REVIEW ARTICLE
Review of Intermediate Uveitis
Frank H.P. Lai, MRCSEd, David T.L. Liu, FRCOphth, FRCS, and Dennis S.C. Lam, MD, FRCOphth
Abstract: The purpose of this article is to highlight evidence about the
medical and surgical management of intermediate uveitis (IU). Updated
understandings of the immunopathology of IU were reviewed in this
retrospective literature review. Literature selection for this review was
based on the PubMed database (National Library of Medicine) and
OVID database (Wolters Kluwer). Articles deemed relevant were se-
lected and highlighted. Intermediate uveitis is most often a benign form
of uveitis. Since intermediate uveitis has been described in association
with different systemic disorders, the initial diagnostic evaluation should
serve to exclude masquerade syndromes and infectious diseases in
which immunosuppression may be ineffective or contraindicated. Al-
though the pathogenesis of intermediate uveitis is not fully understood,
identication of proinammatory molecules involved in the IU has
contributed to the development and implementation of new therapies.
Studies about the use of various immunosuppressants, biological agents
and surgical treatment on IU have provided more evidence for managing
IU. Nevertheless, corticosteroids remain the mainstay of treatment. The
treatment options of intermediate uveitis are evolving, with the devel-
opment of various immunosuppressants and biological agents. The
management of intermediate uveitis should be tailored individually,
based on specic causes of the disease and associated complications.
Key Words: intermediate uveitis, pars planitis, review, management,
immunosuppressant
(Asia-Pac J Ophthalmol 2013;2: 375Y387)
I ntermediate uveitis (IU) is a chronic intraocular inamma-
tory disorder in which the vitreous, pars plana, and peripheral
retina represent the major sites of inammation.1 Intermediate
uveitis was rst described in the literature as chronic cyclitis by
Fuchs2 in 1908. Different terms have been used to describe this
disease.3 With the development of the binocular indirect oph-
thalmoscope, Brockhurst et al4 described changes in the pars
plana and the peripheral retina. The disease was named pe-
ripheral uveitis. Welch et al5 used the term pars planitis to de-
scribe a subset of these patients who developed cellular
exudation or membrane formation over the inferior pars plana.
In 1987, the International Uveitis Study Group6 adopted
the term intermediate uveitis to classify patients who developed
intraocular inammation involving predominantly the vitreous
and peripheral retina. Intermediate uveitis includes diseases of
various causes and different clinical manifestations. Pars planitis
is considered a subset of IU and is characterized by the presence
of white exudates (snowbanks) over the pars plana and ora serrata
or by aggregates of inammatory cells in the vitreous (snowballs)
in the absence of an infectious etiology or a systemic disease.1
From the Department of Ophthalmology & Visual Sciences, The Chinese
University of Hong Kong, Hong Kong SAR, The Peoples Republic of
China.
Received for publication June 11, 2013; accepted June 26, 2013.
The authors have no funding or conicts of interest to declare.
Reprints: David T. L. Liu, FRCOphth, FRCS, Department of Ophthalmology
& Visual Sciences, The Chinese University of Hong Kong, Shatin,
NT, Hong Kong SAR, The Peoples Republic of China.
E-mail: david_tlliu@yahoo.com.
Copyright * 2013 by Asia Pacic Academy of Ophthalmology
ISSN: 2162-0989
DOI: 10.1097/APO.0b013e3182a2c90b
Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013
Copyright 2013 Asia Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
The management of IU is tailored individually, based on
specic causes of the disease and associated complications.
Patients with mild disease are typically observed. Medical and
surgical treatments are available for patients with more severe
disease. The treatment options of IU are evolving, with the de-
velopment of various immunosuppressants and biological agents.
Literature selection for this review was based on the
PubMed database (National Library of Medicine) and OVID
database (Wolters Kluwer). Articles published any date up to
December 2012 were included. The search was limited to arti-
cles of the English language as well as foreign-language pub-
lications with English-language abstracts. Key words were used
in single and combination including uveitis, IU, pars planitis,
chronic cyclitis, vitritis, immunosuppressant, steroid, and sur-
gery. All retrieved articles were cross-referenced, and citations
in the bibliography were retrieved if deemed relevant. Articles
displayed in the related articles link on PubMed were also
utilized when relevant.
EPIDEMIOLOGY
Intermediate uveitis was reported to account for 1.4% to
25% of all uveitis cases7Y11 and around 10% to 20% of uveitis
cases in children.12Y14 It is the second most common form of
uveitis in childhood.15 Intermediate uveitis was found in 3% to
17% of uveitis cases in Asia Pacic region.16Y18 The exact
prevalence is difcult to determine, because the clinical course
can be indolent and patients are often asymptomatic.19 Al-
though IU affects patients in all age groups, it is most commonly
seen in the rst 3 decades of life.8,20 Bilateral involvement is
seen in 70% to 90% of cases.21,22 Intermediate uveitis does not
show denitive predilection for gender or race.3
CLINICAL FEATURES
Symptoms and Signs
The most common presenting symptoms are blurry vision
and oaters (Table 1).23 Sometimes, patients with IU may be
asymptomatic.24 Pain and photophobia are not common. The
symptoms are usually gradual in onset.23,25 The disease is bi-
lateral in around 70% to 90% of cases. Approximately one third
of unilateral cases will eventually become bilateral.26
Anterior chamber cells or are are usually mild.25 However,
children may occasionally present with more severe anterior seg-
ment inammation.27 Occasionally, patients with multiple sclerosis
(MS) develop granulomatous anterior uveitis with characteristic
mutton keratic precipitates. The hallmark of IU is the presence of
cellular aggregates in the vitreous.24 Aggregates of inammatory
cells may appear in the lower vitreous and are referred to as
snowballs (Fig. 1). Grayish yellow exudation, called snow-
bank, is found along the inferior ora serrate (Fig. 2). In severe
cases, this exudation may encircle the entire retinal periphery. The
presence of a snowbank has been reported to be associated with
more severe disease and increased incidence of cystoid macular
edema (CME).28 Optic disc swelling can also be found (Fig. 3).
