prevention of posterior capsule opacification 6

6.1Definition, Types and Natural Behaviour of “After-Cataract”

The term “after-cataract” describes growth oflens epithelial cells (LECs) left behind on thelens capsule following cataract removal [23].These cells proliferate and migrate and finallymay cause visual impairment due to pearl for-mation on, or whitening and shrinkage of thecapsule. The term “after-cataract” should bepreferred over “capsule opacification”, since thecapsule itself remains transparent [23]. Never-theless, the term “posterior capsule opacifica-tion”, or “PCO” has become widespread and itsuse generally accepted also in literature. Morerecently, the term “ACO” has also been widelyused as an abbreviation of “anterior capsuleopacification”. Therefore, both terms will beapplied in the following.

PCO and ACO not only describe different locations, but also different entities of after-cataract, as they are caused by different subpop-ulations of LECs [28], (Figs. 6.1, 6.2).

PCO is mainly caused by the “equatorialLECs”, or “E-cells” that reside in the capsularbag equator. E-cells have an exquisite potentialto migrate and may encroach upon the centre ofthe posterior capsule if not hindered to do so.Asthey tend to form globular structures called“pearls”, the term “pearl after-cataract” has alsobeen used.

When an intraocular lens (IOL) has beenplaced in the capsular bag, the rim of the opticacts as a mechanical barrier against centripetalcell migration. If the extended posterior capsuleis firmly attached to the posterior optic surface,the capsule-optic interface will remain clear

Prevention of Posterior Capsule Opacification

Rupert M. Menapace

6

|

∑ Pearl formation and capsular fibrosis represent the two types of after-cataractthat derive from two different subpopula-tions of the lens epithelial cells (LECs)

∑ Thorough surgical clean-up and the use of a sharp-edge optic implant are readilyavailable methods that effectively reduceposterior capsule opacification

∑ Circumferential overlap of the optic by the rhexis leaf is crucial for the formation of a mechanical barrier along the optic rimwhich is mediated by the capsular bendand mechanical pressure created at theposterior optic edge

∑ Slim haptics designed to conform to thecapsular bag support circumferential barri-er formation, while preserving the integrityof the anterior LEC layer and using opticmaterials with high fibrogenetic potentialenhance the strength and permanence ofthe barrier by maximising fibrotic sealing ofthe capsular leaves along the optic rim

∑ While capsular polishing, therefore, is coun-terproductive, performing a primary poste-rior capsulorhexis is a safe and effective adjunctive method that creates a “secondline of defence” against LECs that may overcome the optic edge barrier

∑ Though we do have methods at our disposal that effectively prevent after-cataract formation, these have been shownto fail in cases (e.g. deficient capsular bagsealing, delayed barrier failures; posterioroptic ongrowth), which nourishes the quest for still more effective alternative approaches

Core Messages

102 Chapter 6 Prevention of Posterior Capsule Opacification

Fig. 6.1. Residual LECs belong-ing to two different subpopula-tions

Fig. 6.2. Lens epithelial cell(LEC) population. Properties ofE- and A-LECs

Fig. 6.3 a–f. “Regeneratory after-cataract” derivedfrom E-LECs. Optic–capsule interspace as visualisedby high-intensity slit-beam illumination (a); as meas-ured by partial coherence laser interferometry (b); ill-

defined syncytial LEC layer (c); pearl monolayer (d);pearl multilayer (e); huge pearls (“bladder cells”) (f)

a b c

d e f

(“no space – no cells”). If, however, the posteri-or capsule stays at a distance to the optic sur-face, cells may eventually gain access to this in-terspace. Once arrived there, E-cells tend toundergo swelling the morphological result ofwhich depends upon the width of the capsule-optic interspace. In a narrow interspace, thesecells form flat structures with a honeycomb-likeappearance which may finally end up in a con-tiguous syncytial cell layer. These optically ho-mogeneous structures do not significantly in-terfere with the patient’s vision. With a widerinterspace, however, the E-cells turn into globu-lar structures, or “pearls”, the borders of whichbecome apparent with retroillumination.With astill wider interspace, these pearls may becomemultilayered or huge (Fig. 6.3). These entitiesare termed “regeneratory” after-cataract. Pearlsmay significantly interfere with the patient’s vi-sion especially when forward-scattered light

causes glare and veiling and frequently requireNd:YAG capsulotomy.

ACO (Fig. 6.4), in contrast, derives from the“anterior LECs”, or “A-cells” that reside on theanterior capsular leaf left back following cap-sulorhexis (rhexis). Though these cells also ex-hibit some potential to migrate, their charac-teristic is the exquisite potential to turn intomyofibroblasts (“myofibroblastic transdiffer-entiation”) where traumatised (rhexis edge) orestablishing contact with IOL material (periph-eral optic, haptic). These cells then tend to con-tract and deposit collagen, which leads toshrinkage and whitening of the anterior cap-sule. This entity is addressed as “fibrotic” after-cataract, “capsular fibrosis”, or simply “fibro-sis”. Fibrosis typically forms in the area ofcontact between the anterior capsule leaf adja-cent to the rhexis (rhexis leaf) and the IOL op-tic, but also on the posterior capsule central to

6.1 Definition, Types and Natural Behaviour of “After-Cataract” 103

Fig. 6.4 a–f. “Fibrotic after-cataract” derived fromA-LECs. Circumferential rhexis-optic overlap withconsecutive fibrosis (“full in-the-bag”) (a); peripher-al posterior capsule fibrosis with round edge optic (b);excessive rhexis contraction (“rhexis phimosis”) (c);

asymmetric rhexis contraction with consecutive op-tic decentration (d); partial rhexis retraction (“but-tonholing”) (e); complete rhexis retraction (full “but-tonholing”,“haptics in – optic out”) with consecutivecentral posterior capsule fibrosis (f)

a b c

d e f

the rhexis edge in a collapsed (e.g. aphakic)capsular bag.

If fibrosis is excessive, significant contrac-tion of the rhexis opening (“rhexis phimosis”)may result. Shrinkage of the anterior capsularleaf may be asymmetric, resulting in sometimessignificant secondary decentration of the IOL optic despite a centred rhexis opening(Fig. 6.4d). As A-cells also migrate, they maygain access to the anterior optic central to therhexis edge (“LEC ongrowth”) to there formtransient and sometimes permanent LEC mem-branes. Also, A-cells may migrate peripherallyto access the posterior capsule. Once arrivedthere, these cells loose their capability to mi-grate, but contract and deposit collagen as a re-sult of transdifferentiation (“posterior capsulefibrosis”). Biomicroscopically, contraction (fo-cal, “wrinkling”; or concentric, “sand-duning”)and whitening of the peripheral posterior cap-sule is seen. With a larger optic, posterior cap-sule fibrosis usually does not approach the visu-al axis.

