Ocular Trauma: A Quick, Illustrated Guide to Treatment, Triage, and Medicolegal
Ocular Trauma: A Quick, Illustrated Guide to Treatment, Triage, and Medicolegal Implications
Authors: Kevin L. Crumpton, MD, Denver Health Medical Center Residency in Emergency Medicine, Denver, CO.
Lee W. Shockley, MD, FACEP, Assistant Professor and Residency Director, Denver Health Medical Center Residency in Emergency Medicine, Denver, CO.
Peer Reviewer: Raghavan K. Chari, MD, FACEP, Associate Director, Emergency Medicine Department, Washington County Hospital, Hagerstown, MD.
Approximately 2.4 million traumatic eye injuries occur each year in the United States,1,2 with up to 15% of these occurring in the workplace.3,4 Optimizing visual outcomes in patients sustaining traumatic ocular injuries requires prompt diagnosis and treatment. Immediate and appropriate intervention in vision-threatening emergencies has the capacity to reduce long-term loss of visual acuity and dramatically affect post-injury quality of life. Mechanisms of eye injury are changing, with recent data reporting a significant incidence of ocular trauma from motor vehicle accidents (MVAs)specifically, from air-bag deploymentassaults, falls, and from sports-related activities.5-11 The majority of these injuries are sustained by young men.
The spectrum of ocular trauma ranges from simple corneal abrasions to orbital fracture and ruptured globe. As might be expected, even injuries that are classified as "minor" can cause considerable morbidity to the patient. In this review, the authors examine recent controversies concerning the management of eye injuries, such as corneal abrasions and hyphemas. They also review the diagnosis and treatment of the most common blunt and penetrating ocular injuries, emphasizing when immediate intervention by the emergency physician or ophthalmologist is mandated. Finally, the medicolegal implications of ocular trauma are highlighted.
The Editor
Eye Assessment and Injury Classification
As with any emergency, accurate diagnosis and outcome-effective management of injuries to the eye hinge on taking good history and performing a targeted physical examination. In the case of ocular trauma, it is essential to establish the details of the injury, its mechanism, and its duration. Any alteration in visual acuity, diplopia, swelling, discharge, or previous ocular injury or dysfunction should be documented. In general, assessment of the eye may be divided into six categories,12 each of which should be systematically evaluated so occult injuries are not overlooked.
• Visual Acuity. Measuring visual acuity is arguably the most important part of the exam; it is essential in all cases for diagnosis, management, and medicolegal concerns. Patients who are unable to read the largest characters on the Snellen eye chart should be assessed for their ability to count fingers; if unable to count fingers, evaluate for finger movement, and finally light perception. A patient who cannot see at all should have his or her acuity documented as NLP (no light perception), rather than "blind" or "unable to see."
• Lid and Orbit. Assess lids for movement, integrity of margins, swelling, erythema, and ecchymosis. Evert the lids upwards over a Q-tip to rule out foreign bodies. Palpate the orbits for bony tenderness and document any perinasal hypesthesia. Do not apply pressure to a globe that may have been ruptured.
• Anterior Segment. The sclera, conjunctiva, and cornea should first be evaluated grossly and then with a slit lamp to detect foreign bodies, lacerations, hemorrhage, or swelling. Fluorescein staining is essential to evaluate abrasions and should be performed only after the anterior chamber has been evaluated for presence of cells (iritis), blood (hyphema), or pus (hypopyon).
• Pupils and Extraocular Movement. In patients with no history of ocular surgery or injury, an irregularly shaped pupil with decreased responsiveness after trauma may indicate a ruptured globe. It is essential to evaluate for both direct and consensual pupillary responses. A delayed consensual pupillary response (Marcus Gunn pupil) is an important piece of information in a patient reporting decreased vision after trauma. A finding of diplopia on upward gaze may indicate an orbital floor fracture with inferior rectus muscle injury, edema, or entrapment.
• Posterior Segment. Rule out lens dislocation, vitreous hemorrhage, and retinal detachment with the direct ophthalmoscopy and the aid of mydriatic agents (e.g., tropicamide, 1%) if the posterior segment cannot be adequately visualized.
• Intraocular Pressure (IOP). Measure IOP with a Schiontz tonometer or Tonopen system; normal values range from 12-20 mmHg. However, do not measure IOP if globe rupture is suspected. Tactile measurements can be made by comparison of eye firmness through a closed lid.
In the past, classification and description of ocular injuries have been problematic and confusing due to the use of such terms as "double-perforating," "double penetrating,"and "partial thickness." Recently, a standardized classification system has been developed so communication about and categorization of ocular injuries can be consistent.13 (See Table 1.) The terms outlined in this classification system are used in this clinical monograph, which will be divided into the following three categories: (1) blunt injuries, including periorbital contusion, subconjunctival hemorrhage, orbital fracture, hyphema, lens injuries, iris injuries, posterior segment injuries, and retrobulbar hemorrhage and indications for lateral canthotomy; (2) penetrating injuries including foreign bodies, eyelid lacerations, and scleral and corneal penetration, and; (3) other injuries including chemical injury, radiation injury, and corneal abrasion.
Blunt ocular injuries are encountered in myriad settings, including MVAs, assaults, falls, and sports and recreation-related activities. Although patients who are being evaluated for injuries sustained in an MVA have critical, life-threatening problems, vision-threatening injuries and newer injuries require early ophthalmological evaluation.
