Ocriplasmin and Its Role in the Management of Vitreoretinal Interface Disorders

Christina Y. Weng, MD, MBA; Jorge A. Fortun, MD; Petros E. Carvounis, MD, FRCSC; Thomas A. Albini, MD


Int Ophthalmol Clin. 2014;54(2):29-38. 

In This Article

Abstract and Introduction


The vitreous gel has an outer cortex consisting primarily of type II collagen that is attached to the internal limiting membrane (ILM) consisting primarily of type IV collagen. The vitreous plays a central role in many common and potentially blinding diseases such as diabetic retinopathy, proliferative vitreoretinopathy, and vitreomacular interface disorders; the latter will be the focus here.

The development of a posterior vitreous detachment is a natural process that occurs typically after the age of 50 years. However, sometimes the posterior hyaloid face does not detach completely and there are focal areas that remain attached to the macula. This is a condition known as vitreomacular adhesion (VMA). In a recent noncomparative case series of 106 eyes with symptomatic idiopathic VMA, spontaneous release of VMA occurred in 34% of eyes during the mean study follow-up period of 23 months.[1] In the cases where VMA does not resolve on its own, traction on the retina may develop, leading to subsequent anatomic distortion; although the terminology is not universally accepted, this anatomic distortion on OCT in the setting of VMA is referred to as vitreomacular traction (VMT).

If left untreated, VMT can sometimes progress into a sight-threatening condition where patients can experience decreased visual acuity, metamorphopsia, and scotomas; full-thickness macular holes can also form as a result of VMT. In a retrospective analysis of 53 consecutive symptomatic eyes with untreated VMT, Hikichi et al[2] found that 64% of eyes experienced a decrease in visual acuity of ≥2 Snellen lines after a median follow-up period of 60 months. Untreated macular holes also carry a poor prognosis with approximately 40% of patients progressing to a visual acuity of 20/200 or worse.[3]

Enzymatic vitreolysis is defined as the induction of a posterior vitreous detachment (PVD) and liquefaction of the vitreous gel, and has been studied since 1998.[4] Enzymes including chondroitinase, hyaluronidase, dispase, and collagenase have been studied, but each has had its drawbacks.[5–7] Plasmin, a key enzyme of the fibrinolytic cascade, has proven to be one of the more promising agents. Plasmin is an 88 kDa nonspecific protease acting on many glycoproteins including laminin and fibronectin, found at the interface of vitreous collagen fibers and the ILM; unlike some other enzymes, it has the advantage that it does not degrade collagen type IV, a major component of the ILM.[8]