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Limited Macular Translocation for Atrophic Maculopathy
Jeffrey D. Benner, MD;
Janet S. Sunness, MD;
Matthias D. Ziegler, BS;
Jalal Soltanian, MSE
Arch Ophthalmol. 2002;120:586-591.
ABSTRACT
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Objectives To report visual improvement following bilateral limited macular translocation
for a patient with atrophic macular disease, and to discuss issues related
to the selection of potential candidates for this technique.
Design Case report.
Results A 78-year-old woman with bilateral atrophic maculopathy and no choroidal
neovascularization had slowly progressive loss of visual acuity for at least
17 months in the right eye and 25 months in the left eye. She underwent bilateral
limited macular translocation, using scleral infolding in the right eye and
scleral outpouching in the left eye. Following translocation of her maculae,
her best-corrected visual acuity improved from 20/200 to 20/30 OD and from
20/180 to 20/100 OS. She remained stable during 30 months of follow-up for
the right eye and 22 months of follow-up for the left eye.
Conclusion Macular translocation may allow visual recovery in selected patients
with atrophic maculopathy, even after a prolonged period of poor vision.
INTRODUCTION
MACULAR translocation was developed as a technique for moving the fovea
relative to underlying choroidal neovascularization. This allows both the
photocoagulation of formerly subfoveal choroidal neovascularization, while
sparing the foveal center, and the repositioning of the fovea over healthier
retinal pigment epithelium (RPE). Machemer and Steinhorst1
first reported success with this technique in 1993 by using a 360° retinotomy
to translocate the macula. Later, de Juan et al2
and Pieramici et al3 used scleral shortening
to perform limited macular translocation without the need for a 360° retinotomy.
Others have confirmed this initial success using both techniques.4-7 This
procedure has preserved and even improved visual acuity. Although the emphasis,
to date, has been on using macular translocation to treat subfoveal choroidal
neovascularization, this technique may possibly be useful for patients with
atrophic macular disease that involves the fovea and affects foveal function.
Atrophic macular disease is generally associated with underlying RPE atrophy,
often with associated loss of choriocapillaris, and the loss of RPE is what
often leads to the loss of photoreceptors and the development of central scotomas.8-10 Theoretically, macular
translocation may be useful for treating atrophic macular disease by placing
the fovea over healthier RPE, which could prevent the loss of photoreceptors
and sustain foveal function. This article presents the results of limited
macular translocation in both eyes of a patient with atrophic macular disease,
presumed to be caused by pattern dystrophy, who had poor visual acuity for
a prolonged period of time prior to the procedure.
REPORT OF A CASE
A 78-year-old woman sought care from her ophthalmologist in May 1996
because of decreased vision in her left eye. At that time, her best-corrected
visual acuity was 20/50 OD with a refractive error of +1.00 -2.00 x
90° and 20/80 OS with a refractive correction of +2.75 -1.50 x
70°. She had macular changes consistent with atrophic maculopathy. By
May 1997, her best-corrected visual acuity had declined to 20/80 OD and 20/100
OS. By March 1998, the visual acuity had further declined to 20/100 OD and
20/200 OS. By July 1998, her visual acuity had declined further to 20/200
OD and 20/400 OS. She was then referred to one of us (J.D.B.) to see if any
treatment was available.
On the initial evaluation in August 1998, the patient's best-corrected
visual acuity was 20/200 OD and 20/400 OS. She had bilateral posterior chamber
intraocular lenses and a circular area of RPE atrophy and pigmentary change
beneath the fovea, with the left eye worse than the right eye (Figure 1A
and Figure 2A). In both eyes, she was
able to accurately fixate foveally and follow a 200-µm diameter spot
projected from the slitlamp (Haag-Streit AG, Köniz, Switzerland). A fluorescein
angiogram showed central blocked hypofluorescence surrounded by a rim of transmission
hyperfluorescence within the macula in the right eye, with more prominent
transmission hyperfluorescence in the left eye (Figure 1B and Figure 2B).
There was no evidence of occult or classic choroidal neovascularization. The
patient asked if any treatment would be available to either improve her vision
or slow the progression of the macular degeneration she had experienced during
the last 4 years. Macular translocation was discussed because it offered the
possibility of relocating the fovea over healthy and viable RPE. After carefully
considering all the known associated risks and potential benefits, she elected
to undergo macular translocation in her right eye. In October 1998, one of
us (J.D.B.) performed a limited macular translocation using circumferential
scleral infolding, as described by de Juan et al.2
The technique included a pars plana vitrectomy and creation of a temporal
retinal detachment by infusing fluid into the subretinal space through a 39-gauge
subretinal needle. Scleral infolding was performed by tying preplaced 5-0
Mersilene (Ethicon Inc, Somerville, NJ) sutures in the superior temporal quadrant.
