`
`FC_DG0511.indd 3FC_DG0511.indd 3
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`Exhibit 1081
`ARGENTUM
`IPR2017-01053
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`

`

`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
`
`CONTINUING EDUCATION
`
`Our Courses on Your Computer!
`
`A team of California optometrists/educators has developed
`a website, OptSpace.com, to provide optometrists and
`their staff educational enrichment in the area of medical
`diagnosis and treatment, and other areas of interest to optometry. OptSpace has partnered
`with us for several video presentations that can be viewed from any computer or electronic
`media of your choice. This is a new way of accessing Melton and Thomasʼ lectures.
`Currently our emphasis is on glaucoma care, with additional topics available in the near
`future. Our series of lectures will be presented exclusively through the genius of OptSpace.
`We invite you to visit www.OptSpace.com for more details.
`
`Come to China with Us!
`June 12 - 23, 2012
`Bridgitte Shen Lee, O.D., a bilingual and bicultural Chinese-American optometrist,
`created iTravelCE LLC and put together a truly first-class (and beyond!) enlightening
`journey into China for COPE-approved
`optometric CE. She will serve as both course
`director and tour guide. For the educational
`component of this exotic voyage, we will
`provide our comprehensive, 20-hour “Current
`Therapy in Ocular Disease” course.
`The itinerary includes:
`• Beijing, the imperial and modern capital
`city, rebuilt by Kublai Khan in 1215 and host
`of the 2008 Olympics
`• Xiʼan, the cradle of Chinese civilization, the
`seat of the Emperor for more than 10 dynasties and the start of the Silk Road
`• Yangtze River, cruise along the longest, most majestic waterway in Asia.
`We invite you to join us for a trip of a lifetime!
`For more details, visit www.iTravelCE.com, e-mail info@iTravelCE.com, or call
`832-390-1393.
`
`Visit our website: www.eyeupdate.com
`
`
`
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`

`

`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
`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-
`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:
`(cid:129) an increased concentration of gatifloxacin (Zymaxid, which is a
`0.5% formulation)
`(cid:129) a decreased concentration of bimatoprost (Lumigan 0.01%)
`(cid:129) a decreased concentration of dexamethasone combined with to-
`bramycin (TobraDex ST)
`(cid:129) another topical antihistamine for once-daily use (Lastacaft)
`(cid:129) a reformulation of moxifloxacin (Moxeza)
`(cid:129) a newer, lipid-based artificial tear (Systane Balance)
`(cid:129) the first once-daily topical NSAID, bromfenac (Bromday)
`(cid:129) 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-
`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
`mission is.
`
`With all best wishes to our esteemed colleagues,
`
`Ron Melton, O.D.
`
`
`
` Randall Thomas, O.D., M.P.H.
`
`CONTENTS
`
`Glaucoma ............................. 2A
`
`Beneath the Surface of
`Dry Eye Disease ................. 12A
`
`Corticosteroids .................. 18A
`
`Topical Antibiotics ............. 22A
`
`Antiviral Strategies ............ 26A
`
`Combination Drugs ............ 29A
`
`Clinical Update on the
`NSAIDs ............................... 32A
`
`Keeping Allergy
`Management Simple .......... 34A
`
`Overview of Oral
`Medicines .......................... 36A
`
`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.
`
`
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`

`Glaucoma
`Glaucoma
`
`New drugs may come and old drugs may go, but the essential question remains:
`At what point does the patient “convert” to glaucoma?
`
`A fter 15 years of basking in
`
`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.
`But don’t forget that a once-daily
`beta-blocker is an excellent second-
`line drug for monotherapy, or as
`additive therapy to a prostaglan-
`din. All others must be used twice
`daily and preferably three times
`a day—but it is rare that patients
`can perform these complex instilla-
`tions with any significant degree of
`consistency.
`
`Q: When new patients present
`to our office on multiple glaucoma
`meds, we want to experiment with
`which meds are optimally effec-
`tive. How long does it usually take
`for a medicine’s effect to stop after
`
`2A
`
`REVIEW OF OPTOMETRY MAY 15, 2011
`
`At what point, clinically, do you begin to inform patients that you are following them
`as a “glaucoma suspect”? This is an optic nerve that has converted to glaucoma.
`Note the inferior erosion of the neuroretinal rim.
`
`discontinuing it?
