■  PERSPECTIVE

Epidemiology and Pathophysiology

Most eye complaints are not immediately sight-threatening and can be managed by an emergency physician. Nontrau-matic diseases, such as glaucoma and peripheral vascular disease leading to retinal ischemia, are more common with advancing age. Ocular injuries are the leading cause of visual impairment and blindness in the United States.1 More patients with postoperative complications can be expected to present to the emergency department as more vision correction sur-geries are performed.

The external and internal anatomy of the eye is depicted in Figure 32-1A and B. The globe has a complex layer of blood vessels in the conjunctiva, sclera, and retina. Redness reflects vascular dilation and may occur with processes that produce inflammation of the eye or surrounding tissues. Eye pain may originate from the cornea, conjunctiva, iris, or vasculature. Each is sensitive to processes causing irritation or inflammation.

■  DIAGNOSTIC APPROACH

Rapid and accurate triage is the most critical consideration in the approach to the red and painful eye. The first question should be, “Did anything get in your eye?” If so, the second question should be, “What do you think it is?” This helps separate trauma from nontrauma, but, more importantly, seeks to identify quickly eyes that may have been exposed to a caustic substance. Patients exposed to caustic substances require rapid decontamination to prevent permanent loss of visual acuity.

Differential Considerations

Diagnoses are classically divided into traumatic and nontrau-matic. Traumatic pain and redness can be caused by caustic fluids and solid materials, low-velocity contact with a host of materials that can fall or be rubbed into the eye, higher veloc-ity blunt-force impacts to the orbit or globe, or potentially penetrating injuries. Causes of nontraumatic pain and redness require a more detailed history, including contact lens use and questions directed toward determining the likelihood of systemic illnesses.

Pivotal Findings

Measurement of the patient’s best corrected visual acuity (i.e., with glasses on, if available) with each eye individually and with both eyes provides vital information when evaluating eye complaints. Only a few situations preclude early and accu-rate visual acuity testing. Eyes exposed to caustic materials should be decontaminated as soon as possible. Patients with sudden and complete visual loss in one eye require prompt funduscopic examination to determine the possibility of acute central retinal artery occlusion. This condition is readily appar-ent as a diffusely pale retina with indistinct or unseen retinal arteries (Fig. 32-2).

Other pivotal findings, which are more likely to be associ-ated with a serious diagnosis, in patients with a red or painful eye are listed in Box 32-1.

History

Chief complaints of pain can be manifestations of a variety of sensations. When carefully questioned, some patients may dif-ferentiate between itching, burning, dull pain, sharp pain, and perception of a foreign body. Itching tends to be more often due to blepharitis, conjunctivitis, or dry eye syndrome. Burning is associated with these conditions and with other mostly extraocular problems such as irritation of a pterygium or pin-guecula, episcleritis, or limbic keratoconjunctivitis. Dull pain may be a manifestation of increased intraocular pressure (IOP) or referred from an extraorbital process such as sinusitis, migraine headache, or temporal arteritis. Sharp pain generally results from abnormalities of the anterior eye, such as keratitis, uveitis, and acute angle-closure glaucoma. A foreign body sen-sation is more typical of corneal irritation or inflammation.

A chief complaint of redness commonly results from palpe-bral or limbal injection of the conjunctiva. However, free blood can be noted behind the bulbar conjunctiva (i.e., subconjunc-tival hemorrhage) or in the anterior chamber (i.e., hyphema). Both of these can be spontaneous or post-traumatic. Spontane-ous subconjunctival hemorrhages may follow coughing or straining or may be due to systemic hypertension. Often, it occurs without any identifiable precipitating incident and is simply noticed by the patient when looking in the mirror. Spontaneous subconjunctival hemorrhage is painless, and the presence of pain raises concern for a more serious cause of the hemorrhage, such as direct globe injury. Hyphema of

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Chapter 32 Red and Painful EyeJoshua L. Wright and John M. Wightman

Figure 32-1.  External (A) and internal (B) anatomy. (From Ragge NK, Easty DL: Immediate Eye Care. St. Louis, Mosby-Year Book, 1990.)

Pupillary margin

Corneaoverlying iris

Sclera

Outer canthus

Iris sphincter

Collarette

Iris crypt

Superior punctum

Inner canthus

Caruncle

Inferior punctum

Limbus (corneoscleraljunction)

Cilia (eyelashes)

External appearance of the eyeA

Ciliary body

Canal of Schlemm

Posterior chamber

Anterior chamber

Lens

Cornea

Limbus

Pars plana

Retina

Fovea

Optic nerve

Cross section of the eye

Iris

B

Figure 32-2.  Key funduscopic findings in acute central retinal artery occlusion include general pallor of the retina (except for a characteristic cherry-red spot where the perfused choroid shows through the thinner fovea) and attenuation of retinal arteries (possibly with retinal veins preserved as in the photograph). (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004, p 297.)

Retinal edema Cherry-red spot

BOX 32-1Pivotal Findings More likely associated with a serious diagnosis in Patients with a red or PainFul eye

Adapted and reprinted, with permission, from Trobe JD: The Physician’s Guide to Eye Care. San Francisco, Foundation of the American Academy of Ophthalmology, 2001.

Severe ocular painPersistently blurred visionProptosisReduced ocular light reflectionCorneal epithelial defect or opacityLimbal injection (i.e., ciliary flush)Pupil unreactive to a direct light stimulusWearer of soft contact lensesNeonateImmunocompromised hostWorsening signs after 3 days of pharmacologic treatment

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sufficient size to be noted by the patient or bystander usually arises with pain and blurred vision.

Other subjective findings may be transient and detected only by history. The patient may relate lid swelling, tearing, discharge, crusting, or sensitivity to light. Lid swelling can be caused by inflammatory and noninflammatory processes. Con-current erythema of the lid favors the former. In the absence of trauma or other external irritant (e.g., contact dermatitis), inflammatory processes include primary lid problems such as hordeolum (i.e., stye) or blepharitis as well as extension from concomitant conjunctivitis or cellulitis in orbital or periorbital structures. When pain is present, tearing is usually secondary. Discharge and crusting are most commonly associated with conjunctivitis, whether allergic, viral, or bacterial. Blepharitis, dacryocystitis, and canaliculitis are other inflammatory pro-cesses that may create a discharge and subsequent crusting.

Other eye status review questions include the following:

■ Are contact lenses used? If so, what type, how are they cleaned, and how old are the lenses? Has there been a change in the pattern of use (especially increased use)? Were the lenses worn for a particularly long period recently? Are there problems with the lenses drying out? Does inser-tion of the lenses worsen or relieve the symptoms?

■ Are glasses worn? If so, when was the last assessment for adequate refraction?

■ Has previous eye surgery or injury occurred?■ What is the patient’s usual state of health?■ What medications are being taken? Are there any allergies,

including environmental allergies?

Physical ExaminationA complete eye examination usually includes eight compo-nents, although many patients require only a limited or directed eye examination, depending on the presentation.2 The mnemonic VVEEPP (pronounced “veep”) plus slit-lamp and funduscopic examinations represent these components (Box 32-2).3 Slit-lamp examination is recommended for any complaint involving trauma and for any medical presentation involving foreign body sensation or alteration of vision.

Funduscopic examination is usually pursued if there is visual loss, visual alteration, or suggestion of serious pathology in the history and initial physical examination. A thorough physical examination can be conducted in the following order.

Visual Acuity

The initial determination of a patient’s visual acuity provides a baseline from which deterioration or improvement may be followed. It is also predictive of functional outcome after ocular trauma. Visual acuity is quantitatively assessed by use of a Snellen chart test at a distance of 20 feet (6 m) or a Rosenbaum chart at a distance of 14 inches. Young patients who cannot yet read letters and numbers should be tested with an Allen chart that depicts easily recognizable shapes. Each eye is tested separately with the opposite eye carefully covered. Patients who present without their prescribed correc-tive lenses may be evaluated by having them view the chart through a pinhole eye cover, which negates most refractive errors in vision.

If the patient cannot distinguish letters or shapes on a chart, visual acuity must be determined qualitatively. Any printed material suffices. The result may be recorded as, for example, “patient able to read newsprint at 3 feet.” If this is not possi-ble, visual acuity is recorded as:

■ Unable/able to count fingers (CF)■ Unable/able to perceive hand motion (HM)■ Unable/able to perceive light (LP)

Visual Field Testing

Confrontation is the most common method of testing visual fields in the emergency department.4 Detection of a scotoma usually represents a retinal problem. However, glaucoma may cause scotomata that can be crescent-shaped, involve just the binasal visual fields, or affect all peripheral vision. Hemi- or quadrantanopia is more commonly a problem of the neural pathways to the brain.

External Examination

Gross abnormalities are assessed by a visual inspection of both eyes simultaneously. Findings may be more apparent if com-pared with the opposite side. Fractures of facial bones are associated with ocular injuries, some of which require immedi-ate intervention by an ophthalmologist.5

Globe position is part of the external examination. Subtle exophthalmos and enophthalmos are rare, and are best detected by looking inferiorly, tangentially across the forehead, from over the patient’s scalp.6 Exophthalmos may have traumatic or nontraumatic causes, but is due to increased pressure or a space-occupying lesion within the orbit, which may mani-fest as pain. Medical causes include cellulitis or intraorbital or lacrimal tumors. Hyperthyroidism may cause enlargement of extraocular muscles. The most important cause of exoph-thalmos in the emergency department is retrobulbar hema-toma, a condition characterized by hemorrhage within the bony orbit, behind the globe. Orbital compartment syndrome pushes the globe forward, stretching the optic nerve and retinal artery and increasing IOP. The resulting microvascular is-chemia is sight-threatening if sufficiently severe and persistent. Orbital emphysema and inflammation caused by a retained foreign body behind the eye are other causes of exophthalmos. The discovery of exophthalmos should prompt ocular tonom-etry measurements to determine the urgency of intervention. Trauma, particularly penetrating globe injury with extrusion

Visual acuity (best possible using correction)Visual fields (tested by confrontation)External examination

Globe position in orbitConjugate gazePeriorbital soft tissues, bones, and sensation

Extraocular muscle movementPupillary evaluation (absolute and relative)Pressure determination (tonometry)Slit-lamp examination

Lids and lashesConjunctiva and scleraCornea (with fluorescein in some cases)Anterior chamberIrisLens

Funduscopic examination

BOX 32-2 coMPlete eye exaMination

Adapted from Wightman JM, Hurley LD: Emergency department management of eye injuries. Crit Decis Emerg Med 12:1, 1998.

