1. FC_DG0511.indd 3 5/11/11 4:41 PM

2. Current Therapy
in Ocular Disease
by Drs. Ron Melton and Randall Thomas
Past recipients of the “Glaucoma Educator of the Year” Award
by the American Academy of Optometry
Authors of Review of Optometry’s annual Clinical Guide to Ophthalmic Drugs
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000_dg0511_R&Rcourse.indd 49 5/11/11 4:36 PM

3. A Brief Overview of the Past Twelve Months Supported by an unrestricted
grant from
Welcome to the 2011 Clinical Guide to Ophthalmic Drugs!
This year, we are attempting to answer many of the questions we
have received during our lectures over this past year. We have col-
lected well over 100 questions, and we are sharing our responses
to as many of them as space allows. We encourage you to read this
CONTENTS
question-and-answer dialogue, as it contains many clinically practical
pearls that we trust you will value
There have been two significant additions to the therapeutic land- Glaucoma ............................. 2A
scape during the past year: Zirgan and generic latanoprost.
But there are also numerous “new and improved” remakes and
enhanced formulations of medicines already in the marketplace: Beneath the Surface of
• an increased concentration of gatifloxacin (Zymaxid, which is a Dry Eye Disease ................. 12A
0.5% formulation)
• a decreased concentration of bimatoprost (Lumigan 0.01%)
• a decreased concentration of dexamethasone combined with to- Corticosteroids .................. 18A
bramycin (TobraDex ST)
• another topical antihistamine for once-daily use (Lastacaft)
• a reformulation of moxifloxacin (Moxeza) Topical Antibiotics ............. 22A
• a newer, lipid-based artificial tear (Systane Balance)
• the first once-daily topical NSAID, bromfenac (Bromday)
Antiviral Strategies ............ 26A
• loteprednol ophthalmic ointment (Lotemax ointment)
So, you can see the waters have been stirred! We will try to put
these changes, and other relevant topics, into a clinically practical per- Combination Drugs ............ 29A
spective for you. It must be absolutely stressed that everything written
in this guide is explicitly aimed at enhancing the lives of the patients
we all serve. We can never lose sight of why we exist and what our Clinical Update on the
mission is. NSAIDs ............................... 32A
With all best wishes to our esteemed colleagues,
Keeping Allergy
Management Simple .......... 34A
Overview of Oral
Medicines .......................... 36A
Ron Melton, O.D. Randall Thomas, O.D., M.P.H.
Questions & Answers
From the Trenches ............. 40A
Note: The clinical views and advice expressed in this publication are those of the authors, and do not necessarily reflect
those of the sponsor, Bausch + Lomb, or the publisher, Review of Optometry.
001_dg0511_intro.indd 3 5/11/11 3:52 PM

4. Glaucoma
New drugs may come and old drugs may go, but the essential question remains:
At what point does the patient “convert” to glaucoma?
fter 15 years of basking in
A the warm sun, the curtain has
fallen on the most successful
glaucoma drug in the history of the
world. Generic latanoprost should
radically re-script glaucoma care
from a financial perspective. This
same fate will soon occur for Lipi-
tor. We think, and hope, this will
bring financial relief to the masses.
Like all of you, we are watching
from the bleachers to see how this
radical transformation will play
out. (See “Latanoprost Goes
Generic,” page 3A.)
There are other glaucoma medi-
cines in research and development,
and we anticipate newer and better
therapies in the coming years. At what point, clinically, do you begin to inform patients that you are following them
But don’t forget that a once-daily as a “glaucoma suspect”? This is an optic nerve that has converted to glaucoma.
beta-blocker is an excellent second- Note the inferior erosion of the neuroretinal rim.
line drug for monotherapy, or as
additive therapy to a prostaglan- discontinuing it? Q: Would you use a prostaglan-
din. All others must be used twice A: Studies have shown that the din to manage increased intraocular
daily and preferably three times effects of prostaglandins last longer pressure in a steroid responder?
a day—but it is rare that patients than the other classes. In our prac- A: Probably not. Most iatro-
can perform these complex instilla- tices, we wait a month to recheck genic intraocular pressure increases
tions with any significant degree of the intraocular pressure after stop- quickly vanish upon the discontinu-
consistency. ping a prostaglandin. We generally ation of the offending corticoste-
assess the effect of such “reverse roid, so additional medical therapy
Q: When new patients present therapeutic trials” in two to three is usually unwarranted.
to our office on multiple glaucoma weeks for the shorter duration-of- If the IOP was high enough to
meds, we want to experiment with action drugs such as the alpha ad- warrant therapeutic intervention
which meds are optimally effec- renergic agonists, the beta blockers, (perhaps over 35mm Hg to 40mm
tive. How long does it usually take and the topical carbonic anhydrase Hg), then we would select a more
for a medicine’s effect to stop after inhibitors. rapid onset medicine such as a beta
2A REVIEW OF OPTOMETRY MAY 15, 2011
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5. Glaucoma
blocker or brimonidine. Prosta- Latanoprost Goes Generic
glandins are relatively slow in their The biggest news in glaucoma in 2011 is that Xalatan lost its
onset of action, and so are rarely patent protection March 28. This means we now have generic
a class of choice when rapid IOP latanoprost. While this is bad news for the drug manufacturers,
reduction is desired. it is good news for glaucoma patients. A basic understanding
of market dynamics explains why Travatan Z and Lumigan
Q: Do you recommend occluding have also reduced their costs (either directly or through rebate
the nasolacrimal ducts to prevent programs, etc.) to be competitive with generic latanoprost.
systemic effects from glaucoma Generally speaking, and when prudent to do so, we prefer to
medicines? prescribe quality brand-name products as opposed to gener-
A: As a general rule, glaucoma ics of unknown quality. For this reason, we plan to prescribe
medicines are very well tolerated, Travatan Z or Lumigan 0.01% as long as the price points are
and therefore there is not a need to similar to the generic latanoprost.
undertake unnecessary medication- We encourage you to call around to your local pharmacies
modifying procedures. to ascertain the cost of these medications. You will be amazed
However, if the medicine was at the differences. At press time, our survey of local pharmacies revealed great disparity
truly needed for glaucoma care, and among prostaglandin prices (anywhere from $25 to $85). Overall, it seems that $38 is
the patient had a rare side effect generally the going price. This brings great relief to the cost-burden of glaucoma therapy.
