As all primary care optometrists need to be familiar with trauma management, this course is designed to review most traumatic injuries and introduce some new concepts in treatment and management.
Brief Epidemiology of Trauma
There are approximately 2.4 million ocular and orbital injuries in the US per year, 20,000 to 68,000 of which are vision-threatening injuries, and some 40,000 persons sustain significant vision loss each year. This is preceded only by cataract as a cause for vision impairment in the US, and trauma is the leading cause of unilateral blindness. There is a much greater probability for males to be affected, especially young males. In the Beaver Dam Eye Study, 20% of adults reported ocular trauma in their lifetimes and those who had experienced an initial trauma were 3 times more likely to experience a further trauma. Sharp objects caused more than half of all injuries reported in the study.
Pathophysiology
There are four main mechanisms that cause ocular trauma: coup, contrecoup, equatorial expansion, and global repositioning. The coup is the initial force that is caused directly by the trauma. The contrecoup is the shock-wave that is imparted by the coup; it is transmitted through the ocular and orbital structures. As the result of trauma, the equator of the globe tends to expand and distort the normal ocular architecture. Finally, the globe returns to its normal shape, but this is not always a benign event.
Classification
In a broad sense, ocular trauma can be divided into two main categories: closed and open globe injuries. When examining a patient with trauma, it is imperative to determine into which of these categories the injury falls because this will direct the immediate management of the condition. Patients with closed globe injuries could have a burn, contusion, or a lamellar laceration. Patients with open globe injuries could have a rupture or a laceration, with the latter being either a penetrating or perforating injury.
Trauma Examination
A 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 allergies.
Visual acuity may be difficult to ascertain and topical anesthesia may be necessary to facilitate this task. Externals should always include pupillary testing, extra-ocular motilities (EOMs), and confrontation visual fields. If the patient has sustained blunt ocular trauma, a cover test (or Maddox rod testing) should be performed, the eyelids and orbital margins should be palpated, and forehead and cheek sensitivity should be evaluated.
The slit-lamp examination should include fluorescein staining, which is necessary for Seidel testing and applanation tonometry, but tonometry should be deferred if there is a known open globe injury. A dilated fundus exam (with or without scleral depression, as appropriate), is also essential during the trauma examination.
Of course, ancillary tests are helpful in determining the patient's condition and can include autorefraction, color vision, gonioscopy, and imaging studies.
Traumatic myopia refers to the transient myopia that can occur 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 thickening of the crystalline lens essentially decreases the anterior and posterior radii of curvature. Ciliochoroidal effusion causes an anterior shift of the lens–iris diaphragm, which also causes the eye to acquire more plus optical power. Traumatic myopia tends to resolve without treatment.
Periorbital ecchymosis, commonly known as a "black eye," is blood accumulation in the eyelids. It is usually more noticeable in the lower lid and occasionally forms an organized hematoma or firm purplish-black mass.
Periorbital Ecchymosis
The treatment of this common condition involves having the patient use a cold compress intermittently for the first 48 hours, followed by hot packs for 3 to 5 days thereafter.
Many types of Eyelid lacerations can occur from trauma. To treat simple, superficial lacerations, clean the wound and surrounding skin (e.g. with Betadine), irrigate it thoroughly with saline, and remove any foreign material that may still be present. Then apply an antibacterial ointment and sterile dressing.
Eyelid Laceration
Deeper lacerations, or those involving the lid margin, typically require sutures so management depends greatly on state scope of practice laws. Complicated lacerations require an oculoplastics consult. These are lacerations that have extensive tissue loss or have damaged the lacrimal drainage system, levator aponeurosis, and/or the medial canthus tendon.
When dealing with any type of eyelid laceration, always consider tetanus prophylaxis, when appropriate.
Subconjunctival hemorrhages typically do not require treatment, although artificial tears tend to enhance comfort for patients who are symptomatic.
Subconjunctival Hemorrhage
Be sure to reassure the patient that the hemorrhage will resolve in 1 to 2 weeks and have the patient discontinue any elective aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) because these can facilitate further hemorrhaging. When appropriate, acetaminophen is generally safe to use for these patients because it does not affect the clotting cascade.
Conjunctival abrasions produce fluorescein staining and may produce some degree of subconjunctival hemorrhage, whereas lacerations usually produce significant hemorrhaging and typically have exposed white sclera.
