Royal College of Ophthalmologists Guidelines (Focus)

Management of Macular Holes

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 


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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