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Conjunctivitis is inflammation of the conjunctiva, the mucous membrane lining the anterior sclera and inner eyelid surfaces, seen in the broad spectrum of conditions, including allergy. Allergic inflammation of the ocular surface (the lid margins, conjunctiva and cornea is one of the commonest eye disorders. • In its mildest form, the conjunctiva becomes inflamed in response to a transient allergen (e.g. pollen in seasonal allergic conjunctivitis), or • A persistent allergen (e.g. house dust mite in perennial allergic conjunctivitis) producing unpleasant symptoms but not threatening sight. At the other end of the spectrum are disorders with blinding complications such as vernal keratoconjunctivitis and Atopic keratoconjunctivitis.
Classification of Allergic Conjunctivitis
• • • • •
Clinical Features of Allergic conjunctivitis
History is important • Other allergic diseases like asthma or eczema suggest allergic conjunctivitis • Use of any topical face/eye preparations — allergic dermatoconjunctivitis • Seasonal history suggest hay fever caused by grass, tree or weed pollen, perennial (all year round) symptoms suggest house dust mites, pets especially cats or moulds • Use of Antihistamines — may alter clinical picture • Contact lens use — irritant or allergic reaction to lens solutions • Hallmark symptom of all types of allergic conjunctivitis is itching (pruritus) —more prominent in acute cases • Photophobia — with or without decreased visual acuity, usually means keratitis is present • It is important to remember that the eyes can be predominantly affected in hay fever, with less rhinitis symptoms, also when patient have been on nasal steroids they will present with conjunctivitis only. Examination • Usually bilateral redness of conjunctiva with swelling (chemosis), periorbital swelling, mucoid discharge • There is often eyelid eczema Three types of conjunctival reaction: • Follicles - these appear as small, pale, elevated nodules, most marked in lower tarsal conjunctiva • Papillae - are less specific red spots. Each papilla has a central vessel running to the surface • Giant Papillae - are less common and much more specific. By definition, they are greater than 1mm in diameter, with domed or flat tops. Large polygonal giant papillae with flat tops form the ‗Cobblestone‘ appearance characteristic of vernal conjunctivitis. Key Features of the Diagnosis of IgE-Mediated Allergic Eye Disease • Pruritus (itching), which is usually intense • Bilateral involvement, and • Associated with atopic respiratory tract disease The absence of any of these is strong evidence against allergy. Acute Allergic Conjunctivitis (Seasonal & perennial allergic conjunctivitis) The pruritus usually distinguishes allergic from other causes of conjunctivitis. Can de diagnosed by doing a conjunctival scrape looking for eosinophils. Treatment Options In perennial conjunctivitis, due to house dust mites or cats, avoidance or allergen reduction measures should be first tried along with antihistamines and if this fails immunotherapy should be considered
Seasonal allergic conjunctivitis or Hay Fever Perennial allergic conjunctivitis Atopic keratoconjunctivitis Vernal keratoconjunctivitis Giant papillary conjunctivitis
but thought to be combination of Type 1 and Type 4 Hypersensitivity reactions Treatment of AKC • Topical steroids for short periods • Antihistamines • Mast cell stabilizers • Cold compresses • Careful follow-up to prevent damage to vision Contact Dermatoconjunctivitis Contact allergy of the eye and periocular area occurs with a variety of cosmetics.Vernal Keratoconjunctivitis This is a chronic. Upper tarsal surface in vernal keratoconjunctivitis showing ‘cobblestone’ appearance. watering. The pathophysiology of AKC is not known. . Eye involvement in AKC include: • Conjunctivitis • Keratoconjunctivitis (combine inflammation of the cornea and conjunctiva) causing painful. bilateral inflammation of the conjunctiva that is most commonly found in children and adolescents. It has been estimated that up to 25% of patients with atopic dermatitis will often have ocular (eye) involvement. The most remarkable finding is the intense itching and giant papillae on the tarsal conjunctiva. Treatment of Vernal conjunctivitis includes: • Aggressive use of mast cell stabilisers e. Males tend to be affected more often than females.g. contact lens solution. sodium cromoglycate • Topical antihistamines • Topical non steroidal anti-inflammatory agents • Topical steroids may be necessary in severe cases Atopic Keratoconjunctivitis (AKC) Atopic dermatitis. soaps. but in severe cases can be perennial. It usually occurs in spring and summer months. The effects of vernal conjunctivitis can be so severe that blindness may result. Symptoms include redness of the conjunctiva and periorbital swelling. Vernal conjunctivitis probably represents a severe and chronic form of allergic conjunctivitis with more intense symptoms and sequelae. red eye with blurring of vision • Cataracts • Increased risk of eye infections The eyelids in atopic keratoconjunctivitis. can have significant eye findings. Like allergic conjunctivitis it is immune mediated. although usually manifested peripherally. Ropy mucoid discharge is also a distinguishing sign. and it usually resolves by early adulthood. and medications.
