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V.B.8. Paradigms Vitreous Floaters and Vision: Current Concepts and Management V.B.8. Paradigms Laura C. Huang, Kenneth M.P. Yee, Christianne A. Wa, Justin N. Nguyen, Alfredo A. Sadun, and J. Sebag Outline Keywords I. Introduction Vitreous • Floaters • Posterior vitreous detachment • II. Background Myopic vitreopathy • Asteroid hyalosis • Light scatter- A. Etiology of Floaters ing • Straylight glare • Contrast sensitivity • VFQ III. Diagnostic Considerations quality of life • Vitrectomy • Retinal detachment • A. Clinical Presentation Oxygen • Cataracts B. Clinical Characterization of Floaters 1. Structural Assessment of Floaters a. Ultrasonography b. Combined OCT/SLO c. Dynamic Light Scattering Key Concepts 2. Effects of Floaters on Vision 1. Floaters result from structural abnormalities in vit- a. Straylight reous. They are a more common complaint than b. Contrast Sensitivity Function previously known and have a more negative impact IV. Therapeutic Considerations on the quality of life than previously appreciated. A. Vitrectomy 1. Efficacy of Vitrectomy for Floaters 2. Vision is adversely affected by vitreous light scat- 2. Safety of Vitrectomy for Floaters tering causing straylight glare and degradation of a. Endophthalmitis contrast sensitivity. This explains the considerable b. Retinal Tears and Retinal Detachment degree of unhappiness experienced by patients suf- c. Cataracts fering from floaters. Conclusions 3. The only proven and safe treatment that effectively References cures floaters and improves vision as well as patient well-being is limited vitrectomy. L.C. Huang, BA VMR Institute for Vitreous Macula Retina, 7677 Center Avenue, suite 400, Huntington Beach, CA 92647, USA Doheny Eye Institute, Department of Ophthalmology, Los Angeles, CA, USA University of Miami Miller School of Medicine, Miami, FL, USA e-mail: [email protected] K.M.P. Yee, BS • C.A. Wa, BA J. Sebag, MD, FACS, FRCOphth, FARVO (*) J.N. Nguyen, BA VMR Institute for Vitreous Macula Retina, VMR Institute for Vitreous Macula Retina, 7677 Center Avenue, suite 400, 7677 Center Avenue, suite 400, Huntington Beach, CA 92647, USA Huntington Beach, CA 92647, USA Doheny Eye Institute, Department of Ophthalmology, A.A. Sadun, MD, PhD, FARVO Los Angeles, CA, USA Doheny Eye Institute/UCLA, e-mail: [email protected]; Los Angeles, CA, USA [email protected]; [email protected] e-mail: [email protected] J. Sebag (ed.), Vitreous: in Health and Disease, 771 DOI 10.1007/978-1-4939-1086-1_45, © Springer Science+Business Media New York 2014 772 L.C. Huang et al. I. Introduction reaction of the vitreous body to disturbances that create liquefaction with the separation of part of its colloid basis Floaters most commonly occur in middle age due to age- (the residual protein) to form appearances evident clinically related changes in vitreous structure and light scattering by as opacities” [10]. This description holds true today as it is the posterior vitreous cortex after collapse of the vitreous body quite consistent with the prevailing theory of the mechanism during posterior vitreous detachment (PVD). In youth, float- by which vitreous undergoes structural changes with age. ers are most often due to myopic vitreopathy. Vitreous float- ers can have a negative impact on visual function and in turn the quality of life. Techniques to characterize floaters clinically A. Etiology of Floaters include ultrasound imaging, optical coherence tomography, and dynamic light scattering for structural characterization. The etiology of floaters is believed to relate to macromolecu- Functional impact can be assessed by straylight measurements, lar changes that alter vitreous organization present during as well as contrast sensitivity testing. When the severity of youth, when hyaluronan (HA) interacts with vitreous colla- floater symptomatology is significant, commonly used thera- gen fibrils to stabilize the gel and keep collagen separated far pies include neodymium:yttrium-aluminum- garnet (YAG) enough to allow light to pass through vitreous with minimal laser and limited 25-gauge vitrectomy. While the former is of or no light scattering, thereby achieving transparency [11]. unproven efficacy, the latter has been shown to be a safe, effec- The vitreous gel structure is maintained by thin, unbranched, tive, and definitive cure that improves patients’ quality of life heterotypic collagen fibrils composed of collagen types II, and eradicates symptomatology produced by light scattering V/XI, and IX [12] and HA that fill the space in between the and diffraction. It is thus reasonable to offer limited vitrectomy fibrils [13]. Liquid vitreous forms as HA dissociates from to individuals who have attempted to cope unsuccessfully and collagen and retains water molecules, sometimes forming in whom functional