19

Ophthalmic Trauma

Jonathan Pargament, MD, Zélia M. Corrêa, MD, PhD, and James J. Augsburger, MD

The eye and periorbital region are subject to a range of injuries with a wide spectrum of severity and sequelae.

INITIAL EVALUATION

Initial evaluation of ophthalmic trauma, whether by a first responder or an emergency department provider, starts with an assessment of the patient’s overall condition to identify and manage any life-threatening problems. Then the circumstances of the injury must be established. The patient’s level of consciousness may be altered due to substance abuse, psychiatric disease or brain injury, so family members or bystanders may provide crucial collateral information. Specific questions should include whether a blunt or sharp object inflicted the injury; whether the injury occurred at high or low velocity; whether the patient has any prior history of ocular disease or surgery; and when and what the patient last ate and drank.

The next step is ophthalmic examination, of which the extent will depend on the patient’s level of cooperation. The first part does not require significant cooperation and begins with an inspection of the eyes and periorbital tissues for any obvious abnormalities such as lacerations, ecchymosis (Figure 19–1), proptosis, corneal clouding, or gross hyphema. In severe ophthalmic trauma, it is critical to examine the eye as atraumatically as possible to avoid exacerbating the damage. The pupils are examined to determine their absolute and relative sizes and shapes and their responses to direct and consensual illumination. If the patient is conscious and cooperative, visual acuity and confrontation visual fields are tested. Keep in mind that the patient may have broken or lost his or her glasses during the trauma. A pinhole for distance acuity and/or near vision chart

835

and presbyopic reading glasses may be crucial.

Figure 19–1. Prominent right eyelid ecchymosis and subconjunctival hemorrhage due to blunt trauma suffered in a fall.

If the initial evaluation reveals an injury that warrants further evaluation, ophthalmology consultation is essential. In addition to reviewing the history, the ophthalmologist will perform an external examination, reassess visual acuity and pupillary responses to light, assess ocular position in each orbit, evaluate ocular alignment and motility, if possible perform slitlamp examination of the anterior segment and measure intraocular pressure, and perform indirect ophthalmoscopy of the fundus.

OCULAR INJURIES

Rapid recognition by emergency care providers of chemical and open globe injuries is particularly important because of the need for emergency intervention to minimize their severity.

Chemical Injuries

In adults, ocular chemical injury is usually due to splash or spray of industrial or agricultural chemical, cleaning solution, automotive fluid, or cement or plaster in the work or home environment or assault with alkali or acid. In children, it is frequently caused by a cleaning solution or detergent.

Regardless of the type of chemical or circumstance of the injury, the most important first step is copious eye irrigation as soon as possible. Tap water will suffice until the patient has been transported to the emergency department, where sterile isotonic saline is preferred. Topical anesthetic drops and the use of an

836

eyelid speculum facilitate effective irrigation and removal of particulate matter in the case of cement or plaster. Irrigation should continue until a neutral pH has been achieved or definitive care by an ophthalmologist has been provided.

The next step is to determine the nature of the chemical involved in the injury, which may be indicated by the reaction of a pH strip prior to irrigation. Acid such as from a car battery precipitates necrotic tissue that acts as a barrier to its deeper penetration. Alkali such as in industrial cleaning solutions, household bleach, cement, and plaster causes more severe damage because it does not form such a barrier and penetrates further. Important signs of severe chemical injury are corneal clouding, limbal whitening, and significant conjunctival chemosis. The lack of redness mistakenly may be interpreted to indicate mild injury.

Further management includes topical antibiotic while there is a corneal epithelial defect; topical cycloplegic to reduce discomfort; topical steroid to reduce inflammation; topical and oral ascorbate (vitamin C) to prevent collagen lysis; topical potassium citrate to chelate calcium to reduce inflammation; oral doxycycline to reduce inflammation and prevent corneal melting; topical lubricants; and oral acetazolamide to treat raised intraocular pressure.

Open Globe Injuries

Open globe injury is an ocular injury that results in a full-thickness defect in the cornea and/or sclera, exposing the intraocular compartments to the external environment. Signs of an open globe injury that can be identified by basic examination include pupillary distortion (usually toward the wound), flat anterior chamber, and extraocular protrusion of uveal tissue (Figure 19–2). Other findings that should arouse suspicion of an open globe injury are massive hemorrhagic chemosis (Figure 19–3), profoundly soft eye, deep eyelid laceration (Figure 19–4), and intraocular blood (hyphema, vitreous hemorrhage). Open globe injuries are categorized as (1) full-thickness eye wall lacerations and (2) globe ruptures.

