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15.6 Optic Disc Pallor (Atrophy)
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15.6.3.3 The Clinical Course ofNAION
On waking up in the morning, the patients usually complain of sudden painless vision loss from
one eye. The vision loss may progress over the
next several hours or even days. The visual acuity
may vary from 6/6 to 6/60.
On examination, they show RAPD in the
affected eye. The ONH is swollen and hyperemic.
It may also show linear haemorrhages. A small
optic disc with no cup is considered a ‘disc at risk’
(Fig.15.19). Since a swollen ONH in the affected
eye does not reveal the presence of a preexisting
cup, examination of the fellow eye may reveal a
disc at risk or even sectoral pallor from a previous
attack of the NAION.If the fellow eye shows a
normal cup, the possibility of an A-AION should
always be considered. More recent data suggest
that instead of crowding the axons in a smaller
optic disc, the cup’s smaller size is signicantly
associated with NAION [106]. On the confrontation eld (CF) testing, the affected eye shows an
altitudinal eld defect, most often in the lower
nasal quadrant or a central scotoma. Standard
automatic perimetry (SAP) should be done to
document the eld defect. On Goldmann perimetry in NAION, absolute inferior nasal quadrantic
defects were found in 22.4% versus 8% altitudinal
elds. The most common was a combination of
inferior altitudinal with an absolute defect in the
lower nasal quadrant (Fig.15.4) [107]. The absolute inferior nasal defect is due to the vulnerable
blood supply of the upper temporal aspect of the
optic disc. When looking for an altitudinal eld or
central defects, CF testing is 75–100% sensitive
Fig. 15.19 A swollen and hyperemic optic nerve head
(a). A small optic disc with no cup is considered a ‘disc at
risk’ for developing anterior ischemic optic neuropathy.
Three weeks later, the ODE resolved (b). Another case of
AION, with splinter peripapillary hemorrhages and ODE
(c). Three years later, there was optic atrophy (d)
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
and has >70% positive predictive value compared
to automated perimetry [108].
The MRI of the optic nerves is usually normal,
and diffusion restriction of the optic nerves can be
observed in a few if MRI is done very early in the
course. However, if the diagnosis of NAION is in
doubt, contrast-enhanced and fat-suppressed MRI
of the brain and orbit should be done to rule out
compressive optic neuropathy and inammatory
optic neuritis [109]. MRI Brain may show microangiopathic changes in addition to implicating
vascular involvement at other sites in the brain.
The ONH swelling may take several weeks for
resolution and leaves behind a sectoral pallor of
the optic disc [110]. In the natural course, signicant improvement in visual acuity may be seen in
up to 30% of eyes. Twenty per cent of eyes may
show progressive deterioration in visual acuity
over the next 3 months [111]. There is a 12–15%
risk of the fellow eye suffering from NAION in
the next 5 years. The same eye may show recurrence in 5% [109].
15.6.3.4 Treatment ofNAION
There is no denitive treatment for
NAION.Patients who present with poor vision,
have persistent ONH edema, any suspicion of
A-AION, or show progressive deterioration of
vision may be treated with oral corticosteroids.
Recognizing the underlying risk factors and minimizing those with appropriate interventions is
important [109].
In a large patient choice study, 70% of patients
with ≥20/70 visual acuity who received oral corticosteroids showed signicant improvement in
vision compared to 40% who did not. The visual
elds improved in 40% of the treatment group
versus 20% in the non-treated group [112].
Recognizing that NAION is a compartment
syndrome, an optic nerve decompression trial was
carried out, which showed that 31% in the careful
follow-up group and 29.4% in the optic nerve
decompression group improved visual acuity by
three lines. Moreover, 21.8% in the control group
versus 20% in the treatment group suffered from
signicant vision loss [111]. The trial was prematurely terminated on detecting that by 6 months of
follow-up, more patients lost vision due to intervention than careful follow-up [113]. Intravitreal
injections of anti-vascular endothelial growth factors or corticosteroids have been used, and although
they hasten the recovery of ONH edema, there is no
benecial effect on visual recovery [114].