Nedocromil sodium is a newer. dog. but have potentially sightthreatening side effects. Secondary infections should be adequately treated. but almost exclusively associated with contact lens wearers. They offer a preventative action and work most effective if taken before the onset of symptoms. Lodoxamide is another recently introduced mast cell stabilizer. • Steriods Topical steroids are very powerful in controlling allergic conjunctivitis. higher potency mast cell stabilizer that compares favourably to cromolyn and can be used twice daily in SAC and PAC. Steroids are generally contraindicated in SAR & PAR. cool compresses. Giant Papillary Conjunctivitis (GPC) GPC is increasingly more common with the advent of extended wear lenses. GPC resembles vernal conjunctivitis. antihistamines.Compounds commonly causing allergic contact dermatoconjunctivitis: • Neomycin • Thiomersal in contact lens solution • Atropine • Papain • Bacitracin • Idoxyuridine • Ppolymxin B • Benzalkonium chloride Investigation: Patch Test Treatment: removal and avoidance of the offending agent. cat. and topical steroids. occasionally they are used in AKC and VKC. frequent enzymatic cleaning of the lens. antihistamines. Topical NSAID are not as potent as steroids but have the advantage of good ocular safety profile and useful in . • Nonsteroidal anti-inflammatory agents Topical NSAIDs appear to have some beneficial effects in allergic conjunctivitis. Both nedocromil and lodoxamide have a more rapid onset of action. mast cell stabilizers. It will usually stop when the patient stops wearing contact lens or the foreign body is removed. They are usually well tolerated with very few side effects. patient must be warned that their eyes might feel worse to start with. all pollens • Non-specific medical therapy: Cold compresses – may be all that is necessary in mild seasonal and perennial conjunctivitis Mucolytic drops – dissolves the abnormal mucus Treatment of facial eczema in AKC – lid margin hygiene • Antihistamines – conventional topical antihistamine • Oral antihistamine preferably non sedating • Mast cell stabilizers These compounds are used topically to reduce mast cell degranulation. And both 2% and 4% drops are available for use up to 4 times per day. and it is believed that this protein coating is responsible for the allergic reaction Clinically. Management of Allergic Conjunctivitis • The skin prick test should always be done to confirm the culprit allergen. Contact lens wearers secrete a protein that coats the lenses. Treatment involves steroid. AS the onset of action is slow (5-7 days) and stinging can occur. • Cyclosporine Topical preparation of 2% cyclosporine has been shown to provide a marked reduction in the symptoms and signs of VKC.g. at the beginning of the pollen season) or early in the disease process. and cyclosporine is particularly helpful as a steroid-sparing agent. mast cell inhibitors act as steroid sparing agents Cromolyn sodium is the longest established of these drugs. GPC is characterized by the presence of large papillae in the tarsal conjunctiva of the upper lid. especially if the patient works with animals • A Patch Test is indicated in contact dermatoconjunctivitis • Immunotherapy for house dust mite. but also have a wide range of other anti-inflammatory effects that may be relevant. GPC is also associated with sutures in the eye and the presence of foreign body It is thought that the antigen responsible for the inflammatory response is located on the surface of the foreign body. IN VKC and AKC. where possible (e. which may evoke fewer stings than the other.
The name itself reflects two aspects of the disease. Palpebral vernal involves the upper tarsal conjunctiva and is characterized by cobblestone papillae (i..html Vernal keratoconjunctivitis (VKC) is a chronic and debilitating external ocular disease.e. Although rare. papillae that have enlarged. Vernal means youth and spring. Most series describe a male preponderance. 1). children are involved in a large percentage of the cases. Fibrin that is enhanced by heat may accumulate on the giant papillae and is known as the Maxwell-Lyons sign. However.4 . there may be lacy scarring that extends superiorly into the fornix (Fig. In general. http://www. DukeElder2 suggests that most symptoms appear in the summer rather than in the spring.treating non sight threatening conditions like SAR and PAR when mast cell stabilizers and antihistamines fail. A sequela that may occur in VKC is conjunctival scarring that has a lacy appearance at the base of the old papillae.1 although one series points out a female preponderance of patients with limbal vernal when cases are stratified by sex. The peak age of onset is 8 to 12 years. although 10% of VKC patients are older than 20 at age of onset.allergyclinic. 2). 3) and enough scarring to cause symblepharon formation. 1 A large number of patients with VKC have symptoms that are exacerbated in the spring.3 Back to Top CLINICAL FINDINGS CONJUNCTIVA Patients with VKC may be divided into two groups based on clinical presentation: palpebral vernal and limbal vernal. these centers consist of the dilated blood vessel at the core of the papilla surrounded by inflammatory cells. Papillae can be distinguished from follicles by their red centers. On rare occasions there may be conjunctival cysts (Fig. • Laser Surgery This can be useful in corneal plaques.co. possibly due to the increase in the pollen count.nz/guides/9. • Surgery Usually limited to the treatment of the sight-reducing corneal disease in AKC & VKC. often having flattened tops (Fig.
