Atopic conjunctivitis is a reactive inflammation of the conjunctiva caused by immune reactions in response to contact with an allergen. Allergic conjunctivitis develops hyperemia and swelling of the mucous membrane of the eye, itching and swelling of the eyelids, lacrimation, photophobia. Diagnosis is based on the collection of an allergic history, skin tests, provocative allergic tests (conjunctival, nasal, sublingual), laboratory tests. Antihistamines (orally and topically), topical corticosteroids, and specific immunotherapy are used in the treatment of atopic conjunctivitis.
H10.1 Acute atopic conjunctivitis
Atopic conjunctivitis occurs in about 15% of the population and is a significant problem of modern ophthalmology and allergology. Allergic damage to the organ of vision in 90% of cases is accompanied by the development of conjunctivitis, less often – atopic blepharitis, dermatitis of the eyelids, atopic keratitis, uveitis, iritis, retinitis, neuritis. Atopic conjunctivitis occurs in persons of both sexes, mainly young age. Atopic conjunctivitis is often combined with other allergoses – allergic rhinitis, bronchial asthma, atopic dermatitis.
Common in the etiology of all forms of atopic conjunctivitis is hypersensitivity to various environmental factors. Due to the peculiarities of the anatomical structure and location of the eyes, they are most susceptible to contact with exogenous allergens. Depending on the etiology , there are:
- Seasonal atopic conjunctivitis. Pollinous conjunctivitis (hay fever, pollen allergy) caused by pollen allergens during flowering of grasses, trees, cereals. Exacerbation of pollinous conjunctivitis is associated with the flowering period of plants in a particular region. Seasonal atopic conjunctivitis in 7% of patients worsens in spring (late April – late May), in 75% – in summer (early June – late July), in 6.3% – in the off-season (late July – mid-September), which correspondingly coincides with the pollination of trees, meadow grasses and weeds.
- Spring conjunctivitis. The etiology of spring conjunctivitis has been little studied. The disease worsens in spring – early summer and regresses in autumn. This form of atopic conjunctivitis usually passes spontaneously during puberty, which suggests a certain role of the endocrine factor in its development.
- Large-capillary conjunctivitis. The main factor of development is considered to be wearing contact lenses and eye prostheses, prolonged contact of the mucous membrane with a foreign body of the eye, the presence of irritating conjunctival sutures after cataract extraction or keratoplasty, calcium deposits in the cornea, etc. In this form of atopic conjunctivitis, the inflammatory reaction is accompanied by the formation of large flattened papillae on the mucosa of the upper eyelid.
- Medicinal conjunctivitis develops as a local allergic reaction in response to topical (90.1%), less often systemic (9.9%) use of medicines. The emergence of medicinal atopic conjunctivitis is facilitated by self-medication, individual intolerance to the components of the drug, polytherapy – a combination of several drugs without taking into account their interaction. Most often, the use of antibacterial and antiviral eye drops and ointments leads to medicinal atopic conjunctivitis.
- Chronic atopic conjunctivitis. It accounts for more than 23% of cases of all allergic eye diseases. With minimal clinical manifestations, the course of chronic atopic conjunctivitis is characterized by a persistent character. The direct allergens in this case are usually household dust, animal hair, dry fish food, feather, fluff, food products, perfumes, cosmetics and household chemicals. Chronic atopic conjunctivitis is often associated with eczema and bronchial asthma.
- Atopic keratoconjunctivitis. It is an allergic disease of multifactorial etiology. It usually develops with systemic immunological reactions, therefore it often occurs against the background of atopic dermatitis, asthma, hay fever, urticaria.
The pathogenesis of atopic conjunctivitis is based on an IgE-mediated hypersensitivity reaction. The trigger factor of atopic conjunctivitis is the direct contact of the allergen with the conjunctiva, leading to the degranulation of mast cells, activation of lymphocytes and eosinophils and a clinical response followed by an inflammatory allergic reaction. Mediators released by mast cells (histamine, serotonin, leukotrienes, etc.) cause the development of characteristic symptoms of atopic conjunctivitis.
The severity of the course of atopic conjunctivitis depends on the concentration of the allergen and the reactivity of the body. The rate of hypersensitivity reaction development in allergic conjunctivitis can be immediate (within 30 minutes from the moment of contact with the allergen) and delayed (after 24-48 or more hours). This classification of allergic conjunctivitis is practically significant for the choice of drug therapy.