15.6.4 Posterior Ischaemic Optic
Neuropathy (PION)
Posterior ischaemic optic neuropathy is uncommon and challenging to diagnose as it does not
have ONH edema or haemorrhages associated
with sudden painless vision loss and visual eld
loss. There are three types. The most common is
perioperative, and the less common are nonarteritic and arteritic. These patients mimic retrobulbar neuritis. It is important to rule out MS and
inltrative and compressive optic neuropathies
by contrast-enhanced MR studies. They have the
same risk factors as NAION except that they do
not have structural characteristics of the ONH, as
seen in NAION.It may not be easy to differentiate a posterior non-arteritic from an arteritic ischaemic optic neuropathy. In a study of 53 eyes of
42 patients with PION, 12 suffered from an arteritic PION due to giant cell arteritis [115]. In
elderly patients in the non-surgical setting who
present with bilateral PION with headache, it is
critical to rule out the arteritic type. ION in nonocular surgeries is extremely rare, and only 1
case per 125,000 was reported in non-cardiac
surgeries at the Mayo Clinic and 0.06% in coronary artery bypass surgeries [116].
On the other hand, ION is more frequent following cardiac surgeries than percutaneous cardiac interventions and spine surgeries [117].
Following spine surgeries, 0.028% developed
ION.Prone position during surgery is a risk factor
[118]. An advisory was issued by the American
Society of Anesthesiologists to rule out high-risk
patients for ION and to warn the patients of such
a complication (American Society of
Anesthesiologists Task Force on Perioperative
Visual Loss; North American NeuroOphthalmology Society; Society for Neuroscience
in Anesthesiology and Critical Care. Practice
Advisory for Perioperative Visual Loss Associated
with Spine Surgery 2019: An Updated Report by
the American Society of Anesthesiologists Task
15.6 Optic Disc Pallor (Atrophy)
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Force on Perioperative Visual Loss, the North
American Neuro- Ophthalmology Society, and the
Society for Neuroscience in Anesthesiology and
Critical Care, [119]).
15.6.5 Arteritic Anterior Ischaemic
Optic Neuropathy
Arteritic anterior ischaemic optic neuropathy
(A-AION) is a devastating complication of small
vessel vasculitis, most commonly giant cell arteritis (GCA). See Box 15.2 for the current diagnostic
Box 15.2 ACR and EULAR Classication of
Giant Cell Arteritis (2022)
Score Criteria
Absolute requirement -age>50years
Additional clinical criteria
2 Morning stiffness in shoulders
and neck
3 Sudden onset loss of vision
2 Jaw or tongue claudication
2 New temporal headache
2 Scalp tenderness
2 Temporal artery -tenderness,
cord-like appearance, or
decreased pulsation
Laboratory, imaging, and biopsy criteria
3 Max. ESR >50mm/h or max.
CRP >10mg/L
5 Positive temporal artery biopsy
or+halo sign on USG of
temporal artery
2 Bilateral axillary artery
involvement -stenosis on
angiography, increased uptake on
FDG-PET, or halo sign on USG.
A sum of scores of ≥6 is deemed+for GCA.
These criteria classify med-large vessel GCA
after excluding other pathologies.
Reproduced from under the Creative
Commons Attribution license (CC BY)
from Szekeres D, Al Othman B. Current
developments in the diagnosis and treatment of giant cell arteritis. Front Med
(Lausanne). 2022 Dec 13;9:1066503. doi:
10.3389/fmed.2022.1066503. PMID:
36582285; PMCID: PMC9792614.
criteria of GCA.Rarely ANCA-associated vasculitis (AAV) may cause A-AION and erroneously
point towards GCA because of temporal artery
involvement in AAV.The two must be differentiated, as the GCA is a granulomatous inammation involving small vessels. On the other hand,
AAV is a necrotizing vasculitis of small and
medium vessels, and the two have vastly different
courses and treatment strategies. Mononeuritis
multiplex and pauci-immune glomerulonephritis
in AAV will help differentiate the two.
A-AION accounts for about 10% of all ischaemic optic neuropathies. Other manifestations
in the eye include central retinal artery occlusion
and the occlusion of posterior ciliary arteries
leading to infarcts of the choroid [120]. Primarily
seen in older women of North European descent,
it causes a sudden painless loss of vision accompanied by headache, jaw claudication, and temporal tenderness. The patients may have a history
of low-grade fever, weight loss, myalgias, and
other constitutional symptoms. In diagnosing
GCA, limb and jaw claudication are more sensitive symptoms than temporal tenderness, temporal artery thickness, or loss of pulsations in the
temporal artery [121]. Patients may have symptoms only in the eye without any systemic
features in ~20% of the patients and are labelled
‘Occult giant cell arteritis’ [120]. The A-AION
has ethnic variations, with the highest incidence
reported from the south of Norway at 32.8 per
100,000 population versus 0.4 per 100,000
African Americans in a US county [122]. In the
Asian -Indian population, an earlier age of onset,
male predominance, and more frequent ocular
involvement were observed [123].
