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Dr. Grandinetti is a senior clinical research pharmacist at the National Cancer Institute, National Institutes of Health, Rockville, Maryland. The views expressed are those of the author and not those of any government agency.

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The World Health Organization estimates that 37 million people are blind, with almost 82% of them aged 50 years or older.^1,2 Cataract causes almost half of blindness globally and occurs more frequently in developing countries.³ Women are at a slightly greater risk than men, with an estimated female-to-male ratio of 1.5 to 2.2.

Cloudy or opaque cataracts on the lens of the eye are generally caused by a denaturing of crystallins, the major lens protein.⁴ In cataracts, less light reaches the retina, impairing vision and decreasing quality of life. Three subtypes, defined by clinical appearance and location, are nuclear, cortical, and posterior subcapsular (PSC) cataracts. Each has different symptoms and risk factors and occurs at different rates in different populations.^1,5-10

The most common cause is aging, but atopic diseases and their treatments, diabetes, trauma, and congenital disorders can cause cataracts, too. Some drugs, such as those causing photosensitivity, and radiation therapy are associated with cataract formation.¹¹ Several studies have associated long-term corticosteroid use (at prednisone doses of ≥10-15 mg/day) with PSC formation.^12-16 This association is stronger with oral steroids than with inhaled steroid use, and children appear to be particularly at risk.⁷ Cataracts may progress even after stopping the corticosteroid. Clinicians should order comprehensive eye exams more frequently in individuals with predisposing risk factors.

Table

At Surgery

Surgery is the only treatment option and should be considered when the cataract impairs the patient's ability to function in daily life.¹⁷ Cataract surgery has a 95% or better success rate in healthy eyes. It involves removing the lens and replacing it with an intraocular lens. During surgery, adequate pupil dilation must be maintained to remove the crystalline lens and implant the corrective intraocular lens without causing trauma to the iris. Prostaglandin release can cause surgically induced miosis and increase the risk of postoperative surgical complications.

Alpha₁ adrenoceptor blockers can increase the likelihood of surgical complications by causing the pupil to suddenly constrict during the operation.⁵ Discontinuing the drug before surgery has not yet been evaluated; however, planned measures, such as iris hooks, iris dilator rings, or viscoelastic devices, can minimize the potential complications.¹⁸ Topical nonsteroidal anti-inflammatory drugs (NSAIDs) are often used to inhibit surgically induced miosis.¹⁹

Table

After Surgery

Although postsurgical complications are infrequent, patients are often started on topical antibiotic, corticosteroid, and NSAID drops to prevent complications.^9,17

Early diagnosis and treatment of endophthalmitis, a serious eye infection, is critical to prevent vision loss. Empiric therapy is based on the suspected microorganism most likely encountered during surgery, from the patient's conjunctiva, eyelids, or nose. The most common microorganisms are gram-positive Staphylococcus aureus and Staphylococcus epidermidis. Gram-negative infections with Pseudomonas spp and Propionbacterium acnes occur less frequently. The treatment includes intravitreal injections of vancomycin and ceftazidime or amikacin (for patients sensitive to beta lactams). Another treatment option is broad-spectrum oral fourth generation fluoroquinolones. The patients are often treated prophylactically before surgery with topical povidoneiodine or topical, subconjunctival, systemic, or intracameral antibiotics.^20,21

Cystoid macular edema (CME), fluid accumulation in the central retina, is the most frequent cause of vision loss. It usually occurs 4 to 6 weeks after surgery, and symptoms include blurred or declining central vision and painless retinal inflammation and swelling. Vision loss is usually temporary. Clinicians should suspect CME in any patient with worse-than-expected vision after surgery.¹⁹ Most patients experience some postoperative inflammation. If left untreated, inflammation may cause discomfort, delay recovery, decrease vision, and lead to other complications.²²

Combination therapy with a topical NSAID and/or corticosteroid is indicated for documented CME and inflammation. CME treatment starts 1 week before surgery and continues for at least 4 weeks, up to several months after surgery. When treating inflammation, NSAIDs are generally started 24 hours after surgery and continued for up to 14 days (Table). Topical steroids are generally administered for 2 to 6 weeks after surgery.^19,22

