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46 The Nurse Practitioner -  Vol. 40, No. 12
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46 The Nurse Practitioner -  Vol. 40, No. 12
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The Nurse Practitioner -  December 2015  47
cular pathologies that require specialized treat-
ment and referral to ophthalmology include:
acute angle-closure glaucoma (AACG), globe
rupture, uveitis, keratitis, scleritis and episcleritis, and
orbital cellulitis.1,2 A thorough history and physical exam
must be performed to differentiate these conditions from
common conjunctiva infections and eyelid abnormali-
ties.3 (See History and physical exam.) NPs should main-
tain a high level of suspicion during the history and
physical exam and ask key questions that can lead to the
correct diagnosis and management of these ocular pa-
thologies. (See Physical findings that warrant an ophthal-
mology referral.)
  AACG
AACG is an uncommon form of glaucoma resulting from
the rapid and complete closure of the angle between the iris
and the trabecular meshwork of the anterior chamber.1 This
closure is mediated by the anterior displacement of the lens
that prevents the outfl ow of aqueous humor, thereby increas-
ing pressure within the anterior chamber. The rise in intra-
ocular pressure (IOP) is abrupt, causing pain, nausea, and
colored halos or rainbows around light.4 Physical fi ndings
are an injected eye with an opaque cornea, IOP greater than
30 mm Hg, shallow anterior chamber, and a characteristic
middilated pupil.5 (See Acute angle-closure glaucoma.) Optic
nerve damage and blindness can result if untreated, and this
condition can occur suddenly as the result moving from an
illuminated room to a dark room with dim lighting or in
patients taking specifi c drugs, such as sulfa drugs and topi-
ramate (both drugs cause swelling of the ciliary body).5
An immediate referral to ophthalmology is necessary if
AACG is suspected. Treatment must be initiated promptly in
the primary care offi ce or ED with an oral dose of acetazol-
amide, and IOP should be measured until the ophthalmologist
can assess the patient.5 Ocular solutions that decrease aqueous
humor production and outfl ow via the trabecular meshwork
are then used with one drop of timolol maleate, apraclonidine,
and pilocarpine.5 Each drop is given 1 minute apart and is
repeated at 5-minute intervals.5 Timolol and apraclonidine
should be used with caution in patients with chronic obstruc-
tive pulmonary disease, asthma, or hypotension.4 Timely treat-
ment prevents permanent vision loss. Possible complications
include repeat episodes, corneal pathologies (edema and cata-
racts), and iris atrophy.5
The American Academy of Ophthalmology (AAO)
does not recommend any specifi c treatment option for
AACG.6 Aqueous humor formation suppression (timolol
and acetazolamide) may be ineffective due to ciliary body
ischemia from marked IOP.6 Instead, ophthalmologic
surgical intervention (iridotomy or lens removal) may be
needed.6 Per the AAO, the level of evidence to support
By Anthony Ossorio, MSN, RN, FNP-BC
2.0
CONTACT HOURS
O
Illustration by Todd Davidson / Almay (c)
Abstract: Severe red eye conditions can be the result of intraocular infl ammation, corneal
insults or infl ammation, and acute glaucoma. These pathologies require the knowledge and
assessment tools of an ophthalmologist. This article will discuss red eye emergencies that the
NP should promptly recognize and refer to ophthalmology.
Keywords: acute angle-closure glaucoma, episcleritis, globe rupture, keratitis, orbital cellulitis, scleritis, uveitis
Red eye emergencies
in primary care
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The Nurse Practitioner -  December 2015  47
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48 The Nurse Practitioner -  Vol. 40, No. 12
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Red eye emergencies in primary care
surgical interventions is A:III, which denotes utmost
clinical importance with evidence obtained from descrip-
tive studies, case reports, and expert committees and
 organizations.6
  Globe rupture
Any eye injury, corneal abrasion, or traumatic orbital
wound should alert the NP to the possibility of globe rup-
ture requiring immediate treatment by an ophthalmologist.
