12/11/2019

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GLAUCOMA FIRESIDE

CHAT

JOSEPH SOWKA, OD

ANTHONY “ANDY” LEONCAVALLO, M.D.

Joseph Sowka, OD is/ has been a Consultant/ Speaker Bureau/ AdvisoryBoard member for Novartis, Alcon, Zeiss, Allergan, Glaukos, and B&L.He is a co-owner of Optometric Education Consultants.

Anthony “Andy” Leoncavallo, M.D.: Nothing to disclose

The ideas, concepts, conclusions and perspectives presented

herein reflect the opinions of the speakers; they have not been

paid, coerced, extorted or otherwise influenced by any third

party individual or entity to present information that conflicts

with their professional viewpoints.

DISCLOSURE:

HOW DO YOU USE OCT, HYSTERESIS,

ELECTRO DIAGNOSTICS, AND OTHER

TECHNOLOGIES?

HOW OFTEN TO REPEAT TESTS?

NEW MEDS VS. CURRENT

BRANDS VS. GENERICS-

WHERE DO WE START

AND WHERE DO WE GO?

VYZULTA™ (latanoprostene bunod ophthalmic solution, 0.024%)

• First prostaglandin analog with one of its metabolites being nitric oxide (NO)

• QD dosing

• Dual mechanism of action– metabolizes into two moieties, latanoprost acid, which primarily works

within the uveoscleral pathway to increase aqueous humor outflow, and butanediol mononitrate, which releases NO to increase outflow

through the trabecular meshwork and Schlemm's canal.

– Blocks RhoKinase and calcium signaling

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ROCK/Norepinephrine Transporter (NET) Inhibitors

Netarsudil 0.02% (Rhopressa TM)-approved 12/18/17

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MLC-PMLC

Rho Kinase (ROCK) Inhibition

Rho activation increases contractility ofTM cells

– Reduces outflow of aqueous humor

Rho kinase inhibition relaxes TM cells

– Reduces actin stress fibers/focal adhesions

– Increases outflow of aqueous humor

Rho kinase inhibition may also:

– Increase ocular blood flow

– Increase retinal ganglion cell survival

New Development in IOP Reduction

Uehata M, et al. Nature 1997;389:990-994

Hirata A, et al. Graefes Arch Clin Exp Ophthalmol. 2008;246(1):51-59

Wang SK, Chang RT. Clin Ophthalmol 2014;8:883-890

Rho Kinases(ROCK1, 2)

Rho-GTP

MLCP-PPase

MLCKLIMK1,2

ActomyosinContractility

Actin Stress FibersAssembly/Stability

Focal AdhesionAssembly/Stability

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Netarsudil ophthalmic solution 0.02% (ROCK-NET Inhibitor) Triple-Action

Ciliary Processes

Cornea

Uveoscleral

Outflow

AR-13324

NETRKI

NETRKI

Trabecular Meshwork

Episcleral Veins

Schlemm’s Canal

1. Wang SK, Chang RT. An emerging treatment option for glaucoma: Rho kinase inhibitors. Clin Ophthal 2014;8:883-890.

2. Wang RF, Williamson JE, Kopczynski C, Serle JB. Effect of 0.04% AR-13324, a ROCK, and norepinephrine transporter inhibitor, on aqueous humor dynamics in normotensive monkey eyes. J Glaucoma 2015. 24(1):51-4.

3. Kiel JW, Kopczynski C. Effect of AR-13324 on episcleral venous pressure (EVP) in Dutch Belted rabbits. ARVO 2014. Abstract 2900

3 Identified IOP-Lowering Mechanisms

ROCK inhibition relaxes TM1, increases outflow1,2

NET inhibition reduces fluid production2

ROCK inhibition lowers Episcleral VenousPressure (EVP)3

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Netarsudil ophthalmic solution 0.02: Rocket 2 study

Rocket 2 is a 12-month Phase 3 study of Netarsidil vs. Timolol

The patient group to be used for Rocket 2 primary endpoint analysis was changed with FDA agreement

Primary endpoint analysis will include only patients with a baseline IOP above 20 mmHg and below 25 mmHg

Rhopressa QD and BID met criterial for non-inferiority to timolol (baseline < 25 mm)

Seems to work best at lower/ modest IOP baseline

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Netarsudil ophthalmic solution 0.02% Rhopressa TM

In two phase III studies, more than half of patients experienced conjunctival hyperemia compared to 8% to 10% of timolol patients.