4. Fig. Mixed vernal is a combination of limbal and palpebral lesions. . Fig. 4). Conjunctival cyst at the limbus. Clinical photograph of the upper palpebral conjunctiva showing cobblestone papillae with their flat-top appearance. 3. Fig. Upper lid retracted with a Desmarres retractor showing the cobblestone papillae of the upper tarsal conjunctiva and lacy scarring of the upper fornix. Limbal vernal begins as a thickening and opacification of the limbus. Limbal vernal: HornerTrantas' dots and elevated gelatinous lesions.Fig. Horner-Trantas' dots are small white elevated lesions that appear at the apices of limbal excresences that consist of desquamated epithelial cells and eosinophils (Fig. 1. elevated lesions that may seem to coalesce and become confluent. Limbal nodules appear as gelatinous. 2.
These ulcers were differentiated from vernal shield ulcers. corneal edema. In addition. Fig. or if uncontrolled it may cause permanent corneal scarring and loss of vision. In general. Vernal corneal ulcers. and three of the four ulcers were polymicrobial. a vernal ulcer is formed. which are indolent and often have a plaque at the base. which stains devitalized cells. Punctate epithelial keratitis is an influx of white cells into the corneal epithelium. Patients report symptomatic relief when the stringy. Kerr and Stern8 described four patients with VKC who developed bacterial corneal ulcers. Vernal ulcer that is horizontal in upper one third of cornea. Staphylococcus aureus grew out of the ulcer from all four. it may form a cast of the cobblestones.END MUCUS VKC is often accompanied by a thick.5 Punctate epithelial erosions are areas of absent epithelium that stain with fluorescein. these ulcers are sterile. When the keratitis coalesces. ropy secretions are removed from the cul-de-sac. tenacious mucous discharge that may be so thick that it adheres to the giant cobblestones of the upper tarsus. When removed.6 Keratitis epithelialis of Tobgy7 is the early phase of vernal keratitis. consisting of minute white dots in the epithelium. also known as shield ulcers. 5). Vernal keratitis is characterized by a combination of punctate epithelial erosions and keratitis. which has been reported to be mucopolysaccharides. There is often white material at the base of the ulcer. These patients showed infiltrates in the cornea. are usually horizontally oval in orientation and involve the upper third of the cornea (Fig. the combination of punctate epithelial keratitis and increased mucus are the necessary ingredients for filamentary keratitis. The epithelium in this area stains with rose bengal. but there have been rare reports of superimposed infectious corneal ulcers occurring in VKC. 5. and hypopyon.CORNEA Corneal involvement may be severe enough to interrupt a child's education. Back to Top PATHOPHYSIOLOGY . iritis.
9 Frankland and Easty10 noted that 93% of their 35 patients from the United Kingdom had manifestations of atopic disease.TYPE I HYPERSENSITIVITY There is evidence that VKC is an allergic disease. Abu El-Asrar and co-workers13 investigated the immunopathology of VKC patients. Allansmith and Frick15 were among the first to provide laboratory evidence of VKC as an allergic disease when they noted antibodies to grass in the tears of patients with VKC.1 who suggested that the prevalence of atopy in their VKC population in Israel was the same as in the general population (10%). Zavaro and colleagues12 studied two patients in depth. In support of this concept. Subsequently. the other had no evidence of atopic disease. specific IgE antibodies to pollen allergens were identified in the tears. one of whom had evidence of atopic disease.18 The role of eosinophil granule major basic protein as a mediator of the immunopathology of VKC has been investigated. However.11 These authors suggested two subgroups based on the presence or absence of IgE in the serum. including histamine and prostaglandins. The mechanism of disease involves fixation of IgE molecules on the surface of mast cells and release of mediators. including asthma.16 and there have been other reports of specific IgE antibodies in the tears. Eosinophil granule major basic protein is the main protein found in the eosinophil granule. having signs of asthma. including elevated serum and tear IgE. Allansmith14 reported IgE as well as IgA and IgD plasma cells in the tarsal conjunctiva of patients with VKC.14 although these authors believed that the increased tear levels were a function of increased serum IgE levels. Further support of the concept of two subclasses of VKC was given by Neumann and associates. eczema. they also found numerous mast cells with IgE on the surface. eczema. serum IgE levels were elevated in 75% of patients with VKC. suggesting local production of antibody in the conjunctiva. Increased IgE levels in the tears of patients with VKC have been reported. It causes desquamation of respiratory epithelium in vitro and mast cell degranulation.20 and in corneal ulcers of these patients.19 in the tissue. appearing in patients who are atopic (i.17 In addition. but rarely IgE. and is deposited at sites of damage in vivo. or hay fever). but 7% did not. MEDIATORS Mediators of immediate hypersensitivity reactions have been found in the tears of patients with VKC. They found numerous plasma cells that were producing IgA and IgG.21 . However. these investigators found higher levels of antibody in the tears than in the serum. In another study. Histamine levels in the tears have been found to be elevated. Zavaro and colleagues12 stated that 80% of their Israeli patients had elevated IgE in the tears and marked eosinophilic infiltration of the conjunctiva.. It has been found in the tears of patients with VKC. or hay fever.e.
