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IREVIEW ARTICLE'

Macular Hole
Vog Raj Sharma, Rajeev Sudan, Ami! Gaur, Raja Rami Reddy

A macular hole is a full thickness defect or tear of the

neurosensory la~ ers ofretina involving the anatomic fovea
of the eye. The majority of macular holes are primary

was sometimes followed by cystoid macular edema

1,1

hich

ruptured later producing macular holes(5).

Soon non trawnatic cases of macular hofes began to

idiopathic macular holes. Secondary macular holes may

be reported(6). Coats was among the first to recognize

occur in association with a variety ofconditions including

blunt trauma, high myopia optic disc coloboma, optic nerve

that macular cystoid degeneration was often 110t related

to trauma and supported cystic degeneration tht:ory or

pit. long standing retinal detachment with long standing

macular hole(4). Intraretinal cystic changes which

('ystoid macular edema resulting from vena-occlusive

coalesced creating full thickness macular holc could be

diseases or diabetic retinopathy, Bes~s disease, adult vitelli

caused by trauma as well as other atraumatic

form macular degeneration. retinal arterio venous

mechanisms. Vascular theory of pathogenesis "as the

cOllununicclliol1. choroidal neovascularizations. topical

other major atrawnatic theory ofmacular hole formation

pilocilll'ine. solar eclipsc macular bluns. and may be fOlmd

which became popular. It was believed that aging and

aflcr successf~" retinal reattachment surgery by scleral

buckling or pneumatic rClinopexy.

other changes of the retinal vasculature led to c~ stoid

retinal degeneration and subsequent macular hole

Historical Perspective and Etiological theories

Ilerman Knapp in 1869 described the first case of
macular hole. in a patient who had sustained a severe
contusion and in whom an initial diagnosis of a macular
hemorrhage was made( I). Two years later Noyes made
the fIrst accurate and detailed ophthalmoscopic description
of a macular hole that was again secondary to blunt
trauma(2).

e\ertheless the entity of macular hole was

not "'dely recogtlized lmtil the tum ofthe centlrry. Trawna

was originally thought to be the primary, ifnot the sole,
etiological cause with traumatic macular holes accounting

formation(7). Lister in 192-1 was the lirst of man\ to

implicate anteroposterior vitreous forces in tho pathogenesis of macular holes(5). Various other proponents of
vitreous theory extended this hypothesis by emphasizing
that the process of posterior vitreous detachment (PVDj
was the critical event in the pathogenesis of a macular
hole causing avulsion of inner retinallayers(8l. As 1'\'1)
is a common event in the age group of those at greatest
risk for idiopadlic macular hole fonnation. it is di fTicult to
ascribe a causal relationship between these two events.
Morgan and Schatz in 1986 proposed a mechanism of

for half of all cases of macular holes in the beginning of

macular hole fonnation that they described as imolutionaJ

this century(3). Hole fomlation was explained by rupture

macular thinning, which incorporates vitreous. I ascular

of I'Olea from mechanical energy created by vitreous

and cystic degeneration theories(9).

Iluid waves and counter coupe macular necrosis or

In 1988. Gass and Johnson described a classification

laccration(4). It was also recognised ,that blunt trauma

scheme for idiopathic macular holes which incorporated

From the Department ofOphlhahnology, Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AllMS, New Delhi.
Correspondence to: Dr. YR. Shanna, Additional Professor ofOphthahnology, AlIMS, New Delhi.
\'01. 4 No.2. April-June 2002

57

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...J.K
their ideas of thc pathogenesis of these lesions. They
concluded that attached \ itrcous was criticallO macular
hole formation. As thc stages of development of a
macular hole caused loss of normal foveal analOmic
depression bUI no e1evalion oftissue above the parafoveal
retina. the) h) pothes~ed that focal shrinkage of the
pre foveolar vitreous cortex and tangential retinal traction,
are responsible for macular hole formation.

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not detected by biomicroscopy (occult hole). The yello\\

ring appears at edge of the centrifugally displaced retinal
receptors. This fmding appears to be specific lO macular
hole formation.
Stage 2

Pathogenesis and Clinical Staging of Macular Hole

Formation

Biomicroscopic finding: Small full thickness retinal

defect 400H) which may be eccentric, oval. crescentic
or horse-shoe shaped at inner of yellow ring or a central
round retinal defect with rim of elevated retina. Hole
may be present with or without a pre foveolar opacity.

Clinical stages of idiopathic macular holes were

originall) descrihed in a reu'ospective series by Gass and
Johnson and \\ere updated in a subsequent prospective
senes(IO.11.12).

Anatomic interpret?tion: A hole(tear) occurs in the

contracted prefoveolar vitreous condensation bridging the
occult retinal hole. so the retinal defect is idenli fiable
biomicroscopically as stage 2 hole. Spontaneous

Stalle IA (Impcnding bole)

vitreofovcal separation may occur creating a semi-trans-

Biomicroscopic finding: A yellow SpOI. I00-200H in

diametcr. centered on the foveola. Associated loss of
101 eal depression (hence fovcal reflection) occurs. No

parent prefoveal opacity (pseudooperculum) that is often larger than the underlying foveolar hole. There is no
loss of foveolar retina and no posterior vitreous detachment from optic disc and macula.

,"itrco foveolar separation.

AnalOmic Interpretation: Spontaneous tangential

traction of thc cxtcrnal part of the prefoveal cortical
\ itreous callses serOllS detachment of foveolar retina

crcating an intraretinal yellow spot. The yellow color

results Irom intraretinal xanthophyll pigment. This finding is not pathognomonic of macular hole.
Siage IB (Impending or occult hole)
Biomicroscopic findings: A yellow'ring. 200-300H in
diameter. centered on the foveala. associated loss of
!c}\eolar depression \\ ith no vitreo foveolar separation.

