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Allergic conjunctivitis
The document provides an overview of allergic conjunctivitis, detailing its types, etiology, pathophysiology, clinical features, diagnosis, and management strategies. It covers various forms such as simple allergic conjunctivitis, vernal keratoconjunctivitis, atopic keratoconjunctivitis, and others, along with their symptoms and treatment options, including antihistamines, mast cell stabilizers, and corticosteroids. The management focuses on avoiding allergens and pharmacological treatments to alleviate symptoms.
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Allergic conjunctivitis
- 1. University of Gondar Departmentof Optometry Allergic conjunctivitis
- 2. ALLERGIC CONJUNCTIVITIS • Itis the inflammation of conjunctiva due to allergic or hypersensitivity reactions which may be immediate(humoral) or delayed (cellular).
- 3. TYPES 1. Simple allergicconjunctivitis Hay fever conjunctivitis Seasonal allergic conjunctivitis (SAC) Perennial allergic conjunctivitis (PAC) 2. Vernal keratoconjunctivitis (VKC) 3. Atopic keratoconjunctivitis (AKC) 4. Giant papillary conjunctivitis (GPC) 5. Phlyctenular keratoconjunctivitis (PKC) 6. Contact dermoconjunctivitis (CDC)
- 4. SIMPLE ALLERGIC CONJUNCTIVITIS •It is a mild, non-specific allergic conjunctivitis characterized by itching, hyperaemia and mild papillary response. • It is an acute or subacute conjunctivalreaction to allergens.
- 5. Etiology Grass pollens Animal dandruff House dust and, Mite
- 6. PATHOPHYSIOLOGY • Pathological featuresof simple allergic conjunctivitis comprise vascular, cellular and conjunctival responses. 1.Vascular response is characterised by sudden and extreme vasodilation and increased permeability of vessels leading to exudation.
- 7. …PATHOPHYSIOLOGY 2.Cellular response isin the form of conjunctival infiltration and exudation in the discharge of eosinophils, plasma cells and mast cells producing histamine and histamine-like substances. 3.Conjunctival response is in the form of boggy swelling of conjunctiva followed by increased connective tissue formation and mild papillary hyperplasia.
- 8. CLINICAL FEATURES Symptoms • intenseitching • Burning sensation • waterydischarge • mild photophobia. Signs • Hyperaemia • chemosis • mild papillary reaction • edema of lids
- 9. DIAGNOSIS • Diagnosisis madefrom: a. typical symptoms and signs b. normal conjunctival flora and c. presence of abundant eosinophils in the discharge
- 10. VERNAL KERATOCONJUNCTIVITIS (VKC)OR SPRING CATARRH • It is a recurrent, bilateral, interstitial, self- limiting, allergic inflammation of the conjunctiva having a periodic seasonal incidence. • It is considered as a hypersensitivity reaction to some exogenous allergens.
- 11.
- 12. PREDISPOSING FACTORS 1.Age • 4-20years 2.sex • more common in boys than girls. 3.Season • More common in summer. • Recently, it is being labelled as 'Warm weather conjunctivitis' 3. Climate. • More prevalent in tropics, less in temperate zones and almost non-existent in coldclimate.
- 13. PATHOPHYSIOLOGY 1.Conjunctival epithelium hyperplasia 2.Markedcellular infiltration in the Adenoid layer 3. Proliferation of fibrous layer which later on undergoes hyaline changes. 4. proliferation,increased permeability and vasodilation of Conjunctival vessels.
- 14. Symptoms • Marked burningand itching sensation - Itching is more marked with palpebral form of disease • Mild photophobia • Lacrimation, • Stringy (ropy) discharge and heaviness of lids
- 15. SIGNS Described in followingthree clinical forms: 1.Palpebral VKC - upper tarsus • papillae - hard, flat topped arranged in a 'cobble-stone' or 'pavement stone', fashion - In severe cases, 'giant papillae'. • white ropy discharge
- 16. …SIGNS 2.Bulbar VKC • Duskyred triangular congestion of bulbar conjunctiva • Gelatinous thickened accumulation of tissue around the limbus • Presence of discrete whitish raised dots along the limbus (Tranta's spots) 3.Mixed VKC It shows combined features of both palpebral and bulbar forms
- 17. KERATOPATHY It is dueto corneal involvement in VKC. The following are some of corneal lesions due to VKC. • Superior punctate epithelial keratitis • Ulcerative vernal keratitis (shield ulceration) • Vernal corneal plaques • Subepithelial scarring • Pseudogerontoxon
- 18. Atopic keratoconjunctivitis (AKC) •Adult equivalent of vernal keratoconjunctivitis and is often associated with atopic dermatitis. Most of the patients are young atopic adults, with male predominance.
