Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit Introduction Ocular trauma is an unfortunate, yet relatively common condition treated in todays optometric practice. As primary eye care providers, optometrists must stay up-to-date with current trauma management principles. The content of this course is designed to review common as well as unusual traumatic conditions that may be seen and/or necessarily ruled-out when examining a patient who has sustained trauma. Additionally, the management of each condition will be discussed in detail. After completing this course, if nothing else, it is very important to always keep in mind that patients with seemingly mild ocular traumatic conditions, such as periorbital ecchymosis and subconjunctival hemorrhages, need to be examined very carefully as these events signal to us that the eye and/or orbit has sustained a substantial injury that may have caused more serious problems. Optometrists must be vigilant when examining these patients and remember to document thoroughly and dilate as appropriate. Follow-up is also critical as sequelae from trauma may be more obvious and profound at a later time. 1.1 Brief Epidemiology There are approximately 3 million ocular and orbital injuries in the US per year. Of those injuries, approximately 20,000 to 68,000 are vision-threatening injuries and some 40,000 sustain significant vision loss. In the US, trauma is the leading cause of unilateral blindness and is preceded only by cataract as a cause for vision impairment. Males are much more likely than females to sustain ocular trauma and this is especially true for young males. In the Beaver Dam Eye Study, 20% of adults reported ocular trauma in their lifetime and these people were 3 times more likely to experience further ocular trauma. In this study, sharp objects caused more than half of all injuries. Surprisingly, the home seems to be more dangerous in terms of traumatic eye injuries than the workplace, but about 23% of all ocular injuries are sports-related. Baseball seems to be the most dangerous sports in terms of these injuries. Interestingly, fishing is the second most dangerous sport with bystanders accounting for 25% of these ocular injuries. Although proven to be effective in saving lives, frontal airbags have caused a two-fold increase in eye injuries related to motor vehicle accidents.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit In the US, the frequency of traumatic ocular conditions is as follows:

Superficial injury of the eye and adnexa (41.6%) Foreign body on the external eye (25.4%) Contusion of the eye and adnexa (16.0%) Open ocular adnexa and eyeball wounds (10.1%) Orbital floor fracture (1.3%) Nerve injury (0.3%)

1.2 Pathophysiology There are four main mechanisms that cause ocular trauma: coup, contrecoup, equatorial expansion and global repositioning. The coup (pronounced koo) is the initial force caused directly by the trauma. The contrecoup is the shockwave that is imparted by the coup and is transmitted throughout the ocular and orbital structures. During blunt trauma, the equator of the globe tends to expand and, therefore, distort the normal ocular architecture. Finally, the globe returns to its normal shape, but this is not always a benign event and can cause damage as well. Keep in mind that this is all occurring to tissues and structures that have varying degrees of elasticity and tensional strength. For example, the sclera is rigid due to collagen fortification and the retina is flexible, but the RPE and Bruchs membrane are less elastic. These differences in mechanical properties play a major role in ocular trauma pathophysiology. 1.3 Classification In a broad sense, the two main categories that ocular trauma can be divided into are closed and open globe injuries. When examining a patient with trauma, it is imperative to determine which of these categories a patient belongs to as this will direct the immediate management of the patients condition. Patients with closed globe injuries have a contusion or a lamellar laceration. Patients with open globe injuries have a rupture or a laceration, with the latter being either a penetrating or perforating injury. While seemingly fairly obvious, differentiating between a closed and open globe injury can be on occasion somewhat difficult. 1.4 Trauma Examination Of course, the problem-oriented exam is used when examining a patient who may have sustained ocular trauma. The case history should be directed particularly to the details of the trauma, pre-injury vision, previous ocular surgery, medical history, current medications and
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit allergies. If the patient is in significant pain, taking their visual acuity can be difficult. In these cases, instilling a topical anesthetic is often necessary to facilitate this task. Externals should always include pupillary testing, extra-ocular motilities (EOMs), and confrontational visual field testing. If the patient has sustained blunt ocular trauma, cover test and/or Maddox rod testing should be performed to look for an ocular deviation. Also, the eyelids and orbital margins should be palpated and the forehead and cheeks should be evaluated for sensitivity loss or imbalance. The slit-lamp examination should include fluorescein staining, which is necessary for Seidel testing and applanation tonometry, but tonometry should always be deferred for any known open globe injuries. A dilated fundus exam, with or without scleral depression when appropriate, is an essential part of the complete examination. Of course, other ancillary tests are sometimes helpful for diagnosing, management and follow-up and include color vision and automated visual field testing, gonioscopy, and imaging studies. Conditions The conditions will be discussed in a general order from anterior to posterior. 2.1 Myopia Traumatic myopia refers to the transient myopic refractive error shift that occur occasionally after blunt ocular trauma. Anywhere from 1 to 9.75D of myopia has been reported in the literature. This condition is thought to be caused by anatomical changes in the ciliary body and crystalline lens. Ciliary body edema causes relaxation of the lens zonules and, therefore, thickening of the crystalline lens essentially decreasing the anterior and posterior radii of curvature. Ciliochoroidal effusion causes an anterior shift of the lensiris diaphragm, which also causes the eye to be a more positively powered optical entity. This condition does not require treatment and tends to resolve without treatment.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.2 Periorbital Ecchymosis Periorbital ecchymosis or what is commonly known as a black eye is blood accumulation in the eyelids. It is usually greater in the lower lid and occasionally forms an organized hematoma or firm purplish-black mass. The treatment of this common condition, have the patient use a cold compress intermittently for the first 48 hours, followed by hot packs for 3 to 5 days thereafter. 2.3 Eyelid Laceration There are basically three types of eyelid lacerations that can occur from trauma and most often are related to sharp objects rather than blunt trauma. Remember, when dealing with any type of eyelid laceration, always consider tetanus prophylaxis when appropriate. To treat simple superficial lacerations, clean the wound and surrounding skin (e.g. Betadine), irrigate it thoroughly with saline and remove any foreign bodies that may still be present. Finally, apply an antibacterial ointment and sterile dressing. Deeper lacerations or those involving the lid margin require sutures so management depends greatly on state scope laws.