deficit can be objectively demonstrated by pools or “lacunae.” No longer separated by HA, vitreous col- testing contrast sensitivity, an important aspect of vision. lagen fibrils cross-link and aggregate [14, 15]. Studies have further shown that type IX collagen, most likely due to its chondroitin sulfate side chains, shields type II collagen from exposure on the collagen fibril surface. Type IX proteogly- II. Background can diminishes with age, further exposing type II collagen and predisposing vitreous collagen fibrils to lateral fusion. Over a century ago, Duke Elder described vitreous as a struc- This additionally contributes to liquefaction [16]. Through ture composed of “loose and delicate filaments surrounded these mechanisms, the human vitreous body undergoes two by fluid” [1]. Throughout the eighteenth century, the com- morphological changes with age that create further light position and structure of vitreous mystified early theorists, diffraction: an increase in the volume of liquefied spaces spawning four different theories regarding vitreous structure. (synchysis) [17] and an increase in optically dense areas In 1741, Demours advocated the “alveolar theory” [2] in due to collagen cross-linking [18] (Figure V.B.8-1) [see which membranes oriented in many directions enclosed com- chapter II.C. Vitreous aging and PVD]. partments, or alveoli, containing the fluid portion of vitreous. This macromolecular inhomogeneity scatters light and Pathologists such as Virchow supported this concept [3]. In creates diffraction. Electron microscopy of vitreous opaci- 1780, Zinn postulated that vitreous is arranged in a concen- ties demonstrates collagen fibrils and cellular debris that tric, lamellar orientation such as the “layers of an onion” [4]. contribute to light scattering and visual disturbances [19] This then constituted the “lamellar theory” and subsequently (Figure V.B.8-2a). Another contributing factor to the devel- gained support from fellow theorists such as von Pappenheim opment of opacities is separation of vitreous away from the [5] and Brucke [6]. In 1845, Hannover proposed the “radial retina that follows gel liquefaction and weakening of vitreo- sector theory” where he postulated that vitreous was com- retinal adhesion, commonly referred to as posterior vitreous posed in sectors that were radially oriented around the central detachment (PVD) [20]. The dense collagen fibril matrix in anteroposterior core containing Cloquet’s canal, similar in the posterior vitreous cortex (Figure V.B.8-2b) causes signif- appearance to a “cut orange” [7]. Lastly, in 1848, Sir William icant light scattering. Thus, the combination of vitreous syn- Bowman introduced the “fibrillar theory” based upon a tech- chysis and syneresis with PVD, which is reported in 53 % nique in which he utilized microscopy to show “nuclear gran- of patients older than 50 years and 65 % in patients older ules” of fine fibrils that formed bundles [8]. than 65 years [20], results in the light scattering that causes Changes during life from the clear, gel-like structure the visual perception of “floaters.” Indeed, the most com- led Szent-Gyorgito to be the first to propose that vitreous mon etiologies of floaters are posterior vitreous detachment structure changes with age [9]. Duke Elder elaborated upon (PVD), followed by myopic vitreopathy, and asteroid hyalo- this with his first description of “floaters” as “the passive sis [21–23]. Other pathologies such as Marfan’s syndrome, V.B.8. Vitreous Floaters and Vision: Current Concepts and Management Paradigms 773 Figure V.B.8-1 Aging changes in human vitreous structure. Dark- posterior aspect of the lens is visible at the bottom of each image. field slit microscopy of fresh unfixed whole human vitreous with the Middle row: Vitreous structure in a 56-year-old (left) and a 59-year-old sclera, choroid, and retina dissected off the vitreous body, which (right) subject features macroscopic fibers in the central vitreous body remains attached to the anterior segment. A slit lamp beam illuminates with an anteroposterior orientation. These form when hyaluronan mol- from the side, creating a horizontal optical section with an illumination- ecules no longer separate collagen fibrils, allowing cross-linking and observation angle of 90°, maximizing the Tyndall effect. The anterior aggregation of collagen fibrils into visible fibers which scatter light, segment is below and the posterior pole is above in all specimens. Top inducing floaters and degrading contrast sensitivity. Bottom row: In old row: The vitreous bodies of an 11-year-old girl (left) and a 14-year-old age, the fibers of the central vitreous become significantly thickened boy (right) demonstrate a homogeneous structure with no significant and tortuous, as demonstrated
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