The presenting visual acuity is less than 6/60,
and nearly 20% may have no light perception.
A-AION is an Ophthalmic emergency, and a
quick diagnosis must be reached as the other eye
may get involved within days [124]. Urgent
C-reactive proteins and ESR should be ordered.
In an older person with A-AION, jaw claudication, C-reactive proteins >2.45 mg/dl, and
ESR>47mm/h are highly sensitive and specic
to reaching a diagnosis of GCA [125]. A temporal artery biopsy should be ordered to conrm the
diagnosis. On USG, the inamed artery shows a
hypoechoic ‘halo sign’ indicating the inamma-
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
Fig. 15.20 Photomicrograph of temporal artery biopsy
shows (a) granulomatous inammation of media of artery
with intimal brous luminal occlusion (a) EVG break of
internal and external elastic lamina (b). (H&E a, EVG- b.a
tory thickening of the temporal artery wall. USG
helps determine the biopsy site to avoid skip
areas of arteritis in the temporal artery
(Fig. 15.20). Skip areas in the temporal artery
biopsy of patients with proven GCA may occasionally show areas that lack either the giant
cells, epithelioid cells, or any inammatory cells)
[126]. Preferably, the USG and the biopsy should
be done before starting intravenous corticosteroids. Once the steroids are started, the wall
×10, b ×40original magnication). Images courtesy of
Prof Rithambra Nada, Professor of Pathology, Post
Graduate Institute of Medical Education and Research,
Chandigarh, India
fully performed confrontation eld testing can
provide a valuable clue to the nature of eld
defects. A sectoral defect or an island of vision is
encountered on visual eld examination. The
eld defects respect the horizontal meridian,
unlike the chiasmal syndromes that respect the
vertical meridian [128]. Compared to the
Goldmann perimeter, both HFA3 and the Octopus
900 kinetic perimeter with the target moving 5°
per second provide equivalent results [129].
thickness disappears within 2–3 days [127]. In
A-AION, the chances of a positive temporal
artery biopsy were nine times higher in the presence of jaw claudication, 3.4 times with neck
pain, two times higher with an ESR of
47–107mm/h, 3.2 times with C-reactive protein
>2.45 mg/dl, and two times higher with age
75years or higher [125].
On clinical examination, these patients show
RAPD, a chalky-white optic disc, and may show
an area of retinal opacication due to a cilioretinal or a branch artery occlusion. More than
50% of the eyes show either a counting nger
vision or no light perception. Although the visual
eld examination is critical in diagnosing ischaemic optic neuropathy, in A-AION, because of
poor visual acuity, it may not be possible to carry
out a visual eld examination on a Goldmann or
Humphrey’s visual eld analyzer (HFA). A care-
15.6.5.1 Treatment ofA-AION
Time is of the essence in initiating treatment in
A-AION primarily to prevent involvement of the
other eye. A-AION must be suspected in elderly
patients with profound vision loss with a temporal headache. GCA is highly sensitive to corticosteroids and shows a response with improved
temporal headache, tenderness, jaw claudication,
and myalgia. The treatment is initiated with intravenous methylprednisolone 1–2 g/day for
2–3 days, followed by oral prednisolone at
1–2mg/kg/day.
Visual function in A-AION may improve in
4% and worsen in 4% of eyes [130, 131].
To minimize the side effects of high corticosteroids, steroid-sparing disease-modifying antirheumatic drugs such as methotrexate have been
used. More recently, recurrences are often seen
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on tapering of steroids. A controlled recently
reported sustained remission with every week or
every other week treatment with tocilizumab
with a 6-month course of corticosteroids [132].
C-reactive proteins and ESR are the two most
sensitive parameters for patients with GCA
[131]. In large series of patients with A-AION,
they could achieve remission with normal ESR
and C-reactive proteins without corticosteroids
only in 7% of patients. GCA ares may cause
permanent visual loss, cerebral ischaemia, or
aortic aneurysms [133]. Methotrexate and tocilizumab are the only two FDA-approved therapies, although several drugs are currently under
trial [133].
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