Retinal changes in IU include tortuosity in arterioles and venules,
sheathing of peripheral veins, neovascularizations, and retinal
detachments.29,30
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Lai et al Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013

TABLE 1. Symptoms and Signs of IU

Symptoms Signs Investigations

Asymptomatic Vitreous cells Basic workup
Blurry vision Anterior chamber cell or ares Complete blood count, erythrocyte sedimentation rate, venereal disease
Floaters Snowball research laboratory, uorescent treponemal antibody absorption test,
Eye redness Snowbank serum enzyme
Eye pain CME Chest radiography
Photophobia Optic disc swelling Additional workup if history or systemic symptoms are suggestive
Vascular tortuosity Fluorescein angiography, OCT, ocular ultrasonography
Sheathing of Magnetic resonance imaging of the brain, computed tomography
peripheral veins of the chest/gallium scan
Lyme antibody testing, Toxocara species antibody testing, human
T-cell lymphotrophic virus type 1 antibody
Cytological evaluation of cerebrospinal uid, diagnostic vitrectomy

Complications Children with IU experience a higher rate of vitreous

Intermediate uveitis is most often a benign form of uveitis.
Complications are usually related to the chronicity of IU and if
left untreated can lead to blindness (Table 2). Intermediate
uveitis is frequently associated with peripheral retinal phlebitis
and is characterized by a high prevalence of CME (Fig. 4). In-
cidence of CME varies from 12% to 51%.24,31 The incidence of
macular edema increases with the duration and severity of the
disease.3,32 Macular edema with cystoid changes and retinal
thickening due to IU is associated with impaired visual acuity
and visual eld changes.33 Other less common causes of visual
loss include cataracts, uveitic glaucoma and vitreous hemor-
rhage, epiretinal membrane and choroidal neovascularization,
retinal detachment, and band keratopathy.23,25,34
Intermediate Uveitis in Children
Pediatric IU has several features different from adult-onset
cases. Children tend to have worse visual acuity, higher risk of
vitreous hemorrhage, higher incidence of anterior segment in-
ammation, and risk of amblyopia.35,36 Children presenting
with IU have worse visual acuity at both initial diagnosis and
follow-up than do adult patients. The reasons for this are not
clear. Childhood IU may be a more aggressive disease process
resulting in a worse prognosis.35 Besides, the relative inability
of children to express their symptoms may lead to a delay in
diagnosis and therefore more advanced disease at presentation.
FIGURE 1. Snowball in vitreous.
hemorrhage. In a study by Lauer and coworkers,37 28% of
children with pars planitis had vitreous hemorrhage, compared
with 6% of adult patients. Besides, children with IU are more
likely to experience anterior segment inammation.38 Some
may present only with anterior uveitis and develop features of
IU later in the course of disease. In contrast, most adults with IU
have minimal anterior segment inammation. Furthermore,
there is a potential for amblyopia when IU or its complications
occur during childhood.27 As treatment of IU alone may not be
sufcient to restore vision, amblyopia therapy should be begun
in a timely manner.
PATHOLOGY
Pathogenesis
The understanding of the pathogenesis of IU is still limited.
A genetic predisposition and involvement of autoimmune pro-
cesses have been suggested.39,40 Several familial cases have been
reported.41Y43 The presence of human leukocyte antigen DR15
(HLA-DR15; a subtype of HLA-DR2, which is also associated
with MS) and HLA-A28 has been demonstrated in patients with
IU.44,45 Other associations include HLA-B8 and HLA-B51.46
Human leukocyte antigen association identies individuals at
risk, but it is not a diagnostic marker.47
Although the exact cause of IU is unknown, several con-
ditions are associated with the syndrome, including MS,48 idi-
opathic optic neuritis,49 autoimmune corneal endotheliopathy,50
sarcoidosis,49 thyroid diseases, inammatory bowel diseases,49
and large cell lymphoma.51 These associations suggest that an
autoimmune process plays a role in pathogenesis. Intermediate
uveitis may be the rst expression of autoimmune diseases in
these patients. Furthermore, IU has been associated with a
number of infectious agents including Borrelia burgdorferi
(Lyme disease), Toxocara canis (toxocariasis), syphilis,52 tu-
berculosis,53 Whipple bacilli (Whipple disease), Epstein-Barr
virus, human T-cell lymphotrophic virus type 1, and HIV.25
Antecedent or subclinical infection has been suggested to ini-
tiate disease through the process of molecular mimicry.54 T-helper
lymphocytes in conjunction with HLAs are likely to be involved
in the development of uveitis.55
Histopathology
In pathologic specimens of IU, a prominent perivascular
lymphocytic cufng (perivasculitis) and wall inltration of the
retinal vessels (vasculitis), primarily involving the venous system

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Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013
FIGURE 2. Bilateral snowbank in pars planitis.
(phlebitis), have been observed. The uveal tract is typically de-
void of inammation.54,56.
