Grand Rounds Vitreous Wick Syndrome and Cystoid Macular Edema Edward Chu, OD, FAAO Abstract: Cystoid macular edema (CME) is a common final endpoint of a number of vascular, inflammatory, or intraocular insults. Vitreous Wick Syndrome is a less common cause of CME that should be considered. Learning Objectives 1) Review pathophysiology and various causes of cystoid macular edema (CME). 2) Review literature on Irvine-Gass syndrome, role of prostaglandin analogs in macular edema, and vitreous wick syndrome. 3) Review treatments for Irvine-Gass syndrome, prostaglandin induced CME, and vitreous wick syndrome. I. Case History a. Patient demographics i. 85 year old Filipino male b. Chief complaint/ Purpose of visit i. Glaucoma follow-up c. Ocular History i. S/P complicated cataract extraction OS x 3 years: posterior capsular tear requiring conversion to extracapsular cataract extraction with anterior vitrectomy OS ii. Vitreous to wound OS treated with YAG laser iii. 6 weeks S/P cataract surgery: diagnosed with pseudophakic cystoid macular edema which was treated successfully with Acular and Pred Forte QID x 1 month iv. Intraocular pressure (IOP) 24/26 and patient is placed on Cosopt BID OU due to possible steroid response v. 1 year later (lost to f/u): diagnosed with glaucoma, pressures still high with good compliance with Cosopt BID OU. After consult with ophthalmology, started on Travatan qhs OU vi. Anatomic narrow angles: S/P peripheral iridotomies OU d. Medical History i. Fatigue, Anemia, High Cholesterol, Hypertension e. Medications i. Glaucoma: Cosopt BID OU and Travatan qhs OU ii. Simvastatin, Lisinopril, Amlodipine II. Pertinent Findings a. Baseline visit (7/28/2008) i. Best corrected visual acuity OD: 20/40 OS: 20/60, previously best corrected 20/40 3 months earlier ii. Pupils: left pupil distorted and peaked at 10:00 with minimal reaction to light, afferent papillary defect (APD) OS by reverse swing test, APD explained by asymmetric glaucoma iii. Versions: smooth, accurate, full, extensive iv. Humphrey Visual Field (3 months prior) 1. OD: mild blind spot enlargement, inferior cluster defect 2. OS: moderate superior arcuate defect, mild inferior arcuate defect v. Anterior segment 1. Cornea OS: positive staining OS due to vitreous wick, mild edema, neovascularization surrounding vitreous to corneal wound, negative Seidel test 2. Patent laser peripheral iridotomies superiorly OU 3. Iris OS: Peaked pupil at 10:00 due to vitreous wick, iris atrophy from complicated cataract surgery. 4. Anterior chamber deep and quiet OU 5. Gonioscopy: thin ciliary body visible 360 OU with vitreous wick in superior/nasal quadrant OS 6. Lens OD: 2+ nuclear sclerosis and 1+ cortical spoking accounting for 20/40 vision 7. PCIOL OS vi. Goldmann tonometry: 12/14 @ 8:57 AM vii. Posterior segment 1. Mild thinning of OD inferior rim consistent with glaucoma, cupping 0.55H x 0.65V 2. Thin inferior and temporal rims with cupping 0.65H x 0.80V 3. OD macula: flat 4. OS macula: central focal pigment changes, yellow cyst, mild elevation viii. Periphery: no holes, breaks, tears 360 OU ix. OCT Macula scan 1. Cystoid spaces in macula OS x. Fluorescein angiography (FA) 1. Petalloid appearance consistent with CME. No venous occlusion or choroidal neovascular membrane detected xi. PLAN: Discontinue Travatan, started Acular QID OS. Continue Cosopt BID OU. Return in 2 months for f/u b. 2nd visit (9/19/08) i. Best corrected visual acuity 1. OD: 20/40 2. OS: 20/40 ii. Anterior segment findings consistent with previous exam iii. Goldmann tonometry 18/21 @ 9:58 AM, elevated since Travatan d/c iv. Posterior segment findings consistent with previous exam except macula OS now flat with no yellow cyst. v. PLAN: Continue Acular QID OS x 2 weeks, then discontinue. Start Alphagan BID OU and continue Cosopt BID OU. Return in 2-3 months for follow-up. rd c. 3 visit (12/30/08) i. Best corrected visual acuity 1. OD: 20/40 2. OS: 20/40+ ii. Anterior segment findings consistent with previous exam iii. Goldmann tonometry 14/15 @ 8:45 AM iv. Posterior segment findings consistent with last exam v. PLAN: Prostaglandin analogs contraindicated due to history of CME. Monitor vitreous wick and plan surgical intervention only with return of CME. Continue Alphagan BID OU and Cosopt BID OU. Return in 3 months for repeat 24-2 humphrey visual field. III. Differential Diagnosis a. Primary i. Cystoid Macular Edema due to complicated cataract surgery, prostaglandin analog use, and vitreous wick b. Others i. Venous Occlusion (CRVO, BRVO) ii. Diabetic Macular Edema iii. Vitreomacular Traction iv. Uveitis v. Epiretinal membrane vi. Retinitis Pigmentosa vii. Tumor IV. Diagnosis and discussion a. Pathophysiology of CME i. Breakdown of blood-retinal barrier (BRB), leaking from perifoveal capillaries, accumulation of fluid in outer plexiform and/or inner nuclear layer b. Irvine Gass Syndrome i. Clinical CME (20/40 or worse or 