Download IS THAT CORNEAL INFILTRATE STERILE OR INFECTIOUS?

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IS THAT CORNEAL
INFILTRATE STERILE
OR INFECTIOUS?
Differentiating between the two requires close observation and analysis.
Here’s a results-oriented approach.
By Jeffrey Sonsino, OD, and Shachar Tauber, MD
D
oes this sound familiar? “Doctor, I don’t
understand what’s
wrong. I have been
wearing my contact
lenses overnight for years and this
has never happened before.” Upon
close examination, you note the
presence of small, grayish aggregates in the corneal epithelium. The
diagnosis? Corneal infiltrates. But
how do you tell if they are sterile or
infectious—harmless, or a potential
serious problem?
As practitioners, we have seen
any number of contact lens-related
complications walk through our
doors. Corneal infiltrates and ulcers
are two such examples that have
long been an unfortunate reality of
patient care. In the 19th century,
treatment of corneal ulcers included
chemical cauterization with silver
nitrate. While we’ve come a long
way since those days in the care we
provide, when such adverse events
occur, differentiating infectious and
sterile infiltrates is still no easy task.
BREAKING IT DOWN
Corneal infiltrates result from the
penetration of white blood cells
into the corneal tissue as part of
the body’s inflammatory response
24
to the presence of bacterial toxins, enzymes and byproducts.1-4 A
corneal ulcer, by comparison, is an
epithelial defect with underlying
inflammation (which typically leads
to necrosis of corneal tissue).
Infiltrates and ulcers are similar
in that they both involve disruption
of the corneal epithelium; indeed, a
staining infiltrate may be the beginning of a corneal ulcer. The difference, however, is that while corneal
infiltrates are not sight-threatening,
corneal ulcers involve active tissue
damage caused either by infectious
or non-infectious etiologies. Infectious ulcers are caused by fungus,
virus, or parasites like Acanthamoeba) or, most commonly, bacteria.5
Alternately, noninfectious ulcers
result from autoimmunity, neurotrophic keratitis, allergy (e.g., shield
ulcers), inflammation from blepharitis or chemical burns, or idiopathic conditions (e.g., Mooren’s ulcer).
In the case of microbial insult,
the damage typically results in an
excavation of the corneal stroma,
which triggers an anterior chamber
response of flare with or without
cells (Figures 1, 2 and 3). For this
reason, the terms microbial keratitis
and bacterial ulcer are sometimes
used interchangeably.
Four subtypes of contact lensrelated corneal infiltrates exist:
microbial keratitis, contact lensinduced peripheral ulcer (CLPU),
contact lens-induced acute red eye
(CLARE) and infiltrative keratitis.
While the etiology of these subtypes
is multifactorial, research shows
significant overlap between their
clinical presentations, suggesting it
is not possible to clinically differentiate between them; rather, they
should be considered as stages of a
single disease spectrum.6
ABOUT THE AUTHORS
Dr. Sonsino is a partner in a
specialty contact lens and
anterior segment practice
in Nashville, Tenn. He is a
diplomate in the cornea,
contact lens, and refractive therapies section of
the AAO, a council member
of the cornea and contact lens section
of the AOA, a fellow of the Scleral Lens
Education Society and an advisory board
member of the GPLI. Dr. Sonsino is boardcertified by the ABO.
Dr. Tauber is an ophthalmologist at Mercy Clinic Eye
Specialists and Surgery
Center. He is a fellow of
the American Academy
of Ophthalmology and a
member of the American
Society of Cataract and Refractive Surgery and International Ocular
Surface Society.
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Fig. 1. Slit beam evaluation of a corneal ulcer. Deviation of the beam shows
corneal excavation.
THE “TWO CORNEAS”
When determining whether the corneal infiltrate is infectious or sterile,
one helpful method is to divide the
cornea into two distinct regions.
Consider that the central cornea
encompasses the 6mm of the
cornea apex whereas the peripheral
cornea is a 2mm to 4mm doughnut, with the limbus as its posterior
border.
Based upon the close approximation of the peripheral cornea to the
limbus (with its preponderance of
stem cells and vascularity), investigators believe the immune response
to be more active in this region
of the cornea. Quantification of
the nerve fibers shows a densely
innervated cornea and a five to six
times lower innervated peripheral
cornea.7 Higher mitotic activity
has also been demonstrated in the
peripheral cornea.8
These observations indicate the
two distinct regions of the cornea
have key anatomic, physiologic and
pathologic differences, allowing for
the generalization that infiltrates
in the periphery of the cornea are
non-infectious while infiltrates in
the central 6mm of the cornea may
have an infectious etiology.9
ALWAYS TAKE NOTES
As with any medical concern that
presents to the clinic, careful history taking can lead the eye care
practitioner to identify the proper
diagnosis and resultant treatment
that gives the patient the best possible outcome with the least risk.
