Abstract
Floaters most commonly occur in the middle age due to age-related changes in vitreous structure and light scattering by the posterior vitreous cortex after collapse of the vitreous body during posterior vitreous detachment (PVD). In youth, floaters are most often due to myopic vitreopathy. Vitreous floaters can have a negative impact on visual function and in turn the quality of life. Techniques to characterize floaters clinically include ultrasound imaging, optical coherence tomography, and dynamic light scattering for structural characterization. Functional impact can be assessed by straylight measurements, as well as contrast sensitivity testing. When the severity of floater symptomatology is significant, commonly used therapies include neodymium:yttrium-aluminum-garnet (YAG) laser and limited 25-gauge vitrectomy. While the former is of unproven efficacy, the latter has been shown to be a safe, effective, and definitive cure that improves patients’ quality of life and eradicates symptomatology produced by light scattering and diffraction. It is thus reasonable to offer limited vitrectomy to individuals who have attempted to cope unsuccessfully and in whom functional deficit can be objectively demonstrated by testing contrast sensitivity, an important aspect of vision.
An erratum to this chapter can be found at http://dx.doi.org/10.1007/978-1-4939-1086-1_57
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Keywords
- Vitreous
- Floaters
- Posterior vitreous detachment
- Myopic vitreopathy
- Asteroid hyalosis
- Light scattering
- Straylight glare
- Contrast sensitivity
- VFQ quality of life
- Vitrectomy
- Retinal detachment • Oxygen
- Cataracts
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1.
Floaters result from structural abnormalities in vitreous. They are a more common complaint than previously known and have a more negative impact on the quality of life than previously appreciated.
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2.
Vision is adversely affected by vitreous light scattering causing straylight glare and degradation of contrast sensitivity. This explains the considerable degree of unhappiness experienced by patients suffering from floaters.
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3.
The only proven and safe treatment that effectively cures floaters and improves vision as well as patient well-being is limited vitrectomy.
I. Introduction
Floaters most commonly occur in middle age due to age-related changes in vitreous structure and light scattering by the posterior vitreous cortex after collapse of the vitreous body during posterior vitreous detachment (PVD). In youth, floaters are most often due to myopic vitreopathy. Vitreous floaters can have a negative impact on visual function and in turn the quality of life. Techniques to characterize floaters clinically include ultrasound imaging, optical coherence tomography, and dynamic light scattering for structural characterization. Functional impact can be assessed by straylight measurements, as well as contrast sensitivity testing. When the severity of floater symptomatology is significant, commonly used therapies include neodymium:yttrium-aluminum-garnet (YAG) laser and limited 25-gauge vitrectomy. While the former is of unproven efficacy, the latter has been shown to be a safe, effective, and definitive cure that improves patients’ quality of life and eradicates symptomatology produced by light scattering and diffraction. It is thus reasonable to offer limited vitrectomy to individuals who have attempted to cope unsuccessfully and in whom functional deficit can be objectively demonstrated by testing contrast sensitivity, an important aspect of vision.
II. Background
Over a century ago, Duke Elder described vitreous as a structure composed of “loose and delicate filaments surrounded by fluid” [1]. Throughout the eighteenth century, the composition and structure of vitreous mystified early theorists, spawning four different theories regarding vitreous structure. In 1741, Demours advocated the “alveolar theory” [2] in which membranes oriented in many directions enclosed compartments, or alveoli, containing the fluid portion of vitreous. Pathologists such as Virchow supported this concept [3]. In 1780, Zinn postulated that vitreous is arranged in a concentric, lamellar orientation such as the “layers of an onion” [4]. This then constituted the “lamellar theory” and subsequently gained support from fellow theorists such as von Pappenheim [5] and Brucke [6]. In 1845, Hannover proposed the “radial sector theory” where he postulated that vitreous was composed in sectors that were radially oriented around the central anteroposterior core containing Cloquet’s canal, similar in appearance to a “cut orange” [7]. Lastly, in 1848, Sir William Bowman introduced the “fibrillar theory” based upon a technique in which he utilized microscopy to show “nuclear granules” of fine fibrils that formed bundles [8].
Changes during life from the clear, gel-like structure led Szent-Gyorgito to be the first to propose that vitreous structure changes with age [9]. Duke Elder elaborated upon this with his first description of “floaters” as “the passive reaction of the vitreous body to disturbances that create liquefaction with the separation of part of its colloid basis (the residual protein) to form appearances evident clinically as opacities” [10]. This description holds true today as it is quite consistent with the prevailing theory of the mechanism by which vitreous undergoes structural changes with age.