Soft-Tissue Ocular Injuries. Periorbital contusion or "black eye" may result from what appears to be a minor amount of force imparted to the orbit. Findings are due to loose subcutaneous tissue underlying the eyelids and orbits, which can become a repository for extravasated blood. Use a low threshold for orbital radiography because concomitant underlying orbital fractures are common.14 In addition, a basilar skull fracture should be considered with these findings, particularly when bilateral periorbital contusions are present ("raccoon’s eyes"). In unusual circumstances, marked periorbital edema may cause a rise in IOP and produce decreased visual acuity. Since the conjunctiva are only loosely adherent to the underlying sclera, accumulation of edema and subconjunctival hemorrhages are common after blunt blows to the eye. (See Figure 1.) These hemorrhages may also occur spontaneously after vigorous coughing, sneezing, or vomiting. If visual acuity is normal or unchanged and there is no foreign body, the treatment for all but the most severe cases of periorbital occlusion is conservative and includes ice, anti-inflammatory agents, rest, and follow-up.
Orbital Fractures. The orbit of the eye, though it is protected anteriorly by a thick anterior rim, is surrounded by relatively weak walls, particularly the floor and medial walls. The pathophysiology of the classic "blow-out fracture" of the orbital floor has been studied in detail and is thought to occur as a result of both hydraulic forces generated by the compressed liquid of the eye and from direct buckling of the inferior floor.15,16 (See Figure 2.) Clinical signs of a blow-out fracture include: enophthalmos from prolapse of orbital fat and increased size of the orbit; impairment of eye movement due to such mechanisms as extraocular muscle entrapment, intramuscular or infraorbital hemorrhage, or nerve damage; orbital emphysema caused by communication with adjoining sinuses; and infraorbital nerve anesthesia causing perinasal and maxillary tingling. Medial wall blow-out fractures associated with floor blow-out fractures occur in between 21%17 and 70%18 of cases.
Other, less common, orbital fractures include "blow-in" fractures, orbital roof fractures, and trochlear fractures. Even when blow-out fractures are associated with enophthalmos, restricted eye movement, or infraorbital nerve anesthesia, emergent surgical repair of orbital fractures is rarely necessary. However, since many studies advocate earlier rather than later repair of such fractures, referral to the facial surgeon is imperative.
The best imaging techniques for visualizing the orbit and orbital floor are plain films (including a Waters view) and CT scanning. (See Figure 3.) A fracture on the Waters view is suggested by either a bony disruption and white-out, an air-fluid level in the adjoining maxillary sinus, or both. When a clinician suspects that a fracture will require surgical repair (i.e., the injury is associated with enophthalmos, nerve anesthesia, restricted eye movement), it is appropriate to forgo the plain films and obtain a CT scan that includes both axial and coronal cuts.
Hyphema. Hyphema is defined as an accumulation of blood in the anterior chamber of the eye resulting from disruption of vessels in the iris or ciliary body.19 (See Figure 4.) Symptoms include pain, photophobia, and blurred vision. Common causes of hyphema include penetrating and blunt trauma from MVAs, assaults, falls, and sports-related injuries.10,11 The patient should be examined for concomitant injuries, including globe rupture, corneal abrasion, orbital fracture, and vitreous hemorrhage.
For reasons that are not entirely clear, lethargy is commonly seen in the setting of hyphema, particularly in children.19 Naturally, further evaluation of head injury is warranted in these cases. The presence of hyphema in the absence of a history of trauma should prompt a search for underlying sickle cell anemia (or trait), hemophilia, leukemia, malignant melanoma of the iris, use of aspirin, other non-steroidal agents, or alcohol.20 Since the red blood cells settle with gravity in the anterior chamber, the characteristic meniscus is usually most easily demonstrated in a patient who is upright. In contrast, the supine patient may have a diffusely dark or steamy appearance in the anterior chamber. Hyphemas are graded 0 through 4 based on amount of blood in the anterior chamber. (See Table 2.) Negative long-term sequelae from hyphema, such as decreased visual acuity and glaucoma, are increased by factors such as hyphema rebleeding (typically, this occurs at 2-5 days after injury), corneal blood staining, persistently elevated IOP, and associated ocular injuries.
ED ophthalmology referral should be sought for all but microscopic hyphemas so that an integrated treatment plan may be initiated. While waiting for the ophthalmologist, avoid administration of aspirin and NSAIDs, keep the patient calm and supine in bed with the head elevated 30-40°, and protect the eye with a metal Fox shield.
