Petros E. Carvounis and Yvonne I. Chu
EPIDEMIOLOGY OF EYE TRAUMA
Worldwide 1.6 million people are estimated to be blind from ocular trauma and another 19 million people suffer from severely impaired vision in one eye due to trauma.1 Published literature from England looking at 15 years of more than 39,000 patients treated for major trauma found that 2.3% of patients had associated ocular injuries. Given that the eyes represent only 0.27% of the total body area, it is a curious phenomenon that the eyes are affected so often. In this series, the most common injuries involved the cornea, optic nerve, conjunctiva, and sclera.2
Men are reported to be four times more likely to suffer from ocular trauma compared to women and in the same series from England, 75.1% of major trauma patients with ocular injuries were men. While ocular trauma most commonly results from motor vehicle accidents, workplace injuries and recreational injuries are also very commonly seen. Most injuries were resulting from sharp objects (54.1%), followed by blunt objects (34.4%), and chemical injuries accounted for 11.5% of ocular injuries.3
EYE TRAUMA TERMINOLOGY AND CLASSIFICATION
Eye trauma is divided first by etiology into mechanical, chemical, thermal, and electric. Thermal (e.g., corneal burn from curling iron) and electric (e.g., lightning) eye traumas are very uncommon and treatment of complications will be by an ophthalmologist in an outpatient setting after discharge from the emergency room/urgent care setting. Chemical injury (alkali and acid burns) is not uncommon and its management will be discussed in detail as immediate intervention by first responders and emergency room physicians can be sight-saving.
Mechanical eye trauma is the most common form of eye injury. It is divided into open globe injury, where the sclera and/or cornea (eyewall) have a full-thickness wound, and closed globe injury where the eyewall does not have a full-thickness wound (Fig. 20-1).4–6 Closed globe injuries are further subdivided into contusion injuries, lamellar laceration (i.e., partial thickness laceration), and superficial foreign body (i.e., foreign body lodged on cornea, conjunctiva, or under the conjunctiva but without full-thickness wound of the eyewall).6 Open globe injuries are further divided into ruptured globes and globe lacerations.4,5 Ruptured globes result from blunt trauma, due to an extreme elevation of intraocular pressure on the moment of impact causing a rupture of the eyewall at the weakest site of the globe (force from inside out), usually away from the site of impact and frequently with significant herniation of intraocular contents.4–6 Globe lacerations result from sharp trauma (usually) due to the direct impact on the eyewall (force from outside inwards).4,5 Perforating injury is a specific type of globe laceration in which the projectile or sharp object has caused an entry as well as an exit full-thickness eyewall wound.4,5 In a penetrating injury only a single full-thickness eyewall wound is present per projectile/object (there is no exit wound).4,5 Finally, an intraocular foreign body (IOFB) is a type of penetrating laceration in which the foreign object is retained within the globe.4–6
FIGURE 20-1 Injury classification.
The above classification is not simply an academic exercise. It provides an effective means of communication between treating physicians but even more importantly the exact type of injury has specific implications to management and prognosis.4–6 Specifically, an open globe needs urgent operative repair, whereas a closed globe typically does not. Among open globes, globe rupture portends a poorer prognosis for final visual outcome than globe laceration.7,8Finally, an IOFB is usually best removed by a vitreoretinal surgeon and may require vitrectomy (sometimes not available in general ophthalmology operating rooms), whereas a penetrating or perforating injury can be managed by any ophthalmologist in an operating room with an ophthalmic operating microscope. Certainly in needed circumstances, primary closure can be achieved and the patient can be referred to a retina specialist for removal of an IOFB at a second procedure.
CLINICAL APPROACH TO EYE TRAUMA
It is imperative that concomitant nonocular injuries be evaluated and assessed on presentation to the emergency room. Involvement of the ophthalmologist in a timely manner and in the absence of life-threatening injury before transfer to the operating room is important. Sight-threatening injury needs to be recognized and treated within an appropriate time interval.
Every effort should be made to take a focused history—if not from the patient (if he or she is unconscious, distracted by other severe injuries, or under the influence of alcohol or drugs), then from relatives, bystanders, or first responders. In the setting of trauma, being time efficient is obviously of the utmost importance.
The most important aspect of the history is the mechanism of injury, as specific mechanisms suggest specific injuries that must be assessed for and treated. For example, hammering is associated with intraocular metallic foreign bodies, while fireworks injury is commonly associated with chemical injury that must be treated emergently (as well as contusion injury—rarely open globe). Injury to the forehead as a result of a bicycle accident followed by loss of consciousness is a common scenario in which traumatic optic neuropathy may develop, while injuries from BB guns are associated with globe lacerations with particularly poor prognosis. Additionally, it is important to elucidate the setting of the injury: penetrating injuries in a rural setting are associated with higher rates of endophthalmitis. Documenting whether protective eyewear was worn at the time of the injury is important for medicolegal reasons.
Patient symptoms are also important: floaters and a visual field defect are highly suggestive of a retinal detachment, while pain with sensitivity to light without compromise in the vision suggests a traumatic iritis (although a globe laceration and even an IOFB remain a possibility).
Past ocular history is important for two reasons. First, it may modify the effects of trauma, for example, in the case of a patient who has previously had a corneal transplant an open globe due to dehiscence of the graft will occur with much less force than normally expected. Similarly, in patients with previous cataract or glaucoma or radial keratotomy surgery the globe ruptures at the site of the previous wound. Second, past ocular history is important as preexisting pathology may dictate different treatment decisions following trauma. For example, the threshold for surgical evacuation of a hyphema would be much lower in a patient with advanced glaucomatous optic neuropathy than in a patient with healthy optic nerves.
Past medical history is similarly important as it can modify treatment decisions. For example, hyphema is managed differently in patients with sickle cell disease. Another example would be patients with pseudoxanthoma elasticum who invariably have angioid streaks and have a much higher risk of choroidal rupture. There are also several systemic conditions that result in eye conditions unrelated to trauma, an obvious example being diabetes mellitus causing diabetic retinopathy that can cause nontraumatic vitreous hemorrhage.
Important aspect of the drug history is whether the patient is on anticoagulants or antiplatelet agents as this will complicate operative repair. Additionally, determining allergies to medications is critical.
Review of systems must assess for the patient’s ability to survive anesthesia and surgical repair. Patients who cannot undergo surgery safely may be better managed medically even though the risk of losing their sight in one eye is evitable rather than dying from complications of anesthesia.
Clinical examination can be challenging due to pain or poor patient cooperation due to the influence of alcohol, drugs, or severe eyelid swelling; yet it is essential for proper diagnosis and management of ophthalmic trauma. The basic tool kit needed for rudimentary eye examination includes: penlight, near vision card, eyelid retractor/speculum, topical anesthetic, fluorescein strip, and eye wash.
It is no exaggeration to state that failure to document the visual acuity is inexcusable and akin to failure to document the pulse! Measuring visual acuity is crucial for three reasons. First, a specific level of vision prompts the examining physician to search for a diagnosis explaining it. For example, vision of hand motions only (HM) is not explained by a subconjunctival hemorrhage and requires the examiner to carefully examine for the other signs of a scleral rupture. Another example would be the patient who had trauma 3 days previously and presents to the emergency room with photosensitivity, mild lid edema, and vision of 20/400: before knowing this level of vision, traumatic iritis could have been contemplated but with vision of 20/400 endophthalmitis with a self-sealed corneal or scleral laceration becomes a strong possibility.
The second reason it is important to measure the visual acuity is to document a baseline so that later in the course it can be established whether there is improvement or deterioration. For example, a patient with a vitreous hemorrhage and vision of HM is seen by a vitreoretinal surgeon for examination to rule out retinal tears and detachment; if a week later the vision is 20/200 (and there are no retinal tears or detachment), further observation is reasonable as it appears that the vitreous hemorrhage is spontaneously resolving. In contrast, if a week later the vision is light perception, this suggests that a retinal detachment has occurred due to an undetected retinal tear.
The final reason why it is important to measure visual acuity is that visual acuity at presentation is a strong predictor for final visual outcome.7,8 Therefore, having an initial visual acuity is essential if discussing the prognosis of the injury with the patient.
Measuring visual acuity is relatively easy. Obviously each eye is tested separately by covering the other eye with an occluder (or the patient’s hand if there is no occluder available). The goal is to determine whether the patient has no light perception (NLP—cannot even see the light from a strong pen torch right in front of the injured eye with the room darkened), light perception only (LPO—can see the light but no hand movements), HM (can see hand movements but cannot count fingers), or vision between 1/200 and 20/20. When trying to measure vision between 1/200 and 20/20, the patient should be wearing his or her spectacles (if these are available). Counting fingers at a distance x is equivalent to x/200 (e.g., counting fingers at 2 ft is vision of 2/200). For vision better than 5/200 a Rosenbaum reading card or a Snellen or ETDRS visual acuity chart can be used. If none of these are available, documentation of ability to read the newspaper title (approximately 20/200) or the normal magazine print (approximately 20/40) is still extremely helpful.
Pupillary Examination (Shape, Reaction, and Relative Afferent Pupillary Defect)
The pupil may be peaked if there the iris is sealing (plugging) a corneal or anterior scleral laceration. The pupil may also be irregular if there has been injury to the iris sphincter muscle (typically a result of blunt trauma, commonly associated with hyphema).
The pupil will be dilated and not react to light if there is compression or damage to the third cranial nerve intracranially (following head trauma); if this is suspected, urgent neurosurgical consultation and computed tomography (CT) imaging is required. Additionally, an orbital compartment syndrome (due to retrobulbar hemorrhage or any cause for swelling within the orbit) may cause compression of the third nerve (and all the other nerves) and result in a fixed dilated pupil. Finally, if there has been damage or ischemia of the iris sphincter (very elevated intraocular pressure or torn iris sphincter), the pupil will not react to light.
A relative afferent pupillary defect (RAPD) is important to document for two reasons: first, its presence means that there is injury to the retina or optic nerve. This is important as it prompts the examiner to carefully consider the diagnoses that may be affecting the retina and optic nerve and not satisfy himself or herself with a diagnosis involving the anterior segment only. Second, the absence of an RAPD is a strong predictor of visual survival, with only 97% of eyes without an RAPD maintaining some vision.9
Measuring an RAPD is by alternately shining a strong light to each eye. At least 2 seconds should be spent shining each eye with 1 second in transit. When the pupils dilate when the light is shone into one of the eyes, it is said that an RAPD is present in that eye. It is important to note that it is the first movement of the pupil when the light is shone into it that matters. From the above, it should be obvious that even in a patient with a pupil that is immobile in the injured eye determination of the presence or absence of an RAPD in that eye is possible since the contralateral pupil movement can be observed while shining the light into the injured eye.
