Disease-a-Month 60 (2014) 247–253
Contents lists available at ScienceDirect
Disease-a-Month journal homepage: www.elsevier.com/locate/disamonth
Management of anterior segment trauma Hercules D. Logothetis, BS, Scott M. Leikin, BA, Thomas Patrianakos, DO
Introduction Ophthalmologic emergencies have the potential to lead to severe morbidity and loss of vision. The ability to recognize and efficiently relay pertinent findings to an ophthalmologist is critical to preventing life-changing damage to the eye. Basic understanding of ocular anatomy, physiology, and pathology will facilitate a successful discussion between an ophthalmologist and the referring physician. As with other specialties, a detailed HPI should be attained that includes basic information such as onset, duration, intensity, and medication use. A useful review of systems includes questions regarding flashing lights, floaters, vision loss, and pain. Additionally, performing an ocular examination that checks visual acuity, intraocular pressure, and pupils will be advantageous to you, the ophthalmologist, and the patient. Anterior segment trauma involves injury to the part of the eye that is visible to the naked eye. Briefly, with the patient's lids open, one should be able to see the conjunctiva, sclera, cornea, iris, and pupil. Identification of these structures is critical and expected of physicians at any level. The variety of anterior segment trauma one may encounter is vast, thus, this article will focus on the presentation, diagnosis, and treatment of chemical burns, corneal abrasions, hyphemas, and traumatic iritis.
Chemical burns Chemical burns are one of the most common causes of ocular trauma and injury.1 Chemical burns are potentially blinding as they can cause ischemic injury to the limbal stem cells leading to deficits in healing and corneal opacification.2 They are most common in males 16–45 years old. They usually occur in industrial accidents, at home, or in connection with criminal assault. Protective eye shields are the most common preventative measure utilized in the work place and should always be encouraged when dealing with dangerous chemicals. The severity of a chemical burn is directly related to the surface area of exposure, the degree of penetration, and the compound.3 An alkali burn usually results in greater damage to the eye than an acidic burn.4 Alkali compounds are more lipophilic and are able to penetrate more easily. They saponify the cell membranes and can penetrate the corneal epithelium, basement membrane, http://dx.doi.org/10.1016/j.disamonth.2014.03.004 0011-5029/& 2014 Elsevier Inc. All rights reserved.
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stroma, and endothelium. In addition to ocular surface injury, alkali compounds can damage other anterior segment structures including the iris, lens, and ciliary body. Acidic compounds on the other hand denature and precipitate proteins. These precipitates can effectively create a barrier preventing further penetration. In general, acidic injuries are not as severe as alkali. However, hydrofluoric acid is one particular acidic agent that is known to penetrate readily.3 The majority of patients present to the emergency department or place a phone call to their primary care physician. The diagnosis is clinical and thus a proper history is important. It is important to illicit at what time the exposure occurred, the specific type of compound, time between exposure and irrigation, duration and type of irrigation, and whether any eye protection was involved. This information determines the severity, prognosis, and treatment. Following immediate irrigation, patients require slit-lamp examination with fluorescein staining to identify any corneal or conjunctival ulceration. Additionally, eyelid eversion is recommended to identify and remove foreign bodies. Obtaining intraocular pressures is suggested as well.4 Roper–Hall and Dua are classification systems used for chemical burns. In a randomized clinical trial, the Dua classification was found to be superior in predicting outcomes. The systems are presented below.5 Roper–Hall classification of ocular chemical injuries. Grade
Prognosis
Cornea
Conjunctival limbus
I II III IV
Good Good Guarded Poor
Corneal epithelial damage Corneal haze and iris details visible Total epithelial loss, stromal haze, and iris details obscured Corneal opaque and iris and pupil details obscured
No limbal ischemia o 1/3 Limbal ischemia 1/3–1/2 Limbal ischemia 4 1/2 Limbal ischemia
Dua classification of ocular chemical injuries. Grade
Prognosis
Clinical findings
Conjunctival involvement
I II III IV V VI
Very good Good Good Good to guarded Guarded to poor Very poor
0 clock hours of limbal involvement o3 clock hours of limbal involvement Between 3 and 6 clock hours of limbal involvement Between 6 and 9 clock hours of limbal involvement Between 9 and 12 clock hours of limbal involvement Total limbus involved
0% o30% 30–50% 50–75% 75–100% Total conjunctival involvement
Chemical burns are classified into mild, moderate, and severe (Fig. 1). Corneal epithelial defects can range from superficial punctate keratopathy to sloughing of the entire epithelium. Mild to moderate burns do not demonstrate areas of perilimbal ischemia. In contrast, ischemic
Fig. 1. (A). Dua Grade VI or Roper-Hall Grade IV. (B). Dua and Roper-Hall Grade II.
