Current Management Approaches For Uveitic Glaucoma

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Current Management Approaches for Uveitic Glaucoma
Article in International ophthalmology clinics · July 2015

DOI: 10.1097/IIO.0000000000000071 · Source: PubMed
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Current Management Approaches
for Uveitic Glaucoma
Mohamed S. Sayed, MD
Richard K. Lee, MD, PhD
’ Introduction
Uveitic glaucoma is a term that encompasses a myriad of disease

entities with different etiologies, mechanisms, and prognoses. The
prevalence of glaucoma in inflammatory diseases of the eye ranges from
10% to 20% in non–population-based studies.1–3 The mechanisms by
which intraocular inflammation causes an elevation of intraocular
pressure (IOP) and subsequent secondary glaucoma vary according to
the specific uveitic etiology, ocular anatomic features, ocular physiology,
and treatment modalities employed which can affect eye pressure.
Aqueous outflow obstruction in uveitis may be either macroscopic (ie,
with synechial seclusion of the pupil, secondary pupillary block and
chronic synechial, and/or neovascular angle closure) or ultrastructural
(ie, with open-angle glaucoma due to microanatomic changes to aqueous
outflow pathways).
In acute uveitis, decreased IOP may be observed due to reduced
aqueous secretion by the inflamed ciliary body (cyclitis),4 and theoretically,
facilitation of aqueous uveoscleral outflow secondary to increased aqueous
concentration of prostaglandins.5,6 Eventually, IOP may paradoxically rise
secondary to increased inflammatory mediators, cells and proteins,
trabecular meshwork (TM) cell dysfunction and trabeculitis, with an
associated increase in resistance to trabecular aqueous outflow.7 In
addition, the prolonged use of topical corticosteroids, a mainstay of uveitis
treatment, and to a lesser extent, periocular or systemic corticosteroids,
may result in trabecular damage and glycosaminoglycan deposition
resulting in steroid-induced glaucoma.8–10 The use of corticosteroid
intravitreal implants in the treatment of uveitic glaucoma has also been
associated with a significant elevation of IOP.11 The corticosteroid-induced
IOP rise appears to be especially pronounced in eyes where damage to the
INTERNATIONAL OPHTHALMOLOGY CLINICS
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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

142 ’ Sayed and Lee
TM and aqueous outflow pathway by the inflammatory process has

already taken place and in patients who are steroid responders.12,13
Anterior uveitis accounts for more cases of uveitic glaucoma than do
intermediate or posterior uveitis.7 Certain uveitic disorders have a
particularly higher risk of developing secondary glaucoma. These
include juvenile idiopathic arthritis (JIA), Fuch heterochromic cyclitis,
Posner-Schlossman syndrome, and herpetic uveitis.14 Elliot in 1915
postulated that infectious diseases such as syphilis, gonorrhea, herpes
zoster ophthalmicus, and tuberculosis were the predominant causes of
uveitic glaucoma.15 The incidence of glaucoma associated with infectious
uveitis has, however, markedly decreased over the years,16 with most
cases now being attributed to noninfectious causes.
Management of uveitic glaucoma is challenging and should be aimed
at controlling both the underlying inflammatory process and secondary
glaucoma. The choice of the appropriate treatment modality depends on
the etiology, extent, and chronicity of inflammation as well as on the
longevity, intensity, and resultant damage of IOP elevation. For example, it
may be sufficient to treat episodic IOP rise during active inflammation if
IOP is acceptably low in between inflammatory episodes. Steroid-respon-
siveness, mechanism of glaucoma, and status of the anterior chamber angle
as determined by gonioscopy also influence the therapeutic approach,
although uveitic glaucoma is often a combined-mechanism glaucoma.
Effective control of intraocular inflammation is crucial for successful
chronic medical and/or surgical IOP control in the treatment of uveitic
glaucoma. In some instances, potent control of inflammation may alone
result in adequate control of IOP, especially in conditions where intraocular
inflammation is the principal mechanism effecting IOP rise, such as Posner-
Schlossman syndrome and herpetic keratouveitis. However, the combined
use of IOP-lowering medications and/or surgical intervention together with
anti-inflammatory agents is typically required. Pupillary block due to
inflammatory synechiae is typically managed by mydriatric agents and laser
peripheral iridotomy (LPI) to create an alternative pathway for aqueous
humor movement from the posterior chamber to the anterior chamber.
Glaucoma in the setting of complete angle closure with 360-degree
peripheral anterior synechiae (PAS) typically requires medical and surgical
intervention, whereas cases with secondary open-angle glaucoma or
incomplete angle closure are initially managed medically. When maximal
tolerated medical therapy of secondary glaucoma fails to sufficiently reduce
IOP and halt glaucoma progression, surgical intervention is considered.
’ Medical Management of Uveitic Glaucoma
The goal of medical therapy in uveitic glaucoma is to provide

symptomatic relief for the patient while protecting the optic nerve by
www.internat-ophthalmology.com

Current Management Approaches for Uveitic Glaucoma ’ 143
reducing IOP to a nondamaging level. Medical management also aims to

minimize the need for surgical intervention and prevent complications
such as recurrent or persistent inflammation and pupillary block.
A combination of anti-inflammatory medications, IOP-lowering medi-
cations, and cycloplegic-mydriatic agents is typically used in the medical
management of uveitic glaucoma.
Anti-Inflammatory Medications
Early management of intraocular inflammation in uveitic glaucoma
is critical as glaucoma is secondary to the inflammatory ocular process.
Inflammation should not be undertreated to avoid a steroid-induced
elevation of IOP, as further trabecular damage and continued posterior
or anterior peripheral synechiae formation might ensue, further
exacerbating glaucoma. Potent topical corticosteroids, for example,
prednisolone acetate 1%, are considered the initial anti-inflammatory
medications of choice in the setting of noninfectious anterior uveitis.
However, continued IOP rise that is often unresponsive to hypotensive
medications may limit their use. This is particularly important in patients
who are corticosteroid responders. Of note, the prevalence of cortico-
steroid response is suggested to be higher in connective tissue diseases
such as JIA or ankylosing spondylitis in which uveitis can be a prominent
feature.17 Other risk factors for corticosteroid response include a history
of glaucoma or glaucoma suspicion,18 family history of glaucoma,19 older
age,20 and high myopia.21 IOP elevation in response to steroid treatment
is often proportional to the potency of the steroid used.22 In uveitis
where the principal cause of ocular hypertension is corticosteroid
response, other classes of corticosteroids, such as rimexolone 1% and
loteprednol etabonate 0.5%, have shown efficacy in controlling intra-
ocular inflammation while producing less IOP elevation.23–26
Topical corticosteroids are generally not effective enough in uveitis
involving the posterior segment, and periocular, intravitreal, and/or
systemic corticosteroids may be required to control ocular inflammation.
Periocular and intravitreal injection of steroids has been shown to have a
higher risk of inducing a significant IOP rise.27–29 Chronic use of
systemic steroids may potentially result in severe systemic side effects
such as weight gain, impaired glucose tolerance, upper gastrointestinal
bleeding, and thromboembolic events.
When corticosteroids are ineffective or the dose required to control
intraocular inflammation is high enough to cause significant IOP rise or
other harmful systemic or ocular side effects, systemic immunomodula-
tory therapy is indicated to lower the dose of corticosteroids or replace
them. Conventional immunosuppressive medications such as antimeta-
bolites (eg, methotrexate, mycophenolate mofetil, and azathioprine),
T-cell inhibitors (eg, cyclosporine and tacrolimus), and alkylating agents

