nw2010 macular hole
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MACULAR HOLE
Nawat Watanachai
Orn (จำ��น�มสกุ�ลใหม�ไม�ได้�)
Ramathibodi Hospital
INTRODUCTION
- Macular Hole (MH) is a full-thickness depletion of the neural tissue in the center of the macula that result in visual loss
History
1869 : Herman Knapp : initial published description of MH
EPIDEMIOLOGY
In USA , MH affect about 100,000 people1.9 % of visual impaired eyes (20/40-
20/200)Female > male (2:1)age 60 – 80 years ( mean 65 years )VA 20/20 - 20/400Incidence of MH in fellow eye : 5-10% not associated with medical dis, refractive
error
Natural Hx
EDCCS : vision/ progression45% loss > 2 snellen lines in 4.5 yrs28% loss > 3 snellen lines in 4.5 yrs30% increased in size in 4.5 yrs8% spont. resolution/regression after 6 yrsonly 3% spont. improve vision
Natural Hx
EDCCS : MH in opposite eye5% at 3 yrs7% at >6 yrs0+ % in pre-existing PVD eyes
rarely associated with RRD, higher incidence in high myopia with posterior staphyloma
Causes
- most common cause is idiopathic- the others
- non-surgical trauma
- surgical trauma
- pathologic myopia
- vascular disease
PATHOGENESIS
idiopathic MH begins with contraction ofprefoveolar vitreous cortex that is adherentto ILM of Mueller cell cone.Foveal pseudocyst formation Dehiscence of pseudocyst and Mueller
cellFull – thickness MH formation (FTMH) +/- avulsion of operculum (Muller cell cone.
ILM, Henle’s layer, cone nuclei)
Pathogenesis
Pathogenesis
Unknown in traumatic MHtangential vit
tractionretinal necrosis?
Estrogen?Elevated serum
fibrinogen levels (EDCCS)
Abnormal traction forces of the vitreous on the macula?
Observed withCL examinationU/SOCTLaser biomicroscopy
CLASSIFICATION
Gass and Johnson classification stage 1 - pre – macular hole lesion
1a yellow spot
1b yellow ring
stage 2 - eccentric or concertric FTMH < 400
stage 3 - FTMH > 400
stage 4 - FTMH with PVD
Stage 1
- localized shrinkage of prefoveal cortical vitreous formed the traction shallow detachment of foveola- loss of normal foveola depression and light reflex - 1a small yellow spot ( 250 -300 ) - 1b yellow ring ( halo form of foveal detachment )
-+/-pseudooperculum- VA < 20/40 , metamorphopsia- 50 % had spontaneous PVD
Stage 2
- eccentric or oval full thickness- defect diameter < 400 micron- VA 20/50 - 20/80- 74 % progress to stage 3
Stage 3
- hole > 400 micron, may be fovealedema & surrounding cuff of subretinal fluid or operculum- VA 20/100 – 20/400- no PVD
Stage 4
- FTMH with complete PVD - may be associated to ERM
- FFA in stage 3 , 4 - mottle hyperfluorescene from RPE thining, RPEdepigment, loss of xanthophyl
MH stage IV
HISTOPATHOLOGY
- MH is the full thickening circular retinal defect at fovea
- size 100 – 800 micron
- operculum composed of ILM, Mueller
cell cone, superficial inner cone fiber and
cone nuclei.
