eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Drug-Induced

Douglas J Rhee, MD, Assistant Professor, Department of Ophthalmology, Harvard Medical School; Consulting Staff, Massachusetts Eye and Ear Infirmary
Steven Gedde, MD, Program Director, Assistant Professor, Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine

Updated: May 18, 2009

Introduction

Background

Several different drugs have the potential to cause the elevation of intraocular pressure (IOP), which can occur via an open-angle mechanism or a closed-angle mechanism. Steroid-induced glaucoma is a form of open-angle glaucoma that usually is associated with topical steroid use, but it may develop with inhaled, oral, intravenous, periocular, or intravitreal steroid administration. Medications prescribed for a variety of systemic conditions (eg, depression, allergies, Parkinson disease) can produce pupillary dilation and precipitate an attack of acute angle-closure glaucoma in anatomically predisposed eyes that have narrow angles.

Open angle

Drug-induced elevation of IOP is more common by an open-angle mechanism. Corticosteroids are a class of drugs that may produce IOP elevation by this mechanism. Not all patients taking corticosteroids will develop elevated IOP. Risk factors include preexisting primary open-angle glaucoma, a family history of glaucoma, high myopia, diabetes mellitus, and history of connective tissue disease (especially rheumatoid arthritis).

Additionally, the number of people responding with an elevated IOP varies with the route of administration. More people respond from topically applied drops (including topically applied creams to the periorbital area) or intravitreal injection. In order of decreasing frequency, incidence of elevated IOP is less with intravenous, parenteral, and inhaled routes of administration. Patients on chronic corticosteroid therapy can remain undiagnosed with an elevated IOP, which can result in glaucomatous optic nerve damage.

Steroid-induced IOP elevation typically occurs within a few weeks of beginning steroid therapy. In most cases, the IOP lowers spontaneously to the baseline within a few weeks to months upon stopping the steroid. In rare instances, the IOP remains elevated. Additionally, there may be some patients whose underlying condition necessitates the continued use of corticosteroids despite the elevated IOP. These patients are treated identically to those with primary open-angle glaucoma.

Closed angle

Most categories of drugs that list glaucoma as a contraindication or adverse effect are concerned with inducing acute angle-closure glaucoma. These medications will incite an attack only in those individuals with occludable angles (ie, very narrow anterior chamber angles). The classes of medications that have the potential to induce angle closure are topical anticholinergic or sympathomimetic dilating drops, tricyclic antidepressants, monoamine oxidase inhibitors, antihistamines, antiparkinsonian drugs, antipsychotic medications, and antispasmolytic agents.

Sulfa containing medications may induce angle-closure glaucoma by a different angle-closure mechanism, involving anterior rotation of the ciliary body. Typically, the angle closure is bilateral and occurs within the first several doses of the sulfonamide-containing medication. Patients with narrow or wide open angles are potentially susceptible to this rare and idiosyncratic reaction.

Pathophysiology

Open angle

Exact pathophysiology of steroid-induced glaucoma is unknown. It is known that steroid-induced IOP elevation is secondary to increased resistance to aqueous outflow. Some evidence indicates that the defect could be increased accumulation of glycosaminoglycans or increased production of trabecular meshwork-inducible glucocorticoid response (TIGR) protein, which could mechanically obstruct outflow. Other evidence points toward corticosteroid-induced cytoskeletal changes that could inhibit pinocytosis of aqueous humor or inhibit the clearing of glycosaminoglycans, resulting in the accumulation of this substance.

Closed angle

The pathophysiology of drug-induced angle-closure glaucoma is usually increased pupillary block (ie, increased iris-lens contact at the pupillary border) from pupillary dilation. Medications have a direct or secondary effect, either to stimulate sympathetic or inhibit parasympathetic activation causing pupillary dilation, which can precipitate acute angle-closure glaucoma in patients with occludable angles. The other possible mechanism is dilation in patients with plateau iris syndrome. See Glaucoma, Angle Closure, Acute. 