Globe rupture is the interruption in the integrity of the
cornea or sclera, which, if not treated immediately, can cause
intraocular infection leading to blindness.5 Symptoms that
alert the NP to globe rupture include: severe pain, decreased
visual acuity, hyphema (blood in anterior chamber), loss of
anterior chamber depth (aqueous humor escape), and a
teardrop-shaped pupil pointing toward the injury (see Globe
rupture).5
Assessing globe rupture requires the Seidel test: fl uores-
cein stain directly to the injury site and wood's lamp exam.5
The Seidel test is positive if the fluorescein stain dilutes
within the aqueous, appearing as a darker formation within
the bright green fl uorescein on wood's lamp exam.5
Treatment includes placement of an eye shield to the
affected eye and computed tomography (CT) images
of the head and orbits (coronal and axial views) to assess
for open globe injuries, foreign bodies, or orbital wall
fractures.7 To help prevent increases in IOP, the patient's
head should be elevated and the patient should be comfort-
able. Pharmacologic treatment includes an antiemetic and
an analgesic for pain. Antibiotic coverage is based on em-
piric guidance and should be started with a cephalosporin
(such as cefazolin) and a fl uoroquinolone (such as cipro-
fl oxacin) I.V. infusion to cover against Streptococcus, Staph-
ylococcus aureus, and Staphylococcus epidermidis species.5
Alternative regimens include intravitreal (intraocular in-
jection administered by the ophthalmologist) and I.V.
antibiotics (such as vancomycin).8
  Uveitis
Uveitis is an infl ammatory process with immune complex
deposition within the blood vessels and the structures of the
anterior uveal tract.9 This process is usually associated with
systemic autoimmune processes or opportunistic infections
within the compromised host. Uveitis has several etiologies:
trauma, the human leukocyte antigen (HLA)-B27 genotype
(associated with ankylosing spondylitis,
Reiter syndrome, infl ammatory bowel
disease [IBD], and psoriatic arthritis),
Behcet disease (triad of uveitis, mouth,
and genital lesions), juvenile rheumatoid
arthritis, and masquerade syndrome
(associated with lymphoma, leukemia,
and malignancies of the choroid).9
Anterior uveitis has two progressions: granulomatous
and nongranulomatous.9 Nongranulomatous uveitis is not
associated with pathologic organisms and is evidenced by
small, white keratic precipitates (KPs) with no iris nodules.9
Granulomatous uveitis follows a microbial infection
 (cytomegalovirus, tuberculosis, syphilis, and toxoplasmosis)
and is associated with large, mutton-fat KPs and iris nodules.9
  History and physical exam1
History
Physical exam
-   Onset: sudden or gradual?
-   Other family members affected with same symptoms?
-   Is the patient using any medications?
-   Was there any trauma to the eye?
-   Is one (both) eye(s) affected?
-   Does the patient use contact lenses, and did the patient
sleep in the lenses?
-   Did the patient have recent eye surgery?
-   Is there decreased vision or pain?
-   Is there any discharge from the affected eye(s)?
-   Is the discharge scant, profuse, watery, or purulent?
-   Does the eye itch?
-   Is there sensitivity to light?
-   Are there any other symptoms associated with the eye?
-   Visual acuity
-   Confrontation testing (peripheral vision)
-   Adnexal assessment of lids, lashes, and surrounding tissues
-   Assessment of the sclera and conjunctiva
-   Extraocular movements
-   Testing of pupils for direct and consensual responses
-   Inspection of the cornea and iris
-   Assessment of the anterior chamber (penlight and slit-lamp
evaluation)
-   Fluorescein stain if corneal integrity is compromised
-   Lens assessment for clarity
-   Fundoscopic exam
-   Tonometry
Assessing globe rupture requires the Seidel
test: fl uorescein stain directly to the injury
site and wood's lamp exam.