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of vitreous, can cause the globe to recede into the orbit, but the most common cause of enophthalmos is actually pseu-doenophthalmos when the contralateral globe is proptotic.

Inspection also involves examination of the upper and lower palpebral sulci for foreign bodies or other abnormalities. The lower sulcus is easily viewed after manual retraction of the lower lid toward the cheek and having the patient gaze upward. The upper sulcus is inspected by pulling its lashes directly forward and looking under the lid with white light. The lid can then be everted by pressing a cotton-tipped applicator in the external lid crease and folding the lid margin over the applicator.

Extraocular Muscle Function

Limitation of ocular movement in one eye may be detected by having the patient follow the examiner’s finger or a bright light through the cardinal movements of gaze. The eyes may move in a disconjugate fashion, or the patient may admit to diplopia if asked. Diplopia on extreme gaze in one direction may indicate entrapment of one of the extraocular muscles within a fracture site, but more often is caused simply by edema or hemorrhage related to the injury and is functional rather than actual entrapment. In the absence of trauma, diplopia is rarely associated with redness or pain.

Pupillary Evaluation

The pupils are inspected for abnormalities of shape, size, and reactivity. These examinations are conducted with light spe-cifically directed into the pupil and by means of the swinging flashlight test.

Previous surgery (e.g., iridotomy for cataract extraction) and synechiae from prior iritis or other inflammatory condition are the most common causes of irregularly shaped pupils. Asym-metrically sized pupils may represent normal or pathologic conditions. Physiologic anisocoria is a slight difference in pupil size that occurs in up to 10% of the population. Topical or systemic medications, drugs, and toxins may cause abnormal pupillary constriction or dilation.

Pathologic reasons for failure of one pupil to constrict with a direct light stimulus include globe injury, abnormalities of afferent or efferent nerves, and paralysis of the ciliaris or sphincter pupillae muscles in the iris. Potentially serious problems, which also cause pain and redness, include uveitis and acute angle-closure glaucoma.

The swinging flashlight test is used to determine whether a relative afferent pupillary defect (RAPD) exists.4 The patient fixes the gaze on a distant object and the examination room is darkened. The size of the pupils in lowered light is noted, and unless there is physiologic anisocoria, the pupils should be equal in size. The direct and consensual light responses of the eyes are compared as a light source, angled into the pupil from in front of the cheeks, is swung back and forth between the two. When the light source shines into an eye with an RAPD, the pupil dilates because the consensual response from withdrawal of light from the opposite eye with normal afferent activity is stronger than the direct constrictive response to light in the affected eye with inhibited afferent activity. It is termed “relative” because the response is compared with that of the opposite side as the light source is alternated between eyes. An RAPD may be partial or complete and due to inhibition of light transmission to the retina because of vitreous hemorrhage, loss of some or all of the retinal surface for light contact because of ischemia or detachment, or the presence of lesions affecting the prechiasmal optic nerve (e.g., optic neuritis).

Pressure Determination

Ocular tonometry is usually the last examination performed in the emergency department. Common methods of determining the IOP in the emergency department include use of elec-tronic, manual (e.g., Schiøtz), or applanation tonometers. IOPs in the 10- to 20-mm Hg range are considered normal. Causes of intraocular hypertension include glaucoma in its many forms, suprachoroidal hemorrhage, and space-occupying retro-bulbar pathology. Patients presenting with IOPs exceeding 20 mm Hg should have ophthalmologic consultation. Rapid treatment is usually not necessary until the pressure exceeds 30 mm Hg.

Slit-Lamp Examination

The slit lamp permits a magnified, binocular view of the con-junctivae and anterior globe for diagnostic purposes and to facilitate delicate procedures. It allows depth perception in otherwise clear structures, such as the cornea, aqueous humor, and lens. The slit-lamp examination can include the following:

■ Lids and lashes may be inspected for blepharitis and point-ing of a lid abscess (i.e., hordeolum). The inner canthus and lacrimal punctum may be better viewed for evidence of dacryocystitis.

■ Punctures, lacerations, and inflammatory patterns of the conjunctiva or sclera may be discovered with magnification.

■ Corneal abrasions, ulcers, foreign bodies, and other abnor-malities may be seen. The depth of these lesions may be accurately assessed with an angled beam. Edema, which appears as a white haze or cloudiness within clear struc-tures, can be differentiated within the epithelium or deeper stroma.

■ The anterior chamber may be examined for cells (e.g., red and white blood cells) and “flare.” Cells are seen as small floating objects caught in the beam of a highly angulated slit-lamp light, as dust floating in the movie theater glows from the reflected light of the projector beam. Flare is a diffuse haziness, related to cells and proteins suspended in the aqueous humor, and is often visible only when illu-minated directly (Fig. 32-3). It usually represents deep

Figure 32-3.  Technique of slit-lamp examination with a short, narrow light beam projected from an extreme temporal angle across the contrasting black pupil to better find cells or “flare” indicative of acute anterior uveitis. (From Ragge NK, Easty DL: Immediate Eye Care. St. Louis, Mosby-Year Book, 1990.)

Reflectionfrom cornea

Space in which tolook for particulatematter, “flare”

Reflectionfrom lens

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inflammation of the eye and is often seen in iritis. Collec-tions of layered blood or pus in the dependent portions of the anterior chamber are called hyphema or hypopyon, respectively, and are graded by the percentage of the verti-cal diameter of the visible iris when the head is upright. Foreign bodies that have penetrated the cornea may be found floating in the anterior chamber.

■ The trabeculated pattern of the iris can be seen in detail. Spiraling muscle fibers may be seen in acute angle-closure glaucoma. If the beam is shown almost coaxially with the examiner’s line of sight such that the red reflex is elicited, tears in the iris may be seen by light returning through the iris itself instead of just through the pupil.

■ The lens should be examined for position, general clarity, and the presence of opacities or foreign bodies. The type and position of any lens implants can also be better assessed during a slit-lamp examination.

Direct Funduscopic Examination

Emergency physicians most commonly perform a nondilated funduscopic examination because there are several eye condi-tions in which dilation may be harmful (e.g., glaucoma). Irido-dialysis, lens dislocation, and conditions requiring early intervention are usually identifiable along the visual axis.

Inability to obtain a red reflex or visualize the fundus of the eye can be due to:

■ Opacification of the cornea, most commonly by edema secondary to injury or infection

■ Hyphema or hypopyon within the anterior chamber■ Extremely miotic pupil■ Cataract of the lens■ Blood in the vitreous or posterior eye wall■ Retinal detachment

In the absence of trauma, few posterior findings are associ-ated with chief complaints of external redness. Findings asso-ciated with visual loss include pallor of the retina indicating ischemia, “cupping” of the optic disk indicating glaucoma, indistinctness of disk margins indicating papilledema or optic neuritis or neuropathy, air or plaque emboli in retinal arteries, and a host of other signs indicating more chronic ocular or systemic pathology not normally amenable to management in the emergency department.

Bedside Testing

Fluorescein solution and the cobalt blue lamp are the best means for identifying damage to the corneal epithelium, including that which cannot be seen with conventional slit-lamp examination. Fluorescein highlights defects, making them easy to identify, because the fluorescing liquid is thicker in defects than it is across the normally smooth corneal surface. Use of fluorescein may reveal corneal abrasions and ulcers as well as damage from keratitides related to chemicals, ultravio-let light, or infections (e.g., herpes).

Relief of discomfort after instillation of a topical anesthetic can be used as a diagnostic test for an external source of pain. In general, abolition of pain by local anesthetic drops indicates pain of corneal origin. Modest but incomplete relief suggests a conjunctival process. Intraocular pain is not diminished by local anesthetic solution.7 When ocular penetration is sug-gested, Seidel’s test can be used. This test involves placing a fluorescein strip directly over an area of possible corneal dis-ruption. The high localized concentration of fluorescein may facilitate identification of the corneal defect with a slit lamp by allowing visualization of leaking aqueous fluid diluting the fluorescein. This test does not work on the conjunctiva overly-

ing the sclera, and a negative test result does not rule out a full-thickness corneal injury.

Ancillary Testing

An erythrocyte sedimentation rate may be used to evaluate for temporal arteritis, which may arise with eye pain and decreased visual acuity.

Infections are usually evident by examination, and labora-tory tests such as a complete blood count are not necessary. Microbiologic cultures are rarely ordered in the emergency department.

Plain radiography is used to identify facial fractures associ-ated with facial or ocular trauma or indirectly by detecting an air-fluid level in the orbit or fluid in the paranasal sinuses. Computed tomography (CT), using 1.5-mm axial and coronal cuts, provides superior imaging, but is not necessary in many cases.

CT also reliably localizes metal and many nonradiopaque foreign bodies in the globe and orbit. It can also detect small amounts of intraocular air following penetrating trauma. Mag-netic resonance imaging (MRI) clearly delineates the orbital and retro-orbital structures, but cannot be employed with metallic (magnetic) foreign bodies, which can migrate to cause additional damage.8 It is less often used in emergency eye assessment, for which, in general, CT is the initial imaging modality of choice.9 Ultrasonography is more sensitive for detecting intraocular foreign bodies, but CT is better at delin-eating the damage caused by them, so they are complementary tests.10

■  DIFFERENTIAL DIAGNOSIS

Clinical findings most indicative of serious eye disorder are listed in Box 32-1.

