Physiology

Light passes through the cornea and then through an opening in the iris, the pupil. The iris is responsible for controlling the amount of light that enters the eye by dilating and constricting the pupil. This light then reaches the lens, which refracts the light rays onto the retina. The anterior chamber is located between the lens and the cornea and contains aqueous humor, which is produced by the ciliary body. This fluid maintains pressure and provides nutrients to the lens and cornea. It is reabsorbed from the anterior chamber into the venous system through the canal of Schlemm. The vitreous chamber, located between the retina and the lens, contains a gelatinous fluid called vitreous humor. Light rays pass through the vitreous humor before reaching the retina. The retina lines the back of the eye and contains photoreceptor cells called rods and cones. Rods help vision in dim light, whereas cones aid light and color vision. The cones are located in the center of the retina in an area called the macula. The fovea is a small depression in the center of the macula that contains the highest concentration of cones. The optic nerve is located behind the retina and is responsible for transmitting signals from the photoreceptor cells to the brain (Fig. 26.1).

Fig. 26.1 Anatomy of the eye (A) and retina (B).

The extraocular muscles (Fig. 26.2) help in stabilization of the eye. Six extraocular muscles assist in horizontal, vertical, and rotational movement. These muscles are controlled by impulses from cranial nerves III, IV, and VI, which tell the muscles to relax or contract.

Fig. 26.2 Extraocular muscles.

(Courtesy Ted Montgomery, OD. Available at www.tedmontgomery.com/the_eye/.)

Epidemiology

More than 3 million Americans suffer from glaucoma, the leading cause of preventable blindness in the United States.³ The term glaucoma refers to a group of disorders that damage the optic nerve and thereby lead to loss of vision. The two main classifications of glaucoma are open angle and angle closure. Acute angle-closure glaucoma is more common in white persons and women. Its peak incidence occurs between the ages of 55 and 70.⁴ African Americans, patients older than 65 years, and people with diabetes and ocular trauma are at increased risk for open-angle glaucoma. Differentiation between the two types of glaucoma lies in the mechanism of obstruction of outflow, as described later. Intraocular pressure (IOP) is determined by the rate of aqueous humor production relative to its outflow and removal. Normal IOP is between 10 and 20 mm Hg. This discussion focuses mainly on acute angle-closure glaucoma.

When the angle of the anterior chamber is reduced, outflow of aqueous humor is blocked, which results in elevated IOP and ultimately visual compromise. Patients with a shallow anterior chamber, hyperopic (farsighted) eyes, and eyes with lens abnormalities such as cataracts are more prone to acute angle-closure glaucoma. Pupillary dilation, caused by events such as presence in a dark room, is the most significant event that can cause an acute attack of glaucoma because the flaccid iris can be pushed against the trabecular meshwork and result in obstruction.

Presenting Signs and Symptoms

Patients with acute angle-closure glaucoma may have a sudden onset of headache or eye pain. Occasionally, nausea and vomiting from vagal stimulation can be the dominant symptoms. Shortly after the onset of pain, blurry vision or halos in the visual field may occur.

The classic physical findings are unilateral eye injection, especially at the limbus; a nonreactive, midsize pupil; shallow anterior chamber; corneal edema or haziness; and high IOP (often 60 to 90 mm Hg). If the attack has been prolonged, ischemia of the ciliary body reduces aqueous humor production with a resultant decrease in IOP. This process is especially important because the ultimate damage depends on the duration of the attack rather than the severity of the elevation in pressure.

With open-angle glaucoma, development of the disease is usually insidious, bilateral, slowly progressive, and painless.

Medical Decision Making

Visual acuity should be recorded in both eyes. Examination of the eye should include a search for the classic signs of glaucoma already described, including a middilated pupil in the affected eye and corneal haziness. A slit lamp should be used to estimate the depth of the anterior chamber. If this depth is less than one fourth the corneal thickness, the anterior chamber angle is very narrow. It is important to measure anterior chamber depth in both eyes; a shallow angle in only one eye argues against acute angle-closure glaucoma. IOP is usually measured with a tonometer; the cornea is flattened, and pressure is determined by measurement of the force needed to flatten it, as well as measurement of the area flattened.

Treatment

Acute angle-closure glaucoma is an ophthalmologic emergency. Because outcome depends on the duration of elevated IOP, treatment should be initiated promptly. Therapy is geared toward decreasing aqueous production, increasing aqueous outflow, and reducing vitreous volume to lower IOP.

Initial treatment includes a topical, nonselective beta-blocker such as 0.5% timolol to reduce aqueous production. Topical beta-blockers are absorbed and can cause systemic effects. Intravenous administration of a carbonic anhydrase inhibitor such as acetazolamide, 500 mg, will also rapidly reduce aqueous humor production. Intravenous mannitol will create an osmotic gradient between the vitreous and blood and thereby cause a reduction in vitreous volume, so it may be useful for severe cases. Tonometry can be performed frequently, even every 15 minutes, to assess progress.

Topical 2% pilocarpine is used to help reopen the angle. Miotics such as the direct-acting parasympathomimetic agent pilocarpine might be less effective at very high IOP because the iris is relatively ischemic and therefore less responsive. Sometimes pilocarpine is used after IOP has been reduced to less than 40 mm Hg. Pilocarpine will therefore be more effective as the initially high pressures are reduced with the initial beta-blocker drops and acetazolamide. Topical 1% prednisolone acetate may sometimes be added to reduce inflammation. For ongoing treatment, topical 2% pilocarpine and prednisolone acetate may be administered every 6 hours and oral acetazolamide two times per day. Sedatives and antiemetics may be administered as needed. When the inflammation has been reduced sufficiently, the patient will be taken for iridotomy by the ophthalmologist.

Disposition

Disposition of the patient is determined in conjunction with the consulting ophthalmologist. Indications for admission include intractable nausea and vomiting and need for careful monitoring to administer systemic agents.

Epidemiology

Retinal artery occlusion affects less than 1 per 100,000 persons annually.^5,6 It is most commonly caused by an embolus from the carotid artery that lodges in a distal branch of the ophthalmic artery. Central retinal artery occlusion most commonly affects elderly patients and men. Although most emboli are formed from cholesterol, they may also be calcific, fat, or bacterial from cardiac valve vegetations.

Pathophysiology

The visual complaints and deficits resulting from retinal artery disease are caused by ischemia. In addition to the embolic causes already described, low-flow states and vasospasm may have the same visual consequences.

