Download Glaucoma and Uveitis

SURVEY OF OPHTHALMOLOGY
VOLUME 58 NUMBER 1 JANUARY–FEBRUARY 2013
MAJOR REVIEW
Glaucoma and Uveitis
Sana S. Siddique, MD,1,2 Ana M. Suelves, MD,1,2 Ujwala Baheti, MD,1,2 and
C. Stephen Foster, MD, FACS, FACR1,2
1
Massachusetts Eye Research and Surgery Institution; and 2Ocular Immunology and Uveitis Foundation, Cambridge,
Massachusetts, USA
Abstract. Despite its relative rarity, uveitis is the third leading cause of preventable blindness
worldwide. Glaucoma associated with uveitis is one of the most serious complications of intraocular
inflammation. We review in detail the epidemiology and pathogenesis of uveitic glaucoma and
the safety and efficacy of the current medical and surgical treatment modalities. (Surv Ophthalmol
58:1--10, 2013. Ó 2013 Elsevier Inc. All rights reserved.)
Key words.
drainage implants
glaucoma
trabeculectomy
I. Introduction
trabectome
uveitis
developing glaucoma not only because of the
uveitis, but also as a side effect of the use of
corticosteroids, the mainstay of uveitis treatment.
The association between uveitis and glaucoma was
first reported by Joseph Beer in 1813 as arthritic
iritis followed by glaucoma and blindness. In 1891
Priesley Smith proposed the first modern classification of uveitic glaucoma (UG). Specific types of UG
were described by Fuchs in 1906 (heterochromic
uveitis) and Posner and Schlossman in 1948
(glaucomatocyclitic crisis).B
UG is one of the most serious complications of
intraocular inflammation. Approximately 20% of
uveitis patients in the United States develop
glaucoma. There is no race, sex, or age predilection.B,56 Glaucoma is much more common in
chronic uveitis, an incidence of 11% after 5 years,
than acute uveitis, with 7.6% after 12 months.33,58
Some authors report no differences in the incidence
of UG between anterior and posterior forms,58 but
a study in 927 patients established anterior uveitis as
the main cause, which is consistent with the overall
distribution of uveitis.12 The occurrence of
In the United States uveitis has an estimated
prevalence of about 38 cases, and an incidence of
15 cases, per 100,000 population.27 One estimate is
that uveitis afflicts 109,000 people in the United
States and that 43,000 new cases a year are
diagnosed.82 Over 2 million people worldwide are
thought to have uveitis. Despite significant advances
in therapeutics, the prevalence of blindness secondary to uveitis has not been reduced in the past
30 years. In the largest population-based study in the
United States, the incidence of uveitis was approximately 3 times that of previous estimates and
increased with the increasing age of patients. Women
had a higher prevalence of uveitis than men, and the
largest differences were in older age groups.30
Unless interventions improve, about 10% of
patients with uveitis will be blinded by it. Epidemiological studies in the United States suggest that this
underestimates the risk by as much as 4- to 5-fold.
The sight-threatening complications of uveitis
include damage to the retina and glaucoma.
Patients with uveitis have an increased risk of
1
Ó 2013 by Elsevier Inc.
All rights reserved.
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http://dx.doi.org/10.1016/j.survophthal.2012.04.006
2
Surv Ophthalmol 58 (1) January--February 2013
secondary glaucoma depends on the type of uveitis,
being more common in Fuchs heterochromic
uveitis, Posner-Schlossman syndrome, uveitis associated with herpes infection, and juvenile idiopathic
arthritis (JIA)—ranging in frequency from 5--46% in
patients with JIA.26,32,43,54,59,69 Additionally, glaucoma is more frequent in uveitic eyes of corticosteroid non-responders than in corticosteroid
responders.68
II. Pathogenesis of Glaucoma Associated
with Uveitis
The mechanisms by which uveitis leads to elevated
intraocular pressure (IOP) are incompletely understood. Imbalance between aqueous production
and resistance to aqueous outflow from inflammation may result in a subsequent change in IOP.
During episodes of intraocular inflammation, IOP is
often reduced because of aqueous humor hyposecretion secondary to ciliary body inflammation,
coupled with increased uveoscleral outflow. Over
time, multiple mechanisms can conspire to increase
the resistance to aqueous outflow during episodes of
uveitis, thereby leading to elevated IOP. In some
cases a rise of IOP in the presence of intraocular
inflammation is a diagnostic challenge. The differential is between insufficient anti-inflammatory
therapy with persistence of active inflammation,
steroid response, and chronic structural damage
secondary to inflammation.
