Posner-Schlossman Syndrome   

Posner-Schlossman syndrome (PSS; also known as glaucomatocyclitic crisis) is a rare inflammatory eye condition that usually affects only one eye and typically develops in the second to fourth decade of life. PSS is characterized by relapsing and remitting episodes of high intraocular pressure (IOP) and mild eye inflammation. IOP increases when normal drainage of the aqueous humor (i.e., fluid that fills the anterior and posterior chambers of the eye) is compromised. The cause of PSS is unknown. It has been variously proposed that PSS is caused by an allergic reaction, a vascular defect, and an autonomic abnormality. The pathophysiology of PSS includes physiologic changes in a type of eye tissue called the trabecular meshwork, which is located around the base of the cornea and is responsible for draining aqueous humor, and possibly also leads to an increased production of aqueous humor. Between episodes of PSS-related signs and symptoms, aqueous humor production and absorption is normal, as is IOP. Some research suggests possible associations between PSS and herpes simplex virus (HSV) infection, cytomegalovirus (CMV) infection, and Helicobacter pylori infection, which causes peptic ulcer disease.

Symptoms of PSS include intermittent episodes of unilateral eye discomfort, mild blurred vision, and halos around lights, but some persons with PSS are asymptomatic. Episodes are self-limiting and can last for hours or weeks; episodes of short duration can be missed by the clinician. The frequency of PSS episodes varies from patient to patient and decreases with age. Assessment of the eyes and vision, including IOP and pupil dilation visual field tests of the side (or peripheral) vision, can determine if the optic nerve is damaged. An ocular exam may reveal mild corneal epithelial edema and elevated IOP during a symptomatic episode. For a diagnosis of PSS to be made, the clinician should rule out other conditions that have signs and symptoms similar to PSS, including herpetic uveitis (i.e., herpetic infection of the middle layer of the eye), sarcoidosis (i.e., a granulomatous inflammatory disease that can affect the eye), and Toxoplasma uveitis (i.e., a toxoplasmosis infection) of the middle layer of the eye. Occasionally PSS may be mistaken for angle closure glaucoma, a nonuveitic condition characterized by a sudden increase in IOP due to blockage of fluid drainage. Prolonged IOP elevation leads to permanent optic nerve damage and visual field defects. 

Medical treatment of PSS includes topical corticosteroids (e.g., prednisolone acetate); antiglaucoma medications such as beta-adrenergic antagonist eye drops to reduce production of aqueous humor (e.g., 0.25-0.5% timolol or 2% dorzolamide); carbonic anhydrase inhibitors (CAIs; e.g., acetazolamide), to reduce aqueous formation; and nonsteroidal anti-inflammatory drugs (NSAIDs; e.g., diclofenac 0.1%; indomethacin), to reduce inflammation by inhibiting production of prostaglandins. The combination of an NSAID and an antiglaucoma drug prevents IOP elevations caused by both PSS and the adverse effects of steroids that some patients experience. Some patients require a surgical procedure (e.g., trabeculoplasty) to prevent high IOP that develops during episodes of PSS. Nurses should promote optimal physiologic function, monitor and reduce risk for complications, and provide emotional support and educate patients about treatment risks and benefits, and the proper way to administer eye medications.