Common Ophthalmologic Emergencies: A Systematic Approach to Evaluation and Management
Common Ophthalmologic Emergencies: A Systematic Approach to Evaluation and Management
Authors: Gregory P. Cuculino, MD, Staff Physician, Department of Emergency Medicine, Crozer Chester Medical Center, Upland, PA; Carlo J. DiMarco, DO, MSc, FOCOO, Director of Ophthalmology Residency, Professor, Department of Ophthalmology, Philadelphia College of Osteopathic Medicine; Chairman, Department of Ophthalmology, Crozer-Springfield Hospital, Springfield, PA, Frankford Bucks Hospital, Langhorne, PA.
Peer Reviewers: Swaminatha V. Mahadevan, MD, FACEP, Assistant Professor of Surgery, Associate Chief, Division of Emergency Medicine, Stanford University School of Medicine, Palo Alto, CA; Theodore C. Chan, MD, FACEP, Associate Professor of Clinical Medicine, Emergency Medicine, University of California San Diego Medical Center.
Ocular complaints are common in the emergency department (ED). It is estimated that approximately 5% of ED visits each year are related to the eye.1,2 Approximately 1.2 million people per year sustain traumatic ocular injuries, with 40,000 of those suffering some degree of visual loss.3
It is essential for the emergency physician to make an accurate diagnosis, begin appropriate therapy, and make the appropriate ophthalmologic consultation to avoid potentially devastating results. Subtle complaints may harbor serious, sight-threatening disease processes. It is imperative to approach each ocular complaint with caution. The armamentarium available to the ED physician to evaluate the eye is limited. Radiographic studies have very limited uses. The physician must rely on his or her knowledge base and ability to complete a thorough ocular exam to make the correct diagnosis and disposition.
This article is intended to be a focused review of common ophthalmologic emergencies. It will outline the ophthalmologic exam, treatment guidelines, and indications for consultation.—The Editor
Common Ophthalmologic Emergencies
Examination. When evaluating a patient with an ocular complaint, certain historical and physical findings are essential to making an accurate diagnosis and conveying adequate information to any ophthalmologic consultants. A complete eye exam should be performed in a step-wise fashion. (See Figure 1 for gross anatomy of the eye.)
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The "vital sign" of the eye, visual acuity, should be obtained on anyone presenting with an ocular complaint. This can be measured with a Snellen eye chart at 20 feet or with a bedside version (Rosenbaum card) that is held at approximately 14 inches. The best, corrected visual acuity is extremely important to determine. This can be established using a pinhole occlusive device. If one is not available, a simple index card with a small hole will suffice.4 The pinhole acts as a refractive device by aligning the beam of light as it enters the eye. It allows a more accurate measure of visual acuity on a patient who is in need of glasses or did not bring glasses or contacts with him. If a patient is unable to cooperate by reading the eye chart or cannot see the largest letter on the eye chart, visual acuity may be measured in grosser terms such as counting fingers, hand motion, and light perception. The distance at which the patient can do all of the above activities should be documented. If pain is a significant factor in patient cooperation, a drop of an ophthalmic anesthetic such as proparacaine hydrochloride may allow the patient to cooperate better with the exam. Pediatric patients may use eye charts encompassing diagrams of age-appropriate images, such as rabbits and cakes, or charts comprised of the letter "E" in various positions. Using this eye chart, the patient must state which direction the "E" is pointing.
The external exam of the eye also should include the eyelids, lashes, peri-orbital bony structures, and the lacrimal system. The lid exam should assess the integrity of the lids’ structure and function. Any lacerations should be documented, as well as whether the laceration involves the lid margins or loss of tissue. Lacerations involving the medial one-third of the eyelids are a risk for disrupting the lacrimal apparatus and require plastic surgery or ophthalmology for closure. The completeness of opening and closing of the lids also should be noted, taking note of any proptosis, ptosis, or enophthalmos. In cases of suspected foreign bodies, the lids should be inverted to examine the cul-de-sac. Double eversion of the eyelid is necessary to evaluate completely the cul-de-sac of the upper eyelid for a retained foreign body. Keep in mind that this should not be done in the case of a suspected globe rupture to avoid any increased pressure on the globe and possible further expulsion of globe contents. Eyelashes should be examined for the presence or absence of discharge or matting. Any lesions also should be documented. The bony orbit should be examined for point tenderness, step off, or crepitus. Crepitus may indicate the presence of a sinus fracture. The peri-orbital area should be examined for the presence of parasthesias, possibly indicating an injury to the infraorbital sensory nerve.
The pupillary exam is extremely important. The size, shape, and reactivity of the pupils, and presence or absence of an afferent defect, should be noted prior to the instillation of eye drops. The size, shape, and reactivity of a pupil can be affected by trauma, medications, and central neurological events, as well as by ocular processes. Any abnormality of the pupillary size or shape should be documented. An eccentric pupil may indicate globe rupture. As the anterior chamber contents are lost, the iris may be pulled into the defect, causing the pupil to look asymmetrical. Often with a globe rupture the pupil is teardrop shaped. An afferent pupillary defect is determined by the swinging flashlight test.5 A light is shone into one pupil for 30 seconds, and then quickly swung to the other side. The first movement of the pupil should be noted. This is repeated, swinging the light to the other side. Normally, pupils will exhibit consensual constriction when a light is shone into one pupil. Therefore, both pupils will react by constricting to a light shone in one eye. In normal eyes, when the light is swung back and forth, the pupils will constrict or remain constricted. Any disease process that blocks light from reaching the optic nerve or blocks transmission of the optic nerve (i.e., optic nerve trauma, large vitreous hemorrhages) will cause an afferent pupillary defect. In these conditions, there is abnormal dilation of the affected pupil when light is shone into it. That eye, in essence, is receiving less light stimulation than normal and dilates in an attempt to bring in more light.
The surface of the globe is composed of the conjunctiva, sclera, and cornea. The conjunctiva is a thin, vascular mucous membrane covering the sclera and internal surface of the eyelids. The sclera is the tough, white, collagenous portion of the eye. Anteriorly, the sclera becomes the clear cornea. The external globe should be examined for any laceration, injection, swelling (chemosis), bleeding, foreign body, or discharge. A fluorescein eye exam will reveal any damage to the epithelium of the cornea. The fluorescein adheres to any exposed portion of the basement membrane of the cornea and fluoresces green under a cobalt blue light.6 A positive Seidel test indicates the presence of an open globe injury. It is positive if the fluorescein appears to be streaming away from the cornea, forming a pool in the cul-de-sac. The streaming is caused by the aqueous humor as it flows out of the defect.
Extraocular movement may be altered in cases of trauma, neurological events, infections, and tumors. There are six muscles controlling eye movement. These are innervated by three cranial nerves (nerves 3, 4, and 6). The superior oblique is innervated by the fourth cranial nerve. The lateral rectus is innervated by the sixth cranial nerve. The remaining muscles (superior rectus, inferior rectus, medial rectus, and inferior oblique) are innervated by the third cranial nerve. The third cranial nerve also controls pupillary constriction and lid elevation. Therefore, any damage to the third nerve can, depending on the severity, cause ptosis and miosis as well as an extraocular muscle deficit. During evaluation of the extraocular muscles, note should be made of any nystagmus. Any resultant diplopia may indicate trauma to the globe with muscle impingement or nerve deficit, whether peripheral or central. In evaluating the extraocular muscles, the patient should be asked to move his eye up, down, left, and right, as well as up and out, down and out, up and in, and down and in. If there is a suspected globe rupture, however, evaluation of the extraocular muscles should be deferred. Diplopia may be either monocular or binocular. Monocular diplopia—diplopia with one eye closed—usually indicates a refractive error in the eye itself. Binocular diplopia—diplopia that is present only when both eyes are open—is the result of a deficiency in the movement of the eye. This may be due to a problem with the muscles themselves, the nerves innervating them, or a central event.
