- •Dedication
- •Foreword
- •Preface
- •Ocular Allergy Overview
- •The ocular surface
- •Clinical examination
- •Immunopathophysiology of ocular allergy
- •Acute allergic conjunctivitis
- •Vernal keratoconjunctivitis
- •Atopic keratoconjunctivitis
- •Giant papillary conjunctivitis
- •Contact dermatitis of the eyelids
- •Blepharoconjunctivitis
- •Bacterial conjunctivitis
- •Viral conjunctivitis
- •Vasomotor conjunctivitis
- •Ocular examination
- •Ophthalmic procedures and testing
- •Summary
- •References
- •Ocular Mast Cells and Mediators
- •Mast cell mediators
- •Preformed granule-associated mediators
- •Biogenic amines
- •Proteoglycans
- •Neutral proteases
- •Newly generated mediators
- •Lipid mediators
- •Cytokines
- •Mast cell heterogeneity
- •Phenotypic heterogeneity
- •Functional heterogeneity
- •Pharmacologic heterogeneity
- •Ocular mast cells
- •The normal eye
- •Mast cells in diseases of the eye
- •Allergic conjunctivitis
- •Vernal conjunctivitis
- •Giant papillary conjunctivitis
- •Experimental autoimmune uveitis
- •Summary
- •References
- •Allergic Conjunctivitis
- •History
- •Examination
- •Seasonal and perennial allergic conjunctivitis
- •Seasonal allergic conjunctivitis
- •Perennial allergic conjunctivitis
- •Procedures
- •Late-phase reaction
- •Treatment
- •Antihistamines
- •Mast cell stabilizers
- •Lodoxamide tromethamine 0.1% (Alomide)
- •Ketorolac tromethamine (Acular)
- •Olopatadine (Patanol, Pataday)
- •Ketotifen (Zaditor)
- •Nedocromil (Alocril)
- •Pemirolast (Alamast)
- •Azelastine (Optivar)
- •Epinastine (Elestat)
- •Corticosteroids (Vexol, Lotemax)
- •Summary
- •References
- •Vernal Conjunctivitis
- •History
- •Epidemiology
- •Clinical manifestation
- •Conjunctival signs
- •Limbal signs
- •Corneal signs
- •Pathogenesis
- •Laboratory evaluation
- •Allergy testing
- •Conjunctival examination
- •Tear evaluation
- •Ocular challenge test
- •Treatment
- •Mast cell stabilizers
- •Antihistamines
- •Corticosteroids
- •Immunosuppressive agents
- •Other medical therapies
- •Surgical therapy
- •Treatment of secondary infections
- •Hyposensitization and immunotherapy
- •Prognosis
- •References
- •Giant Papillary Conjunctivitis
- •Signs and symptoms
- •Stages of giant papillary conjunctivitis
- •Stage 1: preclinical giant papillary conjunctivitis
- •Stage 2: mild giant papillary conjunctivitis
- •Stage 3: moderate giant papillary conjunctivitis
- •Stage 4: severe giant papillary conjunctivitis
- •Epidemiology
- •Histopathology
- •Coated contact lenses
- •Pathophysiology
- •Treatment
- •Treatment for stage 1: preclinical giant papillary conjunctivitis
- •Treatment for stage 2: mild giant papillary conjunctivitis
- •Treatment for stage 3: moderate giant papillary conjunctivitis
- •Treatment for stage 4: severe giant papillary conjunctivitis
- •Summary
- •References
- •Recognizing marginal dry eye disease
- •Contact lens wear in patients with dry eye
- •The use of therapeutic contact lenses in dry eye
- •The use of contact lenses in a patient with ocular allergy
- •Contact lenses and allergic reactions
- •Managing contact lens wear in the patient with ocular allergy
- •Summary of contact lens use in patient with ocular allergy
- •References
- •Mucous membrane pemphigoid
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Linear immunoglobulin A disease
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Epidermolysis bullosa acquisita
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Ocular pemphigus vulgaris
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Summary
- •References
- •Seborrheic dermatitis
- •Treatment
- •Vitiligo
- •Heliotrope rash
- •Port-wine stains
- •Xanthelasmas and plane xanthomas
- •Seborrheic keratosis
- •Skin tags
- •Warts
- •Comedones
- •Syringoma
- •Rosacea
- •Lipoid proteinosis
- •Angioedema
