Mhd Dmour , MD

1. Clinical Cases: NSAIDs for CME
Mhd.Dmour, MD

2. CASE #1: CME POSTVITRECTOMY
 In April 2006 a 60-year-old woman
presented with a macular hole in her right
eye. Visual acuity at presentation was
20/250.
 In early May, the patient underwent
vitrectomy with membrane peel and gas
injection for macular hole repair.
 A routine postoperative course of topical
antibiotics and steroids were prescribed.

3. CASE #1: CME POSTVITRECTOMY
 On follow-up 10 days later, her (IOP) was 42 mm Hg. She was immediately
treated with Cosopt, Alphagan, and travatan.
 Despite treatment, the patient’s IOP reduced only to 39 mm Hg, therefore oral
acetazolamide was started and the topical prednisolone was discontinued.
 Two days later, the IOP measured 14 mm Hg and the pressure- lowering
medications were reduced to timolol 0.5% and brimonidine.

4. CASE #1: CME POSTVITRECTOMY
 In January 2007 (after 7 months)
, the patient’s vision measured
20/40. The IOP measured 14 mm
Hg while continuing timolol 0.5%
and brimonidine.
 OCT showed that the macular
hole was closed and there were
no signs of CME.

5.  In June 2007 (after 14 months) patient had
undergone cataract surgery with improvement in
vision, but noticed a recent decline. Visual acuity
had decreased to 20/80 and CME was detected on
exam.
 OCT confirmed the CME with central retinal
thickness measurement of 674 μm.
 Given her history of steroid response, patient
started on Nepafenac (Nevanac, Alcon) three
times daily.
 When she returned 6 weeks later, vision was
20/70 and notably improved per the patient. IOP
was 16 mm Hg and OCT examination showed
improvement in central retinal thickness
measurement to 489 μm.

6.  In February 2008, the patient’s visual acuity
has improved further to 20/40+ and IOP
measured 19 mm Hg. Retinal thickness
decreased an additional 69 μm to 318 μm.
 Nepafenac has been continued, as the CME
has improved, but has not completely
resolved.

7. CASE #2: CME POST CATARACT SURGERY
 A 79-year-old woman underwent
complicated cataract surgery in the left eye
with placement of an anterior chamber IOL
on January 2006.
 Her vision improved to 20/25+ following
surgery, but developed IOP up to 32 mm Hg
which was controlled with timolol 0.5% and
brimonidine 0.15%.
 She returned in February 2007 with
complaints of decreased vision, which
measured 20/60 in the left eye.

8. CASE #2: CME POST CATARACT SURGERY
 The patient was placed on flurbiprofen
(Ocufen) and Predforte. in addition to her
timolol and brimonidine which led to
increased IOP. In response, predforte was
changed to Lotemax and timolol was
exchanged for cosopt.
 She remained on this treatment for several
months during which the IOP remained
elevated and vision improved, but was
fluctuating, according to the patient.

9. CASE #2
 In August of 2007 (after 20 months), the
patient VA was 20/30 with an IOP of 26 mm
Hg and CME evident on examination.
 OCT confirmed intraretinal cystic changes
and subfoveal fluid with a central retinal
thickness of 367 μm.
 Lotemax and flurbiprofen were discontinued
and she was started on Nepafenac three
times per day.

10. CASE #2
 Six weeks later, vision improved to
20/25+, IOP reduced to 18 mm Hg, and
OCT showed resolution of edema and
fluid with a central retinal thickness
measuring 232 μm.
 Nevanac was discontinued in November
2007 at which time vision measured
20/25+, IOP was 16 mm Hg, and OCT
showed no retinal edema.

11. NSAIDs for CME
• Diclofenac 0.1% (Voltaren, Merck)
• ketorolac 0.5% (Acular, Allergan)
• flurbiprofen
• Indomethacin
NSAIDs prevent prostaglandin
synthesis from arachidonic acid
through the inhibition of
cyclooxygenase.
All demonstrated prophylactic activity against CME in randomized, placebo-controlled trials. In
addition to CME prevention, NSAIDs have been shown to effectively treat both acute and chronic
CME.
Corticosteroids inhibit prostaglandin synthesis by a different mechanism than do NSAIDs and therapy
combining the two has been shown to be more efficacious than monotherapy. It is now fairly
practice to initiate a combination of NSAID and steroid upon documentation of clinical pseudophakic
CME.

12. PENETRATION OF NSAIDS
All topical NSAIDs penetrate the cornea to exert their biologic activity against CME.
Nepafenac 0.1% (Nevanac®) is unique in that it is a prodrug which is converted to its
form, amfenac, by enzymatic hydrolases present in vascular ocular tissues, including the
retina/choroid.
Indeed, one in vivo pharmacodynamics studies comparing nepafenac, ketorolac, and bromfenac have shown that
nepafenac 0.1% reached anterior chamber aqueous concentrations 3.6 times higher than ketorolac 0.4% and eight
times higher than bromfenac. The time to greatest concentration was also shortest for nepafenac signifying faster
penetration.

19. Pseudophakic cystoid macular edema is common after
phacoemulsification cataract surgery. Topical nepafenac
0.3% reduces PCME in patients with pre-operative risk
factors for PCME compared to placebo but shows no
benefit in patients without pre-operative risk factors.