• Contact lenses. Contact lens
use is one identified risk factor for
the development of corneal infiltrates, as evidence shows continuous wear of contact lenses increases
the risk of ocular complications.
However, it is not the primary
cause of corneal infiltrates; rather,
it is simply one of several contributors. Other risk factors for corneal
infiltrate development in continuous wear contact lens patients
include age (i.e., between 18 and
Release Date: April 2015
Expiration Date: April 1, 2018
Goal Statement: This course reviews the etiology, contributing factors and clinical presentations of sterile and infectious corneal
infiltrates. Key points in ocular examination
and treatment will also be discussed.
Faculty/Editorial Board:
Jeffrey Sonsino, OD, and Shachar Tauber, MD
Credit Statement: COPE approval for 1 hour
of continuing education credit is pending
for this course. Check with your state licensing board to see if this counts toward your
29 years) and a history of smoking,
corneal scarring, contact lens acute
red eye or corneal infiltrates.10
Of the different corneal infiltrate
types, microbial keratitis is the most
severe complication of contact lens
wear. In the 1980s and 1990s, risk
of microbial keratitis was found
to be four cases per 10,000 lens
wearers per year for daily wear and
20 cases per 10,000 wearers per
year for extended wear.11,12 Pseudomonas aeruginosa has been identified as the most common bacterial
source of microbial keratitis in
contact lens wearers.13
• Corneal trauma. Risk of microbial keratitis also increases any time
there is a history of corneal trauma
or foreign body presence due to the
possibility of incomplete removal.
This is especially true when the
foreign body is vegetative matter,
which is more likely to be contaminated by pathogens. Corneal
trauma may also include iatrogenic
etiologies, such as retained or broken sutures in penetrating keratoplasty patients.
• History of surgery. Because
anterior segment surgery compromises epithelial barrier function,
any corneal surgery carries a risk
of resultant infiltrative keratitis and
infectious ulcer. In particular, infiltrative keratitis is associated with
astigmatic keratectomy, penetrating
keratoplasty, DSAEK, pterygium
removal, trabeculectomy, LASIK
CE requirements for relicensure.
Joint-Sponsorship Statement: This continuing education course is joint-sponsored
by the Pennsylvania College of Optometry.
Disclosure Statement: Dr. Sonsino consults for SynergEyes, Bausch + Lomb,
Alcon, Visionary Optics and Optovue, has
received grant support from Visioneering,
and owns stock in LVR Technology.
Dr. Tauber consults for AMO and Allergan,
has received grant support from the
Department of Defense, and owns stock in
Calhoun Vision and Ocugenics.
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IS THAT CORNEAL INFILTRATE STERILE OR INFECTIOUS?
Fig. 2. Sodium fluorescein evaluation of a corneal ulcer. The hyperfluorescence
is attributed to staining of the mucous plug.
and cataract surgery.14-17 It is not
clear if the relative risk is greater
with regards to a particular corneal
surgery.
• Ocular surface disease. Sterile
peripheral (i.e., marginal) corneal
infiltrates may result from a compromised ocular surface. Staphlococcal blooms in the lids spill bacterial byproducts onto the cornea,
which triggers a hypersensitivity
reaction that is theorized to lead
to infiltrates.18,19 Often small and
multiple in nature, these infiltrates
are typically positioned roughly
1mm from the limbus. Marginal
infiltrates may be asymptomatic, or
may be accompanied by conjunctival injection. Pathogenesis includes
bacterial, allergic or autoimmune
etiologies.
In the case of severe blepharitis
and meibomian gland dysfunction
(MGD), the bacterial blooms within
the meibomian glands can produce
a hypersensitivity reaction, leading
to peripheral, non-staining subepithelial infiltrates (SEIs). The body
responds to the to antigen presented
by this presence of Staphlococcal
bacteria in the lids by recruiting
white blood cells to the area as part
of an antibody response. For this
reason, the SEIs associated with
26
Staphlococcal marginal keratitis are
typically in the 2 o’clock and 10
o’clock regions and the 4 o’clock
and 8 o’clock regions, contiguous
with the upper and lower lids.