(eg, chlorambucil and cyclophosphamide) have been used either as

adjuvants to corticosteroids or as stand-alone agents.30 However, these
agents have their own severe side effects which may hinder their use.
Biological response modifiers, such as tumor necrosis factor-a inhibitors
(eg, infliximab and adalimumab) are a relatively new class of medications
that can be successfully used as adjuvants to, or in lieu of, corticosteroids
and other immunosuppressive therapies in certain types of uveitis if
there is inadequate response or intolerance to steroid or conventional
immunosuppressive treatment.31
Interestingly, topical, periocular, and intravitreal administration of
nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to
reduce intraocular inflammation in experimental uveitis, and used by
some in the initial treatment of certain uveitic conditions such as Posner-
Schlossman syndrome.32–36 Oral NSAIDs have shown promise in the
treatment of certain types of uveitis, which may reduce dependence on
corticosteroids in chronic or recurrent cases.37,38 The use of NSAIDs in
the management of uveitis is a potential area for further inquiry.
However, some evidence suggests that topical and systemic NSAIDs
may interfere with the ocular hypotensive effects of certain antiglaucoma
medications such as prostaglandin analogs (PGAs) (eg, latanoprost) and
a-agonists (eg, brimonidine).39–41
IOP-lowering Medications
IOP-lowering medications in uveitic glaucoma, as in primary open-
angle glaucoma (POAG), are prescribed in a stepped, incremental fashion.
However, certain considerations need to be taken into account, as these
drugs may behave differently in the presence of intraocular inflammation
or when concomitantly administered with corticosteroids. Topical b-
adrenergic antagonists (b-blockers) have for long been considered the
initial treatment of choice for uveitis-associated IOP elevation due to their
relative efficacy and low incidence of local side effects and low cost. When
systemic contraindications such as bronchial asthma or bradyarrhythmias
do not exist, a twice daily dose of a nonselective b-blocker such as timolol is
prescribed.14 Other nonselective b-blockers such as levobunolol and
carteolol may also be used and have shown similar efficacy to timolol.42,43
Selective b1-blockers, such as betaxolol, have less systemic respiratory side
effects, but are less effective than timolol in lowering IOP.44
Carbonic anhydrase inhibitors (CAIs) suppress aqueous humor
production. Topical formulations, such as dorzolamide, may be used
either alone or as a fixed combination with timolol. However, their IOP-
lowering action may be modest in uveitic glaucoma, and may occasion-
ally result in profound hypotony in long-standing cases.7 Systemic
administration of CAIs is associated with systemic adverse effects
(including diuresis, malaise, gastrointestinal upset, tingling in the

extremities, and metabolic changes) but can be used carefully in select

patients with uveitic glaucoma, especially in cases with poorly controlled
IOP that are pending surgery or when surgery is not a good option.
a-2 adrenergic agonists, such as brimonidine, may be used as second-
line agents. Apraclonidine, a short-acting a-2 agonist, may be used to
treat acute IOP spikes. Miotics, such as pilocarpine and echothiophate
iodide may enhance synechial formation and increase inflammation by
disrupting the blood-aqueous barrier,16 and are therefore better avoided
in uveitic glaucoma.
Of note, a lack of consensus exists on the role of PGAs in the
management of uveitic glaucoma. PGAs, such as latanoprost, travoprost,
and bimatoprost, are potent ocular hypotensive medications that decrease
IOP by increasing uveoscleral outflow of aqueous humor,45 and are first-
line agents in the treatment of POAG. In theory, PGAs may have a
proinflammatory effect inherent to their mechanism of action.46 Studies
have, however, demonstrated that low-dose PGAs may have a regulatory
role in ocular inflammation and even some anti-inflammatory action.47
Although latanoprost has been demonstrated to disrupt the blood-aqueous
barrier in patients with risk factors such as recent history of cataract
surgery,48 no evidence demonstrates that it disrupts blood-aqueous barrier
in subjects without such risk factors.49 Anecdotal reports of reactivation of
preexisting intraocular inflammation in quiescent eyes or exacerbation of
existing inflammation after administration of PGAs exist,50–53 with many
advocating their avoidance or cautious use in uveitic glaucoma. Cystoid
macular edema has also been reported in patients receiving PGAs.52,54–59
However, many of these cases had risk factors such as posterior capsular
rupture in cataract surgery, are case reports, and evidence exists that the
use of PGAs in uveitic patients does not carry an increased risk of cystoid
macular edema development.60
Anecdotal reports of reactivation of herpetic keratitis or keratouveitis
upon treatment with PGAs also exist.61–63 However, it has been shown by
virological measures that latanoprost does not promote ocular shedding
of the virus,64 and population-based epidemiologic studies do not show
any statistically significant association between the use of PGAs and
reactivation of ocular herpes simplex virus.65 Lately, the use of PGAs in
uveitic glaucoma has been gaining popularity, with evidence of their
safety and efficacy when intraocular inflammation is promptly con-
trolled.14,60,66 In the authors’ experience, PGAs appears to be both safe
and effective in controlling IOP in eyes with uveitis, and are used as first-
line agents in uveitic glaucoma.
Cycloplegic-Mydriatic Agents
Topical cycloplegic-mydriatic agents, such as atropine 1%, homa-
tropine 1%, tropicamide 1%, cyclopentolate 1%, and scopolamine, are

muscarinic antagonists that are typically used in intraocular inflamma-

tion to relieve ciliary muscle spasm, minimize posterior synechiae
formation, and break newly formed synechiae. Predominantly mydriatic
agents, such as phenylephrine 2.5%, may also be used to prevent
synechial formation. Potent agents, such as atropine or homatropine,
may be helpful in cases where glaucoma is induced by anterior
displacement of iris lens-diaphragm or anterior rotation of the ciliary
body.67 However, caution must be exercised as the use of these agents
may precipitate acute angle closure,68 and agents with a long-acting
mydriatic action may result in posterior synechiae formation in the
dilated position in the setting of uncontrolled inflammation.
’ Surgical Management of Uveitic Glaucoma
The chronic or recurrent nature of intraocular inflammation usually

associated with uveitic glaucoma results in a gradual destructive process
involving the ciliary body,69 with a greater propensity to develop
postoperative hypotony after glaucoma surgery. Acute inflammatory
episodes result in cyclitis, which may predispose the eye to postoperative
hypotony as well. Ultrasound biomicroscopy imaging has demonstrated
atrophy and inflammation of the ciliary body in patients with uveitis.70
Therefore, the choice of the appropriate surgical procedure in uveitic
glaucoma is influenced by the tendency of the procedure to precipitate
hypotony.
Secondary angle-closure glaucoma with pupillary block in the setting
of uveitic glaucoma is challenging to manage with LPI, as posterior
chamber and broad iridocorneal adhesions may be present, rendering the
procedure less or ineffective with a possibility of inflicting laser trauma to
corneal endothelium.67 Moreover, LPIs can close in the presence of
continued intraocular inflammation and occasionally >1 LPI is necessary
to pupillary block glaucoma associated with inflammation. In cases where a
fibrin membrane occludes the pupil, intracameral injection of tissue
plasminogen activator may be tried.67 When pharmacologic therapy is
ineffective, surgical peripheral iridectomy with or without posterior
synechiolysis and goniosynechiolysis can be attempted. The authors often
place 2 LPIs in association with aggressive steroid treatment in severe
inflammatory pupillary block, as in many such cases at least 1 LPI will
remain patent. Nd:YAG LPI may induce less inflammation and require
fewer applications with a reduction of total energy delivered to the iris as
compared with argon LPI in cases of uveitis.71 The combined use of both
lasers appears to be more effective than argon laser alone in thick brown
irides with a lower incidence of iris bleeding.72
Selective laser trabeculoplasty using 532-nm Q-switched Nd:YAG
laser has been tried when medical treatment fails to control IOP and

before proceeding with surgery.14 However, there is no evidence

supporting its utility in uveitic glaucoma and the authors feel that laser
to an open angle may cause angle closure in the context of ocular
inflammation and do not recommend laser trabeculoplasty for the
treatment of uveitic glaucoma, in addition to the fact that laser
trabeculoplasty is not effective immediately and therefore not helpful
in the treatment of acute uveitic glaucoma.
Issues With Trabeculectomy in Uveitic Glaucoma

