A 70-year-old Hispanic male presented with decreased vision in his left eye that had persisted for a week. He was a practicing physician and explained that he had a retinal problem in his right eye, which had been followed for nearly two years. Recently, he noted a significant visual change in his left eye and quickly became concerned. His medical history was unremarkable, and he did not report the use of any medications.
On examination, his best-corrected visual acuity measured 20/30 O.D. and 20/60 O.S. Confrontation fields were full to careful finger counting O.U. Amsler grid revealed central metamorphopsia in both eyes (O.S.>O.D.). His pupils were equal, round and reactive to light, with no evidence of afferent defect. The anterior segment examination was remarkable for 2+ nuclear sclerotic and cortical cataracts O.D.
Fundus examination showed small cups with good rim coloration and perfusion O.U. The retinal vessels and macula in the right eye appeared normal; however, the left macula showed definitive changes (figure 1). Additionally, we obtained a fluorescein angiogram (figures 2 and 3) of the patient’s left eye, as well as a spectral domain optical coherence tomography (SD-OCT) scan of his right eye (figure 4).
Take the Retina Quiz
1. Fundus photograph of the patient’s left eye shows some interesting macular changes.
1. What is the retinal complication in our patient’s right eye?
a. Vitreofoveal traction (VFT).
b. Cystoid macular edema (CME).
c. Posterior vitreous detachment (PVD).
d. Epiretinal membrane (ERM).
2. What retinal changes do you note in the left eye?
a. Serous retinal detachment.
b. CME.
c. Choroidal neovascular membrane.
d. Choroidal nevus.
3. How should the left eye be managed?
a. Observation.
b. Laser photocoagulation.
c. Anti-VEGF injection.
d. Topical steroids and NSAIDs.
4. How should the right eye be managed?
a. Observation.
b. Immediate pars plana vitrectomy (PPV).
c. PPV, only if the presentation worsens.
d. Ocriplasmin (microplasmin, ThromboGenics) injection.
For answers, scroll down.
Discussion
Clearly, our patient exhibited traction in the fovea of his right eye. Was this presentation, however, representative of vitreomacular traction (VMT) or a milder form, VFT?
VFT describes focal traction on the fovea that, in some instances, may induce a very slight effect on the macula.1 In other cases, however, VFT can progress to CME and/or promote full-thickness macular hole formation.1 There is, however, some existing controversy regarding whether VFT represents a separate syndrome or simply is a variant of VMT.2
Interestingly, our patient had been followed for nearly three years with little or no change in the SD-OCT appearance. At 20/30 O.D., his vision had been stable, so no surgical intervention was recommended.
The traction appeared to be focal and had not induced any architectural changes to his macula beyond the superficial traction that was visible on the SD-OCT. In our patient’s case, we expect that the vitreous either will spontaneously detach on its own or that the traction will increase and cause the formation of a full-thickness macular hole. If the latter occurs, surgical intervention will be considered (unless a more noninvasive option becomes available, which may be very soon).
2, 3. Early- (left) and late-phase (right) fluorescein angiogram of our patient’s left eye.
Ocriplasmin is a pharmacologic treatment for PVD and VMT currently being investigated by the FDA.3 It is a proteolytic enzyme that is injected into the vitreous and has the potential to facilitate PVD development in an effort to relieve VMT.
Specifically, Ocriplasmin erodes the protein structures within the vitreous, creating a lysis between the vitreous cortex and the retina. In a recent phase III study, 652 patients were randomized to receive either a single intravitreal injection or a placebo; 26.4% who received the therapy achieved VMT resolution within 28 days vs. 10.2% of those who received the placebo. Even patients who had full-thickness macular holes demonstrated improvement (40.6% experienced macular hole closure vs. 10.6% in the placebo group).3 Again, Ocriplasmin injection is not yet FDA approved; however, preliminary results are encouraging, and approval is expected later this year.
But let’s not forget the reason why our patient came in to see us. In fact, upon brief inspection, the finding in his left eye is more alarming than that observed in his right eye. On previous visits, our patient had some nonspecific retinal pigment epithelium (RPE) changes in his left macula located nasal to the fovea.
Evidently, since then he developed a choroidal neovascular membrane within the same location. This appeared as a gray/green area that was surrounded by subretinal hemorrhage. Additionally, the RPE looked depigmented around the area of neovascularization. Further, there was a serous retinal detachment in the left macula.
4. Here is the SD-OCT scan of his right eye. What does it reveal?
We treated our patient with an intrevitreal injection of Eylea (aflibercept, Regeneron Pharmaceuticals), which recently received FDA approval in November 2011. Eylea is a fusion protein that effectively binds to VEGF receptor sites and subsequently inhibits their ability to facilitate VEGF uptake.
Currently, Eylea is the only anti-VEGF agent approved for intraocular injection every two months. Furthermore, it is less expensive than Lucentis (ranibizumab, Genentech/Roche)––approximately $1,800 per q2m injection of Eylea vs. more than $2,000 per month for Lucentis.4,5
Overall, our patient did well with Eylea therapy. Over a period of six months, he received two injections and achieved a stabilized visual acuity of 20/50 O.S. Meanwhile, his right eye continues to exhibit persistent VFT. He is debating whether to undergo cataract surgery O.D., which now is his stronger eye despite the presence of macular traction.
1. Davis RP, Smiddy WE, Flynn HW Jr, et al. Surgical management of vitreofoveal traction syndrome: optical coherence tomographic evaluation and clinical outcomes. Ophthalmic Surg Lasers Imaging. 2010 Mar-Apr;41(2):150-6.
2. Johnson MW. Tractional cystoid macular edema: a subtle variant of the vitreomacular traction syndrome. Am J Ophthalmol. 2005 Aug;140(2):184-92.
3. Stalmans P, Benz MS, Gandorfer A, et al. Enzymatic vitreolysis with ocriplasmin for vitreomacular traction and macular holes. N Engl J Med. 2012 Aug 16;367(7):606-15.
4. Stewart MW. Clinical and differential utility of VEGF inhibitors in wet age-related macular degeneration: focus on aflibercept. Clin Ophthalmol. 2012;6:1175-86.
5 Browning DJ, Kaiser PK, Rosenfeld PJ, et al. Aflibercept for age-related macular degeneration: a game-changer or quiet addition? Am J Ophthalmol. 2012 Aug;154(2):222-6.
Answers
1. a
2. c
3. c
4. a