Presenting Signs and Symptoms

Sudden, painless visual loss is the classic manifestation of central retinal artery occlusion. Sometimes patients report transient visual loss before complete compromise. The visual loss is usually profound. Examination can often elicit an afferent pupillary defect (when light is shined into the abnormal eye, the pupil of the affected eye paradoxically dilates instead of constricting). Funduscopic examination typically demonstrates a pale retina with a cherry-red spot at the fovea (Fig. 26.3). Complete evaluation involves auscultation of the carotid arteries for bruits, palpation of the temporal artery for tenderness, and cardiac auscultation and palpation of the pulse to detect atrial fibrillation.

Fig. 26.3 Central retinal artery occlusion.

(Courtesy Ted Montgomery, OD. Available at www.tedmontgomery.com/the_eye/.)

Differential Diagnosis

Sudden, painless visual loss can also result from central retinal vein occlusion, temporal arteritis, ischemic optic neuropathy, amaurosis fugax, retinal detachment, or vitreous hemorrhage. If the loss of vision is accompanied by pain, arterial dissection should be part of the differential diagnosis. The presence of a headache, temporal artery tenderness, and an elevated erythrocyte sedimentation rate (ESR) suggests temporal arteritis. Amaurosis fugax, or unilateral transient obstruction of a retinal artery, does not cause visual loss lasting longer than 15 minutes. Ischemic optic neuropathy causes optic disk pallor and elevation. Retinal detachment and vitreous hemorrhage result in visual disturbances such as floaters in addition to the loss of vision—the occurrence of which is variable with a detached retina. Vitreous hemorrhage causes absence of the normal red reflex of the fundus. A neurologic etiology such as a cerebral infarct must also beconsidered.

Treatment

Treatment must be initiated immediately because the visual loss is generally irreversible after 2 hours of ischemia. Regardless, the outcome is generally poor. Several approaches may be used. Intermittent globe massage can be performed in an effort to dislodge the clot and propel it distally: moderate pressure is applied for 5 second and then released for 5 seconds, and the cycle is repeated. The use of anterior chamber paracentesis for visual loss is based on the principle that decreased IOP allows better perfusion of the retinal artery and may propel the clot distally. Acetazolamide can be administered intravenously for the same purpose. Inhaled carbogen (mixture of 95% oxygen and 5% carbon dioxide) can be used to dilate the vasculature and thereby increase retinal PO₂.

Other treatment options are intraarterial thrombolysis and hyperbaric oxygen; however, studies have shown limited improvement in visual outcome with early administration of both these treatment modalities.^7–10 One retrospective study found that even with thrombolysis, vision did not improve to better than 20/300 in the affected eye.⁷ Another study investigated the outcomes of 32 patients with central retinal artery occlusion, 17 of whom underwent fibrinolysis.⁶ This study found that all but six of the treated patients reported improvement in their visual compromise but that only five of the untreated patients had any improvement. In this study, patients with a duration of symptoms of up to 24 hours were treated.

Patients with sudden visual loss are admitted to the hospital so that the underlying cause can be sought.

Epidemiology

Patients older than 50 years who have cardiovascular disease, hypertension, glaucoma, venous stasis, hypercoagulable conditions, collagen vascular diseases, or diabetes are at risk for central retinal vein occlusion.¹

Pathophysiology

Two types of retinal vein occlusion are distinguished, ischemic and nonischemic. The ischemic type is also known as hemorrhagic retinopathy, and the nonischemic type is also called venous stasis retinopathy. The manifestations and physical findings differ according to the type of occlusion involved.

Presenting Signs and Symptoms

Typically, patients with ischemic retinal vein occlusion report an acute and relatively profound decrease in visual acuity. Those with the nonischemic type have progressively blurry vision that is worse in the morning. An afferent pupillary defect is found in the ischemic type. Funduscopic examination shows an edematous optic disk and macular, dilated retinal veins, retinal hemorrhage, and cotton-wool spots. Sometimes these findings are called the “blood and thunder” appearance of the fundus (Fig. 26.4).

Fig. 26.4 Central retinal vein occlusion.

(From Noble J. Textbook of primary care medicine. 3rd ed. St. Louis: Mosby; 2001.)

Differential Diagnosis

The processes that must be considered when assessing a patient with possible central retinal vein occlusion are the same as those for central retinal artery occlusion. Branch retinal vein occlusion may also occur distal to an arteriovenous crossing, with hemorrhage developing distal to the occlusion site.

Medical Decision Making

No specific diagnostic test can identify central retinal vein occlusion. The diagnosis is based on the clinical history and physical examination, which exclude other processes that also cause painless visual loss.

Treatment

No effective therapeutic regimen exists for central retinal vein occlusion. The emergency physician (EP) should arrange for immediate ophthalmologic consultation. A search for a cause should be performed to protect the contralateral eye from the same problem. The prognosis largely depends on the type of retinal venous occlusion. Nonischemic vein occlusion, unless the macular involvement is extensive, offers a better outcome than the ischemic type does. Spontaneous resolution may occur in some cases.

Although no specific treatment is available, a number of interventions have been proposed and practiced.^11,12 However, these interventions have not been based on evidence of efficacy. Laser photocoagulation, for example, cauterizes leaking vessels with the aim of halting further visual loss. This procedure can be especially helpful for branch retinal vein occlusion. With nonischemic vein occlusion, attempts to reduce macular edema can be helpful. The reduction is accomplished with the administration of topical corticosteroids. Studies have been conducted to determine the benefit of steroids in treating both forms of retinal vein occlusion. Jonas et al.¹¹ conducted a prospective, comparative, nonrandomized clinical interventional study to evaluate the visual outcomes in 32 patients with central retinal vein occlusion after intravitreal administration of triamcinolone acetate. The study included patients with both the ischemic and nonischemic forms of retinal vein occlusion. These researchers found that the medication resulted in temporary (up to 3 months) improvement in visual outcome but also raised IOP. Anticoagulants are not recommended because they may propagate hemorrhage.

Epidemiology

Optic neuritis is inflammation of the optic nerve, and visual loss is due to focal demyelination of the optic nerve. Most affected patients are between 15 and 40 years of age. This disorder can be associated with numerous diseases, including sarcoidosis, systemic lupus erythematosus, measles, leukemia, syphilis, and alcoholism; however, it is most commonly associated with multiple sclerosis. In fact, in up to a third of patients with optic neuritis, multiple sclerosis is eventually diagnosed, and approximately two thirds of patients with multiple sclerosis have optic neuritis. Optic neuritis can also be idiopathic.

