Downloaded 30 times
![EPISCLERITIS
• Simple episcleritis
• Nodular episcleritis
SCLERITIS
o Immune mediated
• Anterior
- Non-
necrotising
- Necrotising
with
inflammation
- Necrotising
without
inflammation
(scleromalacia
perforans)
• Posterior
o Infectious
• Topical steroids - do not affect the natural history of the scleral
inflammation, but may relieve symptoms and oedema in non-necrotizing
disease
• Systemic NSAIDs should be used alone only in non-necrotizing disease
• Periocular steroid injections may be used in non-necrotizing disease
but their effects are usually transient; [contraindicated in necrotizing
scleritis]
• Systemic steroids (e.g. prednisolone is 1–1.5 mg/kg/day) are used
when NSAIDs are inappropriate or inadequate (necrotizing disease).
Intravenous methylprednisolone may be used for emergent cases.
• Immunosuppressives and/or biological blockers - if control is
incomplete with steroids alone, as a steroid-sparing measure
cyclophosphamide, azathioprine, methotrexate, ciclosporin, tacrolimus and
others;
Treatment of immune-mediated scleritis](https://image.slidesharecdn.com/diseasesofscleraeyeamnikhil-221006171741-f8ceb9cc/75/Diseases-of-sclera-43-2048.jpg)
Uploaded byNIKHIL GOTMARE
Diseases of sclera
The document discusses diseases of the sclera, including episcleritis and scleritis. Episcleritis is a benign inflammation of the outer layer of the eyeball that comes in two forms - simple and nodular. Scleritis is a deeper inflammation that involves the entire thickness of the sclera. Scleritis can be immune-mediated, infectious, or necrotizing. Treatment depends on the type but may include topical steroids, NSAIDs, or systemic steroids and immunosuppressive drugs.
More Related Content
Similar to Diseases of sclera
Diseases of sclera
- 1.
- 2.
- 3. Anatomyofsclera It forms theposterior opaque 5/6th part of the external fibrous coat of the eyeball Eye has three coats: Outer – Fibrous Middle – Vascular Inner - Nervous
- 4. • Outer surface- covered by Tenon's capsule • Anterior part - covered by bulbar conjunctiva
- 5. Its inner surface liesin contact with choroid with a potential suprachoroidal space in between
- 6. • In itsanterior most part near limbus there is furrow which encloses the Schlemm’s canal
- 7. Thicknessofsclera • Thinner -children and in females • Thickest - posteriorly (1mm), gradually becomes thin when traced anteriorly • Thinnest - insertion of extraocular muscles (0.3 mm)
- 8. Aperturesofsclera • Anterior - Anteriorciliary vessels, nerves and lymphatics • Middle four vortex veins • Posterior - Short ciliary vessels and nerves - Long ciliary arteries - Optic nerve
- 9. • Anterior - Anteriorciliary vessels, nerves and lymphatics
- 10. • Middle four vortex veins •Posterior - Short ciliary vessels and nerves - Long ciliary arteries - Optic nerve
- 12. Layersofsclera Sclera Episcler a Sclera proper Lamina fusca Thin, dense vascularizedlayer of connective tissue fibroblasts, macrophages and lymphocytes Avascular structure dense bundles of collagen fibres Innermost blends with suprachoroidal and supraciliary laminae of the uveal tract. brownish in colour presence of pigmented cells
- 14. Staphylomas • Localised bulgingof weak and thin outer tunic of the eyeball (cornea or sclera) • Lined by uveal tissue which shines through the thinned out fibrous coat. {‘Staphylo-’ bunch of grapes}
- 15. Classification • posterior • Anterior •Intercalary • Ciliary • Equatorial
- 16. Anteriorstaphyloma • Ass. Withectasia of cornea & iris • Due to perforating corneal ulcer & injury
- 17. Intercalarystaphyloma healing of aperforating injury or a peripheral corneal ulcer to ectasia of weak scar tissue formed at the limbus localised bulge in limbal area lined by root of iris {‘Intercalary’ - Occurring between differentiated tissues}
- 18. Ciliarystaphyloma • Bulge ofweak sclera lined by ciliary body • About 2-3 mm away from the limbus • Thinning of sclera following perforating injury, scleritis and absolute glaucoma
- 19. Equatorialstaphyloma • Bulge ofsclera lined by the choroid in the equatorial region at the regions of sclera which are perforated by vortex veins. • Causes - Scleritis and degeneration of sclera in pathological myopia {‘Equator - 14mm behind limbus}
- 21. Posteriorstaphyloma • Bulge ofweak sclera lined by the choroid behind the equator • Common causes are pathological myopia, posterior scleritis and perforating injuries.
- 22. Diagnosis Ophthalmoscopy • Thearea is excavated with retinal vessels dipping in it
- 24.