(such as taste perversion, a cough, Also note that the prostaglandins exert a therapeutic effect well beyond 24 hours. For
slight shortness of breath, brady- a few of our indigent patients with non-severe glaucoma, we have reduced dosing to
cardia, etc.), then punctal occlusion Monday, Wednesday and Friday.
may be wise. Now let’s think about this rationally and apply some common sense: The goal in glau-
However, we would try switch- coma management is to achieve and maintain an intraocular pressure within the target
ing to another class of drug first, if range deemed to be “safe” for each patient individually. With that in mind, medication
possible. In caring for many hun- management becomes very elementary: We simply check the IOP at one month and at
dreds of patients with glaucoma, two months after dosage-reduction to see if the IOP remains the same as it did with
we have never found the need to once-daily dosing. If that is the case, then we have achieved our IOP goal, and helped the
punctally occlude. patient from not only a health standpoint, but a financial one as well. We simply need to
be thinking, compassionate and attentive doctors.
Q: If a visual field is abnormal,
and repeat testing is normal, do you would repeat the field every six to we provide a standard dilated eye
retest? Or is one normal visual field 12 months to continue to monitor examination.
all you need? for stability or progression. If there is a history of glaucoma
A: Clinically significant visual If the next field shows “progres- suspicion in the family, then we
field defects are largely predictable, sion,” such “progression” MUST would likely obtain pachymetry
and not like a box of chocolates. be confirmed by repeat testing in addition to our always thor-
Generally speaking, if the visual (again, in weeks to months based ough study of the optic nerves via
field is normal, consider it to be on the overall status of the patient’s biomicroscopic-enabled (90D, etc.)
so. If the visual field is defective condition). It is well established ophthalmoscopy.
and the catch trials (fixation losses, that the vast majority of “progres- If the optic nerve(s) appear
etc.) are reasonably normal, and sion” is artifactitious, and disap- compromised in their structure, we
if the optic nerve neuroretinal rim pears upon repeat testing! would then consider accomplishing
tissues are intact, then we would nerve fiber layer assessment, and if
not believe this defective field to be Q: When you see a family mem- this were to be suspicious, then we
a reflection of reality, and therefore ber of a glaucoma suspect patient, would likely obtain a visual field
would repeat the field in a few do you perform a full dilated assessment.
weeks (or even a few months). comprehensive eye exam? Do you Notice that all subsequent testing
However, if there are defects charge them, or is just a quick look is driven by the sequential findings
that correspond to alterations in with the indirect ophthalmoscope during the course of the eye exami-
the optic nerve head anatomy (such sufficient? nation. We do not do tests that are
as polar erosion), then we would A: If it has been over a year since unwarranted, and we always obtain
believe that the defect is true, and the patient has seen an eye doctor, exam elements that are rational,
REVIEW OF OPTOMETRY MAY 15, 2011 3A
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6. Glaucoma
prudent, and medically substanti- We charge a professional fee when Q: At a recent glaucoma lecture,
ated. Appropriate charges are whatever service or procedure per- the specialist stated that nerve fiber
assessed for indicated professional formed is medically prudent. One analysis was pushing back glau-
services and diagnostic testing. could code “glaucoma suspect” if, coma diagnosis by 10 years; that
Some of these may be accomplished in one’s sound clinical judgment, is, initiating treatment for patients
at the initial visit; others may be there is rational justification to in their 50s rather than their 60s.
done days or weeks later, depend- conduct such an examination along Bottom line: With no visual field
ing on assessed risk, the disease with any rational ancillary testing defect, would you treat based on
stage, the patient’s desires, insur- needed to facilitate accurate deci- nerve fiber layer analysis, given the
ance coverage, etc. sion making. potential for long-term consequenc-
es of using glaucoma medicines?
Q: How do you code a claim Q: At what intraocular pressure A: First, glaucoma medicines are
for a family member’s glaucoma would you treat the patient on the generally very well tolerated, even
examination when the results are same day as the exam? in patients who have ocular surface
normal? A: Probably 40mm Hg or disease, so that concern is a mini-
A: How does an orthopedic greater, and even at lower IOP if mal player in decision making. The
surgeon code for a radiographic there were substantial optic nerve larger question is actually much
study if it is normal? The answer: compromise. bigger than structural vs. functional
Topical Glaucoma Drugs
BRAND NAME GENERIC NAME MANUFACTURER CONCENTRATION BOTTLE SIZE
Beta Blockers
Betagan, and generic levobunolol hydrochloride Allergan, and generic 0.25% 5ml, 10ml
0.5% 5ml, 10ml, 15ml
Betimol timolol hemihydrate Vistakon Pharm. 0.25% 5ml
0.5% 5ml, 10ml, 15ml
Betoptic-S betaxolol hydrochloride Alcon 0.25% 5ml, 10ml, 15ml
Istalol timolol maleate Ista 0.5% 5ml
Timoptic, and generic timolol maleate Aton Pharma, and generic 0.25% 5ml, 10ml, 15ml
0.5% 5ml, 10ml, 15ml
Timoptic (preservative-free) timolol maleate Aton Pharma 0.25% unit-dose
0.5% unit-dose
Timoptic-XE, and generic timolol maleate Aton Pharma, and generic 0.25% 2.5ml, 5ml
0.5% 2.5ml, 5ml
Prostaglandin Analogs
Lumigan bimatoprost Allergan 0.01%, 0.03% 2.5ml, 5ml, 7.5ml
Travatan Z travoprost Alcon 0.004% 2.5ml, 5ml
Xalatan, and generic latanoprost Pfizer, and generic 0.005% 2.5ml
Alpha Agonists
Alphagan P, brimonidine Allergan, 0.1%, 5ml, 10ml, 15ml
and generic brimonidine generic 0.15%, 0.2% 5ml, 10ml, 15ml
Carbonic Anhydrase Inhibitors
Azopt brinzolamide Alcon 1% 5ml, 10ml, 15ml
Trusopt, and generic dorzolamide Merck 2% 5ml, 10ml
Combination Glaucoma Medications
Combigan brimonidine/timolol Allergan 0.2%/0.5% 5ml, 10ml
Cosopt dorzolamide/timolol Merck 2%/0.5% 5ml, 10ml
4A REVIEW OF OPTOMETRY MAY 15, 2011
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7. Glaucoma
Select Appropriate Therapy
Let’s assume we have decided for our black patients, and 0.25% ing frequency
a patient merits IOP reduction, for white patients. Furthermore, and compliance.
so what drug do we select? numerous studies clearly support In recognition of
• Prostaglandins. Most the use of these two non-selective this reality, these
of the time, the answer is a beta blockers once daily. It is drugs are general-
prostaglandin, preferably one best to have patients instill beta ly prescribed b.i.d.
of the lower-concentration blockers shortly upon awakening (approximately
formulations (having less for maximum therapeutic effect. every 12 hours).
side effect potential) such Understand that these drugs sup- The CAIs are
as latanoprost 0.005% or press beta adrenergic tone. Our known by their
travoprost 0.004%—and now adrenergic system is active while brand names:
bimatoprost 0.01%. All of the we are awake, and physiologi- Trusopt (dorzol-
prostaglandins lower IOP near- cally asleep while we are asleep. amide, Merck; and generic) and Azopt
ly identically, so prescribing There is little benefit in attempting (brinzolamide, Alcon). Since brimonidine
decisions are based on side to pharmacologically suppress a seems to be slightly more effective than
effect profile and affordability system that is already physiologi- a topical CAI, we generally try it as our
for most patients.1 cally suppressed. This is why it is “Plan B” of choice.
