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Decreased Visual Acuity Associated With Cystoid Macular Edema in Neovascular Age-related Macular Degeneration
T. Daniel Ting, MD, PhD;
Mila Oh, MD;
Terry A. Cox, MD, PhD;
Carsten H. Meyer, MD;
Cynthia A. Toth, MD
Arch Ophthalmol. 2002;120:731-737.
ABSTRACT
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Objective To determine the prevalence and visual significance of cystoid macular
edema (CME) in eyes with subfoveal neovascular age-related macular degeneration
using optical coherence tomography (OCT).
Materials and Methods The medical records of 61 consecutive patients initially seen with nondisciform
subfoveal neovascular age-related macular degeneration were retrospectively
reviewed. All patients underwent fluorescein angiography and OCT imaging.
Eyes with intraretinal hyporeflective spaces in the macula in the OCT images
were considered to have CME.
Results Twenty-eight (46%) of 61 eyes demonstrated CME on the OCT images. The
presence of CME and increased foveal thickness correlated with decreased visual
acuity, but not with the duration of symptoms. Twenty-six (93%) of 28 eyes
with CME contained classic choroidal neovascularization, whereas 16 (48%)
of 33 eyes without CME contained classic choroidal neovascularization.
Conclusions Cystoid macular edema is a common finding in patients with choroidal
neovascularization associated with age-related macular degeneration. The presence
of CME and foveal thickening is associated with worse visual acuity in these
patients. Cystoid macular edema is more common with choroidal neovascularization
containing classic component. The OCT is a useful test to detect the presence
of CME in these patients since CME may be difficult to identify on fluorescein
angiogram.
INTRODUCTION
AGE-RELATED macular degeneration (AMD) is a major cause of legal blindness
in people older than 65 years in the United States and Europe.1-2
The severe visual loss usually results from choroidal neovascularization (CNV).3 These new vessels are accompanied by fibrous tissue4 that can destroy central visual function over months
to years.5
The ophthalmoscopic signs of neovascular AMD include the presence of
a green-gray lesion, subretinal blood, exudate, and often with what has been
described as subretinal fluid.6 Another sign,
cystoid macular edema (CME), has been infrequently reported in neovascular
AMD since it may be difficult to detect angiographically in the presence of
exudation from the CNV.7-8 While
CME can be observed in some patients with neovascular AMD, the prevalence
of CME and whether it may play a role in causing decreased visual acuity is
not well characterized.
Macular structures can be studied in cross-section with optical coherence
tomography (OCT), which allows imaging of a transverse scan of the retina
with high resolution.9 Analogous to B-scan
ultrasonography, OCT measures optical rather than acoustic reflection and
provides noninvasive, noncontact cross-sectional imaging with a resolution
of approximately 10 µm.10 Optical coherence
tomography uses low-coherence interferometry to detect relative changes in
reflectivity at optical interfaces. Optical coherence tomography has been
used to study CME in various macular conditions such as uveitis, epiretinal
membrane, vitreomacular traction, diabetic retinopathy, retinitis pigmentosa,
and branch and central retinal vein occlusion.11-18
This study determined the prevalence of CME in eyes with neovascular AMD using
OCT and evaluated whether CME may play a role in causing decreased visual
acuity.
PATIENTS AND METHODS
A retrospective review was performed on the medical records of 356 consecutive
patients of one of us (C.A.T.). These patients underwent OCT imaging at Duke
Eye Center, Durham, NC, for neovascular AMD as part of an institutional review
board–approved study of OCT imaging of macular lesions from July 1,
1997, through December 31, 1999. The evaluation of patients with neovascular
AMD included a comprehensive ophthalmic examination including a history of
onset and duration of visual loss, slitlamp biomicroscopy, indirect ophthalmoscopy,
stereoscopic fundus photography, and fluorescein angiography (FA). Best-corrected
visual acuity was measured in a standard examination lane with an illuminated
Snellen visual acuity chart.