A. Etiology of Floaters
The etiology of floaters is believed to relate to macromolecular changes that alter vitreous organization present during youth, when hyaluronan (HA) interacts with vitreous collagen fibrils to stabilize the gel and keep collagen separated far enough to allow light to pass through vitreous with minimal or no light scattering, thereby achieving transparency [11]. The vitreous gel structure is maintained by thin, unbranched, heterotypic collagen fibrils composed of collagen types II, V/XI, and IX [12] and HA that fill the space in between the fibrils [13]. Liquid vitreous forms as HA dissociates from collagen and retains water molecules, sometimes forming pools or “lacunae.” No longer separated by HA, vitreous collagen 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 proteoglycan diminishes with age, further exposing type II collagen and predisposing vitreous collagen fibrils to lateral fusion. This additionally contributes to liquefaction [16]. Through these mechanisms, the human vitreous body undergoes two morphological changes with age that create further light diffraction: an increase in the volume of liquefied spaces (synchysis) [17] and an increase in optically dense areas due to collagen cross-linking [18] (Figure V.B.8-1) [see chapter II.C. Vitreous aging and PVD].
This macromolecular inhomogeneity scatters light and creates diffraction. Electron microscopy of vitreous opacities demonstrates collagen fibrils and cellular debris that contribute to light scattering and visual disturbances [19] (Figure V.B.8-2a). Another contributing factor to the development of opacities is separation of vitreous away from the retina that follows gel liquefaction and weakening of vitreoretinal adhesion, commonly referred to as posterior vitreous detachment (PVD) [20]. The dense collagen fibril matrix in the posterior vitreous cortex (Figure V.B.8-2b) causes significant light scattering. Thus, the combination of vitreous synchysis and syneresis with PVD, which is reported in 53 % of patients older than 50 years and 65 % in patients older than 65 years [20], results in the light scattering that causes the visual perception of “floaters.” Indeed, the most common etiologies of floaters are posterior vitreous detachment (PVD), followed by myopic vitreopathy, and asteroid hyalosis [21–23]. Other pathologies such as Marfan’s syndrome, Ehlers-Danlos syndrome, and diabetic vitreopathy [see chapter I.E. Diabetic vitreopathy] also feature aggregation of vitreous collagen fibers resulting in glare due to light scattering.
III. Diagnostic Considerations
Recent studies have found that floaters are more prevalent than previously appreciated. An electronic survey recently administered to 603 people via a smartphone application has demonstrated that 76 % of individuals report seeing floaters and 33 % report impairment in vision due to floaters [24]. Additionally, myopes were 3.5 times more likely to report moderate or severe floaters compared to those with normal vision. While this study suggests a significant prevalence of floaters in younger individuals (< 5 % of participants were above age 50), this may simply be the result of selection bias since younger individuals are more likely to respond to surveys on smartphones than older individuals.
A. Clinical Presentation
The clinical presentation of a patient with floaters includes visual symptoms often described as gray, linear, hair-like structures with round points that appear more prominent against bright backgrounds (a white wall or clear sky), translucent strings, or a “spider web-like” image. The perception of these objects floating occurs during head or eye movements with an overdamping effect. To date, floaters have been viewed by the medical profession as an innocuous and benign process that will improve over time. Recent studies have begun to dismiss this notion of floaters as a benign and innocuous process [25, 26]. These studies employed utility value analysis to determine that floaters have a significantly negative impact upon quality of life and symptoms can be much more disturbing than previously appreciated [27]. In one such study [25], researchers demonstrated that the degree to which floaters lower the visual quality of life is equivalent to age-related macular degeneration and greater than diabetic retinopathy and glaucoma, as well as mild angina, mild stroke, and colon cancer. Additionally, the perceived negative impact of floaters is underscored by the fact that patients would be willing to take an 11 % risk of death and a 7 % risk of blindness and would be willing to trade 1.1 years out of every 10 years remaining in their lives to eradicate floaters.
