Keeping patients educated and adherent to treatment can help prevent further vision loss due to glaucoma.
Glaucoma is the leading cause of blindness. 1 Pathophysiology involves increases in intraocular fluid (aqueous humor), often caused by 1 or more factors preventing eye fluid drainage. Normal intraocular pressure (IOP) ranges from 12 to 22 mm Hg. IOP higher than 22 mm Hg increases risk for optic nerve fiber damage, leading to irreversible vision loss and blindness. Glaucoma can occur, however, in patients with normal eye pressure.2 Additional statistics about glaucoma and its prevalence are presented in Table 13-5.
Initial vision loss is often subtle; peripheral vision is affected first, and is followed by central vision loss. Up to 40% of retinal nerve fibers may be destroyed before patients detect visual loss and seek treatment.2,3 When both eyes are affected, disease progression is not symmetrical.
Glaucoma is a class of diseases with various subtypes. Open-angle glaucoma (OAG) and angle-closure glaucoma (ACG) are the most common. These subtypes are further classified as primary (stemming from physiological eye dysfunction) or secondary (stemming from another condition, such as steroidinduced glaucoma, infections, uveitis, or diabetic neuropathy).
In normal eyes, the aqueous humor flows through an opening where the iris and pupil meet, and drains through tiny channels called the trabecular meshwork. After exiting the trabecular meshwork, the aqueous fluid drains into capillaries and into the bloodstream.1 In OAG (the most common), the trabecular meshwork, although open, becomes partially blocked, resulting in slower drainage and increased IOP. Increased IOP in OAG is asymptomatic.
In ACG, the iris bulges forward, completely blocking the drainage angle and preventing aqueous humor from draining into the trabecular meshwork. Onset is rapid, and acute ACG symptoms include severe eye pain, headache, nausea, vomiting, and visual blurring.1 ACG is common in Asians; approximately 91% of bilateral blindness in China is linked to ACG.3 ACG is considered a medical emergency requiring immediate treatment.
Glaucoma has no cure; treatment focuses on preventing further vision loss. Reducing IOP to prevent further optic nerve damage is the primary goal of treatment. Even with early intervention, approximately 10% of patients still experience additional vision loss.4
Therapeutic options include betablockers, prostaglandins, carbonic anhydrase inhibitors, adrenergic agonists, and miotics. Some agents have serious side effects and are contraindicated with medications used for common conditions (eg, decongestants; see package inserts for contraindications with other agents). Further complicating treatment decisions, many patients require more than 1 agent to achieve optimal IOP. Frequently used combination therapies include brimonidine and timolol, latanoprost and timolol, and dorzolomide and timolol.6,7
Surgical options are second-line treatments when medication fails to reduce IOP. Trabeculectomy is the most common procedure, during which surgeons remove a small piece of the trabecular meshwork and create a new opening for drainage. Other surgical options include laser trabeculoplasty (laser is used to open channels), laser cycloablation (cilliary that produces aqueous humor is destroyed), insertion of aqueous shunt devices, and viscocanalostomy (a superficial sclera flap is created).8 Evidence is lacking demonstrating the superiority of any 1 procedure.9 Following corrective surgery, 50% of patients require medication within 2 years.5
Counseling begins with reviewing the basics; 16% of African Americans and 9% of Caucasians are unfamiliar with glaucoma.4 Up to 50% of the population indicate they have heard of glaucoma, but are not sure of its meaning.4 Table 25,10-13 provides additional points to consider when counseling patients with glaucoma.
Early detection and intervention are the most effective strategies for preventing blindness.3 Toward that objective, pharmacists should take every opportunity for improving public awareness. PT
Table 3. Risk Factors for Glaucoma
· Age (older than 60 years)
· Glaucoma damage in one eye increases risk for damage in the other eye
· Family history of glaucoma
· Ethnic background (eg, African American)
· Severe eye injury
· Prolonged steroid use
· Central corneal thickness less than 0.5 mm
Adapted from references 6 and 7.
Table 4. Agents Frequently Used for Glaucoma Treatment
Topical Non-Selective Beta-Blockers/Agents
· Lower IOPby inhibiting production of aqueous humor
· Standard first-line treatment
· Side effects include irregular heartbeat, depression, impotence, breathing difficulties, fatigue
· Have fewer side effects
· Appear to have nerve-protecting properties
· Increase outflow of aqueous humor
· Used when beta-blockers fail
· Side effects include itching, redness and burning during administration, increased eyelash thickness, joint aches, and flu-like symptoms
· All agents may permanently change eye color from blue or green to brown
Carbonic Anhydrase Inhibitors
· Reduce production of aqueous humor
· Considered second-line treatment, less effective than beta-blockers or prostaglandins, but have fewer side effects
· Oral forms are more effective, but side effects are more severe (frequent urination, depression, stomach problems, fatigue, weight loss)
· Activate muscles that dilate pupils, increasing outflow of fluid
· Brimonidine is particularly effective for long-term use, but is linked to lethargy and mild low blood pressure, 12% risk for allergic reaction
· Side effects for both agents include dry mouth and altered taste
Miotics (Cholinergic Agonists)
· Narrow the iris muscles and constricts the pupil, pulling the iris away from the trabecular meshwork
· Considered standard drug therapy before introduction of newer agents
· Pilocarpine is the preferred miotic, but drops must be applied several times daily
· Can cause nearsightedness, teary eyes, eye pain, and increased risk for cataracts
Adapted from references 1, 5, 8, and 9.
Dr. Zanni is a psychologist and health systems consultant based in Alexandria, Virginia.
1. Andrew DA. Glaucoma. www.medicinenet.com/glaucoma/article.htm. Accessed November 14, 2011.
2. Pan Y, Varma R. Natural history of glaucoma. Indian J Ophthalmol. 2011;59(suppl):S19-S23.
3. Glaucoma Research Foundation. Glaucoma facts and stats. www.glaucoma.org/glaucoma/facts-statistics/glaucoma-facts-and-stats.php. Accessed November 14, 2011.
4. University of Maryland Medical Center. Glaucoma treatment. www.umm.edu/patiented/articles/what_general_guidelines_treating_glaucoma_000025_7.htm. Accessed November 14, 2011.
5. Tsai J. High eye pressure and glaucoma. www.glaucoma.org/gleams/high-eye-pressure-and-glaucoma.php. Accessed November 26, 2011.
6. Agency for Healthcare Research and Quality. National Guideline Clearinghouse. Primary open-angle glaucoma. www.guideline.gov/content.aspx?id=24811. Accessed November 25, 2011.
7. Mayo Clinic Staff. Glaucoma. www.mayoclinic.com/health/glaucoma/DS00283. Accessed November 14, 2011.
8. University of Maryland Medical Center. Glaucoma medications. www.umm.edu/patiented/articles/what_drug_treatments_glaucoma_000025_8.htm. Accessed November 14, 2011.
9. American Health Assistance Foundation. Common glaucoma treatments. www.ahaf.org/glaucoma/treatment/common/. Accessed November 14, 2011.
10. Glaucoma Research Foundation. Medication guide. www.glaucoma.org/treatment/medication-guide.php. Accessed November 14, 2011.
11. Clement CI, Goldberg I. The management of complicated glaucoma. Indian J
12. Sharaawy T, Bhartiya S. Surgical management of glaucoma: evolving paradigms.
Indian J Ophthalmol.2011;59(suppl):S123-S130.
13. Hoyle B. Medication compliance in glaucoma patients varies. www.medscape.com/viewarticle/752251. Accessed November 14, 2011.
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