Treatment Plan

Signs and Symptoms of Posner-Schlossman Syndrome

treatment plan

Signs and Symptoms of Posner-Schlossman Syndrome


A 78-year-old man presented with a complaint of a mildly irritated left eye and slightly blurred vision that began a day earlier. Visual acuity was correctable to 20/25 in each eye, attributable to cataract. The IOP was 16mmHg in the right but 54mmHg in the left. The anterior chamber angles were open (by estimation at the slit lamp) and pupils reacted to light without RAPD. The left anterior chamber showed a mild cellular response. There was neither corneal edema nor staining.

This constellation of symptoms and findings is consistent with Posner-Schlossman syndrome (PSS). A more clinically descriptive term is glaucomatocyclitic crisis. This condition is self-limited and characterized by recurrent episodes of mildly to markedly elevated IOP and mild idiopathic anterior chamber inflammation. It's probably best classified as a secondary inflammatory glaucoma. The original description from nearly 60 years ago included the following clinical findings:

  • Recurrent episodes of mild anterior chamber inflammation characterized by cells.
  • Uniocular involvement.
  • Attacks lasting from a few hours to several weeks.
  • Slightly decreased vision, elevated IOP with open angles and corneal edema.
  • Normal visual fields.
  • Normal optic disc.
  • Normal IOP, outflow facility and all provocative tests between episodes.

Due to recurrence, patients may also show keratic precipitates, heterochromia with anisocoria and a large pupil in the affected eye.

Although we examined this patient for several years, there was no record of any of the findings listed. He didn't fit the typical age range (usually 20 to 50). Apparently his episodes were mild and didn't coincide with scheduled exams or didn't produce threshold symptoms. The lack of KPs, heterochormia and optic disc damage is also evidence of the mild, transient nature of this case.

Treatment and Follow up

My treatment plan included a single dose of acetazolamide (250 mg, PO) and Alphagan-P (brimonidine 0.01%, Allergan) t.i.d. I also prescribed Pred Forte (prednisolone acetate 1%, Allergan) q4 waking hours. Because of the inflammatory component to the IOP increase, I chose not to use a prostaglandin analog.

On follow up later that same day IOP measured 16mmHg in each eye. The anterior chamber reaction had diminished significantly. I continued the topical drops for one additional week. At that time he was free of anterior chamber reaction and had equal IOP (15mmHg).

Variable Courses of Action

Because PSS is a rare condition with variable clinical course and presentations, the exact etiopathological mechanisms remain obscure. What appears to be consistent is that inflammation is responsible for the IOP increase. In addition, some evidence suggests that PSS may be associated with POAG. In patients with a 10-year or longer history of PSS, glaucoma visual field or optic disc changes are three times more likely to develop. These patients may have a predilection for corticosteroid response, which may potentiate elevated IOP. This must remain a precaution in chronic cases or when managing patients for periods of longer than two weeks.

Oral and combination topical medications are standard for PSS. The anti-inflammatory activity of the steroid probably contributes greatly to lowering IOP. But carefully monitor IOP in cases treated for more than weeks. Alternative IOP-lowering drops include beta-blockers and carbonic-anhydrase inhibitors. CLS

Dr. Semes is an associate professor at the University of Alabama at Birmingham School of Optometry.