SPECTRAL-DOMAIN OPTICAL COHERENCE TOMOGRAPHY OF PERIPHERAL LATTICE DEGENERATION OF MYOPIC EYES BEFORE AND AFTER LASER PHOTOCOAGULATION
To investigate the microstructural characteristics of lattice degenerations before and after laser photocoagulation in myopic eyes by spectral-domain optical coherence tomography (SD-OCT).
Twenty-five eyes of 25 consecutive patients at the High Myopia Clinic of the National Taiwan University Hospital were retrospectively reviewed. Myopic eyes with peripheral lattice degeneration were enrolled in the study. Best-corrected visual acuity (BCVA), axial length measurement, color fundus photography was performed. SD-OCT analyses on the lattice degeneration were performed before and after prophylactic laser photocoagulation. All patients were followed for at least 6 months.
In total, 25 myopic eyes with peripheral lattice degenerations were studied. The mean refractive error was −9.92 ± 4.77 Diopters (D) with 21 (84%) of the eye being highly myopic (Over −6.0 D). The average axial length was 27.7 ± 1.86 mm. In these myopic eyes, retinal thinning was the most common finding (92%), followed by vitreoretinal traction (72%), retinoschisis (44%), vitreous membrane with deposits (36%), and retinal break with subretinal fluid (4%). A blunting effect of the vitreoretinal tractions was found after laser photocoagulation.
To our knowledge we firstly investigated the pre- and post-laser photocoagulation microstructural changes using SD-OCT. It demonstrated a beneficial effect of retinoplasty, which released vitreoretinal tractions after laser photocoagulation. Combined with the findings of subtle microstructural retinal breaks and subretinal fluid, early prophylactic laser treatment warrants sincere consideration in these myopic eyes.
Lattice degenerationOptical coherence tomographyMyopiaLaser photocoagulationRetinal detachment
Lattice degeneration is an important clinically recognized vitreoretinal abnormality in myopia. It is an atrophic peripheral retinal degeneration influencing 7–10% of the normal population and the peak of prevalence occurs during the second decade of life.1, 2, 3, 4, 5 Based on a prospective study conducted in India, in a myopic population, the prevalence of retinal degeneration is 42% and lattice degeneration was the most common type.6 In patients with retinal detachment, the presence of lattice degeneration in the fellow eye ranged from 9.2% to 35%.7 One to over twenty lattice lesions could be found in per eye. They appear mostly in the vertical meridian (11–1 o'clock and 5–7 o'clock).8 The pathogenesis of lattice degeneration is still not clear. Theories have suggested developmental anomalies of the internal limiting membrane, abnormal retinovitreous traction, and choroidal abnormalities.2, 4, 8, 9
Lattice degeneration predisposes the eye to rhegmatogenous retinal detachment. Atrophic holes in lattice degeneration cause localized retinal detachment; while most rhegmatogenous retinal detachment is due to tractional retinal tears following posterior vitreous detachment.7, 8, 10 Byer et al. reported that only 1.08% of patients with lattice degeneration developed clinical retinal detachment if left untreated after 10 years of long-term follow-up.3 In a 10-year follow-up study in Taiwan, there were 4.4% of the high myopic patients with untreated lattice degeneration developed macula-off retinal detachment.21 At the present time, no conclusions have been reached about the effectiveness of laser treatment to prevent retinal detachment in eyes with asymptomatic retinal breaks or lattice degeneration, or both.
Retinal focal laser is one of the methods to prevent rhegmatogenous retinal detachment from lattice degeneration. However, the recent literature does not support the benefit of prophylactic treatment on asymptomatic lattice degeneration for the prevention of retinal detachment.11 It does not seem to matter whether the lattice degenerations are associated with or without holes. Retinal focal laser treatment is thought to counteract the traction around the lattice degeneration to prevent further retinal detachment, but the microstructural changes around the lattice degeneration before and after retinal focal laser treatment were unknown.
