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Major review

Current concepts in the treatment of vitreous block,also known as aqueous misdirection

Kevin Kaplowitz, MDa,*, Edward Yung, MDa, Rachel Flynn, BSa,James C. Tsai, MD, MBAb

a Stony Brook University School of Medicine, East Setauket, NY, USAbNew York Eye and Ear Infirmary of Mount Sinai, Icahn School of Medicine at Mount Sinai, New York, NY, USA

a r t i c l e i n f o

Article history:

Received 23 August 2014

Received in revised form

10 December 2014

Accepted 16 December 2014

Available online 27 December 2014

Keywords:

vitreous block

aqueous misdirection

ciliovitreal block

ciliolenticular block

malignant glaucoma

secondary angle-closure glaucoma

* Corresponding author: Kevin Kaplowitz,E-mail address: kevin.kaplowitz@stonybr

0039-6257/$ e see front matter ª 2015 Elsevhttp://dx.doi.org/10.1016/j.survophthal.2014.

a b s t r a c t

Vitreous block (VB), a rare secondary angle-closure caused by anterior rotation of the ciliary

body, occurs in a variety of settings, but most frequently after glaucoma filtering surgery.

The etiology remains unclear, but choroidal expansion and anterior vitreous abnormalities

have been proposed. In the past, treatment of VB has yielded high rates of failure and

recurrence. Advancements in surgical techniques, however, have led to improved visual

outcomes. We review the history of this condition and present a stepwise approach to its

diagnosis and treatment using modern imaging modalities and surgical techniques.

ª 2015 Elsevier Inc. All rights reserved.

1. Background Although traditionally defined in the absence of choroidal

Vitreous block is a secondary angle-closure caused by anterior

rotation of the ciliary body as the result of abnormal fluid

conductivity through the vitreous body. We review the etiol-

ogy, risk factors, diagnosis, and modern treatment strategies

of vitreous block.

Vitreous block (VB), a rare, but aggressive, form of sec-

ondary angle-closure first described by von Graefe in 1869,62 is

characterized by both central and peripheral shallowing of the

anterior chamber (AC) in the presence of a patent iridotomy,

and normal to markedly elevated intraocular pressure (IOP).90

MD, Stony Brook Universookmedicine.edu (K. Kapier Inc. All rights reserve12.004

effusion or hemorrhage, recent evidence suggests that

choroidal effusion is involved in the pathophysiology (see

section 4). Originally called malignant glaucoma because it

presented similarly to relative pupillary block, yet was resis-

tant to traditional methods of treatment including pilocarpine

and iridectomy,103 it is also known by many other names,

including ciliary block,184 ciliovitreal block, ciliolenticular

glaucoma, intravitreal aqueous entrapment, vitreous expan-

sion, vitreous displacement glaucoma, and positive vitreous

pressure glaucoma.55,126 Although the most common name in

the literature is aqueous misdirection, no investigator has

ity School of Medicine, E Setauket, NY 11733.lowitz).d.

s u r v e y o f o p h t h a lmo l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1230

ever been able to demonstrate the presence of a one-way

valve necessary for the misdirection of aqueous to play a

role in its pathophysiology; thus, it is a misnomer. VB occurs

most commonly after incisional surgery for chronic angle-

closure glaucoma,194 particularly in advanced cases.163 In a

consecutive case series of 25 reports of VB, 80% followed

incisional treatment of chronic angle-closure glaucoma.96

Because of the rareness of this condition, the current litera-

ture in the field consists primarily of case reports and series.

