ISCHEMIC OPTIC NEUROPATHY

ISCHEMIC OPTIC NEUROPATHYBY-DR.. DIVYA PATELUPGRADED DEPARTMENT OF OPHTHALMOLOGYMGM MEDICAL COLLEGE AND MYH, INDORE(M.P.)

BLOOD SUPPLY OF OPTIC NERVE HEAD

2ISCHEMIC OPTIC NEUROPATHYIt is circulatory insufficiency to optic nerve headANTERIOR ISCHEMIC OPTIC NEUROPATHYMost common cause of acute optic neuropathy in over 50 yr of ageIt is due to ischemia of anterior part of optic nerve headInvolvement of posterior ciliary artery circulationConsidered in d/d of sudden vision of lossVisual field loss always present

4CLINICAL CLASSIFICATIONDepending upon underlying cause,AION is of two type-

5CHARACTERISTIC ARTERITIC NONARTERITICAGEOver 70 yrs60-70 yrsSEXFemalesnoPRECEDING SYSTEMIC FEATURESJaw claudication,headache,scalp tendernessnoPRECEDING OCULAR SYMPTOMSHighly suggestiveRareVISUAL LOSSHighly suggestive20% casesPAINCommonRareSECOND EYE INVOLVEMENT75% within days or weeks40% in mths or yrsDISC APPEARANCEChalky white swollen discSectoral or pallidFFAChoroidal filling defectNormalESRRaisedNormalCRPRaisedNormalTEMPORAL ART BIOPSYPositiveNegativeRESPONSE TO STEROIDSdefiniteNil6NON-ARTERITIC AIONM.C. cause of acute optic neuropathyOver the age of 50 yr

7PATHOGENESIS- occlusion of short posterior ciliary artery decreased blood supply to optic nerve head infarction of optic nerve head8RISK FACTOR-multifactorial

Noctural arterial hypotension play very imp role

SYSTEMICOCULAR9CLINICAL FEATURES-Sudden painless monocular loss of VAVisual field defect usually inferior altitudinal but can central,paracentric,arcuateDyschromatopsiaDiffuse or sectoral disc swelling(pallid edema) OD of other eye is typically small or absent cupFrequently associated with spinter haemorrages

10It is very imp to distingushed Non-arteriticAION with optic neuritis due to similar picture

NAIONOPTIC NEURITISAGE>5055 yr femaleb/l AION should suggest temporal arteritis17GCA is systemic vasculitis affecting large and medium sized arteries (intenal elastic lamina)

Mostly affects- temporalposterior ciliaryophthalmicvertebral arteries

18CLINICAL FEATURES-SYSTEMIC OCULAR new onset of headache in olderScalp tenderness,jaw claudicationFever, anorexia, wt.loss,malaisePolymyalgia rheumatica(proximal Ms)

Sudden ,profound u/l visual lossMay accompained with painMay preceded by transient visual obscuration and flashing lightdiplopia

19Signs-Chalky white oedematous disc (over 1-2 month optic atrophy ensues)Cotton wool spots(never in NAION)CRAO,OAOOcular ischaemic syndromePION can occurs

20INVESTIGATION-CBCBlood platelet may elevatedESR(westergren more reliable to wintrobe ) usually >60mm/hr,but in 10%,normalC-reactive pretein gold standard Temporal artery biopsy done under local anesthesia ,2-3cm specimen to avoid skip lesion21FLUORESCEIN FUNDUS ANGIOGRAPHY- Delay retinal and choroidal filling defect disc stain in late stage

22TREATMENT- Aim to prevent blindness of the fellow eyeSteroids- treatment of choice oral prednisolone i/v methylprednisolone (80-120mg/d) (1g/d,3days) both are same effective response seen by ESR &CRP Antiplatelet therapyImmunosuppressives

23PROGNOSIS-Only 4% eyes with visual loss improved

Early,adequate steroid therapy prevent visual loss in 96%24CHARACTERISTIC ARTERITIC NONARTERITICAGEOver 70 yrs60-70 yrsSEXFemalesnoPRECEDING SYSTEMIC FEATURESJaw claudication,headache,scalp tendernessnoPRECEDING OCULAR SYMPTOMSHighly suggestiveRareVISUAL LOSSHighly suggestive20% casesPAINCommonRareSECOND EYE INVOLVEMENT75% within days or weeks40% in mths or yrsDISC APPEARANCEChalky white swollen discSectoral or pallidFFAChoroidal filling defectNormalESRRaisedNormalCRPRaisedNormalTEMPORAL ART BIOPSYPositiveNegativeRESPONSE TO STEROIDSdefiniteNil25POSTERIOR ISCHEMIC OPTIC NEUROPATHYUncommonCaused by reterobulbar O.N. ischemia(supplied by pial arteries)Diagnosed only after exclusion of other reterobulbar optic neuropathy

26SUBTYPES-

27PATHOGENESIS-

28CLINICAL FEATURES-Sudden,painless u/l or b/l vision lossRAPDAbsence of optic disc edema

Optic atrophy ensues in 4-6wk29INVESTIGATION-Routine investigationESRCT/MRIVEP-shows decreased amplitude

TREATMENT-There is no effective treatmentSome treatment methods were attempted- corection of hemodynamic derangements systemic corticosteroids antiplatelet therapy measures to lower IOP31