Examination of motility is important to rule out cranial nerve 3–6 injury in head trauma and also to detect muscle entrapment following an orbital fracture (typically inferior rectus muscle entrapment causing a deficit in elevation following an orbital floor fracture—in children this can be associated with severe, even life-threatening bradycardia due to the oculocardiac reflex).
Examination of motility is by asking the patient to follow an extended second digit or pen in all directions of gaze. It is important to ascertain whether the patient has diplopia when looking at any of these directions.
External and Ocular Adnexal Examination
Examination of the ocular adnexa involves looking at the eyelid position with eyes both open and closed, contour, and evidence of laceration. It is important to also evaluate for proptosis and in patients with proptosis, testing for resistance to retropulsion may point toward elevated intraocular pressure and congested orbital compartment. As part of the routine external examination, the examiner should palpate the orbital rim for “step off” in cases of suspected orbital fractures. In cases of suspected orbital floor fractures, testing sensation along the distribution of cranial nerve V on either cheek can be an early sign.
Slit Lamp Biomicroscopy
The slit lamp biomicroscope is the ideal instrument to examine the anterior segment. Portable versions exist for patients who cannot sit up to be examined with the regular slit lamp. If not even a portable slit lamp is available, a direct ophthalmoscope offers high magnification and can be used, and if even this is unavailable, a penlight with a blue filter and a magnifying lens can be used.
Throughout the examination of the anterior segment it is important to remember that pressure should not be exerted on the globe (as it may be open and it is uncomfortable to the patient)—rather the lids should be lifted and held up by applying pressure against the orbital rim.
Examination of the anterior segment starts with inspection of the conjunctiva and sclera. Subconjunctival hemorrhage is a common finding sometimes even after trivial trauma, but can be a sign of an open globe; therefore, the other signs of an open globe should be sought. Additionally, a subconjunctival hemorrhage can be a sign of a retrobulbar hemorrhage, especially if its posterior margin cannot be defined; therefore, the other signs of this condition should also be sought. Uveal tissue, vitreous gel, or even retina is sometimes evident on or under the conjunctiva in cases of scleral rupture or laceration.
Inspection of the cornea should be performed actively searching for a corneal laceration, a corneal foreign body, a corneal abrasion, and a corneal concussive injury to the endothelium (appears as opacity on the endothelium). A corneal abrasion may be more easily seen by applying fluorescein drops or a fluorescein strip in the tear lake and using the cobalt blue filter.
Examination of the anterior chamber should be performed looking for hyphema, hypopyon (layering of white cells inferiorly diagnostic of endophthalmitis in the setting of trauma), a shallow anterior chamber suggestive of open globe, an anterior chamber foreign body, and anterior chamber cell (white cells in the anterior chamber—are seen in endophthalmitis or traumatic iritis). Examination of the iris should be performed looking for iris tears or iris dialyses.
Finally, examination of the lens should be performed to determine whether it is present or not (it may have been lost in the case of a corneal laceration with extrusion of ocular contents or in the case of rupture at the site of prior cataract surgery with extrusion of the intraocular implant), whether it is subluxed, whether there is an intralenticular foreign body, or whether cataractous changes have developed.
There is no need to check the intraocular pressure if the globe is obviously open, but if not, measurement of the intraocular pressure is mandatory. Intraocular pressure is best measured using a Goldmann applanation device used with the slit lamp, but a Tono-Pen is a convenient device for use in the emergency room setting.
A high pressure can be seen with hyphema or with a retrobulbar hemorrhage (due to transmission of the elevated intraorbital pressure), while a low pressure is seen with an open globe or severe intraocular inflammation. It should be noted, however, that the intraocular pressure may on occasion be normal (rarely high) with an open globe.
Dilated fundoscopy is best performed using indirect ophthalmoscopy, a skill beyond the remit of a trauma surgeon. However, a direct ophthalmoscope can establish whether the view is clear or not (if not, either there is a problem with the cornea, anterior chamber, or lens or there is a vitreous hemorrhage), can detect a choroidal rupture and commotio retinae, or can document a normal posterior pole examination. Any patient with a vitreous hemorrhage needs indirect ophthalmoscopy for detection of retinal tears or peripheral retinal detachment.
B-mode ultrasonography is very useful for examination of the posterior segment in the presence of media opacities not allowing ophthalmoscopy. Retinal tears, detachments, and IOFBs can be detected. It should be noted that the investigation is strongly operator dependent and that even in experienced hands severe vitreous hemorrhage cannot be reliably distinguished from a retinal detachment.10
CT imaging is important in evaluating for orbital fractures, orbital foreign bodies, and IOFBs, especially metallic. An orbital CT scan with thin slices should be ordered. Note that the dimensions of foreign bodies are commonly exaggerated on CT images.10 It should also be noted that vegetable matter (such as wood) in the orbit is not well imaged by CT.
Initial Management of the Patient with Ocular Trauma
After the patient is stabilized (i.e., life-threatening injuries have been stabilized) other organ-threatening injuries need to be managed in parallel to evaluating the injured eye. The following are priorities when managing the injured eye:
1. Rule out a chemical injury by history (splash of liquid into the eye, explosion at chemical facility, firework injury). If there is suspicion of a chemical injury, a pH strip should be checked (from the fornix) and irrigation should be started at once (see Section “Chemical Injury”).
2. Rule out an open globe if possible: look for the specific signs (corneal/scleral laceration, prolapse of uveal tissue, hemorrhagic chemosis of the conjunctiva, low intraocular pressure, asymmetry in anterior chamber depth, vitreous hemorrhage). If there is reasonable suspicion of an open globe, exploration in the operating room should still be carried out (such as appendectomy; while one endeavors to reduce the rate of negative exploration, it is better to have a negative exploration than to miss the diagnosis). If there is an open globe or an open globe is suspected:
a. The patient needs urgent (as soon as possible and certainly within 12 hours) repair in the operating room by an ophthalmologist—the necessary arrangements need to be made (this may include transfer to a center with an operating microscope and available ophthalmologist, ophthalmology consult, etc.). Certainly a nil per os (NPO) order needs to be written and intravenous fluids started.
b. Place a shield to cover the eye and instruct the patient not to squeeze his or her lids or strain as this may cause further extrusion of intraocular contents; if a metal shield is not available, a cut Styrofoam cup may be taped over the eye. When taping the shield, it is important that the edge of the shield is secure over the orbital rim (i.e., make sure it is not pressing against the globe).
c. Order a CT scan to rule out an IOFB if the mechanism of injury suggests this is a possibility.
d. Administer tetanus toxoid.
e. Intravenous fluoroquinolone antibiotic (moxifloxacin, levofloxacin, or ciprofloxacin) needs to be considered in penetrating injury, especially when this occurred in a rural setting or if an IOFB is present.
f. Repair of lid lacerations or orbital fractures should never be undertaken before an open globe has been ruled out or repaired.
3. Identify other orbital or ocular injuries and treat accordingly (see Section “Specific Injuries and their Management”).
PROGNOSIS OF EYE TRAUMA
Prognosis of eye trauma involves discussion of three entities: whether the patient is going to retain his or her globe, what the patient may expect his or her vision to be in the long term, and finally whether this will affect the uninjured eye (see discussion on sympathetic ophthalmia below).
Whether a patient is going to retain his or her globe depends on the specifics of the traumatic injury. It is rare that enucleation will be required for an eye sustaining an injury other than an open globe. Primary enucleation is rare (0.17% of open globes) and reserved for eyes where the sclera and cornea have been injured so severely that they cannot be sutured back together (usually due to a blast injury where the eye has been blown away or a gunshot injury directly to the eye).11 Secondary enucleation (reported in 6–20% of open globes) is much more common for ruptures than lacerations and is usually performed for a blind (NLP), painful eye.7,9,11,12 An RAPD, NLP or LPO, visible uveal tissue, and concomitant eyelid laceration at presentation are risk factors for enucleation.7,11,12 Enucleation to prevent sympathetic ophthalmia is also sometimes performed, although it is controversial (see below).
The best system that predicts long-term visual outcome (after appropriate management including surgical treatment) is the ocular trauma score (OTS).8,13 In the OTS a functional outcome (initial visual acuity) and five signs or diagnoses (rupture, endophthalmitis, relative afferent papillary defect, retinal detachment, perforating injury) are used to estimate the likely visual outcome (Table 20-1).8
TABLE 20-1 Determination of Ocular Trauma Score
Many patients worry that a poorly seeing eye will cause “straining” of the other eye—this is unequivocally nonsense. However, the uninjured eye may develop sympathetic ophthalmia, a rare (incidence 0.03/100,000 per year),14bilateral uveitis that may occur 2 weeks to 50 years usually following eye trauma or surgery.15,16 While originally described as a consequence of trauma, currently it is more common following eye surgery.14 This is a consequence of improved management of ocular trauma, including prompt primary repair. Indeed, most cases with sympathetic ophthalmia following eye trauma present to the ophthalmologist several weeks after the initial trauma when the vision in the second eye is affected.17 Tellingly, since World War II there had been no cases of sympathetic ophthalmia reported in any military conflict until a single case in the recent war in Iraq.15 With current treatments, eyes affected with sympathetic ophthalmia commonly maintain functional vision with the majority maintaining reading vision.18 While removing the injured eye (when the vision is NLP) may decrease the rates of sympathetic ophthalmia, this is quite controversial given that sympathetic ophthalmia is rare (especially with appropriate management of the injured eye) and treatable.
SPECIFIC INJURIES AND THEIR MANAGEMENT
Chemical injuries to the eye are true ocular emergencies and time is of essence when treating acute chemical exposure. They represent 7.7–18% of ocular trauma.19–21 Immediate and copious irrigation is vital to limiting the extent of damage to the ocular surface. Alkaline agents tend to penetrate the eye more rapidly due to saponification of cell membranes and lead to liquefactive necrosis. Acidic agents cause coagulative necrosis with protein precipitation within the tissue; thus, acidic injuries tend to cause less severe injury compared to alkali agents due to less penetrative damaging effects.22 The nature of the toxic agent should be identified and brought into the emergency center if possible so that pH can be tested.