- •Contact urticaria
- •Erysipelas
- •Trichinosis
- •Chalazion
- •Hordeolum
- •Nevi
- •Sarcoid
- •Hemangioma
- •Basal cell carcinoma
- •Squamous cell carcinoma
- •Sebaceous carcinoma
- •Malignant melanoma
- •Eyelid dermatitis
- •Atopic dermatitis
- •Contact dermatitis
- •Acute, subacute, and chronic
- •Epidemiology
- •Irritant versus allergic
- •Etiologies
- •Irritation due to mascara and eye cosmetic preservatives
- •Fragrance
- •Irritation due to conjunctival deposition
- •Nail polish
- •Metals
- •Aeroallergens
- •Medications/eyedrops/contact lens solution
- •Paper
- •Plants
- •Histology
- •Diagnosis
- •Herpes simplex
- •Herpes zoster
- •Treatment considerations for the eyelids
- •Eyelid dermatitis
- •Infections
- •Urticaria and angiodema
- •Benign tumors and growths
- •Malignant tumors
- •‘‘Cosmetic’’ lesions of the eyelids
- •Vascular lesions
- •Vitiligo
- •Others
- •References
- •Bacterial conjunctivitis
- •Viral conjunctivitis/herpes simplex virus infections
- •Treatment of infectious conjunctivitis
- •Nasolacrimal duct obstruction
- •Allergic conjunctivitis
- •Neonatal conjunctivitis
- •Congenital glaucoma
- •Uveitis
- •References
- •Ocular Allergy Treatment
- •Ocular allergy treatment algorithm
- •Advisory nonprescription interventions
- •Environmental control
- •Cold compresses
- •Lubrication
- •Contact lenses
- •Decongestants
- •Antihistamines
- •Oral antihistamines
- •Topical antihistamines
- •Topical antihistamines
- •Levocabastine
- •Emedastine
- •Cromoglycate
- •Lodoxamide
- •Pemirolast
- •Ketorolac
- •Multiple action agents
- •Olopatadine
- •Ketotifen
- •Nedocromil
- •Azelastine
- •Epinastine
- •Mizolastine
- •Picumast
- •Amlexanox
- •Topical antihistamines and dry eye
- •Steroids
- •Ophthalmic steroids
- •Intranasal steroids
- •Immunomodulatory agents
- •Cyclosporine
- •Immunotherapy
- •Summary
- •References
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Nasolacrimal duct obstruction
Congenital nasolacrimal obstruction is a common disorder in infants and results in persistent tearing and may lead to infections such as dacryocystitis, orbital cellulitis, and bacterial conjunctivitis [30]. It occurs when a membranous fold obstructs the lower end of the nasolacrimal duct [1]. The condition is usually apparent when the infant is 3 to 12 weeks old [1]. The true incidence of this disorder in healthy newborns remains controversial. The most frequently quoted number of 6% comes from a study of 200 consecutive live births in the 1940s in which nasolacrimal patency was assessed by the presence or absence of discharge on compression of the lacrimal sac [31]. The incidence of the disorder, however, is considered higher in children who have craniofacial disorders and Down syndrome [32].
Epiphora (persistent, overflow tearing) is the most common but least specific presenting sign. The conjunctiva is usually clear, with only one eye typically being a ected [1]. Blepharitis with matting of the lids and lashes is part of the clinical presentation (Fig. 5) [1]. It is essential to determine whether the epiphora is due to overproduction of tears (trichiasis, foreign body, corneal abrasion, or abnormal eyelid position) or obstruction of outflow tract [30]. The patency of the lacrimal outflow system can be assessed using the modified fluorescein disappearance test. Fluorescein mixed with topical anesthetic is placed into the lower conjunctival fornix of each eye and excess solution and tears are blotted with a tissue. After 5 minutes, the child is examined. Light passed through a cobalt blue filter helps to identify residual fluorescein, which should not be present [33,34]. MacEwen and Young [34] found this test to be 90% sensitive and 100% specific for the presence of nasolacrimal obstruction in their prospective study of 80 patients.
