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Is Cataract Surgery a Risk for Developing Nonarteritic Anterior Ischemic Optic Neuropathy?

McCulley, Timothy J. MD; Miller, Neil R. MD

Editor(s): Lee, Andrew G. MD; Van Stavern, Gregory P. MD

Author Information
Journal of Neuro-Ophthalmology: March 2021 - Volume 41 - Issue 1 - p 119-125
doi: 10.1097/WNO.0000000000001109
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Cataract surgery is the most frequently performed ophthalmic surgery and has become safer and more efficient over the past 40 years. There are multiple reports of nonarteritic anterior ischemic optic neuropathy (NAION) associated with cataract extraction, but it remains unclear whether this relationship is coincidental or causal. Two experts debate this topic.

Pro: Timothy J. McCulley, MD

Ischemic optic neuropathies are traditionally categorized in several groups, with NAION representing any variety so long as not related to giant cell arteritis. There are numerous recognized risk factors for NAION, such as factors leading to atherosclerosis, including smoking, hypertension, diabetes, and hyperlipidemia. NAION usually occurs in patients with a structural risk factor, the small or “crowded” optic disc. Other factors such as medications, sleep apnea, and hemodynamic instability may contribute to the development of NAION. Although many intraocular procedures have been reported to trigger NAION, most focus has been on cataract extraction (1–16). Most likely this bias toward cataract extraction is reflective of the large numbers of this type of surgery being performed and is not specific to the procedure.

Two types of cataract extraction associated NAION have been reported; immediate type, cases that occurred within hours or days after surgery, and delayed type, cases that occurred weeks to months after surgery and after a period of good vision (1). The immediate type is almost invariably associated with marked elevation in intraocular pressure (IOP) (2). The delayed type occurs days to months after surgery. The mechanism is likely vascular compression from posterior pole edema (16). Leakage from the optic disc vasculature occurs after intraocular surgery, often but not always in association with cystoid macular edema (CME), and has been documented to precede NAION (17–19). Posterior pole edema involving the optic disc likely leads to vascular compression within the optic disc. This is consistent with the observation that many cases of postsurgical NAION followed surgery that was complicated by posterior capsular tear or CME, where optic disc edema is more apt to develop (3). Although the mechanism of delayed type is unconfirmed, there is an overabundance of evidence in support of a causal relationship between intraocular surgery and NAION. It can be broken down into several categories as follows: anecdotal observations, case-controlled comparisons, temporal analysis, and population-based studies. Each is summarized.

There is an evergrowing wealth of observation-based reports of the association between intraocular surgery and NAION. As far back as 1951, Townes et al described a series of patients who developed an optic neuropathy after cataract extraction (4). In one review of 565 patients who underwent cataract extraction, 4 patients developed optic neuropathies in weeks to months after cataract extraction. Reese and Carrol (1958) and Carrol (1973) authored large case series characterizing patients who developed NAION after cataract extraction (5,6).

In 1980, Hayreh published an important observation (2). He described 13 patients who developed NAION after 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” case differs distinctly from “delayed-type” cases, in that they occur in the perioperative period and have a readily identifiable cause, that is, elevated IOP.

In 2003, McCulley et al identified 18 patients who developed NAION within a year of cataract surgery at the Bascom Palmer Eye Institute (BPEI) in Miami (3). These included patients with the immediate-type and delayed-type postsurgical NAION. As expected, those with the immediate type had elevations in IOP. Patients with the delayed type had a high rate of complication, posterior capsular tear, and CME, consistent with the proposed mechanism of posterior pole edema related to postsurgical inflammation. Subsequently, there have been many smaller series describing NAION after intraocular surgery (7–11,20).

