Retina

 To see retina and associated structures with
the use of an ophthalmoscope.
 Opacities in media of the eye will appear as
black specks or lines against the red reflex of
the Fundus .
 It can be done with direct /indirect
ophthalmoscopy or slit lamp bimicroscopy.
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 When the fundus is viewed without any special lenses
to neutralize the power of the eye it can be called
direct ophthalmoscopy. In this case instead of
neutralizing the power of the eye, it is used as a
magnifying loupe and viewing is made possible.
1.Ease of use to the untrained hand
2.Portability,by the bedside
3.Good for screening
However it also has a few drawbacks such as—
 Poor visibility in case of media opacities
Very limited field of view
Lack of depth perception
Need to get too close to the subject
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 The magnification of the image produced by the
indirect lens used can be easily derived from the
formula
 Magnification = power of eye (+60D)/ power of
lens
For example if using a 20D lens in an emmetropic
eye it would be 60/20=3
 Hence the higher the lens power smaller the image
and vice versa. The lower the power the
condensing lens the farther from the eye it must be
held. The stronger the power the condensing lens
the closer it must be held toward the eye.
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The advantages of I/O are many but the prime
would be---
1. Wide field of view including the fundus
periphery
2. Binocular viewing hence stereopsis
3. Media opacities are less of an issue
4. Dynamic viewing combined with scleral
depression is a boon
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 The non-contact Hruby lens is a high powered
plano concave minus 55 diopter lens (-55D) which
is available for most slit lamp biomicroscopes. The
retinal focus is achieved by effectively neutralizing
the optical power of the eye and extending the
focus of the slit lamp biomicroscope back to the
retina.
The view is erect, but is subject to reflections and a
restricted field of 5-8 degrees or just larger than
one disc diameter. This, plus the need for precise
patient fixations and cooperation makes the Hruby
lens a difficult procedure for screening the
posterior pole.
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 Top: fundus
examination
with Goldmann
3 mirror
contact lens
 Bottom: fundus
examination
with Hruby non
contact lens
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 The magnification on slit lamp biomicroscopy can
be derived from the same formula as for indirect
ophthalmoscopy but the magnification of the slit
lamp will have to be added.
 Thus for a +78D it will be as follows
60/78 = 0.76 X 10 (S/L magnification) = 7.6
 The +60 D lens gives greater magnification than a
+90D lens which would provide a larger field of
view.
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 Retina is a thin {0.2 mm} delicate transparent
membrane.It’s the most internal layer, placed between
vitreous interiorly and choroid externally.
 It extends from the edge of optic disc(1.5mm in diameter)
posteriorly to ora serrata anteriorly .
 The thinnest part of retina is at fovea centralis { center of
macula } .The macula lutea is a yellow spot about 5.5mm
in diameter and temporal to the optic disc
 Fovea centralis(about 1.5 mm in diameter) lies 3.5 mm
lateral to optic disc and it is the most sensitive part for
fine visual discrimination having cones only .The
foveola(0.35mm in diameter) is the central shining pit
 Lamina cribrosa --- the posterior scleral opening through
which optic nerve fibres pass.
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 Pigment epithelium – adherent to choroid and cover
by bowman membrane .It has single layer of flattened
hexagonal cells fine cytoplasmic villi.{cubical cell}.
 Rods and cones- visual receptor { vision in dim light
and vision in bright light }.Rods about 125 million
and cones about 7 million.
 External limiting membrane – formed by the external
ends of Muller s supporting fibres on which rods and
cones rest, and pierced by the fibres of these
photoreceptors.
 Outer nuclear layer – consists of rods and cones
nuclei .
 Outer plexiform layer – consists mainly of the
anastomoses of axons of rods and cones with the
dendrites of bipolar and horizontal cells .
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 Inner nuclear layer - consists of nuclei of bipolar cells
, horizontal and amacrine cells .Nuclei of Muller s
fibers and capillaries of central retinal vessels .
 Inner plexiform layer - consists mainly of the
arborizations of axons of bipolar cells with dendrites
of the ganglion cells and amacrine cells.
 Ganglion cells layer - {2nd order neuron }consists of
large multipolar nerve cells with clear round nuclei.
Their axons forms optic nerve fibres .
 Nerve fibers layer - contain axons of ganglion cells
and retinal vessels .This layer increases in depth as it
converges to the optic disc.
 Internal limiting membrane – A thin lamina made by
inner ends of Muller s fibres and it is in contact with
vitreous.
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Arterial supply
 choriocapillaries {1st to 5th layers}
 Inner layers by branches of Central Retinal
Artery
 Foveal avascular zone{diffusion form
choriocapillaries }
Venous supply
 central retinal vein to cavernous sinus .
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Media - any haziness , opacities , haemorrhage .
Optic disc {papilla}-
 shape – rounded , there may be a physiological cup in its center but
never reaches the disc margin .
 Color – pale pink whiter in the centre.
 Edges – well defined, regular.
 Size – about 1.5 mm {increase in high myopia and decrease in
hypermetropes }.
Blood vessels -
 Arteries – the C.R.A emerges from the physiological cup dividing into
upper and lower trunks each divides into nasal and temporal branches
.They show central light reflex, their color is brighter than veins but
arteries are narrower than veins.
 Veins –follow arteries .Vein is seen normally through arteries at point of
crossing because walls of blood vessels are transparent .
