episcleritis

1. EPISCLERITIS AND SCLERITIS

4. EPISCLERITIS
• It is common benign,recurrent and frequently
bilateral inflammation of the episclera
• Involves the overlying Tenon’s capsule but not
the underlying sclera.
• It typically affects young adults
• Twice as common in women than men.

5. ETIOLOGY
1. Idiopathic Exact etiology is not known in
many cases.
2. Systemic diseases, include gout, rosacea,
psoriasis and connective tissue diseases.
3. Hypersensitivity reaction to endogenous
tubercular or streptococcal toxins.
4. Infectious episcleritis may be caused by
herpes zoster virus, syphillis, Lyme disease
and tuberculosis.

6. PATHOLOGY
• Histologically, there occurs localised
lymphocytic infiltration of episcleral tissue
associated with oedema and congestion of
overlying Tenon’s capsule and conjunctiva.

7. CLINICAL FEATURES
SYMPTOMS-
• Redness
• Mild ocular discomfort -
gritty, burning or foreign
body sensation.
• Rarely, mild photophobia
and lacrimation may occur

8. SIGNS-
O/E-
• Simple episcleritis is ch. by sectorial (occasionally
diffuse) inflammation of episclera. The engorged
episcleral vessels are large and run in radial
direction beneath the conjunctiva .
• Nodular episcleritis is ch. by a pink or purple flat
nodule usually situated 2–3 mm away from the
limbus. The nodule is firm, tender, can be moved
separately from the sclera and the overlying
conjunctiva also moves freely

10. NODULAR EPISCLERITIS

11. CLINICAL COURSE
• Episcleritis runs a limited course of 10 days to
3 weeks and resolves spontaneously. However,
recurrences are common and tend to occur in
bouts. Rarely, a fleeting type of disease
(episcleritis periodica) may occur.

12. D/D
• Simple episcleritis may be confused rarely
with conjunctivitis.
• Nodular episcleritis may be confused with
inflamed pinguecula, swelling and congestion
due to foreign body lodged in bulbar
conjunctiva, phlyctenulosis which is within
rather beneath the conjunctiva and, very
rarely with scleritis.

13. DIFFERENTIAL
DIAGNOSIS
Phlyctenula
r
conjunctiviti
s
Conjunctiviti
s
Scleriti
s

14. TREATMENT
• If mild, no t/t required.
• Treat underlying disease.
• Cold compressus or Topical artificial tears e.g., 0.5%
carboxy methyl cellulose have soothing effect.
• Topical NSAIDs, e.g., ketorolac 0.3% may be useful.
• Topical mild corticosteroid eyedrops e.g.,
fluorometholone(0.1%) or loteprednol(0.5%) instilled
2–3 hourly for 1-2 weeks render the eye more
comfortable and resolve the episcleritis within a few
days.

15. • Systemic nonsteroidal anti-inflammatory
drugs (NSAIDs) such as flurbiprofen (300 mg
OD), indomethacin (25 mg three times a day),
or oxyphenbutazone may be required in
recurrent cases.

16. COMPLICATIONS
• Complications are uncommon.
• If high recurrent rate may lead to Anterior
Uveitis, Intermediate Uveitis, corneal change
but these are rare.

17. SCLERITIS
• Scleritis refers to a inflammation of the sclera
proper.
• It is a comparatively serious disease which
may cause visual impairment and even loss of
the eye if treated inadequately.
• Fortunately, its incidence is much less than
that of episcleritis.
• It usually occurs in elderly patients (40-70
years) involving females more than the males

18. ETIOLOGY
• Autoimmune collagen disorders
 Ankylosing spondylitis
 Rheumatoid arthritis
 Wegner’s granulomatosis
 Systemic lupus
erythematosis
 Psoriatic arthritis
 Ulcerative colitis
• Metabolic disorders like gout and thyrotoxicosis

19. INFECTIOUS SCLERITIS:
Spread of infection from corneal ulcer
Trauma
Excision of a pterygium or adjunctive B irradiation
or mitomycin C
Causative agents:
• Pseudomonas aeruginosa
• Strep. Pneumoniae
• Stap. Aureus
• Varicella zoster virus
Surgically induced scleritis (SIS) is a rare
complication of ocular surgery. It occurs
within 6 months postoperatively.