Case-control studies have compared patient groups with postsurgical NAION to those with spontaneous NAION, with the presumption that a lack of difference would suggest that ischemic events occurring after surgery were coincidental. Conversely, identifying and defining differences would shed light on the role cataract surgery plays. One study found distinct differences between groups; the prevalence of hypertension (29% vs. 68%, P = 0.017) and cup-to-disc ratio ≤0.2 in the involved (60% vs. 94%, P = 0.007) and uninvolved eyes (63% vs. 89%, P = 0.052) was lower in patients with postoperative NAION than those with spontaneous NAION (3). Similar findings were found by the group lead by Neil Miller (21). In their cohort, there were fewer current smokers, fewer patient with hyperlipidemia, and fewer patients with multiple NAION risk factors in the postsurgical NAION than spontaneous NAION group. The relative lack of risk factors, originally reported by McCulley et al and supported by Miller, is consistent with surgery being a causative contributor (3,21).

Another noteworthy finding drawn from the data reported by McCulley et al (3) is that within the group of patients with postoperative NAION 33% had a history of NAION in the contralateral eye. This suggests that a history of NAION in the fellow eye may identify patients at an increased risk of postoperative NAION.

Given the rarity of optic nerve ischemic events after intraocular surgery, a prospective randomized trial is challenging and arguably infeasible. A temporal analysis is a more pragmatic approach. If cases occurring after cataract extraction were by coincidence, a uniform distribution over time would be expected. In 2003, McCulley et al (1) assessed the timing of NAION after cataract extraction. All cases occurred within 6 months of surgery (mean interval, 35 days; range, 1–130 days), which is significantly different from a uniform distribution (P < 0.001). Similarly, in a series of more than 100 cases of postsurgical NAION performed in Canada, most occurrences were within the first 21 days of surgery, which is vastly different from a uniform distribution (P < 0.001) (13). Another study however failed to identify a temporal association (21), but because of the small size and low power of the study, its data are insufficient to exclude a temporal association (22). Taken together, these analyses strongly argue that optic nerve infarction after cataract surgery is not coincidental but rather precipitated by surgery.

Another temporal association is that of patients with bilateral postsurgical NAION. A number of patients have had the misfortune of suffering an ischemic event after sequential surgery in both eyes (3,6,9,10,13,15). Often, the time between surgery and NAION was similar. For example, one such patient described by McCulley et al had onsets on postoperative day 10 and 14 (3). Recently, Bénard-Séguin et al (10) reported (2019) a patient who underwent sequential cataract extraction and developed NAION in both eyes, 3 and 5 weeks postoperatively. In the case series by Ing et al, 4 patients were identified who suffered NAION in both eyes after cataract extraction (13).

A number of population-based assessments have also concluded that intraocular surgery increases the risk of NAION. The occurrence of NAION after lens-related surgery was assessed in a large population at BPEI (15). During a 5-year period, between January 1, 1993, and December 31, 1997, a total of 5,787 cataract extraction cases were performed. Within that group, 3 patients developed NAION within 1 year of the procedure. They occurred postoperatively on days 29, 36, and 117, giving an estimated six-month incidence of 51.8 per 100,000 and six-week incidence of 34.6 per 100,000. This is statistically higher than the previously reported overall incidence of NAION (23,24). In 2017, Al-Madani et al (12) compared groups of patients who did and did not undergo cataract extraction. They reported a significantly higher incidence of ischemic optic neuropathy in the surgical group, similarly concluding, “phacoemulsification is a risk factor for NAION, independent of the presence of medical risk factors.” A recent very large study, using the Korean National Health Insurance Service database, similarly identified cataract extraction as a risk factor for NAION, in their study population of 1,025,340 beneficiaries (16). Although adjusting for other risk factors and comorbidities, patients undergoing cataract extraction had an increased risk of developing NAION compared with the nonsurgical group, hazard ratio 1.80. These studies do not address a mechanism; however, they do strongly support the concept that NAION may be triggered by intraocular surgery, even when onset is not in the immediate postoperative period.

One population-based study failed to demonstrate an increased NAION occurrence rate in patients undergoing cataract extraction (21). These data were based on cases that were identified by searching the medical record database using a single diagnostic code for NAION. This method likely resulted in an underestimation of the true occurrence rate (22). In contradiction to this, the same study found differences in other risk factors between patients with spontaneous and postsurgical NAION, which does suggest that cataract surgery adds to the risk of developing NAION in their patient population.

