Editorial Commentary

Ischemic optic neuropathy and cataract extraction:

What do I need to know?
Timothy J McCulley
The Wilmer Eye Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA
King Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia

Anterior ischemic optic neuropathy (AION) is the most common
optic neuropathy in adults, reported with an estimated annual
incidence in individuals aged 50 years or older of 2.3 to 10.3
per 100,000.[1,2] AION is thought to result from microvascular
hypoperfusion, with a number of recognized risk factors. These
include conditions leading to atherosclerotic disease, such as
hypertension, diabetes and smoking.[3] A “crowded nerve” with a
small cup to disk ratio probably contributes by compressing the
small caliber blood vessels supplying the optic nerve head and is
present in most patients with spontaneous AION.[3]
There is another category of related conditions. These are diseases
or events that may lead to AION in a subset of patients. The most
notorious of these is temporal or giant cell arteritis (GCA).[4] The
occurrence of arteritic AION is frequent enough that the term non-
arteritic AION (NAION) is commonly employed to distinguish
events occurring in patients without GCA. There is growing
evidence that in some cases chronic obstructive sleep apnea may
be contributory.[5] Certain medications including amiodarone
and sildenafil have been implicated in occurrences of NAION,
although the exact nature of their role remains controversial.[6-8]
Others conditions that may trigger NAION include hypotension,
blood loss and anemia. Similarly, and also likely related to
unfavorable hemodynamics, AION and posterior ischemic optic
neuropathy (PION) may be seen in patients undergoing major
surgery, most notably spinal surgery.
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In 1951, Towns and colleagues authored the first published
report of an optic neuropathy following cataract extraction.[9]
In review of 565 patients who underwent cataract extraction,
they identified four who developed optic neuropathies weeks to
months following cataract extraction. In the following years Reese
and Carrol (1958) and Carrol (1973) authored additional series
characterizing patients who developed NAION following cataract
extraction.[10,11] These along with a couple other isolated cases
describe patients with NAION after cataract extraction (and other
types of intraocular surgery), occurring after a period of good
vision, days to weeks following surgery. This has been termed
delayed-type cataract associated NAION.
In 1980 Heyreh described 13 patients who developed NAION
following cataract extraction.[12] His cohort differed from
previously published cases. Onset was within hours of surgery and
cases were “invariably” associated with perioperative elevations in
IOP. This “immediate-type” differs distinctly from “delayed-type”
cases, in that they occur in the peri-operative period and have a
readily identifiable cause, i.e. elevated IOP.
In the year 2003, eighteen patients who developed NAION
(mostly the delayed-type) within a year of cataract surgery were
identified at Bascom Palmer Eye Institute in Miami. Analysis of
the timing of onset relative to surgery argues that these were not
coincidental, but rather precipitated by surgery.[13] Moreover, the
occurrence rate was found to be roughly one per 2000 surgical
cases, significantly higher than expected to occur in the general
population.[14] These studies do not address mechanism; they do
strongly support the concept that NAION may be triggered by
intraocular surgery, even when onset is not in the immediate post-
operative period.

The mechanism in the immediate-type is indisputably elevated

DOI: IOP. The causative link in the delayed-type is not so transparent.
10.4103/0974-620X.106090
Likely the mechanism is a vasculopathy related to intraocular
inflammation. Cystoid macular edema (CME) often follows

Copyright:  2012 McCulley T J. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Correspondence:
Mr. Timothy J McCulley, The Wilmer Eye Institute, Johns Hopkins School of Medicine, 600 North Wolfe Street, Wilmer 110, Baltimore, MD 21287.
E-mail: tmccull5@jhmi.edu

