Hole Update: 2006
E. SMIDDY, MD
topic of macular holes has matured from solely academic interest to being centered
on therapeutics. Better imaging capabilities offered by optical coherent tomography
(OCT) allow more accurate diagnosis especially at early stages, shed light on their
pathogenesis, and may predict or explain postoperative visual results. Interest
in understanding the pathogenesis of macular holes continues, but the focus is making
the surgical success rate higher and more easily achievable for the patient. Specifically,
the intraoperative technique of internal limiting membrane (ILM) peeling, and the
regimen of postoperative positioning have been examined.
The grading scheme introduced by Gass represents an appropriate
framework upon which to build observations and ideas from many investigators, and
interpretation of several imaging modalities,1-3
but pathogenesis is still incompletely understood. A coup-contrecoup force mechanism
of formation has been presumed for traumatically induced macular holes, even though
some holes form days or weeks after trauma.4
Possibly, an intermediate step involves cystoid changes which gradually consolidate
and rupture.5 This might
parallel what may happen in idiopathic macular hole formation the breakdown
of large, consolidated foveal cysts. The development of techniques such as slit-lamp
biomicroscopy and fluorescein angiography allowed reliable distinction between the
cystic changes seen in conditions such as macular holes and the cystoid macular
edema (CME) seen in inflammation-associated conditions.6
However, the subtleties confounding accurate distinction of macular hole, impending
macular hole, and pseudohole conditions are now well recognized.
The steps inducing the cyst and its breakdown are more abstruse.
A firm vitreoretinal adhesion at the fovea and optic disc was demonstrated by clinicopathologic
correlation, first bolstering the evidence for a traction-induced cause.7
Subsequent clinical series implicating the completion of a posterior vitreous detachment
(PVD) abounded, seemingly solidifying traction as the major event, at least in the
majority of cases.8
The first comprehensive study of the histopathology of macular
holes included 3 major findings that might carry implications for pathogenesis.9
First, at least a partial posterior vitreous detachment was observed, but direct
vitreoretinal connections were absent near the hole so no traction was inferred.
Second, cystoid changes were typically more marked in the outer retina than the
inner retina. Third, pigment demarcation delimiting the small area of serous elevation
around the edges of the macular hole was present in some eyes. Secondary findings
included partially separated internal ILM and opercula in several cases. A subsequent
histopathologic study published approximately 10 years later from the same laboratory
reported 12 of 22 full-thickness macular holes with vitreous adherent to a detached
tissue plug (operculum) suspended over the hole, but no agent of tangential vitreous
traction was identified in the full-thickness cases.10
The authors' conclusion was that epiretinal membrane traction might play a role
in the formation of full-thickness macular holes.
Three histopathologic studies of eyes in which macular hole surgery
was successful in closing a macular hole have been reported.11-13
Collectively, these reports noted re-approximation of Mueller cells (and glial cells),
normal-appearing underlying retinal pigment epithelium (RPE),
a lack of inflammatory
response, an apparent resolution of CME, and, interestingly, a lack of ILM around
the margins of the macular hole in some cases, despite no purposeful attempts to
peel that layer at the time of surgery. The authors' consensus was that the holes
closed because removal of cortical vitreous allowed relief of tangential traction
and permitted re-approximation of the edges. They observed that while some photoreceptor
loss must have occurred during the process of macular hole formation, the array
of relatively undisturbed photoreceptors at the area of re-approximation was surprising,
yet consistent with the fairly high degree of visual improvement often obtained
after macular hole surgery.
electron micrographic studies of apparent opercula collected at the time of macular
hole surgery came to opposing conclusions.14-15
One found the opercula in 2 eyes to consist of proliferated fibrous astrocytes and
Mueller cells, emphasizing the absence of distinct retinal neuronal tissue and calling
into question the retinal nature of the operculum.14
The other interpreted the finding of outer retinal, neuronal elements in 7 of 18
specimens and concluded opercula are full-thickness retinal plugs in at least many
This conclusion was supported by their subsequent study utilizing immunochemical
staining techniques that found photoreceptor cell elements in 8 of 12 specimens.16
The authors found poorer anatomic results in those cases in which the operculum
included photoreceptor elements and hypothesized that the variable degree of retinal
elements in the operculum reflects the variable depth of inner retinal cleavage
during hole formation, and probably correlates with the degree of anatomic and visual
success following macular hole surgery. Inherent to this hypothesis is the conclusion
that the extent of foveal damage may be largely predetermined when the macular hole
forms and, therefore, limits visual recovery regardless of surgical technique.