Currently, treatment options for hyphemas are wide-ranging and quite controversial. They may include topical steroids, systemic steroids, cycloplegics, anti-fibrinolytic agents such as aminocaproic acid (amicar), mannitol, acetazolamide, surgical evacuation, and hospitalization.19-27
The management of "low-risk" hyphemas in the outpatient environment has recently become more common because data shows similar outcomes compared with hospitalized patients.28-30 However, patients demonstrating risk factors that increase the chance of rebleeding and that are associated with bad visual outcome should be considered for hospitalization. These risk factors are controversial but generally include the following: sickle cell anemia, sickle trait, and other hemoglobinopathies (these patients are rarely if ever managed as outpatients);20 patients on anti-clotting agents including aspirin, other NSAIDs, and coumadin20; hyphema grade II or greater;20,31 patients evaluated more than one day since the injury31; initial IOP greater than 21-25 mmHg31; and visual acuity 20/200 or worse.31
Iris Injuries. Blunt force to the eye can produce traumatic iritis (or traumatic iridocyclitis). This condition is characterized by photophobia and deep eye pain resulting from ciliary muscle spasm. Slit lamp examination may reveal perilimbal injection (ciliary flush) and cells and flare in the anterior chamber; the appearance of the latter has been likened to seeing dust suspended in a sunlit room. Clues to the diagnosis include continued patient discomfort after instillation of a topical anesthetic32 and pain on accommodation as the patient focuses on his index finger as he moves it from an outstretched position towards his nose.33 Treatment with a long-acting cycloplegia and topical steroids is appropriate. Consultation with an ophthalmologist and arrangement of next-day follow-up for the patient is also mandatory.34,35 Traumatic mydriasis and miosis are seen in both blunt and penetrating trauma when the circular iris sphincters are disrupted. An irregularly shaped or scalloped iris is commonly seen and may last for several months or indefinitely. Surgical treatment is usually avoided unless there is concomitant injury. Iridodialysis is an iris disruption at the limbal border that requires surgical repair only if decreased acuity or diplopia are present.
Lens Injuries. Blunt trauma to the eye may cause disruption of the lens zonule fibers. Resulting lens subluxation or dislocation symptoms include monocular diplopia and marked blurred vision. (See Figure 5.) Examination of the posteriorly subluxed lens will often reveal a trembling or shimmering of the iris with rapid eye movements. These injuries are often watched expectantly and managed only with refractive correction. Anterior dislocation of the lens, a rare entity, is an acute emergency because it may manually block aqueous flow and precipitate acute glaucoma. Traumatic cataracts can occur with blunt or penetrating trauma when there is disruption of the lens capsule and subsequent absorption of fluid and swelling into the normally desiccated lens. Refractive properties are obviously lost in such a setting and future lens replacement may be necessary. Emergency ophthalmology evaluation is warranted for all of these conditions.
Posterior Segment Injuries. Vitreous hemorrhage occurs after blunt trauma when the vascular supply on the inner surface of the globe is disrupted. Symptoms often include "floaters" (described by patients as swirling black dots or strands) that are caused by blood cells floating in the visual axis. The red reflex will be lost, and the fundus will appear hazy due to these cells.
Retinal tears and detachments are painless and may manifest with "floaters" or light flashes. The patient may complain of a dark curtain being pulled across his visual field. Fundoscopic exam reveals a forwardly displaced hazy gray retinal membrane usually with a sharp border. Suspect this injury with a sluggish pupillary response.
Berlin’s edema (or Commitio Retinae) is transient retinal edema caused by a concussive force of blunt trauma. Examination of the fundus reveals a patchy white appearance from retinal ischemia. It requires surgical intervention only when it involves the macula. Confirmation of these uncommon posterior segment injuries by an ophthalmologist is advised.
Retrobulbar Hemorrhage and Indications for Lateral Canthotomy. Acutely decreased vision and proptosis after blunt or penetrating trauma should raise the suspicion of retrobulbar hemorrhage, which often follows disruption of the posterior arterial supply. (See Figure 6.) The resulting increase in IOP within the rigid orbit makes this a true ocular emergency. Decreased vision is thought to occur due to central retinal artery occlusion, direct compressive optic neuropathy, or disruption of the optic nerve vasculature.36,37 The primary indications for decompression of this pressure in the ED are findings of decreased visual acuity, proptosis, and elevated IOP greater than 40-50 mmHg. Other physical findings consistent with the need for emergent orbital decompression are eye pain, afferent pupillary defect (Marcus Gunn pupil), limited extraocular eye movements, macular cherry red spot, or nerve head pallor.38-42 (See Table 3.)
The decompression procedure is a lateral canthotomy with cantholysis, which may be performed by emergency physicians that are skilled at this procedure. These maneuvers allow further proptosis and thus relieve retrobulbar pressure. First, locally anesthetize the area with 2% lidocaine with epinephrine, then apply mosquito hemostats for 30 seconds directed posteriorly and just inferiorly (about 1.5 cm) all the way back to the bony orbit. (See Figure 7.) With fine scissors, cut along the crushed tissue.34 Locate and divide the inferior crus of the lateral canthal tendon (cantholysis) if it was not severed with the initial incision. Retraction of the tissue in a lateral direction during manipulation decreases the chance of a globe injury. The canthotomy will eventually heal without suturing or significant scarring.43
This procedure will significantly lessen IOP37 and temporize the lesion until further evaluation or intraoperative treatment with transethmoidal or transsphenoidal decompression can be completed by the ophthalmic or facial surgeon. Several case reports and expert reviews support lateral canthotomy and cantholysis as a means to decrease long-term loss of visual acuity.34,35,38-45 It should be stressed that with the above indications, minutes count ("time is retina"), and the emergency physician should perform this procedure rather than waiting 20-30 minutes for CT scanning or ophthalmologist evaluation.