20. • Granulomatous diseases-
T.B
Syphilis
Leprosy
Sarcoidosis
• Miscellaneous conditions like irradiation,
chemical burns, Vogt-Koyanagi-Harada
syndrome, Behcet’s disease and rosacea
• Idiopathic In many cases of scleritis, cause is
unknown

21. CLASSIFICATION
Scleritis can be classified as follows:
A. Non-infectious scleritis
I. Anterior scleritis (98%)
a. Non-necrotizing scleritis (85%)
• 1. Diffuse
• 2. Nodular
b. Necrotizing scleritis (13%)
1. with inflammation
2. without inflammation (scleromalacia perforans)
II. Posterior scleritis (2%)
B. Infectious scleritis

22. PATHOLOGY
• Histopathological changes are that of a
chronic granulomatous disorder characterised
by fibrinoid necrosis, destruction of collagen
together with infiltration by
polymorphonuclear cells, lymphocytes,
plasma cells and macrophages. The granuloma
is surrounded by multinucleated epithelioid
giant cells and old and new vessels, some of
which may show evidence of vasculitis.

23. ANTERIOR NON-NECROTISING
SCLERITIS
DIFFUSE SCLERITIS
• It is the commonest variety.
• Relatively benign condition
• Ch. by widespread inflammation involving a
quadrant or more of the anterior sclera.
• The involved area is raised and salmon pink to
purple in colour

24. SYMPTOMS-
• Redness progressing to pain which may
radiate to face and temple.
• Ocular discomfort
• Vision may be blurred

25. SIGNS-
• Vascular congestion and dilatation a/w oedema.
• Redness may be genearised or localised to one
quadrant
• Secondary features can include chemosis, eyelid
swelling, anterior uveitis and raised IOP.
• As the oedema resolved the affected area often
takes slight grey/blue appearance because of
increased scleral translucency. This is due to
rearrangement of scleral fibres rather than a
decrease in scleral thickness.
• Recurrences at the same location are common

27. ANTERIOR NON-NECROTISING
SCLERITIS
NODULAR SCLERITIS:
• It is ch. by one or two hard, purplish elevated
immovable scleral nodules, usually situated
near the limbus.
• Sometimes, the nodules are arranged in a ring
around the limbus (annular scleritis)
• High association with HZO
• Nodule can’t be moved over underlying tissue
visual impairment

28. SYMPTOMS-
• Insidious onset of pain f/b increasing redness,
tenderness of the globe
• Appearance of a scleral nodule.
• Vision is often reduced
SIGNS-
• Scleral nodules may be single or multiple and most
frequently develop in interpalpabrael region close to
limbus. They have a deeper blue-red colour than
episcleral nodules and are immobile.
• In contrast to episcleritis, a slit lamp beam shows an
elevated anterior scleral surface.
• Multiple nodules may expand and coalesce if t/t is
delayed.

29. • Instillation of 10% phenylephrine
drops will constrict the conjunctival
and superficial episcleral vasculature
but not the deep plexus overlying the
nodule.
• As the inflammation in the nodule
subsides, increased translucency of
the sclera becomes apparent.
• More than 10% of patients with
nodular scleritis develop necrotizing
disease, but if treatment is instituted
early superficial necrosis does not
occur and the nodule heals from the
centre leaving a small atrophic scar.

30. Anterior necrotizing scleritis with
inflammation
• Necrotizing disease is the aggressive form of
scleritis.
• The age at onset is later than that of non-
necrotizing scleritis, averaging 60 years.
• The condition is bilateral in 60% of patients
and unless appropriately treated, especially in
its early stages, may result in severe visual
morbidity and even loss of the eye.

31. CLINICAL FEAUTURES
SYMPTOMS-
• Gradual onset of pain that becomes severe
and persistent and radiates to the temple,
brow or jaw.
• It frequently interferes with sleep and
responds poorly to analgesia.