Following toxic chemical exposure to the ocular surface, irrigation should begin immediately with water, saline, or any commercially available eyewash with a neutral pH, and continued if possible while en route to the nearest emergency center. On arrival to the emergency center, an initial pH should be taken by placing pH testing paper in the inferior fornix. Irrigation should continue until the measured pH is neutral (7.2–7.4) for at least 5 minutes after irrigation has stopped. It is important to note that irrigation can last up to an hour or more depending on the severity of the splash injury in order for the eye’s pH to normalize.
Irrigation can be performed by directly pouring saline from intravenous tubing to the surface of the eye. Placing one drop of topical ophthalmic anesthetic such as proparacaine may help the patient to keep the affected eye open. Caution should be exercised when placing irrigation lenses such as a Morgan lens since retained particulate matter or foreign body can be trapped in the fornices of the eye. If an irrigation lens is to be used, the superior eyelid should be everted to look for embedded foreign body and both the superior and inferior fornices should be swept clean with a moist cotton swab to remove any particulate matter.
Chemical injuries are classified using the Roper-Hall classification system (Table 20-2). The size of the corneal epithelial defect and the clock hours of limbal ischemia should be documented after cessation of irrigation by drawing a circle to represent the cornea. Corneal epithelial defects can be easily detected using topical fluorescein staining, such as a moistened fluorescein strip or manufactured combination of fluorescein and topical anesthetic eye drops. Limbal ischemia appears as blanching of normal conjunctival and limbus blood vessels. Hyperemia in the setting of chemical injury presents better prognosis than a white eye.
TABLE 20-2 Classification of Severity of Ocular Surface Burns by Roper-Hall
Successful management of chemical ocular injury is to stop ongoing tissue degradation, promote reepithelialization of the surface, minimize inflammation, and prevent infection. For grade 1 damage, the patient can be treated with an antibiotic (e.g., erythromycin) or antibiotic/steroid mixed combination eye ointment (e.g., dexamethazone/polymyxin/neomycin) four times a day to the affected eye and a topical cycloplegic agent (e.g., atropine) to decrease ciliary spasm and decrease formation of posterior synechiae.22 For grade 2, topical steroid eye drops may need to be added to the regimen to decrease the inflammatory response for the first 1–2 weeks postinjury. In grades 3 and 4, high-dose vitamin C, 10 ascorbate eye drops, and 10% citrate eye drops have been associated with more rapid recovery and better vision.23 Oral doxycycline is a collagenase inhibitor and may reduce the risk of corneal thinning and perforation in severely burned eyes.24,25
Consultation with an ophthalmologist is necessary for follow-up and ensuring that the treatment regimen is leading to clinical improvement. Rarely is immediate surgical intervention needed in chemical injury patients.
Subconjunctival hemorrhage is a very common condition that presents as an ocular emergency. Clinically, subconjunctival hemorrhages appear as flat, bright red blood noted under the bulbar conjunctiva (Fig. 20-2). It can be alarming in appearance and although severity can be variable, in general, it is rather benign and poses no threat to vision.
FIGURE 20-2 Subconjunctival hemorrhage.
Spontaneous subconjunctival hemorrhage can be due to Valsalva maneuvers, coughing, sneezing, vomiting, or heavy lifting. Minor trauma such as excessive eye rubbing can also cause subconjunctival hemorrhages. Often, no specific etiology can be found. When subconjunctival hemorrhage is noted with other signs of facial or ocular trauma, one must rule out occult globe injury. Obtaining a good history is vitally important to determining if further workup is needed. A history of blunt trauma may present with subconjunctival hemorrhage but the patient may also have orbital fractures that need to be evaluated.
Patients who present with complete 360° of subconjunctival hemorrhage from blunt trauma should be examined by an ophthalmologist to rule out possible occult scleral rupture or open globe injury. Clues that may indicate occult open globe injury include: peaked pupil, asymmetric anterior chamber depth, asymmetrically low intraocular pressure, and subconjunctival pigment.
In cases of isolated subconjunctival hemorrhage, no treatment is needed. The hemorrhage will usually resolve spontaneously in a few weeks. Patients need to be informed that the hemorrhage will change color over the next few days and may expand as the bruising process evolves. These patients typically do not require ophthalmic follow-up.
Conjunctival lacerations may present in isolation or in combination with damage to deeper layers of the eyewall and the sclera. Isolated conjunctival lacerations do not require surgical repair unless they are large (e.g., >2 cm) or lie over an extraocular muscle insertion. Often it is difficult to assess if the sclera is involved without manipulation using a cotton tip swab to gently push away the conjunctiva exploring the scleral wall beneath. For large conjunctival lacerations or those that may involve the sclera, ophthalmic consultation is warranted.
Scleral penetration can be associated with vitreous hemorrhage and if the scleral defect is large enough, vitreous prolapse can be seen as well. If there is vitreous hemorrhage, the patient’s vision may be compromised. It is important to not engage the vitreous prolapsed through a scleral defect since traction on the vitreous strands can lead to retinal tears leading to rhegmatogenous retinal detachments.
Patients with corneal abrasions typically present with intense pain and photophobia. Trauma to the cornea from a fingernail, paper cut, thrown objects, and contusive injury (e.g., air bag) can result in the superficial corneal epithelium being stripped away from the underlying stroma. Simple corneal abrasions can be one of the most painful injuries that patients experience because beneath the corneal epithelium lies an extensive plexus of sensory nerves from the ophthalmic division of the trigeminal nerve and when they become exposed, severe pain results.
Corneal abrasions can be diagnosed clinically when topical fluorescein dye is taken up by the area devoid of epithelium and turns bright green viewed with a cobalt blue light. The size and location of the abrasion can be documented using a circle to represent the cornea. Traditional teaching advocated patching for corneal abrasions in the past. Currently, evidence shows that patients heal faster without patching, and also with patching, there is no benefit with regards to pain reduction. Small corneal abrasions without concomitant ocular injury can be managed and treated with antibiotic ophthalmic ointment, topical cycloplegic agent, and topical ophthalmic NSAID (e.g., ketorolac or diclofenac). Although there is no good evidence that topical ophthalmic antibiotic is indicated in cases where there was no recent history of contact lens wear and the injury with organic material, given the devastating sequela of corneal infection and scarring, use of a topical ophthalmic antibiotic is not unreasonable.26–33
History of contact lens wear or injury with organic material raises the risk of infection. These patients should never be patched given the elevated risk of infection, and referred for ophthalmic consultation. Patients with large corneal abrasions may benefit from bandage soft contact lens placed by an eye care professional for comfort. If the affected eye is patched, the patient should follow up next day with an eye care professional to monitor healing and assess for early signs of infection.
Corneal Foreign Bodies
Corneal foreign bodies are one of the most common forms of ocular trauma presenting second in frequency only to corneal abrasions in emergency centers.34 Most patients present with small superficial corneal foreign body with good or mildly affected vision. Individuals can have debris blown into the eye while walking outdoors or while performing high-risk activities such as grinding, drilling, hammering, and using a leaf blower. There are many causes for corneal foreign body, but lack of protective eyewear contributes to increased risk.
Specific questions regarding hammering metal on metal or grinding metal need to be asked and a detailed history regarding exactly the mechanism of injury helps to highlight patients at increased risk for penetrating ocular injury or IOFB. An initial exam should include looking at the corneal surface with magnification; if slit lamp is not readily available, surgical loupes can offer a better exam rather than the naked eye. Often a superficial corneal foreign body will be obvious, but it is important to evert and inspect under the upper eyelid and to look in the inferior fornix as well.
After a penetrating injury has been ruled out, superficial corneal foreign bodies can sometimes be easily removed with a moist cotton swab. Instill a topical ophthalmic anesthetic and moisten a sterile cotton swab with anesthetic, and then gently roll across the surface of the cornea and the foreign body may stick to the cotton tip. Irrigation with eyewash can also be utilized to loosen and remove the foreign body. If these maneuvers fail, ophthalmic consultation should be considered. Those foreign bodies that are moderately embedded in the anterior one third of the cornea can be removed at the slit lamp with a TB syringe or 25-gauge needle. Care must be exercised to not go too deep into the corneal tissue. The average central corneal thickness measures only 550 μm.
After removal of the corneal foreign body, start treatment as a corneal abrasion with ophthalmic ointment, cycloplegic agent, and topical antibiotic. Follow up with eye care provider to access if further debridement is indicated and to look for early signs of infection.
Corneal rupture is unusual unless the patient has had previous penetrating keratoplasty (corneal graft) or radial keratotomy. In the former case, dehiscence at the junction of the graft with the host cornea is common. In the latter, rupture occurs along the keratotomy as the cornea is very thin in that location. Loss of the crystalline lens or intraocular implant through the rupture site is sometimes observed. Management is by emergent operative repair, by closing the rupture site with 10-0 nylon sutures.
Corneal and/or scleral lacerations have better prognosis than ruptures with about 50% retaining vision of 20/40 or better (driving vision).35,36 Scleral/corneal lacerations limited in location to being anterior to the insertion of the recti muscles and those having a length <10 mm are associated with a better prognosis.37 Endophthalmitis is a major concern following penetrating injuries. An IOFB also needs to be ruled out.
A corneal laceration is evident on examination with a slit lamp biomicroscope although it can be usually seen by oblique illumination with a penlight. It is important to realize that smaller corneal lacerations can self-seal or be plugged by iris (which can result in a peaked pupil), allowing normal vision and a formed anterior chamber with normal or near-normal intraocular pressure. It is critically important to realize that eyes that have sustained a self-sealing laceration are first still at risk of endophthalmitis particularly if there is an IOFB and second are at risk for further extrusion of intraocular contents/low intraocular pressure if the patient applies pressure at immediately behind the laceration—say by rubbing the eye. Sadly, we have seen several eyes with undiagnosed self-sealed lacerations that developed endophthalmitis that was erroneously treated as traumatic iritis with steroids by unsuspecting emergency room physicians or pediatricians (with disastrous effects for the eye).
Corneal lacerations can be full thickness or partial thickness (lamellar laceration). A full-thickness laceration is classified under the general diagnosis of open globe. With lamellar or partial thickness lacerations, the globe is considered closed. The diagnosis of a full-thickness corneal laceration is often easy to recognize when there is protruding iris or uveal tissue (Fig. 20-3). In these cases, the anterior chamber may also be shallow or flat, which can be seen when shining a penlight from the lateral or temporal side of the eye.
