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Primary Open-Angle Glaucoma Medication

  • Author: Jerald A Bell, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
 
Updated: Feb 20, 2014
 

Medication Summary

Current medical therapy is limited toward lowering IOP. A rational approach to choosing antiglaucoma medications should minimize the number of medications and the probability of significant adverse effects. The ideal drug for treatment of POAG should have the following characteristics: (1) effectively lower IOP, (2) no adverse effects or systemic exacerbation of disease, and (3) inexpensive with once-a-day dosing. However, because no medicine possesses all of the above, these qualities must be prioritized based on the patient's individual needs and risks; then, therapy should be chosen accordingly.

Once a medicine has been initiated, close follow-up care should be performed to assess its effect. Initial follow-up care should be performed 3-4 weeks after the beginning of therapy. IOP should be rechecked at the drug's peak and trough times to see if the target IOP has been reached and is maintained throughout the day. Look for signs of allergy (eg, hyperemia, skin rash, follicular reaction). Inform the patient of systemic adverse effects and symptoms that may occur. Treatment should be continued if a therapeutic trial has shown effective lowering of IOP without adverse effects. Reevaluation should be performed 2-4 months later depending on the clinical picture.

A monocular therapeutic trial should be considered when first initiating the medical therapy, as the other eye's IOP can be used as a baseline control to gauge effect of a medication (particularly useful in patients with a widely fluctuating diurnal curve). A difference of more than 4 mm Hg between the 2 eyes posttreatment is strongly suggestive of a clinical effect. However, some agents (especially beta-blockers) may have crossover effects on the other eye even with monocular treatment, so clinical correlation must be kept in mind. If monocular therapy is found to be effective, then initiation of binocular therapy may be considered.

Some medications (eg, latanoprost, brimonidine) may have an effect that plateaus at 6-8 weeks in certain patients; keep this effect in mind when scheduling further follow-up examinations. Other patients will be nonresponders to some therapies. If this occurs, the medication should be discontinued and a new drug initiated. While discontinuing or changing therapies, keep in mind that many drugs have a wash-out period of up to 2-4 weeks (especially beta-blockers), during which they may still have some IOP-lowering effect or residual systemic response.

If one medication is not adequate in reaching the target pressure, a second medication should be chosen that has a different mechanism of action, so that the 2 drug therapies will have an additive effect. (Usually, no additive effect is seen if 2 medications from the same drug class are used.)

A specific plan of pharmacotherapy should be administered only after the possible effects of the systemic medications that a patient is taking (eg, beta-blockers, calcium channel blockers, ACE inhibitors) have been taken into consideration.

Before mention of particular medications currently used in most practices, note that as the mechanisms of axonal death by apoptosis are becoming better understood, therapies are being developed to protect nerve fibers from undergoing injury and death by several possible theoretical mechanisms. This halting of processes that is believed to contribute to ganglion cell death in glaucoma has been termed neuroprotection, and several new pharmaceuticals are being developed that hopefully will work in this manner. Agents currently under investigation as neuroprotective include glutamate receptor blockers, calcium channel blockers, inhibitors of nitric oxide synthase, free radical scavengers, and drugs to increase blood flow to the optic nerve.

See Ocular Hypertension and AAO monograph #13 for further in-depth descriptions of particular drugs.

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Beta-adrenergic blockers

Class Summary

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. The patient's pulse rate and blood pressure also should be monitored if symptoms emerge after initiation of treatment. Patients may be instructed to perform punctal occlusion after administering the drops to reduce systemic absorption. Depression or anxiety may be experienced in some patients, and sexual dysfunction may be initiated or exacerbated. Ocular adverse effects may include blurred vision, eye ache, and corneal anesthesia.

Levobunolol 0.25%, 0.5% (Betagan)

 

Nonselective beta-adrenergic blocking agents that lower IOP by reducing aqueous humor production.

Timolol maleate/hemihydrate (Timoptic 0.25%, 0.5%; Timoptic XE, Betimol 0.25%, Istalol)

 

Nonselective agents that may reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.

The brands Timoptic XE and Istalol are both administered qd. However, Timoptic XE is a gel-forming solution, while Istalol is an aqueous solution.

Carteolol ophthalmic (Cartrol, Ocupress)

 

Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects.

Betaxolol ophthalmic (Betoptic-S)

 

Beta1-selective adrenergic antagonist, with possibly less pulmonary effects than nonselective agents. IOP-lowering effect is slightly less than nonselective beta-blockers.

Metipranolol hydrochloride (OptiPranolol)

 

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

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Adrenergic agonists

Class Summary

Alpha2-adrenergic agonists work by decreasing aqueous production. Systemic adverse effects include dry mouth, fatigue, and drowsiness. Ocular adverse effects include allergic (follicular) conjunctivitis and contact dermatitis.

Of this class, the alpha2-selective agonist, brimonidine, is used most commonly to treat POAG. Apraclonidine also is alpha2-selective but is believed to have more of an allergic potential; therefore, it is used less commonly as a long-term medication.