B. Clinical Characterization of Floaters
One of the contributing factors to clinicians’ perception of floaters as a benign condition and not a disease is the lack of a clinical approach to characterize floaters both in terms of structure as well as the impact on visual function. Beyond visual acuity, the evaluation of the impact of floaters on vision is lacking, since rarely do such vitreous opacities affect visual acuity, the most common method for assessing visual function. Thus, both structural [see chapter II.F. To See the Invisible – the Quest of Imaging Vitreous] and functional assessments of floaters are needed.
1. Structural Assessment of Floaters
a. Ultrasonography
Ultrasonography may be used to image opacities within the vitreous body. Ultrasound measures differences in acoustic impedance generated by echoes produced at tissue interfaces between structures of different densities. Ultrasonography imaging within the frequencies of 8–10 MHz can produce wavelengths as small as 0.2 mm to determine pathologies such as PVD, asteroid hyalosis, vitreous hemorrhage, and large foreign bodies [28, 29] (see Figure V.B.8-3). As the vitreous ages, inhomogeneities in density develop via the aforementioned biochemical changes and echoes become more prominent. Acoustic changes or echoes in the vitreous also occur when there is persistence of primary vitreous (vascular) structures, changes induced by myopic vitreopathy, or the presence of intraocular foreign bodies [30]. An advantage of vitreous imaging by ultrasound is the ability to visualize posterior structures regardless of media opacification anteriorly (primarily lens) and the ability to estimate lacunar size and collagen fibril density [31].
Many studies have utilized ultrasonography to image the topography of the vitreous body. In patients being considered for vitrectomy surgery, rapid B-scan imaging is the most useful technique to investigate vitreoretinal pathology [30]. Static A-scan ultrasound demonstrated an 80 % incidence of acoustic interfaces in patients 60 years old and greater, which differed drastically from the 5 % incidence in patients 21–40 years old [32]. This demonstrates the decrease in acoustic homogeneity as the vitreous ages. Additionally, kinetic B-scan ultrasonography was utilized to quantify the vitreous of aged eyes with PVD compared to younger eyes [33]. The speckle density, referring to areas of acoustic hyper-reflectivity in areas of greater acoustic impedance, is increased in older subjects due to aggregation of collagen fibrils. Furthermore, chirp pulse encoding and synthetic focusing with an annular array was utilized to provide imaging of the vitreous with higher resolution and sensitivity through a 20-MHz ultrasound probe [34].
Recently, quantitative ultrasonography was used to analyze increased vitreous echodensity and correlate the findings with contrast sensitivity in patients with floaters of varying severity [35]. Investigators found that quantitative ultrasonography taken at nasal longitudinal, inferotemporal longitudinal, and inferotemporal transverse positions correlated strongly with contrast sensitivity (R = 0.82, p < 0.001) [35]. Quantitative ultrasonography should therefore have great utility to assess the severity of vitreous degeneration and aid in clinical decision-making regarding therapy of floaters.
b. Combined OCT and SLO
Time-domain OCT was previously used to extensively analyze the vitreoretinal interface [36], but utility was limited and fine details of the posterior vitreous were lacking. SD-OCT possesses inherent image resolution enhancement over time domain but also provides advantages in comparison to ultrasound with a greater horizontal resolution as well as better imaging of the vitreoretinal interface [37]. Combined SD-OCT and scanning laser ophthalmoscopy (SLO) provides further insight on vitreous structure and evolving physiologic and pathologic vitreoretinal changes. In one study [31], SD-OCT/SLO imaging examined 202 eyes and demonstrated a high correlation between diagnosis of complete PVD found by both clinical examination and OCT. Additionally, high correlation was found between ultrasound and SD-OCT/SLO results for complete and incomplete PVD. Due to excellent depth of field during coronal plane imaging with the SLO, central vitreous opacities can be very well visualized (see Figure V.B.8-4). Note how the central darkness (umbra) is surrounded by an area of lighter shadow (penumbra) for both floaters. The umbra is the innermost and darkest part of a shadow, while the penumbra is where only part of the light is obscured, resulting in a partial shadow.
