Online CE Newsletter Series for Optometrists
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Eye on GlaucomaTM
Case Chronicles in Glaucoma and
Ocular Surface Disease
CASE 3 IN A SERIES OF 4
Original Release: November 11, 2013
Expiration: November 11, 2016
This course is COPE approved for 1 credit.
COPE Course ID: 39662-GL
Sponsored by The State University of New York College of Optometry
Administrator: MedEdicus LLC
This continuing education activity is supported through an unrestricted educational grant from Merck & Co, Inc.
Murray Fingeret, OD, FAAO (Program Chair)
Chief of the Optometry Section
Brooklyn/St. Albans Campus
Department of Veterans Affairs New York Harbor Healthcare System
State University of New York College of Optometry.
New York, New York
Ian Benjamin Gaddie, OD
Owner and Director
Gaddie Eye Center
Milton Hom, OD
Joseph Sowka, OD
Chief of Advanced Care Service
Director of Glaucoma Service
Nova Southeastern University College of Optometry
Fort Lauderdale-Davie, Florida
LEARNING METHOD AND MEDIUM
This educational activity consists of a case report and ten (10) study questions. The participant should, in order, read the Learning Objectives contained at the beginning of this activity, read the material, answer all questions in the post test, and complete the Activity Evaluation/Credit Request form. To receive credit for this activity, please follow the instructions provided below in the section titled To Obtain CE Credit. This educational activity should take a maximum of 1.0 hour to complete.
This continuing education (CE) activity captures content from a roundtable discussion.
There is a growing awareness of the impact of ocular surface disorders on the successful management of patients with ocular hypertension and glaucoma. Recent studies provide new insights into patient problems and concerns, and an increasing awareness of the significance of preservatives on ocular health. Improved versions of current therapies, and the availability of new therapies, provide opportunities for improved outcomes toward the prevention of glaucoma progression. Recently, a group of experts convened to discuss their insights and approaches for managing these patients. This CE activity brings you highlights from these case discussions in a 4-part series.
This educational activity is intended for optometrists.
Upon completion of this 4-Part CE Case Series, participants will be better able to:
- Assess ocular surface health in patients on ocular antihypertensives
- Review the evidence on the effects of preservatives on the ocular surface as they relate to ocular hypertension treatment regimens
- Employ appropriate ocular antihypertensive strategies in patients with glaucoma or ocular hypertension to manage OSD
ACCREDITATION DESIGNATION STATEMENT
This course is COPE approved for 1.0 hour of CE credit for optometrists.
COPE Course ID: 39662-GL
Murray Fingeret, OD, had a financial agreement or affiliation during the past year with
the following commercial interests in the form of Consultant: Alcon, Inc; Allergan, Inc;
Carl Zeiss Meditec, Inc; Sucampo Pharmaceuticals, Inc; and Topcon Medical Systems,
Inc; Contracted Research: Canon USA, Inc; Carl Zeiss Meditec, Inc; Heidelberg
Engineering; and Topcon Medical Systems, Inc.
Ian Benjamin Gaddie, OD, had a financial agreement or affiliation during the past year
with the following commercial interests in the form of Consultant: Alcon, Inc; Allergan,
Inc; Bausch + Lomb Incorporated; Marco Medical Management LLC; Merck & Co, Inc;
OCuSOFT; and Sucampo Pharmaceuticals, Inc.
Milton Hom, OD, had a financial agreement or affiliation during the past year with the
following commercial interests in the form of Consultant: Allergan, Inc; Bausch + Lomb
Incorporated; NicOx SA; and SARcode Bioscience, Inc; Contracted Research: Abbott
Medical Optics; Allergan, Inc; and Bausch + Lomb Incorporated.
Joseph Sowka, OD, had a financial agreement or affiliation during the past year with
the following commercial interests in the form of Consultant/Advisory Board: Alcon, Inc;
Merck & Co, Inc; and Sucampo Pharmaceuticals, Inc; Fees for promotional, advertising
or non-CME services received directly from commercial interest or their Agents (eg,
Speakers Bureaus): Alcon, Inc; and Carl Zeiss Meditec, Inc.
