SPRING CATARRACH OR VERNAL KERATO CONJUNCTIVITIS

Vernal keratoconjunctivitis (VKC, also Spring catarrh, Vernal catarrh or Warm weather conjunctivitis) is a recurrent, bilateral, and self-limiting type of conjunctivitis (pink eye) having a periodic seasonal incidence

1. VERNAL KERATO CONJUNCTIVITIS OR SPRING CATARRH By Dr.S.ANU R ADHA MS .,

2. ALLERGIC CONJUNCTIVITIS It is defined as the inflammation of the conjunctiva due to allergic or hypersensitivity reactions which may be immediate(humoral) or delayed(cellular)

3. TYPES Simple Allergic Conjunctivitis - Seasonal allergic conjunctivitis -Perennial allergic conjunctivitis Vernal keratoconjunctivitis Atopic keratoconjunctivitis Giant papillary conjunctivitis Phlyctenular keratoconjunctivitis Contact dermatoconjunctivitis

4. INTRODUCTION VKC is one of the type of ALLERGIC CONJUCTIVITIS. ALLERGY is an abnormally high sensitivity to certain substances such as pollen,foods,micro organisms. In greek vernal mean spring.it is commonly occurred in spring season .certain type of pollen is released in the sping season which cause allergy. so it is called SPRING CATARRAH.

5. Allergic Conjunctivitis : Causes POLLEN PET DANDER POLLUTION DUST MITES MOLDS

6. DEFINITION VKC is a chronic,recurrent,interstitial,bilateral,self limiting,external ocular allergic disease having periodic seasonal occurence.

7. ETIOLOGY 1.Exogenous allergen like pollen. 2.family H/O allergic diseases & personal h/o one of the major atopic diseases like ASTHMA,HAY FEVER,ECZEMA may be present. It is consider to be an type 1 IgE mediated hypersensitivity reaction.

8. Conti,,,, 3.Age incidence is about 4 to 20 yrs. 4.Males are affected more than females. 5.disease affects primarly children & young adults.

9. PATHOGENESIS Mainly involved cell is MAST CELL which is present in conjuctiva. Oter sites __ resp.mucosa & connective tissue. 1 cub mm of conjuctiva consits about 5000 mast cells. The surface of mast cell is coated with igE antibody.each mast cell contains about 10000 to 50000 igE ab.

10. Cont,,, The main stimulus for allergic response is exposure of appropriate sensitised igE coated mast cell to air born allergen

11. Allergens Ocular Surface Allergen binds with IgE on mast cell Leads to mast cell activation Preformed Mediators Histamine Chymase Tryptase Proteases Itching , Redness , Swelling Degradation of neighboring cells Inflammatory cells accumulation Newly Formed Mediators Prostaglandins Leukotrienes Platelet-activating factors Cytokines (TNF) Chemokines (IL-8) Redness, swelling Infiltration of eosinophils & neutrophils Calcium enters the cells Mast cell degranulation Release of Mediators

12. Primary Mediator H1 receptor on nerve cells H2 receptor on blood vessels Mast cell Degranulation Histamine released Itching Redness and Swelling

13. Mediators of Allergy :Roles Histamine : Itching, redness, edema Prostaglandins : Sensitized nerves, enhanced pain, edema and redness Leukotrienes : Chemotaxis, edema and vascular permeability Chemotactic factors : Recruitment of eosinophils and neutrophils leading to tissue destruction l

14. Signs & SYMPTOMS 1. Intense itching,watering,photophobia , FB sensation. 2. one of the dignostic sign is mucous discharge __ ropy in nature – thick lardacious,yellowish discharge.it consists of epitheleal cells,eosinophils , neutrophils . Discharge may be found to collected in lower conjuctiva up to medial canthus.patient gets relief after removal of discharge.

15. Cont,,, 3. another diagnostic sign is macro papillae in the upper tarsal conjuctiva. Depending up on the site of formation of papillae it is divided in to 1. palpebral form 2. limbal form 3. mixed ,,

16. PALPEBRAL FORM It is mainly manifested by large papillae on the upper part of conjuctiva. Size vary from 2 mm to 8 mm. Papillae is bluish white , flat topped nodules which are hard. Papillae are arranged in a cobble stone or pavement stone fashion.

17. Cont,,, Papillae consist of dence fibrous tissue, leucocytes, plasma cells,lymphocytes, macrophages. This type is common in males. Allergic madiators which are produced in hypersensitivity reaction play a major role for proliferation of fibroblasts.mainly due to benign hyperplasia of substansia propria of conjuctiva.

18. LIMBAL FORM It is common in tropics & sub tropics , darkly pigmented people. Also known as endemic limbo – conjuctivitis. Recognised by 1.opacification of limbus. Gelatinous thickend accumulation of tissue around limbus. 2.dusky red triangular congetion of bulbar conjuctiva.

19. CONT,, 3. Main characteristic feature is HORNER – TRANTAS dots which are chalcky white, raised superficial dots over the corneo scleral limbus. These are composed of e o sinophills & epithelial debris.

20. VERNAL KERATOPATHY Corneal involvement is seen in 50% of pts. It is due to primary or secondary to extention of limbal lesions. Vernal keratopathy includes 5 types.

21. TYPES OF V.KERATOPATHY 1.SUPERFICIAL PUNCTATE EPITHEAL KERATITS – involves upper cornea with palpebral form. Lesion always stains with rose bengal & invariably fluorescein stain. 2.ULCERATIVE KERATITIS – RARE – horizontal ,oval , shallow ulcers – SHIELDS ULCER – in the upper half of cornea at limbus . It is due to constant rubbing of papillae on cornea.