The time of instillation important to dose beta blockers • Combinations. What about the
should center around when shortly upon awakening. “combination” drugs, such as 0.5%
the patient finds it to be the The vast majority of our glauco- timolol with 0.2% dorzolamide (Cosopt
most convenient. Remember, ma patients are successfully man- [Merck], which has been generic since
compliance is the weak link aged with either a prostaglandin, October 2008) or 0.5% timolol with 0.2%
in the treatment chain, so or a beta blocker, or a combination brimonidine (Combigan [Allergan], an
we need to do whatever we of the two. This is relatively inex- expensive combination of two relatively
can to make adherence most pensive, and requires a drop either inexpensive generic products)? We know
achievable for once daily, or if using both, b.i.d. that timolol is only
each patient. • Carbonic anhydrase inhibitors and needed once daily,
• Beta block- alpha adrenergic agonists. If there is and we know that
ers. Alternatively, a need to move beyond a prostaglandin brimonidine and
if cost is an over- and/or a non-selective beta blocker, then the CAIs are most
riding factor (and do a therapeutic trial of either brimoni- effective at their
cost can compro- dine or a topical CAI—brinzolamide or FDA-approved
mise compliance), dorzolamide. Both of these drugs are labeling of t.i.d.
initiate therapy FDA-approved for t.i.d. therapy, and We suggest try-
with a non-selec- when used as monotherapy, will best ing timolol alone,
tive beta blocker serve the patient as one drop every and to only “add”
such as timolol or eight hours. The problem is that there dorzolamide or
levobunolol. They is an inverse relationship between dos- brimonidine if truly
are available in needed to achieve
0.25% and 0.5% target IOP. These
concentrations, are rare occa-
and are readily sions.
available for about 1. Parrish RK, Palmberg
$4 per 5ml at P, Sheu WP; XLT Study
Group. A comparison of
many pharmacies. latanoprost, bimatoprost,
Since melanin and travoprost in patients
with elevated intraocular
pigments can bind pressure: a 12-week,
some medicines, randomized, masked-
evaluator multicenter
we use the 0.5% study.
concentrations
REVIEW OF OPTOMETRY MAY 15, 2011 5A
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8. Glaucoma
concerns, which is the essence of that can indeed safely use a topical Glaucoma is very similar. With the
this question. The decision is just nonselective beta blocker. We have, limits of our current technology, it
not so dichotomous! in fact, had the occasion to do such, could well be reasonable to pro-
For background, we are currently but only after consultation with the claim a repeatable visual field defect
treating hundreds of patients with patient’s primary care or pulmo- as the “Holy Grail” of glaucoma
glaucoma medicines who do not nary physician. It has recently been confirmation. However, we have
have glaucoma! We obsessively- demonstrated that systemic beta patients with 0.8 cups with no visu-
compulsively assess each of our pa- blockers are in fact therapeutic in al field defects, and we confidently
tients; for those whom we feel are the setting of COPD for many such tell them that they have glaucoma
at considerable risk to develop glau- patients. So, if you have a need to (based on progressive cupping, thin
coma, we intervene therapeutically use a beta blocker in a patient with corneas, and/or high IOPs). So,
in what we believe will prevent the what you might think are systemic in one sense, the question may be
development of glaucoma. Ex- contraindications, consult the pa- more academic and philosophical
amples of such patients are younger tient’s physician—it may well be than clinical and firm.
people with very high intraocular that your therapeutic need can be
pressures; very thin corneas (physi- successfully met. Q: A very similar question: At
ologically, not via keratorefractive what point, clinically, do you begin
surgery); compromised optic to inform patients that you are
nerve head tissues (based on following them as a “glaucoma
either stereoscopic ophthalmos- suspect”?
copy or a nerve fiber layer scan- A: It depends. If there is a
ning device or both, without vi- family history of glaucoma, a
sual field defects); a very strong borderline IOP (around 18mm
family history; or a combination Hg to 26mm Hg), a 0.4 to 0.6
of the above. These decisions cup, a corneal thickness below
are complex and require the as- 510µm, then such patients might
similation of a constellation of be considered “suspicious.”
parameters. But, these various parameters
Lastly, note that doctors of cannot be viewed in a vacuum!
equal competence legitimately The entire clinical picture must
differ on the decisions of treat- be considered collectively. Only
ing vs. attentive monitoring. then can “risk” be rationally
The soundness of whichever de- When does the diagnosis change from ocular assessed.
cision is made usually becomes hypertension to glaucoma?
clear over the ensuing five to 10 Q: When would you discon-
years. A patient is rarely a “glau- Q: When does the diagnosis tinue glaucoma therapy started by
coma suspect” beyond five to eight change from ocular hypertension another clinician?
years, because during this time span to glaucoma? Does the diagnostic A: If, in your clinical opinion,
it should become clear whether definition of glaucoma require a and after a thorough examination,
they have progressive disease or just visual field defect? you feel the patient may not merit
benign risk factors. A: This question is ubiquitous therapy, then a thoughtful “reverse
and haunts most glaucoma clini- therapeutic trial” is very reason-
Q: Are topical nonselective beta cians. Glaucoma is not like a light able. We would have a long conver-
blockers an absolute or a relative switch; either present or absent, but sation with the patient explaining
contraindication in patients hav- rather like a light controlled by a how good doctors commonly have
ing reactive airway disease and/ rheostat. As you begin to reduce the different approaches to the same
or chronic obstructive pulmonary energy flow to the light, the light condition, and that at the least you
disease (COPD)? begins to become less bright—but would like to know the patient’s
A: Only recently has it become when would the average person say true baseline intraocular pressure.
clear to us that the correct answer the luminance goes from “bright” This is something we do commonly,
is “relative.” There are patients to “dim”? There is a zone or range especially if the patient has no
who have lesser expressed asthma in which this declaration is made. positive family history of glaucoma,
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9. Glaucoma
has a thick cornea (greater than tients,” we assume you mean those shortly upon awakening, regardless
580µm—our subjective cutoff), who have a 0.4 to 0.5 or greater of the actual time of the day. Pros-
and/or has healthy-appearing optic cup. If the cup is small and the pres- taglandin efficacy is, by and large,
nerve heads. We also get a Consent sure is normal, this is almost always time of instillation-independent.