Each of the contributing physicians listed above has attested to the following:
- that the relationships/affiliations noted will not bias or otherwise influence his or her involvement in this activity;
- that practice recommendations given relevant to the companies with whom he or she has relationships/affiliations will be supported by the best available evidence or, absent evidence, will be consistent with generally accepted medical practice; and
- that all reasonable clinical alternatives will be discussed when making practice recommendations.
This activity includes off-label discussion of steroids for dry eye. Please consult products for all approved indications and administration.
This CE activity is supported through an unrestricted educational grant from Merck & Co, Inc.
TO OBTAIN CE CREDIT
We offer instant certificate processing and support Green CE. Please take this post test and evaluation online by clicking the Take Exam button at the end of this case. Upon passing, you will receive your certificate immediately. You must answer 7 out of 10 questions correctly in order to pass, and may take the test up to 2 times. Upon registering and successfully completing the post test, your certificate will be made available online and you can print it or file it. Please make sure you take the online post test and evaluation on a device that has printing capabilities. There are no fees for participating in and receiving CE credit for this activity.
The views and opinions expressed in this educational activity are those of the faculty and do not necessarily represent the views of The State University of New York College of Optometry; MedEdicus LLC; Merck & Co, Inc; or Review of Optometry.
Dr Fingeret: A 73-year-old African American male with a 7-year history of primary
open-angle glaucoma (POAG) presented for his quarterly glaucoma evaluation. He
complains of burning and stinging in each eye upon instillation of his ocular
antihypertensive medications. His aversion to the medications has worsened to the
point that he reports often neglecting to administer the medications. His ocular
antihypertensive regimen includes latanoprost (generic formulation) in each eye at
bedtime and timolol/dorzolamide (generic formulation) in each eye twice daily. The
patient also has been using over-the-counter artificial tears for several years. The
artificial tears no longer provide relief for his ocular discomfort.
Allergy History: None
Past Medical History: Hypertension, diabetes (diet-controlled) for 10 years
Nonocular Medications: Hydrochlorothiazide
Ocular History: 7-year history of primary open-angle glaucoma
Visual Acuity (Best Corrected With Low Hyperopic Spectacle Prescription):
20/20 OD 20/20 OS
Anterior Segment Examination: (Figures 1, 2, 3)
1+ conjunctival hyperemia OU
Pouting of meibomian glands with material expressed with gentle pressure
Blepharitis with material present on lid margins OU
Mild-Moderate punctate staining central OU
Tear break-up time <5 seconds OD and OS
Anterior chamber (including angle assessment):
Anterior chamber clear with wide-open angle
All structures visible with gonioscopy
1+ Nuclear sclerosis OU
Figure 1. Examination of the patient's eye showing mild conjunctival hyperemia.
Figure 2. Examination of the patient's eyelid showing pouting of meibomian
Figure 3. Examination of the patient's eyelid showing blepharitis with material on
the lid lashes.
Photos Courtesy of Murray Fingeret, OD
25 mm Hg OD 22 mm Hg OS
525 OD 521 OS
Optic Nerve/Retinal Nerve Fiber Layer (RNFL)/Retina: (Figures 4A, 4B, and 5)
Average disc size OU
Inferior, superior, nasal, and temporal (ISNT) Rule not obeyed
No hemorrhage present
Zone Alpha and Beta Parapapillary atrophy present OU
Mild RNFL loss inferior temporal OU
C/D .7x .7 .65x .6
Optical Coherence Tomography imaging performed showing good quality scans
with overall thinning of the RNFL and statistically abnormal superior and inferior
Fundoscopic Examination (Figures 4A and 4B)
Figure 4A. Photograph of the patient's optic nerve of the right eye.
Figure 4B. Photograph of the patient's optic nerve of the left eye.