837

Figure 19–2. Corneoscleral laceration inferonasally with pupil displaced toward the laceration and iris incarcerated in wound.

Figure 19–3. Massive hemorrhagic chemosis following severe blunt ocular trauma. A globe rupture in the superonasal quadrant was confirmed by surgical exploration.

838

Figure 19–4. Eyelid laceration with concurrent open globe injury. A: Rather innocuous-appearing V-shaped eyelid laceration involving the upper and lower lids and medial canthal skin. B: Total dark red hyphema and hemorrhagic chemosis are evident when the lids are separated. Note also that laceration extends through both lacrimal canaliculi.

A full-thickness eye wall laceration is an ocular injury caused by a sharp object or high-velocity projectile that has cut completely through the cornea, sclera, or both. In some cases, the object that caused the cut is not retained at the site but is withdrawn or extruded prior to emergency evaluation (Figures 19–1 and 19–5). In other cases, the object is retained in the wound (Figure 19–6) or inside the eye (Figure 19–7). In still other cases, the object passes completely through the eye, causing both entry and exit wounds (double perforating injury).

839

Figure 19–5. Pellet gun injury to the right eye resulting in open globe injury. Note massive hemorrhagic chemosis, irregular corneal shape, distorted pupil, and dark brown iris tissue incarcerated into limbal wound.

Figure 19–6. Ocular laceration with retained foreign body. The tip of a metallic foreign body protrudes from the eye at the limbus inferiorly.

Figure 19–7. Metallic intraocular foreign body lying on the surface of the retina.

In full-thickness eye wall lacerations, the lens capsule may be cut at the time of the injury. When the capsule is disrupted, the lens becomes hydrated, swollen,

840

and opaque. Fragments of the lens may also extrude into the anterior chamber and cause severe inflammation. A lensectomy procedure is required but typically is not performed at the time of the globe repair. It may be delayed for treatment of hyphema and/or inflammation and to more accurately measure and plan for intraocular lens placement.

Intraocular foreign bodies retained in the posterior segment can be very challenging to remove without additional injury to ocular structures. Therefore, they should be left alone during the initial globe repair and a vitreoretinal subspecialist consulted about subsequent removal.

Globe rupture is splitting or tearing of the cornea and/or sclera at a relatively weak point by severe blunt ocular trauma. Relatively common sites are posterior to the extraocular muscles (especially in the superonasal quadrant), along incisions from prior intraocular surgery, and at the lamina cribrosa. Globe rupture should be suspected in the setting of any blunt trauma resulting in massive hemorrhagic chemosis or a profoundly soft eye (Figure 19–3).

If an open globe injury is identified or suspected, straightaway a protective shield should be taped over the injured eye and urgent ophthalmology consultation arranged. Analgesic and antiemetic medications should be administered to keep the patient reasonably comfortable and avoid vomiting. Tetanus toxoid vaccine should be administered. In full-thickness eye wall laceration, a computed tomography (CT) scan may be required to identify or rule out a retained intraocular or intraorbital foreign body.

Once an ophthalmologist has confirmed an open globe injury, surgical repair should be undertaken as soon as reasonably possible. General anesthesia should be induced without the use of depolarizing agents (eg, succinylcholine) as this can lead to increased intraocular pressure and extrusion of intraocular contents. The ophthalmologist explores the wound to determine its full extent and plan the surgical repair. In most cases, corneal lacerations and ruptures are closed using 10-0 nylon sutures with buried knots, and scleral discontinuities are closed using 8-0 or 9-0 nylon sutures. Iris and/or ciliary body tissue incarcerated in the wound may be replaced inside the eye (reposited) if it is not necrotic or grossly contaminated. Precise realignment of the wound edges and release of incarcerated corneal and conjunctival epithelium are important. The sutured wound needs to be watertight. If the conjunctiva was lacerated or incised to facilitate exposure of a scleral wound, it is closed with absorbable 7-0 or 8-0 sutures. Antibiotics and corticosteroids are often injected subconjunctivally at the conclusion of the operation and continued as eye drops postoperatively. The

841

patient should be examined frequently in the postoperative period for wound leaks, infection, recurrent intraocular bleeding, hypotony, and ocular hypertension that may require additional treatment.