1.1. Incidence

Debrouwere et al. reported an overall incidence of 2% over an

11 year study.41 Some of the early literature reports signifi-

cantly higher rates of up to 4% of 97 surgical iridectomies.27

Luntz et al. found that from the year 1869 to 1986 only 411

total cases were in the literature.100 Little et al. showed that

over 3 years at a tertiary care center performing over 12,000

cataracts, there were only 7 cases (<0.06%) of postoperative

VB,95 while another series reported an incidence of 0.03% of

32,000 cataract extractions.189 The highest incidence of VB is

after trabeculectomy for angle-closure glaucoma,29,38,41,69,195

the prior surgery in 82% of 118 cases of VB.194 The second

most frequently attributed operative cause is cataract sur-

geryd5% of 118 cases.194

1.2. Etiology

VB occurs in a number of varying clinical scenarios, inclu-

ding after pilocarpine administration,24,36,90,113,123,137 blunt

trauma,166 laser capsulotomy,5 laser iridotomy,19,24,140

neodymium:yttrium-aluminum-garnet (Nd:YAG)70,180 and

diode laser cyclophotocoagulation,7,41 surgical iridectomy,90

cataract surgery (with all techniques including intra-

capsular,68,162,167 extracapsular135,175 or phacoemulsifica-

tion6,74,81,117 represented), trephination,15 iridencleisis,15,141

trabeculectomy,21,39,112,128 bleb needling,3,108,133 bleb revi-

sion,45 deep sclerotomy,35 laser suture lysis after trabeculec-

tomy,42,102 aqueous shunt implantation,64,83,104,105,121,176,188

corneal transplant,65,127,143 and pars plana vitrectomy

(PPV).82,191

Multiple cases of VB have occurred in patients with no

previous surgery, trauma, intraocular inflammation, or miotic

treatment.1,51,61,78,147 There are rare case reports that sug-

gest a possible association with central retinal vein occlu-

sion,18,19,69,182 retinopathy of prematurity,86 and keratoconus

(particularly in Down syndrome).77,110,177 In addition, any

rapid depressurization of the eye may precipitate VB,

including an anterior chamber paracentesis.71,85 Weinreb et al

also reported a single case of bilateral ciliary hyperplasia as a

possible etiology.183 Highlighting the difficulty of establishing

etiology, Loewenstein and Lazar pointed out that in those

cases of VB following laser iridotomy where the history was

described in detail,2,24,158 all had other possible etiologies,

most commonly pre-treatment with pilocarpine.98

In postoperative cases, there is a wide range of times

between surgery and the onset of VB, from possible intra-

operative onset172,185 to up to 16 years after surgery.46 Only

one study is large enough to analyze the timing: Out of 66

cases of VB following trabeculectomy, 54% of cases occurred

within 1 week of surgery, 8% occurred between 1 week and

1 month, 17% occurred between 1 month and 1 year, and 21%

occurred after 1 year.194

1.3. Risk factors

Risk factors for the development of VB include a history of VB

in the fellow eye, nanophthalmos,27,40,54,190 plateau iris,125,173

zonular laxity predisposing to an anterior lens-iris dia-

phragm,137,169,179 larger phakic lenses,14 preoperative shallow

anterior chamber, and preoperative high IOP.27,53 Short axial

length is a common finding, although VB may occur in eyes

with a range of axial lengths.195 The overall mean axial length

in cases of VB reported in the literature is 21.37 �0.28 mm.22,23,38,53,95,96,154,161,181,195 VB appears to be more

common in female patients,41,163,181,194,195 in possible associ-

ation with a more anterior lens and smaller anterior chamber

volume.134 In a study of 50 patients, themean agewas 59 years

old, with a range of 35e81 years.195 In the largest study, the

mean age was 50 � 14 years.194 The youngest reported case of

VB was in an 11-month-old.104 The majority of cases present

unilaterally, though there are cases of simultaneous bilateral

onset.2,75,145

1.4. Pathophysiology

The exact pathophysiology is still unclear. An altered rela-

tionship between the lens, vitreous, and ciliary body may

result in the forward displacement of the lens-iris dia-

phragm.43,164 Chandler proposed that either acute uveal or

vitreous congestion is the inciting event, though a trigger for

this remains unclear.27 Because the earliest reported cases

followed surgical iridectomies, another theory suggests that

penetration of the AC, especially with high IOP, leads to rapid

AC decompression, causing forward displacement of the

ciliary body and lens.26,93 Levene90 and Grant63 hypothesized

that AC decompression exacerbated an underlying structural

predilection to angle closure, but this could not be confirmed

by Epstein and currently is not thought to play a role in the

pathophysiology.48 Early treatment strategies that focused on

deepening the AC by removing the lens proved effective only

when vitreous was lost. Early investigators were also able to

treat VB successfully without lens extraction, further arguing

against lens extraction as the primary treatment.36 VB also

occurrs in aphakic eyes, which led to focusing instead on the

role of the vitreous.152

1.4.1. Vitreous block and vitreous abnormalitiesThe initial theory of pathophysiology of VB came from

observations that the ciliary body and processes were anteri-

orly rotated. Shaffer and Hoskins proposed that physical

misdirection of anteriorly rotated ciliary processes shunted

the produced aqueous into the vitreous rather than the pos-

terior chamber. The vitreous volume then increased enough

to push the lens-iris diaphragm forward, closing the angle.151

Simmons and others added to this theory after he noted

anteriorly displaced ciliary processes coming into contact

with the lens.58,157,185 Ultrasound biomicroscopy (UBM)

confirmed that, during an attack, the ciliary processes were

parallel to the longitudinal muscle, and in some cases the

s u r v e y o f o p h t h a lm o l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1 231

processes indented the posterior iris.169 Following resolution,

the ciliary body and processes rotated back to their anatomic

position21 as the AC deepened.150 Both A-scan107 and B-scan5

ultrasounds later demonstrated aqueous pockets in the vit-

reous as large as 0.7 � 0.4 cm that resolved after successful

treatment. For diverted aqueous to be the cause of VB, there

would have to be a one-way valve allowing aqueous into the

vitreous. No one has been able to demonstrate the presence of

a one-way valve. Although these early theories correctly

identified the anterior rotation of the ciliary body, later studies

provided a much more plausible cause of these findings.