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Red eye emergencies in primary care
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The Nurse Practitioner -  December 2015  49
Patients with anterior uveitis present with: ciliary fl ush,
unilateral pain, redness, photophobia, and acute vision loss.1
Nongranulomatous uveitis symptoms progress acutely, with
circumferential erythema (ciliary fl ush) from the increased
permeability of the uveal vessels.9 Uveitis results in infl am-
matory cells within the anterior chamber that produce the
"cell and fl are" within the aqueous when examined via the
slit lamp.9 KPs can be seen via penlight and magnifying lens
implanted on the corneal epithelium.9 (See Uveitis.)
Treatment must be initiated by the ophthalmologist and
usually takes the form of topical and systemic corticosteroids.1
  Physical fi ndings that warrant
an ophthalmology referral1
Reduced visual acuity
Occurs with serious ocular disease, such as an
infl amed cornea, iritis, or glaucoma. Reduced visual
acuity never occurs in simple conjunctivitis.
Ciliary fl ush
A pattern of injection in which the redness is most
pronounced in a ring at the transition zone between
the cornea and the sclera (limbus), found in uveitis,
corneal infl ammation, or acute glaucoma.
Photophobia
Unusual sensitivity to light that can signify uveitis or
corneal infl ammation/injury.
Severe pain/foreign body sensation
Inability to keep the eye open, indicating corneal
infl ammation or ulceration, uveitis, scleritis, or
glaucoma.
Corneal opacity
Keratic precipitates or cellular deposits on the cornea
within anterior chamber suggestive of uveitis.
Diffuse haze covering cornea suggestive of edema
(acute glaucoma).
Corneal injury
Found on fl uorescein stain (bright green area) or an
irregular light refl ex on penlight exam.
Fixed pupil
Uveitis typically presents with one pupil smaller than
the other due to refl ex spasm of the iris muscle and/or
infl ammatory adhesions (keratic precipitates) to the
site. Acute glaucoma presents with single, fi xed/
middilated pupil that is slightly irregular.
Headache and nausea
Indicates acute angle-closure glaucoma.
Purulent discharge and hyperemia
Suggestive of gonococcal conjunctivitis.
Shallow anterior chamber
Shine penlight from temporal side of eye in a plane
parallel to iris, looking at nasal side of iris, if two-thirds
or more of nasal iris is in shadow, the chamber is
probably narrow.
Increased IOP
Mean IOP is 15 mm Hg (range: 10-21 mm Hg),
elevations above these measurements signify
increased IOP: acute angle glaucoma or iridocyclitis.
Proptosis with painful EOM
Forward displacement of the globe, suggestive of
periorbital and cavernous sinus disease. Best assessed
by tilting chin up and assessing orbits inferiorly from
the chin.
  Acute angle-closure glaucoma
Source: Gerstenblith AT and Rabinowitz MP. The Wills Eye Manual: Offi ce
and Emergency Room Diagnosis and Treatment of Eye Disease. 6th.
Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
 Globe rupture
Source: Gerstenblith AT and Rabinowitz MP. The Wills Eye Manual: Offi ce
and Emergency Room Diagnosis and Treatment of Eye Disease. 6th.
Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
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50 The Nurse Practitioner -  Vol. 40, No. 12
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Red eye emergencies in primary care
Anterior segment inflammation is typically treated with
dexamethasone sodium phosphate 0.1% solution.10 Cholin-
ergic agonists such as atropine 0.5% to 1% eye drops are used
to block the neurotransmission sites in the iris sphincter,
which relieves pain by  immobilizing the iris, preventing adhe-
sions of the iris, and stabilizing the blood-aqueous barrier to
prevent further leakage of cellular material.9
  Keratitis
Keratitis is infl ammation and/or infection of the cornea,
which stems from infectious (bacterial, viral, fungal, or
protozoal) or noninfectious (chemical injuries, dry eyes,
infl ammatory disorders, or severe allergies) causes.11 Patients
with corneal ulcerations present with hyperemia, mucous
secretions within the anterior chamber (hypopyon), and
corneal opacities.1 Patients report pain, photophobia, tear-
ing, and decreased vision.12
Bacterial infections cause epithelial ulceration from
cytokine infiltration reaching Bowman's layer (basement
membrane).13 Corneal opacity (typically a round, white
spot) is the clinical evidence of bacterial keratitis in
 association with red eye, photophobia, and foreign body
sensation.13 These findings are confirmed with fluores-
cein stain and penlight exam. (See Bacterial keratitis.)