Another histopathologic study acknowledged the dilemma of determining
whether the glial proliferation was primary and caused the hole, or whether it was
a secondary reaction.17
The success of macular hole surgical techniques stimulated a resurgence
in understanding the normal anatomy of the vitreoretinal interface. The vitreous
body structure is substantially more complex than it first appears; it is not a
simple, homogenous structure. Cisternal spaces within the vitreous body have been
described long ago,18 and
when exaggerated probably correlate to the vitreoschisis cavities observed clinically,19,20
histologically,21 and echographically.22
Such an anatomic feature may be the basis for commonly encountered persistent cortical
vitreous attachment and provide the conduit for tangential traction. Attached vitreous
remnants demonstrated by scanning electron microscopic study in the perifoveal area
in eyes with apparent posterior vitreous detachment suggest that posterior vitreous
separation may also not be as simple and "clean" as intuition suggests.23
These persistent elements may also provide the substrate for surface traction.
The ILM is attenuated to the point of discontinuity at the central
fovea.24 Henle's nerve fiber
layer, the inverted cone of outer plexiform layer (including Mueller cells) at the
fovea, may be a key site of macular hole initiation since both Henle's layer and
the Mueller cells assume a more oblique orientation in the central fovea (the umbo),
rendering them more structurally vulnerable to tangential, shearing forces and may
proliferate to populate the operculum or complete the hole formation.24-25
Cyst formation may be a preliminary reflection or consequence of such forces.26
The concept of a lamellar macular hole, introduced long ago, was
postulated to occur from rupturing of the inner wall cysts of a patient with CME.27
Apparent histopathologic correlates were studied.9,10
Reports of impending macular holes (Stage 1A) described foveal
cystic changes and, in some cases, a central consolidated cyst that may have represented
a coalescence of previous microcysts.28-30
Although preliminary studies of surgery to prevent progression to full-thickness
macular holes suggested efficacy,31,32
a prospective study of vitrectomy for impending macular holes did not confirm these
findings, possibly due to underrecruitment.33
ROLE OF OCT
A central clinical challenge has been accurately diagnosing early
macular holes which may be mimicked by many other conditions.34,35
No imaging modality has enhanced our diagnostic capability more than the OCT; superior
imaging capabilities have improved diagnostic accuracy, clinical monitoring, and
The OCT unequivocally demonstrates early stages of full-thickness macular holes
(Figure 1), and allows distinction of pseudohole and pre-macular hole conditions
in almost all instances. Fluid accumulation in early, presumed pre-macular hole
stages have been corroborated by OCT observations (Figure 2). Serial images have
been reported showing the progression from apparent impending macular holes to full
thickness macular holes.39-42
It has depicted many other configurations that might be in the spectrum of lamellar
or pre-macular hole conditions (Figure 3 and 4).
Serial OCT exams shed more light on probable pathogenesis and
clinical staging. Resolution of the foveal cystic change/impending macular holes
after posterior cortical vitreous release (aborted Stage 1B) is readily imaged using
OCT (Figure 5).43 The OCT
has documented spontaneous closure (without high vitreous separation) of several
traumatic macular holes44-47
and also an idiopathic macular hole without48
and with high vitreous separation.49,50
Optical coherence tomography renderings of impending holes are
reminiscent of the early reports by Reese which initially suggest vitreofoveal traction
as a macular hole precursor.51,52
While sometimes the OCT images seem to support that hypothesis, static images and
clinical observations do not depict force lines or subsequent events (Figure 6).
Thus, it is possible that the weakened or dehisced central fovea might be a fairly
subtle, early event, and focal proliferation of Mueller or glial cells along the
vitreoretinal adherence produce the same appearance and could be indistinguishable
from the appearance of vitreoretinal traction in a primary role despite the most
accurate of imaging modalities.