 Choroidal blood vessels – can be seen at deeper level .
 Broader without central light reflex {branches and anastomose
freely.
 Arterial pulsation is always pathological while venous is normally
seen at the disc .
Macula - is situated 3mm to the temporal side of edge of optic disc .Its
dark pigmented with central yellow foveal reflex.
General background of Fundus --- color is uniformly red.
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Vein
Disc
Fovea
Artery
Optic cup
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Vein
Artery
Optic cup
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 Uncommon , unilateral condition in old people .
Etiology :
 Thrombosis in D.M , atherosclerosis .
 Emboli {most common } form carotid artery ,
atherosclerosis , valvular heart disease,
rheumatic heart disease .
 Temporal arteritis {if bilateral } ,giant cell arteritis
Vascular spasm as Rayaud s disease .
 Collagen disease .
 Dissecting aneurysm of C.R.A .
 hypertension
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 Sudden painless loss of vision in embolic
disease.
 While vasospastic disease are preceded by
repeated transient episodes of decreased
vision or blindness {Amaurosis fugax} and
finally there is an acute attach in which vision
dose not return.
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 No haemorrhage in Fundus.
 Semi-dilated pupil not reactive to light (no P.L.)
Fundus –
 Early {shortly after the attach } :Retinal artery appear as
thin red threads {narrow}segmentation of blood
column {blood column in the artery is broken into
segments – called cattle track appearence ).Macula is
cherry red {cherry red spot }.Pale edematous retina so it
appears opaque.
 Late {after few weeks or months }:Vessels contracted to
white threads and some vessels refill due to collateral
circulation .Retina appear normal .No cherry spot .White
optic disc .
 Pupil dilated not reactive directly but consensually to light
(no P.L.)
 In obstruction of a branch of the retinal artery an
atheromatous embolus may be visible as a pale refractile
body within the artery called Hollenhorst plaque.
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 Aim to remove the embolus to a more peripheral and
smaller vessel or relief vasospasm{emergency case }.
 Immediate massage of the globe – moderate pressure on
closed lid for few seconds then suddenly release for few
seconds and then repeat the same .
 95% oxygen and 5% Co2 inhalation .
 I.V Diamox {carbonic acid anhydrase inhibitor } to decrease
IOP.
 Anterior chamber paracentesis {puncture of A.C to
decrease IOP --- remove emboli }.
 Vasodilator retrobulbar injection of acetylcholine .
 Anticoagulant {I.V heparin }.
 Treatment must be carried out within 2hours .
 If relief is within 1 hours --- may restore all vision .
 If relief within 2 hours --- may restore peripheral vision .
 If more than 3-4 hours --- permanent visual defect .
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 No severe symptoms .
 Localized milky white sectarian area limited
to the occluded branch which appears thread
like .
 Macula is frequently involved in the superior
temporal branch occlusion with permanent
sector field defect .
 Treatment :Same as C.R.A occlusion .
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 Uncommon , unilateral condition in 6-7th decade.
Etiology :
 In young – usually inflammation as infective
periphlebitis(sarcoidosis ,behcets disease) , optic
neuritis or increase blood
coagulability(polycythaemia, macroglobulinaemia,
cryoglobulinaemia) and stasis as in sickle cell
anaemia .
 In old – hypertension , atherosclerosis , primary open
angle glaucoma .
 Local – as orbital cellulitis .
 Systemic diseases – obstructive pulmonary disease,
D.M , leukaemia , thrombocytopenia purpura , sickle
cell anaemia , lymphoma .
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 Non-ischaemic CRVO(venous stasis
retinopathy/partial CRVO)—in 75% cases.All
symptoms and signs are less
 Ischaemic CRVO(haemorrhagic
retinopathy/complete CRVO)—in 25%
cases.All symptoms and signs are more
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 Gradual painless loss of vision .
 Marked venous congestion and tortousity
{dark blue }.
 Retina show extensive hemorrhage , edema
.Blood and thunder fundus in ischaemic type.
 Cotton wool patches due to retinal ischaemia
and neovascularization .
 Absence of normal physiological venous
pulsation even by pressure on the eye .
 Optic disc may be covered with haemorrhage
which may break into the vitreous
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 New vessels formation at optic disc,
A.C.,Iris{Rubeosis iridis }
 Haemosiderosis of retina .
 Cystoid macular edema .
 Vitreous hemorrhage .
 Secondary glaucoma after about 2-3 months
{100 days glaucoma }due to
neovascularization and vitreous haemorrhage
 Partial re-canalization especially in young .
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 Many patient {especially young }recover with
no treatment or steroids .
 Pan retinal photocoagulation to prevent
neovascular glaucoma .
 Cryo application if media is hazy
 Anticoagulant .
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 More common than C.R.V occlusion .
 The obstruction occur at the site of A-V crossing
and distal to the occlusion .
 The vein is dilated and tortuous .
 Retina with edema , haemorrhage , micro-
aneurysm , cotton wool exudation {sometimes }.
 Capillaries are dilated and leak plasma .
 Surface neovascularization occurs and there may
be proliferative retinopathy and vitreous
haemorrhage .
 The leakage of plasma form capillary cause
central retinal edema with reduced vision
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 If nasal branch is occluded ---- unnoticed visual
loss or branch temporal to macula {good
prognosis }.
 If temporal branch is occluded --- may be
edema or haemorrhage in macula and visual loss.
Treatment :
 Photocoagulation {if neovascularization present }.
 Systemic corticosteroid .
 Anticoagulants .
 Vitrectomy {if vitreous hemorrhage dose not clear
}.
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 Hemorrhage within retina have different
