Vernal kerato conjunctivitis

VERNAL KERATO CONJUNCTIVITIS

SIVATEJA CHALLA

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

IMMUNE PATHOLOGY• type 1 AND type 4 hypersensitivity plays an important role

ALLERGENSOCULAR SURFACEBIND TO MAST CELL IgEACTIVATION OF MAST CELLCALCIUM ENTERS THE CELLDEGRANULATION OF MAST CELLRELEASE OF MEDIATORS

• 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

CLINICAL FEATURESSYMPTOMS1.INTENSE ITCHING2.REDNESS3.TEARING4.PHOTOPHOBIA5.MUCOUS DISCHARGE6.BLEPHAROSPASM(TWITHES)

Some people may experience drooping of eyelids

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

Progression of vernal conjunctivitis Diffuse papillary hypertrophy, most marked on superior tarsus

Formation of cobblestone papillae Rupture of septae - giant papillae

Limbal vernal

Trantas dotsMucoid nodule

Vernal keratopathyOccurs 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

Progression of vernal keratopathy

Punctate epitheliopathy Epithelial macroerosions

Plaque formation (shield ulcer) Subepithelial scarring

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.

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.

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

PHARMACOLOGICAL INTERVENTION

FOR MILD CASES

1.Cool compress2.Ocular lubricants3.Decongestant antihistaminics4.Mast cell stabilisers5.Environment control

FOR MODERATE TO SEVERE CASES

1.topical/oral antihistaminics2.Mast cell stabilisers3.NSAIDS4.Topical steroids5.Acetyl cysteine to eliminate mucous

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

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

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

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

NSAIDSTOPICAL MOAinhibits 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

CYCLOSPORINE 2% QID Severe to intractable VKC MOAImmunosuppressive,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

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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