h ~ , -.
`t ec mies.com
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`EMERGENCY
`MEDICINE CLINICS
`OF NORTH AMERICA
`Ophthalmologic Emergencies
`
`GUEST EDITORS
`Joseph H. Kahn, MD and
`Brendan Magauran, MD
`
`CONSULTING EDITOR
`Arna I Mattu, MD
`
`February 2008 • Volume 26 • Number 1
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`SAUNDERS
`An Imprint of Elsevier, Inc.
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`EMERGENCY MEDICINE CLINICS
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`February 2008
`Editor: Patrick Manley
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`Volume 26, Number 1
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`ELSEVIER
`SAUNDERS
`
`Emerg Med Clin N Am
`26 (2008) 57-72
`
`EMERGENCY
`MEDICINE
`CLINICS OF
`NORTH AMERICA
`
`Ocular Infection and Inflammation
`Jorma B. Mueller, MD\
`Christopher M. McStay, MDb,*
`"Emergency Medicine Residency, Ne w York University/Bellevue Hospital Center,
`462 First Avenue, Ne111 York , NY 10016, USA
`b Department of Emergency Medicine , Ne w York University/ Bellev11e Hospital Center,
`462 First Arenue, N eiv York, NY 10016, USA
`
`Managing the inflamed or infected eye in the emergency setting presents
`a diagnostic and .therapeutic challenge to the emergency physician; the
`causes and prognoses range from benign, self-limited illness to organ-threat(cid:173)
`ening pathology. A careful history, with attention to comorbid illnesses and
`time course, is paramount, as is knowledge of the complete ophthalmologic
`examination. Much of the organ morbidity is ameliorated with prompt ther(cid:173)
`apy in the emergency department (ED) and by initiating ophthalmologic
`consultation.
`
`Conjunctivitis
`
`Inflammation of the bulbar (covering the globe of the eye) and tarsal (lining
`the orbit) conjunctiva can be caused by viral or bacterial infections, trauma,
`toxic exposure, or autoimmune disease. Patients will complain of redness,
`pruritis, and a foreign body sensation that is often associated with discharge.
`Awakening in the'morning with eye crusting is a common complaint. Photo(cid:173)
`phobia and visual loss should not be present. Physical examination will reveal
`injection of the conjunctiva associated with lid edema. Discharge may be scant
`or may range from stringy and fibrinous to copious and purulent. If bacterial
`conjunctivitis is expected, gram stain and culture of the discharge is often
`revealing and can guide initiation of therapy. Most conjunctivitis seen in
`the ED is of viral origin and is self limited. However, the emergency practi(cid:173)
`tioner should be familiar with all causes because the clinical course of conjunc(cid:173)
`tivitis can lead to significant morbidity, depending on the cause.
`
`* Corresponding author.
`E-mail address: chris.mcstay@med .nyu.edu (C.M. McStay).
`
`0733-8627 /08/$ - see front matter © 2008 Elsevier Inc. All rights reserved.
`doi: 10.10 J 6/j.emc.2007 . I 0.004
`
`emed.theclinics.com
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`58
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`MUELLER & MCSTAY
`
`Viral conjunctivitis
`
`Most cases of viral conjunctivitis are caused by adenoviridae, but entero(cid:173)
`viruses and coxsackievirus may also be implicated. Conjunctivitis of viral
`origin is associated with significant redness and pruritis but should have
`less discharge than bacterial conjunctivitis. Chemosis and soft tissue swelling
`may be dramatic. The presence of preauricular lymphadenopathy, conjunc(cid:173)
`tivitis, and a viral prodrome are classic and frequently present. Disease often
`becomes bilateral in the first 24 to 48 hours [ 1,2].
`Viral conjunctivitis is contagious for almost 2 weeks; patients, family, and
`caretakers should be educated in appropriate infection-preventing measures,
`including hand washing. Treatment is symptomatic, with artificial tears,
`cold compresses, and vasoconstrictor-antihistamine combinations for severe
`pruritis.
