Normal visual acuity is 20/40 in a 3-year-old, 20/30 in a 4-year-old, and 20/20 in a 5- to 6-year-old child.
Steroids should not be used for patients with iritis or keratitis until herpes simplex is excluded.
Glaucoma should be suspected in patients who have eye pain and nausea and vomiting.
Neonates with suspected gonococcal conjunctivitis should undergo a complete sepsis workup, including a lumbar puncture. These patients should be admitted for intravenous antibiotics.
Chemical alkali burns to the eye can result in liquefactive necrosis and should be irrigated until the eye pH is between 6 and 8.
Children with eye disorders often come to the emergency department (ED) for evaluation and the emergency physician should make sure to perform a complete eye examination in order to avoid overlooking potentially debilitating ophthalmologic conditions. Visual development starts at birth and accelerates quickly during the first 2 years of life, reaching completion at 9 years of age, any disruption during that time due to ocular disease may result in permanent visual deficits.
A thorough and complete history can often help guide diagnosis and management of ophthalmic disorders. Relevant history includes:
Previous eye problems or surgeries?
Underlying health problems?
Review of eye symptoms including eye redness, eye discharge, vision changes, eye pain, periorbital pain, eye swelling.
A complete review of systems for other symptoms, especially headache, ear pain, fever, vomiting, dizziness, or rash.
Does the patient wear glasses or contact lenses?
What was done for the patient prior to arrival in the ED, including the use of any systemic or topical medications?
Exposure to others with similar conditions?
A thorough and systematic eye examination is divided into eight major categories: vision, extraocular movements, lids and orbit, conjunctiva and sclera, anterior chamber, pupils, posterior segment, and intraocular pressure. Information about the unaffected eye can help guide one in the assessment of the affected eye. The eye examination should be performed in a logical, methodical manner. Patients should be observed for any facial asymmetry. If indicated, dilation and palpation of the globe should only be done after a thorough systematic examination.
A complete physical exam is required in the evaluation of eye disorders, paying particular attention to the neurologic exam, including fontanelles in infants, which can often help in diagnosing acute eye disorders.
For very young children, the ability to focus on an object such as a toy may give a rough assessment of visual acuity. A newborn can fixate on an object 8 to 12 inches away and a 1-month-old infant should be able to follow a moving object. For older children, Snellen letters or Allen figures should be used to check visual acuity in both eyes. Normal visual acuity is 20/40 in a 3-year-old, 20/30 in a 4-year-old, and 20/20 in a 5- to 6-year-old child. Visual fields should be evaluated in older children to help with differential considerations.
Extraocular movements are controlled by cranial nerve innervation of the six extraocular muscles: lateral rectus by the abducens nerve; superior rectus by the trochlear nerve; and the medial rectus, superior rectus, inferior rectus, superior oblique, and inferior oblique, all by the oculomotor nerve. Extraocular movements should be assessed for symmetry, smoothness, abnormal beating (nystagmus), and speed. Abnormalities of extraocular movements may be a result of central or peripheral nerve pathology (increased intracranial pressure or entrapment) or muscle damage.
Conjugate gaze can be evaluated with the corneal light reflex. The light reflection in the pupils should be central when the examiner is standing behind a light upon which the patient is fixated; displacement from center is indicative of abnormal misalignment. Development of conjugate gaze starts at birth and stabilizes by three months of age. Misalignment can be congenital but can also be indicative of an acute process.
The lids are examined by testing the ability to open and close the eyelids and noting any ptosis (drooping of eyelid), erythema, edema, masses, lacerations, or ecchymosis. The glands of Zeis are sebaceous glands attached directly to the hair follicles; the Meibomian glands are sebaceous glands that extend through the tarsal plate and often become inflamed in children. If a foreign body is suspected, the upper lid should be everted by firmly grasping the lashes at the lid margin and using a cotton tip applicator to evert the lid against counter traction at the superior tarsal margin.