25 ASSOCIATED DISEASES Butrus and colleagues26 described ten patients with the hyperimmunoglobulin E syndrome.27 Back to Top PATHOLOGY HISTORY In the nineteenth century. marked elevation in systemic IgE levels. corneal shield ulcer. and plasma cells. Allansmith32 noted that many mast cells are actively degranulating in VKC and for that reason cannot be visualized by light microscopy. and further study has showed these cells to be the type that can induce the production of IgE antibody. which comprises chronic pruritic dermatitis. and coarse facial features. it was generally thought that VKC was a lymphoid disease.22 The increased number of T4 helper/inducer cells has been confirmed. but the mast cell membranes can be seen on electron microscopy. There is also a strong association between ectatic corneal disease. such as keratoconus and pellucid marginal degeneration. severe recurrent systemic infections. Three of these four had ocular findings ―similar to those of vernal conjunctivitis.13 A specific type of delayed hypersensitivity known as cutaneous basophil hypersensitivity has also been implicated.DELAYED HYPERSENSITIVITY It has been suggested that there is a cell-mediated component in vernal conjunctivitis as well. and Trantas' dots. Later on in the disease. and this has been substantiated by studies of the conjunctiva of patients with vernal conjunctivitis.28 In the early twentieth century. and VKC. Herbert29 pointed out the presence of eosinophils in tissue obtained from patients with vernal conjunctivitis. Axenfeld's 1907 study demonstrated the cellular infiltration that included lymphoid cells and plasma cells. This was .23 Abu El-Asrar found numerous stromal lymphocytes. possibly a neoplasm.24 and in an animal model the influx of eosinophils as well as basophils has added evidence that this type of hypersensitivity may be operant.31 He noted that the main feature was the infiltration of inflammatory cells. especially lymphocytes. Four of these patients had systemic atopic symptoms consistent with asthma or allergic rhinoconjunctivitis. He emphasized the increased visibility of the mast cells and the decreased number of plasma cells in the winter when the disease was inactive. eosinophils.30 PATHOLOGY OF PALPEBRAL VERNAL The histopathology of 100 cases of VKC from the Institute of Ophthalmology in London was reviewed by Morgan. collagen fibers are deposited. When the patient is in remission. the plasma cells disintegrate and the mast cells become more numerous.‖ including papillary hypertrophy of the upper tarsal conjunctiva.
some required short-term corticosteroids in addition to cromolyn. Examination of the first report of cromolyn in VKC is important to understand possible differences between various studies. stained.34Thick strands of ropy mucus can be removed. In these cases.13 who noted that the number of cells that had surface staining with IgE was larger than the number of cells identified by light microscopy. These strands are completely filled with eosinophils and eosinophilic granules.35 In this pioneering study. and others required long-term corticosteroids in addition to cromolyn.40 and in the latter study it was thought to be more long-lasting . The efficacy of aspirin was also confirmed in other studies. however.39. This emphasizes the prophylactic nature of the drug and its steroid-sparing qualities. Other mast cell stabilizers have been evaluated. there was less infiltration of inflammatory cells and an absence of eosinophils. when the disease is more severe. However. After treatment with corticosteroids. However. Abelson and his co-workers38 suggested the use of oral aspirin in the treatment of VKC. mast cell stabilizers have been introduced for the treatment of VKC. and there was a lesser degree of degranulation of mast cells. ANTIHISTAMINE-VASOCONSTRICTORS These preparations may have some role in the treatment of mild vernal conjunctivitis. they do not have the potency necessary to control the inflammation. However.36 and lodoxamide (Alomide) has been shown to be more effective than cromolyn in the treatment of VKC. the inflammation should be controlled with topical corticosteroids. most patients with VKC could be controlled with cromolyn alone. and cromolyn should be added as adjunctive therapy to allow the corticosteroids to be tapered. MAST CELL STABILIZERS In recent years.33 Recent evidence has suggested that mast cells are not homogeneous.37 PROSTAGLANDIN INHIBITORS Coincident with his studies on the effect of prostaglandins on the outer eye. and examined under the microscope. this treatment is usually not effective by itself.confirmed by Abu El-Asrar. cromolyn is usually not adequate when the eye is severely inflamed or when there is a vernal ulcer. Back to Top TREATMENT NONSPECIFIC Cold compresses may alleviate the itching in vernal conjunctivitis when it is mild. Nedocromil drops have been shown to be effective when compared with placebo. in the face of onset of any keratitis.