Conjunctival Laceration
With lacerations, the conjunctival edges have a tendency to be rolled due to the conjunctiva's elastic nature. The treatment for these two conditions is an antibiotic ointment TID for 4 to 7 days and pressure patching for 24 hours. If a laceration is greater than 1 to 1.5 cm, consider suturing, but most lacerations will heal without surgical repair.
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 on their composition, location, and the patient's 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 occult palpebral conjunctival foreign bodies, which can cause corneal track marks.
Limbal Foreign Body
It is preferable to use xylocaine (when available) for conjunctival or limbal foreign body removals because it produces deeper 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 because a penetrating object should be considered an open-globe injury and co-managed with an anterior segment or corneal sub-specialist, when available.
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 high-velocity injury, but dilation should routinely be done because the cycloplegic effect enhances patient comfort. After removal of the foreign body, treat as appropriate for an abrasion.
Corneal abrasions produce fluorescein staining with a negative Seidel test. A history of rubbing or scraping the cornea are characteristic findings, and a mild anterior chamber reaction is possible. Always measure the size of the abrasion carefully because this will help your follow-up management, and instruct the patient that his or her visual acuity may decrease initially.
Corneal Abrasion
There are two basic methods used to manage patients with corneal abrasions. The first method, which is preferable for small to moderately sized abrasions and for all contact lens wearers, is to use a fairly tight-fitting bandage contact lens along with topical antibiotic drops that have good anti-pseudomonal activity. Silicone hydrogels are the contact lenses of choice because of their excellent oxygen permeability and the fact that they do not take up fluorescein. This is a particularly nice feature when the patient is seen on follow-up.
The fourth generation fluoroquinolones make excellent antibiotic choices due to their spectrum of activity and low incidence of bacterial resistance. However, less expense drugs like Polytrim tend to also work well.
The second method of treatment is to use an antibiotic ointment and pressure patch the patient. This method tends to work well for moderate to large abrasions. The patch should be removed every day to check on corneal integrity and the patient should be switched to a bandage contact lens when significant healing has begun. Shifting to a bandage lens usually enhances patient comfort and is more aesthetically pleasing.
To treat pain associated with an abrasion, always cycloplege the patient and consider a topical analgesic for mild to moderate pain (first method only) and an oral analgesic for moderate to severe pain.
Corneal laceration patients typically have a history involving cutting or tearing the cornea. The Seidel test can be crucial in 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.
Corneal Laceration
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 you will want to co-mange these patients with a corneal or anterior segment sub-specialist, when available. A full-thickness corneal abrasion should be treated like a ruptured globe (to be discussed later). In these cases, look for iris prolapse, place a protective shield over the patient's eye and order a STAT surgical consult because this is a sight-threatening condition.
Chemical burns are worrisome because of their ability to profoundly affect multiple ocular structures and potentially cause blindness. Alkaline agents are particularly damaging because they are both hydrophilic and lipophilic and can rapidly penetrate cell membranes. Penetration of the anterior chamber is even possible. Ocular damage results from saponification of cell membranes and cell death along with disruption of the extracellular matrix.
Chemical Burn
Acidic agents generally cause less damage than alkalis because many corneal proteins bind acid and act as a chemical buffer. The resulting coagulated tissue acts as a barrier to further penetration of acid. Ocular damage from acids results from collagen fibril shrinkage.
The Roper-Hall classification of chemical burns has been criticized for not being accurate regarding modern, severe burn prognosis, but it continues to serve as a good tool for primary care clinicians. The grade and corresponding prognosis of the burn is determined based on the amount of corneal damage and limbal ischemia, which is any disappearance of the normal conjunctival blood vessel architecture around the cornea. Limbal ischemia is an extremely important clinical factor because it demonstrates the level damage to these limbal vessels and indicates the ability of the corneal stem cells (located at the limbus) to regenerate the damaged cornea. Therefore, unlike all other traumatic ocular conditions, whiter eyes are more alarming then red eyes.
|
GRADE |
PROGNOSIS |
LIMBAL ISCHEMIA |
CORNEAL INVOLVEMENT |
|
I |
Good |
None |
Epithelial Damage |
|
II |
Good |
Less than 1/3 |
Haze but the iris details are visible |
|
III |
Guarded |
1/3 to 1/2 |
Total epithelial loss with haze that obscures the iris details |
|
IV |
Poor |
Greater than 1/2 |
Cornea opaque with the iris and pupil obscured |
Roper-Hall Classification Table
The treatment for a chemical burn should begin on the telephone or immediately when the patient arrives at the office. This is one of the only instances in which visual acuity measurement should be deferred because it is extremely important to begin irrigation as soon as possible and maintain it for at least 30 minutes.