The anterior chamber of the eye is examined with the slit lamp. Biomicroscopy with the slit lamp will detect the presence of blood in the anterior chamber (hyphema), inflammatory cells, and pus. Normally, the anterior chamber is filled with clear aqueous humor and is translucent on bimicroscopy. However, the presence of dark specks within the anterior chamber may indicate the presence of a micro-hyphema. Cells and flare in the anterior chamber are a result of inflammation and take the appearance of white dust particles in a beam of light. Cells are the white blood cells floating in the convection currents of the aqueous humor. Flare is the smoky appearance of the aqueous humor that results from proteins liberated from the inflamed iris or ciliary body. A gross collection of white cells is a hypopyon and a true ocular emergency.
The depth of the anterior chamber is important to note, especially prior to the instillation of dilating drops. This is done easily by shining a penlight across the cornea from the lateral to medial direction. With a normal anterior chamber depth, the light will shine evenly across the iris. A patient with a shallow anterior chamber, however, will exhibit a shadow on the medial aspect of the iris. The shadow is caused by the iris as it bulges outward into the anterior chamber. Currently under debate is the premise that people with shallow anterior chambers are at risk for acute angle closure glaucoma if dilated.7 Past teaching indicated that patients with shallow anterior chambers never should be dilated by a non-ophthalmologist for fear of precipitating an attack of angle closure glaucoma. A shallow anterior chamber also may indicate a globe rupture with loss of aqueous humor.
Intraocular pressures should be measured in all cases except those in which a penetrating globe injury is suspected. A normal intraocular pressure is 8-21 mmHg.4 Pressures can be measured with the slit lamp; however, significant experience and maintenance of the machine is needed. Most physicians use some type of aplanatic tonometer. A Tonopen is an automated, hand-held machine. After calibration, the covered tip is tapped gently against the anesthetized eye with the patient in the supine position. An average of three readings is used. The Schiotz tonometer is a mechanical device that measures pressures by applying weight to the cornea and measuring the resulting indentation of the cornea. If the intraocular pressure is elevated, a given weight will not be able to indent the cornea as much. Therefore, the actual readings on the tonometer are inversely proportional to the intraocular pressure. With the standard 5.5 gram weight, readings of 4 or greater are acceptable. The Schiotz tonometer is equipped with a conversion chart to convert the tonometer reading to pressure measurements.
Increased intraocular pressures are found with chronic glaucoma and acute angle closure glaucoma. Low intraocular pressures, on the other hand, may be found with inflammatory conditions. The exception to this is iritis, which minimally may elevate the intraocular pressure. Globe rupture also will lower the intraocular pressure. However, remember never to assess intraocular pressure with a suspected globe rupture.
Fundoscopic exam is accomplished best with the aid of dilating drops. These drops will last for hours, and their use should be documented carefully, especially in trauma patients. Also, care should be taken with people who have shallow anterior chambers for fear of precipitating an attack of angle closure glaucoma.
The eye drops used to facilitate the exam are divided into three categories: topical anesthetics, mydriatic drops, and cycloplegics. Manufacturers have color-coded the caps on eye drops in an attempt to avoid medication errors. Drops with green caps are miotics. A red cap indicates a mydriatic solution. Blue and yellow caps indicate beta-blocker solutions of 0.25% and 0.5%, respectively. White caps indicate a topical anesthetic agent. The topical anesthetics are proparacaine hydrochloride (ophthetic, Alcaine) 0.5% and tetracaine hydrochloride (pontocaine) 0.5-1.0%. These have immediate onset of action and last approximately 15 minutes. Mydriatic drops are used to dilate the pupil. Tropicamide (mydriacyl) 0.5-1.0% will cause dilatation in approximately 15 minutes, and the effect lasts about six hours. It also has weak cycloplegic effects. Cycloplegic agents cause relaxation of the ciliary body and are useful in conditions such as iritis where the ciliary spasm is extremely painful. Phenylephrine (neo-synephrine, mydfrin) 2.5% takes action in approximately 15 minutes and lasts approximately 2-4 hours. Cyclopentolate (cyclogyl) 1% takes approximately 30 minutes to achieve its effect and lasts 12-18 hours. Homatropine 0.25-0.5 % will last for approximately 1-3 days. Atropine 0.5-1.0% rarely is used because its duration of action is 5-10 days. Once the pupil is dilated adequately, the fundus can be examined with a direct ophthalmoscope.5 Note should be taken of any vitreous abnormalities, the appearance of the optic nerve and disk, retina, macula, and the retinal vessels.
Traumatic Eye Injuries
It is helpful to differentiate ocular complaints based on those with or without a traumatic history. Caution must be taken, however, because often the trauma may not be obvious to the patient. An example of this is a foreign body sensation after hammering a nail. Often a shard of metal can splinter off, striking the eye and possibly penetrating the globe.
Facial Fractures. Beside direct injury to the globe, traumatic facial trauma may have other ocular implications. Orbital wall fractures occur when the pressures within the bony globe compartment are increased as a result of blunt trauma. Physical exam may reveal bony point tenderness along the orbital ridge, crepitus if the sinus cavity has been violated, or parasthesias/hyperathesias along the infraorbital nerve distribution. The eye itself may appear sunken in the globe compartment. Diplopia may be a complaint if any of the extraocular muscles have become entrapped within the fracture. The patient will have limited gaze, often in the vertical direction, and will complain of diplopia or pain when asked to move the eye in certain directions. Computed tomography (CT) scans of the orbits with thin cuts often reveal the fracture as well as give information concerning associated sinus involvement or entrapped contents. The scan should be done with 3 mm cuts with axial and coronal views. Most fractures are at the floor of the orbit, where the bones are weakest. This will cause injury to the maxillary sinus as well as possible entrapment of the inferior rectus and inferior oblique muscles. The fracture may occur through the medial wall into the ethmoid sinus through the lamina papyracea. This may cause entrapment of the medial rectus muscle.
Treatment of simple orbital fractures without any entrapment of orbital contents includes the use of oral antibiotics, ice packs, and decongestants, and the avoidance of nose-blowing and other Valsalva maneuvers, and ophthalmology follow-up. Fractures involving muscle entrapment or evidence of enophthalmos require immediate ophthalmology consultation. The timing of repair is controversial, however. Some experts favor immediate repair, whereas others favor re-evaluation in 10-14 days to allow resolution of edema and possible spontaneous correction.8,9
Eyelid Lacerations. A patient presenting with an eyelid laceration always should be evaluated for the possibility of a penetrating globe injury. Simple partial thickness lacerations may be closed by the ED physician; however, plastic surgeons or ophthalmologists should close any lacerations involving the lid margins or cannicular system and lacerations that include tissue loss or violation of the orbital septum. Fatty tissue present within an eyelid laceration suggests violation of the orbital septum.10 (Please refer to Trauma Reports 2001;4:1-12 for supplemental information.)
