Pediatric Ocular Trauma

    Authors: Sylvia E. Garcia, MD, Pediatric Emergency Medicine Fellow, Children's Hospital, Pittsburgh; Robert Hickey, MD, Assistant Professor of Pediatrics, Children's Hospital, Pittsburgh, University of Pittsburgh School of Medicine.

    Peer Reviewer: John P. Santamaria, MD, FAAP, FACEP, Co-Medical Director, After Hours Pediatrics; Associate Clinical Professor of Pediatrics, USF School of Medicine, Tampa, FL.

Eye injuries are particularly difficult to evaluate in children. Often the child has pain, anxiety, and cannot or will not cooperate with the examination. Because these injuries may be associated with significant morbidity, it is particularly critical to have a thorough knowledge of anatomy, mechanisms of injury, and associated injuries that may place a child at increased risk of an ocular injury. The authors present a review of anatomy, mechanisms of injury, and methods to identify significant eye injuries. They also review methods to examine a traumatized child, medications as they apply to pediatrics, and current management strategies. I hope this review makes the ocular examination of the pediatric patient less stressful in the ED.

-The Editor

Introduction

There are an estimated 2.5 million eye injuries per year in the United States,1 and approximately 15 of every 100,000 children annually suffer an eye injury severe enough to require hospitalization.2 Younger children are injured most often from falls, accidental blows, and motor vehicle accidents, while older children are injured from sports-related activities, burns, and firearms.2 Because eye injuries are a significant cause of morbidity in the pediatric population, emergency medicine physicians should be adept at managing them.

The purpose of this article is to review the management of pediatric ocular trauma. We will begin by reviewing anatomy, relevant historical information, and pertinent findings on physical exam. We will then discuss the management of specific injuries. The discussion of injuries will be organized into two sections: the first, focusing on the anatomic structures involved (corneal abrasion, subconjunctival hemorrhage, etc.) and the second, on selected mechanisms of injury (airbags, fireworks, etc.).

Anatomy

The neurovascular supply to the orbit enters through an opening in the posterior wall of the orbital cavity. The ophthalmic artery is the primary source of arterial blood supply to the orbit and lies beneath the optic nerve in the optic canal. Its first intraorbital branch is the retinal artery.

The orbit consists of the conjunctiva, Tenon's capsule, sclera, cornea, uveal tract, lens, and retina. The conjunctiva is a thin, transparent mucous membrane that is divided into the palpebral conjunctiva lining the inner surface of the eyelids and the bulbar conjunctiva, which is loosely attached to the orbital septum in the fornices and is folded many times. It is continuous with the skin at the lid margin and with the outer edge of the corneal epithelium (limbus). Tenon's capsule (fascia bulbi) is a fibrous membrane that covers the globe from the limbus to the optic nerve. The sclera is the fibrous outer coating of the orbit. It is white and continuous with the cornea anteriorly and the dural sheath of the optic nerve posteriorly. The cornea is an avascular structure composed of transparent tissue. It attaches to the sclera at the limbus. The uveal tract is composed of the iris, the ciliary body, and the choroid. The iris separates the anterior chamber from the posterior chamber and is formed by the anterior extension of the ciliary body. The iris maintains contact with the anterior surface of the lens and is composed of sphincter and dilator muscles. The ciliary body, comprised of ciliary muscles, extends from the anterior end of the choroid to the iris. The ciliary body produces aqueous humor and changes the shape of the lens by contracting or relaxing the zonular fibers. The lens is a biconvex, avascular, colorless, and near transparent structure; it is located posterior to the iris and is connected to the ciliary body by the zonule. The lens is semi-permeable and is without pain fibers. Anterior to the lens lies the aqueous humor, while the vitreous body lies posterior.

Six extraocular muscles are responsible for movement of the globe. Four rectus muscles insert medially, laterally, inferiorly, and superiorly and adduct, abduct, depress, and elevate the globe, respectively. Two oblique muscles control torsional movement along with some vertical movement of the globe. The oculomotor nerve (cranial nerve III) innervates all extraocular muscles except for the superior oblique and lateral rectus muscles. The superior oblique is innervated by the trochlear nerve (cranial nerve IV) and the lateral rectus muscle by the abducens nerve (cranial nerve VI).

Pupillary size is controlled by a balance of sympathetic and parasympathetic input. Parasympathetic fibers travel along cranial nerve III and produce miosis via the constrictor muscles of the iris. Sympathetic fibers arise from the superior cervical ganglia in the neck and innervate the ciliary dilator muscle to produce mydriasis.

The visual cortex receives information through a neural pathway connecting the retina with the cortex. Images imprinted on the retina are relayed through the optic nerve. Input from the temporal retina projects to the ipsilateral optic tract, but the nasal retina input crosses at the optic chiasm to the contralateral tract. The optic tracts end in the lateral geniculate bodies that relay the information to the cortex. Decreased retinal stimulation during neural development can result in amblyopia. If visual stimulation to a retina is absent or markedly diminished, the afferent neurons (which are dependent upon continued stimulation for development) will atrophy or be recruited by the pathways serving the normal eye. Children remain at risk for developing this condition until approximately 9 years of age. The condition may become irreversible if not corrected quickly. Causes for the development of amblyopia include physical occlusion (ptosis, cataract, dislocated lens, prolonged eye patching, and corneal blood staining from a hyphema), unequal refractive errors, and strabismus.