Anatomic interpretation: After the serous foveolar

detachment the foveal retina detaches and elevates to
the level of the surrounding peri foveal retina. elongating
the fO\ eal relina around the u111bo (impending hole). This
is followed b) centri fugal displacement of the retinal
photoreceptors. xanthophyll and radiating nerve fibres
leading lO a dehiscence of the deeper retinal layer at the
umbo. As the o\crlying internal limiting membranes,
horizontal processes of Muller cells, and prefoveolar
,itreous condensation remains intact, the dehiscence is
58

Stage 3
Biomicroscopic finding: Full developed. central alOlUld,
400H diameter hole. with rim of elevated retina. A
prefoveolar opacity mayor may nol be associated.
Anatomic interpretation: A full thickness hole with no
posterior vitreous detachment from optic disc and macula.
vitreofoveal separation ma) form a prefoveal opacit)
(pseudooperculum)
Stage 4
Biomiocroscopic finding: Full thickncss hole rim of
elevated retina and Weiss Ring. A prefoveolar opacil)
mayor may not be present.
Anatomic interpretation: A full thickness hole with
complete posterior vitreous detachment [rom oplic disc
and macula.
Based on their findings, Gass concluded thaI as the
fovea was never elevated anterior to the plane of the
retina, antero-posterior tracti0n with PYD was not the
mechanism for macular hole formation. They proposed
that in the pathogenesis of idiopathic macular hole.
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shrinkage of attached posterior cortical vitreous occurs

degenerated variably in long standing cases. !I. thin la) cr

that generates tangential traction that is transmitted to

ofepiretinal tissue is seen overlying the macula in stage

the foveal retina. The biophysical mechanism for this

1,2 and3 holes and has been found to be posterior cortical

shrinkage of the posterior cortical vitreous is not known.

vitreous. This finding is consistent with Gass's theory that

Guyer and Green proposed three possible mechanisms

prefoveal cortical vitreous plays a role in pathogenesis ()f

for generating tangential traction. Fluid movements.

macular holes. Postmortem studies

cellular remodelling ofthe cortical vitreous. and cellular

had macular hole surgery have also pro\ ided unique: in-

proliferation on the inner surface of the cortical

fonnation. The healed macular hole appears as a dekcl

vitreous( 13). Madreperla and Mc Cuen bave suggested

in the fovea which is occupied by Muller cell processes

a concept of macular hole formation. Initially foveolar

and fibrous astrocytes. Photoreceptors adjacent to thc

011

patients IM\ ing

detaclunent is caused by traction directed at fovea by

healed hole appear normal usually. No RPE abnormal i-

detachment of para foveal cortical vitreous which is at-

ties or CME were found. The size of the healed hole is

tached at tovea. Continued traction from detached para

found to be much smallerthan that noted prcopcrati' el).

fo\ eal cortical \ itreous leads to foveolar dehiscence.

Madreperla and colleagues suggested that surgical relid'

S\\clling offoveal retina occurs with retraction of fO\ cal

of tangential traction and flattening of the cdcmatou . .

hole edges( enlargement of macular hole). Concurrentl}

cdges of the hole allo\\ the setting of the macular hole

glial cells grow from edges of retinal defect along poste-

and reapproximation of the edges. AJ,) residual dekct is

rior face of cortical vitreous. Continued traction from

sealed by glial cells (fibrous astrocytes and Muller eelb).

detached para foveal cortical vitreous leads to break

The presence of normal photoreceptors around the hole

belween glial cclls and macular hole edge. This dehis-

and absence of CI\lE and retinal detachment accounh

cence progresses around the entire circumference of tile

for the observed improvement in vision ancr llllks 11(1\ C

~,=l1tl'""l,\\\ ~"m,alion

of a pseudo operculum

O\crl)ing the lull thickness retinal defect and attached to

posterior cortical \,itreolls( 1-1).
Histopathology of Macular Holes
llistopathologic scries ofpost mortem cases of macular
hole reported by Frangieh et al and Gyer et al have
prO\'ideci information regarding pathogenesis and rationale

been successfully treated( 17).

The prefo,oeal vitreous opacit) pn:scIlt in

mall)

eyes with macular hole was initiall) termed an operculum and was believed to represent retinal lissue that at
one time occupied the hole. Ilistopathologic fealure 01
this tissue oblained during vitrectomy has been sludied
Llsing transmission electron microscopy( 18). The tissue

for management of macular holes( 15, 16)

were composed of Muller cells and Iihrous astroc: Ie .....

with a thin layer of cortical \itreOlls lining the imcrnal

hIli thickness macular holes are characterized b)

absence of all retinallaye. s in an area usually centred at

surface. Importantly there \\ere

the fovea. TIley are usually surrounded by rounded retinal

sented a piece of foveolar retina. It \\as concluded that

edges and a cuO' of detached neurosensory retina with

the pre hole opacity did not represent retinal tissue but

subrClinal Ouid. Lamellar macular holes are character-

rather avulsed gliallissue possibl) im'olved in an altcmpt

ized by partial loss of inner neuro sensory retinal layers

110

photoreceptor, or

neural tissue as would be expected if the tissue repre-

'10

heal the hole and should be referred to as a pseudo

lI'ith no cuff of detached retina. Cystoid macular edema

operculum. It has also been suggested that glial cel'"

(79%) and epiretinal membranes (158%) are the most

present in these tissue may be agents in the primal)

common associated features. RPE changes are not

pathogenesis ofmacwar holes rather than siJ11pl~ elements

uncommon. Photoreceptor adjacent to the hole are

of a reparative process.