Compared to blunt trauma, penetrating trauma is more likely to produce greater long-term loss of visual acuity. With modern microsurgical techniques, functional vision salvage rates in the 60-70% range have been attained.8,46-48 Penetrating or perforating injuries should be suspected with all high-velocity missiles (e.g., metalwork, nail hammering), corneal foreign bodies, and corneal abrasions.
In general, the more anterior the injury or penetration, the better the visual outcome. Damage to the lens, vitreous, or retina usually requires prompt surgical intervention to optimize outcome. Penetrating injuries increase the risk of microbial endophthalmitis with Streptococcus, Staphylococcus, and Bacillus species. These risks are increased when an intraocular foreign body is present. Antibiotic administration with such agents as cefazolin, clindamycin, or an aminoglycoside should be coordinated with the consulting ophthalmologist.
Foreign Bodies. Managing foreign bodies (FBs) in the eye first requires a pressure determination of both its location and whether it penetrated the cornea or sclera to become an intraocular foreign body (IOFB). Corneal penetration can be ruled out with Seidel’s test by heavily staining the cornea with fluorescein; waves of aqueous fluid flowing from a focal site confirms penetration. Gross examination in this instance may also reveal an irregular pupil or a misshapen or flattened anterior chamber. When penetration with a FB is identified, leave the FB in place and place a protective metal shield over the eye until evaluation by an ophthalmologist. Scleral penetration may be suggested by protrusion of the iris or vitreous through the wound. While corneal penetration is a surgical emergency, embedded FBs may require only next-day ophthalmologist examination.
A corneal FB should be removed only after assessment of its depth using a slit lamp. After instilling a topical anesthetic, brace your hand on the patient’s cheek and remove the FB with a moistened Q-tip, hypodermic needle tip (23ga or 25ga), or eye spud. Impress on the patient the importance of keeping the eye perfectly still during the procedure. This can be facilitated by giving the patient a target to fixate upon. The incidence of corneal perforation while removing an FB in this way is very rare.49 If a rust ring is present after metallic FB removal, it should be left to soften for 18-36 hours before attempted removal with needle tip, eye spud, or burr drill.50 Removal of an FB will undoubtedly leave a corneal abrasion; treat as recommended below with topical antibiotics and cycloplegics.
A mechanism of injury involving a high-velocity missile (metalwork, nail hammering) should raise the clinician’s suspicion for an IOFB. When overlooked, these injuries often cause significant morbidity and lead to medicolegal action.51 A high index of suspicion or positive Seidel’s test should prompt evaluation with a CT scan, including axial and coronal views (usually 1.5-2.0 mm cuts). While small pieces of wood, glass, or plastic may not be seen on the CT, the vast majority of IOFBs will be visualized.52-54 Ultrasonography may also have a role in this injury.55 Decision by the ophthalmologist to remove an IOFB depends upon its composition and location in the eye, two factors that will make an impact on the patient’s long-term acuity, comfort, and sequelae.56 For instance, iron and copper tend to be quite irritative and cause sequelae, whereas porcelain, glass, and plastic tend to be inert and are often left in place.57 MRI is contraindicated because its deleterious effects with metallic foreign bodies.58 Visual outcome after BB gun or air pellet injuries to the eye is uniformly poor.59
Lid Lacerations. Eyelid and periocular lacerations should always prompt a thorough evaluation to rule out orbital fracture, globe injury, foreign body, or perforation. Prehospital and pre-repair protection of the eye should be accomplished with a Fox metal shield; soft patching, which has the potential to raise IOP, should be avoided because of the possibility of perforation. Simple superficial lacerations may be repaired by the emergency physician with 6.0 or 7.0 non-absorbable interrupted sutures. Ghezzi and Renner57 have delineated five types of lacerations that should be referred to the ophthalmologist or plastic surgeon.
1. Lacerations involving the lid margins: Improper repair of the tarsal plate frequently causes notching and ectropion.
2. Lacerations involving the canalicular system: Those involving the medial one-third of the inferior eyelid may involve the puncta or canalicular ducts. Repair involves intubation and stenting of the severed duct.
3. Lacerations involving the levator or canthal tendons: If an upper lid or lateral laceration is deep and through these structures, fine repair of the tendons with absorbable sutures is necessary to prevent ptosis or droopy eyelids.
4. Punctures or lacerations through the orbital septum: Disruption of the septum - the fascia covering the orbit circumferentially-will usually cause fat protrusion. These wounds require meticulous multi-layered closure and have a high incidence of post-repair infection.
5. Lacerations with significant tissue loss: Wounds that involve extensive avulsed tissue and tissue loss may require multiple grafting and should be left to the consultant; avoid debridement in these cases.