Complicated lacerations require an oculo-plastics consult. These are lacerations that have extensive tissue loss or have damage to the lacrimal drainage system, levator aponeurosis, and/or the medial canthus tendon.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.4 Subconjunctival Hemorrhage There is usually no treatment necessary for a standard subconjunctival hemorrhage although artificial tears tend to enhance comfort for those symptomatic patients. Be sure to reassure the patient that the condition will resolve in 1 to 2 weeks and discontinue any elective aspirin or non-steroidal antiinflammatory drugs (NSAIDs) as these can facilitate further hemorrhaging. When appropriate, acetaminophen is generally safe to use with these patients as it does not affect the clotting cascade. 2.5 Conjunctival Abrasion and Laceration Conjunctival abrasions have fluorescein staining and tend to have some degree of subconjunctival hemorrhage, whereas lacerations almost always have hemorrhaging and examination typically reveals exposed white sclera. With lacerations, the conjunctival edges have a tendency to be rolled because of the conjunctivas elastic nature. The treatment for these two conditions is varies from artificial tears to using an antibiotic ointment (TID for 4 to 7 days) with pressure patching (for 24 hours). If a laceration is greater than 1 to 1.5cm, consider suturing, but surprisingly, most lacerations will heal without surgical repair. 2.6 External Foreign Body Corneal and conjunctival foreign bodies are commonly seen in primary care practices. Patients can be completely asymptomatic, but generally foreign bodies cause mild to moderate eye pain depending to their composition, location and the patients pain tolerance. When examining a patient with a possible foreign body, it is always important to inspect the fornices thoroughly and evert the eyelids to look for hidden palpebral conjunctival foreign bodies. Corneal track marks, or
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit vertical linear corneal abrasions, are a telltale sign of these occult foreign bodies. For conjunctival or limbal foreign body removals, xylocaine is preferable when available as it causes more anesthesia then proparacaine or tetracaine. Corneal foreign bodies can present with rust rings, corneal infiltrates and mild anterior chamber reactions. Before removing a corneal foreign body, always attempt to localize its depth as a penetrating object should be considered an open-globe injury and co-managed with an anterior segment or corneal subspecialist when available. Personally, I prefer using a large gauge needle over a foreign body spud for most removals as I can be more precise and usually cause less iatrogenic damage. However, you should always approach the patient tangentially to prevent inducing an accidental penetrating injury. Dilating the patient is always important to help rule out an intraocular foreign body (to be discussed later) especially when there is a history of a possible metal-on-metal or high-velocity projectile, but should also be routinely done as the cycloplegic effect greatly enhances patient comfort. After removal, treat the patient as you would if they had an abrasion. 2.7 Corneal Abrasion Fluorescein staining with a negative Seidel test and a history of rubbing or scraping of the cornea are the characteristic findings of a corneal abrasion. It is not unusual to find a mild anterior chamber reaction especially when patient presents after a prolonged amount of time. Always carefully measure the size of the abrasion as this will help your follow-up management and instruct the patient that their visual acuity may initially decrease.

There are two basic methods to manage patients with corneal abrasions. The first method, which is preferable for small to moderately sized abrasions and with all contact lens wearers, is to use a fairly tight-fitting bandage contact lens along with a topical antibiotic drop having good anti-pseudomonal activity. My personal preference is to use a silicone hydrogel contact lenses because of their higher oxygen permeability. In 2005, Engle et al showed that PRK patients who used lotrafilcon A contact lenses had significantly faster corneal reepithelialization and reduced
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit discomfort during the first 48 postoperative hours when compared to etafilcon A lenses. Also, certain silicone hydrogel lenses do not take-up fluorescein, which is a particularly nice feature when you see the patient on follow-up. The fourth generation fluoroquinolones make an excellent choice due to their spectrum of activity and low incidence of bacterial resistance. Another recent choice for prophylactic antibiosis is AzaSite because of its low dosing regimen. However, less expense drugs such as Polytrim tend to also work well for these uses. Remember, that as far as resistance development goes, it is always better to stop an antibiotic at is full dosage early than to prolong its use with a lower dosage frequency. The second method of treatment is to use an antibiotic ointment and pressure patch the patient. Although not necessary for the majority of corneal abrasions, this method is sometimes preferable over a bandage contact lens for moderate to large abrasions. It is extremely important to remove the patch everyday to check on the resolution and ensure that the patient is not developing an infection. Switching the patient to a bandage contact lens as they begin to heal usually further enhances patient comfort and is of course more aesthetically pleasing. To treat the associated pain, always cycloplege the patient and consider a topical analgesic for mild to moderate pain and an oral analgesic for moderate to severe pain. Patients have varying degrees of pain tolerance, but always beware of drug seeking behavior. When writing narcotic prescriptions, always write the number of tables dispensed in both word and number format (example: Disp. ten (10) tablets) to avoid prescription fraud. 2.8 Corneal Laceration As opposed to corneal abrasions, corneal lacerations tend to have a history of cutting or tearing of the cornea. The Seidel test is crucial for determining whether the patient has a full or partial-thickness laceration. When examining these patients, gentle digital pressure may enhance the Seidel test and will allow a general assessment of the IOP if the depth of the laceration is uncertain. For a mild partial-thickness laceration without a gaping wound, treat it like a corneal abrasion. If it is moderate to deep, with or without a gaping wound, suturing is required so depending on state scope laws, co-management of these patients with a corneal or anterior segment sub-specialist
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit may be necessary. A full-thickness corneal abrasion, which may present with iris prolapse, should be treated like a ruptured globe (discussed later). In these cases, place a protective shield on the patient and arrange a STAT surgical consult as this is a sight threatening condition. 2.9 Photokeratitis UV radiation can cause an ocular sunburn in the form of photokeratitis, which is also referred to as a flash burn, UV keratitis, and snow blindness. Essentially, there UV radiation causes an inhibition of mitosis, production of nuclear fragmentation, and loosening of the epithelial layer. The patient history usually gives away this condition as patient present with pain (can be extreme), photophobia, blurred vision, lacrimation, and a foreign body sensation. The unique attribute of the history is the 6 to 12 hour latency in symptoms, which generally means that the onset of symptoms occurs in the evening. This unexplained pattern of corneal sensory loss and return and is thought to indicate a probable photochemical injury rather than a thermal injury to the cornea. The clinical signs associated with photokeratitis are SPK, conjunctival injection and chemosis, lid erythema and edema. Treatment consists of in-office cycloplegia, an antibiotic ointment (TID), copious artificial tears, oral pain medication. Also, if necessary, pressure patching the worse eye can be considered. 2.10 Chemical Burns Generally, there are two main agents that can cause an ocular chemical burn; bases and acids.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.10.1 Bases Alkaline (basic) agents are particularly damaging due to their hydrophilic and lipophilic properties which allows them to rapidly penetrate cell membranes and the anterior chamber within minutes. Damage results from saponification of cell membranes and cell death along with disruption of the extracellular matrix. Although criticized in the literature because of advances in corneal wound therapy and surgical technique, the Roper-Hall classification system is still very useful for primary eye care practitioners.

