December 2008 Z Rahman et al.

- Scleritis 341

MAJOR
REVIEW

Current Approach in Diagnosis and

Management of Scleritis
Dr. Zahedur Rahman MS, Dr. Jyotirmay Biswas MS

Introduction the extraocular recti muscles and becomes continuous

with the perimysium. It also passes backwards to cover
Scleritis is a chronic, painful, and potentially blinding the globe. Posteriorly it becomes inserted into the dural
inflammatory disease that is characterized b y sheath of the optic nerve.
edema and cellular infiltration of the scleral and
episcleral tissues. Because of the potentially devastating The episclera forms the superficial aspect of the sclera.
ocular complications and possible association with It is a thin dense, vascularised layer of connective tissue,
serious systemic disease, the diagnosis of scleritis the fibers of which are continuous with the underlying
should not be missed. Scleritis most often presents sclera. The episclera is immobile, when viewed with a
within 4th–6th decades with a mild preponderance slit-lamp microscope. Lamina fusca is the innermost
towards women over men (1.6:1) 1,2,3. Scleritis is layer of the sclera adjacent to the uvea.
usually suspected from clinical history, and it is In order to reliably differentiate episcleritis and scleritis,
confirmed by its characteristic clinical signs. In a case an understanding of the anatomy of the vascular
of posterior scleritis, ultrasonography and other imaging plexuses contained within the conjunctiva, episclera,
studies may be necessary to confirm the diagnosis. and sclera is essential.. The blood supply to this region
is enormous, being derived from the anterior ciliary
Anatomic considerations arteries, but with extensive collateral arterial
The function of the sclera is to provide a firm protective anastomoses to the posterior ciliary arteries at the root
coat for the intraocular contents. This coat is resilient of the iris . The anterior system is readily visible with
enough to allow for variations in the intraocular the slit lamp and by anterior segment fluorescein
pressure, firm enough to prevent severe distortion of angiography, especially if the eye is inflammed, and its
the contents of the eye on movement or when pressed recognition is of vital importance in the differentiation
on by the muscles or external forces. of episcleral and scleral conditions. The separation and
displacement of these vascular layers give the most
The bulbar conjunctiva is a thin transparent mucous
important clinical clues to the site and the severity of
membrane, the epithelium of which is continuous with
the inflammation. On slit lamp examination, three
the corneal epithelium. Beneath the epithelium lies
layers of vessels are readily visible. The conjunctival
stroma which is a loosely arranged connective tissue.
plexus, which is the most superficial layer of vessels,
Tenon’s capsule is a dense well defined membrane can be moved over the underlying structures. The
which extends backwards from the limbus to ensheath superficial episcleral capillary plexus is a radially
arranged series of vessels lying within the parietal layer
Uvea department, Sankara Nethralaya, 18, College road, Chennai-600 006. of Tenon’s capsule. The vessels in this layer anastomose
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at the limbus with the conjunctival vessels, with other II. Posterior scleritis
members of the same plexus, and with the deep plexus. a) Diffuse
The deep episcleral capillary network is closely applied b) Nodular
to the sclera in the visceral layer of Tenon’s capsule.
Scleritis may be classified etiologically, although it is
The conjunctival and superficial episcleral vessels can
most often idiopathic or associated with a systemic
be blanched with 1:1000 epinephrine or 10%
disease, scleritis can also be post surgical or related to
phenylephrine, but the deep vessels are affected slightly.
an infectious process. In one study, 25–57 % of scleritis
This is of considerable assistance when attempting to
cases were associated with a known systemic
differentiate deep and superficial scleral inflammation.
condition 1,2,3. In the Watson and Hayreh series,
connective tissue disorders were present in 15 % of
Classification the patients, of which rheumatoid arthritis constituted
In 1976,Watson and Hayreh proposed a clinical 10 %. In another series with a higher proportion of
classification of scleritis based upon the anatomic necrotizing scleritis cases, half of the patients had an
location of the inflammation and the observed associated systemic connective tissue or vasculitic