Minimizing intraocular inflammation before proceeding with trabecu-
lectomy in uveitic glaucoma is crucial. A regimen of preoperative topical,
systemic, or depot infraorbital corticosteroids can be useful in reducing the
amount of intraocular inflammation and the inflammatory cell population
in the conjunctiva.73,74 Trabeculectomy success rates may be negatively
influenced by the accelerated wound-healing process because of an
enhanced inflammatory postoperative fibrocellular response,75 and low-
grade anterior chamber inflammation may result in encapsulated blebs.76
Studies reported relatively poor outcomes when trabeculectomy is not
enhanced with adjuvant antimetabolites in uveitic glaucoma, with success
rates ranging from 30% to 54%.77,78 Success rates improved up to 78%
with the use of adjuvant 5-FU. Trabeculectomy augmented with intra-
operative mitomycin C (MMC) has largely replaced trabeculectomy with 5-
FU, although results were comparable to those achieved with 5-FU in
uveitic glaucoma.79–82 Trabeculectomy with MMC was less effective in the
treatment of uveitic glaucoma compared with POAG.83
Cataract is very common in cases of uveitis, and trabeculectomy is
known to enhance cataract formation.84 Eyes with uveitic glaucoma
required cataract surgery more often after trabeculectomy.83 This places
the glaucoma specialist in a challenging situation, as cataract extraction
may compromise the IOP-lowering effectiveness of trabeculectomy,85
and the results of isolated trabeculectomy were reported to be better
than when combined with cataract extraction in some reports.86 It is
therefore ideal to perform cataract surgery before trabeculectomy if
there is preexisting cataract to minimize postoperative inflammation.67
However, the often emergent nature of glaucoma filtration surgery may
preclude such elective planning.
In addition to enhanced cataract formation, complications following
augmented trabeculectomy in uveitic glaucoma include bleb leakage,
overfiltration, hypotony, hypotony maculopathy, choroidal effusion, hy-
phema, macular edema, exacerbation of uveitis, raised IOP, and use of
glaucoma medications to control elevated IOP.79,81,87,88 It is difficult to
precisely determine the incidence and severity of these complications in
uveitic trabeculectomy, as most of the reports of these complications are
anecdotal. As overfiltration and hypotony can have severe consequences in

the uveitic patient, secure scleral flap closure to avoid these complications is
important. The long-term outcome of trabeculectomy in the uveitic patient
may be compromised in the setting of recurrent inflammation. Therefore,
it is crucial to maintain patients on long-term corticosteroid therapy to halt
the fibrocellular response and minimize the healing process to increase the
success of trabeculectomy in IOP control.
The Role of Deep Sclerectomy in Uveitic Glaucoma

Recently, nonpenetrating filtering glaucoma surgery, such as deep
sclerectomy, has become a popular alternative to trabeculectomy in
many centers. The procedure involves creating 2 scleral flaps (superficial
and deep), dissecting the deeper flap, and deroofing Schlemm canal. Its
inherent features such as nonopening of the anterior chamber, lack of a
peripheral iridectomy, and therefore, less postoperative inflammation
may be advantageous when compared with penetrating surgery. The
procedure had commendable success rates and lower incidence of
complications on long-term follow-up as compared with trabeculectomy
in POAG and other types of glaucoma.89–93
Preliminary data suggest that deep sclerectomy may be reasonably
effective and safe in uveitic glaucoma.94 A retrospective study comparing
the safety and efficacy of deep sclerectomy to MMC-augmented
trabeculectomy in uveitic glaucoma demonstrated equivalent IOP
control afforded by both the procedures.95 Although deep sclerectomy
resulted in less early postoperative intraocular inflammation, closer
monitoring for adjustment of IOP-lowering interventions was required.
Deep sclerectomy might therefore be less appropriate for managing
patients in whom close monitoring is difficult. In another retrospective
study, deep sclerectomy had fewer complications than did trabeculec-
tomy in juvenile uveitic glaucoma, but resulted in less IOP reduction and
higher probability of future surgical intervention.96 In a prospective
study by Al Obeidan et al,97 33 eyes of 21 consecutive patients with
uveitic glaucoma underwent MMC-augmented deep sclerectomy. Laser
goniopuncture was performed in cases with uncontrolled postoperative
IOP. Patients were followed up for 33.2 ± 19.8 months after the
procedure. Although the rate of serious complications such as hypotony
with persistent maculopathy was low, additional IOP reduction by means
of laser goniopuncture was frequently required. A large randomized-
controlled trial comparing deep sclerectomy to trabeculectomy in uveitic
glaucoma is necessary to determine the relative long-term safety and
efficacy of the procedure. However, such study would be difficult to
undertake, as uncontrolled assignment of subjects to further anti-
inflammatory or IOP-lowering interventions might be necessitated by
the nature of the disease. The authors feel that deep sclerectomy may be
a useful approach in patients with mild but not severe uveitic glaucoma.

The Role of Minimally Invasive Glaucoma Surgery (MIGS) in

Uveitic Glaucoma
MIGS is a collective term encompassing a range of nonpenetrating
glaucoma procedures. The rationale behind these procedures is to
provide a safer alternative to penetrating glaucoma surgery while still
producing IOP reduction. However, the paucity of safety and efficacy
data of many of these procedures, particularly for secondary glaucomas,
makes it difficult to precisely determine their potential role in the
management of uveitic glaucoma. Moreover, their IOP-lowering effect
and reproducibility as compared to traditional filtering procedures is
unknown.
The Ex-PRESS glaucoma shunt (Alcon Laboratories Inc., Fort
Worth, TX) is a metallic device implanted ab externo under a scleral
flap and drains aqueous into the subconjunctival space. Ex-PRESS
glaucoma shunt has shown favorable outcomes on 5-year analysis
compared with penetrating surgery in POAG.98 Its role in the manage-
ment of uveitic glaucoma has not been extensively studied. However, in a
small series of 5 patients with uveitic glaucoma, the device has
demonstrated promising IOP-lowering effect on short-term follow-
up.99 Larger studies are, however, needed to determine its relative
long-term safety, efficacy, and reproducibility in uveitic glaucoma as
compared with well-established surgical procedures. In addition, as a
scleral flap is required, inflammation from uveitis may limit the long-
term function of the device to levels similar to that of trabeculectomy.
Canaloplasty, another ab externo MIGS, uses circumferential
viscodilation and tensioning of Schlemm canal using a microcatheter
(iTrack 250A; iScience Interventional Corp., Menlo Park, CA). The
procedure has been shown to cause a significant and sustained IOP
reduction in POAG on 3-year analysis.100 As with the Ex-PRESS
glaucoma shunt, only limited data on the safety and efficacy of canal-
oplasty as a primary surgical procedure in uveitic glaucoma exists. A
retrospective case series of 19 eyes with uveitic glaucoma that underwent
canaloplasty with or without simultaneous cataract extraction, with a
mean follow-up of 1-year demonstrated surgical success (IOP < 21 and
> 6mm Hg, and > 20% reduction from baseline on 2 consecutive visits,
without ocular hypotensive medications) in 73.7% of eyes.101 However,
this data needs confirmation with a much larger case series.
Cyclophotocoagulation (CPC) is a cyclodestructive procedure using
a diode laser. Endocyclophotocoagulation (ECP), where ablation of the
ciliary body is achieved through endoscopic diode laser application to
the ciliary processes under direct visualization, has been used in the
management of end-stage glaucoma and pediatric glaucomas, with
success rates comparable to those of transscleral cyclophotocoagulation
(TSCPC).102–105 Some are also using ECP in mild glaucoma in the