A notable exception is the angle closure resulting from sulfa containing medications. The mechanism involves anterior rotation of the ciliary body and/or choroidal effusions, resulting in shallowing of the anterior chamber and blockage of the trabecular meshwork by the iris. Pupillary dilation and a preexisting shallow anterior chamber angle are not necessary. The exact defect that causes the ciliary body swelling is unknown.

Frequency

United States

Open angle

The incidence of steroid-induced IOP elevation in patients on systemic corticosteroids is unknown because most of these patients do not have their IOP checked. These patients may be discovered during a routine eye exam while on their medication, or the glaucoma may have progressed to the point of causing visual symptoms. Patients taking topical steroid drops usually receive follow-up care by an ophthalmologist who monitors IOP.

The risk of developing steroid-induced glaucoma is related to its potency and frequency of administration. People with preexisting primary open-angle glaucoma have a much greater potential to experience an elevated IOP from topical corticosteroids. Patients with primary chronic angle closure and patients with secondary open-angle glaucoma behave similarly to normal eyes with regard to steroid response.

Studies completed by Armaly indicated that approximately one third of normal eyes and more than 90% of patients with primary open-angle glaucoma respond with greater than 6 mm Hg of IOP elevation after receiving a 4-week course of topical dexamethasone 0.1%.^1,2 Following intravitreal injection of triamcinolone, over 50% of nonglaucomatous eyes will have an increase in IOP; this increase in IOP can occur as long as 6 months after the injection.

Closed angle

Prevalence of occludable angles in whites from the Framingham study is 3.8%.

Narrow angles are more common in the Asian population. A study of a Vietnamese population estimated a prevalence of occludable angles at 8.5%.

Mortality/Morbidity

Glaucoma is the third leading cause of blindness in the United States. The risk of becoming legally blind in one eye from open-angle glaucoma is approximately 20%, with bilateral blindness occurring in 9%.

Race

No racial predilection exists for steroid-responsive IOP.

Sex

No sexual predilection exists for steroid-responsive IOP.

Age

Steroid-responsive IOP elevations can occur in people of all ages, although children less frequently are reported to have IOP elevation with steroids.

Clinical

History

Elicit the patient's current medications.

• Symptoms
  • With steroid-induced glaucoma, the pressure elevation is gradual. Therefore, like primary open-angle glaucoma, very few symptoms exist.
  • Visual symptoms of drug-induced acute angle-closure glaucoma are the same as primary acute angle-closure glaucoma.
• Past ocular history/past medical history
  • Elicit history of systemic medical disease, which could require chronic corticosteroid use (eg, uveitis, collagen vascular disease, asthma, dermatitis).
  • Patients with preexisting primary open-angle glaucoma, a family history of primary open-angle glaucoma, diabetes mellitus, high myopia, or connective tissue diseases are at greater risk to be steroid responders.

Physical

Perform a complete ophthalmic examination.

• Vision and refraction - Patients with hyperopia are at an increased risk for narrow angles.
• Pupils - Test for the presence of an afferent pupillary defect if topical use has been unilateral or if the attack has only occurred in one eye.
• External examination - Use a flashlight test to identify an anatomically narrow angle.
• Slit lamp examination - Exclude stigmata of other causes of secondary glaucoma.
  • Cornea - Krukenberg spindle (eg, pigmentary glaucoma), keratic precipitates (eg, uveitic glaucoma, Fuchs heterochromic iridocyclitis)
  • Anterior chamber - Anterior chamber depth to indicate narrow angle
  • Iris - Heterochromia (ie, Fuchs heterochromic iridocyclitis), iris transillumination defects (eg, pseudoexfoliation, pigment dispersion, previous episodes of intermittent angle closure)
  • Lens - Pseudoexfoliation material (pseudoexfoliation glaucoma)
• Gonioscopic evaluation - Examine angle anatomy to determine if the angle is at risk for occlusion with dilation.
• Dilated examination - Inspect the optic nerve for glaucomatous optic nerve damage. See Glaucoma, Primary Open Angle for a description of glaucomatous patterns. Dilate after potentially occludable narrow angles or plateau iris has been excluded by gonioscopy.

