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Article in Insight - the Journal of the American Society of Ophthalmic Registered Nurses · October 2010
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Summary
This article will briefly discuss episcleritis and scleritis as clinical entities. Both are
forms of ocular inflammation but have different clinical, therapeutic and prognos-
tic implications. Episcleritis is a self-limited disease, causing mild discomfort and
infrequently requiring therapeutic intervention. Scleritis is a painful, inflammatory
process, commonly associated with systemic disorders and requires systemic anti-in-
flammatory therapy. It is important to be able to distinguish between the two clinical
conditions, as prompt initiation of therapy for scleritis can be sight saving.
Introduction
Bradley J. Kirkwood, MA, BN, RN
Ophthalmic Nurse Specialist Episcleritis and scleritis are distinct forms of ocular inflammation with different
Professional Eye Centre, Mackay clinical, therapeutic and prognostic implications. Episcleritis is a self-limited disease,
Queensland, Australia commonly idiopathic in nature, and therefore infrequently requires therapeutic
P.O. Box 10122 intervention.1 It involves the superficial aspect of the sclera, with symptoms usually
Mt. Pleasant, Queensland limited to mild discomfort. In direct comparison, scleritis is a painful, severe, destruc-
Australia 4740 tive inflammatory process that poses a significant threat to vision.2 It is frequently
Bradkirkwood@bigpond.com associated with systemic disorders and requires systemic anti-inflammatory therapy.2
Although both episcleritis and scleritis are relatively uncommon, it is important to
Rodney A. Kirkwood, MD, FRANZO be able to distinguish between the two clinical conditions, as prompt initiation of
therapy for scleritis can be sight saving. This article will briefly present the related
anatomy of the sclera and then discuss the clinical and management variations for
episcleritis and scleritis.
Anatomy
The human sclera is the “white” of the eye and is a tough coat of connective tissue that
functions both to protect the intraocular contents and to maintain the shape of the
Disclosure: The authors have disclosed globe. The word sclera is derived from the Greek words sklera mannix, meaning hard
that they do not have a conflicting rela- membrane.3 It accounts for approximately 90% of the outer coat of the eye and begins
tionship of a financial, professional, or at the limbus and terminates at the optic canal.2 The sclera is thickest posteriorly
personal nature related to this activity. (1.0 mm) and thinnest (0.3 mm) behind the insertion of the extraocular muscles.4
Learning Objectives: At the limbus, the sclera is 0.8 mm thick.4
1. Describe two clinical features of For anatomical description, the sclera can be divided into three sections: the episclera,
episcleritis and scleritis. the scleral stroma and the lamina fusca.4 The episclera is the outermost layer and is
2. Differentiate the etiology, onset and comprised of loose connective tissue that lies immediately beneath Tenon’s capsule.
therapeutic interventions for episcleritis It has a rich blood supply from the anterior ciliary arteries which forms a plexus (net-
and scleritis. work). It has two layers: a superficial parietal layer and a deep visceral layer. These two
layers are loosely fused by fine connecting fibers. The superficial parietal layer is vas-
Accreditation: This continuing education cularized by the episcleral capillary plexus, which has a uniquely straight and radially
activity is provided by ASORN. oriented vessel appearance. The visceral layer, which is closely adherent to the sclera,
ASORN is accredited as a provider of con- contains the deep episcleral capillary plexus. The freely anastomosing configuration
tinuing nursing education by the Ameri- of this capillary plexus characterizes this layer. In addition, the episclera also acts as a
can Nurses Credentialing Center’s COA. synovial membrane for smooth movement of the eye.
Post-test: To take this examination for The scleral stroma consists of dense fibrous tissue and fine elastic fibers. Collagen
continuing education credits, go to bundles of varying shapes and sizes are not uniformly orientated, giving it its opaque
www.actioned.org.