Common causes include trauma, recent surgery, and
contact lens use (especially overnight use).13 The most
common organisms involved include S. aureus (MRSA),
Pseudomonas aeruginosa, Pneumococcus, Moraxella, and
staphylococci species.13 Treatment includes the adminis-
tration of fluoroquinolone eye drops.14
Fluoroquinolone eye drops are given an evidence rating
of A:I, noting that they are of key clinical importance and
derived from meta-analysis of randomized controlled trials
with a  low-risk bias.15 Alternatives to fluoroquinolone
therapy include tobramycin solution.15 Referral to an oph-
thalmologist is indicated to ensure proper management.
Gonococcal conjunctivitis is a form of conjunctivitis
that can be sight threatening.13 Transmitted through hand-
genital-eye contact, the bacteria spreads rapidly and can
easily penetrate the corneal surface.13 Symptoms include:
profuse purulent ocular discharge (greater than other
forms of conjunctivitis), conjunctival chemosis, irritation,
preauricular lymphadenopathy, and tenderness to palpa-
tion within 12 hours of infection.13 There may or may not
be concurrent urethritis. If left untreated, corneal perfora-
tion and melting can occur, which makes this a medical
emergency.13 Treatment includes an initial I.M. injection
of ceftriaxone and saline lavage.13 Alternative treatments
include azithromycin as a single-oral dose or doxycycline
therapy for 7 days.15 These treatments are endorsed by AAO
(A:II), which evidences clinically-signifi cant, high-quality
systematic reviews of case-control cohort studies.15
Herpes keratitis takes the form of herpes simplex (HSV)
and herpes zoster (HZV) ocular infections. Viruses colonize
the trigeminal nerve ganglion, which lead to concurrent
reinfections.14 Outbreaks occur with fevers, exposure to
sunlight, stress, or immunocompromised states.14 Patients
typically present with fever, malaise, headache, and peri-
ocular burning, which herald a vesicular, then pustular, then
crusting confl uent ulceration to the trigeminal dermatome.16
Patients may report history of HSV infection, and exam
reveals watery discharge, ciliary fl ush, and decreased visual
acuity.16 Fluorescein staining reveals corneal punctate kera-
titis with both HSV and HZV; however, HSV merge to form
the characteristic branching "dendritic" ulceration.16 Ocular
 Uveitis
Source: Garg SJ. Color Atlas and Synopsis of Clinical Ophthalmology Wills
Eye Institute - Uveitis. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
 Bacterial keratitis
Source: Rapuano CJ. Color Atlas and Synopsis of Clinical Ophthalmology Wills Eye
Institute - Cornea. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
Copyright (c) 2015 Wolters Kluwer Health, Inc. All rights reserved.