Causes

Drug-induced glaucoma can occur via two mechanisms, as follows: open-angle glaucoma is generally steroid induced, and closed-angle glaucoma is generally from pupillary dilation.

Differential Diagnoses

Other Problems to Be Considered

Steroid therapy (eg, posterior subcapsular cataracts)

Workup

Laboratory Studies

• No lab studies are indicated.

Imaging Studies

• No imaging studies are indicated for glaucoma.

Other Tests

• Formal visual field testing (ie, Humphrey, Octopus, Goldmann) is indicated.

Procedures

• No procedures are indicated for glaucoma.

Treatment

Medical Care

• Open angle
  • If the patient's underlying medical condition can tolerate discontinuation of corticosteroids, then cessation of the medication will usually result in normalization of IOP.
  • In the case of topical corticosteroid drops, using a lower potency steroid medication, such as the phosphate forms of prednisolone and dexamethasone, rimexolone, loteprednol etabonate, fluorometholone, or medrysone, should be considered. These lower potency drugs have a lesser chance of raising IOP, but they are usually not as effective as an anti-inflammatory drug. Topical nonsteroidal anti-inflammatory medications (eg, diclofenac, ketorolac) are other alternatives that have no potential to elevate IOP, but they may not have enough anti-inflammatory activity to treat the patient's underlying condition.
  • In the occasional cases in which the patient's IOP does not normalize upon cessation of the steroid or in those patients who must continue on corticosteroid medications, use standard antiglaucoma medications, as described in Glaucoma, Primary Open Angle.
• Closed angle
  • If the etiology is because of sulfa containing medications, the increase in IOP generally will resolve upon stopping the medication. However, severe cases of sulfonamide-induced angle closure (ie, IOP >45 mm Hg) may not respond to simply discontinuing the offending medication. These cases may respond to intravenous Solu-Medrol and mannitol.
  • For other etiologies, treat the same as primary acute angle-closure glaucoma.

Surgical Care

• Open angle
  • When medical therapy is ineffective at lowering the IOP to target pressure or the patient is intolerant of medical therapy, then surgical therapy is indicated.
  • In patients with an open angle and the absence of ocular inflammation, argon laser trabeculoplasty can be attempted to lower the IOP.
  • In patients whom both medical and laser therapy have failed to lower the IOP adequately, surgical therapy is warranted. Usually, trabeculectomy (guarded filtration procedure), with or without intraoperative antimetabolites, is the primary procedure. In cases of eyes with active neovascularization or inflammation, a glaucoma drainage implant may be used as the primary procedure.
• Closed angle: Treat the same as primary acute angle-closure glaucoma.

Consultations

If not able to control IOP, refer the patient to a glaucoma specialist.

Medication

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Bimatoprost (Lumigan) and travoprost (Travatan) are ophthalmic prostaglandin analogs approved for use in the United States. Bimatoprost is a prostamide analog with ocular hypotensive activity. It mimics the IOP-lowering activity of prostamides via the prostamide pathway. Travoprost and bimatoprost are prostaglandin F2-alpha (ie, dinoprost) analogs similar to latanoprost. They are selective FP prostanoid receptor agonists believed to reduce IOP by increasing uveoscleral outflow. They are indicated for the lowering of IOP in patients with open-angle glaucoma or ocular hypertension who are intolerant of other IOP-lowering medications or insufficiently responsive (failed to achieve target IOP determined after multiple measurements over time) to another IOP-lowering medication.

Bimatoprost and travoprost are each administered once daily at bedtime (ie, 1 gtt in affected eye[s] hs); they have not been studied in pediatric patients.

They are contraindicated if hypersensitivity has been documented. No drug interactions have been reported. All are classified as pregnancy category C (ie, fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus).

Like latanoprost, all demonstrate the unusual adverse effect of permanent increase in pigment of the iris (ie, increases brown pigment) and eyelid, and they may increase eyelash growth. Bacterial keratitis may occur. Use is cautioned in uveitis or macular edema. They should not be used if inflammation is present.