alterations in the associated vascular structures .This disease 1 . Necrotizing scleritis has the highest
categorization of disease entities does not infer etiology, association with systemic illness and represents the
but provides valuable information regarding severity most frequent type of scleritis that is the first
of inflammation, prognosis, management options, and manifestation of a systemic condition 1,3. Approximately
association with systemic diseases and with ocular two-thirds of patients with scleromalacia perforans have
complications. Few patients progress to a different form an associated systemic condition 1, most commonly
of scleritis from their initial presentation. longstanding rheumatoid arthritis (47 %) 3. Diffuse
scleritis appears to be the most benign form with the
Scleritis is defined as anterior or posterior based upon
lowest prevalence of associated systemic illness.
the location of inflammation, relative to the equator of
Systemic conditions associated with scleritis are shown
the globe. The majority of scleritis is anterior and can in table 1. Vasculitis is a proposed common factor in
be categorized as non-necrotizing or necrotizing. the pathogenesis of both scleritis and the systemic
Diffuse and nodular scleritis are non- necrotizing and autoimmune disorders. Scleritis may occur following
represent the most common forms of anterior scleritis. ocular trauma . Surgically induced necrotizing scleritis
The necrotizing types of anterior scleritis are less (SINS) can occur after any type of ocular surgery with
common ,but represent a more severe disease entity 1, 3. scleral manipulation, including cataract surgery,
Necrotizing scleritis is classified as either with strabismus surgery, filtering blebs, pterygium surgery,
inflammation or without inflammation, with the latter and operations for retinal detachments. Many
being synonymous with scleromalacia perforans. organisms have been reported as possible causes of
Ultrasonographic classification categorizes posterior scleritis and these are shown in table 2.
scleritis as diffuse or nodular, based upon increased
eye wall thickness or finding of scleral nodule, Table 1 Systemic diseases associated with scleritis
respectively. Rheumatoid arthritis Wegener’s
granulomatosis Inflammatory bowel
disease: Ulcerative colitis and Crohn’s
Classification of scleritis disease Relapsing polychondritis
Systemic lupus erythematosis
I. Anterior scleritis Polyarteritis nodosa
Giant cell arteritis
a) Diffuse
Behçet’s disease
b) Nodular Polymyalgia rheumatica
Reiter’s syndrome
c) Necrotizing Raynaud’s disease
i) With inflammation IgA nephropathy
Ankylosing spondylitis
ii) Without inflammation( scleromalacia perforans)
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Gout In scleritis following a previous herpes zoster
Sarcoidosis
ophthalmicus infection, histologic findings usually
Rosacea
Psoriasis include scleral necrosis, an associated vasculitis, and
Lymphoma (Hodgkin’s) surrounding zonal granulomatous inflammation,
Pyoderma gangrenosum primarily in the anterior sclera 5,6. The inflammation
Cogan’s syndrome
Necrobiotic xanthogranuloma can be non-granulomatous and focal. Although the
scleritis is suspected to be an immune-mediated
Table-2 Infectious scleritis response to the prior infection, the presence of a reactive
Bacterial proliferation of granulation tissue distinguishes this
Pseudomonas form from the rheumatoid type. In infectious scleritis,
Proteus mirabilis
the presence of microabscesses with or without
Staphylococcus epidermidis
Streptococcus pneumoniae histologic identification of a pathogen can be a
Viral distinguishing factor.
Herpes zoster
Herpes simplex Idiopathic necrotizing scleritis is characterized by
Mumps chronic, non-granulomatous inflammation and
Granulomatous
diffuse lymphocytic infiltration of the anterior sclera,
Mycobacterium tuberculosis
Mycobacterium chelonae episclera, and uvea 5,6 The presence of newly formed
Mycobacterium leprae vascular channels and focal granulation tissue with
Syphilis fibroblasts, lymphocytes, and histiocytes in idiopathic
Fungal Aspergillus
Pseudallescheria boydii scleritis may be suggestive of a delayed type of
Sporotrichosis hypersensitivity 8.
Parasitic
Acanthamoeba
Toxocariasis Clinical Presentation of Scleritis
Toxoplasmosis
Onchocerciasis
The clinical presentation of scleritis depends upon
the anatomic site involved and extent of inflammation.
The characteristic feature of scleritis is the severe
Histopathology
pain that may involve the eye and orbit and radiates
Previous pathologic studies were based upon tissue to involve the ear, scalp, face, and jaw. Scleritic pain
