Chapter 5: Conjunctiva
IMMUNOLOGIC (ALLERGIC) CONJUNCTIVITIS
IMMEDIATE HUMORAL HYPERSENSITIVITY REACTIONS
1. HAY FEVER CONJUNCTIVITIS
A mild, nonspecific conjunctival inflammation is commonly associated with hay fever (allergic rhinitis). There is usually a history of allergy to pollens, grasses, animal danders, etc. The patient complains of itching, tearing, and redness of the eyes and often states that the eyes seem to be "sinking into the surrounding tissue." There is mild injection of the palpebral and bulbar conjunctiva, and during acute attacks there is often severe chemosis (which no doubt accounts for the "sinking" description). There may be a small amount of ropy discharge, especially if the patient has been rubbing the eyes. Eosinophils are difficult to find in conjunctival scrapings. A papillary conjunctivitis can occur if the allergen persists (Figure 5-10).
Treatment consists of the instillation of local vasoconstrictors during the acute phase (epinephrine, 1:1000 solution applied topically, will relieve the chemosis and symptoms within 30 minutes). Cold compresses are helpful to relieve itching, and antihistamines by mouth are of some value. The immediate response to treatment is satisfactory, but recurrences are common unless the antigen is eliminated. Fortunately, the frequency of the attacks and the severity of the symptoms tend to moderate as the patient ages.
2. VERNAL KERATOCONJUNCTIVITIS
This disease, also known as "spring catarrh" and "seasonal conjunctivitis" or "warm weather conjunctivitis," is an uncommon bilateral allergic disease that usually begins in the prepubertal years and lasts for 5-10 years. It occurs much oftener in boys than in girls. The specific allergen or allergens are difficult to identify, but patients with vernal keratoconjunctivitis usually show other manifestations of allergy known to be related to grass pollen sensitivity. The disease is less common in temperate than in warm climates and is almost nonexistent in cold climates. It is almost always more severe during the spring, summer, and fall than in the winter. It is most commonly seen in sub-Saharan Africa and the Middle East.
The patient usually complains of extreme itching and a ropy discharge. There is often a family history of allergy (hay fever, eczema, etc) and sometimes in the young patient as well. The conjunctiva has a milky appearance, and there are many fine papillae in the lower tarsal conjunctiva. The upper palpebral conjunctiva often has giant papillae that give a cobblestone appearance (Figure 5-11). Each giant papilla is polygonal, has a flat top, and contains tufts of capillaries.
A stringy conjunctival discharge and a fine, fibrinous pseudomembrane (Maxwell-Lyons sign) may be noted, especially on the upper tarsus on exposure to heat. In some cases, especially in persons of black African ancestry, the most prominent lesions are located at the limbus, where gelatinous swellings (papillae) are noted. A pseudogerontoxon (arcus-like haze) is often noted in the cornea adjacent to the limbal papillae. Trantas' dots are whitish dots seen at the limbus in some patients with vernal keratoconjunctivitis during the active phase of the disease. Many eosinophils and free eosinophilic granules are found in Giemsa-stained smears of the conjunctival exudate and in Trantas' dots.
Micropannus is often seen in both palpebral and limbal vernal keratoconjunctivitis, but gross pannus is unusual. Conjunctival scarring usually does not occur unless the patient has been treated with cryotherapy, surgical removal of the papillae, irradiation, or other damaging procedure. Superficial corneal ("shield") ulcers (oval and located superiorly) may form and may be followed by mild corneal scarring. A characteristic diffuse epithelial keratitis frequently occurs. None of the corneal lesions respond well to standard treatment.
The disease may be associated with keratoconus.
Treatment
Since vernal keratoconjunctivitis is a self-limited disease, it must be recognized that the medication used to treat the symptoms may provide short-term benefit but long-term harm. Topical and systemic steroids, which relieve the itching, affect the corneal disease only minimally, and their side effects (glaucoma, cataract, and other complications) can be severely damaging. Topical cromolyn is a useful prophylactic agent in moderate to severe cases. Vasoconstrictors, cold compresses, and ice packs are helpful, and sleeping (if possible, also working) in cool, air-conditioned rooms can keep the patient reasonably comfortable. Probably the best remedy of all is to move to a cool, moist climate. Patients able to do so are benefited if not completely cured.
