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
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