Intraocular or Intraorbital Foreign Body

A history of explosion, gunshot wound, or striking of metal upon metal should raise suspicion of an intraocular or intraorbital foreign body. If the optical media are still relatively clear, it may be possible for an ophthalmologist to detect or exclude an intraocular foreign body. Otherwise if an open globe injury is suspected or there is massive orbital swelling, CT scan of the eyes and orbits will detect most foreign bodies and determine their general locations (eg, inside the eyeball, in the wall of the globe, in the orbit). Magnetic resonance imaging (MRI) is contraindicated if a magnetic foreign body is suspected.

Closed Globe Injuries

Corneal abrasion, a scratching or scraping away of some of the corneal epithelium (Figure 19–8), is one of the most common ophthalmic injuries encountered in an emergent care setting. Commonly there is a history of an injury, such as from a finger nail or during manipulation of a contact lens. Typically there is severe foreign body sensation, tearing, light sensitivity, and blurred vision. Administration of a topical anesthetic drop usually improves the patient’s symptoms dramatically. Slitlamp examination with fluorescein, which stains the exposed basement membrane, will reveal the extent of the corneal abrasion. Treatment for corneal abrasion should always include topical broadspectrum antibacterial agents. Eye patching may decrease pain. The patient should be examined periodically, especially if there are increased symptoms, to ensure that the cornea is healing and there is no associated corneal infection. Under no circumstance should topical anesthetic drops be given to the patient for self-administration as they delay corneal epithelial healing, mask the subjective findings of a worsening course, and if used for a prolonged period, can cause a chronic neurotrophic corneal ulcer.

842

Figure 19–8. Corneal abrasion stained with fluorescein.

Corneal or conjunctival foreign body occurs when an object with too little momentum to pass completely through the eye wall becomes embedded in the cornea or conjunctiva. The patient will frequently have a recent history of grinding or striking metal. Symptoms are quite similar to a corneal abrasion including foreign body sensation, light sensitivity, and excessive tearing. Larger corneal foreign bodies may be visible on diffuse light examination. Smaller foreign bodies may be evident only on slitlamp examination (Figure 19–9). Linear vertical corneal epithelial defects are often indicative of a foreign body embedded in the tarsal conjunctiva of the upper eyelid and should prompt eversion of the eyelid to examine its conjunctival surface and to remove the foreign body with a sterile cotton-tipped applicator stick.

Figure 19–9. Tiny metallic corneal foreign body appearing as dark brown speck on the cornea (arrow).

Removal of a corneal foreign body requires proficiency with the slitlamp. Depending on the emergency room provider’s training and experience, removal may be attempted. The cornea should first be anesthetized with a topical anesthetic drop. While viewing with the slitlamp, the foreign body is dislodged with a sterile 27-gauge or larger caliber needle. If the foreign body is composed of iron or copper, there may be an associated “rust ring,” which can be removed

843

with a battery-operated drill with a burr tip. A broad-spectrum antibacterial should be administered and treatment continued for a corneal abrasion. If there is any question about whether the foreign body has passed completely through the cornea, an ophthalmologist should be consulted immediately.

Subconjunctival hemorrhage results from cutting or tearing of one or more conjunctival or anterior orbital blood vessels leading to accumulation of blood in the substantia propria of the conjunctiva. If greater than 270 degrees or associated with prominent chemosis, it is suspicious of open globe injury (Figure 19–3) and warrants urgent surgical exploration.

Trauma may cause superficial ocular laceration of the conjunctiva with or without partial thickness laceration of the sclera and/or cornea. Slitlamp biomicroscopy must be used to ascertain the depth of the laceration and assure that it does not extend completely through the eye wall. Most partial-thickness lacerations can be managed as if they were corneal abrasions with an antibacterial and patching. Extensive superficial laceration may warrant suturing by an ophthalmologist.

Ocular trauma can cause posttraumatic inflammatory reaction involving the iris (traumatic iritis) or the iris and ciliary body (traumatic iridocyclitis). Typically, symptom onset is 24–48 hours after the injury with increasing eye pain, photophobia, and blurred vision. On slitlamp examination, there are inflammatory cells and flare in the anterior chamber, finely dispersed keratic precipitates on the cornea, and Vossius ring of dark brown pigment on the anterior lens capsule. Adhesions between the pupillary margin of the iris and the anterior lens capsule (posterior synechiae) and adhesions between the peripheral iris and cornea (peripheral anterior synechiae) may occur. Treatment consists of topical cycloplegic drops (eg, atropine 1%) and frequent corticosteroid drops (eg, prednisolone acetate), which should be prescribed by an ophthalmologist, until the intraocular inflammation subsides. Ophthalmological follow-up is required.