Examination of the orbit involves palpation of the orbital bony structures noting step offs, tenderness, edema, or subcutaneous emphysema. Physicians should note the presence of exophthalmos (abnormal protrusion of the eyeball) or enophthalmos (posterior displacement of eyeball or sunken eyeball). Orbital fractures are often accompanied by ecchymosis, lid swelling, proptosis, and limitation in extraocular movements (see Chapter 98, Traumatic Eye Emergencies).
The conjunctiva is a thin membrane covering the posterior surfaces of the eyelids and the anterior surfaces of the sclera and cornea. The conjunctiva should be examined for swelling, erythema, foreign bodies, hemorrhage, and discharge (purulent, clear, yellow).
The sclera is a white fibrous tissue covering the entire globe continuous with the cornea anteriorly. The sclera, made up mainly of collagen and connective tissue, is the thick vascular covering of the eye. The thin vascular membrane between the sclera and conjunctiva is called the episclera. Scleritis and episcleritis are often hard to distinguish from conjunctivitis, but usually involve a violaceous discoloration of the eye, with scleral thickening or nodules in the absence of discharge. Episcleritis often presents as a distinct area of injected conjunctiva with dilated vessels in the involved layer of tissue. Differentiation may be helpful with the administration of topical phenylephrine, which constricts vessels dilated by conjunctivitis but not those vessels involved in scleritis or episcleritis. Posterior scleritis is often difficult to diagnose with physical exam; a high index of suspicion depending on other factors (age, history, and comorbid disease) in the child with eye pain should prompt further evaluation.
The anterior chamber is comprised of the cornea, uvea (iris, ciliary body, and choroid), and lens, and is filled with aqueous humor.
The cornea is the transparent membrane at the anterior of the eye and should be examined if trauma or foreign body is suspected. Anesthesia with tetracaine or proparacaine drops can be used prior to instilling fluorescein and examining the eye with a slit lamp or Wood lamp. Fluorescein binds to the basement membrane in the cornea, and areas of uptake indicate damage to the cornea. Consider a corneal injury in the crying infant.
Direct observation of the eye can reveal a hypopyon (sterile pus layered out in the anterior chamber, indicative of inflammation in the anterior chamber) or a hyphema (blood in the anterior chamber), which can be helpful in diagnosis. Inflammation of the anterior uvea (anterior uveitis, iritis) is rare in children. Physical examination reveals a miotic pupil and perilimbal injection in the setting of unilateral sudden onset of pain, photophobia, floaters, and redness. Aqueous flare and cells are seen on slit-lamp examination. Aniridia presents as an apparent absence of the iris, but has many variations. The pupil appears as large as the cornea while the iris remains as a small residual structure. The visual acuity for patients with aniridia is extremely poor due to macular hypoplasia; nystagmus and photophobia are often present. Two-thirds of patients have a hereditary autosomal dominant condition, while one-third are sporadic cases. Approximately 20% of infants with sporadic aniridia develop a Wilms tumor, other genitourinary defects, or mental retardation. Other ocular defects associated with aniridia include a displaced lens, cataracts, corneal epithelial dystrophy, and glaucoma.
Pupils should be black, round, symmetric, and equally reactive to light. Changes in the anterior chamber, lens, or vitreous may result in a pupil that is not black. A ruptured globe or intracranial process can lead to pupillary asymmetry. A white pupillary reflex is known as leukocoria, and can be caused by disease in the lens, vitreous, or retina. Pupillary assessment includes evaluation for an afferent pupillary defect known as a Marcus Gunn pupil in which pupillary constriction is delayed and diminished in both eyes when light is shined in the affected eye as compared to the normal eye. A Marcus Gunn pupil is the evidence of injury to the anterior visual system and is a poor prognostic sign.
The posterior segment comprises the retina, choroid, and optic nerve, and is filled with vitreous humor. Direct ophthalmoscope of the retina can be used to examine the optic disc (hemorrhages, blurred margins), vasculature (papilledema, size of arteries), macula (quality of optic nerve, color of fovea), and the overall quality of retina (tears, detachment, intraocular foreign bodies). Chronic conditions including uveitis can cause deposits in the vitreous. In endophthalmitis (infections inside the eye) children will have unilateral severe pain in or around the eye and compromised vision. Purulent exudate in the vitreous will show up as a greenish color on the ophthalmoscopic examination. Posterior uveitis (chorioretinitis) can be diagnosed with exudates on the retina and hazy vitreous humor in the setting of blurred vision and floaters.
