eMedicine Specialties > Ophthalmology > Intraocular Pressure
Posner-Schlossman Syndrome: Treatment & Medication
Updated: Nov 6, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Complete medical care for patients presenting with glaucomatocyclitic crisis includes a reasonably thorough history of present illness, a review of drug allergies and sensitivities, a targeted past medical history and review of systems, a complete eye examination, a careful explanation of the disorder in accordance with the patient's level of understanding, and a commitment to long-term follow-up care of the patient.24
- Medical therapy should be individualized to meet the patient's needs. The favored initial treatment is a combined regimen of a topical nonsteroidal anti-inflammatory drug (NSAID) and an antiglaucoma drug.
- Treatment recommendations include the following:
- Topical steroids - Prednisolone acetate 1% 1 gtt qid, followed by taper
- Topical antiglaucoma drops - Timolol 0.25-0.5% 1 gtt bid or equivalent, or dorzolamide 2% 1 gtt bid/tid or equivalent (Beta-blockers should be avoided in patients with asthma.)
- Systemic carbonic anhydrase inhibitors - Acetazolamide 250 mg PO qid
- Topical NSAIDs - Diclofenac 0.1% 1 gtt tid/qid or equivalent
- Oral NSAIDs - Indomethacin 75-150 mg/d PO
- Miotics and mydriatic agents seldom are used because they may have further deleterious effects on the blood-aqueous barrier, and long-acting periocular steroids are frowned upon because of lingering IOP effects.
- NSAIDs reduce the inflammatory component by inhibiting the production of prostaglandins, and antiglaucoma medications reduce the influx of new aqueous; both these effects rapidly control the IOP. This combination also avoids potential IOP elevations caused by steroids in steroid-responsive patients.
- Well-informed and educated patients often can sense an impending attack based on ocular symptomatology, and they can institute appropriate self-therapy using an aqueous suppressant and a topical NSAID to blunt IOP elevations associated with treatment delays.
- Carefully observe patients periodically for recurrences of attacks and for development of POAG.
- In the absence of underlying chronic glaucoma, antiglaucoma agents do not prevent recurrences of glaucomatocyclitic crisis; therefore, they are not necessary between episodes.
Surgical Care
An occasional patient may require a filtering procedure, which is not effective in preventing recurrences of the episodes of iritis but may be useful in the management of high IOP seen with these episodes.6,25,26 For example, a patient with excessively high pressures threatening vascular perfusion would be a candidate for a filtering procedure. No benefit is gained from laser trabeculoplasty.
Consultations
- An ophthalmologist should be consulted to treat the elevated IOP and to provide long-term follow-up care for patients with POAG.
- Gastroenterology consultation should be sought if the patient has gastric symptoms.
Activity
No restrictions on activity are required.
Medication
A combined regimen of a topical NSAID and an antiglaucoma drug is favored. NSAIDs reduce the inflammatory component by inhibiting the production of prostaglandins, and antiglaucoma medications reduce the influx of new aqueous; both these effects rapidly control the IOP. This combination also avoids potential IOP elevations caused by steroids in steroid-responsive patients.
Corticosteroids
Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Prednisolone acetate (Pred Forte)
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Adult
1 gtt in affected eye qid, followed by taper to optimum clinical response with minimum amount of medication
Pediatric
Not established
Effects may decrease in patients taking phenytoin, barbiturates, and rifampin
Documented hypersensitivity; viral, fungal, or tubercular infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hypertension; known to cause cataract formation with long-term use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate)
Beta-adrenergic blockers
Reduce elevated and normal IOP.
Timolol maleate (Timoptic, Timoptic XE)
Criterion standard for ophthalmic beta-blockers. May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.
Adult
0.25-0.5% 1 gtt in affected eye bid
Pediatric
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, and mental changes (especially in elderly persons)
Alpha-adrenergic agonists
Reduce IOP by reducing the formation of aqueous humor.
Brimonidine tartrate (Alphagan)
Selective alpha-2 receptor that reduces aqueous humor formation and increases uveoscleral outflow.
Adult
1 gtt in affected eye bid
Pediatric
Not established
Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants (eg, barbiturates, opiates, sedatives) may potentiate effects of brimonidine
Documented hypersensitivity; patients receiving MAOIs therapy
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
Carbonic anhydrase inhibitors
Carbonic anhydrase is an enzyme found in many tissues of the body, including the eye. Catalyzes a reversible reaction where carbon dioxide becomes hydrated and carbonic acid dehydrated. By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.
Dorzolamide hydrochloride (Trusopt)
Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
Adult
1 gtt in affected eye bid/tid
Pediatric
Not established
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral carbonic anhydrase inhibitors
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)
Acetazolamide (Diamox, Diamox Sequels)
Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.
Adult
250 mg/d to 1 g/d PO
Pediatric
Not established
Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms also may exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
Diclofenac sodium (Voltaren)
Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which, in turn, decreases formation of prostaglandin precursors. May facilitate outflow of aqueous humor and decrease vascular permeability. Any equivalent topical NSAID also can be used.
Adult
1 gtt in affected eye tid/qid
Pediatric
Not established
Additive effect with systemic NSAIDs may occur
Documented hypersensitivity; avoid during pregnancy
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Corneal thinning may occur
Indomethacin (Indocin)
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Adult
75 mg PO qd
Pediatric
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin levels when administered concurrently
Documented hypersensitivity; GI bleeding; renal insufficiency
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue in persistent leukopenia, granulocytopenia, or thrombocytopenia)
More on Posner-Schlossman Syndrome |
| Overview: Posner-Schlossman Syndrome |
| Differential Diagnoses & Workup: Posner-Schlossman Syndrome |
 Treatment & Medication: Posner-Schlossman Syndrome |
| Follow-up: Posner-Schlossman Syndrome |
| References |
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References
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Further Reading
Keywords
Posner-Schlossman syndrome, PSS, glaucomatocyclitic crisis, secondary inflammatory glaucoma, idiopathic anterior chamber inflammation, mild intraocular inflammation, intraocular pressure, IOP