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I n s i g h t The Journal of the American Society of Ophthalmic Registered Nurses, Inc. | October–December 2010 | Vol. XXXV, No. 4
Continuing Education (CE) Article
6
I n s i g h t The Journal of the American Society of Ophthalmic Registered Nurses, Inc. | October–December 2010 | Vol. XXXV, No. 4
Continuing Education (CE) Article
Scleritis
Scleritis is a severe, potentially destructive disorder with an
entirely different prognosis from episcleritis. The incidence of
scleritis has been estimated to occur in between 0.08% and 4%
of patients1, is most common between 20–60 years of age and
more frequently affects females.6 In general, scleritis can be
divided into two major categories: non-infectious and infec-
tious.9 The first, noninfectious scleritis, is most commonly
caused by immune-mediated disorders such as Wegener’s
Figure 3: Diffuse anterior scleritis
granulomatosis, rheumatoid arthritis and relapsing polychon-
dritis. Scleritis may be the initial presenting clinical sign of these
conditions. Up to 50% of patients with scleritis have evidence scleral tissue becomes thin and translucent. Some areas of ciliary
of an underlying systemic disease.2 The second group, infectious body or choroid may be covered only by conjunctiva.
scleritis, is most commonly caused by surgery or local extension
Necrotizing scleritis without inflammation, also termed
from adjacent ocular tissues. Scleritis is classified on the basis
scleromalacia perforans, is characterized by patients remain-
of clinical appearance and divided into anterior and posterior
ing largely asymptomatic. It is most common in women with
forms.8 Anterior scleritis is further divided into diffuse, nodu-
rheumatoid arthritis.1 Patients may notice a discoloration of
lar, necrotizing with inflammation and necrotizing without
the sclera or present with blurred vision because of astigmatism.
inflammation (scleromalacia perforans).8
Thinned and avascular areas of episclera and sclera with no sur-
Prompt diagnosis of scleritis is essential and differentiation from rounding inflammation can be noted on examination. Despite
the more benign episcleritis can often be made by a detailed his- pronounced thinning in some cases, perforation is rare without
tory, an external examination and a careful slit-lamp examina- scleral trauma or very high intraocular pressure.9
tion to determine which layers of the ocular wall are involved
Posterior scleritis represents 2% to 12% of scleritis cases and is
with the inflammation. Slit-lamp examination also reveals
defined as involvement of the sclera posterior to the insertion of
scleral edema, distortion and tortuosity of both superficial and
the rectus muscles.1 Posterior scleritis may occur in isolation or
deep vascular networks with loss of the normal radial pattern.
can be accompanied by anterior scleritis. Presenting symptoms
Avascular areas with blood vessel closure are indicative signs
can include extreme pain or loss of vision. In more advanced
of scleritis and do not occur in episcleritis. Such an appearance
cases, retinal or choroidal folds, macular edema and glaucoma
strongly suggests necrotizing scleritis. Most scleral disease is
may be noted.1 Diffuse and nodular forms can be delineated
bilateral and recurrent. Patients presenting with scleritis will
with the use of imaging studies such as B-scan ultrasonography
often complain of pain, severe enough to awaken them at night,
and magnetic resonance imaging.2
which may radiate to the forehead, brow or jaw. The pain tends
to be gradual in onset. A history of red eye(s), accompanied by Treatment of scleritis is aimed at reducing morbidity and
photophobia, blurred vision and tenderness to touch will often minimizing complications. Systemic anti-inflammatory and
accompany the ocular pain. The sclera often takes on a bluish- immunosuppressive medications are utilized, as topical therapy
violet color. Visual loss may be caused by keratitis, cataract, alone is ineffective. Initial therapy consists of oral NSAIDs
macular edema or uveitis.1 These complications are rarely pres- and/or oral corticosteroids. Immunosuppressive drugs such as
ent in episcleritis. methotrexate and cyclophosphamide may need to be added or
substituted if unresponsive to the initial therapy. Intravenous
Diffuse anterior scleritis is the most common presentation of
therapy corticosteroids and immunosuppressive drugs may be
scleritis and tends to be the least severe (Figure 3). It often has
required for urgent cases. Rarely, surgical treatment such as a
an insidious onset and may resemble diffuse episcleritis as over-
tectonic scleral graft can be used to preserve the globe.
