| Idiopathic
full thickness macular holes (FTMH) are an important cause of central visual
loss. More than 70 per cent of patients are women in their 60s or 70s who
present with visual distortion and reduction of visual acuity to the level
of 6/36 or worse. Typically these lesions are non-progressive once fully
established. Bilateral FTMH occur in some 10-20 per cent of patients.
In
1988, Gass described his observations on the pathogenesis of FTMH and suggested
a classification of four stages of FTMH which is now widely used.1
In Stage I (impending) macular hole there is a focal detachment of the
foveola which may progress to a small full thickness retinal defect (Stage
II). With time the FTMH usually enlarges, the edges become elevated by
a cuff of subretinal fluid, and a localised posterior vitreous separation
occurs with a small opacity (operculum) lying in front of the retina (Stage
III). In Stage IV there is complete posterior vitreous separation manifested
by the presence of Weiss ring in front of the optic nerve head.
Stage
1 Trial
Unlike
peripheral retinal breaks, FTMH are caused by tangential traction on the
fovea by the adherent posterior cortical vitreous (PCV). This led to the
suggestion that vitrectomy and the removal of the attached PCV could relieve
the vitroretinal traction and prevent the formation of a FTMH. However,
a recently reported randomised trial of vitrectomy for Stage I (impending)
macular holes in the fellow eyes of patients with FTMH failed to demonstrate
a benefit of surgery.2
Kelly
and Wendel were first to report successful treatment of FTMH. In their
series of patients, they performed vitrectomy, removal of PCV and epiretinal
membranes followed by a gas tamponade.3 This resulted in hole
closure in 58 per cent of their patients and visual improvement in 73 per
cent of eyes that had closed holes.
Surgical
Results
Improved
surgical results (60-100 per cent closure rates) have been reported using
a variety of adjuncts applied to the macular hole during surgery such as
growth factors, autologous serum of platelets (Figures 1 and 2). These
adjuncts may promote hole closure by two mechanisms: their viscous nature
(sealant property) and the growth factors they contain are known to induce
a limited healing response. Histological examination of successfully closed
holes shows re-approximation of seemingly healthy photo-receptors to within
16 microns from the centre of the fovea;4 this would explain
the often surprising visual improvement of 6/12 or better in 70 per cent
of such eyes.5
Patients
with FTMH that are relatively small (Stage II) and of recent onset (six
months or less) have the best outcomes, but visual improvement may be obtained
even when FTMH has been present for well over a year.
The
two main components of treatment of FTMH are the relief of all vitreo retinal
traction by meticulous removal of PCV and epiretinal membranes as well
as intraocular tamponade. The latter component is achieved by the intra-operative
injection of long-acting intravitreal gas and strict face-down posturing
for two weeks post-operatively - a tall order for some of our elderly patients.
Those FTMH that do not close after one operation may do so on a second
attempt. The complications of macular hole surgery include those that may
accompany vitrectomy procedures in general such as nuclear cataract, iatrogenic
retinal breaks and detachments. A small proportion of patients may develop
a permanent fold defect, the cause of which is currently a subject of much
debate.6
While
the favourable results of macular hole surgery appear to justify this procedure,
most of the evidence available to date is based on clinical observations
from uncontrolled studies. Controlled randomised treatment trials designed
to assess visual outcome and the usefulness of adjuncts and tamponading
agents are now in progress. We must await these results, which will determine
the optimal method of treatment for our patients with FTMH.
Zdenek
J Gregor FRCOphth
Consultant
Ophthalmic Surgeon
Moorfields
Eye Hospital
References
1. Gass
JDM (1988). Idiopathic senile macular hole: its early stages and pathogenesis.
Arch Ophthalmol; 106: 629-39.
2.
deBustros S (1994). Vitrectomy for prevention of macular holes: results
of a randomised multicentre clinical trial. Ophthalmology; 101: 10559.
3.
Kelly NE, Wendel RT (1991). Vitreous surgery for idiopathic macular
holes: results of a pilot study. Arch Ophthalmol; 109: 654-9.
4.
Madreprla SA, Geiger GL, Funta M, de la Cruz Z, Green WR (1994). Clinicopathologic
correlation of a macular hole treated by cortical vitreous peeling and
gas tamponade. Ophthalmology; 101: 682-6.
5.
Wells JA, Gregor ZJ (1996). Surgical treatment of macular holes using
autologous serum. EYE; 10: 593-9.
6.
Ezra E, Arden GB, Riordan-Eva P, Aylward GW, Gregor ZJ (1996). Visual
field loss following vitrectomy for Stage 2 and 3 macular holes. Brit
J Ophthalmol; 80: 519-25. |