Glaucoma may be open or closed-angle. Openangle glaucoma represents the more common form
of UG. Typically, increased resistance occurs as
a result of mechanical obstruction of the trabecular
meshwork, which may be blocked by inflammatory
cells, proteins, debris, or fibrin liberated from
a disrupted blood-aqueous barrier, inflammatory
precipitates on the meshwork, and swelling or
dysfunction of the trabecular lamellae or endothelium, resulting in increased resistance to the
aqueous outflow.56 Additionally, mediators such as
Rho kinases may cause a constriction of trabecular
endothelium, increasing the outflow resistance.66
Increased levels of protein in the aqueous are
a result of increased permeability of the blood-aqueous barrier, which leads to an aqueous that
more closely resembles serum. This elevated protein
content may lead to IOP elevation. Cytokines
released by inflammatory cells further exacerbate
inflammation and may stimulate neovascularization
in the angle. Some prostaglandins demonstrated in
the aqueous humor of eyes with uveitis are also
known to cause elevated IOP. In chronic cases
of uveitis, obstruction of aqueous outflow may
result from scarring and obliteration of trabecular
SIDDIQUE ET AL
meshwork beams or Schlemm’s canal or from overgrowth of a fibrovascular membrane in the angle.
Additionally, the treatment of uveitis with corticosteroids results in elevated IOP in up to one-third
of patients.9 Although corticosteroids have proven
to be effective in reducing inflammation, prolonged
administration can result in elevated IOP by
decreasing aqueous outflow. Secondary ocular
hypertension from corticosteroid administration is
dependent on the dose, the chemical structure of
the corticosteroid compound, the frequency and
route of delivery, the duration of treatment, and the
patient’s susceptibility to steroid response (‘‘steroid
responders’’). Clinically, a corticosteroid response
usually develops 2 to 6 weeks after initiating therapy,
but may occur at any time. It is often difficult to
distinguish between the side effects of the corticosteroids and the underlying inflammation. Only
about 5% of the normal population demonstrates
corticosteroid responsiveness,14 but with impaired
conventional outflow seen during intraocular
inflammation, the corticosteroid response rate rises
significantly. The risk factors of being a steroid
responder are primary open-angle glaucoma, familial history of glaucoma, rheumatoid arthritis,
extremes of age (children and the elderly), and
diabetes. Children are especially susceptible to an
IOP increase secondary to steroids.5,80,90 Corticosteroids have been reported to cause biochemical and
morphological changes in the trabecular meshwork,
increasing resistance to aqueous outflow, and several
theories have been proposed to explain this
phenomenon, including accumulation of glycosaminoglycans in the trabecular meshwork, inhibition of
phagocytosis by trabecular endothelial cells, and
inhibition of synthesis of certain prostaglandins.B,C
Ultrastructural analysis of trabeculectomy specimens in quiescent uveitic eyes with glaucoma show
an increase of total extracellular material in the
trabecular meshwork and a loss of inner wall
endothelial cells, without an increased accumulation of inflammatory cells as compared to primary
open-angle glaucoma specimens.76
Secondary angle-closure glaucoma can also result
from a number of mechanisms in uveitic eyes. Angle
closure with pupillary block occurs when anterior
chamber inflammation results in 360 of posterior
synechiae (Fig. 1), blocking the flow of aqueous
from the posterior chamber into the anterior
chamber, resulting in iris bombé. Peripheral anterior synechiae, another common complication of
intraocular inflammation (Fig. 2), are typically
broad-based and can result in total closure of the
angle. Less commonly, nonpupillary block angleclosure glaucoma develops when inflammation and
edema cause the ciliary body to rotate forward,
3
GLAUCOMA AND UVEITIS
evaluating the angle.59 Retinal OCT requires a clear
cornea, but anterior segment OCT does not.
Objective evaluation of the optic nerve and nerve
fiber layer may be done through OCT and Heidelberg retinal tomography. It is useful to obtain
baseline photographs of the optic nerve.
IV. Uveitic Disorders Associated
with Glaucoma
Many different types of uveitis have been associated with glaucoma, but certain disorders may have
a relatively higher risk.