for Release of Records from the pa- a plain ol’ normal patient. But, if While slightly more effective when
tient so that we can have the benefit the optic nerve head is suspicious in taken toward the end of a waking
of the prior doctor’s observations appearance, there is a 100% chance period, actual time of instillation is
and thoughts. we will assess the corneal thickness! not a major issue with the prosta-
glandins. So, regardless of the time
Q: Do you obtain pachymetry Q: For patients who work second of the patient’s sleep cycle, it is
on all of your low-normal tension or third shift, how do you recom- always best to instill beta blockers
patients, just to see if the cornea is mend dosing schedules for prosta- shortly upon awakening. While it is
thin? glandins and beta blockers? best to instill the prostaglandins just
A: By “low-normal tension pa- A: Beta blockers are best instilled prior to retiring, time of dosing is
Key Points to Ponder in Glaucoma Management
It is well established that there is some diminution in quality of
• Visual field test results are extremely variable, and it life when a person is diagnosed with glaucoma, as at that point
may take three to five tests over a two to four-year period of their lifestyle is encumbered with medication habituation behav-
time to truly know the extent (if any) and/or rate of progres- ior, as well as cost concerns, and perhaps the ultimate concern
sion of a visual field defect. The exception to this is if there is a of going blind. Note that we, like you, are attentive physicians,
strong clinical correlation. For example, if there is observable infe- and we carefully monitor our patients. If there are any consistent
rior erosion of the optic nerve rim, and there is a dense superior signs of accelerated progression, we would institute therapy. Yet
field defect, then such a defect can be viewed with certainty, and we have learned over the past 30 years to not be trigger-happy,
probably annual retesting is all that is indicated. but rather to be very thoughtful in our management decisions.
The much more common finding, however, is a generalized Standard white-on-white perimetry can facilitate diagnosis, as
scattering of scotomas, or a nonspecific clustering that does not well as provide guidance regarding progression.
correlate with the optic nerve anatomy or a nerve fiber analyzer
scan. It is these vague, non-clinically-correlatable visual field • Always initiate therapy with a lesser concentration of
defects that must be verified by repeat testing, perhaps three to medication if available. Remember, in therapeutic intervention,
five times, in order to know with certainty whether the defect(s) we have a target IOP range in our heads, and our goal should be
is a true reflection of optic nerve damage or simply artifacti- to achieve an IOP within this range with the least medical inter-
tious noise. A classic mistake is to observe what appears to be a vention possible.
change in the visual field and make management decisions based Unfortunately, we have few lower-concentration options in
upon “apparent” demise of the visual field. This is almost always glaucoma therapy: 0.25% timolol (or levobunolol), bimatoprost
an error in clinical judgment and management. 0.01% and pilocarpine 1%. Being faithful to this concept, our rou-
In summary, if the field is normal, believe it to be normal; if it is tine dilating drop only contains 0.25% tropicamide (Paremyd also
borderline or questionable, then repeat the testing. contains 1% hydroxyamphetamine hydrobromide). Thankfully, we
now have the lesser concentration of bimatoprost (0.01%) and the
• It is by and large a myth that short wavelength (blue-on- concentration of BAK has been increased from 0.005% to 0.02%
yellow) or frequency doubling perimetry detects glaucoma (the same as is in latanoprost).
earlier than standard (white-on-white) automated perimetry. A couple of unsubstantiated thoughts come to mind: Because
Furthermore, it truly may not be in the patient’s best interest to BAK enhances drug penetration, it may be that this higher con-
be diagnosed “too early” in the setting of early glaucoma. Recent centration of preservative is what enables the 0.01% bimatoprost
results from the Ocular Hypertension Treatment Study follow-up to provide the same reduction in IOP as the 0.03%, and that it is
showed that delaying IOP reduction for a few years did not result not the BAK potentially causing side effects, but rather the active
in any loss of ultimate control. On average, glaucoma progresses drug itself. The manufacturer claims a significant reduction in
at about 3% per year. With the excellent medicines available to side effects with the 0.01% rendition of the bimatoprost. So keep
us, we can intervene therapeutically in a thoughtful, timely man- in mind that “less is better,” as long as the target IOP goal is
ner to gain good control of the intraocular pressure once the need achieved and maintained.
for control is clearly indicated. (continued on page 9A)
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10. Glaucoma
diagnosis. It is well established that
a subset of the population has quite
marked nocturnal hypotensive epi-
sodes. This could cause a pathologi-
cally low perfusion pressure to the
optic nerve (and brain) during the
sleep cycle.
For this reason, patients with
true low tension glaucoma (and
especially patients who have had
nonarteritic anterior ischemic optic
neuropathy in one eye) should
perhaps only take their blood pres-
sure medicine near breakfast time
and never at bedtime, where this
“piling on” effect could play a key
role in optic nerve tissue demise. A
conversation with the patient’s pre-
Confrontational visual field testing as a screening tool is standard-of-care, but is this scribing physician certainly should
test really adequate? be accomplished.
not a major issue with the prosta- function was treated. I realize it’s a Q: Since breath-holding can
glandins. multifactorial disease, but let’s rule increase episcleral venous pressure
out the easy options. and therefore intraocular pressure,
Q: What is your opinion on A: Thoughtful question. One should we routinely emphasize
confrontational visual field testing would think that thyroid disorders “keep breathing normally” during
as a screening tool in the context of could have an impact on aqueous tonometry?
comprehensive eye examination? production and/or outflow. In all of A: We would suggest that the
This is standard-of-care, but is this our exhaustive reading of the world clinician simply be attentive during
test really adequate? literature, we have never read of the procedure, and perhaps just en-
A: The world’s premier author- any such association with thyroid courage the patient to relax before-
ity in neuro-ophthalmology is Neil dysfunction. We can’t explain your hand. It is usually obese, anxious,
Miller, M.D., at the Wilmer Eye anecdotal observations, and, as you short-waisted, large upper body-
Institute at Johns Hopkins. He rightfully point out, glaucoma is a size patients that often struggle to
stated that 90% of all clinically multifactorial disease, so perhaps properly position themselves at the
significant neurologically-related other factors are at play that are slit lamp. This is why we all need to
visual field defects can be detected not yet fully elucidated. have alternative instruments at the
by confrontation examination. He ready to enable more accurate IOP
recommended that this assessment Q: Since it is known that some assessments in these patients, such
be done as counting-fingers in each low tension glaucoma patients as a handheld (Kowa or Perkins)
quadrant, not bringing in a target may be compromised by nocturnal applanation tonometer or an Icare
from non-seeing areas into see- systemic hypotension, should these Rebound tonometer. Also, beyond
ing areas. We have followed Dr. patients have a sleep study? breath-holding, the blepharospas-
Miller’s guidance since the early A: Perhaps. This is an area of tic patients most always do better
1980s, and have found his observa- ongoing research, and in select with handheld devices than those
tions to be spot-on. patients, knowing their diastolic mounted at the slit lamp.