`Fever, lymphadenopathy, and conjunctivitis with concomitant pharyngi(cid:173)
`tis constitute pharyngoconjunctival fever, caused by certa:in strains of adeno(cid:173)
`viridae. It can have a prolonged course (up to 2 weeks) and resolves
`spontaneously. Preceding upper respiratory infection supports this diagnosis.
`Epidemic keratoconjunctivitis is also caused by strains of adenoviridae
`(usually adenovirus type 8). It generally presents with thicker discharge and
`punctuate keratitis (corneal inflammation seen on fluorescein staining), and
`may result in conjunctiva! membrane formation with scarring. It has an
`even longer clinical course (up to 3 weeks) and corneal opacities may persist
`for months afterwards, affecting vision but ultimately resolving [1 ,2]. Consul(cid:173)
`tation with an ophthalmologist is recommended to decide whether steroids are
`indicated based on the presence and extent of the corneal involvement (Fig. 1).
`
`Bacterial conjunctivitis
`
`The pathogens most commonly associated with bacterial conjunctivitis
`include staphylococci, streptococci, N gonorrohae, and C trachomatis. In
`
`Fig. I. Conjunctivitis in Kawasaki disease. (Courtesy of Christopher McStay, MD, New York,
`NY.)
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`OCULAR INFECTION AND INFLAMMATION
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`59
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`contrast to viral conjunctivitis, discharge may be purulent, and crusting
`marked, typically with less pruritis. Patients who have bacterial pathogens
`may be more likely to report eye crusting that impedes opening each morn(cid:173)
`ing [3]. The process is more likely to be unilateral, but bilateral involvement
`does not rule out a bacterial cause. Acuity should be preserved and photo(cid:173)
`phobia absent; presence of either photophobia or decreased visual acuity
`should raise concern for corneal involvement. In this setting, the practitioner
`should look for signs of keratoconjunctivitis on slit lamp examination. Cor(cid:173)
`neal involvement portends a worse clinical course and is an indication for
`ophthalmologic consultation within the ED. Corneal opacification or hypo(cid:173)
`pyon may indicate a keratitis, which could be vision threatening.
`If a bacterial pathogen is suspected, treatment with topical drops (eg, qui(cid:173)
`nolone, trimethoprim-polymyxin) should be initiated for 7 to 10 days.
`Erythromycin ointment may also be used and is preferred in pediatrics for
`easier compliance. In contact lens wearers, pseudomonal coverage is essen(cid:173)
`tial and a quinolone is first line. Most cases of bacterial conjunctivitis
`resolve spontaneously in a week to 10 days, but antibiotics limit the duration
`and severity of disease [4]. Delaying antibiotic therapy (by 1-3 days) while
`awaiting gram stain and culture results appears to cause little harm and
`may reduce inappropriate antibiotic usage [5]. Ophthalmologic or ED fol(cid:173)
`low-up can be given, with antibiotic choice tailored to culture results. Sup(cid:173)
`portive care, including warm compresses and eye irrigation, are also
`indicated and are of equal importance. Eye patching should be avoided.
`A fulminant course of conjunctivitis in a young, sexually active patient or
`a neonate (24-48 hours postpartum) should raise the possibility of N gonor(cid:173)
`rohae as the causarive organism (Fig. 2). Discharge is often thick, yellowish
`green, and associated with significant underlying chemosis. Concomitant
`and symptomatic genitourinary symptoms may be present, but their absence
`does not rule out the diagnosis. Untreated, corneal involvement leading to
`rupture and endophthalmitis can ultimately occur. The decision as to
`
`Fig. 2. Fulminantgonococcal conjunctivitis. (From Goldman L, Ausiello D, editors. Cecil textbook
`of medicine. 22nd edition. Philadelphia: Saunders (an imprint of Elsevier); 2004; with permission.)