especially when the keratitis is active. repeating the freeze-thaw cycle two to three times. and the treatment regimen is varied. In severe cases. or filamentary keratitis. ACETYLCYSTEINE One of the common clinical findings is the tenacious mucus that develops. Acetylcysteine is known to break the disulfide bonds. because there is already an increased incidence of cataract and infections in patients who are atopic. CORTICOSTEROIDS Corticosteroids inhibit mediator biosynthesis and disrupt intercellular communications by preventing the release of lymphokines. and it is effective for all three types of excessive mucus. which in turn prevents the formation of interleukin-2 and the subsequent recruitment of activated T cells. including glaucoma. Cyclosporin A is a potent immunosuppressive drug used in the prevention of transplant rejections. They concluded that cryotherapy was helpful in the management of VKC. and 21 of their patients were improved on this regimen. cataract. ropy strands of mucus. depending on the severity of the disease. Ketorolac (Acular) is a nonsteroidal anti-inflammatory drug that blocks the release of prostaglandins. they also gave the patients 0. Cyclosporin A binds to cyclophilin. Sankarkumar and colleagues48 treated the conjunctiva of 30 eyes in 15 patients with a glaucoma probe at -60°C and -80°C. This may take any of three forms: mucus adhering to the cobblestones. Patients should be monitored for the complications of corticosteroids.than corticosteroids.43 They are the most effective and the best-proved treatment for VKC. IMMUNOSUPPRESSIVE AGENTS Immunosuppressive medication may be beneficial.5 g of aspirin. Therefore. hourly corticosteroid drop administration may be necessary. It is formulated from commercially available Mucomyst.5 to 1. Gupta and associates41 treated 25 VKC patients with 1% indomethacin drops. systemic corticosteroids may be given to bring the inflammation under control. an intracellular protein. . Corticosteroids can be administered in drop form. diluted to a 5% or 10% solution with artificial tears. In severe conjunctivitis. it is difficult to distinguish the effect of the cryotherapy from that of the aspirin. and is applied four times a day. thick. and external ocular infections.45–47 CRYOTHERAPY Several reports have advocated the use of cryotherapy in the treatment of VKC.44 It has been used successfully in several studies to treat VKC. However.42 Its role in VKC has yet to be determined. thereby dissolving the mucus.
CV Mosby. London. Tse and associates51 found this procedure successful and long-lasting with follow-up. Eye 3:420. Henry Kimpton. Thoft R (eds): The Cornea. 1960 7. p 355. Williams HE: Ocular allergy.49 However. In Duke-Elder S (ed): System of Ophthalmology. Little. Trans Ophthalmol Soc UK 80:665. ß-IRRADIATION Several authors have reported success with ß-irradiation in the treatment of VKC. 1965 3. Boston. St. warns that distorting the tarsus can cause adverse changes in eyelid position. Neumann E. Donshik PC. Jones B: Vernal keratitis. Am J Ophthalmol 147:166. Buckley. Mucous membrane grafting has been reported to improve symptoms in vernal conjunctivitis. 1994 5. Tarsectomy with or without mucous membrane graft has been suggested to physically remove the cobblestone papillae. Arffa RC: Immunologic disorders. p 476.SURGERY Surgical removal of a plaque in the base of a vernal ulcer preventing reepithelialization may promote healing. Blumenkrantz N et al: A review of four hundred cases of vernal conjunctivitis. Part I. Supported in part by a Department of Veterans' Affairs Research Service Merit Review Grant. Duke-Elder S: Diseases of the outer eye. In Smolin G. 1989 4. 1991 . and the lack of publications in the modern literature suggests that this mode of therapy no longer has a place in the treatment of VKC. (ELS) Back to Top REFERENCES 1. 1959 2. Louis. these reports appear to lack long-term follow-up. Tuft SJ. Jones B: The differential diagnosis of punctate keratitis.52 on the other hand. one of the authors of this article (ELS) has seen permanent scarring from this treatment. 1961 6.50 Although there has been controversy in the literature regarding this procedure. Brown. Gutmann MJ. Dart JK. Trans Ophthalmol Soc UK 81:215. Kemeny M: Limbal vernal keratoconjunctivitis: Clinical characteristics and immunoglobulin E expression compared with palpebral vernal.53 However. In Arffa RC (ed): Grayson's Diseases of the Cornea.