The current knowledge regarding lattice degeneration is from clinical studies, autopsy, and electron microscopic reports. Foos et al. reported that in eyes with lattice degeneration, higher rates of posterior vitreous detachment are not the cause of higher rates of retinal detachment because there was no association between the local and central vitreous lesions based on the findings from autopsy eyes.12 However, fellow eyes with PVD and retinal breaks can progress to retinal detachment easily.13 In the process of pathology sample preparation, destruction of the tissue may occur. A pathology study is not the appropriate method to observe the structural characteristics of lattice degeneration in patients. SD-OCT retinal scanning, as a non-invasive method to observe the cross section of the retina, is a new tool that allows the observation of the characteristics of peripheral lattice degeneration in vivo. However, in the past decade, few studies have measured lattice degeneration, and there are even fewer reports using optical coherence tomography to examine lattice degeneration.4
In the present study, we aimed to observe the microstructural morphology of peripheral lattice degeneration by SD-OCT, and describe the different presentations along with the morphological changes before and after laser photocoagulation.
Twenty-five eyes of 25 consecutive myopic patients with peripheral lattice degeneration were retrospectively studied. All 25 patients were found to have peripheral lattice degeneration during their regular fundal examination. These patients were followed at the High Myopic Clinic for individuals with high myopia at the National Taiwan University Hospital in Taiwan. All the OCT exams were performed at the same hospital. No prior ophthalmic surgical history was reported, except for one patient who received LASIK surgery in both eyes and two patients who received scleral buckle surgery in the fellow eye due to retinal detachment. The patients did not report symptoms like photopsia, increased floaters, or decreased vision either in the examined eye or fellow eye 6 months before the exam and during follow-up. Each patient received a basic ophthalmologic examination, including best-corrected visual acuity (BCVA), intraocular pressure, anterior segment and fundal examination, and axial length measurement. Color fundus photography and SD-OCT studies were performed at the lattice degeneration area. We utilized spectral-domain optical coherence tomography (SD-OCT) (RTVue® Model-RT100 version 3.5, Optovue, Inc., Fremont, CA, USA) to scan the areas of lattice degeneration. Because the lattice degenerations were located at the peripheral retina, and the ultimate sites were very close to the equator, the patients were asked to look at a specific direction as hard as they could during the exams to get clearer images. The lesions could be scanned repeatedly guided by the morphology of the lattice degeneration and the color fundus photo. The SD-OCT analyses were performed with a line placed across the lattice degeneration by manual rotation of the line scan. Each line was 5–6 mm in length. The OCT image provides us accurate and direct cross views of the lattice degenerations in vivo.
Laser photocoagulation was performed in all eyes with the Pascal® Synthesis laser system (Topcon, U.S.A; Argon laser, wavelength 532 nm). Approximately three rows of single spots of retinal focal laser were applied around the lattice degeneration (10 μm from the edge of the lattice degeneration, Grade 2 to Grade 3) within two weeks after the OCTs were performed. Each patient was followed for at least 6 months, and no new breaks in the eyes were noticed. OCT was performed immediately before and monthly after the laser photocoagulation for 6 months. Image J was used to analyze the thickness of the lattice degenerations. Institutional Review Board/Ethics Committee of National Taiwan University had approved the study. The patient records/information was anonymized and de-identified.
Twenty-five myopic eyes with peripheral lattice degeneration were scanned with the SD-OCT retinal scanner (Optovue, USA). The mean age of the population in this study was 35.9 years (standard deviation (SD), ±13.2). There were 6 men and 19 women included in the study. Ten of the eyes were right eyes, and 15 were left eyes. The mean myopia was −9.92 (SD, ±4.77 D) D, with 21 (84%) high myopic eyes (over −6.0 D). The average axial length was 27.7 mm (SD, ±1.86 mm); the median visual acuity was 18/20 (Table 1).
Table 1. Baseline demographics and clinical findings of patients with peripheral lattice degeneration.
Total patient number25Age (years, mean ± SD)35.9 ± 13.2Gender (no.; M/F)6/19Laterality (no.; OD/OS)10/15Retinal focal laser (no./%)25 (100)High myopia (no./%)21 (84)Average myopia (diopters; mean ± SD)−9.92 ± 4.77Average Axial length (mm; mean ± SD)27.7 ± 1.86Median BCVA0.9
Regarding the characteristics of lattice degeneration, the average length was 1.48 clock hours long, and in most of the eyes (76%) the lattice degeneration involved one quadrant. The temporal side was the most common area where lattice degeneration occurred. We made detailed recordings of the locations of the lattice degenerations by numbering the areas of lattice degeneration: 1: nasal upper, 2: nasal lower, 3: temporal lower, 4: temporal upper, 5: 2 + 3, 6: 3 + 4, 7: 1 + 4, 8: 2 + 3 + 4, 9: 1 + 3 + 4 (data not shown).
