Review Article

Inflammatory glaucoma
Sonam A. Bodh, Vasu Kumar, Usha K. Raina, B. Ghosh, Meenakshi Thakar
Department of Ophthalmology, Guru Nanak Eye Center, Maulana Azad Medical College, New Delhi - 110 001, India

Glaucoma is seen in about 20% of the patients with
uveitis. Anterior uveitis may be acute, subacute, or
chronic. The mechanisms by which iridocyclitis
leads to obstruction of aqueous outflow include
acute, usually reversible forms (e.g., accumulation of
inflammatory elements in the intertrabecular spaces,
edema of the trabecular lamellae, or angle closure due
to ciliary body swelling) and chronic forms (e.g., scar
formation or membrane overgrowth in the anterior
chamber angle). Careful history and follow-up helps
distinguish steroid-induced glaucoma from uveitic
glaucoma. Treatment of combined iridocyclitis and
glaucoma involves steroidal and nonsteroidal anti-
inflammatory agents and antiglaucoma drugs. However,
glaucoma drugs can often have an unpredictable effect
on intraocular pressure (IOP) in the setting of uveitis.
Surgical intervention is required in case of medical
failure.
Method of Literature Search: Literature on the Medline
database was searched using the PubMed interface.
Keywords: Intraocular pressure, glaucoma,
inflammation, uveitis

Introduction and debris. Unilateral glaucoma should raise the suspicion of

Inflammatory glaucoma, also known as uveitic glaucoma, is a
condition in which ocular inflammation causes apersistent or
recurrent IOP elevation resulting in anatomical and physiological
changes characteristic of primary open angle glaucoma. The
anatomical changes include progressive optic nerve cupping with
corresponding retinal nerve fiber layer loss. When anatomical
changes progress beyond the physiological reserve of the optic
nerve, the visual field defects become detectable. Joseph Beer first
reported the association of uveitis and glaucoma in 1813, describing
it as arthritic iritis.[1] In 1891, Priestley Smith proposed the first
modern classification of uveitic glaucoma.[2] Elliot proposed
several hypotheses for its mechanism: An alteration of aqueous
composition, obstruction of filtering angle by inflammatory cells,
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DOI:
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an inflammatory glaucoma. The overall prevalence of glaucoma
in eyes with uveitis varies from 10 to 20%, but it is much more
common in chronic uveitis and can be as high as 46%.[3]
Method of Literature Search — literature was searched for on the
Medline database using the Pubmed interface.
Pathophysiology: The relationship between IOP and inflammation
is complex. At any one time IOP depends on the comparative
rates of aqueous production and drainage. Both these processes
and intraocular circulation of the aqueous can be altered by
inflammation, its effects on the ocular tissue involved, and its
treatment.
Mechanisms of Intraocular Pressure Elevation
A. Secondary open angle glaucoma
1. Trabecular meshwork (TM) obstruction is the most
common mechanism and can be caused by: Disruption
of the blood aqueous barrier [BAB], which allows entry
of inflammatory cells into the aqueous humor and
entrapment of normal serum components in the aqueous
outflow system.[4] Swelling of trabecular lamellae and

Copyright:  2011 Bodh SA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Correspondence:
Dr. Sonam A. Bodh, Department of Ophthalmology, Guru Nanak Eye Center, Maulana Azad Medical College, J-573, Kalibari Marg, near Birla mandir, New Delhi -
110 001, India. E-mail: dr.angmo@gmail.com

Oman Journal of Ophthalmology, Vol. 4, No. 1, 2011 3

 Bodh, et al.: Inflammatory glaucoma
endothelial cells with both a physical narrowing of
trabecular pores and dysfunction also leads to aqueous
outflow obstruction,[5] ultimately leading to permanent
damage and scarring of the trabecular meshwork.[6]
2. Hypersecretion caused by PGE1- and PGE2-mediated
increase in the rate of aqueous secretion or by a breakdown
in BAB, with an associated increase in aqueous protein
concentration and thus aqueous viscosity.[7]
3. Corticosteroid-induced elevation of IOP
B. Pre-existing primary open angle glaucoma
C. Secondary angle closure glaucoma: The inflammatory cell and
protein in the aqueous humor can form an adhesion between the
iris and lens resulting in the formation of posterior synechiae
leading to pupillary block, iris bombe, and peripheral anterior
synechiae. Subsequently neovascularization of the anterior
chamber angle and its fibrovascular closure may ensue.
