen in rings/clumps : diabetis , old
    • BRVO ,radiation retinopathy,
    • telangiectasias
    • stellate : htn , papilledema,
    • neuroretinitis
    • sub retinal : CNVM, COAT’s, toxocara canis
  • 28.
    • Cotton wool spots.
    • Seen in the NFL layer
    • Cottony appearance with frayed edges central fibrin and peripheral mucopolysaccharide
    • Mechanism :
    • Decreased perfusion ---micro infarcts in the
    • NFL----blockage in the axoplasmic flow---
    • cotton wool exudates are formed
  • 29.
    • Seen in HTN retinopathy , CRVO, HIV, Scleroderma, Pre proliferative DR, systemic vasculitis
  • 30.
    • Pathogenesis
    • 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
    • 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.
  • 31.
    • CHERRY RED SPOT(DD)
    • The mechanism by which a cherry red spotis
    • formed in niemann-pick and tay-sachs is
    • different
    • Due to defective metabolism(lipoidal
    • degeneration) sphingolipids
    • get accumulated---ganglion cells are more
    • susceptible---retina becomes opaque in
    • areas where ganglion cells are more---as
    • ganglion cells are absent in macula it retains it
    • natural colour---appearance of cherry red spot
  • 32.  
  • 33. Central Retinal Artery Occlusion Branch Retinal Artery Occlusion Afferent Pupillary Defect Cherry Red Spot Retinal Edema
  • 34.
    • Pathogenesis:
    • 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
    • Final outcome : organization of hemorrhages, formation of blood vessels on the inner retinal surface extending into vitreous.
  • 35. Central Retinal Vein Occlusion Branch Retinal Vein Occlusion
  • 36.  
  • 37.
    • Fibrino platelet
    • Cholesterol(hollen horst)
    • Calcific
  • 38.  
  • 39.  
  • 40.  
  • 41.  
  • 42.  
  • 43.  
  • 44.
    • Normally the vessels are seen as columns of pigmented RBC’s filling the lumina
    • Retinal arteriolar sclerosis- obscures blood column- light reflex is widened and imparts an orange or coppery hue to the arterioles
    • Process prolonged- perivascular fibrosis may totally hide the blood column – silver wire appearance
  • 45.
    • 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
    • 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).
  • 46.
    • Long standing HTN- Tributary venous occlusions – usually temporal vein is occluded because of more arterial crossings
    • Necrosis of capillary walls- supericial haemorraghes
    • Microinfarcts in the NFL – SOFT EXUDATES
  • 47.
    • Grade I : It consists of mild generalized arteriolar attenuation, particularly of small branches, with broadening of the arteriolar light reflex and vein concealment.
    • Grade II : It comprises marked generalized narrowing and focal attenuation of arterioles associated with deflection of veins at arteriovenous crossings (Salus’ sign).
    • 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.
    • Grade IV : This consists of all changes of Grade III and silver wiring with papilloedema.
  • 48. HTN RETINOPATHY
  • 49.
    • SOFT EXUDATES
  • 50.  
  • 51.
    • MALIGNANT HTN:
    • 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
  • 52.
    • Rarely focal choroidal infarction with patchy proliferation of RPE is evident clinically as elschnig spots and siegrist lines (increased pigmentation along a sclerotic vessel)
  • 53.  
  • 54.
    • Basic pathology : thickening of the basement membrane and ischaema
    • Loss of pericytes ( normal endothelial to pericyte ratio is 1:1. Pericytes have contractile properties and inhibit endothelial proliferation)
    • As the capillaries become acellular and their contractile nature is lost --- microaneurysms are formed---leakage may produce hard exudates
    • Aneurysmal wall break down- dot and blot hemorrhages
  • 55.  
  • 56.
    • 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).
  • 57.  
  • 58.  
  • 59.
    • Venous engorgement --- release of angiogenic factors--- NVD/NVE/ Rete mirabile ---vitreous haemorrhage---fibrovascular proliferation --- RD
  • 60.  
  • 61.  
  • 62.  
  • 63.  
  • 64.  
  • 65.  
  • 66.  
  • 67.  
  • 68.
    • 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
  • 69.  
  • 70.  
  • 71.
    • ACUTE
    • CHRONIC- granulomatous
    • non granulomatous
  • 72.
    • 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
  • 73.  
  • 74.
    • The progress and the severity of the inflammation depends on the element causing it.
    • Tuberculosis
    • Sarcoidosis
    • Syphilis
    • Toxoplasmosis etc
  • 75.
    • 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
    • Vascular walls are thickened and gliotic
    • Remaining outer retina adheres to the bruchs membrane
  • 76.  
  • 77.
    • 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
    • Later RPE dysfunction and death of sub foveal RPE cells – photo receptor degeneration and atrophic macular degeneration
  • 78.  
  • 79.
    • Lipofucsin deposition in the RPE
    • INITIAL EGG YOLK APPEARANCE
    • Egg SCRAMBLING---chorio retinal scarring develops
    • Impaired metabolism of the RPE
  • 80.  
  • 81.
    • Separation of photoreceptor layer from RPE
    • Inflammatory– exudative—either localised /diffuse
    • Tractional – organisation of inflammatory exudates/ haemorrages /glial tissue
    • Rhegmatogenous- break in the retina
  • 82.  
  • 83.  
  • 84.  
  • 85.
    • Seperation of OPL and INL
    • Two types
    • typical- split at OPL
    • reticular – split at NFL
  • 86.  
  • 87.
    • Typical is an exaggerated form of cystoid degeneration
    • Reticular form split at the NFL—if there is an outer hole---may cause RD
  • 88.
    • Discontinuity in the Bruchs mem---thickened and calcified at the level of elastic layer---calcification increases brittleness of bruchs --- sub retinal neovascularisation
    • Seen in hemolytic anaemias , pagets, pseudoxanthoma elasticum
  • 89.
    • Lamellar or full thickness
  • 90.  
  • 91.
    • Age related sclerosis of choriocapillaries
    • Degeneration of the RPE—photo receptor layer degeneration---retinal atrophy---the OLM lies almost in contact with the LAMINA VITREA
    • Hard drusen--- discrete round globular with overlying thinned RPE—beneath the BM of RPE—due to apoptosis of photoreceptors
    • Soft drusen – irregular, granular, in larger areas ---adhere loosely to the bruchs membrane
  • 92.  
  • 93. Bruch ’ s Membrane Drusen
  • 94. Choroidal Neovascularization
  • 95.
    • Lattice like pattern of criss crossing sclerotic vessels
    • 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
  • 96.  
  • 97.  
  • 98.  
  • 99.  
  • 100.  
  • 101.  
  • 102.  
  • 103.  
  • 104.  
  • 105. MALIGNANT MELANOMA CHOROID
  • 106.  
  • 107.  
  • 108.  
  • 109.  
  • 110.  
  • 111.  
  • 112.  
  • 113.  
  • 114.
    • Posterior neovascularisation
    • Peripheral neovascularisation
    • Arterial macroaneurysm
    • PVD with retinal tear
    • Intra ocular tumour
    • Disciform degeneration
    • Ocular trauma
    • CRVO
  • 115.