Limbal involvement is so important because that is where the corneal stem cells that replenish the epithelium are located. 2.10.2 Acids Acids generally cause less damage than bases as many corneal proteins bind acid and act as a chemical buffer and coagulated tissue acts as a barrier to further penetration of acid. Damage usually results from collagen fibril shrinkage, which can cause symblepharon formation.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit The treatment for chemical burns remains somewhat controversial in the literature. It is important to train staff members to instruct patients to immediately irrigate their eyes with water. This significantly reduces the severity of alkali burns and shortens the healing time. If a patient presents to the office, begin irrigation immediately for at least 30 minutes. Sterile saline preferable, but if not available, use tap water and anesthetize as necessary. Mild to moderate burns can be, in most cases, successfully treated in the primary care setting. The patient should be cyclopleged, but only with a cholinergic antagonist. It is important not to use an adrenergic agonist which would further constrict the limbal vascular supply that is potentially already compromised. A prophylactic antibiotic ointment should be dosed every 1-2 hours along with copious artificial tears. Oral pain medication is usually indicated and pressure patching can be considered. Although controversial, a topical steroid should be seriously considered (QID for 7 days, see below for more information). Patient occasionally have elevated IOP, which should be treated if present. Diamox (acetazolamide) is a good choice when treating alkali burns with elevated IOP as it actually decreases the anterior chamber pH and increases ascorbic acid (alkali burns can cause the anterior chamber pH to increase and decreases anterior chamber ascorbate) and a topical -blocker can be added if necessary. The patient needs to be examined daily until full re-epithelialization has occurred. Moderate to Severe burns usually require a referral to a corneal specialist as appropriate and hospital admission may be necessary. As mentioned previously, the use of steroids when managing chemical burns is somewhat controversial as corneoscleral melting after alkali burns has been associated with the use of topical steroids for more than 10 days leading to the theory that steroids enhance the activity of collagenases, which are a group of matrix metalloproteinases that can cause corneal stromal thinning and perforation. However, steroids help block infiltration by PMN cells and should therefore actually help prevent an accumulation of collagenases. It has also been proposed that the decrease in anterior chamber vitamin C seen with alkali burns may actually be the cause of corneal ulceration. Vitamin C use has been shown to stimulate collagen production by fibroblasts and the concurrent use of topical steroids and topical vitamin C has been shown to be safe and effective for treating ocular alkali burns. As topical vitamin C is not currently available in the US, some suggest the use of oral vitamin C of up to 2-g QID. Another advancement in the management of corneal wound healing is the use of amniotic membranes. The idea of using amniotic membranes for wound healing came about because incisions made via the skin of the fetus during fetal surgery performed in the third trimester
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit does not bear any scarring after birth. Although the exact mechanism involved is not yet known and it is not clear if amniotic membranes act like fetal tissue, it is now widely known that amniotic membranes promote rapid corneal epithelialization and reduce inflammation, scarring, and neovascularization. The amniotic membrane are usually sutured to the cornea and can be used with or without limbal stem cell transplantation for patients with severe limbal damage. Additionally, the ProKera medical device, a suture-less amniotic membrane carrier, can now also be considered. 2.11 Microhyphema Microhyphema, by definition, is a small hyphema whereby there are only suspended red blood cells (RBCs) in the anterior chamber without the formation of a layered clot. It is graded from 1+ to 4+ based on the amount of RBCs and may settle into a hyphema as it progresses. The complications of a microhyphema are the same as hyphema including IOP elevation and secondary hemorrhage.

Although to a lesser degree than hyphema management, the treatment of microhyphema is controversial, but as with hyphema, the unified goal is to allow the blood clot to heal completely. In 2002, the Wills Eye Hospital published their protocol for treating microhyphema. The management is as follows:

Discontinuation of elective anticoagulants Bed rest with 30 head elevation (to reduce episcleral venous pressure and allow blood cells to settle faster) for 4 days then the patient may resume light activity for 2 weeks after trauma Full-time protective shield for 2 weeks (use a clear or perforated shield as patients should monitor their vision) Atropine 1% QD to TID for 2 weeks Topical steroids should be considered when not contraindicated Test all Hispanics or African Americans with an IOP greater than 21mmHg for sickle cell disease

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit Compliant, non-sickle cell patients with an IOP less than or equal to 25mmHg should return in 2 weeks or sooner with visual changes (decreased VA, increased pain, increased photophobia). Compliant, non-sickle cell patients with an IOP greater than 25mmHg or sickle cell patients with an IOP greater than 21mmHg should return for follow-up daily for 3 days and should be treated for elevated IOP. This difference in management is due to the fact that since sickle cell patients have a greater risk of developing glaucomatous optic neuropathy at lower levels of IOP. Keep in mind that Diamox is contraindicated in sickle cell patients as it exacerbates the sickling process, but neptazane for diamox if necessary. Alpha-agonists can affect iris vasculature, miotics, epi and prostaglandins can cause inflammation. Use a beta-blocker, then neptazane then paracentesis for sickle cell patients.. Non-compliant patients should not be treated on an outpatient basis. Gonioscopy and scleral depression can be performed only after 2 weeks allowing enough time for the clotting process to be nearly complete. 2.12 Hyphema A hyphema is layering of RBCs in the inferior anterior chamber. During the slit-lamp examination, it is of the utmost importance to measure and document the height of the hyphema as this will dictate both the management and follow-up of the condition. A grade 1+ hyphema has less that 1/3 of the anterior chamber filled with blood. A grade 2+ hyphema has from 1/3 to 1/2 of the anterior chamber filled. A grade 3+ has greater than 1/2 of the anterior chamber filled with blood, but less than a grade 4+ or 8-ball that is a total hyphema in which the entire anterior chamber is filled. As an interesting side note, hyphema patients commonly experience a temporary decrease in accommodative amplitude and may complain about blurred near vision. Again, the management of hyphema is extremely controversial and the literature is littered with variegated opinions on the matter. As a very general guide, outpatient management should only be considered for compliant adults (in terms of medication, activity and follow-up) without sickle cell disease or trait, blood dyscrasia or bleeding diathesis, who have less than a grade 2+ hyphema and an IOP less than or equal to 35mmHg. All other patients require hospitalization during the most critical time for clot formation, which is about 5 to 7 days after the injury. Some of these patients will require surgical evacuation of the clot.
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit