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injury presents as blanching of conjunctival or episcleral vessels. Mild to moderate burns show areas of conjunctival epithelial defect, chemosis (conjunctival edema), hyperemia, hemorrhages, eyelid edema, mild anterior chamber reaction, and first- and second-degree burns of periocular skin.6 Severe ocular burns present with chemosis, conjunctival blanching, corneal edema, corneal opacification, moderate to severe anterior chamber reaction, increased intraocular pressure, and second- and third-degree burns of surrounding skin. Additionally, if the compound penetrates through the sclera, it can potentially cause local necrotic retinopathy.6 Chemical ocular burns require immediate intervention. Treatment must be instituted immediately unless you suspect open globe. Ideally, one can use plastic squeeze bottles of eye irrigation solution or normal saline IV drip with plastic tubing to irrigate the affected eye. However, any source of water may be used as an alternative. Proper irrigation techniques can alter prognosis. Make sure to direct your irrigation toward the temple as to avoid the opposite eye. Irrigate the eye for a minimum of 30 min. The pH can be checked with litmus paper 5–10 min following irrigation. If a neutral pH is not achieved, continue irrigation. The nonophthalmologist should assist with irrigation and contact emergency services. Do not ever attempt to neutralize a compound with another compound. The goal is to dilute the compound the patient was exposed to. This includes alkali (lye, cements, plasters, airbag powder, bleach, and ammonia), acids (battery acid, pool cleaner, and vinegar), solvents, detergents, and irritants. Surgical debridement may be necessary for foreign bodies embedded in conjunctiva, cornea, sclera, and surrounding tissues. After initial management, it is imperative the patient is seen by an ophthalmologist. Subsequent care may include cycloplegics, topical antibiotics, pressure patch, oral pain medications, artificial tears, topical steroids, intraocular pressure management, and daily follow-up until corneal epithelial defect has healed.4,6 Every second following exposure can significantly alter outcome.
Corneal abrasions A corneal abrasion is defined as a defect in the corneal epithelium. The corneal epithelium is 4–5 cell layer stratified non-keratinized squamous epithelium that is critical to corneal clarity. It provides a protective barrier to pathogen invasion. Injury to the corneal epithelium may lead to loss of vision. Corneal abrasions account for approximately 8% of eye presentations in the primary care setting. Unfortunately, the diagnosis is often missed. While they often occur in any setting of corneal epithelial compromise, trauma is one of the most common causes. The injuries tend to heal quickly, but their potential to cause scarring and disturb visual acuity makes them necessary to diagnose and treat early.7 Corneal abrasions are often secondary to corneal epithelial trauma. Injuries can be incurred from foreign bodies, contact lens misuse, vigorously rubbing the eyes, or being poked in the eye amongst other etiologies. Patients with chronically dry eyes are more susceptible to this type of injury. They are often unavoidable and can have significant consequences both personally and professionally. A study of eye injuries at a major US automobile company showed an annual incidence of 15 per 1000 employees. The study found that 86.7% of those injuries were due to foreign body or corneal abrasion. One-third of the total eye injuries led to workers missing 1 day of work.8 Corneal abrasions are diagnosed clinically. The evaluation of these patients should focus on evidence of penetrating trauma, decreased visual acuity, and infection. These are all indications for emergent ophthalmologic referral.7 Patients often present with sharp pain, photophobia, tearing, discomfort with blinking, foreign body sensation, or history of trauma to the eye. On examination, the patient may demonstrate epithelial defect that stains with fluorescein and the absence of underlying corneal opacification. Conjunctival injection, swollen eyelids, and mild anterior chamber reaction may be seen as well. Appropriate workup requires a slit-lamp examination with fluorescein dye, evaluation for anterior chamber reaction, and identification of
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Fig. 2. Corneal abrasion.
corneal laceration or penetrating trauma (Fig. 2). In the setting of vertical or linear abrasions, it is especially important to evert the eyelids in search of any foreign bodies.6 Not every patient with a corneal abrasion will present with the same set of symptoms. It is important to rule out other pathologies that may share similar symptoms. Other possibilities to consider include recurrent corneal erosions, herpes simplex keratitis, confluent superficial punctate keratopathy, dry eye syndrome, conjunctivitis, and acute angle closure glaucoma.6,7 The goal of treatment is to relieve pain, speed healing, and prevent infection. Ophthalmologists often use topical antibiotics, NSAIDS, and cycloplegics during treatment.7 Non-contact lens wearers can be prescribed antibiotic ointments including erythromycin, bacitracin, or bacitracin/polymyxin B. Antibiotic drops including polymyxin B/trimethoprim and fluoroquinolones are alternative options. Contact lens wearers require anti-pseudomonal coverage.6 For pain control, oral Tylenol, NSAIDS, or narcotics can be used. Topical NSAID drops are also considered appropriate. Although a study found that dilute topical proparacaine can be used to alleviate the pain associated with acute corneal injuries,9 it is not recommended due to reports of impaired wound healing. Patching is also not recommended. It can decrease oxygen delivery and promote infection.7 Patching is especially contraindicated if the mechanism of injury involves vegetable matter, fingernails, or if the patient is a contact lens wearer. If one does wear a patch, it is important to be sure that the upper eyelid remains closed in order to prevent further abrasion. A prospective, three-armed, masked, randomized study of patients presenting with superficial corneal foreign bodies compared three different treatment modalities for corneal abrasions. The modalities included pressure patching with ofloxacin ointment, therapeutic contact lens with ofloxacin eye drops, and ofloxacin ointment alone. Primary outcome measure was the difference of the mean corneal abrasion area between the three groups over three different time points. The mean abrasion area was found to be the same amongst all three groups.10 Follow-up depends on the severity. Most abrasions heal within 24–48 h.7 Follow-up by an ophthalmologist may not be needed for abrasions that are 4 mm or less with a patient who has no visual acuity defects and symptoms that seem to be resolving. Central and large corneal abrasions require a follow-up the next day. An ophthalmologist should be consulted when the patient has symptoms that worsen on reexamination, any corneal infiltrates or ulcers, penetrating eye injuries, or visual acuity defects that are significant. Ultimately, healing time depends on the abrasion surface area. The larger the size, the longer it will take to heal. Traumatic abrasion patients treated in ophthalmology offices had recurrent symptoms for 3–4 months 28% of the time.11 Contact lenses should not be worn while healing and may be reintroduced once the eye feels normal for a week and appropriate medications have stopped.