Pathophysiology

Optic neuritis results from an autoimmune reaction that ultimately causes demyelinating inflammation. In idiopathic and multiple sclerosis–related optic neuritis, lesions are characterized by areas of loss of the myelin sheath with preservation of axons. In acute disease, remyelination may occur. In chronic disease, because of the accumulation of scar tissue, the process becomes irreversible. The lesions in multiple sclerosis–associated optic neuritis are pathologically the same as those in the brain.

Presenting Signs and Symptoms

Symptoms of optic neuritis are generally unilateral. Patients complain of pain, especially with eye movement. Visual loss, which can range from minimal loss to complete loss of light perception, usually occurs over a number of hours or days. Patients may also experience dulling of color vision, worse vision after exertion or exposure to steam, brief light flashes, and central scotoma. An afferent pupillary defect is always present. Funduscopic examination may show disk pallor, swelling, or elevation. However, because up to two thirds of cases are retrobulbar, the fundus can appear normal.

Differential Diagnosis and Medical Decision Making

Any condition that causes visual disturbance along with eye pain must be considered in the differential diagnosis of optic neuritis. Orbital cellulitis can cause this clinical picture but does not include an afferent pupillary defect; furthermore, inspection alone should allow differentiation between the two diseases. Glaucoma can also cause the combination of ocular pain and visual impairment. Physical examination, including assessment of pupil size and reactivity, as well as corneal inspection, allows distinction between glaucoma and optic neuritis.

Unilateral ocular pain with visual compromise should always raise clinical suspicion for optic neuritis. If no afferent pupillary defect is found on physical examination, another diagnosis is almost ensured. Although imaging is usually not indicated, magnetic resonance imaging (MRI) provides adequate visualization of the optic nerve.

Treatment and Disposition

Ophthalmologic and neurologic consultation should be obtained if optic neuritis is suspected. Approximately 31% of patients with optic neuritis have a recurrence within 10 years of the initial episode.¹³ The goals of treatment are to restore visual acuity and prevent propagation of the underlying disease process. The Optic Neuritis Treatment Trial was a randomized, 15-center clinical trial involving 457 patients that was performed to evaluate both the benefit of corticosteroid treatment of optic neuritis and the relationship of this entity to multiple sclerosis. Use of intravenous steroids in conjunction with oral steroids reduced the short-term risk for the development of multiple sclerosis as determined by MRI evaluation. No long-term immunity from or benefit for multiple sclerosis was reported, however. The study concluded that although intravenous steroids have only minimal, if any effect on the patient’s ultimate visual acuity, they do expedite recovery from optic neuritis. Use of oral steroids alone is associated with a higher recurrence rate of optic neuritis. The dosage regimen recommended on the basis of the study results was methylprednisolone, 250 mg intravenously every 6 hours for 3 days, followed by prednisone, 1 mg/kg/day orally for 11 days.¹⁴

Pathophysiology and Anatomy

The retina has two layers, the inner neuronal layer and the outer pigment epithelial layer (the choroid). Retinal detachment refers to separation of the two layers. Rhegmatogenous retinal detachment, the most common of the three types, is caused by a tear or hole in the neuronal layer, which leads to extrusion of fluid from the vitreous cavity into the potential space between the two retinal layers. It is more common in patients older than 45 years and those with severe myopia. When caused by trauma, this type of detachment can affect any age group. Exudative retinal detachment is caused by leakage of fluid or blood from within the retina itself. Predisposing factors for this type include hypertension, vasculitis, and central retinal venous occlusion. Traction retinal detachment results from the formation and subsequent contraction of fibrous bands in the vitreous.

Presenting Signs and Symptoms

Retinal detachment can occasionally be asymptomatic. More commonly, patients complain of flashes of light, floaters, or fine dots or cobwebs in their visual fields. Generally, a new onset of floaters associated with flashing lights is indicative of retinal detachment unless proved otherwise. Visual acuity correlates with the extent of macular involvement and can be minimally changed to severely decreased. The loss of vision is usually sudden in onset and starts peripherally, with propagation to the central visual field. The visual loss is commonly described as a filmy, cloudy, or curtainlike appearance. Visual field cuts relate to the location of the retinal detachment, and an afferent pupillary defect occurs if the detachment is large enough. Retinal detachment is painless. On examination, the detached retina may appear gray or translucent or may seem out of focus (Fig. 26.5). Retinal folds may be seen. The visual field defects are variable, depending on the involvement of the retina and macula. Bedside ED ultrasonography has been shown to be helpful in confirming the presence of retinal detachment.¹⁵ Left untreated, all cases of retinal detachment progress to involve the macula and result in complete loss of vision in the affected eye.

Fig. 26.5 Retinal detachment.

(Courtesy Ted Montgomery, OD. Available at www.tedmontgomery.com/the_eye/.)

Differential Diagnosis and Medical Decision Making

Vitreous hemorrhage, which results from bleeding into either the preretinal space or the vitreous cavity itself, can be difficult to distinguish from retinal detachment. Complaints with this disorder range from floaters or cobwebs in the visual field to severe, painless loss of vision. Vitreous hemorrhage without concomitant retinal detachment should not, however, cause an afferent pupillary defect. Ophthalmoscopy usually demonstrates discoloration (ranging from reddish to black) with fundal structural details difficult to discern. Therapy for vitreous hemorrhage consists of bed rest with head elevation followed by possible interventional procedures such as laser photocoagulation and cryotherapy.

All macular disorders can cause painless visual loss. They are manifested as loss of central vision with preservation of peripheral vision, as well as findings of retinal abnormalities. A careful history and physical examination can exclude macular degeneration as a cause of central visual loss. Funduscopic examination in individuals with age-related macular degeneration shows the presence of drusen—small, yellow masses scattered on the retina. A gray-green subretinal neovascular membrane may also be seen. Inflammatory processes involving the retina often cause inflammatory proteins to fill the vitreous, thus making it appear cloudy.

Treatment

The sooner that treatment of retinal detachment is initiated, the greater the chance of visual preservation and recovery. After detachment, retinal ischemia ensues because of loss of the choroidal blood supply. Patients with suspected or confirmed retinal breaks or detachments require emergency ophthalmologic consultation. Contrary to traditional belief, not all detachments are managed surgically. Laser photocoagulation or cryotherapy is frequently used to create small burns around the area of detachment to prevent further leakage of fluid between the retinal layers. Intraocular gas is sometimes used to tamponade the tear. These procedures are approximately 95% effective in halting the disease process.¹⁶ Surgical intervention may be needed to repair the tear and simultaneously remove the traction forces on the retina. The modality of treatment is at the discretion of the consulting ophthalmologist.