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Red eye emergencies in primary care
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The Nurse Practitioner -  December 2015  51
signs of viral infection include conjunctivitis, episcleritis,
and uveitis.14
Treatment for corneal HSV infections includes cor-
neal debridement, antiviral therapy with  trifl uridine eye
drops until reepithelialization occurs (21 days).14 Ganci-
clovir 0.15% ophthalmic gel 1 drop 5 times daily until
ulceration heals, then 3 times daily for 7 days.17 Cortico-
steroid eye drops, prescribed by the ophthalmologist, are
usually added to the treatment regimen.11 Treatment of
HZV infection also  includes high-dose oral acyclovir
therapy.14 Alternative treatments to oral therapy are indi-
cated if the patient has had multiple HSV keratitis infec-
tions indicating possible  acyclovir resistance.17 Systemic
treatment with foscarnet is advised if resistance is sus-
pected.17 AAO supports these treatment regimens with
level A:I evidence, indicating systematic  reviews of ran-
domized  controlled trials.17
Chemical injuries are another source of emergent
corneal injury, with alkali substances being more injurious
than acidic contacts.5 The injury's severity is variable de-
pending on the pH concentration and chemical nature of
the solution.5 Photophobia, foreign body sensation, severe
pain, and blurred vision ensue almost instantaneously
after exposure to the chemical.5 Patients will constantly
blink (refl ex blepharospasm) in almost all chemical inju-
ries.5 Severe alkali exposures cause conjunctival and scler-
al ischemia, causing a "porcelainized" corneal appearance.5
(See Chemical burn.)
A visual acuity exam should not be performed in this
setting, and immediate irrigation should ensue. Ocular
pH should be tested by placing pH paper between the
eyelid and the globe; normal ocular pH is "neutral" be-
tween 7.0 and 7.3.5 This pH measurement is used to guide
therapy. Before irrigation, an ocular anesthetic such as
tetracaine should be instilled and a Morgan lens placed to
irrigate with 0.9% sodium chloride or lactated Ringer's
solution.5 Irrigation should continue until pH returns to
7.0.5 An antibiotic such as ofl oxacin drops can be instilled
after stabilization occurs to prevent infection.5
  Scleritis and episcleritis
Scleral inflammation comes in the form of episcleritis
 (superfi cial) and scleritis (deeper and more destructive)
infl ammation.18 Both processes are usually associated with
systemic autoimmune processes; however, episcleritis is more
benign and can be the result of dry eye and viral infections.18
Approximately 39% to 50% of cases are associated with
systemic disease, with the most common tissue disorders
being rheumatoid arthritis and Wegener granulomatosis.19
Scleritis carries more ocular risks, including keratitis, uveitis,
and glaucoma.18 The majority of patients have underlying
autoimmune diseases, such as rheumatoid arthritis, IBD, or
systemic lupus erythematosus.18
Immunoglobulin E degranulation, systemic vasculitic
diseases (tuberculosis and syphilis), and granulomatous
diseases are the causes of immune-mediated episcleritis.18
Episcleritis presents with bilateral ocular pain and periph-
eral injection pattern with minimal lacrimation or photo-
phobia.18 (See Episcleritis.)
Scleritis presents with a deeper red injection to all layers
of the sclera and globe, edema, and ocular tenderness.20 (See
Scleritis.) Scleritis can lead to necrotizing scleral ulceration
and perforation; therefore, ophthalmologic consult is re-
quired.20 Instillation of topical phenylephrine is utilized to
differentiate scleritis from episcleritis or conjunctivitis. If the
diagnosis is episcleritis or conjunctivitis, hyperemia clears;
 Chemical burn
Source: Chern KC, Saidel MA. Ophthalmology Review Manual. 2nd.
 Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
 Episcleritis
Source: Rapuano CJ. Color Atlas and Synopsis of Clinical Ophthalmology
Wills Eye Institute - Cornea. 2nd ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2012.