1.4.2. Choroidal expansionThe current etiological hypothesis supported by the most

evidence is choroidal expansion pushing the vitreous for-

ward.13,116,131 Inward expansion of the choroid is normally

opposed by IOP. Some inciting event, such as intraoperative

inflammation or hypotony, could lead to breakdown of the

bloodechoroid barrier and may lead to protein exudate in the

extravascular choroid. The normal osmotic force pulling fluid

into the choroidal vessels is lost, and this leads to choroidal

volume expansion, which in turn increases the IOP in the

posterior vitreous.129 The vitreous does offer some resistance

to fluid flow52,130 that could recursively increase as the pres-

sure differential builds across the vitreous.48 Indirect support

for the theory of choroidal expansion includes the finding of

choroidal effusions in 43% of 70 eyes in acute angle-closure

glaucoma and in 9% of eyes only with narrow angles with no

history of angle-closure, suggesting a possible link between

uveal edema and angle closure.144 Another study found that

angle-closure patients had a thicker choroid than did healthy

control and open-angle glaucoma patients and suggested that

some of these eyes are more prone to choroidal expansion.4

Choroidal expansion could also explain more recent evi-

dence showing a high incidence of uveal edema in VB.44 One

group found that with routine UBM use at a large tertiary care

center, 50% of cases originally diagnosed as VB had a ciliary

body detachment.91 This high incidence when UBM scanning

was done for every presumed case of VB could suggest that

many previously published cases also had uveal edema,

where either imaging was not available or the edema was not

significant enough to be seen on UBM,84 since only a 50-

micron choroidal expansion leads to a large increase in IOP.129

Epstein et al demonstrated in a landmark experimental

study that, at high pressures (40e60mmHg), the vitreous does

offer significantly more resistance to outflow than the AC.48

The pressure differential leads to vitreous expansion139 and

shallowing of the AC. The building pressure in the posterior

vitreous would cause it to become compressed and move

anteriorly, until the anterior portion of the vitreous directly

contacts the lens or ciliary body. This reduction in open sur-

face area of the anterior vitreous further limits the diffusion of

aqueous out of the posterior chamber.63 The process would be

accelerated in eyes prone to angle-closure with shorter axial

lengths (shallower posterior segment with less distance for

the vitreous to travel before impacting the lens and more

resistance to posterior diffusion of the choroidal overflow

through a thicker sclera) and relatively larger lenses thatmore

effectively block anterior fluid flow and decrease the space

between the lens and iris.131

Schwartz et al reported that the anterior vitreous in cases

of VB is abnormally compressed intraoperatively,147 causing

positive pressure.168 In some cases, it is densely adherent to

the ciliary body.152 Additionally, iridovitreal, iridocapsular,

and vitreocapsular adhesions, as well as vitreous adhesions

around peripheral iridectomies,69 are described.

In phakic cases, the abnormally dense anterior vitreous

can push the lens anteriorly into the iris, resulting in a type

of phacomorphic27 angle-closure. In aphakic cases, rather

than the lens pushing the iris forward, it is thought that the

anterior hyaloid directly pushes the ciliary body and iris

forward.147 Both cases lead to the lens-iris diaphragm

moving anteriorly.120 Axial shallowing would be exacer-

bated if a small plug of vitreous occluded the pupil, which

simultaneously increases the pressure gradient between the

posterior and anterior chamber and decreases the surface

area for forward diffusion of aqueous out of the posterior

chamber.63,136 In support of this theory, an intact anterior

hyaloid has been visualized in the anterior chamber.110

Although the inciting event for positive pressure leading to

anterior ciliary body rotation is still under debate, most of

the literature concurs that the lens-iris diaphragm is pushed

forward directly both centrally and peripherally, causing

acute angle-closure. Unlike in relative pupillary block,

where the facility of outflow is not affected until there is

iridotrabecular block, anterior movement of the lens or

ciliary body compresses the trabecular meshwork (probably

through anterior forces on the scleral spur) and immediately

reduces the facility of outflow, regardless of the position of

the iris.63

The realization that the final pathway was anterior rota-

tion of the ciliary body and lens-iris diaphragm led to the first

consistently successful treatment of VB: a combination of

topical 1% atropine and 10% phenylephrine to cause relaxa-

tion of the ciliary sphincter, thus increasing the radial pull of

the zonules.29 Making the zonules taut pulls the ciliary pro-

cesses and lens posteriorly to resist the positive posterior

pressure and prevents the angle from being narrowed. At the

same time, themydriasis increases the free surface area of the

anterior hyaloid, improving anterior diffusion of aqueous.19

Although medical treatment may counteract the anterior

rotation, this does not address the inciting event, leading

to numerous reports of relapses within days of stopping

medications.2,29,137

1.4.3. Secondary causesCases of secondary VB, where there is a known etiology for

anterior displacement of the ciliary body, should be classified

separately because in those cases treatment should target the

underlying cause. If there are adhesions (peripheral anterior

synechiae, posterior synechiae,119 or zonular-capsular adhe-

sions87), limited evidence suggests that these should be

removed to restore normal anatomy.122 Care must be taken as

a retinal detachment occurred after an attempt to remove

ciliovitreal adhesions without performing a core vitrec-

tomy.153 Angle-closure resembling VB may develop when

sufficient foreign material (such as injected balanced saline

solution,174 viscoelastic,12 perfluoropropane gas,132 or an in-

fectious fungal mass33,80) is deposited in the anterior vitreous

and causes enough positive pressure to close the angle.

s u r v e y o f o p h t h a lmo l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1232