32. SIGNS-
Vary according to the
following three types of
necrotizing disease:
Vaso-occlusive is
commonly a/w
rheumatoid arthritis.
Isolated patches of scleral
oedema with overlying
non-perfused episclera
and conjunctiva are
seen.The patches coalesce
and if unchecked rapidly
proceed to scleral necrosis

33. • Granuloma formation may occur in conjunction
with conditions such as granulomatosis with
polyangiitis or polyarteritis nodosa. The
disease typically starts with injection adjacent
to the limbus and then extends posteriorly.
Within 24 hours, the sclera, episclera,
conjunctiva and adjacent cornea become
irregularly raised and oedematous.

34. • Surgically induced scleritis
typically starts within 3 weeks
of a procedure, though much
longer intervals have been
reported.
• It may be induced by any type
of surgery including
strabismus repair,
trabeculectomy with excessive
exposure to mitomycin C ,
excision of pterygium and
scleral buckling.
• The necrotizing process starts
at the site of surgery and
extends outwards, but tends
to remain localized to one
sector

35. INVESTIGATIONS
Laboratory.
• ESR
• CRP
• CBC
• ANA
• ANCA
• CCP
• S.Uric acid
• Syphilis serology
• Lyme serology
Radiological imaging
• Chest, sinus, joint and other imaging

36. • Angiography Fluorescein angiography of the
anterior segment helps to distinguish
necrotizing disease by the presence of non-
perfusion and can be used for monitoring.
• Ultrasonography can help to detect associated
posterior scleritis.
• Biopsy. This may be considered in resistant
cases, especially if infection is suspected.

37. COMPLICATIONS
• Acute infiltrative stromal keratitis may be localized or
diffuse
• Sclerosing keratitis, characterized by chronic thinning and
opacification in which the peripheral cornea adjacent to the
site of scleritis resembles sclera.
• Peripheral ulcerative keratitis
• Uveitis
• Glaucoma is the most common cause of eventual loss of
vision. The intraocular pressure can be very difficult to
control in the presence of active scleritis.
• Hypotony (rarely phthisis) may be the result of ciliary body
detachment, inflammatory damage or ischaemia.
• Perforation of the sclera as a result of the inflammatory
process alone is extremely rare.

38. SCLEROMALACIA PERFORANS
• It is a specific type of progressive scleral thinning without
inflammation
• It typically affects elderly women with longstanding
rheumatoid arthritis, but has also been described in
association with other systemic disorders.
• Despite the nomenclature, perforation of the globe is rare
as integrity is maintained by a thin layer of fibrous tissue.
• D/d-innocuous scleral hyaline plaque and senile
scleromalacia
Symptoms:
• Mild non-specific irritation.
• Pain is absent and vision unaffected
• keratoconjunctivitis sicca may be suspected.

39. Signs
• Necrotic scleral
plaques near the
limbus without
vascular
congestion
• Coalescence and
enlargement of
necrotic areas.
Slow progression
of scleral thinning,
with exposure of
underlying uvea.

40. TREATMENT
• Effective in patients with early disease, less useful
in advanced disease.
• No consistent benefit from any specific agent has
been demonstrated.
• Frequent lubricant instillation, local or systemic
anticollagenase agents, immunosuppressives
(including topical and oral, but not periocular
injection of, steroids and topical cyclosporin) and
biological blockers have been used.
• Underlying systemic disease should be treated.
• Protection from trauma is important.
• Surgical repair of scleral perforation (e.g. patch
grafting) may be required to prevent phthisis bulbi

41. POSTERIOR SCLERITIS
• It is a potentially blinding condition in which
diagnosis is commonly delayed, with an adverse
prognostic effect.
• The inflammatory changes in posterior and
anterior scleral disease are identical and can arise
in both segments simultaneously or separately.
• The age at onset is often less than 40 years.
Young patients are usually otherwise healthy, but
about a third over the age of 55 have associated
systemic disease

42. DIAGNOSIS
Symptoms:
Pain does not correlate well with the severity of
inflammation but tends to be more severe in those
with accompanying orbital myositis.
Signs:
• The disease is bilateral in 35%.
• Choroidal folds are usually confined to the
posterior pole and orientated horizontally
• Exudative retinal detachment occurs in around
25%. The yellowish-brown subretinal exudative
material can be mistaken for a choroidal tumour.

