Nearly all glaucoma medications are prescribed for reducing eye pressure.
Topical beta adrenoceptor blockers (commonly called beta-blockers) are the drugs most often prescribed to treat glaucoma. They lower the pressure inside the eye by inhibiting the production of aqueous humor.
Brands. These drugs are categorized as either nonselective or selective beta-blockers:
All beta-blockers work well and generally well tolerated. Because they cause less eye irritation than many other glaucoma medications, they are often prescribed for patients who also have cataracts.
Side Effects and Complications. After the beta-blocker is administered, only a tiny amount of the drug is absorbed by the cornea. Most of it enters in the bloodstream. These drugs, therefore, can cause side effects in parts of the body other than the eyes ("systemic" side effects):
Interactions with Other Medications. The effects of the eye medication can interact with other oral medications, such as oral beta-blockers, calcium-channel blockers, or the antiarrhythmic drug quinidine. People with diabetes who take insulin or hypoglycemic medications should realize that beta-blocker side effects may mask the symptoms of hypoglycemia (low blood sugar).
Prostaglandins are hormone-like substances that help open blood vessels. Drugs that resemble prostaglandins increase outflow of aqueous humor (the watery substance in the eye). Drainage of aqueous humor helps reduce intraocular pressure.
Brands. Latanoprost (Xalatan) and unoprostone (Rescula) are the standard brands. Latanoprost was the first prostaglandin to be approved as first-line treatment for elevated eye pressure. Two newer prostaglandins, travoprost (Travatan) and bimatoprost (Lumigan), may help some patients who do not respond to latanoprost. These drugs may also benefit patients with normal-tension glaucoma.
Side Effects. These drugs do not slow down the heart rate and also appear to be safe for people with asthma. Side effects include itching, redness, and burning during administration. Muscle and joint pain may also occur. All of these drugs may permanently change eye color from blue or green to brown.
Carbonic anhydrase inhibitors (CAIs) decrease eye pressure by reducing the fluid in the chambers of the eye (aqueous humor). These drugs are used for glaucoma when other drugs do not work. They may be combined with other medications.
CAIs may also improve blood flow in the retina and optic nerve (beta-blockers do not). Improving blood flow can keep the disease from getting worse.
Brands and Side Effects. CAIs are available in the following forms:
Adrenergic agonists activate muscles in the eye that dilate pupils and, therefore, increase outflow of aqueous fluid. Newer variations called alpha 2-adrenergic agonists reduce production of aqueous humor and also increase outflow through the uveoscleral pathway (the alternative channel to the trabecular meshwork).
Apraclonidine (Iopidine) and brimonidine (Alphagan) are alpha 2-adrenergic agonists. These are generally been used before glaucoma surgery, but may be useful as primary therapy when used in combination with beta-blockers or other standard drugs.
Brimonidine is proving to be particularly effective for long-term therapy. (Apraclonidine is used for the short term.) It also may have nerve-protecting properties and may be safer than other drugs during pregnancy and for patients with asthma.
The most common side effects of brimonidine and apraclonidine are dry mouth and altered taste. They also commonly trigger an allergic reaction that causes red and itching eyes and lids,. Brimonidine causes less of an allergic response than apraclonidine. Unlike apraclonidine, however, it can cause lethargy and mild low blood pressure.
Miotics, also called cholinergic agonists, narrow the iris muscles and constrict the pupil. This action pulls the iris away from the trabecular meshwork and allows the aqueous humor to flow out through the drainage channels, reducing the pressure inside the front of the eye.
Brands. Pilocarpine (Pilocar, Adsorbocarpine, Almocarpine, Isoptocarpine, Ocusert) was the most widely used anti-glaucoma drug before timolol was introduced. It is the preferred miotic. Because pilocarpine is used up by the body fairly quickly, however, patients must take it several times a day; many people, therefore, fail to take their medication regularly. A combination of timolol or latanoprost with pilocarpine is more effective than either drug used alone. Carbachol is another miotic.
Epinephrine and its derivatives are the older anticholinergics. Epinephrine is now rarely prescribed because of side effects. Dipivefrin (Dipivefrin), a newer form of epinephrine, remains inactive until it reacts with enzymes in the cornea. It is effective in low doses and causes few systemic side effects.
Side Effects. Side effects include:
Studies indicate that many patients skip doses of their glaucoma medications, sometimes because of side effects and sometimes because of confusing or time-consuming regimens. Skipping even a few doses can greatly increase the risk of visual loss. It is essential that patients tell their doctor if they are not regularly taking their medication. Otherwise, the doctor may increase the dosage, thereby causing unwelcome side effects.
Patients who do not regularly take their glaucoma medication are at high risk for blindness. If you have problems taking your medications or sticking to the dosing regimen, talk with your doctor.
Hints for Managing a Regimen.