CLINICAL AND DIAGNOSIS
VA loss 20/80 – 20/400 mean 20/200
Central scotoma / Amsler grid metamorphopsia
• Watzke – Allen test ( WAT )
• laser aiming beam test ( LAM )
CLINICAL AND DIAGNOSIS
CLINICAL AND DIAGNOSIS
FFA - transmission defect at hole or partial blockage at surrounding subretinal fluid
OCT and SLOMacular perimetry - absolute
scotoma surrounding with relative scotoma
MH WITH SPECIFIC CAUSE
1. TRAUMA
- trauma with cystic macular degeneration
associated with MH formation
- concussion effect & residual macular
traction after incomplete PVD
traumatic MH
traumatic MH
2.PATHOLOGIC MYOPIA
- progressive thining and strechingof posterior pole, loss of choriocapillarislead to cystic formation and macularatrophy
- FFA - abnormal slow choroidaland retinal blood flow
3. LASER
- LASER eg. Argon, dye laser, Xenon,
Krypton, YAG - Thermal pigment absorption
LASER
LIGHTNING
4.ELECTRIC CURRENT
- electric current can cause of cataract by current pass to the eye
- study ; 2 from 159 electric burn
patient develop MH
5.ORTHERS
- pilocarpine
- Best’s disease
- intravitreous ceftazidime
- Alport
- Von Hippel
NATURAL COURSE
Different between stage 1 – 4stage 1 - MH s PVD progress to FTMH 33-52 %
- MH c PVD not turn to FTMHstage 2 - most turn to stage 3, 4stage 3,4 – almost always stable or slowly
progress
Chance of FTMH in fellow eye
1. if no PVD in both eyes - high risk 2. if PVD in FTMH eye but no PVD in fellow eye - intermediate risk 3. if PVD in fellow eye - no/very low risk
DIFFERENTIAL DIAGNOSIS
1. PSEUDOHOLE- may be retinal excavation without
tissue loss, RPE atrophy, granular pigmentchange around normal foveal depression
- may because of dehiscence of gliotic preretinal membrane on the macular
- associated with ERM, vitreomaculartraction syndrome, PDR, RRD, inflammation
- VA normal or slightly reduce or
distortion
- FFA normal
- good prognosis
- no evidence of leser therapy
- vitrectomy surgery or membrane
peeling when VA < 20/80 or distortion
pseudohole
2.MACULAR CYST - intact inner and outer retinal
layer, Intraretinal fluid cystic maculardegeneration with loss of nerve fiberlayer, ganglion cell, IPL , inner aspect ofInner nuclear layer
- large cyst in chronic or severeCystoid macular edema looklike MH
- Watzke – Allen test normal- VA 20/20 – 20/100
- FFA - pooling in cystic space inlate venous phase
- CME associated with intraocularGas, trauma, inflammation, exudate macular degeneration, DM
- fluid accumulated between innernuclear and outer plexiform layer
- prognosis depend on underlyingCause, size, chronicity of cytoid edema
- no treatment
3.PARTIAL THICKNESS HOLE
- outer lamella hole (OLH ) - inner lamella hole ( ILH )
• outer lamella hole ( OLH )
- collapse of outer wall of Cyst follow break down of outer BRB at RPE
- associated with Berlin’ s edema,macular schisis, LASER
- slightly irregular deep round or ovalExcavation with intact inner retinal tissue
- VA 20/20 – 20/400- FFA - window defect
• Inner lamella hole ( ILH )
- common, may be intermediate stageto develop FTMH
- rarely develop from chronic CME, spontaneous rupture at inner wall of cyst result in round oval excavation in retinasize < 500 micron
- may develop from radiation, gasC3F8, telangiectasia
- VA 20/20 – 20/80
- FFA - no transmitted fluorescene,minimal window defect or accumulated inperifoveal cystoid space
Treatment
Kelly and Wendel 1991
conceptsrelease traction forcere-position the
displaced neural tissue
TREATMENTBasic step of MH surgeryPPV Remove of post. HyaloidERM dissectionCheck peripheral retinal breakFAXInject adjunctive agent ( if use )Air – gas/SO exchange prone position
1. PPV and delamination of vitreous cortex- remove AP, tangential,circumferential force
- fish – strike or diving rod sign
2. Delamination of ERM- peeling of visible ERM and / or
ILM- prevalence of ERM
- 80% in Pseudophakic eye- 63 % in phakic eye
3.Delamination of ILM
- fibroblast like cell- +/- 0.2 -0.4 cc. Of 0.5% ICG stain- complication s
- trauma to retina - Light toxicity – 15 min - ICG RPE toxicity
4.Adjuvant
- growth factor B2, collagen plug,thrombin – activated fibrinogen, thrombinautologous platlet concentration, \autologous serum
- endolaser
5.Temponade of MH
- gas or silicone oil- postop. 12 -16 % C3F8 facedown
1-3 wks then 6 hr. per day until no gas( 4 – 6 wks )
6.Elimination or reducing duration position- short acting gas ( 4 days )
- SO 6 – 12 wks
7.Orther
- macular scleral buckle may beUsed in high myopia, post. StaphylomaOr MH with extensive subretinal fluid
8.Repaired reopened MH- repeat vitrectomy or FGX, FGX
With laser photocoagulation
Other alternatives
macular buckleminimal vitrectomy (Rick Spaide)pharmacological vitreolysis eg plasmin,
hyaluronidase, TPA, urokinase, plasminogen
RPE laser treatment
RESULT OF SURGERY
Stage 1 lesion
- no benefit to PPV
- stage 1
- VA 20/40 30% turn FTMH
- VA 20/50 – 20/80 % turn FTMH
Stage 2 – 4
position of hole - elevate or flat
edges of hole - open or closed
Anatomical outcome
1. elevate/oper - failed surgical2. flat/open - VA rarely better than
20/503. flat/close - VA > 20/30
COMPLICATIONS
cataract 70% in 2 yrsRD 2 – 11%ERMPeriphery iatrogenic retinal break 5.5 %VF defect ( temporal wedge)Increase IOPRPE changeEndophthalmitis < 1 : 1000Ulnar neuropathy
THANK YOU
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