shapes depending on the layer in which they
occur .
 Preretinal hemorrhage --- occur between
retina and vitreous , hemispherical shape.It
indicates blood dyscrasias or trauma .
 Retinal hemorrhage --- may be flame shaped
which occur in the nerve fiber layer or round
dot and blot haemorrhage which occur within
the deep capillaries of retina --- inner
nuclear layer .
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 Trauma : vascular obstruction {C.R.V
occlusion , papilledema , subarachnoid
haemorrhage }.
 Inflammation : {vasculitis }, toxic vascular
disease {hypertension , D.M }, haemophilia
 Leukemia , purpura , retinal tear .
 N.B :- Retinal and preretinal {subhyaloid }
hemorrhages occur more commonly in
patient with subarachnoid and subdural
hemorrhage .
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 Micro-aneurysms :A common retinal abnormality
.Usually on the venous side of capillary network and
Can be identified by fluorescein angiography or
histological exam .
 Micro-aneurysms leak plasma and are often
surrounded by edema which gives the hazy
appearance of retina and occur in { D.M , C.R.A or
branch R.V stasis , coat s disease , periphlebitis ,
blood hyper-viscosity}.
 Exudates :These are opacities resulting from
inflammation .They are dirty white with ill-defined
margins .
Types :
 Hard exudates : small and take long time to develop
seen in D.M , hypertension .
 Soft exudates(cotton wool spots) : large appear
rapidly , they are micro-infarcts of retina in nerve
fiber layer .
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 More common in the outer part of outer plexiform
layer {fluid accumulation }—edema .
Cause :
 D.M , C.R.A , C.R.V occlusions , hypertension , retinal
angiomas , traction by vitreous inflammation of
vitreous or retina .
 Macro-aneurysms after ocular surgery .
Clinically :
 Blurred vision when macula is edematous .
 Retina thicker and opaque with blurred irregular
foveal reflex .
 In chronic edema –retina slightly raised , white .
 Irvine Gass syndrome : retinal edema , rapid temporal
loss of vision in aphakic patient {commonly after
intra-capsular cataract extraction } which allows
vitreous to adhere to iris
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 If macular edema is due to inflammation give
corticosteroid to prevent scaring .
 Focal edema due to vasculo- patient {D.M}
may respond to photocoagulation .
 Prognosis :Persistent macular edema may
become Cystoid with irreversible loss of
central vision
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 Bilateral retinal vascularization abnormality in
premature infants(birth weight less than 1500
gm) who require high oxygen environment .
 Seen few days after birth it s due to spasm {vaso-
constriction } of immature retinal blood vessels in
response to excess oxygen so leading to
suppression of normal retinal vascularization
{obliteration --- new vessel (late)}.
 There after the infant s new retinal vessels
become sensitive to oxygen so although
exposure to normal oxygen levels the vessels
dilate and new fibrovascular proliferation into
vitreous causing retinal detachment .
 In severe case --- retrolental space is filled with
fibrous tissue(pseudo-glioma) --- blindness .
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 I-formation of a demarcation line between
vascular and avascula zone
 II-formation of retinal ridge
 III-ridge with extraretinal fibrovascular
proliferation
 IV-sub-total tractional retinal detachment
 V-total retinal detachment
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 Prophylaxis :
 supplemental oxygen in premature infants {30-
35% O2 concentration }.
 Keep pupil dilated to be examined by {indirect
ophthalmoscope }to detect earlier stage of
retinopathy of pre-maturity{temporal peripheral
retina first affected .
Therapy :
 Early diagnosis --- complete regression .
 Late ---- irreversible blindness .
 Vit A and photocoagulation .
 N.B:Patient of retinopathy of pre-maturity are
more commonly with strabismus , myopia ,
macular pigmentation and rhegmatogenous R.D
.
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 A group of retinal degeneration hereditary
progressive disorders of retinal receptors ,
transmitted as autosomal recessive most
common or autosomal dominant least severe
or x –linked traits most severe .
 Rods slowly degenerate with secondary
atrophy of the remaining retina and pigment
epithelium .
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 Night blindness {1st symptom }nyctalopia .
 Constriction of visual field : begins as a ring
scotoma then extends peripherally and centrally
until only a small contracted visual field remains
{Gun barrel vision }.
 At50 – 60 Y {tubular vision } macular vision may
also be loss .
 Fundus: appears normal at first , later it shows
small retinal pigment epithelium holes with grey
appearance and areas of hyper and hypo
pigmentation .
 arteriolar attenuation .
 there are accumulations of pigments, shaped as
bone corpuscles .
 yellow waxy pale optic disc .
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 Electro-retino-gram(ERG) is reduced or
absent .
 Electro-oculo-gram(EOG) is flat .
 1/3 no family history.
 Commonly associated with myopia , posterior
subcapsular cataract , O.A.Glaucoma ,
 Cystoid macular edema in 70% cases , optic
disc hamartomas , keratoconus .
 Cellophane maculopathy/atrophic
maculopathy
 In late stages the unmasking of of the larger
choroidal vessels(tessellated fundus)
 Retinitis pigmentosa :Is usually bilateral .
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 Laurence-Moon-Biedl syndrome :Retinitis
pigmentosa ,autosomal recessive, obesity ,
mental retardation , hypo genital and
polydactyly {more then 5 digits on hand or
foot }.
 Bassen – kornzweig syndrome :Retinitis
pigmentosa , autosomal recessive
,steatorrhea , Friedreich s ataxia due to beta-
lipo-proteinaemia
 Usher s syndrome :Retinitis pigmentosa
,autosomal recessive, congenital
neurosensory deafness .
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 Refsum s disease:autosomal
recessive,RP,peripheral neuropathy,cerebellar