If the patient is in the office, sterile saline is preferable as an irrigation solution, but, if it is not available, tap water can be used. Anesthetize the eye as necessary to facilitate proper irrigation. Check the pH of the tears with litmus paper if available every 5 minutes and continue until the pH is neutral (the paper turns blue for base and red for acid). The addition of acids or bases should never be considered to neutralize the ocular tissues.
Patients with mild to moderate burns should be cyclopleged with cholinergic antagonists only so as to not cause any further blood vessel constriction. An antibiotic ointment should be applied every 1 to 2 hours along with copious quantities of artificial tears and oral pain medication as necessary. Topical steroids are important because they help block neutrophil infiltration and thus prevent an accumulation of collagenases, but steroids should not be used for more than 1 week because of a risk of corneoscleral melting. In addition, some suggest using oral vitamin C (up to 2-g QID) because it has been shown to stimulate collagen production by fibroblasts.
Elevated IOP should be treated with Diamox if indicated, but topical beta-blockers can used alone or added when necessary.
Pressure patching can be considered, and the patient needs to be re-examined daily until complete epithelialization has occurred.
Moderate to severe burns should be referred to a corneal sub-specialist, when available, and hospital admission may be necessary. Amniotic membranes (AM) have been shown to facilitate migration of epithelial cells, reinforce adhesion of basal epithelial cells, prevent epithelial apoptosis, and promote epithelial differentiation. AM grafts have been used to help to reduce scarring, inflammation, and neovascularization of traumatized eyes; AM contact lenses are currently being investigated for this purpose.
Microhyphema is a small hyphema in which there are only suspended red blood cells (RBCs) in the anterior chamber. A layered clot is not present. Microhyphema is graded from 1+ to 4+ based on the quantity of RBCs, which may settle and form an actual hyphema as the condition progresses.
Microhyphema
The complications of a microhyphema include IOP elevation and secondary hemorrhage. Although to a lesser degree than for hyphema management, the treatment of microhyphema is controversial, but the goal is to allow the blood clot to stay in place long enough to heal the blood vessel rupture completely. In 2002, the Wills Eye Hospital published their protocol for treating microhyphema. It includes discontinuing elective anticoagulants, and bed rest with 30° head elevation for 4 days (this reduces episcleral venous pressure and allows cells to settle faster). Then the patient may resume light activity for 2 weeks after trauma. A full-time protective shield is worn for 2 weeks (a clear or perforated shield should be used so that patient can monitor his or her own vision). Atropine 1% QD to TID should be used for 2 weeks, topical steroids can be considered when not contraindicated, and all Hispanics or African Americans with an IOP greater than 21mm Hg need to be tested for sickle cell anemia.
Compliant, non-sickle cell patients with an IOP less than or equal to 25mm Hg should return in 2 weeks or sooner if visual changes occur (e.g., decreased VA, increased pain, increased photophobia). Compliant, non-sickle cell patients with an IOP greater than 25mm Hg and sickle cell patients with an IOP greater than 21mm Hg should return for follow-up daily for 3 days and should be treated for elevated IOP. This is because sickle cell patients have a greater risk of developing glaucomatous optic neuropathy at lower levels of IOP. It should be kept in mind that Diamox is contraindicated in sickle cell patients because it exacerbates the sickling process. Non-compliant patients should not be treated on an outpatient basis. Gonioscopy and scleral depression can be performed only after 2 weeks, which allows enough time for the clotting process to be nearly complete.
Hyphema is layering of RBCs in the inferior anterior chamber. During the slit-lamp examination, it is of the utmost importance to measure the hyphema height in millimeters, because this will dictate both the management and follow-up of the condition.
Hyphemia
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 but less than complete filling of the anterior chamber. In a grade 4+, or "8-ball," or total hyphema, the entire anterior chamber is filled.
As an interesting side-note, hyphema patients commonly experience a 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 (i.e., those who can be trusted to follow instructions regarding medication, activity, and follow-up) who do not have 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 35 mm Hg. All other patients require hospitalization during the most critical time for clot formation; about 5 to 7 days after the injury.