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52 The Nurse Practitioner -  Vol. 40, No. 12
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Red eye emergencies in primary care
however, if deeper layers are affected, scleral  erythema will
not clear, and scleritis should be suspected.18
Treatment of episcleritis involves polyethylene glycol
400 and propylene glycol eye drops as needed, oral nonste-
roidal anti-inflammatory drugs (NSAIDs), and topical
corticosteroids as needed.18 Scleritis involves the use of
NSAIDs and oral prednisone initially.18 Bolus or pulse
therapy with I.V. glucocorticoids may be given followed by
oral prednisone.21 Ophthalmologic referral is necessary for
both to ensure proper diagnosis and management.18
  Orbital cellulitis
Orbital cellulitis is an infection that involves the orbit
(fat and ocular muscles).22 It is differentiated by preseptal
(infection involving tissue anterior to the orbital septum)
and periorbital (infection of tissue posterior to the sep-
tum).22 (See Preseptal cellulitis.) Orbital cellulitis stems
from unresolved ethmoid sinus infection, orbital trauma,
and ocular surgery.22 Preseptal cellulitis stems from: si-
nusitis, soft tissue infection of face or eyelid, trauma,
insect bites, and foreign bodies.22 Bacterial causes include
staphylococcus species S. aureus, S. epidermidis, and the
following streptococcus species:  Streptococcus anginosus,
Streptococcus pneumoniae,  Haemophilus infl uenzae, Mo-
raxella catarrhalis, and group AB-hemolytic streptococci.23
Without proper and rapid treatment, preseptal presenta-
tions can result in orbital infections, and orbital infections
can cause blindness, meningeal infections, optic nerve
involvement, and cavernous sinus thrombosis.22 Patients
with preseptal cellulitis present with lid swelling, conjunc-
tival congestion, and pain. Patients with orbital cellulitis
present with the same symptoms; however, they also have
proptosis, increased IOP, and pain with extraocular move-
ments (EOM).22
Empiric treatment of preseptal cellulitis includes oral
clindamycin alone or in conjunction with amoxicillin-
clavulanate or cefpodoxime twice daily with close follow
up.22 Orbital cellulitis requires CT imaging, hospitalization,
and I.V. antibiotics, including: vancomycin, ceftriaxone, and
metronidazole.22 Alternative treatment regimens include
inpatient versus outpatient antibiotic therapy.24 A referral
to the ophthalmologist is indicated to ensure that there are
no intraocular pathologies associated with the orbital infec-
tions.22
 An increased suspicion and rapid recognition of these
red eye emergencies by nurse practitioners in all practice
settings will help ensure improved patient outcomes with
the best chances to preserve eyesight. Although many ocu-
lar conditions can be treated in the primary care offi ce, there
are these select cases that require specialist consultation.
Primary care NPs should never hesitate to call on the ex-
perience and knowledge of a  trusted ophthalmologist to
ensure proper patient care.
REFERENCES
 1.  Harper RA. The red eye. In: Harper RA, ed. Basic Ophthalmology. 9th ed.
San Francisco, CA: American Academy of Ophthalmology; 2010:73-95.
 2.  Cronau H, Kankanala RR, Mauger T. Diagnosis and management of red eye
in primary care. Am Fam Physician. 2010;81(2):137-144.
 3.  Harper RA. The eye examination. In: Harper RA, ed. Basic Ophthalmol-
ogy. 9th ed. San Francisco, CA: American Academy of Ophthalmology;
2010:1-29.
 4.  Harper RA. Chronic vision loss. In: Harper RA, ed. Basic Ophthalmology.
9th ed. San Francisco, CA: American Academy of Ophthalmology; 2010:
47-71.
 5.  Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007;
76(6):829-836.
 Preseptal cellulitis
Source: Dinn RB, Graff M. Preseptal cellulitis. University of Iowa Health Care:
Opthalmology and Visual Sciences. Updated February 2, 2010. Used with
permission from EyeRounds.org and The University of Iowa: www.EyeRounds.org.
 Scleritis
Source: Rapuano CJ. Color Atlas and Synopsis of Clinical Ophthalmology
Wills Eye Institute - Cornea. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2012.
Copyright (c) 2015 Wolters Kluwer Health, Inc. All rights reserved.

Page 8
Red eye emergencies in primary care
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The Nurse Practitioner -  December 2015  53
 6.  Primary Angle Closure. Preferred Practice Pattern. American Academy of
Ophthalmology 2010 Oct. (Clinical Practice Guideline.)