Exclusionary criteria for the study eye were macular disease other than
AMD, patient aged younger than 55 years, previous laser photocoagulation or
surgical treatment for the CNV, disciform scar, and the absence of subfoveal
CNV. Patients with inadequate FA or OCT imaging for analysis were excluded.
Fluorescein angiograms were reviewed (T.D.T., C.H.M., and C.A.T.) for
inclusionary criteria and categorization. The FA reviewers were masked to
visual acuity and OCT findings. Interpretation was based on the Macular Photocoagulation
Study Group19 guidelines. Only eyes with subfoveal
CNV as demonstrated on FA were included in the study. The total lesion size
was determined from the FA. The size of any classic component present within
the lesion was also determined from the FA and was represented as a percentage
of the total lesion.
Optical coherence tomograpic imaging of the macula was obtained for
all patients (Zeiss Humphrey Systems, Dublin, Calif). Optical coherence tomograpic
images are depicted in a false-color scheme. Red and white represent areas
of high optical reflectivity, blue represents lower relative reflectivity,
and black represents the absence of reflectivity. Areas of intraretinal or
subretinal fluid have low reflectivity.11 Multiple
scans of the macula in the vertical and horizontal axes were performed for
each eye. At least one of the scans included fixation. In cases where fixation
was equivocal, a scan through the foveal depression was used. Each tomogram
has a scan depth of 1.5 mm that is represented by 300 pixels. Scan lengths
varied from patient to patient and ranged from 2.50 to 6 mm. Analyses of foveal
thickness, subretinal fluid, and cystoid spaces were performed on OCT images
transferred to Adobe Photoshop (Adobe Systems Inc, San Jose, Calif).
Eyes demonstrating cystoid spaces in the macula on OCT were considered
to have CME and are shown in Figure 1
and Figure 2. Cystoid space was
defined in this study as an intraretinal area of low reflectivity encompassing
a minimal block of 4 x 5-contiguous pixels (Figure 1B asterisks). Eyes that did not demonstrate cystoid spaces
are shown in Figure 3. The foveal
center was determined on OCT by the presence of the foveal depression. In
eyes in which the foveal depression was not visible owing to retinal thickening
or the presence of subretinal fluid, the OCT video image was used to determine
the most appropriate scan through the fovea.
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Figure 1. Example of an eye with age-related
macular degeneration, subfoveal occult choroidal neovascularization (CNV),
and cystoid macular edema. A, Color fundus photograph demonstrates the presence
of drusen, blurring of retinal features in the area of CNV, subretinal hemorrhage,
and subretinal lipid. The arrow indicates the location and direction of the
optical coherence tomographic (OCT) scan. B, The OCT image demonstrates thickening
of the macula with several large hyporeflective cystoid spaces (asterisks)
in the fovea. Beneath this, there is hyperreflective thickening above the
normal location of the retinal pigment epithelial–choriocapillaris layer,
consistent with CNV. C and D, The fluorescein angiogram demonstrates late
leakage from the primarily occult CNV and fluorescein pooling in the cystic
spaces.
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Figure 2. Example of an eye with age-related
macular degeneration, subfoveal classic choroidal neovascularization (CNV),
and cystoid macular edema. A, Color fundus photograph demonstrates the presence
of a green-gray subretinal lesion with minimal hemorrhage. The arrow indicates
the location and direction of the optical coherence tomographic (OCT) scan.
B, The OCT image demonstrates loss of the foveal depression with cystoid spaces.
C and D, Fluorescein angiography demonstrates a classic CNV with early hyperfluorescence,
well-demarcated boundaries, and late leakage.
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Figure 3. Example of an eye with age-related
macular degeneration, subfoveal choroidal neovascularization (CNV), and no
cystoid macular edema. A, Color fundus photograph demonstrates the presence
of drusen, a green-gray subretinal lesion, and subretinal fluid. The arrow
indicates the location and direction of the optical coherence tomographic
(OCT) scan. B, The OCT image demonstrates no cystoid spaces in the macula.
