Retinal lesions Pathophysiology
Upcoming SlideShare
Loading in...5

Retinal lesions Pathophysiology






Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

Retinal lesions Pathophysiology Retinal lesions Pathophysiology Presentation Transcript

    • 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.
    • 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
    • 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-
    • 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.
  • 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…
    • 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
    • This reaction is peculiar only to incompletely vascularised retina.
    • A fully vascularised retina does not react to hyperoxygenation in this way
    • Due to abnormal closure of fetal fissure mostly inferonasal
    • The RPE is totally absent in the coloboma
    • region or merely represented.
    • 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
    • Gross absence of macula / hypoplasia of
    • macula
    • Total absence of Rods. Abnormal no of
    • cones present. Retardation of dark
    • adaptation.
    • Dev. Aberration(proliferation and infolding of
    • outer layers of retina) which is present at
    • birth.
    • Pre retinal hemorrage
    • Seen in proliferative retinopthy , trauma, subarachnoid hemorrhage, valsalva retinopathy, shaken baby syndrome etc..
    • Round or boat
    • shaped
    • 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
    • Haemorrhages with white centres
    • Seen in anaemias , leukemias, HIV
    • retinopathy, SABE etc
    • 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
    • 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
    • Between RPE and bruch’s membrane
    • Choroidal neovascularisation is the common cause.
    • 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
    • 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
    • Seen in HTN retinopathy , CRVO, HIV, Scleroderma, Pre proliferative DR, systemic vasculitis
    • 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.
    • 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
  • Central Retinal Artery Occlusion Branch Retinal Artery Occlusion Afferent Pupillary Defect Cherry Red Spot Retinal Edema
    • 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.
  • Central Retinal Vein Occlusion Branch Retinal Vein Occlusion
    • Fibrino platelet
    • Cholesterol(hollen horst)
    • Calcific
    • 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
    • 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).
    • 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
    • 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.
    • 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
    • Rarely focal choroidal infarction with patchy proliferation of RPE is evident clinically as elschnig spots and siegrist lines (increased pigmentation along a sclerotic vessel)
    • 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
    • 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).
    • Venous engorgement --- release of angiogenic factors--- NVD/NVE/ Rete mirabile ---vitreous haemorrhage---fibrovascular proliferation --- RD
    • 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
    • ACUTE
    • CHRONIC- granulomatous
    • non granulomatous
    • 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
    • The progress and the severity of the inflammation depends on the element causing it.
    • Tuberculosis
    • Sarcoidosis
    • Syphilis
    • Toxoplasmosis etc
    • 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
    • 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
    • Lipofucsin deposition in the RPE
    • Egg SCRAMBLING---chorio retinal scarring develops
    • Impaired metabolism of the RPE
    • Separation of photoreceptor layer from RPE
    • Inflammatory– exudative—either localised /diffuse
    • Tractional – organisation of inflammatory exudates/ haemorrages /glial tissue
    • Rhegmatogenous- break in the retina
    • Seperation of OPL and INL
    • Two types
    • typical- split at OPL
    • reticular – split at NFL
    • Typical is an exaggerated form of cystoid degeneration
    • Reticular form split at the NFL—if there is an outer hole---may cause RD
    • 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
    • Lamellar or full thickness
    • 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
  • Bruch ’ s Membrane Drusen
  • Choroidal Neovascularization
    • 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
    • Posterior neovascularisation
    • Peripheral neovascularisation
    • Arterial macroaneurysm
    • PVD with retinal tear
    • Intra ocular tumour
    • Disciform degeneration
    • Ocular trauma
    • CRVO