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Vitreous occupies about four-fifths of the volume of the eye and weighs approximately 4 g. The vitreous body is somewhat spherical with slight flattening meridionally and has a cup-shaped depression anteriorly, known as the patellar fossa. The vitreous body is attached to all contiguous structures, but the firmness of the attachment varies with topography and age [1–3]. It is most firmly attached at the vitreous base, a 3-dimensional doughnutlike structure that is 3–6 mm wide and straddles the ora serrata. The vitreous base includes the posterior 2 mm of the pars plana and from 1 to 4 mm of the anterior retina posterior to the ora serrata. The posterior border of the vitreous base is located farther posteriorly in older individuals [4] and is more anterior nasally than temporally [5], which may underlie the greater frequency of retinal tears temporally than elsewhere in the peripheral retina [4]. The density of vitreous collagen is greatest within the vitreous base, and the collagen fibers are oriented perpendicular to the retinal plane, whereas elsewhere the orientation is tangential to this plane. The vitreous base contains remnants of the fetal hyaloid vasculature, and it has been suggested that fetal antigens in this region of the vitreous [6] or degenerative products of the vitreous [7] may be immunogenic and play a role in ocular inflammatory diseases, such as pars planitis.

Unmet needs in the treatment of vitreoretinal (VR) disorders provide the impetus to explore new pharmacologic treatments to complement the ever-improving quality and miniaturization of mechanical surgical tools [1, 2]. This is true today as it was 20 years ago when we undertook a novel exploration in biochemical manipulation of the VR interface. Plasmin, a nonspecific serine protease, was first used in 1990 in an experimental animal model to assess its potential to cleave the VR interface [1]. The physiologic adhesion between the inner retina and the posterior vitreous cortex is primarily attributed to glycoproteins, including laminin and fibronectin [see chapter II.E. Vitreoretinal interface and the ILM]. These molecules interact with the internal limiting membrane (ILM) of the retina and the posterior vitreous cortex collagens [3, 4], which over the posterior pole are mostly running parallel to the ILM, whereas perpendicular insertion of vitreous collagen fibrils is seen at the vitreous base [5]. Laminin is primarily located in the basement membrane and attached to collagen type IV. Fibronectin is seen preferentially around blood vessels, in the basement membrane of most cells, and in the extracellular matrix. In the eye, it is present in the vitreous and in the ILM. These glycoproteins are also present in lens zonules, the lamina cribrosa, and the ciliary body. Variations in the distribution of laminin and fibronectin may underlie variability in the strength of the VR adhesion. Some pathologic conditions, like diabetes, can lead to a buildup of laminin and fibronectin at the VR interface [6, 7].

Anterior proliferative vitreoretinopathy (PVR) is the greatest challenge facing the surgeon attempting to repair recurrent retinal detachment [1]. The Retina Society recognized this and, to create a more prognostic classification, added anterior proliferation and posterior proliferation (extensive macular pucker) to its ABCD classification of PVR [2] (Figure V.B.6-1). The traction forces at the vitreous base were classified as circumferential or anterior (Figure V.B.6-2), acknowledging the complexity of contraction of fibrous tissue formation in this zone. Machemer first described retinotomy in 1981 [3] for incarcerated retina in a ruptured globe. Zivonovich described its application for severe traction membranes [4]. Subsequent reports followed [5–9] and emphasized the importance of removing retina anterior to the retinotomy to prevent re-proliferation, extending the retinotomy to an adequate size, the importance of long-term tamponade, and the benefit of perfluorocarbon liquids. In the PVR Silicone Oil Study, retinotomy was performed in 29 % of cases [10].

Up to 10% of rhegmatogenous retinal detachments are complicated by proliferative vitreoretinopathy (PVR), which leads to failure of retinal detachment repair. A related more anterior process, though less well defined clinicopathologically, has been described clinically. Termed anterior loop traction,1 peripheral proliferative vitreoretinopathy (PPVR)2, or anterior proliferative vitreoretinopathy (APVR)3,4 (also see Part I of this chapter) on clinical bases, this process complicates rhegmatogenous retinal detachments, though less frequently than PVR. Adherent APVR membranes and vitreous extend from the peripheral retina near the vitreous base to the ciliary body, iris, or pupillary margin. APVR membrane and vitreous contraction pull the peripheral retina anteriorly, thereby producing a circumferential retinal fold with a trough of variable depth and width between the circumferential retinal fold and the pars plana of the ciliary body.1,3,4 (Part I) Circumferential contraction produces radial retinal folds extending posteriorly and from the circumferential retinal fold.4 (Part I)

Proliferative vitreoretinopathy (PVR) is the most common cause of failure in retinal reattachment surgery.1 The basic pathologic process is growth and contracture of cellular membranes on both sides of the retina and on the posterior vitreous surface.2–5 This results in centripetal and postero-anterior traction on the peripheral retina from contracture in the region of the vitreous base. Fixed folds of the posterior retina occur due to contraction of epiretinal membranes (Fig. 1).

Oral tears occur at the ora serrata, whereas intrabasal tears are located within the vitreous base. Juxtabasal tears are located at the posterior border of the vitreous base. Extrabasal tears are located within the region bounded by the equator and posterior border of the vitreous base. Retinal tears can be partial thickness involving the inner (vitreal) portion of the neurosensory retina or they can be through and through, in which case they are termed full-thickness retinal tears (see Table 5.1).

In 1983, the Retina Society devised a grading system for proliferative vitreoretinopathy (PVR) in hopes that a standardized grading system would make it possible to compare techniques and results of treatment for PVR from different surgeons.1 The system defines PVR as grade “A” if there is pigment proliferation in the vitreous, grade “B” if there are partial thickness retinal wrinkles and rolled edges on retinal breaks due to pre-retinal membrane contraction, grade “C” if periretinal membrane contraction produces full-thickness retinal folds involving 9 clock hours of the retina or less, and grade “D” if more than 9 clock hours of the retina are involved by such fixed folds. The “C” category is subdivided according to the number of clock hours of the retina involved by fixed folds (C-l, 1–3 clock hours; C-2, 4–6 clock hours; C-3, 7-9 clock hours). The D category is subdivided according to the degree of “funnelling” the fixed folds produce around the optic nerve (D-l, a wide open funnel; D-2, a narrow funnel defined as having its “mouth” less than 45°; and D-3, a closed funnel, such that the disc is entirely hidden at the apex of the funnel).

Vitreous embryology can be considered from three interrelated, yet separable perspectives (Table II-1). The first is the classical perspective of anatomists and histologists, who described vitreous embryogenesis in terms of structural events. A second perspective concerns cellular development of the vitreous, in particular the origin and development of the resident cells of the adult vitreous: hyalocytes and fibroblasts. A third perspective considers vitreous embryogenesis from the standpoint of the major molecular constituents (collagen and hyaluronic acid) and their influence upon vitreous and ocular development (see also Chapter IV-A). The following considers vitreous embryogenes is from each of these three perspectives.

When retinal detachments are complicated by advanced proliferative vitreoretinopathy (PVR), scleral buckling surgery alone is generally not sufficient to result in permanent retinal reattachment. The continued evolution of vitreous surgical instrumentation and techniques in the 1980s has resulted in a dramatically improved prognosis in the treatment of such advanced PVR cases. This paper highlights the current surgical approaches used at the Duke University Eye Center in these most severe cases.