Photos Courtesy of Murray Fingeret, OD
Optic Nerve Head and Retinal Nerve Fiber Layer Images: (Figure 5)
Figure 5. Optic nerve head and retinal nerve fiber layer imaging analysis
of both eyes of the patient.
Figure Courtesy of Murray Fingeret, OD
Visual fields (SITA Standard):
Borderline reliability – OD, OS
OD: arcuate scotoma; OS : partial arcuate scotoma
Visual Field Images (Figures 6A and 6B)
Figure 6A. Visual field of the patient's right eye.
Figure 6B. Visual field of the patient's left eye.
Figures Courtesy of Murray Fingeret, OD
PERTINENT EXAMINATION FINDINGS
External eye examination finds mild conjunctival hyperemia and pouting of the
meibomian glands with clear material expressed upon gentle pressure of the patient's
eyelids. A moderate amount of debris is visualized on his eyelashes. He also has some
corneal punctate staining. His tear break-up time is very fast. His current intraocular
pressures (IOPs), 25 mm Hg OD and 22 mm Hg OS, are 7 to 8 points higher than in
previous visits and are approaching pretreatment levels. The patient reports that he is
not using his ocular antihypertensive medications because of the irritation he
experiences when administering them, and he also states that his eyes feel irritated
This patient's POAG is complicated by ocular surface disease (OSD), which interferes
with his adherence to glaucoma therapies.
Dr Fingeret: What would be the other panelists' considerations for treating this
patient's glaucoma and OSD?
Dr Sowka: Before attempting to modify his ocular antihypertensives, I would embark
upon treating his meibomian gland dysfunction (MGD) and blepharitis. My
recommendation would be to apply profound lid hygiene: lid scrubs, hot compresses,
digital massage, and perhaps a course of oral doxycycline or topical azithromycin.
Getting his MGD treated first will likely improve his chances of tolerating any new ocular
Dr Fingeret: Would you consider the use of topical steroids on his eyelids?
Dr Sowka: I would consider topical steroids only for severe dry eye. Using a
steroid is always risky because it can cause an IOP spike—an added risk here because
this patient has not been using his glaucoma therapies.
If this option is pursued, however, because of extremely severe OSD and uncomfortable
dry eye, I would use only a small dose for a short period of time. I recently have done
this with a patient of mine. Loteprednol, 0.2%, (brand formulation) was too expensive,
so I prescribed the generic fluorometholone. Both steroids have a low propensity to elevate IOP.1,2 In my patient's case, a week of steroid treatment was life changing and
so far, no IOP rise, thankfully. Applying a steroid topically to this case patient's eyelid
rather than instilling a steroid directly into his eye may minimize the risk of steroid-induced IOP increases.
Dr Fingeret: Dr Sowka, are you suggesting discontinuing all his glaucoma
medications—so long as the patient does not have advanced glaucoma—and treating
the eyelids and the ocular surface until the MGD and blepharitis resolve?
Dr Sowka: Yes, with an additional caveat: If this patient had a pretreatment IOP above
40 mm Hg, I would not discontinue his glaucoma medications. Another option is to
reduce the glaucoma medications down to 1 agent and to proceed on the course of
Dr Hom: I would take a diagnostic approach initially, investigating for Demodex mite
infestation. There are several reasons to first rule out Demodex as the cause of his
ocular signs and symptoms. Firstly, in patients who are aged 70 years and older, the
prevalence of Demodex approaches 100%,3 and this patient is 73 years old, placing him
in the high-risk age group. Secondly, consider that Demodex might be a cause of the
patient's blepharitis4 and worsening MGD.5,6 A 2011 study conducted in the Philippines
showed that 85% of patients with MGD had underlying Demodex infestation.7 Thirdly,
the images of the patient's eyes indicate some lid debris at the base of the eyelashes. (Figure 2) That debris could be cylindrical dandruff, although it is difficult to visualize
against the patient's dark skin. In a 2005 study, Gao and colleagues found that
cylindrical dandruff is 80% pathognomonic for Demodex.4 (Figure 7) Lid debris typically
appears farther down the lash, but in Demodex infestation, a more typical presentation
of lid debris appears at the eyelash base.4 This cylindrical debris is caused either by Demodex folliculorum mites that live in the follicle and/or by Demodex brevis mites that
live deep in the eyelash's sebaceous glands and in the meibomian gland.4 The lid debris
is the waste products that the mites leak out from the follicle.
