Evaluation and Management of Macular Holes - Dr James Beatty

1. Evaluation and Management of
Macular Holes
Focal Points, March
2003

2. Introduction
 Idiopathic (most common)
 Nonsurgical trauma
 Surgical trauma
 Pathological myopia
 Retinal vascular disease

3. Epidemiology and Natural History
 2 x more in F than in M
 7th
to 8th
decade
 9% due to trauma
 1,9% of visually impaired (BES)
 Not associated with medical disease or
refractive errors
 Full thickness = significant visual loss(EDCCS)
 Holes will progress in size and stage (EDCCS)

4. Microscopic Anatomy of the Macula
 Macula: 2x ganglion nuclei, ILM
 Fovea: no nerve fiber, ganglion cell or inner
plexiform layers
 Foveola: only cones, Muller cell cone (NB
support, vitreous attached)

5. Pathogenesis
 Idiopathic:
– Contraction of the prefoveolar vitreous cortex
– Foveal pseudocyst formation
– Dehiscence of pseudocyst and the Muller cell cone leads to
full thickness macular hole
– +- Contraction of internal limiting membrane
 Traumatic:
– ? Unknown

6. Classification
 Stage 1 (a or b)
– Perifoveal PVD
– Yellow spot (a) or ring (b)
– Contraction > split Muller cell cone
– Foveal pseudocyst, not full-thickness
– Metamorphopsia, VA 20/40
– > Full thickness hole (30%), partial thickness, stay
same, 50% show improvement

7.  Stage 2
– Eccentric or oval full thickness
– < 400um
– VA 20/50 to 20/80
– 74% progress to stage 3

8.  Stage 3.
– >400um.
– Foveal oedema + surrounding neuroretinal rim
detachment.
– Operculum (ILM, muller cell cone, Henles layer and
cone nuclei).
– VA 20/100 to 20/400.

9.  Stage 4
– Full thickness
– Complete vitreous seperation (PVD)

10. Histopathology
 Full thickness circular retinal defect at fovea +-
an operculum (?Photoreceptors)
 100 – 800um
 Subretinal fluid, cystoid foveal oedema

11. Presentation and Diagnosis
 Central scotoma, metamorphopsia
 Amsler grid
 VA (20/80 to 20/100)
 Contact lens
 FFA (transmission defect)
 Optical coherence tomography (Gass hypothesis)
 Scanning laser ophthalmoscopy
 Watzke-Allen
 Laser aiming beam test

12. Differential Diagnosis
 Pseudo-hole (in epiretinal membrane)
 Foveal RPE atrophy
 CME
 Idiopathic central serous chorioretinopathy
 Foveal drusen
 RPE detachment
 Choroidal neovascularization
 Lamellar macular lesions

13. Treatment
 PPV/ Delamination of vitreous cortex
– Remove tractional forces
– Technique using cannula, vitreous cutter

14.  Delamination of the epiretinal membrane
– Especially visible ones
– Vitrectomy for macular hole study group (80%, 63%)
– Seems reasonable

15.  Delamination of the internal limiting membrane
– Myofibrocytes and fibrous astrocytes in memb.
>Hole patency and enlargement
– Indocyanine green (ICG)
– Controvercy (trauma, light and ICG toxicity)

16.  Adjuvants
 Tamponade of macular hole
– Gas or silicone oil
– Long acting gas (12-16% C3F8)
– Face down positioning (1-2 weeks)/ controversy
 Other options (minimal vitrectomy, macular and
scleral buckel)

17. Results of Macular Hole Surgery
 Stage 1 lesions (foveal cysts)
– Nil surgery
– Vitrectomy for prevention macular hole study (30%
pts with 20/40 vision progress to full thickness, ?
role of enzymatic PVD), no clear benefit for
vitrectomy

18.  Full-thickness macular holes (stage 2-4)
– Elevated or flat / open or closed
– Elevated/open – failed
– Flat/open – VA <20/50
– Flat /closed – VA >20/30

19. – >VA, >stereopsis, <distortion, <scotoma
– Better results with better preop VA, shorter preop
duration and more complete ILM peeling
– ILM peeling improves VA and eliminates reopening
of of holes > than 300um
– Current surgery = 90% closure, majority >VA
– Also good results without face down positioning
– Chronic holes also have an improvement in vision

20.  Reopened or persistent macular holes.
– 2nd
vitrectomy (83% closure).
– Outpatient fluid gas exchange + lazer of foveal RPE
12/13 and 13/15).
– Surgical fluid gas exchange (17/23).

21.  Macular holes in high myopes
– PPV and gas >lower closure rate
– Better results with ILM peeling

22. Complications of Surgery
 Retinal detachment (2-11%)
 Retinal breaks (5.5%)
 Raised IOP (1st
week)
 RPE (endoillumination /uncommon)
 Endophthalmitis (0.1 %)
 Late reopening (5 – 9.5%)
 Ulnar neuropathy
 Cataract

23. Conclusion
 Significant cause of loss in central VA.
 Becoming more common.
 Increased surgical closure rate (58% to 90%).
 Decreased complication rate.
 VA and visual function improve in the majority
of patients.