Similarly, ocular rosacea can
lead to MGD. However, with
severe rosacea, potential outcomes
include marginal infiltrates, chronic
conjunctivitis, sterile ulceration,
corneal neovascularization and
corneal scarring (Figures 4 and 5).
It is also critical to rule out herpes
simplex keratitis (HSK), which
may resemble the infiltrates seen in
Staphlococcal marginal keratitis.
HSK lesions, however, are typically
harder to treat and appear with
deeper stromal inflammation.20
• Allergic conjunctivitis. All
eye care practitioners are familiar
with the signs and symptoms of
Fig. 3. Contact lens-related microbial
keratitis. Ulcer filled with mucous
plug.
seasonal allergic conjunctivitis,
atopic conjunctivitis and papillary
conjunctivitis. Perhaps less commonly encountered, however, is
a variant of allergic conjunctivitis
found most often in young boys.
Vernal conjunctivitis is a severe
bilateral condition characterized
by photophobia, chemosis, sticky
discharge, eosinophils at the limbus
(i.e., Horner-Trantas dots) and
shield ulcers.21 Secondary bacterial
keratitis typically results from 10%
of shield ulcers.22
• Medications. Contamination
of ocular medications has been
implicated in numerous case studies
of corneal ulceration; the pathogen
may originate in topical medication
dropper tips or within the medications themselves.23,24
LOOK FOR THE SIGNS
The next step after collecting a
complete patient history is to conduct an ocular examination, which
can help determine whether an
infiltrate is sterile or infectious. The
following are all key elements of a
physical examination that can help
with proper diagnosis:
• Does the patient report symptoms of pain, photophobia or loss
of vision? What about corneal sensation? Pain out of proportion with
the signs points to Acanthamoeba,
while loss of corneal sensation (i.e.,
lack of pain upon history or with
the corneal wisp test) signals HSK.
• Do you observe blepharitis,
nasolacrimal duct obstruction,
poor or incomplete blink or lagophthalmos, entropion/ectropion
or conjunctival injection? Is the
conjunctival injection localized or
diffuse? How about circumlimbal?
Be sure to grade the injection (i.e.,
1-4+). What about corneal foreign
bodies?
• Is there discharge and, if so,
what are its characteristics?
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Fig. 4. Severe ocular rosacea. Visible on the lid is tyalosis, scalloped lid
margin and telangiectasia, which signals severe inflammation within the
meibomian glands.
• What is the location, depth and
size of the infiltrate(s)? Do you observe stromal loss?
• Is there visible loss of corneal
endothelium? What about plaque
or pigment on the endothelium?
• What is the status of the patient’s
corneal graft, if they have one?
• Do you observe any stromal
haze and edema?
• Do you observe anterior chamber reaction, cells/flare or hypopyon?
• Are there vitreous cells present?
Note, a corneal ulcer will rarely
lead to endophthalmitis with vitreous cells present.
THE CULTURAL REVOLUTION
In the last 20 years, a major shift
in thought regarding the need to
obtain corneal material to identify
offending organisms and determine sensitivity to antibiotics has
occurred. Today, broad-spectrum
fluoroquinolones are readily available as the primary treatment for
a corneal infiltrate believed to be
infectious. Thus, the majority of
community-acquired cases of bacterial keratitis are typically resolved
with empiric therapy and managed
without smears or cultures.
However, such tests are indicated
in certain cases, including those that
involve a corneal infiltrate that is
central, large and extends to the mid
to deep stroma, particularly with
significant thinning of the cornea or
scleral extension; those chronic in
nature or unresponsive to broadspectrum antibiotics; and those that
present with atypical clinical features suggestive of fungal, amoebic
or mycobacterial keratitis.25 Smears
and cultures may also be helpful
in cases with an unusual history,
such as trauma caused by vegetable
matter or if the patient wore contact
lenses while in a hot tub.25
Additional specialized studies can
help identify atypical organisms, for
example in sight-threatening or severe keratitis of suspected microbial
origin.25 However, the American
Academy of Ophthalmology—noting that the hypopyon that occurs
in eyes with bacterial keratitis is
usually sterile—recommends aqueous or vitreous taps should not be
performed unless there is a high
suspicion of microbial endophthalmitis, such as following an intraocular surgery, perforating trauma
or sepsis.25
When obtaining corneal material, proper technique is critical
to identify the causative organism
and select the proper antibiotic,
antiviral, antifungal or antiprotozoal medications. The process of
obtaining corneal material should
first involve the instillation of a
topical anesthetic agent (note that
tetracaine should be avoided due to
its antimicrobial effect) followed by
the use of a heat-sterilized platinum
spatula, blade, jeweler’s forceps
or other similar sterile instrument
to obtain scrapings of material
from the advancing borders of the
infected area of the cornea. Culture
yield may be improved by avoiding
anesthetics with preservatives.
