- •Contents
- •Preface
- •Abbreviations
- •Introduction
- •Orbit and external eye
- •Extraocular muscles
- •Anterior segment
- •Posterior segment
- •Introduction
- •Ocular examination
- •The ‘red reflex’
- •Assessment of vision and visual acuity
- •Cover test for strabismus
- •Light reflex testing
- •Color vision testing
- •Assessment of stereoacuity
- •Ophthalmoscopy
- •Vision screening
- •Photoscreening
- •Autorefraction
- •Visual evoked potential
- •Strabismus
- •Comitant strabismus
- •Congenital esotropia
- •Accommodative esotropia
- •Congenital exotropia
- •Intermittent exotropia
- •Incomitant strabismus
- •Third cranial nerve palsy
- •Fourth nerve palsy
- •Sixth nerve palsy
- •Strabismus syndromes
- •Duane’s syndrome
- •Brown’s syndrome
- •Monocular elevation deficiency (MED)
- •Möbius syndrome
- •Introduction
- •Conjunctivitis
- •Bacterial conjunctivitis
- •Viral conjunctivitis
- •Herpes conjunctivitis
- •Giant papillary conjunctivitis
- •Allergic conjunctivitis
- •Vernal keratoconjunctivitis
- •Phlyctenular keratoconjunctivitis (phlyctenulosis)
- •Ophthalmia neonatorum
- •Introduction
- •Congenital corneal opacity
- •Embryology
- •Peters anomaly
- •Sclerocornea
- •Congenital dermoid
- •Birth trauma
- •Congenital hereditary endothelial dystrophy
- •Congenital hereditary stromal dystrophy
- •Posterior polymorphous membrane dystrophy
- •Metabolic diseases
- •Mucopolysaccharidosis
- •Hurler’s syndrome (MPS I-H)
- •Scheie’s syndrome (MPS I-S)
- •Hunter’s syndrome (MPS II)
- •Sly’s syndrome (MPS VII)
- •Mucolipidosis
- •Sialidosis (ML I)
- •I-Cell disease (ML II)
- •Pseudo-Hurler dystrophy (ML III)
- •Miscellaneous metabolic diseases
- •Fabry’s disease
- •Cystinosis
- •Tyrosinemia
- •Infectious diseases
- •Herpes simplex virus (HSV)
- •Congenital syphilis
- •Rubella
- •Introduction
- •Structural lens abnormalities
- •Aphakia
- •Spherophakia (microspherophakia)
- •Coloboma
- •Subluxation (ectopia lentis)
- •Lenticonus
- •Persistant fetal vasculature
- •Cataracts
- •Nuclear cataracts
- •Lamellar cataracts
- •Anterior polar cataracts
- •Posterior polar cataracts
- •Sutural cataracts
- •Anterior subcapsular cataracts
- •Posterior subcapsular cataracts
- •Cerulean (blue-dot) cataracts
- •Complete cataracts
- •Etiology of cataracts
- •Genetic and metabolic diseases
- •Trauma
- •Medication and toxicity
- •Maternal infection
- •Diagnosis of cataracts
- •Management/treatment of cataracts
- •Visual significance
- •Surgery
- •Aphakia
- •Pseudophakia
- •Amblyopia
- •Cataract prognosis
- •Introduction
- •Diagnosis of pediatric glaucoma
- •Ocular examination
- •Differential diagnosis of pediatric glaucoma
- •Primary infantile glaucoma
- •Juvenile open-angle glaucoma
- •Primary pediatric glaucoma associated with systemic disease
- •Lowe’s syndrome
- •Sturge–Weber syndrome
- •Neurofibromatosis
- •Axenfeld–Rieger syndrome
- •Aniridia
- •Peters anomaly
- •Secondary childhood glaucoma
- •Trauma
- •Neoplasia
- •Glaucoma following pediatric cataract surgery
- •Other causes of secondary glaucoma in children
- •Treatment of pediatric glaucoma
- •Drug treatment
- •Surgical management
- •Summary
- •Introduction
- •Coats’ disease
- •Leber’s congenital amaurosis
- •X-linked congenital stationary night blindness
- •Achromatopsia
- •Stargardt disease
- •Best’s disease
- •Persistent fetal vasculature
- •X-linked juvenile retinoschisis
- •Albinism
- •Retinal dystrophies with systemic disorders (ciliopathies)
- •Introduction
- •Common clinical features
- •Classification
- •Anterior uveitis
- •Juvenile idiopathic arthritis
- •Juvenile spondyloarthropathies
- •Sarcoidosis
- •Herpetic iridocyclitis
- •Intermediate uveitis
- •Posterior uveitis
- •Toxoplasmosis
- •Toxocariasis
- •Vogt–Koyanagi–Harada syndrome
- •Sympathetic ophthalmia
- •Masquerade syndromes
