vkc/spring catarrah/allergic conjunctivitis

1. VERNAL KERATO
CONJUNCTIVITIS
SIVATEJACHALLA

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

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

9. Limbal vernal
Trantas dotsMucoid nodule

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.

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

24. THANK YOU