43. • Uveal effusion with choroidal
detachment may be present.
• Disc oedema with accompanying
reduction of vision is common and is
caused by spread of inflammation into
the orbital tissue and optic nerve.
Treatment must not be delayed in these
patients as permanent visual loss can
rapidly ensue.
• Myositis is common and gives rise to
diplopia, pain on eye movement,
tenderness to touch and redness around
a muscle insertion.
• Proptosis is usually mild and is
frequently associated with ptosis.
• Occasional features include raised IOP,
periorbital oedema and chemosis.

45. • Ultrasonography may show increased scleral
thickness, scleral nodules, separation of
Tenon capsule from sclera, disc oedema,
choroidal folds and retinal detachment.
• Fluid in the Tenon space may give a
characteristic ‘T’ sign, the stem of the T
being formed by the optic nerve and the
cross bar by the fluid-containing gap.

46. • MR and CT may show scleral thickening and
proptosis.

47. D/D
• Subretinal mass
• Choroidal folds, retinal striae and disc oedema
may also occur in orbital tumours, orbital
inflammatory disease, thyroid eye disease,
papilloedema and hypotony.
• Exudative retinal detachment-Vogt–Koyanagi–
Harada (VKH) syndrome and central serous
retinopathy
• Orbital cellulitis may cause proptosis and
periocular oedema but is associated with marked
pyrexia

48. TREATMENT OF IMMUNE MEDIATED
SCLERITIS
A. Non-infectious scleritis
I. Non-necrotizing scleritis. It is treated by:
• Topical steroid eyedrops
• Systemic NSAID’s like indomethacin 75 mg twice a day until
inflammation resolves.
• Systemic Prednisolone-1-1.5 mg/kg/day are used when NSAID’s
are inadequate. IV methylprednisolone(0.5-1g daily for 3 days)
may be used for severe cases.
• Subconjunctival steroid injections: Triamcinolone acetonide
(40mg/ml) .Only for non-necrotizing type.

49. II. Necrotizing scleritis. It is treated by:
• Topical steroids
• Oral steroids on heavy doses, tapered slowly.
• Immunosuppressives and/or
immunomodulatory agents should be considered
if control is
(a) incomplete with steroids alone
(b)as a steroid-sparing measure in long-term
treatment
(c) to treat underlying systemic disease.

50. A wide range of drugs are available, including
cytostatics (e.g. cyclophosphamide, azathioprine,
methotrexate), drugs acting on immunophilins (e.g.
ciclosporin, tacrolimus) and biologicals.
In necrotizing disease, rituximab is particularly
effective
• Subconjunctival steroids are contraindicated
because they may lead to scleral thinning and
perforation.
• Surgical treatment, in the form of scleral patch
graft may be required to preserve integrity of the
globe in extensive scleral melt and thinning.

51. INFECTIOUS SCLERITIS
• Infectious scleritis accounts for 5–10% of all cases.
• In the early stage diagnosis becomes difficult as
presentation is similar to as non-infectious scleritis.
• Scleritis with purulent exudates or infiltrates should
raise the suspicion of an infectious etiology.
• Formation of fistulae, painful nodules, conjunctival and
scleral ulcers are usually the signs of infectious scleritis
Causes –
• Herpes zoster is the most common infective cause.
• Tuberculous scleritis is rare and difficult to diagnose.
The sclera may be infected by direct spread from a local
conjunctival or choroidal lesion, or more commonly by
haematogenous spread. Involvement may be nodular or
necrotizing.

52. • Leprosy Recurrent necrotizing scleritis can occur,
even after apparent systemic cure. Nodular
disease may be seen in lepromatous leprosy.
• Syphilis Diffuse anterior scleritis may occur in
secondary syphilis and occasionally scleral
nodules may be a feature of tertiary syphilis.
• Lyme disease Scleritis is common but typically
occurs long after initial infection.
• Other causes include fungi, Pseudomonas
aeruginosa and Nocardia

53. TREATMENT
• Most of the time diagnosis is delayed and
patients are put on topical and oral steroids
which worsen the infective scleritis.
• Antimicrobial therapy, both with topical and
oral agents is required in an aggressive
manner.
• Surgical debridement is found useful by
debulking the infected scleral tissue and also
facilitating the effect of antibiotics

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