Vernal kerato conjunctivitis

vkc/spring catarrah/allergic conjunctivitis

1. VERNAL KERATO CONJUNCTIVITIS SIVATEJA CHALLA

2. Recurrent,bilateral,seasonal external ocular allergy primarily affects children and young adults Predisposing factors :: AGE- 80% <14 yrs SEX- Males>Females SEASON-exacerbates during spring FAMILY H/O allergic disease PERSONAL H/O atopic diseases like asthma,hay fever DRY and HOT environments

3. IMMUNE PATHOLOGY type 1 AND type 4 hypersensitivity plays an important role ALLERGENS  OCULAR SURFACE BIND TO MAST CELL IgE  ACTIVATION OF MAST CELL CALCIUM ENTERS THE CELL DEGRANULATION OF MAST CELL RELEASE OF MEDIATORS

4. Early phase mediators like histamine,protease cause itching redness swelling degradation of neighbouring cells and inflammatory cell accumulation Other mediators like PG’S,LT’S,PAF,CYTOKINES,CHEMOKINES also mediate redness,swelling,infiltration of eosinophils and neutrophils EOSINOPHILS release MBP and ECP are epitheliotoxic and involved in corneal damage Tear levels of ECP are considered as local markers of eosinophil activation and correlated with clinical signs and symptoms

5. CLINICAL FEATURES SYMPTOMS 1.INTENSE ITCHING 2.REDNESS 3.TEARING 4.PHOTOPHOBIA 5.MUCOUS DISCHARGE 6.BLEPHAROSPASM(TWITHES) Some people may experience drooping of eyelids

6. SIGNS Papillary reaction. Conj redness and edema GPC. Limbal gelatinous infiltrate. Trantas dots. Mucus discharge. Pseudoptosis . Tarsal conjunctival fibrosis. THREE clinical forms 1.Palpebral type 2.Limbal type 3.Mixed type

7. Progression of vernal conjunctivitis Diffuse papillary hypertrophy, most marked on superior tarsus Formation of cobblestone papillae Rupture of septae - giant papillae

8. Limbal vernal Trantas dots Mucoid nodule

9. Vernal keratopathy Occurs in about 50% patients of VKC starts as superficial punctate keratitis Epithelial erosion Ulcerative venal keratitis(shield ulcer) Vernal corneal plaques Sub epithelial scarring Pseudogerentoxon keratoconus

10. Progression of vernal keratopathy Punctate epitheliopathy Epithelial macroerosions Plaque formation (shield ulcer) Subepithelial scarring

11. Diagnostic approaches: Clinically. Specific IgE maybe assayed in serum and tears. CBC for eosinophilia. Tear levels of tryptase Conj scraping and tear cytology: Eosinophils . Basophils. Neutrophils .

12. Histopathology: Proliferative and degenerative changes in the epithelium: Occur early with marked acanthosis , and intraepithelial pseudocysts . Prominent cellular infiltration in the substantia propria : Eosinophils , neutrophils, basophils, lymphocytes, and plasma cells. Resident plasma cells and fibroblasts are also increased . Typically mast cells contain enzymes tryptase and chymase Hyperplasia of the connective tissues: Mainly type III collagen, they run parallel to the surface forming the fibrous structure for giant papillae.

13. TREATMENT NON PHARMACOLOGICAL INTERVENTION Avoidance of allergens remains the first step Cold compression provide symptomatic relief especially itching Lubrication with preservative free drops may wash out allergans from conjunctival sac Change of climate

14. PHARMACOLOGICAL INTERVENTION FOR MILD CASES 1.Cool compress 2.Ocular lubricants 3.Decongestant antihistaminics 4.Mast cell stabilisers 5.Environment control FOR MODERATE TO SEVERE CASES 1.topical/oral antihistaminics 2.Mast cell stabilisers 3.NSAIDS 4.Topical steroids 5.Acetyl cysteine to eliminate mucous

15. ANTI HISTAMINICS TOPICAL Antihistamine– emadastine 1 drop qid S/E headache Antihistamine+decongestant -- naphazoline 0.025%+ pheneramine 0.3% -- S/E rebound congestion ORAL Benadryl chlorpheneramine maleate Cetrizine HCL S/E somnolence,dry mouth

16. STEROIDS TOPICAL STEROIDS For moderate to severe forms Careful monitoring to detect steroid induced glaucoma and steriod responder MOA- inhibitis phospholipase which convert phospholipids to arachodonic acid EXAMPLES- 1.Prednisolone 0.01 to 1% hourly to BID 2.loteprednol 0.2 to 0.5% QID 3.flouromethalone BID TO QID S/E may cause IOP raise and cataract formation PULSE THERAPY

17. MAST CELL STABILISERS Plays an important role Most effective when began before the onset of symptoms,may need 14 days for clinical effects to occur Until then topical antihistaminics and steroids can be used Examples 1.cromolyn sodium QID 2.lodaxamide 0.1% QID MOA  Block influx along mast cell mem,inhibits degradation S/E Burning/sting LODAXAMIDE IS 2500 TIMES MORE POTENT

18. MAST CELL STABILISERS+ANTI HISTAMINICS Dual acting drugs MOA  inhibits mast cell degaranulation  also block the H1 receptors  blocks type1 hypersensitivity reaction S/E headache Examples -- olapatdine hcl 0.1% 1drop BID -- olapatidine hcl 0.2% 1drop once daily -- ketotifen 0.025% 1 drop BID S/E hyperemia -- Azolastine 0.05% 1drop BID S/E burn/sting

19. NSAIDS TOPICAL MOA inhibits cox pathway Examples --ketorolac 0.5% --indomethacin 1% -- flubiprofen 0.03% S/E burn/sting ORAL 650 mg tid can be tried in severe to intractable cases along with mast cell stabilisers

20. CYCLOSPORINE 2% QID Severe to intractable VKC MOA Immunosuppressive,T CELL inhibition reduce collagen producn and coz apoptosis of fibroblasts S/E burning sensation Subjective and objectve improvement occurs in 3 days and complete improvement will occur in 6 weeks

21. SURGICAL SHIELD ULCER --vision threatining complication of vkc --treat with topical antibiotic and steriod eye ointment --occlusive therapy --if plaque forms in ulcer bed sup keratectomy may be beneficial for epithelium healing --non resolving shield ulcer may requrie keratectomy with amniotic membrane grafting GAINT PAPILLAE -- surgical excision -- cryotherapy for upper tarsus -- supratarsal steroid injection --topical tacrolimus for refractile cases

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