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`60
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`MUELLER & MCSTAY
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`whether to treat for gonococcal conjunctivitis is based on the history, fulmi(cid:173)
`nant course, and gram stain (chocolate agar cultures should also be sent).
`The practitioner should ask about sexual practices, partners, and symptoms
`[6]. Treatment is typically more aggressive, and hospital admission for intra(cid:173)
`venous and topical antibiotics may be warranted. For milder cases, one
`gram of ceftriaxone intramuscularly and appropriate coverage for concom(cid:173)
`itant Chlamydia infections (doxycycline or azithromycin) is indicated, in
`addition to ophthalmic antibiotics (bacitracin, erythromycin ointment). The
`high risk of corneal involvement warrants daily ophthalmologic follow-up.
`Sexual partners should seek appropriate medical care.
`
`Neonatal conjunctivitis
`
`In the neonatal period, conjunctivitis can occur and the causes are closely
`linked with postpartum age at presentation. Conjunctivitis in the first 36
`hours postpartum is often chemically induced, caused by silver nitrate
`used to prevent maternal transmission of gonococcus, Chlamydia, and other
`bacteria. Almost all infants treated with silver nitrate will develop a transient
`conjunctivitis that resolves in 1 to 2 days. Silver nitrate drops have largely
`been replaced by topical erythromycin in the United States. Neonatal symp(cid:173)
`toms occurring 24 to 48 hours postpartum are often due to N gu•10rrhoeae
`and should be treated with intravenous penicillin, or intra~uscular ceftriax(cid:173)
`one or cefotaxime, in addition to saline washes. Topical antibiotics are also
`indicated; penicillin or erythromycin ointment should be used every 2 hours
`while discharge persists. Blood cultures and cerebrospinal fluid gram stain
`and culture are also recommended but are controversial. These patients
`should also be treated for concomitant Chlamydia infection [7]. Other bac(cid:173)
`terial causes often occur on days 2 through 5 postpartum and treatment
`should be guided by gram stain (erythromycin ointment for gram-positive
`organisms, gentamicin or tobramycin drops for gram-negative organisms).
`Chlamydia! conjunctivitis often occurs on days 5 through 12 postpartum
`and should be treated with oral erythromycin for 2 weeks.
`
`Episcleritis
`
`Inflammation of the episclera and sclera may be difficult to distinguish.
`Because their causes and prognoses differ considerably, it is important to
`differentiate between the two. Both have significant association with sys(cid:173)
`temic disease, so primary care or ophthalmologic follow-up is indicated,
`based on patient comorbidities and severity of symptoms.
`Inflammation of the episclera, generally a benign, self-limited condition,
`presents as acute redness, tearing, pruritis, and foreign body sensation
`("grittiness"), with minimal-to-moderate pain in one or both eyes. It typi(cid:173)
`cally occurs in young adults and may be recurrent. Examination will reveal
`dilated episcleral vessels and an overall injected appearance. The differential
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`61
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`diagnosis also includes conjunctivitis, scleritis, keratitis, and glaucoma.
`A slit lamp examination should also be performed to rule out other common
`causes of ocular inflammation. A true change in acuity should prompt the
`clinician to consider other causes.
`To differentiate episcleritis from conjunctivitis, topical anesthetic should
`be applied and, under slit lamp, the ocular surface probed with a cotton-tip(cid:173)
`ped applicator. Conjunctiva! vessels will be highly mobile, whereas episcleral
`vessels should remain relatively fixed. In contrast to conjunctivitis, the find(cid:173)
`ings are generally limited to one segment of the bulbar surface. Conjunctiva!
`involvement may also occur in episcleritis but should be focal [8,9]. The epis(cid:173)
`cleral vessels should also blanch with application of a topical vasoconstrictor,
`which will help the clinician differentiate between episcleritis and scleritis.