Figure 7. Cylindrical dandruff indicative of Demodex mite infestation.
Photo Courtesy of Milton Hom, OD
To check for the presence of the parasites, epilate the lash and look at the eyelash
underneath a light microscope to see if there are any mites visible. The presence of the Demodex mites could explain the patient's discomfort. And if Demodex is indeed the
cause of discomfort, my suggestion is to treat the patient with in-office tea tree oil
treatments.5 Clinicians should be aware that Demodex might be the culprit in many lid
disease cases that are resistant to routine therapies. If a patient is not getting better with
routine treatment, Demodex could be the reason.
An important point with respect to Demodex treatment is that Demodex infestation is
usually related to rosacea.3,8 Treatment for acne rosacea usually involves steroid
therapy. However, steroids should be avoided in patients with Demodex because
steroids may increase mite counts.9 Thus, treatment of the rosacea with steroids
actually could cause the Demodex infestation to worsen.10 Optometrists are often reluctant to use steroids in a patient with glaucoma in the first
place because of its effect on IOP. Thus, if this patient has Demodex infestation, I would
not use steroids on the patient's eyelids.
Dr Gaddie: I agree completely with Dr Hom that this appears to be a case complicated
by Demodex. While the prevalence is close to 100% at this age3, not everyone with Demodex has symptoms or requires treatment.6 But certainly in this case the condition
does warrant treatment, and I think you could do so without stopping glaucoma therapy.
I also use a tea tree oil treatment for Demodex and doing so does not necessitate discontinuation of glaucoma treatment. In my clinical experience I have found that
patients who are on prostaglandin analogs are more susceptible to Demodex, possibly
as a result of the inflammatory mechanisms of the drugs.
Certainly laser trabeculoplasty would be a great option to otherwise reduce the load of
topical medications and their associated preservatives vs a preservative-free medication
Dr Fingeret: Allow me to relate how I managed this patient's glaucoma in light of his
OSD. I treated his OSD condition with warm compresses, meibomian gland
expression, and eyelid cleaning. I added omega-3 fatty acid therapy11,12,13 and switched
him to preservative-free ocular antihypertensives: tafluprost (brand formulation) and the
combination preservative-free dorzolamide/timolol (brand formulation). When the patient
returned a month later, he felt better. His eyes looked relatively white, and he reported
that the ocular antihypertensive medications were not causing stinging in his eyes. His
IOPs were 13 mm Hg OD and 14 mm Hg OS, which confirmed that his previously poorly
controlled IOP was related to poor adherence to glaucoma therapy.
The question then arises: Were the patient's OSD symptoms independent of his ocular
antihypertensive medications, or did the medications contribute to the OSD? My
assessment was the latter. Although his medications may not have been the instigators
of or culprits in the OSD, they were at least contributing to it. Consequently, switching to
a preservative-free ocular antihypertensive eliminated any contribution of the
benzalkonium chloride (BAK)-preserved ocular antihypertensives aggravating the
When corneal staining and hyperemia are present with an unclear cause, my
assessment is that BAK may be exacerbating OSD. In a 2008 study examining the
prevalence of OSD in patients with glaucoma, Leung and colleagues found that 59% of
patients reported symptoms of OSD.12 The researchers also investigated the link
between the number of BAK-containing drops and clinical test results for OSD. After
controlling for age and sex, each additional BAK-containing drop was associated with
approximately twice the risk of abnormal results on corneal and conjunctival lissamine
green staining (odds ratio = 2.03; 95% confidence interval = 1.06 – 3.89; P=.034).14 BAK
has been found to exacerbate conditions that are deleterious to the ocular surface,
including blepharitis, MGD, tear film instability, conjunctival inflammation, and keratitis.15 Compared with preservative-free ocular antihypertensives, preserved ocular
antihypertensives, particularly those containing BAK, can aggravate dry eye disease
and can cause a markedly increased prevalence and frequency of symptoms of
burning, stinging, and discomfort.15 Even if there had been preexisting OSD prior to BAK
exposure in this case patient, my thought was that a preservative-free ocular antihypertensive would avoid additional insult to the eye and might make the patient's
eyes feel better.