Fig. 1. Posterior synechiae involving most of the pupillary margin.
closing the angle,C a mechanism described in
patients with Vogt-Koyanagi-Harada syndrome.47
III. Signs and Symptoms
The patient may present with blurred vision,
ocular pain, brow ache, redness, and other ocular
disturbances. Some patients with markedly elevated
IOP often have severe eye pain and nausea
associated with corneal edema. Topical glycerol
may decrease corneal edema so that the ophthalmologist may adequately assess the eye. Patients may
also complain of photophobia and colored halos.
Examination should include evaluation of the optic
nerve and visual field to assess glaucomatous
damage, along with gonioscopy to detect the
presence of peripheral anterior synechiae and to
assess the angle. If the cornea cannot be adequately
cleared, ultrasound biomicroscopy and optical
coherence tomography (OCT) are useful tools for
Fig. 2. Anterior synechiae adjacent to the temporal
limbus and Ahmed valve tube visible superiorly.
A. FUCHS HETEROCHROMIC UVEITIS
Fuchs heterochromic uveitis (FHU) was described
by Ernst Fuchs in 1906 as a triad of anterior uveitis,
heterochromia, and cataract. It is typically unilateral,
affecting the hypochromic eye; in 13% of the cases it
presents bilaterally. In some series FHU represents 2-5% of total uveitis cases and around 15% of anterior
uveitis. It is believed to be underdiagnosed, especially
in bilateral cases in which heterochromia is not well
seen. The typical age of onset is 20--40 years of age,
with men and women affected equally.46 FHU is
a rare, idiopathic, chronic, low-grade iridocyclitis,
without synechiae, with heterochromia, low-grade
anterior chamber reaction with diffuse, small stellate
keratic precipitates, posterior subcapsular cataract,
and secondary open-angle glaucoma. An association
between FHU and rubella virus has been described.10,64 The uveitis is typically poorly responsive
to corticosteroid therapy, and in fact steroids may
worsen the IOP elevation. Treatment of the glaucoma is initiated with medical therapy.
The reported incidence of glaucoma in FHU
varies from 13--59%, with higher figures seen on
long-term follow-up. Glaucoma is believed to be the
major long-term threat to vision in FHU patients.
Typically, glaucoma more commonly develops in
persons of African descent and in bilateral cases.1
Glaucoma generally persists after uveitis has subsided and does not respond to steroids. Controlling
inflammation has little or no effect on IOP, and
many physicians do not treat the associated
inflammation. Medications, particularly aqueous
suppressants, may be effective in controlling glaucoma initially, but characteristically FHU-associated
glaucoma is relatively resistant to medical therapy,
and surgery is often necessary.35,50 Treatment of the
inflammation with corticosteroids may do little
more than accelerate cataract formation and increase IOP further. Glaucoma is the major threat to
vision in patients with FHU, and though frequently
intermittent and well controlled initially, it may
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Surv Ophthalmol 58 (1) January--February 2013
become chronic and difficult to treat. Unless
glaucoma develops, FHU is a benign disorder and
does not require therapy.
B. POSNER-SCHLOSSMAN SYNDROME
Posner-Schlossman syndrome, also known as
glaucomatocyclitic crisis, was first described in
1948. It presents between 20 and 60 years of age,
typically with unilateral recurrent episodes of mild
cyclitis and heterochromia. Though inflammatory
signs may be minimal, rise of intraocular pressure
may be in the range of 40--70 mm Hg during an
acute attack, but this usually resolves spontaneously.
The levels of prostaglandins in the aqueous humor
are correlated with the level of IOP.37 The prognosis
for patients with Posner-Schlossman syndrome is
benign, except when they develop glaucomatous
damage, which occurs in about 25% of cases.
Raitta and Vannas believed that there may be
a relationship between this syndrome and the
eventual development of primary open-angle glaucoma.65 Although the pathogenesis of PosnerSchlossman syndrome remains unknown, suggested
possible associations include an immunogenetic
factor involving HLA-Bw54,35 viral infections
(Herpes simplex and cytomegalovirus),11,89 gastrointestinal disease, and various allergic conditions
including angioneurotic edema, eczema, urticaria,
contact dermatitis, asthma, rhinitis, food allergies,
and intolerance to aspirin.48 A vascular cause has
been postulated based on the demonstration of
segmental iris ischemia on fluorescein angiography.