Outpatient treatment consists of: discontinuing any elective anticoagulants, atropine 1% (from QD to TID), reduce patient to bed rest with ambulatory activities kept to a minimum and no strenuous activities for 2 weeks, and antiglaucoma medication as needed. Avoid sedative medication as patients with hyphema sometimes become somnolent so use mild analgesics only (e.g. Tylenol). In bed, the patients head should be elevated 30, they should wear a fulltime clear or perforated protective shield for 2 weeks, and need to be seen daily for 3 days, then several days to a week thereafter depending on their progress. They can gradually resume normal activities after about 2 weeks if they are doing well and dont experience a rebleed. Gonioscopy and scleral depression should be deferred for 2 to 4 weeks after trauma. Amicar (-aminocaproic acid) is an antifibrinolytic agent that has been used 50 mg/kg PO every 4 hours for 5 days and has been shown to decrease the rate of rebleeding, but its use is controversial due to a lack of improved visual acuity outcome data and side affects such as nausea, vomiting, diarrhea, muscle weakness, abdominal cramps, bradycardia, postural hypotension, and potentially, increased IOP. Although not currently marketed, a topical gel preparation of aminocaproic acid has been shown to be as effective and Amicar and has an improved safety profile. Corticosteroids have also been studied because they are known to stabilize the blood-ocular barrier and directly inhibit fibrinolysis. Oral steroids, used 40 mg a day in divided doses, have been shown in some studies to be as effective as or better than Amicar at reducing secondary bleeding and are much less expensive. Topical steroids may be as effective as oral steroids, but this is not well established. When managing a patient with hyphema, keep in mind that 3.5 to 38% rebleed usually 2 to 5 days after the injury, about 30% have temporarily elevated IOP for 5 to 7 days. Also, about 5% require surgical intervention and approximately 75% demonstrate some degree of angle recession or iridodialysis, but only 5% will develop secondary glaucoma. Due to the relatively high percentage of rebleeds, which can actually be worse than the original hyphema, Romano and Phillips (2000) have now published several times on a hands off approach, which has been shown to have excellent results. This method requires oral steroid use and hospitalization for all hyphema patients and there is absolutely no routine tonometry or eye drops used in order to limit ocular manipulation and, therefore, decrease the chance of clot dislodgement. Indeed, the proper management of this condition is still quite debatable.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.13 Hemosiderosis Hemosiderosis is the clinical entity whereby the cornea becomes stained by blood; specifically by the iron contained within the RBCs. It is more likely to occur when a 50% or greater hyphema is present for a week or more, when the IOP is elevated, or if there is concomitant endothelial damage. Although not recommended, some advocate patching hyphema patients as prolonged light exposure causes endothelial dysfunction and corneal staining. Interestingly, the staining resolves from the limbus towards the central cornea. 2.14 Angle Recession Angle recession is often overlooked on gonioscopy, but occurs commonly with blunt ocular trauma. Studies show that 56 to 100% of patients with a past history of traumatic hyphema have some degree of angle recession. Mechanistically, the pathogenesis of angle recession is easy to understand. When the globe is hit, the IOP is suddenly elevated and causes a posterior displacement of the iris. A valve-like action of the iris prevents aqueous from flowing back through the pupil and, therefore, causes a portion of the force from the blow to be redirected towards the angle. This manifests as a tearing of the uveal meshwork (mild) and possibly between the longitudinal and circular fibers of the ciliary muscle (moderate) and is associated with immediate and subsequent damage to the corneoscleral trabecular meshwork. To observe angle recession, it is often helpful to compare both eyes and look for a discrepancy in anterior chamber depth and ciliary body band width of corresponding quadrants on gonioscopy. Also, look for tears in iris processes, a whitening and enhanced visibility of the scleral spur, tears of the uveal meshwork covering the ciliary muscle giving it a bare appearance, and for indications of past trauma such as eyelid scars or iris sphincter tears. Patients with angle recession without glaucoma need to be followed annually for the development of glaucoma and patient education is the key to success.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.15 Glaucoma Traumatic glaucoma is a secondary open-angle glaucoma and may occur in 2-10% of those with angle recession over a 10 year period. It is more likely to occur with 180 or more of angle recession. There are primarily two types (some references list three distinct types) based on onset of permanently elevated IOP: early and late. The early type of angle recession glaucoma develops from a few weeks to a year or two after trauma with the severity usually relating to the visible extent of the injury. This is more common than the late type and the obstruction to aqueous outflow is, at least in part, a direct consequence of damage to the trabecular meshwork. The late type of angle recession glaucoma usually arises 10 or more years after the injury and is more likely to occur in eye with 270 or more of angle recession. The small percentage of patients that develop this type could have an underlying predisposition to the development of primary open-angle glaucoma as evidenced by the fact that it is rare to develop truly unilateral glaucoma years after blunt trauma. The management of traumatic glaucoma is generally the same as currently with primary open-angle glaucoma, that is to choose a drug that inhibits aqueous formation or increases uveoscleral outflow. Pilocarpine is not indicated as it may cause a paradoxical increase in IOP because it decreases uveoscleral outflow. In refractory cases, surgical intervention may be necessary, but success rates are lower than with primary open-angle glaucoma. 2.16 Cyclodialysis Cleft A cyclodialysis cleft is a separation of the longitudinal muscle of the ciliary body from the sclera. This separation creates a path for aqueous to exit the anterior chamber directly to the subchoroidal space, so there will obviously be some degree of hypotony. Look for a white area below the scleral spur on gonioscopy, but ultrasound biomicroscopy (UBM) will be helpful if available. The treatment of choice is atropine 1% BID to TID for 6 to 8 weeks. If this fails, argon laser photocoagulation can be helpful, but surgical intervention will be otherwise required.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.17 Iridodialysis Iridodialysis is a detachment of the iris root from the ciliary body and can produce corectopia (irregular pupil shape), pseudopolycoria, and diplopia. These patients must be monitored for glaucoma as they are at a higher risk for developing increased IOP. If the patient experiences bothersome diplopia, consider opaque soft contact lens with a clear pupil. Surgery, while usually not necessary, decreases the likelihood of peripheral anterior synechia formation. 2.18 Iritis Besides the history of trauma, a traumatic iritis presents very much like other types of anterior uveitides although tends to be more painful than other varieties. There tends to be photophobia in involved and uninvolved eye (because of consensual pupillary constriction), perilimbal injection and cells and flare in the anterior chamber. Treatment consists primarily of using a cycloplegic agent. Topical steroids are usually not necessary because the stimulus for the iritits, that is the trauma itself, is no longer present. However, topical steroids are helpful for refractory cases or when the patient is in significant pain. Unless necessary, defer scleral depression until the eye is quiescent.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.19 Vossius' Ring Vossius ring is a traumatic imprint of the iris pigment epithelium on the anterior lens capsule and usually fades with time. It should be differentiated from posterior synechia remnants from a prior uveitis.