Histologic studies of the peripheral retina and ciliary body
demonstrate condensed vitreous, broblasts, spindle cells, hy-
perplastic nonpigmented pars plana epithelium, lymphocytes,
and blood vessels.56,57 Peripheral snowbanks are composed
mainly of glial elements, Muller cells, and organized collagen
and may be associated with new vessels.58,59 Vitreous biopsy at
the time of active disease demonstrates lymphocytes, epithelioid
cells, macrophages, and giant cells. Vitreous lymphocytes are
mostly T cells with variable numbers of macrophages and few B
cells.57,60 A preponderance of CD4+ T lymphocytes has been
found in the pars plana and snowbank, and these outnumber
CD8+ T lymphocytes by 10:1. CD4+ T cells expressing the acti-
vation marker CD69 in either peripheral blood or the aqueous
humor of patients with idiopathic uveitis support the hypoth-
esis that T-helper cells are involved in inducing and sustain-
ing the inammatory process.61 Increased frequency of effector-
memory CD57+ T cells was also shown to be associated with
pars planitis.62
Immunopathology
Circulating T lymphocytes, which recognize several retinal
antigens, have been identied but are not specic to IU.63 Pa-
tients with MS, with or without IU, may have increased circu-
lating T lymphocytes, particularly CD54+64 and antibodies that
recognize a series of glial proteins. Signicantly elevated con-
centrations of multiple intraocular cytokines were found in IU
patients, especially interleukin 6 (IL-6) and IL-8 in those with
CME and active disease.65,66 Serum IL-1 receptors, which
down-regulate the immune response, become elevated with
successful treatment.67 Elevated serum levels of tumor necrosis
FIGURE 3. Optic disc swelling in IU.
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Review of Intermediate Uveitis
factor > (TNF->), independent of the presence of associated
systemic disease, were found in IU patients, but the serum TNF->
level would decrease under immunosuppressive treatment. How-
ever, intraocular TNF-> levels of IU patients were not increased,
and the levels of diverse cytokines and chemokines in their in-
traocular uids did not correlate with their serum levels.66 The
identication of proinammatory molecules involved in the IU
could contribute to the development and implementation of
new therapies.
The polymorphism of interferon F and IL-10 genes were
shown to be associated with a worse visual acuity at 5 years
from presentation of IU.68 Complement factor H-rs800292 and
KIAA1109-rs4505848 genes are associated with noninfectious
intermediate and posterior uveitis. Besides, gender susceptibil-
ity for uveitis might be involved in the KIAA1109 gene.69 It
demonstrated that outcome in IU may be partly determined by a
complex interplay among genes of cytokine and complement
system. This observation may have implications for future
treatment with biological agents that target these cytokines or
complement systems.
CLINICAL COURSE
A signicant proportion of patients with IU maintain a
good visual function.32,70 Malinowski et al34 found that long-
term visual acuity (20/44) in patients followed up for an aver-
age of 90 months was not statistically different from the
presenting visual acuity (20/46). Rothova et al71 found that 72%
of patients with IU did not experience visual impairment.
The most common cause of visual loss in these patients is
CME.38 In addition, formation of epiretinal membrane, cataract,
macular ischemia, detachment of the macula, and vitreous
hemorrhage from retinal neovascularization are other causes of
visual loss.24
A number of schemes have been used to classify IU,4,72,73
but none can predict the overall prognosis of the disease
TABLE 2. Complications of IU
CME
Cataract
Retinal phlebitis
Epiretinal membrane
Uveitic glaucoma
Neovascularization
Vitreous hemorrhage
Band keratopathy
Retinal detachment
Choroidal neovascularization
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Lai et al Asia-Pacic Journal of Ophthalmology
FIGURE 4. Bilateral CME in IU.
accurately. The disease is typically chronically active or follows
a course of intermittent exacerbation punctuated by periods of
quiescence.38 A permanent resolution of the disease is uncom-
mon.24,38 The SUN Working Group has dened remission as
inactive disease at least 3 months after discontinuing all treat-
ment.1 In a retrospective cohort study of 29 IU patients with
follow-up of at least 10 years,38 one third them achieved a re-
mission of their intraocular inammation for longer than 1 year
and had a mean time to remission of 8.6 years. When properly
treated, around two thirds of IU patients can maintain a visual
acuity of 20/40 or better.24,70
In the pediatric group, the majority of IU was bilateral and
chronic74,75 and it is associated with a worse presenting visual
acuity.36 Poorer outcomes may be related to delayed presentation/
diagnosis, the inherent difculties of immunosuppression in
children, or a more aggressive disease.35 A remission of disease
for at least 1 year could be found in 47% of pediatric patients.74
A case series of 35 patients suggested that children diagnosed
before age 7 years have poorer visual outcomes than those who
are diagnosed at an older age.35 Patients who were younger at
onset of IU were less likely to achieve remission than those who
were older at onset.
INVESTIGATIONS
Diagnostic Tests
The diagnostic approach to IU should center on the history
and clinical examination. Approximately two thirds of patients
would have idiopathic IU.11 Since IU has been described in
association with several systemic disorders, the initial diag-
nostic evaluation should serve to exclude masquerade syn-
dromes and infectious diseases in which immunosuppression
may be ineffective or contraindicated. There is no specic lab-
oratory test for diagnosis of IU. Investigations are performed to
rule out underlying causes of vitreous inammation, to evaluate
extent of inammation, to dene the cause of decreased vision,
and to guide treatment (Table 1).
The patients history should concentrate on the duration of
symptoms, the number of recurrences, and ndings that might
be associated with systemic disorders. Fever, fatigue, or night
sweats are typical signs of sarcoidosis and tuberculosis. Pares-
thesias of the hands, arms, or legs raise the suspicion of MS.
Signs of dermatitis may point to Lyme disease, syphilis, or tu-
berculosis. Arthritis of the knee may be related to Lyme disease,
and contact with cats may suggest possibility of Bartonella
infection.
The initial laboratory investigation may include complete
blood count with differential, erythrocyte sedimentation rate,
venereal disease research laboratory, and uorescent trepone-
mal antibody absorption test. Serum and urinary calcium as
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& Volume 2, Number 6, November/December 2013
well as serum angiotensin-converting enzyme can be checked
if sarcoidosis is suspected. Chest radiography is used to look
for tuberculosis and sarcoidosis. The laboratory workup can
be expanded, depending on the clinical history and physical
ndings.