A gas bubble using sulfur hexafluoride gas was placed in the vitreous cavity,
and the patient was positioned nasal side up for 5 minutes. She was then positioned
upright to allow the gas bubble to translocate the macula inferiorly and reattach
the retina. Postoperatively, her course was uncomplicated, with spontaneous
reattachment of the retina and good translocation of the macula (1191 µm).
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Figure 1. Right eye: A preoperative fundus
photograph (A) shows atrophic macular changes. On the color photograph, xanthophyll
was apparent within the atrophic lesion. A preoperative fluorescein angiogram
frame (B) shows areas of blockage and hyperfluorescence. No evidence of choroidal
neovascularization is present, and the fluorescein pattern is not characteristic
of geographic atrophy or Stargardt disease. An 8-month postoperative argon
blue scanning laser ophthalmoscope (SLO) image (C) shows the xanthophyll entirely
outside the atrophic lesion. An infrared SLO image (D) from 8 months after
macular translocation shows the retina shifted inferiorly relative to the
retinal pigment epithelium (RPE) lesion. Fixation is inferior to the atrophic
lesion. The retina now overlying the atrophic lesion has a dense scotoma.
The cross indicates fixation; shaded circles, stimulus that has been seen;
and open triangles, stimulus that has not been seen (scotoma). Several stimulus
intensities were employed, with the brighter symbols indicating a dimmer stimulus.
An 8-month postoperative SLO autofluorescence image (E) shows a patchy loss
of autofluorescence in the region of the atrophic RPE. A 22-month postoperative
argon blue SLO image (F) shows that the RPE atrophy has become more pronounced
and has an overlying dense scotoma. The xanthophyll appearance is unchanged.
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Figure 2. Left eye: A preoperative fundus
photograph (A) shows a central atrophic lesion, within which xanthophyll is
visible in the color photograph. A preoperative fluorescein angiogram frame
(B) shows patchy transmission hyperfluorescence, consistent with atrophic
maculopathy. A preoperative infrared scanning laser ophthalmoscope (SLO) image
(C) shows fixation within the atrophic lesion. The cross indicates fixation;
shaded circles, stimulus that has been seen; and open triangles, stimulus
that has not been seen (scotoma). A number of stimulus intensities were employed,
with the brighter symbols indicating a dimmer stimulus. When the cross was
fixated within the atrophic lesion, few stimuli were detected near it. When
the cross was moved out of the field, the area had a significant relative
scotoma (but not a full dense scotoma). A preoperative argon blue SLO image
(D) shows the presence of xanthophyll (dark area) within the atrophic lesion.
A preoperative autofluorescence SLO image (E) shows a mottled, but not complete,
loss of autofluorescence in the atrophic region. An argon blue SLO image (F)
from 14 months after macular translocation shows that some of the xanthophyll
is still overlying the atrophic lesion. A 14-month postoperative infrared
SLO image (G) shows that fixation is inferior to the atrophic region, in the
area of xanthophyll seen in F. There is a dense scotoma in the retinal area
now overlying the atrophic region.
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Two months after surgery, her visual acuity had improved to 20/70-1
OD, but her refractive error had increased dramatically, with a significant
amount of induced astigmatism. Her new refractive error in the right eye had
changed from her baseline of +1.00 -2.00 x 90° (which had
been confirmed on several occasions preoperatively by refraction, keratometry,
low vision evaluation, and automated refraction) to +5.00 -6.75 x
80°. Four months after surgery, her visual acuity had improved to 20/50
+ 2 OD with the same refractive error. To help eliminate the anisometropia
caused by the induced astigmatism, she underwent an astigmatic keratotomy
in the right eye. Eleven months after translocation surgery, her visual acuity
had improved to 20/40 + 2 OD with a refractive error of +2.00 -0.75
x 60°. Her acuity had generally been in the 20/40 to 20/50 range,
but at her most recent visit, 30 months postoperatively, her best-corrected
visual acuity was 20/30 OD.