If contraction of the posterior capsule be-hind the optic periphery exceeds that of the an-terior capsule, the rhexis edge may be retractedto finally be flipped over and around the optic tothen establish contact with the posterior cap-sule behind the IOL optic. This leaves the opticpartly or even totally captured, or “button-holed” [18, 31] (Fig. 6.4e,f). This is less seen withthinner high-refractive silicone and acrylicIOLs featuring a smaller optic thickness and aless convex anterior optic surface, or a reducedfibrogenetic potential [30]. A-cells then migratecentrally from the rhexis edge unto the posteri-or capsule where they undergo transdifferentia-tion. Though migration again is thus limited,the resulting capsular fibrosis may significantlynarrow the free optical zone especially withsmall-optic IOLs (Fig. 6.4f).

The severity of ACO resulting from contactbetween rhexis leaf and IOL optic is materialdependent, the latter varying in its potential to“catalyse” transdifferentiation. Some materials(e.g. silicones) induce more fibrosis than others(e.g. some hydrophilic acrylics). With a smalloptic diameter and an optic material thatstrongly triggers A-LEC transdifferentiation,the risk of central encroachment of the posteri-

or capsule by fibrosis increases. This is true forany amount and extent of rhexis-optic overlap(lacking or incomplete overlap; full in-the-bag,partly or fully buttonholed optic).

Fibrosis of the central posterior capsule in-terferes less with visual acuity and contrast vi-sion than pearl formation [9], but may also re-quire Nd:YAG capsulotomy. When necessary,however, performing the Nd:YAG capsulotomymay be difficult: With regeneratory after-cataract, the capsule is thin and vulnerable, andat a distance to the optic, which usually allowsfor posterior defocus and requires only lowlaser energy, thus posing a low risk of opticdamage. With vision-impairing fibrotic after-cataract, however, the capsule is thickened andtough. As capsular whitening hinders posteriorlaser defocus and as the capsule is usually firm-ly attached to the optic, considerable damage ofthe optic may be unavoidable.

Fibrotic after-cataract formation usuallyceases after 3 to 6 months, while regeneratoryafter-cataract develops over a much longer timeto become visually disturbing after 1–3 years. Ina 1998 meta-analysis, the reported PCO rates ofafter extracapsular cataract surgery with IOLimplantation were 11.8% at 1 year, 20.7% after3 years, and 28.4% after 5 years [3].

Summary for the Clinician

∑ Visual disturbance is mainly caused byequatorial LECs that gain access to the posterior optic-capsule interspace and form pearls

∑ Anterior LECs tend to cause capsularwhitening and shrinkage following myofibroblastic transdifferentiation upon contact to the IOL

∑ “Regeneratory after-cataract of the posterior capsule”, and “fibrotic after-cataract of the anterior or peripheral posterior capsule” more appropriately describe what has been generally termed“PCO” and “ACO”

∑ Fibrotic after-cataract formation mainly occurs during the first 3 months, while regeneratory after-cataract formation startslater, culminating between the years 2 and3, and occasionally lasting up to 5 years


6.2Quantification of After-Cataract

Efforts have been made to create methods toquantify the extent and severity of after-cataract. Different approaches are necessary forPCO and ACO.

For regeneratory PCO, retroillumination im-ages are currently used for evaluation. Subjec-tive grading, which is largely based on intuition,has been replaced by three methods: (1) Manu-ally outlining areas of different severity andthen multiplying area by severity (EPCO) [51];(2) automatically calculating the total area ofopacification (POCO-A) [2]; and (3) automati-cally calculating a score for area and severity byeither: (a) implementing an additional mathe-matical algorithm into the POCO-A system(POCO-S, so far unpublished), or (b) by apply-ing a fully-automated mathematical algorithmbased on the evaluation of pixel entropy of theimage (AQUA) [14]. The latter was developed inVienna and is used as our standard evaluationmethod since it has shown a very high repro-ducibility and correlation with subjective grad-ing and EPCO scoring while the POCO-A sys-tem was not adopted because it exhibited tooearly saturation and thus overestimation of low-grade and intermediate PCO [14].

Any evaluation method can only pick up thevariability displayed by the image. Thus effortshave been made to devise a photographic set-upoptimising sagittal alignment [44]. Inherently,reflected-light images better display morpho-logical details than retroillumination images[8]. However, full area coverage is impractical,and evaluation software is not available. Thus,assessment of retroillumination images has be-come the standard. As an alternative, area den-sitometry with the Scheimpflug camera systemhas been used, and has been shown to correlatewell with the patient’s visual acuity [19].

For ACO, reflected-light images are manda-tory, as only these accordingly display the de-gree of whitening and wrinkling, or fibrosis.Apart from subjective grading, an automatedevaluation method has been developed by ap-plying the Photoshop software on standardisedreflected-light images [47].


∑ Current methods of PCO quantification relyon retroilluminated imaging

∑ The subjective EPCO system and the objec-tive AQUA system correlate well with eachother, while both also do so with subjectivegrading

∑ For ACO grading the degree of whitening isassessed either subjectively or using stan-dard image analysis software (Photoshop)

∑ Future technologies may focus on reflected-light image evaluation which better displaymorphological details

6.3Prevention of After-Cataract

6.3.1Removing LEC from the Equator to Reduce the Proliferative Potential

A logical approach is to selectively target thoseLECs that finally interfere with the patient’s vi-sion, i.e. the equatorial LEC population with itsexquisite potential to migrate centrally and tothen form pearls within the retro-optical inter-space.However, these cells cannot be directly re-moved as they are remote in the flaccid equato-rial capsule and cannot be directly visualised.Thus, direct and complete aspiration is not fea-sible. However, reducing the number of E-LECsmay at least retard and mitigate after-cataractformation though it will not totally preclude it.Therefore, efforts should be made to remove asmany of these cells as possible during surgery.Direct abrasion of E-cells using dusted curettes,and ultrasound or diathermy probes has beenattempted. However, these procedures are poor-ly controlled, and E-LEC removal is inherentlyincomplete. Damage to the capsule, zonules, andciliary tissue cannot be excluded.

Lens fibres are derived from LECs in the lensbow which have differentiated to build up thelens. Incomplete removal may result in prolifer-ation of these cells known as Soemmering’s ringformation. Therefore, every effort should bemade to indirectly reduce the amount of cellularmaterial in the capsular equator by aiming at

6.3 Prevention of After-Cataract 105

the complete removal of all lens fibres, using amethod that may be termed cortical fibre strip-ping: Following aspiration of the cortical mass-es left behind after phacoemulsification, resid-ual lens fibres may be detected adhering to theposterior capsule when focussing it at highermagnification. When jetting water through athin cannula, the central end of these fibres isdetached from the capsule to then float freely.Using an aspiration cannula, the ends of thesecells can be aspirated and occlusion attained byadditionally engaging the underlying capsule.Thus, the residual lens fibre bundles may beefficiently stripped off towards the periphery.With appropriate instrumentation and flow/vacuum settings (e.g. Brauweiler cannula byGeuder: 7 ml/min, 100 mmHg), this has beenroutinely performed by the author without asingle case of posterior capsule damage. Thegoal is: (a) to completely remove all lens fibrematerial, thus precluding Soemmering’s ringformation, and (b) to potentially also catch holdof contiguous E-cells of the capsular bag equa-tor, which my also reduce their proliferativepotential.


