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INTRODUCTION-ION
• Ischemic Optic Neuropathy- Acute ischemia of the optic nerve
• Common Optic Neuropathy in elderly.
• ~Age of 55 to 77years old.

Acute ischemia Acute ischemia

of the anterior of the posterior
part of the optic part of the optic
nerve (ONH), nerve
which is
supplied mainly Giant cell arteritis
by the posterior
ciliary arteries.

Non-inflammatory cause
INTRODUCTION-ION
Symptoms:
• Acute vision loss one or both eyes
• Painless

Signs:
• VF loss
• RAPD +ve
• Swollen Optic Disc (AION) + flame
haemorhage
INTRODUCTION
•This is the most SERIOUS type of ION
•Primary cause of AAION is due to a disease
called giant cell arteritis(GCA) or temporal
arteritis.
• Giant cell arteritis is a systemic inflammatory
(vasculitis) condition that causes swelling of the
medium-sized and large arteries in the head.
• GCAtypically affects the superficial temporal
arteries.
•Other rare causes include other types of
vasculitis, e.g. , polyarteritis nodosa, systemic
lupus erythematosus, and herpeszoster
•Female, 60’s
PATHOGENE
• In the eye, GCA has a special predilection to involve the posterior ciliary artery,
SIS
resulting in its thrombotic occlusion, cause the development of AAION and visual
loss.
 (Hayreh, S.S. 1974)

PATHOGENESIS
Occlusion of the posterior ciliary artery results in
infarction of a segment or the entire optic nerve
head
Depending upon the area of the optic nerve head
supplied by the occluded posterior ciliary artery

Abbreviations: A = arachnoid; C = choroid; CRA = central retinal artery; Col. Br. = Collateral branches; CRV = central retinal vein; D = dura; LC = lamina
cribrosa; NFL = surface nerve fiber layer of the disc; OD = optic disc; ON = optic nerve; P = pia; PCA = posterior ciliary artery; PR / PLR = prelaminar
region; R = retina; RA = retinal arteriole; S = sclera; SAS = subarachnoid space.
RISKFACTOR
1. Age: Fifty years of age or older at onset.
2. Gender : 3 times more common in women than
in men
3. Race: Common among Caucasians > other races
4. Giant cell arteritis
5. New onset of localized headache.
6. Temporal artery pulse.
7. Elevated ESR.
8. Positive temporal arterybiopsy.
CLINICAL FEATURES(Ocular)
CLINICAL FEATURES:
Pale and swollen opticdisc

Pale optic disc edema with adjacent Chalky white pale,swollen and
retina infarcted hyperemic optic disc
CLINICAL FEATURES -Optic Disc

Fundus photographs of right eye

with A-AION:
(A)Before developing A-AION
(B)One week after developing A-
AION with chalky white optic disc
edema and
(C)4 months later showing optic
disc cupping with a cup/disc ratio
of 0.8 (note no cup in A)

Hayreh SS (2009) Ischemic optic neuropathy.

Progress in retinal and eye research 28: 34-62
CLINICAL FEATURES:
Visual field defect (Altitudinal & inferiorly)
PRESENTATION (Physical)
WORK UP :AAION
• The diagnostic work-up for GCAincludes

1. Erythrocyte sedimentation rate(ESR) >47mm

2. C-reactive protein >2.45MG/DL
3. Fluorescein fundus angiographic (FFA): Critical
diagnostic test for A-AION during the early stages
  shows thrombosis and occlusion of the posterior
ciliary artery inGCA
4. JawClaudication
5. Neck pain

(Kanski, 2003 & Hayreh, 2011)

WORK UP: FFAfinding

Fundus photograph (A) and fluorescein fundus angiogram (B) of right eye with A-AION and
cilioretinal artery occlusion during the initial stages. (A) Fundus photograph shows chalky white
optic disc edema with retinal infarct in the distribution of occluded cilioretinal artery. (B)
Fluorescein fundus angiogram shows evidence of occlusion of the medial posterior ciliary artery
and no filling of the cilioretinal artery.
Hayreh SS (2009) Ischemic optic neuropathy.
Progress in retinal and eye research 28: 34-62
TREATMENT & PROGNOSIS
• AAION is EMERGENCY case. Early treatmentis essential.
• Aim of treatment: To prevent blindness of the fellow eye.
• Treatment: (steroidtherapy)
• High dose systemic corticosteroid (IV methylprednisolone & oralprednisolone) for
several months.
• Temporal artery biopsy- within 3days of treatment

• Duration of treatment: ~1 to 2 years

• Prognosis-POOR
• Visual loss is usuallypermanent.
• Visual recovery of the affected eye that has treatment is poor with a 15-34%
improvement rate.
PATHOGENESIS
Partial OR total
infarction of the
optic nervehead
caused by
occlusion of the
short posterior
ciliary arteries.
PREDISPOSITION
1. Structural crowding of the ONH
2. Hypertension
3. Diabetes Mellitus
4. Hypercholesterolemia
5. Sudden Hypotensive event
6. Sleep ApnoeaSyndrome
7. Administration of sildenafil
PRESENTATION
1. Sudden onset
2. Painless VISUAL LOSS
3. Monocular
4. Always discovered onawakening
5. Nocturnal Hypotension
SIGNS
PARAMETER FINDING
Visual Acuity Often better than 20/100.
Visual Field Typically Inferior Altitudinaldefect.
ColourVision May be severely impaired when VAis good.
Ophthalmic ExamFindings Diffuse OR sectorialhyperaemic disc swelling
associated with FEW peripapillary splinter-
shaped haemorrhages.
Small ORcupless disc in fellow eye.
Swelling gradually resolves and pallor in 3-6
weeks after onset.
FAFinding Acute Stage: localizeddisc hyperfluorescence,
intense, eventually involves entire disc.
Laboratory Evaluation No associated laboratoryabnormalities.
TREATMENT
• No definitive treatment.
• Aspirin is effective in reducing systemic vascular events.
• But does not reduce risk of involvement of the fellow eye.
PROGNOSIS
Condition Prognosis
No further loss of vision Very smallpercentage
Recurrences in the same eye ~6%
Involvement of the FELLOW eye ~10% after 2years
~15% after 5years
2 Important Factors caused Poor VA in 1st eye
involvement of FELLOW eye
DM
Signs of FELLOW eye involvement 1 eye optic atrophy
(Pseudo-Foster Kennedy Syndrome) Another eye discedema
DIFFERENTIATION :
AAION FROMNAAION
1. Systemic symptoms GCA: Patients with NA-AION have no systemic symptoms of giant
cell arteritis.
2. Visual symptoms: Amaurosis fugax is highly suggestive of AAION and is extremely rare
in NA-AION.
3. Hematologic abnormalities:Elevated ESRand CRP,particularly CRP,is helpful in the
diagnosis of GCA. Patients with NA-AION do not show any of these abnormalities.
4. Early massive visual loss: Extremely suggestive of A-AION.
5. Chalky white optic disc edema: This is almost diagnostic of A-AION and is seen in 69%
of AAION eyes. In NAAION, chalky white optic disc edema occurs only very rarely with
embolic occlusion of the posterior ciliary artery.
6. AAION associated with cilioretinal artery occlusion . This is almost diagnostic of
AAION.
7. Fluorescein fundus angiography: Evidence ofposterior ciliary artery occlusion in
AAION.
8. Temporal artery biopsy.
OPTOMETRIC MANAGEMENT:
AION & AAION

•Provides low vision aids for distance and near.

• For example: Magnifier, telescopeetc.
•Explain on monocular cues.
•Advise patient to take care of remaining good eye.
THANKYOU