The risk of postsurgical NAION is likely decreasing as our surgical techniques evolve. In the 1950s, the occurrence rate in Townes et al cohort was roughly 1 per 150 cases (4 occurrences of the 565 surgeries) (4). At that time, cataract surgery was performed using large scleral incisions with extracapsular or intracapsular techniques. The amount of inflammation associated with such surgeries is much greater than that associated with small incision surgery. In the 1990s, after the advent of phacoemulsification, the estimate occurrence rate was lower, roughly 1 per 2000 cases (3 occurrences of the 5,787 cases) (15). More recently (2020), the occurrence rate was estimated to be less than 1 in 10,000 cases (13). 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 surgery-related NAION.

Although the overall incidence of postsurgical NAION may be very low, the danger in downplaying the risk of postsurgical NAION lies in the more tangible risk for patients with a history of NAION in the fellow eye. Patients with a history of NAION in the fellow eye are likely at an increased risk of postsurgical NAION. Reese and Carroll described this in the 1950s (5,6). Combining patients from their 2 series, 8 of 17 patients with a history of NAION after cataract extraction developed NAION after cataract extraction in the second eye. In the series of postoperative NAION assessed by McCulley et al (3), a total of 6 (33%) of 18 cases occurred in patients who had a history of NAION in the contralateral eye. Also included in this cohort were 2 subjects who underwent a second cataract extraction in the fellow eye. One developed NAION after both surgeries. In 2007, Lam et al assessed cataract extraction as a risk factor for NAION in patients with a history of NAION in the fellow eye (14). They found that cataract extraction increased the risk of NAION occurrence by 3.6 times (Cox regression, P = 0.001).

In closing, the evidence overwhelmingly supports the observation that intraocular surgery may cause NAION. The risk is likely decreasing as surgical techniques improve. However, until cataract and other intraocular surgery can be performed without any chance of elevation in IOP or postoperative inflammation, some risk will remain. The hazard in underestimating the risk of NAION associated with cataract surgery lies in second eye involvement. It has been estimated that upward of 50% of patients, with a history of NAION, may develop NAION in the fellow eye after cataract extraction (14). In patients with a history of NAION in the fellow eye, prudence is warranted. Considerations include delaying surgery if not essential and judicial control of IOP and postoperative inflammation.

Con: Neil R. Miller, MD

Cataract surgery is one of the most common and safe procedures performed throughout the world. Nevertheless, rare complications occur, including hemorrhage, infection, and retinal detachment, all of which can cause severe and permanent visual loss (8). In addition to these potential causes of visual loss, an optic neuropathy resembling NAION has been documented to occur after apparently uncomplicated cataract surgery (2,8,25–28), resulting in devastating visual morbidity. In some cases of postcataract surgery optic neuropathy (PCSON), visual loss is present immediately after surgery (the immediate form) (7,8), whereas in others, symptoms develop several days, weeks, or months postoperatively (the delayed form) (1,3–5,7,8,15,20). Some authors have suggested that increased IOP, raised intraorbital pressure from a retrobulbar or peribulbar anesthetic, systemic perioperative hypotension, or a combination of these factors might be responsible for the immediate form (1,2,6,15,29), whereas the causative factors for the delayed form were unclear, although intraocular surgery–related posterior pole edema, resulting in vascular compression of the optic nerve, were proposed (3,30).