Subconjunctival Hemorrhage. Subconjunctival hemorrhage is defined as bleeding of the conjunctival or episcleral vessels into the subconjunctival space. It usually is a self-limiting process. Patients may present with painless, red eyes. There may be some mild irritation. Causes are numerous and include Valsalva maneuvers such as coughing or straining, trauma, hypertension, coagulapathy, febrile illness, or idiopathic causes. Care must be taken with traumatic cases to rule out the presence of a globe rupture or retrobulbar hemorrhage. Treatment is supportive and directed to prevent further bleeding. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin should be discontinued for 24-48 hours. Valsalva maneuvers should be avoided, and artificial tears should be used for mild irritation. The natural course mimics that of hematoma. As the blood is broken down, it will change color from green to yellow, and then to brown. There may be a slight early spreading of the discoloration, but it should resolve within two weeks. Post-operative hemorrhages or any hemorrhage associated with globe tenderness should be evaluated for the presence of an occult infection.11
Corneal Abrasion. A corneal abrasion is defined as a defect in the cornea that does not penetrate Bowman’s layer. Corneal abrasions are very common and account for approximately 10% of eye-related visits to the ED annually. Patients may present with pain, photophobia, tearing, and a foreign body sensation. Fluorescein examination of the cornea will reveal an area of green fluorescence under cobalt blue light. Multiple linear areas of fluorescein uptake suggest a foreign body adhered to the inner surface of the conjunctiva, causing repeated abrasions to the cornea as the eye opens and closes. It is important to perform a double eversion of the eyelid to assess for a retained foreign body. There may or may not be a history of trauma. Contact lens wearers have an increased risk of "non-traumatic" abrasions. The relatively sharp edges of hard contacts often cause small defects during normal use. Extended-wear contacts cause epithelial hypoxia, which impairs the attachment of the epithelial cells to Bowman’s membrane. This weakened attachment makes the epithelium more susceptible to damage due to minimal trauma, such as rubbing the eyes.
Treatment of corneal abrasions consists of topical antibiotics, tetanus prophylaxis, and pain control. Cycloplegic agents also may be considered for patients exhibiting significant ciliary spasm. Contact lens use should be discontinued until the abrasion has healed completely. The decision to patch a corneal injury is made on a case-by-case evaluation.12-17 Patching of the eye may slow healing and may increase the rate of infection and is rarely done. However, it still may be used briefly for patients with significant ciliary spasm and photophobia. A patch should not be used for abrasions in contact lens wearers or abrasions caused by vegetable matter or artificial fingernails. The antibiotics generally used are broad-spectrum with additional pseudomonal coverage for those caused by vegetable matter or in patients with contact lenses.18 (See Table 1.) Ointments often are considered to offer soothing lubrication to the eye, but they blur vision for a short period. Drops, on the other hand, do not blur vision but may be more difficult to instill. Pain control may include topical NSAID drops or systemic medications.19 Topical anesthetic agents never should be prescribed for a patient. They impede epithelial repair and may predispose patients to further trauma as the protective reflexes of the eye are lost.
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Corneal abrasions heal rapidly, and most are improved significantly within 24 hours and do not cause any vision deficits. However, they may be complicated by a corneal ulcer or cause decreased visual acuity if they involve the visual axis. Traumatic iritis may develop 24-72 hours post-injury. Recurrent erosion syndrome is defined as a recurrent abrasion days to years after a previous injury. Often, the patients will present with sudden severe pain experienced when they opened their eyelids upon waking. This is caused by a weakness in the attachment to Bowman’s membrane in the previously injured area. Upon waking, the eyelids pull off the corneal epithelium over the weakened area, resulting in a corneal abrasion and pain. Patients at risk for this type of abrasion are those presenting with large abrasions or those abrasions caused by fingernails or hard contact lenses.20
Corneal Foreign Bodies. The subjective sensation of a corneal foreign body is one of the most common reasons for a visit to the ED. The patient will present with pain, a foreign body sensation, a red eye, tearing, and photophobia. Care must be taken to obtain an accurate history of the nature of the exposure. High-velocity objects may cause corneal perforation. A corneal perforation should be suspected if the patient presents with a diffuse subconjunctival hemorrhage, diffuse corneal damage, abnormal pupillary shape, a hyphema, or a change in anterior chamber depth vs. the noninvolved eye.
Prior to examination and removal of a foreign body, topical anesthesia is needed. The depth of the foreign body should be evaluated with biomicroscopy. Deeply embedded foreign bodies and those involving the visual axis should be removed by an ophthalmologist. Superficial foreign bodies may be removed with a moist cotton applicator, a foreign body spud, or the bevel of a 25- or 27-gauge needle. The foreign body should be approached from the side and gently removed. Antibiotic drops should be instilled pre- and post-removal. Iron-containing products may leave a residual rust ring. These can be removed 24-28 hours later by the ophthalmologist. A negative Seidel test should be documented post-removal of the foreign body to ensure that an iatrogenic corneal perforation did not occur. Once the foreign body is removed, treatment is the same as that for a corneal abrasion.21
Ocular Burns/Chemical Exposure. Ocular burns may result from chemical, thermal, or ultraviolet injury. Approximately 20% result in significant visual or cosmetic disability. Chemical eye exposures account for 10% of all ocular complaints and 80% of all ocular burns. Sixty percent of chemical exposures occur in the workplace.21
The chief determinants of the degree of injury in a chemical exposure are the pH of the material, length of exposure, and permeability of the agent. Acidic materials often coagulate upon contact and limit the exposure and penetration. An exception to this is the weak acid, hydrofluoric acid. Hydrofluoric acid does not cause coagulation of the cornea and is absorbed into the globe. It is an extremely dangerous substance and can cause fatal systemic complications, such as hypocalcemia and cardiac dysrhythmias. All hydrofluoric acid ocular exposures require immediate ophthalmologic consultation and irrigation with 1% calcium gluconate. Significant exposures with hydrofluoric acid require systemic treatment and decontamination. Alkali substances are lipophilic. They cause saponification of tissues and can penetrate the eye deeply. Alkali substances induce a severe inflammatory response that releases protealytic enzymes that cause liquefaction necrosis. (See Table 2.)
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Treatment of all chemical exposures is immediate decontamination. Any particulate matter should be removed immediately. The eye is irrigated with at least 1-2 liters of normal saline solution or lactated ringer’s solution until a neutral pH is obtained.22 The eye must be allowed to equilibrate for 5-10 minutes before determining the pH. Cycloplegic/mydriatics may be used to relieve the painful ciliary spasm. Mild chemical injuries may be treated as corneal abrasions and followed up on an outpatient basis. However, moderate to severe chemical burns necessitate immediate ophthalmology evaluation. The ophthalmologist may decide to initiate treatment to reduce inflammation, promote epithelial healing, decrease intraocular pressure, or even debride the injured area. These are done in an effort to prevent scarring, cataract formation, perforation, and glaucoma.
Ultraviolet (UV) burns often present 6-12 hours after the injury.23 These burns often occur in welders who do not wear protective eyewear or in people who are out in the snow on a very sunny day. These people often are unaware that the UV light from the welder’s arc or reflected from the snow is causing epithelial damage. Just as with a sunburn, the pain often is delayed but severe. Physical exam will demonstrate punctate keratitis, often in a distribution on the exposed surface only. Simple thermal and ultraviolet burns are treated as corneal abrasions with pain control and antibiotic prophylaxis.
Cyanocrylate Glues. Direct exposure to cyanoacrylate glues may cause a chemical keratitis. If the eyelids are bonded together, gently rubbing them with a petroleum-based ointment such as bacitracin or erythromycin may allow the eyelids to be separated. However, forceful retraction should not be used, and patients who do not respond to the petroleum-based ointment should be referred to an ophthalmologist.