`A: Studies have shown that the
`effects of prostaglandins last longer
`than the other classes. In our prac-
`tices, we wait a month to recheck
`the intraocular pressure after stop-
`ping a prostaglandin. We generally
`assess the effect of such “reverse
`therapeutic trials” in two to three
`weeks for the shorter duration-of-
`action drugs such as the alpha ad-
`renergic agonists, the beta blockers,
`and the topical carbonic anhydrase
`inhibitors.
`
`Q: Would you use a prostaglan-
`din to manage increased intraocular
`pressure in a steroid responder?
`A: Probably not. Most iatro-
`genic intraocular pressure increases
`quickly vanish upon the discontinu-
`ation of the offending corticoste-
`roid, so additional medical therapy
`is usually unwarranted.
`If the IOP was high enough to
`warrant therapeutic intervention
`(perhaps over 35mm Hg to 40mm
`Hg), then we would select a more
`rapid onset medicine such as a beta
`
`
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`

`
`
`GlaucomaGlaucoma
`
`blocker or brimonidine. Prosta-
`glandins are relatively slow in their
`onset of action, and so are rarely
`a class of choice when rapid IOP
`reduction is desired.
`
`Q: Do you recommend occluding
`the nasolacrimal ducts to prevent
`systemic effects from glaucoma
`medicines?
`A: As a general rule, glaucoma
`medicines are very well tolerated,
`and therefore there is not a need to
`undertake unnecessary medication-
`modifying procedures.
`However, if the medicine was
`truly needed for glaucoma care, and
`the patient had a rare side effect
`(such as taste perversion, a cough,
`slight shortness of breath, brady-
`cardia, etc.), then punctal occlusion
`may be wise.
`However, we would try switch-
`ing to another class of drug first, if
`possible. In caring for many hun-
`dreds of patients with glaucoma,
`we have never found the need to
`punctally occlude.
`
`Q: If a visual field is abnormal,
`and repeat testing is normal, do you
`retest? Or is one normal visual field
`all you need?
`A: Clinically significant visual
`field defects are largely predictable,
`and not like a box of chocolates.
`Generally speaking, if the visual
`field is normal, consider it to be
`so. If the visual field is defective
`and the catch trials (fixation losses,
`etc.) are reasonably normal, and
`if the optic nerve neuroretinal rim
`tissues are intact, then we would
`not believe this defective field to be
`a reflection of reality, and therefore
`would repeat the field in a few
`weeks (or even a few months).
`However, if there are defects
`that correspond to alterations in
`the optic nerve head anatomy (such
`as polar erosion), then we would
`believe that the defect is true, and
`
`Latanoprost Goes Generic
`The biggest news in glaucoma in 2011 is that Xalatan lost its
`patent protection March 28. This means we now have generic
`latanoprost. While this is bad news for the drug manufacturers,
`it is good news for glaucoma patients. A basic understanding
`of market dynamics explains why Travatan Z and Lumigan
`have also reduced their costs (either directly or through rebate
`programs, etc.) to be competitive with generic latanoprost.
`Generally speaking, and when prudent to do so, we prefer to
`prescribe quality brand-name products as opposed to gener-
`ics of unknown quality. For this reason, we plan to prescribe
`Travatan Z or Lumigan 0.01% as long as the price points are
`similar to the generic latanoprost.
`We encourage you to call around to your local pharmacies
`to ascertain the cost of these medications. You will be amazed
`at the differences. At press time, our survey of local pharmacies revealed great disparity
`among prostaglandin prices (anywhere from $25 to $85). Overall, it seems that $38 is
`generally the going price. This brings great relief to the cost-burden of glaucoma therapy.
`Also note that the prostaglandins exert a therapeutic effect well beyond 24 hours. For
`a few of our indigent patients with non-severe glaucoma, we have reduced dosing to
`Monday, Wednesday and Friday.
`Now let’s think about this rationally and apply some common sense: The goal in glau-
`coma management is to achieve and maintain an intraocular pressure within the target
`range deemed to be “safe” for each patient individually. With that in mind, medication
`management becomes very elementary: We simply check the IOP at one month and at
`two months after dosage-reduction to see if the IOP remains the same as it did with
`once-daily dosing. If that is the case, then we have achieved our IOP goal, and helped the
`patient from not only a health standpoint, but a financial one as well. We simply need to
`be thinking, compassionate and attentive doctors.