Furthermore, with longitudinal OCT imaging, the floater-induced attenuation of incident light transmission to the fundus results in shadowing and poor resolution of fundus structure, in particular, the retinal pigment epithelium/Bruch’s membrane complex, that maps the floater shadow upon the fundus and may serve as a means of quantifying the density of these structures (see Figure V.B.8-5).
c. Dynamic Light Scattering
Dynamic light scattering (DLS) is a laser-based nanodetector that can measure the size of particles from 3 nm to 3 μm in the cornea, lens, aqueous, and vitreous [38], thus enabling the mapping of three-dimensional distribution of vitreous macromolecules [39]. Ophthalmic usages of DLS include characterizing diabetic vitreopathy by detecting aggregation of vitreous collagen fibrils in diabetes [40–43], identifying patients at high risk for cataracts by detecting a decreased alpha-crystallin index [44], monitoring inflammatory processes following refractive surgery [45], and evaluating the molecular effects of pharmacologic vitreolysis [46]. In a comprehensive study of the last mentioned [43], DLS reproducibility demonstrated a coefficient of variance less than 3.3 % in all but one specimen. Thus, DLS was utilized to measure vitreous macromolecule sizes before, during, and after injection of ocriplasmin, hyaluronidase, and collagenase into solutions of respective substrates as well as whole bovine vitreous. This was made possible by measuring the diffusion coefficients of the molecules to determine size and detecting the increase in Brownian motion produced when the particle size decreased following pharmacologic vitreolysis. Therefore, the use of DLS in pharmacologic vitreolysis may play a paramount role in the future of vitreoretinal pharmacotherapy of various types, especially pharmacologic vitreolysis [see chapter VI.A. Pharmacologic vitreolysis].
2. Effects of Floaters on Vision
a. Straylight
Light scattering produced by opacities within the vitreous body can be quantified by the use of the C-quant (C-Quant; Oculus Optikgeräte, Wetzlar-Dutenhofen, Germany) straylight meter [47, 48]. Straylight, or disability glare, refers to a perceived spreading of light around a bright light source. Straylight was first described by Cobb in the early 1900s as “equivalent veiling luminance” (Leq), the external luminance that has the same visual effect as the glare source [24]. Symptoms of straylight appear to the patient as haziness, decreased color and contrast, difficulty recognizing faces, and glare hindrance. Factors affecting straylight in normal patients include age (2× increased straylight values at 65 years old and 3× increased straylight values at 77 years old) [44, 49] and pigmentation – blue-eyed Caucasians had increased values 0.1–0.4 log units higher compared to pigmented non-Caucasians [50]. One study [51] recommended the utilization of the C-quant straylight meter to assess long-term effect of surgical procedures on quality of vision based on its high reproducibility. The C-quant straylight meter thus provides a functional measure for the intensity of light spreading seen by the patient and demonstrates the increasing role of glare and contrast sensitivity in impairing vision.
b. Contrast Sensitivity Function
Measuring contrast sensitivity function (CSF) provides a useful method to quantify floaters and the impact on vision. The measure of CSF is often used to supplement visual acuity measurements in evaluating posterior capsular opacification after cataract surgery [52] as well as demonstrate reduced visual function in patients with cataracts whose acuity is only slightly impaired [53, 54]. In one study, multiple logistic regression analysis demonstrated that reduced contrast sensitivity was independently associated with a vision disability score affecting tasks such as judging distance, night driving, and mobility issues [55]. In addition to anterior ocular media opacities, vitreous opacities may also degrade CSF.
This hypothesis was tested in a study [56] at the VMR Institute for Vitreous Macula Retina in California, that utilized computer-based Freiburg Acuity Contrast test (FrACT) to evaluate CSF [57–59]. This CSF testing method had a reproducibility of 92.1 % when employing the Weber index (%W = (Luminancemax − Luminancemin)/Luminancemax) [52, 60] as the outcome measure. Studies have previously demonstrated that FrACT yields results similar to those of Pelli-Robson and is not significantly affected by group differences in visual acuity [61]. Patients with bothersome floaters have been reported to have CSF that is diminished by 67.4 % (4.0 ± 2.3 %W; N = 16) compared to age-matched controls (2.4 ± 0.9 %W; N = 16; P < 0.01). Since publication of these preliminary findings, this study has continued with increased enrollment (n = 38) obtaining similar results: in floater patients, CSF is degraded by 72.3 % (4.14 ± 1.95 %W) compared to controls (P < 0.01).