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Clinical Characteristics and Epidemiology of

Macular Holes (19.20.21)

monocular. Some patients may remain entirely

near the inner edge oCthe yellow ring. Stage 2 holes can
be centric and eccentric. Small stage 2 holes can be
difficult to see and use of nanow high imensit) slit beam
and high magnification can aid their dctection. In stage 3
& 4 holes, a round excarvated lesion (>400m) is secn
interrupting the beam of slit lamp. In majorit) ofpatiems.
an opacity (pseudooperculum) can be seen suspended
over the hole. Often there is a surrounding culT of edema
and subretinal nuid. lIistopathologic studies show that
only a very small amount of actual retinal detachment
occurs and most of the perceived cuff at the border of
the holes is due to surrowlding C) stic edema of retina.
Retinal pigmcnt epitheliwn (RPE) at base of hole appears intact and nonnal in acute holes. but c1uonic changes
include pigmcntary atrophy and hyperplasia Icading to a
granular appearance. Characteristic yellow refractile dot
like deposits may be seen at the base of holc( 42% of
cases), these may represent lipofuscinladenmacrophages
or nodular proliferations ofRPE overlying eosinophilic

as) mptomatic and the hole is diagnosed only on routine

material. Epiretinal membrane formation

ophthalmologic examination or by the optometrists who

are alerted to the condition by the poor visual acuity. The
,isual acui\) of stage I hole is often as good as 6/9 or 6/
12. Once full thickness hole is identifiable (stage 2
onwards) vision varies between 6/18 to 3/60. Patients
\\ ith recent. small eccentric stage 2 hole may retain
excellent visual acuity (6/9-6/12). As a rule ofthurnb, a
lull thickness macular hole does not maintain a visual
acuity 6/18 or better for more than 3 months.
Metamorphopsia is caused by elevation of neuro sensory
retina around thc hole.

present in some cases. Weiss Ring (complcte PVD)

is seen in stage 4. Macular holes may val') in size
depending in part on their duration. Average hole measure
500-800H

Idiopathic macular holes are most common accounting

for 83% of cases. 15% Cases are due to trauma
(accidental or surgical) and rest are secondary macular

holes associated \\ ith other conditions mentioned above.

rhe peak incidence of idiopathic macular hole
de'elopment is in the seventh decade of life. A female
preponderance is observed(80%).
Symptoms
rhe majorit) of idiopathic macular holes are
as) mplomatic in the carly stages. Patients who are symptomatic with macular holes complain of blurred central
vision or a cemral scotoma and metamorphopsia. Usually
they notice only a mild loss of vision particularly apparent
when reading or driving. Symptoms develop relatively
graduall) and it ma) be some time before they cover one
C) e and detect that the central decrease in acuity is

Clinical examination

rhe detec'ion of macular hole is best achieved by slit

lamp biomicroscopy using a contact Iron contract/non
lens. The Gass classi fication system is used most widely
to describe the clinical appearance and evaluation of
macular holes. In stage lA (impending hole) a yellow
spot is seen. a yellow ring is noted in stage'I B (impending
or occult hole) Stage 2 is diagnosed when a full thickness
defect <400 m in diameter is first noted clinically, usually
60

1113)

be

Aueilliary Tests
Although clinical examination remains the gold
standard for diagnosis. these tests assist in making a
diagnosis ofmacular hole and in differentiation from other
pseudo hole conditions.
a)
Fluorescein Angiography: This may be a useful
adjunct to biomicroscopy. In stage I faint hyper nuorescence or more typically no abnomlality at all is seen on
fluorescein angiography. In stage 2 holes, nuorescein
angiography may reveal a round area of window defect
or may remain normal. Stage 3 and 4 holes typicall)
produce a window dcfect with early transmission of
fluorescence in phase with choroidal filling through the
central retinal defect. No late leakage or accwnulation
of dye is seen. In some cases particularly those involving
very small holes or holes accompanied by RPE
Vol. 4 No.2. April-June

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abnormalities. distinguishing the characteristic hallmark

window defect may be difficult.
b)
Watzke Allen Test: This is perfonned by placing a
thin vertical slit lamp beam directly on hole during contact
lens biomicroscopic examination. Patient with positive
Walzke Allen sign will perceive an interruption in the
light beam. A normal appearing or only narrowed beam
is a negative result. This is a highly sensitive and specific
clinical test distinguishing full thickness macular holes from
pseudo-holes.lfncgative with vertical beam, a horizontal
beam can be tried. Another useful maneuver is moving
the slillamp beam slowly across the macula and asking
the patient whether at any time the beam is clotted or
broken.
c)
Laser Microperimerry: The aiming beam on a laser
delivery system is also a good test for assessing th~
presence or absence of a full thickness macular hole.
The patient is seated at the laser with contact lens in
place. A 50 Painting beam is used to test central areas of
retina focally for sensitivity. The inability ofthe patient to
percei\e the SPOI in the area of presnmed macular hole
(absolute scotoma) confirms the lack of retinal tissue'in
thallocation (full thickness hole).
d)
Optical Coherence Tomography(OCT): Tbis is a
. new diagnostic imaging technique for high resolution
imaging ofthe retina(22). Cross sectional images ofretina
can be obtained with 10 longitudinal resolution. OCT is
perfomled with patient sitting at slit lamp into which a
78D lens has been mounted. A superluminescent diode
laser produces a probe beam of wavelength 840 units
(infrared) that is focussed in the retina. A pair of
galvanometrically driven ortho gonal scarming mirror
scans the beam within the eye and area of retina scarmed
can be visualised with an infra red camera. Cross sectional images of retina are displaced in colours corresponding to regions of high relative optical reflectivity
(red and while) or low reflectivity (blue to black). High
resolution tomographic images provided by OCT can help
differentiate true macular holes from pseudo holes and
lamellar holes.
Vol.l No.2. April-June 2002

e)

Scanning laser ophthalmoscope and

f)
Retinal thickness analyzer also have been used to
differentiate between macular holes and mimicking
conditions.
Differential Diagnosis