∑ Complete removal of all LECs from the capsular equator by “capsule polishing”techniques is impracticable

∑ Thorough cortical clean-up using “hydrodissection” and “lens fibre stripping” may prevent Soemmering’s ring and PCO formation by reducing thenumber and thus the proliferative potentialof the equatorial LEC population

6.3.2Erecting Mechanical Barriers to Prevent LEC Migration

Since complete mechanical E-LEC removal can-not be achieved, efforts must be made to pre-vent LECs from migrating centrally and reach-ing the visual axis. The rim of the IOL optic isknown to form a mechanical barrier. The im-portance of the rim shape, however, became ob-vious only more recently when a sharp sharp-edged IOL (Acrysof MA60BM) was shown toallow for significantly less PCO than IOLs withround edges. Meanwhile, the sharp posterioroptic edge design has been implemented intoessentially all new lenses on the market with theeffect of significantly lower Nd:YAG capsuloto-my rates (Fig. 6.5).


Fig. 6.5 a, b. “Hybrid IOLs” with round (sharp) optic edge oriented nasally (temporally). Note fibrotic/regen-eratory after-cataract trespassing round optic edge

a b

6.3.2.1Mechanism of Optic Edge Barrier Effect

Apart from its sharpness, the efficacy of theposterior optic edge to permanently preventLEC migration is strongly dependent upon theoptic overlap by the rhexis leaf. Without suchoverlap, the barrier effect generally is only weakand transient. This is understood when lookingat the postoperative changes of the capsular bagfollowing IOL implantation as discussed in thefollowing sections.

Capsular Bag Closure

“Capsular fusion”: Within days after the evacu-ation of the lens contents, the capsular bagstarts shrinking. Setting out from the bag equa-tor, the anterior and posterior capsule leaves

progressively fuse. Depending upon the designof the IOL, this fusion process is more or lessasymmetric and incomplete, as the haptics vari-ably distort the contour of the capsular bag andthe IOL interferes with the approximation of thecapsular leaves. With a three-piece open-loopIOL and a circumferential rhexis-optic overlap,however, this generally ends up with the twocapsule leaves tightly fused around the opticrim, with the rhexis leaf stretched out and set-tled down on the optic in the area of overlap,and with the posterior capsule pulled up aroundthe posterior edge of the optic to then join theanterior capsule (Fig. 6.6a–c)

“Capsular sealing”: When during the courseof capsular bag closure the rhexis leaf settlesdown on the optic surface, the anterior LECstake up contact with the optic material andtransform into myofibroblasts, which contract


Fig. 6.6 a–d. Capsular bag closure. a–c High-resolu-tion OCT imaging of capsular fusion process. a Day 1:capsular bag widely open. Note pronounced distanceof rhexis leaf to optic surface and posterior capsule.b Week 1: capsular fusion in progress: rhexis leaf set-

tling down on optic surface. c Month 1: capsular fu-sion finalised; posterior capsule wrapped aroundposterior optic edge. d Capsular sealing: fibrosis pro-viding strong and permanent “shrink wrapping”

a b

c d

and deposit collagen. The collagen depositedalong the optic rim seals the two capsular leavestogether, thus creating a strong and permanentsealing line (Fig. 6.6d).

The speed and completeness of capsular fu-sion varies and is influenced by the design andmaterial characteristics of the implant [21, 42].The firmness of capsular sealing is determinedby the catalysing potential of the optic materialand the extensiveness and intensity of contactbetween optic and capsule. Its potentialstrength may be experienced when trying tosurgically reopen a well-sealed capsular bag.

Capsular Bending

During the course of capsular closure the poste-rior capsule is distended and pulled around theoptic rim.This has been shown to result in a me-chanical barrier against LEC migration. There isstill controversy on the causative factor for thiseffect. It has been attributed to the capsularbending itself and the resulting “contact inhibi-tion” [39], or to the mechanical pressure build-ing up along the line of capsular apposition [4,5, 34]. Both factors may most likely be involved[36]. The strength of the barrier depends uponthe tension of the capsule and the angle ofthe posterior optic edge, and is greatest with atense capsule and a sharp optic edge. As the A-cell-mediated contraction of the anterior and

adjacent posterior capsule tightly wraps thecapsular bag around the implant (“shrink-wrapping”), the posterior capsule is tightlypulled around the posterior optic edge, thus cre-ating a sharp bend and maximising the pressureexerted along the contact line between thesharp posterior optic edge and posterior cap-sule. With a lacking capsular overlap, however,such a bend cannot form. Though collagenousattachment may also form along the contact linebetween rhexis edge not overlapping the opticrim and the posterior capsule [23], this barrieris more easily overcome by migrating LECs, as isthe optic rim when not overlapped by the rhex-is leaf (Fig. 6.7).

6.3.2.2Clinical Evidence for Sharp Optic Edge Efficacy

The role of a sharp implant edge as a migrationinhibiting factor and the mechanism of capsu-lar bending was for the first time realised in themid-1990s. Before, the reduced PCO formationobserved with the Acrysof MA60BM three-piece IOL was thought to reflect a specific in-hibitory material property. However, attentionwas drawn to the edge design when it becameapparent that most of the PCO inhibitory effectwas lost with a lacking rhexis/optic overlap(Fig. 6.7). Thus, the formation of a capsular


Fig. 6.7. Absent rhexis–optic overlap resulting in “primary barrier failure”

bend along the sharp posterior optic edge of theAcrysof when circumferentially overlapped bythe rhexis leaf was isolated as the cardinal factorexplaining for the PCO inhibiting effect of thisIOL. In a number of pertinent animal studies,Nishi corroborated the effectiveness of thesharp posterior edge for various optic materi-als. Conversely, he was able to show that most ofthe PCO-inhibiting effect of the Acrysof IOLwas lost when the edge was blunted or rounded[40]. This was experimental proof that the pre-ventive effect of the Acrysof IOL on PCO was es-sentially the effect of its rectangular, sharp-edged design rather than the adhesiveness orbioactivity of the specific acrylic material asforwarded by others [26, 43].

