Year : 2012 | Volume
: 5 | Issue : 3 | Page : 141--143
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 and King Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia
Timothy J McCulley
The Wilmer Eye Institute, Johns Hopkins School of Medicine, 600 North Wolfe Street, Wilmer 110, Baltimore, MD 21287, USA
|How to cite this article:|
McCulley TJ. Ischemic optic neuropathy and cataract extraction: What do I need to know?.Oman J Ophthalmol 2012;5:141-143
|How to cite this URL:|
McCulley TJ. Ischemic optic neuropathy and cataract extraction: What do I need to know?. Oman J Ophthalmol [serial online] 2012 [cited 2022 Jan 29 ];5:141-143
Available from: https://www.ojoonline.org/text.asp?2012/5/3/141/106090
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. , 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.  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. 
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).  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.  Certain medications including amiodarone and sildenafil have been implicated in occurrences of NAION, although the exact nature of their role remains controversial. ,, 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.
In 1951, Towns and colleagues authored the first published report of an optic neuropathy following cataract extraction.  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. , 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.  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.  Moreover, the occurrence rate was found to be roughly one per 2000 surgical cases, significantly higher than expected to occur in the general population.  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 IOP. The causative link in the delayed-type is not so transparent. Likely the mechanism is a vasculopathy related to intraocular inflammation. Cystoid macular edema (CME) often follows 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. , 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).  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 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.
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