- 19. Pathophysiology • The underlyingmechanism is thought to be a combined type I and type IV hypersensitivity response. • AKC has a protracted course with exacerbations and remissions. AKC tends to be perennial and is often worse in the winter. • Like vernal keratoconjunctivitis it tends to become inactive when the patient reaches the fifth decade.
- 20. Symptoms • Itching, soreness,dry sensation. • Mucoid discharge. • Photophobia • blurred vision
- 21. Signs • Lid marginsare chronically inflamed with rounded posterior borders. • Tarsal conjunctiva has a milky appearance. There are very fine papillae, hyperaemia and scarring with shrinkage. • Cornea may show punctate epithelial keratitis, often more severe in lower half. There may also occur corneal vascularization, thinning and plaques.
- 22. Diagnosis • Diagnosis isclinical but can be aided by raised serum and tear IgE levels. • Symptoms are similar to those of VKC, but are frequently more severe and unremitting. • Discharge is generally more watery than the stringy mucoid discharge in VKC.
- 23. GIANT PAPILLARY CONJUNCTIVITIS(GPC) • It is the inflammation of conjunctiva with formation of very large sized papillae.
- 24. Etiology • It isa localised allergic response to a physically rough or deposited surface (contact lens, prosthesis, left out nylon sutures). Probably it is a sensitivity reaction to components of the plastic leached out by the action of tears.
- 25. Pathophysiology • GPC canoccur secondary to a variety of mechanical stimuli of the tarsal conjunctiva. It is most frequently encountered with contact lens (CL) wear, termed as when it is termed contact lens-associated papillary conjunctivitis (CLPC).
- 26. Signs and Symptoms •Itching, stringy discharge and reduced wearing time of contact lens. • Signs Papillary hypertrophy (1 mm in diameter) of the upper tarsal conjunctiva, similar to that seen in palpebral form of VKC with hyperaemia are the main sign. Substantial CL protein deposits may be present.
- 27. PHLYCTENULAR KERATOCONJUNCTIVITIS • Phlyctenularkeratoconjunctivitis is a characteristic nodular affection occurring as an allergic response of the conjunctival and corneal epithelium to some endogenous allergens to which they have become sensitized.
- 28. Etiology • It isbelieved to be a delayed hypersensitivity (Type IV-cell mediated) response to endogenous microbial proteins. I. Causative allergens Staphylococcus proteins Other allergens may be proteins of Moraxella Axenfeld bacillius and certain parasites (worm infestation).
- 29. Pathophysiology 1. Stage ofnodule formation : exudation and infiltration of leucocytes into the deeper layers of conjunctiva leading to a nodule formation. 2. Stage of ulceration. Later on necrosis occurs at the apex of the nodule and an ulcer is formed. 3. Stage of granulation. Eventually floor of the ulcer becomes covered by granulation tissue. 4. Stage of healing. Healing occurs usually with minimal scarring.
- 30. Symptoms • mild discomfortin the eye • irritation and reflex watering. • May be associated mucopurulent conjunctivitis due to secondary bacterial infection.
- 31. Signs. • The phlyctenularconjunctivitis can present in three forms. 1. Simple phylctenular conjunctivitis. It is characterised by the presence of a typical pinkish white nodule surrounded by hyperaemia on the bulbar conjunctiva, usually near the limbus. 2. Necrotizing phlyctenular conjunctivitis is characterised by the presence of a very large phlycten with necrosis and ulceration leading to a severe pustular conjunctivitis. 3. Miliary phlyctenular conjunctivitis: characterised by the presence of multiple phlyctens which may be arranged in the form of a ring around the limbus and may even form a ring ulcer.