D. Pre-existing predisposition to primary angle closure glaucoma:
In eyes with shallow anterior chamber.
E. Combined mechanism glaucoma: Scarring and obstruction of
outflow channels.
General Symptoms and Signs
Symptoms with acute iridocyclitis may include blurred vision,
ocular pain, brow ache, and other ocular disturbances like
photophobia and colored haloes. The cornea may reveal band
keratopathy, epithelial dendrites, or stromal scarring from
herpetic infections. The iris should be examined for evidence
of stromal atrophy, nodules, posterior synechiae, peripheral
anterior synechiae (PAS), and neovascularization of iris (NVI).
The lens may have a pigment on the anterior capsule, and the
posterior subcapsular opacification may be due to uveitis or to
chronic corticosteroid therapy. These patients require regular IOP
monitoring. Note has to be made on the timing and the extent
of the pressure rise. If the pressure is elevated at the time of
diagnosis, it is more likely that the inflammation is contributing
to pressure elevation. In this case, the priority has to be in the
escalating anti-inflammatory treatment, until the inflammation
has been controlled. Gonioscopy must be performed to detect the
presence of PAS and to assess the degree of angle closure. The
posterior segment must be examined, paying particular attention
to the optic nerve, to document the morphological changes
consistent with glaucoma. Other possible posterior segment
findings include cystoid macular edema, retinitis, perivascular
sheathing, choroidal infiltrates, or retinal detachment.
Major Ocular Inflammations Associated with
Secondary Glaucoma
Fuch’s Heterochromic Iridocyclitis (FHIC): First described by Fuch’s
in 1906, FHIC is an idiopathic, painless, chronic, low-grade
iridocyclitis with heterochromia, due to iris stromal atrophy. The
typical age of onset is 20 – 40 years of age, with men and women
affected equally.[8] It is typically unilateral, but in 13% of the
cases it has presented bilaterally.[9] Slit lamp examination shows
fine, diffuse, scattered, stellate-shaped keratic precipitates (KP)
4
with fine filaments between them, with iris atrophy and patchy
transillumination, secondary to loss of pigment epithelium, with
characteristic moth-eaten appearance.[8] Histology reveals anterior
stromal depigmentation, hyalinization of blood vessels, cellular
infiltrations and Russell bodies. Infiltration of TM by mononuclear
inflammatory cells, typically lymphocytes and plasma cells,
causes rubeosis, trabeculitis, and collapse of the Schelmm’s
canal, leading to TM obstruction and rise in IOP.[10] Gonioscopic
examination typically reveals an open angle and possible
neovascularization, which may bleed with minor trauma.[11]
Iris angiography can show leakage of the iris vessels and possibly
ischemic changes of the iris. Complications are posterior
subcapsular cataract (PSC) and secondary glaucoma. Reported
incidence of glaucoma varies from 13 – 59%, with higher figures
seen on long-term follow-up. Typically, glaucoma more commonly
develops in persons of African descent and bilateral cases.[9] The
glaucoma typically persists after uveitis has subsided and does
not respond to steroids. Fuch’s rarely causes synechiae formation.
Unless glaucoma develops, Fuch’s cyclitis is a benign disorder and
does not require therapy. Use of steroids may only accelerate PSC
formation and increase IOP.