– More complaints of eye redness with Rhopressa.

9% and 5% of Rhopressa once-daily patients reported corneal deposits across the two phase III studies compared to 0.4% and 0% of the timolol patients.

Blurry vision was reported by 7% and 5% of Rhopressa patients compared to 3% and 0.5% of timolol patients in the studies.

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Fixed Combination of Rhopressa with Latanoprost

Ciliary Processes

Cornea

Uveoscleral Outflow

NETRKI

NETRKI

Trabecular Meshwork

Episcleral Veins

Schlemm’sCanal

Latanoprost

Quadruple-Action (ROCK-NET Inhibitor/latanoprost)- Rocklatan

1.Wang SK, Chang RT. An emerging treatment option for glaucoma: Rho kinase inhibitors. Clin Ophthal 2014;8:883-890.

2.Wang RF, Williamson JE, Kopczynski C, Serle JB. Effect of 0.04% AR-13324, a ROCK, and norepinephrine transporter inhibitor, on aqueous humor dynamics in normotensive monkey eyes. J Glaucoma 2015. 24(1):51-4.

3.Kiel JW, Kopczynski C. Effect of AR-13324 on episcleral venous pressure (EVP) in Dutch Belted rabbits. ARVO 2014. Abstract 2900

4.Latanoprost prescribing information

ROCK inhibition relaxes TM1, increases outflow1,2

NET inhibition reduces fluid production2

ROCK inhibitionlowers EVP3

PGA receptor activationincreases uveoscleraloutflow4

4 IdentifiedIOP-Lowering Mechanisms

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IS GLAUCOMA A

MEDICAL OR SURGICAL

DISEASE?

LET’S TALK ABOUT THE

LIGHT AND ZAP STUDIES

MIGS

Appear to have improved safety profile

over trabeculectomy, but reduced efficacy

Procedures:

- Canaloplasty

- Trabectome*

- Glaukos iStent

- ECP

- Cypass

- XEN Gel stent

• Bleb forming

- Kahook Dual Blade*

* Modified goniotomy

Postoperative (6 month)

TRABECTOME (NEOMEDIX)

FDA Approved 2004

A thermal cautery device with irrigation and aspiration

Used to remove a 2-4 clock hour segment of TM/SC

Less traumatic and safer than trabeculectomy surgery

Is combined with CE

Modest IOP lowering

CANALOPLASTY (ISCIENCE)

FDA Approved 2008

The goal of this procedure is to enlarge

Schlemm's canal and enhance outflow.

A prolene suture is passed 360 degrees

through Schlemm's canal with the aid of

a microcatheter and viscoelastic to

dilate the canal.

One drawback of this procedure is that

it is technically challenging.

ISTENT (GLAUKOS CORP.)

iStent: Trabecular

Micro-Bypass Stent

• FDA Approved 2012 for:

Mild to Moderate

glaucoma in patients

who need cataract

surgery

No Bleb is formed

• Few complications

Relatively Easy to

perform

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ISTENT ADVANCEMENTS

iStent inject

- Preloaded needle that injects two stents, for which

Glaukos has completed a phase 1 clinical trial.

• Involving patients unresponsive to two glaucoma medications,

patients were randomized to receive one, two or three stents

• Each additional stent gives an incremental decrease in

intraocular pressure.

CYPASS

Supraciliary

microstent that

increases uveoscleral

outflow.