The severe symptoms of an extremely photophobic patient who is unable to function can often be relieved by a short course of topical or systemic steroids followed by vasoconstrictors, cold packs, and regular use of histamine-blocking agents as eyedrops. Newer nonsteroidal anti-inflammatory medications, including ketorolac and lodoxamide, may provide significant symptomatic relief. (See discussion in Chapter 3.) As has already been indicated, the prolonged use of steroids must be avoided since it is all too often followed by herpes simplex keratitis, cataract, glaucoma, and fungal and other opportunistic corneal ulcers. Recent clinical studies have shown that topical 2% cyclosporine eye drops are effective in severe unresponsive cases. Supratarsal injection of depot corticosteroids has been demonstrated to be effective for vernal shield ulcers.
Desensitization to grass pollens and other antigens has not been rewarding. Staphylococcal blepharitis and conjunctivitis are frequent complications and should be treated. Recurrences are the rule, particularly in the spring and summer; but after a number of recurrences the papillae disappear completely, leaving no scars.
3. ATOPIC KERATOCONJUNCTIVITIS
Patients with atopic dermatitis (eczema) often also have atopic keratoconjunctivitis. The symptoms and signs are a burning sensation, mucoid discharge, redness, and photophobia. The lid margins are erythematous, and the conjunctiva has a milky appearance. There are fine papillae, but giant papillae are less developed than in vernal keratoconjunctivitis and occur more frequently on the lower tarsus-unlike the giant papillae of vernal keratoconjunctivitis, which are on the upper tarsus (Figure 5-12). Severe corneal signs appear late in the disease after repeated exacerbations of the conjunctivitis. Superficial peripheral keratitis develops and is followed by vascularization. In severe cases, the entire cornea becomes hazy and vascularized, and visual acuity is reduced. The disease may be associated with keratoconus.
There is usually a history of allergy (hay fever, asthma, or eczema) in the patient or the patient's family. Most patients have had atopic dermatitis since infancy. Scarring of the flexure creases of the antecubital folds and of the wrists and knees is common. Like the dermatitis with which it is associated, atopic keratoconjunctivitis has a protracted course and is subject to exacerbations and remissions. Like vernal keratoconjunctivitis, it tends to become less active when the patient reaches the fifth decade.
Scrapings of the conjunctiva show eosinophils, though not nearly as many as are seen in vernal keratoconjunctivitis. Scarring of both the conjunctiva and cornea is often seen, and an atopic cataract, a posterior subcapsular plaque, or an anterior shield-like cataract may develop. Keratoconus, retinal detachment, and herpes simplex keratitis are all more than usually frequent in patients with atopic keratoconjunctivitis, and there are many cases of secondary bacterial blepharitis and conjunctivitis, usually staphylococcal.
The management of atopic keratoconjunctivitis is often discouraging. Any secondary infection must be treated. Environmental control should be considered. Oral antihistamines including terfenadine (60-120 mg twice daily), astemizole (10 mg four times daily), or hydroxyzine (50 mg at bedtime, increasing to 200 mg at bedtime) have been shown to be of value. Newer nonsteroidal anti-inflammatory medications, including ketorolac and lodoxamide, show promise for symptomatic relief for these patients (see Chapter 3). A short course of topical steroids may relieve symptoms. In severe cases, plasmapheresis may be an adjunct to therapy. In advanced cases with severe corneal complications, corneal transplantation may be needed to improve the visual acuity.