ataxia,elevated CSF protein,deafness,icthyosis
 Cockaynes syndrome:autosomal
recessive,RP,dwarfism,bird like faacies,mental
retardation,premature aging
 Kearns-sayre syndrome:external
ophthalmoplegia,myopathy,heart block
 Friedreichs ataxia:RP,post column
disease,ataxia,nystagmun,sub aortic stenosis
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 Prognosis ;25% of patient good .A few patient <
25 Y decrease in visual acuity and at 50 Y
decrease in visual acuity .
 Treatment :
 no specific therapy .
 vitamins A & E .
 to preserve vision in one eye by excluding it from
light with an opaque shell or very dark glasses
because it s believed that exposure to light
accelerates the degenerative process in retinitis
pigmentosa .
 genetic counseling should be offered to prevent
propagation of the disease .
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 Using gene therapy, scientists have restored
complex visual responses in mice with
retinitis pigmentosa (RP), according to a
paper
 The researchers used an adeno-associated
viral vector with cell-specific promoters to
ferry the halorhodopsin gene into the cones
of two mouse RP models
 If there are no immune reactions, then we can
come to humans in three to five years.
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 Retinal periphlebitis of unknown cause affecting
both eyes of young males .
 The signs of recurrent vitreous haemorrhage and
recurrent retinal haemorrhage .
 No symptoms or loss of vision caused by vitreous
haemorrhage .
 Segmented , dilated , beaded veins, with
sheathing or exudation and haemorrhage .
 Some cases develop Rubeosis iridis , neovasclar
glaucoma , cataract , uveitis .
 Treatment :-Photocoagulation to destroy
neovasclar tissue and Vitrectomy in certain case.
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 Paving stone degeneration :Pigment epithelium and outer
retinal layers are damaged or absent and it more in lower
quadrants .Common in adults .Patient is unaware of its
presence {harmless }.
 Lattice degeneration :Elongated canal in peripheral retina ,
surrounded by a narrow film where vitreous is attached
.Glisting white spots are common on retinal surface giving
a snail track appearance to some lattice areas .Retinal
vessels are thickened and form a white lattice –work {so
the name lattice }.Lattice lesion generally lie parallel to the
ora serrata .They are as many as 20 lesions in one eye
forming 2 or more parallel rows .
 Lattice degeneration is an etiologic factor in some cases of
rhegmatogenous R.D this is because of the vitreo-retinal
adhesion which may produce a retinal tear by the stress of
vitreous on post border of lattice lesion .People with lattice
degeneration enjoy or normal asymptomatic life ---- so to
be checked periodically and seen immediately if symptoms
are reported .
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 Retinal Holes :Retinal holes are small retinal break usually
circular without any virteous traction either tears or
atrophic holes .Common site are fovea and peripheral
retina .
 Retinal tears :Commonest cause is vitreous traction which
may be constant or intermittent .It is horse shoe shaped
with the tractional element and more dangerous than a
hole.
 Constant vitreous traction ; occur in proliferative diabetic
retinopathy , penetrating injury , other disorders causing
scarring of vitreous.
 Intermittent vitreous traction : occurs when vitreous is
partly liquefied and detached from retina ---- acceleration
or deceleration of the globe {by trauma or normal eye
movements }will cause whip like motions to vitreous gel
causing stress ---- retinal tear at vitreo-retinal
attachment points .
 Other causes of retinal tears :Blunt trauma & anomalous
zonular attachments to retina .
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 Due to retinal tears ---- capillary are ruptured RBC in
retrovitreal space --- black spots seen by the patient
.
 Most retinal tears retains a partial attachment so that
vitreous continues to exert traction on retina .But
they are not treated unless :
 Vitreous cavity is very large .
 Retinal holes are multiple large or far behind ora
serrata .
 History of R.D in the fellow eye or family history of
R.D .
 There are recent symptoms of vitreous detachment .
 Atrophic retinal holes
 Caused by lattice degeneration , retinoschisis
{splitting of retina due to degeneration with cyst
formation between the 2 layers } or idiopathic .
 Most are asymptomatic .
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 There are 3 ways to seat a retinal hole .The
mechanism is the same to cause an
inflammatory choroidal and retinal response
that will bind them together .These 3 ways
are :
 Cryothermy : by freezing .
 Photocoagulation: burring by light using
xenon argon or argon laser as the light
source .
 Diathermy:burring by high frequency
current{electricity }
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 It is the separation of sensory retina from retinal
pigment epithelium allowing fluid to accumulate
between them.
Predisposing factors :
 Males more affected than female .
 Degenerative myopia , retinoschisis .
 Old age , snail track degeneration .
 Aphakia {100 times than normal }.
 After complicated cataract extraction .
 History of trauma {blunt or perforating
}commotio retinae (Called Berlin's Edema If
Invoved the Macula [Added By Wesmosis!] )
contrecoup injury to the retina
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 most common.Retinal separation with hole
formation Due to :
 break in continuity of sensory layer by
vitreous traction and retinal degeneration .
 laceration or contusion of the eye.
 Separation or retina at ora serrata by trauma .
 Congenital .
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 High myopia .
 Vitreous degeneration .
 Snail track degeneration .
 Retinoschisis {juvenile type}.
 Trauma & commotio retinea .
 After cataract surgery with vitreous loss .
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 A retinal hole .
 Liquid in vitreous with free access to the hole
.
 A force sufficient to break the band between
retina and pigment epithelium .
6/17/2015
(Ophth) 95