2. Diagnosis and workup

2.1. Clinical criteria

VB is characterized by central and peripheral shallowing of

the anterior chamber in the presence of a patent peripheral

iridotomy and in the absence of choroidal effusion or hem-

orrhage. The average anterior chamber depth in 25 consecu-

tive cases was 0.37mm,which improved to 2.39mm following

successful treatment.96 The IOP is usually elevated. Particu-

larly in cases following trabeculectomy, the IOP may be

normal or as low as 3 mm Hg21,168 because of hyperfiltration,

wound leak, or choroidal detachments. In postoperative

glaucoma cases, after ruling out hyperfiltration and wound

leak (both associated with a low IOP), a progressively shal-

lowing ACwith a rising IOP should prompt evaluation for VB.64

Attempts to refill the AC in VB will not deepen the AC and the

IOP continues to increase.153 A careful fundus examination or

ultrasound imaging is necessary to rule out posterior segment

abnormalities, most importantly suprachoroidal hemorrhage

and choroidal effusion.53,92

Slit-lamp examination shows anterior displacement of the

lens-iris diaphragm centrally and peripherally. The elevated

IOP (> 35 mmHg in 100% of 50 patients)163 leads to the typical

signs of congestive glaucomadthat is, conjunctival injection

and microcystic corneal edema. A less common finding is a

myopic shift124,147,156 due to forward rotation of the lens-iris

diaphragm. Eyes that have undergone trabeculectomy will

usually have an elevated filtering bleb.21

2.2. Anterior segment imaging

Anterior segment imaging has led to improved diagnosis of

VB and can complement clinical examination.155 UBM has

demonstrated narrowing of the anterior chamber, anterior

rotation of the ciliary body,37,66,122,146,150,155,165,169 anterior

rotation of the ciliary processes and zonules until they contact

the lens, and forward displacement of the lens-iris dia-

phragm.122 Quantitative measurements showed that the

angle between the posterior corneal surface and the anterior

ciliary body in affected cases was less than half of those in the

unaffected fellow eye.181 Another sign on UBM is the inability

to find the posterior chamber, which reappears following

successful treatment.195 Finally, UBM can also be used to

confirm the patency of the iridotomy.37,155 Although optical

coherence tomography can visualize the angle closure and

part of the lens,72 UBM is better for visualizing the deeper

structures (ciliary body and posterior chamber) essential

to identifying VB.60 Finally, UBM can also be used after a

procedure to verify that the anterior hyaloid has been

disrupted.56,155

2.3. Differential diagnosis

The main differential diagnosis, acute angle-closure glau-

coma from relative pupillary block, sharesmany of the clinical

features, can also occur postoperatively, and in some cases

improves with cycloplegics.17 With pupillary block, however,

as the aqueous trapped between the iris and lens causes

peripheral iris bowing, the central anterior chamber depth is

greater than at the periphery.90 Also with pupillary block, the

lens (if present) should be in the normal anatomic position,

whereas in VB the lens can be displaced anteriorly. The fellow

angle in a case of pupillary block would also be expected to be

narrow, whereas VB shows more of a disparity in angle depth

between the two eyes.91 The only reliable way to distinguish

the two is to treat any possible pupillary block component by

performing an iridotomy. If there is an existing iridotomy, it

must be determined that it is not occluded by ciliary pro-

cesses, fibrin, or vitreous. If this cannot be confirmed, then

another iridotomy should be made. Other entities in the

differential include choroidal effusion or suprachoroidal

hemorrhage. UBM can often identify these even when

ophthalmoscopy cannot.92 Also included in the differential is

any mass of the iris, ciliary body, or retina (such as a sub-

retinal hemorrhage) large enough to displace the ciliary body

anteriorly.192

3. Treatment

3.1. Treatment strategy

The goal of treatment is to reestablish the free diffusion of

aqueous from the vitreous into the AC to allow the ciliary body

to rotate back into its anatomic position. This relieves the

compression of the TM, allowing aqueous to resume outflow

and reforms the anterior and posterior chamber. The recom-

mended treatment is a stepwise approach,41 beginning with a

trial of medical therapy. The goal of treatment is an immedi-

ate deepening of the AC. Failure of medical therapy to lower

the IOP calls for laser or other surgical intervention.

3.2. Medical treatment

3.2.1. CycloplegicsMedical therapy, as the least invasive option with the least

number of side effects, is the first line of treatment for VB. In

1962, Chandler and Grant proposed a combination of cyclo-

plegic and mydriatic agents.29 The use of cycloplegics was

thought to improve aqueous flow by tightening of the lens

zonules, subsequently pulling the lens posteriorly to reverse

the shallowing of the anterior chamber. Sensitization

to atropine drops may become an issue because there are

few alternatives.24,142 Systemic side effects, such as urinary

retention or tachycardia, are rare.155

3.2.2. HyperosmoticsWeiss et al used intravenous mannitol to reduce vitreous

volume in the treatment of VB.185 They noted that mannitol

deepened the AC in many types of glaucoma, and thought the

hyper-osmotic agent would draw aqueous out of the posterior

segment while further dehydrating the vitreous. A similar

explanation has been proposed for the successful use of

intravenous urea.59,178 An additional mechanism may be the

reduction of extravascular choroidal volume, subsequently

lowering posterior pressure. Simmons used a systemic agent

in combination with cycloplegia for 5 days (i.e., phenylephrine

10% four times a day, atropine 2% four times a day, and

s u r v e y o f o p h t h a lm o l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1 233

acetazolamide 250 mg four times a day) in early studies,

reporting a 50% success rate.157 He suggested attempting

medical treatment alone for no longer than 5 days after noting

that most successfully treated cases showed deepening of the

AC after only 2e3 days. Reduction of aqueous production with

topical beta blockers, alpha agonists, and carbonic anhydrase

inhibitors is also used as adjunctive therapy.53,195

Indefinite treatment with atropine may be necessary to

prevent recurrence,34 because a reshallowing of the AC and

increased IOPmay occur within days of stopping atropine.2,137

Medical therapy can be repeated if the condition recurs. The

presence of physical lens-cornea touch or excessively high

IOP, however, precludes continued medical management.100

Once there is lens-cornea touch, surgical intervention within

24 hours100 is warranted to prevent the development of pe-

ripheral anterior synechiae (which can lead to chronic angle-

closure glaucoma even after the VB is corrected),171 posterior

synechiae, cataract, and corneal endothelial damage.142

3.2.3. Recurrence rateThe twomain problems with medical treatment alone are the

low immediate success rate and the high risk of recurrence.41

Although multiple studies have found an immediate success

rate of around 50%,41,157,169 and theoretically no other treat-

ment may ever be needed, the duration of success has not

been detailed well. Even in Chandler and Grant’s seminal

paper29 advocating medical treatment, the follow-up ranged

only from 6 days to 6 months. In that short time, 50% of cases

required subsequent surgical treatment. Other studies

showedmuch lower success rates withmedical treatment: 8%

of 50 eyes,163 9% of 57 eyes,195 and 14% of 28 eyes.38 Debrou-

were et al found that among 9 patients treated medically, 3

could not be broken,41 and after an average of 112 days, all had

recurred. Despite this, virtually every study reports starting

treatment with medical treatment alone.