Vasculature incompetence could be associated with
a release of prostaglandins, inflammation, and
a subsequent rise in intraocular pressure.52 Prostaglandin inhibitors, oral indomethacin, and subconjunctival polyphloretin (a prostaglandin antagonist)
have been shown to lower intraocular pressures
during attacks, further supporting this theory.37,52
The prognosis for control of IOP in patients with
glaucomatocyclitic crisis is good.39 Chandler and
Grant recommended corticosteroid therapy to
control inflammation and topical hypotensive medications, including beta-blockers and carbonic anhydrase inhibitors, to control pressure during acute
attacks.2 Currently, the favored initial treatment is
a topical nonsteroidal anti-inflammatory drug
(NSAID) to control the inflammation (diclofenac
0.1% 1 gutta three or four times daily).39 Topical
steroids (prednisolone acetate 1% 1 gutta three
times daily, followed by taper), oral NSAIDs
(indomethacin 75--150 mg/day), or carbonic anhydrase inhibitors (acetazolamide 250 mg by mouth
three times daily) may also be used. Antiprostaglandin therapy may play a role in the future.
SIDDIQUE ET AL
C. JUVENILE IDIOPATHIC ARTHRITIS
The prevalence of glaucoma in JIA-associated
uveitis has been reported in the range of
14--27%43,45,86 our group,26 however, found a higher
prevalence: 42% of patients with JIA-uveitis had
associated glaucoma or ocular hypertension. Patients
who experience persistent low-grade intraocular
inflammation are at greatest risk for developing
glaucoma, and an earlier referral to a glaucoma
specialist and an aggressive approach to treatment
of UG may reduce the risk of blindness in this
population. The glaucoma associated with JIA
commonly occurs with open angles, but may be of
the pupillary block, secondary angle-closure type, as
a result of the formation of posterior synechiae. We
acknowledge the difficulty of treating glaucoma
associated with JIA-uveitis and have outlined our
approach.26 We treat our patients with a stepladder
algorithm beginning with topical steroids and cycloplegics, possibly followed by regional injection steroid
therapy and brief systemic steroid therapy. If inflammation recurs with steroid withdrawal, an oral
NSAID is used. Immunomodulatory therapy, usually
methotrexate, is the final step in our algorithm, with
resulting high efficacy and low toxicity. Biologic
response modifier therapy has been reserved for
treatment failures. Medical treatment of glaucoma is
initiated with a step-by-step approach starting with
topical beta blocker and sympathomimetics, adding
topical carbonic anhydrase inhibitors (oral if necessary) and latanoprost if required. We believe that it is
beneficial to consider filtering surgery (mitomycin C
[MMC] trabeculectomy with or without fluorouracil
[5-FU] and draining devices) early on if pressures
remain uncontrolled. Some consider goniotomy as
the first-line surgical intervention for childhood
glaucoma.28,36 Freedman and associates28 conducted
a retrospective review of patients with refractory
glaucoma associated with chronic childhood uveitis
to evaluate the safety and efficacy of goniotomy in
these patients. They evaluated 12 patients with childhood UG and found a high overall success rate of 75%
with a mean follow-up of 32.4 months. Similarly, Ho
and colleagues36 conducted a study of the long-term
results of standard goniotomy in childhood glaucoma
and reported success in 72% of eyes (55% without
medications) with a mean follow-up of more than 8
years. Compared with other surgical options, goniotomy offers comparable or even higher rates of success,
but with fewer risks of complications such as infection,
exacerbation of uveitis, iatrogenic damage to intraocular structures, or hypotony. Thus, goniosurgery
is considered an effective, low-risk surgical intervention that can be utilized in the face of failure with
maximal medical therapy.
5
GLAUCOMA AND UVEITIS
D. HERPETIC UVEITIS
The association between virus infections of the
anterior uvea and glaucoma was described more
than 40 years ago.75 Secondary glaucoma is the most
common complication in patients with herpetic
uveitis.55 An estimated 28--45% of patients with
Herpes simplex virus (HSV) keratouveitis (Figs. 3, 4)
develop transient elevated IOP,44 and 10%44 to
54%55 may present with secondary glaucoma.55
An acute increase in IOP in the presence of active
iridocyclitis is the hallmark of a herpetic etiology,
associated most commonly with either HSV or
varicella zoster virus (VZV).55 These hypertensive
episodes are attributed to inflammation of the
trabecular meshwork,22 similar to PosnerSchlossman crises. This is supported by the normalization of IOP in response to topical corticosteroids.