Chemical Injuries. Caustic chemical splashes to the eye are a true ocular emergency. Immediate treatment and evaluation are required to minimize long-term damage. Alkali injuries often cause severe damage because they rapidly penetrate the cornea and induce tissue saponification and denaturation.61 Common alkali splashes include ammonia, lye, drain cleaners, refrigerants, and lime powder (as in plaster and concrete). Acid splashes tend not to be as destructive, with the exception of hydrofluoric acid whose fluoride ion complexes with cellular calcium and magnesium to cause tissue destruction and systemic toxicity.62 Sulfuric acid (as in batteries), acetic acid, and hydrochloric acid, when treated promptly, generally do not cause long-term sequelae. Treat all chemical splashes immediately upon arrival with instillation of topical anesthetic and irrigation with 2 L of normal saline or lactated ringers in each affected eye before further evaluation is begun. If pH after irrigation is not 7.4, examine the eye for particulate matter, remove as needed, and continue irrigation until this pH is attained. Evaluate further at this point for visual acuity, foreign bodies, and peri-ocular injury. When this is completed instill a cycloplegic (e.g., homatropine 2%) and antibiotic ointment. Severe exposures often require hospitalization. Ophthalmologist referral, discussion of steroid treatment (controversial), and close follow-up are recommended for all but the most minor of exposures.63
Ultraviolet Injury. Welder’s arc exposure, tanning lamps, and high-altitude snow covered environments may induce ultraviolet injury with subsequent edema and sloughing of the corneal epithelium.64 The patient notices onset of foreign body sensation, pain, tearing, blepharospasm, photophobia, and decreased visual acuity 6-10 hours after onset of the exposure(s) due to delay in breakdown of the injured cells. Fluorescein staining will typically show punctate uptake. Treatment is the same for standard corneal abrasions with topical antibiotics, cycloplegia, and oral narcotic analgesia. These lesions usually heal well in 24-36 hours.
Corneal Abrasions. Corneal abrasions are frequently encountered in the ED and should be suspected in patients with complaints of eye pain, tearing, blepharospasm, photophobia, and conjunctival erythema. In infants, corneal abrasions may provoke persistent fussiness with lack of other systemic findings.65 Corneal abrasions should be diagnosed after ruling out other ocular injuries; instill topical anesthesia, stain with fluorescein, and examine with cobalt blue light. Document the size of the abrasion and whether the central visual axis is involved.
Treatment practices of corneal abrasions recently have been challenged. Antibiotic drops or ointment such as sulfacetamide, bacitracin/neomycin/polymyxin, or erythromycin, are employed, as are cycloplegics such as tropicamide 1% or homatropine 2%, especially when there is significant abrasion or photophobia. Although the value of tetanus prophylaxis with simple abrasions has recently been challenged, maintain a low threshold for its administration in patients not currently immune.66,67 Avoid prescription of topical anesthetics because they both impede corneal regeneration68 and suppress protective ocular reflexes that may prevent further injury. Oral narcotics are appropriate for discomfort. Patching the eye after abrasion has been a time-honored tradition supported by scant objective data. Recent prospective studies have challenged this practice69-71 and have shown not only lack of additional benefit in terms of pain or increased healing but also possible detrimental effects.72 Without clear benefit, the loss of binocular vision (and skills such as driving or reading) caused by patching make the practice questionable at best.
Ocular trauma cases may account for 6-9% of all ophthalmology-related litigation.73,74 Emergency physicians act as both the primary treatment provider and as an interface for the care provided by consultants in the department. Partial or complete loss of vision is an emotionally charged injury that will likely decrease a patient’s quality of life and may make him or her more likely to seek litigation. The following five steps will minimize the medicolegal risk of the emergency physician when dealing with such cases:
1. Document Compulsively. Prosecution of medical malpractice cases often does not occur until 2-5 years after the injury.75 Thorough documentation is frequently the physician’s best defense and can actually prevent seemingly frivolous litigation. Document visual acuity before and after any procedure and record your examination of both the other five divisions of the ophthalmologic exam as listed above and the unaffected eye. Document in the chart the over-the-phone consultation with ophthalmologist and plans for follow-up. Remember the axiom, "If it wasn’t documented, it wasn’t done." Finally, never embellish or alter the medical record after a claim has been brought.
2. Explain Potential Risks and Long-Term Sequelae. Several sequelae of ocular trauma, such as glaucoma, cataract, and retinal detachment, often do not occur for months to years after the injury. For this reason referral to the ophthalmologist for serial examinations is recommended in almost all cases of significant trauma.51 Make the patient aware of these potential complications at the time of the injury; such information may minimize future litigation.76 In addition, warn the patient of the corneal abrasion caused by removal of their corneal foreign body.
3. Rule-Out IOFB. Missed IOFBs are a common source of litigation.51 If suspected, as with high-velocity metal objects, get the CT scan or plain film.
4. Only Use Steroids In Consultation with an Ophthalmologist. Use of steroids, particularly for prolonged periods of time, increases the risk of subsequent viral and fungal infections and cataracts. However, in certain conditions, such as severe traumatic iritis, they are clearly indicated.
5. Maintain Good Patient Rapport. A recent study confirmed what has long been suspected by physicians-that personal communication and interpersonal skills of the doctor with an emphasis on patient understanding will minimize the risk of medical malpractice.77
The emergency physician should have a working knowledge of the most common ocular topical anesthetics, antibiotics, and mydriatics/cycloplegics. Table 4 and Table 5 demonstrate the onset, duration, reactions, and other important information for the most common examples of each of these classes of agents. Oral and parenteral drugs in the treatment of ocular emergencies (e.g. acetazolamide, amicar, and parenteral antibiotics) should almost always be administered in direct consultation with the ophthalmologist who will care for the patient.
Topical anesthetics should be used in most ocular evaluations; a drop in the unaffected will facilitate the examination. The choice of a mydriatic/cycloplegic depends on the desired effect; if only posterior segment examination is desired, a shorter acting agent such as Phenylephrine or Tropicamide is desirable. If iritis is suspected and longer term iris and ciliary body paralysis would increase the patient’s comfort, choose a longer acting agent such as Cyclopentolate or Homatropine. The duration of a cycloplegic depends on both its concentration and the number of drops instilled into the eye.