Adrenergic agonists

Topical agents (sympathomimetics) decrease aqueous production and reduce resistance to aqueous outflow. Often used with cholinergic agonists like pilocarpine. Adverse effects include dry mouth and allergenicity.

Brimonidine (Alphagan)

Selective alpha2-receptor agonist that reduces aqueous humor formation and possibly increases uveoscleral outflow.

Dosing

Adult

1 gtt OU bid

Pediatric

Not established; serious systemic adverse effects have been reported

Interactions

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

Contraindications

Documented hypersensitivity; patients receiving MAOIs

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in cardiovascular disease, depression, cerebral or coronary insufficiency, orthostatic hypotension, Raynaud syndrome; punctal occlusion may help minimize adverse effects

Apraclonidine (Iopidine) 0.5%, 1%

Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist without significant local anesthetic activity. Has minimal cardiovascular effect.

Dosing

Adult

1 gtt tid

Pediatric

Not established

Interactions

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs

Contraindications

Documented hypersensitivity; patients on MAOIs or have taken them in the past 14 d

Precautions

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 coronary insufficiency, chronic renal failure, recent myocardial infarction, cerebrovascular disease, Raynaud disease, thromboangiitis obliterans, and in patients who are depressed

Beta-blockers

Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects are due to systemic absorption of the drug, decreased cardiac output, and bronchoconstriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Monitor the patient's pulse rate and blood pressure; patients may be instructed to perform punctal occlusion after administering the drops. Depression or anxiety may be experienced in some patients, and sexual dysfunction may be initiated or exacerbated.

Levobunolol (Betagan) 0.25%, 0.5%

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Contraindications

Documented hypersensitivity; bronchial asthma; severe COPD; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock

Precautions

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

Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Timolol (Betimol, Timoptic) 0.25%, 0.5%

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Administer as in adults

Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Contraindications

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe COPD; overt cardiac failure; cardiogenic shock

Precautions

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

Betaxolol (Betoptic) 0.25%, 0.5%

Relatively selective in blocking beta1-adrenergic receptors. Reduces IOP by reducing production of aqueous humor.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Interactions

May have additive systemic effects if patient is already on systemic beta-blockers

Contraindications

Documented hypersensitivity; bronchial asthma; severe COPD; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock

Precautions

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

Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons

Carteolol (Cartrol, Ocupress) 1%

Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic effects.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Administer as in adults

Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Contraindications

Documented hypersensitivity; congestive heart failure; asthma; cardiac conduction defects; breastfeeding

Precautions

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 certain susceptible persons

Metipranolol (OptiPranolol) 0.3%

Beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane stabilizing activity. Has little local anesthetic activity. Reduces IOP by reducing production of aqueous humor.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Interactions

Caution in patients on systemic beta-blockers because added dose may be sufficient to cause systemic adverse effects

Contraindications

Documented hypersensitivity; sinus tachycardia; cardiac failure; cardiogenic shock; second- and third-degree AV block

Precautions

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 diabetes mellitus, bradycardia, asthma, cardiac failure, and AV block

Sympathomimetics

Increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action. Up to one third of patients will not respond to these drugs.

Epinephrine (Epifrin) 0.5%, 1%, 2%

Lower IOP by increasing outflow and reducing production of aqueous humor. Used as adjunct to miotic or beta-blocker therapy. Combination of miotic and sympathomimetic will have additive effects in lowering IOP.

Dosing

Adult

1 gtt in affected eye(s) qd/bid

Pediatric

Not established

Interactions

Increases toxicity of beta- and alpha-blocking agents and halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; narrow- or shallow-angle glaucoma; aphakia

Precautions

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 elderly persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Dipivefrin (AKPro, Propine)

Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.