Many ocular injuries damage blood vessels of the iris causing hemorrhage into the anterior chamber (traumatic hyphema). If the amount of intraocular bleeding is not too severe, the blood becomes layered out gravitationally (Figure 19–10). Symptoms are similar to those of a traumatic iritis and include blurred vision, eye pain, and light sensitivity. Gross hyphema will be visible on external diffuse light examination, but slitlamp examination is required to detect limited red blood cells in the anterior chamber. Hyphema can be a sign of an open globe injury, so a comprehensive ophthalmic examination is required. Potential complications of hyphema include raised intraocular pressure and corneal blood

844

staining. Treatment of hyphema includes bed rest, ocular antihypertensive drops, frequent topical corticosteroid, and cycloplegic drops. Oral aminocaproic acid reduces breakdown of clot and reduces the risk of re-bleeding.

Figure 19–10. Traumatic hyphema and associated subconjunctival hemorrhage.

The concussive shock wave from blunt ocular trauma can damage the iris, ciliary body, and trabecular meshwork. There may be small radial tears through the iris sphincter muscle at the pupillary margin (traumatic iris sphincter tears). Iridodialysis is more extensive circumferential tear of the iris at the iridociliary junction. Cyclodialysis is circumferential separation of the peripheral iris and ciliary body from the sclera at the scleral spur. Angle recession is circumferential tear through the trabecular meshwork and is identified as widening of the anterior chamber angle on gonioscopy. These abnormalities typically are accompanied by hyphema and may not be evident until the blood clears. Impairment of the trabecular meshwork function from hyphema and angle recession leads to secondary glaucoma in many cases. Low intraocular pressure (hypotony) can occur with cyclodialysis because the aqueous fluid has direct access to the suprachoroidal space. Ultrasound biomicroscopy is useful for identifying angle recession as well as cyclodialysis with associated ciliochoroidal effusion. These conditions can resolve spontaneously, but surgical intervention may be required for large iridodialysis, cyclodialysis with hypotony, and angle recession glaucoma. Open globe injury with displacement of intraocular contents or blunt ocular injury may cause displacement of the (crystalline) lens (traumatic lens dislocation). It is more likely if there is pre-existing weakness of the zonules, such as in Marfan’s syndrome and homocystinuria. On slitlamp examination, there may be abnormal movements of the lens with eye movements (phakodensis), abnormal position (subluxation) of the lens, or complete dislocation of the lens into the anterior chamber or vitreous. Depending on the extent of the dislocation, nonurgent

845

surgery may be required.

Severe ocular contusion may cause focal or geographic retinal whitening (commotio retinae) that usually is located opposite the site of impact. Typically it develops within 24 hours after the injury and gradually fades over several days to weeks. If the macula is affected, the visual acuity may be profoundly reduced. There is no active treatment.

Blunt or sharp trauma to the periorbital region can damage the optic nerve (traumatic optic neuropathy). Severe blunt trauma to the head, particularly the frontal region, or to the face, particularly if there is a fracture at the orbital apex, may injure the optic nerve as it passes through the optic canal. Penetrating orbital injuries, periocular soft tissue lacerations, and eye gouging can damage the optic nerve without necessarily causing an open globe injury. Depending on the severity of the injury, the visual acuity ranges from normal to no light perception. Treatment with systemic corticosteroids is controversial, and prognosis is variable.

Severe ocular contusion can cause tearing of the retinal pigment epithelium (choroidal rupture) in a crescentic or curvilinear pattern that is typically concentric to the optic disk margin (Figure 19–11). Involvement of the central macula can cause permanent profound reduction of visual acuity. Choroidal neovascularization arising from the edge of the choroidal rupture may also cause reduction of visual acuity, but treatments are available.

Figure 19–11. Traumatic choroidal ruptures with associated subretinal blood.

Ocular contusion injury in which the shock wave impacts directly on the fovea can cause a full-thickness retinal hole (traumatic macular hole) (Figure 19–12). Vitreoretinal surgery may be indicated, but visual acuity frequently does not improve.