Traumatic eye injuries are common presenting complaints in an emergency practice. The myriad of these injuries presents a challenging array of therapeutic options when the stakes are high because vision may be threatened. Of recent note, treatment paradigms have shifted with regard to foregoing the corneal abrasion patch, managing more hyphemas on an outpatient basis, and aggressively decompressing the orbit with canthotomy and cantholysis when indicated. Armed with the knowledge of traumatic ocular injuries, the emergency physician can perform a thorough, systematic exam, instigate immediate treatment and referral as needed, and maximize the patient’s visual outcome.
References
1. Parver LM. Eye trauma: The neglected disorder. Arch Ophthalmol 1986;104:1452-1453.
2. Parver LM, Dannenberg AL, Blacklow B, et al. Characteristics and causes of penetrating eye injuries reported to the National Eye Trauma System Registry, 1985-1991. Public Health Rep 1993;108:625-632.
3. National Society to Prevent Blindness. A Guide for Controlling Eye Injuries in Industry. New York: National Society to Prevent Blindness; 1990.
4. Karlson TA, Klein BEK. The incidence of acute hospital-treated eye injuries. Arch Ophthalmol 1986;104:1473-1476.
5. Sastry SM, Paul BK, Bain L, et al. Ocular trauma among major trauma victims in a regional trauma center. J Trauma 1993;34:223-226.
6. Duma SM, Kress TA, Porta DJ, et al. Airbag-induced eye injuries: A report of 25 cases. J Trauma 1996;41:114-119.
7. Vichnin MC, Jaeger EA, Gault JA, et al. Ocular injuries related to air-bag inflation. Ophthalmic Surg Lasers 1995;26:542-548.
8. Hemady RK. Ocular injuries from violence treated at an inner-city hospital. J Trauma 1994;37:5-8.
9. Klopfer J, Tielsch JM, Vitale S, et al. Ocular trauma in the United States. Eye injuries resulting in hospitalization, 1984 through 1987. Arch Ophthalmol 1992;110:838-842.
10. Kennedy RH, Brubaker RF. Traumatic hyphema in a defined population. Am J Ophthalmol 1988;106:123-130.
11. Spoor TC, Kwitko GM, O’Grady JM, et al. Traumatic hyphema in an urban population. Am J Ophthalmol 1990;109:23-27.
12. Shingleton, BJ. Eye injuries. N Engl J Med 1991;325:408-413.
13. Kuhn F, Morris R, Witherspoon CD, et al. A standardized classification of ocular trauma. Ophthalmology 1996;103:240-243.
14. Giovinazzo VJ. The ocular sequelae of blunt trauma. Adv Ophthalmic Plast Reconstr Surg 1987;6:107-114.
15. Tajima S, Sugimoto C, Tanino R, et al. Surgical treatment of malunited fracture of zygoma with diplopia and with comments on blow-out fracture. J Maxillofac Surg 1974;2:201-210.
16. Jones DEP, Evans JNG. "Blow-out" fractures of the orbit: An investigation into their anatomical basis. J Laryngol Otol 1967;81:1109-1120.
17. Dulley B, Fells P. Orbital blow-out fractures: To operate or not to operate, that is the question. Br Orthop J 1974;31:47-53.
18. Pearl RM, Vistnes LM. Orbital blowout fractures: An approach to management. Ann Plast Surg 1978;1:267-270.
19. Wilson FM. Traumatic hyphema. Pathogenesis and management. Ophthalmology 1980;87:910-919.
20. Gottsch JD. Hyphema: Diagnosis and management. Retina 1990;10(Suppl 1):S65-71.
21. Uusitalo RJ, Ranta-Kemppainen L, Tarkkanen A. Management of traumatic hyphema in children. An analysis of 340 cases. Arch Ophthalmol 1988;106:1207-1209.
22. Kutner B, Fourman S, Brein K, et al. Aminocaproic acid reduced the risk of secondary hemorrhage in patients with traumatic hyphema. Arch Ophthalmol 1987;105:206-208.
23. Volpe NJ, Larrison WI, Hersh PS, et al. Secondary hemorrhage in traumatic hyphema. Am J Ophthalmol 1991;112:507-513.
24. Loewy DM, Willliams PB, Crouch ER Jr., et al. Systemic aninocaproic acid reduces fibrinolsysis in aqueous humor. Arch Ophthalmol 1987;105:272-276.
25. Spoor TC, Hammer M, Belloso H. Traumatic hyphema. Failure of steroids to alter its course: A double-blind prospective study. Arch Ophthalmol 1980;98:116-119.
26. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid versus prednisone for the treatment of traumatic hyphema. A randomized clinical trial. Ophthalmology 1991;98:279-286.
27. Ng CS, Strong NP, Sparrow JM, et al. Factors related to the incidence of secondary haemorrhage in 462 patients with traumatic hyphaema. Eye 1992;6:308-312
28. Wilson TW, Nelson LB, Jeffers JB, et al. Outpatient management of traumatic microhyphemas. Ann Ophthalmol 1990;22:366-368.