Brimonidine (Alphagan-P 0.2%, 0.15%, 0.1%)

 

Lowering of IOP of up to 27% reported. Bid dosing used initially, especially if in combination with other classes of agents. Tid dosing used most often in single-agent therapy that does not adequately control IOP with bid dosing. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine.

The brand Alphagan-P contains the preservative Purite and has been shown to be much better tolerated than its counterpart Alphagan or generic brimonidine.

Apraclonidine 0.5%, 1% (Iopidine)

 

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

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Less-selective sympathomimetics

Class Summary

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

Less-selective adrenergics, such as epinephrine and dipivefrin, also can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, or cystoid macular edema (CME). These less-selective agents are used infrequently.

Dipivefrin (AKPro, Propine)

 

Prodrug 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.

Epinephrine (Epifrin)

 

Lowers 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.

Dipivefrin is 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.

Memantine (Namenda, Axura)

 

Indicated for moderate-to-severe Alzheimer disease; failed initial phase III trial endpoints for glaucoma indication, although subgroup analysis shows possible efficacy for patients with severe visual loss from glaucoma; possible neuroprotective systemic treatment of glaucoma, although as of now, this is a non-FDA approved off-label use of the drug. N-methyl-D-aspartate (NMDA) antagonist. NMDA receptor stimulation in the CNS by glutamate (an excitatory amino acid) is hypothesized to contribute to Alzheimer symptoms, as well as apoptosis (programmed cell death) and neuronal degeneration.

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Carbonic anhydrase inhibitors

Class Summary

Reduce secretion of aqueous humor by inhibiting carbonic anhydrase (CA) 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, anorexia, nausea, depression, dysgeusia, and lassitude.

Oral agents, such as acetazolamide and methazolamide, primarily are used only for the treatment of refractory POAG and secondary glaucomas because they have increased systemic adverse effects. However, oral CAIs can have a slightly greater effect than topical CAI medications and are appropriate to use in certain clinical situations. The mechanism of IOP reduction is similar to other CAIs, being accomplished by reduction of bicarbonate accumulation in the posterior chamber, with a resultant decrease in sodium and associated fluid movement linked to the bicarbonate ion. An additional IOP-lowering effect exists by the creation of a relative metabolic acidosis.

Dorzolamide (Trusopt)

 

More commonly used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer drugs at least 10 min apart. Either drug reversibly inhibits CA, reducing hydrogen ion secretion at renal tubule, and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Brinzolamide (Azopt)

 

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.

May cause less ocular discomfort on instillation, secondary to a buffered pH, but can still cause foreign body sensation.

If more than one topical ophthalmic drug being used, administer drugs at least 10 min apart.

Acetazolamide (Diamox)

 

Reduces rate of aqueous humor formation by direct inhibition of enzyme carbonic anhydrase (CA) on secretory ciliary epithelium, causing in turn a reduction in intraocular pressure (IOP). More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated.

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

Methazolamide (Neptazane)

 

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

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Antiglaucoma, Combos

Class Summary

Combination solution may further decrease aqueous humor secretion compared to each solution used as monotherapy, while improving compliance.

Timolol/brimonidine (Combigan)

 

Brimonidine is a selective alpha2 adrenergic receptor agonist and timolol is a nonselective beta-adrenergic receptor inhibitor. Each of these agents decrease elevated IOP, whether or not associated with glaucoma.

Timolol/dorzolamide (Cosopt)

 

Dorzolamide is a carbonic anhydrase inhibitor that decreases aqueous humor secretion, causing a decrease in IOP. This agent presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport. Timolol is a 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.

Brinzolamide/brimonidine (Simbrinza)

 

This combination product contains the carbonic anhydrase inhibitor brinzolamide and the alpha2 adrenergic receptor agonist brimonidine. It is indicated for reduction of elevated intraocular pressure in patients with primary open-angle glaucoma.

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Prostaglandin analogs

Class Summary

Increase uveoscleral outflow of aqueous. One mechanism of action may be through induction of metalloproteinases in the ciliary body, which breakdown the extracellular matrix, thereby reducing resistance to outflow through the uveoscleral pathway. Can be used in conjunction with beta-blockers, alpha-agonists, or topical CAIs. Many patients respond well to these agents; other patients do not respond at all. Adverse effects include conjunctival hyperemia, iris pigmentation, CME, and uveitis.

Latanoprost 0.005% (Xalatan)

 

Decreases IOP by increasing outflow of aqueous humor through uveoscleral pathways.

Bimatoprost (Lumigan)

 

Prostaglandin agonist that selectively mimics effects of naturally occurring substances, prostamides. Exact mechanism of action unknown but believed to reduce IOP by increasing outflow of aqueous humor through trabecular meshwork and uveoscleral routes. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthamic solution (Travatan)

 

Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.

Unoprostone (Rescula)

 

Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.

