Posterior vitreous detachment (PVD) is largely viewed as a fairly simplistic event; however, this is not necessarily the case. PVD is composed of 2 biologic phases that must work in synchrony— liquefaction of the vitreous and separation of the vitreous from the retina. If these 2 phases do not work in synchrony, a normal vitreous detachment will not occur. Instead, what results is known as an anomalous, or pathologic, vitreous detachment and vitreomacular adhesion (VMA), in which an area of attachment of the vitreous exists where it should not. VMA at the macula causes metamorphopsia, or visual distortion.

Historically, we have had agents that can induce 1 phase of the PVD, but again, liquefaction and separation must occur in synchrony. Hyaluronidase was first introduced in 1943 and was more recently reintroduced as Vitrase (Ista). This agent did not work well because it achieves only liquefaction, not separation. Another agent, dispase, which is a cleaving agent, also did not work well because, conversely, it causes interface separation without liquefaction. Ocriplasmin (ThromboGenics) is the only agent that induces both liquefaction and separation of the vitreous from the retinal interface.

Currently, for most patients with VMA who maintain good vision, the only reasonable available option is observation, due to the risks involved with a surgical intervention. This can be frustrating to patients because they come to our offices with true symptoms of poor vision and distortion and, because we can do nothing for them, they leave unhappy.

By choosing watchful waiting, we are hoping for spontaneous separation of the vitreous from the retina. As David Williams, MD, MBA, discusses in his article beginning on page 6, however, spontaneous separation is a relatively rare event. Rather, what seems to happen more frequently is vitreomacular traction (VMT), resulting in cystic and retinal pigment epithelium changes and subsequent visual acuity loss. Macular hole is another possible consequence of VMA that is left to observation.

Advanced Imaging and VMA

The condition in the top panel of Figure 1 can be described by a number of names: VMT, stage 1 macular hole, or macular cyst. Therefore, the lack of accuracy of our nomenclature betrays continued understanding of this condition.

Because we now have access to advanced imaging techniques, from time-domain optical coherence tomography (OCT) to spectral-domain (SD) OCT, we are further ahead in our understanding of VMA, VMT, and macular hole. Our nomenclature, however, lags far behind, which can lead to confusion and misunderstanding.

It is quite formidable to think of how far we have come with our imaging technology. When I performed my medical retina fellowship with J. Donald M. Gass, MD, he was using a Hruby lens, which no one else was using at the time, and was able to see pathology in an unprecedented fashion. Imagine what he could have done using our current imaging technologies.

Even with older time-domain OCT, it is apparent that VMA plays a larger role in retinal disease than was previously understood. The advances in OCT technology are related to an increased understanding as to the prevalence of VMA. SD-OCT has allowed improved visualization of the vitreoretinal interface and has revealed the larger role that VMA plays in retinal disorders such as age-related macular degeneration, diabetic retinopathy, epiretinal membrane, cystoid macular edema, and retinal vein occlusion(RVO).1-9 Based on this new understanding, a new ICD-9 diagnostic code 379.27 was designated for VMA.

Applying Pharmacologic Vitreolysis

Figure 2 shows a patient with 20/30 vision and metamorphopsia. Although this patient might complain about poor vision, I would not consider surgery because the vision is too good and so the benefits of surgery do not outweigh the risks. This patient, in my opinion, would be a perfect candidate for ocriplasmin.

I would also use ocriplasmin in a patient with a fullthickness macular hole, or for a patient who has VMA causing a macular cyst or a stage I macular hole.

For patients with RVO and macular edema, I would consider using ocriplasmin to increase the sustainability of anti-VEGF injections.

Summary

Currently, we have a convergence of several forces, 2 of which I have discussed. The first is the increased understanding of the role that the vitreous plays in retinal disease, fueled by advances in ocular imaging. The second is the availability of an agent that can achieve what could only be achieved previously by a surgical procedure. More data on all the available approaches to symptomatic VMA, along with information that shows its role in other retinal disease states, will be discussed in the following pages.

Pravin U. Dugel, MD, is Managing Partner of Retinal Consultants of Arizona in Phoenix; Clinical Associate Professor of Ophthalmology, Doheny Eye Institute, Keck School of Medicine at the University of Southern California, Los Angeles; and Founding Member of the Spectra Eye Institute in Sun City, AZ. He can be reached at pdugel@gmail.com.

  1. Ezra E. Idiopathic full thickness macular hole: natural history and pathogenesis. Br J Ophthalmol. 2001;85(1):102-108.
  2. Koerner F, Garweg J. Vitrectomy for macular pucker and vitreomacular traction syndrome. Doc Ophthalmol. 1999;97(3-4):449-458.
  3. Krebs I, Brannath W, Glittenberg C, Zeiler F, Sebag J, Binder S. Posterior vitreomacular adhesion: a potential risk factor for exudative age-related macular degeneration? Am J Ophthalmol. 2007;144(5):741-746.
  4. Bertelmann T, Ki'ová N, Messerschmidt-Roth A, Irle S, Sekundo W, Mennel S. The vitreomacular interface in retinal vein occlusion. Acta Ophthalmol. 2011;89(4):e327-331.
  5. Kakehashi A, Schepens CL, Trempe CL. Vitreomacular observations. I. Vitreomacular adhesion and hole in the premacular hyaloid. Ophthalmology. 1994;101(9):1515-1521.
  6. Ghazi NG, Ciralsky JB, Shah SM, Campochiaro PA, Haller JA. Optical coherence tomography findings in persistent diabetic macular edema: the vitreomacular interface. Am J Ophthalmol. 2007;144(5):747-754.
  7. Robison CD, Krebs I, Binder S, et al. Vitreomacular adhesion in active and end-stage agerelated macular degeneration. Am J Ophthalmol. 2009;148(1):79-82.
  8. Krebs I, Brannath W, Glittenberg C, Zeiler F, Sebag J, Binder S. Posterior vitreomacular adhesion: a potential risk factor for exudative age-related macular degeneration? Am J Ophthalmol. 2007;144(5):741-746.
  9. Carpineto P, Di Antonio L, Aharrh-Gnama A, Ciciarelli V, Mastropasqua L. Diagnosing and treating vitreomacular adhesion. Eur Ophthalmic Rev. 2011;5:69-73.