Management Options for Vitreous Opacities

A practical approach to managing patients with floaters.

By Steve Charles, MD, and Mohammad Rafieetary, OD

The alteration of the vitreous humor due to aging and to degenerative and pathologic processes can result in highly variable visual symptoms, including functional vision loss in some patients. This slow process, resulting in an evolving separation of the posterior vitreous over time and crosslinking of vitreous collagen, is thought to be associated with advanced glycation end products (AGEs) in the vitreous.1,2 AGEs lead to irreversible crosslinking of many macromolecules, including those in the vitreous, and this crosslinking has been detected at a higher rate with aging and at an accelerated rate in patients with diabetes.1 These changes often lead to macular conditions such as vitreomacular adhesion (VMA), vitreomacular traction (VMT), epimacular membrane (EMM), vitreomacular schisis, and partial- and full-thickness macular holes (MH).

In the VAST study,3 which included 1,475 eyes of 760 patients, the prevalence of VMA in patients 40 years and older was estimated to be more than 40%. In random sampling, VMA has been detected by optical coherence tomography (OCT) in nearly 15% of the population.4

By contrast, the vitreoretinal interface changes, particularly during an acute posterior vitreous separation (PVS), more commonly referred to as posterior vitreous detachment (PVD), can result in retinal tears and breaks with potential progression to rhegmatogenous retinal detachment (RRD).5

SYMPTOMS

Nonpathologic vitreous opacities, often called floaters, are a common complaint among the general population.6 In a study of smartphone users 18 years and older, Webb et al reported that 76% had floaters and 33% described the floaters to be bothersome, interfering with their vision.7

Figure 1. Collagen fibrils (arrows) within the vitreous cavity can be seen on high-resolution spectral-domain optical coherence tomography (HR SD-OCT).

Figure 2. Posterior vitreous cortex (PVC) is seen on HR SD-OCT.

Figure 3. Anterior shifting of the PVC and precortical vitreous pockets seen on OCT. Note the clumping and condensation of the vitreous (arrow).

A variety of visual complaints described by patients with floaters can be due to a number of factors: crosslinking of collagen fibrils in the vitreous humor (Figure 1), crosslinking of the collagen layers of the posterior or anterior vitreous cortex (Figure 2), or clumping of collagen fibers (Figure 3). These may or may not be accompanied by PVD or PVS.6 The visual disturbances experienced by patients may be caused by light scattering or obscuration of image formation by the semitransparent vitreous cortex or vitreous opacities (Figure 4).

CONSERVATIVE MANAGEMENT

In many cases these complaints are transient. Opacities may move anteriorly out of the focal plane or inferiorly below the visual axis (Figure 5), or patients may undergo neural adaptation and report “getting used to” the visual disturbance.

Figure 4. Vitreous opacities are visible on infrared photograph (A) and are seen to be causing a blocking interference on OCT scan (arrow, B), corresponding to patient’s reported symptoms.

Figure 5. Symptoms caused by anterior displacement of the vitreous cortex and early posterior vitreous detachment (PVD) and/or vitreous condensation were spontaneously alleviated in 2 months in one patient (A) and 1 month in another patient (B) due to further anterior and inferior movement of the visually disturbing opacities outside of the patients’ visual axis and focal point to a nodal point.

When visual complaints persist, affecting patients’ activities of daily living, intervention may be required. A number of management options have been described over the years with variable degrees of success. Before any intervention, a number of factors must be addressed, the most pertinent being patient education. Patients must be aware that, in the absence of any other associated pathology, vitreous opacities are generally not progressive, nor do they result in permanent vision loss or blindness. The psychiatric state of the patient must be considered, as well as patient expectations.

Figure 6. Fundus photographs of a patient before (A) and after (B) pars plana vitrectomy (PPV). Note complete resolution of clumped vitreous opacities (arrow, A).

Figure 7. Although vitreous opacities are somewhat visible on fundus photographs (A and B) of a patient complaining of floaters in both eyes, the floaters are easier to detect on infrared (IR) photographs (C and D).

Figure 8. A large floater is seen in the inferior field of an IR photograph (A). The mobility of the floaters is evident as they shift in the field of fundus autofluorescence images (B and C).

Figure 9. Wideangle 55° SD-OCT (Spectralis; Heidelberg Engineering) images; patient with partial PVD (A) and patient with complete separation of PVC from retinal surface (B).

The earliest attempts to resolve vitreous opacities used an enzymatic approach.8 Use of alpha-chymotrypsin in the 1960s failed, as the enzyme caused breakdown of the lens zonules. It was subsequently used in intracapsular cataract extraction.9 Hyaluronidase (Vitrase; Bausch + Lomb) also failed to show positive results in treatment of vitreous hemorrhage and floaters.10 Plasmin and microplasmin have since been used for treatment of a variety of ophthalmic disorders and have shown limited success for enzymatic vitreolysis.8 An integrin peptide, ALG-1001 (Luminate, Allegro Ophthalmics) is undergoing clinical trials for this purpose.11

Nd:YAG vitreolysis has also been promoted by some.12 There is no scientific evidence that this management strategy is an effective way to reduce patients’ symptoms. Delany et al compared Nd:YAG to pars plana vitrectomy (PPV) in 42 eyes of 31 patients (54 procedures) and concluded that laser was a moderately effective modality.13 The problem with laser vitreolysis is that the symptomatic vitreous opacities are broken into smaller fragments that may actually increase the patient’s complaints. Risks associated with laser vitreolysis include retinal breaks, hemorrhage, and disruption of the lens capsule resulting in cataract formation.

