Healio
Healio
April 01, 2007
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Evolution of NSAIDs in CME prevention

Nonsteroidal anti-inflammatory drugs are helpful in preventing cystoid macular edema. Cystoid macular edema is the leading cause of poor vision after routine, uncomplicated cataract surgery.

Patients experience a decrease in vision more commonly as a result of cystoid macular edema than endophthalmitis. Although improved surgical techniques have resulted in subtler cases of CME, CME remains a concern.

Diagnosing CME

Ophthalmologists examine quality of vision and contrast sensitivity in addition to Snellen visual acuity to define CME as the cause of vision loss after cataract surgery. Originally detected by performing angiography, CME is now detectable by optical coherence tomography (OCT), because it allows for examination of cross-sections of the retina. OCT examinations of patients with uveitis and patients following cataract extraction who develop macular thickening showed that subtler cases of CME are better defined by ultrahigh resolution OCT because it displays detail of the retinal architecture (Figure). Fundus examinations are also effective in diagnosing CME. 1

Figure

Figure: Ultrahigh Resolution OCT helps define subtler cases of CME
Ultrahigh resolution OCT helps define subtler cases of CME.

Images: Raizman, MB

Incidence of CME

With extracapsular techniques, the incidence of CME may be as high as 30%. With cornea phacoemulsification, the incidence is between 0.2% and 12%. In patients with diabetes who undergo phacoemulsification, the incidence of CME is as high as 32%. Of patients with diabetes with a history of diabetic retinopathy, 16% to 52% were shown to have increased thickening of the retina in at least one study. CME can result from trauma in the eye as well as complicated cataract surgery with a broken capsule, retained lens fragments and IOLs in a poor position. However, CME can also occur after perfect surgery. 1

Risk factors for CME include preexisting ocular inflammation, epiretinal or vitreoretinal interface membrane complications, diabetic retinopathy, ocular vascular disease, cardiovascular disease and history of retinitis pigmentosa.1

NSAIDs to treat CME

Most ophthalmologists use NSAIDs for prophylaxis in every cataract surgery because they are effective in preventing postoperative CME and improve vision function.2 One percent of patients who develop CME after cataract surgery will never attain improved vision despite therapy. Thus, postoperative treatment of CME is not always effective.

Most ophthalmologists use NSAIDs for prophylaxis in every cataract surgery because they are effective in preventing postoperative CME and improve vision function.

— Michael B. Raizman, MD

NSAIDs should be used with corticosteroids to allow for optimum control of inflammation.2 Furthermore, NSAIDs inhibit prostaglandins, which increase ocular vascular permeability, resulting in inflammation, miosis and pain.3 Prostaglandins are released in the anterior portion of the eye and diffuse to the posterior portion of the eye. NSAID prophylaxis prevents intraoperative miosis during cataract surgery, manages postoperative inflammation, prevents and treats CME following cataract surgery and reduces pain and discomfort following cataract and refractive surgery.3-9

NSAIDs meet patient expectations

More than 8 years ago I performed a study showing that NSAIDs should be used routinely in cataract surgery.10 I examined a group of patients undergoing cataract surgery who had no risk factors for CME. All patients received diclofenac sodium ophthalmic solution 0.1% for 2 days before surgery and just before surgery. Then half of the patients received diclofenac and corticosteroids, whereas the other half received only corticosteroids. Twelve percent of the patients who received only corticosteroids developed CME, compared with none of the patients who received diclofenac and corticosteroids.