Pathophysiology

Vessels affected by giant cell arteritis are infiltrated with lymphocytes, plasma cells, and multinucleated giant cells in patches or segmental patterns. A cell-mediated immune response is thought to account for the vascular changes seen with this disorder. Inflammation of branches of the ophthalmic artery, especially the posterior ciliary artery, leads to ischemic optic neuritis, which compromises vision. The central retinal artery is also often affected. Inflammation of the temporal artery causes the classic headache associated with this diagnosis.

Presenting Signs and Symptoms

Unilateral headache, jaw or tongue claudication, constitutional symptoms, including anorexia and malaise, and visual impairment are common initial symptoms of temporal arteritis. Occasionally, the visual loss is preceded by amaurosis fugax. In one series of patients, visual loss was unilateral in 46%, sequential in 37%, and simultaneously bilateral in 17%.¹⁷ Patients with polymyalgia rheumatica may also complain of pain and stiffness in the shoulders or hips.

Examination may demonstrate tenderness and decreased pulsations over the involved temporal artery. Funduscopic findings may be normal or consist of optic disk edema or pallor, scattered cotton-wool spots, flame-shaped retinal hemorrhages, and distended retinal veins. An afferent pupillary defect may be present. When vision is evaluated, horizontal field defects and involvement of the extraocular muscles are often detected.

Differential Diagnosis and Medical Decision Making

In patients who do not have visual complaints, a differential diagnosis for headache must be investigated. Migraines, tension headaches, and subarachnoid hemorrhage may mimic temporal arteritis. Palpation of the temporal artery along with a careful history, including questions about jaw symptoms, may allow distinction. Because temporal arteritis is a medical emergency associated with high morbidity if not recognized and treated promptly, it must be definitively excluded on the basis of the history and physical or laboratory findings before the patient’s symptoms are attributed to another entity. Acute angle-closure glaucoma is also high on the differential diagnosis list, regardless of whether visual symptoms are present. Occasionally, headache can be the dominant symptom of glaucoma. In glaucoma, however, physical examination should find a middilated, nonreactive pupil with corneal haziness and a shallow anterior chamber.

Although temporal arteritis can rarely be accompanied by a normal ESR, this parameter is almost always elevated. The upper limit of normal ESR increases with age. A rough approximation of the upper limit of normal for men is age in years divided by 2. For women it is age in years plus 10, with the sum divided by 2, or half the age in years plus 5. Elderly patients with new-onset headaches, visual loss, and an elevated ESR should always be treated for temporal arteritis. Generally, the ESR is higher than 80 mm/hr in individuals with temporal arteritis. Temporal biopsy confirms the presence of the disease. Early in the course of the disease, however, biopsy findings may be normal. Ultrasound has been proposed as a possible diagnostic modality for temporal arteritis, but studies have yielded conflicting results. Further investigation is necessary before a definitive conclusion can be drawn about its standard use.

Treatment

Treatment of temporal arteritis should never be delayed to await the results of biopsy because outcome is contingent on early medical treatment. Initial treatment should consist of prednisone, 60 to 80 mg, or high-dose intravenous methylprednisolone. The exact duration and regimen of steroid therapy are determined on a case-by-case basis. Generally, treatment is continued until the symptoms improve and the ESR begins to normalize. It has also been suggested that methotrexate, infliximab, and aspirin may also halt progression of the visual symptoms, but further studies are necessary to establish practice patterns.¹⁸

Anatomy and Pathophysiology

Orbital cellulitis is inflammation of any of the tissues within the orbit posterior to the orbital septum, whereas preorbital cellulitis is confined to the tissues anterior to the septum. Making this distinction is extremely important for management. Because of the gravity of the potential consequences of orbital cellulitis and the fact that most cases of orbital cellulitis have a concomitant periorbital component, the EP evaluating an infected, erythematous orbit should always assume that the patient has orbital cellulitis until it can be definitively excluded.

Approximately 75% of cases of orbital and periorbital cellulitis have identifiable antecedent causes. Sinusitis is the most common predisposing condition. Because the inferior, medial, and superior walls of the orbit lie adjacent to the sinuses, it is easy to understand how extension of infection may occur. The ethmoid sinus is most commonly involved. Infection after trauma or surgery with direct inoculation of pathogens and hematogenous spread from other sources of bacteremia are other methods of acquiring the infection. The pathogen involved is contingent on the mode of infection. Aerobic, non–spore-forming organisms are most frequently the culprits. Anaerobic organisms tend to be causative when infection results from chronic sinusitis.

Presenting Signs and Symptoms

Patients with infection limited to the periorbital tissues typically have erythema, edema, and warmth of the external eye tissues. Though generally unilateral, the infection can be bilateral. Constitutional symptoms, including fever and malaise, may be present. The presence of ocular pain, ophthalmoplegia, and pain with extraocular movement suggests orbital involvement. Patients with orbital infection may also have decreased visual acuity and pupillary paralysis. Elevated IOP, preseptal (periorbital) cellulitis, conjunctival injection, and proptosis may additionally be present (Fig. 26.6).

Fig. 26.6 Orbital cellulitis.

(From Long SS, Pickering LK, Prober CG, editors. Principles and practice of pediatric infectious diseases. 2nd ed. Philadelphia: Churchill Livingstone; 2003.)

Differential Diagnosis and Medical Decision Making

The signs of periorbital infection can be similar to those of allergic periorbital swelling, especially when the involvement is bilateral. With an allergic reaction, cobblestoning may be noted on the interior aspect of the upper lid, and the condition should improve with the administration of diphenhydramine or another antihistamine. It can be difficult to distinguish orbital cellulitis from subperiosteal and orbital abscesses and even from cavernous sinus thrombosis, which carries a dismal prognosis. With subperiosteal abscesses, the globe is often displaced by the abscess; the displacement should be obvious on inspection. Orbital abscesses are located in postseptal tissues. They may cause obvious pus, significant ophthalmoplegia, and exophthalmos, as well as globe displacement. Cavernous sinus thrombosis typically starts unilaterally and progresses to contralateral involvement. Examination should detect dilation of the episcleral vessels and venous engorgement of the fundus; the pupil may be fixed and dilated. Depending on the time course, orbital neoplasm with associated inflammation may cause similar symptoms.