FIGURE 20-3 Corneal laceration with protrusion of iris.
Some corneal lacerations may be combined and encompass the limbus and extend into sclera (aka corneal–scleral laceration). As with all open globe injuries, extreme care must be taken to prevent any direct pressure on the eye that may result in extrusion of intraocular contents. If corneal laceration is suspected, a metal shield (aka Fox shield) should be placed over the affected eye. The goal is to prevent any direct pressure or contact on the globe; soft eye patch should be avoided.
For partial thickness lacerations, depending on the size and depth of the laceration, simple observation with topical antibiotic prophylaxis up to suturing the partial thickness flap may be warranted. Due to the expertise needed to evaluate the depth of the laceration with a slit lamp, ophthalmic consultation should be sought in corneal lacerations.
Sclera Laceration or Rupture
Scleral rupture occurs in about 3.5% of eyes with severe blunt trauma.38 It most commonly involves the sclera immediately posterior to the recti muscle insertion (about 6–7 mm posterior to the limbus) as the sclera is thinnest at that location; in patients who have had previous surgery involving the sclera (most commonly a glaucoma filtration surgery) rupture at the site of the previous scleral wound may also occur.
Scleral rupture is invariably accompanied by rupture of the highly vascular choroid or ciliary body. As a result, hemorrhagic chemosis, hyphema, vitreous hemorrhage, or a combination of these is invariably present.38 Prolapsed uveal tissue appears dark brown or black while prolapsed vitreous gel appears as a transparent or blood-tinged blob of gel; since the mechanism of scleral rupture is due to an extreme elevation of intraocular pressure at the moment of blunt impact, the force causing the rupture is from the inside—prolapse of intraocular contents is therefore not uncommon, although it can be difficult to discern clinically as it may be covered by the hemorrhagic chemosis of the conjunctiva. Signs with the greatest specificity are a low intraocular pressure (<6 mm Hg), anterior chamber depth asymmetry (can be abnormally shallow or deep compared to fellow eye), and vision poorer than hand motions.35,38
Scleral rupture generally has poor outcomes with only 30–35% of eyes regaining ambulatory vision (i.e., vision that allows getting around without a guide).36 Moreover, scleral rupture is a risk factor for enucleation with up to 40% of eyes with scleral rupture being enucleated.7,12,35,36 Particularly poor predictors are scleral rupture greater than 11 mm, golf ball injury, and presenting vision of hand motions or worse.12,35
Treatment is by operative repair for scleral ruptures anterior to the equator that consists of excising necrotic uveal tissue, repositing viable uveal tissue and retina into the globe, and approximating the scleral edges using 8-0 nylon sutures. Posterior scleral ruptures are not accessible for repair (to access the posterior sclera, one would have to disinsert one or more of the recti muscles and pull to turn the eye that would cause further extrusion of intraocular contents making matters worse) and are allowed to heal by secondary intention.
Special Situation: Trauma in LASIK Patients
In 2007, more than 800,000 Americans underwent Laser-Assisted In Situ Keratomileusis (LASIK) vision correction surgery.39 The first clinical trial for LASIK refractive surgery was performed in 1995 and it has been a growing surgical procedure for the past 10 years. To perform LASIK, a thin corneal flap is first made and folded back to allow for laser remodeling of the corneal stroma. The flap is most commonly hinged either superiorly or nasally and floated back into position once laser remodeling is completed without any need for suturing. Since this is commonly done as an outpatient procedure in an ophthalmologist’s office or laser center, most patients do not consider this a significant part of their medical history.
It is important to recognize that both early and late traumatic flap dislocation and amputation have been reported in the literature. There are case reports of LASIK flap complications up to 7 years postsurgery. Minor blunt traumas with fingernail or sports-related injuries have been the reported cause of flap dislocation and amputation.40–42 Patients with LASIK flap dislocation and amputation will typically present with decreased vision and pain, and a very similar history to simple traumatic corneal abrasion patients. In fact, a complete amputation of the LASIK flap can look very much like a large corneal abrasion with fluorescein staining since the corneal epithelium is lost with the flap.
LASIK flap dislocation and amputations are treated very differently than a simple traumatic corneal abrasion and patients will need consultation with an ophthalmologist, preferably a corneal-refractive surgeon. Prognosis for early flap dislocation has generally been good and with later flap dislocation, vision recovery is generally acceptable. For patients with flap amputation, prognosis is poor due to development of irregular astigmatism and corneal haze and scarring. Given the large number of patients who have undergone this very popular procedure over the past 15 years, it is crucial to always ask specifically regarding prior history of refractive or LASIK surgery.
Hyphema is when blood accumulates in the anterior chamber (Fig. 20-4). It can present even after minor trauma in patients with impaired coagulation either idiopathic or medically induced. The presentation includes pain, photophobia, and decreased vision and on further examination with a penlight, a reddish pool of blood can be seen layered toward the inferior half of the anterior chamber due to gravity. If a patient has been recumbent, due to gravity, the hyphema may be layered over the pupil precluding a clear view to the posterior segment.
FIGURE 20-4 Hyphema.
The estimated annual incidence of hyphema is 17 patients in 100,000. The mean age of presentation is 25 years old with a higher prevalence in men over women. A hyphema does not rule out an open globe injury and up to one third of patients with traumatic hyphema can have concomitant open globe injury.43 Patients can also present with eyelid injuries or orbital fractures concurrently with hyphema (Fig. 20-5).
FIGURE 20-5 Hyphema and lid lac.
Concussive injury causes equatorial expansion of the eyeball with resulting damage to the iris, ciliary body, and major arterial circle of the anterior segment. Depending on the level of force exerted, differing levels of bleeding can be seen. Some patients may only have a microhyphema where a very small amount of red blood cells circulates in the anterior chamber but not enough blood is present to collect in the inferior part of the anterior chamber. These patients generally have very mild symptoms and can be managed similarly to traumatic iritis patients.
For patients who suffer more severe bleeding, the hyphema may completely fill the anterior chamber, also known as an “eight-ball” hyphema obscuring all anterior chamber details. Typically, the grading scale for hyphema is described by using an estimated percent layered in the anterior chamber. For example, a hyphema reaching mid-pupil level could be described as “50%” layered hyphema.
At the initial encounter, visual acuity, intraocular pressure, and grading of the hyphema severity should be documented. For patients of African American descent and others with known risk factors for hemoglobinopathies, a sickle cell prep or hemoglobin electrophoresis should be ordered along with other initial laboratory workup. This will provide important information for intraocular pressure management. For individuals with sickling hemoglobinopathies, carbonic anhydrase inhibitors are contraindicated and, thus, those who have elevated intraocular pressures may need surgical intervention.
For any patient with a layered hyphema regardless of percentage, an ophthalmic consultation is warranted since these patients will need close follow-up for the first 5 days after initial injury when the risk of rebleeding is highest. Also, patients who suffer concussive injury great enough to cause a layered hyphema are likely to have concomitant injury to other intraocular structures and have an increased risk of traumatic glaucoma resulting in permanent blindness in the future.
For patients who will need to be transferred for ophthalmic consultation, a clear or metal eye shield should be placed on the affected eye to protect from further injury. Depending on the interval until the patient is seen by an ophthalmologist, routine treatment for hyphema can be initiated with topical steroid eye drops (i.e., prednisolone acetate 1%) four times a day and a topical cycloplegic agent (i.e., 1% atropine) twice a day.
Traumatic Iritis/Mydriasis/Iris Sphincter Tears/Iridodialysis
With minimal blunt trauma to the eye, patients may suffer a mild inflammatory reaction known as traumatic anterior uveitis or traumatic iritis. Patients generally present with mild blurry vision, eye pain, and light sensitivity or photophobia. The symptoms can be immediate or delayed for 24–48 hours and examination often will reveal nothing more than mildly red eyes or conjunctival injection. However, if a slit lamp examination is done, an inflammatory reaction with circulating cells and flare can be seen in the anterior chamber.
Most cases will resolve within 1–2 weeks with topical steroid eye drop (1% prednisolone acetate, four times a day) and topical cycloplegic agent (1% atropine, twice a day). When prescribing cycloplegic agents, it is important to inform the patient that objects at near will be blurry in the treated eye due to the loss of accommodation from pharmacologic dilation. In patients who have long-standing anterior uveitis from any etiology, posterior synechiae or iris–lens adhesions can form. The use of a topical cycloplegic agent is not only for patient comfort but also as a preventative measure against formation of posterior synechiae (Fig. 20-6).
FIGURE 20-6 Posterior synechiae.
With more forceful blunt trauma, patients may suffer direct damage to the iris sphincter causing tears or traumatic mydriasis (seen near the pupil) or to the iris base causing iridodialysis (seen near the limbus). On initial examination, patients with traumatic mydriasis (dilation) or iris sphincter tears will have unequal pupil size and contour. Most patients may not complain acutely of symptoms but some will note the difference between the affected and unaffected eye in a mirror and question the etiology. There is no acute treatment for sphincter tears and traumatic mydriasis other than to treat the associated traumatic iritis.
With significant blunt force trauma, the longitudinal and radial fibers of the iris root can be torn apart at the ciliary body causing an iridodialysis. The diagnosis can easily be made with a penlight exam. The separation can occur at any clock hour and often will look as though a second pupil has been formed near the limbus. Sometimes, patients with large iridodialysis will complain of diplopia (seeing double) in the affected eye due to images being projected through the pupil and also simultaneously, the new iris defect.
Patients who suffer iris trauma need to be followed up with an ophthalmologist to monitor resolution of the inflammatory reaction and intraocular pressure, and assess potential damage to other anterior segment structures. For some patients with extensive iris damage, reconstructive anterior segment surgery may be warranted.
Traumatic Lens Injury
The lens is suspended like a hammock behind the iris by fibers called zonules that attach to the ciliary body and to the equator of the lens capsule. The lens is part of the total visual system and helps with vision and accommodation. Without the natural lens in position, patients would need a contact lens or intraocular lens placed to help visual rehabilitation. Thus, patients who suffer from lens dislocation will complain of decreased vision as well.