Critical Diagnoses

Caustic injury to the eye can rapidly lead to a destructive kera-toconjunctivitis (Fig. 32-4A and B) if the agent is not removed immediately. The diagnosis is made on history alone, before any other examination is performed. Early and copious irriga-tion is indicated. Many patients have already undergone extensive irrigation at the job site, but when the exposure has occurred in the home, irrigation prior to arrival in the emer-gency department is uncommon. Alkaline caustic agents cause a liquefactive necrosis of the cornea by progressively reacting with the corneal layers, and destruction is severe and relent-less. Continuous irrigation is the only effective method to terminate the reaction and should be continued for at least 30 minutes. Acid injury is much less severe and requires less irrigation than alkaline exposures, but irrigation should continue until the pH of the tears is neutral or the patient is essentially asymptomatic.

Acute angle-closure glaucoma is a relatively rare but impor-tant critical diagnosis to make in the emergency department. Patients present with pain, the onset of which is often sudden in low-light conditions requiring pupillary dilation through contraction and thickening of the iris peripherally. The iris becomes immobile and often irregular, and the pupil is com-monly fixed at 5 to 6 mm in diameter. Inability of the pupil to constrict may result in photophobia, and accommodation may be affected. These reactions and the increased IOP can lead to frontal headache, nausea, and vomiting. As inflammation progresses, limbal injection of the conjunctiva is almost universally seen. Figure 32-5 demonstrates many of these findings. Immediate medical intervention in the emergency

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corneal origin of the process and facilitating examination and definitive diagnosis.6 Corneal abrasions are very common and may be identified by white light or fluorescein-facilitated blue light using a slit lamp or any other magnification (Fig. 32-6). Following thorough irrigation, thermal and chemical burns must receive a careful slit-lamp examination for potential full-thickness injury. If this is not found, the corneal injury may be treated similarly to an abrasion.

In immunocompetent hosts, corneal ulcerations are most commonly due to overuse of contact lenses. They are seen as a denuding of epithelium with surrounding edema, the increased interstitial water of which is seen as whitish clouding of the normally clear tissue (Fig. 32-7). Almost all ulcerations require same-day evaluation by an ophthalmologist. Infections of the cornea with herpes simplex virus can rapidly lead to opacification and significant visual loss. It is most commonly recognized by a characteristic dendritic pattern of fluorescein pooling under blue light (Fig. 32-8). Anterior uveitis, which includes iritis and iridocyclitis, often occurs secondary to a traumatic injury or infectious process or can be associated with serious systemic immune diseases, such as adult and juvenile rheumatoid arthritis, sarcoidosis, and ankylosing spondylitis.

Scleritis is rare and may be difficult to differentiate from episcleritis, which is somewhat more common and a more

Figure 32-4.  A, Alkali burn demonstrating corneal burns and conjunctival injection on the day of the accident. B, Complete corneal tissue destruction 7 days after alkali burn. (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Corneal alkali burn Corneal alkali burn

A B

Figure 32-5.  Primary angle-closure glaucoma with very shallow anterior chamber and iridocorneal touch (no space between slit-beam view of cornea and iris). (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Posterior cornea Slit-beam Iris surface

department and urgent ophthalmologic consultation are warranted.

Retrobulbar hematoma (blood) is usually caused by orbital trauma, but it can also occur spontaneously in patients with coagulopathy. Retrobulbar abscess (pus) or emphysema (air) can also occur.11,12 Elevated IOP in any of these conditions constitutes orbital compartment syndrome and a surgical emergency. Emergency intervention is to decompress the orbit by performing lateral canthotomy and cantholysis.13,14

Emergent Diagnoses

Most emergent diagnoses involve some kind of inflammation secondary to trauma, infection, or systemic disease. These include keratitis, anterior uveitis, scleritis, and endophthalmi-tis. Any of these may be complications of surgical procedures, and an appropriate ophthalmologic history must be obtained.

Keratitis, or inflammation of the cornea, is most commonly viral in origin but can also be caused by exposure to intense ultraviolet light (e.g., snow blindness, arc welder’s blindness), various chemicals, or ischemia related to contact lens use. Patients present with an intense foreign-body sensation, ciliary spasm causes photophobia that is often severe, and the affected eyes are often clenched shut. Topical anesthesia provides immediate (but temporary) relief of pain, thus reinforcing the

Figure 32-6.  Corneal abrasion demonstrating fluorescein pooling of a small inferior epithelial defect. (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Corneal abrasion

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translucent, sclera (Fig. 32-9). Scleritis may be associated with anterior uveitis, cataract, and secondary glaucoma.

Endophthalmitis usually results from an infection of struc-tures inside the globe. It is most common following penetrat-ing trauma but may begin after hematogenous seeding from a remote or systemic infection, particularly in immunocompro-mised hosts. Unless it is detected early, and is responsive to aggressive antimicrobial therapy, endophthalmitis is a devas-tating process that frequently requires enucleation.

Urgent Diagnoses

Penetrating ocular trauma is evaluated by history (e.g., working with high-speed grinding equipment), examination (extrusion of aqueous humor or other globe content; direct visualization of a foreign body in the anterior chamber, vitreous, or retina), or identification of the offending object by biplanar plain radi-ography, thin-cut CT, or ultrasonography. MRI should not be used if there is any possibility that the foreign object may be metallic. Indirect indicators of globe penetration are hyphema, an irregularly shaped pupil from traction on or injury to the iris’ attachments, or lack of a red reflex. If penetrating ocular injury is confirmed or if the possibility persists after evaluation, an ophthalmologic consultation is indicated.4

Spontaneous or traumatic hyphema is often managed con-servatively. Blood in the anterior chamber is usually the result of direct ocular trauma and may be associated with traumatic mydriasis or an obvious tear of the iris. If penetration and rupture can be reasonably excluded, the hyphema should be graded and IOP determined. Intraocular hypertension (or hypotension in the case of occult globe rupture) following trauma must also be evaluated by an ophthalmologist urgently. Inability to view posterior structures through the anterior blood may necessitate radiologic or ultrasonographic imaging.

Diagnostic Algorithm

A recommended algorithmic approach to the patient with an acute red eye is provided in Figure 32-10.

Figure 32-7.  Bacterial keratitis demonstrating large, central Streptococcus pneumoniae corneal ulcer. Note the dense, white corneal infiltrate and the extreme conjunctival injection. (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Neovascularization Corneal ulcer

Figure 32-8.  Patient demonstrating fluorescein pooling of herpes simplex virus dendrite. (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Herpes simplex virus dendrite

benign inflammation. The former is commonly idiopathic but may be associated with a systemic inflammatory process, such as a connective tissue disease, gout, or infection (e.g., Lyme disease, syphilis, tuberculosis). Eye redness in episcleritis results from dilation of the episcleral blood vessels just under-neath the conjunctiva, usually in a small sector of the visible portion of the globe. If the location of the involved layer is in doubt, a topical anesthetic allows the examiner to move the conjunctiva and its contained vessels with a cotton-tipped applicator, thus differentiating between vessels of scleral or conjunctival origin. The pain of scleritis is typically slower in onset but is often described as a severe “boring” pain that radiates to the ipsilateral forehead, cheek, or jaw. Engorge-ment of scleral vessels is usually more prominent and more diffuse than that of the episcleral vessels in episcleritis. A bluish hue may be seen as the underlying pigmented epithelium shows through the edematous, and hence more

Figure 32-9.  Diffuse scleritis with slight bluish region in addition to injection of scleral, episcleral, and conjunctival vessels. (From Kaiser PK, Friedman NJ, Pineda R, II: The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology, 2nd ed. Philadelphia, WB Saunders, 2004.)

Necrotizing scleritis

Ch

apter 32 / R

ed and Painful E

ye233

Figure 32-10.  Diagnostic algorithm for red eyes. *Indicates potentially serious diagnoses if not identified on initial emergency department evaluation. †Purulent implies true pus, as opposed to the mucoid discharge more commonly associated with nonbacterial causes of conjunctivitis. a.k.a., also known as; FB, foreign body; incl, including. (Modified from Trobe JB: The Physician’s Guide to Eye Care. San Francisco, Foundation of the American Academy of Ophthalmology, 2001.)

Causticcontamination?

Proptosis orexternal swelling? Yes

Yes1. Caustic keratoconjunctivitis*

2. Blepharitis 3. Chalazion 4. Dacrocystitis and dacroadenitis 5. Hordeolum (a.k.a. stye) 6. Inflammatory pseudotumor* 7. Orbital celluitis* 8. Orbital tumor* 9. Periorbital cellulitis or erysipelas10. Retrobulbar abscess*11. Retrobulbar emphysema*12. Retrobulbar hematoma*

13. Keratitis* (incl abrasion and ulcer)14. Keratoconjunctivitis15. Episcleritis16. Scleritis*17. Anterior uveitis and hypopyon*18. Acute angle-closure glaucoma*19. Hyphema*20. Endophthalmitis*

21. Inflamed pingueculum22. Inflamed pterygium23. Scleral penetration*24. Subconjunctival hemorrhage

25. Bacterial conjunctivitis*

26. Allergic conjunctivitis

Yes

Yes

Yes

Yes

27. Contact dermatoconjunctivitis28. Toxic conjunctivitis

29. Chlamydia conjunctivitis30. Viral conjunctivitis

Yes

No

No

No

No

No

No

No

Severe pain, FBsensation, or

limbal injection?

Focal rednessof bulbar

conjunctiva?

Purulentdischarge?†

Itching sensationwith or without

other symptoms?

