|
 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.
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