Case Report

Nonarteritic Ischemic Optic Neuropathy Due to the Increased Intraocular Pressure During Cataract Surgery: A Case Report


  • Sadık Etka Bayramoğlu
  • Nihat Sayın
  • Mehmet Erdoğan
  • Dilbade Yıldız Ekinci

Received Date: 23.03.2017 Accepted Date: 02.05.2017 Med Bull Haseki 2017;55(3):243-247

A 46-year-old patient diagnosed with rheumatoid arthritis underwent cataract surgery for a subcapsular cataract. Perioperative intraocular pressure (IOP) increased after two sideport incisions. Despite administration of 300 cc of 20% mannitol, the elevated IOP persisted for 30 minutes. IOP decreased after pressing the posterior surface of the sideports with a 25 G cannula. The other steps of cataract surgery and intraocular lens implantation were performed uneventfully. On the first postoperative day, the diagnosis of nonarteritic ischemic optic neuropathy (NAION), which was thought to be the result of increased IOP in the perioperative period, was recorded. Cataract surgeons keep in mind and urgently perform simple maneuvers to lower IOP in order to prevent unexpected vision-threatening complications, such as NAION. In addition, for patients who have a crowded optic nerve head with a small cup-to-disc ratio or a previous episode of NAION in the other eye, perioperative and postoperative ocular pressure must be attentively managed.

Keywords: Cataract surgery,optic neuropathy,complication


Cataract surgery is the most common eye procedure in older patients. With increasing surgical experience and developing technology, complications due to surgery have decreased. Cataract surgery is performed on patients for refractive aims and to improve low vision. However, tolerance to complications decreases with increasing expectations. Although regarded as a safe surgery, many complications can develop which threaten vision, including nucleus drop, endophthalmitis, and corneal decompensation. Complications can be related to the experience of the surgeon, techniques, and devices used, the sterilization conditions, and patient-related factors. Neuroophthalmologic complications secondary to cataract surgery is rarely encountered.

Nonarteritic ischemic optic neuropathy (NAION) is the most frequently diagnosed acute optic neuropathy in adults over 50 years of age. Diagnostic criteria are sudden loss of vision frequently accompanied by altitudinal visual field defects, optic nerve head oedema, relative afferent pupillary defect and excluding other acute optic neuropathies (1). In two studies conducted in people over the age of 50, the incidence of NAION development was estimated to be 2.3 and 10.2 per 100.000 people (2,3). The rate of NAION development after cataract surgery has been reported as 0.2%, which indicates increased NAION risk with cataract surgery (4). Even though intravenous methylprednisolone is frequently used in treatment, its efficacy has not been proven by randomized large-scale trials (5).

Here, we present a patient with NAION secondary to increased intraocular pressure (IOP) during cataract surgery.


A 46-year-old male patient with a previous diagnosis of rheumatoid arthritis underwent bilateral cataract surgery for posterior subcapsular cataract secondary to steroid treatment. Surgery was performed with topical anesthesia using 0.5% proparacaine hydrochloride (Alcaine, Alcon, USA) eye drop. Preoperative corrected distance visual acuity (CDVA) of the right eye and left eye were 10/50 and 20/50, respectively. IOP of the right and left eye was 14 and 15 mmHg, respectively. Biomicroscopic examination revealed no pathology except posterior subcapsular cataract. Fundus examination revealed normal optic nerves with a small cup-disc ratio. The patient was diagnosed with rheumatoid arthritis 10 years ago and was medicated with steroid treatment. There was no history of ocular involvement or examination findings of rheumatoid arthritis related ocular involvement, such as uveitis, scleritis, and episcleritis. After surgery of the right eye, the CDVA was 50/50 and ophthalmic examination was normal. The left eye surgery was performed one week after the right eye surgery. Perioperative IOP increased after two sideport incisions (Figure 1). Iris also had a tendency to prolapse from the sideports. Intravenous mannitol infusion was given because IOP did not decrease after the anterior chamber discharging procedure. Despite 300 cc of 20% mannitol administration, elevated IOP persisted for 30 minutes. IOP decreased when the posterior surface of the sideports were pressed with a 25 G cannula by a more experienced surgeon. After IOP decreased, the other steps of the cataract surgery and intraocular lens implantation were performed uneventfully. CDVA on the postoperative first day was 10/50. IOP was 14 mmHg for both eyes. Optic disc swelling, leakage from the optic disc at late phases on fundus fluorescein angiography, thickening of the retinal nerve fiber layer, and enlargement of the blind spot on visual field were detected (Figures 2, 3, 4). The patient was diagnosed with NAION. The natural course of the disease and treatment options were discussed with the patient and steroid treatment was deemed to be the choice of treatment.