- •Retinoblastoma
- •Leukemia
- •Introduction
- •Optic nerve hypoplasia
- •Morning glory disc anomaly
- •Optic disc coloboma
- •Peripapillary staphyloma
- •Congenital tilted disc
- •Optic pit
- •Myelinated retinal nerve fibers
- •Papilledema
- •Pseudopapilledema
- •Optic disc drusen
- •Introduction
- •Dacryocele
- •Nasolacrimal duct obstruction
- •Lacrimal sac fistula
- •Decreased tear production
- •Dacryoadenitis
- •Introduction
- •Cryptophthalmos and ankyloblepharon
- •Coloboma of the eyelid
- •Blepharoptosis
- •Epicanthal folds and euryblepharon
- •Lagophthalmos
- •Lid retraction
- •Ectropion, entropion, and epiblepharon
- •Blepharospasm
- •Blepharitis
- •Hordeolum
- •Chalazion
- •Tumors of the eyelid
- •Preseptal and orbital cellulitis
- •Herpes simplex, molluscum contagiosum, and verruca vulgaris
- •Allergic conjunctivitis
- •Trauma
- •Summary
- •Introduction
- •Cystinosis
- •Marfan’s syndrome
- •Homocystinuria
- •Wilson’s disease
- •Fabry disease
- •Osteogenesis imperfecta
- •The mucopolysaccharidoses
- •Sickle cell disease
- •Albinism
- •Congenital rubella
- •Introduction
- •Genetics
- •Malignant potential
- •Formes frustes
- •Neurofibromatosis (von Recklinghausen’s syndrome)
- •Retinocerebellar hemangioblastomatosis (von Hippel–Lindau syndrome)
- •Racemose hemangiomatosis (Wyburn-Mason syndrome)
- •Encephalofacial cavernous hemangiomatosis (Sturge–Weber syndrome)
- •Oculoneurocutaneous cavernous hemangiomatosis
- •Organoid nevus syndrome
- •Introduction
- •Cortical visual impairment
- •Migraine headache
- •Spasmus nutans
- •Opsoclonus
- •Horner’s syndrome
- •Congenital ocular motor apraxia
- •Myasthenia gravis
- •Introduction
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Diagnostic approaches
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Therapeutic approaches
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Eyelid tumors
- •Capillary hemangioma
- •Facial nevus flammeus
- •Kaposi’s sarcoma
- •Basal cell carcinoma
- •Melanocytic nevus
- •Neurofibroma
- •Neurilemoma (schwannoma)
- •Conjunctival tumors
- •Introduction
- •Choristomatous conjunctival tumors
- •Epithelial conjunctival tumors
- •Melanocytic conjunctival tumors
- •Vascular conjunctival tumors
- •Xanthomatous conjunctival tumors
- •Lymphoid/leukemic conjunctival tumors
- •Non-neoplastic lesions that simulate conjunctival tumors
- •Conclusions
- •Intraocular tumors
- •Retinoblastoma
- •Retinal capillary hemangioma
- •Retinal cavernous hemangioma
- •Retinal racemose hemangioma
- •Astrocytic hamartoma of the retina
- •Melanocytoma of the optic nerve
- •Intraocular medulloepithelioma
- •Choroidal hemangioma
- •Choroidal osteoma
- •Uveal nevus
- •Uveal melanoma
- •Congenital hypertrophy of retinal pigment epithelium
- •Leukemia
- •Orbital tumors
- •Dermoid cyst
- •Teratoma
- •Capillary hemangioma
- •Lymphangioma
- •Juvenile pilocytic astrocytoma
- •Rhabdomyosarcoma
- •Granulocytic sarcoma (‘chloroma’)
- •Lymphoma
- •Langerhan’s cell histiocytosis
- •Metastatic neuroblastoma
- •Introduction
- •Eyelid
- •Open globe
- •Ocular surface injury
- •Intraocular trauma
- •Iridodialysis
- •Cataract
- •Retina
- •Optic nerve injury
- •Orbital fracture
- •Other orbital injury
- •Child abuse
- •Shaking injury
- •Index
74 CHAPTER 6 Conjunctiva
Viral conjunctivitis
DEFINITION/OVERVIEW
A common misperception of conjunctivitis is that it is routinely secondary to viral and not bacterial infection. Even the most current version of the AAP Red Book lists viral conjunctivitis as the most common form of the disease in children.8 However, the literature does not support this assertion. Nevertheless, viral conjunctivitis is common and practitioners should be particularly attuned to its signs and symptoms since it should not be treated with antibiotics.