Glaucomatocyclitic crisis: First described by Posner and
Schlossman in 1948, presents in the 20 – 60 years age group,
typically with unilateral recurrent episodes of mild cyclitis and
heterochromia. Its pathogenesis still remains unknown, with
suggested possible associations including an immunogenetic
factor involving HLA-Bw54,[12] viral infections (HSV and
CMV),[13,14] gastrointestinal disease, and various allergic factors.[15]
The IOP is in the range of 40 – 70 mmHg during an acute attack
and usually resolves spontaneously. The levels of prostaglandins
in the aqueous humor have been found to be correlated with the
level of IOP.[16] Slit lamp examination shows fine, small, flat, non-
pigmented KP’s in inferior corneal endothelium.[17] Gonioscopy
reveals an open angle, with occasional trabecular precipitates. The
treatment includes corticosteroids to control inflammation, and
antiglaucoma medications notably beta-blockers and carbonic
anhydrase inhibitors to control IOP. Apraclonidine has been
shown to be effective during acute attacks.[18] Oral indomethacin
may be effective because prostaglandins have been implicated
in the disease.[16] If severe residual glaucoma persists after being
maximally treated by medications, filtration surgery is indicated.
Grant’s syndrome: First described by Chandler and Grant, it is
an acute onset bilateral condition, affecting patients above 50
years of age.[18,19] Patients are usually asymptomatic. Gonioscopy
reveals gray-to-yellowish inflammatory precipitates on the TM.
The magnitude of IOP does not correspond to the amount of
precipitates. It shows a good response to topical steroids and is
typically unresponsive to antiglaucoma medication, but shows
an excellent response to topical corticosteroid therapy. In most
cases, the IOP returns to a normal level within one to two weeks
after administration of topical corticosteroid, which clears the
inflammatory precipitates. If severe angle closure is present
secondary to the formation of extensive PAS, filtration surgery
may be indicated.
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 Bodh, et al.: Inflammatory glaucoma
Sarcoidosis: Sarcoidosis is a multisystem inflammatory disorder
seen in the 20 – 40 year age group. It is more common in females
than males and in blacks more than whites.[20] The ocular findings
seen are panuveitis, mutton fat KP’s, Bussaca and Koeppe’s nodules,
snow balls, candle wax dripping, and phlebitis. Glaucoma is seen
in 11% of the cases. Gonioscopy shows obstruction of TM by
inflammatory debris or nodules. Corticosteroids are the mainstay
of the treatment.[21]
Juvenile Rheumatoid Arthritis (JRA): JRA is an autoimmune
disease typically affecting children under the age of 16 years and
lasts more than six months.[22] The uveitis is typically bilateral,
nongranulomatous, asymptomatic anterior uveitis, usually
preceded by arthritis.[23] Children with iridocyclitis rarely have
a positive serology for a rheumatoid factor, but they frequently
have antinuclear antibody[23,24] and HLA-B27 antigen, and some
eventually are found to have typical ankylosing spondylitis.[24]
Secondary glaucoma is seen in 19-25% of the patients with
longstanding uveitis, due to secondary pupillary block acute
angle closure. Topical steroids and mydriatics are the mainstay
of treatment. The antiglaucoma drugs are required for control
of IOP. In many cases, visual acuity is threatened enough to
warrant further glaucoma surgery. Trabeculectomy or tube shunt
surgeries are the first-line procedures. Goniotomy has been
reported to be a safe and effective procedure and could be a first-
line surgical treatment for JRA patients, although many patients
may continue to require medication even after surgery.[25] Other
potential surgical options that have been shown to have some
positive outcomes include, nonpenetrating deep sclerectomy
with the collagen glaucoma drainage device[26] and Molteno
implant.[27] The complications that may cause significant visual
loss in children with iridocyclitis and JRA include cataracts, band
keratopathy, and glaucoma.