2.20 Cataract A traumatic cataract, or contusion rosette, may not be apparent for years after trauma. While anterior and/or posterior subcapsular opacities can occur with trauma, a petalliform cataract is most commonly found and is a compact white starshaped opacity, usually in the anterior cortex. The cataract may not appear until years after the trauma and this delayed-onset is thought to be due to a change in metabolism. There is no difference in the management of this cataract compared with the age-related variety although the patient should be made aware that there is an increased risk of zonular dehiscence during cataract extraction.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.21 Lens Subluxation Lens subluxation is a partially dislocated crystalline lens due to incomplete zonular dehiscence secondary to equatorial expansion of the globe after trauma. Although a visible lens equator (sometimes with visible zonules) is the hallmark of this condition, iridodonesis and/or phakodonesis (quivering of the iris and lens with eye movements, respectively) are commonly present. These patients can be bothered by acquired myopia, marked astigmatism and diplopia and these symptoms can vary with head position. Depending on the extent of subluxation, patients can be managed with miotics, mydriatics and aphakic correction, or extracapsular vs. intracapsular cataract extraction. If the dislocation seems severe in comparison to the amount of trauma, one should explore the possibility of Marfans disease, homocystinuria, Weill-Marchesani syndrome, Ehlers-Danlos syndrome, and syphilis.

2.22 Lens Dislocation Lens dislocation is caused by complete zonular dehiscence. The dislocated lens can be positioned either in the posterior segment or the anterior chamber. If the lens is found in the anterior chamber, try to reposition the lens by maximally dilating the pupil, placing the patient in a supine position and indenting the cornea with a gonioprism. Once lens is repositioned and the lens is not surgically removed, the patient should have a peripheral iridotomy and treated with chronic 0.51% pilocarpine.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit If dislocated lens is found in the posterior segment with an intact capsule, symptomatic patients can be treated with an aphakic contact lens or can undergo intra-ocular lens implantation. If the capsule is damaged, pars plana lensectomy is necessary to avoid a massive inflammatory response that can result in blindness.

2.23 Globe Rupture A globe rupture is one of the most ghastly consequences of ocular trauma and must always be considered when evaluating a patient that has sustained blunt trauma or a lacerating injury. The signs are: severe subconjunctival hemorrhage, deep or shallow anterior chamber compared with the contralateral eye, hyphema, irregularly shaped pupil that tends to be peaked towards the wound, exposed uveal tissue (appears brownishred), an EOM restriction that is greatest in the direction of the rupture, and hypotony although elevated IOP does not rule out a rupture. If the diagnosis is uncertain, place a Fox shield on the patients eye and order a STAT CT scan to localize the site of the rupture (look for a flat tire sign) and determine if there is an intraocular or intraorbital foreign body. Once you have made the diagnosis, a STAT surgical consult is needed. Some surgeons will consider enucleation within 7 to 14 days to avoid sympathetic ophthalmia if the eye is NLP or severely traumatized. 2.24 Orbital Fracture Orbital fractures are a relatively common consequence of blunt trauma. As such, one must always evaluate the orbital integrity when examining a patient. To do so, palpate the orbital margins for a bony step-off that would be a clear sign of a fracture. Also, palpate the eyelids for crepitus or subcutaneous emphysema. A positive finding indicates that air from a sinus has
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit formed pockets within the orbital tissues. Check EOMs for muscle entrapment and/or a nerve palsy. These can be differentiated with forced-duction testing. Finally, compare the sensation of the ipsilateral and contralateral cheek and forehead. Recall that the infraorbital nerve, a division of the maxillary nerve (cranial nerve V2), travels within the maxillary air sinus, exits through the infraorbital foramen and provides the cheek and upper lip with general somatic afferent (GSA) or sensory fibers. The supraorbital and supratrochlear nerves, divisions of the ophthalmic nerve (cranial nerve V1), travel from within the orbit and supply the forehead and scalp with GSA fibers. 2.24.1 Medial Wall Fracture If a patient has sustained a medial wall or ethmoidal fracture, the patient may give a history of eyelid swelling after blowing their nose. Look for lateral displacement of the medial canthus or telecanthus and a narrowing of the palpebral aperture. A CT with axial views is indicated.

2.24.2 Blow-out Fracture There three main theories as to the mechanism of a blow-out fracture: a hydraulic theory, the contact of globe-to-orbital wall theory, and a bone buckling theory. Although once somewhat controversial, the mechanism of the fracture is unlikely due to a hydraulic mechanism or direct contact with the globe, given the low incidence of concomitant globe injury, and more likely due to bone buckling in most cases. A blow-out fracture of the orbital floor generally presents with vertical diplopia due to inferior rectus belly entrapment that results in restricted down and upgaze. Also look for infraorbital hypesthesia and enophthalmos.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit A trapdoor fracture is a relatively small orbital floor fracture with clinically significant muscle entrapment and is common in the pediatric population. Unlike a blow-out fracture though, prompt surgical intervention is necessary to avoid early tissue necrosis resulting from compromised vascular supply. Look for the same findings of a blow-out fracture, plus no supraduction, nausea, vomiting and the patient will usually exhibit intense pain. Like a blow-out fracture, a CT scan with coronal views is also indicated. 2.24.3 Tripod Fracture A tripod fracture of the lateral wall is also known as a zygomatico-complex fracture and typically involves a disruption of the zygoma at the zygomaticofrontal, temporal, and maxillary sutures. Look for a flattening of the malar region of the face and an inferior displacement of the lateral canthus. Generally, a CT scan will coronal views will help diagnosis this condition.