A thiol or thioglycollate brothmoistened dacron/calcium alginate
or sterile cotton swab can also be
used to obtain material.25 However,
solid as well as liquid plating media
is always recommended.26 If treatment is refractory and cultures do
not yield results, it is advisable to
halt antibiotics in order to isolate
the exact pathogen for further
treatment. It is also important to
consider culturing contact lenses,
contact lens cases and contact lens
solutions if appropriate and available.
TREATMENT OPTIONS
Topical antibiotics are the first-line
therapy for suspected or cultureproven bacterial keratitis; however,
the selection depends on severity. A
peripheral infiltrate associated with
lid margin disease may be appropriately managed with inexpensive
early fluoroquinolones such as
ofloxacin, ciprofloxacin, azithromycin or a polymixin-bacitracin
ointment, while central or more
aggressive infiltrates warrant use of
fourth-generation fluoroquinolones
such as gatifloxacin, moxifloxacin
or levofloxacin.
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IS THAT CORNEAL INFILTRATE STERILE OR INFECTIOUS?
Fig. 5. Corneal scarring with severe
ocular rosacea.
For more serious keratitis, the use
of besifloxacin has recently been
advocated. This new fluoroquinolone has high MIC values for many
common ophthalmic pathogens
and a unique compound containing
polycarbophil, edetate disodium
dihydrate and sodium chloride,
which allows for greater ocular
surface contact time. Additionally,
its position as the only ophthalmic
fluoroquinolone not used systemically makes it unique by reducing
the risk of antibiotic resistance.
In severe situations with risk for
perforation, failure to respond to
monotherapy or central aggressive
ulcers with the potential for vision
loss, the use of combination fortified-antibiotic therapy should be
considered. This should be formulated by a compounding pharmacy
that is a member of the Pharmacy
Compounding Accreditation Board.
Note that methicillin-resistant
Staphylococcus aureus (MRSA)
has been isolated with increasing
frequency from patients with bacterial keratitis. Fluoroquinolones are
generally poorly effective against
MRSA ocular isolates; however,
vancomycin has demonstrated some
success.27 In cases of severe ulcer,
consider more complete coverage
with combination therapy.28
Systemic antibiotics are rarely
needed, but may be considered in
severe cases where the infectious
process has moved to adjacent tissues (e.g., the sclera) or when there
28
is impending or frank perforation
of the cornea. Research shows oral
tetracycline controls the anticollagenase activity commonly seen
in necrotizing infections such as
Pseudomonas.29 Systemic therapy
is necessary in gonococcal keratitis
because of the extremely aggressive
nature of this organism (corneal
penetration in 24 hours with inadequate treatment). For this reason,
the CDC recommends immediate
hospitalization with IV antibiotics
for adult gonococcal infection.
Treating viral, fungal and amoebic keratitis may be challenging and
is beyond the scope of this article.
Regardless, the eye care provider
who has clinical suspicion or laboratory data supporting any of these
infectious processes should be fluent
in their current treatment options
or have available the appropriate
consultants to offer prompt referral.
Determining whether an infiltrate
is sterile or infectious is not an easy
task for even the best clinicians.
However, with careful history taking, physical examination, differential diagnosis and proper treatment,
patients have the best chance of
making the best of a bad situation.
RCCL
1. Josephson JE, Caffery BE. Infiltrative keratitis
in hydrogel lens wearers. Int Contact Lens Clin.
1979;6:223–41.
2. Szczotka-Flynn L, Lass JH, Sethi A, et al. Risk
factors for corneal infiltrative events during continuous wear of silicone hydrogel contact lenses.
Invest Ophthalmol Vis Sci. 2010 Nov;51(11):5421-30.
3. Pearlman E, Johnson A, Adhikary G, et al.
Toll-like receptors at the ocular surface. Ocul Surf.
2008;6:108–16.
4. Sweeney DF, Naduvilath TJ. Are inflammatory
events a marker for an increased risk of microbial
keratitis? Eye Contact Lens. 2007 Nov;33(6 Pt
2):383-7; discussion 399-400.