Corneal Laceration. A corneal laceration is a full-thickness injury. Many are self-sealing and may be difficult to visualize. Therefore, a high index of suspicion should be maintained. Clues to the possibility of a full-thickness injury may be the presence of a teardrop pupil, a flat anterior chamber, or hyphema. Once a laceration is identified, the patient should have the eye covered with a hard shield and should be instructed not to move the eye in an effort to prevent expulsion of intraocular contents. Intraocular pressures should not be measured in cases of suspected full-thickness lacerations. The patient should be kept at a 30- to 45-degree angle at all times in case of an associated hyphema. Immediate ophthalmology consultation should be made. Prophylactic antibiotics and tetanus prophylaxis often are initiated. Antiemetics may be used to prevent any increase in intraocular pressure from vomiting.
Intraocular Foreign Bodies. Metallic particles comprise 80% of all intraocular foreign bodies.24 A physician should maintain a high index of suspicion for the possibility of an occult intraocular foreign body when there is a history of metal striking metal or any mechanism indicating a high velocity projectile. The patient will present with pain, irritation, and injection. On biomicroscopy the entry site may be visible as a disruption of the smooth corneal surface with surrounding edema. Fluorescein staining may demonstrate a positive Seidel sign, which is a streaking of the fluorescein as aqueous humor leaks out of the globe. Remember that in any suspected case of an intraocular foreign body, measurement of the intraocular pressure is contraindicated. Work-up of a potential intraocular foreign body includes plain films of the orbits if the suspected material is radio-opaque. However, CT scan of the orbits is the preferred imaging study.25,26 Ultrasound also may detect some foreign bodies and has the added benefit of identifying retinal detachments.27 Magnetic resonance imaging (MRI) may be useful for foreign bodies not visualized on CT, but should be avoided if the foreign body in question is metallic.
ED treatment of intraocular foreign bodies consists of protecting the eye from further injury with a hard protective shield. Care should be taken not to apply any pressure to the globe. Tetanus prophylaxis should be addressed and immediate ophthalmology consultation made. Intravenous (IV) antibiotic prophylaxis often is initiated in the ED. Approximately 10% of intraocular foreign bodies become infected. The incidence of endophthalmitis increases from 3.5% to 13.4% with a delay of just 24 hours in removing the foreign body.25 Beside standard gram-positive organism coverage, antipseudomonal coverage is needed if the material is dirt or vegetable matter such as a tree branch. Endophthalmitis secondary to Bacillus species is extremely debilitating and often leads to irreversible vision loss in fewer than 24 hours.28-30 Antiemetics again may be necessary to prevent vomiting and a resultant increase in intraocular pressure.
Globe Rupture. A globe rupture may occur from direct blunt trauma to the eye. As the intraocular pressure is increased suddenly, rupture of the sclera where it is thinnest may occur—the limbus, the site of insertion for extraocular muscle (EOM), and the site of the optic nerve insertion.31 Physical exam may reveal a total subconjunctival hemorrhage, enophthalmos, a teardrop pupil, or a flattened anterior chamber. If uveal prolapse has occurred, a small patch of brown or black material may be visible on the sclera. This is not a foreign body but, rather, uveal tissue exposed through the sclera. If any of these conditions is present, intraocular pressure measurements should be avoided to prevent further damage to the eye. Treatment for a globe rupture is the same as that for an intraocular foreign body or corneal laceration.
Hyphema. A hyphema is defined as blood within the anterior chamber. Patients may present with a history of trauma, decreased vision, and pain. The degree of hyphema may vary from cells visible only on biomicroscopy to large total (so-called "eight-ball") hyphemas where the iris is obscured by gross blood. An underlying coagulopathy may be the cause of an atraumatic hyphema. The size of the hyphema determines the visual outcome. Larger hyphemas are associated with a worse prognosis.32 All hyphemas require immediate ophthalmology consultation, because even small hyphemas may indicate significant ocular injury. Treatment is aimed at reducing the risk of re-bleeding as well as preventing complications such as glaucoma. Small hyphemas may be treated on an outpatient basis in a compliant patient with appropriate ophthalmology consultation and follow-up.33 Treatment consists of total bed rest with the head of the bed elevated 30-45 degrees, strict eye rest, and cycloplegics. The eye should remain shielded to avoid any further injury, and antiplatelet agents should be avoided. Larger hyphemas may be monitored as an inpatient. Intraocular pressures must be obtained and monitored because of the increased risk of glaucoma.34
Lens Dislocation/Subluxation. Trauma to the eye may disrupt the zonular fibers that maintain the lens in its correct position. Partial disruption will cause the lens to sublux. The lens, however, still remains in the pupillary aperture. Patients will complain of pain and monocular diplopia, and the edge of the lens will be visible through the pupillary aperture. A total disruption of the zonular fibers will cause the lens to dislocate into the posterior chamber. This may lead to an acute rise in intraocular pressure. Both conditions require immediate ophthalmology evaluation. A lens dislocation or subluxation may occur with minimal trauma in patients with Marfan’s syndrome, homocystinuria, or syphilis.
Iridodialysis. Direct trauma to the eye may cause the iris to be torn from the ciliary body. This will cause the appearance of a second pupil. A secondary hyphema often develops and the patient may complain of monocular diplopia if the defect in the iris is large. Treatment consists of treating the hyphema and obtaining immediate ophthalmology consultation.
Optic Nerve Trauma. Occasionally trauma to the eye will cause direct trauma to the optic nerve. Patients will present with a decrease in vision and an afferent pupillary defect unrelated to any other associated eye injury. Care must be taken to rule out the presence of other injuries, such as retinal tears or a hyphema, as the cause of the vision loss. Initially the fundoscopic exam may be normal. Immediate ophthalmology consultation is necessary.
Retrobulbar Hemorrhage (Orbital Compartment Syndrome). Most cases of retrobulbar hemorrhage are post-traumatic or post-operative, although there are rare cases of spontaneous hemorrhages. Patients may present with acute proptosis, pain, elevated intraocular pressures, swelling, and decreased range-of-motion, the result of extravasated blood within the bony orbital walls. As the blood accumulates, it causes pressure on the globe with resultant proptosis, increased intraocular pressure, and decreased range-of-motion. There is a resistance to retropulsion of the globe.35 Irreversible vision loss occurs within 60 minutes, so aggressive management is the key. The intraocular pressure must be reduced. Topical beta-blockers such as timolol 0.5 % (1 drop every 30 minutes for 1 hour) decrease production of aqueous humor. Carbonic anhydrase inhibitors such as acetazolamide (500 mg PO/IV/IM then 250mg PO/IV/IM every 6 hours) also reduce production of aqueous humor. Hyperosmotic agents, such as mannitol 1.0-1.5 mg/kg, reduce vitreous volume. In severe cases, a lateral canthotomy will allow the globe to protrude out of the confines of the orbit with a resultant decrease in intraocular pressure. Immediate ophthalmology consultation is necessary.
Globe Luxation. Probably one of the most dramatic traumatic eye presentations, globe luxation requires immediate attention. In these cases, the entire globe will be found external to the bony orbit. Early reduction to minimize traction on the optic nerve is recommended, with gentle pressure as the eyelids are retracted. Edema and retrobulbar hemorrhage may make this impossible outside the operating room.
Non-Traumatic Eye Injuries: External Diseases
Pinguecula/Pterygium. These are extra tissue growths of conjunctiva. They both are related to UV exposure as well as age. A pinguecula is a cream-colored or white raised growth of the conjunctiva. A pterygium is a triangular fibrous tissue overgrowth of conjunctiva onto the cornea. Treatment generally is not indicated. However, a pterygium may compromise the visual axis and, at that point, surgery may be undertaken. Recurrence is common. The pterygium also may become inflamed and painful, causing the patient to seek emergency care. Topical vasoconstrictors such as naphazoline may be used to decrease the inflammation.