History

It is important to obtain a complete medical history on the patient who presents with an ocular injury. The method of injury, the location where the injury took place, the use (or lack) of eye protection, the object involved, and the speed of the object should all be elicited. Medical history, previous ocular injury or ocular surgery, current medications, history of drug allergies, family history, and immunization history (especially tetanus status) should also be obtained. Taking into consideration the regular recommendations for age, tetanus toxoid is recommended for the patient with orbital penetration, heavily contaminated wounds, and wounds with delayed care.3

Examination

It is important that the exam not result in further injury to the eye. If the globe is intact, inadvertent application of pressure to the eye could result in extravasation of the eye contents. Therefore, if it becomes apparent that the globe has been ruptured, the exam should stop immediately, a rigid eye-shield should be placed, and an ophthalmologist consulted.

If gross examination of the eye does not reveal the possibility of a ruptured globe, the examination should continue with a systematic assessment of visual acuity and an external to internal evaluation of ocular structures.

The assessment of visual acuity should be age-appropriate. Infants develop the ability to fix on objects within the first 1-2 months of life, and, by age 3 months, they will fix on and follow an object directly in front of them. By age 5-6 months, a child will follow an object into all fields of a gaze. Allen object recognition cards, which are simple pictures of common objects, can be used to test 2 and one-half to 3 and one-half year old children. The pictures are shown at increasing distances until the patient recognizes or fails to recognize the cards. The Sheridan-Gardiner or HOTV test is an appropriate test of visual acuity in those aged 3-5 years. The letters H, O, T, and V are individually presented to the child who then matches them to the corresponding card held on their lap. The tumbling-E, where the letter E is presented in decreasing size and differing orientations, is also appropriate for this age group. Snellen letters represent the "gold standard" for assessment of visual acuity, and are used in children aged 6 years and older. Although a significant change in visual acuity may signify a serious eye injury, it is important to recognize that serious injuries (including a ruptured globe) can occasionally present with normal visual acuity.

The external to internal evaluation of ocular structures begins with palpation and gross inspection of the surrounding periocular structures and the orbit. The orbital rim should be carefully palpated for tenderness or any bony deformities. The unruptured globe can be palpated through closed eyelids for gross assessment of intraocular pressure. A more exact measure of intraocular pressure can be obtained with the use of tonometers, but this requires a cooperative or sedated patient and is best performed by experienced clinicians or ophthalmologists. Patients with lacerations involving the eyelids should be carefully evaluated for associated intracranial injury or injury involving the globe, tarsal plate, or lacrimal system. Proptosis, if present, should alert the examiner to the possibility of increased pressure behind the globe secondary to hemorrhage.

Next, the position of the eye and the range of motion should be assessed. Limited range of motion can occur secondary to cranial nerve palsies or muscle entrapments. A penlight simultaneously shown into both eyes can be used to evaluate alignment. If aligned, the light will reflect off of the same location in both corneas. In an esotropic (inwardly misaligned) eye, the light reflection will be displaced in a temporal direction compared to the other eye. In an exotropic (outwardly misaligned) eye, the light reflection will be displaced in a nasal direction. The term hypertropia is used to describe upward or downward displacement of the globe. Limitation in range of motion or misalignment is often accompanied by a complaint of diplopia. Typically, the diplopia is binocular (resolves when either eye is covered). The cause is misalignment of the globe, with one eye fixating on the object and the other seeing it as displaced. Binocular diplopia may be seen with blow-out fracture, traumatic cranial nerve palsy, iris injuries, inflammation, neoplasm, or strabismus. With monocular diplopia, double vision is present even when one eye is covered. The differential diagnosis for monocular diplopia includes uncorrected refractory error, cataract, displaced lens, and conversion disorder.

Pupillary shape, size, and reaction to direct light should be recorded. Abnormal pupil shape can be seen with rupture of the globe or injuries of the iris. For example, a D-shaped aperture can be seen with iris injuries.

A difference in pupillary size (anisocoria) of more than 1 mm in dim light is clinically significant. The differential diagnosis of anisocoria includes: Horner's syndrome, cranial nerve III injury, Adie's syndrome, Argyll Robertson pupil, ocular trauma, ocular inflammation, and normal physiologic variation. Horner's syndrome is caused by lesions along the sympathetic pathway and presents with miosis, ptosis, and anhydrosis. Cranial nerve III injury presents with ptosis, extraocular muscle weakness, and, because of the associated parasympathetic involvement, mydriasis. Adie's syndrome is a condition of unknown etiology characterized by anisocoria and diminished tendon reflexes. The Argyll Robertson pupil is a consequence of a midbrain lesion (classically associated with syphilis) resulting in a pupil that constricts during accommodation but not to direct light. Ocular trauma or inflammation may cause anisocoria through disruption or spasm of the dilator and/or constrictor mechanisms. The diagnosis of normal physiologic variation is made by history. An old photograph of the patient, if available, may help differentiate normal physiologic variation from new onset disease.

The pupillary light reflex is a reflex arc, with the stimulus being light transmission to the retina and the response being constriction of the pupil. The pathway is mediated through the midbrain and incorporates crossover innervation so that both pupils will constrict even when light is shown into only one eye. The pathway is assessed by the swinging light test. The test is performed by shining a light into one eye, noting the reaction of the pupil, and then swinging the light over to the opposite eye. Normally, both pupils will constrict with direct light to one of the pupils, and no change in pupillary size is noted when light is quickly directed to the opposite eye. If a defect exists in the afferent (sensory) part of the reflex arc, both pupils dilate when the light is swung to the affected eye. An abnormal test is referred to as an afferent pupillary defect, and the abnormal pupil is known as a Marcus Gunn pupil. Retinal arterial or venous occlusions, retinal detachment, ischemic optic neuropathy, and tumors can result in a relative pupillary defect.

The accommodation pathway mitigates changes in pupil size and lens shape in order to maintain focus through a range of distances. As an eye maintains focus on an object moving from far to near, the pupil will constrict and the lens thickens. Both actions are mediated by cranial nerve III.