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Fig. 3. Acute hyphema.
Hyphema The accumulation of blood in the anterior chamber is known as hyphema (Fig. 3). Minimal amounts of blood only observable by slit-lamp examination are referred to as microhyphemas. In contrast, larger hyphemas can often be observed by penlight examination alone. The patient's history usually includes recent trauma or ocular surgery. Patients present with pain, blurred vision, and blood in the anterior chamber that is grossly visible. The blood may appear black (8-ball) or red.6 The most common cause of hyphema is blunt trauma. Iris vasculature, ciliary body, and trabecular meshwork can be damaged from the compressive forces of such trauma. Any cause of intraocular inflammation in the anterior chamber may lead iris neovascularization and resulting accumulation of blood in the anterior chamber.12 In addition to trauma and surgery, hyphema can also occur spontaneously. Etiologies include iris melanoma, myotonic dystrophy, leukemia, hemophilia, von Willebrand disease, and the use of warfarin amongst other anticoagulant medications.13 Ascertaining the mechanism of injury is a crucial step in evaluation. Understanding the force, velocity, type, and direction of injury will facilitate more effective treatment. One should also ascertain whether protective eyewear was worn, the time of injury, and extent of visual loss. If the patient presents with decreasing vision over time, it may suggest an active bleed. The medication list should be examined for anticoagulants such as aspirin, warfarin, clopidogrel, or NSAIDS. Additionally, the patient should be asked about sickle cell disease and coagulopathies. Patients with underlying coagulopathies have a higher rate of rebleeding and elevated intraocular pressures. Carbonic anhydrase inhibitors should be avoided in these patients due to increased sickling of red blood cells making it harder for the hyphema to clear. The ocular examination should include assessment for ruptured globe, intraocular pressure measurement, fundoscopic examination, and possible use of B-scan ultrasound (ultrasound of the eye) if the fundoscopic view is poor. CT scan of the orbits and brain may be indicated in some cases.6 Hyphemas can be graded 0–IV.14 Familiarity with this grading system will facilitate effective communication with the patient's ophthalmologist. Grade Grade Grade Grade Grade
0 I II III IV
Microhyphema and no gross visible blood in the AC Layered blood occupying less than one-third of the AC Blood fills one-third to one-half of the AC Blood fills one-half to less than total of the AC Total clotted blood, referred to as “8-ball” or “blackball” hyphema
The etiologies for hyphemas include a broad differential. These include trauma, intraocular surgery, neovascularization, neoplasia, infection, and vascular anomaly.15 Traumatic hyphema is related to rapid increases in intraocular pressure as well as the distortion of ocular structures. These include the iris, pupillary sphincter, trabecular meshwork, lens, zonules, vitreous, retina, and optic nerve.12
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The severity of hyphemas dictates management. Most will resolve with no sequelae or residual vision deficits. There are currently many differing opinions regarding management of hyphemas. Uncomplicated hyphemas can be managed with use of an eye shield, limited activity, and head elevation. There are multiple benefits to having the head elevated at a 451 angle. It allows the blood to settle inferiorly and thus not obstruct central vision. Additionally, it limits the amount of RBC exposure to the trabecular meshwork.4 Hospitalization should be considered in severe ocular injuries, non-compliant patients, or other scenarios deemed appropriate by the treating ophthalmologist. Protective eyewear is recommended during the day and night. The use of patches is discouraged as it prevents the patient from recognizing sudden visual changes. Mild analgesics such as acetaminophen can be prescribed for pain. Defer the remainder of necessary eye medications to the treating ophthalmologist. These will likely include topical steroids and cycloplegics. Additionally, screening for elevated intraocular pressure should be done by an ophthalmologist. The follow-up for these patients is usually daily for the first 5 days after the injury. Patients should be encouraged to return if there is a sudden increase in pain or decrease in visual acuity. Patients should be instructed to avoid strenuous activity for at least a week following injury and ideally until after resolution of hyphema.6 Surgical interventions include anterior chamber washout. This consists of anterior chamber irrigation and aspiration. Clot irrigation with trabeculectomy is an alternative option.12 Postoperative hyphemas may be seen at the time of surgery or within 3 days of surgery. Intraoperative hyphemas may necessitate coagulation.14 A recent retrospective chart review of 138 cases of pediatric unilateral traumatic hyphema showed that only three of the patients had a visual acuity of o20/40 after 1 month, and there were no cases of rebleeds. Of the 33 patients with elevated intraocular pressure, only four (12%) needed surgical intervention.16