Additionally, the increase of IOP can be secondary
to swelling and obstruction of trabecular meshwork
by inflammatory cells and debris. Typically, herpetic
iridocyclitis episodes are unilateral, synechiaeforming, and explosive in nature; with hypopyon,
hyphema, or fibrin deposition noted at exam in
severe cases.31,49 Diffuse or sectorial iris atrophy
demonstrated by retroillumination at the slit lamp is
no longer considered pathognomonic of VZV, but it
is a characteristic of herpetic iritis, including HSV,
VZV, or cytomegalovirus iridocyclitis.
Management of secondary glaucoma in patients
with herpetic uveitis may be difficult. In severe cases
long-term anti-glaucoma therapy and surgical
approach may be warranted even after the active
inflammation has subsided. Along with management
of glaucoma, long-term antiviral prophylaxis such as
oral acyclovir, valacyclovir, or famciclovir is usually
required to prevent recurrences.77,81 We normally
prescribe acyclovir 800 mg twice a day or valacyclovir
Fig. 4. Large patches of iris atrophy in a patient with
HSV-related uveitis. Note the transillumination defects
and the visualization of the haptic inferiorly.
prophylactically for patients with herpes simplex
disease and double the dose for varicella zoster
disease. Topical antiviral therapy is indicated in
patients with keratouveitis to prevent viral replication
during the use of topical steroid treatment, but it is
considered ineffective in herpetic uveitis.
V. Management
Treatment of glaucoma in uveitis depends on the
underlying disease. One should treat any underlying
systemic disease, the ocular inflammation, and the
glaucoma. The ocular inflammation and glaucoma
usually can be controlled with anti-glaucoma and
anti-inflammatory agents. Often, treatment of the
inflammation will control the IOP. Patients treated
aggressively with anti-inflammatory therapy have
a better clinical course of uveitic glaucoma. We use
potent topical corticosteroids such as difluprednate
or betamethasone.25 Invasive options are considered
if glaucoma medical management does not suffice,
which occurs in 25--30% of cases.
A. MEDICAL
Fig. 3. Slit-lamp photograph of a 23-year-old man with
HSV-related transillumination defects and iris atrophy
spreading from 9 o’clock to 5 o’clock.
Traditionally, the first-line agents used to treat
increased IOP associated with uveitis were topical
beta-blockers and carbonic-anhydrase inhibitors.
Absorption of topical medication may be decreased
in the face of inflammation, and systemic carbonic
anhydrase inhibitors should be considered if topical
medications fail to have the desired effect. Oral or
intravenous hyperosmotic agents may also be used.
Prostaglandin analogs are now the first-line drugs,
and, although they have been reported to reinduce
or cause exacerbations of inflammation,23,70,71,84,85
they may be used in patients in whom the uveitis is
6
Surv Ophthalmol 58 (1) January--February 2013
quiescent. Our group followed 42 patients (59 eyes)
with anterior, intermediate, or posterior uveitis
treated with the prostaglandin bimatoprost and
concluded that bimatoprost is an effective and safe
agent in lowering IOP in patients with uveitic
glaucoma where the uveitis is controlled on immunomodulatory therapy. Other studies support the
efficacy and safety of other prostaglandin analogs as
IOP-lowering agents in UG, even in herpetic
keratouveitis.51,68 Additionally, prostamides do not
increase the flares of uveitis,24 nor do they result in
clinically significant cystoid macular edema.17
Typically we start with a topical prostaglandin
such as bimatoprost, latanoprost, or travoprost once
a day. If this alone fails to control the IOP, we add
another topical agent such as a beta-blocker
(timolol) up to twice a day, carbonic anhydrase
inhibitor (dorzolamide or brinzolamide) up to two
to three times per day, or an alpha agonist such as
brimonidine up to twice a day. If maximal topical
therapy fails to control the IOP, we add an oral
carbonic anhydrase inhibitor such as acetazolamide
250--1,000 mg per day. If all medical efforts fail, we
move along to other options such as selective laser
trabeculoplasty (SLT) which, in our experience,63,A
works well in patients with UG. If further intervention is needed, we use the Ahmed valve or MMC
trabeculectomy.