For three days, we administrated intravenous 1 gr methylprednisolone, and for one month, we administrated oral methylprednisolone with dose tapering. CDVA was 20/50 and 30/50 after three days and one month of treatment, respectively. One year later, CDVA was 50/50 and visual field examination and optic disc nerve analysis was normal.


NAION is the most common form of anterior ischemic optic neuropathy and is usually the result of transient insufficiency of the oxygen supply in the choroid encircling the optic disk (6). Decreased perfusion pressure, reduced oxygen-carrying capacity, and increased resistance to blood flow results in decreased oxygen delivery. The difference between arterial pressure and venous pressure or IOP if that exceeds venous pressure composes the perfusion pressure of the optic nerve head. Hypertension, diabetes mellitus, hypercholesterolemia, ischemic heart disease, coagulopathies, acute blood loss, anemia, hypotension, nocturnal hypotension, cerebrovascular diseases, migraine, and sleep apnea have been identified as systemic risk factors for the development of NAION (5,7,8).

Our patient had rheumatoid arthritis which might have predisposed him to NAION. We know that inflammatory diseases, such as rheumatoid arthritis are associated with NAION (8).

There are several reports of NAION after non-ocular surgeries. Systemic perioperative risk factors of NAION are; increased venous pressure after head and neck surgery (9), spinal fusion surgery (10), excessive blood loss (11), intraoperative hypotension secondary to cardiopulmonary bypass surgery (12), high-volume crystalloid loading (13,14), prone position with head-down posture (14, 15), and any pathology that may cause intraoperative hypotension (16). The main perioperative ocular risk factor of NAION is increased IOP during surgery (17). According to our knowledge, the development of NAION due to topical anesthesia has not been reported in the literature. Only increased IOP was present as perioperative risk factor in our patient.

The risk of developing NAION, in the fellow eye of patients who had unilateral NAION, has been found to be 18% within one year and 35% within five years (18). Increased IOP, small optic disc, and small optic cup are ocular risk factors for NAION. Small scleral canal diameter has been shown to cause axonal congestion in the lamina cribrosa level in eyes with small optical disc and small optic cup (17). This leads to a decrease in regional blood flow leading to infarction of the optic nerve head (19).

Increased IOP in the first 24 hours after cataract surgery plays an important role in the pathophysiology of early-onset NAION. Early-onset NAION after cataract surgery occurs within a few days after surgery (1,20); whereas, delayed NAION occurs weeks or months after surgery (21-24). Early-onset NAION is known to be associated with increased IOP, but evidence for surgical linkage in delayed NAION is inadequate (25). If NAION develops in one eye after cataract surgery, the risk of developing NAION after subsequent cataract surgery in the fellow eye has been reported to be 30-50% (18,26).

Ocular hypotensive effect for intravenous infusion of mannitol begins within 30 minutes. In our case, IOP did not decreased even 30 minutes after mannitol infusion. IOP decreased after pressing sideports with a cannula by another surgeon. The experience of the surgeon may have influenced the success of the maneuver. We think that increased IOP, which persists for 30 minutes during the operation, is the main reason for the early onset of NAION. We assume that the main reason for early-onset NAION was increased IOP, which persisted for 30 minutes during the operation.

