Transcript
DR. PARAMESWARA RAO(PROFESSOR) DR.SIVA KUMAR( PG)
AT BIRTHFovea contains many layersOra serrata is less developedThere is a fold of redundant retina called Lange’s fold.Thicker retinaPeripheral retina circulation develops only in the last trimester of gestation.
WITH AGE1. 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- 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.
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
COLOBOMA Due to abnormal closure of fetal fissure
mostly inferonasalThe RPE is totally absent in the coloboma region or merely represented.
MEDULLATED NERVE FIBRESNormal 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
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.
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 etcFlame 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
ROTH SPOTSHaemorrhages with white centresSeen in anaemias , leukemias, HIV retinopathy, SABE etc
Deep hemorrhagesAlso 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
PathogenesisArterial 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.
CHERRY RED SPOT(DD)The mechanism by which a cherry red spotis formed in niemann-pick and tay-sachs is differentDue 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 DefectCherry Red SpotRetinal 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.
HTN RETINOPATHY
SOFT EXUDATES
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
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 INITIAL EGG YOLK APPEARANCE 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
BruchBruch’’ssMembraneMembrane
BruchBruch’’ssMembraneMembrane
DrusenDrusenDrusenDrusen
ChoroidalChoroidalNeovascularizatioNeovascularizationn
ChoroidalChoroidalNeovascularizatioNeovascularizationn
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
MALIGNANT MELANOMA CHOROID
Posterior neovascularisation
Peripheral neovascularisation
Arterial macroaneurysm
PVD with retinal tear
Intra ocular tumour
Disciform degeneration
Ocular trauma CRVO
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