The conjunctiva and cornea should be inspected for foreign bodies and isolated injuries. To examine the conjunctiva, the patient is asked to look down as the upper eyelid is everted with the use of a cotton swab. Downward pressure is placed on the superior border of the tarsal plate with the swab as the lid margin is lifted and the swab rotated to expose the tarsal surface. This can also be accomplished using the examiner's index finger instead of a cotton swab. Alternatively, eversion of the eyelid may be accomplished with a Desmarre retractor. To inspect the lower lid, the patient is asked to look up as the lower lid is pulled down and out. Visualization of corneal and conjunctival abrasions are facilitated by the use of fluorescein dye (2% solution or impregnated strips) and ultraviolet light. When administering fluorescein dye, check for the presence of contact lenses, as fluorescein will permanently stain them.

Chemosis (conjunctival swelling) is associated with scleral rupture or retained foreign body. A cystic appearing conjunctiva with crepitus (subconjunctival emphysema) is associated with medial wall fractures.

Full-thickness ruptures of the cornea or sclera can result in a peaked or tented pupil and compromised visual acuity. If the possibility of globe rupture exists, the eye must be shielded and ophthalmology emergently consulted.

Gross integrity of posterior ocular structures can be assessed by visualizing the red reflex. An absent or dull red reflex may indicate a vitreous hemorrhage, cataract, hyphema, opacity of the cornea, enophthalmos, or misalignment of the globe. In the patient with no history of trauma, the possibility of a tumor must be considered. Direct or indirect ophthalmoscopy is used to more extensively evaluate the vitreous, retina, and optic nerve.

Table 1. Ophthalmic Medications

ANESTHETICS

ONSET

DURATION

SIDE EFFECTS

COMMENTS

Proparacaine hydrochloride 0.5% (Alcaine, Ophthetic)

1 min

15-20 min

Epthelial keratitis with habitual use, iritis Conjunctival congestion Corneal opacification (rare)*

Used to aid in removal of corneal foreign body Use with caution in patients with hyperthyroidism

Tetracaine hydrochloride 0.5% (Pontocaine, Anacel)

1 min

1.5-3 hrs

Same as above Cardiac arrest (rare), bradycardia (rare), central nervous system depression/stimulation (rare), respiratory arrest (rare)_

Used to aid in removal of corneal foreign body Pediatric safety, efficacy not established*

Mydriatics and Cycloplegics

Tropicamide 0.5%, 1% (Mydriacyl, Tropicacyl, Ocu-Tropic)

30 min

4-6 hrs

Dry mouth, elevated intraocular pressure (rare). Tachycardia (rare)* headache*, drowsiness*, blood pressure (rare)_, cardiorespiratory collapse_, and behavioral disturbances (rare)_

Contraindicated in narrow angle glaucoma. Used to treat some cases of acute iritis, iridocyclitis, keratitis. 0.5% solution preferred for mydriasis_; 1% solution preferred for cytoplegia_; Useful in ED for direct ophthalmoscopy

Cyclopentolate hydrochloride 0.5%, 1%, 2% (Cyclogyl, AK Pentolate)

15 min

12-24 hrs

Tachycardia, hypertension, restlessness, (1% and 2% concentrations) Toxic reactions in pediatric populations (2% concentrations); (psychotic reaction, ataxia, hallucinations [rare])

Contraindicated in narrow angle glaucoma. 0.5% for newborns, infants_; Useful for treatment of ciliary spasm.

Cyclopentolate hydrochloride 0.2% and phenylephrine hydrochloride 1%

3-6 min

< 24 hrs

Same as reactions in Cyclopentolate hydrochloride

Contraindicated in narrow angle glaucoma. Useful in newborns, infants, and children_

    * McGhee B, et al. Pediatric Drug Therapy Handbook and Formulary 1998-1999.

    _ Apt L. Pharmacology. In: Isenberg SJ. The Eye in Infancy. Chicago: Year Book: 1989:91-99.

    _ Awan KJ. Adverse systemic reactions of topical cyclopentolate hydrochloride. Am Ophthalmol 1976;8:695-698.

Medications

Table 1 lists selected medications (anesthetics, dilators) that may be useful in aiding the physician to complete a thorough examination of the eye.4,5 Topical anesthetics act on the trigeminal nerve to anesthetize the cornea and conjunctiva. When administering topical anesthetic drops, the patient should be warned of a stinging sensation for several seconds and that they should not rub the eye for 20-30 minutes, as a corneal abrasion may result. Both sympathomimetic and parasympatholytic drops will cause mydriasis by acting on the iris sphincter muscle. However, parasympatholytic agents will result in more complete dilation because they also paralyze the ciliary muscle (cycloplegia). Pilocarpine should be readily available when mydriatics are used so that effects may be quickly reversed if necessary.

Anatomic Lesions

Fractures. Medial wall fractures can occur in association with nasal trauma. Along with a nasal fracture, deviation of the nasal septum and laceration of the lacrimal canaliculi may be present. It may be possible to palpate a bony avulsion fracture at the insertion site of the medial canthal ligament. Disruption of the ligament will give the eye the appearance of esotropia (pseudo-esotropia). Direct trauma to the medial wall can also result in fracture of the thin lamina papyracea of the ethmoid bone. This may be seen on radiography as air in the orbit and clinically as subcutaneous and subconjunctival emphysema that worsens with nose blowing (although impressive in appearance, this condition is often self-limited).

Superior wall (orbital roof) fractures involve the frontal sinus or cribriform plate. They can be associated with cerebral spinal fluid rhinorrhea. The rare finding of pulsating enophthalmos mandates an immediate consultation with an ophthalmologist.6

Basilar skull fractures can present with eyelid ecchymosis (raccoon eyes) and associated conjunctival hemorrhage.

