A 63-year-old white male presented with blurred vision in his right eye. He said his eye had been this way for the past two months. The patient"s optometrist could not find an explanation for the reduced acuity, so he referred the patient to our clinic.

The patient"s ocular history was unremarkable, though his medical history was significant for elevated cholesterol, for which he takes Lipitor (atorvastatin, Pfizer).
Best-corrected visual acuity at this visit measured 20/50 O.D. and 20/20 O.S.

Confrontation visual fields were full to careful finger counting O.U., and his pupils were equally round and reactive with no afferent pupillary defect. Extraocular motility testing was normal. Amsler grid revealed slight central metamorphopsia in the right eye; the left eye was normal. The anterior segment exam was significant only for mild arcus.

The dilated fundus exam revealed healthy optic nerves with small cups (figure 1). The dilated fundus exam of the left eye was unremarkable. We also ordered fluorescein angiography (figures 2 and 3) and optical coherence tomography (figures 4 and 5).

1. The dilated fundus exam of our patient"s right eye was essentially normal. Even when you look closely at the macula, the eye appears
normal. 2, 3. Fluorescein angiogram of the patient"s right eye (shown here at 22 seconds and 3 minutes) appeared normal.

4. OCT with a vertical cut through the macula showed a focal area of vitreous that was attached to the retina.

5. Retinal map around the macula revealed a localized area of retinal thickening (as outlined in red) measuring 315m to 340m.

Take the Retina Quiz

1. What does the fundus photo show?
a. Serous detachment of the retina.
b. Epiretinal membrane (ERM).
c. Stage 1 macular hole.
d. Normal-appearing retina.
2. What is the significant finding of the fluorescein angiogram?
a. Diffuse hyperfluorescence from serous detachment.
b. Delayed filling of the retinal arteries.
c. Focal defect of hyperfluorescence.
d. Essentially normal fluorescein angiogram.
3. What is the significant finding on the OCT?
a. Vitreomacular traction.
b. Pseudocyst.
c. Retinal tear.
d. Neurosensory retinal detachment.
4. What is the correct diagnosis?
a. Idiopathic central serous chorioretinopathy.
b. Stage 1 macular hole.
c. Epiretinal membrane.
d. Vitreomacular traction.
5. What is the most appropriate management?
a. Focal laser.
b. Vitrectomy.
c. Membrane peel.
d. Observation.

For answers to this month"s quiz, please click here.


The reduced visual acuity in this patient"s right eye was a diagnostic dilemma. The fundus exam of the eye was essentially normal. There was no epiretinal membrane present, nor was there any subretinal fluid or hemorrhage that would explain his reduced acuity. The macula appeared normal. The fluorescein angiogram also was normal, and a second, more careful exam of the macula--with a fundus contact lens--was not helpful.
Next, we ordered optical coherence tomography, which yielded some surprising results. Each OCT cut through the macula showed a focal area of vitreous attached to the retina. This vitreoretinal adhesion, in turn, caused macular traction. We can see the effects of this on the retinal thickness map, on which a localized area of retinal thickening (outlined in red) measures 315m to 340m. Given these findings, we diagnosed the patient with vitreomacular traction.

Vitreomacular traction (VMT) was originally described as a syndrome in which patients presented with vitreous traction at the macula as a result of an incomplete, or partial, PVD at the optic nerve.1 Specifically, the vitreous pulled and tugged around the macula, where it remained attached, often resulting in cystoid macular edema (CME). In many of these original cases, clinicians were able to make the diagnosis after visualizing the vitreous bands at the macula and over the optic nerve where the vitreous was beginning to detach. As we see from our patient, VMT can still be present even though the vitreous adhesions on the retina cannot be visualized .

Improved diagnostic equipment such as OCT has shown that vitreomacular traction is more common than once believed. In many instances, clinicians have diagnosed VMT based solely on the OCT findings in patients whose fundus and vitreous both appear normal.

The typical OCT findings in VMT show that a strand of vitreous adheres to the retina, as we observed in our patient. There can be varying degrees of traction and retinal thickening. More severe cases can lead to CME and/or macular hole formation. Milder cases such as ours can show retinal thickening.

As such, we now consider vitreomacular traction to be a spectrum of diseases that result from incomplete posterior vitreous detachment, idiopathically (as with our patient) or from epiretinal membrane. Consider VMT as part of the differential diagnosis when patients present with reduced acuity and a normal appearing fundus but no other explanation can found.

The initial management for VMT depends on the severity of the traction and on whether structural changes occur in the macula. Pars plana vitrectomy may be warranted in patients who develop CME.

In milder cases, such as the one in our patient, a more conservative approach with close observation may be appropriate. The hope is that the vitreous will spontaneously detach on its own, allowing the retina to flatten.

We have followed our patient for the past six months and observed no change in his condition. Vitrectomy will be indicated if his vision deteriorates or if CME develops.

1. Smiddy WE, Green WR, Michels RG, de la Cruz Z. Ultrastructural studies of vitreomacular traction syndrome. Am J Ophthalmol 1989 Feb 15;107(2):177-85.

Vol. No: 141:10Issue: 10/23/04