- 32. Differential diagnosis • Phlyctenularconjunctivitis needs to be differentiated from episcleritis, scleritis. • Presence of one or more whitish raised nodules on the bulbar conjunctiva near the limbus, with hyperaemia usually of the surrounding conjunctiva, are the diagnostic features of the phlyctenular conjunctivitis.
- 33. CONTACT DERMOCONJUNCTIVITIS • Itis an allergic disorder, involving conjunctiva and skin of lids along with surrounding area of face.
- 34. Etiology • It isin fact a delayed hypersensitivity (type IV) response to prolonged contact with chemicals and drugs. A few common topical ophthalmic medications known to produce contact dermoconjunctivitis are atropine, penicillin, neomycin, soframycin and gentamycin.
- 35. Clinical features • Cutaneousinvolvement is in the form of weeping eczematous reaction, involving all areas with which medication comes in contact. • Conjunctival response is in the form of hyperaemia with a generalised papillary response affecting the lower fornix and lower palpebral conjunctiva more than the upper.
- 36. Diagnosis • Typical clinicalpicture. • Conjunctival cytology shows a lymphocytic response with masses of eosinophils. • Skin test to the causative allergen is positive in most of the cases.
- 37. Managements startegies ofallergic conjunctivitis • Avoiding allergen that trigger may be the best solution. • Definitive( pharmachologic) management • Supportive management
- 38. 1.Ocular Decongestants Mechanism ofaction • This drugs are adrenergic agonist mainly alpha 1 receptor • Local vasoconstrictor, temporarily reduces redness and swallowen blood vessel Example : Phenylephrine (action-selective alpha one agonist).
- 39. Mechanism of action •Blocks H1 receptors which control .Itching .Capillary dilation .Increase in capillary permeability • Thus providing symptomatic relief from histamine activity. Antihistamins
- 40. Some antihistamine drugs •Pheniramine, antazoline combined with naphazoline • Levocabastine HCl ophthalmic suspension 0.5% (Livostin) • Emedastine difumarate 0.05% (Emadine)
- 41. Mast cell stabilizer Mechanismof action -Mast cell stabilizers work by inhibiting mast cell degranulation thereby reducing the release of inflammatory substances. - However, these agents do not eliminate inflammatory mediators that have released prior to drug instillation. Effective for VKC,AKC,GPC Examples •Cromolyn Sodium (Sodium cromoglycate) 4% • Lodoxaminde 0.1% • Pemirolast potassium 0.1% (Alamast) • Nedocromil sodium 2% (Alocril)
- 42. Corticosteroids Mechanism ofaction -By inhibiting phospholipase A2 ,block the release of arachidonic acid and its subsequent conversion to eicosanoids. -Inhibition of degranulation of mast cells, basophils and neutrophils. Examples • Dexamethasone/0.1%/ • Fluorometholone 0.1% • prednisolone acetate (0.125% and 1.0%) N.B corticosteroids should be tapered, as our body has corticoid hormones.