22. TYPES 3.VERNAL CORNEAL PLAQUES – due to coating of bare area of epitheal macro erotion with a layer of altered exudates. 4.SUBEPITHELIAL SCARRING – ring scar . 5. PSEUDOGERONTOXON – clasical cupids bow out line. Prone for keratoconus .

23. COMPLICATIONS 1.Sheild’s ulcer. 2.opacification of bowmans membrane. 3.peripharal corneal degeneration – rarely – leads to astigmatism. 4.keratoconus & keratoglobus– rare. 5.Severe dry eyes

24. D/D 1.TRACHOMA 2.GIANT PAPILLARY CONJUCTIVITIS 3.PHYCTENULAR CONJUCTIVITIS

25. TREATMENT Medical treatment – most effective. Surgical treament

26. Medical Management Vasoconstrictors/Decongestant Antihistaminic agents Mast Cell Stabilizers Steroids Immuno supressants Artificial tear drops NSAIDS General measures

27. Vasoconstrictors Acts by constricting the inflamed , dilated vessels. Act on the alpha adrenergic receptors in the arterioles of the conjunctiva resulting in decreased conjunctival congestion Eg : naphazoline

28. ANTI HISTAMANICS Block histamine receptors on nerve endings and blood-vessel walls . 2 types of histamine receptors are important H1 receptors mediate itching H2 receptor mediate redness. E.g Levocabastine , Emedastine ( not available in India)

29. Antihistamine : Mode of Action Antihistamines effectively block the action of histamine on: ► nerve endings (itching) ► blood vessel walls (redness) ► eyelids (edema). Antihistamines do not influence the effects of other, preformed mediators.

30. Mast Cell Stabilizer Prevent degranulation of mast cells by Preventing calcium intake step that normally follows allergen –IgE binding. Able to alleviate allergy symptoms in the long-term. Ineffective at stopping the immediate itching. Are used as prophylactic agents , for prevention of allergy rather than treatment Sodium Cromoglycate , Lodoxamide, Nedocromil and Pemirolast

31. Mast Cell Stabilizer Prevent degranulation of mast cells by Preventing calcium intake step that normally follows allergen –IgE binding. Able to alleviate allergy symptoms in the long-term. Ineffective at stopping the immediate itching. Are used as prophylactic agents , for prevention of allergy rather than treatment Sodium Cromoglycate , Lodoxamide, Nedocromil and Pemirolast

32. Drug Categories : Indications Drug Category Example Indication Vasoconstrictor Naphazoline For managing redness Steroids Loteprednol For sever conditions like VKC , manage severe inflammatory conditions Antihistamines Levocabastine , Emedastine When intensity of itching is higher , antihistamines are preferred. Mast Cell Stabilizer Sodium cromoglycate , nedocromil For prophylaxis , prevention of allergy loading doses are administered, also along with antihistaminic agents

33. Dual Acting Agents : Rationale Antihistamines can halt the most immediate symptoms of allergy . Mast cell stabilizers give relief from allergic symptoms in the long-term Thus combination agents come into effect immediately relieving from ocular itch as well as the long -term symptoms of ocular allergy. e.g Epinastine, Olopatadine , Ketotifen , Azelastine ,

34. Dual Acting Agent Features Azelastine Onset of action within 15 mins. Blood –brain barrier No data available Burning, stinging (30%), headaches (15%) and bitter taste (a 10%). The level of discomfort and taste perversion in patients treated with azelastine limit its use. H1, H2 binding no specific data Ketotifen Onset within 3 mins Blood – brain barrier No data available Vision blurring dry eye, eyelid disorder, conjunctivitis, photophobia , tearing Only H1 receptor binding Olopatadine Onset within 3 mins Does not cross blood brain barrier Occurrence of dry eyes post long term use Reduction in tear volume post administration Olopatadine has high affinity for H1 receptors and only some affinity for H2 receptors

35. Epinastine: Multiple mechanism of Action Antihistaminic blockade of the histamine H1 and H2 receptors , Mast cell stabilization , Other anti-inflammatory activities

36. Epinastine :Onset and Duration Of Action Rapid onset of action within 3 to 5 minutes Duration of effect was approximately 8 to 12 hours.

37. Steroids Preferred in severe conditions like VKC. When the inflammation is not controlled by other therapeutic agents . Have serious adverse effect profile E.g Prednisolone , Loteprednol etabonate *, Fluorometholone *. * - Safer compared with prednisolone

38. IMMUNO SUPRRESENTS Cyclosporin A is apotent immunosuppresent. It control cell mediated immunity by inhibiting activated T- LYMPHOCYTES. Uncontrolled cases even after tt with sodium cromoglycate, steroids, it is indicated. Improvement occur with in 3 days ,complete improvement achieved in 60% of pt after 6 weeks.

39. LUBRICANTS Artificial tear drops – this agents will wash off the allergens which are present in the conjuctival sac. Also reduce the dryness which is produced by other drugs.

40. GENERAL TREATMENT General tt –1. dark goggles to prevent photophobia. 2. avoidence of allergen 3. cold compresses

41. SURGICAL TREATMENT Superficial keretectomy – to remove plaques.the epithelium is removed to the edge of the calcified region.medical tt is maintained until cornea has reepithelialised to prevent recurrence. Eximer laser phototherapatic keretectomy is alternative.

42. Contt,, Amniotic membrane graft – with tarsorraphy or lamellar keratoplasty – required in severe persistant epithelial defects with ulceration. Large papillae is removed by cryo application or beta irradiation.

43. PROGNOSIS Good prognosis as the disease is self limiting in most of the children