`Distribution of the findings may be simple or nodular. In simple disease,
`sectoral involvement of the episclera is generally seen, with only part of the
`episclera involved. Nodular densities with surrounding injection of the
`sclera vessels appear in nodular episcleritis.
`Episcleritis is of idiopathic origin in two thirds of cases and generally im(cid:173)
`proves after a week or so. Supportive treatment includes the use of artificial
`tears. The use of topical corticosteroids and nonsteroidal anti-inflammatory
`drugs has been suggested but both are controversial. A recent study found
`the duration and severity of symptoms the same with topical ketorolac
`and artificial tears. Patients treated with ketorolac were more likely to com(cid:173)
`plain of stinging [10]. If treatment has failed by 2 weeks, ophthalmologic re(cid:173)
`ferral is indicated. In one third of cases, systemic disease is present.
`Evaluation for connective tissue, autoimmune vascular, or rheumatoid
`(more common in nodular subtypes) disease may be indicated. Rosacea
`and atopy are also commonly associated with episcleritis.
`Inflammation of the sclera itself has a more insidious onset, more pro(cid:173)
`nounced pain, and a greater number of complications and systemic asso(cid:173)
`ciations (Fig. 3). It is most often idiopathic in origin, but patients may
`
`Fig. 3. Scleritis. (From Sen HN, Suhler EB, Al-Khatib SQ, et al. Mycophenolate mofetil for the
`treatment of scleritis. Ophthalmol 2003; I 10(9): 1750-5; with permission.)
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`62
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`MUELLER & MCSTAY
`
`give a history of recent eye surgery, infection, new malignancy, or new
`drug therapy. Patients may describe the onset of progressive pain and vi(cid:173)
`sual deterioration over the course of days to weeks. Pain may radiate from
`the eye to the face and may be intense and boring in nature. Photophobia,
`tearing, and pain with ocular motion may be present. Patients may notice
`marked scleral swelling and globe tenderness if the anterior sclera is in(cid:173)
`volved. On examination, swelling may be focal and limited to one part
`of the globe or may involve the entire visible sclera. The overlying epis(cid:173)
`cleral and conjunctiva! vessels may be dilated and inflamed, making the
`diagnosis difficult. Engorgement of vessels with a surrounding violaceous
`hue is indicative of scleritis. Topical vasoconstrictors will blanch the con(cid:173)
`junctiva! and episcleral vessels, but the sclera itself should remain swollen
`and inflamed. Findings adjacent to the cornea may also show a keratitis.
`Areas of necrosis should raise the possibility of an infectious cause of
`scleritis, including tuberculosis. Necrotizing scleritis will also reveal areas
`of capillary nonperfusion and represents an immediate threat to globein(cid:173)
`tegrity [8,9].
`In patients who do not have involvement of the anterior sclera, posterior
`scleritis is easily missed. Patients may have similar presenting symptoms and
`may also have proptosis. Alternatively, patients may present with minimal
`pain, complaining only of visual loss in a rare variant of necrotizing poste(cid:173)
`rior scleritis. Concomitant, secondary uveitis, either anterior or posterior, is
`not uncommon and the ED practitioner can easily be fooled into thinking
`this is the primary diagnosis. Retinal detachment or other retinal pathology
`may also accompany posterior scleritis, but the painful nature of the condi(cid:173)
`tion should initiate a more thorough workup. Diagnosis by ultrasound is
`preferred. CT with intravenous contrast may be helpful in these cases and
`can show a thickened scleral component. MRI is also useful but is not rou(cid:173)
`tinely available in the ED [8,9,11].
`One half of all cases of scleritis are associated with systemic disease. The
`most commonly associated disease is rheumatoid arthritis. Other associa(cid:173)
`tions include Wegener's grairnlomatosis, relapsing polychondritis, systemic
`lupus erythematosus, and polyarteritis nodosa. Workup for these conditions
`can begin in the ED or with the patient's primary care provider. All patients
`should have screening tests for syphilis. Tuberculosis and Hansen's disease
`can also cause a granulomatous scleritis.