Macular holes are often misdiagnosed. Careful

biomicroscopic examination with a contact lens is required
to make an accurate diagnosis. Various ancillary tests
mentioned above help in di fferentiation. A true full
thickness macular hole has a distinct and circular margin.
often with a surrounding cuff of subretinal fluid and an
overlying pseudo-operculum. Vision is usually 6/18 or
worse while macular pseudo hoJes fare betteF.
a)
Hole in epiretinal (epimacular membrane): Most
commonly confused lesion is an epiretinal membrane that
has a hole, contraction or circumlinear edge in or near
the fovea. Contact lens biomicroscopy shows the
membrane itself with contracture and macular puckering with nonnal retina beneath the membrane. No cuff
of subretinal fluid and retinal edema is found around the
hole and fluorescein angiography shows no window
defect. It is important to note that epiretinalmembranes
may be found in association with macular holes as well,
so presence of one does not rule out the diagnosis of
macular hole.
b)
Age related macular degeneration (ARMD):
Geographic atrophy of RPE and overlying retina may.
when sharply demarcated circular and central. mimic the
appearance of macular hole.
c)
Cystoid macular edema(CME): When a large
central cyst is present it may simulate the presence of
full thickness macular hole. Other ocular conditions
associated with CME (recent intraocular surgery, ocular
inflanunatory condition etc.) and fluorescein angiography
help in differentiation.
d)
Lamellar macular holes: These are partial thickness defect of macular retina most often the result of
aborted macular hole formation or seen in cases ofchrome
CME when the tbin inner layer of the cyst breaks. A
61

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pseudo-operculum may be observed overlying the lamellar

macular hole contributing to misdiagnosis. Neither cuff
of retinal edema or subretinal fluid nor central window
defect on fluoresLein angiography are demonstrated.
Borders oflamellar hole are less slowly defined and have
more sloping edges.
e)
Sub foveal choroidal neovascularization with a
foveal cyst and intra retinal edema may mimic a macular
hole.
Vitreo macular teaction with a cystic fovea may
also masquerade as a macular hole.
f)

g)
Various conditicms that may be misdiagnosed as
stage I macular hole (impending hole) include ARMD
with a large central drusen, central serous retinopathy,
cystoid macular edema, vitreomacular traction syndrome
or a foveal yellow lesion associated with solar retinopathy.

In a follow up study to the EDCCS. rate of development

of macular hole in the fellow eye was 4.3-7.1 % on 3-6

years of follow up(23). Other studies have reported risk
of fellow eye involvement to be from 3-22%(24). The
risk of development is high (40%), if the fellow eyes
showed premacular hole change (Stage I lesions). while
normal fellow eyes have a very low incidence (0.2%)
particularly if there is a pre-existent posterior vitreous
detachment.
Natural History of Macular Holes
Natural history ofsmall full thickness macular hole is
one of hole enlargement accompanied by deterioration
of visual acuity.
Stage 1 lesions

Risk factors for idiopathic macular hole

Vitrectomy for Prevention of Macular Hole Stud)

Group, a multicenter, randomized, controlled clinical trial

The eye disease case cortrol studv group (EDCCS)

reported on the demographic and risk factors for idiopathic
macular hole comparing 198 subjects with macular hole
with 1023 matched controls. 72% ofsubjects with macular
hole were female. Only 3% of subject were less than 55
years of age. In the final multivariate logistic regression
model that included all cases, higher fibrinogen levels and
history ofglaucoma were the only significant risk factors.
In women. current users of exogenous estrogen had
reduced risk. Other risk factor like cardi..lVascular disease.
hypertension. history ofhysterectomy, total protein, serum
beta carotene. which have been suggested as risk factors
in previous studies were not found to be associated significantly as risk factor for macular hole in the EDCCS.

was performed to better understand the natural histo~

of early stages of macular hole (25). Forty percent 01
oatients with stage I lesion progress to a full thickne.
macular hole over a 2 year follow up period while 60\
ofstage I lesions abort macular hole formation. Resoluti
of stage I lesion is accompanied by \ itreofO\e
separatiorL Resolved fovea may appear normal or mao
show a lamellar macular hole. Lamellar macular hoi.
do not progress to macular holes (12). Posterior vitre
detachment confers protection from macular h
evolution (24). Eyes with stage I macular hole and
corrected visual acuity between 6/18-6/24 had a 66
rate of progression to ,'nil thickness macular hole. \\
eyes with 6/6-6112 had a 30% risk of progression (26

Risk to the fellow eye

Stage 2 lesions

This is important point for consideration as patients

with a unilateral macular hole will be concerned about
the prognosis for their fellow eye. Risk to the fellow eye
also needs to be considered when surgical treatment of
f,ill thickness macular hole is planned.

Majority of stage 2 holes demonstrate progression

stage 3 and 4 macular holes with subsequent loss ofvis'
usually within 6 months. Hikichi reported 96% of stag<
lesion progress to stage 3 and 4 lesions, in 85% the h
enlarges, visual acuity loss of2 or more snellen lines oc
in 71 % ofeyes with no eyes demonstrating resolution

The vast majority of fellow eyes will not develop a

macular hole. but there is definite incidence ofbilaterality.
62

median follow up period of 4 years(27).

Vol. 4 No.2. April-June2

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Stage 3 and 4 macular holes
The frequency of hole enlargement and visual
deterioration is less with stage 3 and 4 lesions. Hikichi
reported 55% of stage 3 lesion and 16% of stage 4 lesion,
undergo macular hole enlargement during median follow
up of 3 year period and visual acuity loss of 2 or more
snellen lines occur in 29% of eyes with stage 3 lesion and
13% with stage 4 lesion. Progressive visual deterioration
in stage 3 and 4 holes is due to increasing cuffofsubretinal
fluid, cystoid retinal changes and photoreceptor atrophy.
5-12% of stage 3 or 4 lesions may spontaneously flatten
with improvement in visual acuity (16).
Management of macular hole : Historical
Background
Until recently majority of patients with macular hole
were considered untreatable with patient usually
becoming legally blind in the affected eye. Surgeons
focussed their attention on macular hole only if retinal
detachments were associated. Surgery involved scleral
buckling techniques with subretinal fluid drainage and light
laser photocoagulation to flatten a macular hole. Other
variations included Y shaped plombs, armed silicone
implants, diatllenny, cryotherapy, silicone oil or intravitreal
gas injection without vitrectomy (28).
Vitrectomy with gas tamponade to achieve retinal
realtachment in eye with large retinal detachment and
macular holes was reported in i 982 (29). Bidwell et al
reponed spontaneous recovery of excellent vision (6/6)
and disappearance of the macular hole in one eye and
retinal reattachment with disappearance ofthe hole and
6/6 vision after vitrectomy and gas tamponade in one
eye(30).1n 1988 Gass introduced the concept of Iangential \ itreous traction on the posterior pole in macular holes
and a classificatioin and hypothesis for their
pathogenesis( I0, II). Kelly and Wendel are to be credited
for the introduction and developments of vitreous surgery for full thickness macular holes. They hypothesized
that vision might stablize or improve if it were possible to
surgically relieve the tangential traction, reduce the cystic
changes and reattach the cuff of detached retina
Vol. 4No.2. April-June 2002