2.24.4 Orbital Roof Fracture An orbital roof fracture is a life threatening injury that involves a fracture along the orbital surface of the frontal bone. A neurosurgical consult is needed as a potential communication has been established between the orbit and the anterior cranial fossa. Generally, a CT scan will coronal views will help diagnosis this condition.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.24.5 Apex Fracture Finally, an apex or optic canal fracture is rare, but can occur with severe trauma. Because of the proximity to the optic nerve, optic neuropathy or optic nerve transaction is quite possible. A CT scan with axial views indicated for a suspected apex fracture.

In summary, when evaluating a patient that may have sustained an orbital fracture, order a CT scan (not MRI as it is not as sensitive as CT for looking at bony tissue) of orbits and brain with 3mm cuts generally being sufficient. A broad-spectrum oral antibiotic should be prescribed for 10 to 14 days to avoid orbital cellulitis. Instruct the patient not to blow their nose and use a cold compress for 24 to 48 hours. Immediate consults are only necessary for an orbital roof fracture (neurosurgical consult) or a trapdoor fracture (oculoplastics consult). Get an oculoplastics consult in up to 7 to 14 days for a large fracture or cosmetically unacceptable enophthalmos, and up to 3 to 6 weeks for persistent diplopia. All other patients should be followed periodically and tend to recover without surgical intervention. 2.25 Vitreous Involvement The vitreous can be involved in ocular trauma. Inspect the vitreous for cells, hemorrhage, liberated pigment, and flocculent lens material. If the patient has a vitreous hemorrhage, assume a retinal tear is present until proven otherwise. 2.26 Intraocular Foreign Body An intraocular foreign body (IOFB) should be considered for all high-velocity ocular injuries, particularly with metal-on-metal activities. Look for a self-sealing laceration, iris tear, lens opacities, shallow anterior chamber, or low IOP. These patients may only experience a transient foreign body sensation, but to rule out, consider using B-scan ultrasonography, orbital CT scan with 1.0 -1.5mm cuts in both the axial and coronal planes, or a UBM if available. When ordering a CT scan, a piece of the suspected FB (is available) can be taped onto the patients
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit forehead or cheek during the scan to help the technician/radiologist know what they are to look for. Remember that an MRI is contraindicated until metallic IOFB is ruled out. Endophthalmitis occurs in up to 48% of eyes with an IOFB injury and only timing of surgery (>24 hours) and type of FB (e.g. wood) are associated with higher rates. The clinical findings of endophthalmitis are: retinal periphlebitis, marked anterior chamber reaction or hypopyon, and severe vitreal inflammation. Metallic IOFBs can cause toxic retinal metallosis and metals with low redox potentials (easily lose electrons) such as iron or cooper are more likely to cause metallosis. Inert IOFBs can cause proliferative vitreoretinopathy and/or debilitating ocular inflammation. The treatment is prompt surgical removal via pars plana vitrectomy (with or without lensectomy) with rare-earth magnet and/or forceps assisted IOFB removal. 2.27 Intraorbital Foreign Body An intraorbital foreign body (IOrbFB) should be considered for all high-velocity periocular injuries. With inorganic IOrbFBs, the vision loss is usually due to the initial trauma, whereas with organic IOrbFBs there is a higher incidence of severe orbital infection after the trauma. To rule-out an IOrbFB, order a CT scan and follow this with an MRI if a wooden IOrbFB is suspected. The patient should receive anti-tetanus prophylaxis and a broad-spectrum oral antibiotic. Surgical removal is indicated for all organic IOrbFBs and inorganic IOrbFBs that can potentially cause orbital complications.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.28 Commotio Retinae Commotio retinae is also known as Berlins edema, but the latter term is a bit of a misnomer. With this condition, there will be a confluent area of retinal whitening, due to outer photoreceptor disruption and RPE damage, that mimics, but is not actually edema. Blood vessels are seen distinctly and undisturbed under the retinal whitening. This can occur anywhere in the retina, but typically maximal in the area opposite to the blow. The pathophysiology of the condition is interesting. The retinal changes are caused by a contrecoup that is created by blunt trauma, with the force being transmitted through the vitreous and finally onto the retina and choroid. There is usually no treatment required as it tends to resolve without significant sequelae.