In many cases it may be possible to exclude orbital involvement on the basis of the history and physical examination alone. If there is any doubt or another entity or complication such as abscess is suspected, computed tomography (CT) is the diagnostic modality of choice. It is not necessary to use intravenous contrast material. MRI is another acceptable mode of diagnosis.

Treatment and Disposition

In adults, preorbital infection should be treated with oral antibiotics, and close outpatient follow-up should be arranged. An antibiotic that provides coverage for staphylococci, streptococci, and Enterobacteriaceae is appropriate. Orbital cellulitis should be treated with broad-spectrum intravenous antibiotics, the patient should be admitted to the hospital, and consideration should be given to incision and drainage if imaging reveals a collection. Because of the increased incidence of community-acquired methicillin-resistant Staphylococcus aureus, empiric coverage for this pathogen may also be considered. For periorbital infection in children, the threshold for admission to the hospital should be lower. Patients with mild periorbital cellulitis can be discharged with arrangements for extremely close outpatient follow-up. For patients with more involved cases, including any underlying comorbid conditions, admission for observation should be considered.

Pathophysiology and Anatomy

An eye appears red because of dilation of blood vessels. Ciliary injection, caused by dilation of branches of the anterior ciliary arteries, indicates inflammation of the cornea, iris, or ciliary body. Conjunctival injection results from dilation of the more posterior, superficial conjunctival vessels. Because of the conjunctiva’s more superficial location, vascular dilation causes more dramatic injection there than in the ciliary body.

Conjunctivitis refers to inflammation of the mucous membrane that lines the anterior sclera and inner eyelids. The conjunctiva is a key player in maintaining lubrication of the eye. Infection can result in scarring and abnormal tear formation in the affected eye.

Conjunctivitis can have a viral, bacterial, fungal, toxic, chemical, or allergic cause. The clinical findings and treatment differ with the underlying etiology. Sometimes it may be difficult to determine the underlying cause.

Presenting Signs and Symptoms

Generally, bilateral conjunctivitis signifies an infectious or allergic cause. However, such is not always the case. Viral infection is the most common cause of conjunctivitis. Adenovirus infection, which is highly contagious, is extremely common. Other viral causes include coxsackievirus and enteroviruses. Patients have significant injection, itching, irritation, and watery discharge. They may have accompanying preauricular adenopathy. Patients often have associated mild systemic symptoms because the conjunctivitis occurs in concert with a viral syndrome. Epidemic keratoconjunctivitis, which may result in the development of pseudomembranes, is caused by adenovirus types 8 and 19; this is the classic pink eye. Patients are contagious for up to 2 weeks.

Herpes simplex conjunctivitis is manifested as unilateral conjunctival injection with a clear discharge. Patients complain of a foreign body sensation and photophobia. With gross inspection alone it may be impossible to distinguish herpes simplex from other viral causes. Patients may have facial or lid vesicles. This infection can spread rapidly and cause corneal damage, which is seen as a dendritic pattern on fluorescein examination. Depending on the location, size, and depth of corneal involvement, patients may have decreased visual acuity.

Herpes zoster ophthalmicus is caused by activation of the virus along the ophthalmic branch of the trigeminal nerve. A vesicular rash is present along the involved dermatome and results in forehead and upper eyelid lesions. Lesions on the tip of the nose, called the Hutchinson sign, signify involvement of the nasociliary branch of the fifth cranial nerve. The presence of the Hutchinson sign indicates a much higher likelihood of ocular involvement (76% risk versus a 34% risk in the absence of such lesions). Fluorescein examination may show punctate, ulcerated, or dendritic corneal lesions (Fig. 26.7).

Fig. 26.7 Herpes zoster ophthalmicus.

(Available from www.emedicine.com.)

Patients with bacterial conjunctivitis have conjunctival erythema, a foreign body sensation, purulent drainage, and morning crusting of the eye. They do not usually experience photophobia or loss of visual acuity. The most common causative organisms are Staphylococcus, Streptococcus, and Haemophilus (although with immunization this last pathogen is being seen decreasingly).

Gonococcal infection generally results in unilateral conjunctival injection, copious purulent discharge, and edema and erythema of the lids. The infection is sudden in onset and progresses rapidly.¹⁹ Patient populations usually affected are infants, health care workers, and sexually active young adults. The amount of discharge helps distinguish gonococcal infection from other bacterial pathogens. Patients may have associated urethral discharge or arthritis.

Pseudomonas aeruginosa infection should be suspected in patients who are immunosuppressed or wear contact lenses. Usually, a sticky, mucopurulent, yellow-green discharge is present. The cornea should be inspected carefully for ulceration because corneal perforation with progression of the infection is a major concern with this organism.

Fungal pathogens that cause conjunctivitis include Actinomyces, Aspergillus, Candida, Coccidioides, and Mucor (in diabetic patients). These organisms should be considered in any immunosuppressed patient, as well as any individual who has sustained eye trauma involving vegetable matter. Examination may show a corneal infiltrate with underlying endothelial plaque and hypopyon, which is the presence of pus cells in the anterior chamber.

Chlamydial conjunctivitis is fairly common, especially in sexually active young adults. It is also a frequent cause of neonatal conjunctivitis. Patients may have associated gonococcal disease and should thus be asked about urethral discharge and arthritis. Patients with chlamydial conjunctivitis have a scant seropurulent eye discharge and fair to moderate conjunctival injection. Preauricular adenopathy is occasionally associated with this disorder.

Allergic conjunctivitis gives rise to significant pruritus and chemosis. Generally, an associated clear discharge is present in varying amounts. Cobblestoning may be seen on the inner eyelids.

Diagnosis

The diagnosis of conjunctivitis is based on the history, physical examination, and appropriate exclusion of other causes of red eye. It is important, in the correct setting, to perform a thorough examination to rule out both other causes of red eye and potential complications of conjunctivitis such as corneal ulceration. When particularly virulent pathogens are a consideration, Gram stain and cultures may be necessary. Because the diagnosis of viral conjunctivitis can be made clinically, viral culture and laboratory investigation are not necessary.²⁰

Treatment and Disposition

Some basic tenets should be followed in the treatment of conjunctivitis, with separate consideration for the specific cause as detailed later.