ETIOLOGY
Children with viral conjunctivitis are contagious for at least 7 days from the first appearance of their symptoms. Although the spread of the disease is thought to be caused mainly by direct contact with the virus by contaminated fingers to the eye, the virus may also be spread by coughing and sneezing of airborne particles. For this reason, the most important strategy to halt the spread of the virus is good hygiene and washing hands. The child should be isolated to prevent spread of the contagion. Adenovirus is the most common etiology of viral conjunctivitis, and as discussed previously, is seen more commonly in the fall and winter months.
CLINICAL PRESENTATION
Table 8 presents the signs and symptoms of viral conjunctivitis. There is an acute onset of unilateral symptoms that can rapidly spread to being bilateral through cross contamination of the fellow eye. A watery or serous discharge is present, along with the conjunctival injection (75). A hemorrhagic component may be seen in some cases (76). The presence of acute preauricular and/or submandibular lymphadenopathy may help to confirm the diagnosis. The child may be febrile and may have a pharyngitis associated with the conjunctivitis. Follicles of the conjunctiva can be seen if the lower lid is pulled down slightly (77). Acute follicular conjunctivitis is usually associated with a viral etiology (epidemic keratoconjunctivitis, herpes zoster keratoconjunctivitis, infectious mononucleosis, Epstein–Barr virus infection) or chlamydial infections (inclusion conjunctivitis), while chronic follicular changes can be seen in chronic chlamydial infection (trachoma, lymphogranuloma venereum) or as a toxic or reactive inflammatory response to topical medications and molluscum contagiosum. The follicles appear as gray-white, round to oval elevations which measure 0.5–1.5 mm in diameter and can be seen in the inferior and superior tarsal conjunctivae, and less often, on bulbar or limbal conjunctiva.
Table 8 Signs and symptoms of viral conjunctivitis |
|
|
|
Adenoviral |
|
|
|
• |
Water discharge |
• |
Frequent preauricular lymphadenopathy |
• |
Hyperemia |
• Serous, mucoid, or mucopurulent discharge |
|
• |
Petechial hemorrhages |
• |
Pharyngitis |
|
Punctate keratitis |
|
|
Herpetic |
|
|
|
• |
Usually unilateral |
• |
Serous–mucoid discharge |
• |
Vesicular eruptions on eyelids |
• |
Occasional preauricular lymphadenopathy |
• |
Diffuse hyperemia |
• |
Dendritic epithelial keratitis of conjunctiva |
• |
Follicles |
|
or cornea |
|
|
|
|
Viral conjunctivitis 75
MANAGEMENT/TREATMENT
Supportive care and isolation of the child to decrease the spread of the contagion is the only treatment indicated for routine viral conjunctivitis. Because the necessity of isolation requires children to miss school, afterschool, and daycare, parents often request a ‘drop’ to get their child back into their daily routine. Most schools or daycare will only allow a child back if they are ‘on a drop’, but this is not even standardized from community to community.25 Nevertheless, the use of an antibiotic drop is inappropriate when the etiology is presumed to be viral in nature.
75
75 Viral conjunctivitis.(Courtesy of Robert D. Gross,MD,MPH.)
The use of an antibiotic has no effect on the infection, other than to eradicate the normal bacterial flora of the conjunctiva. Moreover, the child is no less contagious, and may actually spread the virus quicker because good hygiene and hand washing may be less rigorous if the caregiver thinks that the antibiotic is having an effect on the disease process.
Most cases of viral conjunctivitis are selflimiting and overtreatment should be avoided. Corneal subepithelial infiltrates may be seen in some cases of epidemic keratoconjunctivitis (78).
76
76 Hemorrhagic conjunctivitis.(Courtesy of Casey Eye Institute,Oregon Health Sciences University.)
|
77 |
|
|
78 |
|
|
|
|
|
|
|
|
|
|
77 Conjunctival follicles.(Courtesy of Casey Eye Institute,Oregon Health Sciences University.)
78 Adenoviral conjunctivitis,corneal infiltrates. (Courtesy of Casey Eye Institute,Oregon Health Sciences University.)
76 CHAPTER 6 Conjunctiva
Herpes conjunctivitis
Viral conjunctivitis caused by the herpes simplex (HSV) or herpes zoster (HZV) viruses can cause serious and permanent damage to the eye and vision. Herpes zoster infections are not as common as herpes simplex in the pediatric patient. These infections can show periocular as well as ocular involvement, and are most often unilateral in nature. Herpes simplex infections can also be recurrent, causing repeated bouts of conjunctivitis, keratitis, and periorbital disease.