It is implanted through

a clear corneal

incision and can be

combined with

cataract surgery

KAHOOK DUAL BLADE

Single use, ophthalmic blade

Utilizes ab interno approach through a clear cornea

micro incision

Precision engineered to fit in the canal of Schlemm

Dual blades positioned for precise parallel incisions

of the trabecular meshwork with minimal residual

leaflets

Maintains natural physiologic outflow pathways

KAHOOK DUAL BLADE

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XEN GEL STENT

FDA approved the XEN45 Gel Stent and the

XEN Injector for patients with refractory

glaucoma who failed previous surgical

treatment or in patients with primary open

angle glaucoma, pseudoexfoliative or

pigmentary glaucoma with open angles that

are unresponsive to maximum tolerated

medical therapy

“Lower maintenance” bleb-forming

procedure

Potential for low (<15 mm) IOP

WHEN DO YOU NOT

BELIEVE YOUR OCT?

ISSUES IN IMAGING

OCT technology is readily available and

present in contemporary practice

No one single parameter is more

important than the others.

Never base a clinical decision based

upon only one piece of data.

OCT is not a Silicon Valley

Rumplestilskin. You cannot put in

straw and get out gold

ISSUES IN IMAGING

Interpretation is a three-step process

1. Understand what the printout says

2. Apply experience and value judgement

3. Correlate to the clinical findings

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ISSUES IN IMAGING

You cannot make a diagnosis of glaucoma

based solely upon imaging results.

The use and overemphasis of imaging

technology to the exclusion of additional

clinical findings and assessment of risk will

put patients in peril.

Exactly how much confidence should an OCT

give you as to whether or not a patient has

glaucoma?

- Depends how much confidence you had before you

imaged the patient.

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ISSUES IN IMAGING

Normative Database

Signal Quality

Blink/Saccades

Segmentation Errors

Media Opacities

Axial Length

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OCT DATABASE INFORMATION

Spectralis: 201 patients

- All Caucasian

- Age 18-78

- New database more representative of US population

Cirrus: 284 eyes

- Age 19-84

- Ethnic Groups: Causasian, Asian, African-American,

Hispanic

RTVue: 600 eyes

- Disc Size

- African-American, Chinese, Japanese, Caucasian,

Hispanic, Indian

WHAT TO LOOK FOR WHEN

INTERPRETING OCT SCANS

Quality score

Illumination

Focus clarity

Image centered

Any signs of eye movement

Segmentation accuracy

B Scan Centration

Missing data

Media issues

Maculopathy for GCC scans37

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RTVue-100

EYE MOVEMENT

Accidentally find CSC when looking

for glaucoma

Cirrus

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RTVue-100

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Spectralis

IF YOU THINK DEVICES MEASURE

TISSUE ACCURATELY EVERY TIME…

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Spectralis

46

Spectralis

47

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Don’t make clinical decisions based

upon bad data

IS SUSTAINED RELEASE

THE NEXT ‘HOT THING’?

Allergan is currently performing phase 3

clinical trials on its bimatoprost sustained-

release implant (bimatoprost SR), which is an

intracameral depot implant injected into the

anterior chamber.

Implant comprising a prostamide associated

with a biodegradable polymer matrix that

releases an amount of a prostamide

BIMATOPROST SR

Phase 2 trials of the implant showed mean

overall IOP reductions from baseline through

week 16 after the first implantation of the

bimatoprost sustained-release device

- 7.2, 7.4, 8.1, and 9.5 mm Hg with the 6-, 10-, 15-, and

20-microgram doses compared with an 8.4 mm Hg

decrease in the pooled fellow eyes treated with topical

bimatoprost (0.03%).

BIMATOPROST SR

The implant lowered IOP in 92% of patients at 4

months and 71% at 6 months.

- Did not need additional rescue therapy

There were no serious adverse ocular events

- The most common adverse event was transient conjunctival

hyperemia (median duration of 5 days), which developed within 2

days after the implant was injected.

In 24 eyes that did require another treatment to

control IOP, the overall mean IOP reduction from the

baseline IOP was 8.0 mm Hg through 16 weeks after

the repeat bimatoprost sustained-release treatment.

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HELIOS (FORSIGHT VISION5)

Bimatoprost-laden polymer-matrix insert

embedded in a compliant ring.

The ring is positioned under the upper and

lower eyelids and rests on the conjunctiva.

It is visible only at the caruncle once it is in

place.

The ring is designed to be replaced by an

optometrist or ophthalmologist

every 6 months.