Some patients will require surgical evacuation of the clot.
Outpatient treatment consists of discontinuing any elective anticoagulants, using only mild analgesics (e.g. Tylenol), atropine 1% QD to TID, bed rest with ambulatory activities kept to a minimum and no strenuous activities for 2 weeks, and antiglaucoma medication as needed. In bed, the patient's head should be elevated 30°, and a clear or perforated protective shield should be worn full-time for 2 weeks. The patient needs to be seen daily for 3 days, then several days to a week thereafter depending on his or her progress. The patient can gradually resume normal activities after about 2 weeks if he or she is doing well and doesn't experience a rebleed.
Gonioscopy and scleral depression should be deferred for 2 to 4 weeks after trauma.
Amicar (E-aminocaproic acid) is an antifibrinolytic agent that has been used 50 mg/kg PO q4h for 5 days and has been shown to decrease the rate of rebleeding, but its use is controversial due to a lack of improved VA outcome data and side-effects such as nausea, vomiting, diarrhea, muscle weakness, abdominal cramps, bradycardia, and postural hypotension. However, a topical gel preparation of Amicar has been shown to be effective 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/day in divided doses have been shown in some studies to be as effective as or better than Amicar at reducing secondary bleeding and they are much less expensive. Topical steroids may be as effective as oral steroids, but this is not well established.
When dealing with a hyphema, keep in mind that 3.5 to 38% of patients rebleed, usually 2 to 5 days after the injury; about 30% have temporarily elevated IOP for 5 to 7 days; 5% require surgical intervention; and about 75% demonstrate some degree of angle recession or iridodialysis, but only 5% will develop secondary glaucoma.
Due to the relatively high percentage of rebleeds that can be worse than the original bleed, a "hands off" approach has been suggested and shown to have excellent results. This method requires hospitalization for all hyphema patients and there is absolutely no routine tonometry or eye drops used in order to limit ocular manipulation and decrease the chance of clot dislodgment.
Indeed, the proper management of this condition remains quite debatable.
Hemosiderosis is the clinical entity in which the cornea becomes stained by blood; specifically by the iron contained within the RBCs.
Hemosiderosis
Hemosiderosis is more likely to occur when a 50% or greater hyphema is present for a week or more, when the IOP is elevated, or when there is concomitant endothelial damage. Although not recommended, some advocate patching hyphema patients because prolonged light exposure can cause endothelial dysfunction and corneal staining.
Hemosiderosis staining typically resolves from the limbus towards the central cornea.
Traumatic iritis presents very much like other types of anterior uveitides, however a history of trauma is critical in making a correct diagnosis. There tends to be photophobia in both the involved and the uninvolved eye (because of consensual pupillary constriction), perilimbal injection, and cells and flare in the anterior chamber.
Traumatic Iritis
Treatment consists primarily of using a cycloplegic agent. Topical steroids are usually not necessary because the stimulus for the iritis, that is the trauma itself, is no longer present. However, topical steroids can be helpful for refractory cases or when the patient is in pain.
Unless necessary, defer scleral depression until the eye is quiet.
Angle recession is often overlooked on gonioscopy, but it occurs commonly with blunt ocular trauma.
Angle Recession
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, which causes a posterior displacement of the iris. A valve-like action of the iris prevents aqueous from flowing back through the pupil and this causes a portion of the force from the blow to be redirected towards the angle. This can cause a tearing of the uveal meshwork if the force is mild, whereas moderate force can cause a separation between the longitudinal and circular fibers of the ciliary muscle. Either way, this results in immediate and subsequent damage to the corneoscleral trabecular meshwork.
To observe angle recession, it is often helpful to use gonioscopy and compare both eyes looking for a discrepancy in anterior chamber depth and ciliary body band width of corresponding quadrants. 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 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; patient education is a key to successful management.
Traumatic glaucoma is a secondary open-angle glaucoma that may occur in 2-10% of those with angle recession within a 10 year period. It is more likely to occur with 180° or more of angle recession.