2.29 Pre-Retinal Hemorrhage A pre-retinal hemorrhage is a retinal hemorrhage that is confined between the nerve fiber layer and the internal limiting membrane and is often associated with a choroidal rupture. The visual acuity can be severely reduced if the hemorrhage lies in front of the macula. Gravity will cause the blood to settle into the quintessential keel-shape with the blood being darker on the bottom. A patient that has a pre-retinal hemorrhage needs to be dilated every 1 to 2 weeks until the choroid can be well visualized.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.30 Choroidal Rupture If a choroidal rupture is present, look for a yellow or white crescent-shaped subretinal streak that is often concentric with the optic nerve. They can be single or multiple and may be obscured for several days to weeks by overlying pre or subretinal hemorrhage. These patients are at a greater risk of developing a sub-retinal neovascular membrane, so they should be followed every 3 to 6 months and daily Amsler grid monitoring is appropriate. Fortunately, many neovascular membranes due to choroidal rupture regress spontaneously. 2.31 Retinitis Sclopeteria Retinitis sclopeteria or chorioretinitis sclopeteria is a rare condition whereby the patient sustains both a choroidal and retinal rupture. This rare clinical entity is caused by a highvelocity object grazing the globe, but not rupturing the sclera. These patients require a prompt retinal consult as surgical intervention may be necessary. 2.32 Macular Hole A traumatic macular hole is clinically similar to the idiopathic variety in appearance as it presents as a round, red spot in the center of the macula with or without a surrounding cuff of edema that can look like a grey halo. The patients visual acuity is usually around 20/200 and the Watzke-Allen test is usually positive. To perform the Watzke-Allen test, direct a slit beam on the fovea during slit-lamp fundoscopy and ask the patient if they see an unbroken (negative) or broken (positive) bar. While the pathophysiology of this condition is not entirely certain, when a hole develops immediately after trauma, it seems likely that the dehiscence of the fovea is due to exaggerated vitreal tractional forces that peak when the globe is returning to its normal shape after a blunt injury has occurred. Simply put, when the eye is hit the equatorial expansion of the globe causes a flattening of the posterior pole and when the globe returns to its normal shape, the
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit vitreous exerts tangential tractional forces on the anatomically thin fovea, thereby resulting in foveal dehiscence and macular hole formation. There are two theories on delayed traumatic macular hole development. A small hole is thought to be secondary to persistent vitreofoveal adhesion, whereas a large hole may be due to post-concussion retinal necrosis. Patients with a traumatic macular hole should be dilated every month for up to 4 months before surgery is recommended as spontaneous closure up to 4 months after the initial injury has been shown to occur in a significant number of cases, although these patients tend to be younger males. All patients should be educated about the signs and symptoms of a retinal detachment as this is an unlikely, but possible consequence. 2.33 Purtscher's Retinopathy Purtschers retinopathy is an interesting clinical condition that occurs after an injury, involving either major chest compression or head trauma, as well as pancreatitis and other systemic conditions. Classically, the patient presents with cotton-wool spots and hemorrhages along the retinal arcades and, as such, this diagnosis is driven first by history and then by clinical presentation. Although not completely understood, Purtschers retinopathy can be due to arterial and venous back-flow into the retinal vessels. Patients should be dilated every 2 to 3 weeks until it resolves, which typically occurs without treatment. This condition carries a guarded prognosis, but 50% of patients have at least a 2 Snellen line visual acuity increase from initial presentation. 2.34 Retinal Detachment Trauma accounts for up to 35% of all retinal detachements. A traumatic retinal detachment (RD) is by definition a rhegmatogenous detachment that can be due to retinal cyclodialysis or a retinal tear. B-scan ultrasonography is necessary to rule out an RD if there is a poor view of the fundus. When appropriate, utilize scleral depression after trauma to help rule-out retinal cyclodialysis. A patient with a macula-on RD should receive a retinal consult and undergo surgery within 1 to
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2 days of diagnosis and these patients should be confined to bed rest until surgery. A macula-off RD is less urgent and these patients should have a retinal consult and surgery within approximately one week. 2.35 Retrobulbar Hemorrhage Retrobulbar hemorrhage occurs when an orbital vessel ruptures thereby leaking blood products into the orbit. Since this space is a closed environment, any added contents will inevitable increase the pressure inside of the orbit and have the potential to negatively impact the ocular structures. These patients will exhibit non-pulsating exophthalmos with resistance to retropulsion, elevated IOP, an EOM restriction, central retinal artery pulsation (indicating a possible impending central retinal artery occlusion), choroidal folds, and possibly signs of optic neuropathy (see below). These patients require imaging and MRI is preferable over CT scanning because it is more important to visualize soft tissue structures with this condition. If vision is not immediately threatened, attempt to medically lower the patients IOP. However, if there are any signs of optic neuropathy, institute pharmaceuticals to lower the IOP and order an immediate surgical consult for a lateral canthotomy and cantholysis to reduce orbital pressure. This procedure involves the surgeon making a horizontal incision across the lateral canthus and then the inferior arm of the lateral canthal tendon is cut. An emergent orbital decompression will be necessary if the above are unsuccessful in relieving orbital pressure.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.36 Carotid-Cavernous Fistula A carotid-cavernous fistula is a high-flow arterial venous fistula that is usually caused by a traumatic basal skull fracture. The clinical findings can include an audible orbital bruit, pulsatile proptosis (as opposed the the non-pulsatile proptosis found with a retrobulbar hemorrhage), chemosis, orbital swelling, elevated IOP, ophthalmoplegia, and retinal vessel congestion. An immediate neurosurgical consult is indicated for the management of this condition. 2.37 Optic Neuropathy Traumatic optic neuropathy can be caused by optic nerve compression from displaced surrounding tissue or optic nerve transection due to fractured bone or penetrating trauma. Indirect traumatic optic neuropathy is the most common type and occurs in 0.5% - 5% of all closed head injuries. The clinical findings are decreased visual acuity, impaired color vision, afferent pupillary defect without significant retinal pathology, but keep in mind that optic nerve head pallor may not appear for weeks and optic nerve head cupping is atypical of optic neuropathy. If suspected, order a CT scan with thin slices through the optic canal. If given in the first 8 hours, a short course (48 to 72 hours) of megadose intravenous steroids may be beneficial (based on spinal chord injury research), although optic canal decompression surgery can be necessary.

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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit 2.38 Optic Nerve Avulsion Optic nerve avulsion is a rare clinical entity that occurs when there is a partial or complete tearing of the optic nerve from the globe at the level of the lamina cribrosa. Obviously, this tearing causes tremendous axonal disruption. Optic nerve avulsion can occur after severe trauma or relatively minor insults, but always results in devastating loss of vision. Conclusion The ocular effects of trauma can be far reaching and profound and should, therefore, never be underestimated. Using a thorough systematic approach (including dilation as usually appropriate) when examining for ocular trauma will serve the clinician and the patient alike. Detailed documentation of these cases is extremely important for clinical as well as medicolegal reasons. While this course was not designed to be completely inclusive of all possible scenarios that a clinician may encounter while examining a patient who has sustained trauma, it should serve as a good reference for most primary care situations.