`Complications of scleritis include necrosis, scleral thinning, and visual
`loss. Treatment with oral indomethacin is the standard of care in patients
`who have active anterior scleritis. Necrotizing or posterior scleritis should
`be treated in concert with ophthalmologic consultation; treatment should in(cid:173)
`clude systemic and intraocular steroid injection. If disease is mild, with no
`tenting of the sclera, and with no secondary iritis or uveitis, treatment can
`be deferred, with close ophthalmologic follow-up. If an infectious cause is
`suspected (postsurgical patients, necrosis, immunocompromised hosts),
`treatment decisions should be made with an ophthalmologic consultant.
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`OCULAR. JNFECTfON AND INFLAMMATION
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`63
`
`Anti".Jiotic penetration into the sclera is generally poor, owing to its avascu(cid:173)
`Iar nature [8,9].
`
`I(eratitis
`
`Inflammation of the cornea with or without violation of its epithelium
`constitutes keratitis. Patients will present with an acutely red, painful eye
`and often complain of foreign body sensation, photophobia, tearing, and vi(cid:173)
`sion change. Infectious causes may be associated with secondary lid edema,
`conjunctiva! reaction, hypopyon, and anterior chamber reaction. Photopho(cid:173)
`bia is due to ciliary spasm . Keratitis is most often viral or bacterial in origin,
`but exposurt to intense ultraviolet light, chemicals, and contact lenses may
`be implicated. Contact lens use itself imparts a 10-fold risk of developing an
`infectious keratitis. Corneal abrasions may accompany (or mimic) a keratitis
`because of excessive rubbing or scratching of the affected eye. Prompt diag(cid:173)
`nosis, treatment, and identification of cause are paramount to prevent vision
`loss due to ulceration, necrosis, and scarring [12,13].
`Patients should receive a full ophthalmologic examination. The presence
`of corneal opacification, ulceration, hypopyon, or other irregularities
`strengthen the diagnosis. Fluorescein staining is essential to evaluate for
`epithelial disruption, and its pattern can also help reveal the cause.
`
`Viral !ceratitis
`
`The herpesviridae (herpes simplex virus [HSV]-1, HSV-2, varicella zoster
`virus [VZV], Epstein-Barr virus [EBY], cytomegalovirus [CMY]) are the
`viral agents most commonly associated with keratitis. Their clinical presen(cid:173)
`tations and treatments have considerable overlap.
`HSV can present with ocular involvement in primary or recurrent infec(cid:173)
`tions. Primary infections often occur in neonates (by way of maternal deliv(cid:173)
`ery with active lesions) or at 6 months of age (by way of saliva), when
`maternal antibodies no longer protect the infant from HSV transmission.
`A follicular conjunctivitis with the presence of lid or periorbital vesicles
`should alert the clinician to HSY infection. Slit lamp examination may
`show staining of the cornea in a dendritic pattern. Ophthalmologic antivi(cid:173)
`rals and systemic antivirals (acyclovir) should be initiated promptly. Corneal
`involvement may lag behind and persist after conjunctiva! and dermatologic
`involvement.
`Most HSV pathology is caused by recurrent disease and may present
`without dermatologic findings. Patients may complain simply of eye pain,
`redness, and change in vision. Slit lamp examination should reveal a corneal
`ulcer with fluorescein uptake in a characteristic dendritic branching pattern
`that extends outward. Sometimes, the ulcer alone may stain with fluorescein,
`without staining of the advancing dendritic cells. In these cases, ophthalmo(cid:173)
`logic consultation for rose bengal or other dye staining will reveal the
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`64
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`MUELLER & MCSTAY
`
`pattern. Advanced or recurrent disease may lead to stromal (subepithelial
`corneal matrix) involvement with opacification, thinning, and edema present
`on slit lamp examination [14].