Blepharitis. Blepharitis is an inflammation of the eyelid margins due to a superficial infection of Staphylococcus aureus. Patients present with irritation and burning of the eyelashes, with or without signs of associated conjunctivitis. There often is a fibrinous material on the lashes. Treatment includes proper lid hygiene with gentle detergents, such as baby shampoo, and antibiotic ointment.
Dacryocystitis. Patients often will present with unilateral pain, swelling, and erythema over the lacrimal sac beneath the medial canthus of the eye. There is a bimodal distribution of this disease, with peaks occurring in those younger than 2 years and older than 40 years.36 Purulent material may be expressed from the punctum when the lacrimal gland is massaged. Treatment consists of warm compresses, oral antibiotics covering normal skin flora, and pain control. Patients should be referred to an ophthalmologist for follow-up.
Hordeolum. Also known as a stye, a hordeolum is a localized inflammation of the eyelid margin. It is caused by inflammation in the Zeis or Meibomian glands. S. aureus is the causative pathogen in 90-95% of cases. The area often is erythematous and tender. Some cases may progress to periorbital cellulitis. Treatment consists of warm compresses, topical antibiotics, and follow-up with an ophthalmologist. Most hordeolum spontaneously drain and resolve within 5-7 days.37 However, large symptomatic abscesses may be drained, preferably from the conjunctival side. A small vertical incision is made to minimize any corneal irritation from the healing wound. The eyelid margins never should be incised unless by an ophthalmologist. Children normally have a high recurrence rate; however, multiple recurrences in an adult may indicate the presence of a basal cell carcinoma or sebaceous cell carcinoma.
Chalazia. Chalazia is the Greek word for hailstone. Chalazias are caused by chronic inflammation of the Meibomian or Zeis glands, secondary to obstruction. A chalazia is non-tender, which differentiates it from a hordeolum. Most point toward the conjuctival surface; however, larger ones may extend to the external surface of the eyelid. The development of chalazia is associated with seborrhea, acne rosacea, chronic blepharitis, and hyperlipidemia. Treatment usually includes warm compresses until the inflammation subsides. Incision and curettage is an option. Emphasis also is placed on prevention, with regular massage of the eyelids with baby shampoo to prevent obstruction of the glands.38
The Red Eye
A patient presenting to the ED with a red eye may harbor an innocent, self-limiting disease or a sight-threatening process. The physician must take care to differentiate the two and obtain appropriate ophthalmologic consultation.
Conjunctivitis. Conjunctivitis is defined as an inflammation of the mucous membrane of the eye. Most often it is secondary to bacterial or viral infections. Physical exam reveals injected conjunctiva, discharge, and edema of the eyelids. The discharge often will be thin and watery with viral infections and mucopurulent with bacterial cases. Severe injection with copious purulent discharge is found in gonoccocal conjunctivitis (hyperacute conjunctivitis). Patients often will have pre-auricular adenopathy. The remainder of the eye exam should be normal, with no pupillary changes or changes in visual acuity. There is no corneal involvement. This condition is extremely contagious, and the physician should take care to wear gloves and wash thoroughly to avoid cross-contaminating the other eye or infecting himself and other patients.
The offending bacterial agents are mainly Staphylococcus and Streptococcus. Pseudomonal infections increase in frequency in contact lens wearers. Gonorrhea and chlamydia affect mainly neonates. Viral agents are mainly adenovirus and herpes simplex virus. Pharyngoconjunctivitis is caused by adenovirus types 3, 4, and 7. The clinical scenario is that of fever, pharyngitis, and conjunctivitis.39 Epidemic keratoconjunctivitis is caused by adenovirus 8 and 19. It is extremely contagious and may last for 7-21 days. Herpetic conjunctivitis also may be related to primary herpetic disease (chickenpox). This usually occurs in children younger than 5 years. It also may be related to a herpes zoster infection.
General treatment of conjunctivitis is comprised of empiric antibiotic drops/ointments, cold compresses for symptomatic relief, and proper hygiene to avoid spread. (See Table 1 for some commonly used antibiotic ointments.) Broader spectrum agents are used to cover potential pseudomonas in patients who wear contacts or who were exposed to organic matter. Exceptions to this empiric treatment are made for conjunctivitis secondary to gonorrhea, chlamydia, and herpes simplex infections. Conjunctivitis may be complicated by membrane formation, scarring of the punctum of the eyelids, corneal ulceration, and endophthalmitis.40
Gonococcal conjunctivitis, also known as hyperacute conjunctivitis, necessitates systemic treatment and immediate ophthalmology consultation. It may progress rapidly to corneal ulceration. In the neonate, it is treated with penicillin G 100 units/kg divided QID IV for 7 days.40 In adults it is treated with 1 gram of ceftriaxone IM and doxycycline 100 mg by mouth BID for 14 days. Chlamydia infections in the neonate are treated with erythromycin liquid 50 mg/kg/day divided QID for 14 days as well as erythromycin ophthalmic ointment QID.41 Adults with a chlamydial infection are treated with doxycycline 100 mg PO BID for 7 days. Although less common in the United States, chlamydia eye disease is the leading cause of blindness in the world. Untreated chlamydia infections lead to the formation of a trachoma. As the conjunctivitis progresses, it causes scarring of the palpebral conjunctiva and eyelid deformities. These deformities cause constant abrasions of the cornea as the eyes are opened and closed. Eventually, this causes scarring, erosion of the cornea, and blindness.
A key to herpetic ocular involvement may be the presence of cutaneous vesicles elsewhere on the face. In cases of a herpes zoster infection, a vesicle on the tip of the nose is referred to as Hutchinson’s sign and indicates involvement of the V1 dermatome of the facial nerve and potential ocular involvement. Fluorescein staining of the eye typically reveals a dendritic lesion. However, not all herpetic lesions are dendritic. Treatment of herpetic ocular lesions includes a topical antiviral such as trifluridine (one drop 5 times a day for 10 days) or vidarabine 3% (0.5-inch applied to the eye 5 times a day). Although primary ocular herpes usually is self-limited, antiviral therapy still is initiated to limit corneal involvement. Of note, herpetic ocular involvement presents as conjunctivitis in 54% of cases. Therefore, it is important to conduct fluorescein staining on all cases of conjunctivitis to rule out the presence of a dendritic lesion.42 Topical steroid use in the presence of an ocular herpetic infection may lead to corneal perforation and should be done only by an ophthalmologist. All cases of suspected herpetic ocular involvement should be referred to an ophthalmologist.
Not every case of conjunctivitis is infectious. Acute atopic conjunctivitis is a type 1 allergic reaction. It is mediated by an IgE released in response to airborne pathogens. Patients present with itchy, burning eyes that are hyperemic and swollen (chemotic). Treatment consists of cold compresses and antihistamines.