`
`would repeat the field every six to
`12 months to continue to monitor
`for stability or progression.
`If the next field shows “progres-
`sion,” such “progression” MUST
`be confirmed by repeat testing
`(again, in weeks to months based
`on the overall status of the patient’s
`condition). It is well established
`that the vast majority of “progres-
`sion” is artifactitious, and disap-
`pears upon repeat testing!
`
`Q: When you see a family mem-
`ber of a glaucoma suspect patient,
`do you perform a full dilated
`comprehensive eye exam? Do you
`charge them, or is just a quick look
`with the indirect ophthalmoscope
`sufficient?
`A: If it has been over a year since
`the patient has seen an eye doctor,
`
`we provide a standard dilated eye
`examination.
`If there is a history of glaucoma
`suspicion in the family, then we
`would likely obtain pachymetry
`in addition to our always thor-
`ough study of the optic nerves via
`biomicroscopic-enabled (90D, etc.)
`ophthalmoscopy.
`If the optic nerve(s) appear
`compromised in their structure, we
`would then consider accomplishing
`nerve fiber layer assessment, and if
`this were to be suspicious, then we
`would likely obtain a visual field
`assessment.
`Notice that all subsequent testing
`is driven by the sequential findings
`during the course of the eye exami-
`nation. We do not do tests that are
`unwarranted, and we always obtain
`exam elements that are rational,
`
`
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`

`
`
`GlaucomaGlaucoma
`
`prudent, and medically substanti-
`ated. Appropriate charges are
`assessed for indicated professional
`services and diagnostic testing.
`Some of these may be accomplished
`at the initial visit; others may be
`done days or weeks later, depend-
`ing on assessed risk, the disease
`stage, the patient’s desires, insur-
`ance coverage, etc.
`
`We charge a professional fee when
`whatever service or procedure per-
`formed is medically prudent. One
`could code “glaucoma suspect” if,
`in one’s sound clinical judgment,
`there is rational justification to
`conduct such an examination along
`with any rational ancillary testing
`needed to facilitate accurate deci-
`sion making.
`
`Q: How do you code a claim
`for a family member’s glaucoma
`examination when the results are
`normal?
`A: How does an orthopedic
`surgeon code for a radiographic
`study if it is normal? The answer:
`
`Q: At what intraocular pressure
`would you treat the patient on the
`same day as the exam?
`A: Probably 40mm Hg or
`greater, and even at lower IOP if
`there were substantial optic nerve
`compromise.
`
`Q: At a recent glaucoma lecture,
`the specialist stated that nerve fiber
`analysis was pushing back glau-
`coma diagnosis by 10 years; that
`is, initiating treatment for patients
`in their 50s rather than their 60s.
`Bottom line: With no visual field
`defect, would you treat based on
`nerve fiber layer analysis, given the
`potential for long-term consequenc-
`es of using glaucoma medicines?
`A: First, glaucoma medicines are
`generally very well tolerated, even
`in patients who have ocular surface
`disease, so that concern is a mini-
`mal player in decision making. The
`larger question is actually much
`bigger than structural vs. functional
`
`Topical Glaucoma Drugs
`BRAND NAME
`GENERIC NAME
`Beta Blockers
`levobunolol hydrochloride
`Betagan, and generic
`
`
`timolol hemihydrate
`Betimol
`
`
`betaxolol hydrochloride
`Betoptic-S
`timolol maleate
`Istalol
`timolol maleate
`Timoptic, and generic
`
`
`Timoptic (preservative-free) timolol maleate
`
`
`Timoptic-XE, and generic
`timolol maleate
`
`
`
`MANUFACTURER
`
`CONCENTRATION
`
`BOTTLE SIZE
`
`Allergan, and generic
`
`Vistakon Pharm.