There are primarily two types based on the onset of permanently elevated IOP: early and late. The early type of angle recession glaucoma develops a few weeks to a year or two after trauma with the severity usually related 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 an eye with 270° or more of angle recession. The small percentage of patients that develop this type of glaucoma could have an underlying predisposition to the development of primary open-angle glaucoma (POAG) 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 used for with POAG, that a drug is chosen that inhibits aqueous formation or increases uveoscleral outflow. Pilocarpine is not indicated because it may cause a paradoxical increase in IOP via a decrease in the uveoscleral outflow. In refractory cases, surgical intervention may be necessary, but success rates are lower than with POAG.
Cyclodialysis cleft is a separation of the longitudinal muscle of the ciliary body from the sclera. This separation allows 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 required otherwise.
Iridodialysis is a detachment of the iris root from the ciliary body and can produce corectopia (irregular pupil shape), pseudopolycoria, and diplopia.
Iridodialysis
Patients with this condition must be monitored for glaucoma because they are at a higher risk for developing increased IOP. If the patient experiences bothersome diplopia, consider an opaque soft contact lens with a clear pupil. Surgery, while usually not necessary, decreases the likelihood of peripheral anterior synechia formation.
Vossius' ring is a traumatic deposit of iris pigment epithelium on the anterior lens capsule and usually fades with time.
Vossius' Ring
Vossius' ring should be differentiated from posterior synechia remnants caused by a prior uveitis.
Traumatic cataract, or contusion rosette, may not be apparent until years after a trauma. Although anterior and/or posterior subcapsular opacities can occur with trauma, a petalliform cataract with a compact white star-shaped opacity, usually in the anterior cortex, is most commonly found.
Contusion Rosette Cataract
There is no difference in the management of this cataract compared with the age-related variety, but the patient should be made aware that there is an increased risk of zonular dehiscence during cataract extraction.
Lens subluxation is a partially dislocated crystalline lens caused by incomplete zonular dehiscence secondary to equatorial expansion of the globe from trauma. Although a visible lens equator (sometimes with visible zonules) is the hallmark of this condition, iridodonesis and/or phakodonesis (i.e., quivering of the iris and lens with eye movements, respectively) are commonly present.
Lens Subluxation
Patients with lens subluxation can be bothered by acquired myopia, marked astigmatism, and diplopia; these symptoms may vary with head position. Depending on the extent of subluxation, patients can be managed with miotics, mydriatics (with aphakic correction), or with extracapsular vs. intracapsular cataract extraction.
If the dislocation seems severe in comparison to the amount of trauma, one should explore the possibility of Marfan's disease, homocystinuria, Weill-Marchesani syndrome, Ehlers-Danlos syndrome, and syphilis.
Lens dislocation is caused by complete zonular dehiscence. The dislocated lens can be positioned either in the posterior segment or the anterior chamber.
Anterior Lens Dislocation
If the lens is found in the anterior chamber, try to reposition it by maximally dilating the pupil, placing the patient in a supine position, and indenting the cornea with a gonioprism.
If the 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.
Posterior Lens Dislocation
If the capsule is damaged, pars plana lensectomy is necessary to avoid a massive inflammatory response that can result in blindness.
Intraorbital foreign body (IOrbFB) should be considered for all high-velocity periocular injuries. With inorganic IOrbFBs, 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.
Intraorbital Foreign Body
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 cause orbital complications.
Globe rupture is one of the most ghastly consequences of ocular trauma and must always be considered when evaluating a patient who has sustained blunt trauma or a lacerating injury.
Globe Rupture
The signs of globe rupture include 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 brownish-red), 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 patient's eye and order a STAT CT scan to localize the site of any rupture (look for a "flat tire" sign) and to determine if there is an intraocular or intraorbital foreign body. Once the diagnosis is made, 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.
Retrobulbar hemorrhage occurs when an orbital vessel ruptures and leaks blood products into the orbit. Since this space is a closed environment, any added contents will inevitable increase the pressure inside the orbit and have the potential to negatively impact the ocular structures.
Retrobulbar Hemorrhage
Patients with retrobulbar hemorrhages can 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. An MRI is preferable over CT scanning because it is more important to visualize soft tissue structures if a hemorrhage is suspected.
If vision is not immediately threatened, attempt to medically lower the patient's IOP. However, if there are any signs of optic neuropathy, institute pharmaceutical treatment to lower the IOP and order an immediate surgical consult for a lateral canthotomy and cantholysis to reduce orbital pressure. An emergent orbital decompression will be necessary if the above are unsuccessful in relieving orbital pressure.