nocturnal blood pressure profile
Q: Why isn’t thyroid function could potentially be very helpful. Q: Do prostaglandins cause or
part of the glaucoma workup? Along this same line of thought is increase the risk of recurrent cor-
I have seen three patients, and the consideration of the patient’s neal erosions?
heard of more, with high IOP that medical treatment for systemic A: This question acknowledges
normalized after their thyroid dys- hypertension, if they carry that two clinical realities:
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11. Glaucoma
(continued from page 7A) • If you have not yet acquired a nerve fiber layer imaging
instrument, we encourage you to do so as soon as you can
• Do not “micromanage” any single component of the justify the cost of the purchase. Without debate, the technology
glaucoma workup. For example, refrain from performing a quan- to acquire is an ocular coherence tomography (OCT) unit. We rec-
titative analysis on central corneal thickness: the cornea is simply ommend spectral-domain OCT technology because it can give you
thick, thin, or normal. Here are our entirely subjective breakpoints: quantitative information on the retina nerve fiber layer for glauco-
thick is >580µm to 590µm, and thin is <500µm to 510µm. ma assistance, and also provide diagnostic help for hydroxychlo-
What’s in the middle is essentially normal, and minimally impact- roquine and other screenings, as well as for macular conditions
ful to our decision-making process. such as central serous retinopathy, macular edema, etc.
By the way, the cornea reaches adult thickness by age 10. We While the Fourier (spectral)-domain platform is the most
have already discussed how incredibly subjective visual field data sophisticated technology available, the truth is that a basic OCT
are. Even so-called “objective” tests, such as nerve fiber layer is amply adequate to meet the vast majority of the clinical needs
analyses, are not precisely objective; they are simply less variable. of practicing eye doctors. We’d much rather see an O.D. have
We have seen nerve fiber layers “thicken” a bit year to year, and a time-domain OCT than not have an OCT in his/her diagnostic
test to test, but short of retinal edema, nerve fiber layer thickness armamentarium at all. One can always upgrade later. We have
stays the same or slowly thins. So we know an “improved” nerve never encountered an O.D. who acquired an OCT who was not
fiber layer is just a change relative to a prior test. As with visual thrilled to have it. Do note, though, that the time-domain OCT
fields, do not make a management change based on the result of technology is not adequate for hydroxychloroquine screening. This
a single test, even those that are supposedly objective. is the most notable shortcoming of the time-domain technology.
With IOP, we know it can fluctuate wildly. Thus, if the IOP is up
on one visit and down the next, we do not make proclamations • We think there is now a
such as “You’re doing great!” or “You’re getting worse;” rather, technology “ready for prime
we proclaim that “overall, it appears that your pressure control is time” (it is awaiting FDA-
pretty stable,” or some other appropriate statement. We most cer- approval) to allow patients
tainly do not know what each individual’s IOP is during sleep. to do self-tonometry. It is
It is well established that there is considerable inter- and intra- from Icare, the inventor of
observer variability in the numeric assessment of the optic disc the Icare Rebound tonometer
anatomy (i.e., the cup-to-disc ratio). It would perhaps be over- (www.Icaretonometer.com).
confident to chart “cup has enlarged from 0.3 to 0.4, therefore It uses the same exact
will initiate therapy,” etc. One would more likely have to see a 0.2 rebound technology as the
change, or perhaps even a 0.3 change in order to state with any standard, handheld unit, but is
authority that there has been progressive optic neuropathy. placed in a special handheld frame type device that should allow
So, it can be seen that there are several opportunities to most adults to competently obtain a series of measurements
become bogged down with minutiae in the global context of the on their own, and outside of typical office hours. This should
comprehensive glaucoma evaluation. There are plenty of data be a huge help to learn our glaucoma suspects’ and glaucoma
points, plenty of parts, so that a thoughtful doctor should be able patients’ IOP behaviors early in the mornings, late in the evenings,
to assimilate these various pieces and arrive at a rational stratifi- and perhaps even mid-sleep, for those patients who habitually
cation of risks for, or stage of, glaucoma. awake during the night to use the bathroom.
(1) Prostaglandins potentiate the stage for epithelial erosions. glaucoma suspects. I have a large
cytoarchitecture remodeling ability While this question is quite intel- geriatric population, but is that
of extracellular matrix metallopro- lectual, and obviously has a sound percentage too much?
teinases. This is indeed the mecha- scientific basis, we are not aware A: It seems reasonable that your
nism of action by which prostaglan- of any studies that point toward percentage is in keeping with the
dins enhance uveoscleral outflow. an increased tendency in patients prevalence of glaucoma suspects
(2) There is an abundance of to experience recurrent corneal in an aged population. We do
matrix metalloproteinases at sites erosions while using prostaglandin know that increased age is a key
within the cornea where the epi- eyedrops. risk factor for the development
thelium is loosely adherent. These of glaucoma. We commend your
destructive enzymes weaken the Q: I’ve carefully studied my keen attention to your patients, and
epithelial-basement membrane-an- patients’ optic nerves, and I esti- further commend your focus on the
terior stromal complex, setting the mate that 5% to 10% of them are optic nerve, not the IOP. ■
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12. Glaucoma
Medical Management of Acute
Angle-closure Glaucoma
Almost all cases of angle-closure glau-
coma can be successfully—and calmly—
managed in the office. First, one needs
to have on hand all the meds that might
be useful in such a rare presentation.
These would include acetazolamide tab-
lets, either 250mg or 500mg. Do not use
the 500mg Diamox Sequels because an
extended, time-release of the medicine is
not as impactful as the quicker onset of
action that one gets from the tablet forms.