SIDDIQUE ET AL
in the range of 14--40%.18,19,40 In a recent review on
SLT in patients with non-uveitic glaucoma, it was
concluded, based on five prospective and two
retrospective studies comparing SLT with ALT, that
the IOP lowering efficacy of SLT is similar to ALT
with statistically equivalent mean IOP reductions.67
SLT, in comparison to ALT, induces less inflammation and does not alter the structural integrity of the
trabecular meshwork (TM), an important consideration in UG, where permanent structural alterations
can contribute to glaucoma.8,56 SLT has been
effective in controlling IOP in patients with UG
and we use it as the next step after maximal medical
therapy fails. We recently conducted a retrospective
analysis of 84 eyes of 84 patients with UG who
underwent selective laser trabeculoplasty. The
patients were divided based on the presence or
absence of prior glaucoma surgery (trabeculoplasty/
valve), and outcomes were analyzed at 1, 3, 6, and 12
months. SLT was successful in reducing mean IOP
percentage in naı̈ve eyes from baseline at 1, 3, 6, and
12 months by 15.2%, 16.8%, 23.3%, and 19.8%,
respectively (all statistically significant levels). SLT
was less effective in eyes with previous glaucoma
surgery, though 50% of the eyes at all follow-up visits
had a pressure decrease of $ 1 mm Hg. There was
no statistically significant difference between numbers of flare-ups prior to SLT compared with flareups during follow-up.63,A
B. SURGICAL
If medical management fails to get the IOP under
control, the next step is to use surgical options,
including laser therapy, trabeculectomy, drainage
implants, and cycloablation. The severity of uveitis
may increase after surgical intervention.
1. Laser Iridotomy
Pupillary-block glaucoma may occur from posterior synechiae formation or a fibrin membrane.
A laser iridotomy with an argon and/or Nd:YAG laser
may relieve the block. Sometimes more than one
iridotomy may be required. In some cases, a surgical
iridectomy may be required if the laser iridotomy
seals secondary to intense inflammation.13,70 This is
especially likely in patients with brown irides.
Argon laser trabeculoplasty (ALT) usually fails to
control the IOP in uveitic eyes because of angle
alterations, and we do not advocate ALT in patients
with UG. SLT is done with a 532-nm Q-switched
Nd:YAG laser that specifically targets pigmented
cells in the trabecular meshwork, using low power
and ultra-short durations, and spares the adjacent
cells from collateral thermal damage and preserves
structural integrity. Various studies have reported
a mean reduction of IOP at various follow-up times
2. Trabeculectomy
Trabeculectomy is indicated for eyes with closedangle, open-angle, or combined mechanism glaucoma when IOP is believed to be too high despite
maximum tolerated medical and laser therapy. The
results of unaugmented trabeculectomy are variable
and are particularly poor in young patients with
UG,73 as a result of an accelerated wound-healing
response. Anterior idiopathic uveitis, Fuchs cyclitis,
and aphakia have traditionally been associated with
a higher risk of surgical failure. Combined surgery
with phacoemulsification has a high risk of surgical
failure in patients with intermediate uveitis.15
Hoskins and associates38 reported successful control
of IOP (! 21 mm Hg) in six of their nine patients
with uveitis who underwent trabeculectomy. Stavrou
and colleagues74 achieved an overall 1- and - year
success rates of 92% and 83%, respectively, in 33 eyes
treated with trabeculectomy for UG. Hill and
associates34 reported successful trabeculectomy in
13 (81%) of 16 patients with uveitic glaucoma after
1 year and in 11 (73%) patients after 2 years. They
also reported that in five of seven patients with
significant postoperative inflammation, the filtering
surgery failed.
7
GLAUCOMA AND UVEITIS
Trabeculectomy with wound healing modulators,
such as 5-FU and MMC, has been used in an effort to
minimize scarring of the filtration bleb in patients
with UG and to improve the success rate in patients
with a high risk of failure.5,62,87,88 MMC can be
applied to the eye for a variable duration prior to or
after dissection of the scleral flap; irrigation of the
subconjunctival tissues should be carried out to
prevent intraocular exposure, however.
Towler and associates79 reported on 28 uveitic
eyes undergoing trabeculectomy with and without
5-FU. In 17 eyes trabeculectomy was followed by
subconjunctival 5-FU beginning on the day after
surgery. Ten 200-ml injections of 5 mg 5-FU in sterile
saline were given into the lower fornix daily for
7 days, then on alternate days for the next 7 days.