Most of the initial studies of PCSON included small numbers of patients and there was, for many years, no acceptance of this concept; however, McCulley et al (15) evaluated the incidence of PCSON among 5,787 patients who underwent noncomplex cataract surgery between 1993 and 1997 and identified 3 patients who experienced an acute anterior optic neuropathy within 1 year of the surgery, with an estimated 6-week incidence of 34.6 in 100,000 and a 6-month incidence of 51.8 in 100,000 (95% confidence interval [CI], 10.7–151). These rates were significantly higher than the previously reported incidence of NAION, estimated to be 2.3–10.2 per 100,000 in the general population of people 50 years and older (14,23). The authors thus concluded that cataract surgery was indeed associated with an increased incidence of an acute anterior optic neuropathy. In a subsequent study, McCulley et al (1) evaluated the temporal relationship of cataract surgery to the development of a subsequent anterior optic neuropathy. These investigators reviewed the records of all patients who developed an anterior optic neuropathy between 1993 and 1999 and identified 18 eyes of 17 patients who experienced this disorder within 1 year after surgery. They found that most of these patients developed the optic neuropathy within 6 weeks of surgery, suggesting a decreasing temporal association between the surgery and the optic neuropathy.

Because of the resemblance of PCSON to NAION, Lam et al (14) evaluated the risk of PCSON in the fellow eye of 325 patients with previous unilateral spontaneous NAION who were evaluated at the BPEI between 1986 and 2001. Nine of 17 patients (53%) with spontaneous NAION in one eye and who subsequently underwent cataract surgery in the fellow eye developed NAION in that eye, whereas 59 of 308 patients (19%) with spontaneous NAION in one eye but who did not undergo cataract surgery in the fellow eye developed spontaneous NAION in that eye. The figure of 53% was similar to that of Carroll (6) for the risk of PCSON in the fellow eye of patients who previously had experienced PCSON in their first eye. Lam et al thus concluded that PCSON is a form of NAION and that patients who experience an attack of unilateral spontaneous NAION also have a significantly (3.6-fold) increased risk of PCSON in the fellow eye (95% CI, 1.7–7.7) (20), the development of which has potentially disastrous visual consequences for an elderly patient already debilitated from visual loss in one eye. In addition, a survey of Canadian cataract surgeons collected by Ing et al (13) found that 26% of those cataract surgeons who replied had at least one patient who had experienced PCSON and that the pooled estimate incidence was 2.8 cases per 100,000 procedures during the year after the surgery, with 77% of cases occurring within 3 weeks. Another recent series from South Korea also concluded that there was an increased risk of an acute optic neuropathy after apparently uncomplicated cataract surgery (16). However, there have been substantial changes in both anesthetic and surgical techniques since the work of McCulley et al—specifically, most cataract surgery now is performed under topical rather than retrobulbar or peribulbar anesthesia and the actual surgery takes less than 10 minutes in experienced hands. In addition, there is considerable bias in the retrospective study by Ing et al—as the authors acknowledge in the article—including limited sample size, selection bias from sampling bias, and information biases, including nonresponse bias, response bias, surgeon recall bias, and response inconsistency (13), and the Korean authors acknowledged that in their study, only 9% of patients developed an acute optic neuropathy within 3 days and most occurred more than 1 year after the surgery (16). Finally, there is at least one recent retrospective study that calls into question the relationship between “modern” cataract surgery performed under topical anesthesia and PCSON. Moradi et al (full disclosure: I am a co-author of this report) performed a retrospective study of patients seen at the Wilmer Eye Institute or one of its satellites to determine if these changes had affected the incidence and prevalence of PCSON (21). In this study, 9.6% of patients had a history of cataract surgery during the year subsequent to developing NAION. Of these patients, none developed visual loss in the immediate postoperative period. This is in contrast to the cohort reported by McCulley et al (1), in which 22% developed visual loss within a few days after surgery and the report by Ing et al (13) that 77% developed visual loss within 3 weeks after surgery. In addition, a comparison by Moradi et al of the timeframe of the cases of NAION after cataract surgery against an expected uniform distribution across consecutive 3-month time intervals resulted in their conclusion that their “PCSON” cases were more likely spontaneous NAION and not related to the cataract surgery (21). Over a 5-year study period, among more than 18,000 patients who underwent cataract surgery at the Wilmer Eye Institute or one of its satellites, 2 experienced an attack of “NAION” within 1 year of undergoing surgery—an incidence of 10.9 per 100,000 (95% CI, 1.3–39.4). This rate is virtually identical with the previously reported rate by Hattenhauer et al of 10.3 (95% CI, 6.5–15.6) per 100,000 cases of spontaneous NAION in the general population aged ≥50 years (23). In addition, the estimated incidence of NAION within 6 months after cataract surgery in their study was 5.5 (95% CI, 0.1–30.3) in 100,000. Although the associated CIs of their study were wide and overlapped those of previous studies, the estimated incidence of PCSON in their study was 10-fold lower than the rate previously reported by McCulley et al (15) of 51.8 in 100,000 that also had a wide CI (95% CI, 10.7–151).