5. Online Merck Manual. Corneal Ulcer. Available
at: www.merckmanuals.com/professional/eye_
disorders/corneal_disorders/corneal_ulcer.html.
Accessed March 10, 2015.
6. Efron N, Morgan PB. Can subtypes of contact
lens-associated corneal infiltrative events be clinically differentiated? Cornea. 2006 Jun;25(5):540-4.
7. Müller, Vrensen, Pels, et al. Architecture of Human Corneal Nerves. Invest Ophthalmol Vis Sci.
April 1997;38(5):985-94.
8. Lemp MA, Mathers WD. Corneal Epithelial Cell
Movement in Humans. Eye. 1989;3:438-45.
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9. Mah FS. Corneal infiltrates merit care: Differentiating sterile and infectious conditions key to
diagnosis, treatment. Ophthalmology Times. 2010
Oct;35(19):42.
10. McNally JJ, Chalmers RL, McKenney CD,
Robirds S. Risk factors for corneal infiltrative
events with 30-night continuous wear of silicone
hydrogel lenses. Eye Contact Lens. 2003 Jan;29(1
Suppl):S153-6; discussion S166, S192-4.
11. Poggio EC, Glynn RJ, Schein OD, et al. The
incidence of ulcerative keratitis among users
of daily-wear and extended-wear soft contact
lenses. N Engl J Med. 1989;321:779–83.
12. Cheng KH, Leung SL, et al. Incidence of
contact-lens-associated microbial keratitis and its
related morbidity. Lancet. 1999;354:181–5.
13. Mondino BJ, Weissman BA, Farb MD, et al.
Corneal ulcers associated with daily-wear and
extended-wear contact lenses. Am J Ophthalmol.
1986;102:58–65.
14. Adrean SD, Cochrane R, Reilly CD, Mannis MJ.
Infectious keratitis after astigmatic keratotomy in
penetrating keratoplasty: review of three cases.
Cornea. 2005 Jul;24(5):626-8.
15. Moon SW, Kim YH, Lee SC, Lee MA, Jin KH. Bilateral peripheral infiltrative keratitis after LASIK.
Korean J Ophthalmol. 2007 Sep;21(3):172-4.
16. Villarrubia A, Cano-Ortiz A. Candida keratitis
after Descemet stripping with automated endothelial keratoplasty. Eur J Ophthalmol. 2014
Nov-Dec;24(6):964-7.
17. Akpek EK, Demetriades AM, Gottsch JD.
Peripheral ulcerative keratitis after clear corneal
cataract extraction(1). J Cataract Refract Surg.
2000 Sep;26(9):1424-7.
18. Mondino BJ. Inflammatory diseases of the
peripheral cornea. Ophthalmol 1998;95:463-12.
19. Mondino BJ, Lahedi AK, Adamu SA. Ocular
immunity to Staphylococcus aureus. Invest Ophthalmol Vis Sci 1987;28:560.
20. One Network. Herpes Simplex Virus.
Available at: one.aao.org/focalpointssnippetdetail.aspx?id=356f0d13-8853-410f-ac6b7ff5e0257800. Accessed March 25, 2015.
21. Bonini S, Coassin M, Aronni S, Lambiase A.
Vernal keratoconjunctivitis. Eye. 2004;18:345–51.
22. Reddy JC, Basu S, Saboo US, et al. Management, clinical outcomes, and complications of
shield ulcers in vernal keratoconjunctivitis. Am J
Ophthalmol. 2013 Mar;155(3):550-9.
23. Donzis PB. Corneal ulcer associated with
contamination of aerosol saline spray tip. Am J
Ophthalmol. 1997 Sep;124(3):394-5.
24. Schein OD, Wasson PJ, et al. Microbial keratitis
associated with contaminated ocular medications. Am J Ophthalmol. 1988 Apr 15;105(4):361-5.
25. American Academy of Ophthalmology
Cornea/External Disease Panel. Bacterial keratitis.
Limited revision. San Francisco (CA): American
Academy of Ophthalmology (AAO); 2011.
26. Bhadange Y, Sharma S, Das S, Sahu SK. Role
of liquid culture media in the laboratory diagnosis
of microbial keratitis. Am J Ophthalmol. 2013
Oct;156(4):745-51
27. Eiferman RA, O'Neill KP, Morrison NA. Methicillin-resistant Staphylococcus aureus corneal
ulcers. Ann Ophthalmol. 1991 Nov;23(11):414-5.)