Either infection or injury to the anterior chamber can lead to increased intraocular pressure. Glaucoma can manifest any time after an insult to the eye. Pain and blurred vision should alert one to the possibility of glaucoma. The pupil is nonreactive and dilated, and patients may complain of seeing halos around objects. Accurate measurement is accomplished by slit-lamp tonometry or with a handheld tonometer. This should not be undertaken, however, if the possibility of a ruptured globe exists. In patients with acute glaucoma, rough tactile measurement of intraocular pressure can be made by gentle palpation of the globes with the fingers through the eyelids. An extremely firm eye can easily be detected. Normal eye pressure in children ranges from 10 to 22 mmHg.1
The optic nerve is responsible for the transmission of visual information to the cortex. Disruptions in this transmission can lead to visual loss. Optic neuritis is usually due to inflammation or demyelination. It is characterized by an abrupt, rapid, unilateral loss of vision, while pain is variable. Rarely does optic neuritis present as a separate entity in children. Most often it is caused by meningitis, viral infections, encephalomyelitis, and demyelinating diseases. Lead poisoning and long-term chloramphenicol therapy are other known culprits.
Various toxins have been associated with impaired vision. Most act on the ganglion cells of the retina or optic nerve, causing visual defects. Methyl alcohol can cause sudden, permanent blindness. Other recognized toxins include sulfanilamide, quinine, quinidine, and halogenated hydrocarbons.
Finally, one must consider that visual loss can result from impedance within the visual cortex of the brain. Head trauma, hypoglycemia, leukemia, cerebrovascular accidents, and anesthetic accidents can all be associated with cortical blindness.
In the pediatric patient presenting to the emergency room with acute-onset misalignment of eyes, a sixth or third cranial nerve palsy should be suspected and prompt evaluation for increased intracranial pressure (secondary to infection, trauma, mass) should be undertaken. In the setting of trauma to the eye, an orbital fracture should be suspected. Orbital cellulitis and orbital foreign bodies can also present with misalignment (see below). Treatment includes identifying the underlying process and prompt treatment with antibiotics and neurosurgical or ophthalmologic consultation.
In a patient older than 6 months with subacute, chronic, or congenital misalignment, prompt referral to ophthalmology should be made for outpatient treatment to prevent amblyopia.
Ptosis is the abnormal drooping of the eyelid and is usually produced by an neurologic abnormality along the nerves that enervate the eyelids including parasympathetic enervation, the oculomotor nerve (cranial nerve three) and the facial nerve (cranial nerve seven) or an abnormality in the one of the muscles they enervate. The differential diagnosis of ptosis depends on acuity, progressiveness, family history, progression through day, and other associated symptoms (headache, diplopia). If the ptosis is associated with ipsilateral miosis and anhidrosis, it is referred to as Horner syndrome and is a defect along the sympathetic pathway that supplies the head and neck. Most of the time a specific lesion is not identified, but neuroimaging should be undertaken to rule out acute lesions. If the ptosis is variable throughout the day it is usually associated with myasthenia gravis, an autoimmune disorder of the neuromuscular junction.
Blepharitis (eyelid inflammation) is frequent throughout childhood and often involves one of the sebaceous glands of Zeis (in the margin of the eyelid) or Meibomian (in the tarsal plate in the rim of the eyelid).
Hordeolum is a suppurative inflammation, sterile or infectious, of the gland of Zeis (external hordeolum) or gland of Meibomian (internal hordeolum). Differential of a hordeolum includes preseptal cellulitis and chalazion. Hordeolums are usually localized (unlike preseptal cellulitis) and acute (unlike a chalazion). Treatment of a hordeolum consists of warm compresses in 15-minute increments several times a day. Use of topical antibiotics in the treatment of hordeolum is employed by some clinicians; however, no clear evidence shows its effectiveness. If there is no improvement with conservative treatment, the patient should be referred to ophthalmology.