We noticed some characteristics of the lattice degeneration with SD-OCT. In our population, retinal thinning was the most common finding (92%), followed by vitreoretinal traction (72%), retinoschisis (44%), vitreous membrane with deposits (36%) and retinal breaks with subretinal fluid (4%) (Table 2).
Table 2. Characteristics of the peripheral lattice degeneration on optical coherence tomography (OCT) images.
CharacteristicsCase number(s)Percentage (%)Thinning2392Membrane formation936Vitreoretinal traction1872Retinoschisis1144Retinal break with subretinal fluid14
The local findings are summarized as followed.
In 23 patients (92%), retinal thinning was noted in the lattice degeneration area. In those lattice degenerations with the change of thinning, the thickness of the lattice degeneration was thinner than the surrounding retina. For example, the thickness of the lattice degeneration was 63.0% of the surrounding retinal tissue in Fig. 1B. There was no obvious destruction of the inner and outer retinal layers. Some local thinning of the retina was observed (Fig. 1A, B).
There were 18 patients (72%) showing vitreo-retinal traction around the lattice degeneration. The vitreous strand was attached to the retina near the lattice degeneration, and pull the surrounded retina in the anterior direction (Fig. 1C, D).
In 11 (44%) of the patients, retinoschisis was observed in the lattice degeneration. The retina split into two to three layers, with some space between the split layers. One of these cases also had SRF between the neuroretina and pigmented layer (Fig. 1D).
In 9 (36%) patients, a vitreous membrane with deposits was observed between the posterior hyaloid and retina (Fig. 2).
In one eye (4%) with lattice degeneration, we observed subretinal fluid with a retinal break. However, there was no visible subretinal fluid or break in the fundus color photography of the same area (Fig. 3).
The change in the characteristics of the retinal and vitreous around the lattice degeneration before and after retinal focal laser was also detected. Laser retinoplasty caused blunting of vitreous traction. The traction did not release or intensify from the area of photocoagulation.
The micromorphology of the lattice degeneration after focal laser treatment revealed blunting of the vitreous traction due to a retinoplasty effect compared to the condition that existed before focal laser. The blunting effect could be observed 2–3 months after laser photocoagulation. Ninety-two percent (23 out of 25) of our patients receiving laser photocoagulation had the change of blunting vitreous traction. The scarring of the ellipsoid zone around the lattice degeneration indicated the laser area. In areas in the lattice degeneration, the vitreous traction did not appear to release or progress further after laser photocoagulation (Fig. 4).
In our study population, there were more women than men, and the ages were distributed from 14 to 64 years. Most of the patients were between 20 and 50 years of age. The average myopic refractive error was high and 84% of the patients had high myopia, which reflected the general myopia prevalence in Taiwan.14 The average axial length was also much longer than that of the general population, which was compatible with the high myopic population in this study.14 In our population, the moderate to severe myopia and the range of axial length conferred a high risk of developing a retinal detachment.15, 16 Depending on the high myopia and presence of lattice degeneration, the incidence of retinal detachment of these patients was high despite the relatively young age of this cohort of patients.17 Despite the highly myopic eyes and peripheral retinal degeneration, the mean VA in this group was relatively good.
In our study, the most common finding of lattice degeneration in SD-OCT was focal retinal thinning, which is consistent with the histological findings from autopsy.18 The occasional absence of an internal limiting membrane at the center of the lattice degeneration observed on SD-OCT was also compatible with the findings observed with electron microscopy in autopsy eyes.18 The vitreous membrane with deposits observed on SD-OCT was probably related to vitreous condensation and the proliferation and accumulation of glial cellspreviously found in autopsies of myopic eyes with lattice degeneration.18 In addition to the vitreous condensation, exaggerated vitreoretinal adherence at the edge of the lesion was also found in autopsied myopic eyes. The vitreoretinal traction was found in vivo by SD-OCT in our study, and could be the traction force near the lattice degeneration. This was probably related to the retinoschisis and further subretinal fluid around the area of lattice degeneration.18
The etiology of lattice degeneration remained unclear until now, and the subretinal fluid or retinal detachments around the lattice degeneration were thought to be related to atrophic holes rather than tractional force around the degeneration. However, based on our image findings, 72% of the cases in our study presented with vitreoretinal traction around their areas of lattice degeneration. Some of the eyes even showed retinoschisis within the lattice degeneration. The traction or retinoschisis may further develop subretinal fluid and retinal detachment in the follow-up.
