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VERNAL KERATO
CONJUNCTIVITIS
SIVATEJACHALLA
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
ALLERGENS
OCULAR SURFACE
BIND TO MAST CELL IgE
ACTIVATION OF MAST CELL
CALCIUM ENTERS THE CELL
DEGRANULATION OF MAST CELL
RELEASE 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
SYMPTOMS
1.INTENSE ITCHING
2.REDNESS
3.TEARING
4.PHOTOPHOBIA
5.MUCOUS DISCHARGE
6.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 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
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 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
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
 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
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
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
THANK YOU

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Vernal kerato conjunctivitis

  • 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.
  • 5. • 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
  • 6. 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
  • 7. 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
  • 8. Progression of vernal conjunctivitis Diffuse papillary hypertrophy, most marked on superior tarsus Formation of cobblestone papillae Rupture of septae - giant papillae
  • 10. 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
  • 11. Progression of vernal keratopathy Punctate epitheliopathy Epithelial macroerosions Plaque formation (shield ulcer) Subepithelial scarring
  • 12. 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.
  • 13. 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.
  • 14.
  • 15. 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
  • 16. 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
  • 17. 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
  • 18. 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
  • 19. 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
  • 20. 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
  • 21. 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
  • 22. 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
  • 23. 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