Once having realised the importance of thesharp optic edge design, clinical studies wereinitiated to confirm this for, and to isolate possi-ble differences between the various IOL opticmaterials. Most of these studies, however, inves-tigated IOLs differing in the material and theoptic edge design and/or the haptic construc-tion [1, 20, 53]. At the University of Vienna, theauthor and his group (Vienna IOL Study Group)started conducting a series of prospective clini-cal implant studies systematically evaluatingthe influence of the IOL design and material,and that of surgical measures by only varyingone single parameter in each study. The eyeswere randomised and compared intraindividu-ally, since LEC proliferation rates and conflu-ence times have been shown to be age depend-ent and to correlate closely between pairs ofeyes [12]. One series compared lenses of a spe-cific IOL material [poly(methyl methacrylate)(PMMA), silicone, hydrophobic acrylic] thatdiffered solely in the design of the optic edge.The sharp-edged PMMA and silicone IOLs usedin the early series were custom-made IOLs pro-vided by Dr. Schmidt Intraokularlinsen (St. Au-gustin, Germany). The acrylic and silicone IOLsinvestigated later were provided by Allergan(now AMO, Irvine, CA). All IOLs were investi-gational IOL models now marketed by Dr.Schmidt Intraokularlinsen as MicroPlex MC220(PMMA) and MicroSeal MS 612 (silicone), andby AMO as Sensar AR40e (hydrophobic acrylic)and ClariFlex CLFLX B (silicone). The edge de-sign of the two companies differed in that those

provided by Dr. Schmidt Intraokularlinsen fea-tured both a posterior and an anterior sharpedge (truncated edge), while those by Aller-gan/AMO had a squared posterior edge whilethe side edge was sloping and the anterior edgeround (patented “OptiEdge” design).

Meanwhile, 3- to 5-year follow-up data areavailable for all three materials (MicroPlexMC220, MicroSil MS612, Sensar AR40e;Table 6.1). The fact that with all IOL materialsthe sharp-edged models showed significantlylower PCO rates unanimously supports the con-cept that the sharp optic edge, at least with thematerials and designs (open-loop) used, is thedominating PCO inhibiting factor. The crucialrole of a sharp posterior edge is evidenced bythe fact that IOLs with a sharp posterior and arounded anterior edge profile performed com-parably well as those with a truncated edge [6,7]. The subordinate though well-evidenced roleof the IOL optic material has been demonstrat-ed by the above-mentioned animal experimentconducted by Nishi, where blunting or roundingoff the edges of optic resulted in a loss of thePCO inhibiting effect of the Acrysof IOL [40].

A sharp posterior optic edge and a circum-ferential rhexis overlap as the prerequisite to al-low for posterior capsule bending have thusbeen isolated as the causative factors for effec-tively inhibiting LEC migration at the optic rim.


∑ The formation of a capsular bend at theposterior optic edge is the substrate of thebarrier effect observed at the optic rim

∑ Full circumferential rhexis-optic overlap isa prerequisite for capsular bend and thus barrier formation along the posterioroptic edge

∑ The barrier effect is attributed to the mechanical pressure and/or the contact inhibition caused by the capsular bend

∑ The influence of IOL design and optic material characteristics, and the surgicaltechnique has been isolated in prospectiverandomised bilateral clinical studies withonly one single varying parameter



Tab

le6

.1.

PCO

and

YA

G r

ates

wit

h di

ffer

ent I

OL

styl

es,m

ater

ials

and

sur

gica

l pro

cedu

res

Follo

w-u

p1

Year

2Ye

ars

3Ye

ars

4Ye

ars

pVa

lues

c

Para

met

erSu

bja

YAG

Subj

YAG

Subj

YAG

Subj

YAG

AQ

UA

bA

QU

AA

QU

AA

QU

A

PMM

Ad

––––

–2/

6Tr

unca

ted-

edge

/rou

nd2.

0/4.

2(n

=16

)<

0.00

1

Silic

onee

––––

–0/

4Tr

unca

ted-

edge

/rou

nd1.

0/2.

6(n

=25

)<

0.00

1

Silic

onef

0.3/

1.3

0/1

<0.

001

Opt

iEdg

e/ro

und

0.7/

1.4

(n=

40)

<0.

001

Acr

ylic

g0.

4/1.

50/

11.

2/3.

21/

12<

0.00

1O

ptiE

dge/

roun

d1.

0/2.

2(n

=31

)1.

8/3.

1(n

=31

)<

0.00

1

Trun

cate

d0.

7/1.

40.

051

Silic

oneh

vs a

cryl

ici

1.9/

2.2

0.28

[sub

j.AC

O-s

core

:][1

.4/1

.1]

Cap

sula

r be

ndin

g ri

ng:

––––

–1/

11C

BRj /C

ontr

ol2.

0/4.

4(n

=28

)<

0.00

1

Rou

nd-e

dge

silic

onek

––––

–9/

2––

–––

18/1

1Po

lish/

non-

polis

h1.

8/1.

6(n

=33

)3.

7/3.

3(n

=33

)p=

0.79

p=0.

1

Trun

cate

d-ed

ge s

ilico

neh

––––

–1/

0Po

lish

vs n

on-p

olis

h1.

5/1.

2(n

=43

)0.

052

Trun

cate

d ac

rylic

(0.1

/0.6

)0.

7/1.

1N

o YA

G1-

piec

ei vs

3-pi

ecel

(0.9

/1.3

)1.

3/1.

5p<

0.05

p>0.

05

PPC

CC

rou

nd-e

dge

IOL

––––

–2/

2Si

licon

ekvs

Hyd

roge

lm2.

3/3.

2n(Y

AG

or A

VE)

0.03

(4.3

/4.7

)o(0

.25)

a Sub

ject

ive

PCO

sco

re [

11];

b Obj

ecti

ve P

CO

sco

re (

AQ

UA

[11

]);c P

-val

ue f

or P

CO

sco

res

at l

ast

follo

w-u

p;d M

icro

Plex

MC

220

(Dr.

Schm

idt

Intr

aoku

larl

inse

n,St

.Aug

usti

n,G

erm

any)

;e M

icro

Sil

MS6

12 (

Dr.

Schm

idt

Intr

aoku

larl

inse

n);

f Cla

riFl

ex (

AM

O,

Irvi

ne,

CA

);g S

ensa

r (A

MO

);h C

eeO

n Ed

ge 9

11A

(Ph

arm

acia

,G

roni

ngen

,The

Net

herl

ands

);i A

crys

ofSA

60AT

(A

lcon

);j C

apsu

lar

Ben

ding

Rin

g Ty

pe 1

4E (

Mor

cher

,Stu

ttga

rt,G

erm

any)

;k SI4

0 (A

MO

),Si

lens

6 (D

omile

ns,

Lyon

,Fra

nce)

;l Acr

ysof

MA

60BM

(Alc

on,F

ort W

orth

,TX

);m

Hyd

rovi

ew (S

torz

Oph

thal

mic

s,St

Lou

is,M

O);

n Ins

ide

PCC

C;o C

apsu

le o

utsi

de P

CC

C.