 sudden rapid painless loss of vision but when
R.D spreads very slowly the patient is not aware
of any problem until macula is involved.
 Photopsia – flashes of light without retinal
stimulation by light it is caused by vitreous
traction on retina .
 Sudden black dots in peripheral visual field due
to minute vitreous haemorrhage at point of
retinal separation .
 Visual field defect corresponding to detached
area .
6/17/2015
(Ophth) 96

 Red reflex becomes greyish in color .
 The detached retina is grey or translucent .
 Pattern of normal choroid cannot be seen.
 Tortuous retinal vessel and dark red in the area of
detachment and have undulating course .
 Retina thrown into folds that change in location or
shape with shifting in eye position
 Arteries and veins may appear to have same blood
color .
 Retinal breaks are recognized by the bright red reflex
of choroid shining through the greyish opaque
detached retina .
 Vitreous show tobacco dust
 Relative afferent papillary defect(Marcus-Gunn pupil)
in eyes with extensive RD
 Mild anterior uveitis
 Low IOP --- due to absorption of sub retinal fluid by
the vascular choroid .
6/17/2015
(Ophth) 97

 Retinal thinning with sub-retinal demarcation
linings
 Secondary intraretinal cysts
 Opaque threads of subretinal fibrosis
 Proliferative vitreo-retinopathy
 RD becomes total
 Complicated cataract,chronic
uveitis,hypotony,phthisis bulbi
6/17/2015
(Ophth) 98

 Horse shoe shaped tears with concavity
towards ora serrata common in upper
temporal region .
 Small round holes seen anywhere especially
macular and perimacular region .
 Retinal disinsertion {anterior dialysis }-tearing
of retina from ciliary body at ora serrata
usually in lower quadrants
6/17/2015
(Ophth) 99

 Sudden and rapid visual loss
 Floaters present but photopsia absent as there is
no vitrei-retinal tractions
 No break in continuity of inner retina
 RD configuration is convex,smooth,non
corrugated and bullous and even it may touch
lens
 Exudative detachment by choroiditis .
 Solid malignant detachment by malignant
melanoma .
 In rheumatoid arthritis, haradas disease,
toxaemia of pregnancy
6/17/2015
(Ophth)
10
0