context of cataract surgery to decrease the amount of medical IOP-

lowering therapy. The scope of ECP has gradually expanded, with more
eyes with better visual potential now undergoing the procedure.106,107
The major postoperative complication with TSCPC is intense intraocular
inflammation, with the majority of eyes developing postoperative
inflammation/uveitis.108 Intraocular inflammation is also the most
common complications of ECP.104 As with TSCPC, another main risk
of ECP is postoperative hypotony, which is a major concern in uveitic
glaucoma. However, postoperative hypotony seems to be less of a
problem with ECP,104,109 and ECP appears to have a better overall
adverse event profile than does TSCPC.104,105,110 To our knowledge, the
role of ECP in the management of uveitic glaucoma has not been
investigated. The potential risks of postoperative inflammation and
hypotony, however, limit the role of CPC in the treatment of uveitic
glaucoma and may exacerbate uveitis with increased inflammation. The
authors do not in general recommend the use of CPC for the treatment
of uveitic glaucoma because of the possible increased inflammation and
possible overtreatment with hypotony.
The trabectome (Neomedix Corp., Tustin, CA) is a thermal cautery
device used to perform a procedure that is sometimes referred to as ab
interno trabeculectomy, where a segment of the TM and Schlemm canal
is ablated under direct vision using a gonioscopy lens. The trabectome
may be performed simultaneously with cataract extraction. The trabec-
tome procedure had promising IOP-lowering effects and decreased
number of antiglaucoma medications in POAG and many secondary
glaucomas.111–116 Jordan et al117 conducted a large single-center pro-
spective observational study looking at the safety and efficacy of the
trabectome procedure in POAG and secondary open-angle glaucomas.
They enrolled 22 patients with uveitic glaucoma who underwent the
trabectome procedure. The mean preoperative IOP and medications
used for the uveitic glaucoma subgroup were 31.7 ± 10.7 and
1.7 ± 1.3 mm Hg, respectively. The mean postoperative IOP and
medications used were 25.7 ± 11.9 and 1.6 ± 1.1 mm Hg, respectively.
Unfortunately, no further subgroup analysis was performed. Long-term
follow-up of the trabectome is needed to determine its efficacy as the
angle may have an increased risk of closure in the context of
inflammation from uveitis.
The Role of Glaucoma Drainage Implants (GDIs) in Uveitic

Glaucoma
Two categories of GDIs exist: valved [eg, Ahmed glaucoma implant
(AGI; New World Medical Inc., Rancho Cucamonga, CA)] and non-
valved [eg, Molteno glaucoma implant (MGI; Molteno Ophthalmic Ltd.,
Dunedin, New Zealand) and Baerveldt glaucoma implant (BGI; AMO

Inc., Irvine, CA)]. A Cochrane review in 2006 concluded from meta-

analysis of available literature at the time that no evidence that one GDI
type is clearly superior to another exists.118 The traditional indications
for the use of GDIs in uveitic glaucoma have been uveitic glaucoma
secondary to JIA, previous failed trabeculectomy, aphakia, eyes with
prior silicone oil injection, and cases complicated by neovasculariza-
tion.67 However, a trend to use GDIs as the primary surgical procedure
of choice in uveitic glaucoma is growing.119
AGI houses a valve composed of 2 thin elastic membranes that close
when IOP falls <8 to 12 mm Hg and open if IOP is higher. Theoretically,
this makes valved GDIs less prone to postoperative hypotony. However,
transient hypotony is not uncommon following AGI implantation,120 and
has been reported to be as high as 42.8% in eyes with uveitic
glaucoma.121 Persistent hypotony may result from valve failure or
operative damage. In a retrospective noncomparative case series, AGI
implantation in 21 eyes with uveitic glaucoma with an average post-
operative follow-up of 24.5 months122 had IOPs between 5 and 18 mm
Hg at the most recent follow-up visit, and the average number of
antiglaucoma medications required to achieve target pressure decreased
from 3.5 before surgery to 0.6 after surgery. No eyes lost any lines of
Snellen acuity. One eye developed early postoperative hypotony that
resolved with no intervention, and another eye developed hypotony
with maculopathy after 20 months of follow-up. The reason for
hypotony in the latter was believed to be related to thinning of the
pseudocapsule surrounding the implant plate. Intrableb autologous
blood injection and tube ligature to narrow the lumen were required to
correct the hypotony.
In another interventional retrospective case series, 4-year outcomes
were evaluated in 60 eyes with uveitic glaucoma that underwent AGI
implantation (mean follow-up time was 30 mo).123 Success rates at 1 and
4 years were 77% and 50%, respectively (success was defined as IOP 5 to
21 mm Hg, reduced by 25% from preimplantation IOP). However,
success rates were lower at the same timepoints (57% and 39%,
respectively) when eyes with sight-threatening complications (eg, hypot-
ony maculopathy, retinal detachment, corneal decompensation, endoph-
thalmitis, or phthisis bulbi) were excluded. The overall rate of
complications was 12%/person-years. The rate of severe hypotony
associated with maculopathy, flat anterior chamber, and/or choroidal
effusion was 1.2%/person-years.
Nonvalved glaucoma implants lack fluid egress restriction mecha-
nisms. Therefore, complete tube occlusion with fluid-tight absorbable
external ligatures is necessary to prevent severe early postoperative
hypotony until sufficient plate encapsulation occurs, which would provide
the necessary aqueous egress resistance to prevent severe hypotony.
Internal stenting of the tube may be employed in addition to, or in lieu

of, external ligature. Early postoperative elevated IOP may be minimized

by tube fenestrations proximal to ligatures, topical antiglaucoma medi-
cations, and if necessary, systemic CAIs. However, sudden decompression,
severe hypotony, and choroidal effusion may still occur after ligatures
absorb, particularly in implants with a large plate surface area.
Insertion of MGI was found to be a reasonably successful strategy in
the primary surgical management of uveitic glaucoma. Outcomes better
than trabeculectomy was observed in eyes with marked inflammation.124
Molteno et al125 reported an IOP control success rate of 76% on long-
term follow-up (mean, 7.1 y) in 40 study eyes with uveitic glaucoma
followed prospectively followed MGI surgery. GDI failures were
attributed mainly to previous surgery, persistent inflammation, and
advanced disease. Complications were mainly related to blockage of the
drainage tube resulting in elevated IOP, or hypotony resulting in flat
anterior chamber and choroidal detachment. Postoperative hypotony or
phthisis bulbi occurred in 15% of cases. However, they were associated
more frequently with the older 2-plate implant, and this incidence was
higher in eyes that were blind preoperatively. Although IOP reduction
achieved by MGI may be suboptimal in the early postoperative period,
IOP continued to decrease during the first year after surgery, and
antiglaucoma medications were slowly tapered for up to 3 postoperative
years.126 Late postoperative hypotony was a complication in 2 of 30 eyes.
Three cases of hypotony with flat anterior chamber of 27 eyes of patients
with JIA were reported in whom MGI was implanted.127 Hypotony
resolved spontaneously in all 3 eyes, and no eyes developed persistent
hypotony with an IOP<6 mm Hg.
BGI, like the MGI, is a nonvalved glaucoma drainage implant. The
large surface area of the plate is believed to contribute to the continued
IOP-lowering effect of the implant. In a retrospective case series of 24
eyes with intractable uveitic glaucoma that underwent BGI implantation,
surgical success rate was 91.7% at 1 and 2 years, with success defined as
IOPr21 and Z5 mm Hg without antiglaucoma medications or further
glaucoma surgery, and with no loss of light perception vision, chronic
hypotony, or phthisis bulbi. Three eyes had hypotony maculopathy and
4 eyes had choroidal effusions. Intractable postoperative hypotony was
the cause of failure in 2 eyes. Common characteristics in these 2 cases
were young age at time of surgery (18 and 21 y old) female sex, and
aphakia. Both eyes received an implant with a plate size of 350 mm2,
which was used in 21 of 24 eyes.
To the best of our knowledge, no studies comparing valved and
nonvalved glaucoma drainage implants in uveitic glaucoma exist to date.
The Ahmed-Baerveldt Comparison study found that AGI implantation
was associated with a significantly higher IOP at 1 year of follow-up,
whereas BGI implantation resulted in a significantly higher rate of overall
postoperative complications and a higher rate of sight-threatening

complications.128 However, only 2 of 133 eyes in the BGI group

experienced persistent hypotony. The Ahmed versus Baerveldt study
enrolled 238 eyes, 23 of which were uveitic glaucoma eyes (10 received
AGI; 13 received BGI).129 Three-year results showed higher surgical
success rate in the BGI group, but the hypotony-related complications
(suprachoroidal hemorrhage, choroidal/retinal detachment, and persistent
severe hypotony requiring explantation) were significantly higher in that
group (6 eyes (7%); compared with no eyes in the AGI group). No
glaucoma-type subset analysis showing specific success or complication
rates was done. A BGI (with a plate surface area of 350 mm2) is the authors’
current primary surgical procedure of choice in uveitic glaucoma.
Corticosteroid Implants in Uveitic Glaucoma: Risks and

