ISCHEMIC OPTIC NEUROPATHY

1. BY-DR.. DIVYA PATEL
UPGRADED DEPARTMENT OF OPHTHALMOLOGY
MGM MEDICAL COLLEGE AND MYH, INDORE(M.P.)

2. BLOOD SUPPLY OF OPTIC NERVE
HEAD

3. ISCHEMIC OPTIC NEUROPATHY
 It is circulatory insufficiency to optic nerve head
ISCHEMIC
OPTIC
NEUROPATHY
ANTERIOR
ISCHEMIC OPTIC
NEUROPATHY
ARTERITIC
NoNARTERIT
IC
POSTERIOR
ISCHEMIC
OPTIC
NEUROPATHY
ARTERITIC NON-ARTERITIC
POST
OPRETIVE

4. 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

5. 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

6. CHARACTERISTIC ARTERITIC NONARTERITIC
AGE Over 70 yrs 60-70 yrs
SEX Females no
PRECEDING SYSTEMIC
Jaw claudication,headache,scalp
no
FEATURES
tenderness
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
Positive Negative
BIOPSY
RESPONSE TO
STEROIDS
definite Nil

7. NON-ARTERITIC AION
 M.C. cause of acute optic neuropathy
 Over the age of 50 yr

8. PATHOGENESIS-occlusion
of short posterior ciliary artery
decreased blood supply to optic nerve head
infarction of optic nerve head

9. RISK FACTOR-multifactorial
HTN/DM
H’RGIC
SHOCK
VASOSPASTIC
DISORDER
THYROID DS
CARDIAC
DS
COLLEGEN
VASCULAR
DS
Absent
cup
Noctural arterial hypotension play very imp role
Raised
iop
Prolong
pressure
on eyeball
Small
SYSTEMIC cup OCULAR

10. 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

11.  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

12. INVESTIGATION-
 Routine investigation
 Lipid profile
 BP &Cardiac evaluation
 ESR(rule out arteritic AION)
 MRI

13. Fluorescein fundus angiography
In early stage shows filling defect in optic disc,peripapillary
choroid or choroidal watershed area

14. TREATMENT-no
proven definitive treatment
some proposed t/t –aspirin
levodopa or carbidopa
hyperbaric o2
topical- brimonidine

15. 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.

16. 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)

17. 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

18.  GCA is systemic vasculitis affecting large and medium
sized arteries (intenal elastic lamina)
Mostly affects-
 temporal
 posterior ciliary
 ophthalmic
 vertebral arteries

19. CLINICAL FEATURES-SYSTEMIC
OCULAR
 new onset of
headache in older
 Scalp
tenderness,jaw
claudication
 Fever, anorexia,
wt.loss,malaise
 Polymyalgia
rheumatica(proxim
al Ms)
 Sudden ,profound
u/l visual loss
 May accompained
with pain
 May preceded by
transient visual
obscuration and
flashing light
 diplopia

20. 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

21. 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

22.  FLUORESCEIN FUNDUS ANGIOGRAPHY-Delay
retinal and choroidal filling defect
disc stain in late stage

23. 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

24. PROGNOSIS-
 Only 4% eyes with visual loss improved
 Early,adequate steroid therapy prevent visual loss in
96%

25. POSTERIOR ISCHEMIC OPTIC
NEUROPATHY
 Uncommon
 Caused by reterobulbar O.N. ischemia(supplied by pial
arteries)
 Diagnosed only after exclusion of other reterobulbar
optic neuropathy

26. SUBTYPES-
• Within hours to days
• Mainly spinal.cardiac bypass sx
PERIOPERATIVE
• Associated with GCA
ARTERITIC • Poor visual prognosis
• Same risk factor of NAION
• Not associated with crowed optic
disc
NONARTERITIC

27.  PATHOGENESIS-PION
DECREASED
OXYGEN
CARRYING
CAPACITY
HYPOTENSION
LEADS TO
DECREASED
PERFUSION
PRESSURE
INCREASED
RESISTANCE TO
BLOOD FLOW

28. CLINICAL FEATURES-
 Sudden,painless u/l or b/l vision loss
 RAPD
 Absence of optic disc edema
o Optic atrophy ensues in 4-6wk

29. INVESTIGATION-
 Routine investigation
 ESR
 CT/MRI
 VEP-shows decreased amplitude

30. TREATMENT-
• There is no effective treatment
• Some treatment methods were attempted-corection
of hemodynamic derangements
systemic corticosteroids
antiplatelet therapy
measures to lower IOP