3.3. Laser treatment

3.3.1. CapsulotomyLaser has been used for the treatment of VB to restore normal

aqueous flow. Posterior capsulotomy allows for decompres-

sion of the anterior vitreous, resulting in equalization of IOP in

the anterior and posterior chambers.47,97,138 Of 7 cases of

pseudophakic VB, a YAG capsulotomy broke the attack in 5

(71%) with no recurrences over 9 months.95 No complications

were noted. It is quite possible that the laser energy not only

disrupts the capsule, but also the anterior hyaloid, which is

almost always needed for complete resolution.73,106 The cap-

sulotomy should be attempted outside of the artificial lens

optic, through a peripheral iridotomy if necessary, in order

to allow sufficient space for aqueous to flow through the

channel.

3.3.2. HyaloidotomyNd:YAG laser hyaloidotomy can be used to disrupt the ante-

rior hyaloid in combination with posterior capsulotomy,

creating a direct communication between the vitreous cavity

and the AC.20,49,67,94 Reported settings for Nd:YAG hyaloidot-

omy ranged from 1e2 mJ for 2e5 shots,38 to 3e5 mJ for 20e40

shots.111,168 A peripheral disruption of the anterior vitreous is

also preferable, so that the forward flow of aqueous is not

blocked by the lens optic.160 A successful response is deep-

ening of the AC within 12e24 hours, which is more important

than the accompanying IOP decrease, because the AC deep-

ening should signify that the positive posterior pressure is

resolving and may occur immediately.34 In one series, a hya-

loidotomy was only successful in 57% of 7 cases with

14 months of follow-up.64 Another study found that initial

success occurred only in 67% of 15 cases, and of those cases

with initial success, 30% had a recurrence within only

3 months.38 Although Little reported higher initial success

rates (71% of 7 cases), the length of follow-up was not given.95

Because a hyaloidotomy allows vitreous to move forward

into the AC, there is the potential risk of retinal detachment.7

A clear view is needed, and multiple hyaloidotomies may be

necessary.20,111 Although initial success rates ranged from

57% of 7 cases64 to 100% of 4 cases,41 the recurrence rate is

high, with Debrouwere reporting that 3 of 4 cases recurred

within only 80 days.41 The main reservation with recom-

mending hyaloidotomy as first-line treatment is the lack of

long-term follow-up demonstrating that it yields more than

only a temporary benefit, because many cases have follow-up

for less than a year.67 Also, laser application to posterior

structures is generally not an option in phakic cases.142

3.3.3. Argon cyclophotocoagulationArgon laser iridoplasty attempts to deepen the AC, but

because this does not address the underlying problem of vit-

reous expansion, this would not be expected to be sufficient.69

Other studies have looked at external cyclophotocoagulation

with argon laser to try to move the ciliary processes posteri-

orly. The laser has been used through a goniolens88,182 or

through an iridectomy73 on at least 4 but preferably 10 ciliary

processes89 (at 100e200 microns spot size, 300e1000 mW for

0.1 seconds) to shrink them and correct the anterior rotation,

avoiding any visible capillaries. As with capsulotomy, the

mechanism of treatment is unclear because the laser energy

may also disrupt the anterior vitreous or adhesions between

the vitreous and ciliary processes.73 A successful response is

immediate AC deepening that improves over the following

3e5 days.73

The largest series of external ciliary process laser followed

6 patients for an average of 16 months.73 Although all

continued to take atropine both before and after the laser,

only 1 (17%) had a recurrence and needed further treatment.

This study highlights the possibility that for any procedure

done after only a short trial with medications, the successful

outcome may simply be a delayed response to medication

alone.73 The number of reported cases is too small to deter-

mine the overall success and relapse rate. After the reports of

the success of argon photocoagulation of ciliary processes,

treatment of the ciliary body, first by cryotherapy then by

transscleral cyclophotocoagulation (CPC), was also reported.11

3.3.4. Transscleral cyclophotocoagulationCPC may work by causing shrinkage of the ciliary processes

and decreased aqueous production from coagulative necrosis

of the ciliary processes.50,117,149 As with laser hyaloidotomy, it

is possible that the actual reason for success is the disruption

of the anterior vitreous by laser energy or the subsequent

s u r v e y o f o p h t h a lmo l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1234

inflammation.106 UBM showed that only 24 hours after CPC,

the ciliary body and many of the processes had returned to

their normal anatomic position.23

Beyond case reports, there are 3 series describing CPC as a

treatment option. Carassa reported 5 cases treated with CPC

after failed hyaloidotomy, with all 5 responding promptly to

CPC with no recurrences over an average follow-up of only

12 months.23 The second study also had 5 patients treated

over approximately 180� and found only 1 recurrence after an

average follow-up of 4.7 years.161 The third study reported

success in 12 (80%) of 15 cases.38 The 3 failures consisted of a

case that did not respond initially and 2 recurrences (13%)