obtained from enucleated eyes with advanced is typically dull and boring in nature, exacerbated
disease 4. Scleral biopsies have rarely been performed by eye movement. It is worse at night often interfering
because of the high rate of associated complications. with sleep, and characteristicall y wakens the
The pathologic findings of scleritis are classified as patient from sleep early in the morning. The pain is
(1) rheumatoid and rheumatoid- like necrotizing usually severe in nature and resistant to mild
scleritis, (2) idiopathic necrotizing scleritis, (3) post analgesic.
infectious scleral inflammation, and (4) sarcoidal
Scleritis typically has a gradual onset of redness with
inflammation 5,6 .
increasing inflammation over several days 3. In contrast
The typical feature of rheumatoid or rheumatoid-like to the brighter redness of episcleritis, scleritis is usually
scleritis is central scleral necrosis with a distinct a darker violaceous-red hue due to the depth of the
surrounding zone of granulomatous inflammation 5,6,7. congested vascular plexus.
Inflammatory cell infiltration with polymorphonuclear
The patient with anterior scleritis usually notices
leukocytes, histiocytes, and lymphocytes within the
redness and tenderness of the globe. There may be
episcleral tissue and suprachoroidal area, the presence
photophobia and lacrimation. Patient with posterior
of an associated necrotizing vasculitis, and scleral fibre
scleritis may present with reduced vision with or
necrosis between the pars plana and limbus are other
without pain. Patients may have features of an
notable findings in rheumatoid scleritis.
underlying systemic disorder.
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Physical examination: ocular signs nodules. Typically, the nodule is a darker hue of red,
separate from the overlying episclera, immobile, and
The key clinical observations in patients with scleral
tender to palpation. These features distinguish this form
inflammation involve determining the relationship of
of scleritis from nodular episcleritis. The lack of necrosis
the vascular plexuses to each other and the site of
within the nodule and the containment of inflammation
maximum vascular involvement best seen with red-free
within the borders of the nodules differentiate this form
light on slit- lamp biomicroscope. Deep discoloration,
from necrotizing anterior scleritis with inflammation.
extent of scleral edema, and areas of increased
All of the vascular layers overlying the nodule are
transparency are best appreciated in natural day light 3.
displaced forward (Fig. 2).
A hallmark finding that distinguishes scleritis from
episcleritis is the presence of scleral edema. Edematous
sclera can bow forward, displacing the deep episcleral
vascular plexus and exacerbating deep vascular
congestion. To assess the degree of scleral involvement,
blanching the superficial conjunctival and episcleral
vasculature with topical 10 % phenylephrine can
improve visualization of the underlying tissue. Further
examination using a red-free filter is instrumental in
evaluating the vascular architecture, areas of
avascularity, and cellular infiltration of the episclera. Fig 2. Nodular anterior scleritis
The anatomic location of the inflammation and typical
alterations in the vessels form the basis of the Necrotizing scleritis with inflammation:
classification of the vascular layers overlying the nodule Necrotizing scleritis, the most severe form of scleritis
are displaced forward 3. is a serious threat to vision and integrity of the eye.
Diffuse anterior scleritis: It is the most benign and Aching pain, particularly in head, is usually the
most common form of scleritis characterized by diffuse predominant feature. The scleral involvement is
involvement of anterior sclera by oedema and dilatation characterized by severe vasculitis and there are visible
of deep episcleral vascular plexus. These changes lead areas of capillary non perfusion on clinical examination.
to distortion of the normal vascular pattern which Ischemia subsequently leads to scleral infarction and
remains as permanent marker of past scleral necrosis. The edges of the affected area is usually far
inflammation. The swollen sclera loses its normal more inflammed than its centre where destructive
appearance and takes on a dusky hue which is much changes are occurring.
more obvious when viewed in daylight (Fig.1). The Thinning of the sclera with increased visualization of
globe is usually tender to touch. the underlying uveal tissue may result in a bluish-grey
hue to the sclera. If any form of necrotizing scleritis
remains untreated then tissue loss occurs, producing