 Photopsia and floaters are usually absent
because vitreo-retinal traction develops
slowly
 Slow and progressive loss of visual fields
 Retinal breaks are absent
 RD configuration is concave
 Mobility of detached retina is severely
reduced
 Sub-retinal demarcation lines are absent
6/17/2015
(Ophth)
10
1

6/17/2015
(Ophth)
10
2

6/17/2015
(Ophth)
10
3

 Red reflex .
 Ophthalmoscopy {direct and indirect }.
 Biomicroscopy for peripheral retinal .
 Visual fields .
 Ultrasound(B-scan)
D/D :-
 Senile retinoschisis no retinal tear , no R.D ,
cystic spaces between retinal layers.
 Choroidal detachment : retina smooth , pigment
epithelium still visible not much visual loss .
 Malignant melanoma of choroid : sub retinal fluid
shifts on changing patient s position.
6/17/2015
(Ophth)
10
4

 The aim is to seal the holes and prevent further holes
from developing .
 In severe cases --- relief vitreous traction by
reducing volume of vitreous compartment and
distorting it by vitrectomy .
 Retinal is placed in contact with choroid to seal the
retinal breaks and tissues stimulated by diathermy
,Cryotherapy , laser photocoagulation to establish a
permanent chorioretinal band around the hole .
 Multiple holes ---- encirclage operation .
 Generally is done by scleral buckle operation in which
sclera is depressed so that it bulges inward pushing
choroid to the detached retina .
 Sub-retinal fluid drainage
 Intra vitreal injection of air/ringer lactate if eye is too
soft
 Pars plana vitrectomy with internal gas/silicon oil to
remove tractions
6/17/2015
(Ophth)
10
5

 The course of R.D depends on type and location of the
retinal breaks :
 Horse shoe shaped tear – in upper temporal region will
early lead to symptoms .When patient is erect the
detachment will increase from above downward and will
soon involve the macula --- decrease central vision { in
addition to field defect }.
 If the retinal tear occur in the upper nasal quadrant the
firm adhesion of retinal to margins of optic nerve head will
prevent rapid extension of the detachment toward macula
.
 Disinsertion from lower retina {at ora serrata } take long
time to develops field defect and loss of visual acuity
 The prognosis is related to size of retinal tear , time
interval between detachment and its diagnosis and
surgical treatment .Disinsertion at ora have the best
prognosis .90% of cases have good results if diagnosed
early.Prognosis is bad in case of old standing R.D
{>9months }large multiple holes , extensive dialysis ,
massive vitreous retraction .
6/17/2015
(Ophth)
10
6

 Recurrence .
 Scleral necrosis.
 Vitreous and retinal haemorrhage .
 Uveitis .
 Complicated cataract .
6/17/2015
(Ophth)
10
7

 Unknown etiology , male more affected ,
unilateral .
 Sudden disturbances of vision in one eye .
 There are small defect in retinal pigment
epithelium --- fluid leakage form
choriocapillaries to sub retinal space leading to
serous detachment of macula .
 By ophthalmoscope – slight elevation of macula
due to detachment of retinal pigment epithelium
in that area , cloudy macula , loss of foveal reflex
,sometime foveal ring reflex.
 Visual acuity is reduced to a variable degree ,
there’s slight shift toward hypermetropia
 Fundus fluorescein angiography showing smoke-
stack pattern or ink-blot pattern
6/17/2015
(Ophth)
10
8

6/17/2015
(Ophth)
10
9

6/17/2015
(Ophth)
11
0

 Most cases(80-90%) heal spontaneously
though it may take {attacks }several weeks to
months
 40% cases develop recurrent attacks
 The duration of the disease can be shortened
by closing the leakage point with light
coagulation (argon laser photocoagulation).
 Mild metamorphopsia or micropsia may
persist for a longer period
6/17/2015
(Ophth)
11
1

 It is an accumulation of fluid in the outer
plexiform (Henles) layer and inner nuclear layer
of the retina, in the macular area.
 Aetiology—
 Irvine-Gass syndrome—most common cause of
CME specially after complicated cataract
extraction
 Back-ground diabetic retinopathy
 CRVO / BRVO
 Acute iridocyclitis / pars planitis
 Retinitis pigmentoisa (70% cases)
 Epinrpherine eye drop specially in aphakic
6/17/2015
(Ophth)
11
2

 Visual acuity reduced to 6/60
 Irregular and blurred foveal reflex
 Macula edematous with multiple cystic
changes
 In long standing cases even macular hole
 Fundus fluorescein angiography shows flower
petal appearance in the macular region
6/17/2015
(Ophth)
11
3

6/17/2015
(Ophth)
11
4

 Usually self-limiting
 Systemic steroids for vascular and inflammatory
conditions
 Sub tenon and long acting steroids
 Systemic and local non steroidal anti inflammatory
drugs
 In the postoperative period, if they don't refract to
a crisp 20/20 or better, get high-resolution optical
coherence tomography of the fovea to make sure
there is no cystoid macular edema before tapering
their anti-inflammatory regimen.
6/17/2015
(Ophth)
11
5