References Agrawal A, McKibbin M. Purtscher's retinopathy: Epidemiology, clinical features and outcome. Br J Ophthalmol 2007; Jun 7 [Epub ahead of print]. Alexander LJ. Primary Care of the Posterior Segment: second edition. Appleton & Lange, Stamford. 1994. Arffa RC. Grayson Disease of the Cornea: fourth edition. Mosby Year, St. Louis. 1997. Bansagi ZC, Meyer DR (2000). Internal Orbital Fractures in the Pediatric Age Group. Ophthalmology 107(5): 829-36. Bleiman BS, Schwartz AL (1979). Paradoxical Intraocular Pressure Response to Pilocarpine: A Proposed Mechanism and Treatment. Arch Ophthalmol 97(7): 1305-6.
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Author: Joseph Rappon, OD COPE #21042-AS 3 credit Brandonisio TM, Newman TL (2002). Hypotonous Maculopathy and Normal Visual Acuity Secondary to Post-traumatic Cyclodialysis Cleft. Optometry 73(10): 620-5. Brodovsky SC et al (2000). Management of Alkali Burns. Ophthalmology 107(10): 1829-35. Carolina Eye Associates. Clinical Photo Library, 2000. Catania LJ. Primary Care of the Anterior Segment: second edition. Appleton & Lange, Stamford. 1995. Dua HS, Azuara-Blanco A. Amniotic membrane transplantation. Br J Ophthalmol. 1999; 83: 74852. Davis AR et al (1997). Topical steroid use in the treatment of ocular alkali burns. Br J Ophthalmol 81:732-4. Engle AT, et al. Masked comparison of silicone hydrogel lotrafilcon A and etafilcon A extendedwear bandage contact lenses after photorefractive keratectomy. J Cataract Refract Surg 2005; 31:681-686. Epstein DL. Chandler and Grants Glaucoma (third edition). Lea & Febiger, Philadelphia. 1986. Friedman NE, Bullimore MA. The Anterior Segment. In: The Ocular Examination: Measurements and Findings. Zadnik K. ed. Saunders, Philadelphia. 1997. Fulcher TP, McNab AA, Sullivan TJ (2002). Clinical Features and Management of Intraorbital Foreign Bodies. Ophthalmology 109(3): 494-500. Greven CM et al (2000). Intraocular Foreign Bodies. Ophthalmology 107(3): 608-12. Hamill MB (1992). Repair of the Traumatized Anterior Segment. Focal Points; volume X, number 1. Hart, WM. Adlers Physiology of the Eye (ninth edition). Mosby Year, St. Louis. 1992. He D, Blomquist PH, Ellis E 3rd. Association between ocular injuries and internal orbital fractures. J Oral Maxillofac Surg 2007;65(4):713-20.
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Author: Joseph Rappon, OD COPE #21042-AS 3 credit Herschler J, Cobo M. Trauma and Elevated Intraocular Pressure. In: Glaucomas. Ritch R, Shields MB, Krupin T eds. Mosby-Year, St. Louis. 1996. Ikeda N et al (2002). Pathogenesis of Transient High Myopia after Blunt Eye Trauma. Ophthalmology 109(3): 501-7. Ikeda N, Hayasaka S, Hayasaka Y, Watanabe K. Alkali burns of the eye: effect of immediate copious irrigation with tap water on their severity. Ophthalmologica. 2006; 220(4): 225-8. Johnson RN et al (2001). Traumatic Macular Hole. Ophthalmology 108(5): 853-7. Jonas JB, Knorr HLJ, Budde WM (2000). Prognostic Factors in Ocular Injuries Caused by Intraocular or Retrobulbar Foreign Bodies. Ophthalmology 107(5): 823-8. Kanski JJ, Nischal KK. Ophthalmology Picture Tests: second edition. Churchill Livingstone, New York. 1997. Kanski JJ, Nischal KK. Ophthalmology: Clinical Signs and Differential Diagnosis. Mosby Year, St. Louis. 1999. Kanski, JJ. Clinical Ophthalmology (third edition). Butterworth Heinemann, Oxford. 1994. Krachmer JH, Palay DA. Cornea Color Atlas. Mosby-Year, St. Louis. 1995. Kuhn F, Morris R (2000). Posterior Segment Intraocular Foreign Bodies. Ophthalmology 107(5): 821-2. Lueder GT (2000). Air Bag-associated Ocular Trauma in Children. Ophthalmology 107(8): 14725. MacCumber MW, Zanger MW (2001). Open-globe Injuries. Focal Points; volume XIX (7). Mandava S, Sweeney T, Guyer D. Color Atlas of Ophthalmology: The Manhattan Eye, Ear & Throat Hospital Pocket Guide. Thieme, New York. 1999. Mauriello JA, Lee HJ, Nguyen L (1999). CT of Soft Tissue Injury and Orbital Fractures. Radiologic Clinics of North America 37(1): 241-52.
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Primary Care Ocular Trauma Management

Author: Joseph Rappon, OD COPE #21042-AS 3 credit McGwin G Jr, Owsley C. Risk factors for motor vehicle collision-related eye injuries. Arch Ophthalmol. 2005; 123(1): 89-95. Mermoud A, et al (1993). Post-traumatic Angle Recession Glaucoma: A Risk Factor for Bleb Failure after Trabeculectomy. Brit J Ophthalmol 77(10): 631-4. Mermoud A, et al (1993). Surgical Management of Post-traumatic Angle Recession Glaucoma. Ophthalmol 100(5): 634-42. Myers JS, Katz LJ, Spaeth GL. Glaucoma Following Trauma. In: Duanes Clinical Ophthalmology; 3(54C):1-9. Pieramici DJ et al. A Phase III, Multicenter, Randomized, Placebo-Controlled Clinical Trial of Topical Aminocaproic Acid (Caprogel) in the Management of Traumatic Hyphema. Ophthalmology. 2003; 110(11): 2106-12. Ray SK and Jakobiec FA. Ocular Trauma. Lippincott Williams & Wilkins, Philadelphia. 2002. Recchia FM et al (2002). Outpatient Management of Traumatic Microhyphema. Ophthalmology 109(8):1465-71. Rhea JT, Rao PM, Novelline RA (1999). Helical CT and Three-Dimensional CT of Facial and Orbital Injury. Radiologic Clinics of North America 37(3): 489-513. Rhee DJ, Pyfer MF editors. The Wills Eye Manual: third edition. Lippincott Williams & Wilkins, Philadelphia. 1999. Romano PE (2000). Systemic Prednisolone Prevents Rebleeding in Traumatic Hyphema. Ophthalmology 107(5): 812-4. Romano PE and Phillips PJ(2000). Traumatic hyphema: a critical review of the scientifically catastrophic history of steroid treatment therefore; and A report of 24 additional cases with no rebleeding after treatment with the Yasuna systemic steroid, no touch PLUS protocol. Binocul Vis Strabismus Q 15(2): 187-196. Rubin PAD, Bilyk JR, Shore JW. Management of Orbital Trauma: Fractures, Hemorrhage, and Traumatic Optic Neuropathy. Focal Points, volume XII (7).
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Copyright Pacific University, Forest Grove, Oregon, USA Documents and materials located on the Pacific University gopher, WAIS, WWW, phonebook, and FTP servers are copyrighted by the Pacific University, or by the authors of the individual documents, and are provided for the convenience of university faculty, students, and staff, with no warranty of accuracy or usability. www.pacificu.edu/optometry/ce Page 33 of 33