Apparent contradictions of a vitreofoveal traction theory include
the occurrence of full-thickness macular holes long after observing complete PVD,53
following scleral buckling procedure for rhegmatogenous detachments that presumably
were due to complete PVD,54,55
and even well after vitrectomy for an unrelated diagnosis.56
In these eyes the cortical vitreous presumably was not available to mediate traction;
perhaps a weakened, degenerated, inner retinal surface became attenuated independent
Regardless of the initiating mechanism, once the vitreous separates,
an early (occult) macular hole could repair itself (especially if very small) via
glial proliferation with little or no clinical symptoms or signs. If a full-thickness
macular hole first presents as reopening of a previously undetected, self-healed
macular hole, this could account for the predominance of (hyperplastic) Mueller
cells and glial cells found in the removed opercula. If the discontinuity is too
large, migration of reparative, proliferating glial cells is impeded,57
so a macular hole would enlarge as the glial cells which migrated around the hole
edge onto the perifoveal internal limiting membrane progressively contract. The
hydration theory is a novel concept that describes a mechanism by which a tiny dehiscence
might permit increasing degrees of perifoveal cystic changes, and subsequently a
dehiscence of a larger unit of inner retina (Figure 3).58
The OCT may have a role in identifying prognostic characteristics
or in explaining postoperative results. Most patients with macular holes regain
a gratifying amount of vision. The magnitude of improvement is variable, and may
be disappointing in some. While patients with better preoperative visual acuity,
shorter duration,59 earlier
stage,60 and smaller macular
hole size61,62 have better
anatomic and visual success rates, these characteristics do not predict individual
prognosis specifically. Other tests have also failed to offer a more specific prognosis,
suggesting that a more complex interaction of factors is operative.63
Kusuhara, et al64 used an
earlier model (OCT1), defined parameters, and attempted to identify a reproducible,
accurate, and straightforwardly ascertainable prognostic algorithm, but without
a substantial improvement in specificity. This was the first attempt to use the
OCT as a prognostic tool.
have attempted to correlate or to explain postoperative vision with OCT characteristics.
The OCT foveal morphology has been correlated to macular function in patients with
closed macular holes with conflicting results.65,66
Kang positively correlated closure type (with or without neurosensory defect) and
final visual outcome, but did not evaluate specific structural characteristics of
the foveal region.65
Uemoto, using a similar approach, evaluated foveal contour (good shape and poor
shape) and visual acuity in 86 eyes after successful macular hole surgery, but did
not find a correlation when using a simple approach of grading the foveal shape.66
It would seem that an intact, layered neurosensory retina should
correlate with visual acuity. However, foveal OCT findings in patients with anatomically
closed holes frequently seem to contradict intuition some patients with good
visual acuity may have an asymmetric, odd-looking fovea, while others with poor
visual acuity after successful macular hole surgery may present with a symmetric,
near-normal foveal configuration. A study examining such eyes using OCT found, however,
that certain specific structural features within the foveal architecture may be
more important than others to restore visual function in patients with closed macular
holes.67 Specifically, average
photoreceptor thickness correlated with final visual acuity, confirming that physical
integrity of the photoreceptor layer is most important for visual function. Furthermore,
the integrity of the high reflective band representing the transition zone between
inner and outer photoreceptor segments and the low reflective space between the
transition zone and the RPE-choriocapillaris area, were found to be key features
correlating with visual acuity. These may be useful indicators for follow-up management
such as when considering cataract extraction in patients with previous macular hole
surgery. Thus, the outer retina seems more important than the inner retina in terms
of restoring optimal postoperative visual acuity, while the inner retina is likely
more important to induce anatomic closure and clinical foveal morphology. However,
clinical foveal morphology seems to be a relatively unimportant determinant of visual
The therapeutic objectives in macular hole surgery involve one
or more of the following: glial proliferation induction, relief of traction on the
edges of the hole (surface or vitreoretinal), and providing a smooth template (gas
bubble or hyaloid) for cell migration. While in selected cases surgery limited to
surgical release of such a vitreofoveal adherence has been reported to be sufficient
to induce closure of the macular hole,68
the usual case requires more relief of traction or stimulation of gliosis. Peeling
of the ILM has become a commonly preferred step in contemporary macular hole surgical
technique because it seems to improve closure rate, possibly by enhancing results.60-74
ILM peeling itself appears to be safe. Minor inner retinal damage has been demonstrated
by transmission electron microscopy (TEM) in cadaver eyes undergoing ILM peeling.75
Clinically apparent effects were not seen despite the frequent, incidental finding
of ILM fragments in TEM studies in the majority of removed epiretinal membrane (ERM)
specimens.76 Poorer visual
acuity was found when large ILM fragments were present in light micrographs of removed
ERM specimens,77 as well
as infrequent morphologic consequences. Subclinical microperimetry defects78
and subclinical paracentral scotomata scanning laser ophthalmoscopic (SLO) perimetry
have also been reported.73
Iatrogenic punctate chorioretinopathy may occur due to repeated attempts at engaging
an edge79 and self-limited
have been reported with ILM removal.