Hayreh and Zimmerman (27) performed a nonrandomized, open-label study of systemic corticosteroids for acute NAION and reported that corticosteroids were effective in improving visual function compared with the natural history. Despite that, a subsequent study by Rebolleda et al. (28) revealed no difference in visual outcome with corticosteroid treatment. Although there are up-to-date case series that show successful results for anti-vascular endothelial growth factor (VEGF) agents, the number of patients in these series is low and long-term follow-up is limited (29,30). In addition, NAION occurrence after intravitreal anti-VEGF injection has been reported as a complication (31). Although there is no consensus on treatment, steroid treatment is the most applied treatment in NAON treatment in current practice (5). We discussed with the patient and explained him about the risks and benefits, and performed corticosteroid treatment. After steroid treatment, the patient’s visual acuity increased and there was no side effect due to steroid. Optic nerve sheath fenestration (32) and hyperbaric oxygen treatment (33) have been reported in the literature for NAION but these treatment modalities did not show beneficial effect on visual outcome.

Patients who used aspirin for the first two years after developing NAION in one eye were reported to have lower risk of developing NAION when compared with patients who have not used aspirin after developing NAION in one eye (34).


We propose that there are three risk factors associated with NAION: increased ocular pressure during the perioperative period, a crowded optic nerve head with a small cup-disk ratio, and diagnosis of rheumatoid arthritis. Therefore, the perioperative and postoperative ocular pressure must be attentively managed in patients with risk factors of NAION in order to prevent NAION. We suggest that cataract surgeons keep these risks factors in mind and perform simple lowering IOP maneuvers, as described on this case, to prevent unexpected vision threatening complications such as NAION.


Informed Consent: It was taken.

Peer-review: Externally and internally peer-reviewed.

Authorship Contributions

Surgical and Medical Practices: S.E.B., N.S. Concept: S.E.B. Design: S.E.B. Data Collection or Processing: S.E.B. Analysis or Interpretation: S.E.B., N.S., D.Y.E., M.E. Literature Search: S.E.B. Writing: S.E.B.

Conflict of Interest: No conflict of interest was declared by the authors.

Financial Disclosure: The authors declared that this study received no financial support.