Administering Eye Drops. A common reason that medicine does not work is that patients do not take it correctly. Patients should ask the ophthalmologist to watch while they place the drops in their own eyes to make sure the procedure is being done correctly. The following are some recommended steps:
Acute closed-angle glaucoma is an emergency situation. Doctors may administer a combination of two or more anti-glaucoma medications to reduce eye pressure quickly before it can damage the optic nerve and cause visual loss. Apraclonidine (Iopidine) is a powerful drug used before and after laser surgery to prevent an increase in fluid pressure and is more effective than other medications. In addition to standard drugs, doctors may also administer glycerin (Glyrol, Osmoglyn) by mouth or mannitol or acetazolamide intravenously. Surgery is almost always performed once the pressure is reduced.
Aptel F, Cucherat M, Denis P. Efficacy and tolerability of prostaglandin analogs: a meta-analysis of randomized controlled clinical trials. J Glaucoma. 2008 Dec;17(8):667-73.
Burr JM, Mowatt G, HernĂˇndez R, Siddiqui MA, Cook J, Lourenco T, et al. The clinical effectiveness and cost-effectiveness of screening for open angle glaucoma: a systematic review and economic evaluation. Health Technol Assess. 2007 Oct;11(41):iii-iv, ix-x, 1-190.
Chang R, Budenz DL. New developments in optical coherence tomography for glaucoma. Curr Opin Ophthalmol. 2008 Mar;19(2):127-35.
Cheng JW, Wei RL, Cai JP, Li Y. Efficacy and tolerability of nonpenetrating filtering surgery with and without implant in treatment of open angle glaucoma: a quantitative evaluation of the evidence. J Glaucoma. 2009 Mar;18(3):233-7.
Dueker DK, Singh K, Lin SC, Fechtner RD, Minckler DS, Samples JR, et al. Corneal thickness measurement in the management of primary open-angle glaucoma: a report by the American Academy of Ophthalmology. Ophthalmology. 2007 Sep;114(9):1779-87.
Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL. Treatment outcomes in the tube versus trabeculectomy study after one year of follow-up. Am J Ophthalmol. 2007 Jan;143(1):9-22.
Hatt S, Wormald R, Burr J. Screening for prevention of optic nerve damage due to chronic open angle glaucoma. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD006129.
HernĂˇndez R, Rabindranath K, Fraser C, Vale L, Blanco AA, Burr JM; OAG Screening Project Group. Screening for open angle glaucoma: systematic review of cost-effectiveness studies. J Glaucoma. 2008 Apr-May;17(3):159-68.
Higginbotham EJ. Managing glaucoma during pregnancy. JAMA. 2006 Sep 13;296(10):1284-5.
Hodge WG, Lachaine J, Steffensen I, Murray C, Barnes D, Foerster V, et al. The efficacy and harm of prostaglandin analogues for IOP reduction in glaucoma patients compared to dorzolamide and brimonidine: a systematic review. Br J Ophthalmol. 2008 Jan;92(1):7-12.
Kwon YH, Fingert JH, Kuehn MH, Alward WL. Primary open-angle glaucoma. N Engl J Med. 2009 Mar 12;360(11):1113-24.
Lam DS, Tham CC, Lai JS, Leung DY. Current approaches to the management of acute primary angle closure. Curr Opin Ophthalmol. 2007 Mar;18(2):146-51.
Lemij HG, Reus NJ. New developments in scanning laser polarimetry for glaucoma. Curr Opin Ophthalmol. 2008 Mar;19(2):136-40.
Leske MC, Heijl A, Hyman L, Bengtsson B, Dong L, Yang Z; EMGT Group. Predictors of long-term progression in the early manifest glaucoma trial. Ophthalmology. 2007 Nov;114(11):1965-72. Epub 2007 Jul 12.
Rivera JL, Bell NP, Feldman RM. Risk factors for primary open angle glaucoma progression: what we know and what we need to know. Curr Opin Ophthalmol. 2008 Mar;19(2):102-6.
Rolim de Moura C, Paranhos A Jr, Wormald R. Laser trabeculoplasty for open angle glaucoma. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003919.
Rosenberg EA, Sperazza LC. The visually impaired patient. Am Fam Physician. 2008 May 15;77(10):1431-6.
Stewart WC, Konstas AG, Nelson LA, Kruft B. Meta-analysis of 24-hour intraocular pressure studies evaluating the efficacy of glaucoma medicines. Ophthalmology. 2008 Jul;115(7):1117-1122.e1. Epub 2008 Feb 20.
Vass C, Hirn C, Sycha T, Findl O, Bauer P, Schmetterer L. Medical interventions for primary open angle glaucoma and ocular hypertension. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003167.
Wishart MS, Dagres E. Seven-year follow-up of combined cataract extraction and viscocanalostomy. J Cataract Refract Surg. 2006 Dec;32(12):2043-9.
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