`The cornea should be debrided of infected cells using a cotton applicator,
`starting with the ulcer. This procedure can be done by the ED practitioner
`or, preferably, by the ophthalmologic consultant. Pharmacologic treatment
`of HSV keratitis consists of ophthalmic antiviral drops (acyclovir or idoxur(cid:173)
`idine) or systemic antiviral medication (oral acyclovir) . ED ophthalmologic
`consultation is indicated and close follow-up or admission is appropriate.
`Topical drops may be associated with corneal toxicity and could prolong
`healing, so some clinicians prefer oral agents. Some research suggests that
`topical ganciclovir gel may also be effective. Daily ophthalmologic follow(cid:173)
`up or admission is indicated (Fig. 4) [14,15].
`Reactivation of herpes zoster virus in the trigeminal distribution can
`cause significant ocular disease, including a keratitis. Zoster is often pre(cid:173)
`ceded by a viral prodrome of malaise, fever, headache, and neuralgia. Ocu(cid:173)
`lar and periorbital disease can then follow, with the conjunctiva, lid, and
`periorbital skin showing crops of vesicular lesions. The rash is typically uni(cid:173)
`lateral, does not cross the midline, and involves only the upper portion of
`the lid. The presence of vesicular lesions on the tip of the nose (nasociliary
`branch of the ophthalmic division of trigeminal Vl), or Hutchinson's sign,
`should prompt the clinician to evaluate the cornea for involvement. Disease
`can be marked and conjunctiva! vesicles with scarring can occur [16].
`Corneal involvement usually occurs after other manifestations and may
`present after other symptoms have resolved, or separately from them. Fluo(cid:173)
`rescein staining will reveal dendritic branching that is thicker and more
`rope-like than the lace-like pattern ofHSV keratitis. Terminal bulbs, present
`in HSV keratitis, should be absent in VZV. Fluorescein uptake is much less
`pronounced on the VZV dendrites, so inspection under slit lamp must be
`
`Fig. 4. HSV keratitis with characteristic dendritic pattern of staining. (From Goldmi n L,
`Ausiello D , editors. Cecil textbook of medicine. 22nd edition. Philadelphia: Saunders (an im(cid:173)
`print of Elsevier); 2004; with permission.)
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`OCULAR INFECTION AND INFLAMMATION
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`65
`
`ca1eful so as to avoid missing the lesions. Complications include uveitis and
`keratitis (even bacterial coinfection). Ophthalmologic consultation is indi(cid:173)
`cated to start oral versus topical antivirals. Steroids are controversial and
`should not be started by the emergency practitioner [15,16].
`EBV and CMV can also cause a keratitis, but this is much more likely in
`the immunocompromised host. A dendritic corneal branching pattern is of(cid:173)
`ten seen with EBV and the conjunctiva and soft tissue may be affected as in
`HSY infection. Diagnosis is made by way of polymerase chain reaction of
`infected cells. Supportive care is indicated; the use of systemic antivirals is
`controversial. In the ED, where it will be difficult to distinguish cause, start(cid:173)
`ing the patient on oral acyclovir may be appropriate. CMV keratitis has
`been reported but is uncommon. Its corneal findings are almost identical
`to vzv t11].
`
`Bacterial keratitis
`
`The propensity to cause visual loss makes bacterial keratitis an ophthal(cid:173)
`mologic emergency. Its incidence is increasing in the setting of contact lens
`use. Most cases are caused by staphylococcal species, but in contact lens
`wearers, pseudomonas species may predominate. Both organisms have in(cid:173)
`creased because of contact lens use; in the non-contact lens wearer, strepto(cid:173)
`coccal species are common. In immunocompromised patients, M oraxella
`catarrhalis should be considered. Patients will complain of pain, tearing,
`and decreased vision. N gonorrohae and C trachomatis should be considered
`in the sexually active patient, particularly if conjunctivitis is present. Depend(cid:173)
`ing on the causative organism and the condition of the underlying cornea,
`physical examination may reveal a corneal ulcer, with or without surrounding
`stromal involvement. The overlying epithelium may be absent. The cornea
`will often be opacified and edematous, and hypopyon may be present. The
`surrounding conjunctiva may show injection with vessel dilatation [18].