In the case with subretinal fluid noticed by SD-OCT, a true retinal breaks were detected using SD-OCT imaging, but not using color fundus photography. In clinical practice, SD-OCT can help to detect the possible retinal breaks in the lattice degeneration which are invisible by funduscope. Prophylactic retinal focal laser treatment could be performed early to prevent further retinal detachment in these cases.
There was no prospective study found in the literature review regarding the prophylactic treatment of asymptomatic retinal breaks or lattice degenerations for preventing retinal detachment.19 There is no efficient evidence of effective prophylactic treatment of retinal lesions except for that with symptomatic flap tears.11 The treatment of lattice degeneration is basically observation unless further symptoms or breaks develop. Folk et al. reported a significantly reduced incidence of new breaks or retinal detachment over 7 years in the fellow eye of RD after prophylactic treatment of the lattice degeneration (19.4 versus 7.5%, P = 0.0002).20 However, myopia and lattice degeneration are still risk factors in rhegmatogenous retinal detachment.17 In our observations via SD-OCT, retinal vitreoretinal traction occurs around some lattice degenerations (72%), and some of them are combined with retinal breaks even subretinal fluid, which are not detectable simply by indirect ophthalmoscope examination. SD-OCT provides us further information about lattice degeneration. By comparing the traction before and after focal laser treatment, the traction did not pull farther and became more stable after treatment. In eyes with blunting effect, the traction angle was less sharp, indicating the probable released traction by retinoplasty effect. Since the traction around the lattice degeneration is the major force causing the tractional tear, the release of the traction may prevent further tear at the lattice degeneration. Prophylactic focal retinal laser is indicated in some lattice degenerations to prevent retinal detachment under SD-OCT examination.
Traditional data indicate that patients with lattice degeneration with or without retinal holes are at a very low risk for progression to clinical retinal detachment without a previous rhegmatogenous retinal detachment in the fellow eye.3, 19 Only approximately 0.7% eyes or 1.08% patients developed clinical retinal detachments due to round holes in lattice lesions or asymptomatic tractional tear.3 However, our long-term follow-up data showed that highly myopic eyes are prone to develop macula-off retinal detachment.21 Thus, sincere consideration of prophylactic laser photocoagulation should be made in highly myopic eyes and those eyes with susceptible microstructural characteristics, such as: severe vitreoretinal traction, retinal breaks, and subretinal fluid.
The blunting effect of laser photocoagulation implicated that prophylactic laser was effective in partially releasing the vitreous traction. In addition, the chorioretinal adhesion created by the laser photocoagulation should further secure the lattice degeneration. Overall, laser photocoagulation was effective and safe in this SD-OCT study.
There are still some limitations in this study. First, the lattice degenerations are usually at the peripheral retina, even to the level of equator. The OCT images of the peripheral retina in high myopic patients may not be as clear as central retina with OCT. But we can still get useful information based on the current images we have got. Secondly, this is a retrospective study of patients with high myopia. The OCT images from lattice degenerations of non-high myopic eyes are also of importance and may provide more information to this field. In our next study, we plan to collect non-high myopic eyes and make some comparisons. Some changes associated with lattice degeneration were not found in our cases such as sclerosing or whitening vessels, hyperpigmentary change and snail tracts. Their OCT findings remains to be determined in future study.
In conclusion, to the best of our knowledge this is the first study to observe the large number of peripheral lattice degenerations in myopic eyes using SD-OCT, and also the first study to compare the vitreoretinal structure changes before and after retinal focal laser photocoagulation for lattice degeneration. These results show the characteristics in cross-view of the lattice degenerations, and the subretinal fluid with retinal break, which is undetectable under color fundus photography. Blunted traction by retinoplasty effects after retinal focal laser is a new finding. In clinical practice, the usage of SD-OCT at peripheral lattice degenerations provides us information about the vitreoretinal traction, which was not detected by indirect ophthalmoscope or fundus photography. Early retinal focal laser can be applied in an attempt to prevent further retinal detachment according to SD-OCT studies.
The authors have no conflicts of interest relevant to this article.
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