lying episcleral injection is present. Nodular anterior scleritis
presents with a nodule that is firm, immobile and tender on Infections of the sclera are uncommon, accounting for approxi-
palpation. Necrotizing anterior scleritis with inflammation mately 5% to 15% of cases.10 Scleral infections may be classi-
is the most severe type of scleritis and is associated with the fied into two groups: exogenous and endogenous infections.9
greatest potential for visual loss. Avascular areas of sclera and The first, exogenous infections, are most common and include
conjunctiva, with surrounding scleral oedema and congestion, post-traumatic and post-surgical infections (Figure 4). These
are frequently seen. Uveal tissue may be seen as the overlying exogenous infections tend to be acute, suppurative and destruc-
tive. The second group, endogenous infections, is less common
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I n s i g h t The Journal of the American Society of Ophthalmic Registered Nurses, Inc. | October–December 2010 | Vol. XXXV, No. 4
Continuing Education (CE) Article
Conclusion
Episcleritis and scleritis are distinct clinical entities. Differentia-
tion between the two disorders can be made through a detailed
history, an external examination and a careful slit-lamp exami- Figure 4: Infectious necrotising scleritis following pterygium surgery
nation. Episcleritis is a relatively benign, self-limited disease,
infrequently requiring therapeutic intervention. Scleritis is a
painful, inflammatory process, requiring systemic anti-inflam- 5. Pearlstein E. Chapter 118: Episcleritis. In: Krachmer J, Mannis M, Holland
E, editors. Cornea Text & Color Atlas CD-ROM: Mosby CD online;
matory therapy and frequently associated with systemic autoim- 1998.
mune disorders. A prompt diagnosis of scleritis and initiation of
6. Jones W. Chapter 28: Diseases of the sclera. In: Bartlett J, Jaanus S, editors.
therapy is essential to assist in minimizing ocular complications. Clinical ocular pharmacology. 4th ed. Woburn: Butterworth-Heine-
mann; 2001; pp. 701–713.
References 7. Margo C. Recurrent episcleritis and emotional stress. Arch Ophthalmol.
1. Soukiasian S. Episcleritis and Scleritis: Diagnosis and Therapy. Sem Ophthal- 1984;102(6):821–24.
mol 1996;11(1):79–92. 8. Watson P. Vol. 4, Chapter 26: Diseases of the sclera and episclera. In: Tas-
2. Okhravi N, Odufuwa B, McCluskey P, Lightman S. Scleritis. Surv Ophthal- man W, Jaeger E, editors. Duane’s Ophthalmology on CD-ROM 2006
mol 2005;50(4):351–63. Edition. Philadelphia: Lippincott, Williams and Wilkins; 2006.
3. Sainz de la Maza M, Foster C. Vol. 1, Chapter 23: Sclera. In: Tasman W, 9. Schwam B, Raizman M. Chapter 119: Scleritis. In: Krachmer J, Mannis M,
Jaeger E, editors. Duane’s Ophthalmology on CD-ROM 2006 Edition. Holland E, editors. Cornea Text & Color Atlas CD-ROM: Mosby CD
Philadelphia: Lippincott, Williams and Wilkins; 2006. online; 1998.
4. Snell R, Lemp M. Clinical anatomy of the eye. 2nd ed. Malden: Blackwell 10. Raizman M. Chapter 80: Microbial scleritis. In: Pepose J, Holland G,
Science; 1998; pp. 139–143. Wilhelmus K, editors. Ocular infection and immunity. St. Louis:
Mosby; 1996; p. 1081–7.
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