846

Figure 19–12. Traumatic macular hole (larger arrow) with surrounding exudative subretinal fluid (smaller arrow).

Mechanical ocular injuries often tear superficial retinal blood vessels, leading to traumatic vitreous hemorrhage, which can range from mild to severe. Typically, there is an associated partial or complete posterior vitreous detachment. As long as the retina is not torn, the intravitreal blood usually clears spontaneously within a few weeks to months. If the retina is torn, retinal detachment frequently develops, requiring surgery.

ORBITAL INJURIES

Trauma to the periorbital region can result in a variety of injuries including contusions, abrasions, avulsions, and lacerations. The initial evaluation should include a thorough examination of the eyelid margin, nasolacrimal system, and canthi. Contusions and abrasions can be treated conservatively with topical antibacterial ointment. Superficial eyelid lacerations not involving the eyelid margin may be closed as with any skin laceration. Injuries involving the full thickness of the eyelid margin or the nasolacrimal system (Figure 19–13) require an ophthalmology or oculoplastic consultation. Surgery is usually required to achieve precise alignment of the tarsal plate, mucocutaneous junction, lash line, and canaliculus so as to prevent a lid notch and reduced the risk of epiphora. All periorbital lacerations should receive a thorough examination to rule out associated ocular injury.

847

Figure 19–13. Full-thickness laceration of left lower eyelid involving its medial margin with underlying eye wall laceration and uveal prolapse.

Blunt and penetrating injuries to the periorbital region are frequently associated with orbital fractures, either from direct impact with transmission of force through the bones or indirectly by injury to the thin bone of the orbital walls from elevation of intraorbital pressure (“blowout fracture”), which most commonly affects the orbital floor and may result in entrapment of orbital tissue sometimes including an extraocular muscle. Clinical signs of an orbital fracture include step defect of the orbital rim, enophthalmos or exophthalmos, paresthesias and numbness in the distribution of the first or second division of the trigeminal nerve, diplopia, and orbital crepitus. Entrapment of an extraocular muscle may cause severe pain and autonomic disturbance with bradycardia and vomiting on attempted eye movement. Particularly in children, blowout fracture with extraocular muscle entrapment may not be accompanied by orbital soft tissue signs (“white-eyed blowout”). CT scan of head and orbits, preferably reviewed by a neuroradiologist, will identify most orbital fractures (Figure 19– 14), whether there is entrapment of orbital soft tissues, and whether there are facial or skull fractures requiring maxillofacial or neurosurgical assessment.

Figure 19–14. Coronal computed tomography scan of orbits showing right orbital floor fracture (arrows).

848

Not all orbital fractures need to be repaired, and in many cases, surgery can be delayed by 1–2 weeks to allow resolution of orbital swelling and reduction of the risk of dangerously high intraorbital pressure during surgery. Blowout fractures with severe pain and/or autonomic disturbance require urgent surgical intervention. Blowout fractures with troublesome double vision or risk of persistent enophthalmos benefit from surgery, with optimal timing being determined by individual circumstances. Whether orbital fractures with displaced bony fragments impinging on the optic nerve should be repaired is debatable because existing optic nerve damage is unlikely to be improved and surgery entails a risk of further optic nerve injury.

A wide variety of injuries including from firearms and explosions may result in intraorbital foreign bodies. Depending on their composition and location, surgical removal may be attempted, but often it is better avoided unless necessitated by infection or inflammation. CT shows metals well. MRI is contraindicated if the foreign body is known to be or could be magnetic. Copper may cause an inflammatory reaction and, along with iron, may cause retinal toxicity (see below). Lead is relatively inert. Organic foreign bodies including wood may be difficult to appreciate with CT scan and more apparent on MRI. They predispose to orbital infection and should be removed if possible.

Blunt or sharp trauma can cause retrobulbar hemorrhage, especially in patients on anticoagulants. Symptoms include marked orbital swelling with lid ecchymosis and subconjunctival hemorrhage, decreased vision, and double vision. On examination, the orbit is tense to retropulsion with increased intraocular pressure and decreased movements of the globe. Markedly increased intraocular pressure and a relative afferent pupillary defect require emergent lateral canthotomy and cantholysis. Ophthalmology consultation should occur without delay.