There are limitations to the study by Moradi et al (21), including potential selection bias. In particular, cases of PCSON may have been missed because of incorrect coding (e.g., 377 [nonspecific optic neuropathy], 377.3 [optic neuritis], and 377.1 [optic atrophy]). In addition, the diagnosis of NAION may have been incorrect. Moradi et al addressed these issues, noting that the Wilmer Eye Institute's Neuro-Ophthalmology Division requires that all patients who present to ophthalmology residents in either the Johns Hopkins Emergency Department or the Wilmer General Eye Service with known or presumed neuro-ophthalmologic symptoms or signs be discussed with one of the faculty neuro-ophthalmologists, thus making it less likely that a patient with NAION would receive an incorrect diagnosis. In addition, Moradi et al indicated that it is common practice at Wilmer, including its satellites, for all patients seen by Wilmer faculty in other divisions with known or presumed neuro-ophthalmologic symptoms or signs to be immediately discussed with a member of the Neuro-Ophthalmology Division. Thus, although it obviously is possible that some patients with NAION were miscoded, Moradi et al considered this unlikely. Moradi et al also reviewed the records of all patients coded as NAION (377.41), and in cases in which there was incomplete information, the authors contacted the patient, the patient's surgeon, the patient's ophthalmologist, the patient's primary care provider, or a combination of these individuals to obtain a complete understanding of the situation. Among 651 cases diagnosed as NAION in their database, the authors excluded 463 (71.1%) from further consideration because the patients had experienced their episode of NAION before the study period (n = 165), because of lack of sufficient evidence to support the diagnosis of NAION (e.g., disc swelling never observed, n = 114), or because subsequent assessment revealed that the diagnosis of NAION was incorrect and the visual loss was caused by another etiology (n = 184). Thus, their strict inclusion criteria would seem to have ensured that the 188 patients who were included in the study truly had PCSON. Of course, they did assume that if a patient developed NAION after having undergone cataract surgery at the Wilmer Eye Institute or one of its satellites, he or she would have returned to the Wilmer Eye Institute or one of its satellites for an evaluation. This might have resulted in an underestimated incidence of PCSON. Furthermore, they carefully reviewed all eye records to ensure that optic disc swelling was present to support a diagnosis of a postcataract NAION-like clinical picture. Patients with evidence of an optic neuropathy but in whom optic disc swelling was never documented thus were excluded from this study, also potentially underestimating the prevalence of PCSON, particularly if it was posterior rather than anterior. Although they might have neglected to appreciate other potential risk factors for the development of NAION, such as recent cardiac surgery using cardiopulmonary bypass or prone-position spine surgery, perioperative AION after cardiac surgery occurs acutely and would be unlikely to be confused with spontaneous NAION, and virtually all cases of perioperative ION after spine surgery are posterior (i.e., retrobulbar) not anterior (24). Finally, the number of patients who had cataract surgery in the fellow eye after having developed unilateral NAION in one eye was small (n = 7), making it difficult to evaluate the risk of PCSON in the fellow eye of patients with unilateral NAION. In conclusion, the data obtained by Moradi et al (21) suggest that both the prevalence and incidence of NAION after “modern” cataract surgery are comparable with those of the general population, with no significant temporal relationship between modern cataract surgery and the subsequent development of NAION in the operated eye.