Arrows depict the distance between the inner and outer neurosensory retinal
surfaces. Beneath the retina is a focal hyporeflective region of presumed
subretinal fluid (asterisk). Note the reflective vitreous strand extending
to an attachment site at the fovea. C and D, Fluorescein angiography demonstrates
a primarily classic CNV.
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Retinal thickness was defined as the distance between the inner and
outer neurosensory retinal surfaces (Figure
3B arrows). Therefore, subretinal hyporeflective zones representing
subretinal fluid were not considered retinal components (Figure 3B asterisk). Retinal thickness measurements were obtained
from the single best tomogram of the foveal center from each eye.
The prevalence of subretinal fluid in neovascular AMD was determined
using OCT imaging. An eye that contained a hyporeflective zone between the
outer retinal surface and the retinal pigment epithelium on any OCT image
was considered to have subretinal fluid. The prevalence of subfoveal fluid
was also determined on OCT imaging. Eyes that contain a subfoveal hyporeflective
zone were considered to have subfoveal fluid.
Statistical analysis of the data was performed using either SAS 8.0
for Windows (SAS Institute Inc, Cary, NC) or StatXact 4 for Windows (CYTEL
Software Corp, Cambridge, Mass). Statistical methods included the Fisher exact
test, Wilcoxon rank sum test, and the mean score test. All statistical tests
were 2-tailed.
RESULTS
A total of 61 eyes of 61 patients met the inclusionary criteria for
this study. The mean age of the patients was 75.9 years (age range, 58-90
years). There were 29 men and 32 women enrolled in the study. Mean duration
of symptoms was 83.2 days (range, 1 day to 1 year). Visual acuity measurements
ranged from 20/30 to 8/200. On biomicroscopic examination, all eyes contained
drusen as well as signs of neovascular AMD such as serous or hemorrhagic detachment
of the retinal pigment epithelium, subretinal fluid, subretinal lipid, or
intraretinal or subretinal hemorrhage.
OCT FINDINGS
Using the aforementioned criteria, CME was found on OCT imaging in 28
(46%) of 61 eyes. The average age of patients with and without CME was 75.2
and 76.5 years, respectively. The mean duration of symptoms was 88 days for
eyes with CME and 69 days for eyes without CME. There was no statistically
significant difference in the age of the patient or the duration of the symptoms
between the 2 groups. Nine (32%) of 28 eyes with CME and 11 (33%) of 33 eyes
without CME were pseudophakic. The average foveal thickness of the neovascular
AMD study eyes was 185 µm compared with an average foveal thickness
of 103 µm in eyes from 17 age-matched individuals without ocular disease.
Average foveal thickness was significantly greater in eyes with CME (264 µm)
compared with eyes without CME (118 µm) (P<.001).
The results are summarized in Table 1.
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Comparison of Patients With and Without Cystoid Macular Edema (CME)*
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VISUAL ACUITY AND FOVEAL THICKNESS
The mean visual acuity for all 61 patients was 20/110. The mean visual
acuity in eyes with CME was 20/150 and in eyes without CME was 20/85. This
difference in visual acuity between the 2 groups (Figure 4) was statistically significant (P
= .004). Only 3 (11%) of 28 eyes with CME had visual acuity better than or
equal to 20/60, while 9 (27%) of 33 eyes without CME had visual acuity better
than or equal to 20/60.
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Figure 4. Best-corrected Snellen visual
acuity in eyes with and without cystoid macular edema (CME).
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The correlation between foveal thickness and visual acuity for all 61
eyes is shown in Figure 5. Linear
regression analysis demonstrated foveal thickness was a significant predictor
(P = .02) for logMAR visual acuity.
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Figure 5. Correlation between foveal thickness
and logMAR visual acuity.
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VISUAL ACUITY AND SUBRETINAL FLUID
The presence of submacular fluid had no significant influence on visual
acuity. Submacular fluid was found in 33 (54%) of 61 total eyes, and subfoveal
fluid was found in 14 (23%) of 61 total eyes. There was no statistical difference
in the mean logMAR visual acuity in eyes with and without submacular or subfoveal
fluid (20/110 in all groups).