THERMAL BURNS

Thermal burns of the periocular region occur most commonly from fires and explosions. Mild cases may present with redness and pain. Severe thermal burns will present with severe swelling, redness or whitening, blistering, and charring of the involved tissues. Initial treatment consists of topical antibiotic ointment to keep the tissues lubricated and prevent secondary infection. Full-thickness burns can cause ectropion and lid retraction within a few days, necessitating

849

tarsorrhaphies or skin grafts to prevent corneal exposure. Repeat procedures are frequently required over the ensuing weeks to months in such patients.

Thermal burns to the ocular surface are much less frequent than thermal burns to the eyelids. However, full-thickness eyelid burns frequently result in necrosis and retraction of eyelid tissues, which can lead to ocular surface exposure, fusion of the eyelids to the surface of the eye (symblepharon), microbial keratitis, corneal perforation, intraocular infection, and blindness.

The most common electromagnetic injury to the eye is ultraviolet radiation– induced superficial keratoconjunctivitis due to absorption of ultraviolet radiation energy by the corneal and conjunctival epithelium during activities such as arc welding, prolonged exposure to reflected light off of snow, water or white sand, and use of tanning beds. Typically, patients will report a painful red eye with foreign body sensation and tearing several hours after the exposure. Topical anesthetic drops may be required to provide temporary relief sufficient to allow slitlamp examination. Treatment is similar to that described earlier for corneal abrasions.

LATE SEQUELAE OF OPHTHALMIC TRAUMA

Corneal full-thickness lacerations and ruptures frequently heal with sufficient irregular warping to cause profound impairment of visual acuity. Rigid contact lens, corneal laser treatment, or corneal grafting (usually delayed until at least 6 months after the injury) may be required.

Following severe chemical injuries and some thermal injuries, the corneal stroma becomes partially or completely opaque. Also most or all of the limbal stem cells that normally repopulate the corneal epithelium are lost, which results in progressive conjunctivalization of the corneal surface. Limbal stem cell transplantation followed by penetrating keratoplasty or implantation of a prosthetic cornea may restore some vision.

Ocular hypotony means low intraocular pressure, typically defined as less than 6 mm Hg. It leads to corneal folds, diffuse corneal and uveal congestion, and macular edema, which can cause mild to profound visual impairment. It may be caused by exudative ciliochoroidal effusion, cyclodialysis, retinal detachment, unrecognized globe rupture, and posttraumatic intraocular inflammation. If hypotony is not effectively treated, the eye may become shrunken and blind

850

(phthisis bulbi).

Microbial infection is a serious and potentially blinding complication of many ocular injuries. It may be limited to the specific site of injury (eg, cornea, lid) or may extend throughout the eye (endophthalmitis) or orbit (panophthalmitis). It is much more likely after trauma involving a contaminated object and in open globe injuries.

Corneal blood staining complicates ophthalmic trauma associated with major hyphema and concomitant substantial elevation of intraocular pressure. Red blood cells are forced into the stroma of the cornea by the high intraocular pressure. As the red blood cells break down, reddish brown hemosiderin pigment is deposited in the corneal stroma. Typically, the staining is most pronounced centrally and inferiorly and least pronounced peripherally and superiorly. If the blood eventually clears from the anterior chamber and intraocular pressure returns to normal, the corneal blood staining will resolve slowly over many months. While this is a tolerable problem for most adults, it is a potential cause of amblyopia in young children. Therefore, sustained raised intraocular pressure in a child with hyphema should be treated aggressively, possibly including anterior chamber washout.

Iron and copper are toxic to intraocular structures. Iron released from a retained foreign body is absorbed by many intraocular tissues including the cornea, lens, and retina, leading to greenish discoloration (siderosis oculi). Copper (chalcosis oculi) is deposited particularly in the Descemet’s membrane, lens capsule, and retina. In either case, permanent vision loss can occur due to retinal toxicity. Thus intraocular foreign bodies containing iron or copper should be removed whenever possible.

After external exposure of uveal tissue, an autoimmune granulomatous inflammation may develop in both the injured and uninjured eye (sympathetic ophthalmia) (see Chapter 7). It is most commonly associated with extensive corneoscleral laceration. Symptoms may begin as early as 1–2 weeks after the trauma but may not develop for several years. Untreated, the inflammation can lead to profound loss of vision in both eyes. Local and systemic immunosuppression with steroids and other agents is required to preserve vision. Removal of a severely traumatized eye within 7–10 days of the injury reduces the likelihood of sympathetic ophthalmia.