Traumatic iritis The uvea is considered the vascular “middle” layer of the eye and is composed of the iris, ciliary body, and choroid. The iris is a circular structure in the eye best known for providing “eye color.” It controls the amount of light permitted to reach the retina by its ability to constrict or dilate. The first of two layers is known as the stroma. It is a pigmented fibrovascular tissue connected to muscles that effectively dilate or constrict the pupil. Those include the iris dilator muscle and iris sphincter muscle. The second and more posterior layer consists of pigmented epithelium. The pigment inhibits the passage of light assuring the pupil is the primary regulator of light reaching the retina. Inflammation of the iris is referred to as iritis.17 Iritis can be caused by infection, autoimmune disease, malignancy, and blunt trauma. Disorders such as syphilis, HIV, and sarcoidosis should be considered. It may be appropriate to order chest films for sarcoidosis and serology for syphilis.18 When the eye experiences trauma, the iris can be torn, cut, or even bruised. The damage incurred induces an inflammatory response in the anterior portion of the eye. The inflammatory response can cause the iris to become stuck to other structures in the eye such as the lens. Damage to the ciliary body and the accumulation of debris in the trabecular meshwork can cause changes in intraocular pressure.19 Traumatic iritis patients tend to present with dull or aching pain, photophobia, diminished vision, and tearing within 3 days of trauma. A thorough history will help elicit the mechanism of injury and time since its occurrence. A slit-lamp examination will demonstrate cells and flare in the anterior chamber. The patient may also have changes in intraocular pressure, mydriasis, miosis, conjunctival injection surrounding the limbus, decreased vision, and floaters. A complete ophthalmic examination including IOP measurements and dilated fundus examinations are necessary.6 The differential diagnosis of iritis is very broad, and as such, these patients should see a specialist and undergo an appropriate vasculitis workup to look for underlying systemic causes.6 Patients presenting with traumatic iritis should be referred to an ophthalmologist immediately. The mainstays of treatment are cycloplegic agents and steroid drops. Continued
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follow-up examinations by an ophthalmologist are necessary in order to rule out associated complications such as angle recession and retinal detachments.6 References 1. Clare G, Suleman H, Bunce C, Dua H. Amniotic membrane transplantation for acute ocular burns. Cochrane Database Syst Rev. 2012;9. [CD009379]. 2. Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41(4):275–313. 3. Barouch F, Colby KA. Evaluation and initial management of patients with ocular and adnexal trauma. In: Miller JW, Azar DT, Blodi B, eds. Albert and Jakobiec’s Principles and Practice of Ophthalmology, 3rd ed. Philadelphia: WB Saunders Elsevier. 2008:5071–5092. 4. Bradford Cynthia. Ocular and orbital injuries. In: Bradford Cynthia, editor. Basic Ophthalmology. 8th ed. San Francisco, CA: American Academy of Ophthalmology. 2004:108–110. 5. Gupta N, Kalaivani M, Tandon R. Comparison of prognostic value of Roper Hall and Dua classification systems in acute ocular burns. Br J Ophthalmol. 2011;95(2):194–198. 6. Gerstenblith AT. Trauma. In: Friedberg M, Rapuano C, eds. The Wills Eye Manual. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2012:13–17. [20–22]. 7. Wipperman JL, Dorsch JN. Evaluation and management of corneal abrasions. Am Fam Physician. 2013;87(2):114–120. 8. Wong TY, Lincoln A, Tielsch JM, Baker SP. The epidemiology of ocular injury in a major US automobile corporation. Eye (London). 1998;12(Pt 5):870–874. 9. Ball IM, Seabrook J, Desai N, Allen L, Anderson S. Dilute proparacaine for the management of acute corneal injuries in the emergency department. CJEM. 2010;12(5):389–396. 10. Menghini M, Knecht B, Kaufmann C, et al. Treatment of traumatic corneal abrasions: a three-arm, prospective, randomized study. Ophthalmic Res. 2013;50(1):13–18 http://dx.doi.org/10.1159/000347125. [Epub 2013 May 3]. 11. Eke T, Morrison DA, Austin DJ. Recurrent symptoms following traumatic corneal abrasion: prevalence, severity, and the effect of a simple regimen of prophylaxis. Eye. 1999;13(11a):345–347. 12. Basic and Clinical Science Course, 1st Ed. Glaucoma. American Academy of Ophthalmology, 2009-10:114–116. 13. Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. 2002;47(4): 297–334. 14. Sheppard J Jr., Crouch E, Williams P, Crouch E Jr., Rastogi S, Garcia-Venezuela E. Hyphema. Medscape Ref. 2009:1–19. 15. Viajalakshmi P, Shetty S, Jethani J, Devi TB. Bilateral spontaneous hyphaema in juvenile xanthogranuloma. Indian J Ophthalmol. 2006;Vol 56(1):45–46. 16. Soohoo J, Davies B, Braverman R, Enzenauer R, McCourt E. Pediatric traumatic hyphema: a review of 138 consecutive cases. J AAPOS. 2013;S1091-8531(13). [00285-1]. 17. Fine BS, Yanoff M, editors. Ocular Histology: A Text and Atlas. 2nd ed. New York: Harper & Row; 1972:168–212. 18. Deibel JP, Cowling K. Ocular inflammation and infection. Emerg Med Clin North Am. 2013;31(2):387–397. 19. Catania Louis J. Primary Care of the Anterior Segment. 2nd Ed. New York, NY: Appleton & Lange. 1995.