Frequently, treatment is supportive. Cold compresses help alleviate the swelling and lid discomfort. Broad-spectrum antibiotic drops are used for bacterial conjunctivitis and often to prevent superinfection with other organisms. Erythromycin is appropriate for uncomplicated cases. A fluoroquinolone that provides coverage against Pseudomonas should be given to contact lens wearers. Topical corticosteroids should be prescribed only after consultation with an ophthalmologist and should never be used in a patient with suspected or confirmed herpes infection. Artificial tears alleviate keratitis and photophobia.

Pathophysiology

Corneal abrasions are defects in the corneal surface that are typically limited to the epithelial layer. Sometimes the bulbar conjunctiva is also affected. Severe injuries can involve the deeper, thicker stromal layer of the cornea.

Presenting Signs and Symptoms

Common complaints of patients with corneal abrasions include photophobia, foreign body sensation, pain, and tearing. Conjunctival injection and blepharospasm may or may not be seen. Depending on the location and size of the abrasion, patients may also complain of decreased visual acuity. Fluorescein examination demonstrates the abrasion as a staining defect (Fig. 26.8). If a linear abrasion is noted, the EP should search carefully for a retained foreign body on the inner side of the upper eyelid. Corneal ulceration should be excluded with a slit-lamp examination, especially in contact lens wearers. A topical anesthetic should be administered to facilitate the examination.

Fig. 26.8 Corneal abrasions.

(From Goldman L, Ausiello D, editors. Cecil medicine. 23rd ed. Philadelphia: Saunders; 2007.)

Differential Diagnosis

All entities that cause eye pain should be included in the differential diagnosis for corneal abrasion. Because erythema and changes in visual acuity may or may not be present, the differential diagnosis has to be tailored to the individual case. Examination and measurement of IOP should eliminate glaucoma as a cause of the symptoms. Slit-lamp examination demonstrates cells and flare in the anterior chamber in a patient with iritis. Lack of infiltrate and ulcer morphology exclude corneal ulcers. The EP should look carefully for a foreign body to eliminate it as a cause of the complaints.

Treatment

Providing comfort for the patient is the goal of treatment of corneal abrasion. Although topical antibiotics may be administered to facilitate evaluation, patients should never be discharged with such medications. Continued use of topical ocular anesthetics may cause injury through loss of the protective reflexes and drying of the eye. Systemic analgesia should be prescribed as needed. Studies have suggested that topical nonsteroidal antiinflammatory drugs also provide relief and may reduce the need for oral narcotic agents. A cycloplegic agent such as homatropine provides relief from photophobia and blepharospasm.

The practice of routinely prescribing topical antibiotics for corneal abrasions to prevent corneal ulceration is not clearly based on evidence, although some studies have suggested that it is beneficial. For example, a prospective study investigating the incidence of corneal ulceration in close to 35,000 patients in whom corneal abrasions were diagnosed demonstrated that none of the patients who received antibiotics had ulceration. Contact lens wearers should be treated with agents that provide coverage against Pseudomonas. Eye patching should be avoided, especially in contact lens wearers and patients whose abrasions were cause by organic material, because it may encourage infection. Evidence suggests that patching may be harmful, but current data are not available. Patients with abrasions should discontinue contact lens wear during the healing period.

Tetanus prophylaxis has been a long-standing component of the treatment of corneal abrasions, but evidence suggests that this practice is not routinely indicated. In the absence of infection, corneal perforation, or devitalized tissue, no benefit is seen with the routine administration of a tetanus booster. However, current Centers for Disease Control and Prevention guidelines recommend a tetanus booster within 5 years if the event causing the corneal abrasion involved a dirty vector such as vegetable matter and within 10 years if the corneal injury was caused by a clean, uncontaminated vector.^22,23 Corneal abrasions heal within 3 to 5 days, and patients can be discharged with arrangements for close outpatient follow-up.

Pathophysiology

Even seemingly minor trauma involving the cornea can create a break, which serves as a port of entry for bacteria. Conditions such as lack of lubrication and malnutrition make the cornea more susceptible to injury.

Presenting Signs and Symptoms

Corneal ulcers cause significant eye pain, ciliary injection, tearing, foreign body sensation, blurry vision, and photophobia. Eyelid swelling and purulent drainage may be present. Depending on the location and extent of the lesion, visual acuity may be decreased. Inspection may show eyelid swelling and erythema. Large ulcers can be seen as round or oval white spots on the cornea with the naked eye. Fluorescein and slit-lamp examinations demonstrate a corneal defect, usually with sharply demarcated borders and a gray appearance of the infiltrated ulcer base. On examination of the anterior chamber, hypopyon or a flare consistent with iritis is often seen. With the exception of the classic dendritic lesions that occur with herpes simplex virus infection, no pathognomonic signs or symptoms can be used to diagnose the cause of the ulcer seen on examination (Fig. 26.9).

Fig. 26.9 Corneal ulcers.

(From Auerbach PS, editor. Wilderness medicine. 5th ed. Philadelphia: Mosby; 2007.)

Differential Diagnosis

The same conditions that must be considered in the differential diagnosis for patients with corneal abrasions must be considered for those with corneal ulcers.

Treatment and Disposition

Immediate ophthalmologic consultation should be obtained for a patient with a corneal ulcer. Some ophthalmologists advocate discharge with follow-up the next day. A cycloplegic agent such as homatropine is given for comfort. Frequent topical antibiotic therapy should be prescribed. The typical regimen involves administration of the drops every 1 to 2 hours until the follow-up appointment the next day.

Pathophysiology

Objects, especially those projected with considerable force, may become embedded in the corneal epithelium or deeper into the stroma. The associated irritation triggers a cascade of events, including vascular dilation, which is manifested as conjunctival injection and lid edema.

Presenting Signs and Symptoms

Typical symptoms of an ocular foreign body include pain, photophobia, tearing, conjunctival injection, and a foreign body sensation. Examination may show conjunctival injection, a visible foreign body, a corneal epithelial defect, and corneal edema. White blood cell mobilization may occur and can be detected as anterior chamber flare and the presence of cells. Visual acuity can be decreased. Metallic foreign bodies can cause visible rust rings (Fig. 26.10).

Fig. 26.10 Rust ring seen after removal of a metallic foreign body.

(Courtesy Ted Montgomery, OD. Available at www.tedmontgomery.com/the_eye/.)