`
`Alcon
`Ista
`Aton Pharma, and generic
`
`Aton Pharma
`
`Aton Pharma, and generic
`
`
`0.25%
`0.5%
`0.25%
`0.5%
`0.25%
`0.5%
`0.25%
`0.5%
`0.25%
`0.5%
`0.25%
`0.5%
`
`5ml, 10ml
`5ml, 10ml, 15ml
`5ml
`5ml, 10ml, 15ml
`5ml, 10ml, 15ml
`5ml
`5ml, 10ml, 15ml
`5ml, 10ml, 15ml
`unit-dose
`unit-dose
`2.5ml, 5ml
`2.5ml, 5ml
`
`Prostaglandin Analogs
`Lumigan
`Travatan Z
`Xalatan, and generic
`
`Alpha Agonists
`Alphagan P,
`and generic
`
`bimatoprost
`travoprost
`latanoprost
`
`brimonidine
`brimonidine
`
`Carbonic Anhydrase Inhibitors
`Azopt
`brinzolamide
`Trusopt, and generic
`dorzolamide
`
`Combination Glaucoma Medications
`Combigan
`brimonidine/timolol
`Cosopt
`dorzolamide/timolol
`
`Allergan
`Alcon
`Pfizer, and generic
`
`0.01%, 0.03%
`0.004%
`0.005%
`
`2.5ml, 5ml, 7.5ml
`2.5ml, 5ml
`2.5ml
`
`Allergan,
`generic
`
`Alcon
`Merck
`
`Allergan
`Merck
`
`0.1%,
`0.15%, 0.2%
`
`5ml, 10ml, 15ml
`5ml, 10ml, 15ml
`
`1%
`2%
`
`5ml, 10ml, 15ml
`5ml, 10ml
`
`0.2%/0.5%
`2%/0.5%
`
`5ml, 10ml
`5ml, 10ml
`
`4A
`
`REVIEW OF OPTOMETRY MAY 15, 2011
`
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`for our black patients, and 0.25%
`for white patients. Furthermore,
`numerous studies clearly support
`the use of these two non-selective
`beta blockers once daily. It is
`best to have patients instill beta
`blockers shortly upon awakening
`for maximum therapeutic effect.
`Understand that these drugs sup-
`press beta adrenergic tone. Our
`adrenergic system is active while
`we are awake, and physiologi-
`cally asleep while we are asleep.
`There is little benefit in attempting
`to pharmacologically suppress a
`system that is already physiologi-
`cally suppressed. This is why it is
`important to dose beta blockers
`shortly upon awakening.
`The vast majority of our glauco-
`ma patients are successfully man-
`aged with either a prostaglandin,
`or a beta blocker, or a combination
`of the two. This is relatively inex-
`pensive, and requires a drop either
`once daily, or if using both, b.i.d.
`(cid:129) Carbonic anhydrase inhibitors and
`alpha adrenergic agonists. If there is
`a need to move beyond a prostaglandin
`and/or a non-selective beta blocker, then
`do a therapeutic trial of either brimoni-
`dine or a topical CAI—brinzolamide or
`dorzolamide. Both of these drugs are
`FDA-approved for t.i.d. therapy, and
`when used as monotherapy, will best
`serve the patient as one drop every
`eight hours. The problem is that there
`is an inverse relationship between dos-
`
`Select Appropriate Therapy
`Let’s assume we have decided
`a patient merits IOP reduction,
`so what drug do we select?
`(cid:129) Prostaglandins. Most
`of the time, the answer is a
`prostaglandin, preferably one
`of the lower-concentration
`formulations (having less
`side effect potential) such
`as latanoprost 0.005% or
`travoprost 0.004%—and now
`bimatoprost 0.01%. All of the
`prostaglandins lower IOP near-
`ly identically, so prescribing
`decisions are based on side
`effect profile and affordability
`for most patients.1
`The time of instillation
`should center around when
`the patient finds it to be the
`most convenient. Remember,
`compliance is the weak link
`in the treatment chain, so
`we need to do whatever we
`can to make adherence most
`achievable for
`each patient.
`(cid:129) Beta block-
`ers. Alternatively,
`if cost is an over-
`riding factor (and
`cost can compro-
`mise compliance),
`initiate therapy
`with a non-selec-
`tive beta blocker
`such as timolol or
`levobunolol. They
`are available in
`0.25% and 0.5%
`concentrations,
`and are readily
`available for about
`$4 per 5ml at
`many pharmacies.
`Since melanin
`pigments can bind
`some medicines,
`we use the 0.5%
`concentrations
`
`
`
`GlaucomaGlaucoma
`
`ing frequency
`and compliance.
`In recognition of
`this reality, these
`drugs are general-
`ly prescribed b.i.d.
`(approximately
`every 12 hours).