Patients from endemic areas for Lyme disease with a his-
tory of a rash typical of erythema migrans, chronic arthritis, or
cranial nerve palsies should be checked for antibodies to B.
burgdorferi (Lyme disease). If patients develop neurologic
symptoms or have a history of optic neuritis, a magnetic reso-
nance imaging of the brain and subsequent consultation with a
neurologist should be considered to rule out MS. A computed
tomography of the chest or a gallium scan can be considered
when there is a high clinical suspicion of sarcoidosis. Consul-
tation with a gastroenterologist may be required in patients with
symptoms suggestive of inammatory bowel disease or Whip-
ple disease. Older patients presenting with vitreous cells should
raise the suspicion for intraocular lymphoma. Diagnostic vitrec-
tomy, cytological evaluation of cerebrospinal uid, and neuroim-
aging may be necessary.
Fluorescein angiography is useful in documenting macular
(Fig. 5) and disc edema, retinal vasculitis, ischemia, and neov-
ascularization. Characteristic uorescein angiography ndings
include large vein staining, peripheral venous leakage, and optic
disc hyperuorescence76 (Fig. 6).
Optical coherence tomography (OCT) is a noninvasive
technique that provides detailed information about macular
edema (Fig. 7), subretinal and epiretinal membranes, and macular
hole,77 even in the presence of moderate vitreous opacities or
small pupils. Sequential OCT scans are also useful on follow-up.
FIGURE 5. Typical petalloid pattern of CME.
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Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013
FIGURE 6. Optic disc and venous capillary hyperfluorescence.
Ultrasonography can be useful when there are media opaci-
ties that prevent visualization of the retina, including vitreous
hemorrhage, inammatory debris, cyclitic membrane, or cataract.
It helps to determine degree of vitreous involvement and retinal
anatomic status such as tractional or rhegmatogenous retinal
detachment. Ultrasound biomicroscopy is indicated in cases when
posterior synechiae, cataract, or vitreous opacities do not allow
a good exploration of pars plana and peripheral retina.
In a retrospective cohort of 51 patients with IU, 8 cases
were found to have new associated diagnoses after at least
5 years of follow-up.78 Therefore, initial workup of the patient
with IU is not sufciently sensitive. A careful follow-up of
these patients considerably improves the diagnosis of associ-
ated disease.
MANAGEMENT APPROACH OF
INTERMEDIATE UVEITIS
General Approach
Intermediate uveitis due to infectious or systemic causes
should be treated for the underlying illnesses. A signicant
proportion of patients with IU maintain a good visual func-
tion.32,70 Rothova et al71 found that 72% of patients with IU did
not experience visual impairment.
Therefore, not all cases of IU require treatment. Kaplans79
algorithm is the most popular treatment strategy for IU. The
FIGURE 7. Appearance of CME in OCT.
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Review of Intermediate Uveitis
indications of treatment include (1) visual acuity worse than
20/40, (2) cystoid macula edema, (3) secondary retinal vascu-
litis or neovascularization, and (4) patients bothered by visual
oaters (Fig. 8). Smoking cessation should be strongly en-
couraged as Thorne et al22 found a 4-fold increased risk of
uveitic CME in smokers with IU. Intermediate uveitis patients
should be followed up every 1 to 4 weeks during the active
phase of the disease, more frequently if cystoid macula edema
or severe inammation is present. Because IU is a long-term
and recurrent disease, patients should be educated to recog-
nize symptoms of a are-up (eg, oaters, blurred vision, eye
redness, discomfort) and seek medical advice appropriately.
MEDICAL TREATMENT
Corticosteroids
Although the number of prospective studies in the treat-
ment of noninfectious uveitis has increased in recent years, the
vast majority of published studies in IU are case series or
nonrandomized trials. There remains a lack of level 1 evidence
to guide the choice and duration of therapy.80 Nevertheless,
corticosteroids remain the mainstay of therapy,3,81 based on
their established advantages over alternative approaches that
was afrmed by an expert panel review conducted in 2000.82
Choice of treatment modalities can be determined by the severity
of inammation, response to treatment, presence of complica-
tions, and bilateral involvement of the disease (Table 3).
Anterior segment inammation can be managed with top-
ical corticosteroid (prednisolone acetate 1% or prednisolone
sodium phosphate 1%). Because of limited intraocular pene-
tration, topical corticosteroids are useful only to control anterior
segment inammation.83 In patients with unilateral or asym-
metric bilateral disease or in whom systemic administration of
corticosteroid is less desirable, for example, during pregnancy
or in patients with a history of gastric ulceration,25,84 periocular
injections of corticosteroids are preferentially given. Depot
preparation of either a long-acting methylprednisolone (40 mg)
or triamcinolone acetonide (20 mg) can be administered super-
otemporally into the sub-Tenon space or through the inferior
eyelid into the retroseptal space. The precise mechanisms by
which locally injected corticosteroids enter the eye are not
known,85 but systemic drug levels remain low, and corticoste-
roids can be found in all layers of the eye, even at 30 days after
a single sub-Tenon injection of triamcinolone acetate.86 Helm
and Holland87 showed that 67% of patients experienced im-
provement in Snellen visual acuity, improving by at least 2 lines.
Adverse effects are similar to topical corticosteroids, with ap-
proximately 30% of patients having a rise in intraocular pressure
as well as cataract and very rarely inadvertent ocular penetration.
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Lai et al Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013

FIGURE 8. Suggested management algorithm for IU.