The natural course of the disease appears to be spontaneous remission. In MacEwen and Young’s [35] study of 4792 infants in Scotland, they saw spontaneous remission throughout the first year of life, with 96% of the cases resolving before the age of 1 year and 350 cases resolving within the
Fig. 5. Watery discharge in a child who has congenital nasolacrimal duct obstruction.
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first month alone. Conservative treatment consists of topical antibiotics and lacrimal sac massage. A topical antibiotic ointment may aid the inflammation at the lid margin [1,36]. Lacrimal sac massage, first described by Crigler [36], is the technique of placing one finger over the common canaliculus to block upward flow and then stroking downward along the lacrimal sac to increase hydrostatic pressure and attempt to break a membrane at the opening of the nasolacrimal duct into the nose (Fig. 6). Although studies quote varying degrees of success for lacrimal sac massage, it is not harmful.
Most investigators recommend probing and irrigation as the next intervention after conservative management. The procedure to probe and irrigate the nasolacrimal duct canal is performed under general anesthesia [1]. Early intervention occurs when the procedure is performed on a child younger than 1 year. Advantages to early probing are earlier relief of symptoms, the avoidance of complications of nasolacrimal obstruction (the development of acute dacryocystitis, conjunctivitis, and cellulitis), and decreasing the chance of fibrosis and scarring of the nasolacrimal system that would make further treatment di cult [30]. The main disadvantages to early probing are that it requires surgical intervention in patients who might have complete resolution of symptoms with conservative management and places the infant at risk for complications such as the creation of false passages and the morbidity from general anesthesia [30]. After the age 1 year, the success rate of probing decreases with increasing age. The addition of balloon catheter dilatation of the lacrimal sac (Lacri-Cath) at the time of probing may result in improved success rates. When probing is not successful, a silicone tube may be placed into the nasolacrimal canal.
Allergic conjunctivitis
Children are subject to the same ocular allergies as their adult counterparts. Allergic conjunctivitis can be divided into acute and chronic
Fig. 6. Mucous expressed from the lacrimal puncta with digital pressure over the lacrimal sac is diagnostic of congenital nasolacrimal duct obstruction.
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Fig. 7. Acute conjunctival chemosis (edema) in allergic conjunctivitis.
disorders. Seasonal allergic conjunctivitis and perennial allergic conjunctivitis can be placed into the acute disorder category, whereas chronic allergic diseases are made up of vernal keratoconjunctivitis, atopic keratoconjunctivitis, and giant papillary conjunctivitis. The inflammation encountered on the ocular surface results in itching, tearing, and lid/conjunctival edema (Fig. 7).
The allergic response in conjunctivitis is typically elicited by ocular exposure to allergens that causes cross-linkage of membrane-bound immunoglobulin (Ig)E, which triggers mast cell degranulation, releasing a cascade of allergic and inflammatory mediators [37]. Allergens may be seasonal culprits (pollen, weeds, molds, grasses) or perennial ones (animal dander, dust mites, cockroaches) [1]. Vernal conjunctivitis occurs in two forms: limbal vernal, with the infiltration of eosinophils at the superior limbus; and a form with large papules forming on the palpebral conjunctiva. Both forms are particularly di cult to treat and may require a topical steroid in addition to a combination antihistamine–mast cell stabilizer (Fig. 8).
Fig. 8. Eosinophilic infiltrate on superior limbus in limbal vernal conjunctivitis.
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Treatment with cold compresses, eyewashes with artificial tears, and avoidance of allergens (dust mite covers) are nonspecific measures to counsel the allergic patient. The use of topical therapy allows for direct and local application while avoiding the ocular drying e ects evident with the use of systemic oral antihistamines [38]. Combinations of antihistamines and topical vasoconstrictors provide relief from itch but are not recommended for long-term use because they may cause a reduction in body temperature, central nervous system depression, headache, cardiac arrhythmias, and papillary dilation [25]. Naphcon-A, which contains naphazoline hydrochloride and pheniramine maleate, is presently available over-the-counter for children older than 6 years (Table 2) [1].