Three major traumatic injuries to the lens are lens dislocation/subluxation, traumatic cataract, and intralenticular foreign body. With blunt trauma, the zonules may break and cause the lens to dislocate either partially or completely depending on the amount of support remaining. A sign of zonular fiber loss may be seen at the slit lamp as iridodonesis, where the iris “jiggles” with rapid eye movements, or phacodonesis, where the lens shakes or moves with rapid eye movements. Typically, emergent intervention is not needed for lens subluxation or dislocation unless the lens is dislocated into the anterior chamber causing pupillary block, where the lens is obstructing aqueous flow from behind the pupil, or corneal endothelial decompensation, where the lens is in contact with the corneal endothelium.
Patients who have a history of prior cataract surgery with artificial intraocular lens placement can also experience artificial lens dislocation. They will also experience a decrease in vision since the artificial lens acts as a substitute for the natural lens and is part of the total visual system. Surgical intervention can usually be done to reposition or replace the intraocular lens as an outpatient on an elective basis.
Traumatic cataracts are generally seen months to years after the acute episode. They can result from blunt trauma, penetrating trauma, electrical shock, and ionizing radiation. Unilateral vision loss in young adults is most commonly due to unilateral traumatic cataract, most likely due to not only accidental trauma but also sports-related activities that routinely have associated blunt trauma such as boxing, soccer, and martial arts. Although traumatic cataracts may pose additional intraoperative risks, modern techniques for cataract removal are quite successful and yield excellent vision provided there are no retinal or optic nerve abnormalities.
Lenticular Foreign Body
Lenticular foreign body refers to the unusual occurrence of a small foreign body, usually metallic, being retained within the crystalline lens.44–46 On many occasions these have been well tolerated for many years without adverse effect as the anterior capsule heals over the site of entry into the crystalline lens. Indeed, toxicity would be expected to manifest by cataract formation and then prompt surgical removal by phacoemulsification would be advised.
Vitreous hemorrhage occurs in 30% of eyes with serious trauma. Its presence attests to the severity of the injury and is a marker for concomitant injury that is harder to detect due to its presence. Vitreous hemorrhage is invariably present in eyes with scleral rupture and may be present in penetrating injuries. In closed globe injury, it may be associated with iris sphincter tears, hyphema, and lens dislocation, while in the posterior segment associated findings include retina tear/detachment, traumatic macular hole, choroidal rupture, and traumatic optic neuropathy.47
Eyes with vitreous hemorrhage need to be examined carefully to rule out occult scleral rupture or laceration and concurrent retinal tears or detachment. If the severity of the vitreous hemorrhage does not allow sufficient visualization of the retina, B-mode ocular echography to detect retinal tears or detachment can be utilized as an acceptable alternative to direct visualization. It should be noted that when the vitreous hemorrhage is very severe, it is impossible to reliably detect a retinal detachment.
In the case of closed globe injury, management includes observation for 4–6 weeks as spontaneous resolution is common, with vitrectomy if faster visual rehabilitation is desired. Recently it has been suggested that early vitrectomy can prevent retinal complications, although convincing evidence for this is lacking thus far.
Intraocular Foreign Body
IOFBs are present in 30–40% of open globe injuries.48–50 In the vast majority (>85%) the patient is male.48,50–52 The IOFB is typically metallic (90%), usually iron, and results from hammering (60–70%) or use of a high-speed rotary tool.49,51,52 Glass foreign bodies can be found after car accidents, explosive blast injuries typically associated with terrorism, or assault with beer bottle.53 Stone and concrete represent less than 2% of IOFB, except in combat trauma where they are common after eye injury following explosion of roadside improvised explosive devices (IEDs).49–51 The majority of IOFBs are in the posterior segment (75%).52
Patient symptoms are dictated by the possible concomitant injury or complication (corneal laceration, scleral laceration, cataract, vitreous hemorrhage, endophthalmitis, retinal detachment). In every case of corneal or scleral laceration, even when self-sealing (i.e., not requiring operative repair), it is critically important to rule out IOFB by helical CT of the orbits. Additionally, any time a patient presents with ocular pain after hammering and subconjunctival hemorrhage, CT is essential to rule out IOFB as a scleral laceration may be present under the hemorrhage.
IOFBs are associated with an increased incidence of endophthalmitis that results in poorer visual outcomes after penetrating injury.54,55 Additionally, copper foreign bodies may incite severe inflammation and in the long term retained IOFBs may lead to retinal toxicity (e.g., iron IOFBs lead to ocular siderosis which among other effects leads to loss of vision due to retinal toxicity).56
While there is agreement that primary repair of open globe injury should be undertaken emergently, the timing of IOFB removal is controversial.52,54,57–59 IOFB removal from the posterior segment is usually performed by pars plana vitrectomy although for ferromagnetic IOFBs an external magnet can be used for smaller IOFBs if the requisite expertise for performing pars plana vitrectomy is not available.58–60
Commotio retinae (Berlin’s edema) is the term used to describe the opacified retina observed as a result of closed globe contusion injury to the retina. If the macula is involved, the vision will be affected. Spontaneous resolution is the rule with the long-term prognosis determined by concomitant retinal pigment epithelium injury.
Contusion of the retinal pigment epithelium is infrequently described, yet it is a common sequela of closed globe injury characterized by atrophic changes and mottling of the retinal pigment epithelium in the long term. It is an important cause of limited vision following such injury.61
Retinal tears/dialyses and detachment may arise following closed or open globe injury. The difference between retinal tears and dialyses is beyond the scope of this text but is significant when considering surgical repair of a detachment.
Following closed globe injury, the sudden expansion of the equatorial region of the eye results in the forced separation of the vitreous from the retina; in young individuals the vitreous may adhere strongly to the retina and its forced separation may result in tears in the retina or retinal dialysis. Usually vitreous hemorrhage (which can be very minor) occurs concomitantly due to bleeding from the vascular retina. In about 85% of patients with retinal tears or dialyses fluid passes under the tear/dialysis causing the retina to float away from the choroid, which is a retinal detachment.62
Patients with retinal tears may report floaters (black dots or “spider”-like opacities in their vision that move as the eye moves), while patients with a retinal detachment report a visual field defect (“dark area” or “curtain” in the vision, “like seeing underwater”). If the retinal detachment advances to include the fovea, patients will also report blurred vision. Timely treatment of retinal tears with laser retinopexy (or cryopexy) to reinforce the adhesion between retina and retinal pigment epithelium will prevent retinal detachment. Given that most traumas involve young individuals whose vitreous is more gel than fluid, only 12–30% of traumatic retinal detachments present immediately after trauma while 20% present more than 1 year after trauma.62–64 There is therefore ample opportunity to prevent retinal detachment after closed globe injury and it is imperative that a thorough examination of the fundus by indirect ophthalmoscopy by an experienced ophthalmologist is performed within a few days after such injury.
If a retinal detachment occurs, timely treatment (before the fovea is involved) can lead to preservation of excellent vision—therefore, a retinal detachment not involving the fovea needs to be repaired within 24 hours. Once the fovea is involved, the vision will never be normal; patients presenting with fovea-in-volving retinal detachments need to undergo repair within 1 week of presentation. When retinal detachments are not treated promptly, proliferative vitreoretinopathy (a process of scar formation in the vitreous cavity) supervenes and surgical outcomes are poorer (both anatomic and visual outcomes) and there is a greater risk of phthisis bulbi (globe becoming shrunk with opacification of the cornea). Treatment of retinal detachments is by scleral buckling if the cause is a dialysis, pars plana vitrectomy if there is a giant retinal tear, and pars plana vitrectomy or scleral buckling if the cause is a retinal tear.65,66
In open globe injury retinal tears commonly arise by the same mechanisms as in closed globe injury but may also be the direct result of the penetrating or perforating injury (e.g., a sharp projectile penetrating the eyewall and the choroid and retina causing a retinal tear); IOFBs may cause further retinal tears at the site of internal impact on the retina. Moreover, a hemorrhagic retinal detachment may arise from bleeding under the retina. Retinal detachment occurs in approximately 20% of open globe injuries.67 Treatment is by pars plana vitrectomy.
Traumatic Macular Hole
Traumatic macular holes usually arise as a consequence of blunt ocular trauma, typically from a fist or finger, a champagne cork, a ball (baseball, softball, soccer ball, tennis ball usually), or rubber band.68–70The typical symptom is a blurring of the central vision. It should be noted that development of a traumatic macular hole may be delayed by a few days or weeks following trauma.
Anatomic closure occurs spontaneously in 44–64% within the first 4–6 months.71,72 Pars plana vitrectomy with lifting of posterior hyaloid face and gas endotamponade successfully closes macular holes in up to 96% of patients and is indicated after a period of observation for spontaneous closure, 3–4 months.68–70 Improvement in vision usually accompanies anatomic closure but may be limited by RPE mottling/atrophic changes due to RPE concussive injury.
Chorioretinitis sclopetaria is a rare type of closed globe contusion injury due to a high-velocity projectile grazing the globe without penetrating it. Ophthalmoscopically there is a white area as sclera is visible surrounded by hyperpigmentation adjacent to the path of the projectile while remote to the path of the projectile is an area of hyperpigmentation and RPE atrophic changes with a characteristic severe epiretinal membrane, usually at the macular area.73,74 These appearances become apparent several weeks after the injury while immediately they are typically obscured by vitreous hemorrhage.73,74
Endophthalmitis is a devastating complication of ocular trauma occurring in 1–11% open globes,52,55,75–78 with a higher incidence (4–30%) when IOFBs are present.52,54,76 Delayed primary closure, presence of IOFB, disruption of the lens capsule, rural setting of injury, and possibly posterior segment involvement increase the risk of endophthalmitis.54,55,75,78 Common microorganisms are streptococci, staphylococci (especially with IOFBs), and Bacillus cereus, while gram-negative organisms occur in about 10% and fungi in fewer than 5% of injuries.54,77–79
Symptoms include severe to extreme pain, sensitivity to light, and decreased vision. Hypopyon (white blood cells/pus collection in the anterior chamber), fibrin in the anterior chamber (Fig. 20-7), vitreous inflammation, and sheathing of vessels are characteristic.78 Other signs commonly present are chemosis and erythema of the conjunctiva (which can be severe), severe tenderness, and lid edema. Sadly, we have seen several patients over the years misdiagnosed as having only traumatic iritis, which rarely would present with hypopyon or severe tenderness.
FIGURE 20-7 Hypopyon in an eye with corneal laceration and iris protrusion.