Airborne allergen,topical med, or

cosmetics?

■  EMPIRICAL MANAGEMENT

Irrigation

Any clean water is appropriate for irrigation, and prompt initiation takes precedence over procurement of a particular irrigating solution. The most important principles are rapid and copious dilution and removal of the offending material. An eyewash station or faucet with tap water may be employed.

Normal saline may be instilled through the end of macrodrip intravenous administration tubing. If there is no gross eye injury, a Morgan lens may be attached to this tubing, but emergency department staff do not have to help the patient hold the eye open. Quickly administering two drops of topical anesthetic and allowing 30 seconds or so for the anesthetic to become effective greatly facilitates patients’ tolerance of the prolonged irrigation required. It is recom-mended that the first 500 to 1000 mL of irrigation fluid be

234PA

RT 

I ■

Fun

dam

enta

l Clin

ical

Con

cept

s /

SeC

tio

n t

wo

• C

ardi

nal P

rese

ntat

ions

administered while examining the eye; then the Morgan lens may be placed.

Pain Relief

Pain often interferes with obtaining an adequate assessment. A topical anesthetic, such as proparacaine 0.5%, may facilitate cooperation in patients with possible injury or inflammation of the anterior eye by reducing pain and blepharospasm long enough to obtain a targeted history and focused examination. Topical anesthetic agents should not be given to patients to use at home. Parenteral or oral analgesics can be used for severe deep pain not amenable to topical relief in the emer-gency department, or for outpatient management of discom-fort after discharge.

Mydriatic and Cycloplegic Agents

Dilation of the pupil is not usually necessary in the emergency department for funduscopic examination, but may relieve pain associated with ciliary spasm in anterior uveitis. Mydriatic agents (e.g., phenylephrine, tropicamide) merely prevent con-striction of the pupil by paralyzing the sphincter pupillae muscle of the iris. Cycloplegic agents (e.g., cyclopentolate, homatropine) paralyze the ciliaris muscle, with an accompany-ing mydriatic effect. The agent chosen should be guided by the desired length of time of mydriasis for the particular condi-tion being treated (Table 32-1). Mydriatic agents are contra-indicated in patients with narrow-angle glaucoma.

Antimicrobial Agents

Most conjunctivitis is viral in origin, but it is often difficult to distinguish bacterial from viral types of conjunctivitis based solely on clinical grounds.15,16 Although no definitive empirical evidence dictates the use of antibiotic solutions or ointments for surface infections, the use of broad-spectrum topical antibiotics in cases of proven bacterial conjunctivitis is associated with benefit showing significantly higher clinical remission rates.17 Antimicrobial prophylaxis should be used for penetrating wounds to prevent bacterial keratitis or endophthalmitis.

Antibiotics are typically used to treat identified or suggested bacterial infections, even if the exact bacterial agent has not been determined. The most common causes of bacterial con-junctivitis are nontypable Haemophylis influenzae, Streptococcus pneumoniae, and Staphylococcus aureus.18,19 Trachoma, a chronic keratoconjunctivitis caused by Chlamydia trachomatis, is the

most common infectious cause of blindness.20 Bacterial kera-titis is usually seen in contact lens wearers, particularly those who wear them overnight.21 In descending order of frequency of cultured organisms, microbial keratitis is caused by Pseudo-monas aeruginosa, streptococcal or staphylococcal species, filamentous fungi, nonpseudomonal gram-negative rods, Acanthamoeba, other bacteria, and yeast.22

The most common organisms cultured from deeper eye structures, particularly following open-globe injuries, are Bacillus cereus, Propionibacterium acnes, and various species of Bacillus, Streptococcus, and Staphylococcus.23,24 While awaiting emergent ophthalmologic consultation for possible vitrectomy, empirical parenteral antibiotic combinations include cefazolin plus gentamicin or vancomycin plus cefotaxime, ceftazidime, or ceftriaxone. Possible cases of mycotic endophthalmitis have historically been treated with amphotericin B,23 though voriconazole has been shown to have good intraocular penetra-tion, broad-spectrum activity, and relatively low systemic toxicity.25

Open wounds also require tetanus prophylaxis, if the patient’s immunization status is not up to date. There is no current evidence supporting the practice of administering tetanus immunization to patients with superficial corneal abrasions.

Other Protective Interventions

Significantly increased IOP must be reversed as rapidly as possible, often before the specific cause is known. After placing the patient in at least a 30° head-up position, two drops of timolol 0.5%, a topical beta-adrenergic blocking medication, should be administered as a first-line agent to decrease the production of aqueous humor. This may be followed by two drops of dorzolamide 2%, a topical carbonic anhydrase inhibitor, to reduce aqueous humor production further. If not available, 500 mg of acetazolamide may be given orally or intravenously. If the patient has sickle cell disease or trait, oral methazolamide 50 mg must be used instead. Patients with suggested intraocular hypertension who also have nausea or vomiting should receive a parenteral antiemetic so that they do not gag or vomit, which may further increase IOP.

Specific Management

Management of the specific entities listed in the diagnostic algorithm presented in Figure 32-10 is presented in Table 32-2. Specific management of ophthalmologic conditions is also discussed in Chapter 69.

■  SPECIAL CONSIDERATIONS

Pediatrics

A red eye in a neonate or infant is always abnormal. It is usually caused by corneal abrasion or infection. Corneal abrasions can also be a cause of inconsolable crying in an infant. Fluorescein examination helps to identify abrasions and herpes keratitis, acquired from the birth canal. Chlamydia infections may also be acquired during vaginal deliveries but may not arise for weeks. These infections should be treated with oral azithro-mycin as well as parenteral ceftriaxone to cover Neisseria gonor-rhoeae. Conjunctivitis associated with respiratory symptoms or infiltrates on a chest radiograph in an infant younger than 3 months should be treated with an oral macrolide. Oral antibiot-ics are also indicated for conjunctivitis associated with otitis media. Mycoplasma is a common infectious agent in these cases, and a macrolide is indicated.14

Table 32-1  Duration of Action for Common Mydriatic and Cycloplegic Medications

NAMECONCENTRATION (%)

COMMON DURATION

MAXIMUM DURATION

Ephedrine* 5.0 0.5–1 hr 3 hrPhenylephrine* 2.5 0.5–1 hr 3 hrTropicamide 0.5 3–4 hr 6 hrCyclopentolate 0.5 12–18 hr 24 hrHomatropine 1.0 1–2 days 3 daysScopolamine 0.5 2–5 days 7 daysAtropine 0.5 5–10 days 14 days

*Mydriatic action only, no cycloplegic effect. Combination products such as Cyclomydril, which is cyclopentolate 0.2% and phenylephrine 10%, are also available.

Ch

apter 32 / R

ed and Painful E

ye235

Tabl

e 32

-2 

Man

agem

ent 

Alg

ori

thm

 fo

r R

ed E

yes 

Exte

nd

ed f

rom

 Dia

gn

ost

ic A

lgo

rith

m in

 Fig

ure

 32

-10

DIA

GN

OSI

S FR

OM

 FIG

UR

E 3

2-1

0M

AN

AG

EMEN

TC

ON

SULT

ATI

ON

DIS

PO

SITI

ON

1.

Cau

stic

ker

atoc

onju

ncti

viti

sIm

med

iate

and

cop

ious

irri

gati

on w

ith

tap

wat

er o

r st

erile

nor

mal

sal

ine

unti

l tea

r-fil

m p

H =

7.

Oph

thal

mol

ogis

t m

ust

com

e to

ED

if

ther

e is

any

abn

orm

al v

isua

l acu

ity

or o

bjec

tive

find

ing

on e

xam

inat

ion

afte

r su

ffici

ent

irri

gati

on, w

ith

exce

ptio

n of

exp

ecte

d in

ject

ion

of

conj

unct

iva

seco

ndar

y to

tre

atm

ent.

May

dis

char

ge o

nly

if t

ear

film

pH

= 7

and

no

find

ings

on

exam

inat

ion

exce

pt

conj

unct

ival

inje

ctio

n an

d op

htha

lmol

ogis

t ca

n re

eval

uate

nex

t da

y.So

lids:

lift

part

icle

s ou

t w

ith

dry

swab

bef

ore

irri

gati

onA

cids

: min

imum

of

2 L

and

20

min

Alk

alis

: min

imum

of

4 L

and

40

min

2.

Ble

phar

itis

Infl

amm

atio

n of

eye

lid m

argi

ns

ofte

n a/

w c

rust

s on

aw

aken

ing,

FB

sen

sati

on,

and

tear

ing.

Non

e ex

cept

art

ifici

al t

ears

for

dry

eye

.O

utpa

tien

t re

ferr

al o

nly

for

trea

tmen

t fa

ilure

aft

er 2

wk.

Dis

char

ge w

ith

inst

ruct

ions

to

appl

y w

arm

co

mpr

esse

s to

eye

lids

for

15 m

in q

id a

nd

scru

b lid

mar

gins

and

lash

es w

ith

mild

sh

ampo

o on

was

hclo

th b

id.

3.

Cha

lazi

on I

nflam

mat

ion

of m

eibo

mia

n gl

and

caus

ing

subc

utan

eous

nod

ule

wit

hin

the

eyel

id.

Non

e.O

utpa

tien

t re

ferr

al o

nly

for

trea

tmen

t fa

ilure

aft

er 2

wk.

Dis

char

ge w

ith

inst

ruct

ions

to

appl

y w

arm

co

mpr

esse

s to

eye

lids

for

15 m

in a

nd

gent

ly m

assa

ge n

odul

e qi

d.4.

D

acro

cyst

itis

and

dac

road

enit

is E

ye t

eari

ng

and

infla

mm

atio

n of

low

er e

yelid

infe

rior

to

lacr

imal

pun

ctum

find

ing

redn

ess

and

tend

erne

ss o

ver

nasa

l asp

ect

of lo

wer

lid

and

adja

cent

per

iorb

ital

ski

n.