H1 receptor antagonists such as levocabastine hydrochloride (Livostin 0.05%) are available for use in patients 12 years and older, with a suggested application regimen of four times daily to relieve ocular pruritus [1]. Azelastine (Optivar) is a second-generation H1 receptor antagonist with the added component of being an inhibitor of histamine–mast cell release. It can be prescribed in children older than 3 years and applied twice daily for relief. Comparisons of the two agents show a similar profile of tolerability and symptomatic relief [39].
Combination antihistamine–mast cell stabilizers have the advantage of rapid symptomatic relief given by immediate histamine receptor antagonism along with the long-term disease-modifying benefit of mast cell stabilizers. It should be noted that not all medications of this class are equivalent [37]. Olopatadine, ketotifen, and epinastine ophthalmic solutions have indications for the treatment of allergic conjunctivitis in patients age 3 years and older.
Another class of medications includes corticosteroids; however, caution is advised considering the potential side e ects (cataracts, increased intraocular pressure, and corneal melts). The use of corticosteroids is typically reserved for patients not responsive to the previously mentioned therapies or for severe forms of allergy; namely, vernal keratoconjunctivitis and atopic keratoconjunctivitis [37]. As mentioned previously, the use of topical corticosteroids in patients who have herpetic conjunctival disease can cause rapid proliferation of the virus and corneal scarring. If needed, rimexolone (Vexol), a derivative of prednisolone approved for the treatment of allergic conjunctivitis that becomes inactivated in the anterior chamber of the eye, may be an option [40] because it demonstrates e cacy while decreasing safety concerns (intraocular pressure) [41,42].
Topical nonsteroidal anti-inflammatory drugs (NSAIDs) are e ective for use in allergic conjunctivitis through their interruption of prostaglandin synthesis. Ketorolac (Acular) has been shown to diminish the ocular itching and conjunctival hyperemia associated with allergic conjunctivitis [43]. The advantage of this class of agents over corticosteroids is that NSAIDs do not increase intraocular pressure, induce cataract formation, or interfere with wound healing. Ocular irritation, however, is commonly associated
Table 2
Treatment of allergic conjunctivitis
Medication |
Class |
Dosage |
Adverse e ects |
Approximate cost |
|
|
|
|
|
Naphazoline-pheniramine |
Antihistamine/decongestant |
Age O6 y: 1–2 drops each |
Mydriasis, irritation, redness, |
15 mL ¼ $12.00 |
(Naphcon-A) |
(over-the-counter) |
eye q 3–4 h prn |
blurred vision, headache |
|
|
|
|
Serious: central nervous |
|
|
|
|
system depression, |
|
|
|
|
increased intraocular |
|
|
|
|
pressure |
10 mL ¼ $150.00 |
Ketoralac 0.5% (Acular) |
Nonsteroidal anti- |
Age O12 y: 1 drop each |
Burning, stinging, hyperemia, |
|
|
inflammatory drug |
eye qid 1 wk |
corneal infiltrate |
|
|
|
|
Serious: corneal ulcer, erosion |
|
|
|
|
or perforation, keratitis |
|
Azelastine 0.05% (Optivar) |
H1 receptor antagonist |
Age O3 y: 1 drop each |
Burning, stinging, bitter taste, |
6 mL ¼ $78.03 |
|
|
eye bid |
ocular pain |
|
Olopatadine 0.2% (Pataday) |
H1 receptor antagonist/ |
Age O3 y: 1 drop each |
Headache, burning, dry eye, |
2.5 mL in a 4 mL |
|
mast cell stabilizer |
eye qd |
hyperemia, foreign-body |
bottle ¼ $80.00 |
|
|
|
sensation |
|
Epinastine 0.05% solution |
H1 receptor antagonist/ |
Age O3 y: 1 drop each |
Ocular burning, hyperemia, |
5 mL ¼ $83.28 |
(Elestat) |
mast cell stabilizer |
eye bid |
pruritus, upper respiratory |
|
|
|
|
infection, headache, cough, |
|
|
|
|
folliculosis |
5 mL ¼ $28.99 |
Rimexolone 1% (Vexol) |
Corticosteriod |
Adult dosing: 1–2 drops |
Blurred vision, burning, |
|
|
|
each eye qid 2 wk |
redness |
|
|
|
|
Serious: cataract, loss |
|
|
|
|
of vision, superinfection |
|
|
|
|
|
|
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