surrounding a macular hole using traditional vitrectomy

techniques. The pilot surgical series was published in 1991
and was updated in 1993(31,32). After this extraordinary
report and remarkable success in improving vision by
sealing full thickness macular holes, interest was renewed
in this order which was previously considered untreatable.
There was quick acceptance by many vitreous surgeons
ofthe technique reported by Kelly and Wendel and results
have been duplicated by other investigators around the
world, The surgical techniques have been gradually
improving along with improvement in visual results.
Surgical techniques for full thickness holes
Indications for surgical intervention are vision loss and
the presence ofa full thickness retinal break. The surgical
objectives are to relieve all vitreomacular traction and to
affect retinal tamponade. Tangential traction is released
by identification and removal ofthe conical vitreous and
by removal of fine epiretinal membrane (ERMs)
surrounding the hole. Tamponade is usually provided by
total gas fluid exchange and strict post operative prone
positioning.
A standard three port pars plana vitrectomy is
performed to remove anterior and middle vitreous. Then
a critical surgical step is the technique of induction of a
complete posterior vitreous detachment (PVD). Various
surgical techniques have been described including use of
tapered extrusion (suction) needle, use of rnicrovitreoretinal blade to incise the posterior hyaloid at optic disc
margm.
But the easiest and safest is the use ofsoft tipped silicone
cannula. Using active suction (150-250mmHg), the cannula
is swept gently over the retinal surfaces near the major
vascular arcades, around the optic nerve or temporal to
macula. The area aroWld the macular hole is avoided as tl,e
cuff of detached retina is mobile and easily incarcerates
into the pon, Engagement ofcortical vitreous results in flexion
ofthe silicone tip ("fish strike" sign). The tip ofcannula should
be kept I nun away from retinal sw'face. As long as vitreous
cortex is present this maneuver is safe as vitreous plugs tl,e
port preventing retinal incarceration. Care should be taken
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if intraoperatively or preoperatively PVD has occcured

(Stage 4 hole), as the retina can be aspirated into the p0l1
and tom. As the cortical vitreous can be difficult to identify,
use ofautologous blood to stain this tissue has been reported.
Once the surgeon becomes familiar with identifying the
vitreous cortex, a faster and easier method is suggested in
which the vitreous cutter set on "suction only" is directed
posteriorly and gendy swept over the retina till cortical vitreous
fibres are seen streaming into the port.

surrolUlding the macular hole to the subjacent RPE. Tlus

Once vitreous is engaged, a PVD is created with

is usually associated with a decrease in size of hole with

persistent, gentle traction as the tip of cannula is moved

over retinal surface to the posterior equatorial zone. Once
elevated the cortici'l vitreous is seen as a thickened
translucent sheet. A ring ofperipapillary vitreous (Weiss's
ring) and a pseudo-operculum can be detected usually.
These are removed with the vitreous cutter.

the edges appearing to have slid together and becoming

Preoperative examination made to detect the extent

and location of ERMs help in their intraoperative
identification and surgical removal. ERMs associated with
macular holes are finer more friable, and more tightly
adherent to d,e retina. A bent MVR blade is used to
create an edge and then elevated with a membrance pick.
The free edge is grasped with intraocular tissue forceps
and stripped.
After completing the vitrectomy, a careful indirect
ophthalmoscopic examination ofthe peripheral retina for
iatrogenic retina tear is made. A total air-fluid exchange is
performed. Waiting for a few minutes will allow residual
intraocular fluid to collect posteriorly which is then removed
to completely dehydrate the vitreous cavity. Once all the
fluid has been removed the residual fluid in the base ofthe
macular hole may be aspirated using a 33 G metal tapered
tip aspiration needle, taking care to avoid touching the retinal
pigment epithelilUu. TIus step is not attempted in stage 2
holes to avoid inadvertent progression to stage 3.
A non expansile concentration oflong acting gas (20%
SF" 14% C,F 8) is exchanged for the air. In cases where
surgery is performed lUlder general anaesthesia, it is
important to stop tutrous oxide administration 30 minutes
before gas air exchange.
64

Post operatively 24 hours a day strict prone positioning for I week is mandatory to ensure success. An
alternative approach in case where this is not possible is
use ofsilicone oil for tanlponade wid'Out prone positioning.
Results
Anatomic success in macular hole surgery is defined
as attachment of the previously elevated cuff of retina

imperceptible in some cases. In every anatomical II

successful case, the cystic retinal changes around tb,
edges of the hole resolve. These clinical observations
have been confIrmed histopathologically (17). It has been
suggested that the surgical relief of tangential traction
and flattening of the edematous edges of the hole allo\\
settling of the macular hole and reapproximation oftb,
edges. Any residual defect is then sealed by glial cells
(fibrous astrocytes and Muller cells). The presence of
nonnal photoreceptors arolUld the surgically treated hole.
absence of CME and retinal detacl:unent and the laci
that there is no actual loss of retinal tissue in macular
hole accounts for the observed improvement in vision
after holes have been successfully treated. Besides
closure of macular hole and visual improvement aftel
surgery, other changes observed are resolution of central
hyperfluorescence (window defect) on fluorescein
angiography and absence of absolute scotoma delect~
by preoperative microperimetry.
In the landmark pilot series of 20 cases persented ~
.Kelly and Wendel, overall results were of 58% anatoml
success rate and visual improvement of two or more lino
in 42% of eyes (31). Later in a larger series of 17
consecutive cases ofmacular holer surgery they report.
improved over all results to 73% anatomic success aIIl
55% patients improving two or more lines ofvisual acuin
(32). Various subsequent surgical series (33-35) confinn.