Dosing

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Interactions

Increased or synergistic effects are seen when used concurrently with agents that lower IOP

Contraindications

Documented hypersensitivity; narrow angles; dilation of pupil may predispose patient to attack of angle-closure glaucoma

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Macular edema occurs in up to 30% of aphakic patients treated with epinephrine; discontinuation of treatment generally results in reversal of maculopathy; caution in vascular hypertension

Carbonic anhydrase inhibitors

Reduce secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. In acute angle-closure glaucoma, administer systemically; apply topically in patients with open-angle glaucoma. These drugs are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects are relatively rare but include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude.

Dorzolamide HCl (Trusopt) 2%

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.
Dorzolamide is a reversible carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably, it slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Systemic absorption can affect carbonic anhydrase in the kidney, reducing hydrogen ion secretion at renal tubule, and increases renal excretion of sodium, potassium bicarbonate, and water.

Dosing

Adult

1 gtt in affected eye(s) tid

Pediatric

Not established

Interactions

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CA inhibitors

Contraindications

Documented hypersensitivity

Precautions

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 (discontinue therapy and evaluate patient before restarting therapy)

Brinzolamide (Azopt) 1%

Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is used, administer drugs at least 10 min apart.

Dosing

Adult

1 gtt in affected eye(s) tid

Pediatric

Not established

Interactions

May have additive systemic effects if patient is already on oral CA inhibitors

Contraindications

Documented hypersensitivity

Precautions

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)

Dorzolamide HCl/timolol maleate (Cosopt)

Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Timolol is nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion.
Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.

Dosing

Adult

1 gtt into affected eye(s) bid; if more than one topical ophthalmic drug is being used, administer at least 10 min apart

Pediatric

Not established

Interactions

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CA inhibitors

Contraindications

Documented hypersensitivity; COPD

Precautions

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); product may have sulfites, which may cause allergic-type reactions in susceptible patients

Miotic agents (parasympathomimetics)

Contract the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of aqueous. Miosis results from the action of these drugs on pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.

Pilocarpine (Pilocar, Pilagan, Pilogel) 1%, 2%, 4%

Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.
Instillation frequency and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths.
If other glaucoma medication also is being used, at bedtime, use drops at least 5 min before gel.

Dosing

Adult

Solution: 1 or 2 gtt tid/qid
Gel: 0.5-inch ribbon in lower conjunctival sac of affected eye(s) hs

Pediatric

Not established

Interactions

May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents

Contraindications

Documented hypersensitivity; acute inflammatory disease of anterior chamber

Precautions

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 acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension

Prostaglandin analogs

Increase uveoscleral outflow of aqueous. One mechanism of action may be through induction of metalloproteinases in the ciliary body, which breakdown the extracellular matrix, reducing resistance to outflow through the ciliary body. They can be used in conjunction with beta-blockers, alpha-agonists, or topical carbonic anhydrase inhibitors. Many patients respond well to these agents; others do not respond at all. Adverse effects include iris pigmentation, cystoid macular edema, and uveitis.

Latanoprost (Xalatan) 0.005%

Decreases IOP by increasing outflow of aqueous humor.

Dosing

Adult

1 gtt (1.5 mcg) in affected eye(s) qhs; higher frequency administrations may decrease effectiveness

Pediatric

Not established

Interactions

Coadministration with eye drops, containing the preservative thimerosal, may reduce effects (administer at intervals of 5 min between applications)

Contraindications

Documented hypersensitivity; CHF; asthma

Precautions

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

Do not administer while wearing contact lenses; may increase brown pigment in iris and change eye color gradually (unknown effect)

Follow-up

Further Outpatient Care

• Open angle
  • It is recommended that all patients who use chronic corticosteroid medications in any capacity should have a full ophthalmologic evaluation.
  • Patients on topical corticosteroid therapy should receive follow-up care at regular intervals by an ophthalmologist to monitor their ocular condition and IOP. Steroid-induced IOP elevation typically occurs within 2-6 weeks of beginning steroid therapy.
  • Upon stopping corticosteroids, the IOP usually normalizes in a few weeks to months. For patients on medical therapy alone, the interval of follow-up care is determined by the extent of the IOP elevation and the degree of optic nerve and visual field damage.
  • Patients who have had surgical intervention should have follow-up care consistent with routine postoperative care for the appropriate procedure.
• Closed angle
  • It is recommended that people older than the 40 years should have routine eye examinations to screen for various conditions. One of these conditions should be the presence of narrow anterior chamber angles.
  • Treat the same as primary acute angle-closure glaucoma.