Oman Journal of Ophthalmology, Vol. 5, No. 3, 2012 141

 McCulley: AION and cataract extraction
cataract extraction by weeks and even months and a mechanistic
link is not questioned. Leaking vessels are thought to develop
secondary to “mediators” released with surgically incited
inflammation. It follows that the vessels supplying the optic nerve
might also be affected by mediators released following surgery.
Optic disk vasculature leakage and subsequent swelling related to
surgery may lead to NAION in a subgroup of patients, specifically
those who already have tenuous blood flow to the optic nerve
head. Optic nerve edema without associated infarction has been
reported weeks to months following cataract extraction.[15,16]
Interstitial fluid in the optic nerve head may compress small
caliber blood vessels leading to NAION.
The hypothesis of inflammatory mediator related vasculopathy
and ensuing edema leading to NAION would dictate that one’s
risk increases proportional to the degree of incited inflammation.
Existing data is in concordance with this theory. At the time
of the initial publication by Towns and associates, cataract
surgery was being performed using large scleral incisions with
extra capsular or intra capsular techniques. The amount of
inflammation associated with such surgeries would be expected
to be much greater than that associated with small incision
surgery (i.e. phacoemulsification). In fact, three of the four
patients described by Towns and colleagues were noted to
have intraocular inflammation at the time the optic neuropathy
developed. The occurrence rate in Towns and colleagues cohort
was roughly 1 per 150 cases (4 occurrences out of 565 surgeries).
The rate was much lower; roughly 1 per 2000 cases (3 occurrences
out of 5787 cases) in the cohort assessed at Bascom Palmer,
where more modern cataract surgery techniques were utilized.
Moreover, it was noted that a number of patients in the Bascom
Palmer cohort had complicated surgeries, consistent with a link
between inflammation and delayed-type post-cataract NAION. As
our surgical techniques gain sophistication, complication rates
decrease and trauma sustained by the eye diminishes. With less
inflammation incited, we may see a further decline in the number
of cases of surgically related NAION.
Patients with a history of NAION in the fellow eye are at
increased risk of developing optic disk ischemia following
intraocular surgery. In an assessment of patients undergoing
cataract extraction, Lam and colleagues found, in patients with
a history of NAION, cataract extraction increased the risk of
NAION occurrence in the fellow eye by 3.6 times (Cox regression,
p = 0.001).[17] Stated more tangibly, 9 of 17 (53%) NAION patients
who underwent cataract extraction in the fellow eye developed
NAION after cataract extraction. Unfortunately, without a history
of NAION, we are unable to predict whois apt to develop NAION
following intraocular surgery.
When approached by physicians and patients, my advice is as
follows. If there is no history of NAION, I stress that there is only
a very small chance of developing NAION and recommend no
precautions, beyond that appropriate for any patient undergoing
intraocular surgery. In patients with a history of NAION (with or
without cataract extraction) the chance of precipitating NAION
142
is high, possibly as great as 50%. In these cases I recommend the
following precautions. 1) Avoid surgery if possible. Wait until
cataract related visual decline reaches the point where quality of
life is significantly impacted, and the benefit of surgery arguably
outweighs the risk of causing NAION. 2) Take measures to
ensure an IOP spike does not occur. Peri-operative medications
may be helpful. Diligent clearing of viscoelastics from the anterior
chamber is of course essentialto avoid dangerously high post-
operative IOP elevations. Beyond these two generalizations, I
leave the specifics (e.g. which medication is most effective) to
the discretion of the surgeon. 3) Avoid breaching the posterior
capsule. Post-operative inflammation and its effect on the
posterior pole vasculature, likely play a role in the development
of delayed post-operative NAION. Just as CME is less likely with
an intact posterior capsule, post-operative NAION is probably less
likely. Potential protective steps might include avoiding surgery
by first year residents in patients with a history of NAION. 4) If
appropriate use a clear corneal incision. It has been shown that
fewer inflammatory mediators are liberated with a clear cornea
incision relative to a scleral tunnel. This in turn may decrease
the effect such mediators have on posterior pole vasculature and
hence reduce the risk of NAION.
In conclusion, NAION should be considered a potential
complication of intraocular surgery, most notably cataract
extraction where it occurs in roughly one out of 2000 cases.
There are two distinct categories of intraocular surgery associated
NAION. 1) The immediate-type, which occurs within hours to
days after surgery, and is invariably associated with elevations in
IOP. 2) The delayed-type, which occurs weeks to months after
surgery following a period of good vision, and likely results from
an inflammatory mediated vascular effect on the posterior pole
and optic disk. Patients with a history of NAION in the fellow
eye are at increased risk, possibly up to 50%. In such patients, the
following precautions are advisable: 1) avoid surgery if possible, 2)
control IOP, 3) maintain the posterior capsule, and 4) consider
using a clear corneal incision.
References
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2. Hattenhauer MG, Leavitt JA, Hodge DO, Grill R, Gray DT. Incidence
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