Fig1.Diffuse anterior scleritis

Nodular anterior scleritis: Nodular anterior

scleritis can present with single or multiple scleral Fig. 3. Necrotizing scleritis with inflammation
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milky white areas of necrotic sclera, episclera, and overlying serous detachment of the neurosensory retina,
conjunctiva. With time this dead tissue is absorbed, which represents the most common sign of posterior
leaving areas of dark choroid covered only by a thin scleritis 9, 10 . Ultrasound remains the key to diagnosis
layer of atrophic conjunctiva (Fig. 3). with which the thickened posterior coat of the eye
(usually greater than 2 mm) can be identified (Fig. 5.)
Scleromalacia perforans: Scleromalacia perforans
does not produce the acute signs of necrotizing scleritis, Surgically induced necrotizing scleritis :
may present with blurred vision from high astigmatism Surgically induced necrotizing scleritis (SINS) can occur
due scleral thinning leading to loss of scleral rigidity. after any type of ocular surgery with scleral manipulation,
The sclera may appear porcelain-like, as the vascularity including cataract surgery, strabismus surgery, filtering
diminishes. Necrotic sclera can slough or become blebs, pterygium surgery, and operations for retinal
sequestered. With severe scleral thinning, increased detachments 11,12,13,14. Inflammation is typically localized
visualization of the dark underlying uvea may occur. to the site or adjacent to the site of surgery, but may
Due to decreased scleral vascularity attributed to progress to involve the entire sclera 11,13 . Patients who
arteriolar vaso-occlusion, large abnormal vessels have SINS need careful systemic investigation as
may cross and surround the areas of affected region 62-90 % of patients in one study were later diagnosed
(Fig. 4). with autoimmune vasculitic disease which required
immunosuppessive therapy. 11,12,13
Investigations :
Because so many patients with scleral disease have
systemic disease, a thorough physical examination is
essential.
The following routine investigations should be
performed:
1. Hemoglobin
Fig. 4. Scleromalacia Perforans
2. White blood cell count and differential count
Posterior Scleritis: The presentation of posterior 3. Erythrocyte sedimentation rate
scleritis depends upon the severity, extent, and location 4. If connective tissue disease is suspected, full
of inflammation. The common signs of posterior scleritis immunologic investigations are undertaken, including
are posterior extension of anterior scleritis, a serous or levels of immunoglobulins and immunofluorescent
exudative retinal detachment, optic disc edema, studies for autoantibodies (including rheumatoid
circumscribed subretinal mass, choroidal folds, retinal factor and antinuclear and anti- ds- DNA antibodies);
striae, elevated intraocular pressure, and a bullous or circulating immune complexes are searched for.
annular choroidal detachment 9. Extension of scleral If Wegener’s granulomatosis or polyarteritis nodosa
inflammation to the adjacent choroid can lead to an are suspected, the anti-nuclear cytoplasmic antibody
(ANCA) tests should be performed. The C-reactive
protein is the best indicator of an active generalized
inflammatory response.
5. Serum uric acid
6. Full serologic tests for syphilis
7. X-ray chest
B-scan ultrasonography should never be omitted from
the examination of patients with scleritis. Now that
Fig.5. Posterior scleritis high-quality ultrasonography has become available, the
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extent and severity of the inflammation can be patients with posterior scleritis have an anterior uveitis.
determined with great accuracy. Many patients who Corneal changes are most frequently seen in patients
were formerly thought to have only anterior segment with necrotizing scleritis including peripheral corneal
disease have been found to have extensive and sight- thinning, stromal keratitis, and peripheral ulcerative
threatening posterior scleritis as well. It also has become keratitis 18. Patients with scleritis and keratopathy have
known that many patients with posterior scleritis with more chance of being associated with systemic diseases.
few symptoms and signs have much more extensive
During any stage of scleral inflammation, the
disease than had previously been considered possible.
intraocular pressure may be elevated due to several
The hallmark features of posterior scleritis seen with
different mechanisms, such as obstruction of the
B-scan ultrasonography are helpful in differentiating
aqueous outflow channels, elevated episcleral pressure,
posterior scleritis from other conditions. B -scan
angle closure, or secondary to a steroid response.
ultrasonography may reveal the characteristic flattening
Cataract formation may be accelerated by long-standing
of the posterior aspect of the globe due to retrobulbar
inflammation or secondary to steroid use. Scleral
edema 15. Abnormally increased thickening of the
thinning most commonly occurs in necrotizing scleritis
posterior ocular coats of the globe >2 mm, optic disc
and may progress to staphyloma in the presence of
swelling, distension of the optic nerve sheath, retinal
raised intraocular pressure.
detachments, and choroidal detachments can be
detected. Fluid can accumulate in the posterior
Medical management:
episcleral space and extend around the optic nerve,
forming the characteristic “T-sign”on B-scan 9,15,16. The aim of treatment is to treat the cause, to control
Ultrasound biomicroscopy :This can be valuable the inflammatory process and thereby reduce the
for better delineation of scleral thinning and ruling out damage to the eye. Treatment almost always requires
any malignanc y. An underlying squamous cell systemic therapy. Patients with an associated disease
carcinoma, medulloepithelioma can extend to the need specific treatment.
sclera. Treatmen t of n o n inf ectio u s scleritis:
Complications of Scleritis : Nonsteroidal anti-inflammatory drugs (NSAIDs),
corticosteroids, or immunomodulatory drugs are
Decreased visual acuity, keratitis, cataract, uveitis, and
indicated. Topical therapy is routinely insufficient.
glaucoma are ocular associations indicating the spread
This treatment must be individualized for the
of scleral inflammation to adjacent tissues 1,2,3 .
severity of the scleritis, response to treatment,
Complications are more frequent in severe necrotizing
adverse effects, and presence of the associated
scleritis and posterior scleritis 1,2,3. Due to potential
disease.
ocular complications related to scleritis, early diagnosis
and treatment of scleritis and its associated ocular
manifestations are critical. Diffuse scleritis or nodular scleritis:

Vision may be limited due to keratitis, anterior uveitis, The initial therapy consists of an NSAID (eg:
cataract, change of refractive status, macular oedema, Indomethacin 75mg twice daily after meal). In case
optic disc oedema, or atrophy, retinal detachment, of therapeutic failure, 2 different NSAIDs should be
epiretinal membrane formation, macular cyst or hole, or tried in succession with the first drug. In high-risk
raised intraocular pressure. Decreased vision occurs most patients, consider appropriate gastrointestinal
frequently with posterior scleritis (45-84 %), necrotizing protection with misoprostol or omeprazole.
scleritis (74-82 %), nodular scleritis (26 %) and least If NSAIDs are not effective or have untoward
often with diffuse anterior scleritis (9 %) 1,2 complications, oral corticosteroid s (tab:
A mild to moderate anterior uveitis has been observed Prednisolone) at doses of 1 mg/ kg body weight
in 30–42 % of patients with scleritis, most frequently can be substituted. Remission may be maintained
(69 %) with necrotizing scleritis 3,17. Almost half of the with continued NSAIDs.
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Periorbital and subconjunctival steroid injections Surgical care:
(Inj.Triamcinolone acetonide 40 mg/ml) are
Tectonic surgical procedures rarely may be required to
also effective in non-necrotizing anterior scleritis
preserve the integrity of the globe.
(Fig. 6, Fig.7, Fig. 8). In case of therapeutic failure
of corticosteroids, immunosuppressive drugs
should be added or substituted. Methotrexate (initial
dose-15 mg/week and tapered monthly) can be the
first choice, but azathioprine, cyclophosphamide,
or cyclosporine may be helpful. Tumor necrosis
factor alpha (Tumour necrosis factor (TNF)-alpha)
inhibitor infliximab, may be effective, although
further investigation is warranted.

Necrotizing scleritis : Fig. 6. Sub-conjuntival triamcinolone acetonide injection in

a case of anterior scleritis
Cyclophosphamide(100 mg per day orally and
tapered monthly) should be the first choice in
treating patients with associated potentially lethal
vasculitic diseases, such as Wegener’s granulomatosis
or polyarteritis nodosa.
The initial therapy consists of immunosuppressive
drugs that are supplemented with corticosteroids
during the first month; the latter is tapered slowly,
if possible. Cyclophosphamide is the most effective
drug.
Fig. 7. Diffuse anterior scleritis before giving subtenon
In case of therapeutic failure, another injection of triamcinolone acetonide.
immunomodulatory drug, such as infliximab, may
be effective. Other alternatives are daclizumab and
rituximab, although their efficacy awaits further
study.
Periocular steroid injections should be applied with
great caution in cases of necrotizing scleritis or
peripheral ulcerative keratitis. Some authors believe
that depot steroids actually may exacerbate
necrotizing disease or an underlying infection.
Pulse intravenous cyclophosphamide with or Fig. 8. Resolution of diffuse anterior scleritis two days after
giving sub-conjunctival injection triamcinolone
without pulse intravenous corticosteroids may be acetonide.
required in case of emergencies and may be followed
by maintenance therapy.
Treatment of infectious scleritis: Systemic Scleral grafts are fresh sclera or glycerin-preserved
treatment with or without topical antimicrobial therapy sclera that is available through eye banks. Grafts
always is required. Differentiating infectious scleritis may be performed in cases of pending perforation
from non-infectious scleritis is important because during the time before the effects of systemic
corticosteroid therapy and immunosuppressive therapy immunosuppressive agents manifest (Fig.9).
(often used in noninfectious autoimmune scleritis) are Corneal tissue may be used for associated corneal
contraindicated in active infections. disease.
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2. Tuft SJ, Watson PG. Progression of scleral disease.
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3. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J
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4. Fraunfelder FT, Watson PG.Evaluation of eyes
enucleated for scleritis. Br J Ophthalmol. 1976;60:
227–230
5. Rao NA, Marak GE, Hidayat AA.Necrotizing scleritis: a
Fig.9. Scleral patch graft clinico-pathologic study of 41 cases. Ophthalmology.
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6. Riono WP,Hidayat AA, Rao NA. Scleritis: a
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7. Fong LP, Sainz de la Maza M, Rice BA, Kupferman AE,
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8. Rao NA, Phillips TM,Wong VG, et al. (1985) Etiology
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clinical history, detailed ocular examination, and use Posterior scleritis: Clinical profile and imaging
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associated uveitis. Ophthalmology.1997;104: 58–63
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