ETIOLOGY
Most cases of secondary conjunctivitis are caused by HSV-1 and are associated with recurrent orolabial infection (cold sores). HSV-2 is associated with genital infection and is the more common cause of neonatal eye infections.
CLINICAL PRESENTATION
Patients can exhibit a serous discharge, bulbar and tarsal conjunctival injection, photophobia, epiphora, lid edema, and vesicular eruptions of the lids. There may also be dendritic ulcerations of the cornea which can leave permanent scarring and visual acuity damage. The dendrites will stain with fluorescein and be visible with a
Wood’s light or cobalt blue light (79). They will also stain with Rose Bengal, which stains devitalized cells of the cornea, giving the classic dendrite appearance. A Wood’s light is not necessary to observe the staining with Rose Bengal. If herpetic involvement is suspected in a child with conjunctivitis, a referral to an ophthalmologist is warranted.26 The use by a primary care provider of any ophthalmic drop containing a steroid is contraindicated and it should only be prescribed by an ophthalmologist because of the possibility of herpetic involvement. The use of a steroid in a child with herpes can cause permanent and possibly devastating complications, including acute corneal perforation.
MANAGEMENT/TREATMENT
Treatment of viral conjunctival disease may shorten its duration but does not seem to otherwise alter the course of disease. Treatment is indicated when the cornea is involved. Oral acyclovir (aciclovir) has been shown to be effective for treatment of herpetic epithelial keratitis and for reducing the rate of recurrence when used prophylactically. Topical antiviral medications carry a risk of corneal toxicity and their use should be reserved for patients under the care of an ophthalmologist.
79
79 Corneal dendrites.(Courtesy of Casey Eye Institute,Oregon Health Sciences University.)
Giant papillary conjunctivitis 77
Giant papillary conjunctivitis
ETIOLOGY
GPC is a noninfectious condition that occurs when there is a chronic foreign body irritation of the eye. In the past, it was most frequently seen in children and young adults with an ocular prosthesis and in patients with exposed sutures or scleral buckles after retinal detachment surgery. GPC is also associated with patients who have undergone glaucoma filtering procedures with the formation of a conjunctival bleb, or elevation of the conjunctiva near or at the limbus, to allow the aqueous humor to escape the anterior chamber, therefore maintaining a controlled intraocular pressure.39 However, as the use of cosmetic contact lenses finds its way into younger and younger children, GPC is now commonly being seen with the use, and misuse, of contact lenses in both children and adults. Rigid, gas-permeable lenses as well as soft contact lenses have both been associated with GPC, although the incidence of GPC with the use of rigid gas-permeable lenses is less than with soft contact lens use.
The symptoms of GPC are low grade as the condition starts to evolve. There may be a mild amount of itching, or mild contact lens discomfort. However, since many of the patients are extremely motivated to continue their contact lens wear, the symptoms will worsen with increasing itching, blurring of vision, mucoid production, and then finally contact lens intolerance. Involvement of the cornea is rare, but with continued use of soft contact lenses, even in the presence of increasing conjunctival irritation, pannus formation can occur.
CLINICAL PRESENTATION
The symptoms of GPC can begin months or even years after the patient starts to wear his or her contact lenses. There is no sex or racial predilection, but the symptoms of GPC seem to be more aggressive in children who wear contact lenses. Papillae are seen on the superior tarsal conjunctiva and can measure up to 1 mm in diameter (80). The same type of papillae are seen in VKC, but the giant papillae in VKC are usually larger than in GPC, and the permanent ocular changes seen in VKC are not seen in GPC. However, pannus formation can be seen in
children from chronic misuse of their contact lenses. Itching on initial insertion of the contact lenses is an early symptom of GPC. If not treated properly, progression to complete contact lens intolerance may occur.
MANAGEMENT/TREATMENT
The only definitive treatment for patients who are experiencing signs and symptoms of GPC is removal of the foreign material from contact with the eye. This means removing exposed scleral buckles, altering an ocular prosthesis to create less conjunctival irritation, or discontinuation of the use of contact lenses until the symptoms resolve. Since, as previously mentioned, the motivation of these patients to continue their cosmetic contact lens wear is usually high, complete discontinuation may be very difficult to accomplish. In these cases, improving the patient’s compliance with hygiene in handling their lenses, decreasing the time that the contact lenses are inserted, the use of disposable lenses, or a different lens material should be employed. Since the primary care provider does not have expertise in this area, the importance of compliance should be stressed, and the patient should be referred back to the eye care professional providing the contact lenses.
PROGNOSIS
The symptoms of most patients can be controlled with topical medications. In those cases that cannot, removal of the offending agent is generally curative.
80
80 Giant papillary conjunctivitis.(Courtesy of Casey Eye Institute,Oregon Health Sciences University.)
