Evaluation and Management of
Macular Holes
Focal Points, March
2003
Introduction
 Idiopathic (most common)
 Nonsurgical trauma
 Surgical trauma
 Pathological myopia
 Retinal vascular disease
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)
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)
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
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
 Stage 2
– Eccentric or oval full thickness
– < 400um
– VA 20/50 to 20/80
– 74% progress to stage 3
 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.
 Stage 4
– Full thickness
– Complete vitreous seperation (PVD)
Histopathology
 Full thickness circular retinal defect at fovea +-
an operculum (?Photoreceptors)
 100 – 800um
 Subretinal fluid, cystoid foveal oedema
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
Differential Diagnosis
 Pseudo-hole (in epiretinal membrane)
 Foveal RPE atrophy
 CME
 Idiopathic central serous chorioretinopathy
 Foveal drusen
 RPE detachment
 Choroidal neovascularization
 Lamellar macular lesions
Treatment
 PPV/ Delamination of vitreous cortex
– Remove tractional forces
– Technique using cannula, vitreous cutter
 Delamination of the epiretinal membrane
– Especially visible ones
– Vitrectomy for macular hole study group (80%, 63%)
– Seems reasonable
 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)
 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)
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
 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
– >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
 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).
 Macular holes in high myopes
– PPV and gas >lower closure rate
– Better results with ILM peeling
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
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.

Evaluation and Management of Macular Holes

  • 1.
    Evaluation and Managementof Macular Holes Focal Points, March 2003
  • 2.
    Introduction  Idiopathic (mostcommon)  Nonsurgical trauma  Surgical trauma  Pathological myopia  Retinal vascular disease
  • 3.
    Epidemiology and NaturalHistory  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 ofthe 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: – Contractionof 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 thicknesscircular 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/ Delaminationof vitreous cortex – Remove tractional forces – Technique using cannula, vitreous cutter
  • 14.
     Delamination ofthe epiretinal membrane – Especially visible ones – Vitrectomy for macular hole study group (80%, 63%) – Seems reasonable
  • 15.
     Delamination ofthe internal limiting membrane – Myofibrocytes and fibrous astrocytes in memb. >Hole patency and enlargement – Indocyanine green (ICG) – Controvercy (trauma, light and ICG toxicity)
  • 16.
     Adjuvants  Tamponadeof 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 MacularHole 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 macularholes (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 orpersistent 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 holesin 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 causeof 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.

Editor's Notes

  • #4 20/40 to 20/400, 45% loss of 2 lines, 28% loss of three lines, opposite eye 4.6 to 6.5%
  • #6 (foveal center is weak point due to lack of photoreceptor zonular attachments in this area) Adhearent to the ILM, of muller cell cone.
  • #12 Pathogenisis is realated to traction from the vitreous
  • #13 Oval, no or little ffa changes, minimal va watsky and laser neg Partial thickness with overlying retina intact