You also need to have 0.5% nonselec-
tive beta blocker, brimonidine, and 2%
pilocarpine at the ready. There is little
to no value in the use of a prostaglandin
in the setting of acute angle-closure
glaucoma, as the aforementioned rapid- A gonioscopic image (above) of an counterproductive to opening the angle.
onset medications perform very nicely. angle in closure. In a different eye in The 2% seems to be the optimum bal-
The prostaglandins’ speed-of-onset is acute angle closure (below), note the ance between effectively stimulating the
relatively slow, and is simply not needed fixed, mid-dilated pupil in a red eye. parasympathomimetically innervated
(like too many cooks in the kitchen) in this musculature of the iris sphincter, and
situation. not creating overall iris volume expan-
In the event the patient is vomiting, sion. Keep in mind that the iris sphincter
have Compazine (prochlorperazine) sup- becomes very lethargic when the IOP
positories stored in the refrigerator. It is exceeds around 60mm Hg, so the pilocar-
counterproductive, if not impossible, to pine will be most pharmacologically active
get oral acetazolamide tablets into the once the intraocular pressure drops into
patient’s system when the patient has the 50s or 40s.
uncontrolled vomiting. A single antiemetic This is why the aqueous suppressants
suppository quickly calms the storm are used first, and pilocarpine shortly
in most cases, and thereby allows the after. Of course, once the IOP is con-
appropriate administration of oral medi- trolled, the patient is kept on the 2% pilo-
cation. (Note that most patients prefer drops, and then a second drop of brimo- carpine q.i.d. until a YAG photoiridotomy
to insert the suppositories themselves; nidine in two to three minutes. Both beta can be performed—which may take a
another good reason to keep gloves avail- blockers and alpha adrenergic agonists day or two to schedule, depending upon
able in the office.) rapidly decrease aqueous production via the location and availability of this ser-
Since all carbonic anhydrase inhibitors separate pharmacologic mechanisms. vice. Of note, there can be considerable
contain a sulfa moiety, there is perhaps In 10 minutes or so, instill 2% pilocar- conjunctival injection present as well, and
a slight chance of a sulfa allergy even in pine. It is the pilocarpine that will actually if so, then a potent corticosteroid, such
these non-sulfonamide medicines. Just to physically open the angle—the other as Lotemax, Durezol or Pred Forte used
be thorough, always inquire if there is a three meds simply reduce the IOP by radi- q.i.d., can help the eye look and feel bet-
history of severe allergic reaction to sulfa. cally subduing aqueous production. ter, particularly if there is any associated
If there is no history of such, then have Why not use 4% pilocarpine? anterior uveal inflammation present.
the patient take 500mg of acetazolamide Pilocarpine is an acetylcholinergic agonist In summary, the diagnosis and treat-
right away. If there is no asthma, then (parasympathomimetic) and can cause ment plan for the uncommon presentation
instill a drop of beta blocker, followed by blood vessel dilation, thus enlarging the of acute angle-closure glaucoma is very
a second drop in two to three minutes. mass volume of the iris, and in turn caus- straightforward. The key is to have all the
Get in a drop of brimonidine in between ing some anterior-posterior dimensional medications necessary at the ready to
the two administrations of beta blocker swelling of the peripheral iris, which is treat the patient quickly and efficiently.
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13. Glaucoma
Glaucoma Pearls
• Even glaucoma subspecialists cannot always judge optic
• Childhood glaucoma is very rare. Note that virtually all nerve glaucomatous “progression” from sequential optic
cases of childhood glaucoma have significantly increased intra- nerve head photographs. “Interobserver agreement among
ocular pressure. glaucoma specialists in judging progressive optic disc change
The key in such suspicious cases is to examine the optic from stereophotographs was slight to fair. After masked adju-
nerves of parents and/or siblings, to photodocument the optic dication, in 40% of the cases in which the optic disc appeared
nerves, and to attentively follow these children every six to 12 to have progressed in glaucoma severity, the photograph of the
months until it becomes clear whether these suspicious optic ‘worse’ optic disc was in fact taken at the start of the study.
nerves are either a physiological variant, or there is evidence of Caution must be exercised when using disc change on photo-
progression. Bear in mind that asymmetry of approximately 0.2 graphs as the “gold standard” for diagnosing open-angle glau-
cup-to-disc ratio is a common physiological finding.1 coma or determining its progression.”4
It may take longer than the five to 50 months (median 26
• Central corneal thickness reaches adult status by age months) of analysis performed in this study to accurately discern
10. changes in optic nerve anatomy. Because glaucoma progresses
on average at a rate of 3% per year, it may take more like eight
• Most patients with ophthalmoscopically visible optic to 10 years to competently and accurately judge progression
nerve drusen manifest wide-ranging variations of visual field using optic disc photography. We think sequential nerve fiber
defects. If these patients are observed to have high intraocular layer scanning technology may be a more refined manner to
pressure, or if there is a documented steady increase in IOP over assess progression.
time (years), then it may be prudent to institute IOP-lowering
therapy. By and large, visual field and nerve fiber layer scanning • “Objective” technology is not absolutely objective, only
data will be relatively useless, and so keeping IOP at physiologi- objective relative to other subjective tests. It is well under-
cal levels is likely the wisest course. stood that visual field testing can be highly variable from test
to test. We love our nerve fiber layer scanning instruments, and
• The single most challenging decision in the care of depend upon them to aid us in the assessment of our glaucoma
patients who are glaucoma suspects endures: When should patients, but even these wonderful “objective” tests can vary
therapy be initiated? “In the end, the physician is struck with slightly from test to test.
the persistent problem of whom to treat and whom to watch… Our advice: Never micromanage any single component of the
The endless symposium and debate on how to best manage glaucoma evaluation, but rather look for repeatable trends over
with ocular hypertension will probably continue unabated.”2 time (years).
This seminal declaration precisely establishes the imprecision Regarding visual field testing, we recommend the Humphrey
of decision-making and caring for patients with glaucoma. One 24-2 SITA-Standard or SITA-Fast, using standard white-on-white
doctor may judge the best course of care to be watchful waiting, perimetry (standard achromatic perimetry, SAP). Newer research
while another may pursue a course of active treatment. In these as shown that there is little or no advantage to using blue-on-yel-
unclear cases, one doctor cannot declare the other errant in clini- low (short-wavelength automated perimetry, SWAP) or frequency
cal judgment. The truth is, it may require many years of following doubling technologies.5-7
such a patient in order to know with certainty which course con-
1. Beck A. Evaluating and Managing Optic Disc Cupping in Children. Glaucoma Today.
fers the greater benefit to the patient. Jan-Feb 2009.