`Topical aminoglycosides, quinolones, or cephalosporins should be used,
`based on history and gram stain. If gram stain is unavailable or the causative
`organism is unlikely to be discovered in the ED, broad-spectrum coverage
`using two antibiotics should be initiated with rapid alternating of agent
`(eg, two drops aminoglycoside followed by two drops of cephalosporin every
`5 minutes for the first hour followed by applications every 15 minutes to 1
`hour around the clock). Alternatively, quinolone monotherapy may be effec(cid:173)
`tive. ED ophthalmologic consultation should pe obtained and the patient
`admitted [18].
`
`Keratitis due to light exposure
`
`Prolonged exposure to ultraviolet light, or brief exposure to intense ultra(cid:173)
`violet flashes, can produce a photokeratitis or photokeratoconjurictivitis of
`noninfectious origin. Patients may complain of eye pain, change in vision,
`
`Mylan Exhibit 1060
`Mylan v. Regeneron, IPR2022-01226
`Page 11
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`66
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`MUELLER& MCSTAY
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`and redne~s. The staining pattern is generally punctuated with some degree of
`corneal opacification. Ancillary signs of infection (purulent discharge, cellu(cid:173)
`litic changes) are generally absent. In punctuate keratitis due to welding expo(cid:173)
`sure, symptoms begin hours after exposure. In patients who have had
`prolonged ultraviolet exposure (ie, snow blindness), time to onset may be vari(cid:173)
`able [19]. Topical antibiotics are indicated to prevent bacterial superinfection.
`
`Uveitis
`
`Understanding the anatomy of the uvea is essential in diagnosing and
`treating the different forms ofuveitis. The uvea is the middle eye. Anteriorly,
`this includes the iris and ciliary body, with the posterior reflection of these
`structures known as the choroid. Inflammation of the anterior structures
`presents with anterior chamber reaction and is easily seen and diagnosed in
`the ED. Inflammation of the anterior chamber (anterior uveitis) is a much
`more common presentation in the ED than middle or posterior involvement.
`Posterior involvement is synonymous with retinitis. Inflammation of the
`uveal structures can be a primary, idiopathic process, or can occur secondary
`to other ophthalmologic infections or inflammatory conditions.
`
`Anterior uveitis
`
`Patients who have anterior uveitis (commonly called iritis) can present
`with a remarkable range of complaints, from mild visual disturbance to
`severe pain and loss of vision. Approximately 50% of cases are considered
`idiopathic and the next most common cause is thought to be HLA-B27
`associated. Patients typically present with eye pain, redness, decreased
`vision, photophobia, and headache. The symptoms may mimic glaucoma,
`which must be ruled out first by measuring intraocular pressure. When pres(cid:173)
`ent, scleral injection and anterior chamber cells and flare make the diagnosis
`clear. The limbus is characteristically injected (known as ciliary flush) and
`the pupil is often constricted. In idiopathic anterior uveitis, small keratic
`precipitates may be present in the anterior chamber. Larger, granulomatous
`or clumpy precipitates should lead the physician to consider specific causes,
`including syphilis, toxoplasmosis, and tuberculosis. Hypopyon, when pres(cid:173)
`ent, should prompt the clinician to think of HLA-B27-associated disease,
`and referral to a rheumatologist is appropriate [20].
`In patients who have HIV, the antibiotic rifabutin and the antiviral cido(cid:173)
`fovir should be considered as possible causes. Both have been associated
`with anterior uveitis, and withdrawal of the drug, or reduction of the
`dose, is often enough to stop or reduce symptoms [21]. Anterior chamber
`react