Nonarteritic Anterior Ischemic Optic Neuropathy Associated With Acute Glaucoma Secondary to Posner-Schlossman Syndrome

The occurrence of nonarteritic anterior ischemic optic neuropathy (NAION) has been well described following cataract surgery. It has been postulated that a perioperative increase in intraocular pressure leads to a decrease in optic nerve head perfusion pressure, which results in ischemia of the optic disc.¹ Acute rises in pressure secondary to other causes could also result in NAION. The lack of cases in the literature reporting NAION following episodes of acute glaucoma is thus surprising. Although vision loss in acute glaucoma has always been thought to be secondary to optic nerve head ischemia, to our knowledge, NAION following acute glaucoma has only been described in one report.² We report a case of NAION occurring during an episode of acute glaucoma secondary to Posner-Schlossman syndrome.

A 71-year-old white woman with a history of hypertension and hypercholesterolemia sought treatment for a 1-week history of intermittent left eye pain and decreased vision. Results of a right eye examination were normal. Initial visual acuity was 20/200 OS, and a relative afferent pupillary defect was present in the left eye. Corneal edema and trace anterior chamber cell and flare were noted. Intraocular pressure was 69 mmHg. Gonioscopy revealed grade IV angles with light trabecular meshwork pigmentation and no peripheral anterior synechiae.

A dilated fundus examination revealed a mildly edematous left optic nerve and a crowded right optic nerve with a cup-disc ratio of 0.2. Humphrey visual field tests detected an inferior altitudinal defect in the left eye. The erythrocyte sedimentation rate was 16 mm/h. Once the pressure was controlled, the patient had no further complaints of eye pain. The patient had no family history of stroke at a young age, blood clots, unexplained loss of vision, or glaucoma. The patient denied having other neurologic symptoms, including symptoms suggestive of giant cell arteritis. Results of tests for homocysteine, anticardiolipin antibody, lupus anticoagulant, rapid plasma reagin, fluorescent treponemal antibody absorption, and antinuclear antibody were all within reference ranges. Left NAION was diagnosed. The patient was advised to take an aspirin daily.

The patient's intraocular pressure was acutely controlled with eye drops to treat glaucoma and oral acetazolamide. After resolution of the corneal edema, the patient's vision improved to 20/20. During the next year our patient experienced recurrent episodes of elevated intraocular pressure and was diagnosed as having Posner-Schlossman syndrome. There was no further visual field loss associated with her subsequent attacks of elevated pressures and no evidence of recurrence of NAION. Her visual field deficit showed mild improvement at the 1-month visit but remained stable thereafter. Two months later, her left optic nerve showed mild temporal pallor and resolved edema.

Perfusion of the optic disc is directly proportional to mean arterial pressure and inversely proportional to intraocular pressure.³ In our case, the presumed mechanism causing NAION was decreased perfusion to the optic disc secondary to the rise in intraocular pressure. In addition, our patient had a small cup-disc ratio, which implies crowding of the nerve fibers as they pass through a smaller scleral canal. This renders the disc more susceptible to fluctuations in perfusion pressure.⁴ Recurrence of NAION in the same eye is rare, probably because after the initial episode, a reduction in the number of nerve fibers results in decompression of the crowded disc. Interestingly, this may explain why our patient had no further detectable visual field loss with recurrent rises in intraocular pressure. This case further suggests that the mechanism of NAION is related to decreased perfusion of the optic nerve. It also illustrates the importance of pressure control in all cases to prevent NAION.

Corresponding author: Gregory Van Stavern, MD, Kresge Eye Institute, 4717 St Antoine, Detroit, MI 48201 (e-mail: gvanstaver@aol.com).