Chalazion is formed by lipid obstruction followed by a granulomatous inflammation of the glands of Zeis or Meibomian resulting in a hard, painless nodule. Initially the swelling may be diffuse, but usually becomes localized to the lid margin. The differential diagnosis of a chalazion includes rhabdomyosarcoma, capillary hemangiomas, dermoids, orbital cysts, molluscum contagiosum, sarcoidosis, fungal infections, foreign bodies, and juvenile xanthogranuloma. Differentiation is made by lack of response to local therapy and/or biopsy. Treatment of a chalazion is similar to that of a hordeolum with hot compresses and referral to ophthalmology if no improvement for curettage.
Impetigo Contagiosa is a pyoderma usually presenting with vesicles; it then develops a yellowish crust, which occurs due to local invasion by staphylococci or streptococci. In patients with impetigo, there can often be an underlying seborrheic dermatitis. Impetigo contagiosa should be treated by removing crusts and with topical antistaphylococcal and streptococcal antibiotics. A cotton-tip applicator soaked in baby shampoo can be used to clean the lid margins. Bacitracin ophthalmic ointment is often effective; however, topical erythromycin and gentamicin can be used. If systemic impetigo is present, oral antibiotics should be initiated.
Herpes Simplex can present on the eyelids of children and can lead to latent infection, which may persist throughout life and be reactivated. Recurrent infection often involves the cornea. Impetigo contagiosa and herpes simplex can be easily confused. Cultures should be obtained to ascertain etiology.
Molluscum Contagiosum is a poxvirus that presents with flesh-colored, often umbilicated papules. Differential includes herpes simplex and impetigo contagiosum; however, molluscum is not vesicular or crusted. Molluscum is self-limited and resolves within a year. If necessary, referral to dermatology for excision or cryotherapy can be made.2
Periorbital infections are common in childhood and usually resolve with appropriate therapy and without sequelae. The anatomic development of the sinuses in children is thought to play a major role in the development of orbital and periorbital infections.
Periorbital infections, particularly sinusitis, may cause infection or severe inflammation in the orbital tissues leading to a preseptal or orbital cellulitis. The proximity of the paranasal sinuses to the orbital walls and the interconnection between the venous system of the orbit and the face allow infection to spread from the sinuses to the orbit either directly or via the bloodstream. Orbital and facial infections can lead to cavernous venous thrombosis.
The orbital periosteum and septum are important anatomic structures which help to limit direct spread of infection. The orbital periosteum acts as a barrier to the spread of infection from the sinuses; however, it may become eroded if a periorbital abscess develops. The orbital septum may also limit the spread of infection from the preseptal space to the orbit. The following classification system has been described for orbital infections:
Class I: Periorbital or preseptal cellulitis (Fig. 99-1)—Cellulitis is confined to the anterior lamella tissue. Lid edema and erythema may be mild or severe. The globe ordinarily is not involved, so vision and function remain normal.
Class II: Orbital cellulitis—Orbital tissue is infiltrated with bacteria and cells, which extend through the septum into the orbital fat and other tissues. Manifestations usually include proptosis, impaired or painful movement, and periocular pain. Visual acuity may be impaired and septicemia may be present.
Class III: Subperiosteal abscess (Fig. 99-2)—Purulent material collects between the periosteum and the orbital wall. Medial wall involvement causes the globe to be displaced inferiorly or laterally. Symptoms include edema, chemosis, and tenderness with ocular movement, while vision loss and proptosis vary in severity.
Class IV: Orbital abscess—When pus accumulates within the orbital fat inside or outside the muscle cone, an orbital abscess has developed. The infectious process becomes localized and encapsulated, unlike orbital cellulitis, which tends to be more diffuse. Exophthalmos, chemosis, ophthalmoplegia, and visual impairment are generally severe; systemic toxicity may be impressive.