As demonstrated in Figure V.B.8-6, diminished contrast sensitivity is often a clinically significant consequence of light scattering by ocular media opacities. An opaque object with a smooth surface (e.g., an asteroid hyalosis body) will block light rays that create an umbra and a penumbra (see “a” in Figure V.B.8-6). A floater of the same size but with uneven surfaces and edges will scatter more light rays, creating a smaller umbra and a larger penumbra than a smooth body (see “b” in Figure V.B.8-6). Although the objects are of the same size, the uneven surface of a floater will scatter more light, and the larger penumbra will degrade contrast sensitivity. As light interacts with collagen fibers in the vitreous (Figure V.B.8-7), the spacing of the collagen fibrils, or interfibrillar distance, can influence the transmission of light to the retina. When the interfibrillar distance is decreased as in aged vitreous with syneresis (b in Figure V.B.8-7), increased scattered light will create a larger penumbra and degrade contrast sensitivity.
IV. Therapeutic Considerations
To date, treatment options for patients with bothersome floaters have been limited. Because floaters are generally viewed by doctors as benign and innocuous, patients are often told to cope with symptoms and hope for either improvement via settling inferiorly or acceptance over time. For patients unwilling to accept this advice, eyedrops and Nd:YAG (neodymium:yttrium-aluminum-garnet (YAG) laser) are sometimes offered as therapies, though efficacy has never been demonstrated and reports are conflicting [62–64]. In one study, Nd:YAG vitreolysis eradicated floater symptoms in only 1/3 of patients with moderate clinical improvement and worsened symptoms in 7.7 % of patients [62]. As a result, the authors concluded that Nd:YAG vitreolysis provided a safe, but only mildly if at all effective, treatment for the eradication of floater symptoms. Additionally, posteriorly located vitreous opacities, which often cause the most disturbing symptoms, cannot be safely treated by YAG laser [64].
A. Vitrectomy
Pars plana vitrectomy (PPV) provides the most effective treatment for floaters as it offers a definitive cure with complete resolution of symptoms. However, this procedure is invasive with the possibility of complications such as endophthalmitis, retinal tears and detachments, cataract formation, glaucoma, vitreoretinal hemorrhage, and macular edema [65]. Therefore, it is important to only advocate vitrectomy to cure floaters for patients who understand the desired surgical goal and accept the risks, albeit minimal, and who have objective findings of visual dysfunction, such as contrast sensitivity or, if sufficiently severe, visual acuity. With the use of 25-gauge instruments and sutureless, technique with limited vitrectomy, postoperative complications can be diminished significantly to provide a safe and effective cure for clinically significant floaters [56, 65].
1. Efficacy of Vitrectomy for Floaters
Vitrectomy can cure floaters by decreasing light scattering and thus decrease straylight, increase contrast sensitivity function (CSF), and improve the quality of life. It has been demonstrated that straylight measurements improve following vitrectomy [66]. Improvement in recognizing faces and glare hindrance occurred in 38 of 39 cases (97 %) with a statistically significant decrease in straylight glare measurements post vitrectomy, with 69 % of cases having straylight values within the normal range compared to 21 % preoperatively. The overall improvement, however, was only 18.2 % in the 39 floater cases of that study, perhaps related to the fact that 21 % of the cases had preoperative straylight measurements that were within the normal range.
Light scattering also degrades contrast sensitivity [47] underscoring that floaters negatively impact patients’ vision in more than one way. In the aforementioned prospective study of 16 cases [56], investigators at the VMR Institute in Huntington Beach, California, found that patients with floaters had a 67 % diminution in CSF when compared to age-matched controls (P < 0.013). Following limited vitrectomy, CSF normalized at 1 week (P < 0.01) and remained normal at 1 month (P < 0.003) and at greater than 3 months (P < 0.018). Following publication in 2013, this study has been continued with enrollment now up to 38 subjects. CSF improved in every single subject at 1 week (P = 1.4 × 10−6; N = 36), 1 month (P < 0.0001; N = 38), 3 months (P = 1.07 × 10−5; N = 21), 6 months (P = 0.008; N = 19), and >9 months (P = 0.009; N = 15) after limited vitrectomy (Figure V.B.8-8).