29. Clever VG. Home care of hyphemas. Ann Ophthalmol 1982;14:25-27.
30. Williams C, Laidlaw A, Diamond J, et al. Outpatient management of small traumatic hyphemas: Is it safe? Eye 1993;7:155-157.
31. Fong LP. Secondary hemorrhage in traumatic hyphema. Predictive factors for selective prophylaxis. Ophthalmology 1994;101:1583-1588.
32. Sklar DP, Lauth JE, Johnson DR. Topcial anesthesia of the eye as a diagnostic test. Ann Emerg Med 1989;18:1209-1211.
33. Talbot EM. A simple test to diagnose iritis. Br Med J 1987;295:812-813.
34. Joondeph BC. Blunt ocular trauma. Emerg Med Clin North Am 1988;6:165-167.
35. Weisman RA, Savino PJ. Management of patients with facial trauma and associated ocular / orbital injuries. Otolaryngol Clin North Am 1991;24:37-40.
36. Dolman PJ, Glazer LC, Harris GJ, et al. Mechanisms of visual loss in severe proptosis. Ophthal Plast Reconstr Surg 1991;7:256-260.
37. Yung CW, Moorthy RS, Lindley D, et al. Efficacy of lateral canthotomy and cantholysis in orbital hemorrhage. Ophthal Plast Reconstr Surg 1994;10:137-141.
38. Grewal RK, Dhaliwal DK, Hersh PS, et al. Anterior segment injuries. In: Zagelbaum B, ed. Sports Ophthalmology. Cambridge, MA: Blackwell Science; 1996:184-209.
39. Khan JA. Blunt trauma to orbital soft tissues. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye Trauma. St. Louis, MO: Mosby-Year Book, Inc.; 1991:292-293.
40. Hislop WS, Dutton GN, Douglas PS. Treatment of retrobulbar haemorrhage in accident and emergency departments. Br J Oral Maxillofac Surg 1996;34:289-292.
41. Hislop WS, Dutton GN. Retrobulbar haemorrhage: Can blindness be prevented? Injury 1994;25:663-665.
42. Bailey KW, Kuo PC, Evans LS. Diagnosis and treatment of retrobulbar hemorrhage. J Oral Maxilllofac Surg 1992;51:780-784.
43. Samples, JR. Ophthalmologic procedures. In: Roberts JR, Hedges JR, eds., Clinical Procedures in Emergency Medicine, 3rd ed., Philadelphia: W.B.Saunders, 1998:1089-1119.
44. Goldberg RA, Marmor MF, Shorr N, et al. Blindness following blepharoplasty: Two case reports and a discussion of management. Ophthalmic Surg 1990;21:85-89.
45. Katz B, Herschler J, Brick DC. Orbital haemorrhage and prolonged blindness: A treatable posterior optic neuropathy. Br J Ophthalmol 1983;67:549-553.
46. Esmaeli B, Elner SG, Schork MA, et al. Visual outcome and ocular survival after penetrating trauma. A clincopathologic study. Ophthalmology 1995;102:393-400.
47. Sternberg P, de Juan E, Michels RG. Penetrating ocular injuries in young patients. Initial injuries and visual results. Retina 1984;4:5-8.
48. Barr CC. Progressive factors in corneoscleral lacerations. Arch Ophthalmol 1983;101:919-924.
49. Barr DH, Samples JR, Hedges JR. Ophthalmologic, otolaryngolic, and dental procedures. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency Medicine, 2nd ed., Philadelphia,: W.B.Saunders, 1991:995-1019.
50. Santen SA, Scott JL. Ophthalmologic procedures. Emerg Med Clin North Am 1995;13:681-701.
51. Umbarger DM. The traumatized patient. Legal considerations. Ophthalmol Clin North Am. 1995;8:723-729.
52. Lobes LA, Grand MG, Reece J, et al. Computerized axial tomography in the detection of intraocular foreign bodies. Ophthalmology 1981;88:26-29.
53. Maguire AM, Enger C, Elliott D, et al. Computerized tomography in the evaluation of penetrating ocular injuries. Retina 1991;11:405-411.
54. Chacko JG, Figueroa RE, Johnson MH, et al. Detection and localization of steel intraocular foreign bodies using computed tomography. Ophthalmology 1997;104:319-323.
55. McNicholas MMJ, Brophy DP, Power WJ, et al. Ocular trauma: Evaluation with US. Radiology 1995;195:423-427.
56. Finkelstein M, Legmann A, Rubin PAD. Projectile metallic foreign bodies in the orbit. A retrospective study of epidemiologic factors, management, and outcomes. Ophthalmology 1997;104:96-103.
57. Schwartz JG, Somerset JS, Harrison JM, et al. Eye injuries with metal missiles presenting to an emergency center: A three-year study. Am J Emerg Med 1991;9:313-317.
58. Kelly WN, Paglen PG, Pearson JA, et al. Ferromagnetism of intraocular foreign body causes unilateral blindness after MR study. Am J Neurol Rev 1986;7:243-245.
59. Sternberg P, de Juan E, Green WR, et al. Ocular BB injuries. Ophthalmology 1984;91:1269-1277.
60. Ghezzi K, Renner GS. Ophthalmologic disorders. In: Rosen P, Barkin RM, et al eds., Emergency Medicine, Concepts and Clinical Practice, 3rd ed. St. Louis: Mosby-Year Book, 1992:2444-2445.