despite a short follow-up of only 6months. Although there are

two case reports of VB developing after CPC,7,41 this is a po-

tential problem with all treatment strategies. The only treat-

ment of VB that has to date not been reported as a possible

inciting cause is laser hyaloidotomy. Also, the clinical details

were only provided in one of the two cases that describes a

complicated ocular history including a chemical burn with

corneal perforation, corneoscleral graft, cataract extraction,

and aqueous shunt placement only weeks before the CPC.7

The lack of long-term follow-up and small number of

reports make it difficult to assess the role of CPC in the

treatment algorithm. Although it can be done through opaque

media and causes less conjunctival scarring than PPV, CPC

does carry the risk of hypotony, phthisis, and rarely sympa-

thetic ophthalmia. Because of these rare, but serious, poten-

tial risks and the lack of more long-term follow-up, it is likely

that, as for primary open-angle glaucoma, CPC is reserved for

cases with poor visual prognosis (i.e., visual acuity worse than

20/200).38

3.4. Surgical treatment

3.4.1. Vitreous aspirationWhen medical or laser therapy has failed to induce or main-

tain resolution of VB, surgical intervention is necessary. As

previously mentioned, the presence of lens-cornea touch

necessitates surgical intervention within 24 hours.100 Initial

attempts at reformation of the anterior chamber resulted in

elevated IOP. It was not until a penetrating incision through

the anterior hyaloid was performed that forward flow was

restored. Chandler and others148 proposed an anterior

approach to disrupt the vitreous.28 He suggested passing an

18-gauge needle posteriorly through a scleral flap and noted

the expulsion of fluid through the needle, suggesting that

aqueous trapped in the vitreous cavity had been evacuated.30

Some surgeons also swept the needle within the vitreous for

2e3 mm in order to ensure that the vitreous was disrupted.114

This technique was subsequently abandoned because of high

rates of cataract formation and the risk of retinal detachment.

To reduce the chance of retinal detachment, Balakrishnan

refined the technique by directing the needle through the

limbus, through a surgical iridectomy to a depth of only

5e7 mm, and withdrawing 0.5 cc of vitreous.9 Still, 50% of

cases relapsed after a vitreous tap.9 Recently, Francis et al

proposed the use of slit-lamp needling of the anterior vitre-

ous.57 A 27-gauge needle is inserted through a paracentesis

and a pre-existing iridectomy and is used to sweep and

disrupt the anterior hyaloid, followed by aspiration and then

reformation of the AC. Although this technique successfully

averted the need for vitrectomy in the two reported cases,57

mechanical disruption of the anterior vitreous carries the

risk of retinal detachment and would be of limited use in a

phakic patient. It also requires the presence of a large surgical

iridectomy, which may not readily be available. No further

reports of this technique exist. A similar operative technique

was performed using a vitrector through an anterior approach

to successfully disrupt the anterior vitreous in two patients

without recurrence over 5 months.10

3.4.2. Core vitrectomyAs microsurgical instrumentation improved, a core PPV could

be done rather than a vitreous tap. Weiss et al noted a

decreased recurrence rate following core PPV (0% of 7 cases) as

compared with 38% following a vitreous tap.186 A large surgi-

cal study had 50 cases that all received a core PPV and had

only a 6% recurrence rate.195 In phakic cases, it was not

initially clear if the lens needed to be removed.

When comparing outcomes of PPV for VB, the success

rates were higher in cases presenting with pseudophakia as

compared to phakic cases. In the study byHarbour et al, 90% of

10 pseudophakic cases were successful.69 In another study of

20 PPVs with follow-up averaging 16 months, the recurrence

rate was 50% in the 10 phakic eyes versus only 10% in the 10

pseudophakic eyes. In phakic eyes, studies found that lower

failure rates (failure to break the misdirection or recurrence)

occurred when a PPV was combined with cataract extraction.

One study found a failure rate for core PPV of 75% of 4 cases

versus 17% of 6 cases treated with combined lensectomy and

pars plana core vitrectomy without trimming of the vitreous

base.170 Harbour found that combined PPV/lensectomy led to

resolution in 100% of 7 cases versus only 71% of 7 cases treated

with PPV without lensectomy.69 This led to the recommen-

dation that in phakic cases of VB, PPV should be combined

with lensectomy. The main reason postulated for higher

success rates in pseudophakic cases versus phakic ones was

easier visualization and assured disruption of the anterior

hyaloid without a lens.25,170

Another reason to support lens extraction with PPV is the

risk of iatrogenic cataract formation while maneuvering

around the lens in an attempt to completely remove the

anterior hyaloid.25 Out of 10 phakic cases treated only with

PPV, that a cataract developed in 30% after only 16months.22 A

less aggressive approach would be to proceed with lensec-

tomy if PPV alone fails to deepen the AC.109 Removing the lens

also allows for creating a posterior capsulotomy to further

ensure a unicameral eye, as has been suggested in two

studies.96,170

If a PPV is combined with cataract extraction, one tech-

nique is to first perform a limited core PPV in order to reduce

positive posterior pressure and allow more space for lens

removal, decreasing the risk of posterior capsule rupture.154

This also allows for improved pupil enlargement to ensure

adequate visualization of the anterior vitreous.195 Following

lens implantation, the residual PPV can be completed. Finally,

in order to create a unicameral eye, they recommended using

the vitrector to create a zonulohyaloidectomy and iridot-

omy.195 This technique had previously been used in cases

where the AC wouldn’t deepen with core PPV alone.101 Using

s u r v e y o f o p h t h a lm o l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1 235

this technique, Zhou et al found no recurrences in 4 cases

after a mean follow-up of 16 months.

