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Did cataract surgery cause this patient’s NAION?

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Figure 1. Fundus examination revealed inferior-nasal optic disc oedema and no haemorrhages

______________________________

Andy Mackner BA
Pacific University College of Optometry, Forest Grove, Oregon

Dr Leonid Skorin Jr
OD DO MS FAAO FAOCO
Department of Ophthalmology, Mayo Clinic Health System, Albert Lea, Minnesota 

CASE REPORT

A 78-year-old Caucasian male presented for a cataract evaluation. The patient reported that his right eye seemed worse than his left eye. The patient was scheduled for cataract extraction of the right eye. His ocular history was significant for cataracts and blepharoplasty. His medical history was significant for Alzheimer’s disease with moderate dementia.

At the initial visit, the patient’s best corrected acuities were 6/45-2 in the right eye and 6/20+2 in the left eye. Pupil testing was unremarkable and his eye movements were full, as were confrontation fields. His intraocular pressures (IOPs) were 13 mmHg in both eyes. Slitlamp examination of the right eye revealed grade 2+ nuclear sclerotic and grade 2+ posterior subcapsular cataracts. The left eye exhibited grade 2+ nuclear sclerotic and grade 1+ posterior subcapsular cataracts. All other anterior structures were unremarkable. The posterior examination of both eyes revealed maculae that were flat and dry, optic nerves were perfused with a cup-to-disc ratios of .45 x .45 and the peripheral retinas were flat and intact. The patient underwent successful phacoemulsification cataract surgery with a posterior chamber IOL in the right eye.

The patient’s one-day post-operative examination was unremarkable. Post-operative medications included prednisolone acetate 1%, moxifloxacin 0.5% and ketorolac 0.5% four times a day in the right eye. Uncorrected acuities were 6/18-1 in the right eye and 6/18+2 in the left eye. IOPs were 17 mmHg right eye and 16 mmHg left eye. The right eye anterior chamber was deep with trace cells, posterior chamber IOL was stable, surgical incisions were intact and there was no Siedel sign.

The patient was then scheduled for left eye cataract surgery the following week.

As the patient was being checked into surgery the following week, he reported that the vision in his right eye seemed to be better but he was unable to see anything in his superior visual field. On further questioning, his wife reported that he had noticed a spot in his vision prior to his first cataract extraction but they had not thought anything of it and attributed it to his cataracts.

Because of this new complaint, the left eye surgery was cancelled and the patient was re-evaluated. His right eye acuity was 6/21 with pinhole 6/12. The IOP was 11 mmHg in the right eye. Pupils were equal, round, reactive to light with no relative afferent pupillary defect. Confrontation fields suggested a superior field defect in the right eye. Anterior segment findings were unremarkable. Fundus examination revealed inferior-nasal optic disc oedema and no haemorrhages (Figure 1). The computerised visual field exhibited a superior altitudinal defect. The left eye visual field was unremarkable.

Although the patient denied any jaw claudication, scalp tenderness or temple pain, we proceeded to order an erythrocyte sedimentation rate and C-reactive protein (CRP) test to rule out temporal arteritis. Laboratory results showed an elevated ESR at 62 mm/hr and a normal CRP at 4.2 mg/L.

We started the patient on 60 mg oral prednisone daily and scheduled a temporal artery biopsy. The temporal artery biopsy was negative for inflammation. The oral prednisone was discontinued and the patient was diagnosed with non-arteritic anterior ischaemic optic neuropathy (NAION). The patient was then scheduled for cataract extraction of his left eye. The patient underwent successful cataract extraction of the left eye with no complications.

Discussion

This case report highlights the importance of listening to our patients and the rare association of cataract extraction and non-arteritic anterior ischaemic optic neuropathy.

Anterior ischaemic optic neuropathy can present in two forms: arteritic (AAION) and non-arteritic (NAION).1,2 Although the exact mechanism is still unclear, it is thought that NAION is a result of acute ischaemia to the optic disc.1-3 NAION is characterised by a sudden, painless decrease in vision with optic disc oedema and visual field defect.1,3 The most common visual field defect is an altitudinal defect. However, other common visual field defects may include central, centrocecal, arcuate or a generalised depression.1

The patient may also present with reduced visual acuity, dyschromatopsia, afferent pupillary defect, peripapillary splinter haemorrhages and a small or crowded disc, also referred to as a disc at risk.4,5 Other risk factors include sleep apnoea, diabetes mellitus, hypertension and hypercholesterolaemia.4 In addition, the use of phosphodiesterase-5 inhibitors and amiodarone have been associated with the development of NAION.5