Endophthalmitis is a true ophthalmic emergency and in the case of virulent microorganisms such as Bacillus a few hours can make the difference between retaining the globe and losing it to phthisis. Suspicion of endophthalmitis should prompt an emergent ophthalmology consult and institution of systemic treatment with a fluoroquinolone (ideally fourth generation) as fluoroquinolones have excellent penetration into the vitreous and they are effective against B. cereus.80 Definitive management is by injection of intravitreous antibiotics with vitrectomy for selected cases.
Rupture of the choroid accompanies closed globe trauma more often than open globe trauma and is usually a consequence of injury with a ball (soccer ball), other large projectile (rock, shoe, etc.), or fist.81,82The choroidal rupture appears as a white crescent, typically concentric to the optic nerve and within the macula (>70%).81,82 Vision immediately following injury may be limited if the choroidal rupture is through or adjacent to the fovea or from associated subretinal hemorrhage (which resolves).
A treatable, long-term complication of choroidal ruptures in the macula, especially in older individuals, is choroidal neovascular membranes (CNVM: growth of new vessels from the choroid under the retina which tend to leak fluid or cause hemorrhage). Off-label intravitreous injection of bevacizumab or photodynamic therapy for CNVM due to choroidal rupture may lead to excellent visual outcomes if the patient presents early.83,84 Therefore, it is critically important to educate patients with choroidal rupture at risk of developing CNVM that if they develop a sudden change in vision or metamorphopsia (distortion in vision so that straight lines appear curved), they should see an ophthalmologist at once.
Traumatic Optic Neuropathy
Sharp objects, projectiles, or bone fragments may directly damage the optic nerve (direct traumatic optic neuropathy). Direct optic neuropathy is associated with severe loss of vision with little prospect of improvement. If suspected, imaging of the optic nerve (orbital CT) is recommended to detect the rare case where surgical relief of impingement of the optic nerve may improve vision.
More commonly, however, traumatic optic neuropathy results from concussive head injury, especially involving impact to the forehead (indirect traumatic optic neuropathy). In indirect optic neuropathy, impact forces are transmitted from the frontal bone to the orbital bones and concentrated in the area of the optic canal causing a shearing injury to neuronal axons of the intracanalicular portion of the optic nerve.85,86
Patients with indirect traumatic optic neuropathy are usually young, male (85%), have commonly lost consciousness, and have typically sustained their injury as a result of involvement in a motor vehicle or bicycle accident (about 50%), fall, or assault.87,88 Patients notice a typically unilateral decrease in vision immediately or after regaining consciousness.87,88 The severity of visual loss is often dramatic (40% have NLP and a further 23% only have light perception or hand motions vision). In cases with less dramatic visual loss, symptoms may include visual field defects and abnormalities of color vision.87,88 On examination an RAPD is present but the fundoscopic examination is normal until several weeks after the injury when optic nerve pallor/atrophy becomes apparent.
Spontaneous improvement has been reported in up to 57% of patients with indirect traumatic optic neuropathy.87,88 The regimen employed in the Second National Acute Spinal Cord Injury Study (NASCIS) of an initial dose of 30 mg/kg methylprednisolone followed by continuous infusion of 5.4 mg/(kg h) for 24–48 hours has been used for the treatment of traumatic optic neuropathy despite lack of evidence for efficacy in this condition.87–92 Indeed, several comparative studies have failed to show benefit from the use of megadose or high-dose corticosteroids over placebo for indirect traumatic optic neuropathy.87,88,93 Moreover, recently the CRASH study demonstrated excess mortality for patients with significant closed head injury who were given corticosteroids compared to placebo.94 Therefore, the role, if any, of megadose steroids in the treatment of this condition is controversial. Finally, surgical decompression has been performed with encouraging results in several case series but with no evidence that results are superior to observation.95
Optic Nerve Avulsion
Optic nerve avulsion is a specific type of indirect traumatic optic neuropathy with a distinct pathogenesis. In optic nerve avulsion a blunt object (typically a finger, unusually a snooker cue or golf club) is inserted between the globe and orbit and causes abrupt rotation of the globe as well as a sudden increase in intraocular pressure resulting in retraction of the optic nerve within its dural sheath. The clinical appearance is striking once the accompanying hyphema or vitreous/subhyaloid hemorrhage clears: there is a hole or cavity where the optic disc has retracted within its dural sheath.96,97 Prognosis is guarded, with limited potential for spontaneous improvement and no effective treatment.
The approach to a patient with eyelid trauma must be systematic and take into account a detailed history to rule out open globe injuries that may preclude repair of the eyelid until the globe can be surgically closed. There are multiple types of eyelid injury and a patient can have more than one type depending on the mechanism of injury. These include:
1. Contusion: blunt impact injury with superficial soft tissue swelling and ecchymoses
2. Abrasion: scraping causing superficial epithelial skin loss
3. Avulsion: shearing or tearing away of tissue
4. Puncture: defect through multiple tissue planes caused usually by sharp objects
5. Laceration: cut tissue can be superficial or deep, usually caused by sharp objects
For patients with isolated eyelid contusion and abrasion, conservative medical management with ice packs and antibiotic ointment is usually all that is required. Given time, the healing and reepithelialization of the skin gives good results.
For eyelid avulsion, puncture, and laceration, surgical repair is generally needed. Depending on the patient’s age, mental status, and size of injury, repair may be done at the bedside with local anesthesia, preferably with 2% lidocaine with epinephrine for better hemostasis. Deeper tissue involvement, full thickness, marginal, or lacrimal duct involvement will generally require involvement of an ophthalmologist or oculoplastic surgeon to repair. Signs that may clue into deeper tissue involvement include orbital fat prolapse, exposed sclera under the laceration, and medial canthal involvement.
Once an eyelid laceration is suspected, a plan to explore the extent of the injury needs to be formulated. Since soft tissue swelling can distort the natural anatomy and create the false impression of missing tissue due to excessive tension when approximating tissue margins, ice packs applied to the wound can help to decrease swelling before manipulation. Importance is given to be sure that an occult open globe injury has been ruled out before exploration of the eyelid laceration (Fig. 20-8).
FIGURE 20-8 Lid lac.
When exploring an eyelid laceration, anesthetize the tissues prior to cleansing and gently pull lacerated tissues apart during your inspection as fibrin tends to hold these lacerated edges together giving an inaccurate impression on the level of deep tissue involved. It is important to reapproximate the deep tissue layers to avoid undue excess tension on the superficial layers. The timing of eyelid laceration repair is more forgiving than most other ocular injuries due to the well-vascularized tissues of the eyelid. In some cases of extensive swelling, waiting 24–72 for eyelid repair can give a better anatomic and cosmetic result.
For subcutaneous closure, an absorbable suture is preferred such as 5-0 polyglactic acid (Vicryl®, Ethicon, Somerville, NJ) on a spatulated needle to close deeper tissues. This same suture size can be used above and below the brow or to secure tissue to the periosteum. For skin closure, nylon suture is preferred because it creates the least amount of inflammation, but if follow-up for removal of the sutures in 7–10 days cannot be assured, it is better to use an absorbable suture. 6-0 sutures can be used for closure above and below the brow; some oculoplastic surgeons advocate using a smaller suture size such as 7-0 for closure below the brow.
Patients with orbital injuries such as orbital wall and floor fractures typically will have concomitantly significant facial trauma. These patients will need to be simultaneously managed with head and neck, oral maxillofacial, or plastic surgeons. An orbital CT scan should be obtained to optimally diagnose and manage orbital injuries. Many times, specific orbital cuts can be added to a standard face CT scan protocol when initially ordered to evaluate the patient with facial trauma.
Neurosurgery consultation may be necessary for patients with orbital roof fractures, which can happen after significant trauma, usually from motor vehicle accidents or falls from heights. These fractures can often include complications of CSF leaks due to dural tears, intracranial hemorrhage, traumatic encephalocele, and brain abscesses or meningitis.
The orbit is comprised of many bony structures with the purpose of protecting the globe. The orbital roof and lateral wall have the thickest walls. The thinnest wall is the medial wall comprised of the ethmoidal bone, also known as the lamina papyracea, and the orbital floor medal to the infraorbital groove. Contusive orbital injuries can lead to a “blowout” fracture of these thin areas.
The quality of the thin bones in orbital blowout fractures actually provides a protective feature, where a large area of the orbital floor and medial wall has given way allowing for decompression of the orbital contents. This expanded volume into the sinuses allows for decreased congestion in the orbital space. A pure blowout fracture does not include fracturing of the orbital rim.
When evaluating a patient with potential orbital fracture, one of the clues to diagnosing an orbital floor fracture is decreased skin sensation on the cheek of the affected side. The infraorbital nerve, a branch of the trigeminal nerve, travels through the infraorbital canal and within the floor to exit just under the inferior orbital rim at the infraorbital foramen. This nerve is often affected when traumatized by orbital floor fractures and presenting with hypoesthesia of the cheek. Another clue can be subcutaneous emphysema that often results from the patient blowing his or her nose forcing air into the tissues.
Since up to one third of patients with orbital blowout fractures will have other accompanying ocular injuries, such as corneal abrasion, iritis, hyphema, ruptured globe, retinal detachment, and retinal hemorrhage, it is important to examine these patients systematically with the eight-point eye exam to diagnose correctly and treat more sight-threatening conditions first.
Once an orbital wall or floor fracture has been diagnosed, patients must be given instructions to not blow their nose since this can cause further expansion of air into the orbital tissue and can lead to a tight orbit and elevated intraocular pressure. Patients can use ice packs during the first 48 hours to help with reduction of the soft tissue swelling and for patients who need surgical repair, this is usually done in the next 1–2 weeks.
Management and treatment of orbital floor fractures will be discussed in Chapter 21.
Intraorbital Foreign Bodies
Intraorbital foreign bodies can result from both blunt and sharp objects, usually as a result of assault, industrial accidents, accidents at home, or recreational activities. They can cause vision loss if the globe is involved, or in case of neurologic damage from intracranial extensions. A high index of suspicion is important in evaluating patients with recent or remote history with persistent periocular inflammation. Signs and symptoms of retained intraorbital foreign bodies include:
1. Orbital mass
3. Painful or restricted eye movements
7. Orbital cellulitis
8. Draining sinus tract
9. Gaze-evoked amaurosis (transient loss of vision)
An orbital CT scan is the preferred imaging modality since metallic foreign bodies are contraindicated for MRI scan; once a metallic foreign body is ruled out, an MRI scan may be better at detecting organic matter such as wood. Depending on the size and extension of the foreign body, neurosurgery and/or otorhinolaryngology consultation may be necessary to safely remove the foreign body.