3.4.3. Anterior vitrectomyAn anterior vitrectomy may be performed in place of a PPV.

An anterior approach consisting of an iridectomy, zon-

ulohyaloidectomy, and anterior vitrectomy has been reported

to have no recurrences in 7 cases, all of which had less than

1 year of follow-up.10,16,99 A larger case series recently

reported no recurrences with this anterior technique in 10

pseudophakic eyes with a mean follow-up time of 1 year.193

Liu et al found no recurrences in 25 phakic eyes treated with

phacoemulsification, posterior capsulectomy, and anterior

vitrectomy with 23 months average follow-up.96 A smaller

series found no recurrences in 4 cases treated with anterior

vitrectomywith phacoemulsification followed for amaximum

of 2 years.115

Only one study41 had comparative (retrospective) data on

the efficacy of anterior vitrectomy versus PPV. In both treat-

ment groups, an iridectomy and zonulectomy was done and

phakic cases received phacoemulsification as well. Although

initial success occurred in all cases, the recurrence rates

favored PPV. After a mean follow-up of 61 days, 2 out of 3

recurred after a combined anterior vitrectomy versus none of

15 cases treated with combined PPV.41

3.4.4. Recurrence ratesThere has been recurrence of VB after core PPV in numerous

cases.22,76,82,168,170,191 The most likely explanation for the

recurrence of VB after PPV is that part of the anterior vitreous,

which can be especially challenging to remove in phakic pa-

tients without damaging the lens, was left intact.22,106 It has

been recommended to continue with the vitrectomy until the

AC deepens intraoperatively,109 which should reduce the risk

of leaving remnant vitreous at the base that can later cause a

recurrence.187 In order to assure that the anterior vitreous is

removed, the vitreous can be stained with fluorescein32 or

triamcinolone118 to improve visualization of uncut vitreous.

Although the preponderance of evidence suggests that in

phakic cases the lens should be removed, a prospective

comparative trial is needed to demonstrate if a PPV is clearly

superior to an anterior vitrectomy in lowering recurrence

rates and to demonstrate whether a zonulohyaloidectomy is

needed at the first presentation of VB.

4. Postoperative complications

Besides the rare sensitization to atropine,155 none of the

studies report a complication following medical treatment

other than the high rate of recurrence. Nor are there reports of

any complications following laser capsulotomy or hyaloidot-

omy for VB. No vision-threatening consequences following

CPC for VB are reported, although this is likely a function of

the small number of cases. Following PPV in 24 cases, there

were 6 cases of bullous keratopathy (25%), 2 cases of choroidal

detachments (8%), 1 exudative retinal detachment (4%), and 1

suprachoroidal hemorrhage (4%).69 In another retrospec-

tive series with 50 PPVs (with cataract extraction in phakic

cases), 6% developed bullous keratopathy, 6% had choroidal

detachments, and 6% had a retinal detachment.195 Failure of

an existing trabeculectomy bleb occurs (e.g., in 33% of 9 tra-

beculectomies,69 44% of 9,109 and 24% of 50 trabeculec-

tomies195), but without a control group it is difficult to

attribute this only to the PPV. UBM has shown that during an

attack of VB, severe AC shallowing blocks the sclerostomy,23

and the lack of fluid flow may allow scar tissue to form.195

5. Prevention

Because the condition is rare, it is difficult to prove if any

prophylactic measure is successful. The first step of preven-

tion would be identifying eyes that are at higher risk of

developing VB following surgery. The most commonly re-

ported risk factor is a history of VB in the other eye.29 An

ongoing area of research is using UBM to predictwhowould be

at highest risk, with Prata et al finding a plateau iris configu-

ration in 85% of a series of patients who later developed

postoperative VB.125

5.1. Iridotomy

One study compared UBM findings in unaffected fellow eyes

with a matched control group of patients with narrow angle

but no history of VB in either eye.181 They noted that, even in

the unaffected fellow eyes in cases of contralateral VB, the

ciliary body was more anteriorly rotated than the control

group. After an episode of VB, iridotomyhas been proposed for

the unaffected fellow eye, even if that angle does not appear

narrow.29,90 Although this would prevent pupillary block, it is

not clear why this would prevent VB.91 If a prophylactic iri-

dotomy is done, atropine and phenylephrine should be given

immediately afterward to protect against an iridotomy-

induced VB.34

5.2. Prophylactic surgical procedures

Most of the reported preventive techniques focus on altering

surgical techniques to reduce the chance of postoperative VB.

The first suggestion was to lower the IOP as much as possible

prior to any surgery. In cases at high risk for VB, the AC should

be maintained at all times intraoperatively, and during a tra-

beculectomy preplaced sutures should be used to minimize

hypotony.53 If the fellow eye in a patient with a history of VB

requires any intraocular surgery, Chandler recommended

adding lens extraction to the procedure in order to decom-

press the posterior chamber.27 Others suggested that cataract

extraction should be combined with prophylactic PPV and

zonulohyaloidectomy.31,154 For phacoemulsification, an arti-

ficial lens with a small diameter should be considered in order

to occupy less space in the posterior chamber.195

6. Prognosis

VB was originally termed malignant glaucoma as it resis-

ted then conventional treatments and consequently had

a poor prognosis. With the improvement of surgical tech-

niques, however, VB now has a much-improved prognosis, as

Table 1 e Recurrence rates after surgery

Type of surgery Number ofpatients

Averagefollow-up time

Rate ofrecurrence (%)

Anterior vitrectomy

Anterior vitrectomy (phakic with lensectomy and posterior capsulotomy)

Liu96 25 23 mos 0

Anterior vitrectomy (pseudophakic)

Tsai170 6 11 mos 40

Anterior vitrectomy with iridectomy/hyaloidectomy/zonulectomy

Bitrian16 5 7.6 mos 0

Lois99 5 5 mos 0

Debrouwere41 3 24 days 67

Zarnowski193 10 12 mos 0

Core vitrectomy

Core vitrectomy (phakic without lens extraction)

Tsai170 4 3 mos 75

Harbour69 7 21 mos 29

Byrnes22 10 16 mos 50

Weiss185 2 Not reported 0

Core vitrectomy (phakic with lens extraction)

Tsai170 6 14 mos 67

Harbour69 7 21 mos 0

Debrouwere41 2 8 days 100

Zhou195 38 34 mos 3

Core vitrectomy (aphakic)

Weiss185 6 Not reported 0

Core vitrectomy (pseudophakic)

Harbour69 10 16 mos 10

Byrnes22 10 16 mos 10

Debrouwere41 2 12 days 50

Zhou195 10 34 mos 20

Weiss185 1 Not reported 0

Hosoda76 2 4 mos 100

Core vitrectomy with iridectomy/hyaloidectomy/zonulectomy

Sharma154 4 16 mos 0

Dave38 3 192 days 0

Debrouwere41 15 61 days 0

s u r v e y o f o p h t h a lmo l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1236

evidenced by Dave et al reporting that 96% of 28 cases of VB

resolved with medication or surgery.38 Table 1 lists the

recurrence rates with modern surgical techniques.