Arteriovenous fistulas can be classified as high-flow or low-flow types. Carotid-cavernous or high-flow fistulas have an abrupt onset because they are usually caused by a traumatic basal skull fracture.
High-Flow Arteriovenous fistula
The clinical findings associated with a high-flow fistula include an audible orbital bruit, pulsatile proptosis, chemosis, orbital swelling, elevated IOP, ophthalmoplegia, and retinal vessel congestion.
A dural-cavernous or low-flow fistula, on the other hand, tends to have more of an insidious onset and is not usually caused by trauma.
Low-Flow Arteriovenous fistula
Low-flow fistulas are typically associated with hypertension and arteriosclerosis, especially in post-menopausal women. The clinical findings are mild orbital congestion from torturous and dilated conjunctival blood vessels, proptosis, low or no orbital bruit, and normal to elevated IOP. These findings may be subtle and can fluctuate. It is somewhat alarming to consider that when the IOP is elevated, this condition can masquerade as POAG.
The diagnosis is made by way of an orbital CT scan or an MRI with MRA to rule out an enlarged superior ophthalmic vein, which is pathognomonic of an arteriovenous fistula.
Orbital fractures are a relatively common consequence of blunt trauma. As such, one must always evaluate orbital integrity when examining a trauma patient. To do this, 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 formed pockets within the orbital tissues.
Check the EOMs for muscle entrapment and/or a nerve palsy. These can be differentiated with forced-duction testing.
Finally, compare ipsilateral and contralateral cheek and forehead sensitivity. 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.
A medial wall or ethmoidal fracture should be suspected if the patient has sustained facial trauma and gives a history of eyelid swelling after blowing his or her nose.
Medial Wall Fracture
Look for lateral displacement of the medial canthus or telecanthus and a narrowing of the palpebral aperture. A CT scan with axial views is indicated.
Blow-out fracture of the orbital floor generally presents with symptoms of vertical diplopia due to inferior rectus belly entrapment that results in restricted down and upgaze. Also look for infraorbital hypesthesia and enophthalmos.
Blowout Fracture
Trapdoor fracture is a relatively small orbital floor fracture with clinically significant muscle entrapment. It is common in the pediatric population. Unlike a blow-out fracture, prompt surgical intervention is necessary to avoid early tissue necrosis resulting from a compromised vascular supply. Look for the same findings as for a blow-out fracture, plus no supraduction, nausea, vomiting, and intense pain. A CT scan with coronal views is indicated.
Trapdoor Fracture
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.
Tripod Fracture
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.
Orbital Roof 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 transection is quite possible. A CT scan with axial views is indicated.
Orbital Apex Fracture
In summary, when evaluating a patient who may have sustained an orbital fracture, order a CT scan (not an MRI) of orbits and brain, typically with 3-mm cuts. A broad-spectrum oral antibiotic should be prescribed for 10 to 14 days to avoid orbital cellulitis. Instruct the patient not to blow his or her nose and to 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 after 7 to 14 days for a large fracture or cosmetically unacceptable enophthalmos, and after 3 to 6 weeks for persistent diplopia. All other patients should be followed periodically and tend to recover without surgical intervention.
The vitreous and retina 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.
Intraocular foreign body (IOFB) should be considered for all high-velocity ocular injuries, particularly those resulting from metal-on-metal activities.
Intraocular Foreign Body
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 an IOFB, consider using B-scan ultrasonography, an orbital CT scan with 1.0 - 1.5 mm cuts in both the axial and coronal planes, or a UBM, if available. Remember that an MRI is contraindicated until the presence of a metallic IOFB is ruled out.
Endophthalmitis occurs in up to 48% of eyes with an IOFB injury and only the timing of surgery (>24 hours) and the type of FB (e.g. wood) are associated with higher rates. The clinical findings include retinal periphlebitis, marked anterior chamber reaction or hypopyon, and severe vitreal inflammation.
Metallic IOFBs can cause toxic retinal metallosis, but even 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) involving magnetic and/or forceps assisted IOFB removal.
Commotio retinae is also known as Berlin's 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, but not edema. Blood vessels are seen distinctly and are undisturbed under the retinal whitening.
Commotio Retinae
Commotio retinae can occur anywhere in the retina, but it is usually 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 because commotio retinae tends to resolve without sequelae.