A blow-out fracture results when the orbit is struck with an object larger than the orbital diameter, causing increased intraocular pressure that is transmitted to the orbital walls. The orbital floor, the weakest part of the orbit, is fractured. This can result in a prolapse of the orbital contents into the maxillary sinus, with narrowing of the palpebral fissure, slight enophthalmos, and entrapment of the inferior rectus muscle. Entrapment or spasm of the inferior rectus will result in limitation of upward gaze. Hypesthesia of the ipsilateral cheek and upper lip from injury to the infraorbital nerve (which runs through the orbital floor) may also be present. Radiographs (including the Waters view) may demonstrate an air-fluid level or increased density in the maxillary sinus from extravasation of blood or orbital contents. Computed tomography is more sensitive for showing subtle soft tissue and bony abnormalities and should include views of the optic canal and cavernous sinus. If entrapment of the inferior rectus muscle is suspected, a CT scan is indicated to determine if the fracture is a "trap-door" fracture caused by a bone fragment that flexes into the sinus and then snaps back into position, entrapping the inferior rectus muscle.7 Some physicians recommend emergent surgery to repair trap-door blow-out fractures because of the potential for compromise of the blood supply to the inferior rectus muscle.7 Otherwise, the decision to operatively repair a blow-out fracture can be delayed for a period of 10-14 days. Interim therapy includes antibiotics, nasal decongestants, and ice packs.

Traumatic optic neuropathy is a serious, though uncommon, complication of blow-out fractures. Patients typically present with an immediate loss of vision and an afferent pupil defect secondary to contusion, compression, or avulsion of the optic nerve.8 Computed tomography with coronal and axial views should be emergently obtained. Treatment is immediate decompression of the optic nerve sheath or canal.9

Orbital hematoma. Orbital hematoma is caused by diffuse hemorrhage located, most commonly, subperiosteally. Increased intraorbital pressure can be transmitted to the optic nerve and globe. Patients may present with diplopia, reduced visual acuity, and pain. Physical findings include periorbital ecchymosis, conjunctival chemosis and hemorrhage, corneal edema, optic disc edema, and a tense proptotic-appearing eye. Compression of the optic nerve can result in decreased visual acuity and an afferent pupil defect. Patients with visual loss should have emergent surgical decompression. Time is critical for patients requiring emergent decompression; consultation and management should not be delayed by computed tomography.10 Patients not requiring emergent surgical decompression are admitted and monitored for changes in visual acuity and recurrent hemorrhage.

Eyelid trauma. Eyelid ecchymosis is typically a result of blunt injury. On examination, the physician should carefully search for associated injuries including hyphema, ruptured globe, orbital hematoma, and blow-out fractures. A superior conjunctival hemorrhage, associated with eyelid edema and ecchymosis, is suggestive of an orbital roof or superior wall, fracture, while an inferior conjunctival hemorrhage with lower lid ecchymosis suggests an orbital floor fracture.11 Ptosis of the eye can result from injury to the levator palpebrae muscle and may be permanent if the aponeurosis is stretched or torn. Patients with ptosis that persists following resolution of an eyelid hematoma should be referred to an ophthalmologist for continued observation and possible surgical repair. If no other complications exist, eyelid ecchymosis can be simply managed with cold compresses.

Eyelid lacerations may be caused by blunt or penetrating trauma. Again, the eye must be inspected for retained foreign bodies, open globe injury, and canalicular damage. There should be a high index of suspicion for damage to the canalicular system in lacerations involving the inner third of the eyelid. Laceration of the upper lid has a higher risk for associated intracranial injury. If orbital fat is protruding from the wound, the orbital septum has been violated and the levator palpebrae muscle has been injured.

The necessity of antibiotic prophylaxis in clean wounds is controversial. Most clinicians generally agree on the use of antibiotics for wounds secondary to human or animal bites.

Corneal abrasion. Twenty-five percent of reported ocular injuries are corneal abrasions.12 Abrasions can be secondary to transient debris, retained foreign bodies, or irritation from contact lenses.13 A patient with a corneal abrasion typically complains of pain, tearing, photophobia, and changes in visual acuity. A corneal abrasion is a well-described occult cause of irritability and prolonged crying in an otherwise healthy infant.14,15 A corneal abrasion defect may be seen with a direct light source, but the use of fluorescein dye and a cobalt lamp facilitate detection. Multiple vertical abrasions should alert the examiner to the presence of a retained foreign body. Abrasions caused by contact lens use predispose the patient to fungal and bacterial infections, which create a higher risk for developing corneal ulcerations.13 It is important not to mistake a herpes infection for a corneal abrasion. Herpes lesions arise from reactivation of latent virus in the trigeminal nerve. They have a dendritic appearance and may be associated with a vesicle at the tip of the nose (also innervated by the trigeminal). Failure to recognize and treat a herpetic lesion can have catastrophic consequences. These patients should be immediately referred to an ophthalmologist, as loss of vision is a substantial risk. Treatment includes the use of topical antiherpetic agents.

Most uncomplicated abrasions can be treated with topical antibiotic drops or ointment alone.16 Ointment may be a better lubricant and provide longer protection than drops, but is not well tolerated in older patients because they dislike the blurred vision caused by the ointment.17 For these reasons, in general, ointment should be used in children younger than 1 year of age. Cycloplegic drops can be used to relieve the intense pain created by the ciliary muscle spasm accompanying significant abrasions.17-19 Topical anesthetics can be used to facilitate the exam in the ED but should not be included in discharge medications because they can lead to neurotrophic keratitis. In addition, worsening pain is an important warning sign that should prompt the clinician to consider a poorly healing abrasion or an abrasion progressing to an ulcer.