Not all orbital foreign bodies need to be removed. Certain inert metals, glass, plastic, and silicone can be left in place as long as there is no optic nerve impingement. Foreign bodies made from iron should be removed since long-term toxicity can occur leading to vision loss and retinal damage from siderosis.
Orbital Compartment Syndrome
The orbit is susceptible to compartment syndrome due to its small size and the bony walls of the orbit lacking the ability to stretch or flex. The normal orbital volume is 30 cm3. Trauma directly to the orbit or to other regions of the face resulting in fractures can cause bleeding into retrobulbar, subperiosteal, extraconal, and/or intraconal spaces of the orbit with rapid expansion in orbital distention. Rapid escalation in orbital compartmental pressure can cause ischemia of the orbital tissues and increased intraocular pressure can lead to damage and permanent vision loss. Patients with large orbital floor and wall fractures have less risk for developing orbital compartment syndrome since the orbital contents can be decompressed into the sinuses.
Proptosis and taut orbital content or increased resistance to retropulsion on examination is always seen in orbital compartment syndrome. Depending on the extent of orbital congestion, patients with mild compartment syndrome have only mildly elevated intraocular pressures without visual compromise, and can be treated with glaucoma agents topically or orally. Once intraocular pressures exceed 40 mm Hg despite antiglaucoma therapy in an orbital compartment syndrome patient, close monitoring of vision and pupillary response will help guide need for lateral canthotomy and cantholysis.
On the rare occasion, a patient may have bleeding into the optic nerve sheath causing direct impingement and compression of the optic nerve, or a bony fragment from posterior fractures can compress on the optic nerve causing an RAPD. Thus, reviewing the orbital imaging is important to rule out such cases that will need to be referred to an oculoplastic surgeon for urgent optic nerve sheath fenestration.
Patients with mild compartment syndrome should not have any signs of optic nerve compromise and a patient with an RAPD and decreased vision may need urgent decompression with emergent canthotomy and cantholysis of the lateral canthal tendon performed at the bedside. This works to allow the taut orbital content to prolapse anteriorly out of the orbit. Success is measured by improved vision, lower intraocular pressure, and reversal of optic nerve compromise or RAPD. If the orbital compartment syndrome is not decompressed adequately with a lateral canthotomy and cantholysis, consultation with an oculoplastic surgeon is warranted to decompress the orbit via bony decompression.
Steps to perform a lateral canthotomy and inferior cantholysis are as follows:
1. Obtain informed consent if patient is able to cooperate.
2. Prep and drape the affected eye.
3. Anesthetize with 2% lidocaine with epinephrine in the lateral canthal region. Make sure to infiltrate subcutaneously and subconjunctivally.
4. Allow the anesthetic to take effect and clamp a hemostat over the lateral canthus vertically; this will help direct the cut in the next step.
5. Using Steven scissors, place one blade on the conjuntival side of the later canthus and the other blade on the skin surface, and then cut the lateral corner of the eyelid while applying lateral pressure.
6. The inferior crus of the lateral canthal tendon will need to be cut to release the lower eyelid from the lateral orbital wall. Taking the scissors with blades closed, strum the inferior tendon inside the cut canthotomy wound. The attachment should feel like a firm, tense cord. Now, open the blades of the scissors and cut the cordlike structure until the lower eyelid becomes freely mobile.
7. Hemostasis can be achieved with pressure or the use of handheld cautery if available.
WHEN TO OBTAIN CONSULTATION WITH AN OPHTHALMOLOGIST
While some cases will be grossly evident in need of a consultation with ophthalmology (Fig. 20-9), others may be more subtle, such as an occult scleral laceration or open globe injury from a full-thickness eyelid laceration (Fig. 20-10). The key in successfully managing patients with ocular injury is to perform a systematic exam and use a common vocabulary to communicate those findings with the consultant.
FIGURE 20-9 Intraocular foreign body.
FIGURE 20-10 Open globe.
The role of the emergency care provider or trauma surgeon with regards to ocular trauma is to recognize common traumatic eye injuries that can be managed immediately and be able to refer sight-threatening conditions appropriately for ophthalmic follow-up. While there are a few true ophthalmic emergencies—open globe, chemical injury, endophthalmitis, and orbital compartment syndrome—many isolated ocular injuries in an otherwise healthy individual can often be managed outside of the emergency room setting. Like injury to any other organ system, potential long-term complications require follow-up with specialists.
1. Negrel AD, Thylefors B. The global impact of eye injuries. Ophthalmic Epidemiol. 1998;5:143–169.
2. Guly CM, Guly HR, Bouamra O, et al. Ocular injuries in patients with major trauma. Emerg Med J. 2006;23:915–917.
3. Klein BE, Klein R. Lifestyle exposures and eye diseases in adults. Am J Ophthalmol. 2007;144(6):961–969.
4. Kuhn F, Morris R, Witherspoon CD, et al. A standardized classification of ocular trauma. Ophthalmology. 1996;103:240–243.
5. Kuhn F, Morris R, Witherspoon CD, et al. A standardized classification of ocular trauma. Graefes Arch Clin Exp Ophthalmol. 1996;234:399–403.
6. Pieramici D, Sternberg P, Aabert TM, et al. A system for classifying mechanical injuries of the eye (globe). Am J Ophthalmol. 1997;123: 820–831.
7. Rahman I, Maino A, Devadason D, Letherbarrow B. Open globe injuries: factors predictive of poor outcome. Eye. 2006;20:1336–1341.
8. Kuhn F, Maisiak R, Mann L, et al. The ocular trauma score. Ophthalmol Clin North Am. 2002;15:163–166.
9. Schmidt GW, Broman AT, Hindman HB, Grant MP. Vision survival after open globe injury predicted by classification and regression tree analysis. Ophthalmology. 2008;115:202–209.
10. Kuhn F. Ocular Traumatology. New York: Springer; 2008.
11. Savar A, Andreoli MT, Kloek CE, Andreoli CM. Enucleation for open globe injury. Am J Ophthalmol. 2009;147:595–600.
12. Hyun Lee S, Ahn JK. Emergent risk factors associated with eyeball loss and ambulatory vision loss after globe injuries. J Trauma. 2010;69: 195–198. DOI:10.1097/TA.0b013e3181bbd23b.
13. Man CYW, Steel D. Visual outcome after open globe injury: a comparison of two prognostic models—the ocular trauma score and the classification and regression tree. Eye. 2010;24:84–89.
14. Kilmartin DJ, Dick AD, Forrester JV. Prospective surveillance of sympathetic ophthalmia in the UK and Republic of Ireland. Br J Ophthalmol. 2000;84:259–263.
15. Castiblanco CP, Adelman RA. Sympathetic ophthalmia. Graefes Arch Clin Exp Ophthalmol. 2009;247:289–302.
16. Sen HN, Nussenblatt RB. Sympathetic ophthalmia: what have we learned? Am J Ophthalmol. 2009;148:632–633.
17. du Toit N, Motala MI, Richards J, et al. The risk of sympathetic ophthalmia following evisceration for penetrating injuries at Groote Schuur Hospital. Br J Ophthalmol. 2008;92:61–63.
18. Galor A, Davis JL, Flynn HW, et al. Sympathetic ophthalmia: incidence of ocular complications and vision loss in the sympathizing eye. Am J Ophthalmol. 2009;148:704–710.
19. Jones NP, Hayward JM, Khaw PT, et al. Function of an ophthalmic accident and emergency department: results of a six month survey. Br Med J. 1986;292:188.
20. Pfister RR. Chemical injury of the eye. Ophthalmology. 1983;90:1246.
21. Liggett P. Ocular trauma in an urban population. Ophthalmology. 1989;97:581.
22. Yu JS, Ralph RA, Rubenstein JB. Ocular burns. In: MacCumber MW, ed. Management of Ocular Injuries and Emergencies. Philadelphia: Lippincott-Raven; 1998:163–171.
23. Brodovsky SC, McCarty CA, Snibson G, et al. Management of alkali burns: an 11 year retrospective review. Ophthalmology. 2000;107(10): 1829.
24. Perry HD, Hodes LW, Seedor JA, et al. Effect of doxycycline hyclate on cornel epithelial wound healing in the rabbit alkali-burn model: preliminary observation. Cornea. 1993;12(5):379.
25. Ralph RA. Tetracyclines and the treatment of corneal stromal ulceration: a review. Cornea. 2000;19:274.
26. Patterson J, Fetzer D, Krau J, et al. Eye patch treatment for the pain of corneal abrasion. South Med J. 1996;89:227.
27. Hart A, White S, Conboy P, et al. The management of corneal abrasion in accident and emergency. Injury. 1997;28:527.
28. Arbour JD, Brunette I, Boisjoly HM, et al. Should we patch corneal erosions? Arch Ophthalmol. 1997;115:313.
29. Solomon A, Halpert M, Frucht-Perry T. The use of topical indomethacin and eye patching for minor corneal trauma. Arch Ophthalmol. 2000;32:316.
30. Kaiser PK, Pineda R. A study of topical non-steroidal anti-inflammatory drops and no pressure patching in the treatment of corneal abrasions. Corneal Abrasion Patching Study Group. Ophthalmology. 1997;104:1353.
31. May DR, Kuhn FP, Morris RE, et al. The epidemiology of serious eye injuries from the United States Eye Injury Registry. Graefes Arch Clin Exp Ophthalmol. 2000;238:153.
32. Xiang H, Stallones L, Guanmin C, et al. Work-related eye injuries treated in hospital emergency departments in the U.S. Am J Ind Med. 2005;48:57.
33. Hemady RK. Ocular injury from violence treated at city hospital. J Trauma. 1994;37:5.
34. Hamill MB. Corneal injury. In: Brachmer JH, Mannus MJ, Holland EJ, eds. Cornea: Fundamentals of Cornea and External Disease. Vol. 2. St. Louis: Mosby; 1997:1416–1419.
35. Russell SR, Olsen KR, Folk JC. Predictors of scleral rupture and the role of vitrectomy in severe blunt ocular trauma. Am J Ophthalmol. 1988;105:253–257.
