cystoidmacularedema
TO ALL CYSTOID MACULAR EDEMA SUFFERERS.
I refer to article :
May 1998 Cystoid macular edema associated with latanoprost use
Jeffrey S Heier, Roger F Steinert, Albert R Frederick.
Arch Ophthalmol. 1998; 116(5): 680- 682. doi:
Latanoprost is a prostaglandin analog that is being used to reduce intraocular pressure in patients with glaucoma. The convenience of its once a day dosing, relative safety, and apparent efficacy have resulted in wide acceptance of latanoprost as a valuable adjunct in the treatment of glaucoma.
We report of a case in which cystoid macular edema (CME) occurred after the initiation of topical latanoprost. The CME resolved after discontinuation of the drug, without additional intervention.
Case Report
An 81 year old white woman had decreased vision in her left eye 3 weeks after being prescribed latanoprost for chronic open angle glaucoma. Her ocular history, in addition to glaucoma, was remarkable for pseudophakic bullous keratopathy after cataract extraction of the left eye in 1993 with placement of an anterior chamber intraocular lens because of intraoperative capsular rupture. She underwent penetrating keratoplasty and intraocular lens exchange with transscleral suturing in of a posterior chamber intraocular lens in 1994.
The patient's visual acuity stabilised at 20/30 OS, but the intraocular pressure remained in the range of the mid 20s mm Hg despite treatment with 0.5 % timolol twice daily. Latanoprost treatment was started once daily in the left eye.
The patient was seen 3 weeks later complaining of decreased vision in the left eye. Examination revealed best corrected visual acuity of 20/60 OS. Intraocular pressure was 13 mm Hg. Anterior segment examination of the left eye showed a clear and compact graft a deep and quiet anterior chamber and a well centred posterior chamber intraocular lens. Biomicroscopic fundus examination of the left eye revealed prominent cystoid spaces in the macula . Fluorescein angiography revealed numerous perifoveolar punctate hyperfluorescent lesions in the left macula in the early phases. These lesions became increasingly more prominent in the mid phase of the angiogram and showed leakage in a petalloid pattern in the late phase. In addition there
was mild staining of the optic disc. The diagnosis of CME was made. Because of the sudden occurrence of the CME with the initiation of latanoprost therapy the medication was stopped and no additional treatment was initiated.
The patient noted improvement in vision within days of stopping latanoprost treatment. Three weeks after discontinuing latanoprost treatment her visual acuity had improved to 20/40 OS and the CME was less prominent. Seven weeks later her vision had recovered to her pre CME level of 20/ 30 OS . The fundus appeared normal. Fluorescein angiography revealed mild leakage in the left macula.
Investigators have speculated that prostaglandins can cause retinal vasodilation and vascular leakage resulting in CME.
I refer to article:
Prostaglandin induced cystoid macular edema following routine cataract extraction
Negin Agange and Sameh Mosaed
Department of Ophthalmology University of California, Irvine CA 92697, USA 4 July 2010
Introduction: The National Eye Institute estimates that there are 1.5 million surgeries for cataracts each year in the U.S. A common clinical scenario in a percentage of patients undergoing cataract extraction is receiving treatment for co morbidities like glaucoma with hypertensive lipids. We report of a case of a 59 year old man who developed recurrent cystoid macular edema with 3 separate trials of prostaglandin analogs following uncomplicated phacoemulsification with intraocular lens implantation. Currently, we have no prospective blinded control trials to better define the ideal preoperative strategies in this patient population.
Case Report: Our patient has a history of advanced pigmentary glaucoma in both eyes which was controlled preoperatively for many years with XALATAN (Latanoprost), COSOPT (Timolol/ Dorzolamide) and ALPHAGAN (Brimonidine). The patient developed visually significant cataracts in both eyes with visual acuity dropping below 20/40 OU prior to surgery. He had uncomplicated cataract extraction with IOL implant OD, followed 1 month later by OS. His best corrected visual acuity in each eye was 20/20 OU by one week post op. His immediate post op regimen was AVELOX (Moxifloxacin) QID for 1 week, diclofenac QID for 1 month and PRED FORTE (prednisolone) QID for 1 week and then tapered off over the next 3 weeks. His XALATAN (Latanoprost) was resumed immediately post op.