Fir

st r

/o p

erio

rbit

al c

ellu

litis

(#9

) an

d or

bita

l ce

llulit

is (

#7).

Insp

ect

for

obst

ruct

ion

of

punc

tum

by

SLE

, may

exp

ress

pus

by

pres

sing

on

sac,

PO

Rx

for

nasa

l and

ski

n flo

ra if

not

adm

itti

ng.

Oph

thal

mol

ogis

t m

ay a

dmit

if

syst

emic

ally

ill,

case

is m

oder

ate

or

seve

re, o

r no

soc

ial s

uppo

rt f

or

pati

ent.

Ask

abo

ut c

ultu

ring

bef

ore

Rx

if a

dmit

ting

, the

n R

x sa

me

as

for

peri

orbi

tal c

ellu

ltit

is (

#9).

May

dis

char

ge m

ild c

ases

wit

h P

O

anal

gesi

cs a

nd a

ntib

ioti

cs (

e.g.

, am

oxic

illin

/cla

vula

nate

), an

d in

stru

ctio

ns

to a

pply

war

m c

ompr

esse

s to

eye

lids

for

15 m

in a

nd g

entl

y m

assa

ge in

ner

cant

hal

area

qid

.5.

H

orde

olum

(a.

k.a.

sty

e) A

bsce

ss in

eye

lash

fo

llicl

e or

mod

ified

seb

aceo

us g

land

at

lid

mar

gin:

ext

erna

l or

inte

rnal

bas

ed o

n si

de o

f lid

m

argi

n th

at a

bsce

ss is

poi

ntin

g.

Ext

erna

l: W

arm

com

pres

ses

ofte

n al

l tha

t is

ne

eded

, may

Rx

anti

-Sta

ph o

intm

ent

bid.

In

tern

al: P

O R

x fo

r β-

lact

amas

e St

aph.

Out

pati

ent

refe

rral

onl

y fo

r tr

eatm

ent

failu

re a

fter

2 w

k.D

isch

arge

wit

h in

stru

ctio

ns t

o ap

ply

war

m

com

pres

ses

to e

yelid

s fo

r 15

min

and

ge

ntly

mas

sage

abs

cess

qid

.

6.

Infla

mm

ator

y ps

eudo

tum

or*

Non

spec

ific

idio

path

ic r

etro

bulb

ar in

flam

mat

ion

wit

h ey

elid

sw

ellin

g, p

albe

bral

inje

ctio

n of

co

njun

ctiv

a, c

hem

osis

, pro

ptos

is, b

lurr

ed

visi

on, p

ainf

ul o

r lim

ited

ocu

lar

mob

ility

, bi

nocu

lar

dipl

opia

, ede

ma

of o

ptic

dis

k, o

r ve

nous

eng

orge

men

t of

ret

ina.

Mea

sure

IO

P. E

valu

ate

for

infe

ctio

n,

diab

etes

mel

litus

, and

vas

culit

is w

ith

CB

C, B

MP,

UA

, and

ESR

. Obt

ain

axia

l C

T o

f br

ain

and

axia

l and

cor

onal

CT

of

orbi

ts a

nd s

inus

es.

IOP

> 2

0 m

m H

g m

ay b

e su

rgic

al

emer

genc

y, R

x to

dec

reas

e IO

P in

E

D.

May

dis

char

ge if

no

syst

emic

pro

blem

s, n

o fin

ding

s of

par

ticu

lar

conc

ern

on C

T, a

nd

IOP

> 2

0 m

m H

g. S

tart

hig

h-do

se P

O

ster

oids

aft

er d

iscu

ssio

n w

ith

opht

halm

olog

ist

and

ensu

re r

eeva

luat

ion

in 2

–3 d

ays.

7.

Orb

ital

cel

lulit

is*

Eye

lid s

wel

ling,

red

ness

an

d w

arm

th o

f sk

in o

verl

ying

orb

it,

tend

erne

ss o

f sk

in o

verl

ying

bon

e pa

lbeb

ral

inje

ctio

n of

con

junc

tiva

, and

che

mos

is.

Dif

fere

ntia

ted

from

per

iorb

ital

cel

lulit

is b

y pr

esen

ce o

f an

y fin

ding

of

feve

r, ill

app

eara

nce,

bl

urre

d vi

sion

, pro

ptos

is, p

ainf

ul o

r lim

ited

oc

ular

mob

ility

, bin

ocul

ar d

iplo

pia,

ede

ma

of

opti

c di

sk, o

r ve

nous

eng

orge

men

t of

ret

ina.

Mea

sure

IO

P. S

tart

IV

Rx

wit

h se

cond

-ge

nera

tion

cep

halo

spor

in (

e.g.

, ce

furo

xim

e, c

efox

itin

, or

cefo

teta

n) o

r w

ith

ampi

cilli

n/su

lbac

tam

to

cove

r si

nus

and

skin

flor

a. A

lter

nati

ve R

x is

tic

arci

llin/

clav

ulan

ate,

pip

erac

illin

/taz

obac

tam

, va

ncom

ycin

, or

clin

dam

ycin

+ t

hird

-ge

nera

tion

cep

halo

spor

in (

e.g.

, cef

otax

ime

or c

eftr

iaxo

ne).

IOP

> 2

0 m

m H

g m

ay b

e su

rgic

al

emer

genc

y, R

x to

dec

reas

e IO

P in

E

D. O

btai

n bl

ood

cult

ures

and

st

art

anti

biot

ics.

Axi

al a

nd c

oron

al

CT

of

orbi

ts a

nd s

inus

es t

o r/

o F

B,

retr

obul

bar

absc

ess,

orb

ital

gas

, su

bper

iost

eal a

bsce

ss, o

steo

mye

litis

, an

d ch

ange

s in

cav

erno

us s

inus

. C

onsi

der

LP.

Adm

it a

ll ca

ses

of o

rbit

al c

ellu

litis

.

8.

Orb

ital

tum

or*

Blu

rred

vis

ion,

pro

ptos

is o

r ot

her

disp

lace

men

t of

glo

be, p

ainf

ul o

r lim

ited

ocu

lar

mob

ility

, or

bino

cula

r di

plop

ia

(but

can

be

asym

ptom

atic

).

Mea

sure

IO

P. E

valu

ate

for

extr

aocu

lar

sign

s of

mal

igna

ncy.

Obt

ain

axia

l CT

of

brai

n an

d ax

ial a

nd c

oron

al C

T o

f or

bits

and

si

nuse

s.

IOP

> 2

0 m

m H

g m

ay b

e su

rgic

al

emer

genc

y, R

x to

dec

reas

e IO

P in

E

D. O

phth

alm

olog

ist

may

wan

t M

RI,

MR

A, o

r or

bita

l US.

Bas

ed o

n fin

ding

s an

d di

scus

sion

wit

h co

nsul

tant

.

Con

tinue

d

236PA

RT 

I ■

Fun

dam

enta

l Clin

ical

Con

cept

s /

SeC

tio

n t

wo

• C

ardi

nal P

rese

ntat

ions

Tabl

e 32

-2 

Man

agem

ent 

Alg

ori

thm

 fo

r R

ed E

yes 

Exte

nd

ed f

rom

 Dia

gn

ost

ic A

lgo

rith

m in

 Fig

ure

 32

-10

—co

nt’d

DIA

GN

OSI

S FR

OM

 FIG

UR

E 3

2-1

0M

AN

AG

EMEN

TC

ON

SULT

ATI

ON

DIS

PO

SITI

ON

9.

Per

iorb

ital

cel

lulit

is o

r er

ysip

elas

Eye

lid

swel

ling,

red

ness

and

war

mth

of

skin

ov

erly

ing

orbi

t, te

nder

ness

of

skin

ove

rlyi

ng

bone

, pal

bebr

al in

ject

ion

of c

onju

ncti

va, a

nd

chem

osis

.D

iffe

rent

iate

d fr

om o

rbit

al c

ellu

litis

by

abse

nce

of a

ny o

ther

find

ing

liste

d in

#7.

Fir

st r

/o o

rbit

al c

ellu

litis

(#7

). P

O R

x fo

r si

nus

and

skin

flor

a if

not

adm

itti

ng.

Oph

thal

mol

ogis

t m

ay a

dmit

if

syst

emic

ally

ill,

case

is m

oder

ate

or

seve

re, o

r no

soc

ial s

uppo

rt f

or

pati

ent.

May

dis

char

ge m

ild c

ases

wit

h P

O

anti

biot

ics.

Oph

thal

mol

ogis

t m

ust

reev

alua

te n

ext

day

to e

nsur

e no

orb

ital

ex

tens

ion.

10.

Ret

robu

lbar

abs

cess

* F

indi

ngs

of o

rbit

al

cellu

litis

(#7

) bu

t a/

w in

crea

sed

IOP.

Mea

sure

IO

P u

nles

s po

ssib

ility

of

rupt

ured

gl

obe.

IO

P >

30

mm

Hg

may

req

uire

em

erge

nt n

eedl

e as

pira

tion

or

late

ral

cant

hoto

my

and

cant

holy

sis

in E

D.

IOP

> 2

0 m

m H

g m

ay b

e su

rgic

al

emer

genc

y, R

x to

dec

reas

e IO

P in

E

D. O

btai

n ax

ial C

T o

f br

ain

and

axia

l and

cor

onal

CT

of

orbi

ts a

nd

sinu

ses.

Adm

it a

ll ca

ses

of r

etro

bulb

ar p

atho

logy

ca

usin

g in

crea

sed

IOP.

Oth

ers

mig

ht b

e ca

ndid

ates

for

dis

char

ge d

epen

ding

on

caus

e of

pro

blem

.

11.