`The CAIs are
`known by their
`brand names:
`Trusopt (dorzol-
`amide, Merck; and generic) and Azopt
`(brinzolamide, Alcon). Since brimonidine
`seems to be slightly more effective than
`a topical CAI, we generally try it as our
`“Plan B” of choice.
`(cid:129) Combinations. What about the
`“combination” drugs, such as 0.5%
`timolol with 0.2% dorzolamide (Cosopt
`[Merck], which has been generic since
`October 2008) or 0.5% timolol with 0.2%
`brimonidine (Combigan [Allergan], an
`expensive combination of two relatively
`inexpensive generic products)? We know
`that timolol is only
`needed once daily,
`and we know that
`brimonidine and
`the CAIs are most
`effective at their
`FDA-approved
`labeling of t.i.d.
`We suggest try-
`ing timolol alone,
`and to only “add”
`dorzolamide or
`brimonidine if truly
`needed to achieve
`target IOP. These
`are rare occa-
`sions.
`
`1. Parrish RK, Palmberg
`P, Sheu WP; XLT Study
`Group. A comparison of
`latanoprost, bimatoprost,
`and travoprost in patients
`with elevated intraocular
`pressure: a 12-week,
`randomized, masked-
`evaluator multicenter
`study.
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`

`that can indeed safely use a topical
`nonselective beta blocker. We have,
`in fact, had the occasion to do such,
`but only after consultation with the
`patient’s primary care or pulmo-
`nary physician. It has recently been
`demonstrated that systemic beta
`blockers are in fact therapeutic in
`the setting of COPD for many such
`patients. So, if you have a need to
`use a beta blocker in a patient with
`what you might think are systemic
`contraindications, consult the pa-
`tient’s physician—it may well be
`that your therapeutic need can be
`successfully met.
`
`When does the diagnosis change from ocular
`hypertension to glaucoma?
`
`
`
`GlaucomaGlaucoma
`
`concerns, which is the essence of
`this question. The decision is just
`not so dichotomous!
`For background, we are currently
`treating hundreds of patients with
`glaucoma medicines who do not
`have glaucoma! We obsessively-
`compulsively assess each of our pa-
`tients; for those whom we feel are
`at considerable risk to develop glau-
`coma, we intervene therapeutically
`in what we believe will prevent the
`development of glaucoma. Ex-
`amples of such patients are younger
`people with very high intraocular
`pressures; very thin corneas (physi-
`ologically, not via keratorefractive
`surgery); compromised optic
`nerve head tissues (based on
`either stereoscopic ophthalmos-
`copy or a nerve fiber layer scan-
`ning device or both, without vi-
`sual field defects); a very strong
`family history; or a combination
`of the above. These decisions
`are complex and require the as-
`similation of a constellation of
`parameters.
`Lastly, note that doctors of
`equal competence legitimately
`differ on the decisions of treat-
`ing vs. attentive monitoring.
`The soundness of whichever de-
`cision is made usually becomes
`clear over the ensuing five to 10
`years. A patient is rarely a “glau-
`coma suspect” beyond five to eight
`years, because during this time span
`it should become clear whether
`they have progressive disease or just
`benign risk factors.
`
`Q: When does the diagnosis
`change from ocular hypertension
`to glaucoma? Does the diagnostic
`definition of glaucoma require a
`visual field defect?
`A: This question is ubiquitous
`and haunts most glaucoma clini-
`cians. Glaucoma is not like a light
`switch; either present or absent, but
`rather like a light controlled by a
`rheostat. As you begin to reduce the
`energy flow to the light, the light
`begins to become less bright—but
`when would the average person say
`the luminance goes from “bright”
`to “dim”? There is a zone or range
`in which this declaration is made.
`
`Q: Are topical nonselective beta
`blockers an absolute or a relative
`contraindication in patients hav-
`ing reactive airway disease and/
`or chronic obstructive pulmonary
`disease (COPD)?
`A: Only recently has it become
`clear to us that the correct answer
`is “relative.” There are patients
`who have lesser expressed asthma
`
`6A
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`REVIEW OF OPTOMETRY MAY 15, 2011
`
`Glaucoma is very similar. With the
`limits of our current technology, it
`could well be reasonable to pro-
`claim a repeatable visual field defect
`as the “Holy Grail” of glaucoma
`confirmation. However, we have
`patients with 0.8 cups with no visu-
`al field defects, and we confidently
`tell them that they have glaucoma
`(based on progressive cupping, thin
`corneas, and/or high IOPs). So,
`in one sense, the question may be
`more academic and philosophical
`than clinical and firm.