The issue of pressure patching has been investigated by several authors. It has been found to have no clinically significant effect on the healing rate of corneal abrasion and might even delay healing.16-20 The potential for a delay in healing is hypothesized to be secondary to the hypoxic environment that is produced by patching, as well as the constant pressure of the patch delaying reepitheliazation.17-19 Patching of both eyes has been associated with more rapid healing, probably by reducing conjugate ocular movement, but does not seem practical in clinical use.18-20 Treatment of corneal abrasions without patching is preferred in most cases.

Most corneal abrasions heal within 24-72 hours. Re-evaluation of the abrasion should be performed in 24 hours to observe for signs of infection and to document improvement. For most patients, this entails a repeat physical exam. However, in highly compliant and reliable patients with minor abrasions that are not associated with contact lenses, a phone call documenting complete resolution of symptoms may be sufficient follow-up. Patients with contact-lens related injuries are at high risk for developing corneal ulcers and should be followed more closely. Similarly, patients with a history of ocular herpes should be thoroughly evaluated and compulsively followed for signs of recurrence.

Corneal and conjunctival lacerations. Corneal and conjunctival lacerations are usually a result of penetrating trauma. Prolapse of the iris, creating a tear-drop distortion in shape, is pathognomonic for a corneal laceration. Other associated injuries include extension of the laceration into the sclera or aqueous/vitreous humor, iridodialysis (iris torn from the sclera), traumatic cataract, and a retained foreign body. In conjunctival lacerations, the affected area is surrounded by hemorrhage, with the laceration appearing as a white crescent-shaped lesion (prolapse of Tenon's capsule). The Seidel test can be helpful for diagnosing full-thickness injuries. In this test, a fluorescein strip touched to the lacerated area will demonstrate a stream of florescent dye if there is actively leaking aqueous humor.13 However, small full-thickness corneal and conjunctival lacerations can self-seal and yield a false-negative test. A slit-lamp examination can clarify the depth of the laceration. If a full-thickness laceration exists or is suspected from the exam, a rigid eye shield should be placed and a systemic, broad-spectrum antibiotic initiated while awaiting the arrival of the ophthalmologist. Glaucoma, traumatic cataract, and amblyopia are late complications.

Subconjunctival hemorrhage. Subconjunctival hemorrhage is painless bleeding into the conjunctiva. In the absence of related injuries (penetrating injury, retained foreign body, associated fractures), the condition is self-limited, and only reassurance is necessary. The patients and parents should be warned that the hemorrhage may appear larger before reabsorbing in 2-3 weeks.

Hyphema. Hyphema is a collection of blood in the anterior chamber of the eye. The incidence of hyphema is approximately 9 out of every 100,000 children.2 The mechanism is compression of the eyeball resulting in distortion of the iris and tearing of the anterior ciliary body. Almost one-third of the patients will have associated ocular injuries.21 Patients with hyphema will complain of photophobia and pain. Young children may be lethargic. The history should focus on the mechanism of injury, risk factors for bleeding dyscrasias, risk for sickle cell disease, current medications (especially aspirin products), and history of renal or liver disease. Hyphemas are classified by estimating the volume of the anterior chamber that is filled with blood (grade I: < one-third, grade II: one-third to one-half, grade III: > one-half, grade IV: complete). The blood is usually reabsorbed in 2-3 days, but rebleeding can occur as the clot retracts and can be of greater magnitude and result in higher intraocular pressures than the original bleed. Rebleeding is most common 2-5 days after the initial injury.22 Patients with grade I hyphemas have a 15% risk of rebleeding, whereas those with grades II or III have a 60% risk.3

Patients with sickle cell trait or sickle cell disease require special consideration. The anterior chamber has a low pH and low PO2, which promotes sickling of the extravasated red blood cells. The sickled cells cannot easily be cleared from the anterior chamber, and the drainage system becomes blocked, causing intraocular pressure to rise. A vicious cycle then ensues with continued sickling and progressive increase in intraocular pressure. Patients with sickle cell disease and even minimal elevations in intraocular pressure are at increased risk for developing optic atrophy.3

Traditionally, patients with hyphema were hospitalized, maintained on strict bed rest, and had bilateral patching and sedation.23 This approach fell out of favor when it was demonstrated that most patients can be managed as outpatients with ad lib activity and do well. One reasonable approach is to reserve hospitalization for patients with grade II or III hyphemas, sickle cell disease, evidence of increased intraocular pressure, or social circumstances precluding close follow-up.3

Medical management should include the use of a rigid eye shield and elevation of the head of the bed. Cycloplegics, topical steroids, and antifibrinolytics are optional therapies. Topical cycloplegics can be used to relieve associated ciliary spasm. Topical corticosteroids attenuate anterior chamber inflammation, and may decrease the incidence of rebleeding.24 Antifibrinolytic agents, such as aminocaproic acid (Amicar), stabilize the clot by preventing fibrin lysis and clot retraction, allowing the damaged vessel to heal. Aminocaproic acid has traditionally been delivered either intravenously or orally. The intravenous route requires hospitalization with its attendant disadvantages (cost, inconvenience). Oral administration, although less costly, can result in important side effects including nausea, vomiting, and postural hypotension. Because of these side effects and disagreement about relative efficacy, there is no consensus on indications for use of systemic amino caproic acid. More recently, topical aminocaproic acid has become available and is undergoing treatment trials. A comprehensive discussion of antifibrinolytic therapy and ongoing treatment trials of topical aminocaproic acid has recently been published.22

The initial hyphema or subsequent rebleeding can result in glaucoma, decreased visual acuity, and blood-staining of the cornea. Corneal staining assumes special consideration in the pediatric population because of the risk of amblyopia.3 Non-traumatic causes of hyphema include tumors (retinoblastoma, leukemia), hemophilia, juvenile xanthogranuloma, factious history, and physical abuse.