Bacterial Keratitis. This is a sight-threatening disease that is characterized by rapid progression, corneal ulceration, edema, and anterior segment inflammation. Patients present with conjunctival injection, pain, foreign body sensation, discharge, photophobia due to ciliary spasm, and cells in the anterior chamber. These cells actually may layer out and form a hypopyon. The corneal ulcer is seen as a white area on the cornea and often is called a corneal infiltrate. Most cases are infectious in nature and tend to occur after an insult to the cornea (e.g., an abrasion). The exception is viral etiologies, which may occur with an intact corneal epithelium. Host factors that may hinder corneal integrity, such as contact lens use, steroid use, and other forms of immunosuppression, also predispose patients to developing keratitis. Nineteen to 24% of patients with bacterial keratitis are contact lens wearers.43 Bacterial pathogens include streptococcus, staphylococcus, pseudomonas, and enterobacteriaceae. The primary viral pathogen is the herpes virus. In the United States, herpes simplex virus is the most common cause of a corneal ulcer, and up to 40% of cases have a resultant visual disability.42
Treatment of keratitis consists of broad spectrum antibiotics and immediate ophthalmology consultation. Aminoglycosides are used alternating with fluoroquinolones every 15-30 minutes. Steroids may be used under the guidance of ophthalmology and in the absence of a herpetic lesion. Complications of keratitis include scarring, visual loss, and glaucoma.
Uveitis. The uveal tract is composed of the iris, ciliary body, and choroid. The term uveitis is used to denote inflammation in any of these areas. Usually the inflammation is limited to the anterior structures—the iris and ciliary body. This commonly is referred to as iritis or iridocyclitis. Posterior involvement is rare except in cases of cytomegalovirus (CMV) retinitis and HIV retinopathy. The incidence of uveitis is 15 per 100,000, and it occurs primarily in the 20- to 30-year-old age group. Causes of iritis include post-traumatic, autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and idiopathic causes. More than 50% of patients with uveitis have the HLA-B27 or HLA-B8.44 Patients present with intense pain, photophobia, and conjunctival injection. Most cases are unilateral. Posterior involvement may present as blurred vision and floaters, but may have less pronounced pain and photophobia. Physical exam will reveal perilimbal injection, a mioitic pupil due to ciliary spasm, consensual photophobia, and cells/flare in the anterior chamber. Extraocular movements are intact, and intraocular pressure usually is low or minimally elevated.
Treatment is directed at decreasing pain and inflammation. This is done with the use of cycloplegics. Topical steroids often are used, but only after consultation with ophthalmology.
Scleritis and Episcleritis. Both of these conditions have a high association with systemic illness such as rheumatoid arthritis, Sjogren’s syndrome, and syphilis. Episcleritis is limited to an isolated patch of the sclera and is unilateral approximately 70% of the time. The pain is usually minimal. It resembles localized conjunctivitis. Episcleritis improves with topical vasoconstrictors and is self-limited. Scleritis is diffuse and may be bilateral 50% of the time. In contrast to episcleritis, scleritis does not improve with topical vasoconstrictors and may extend to damage ocular tissues. It requires immediate ophthalmologic consultation. The pain associated with scleritis often is described as deep and aching.
In both conditions, the globe is tender and may exhibit a violet discoloration secondary to engorgement of the deep venous plexus. Treatment consists of pain control and topical steroids and cycloplegics. Severe cases may require systemic steroids.44,45
Endophthalmitis. This is an inflammation of the intraocular cavity and is primarily infectious in etiology. The source of bacteria may be endogenous or exogenous. Post-operative infections are common causes. People with endophthalmitis related to an endogenous source usually have significant comorbitities such as DM, AIDS, ESRD, or chronic immunosuppression. The incidence is 5 per 10000, with the right eye involved more commonly than the left. It is theorized that the take-off of the internal carotid artery is more direct on the right and, therefore, the more common route of infectious organisms. Fungal organisms are a common etiologic agent with Candida being the most common followed by Aspergillus. Exogenous endophthalmitis is related to penetrating ocular injuries. Two to three percent of all penetrating injuries result in endophthalmitis. Bacterial pathogens are primarily Staphylococcus epidermidis, S. aureus, streptococcus, and bacillus. If related to a penetrating injury, additional organisms include gram-negatives and pseudomonas. Patients will present with pain, decreased visual acuity, headache, and photophobia. Physical exam will reveal edema of the cornea, chemosis, hypopyon, injection, fever, ocular discharge, and cotton wool spots on the retina. Treatment involves immediate ophthalmologic consultation for systemic as well as intravitreal antibiotics and often enucleation of the affected eye.47
Glaucoma. As intraocular pressure increases, it causes damage to the optic nerve. Open angle glaucoma is a gradual process that causes vision loss without other symptoms. Acute angle closure glaucoma, on the other hand, is a true ophthalmologic emergency. Irreversible optic nerve damage begins to occur within 60 minutes of the onset of symptoms. The frequency of acute angle glaucoma is 100 cases per 100,000, with a peak age of 5570 years. Asians and Eskimos have a higher occurrence rate, as do people with shallow anterior chambers.48 An attack often is precipitated by entering a well-lit room after being subject to relative darkness, or possibly by the use of mydriatic agents in people with shallow anterior chambers. Inflammatory conditions also may precipitate an attack by pulling the iris forward. As the pupil dilates, it obstructs the Schlemm’s canal, which is the route by which most aqueous humor leaves the eye. As the aqueous humor backs up, the intraocular pressure increases, resulting in damage to the optic nerve. The history of an attack is usually the sudden onset of pain, blurred vision, lacrimation, nausea, and vomiting. The pain often is described as deep and aching. Resulting corneal edema may cause the appearance of halos around lights. Physical exam may reveal decreased visual acuity, conjuctival injection, a fixed mid-position pupil, and a hazy, edematous, cornea. Palpation of the globe may demonstrate that one globe feels firmer than the other.
Treatment is aimed at decreasing the intraocular pressure by decreasing the production of aqueous humor, reducing vitreal volume, and facilitating the drainage of aqueous humor. Topical beta-adrenergic antagonists such as timolol (timoptic 0.5% one drop every 30 to 60 minutes) and carbonic ahydrase inhibitors such as acetazolamide (acetazolamide 500 mg PPO/IV/IM then 250 mg PO/IV/IM every 6 hours) work to decrease the production of aqueous humor. Patients with a sulfa allergy should not receive acetazolamide. Hyperosmotic agents such as mannitol 12 mg/kg IV are used to decrease vitreous volume. Pilocarpine drops are miotic agents and are used to facilitate drainage of aqueous humor. Pilocarpine 2% solution can be used in patients with light-colored eyes. The 4% solution should be used in patients with dark-colored eyes. The difference is related to the amount of melanin in the eye. The dose is one drop every 15 minutes for 2 hours. Definitive treatment is iridotomy. The hole that is created in the iris allows the aqueous humor to flow anterior to the iris and return the iris to the normal position. This re-establishes flow within the Schlemm’s canal.
Periorbital Cellulitis (Preseptal Cellulitis)/Orbital Cellu-litis. Differentiation between these two conditions is vital. Periorbital cellulitis will manifest as swollen, erythematous eyelids with mild conjunctival injection. The patient may give a remote history of an inciting event, such as a bug bite or a history of sinus disease. The patient should have normal visual acuity, full range-of-motion of the eye without pain, and no evidence of proptosis.
Treatment usually consists of empiric amoxicillin/clavulonic acid to cover skin and sinus pathogens. Early infections with good follow-up and compliance may be treated on an outpatient basis; however, some cases are treated as inpatients with IV antibiotics. Indications for admission include failed outpatient therapy, intractable vomiting, or a patient who appears toxic. Other factors, such as ability of follow up and compliance, may push the physician toward admitting the patient to the hospital.