Differential Diagnosis

Conditions that may mimic corneal abrasion and corneal ulceration must also be considered in patients with an ocular foreign body. Application of topical anesthesia blunts or obliterates the pain and photophobia associated with superficial corneal processes. This response can be helpful in distinguishing among the various eye disorders.

Diagnosis

The diagnosis of an ocular foreign body is based on the history and physical findings. If there is concern about a foreign body that is not visible, especially an intraocular foreign body, a CT scan should be obtained. MRI is contraindicated if it is possible that the foreign body is metallic. Ultrasonography can be used to visualize a superficial foreign body, but this modality is limited by the type of particle, as well as possible obscuration of findings by processes such as subconjunctival hemorrhage. A Seidel test should be performed to look for corneal rupture if deep projection is suspected. The lids should be everted and a possible lodged foreign body sought.

Treatment and Disposition

Treatment consists first of removal of the foreign body. Topical anesthesia should be provided and a cycloplegic agent considered. Superficial foreign bodies are removed with a spud or needle. A cotton-tipped applicator should be used with great caution because its large surface area may result in abrasion. The foreign body should be removed under magnification with a slit lamp. The EP should approach the foreign body with the removal device held parallel to the surface of the eye to avoid inadvertent perforation. Retained rust rings after removal of a metallic foreign body must be removed with a rust ring drill; an ophthalmologist should be consulted for this maneuver.

After removal of the foreign body, the patient should be given topical antibiotics. Patching of the eye for comfort is not necessary and is strictly contraindicated in those with severe corneal injury because it may foster infection. Pain control should be adequate, and arrangements should be made for prompt follow-up.

Differential Diagnosis

If the eye with the foreign body appears normal externally, inspection alone excludes several painful eye disorders, such as iritis. Application of topical anesthetics should not affect the pain caused by an intraocular foreign body—in contrast to the pain associated with a corneal foreign body or abrasion. A careful examination can exclude glaucoma as the cause of the patient’s symptoms.

Treatment

Consultation with an ophthalmologist should be sought immediately. The patient should not eat or drink, and antibiotics and pain medications should be administered. Tetanus status should be updated as necessary. Generally, intraocular foreign bodies are removed surgically. The technique and approach are chosen by the ophthalmologist. Patients with an intraocular foreign body should be admitted to the hospital.

Pathophysiology

Burns cause tissue damage by denaturing and coagulating cellular proteins and by leading to vascular ischemia. Thermal burns usually cause superficial epithelial destruction, but deep penetration can occur. Radiation injury causes punctuate keratitis, which is extremely painful. Patients with radiation ocular burns report exposure to sun lamps, tanning booths, high altitudes, or welder’s arcs. Acidic burns cause coagulation necrosis, which serves as a barrier and limits the extent of penetration. Alkaline chemicals can cause devastating injury. Such a chemical causes liquefaction necrosis, which continually penetrates and dissolves tissue until the chemical is removed. At pH values greater than 11.5, the damage is generally irreversible.

Presenting Signs and Symptoms

Patients usually complain of eye pain and limited visual acuity. Examination in the acute phase often shows corneal cloudiness and scleral whitening. The eye may be erythematous or whitened. Findings consistent with anterior chamber reaction, chemosis, and vascular engorgement may be present. Radiation burn or ultraviolet keratitis causes intense pain, tearing, photophobia, blepharospasm, and a foreign body sensation. Physical findings include punctate lesions on the corneal epithelium, conjunctival injection, and decreased visual acuity. Thermal burns are almost always limited to the corneal epithelium.

Differential Diagnosis

A history of exposure usually leads to a clear diagnosis. Radiation burns are not always so clear-cut because symptoms develop 6 to 10 hours after exposure to the light source. Other conditions to consider are iritis, glaucoma, corneal ulcer, corneal abrasion, and a retained foreign body. Slit-lamp and fluorescein examinations allow differentiation among the various entities.

Diagnosis

The type of chemical burn can be diagnosed by determination of the pH of the affected eye. Findings depend on the concentration of the chemical and the duration of exposure to it. Most burns can be diagnosed from the history alone. Radiation burns can be a bit more challenging to diagnose because of extreme patient discomfort. Providing adequate topical analgesia should enable examination.

Treatment and Disposition

The most important component in the treatment of chemical burns is copious irrigation. Eye irrigation should be started immediately—with no waiting even for measurement of visual acuity. After irrigation for 30 minutes, the pH should be checked. The EP should not withhold irrigation or delay its initiation even if the patient underwent prehospital irrigation. Irrigation should continue until a normal pH is recorded. Once a normal pH is obtained, the measurement should be repeated 10 to 15 minutes later to confirm neutrality. Topical anesthetics and manual lid retraction may be necessary for proper irrigation. Any particles should be removed from the fornices with a cotton swab.

After adequate irrigation, complete examination of the eye, including slit-lamp examination and determination of visual acuity, should be performed. Patients with minor burns can be discharged home with topical antibiotics, oral analgesics, and cycloplegics as necessary with arrangements for follow-up in 24 hours. An ophthalmologist should be consulted for all but the most minor ocular burns. Severe burns may cause secondary glaucoma, which is treated in consultation with the ophthalmologist. Patients with severe burns require admission for monitoring, including IOP measurements, and adequate analgesia.

Most thermal burns, which are relatively minor and restricted to the lid and corneal epithelium, can be treated the same as corneal abrasions. Initial irrigation may provide relief. Topical antibiotics, oral pain medications, and cold compresses should be provided. Patients can be discharged with outpatient follow-up. An ophthalmologist should be consulted for more severe burns.

Radiation burns are treated with cycloplegic agents and topical antibiotics. Eye patching can be considered for comfort, and oral pain medications should be prescribed. Topical anesthetics delay healing and can lead to corneal ulcer formation. Follow-up in 24 hours should be arranged.

Presenting Signs and Symptoms

Severe eye pain, nausea, vomiting, diplopia, and decreases in both visual acuity and eye movement are common complaints at initial evaluation of a patient with retrobulbar hematoma. Physical findings include proptosis, decreased ocular motility, visual loss, elevated IOP, and hemorrhagic chemosis. An afferent pupillary defect is common (Fig. 26.11).

Fig. 26.11 A and B, Retrobulbar hematoma.

(B, from Pacific University: Online Optometry Education. Available at http://www.opt.pacificu.edu/ce/catalog/10310-SD/Trauma%20Pictures/Retrobulbar%20Heme.jpg.)