6.4Rationale for Investigating Alternatives:“Optic Edge Barrier Failures”

When thinking about alternatives to the “sharpposterior optic edge concept”, one questionmay immediately arise:“If a sharp posterior op-tic edge so effectively prevents migrating LECsfrom entering the retro-optical space, why thenshould we search for alternatives?” Much moreso, as the technology can be implemented in al-most any IOL style and does not require addi-tional surgical skills or implant devices. The an-swer is: “To explore even more effective oradjunctive approaches, as a sharp posterior op-tic edge does not completely and permanentlyprevent PCO in all eyes, especially over longertime periods (1–2 years and thereafter)”. Thisbecomes obvious when not only looking at sta-tistical differences between sharp and roundIOLs, but when analysing the unfavourable cas-es in the sharp-edged cohort.

6.4.3.1Primary Barrier Failures

Additional to the circumferential overlap of theoptic by the rhexis leaf, centripetal fusion of thetwo capsular leaves resulting in capsular bagclosure during the first weeks postoperatively isanother prerequisite for capsular bend and thusbarrier formation at the posterior optic edge.However, in some cases, this process of capsularclosure may been incomplete, or even lacking.This may be termed “primary barrier failure”.LECs then are only temporarily, if at all, with-held at the optic edge to then invade the retro-lental space (Fig. 6.8)

Incomplete or Lacking Capsular Bag Closure

In some cases, the capsular bag fails to closewithout detectable reasons. In others, excessivestretch exerted by an oversized IOL may be iso-lated as the cause of symmetric barrier failures

6.4 Rationale for Investigating Alternatives: “Optic Edge Barrier Failures” 111

Fig. 6.8 a–d. Barrier fail-ures. A long axial capsularstress lines (rigid over-sized haptics) (a, b);at optic–haptic junction(one-piece IOLs) (c, d)

a b

c d

occurring along the capsular stress lines(Fig. 6.8a,b). Large optics also seem to hamperbag closure and bend formation [37].

“Junction Phenomenon”

Even at a slim haptic–optic junction, capsularfusion and consecutive bending is compro-mised (Fig. 6.9). Consequently, the barrier ispartly interrupted or at least weakened at thesesites. This is particularly true for any one-pieceIOL featuring plate haptics, but also those with broad-based loops [37]. Capsular bend-ing cannot occur even with the sharp optic edge continuing beneath the junction, thus allowing LECs to enter the retro-optical spa-ce (Fig. 6.8c,d). This has been termed “junc-tion phenomenon”. The positive effect oflooped haptics on capsular fusion may be part-ly neutralized if they are oversized and/or toorigid [49].

6.4.3.2Secondary Barrier Failure

In cases with primarily complete capsular clo-sure and bending around the optic, secondaryreopening of the barrier with consecutive LECinvasion of the retro-optical space has been ob-served (“secondary barrier failure”). The reasonfor this is understood when considering the nat-ural course of E-cell proliferation. Close consec-utive in vivo observation of capsular bag clo-sure and LEC migration suggests two phases ofE-LEC migration and proliferation: In the firstdays and weeks postoperatively, and before theprocess of capsular bag fusion is finalised, earlyLEC migration can already be observed. Thus,E-LECs may already have reached the retro-op-tical capsule when capsular fusion has pro-gressed far enough to implement capsularbending. E-LECs thus trapped in the retrolentalspace, supposedly due to the lack of nutrients,do not proliferate any further and seeminglyundergo apoptosis. Such early LEC invasion of


Fig. 6.9 a–d. “Junctionphenomenon”. Broad-based optic–haptic junc-tion (below) interferingwith capsular bending.Note “sealing line” detach-ing from optic rim at junction

a b

c d

the retro-optical space seems to be influencedby the haptic–optic angulation, since angulatedhaptics provide for circular attachment of thesharp optic edge and induce capsular bendingfrom the very beginning. In the months andyears to follow, a second phase of E-LEC migra-tion and proliferation can be observed: Partlyamorphous and partly globular material formsin the capsular equator (Soemmering’s ring[23]), which increases in volume and tends tomechanically reopen the once closed capsulebag. Once arrived at the optic, progression ishalted by the collagenous sealing of the two cap-sule leaves along the anterior and lateral aspectsof the lens optic and by the permanent posteri-or capsular bending thus induced (Fig. 6.6d)which both resist the mechanical force exertedby the proliferating LEC masses. If collagenoussealing is weak relative to the proliferative pres-sure, however, the sealing line itself and/or thecapsular bend thereby induced may break upsecondarily, and LECs may enter the retrolentalspace (Fig. 6.10). As the collagenous sealing ismediated by the A-LECs that undergo myofi-broblastic transdifferentiation upon optic con-tact, the optic material is an important determi-nant for the firmness and thus resistance of

capsular sealing. The various IOL materials dif-fer in their inherent ability to catalyse myofi-broblastic transdifferentiation leading to colla-gen deposition and capsular contraction.Silicones exhibit the highest and hydrophilicacrylics the lowest catalysing effect,while that ofhydrophobic acrylics is labelled intermediate.Thus, the PCO score of IOLs that show relative-ly low PCO rates during the first 1–2 years mayincrease thereafter due to secondary barrierfailure (e.g. hydrophobic acrylics), while suchdecay of PCO performance is less observed withother materials (e.g. silicones).


∑ A sharp posterior optic edge, though easy-to-implement and effective, does not com-pletely and permanently prevent PCO in alleyes, especially over longer time periods

∑ Capsular bag closure is a prerequisite forcapsular bend formation

∑ Primary disturbances of capsular bag closure are caused by capsular stress linesinduced by oversized IOLs or at theoptic–haptic junction of IOLs with a broadhaptic base (primary barrier failure)


Fig. 6.10. “Secondary barrier failure” with reopening of fused capsules following weak fibrotic sealing

∑ A once closed capsular bag may be second-arily reopened by the mechanical pressureexerted by proliferating equatorial cells(secondary barrier failure)

∑ The material-dependent strength ofcollagenous sealing along the optic rimavoids secondary barrier failures as it resists the mechanical force exerted by LEC proliferation

6.34.4Factors Influencing Fibrotic After-Cataract Formation

The extent and severity of ACO is influenced bythe extent and intensity of the contact betweenthe anterior capsule and the optic surface.With-out such contact, the rhexis leaf remains clear,as the A-LECs do not transdifferentiate. This isbest seen in eyes where a capsular bending ring(CBR) keeps the rhexis leaf at a pronounced dis-tance to the optic surface.