Contents lists available at ScienceDirect
Disease-a-Month journal homepage: www.elsevier.com/locate/disamonth
Management of anterior segment trauma Hercules D. Logothetis, BS, Scott M. Leikin, BA, Thomas Patrianakos, DO
Introduction Ophthalmologic emergencies have the potential to lead to severe morbidity and loss of vision. The ability to recognize and efficiently relay pertinent findings to an ophthalmologist is critical to preventing life-changing damage to the eye. Basic understanding of ocular anatomy, physiology, and pathology will facilitate a successful discussion between an ophthalmologist and the referring physician. As with other specialties, a detailed HPI should be attained that includes basic information such as onset, duration, intensity, and medication use. A useful review of systems includes questions regarding flashing lights, floaters, vision loss, and pain. Additionally, performing an ocular examination that checks visual acuity, intraocular pressure, and pupils will be advantageous to you, the ophthalmologist, and the patient. Anterior segment trauma involves injury to the part of the eye that is visible to the naked eye. Briefly, with the patient's lids open, one should be able to see the conjunctiva, sclera, cornea, iris, and pupil. Identification of these structures is critical and expected of physicians at any level. The variety of anterior segment trauma one may encounter is vast, thus, this article will focus on the presentation, diagnosis, and treatment of chemical burns, corneal abrasions, hyphemas, and traumatic iritis.
Chemical burns Chemical burns are one of the most common causes of ocular trauma and injury.1 Chemical burns are potentially blinding as they can cause ischemic injury to the limbal stem cells leading to deficits in healing and corneal opacification.2 They are most common in males 16–45 years old. They usually occur in industrial accidents, at home, or in connection with criminal assault. Protective eye shields are the most common preventative measure utilized in the work place and should always be encouraged when dealing with dangerous chemicals. The severity of a chemical burn is directly related to the surface area of exposure, the degree of penetration, and the compound.3 An alkali burn usually results in greater damage to the eye than an acidic burn.4 Alkali compounds are more lipophilic and are able to penetrate more easily. They saponify the cell membranes and can penetrate the corneal epithelium, basement membrane, http://dx.doi.org/10.1016/j.disamonth.2014.03.004 0011-5029/& 2014 Elsevier Inc. All rights reserved.
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stroma, and endothelium. In addition to ocular surface injury, alkali compounds can damage other anterior segment structures including the iris, lens, and ciliary body. Acidic compounds on the other hand denature and precipitate proteins. These precipitates can effectively create a barrier preventing further penetration. In general, acidic injuries are not as severe as alkali. However, hydrofluoric acid is one particular acidic agent that is known to penetrate readily.3 The majority of patients present to the emergency department or place a phone call to their primary care physician. The diagnosis is clinical and thus a proper history is important. It is important to illicit at what time the exposure occurred, the specific type of compound, time between exposure and irrigation, duration and type of irrigation, and whether any eye protection was involved. This information determines the severity, prognosis, and treatment. Following immediate irrigation, patients require slit-lamp examination with fluorescein staining to identify any corneal or conjunctival ulceration. Additionally, eyelid eversion is recommended to identify and remove foreign bodies. Obtaining intraocular pressures is suggested as well.4 Roper–Hall and Dua are classification systems used for chemical burns. In a randomized clinical trial, the Dua classification was found to be superior in predicting outcomes. The systems are presented below.5 Roper–Hall classification of ocular chemical injuries. Grade
Prognosis
Cornea
Conjunctival limbus
I II III IV
Good Good Guarded Poor
Corneal epithelial damage Corneal haze and iris details visible Total epithelial loss, stromal haze, and iris details obscured Corneal opaque and iris and pupil details obscured
No limbal ischemia o 1/3 Limbal ischemia 1/3–1/2 Limbal ischemia 4 1/2 Limbal ischemia
Dua classification of ocular chemical injuries. Grade
Prognosis
Clinical findings
Conjunctival involvement
I II III IV V VI
Very good Good Good Good to guarded Guarded to poor Very poor
0 clock hours of limbal involvement o3 clock hours of limbal involvement Between 3 and 6 clock hours of limbal involvement Between 6 and 9 clock hours of limbal involvement Between 9 and 12 clock hours of limbal involvement Total limbus involved
0% o30% 30–50% 50–75% 75–100% Total conjunctival involvement
Chemical burns are classified into mild, moderate, and severe (Fig. 1). Corneal epithelial defects can range from superficial punctate keratopathy to sloughing of the entire epithelium. Mild to moderate burns do not demonstrate areas of perilimbal ischemia. In contrast, ischemic
Fig. 1. (A). Dua Grade VI or Roper-Hall Grade IV. (B). Dua and Roper-Hall Grade II.
