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Sclera
19

3-SKLERA

Nov 28, 2015

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Page 1: 3-SKLERA

Sclera

Page 2: 3-SKLERA

Anatomy of The Sclera

• Composed primarily of type I collagen and proteoglycans

• Avascular, execpt :– superficial vesels of the episclera– intrascleral vascular plexus at posterior of the

limbus

• Anteriorly, consists of dense vascular connective tissue

Page 3: 3-SKLERA

Hypersensitivity Reaction and Ocular Disease

• Type I ( Anaphylactic or Atopic Reactions)– An antigen binds with two adjacent IgE --->

release of histamine and other mediator

• Type II (Cytotoxic Hypersensitivity)– Interaction of immunoglobines with antigens

--> cell lysis by complement activation– Killer cells are involved in antibodydependent

cell cytotoxity

Page 4: 3-SKLERA

• Type III (Immune-Complex Reactions)– follows the deposition of antigen-antibody

complexes in ocular tissue with complement activation and neutrophil recruitment

• Type IV (Delayed Hypersensitivity)– Antigens inter act with receptors on the surface

of T lymphocytes and result in the release of lymphokines

Page 5: 3-SKLERA

Type Ocular Disease I Allergic conjungtivitis Atopic keratoconjungtivitis & dermatitis II Ocular cicatrical pemphigoid Mooren ulcer III Scleritis IV Contact dermatitis

Phlyctenulosis

Hypersensitivity Reactions and Ocular Disease

Page 6: 3-SKLERA

Inflammation of the Sclera

• Episcleritis– benign inflammatory of the deep

subconjungtival connective tissues– occasionally fleeting, frequently repeated

(episcleritis periodica fugax)

Page 7: 3-SKLERA

– E/ : allergic reaction to an endogenous toxin– Clinical finding :

• Dense lymphatic infiltration of the subconjunctival and episcleral tissues

Page 8: 3-SKLERA

• Little or no pain, usually there is a feeling of discomfort and tenderness on pressure, often severe neuralgia

• Treatment :– corticosteroid drops/ointment– NSAID drops

Page 9: 3-SKLERA

• Scleritis– bilateral, occurred most frequently in women– more rare than episcleritis– may extend entirely round the cornea, forming

a very serious condition known as annular scleritis

– sometimes extend to cornea causing slerosing keratitis

– E/: immune-mediated vasculitis that inflames and destroys the sclera

– associated with systemic disease :• SLE, polyarteritis nodosa

Page 10: 3-SKLERA

• Clinical presentation– The swelling is at first dark red or bluish, later

it becomes purple and semi transparent– Onset usually gradual over several days

Subtypes And Prevalence of Scleritis

Location Subtype PrevalenceAnterior sclera Diffuse scleritis 40%

Nodular scleritis 44%Necrotizing scleritis 14% with inflammation (10%) without inflammation (4%)

Posterior sclera 2%

Page 11: 3-SKLERA

• Diffuse or nodular anterior scleritis– characterized by scleral edema and redness zone– scleral nodule is a deep red to purple colour, immobile,

and separated from the overlying episcleral tissue which is elevated by the nodule

Page 12: 3-SKLERA

• Necrotizing scleritis– the most destructive form– a localized patch of inflammation with the edge of

lesion more inflamed than the center– sclera becomes blue-gray appearance and an altered

deep episcleral blood vessel pattern

Page 13: 3-SKLERA

• Necrotizing scleritis without signs of inflammation (scleromalacia perforans)– in patiens with long-standing rheumatoid

arthritis (55% of cases)– signs are minimal and generally no pain– sclera thins and the underlying dark uveal tissue

become visible --> uvea is covered with only thin connective tissue and conjunctiva

Page 14: 3-SKLERA

• Posterior scleritis– occur in isolation or concomitant with anterior scleritis– signs are pain, tenderness, proptosis, visual loss and

restricted motility, retraction of the lower eyelid caused by infiltration of muscle in the region of posterior scleritis

– pain maybe reffered to other other parts of head --> D/ can be missed

Page 15: 3-SKLERA

Complications of scleritis

• Complication are frequent and include :– peripheral keratitis (37%)– uveitis (30%)– cataract (7%)– glaucoma (18%)– scleral thinning (33%)

• anterior uveitis as spillover phenomenon : anterior scleritis

• posterior uveitis : ant and post scleritis

Page 16: 3-SKLERA

Management of Scleritis

• In mild cases of diffuse anterior & nodular scleritis : topical corticosteroid

• NSAID (indomethacine, naproxen, diclofenac, etc) are also effective

• Oral and high dose IV steroid may be effective in necroting sleritis sclerokeratitis

Page 17: 3-SKLERA

Congenital Anomalies of Sclera

• Blue Sclera– Related to generalized thinning with increased

visibility of underlying uvea– Syndromes associated with :

• Osteogenesis imperfecta type I

• Ehlers-Danlos syndrome type VI (EDS VI)

• EDS VI with normal lysyl hydroxylase

Page 18: 3-SKLERA

– Clinical findings : All three syndrome share each other

– Management : regular hearing evaluation after adolescence

Page 19: 3-SKLERA

Degenerative Process of the Sclera

• Senile Plaques– E/:

• scleral reigidity• decrease of scleral hydration• decrease of mucopolysaccharide

– Accompanied by subconjungtival deposition of fat

– The plaques do not elicit inflammation and rarely extrude