Ret

robu

lbar

em

phys

ema*

Fin

ding

s of

ps

eudo

tum

or (

#6)

but

a/w

incr

ease

d IO

P.A

bsce

ss: A

ntib

ioti

cs a

s in

orb

ital

cel

lulit

is

(#7)

. Em

phys

ema:

Pro

phyl

ax w

ith

anti

biot

ics

to c

over

sin

us fl

ora.

Hem

atom

a:

Cor

rect

any

coa

gulo

path

y or

th

rom

bocy

tope

nia.

12.

Ret

robu

lbar

hem

atom

a* F

indi

ngs

of

pseu

dotu

mor

(#6

) bu

t oc

curs

due

to

trau

ma,

co

agul

opat

hy, o

r th

rom

bocy

tope

nia

and

a/w

di

ffus

e su

bcon

junc

tiva

l hem

orrh

age

ante

rior

ly

and

exte

ndin

g po

ster

iorl

y as

wel

l as

incr

ease

d IO

P.13

. K

erat

itis

(ab

rasi

on o

r U

V in

jury

) P

ain,

FB

se

nsat

ion,

ble

phar

ospa

sm, t

eari

ng,

phot

opho

bia,

epi

thel

ial d

isru

ptio

n on

in

spec

tion

und

er w

hite

ligh

t or

fluo

resc

ein

pool

ing

unde

r bl

ue li

ght.

SPK

app

ears

as

stip

plin

g of

cor

neal

sur

face

[of

ten

low

er 2

/3 o

f co

rnea

if d

ue t

o lig

ht e

xpos

ure]

.

Fir

st r

/o c

orne

al p

enet

rati

on e

ithe

r gr

ossl

y or

em

ploy

ing

Seid

el’s

tes

t. R

elie

ve p

ain

and

blep

haro

spas

m w

ith

topi

cal a

nest

heti

c.

Insp

ect

all c

onju

ncti

val r

eces

ses

and

supe

rfici

al c

orne

a fo

r an

y fo

reig

n m

ater

ial

that

can

be

rem

oved

by

irri

gati

on o

r m

anua

lly li

fted

fro

m s

urfa

ce. T

etan

us

prop

hyla

xis

is s

tand

ard

of c

are

even

if

corn

ea n

ot p

enet

rate

d.

Oph

thal

mol

ogis

t m

ust

com

e to

ED

if

ther

e is

any

con

cern

for

glo

be

pene

trat

ion.

Oth

erw

ise

cons

ult

for

follo

w-u

p ex

amin

atio

n in

1–2

day

s.

One

-tim

e ad

min

istr

atio

n of

cy

clop

legi

c ag

ent

may

lim

it

phot

opho

bia

unti

l fol

low

-up

exam

inat

ion.

May

dis

char

ge c

ases

not

infe

cted

or

ulce

rate

d on

top

ical

ant

ibio

tic

prop

hyla

xis

usin

g po

lym

yxin

B c

ombi

nati

ons

wit

h ba

citr

acin

(oi

ntm

ent)

or

trim

etho

prim

(s

olut

ion)

. Gen

tam

icin

and

sul

face

tam

ide

are

less

des

irab

le s

ingl

e-ag

ent

alte

rnat

ives

. PO

NSA

IDs

or n

arco

tics

for

an

alge

sia.

Pat

chin

g no

t ne

cess

ary.

Ker

atit

is (

ulce

rati

on)*

Sym

ptom

s an

d si

gns

as

abov

e. U

lcer

atio

n fr

om c

ompl

icat

ions

of

cont

act

wea

r or

neg

lect

ed c

orne

al a

bras

ion

has

“sco

oped

out

” ep

ithe

lium

wit

h su

rrou

ndin

g ed

ema

appe

arin

g as

whi

te

“clo

udin

ess”

in c

lear

tis

sue.

Rel

ieve

pai

n an

d bl

epha

rosp

asm

wit

h to

pica

l an

esth

etic

. Sta

ph. a

nd S

trep

. spe

cies

sti

ll m

ost

com

mon

org

anis

ms,

but

Pse

udom

onas

gr

eate

r pe

rcen

tage

in e

xist

ing

infe

ctio

ns

(esp

ecia

lly c

onta

ct le

ns w

eare

r), s

o R

x w

ith

topi

cal fl

uoro

quin

olon

e is

pre

ferr

ed.

Dis

cuss

any

pot

enti

al n

eed

to d

ébri

de

or c

ultu

re b

efor

e st

arti

ng a

ntib

ioti

c.B

ased

on

findi

ngs

and

disc

ussi

on w

ith

cons

ulta

nt. T

ypic

al c

ipro

floxa

cin

dosi

ng is

1

gt. q

15

min

for

1 h

r, th

en 1

gt.

q hr

for

8

hr, t

hen

1 gt

. q 4

hr

unti

l see

n by

co

nsul

tant

nex

t da

y. P

O N

SAID

s or

na

rcot

ics

for

anal

gesi

a. N

o pa

tch.

Ker

atit

is (

herp

etic

infe

ctio

n)*

Sym

ptom

s an

d si

gns

as a

bove

. Loo

k fo

r ot

her

sign

s of

he

rpes

, var

icel

la, z

oste

r (o

r C

MV

infe

ctio

n in

imm

unoc

ompr

omis

ed p

atie

nt).

Loo

k fo

r “d

endr

itic

” de

fect

s of

cor

nea

wit

h flu

ores

cein

und

er b

lue

light

.

Rel

ieve

pai

n an

d bl

epha

rosp

asm

wit

h to

pica

l an

esth

etic

. Rx

wit

h tr

iflur

idin

e 1%

so

luti

on, v

idar

abin

e oi

ntm

ent,

or a

cycl

ovir

oi

ntm

ent.

Vari

cella

-zos

ter

and

CM

V n

ot

norm

ally

giv

en a

ntiv

iral

s if

im

mun

ocom

pete

nt.

Dis

cuss

wit

h op

htha

lmol

ogis

t an

y po

tent

ial n

eed

to d

ébri

de o

r cu

ltur

e be

fore

sta

rtin

g an

tivi

ral.

Bas

ed o

n fin

ding

s an

d di

scus

sion

wit

h co

nsul

tant

. Typ

ical

tri

fluri

dine

dos

ing

is

1 gt

. q 2

hr

for

7 da

ys, t

hen

tape

r ov

er 2

m

ore

wk.

Typ

ical

vid

arab

ine

or a

cycl

ovir

do

sing

is fi

ve t

imes

a d

ay f

or 7

day

s, t

hen

tape

r ov

er 2

mor

e w

k. P

O N

SAID

s or

na

rcot

ics

for

anal

gesi

a. N

o pa

tch.

Ch

apter 32 / R

ed and Painful E

ye237

DIA

GN

OSI

S FR

OM

 FIG

UR

E 3

2-1

0M

AN

AG

EMEN

TC

ON

SULT

ATI

ON

DIS

PO

SITI

ON

14.

Ker

atoc

onju

ncti

viti

s C

onju

ncti

viti

s w

ith

sube

pith

elia

l infi

ltra

tes

in c

orne

a ca

usin

g pa

in

and

decr

ease

d vi

sion

, pos

sibl

y w

ith

halo

s re

port

ed.

Tre

at f

or c

onju

ncti

viti

s by

like

ly e

tiol

ogic

ca

tego

ry (

#25–

30).

Dis

cuss

find

ings

and

use

of

pred

niso

lone

ace

tate

1%

(fr

eque

ncy

dete

rmin

ed b

y op

htha

lmol

ogis

t).

May

dis

char

ge p

atie

nt w

ith

med

icat

ions

re

com

men

ded

by o

phth

alm

olog

ist

and

ensu

re r

eeva

luat

ion

in 2

–3 d

ays.

15.

Epi

scle

riti

s R

apid

ons

et o

f lo

caliz

ed p

ain,

in

ject

ion

of e

pisc

lera

l ves

sels

, and

loca

lized

te

nder

ness

.

Rel

ieve

irri

tati

on w

ith

arti

ficia

l tea

rs a

nd

decr

ease

infla

mm

atio

n w

ith

keto

rola

c gt

t.O

utpa

tien

t re

ferr

al o

nly

for

trea

tmen

t fa

ilure

aft

er 2

wk.

May

dis

char

ge p

atie

nt w

ith

PO

NSA

IDs

alon

e or

in c

ombi

nati

on w

ith

topi

cal

keta

rola

c gt

t.16

. Sc

leri

tis*

Pro

gres

sive

ly in

crea

sing

eye

pai

n w

ith

radi

atio

n to

ipsi

late

ral f

ace

and

decr

easi

ng v

isio

n, p

hoto

phob

ia, t

eari

ng, a

nd

poss

ible

pai

n w

ith

eye

mot

ion.

Dec

reas

e in

flam

mat

ion

wit

h P

O N

SAID

s.D

iscu

ss fi

ndin

gs a

nd u

se o

f to

pica

l or

PO

ste

roid

s.M

ay d

isch

arge

pat

ient

wit

h m

edic

atio

ns

reco

mm

ende

d by

oph

thal

mol

ogis

t an

d en

sure

ree

valu

atio

n in

2–3

day

s.

17.

Ant

erio

r uv

eiti

s an

d hy

popy

on*

Eye

pai

n,

phot

opho

bia,

tea

ring

, lim

bal i

njec

tion

of

conj

unct

iva,

and

cel

ls o

r fla

re in

ant

erio

r ch

ambe

r. H

ypop

yon

is la

yeri

ng o

f w

hite

cel

ls

(pus

) in

ant

erio

r ch

ambe

r.

Fir

st r

/o g

lauc

oma

wit

h IO

P m

easu

rem

ent.

Rx

in E

D if

IO

P >

20

mm

Hg.

Oth

erw

ise

OK

to

dila

te p

upil

wit

h 2

gtt.

of

cycl

open

tola

te 1

%.