Benefits
Corticosteroid sustained-release implants may be indicated in uveitic
cases that are resistant to or require multiple direct injections of
corticosteroids into the vitreous, such as cases with severe macular
edema. Devices releasing triamcinolone acetonide (eg, I-vation; Sur-
Modics, Eden Prairie, MN), fluocinolone acetonide (eg, Retisert; Bausch
and Lomb, Rochester, NY), and dexamethasone (eg, Ozurdex; Allergan
Inc., Irvine, CA) are available commercially. Despite the efficacy of these
implants in controlling inflammation and reducing macular edema, IOP
elevation is a common complication.130,131 A 45% glaucoma surgery rate
was observed in eyes that received a fluocinolone acetonide implant.132
The Multicenter Uveitis Steroid Treatment Trial showed that fluocino-
lone acetonide implants had a >4-fold higher risk of IOP elevation of
10 mm Hg or more, absolute IOP of 30 mm Hg or more, and of needing
medical or surgical treatment for IOP elevation as compared with
systemic anti-inflammatory therapy.133 However, dexamethasone im-
plants appear to have a lower incidence of IOP elevation than do
fluocinolone acetonide implants,134 which may be related to the shorter
duration of steroid release into the vitreous in dexamethasone implants.
Simultaneous implantation of a GDI and a corticosteroid implant in
uveitic eyes is a reasonable option. This is particularly true in eyes with
preexisting IOP elevation and eyes that are prone to develop glaucoma,
such as eyes with posterior and/or PAS. Patients who are known to have a
corticosteroid response or have risk factors are also candidates for the
combined procedure. In advanced cases in which posterior synechiae,
PAS, and/or cataract are present, it is possible to also perform posterior
synechiolysis, goniosynechiolysis, and cataract extraction. The outcome
of such combined procedures will be influenced by the degree of
inflammation, magnitude of IOP elevation, extent of glaucomatous
damage, and mechanism of glaucoma, among other factors.

’ Conclusions
Uveitic glaucomas are complex in cause of disease and response to

treatment and often require comanagement by uveitis and glaucoma
specialists. Recently, a multitude of novel medical therapies and surgical
techniques have been added to the armamentarium of existing
therapeutic modalities. More basic research and randomized-controlled
clinical trials are necessary to shed light onto the role of different anti-
inflammatory and IOP-lowering therapies and surgical interventions in
uveitic glaucoma. Despite the many controversies, continuing refine-
ment of management approaches based on our expanding experience
and evidence-based knowledge affords uveitic glaucoma patients better
opportunities for improving symptoms and preserving vision on the
long run.
The authors declare that they have no conflicts of interest to disclose.
’ References
1. Merayo-Lloves J, Power WJ, Rodriguez A, et al. Secondary glaucoma in patients with
uveitis. Ophthalmologica. 1999;213:300–304.
2. Takahashi T, Ohtani S, Miyata K, et al. A clinical evaluation of uveitis-associated
secondary glaucoma. Jpn J Ophthalmol. 2002;46:556–562.
3. Herbert HM, Viswanathan A, Jackson H, et al. Risk factors for elevated intraocular
pressure in uveitis. J Glaucoma. 2004;13:96–99.
4. Toris CB, Pederson JE. Aqueous humor dynamics in experimental iridocyclitis.
Invest Ophthalmol Vis Sci. 1987;28:477–481.
5. Weinreb RN, Toris CB, Gabelt BT, et al. Effects of prostaglandins on the aqueous
humor outflow pathways. Surv Ophthalmol. 2002;47(suppl 1):S53–S64.
6. Eakins KE, Whitelocke RA, Bennett A, et al. Prostaglandin-like activity in ocular
inflammation. Br Med J. 1972;3:452–453.
7. Kok H, Barton K. Uveitic glaucoma. Ophthalmol Clin North Am. 2002;15:375–387, viii.
8. Wilson K, McCartney MD, Miggans ST, et al. Dexamethasone induced ultra-
structural changes in cultured human trabecular meshwork cells. Curr Eye Res. 1993;
12:783–793.
9. Clark AF, Wilson K, de Kater AW, et al. Dexamethasone-induced ocular hyper-
tension in perfusion-cultured human eyes. Invest Ophthalmol Vis Sci. 1995;36:
478–489.
10. Johnson DH, Bradley JM, Acott TS. The effect of dexamethasone on glycosamino-
glycans of human trabecular meshwork in perfusion organ culture. Invest Ophthalmol
Vis Sci. 1990;31:2568–2571.
11. Goldstein DA, Godfrey DG, Hall A, et al. Intraocular pressure in patients with uveitis
treated with fluocinolone acetonide implants. Arch Ophthalmol. 2007;125:1478–1485.
12. Tektas OY, Heinz C, Heiligenhaus A, et al. Morphological changes of trabeculectomy
specimens in different kinds of uveitic glaucoma. Curr Eye Res. 2011;36:442–448.

13. Sallam A, Sheth HG, Habot-Wilner Z, et al. Outcome of raised intraocular pressure
in uveitic eyes with and without a corticosteroid-induced hypertensive response. Am
J Ophthalmol. 2009;148:207–13 e1.
14. Siddique SS, Suelves AM, Baheti U, et al. Glaucoma and uveitis. Surv Ophthalmol.
2013;58:1–10.
15. Elliot RH. A Treatise on Glaucoma. London: Oxford Medical Publications; 1918.
16. Moorthy RS, Mermoud A, Baerveldt G, et al. Glaucoma associated with uveitis. Surv
Ophthalmol. 1997;41:361–394.
17. Gaston H, Absolon MJ, Thurtle OA, et al. Steroid responsiveness in connective tissue
diseases. Br J Ophthalmol. 1983;67:487–490.
18. Becker B, Mills DW. Corticosteroids and intraocular pressure. Arch Ophthalmol.
1963;70:500–507.
19. Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol.
1965;4:198–205.
20. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics. I.
The effect of dexamethasone in the normal eye. Arch Ophthalmol. 1963;70:482–491.
21. Podos SM, Becker B, Morton WR. High myopia and primary open-angle glaucoma.
Am J Ophthalmol. 1966;62:1038–1043.
22. Cantrill HL, Palmberg PF, Zink HA, et al. Comparison of in vitro potency of
corticosteroids with ability to raise intraocular pressure. Am J Ophthalmol. 1975;79:
1012–1017.
23. Assil KK, Massry G, Lehmann R, et al. Control of ocular inflammation after cataract
extraction with rimexolone 1% ophthalmic suspension. J Cataract Refract Surg.
1997;23:750–757.
24. Foster CS, Alter G, DeBarge LR, et al. Efficacy and safety of rimexolone 1%
ophthalmic suspension vs 1% prednisolone acetate in the treatment of uveitis. Am J
Ophthalmol. 1996;122:171–182.
25. Bron A, Denis P, Hoang-Xuan TC, et al. The effects of Rimexolone 1% in
postoperative inflammation after cataract extraction. A double-masked placebo-
controlled study. Eur J Ophthalmol. 1998;8:16–21.
26. Amon M, Busin M. Loteprednol etabonate ophthalmic suspension 0.5%: efficacy
and safety for postoperative anti-inflammatory use. Int Ophthalmol. 2012;32:
507–517.
27. Kalina RE. Increased intraocular pressure following subconjunctival corticosteroid
administration. Arch Ophthalmol. 1969;81:788–790.
28. Fitzgerald JT, Saunders L, Ridge B, et al. Severe intraocular pressure response to
periocular or intravitreal steroid treatment in Australia and New Zealand: data from
the Australian and New Zealand Ophthalmic Surveillance Unit. Clin Experiment
Ophthalmol. 2014. Available at: http://onlinelibrary.wiley.com/doi/10.1111/ceo.12433/
abstract.
29. Rhee DJ, Peck RE, Belmont J, et al. Intraocular pressure alterations following
intravitreal triamcinolone acetonide. Br J Ophthalmol. 2006;90:999–1003.
30. Jabs DA, Rosenbaum JT, Foster CS, et al. Guidelines for the use of immunosup-
pressive drugs in patients with ocular inflammatory disorders: recommendations of
an expert panel. Am J Ophthalmol. 2000;130:492–513.
31. Pasadhika S, Rosenbaum JT. Update on the use of systemic biologic agents in the
treatment of noninfectious uveitis. Biologics. 2014;8:67–81.
32. Bucolo C, Marrazzo G, Platania CB, et al. Effects of topical indomethacin, bromfenac
and nepafenac on lipopolysaccharide-induced ocular inflammation. J Pharm
Pharmacol. 2014;66:954–960.
33. Hayasaka Y, Hayasaka S, Zhang XY, et al. Effects of topical anti-inflammatory and
antiallergic eyedrops on prostaglandin E2-induced aqueous flare elevation in
pigmented rabbits. Arch Ophthalmol. 2002;120:950–953.