4. GIANT PAPILLARY CONJUNCTIVITIS
Giant papillary conjunctivitis with signs and symptoms resembling those of vernal conjunctivitis may develop in patients wearing plastic artificial eyes or contact lenses. It is probably a basophil-rich delayed hypersensitivity disorder (Jones-Mote hypersensitivity), perhaps with an IgE humoral component. Use of glass instead of plastic for prostheses and spectacle lenses instead of contact lenses is curative. If the goal is to maintain contact lens wear, additional therapy will be required. Careful contact lens care, including preservative-free agents, is essential. Hydrogen peroxide disinfection and enzymatic cleaning of contact lenses may also help. Changing to a different brand or style of contact lenses may be necessary if other measures fail. If these treatments are unsuccessful, contact lenses should be discontinued.
DELAYED HYPERSENSITIVITY REACTIONS
1. PHLYCTENULOSIS
Phlyctenular keratoconjunctivitis is a delayed hypersensitivity response to microbial proteins, including the proteins of the tubercle bacillus, Staphylococcus species, Candida albicans, Coccidioides immitis, Haemophilus aegyptius, and Chlamydia trachomatis serotypes L1, L2, and L3. Until recently, by far the most frequent cause of phlyctenulosis in the USA was delayed hypersensitivity to the protein of the human tubercle bacillus. This is still the commonest cause in regions where tuberculosis is still prevalent. In the USA, however, most cases are now associated with delayed hypersensitivity to S aureus.
The conjunctival phlyctenule begins as a small lesion (usually 1-3 mm in diameter) that is hard, red, elevated, and surrounded by a zone of hyperemia. At the limbus it is often triangular in shape, with its apex toward the cornea. In this location it develops a grayish-white center that soon ulcerates and then subsides within 10-12 days. The patient's first phlyctenule and most of the recurrences develop at the limbus, but there may also be corneal, bulbar, and, very rarely, even tarsal phlyctenules.
Unlike the conjunctival phlyctenule, which leaves no scar, the corneal phlyctenule develops as an amorphous gray infiltrate and always leaves a scar. Consistent with this difference is the fact that scars form on the corneal side of the limbal lesion and not on the conjunctival side. The result is a triangular scar with its base at the limbus-a valuable sign of old phlyctenulosis when the limbus has been involved.
Conjunctival phlyctenules usually produce only irritation and tearing, but corneal and limbal phlyctenules are usually accompanied by intense photophobia (Figure 5-13). Phlyctenulosis is often triggered by active blepharitis, acute bacterial conjunctivitis, and dietary deficiencies. Phlyctenular scarring, which may be minimal or extensive, is often followed by Salzmann's nodular degeneration.
Histologically, the phlyctenule is a focal subepithelial and perivascular infiltration of small round cells, followed by a preponderance of polymorphonuclear cells when the overlying epithelium necrotizes and sloughs-a sequence of events characteristic of the delayed tuberculin type hypersensitivity reaction.
Phlyctenulosis induced by tuberculoprotein and the proteins of other systemic infections responds dramatically to topical corticosteroids. There is a major reduction of symptoms within 24 hours and disappearance of the lesion in another 24 hours. Phlyctenulosis produced by staphylococcal proteins responds somewhat more slowly. Topical antibiotics should be added for active staphylococcal blepharoconjunctivitis. Treatment should be aimed at the underlying disease, and the steroids, when effective, should be used only to control acute symptoms and persistent corneal scarring. Severe corneal scarring may call for corneal transplantation.
2. MILD CONJUNCTIVITIS SECONDARY TO CONTACT BLEPHARITIS
Contact blepharitis caused by atropine, neomycin, broad-spectrum antibiotics, and other topically applied medications is often followed by a mild infiltrative conjunctivitis that produces hyperemia, mild papillary hypertrophy, a mild mucoid discharge, and some irritation (Figure 5-14). Examination of Giemsa-stained scrapings often discloses only a few degenerated epithelial cells, a few polymorphonuclear and mononuclear cells, and no eosinophils.
Treatment should be directed toward finding the offending agent and eliminating it. The contact blepharitis may clear rapidly with topical cortico-steroids, but their use should be limited. Long-term use of steroids on the lids may lead to steroid glaucoma and to skin atrophy with disfiguring telangiectasis.
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10.1036/1535-8860.ch5