Certain pathologies predispose to excessivefibrotic shrinkage (“phimosis”) which may endup in total closure of the rhexis opening, espe-cially with an extensive primary rhexis–opticoverlap. The causative factor is either zonularweakness (e.g. pseudoexfoliation syndrome,uveitis, pars planitis, high myopia, retinitis pig-mentosa) and/or abnormal myofibroblastic ac-tivity (e.g. myotonic dystrophy [35]). The lensstyle determines the type of capsular fibrosis:Slim-looped IOLs, especially those with siliconeoptics [18, 31], often provoke half- or even full-circumference buttonholing, while the broadjunction of plate-lenses inherently reduces thisrisk. On the other hand, silicone plate-lensesshow a strong tendency to induce rhexis phimo-sis [11], while this is much less the case withopen-looped silicone IOLs. The optic edge pro-file also influences ACO: IOLs with a sharp pos-terior optic edge hinder A-LECs from “escap-ing” into the retrolental space. As a result,fibrosis of the peripheral posterior capsule de-creases, while anterior capsule fibrosis increas-es, as evidenced by the enhanced whitening andshrinkage observed [48]. As mentioned above,fibrosis also strongly depends upon the IOL ma-terial. There are significant differences in the

ability to catalyse myofibroblastic transdiffer-entiation upon contact [52], with silicones beingthe most potent ones. In conjunction with asharp-edged open-loop IOL and symmetricalrhexis-optic overlap, however, this property ofthe silicone material provides the desired cap-sular wrapping and sealing of the optic ad-dressed above. The pressure thus created be-tween the posterior capsule and optic edgeprovides a strong and permanent barrieragainst (early) A-cell as well as (delayed) E-cellimmigration and prevents fibrotic and regener-atory after-cataract formation behind the optic.

How can excessive fibrosis and its negativesequelae be counteracted? Apart from hinder-ing the rhexis leaf to establish contact with theIOL optic by inserting a capsular bending, ordistance ring, fibrotic capsular opacificationcan be avoided by anterior capsule polishing,thereby removing the A-LEC layer as the sub-strate of myofibroblastic transdifferentiation. Incases predisposed for excessive anterior capsulefibrosis and shrinkage, this protective effect of anterior capsule polishing may outweigh the disadvantages of a compromised barrierformation at the optic edge (see Sects. 6.3.7.2,6.3.7.4).


∑ The extent and severity of ACO is influ-enced by the extent and intensity of thecontact between the anterior capsule andthe optic surface

∑ Certain pathologies predispose to excessive fibrotic shrinkage of the rhexisleaf (“rhexis phimosis”)

∑ IOL determinants of ACO type and intensity are material, but also lens styleand optic edge profile

∑ Use of a capsular bending ring and anteriorcapsule polishing effectively counteractrhexis whitening and shrinkage, but weakenthe barrier at the optic edge


6.4.5The Role of Optic Material

Originally, the PCO inhibitory effect was attrib-uted to the IOL material. Conversely, when thesharp posterior edge was recognised as a keyfactor, it became widespread to underestimateor even ignore the influence of the material.Theoretically, the optic material may influencePCO development at three different stages:(1) capsular bag closure (bend formation), (2)fibrotic edge sealing (bend maintenance), and(3) LEC migration and proliferation in the op-tic–capsule interspace. Most clinical studiescomparing IOLs with regard to PCO perform-ance have been using IOLs that differed both inmaterial and design. Considering these limita-tions, the following may be stated: (1) Speed ofcapsular bag closure is significantly faster withthe silicone and acrylic IOL compared to thePMMA IOL, and significantly faster with the sil-icone IOL than with the acrylic IOL. This wasdemonstrated by observing capsular bend for-mation at the optic edge and apposition of cap-sule to the optic using the slit-lamp microscope[42] and Scheimpflug videophotography [21],respectively. (2) Firmness and thus permanenceof fibrotic capsular sealing at the optic edge issignificantly greater with silicone than withacrylics. This is evidenced by studies showingthat round-edge silicone IOLs perform similar-ly well as sharp-edge acrylic, and significantlybetter than round-edge PMMA IOLs [20]. Dif-ferences in adhesiveness [43] and bioactivebonding [26] between optic and capsule havebeen attributed as factors inhibiting migrationof LECs once arriving in the optic–capsule in-terspace. Others have described regression ofPCO with specific IOL materials [22]. However,the clinical impact of these parameters remainsto be established.

To clearly define the influence of each factor,however, IOLs have to be investigated that differonly in one single criterion [material, or optic(edge) design, or haptic design]. More recent in-tra- and inter-patient studies indicate thatsharp-edge silicone IOL may outperform sharp-edge acrylic IOL in the long run [45] (Tables 6.1and 6.2).


∑ Speed of capsular bag closure is fastest with silicone IOLs, and faster with acrylicthan with PMMA IOLs of similar design

∑ Firmness and thus permanence offibrotic capsular sealing at the optic edge is significantly greater with silicone thanwith acrylic IOLs

∑ The clinical impact of material adhesive-ness and bioactive bonding on after-catar-act formation remains to be established

6.4.6The Role of Patient Age

Organ culture experiments with human LECshave revealed an age dependency between pro-liferation rates and confluence times [12]. Ac-cordingly, children exhibit high LEC prolifera-tion rates. The proliferative pressure is strongenough to regularly break open and breach thecapsular sealing line. A primary posterior cap-sulorhexis (PPCCC) as a second line of defenceis also easily overrun by exuberantly proliferat-ing LECs which use the anterior hyaloid surfaceas a scaffold. Regarding preventive surgicalmeasures there is general consensus with regardto the necessity of performing a PPCCC in in-fants and children. However, there is controver-sy on the need and type of additional measures.According to Koch and Kohnen a PPCCC must becombined with anterior vitrectomy (AVE) to bean effective method of preventing or delayingsecondary cataract formation in these patients[24]. For children younger than 7 years the ne-cessity of additionally performing a AVE hasbeen confirmed for the sharp-edge three-pieceacrylic IOL Acrysof [25]. The efficacy of captur-ing the IOL optic through the PPCCC opening


Table 6.2. Prerequisites for optimal optic edge bar-rier

Circumferential rhexis/optic overlap

Sharp posterior optic edge

Slim haptic/optic junction

Fibrosis-inducing optic material

as a sole measure without AVE has been contro-versially valued [17, 24, 55]. It may be consideredas a simple and potentially useful additive meas-ure against after-cataract formation which alsoimproves optic centration, though lens depositsand posterior synechiae may more often form. Inchildren older than 7 years, AVE may not be nec-essary with modern sharp-edge IOLs [25], whileothers consider an additional AVE as a mandato-ry procedure for children up to 12 years even withposterior optic capture [55] (Table 6.3).


∑ Children exhibit high LEC proliferation rates∑ There is general consensus with regard to

the necessity of performing a PPCCC in infants and children, but controversy on theneed and type of additional measures

∑ Combining the PPCCC with anterior vitrectomy up to an age of at least 7 yearshas been strongly recommended

∑ Capturing the IOL optic through the PPCCC opening may be considered as asimple and potentially useful additivemeasure against after-cataract formation,and also improves optic centration

6.4.7Alternatives to the Sharp-Edged Optic

Several approaches have been investigated aspossible alternative or adjunctive measures toprevent PCO formation. These are discussed inthe following sections.

