Aphakic and Pseudophakic Glaucoma Medication

  • Author: Robert H Graham, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 15, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Beta-adrenergic blockers

Class Summary

The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous humor production or inhibition of inflow.

Timolol ophthalmic (Timoptic, Timoptic XE, Blocadren)

 

May reduce elevated and normal IOP, with or without glaucoma, possibly by inhibiting inflow.

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Alpha-adrenergic agonists

Class Summary

Decrease IOP possibly by reducing aqueous humor production.

Apraclonidine (Iopidine)

 

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

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Cholinergic agents

Class Summary

Stimulate muscarinic receptors, causing miosis in the eye and may reduce aqueous humor outflow.

Pilocarpine gel (Pilopine HS)

 

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.

Patients may be maintained on pilocarpine as long as IOP is controlled and there is no deterioration in visual fields. May use alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.

Carbachol (Carbastat, Carboptic, Isopto Carbachol)

 

Direct acting cholinergic agent that lowers IOP.

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Carbonic anhydrase inhibitors

Class Summary

Carbonic anhydrase (CA) 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 CA in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Acetazolamide (Diamox, Diamox Sequels)

 

Inhibits enzyme CA, 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.

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Prostaglandin analogs

Class Summary

Increase uveoscleral outflow of the aqueous. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through ciliary body.

Latanoprost (Xalatan) 0.005%

 

Decreases IOP by increasing outflow of aqueous humor.

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 (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.

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Contributor Information and Disclosures
Author

Robert H Graham, MD  Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona

Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Arizona Ophthalmological Society

Disclosure: WebMD/eMedicine Salary Employment

Specialty Editor Board

Bradford Shingleton, MD  Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

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.

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: Nothing to disclose.

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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors, Sai Gandham, MD, and DooHo Brian Kim, BA, to the development and writing of this article.

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