`
`Q: A very similar question: At
`what point, clinically, do you begin
`to inform patients that you are
`following them as a “glaucoma
`suspect”?
`A: It depends. If there is a
`family history of glaucoma, a
`borderline IOP (around 18mm
`Hg to 26mm Hg), a 0.4 to 0.6
`cup, a corneal thickness below
`510µm, then such patients might
`be considered “suspicious.”
`But, these various parameters
`cannot be viewed in a vacuum!
`The entire clinical picture must
`be considered collectively. Only
`then can “risk” be rationally
`assessed.
`
`Q: When would you discon-
`tinue glaucoma therapy started by
`another clinician?
`A: If, in your clinical opinion,
`and after a thorough examination,
`you feel the patient may not merit
`therapy, then a thoughtful “reverse
`therapeutic trial” is very reason-
`able. We would have a long conver-
`sation with the patient explaining
`how good doctors commonly have
`different approaches to the same
`condition, and that at the least you
`would like to know the patient’s
`true baseline intraocular pressure.
`This is something we do commonly,
`especially if the patient has no
`positive family history of glaucoma,
`
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`has a thick cornea (greater than
`580µm—our subjective cutoff),
`and/or has healthy-appearing optic
`nerve heads. We also get a Consent
`for Release of Records from the pa-
`tient so that we can have the benefit
`of the prior doctor’s observations
`and thoughts.
`
`tients,” we assume you mean those
`who have a 0.4 to 0.5 or greater
`cup. If the cup is small and the pres-
`sure is normal, this is almost always
`a plain ol’ normal patient. But, if
`the optic nerve head is suspicious in
`appearance, there is a 100% chance
`we will assess the corneal thickness!
`
`Q: Do you obtain pachymetry
`on all of your low-normal tension
`patients, just to see if the cornea is
`thin?
`A: By “low-normal tension pa-
`
`Q: For patients who work second
`or third shift, how do you recom-
`mend dosing schedules for prosta-
`glandins and beta blockers?
`A: Beta blockers are best instilled
`
`
`
`GlaucomaGlaucoma
`
`shortly upon awakening, regardless
`of the actual time of the day. Pros-
`taglandin efficacy is, by and large,
`time of instillation-independent.
`While slightly more effective when
`taken toward the end of a waking
`period, actual time of instillation is
`not a major issue with the prosta-
`glandins. So, regardless of the time
`of the patient’s sleep cycle, it is
`always best to instill beta blockers
`shortly upon awakening. While it is
`best to instill the prostaglandins just
`prior to retiring, time of dosing is
`
`Key Points to Ponder in Glaucoma Management
`
`(cid:129) Visual field test results are extremely variable, and it
`may take three to five tests over a two to four-year period of
`time to truly know the extent (if any) and/or rate of progres-
`sion of a visual field defect. The exception to this is if there is a
`strong clinical correlation. For example, if there is observable infe-
`rior erosion of the optic nerve rim, and there is a dense superior
`field defect, then such a defect can be viewed with certainty, and
`probably annual retesting is all that is indicated.
`The much more common finding, however, is a generalized
`scattering of scotomas, or a nonspecific clustering that does not
`correlate with the optic nerve anatomy or a nerve fiber analyzer
`scan. It is these vague, non-clinically-correlatable visual field
`defects that must be verified by repeat testing, perhaps three to
`five times, in order to know with certainty whether the defect(s)
`is a true reflection of optic nerve damage or simply artifacti-
`tious noise. A classic mistake is to observe what appears to be a
`change in the visual field and make management decisions based
`upon “apparent” demise of the visual field. This is almost always
`an error in clinical judgment and management.
`In summary, if the field is normal, believe it to be normal; if it is
`borderline or questionable, then repeat the testing.
`
`(cid:129) It is by and large a myth that short wavelength (blue-on-
`yellow) or frequency doubling perimetry detects glaucoma
`earlier than standard (white-on-white) automated perimetry.