Most adverse events following topical NSAIDs are local, such as burning, stinging, conjunctivitis, atonic mydriasis, and local anesthetic effects, as well as pruritus, erythema, and edema of the bulbar conjunctiva and lids. Systemic reactions occur rarely. Increased intraocular pressure and delayed wound healing are associated with topical corticosteroids. NSAIDs are useful alternatives for patients who develop increased intraocular pressure while using topical steroids.¹⁹

Pharmacists treating cataract patients should use their clinical expertise to monitor appropriate medication use—especially nursing and patient adherence to the medication regimen—and promote appropriate follow-up care and routine eye examinations.

References

1. Abraham AG, Condon NG, West Gower E. The new epidemiology of cataract. Ophthalmol Clin North Am. 2006;19:415-425.
2. Resnikoff S, Pascolini D, Etya'ale D, et al. Global data on visual impairment in the year 2002. Bull World Health Organ. 2004;82:844-851.
3. Foster A, Resnikoff S. The impact of Vision 2020 on global blindness. Eye. 2005;19:1133-1135.
4. Andley UP. Crystallins in the eye: Function and pathology. Prog Retin Eye Res. 2007;26:78-98.
5. Allen D, Vasavada A. Cataract and surgery for cataract. BMJ. 2006;333:128-132.
6. Asbell PA, Dualan I, Mindel J, Brocks D, Ahmad M, Epstein S. Age-related cataract. Lancet. 2005;365:599-609.
7. Urban RC, Jr., Cotlier E. Corticosteroid-induced cataracts. Surv Ophthalmol. 1986;31:102-110.
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10. Kelly SP, Thornton J, Edwards R, Sahu A, Harrison R. Smoking and cataract: review of causal association. J Cataract Refract Surg. 2005;31:2395-2404.
11. Abel SR, Sorensen SJ. Eye Disorders. In: Koda-Kimble MA, Young LY, Kradjen WA, Gugliemo BJ, Alldredge BK, eds. Applied Therapeutics: The Clinical Use of Drugs. 8th Edition. Pennsylvania: Lippincott Williams and Wilkins; 2005:51-13-51-16.
12. Szefler SJ, Lyzell E, Fitzpatrick S, Cruz-Rivera M. Safety profile of budesonide inhalation suspension in the pediatric population: worldwide experience. Ann Allergy Asthma Immunol. 2004;93:83-90.
13. Walsh LJ, Wong CA, Oborne J, et al. Adverse effects of oral corticosteroids in relation to dose in patients with lung disease. Thorax. 2001;56:279-284.
14. Li JT, Ford LB, Chervinsky P, et al. Fluticasone propionate powder and lack of clinically significant effects on hypothalamic-pituitary-adrenal axis and bone mineral density over 2 years in adults with mild asthma. J Allergy Clin Immunol. 1999;103:1062-1068.
15. Dasgupta B, Dolan AL, Panayi GS, Fernandes L. An initially double-blind controlled 96 week trial of depot methylprednisolone against oral prednisolone in the treatment of polymyalgia rheumatica. Br J Rheumatol. 1998;37:189-195.
16. Simons FE, Persaud MP, Gillespie CA, Cheang M, Shuckett EP. Absence of posterior subcapsular cataracts in young patients treated with inhaled glucocorticoids. Lancet. 1993;342:776-778.
17. Solomon R, Donnenfeld ED. Recent advances and future frontiers in treating age-related cataracts. JAMA. 2003; 290:248-251.
18. Manvikar S, Allen D. Cataract surgery management in patients taking tamsulosin staged approach. J Cataract Refract Surg. 2006;32:1611-1614.
19. Colin J. The role of NSAIDs in the management of postoperative ophthalmic inflammation. Drugs. 2007;67:1291-1308.
20. Kim JY, Ali R, Cremers SL, Henderson BA. Perioperative prophylaxis for postcataract extraction endophthalmitis. Int Ophthalmol Clin. 2007;47:1-14.
21. Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina. 2007;27:662-680.
22. McColgin AZ, Heier JS. Control of intraocular inflammation associated with cataract surgery. Curr Opin Ophthalmol. February 2000;11:3-6.