Allergic Conjuncitivitis


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The EBAI CME 2013 - 21st and 22nd of September 2013, Golden Valley Resort, Ghodbunder Road, Thane West, Mumbai.

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Allergic Conjuncitivitis

  1. 1. Introduction  Allergic conjunctivitis is a group of ocular surface diseases that are typically associated with type 1 hypersensitivity reactions .  May be associated with rhinitis and asthma
  2. 2. Allergic conjunctivitis Seasonal allergic conjunctivitivitis coincides with regional seasonal increases in circulating allergens, such as grass pollens Perennial allergic conjunctivitivitis symptoms throughout the year; however seasonal spikes can occur, Animal dander, house dust, molds Vernal keratoconjunctivitis associated with conjunctival scarring, ptosis, corneal neovascularisation, ulceration, thinning, Keratoconus, vision loss Atopic keratoconjunctivitis eyelid tightening, loss of eyelashes, and cataracts
  3. 3. VKC  Younger , 1st decade  Not so  Males more  Resolves at puberty  Upper tarsus  Forniceal shortening rare  Shield ulcer  Corneal vascularization not common  Periocular skin normal AKC  Older 2nd to 5th decade  Associated with atopic dermatitis  No predilection  Chronic  Lower tarsus  Forniceal shortening and subepithelial scarring  Persistent epithelial defect  Corneal vascularization common  Periocular skin, scaly, dry, lid thickened, madarosis, cicatricial ectropion
  4. 4. Sheild Ulcer in severe VKC Cobblestone papillae
  5. 5. Atopic keratoconjunctivitis
  6. 6. OD
  7. 7. OS
  8. 8. Symptoms  Itching (pruritus) and  Redness  Burning,  Stinging, Photophobia  Tearing (epiphora)  watery or mucoid ropy discharge
  9. 9. Signs  Conjunctiva pinkish or milky appearance (obscuration of conjunctival vessels due to chemosis)  Papillary hypertrophy upper tarsus, limbal  Tarsal papillae 1mm or more, cobblestone like (differentiate VKC from SAC, PAC)  Limbal papillae confluent, gelatinous
  10. 10. Signs  Horner Trantas dots along the limbus ( white dots are a collection of eosinophils and epithelial cells an indicator of active allergy)  Spotty pigmentation of interpalpebral conjunctiva in brown individuals  Punctate epithelial erosions on Cornea  Peripheral cornea superficial stromal grey white deposition Pseudogerontoxon
  11. 11. Limbal VKC Horner trantas spots pseudogerontoxon Subepithelial scarring Corneal scarring
  12. 12. Limbal VKC & cataract4 weeks post cataract surgery 6 months post op after stopping treatment Shield ulcer Limbal thickening Limbal thickening Steroid induced cataract OS
  13. 13. Limbal VKC 6 weeks of medical management 6 months later after discontinuing treatment Partial stem cell deficiency OD
  14. 14. Limbal VKC  Fulminant & long standing limbal VKC can result in stem cell deficiency  Under recognised and frequently missed  In established limbal stem cell deficiency limbal allograft- direct or cultivated  Immunosuppression
  15. 15.  the greater the papillary size, the more probable is the persistence or worsening of symptoms in the long term follow up period Giant papillae in VKC
  16. 16. Giant papillae in VKC Supratarsal Steroid injection  Short acting dexamethasone 4mg  Intermediate acting triamcinolone acetonide 20mg  Improvement in 2 weeks  Both effective  Recurrences less with triamcinolone Holsclaw DS et al, Am J Ophthalmol 1996 Saini JS et al, Acta Ophthalmol Scand,1999 Oct
  17. 17. Giant papillae in VKC After supratarsal steroid injection tricort
  18. 18. Differential features of allergic conjunctivitis
  19. 19. Pathophysiology  type I (IgE-dependent) immediate hypersensitivity reaction in VKC  B lymphocytes from the lymphoid follicle of the conjunctiva locally produce IgE.  Mast cell degranulation results in the release of a range of mediators such as histamine, leading to the classical allergic reactions of vasodilatation, oedema, hyperaemia,  And recruitment of other inflammatory cells.
