vernal kerato conjunctivitis
DESCRIPTION
vkc/spring catarrah/allergic conjunctivitisTRANSCRIPT
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 FEATURES
SYMPTOMS1.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
NSAIDS
TOPICAL 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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