Given her success with surgery in the right eye, the patient inquired
about surgery on the left eye. The patient was assessed at the Wilmer Eye
Institute, Baltimore, Md, in June 1999. The patient reported that her left
eye had always been her weaker eye. She also reported that she was occasionally
aware of a blind spot in her left eye and that she had been aware of a blind
spot in the right eye, but that this had resolved following the translocation
surgery. The patient reported some difficulty with night vision but normal
color vision and peripheral vision. Her best-corrected visual acuity, measured
with an ETDRS (Early Treatment of Diabetic Retinopathy Study) chart, was 20/50
OD and 20/180 OS. The patient missed the middle letters of some lines with
her left eye. Her Pelli-Robson contrast sensitivity was reduced to 1.35 OD
and 1.20 OS (normal,  1.65). No relative afferent pupillary defect was
present. A dilated examination of the right fundus (Figure 1C) revealed an atrophic lesion located superior to the fovea
that was not as discrete and "punched out" as advanced geographic RPE atrophy
generally appears. In the left eye, there was an atrophic lesion of similar
character involving the foveal center (Figure
2A). The patient did not have high-risk drusen or the pigmentary
alterations typically associated with a pattern dystrophy in either eye.
Scanning laser ophthalmoscope (SLO) macular perimetry showed that fixation
was inferior (on the retina) to the atrophic RPE lesion in the right eye and
that the area over the atrophic RPE lesion had a dense scotoma (Figure 1D). There was a mild reduction in general retinal sensitivity
outside the area of her lesion. With argon blue imaging, the area of xanthophyll
was prominent and outside the atrophic lesion (Figure 1C). Autofluorescence imaging showed patchy black areas within
the atrophic lesion rather than the solid black appearance seen in geographic
atrophy with loss of RPE (Figure 1E).
In the left eye, the patient fixated within the area of the central atrophic
lesion (Figure 2C). In this lesion,
only the brightest SLO stimulus (0 dB with a Goldmann III–sized target)
could be seen. Peripherally, there was normal sensitivity, except for a mild
relative scotoma inferonasally. Argon blue imaging showed xanthophyll present
within the atrophic lesion (Figure 2D),
and autofluorescence imaging showed patchy black areas within the region of
this lesion (Figure 2E).
To better define the cause of her macular lesions, electrophysiological
and visual function testing was performed. Electro-oculography was performed
to evaluate any evidence of Best disease. The Arden ratio was normal in both
eyes (2.64 OD and 2.84 OS; normal, 1.80). Electroretinography was performed
to assess the presence of diffuse retinal disease as a cause of the macular
lesions. The scotopic responses were normal. The flicker responses were reduced
to approximately 50% of normal in the right eye and 80% of normal in the left
eye, and the photopic flash response was reduced to about 80% of normal in
the right eye and was normal in amplitude in the left eye, but these responses
were somewhat delayed. The Farnsworth D15 panel color vision was normal in
the right eye and showed 1 minor error in the left eye.
The macular lesion in the left eye showed evidence of preserved photoreceptor
function within the lesion. This conclusion was based on the patient's ability
to fixate centrally in the left eye, the ability to see bright stimuli within
the lesion, the presence of xanthophyll within the lesion, as demonstrated
by argon blue imaging, and the absence of a completely black appearance on
autofluorescence imaging. Although her vision had been decreased to 20/100
or worse in this eye for 25 months, the results of all her measurements suggested
that there was a reasonable chance for improvement in foveal function if macular
translocation were performed.
The patient therefore underwent limited macular translocation in the
left eye by one of us (J.D.B.) in June 1999. This time, a different technique
was performed, using radial scleral outpouching.7
The technique was otherwise identical to that performed in the right eye,
except that scleral shortening was performed by creating a radial scleral
outfold. A scleral folding clamp was used to create a radial scleral outfold,
followed by placement of a full-thickness 6-0 Prolene (Ethicon Inc) horizontal
mattress suture to secure the radial fold. Postoperatively, her course was
uncomplicated, with macular translocation of 832 µm and prompt retinal
reattachment. Postoperatively, her visual acuity remained in the 20/200 to
20/400 OS range, although at the Wilmer Eye Institute, she attained 20/100-2
with an ETDRS chart (improved from 20/180 preoperatively at the Wilmer Eye
Institute) and 20/100 (Snellen) at 1 other visit. Her refractive error was
essentially unchanged from the preoperative level, with no induced astigmatism
in the left eye. At a follow-up visit 22 months postoperatively, her best-corrected
visual acuity was 20/200.
