This document discusses episcleritis and scleritis. It begins with an introduction to the anatomy of the sclera and its blood supply, innervation and functions. It then discusses episcleritis, describing it as a common, self-limiting condition characterized by redness and mild discomfort. Scleritis is defined as inflammation of the sclera proper and can be classified as anterior or posterior. Anterior scleritis is further classified as non-necrotizing or necrotizing. Signs, symptoms, investigations, and treatments are provided for both conditions. Complications are also mentioned. The document concludes by briefly discussing blue sclera caused by thinning of the scleral collagen.

1. TOPIC:
EPISCLERITIS AND SCLERITIS
LUMBINI MEDICAL COLLEGE AND
TEACHING HOPSITAL PVT. LTD.
BY-------- INTERN VISHAL BARUN

2. CONTENTS:
I. Introduction
II. Anatomy
III. Episcleritis
IV. Immune mediated scleritis
V. Scleral discoloration
VI. Blue sclera
VII.Reference

3. INTRODUCTION:
 The sclera forms the posterior opaque 5/6 part of the
external fibrous tunic of the eyeball.
 Whole outer surface : Tenon’s capsule
 Anterior part: bulbar conjunctiva
 Inner surface: contact with choroid with a potential
suprachoroidal space in between.

4.  Thickness varies with individual, with age
 Thinner: children, elder, F>M
 Thickest posteriorly
 Gradually becomes thinner when traced anteriorly
 Thin at insertion of extra-ocular muscle.

6. Blood Supply
 Episclera: anterior and posterior ciliary arteries.
 Scleral stroma: relatively avasculature structure.

8. Venous Drainage
• Episclera collecting veins
• Vortex veins
Anterior ciliary vein

9. Nerve Supply
• Rich in nerve supply.
• Anterior sclera: long posterior ciliary nerves which
pierce it 2-4mm from the limbus to form a plexus.
• Posterior sclera: short posterior ciliary nerves.

10. Functions
Protects intraocular components from trauma, light
and mechanical displacement.
Withstands the considerable expansive force
generated by the intraocular pressure maintaining
the shape of the globe.
Provides attachment sites for the extra ocular
muscles.

11. EMBRYOLOGY:
• Sclera: >derived from mesenchyme > derived from
neural crest.

12. EPISCELRITIS:
o It is a common benign usually idiopathic, recurrent
and frequently bilateral condition.
o Self limiting
o Attacks : last a few days.
o Types: 2
I. Simple
II. Nodular

13. ETIOLOGY
1. Idiopathic
2. Systemic disease: gout, psoriasis, connective tissue
disease
3. Hypersensitivity reaction: endogenous tubercular,
streptococcal toxins.
4. Infectious : herpes zoster virus, syphilis, Lyme
disease, tuberculosis

14. Pathology
• Localized lymphocytic infiltration of episcleral
tissue.
• Oedema and congestion of overlying Tenon’s
capsule and conjunctiva.

15. Incidence
 female adults are affected more commonly than
male adults

16. SYMPTOMS
• Redness
• Mild ocular discomfort described as gritty, burning
or foreign body sensation.
• Rarely : mild photophobia and lacrimation

17. SIGN
(A)Diffuse :
• Whole eye may be involved to some extent
• The maximum inflammation is confined to one or two quadrant.
(B)Nodular:
• A pink or purple flat nodule surrounded by injection is seen, 2-3mm away from the
limbus.
• Nodule is firm, tender & overlying conjunctiva moves freely.
(A) (B)

18. CLINICAL COURSE
• Limited course of 10 days to 3 weeks and resolves
spontaneously
• Recurrence are common and tend to occur in bouts.
• A fleeting type of disease(episcleritis periodica) may
occur.

19. TREATMENT
• Cool artificial tear
• Topical corticosteroids eye drops 2-3 hourly
• Cold compression
• Oral NSAIDS:
I. flurbiprofen 100 mg T.I.D for 10 days
II. Indomethacin 25 mg Q.I.D
III. Oxyphenbutazone in (recurrent cases)

20. Differential Diagnosis
• Inflammed pinguecula
• Scleritis
• Foreign body reaction on bulbar conjunctiva

21. SCLERITIS
• It is a chronic inflammation of the
sclera proper.
• F>m
• Elderly : 40-70 years of age

22. A. Auto immune collagen disorder:
I. RA (common)
II. Wegner’s granulomatosis
III. SLE
B. Infections :
I. Herpes zoster ophthalmicus
II. Streptococcal infection
ETIOLOGY

23. C. Granulomatous disease:
I. TB, syphilis, sarcoidosis, leprosy
D. Miscellaneous condition:
I. irradiation, chemical burns.
E. Surgically induced scleritis: ocular surgery within 6
months post-operatively
F. Idiopathic

24. PATHOLOGY
Infiltration by PMNL, lymphocytes, plasma cells and macrophages
Fibrinoid necrosis, destruction of collagen
Granuloma surrounded by multinucleated epitheloid giant cells.