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injury presents as blanching of conjunctival or episcleral vessels. Mild to moderate burns show areas of conjunctival epithelial defect, chemosis (conjunctival edema), hyperemia, hemorrhages, eyelid edema, mild anterior chamber reaction, and first- and second-degree burns of periocular skin.6 Severe ocular burns present with chemosis, conjunctival blanching, corneal edema, corneal opacification, moderate to severe anterior chamber reaction, increased intraocular pressure, and second- and third-degree burns of surrounding skin. Additionally, if the compound penetrates through the sclera, it can potentially cause local necrotic retinopathy.6 Chemical ocular burns require immediate intervention. Treatment must be instituted immediately unless you suspect open globe. Ideally, one can use plastic squeeze bottles of eye irrigation solution or normal saline IV drip with plastic tubing to irrigate the affected eye. However, any source of water may be used as an alternative. Proper irrigation techniques can alter prognosis. Make sure to direct your irrigation toward the temple as to avoid the opposite eye. Irrigate the eye for a minimum of 30 min. The pH can be checked with litmus paper 5–10 min following irrigation. If a neutral pH is not achieved, continue irrigation. The nonophthalmologist should assist with irrigation and contact emergency services. Do not ever attempt to neutralize a compound with another compound. The goal is to dilute the compound the patient was exposed to. This includes alkali (lye, cements, plasters, airbag powder, bleach, and ammonia), acids (battery acid, pool cleaner, and vinegar), solvents, detergents, and irritants. Surgical debridement may be necessary for foreign bodies embedded in conjunctiva, cornea, sclera, and surrounding tissues. After initial management, it is imperative the patient is seen by an ophthalmologist. Subsequent care may include cycloplegics, topical antibiotics, pressure patch, oral pain medications, artificial tears, topical steroids, intraocular pressure management, and daily follow-up until corneal epithelial defect has healed.4,6 Every second following exposure can significantly alter outcome.
Corneal abrasions A corneal abrasion is defined as a defect in the corneal epithelium. The corneal epithelium is 4–5 cell layer stratified non-keratinized squamous epithelium that is critical to corneal clarity. It provides a protective barrier to pathogen invasion. Injury to the corneal epithelium may lead to loss of vision. Corneal abrasions account for approximately 8% of eye presentations in the primary care setting. Unfortunately, the diagnosis is often missed. While they often occur in any setting of corneal epithelial compromise, trauma is one of the most common causes. The injuries tend to heal quickly, but their potential to cause scarring and disturb visual acuity makes them necessary to diagnose and treat early.7 Corneal abrasions are often secondary to corneal epithelial trauma. Injuries can be incurred from foreign bodies, contact lens misuse, vigorously rubbing the eyes, or being poked in the eye amongst other etiologies. Patients with chronically dry eyes are more susceptible to this type of injury. They are often unavoidable and can have significant consequences both personally and professionally. A study of eye injuries at a major US automobile company showed an annual incidence of 15 per 1000 employees. The study found that 86.7% of those injuries were due to foreign body or corneal abrasion. One-third of the total eye injuries led to workers missing 1 day of work.8 Corneal abrasions are diagnosed clinically. The evaluation of these patients should focus on evidence of penetrating trauma, decreased visual acuity, and infection. These are all indications for emergent ophthalmologic referral.7 Patients often present with sharp pain, photophobia, tearing, discomfort with blinking, foreign body sensation, or history of trauma to the eye. On examination, the patient may demonstrate epithelial defect that stains with fluorescein and the absence of underlying corneal opacification. Conjunctival injection, swollen eyelids, and mild anterior chamber reaction may be seen as well. Appropriate workup requires a slit-lamp examination with fluorescein dye, evaluation for anterior chamber reaction, and identification of
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Fig. 2. Corneal abrasion.
corneal laceration or penetrating trauma (Fig. 2). In the setting of vertical or linear abrasions, it is especially important to evert the eyelids in search of any foreign bodies.6 Not every patient with a corneal abrasion will present with the same set of symptoms. It is important to rule out other pathologies that may share similar symptoms. Other possibilities to consider include recurrent corneal erosions, herpes simplex keratitis, confluent superficial punctate keratopathy, dry eye syndrome, conjunctivitis, and acute angle closure glaucoma.6,7 The goal of treatment is to relieve pain, speed healing, and prevent infection. Ophthalmologists often use topical antibiotics, NSAIDS, and cycloplegics during treatment.7 Non-contact lens wearers can be prescribed antibiotic ointments including erythromycin, bacitracin, or bacitracin/polymyxin B. Antibiotic drops including polymyxin B/trimethoprim and fluoroquinolones are alternative options. Contact lens wearers require anti-pseudomonal coverage.6 For pain control, oral Tylenol, NSAIDS, or narcotics can be used. Topical NSAID drops are also considered appropriate. Although a study found that dilute topical proparacaine can be used to alleviate the pain associated with acute corneal injuries,9 it is not recommended due to reports of impaired wound healing. Patching is also not recommended. It can decrease oxygen delivery and promote infection.7 Patching is especially contraindicated if the mechanism of injury involves vegetable matter, fingernails, or if the patient is a contact lens wearer. If one does wear a patch, it is important to be sure that the upper eyelid remains closed in order to prevent further abrasion. A prospective, three-armed, masked, randomized study of patients presenting with superficial corneal foreign bodies compared three different treatment modalities for corneal abrasions. The modalities included pressure patching with ofloxacin ointment, therapeutic contact lens with ofloxacin eye drops, and ofloxacin ointment alone. Primary outcome measure was the difference of the mean corneal abrasion area between the three groups over three different time points. The mean abrasion area was found to be the same amongst all three groups.10 Follow-up depends on the severity. Most abrasions heal within 24–48 h.7 Follow-up by an ophthalmologist may not be needed for abrasions that are 4 mm or less with a patient who has no visual acuity defects and symptoms that seem to be resolving. Central and large corneal abrasions require a follow-up the next day. An ophthalmologist should be consulted when the patient has symptoms that worsen on reexamination, any corneal infiltrates or ulcers, penetrating eye injuries, or visual acuity defects that are significant. Ultimately, healing time depends on the abrasion surface area. The larger the size, the longer it will take to heal. Traumatic abrasion patients treated in ophthalmology offices had recurrent symptoms for 3–4 months 28% of the time.11 Contact lenses should not be worn while healing and may be reintroduced once the eye feels normal for a week and appropriate medications have stopped.