Herpetic Keratouveitis: This viral infection may cause recurrent
conjunctivitis, keratitis, and uveitis. In one study of patients with
herpes simplex keratouveitis, 28% had IOP elevation and 10%
had glaucomatous damage.[28] The period of elevated IOP from
herpetic keratouveitis has a mean duration of two months. Increase
in IOP is due to an increase in the aqueous viscosity, trabecular
blockade due to inflammatory debris, and trabeculitis with edema
of the meshwork. Management of this condition requires that
attention be given to the infection, inflammation, and glaucoma,
and one suggested regimen includes topical trifluorothymidine,
corticosteroids, and cycloplegics, along with antiglaucoma agents
that reduce aqueous production.[29]
Syphilis: Fifteen percent of the patients of syphilis develop
interstitial keratitis, of which 96% are bilateral. Twenty percent
of the patients with interstitial keratitis (IK) develop secondary
glaucoma. Both open and closed types of glaucoma have been
reported.[30] In the open-angle, deep chamber type, there is
usually no active inflammation. The glaucoma appears later
in life, with an elevated IOP. The anterior chamber may have
irregular pigmentation with varying amount of synechiae.
Gonioscopy reveals open angles with a ‘dirty appearance,’ having
Oman Journal of Ophthalmology, Vol. 4, No. 1, 2011
varying amounts of old PAS that do not correlate with the amount
of outflow obstruction.[30] The pathological mechanism of the
condition appears to be endothelialization of the open portions of
the angle, with formation of a hyaline membrane. The glaucoma
tends to respond poorly to antiglaucoma medications and
eventually requires filtering surgery. The closed-angle, narrow
chamber type is characterized by small anterior segments, which
could be due to IK in early infancy.[31] Peripheral iridectomy can
be curative in eyes without permanent synechial angle closure.[30]
In other eyes with permanent PAS, medical therapy, surgical
goniosynechialysis, or filtering surgery may be necessary.
Scleritis: Scleritis is a painful ocular inflammation, which may
primarily involve the anterior or posterior segment of the eye.[32]
It affects patients in the 40 – 60 year age group; 12 – 46% of the
patients of posterior scleritis show elevated IOP.[33] Unilateral acute
angle closure glaucoma could be the presenting feature of scleritis
due to choroidal effusion and subsequent detachment. Other
mechanisms of glaucoma are uveitis, trabeculitis, primary angle
closure glaucoma, pupillary block glaucoma, and neovascular
glaucoma.[34] Treatment includes systemic anti-inflammatory
agents, antiglaucoma medication, and laser iridotomy for pupillary
block glaucoma.
Episleritis: Four percent of the patients develop open angle
secondary glaucoma due to inflammation of the angle structure
or due to steroids.[35]
Investigations
In any patient with recurrent or bilateral uveitis, an underlying
ocular or systemic cause should be sought. The ocular syndrome
will dictate the workup and directed history. An appropriate
systemic workup, focusing on arthritis, infections, mucosa or
skin lesions, and cough should be conducted. A complete blood
count and syphilis serology may be appropriate for all patients,
while specific tests such as angiotensin converting enzyme and
chest x-ray may be advisable for patients of African descent. Many
syndromes may have unique characteristic features, either in the
clinical presentation or examination findings. Findings such as
disciform keratitis or a characteristic distribution of skin lesions
may implicate herpetic infection. A rapid episodic rise in IOP
with minimal cellular reaction may suggest Posner-Schlossman
syndrome.
Treatment
Treatment of uveitic glaucoma is aimed at controlling the
intraocular inflammation and elevated IOP, as well as treating any
underlying systemic disease.
Treatment of the inflammation: The major goals of treatment of
inflammation are to provide symptomatic relief, prevent posterior
synechiae formation, and reduce the severity and frequency of
attacks or exacerbation of uveitis.
5
 Bodh, et al.: Inflammatory glaucoma
Corticosteroids
Corticosteroids remain the first line treatment in noninfectious
ocular inflammation and can be administered topically,
periocularly, intravitreally, and systemically. They exert anti-
inflammatory effects by inhibiting the release of arachidonic acid
and a subsequent production of prostaglandins. Topical steroids
are favored for anterior segment disease.[36] If a long-term anti-
inflammatory is needed, corticosteroid-sparing medications, or less
potent corticosteroids, should be slowly replaced because of the
potential side effects of long-term use, such as cataract, glaucoma,
and local immunosuppression.[37] Periocular administration is
used when more posterior effects are needed or when a patient’s
compliance is unsure. Several techniques have been advocated
for the periocular application of corticosteroid, including
subconjuctival, sub-Tenon’s capsule, transeptal, orbital floor, and
retrobulbar injections. Intravitreal injections of triamcinolone
(IVTA) can also be used to deliver a high concentration of
corticosteroids, to treat inflammation involving both anterior and
posterior segments. IVTA is associated with over a 50% chance
of an IOP elevation, although only 1 – 2% of these elevations
necessitate surgical intervention.[38] Systemic steroids can be used
to treat ocular inflammation recalcitrant to topical and periocular
injections or when the uveitis is associated with systemic disease.