We urge the clinician to provide all glaucoma suspects a 2. Sommer A. Treatment of ocular hypertension: Hamlet’s Lament revisited. Arch Ophthal-
mol. 2010 Mar;128(3):363-4.
state-of-the-art assessment, develop a solid patient care plan, 3. Barkana Y, Dorairaj SK, Gerber Y, et al. Agreement between gonioscopy and ultra-
and be confident in that care plan. Do not concern yourself with sound biomicroscopy in detecting iridotrabecular apposition. Arch Ophthalmol. 2007
Oct;125(10):1331-5.
the potential for another clinician’s different approach. Above all, 4. Jampel HD, Friedman D, Quigley H, et al. Agreement among glaucoma specialists in
carefully, attentively follow the patient.2 assessing progressive disc changes from photographs in open-angle glaucoma patients.
Am J Ophthalmol. 2009 Jan;147(1):39-44.e1.
5. van der Schoot J, Reus NJ, Colen TP, Lemij HG. The ability of short-wavelength auto-
• The website gonioscopy.org is a magnificent way to mated perimetry to predict conversion to glaucoma. Ophthalmology. 2010 Jan;117(1):30-4.
6. Bengtsson B, Heijl A. Diagnostic sensitivity of fast blue-yellow and standard automated
improve your assessment of the iridocorneal angle anatomy. perimetry in early glaucoma: a comparison between different test programs. Ophthalmol-
“In routine clinical practice, gonioscopy should be performed in ogy. 2006 Jul;113(7):1092-7.
7. SWAP or DOUBLE? International Glaucoma Review: The Journal for the World Glau-
a dark room to avoid misdiagnosis of treatable iridotrabecular coma Association. 2008 Sep; 10-2. Available at: www.e-igr.com/SP/index.php?issue=102
apposition.”3 &supID=7&pageID=146.
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14. Beneath the Surface of
Dry Eye Disease
We now understand that most ocular surface dryness is related in one way or
another to meibomian gland dysfunction, which affects the tear film lipid layer.
rom a disease management
F perspective, the single most
common clinical challenge we
face each day is helping patients
who suffer from ocular surface
disease, predominantly ocular
surface dryness. It is now realized
that most ocular surface dryness
is related in one way or another
to meibomian gland dysfunction.1
This leads to a poorly perform-
ing tear film lipid layer. Logical
thought would then move us to
recommend a lipid-based artificial
tear as initial therapy. Dry spots on the corneal surface are associated with reduced tear film break-up time.
In addition, we start all of our
dry eye patients on 2,000mg of hances meibomian gland function. the ultimate treatment/management
fish oil. We urge them to take such This gives more rapid improvement of meibomian gland disease is heat
with breakfast. We do not get of patient comfort and simultane- and massage, not medical.
hung up on micromanaging this ously buys time for the fish oils With this comprehensive back-
oral supplement with regard to the to kick in. (For those few patients ground, we now answer questions
debate over triglyceride versus ethyl who cannot swallow these rather regarding dry eye.
ester formulations—just fish oil. By large capsules, Nordic Naturals,
the way, and just for perspective, Coromega and others make very Q: If a patient were to be allergic
cardiologists commonly prescribe palatable liquid formulations.) to doxycycline, what would you
Lovaza (GlaxoSmithKline), a puri- A more thorough discussion of recommend for treating meibomian
fied omega-3 fish oil supplement of meibomian gland gland dysfunction?
an ethyl ester variety. treatment is found A: We have never encountered
While fish oil can help with mei- on page 12A, but this; the answer is probably oral
bomian gland secretions, it often erythromycin or oral azithromycin.
takes four to six months to begin We might even prescribe a 5mg
to see an effect. For this reason, we steroid Dosepak, just to potentiate
often prescribe 50mg of oral doxy- the mild anti-inflammatory proper-
cycline once daily for two to three ties of these two antibiotics.
months. From our observations, it
more quickly and more potently en- Q: In the setting of dry eye,
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15. Dry Eye
which drop works best with contact
lenses?
A: We would generally select
any artificial tear that is not BAK-
preserved, and have the patient use
it as often as is needed to achieve
and maintain comfort. We like to
use punctal plugs to diminish the
frequency of, or need for, any artifi-
cial tear. Don’t forget to use fish oil
supplements as well. We commonly
recommend 2,000mg taken every
day with breakfast.
Q: For dry eye, Leiterspharmacy.
com will fill an Rx for 5% albumin Most ocular surface dryness is related in one way or another to meibomian gland
drops—any comments? dysfunction. This leads to a poorly performing tear film lipid layer. Logical thought
A: We have never used this ap- would then move us to recommend a lipid-based artificial tear as initial therapy.
proach with any of our patients, but
for those few dry eye patients for
whom the “kitchen sink” approach New MGD Device on the Way
has not achieved control and relief, While not yet FDA approved, there is an incredibly ingenious device known as the
this would likely be worth a try. LipiFlow Thermal Pulsation System (TearScience Inc.), which both heats the eyelid
Another approach that is talked (from the tarsal conjunctival side
about in these more challenging where adequate heat levels can
cases is the use of autologous serum, be achieved), while simultane-
which we have each used on rare oc- ously massaging/expressing the
casions with success, and think that glands. Both the heat application
this more comprehensive source of and compression pressure are
ocular nutrition would be superior precisely controlled for optimum
to albumin. patient care.
We foresee the day when a
Q: How do you approach the patient who needs meibomian
contact lens-wearing dry eye pa- gland therapy will schedule a
tient? follow-up appointment to come
A: There are a number of ap- into the office for a “meibomian
proaches. Here’s what we usually expression treatment” session
do: using the LipiFlow technol-
• Quantify the degree of ocular ogy. Such a therapeutic session
surface dryness. has the potential to reduce or
• Replace “rewetting drops” with eliminate symptoms for six to 12
a top-quality artificial tear. We have months.
had excellent success with lipid- Necessity is the mother of
based tears. invention, and the LipiFlow tech-
• We recommend 2,000mg of fish nology may just be what the doc-
oil supplementation every day for tor will soon order. It should come
nearly all of our dry eye patients. as no surprise that the inventor
Note that it may be three to six of this technology is Donald Korb,
months before an effect can be ap- O.D. He has done so much over
preciated. Whatever the case, fish oil the years to enhance patient care
is a very healthy substance, and is and make our profession proud.