The median time to improvement was 3 weeks.87 If the disease is Systemic corticosteroids are generally advocated for IU
not controlled after 2 to 3 injections given over an 8-week period, that is bilateral, resistant to periocular steroids, or associ-
systemic prednisone can be considered.88 ated with systemic disease.25,84 Before starting systemic

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Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013 Review of Intermediate Uveitis

TABLE 3. Treatment Options of IU

Treatment Indications Side Effects

Medical
Corticosteroids
Topical Anterior segment inammation Rise in intraocular pressure, cataract, inadvertent ocular
Periocular Unilateral or asymmetric bilateral disease, penetration (periocular administration)
systemic corticosteroid not desirable
Systemic Bilateral disease, resistance to periocular Gastric ulcers, weight gain, psychological disturbances,
steroids, association with systemic disease osteoporosis, diabetes, hypertension, are-up of
infection, suppression of growth in children
Intravitreal CME not responsive to sub-Tenon or systemic Rise in intraocular pressure, cataract, risk of
corticosteroid endophthalmitis and retinal detachment
Intraocular implant Long-term release of corticosteroid for control
of inammation
Intravitreal ranibizumab/ Control of CME Lens injury, risk of endophthalmitis, and retinal
bevacizumab detachment
Corticosteroid-sparing High-dose steroids required for control of ocular Gastrointestinal upset, hepatotoxicity, nephrotoxicity,
agents inammation, chronic doses 97.5 mg, myelosuppression, metabolic abnormalities,
signicant adverse effects from steroids opportunistic infections
Biological therapies Intolerance or failed response to corticosteroid Flulike symptoms, fatigue, increased liver enzymes,
or other systemic immunosuppressive drugs opportunistic infections
Surgical
Cryotherapy or indirect Failed medical therapy, contraindications to CME, epiretinal membrane, vitreous hemorrhage,
laser photocoagulation corticosteroid and immunomodulatory therapy inadvertent placement of laser or cryotherapy
PPV Failed medical therapy, failed cryotherapy, or Epiretinal membrane, macular edema, retinal
indirect laser photocoagulation detachment, vitreous hemorrhage, endophthalmitis

corticosteroids, screening for tuberculosis and viral hepatitis
should be performed to prevent are-up of these diseases
during the treatment. Oral prednisolone is started at 1 mg/kg
per day. Adverse effects of oral corticosteroids include gastric
ulcers, weight gain, psychological disturbances, osteoporosis,
diabetes, hypertension, and suppression of growth in chil-
dren.84 A histamine H2 receptor antagonist or a proton pump
inhibitor can be prescribed adjunctively to help prevent peptic
ulcer. Patients should have intraocular pressure monitored to
look for any steroid responsive glaucoma. Oral prednisolone
can be tapered according to disease activity when the in-
ammation stabilizes. The aim is for good control of inam-
mation at a dose of 7.5 mg or less, and if this cannot be
achieved, the use of an adjunct second-line agent should be
considered.84 Tapering can be initiated as soon as 2 weeks
after treatment was started, according to the clinical response
of the patient. The minimal effective dose controlling the in-
ammation should be maintained for at least 4 months.88
To manage CME not responsive to sub-Tenon or systemic
corticosteroid, intravitreal triamcinolone acetonide injections
have been used. The dose most commonly used is 4 mg, and the
typical duration of the effect is 4 to 5 months, with the maxi-
mum effect on visual acuity occurring at 1 to 6 months after
injection.89 Kok et al90 studied the outcome of intravitreal tri-
amcinolone (4 mg/0.1 mL) in 65 cases of uveitis-related CME
inadequately responsive to treatment combinations of oral cor-
ticosteroids, periocular orbital oor corticosteroid injections,
and second-line immunosuppressive agents. They reported a
mean improvement of visual acuity of logMAR (logarithm of
the minimum angle of resolution) 0.26, after a mean period of
4 weeks.90 The improvement in visual acuity was more signif-
icant if the duration of CME before intravitreal triamcinolone
was less than 12 months and if patients were younger than
60 years. Forty-three percent experienced an intraocular pres-
sure increase of greater than 10 mm Hg. The dosage of oral
corticosteroids and/or second-line immunosuppressive medica-
tion was reduced or stopped altogether in 55% cases. In a case
series by Hogewind et al,91 of 33 eyes with intermediate or
posterior uveitis and refractory CME, 50% improved greater
than 2 lines at 3 months after intravitreal injection of 10 mg
triamcinolone acetonide. On the other hand, Sallam et al92
reported a mean improvement of visual acuity of logMAR 0.6 a
mean of 3 weeks after intravitreal injection of triamcinolone, in
8 cases of childhood CME from IU. Resolution of CME was
achieved in all of the treated eyes, but 3 cases (38%) had re-
current CME after a median period of 7 months.92
Several small case series have explored the use of intra-
muscular somatostatin analogs (octreotide) and intravitreal
bevacizumab (Avastin) in patients with refractory uveitic CME.93,94
Missotten et al95 studied 20 patients with recurrent CME during
otherwise quiescent uveitis. Intramuscular octreotide reduced CME
in 70% of cases, after a mean of 3 months of treatment. In 36%
of successfully treated episodes, CME was absent for more than
1 year. In a recent randomized trial comparing the effects of
intravitreal injections of bevacizumab and triamcinolone aceto-
nide for the treatment of persistent macular edema in noninfectious
uveitis, improvement in visual acuity at 6 months was achieved
in 96% of eyes in triamcinolone group and in 83% eyes in
bevacizumab group. Although there was no signicant difference in
improvement of visual acuity, triamcinolone could achieve a greater
reduction in central macular thickness.96 In a series of 7 patients
with refractory uveitic macular edema, intravitreal ranibizumab
(Lucentis) was also shown to reduce the central retinal thickness
and improve the visual acuity at 3 and 6 months.97 For patients not
suitable for intravitreal triamcinolone, these drugs provide an al-
ternative to manage refractory CME.