6.1. Course of intraocular pressure control

The lack of large studies combined with short follow-up

makes it difficult to estimate the visual prognosis following

VB. As with most causes of angle closure, the duration and

maximum IOP with resulting glaucomatous optic neuropathy

would be expected to be a main determinant of the final

outcome. The average duration of an attack was 13 days in 28

cases.38 Unfortunately, there is very little data analyzing the

optic nerve status, and no studies with any controls or

retrospective case matching. When IOP is reported, it usually

responds promptly to adequate treatment of the VB. In one

study the mean IOP at presentation was 34 mm Hg and

decreased to 14 mm Hg (58% decrease) after treatment.38 The

single study that focused on late IOP outcomes demonstrated

elevated IOP even 1 year after the attack.109 They divided

their analysis of VB into cases with and without a pre-

existing history of glaucoma. One year after resolution of

VB, the group of patients with a previous history of glaucoma

were still on one additional medication over baseline,

whereas the group of nonglaucomatous cases was main-

tained on a mean of four medications with an average IOP of

20 mm Hg.109

In a series of 19 eyes that required surgery to break the

attack, 32% went on to need later glaucoma surgeries for IOP

control.170 In the study (n ¼ 57) with the longest follow-up,

the final IOP averaged 17.5 mm Hg on a mean of 0.1 medi-

cations.195 The reason for late IOP increases without a

recurrence of VB has not been well detailed, but there are a

number of risk factors these patients share, including narrow

or closed angles and postsurgical scarring. The most defini-

tive treatment of the increased IOP appears to be a pars plana

aqueous shunt,8,159 since this is combined with a PPV and

leaves a direct tract for fluid to exit the vitreous. Placing a

pars plana shunt to treat an attack has been recommended in

cases of existing advanced glaucomatous optic neuropathy8

or extensive peripheral anterior synechiae (particularly

synechial angle closure for more than 180� for 1 year or

longer). Otherwise, adding a glaucoma procedure is not

routinely recommended.79 Perioperative topical steroids and

cycloplegics should be used to reduce postoperative recur-

rence of VB.91

s u r v e y o f o p h t h a lm o l o g y 6 0 ( 2 0 1 5 ) 2 2 9e2 4 1 237

6.2. Visual acuity outcomes

Another factor confounding the final visual outcome is a

complicated ocular history since the majority of cases of VB

are postoperative, making it difficult to ascertain the specific

cause of vision loss. The most common association of VB is

with chronic angle-closure glaucoma, which is generally a

progressive disease.38 In one study where 6 (21%) of 28 cases

lost two or more lines of Snellen visual acuity, it was specif-

ically noted that none of the cases lost vision because of

glaucomatous optic neuropathy.38 In a series of 24 cases

requiring PPV, only 6 cases (25%) lost two or more lines of

visual acuity.69 Dave et al reported 28 cases where 50% of

patients had no change in vision compared to baseline, 29%

gained �2 lines of Snellen visual acuity, and 21% lost �2

lines.38

A trial with a large cohort (57 cases) also had the longest

follow-up (mean: 34 months).195 Only 9% responded to medi-

cation, and the remainder received a core PPV (with cataract

extraction in phakic cases). Following treatment, the vision

improved in only 58% of cases. The mean IOP decreased from

a baseline of 32 mm Hg to 17.5 mm Hg (41% decrease) and the

number of medications decreased from 3.1 to 0.1. Risk factors

for poor outcome (thiswas the only study to report on a formal

risk factor analysis following treatment) were higher baseline

IOP and shorter axial length.195 This is also the only studywith

a survival analysis, and the authors found that a successful

outcome (defined as IOP < 21 mm Hg, formed AC, and vision

better than no light perception) occurred in approximately

75% of cases after 3.5 years and fell below 50% after 9 years.

The specific reason for failure was not specified, although

recurrence of VB only occurred in 6% of the 50 cases who had

received PPV as part of their treatment.

7. Conclusion

VB is a rare, but devastating, complication occurring most

commonly in eyes with chronic angle-closure glaucoma after

glaucoma filtering surgery. The exact mechanism of VB is

still unproven, but is likely choroidal expansion and an

abnormal diffusion of aqueous through the vitreous, leading

to anterior rotation of the ciliary body. Because of its low

prevalence, no treatment technique has emerged as the gold

standard. To date, the most successful results with the

fewest recurrences follow core vitrectomy and assuring a

unicameral eye. Using these techniques, the visual prognosis

has greatly improved.

8. Method of literature search

We used the following search terms: aqueous misdirection,

malignant glaucoma, ciliary block, ciliovitreal block, ciliolenticular

block. We searched the following databases: Pubmed, Ovid,

andWeb of Science/ISI. The search focused on articles written

in English, but we reviewed all abstracts available in these

search engines, translating and including other articles that

either added novel information or consisted ofmore than case

reports.

9. Disclosures

All authors report no proprietary or commercial interest in

any product mentioned or concept discussed in this article.

Supported in part by an unrestricted departmental grant from

Research to Prevent Blindness, Inc., New York, NY (to JCT).

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