Tafluprost (Zioptan)

 

Tafluprost is a preservative-free, topical, ophthalmic prostaglandin analog indicated for elevated IOP associated with open-angle glaucoma or ocular hypertension. The exact mechanism by which it reduces IOP is unknown, but it is thought to increase uveoscleral outflow.

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Miotic agents (parasympathomimetics)

Class Summary

Miotics work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of aqueous through traditional pathways. Miosis results from action of these drugs on the pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light. These agents are used less commonly today since the advent of newer drugs with fewer adverse effects.

Pilocarpine is one of the more commonly used agents in this class. Less frequently used miotics include phospholine iodide (0.03%, 0.06%, 0.125%, 0.25% qd/bid) and carbachol (0.75%, 1.5%, 3% tid/qid).

Pilocarpine ophthalmic (Pilocar, Pilagan, Pilogel, Ocusert)

 

A naturally occurring alkaloid, pilocarpine mimics the muscarinic effects of acetylcholine at postganglionic parasympathetic nerves. 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 gtt at least 5 min before gel.

Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields occurs.

May use alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, CAIs, or hyperosmotic agents to decrease IOP. Use with prostaglandin analogs can have a small additive effect.

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Hyperosmotic agents

Class Summary

These agents are used infrequently, most commonly to reduce extremely elevated IOP in acute situations of angle-closure or certain secondary glaucomas, or selectively as a preoperative measure before intraocular surgery.

Osmotics lower IOP by increasing the osmotic gradient between the blood and ocular fluids, resulting in loss of water from the eye (especially the vitreous) into the hyperosmotic blood plasma, with concomitant lowering of IOP, but an increase in intravascular volume. Therefore, care should be used in any patient with cardiac, renal, or hepatic abnormalities.

Systemic adverse effects include nausea, vomiting, headache, increased thirst, chills, fever, confusion or disorientation, electrolyte imbalances, and urinary retention.

Isosorbide dinitrate (Ismotic)

 

In the eyes, may create an osmotic gradient between plasma and ocular fluids and induce diuresis by elevating osmolarity of glomerular filtrate. Effects may, in turn, inhibit tubular reabsorption of water. Treatment is preferred when less risk of nausea and vomiting than that posed by other oral hyperosmotic agents desired. Palatability best if poured over ice before ingestion. May use in patients with diabetes.

Mannitol (Osmitrol, Resectisol)

 

Reduces elevated IOP when the pressure cannot be lowered by other means.

Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.

In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.

The 20% w/v solution most commonly is used IV. Alternatively, concentrations of 10%, 15%, or 25% may be used.

Glycerin (Ophthalgan, Osmoglyn)

 

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h.

Used for diagnostics. Facilitates ophthalmoscopic and gonioscopic examination in acute glaucoma. Used only for topical application to cornea. By virtue of osmotic action (attraction of water through the semipermeable corneal epithelium), promptly reduces edema and causes clearing of corneal haze. Action is transient and therefore used primarily for diagnostic purposes.

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Contributor Information and Disclosures
Author

Jerald A Bell, MD Staff Physician, Department of Ophthalmology, Billings Clinic

Jerald A Bell, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Inci Irak Dersu, MD, MPH Associate Professor of Clinical Ophthalmology, State University of New York Downstate College of Medicine; Attending Physician, SUNY Downstate Medical Center, Kings County Hospital, and VA Harbor Health Care System

Inci Irak Dersu, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Additional Contributors

Neil T Choplin, MD Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences

Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society, California Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors, Robert J Noecker, MD, and Emily Patterson, MD, to the development and writing of this article.

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Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields, MD.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, field loss among individuals with pressures in the upper teens can occur. Also, note that the average pressure among those with glaucomas is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.
Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally shaded lines) and/or damage from glaucoma (vertically shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are also those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). Courtesy of M. Bruce Shields, MD.OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines
Humphrey visual field, right eye, showing patient with advanced glaucomatous field loss. Notice both the arcuate extension from the blind spot (Bjerrum scotoma) and the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields, MD.
Illustration of progressive optic nerve damage. Notice the deepening (saucerization) along the neural rim, along with notching and increased excavation/sloping of the optic nerve and circumlinear vessel inferiorly. Courtesy of M. Bruce Shields, MD.
Example of progressive visual field loss over time (from top to bottom) in a patient with glaucoma. Notice the early appearance of an inferior nasal step and arcuate loss, with progressive enlargement and increasing density of the scotomata over time. Courtesy of M. Bruce Shields, MD.
Optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly (similar to Image 5). Courtesy of M. Bruce Shields, MD.
Glaucomatous optic nerve damage, with sloping and nerve fiber layer rim hemorrhage at the 7-o'clock position. Hemorrhage is indicative of progressive damage, usually due to inadequate pressure control. Further notching and pallor corresponding to the area of hemorrhage usually is seen several weeks after resorption of the blood. Courtesy of M. Bruce Shields, MD.
Correction values according to corneal thickness.
Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).
Intraocular pressure measurements. Adapted from Reichert Ophthalmic Instruments, Ocular Response Analyzer, How does it work Web page.
 
 
 
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