Dr.Narang

Retina

ANATOMY OF RETINA

Gross Anatomy•R

etina extends from the optic disc to the ora serrata.•I

t is divided into two distinct regions: -p

osterior pole and-p

eripheral retina separated by the so called retinal equator.

Posterior pole •I

t refers to the area of the retina posterior to the retinal equator.

•The posterior pole of the retina includes two distinct areas:

-optic disc and

-macula lutea

Macula lutea. •I

t is also called the yellow spot.•I

t is comparatively deeper red than the surrounding fundus and is situated at the posterior pole temporal to the optic disc.

•Fovea centralis is the central depressed part of the macula. It is about 1.5 mm in diameter and is the most sensitive part of the retina. In its Center is a shining pit called foveola.

•An area about 0.8 mm in diameter (including foveola and some surrounding area) does not contain any retinal capillaries and is called foveal avascular zone (FAZ).

•Surrounding the fovea are the parafoveal and perifoveal areas.

Structure of fovea centralis•I

n this area, there are no rods.•C

ones are tightly packed and other layers of retina are very thin.

•Its central part (foveola) largely consists of cones and their nuclei covered by a thin internal limiting membrane.

•All other retinal layers are absent in this region.

•In the foveal region surrounding the foveola, the cone axons are arranged obliquely (Henle’s layer or outer plexiform layer) to reach the margin of the fovea.

Fovea centralis

Peripheral retina It refers to the area bounded posteriorly by the retinal equator and anteriorly by the ora serrata.

Optic disc•I

t is a pink coloured , well-defined circular area of 1.5-mm diameter.

•At the optic disc all the retinal layers terminate except the nerve fibres, which pass through the lamina cribrosa to run into the optic nerve.

• A depression seen in the disc is called the physiological cup. The central retinal artery and vein emerge through the centre of this cup.

LAYERS OF RETINA :•M

NEMONIC:•I

N –INTERNAL LIMITING MEMBRANE•N

EW –NERVE FIBER LAYER•G

ENERATION –GANGLIONIC LAYER•I

T –INTERNAL PLEXIFORM LAYER•I

S –INTERNAL NUCLEAR LAYER•O

NLY –OUTER PLEXIFORM LAYER•O

PHTHALMOLOGIST’S –OUTER NUCLEAR LAYER•E

XAMINING –EXTERNAL LIMITING MEMBRANE•P

ATIENTS –PHOTORECEPTORS •R

ETINA –RETINAL PIGMENT EPITHELIUM

Internal limiting membrane•I

t is the innermost layer and separates the retina from vitreous.

•It is formed by the union of terminal expansions of the Muller’s fibres.

•It is essentially a basement membrane.

Nerve fibre layer (stratum opticum) •I

t consists of axons of the ganglion cells, running parallel to retinal surface.

•The layers increase in depth as it converges to optic disc.

•The nerve fibers are fine and non-medullated

•It pass through the lamina cribrosa to form the optic nerve

Ganglion cell layer•I

t mainly contains the cell bodies of ganglion cells (the second order neurons of visual pathway).

• There are two types of ganglion cells:

- The midget ganglion -cells are present in the macular region. each such cell synapses with single bipolar cell.

- Polysynaptic ganglion -cells lie predominantly in peripheral retina .Each such cell may synapse with upto a hundred bipolar cells

Inner plexiform layer•I

t essentially consists of connections of bipolar cells with the ganglion cells and amacrine cells.

Inner nuclear layer•I

t mainly consists of nuclei of bipolar cells. •I

t also contains nuclei of amacrine and Muller’s cells •C

apillaries of central artery of retina, but outer layers are avascular.

•The bipolar cells constitute the first order neurons.

Outer plexiform layer•T

he Innermost portion of each rod and cone cell is swollen with lateral processes known as spherules and pedicles respectively.

•This layer consists of connections of rod spherules and cone pedicles with the dendrites of bipolar cells and horizontal cells.

Outer nuclear layer•I

t consists of nuclei of the rods and cones.•C

one nuclei are larger and more oval and carry a layer of cytoplasm

External limiting membrane•I

t is a fenestrated membrane, on which rods and cones rest and their processes pierce

Photoreceptor layer•

Rods and cones are the end organs of vision and are also known as photoreceptors.

•Rods contain a photosensitive substance visual purple (rhodopsin) and subserve the peripheral vision and vision of low illumination (scotopic vision).