Injuries to the iris. Traumatic iritis. Miosis or mydriasis can occur following iris injuries secondary to ciliary body spasm or iris sphincter muscle paralysis, respectively. Patients will complain of pain, photophobia, and blurred vision. Examination may reveal perilimbal conjunctival injection and anisocoria. An accommodative pupillary spasm (the affected pupil will slowly constrict with bright light and have delayed dilatation in dim light) may be present. Slit lamp examination may show a tear in the iris sphincter muscle and a "flare and cell" effect in the anterior chamber. Plasma proteins released into the anterior chamber create the flare. The specks of dust ("cell") seen in the flare are white blood cells and iris pigment cells. White blood cells may also be seen as an inflammatory response to untreated corneal abrasions, traumatic retinal detachments, and endophthalmitis secondary to a retained foreign body. Mydriasis caused by injury to the ciliary ganglion, which can be associated with an orbital floor fracture, should also be considered in the differential diagnosis. Cycloplegics help decrease spasm and relieve pain. Topical corticosteroids reduce inflammation and decrease the likelihood of the formation of adhesions from the iris to the cornea and/or the lens (synechiae).

When the iris is torn at its root (iridodialysis), patients may complain of diplopia, photophobia, and glare. The eye will appear to have more than one pupil (polycoria) or the opening of the pupil will appear D-shaped. Hyphema is often associated with this injury.

Lens injuries. Lens dislocation. Dislocation of the lens results from traumatic rupture at the zonule(s). A subluxated lens is only partially dislocated and remains within the posterior chamber. In contrast, a dislocated lens migrates into the anterior chamber or posteriorly into the vitreous humor. Symptoms of subluxation/dislocation include monocular diplopia, glare, and decreased visual acuity.25 Patients with dislocation will always have symptoms on presentation. However, patients with subluxation may remain asymptomatic for weeks or months following the traumatic event, making diagnosis difficult. A shallow appearance to the anterior chamber and movement of the iris and lens with ocular movement may be seen. If the vitreous can be seen in the anterior chamber or if the edge of the lens is seen within the pupil, the diagnosis of subluxation is confirmed. Patients with the lens edge lying in the visual field may experience monocular diplopia and astigmatism.

Removal of the lens is indicated if is there is significant visual impairment. Indications for emergent surgical removal include pupillary block (obstruction of aqueous flow from the anterior to the posterior chamber), corneal touch (the lens touches the cornea and permanently damages the endothelium), and severe inflammation. The differential diagnosis of non-traumatic lens displacement includes Marfan's syndrome, homocystinuria, inflammation, and congenital dislocation.

Lens capsule rupture. Rupture of the lens capsule progresses to cataract formation within hours of injury. Patients will complain of decreased vision and present with a cloudy lens, increased intraocular pressure, and signs of inflammation. Surgical removal is indicated.

Retinal detachment. A retinal detachment is a separation of the sensory portion of the retina (rods and cones) from the pigment layer. Symptoms include flashes, floaters, and visual defects. Traction at the retinal periphery is manifested as brief flashing lights. If there is progression, fibrous aggregates on the posterior surface of the vitreous block light to the retina and the patient sees "floaters." Extravasation of blood into the vitreous causes blurred vision. With a severe detachment, a full-thickness hole in the retina may result, allowing the vitreous to separate the sensory portion of the retina from the pigment layer. Once a retinal detachment occurs, a loss of vision in the affected area will occur. Ophthalmology should be consulted to evaluate all patients with complaints of flashes and floaters to prevent the progression of partial tears to complete detachment.

Ruptured globe. The most common sites for rupture of the globe are at the limbus and immediately posterior to the insertion of the rectus muscle, which are the weakest points of the sclera. Alternatively, the globe can rupture through the cornea. Physical findings include conjunctival chemosis, asymmetric anterior chamber, peaked or tented pupil, exposed uveal tissue (appearing as a pigmented area), hyphema, and vitreous hemorrhage. Treatment, other than immediate placement of a rigid eye shield and emergent consultation with ophthalmology, includes intravenous antibiotics, not allowing the patient to eat, and providing antiemetics as needed. Agents that increase intraocular pressure could theoretically result in further extravasation of orbital contents. For example, succinylcholine is frequently mentioned as a drug that is believed to increase intraocular pressure and, therefore, avoided. However, other authors have promoted the position that the increased intraocular pressure associated with succinylcholine is clinically insignificant and should be balanced against its known benefits.26 Some authors recommend avoiding the use of narcotics because of the risk of vomiting, and sedatives because of the risk of a paradoxical agitation response.27 Concerns about potential side effects of narcotics and sedatives should be weighed against the possible benefit in a child who is grimacing/crying in pain or agitated from anxiety.

Specific Mechanisms of Injury

Burns. Chemical. Chemical burns to the eye represent a true ocular emergency. The severity of the injury is dependent on the solution's pH, volume, and penetrability, and its duration of contact with the eye. Particulate matter is more damaging to the eye than solution because it remains in contact with the eye for a longer duration. Alkali solutions are more damaging than acids because they cause saponification of fatty acids in cell membranes, making the eye further susceptible to degradative enzymes. In contrast, acid solutions coagulate proteins in the corneal epithelium and superficial stroma of the eye, forming a protective barrier against continued penetration.