Pre-retinal hemorrhage is confined between the nerve fiber layer and the internal limiting membrane of the retina and is often associated with a choroidal rupture. The visual acuity can be severely reduced if it lies in front of the macula.
Pre-retinal Hemorrhage
Gravity will cause the blood to settle into the quintessential "keel-shape" with the blood being darker on the bottom. A patient who has a pre-retinal hemorrhage needs to be dilated every 1 to 2 weeks until the choroid can be well visualized.
Choroidal rupture is detectable as a yellow or white crescent-shaped subretinal streak that is often concentric with the optic nerve.
Choroidal Rupture
The rupture can be single or multiple and may be obscured for several days to weeks by overlying pre- or sub-retinal hemorrhage. Patients with this condition are at a greater risk for developing a sub-retinal neovascular membrane, so they should be followed every 3 to 6 months. They should also be instructed to monitor their vision daily with an Amsler grid and to report any significant changes.
Retinitis sclopeteria or chorioretinitis sclopeteria is a rare condition in which the patient sustains both a choroidal and retinal rupture.
Retinitis sclopeteria
This condition occurs when a high-velocity object grazes the globe, but does not rupture the sclera. Patients with retinitis sclopeteria require a prompt retinal consult because surgical intervention may be necessary.
Traumatic macular hole is clinically similar to the idiopathic variety in appearance. 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.
Traumatic Macular Hole
The patient's visual acuity is usually around 20/200 and the Watzke-Allen test is usually positive. (This is a test in which a slit beam is imaged on the macular area and the patient is asked to describe the appearance of the beam.)
The pathophysiology of this condition is not entirely certain, but 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 following a blunt impact.
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 because spontaneous closure has been shown to occur in a significant number of cases up to 4 months after the initial injury - although these patients tend to be younger males.
All patients should be educated about the signs and symptoms of retinal detachment because this is an unlikely, but possible consequence.
Purtscher's retinopathy is an interesting clinical condition that occurs after an injury that includes either major chest compression or head trauma. Classically, the patient presents with cotton-wool spots and hemorrhages along the retinal arcades, so this diagnosis is driven first by history and then by the clinical presentation.
Purtscher's retinopathy
Although not completely understood, Purtscher's retinopathy may be due to arterial and venous back-flow into the retinal vessels. Patients should be reassured that the condition tends to resolve without treatment, but they should be dilated every 2 to 3 weeks until resolution occurs.
Traumatic retinal detachment (RD) is a rhegmatogenous detachment that can be caused by 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 (i.e., the macular region of the retina is intact) should receive a retinal consult and undergo surgery within 1 to 2 days of diagnosis. These patients should be confined to bed rest until surgery. A macula-off RD (i.e., the macular region has detached) is less urgent and these patients should have a retinal consult and surgery within approximately one week.
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. However, it most commonly arises from indirect damage, occurring in 0.5% to 5% of all closed head trauma.
Traumatic Optic Neuropathy
The findings are decreased VA, impaired color vision, and 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, although optic canal decompression surgery may be necessary.
The presence of blood within the posterior ethmoidal cells, a patient age over 40 years, loss of consciousness associated with traumatic optic neuropathy, and absence of recovery after 48 hours of steroid treatment have been shown to significantly increase the probability that the patient's visual acuity will not recover.
Optic nerve avulsion is a rare clinical entity that occurs when there is partial or complete tearing of the optic nerve from the globe at the level of the lamina cribrosa. This obviously causes tremendous axonal disruption.
Optic Nerve Avulsion
Avulsion can occur after severe trauma or relatively minor insults, but always results in devastating loss of vision.
The ocular effects of trauma can be far reaching and profound. They must never be underestimated. Using a thorough, systematic approach (including a complete history and a dilation, as appropriate) when examining for ocular trauma will serve the clinician and the patient alike.
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Joseph M. Rappon, OD, MS, FAAO 1013 East Freway Drive Conyers GA 30094 drrappon@yahoo.comPacific University College of Optometry provides On-Line CE as a service to optometrists. The college does not endorse or recommend any products, equipment, or services that might be discussed in the courses. Courses are prepared by individuals believed to be experts in their areas of specialization who are compensated for their efforts. The College relies on their expertise to produce accurate and timely courses. Questions or concerns about courses should be directed to the individual authors and/or the Continuing Education Department at the College of Optometry at kundart@pacificu.edu .
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