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Gellis S et al: Vernal conjunctivitis in the hyperimmunoglobulin E syndrome. Bull Mem Soc Fr Ophtalmol 24:1. 1971 32. Am J Ophthalmol 94:205. Collin HB. Trans Ophthalmol Soc UK 91:491. Beigelman MN: Vernal Conjunctivitis. Fujikawa LS. Ophthalmology 91:1213. Proc Natl Acad Sci USA 83:4464. Bonini S. Schecter NM. Am J Ophthalmol 9:71. 1971 36. Stock EL.22. Maggi E. 1950 29. Del Prete G et al: Accumulation of Th-2-like helper T cells in the conjunctiva of patients with vernal conjunctivitis. Barney NP. Herbert H: Preliminary notes on the pathology and diagnosis of spring catarrh. 1984 27. Craig SS et al: Two types of mast cells that have distinct neutral protease compositions. Ophthalmology 96:1615. J Immunol 146:1169. 1977 25. Invest Ophthalmol Vis Sci 16:858. Trans Ophthalmol Soc UK 190:98. Irani AA. Br Med J II:735. Morgan G: The pathology of vernal conjunctivitis. Merrett T et al: Immunologic investigations in vernal eye disease. 1981 33. 1986 35. 1907 31. University of Southern California Press. Schiavone M et al: Effectiveness of nedocromil sodium 2% eyedrops on clinical symptoms and tear fluid cytology of . Meisler DM: Cutaneous basophil hypersensitivity in the guinea pig conjunctiva. Leung DYM. Easty DL. Bhan AK. 1903 30. 1991 24. Allansmith MR: Basophils in vernal conjunctivitis in humans: An electron microscope study. Biswas P. Allansmith MR. Rice NSC. Los Angeles. Badr IA: Corneal ectasia in vernal keratoconjunctivitis. 1989 28. Foster CS: T-cell subsets and Langerhans cells in normal and diseased conjunctiva. Cameron JA. Jones B: Disodium cromoglycate (Intal) in the treatment of vernal keratoconjunctivitis. Easty D. Trans Ophthalmol Soc UK 91:467. Curr Eye Res 2:887. Baird RS: Percentage of degranulated mast cells in vernal conjunctivitis and giant papillary conjunctivitis associated with contact lens wear. Birkenshaw M. Butrus SI. 1982/1983 26. 1982 23. Axenfeld T: Rapport sur le catarrhe printanier. Al-Rajhi AA. 1980 34.
Brodsky M et al: Cyclosporin eye drops for the treatment of severe vernal keratoconjunctivitis. Haynes RC Jr: Adrenocorticotropic hormone. Am J Ophthalmol 124:253. In Gilman AG. Br J Ophthalmol 71:497. Sankarkumar T. Surv Ophthalmol (suppl) 38:133. Kaufman H et al: Double masked. Am J Ophthalmol 53:429. adrenocortical steroids and their synthetic analogs. 1992 38. Meyer E. Zonis S: Efficacy of antiprostaglandin therapy in vernal conjunctivitis. Khurana AK. Angra SK: Efficacy of cryotherapy in vernal catarrh. Am J Ophthalmol 113:632. Butrus S. Sebbahi et al: Traitement de la conjonctivite printanière par l'aspirine. Caldwell DR. Tognon MS. pp 1442–1460. Hartwich-Young R et al: Efficacy and safety of lodoxamide 0. Trans . Kraus E. New York. Ahluwalia BK et al: Topical indomethacin for vernal keratoconjunctivitis. Eye 65:648. Abelson MB.5% ophthalmic solution compared with placebo eye drops in the treatment of seasonal allergic conjunctivitis. Panda A. inhibitors of the synthesis and actions of adrenocortical hormone. Pe'er J. Leonardi A: Topical use of cyclosporine in the treatment of vernal keratoconjunctivitis. 1993 43. 8th ed. Pergamon Press. Rev Int Trach Pathol Ocul Trop Subtrop Sante Publique 66:119. 1992 49. Secchi AG. Cross AG: Surgical treatment of persistent vernal catarrh. Acta Ophthalmol 69:95. Ophthalmology 98:1679. Pendleton RB: Pharmacological treatment of ocular allergic diseases. Lemrini F.1% vs cromolyn sodium 4% in patients with vernal keratoconjunctivitis. Am J Ophthalmol 95:502. 1983 39. Sugar HS: Tarsectomy for proliferative palpebral vernal conjunctivitis. Nies AS et al (eds): The Pharmacological Basis of Therapeutics. 1993 45. 1991 42. Gupta S. Am J Ophthalmol 101:278. Bleik JH. 1989 41. 1987 40. Rupp G. paired comparison clinical study of ketorolac tromethamine 0. Am J Ophthalmol 110:641.patients with vernal conjunctivitis. Rail TW. 1986 46. Tabbara KF: Topical cyclosporine in vernal keratoconjunctivitis. Weston JH: Aspirin therapy in vernal conjunctivitis. 1990 44. 1991 47. Int Ophthalmol Clin 33:47. 1992 37. Philippe V. BenEzra D. 1962 50. Tinkelman DG. Stock EL. Dafrallah L. 1990 48.