Internal limiting membrane peeling is not an absolute requirement
to induce macular hole closure,69,70
but generally increased anatomic and visual success rates reported as ILM peeling
has been used more widely have led to its general acceptance.71,72,74,81,82
High success rates in lower prognosis macular hole cases, such as traumatic83
or highly myopic eyes,84
is compelling evidence of its efficacy.
Under the reasonable presumption that ILM removal is helpful,
there has been much interest in perfecting its effective removal, including customized
ILM staining to allow its visualization most extensively studied using indocyanine
green (ICG).87-96 Removing
the ILM is unquestionably easier using ICG, but concerns regarding possible toxicity
have been raised. ICG persists postoperatively for up to several months.97-103
It has been shown in vitro to be toxic due to external diffusion,104
and it induces a hyposmolality effect in cultured RPE cells.105
A host of other effects has been documented in vitro and in animal models suggesting
a focus of toxicity on apoptosis of the RPE cells and through alteration of gene
expression.106-112 ICG has
been demonstrated to induce death of cultured glial cells at high concentrations,113
and in retinal ganglion cells.114
It has caused histological and ERG changes in rabbit eyes.115
Possible clinical examples of ICG toxicity have been reported as RPE atrophy,116,117
potentiation of phototoxicity,118
visual field defects,119
alteration of the ILM-retinal cleavage plane by allowing more inner retinal element
adherence to the removed ILM,120
and optic neuropathy.121
reports have also suggested ICG toxicity. A clinical study showed no visual improvement
in a series of 20 patients undergoing macular hole surgery using ICG.122
Histologic examination of removed epiretinal membrane specimens showed more cellular
debris from eyes in which ICG was used compared to eyes without ICG, but more visual
improvement was seen in ICG cases.123
Another report of 18 patients undergoing macular hole surgery found lower functional
visual outcomes and more common visual field defects with ICG and questioned whether
this was a toxic or mechanical effect.124
The hypothesis that light toxicity is potentiated by ICG is consistent with its
spectral absorption, its effects on cultured RPE cells, cadaver eye studies, and
the incidental finding of increased diode laser update in ICG stained eyes.125-129
Other studies, however, have not found evidence of the ICG toxicity.
No effects were seen in an experimental study after exposing cultured RPE cells
for 5 minutes, but after 10 minutes morphologic effects were found.130
Toxic effects were not seen in a clinical study of 18 eyes examined with SLO perimetry
exams and photographs.131
A series of 37 eyes in which ICG was used showed a 97% anatomic success rate and
62% visual improvement rate including some to 20/20 indicating analogous results
with standard series.132
Similar results were found in another study.88
These and other aspects defending the safety of ICG have been recently reviewed.133
Nevertheless, the conflicting opinions and results have caused
many to advocate caution, further study, modifications in technique, or even restraint
regarding the use of ICG.134,135
Sodium hyaluronate use has been suggested to block ingress of the ICG through the
macular hole to the subretinal space.136
Alternate preparations of dye have been studied (eg, infracyanine green) without
a definitive conclusion of a better toxicity profile.137-139
The technique of ICG staining has been described with a few permutations. Probably
the most common concentration used has decreased from the 0.5%104,118-121
in initial reports to 0.1% or even 0.05%.122-124,131
However, less effective staining at lower concentrations may necessitate longer
or repeated staining maneuvers.140,141
Shorter exposure times (15 seconds rather than 30 seconds to 3 minutes) have also
been proposed as a means of minimizing toxicity risk.141,142
There is a general consensus to use as low of a concentration and time of exposure
to the stain as possible. Some inject the dye without doing a temporary fluid-gas
exchange, while others instill the dye into a small pool of residual fluid overlying
the macula (as in the current study). A valid concern with the latter strategy is
that partial fluid-air exchange effectively exposes the retina to a higher concentration,
but yields a very faint staining which seemed to be at the visual threshold necessary
to see an effect.