The single most important factor determining long-term prognosis is related to intervention at the site of the accident. The eye should be irrigated as soon as possible after the injury has occurred. The single exception is particulate material. The childeyes should be placed under the water faucet, with the lids held open by the parent. Direct, constant irrigation of the eyes should then occur with cool tap water. On arrival to the emergency room, a quick assessment of visual acuity (Rosenbaum card, fingers before the face, or light perception) should be attempted. The fornices and tarsal areas should be examined and any retained particulate matter removed. The pH of the tears should be determined, topical anesthetics placed, and irrigation continued with an isotonic solution. Irrigation is recommended until the pH of the eye is approximately 7.4 (typically requiring 1-3 liters). The pH should not be tested until five minutes after the completion of irrigation because earlier testing may reflect the pH of the solution.28 The pH should be checked again at 30 minutes following irrigation to ensure that the pH is stable. If the pH is not stable, the eye should be reinspected for retained foreign material. Visual acuity should be reassessed and the eye checked for corneal opacification or conjunctival blanching. If opacification or blanching is seen, severe scarring and secondary glaucoma are more likely, and an ophthalmologist should be consulted emergently. Any child with serious alkali burn to the eye should be referred to an ophthalmologist. If no opacification or blanching is noted, the cornea should be stained with fluorescein to identify residual epithelial defects.

Treatment options for significant burns include topical corticosteroid, cycloplegic, antibiotics, and bandage-type contact lenses.

Thermal. Direct thermal injury to the globe is often prevented by reflex closing of the eyelids. Therefore, burns will usually be confined to the eyelid. These can become serious injuries if scarring results in incomplete apposition of the lids, which exposes the globe to drying.

Radiant injury. Eyes that have had prolonged exposure to bright light arcs ("Welder's keratitis"), snowfields, or sun lamps are susceptible to ultraviolet burns of the cornea. Symptoms include foreign body sensation, lacrimation, and photophobia, and may be delayed. Examination with fluorescein dye reveals a diffuse punctate pattern of staining. The condition is self-limited, and the goal of management is to provide symptomatic relief.

Super glue. Exposure of the eyelid and the globe to super glue results in a rapid fusion of structures. If gentle traction fails to separate the lids, saline compresses or neosporin ophthalmic ointment should be applied for 24 hours. `Super glue remover,' which has acetone, should not be used in the eye, as acetone can dissolve the epithelial layer of the cornea.

Conjunctival and corneal foreign bodies. Patients with a foreign body in the cornea or conjunctiva often complain of pain and foreign body sensation. Topical anesthetics can be used to ease the discomfort of the exam and foreign body removal. The exam should include eversion of the lids and close inspection of the palpebral conjunctiva and cul-de-sac. Several methods of removal have been described. Irrigation is the gentlest method and should be attempted first. If the foreign body remains adherent to the surface of the cornea or conjunctiva, a moistened cotton swab, foreign-body spud, a fine forceps, or a medium bore needle (22 gauge) can be used in conjunction with a slit lamp. Sharp tools should be used only in a cooperative patient who will remain still and allow the physician's hand to rest on his or her cheek (minimizing the risk of further injury secondary to sudden movement). Removal should not be attempted if the foreign body appears to perforate deeper structures.

If the foreign body should not or cannot be removed, a rigid shield should be placed over the eye and ophthalmology consulted. Continued foreign body sensation in the absence of an identified foreign body may be indicative of deeper ocular injury and should also be referred. Embedded metallic corneal foreign bodies can cause rust rings with permanent staining if left in place. Always remove metallic foreign bodies promptly and refer to an ophthalmologist for rust ring removal if present.

Intraocular foreign bodies. Size, velocity, composition, and ocular location all affect the management of intraocular foreign bodies. Intraocular foreign bodies are most commonly caused by either large objects traveling at low speed (e.g., pencils, plant debris) or small, sharp objects at high velocity (e.g., metal particles from hammering metal on metal). The large object typically results in impressive signs and symptoms, whereas the small, sharp object can present occultly. Of intraocular foreign bodies, 80-90% are metallic, with the remainder being categorized as non-metallic or organic. Injury from metallic foreign bodies occurs when two metal objects strike together and small flecks of metal fly from the impact. The examiner should maintain a high index of suspicion for ocular penetration. A history of metal on metal may be the only clue; the physical examination may be completely normal.

Foreign bodies in the eye, as elsewhere in the body, can remain asymptomatic, develop delayed symptoms, or cause an immediate, intense, suppurative inflammatory reaction. An additional consideration in the eye is the risk of staining and local toxicity (commonly from iron or copper foreign bodies). Non-organic foreign bodies are the most likely to remain asymptomatic, and, if detected as an incidental finding, are often left in place. Management of foreign bodies detected at the time of initial injury is controversial. Whereas some clinicians elect to leave low-risk foreign bodies in place, others point to evidence that visual outcome is improved and the risk of endophthalmitis is minimized with early removal.29

Multisystem Trauma. In the multiply injured patient, assessment of ocular injuries is an important component of the secondary survey. The window of opportunity can be limited by sedation, paralysis, and evolving facial swelling. Therefore, documenting the integrity of the visual axis (at the very minimum, the pupillary light reflex) and gross assessment of the eye for contact lenses, retained foreign bodies, hyphemas, and injuries to the orbit is critical. If the patient is conscious and cooperative, visual acuity can be tested using a Rosenbaum card, held 14 inches from the eye. Hard contact lenses can be removed with the use of a moistened lens suction cup. Soft contact lenses are removed by gently pinching off the lens. If severe facial injuries limit the exam or there is a possibility of a ruptured globe, the eyes should be protected by a hard shield.

