Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy.Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), e...
Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy.Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), edema (swelling) of the conjunctiva, itching, and increased lacrimation (production of tears). If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis.
The symptoms are due to release of histamine and other active substances by mast cells, which stimulate dilation of blood vessels, irritate nerve endings, and increase secretion of tears.
Treatment of allergic conjunctivitis is by avoiding the allergen (e.g., avoiding grass in bloom during "hay fever season") and treatment with antihistamines, either topical (in the form of eye drops), or systemic (in the form of tablets). Antihistamines, medications that stabilize mast cells, and nonsteroidal anti-inflammatory drugs (NSAIDs) are generally safe and usually effective.
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University of Gondar Department of Optometry Allergic conjunctivitis by Getachew . k
ALLERGIC CONJUNCTIVITIS It is the inflammation of conjunctiva due to allergic or hypersensitivity reactions which may be immediate( humoral ) or delayed (cellular).
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.
Etiology Grass pollens Animal dandruff House dust and, Mite
PATHOPHYSIOLOGY Pathological features of 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.
…PATHOPHYSIOLOGY 2. Cellular response is in 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 .
CLINICAL FEATURES Symptoms intense itching Burning sensation waterydischarge mild photophobia. Signs Hyperaemia chemosis mild papillary reaction edema of lids
DIAGNOSIS Diagnosisis made from: typical symptoms and signs normal conjunctival flora and presence of abundant eosinophils in the discharge
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.
ETHIOLOGY grass pollens
PREDISPOSING FACTORS 1 .Age 4-20 years 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 .
PATHOPHYSIOLOGY 1.Conjunctival epithelium hyperplasia 2.Marked cellular 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.
Symptoms M arked burning and itching sensation - Itching is more marked with palpebral form of disease Mild photophobia L acrimation , S tringy (ropy) discharge and heaviness of lids
SIGNS Described in following three 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
…SIGNS 2. Bulbar VKC D usky red 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
KERATOPATHY It is due to corneal involvement in VKC. The following are some of corneal lesions due to VKC . Superior p unctate epithelial keratitis Ulcerative vernal keratitis (shield ulceration ) Vernal corneal plaques Subepithelial scarring Pseudogerontoxon
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.
Pathophysiology The underlying mechanism 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.
Signs Lid margins are 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.
Diagnosis Diagnosis is clinical 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.
GIANT PAPILLARY CONJUNCTIVITIS (GPC) It is the inflammation of conjunctiva with formation of very large sized papillae.
Etiology It is a 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.
Pathophysiology GPC can occur 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).
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.
PHLYCTENULAR KERATOCONJUNCTIVITIS Phlyctenular keratoconjunctivitis 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.
Etiology It is believed 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).
Pathophysiology 1. Stage of nodule 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.
Symptoms mild discomfort in the eye irritation and reflex watering. May be associated mucopurulent conjunctivitis due to secondary bacterial infection.
Signs. The phlyctenular conjunctivitis 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.
Differential diagnosis Phlyctenular conjunctivitis 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.
CONTACT DERMOCONJUNCTIVITIS It is an allergic disorder, involving conjunctiva and skin of lids along with surrounding area of face.
Etiology It is in 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 .
Clinical features Cutaneous involvement 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.
Diagnosis Typical clinical picture. Conjunctival cytology shows a lymphocytic response with masses of eosinophils . Skin test to the causative allergen is positive in most of the cases.
Managements startegies of allergic conjunctivitis Avoiding allergen that trigger may be the best solution. Definitive( pharmachologic) management Supportive management
1.Ocular Decongestants Mechanism of action 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).
Mechanism of action Blocks H1 receptors which control . Itching . Capillary dilation . Increase in capillary permeability Thus providing symptomatic relief from histamine activity. Antihistamins
Mast cell stabilizer Mechanism of 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 )
Corticosteroids Mechanism of action 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.
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
some supportive managements Cold compress Artificial tear