the potential role ofvitreous surgery to close full thicknei

Vol. 4 No.2. AprilJuue 200

______________

J~:~JK SCIENCE

macular holes with possible recovery of central visual

anatomic and visual success rates by refining various

flmction with increasing repotted success rates and visual

stages of the surgical techniques. Histopathologic studies

acuity recovery rates. A series of sW'gery for stage 2

have demonstrated that with macular hole resolution.

macular holes in 1994 demonstrated that 61 % improved

either spontaneously or after successful m,-H':lllar hole

isual acuity. 27% rcmained stable and 12% progressed

surgery. the edges are reapproximated. and the residual

to a stage 3 macular hole with \vorse vision (36). As

1110st of these series were uncontrolled, Freeman

organised the Vitrectomy for Macular Hole Study Group
"hich investigated the natural history of fuJI thickness
macular holes and role of vitrectomy sW'gery versus
obscrvation for full thickness macular holes in a
prospective. randomized controlled clinical tTial (37). In
the Earl) Full Thickness Macular Hole Study, stage 2

defect filled with fibroglial cells( 17). Surgical rationale

for using adjunctive therapy regimens is lhc stimulation
offibroglial proliferation to close the hole, al'oiding trauma
to adjacant functional retinal elements. Various adjll\ ants
which have been used are biological tissue adhesi\ l'.
transforming gro\>.rth factor-beta, (TGF-~, ) autologous
serum, aUlologus platelet concentrale.

macular holes were included (38). At 12 months,

Biologicallissue adhesive. a commercially mailable

progression frol11 stage 2 to a stage 3 or 4 macular hole

product composed ofbovine thrombin and pooled human

II as

significantly less frequent in the smgery group (20%)

fibrinogen, was the first adjunctive therapy reported( -\ 1).

than in the obscrvation group (71 %). Visual function

The clinical results were encouraging and subsequentl)

assessillent b\

ord rcading and PAM was significantly

various investigators have used the straleg) of thrombin

II

better in surgery group then in observation group at 12

\"rith a fibrinogen containing activator. such as autologou:..

mdnlh lallow up. but no statistically significant difference

plasma or cryo preci

hetween the two groups was seen in the ETDRS acuity

serum(-l-2.-+3). As there \\'1a~ faJ

or contrast sensitivity assessments. TIlis may be related

of controls in these sludies. the conclusion on to thl'

to the high rate or development of nuclear sclerosis arter

efficacy oflhcse agents arc limitc~1. Besidcs. tht.'r~ i"

litrc,.\()Ill). The Fully Devcloped Full Thickness Macular

report

Iiole Study analvsed stage 3 and 4 holes(39). At 6 month

lollowup \'itrcotls surger: resulted in signilicant increase
itllllaCular hole closure (69 0(0) and significantly bctkr

in

Clllltrnlkd Vitrcctomy Mculat' I laic

Study I,;onfirmcd the abilil)

llf

\'itreolls surgeI') to close

'c to randomil..c and lack

i.1

hemorrhage i1 11 9% and h:

pOp: l)[1

of palie!1ts lllHJergoing trcatment \\ ith

hil\ I Ill'

tl1l'<'l11hil1 (-\-\ I.
I (,I (i "illl11Li,lt(:~ collagen and gl: coproh:in ":- nthL:si~

\ isioll on I: rDRS \ ision testing than in observed C) eS.

rh~ ralldomized

RO(o

r iIII raret iJl<ll

deriYed from autologous

and induce..; c... !lular prl)lilCration and llligralhlll ... \

prOS\K'ct i\ L'

plll)1 . . . Iud:- 0

U,O C: l'S ill \\ hicll h\)\ 111(: lkri \ ed

~,\\as lh~d sho\\cd \cr: e!lCOUr~lglllg

macular holes. thus pr<l\'iding sllpport lor the linding or

rCiI

the prel iOllsh pllhlished non-r"ndomiled stlldics. With

!\natnmic clnsurc "as induced ill nil IhL' ~) P:IIILnh

refinement in surgicall('clltliqllL's success rate is impnn ing

rcccj\illgatk:lst

in 1ll0st centres \\ ith ";UCCesS rate or 85-9-l-0 for (11l~1

\islul

IOmical clol.;ure and 5()-~-l-"o improvingallc<lsl two lines

ca <';L'S( -l5) ..'\

OraCuil) or nwre (-\0).

'lO patients L:l)n\irrm':ll \hL'

Role ofPharmacologil' Ad .i 11\.:Ints in Macular

Hole
,

Surg('r~

The extremcl) encouragIng results of macuJar hole

surgery prompted investigators to attempt to improve the

Vol. -t No.2.

APlll-ll1l1 l ' 2(111~

n:sult ...

)~()hg()t"hn\iJlcdL'l"i\cdl(il-~1

.1cuit: illlprc)\ing <ll ki.1<.;1 l\\l' II11<.:s

Sll hSL'l! l1C'l1t pro~pcCI

bccause bo\ inc dcri"xl I (jF-~

hl'I OI ot

i \ \..' random i";\..'L! tri:1I

L'\TiL:aL~

(jJ'-P2 \\11('n compared \\ilh a

III

.\\ilh
I

ul' bn\ In\..' lkri\...:d

pL.ll'L'l"h1IJ( I

\\a~

\'

1(1

1Ill\\C\Cr.

ul~ll;.

lur lart!-l'

scale prodliCliol1. recombinant I (il-P, \\as dl'\el(lpL'd.