Rebuttal: Timothy J. McCulley, MD

The findings of one study, of which Dr. Miller was the senior investigator, in part are incongruous with the collective findings of existing literature (21). Although they did find a difference in preexisting NAION risk factors between patients with postsurgical and spontaneous NAION, their study failed to identify a temporal association or increased incidence of NAION after cataract extraction. The primary limitation in this study lies in the use of a single diagnostic code to identify cases of NAION. Dr. Miller points out that the policy at Wilmer is, at minimum, to have every patient with neuro-ophthalmic disease discussed with a member of the neuro-ophthalmology division. This is of course correct, and I too would like to believe that our diagnostic accuracy is unparalleled. Where our opinions diverge, concerns coding. Dr. Miller implies that the use of a code other than 377.41 for a patient with NAION would be incorrect. My perspective is that codes for optic disc edema, visual field defect, and any other number of options are also accurate. As a member of the Wilmer Neuro-Ophthalmology team, I can state with certainty that uniform coding is not one of our attributes. A more encompassing study design is to take into account coding practices of the entire division and department. It is very likely that the incidence of NAION after surgery at Wilmer was underestimated by Dr. Moradi et al (21). That said, I agree completely with Dr. Miller in that the incidence of postsurgical NAION is most likely decreasing and in ideal circumstances may be negligible.

The risk of NAION after intraocular surgery has likely decreased as surgical techniques improved. Dr. Miller stresses that in noncomplicated surgery, performed with topical anesthesia, the risk of optic nerve ischemia may be similar to the risk of developing an unrelated NAION. This may be close to accurate. However, until cataract and other intraocular surgeries are performed without any chance of elevation in IOP, posterior capsule tear, or postoperative inflammation, some risk will remain. The most discernible hazard in underestimating the risk of NAION associated with cataract surgery lies in second eye involvement, given that upward of 50% of patients, with a history of NAION, may develop NAION in the fellow eye after surgery (14). I also very much agree with Dr. Miller's stance that denying surgery to patients with visually crippling cataracts would be a gross overreaction. However, in patients with a history of NAION in the fellow eye, prudence is warranted. For example, avoiding surgery in a patient with a history of NAION in the fellow eye, with a primary complaint of glare with 20/30 acuity, in my opinion, is a reasonable consideration. For at risk populations, judicial control of IOP and postoperative inflammation is also essential.

In closing, intraocular surgery including cataract extraction is a risk factor for NAION. Dr. Miller and I agree that this risk has almost certainly decreased with advances in the surgical technique. Although in ideal circumstances, the risk of postsurgical NAION may be near inconsequential, there likely remains a significant risk for patients with a history of NAION in the fellow eye. In such cases, prudence is warranted.

Rebuttal: Neil R. Miller, MD

The seminal work performed by McCulley et al that established a clear-cut relationship between apparently uncomplicated cataract surgery and postoperative optic neuropathy (1,2,5,14,15,22) as well as the recent articles by Ing et al (13) and Yang et al (16); notwithstanding, in my opinion, there currently is no unequivocal evidence that patients who have experienced NAION in one eye have an increased risk of NAION after noncomplex cataract surgery in the fellow eye under topical anesthesia. Thus, although it remains possible that even modern cataract surgery in some way predisposes susceptible patients to develop an acute optic neuropathy after apparently uncomplicated cataract surgery, and although I agree with Dr. McCulley that this issue should be discussed with any patient contemplating surgery in this setting, I would not hesitate to recommend cataract surgery (under topical anesthesia) for the patient who has experienced either an acute optic neuropathy within 1 year of apparently uncomplicated cataract surgery or after spontaneous NAION in one eye and who is visually debilitated from a progressive cataract in the fellow eye.

Conclusions: Andrew G. Lee, MD and Gregory P. Van Stavern, MD

Although a causal relationship between uncomplicated cataract surgery and NAION may not be conclusively established, there is enough evidence pointing in that direction to warrant some caution and preoperative discussion when operating on the fellow eye in a patient with previous NAION. The risk should be discussed with the patient and every effort should be made to control perioperative IOP and inflammation.

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