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PERIPHERAL ULCERATIVE KERATITIS
Peripheral ulcerative keratitis is characterized by crescent-shaped inflammation of the corneal stroma, often associated with autoimmune disorders and various ocular conditions. Differential diagnoses include several forms of keratitis and degeneration, while treatment typically involves steroids, immunosuppression, and surgical options such as amniotic membrane grafts. The condition requires careful management due to its association with systemic diseases and potential for severe ocular complications.
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PERIPHERAL ULCERATIVE KERATITIS
- 1. PERIPHERAL ULCERATIVE KERATITIS DR. K.VASANTHA M.S.,F.R.C.S. Ed Director RIO Chennai (Rtd)
- 2. Definition • Crescent shapeddestructive inflammation of the juxta limbal corneal stroma • associated with epithelial defect, • stromal inflammatory cells • and stromal degradation
- 3. • Usually conjunctiva,episclera and sclera are also involved. • Biopsy will show micro angiopathy. • Antibodies to corneal epithelium is also found. • In ANCA +ve vasculitides cell mediated cytotoxicity is also found
- 4. DIFFERENCIAL DIAGNOSIS • Peripheraldegenerations like • Arcus, White limbal girdle of Vogt • Idiopathic furrow degeneration – thinning in the area of arcus • Marginal keratitis
- 5. D.D • Post irradiationesp. Beta radiation • Terrien’s marginal degeneration • Bilateral, young males, superior, stromal thinning, ectasia, lucid interval between the lesion and the limbus. • Yellow lipid border at the advancing edge.
- 6. CLINICAL ASSOCIATIONS AUTOIMMUNE DISORDERS RA, PAN, WG,SLE, Sjogrensdis Behcets dis, relapsing polychondritis SYSTEMIC INFECTIONS Hepatitis C Syphilis salmonella OCULAR CONDITIONS Herpes simplex Fungi varicella zoster acanthamoeba
- 8. Why limbus isinvolved? • Limbal arcades • Inflamed vessels draw inflammatory cells which cause destruction • Tight collagen bundles in the periphery facilitates collection of IgM, C1 and other high molecular weight molecules • Immune complex deposits at the limbus and corneal periphery
- 9. Why? • Presence ofLangerhans cells in the conj., and corneal periphery • Limbal macrophages (antigen presenting cells) will be up regulated when there is inf., and immune mediated events occur • Channels from sub conj lymphatics enter the periphery of the cornea- afferent arm • Limbus is a reservoir of effector cells of immune sys., cytokines
- 10. RHEUMATOID ARTHRITIS • Autoimmune •Typical joint deformities • Ocular surface disorders more common • Corneal melting can occur • Following surgery PUK more common
- 11. Systemic Lupus Erythymatosis •Dysfunction of immune regulation by T cells and B cells • Ocular surface disorder is more common
- 12. Wegener’s • Necrotizing granulomatousvasculitis • Bilateral PUK • Lead on to ring ulcer • Scleral inflammation is severe, may lead on to necrosis • Steroids not effective
- 13. Relapsing poly chondritis •Cartilages involved • Auditory impairment, tinnitus and vertigo • Other collagen vascular disorders may co exist • Ring ulcer with scleritis, bilateral – rare • Lid edema, iritis, retinopathy, optic neuritis • Cornea has glycosamino glycans- same as sclera, aortic wall, cartilage and inner ear
- 14. Poly arteritis nodosa •Non granumatous necrotizing vasculitis both small and medium • URI, drug abuse, hepatitis b and c • Pseudo tumor, papilledema, papillitis, muscle involvement • Mooren’s like PUK • Interferon alfa 2b. Steroids alone not effective, cyclophosmamide to be added
- 15. MICRO POLYANGIITIS • ANCAagainst myeloperoxidase • Mooren’s like PUK, often bilateral with scleral involvement • Uveitis, ischemic optic neuropathy, muscle palsies
- 16. MOOREN’S ULCER • Firstdescribed by Bowman in 1949 • Mooren published a paper later • Type iii hypersensitivity ? • Diagnosis by exclusion • PUK may be the presenting feature of collagen vascular diseases
- 17. • Primary –classic, idiopathic • Secondary – trauma, surgical, chemical injury, Herpes, syphilis, tuberculosis, Hepatitis C, helminthiasis both ascariasis and ancylostoma
- 18. • Fulminating, • centrallyprogressive, • painful • more common in males • Under mining edge • Sclera not usually involved • Absence of any systemic disorder
- 19. Benign • Older patients •Unilateral • Responds to steroids
- 21. Severe • Younger • Bilateral •Progressive • Sclera and episclera may be involved
- 22. Histology • Necrosis ofcollagen tissue • Chronic inflammatory cells • Vascularisation of limbal margin • Auto anti bodies to epithelium • Polymorphs which are responsible for collagenolysis
- 23. TREATMENT • Steroids everyhour • Conjunctival excision- not just peritomy • This helps by removing the causative factors • Tissue adhesives – excludes neutrophils from reaching the involved area • Tetra cyclines to prevent collagenolysis
- 24. Immuno suppression • Methotrexate7.5 to 15 mg/week • Azathioprine 2 mg/kg/day • Cyclophosphamide 2 mg/kg/day • The above three must be given for 6 months and then tapered • For Mooren’s topical cyclosporine can be used • Before cataract surgery immune suppression
- 25. surgical • Amniotic membranegraft • Tectonic kp to prevent the immune complexes from reaching the cornea • Palliative, temporizing, inadequate to prevent recurrences as immunologic process continues
- 29.