Eleven eyes underwent unaugmented trabeculectomy. During the first 2 years more than 90% of the
5-FU group achieved control of the IOP compared
with 80% of the non 5-FU patients. Complete
surgical success was defined as IOP # 20 mm Hg
without topical anti-glaucoma drops and partial
success was defined as IOP # 20 mm Hg with
topical anti-glaucoma therapy. The success of IOP
control was analyzed by combining the two groups.
The median survival of primary trabeculectomy in
the 5-FU--treated eyes was 60 months, compared
with 42 months for untreated eyes. After 5 years only
50% of the eyes that underwent trabeculectomy with
5-FU were controlled and only 30% of the eyes that
did not receive 5-FU were controlled. This same
group reported a larger series with a success rate of
67% after 5 years in eyes with UG treated with
trabeculectomy plus intraoperative 5-FU.78
Similarly, Patitsas and colleagues61 reported a 71%
success rate in eyes undergoing trabeculectomy with
5-FU after a mean follow-up of 34 months. Ceballos
and colleagues16 reported a cumulative probability of
success of 78% and 62% with trabeculectomy with
5-FU or MMC at 1 and 2 years, respectively. They also
reported male sex as the only statistically significant
risk factor for trabeculectomy failure.
A more recent study by Kaburaki41 demonstrated
no differences in rate of IOP control after 5 years in
53 eyes with inactive uveitis and secondary glaucoma
compared with 80 eyes with primary open-angle
glaucoma that underwent a trabeculectomy plus
MMC. This study showed similar incidence of
postoperative complications, but hypotonic maculopathy was more frequent in UG.
Even though subconjunctival bevacizumab has
been used successfully in controlling wound healing
after glaucoma filtration surgery, there is no
published data evaluating the safety and efficacy of
intraoperative use of bevacizumab as adjunct to
trabeculectomy in UG.
3. Non-penetrating Glaucoma Surgery
Non-penetrating glaucoma surgery (NPGS) is
a large trabeculectomy with the final thin layer of
Descemet’s membrane left intact. The aqueous fluid
percolates through the membrane into a ‘‘lake’’ in
a pocket of the sclera. The fluid is absorbed into
blood vessels, rather than getting to the subconjunctival space to be absorbed there. There are two
variations of NPGS: viscocanalostomy and nonpenetrating deep sclerectomy (NPDS). Both involve
removal of a deep scleral flap, the external wall of
Schlemm’s canal and corneal stroma behind the
anterior trabeculum and Descemet’s membrane,
thus creating an intrascleral space. The aqueous
humor leaves the anterior chamber through the
intact trabeculo-Descemet’s membrane into the
scleral space, hence it will egress into different
pathways. The risk of IOP being too low is lessened
because there is no complete hole through the wall
of the eye. The best patients for NPGS are those in
whom an IOP of 17--18 mm Hg would be adequate.
An implant is normally used in deep sclerectomy,
but no routine antiproliferative agents are used, and
the IOPs are not as low as those seen with
trabeculectomy.
Several small, prospective, randomized trials have
been conducted to compare the efficacy and sideeffect profile of NPDS with that of trabeculectomy.4
Although these had limited follow-up, they did
generally demonstrate that postoperative IOP reduction was equivalent or slightly lower compared
with that of trabeculectomy, but with a lower
frequency of complications. Some retrospective
reviews of NPGS found NPDS to be significantly
safer than trabeculectomy while retaining good IOP
control.21,53 NPDS with implant, and intraoperative
MMC, has also been used in UG with a high success
rate,3,7,72 but the series are small, retrospective, and
non-comparative. So far, no cases of endophthalmitis have been reported following NPDS, even when
augmented with intraoperative antimetabolites, and
this is likely to be related to the barrier provided by
the trabeculo-Descemet’s membrane. There is
currently no evidence in the form of adequately
powered randomized trials with sufficiently long
follow-up periods to conclusively demonstrate that
NPGS has a significantly lower risk of endophthalmitis and infection when compared to trabeculectomy and glaucoma drainage device implantation,
however. Regardless of the surgical procedure, it is
of utmost importance to educate the patient about
the symptoms of bleb-related infection to allow early
intervention.4 NPGS has been used in patients with
UG, but no long-term data have yet been published
on its safety and efficacy.
