Pseudophakic cystoid macular edema case presentation

A presentation about CME that occurs as a complication post cataract surgery

1. Pseudophakic cme DR.PRAKRITI YAGNAM.K

2. Definition : Occurs after cataract surgery Also called Irvine- Gass syndrome One of the most common cause of visual loss after cataract surgery Higher incidence in ICCE compared to ECCE

3. Clinical : associated with decreased visual acuity Angiographic CME : seen on FFA Acute : within 6 months Chronic : more than 6 months

4. Pathophysiology : Disruption of BRB Leakage from perifoveal capillaries Accumulation of fluid in intracellular spaces mainly in OPL and INL(Henleys layer) Photoreceptor architecture disruption Visual loss

5. Preoperative risk factors : Severe NPDR or PDR DME : P ostoperative macular edema usually develops in those with a prior history of DME * Uveitis : Eyes with active inflammation within 3 months of surgery had a 6 fold increased risk of developing CME**  Topical AGM – Prostaglandins RVO ERM * Jiramongkolchai K, Lalezary M, Kim SJ. Influence of previous vitrectomy on incidence of macular oedema after cataract surgery in diabetic eyes. Br J Ophthalmol 2011;95(4):524-529. **Belair ML, Kim SJ, Thorne JE, et al. Incidence of cystoid macular edema after cataract surgery in patients with and without uveitis using optical coherence tomography. Am J Ophthalmol 2009;148(1):128-135.

6. Intraoperative risk factors : PCR and vitreous loss Vitreous traction at incision sites Vitrectomy for retained lens fragments Iris trauma Early postoperative yag capsulotomy Iris fixated IOL ACIOL

7. Symptoms : Decreased vision Metamorphopsia,micropsia Central scotoma Decreased colour vision and contrast sensitivity Occurrence peaks at 4 to 6 weeks postoperatively

8. Signs : Loss of foveal reflex with cystic spaces Clinically significant foveal edema Vitritis ONH swelling or lamellar hole in severe cases Slit lamp biomicroscopy may not show abnormality in 5-10% of cases

9. OCT : Loss of the foveal depression, retinal thickening, and cystic hyporeflective areas within the macula.  In severe cases,subfoveal fluid may be evident Others – VMT abnormalities,ERM

10. FFA : Early phase – capillary dilatation in perifoveal region Late phase (5-15 min) – Leakage into cystoid spaces radially into henleys layer – petaloid leaking pattern/expansile dot pattern Late staining of optic disc Gold standard FFA also rules out other causes of CME such as DME and RVO FAF : Hyperautoflurescent intraretinal cysts

11. OCTA : D isruption of parafoveal capillary arcade and cystoid spaces in the deep capillary plexus. L arger foveal avascular zone and reduced vessel density of full-thickness retina and DCP.

12. FFA is the gold standard in diagnosing pseudophakic CME, but treatment responses would be more conveniently monitored by biomicroscopy , visual acuity and OCT.

13. Management : No standardized treatment or prophylactic protocol Prophylaxis : Topical   NSAIDs  in combination with topical steroids are the mainstay of perioperative pseudophakic CME prophylaxis . Most commonly used – 0.1% nepafenac or 0.09% bromfenac  along with prednisolone acetate.

14. Treatment : NSAIDs and Corticosteroids : Minimal evidence regarding treatment of acute episodes Mainstay and initial mode will be combination of steroids and NSAIDs as it has been superior compared to individual therapies.* Refractory cases – periocular(posterior subtenon ) or intravitreal triamcinolone Persistent macular edema – sustained drug delivery systems – Ozurdex * Heier JS, Topping TM, Baumann W, et al. Ketorolac versus prednisolone versus combination therapy in the treatment of acute pseudophakic cystoid macular edema. Ophthalmology 2000;107(11):2034-2038;discussion 2039.

15. Anti VEGFs : VEGF plays an important role in the inflammation and capillary permeability that causes CME . Can be used in persistent or refractory cases. Mainly useful in steroid responders. “Triple therapy” with intravitreal triamcinolone, intravitreal bevacizumab and topical NSAIDs has been shown to be effective as well, although the effects of the intravitreal medications were transient.* *Warren KA, Bahrani H, Fox JE. NSAIDs in combination therapy for the treatment of chronic pseudophakic cystoid macular edema. Retina 2010;30(2):260-266. This is the first study to examine triple therapy with intravitreal triamcinolone, intravitreal bevacizumab, and a topical NSAID.

16. CAIs : Oral  carbonic anhydrase inhibitors may be considered in refractory pseudophakic CME. They are thought to improve the pumping action of the retinal pigment epithelium, to decrease intraretinal fluid.  Topical CAIs have not yet been investigated in pseudophakic CME . Immunomodulator therapy : Recent small pilot studies have started to examine subconjunctival interferon alpha* and intravitreal infliximab** with mixed results. * Deuter CM, Gelisken F, Stubiger N, et al. Successful treatment of chronic pseudophakic macular edema ( irvine-gass syndrome) with interferon alpha: a report of three cases. Ocul Immunol Inflamm 2011;19(3):216-218. **Wu L, Fernando Arevalo J, Hernandez- Bogantes E, Roca JA. Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group. Int Ophthalmol 2010; Apr 8 [ Epub ahead of print]

17. Surgical therapy : Laser vitreolysis Pars plana vitrectomy

18. Differential diagnosis: DME Pars planitis / Uveitis Retinitis pigmentosa Vein occlusions Leakage on FFA Post surgeries – PPV,laser photocoagulation,cryopexy,filtration procedures Medications – epinephrine,E2 prostaglandins

19. No leakage on FFA : Juvenile retinoschisis Vitreomacular traction Goldmann -Favre syndrome Certain types of RP

20. Conclusion : One of the most common complication post cataract surgery. Most acute cases resolve sponataneously with good vision restoration. DME and severe DR should be stabilized before undergoing cataract extraction. A dequate preoperative and postoperative control of inflammation is paramount for successful cataract extraction Management : Topical steroids + NSAIDS PST TA Intravitreal TA/Implant/anti VEGF

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