Traumatic diplopia can be monocular or binocular. Monocular double vision persists with closure of the fellow eye, whereas binocular double vision resolves when either eye is closed. Significant injury to the cornea will frequently cause

851

substantial corneal warping (irregular astigmatism) leading to monocular diplopia. Binocular diplopia can be caused by injury to the third, fourth, or sixth cranial nerves or to the extraocular muscles. Orbital fractures are a common cause. After surgical repair and release of extraocular muscle entrapment, diplopia may persist because of neuromuscular damage, and extraocular muscle surgery may be required.

Injuries to the nasolacrimal system can occur anywhere from the punctum to the nasolacrimal duct. Obstruction of any component of the nasolacrimal system leads to chronic overflow of tears (epiphora). Isolated obstruction of the nasolacrimal duct can also lead to infection of the lacrimal sac (dacryocystitis). Stenosis of the punctum can be treated easily with punctoplasty. Obstruction of the canaliculus or nasolacrimal duct may require dacryocystorhinostomy or a Jones tube.

NONOPHTHALMIC INJURIES

Ophthalmic traumas are rarely isolated injuries. Mechanisms of injury capable of causing ocular and periorbital injury are often sufficient to cause severe facial and brain injury (Figure 19–15). A team-based approach, often with maxillofacial surgeons, plastic surgeons, and neurosurgeons, is necessary to provide the best possible cosmetic and functional outcome for the patient.

Figure 19–15. Three-dimensional reconstructed computed tomography scan of unhelmeted motorcycle accident victim with bilateral panorbital fractures, frontal sinus fractures, and mandibular fracture.

852

REFERENCES

Al Wadeai EA et al: Epidemiological features of pediatric ocular trauma in Egypt. J Ophthalmol 2016;2016:7874084. [PMID: 27800177]

Baharestani S et al: Eyelid reconstruction techniques. In: Ichpujani P et al (eds): Expert Techniques in Ophthalmic Surgery. Jaypee Brothers Medical Publishers, 2015.

Bansal S et al: Controversies in the pathophysiology and management of hyphema. Surv Ophthalmol 2016;61:297. [PMID: 26632664]

Baradaran-Rafii A et al: Current and upcoming therapies for ocular surface chemical injuries. Ocul Surf 2017;15:48. [PMID: 27650263]

Batur M et al: Epidemiology of adult open globe injury. J Craniofac Surg 2016;27:1636. [PMID: 27526252]

Bossert RP et al: Blindness following facial fracture: Treatment modalities and outcomes. Craniomaxillofac Trauma Reconstr 2009;2:117. [PMID: 22110805]

Damgaard OE et al: Surgical timing of the orbital “blowout” fracture: A systematic review and meta-analysis. Otolaryngol Head Neck Surg 2016;155:387. [PMID: 27165680]

Eslani M et al: The ocular surface chemical burns. J Ophthalmol 2014;2014:196827. [PMID: 25105018]

Gharaibeh A et al: Medical interventions for traumatic hyphema. Cochrane Database Syst Rev 2013;12:CD005431. [PMID: 24302299]

Guzman-Salas PJ et al: Characteristics of sympathetic ophthalmia in a single international center. Open Ophthalmol J 2016;10:154. [PMID: 27651849]

Haring RS et al: Epidemiologic trends of chemical ocular burns in the United States. JAMA Ophthalmol 2016;134:1119. [PMID: 27490908]

Jung H et al: Prognostic CT findings of diplopia after surgical repair of pure orbital blowout fracture. J Craniomaxillofac Surg 2016;44:1479. [PMID: 27427337]

Kalin-Hajdu E et al: Controversies of the lacrimal system. Surv Ophthalmol 2016;61:309. [PMID: 26700821]

853

Kim SM et al: Prediction of the development of late enophthalmos in pure blowout fractures: Delayed orbital tissue atrophy plays a major role. Eur J Ophthalmol 2017;27:104. [PMID: 27198642]

Kong Y et al: Six-year clinical study of firework-related eye injuries in North China. Postgrad Med J 2015;91:26. [PMID: 25583736]

Leonard R: Statistics on Vision Impairment: A Resource Manual, 2000. Lighthouse International, 2000.

