BY-DR.. DIVYA PATEL

UPGRADED DEPARTMENT OF OPHTHALMOLOGY

MGM MEDICAL COLLEGE AND MYH, INDORE(M.P.)

BLOOD SUPPLY OF OPTIC NERVE HEAD

ISCHEMIC OPTIC NEUROPATHY It is circulatory insufficiency to optic nerve head

ISCHEMIC OPTIC

NEUROPATHY

ANTERIOR ISCHEMIC OPTIC

NEUROPATHY

ARTERITICNoNARTERIT

IC

POSTERIOR ISCHEMIC

OPTIC NEUROPATHY

ARTERITIC NON-ARTERITIC

POST

OPRETIVE

ANTERIOR ISCHEMIC OPTIC NEUROPATHY Most common cause of acute optic neuropathy in over

50 yr of age

It is due to ischemia of anterior part of optic nerve head

Involvement of posterior ciliary artery circulation

Considered in d/d of sudden vision of loss

Visual field loss always present

CLINICAL CLASSIFICATION Depending upon underlying cause,AION is of two

type-

ARTERITIC

• Most serious type

• Mainly due to gaint cell arteritis

NON-ARTERITIC

• Most common

• Consist of all other cause than GCA

CHARACTERISTIC ARTERITIC NONARTERITIC

AGE Over 70 yrs 60-70 yrs

SEX Females no

PRECEDING SYSTEMIC FEATURES

Jaw claudication,headache,scalptenderness

no

PRECEDING OCULAR SYMPTOMS

Highly suggestive Rare

VISUAL LOSS Highly suggestive 20% cases

PAIN Common Rare

SECOND EYE INVOLVEMENT

75% within days or weeks 40% in mths or yrs

DISC APPEARANCE Chalky white swollen disc Sectoral or pallid

FFA Choroidal filling defect Normal

ESR Raised Normal

CRP Raised Normal

TEMPORAL ART BIOPSY

Positive Negative

RESPONSE TO STEROIDS

definite Nil

NON-ARTERITIC AION M.C. cause of acute optic neuropathy

Over the age of 50 yr

PATHOGENESIS-

occlusion of short posterior ciliary artery

decreased blood supply to optic nerve head

infarction of optic nerve head

RISK FACTOR-multifactorial

Noctural arterial hypotension play very imp role

HTN/DM

H’RGIC SHOCK

VASOSPASTIC DISORDER

THYROID DS

COLLEGEN VASCULAR

DS

CARDIAC DS

Absent cup

Raised iop

Prolong pressure

on eyeball

Small cupSYSTEMIC OCULAR

CLINICAL FEATURES-

Sudden painless monocular loss of VA

Visual field defect usually inferior altitudinal but can central,paracentric,arcuate

Dyschromatopsia

Diffuse or sectoral disc swelling(pallid edema)

OD of other eye is typically small or absent cup

Frequently associated with spinter haemorrages

It is very imp to distingushed Non-arteriticAION with optic neuritis due to similar picture

NAION OPTIC NEURITIS

AGE >50 <40

PAIN unsual +nt

PUPIL +RAPD +RAPD

VISUAL FIELD DEFECT altitudinal central

OPTIC DISC Edema,may be pale Edema,hyperemic

RETINAL HEMORRHAGE

common unusual

FA Delayed disc filling No delayed

MRI SCAN No ON enhancement ON enhancement

INVESTIGATION-

Routine investigation

Lipid profile

BP &Cardiac evaluation

ESR(rule out arteritic AION)

MRI

Fluorescein fundus angiography In early stage shows filling defect in optic disc,peripapillarychoroid or choroidal watershed area

TREATMENT-

no proven definitive treatment

some proposed t/t –aspirin

levodopa or carbidopa

hyperbaric o2

topical- brimonidine

SURGICAL TREATMENT-

• Transvitreal optic neurotomy-nasal margin of disc widen the scleral canal

• Vitrectomy-to reduse episcleral traction

ISCHEMIC OPTIC NEUROPATHY DECOMPRESSION TRIAL (IONDT)

it shows no effect of surgery on visual outcome.

PROGNOSIS-

Optic disc become atrophic within 4-8wks

Rate of recurrence - same eye6.4%

fellow eye 10%after 2yr

& 15% after 5yr

When second eye involved,optic atrophy in one eye

and edema in other gives PEUDO-FOSTER-KENNEDY SYNDROME.(in contrast true foster

kennedy syndrome ,secondary to intracranial mass)

ARTERITIC AION It mainly caused by giant cell arteritis

Other rare cause-SLE

polyarteritis nodusa

herpes zoster

Mostly in age>55 yr female

b/l AION should suggest temporal arteritis

GCA is systemic vasculitis affecting large and medium sized arteries (intenal elastic lamina)

Mostly affects-

temporal

posterior ciliary

ophthalmic

vertebral arteries

CLINICAL FEATURES-

SYSTEMIC OCULAR

new onset of headache in older

Scalp tenderness,jawclaudication

Fever, anorexia, wt.loss,malaise

Polymyalgiarheumatica(proximal Ms)

Sudden ,profound u/l visual loss

May accompainedwith pain

May preceded by transient visual obscuration and flashing light

diplopia

Signs-

Chalky white oedematous disc (over 1-2 month optic atrophy ensues)

Cotton wool spots(never in NAION)

CRAO,OAO

Ocular ischaemic syndrome

PION can occurs

INVESTIGATION-

CBC

Blood platelet may elevated

ESR(westergren more reliable to wintrobe )

usually >60mm/hr,but in 10%,normal

C-reactive pretein

gold standard Temporal artery biopsy

done under local anesthesia ,2-3cm specimen to avoid skip lesion

FLUORESCEIN FUNDUS ANGIOGRAPHY-

Delay retinal and choroidal filling defect

disc stain in late stage

TREATMENT-Aim to prevent blindness of the fellow eye

Steroids- treatment of choice

oral prednisolone i/v methylprednisolone(80-120mg/d) (1g/d,3days)

‘ both are same effective’response seen by ESR &CRP

Antiplatelet therapy Immunosuppressives

PROGNOSIS-

Only 4% eyes with visual loss improved

Early,adequate steroid therapy prevent visual loss in 96%

POSTERIOR ISCHEMIC OPTIC NEUROPATHY Uncommon

Caused by reterobulbar O.N. ischemia(supplied by pialarteries)

Diagnosed only after exclusion of other reterobulbaroptic neuropathy

SUBTYPES-

• Within hours to days

• Mainly spinal.cardiac bypass sxPERIOPERATIVE

• Associated with GCA

• Poor visual prognosisARTERITIC

• Same risk factor of NAION

• Not associated with crowed optic disc

NONARTERITIC

PATHOGENESIS-

PION

DECREASED OXYGEN

CARRYING CAPACITY

HYPOTENSION

LEADS TO DECREASED PERFUSION PRESSURE

INCREASED RESISTANCE TO BLOOD FLOW

CLINICAL FEATURES-

Sudden,painless u/l or b/l vision loss

RAPD

Absence of optic disc edema

o Optic atrophy ensues in 4-6wk

INVESTIGATION-

Routine investigation

ESR

CT/MRI

VEP-shows decreased amplitude

TREATMENT-

• There is no effective treatment

• Some treatment methods were attempted-

corection of hemodynamic derangements

systemic corticosteroids

antiplatelet therapy

measures to lower IOP