  20. 20.  Role of eosinophil in ocular allergy important their consistent presence in conjunctival biopsy tissues affected by ocular allergy and by eosinophilic cationic protein levels in tears.  Activated eosinophils elicit ocular surface inflammation by their soluble mediators (EMBP, ECP) can lead to corneal epithelial breakdown Pathophysiology
  21. 21.  There is also growing evidence for the involvement of a CD4T helper 2 (Th2)- driven type IV (delayed or cell- mediated)hypersensitivity reaction as well.  Once activated, these Th2 lymphocytes play a role in recruitment and activation of mast cells and eosinophils, and in B cell switching to the production of IgE. Pathophysiology
  22. 22. Antigen presentation to T lymphocytes Naïve T cell Interaction between T Helper Lymphocytes and antibody producing cells
  23. 23. Interleukins, 1,3,4,5,6, TNF over hours In minutesimmediate
  24. 24. Differential diagnosis  Bacterial / viral conjunctivitis,  rhinitis, dry eye,  meibomian gland disease (resulting in tear film abnormality or insufficiency),  blepharitis  Contact lens wear  A medical history and assessment of environmental risk factors
  25. 25.  Signs and symptoms (itching, redness, and chemosis)  Symptom duration  Discharge  Unilateral or bilateral presentation  Allergy, asthma, or eczema  Topical and systemic medication use (i.e. overthe-counter eyedrops and systemic allergy medications) Differential diagnosis
  26. 26. Severe VKC  23 % have perennial form  16% seasonal form becomes perennial after 3years from disease onset  9.7% develop shield ulcers  6% develop visual impairment –due to corneal damage, cataract, glaucoma Bonnini S et al Ophthalmology June 2000
  27. 27. Shield ulcer  Sight threatening complication of VKC  Superficial Epithelial erosions Macroerosion Collected cellular debris & mucus- vernal plaque or shield ulcer
  28. 28. Pathogenesis  Mechanical Hypothesis Abrasion of cornea by giant papillae on upper tarsal conjunctiva  Hence superior location of shield ulcer
  29. 29. Pathogenesis  Toxin Hypothesis Eosinophil granule major basic protein Cytotoxic, inhibits epithelial healing  Hence removal of inflammatory debris promotes epithelisation
  30. 30. Grades Grade I  Transparent clear base  Respond to medical management  Minimal scarring, no vascularisation  Good outcome
  31. 31. Shield ulcer  Grade I-II Central base clear Peripheral translucency
  32. 32. Grades Grade II  Inflammatory debris in Ulcer base  Respond poorly to medical management  Surgical debridement of ulcer base required  Re-epithelisation in a week Cameroon JA, Ophthalmology 1995 Ozbek Z, Rapuano CJ, Cornea. 2006 May
  33. 33. Shield ulcer  Grade II After amniotic membrane transplantation Translucent base
  34. 34. Grades Grade III  Elevated plaque above surrounding epithelium  Responds best to surgical treatment
  35. 35. Shield ulcer  Grade III Giant papillae Shield ulcer with plaque After AMG
  36. 36. Shield ulcer Complications  Secondary infection  Corneal vascularisation  Corneal scarring  Amblyopia  Strabismus Cameroon JA, Ophthalmology 1995 Cameroon JA et al,J Pediatr Ophthalmol Strabismus 1997
  37. 37. Management  No improvement or evidence of epithelisation after 1 week of medical treatment – surgical debridement for grade I & II.  Surgical debridement needed for grade III
  38. 38. Amniotic membrane for Shield Ulcer  For nonresponsive cases –AMG  Promotes epithelisation  Antiscarring  Antivascularisation  Anti inflammatory  Acts like a BCL M.S.Sridhar et al, Ophthalmology July 2001
  39. 39. Excimer PTK for Shield ulcer  After removal of the plaque & control of inflammation  Excimer laser PTK beneficial in certain cases  Produces smooth surface  Removes toxic inflammatory products  Allows epithelisation  Reduces scarring Cameron JA, et al J Refract Surg 1995