28. Asbell PA, Colby KA, Deng S, et al. Ocular
TRUST: nationwide antimicrobial susceptibility
patterns in ocular isolates. Am J Ophthalmol
2008;145:951-8.
29. Ralph RA. Tetracyclines and the treatment
of corneal stromal ulceration: a review. Cornea.
2000 May;19(3):274-7.
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CE TEST ~ APRIL 2015
EXAMINATION ANSWER SHEET
Is That Corneal Infiltrate Sterile or Infectious?
1.
a.
b.
c.
d.
All of the following are likely symptoms or signs of corneal infection EXCEPT:
Pain and photophobia.
Discharge and foreign body sensation.
Anterior chamber reaction that includes cell and flare.
Lack of debris at the tear menuscus.
2. There are many reasons to culture corneal ulcers. Which of the following
is NOT one of them?
a. Culturing would be a helpful medico-legal component of your record in case
the ulcer doesn’t respond to empiric treatment.
b. Culturing reveals sensitivities of the organism(s).
c. Because no single agent is generally effective for all infections.
d. Because ineffectively treated organisms are difficult to isolate.
3. Currently, the most effective/complete treatment plan for resistant
bacterial infection is:
a. Vancomycin and ceftazidime.
b. Tobramycin.
c. Gentamycin and Ocuflox.
d. Ocuflox and erythromycin.
4. Which of the following statements is true regarding corneal infiltrates?
a. Sterile infiltrates are often single in number and are found closer to the visual
axis.
b. Corneal infiltrates at least histologically present in all infections.
c. Large, central infiltrates with overlying stains are probably sterile.
d. Corneal infiltrates associated with microbial keratitis generally produce little
to no pain and photophobia.
5.
a.
b.
c.
d.
The most common cause of perennial allergic conjunctivitis is:
Ragweed or tree pollen.
Summer grasses.
Home allergens, such as dust mites and animal dander.
Multipurpose disinfecting solutions used in contact lens care.
6. Which of the following is not true regarding the use of systemic
antibiotics?
a. They often provide a more effective dose to the cornea than topicals alone.
b. They have a lower chance of producing an allergic response.
c. They are often ineffective when the infection has scleral extension.
d. Tetracycline may aid in patients with an impending corneal melt.
7.
a.
b.
c.
d.
Risk for infiltrative keratitis is increased with all of the following EXCEPT:
Poor compliance/hygiene.
Smoking.
History of corneal scarring and CLARE.
Age 39 to 40.
Valid for credit through April 1, 2018
Online: This exam can also be taken online at www.reviewofcontactlenses.com.
Upon passing the exam, you can view your results immediately. You can also
view your test history at any time from the website.
Directions: Select one answer for each question in the exam and completely
darken the appropriate circle. A minimum score of 70% is required to earn credit.
Mail to: Jobson Optometric CE, Canal Street Station, PO Box 488 New York, NY 10013
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Credit: COPE approval for 1 hour of CE credit is pending for this course.
Sponsorship: Joint-sponsored by the Pennsylvania College of Optometry
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Answers to CE exam:
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Identifying information (please print clearly):
First Name
Last Name
Email
8. The incidence rate for microbial keratitis has been estimated to range from
what to what per 10,000 extended-wear lens patients per year:
a. 18 to 20.
b. 4 to 5.
c. 34 to 38.
d. 1 to 2.
The following is your:
Home Address
Business Address
Business Name
Address
City
9. Which of the following is NOT a risk for microbial keratitis?
a. Wearing contact lenses overnight.
b. History of corneal trauma or foreign body.
c. Prior corneal surgery.
d. Daily use of aspirin.
10. Which of the following is true regarding monotherapy use in presumed
microbial keratitis?
a. A fourth-generation fluoroquinolone is probably the best overall option and
can be used alone for deep central ulcers.
b. Besivance is likely the best option for MRSA infections.
c. Monotherapy should be reserved for use in central infiltrates only.
d. Erythromycin is generally the best treatment option pending culture results.
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By submitting this answer sheet, I certify that I have read the lesson in its entirety
and completed the self-assessment exam personally based on the material presented. I have not obtained the answers to this exam by fraudulent or improper means.
Signature: ________________________________________ Date: _____________
Please retain a copy for your records.
LESSON 111206, RO-RCCL-0415
REVIEW OF CORNEA & CONTACT LENSES | APRIL 2015
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