6.4.7.1Posteriorly Vaulted Posterior–Convex Optic

The idea is highlighted by the “super-reversedoptic” concept originally forwarded by Fechner[13]. It was aimed at maximising the posteriorlydirected vector force of a posterior convex op-tic, thereby achieving tight attachment betweenoptic and distended posterior capsule. In theo-ry, no interspace would be left at all, or at leastnot wide enough to allow LECs to form out vi-sion-disturbing pearls (“No space – no cells”, or“small space – no pearls”). With current IOLs,such posterior vaulting characteristics can beimplemented in three-piece IOLs with angulat-ed loops made from permanent memory mate-rials (e.g. polyimide), or in one-piece IOLs withangulated broad-based loop or plate hapticsmade from foldable acrylic or silicone. Withplate-haptic IOLs,posterior haptic angulation isnot a prerequisite, since posterior vaulting isinitiated as the anterior capsule starts shrinking(e.g. STAAR AA4203) [10].

To prove the validity of this approach, we investigated the frequency and width of lens–capsule interspace as detectable with high-in-tensity slitlamp illumination and/or partial co-herence laser interferometry with different IOLstyles [15]. Interestingly, no statistically signifi-cant difference was found. Notably, the IOLswith the strongest permanent backward vault(Corneal ACR6D SE, STAAR AA4203) exhibitedthe widest mean space (160mm) of all lenses in-vestigated. Also, we have seen significant regen-eratory PCO formation with a posteriorly vault-ed plate IOL (IOGEL) [29]. In conclusion, thisconcept must be considered ineffective.


Table 6.3. Indications for alternatives to sharp-edgeoptic

Primary posterior capsulorhexis

Primary posterior capsule fibrosis (thick plaque: HF-diathermy)

Non-availability of patient (non-compliant,immobile, remote)

Multifocal IOLs (early loss of contrast)

Synchysis scintillans (trans-rhexis AVE)

Children (combined with AVE up to at least school-age)

High myopes (weakened barrier effect at implant edge)

Capsular bending ring

In children (in addition to PPCCC)

Possible/planned vitreoretinal surgery

Capsule polishing

Risk for rhexis phimosis (pseudoexfoliation,uveitis, pars planitis, high myopia, retinitis pigmentosa; myotonic dystrophy)

6.4.7.2Capsular Bending Ring

The capsular bending ring (CBR) was conceivedand first investigated in rabbit eyes by Nishi[38]. After having proven the safety and shortterm efficacy in a human pilot study, trials wereinitiated at the Nishi and University Eye Hospi-tals in Osaka and Vienna intraindividually com-paring the effect of a CBR (Morcher Type 14E;Morcher, Stuttgart, Germany) on after-cataractformation. The device was conceived to act intwo ways. Firstly, to keep the entire posteriorcapsule clear up to the very periphery by induc-ing a capsular bend at the equator. Secondly, toalso keep the anterior capsule clear by keeping itat a pronounced distance to the posterior cap-sule and the anterior optic surface (“capsulardistance ring”, or “CDR”). In fact, the CBRshowed effectiveness in both aspects during a 2-year follow-up period [32, 41]. However, in asmall number of CBR eyes some amount of re-generatory LEC invasion was still observed.Some of these failures could be explained by thegap between the ring eyelets in a large bag al-lowing LECs to gain access to the posterior cap-sule. This was remedied by modifying the de-sign of the ring (injectable CBR Morcher Type14F after Menapace and Nishi). This still left uswith some cases of regeneratory after-cataractformation without a detectable cause. Our onlyexplanation is that in these cases E-cells maystill be residing central to the posterior bendingline. These small numbers of “fenced in” LECswould eventually also invade the posterior cap-sule. Since with a CBR in place capsular bendingat the optic rim can no longer occur, LECs caneasily access the space between the tense poste-rior capsule and the periphery of a posteriorlyconvex optic, though they cannot readily accessthe very centre of the optic as the apex of suchan optic is firmly attached to the capsule. Never-theless, in our randomised study, differences inPCO were highly significant: After 1 year, theEPCO PCO score within the 6 mm zone was 0.4in the CBR as opposed to 0.8 in the controlgroup. After 3 years, the AQUA score was 2.4 inthe CBR versus 4.4 in the control group. Of the28 patients, only one patient had requiredNd:YAG capsulotomy in the CTR eye, as op-

posed to 11 patients with a YAG capsulotomy inthe control eye. In conclusion, the CBR conceptdoes work, but (at least with the IOL styles cur-rently available) not efficiently enough to justi-fy the routine use of such an additional implant.

6.4.7.3Primary Posterior Capsulorhexis (PPCCC)

LECs use the posterior capsule as a scaffoldwhen migrating centrally. Consequently, vision-disturbing after-cataract should be excludedwhen the central posterior capsule is removed.Even though, cases with vision-disturbing after-cataract formation have been reported withPPCCC. In children, the hyaloid surface isknown to serve as an alternative scaffold for E-LEC migration. Despite the differences inhyaloid anatomy, such failures have also beenreported in adults. Our theory was that in adultsthe posterior optic surface may alternativelyserve as a scaffold. We conducted a randomisedprospective clinical trial intraindividually com-paring the efficacy of PPCCC with different op-tic materials (silicone as a hydrophobic versushydrogel as a hydrophilic material) using IOLswith a similar design [16]. The main outcomemeasure was LEC ongrowth within the PPCCCopening in cases with optic edge barrier failure.A capsular tension ring was additionally used inthis series to provide for a fully distended pos-terior capsule and thus circular attachment ofthe PPCCC margin to the optic. In our study,PPCCC was demonstrated to be safe with nocase of associated retinal complication, as alsodemonstrated by others [54]. In 58 eyes of 29 pa-tients completing the 2-year follow-up, the PPCCC opening remained clear with 66% of thesilicone IOLs as opposed to only 41% of the hydrogel IOLs. Partial closure of the PPCCC wasobserved with 55% of the hydrogel IOLs butwith only 28% of the silicone IOLs. Total closureof the PCCC occurred in three eyes, two in thehydrogel group and one in the silicone group.PCO score within the PPCCC opening was sig-nificantly lower with silicone IOLs as comparedto hydrogel IOLs (AQUA-score 2.3 versus 3.2,p=0.03; Table 6.1). Biomicroscopy, and the de-pendency on optic material confirmed that itwas the optic surface that had served as a scaf-


fold in these cases. In conclusion, PPCCC is ef-fective but, as it requires additional surgicalskills, may be reserved to supplement the use ofa sharp-edged optic in cases with a higher PCOrisk (children and young patients, high myopes)or those who are difficult to follow-up or treat(non-compliant or remote patients). In adultssilicone optics should be preferred at least overhydrophilic acrylic IOLs because of greaterPPCCC efficacy while no retinal complicationshave been observed so far.