  40. 40. Corneal edema, small infiltrate Healed with scarring and resolution of edema
  41. 41. 26 % on topography 7% on slit lamp and keratometry Ophthalomology 2001
  42. 42. Treatment  Topical Antihistamines  Mast cell stabiliser  Antihistamine and mast cell stabiliser combination  Topical steroids  Immunomodulators
  43. 43. Severity of Allergic conjunctivitis
  44. 44. Lifestyle modification  Allergen avoidance – avoid being outdoors  Avoidance of animal exposure for sensitive individuals  Hypoallergenic bedding  Washing sheets in hot water, which denatures allergenic proteins (i.e. those from dust mites)  Showering and shampooing at bedtime to remove allergens  Sunglasses, which serve as a barrier to airborne allergens  Avoidance of eye rubbing –release of more inflammatory mediators  Cool compresses – help to alleviate ocular itching
  45. 45. Topical antihistamine  The benefits of these agents are that  they block histamine, stabilize the mast cell, and inhibit eosinophil activation and migration .  antihistamines address the signs and symptoms of ocular allergy, particularly itching  Onset of action quick but duration short up to 4 times daily
  46. 46.  Levocabastine  Chlorpheniramine  Antazoline  Systemic antihistamines increase dryness can be given for rhinitis Topical antihistamine
  47. 47. Mast cell stabiliser  Mast cell stabilizers (inhibitors) prevent degranulation of mast cells.  These agents are particularly effective in SAC and PAC in which the predominant cell types are the mast cell and eosinophil.  Mast cell stabilizers address both the early and late phases of the allergic response  clinically effect takes 1-2 weeks
  48. 48.  Disodium cromoglycate (Cromolyn) 4% twice a day  Lodoxamide (Alomide 0.1 %) twice a day  Nedocromil 2% twice a day Mast cell stabiliser
  49. 49. Antihistamine and mast cell stabiliser combination  These dual-acting medications relieve redness, itching, and irritation.  They have a quick onset of action, which is likely to improve patient adherence compared with the pure mast cell stabilizers  require only once-a-day or twice-a-day dosing.  Side-effects, which tend to be transient and mild, include: stinging, burning, bitter taste, and sedation.
  50. 50.  Ketotifen 0.025%  Epinastine 0.05% b.d is a multi-action agent  potent H1 and H2-receptor antagonist, mast cell-stabilizing properties and anti- inflammatory actions  Epinastine not only inhibits activation of neutrophils and eosinophils but also interferes with CD4+ T-cell signaling, and thus decrease of TH2 cytokine production  Onset of action 3 minutes, duration 8 hours Antihistamine and mast cell stabiliser combination
  51. 51.  Olopatadine  It also has anti-inflammatory properties such as inhibition of cytokine secretion , inhibition of TNF-α release from human conjunctival mast cell , with a subsequent decrease in ICAM-1 expression and thereby a decrease in chemotaxis of inflammatory cells such as eosinophils.  rapid onset (within 20 min), with at least 8h duration of action .  The 0.1% b.d / 0.2% o.d (24 hours action) . Antihistamine and mast cell stabiliser combination
  52. 52. NSAIDS  NSAIDs can address the itching associated with allergic conjunctivitis  These agents can cause discomfort upon instillation, which can in turn lead to reduced patient adherence, not ideal in presence of epithelial erosions
  53. 53. Corticosteroids  Corticosteroids are the most effective anti- inflammatory drugs available  Productions of several pro-inflammatory cytokines such as IL-1, IL-4, IL-5and TNF-a are directly ‘repressed’ by corticosteroids  decrease expression of adhesion molecules  decrease in numbers of eosinophils neutrophils, mast cells and lymphocytes at the site of inflammation  Topical application high local tissue concentration