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Fig. 3. Acute hyphema.
Hyphema The accumulation of blood in the anterior chamber is known as hyphema (Fig. 3). Minimal amounts of blood only observable by slit-lamp examination are referred to as microhyphemas. In contrast, larger hyphemas can often be observed by penlight examination alone. The patient's history usually includes recent trauma or ocular surgery. Patients present with pain, blurred vision, and blood in the anterior chamber that is grossly visible. The blood may appear black (8-ball) or red.6 The most common cause of hyphema is blunt trauma. Iris vasculature, ciliary body, and trabecular meshwork can be damaged from the compressive forces of such trauma. Any cause of intraocular inflammation in the anterior chamber may lead iris neovascularization and resulting accumulation of blood in the anterior chamber.12 In addition to trauma and surgery, hyphema can also occur spontaneously. Etiologies include iris melanoma, myotonic dystrophy, leukemia, hemophilia, von Willebrand disease, and the use of warfarin amongst other anticoagulant medications.13 Ascertaining the mechanism of injury is a crucial step in evaluation. Understanding the force, velocity, type, and direction of injury will facilitate more effective treatment. One should also ascertain whether protective eyewear was worn, the time of injury, and extent of visual loss. If the patient presents with decreasing vision over time, it may suggest an active bleed. The medication list should be examined for anticoagulants such as aspirin, warfarin, clopidogrel, or NSAIDS. Additionally, the patient should be asked about sickle cell disease and coagulopathies. Patients with underlying coagulopathies have a higher rate of rebleeding and elevated intraocular pressures. Carbonic anhydrase inhibitors should be avoided in these patients due to increased sickling of red blood cells making it harder for the hyphema to clear. The ocular examination should include assessment for ruptured globe, intraocular pressure measurement, fundoscopic examination, and possible use of B-scan ultrasound (ultrasound of the eye) if the fundoscopic view is poor. CT scan of the orbits and brain may be indicated in some cases.6 Hyphemas can be graded 0–IV.14 Familiarity with this grading system will facilitate effective communication with the patient's ophthalmologist. Grade Grade Grade Grade Grade
0 I II III IV
Microhyphema and no gross visible blood in the AC Layered blood occupying less than one-third of the AC Blood fills one-third to one-half of the AC Blood fills one-half to less than total of the AC Total clotted blood, referred to as “8-ball” or “blackball” hyphema
The etiologies for hyphemas include a broad differential. These include trauma, intraocular surgery, neovascularization, neoplasia, infection, and vascular anomaly.15 Traumatic hyphema is related to rapid increases in intraocular pressure as well as the distortion of ocular structures. These include the iris, pupillary sphincter, trabecular meshwork, lens, zonules, vitreous, retina, and optic nerve.12
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The severity of hyphemas dictates management. Most will resolve with no sequelae or residual vision deficits. There are currently many differing opinions regarding management of hyphemas. Uncomplicated hyphemas can be managed with use of an eye shield, limited activity, and head elevation. There are multiple benefits to having the head elevated at a 451 angle. It allows the blood to settle inferiorly and thus not obstruct central vision. Additionally, it limits the amount of RBC exposure to the trabecular meshwork.4 Hospitalization should be considered in severe ocular injuries, non-compliant patients, or other scenarios deemed appropriate by the treating ophthalmologist. Protective eyewear is recommended during the day and night. The use of patches is discouraged as it prevents the patient from recognizing sudden visual changes. Mild analgesics such as acetaminophen can be prescribed for pain. Defer the remainder of necessary eye medications to the treating ophthalmologist. These will likely include topical steroids and cycloplegics. Additionally, screening for elevated intraocular pressure should be done by an ophthalmologist. The follow-up for these patients is usually daily for the first 5 days after the injury. Patients should be encouraged to return if there is a sudden increase in pain or decrease in visual acuity. Patients should be instructed to avoid strenuous activity for at least a week following injury and ideally until after resolution of hyphema.6 Surgical interventions include anterior chamber washout. This consists of anterior chamber irrigation and aspiration. Clot irrigation with trabeculectomy is an alternative option.12 Postoperative hyphemas may be seen at the time of surgery or within 3 days of surgery. Intraoperative hyphemas may necessitate coagulation.14 A recent retrospective chart review of 138 cases of pediatric unilateral traumatic hyphema showed that only three of the patients had a visual acuity of o20/40 after 1 month, and there were no cases of rebleeds. Of the 33 patients with elevated intraocular pressure, only four (12%) needed surgical intervention.16