Figure 10. Three patients shown in three rows of images. In the top row (A), partial attachment of vitreous is noted in both the peripapillary and the perifoveal areas. In the second row (B), patient with recent-onset floaters (yellow arrow) exhibits separation of the perifoveal vitreous cortex and visible vitreous opacities (red arrow); however, persistent peripapillary partial vitreous attachment is also evident (green arrows). In the third row (C), a symptomatic patient with floaters (red arrows) demonstrates separation of peripapillary vitreous cortex; however, vitreous is visibly attached to the macula (green arrows).

Figure 11. Peripapillary nerve fiber layer analysis scans provide a good way to evaluate attachment of the vitreous. In this time-lapse example, the separation of the peripapillary vitreous over a span of 5 years is demonstrated.

VITRECTOMY

The only definitive way to rid a patient of vitreous opacities is PPV (Figure 6). The advances made in sutureless small-gauge PPV in recent years have made it a safer technique for any vitreoretinal conditions for which PPV is indicated. PPV was found to be superior to Nd:YAG in the aforementioned study by Delaney et al.13

The most important factor in considering PPV is patient selection. Patients with symptoms of recent onset with no other associated pathology should be given ample time for spontaneous resolution of their symptoms. In patients with chronic and significant complaints affecting their quality of life, the criteria to select patients for PPV include the following:

• visibility of vitreous opacities at slit-lamp fundus examination (Figure 7) and on infrared or fundus autofluorescence images (Figures 4, 7, and 8)
• the presence of a PVD from both the peripapillary and prefoveal regions, documented on high-resolution spectral-domain OCT (Figures 9-11).

Absence of PVD should exclude patients from surgical intervention. Inducing an intraoperative PVD must absolutely be avoided, as it will significantly increase the risk of postoperative complications. Additionally, careful examination of the peripheral retina is necessary to detect or rule out any peripheral retinal holes or breaks that need management before or during PPV. Finally, patients with any psychiatric conditions should be advised against surgical intervention.

All patients should also be made aware of the potential risks of PPV. The most significant downside is the hastening of progression of nuclear sclerotic cataracts. The likelihood of endophthalmitis, peripheral retinal tears, or retinal detachment is extremely low. However, careful postoperative care is needed to assure a successful outcome.

CONCLUSION

Physiologic and age-related alteration of the vitreous may result in visual symptoms affecting quality of life in many patients. In appropriately selected patients, PPV is an effective modality to decrease patient symptoms and therefore improve quality of life.

1. Glenn J, Stitt A. The role of advanced glycation end products in retinal aging and disease. Biochim Biophys Acta. 2009;1790(10):1109-1116.

2. Stitt A, Moore J, Sharkley J, et al. Advanced glycation end products in vitreous: structural and functional implications for diabetic vitreopathy. Invest Ophthalmol Vis Sci. 1998;39(13):2517-2523.

3. Rodman J, Shechtman D, Haynie J, et al. The prevalence of vitreomacular adhesion in patients 40 years and older-VAST Study. Invest Ophthalmol Vis Sci. 2015;56(7):1226.

4. Reichel E, Jaffe G, Sadda S, et al. Prevalence of vitreomacular adhesion: an optical coherence tomography analysis in the retina clinic setting. Clin Opthalmol. 2016;10:627-633.

5. Mitry D, Fleck BW, Wright AF, Campbell H, Charteris DG. Pathogenesis of rhegmatogenous retinal detachment: predisposing anatomy and cell biology. Retina. 2010;30(10):1561-1572.

6. Roufail E, Polkinghorne P. Vitreous floaters. Compr Ophthalmol Update. 2006;7(4):171-177.

7. Webb B, Webb J, Schroeder M, North C. Prevalence of vitreous floaters in community sample of smartphone users. Int J Ophthalmol. 2013;6(3):402-405.

8. Williams G. Enzymatic vitreolysis for retinal disorders. Review of Ophthalmology. May 2008.

9. Rizzuti A. Alpha-chymotrypsin (quimotrase) in cataract surgery. AMA Arch Ophthalmol. 1959;61(1):135-140.

10. Kuppermann B, Thomas E, de Smet M, et al. Safety results of two phase III trials of an intravitreous injection of highly purified ovine hyaluronidase (Vitrase) for the management of vitreous hemorrhage. Am J Ophthalmol. 2005;140(4):585-597.

11. A clinical trial designed to evaluate the safety and efficacy study of Luminate in inducing PVD in non-proliferative diabetic retinopathy. Clinicaltrials.gov: NCT02435862. Accessed August 1, 2017.

12. Tsai W, Chen F, Su C. Treatment of vitreous floaters with neodymium YAG laser. Br J Ophthalmol. 1993;77(8):485-488.

13. Delaney Y, Oyinloye A, Benjamin L. Nd:YAG vitreolysis and pars plana vitrectomy: surgical treatment for vitreous floaters. Eye (Lond). 2002;16(1):21-26.

Steve Charles, MD, FACS, FICS
• founder, Charles Retina Institute, Germantown, Tenn.
• financial disclosure: advisory board member and clinical investigator, Heidelberg Engineering
scharles@att.com

Mohammad Rafieetary, OD, FAAO
• consultative optometric physician, Charles Retina Institute, Germantown, Tenn.
• financial disclosure: consultant and clinical investigator, Alcon Surgical
mrafieetary@charlesretina.com