• Cones also contain a photosensitive substance and are primarily responsible for highly discriminatory central vision (photopic vision) and colour vision.

Pigment epithelium. •I

t is the outermost layer of retina.•I

t consists of a single layer of cells containing pigment.•T

he cells of RPE contain varying amount of melanin.•C

ells are taller at fovea and contain more pigment.•A

round the Optic disc they are heaped up as ‘choroidal ring’•I

t is firmly adherent to the underlying basal lamina (Bruch’s membrane) of the choroid.

Blood supply•O

uter four layers of the retina- choroidal vessels•I

nner six layers- central retinal artery, which is a branch of the ophthalmic artery.

CRAO•C

entral retinal artery emerges from centre of the physiological cup of the optic disc and divides into four branches.

•These are end arteries i.e., they do not anastomose with each other.

Predisposing factors:•H

ypertension•C

ardiovascular diseases

Etiology•T

hrombophilic disorders.•E

mboli from the carotid artery and those of cardiac origin(20%)

•Atherosclerosis-related thrombosis at the level of lamina cribrosa(75%).

•Arteritis with obliteration.

•Angiospasm

•Raised intraocular pressure

Symptoms :•S

udden,painless loss of vision.•A

maurosis fugax

Sign’s•R

ed reflex absent.•M

arked narrowing of large arteries, arterioles invisible.•W

ithin few hours retina become milky white because of oedema.•W

ithin a day or two macular area show cherry red spots because of choroid shining through thin retina.

•When obstruction is incomplete, column of venous blood has cattle tract appearance.

•After few weeks oedema subsides , atrophic changes occur(optic nerve atrophy/attenuated thread like arteries).

•No PL/PR

Treatment•I

mmediate lowering of IOP –massage /IV mannitol /A.C. paracentesis .

•Vasodilator and inhalation of mixture of 5%CO2 and 95%O2.

•Anticoagulants –IV heparin

•IV steroids –giant cell arteritis

Prognosis:•>

6 hours –No return of central vision.

CRVO•T

he retinal veins: These follow the pattern of the retinal arteries.

•The central retinal vein drains into the cavernous sinus directly or through the superior ophthalmic vein

Predisposing Factors•A

ge :6th/7th decade(2nd decade in case of non ischaemic)•S

ystemic hypertension•R

aised IOP•D

iabetes•H

yperviscosity syndrome•P

eriphlebitis

Pathogenesis•E

xternal compression on the vein•V

enous stasis•D

egenerative disease of venous endothelium

Types:•N

on Ischaemic/Venous stasis retinopathy/Partial CRVO=75%•I

shchaemic CRVO/haemorrhagic CRVO/Complete CRVO=25%

Non Ischaemic Symptom:•V

ague U/L fogginess of vision initially.•V

/A remains good.•V

itreous hemorrhage never present•M

ild pupillary defect

Signs:•M

ild tortuosity and dilatation of retinal veins.•D

ot and blot and flame shaped haemorrhage.•O

ptic disc swelling•M

acular oedema may or not- permanent impaired vision but normally 50% regain VA as Macular oedema resolves.

•Circulating IgM raised in most,leading to phlebitis of central vein in optic head ,hence fundus picture resemble venous thrombosis

Ischaemic CRVO Symptoms :•V

A- marked reduced

Signs•M

arked tortuosity and engorged retinal veins.•M

assive superficial and deep haemorrhages.•C

otton wool exudates.•O

ptic disc swelling and hyperaemia.•M

acular oedema and haemorrhage.•B

unches of tortuous new vessels formed upon optic disc.•E

ventual atrophy of affected retina.•F

undus described as BLOOD AND THUNDER FUNDUS•O

bstruction of central vein just behind lamina cribrosa ,peripheral at bifurcation as in arterisclerotic

Prognosis:•5

0% develop rubeosis and neovascular glaucoma within 3 months of initial occlusion aka 90 days glaucoma.

•Pre-retinal or vitreous haemorrhage secondary to NVD

Management•I

t is usually not required.•T

he condition resolves with almost normal vision in about 50 percent cases.

•Visual loss in rest of the cases is due to chronic cystoid macular oedema, for which no treatment is effective.

•However, a course of oral steroids for 8-12 weeks may be effective.

•Patient should be followed up closely for rubeosis iridis, as prompt treatment in early cases by PRP.

THANKS FOR PATIENCE…!