14
QUESTION
HOW DO I FIGURE OUT WHETHER OR NOT MY PATIENT HAS A POSTERIOR VITREOUS DETACHMENT? DOES THERE HAVE TO BE A WEISS RING TO MAKE THE DIAGNOSIS?
Stephen G. Schwartz, MD, MBA
Harry W. Flynn, Jr., MD
Ingrid U. Scott, MD, MPH
Posterior vitreous detachment (PVD) is a common age-related event that may be associated with multiple vision-threatening retinal conditions, including retinal break, rhegmatogenous retinal detachment (RRD), vitreomacular interface disorders, proliferative diabetic retinopathy (PDR) in persons with diabetes, and others.1 Interestingly, this common and important finding lacks a clinically validated diagnostic endpoint. The Weiss ring (Figure 14-1) traditionally has been considered a specific sign of a completed PVD, in the sense that a patient with an ophthalmoscopically visible Weiss ring is thought to have a PVD.2
The Weiss ring, however, is not a definitive sign of a PVD, and some eyes with PVD do not have a Weiss ring.3 For example, in one series of 200 eyes with a PVD diagnosed using biomicroscopy, the authors reported a complete Weiss ring in 51%, an incomplete Weiss ring in 36%, and no Weiss ring in 13%.4
B-scan echography (Figure 14-2) may be a more sensitive test for PVD than biomicroscopy. The Phase III Microplasmin for Intravitreous Injection–Traction Release Without Surgical Treatment clinical trial specified the use of B-scan “to evaluate the status of the posterior vitreous cortex.”5 More recently, swept source optical coherence tomography (OCT) has been reported to image the posterior vitreous cortex and differentiate partial from complete PVD.6
The use of ancillary testing to diagnose PVD in routine clinical care is variable. Some authors report that ultrasonography is routinely used to diagnose or confirm PVD,7 but we tend not to use this technique (or OCT) frequently in clinical practice for the purpose of diagnosing or confirming PVD. Typically, a PVD is documented if a complete or partial Weiss ring can be determined by biomicroscopy, and vitreous syneresis or possible PVD is used to describe the status of the vitreous in which a Weiss ring is not detected.
Figure 14-1. Color fundus photograph, left eye, demonstrating a broken Weiss ring in a patient with a complete PVD.
Figure 14-2. B-scan echography, right eye, demonstrating a complete PVD. The area of increased signal along the posterior hyaloid represents the Weiss ring.
Therefore, the short answers to the questions, “How do I figure out whether or not my patient has a PVD?” and “Does there have to be a Weiss ring to diagnose the diagnosis?” are “with clinical examination and, optionally, B-scan echography or OCT” and “no.” Perhaps an additional question at this juncture is, “Does it matter?”
During pars plana vitrectomy (PPV), induction of a PVD in an eye with an attached posterior hyaloid may be an important step in the surgery. In one series of 96 eyes with high myopia that underwent PPV, intraoperative diagnosis (usually with staining agents) of complete PVD was made in 52% of eyes, and the finding of PVD was significantly associated with the preoperative diagnosis. Specifically, PVD was noted in 85% of eyes with RRD and 74% with epiretinal membrane, but only 14% of eyes with myopic foveal schisis and 10% with macular hole.8
Outside the context of PPV, does the definitive diagnosis of a PVD affect clinical management decisions? In the very common situation of a patient with new-onset or worsening complaints of flashes or floaters, we suggest that the clinical management (in this case, dilated fundus examination including scleral depression as needed) is the same regardless of the presence or absence of a PVD.
The status of the posterior vitreous may be important in the pathogenesis of certain retinal diseases. It has been taught traditionally that vitreomacular traction (VMT) is important in the development of full-thickness macular hole,9 but some macular holes occur months or years following documented release of VMT10 or PPV for RRD.11 Similarly, it has been taught traditionally that retinal neovascularization in PDR grows along the scaffold of the posterior hyaloid.12 To that effect, a Phase II randomized clinical trial evaluating the use of ocriplasmin to induce a PVD in an attempt to reduce the development of PDR is currently recruiting patients.13 However, a case of recurrent PDR with 2 areas of neovascularization elsewhere has been reported in an eye with a complete PVD, determined by the presence of a Weiss ring and confirmed using B-scan echography and OCT.14 Thus, a PVD does not guarantee that a patient will not subsequently develop a macular hole or PDR in that eye.