FA FINDINGS
The FA characteristic of representative eyes with and without CME is
shown in Figure 1C, Figure 2C, and Figure 3C.
The average CNV size in all eyes was 5.4 Macular Photocoagulation Study (MPS)
disc areas. The average CNV size in eyes with CME was 5.3 MPS disc areas and
without CME was 5.6 MPS disc areas. There was no statistical significance
between lesion size and visual acuity.
Eyes with CME had a proportionally greater area of classic CNV than
eyes without CME (Figure 6). Classic
CNV composed an average of 54% of the lesion in eyes with CME and 20% of the
lesion in eyes without CME. Eyes with CME were also more likely to contain
100% classic CNV than eyes without CME. Eyes without CME were more likely
to have 100% occult CNV (Table 1).
There is a strong association between CME and classic CNV (P<.001). The association between visual acuity (logMAR) and CME
remains significant (P = .008) when classic CNV is
controlled for in a linear model.
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Figure 6. Fluorescein angiographic (FA)
findings in eyes with and without cystoid macular edema (CME).
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COMMENT
Visual acuity in eyes with neovascular subfoveal CNV can vary widely,
even among groups with similar angiographic components and duration of disease.5, 20 Many factors have been associated
with the loss of vision from AMD. Although this study was retrospective and
was limited to a few patients from a tertiary referral center, the number
of patients was sufficient to demonstrate a correlation between both the presence
of CME and retinal thickness with vision loss associated neovascular AMD.
The presence of CME in neovascular AMD may be difficult to identify
angiographically in the setting of leakage from the CNV. Bressler et al have
noted the presence of a "well-demarcated area of hyperfluorescence which represented
pooling of fluorescein in a compartmentalized (loculated) space anterior to
the choroidal neovascular leakage"7(p211) in
one third of the eyes with well-defined subfoveal CNV associated with AMD.
The authors stated that the observed "loculated fluid" may conform to a pattern
of typical CME, but may also pool within an area deep to the sensory retina
in a shape that does not resemble CME.
In a retrospective review of 100 eyes with CNV secondary to AMD and
concurrent CME, Soubrane et al8 detected CME
in all forms of neovascular AMD, including classic CNV, occult CNV, pigment
epithelial detachments, and disciform scars. The authors obtained photographs
with blue monochromatic light and stereoscopic FAs to detect the presence
of CME. The authors stressed the importance of distinguishing fluorescein
leakage due to CME from leakage due to CNV on FA. This study demonstrated
that the presence of CME was not related to the duration of symptoms, nor
to the location, extent, or type of CNV. The study also noted that the presence
of CME was compatible with preservation of useful vision, especially in patients
with occult CNV.
Similar to Soubrane et al,8 this study
found no association between the duration of symptoms and presence of CME.
However, unlike Soubrane et al, this study found a correlation between CME
and decreased visual acuity. Using OCT techniques, this study demonstrated
that CME was found in 46% of patients with nondisciform subfoveal CNV secondary
to AMD. Both increased retinal thickness and the presence of CME were correlated
with decreased visual acuity. A direct correlation between foveal thickness
measured by OCT and visual acuity has also been reported in diabetic retinopathy11 and in epiretinal membrane.18
While retinal thickening is certainly not the only factor that leads to decreased
visual acuity in patients with neovascular AMD, it may be a contributing factor.
However, retinal thickening may simply be a marker associated with retinal
damage sufficient to decrease visual acuity.
Subretinal fluid identified on OCT was not included as a component of
retinal thickening in this study. This delineation of components of retinal
elevation over a CNV using OCT is different from the 1988 blue light photographic
examination of the retina8 in attempts to discern
retinal edema. The difference in macular examination techniques may have resulted
in our differentiating subretinal fluid from CME in eyes with nondisciform
CNV. Subretinal fluid, in contrast to retinal edema, was not associated with
worse visual acuity in our group of patients. These results based on OCT imaging
suggest that macular edema rather than subretinal fluid plays a greater role
in causing decreased visual acuity in eyes with neovascular AMD.