Implantation of intraocular slow-release drug delivery devices
using fluocinolone acetonide has been studied,[39,40] and could be
a potential surgical treatment of uveitis. A concerning ocular side
effect of corticosteroids is ocular hypertension especially with
long-term use (more than three months).[41,42]
Cycloplegics
Cycloplegics are frequently prescribed together with
corticosteroids to decrease the photophobia and pain caused by
ciliary muscle or iris sphincter spasm. Cycloplegia can also break
or prevent the formation of posterior synechiae.
Immunosuppressive agents
Immunosuppressive agents like antimetabolites, T-cell
suppressors, and cytotoxic agents are generally reserved for
cases refractory to corticosteroids or when chronic side effects of
systemic corticosteroids, such as, bone demineralization, diabetes,
or psychosis, are being avoided. Most immunosuppressive agents
take several weeks to achieve efficacy and should be used in
conjunction with oral corticosteroids, initially. Patients should be
monitored very closely.
Antimetabolites
Methotrexate: Methotrexate (MTX) is an effective first-line
corticosteroid-sparing medication. In a retrospective case series
review of 160 patients, control of inflammation was achieved in
more than 70% of the uveitic patients, with 90% having improved
or stable visual acuity.[43] However, MTX is associated with a
30% discontinuation rate in the first year, due to toxicity, which
includes liver dysfunction, nausea and vomiting, and alopecia.
6
Folate supplementation should be used concurrently, to minimize
the toxicity.
Mycophenolate Mofetil: Mycophenolate mofetil (MMF) is another
corticosteroid-sparing medication that has favorable outcomes
in treating ocular inflammation, with a low risk of side effects.
MMF could be a potentially valuable alternative to other
immunosuppressive therapy.[44]
T-cell Suppressors
Cyclosporine: Cyclosporine is an effective second-line agent in
treating uveitis, but its therapeutic use is greatly limited by its
toxicity, namely, renal dysfunction and systemic hypertension,
even with low-dose regimens.[45]
Cytotoxic Agents
Cyclophosphamide: Cyclophosphamide has been used as a second-
line immunosuppressive agent and has been seen to have stronger
immunosuppressive power than MTX and MMF. Scleritis has an
excellent response rate to cyclophosphamide.[46]
Chlorambucil: Chlorambucil is an alkylating agent of the nitrogen
mustard type. It is recommended for use in patients with (1) severe
ocular inflammation unresponsive to corticosteroids and / or a
corticosteroid-sparing agent, (2) serious progressive reduction
in vision despite other treatments, or (3) when blindness is an
unavoidable consequence without further attempted therapy.[47]
Treatment of Glaucoma
Usually, abating the ocular inflammation normalizes the IOP,
but in refractory cases, antiglaucoma medications, surgical
management, or cyclodestructive laser treatment of glaucoma
may be required.
Antiglaucoma Agents
Beta-blockers: Beta-blockers are first-line drugs to lower IOP in
inflammatory glaucoma by reducing aqueous humor production.
They are usually administered once or twice daily.[48]
Carbonic anhydrase inhibitors: Carbonic anhydrase inhibitors
(CAIs) reduce aqueous production through an alteration of
ion transport mechanism in the ciliary epithelium. CAIs can
be administered topically, orally, or intravenously. Topical
administration has the least potential for side effects, but also the
least potent IOP-lowering effect
Selective alpha-2 adrenergic agonists: Alpha-2 adrenergic
agonists lower IOP primarily by decreasing aqueous production.