Dis

cuss

find

ings

and

use

of

pred

niso

lone

ace

tate

1%

(fr

eque

ncy

dete

rmin

ed b

y op

htha

lmol

ogis

t bu

t ra

nge

is q

1–6

hr)

.

May

dis

char

ge p

atie

nt w

ith

med

icat

ions

re

com

men

ded

by o

phth

alm

olog

ist

and

ensu

re r

eeva

luat

ion

in 2

–3 d

ays.

Pat

ient

s w

ith

hypo

pyon

are

gen

eral

ly a

dmit

ted.

18.

Acu

te a

ngle

-clo

sure

gla

ucom

a Su

dden

-ons

et

eye

pain

and

blu

rred

vis

ion

that

may

be

a/w

fr

onta

l hea

dach

e, n

ause

a, a

nd v

omit

ing.

A

nter

ior

eye

may

man

ifes

t sh

allo

w o

r cl

osed

an

gle

betw

een

iris

and

cor

nea,

pup

il fix

ed in

m

id-d

ilati

on, o

r lim

bal i

njec

tion

of

conj

unct

iva.

Dec

reas

e pr

oduc

tion

of

aque

ous

hum

or.

Dis

cuss

any

IO

P >

20

mm

Hg

wit

h op

htha

lmol

ogis

t.B

ased

on

findi

ngs

and

disc

ussi

on w

ith

cons

ulta

nt, w

hich

pri

mar

ily d

epen

ds o

n sp

eed

of o

nset

and

res

pons

e to

tre

atm

ent.

T

imol

ol 0

.5%

1 g

t., t

hen

repe

at in

30

min

.

Apr

aclo

nidi

ne 1

% 1

gt.

once

.

Dor

zola

mid

e 2%

2 g

tt. o

r if

sick

le c

ell

dise

ase

or tr

ait t

hen

met

hazo

lam

ide

50 m

g P

O. D

ecre

ase

infla

mm

atio

n.

Pre

dnis

olon

e 1%

1 g

t. ev

ery

15 m

in f

our

tim

es.

Rx

in E

D if

IO

P >

30

mm

Hg.

Con

stri

ct p

upil.

P

iloca

rpin

e 4%

1 g

t., t

hen

repe

at in

15

min

Con

side

r es

tabl

ishi

ng o

smot

ic g

radi

ent

M

anni

tol 2

g/k

g IV

.19

. H

yphe

ma*

Pai

n, d

ecre

ased

vis

ual a

cuit

y,

gros

s or

mic

rosc

opic

blo

od in

ant

erio

r ch

ambe

r, m

ay b

e a/

w d

ilate

d an

d fix

ed p

upil

follo

win

g bl

unt

trau

ma.

Gra

ded

by a

mou

nt o

f bl

ood

P

erce

ntag

e of

ver

tica

l dia

met

er o

f an

teri

or

cham

ber

whe

n bl

ood

laye

rs w

ith

pati

ent

in

upri

ght

posi

tion

.

Mic

rohy

phem

a sh

ows

no la

yeri

ng a

nd o

nly

susp

ende

d re

d bl

ood

cells

.

Fir

st r

/o g

lobe

rup

ture

. May

req

uire

ul

tras

ound

if c

anno

t vi

sual

ize

post

erio

r st

ruct

ures

. Mea

sure

IO

P u

nles

s po

ssib

ility

of

rup

ture

d gl

obe.

IO

P >

30

mm

Hg

may

re

quir

e ac

ute

trea

tmen

t as

in g

lauc

oma

(#18

). If

IO

P >

20

mm

Hg

and

no

irid

odia

lysi

s, m

ay u

se c

yclo

pleg

ic t

o pr

even

t ir

is m

otio

n.

Dis

cuss

find

ings

and

use

of

ε-am

inoc

apro

ic a

cid

and

ster

oids

, ot

her

med

ical

the

rapy

, bes

t di

spos

itio

n, a

nd f

ollo

w-u

p ex

amin

atio

n by

oph

thal

mol

ogis

t w

ithi

n 2

days

. Som

e pa

tien

ts m

ay

be a

dmit

ted

for

obse

rvat

ion,

bed

-re

st, h

ead

elev

atio

n, a

nd f

requ

ent

med

icat

ion

adm

inis

trat

ion.

Mos

t pa

tien

ts c

an b

e di

scha

rged

wit

h ca

refu

l ins

truc

tion

s to

ret

urn

for

any

incr

ease

d pa

in o

r ch

ange

in v

isio

n.

Pat

ient

s sh

ould

dec

reas

e ph

ysic

al a

ctiv

ity

and

slee

p w

ith

an e

ye s

hiel

d in

pla

ce.

Eye

s sh

ould

be

left

ope

n w

hile

aw

ake,

so

any

chan

ge in

vis

ion

can

be im

med

iate

ly

reco

gniz

ed. P

O N

SAID

s or

nar

coti

cs f

or

anal

gesi

a.

Con

tinue

d

238PA

RT 

I ■

Fun

dam

enta

l Clin

ical

Con

cept

s /

SeC

tio

n t

wo

• C

ardi

nal P

rese

ntat

ions

DIA

GN

OSI

S FR

OM

 FIG

UR

E 3

2-1

0M

AN

AG

EMEN

TC

ON

SULT

ATI

ON

DIS

PO

SITI

ON

20.

End

opht

halm

itis

* P

rogr

essi

vely

incr

easi

ng

eye

pain

and

dec

reas

ing

visi

on, d

imin

ishe

d re

d re

flex,

cel

ls a

nd fl

are

(and

pos

sibl

y hy

popy

on)

in a

nter

ior

cham

ber,

chem

osis

, and

ey

elid

ede

ma.

Em

piri

cal p

aren

tera

l ant

ibio

tic

adm

inis

trat

ion

wit

h ce

fazo

lin +

gen

tam

icin

or

van

com

ycin

+ c

efot

axim

e, c

efta

zidi

me,

or

cef

tria

xone

to

cove

r B

acill

us,

ente

roco

ccus

, and

Sta

phyl

ococ

cus

spp.

Oph

thal

mol

ogis

t m

ust

adm

it f

or

pare

nter

al a

nd p

ossi

bly

intr

aocu

lar

anti

biot

ics.

Adm

it a

ll ca

ses

of e

ndop

htha

lmit

is.

21.

Infla

med

pin

guec

ulum

Infl

amm

atio

n of

sof

t ye

llow

pat

ches

in t

empo

ral a

nd n

asal

edg

es o

f lim

bal m

argi

n.

Dec

reas

e in

flam

mat

ion

wit

h na

phaz

olin

e or

ke

toro

lac

gtt.

Out

pati

ent

refe

rral

onl

y fo

r tr

eatm

ent

failu

re a

fter

2 w

k.D

isch

arge

to

follo

w-u

p w

ith

opht

halm

olog

ist

for

poss

ible

ste

roid

the

rapy

or

surg

ical

re

mov

al.

22.

Infla

med

pte

rygi

um I

nflam

mat

ion

of fi

rmer

w

hite

nod

ules

ext

endi

ng f

rom

lim

bal

conj

unct

iva

onto

cor

nea.

Sam

e as

#21

Sam

e as

#21

Sam

e as

#21

23.

Scle

ral p

enet

rati

on*

Loc

aliz

ed r

edne

ss a

t si

te

of e

ntry

, tea

rdro

p pu

pil,

bloo

d in

ant

erio

r ch

ambe

r or

loss

of

red

refle

x.

Pro

tect

eye

fro

m f

urth

er p

ress

ure,

pro

vide

pa

in r

elie

f, an

d pr

even

t vo

mit

ing.

Tet

anus

pr

ophy

laxi

s.

Oph

thal

mol

ogis

t m

ust

com

e to

ED

if

ther

e is

any

con

cern

for

glo

be

pene

trat

ion.

Adm

it f

or I

V a

ntib

ioti

cs a

nd p

ossi

ble

proc

edur

al in

terv

enti

on.

24.

Subc

onju

ncti

val h

emor

rhag

e R

ed b

lood

be

neat

h cl

ear

conj

unct

ival

mem

bran

e.E

xclu

de c

oagu

lopa

thy

or t

hrom

bocy

tope

nia,

if

indi

cate

d by

his

tory

.N

one

requ

ired

if n

o co

mpl

icat

ions

.R

eass

ure

pati

ent

that

red

sho

uld

reso

lve

over

2–3

wk.

25.

Bac

teri

al c

onju

ncti

viti

s* H

yper

puru

lent

di

scha

rge

not

typi

cal o

f co

mm

on “

pink

eye

” an

d m

ore

com

mon

ly u

nila

tera

l in

adul

ts.

Infla

mm

atio

n of

eye

lid m

argi

ns a

/w li

d ed

ema,

che

mos

is, a

nd p

ossi

bly

subc

onju

ncti

val h

emor

rhag

e, b

ut u

sual

ly n

o fo

llicu

lar

“cob

bles

toni

ng.”

Top

ical

pol

ymyx

in B

tri

met

hopr

im in

in

fant

s an

d ch

ildre

n, b

ecau

se m

ore

Stap

h.

spp.

Top

ical

sul

face

tam

ide

or g

enta

mic

in

clin

ical

ly e

ffec

tive

in 9

0% o

f un

com

plic

ated

adu

lt c

ases

. Use

top

ical

flu

oroq

uino

lone

if P

seud

omon

as p

ossi

ble.

Cul

ture

dra

inag

e an

d op

htha

lmol

ogy

cons

ult

in a

ll ne

onat

es a

nd t

hose

at

risk

for

vis

ion

loss

or

syst

emic

se

psis

. Nei

sser

ia g

onor

rhoe

ae c

an b

e ra

pidl

y si

ght-

thre

aten

ing.