Diagnosis

Clinical examination suggests the diagnosis. If the diagnosis is in doubt, CT can be performed to demonstrate the hematoma.

Treatment

The rate of development of retrobulbar hematoma dictates the treatment. If the condition develops over minutes, the eye must be decompressed immediately via lateral canthotomy (Fig. 26.12). Orbital CT demonstrates the hematoma; however, treatment should not be delayed while waiting for imaging to be performed. If the process is slower and develops over a period of hours, conservative management can be effective and consists of head elevation, ice packs to reduce swelling, intravenous acetazolamide and mannitol, and topical beta-blockers. Progress is monitored through serial measurements of IOP and pupillary reactivity. An ophthalmologist should be notified for consultation as soon as the diagnosis is suspected. Patients with retrobulbar hematoma are admitted to the hospital to monitor progress.

Fig. 26.12 Lateral canthotomy.

Presenting Signs and Symptoms

Patient symptoms and findings on examination correlate with the size of the hyphema. Typically, patients complain of eye pain, decreased visual acuity, and photophobia. If the patient is upright, the hyphema usually layers out in the inferior portion of the anterior chamber. Depending on the size of the hyphema, it can be seen with either the naked eye or a slit-lamp examination. If the hyphema is large, IOP can be elevated. IOP is elevated in approximately 27% of patients acutely but is usually mild and self-limited. Pressures greater than 35 mm Hg with durations greater than 5 to 14 days are more likely to be associated with optic atrophy.²⁰ Generally, no afferent pupillary defect is present (Fig. 26.13).

Fig. 26.13 Hyphema.

(From Auerbach PS, editor. Wilderness medicine. 5th ed. Philadelphia: Mosby; 2007.)

Diagnosis

The diagnosis is made by visualization of blood in the anterior chamber.

Treatment and Disposition

All patients with hyphemas should be seen by an ophthalmologist. The goal is to stop damage to the visual process by preventing or curbing elevations in IOP. The patient’s head should be elevated to allow inferior settling of the red blood cells. Such settling will prevent clogging of the trabecular meshwork. The pupil should be dilated to avoid “pupillary play”—movements of the iris to accommodate changing light conditions; this step should be taken in consultation with the ophthalmologist. Dilation does not block drainage of aqueous humor in normal eyes. Topical beta-blockers should be used to lower IOP. Topical α-agonists, topical carbonic anhydrase inhibitors, and systemic acetazolamide or mannitol may also be considered. Adequate analgesia should be given, with care taken to avoid aspirin and other antiplatelet agents.

Surgery may be necessary if the elevated IOP is refractory to medical therapy or to remove a large clot. Patients with hyphemas larger than 50%, decreased vision, increased IOP, and sickle cell disease should all be considered for admission.²⁴ In consultation with an ophthalmologist it may be determined that a patient with an extremely small hyphema can receive outpatient management. The major complication of hyphema is rebleeding after 2 to 5 days when the initial clot loosens, which results in potentially severe elevations in IOP. The reported incidence of rebleeding is between 6% and 33%.²⁰

Presenting Signs and Symptoms

The signs and symptoms in patients with an orbital wall or blow-out fracture can be highly variable and range from mild swelling and ecchymosis to impairment of vision. Patients may exhibit tenderness with palpation of the orbit. Subcutaneous orbital emphysema can often be found by examination. Inferior wall fractures can cause entrapment of the inferior rectus and inferior oblique muscles and orbital fat. Patients may have restricted upward gaze and diplopia, anesthesia of the ipsilateral cheek and upper lip, and ptosis. Epistaxis and diplopia can be seen with medial wall fractures. On rare occasion, orbital emphysema can cause a mass effect in which the optic nerve is compressed and blindness ensues.

Diagnosis

A Waters view radiograph can show indirect signs of fracture: a cloudy sinus, a bulge extending from the orbit into the maxillary sinus (the teardrop sign), or an air-fluid level in the maxillary sinus. CT is the diagnostic study of choice because it demonstrates the fracture, as well as other injuries. The use of bedside ultrasound has also shown to be helpful in the identification of orbital wall fractures.²⁵

Treatment and Disposition

Indications for surgical repair include muscle entrapment and cosmetic deformity with significant enophthalmos. Immediate surgery is not necessary. Surgery is delayed to allow abatement of the swelling and a better examination. The preferred time frame for operative repair is 10 to 14 days, which optimizes the balance between reduced swelling and absence of scar tissue formation. Administration of prophylactic antibiotics for an orbital wall or blow-out fracture without evidence of sinus infection is controversial. Data are inadequate for a definitive recommendation, as review of 214 studies to examine this very question found.^26,27

Presenting Signs and Symptoms

Patients with globe rupture complain of eye pain and decreased visual acuity. Because this entity is associated with a high rate of concomitant orbital floor fractures, patients may report diplopia. Rupture may not be easily apparent on examination. A shallow anterior chamber on slit-lamp examination, hyphema, and an irregular (teardrop) pupil are possible findings. A Seidel test can identify wound leaks from the anterior chamber.

Diagnosis

Diagnosis is not always easy. The history and physical findings described lead to the diagnosis. Though not always indicated, CT can detect occult tears, as well as retained foreign bodies. Plain radiographs may show foreign bodies.

Treatment and Disposition

Direct pressure should never be applied to a globe that is suspected or confirmed to be ruptured because of the risk for extrusion of intraocular contents. Although a lower than normal IOP is a good indication of rupture, tonometry should not be performed in patients with suspicion of globe rupture. A protective eye shield should be placed, and an ophthalmologist should be contacted immediately. The patient’s tetanus status should be checked and updated if necessary, and a dose of prophylactic antibiotics should be given to prevent endophthalmitis. Because skin flora is typically involved in infections of a ruptured globe, cefazolin or ciprofloxacin plus clindamycin is a good choice. Adequate antiemetics should be given to prevent Valsalva maneuvers. Surgery is performed expeditiously, and all patients with globe rupture are admitted to the hospital.

Presenting Signs and Symptoms and Diagnosis

Eye pain and photophobia are the most common patient complaints with traumatic iritis. Patients report impaired vision. Evaluation shows perilimbal conjunctival injection, cells and flare in the anterior chamber, and a constricted, weakly dilating pupil.

Treatment and Disposition

Treatment involves administration of a long-acting cycloplegic agent such as 5% homatropine, a topical steroid chosen in consultation with an ophthalmologist, and oral analgesics. Patients can be discharged with arrangements for ophthalmologic follow-up.