Orbital cellulitis extends beyond the orbital septum and causes diminished visual acuity, proptosis, and painful or reduced motion of the eye in addition to edema and erythema of the eyelids. These patients should undergo a CT of the orbit and sinuses to evaluate for the possibility of an abscess and should be admitted to the hospital for intravenous antibiotics and appropriate ENT and ophthalmology consultation. Bacteria associated with sinus disease are the most common etiologic agents in orbital cellulitis—S. aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Haemophilus influenzae. Diabetics and other immunocompromised patients are at risk for fungal infections (mucormycoses), which quickly can become fatal. Antimicrobial therapy should be directed against these organisms.
Sudden Visual Loss
Certain conditions may cause sudden visual loss or disturbances without pain or external findings. These cases require prompt diagnosis and, at times, immediate ophthalmologic consultation.
Vitreous Hemorrhage. This is caused by extravasations of blood into the vitreous cavity from retinal tears or neovascularization of the retina. Risk factors include coagulopathies, trauma, and proliferative retinal diseases such as proliferative diabetic retinopathy and proliferative sickle cell retinopathy. The history usually is the sudden development of new "floaters," cloudy vision, "shadows" or "cobwebs" in the visual fields, and possible photophobia. Diabetics with retinal disease may have a history of a previous hemorrhage.
Physical exam may reveal evidence of proliferative retinopathy or the actual hemorrhage may be visualized as black or red areas within the vitreous. However, indirect ophthalmoscopy often is necessary to visualize the blood and flourescein angiography to visualize the leaky vessel. At times, the amount of blood obscures visualization of the retina, and in severe cases, decreases the red reflex. If the retina cannot be visualized, an ultrasound is necessary to rule out a retinal detachment.28
Treatment consists of bed rest with the head of the bed elevated 30-45 degrees, the avoidance of NSAIDs and aspirin, and ophthalmology follow-up.
Terson’s syndrome is characterized by a subarachnoid hemorrhage with associated vitreous bleeding. Approximately 33% of patients with subarachnoid hemorrhages will have associated intraocular bleeds.49
Retinal Detachments. A retinal detachment may occur related to trauma or proliferative retinopathy. It will present as new onset of floaters, flashes of light, or a curtain or shadow coming vertically across the visual field. If the detachment involves the periphery, the patient will demonstrate a visual field deficit. If the fovea is involved, visual acuity will be decreased.50 Physical exam will reveal a billowing of the retina. If the detachment is related to trauma, a significant hyphema may obscure the fundus. In that instance, a beta scan ultrasound may diagnose the detachment. With rapid recognition and treatment, patients have an excellent prognosis. Treatment consists of ophthalmology consultation for laser or surgical repair.
Central Retinal Artery Occlusion (CRAO). CRAO is a true emergency because irreversible retinal damage occurs after just 60 minutes. Patients will present with a severe, sudden onset of decreased visual acuity. The vision loss is often dramatic and usually the patient will exhibit only a visual acuity of counting fingers or light perception. This condition was described first by van Graefe in 1859 in a patient with endocarditis. Its prevalence is 1 in 10,000 patients, with a greater predominance in males.50,51 The age group most commonly affected is 60 years or older. The source of the occlusion usually is cholesterol emboli called Hollenhorst plaques. They appear as bright refractile objects on fundoscopic exam. As the plaque impedes blood flow to the retina, the retina becomes pale and yellow. The fovea becomes somewhat reddened and is called a "cherry-red" spot. This reddening occurs for two reasons. The first is that the fovea has a secondary blood supply, the choriocapillaris. The second reason is that the intact retinal pigmented epithelium and choroids are visualized under the fovea and contribute to the red color. It may take a few hours for the cherry-red spot to develop. Unconscious patients also may develop a CRAO. Constant pressure on the globe with resultant increase in intraocular pressure can precipitate a clot in the central retinal artery. Giant cell arteritis is the etiology in 12% of cases of CRAO, and any patient older than age 50 should have a sedimentation rate checked to rule out giant cell arteritis.
Treatment is initiated to dislodge the emboli and cause them to travel toward the periphery. Although reversible and damage occurs after 60 minutes, treatment still is initiated if a patient presents within 24 hours of onset. Ocular massage is done in an attempt to dislodge the clot. Firm pressure is placed on the globe for 15 seconds, then rapidly released. This is repeated multiple times. Intraocular pressures are lowered as well. This is done using topical beta-blockers, mannitol, and acetazolamide. Carbogen therapy is used to cause vasodilatation of the retinal arterioles. The patient inhales a mixture of 95% O2 and 5% CO2 for 10 minutes every two hours for 48 hours. In the absence of Carbogen, the patient can breathe into a paper bag for 10 minutes each hour. Anterior chamber paracentesis also may be done. After the eye is anesthetized, antibiotic drops are instilled as prophylaxis. With a 30-gauge needle on a TB syringe, approximately 0.10.2 cc of aqueous humor is removed. The anterior chamber is entered at the limbus temporally with the bevel of the needle pointing up. This should be done by an ophthalmologist; however, in extreme circumstances it may be done by the ED physician.
Patients suffering from a CRAO have an increased mortality rate compared to age-matched cohorts. (56% vs. 27% during a 9-year period). Forty-five percent of patients have carotid athreosclerotic disease.50,51
A branch retinal artery occlusion presents with a sudden visual field deficit as a segment of the retina infarcts. Care must be taken to distinguish this visual field deficit from a central neurological event.
Central Retinal Vein Occlusion. This entity is a disease primarily of the elderly and may be divided further into two categories—ischemic and non-ischemic. The non-ischemic form generally is milder.53 The ischemic form usually presents with a severe visual loss with retinal hemorrhages and exudates and an afferent pupillary defect. Keep in mind that the visual loss may be gradual. It occurs with a thrombotic occlusion of the central retinal vein with a resultant backup of blood and engorgement of retinal veins. The resultant fundoscopic exam is called "blood and thunder" and results from significant retinal hemorrhages and cotton wool spots.54
Immediate ophthalmology consultation for possible future photocoagulation is the only ED treatment. Just as with retinal artery occlusion, the venous occlusion may just affect a branch vein and present with a visual field deficit. Fundoscopic exam may reveal venous engorgement and hemorrhages distal to the obstruction.
Neuroophthalmology
Anisocoria. Approximately 20% of the population will have unequal pupils (anisocoria). However, the determination between physiologic anisocoria and pathological anisocoria may become an emergency issue. The first step is to determine which pupil is abnormal. Is the small pupil abnormally constricted or is the large pupil abnormally dilated? If in dim illumination the anisocoria is more pronounced and there is a good light reaction, then the smaller pupil is abnormal. If the anisocoria is more pronounced in bright light and there is a poor light reflex, then the larger pupil is abnormal.
If the pupils both are equally reactive, the cause is either a Horner’s syndrome or physiologic anisocoria. If the pupil has an abnormal response to light, then the cause is either damage to the iris, Adie’s tonic pupil, third cranial nerve palsy, or iatrogenic from eye drops.
To differentiate between physiologic anisocoria and Horner’s syndrome, a 10% cocaine solution is placed in the eyes. If both eyes dilate equally, the anisocoria is physiologic. If the smaller pupil fails to dilate or dilates weakly, the cause is a Horner’s syndrome. Associated findings in Horner’s syndrome consist of ptosis and anhydrosis on the affected side. The anhydrosis may or may not be present, depending on the level of the sympathetic lesion. Causes of a Horner’s syndrome include lung masses, internal carotid artery dissections/aneurysms, brachial plexus trauma, aortic aneurysms, and infarction.