34. Rabiah PK, Fiscella RG, Tessler HH. Intraocular penetration of periocular ketorolac
and efficacy in experimental uveitis. Invest Ophthalmol Vis Sci. 1996;37:613–618.
35. Baranano DE, Kim SJ, Edelhauser HF, et al. Efficacy and pharmacokinetics of
intravitreal non-steroidal anti-inflammatory drugs for intraocular inflammation. Br J
Ophthalmol. 2009;93:1387–1390.
36. Hung PT, Chang JM. Treatment of glaucomatocyclitic crises. Am J Ophthalmol.
1974;77:169–172.
37. Fiorelli VM, Bhat P, Foster CS. Nonsteroidal anti-inflammatory therapy and
recurrent acute anterior uveitis. Ocul Immunol Inflamm. 2010;18:116–120.
38. Suelves AM, Martinez-Castillo S, Salavert M, et al. Celecoxib for recurrent
sclerouveitis after syphilitic panuveitis. A case report. J Ophthalmic Inflamm Infect.
2011;1:185–187.
39. Kashiwagi K, Tsukahara S. Effect of non-steroidal anti-inflammatory ophthalmic
solution on intraocular pressure reduction by latanoprost. Br J Ophthalmol.
2003;87:297–301.
40. Sponsel WE, Paris G, Trigo Y, et al. Latanoprost and brimonidine: therapeutic and
physiologic assessment before and after oral nonsteroidal anti-inflammatory
therapy. Am J Ophthalmol. 2002;133:11–18.
41. Chiba T, Kashiwagi K, Chiba N, et al. Effect of non-steroidal anti-inflammatory
ophthalmic solution on intraocular pressure reduction by latanoprost in patients
with primary open angle glaucoma or ocular hypertension. Br J Ophthalmol.
2006;90:314–317.
42. Akafo SK, Thompson JR, Rosenthal AR. A cross-over trial comparing once daily
levobunolol with once and twice daily timolol. Eur J Ophthalmol. 1995;5:172–176.
43. Ohno S, Ichiishi A, Matsuda H. Hypotensive effect of carteolol on intraocular
pressure elevation and secondary glaucoma associated with endogenous uveitis.
Ophthalmologica. 1989;199:41–45.
44. Berry DP Jr, Van Buskirk EM, Shields MB. Betaxolol and timolol. A comparison of
efficacy and side effects. Arch Ophthalmol. 1984;102:42–45.
45. Toris CB, Camras CB, Yablonski ME. Effects of PhXA41, a new prostaglandin F2
alpha analog, on aqueous humor dynamics in human eyes. Ophthalmology.
1993;100:1297–1304.
46. Eakins KE. Prostaglandin and non-prostaglandin mediated breeakdown of the
blood-aqueous barrier. Exp Eye Res. 1977;25(suppl):483–498.
47. Bazan NG, Allan G. Signal transduction and gene expression in the eye: a
contemporary view of the pro-inflammatory, anti-inflammatory and modulatory
roles of prostaglandins and other bioactive lipids. Surv Ophthalmol. 1997;41(suppl 2):
S23–S34.
48. Miyake K, Ota I, Maekubo K, et al. Latanoprost accelerates disruption of the blood-
aqueous barrier and the incidence of angiographic cystoid macular edema in early
postoperative pseudophakias. Arch Ophthalmol. 1999;117:34–40.
49. Stjernschantz JW. From PGF(2alpha)-isopropyl ester to latanoprost: a review of the
development of xalatan: the Proctor Lecture. Invest Ophthalmol Vis Sci.
2001;42:1134–1145.
50. Smith SL, Pruitt CA, Sine CS, et al. Latanoprost 0.005% and anterior segment
uveitis. Acta Ophthalmol Scand. 1999;77:668–672.
51. Fechtner RD, Khouri AS, Zimmerman TJ, et al. Anterior uveitis associated with
latanoprost. Am J Ophthalmol. 1998;126:37–41.
52. Wand M, Gaudio AR, Shields MB. Latanoprost and cystoid macular edema in high-
risk aphakic or pseudophakic eyes. J Cataract Refract Surg. 2001;27:1397–1401.
53. Warwar RE, Bullock JD, Ballal D. Cystoid macular edema and anterior uveitis
associated with latanoprost use. Experience and incidence in a retrospective review
of 94 patients. Ophthalmology. 1998;105:263–268.