Recommended NSAID dosing for patients at risk for CME is 1 week before surgery and 4 weeks to several months after surgery. Recommended NSAID dosing for patients not at risk is 1 to 3 days before surgery and 4 weeks after surgery. 11

OCT is effective in detecting subtle cases of CME. One of the patients in this study had 20/25 vision after cataract surgery. After a fundus examination failed to yield definitive information, I examined the patient with OCT. In the past, 20/25 vision was considered an excellent result after cataract surgery. However, the OCT examination showed thickening in the fovea and blunting of the typical foveal pit. This type of subtle macular thickening is clinically significant and common in patients. It is important to recognize that a patient can have 20/20 vision and have clinical CME. I treated a patient with 20/20 vision who reported that vision in one eye was not as good as the vision in the eye I had performed surgery on approximately 1 month earlier. An Amsler grid examination showed metamorphopsia and wavy lines, and OCT demonstrated perifoveal thickening, with a normal foveal pit in the eye with decreased vision.

In 2005, Eric D. Donnenfeld, MD, and colleagues presented a study in which 12% of patients who received placebo developed CME after cataract surgery compared with no patients who received ketorolac tromethamine ophthalmic solution 0.4%.12 John R. Wittpenn, MD, presented a poster at the 2006 annual meeting of the American Academy of Ophthalmology illustrating a study in which 8% of patients who did not receive NSAIDs postoperatively developed CME after routine cataract surgery.13 The study compared combination therapy with ketorolac 0.4% and corticosteroids and corticosteroids alone to prevent macular leakage after cataract surgery.

Future indications for NSAIDs

The preoperative and postoperative use of NSAIDs is important in preventing CME. NSAIDs have also been shown to facilitate visual recovery time. Studies must continue to be conducted to gauge future indications for NSAID use after cataract and refractive surgery.

References

  1. Heier JS. Preventing post-cataract extraction CME: Early identification of patients at risk and prophylactic treatment may avert vision loss. Ophthalmology Management. October 2004:63-72.
  2. Saminy N, Foster CS. The role of nonsteroidal antiinflammatory drugs in ocular inflammation. Int Ophthalmol Clin.1996;36:195-206.
  3. Flach AJ. Topical nonsteroidal antiinflammatory drugs in ophthalmology. Int Ophthalmol Clin. 2002;42:1-11.
  4. Jampol LM. Pharmacologic therapy of aphakic cystoid macular edema: A review. Ophthalmology. 1982;89:891-897.
  5. Jampol LM. Pharmacologic therapy of aphakic and pseudophakic cystoid macular edema: 1985 update. Ophthalmology. 1985;92:807-810.
  6. Yee RW. Analgesic efficacy and safety of nonpreserved ketorolac tromethamine ophthalmic solution following radial keratotomy. Ketorolac Radial Keratotomy Study Group. Am J Ophthalmol. 1998;125:472-480.
  7. Eiferman RA, Hoffman RS, Sher NA. Topical diclofenac reduced pain following photorefractive keratectomy. Arch Ophthalmol. 1993;111:1022.
  8. Szerenyi K, Sorken K, Garbus JJ, Lee M, McDonnell PJ. Decrease in normal human corneal sensitivity with topical diclofenac sodium. Am J Ophthalmol. 1994;118:312-315.
  9. Price MO, Price FW. Efficacy of topical ketorolac tromethamine 0.4% for control of pain or discomfort associated with cataract surgery. Curr Med Res Opin. 2004;20:2015-2019.
  10. McColgin AZ, Raizman MB. Efficacy of topical diclofenac in reducing the incidence of postoperative cystoid macular edema. Invest Ophthalmol Vis Sci. 1999;40:289.
  11. O’Brien TP. Emerging guidelines for use of NSAID therapy to optimize cataract surgery patient care. Curr Med Res & Opin. 2005;21:1131-1137.
  12. Donnenfeld ED, Perry HD, Wittpenn JR, Solomon R, Nattis A, Chou T. Preoperative ketorolac tromethamine 0.4% in phacoemulsification outcomes: Pharmacokinetic-response curve. J Cataract Refract Surg. 2006;32:1474-1482.
  13. Wittpenn JR. A masked comparison of Acular LS plus steroid alone for the prevention of macular leakage in cataract patients. Poster presented at: Annual meeting of the American Academy of Ophthalmology; November 12, 2006; Las Vegas, Nev.