36. Pieramici DJ, MacCumber MW, Humayun MU, et al. Open-globe injury update on types of injuries and visual outcomes. Ophthalmology. 1996;103:1798–1803.
37. Sternburg P, De Juan E, Michels RG, Auer C. Multivariate analysis of prognostic factors in penetrating ocular injuries. Am J Ophthalmol. 1984;98:467–472.
38. Klystra JA, Lamkin JC, Runyan DK. Clinical predictors of scleral rupture after blunt ocular trauma. Am J Ophthalmol. 1993;115:530–535.
39. LASIK eye surgery. New York Times. Available at: http://www.nytimes.com. Accessed April 24, 2008.
40. Tetz M, Werner L, Muller M, et al. Late traumatic LASIK flap loss during contact sport. J Refract Surg. 2007;33:1332–1335.
41. Srinivasan M, Prasad S, Prajna P. Late dislocation of Lasik flap following fingernail injury. Indian J Ophthalmol. 2004;52:327–328.
42. Cheng AC, Rao SK, Leung GY, et al. Late traumatic flap dislocations after LASIK. J Refract Surg. 2006;22(5):500–504.
43. Walton W, Von Hagen S, Grigorian R, et al. Management of traumatic hyphema. Surv Ophthalmol. 2002;47(4):297–334.
44. Cazabon W, Dabbs TR. Intralenticular metallic foreign body. J Cataract Refract Surg. 2002;28:2233–2234.
45. Dhawahir-Scala FE, Kamal A. Intralenticular foreign body: a D-day reminder. Clin Exp Ophthalmol. 2005;33:659–664.
46. Tokoro M, Yasukawa T, Okada M, et al. Copper foreign body in the lens without damage of iris and lens capsule. Int Ophthalmol. 2007;27: 329–331.
47. Yeung L, Chen TL, Kuo YH, et al. Severe vitreous hemorrhage associated with closed-globe injury. Graefes Arch Clin Exp Ophthalmol. 2006;244: 52–57.
48. Cillino S, Casuccio A, Di Pace F, et al. A five-year retrospective study of the epidemiological characteristics and visual outcomes of patients hospitalized for ocular trauma in a Mediterranean area. BMC Ophthalmol. 2008;8:6. DOI:10.1186/1471-12415-8-6.
49. Imrie FR, Cox A, Foot B, MacEwen CJ. Surveillance of intraocular foreign bodies in the UK. Eye. 2008;22:1141–1147.
50. Weichel ED, Colyer MH, Ludlow SE, et al. Combat ocular trauma visual outcomes during operations Iraqi and Enduring Freedom. Ophthalmology. 2008;115:2235–2245.
51. Woodstock MGL, Scott RAH, Huntbach J, Kirkby GR. Mass and shape as factors in intraocular foreign body injuries. Ophthalmology. 2006;113:2262–2269.
52. Ehlers JP, Kunimoto DY, Ittoop S, et al. Metallic intraocular foreign bodies: characteristics, interventions, and prognostic factors for visual outcome and globe survival. Am J Ophthalmol. 2008;146:427–433.
53. Ghoraba H. Posterior segment glass intraocular foreign bodies following car accident or explosion. Graefes Arch Clin Exp Ophthalmol. 2002;240:524–528.
54. Essex RW, Yi Q, Charles PGP, Allen PJ. Post-traumatic endophthalmitis. Ophthalmology. 2004;111:2015–2022.
55. Andreoli CM, Andreoli MT, Kloek CE, et al. Low rate of endophthalmitis in a large series of open globe injuries. Am J Ophthalmol. 2009;147: 601–608.
56. Cibis PA, Yamashita T, Rodriguez F. Clinical aspects of ocular siderosis and hemosiderosis. Arch Ophthalmol. 1959;62:180–187.
57. Chaudhry IA, Shamsi FA, Al-Harthi E, et al. Incidence and outcome of endophthalmitis associated with intralenticular foreign body. Graefes Arch Clin Exp Ophthalmol. 2008;246:181–186.
58. Colyer MH, Weber ED, Weichel ED, et al. Delayed intraocular foreign body removal without endophthalmitis during operations Iraqi Freedom and Enduring Freedom. Ophthalmology. 2007;114:1439–1447.
59. Wani VB, Al-Ajmi M, Thalib L, et al. Vitrectomy for posterior segment intraocular foreign bodies. Retina. 2003;23:654–660.
60. Greven CM, Engelbrecht NE, Slusher MM, Nagy SS. Intraocular foreign bodies management, prognostic factors and visual outcomes. Ophthalmology. 2000;107:608–612.
61. Seider MI, Lujan BJ, Gregori G, et al. Ultrahigh resolution spectral domain optical coherence tomography of traumatic maculopathy. Ophthalmic Surg Lasers Imaging. 2010;41:144.
62. Johnston PB. Traumatic retinal detachment. Br J Ophthalmol. 1991; 75:18–21.
63. Goffstein R, Burton TC. Differentiating traumatic from non-traumatic retinal detachment. Ophthalmology. 1982;89:361–368.
64. Cox MS, Schepens CL, Freeman HM. Retinal detachment due to ocular contusion. Arch Ophthalmol. 1966;76:678–685.
65. Ersanli D, Sonmez M, Unal M, Gulecek O. Management of retinal detachment due to closed globe injury with pars plana vitrectomy with and without scleral buckling. Retina. 2006;26:32–36.
66. Aylward GW, Cooling RJ, Leaver PK. Trauma-induced retinal detachment associated with giant retinal tears. Retina. 1993;13:136–141.
67. Liggett PE, Gauderman WJ, Moreira CM, et al. Pars plana vitrectomy for acute retinal detachment in penetrating injuries. Arch Ophthalmol. 1990;108:1724–1728.
68. Johnson RN, McDonald HR, Lewis H, et al. Traumatic macular hole—observations, pathogenesis, and results of vitrectomy surgery. Ophthalmology. 2001;108:853–857.
69. Amari F, Ogino N, Matsumura M, et al. Vitreous surgery for traumatic macular holes. Retina. 1999;19:410–413.
70. Chow DR, Williams GA, Trese MT, et al. Successful closure of traumatic macular holes. Retina. 1999;19:405–409.
71. Yamashita T, Uemara A, Uchico E, et al. Spontaneous closure of traumatic macular hole. Am J Ophthalmol. 2002;133:230–235.
72. Mitamura Y, Saito W, Ishida M, et al. Spontaneous closure of traumatic macular hole. Retina. 2001;21:385–389.
73. Beatty S, Smyth K, Au Eong KG, Lavin MJ. Chorioretinitis sclopetaria. Injury. 2000;31:55–60.
74. Martin DF, Awh CC, McCuen BW, et al. Treatment and pathogenesis of traumatic chorioretinal rupture (sclopetaria). Am J Ophthalmol. 1994;117:190–200.
75. Duch-Samper AM, Menezo JL, Hurtado-Sarrio M. Endophthalmitis following penetrating eye injuries. Acta Ophthalmol Scand. 1997;75: 104–106.
76. Verbraeken H, Rysselaere M. Post-traumatic endophthalmitis. Eur J Ophthalmol. 1994;4:1–5.
77. Chhabra S, Kunimoto DY, Kazi L, et al. Endophthalmitis after open globe injury: microbiologic spectrum and susceptibilities. Am J Ophthalmol. 2006;143:852–856.
78. Zhang Y, Zhang MN, Jiang CH, et al. Endophthalmitis after open globe injury. Br J Ophthalmol. 2010;94:111–114.
79. Lieb DF, Scott IU, Flynn HW, et al. Open globe injuries with positive intraocular cultures. Ophthalmology. 2003;110;1560–1566.
80. Cebulla CM, Flynn HW. Endophthalmitis after open globe injuries. Am J Ophthalmol. 2009;147:568–569.
81. Shortsleeve Ament C, Zacks DN, Lane AM, et al. Predictors of visual outcome and choroidal neovascular membrane formation after traumatic choroidal rupture. Arch Ophthalmol. 2006;124:957–966.
82. Wyszynski RE, Grossniklaus HE, Frank KE. Indirect choroidal rupture secondary to blunt ocular trauma. Retina. 1988;8:237–243.
83. Artunay O, Rasier R, Yuzbasioglu E, et al. Intravitreal bevacizumab injection in patients with choroidal neovascularization due to choroid rupture after blunt-head trauma. Int Ophthalmol. 2009;29: 289–291.
84. Harissi-Dagher M, Sebag M, Gauthier D, et al. Photodynamic therapy in young patients with choroidal neovascularization following traumatic choroidal rupture. Am J Ophthalmol. 2005;139:726–728.
85. Anderson RL, Panje WR, Gross CE. Optic nerve blindness following blunt forehead trauma. Ophthalmology. 1992;89:445–455.
86. Gross CE, DeKock JR, Panje WR, Hershkowitz N, Newman J. Evidence for orbital deformation that may contribute to monocular blindness following minor frontal head trauma. J Neurosurg. 1981;55: 963–966.
87. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy. The International Optic Nerve Trauma Study. Ophthalmology. 1999;106:1268–1277.
88. Lessell S. Indirect optic nerve trauma. Arch Ophthalmol. 1989;107: 382–386.
89. Wolin MJ, Lavin, PJM. Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am J Ophthalmol. 1990;109: 430–435.
90. Wu N, Yin ZQ, Wang Y. Traumatic optic neuropathy therapy: an update of clinical and experimental studies. J Int Med Res. 2008;36:883–889.
91. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisone or naloxone in the treatment of acute spinalcord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322:1405–1411.
92. Steinsapir KD. Treatment of traumatic optic neuropathy with high-dose corticosteroid. J Neuroophthalmol. 2006;26:65–67.
93. Entezari M, Rajavi Z, Sedighi N, et al. High-dose intravenous methylprednisone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol. 2007;245:1267–1271.
94. CRASH Trial Collaborators. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004;364:1321–1328.
95. Yu-Wai-Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. 2005;(4):CD005024. DOI: 10.1002/14651858.CD005024.pub2.
96. Foster BS, March GA, Lucarelli MJ, et al. Optic nerve avulsion. Arch Ophthalmol. 1997;115:623–630.
97. Cirovic S, Bhola RM, Hose DR, et al. Computer modeling study of the mechanism of optic nerve injury in blunt trauma. Br J Ophthalmol. 2006;90:778–783.