54. Rowe JA, Hattenhauer MG, Herman DC. Adverse side effects associated with
latanoprost. Am J Ophthalmol. 1997;124:683–685.
55. Heier JS, Steinert RF, Frederick AR Jr. Cystoid macular edema associated with
latanoprost use. Arch Ophthalmol. 1998;116:680–682.
56. Callanan D, Fellman RL, Savage JA. Latanoprost-associated cystoid macular edema.
Am J Ophthalmol. 1998;126:134–135.
57. Wand M, Gaudio AR. Cystoid macular edema associated with ocular
hypotensive lipids. Am J Ophthalmol. 2002;133:403–405.
58. Moroi SE, Gottfredsdottir MS, Schteingart MT, et al. Cystoid macular edema
associated with latanoprost therapy in a case series of patients with glaucoma and
ocular hypertension. Ophthalmology. 1999;106:1024–1029.
59. Lima MC, Paranhos A Jr, Salim S, et al. Visually significant cystoid macular edema in
pseudophakic and aphakic patients with glaucoma receiving latanoprost. J Glaucoma.
2000;9:317–321.
60. Chang JH, McCluskey P, Missotten T, et al. Use of ocular hypotensive prostaglandin
analogues in patients with uveitis: does their use increase anterior uveitis and cystoid
macular oedema? Br J Ophthalmol. 2008;92:916–921.
61. Kroll DM, Schuman JS. Reactivation of herpes simplex virus keratitis after initiating
bimatoprost treatment for glaucoma. Am J Ophthalmol. 2002;133:401–403.
62. Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J
Ophthalmol. 1999;127:602–604.
63. Ekatomatis P. Herpes simplex dendritic keratitis after treatment with latanoprost for
primary open angle glaucoma. Br J Ophthalmol. 2001;85:1008–1009.
64. Gordon YJ, Yates KA, Mah FS, et al. The effects of Xalatan on the recovery of ocular
herpes simplex virus type 1 (HSV-1) in the induced reactivation and spontaneous
shedding rabbit models. J Ocul Pharmacol Ther. 2003;19:233–245.
65. Bean G, Reardon G, Zimmerman TJ. Association between ocular herpes simplex
virus and topical ocular hypotensive therapy. J Glaucoma. 2004;13:361–364.
66. Horsley MB, Chen TC. The use of prostaglandin analogs in the uveitic patient. Semin
Ophthalmol. 2011;26:285–289.
67. Kulkarni A, Barton K. Uveitic glaucoma. In: Shaarawy TM, Sherwood MB,
Hitchings RA, Crowston JC, eds. Glaucoma Volume I, 2nd edition; St. Louis, MO:
Saunders Ltd.; 2015.
68. Brooks AM, West RH, Gillies WE. The risks of precipitating acute angle-closure
glaucoma with the clinical use of mydriatic agents. Med J Aust. 1986;145:
34–36.
69. Gilger BC, Malok E, Cutter KV, et al. Characterization of T-lymphocytes in the
anterior uvea of eyes with chronic equine recurrent uveitis. Vet Immunol Immunopa-
thol. 1999;71:17–28.
70. Roters S, Szurman P, Engels BF, et al. Ultrasound biomicroscopy in chronic ocular
hypotony: its impact on diagnosis and management. Retina. 2002;22:581–588.
71. Robin AL, Pollack IP. A comparison of neodymium: YAG and argon laser
iridotomies. Ophthalmology. 1984;91:1011–1016.
72. McAllister JA, Schwartz LW, Moster M, et al. Laser peripheral iridectomy comparing
Q-switched neodymium YAG with argon. Trans Ophthalmol Soc U K. 1985;104(pt 1):
67–69.
73. Broadway DC, Bates AK, Lightman SL, et al. The importance of cellular changes in
the conjunctiva of patients with uveitic glaucoma undergoing trabeculectomy. Eye
(Lond). 1993;7(pt 4):495–501.
74. Sung VC, Barton K. Management of inflammatory glaucomas. Curr Opin Ophthalmol.
2004;15:136–140.
75. Skuta GL, Parrish RK II. Wound healing in glaucoma filtering surgery. Surv
Ophthalmol. 1987;32:149–170.

76. Ophir A, Ticho U. Delayed filtering bleb encapsulation. Ophthalmic Surg. 1992;23:
38–39.
77. Stavrou P, Murray PI. Long-term follow-up of trabeculectomy without antimetabo-
lites in patients with uveitis. Am J Ophthalmol. 1999;128:434–439.
78. Towler HM, Bates AK, Broadway DC, et al. Primary trabeculectomy with q5-
fluorouracil for glaucoma secondary to uveitis. Ocul Immunol Inflamm. 1995;3:163–170.
79. Ceballos EM, Beck AD, Lynn MJ. Trabeculectomy with antiproliferative agents in
uveitic glaucoma. J Glaucoma. 2002;11:189–196.
80. Prata JA Jr, Neves RA, Minckler DS, et al. Trabeculectomy with mitomycin
C in glaucoma associated with uveitis. Ophthalmic Surg. 1994;25:616–620.
81. Novak-Laus K, Mandic Z, Ivekovic R, et al. Trabeculectomy with mitomycin C in
glaucoma associated with uveitis. Coll Antropol. 2005;29(suppl 1):17–20.
82. Wright MM, McGehee RF, Pederson JE. Intraoperative mitomycin-C for glaucoma
associated with ocular inflammation. Ophthalmic Surg Lasers. 1997;28:370–376.
83. Iwao K, Inatani M, Seto T, et al. Long-term outcomes and prognostic factors for
trabeculectomy with mitomycin C in eyes with uveitic glaucoma: a retrospective
cohort study. J Glaucoma. 2014;23:88–94.
84. Lichter PR, Musch DC, Gillespie BW, et al. Interim clinical outcomes in the
Collaborative Initial Glaucoma Treatment Study comparing initial treatment
randomized to medications or surgery. Ophthalmology. 2001;108:1943–1953.
85. Chen PP, Weaver YK, Budenz DL, et al. Trabeculectomy function after cataract
extraction. Ophthalmology. 1998;105:1928–1935.
86. Park HJ, Weitzman M, Caprioli J. Temporal corneal phacoemulsification combined
with superior trabeculectomy. A retrospective case-control study. Arch Ophthalmol.
1997;115:318–323.
87. Yalvac IS, Sungur G, Turhan E, et al. Trabeculectomy with mitomycin-C in uveitic
glaucoma associated with Behcet disease. J Glaucoma. 2004;13:450–453.
88. Noble J, Derzko-Dzulynsky L, Rabinovitch T, et al. Outcome of trabeculectomy with
intraoperative mitomycin C for uveitic glaucoma. Can J Ophthalmol. 2007;42:
89–94.
89. Mermoud A, Schnyder CC, Sickenberg M, et al. Comparison of deep sclerectomy
with collagen implant and trabeculectomy in open-angle glaucoma. J Cataract Refract
Surg. 1999;25:323–331.
90. Roy S, Mermoud A. Deep sclerectomy. Dev Ophthalmol. 2012;50:29–36.
91. Shaarawy T, Karlen M, Schnyder C, et al. Five-year results of deep sclerectomy with
collagen implant. J Cataract Refract Surg. 2001;27:1770–1778.
92. Roy S, Mermoud A. How does nonpenetrating surgery work? J Fr Ophtalmol.
2006;29:1167–1174.
93. Bissig A, Rivier D, Zaninetti M, et al. Ten years follow-up after deep sclerectomy with
collagen implant. J Glaucoma. 2008;17:680–686.
94. Auer C, Mermoud A, Herbort CP. Deep sclerectomy for the management of
uncontrolled uveitic glaucoma: preliminary data. Klin Monbl Augenheilkd.
2004;221:339–342.
95. Dupas B, Fardeau C, Cassoux N, et al. Deep sclerectomy and trabeculectomy in
uveitic glaucoma. Eye (Lond). 2010;24:310–314.
96. Heinz C, Koch JM, Heiligenhaus A. Trabeculectomy or modified deep sclerectomy
in juvenile uveitic glaucoma. J Ophthalmic Inflamm Infect. 2011;1:165–170.
97. Al Obeidan SA, Osman EA, Mousa A, et al. Long-term evaluation of efficacy and
safety of deep sclerectomy in uveitic glaucoma. Ocul Immunol Inflamm.
2015;23:82–89.
98. de Jong L, Lafuma A, Aguade AS, et al. Five-year extension of a clinical trial
comparing the EX-PRESS glaucoma filtration device and trabeculectomy in primary
open-angle glaucoma. Clin Ophthalmol. 2011;5:527–533.