Other staining techniques utilizing trypan blue143-145
or triamcinolone acetonide146-150
may offer less toxicity while still facilitating reproducible and complete ILM removal.
However, more studies are necessary to confirm pilot studies, especially regarding
toxicities, as preliminary reports suggest possible toxicity with trypan blue,151-152
and induced intraocular pressure and cataracts are well-recognized potential complications
of intraocular corticosteroids.153
Studies comparing ICG to trypan blue have generally shown a better toxicity profile
for trypan blue.154-156
A reasonable clinical algorithm in the face of uncertainty regarding
ICG use is to peel ILM without using ICG, as is usually possible, but if difficulty
is anticipated or encountered, then ICG should be considered as a reasonable option.
Cases ideal for ICG include those with compromised visibility or anatomic complexity.157
The element considered by most to be essential for success also
presents the most formidable challenge to the patient face-down positioning.
Early investigators recommended up to 4-weeks positioning, but this has gradually
been reduced to about 1 week without apparently compromising results. Some have
suggested shorter intervals or even no positioning,158
but the success rates in some of those reports might not be as good as techniques
using positioning, or may only be applicable in selected cases.159
Some patients are unable due to arthritis or dementia, or are unwilling to comply
with a prone-positioning regimen. Complications have been reported with prolonged
In addition, air travel constraints may limit gas bubble use. These factors have
forced surgeons to consider alternate treatment techniques.
Silicone oil tamponade has been evaluated as a solution to these
constraints. An extra potential benefit of silicone oil would be more rapid recovery
of postoperative vision. However, the need for re-operation to remove the oil must
be considered, although it may be combined with cataract extraction in many patients.
Initial results were encouraging,161,162
but later studies demonstrated anatomic results equivalent (at best) to using gas,
but inferior visual results.163-165
Several reports have discussed possible retinal toxicity associated with silicone
oil. Goldbaum discussed possible photoreceptor toxicity resulting from silicone
oil exposure.161 Saitoh showed
that 6-month silicone oil tamponade in a rabbit model may result in the accumulation
of oil vacuoles within the optic nerve on electron microscopy.166
Similar accumulations may account for poor visual outcomes in macular hole patients.
gas tamponade remains the preferred surgical technique for patients undergoing macular
hole repair, even if face-down positioning cannot be pursued. Shorter acting gas
mixtures are preferable for patients desiring early air travel.
Macular holes have gone from being an untreatable curiosity to
become one of the most common and satisfying conditions for the vitreoretinal surgeon
to treat. OCT imaging has offered markedly enhanced imaging of macular anatomy,
allowing more accurate diagnosis and assessment of anatomic results, and it may
offer some prognostic information. While pathogenesis is still incompletely understood,
relief of vitreoretinal and tangential traction (whether causative or secondary)
is a key objective of surgical repair. ILM peeling may not be necessary in all cases,
but increases overall success rates without damaging retinal function, so it is
pursued to achieve the traction relief objective. ICG seems safe, but because there
are considerable questions about its possible toxicity it is probably best reserved
for selected cases. While some relief in the postoperative face-down positioning
regimen may be safe, silicone oil probably should be avoided as a tool to facilitate
Macular hole surgery, though highly successful by vitreoretinal
surgical standards, may always be improved.
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E. Smiddy, MD, is professor of ophthalmology specializing in macular holes, diabetic
retinopathy, macular degeneration, macular disease, and vitreoretinal diseases and
surgery at the Bascom Palmer Eye Institute in Miami, Fla. Dr. Smiddy has no financial
interest in any of the information contained in this article. He can be e-mailed
Retinal Physician, Issue: July 2006