Dis

char

ge u

ncom

plic

ated

cas

es w

ith

10 d

ays

of t

opic

al a

ntib

ioti

cs in

bot

h ey

es,

rega

rdle

ss o

f la

tera

lity

of a

ppar

ent

infe

ctio

n. U

se o

intm

ents

in in

fant

s an

d gt

t. in

oth

ers.

26.

Alle

rgic

con

junc

tivi

tis

Oft

en b

ilate

ral

palp

ebra

l inj

ecti

on o

f co

njun

ctiv

a an

d fo

llicu

lar

cobb

lest

onin

g of

inne

r su

rfac

e of

lid

s th

at m

ay b

e se

ason

al a

nd a

/w o

ther

al

lerg

ic s

ympt

oms

such

as

rhin

itis

.

Dec

reas

e ir

rita

tion

wit

h na

phaz

olin

e gt

t.O

utpa

tien

t re

ferr

al o

nly

for

trea

tmen

t fa

ilure

aft

er 2

wk.

Iden

tify

ant

igen

if p

ossi

ble.

Con

side

r tr

eati

ng o

ther

alle

rgic

sym

ptom

s w

ith

P

O a

ntih

ista

min

es.

27.

Con

tact

der

mat

ocon

junc

tivi

tis

Loc

aliz

ed li

d an

d co

njun

ctiv

al r

edne

ss a

nd e

dem

a.Ir

riga

tion

wit

h ta

p w

ater

or

ster

ile n

orm

al

salin

e. D

ecre

ase

irri

tati

on w

ith

naph

azol

ine

gtt.

Out

pati

ent

refe

rral

onl

y fo

r se

vere

ca

ses

or t

reat

men

t fa

ilure

aft

er

2 w

k.

Iden

tify

off

endi

ng a

gent

and

avo

id

subs

eque

nt e

xpos

ure.

Dis

char

ge

unco

mpl

icat

ed c

ases

on

cont

inue

d na

phaz

olin

e.28

. T

oxic

con

junc

tivi

tis

Dif

fuse

con

junc

tiva

l in

ject

ion,

che

mos

is, a

nd li

d ed

ema.

Sam

e as

#27

Sam

e as

#27

Sam

e as

#27

29.

Chl

amyd

ia c

onju

ncti

viti

s O

ften

bila

tera

l pa

lpeb

ral i

njec

tion

of

conj

unct

iva

in n

eona

te

or o

ther

indi

vidu

al a

t ri

sk f

or s

exua

lly

tran

smit

ted

dise

ase.

Rx

PO

azi

thro

myc

in f

or C

hlam

ydia

. Con

side

r pa

rent

eral

cef

tria

xone

for

con

curr

ent

Nei

sser

ia g

onor

rhoe

ae.

Cul

ture

dra

inag

e an

d co

nsul

t op

htha

lmol

ogy

in a

ll ne

onat

es a

nd

thos

e at

ris

k fo

r vi

sion

loss

or

syst

emic

sep

sis.

Dis

char

ge u

ncom

plic

ated

cas

es o

n 5

days

of

PO

azi

thro

myc

in.

30.

Vir

al c

onju

ncti

viti

s O

ften

bila

tera

l pal

pebr

al

inje

ctio

n of

con

junc

tiva

and

fol

licul

ar

cobb

lest

onin

g of

inne

r su

rfac

e of

lids

.In

flam

mat

ion

of e

yelid

mar

gins

oft

en a

/w

crus

ts o

n aw

aken

ing,

FB

sen

sati

on, a

nd

tear

ing.

Dec

reas

e ir

rita

tion

wit

h ar

tific

al t

ears

, na

phaz

olin

e, o

r ke

toro

lac

gtt.

Cul

ture

dra

inag

e an

d co

nsul

t op

htha

lmol

ogy

in a

ll ne

onat

es a

nd

thos

e at

ris

k fo

r vi

sion

loss

or

syst

emic

sep

sis.

Ask

abo

ut p

regn

ant

mot

hers

, inf

ants

, and

im

mun

ocom

prom

ised

indi

vidu

als

in c

lose

co

ntac

t. D

isch

arge

unc

ompl

icat

ed c

ases

w

ith

inst

ruct

ions

on

resp

irat

ory

and

dire

ct-c

onta

ct c

onta

gion

for

2 w

k.

a.k.

a., a

lso

 kn

ow

n a

s; a

/w, a

sso

ciat

ed w

ith

; bid

; tw

ice 

dai

ly; B

MP, 

bas

ic m

etab

olic

 pro

file 

(incl

ud

es e

lect

roly

tes, 

glu

cose

, an

d r

enal

 fu

nct

ion

 tes

ts); 

CB

C, c

om

ple

te b

loo

d c

ou

nt; 

CM

V, c

yto

meg

alov

iru

s; C

T, c

om

pu

ted

 to

mo

gra

ph

y; 

ED, e

mer

gen

cy d

epar

tmen

t; ES

R, e

ryth

rocy

te s

edim

enta

tio

n r

ate;

 FB,

 fore

ign

 bo

dy;

 gt.,

 dro

p; g

tt. d

rop

s; IO

P, in

trao

cula

r p

ress

ure

; LP, 

lum

bar

 pu

nct

ure

; MR

A, m

agn

etic

 res

on

ance

 an

gio

gra

ph

y; M

RI, m

agn

etic

 res

on

ance

 imag

ing

;  N

SAID

s, n

on

ster

oid

al a

nti

-in

flam

mat

ory

 dru

gs;

 PO

, ora

l; q

, eve

ry; q

id, 4

 tim

es a

 day

; r/o

, ru

le o

ut; 

Rx, p

resc

rib

e; S

LE, s

lit-l

amp

 exa

min

atio

n; S

PK, s

up

erfic

ial p

un

ctu

ate 

kera

titi

s; s

pp

, sp

ecie

s; S

taph

., St

aphy

loco

ccus

; Str

ep.,

Stre

ptoc

occu

s; U

A; u

rin

alys

is; U

S, u

ltra

son

og

rap

hy;

 UV,

 ult

ravi

ole

t.

*Po

ten

tial

ly s

erio

us 

dia

gn

ose

s if 

no

t id

enti

fied

 on

 init

ial e

mer

gen

cy d

epar

tmen

t ev

alu

atio

n. A

nti

bio

tic 

cho

ices

 sh

ou

ld b

e b

ased

 on

 cu

rren

t p

ract

ice.

Tabl

e 32

-2 

Man

agem

ent 

Alg

ori

thm

 fo

r R

ed E

yes 

Exte

nd

ed f

rom

 Dia

gn

ost

ic A

lgo

rith

m in

 Fig

ure

 32

-10

—co

nt’d

Ch

apter 32 / R

ed and Painful E

ye239

Trauma

Blunt trauma is a common cause of a red and painful eye. Large hyphemas and those with clots are likely to require hospitalization for bedrest with 30° of head elevation. Sys-temic analgesia and, if required, antiemetics are indicated. Medications affecting platelet function should be avoided. Treatment may be indicated when the IOP exceeds 30 mm Hg, as it is in acute angle-closure glaucoma. If the iris is not injured, a long-acting cycloplegic agent (e.g., topical homatropine) may be recommended to prevent repetitive motion of the iris. Some reliable adult patients may be discharged with daily follow-up by a specialist. Strong analgesia and patching are not indicated, so that the patient may immediately identify increases in pain or decreases in visual acuity.

Corneal abrasions are common problems in the emergency department. When the emergency physician is convinced that the cornea has not received a full-thickness laceration or pen-etration by a foreign body, management is relatively simple. Foreign bodies (on or in the epithelium only) should be removed when possible. These may frequently adhere to a saline-moistened cotton-tipped applicator. Ones that do not may sometimes be lifted off with a blunt-tipped tool (“spud”) under the binocular magnification of a slit lamp. The common use of hypodermic needle removal may damage surrounding cornea and is not recommended. Whether or not the object can be successfully removed, management is the same as for corneal abrasions. Rust staining of the corneal epithelium does not require removal in the emergency department, but patients are referred to a specialist for examination within 3 days. Pro-phylactic topical antibiotics are indicated for all epithelial defects of the cornea. Patching is not necessary and may be harmful. Systemic analgesia appropriate to the patient’s level of pain should be provided. Larger lesions may require a pro-phylactic mydriatic or cycloplegic agent anticipating a second-ary iritis. Topical anesthetics should not be given to the patient for home use.4

■  DISPOSITION

Most emergency department patients with eye complaints are candidates for discharge and, if indicated, follow-up in the

emergency department or with an ophthalmologist in 1 to 2 days. Others may require referral only if there is lack of resolu-tion or treatment fails. A few patients require admission for procedural intervention, parenteral antibiotic regimens, man-agement of intractable pain, or further diagnostic evaluation. General consultation and disposition considerations for the most important entities are outlined in Table 32-2.

The references for this chapter can be found online by accessing the accompanying Expert Consult website.

KEY CONCEPTS

■  Prompt and prolonged irrigation is advised for patients who experience caustic injury to the eye.

■  Headache and nausea may be prominent symptoms in patients with acute angle-closure glaucoma.

■  Keratitis, inflammation of the cornea, is most commonly caused by a viral infection, but may also be caused by recent ultraviolet light exposure, chemical injury, or hypoxic injury from contact lens use.

■  A localized corneal defect with edematous, inflammatory changes may signal corneal ulceration.

■  A corneal dendritic pattern may signal a herpetic infection, which can progress to corneal opacification and visual loss.

■  Pain, consensual photophobia, perilimbic conjunctivial infection, and a miotic pupil that is caused by ciliary spasm could signal iritis, which is inflammation of the iris and ciliary body, or uveitis, inflammation of the iris, ciliary body, and also choroids. The cause may be trauma or underlying autoimmune disease. The presence of cells and flare in the anterior chamber can help signal these conditions.