99. Lee JW, Chan JC, Qing L, et al. Early postoperative results and complications of
using the EX-PRESS shunt in uncontrolled uveitic glaucoma: a case series of
preliminary results. J Curr Glaucoma Pract. 2014;8:20–24.
100. Lewis RA, von Wolff K, Tetz M, et al. Canaloplasty: three-year results of circum-
ferential viscodilation and tensioning of Schlemm canal using a microcatheter to
treat open-angle glaucoma. J Cataract Refract Surg. 2011;37:682–690.
101. Kalin-Hajdu E, Hammamji K, Gagne S, et al. Outcome of viscodilation and
tensioning of Schlemm’s canal for uveitic glaucoma. Can J Ophthalmol. 2014;49:
414–419.
102. Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of
refractory glaucoma. J Glaucoma. 2008;17:238–247.
103. Kraus CL, Tychsen L, Lueder GT, et al. Comparison of the effectiveness and safety of
transscleral cyclophotocoagulation and endoscopic cyclophotocoagulation in pedia-
tric glaucoma. J Pediatr Ophthalmol Strabismus. 2014;51:120–127.
104. Chen J, Cohn RA, Lin SC, et al. Endoscopic photocoagulation of the ciliary body for
treatment of refractory glaucomas. Am J Ophthalmol. 1997;124:787–796.
105. Neely DE, Plager DA. Endocyclophotocoagulation for management of difficult
pediatric glaucomas. J AAPOS. 2001;5:221–229.
106. Kahook MY, Lathrop KL, Noecker RJ. One-site versus two-site endoscopic cyclo-
photocoagulation. J Glaucoma. 2007;16:527–530.
107. Kahook MY, Schuman JS, Noecker RJ. Endoscopic cyclophotocoagulation using iris
hooks versus viscoelastic devices. Ophthalmic Surg Lasers Imaging. 2007;38:
170–172.
108. Hawkins TA, Stewart WC. One-year results of semiconductor transscleral
cyclophotocoagulation in patients with glaucoma. Arch Ophthalmol. 1993;111:
488–491.
109. Lin SC, Chen MJ, Lin MS, et al. Vascular effects on ciliary tissue from endoscopic
versus trans-scleral cyclophotocoagulation. Br J Ophthalmol. 2006;90:496–500.
110. Bloom PA, Dharmaraj S. Endoscopic and transscleral cyclophotocoagulation. Br J
Ophthalmol. 2006;90:666–668.
111. Minckler D, Mosaed S, Dustin L, et al. Trabectome (trabeculectomy-internal
approach): additional experience and extended follow-up. Trans Am Ophthalmol
Soc. 2008;106:149–159, discussion 59-60.
112. Wecker T, Jordan JF. Minimally invasive glaucoma surgery using the trabectome.
Klin Monbl Augenheilkd. 2015;232:303–309.
113. Werth JP, Gesser C, Klemm M. Diverse effectiveness of the trabectome for different
types of glaucoma. Klin Monbl Augenheilkd. 2015;232:72–78.
114. Godfrey DG, Fellman RL, Neelakantan A. Canal surgery in adult glaucomas. Curr
Opin Ophthalmol. 2009;20:116–121.
115. Mizoguchi T, Kuroda S, Terauchi H, et al. Trabeculotomy combined with
phacoemulsification and implantation of intraocular lens for primary open-angle
glaucoma. Semin Ophthalmol. 2001;16:162–167.
116. Minckler D, Mosaed S, Francis B, et al. Clinical results of ab interno trabeculotomy
using the trabectome for open-angle glaucoma: the Mayo Clinic series in Rochester,
Minnesota. Am J Ophthalmol. 2014;157:1325–1326.
117. Jordan JF, Wecker T, van Oterendorp C, et al. Trabectome surgery for primary and
secondary open angle glaucomas. Graefes Arch Clin Exp Ophthalmol. 2013;251:
2753–2760.
118. Minckler DS, Vedula SS, Li TJ, et al. Aqueous shunts for glaucoma. Cochrane Database
Syst Rev. 2006;CD004918.
119. Joshi AB, Parrish RK II, Feuer WF. 2002 survey of the American Glaucoma Society:
practice preferences for glaucoma surgery and antifibrotic use. J Glaucoma. 2005;
14:172–174.

120. Souza C, Tran DH, Loman J, et al. Long-term outcomes of Ahmed glaucoma valve
implantation in refractory glaucomas. Am J Ophthalmol. 2007;144:893–900.
121. Gil-Carrasco F, Salinas-VanOrman E, Recillas-Gispert C, et al. Ahmed valve implant
for uncontrolled uveitic glaucoma. Ocul Immunol Inflamm. 1998;6:27–37.
122. Da Mata A, Burk SE, Netland PA, et al. Management of uveitic glaucoma with
Ahmed glaucoma valve implantation. Ophthalmology. 1999;106:2168–2172.
123. Papadaki TG, Zacharopoulos IP, Pasquale LR, et al. Long-term results of Ahmed
glaucoma valve implantation for uveitic glaucoma. Am J Ophthalmol. 2007;144:62–69.
124. Hill RA, Nguyen QH, Baerveldt G, et al. Trabeculectomy and Molteno implantation
for glaucomas associated with uveitis. Ophthalmology. 1993;100:903–908.
125. Molteno AC, Sayawat N, Herbison P. Otago glaucoma surgery outcome study: long-
term results of uveitis with secondary glaucoma drained by Molteno implants.
Ophthalmology. 2001;108:605–613.
126. Vuori ML. Molteno aqueous shunt as a primary surgical intervention for uveitic
glaucoma: long-term results. Acta Ophthalmol. 2010;88:33–36.
127. Valimaki J, Airaksinen PJ, Tuulonen A. Molteno implantation for secondary
glaucoma in juvenile rheumatoid arthritis. Arch Ophthalmol. 1997;115:1253–1256.
128. Budenz DL, Barton K, Feuer WJ, et al. Treatment outcomes in the Ahmed Baerveldt
Comparison Study after 1 year of follow-up. Ophthalmology. 2011;118:443–452.
129. Christakis PG, Tsai JC, Kalenak JW, et al. The Ahmed versus Baerveldt study: three-
year treatment outcomes. Ophthalmology. 2013;120:2232–2240.
130. Callanan DG, Jaffe GJ, Martin DF, et al. Treatment of posterior uveitis with a
fluocinolone acetonide implant: three-year clinical trial results. Arch Ophthalmol.
2008;126:1191–1201.
131. Adan A, Pelegrin L, Rey A, et al. Dexamethasone intravitreal implant for treatment
of uveitic persistent cystoid macular edema in vitrectomized patients. Retina.
2013;33:1435–1440.
132. Bollinger K, Kim J, Lowder CY, et al. Intraocular pressure outcome of patients with
fluocinolone acetonide intravitreal implant for noninfectious uveitis. Ophthalmology.
2011;118:1927–1931.
133. Multicenter Uveitis Steroid Treatment Trial Research G, Kempen JH, Altaweel MM,
et al. Randomized comparison of systemic anti-inflammatory therapy versus
fluocinolone acetonide implant for intermediate, posterior, and panuveitis: the
Multicenter Uveitis Steroid Treatment Trial. Ophthalmology. 2011;118:1916–1926.
134. Hunter RS, Lobo AM. Dexamethasone intravitreal implant for the treatment of
noninfectious uveitis. Clin Ophthalmol. 2011;5:1613–1621.

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Current Management Approaches for Uveitic Glaucoma

Article in International ophthalmology clinics · July 2015

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Uveitic glaucoma is a term that encompasses a myriad of disease

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

TM and aqueous outflow pathway by the inflammatory process has

’ Medical Management of Uveitic Glaucoma

The goal of medical therapy in uveitic glaucoma is to provide

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

reducing IOP to a nondamaging level. Medical management also aims to

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(eg, chlorambucil and cyclophosphamide) have been used either as

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extremities, and metabolic changes) but can be used carefully in select

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muscarinic antagonists that are typically used in intraocular inflamma-

’ Surgical Management of Uveitic Glaucoma

The chronic or recurrent nature of intraocular inflammation usually

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before proceeding with surgery.14 However, there is no evidence

Issues With Trabeculectomy in Uveitic Glaucoma

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The Role of Deep Sclerectomy in Uveitic Glaucoma

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The Role of Minimally Invasive Glaucoma Surgery (MIGS) in

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context of cataract surgery to decrease the amount of medical IOP-

The Role of Glaucoma Drainage Implants (GDIs) in Uveitic

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Inc., Irvine, CA)]. A Cochrane review in 2006 concluded from meta-

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of, external ligature. Early postoperative elevated IOP may be minimized

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complications.128 However, only 2 of 133 eyes in the BGI group

Corticosteroid Implants in Uveitic Glaucoma: Risks and

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Uveitic glaucomas are complex in cause of disease and response to

The authors declare that they have no conflicts of interest to disclose.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

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