In addition, unlike the biomicroscopic examination-based study,8 this study found a correlation between CME and the
presence of FA classic CNV. Classic CNV composed a greater percentage of the
total lesion in eyes with CME than eyes without CME. Lesions containing mainly
classic CNV were more common in eyes with CME than eyes without CME. Conversely,
lesions containing mainly occult CNV were more common in eyes without CME
than eyes with CME. Thus, CME, a retinal structural finding, may be "hidden"
in FAs by the hyperfluorescence of classic CNV, but is frequently found in
classic CNV when nonangiographic structural imaging is used. Previous reports
have demonstrated that visual acuity is worse in eyes with AMD that have predominantly
classic subfoveal CNV than in eyes with occult CNV.5, 21-22
This study found that an association between decreased visual acuity and the
presence of CME exists even when classic CNV is controlled for in a statistical
model. This raises the possibility that macular edema may play a role in contributing
to the worse visual acuity found in eyes containing predominantly classic
subfoveal CNV compared with eyes containing occult CNV. Additional studies
will need to be conducted to test this hypothesis.
The cause of CME in patients with neovascular AMD is not well elucidated.
Gass23 hypothesized that the extension of a
CNV into the capillary-free zone in the macula may disrupt the photoreceptor-external
limiting membrane complex and lead to CME. The capillary-free zone may be
particularly at risk due to structural weakness of the external limiting membrane
where Müller cell processes are reduced in number and due to the scarcity
of retinal vessels to provide a pathway of return of the extracellular fluid
to the intravascular compartment.23
Disruption of retinal pigment epithelial metabolism has been implicated
to alter the structure and permeability of the retinal capillary circulation.24-25 If this implication is true, the
formation of CNV may disrupt retinal pigment epithelial metabolism and cause
CME by altering the permeability of retinal capillaries. Alternatively, CME
formation in neovascular AMD may be mediated by an inflammatory pathway as
electron microscopic studies have identified inflammatory cells such as macrophages,
fibroblasts, lymphocytes, and mast cells in CNV associated with AMD.26
In some treatments of AMD, vision improvement may be associated with
a decrease in retinal thickening. Monitoring retinal thickness may also be
useful in evaluating efficacy of treatment. The OCT is a useful tool for detecting
and monitoring the presence of CME. Further studies will be needed to determine
the cause of CME in patients with neovascular AMD. Further studies will also
be needed to determine if treatments such as surgical removal of CNV, restoring
interaction with normal retinal pigment epithelium through macular translocation,
photodynamic therapy, transpupillary thermotherapy, or injection of periocular
steroid may improve vision by decreasing macular edema.
AUTHOR INFORMATION
Submitted for publication July 24, 2001; final revision received February
12, 2002; accepted February 28, 2002.
This research was supported in part by the grant 5 R24 EY-13015-02,
from the National Institutes of Health, Bethesda, Md; the Heed-Knapp Foundation
Fellowship Award, Cleveland, Ohio (Dr Ting); the Adler Foundation, Rye, NY
(Dr Meyer); and the McLaughlin Foundation, Toronto, Ontario (Dr Oh).
We thank Melissa Keller for excellent technical assistance and Katrina
Winter for preparation of the manuscript and figures.
Corresponding author: Cynthia A. Toth, MD, Duke University Medical
Center, Box 3802, Erwin Road, Durham, NC 27710 (e-mail: toth0004{at}mc.duke.edu).
From the Departments of Ophthalmology (Drs Ting, Oh, Cox, Meyer, and
Toth) and Biostatistics and Bioinformatics (Dr Cox), Duke University Medical
Center, Durham, NC. The authors have no commerical, proprietary, or financial
interest in the products or companies described in this article.
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