`Furthermore, it truly may not be in the patient’s best interest to
`be diagnosed “too early” in the setting of early glaucoma. Recent
`results from the Ocular Hypertension Treatment Study follow-up
`showed that delaying IOP reduction for a few years did not result
`in any loss of ultimate control. On average, glaucoma progresses
`at about 3% per year. With the excellent medicines available to
`us, we can intervene therapeutically in a thoughtful, timely man-
`ner to gain good control of the intraocular pressure once the need
`for control is clearly indicated.
`
`It is well established that there is some diminution in quality of
`life when a person is diagnosed with glaucoma, as at that point
`their lifestyle is encumbered with medication habituation behav-
`ior, as well as cost concerns, and perhaps the ultimate concern
`of going blind. Note that we, like you, are attentive physicians,
`and we carefully monitor our patients. If there are any consistent
`signs of accelerated progression, we would institute therapy. Yet
`we have learned over the past 30 years to not be trigger-happy,
`but rather to be very thoughtful in our management decisions.
`Standard white-on-white perimetry can facilitate diagnosis, as
`well as provide guidance regarding progression.
`
`(cid:129) Always initiate therapy with a lesser concentration of
`medication if available. Remember, in therapeutic intervention,
`we have a target IOP range in our heads, and our goal should be
`to achieve an IOP within this range with the least medical inter-
`vention possible.
`Unfortunately, we have few lower-concentration options in
`glaucoma therapy: 0.25% timolol (or levobunolol), bimatoprost
`0.01% and pilocarpine 1%. Being faithful to this concept, our rou-
`tine dilating drop only contains 0.25% tropicamide (Paremyd also
`contains 1% hydroxyamphetamine hydrobromide). Thankfully, we
`now have the lesser concentration of bimatoprost (0.01%) and the
`concentration of BAK has been increased from 0.005% to 0.02%
`(the same as is in latanoprost).
`A couple of unsubstantiated thoughts come to mind: Because
`BAK enhances drug penetration, it may be that this higher con-
`centration of preservative is what enables the 0.01% bimatoprost
`to provide the same reduction in IOP as the 0.03%, and that it is
`not the BAK potentially causing side effects, but rather the active
`drug itself. The manufacturer claims a significant reduction in
`side effects with the 0.01% rendition of the bimatoprost. So keep
`in mind that “less is better,” as long as the target IOP goal is
`achieved and maintained.
`
`(continued on page 9A)
`
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`
`
`GlaucomaGlaucoma
`
`Confrontational visual field testing as a screening tool is standard-of-care, but is this
`test really adequate?
`
`not a major issue with the prosta-
`glandins.
`
`Q: What is your opinion on
`confrontational visual field testing
`as a screening tool in the context of
`comprehensive eye examination?
`This is standard-of-care, but is this
`test really adequate?
`A: The world’s premier author-
`ity in neuro-ophthalmology is Neil
`Miller, M.D., at the Wilmer Eye
`Institute at Johns Hopkins. He
`stated that 90% of all clinically
`significant neurologically-related
`visual field defects can be detected
`by confrontation examination. He
`recommended that this assessment
`be done as counting-fingers in each
`quadrant, not bringing in a target
`from non-seeing areas into see-
`ing areas. We have followed Dr.
`Miller’s guidance since the early
`1980s, and have found his observa-
`tions to be spot-on.
`
`Q: Why isn’t thyroid function
`part of the glaucoma workup?
`I have seen three patients, and
`heard of more, with high IOP that
`normalized after their thyroid dys-
`
`function was treated. I realize it’s a
`multifactorial disease, but let’s rule
`out the easy options.
`A: Thoughtful question. One
`would think that thyroid disorders
`could have an impact on aqueous
`production and/or outflow. In all of
`our exhaustive reading of the world
`literature, we have never read of
`any such association with thyroid
`dysfunction. We can’t explain your
`anecdotal observations, and, as you
`rightfully point out, glaucoma is a
`multifactorial disease, so perhaps
`other factors are at play that are
`not yet fully elucidated.
`
`Q: Since it is known that some
`low tension glaucoma patients
`may be compromised by nocturnal
`systemic hypotension, should these
`patients have a sleep study?
`A: Perhaps. This is an area of
`ongoing research, and in select
`patients, knowing their diastolic
`nocturnal blood pressure profile
`could potentially be very helpful.
`Along this same line of thought is
`the consideration of the patient’s
`medical treatment for systemic
`hypertension, if they carry that
`
`8A
`
`REVIEW OF OPTOMETRY MAY 15, 2011
`
`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