Brimonidine may have a delayed onset of enhanced uveoscleral
outflow as well.[49,50] Nonselective adrenergic agents, such as
epinephrine and dipivefrin, are not typically used. However, the
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 Bodh, et al.: Inflammatory glaucoma
mydriatic effect of epinephrine can be used to prevent posterior
synechiae.
Prostaglandin analogs: Use of prostaglandin analogs (PGAs) in
the setting of uveitic glaucoma has been limited due to potential
concerns of worsening inflammation and increasing the risk of
cystoid macular edema.[51,52] Although prostaglandins are to be
avoided as the first-line therapy, they may prove to be very useful
in a quiet eye with continuous pressure elevation.
Hyperosmotic agents: Hyperosmotic agents reduce IOP by
dehydrating the vitreous, and thus, reducing the vitreous volume.
They are used to lower IOP rapidly in an acute setting. However,
hyperosmotic agents carry a significant risk of intravascular fluid
overload in a patient with suppressed cardiovascular function.
Miotics: Miotics should not be used in uveitic glaucoma due
to their potential to induce formation of posterior synechiae,
aggravate the symptoms of inflammation caused by ciliary spasm,
and worsen inflammation by disrupting the BAB.
Surgical Treatment
Surgery for uveitic glaucoma is reserved for uncontrolled elevated
IOP, despite maximally tolerated medical therapy, as well as in
cases of pupillary-block angle-closure glaucoma. Intraocular
surgery should be avoided whenever possible in eyes with active
inflammation. However, when medical therapy is inadequate,
surgery may be required. In these cases, it is best to do the least
amount of surgery possible. A laser iridotomy is safer than an
incisional iridectomy when an angle closure mechanism is
present, although the fibrin may tend to close a small iridotomy
in an inflamed eye. Antimetabolite therapy in association with
trabeculectomy has been shown to improve the success rate of
trabeculectomy in patients with a high risk of failure.[36] A study
by Kaburaki et al.,[53] has concluded that initial trabeculectomy
with mitomycin C in uveitic glaucoma eyes with inactive uveitis
that had not undergone any previous ocular surgery had results
comparable to those of primary open angle glaucoma, suggesting
that pre-existing uveitis itself is not a risk factor for failure of
trabeculectomy, with mitomycin C, when uveitis is under control.
Drainage implants are particularly useful in cases with significant
conjunctival scarring due to previous surgery. Drainage valves,
such as the Ahmed valve, may be safer than trabeculectomy, as
less risk of hypotony exists, which can be seen in postoperative
uveitic eyes due to decreased aqueous production.[54-58] Standard
goniotomy represents an alternative, safe, and effective surgical
option for the treatment of young patients with medically refractory
glaucoma, complicating chronic childhood uveitis. Candidates
for goniotomy include children and young adults, both phakic
and after cataract surgery. Angle surgery should be considered in
these young patients, as it may be appropriate to utilize before
more invasive surgical techniques such as trabeculectomy and
glaucoma implant surgery. Future consideration of goniotomy
for the surgical treatment of glaucoma, secondary to adult-onset
uveitis, might also be warranted.
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Freedman et al.[59] reported an overall success rate of 75% with
standard goniotomy surgery for the treatment of young patients
with medically refractory glaucoma associated with chronic
childhood uveitis, with few complications, and without worsening
of the existing uveitis. Trabeculodialysis is a modified goniotomy
used in children and young adults with uncontrolled uveitic
glaucoma.[60] Diode or Nd: YAG laser cyclophotocoagulation
can be used to destroy the secretory ciliary epithelium, leading
to decreased aqueous production. Unfortunately, cycloablative
procedures often exacerbate the inflammation. These methods are
reserved for eyes with poor visual potential, due to the relatively
high risk of further vision loss and phthisis bulbi.
Few published reports are available that address the results of
surgery in patients with uveitic glaucoma.