Given the aforementioned impacts of floaters on vision and patient well-being, it is reasonable to expect that following vitrectomy, patients would perceive an improvement in their quality of life. One study [67] of 110 patients who underwent vitrectomy to cure bothersome floaters demonstrated 85 % patient satisfaction. Additionally, 84 % of patients were completely cured of floaters, while 9.3 % of patients were less troubled by floaters. Several studies have utilized the National Eye Institute Visual Function Questionnaire (NEI VFQ-39) to quantify patients’ improved visual quality of life following surgery. In the aforementioned prospective study at the VMR Institute in Huntington Beach, California [56],VFQ testing in the original 16 cases demonstrated VFQ improvement of 29.2 % (P < 0.001) at 1 month postoperatively that was sustained at 3–9 months following surgery. Continued study at the VMR Institute in Huntington Beach has increased this series and found an average postoperative improvement in the composite index of NEI VFQ-36 of 32 % (P < 0.001). Similar improvements have been demonstrated in other studies utilizing the NEI VFQ [68–70] and other methods [71, 72] to assess patient visual quality of life before and after vitrectomy.
2. Safety of Vitrectomy for Floaters
As described above, vitrectomy offers an effective cure of floaters that improves vision and quality of life for patients who cannot cope with the symptoms of floaters, presumably because of profound diminution in contrast sensitivity. As an invasive procedure, however, vitrectomy has known potential complications [73–76]. Fortunately, a study by Delaney et al. [62] demonstrated a lower postoperative complication rate associated with vitrectomy for floaters as opposed to other vitreoretinal diseases. In a study of 31 patients (42 eyes) who underwent either Nd:YAG vitreolysis or pars plana vitrectomy for floaters, the authors compared the efficacy of the two treatments to eradicate floater symptomatology. Of these, 15 eyes underwent vitrectomy for floaters: 4 eyes underwent vitrectomy as a primary treatment for floaters, while 11 patients had vitrectomy subsequent to Nd:YAG laser treatment for floaters. In this admittedly small and limited study, 93.3 % of patients demonstrated complete resolution of floaters following vitrectomy with an average follow-up post vitrectomy of 31.5 months (range 6–108 months). Reported complications included postoperative cataract development that underwent successful phacoemulsification surgery and postoperative retinal detachment occurring 7 weeks after a combined vitrectomy with phacoemulsification. Another study found a relatively low rate of immediate post-floater vitrectomy retinal detachment with a slightly increased risk during long-term follow-up [77]. Out of 73 eyes that underwent vitrectomy for severe and persistent floaters ≥6 months’ duration, a total of five (6.8 %) developed retinal detachments, four occurring 24–44 months after vitrectomy.
The current approach to curing floaters with vitrectomy must take into consideration the following specific risks and incorporate measures to mitigate these risks.
a. Endophthalmitis
Endophthalmitis is a rare but severe complication of vitrectomy [78]. However, instrument size (microincisional 23- or 25-gauge vs. conventional 20-gauge), beveled entry technique, and cannula removal with a blunt probe have all been demonstrated to lower the risk of this postsurgical complication. Recent literature has reported that there is inconclusive evidence that 25-gauge PPV has a higher rate of endophthalmitis than 20-gauge PPV [79–82]. The one exception is the use of a straight approach to cannula insertion, which has an increased risk for endophthalmitis as compared to a beveled approach [83, 84]. This probably relates to a reduction of vitreous incarceration, which will not only mitigate endophthalmitis [85, 86] but also peripheral retinal tears [87–89] and fibrovascular proliferation in diabetic patients [90]. Regarding endophthalmitis, incisional vitreous incarceration is believed to improve postoperative sclerotomy closure, preventing the entry of bacteria into vitreous via an incisional vitreous wick [85]. Cannula removal at the end of surgery also influences the risk of postoperative endophthalmitis. In a prospective study of 118 cadaveric pig eyes that underwent vitrectomy with 23-gauge transconjunctival sclerotomies, two techniques of cannula removal were employed: the superior cannula was extracted with the illumination probe inserted through it and the other cannula was removed with a cannula plug inserted [86]. Postoperative incisional vitreous entrapment was subsequently evaluated and demonstrated vitreous entrapment in 95.8 % of entry sites whose cannulas were extracted with the plug inserted, whereas incarceration only occurred in 93.2 % of incisions whose cannulas were extracted with the light probe inside. While this was not a big difference, the authors report that this difference may be due to the peripheral vitreous being displaced to the inner face of sclerotomies when a plug is inserted, thus leading to a greater degree of vitreous incarceration. The use of non-hollow probes for cannula extraction may have contributed to the safety profile observed in the ongoing study at the VMR Institute in Huntington Beach, California [56], that employs 25-gauge vitrectomy with beveled incisions and illumination probe insertion for cannula removal at the end of the case. In 98 eyes with severe floaters, there have been no cases of endophthalmitis. Additionally, a reduction in vitreous incarceration may also decrease post-vitrectomy retinal detachment rate [89].
b. Retinal Tears and Retinal Detachment
Retinal tears and detachments occurring intraoperatively or postoperatively are well-documented potential complications [91, 92]. However, smaller instrument size (microincisional 23- or 25-gauge vs. conventional 20-gauge), avoiding surgical induction of PVD, and performing cannula removal as described above can decrease the incidence of retinal tears and detachment.
