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Clinicopathologic Reports, Case Reports, and Small Case Series
August 2001

Anterior Ischemic Optic Neuropathy Following Acute Angle-Closure Glaucoma

Arch Ophthalmol. 2001;119(8):1215. doi:

Nonarteritic anterior ischemic optic neuropathy (NAION) is believed to be caused by acute occlusion of small vessels to the optic nerve, resulting in lacunar infarction. Most involved optic nerves are anatomically crowded with a cup-disc ratio that is small and usually less than 30%.1 Nonarteritic anterior ischemic optic neuropathy may also follow other episodes of hemodynamic instability, such as cerebral hypoperfusion (shock optic neuropathy) or blood loss. It has been described after uncomplicated cataract extraction, in which it is presumed to be due to perioperative elevation of intraocular pressure.2 We report a case of NAION developing in each eye of a man with sequential acute angle-closure glaucoma. In each eye, the vision loss followed the bout of glaucoma by approximately 2½ weeks.

Report of a Case

A 70-year-old man with angina pectoris and hypercholesterolemia developed acute pain and markedly diminished vision in his left eye due to angle-closure glaucoma. Visual acuity was noted to be 5/200, corneal edema was present, and intraocular pressure was 50 mm Hg. Medications (timolol maleate, brimonidine tartrate, latanoprost, 1% pilocarpine hydrochloride, prednisolone, and oral acetazolamide), and subsequent laser iridotomy were successful in reversing the process. He was maintained on timolol and latanoprost after the third day. Visual acuity was noted to be 20/40 after 11 days. Ophthalmoscopy showed a healthy left optic nerve with a 0.1 cup-disc ratio. At this time, the patient was advised, but refused, to have prophylactic iridotomy in the fellow eye. One week later, vision loss in the left eye recurred. There was no associated eye pain, headache, jaw claudication, or polymyalgia rheumatica. On examination, visual acuity was hand movements, and a remaining inferotemporal island of vision was detected on confrontation visual field testing. Slitlamp examination results were unremarkable, and intraocular pressure was normal. A left afferent pupil defect was present. The left optic nerve was swollen with overlying hemorrhages. Westergren erythrocyte sedimentation rate was normal. Left NAION was diagnosed.

One month after the bout of angle-closure glaucoma in the left eye, the patient experienced sudden vision loss in the right eye due to angle-closure glaucoma. The intraocular tension was 56 mm Hg. Medications (the same used as in fellow eye) and laser iridotomy again were successfully employed, and 10 days later, visual acuity recovered to 20/50. One week later, however, there was marked worsening of vision in the right eye. Neuro-ophthalmologic consultation was sought, and examination revealed a best-corrected visual acuity of 20/200 OD and 2/200 OS. Each pupil was dilated and unresponsive to light. Glaucomflecken was noted on the left lens. Goldmann visual fields showed bilateral central scotomas with peripheral inferior extension. Ophthalmoscopy revealed pale swelling of the right optic disc and resolving optic disc edema in the left eye, with marked optic atrophy. Retinal arterioles were attenuated bilaterally. Sequential NAION was diagnosed. On subsequent follow-up there was no improvement of visual acuity or visual fields in either eye, and bilateral optic atrophy was noted.


In our case, vision loss due to NAION was most likely precipitated by hemodynamic instability to the optic nerve from the marked rise and subsequent stabilization of intraocular pressure. Although permanent vision loss, which occurs at the time of angle-closure glaucoma, is thought to be caused by an ischemic event to the optic nerve, NAION following such a bout has not (to our knowledge) previously been reported. The explanation for the duration between the angle-closure episode and the onset of NAION is unknown. We postulate that in our case, subclinical low-grade optic nerve ischemia occurred at the time of the pressure rise with subsequent progressive ischemia until frank vision loss ensued. Perhaps a vicious cycle consisting of ischemia, optic disc swelling, and additional ischemia occurred. Hayreh3 has described several cases of subclinical optic disc edema resulting in frank bouts of symptomatic NAION months later. Perhaps our case and those of Hayreh shed some light on the possible mechanism as to why some cases of NAION following cataract extraction have a demonstrable interval between surgery and vision loss.4 In any event, acute rise in intraocular pressure is to be considered a risk factor in NAION. Whenever possible, precautions should be taken to avoid pressure rise, especially in eyes with optic discs that are developmentally small, with small cup-disk ratios.

Corresponding author and reprints: Michael L. Slavin, MD, Division of Neuro-ophthalmology, Department of Ophthalmology, Long Island Jewish Medical Center, the Albert Einstein College of Medicine, 600 Northern Blvd, Great Neck, NY 11021 (e-mail: DrSlavin4@aol.com).

Beck  RWSavino  PJRepka  MX  et al.  Optic disc structure in anterior ischemic optic neuropathy.  Ophthalmology. 1984;911334- 1337Google ScholarCrossref
Hayreh  SS Anterior ischemic optic neuropathy, IV: occurrence after cataract extraction.  Arch Ophthalmol. 1980;981410- 1416Google ScholarCrossref
Hayreh  SS Anterior ischemic optic neuropathy, V: optic disc edema as early sign.  Arch Ophthalmol. 1981;991030- 1040Google ScholarCrossref
Carroll  FD Optic nerve complications of cataract extraction.  Trans Am Acad Ophthalmol Otolaryngol. 1973;77623- 629Google Scholar