Tse DT.nih. The presence of an antigen starts the allergic cascade.com/lessons/html/conjunct2001. nonsteroidal anti-inflammatory drugs. Buckley RJ: Vernal keratoconjunctivitis. 1983 52.php?img=2629892_kjo-21-251-g001&req=4 http://secure. mast cell stabilizers. and. Diagnosis of allergic conjunctivitis is generally made by thorough history and careful clinical observation (see Clinical). The major type I hypersensitivity reactions involving the conjunctiva are commonly referred to as allergic conjunctivitis. Epstein S et al: Mucous membrane grafting for severe palpebral vernal conjunctivitis.net/downaton502/prof/ebook/duanes/pages/v4/v4c009.oculist. See the following for more information: Acute Hemorrhagic Conjunctivitis Atopic Keratoconjunctivitis Bacterial Conjunctivitis Emergent Treatment of Acute Conjunctivitis Epidemic Keratoconjunctivitis Giant Papillary Conjunctivitis Keratoconjunctivitis Sicca Neonatal Conjunctivitis Superior Limbic Keratoconjunctivitis Viral Conjunctivitis Immunologic reactions of conjunctiva and cornea . Trans Am Ophthalmol Soc 50:469.com/minor/ophthalmology/vernal-keratoconjunctivitis-vkc-or-spring-catarrah/ http://www.pharmacytimes. avoidance of the offending antigen is the primary behavioral modification for all types of allergic conjunctivitis. thus. Int Ophthalmol Clin 28:303.htm The ocular surface may exhibit a wide variety of immunologic responses resulting in inflammation of the conjunctiva and cornea. 1952 http://www.com/Singapore/pub/topic/Medical%20Progress/201204/Conjunctivitis%20Dont%20Miss%20the%20Serious%20Causes%20%20 http://openi.html http://medchrome. and corticosteroids (see Treatment). In other respects.gov/detailedresult. Arch Ophthalmol 101:1879. 5 types of reactions are recognized. 1988 53. Allergic conjunctivitis can be treated with a variety of drugs. Hughes WF Jr: Beta radiation therapy in ophthalmology.Ophthalmol Soc UK 79:45. Mandelbaum S. management of allergic conjunctivitis varies somewhat according to the specific subtype.mims.nlm. 1959 51. including topical antihistamines. In the Gell and Coombs classification system for various immunologic hypersensitivity reactions.
For patient education information. see the Eye and Vision Center. may provoke the symptoms of acute allergic conjunctivitis. The mast cell’s degranulation releases various preformed and newly formed mediators of the inflammatory cascade. Immunoglobulin E (IgE) has a strong affinity for mast cells. Ocular examples of type IV hypersensitivity include phlyctenular keratoconjunctivitis. which is an immediate hypersensitivity. These type III reactions can often induce a corneal immune (Wesley) ring that dissolves when the inflammatory reaction subsides. in contrast to the type I reaction. the prognosis is favorable. in summer. together with various chemotactic factors. thromboxanes. result in an increase in vascular permeability and migration of eosinophils and neutrophils. The main distinction between SAC and PAC. individuals with PAC may have symptoms that last the year round. persons with SAC are symptom-free during the winter months in cooler climates because of the decreased airborne transmission of these allergens. Type III hypersensitivity reactions result in antigen-antibody immune complexes. and How to Instill Your Eyedrops. and the cross-linking of 2 adjacent IgE molecules by the antigen triggers mast cell degranulation. and ocular type III hypersensitivity reactions include Stevens-Johnson syndrome and marginal infiltrates of the cornea. Type IV hypersensitivity reactions. Prognosis Since allergic conjunctivitis generally clears up readily. heparin. burning. Common airborne antigens. since its onset is generally after 48 hours. when the predominant airborne allergen is tree pollen. which deposit in tissues and cause inflammation. Complications are very rare. and weeds.Type I (immediate) hypersensitivity reactions occur when a sensitized individual comes in contact with a specific antigen. also known as cell-mediated immunity. chymase. Vernal keratoconjunctivitis (VKC). is the timing of symptoms. it rarely causes any visual loss. In contrast. allergic inflammation did not cause permanent tear film instability. such as ocular itching. with corneal ulcers or keratoconus occurring rarely. prostaglandins. and drug allergies. atopic keratoconjunctivitis (AKC). or in fall. Most notable of these inflammatory mediators are histamine. and giant papillary conjunctivitis (GPC) constitute the remaining subtypes of allergic conjunctivitis. and tearing. A classic systemic type III reaction is the Arthus reaction. as well as Pinkeye. This inflammatory cell-driven reaction