The use of 25-gauge vitrectomy instruments allows for an incision with an oblique scleral tunnel that can be self-sealing without any sutures, decreasing operating time and hastening postoperative recovery [93–95]. Furthermore, the use of self-retaining cannulas preserves the edge of the incisions during instrument insertion and removal and allows more effective self-sealing during sutureless surgery [96, 97]. Iatrogenic intraoperative peripheral retinal break incidence during 23-gauge vitrectomy was compared to conventional 20-gauge vitrectomy, and retinal breaks occurred significantly less often during 23-gauge (16 of 973 cases, 1.6 %) compared to conventional vitrectomy (25 of 402 cases, 6.2 %) [98]. This is consistent with another study that found a 4.9 % retinal detachment rate 14 months after vitreo-macular surgery with 20-gauge instruments versus a 1.1 % retinal detachment rate with 23-gauge instruments [99].
Additionally, the use of 360° indirect ophthalmoscopy with scleral depression to identify retinal breaks or tears for prophylactic treatment prior to or during surgery has also been shown to decrease the incidence of postoperative retinal detachments [100]. In a study of 415 eyes of 381 patients that underwent primary, standard, three-port vitrectomy, 65 retinal breaks were found in 48/415 eyes (11.6 %) that were treated perioperatively. Of 366 eyes in which no breaks were identified during vitrectomy, postoperative retinal detachment occurred in 8 (2.2 %) eyes; all occurring at least 3 months following vitrectomy. This demonstrates the importance of avoiding, detecting, and treating breaks during surgery to decrease the incidence of postoperative RD. In a study performed by Sebag et al. [56], 24/98 (24.5 %) cases received localized prophylactic laser or cryopexy to peripheral retinal breaks a minimum of 3 months prior to vitrectomy for floaters. This further contributed to the safety profile of the procedure, with no cases of retinal detachment occurring at a mean follow-up of 16.2 months (range = 3–51 months).
Lastly, avoiding the induction of PVD during vitrectomy will also help decrease the incidence of intraoperative or postoperative retinal breaks. A study of 311 patients undergoing vitrectomy for treatment of premacular membrane with macular pucker or macular hole demonstrates a decreased incidence of retinal tears when surgical PVD was avoided in both groups [101]. For patients undergoing vitrectomy for macular pucker, 32.1 % had retinal breaks with induction of PVD compared to 2.1 % that had retinal breaks without induction of PVD (P = 0.006). For patients undergoing vitrectomy for macular hole, 12.7 % had retinal breaks with induction of PVD while only 3.1 % had breaks without induction of PVD (P = 0.008). Additionally, in a previous study that induced PVD during vitrectomy for floaters, retinal breaks occurred in 9/30 (30.5 %) cases [102], compared to 0/60 (0 %) that developed retinal breaks or detachments without induction of PVD (P < 0.007) [56]. Since that publication, a total of 98 cases have been performed at the VMR Institute in Huntington Beach without PVD induction. There have been no cases of retinal breaks or detachment.
c. Cataracts
Increased risk of cataract formation due to increased intravitreal levels of oxygen following vitrectomy [103–108] may be mitigated by leaving the anterior vitreous and posterior vitreous intact to protect the lens against oxygen free radicals. Previous studies [103, 106] have demonstrated that vitreous maintains an intraocular oxygen concentration gradient from the retina to the vitreous gel [see chapter IV.B. Oxygen in vitreo-retinal physiology and pathology]. Following vitrectomy, the oxygen gradient no longer exists due to the removal of the vitreous. One study demonstrated that the difference in oxygen tension pre- and post vitrectomy is statistically significant with oxygen tension levels in the mid-vitreous and near the lens increasing greatly, remaining elevated, and becoming more uniform in distribution in patients who had previous removal of vitreous gel [103]. This led to the conclusion that vitrectomy significantly increases intraocular oxygen tension after surgery causing exposure of the crystalline lens to reactive oxygen species that contribute to cataract formation. Similar reports of vitrectomy in animal models have further confirmed that oxygen measurements taken in the nucleus of the lens post vitrectomy had increased oxygen levels due to diffusion from elevated oxygen tension in the vitreous [106].