Traumatic iritis The uvea is considered the vascular “middle” layer of the eye and is composed of the iris, ciliary body, and choroid. The iris is a circular structure in the eye best known for providing “eye color.” It controls the amount of light permitted to reach the retina by its ability to constrict or dilate. The first of two layers is known as the stroma. It is a pigmented fibrovascular tissue connected to muscles that effectively dilate or constrict the pupil. Those include the iris dilator muscle and iris sphincter muscle. The second and more posterior layer consists of pigmented epithelium. The pigment inhibits the passage of light assuring the pupil is the primary regulator of light reaching the retina. Inflammation of the iris is referred to as iritis.17 Iritis can be caused by infection, autoimmune disease, malignancy, and blunt trauma. Disorders such as syphilis, HIV, and sarcoidosis should be considered. It may be appropriate to order chest films for sarcoidosis and serology for syphilis.18 When the eye experiences trauma, the iris can be torn, cut, or even bruised. The damage incurred induces an inflammatory response in the anterior portion of the eye. The inflammatory response can cause the iris to become stuck to other structures in the eye such as the lens. Damage to the ciliary body and the accumulation of debris in the trabecular meshwork can cause changes in intraocular pressure.19 Traumatic iritis patients tend to present with dull or aching pain, photophobia, diminished vision, and tearing within 3 days of trauma. A thorough history will help elicit the mechanism of injury and time since its occurrence. A slit-lamp examination will demonstrate cells and flare in the anterior chamber. The patient may also have changes in intraocular pressure, mydriasis, miosis, conjunctival injection surrounding the limbus, decreased vision, and floaters. A complete ophthalmic examination including IOP measurements and dilated fundus examinations are necessary.6 The differential diagnosis of iritis is very broad, and as such, these patients should see a specialist and undergo an appropriate vasculitis workup to look for underlying systemic causes.6 Patients presenting with traumatic iritis should be referred to an ophthalmologist immediately. The mainstays of treatment are cycloplegic agents and steroid drops. Continued
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follow-up examinations by an ophthalmologist are necessary in order to rule out associated complications such as angle recession and retinal detachments.6 References 1. Clare G, Suleman H, Bunce C, Dua H. Amniotic membrane transplantation for acute ocular burns. Cochrane Database Syst Rev. 2012;9. [CD009379]. 2. Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41(4):275–313. 3. Barouch F, Colby KA. Evaluation and initial management of patients with ocular and adnexal trauma. In: Miller JW, Azar DT, Blodi B, eds. Albert and Jakobiec’s Principles and Practice of Ophthalmology, 3rd ed. Philadelphia: WB Saunders Elsevier. 2008:5071–5092. 4. Bradford Cynthia. Ocular and orbital injuries. In: Bradford Cynthia, editor. Basic Ophthalmology. 8th ed. San Francisco, CA: American Academy of Ophthalmology. 2004:108–110. 5. Gupta N, Kalaivani M, Tandon R. Comparison of prognostic value of Roper Hall and Dua classification systems in acute ocular burns. Br J Ophthalmol. 2011;95(2):194–198. 6. Gerstenblith AT. Trauma. In: Friedberg M, Rapuano C, eds. The Wills Eye Manual. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2012:13–17. [20–22]. 7. Wipperman JL, Dorsch JN. Evaluation and management of corneal abrasions. Am Fam Physician. 2013;87(2):114–120. 8. Wong TY, Lincoln A, Tielsch JM, Baker SP. The epidemiology of ocular injury in a major US automobile corporation. Eye (London). 1998;12(Pt 5):870–874. 9. Ball IM, Seabrook J, Desai N, Allen L, Anderson S. Dilute proparacaine for the management of acute corneal injuries in the emergency department. CJEM. 2010;12(5):389–396. 10. Menghini M, Knecht B, Kaufmann C, et al. Treatment of traumatic corneal abrasions: a three-arm, prospective, randomized study. Ophthalmic Res. 2013;50(1):13–18 http://dx.doi.org/10.1159/000347125. [Epub 2013 May 3]. 11. Eke T, Morrison DA, Austin DJ. Recurrent symptoms following traumatic corneal abrasion: prevalence, severity, and the effect of a simple regimen of prophylaxis. Eye. 1999;13(11a):345–347. 12. Basic and Clinical Science Course, 1st Ed. Glaucoma. American Academy of Ophthalmology, 2009-10:114–116. 13. Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. 2002;47(4): 297–334. 14. Sheppard J Jr., Crouch E, Williams P, Crouch E Jr., Rastogi S, Garcia-Venezuela E. Hyphema. Medscape Ref. 2009:1–19. 15. Viajalakshmi P, Shetty S, Jethani J, Devi TB. Bilateral spontaneous hyphaema in juvenile xanthogranuloma. Indian J Ophthalmol. 2006;Vol 56(1):45–46. 16. Soohoo J, Davies B, Braverman R, Enzenauer R, McCourt E. Pediatric traumatic hyphema: a review of 138 consecutive cases. J AAPOS. 2013;S1091-8531(13). [00285-1]. 17. Fine BS, Yanoff M, editors. Ocular Histology: A Text and Atlas. 2nd ed. New York: Harper & Row; 1972:168–212. 18. Deibel JP, Cowling K. Ocular inflammation and infection. Emerg Med Clin North Am. 2013;31(2):387–397. 19. Catania Louis J. Primary Care of the Anterior Segment. 2nd Ed. New York, NY: Appleton & Lange. 1995.