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Lai et al Asia-Pacic Journal of Ophthalmology
For cases that require a high dose of systemic corticoste-
roids or frequent periocular injections to control are-ups of the
disease, the surgical implantation of a device releasing cortico-
steroid in the vitreous can be considered.98,99 Steroid implants
offer the benet of sustained corticosteroid delivery to the eye
while avoiding systemic complications of other therapies.
The uocinolone acetonide implant (Retisert; Baush and
Lomb, Rochester, NY) was developed to deliver corticosteroids
for up to 30 months and is currently approved in the United
States as a 0.59-mg uocinolone acetonic implant for chronic
noninfectious posterior uveitis. In the Multicenter Uveitis Steroid
Treatment Trial, the effect of uocinolone acetonide implant
was comparable to systemic anti-inammatory therapy in control-
ling IU.100 The implant and systemic therapy groups had an im-
provement in visual acuity of 6.0 and 3.2 letters after 24 months
follow-up. Over the 24-month period, implant-assigned eyes had
a higher risk of cataract surgery (80%) and glaucoma (17%). On
the other hand, patients assigned to systemic therapy had more
prescription-requiring infections than patients assigned to implant
therapy (0.60 vs 0.36/person-years). They concluded that the
choice between uocinolone acetonide implant and systemic
therapy should be judged on the individual basis.
Besides, dexamethasone implant (DEX implant Ozurdex;
Allergan, Inc, Irvine, Calif ) has recently been studied for its
benet in IU. It has been shown to improve intraocular inam-
mation and visual acuity persisting for 6 months.99 The efcacy of
Ozurdex for noninfectious intermediate or posterior uveitis was
assessed in a 26-week, multicenter, double-masked, randomized
clinical trial. Forty-seven percent of treated patients achieved a
vitreous haze score of 0 (no inammation) at 8 weeks, and 43% of
treated patients achieved a 3-line improvement in best corrected
vision. The most common ocular complications included intra-
ocular pressure elevation (25%) and conjunctival hemorrhage
(22%). Cataract occurred in 5% cases.
Corticosteroid-Sparing Agents
Corticosteroid-sparing agents are indicated when inam-
mation requires high-dose steroids for control of ocular in-
ammation for more than 1 month (960 mg or G60 mg based on
the weight of individual dose 1 mg/kg), chronic doses greater
than 7.5 mg, or adverse effects requiring discontinuation of
steroids.82 Patients are typically transitioned to steroid-sparing
therapy, and the steroid is slowly tapered once the ocular in-
ammation is quiet. Standard initial treatment for steroid-
resistant disease is to add a single immunosuppressant to the
regimen, with additional agents being substituted or added as
required. Combination of 2 immunosuppressants in addition
to steroids may be indicated especially in chronic inamma-
tion. There are several classes of agents including antimetabo-
lites, T-cell inhibitors, alkylating agents, and biologic agents.
Methotrexate, azathioprine, and mycophenolate mofetil are
the most commonly used agents with documented efcacy.80,81
They are antimetabolites interfering with the production of nu-
cleotides required for DNA replication, hence inhibiting rapidly
dividing cells including lymphocytes. Methotrexate has gained
its popularity for its good record of safety and tolerability.81 The
initial dose is 7.5 to 12.5 mg/wk. The maximum dose is 25 mg/wk.
Samson et al101 reported a control rate of 89% in patients with
IU. In the Systemic Immunosuppressive Therapy for Eye Dis-
eases Cohort Study, 47% IU had complete suppression of in-
ammation sustained for 28 days or more within 6 months after
addition of methotrexate to an anti-inammatory regimen;
71.5% patients required 17.5 mg/wk or less. Corticosteroid-
sparing success (sustained suppression of inammation with
prednisone 10 mg/d) was achieved in 41.3% of cases within
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& Volume 2, Number 6, November/December 2013
6 months.102 Methotrexate has also been used safely in children
with IU.103 The dose of oral steroid could be decreased from a
mean of 18 mg/d to 2.85 mg/d.
Azathioprine (initial dose, 1 mg/kg per day) and mycophenolate
mofetil (initial dose, 500 mg twice a day) have a similar immu-
nosuppressive effect on T and B lymphocytes, but mycophenolate
mofetil may have a better adverse effect prole.104,105 Ninety
percent of patients taking azathioprine could achieve complete
control of inammation sustained for at least 28 days, and 68%
patients could obtain a corticosteroid-sparing benet.106 On the
other hand, 83% and 39% patients using mycophenolate mofetil
could obtain control of inammation and obtain steroid-sparing
benet, respectively, in 6 months.107 Adverse effects of this group
of immunosuppressants include gastrointestinal upset, hepato-
toxicity, nephrotoxicity, and myelosuppression.
Cyclosporine (initial dose, 2.5-5.0 mg/kg per day) and
tacrolimus (initial dose, 0.15-0.30 mg/kg per day) both in-
hibit calcineurin-dependent transcription of IL-2 by activated
T lymphocytes.108 Murphy et al109 prospectively evaluated the
efcacy and the safety of cyclosporine and tacrolimus in pa-
tients with posterior and IU. Sixty-eight percent of patients
taking tacrolimus and 67% of patients taking cyclosporine
responded to treatment. The median durations of response to
cyclosporine and tacrolimus were 7 and 6 months, respectively.
Kacmaz et al108 also reported that 74% of IU patients using
cyclosporine had controlled inammation, with no activity or
slight activity within 6 months of treatment. The 2 drugs
showed a similar response rate, but cyclosporine was associated
with a higher incidence of adverse effects, including headache,
gingival hyperplasia, fatigue, and palpitations. The adverse ef-
fects of cyclosporine and tacrolimus include renal impairment,
systemic hypertension, and metabolic abnormalities.