Beebe et al. [104] further elucidated the concept of oxidative damage and its role in cataract formation. They demonstrated that patients with ischemic diabetic retinopathy had lower oxygen levels in the vitreous and thus had partial protection from nuclear cataract development within the first year after vitrectomy. Other studies have also suggested that the rate of cataract extraction following vitrectomy in diabetic patients is lower than in nondiabetic patients undergoing vitrectomy [108]. Additionally, PVD has been implicated in possible acceleration of nuclear cataract formation due to increased oxygen tension levels following PVD. Pharmacologic vitreolysis induction of posterior vitreous detachment with ocriplasmin has also been demonstrated to increase vitreous oxygen concentration in comparison to control eyes and hyaluronidase-injected (without PVD) eyes [109]. In another study, intravitreal ocriplasmin injection that produced liquefaction and PVD was associated with a 68 % increase in lens nuclear oxygen tension compared to intravitreal hyaluronidase that only produced liquefaction and not PVD [110].
Thus, based on the strong association between increased oxygen levels and nuclear cataract formation [103, 111, 112], age-related PVD may be related to an acceleration of nuclear cataract development. Due to the increased oxygen tension levels that occur with induction of PVD and removal of the vitreous in vitrectomy, this suggests that leaving the anterior and posterior vitreous intact during surgery may result in decreased cataract formation postoperatively. In the VMR Institute study of 98 eyes with limited vitrectomy for clinically significant floaters, only 14/60 phakic eyes (23 %) needed cataract surgery, all in patients with a mean age 64.1 years and average time between vitrectomy and cataract surgery of 13 months. No patients under 53 years of age required cataract surgery. These findings support the concept of cataract mitigation by not inducing PVD and leaving vitreous (and its constituent antioxidants) intact behind the lens (see Figure V.B.8-9).
Conclusions
Patients are disturbed by floaters due to a reduction in contrast sensitivity, an important, albeit underappreciated, aspect of vision. As the medical community begins to better understand the impact of floaters on patients’ vision and the impact on quality of life, it is advisable to consider the treatment that has proven to be most effective and safe. Today, for patients who are unable to cope with chronically symptomatic vitreous opacities, the use of sutureless, limited vitrectomy using small-gauge instrumentation can safely eradicate symptoms, improve vision, and increase quality of life. Future directions to help patients with floaters include the use of optical methods to counteract or neutralize the visual effects, improved surgical instrumentation to further decrease risks, and pharmacologic vitreolysis (see Part VII. Pharmacologic vitreolysis) to obviate the need for vitrectomy and minimize the invasive nature of the treatment by pharmacologically breaking down vitreous macromolecules, especially the aggregates of collagen that underlie the formation of floaters [46, 113–123].
It is important that the medical profession heed the cry of reasonable patients afflicted with clinically significant floaters, defined by quantitative ultrasound and contrast sensitivity testing, to achieve the goal of modern medicine [124]:
To help people die young, as late in life as possible
Ernst L. Wynder MD
Founding President of the American Health Foundation
- CSF:
-
Contrast sensitivity function
- DLS:
-
Dynamic light scattering
- FrACT:
-
Freiburg acuity contrast test
- HA:
-
Hyaluronan
- Leq:
-
Equivalent veiling luminance
- mmHg:
-
Millimeters of mercury
- Nd:YAG:
-
Neodymium:yttrium-aluminum-garnet
- NEI VFQ-39:
-
National Eye Institute visual function questionnaire
- pO2 :
-
Partial pressure of oxygen
- PPV:
-
Pars plana vitrectomy
- PVD:
-
Posterior vitreous detachment
- RD:
-
Retinal detachment
- SD-OCT:
-
Spectral-domain optical coherence tomography
- SLO:
-
Scanning laser ophthalmoscopy
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Huang, L.C., Yee, K.M.P., Wa, C.A., Nguyen, J.N., Sadun, A.A., Sebag, J. (2014). V.B.8. Vitreous Floaters and Vision: Current Concepts and Management Paradigms. In: Sebag, J. (eds) Vitreous. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-1086-1_45
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