65

_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ ,~,~_JK SCIENCE

l Tnfonunatel~. the results of phase III. prospective.

for the use of adjuvants. They may also help to shoner

randomized placebo controlled trial did nOI sho\\ a

the duration of face down positioning.

stastically significant difference between recombinant

Internal Limiting Membrane Removal in Macular

TGF-p,and placebo: conscqcntly. further investigations

Hole Surgery

\\ ith TGF-p, have been suspended (47).

As bO\ ine TGF-p, is expensive and availability is

11,e role ofintcmallimiting membrane (lLM) rcmO\al

Ihal othcr fa\ourably bioactive cytokines or growth factor

ill111acular hole surgery is currentl) the subject ora great

deal of debate. Morris et al in 1994 had suggested role 01
rLM removal in all forms oftraction maculopathy including
macular hole. It was observed. following macular hole
surgery. that eyes from which an ERM(52).has been

may exist prompted its investigation. Several studies

removed had higher success rate compared \\ith eyes

subscquent to a pilot sludy in II human eyes. reported

that bad no detachable ERM. This led to hy pothesis lhat

anatomic and ,"isual success (48). Ho\-vever. a recent

removing the ERM from inner surface of retina (\\ hich

randomized trial has failcd to demonstrate a significant

often includes portions ILM) might mobilize the rClina

limited. in\ estigators tried other means of deli vcring a

prOIllOler or cellular growth. Although concentration of

I"(JI-P. in aUlologous scrum is velY low. the possibility

bendicial effcct of autologous serum (49).

around the macular hole so that it \\as more flexible and

"Is the alpha granulcs of platelets contain various

easier to flatten against the underlying retinal pigmcnt

grIm th factors including TGF-P,. autologus platelet

epithelium. In a study involving 126 macular hole

concentrate has bccn uscd as an adjuvant for macular

surgeries. removal of ERM or an absence of an ERM.

holc surgcry, A rcccnt multicentric randomized trial that

the presumed ILM was carricd out in conjunction with

includcd 110 cycs rcported 94% success rate at 6 months

macular hole surgery. Increased success rate in closure

compared to 81 % in control group (50).

of macular holes without adversely alfecting thc \ isual

rhus. 011" the use ofho\inc TGF-p, and autologous

platelets hm e demonstrated an enhanced anatomic

results was observed (53).

ILM remo\'al requires modi fied or no\'e1 instrumenta

outcome in randomized trials. Bovine-p, is not available

tion due to extremely thin structure of ILM. Usuall) a

lor hurnan use and autologous platelet preparation requires

bent MVR blade is used to create a defect in ILM. An

help of a hematology laboratory.

ILM elevator is used to elevate the ILM. It is then grasped

Allhough cOl1\entional surgery for macular holes is

able to aehie\ e a success rate of 80% or more in most

casc~, the use of biological adjuvants such as autologous
platelets signiiicanlly improves the hole closure rate.
Ilo\\cvcr. thc qucstion of thc usefulness of adjunctive
therapics for macular hole surgcry is not well established
and a recent survey on macular hole surgelY in United
States rcvcalcd that 80% of surgeons questioned do not

with either conventional membrane forceps or ILM

forceps (Grieshaber). The ILM can be grasped in the
inferior and superior part and peeled tangentially or.
capsulorrhexis type of peeling can be used to remo""
disc shaped patch oflLM offthc central macula, A small
amount of bleeding often takes place as ILM is liftcd oft'
which stops quickly. spontaneously or ifinfusion bottle is
elevated to raise the intraocular pressure.

belie\'e that adjll\ ants can be useful(51).. It can be argued

Fluidic Internal Limiting Membrane Separatio

that adju\ ants should be lIsed only in cases with poor

(FILMS) teclmique has also been described in \\ hich II II

prognosis. Failure of prior surgery'. re-opening ohhe hole.

cannula is used to pierce the ILM and cannulate the sub-

long standing holcs. traumatic holes or holes in highly

ILM space. Viscoelastic is then injected with an injecti

my opic eyes \\ould be in this perspective good indication

to elevate the ILM (54).

66

Vol. 4 No.2. Aprit-June 200

_____________

J.;.~JK

ILM removal remains controversial because it is

technically difficult and may prolong macular surgery
Greater experience will help to define the role of ILM

SCIENCE

impairment. Continued traction iJ1\'olving the cortical

vitreous results in a full thickness macular defect and

positioning for 1-2 weeks post operatively as important

corresponding vision loss. where as spontaneous release

ofvitreous traction can result in subsidence 01'5) mptoll1s.
To test the efficacy of prophylactic vitrectom) on
impending macular holes. a multicenter. prospecti\'c
randomized clinical trial was conducted(57). 62 patients
were randomly assigned to observation or surger:. The
differences between the two groups was not statisticall,

for staining hole closure (31.55). Certain patients are

significant so no definitive conclusions could hc reached.

unable or unvvilling to assume a face down position

Current opinion is vitreous surgery for impending

macular holes should not be considered routinel) lor the
following reasons: (I) difficulty in making the correct
diagnosis in impending macular holes. (2) unproved
benefit, (3) cost and morbidity ofsmgery. (4) spontaneous
recovery in many patients and (5) good anatomic and
functional results after macular hole surgery lor carh
full thickness macular holes. But in futurc ",ith
improvement in diagnostic techniques and ic!enti fication
of risk factors and improvement in surgical techniques. a
reversal to surgical approach in impending macular holes
cannot be ruled out.

dissection in treatment of macular holes.

Silicone Oil in the treatment of Idiopathic Macular Holes

Long acting gas tamponade (Sulfur hexafluoride or

perfiuoropropane) is usually used in macular hole smgery.
Various studies have stressed on strict face down

elfectivcl). In such patients use of silicone oil for

intraocular tamponade has a role. When silicone oil is

Llsed for tamponade, careful attention to achieving as
complcte a silicone oil fill as possible during the procedure
is important in maximising successful results. Patients
are asked to maintain a face down position until the
morning of the first post-operative day, following which
the) are instructed only to avoid extended supine
positioning. Silicone oil is removed a\ the patients
t.:onvenience 4-8 weeks post operatively. The surgical

success rale us~ng silicone oil as a tamponade is similar

to that in previous reports of surgery using gas (56). With
silicone oil. no face down positioning is required and patient

can retllrn to near normal activity almost illlJnediately.