Dr Sowka: Based on the success of Dr Fingeret's treatment plan, the patient's
condition was unlikely to have been caused by Demodex infestation. Nonetheless,
optometrists should consider adding Demodex to the differential diagnosis in a patient
presenting with some of the following signs and symptoms: blepharitis, MGD, OSD,
debris near the eyelash base. Also, a Demodex treatment plan is a helpful addition to
the optometrist's armamentarium. Regardless of why the treatment for this patient was
a success, whether it was due to the blepharitis treatment or to the switch to a
preservative-free ocular antihypertensive, the end result was a positive outcome—a
patient with glaucoma who is now comfortable using his ocular antihypertensive
- Comstock TL, Decory HH. Advances in corticosteroid therapy for ocular inflammation:
loteprednol etabonate. Int J Inflam. 2012;2012:789623. doi: 10.1155/2012/789623. Epub
2012 Mar 28.
- Yang CQ, Sun W, Gu YS. A clinical study of the efficacy of topical corticosteroids on
dry eye. J Zhejiang Univ Sci B. 2006;7(8):675-678.
- Hom MM, Mastrota KM, Schachter SE. Demodex. Optom Vis Sci. 2013;90(7):e198-e205.
- Gao YY, Di Pascuale MA, Li W, et al. High prevalence of Demodex in eyelashes with
cylindrical dandruff. Invest Ophthalmol Vis Sci. 2005;46(9):3089-3094.
- Gao YY, Xu DL, Huang lJ, Wang R, Tseng SC. Treatment of ocular itching associated
with ocular demodicosis by 5% tea tree oil ointment. Cornea. 2012;31(1):14-17.
- Gao YY, Di Pascuale MA, Elizondo A, Tseng SC. Clinical treatment of ocular
demodecosis by lid scrub with tea tree oil. Cornea. 2007;26(2):136-143.
- de Venecia III AB, Slong RLB. Demodex sp. infestation in anterior blepharitis,
meibomian-gland dysfunction, and mixed blepharitis. Philipp J Ophthalmol. 2011;36(1):15-22.
- Demodex Convenience Kit [package insert]. Rosenberg, TX: OCuSOFT, Inc; 2010.
- Forton F, Germaux MA, Brasseur T, et al. Demodicosis and rosacea: epidemiology and
significance in daily dermatologic practice. J Am Acad Dermatol. 2005;52(1):74-87.
- Bonnar E, Eustace P, Powell FC. The Demodex mite population in rosacea. J Am Acad
- Miljanović B, Trivedi KA, Dana MR, Gilbard JP, Buring JE, Schaumberg DA. Relation
between dietary n-3 and n-6 fatty acids and clinically diagnosed dry eye syndrome in
women. Am J Clin Nutr. 2005;82(4):887-893.
- Rashid S, Jin Y, Ecoiffier T, Barabino S, Schaumberg DA, Dana MR. Topical omega-3
and omega-6 fatty acids for treatment of dry eye. Arch Ophthalmol. 2008;126(2):219-
- Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian
gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106:336-356.
- Leung EW, Medeiros FA, Weinreb RN. Prevalence of ocular surface disease in glaucoma
patients. J Glaucoma. 2008;17(5):350-355.
- Stalmans I, Sunaric Mégevand G, Cordeiro MF, et al. Preservative-free treatment in
glaucoma: who, when, and why? Eur J Ophthalmol. 2013;23(4):518-525.