1. Hayreh SS. Anterior ischemic optic neuropathy: IV. Occurrence after cataract extraction. Arch Ophthalmol 1980;98:1410-6.
2. Johnson LN, Arnold AC. Incidence of nonarteritic and arteritic anterior ischemic optic neuropathy: population-based study in the state of Missouri and Los Angeles County, California. J Neuroophthalmology 1994;14:38-44.
3. Hattenhauer MG, Leavitt JA, Hodge DO, Grill R, Gray DT. Incidence of nonarteritic anteripr ischemic optic neuropathy. Am J Ophthalmol 1997;123:103-7.
4. McCulley TJ, Lam BL, Feuer WJ. Nonarteritic anterior ischemic optic neuropathy and surgery of the anterior segment: temporal relationship analysis. Am J Ophthalmol 2003;136:1171-2.
5. Miller NR, Arnold AC. Current concepts in the diagnosis, pathogenesis and management of nonarteritic anterior ischaemic optic neuropathy. Eye (Lond) 2015;29:65-79.
6. Hayreh SS. The role of optic nerve sheath fenestration in management of anterior ischemic optic neuropathy. Arch Ophthalmol 1990;108:1063-5.
7. Biousse V, Newman NJ. Ischemic optic neuropathies. N Engl J Med 2015;372:2428-36.
8. Kay MC. Ischemic optic neuropathy. Neurol Clin 1991;9:115-29.
9. Bouzaiene M, Deboise A, Kheyar A, Le Queau F, Lemogne M, Baudoin La Cour S. Cécité bilatérale irréversible après curage cervical fonctionnel bilatéral. A propos d’un cas et revue de la littérature. Revue de Stomatologie et de Chirurgie Maxillo-Faciale 1994;95:226-32.
10. Rubin DS, Parakati I, Lee LA, Moss HE, Joslin CE, Roth S. Perioperative Visual Loss in Spine Fusion Surgery: Ischemic Optic Neuropathy in the United States from 1998 to 2012 in the Nationwide Inpatient Sample. Anesthesiology 2016;125:457-64.
11. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008;145:604-10.
12. Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982;32:560-2.
13. Ripart J, Desmonts JM. Loss of vision after anaesthesia for nonophthalmic surgery: a persistent problem. Eur J Anaesthesiol 2009;26:524-6.
14. Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: the Johns Hopkins Hospital Experience. Spine (Phila Pa 1976) 2005;30:1299-302.
15. Hunt K, Bajekal R, Calder I, Meacher R, Eliahoo J, Acheson JF. Changes in intraocular pressure in anesthetized prone patients. J Neurosurg Anesthesiol 2004;16:287-90.
16. Brown RH, Schauble JF, Miller NR. Anemia and hypotension as contributors to perioperative loss of vision. Anesthesiology 1994;80:222-6.
17. Tomsak RL, Remler BF. Anterior ischemic optic neuropathy and increased intraocular pressure. J Clin Neuroophthalmol 1989;9:116-8.
18. Beri M, Klugman MR, Kohler JA, Hayreh SS. Anterior ischemic optic neuropathy. VII. Incidence of bilaterality and various influencing factors. Ophthalmology 1987;94:1020-8.
19. Beck RW, Servais GE, Hayreh SS. Anterior ischemic optic neuropathy. IX. Cup-to-disc ratio and its role in pathogenesis. Ophthalmology 1987;94:1503-8.
20. Serrano LA, Behrens MM, Carroll FD. Postcataract extraction ischemic optic neuropathy. Arch Ophthalmol 1982;100:1177-8.
21. Carroll FD. Optic nerve complications of cataract extraction. Trans Am Acad Ophthalmol Otolaryngol 1973;77:OP623-9.
22. Gartner S. Optic Neuritis and Macular Edema Following Cataract Extraction. Eye Ear Nose Throat Mon 1964;43:45-9.
23. Michaels DD, Zugsmith GS. Optic neuropathy following cataract extraction. Ann Ophthalmol 1973;5:303-6.
24. Reese AB, Carroll FD. Optic neuritis following cataract extraction. Am J Ophthalmol 1958;45:659-62.
25. Lee H, Kim CY, Seong GJ, Ma KT. A case of decreased visual field after uneventful cataract surgery: nonarteritic anterior ischemic optic neuropathy. Korean J Ophthalmol 2010;24:57-61.
26. Lam BL, Jabaly-Habib H, Al-Sheikh N, et al. Risk of non-arteritic anterior ischaemic optic neuropathy (NAION) after cataract extraction in the fellow eye of patients with prior unilateral NAION. Bri J Ophthalmol 2007;91:585-7.
27. Hayreh SS, Zimmerman MB. Non-arteritic anterior ischemic optic neuropathy: role of systemic corticosteroid therapy. Graefes Arch Clin Exp Ophthalmol 2008;246:1029-46.
28. Rebolleda G, Perez-Lopez M, Casas-Llera P, Munoz-Negrete FJ. Treatment of non-arteritic anterior ischemic optic neuropathy with high-dose systemic corticosteroids. Graefes Arch Clin Exp Ophthalmol 2013;251:1031-2.
29. Rootman DB, Gill HS, Margolin EA. Intravitreal bevacizumab for the treatment of nonarteritic anterior ischemic optic neuropathy: a prospective trial. Eye (Lond) 2013;27:538-44.
30. Ayhan Z, Kocaoglu G, Yaman A, Bajin MS, Saatci AO. Single intravitreal aflibercept injection for unilateral acute nonarteritic ischemic optic neuropathy. Case Rep Ophthalmol Med 2015;2015:783241.
31. Mansour AM, Shahin M, Kofoed PK, et al. Insight into 144 patients with ocular vascular events during VEGF antagonist injections. Clin Ophthalmol 2012;6:343-63.
32. No authors listed. Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the Ischemic Optic Neuropathy Decompression Trial. Arch Ophthalmol 1996;114:1366-74.
33. Arnold AC, Hepler RS, Lieber M, Alexander JM. Hyperbaric oxygen therapy for nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1996;122:535-41.
34. Beck RW, Hayreh SS, Podhajsky PA, Tan ES, Moke PS. Aspirin therapy in nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123:212-7.