is also referred to as delayed-type hypersensitivity. Other common household allergens. the same allergens that trigger allergic rhinitis may be involved in the pathogenesis of allergic conjunctivitis. One study found that outside the pollen season. contact dermatitis. This type I hypersensitivity reaction is the most common allergic response of the eye. Early diagnosis and treatment will help prevent the rare complications that can occur with this disease. although they may play a role. grass. Pathophysiology Seasonal and perennial allergic conjunctivitis Since the conjunctiva is a mucosal surface similar to the nasal mucosa. Eye Allergies. redness. Type IV hypersensitivity reactions imply immunocompetence on the part of the individual since an intact immune system is required to mount the cell-mediated response. These various inflammatory mediators. Typically. PAC may not be caused exclusively by seasonal allergens. when the predominant allergen is weed pollen. including pollen. Individuals with SAC typically have symptoms of acute allergic conjunctivitis for a defined period of time. such as cicatricial pemphigoid and Mooren ulcer. that is. such as dust . Seasonal allergic conjunctivitis can manifest itself through tear film instability and symptoms of eye discomfort during the pollen season. in spring. and leukotrienes. thus. Allergic conjunctivitis subtypes Allergic conjunctivitis may be divided into 5 major subcategories. Although allergic conjunctivitis may commonly reoccur. Seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC) are commonly grouped together. corneal allograft rejection. tryptase. as implied by the names. Patient education Patients should make every attempt to identify the allergen causing the problem and to avoid the offending antigen. chondroitin sulfate. are interceded by T lymphocytes. when the predominant allergen is grass pollen. These immune-derived reactions may be the underlying cause of various ocular conditions.
which are typically greater than 0. It is also a type I hypersensitivity disorder with many similarities to VKC. may be responsible for the symptoms of PAC. which stimulates the immunological reaction and the development of GPC. Epidemiology Allergic conjunctivitis occurs very frequently and is seen most commonly in areas with high seasonal allergens. the primary finding is the presence of "giant" papillae. yet AKC is distinct in a number of ways.com/article/1191467-overview#showall . Hogan first described the association between atopic dermatitis and conjunctival inflammation. of these. Approximately 3% of the population is afflicted with atopic dermatitis. such as the Mediterranean. Atopic dermatitis is a common hereditary disorder that usually has its onset in childhood. A combination of type I and type IV hypersensitivity reactions may be responsible for the pathogenesis of GPC. Atopic keratoconjunctivitis AKC is a bilateral inflammation of conjunctiva and eyelids. The onset of VKC is generally in the first decade and persists for the first 2 decades. the Middle East. extruded scleral buckles. It is believed that an antigen is present. and Africa. airborne allergens. More than 90% of patients with VKC exhibit one or more atopic conditions. http://emedicine. Vernal keratoconjunctivitis VKC is a chronic bilateral inflammation of the conjunctiva. and. approximately 25% have ocular involvement. Giant papillary conjunctivitis GPC is an immune-mediated inflammatory disorder of the superior tarsal conjunctiva.medscape. ocular prostheses. which has a strong association with atopic dermatitis. Sexual and age-related differences in incidence VKC has a significant male preponderance. Prolonged mechanical irritation to the superior tarsal conjunctiva. Although contact lenses (hard and soft) are the most common irritant.mite. commonly associated with a personal and/or family history of atopy. VKC occurs predominantly in areas with tropical and temperate climates. from any of a variety of foreign bodies may also be a contributing factor in GPC. eczema. such as asthma.  He reported 5 cases of conjunctival inflammation in male patients with atopic dermatitis. of the upper lid. in predisposed individuals. In 1953. As the name implies. symptoms may regress with advancing age. typically affecting young males. cockroach dust. cigarette smoke. Symptoms usually peak prior to the onset of puberty and then subside. or seasonal allergic rhinitis.3 mm in diameter. The limbal form of VKC commonly occurs in dark-skinned individuals from Africa and India. and pet dander. and exposed sutures following previous surgical intervention may also precipitate GPC.