 It is a development disorder of vitreous
 Usually unilateral and first noted in neonatal
period
 Associated with microphthalmos, cataract ,
elongated ciliary processes
 May be associated with high IOP
 Ultrasound(B-scan) confirms the diagnosis
6/17/2015
(Ophth)
11
6

 Nutrition of the macula is derived from
choriocapillaries so oxygen and nutrient have
to pass Bruchs membrane and pigment
epithelium .
 So macula is affected wherever there’s
sclerosis of choriocapillaries ,pathologic
changes in pigment epithelium , senile
changes in Bruch s membrane .
 Macular degeneration affect 50% of person
above age of 80 Y .
6/17/2015
(Ophth)
11
7

Macular Degeneration
 People with macular degeneration gradually
lose their central vision—the part of vision
needed for reading and seeing fine details.
Their peripheral (side) vision remains
unharmed.
6/17/2015
(Ophth)
11
8

 AGE RELATED MACULAR DEGENERATION
 TWO TYPES
6/17/2015
(Ophth)
11
9

 The most common type of ARMD
 Atrophic pale area in the centre , loss of
foveal reflex .
 Partial slow and progressive atrophy of
pigment epithelium ,photoreceptors, Bruch s
membrane and choriocapillaries .
 There are usually a number of
drusen(amorphous material appear as yellow
spots) located in degenerated retinal pigment
cell .
 No treatment .
6/17/2015
(Ophth)
12
0

6/17/2015
(Ophth)
12
1

6/17/2015
(Ophth)
12
2

 It represents a progressive Exudative and
proliferating senile macular degeneration .
 There is a defect in Bruch s membrane
leading of serous fluid or blood from choroid
through the small defects causing focal
elevation of the retinal pigment epithelium
and haemorrhagic detachment of the
epithelium .
 The blood vessels leaking through defect in
Bruch s membrane will cause sub retinal
neovascularisation membrane(SRNVM) into
pigment epithelium .
6/17/2015
(Ophth)
12
3

6/17/2015
(Ophth)
12
4

6/17/2015
(Ophth)
12
5

 Rapid loss of vision .
 Metamorphopsia {distorted objects }
Complications of exudative ARMD—
 Haemorrhagic detachment of
RPE/neurosensory retina
 Vitreous haemorrhage
 Disciform scarring of the macula
 Exudative retinal detachment
Treatment :Argon(blue-green) laser
photocoagulation only if sub retinal
neovascularization developed must be done
as soon as possible before involvement of
fovea .Before laser fundus fluorescein
angiography is done to localise the lesion.6/17/2015
(Ophth)
12
6

Etiology :
 May be secondary to trauma , vascular
disease of retina , intraocular inflammations ,
myopia , R.D or as a congenital anomaly ,
cystoid macular degeneration .
Clinically :
 Instead of macula we see a red spot .
 No fovea reflex .
Treatment :Not necessary because the hole is
stationary and never leads to R.D.
6/17/2015
(Ophth)
12
7

6/17/2015
(Ophth)
12
8

 Malignant intraocular tumour that originates in the outer nuclear
layer of retina .Most cases appear before 3 years of life(average
age of diagnosis 18 month), unilateral cases being diagnosed at
around 24 months and bilateral cases before 12 months
 Most common intraocular tumour of childhood .
 30 – 25% of cases are bilateral .
 Family history present in 6% cases(autosomal dominant)
and remaining 94% are sporadic
 Chromosomal abnormality deletion of the long arm of
chromosome-13 and with trisomy-21
 all bilateral cases are related to hereditary and 5 – 10% of
unilateral are hereditary also.
 Other cases are thought to arise by chromosomal mutation .
 Orbital sarcoma may occur in the irradiated orbits after
enucleation of retinoblastoma
 Osteogenic sarcoma of femur and skull in patients who have
survived from bilateral retinoblastoma
 Trilateral retinoblastoma is bilateral retinoblastoma with6/17/2015
(Ophth)
12
9

 Amaurotic cat s eye(leukocoria)- white mass
or greyish red reflex in pupil (most common
presentation about 60%)
 red painful eye {tumor necrosis }.
 Squint {in 20% cases }.
 Enlargement of the globe {2ry glaucoma }.
 Proptosis due to orbital involvement
 Endophthalmitis/anterior uveitis
 Visual difficulties
 Nystagmus in bilateral case
6/17/2015
(Ophth)
13
0

6/17/2015
(Ophth)
13
1

 Leucocoria 56%
 Strabismus 20%
 Red painful eye 7%
 Poor vision 5%
 Asymptomatic 3%
 Orbital Cellulitis 3%
 Unilateral Mydriasis 2%
 Heterochromia Iridis 1%
 Hyphaema 1%
6/17/2015
(Ophth)
13
2