• Wright et al. reported that three of the 24 patients undergoing
trabeculectomy with mitomycin-C required subsequent
drainage implants and that seven of the 24 patients lost two
or more lines of Snellen acuity.[61]
• Hill et al. reported a success rate of 79% in eyes undergoing
Molteno tube implantation.[62]
• Ceballos et al. reported a two-year success rate of 91.7% in
eyes undergoing Baerveldt drainage device placement for
uveitic glaucoma. There were no intraoperative complications
in this series. Ten eyes had postoperative complications.
The most common were choroidal effusions (four eyes,
16.7%), hypotony maculopathy (three eyes, 12.5%), cystoid
macular edema (three eyes, 12.5%), and failure of corneal
grafts (two eyes, 8.3%). One patient in whom a corneal graft
failed had undergone penetrating keratoplasty, three months
before placement of the Baerveldt implant. The corneal graft
remained clear for two years and then slowly failed. The
second patient in whom a corneal graft failed had undergone
penetrating keratoplasty at the same time as placement of the
Baerveldt implant. Her corneal graft failed 12 months after
surgery, at which time she underwent a second penetrating
keratoplasty. Most complications were transient and of no
visual consequence.[63]
• Ozdal et al. showed a two-year success rate of 68.4% in eyes
undergoing the Ahmed drainage device placement for uveitic
glaucoma.[64] Postoperative complications were observed in
57.9% eyes. The majority of these complications were resolved
either spontaneously or with an additional surgical procedure.
Occlusion of the valve was the most common complication and
occurred in 26.3% in which one additionally had extrusion of
the valve. In one of these eyes, the AV implant was replaced
and the second implant worked successfully. Another one was
treated with irrigation of the implant. The remaining three
eyes in which two had neovascular glaucoma (NVG) were
considered as a failure. A success rate in eyes with NVG has
been reported to be significantly lower. Another complication
that required additional surgery was corneal decompensation
due to the corneal-tube touch and was observed in one eye.
Penetrating keratoplasty was performed in this eye. Choroidal
effusion was observed in one and treated with systemic
corticosteroid. Other complications such as hyphema
7
 Bodh, et al.: Inflammatory glaucoma
(5.3%) and postoperative hypotony (15.8%) were resolved
spontaneously within few days.
• Rachmiel et al. reported a 30-month success rate of 60% in both
primary open angle glaucoma and uveitic glaucoma in patients
undergoing Ahmed glaucoma valve implantation. The most
common side effect in the two groups was uveitis, 24.5% and
33.3% in the primary open angle glaucoma and uveitic groups,
respectively, which was controlled with topical steroids. Other
complications, such as wound dehiscence, choroidal effusion,
and transient diplopia were comparable in the two groups
and resolved spontaneously with no intervention. The single
significant complication in the uveitic group was tube removal
in three eyes (13.3%; P = 0.02) due to tube exposure in two
cases and plate exposure in one case.[65]
Summary
Glaucoma is a common and potentially blinding complication of
uveitis and is seen in about 20% of these patients. The pathogenic
processes responsible for the underlying elevation in intraocular
pressure are multiple involving both open angle and closed
angle mechanisms.[66,67] The mechanisms by which iridocyclitis
leads to obstruction of aqueous outflow include acute, usually
reversible forms (e.g., accumulation of inflammatory elements
in the intertrabecular spaces, edema of the trabecular lamellae,
or angle closure due to ciliary body swelling) and chronic forms
(e.g., scar formation or membrane overgrowth in the anterior
chamber angle). Careful history and follow-up helps distinguish
steroid-induced glaucoma from uveitic glaucoma. Successful
management of uvetic glaucoma depends on recognition of the
uveitis syndrome and clarification of the mechanisms contributing
to it. Both the inflammation and raised intraocular pressure
require treatment. The anti-inflammatory regimen includes
corticosteroids, cytotoxic agents, and other immunosuppressive
agents. When the angle is open IOP reduction may be achieved
medically. When medical treatment fails surgical intervention
may be required.
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Cite this article as: Bodh SA, Kumar V, Raina UK, Ghosh B, Thakar M.
Inflammatory glaucoma. Oman J Ophthalmol 2011;4:3-9.
Source of Support: Nil, Conflict of Interest: None declared.
9
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