When considering anomalous posterior vitreous detachment (PVD) and vitreomacular adhesion (VMA), it is useful to have some sort of conceptual framework on which to hang your thought processes in understanding what is happening within the eye.
Partial-thickness vitreous detachment traditionally has been called vitreoschisis, which is typically seen in complex diabetic pathology such as a diabetic tractional detachment. Vitreoschisis, however, is a more common occurrence than previously thought.
Partial thickness vitreous detachment may lead to epiretinal membranes (ERMs), which in the setting of centrifugal traction may lead to macular hole or macular pucker. Figure 1 shows the relationship of anomalous PVD to several retinal disorders.
What are our options for macular holes? For stage 1 macular holes, the most common strategy is watchful waiting because many of these will resolve. Once it becomes a full-thickness macular hole, spontaneous closure is uncommon, and if the patient is sufficiently symptomatic, surgical intervention, which will be discussed in an article beginning on page 8, is appropriate.
VMA + VMT: Natural History
The majority of patients with VMA and vitreomacular traction (VMT) present with cystoid changes in the macula. Microscopically, small cysts may be present, which are easier to visualize with spectral-domain OCT (SD-OCT). Hikichi et al1 showed that 81% of patients in their study presented with cystoid changes in the retina at the time of diagnosis of VMT; only 19% had no cystoid changes at the time of diagnosis. Over a median of 60 months, more than 90% of those with cystoid changes experienced severe vision loss, persistent cystoid changes, or development of new cystoid changes. In terms of visual acuity, 64% of the patients in this study lost more than 2 lines of vision, and 32% lost more than 6 lines of vision at 60 months.
The experience in this study with the natural history of VMT leads us to believe that the watch-and-wait approach may not be the best for many of our patients.
Figure 2 shows the fluorescein angiography and corresponding OCT image of an eye of a patient with dry age-related macular degeneration. Macular changes and an attachment of the vitreous to the central macula can be seen, but there is no elevation of the macula and no visible cystoid changes. This is the type of case I see often on referral. Although there is a persistent VMA, I can see no traction and the patient's vision is 20/40, so I will not jump the gun with surgery.
Figure 3, however, shows a different case. This patient has a classic VMT, and the tractional effects are visible. Some ERM is present, and there are chronic cystoid changes to the retina. We know from experience that a case like this is unlikely to resolve, so if the patient is symptomatic and is bothered the visual distortion, I then intervene. In the past, I have performed surgery, but this is a perfect case for a medical intervention with a pharmacolytic agent if it were available.
There is nothing wrong with waiting, and there was a time when we would wait until the visual acuity was 20/70 or worse. Patients' expectations, however, have changed, and they tend to be less tolerant of metamorphopsia than in years past. This is an important point. I am hesitant to operate on a patient who does not necessarily appreciate that they have a problem because he or she may very well notice the symptoms after I have operated and misinterpret them to be a result of the surgical procedure.
Watchful waiting remains a reasonable approach to some cases of asymptomatic VMA; however, increased patient expectations have created a situation in which having a pharmacologic solution that can address visual symptoms without the risks of surgical intervention would be advantageous. The surgical approach to VMA and the associated risks will be discussed by Timothy G. Murray, MD, MBA, FACS, in the next article in this supplement.
David F. Williams, MD, MBA, is in private practice at VitreoRetinal Surgery PA in the Twin Cities of Minnesota, and is an Assistant Clinical Professor of Ophthalmology at the University of Minnesota.
- Hikichi T, Yoshida A, Trempe CL. Course of vitreomacular traction syndrome. Am J Ophthalmol. 1995;119(1):55-61.