with the use of these agents, especially in contact lens wearers. Use of topical NSAIDs is limited to age 12 years and older.

Immunotherapy, which involves administration of selected allergens to which the patient is allergic by way of a subcutaneous, gastrointestinal, mucosal, or sublingual route, has aided greatly in the treatment of allergic rhinitis symptoms [40]. Some clinical studies have focused on the improvement in ocular symptoms with immunotherapy [44,45]. Benefits of this modality must be weighed against the time commitment, risk of systemic reactions, and di culty in administering injections to the pediatric population.

Neonatal conjunctivitis

Conjunctivitis in the first month of life (ophthalmia neonatorum) is the most common infection in the neonatal period [10,11,46]. It occurs in 1.6% to 12% of newborns [20]. The etiologies include chemical, bacterial, and viral [46]. The most common cause is from chemical irritation followed by C trachomatis infection [20]. Chemical conjunctivitis is commonly induced by the use of eye drop prophylaxis, especially silver nitrate but also erythromycin and tetracycline ointments [46]. It typically appears within 6 to 8 hours of application and remits spontaneously in 1 to 2 days. No treatment is necessary and Gram stain shows no organisms [46].

Regarding infectious etiology, the most common infectious cause is due to C trachomatis acquired during delivery from mother to child: a vaginally born infant to a mother who has an active chlamydial infection has a 50% chance of acquiring the organism [46]. Of these infants, roughly one fourth to one half develop conjunctivitis [4]. Symptoms typically begin at age 5 to 14 days (it can be seen earlier if amniotic membranes rupture prematurely) [47] and vary widely, from conjunctival injection to severe edema with mucopurulent discharge. The inflammatory reaction consists mostly of polymorphonuclear leukocytes, and pseudomembrane formation may occur as the exudate adheres to the conjunctiva [47]. The pseudomembranes may be appreciated by everting the eyelid. The cornea is usually spared, and systemic treatment with erythromycin (oral erythromycin base or ethylsuccinate, 50 mg/kg/d in four divided doses for 14 days) usually results in healing without complications (Fig. 9) [47]. Sometimes a second course of erythromycin is needed because the e cacy of erythromycin is approximately 80% [4]. Untreated infection may persist and carries the risk of corneal and conjunctival scarring [47]. The preferred method for diagnosis is culture of the conjunctiva (from the everted eyelid) and pharynx. Nonculture tests that are acceptable to the Food and Drug Administration for use with conjunctival specimens include (1) an enzyme immunoassay that uses enzyme-labeled chlamydial-specific antibodies to detect chlamydial lipopolysaccharide and (2) direct fluorescent antibody assays that use

dose or cefotaxime, 100 mg/kg, administered IV or IM for one dose) [4] and with aggressive irrigation several times a day until the purulence subsides [4,46]. The patient should also be evaluated for disseminated infection such as arthritis, meningitis, or sepsis because the conjunctivae serve as portals of entry [48]. Isolation of Neisseria gonorrhoeae by culture performed on conjunctival exudates, blood, synovial fluid, or cerebrospinal fluid is standard for diagnosis [48]. The mother and her sexual contacts should also be treated for gonorrhea [46].

Other potential microbes for neonatal conjunctivitis are H influenzae,

Streptococcus pneumoniae, Staphylococcus aureus, Neisseria cineria, Pseudomonas sp, Proteus sp, Klebisella pneumoniae, enterococci, HSV, and adenoviruses [48]. Infections with most of these other organisms may be treated with topical antibiotics except for Pseudomonas aeruginosa [46]. This infection presents with edema, erythema, purulent discharge, or endophthalmitis [46,49] and can cause corneal perforations, blindness, and death [46]. Presumptive diagnosis is made when gram-negative rods are seen on Gram stain of exudates, with growth in culture confirming the diagnosis [46]. Treatment with topical and systemic aminoglycosides is necessary [49].

Congenital glaucoma

The primary clinical manifestations of congenital glaucoma are tearing, photophobia, corneal clouding and edema, redness, and enlargement of the eye [1]. Some of these symptoms (tearing, redness, edema) may prompt physicians to think of conjunctivitis. The abnormality of congenital glaucoma is a defect in the iridocorneal angle of the anterior chamber that obstructs the outflow of aqueous fluid [1]. The consequent rise in intraocular pressure leads to corneal edema and enlargement. Surgery is necessary to reduce this rise in intraocular pressure [1]. Glaucoma classification is vast, and this disease has associations with systemic abnormalities such as SturgeWeber syndrome, neurofibromatosis type 1, Marfan syndrome, trisomy 13 syndrome, trisomy 21 syndrome, and Rubinstein-Taybi syndrome [50].

Uveitis

Uveitis includes inflammation of the iris (iritis), ciliary body (cyclitis), and choroid (choroiditis) [6]. It can be classified anatomically into the following categories: anterior, intermediate, posterior, and di use [1]. Patients complain of decreased or hazy vision, pain, and photophobia, with a sensation of black floating spots [1]. Typical presentation for anterior uveitis is conjunctival injection with a miotic pupil and ciliary flush (Fig. 11) [6]. Due to its primary presentation with tearing and red eye, uveitis may be confused with conjunctivitis.

Fig. 11. Irregularly shaped pupil secondary to synechia formation in recurrent anterior uveitis.

Children represent 5% to 10% of patients seen at tertiary referral centers for uveitis, with slightly more cases seen in female patients [51]. A retrospective, multicenter observational study in England of patients younger than 16 years who had uveitis found a prevalence of 4.9 in 100,000 [52]. Anterior and posterior uveitis account for most cases (30%–40% and 40%–50%, respectively), with intermediate uveitis accounting for 10% to 20% and di use uveitis accounting for 5% to 10% of cases [51]. In children, the most common cause of anterior uveitis is juvenile rheumatoid arthritis [51]. Toxoplasmic retinochoroiditis is the most frequent type of posterior uveitis [51]. Intermediate uveitis and di use uveitis are mostly bilateral, chronic, and of idiopathic etiology [51]. Cunningham [51] described the most common complications in children to be cataract formation, band keratopathy, glaucoma, and cystoid macular edema, with one fourth to one third of uveitis patients being left with severe vision loss.

Anterior uveitis may be granulomatous or nongranulomatous [6]. Granulomatous causes include sarcoidosis, tuberculosis, syphilis, and toxoplasmosis [6]. Nongranulomatous anterior uveitis is associated with ankylosing spondylitis, sacroiliitis, Reiter syndrome, psoriasis, Behc¸et’s syndrome, and infections (HSV, varicella-zoster virus) [6]. The sequelae of anterior uveitis are formation of synechia (adhesions of the posterior iris to the anterior capsule of the lens), angle closure glaucoma, and cataract formation [1].

Posterior uveitis presents with inflammatory cells in the vitreous, retinal vasculitis, and macular edema, which threaten visual acuity [1]. Causes of posterior uveitis include congenitally transmitted toxoplamosis, toxocariasis, tuberculosis, syphilis, Lyme disease, cat-scratch disease, rubella retinitis, HSV, and cytomegalovirus [51]. Panuveitis involves all three portions of the uveal track and, in one Israeli study, it was linked to a systemic autoimmune disease in over 95% of cases [53].