Alkylating agents (cyclophosphamide and chlorambucil)
cause cross-linking of DNA, which prevents RNA transcription and
DNA replication. Cyclophosphamide can be administered both
orally (1Y2 mg/kg daily) and intravenously (750Y1000 mg/m2
body surface area every 3Y4 weeks), whereas chlorambucil can
be administered orally at 0.1 mg/kg per day.110,111 They profoundly
suppress the function of both T and B cells, broadly inhibiting
the immune system. Severe adverse effects include bone marrow
suppression, infertility, teratogenicity, and increased risk of malig-
nancy. In view of their potential toxicity, cyclophosphamide and
chlorambucil are usually reserved for cases of uveitis resistant
to other forms of second-line immunosuppression.80 For cyclo-
phosphamide, a complete control of inammation for at least
28 days was observed in 50% of patients with noninfectious uveitis,
whereas 31% of patients obtained a steroid-sparing benet.110 A
response rate of 68% has been reported for treatment-resistant
noninfectious uveitis treated with chlorambucil.112
BIOLOGICAL THERAPIES
Interferon A, which has an established value in the treat-
ment of MS, appears to have a positive effect in terms of visual
acuity, CME, and aqueous and vitreous inammation in IU as-
sociated with MS. There has been a report of the use of inter-
feron A in the treatment of IU related to MS. In this pilot study
of 13 patients, aqueous and vitreous inammation improved in
100% and CME improved in 82% of those affected.113 Seventy-
one percent of cases obtained improved visual acuity. Inter-
feron > has also been shown to be effective in controlling
CME.114 Interferon > was also introduced to treat severe, sight-
threatening refractory uveitis.115 Interferon > was shown to be
effective to achieve complete resolution of CME within 3 months
in 63% of noninfectious uveitis, including IU. Common adverse
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Asia-Pacic Journal of Ophthalmology & Volume 2, Number 6, November/December 2013
effects include ulike symptoms, fatigue, or increased liver
enzymes.
During the last few years, there have been reports on the
role of TNF-> and other interleukins in the pathogenesis of
ocular inammation.116 These have been used as targets for
treating uveitis. Daclizumab (Zenapax; Hoffman-La Roche,
Nutley, NJ), iniximab (Remicade; Centocor, Horsham, Pa),
and adalimumab (Humira; Abbott, North Chicago, Ill) are the
major biologic agents that have been used to treat uveitis.117
Daclizumab, a humanized IL-2 receptorYblocking antibody,
is administered as 1 to 2 mg/kg infusions every 2 to 4 weeks.
Subcutaneous administration is also used. Adverse effects in-
clude rash, edema, granulomatous reactions, viral respiratory
infections, elevated liver enzymes, and leukopenia.118 In a
multicenter nonrandomized interventional case series, it allowed
control of ocular inammation with stability in visual acuity
with reduction of concomitant immunosuppression by at least
50% in 67% of patients with noninfectious IU, posterior uveitis,
or panuveitis receiving subcutaneous daclizumab treatment.119
Yeh et al120 reported the use of high-dose daclizumab in 5 pa-
tients with noninfectious intermediate or posterior uveitis and
demonstrated an improvement in vitreous haze in 4 of 5 patients
by the fourth week of follow-up. It was well tolerated, but there
might be a potential increased risk of infection associated with
immunosuppression.120 Despite the success of daclizumab in
treating uveitis, it was recently pulled from the market because
of diminishing market demand and availability of alternative
agents (based on a September 2009 Hoffmann-La Roche Inc
drug announcement).
Tumor necrosis factor > inhibitors include iniximab and
adalimumab, which are monoclonal antibodies against TNF->.
Iniximab (Remicade; Centocor Ortho Biotech, Malvern, Pa)
is a 149-kd chimeric immunoglobulin G1 monoclonal antibody
composed of human constant and murine variable regions. It
is given intravenously. The use of iniximab has been shown to
be effective in improving macular thickness and visual acuity
in patients with uveitic refractory CME due to IU or other
noninfectious uveitis.121 Markomichelakis et al122 and Rajaraman
et al123 found that iniximab achieved reduction in intraocular in-
ammation with concurrent decrease in steroid requirements in
both adult and pediatric populations. Adverse effects include
development of an infusion reaction, opportunistic infections in-
cluding latent tuberculosis, malignancies, lupus-like reactions,
and elevations of autoantibodies and transaminases. Patients must
be screened for hepatitis B and C as well as tuberculosis with
chest radiography and tuberculin skin test.124
The experience with the use of adalimumab (a fully hu-
man monoclonal antibody) in the treatment of uveitis is limited,
but the preliminary results show its promising role in the man-
agement of uveitis. Recently, a prospective case series on the
efcacy on the use of adalimumab for the treatment of refractory
uveitis was performed. A total of 131 patients, including 16 pars
planitis patients, who are intolerant or failed to respond to
prednisone and at least 1 other systemic immunosuppressive
drug, were included. Diaz-Llopis et al125 showed that all patients
had good response with adalimumab, as demonstrated by de-
crease in anterior chamber and vitreous cavity inammation,
overall gain in visual acuity, reduction of macular thickness, or
decrease of the immunosuppression load after 6 months of
treatment with 40-mg subcutaneous injections of adalimumab.
Eighty-ve percent of patients were able to reduce at least
50% of their baseline immunosuppression load.125 Long-term
data on the effectiveness of adalimumab therapy in patients
with noninfectious refractory uveitis, including IU, are war-
ranted. Adalimumab has so far demonstrated some preliminary
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Review of Intermediate Uveitis
advantages over iniximab, including its subcutaneous route
of administration, no need for hospitalization, being less im-
munogenic and less expensive, and having a more protracted
therapeutic response in uveitis.126 However, adalimumab is sub-
stantially more expensive than many other immunosuppressive
drugs, and it is suitable for only selected patients.
SURGICAL TREATMENT
For IU patients who fail corticosteroid treatment or have
contraindications to corticosteroids and immunomodulatory
therapy, peripheral ablation with cryotherapy or indirect laser
photocoagulation to the peripheral retina can be considered.