Allergic eye lesions can occur in the form of pollinous conjunctivitis, spring keratoconjunctivitis, large-capillary conjunctivitis, medicinal conjunctivitis, chronic atopic conjunctivitis, atopic keratoconjunctivitis. Along the course, allergic conjunctivitis can be acute, subacute or chronic; according to the time of occurrence, seasonal or year–round.
With allergies, as a rule, both eyes are affected. Symptoms develop within a few minutes to 1-2 days from the moment of exposure to the allergen. Atopic conjunctivitis is characterized by severe itching of the eyes, burning under the eyelids, lacrimation, swelling and hyperemia of the conjunctiva; in severe cases – the development of photophobia, blepharospasm, ptosis.
Itching in atopic conjunctivitis is so intense that it forces the patient to constantly rub his eyes, which, in turn, further enhances the remaining clinical manifestations. Small papillae or follicles may form on the mucous membrane. The discharge from the eyes is usually slimy, transparent, sometimes viscous, filamentous. When the infection is layered in the corners of the eyes, a purulent secret appears.
In some forms (spring and atopic keratoconjunctivitis), corneal damage occurs. With drug allergies, lesions of the skin of the eyelids, cornea, retina, choroid, optic nerve may be observed. Acute drug conjunctivitis is sometimes aggravated by anaphylactic shock, Quincke’s edema, acute urticaria, systemic capillarotoxicosis.
With chronic allergic conjunctivitis, the symptoms are poorly expressed: complaints of periodic itching of the eyelids, burning of the eyes, redness of the eyelids, lacrimation, a moderate amount of discharge are characteristic. Chronic allergic conjunctivitis is spoken of if the disease lasts 6-12 months.
In the diagnosis and treatment of atopic conjunctivitis, the coordinated interaction of the attending ophthalmologist and the allergist-immunologist is important. If there is a clear connection between conjunctivitis and exposure to an external allergen in the anamnesis, the diagnosis, as a rule, is not in doubt. To confirm the diagnosis is carried out:
- Ophthalmological examination. Reveals conjunctival changes (edema, hyperemia, papillary hyperplasia, etc.). Microscopic examination of conjunctival scraping allows you to detect eosinophils (from 10% and above). In the blood, an increase in IgE of more than 100-150 IU is typical.
- Allergological examination. To determine the cause of disease, tests are carried out: elimination, when contact with a suspected allergen is excluded against the background of clinical manifestations, and exposure, consisting in repeated exposure to this allergen after the symptoms subside. After the acute allergic manifestations of conjunctivitis subside, skin-allergic tests are performed (application, scarification, electrophoresis, prick test). During remission, provocative tests are resorted to – conjunctival, sublingual and nasal.
- Laboratory examination. In chronic form, a study of eyelashes for demodex is indicated. If an infectious lesion of the eyes is suspected, a bacteriological examination of a smear from the conjunctiva to the microflora is carried out.
Atopic conjunctivitis treatment
The basic principles of the treatment include: elimination (exclusion) of the allergen, local and systemic desensitizing therapy, symptomatic drug therapy, specific immunotherapy, prevention of secondary infections and complications. With large-capillary conjunctivitis, it is necessary to stop wearing contact lenses, eye prostheses, removal of postoperative sutures or removal of a foreign body.
With allergic conjunctivitis, oral antihistamines (claritin, ketotifen, etc.) and the use of antiallergic eye drops (levocabastine, azelastine, olopatadine) 2-4 times a day are prescribed. Local use in the form of drops of cromoglycic acid derivatives (mast cell stabilizers) is also shown. With the development of dry eye syndrome, tear substitutes are prescribed; with corneal damage, eye drops with dexpanthenol and vitamins.
Severe forms may require the appointment of topical corticosteroids (eye drops or ointments with dexamethasone, hydrocortisone), topical NSAIDs (eye drops with diclofenac). Persistently recurrent allergic conjunctivitis is the basis for specific immunotherapy.
Prognosis and prevention
In most cases, when an allergen is detected and eliminated, the prognosis is favorable. In the absence of treatment, it is possible to attach an infection with the development of secondary herpetic or bacterial keratitis, a decrease in visual acuity. In order to prevent atopic conjunctivitis, contact with known allergens should be excluded if possible. With seasonal forms of atopic conjunctivitis, it is necessary to conduct preventive courses of desensitizing therapy. Patients should be monitored by an ophthalmologist and an allergist.