She was reevaluated at Wilmer Eye Institute by one of us (J.S.S.) in
August 2000, which was 22 months postoperatively in the right eye (Figure 1F) and 14 months postoperatively
in the left eye (Figure 2F). She
reported that the vision in the right eye had gotten better and the vision
in her left eye was better than it had been preoperatively. She reported that
her night vision continued to be somewhat reduced, as it had been all her
life. She denied having diplopia, except when looking at Christmas lights.
On this visit, her best-corrected visual acuity was 20/50-1 OD and 20/100-2
OS (ETDRS chart). She was able to read 1 M print with the right eye and 2.5
M print with the left eye at 40 cm. The SLO macular perimetry showed a dense
scotoma over the areas of RPE atrophy in each eye (Figure 2G). Argon blue SLO imaging of the left eye demonstrated
that the xanthophyll area had been translocated inferior to the atrophic lesion,
except for the superior-most portion, which remained partially over the atrophic
RPE (Figure 2F). This was in contrast
to the right eye, where the entire xanthophyll area had completely cleared
the atrophic lesion (Figure 1F).
COMMENT
VISUAL IMPROVEMENT
Several aspects of this case are remarkable. This patient had a significant
improvement in vision in her right eye after having had slowly progressive
visual acuity loss, with acuity at 20/80 or worse for at least 17 months prior
to the procedure in her right eye and for at least 37 months prior to the
procedure in her left eye. Her visual acuity improved from 20/200 to 20/30
OD (best acuity, with acuities ranging from 20/30 to 20/50) and from 20/186
to 20/100 OS (best acuity, with acuities ranging from 20/100 to 20/200). The
amount of foveal translocation was greater in the right eye (1191 µm)
than the left eye (832 µm). As a result, the fovea (as delineated by
the xanthophyll) was relocated completely outside the atrophic RPE in the
right eye and only partially outside the slightly larger atrophic area in
the left eye. The more atrophic appearance of the lesion preoperatively and
the longer duration of visual loss may have accounted for the more limited
amount of improvement in the left eye. That her vision improved after having
been decreased for so long suggests that her foveal photoreceptors had remained
viable over the atrophic lesion during this time. After they were relocated
to a new site over healthy RPE, the photoreceptors apparently were able to
function more effectively, and her vision improved.
PATIENT SELECTION
This case illustrates the use of macular translocation for patients
with atrophic macular disease. Preoperative evaluation of visual function
may provide insight into which eyes are likely to benefit from translocation.
The most critical element is residual photoreceptor function and foveal fixation
within the atrophic region prior to the procedure. In this patient, the SLO
evaluation was used to make this determination in the left eye, and a 200-µm
diameter slitlamp spot was used to assess fixation in both eyes. Another indirect
measure of viability and residual photoreceptor function is the presence of
xanthophyll within the atrophic lesion.11 Xanthophyll
may be visualized by ophthalmoscopic examination and standard fundus photography,
but its visualization is enhanced using either argon blue SLO imaging or fundus
photography with an appropriate filter for detecting xanthophyll. Finally,
the SLO can be used to identify residual RPE within the atrophic area. The
SLO macular perimetry preoperatively showed fixation and residual function
within the atrophic lesion (although postoperatively there was a dense scotoma
of the retina now overlying the atrophic lesion). Our patient had mottled,
rather than totally black, autofluorescence in the atrophic lesion. This provides
further suggestive evidence that the photoreceptors are viable and complements
macular perimetry over the atrophic lesion.12
The exact cause of this patient's atrophic maculopathy is unclear. Her
progressive visual loss in her late 70s and the well-circumscribed area of
subfoveal RPE atrophy are consistent with age-related macular degeneration.
Yet, the absence of drusen, the blocked hypofluorescence on the fluorescein
angiogram, and the retention of fixation within the lesion are more consistent
with a pattern dystrophy of the macula. Additionally, the pattern of a patchy
decrease in autofluorescence seen with the SLO in this patient was different
from the homogeneously black area (loss of autofluorescence) seen in patients
with geographic atrophy from age-related macular degeneration.12-15
The electro-oculogram was normal, so Best disease was not the cause. The electroretinogram
showed a mild reduction in cone amplitudes and some delay in cone responses,
suggesting a cone dystrophy, but the color vision was essentially normal.
The patient did not have a dark choroid or flecks that would suggest Stargardt
disease. The most likely diagnosis is RPE atrophy, resulting from pattern
dystrophy. Early RPE changes and atrophy, from age-related macular degeneration
and related conditions, may be associated with decreased retinal function
even before frank geographic atrophy occurs16-17;
this decreased function may reverse with translocation to a healthier area
of RPE.