- 43. NSAIDs Mechanism of action •NSAIDs inhibit prostaglandin production from arachidonic acid by blocking cyclooxygenase. which results in vasoconstriction, decrease in vascular permeability. • It penetrates the cornea & reaches concentrations that reduces prostaglandin E levels in the aqueous humor. example : Ketorolac tromethamine 0.5% Used for
- 44. some supportive managements •Cold compress • Artificial tear
Editor's Notes
- #10 Treatment 1. Elimination of allergens if possible. 2. Local palliative measures which provide immediate relief include: i. Vasoconstrictors like adrenaline, ephedrine, and naphazoline. ii. Sodium cromoglycate drops are very effective in preventing recurrent atopic cases. iii. Steroid eye drops should be avoided. However, these may be prescribed for short duration in severe and non-responsive patients. 3. Systemic antihistaminic drugs are useful in acute cases with marked itching. 4. Desensitization has been tried without much rewarding results. However, a trial may be given in recurrent cases
- #18 Local therapy 1. Topical steroids. These are effective in all forms of spring catarrh. However, their use should be minimised, as they frequently cause steroid induced glaucoma. Therefore, monitoring of intraocular pressure is very important during steroid therapy. Frequent instillation (4 hourly) to start with (2 days) should be followed by maintenance therapy for 3-4 times a day for 2 weeks. Commonly used steroid solutions are of fluorometholone medrysone, betamethasone or dexamethasone. Medrysone and fluorometholone are safest of all these. 2. Mast cell stabilizers such as sodium cromoglycate (2%) drops 4-5 times a day are quite effective in controlling VKC, especially atopic cases. It is mast cell stabilizer. Azelastine eye drops are also effective in controlling VKC. 3. Topical antihistaminics are also effective. 4. Acetyl cysteine (0.5%) used topically has mucolytic properties and is useful in the treatment of early plaque formation. 5. Topical cyclosporine (1%) drops have been recently reported to be effective in severe unresponsive cases
- #23 Treatment is often frustrating. Treat facial eczema and lid margin disease Sodium cromoglycate drops, steroids and tear supplements may be helpful for conjunctival lesions.
- #26 The risk is increased by the build-up of proteinaceous deposits and cellular debris on the contact lens surface. Ocular prostheses (Fig. 5.18), exposed sutures and scleral buckles, corneal surface irregularity and filtering blebs can all be responsible.
- #27 Treatment 1. The offending cause should be removed. After discontinuation of contact lens or artificial eye or removal of nylon sutures, the papillae resolve over a period of one month. 2. Disodium cromoglycate is known to relieve the symptoms and enhance the rate of resolution. 3. Steroids are not of much use in this condition
- #29 I. Causative allergens Tuberculous proteins were considered, previously, as the most common cause. 2. Staphylococcus proteins are now thought to account for most of the cases. 3. Other allergens may be proteins of Moraxella Axenfeld bacillius and certain parasites (worm infestation).
- #30 Pathology 1. Stage of nodule formation. In this stage there occurs exudation and infiltration of leucocytes into the deeper layers of conjunctiva leading to a nodule formation. The central cells are polymorphonuclear and peripheral cells are lymphocytes. The neighbouring blood vessels dilate and their endothelium proliferates. 2. Stage of ulceration. Later on necrosis occurs at the apex of the nodule and an ulcer is formed. Leucocytic infiltration increases with plasma cells and mast cells. 3. Stage of granulation. Eventually floor of the ulcer becomes covered by granulation tissue. 4. Stage of healing. Healing occurs usually with minimal scarring.
- #32 The phlyctenular conjunctivitis can present in three forms. 1. Simple phylctenular conjunctivitis. It is the most commonly seen variety. It is characterised by the presence of a typical pinkish white nodule surrounded by hyperaemia on the bulbar conjunctiva, usually near the limbus. Most of the times there is solitary nodule but at times there may be two nodules In a few days the nodule ulcerates at apex which later on gets epithelised. Rest of the conjunctiva is normal. 2. Necrotizing phlyctenular conjunctivitis is characterised by the presence of a very large phlycten with necrosis and ulceration leading to a severe pustular conjunctivitis. 3. Miliary phlyctenular conjunctivitis is characterised by the presence of multiple phlyctens which may be arranged haphazardly or in the form of a ring around the limbus and may even form a ring ulcer.
- #33 Management It includes treatment of phlyctenular conjunctivitis by local therapy, investigations and specific therapy aimed at eliminating the causative allergen and general measures to improve the health of the child. Local therapy. i. Topical steroids, in the form of eye drops or ointment (dexamethasone or betamethasone) produce dramatic effect in phlyctenular keratoconjunctivitis. ii. Antibiotic drops and ointment should be added to take care of the associated secondary infection (mucopurulent conjunctivitis). iii. Atropine (1%) eye ointment should be applied once daily when cornea is involved.
- #43 There by blocking release of arachidonic acid and its subsequent conversion to eicosanoids. -Inhibition of degranulation of mast cells, basophils and neutrophils -This drugs are lipophilic which can easily cross cell membrane and gain access to cytoplasm.