6/17/2015
(Ophth)
13
3

 Pseudohypopyon
 Spontaneous hyphema
 Vitreous hemorrhage
 Phthisis bulbi
 Preseptal or orbital cellulites
6/17/2015
(Ophth)
13
4

6/17/2015
(Ophth)
13
5

6/17/2015
(Ophth)
13
6

6/17/2015
(Ophth)
13
7

6/17/2015
(Ophth)
13
8

 Mid dilated pupil non reactive .
 White mass behind lens .
 Ophthalmoscopically ---- white or pale pink mass with newly
formed blood vessels on its surface .
 The tumor may grow outwards separating retina from choroid ,
with/without total exudative RD & difficult to see, {Glioma
exophytum } and retinal vessels are seen over the tumor.
 grows inwards toward vitreous, seen as white or pink colored
mass with calcium deposits –{Glioma endophytum }. The retinal
vessels are not seen on the tumor surface.
 Growth of the tumor ---- enlargement of globe --- iris pushed
forward against trabecular meshwork ---- increase IOP --- 2ry
glaucoma .
 strabimus
 Increase level of aqueous humor lactate dehydrogenase .
 Extraocular extension of the tumor to optic nerve , break through
limbus as large fungating mass .
 Metastasis ---- locally direct to intra ocular tissues and extra
ocular tissues , orbital bones & CNS via optic nerve and regional
pre-auricular & cervical lymph nodes { blood metastasis is rare to
bone ,liver ,lungs } 6/17/2015
(Ophth)
13
9

6/17/2015
(Ophth)
14
0

6/17/2015
(Ophth)
14
1

6/17/2015
(Ophth)
14
2

6/17/2015
(Ophth)
14
3

6/17/2015
(Ophth)
14
4

6/17/2015
(Ophth)
14
5

6/17/2015
(Ophth)
14
6

6/17/2015
(Ophth)
14
7

6/17/2015
(Ophth)
14
8

6/17/2015
(Ophth)
14
9

 1-quiescent stage(6-12 months)
 2-Glaucomatous stage
 3-Stage of extra ocular extension
 4-Stage of metastasis
6/17/2015
(Ophth)
15
0

 Congenital cataract .
 Persistent hyperplastic , 1ry vitreous ,
vitreous hemorrhage .
 Toxocara canis infestation .
 Total R.D .
 Coat s disease .
 Endophthalmitis.
 Retinopathy of pre-maturity .
6/17/2015
(Ophth)
15
1

 Direct/indirect ophthalmoscopy
 X-ray of orbit for calcification and erosion of optic
foramen
 Ultrasound(B-scan)
 CT-scan
 Aqueous humour paracentesis for cytology & LDH
enzyme assay
 Carcino embryonic antigen
 ELISA-for toxocara endophthalmitis
 Lumber puncture and bone marrow aspiration for
metastasis
 Fine needle aspiration cytology(FNAC)when diagnosis
is not confirmed
 Fluorescein angiography
6/17/2015
(Ophth)
15
2

6/17/2015
(Ophth)
15
3

6/17/2015
(Ophth)
15
4

 Depends on size , location and number or tumors
 Small tumor can be treated with radiotherapy(cobalt-
60) sometimes combined with chemotherapy .
 Cryotherapy or photocoagulation(xenon arc)—for
small tumours .
 Large tumor ---- Enucleation with long piece of optic
nerve.
 Orbital involvement—exentration
 Advanced cases with distant metastasis—
chemotherapy(cyclophosphamide & vincristine)
 Genetic counselling—if two or more cases in the
family
 If retinoblastoma is unilateral ---- annual exam of
fellow eye {after treatment of affected eye }.
 If bilateral ---- Enucleation of more advanced eye
and medical therapy in other eye .
6/17/2015
(Ophth)
15
5

 This is chronic,progressive vascular abnormality in
which telengiectatic retinal vessels leak fluid which
causes exudative bullous retinal detachment
 Usually unilateral in boys between 18 months to 18
years
 Decreased visual acuity/white papillary reflex
 Ophthalmoscopically yellowish white exudative patch
behind the retinal blood vessels which are
tortuous,fusiform dilatation,aneurysms,vitreous
haemorrhage
 Retinal detachment with iritis
 Cataract and glaucoma
Treatment--early photocoagulation or cryotherapy may
be helpful
6/17/2015
(Ophth)
15
6

 Normal pregnancy : 50% of pregnant show
increase BP so arteries of retinal show
attenuation , this is only a tonic functional
contraction which disappears after delivery
 Toxemia of pregnancy : retinal vessels are
attenuated {constricted } .Ischemic retinal
changes , retinal edema , haemorrhage
,haemorrhagic infarction , cotton wool exudates
.Milky white edema of optic nerve head .Macular
star – edema , exudates in macula.
{the attenuation of retinal arterioles may be
general or signs .Changes are usually
reversible.but only if toxemia is 2ry to kidney
disease is irreversible
6/17/2015
(Ophth)
15
7

6/17/2015
(Ophth)
15
8

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