 7.  Pieramici DJ. Open-globe injuries are rarely hopeless: Managing the open
globe calls for creativity and fl exibility of surgical approach tailored to the
specifi c case. Review of Ophthalmology. 2005. www.revophth.com/content/d/
retinal_insider/i/1315/c/25307/.
 8.  Durand ML. Endophthalmitis. Clin Microbiol Infect. 2013;19(3):227-234.
 9.  Alexander KL, Dul MW, Lalle PA, Magnus DE, Onofrey B.American Opto-
metric Association. Optometric clinical practice guideline. 2004: Care of the
patient with anterior uveitis. www.aoa.org/documents/CPG-7.pdf.
10.  Cunningham ET Jr, Wender JD. Practical approach to the use of corticoste-
roids in patients with uveitis. Can J Ophthalmol. 2010;45(4):352-358.
11.  Vemuganti GK, Murthy SI, Das S. Update on pathologic diagnosis of
corneal infections and infl ammations. Middle East Afr J Ophthalmol.
2011;18(4):277-284.
12.  American Academy of Opthalmology. Preferred practice pattern: Bacterial
keratitis. 2013. http://one.aao.org/preferred-practice-pattern/bacterial-
keratitis-ppp-2013.
13.  Kumar P. Gonorrhoea presenting as red eye: rare case. Indian J Sex Transm
Dis. 2012;33(1):47-48.
14.  Riordan-Eva P. Disorders of the eyes and lids. In: Papadakis MA, McPhee SJ,
eds. Current Medical Diagnosis and Treatment 2014. 53rd ed. USA: McGraw-
Hill Education; 2014:159-192.
15.  Bacterial Keratitis. Preferred Practice Pattern. American Academy of Ophthal-
mology 2013 Sept. (Clinical Practice Guideline.)
16.  Guess S, Stone DU, Chodosh J. Evidence-based treatment of herpes simplex
virus keratitis: a systematic review. Ocul Surf. 2007;5(3):240-250.
17.  White ML, Chodosh J. Herpes simplex virus keratitis: A treatment guideline.
Ocular Microbiology and Immunology Group and American Academy of
Ophthalmology June 2014. (Clinical Practice Guideline.)
18.  Jabs DA, Mudun A, Dunn JP, Marsh MJ. Episcleritis and scleritis: clinical
features and treatment results. Am J Ophthalmol. 2000;130(4):469-476.
19.  Mahmood AR, Narang AT. Diagnosis and management of the acute red eye.
Emerg Med Clin North Am. 2008;26(1):35-55.
20.  Okhravi N, Odufuwa B, McCluskey P, Lightman S. Scleritis. Surv Ophthal-
mol. 2005;50(4):351-363.
21.  Reza DA. Treatment of scleritis. In: UpToDate, Post TW, eds. UpToDate.
Waltham, MA. 2015.
22.  Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatr Rev. 2010;
31(6):242-249.
23.  Seltz LB, Smith J, Durairaj VD, Enzenauer R, Todd J. Microbiology and
antibiotic management of orbital cellulitis. Pediatrics. 2011;127(3):
e566-e572.
24.  Alteveer JG, McCans KM. The red eye, the swollen eye, and acute vision
loss: handling non-traumatic eye disorders in the ED. Emergency Medicine
Practice: An evidenced-based approach to Emergency Medicine. 2002;4(6):
1-28.
Anthony Ossorio is an advanced registered nurse practitioner student at the
University of North Florida, Jacksonville, Fla.
The author and planners have disclosed no fi nancial relationships related to this
article.
DOI-10.1097/01.NPR.0000473384.55251.25
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CE Group, 74 Brick Blvd., Bldg. 4, Suite 206, Brick, NJ
08723. We will mail your certifi cate in 4 to 6 weeks.
For faster service, include a fax number and
we will fax your certifi cate within 2 business days of
receiving your enrollment form.
-  You will receive your CE certifi cate of earned con-
tact hours and an answer key to review your results.
There is no minimum  passing grade.
-  Registration deadline is December 31, 2017.
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