The relationship between PVD and response to anti-vascular endothelial growth factor (anti-VEGF) treatment for neovascular age-related macular degeneration (AMD) is unknown. In one retrospective series of 61 eyes treated with anti-VEGF agents, the presence of PVD was determined using B-scan echography, and patients with and without PVD were compared. Presence of a PVD was associated with significantly larger visual acuity improvement, but not with greater reduction in OCT-measured central subfield thickness.15 In one prospective series of 93 patients treated with anti-VEGF therapy for neovascular AMD, the presence of PVD was not significantly associated with the magnitude of visual acuity improvement nor with magnitude of central subfield thickness reduction on OCT.16
Clinicians strive to perform the best clinical examination that they can. A definitive answer to the question “Does my patient have a PVD?” may be very important in a research setting, a prospective clinical trial, or a patient being considered for PPV. For the vast majority of patients, however, this question may not affect subsequent clinical management. The presence of a PVD traditionally has suggested a lower risk of future PDR, RRD, macular hole, and other conditions, although the presence of a PVD does not prevent any of these entities and, in our opinion, treatment recommendations and follow-up intervals are generally not affected by the presence or absence of a Weiss ring.
References
1. Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages. Am J Ophthalmol. 2010;149(3):371-382.
2. De Bustros S. Vitrectomy for prevention of macular holes. Results of a randomized multicenter clinical trial. Vitrectomy for Prevention of Macular Hole Study Group. Ophthalmology. 1994;101(6):1055-1059.
3. Murakami K, Jalkh AE, Avila MP, Trempe CL, Schepens CL. Vitreous floaters. Ophthalmology. 1983;90(11):1271-1276.
4. Kakehashi A, Inoda S, Shimizu Y, Makino S, Shimizu H. Predictive value of floaters in the diagnosis of posterior vitreous detachment. Am J Ophthalmol. 1998;125(1):113-115.
5. Stalmans P, Benz MS, Gandorfer A, et al. Enzymatic vitreolysis with ocriplasmin for vitreomacular traction and macular holes. N Engl J Med. 2012;367(7):606-615.
6. Bertelmann T, Goos C, Sekundo W, Schulze S, Mennel S. Is optical coherence tomography a useful tool to objectively detect actual posterior vitreous adhesion status? Case Rep Ophthalmol Med. 2016;2016:3953147.
7. Milston R, Madigan MC, Sebag J. Vitreous floaters: etiology, diagnostics, and management. Surv Ophthalmol. 2016;61(2):211-227.
8. Philippakis E, Couturier A, Gaucher D, et al. Posterior vitreous detachment in highly myopic eyes undergoing vitrectomy. Retina. 2016;36(6)1070-1075.
9. Smiddy WE, Flynn HW Jr. Pathogenesis of macular holes and therapeutic implications. Am J Ophthalmol. 2004;137(3):525-537.
10. Smiddy WE. Macular hole formation without vitreofoveal traction. Arch Ophthalmol. 2008;126(5):737-738.
11. Medina CA, Ortiz AG, Relhan N, et al. Macular hole after pars plana vitrectomy for rhegmatogenous retinal detachment. Retina. 2017;37(6):1065-1072.
12. Akiba J, Arzabe CW, Trempe CL. Posterior vitreous detachment and neovascularization in diabetic retinopathy. Ophthalmology. 1990;97(7):889-891.
13. ThromboGenics. A Study to Evaluate the Efficacy and Safety of Ocriplasmin in Inducing Total PVD in Subjects With NPDR (CIRCLE). ClinicalTrials.gov. https://clinicaltrials.gov/ct2/show/NCT02681809. Updated January 4, 2018. Accessed April 25, 2018.
14. Shiraya T, Kato S, Fukushima T, Tanabe T. A case of diabetic retinopathy with both retinal neovascularization and complete posterior vitreous detachment. Eur J Ophthalmol. 2006;16(4):644-646.
15. Uney GO, Unlu N, Acar MA, et al. Role of posterior vitreous detachment on outcome of anti-vascular endothelial growth factor treatment in age-related macular degeneration. Retina. 2014;34(1):32-37.
16. McKibbin MA, Suter CA, Willis TA. The influence of vitreomacular adhesion on outcomes after aflibercept therapy for neovascular age-related macular degeneration. Retina. 2015;35(10):1951-1956.
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