Specific situations in which smgety with silicone oil might
be considered include patients who are lmable or lmwilling
to maintain a post operative face down position. need to
return to normal activities in the early post operative
period, need to lIy or travel to high altitudes, and are
monocular and need restoration of visual function as
rapidly as possible'.

&\>; ,he other hand, use of silicone oil in macular hole

surgery means l\VO surgeries are necessary, one for the
initial vitrectomy and one later to remove the oiL This
also increases the total expense of the surgety.
Role of Macular Hole Surgery in Impending
Macular Holes (Stage In and lb) ,

Treatment of Pel'sistent or Recurrent Macular Holes

Approximately 10-15% ofpatients can have failurc of

'macular hole surgety through persistence or recurrence
ofthe hole. Three methods of relreatment lor persistent
or recurrent macular holes have been reported.

a) First is repeat vitrectomy with membrane dissection

and gas fluid exchange. Anatomic success rate follovving
macular hole surgery without adjuvants in persislcm and
recurrent macular holes is reported to be 87%(58). 80%
and 83% success rates have been reported in other srudies
in which autologous senun and bovine TGF-p, werc used
as adjuncts respectively (59,60).
b) Second method reported is laser photocoagulation
followed by gas fluid exchange. Three to six 50 spots of
Krypton laser at 0.2 second duration and 90-120 m\\
are applied to the retina at the border of macular hole

In the early stages of macular hole (impending macular

using slit lamp delivery syslem. Another technique is 12-

holes) paticnts arc asymptomatic or experience mild visual

27 spots of yellow laser (50-1 OOmw) are applied at O. I

Vol. 4 No.2. April-June 2002

67

\'dK SCIENCE

------------~-,~,;,;.;;;,;;,;,,;;,;,,;,;;;,;;;.----------second dural ion and 45-100 mw to the pigment epitheliumjust inside the border of macular hole, approximalely

shallowing of the anterior chamber with relali, e angle

closure and use of expansile gases and silicone oil for

one burn" idth parL nOllreating the neurosensory retina.

A recent series reponed an 870/0 anatomic success
ralq61 ).

tamponade.

c) Third approach is gas fluid exchange alone, A 74%

success rate "as noted in patients with persistent holes
1'0110\\ ing \ itrccIOI11).
fhough resulls of anatomic success and visual acuity
all three approaches are similar, vitrectomy with
membrane dissection for recurrent holes has the highest
In

single surgeI') anatomic success rate.

CWTent opinion is, in pcrsistent holes, ifno ILM peeling

"as donc, ,itreclomy wilh ILM peeling is best approach.
IfilM pccling "as donc io persislent hole. any of three
approach can be recommended. No compelling evidence
is secn [or lascr. TGF-B, or autologus serum as adjuvants.
Therefore gas fluid cxchange alone or vitrectomy with
membrane dissection would be favoured (62).
Complications of Macular' Hole Surgery
/\s experience with macular hole surgery is increas-

ing and long tcrm lollow up has become available, post

opcrali\e complications, as with all procedures are bcing
incrcasingly recognised. Most ofthese complications are
common
a)

10

'itrectom) performed for other diseases.

Calaract

rhe most C0l111110n complication of macular hole

...urger) is progression of nuclear sclerotic cataract.

'iludies hay e reported incidence in the range of 13-95%

alkr' itreClOm) lor fulllhickness holes(63).. Altered lens
metabolism aner, itrectomy is believed to playa role.
b) Glaucoma
rhe pre"lIence of 101' increase of more than 30mm
Hg after macular hole surgery has ranged from 4% to
39. and most commonly occurs within 2 weeks of
surgery(64), The eliolog) of increased TOP after macular hole surgery is multifactorial including decreased
aqueous outflow from POSI operative inflammation,
68

c) Visual field loss

Peripheral visual field loss after macular hole surge'}
has been recognized orny recently with incidence ranging
from 7%-160/0(65). The pathophysiology ofvisual field loss
is a subject ofdebate, One hypothesis is inad'enent trawna
to the optic nerve with silicone tipped cannula during fluid
air exchange or damage to nerve fibre layer during
separation ofthe posterior hyaloid. Another theoT) is that
dessication of the supero temporal relina by the jel of air
from inferotemporally placed cannula during fluid air ex,
change, Additional possibilities includc retinal. choroclia! or
optic nerve ischemia, gas toxicity and lightloxicity.
d) Retina! Detaclunent
Rhegmatogenous relinal delachment is uncommon
(1-18%) but potentially serious complicalion.
e) Retinal pigment epitheliopathy
Severe RPE disturbance with decrease in visual

acuit~

is seen in 11.5% of cases (66).Causalive mechanism is

multifactorial involving suceptibility to light and rcsOlption
of subretinal fluid.
f)

Retinal breaks

Iatrogenic retinal breaks are a relatively common

complication ofmacular hole surgery, occuring in 2-17
ofcases (67).The majority are peripheral. It is imponan
to carefully examine for retinal breaks prior 10 fluid ~
exchange, as small break are overlooked easil) ,,11<
the vitreous cavity is filled with air,
Other complication reponed are ialrogenic macu!
hole, enlargement of macular hole, lale reopening
macular hole, retinal dialysis, exudative relin,,1 delat
ment, branch retinal artery occulsion, endophlbalmib
filaments, anterior ischemic oplic neuropathy a
choroidalneovascular membrane. Gaining further insi,.into the mechanisms ofthese complicalions may mak'
possible to further minimise the risks associated lit
macular hole surgery,
Vol. 4 No.2. April.JullC:

--------------J: JK SCLENCE
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ayes 110. Detachment of the retina with laceration at the

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