A less commonly cited association with NAION is cataract extraction. The association with cataract surgery is rare but it is also one of the most visually devastating complications.6 Past studies have shown that there is an increased risk of NAION with cataract surgery that is greater than the overall incidence of NAION.7 The incidence of NAION following cataract extraction is estimated to be one case per 2,000 whereas studies suggest that the overall incidence of NAION is 2.3 to 10.2 cases per 100,000 in individuals over the age of 50 years.7,8,9

However, a more recent study suggests that the increased incidence may reflect the use of retrobulbar and peribulbar anaesthesia as well as intracapsular and extracapsular surgical techniques. More modern surgical methods using phacoemulsification and topical anaesthesia have a prevalence and incidence of NAION after cataract surgery comparable to that of the general population.9 Additionally, this study found no evidence suggesting that patients who have experienced NAION in one eye have an increased risk of NAION following a non-complex cataract surgery in the fellow eye.9

Although new evidence suggests that concern for NAION in the fellow eye following cataract surgery may be unwarranted, it is still important to educate our patients about the associated risks. Currently, there is no treatment for NAION. Surgical intervention with optic nerve sheath decompression has been shown to be ineffective and possibly harmful.10,11,12 Other strategies to improve recovery by improving perfusion to the nerve have been attempted. Aspirin, vasodilators, systemic steroids and intravitreal steroids have been trialled but none has been proved to be effective.12  

During the patients pre-operative visit there were no signs of ischaemic optic neuropathy. The patient explained to us that he noticed the decrease in vision after the initial visit, prior to his first eye cataract surgery, and attributed the change in his vision to the cataracts. However, after right eye cataract surgery, he became more aware of the visual field defect in his right eye and brought it to our attention prior to the surgery in his left eye.

In this case the NAION was not related to the cataract surgery but when consulting our patients with a history of NAION who are interested in undergoing cataract surgery, we should educate them on the associated risks and reassure them that risk of NAION in the fellow eye is low.9 Ultimately, it is the patient’s decision to undergo cataract surgery but it is our responsibility to be aware of associated risks and provide guidance to our patients.

 

  1. Tamhankar M, Volpe N. Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis.  In: UpToDate, Post TW (Ed), Waltham, MA. Accessed June 26, 2017.
  2. McCulley T, Lam B, Feuer W. A comparison of risk factors for postoperative and spontaneous nonarteritic anterior ischemic optic neuropathy. Neuro-Ophthalmology 2005; 25: 22-24.
  3. Hata M, Oishi A, Muraoka U, et al. Structural and functional analyses in nonarteritic anterior ischemic optic neuropathy: Optical coherence tomography angiography study. Neuro-Ophthalmology 2017; 37: 140-148.
  4. Kabat AG, Skorin L: Nonarteritic ischemic optic neuropathy. In: Onofrey B, Skorin L, Holdeman N, eds. Ocular Therapeutics Handbook: A Clinical Manual, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2011; 591-593.
  5. McCulley T, Lam B, Feuer W. Nonarteritic anterior ischemic optic neuropathy and intraocular surgery. Amer J Ophthalmol 2017; 175: 14-16.
  6. Ruskiewicz J. NAION follows cataract surgery. Review Optometry 2013; 18: 58-70.
  7. MCulley T, Lam B, Feuer W. Incidence of nonarteritic anterior ischemic optic neuropathy associated with cataract extraction. Ophthalmology 2001; 108: 1275-1278.
  8. Lam B, Jabaly-Habib H, Al-Sheikh, et al. Risk of non-arteritic anterior ischemic optic neuropathy (NAION) after cataract extraction in the fellow eye of patients with prior unilateral NAION. Brit J Ophthalmol 2007; 91: 585-587.
  9. Moradi A, Kanagalingam S, Diener-West M, Miller N. Post-cataract surgery optic neuropathy: prevalence, incidence, temporal relationship, and fellow eye involvement. Amer J Ophthalmol 2017; 175: 183-195.
  10. Yee R, Selky A, Purvin V. Outcomes of optic nerve sheath decompression for nonarteritic ischemic optic neuropathy. J Neuro-Ophthalmology 1994; 14: 70-76.
  11. Dickerson K, Everett D, Feldon S, et al. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. J Amer Med Assoc 1995; 273: 625-632.
  12. Atkins EA, Bruse BB, Newman NJ, Biousse V. Treatment of non-arteritic ischemic optic neuropathy. Survey Ophthalmol 2010; 55: 47-63.


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