Our patient first developed CME in his right eye 4 months post cataract extraction when he presented with complaints of blurry vision and central distortion. A dilated fundus examination revealed CME confirmed by OTC. The BCVA had dropped from 20/20to 20/70 . XALATAN (Latanoprost) was discontinued and diclofenac was initiated. After 1 month his BCVA and
intraocular pressure OD were 20/70 and 16 mm of Hg respectively. Over the next 2 months while off the XALATAN (Latanoprost) the patient's CME improved and the visual acuity improved to 20/30 +2 but intraocular pressure climbed to 28 mm Hg.
Within 3 weeks of initiating LUMIGAN (Bimatoprost) in an effort to control his increased IOP his CME symptoms recurred for a second time, and his BCVA dropped again to 20/60. The patient's CME was again re - treated with a combination of topical diclofenac QID . Prostaglandin therapy was avoided for a period of 13 months. His BCVA after resolution of the second episode of CME was 20/25 and remained stable for 13 months.
For 1 year after the second episode of CME the IOP remained in the borderline acceptable range on ALPHAGAN (Brimonidine) and COSOPT (Timolol/Dorzolamide) fixed combination OU. He became progressively worse when he presented with an IOP of 28 mm Hg at which time a trial of TRAVATAN ( Travoprost) was attempted. Within 3 weeks the patient presented with a third round of CME in the right eye . TRAVATAN (Travoprost) was the third prostaglandin therapy to date that seems to have triggered CME in our pseudophakic patient and was again discontinued. The patient's third episode of CME eventually resolved with the prior treatments and his BCVA stabilised at 20/25. His IOP at the time of this report is controlled with COSOPT (Timolol/Dorzolamide) fixed combination and ALPHAGAN (Brimonidine) .
Discussion: The association between ocular hypotensive lipids and CME continues to be subject of debate. It has been suggested that it is unlikely that topical XALATAN (Latanoprost) induces CME in eyes with a normally functioning blood ocular barrier. Interestingly, our patient who had been uneventfully treated with XALATAN (Latanoprost) for several years, developed CME that worsened with rechallenge of LUMIGAN (Bimatoprost) and TRAVATAN (Travoprost) even more than 1 year after uncomplicated anterior segment surgery. CME associated with XALATAN (Latanoprost) has been reported after uncomplicated cataract surgery but it is an uncommon complication. In one retrospective review of a cohort of patients after uneventful phacoemulsification 3% developed clinically significant CME. It has also been associated with LUMIGAN (Bimatoprost) in an eye with high risk profile. To our knowledge, this case represents the only report in the literature that definitely identifies prostaglandin analogs as the inciting agent in recurrent CME.
Despite multiple case reports of individual prostaglandin analogs being suggested as the cause of CME, there is currently no consensus or recommendation regarding the use of these medications in the perioperative period.
FOOTNOTE
What happens to the poor, unfortunate patient who is being treated for glaucoma with a prostaglandin analog, and undergoes cataract extraction, and develops CME after the cataract extraction due to the continued use of the prostaglandin analog, and cannot find a substitute for the prostaglandin analog? Trabeculectomy or MIGS?
SOURCES
https://sites.google.com/view/keratoconus
https://sites.google.com/view/markmcgowan
https://sites.google.com/view/royalperthhospital
https://sites.google.com/view/lionseyeinstituteofwa
https://sites.google.com/view/haigis
https://sites.google.com/view/dryeye
https://sites.google.com/view/haigis
https://sites.google.com/view/xengelstent
https://sites.google.com/view/xen45
https://sites.google.com/view/cataractoperation
https://sites.google.com/view/cystoidmacularedema
https://sites.google.com/view/cypass
https://sites.google.com/view/zioptan
https://sites.google.com/view/glaucomawa
https://sites.google.com/view/haigis2
https://sites.google.com/view/istent
https://sites.google.com/view/prognosis2
https://sites.google.com/view/keratoconus3
https://sites.google.com/view/cataract2
https://sites.google.com/view/keratoconus4
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