  54. 54.  Important side effect of ocular steroids is increase in ocular pressure (IOP)  Cataract, secondary infection  newer ‘soft’ corticosteroids with the alteration of the ketone structure to ester at carbonC20 of the corticosteroid structure has led to a marked decrease in this side effect in both IOP and cataract formation  Loteprednol etabonate  is thus a preferred topical steroid 0.2% Corticosteroids
  55. 55. Topical cyclosporin and Tacrolimus  Moderate to severe AKC and VKC  Topical Cyclosporin or Tacrolimus  actions of both agents are inhibition of T-cell activation and inhibition of release of IgE- dependent mediators and cytokines from mast cells and other related cells  cyclosporine A (CsA) inhibits proliferation and cytokine production from conjunctival fibroblasts thus suppressing the inflammatory cascade
  56. 56. Topical cyclosporin  1% - 2% in olive oil, castor oil, lubricants  Burning sensation on topical application  Can affect compliance  0.1 % - 0.05% less burning, not so effective  Aurosporin 2% cyclosporin from Aurolab
  57. 57. Topical Tacrolimus  0.1% - 0.03% ointment  0.03% can be applied in lower fornix 2 times a day  Minimal stinging on topical application  Tacliment 0.03% from Aurolab  Beneficial effects reported in VKC, AKC, GPC in 4 weeks
  58. 58.  No systemic adverse effects reported with both Cyclosporin and Tacrolimus on topical use.  Burning and stinging less with Tacrolimus ointment  HSV keratitis reported by some on tacrolimus use. Topical cyclosporin and Tacrolimus
  59. 59.  Because allergic conjunctivitis usually accompanies allergic rhinitis, most of the studies of allergen immunotherapy were conducted in patients with symptoms of both organ systems.  As a consequence, ocular symptoms were shown to be improved together with rhinitis symptoms  Needs to be given for atleast a year. Sublingual immunotherapy
  60. 60. Sublingual immunotherapy  Sublingual immunotherapy is taken as drops or tablets, containing specific allergen extracts which interact with the immune system to decrease allergic sensitivity.  Increasing doses of the allergen are administered by sublingual immunotherapy route to achieve hyposensitization and creating immune tolerance to antigens.  Long term changes that occur with immunotherapy include a decrease in mast cell sensitivity and a decrease in IgE production by mucosal B-cells.  There is a decrease in the IgE/IgG4 and a decrease in the TH1/TH2 ratio.
  61. 61.  recently published metaanalysis results of SLIT for allergic conjunctivitis.  not only improved patients’ eye symptoms (red eyes, itching, watery eyes) but also increased allergen threshold  May benefit VKC , AKC Sublingual immunotherapy
  62. 62. Conclusion  a proactive, multifaceted approach based on severity of the disease.  Co management with an allergy specialist in severe cases  Immunomodulators for severe VKC, AKC  Patients going for elective laser vision correction or cataract surgery should be well controlled
  63. 63. October 2013
  64. 64. Giant papillae in VKC  Surgical resection of giant papillae and autologous conjunctival graft in refractory cases  No recurrence over 9-27 months Nishiwaki-Dantas MC, et al Ophthal Plast Reconstr Surg. 2000 Nov
  65. 65. Giant papillae in VKC  Surgical Resection and cryotherapy Drawback  Irregular conjunctival scarring can produce palpebral deformity & surface irregularity of superior palpebral conjunctiva
  66. 66. Giant papillae in VKC  Superficial tarsectomy Compromises accessory lacrimal and meibomian gland function  Surgical resection & Buccal mucous membrane graft
  67. 67. Giant papillae in VKC  Removal of giant vernal papillae by CO2 laser. Belfair N et al Can J Ophthalmol. 2005 Aug  Only mechanical trauma eliminated, immunologic process controlled medically