Class V: Cavernous sinus thrombosis—Thrombosis results from extension of an orbital infection into the cavernous sinus. Nausea, vomiting, headache, fever, pupillary dilation, and other systemic signs may be present. There is marked lid edema and early onset of third, fourth, and sixth cranial nerve palsies.
The bacteriology involved in orbital infections depends on the age of the patient and the underlying problem. In newborn infants and in those up to the age of 5 years, Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis are predominant, particularly in children with upper respiratory tract infections, conjunctivitis, sinusitis, or otitis media. The incidence of infections due to H. influenzae type B has dropped since the advent of routine vaccination against this pathogen.3 In patients with a history of skin infections or trauma, Staphylococcus aureus and streptococcal species are the main offending agents. The incidence of infections with community-acquired Methicillin-resistant S. aureus continues to increase.4 Polymicrobial and anaerobic infections are more common in older children. Children with cystic fibrosis are susceptible to infections with Pseudomonas aeruginosa.
Fungal orbital cellulitis is uncommon in children. A slowly progressive course of orbital swelling in children with vomiting or dehydration may indicate an underlying fungal infection; immunocompromised and diabetic children may be at greatest risk. Rhizopus and Mucor are the most common fungi causing infections.
Most of the clinical findings are described with each class of infection. Preseptal or periorbital cellulitis is marked by periorbital edema, erythema, and tenderness but is not accompanied by proptosis, ophthalmoplegia, or loss of visual acuity. Chemosis and conjunctivitis may be present, as well as fever and leukocytosis. Patients with orbital cellulitis present similarly but have further development of ophthalmoplegia, proptosis, pain on eye movement, worsening chemosis, and changes in vision. Fever and leukocytosis are often seen. Blood cultures are positive in up to 25% of patients. If the orbital cellulitis is secondary to sinusitis, headache, rhinorrhea, and swelling of the nasal mucosa may also be present. Swelling of the eyelid may sometimes be so severe that further evaluation is necessary. Computed tomography (CT) has been useful in the delineation of periorbital cellulitis from orbital cellulitis.
In patients with mild periorbital cellulitis and no history of fever or other systemic illness, a thorough physical examination is recommended but laboratory investigation may be unnecessary. Mild cases of preseptal cellulitis due to local trauma or conjunctivitis can be treated with oral antibiotics such as amoxicillin-clavulanate (20–40 mg/kg/d) to cover against S. aureus. Cellulitis associated with an upper respiratory infection may also be treated with amoxicillin-clavulanate or with cefuroxime. For cellulitis secondary to bug bites, oral antihistamines and warm compresses may also be helpful. Close follow-up is mandatory.
For patients requiring hospitalization, a complete blood cell count, lumbar puncture, cultures of the blood, nasal mucosa, throat and conjunctiva, and CT of the head may be warranted. A lumbar puncture should be considered to rule out meningitis if patients appear toxic and are younger than 2 years or if infection with H. influenzae is suspected. The following management scheme has been recommended by several authors:
All patients hospitalized for orbital inflammation should receive ophthalmologic and otolaryngology consultation.
Broad-spectrum antimicrobial therapy should be instituted at once while awaiting blood or intraoperative culture results. Children younger than 5 years of age without a history of trauma should be placed on appropriate coverage against H. influenzae type B, S. pneumoniae, and group A streptococcus. A suggested initial regimen consists of ceftriaxone, 100 mg/kg/d, with the addition of vancomycin, 40 mg/kg/d in severe cases. Children older than 5 years or those fully immunized with the Haemophilus vaccine do not generally require coverage for Haemophilus; appropriate antimicrobials are similar to those used for treatment of severe sinusitis.
Attempts must be made to delineate if the cellulitis is of preseptal or postseptal origin. CT of the head is a helpful diagnostic aid but may not differentiate between subperiosteal abscess and reactive periosteal edema.
Surgical indications include diminishing visual acuity, lack of improvement despite adequate antibiotics, or spiking fevers, suggesting possible development of orbital abscess or cavernous venous thrombosis.
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