6.4.7.4“Capsule Polishing”

In theory, the most straight-forward and effec-tive way to exclude any form of after-cataractwould be to completely remove all LECs duringcataract surgery. In principle, this may beachieved by the application of chemicals or im-munotoxins selectively targeting LECs. This,however, has so far not been possible, postoper-ative uveitis with clinically effective doses con-stituting the main problem. So far, no methodhas been shown to be safe for clinical use [27].

Alternatively, efforts have been made to me-chanically abrade the lens epithelium. Rentschdeveloped a ring curette to be entered throughthe cataract incision (“Ring curettes”, Geuder).However, a set of three differently angulatedcurettes is required to cope with the varying an-gles of approach. Also, the efficiency of the pol-ishing procedure itself is low as the curetteshave to be actively pressed against the flaccidand slippery capsule in a bag expanded withviscoelastic. In general, 5 min under brightcoaxial illumination are usually required. Inher-ently equatorial LEC removal and its complete-ness cannot be assured. Thus, in an uncon-trolled retrospective study conducted byRentsch [46], 12% of the eyes that had under-gone full circumferential polishing using thismethod still required Nd:YAG capsulotomywithin 3 years.

Therefore, an alternative instrument was de-veloped by Menapace before embarking on acontrolled prospective bilateral study to eluci-date the efficacy of capsule polishing (“aspira-tion curette”, Geuder). Since mechanical polish-ing of the equator is inherently uncontrolled

and incomplete, this instrument was specifical-ly designed for efficient polishing of anteriorcapsule only. Thus, the A-LEC and those E-LECsthat reside on the peripheral anterior capsularare targeted. The cannula features an upward-facing slit-like opening with sharp edges onboth flanks and rounded edges at the flexes. Theuniplanar configuration of the entry allows forfirm occlusion when brought into contact withthe back surface of the anterior capsular leaf. Abypass hole allows for smooth vacuum build-up. The cannula is compatible with the bimanu-al cortex aspiration set designed by Brauweiler(Geuder). The cannula is consecutively enteredthrough three paracentesis openings each 120°apart and the slit-like opening lifted up againstthe contralateral rhexis leaf to allow for occlu-sion and vacuum build-up. When the cannula isthen moved from one side to the other like awindshield wiper, the sharp slit edges efficient-ly shear off the anterior lens epithelium.Through each paracentesis, one third of thecontralateral rhexis circumference is thus deep-ithelialized. The procedure is visually con-trolled, and in several hundred cases the cannu-la has proven to be safe (no case of capsular orzonular damage) and efficient (mean cleaningtime 1.5 min).

A prospective study was carried out intrain-dividually comparing the efficacy of anteriorcapsule polishing with regard to after-cataractprevention. On a randomised basis one eye un-derwent extensive polishing using the aspira-tion curette described above, while the other eyewas left unpolished. Round-edge open-loop sil-icone IOLs were implanted. Main outcomemeasures were: (a) PCO scores and YAG capsu-lotomy rates after 1 and 3 years, and (b) ACO andfibrotic PCO after 3 years.

The study produced the following results: (a)Fibrotic after-cataract [50]: ACO in the polishedeyes was significantly reduced, with almost nowhitening and contraction of the rhexis leaf asopposed to the non-polished eyes. Mean ACOwas 17% for the polished eyes and 26% for theunpolished eyes (p<0.01). Mean fibrotic PCOscore was 0.5 and 1.0, respectively (p<0.01). Effi-cacy with regard to fibrotic ACO and PCO pre-vention thus was very satisfactory. (b) Regener-atory after-cataract [56] (Table 6.1).


At year 1, the polished eyes did not show sig-nificantly lower PCO scores than the unpolishedeyes. When sorting the eyes according to PCOseverity, the worst cases were predominantlyfound in the polished group.At year 1, no capsu-lotomy was required in either group.At between1 and 3 years, nine of the polished and two of theunpolished eyes required Nd:YAG capsulotomy.After 3 years, nine additional eyes in each groupneeded KT. Thus, the cumulative KT rate was 18in the polished eyes and 11 in the unpolishedgroup.AQUA scores, however, did not differ sig-nificantly. This discrepancy may be explainedby an obvious morphological difference: PCO inpolished eyes tended to be more homogeneous,while in unpolished eyes it exhibited greaterpropensity to form well-defined pearls. Thislayer of poorly delineated PCO after polishing is not adequately depicted on photographsretroilluminated by reflected or backward scat-tered light.Any evaluation based on retroillumi-nated images may largely underscore PCO,while the patient’s vision is significantly de-graded by glare and blur due to forward scat-tered light.

In conclusion, polishing was effective in pre-venting fibrotic, but ineffective in reducing regeneratory after-cataract. Nd:YAG capsulo-tomies had to be performed more often (18 vs 11out of 33 eyes) and at an earlier time (nine vstwo during years 1–3).

Unfavorable results of capsule polishing withregard to regeneratory after-cataract have alsobeen reported by another study using the “ringcurettes”: In a large study comprising over 1200eyes, Miller et al. reported a cumulative Nd:YAGcapsulotomy rate of 46% in the polished groupversus 20% in non-polished eyes in the not pol-ished group (p=0.0001) [33]. This strongly sup-ports the concept of capsular fibrosis as a cru-cial factor for the barrier formation at the opticedge: Without capsule polishing, both the A-and E-cell population are left untouched. Fol-lowing capsular closure, the A-cells cause fibro-sis, thereby firmly sealing the capsular leaves to-gether along the optic circumference. Thisforms a strong barrier against the delayed mi-gration and proliferation of E-cells. Followingcapsule polishing, the A-cells and the more an-teriorly located E-cells are removed. However,

the more remote equatorial portion of E-cells isleft at least partly in situ and viable. Though re-duced in number, these residual E-cells will alsomigrate and proliferate, and finally get numer-ous enough to reach the optic rim. Since no fi-brotic sealing of the capsules at the optic rimhas occurred, the fusion line is easily overcome,thus allowing the migrating LECs to gain accessto the retro-optical space along the whole cir-cumference. Preliminary data from a more re-cent study indicate that polishing also compro-mises the barrier effect of sharp-edged optics,though seemingly to a lesser extent (Table 6.1).


∑ The concept of avoiding PCO by creating astrong and permanent posterior optic vaulthas failed

∑ The capsular bending ring significantly reduces regeneratory after-cataract, while at the same time it avoids ACO (distance effect); however, its limited efficacy withcurrently available IOLs and the need for anadditional implant limits its application

∑ Primary posterior capsulorhexis is safe andeffective, and supplements the efficacy of asharp-edge optic IOL forming a “secondline of defence”; however, the surgical skillrequired limits its widespread use

∑ “Capsular polishing” is counterproductive,as it interferes with fibrotic sealing of thecapsular leaves along the optic rim, predis-posing for secondary barrier failures and,consequently, unimpeded access of E-cellsto the retro-optical space

Acknowledgements. The author wishes to ex-press his gratitude to his co-workers at the Vien-na IOL Study Group who helped compile thedata on which this chapter is based.


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