25. CLASSIFICATION
1. Anterior scleritis (98%)
 Non- necrotizing scleritis (85%)
A. Diffuse B. Nodular
 Necrotizing scleritis (13%)
A. with inflammation
B. without inflammation (scleromlacia perforans)
2. Posterior scleritis (2%)

26. Symptom
I. Moderate to severe pain:
* Deep and boring in character nd often
* Wakes the patient early in the morning
* Radiates to the jaw and temple.
II. Localized or diffuse redness
III. Mild to severe photophobia
IV. lacrimation

27. SIGNS
NON-NECROTIZING ANTERIOR DIFFUSE SCLERITIS:
• Vascular congestion and dilation associated with oedema
• Develop: redness generalized or localized to one quadrant.
Edema resolves affected area often takes place slight grey and blue appearance

28. NON-NECROTIZING ANTERIOR NODULAR SCLERITIS:
• Scleral nodules: single or multiple (a)
• Develop: inter palpable region 3-4mm away from the limbus
• Deeper blue red color than episcleral nodules
• Immobile
• SLIT LAMP EXAM.: slit beam is displaced by the scleral
nodule (b)

29. ANTERIOR NECROTIZING SCLERITIS WITH
INFLAMMATION:
• Aggressive form of scleritis
• Present in 6th decade
• Results : severe visual morbidity and loss of the eye.
SIGN: 3 types of necrotizing disease:
1. vaso-occlusive: associated RA.
2. Granulomatous: associated wegner granulomatosis and polyarteritis
nodosa.
3. Surgically induced scleritis: starts within 3-6 weeks of the surgical
procedure.

30. Vaso-occlusive necrotizing scleritis Granulomatous necrotizing scleritis
With inflammation with inflammation
(a) Early stage surgically induced scleritis
(b) Advanced stage (a) following trabeculectomy
(b) following scleral buckling
(c) following use of mitomycin c

31. SCLEROMALACIA PERFORANS:
It is a specific type of necrotizing scleritis without
inflammation.
Affects: elderly women with long standing RA.
Clinical features:
Presentation:
• Slight non specific irritation
• Keratoconjuctivitis sicca-suspected
• Pain-absent
• Vision- unaffected

32. SIGNS:
1. Necrotic scleral plaques near the limbus without vascular congestion.
2. very slow progression of scleral thinning out exposure of underlying uvea.

33. Posterior scleritis
1. The sclera behind the equator
2. Frequently misdiagnosed
3. Associated inflammation of adjacent structures:
 Exudative retinal detachment
 Macular edema
 Proptosis
 Limitation of ocular movements

34. COMPLICATION
• 2’ Glaucoma (due to uveitis)
• Complicated cataract
• Sclerosing keratitis
• Keraotlysis

35. INVESTIGATION:
1. TLC, DLC & ESR
2. Immunological assay: Serum levels of complement(c3),
immune complexes, RA factor, antinuclear antibodies
3. Syphilis: FTA-ABS, VDRL
4. Gout: serum uric acid
5. Urine analysis
6. Mantoux test
7. Nodular scleritis: x-ray of chest, paranasal sinuses, sacroiliac
joint and orbit.

36. TREATMENT
(A)NON-NECROTISING SCLERITIS:
• topical steroid eye drop
• systemic : indomethacin 100 mg daily for a day and then 75 mg daily
until inflammation resolves.
(B) NECROTISING SCLERITIS:
• topical steroids and heavy doses of oral steroids tapered slowly
• NON RESPONSIVE: methotrexate and cyclophos-phamide
(immunosuppressive agents)

37. BLUE SCLERA
It is caused by thinning or transparency of scleral collagen
with visualization of the underlying uvea.
ETIOLOGY:
I. Osteogenesis imperfecta
II. Ehlers – Danlos syndrome Type VI (ocular sclerotic)

38. REFERENCE
Kanski's Clinical Ophthalmology 7th Edition
A. K. Khurana comprehensive ophthalmology fifth
edition
 Wikipedia
American Academy Of Ophthalmology
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