When evaluating abnormally large pupils, pilocarpine drops are used to distinguish between Adie’s tonic pupil and a third nerve palsy. With Adie’s tonic pupil, the abnormally large pupil will constrict dramatically with the instillation of 0.1% pilocarpine, whereas the normal pupil will not. Adie’s tonic pupil is a disease that causes pupillary asymmetry and blurred vision. Its etiology often is unknown It strikes females more often than males, with an age predominance of 20-40 years old. There is no ED treatment except arranging ophthalmology follow up. If both pupils fail to constrict with pilocarpine 0.1%, the etiology of the abnormal pupil is either a third-nerve palsy, damage to the iris itself, or pharmacologic. The next test is to instill pilocarpine 1% drops. If both pupils constrict, the etiology is a third-nerve palsy. If neither pupil responds to 1% pilocarpine, the cause is iatrogenic (i.e., eye drops).
A third-nerve palsy is a true medical emergency. Etiologies include cerebral infarction, uncal herniation, giant cell arteritis, posterior communicating aneurysms, and demyelinating diseases. Other clinical findings include ptosis and decreased motion of the eye, as all muscles innervated by the third cranial nerve are involved. If the pupillary response to light is abnormal, a posterior communicating aneurysm must be excluded immediately. If the light reflex is normal, then ischemic microvascular disease from diabetes or hypertension is usually the cause. The reason is that the sympathetic nerve fibers that control pupillary response to light are carried on the periphery of the cranial nerve with a secondary blood supply from the vaso vasorum. In ischemic events, these fibers generally are spared because of this accessory blood flow. Therefore, the pupillary light response is normal. However, as a posterior communicating aneurysm expands, it compresses the third nerve along with the sympathetic fibers causing a pupil-involving third-nerve palsy.
Cavernous Sinus Thrombosis. Cavernous sinus thrombosis is a deadly entity with a 30% mortality despite appropriate treatment.41 Etiologies include trauma, small vessel vasculitis, sickle cell disease, mass lesions, and septic causes such as sinusitis and facial, orbital, and dental infections. Patients present with headaches, nausea and vomiting, vision loss, edema of the eye, diplopia, and proptosis. Initially there may be a sixth nerve palsy, which may extend into a third and fourth nerve palsy. Treatment consists of heparin, antibiotics if related to an infection, and surgery to drain an abscess or remove a mass lesion.
Internuclear Ophthalmoplegia. This specific disorder deserves mention because of its high association with demylenating disorders. Patients will complain of binocular diplopia. On exam, the ipsilateral eye is slow to adduct, while the contralateral eye exhibits nystagmus on abduction.
Optic Neuritis. Optic neuritis is a gradual, unilateral loss of vision. It may develop over hours, but most commonly the vision loss will develop over days. Patients are typically 18-45 years old. The classic complaint is pain on movement of the eye. Physical exam may reveal an afferent pupillary defect with an edematous disk. Patients with optic neuritis have an increased risk of developing multiple sclerosis. Treatment should consist of intravenous steroids and ophthalmology follow-up. Twenty to 30% of patients will have a recurrence.55
Giant Cell Arteritis. This is a disease generally seen in patients older than age 55, with a peak age group between 70 and 80 years old. Females more often are affected than males. It presents as a unilateral, painless, acute loss of vision. Patients will exhibit an afferent pupillary defect. They may complain of associated systemic symptoms, such as headache, jaw claudication, scalp tenderness over the temporal artery, weight loss, fever, and proximal muscle weakness. The sedimentation rate often is elevated over 55. A definitive diagnosis requires biopsy of the temporal artery. Treatment is high-dose IV steroids, which should be instituted prior to the definitive diagnosis to avoid progression of the disease and permanent visual loss. There is an approximate seven-day window before biopsy results will be affected by the steroids. Without treatment, the second eye will be affected within 10 days in 70% of cases.56
Ocular Manifestations of Systemic Disease
Diabetic Retinopathy. Diabetic retinopathy retinal changes occur in 25% of people with diabetes. Nonproliferative retinopathy is confined just to the retina. However, in proliferative retinopathy new blood vessels grow from the retina into the vitreous cavity. Neovascularization of the iris also may cause abnormal blood vessels to grow into the vitreous space. These vessels may bleed suddenly, causing a vitreous hemorrhage or a tractional pull on the retina that may cause a detachment. Sudden visual deficits in people with diabetes usually are related to a vitreous hemorrhage or a retinal detachment, whereas gradual visual changes are related to macular degeneration, ischemia, or cataract formation. Currently, 5% of patients with diabetic retinopathy progress to blindness.57 Sickle cell disease also has an effect on the eye, with formation of proliferative retinopathy and increased risk for recurrent hyphemas secondary to neovascularization of the iris. A hyphema in a sickle cell patient has an increased risk of causing glaucoma and needs to be monitored carefully.
Hypertensive Retinopathy. Chronic hypertension will cause changes in the retina. Fundoscopic exam will reveal arterial-venous nicking followed by a copper wire appearance of the arterioles. Eventually a proliferative retinopathy can develop. Malignant hypertension is a hypertensive emergency where the end organ involved is the retina. In this instance, the optic nerve will be swollen, and there will be hemorrhages and exudates on fundoscopic exam. This is a true medical emergency, and the blood pressure must be lowered acutely.
Pseudotumor Cerebri. Pseudotumor cerebri is more common in females than in males. Risk factors include obesity, pregnancy, hypertension, oral contraceptive use, vitamin A ingestion, and use of certain drugs such as tetracycline. Patients present with headache, nausea, vomiting, and vision loss. The vision loss may be transient episodes lasting only seconds. There may or may not be a sixth-nerve palsy. Fundoscopic exam will reveal papilledema. Once an intracranial mass lesion is ruled out, lumbar puncture will demonstrate an elevated opening pressure. Treatment consists of weight loss, discontinuing any offending agents, acetazolamide, and repeat lumbar punctures to relieve pressure. Occasionally optic nerve sheath decompression may be done.
CMV Retinitis. Primarily a disease associated with immunodeficiency, CMV retinitis presents with floaters, flashing lights, and decreased visual acuity. It occurs in 16-40% of AIDS patients, and usually the CD 4 count is less than 50. Physical exam will reveal very little, if any, cells in the anterior chamber. The retinal exam will exhibit hemorrhages and focal areas of necrosis.58 The retinal findings often are in a wedge-shaped distribution. Retinal detachment and pappilitis often are seen as well. Treatment consists of systemic or intravitreal antivirals. Sustained release antiviral implants also may be used.
Consulting the Ophthalmologist
Many of the ocular conditions discussed require close follow-up, often within 24 hours. Therefore, it is important to maintain an open channel of communication between the ED physician and the ophthalmologist. When speaking with the consulting ophthalmologist, it is important to present the entire history and examination as well as the differential diagnosis. At that time, a treatment plan can be made that includes timing of follow-up for the patient. One important key is to express the certainty (or uncertainty) of the diagnosis. If the ED physician is unsure of the diagnosis or cannot complete the examination, it is important to express that to the ophthalmologist so that he or she may evaluate the patient.
Summary
Ocular injuries and disorders can be devastating. The emergency physician always must be on the lookout for sight-threatening conditions. The definitive treatment for many of these disorders is well beyond the scope of emergency medicine and falls on the ophthalmologist’s shoulders. Therefore, it is the job of the emergency physician to identify true ophthalmologic emergencies, begin appropriate treatment if possible, and, most importantly, make the appropriate ophthalmologic consultation. To do so, the emergency physician should have a thorough understanding of common ophthalmologic emergencies, be able to complete a thorough ophthalmologic exam, and be able to convey this information to the ophthalmologist.
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