Child Abuse. In a 1995 survey by the National Committee to Prevent Child Abuse, there were 996,000 confirmed cases of child abuse.30 Caffey first described the constellation of intracranial and retinal hemorrhages (often in the absence of external signs of abuse) in infants subjected to vigorous shaking.31 This has subsequently been called "shaken baby syndrome." Retinal and/or vitreous hemorrhages are found in 50-80% of patients with shaken baby syndrome, and in 6-24% of all abused children.31-33 Retinal hemorrhages appear as flame shaped and boat shaped lesions. The hemorrhages are believed to be secondary to increased intracranial venous pressure that is transmitted from the thorax (from squeezing or choking) and from acceleration/deceleration injury causing tears in the retinal vessels.33

Less common causes of retinal hemorrhages include blood dyscrasias, infectious agents, intracranial lesions, anesthesia, intraocular surgery, accidental trauma associated with head or chest injury and, Extracorporeal Membrane Oxygenator/Oxygenation.33-37 Up to 50% of vaginally delivered newborns have retinal hemorrhages secondary to birth trauma.33,38

Retinal hemorrhages are an uncommon result of cardiopulmonary resuscitation.36,39 Kanter reported on the fundoscopic findings of 54 patients undergoing CPR.36 Five of nine patients with intentional or unintentional trauma as a precipitating cause of their arrest had retinal hemorrhages; these hemorrhages were most likely a result of the preceding trauma rather than the subsequent CPR. In support of this, only one of the 45 patients without a history of trauma had retinal hemorrhages. Goetting reported on the fundoscopic findings of 20 children undergoing CPR.39 Two children had retinal hemorrhages. One child underwent 40 minutes of CPR following water immersion and the other child underwent 75 minutes of CPR after arresting in the hospital while admitted for presumed sepsis. Although these studies demonstrate that retinal hemorrhages can be a result of CPR, they also underscore the importance of considering more likely (and more insidious) mechanisms involving intentional and unintentional injury.

Sports-related injuries. Approximately one-third of all significant ocular injuries seen in the pediatric population are sports-related, with four sports accounting for more than half the injuries: basketball (17.2%); baseball (16.8%); water sports (10.3%); and racquet sports (8.6%).40,41 Enucleations are particularly common in hockey and golf-related injuries.42 It is estimated that 90% of sports-related eye injuries can be prevented with protective eyewear.40,43-45 Guidelines for protective eyewear have been published in a joint statement by the American Academy of Pediatrics and the American Academy of Ophthalmology.44-45 Special consideration should be given to the functionally monocular patient and patients with previous ocular injuries or eye surgery. These patients are at particular risk because damage to the normal eye could have devastating consequences; they should always wear protective eyewear when participating in sports, and they should avoid sports where protective eyewear cannot be worn (boxing, karate, wrestling, etc.).44-45

Fireworks. There are approximately 12,600 people in the United States who are treated for fireworks-related injuries per year.46 More than half of these injuries occur in children, and approximately 20% involve the eye.47-48 One-third of fireworks-related ocular injuries result in permanent blindness.49 Forty-five percent of those injured are bystanders,48 and, in approximately half of the cases in which children are injured, there is adult supervision.50 Legally available class C fireworks (firecrackers, bottle rockets) are responsible for two-thirds of accidents.50 The most severe injuries are associated with the use of rockets and class B fireworks (cherry bombs), which are legally banned.48 Most accidents are caused by improper use, misfirings, erratic behavior of the firework, and ricochet of the device off a hard surface.48 It is instructive to note that in states where the sale of various fireworks is permitted, there is a greater than seven-fold increase in fireworks-related injuries.50-51

Airbag-induced injuries. Duma et al reported a series of 25 patients with air-bag related injuries (patients aged 2-75 years).52 Contusions to the face, eyelid, or eyeball occurred in all 25. Seven patients had corneal abrasions, seven had lacerations to the eyelid and face, and four had retinal and vitreous detachments. In a separate series published by Ghafouri, three of 11 patients had bilateral ocular injuries, despite monocular complaints.53

Sodium hydroxide, a highly alkaline agent, is released in the chemical reaction used to deploy the air-bag.54,55 Chemical keratitis, presumably as a result of exposure to sodium hydroxide during air-bag deployment, has been reported.54,55

Lawnmower-related injuries. There are 70,000 lawnmower accidents reported per year in the United States, and an estimated 5% will include ocular injuries.56,57 The majority of injuries are caused by tractor and rider type mowers.58 Injuries to children are associated with: riding with the driver, playing near the mower, using the mower unsupervised, and entering the area unknown to the mower.59 John et al reviewed patients reported to the Eye Injury Registry of Alabama over a five-year period and found that all ocular injuries associated with lawnmowers were secondary to projectiles, most commonly rocks.57 Injuries included hyphemas, traumatic retinopathy, ruptured globes, intraocular hemorrhages, and intraocular foreign bodies. It is recommended that eye protection be used when operating the lawnmower and that children be kept away.57

Air gun-related injuries. There are approximately 1300 cases of pediatric ocular injuries associated with air guns per year in the United States.1 Of these injuries, 4-15% result in severe injuries.41,60 Visual outcome is poor, and enucleation of the perforated eye is commonly required.61-62

Table 2. Indications for Ophthalmologic Consultations

Ruptured globe

Orbital hematoma

Severe chemical burns

· corneal clouding

· burns

· decreased visual acuity

Hyphema

Retinal/vitreous detachment

Intraocular foreign bodies

Contact lens abrasions

Complicated eyelid lacerations

· canthus/lacrimal duct involvement

· associated ptosis

· eyelid margins

Clinical Findings

Marked changes in visual acuity

Misalignment of globe

Limitation in range of motion

Abnormal pupillary shape

Afferent pupil defect

Summary

The approach to ocular injuries is simplified by recalling anatomic relationships and understanding pathophysiologic considerations. A systematic evaluation of visual acuity and orbital structures will facilitate diagnosis and management and help the clinician to determine the need for consultation. (See Table 2.) In addition to understanding the structure and function of the injured components of the eye, emergency medicine physicians should be familiar with specific mechanisms of injury (many of which are preventable and/or result in a unique injury).

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