Cryotherapy has been shown to be effective in treatment of
IU.127 It may be used after periocular or systemic corticosteroid
therapy failure and is often combined with a periocular steroid
injection. Peribulbar anesthesia is required for this procedure.
Destruction and elimination of the neovascularization and is-
chemic tissue seem to be the mechanism behind the success of
this treatment.19 The effect is noted after several weeks but may
need to be repeated after 3 to 6 months. Devenyi et al128
reported that 90% of steroid-resistant eyes can be managed
without corticosteroid treatment after cryotherapy, and in 78%
of cases, vitritis was eliminated. Patients with smaller snowbank
may have better visual improvement.127 Complications included
transient worsening of vitreous inammation, decreased accom-
modative potential, cataract, hyphema, epiretinal membranes, and
retinal detachment.25
A retrospective review of 22 eyes with pars planitis that
had undergone peripheral retinal laser photocoagulation was
conducted by Pulido et al.129 Although there was no signicant
improvement in visual acuity, laser photocoagulation could de-
crease need of corticosteroids in 60% cases. Moreover, vitritis,
neovascularization of the vitreous base, and CME were sig-
nicantly reduced after the laser treatment. An increase in
epiretinal membranes had been reported after laser.129 Park
et al130 also evaluated the use of peripheral scatter photocoag-
ulation in 10 eyes with steroid-resistant pars planitis. All cases
obtained the regression of neovascularization regressed, stabi-
lized inammation, and improvement in CME, without com-
plications of the treatment.
Being compared with cryotherapy, laser photocoagulation
is easier to administer and produces less pain and possibly fewer
complications.
Since 1978, numerous authors, beginning with Diamond and
Kaplan,134 have documented the benecial effect of pars plana
vitrectomy (PPV) on visual acuity in patients with intermediate
uveitis. Reductions in clinically signicant CME, uveitis relapses,
and systemic therapy use were additional benets.131Y137
Retinal detachment, cataract, and recurrent vitreous hem-
orrhage are known complications. A review about the role of
PPV in treatment of IU was conducted by Becker and Davis.131
In 282 cases of IU from 9 studies with a mean percentage of IU
cases of more than 59%, PPV could achieve improvement of
vision in a mean 66% of cases and could reduce the CME from
a median 42.1% to 12.5%.131 Trittibach et al138 established the
positive effects of PPV on the course and complications of pe-
diatric and juvenile chronic uveitis. A signicant reduction in
postoperative CME and improvement in visual acuity were
found after the PPV.138 Their ndings revealed that a low pre-
operative visual acuity and the presence of CME had a negative
inuence on the nal visual acuity. Early treatment of IU in
children and adolescents has been recommended if regional
corticosteroid treatment and cryoretinopexy fail to control dis-
ease; 22 of 25 patients had visual improvement, and 7 patients
with chronic macular edema had complete regression after the
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Lai et al Asia-Pacic Journal of Ophthalmology
vitrectomy.139 Quinones et al140 have recently conducted a
prospective randomized study to compare the benet of PPV
with immunomodulatory therapy for patients with recalcitrant
IU. They showed that 82% (9/11 eyes) of those treated with PPV
showed resolution of inammation at follow-up at 5.93 years,
whereas 57% (4 of 7 eyes) had persistent inammation requir-
ing subsequent PPV. Three PPV patients had CME initially; all
resolved postoperatively. Cystoid macular edema improved in 2
of 3 eyes using immunosuppressive therapy. Patients with PPV
showed greater improvement in visual acuity, intraocular pressure,
and vitreous cell reduction.
A large proportion of patients with IU develop cataract,
either secondary to the disease process or corticosteroid treat-
ment.38 Preoperative suppression of inammation is important
before cataract surgery.141 Phacoemulsication and intraocular
lens implantation are safe in patients with IU.142 Ninety-one
percent of patients could achieve visual improvement after the
cataract surgery, but CME or reactivation of pars planitis was
observed in around 50% of cases. Fogla et al143 studied 54 cases
of cataract surgery in IU patients. Visual acuity improved fol-
lowing surgery in 94.2% of eyes, and 71.2% of eyes achieved a
nal visual acuity better than or equal to 20/60. They concluded
that absolute control of inammation, atraumatic surgery, and
regular postoperative follow-up could improve the results of the
cataract surgery.143
FUTURE RESEARCH AREAS
Although the pathogenesis of IU is not fully understood,
identication of proinammatory molecules involved in the IU
has contributed to the development and implementation of new
therapies. Tumor necrosis factor > inhibitors, such as iniximab121
and adalimumab,125 have been shown to be effectively treating
IU. Signicantly elevated concentrations of multiple intraocular
cytokines were found in IU patients, especially IL-6 and IL-8 in
those with CME and active disease.65,66 These observations may
have implications for future treatment with biological agents that
target these cytokine or complement systems. Moreover, there is
still a paucity of long-term results of these biological agents,
which will provide more evidences about the efcacy and safety
of these treatments.
Genetic polymorphisms have been shown to be associated
with the outcomes of IU.68 It demonstrated that outcome in IU
may be partly determined by a complex interplay among genes
of cytokine and complement system. The prevalence of IU
among different ethnic populations as well as the treatment re-
sponse to those new biological agents is going to be an inter-
esting area for further research in the future.
CONCLUSIONS
Intermediate uveitis is most often a benign form of uveitis.
The management of IU is tailored individually, based on spe-
cic causes of the disease and associated complications. Choice
of treatment modalities can be determined by the severity of
inammation, response to treatment, presence of complications,
and bilateral involvement of the disease. The treatment options
of IU are evolving, with the development of various immuno-
suppressants and biological agents. Nevertheless, corticosteroids
remain the mainstay of treatment.
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