Other forms of atrophic macular disease may not benefit from translocation
surgery, so careful consideration must be given to the likelihood of visual
improvement. Geographic atrophy that already involves the fovea, with a dense
central scotoma, will likely not benefit from translocation. Translocation
that will move the fovea to an area that will likely develop frank RPE atrophy
in the future is not likely to benefit the patient. For example, in a patient
with a bull's-eye scotoma surrounding the foveal center, macular translocation
might relocate the fovea to a site with a higher risk of becoming atrophic
than the foveal center itself. Because geographic atrophy often develops in
the parafoveal region first, thought must be given to the health of the RPE
in the area to which translocation is contemplated. The patient with geographic
atrophy from age-related macular degeneration most likely to benefit from
macular translocation is one with recent visual loss who has an isolated atrophic
lesion just superior to the fovea that is threatening to spread into the foveal
center. In this case, macular translocation would move the foveal center away
from the atrophic RPE, reducing the likelihood that atrophy would spread to
involve the new foveal center.
This case suggests that limited macular translocation may be helpful
for patients with certain other atrophic maculopathies. However, the disease
process causing the atrophy may well be a factor in determining whether surgery
would be likely to be beneficial. If enlargement of atrophy over time is anticipated,
one might have to contemplate performing further translocation at a later
time. In limited macular translocation, the fovea is generally translocated
inferiorly because of anatomical and surgical limitations. In terms of visual
function, when the fovea is moved inferiorly, the atrophic lesion is then
positioned beneath a focal area of retina superior to the fovea. The patient
will then have a scotoma inferior to fixation (corresponding to the superior
retina that overlies the atrophic lesion), which is a disadvantageous position.18-19 (Presumably, the recovery of central
vision outweighs the disadvantage of having an inferior scotoma.) One possibility
for avoiding an inferior scotoma is to perform a 360° retinotomy to allow
enough superior movement of the fovea to be beneficial. Whether the additional
risk associated with this technique is warranted remains to be seen.
POSTOPERATIVE LOSS OF FUNCTION OF RETINA OVERLYING THE ATROPHIC LESION
An interesting observation was the loss of functioning retina in the
region that came to reside over the RPE atrophy in each eye after surgery.
This was demonstrated at 8 months postoperatively in this case. The loss of
function of the previously normal retina overlying the RPE atrophy following
macular translocation has been shown to develop as early as 1 week postoperatively
(G. Y. Fujii, MD, and J.S.S., unpublished data, 2000). Prior to translocation,
our patient had a relative scotoma in the fovea overlying the RPE atrophy,
but she could still see the brightest stimulus. Following the translocation
surgery, the retina that was relocated over the RPE atrophy, and had previously
tested normal with the SLO, now had a dense scotoma. The fact that function
remained in the foveal retinal area overlying the RPE prior to translocation
could be due to specific protection conferred on the foveal photoreceptors,
or it may reflect additional damage to the RPE-photoreceptor interface following
translocation.
AUTHOR INFORMATION
Submitted for publication May 31, 2001; final revision received December
28, 2001; accepted January 24, 2002.
This study was supported in part by grant NEI EY08552 from the National
Eye Institute, Bethesda, Md, and the James S. Adams Research to Prevent Blindness
Special Scholar Award, New York, NY (Dr Sunness); the John A. Hartford Foundation/American
Federation of Aging Research Medical Student Geriatric Scholars Program, New
York (Dr Sunness and Mr Soltanian); the Panitch Fund to Stop Age-Related Macular
Degeneration, Baltimore; core grant NEI 2 P30 EY01765-24 from the National
Eye Institute; and an unrestricted research grant from Research to Prevent
Blindness to the Wilmer Eye Institute.
This study was presented in part at the annual meeting of the Association
for Research in Vision and Ophthalmology, Ft Lauderdale, Fla, May 2, 2001,
and at the annual meeting of the Macula Society, Scottsdale, Ariz, February
28, 2001.
We thank Morton F. Goldberg, MD, for his critical review of the manuscript.
Corresponding author and reprints: Janet S. Sunness, MD, 550 N Broadway,
Sixth Floor, Baltimore, MD 21205 (e-mail: jsunness{at}jhmi.edu).
From the Delmarva Vitreoretinal Center, Salisbury, Md, and the University
of Maryland, Baltimore (Dr Benner); and Wilmer Lions Vision Center, Johns
Hopkins University School of Medicine, Baltimore (Dr Sunness and Messrs Ziegler
and Soltanian).
The authors have no commercial or proprietary interest
in any device discussed herein.
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