2 lines less than BCVA) 1-2% of patients, as high as 20% in complicated CE ii. Angiographic CME (on FA or OCT w/o vision loss) seen in up to 30% iii. Usually 3-12 weeks postoperatively, but can be delayed months or years iv. Resolves spontaneously over several months in 80% patients v. Preoperative weakening of BAB and BRB can increase risk of postoperative CME vi. Pathophysiology 1. Surgical trauma to lens, iris, or ciliary body powerful pro-inflammatory event 2. Prostaglandins synthesized in aqueous, leads to breakdown of bloodaqueous barrier (BAB), accumulation of more inflammatory mediators which can diffuse to vitreous and disrupt BRB, causing leakage of fluid into retinal tissue 3. Disruptions of BAB and BRB are parallel in nature c. Prostaglandin Analog (PA) induced CME i. Drop mimics effects of endogenous prostaglandins (inflammatory mediator) ii. When used in early postoperative pseudophakias, associated with destruction of BAB and higher incidence of angiographic CME iii. Average onset 7-30 days after initiation of PA iv. Generally unlikely that PA will induce CME in eyes w/ normal blood ocular barrier v. CME resolved in 60% of patients where discontinuation of medication was only intervention vi. Other patients treated successfully with NSAID and/or topical steroid d. Vitreous Wick Syndrome i. Aqueous leak due to surgery allows vitreous to move anterior, mucus threadlike strand prolapses through wound site out to external ocular surface ii. Signs: peaked pupil, corneal haze, hypopyon, redness, discharge iii. Typical onset 2-4 weeks after surgery (cataract, limbal relaxive incision, retinal surgery iv. Patient may present with mild discomfort to extreme pain v. Risk to develop: CME, Endophthalmitis, Pupillary Block Glaucoma, retinal tear, chronic inflammation vi. Wick formation 1. Poor suture technique resulting in tightly compressed corneal tissue can create enlarged suture tract and fistula 2. Phacoemulsification: clear corneal tongue creates barrier for wound closure and can lead to leakage vii. Treatment 1. YAG laser to cut strand 2. Anterior vitrectomy V. Conclusion a. Recognize potential causes of CME i. Diabetes, venous occlusion, VMT, ERM, Uveitis, surgery b. Clinical CME 2% of cataract surgeries, up to 20% in complicated surgeries c. Prostaglandin analogs can cause CME, but more likely in patients with compromised BRB i. Avoid in patients with history of CME or active inflammation ii. Use with cuation in patients with previous BRB insult d. Recognize vitreous wick and potential to cause CME i. Peaked pupil, mucus strand ii. Watch for endopthalmitis and pupillary block Bibliography Ayyala R et al. Cystoid Macular Edema Associated with Latanoprost in Aphakic and Pseudophakic Eyes. American j of Ophthalmology 1998; 126: 602-604. Callanan D et al. Latanoprost-associated Cystoid Macular Edema. American J of Ophthalmology 1998; 126: 134-135. Chavan R. Overnight visual improvement after early surgical intervention in Irvine-Gass Syndrome. Eye (2007) 21, 137-139. 9 June 2006. Di Pascuale et al. Corneal Melting After Use of Nepafenac in a Patient with Chronic CME After Cataract Surgery Eye and Contact Lens 34 (2): 129-130, 2008. Harbour JW et al. Pars plana vitrectomy for chronic pseudophakic cystoid macular edema. Am J Ophthalmol 1995; 120: 302-307 Henderson B et al. Clinical pseudophakic cystoid macular edema: Risk factors for development and duration after treatment. J Cataract Refract Surg 2007; 33: 1550-1558. Moroi S et al. Cystoid Macular Edema Associated with Latanoprost Therapy in a Case Series of Patients with Glaucoma and Ocular Hypertension. Ophthalmology 1999; 106: 10241029. Miyake K et al. Prostaglandins and Cystoid Macular Edema. Survey of Ophthalmology 47: S203S218, 2002. Rice TA, Michels RG. Current surgical management of the vitreous wick syndrome. Am J Ophthalmology 1978; 85: 656-661. Roque M. Vitreous Wick Syndrome. Emedicine.com. 2007. Rouw J, Shaver J. Vitreous wicking syndrome as a complication of extracapsular cataract extraction. 2008. Optometry 2008; 79:193-196. Ruiz, RS, Teeters WV. The vitreous wick sydrome. Am J Ophthalmology 1970; 70: 483-490 Srinivasan BD, Hofeldt A, Coleman DJ, et al. Vitreous wick syndrome. Am J Ophthalmology 1979; 87: 662-664. Tam DY, Vagefi MR, Naseri A. The clear corneal tongue: a mechanism for wound incompetence after phacoemulsification. Am J Ophthalmol 2007; 43: 526-528 Tranos P et al. Macular Edema: Major Review. Survey of Ophthalmology 49: 470-490, 2004. Weisz JM et al. Ketorolac treatment of pseudophakic cystoid macular edema identified more than 24 months after cataract extractdion. Ophthalmology 106: 1656-1659. Wolf E et al. Incidence of visually significant pseudophakic macular edema after uneventful phaocemulsification in patients treated with nepafenac. J Cataract Refract Surg 2007; 33: 1546-1549. Yeh P et al. Latanoprost and clinically significant cystoid macular edema after