Inpatient & Outpatient Medications

• See Medication.

Deterrence/Prevention

• Drugs that have the potential of inducing glaucoma should only be used if truly indicated.
• If drugs must be used, IOP should be monitored closely.

Complications

• Untreated glaucoma can lead to permanent visual damage and blindness.

Prognosis

• A favorable outlook exists if IOP is controlled.

Patient Education

• It is recommended that all patients who use chronic corticosteroid medications in any capacity should have a full ophthalmologic evaluation.
• For excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see eMedicine's patient education articles Glaucoma Overview, Glaucoma FAQs, Understanding Glaucoma Medications, and Angle Recession Glaucoma.

Miscellaneous

Medicolegal Pitfalls

• Patients taking drugs that have the potential to increase IOP should have tests to detect this condition and to allow early diagnosis.

References

1. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics. I. The effect of dexamethasone in the normal eye. Arch Ophthalmol. 1963;70:482.

2. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics. II. The effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol. 1963;70:492.

3. Nguyen N, Mora JS, Gaffney MM, et al. A high prevalence of occludable angles in a Vietnamese population. Ophthalmology. Sep 1996;103(9):1426-31. [Medline].

4. Ohji M, Kinoshita S, Ohmi E, et al. Marked intraocular pressure response to instillation of corticosteroids in children. Am J Ophthalmol. Oct 15 1991;112(4):450-4. [Medline].

5. Panday VA, Rhee DJ. Review of sulfonamide-induced acute myopia and acute bilateral angle-closure glaucoma. Compr Ophthalmol Update. Sep-Oct 2007;8(5):271-6. [Medline].

6. Polansky JR. Side effects of ophthalmic therapy with anti-inflammatory steroids. Curr Opin Ophthalmol. 1992;3:259-272.

7. Rhee DJ, Peck RE, Belmont J, et al. Intraocular pressure alterations following intravitreal triamcinolone acetonide. Br J Ophthalmol. Aug 2006;90(8):999-1003. [Medline].

8. Rhee DJ, Ramos-Esteban JC, Nipper KS. Rapid resolution of topiramate-induced angle-closure glaucoma with methylprednisolone and mannitol. Am J Ophthalmol. Jun 2006;141(6):1133-4. [Medline].

9. Wolfs RC, Grobbee DE, Hofman A, et al. Risk of acute angle-closure glaucoma after diagnostic mydriasis in nonselected subjects: the Rotterdam Study. Invest Ophthalmol Vis Sci. Nov 1997;38(12):2683-7. [Medline].

Keywords

drug-induced glaucoma, drug induced glaucoma, steroid-induced glaucoma, open-angle glaucoma, closed-angle glaucoma, acute angle-closure glaucoma, intraocular pressure, IOP, vision loss, visual deficit, blindness

Contributor Information and Disclosures

Author

Douglas J Rhee, MD, Assistant Professor, Department of Ophthalmology, Harvard Medical School; Consulting Staff, Massachusetts Eye and Ear Infirmary
Douglas J Rhee, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Glaucoma Society, American Medical Association, Association for Research in Vision and Ophthalmology, and Phi Beta Kappa
Disclosure: Alcon Honoraria Speaking and teaching; Allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Johnson & Johnson Consulting fee Consulting; Santen Consulting fee Consulting

Coauthor(s)

Steven Gedde, MD, Program Director, Assistant Professor, Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine
Steven Gedde, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Andrew I Rabinowitz, MD, Consulting Staff, Department of Ophthalmology, Barnet Dulaney Perkins Eye Center
Andrew I Rabinowitz, MD is a member of the following medical societies: Aerospace Medical Association, American Academy of Ophthalmology, and American Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)