- 25. Bluesclera Marked, generalised bluediscolouration of sclera due to thinning
- 26. CausesofBluesclera • Mnemonic- {H O P E S are too big } H - High myopia, Hurlers and Healed scleritis O - Osteogenesis imperfecta - Oculodermal melanosis P - Pseudoxanthoma elasticum E - Ehlers-Danlos syndrome S – Scleritis, Staphyloma, Scleromalacia perforans Are - Marfan's syndrome Too – Turner’s
- 27. Inflammations of sclera •Episcleritis(superficial) •Scleritis (deep)
- 28. Anterior scleritis (98%)Posterior scleritis (2%) Necrotizing scleritis with inflammation Non-necrotizing scleritis (85%) (a) Diffuse (b) Nodular Inflammationsofsclera EPISCLERITIS (SUPERFICIAL) SCLERITIS (DEEP) • Simple episcleritis • Nodular episcleritis Immune mediated Infectiou s Necrotizing scleritis without inflammation (Scleromalacia perforans)
- 29. Episcleritis • Benign, recurrentinflammation of the episclera, involving the overlying Tenon's capsule but not the underlying sclera • Common • Usually idiopathic • Females > males • Middle age EPISCLERITIS • Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 30. Simple episcleritis • Accountsfor 75% of cases • Tendency to recur (60%) • Features often peak within 24 hours, gradually fading over the next few days EPISCLERITIS • Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 31. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious Nodular episcleritis • Less acute onset and a more prolonged course • Red eye typically first noted on waking, over next 2-3 days area of redness enlarges and becomes more uncomfortable • Tender red vascular nodule (Interpalpebral area) • Underlying flat anterior scleral surface deep beam is not displaced above the scleral surface
- 32. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious Treatment • If mild – No treatment, cold compress or refrigerated artificial tears • Weak topical corticosteroid eyedrops, four times a day 1-2 weeks • Topical NSAID is an alternative, though maybe less effective • Oral NSAID is occasionally
- 33. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious SCLERITI S • Oedema and cellular infiltration of the entire thickness of sclera
- 34. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious Immune mediated scleritis • Most common type • Much less common than episcleritis • Spectrum – from trivial and self limiting disease to a necrotizing process that can involve adjacent tissue and threaten vision
- 35. Non- necrotizing Diffus e Nodular superficial displaceme nt of the entire beam EPISCLERITIS •Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 36. Non- necrotizing EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious • Female > males • 5th decade • Redness – bluish hue, vessels do not blanch with 10% phenylephrine, immobile • Pain may radiate to face and temple, discomfort wakes patient in early hours of morning • When edema/inflammation subsides affected area takes grey/bluish appearance • Duration- avg- 6 years with frequent reccurences decreasing after first 18months • Long term visual prognosis is good
- 37. Necrotizing scleritis EPISCLERITIS • Simpleepiscleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious ○ Vaso-occlusive • commonly associated with rheumatoid arthritis • Isolated patches of scleral oedema with overlying non- perfused episclera and conjunctiva • Patches coalesce, and if unchecked rapidly proceed to scleral necrosis ○ Granulomatous • may occur in conjunction with conditions such as granulomatosis or polyarteritis nodosa • Within 24 hours, the sclera, episclera, conjunctiva and adjacent cornea become irregularly raised and oedematous
- 38. ○ Surgically inducedscleritis • typically starts within 3 weeks of a procedure- strabismus repair, trabeculectomy and scleral buckling, and excision of pterygium with adjunctive mitomycin C. • The necrotizing process starts at the site of surgery and extends outwards, but tends to remain localized to one sector. EPISCLERITIS • Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 39. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious Scleromalacia perforans • 5% of scleritis • Progressive scleral thinning without inflammation • Affects elderly women with longstanding rheumatoid arthritis (but has also been described in association with other systemic disorders) Symptoms • Mild non-specific irritation • pain is absent and vision unaffected 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. Posterior scleritis • Sclerabehind the equator • frequently misdiagnosed • Choroidal folds at posterior pole, oriented horizontally • Exudative RD EPISCLERITIS • Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 41. Fluid in theTenon 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 EPISCLERITIS • Simple episcleritis • Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious
- 42. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious Investigations • Laboratory: ESR, CRP, ANA, C-ANCA, P-ANCA, CCP, syphilis serology, Lyme serology, hepatitis B surface antigen and antiphospholipidantibodies. • Investigation for tuberculosis, sarcoidosis or ankylosing spondylitis • Radiological imaging: Chest, sinus, joint and other imaging may be indicated in the investigation of a range of conditions such as tuberculosis, sarcoidosis, Churg–Strauss syndrome, Wegener granulomatosis, ankylosing spondylitis and other condition
- 43. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious • Topical steroids - do not affect the natural history of the scleral inflammation, but may relieve symptoms and oedema in non-necrotizing disease • Systemic NSAIDs should be used alone only in non-necrotizing disease • Periocular steroid injections may be used in non-necrotizing disease but their effects are usually transient; [contraindicated in necrotizing scleritis] • Systemic steroids (e.g. prednisolone is 1–1.5 mg/kg/day) are used when NSAIDs are inappropriate or inadequate (necrotizing disease). Intravenous methylprednisolone may be used for emergent cases. • Immunosuppressives and/or biological blockers - if control is incomplete with steroids alone, as a steroid-sparing measure cyclophosphamide, azathioprine, methotrexate, ciclosporin, tacrolimus and others; Treatment of immune-mediated scleritis
- 44. EPISCLERITIS • Simple episcleritis •Nodular episcleritis SCLERITIS o Immune mediated • Anterior - Non- necrotising - Necrotising with inflammation - Necrotising without inflammation (scleromalacia perforans) • Posterior o Infectious • Rare • But may present diagnostic difficulty as the initial clinical features are similar to those of immune-mediated disease Causes • Herpes zoster is the most common infective cause. • Tuberculous scleritis is rare and difficult to diagnose. • Leprosy. • Syphilis. • Lyme disease. • Other causes include fungi (Fig. 8.14D), Pseudomonasaeruginosa and Nocardia. Treatment • Once the infective agent has been identified, specific antimicrobial therapy initiated • Topical and systemic steroids may also be used to reduce the inflammatory reaction • If appropriate, surgical debridement - to debulk a focus of infection and facilitates the penetration of antibiotics Infectious scleritis
- 46.