likely beneficial to total body health,
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16. Dry E ye
whether it improves tear function subject patients to more office visits of action than omega-3 supplemen-
or not. than needed? We never use intra- tation, so for our more symptom-
• Try loteprednol 0.5% b.i.d. (a canalicular plugs because of an atic and inflamed dry eye patients
drop in the morning a few min- increased risk of canaliculitis, and we often prescribe 100mg (50mg
utes prior to lens insertion, and a we like to be able to see the plug at b.i.d.) of generic oral doxycycline
second drop after lens removal in the punctum. This way, we—and for a week or two, then decrease to
the evening) in the setting of acute our patients—can tell if the plug is 50mg once daily for two to three
inflammation. It is exceedingly rare present or not. more months. After having been
that an individual has a legitimate on the doxycycline for two
reason (laziness is not one of them) months, we often start fish oil
to sleep in contact lenses. as well. So, as we finish the
• If, after a month of the above course of doxycycline, the fish
maneuvers, the patient remains oil should be able to pick right
symptomatic, try a punctal plug in up where the doxycycline
the lower eyelid of the more symp- leaves off. Both doxycycline
tomatic eye, and then evaluate the and fish oil render a benefit
results in another month. to meibomian gland func-
• Try a different brand of contact tion. The topical steroid helps
lenses. to quiet the ocular surface
• Try Restasis (cyclosporine, Al- If the patient remains symptomatic after a inflammation, while the doxy-
lergan). It may do the trick in some month of usual maneuvers, try a punctal plug in cycline and/or fish oil supple-
patients. Like fish oil, it takes three the lower eyelid of the more symptomatic eye. mentation aids meibomian
to six months to produce an effect. gland function, which yields
• Try a different disinfecting While all punctal plugs work a two-pronged approach in helping
system, such as a hydrogen perox- well, we have evolved into using the the dry eye patient.
ide system. Odyssey brand because of ease of
By attentively and systematically insertion and retention properties. Q: If you do get an increased
considering the above interven- We do measure punctal diameter in intraocular pressure while using
tions, most patients can be helped an attempt to obtain the most op- Lotemax, what do you suggest?
considerably. timum fit. Note that punctal plugs A: It depends on how well the
create some beneficial scarring once patient has responded to this ther-
Q: Is it safe to use OTC Vase- the plug has resided in the punc- apy, and the degree of intraocular
line petroleum jelly directly into tal tissues for several weeks. This pressure increase. If the patient was
the lower cul-de-sac at bedtime for explains why many patients do not getting a good response to the cor-
chronic nocturnal lagophthalmos? revert to symptomatic status once a ticosteroid, then we would consider
The cost is very minimal compared plug has been lost or extruded. switching to the 0.2% loteprednol
to a tiny tube of petrolatum jelly/ (Alrex) if the IOP increase was less
mineral oil combination. Q: I recently read that flaxseed than 10mm Hg above baseline, and
A: It must be safe, because we oil causes inflammation of the monitor the intraocular pressure.
have had many, many patients over prostate. Has this influenced your If the IOP increase is greater
the years use Vaseline-type products recommendation for the male dry than 10mm Hg, then we would try
in their eyes without a problem. eye patient? a topical NSAID or cyclosporine
A: Yes, it has. We instead recom- IF the patient had a positive initial
Q: Which punctal plug do you mend fish oil (2,000mg per day) for response to anti-inflammatory
use for maximum patient comfort all of our dry eye patients. therapy. If there was little initial
and efficacy, and do you ever use response to the steroid, we see little
dissolvable/temporary plugs? Q: If you are using Lotemax in potential to try other anti-inflam-
A: From the outset, we have the setting of managing dry eyes, matory approaches.
always used permanent plugs. It is when would you consider add- 1. Green-Church KB, Butovich I, Willcox M, et al. The inter-
our clinical impression that well- ing oral doxycycline, and for how national workshop on meibomian gland dysfunction: report
of the subcommittee on tear film lipids and lipid-protein
trained clinicians can determine the long? interactions in health and disease. Invest Ophthalmol Vis Sci.
need for occlusion or not, so why A: Doxycycline has a faster onset 2011 Mar 30;52(4):1979-93.
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17. Dry Eye
A Scientific View on
Blepharitis and MGD
Recent literature has used the terms posterior blepharitis and meibomian gland
dysfunction as if they were synonymous, but these terms are not interchangeable.
hanks to the recent report MGD Report Released
T from the International Work-
shop on Meibomian Gland
Dysfunction, organized by the Tear
Just as the Dry Eye WorkShop (DEWS) report brought greater
understanding of dry eye in 2007, the International Workshop
on Meibomian Gland Dysfunction report published in March
Film & Ocular Surface Society, 2011 brings greater understanding of meibomian gland dys-
we have new and more scientifi- function. All optometrists should read this report, if not in
cally proper nomenclature for these its entirety, then at least the “executive summary.” These
(mostly) distinct clinical entities. can be viewed via www.tearfilm.org/mgdworkshop.
Here is the definition from the Although several critical questions remain unanswered,
MGD workshop: this landmark report advances our understanding of
“Posterior blepharitis is used to meibomian gland functions and their clinical significance.
describe inflammatory conditions Because it is well known that most “dry eye” is underpinned by
of the posterior lid margin, includ- meibomian gland dysfunction and disease, it is imperative that all O.D.s acquaint them-
ing MGD. Indeed, recent litera- selves with this report.
ture has used the terms posterior
blepharitis and meibomian gland constitutes the vast majority of “professional” therapeutic modal-
dysfunction or MGD as if they afflictions to the posterior tissues ity, and should completely replace
were synonymous, but these terms of the eyelids. So, to keep things the older, out-of-date baby sham-
are not interchangeable. Distinct simple, blepharitis is an anterior poo approach.
from the portion of lid margin ante- infectious/inflammatory condition, There are those patients who do
rior to the gray line, which includes while MGD represents the prepon- have clinically significant eyelid
the skin and eyelashes, the posterior derance of posterior eyelid disease. erythema and other signs of inflam-
lid margin contains the marginal They are managed very differently. mation, such as lash misdirection
mucosa, the mucocutaneous junc- and madarosis. These inflammatory
tion, the meibomian gland orifices Blepharitis signs are predominantly manifested
and associated terminal ductules, Blepharitis (like rheumatoid as a response to staphylococcal
and the neighboring keratinized arthritis and dandruff) is a chronic exotoxins. When there is clinically
skin. Posterior blepharitis is a term disease, and the absolute mainstay significant eyelid inflammation,
used to describe inflammatory con- for control (not cure) is initial and medical therapy is indicated to help
ditions of the posterior lid margin, enduring eyelid hygiene. Forget achieve tissue restoration. This can
of which MGD is only one cause. baby shampoo; this is obsolete be accomplished in several ways.
Other causes include infectious or when compared to commercially One way is the use of combination
allergic conjunctivitis and systemic available eyelid scrub products such antibiotic/steroid eye drops q.i.d.
conditions such as acne rosacea.”1 as OCuSOFT Eyelid Cleanser or for two to four weeks. Options here
It has been our observation that SteriLid (TheraTears). These have include Zylet, generic TobraDex,
MGD, with or without rosacea, the appearance and function of a TobraDex ST, or generic Maxitrol.
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