8
Surv Ophthalmol 58 (1) January--February 2013
4. Glaucoma Drainage Device Implantation
Drainage implants are designed to route aqueous
from the anterior chamber to a posterior reservoir.
They are particularly useful in cases with significant
conjunctival scarring due to previous surgery.
Drainage valves, such as the Ahmed valve (Fig. 2),
may be safer than trabeculectomy with less risk of
hypotony. They have been used with increasing
frequency in the management of UG, either as the
initial glaucoma surgery or when trabeculectomy
has failed, and have proved to be an effective tool.
We have found a cumulative probability of success
of up to 94% at one year, following (between 1995
and 1998) 19 patients (21 eyes) with chronic uveitis
who underwent Ahmed glaucoma valve implantation for uncontrolled glaucoma.20 Gil-Carrasco and
associates29 reported successful glaucoma management after Ahmed glaucoma valve implantation in
8 of 14 uveitic eyes (57%) after an average follow-up
of 14 months. Hill and colleagues34 included
11 patients with uveitic glaucoma with failed
trabeculectomy filtering blebs who subsequently
received Molteno drainage implants. Safety and
efficacy of the Ahmed valve has also been demonstrated in children.42,57
We recently published the long-term results of
Ahmed glaucoma valve implantation in uveitic
glaucoma, with success rates of 77% and 50% at
1 and 4 years, respectively.60 Ceballos and
colleagues,16 using the Baerveldt glaucoma drainage
implant in 24 eyes, had a success rate of 92% at
1 year, with most patients requiring no adjunctive
medical therapy.
A retrospective comparative study in refractory UG
eyes versus primary open-angle glaucoma disclosed
no significant differences in IOP control or long-term
complications, except for an increased need of
removing the tube observed in uveitic eyes.60
5. Stents
No data on the use of stents in UG have been
published.
6. Cycloablation
As a last resort, cycloablative techniques can be
used to decrease aqueous production by destruction
of the ciliary body using transcleral or intraocular
diode Nd:YAG laser cyclophotocoagulation. An 810nm infrared diode laser may also be used.
Unfortunately, cycloablative procedures often exacerbate inflammation and lead to postoperative
hypotony and phthisis bulbi. Therefore, cycloablation is only used as a last resort for refractory
glaucoma in eyes with poor visual potential in which
conventional drainage surgery has failed.6,83
SIDDIQUE ET AL
VI. Conclusion
Uveitic glaucoma is potentially blinding and
should be managed aggressively. In the minority of
patients who fail medical management, trabeculectomy with antifibrotic agents or drainage implants
must be used. Maximum control of the inflammation by topical, regional, and/or oral steroids or
other immunomodulatory therapy is critical for
a favorable long-term visual outcome.
VII. Method of Literature Search
Literature selection for this review was based on
a Medline database search from the period 1955 to
2011, using the following key words and various
combinations: uveitis and glaucoma.
VIII. Disclosure
The authors report no proprietary or commercial
interest in any product mentioned or concept
discussed in this article.
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Other Cited Materials
A. Unpublished data
B. Herdnon L Jr. Glaucoma, uveitic treatment, and management. http://emedicine.medscape.com/article/1206838overview. Accession date 30 May 2012
C. Salim S, Boyle JW, Netland PA. Pathophysiology and
management uveitic glaucoma. Ophthalmic Pearls: Glaucoma (Sep 2008). http://www.aao.org/publications/
eyenet/200809/pearls.cfm. Accession date 29 May 2012
Reprint address: C. Stephen Foster, MD, FACS, FACR, Massachusetts Eye Research and Surgery Institution, 5 Cambridge Center, 8th
floor, Cambridge, MA 02412. e-mail: [email protected].
Outline
I. Introduction
II. Pathogenesis of glaucoma associated with
uveitis
III. Signs and symptoms
IV. Uveitic disorders associated with glaucoma
A.
B.
C.
D.
Fuchs heterochromic uveitis
Posner-Schlossman syndrome
Juvenile idiopathic arthritis
Herpetic uveitis
V. Management
A. Medical
B. Surgical
1.
2.
3.
4.
5.
6.
Laser iridotomy
Trabeculectomy
Non-penetrating glaucoma surgery
Glaucoma drainage device implantation
Stents
Cycloablation
VI. Conclusion
VII. Method of literature search
VIII. Disclosure