Loporchio D et al: Intraocular foreign bodies: A review. Surv Ophthalmol 2016;61:582. [PMID: 26994871]

Messman AM: Ocular injuries: New strategies in emergency department management. Emerg Med Pract 2015;17:1. [PMID: 26466300]

Movahedan A et al: Long-term management of severe ocular surface injury due to methamphetamine production accidents. Cornea 2015;34:433. [PMID: 25642642]

Nam SM: Microscope-assisted reconstruction of canalicular laceration using Mini-Monoka. J Craniofac Surg 2013;24:2056. [PMID: 24220405]

Neovius E et al: Persistent diplopia after fractures involving the orbit related to nerve injury. J Plast Reconstr Aesthet Surg 2015;68:219. [PMID: 25488468]

Page RD et al: Risk factors for poor outcomes in patients with open-globe injuries. Clin Ophthalmol 2016;10:1461. [PMID: 27536059]

Pargament JM et al: Physical and chemical injuries to eyes and eyelids. Clin Dermatol 2015;33:234-237. [PMID: 25704943]

Rajkumar GC et al: Ocular injuries associated with midface fractures: A 5 year survey. J Maxillofac Oral Surg 2015;14:925. [PMID: 26604465]

Read SP et al: Traumatic open globe injury in young pediatric patients: Characterization of a novel prognostic score. J AAPOS 2016;20:141. [PMID: 27079595]

Rodman RE et al: Controversies in the management of the trauma patient. Facial Plast Surg Clin North Am 2016;24:299. [PMID: 27400843]

Rudnisky CJ et al: Visual acuity outcomes of the Boston keratoprosthesis type 1: Multicenter study results. Am J Ophthalmol 2016;162:89. [PMID: 26550696]

854

Sadiq MA et al: Eyelid lacerations due to dog bite in children. J Pediatr Ophthalmol Strabismus 2015;52:360. [PMID: 26371465]

Scruggs D et al: Ocular injuries in trauma patients: An analysis of 28,340 trauma admissions in the 2003-2007 National Trauma Data Bank National Sample Program. J Trauma Acute Care Surg 2012;73:1308. [PMID: 22914085]

Septa D et al: Etiology, incidence and patterns of mid-face fractures and associated ocular injuries. J Maxillofac Oral Surg 2014;13:115. [PMID: 24822001]

SooHoo JR et al: Pediatric traumatic hyphema: A review of 138 consecutive cases. J AAPOS 2013;17:565. [PMID: 24215806]

Sosin M et al: Treatment outcomes following traumatic optic neuropathy. Plast Reconstr Surg 2016;137:231. [PMID: 26710028]

Su Y et al: Predictive factors for residual diplopia after surgical repair in pediatric patients with orbital blowout fracture. J Craniomaxillofac Surg 2016;44:1463. [PMID: 27530668]

Sung EK et al: Injuries of the globe: What can the radiologist offer? Radiographics 2014;34:764. [PMID: 24819794]

Tabatabaei SA et al: Systemic oral antibiotics as a prophylactic measure to prevent endophthalmitis in patients with open globe injuries in comparison with intravenous antibiotics. Retina 2016;36:360. [PMID: 26815932]

Toride A et al: Visual outcome after emergency surgery for open globe eye injury in Japan. Clin Ophthalmol 2016;10:1731. [PMID: 27660410]

Vaca EE et al: Facial fractures with concomitant open globe injury: Mechanisms and fracture patterns associated with blindness. Plast Reconstr Surg 2013;131:1317. [PMID: 23416437]

Voss JO et al: The “tight orbit”: Incidence and management of the orbital compartment syndrome. J Craniomaxillofac Surg 2016;44:1008. [PMID: 27259677]

Westekemper H et al: Clinical outcomes of amniotic membrane transplantation in the management of acute ocular chemical injury. Br J Ophthalmol 2017;101:103. [PMID: 27150827]

Yardley AE et al: Paediatric ocular and adnexal injuries requiring hospitalisation in Western Australia. Clin Exp Optom 2016 Oct 20. [Epub

855

ahead of print] [PMID: 27762442]

Yildiz M et al: An important cause of blindness in children: Open globe injuries. J Ophthalmol 2016;2016:7173515. [PMID: 27247799]

Yucel OE et al: Clinical characteristics and prognostic factors of scleral rupture due to blunt ocular trauma. Eye (Lond) 2016;30:1606. [PMID: 27589050]

Zhu L et al: Ocular trauma score in siderosis bulbi with retained intraocular foreign body. Medicine (Baltimore) 2015;94:e1533. [PMID: 26426616]

856