61. Rosenbaum D, Baruchin AM, Dafna Z. Chemical burns of the eye with special reference to alkali burns. Burns 1991;17:136-140.
62. Rubinfield RS, Silbert DI, Artensen JJ, et al. Ocular hydrofluoric acid burns. Am J Ophthalmol 1992;114:420-423.
63. Wagoner MD, Kenyon KR. Chemical injuries. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye Trauma. St. Louis: Mosby-Year Book; 1991:79-94.
64. Lubeck D, Greene JS. Corneal injuries. In: Mathews J, Zun LS, eds. Emerg Med Clin North Am Philadelphia: W.B. Saunders Co; 1988;6:73-94
65. Poole SR. Corneal abrasions in infants. Pediatr Emerg Care 1995;11:25-26.
66. Benson WH, Snyder IS, Granus V, et al. Tetanus prophylaxis following ocular injuries. J Emerg Med 1993;11:677-683.
67. Ostler HB. Risk of tetanus from corneal injuries. JAMA 1988;260:553.
68. Bisla K, Tanelian DL. Concentration-dependent effects of lidocaine on corneal epithelial wound healing. Invest Ophthalmol Vis Sci 1992;33:3029-3033.
69. Kirkpatrick JNP, Hoh HB, Cook SD. No eye pad for corneal abrasion. Eye 1993;7:468-471.
70. Patterson J, Fetzer D, Krall J, et al. Eye patch treatment for the pain of corneal abrasion. South Med J 1996;88:227-229.
71. Hulbert MFG. Efficacy of eyepad in corneal healing after corneal foreign body removal. Lancet 1991;337:643.
72. Frucht-Pery J, Stiebel H, Hemo I, et al. Effect of eye patching on ocular surface. Am J Ophthal 1993;115:629-633.
73. Bettman JM. Seven hundred medicolegal cases in ophthalmology. Ophthalmology 1990;97:1379-1384.
74. Kraushar MF, Turner MF. Medical malpractice litigation in ophthalmology: the New Jersey experience. Ophthalmic Surg 1986;17:671-674.
75. Shelton PA. Medicolegal concerns. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye Trauma. St. Louis: Mosby-Year Book, 1991:403-408.
76. Bettman JW. How to reduce medicolegal involvement in cases of trauma. Ophthalmology 1980;87:432-434.
77. Hickson GB, Clayton EW, Entman SS, et al. Obstetrician’s prior malpractice experience and patients’ satisfaction with care. JAMA 1994;272:1583-1587.
Physician CME Questions
73. Which of the following are the primary indications for lateral canthotomy following trauma?
A. Decreased visual acuity, proptosis, IOP greater than 40
B. Decreased visual acuity, proptosis, afferent pupillary defect
C. Proptosis, afferent pupillary defect, macular cherry red spot
D. Decreased visual acuity, afferent pupillary defect
E. Proptosis, afferent pupillary defect, ophthalmoplegia
74. Indications of a penetrated globe may include?
A. Positive Seidel’s test
B. Misshapen pupil
C. Flattened anterior chamber
D. High velocity missile with lodged corneal FB
75. Which of the following conditions warrant emergent (immediate) rather than urgent (12-24 hour) evaluation by the ophthalmologist?
A. Embedded corneal FB without penetration
B. Traumatic lens dislocation
C. Corneal rust ring
D. Traumatic iritis
E. Microscopic hyphema
76. Which of the following best describes the sequence of treatment for chemical splashes?
A. pH, irrigation, acuity testing, rest of exam
B. irrigation, pH, further irrigation if needed, acuity testing, rest of exam
C. acuity testing, slit lamp exam, pH, irrigation, pH, rest of exam
D. irrigation, acuity testing, rest of exam, pH
E. pH, acuity testing, irrigation, pH, rest of exam
77. Patching after corneal abrasions is now being questioned as a treatment because?
A. Prospective studies show lack of benefit in terms of pain.
B. Prospective studies show lack of benefit in terms of healing.
C. Studies show some people cannot tolerate patching due to discomfort.
D. Loss of binocular vision with patching is an important consideration.
78. Which of the following patients with traumatic hyphema most warrants hospitalization?
A. Grade II hyphema, patient takes an aspirin daily for MI prophylaxis
B. Grade III hyphema, no other risk factors
C. Grade II hyphema, sickle cell trait, IOP 21 mmHg
D. Grade II hyphema, new visual acuity in affected eye 20/100
E. Microscopic hyphema, trauma occurred 24 hours ago, patients thinks one of his medicines could be "coumadin"
79. Patients presenting with symptoms of "floaters" or "flashing lights" after trauma should be ruled- out for what disorder?
A. "Blow-out" fracture of the orbit
B. Traumatic hyphema
C. Commitio Retinae or Berlin’s Edema
D. Retinal Detachment
E. Anterior chamber penetration
80. Which of the following agents would be optimal choices for ophthalmoscopy?
A. Phenylephrine 2.5% or Tropicamide 0.5%
B. Tropicamide 0.5% or Homatropine 5%
C. Cyclopentolate 0.5% or Scopolamine 0.25%
D. Cyclopentolate 0.5% or Atropine 0.25%
E. Homatropine 2% or Cyclopentolate 0.5%
Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.