HELIOS (FORSIGHT VISION5)

GREAT THINGS ABOUT SUSTAINED

DELIVERY

Compliance is greatly enhanced

Potentially fewer issues for patients

NOT SO GREAT THINGS ABOUT

SUSTAINED DELIVERY

Injectable meds and implants- if med doesn’t

work topically or has adverse effects, drop is

stopped; can’t easily stop implantable

devices.

Implants can theoretically block parts of the

angle

Complications with invasive options

- Endophthalmitis

Decreased access to care?

NOT SO GREAT THINGS ABOUT

SUSTAINED DELIVERY

Patients still have to verify if plug or ring is

still in place

- May be challenging for some

• If patients have to check daily- why not just use a drop?

Contact lens-delivery system:

- Older patients handling lenses?

- Issues with infectious keratitis

NOT SO GREAT THINGS ABOUT

SUSTAINED DELIVERY

Limitations- how many drugs can you load

into a ring or put in the anterior chamber?

Patients only have 2 puncta per eye- may still

need topical therapy as well

Drugs may work better in pulsatile form and

not so well in constant delivery

PGAs less effective at BID dosing- receptor

supersaturation and desensitization

- Downtime between drops prevents desensitization

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NOT SO GREAT THINGS ABOUT

SUSTAINED DELIVERY

SR products seem less effective than drops

Will insurance pay for it just to increase

compliance?

ANTI-VEGF MODEL FOR AMD

Compared to clinical trials, VA outcomes are worse

and there are fewer injections done in the real world.

Patients lost to follow-up are doing poorly.

Drop out rate 20%-30%

WILL PATIENTS GO FOR IT?

Electronic surveys were administered to 150 individuals at two

glaucoma clinics

The majority of participants would accept contacts (59%), rings (51%),

plugs (57%) and subconjunctival injections (52%) if they obviated

glaucoma surgery

Fewer would accept these devices if they reduced (23% to 35%) or

eliminated (27% to 42%) drops. Most participants would also accept

contacts (56%), plugs (55%) and subconjunctival injections (53%) if

they were more effective than eye drops, while only 47% would accept

a ring; fewer would accept any device if it were equally or less effective

than drops. Participants were also 36% less likely to accept rings and

32% less likely to accept subconjunctival injections as compared to

contacts.

Researchers determined that most glaucoma patients considered

sustained drug-delivery modalities acceptable alternatives to IOP-

lowering eye drops, but only when they were said to obviate surgery or

demonstrate greater efficacy than eye drops.

Varadaraj V, Kahook MY, Ramulu PY, et al. Patient acceptance of sustained glaucoma treatment

strategies. J Glaucoma. 2018; Feb 16.

WILL PATIENTS GO FOR IT?

WHEN IS SURGERY WRONG FOR

THE PATIENT?

ANSWER:

When the risk of surgery is greater than its

expected benefit.

When it is more dangerous to undergo a

surgical procedure than to continue on the

same medical treatment.

When you would not recommend the same

intervention to your family members

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GLAUCOMA SURGICAL DECISION

MAKING

Establishing the course of treatment

- Is the disc or field status stable or worse?

- If progression has occurred, over what time period?

- What is the rate of change?

- What is the risk of visual disability in the patient’s

lifetime?

- Is the patient aware of either decreased central visual

acuity or peripheral visual field loss?

• Classic question: Is it the cataract or the glaucoma or the age

related macular degeneration?

IMPORTANT QUESTIONS ABOUT

VALUE OF SURGICAL INTERVENTION

– HOW FAR TO GO?

- Does the patient value the visual acuity of Hand Motions or

Light Perception or remaining visual field?

- What is the status of the fellow eye?

- Is glaucoma a primary condition or related to a cause

(proliferative diabetic retinopathy, central retinal vein

occlusion, trauma)?

- Has a family member become visually disabled from

glaucoma?

- Has a family member lost vision after glaucoma surgery?

RISKS OF GLAUCOMA SURGERY

Trabeculectomy

- Immediate postoperative period

• Hypotony – flat anterior chamber, acute cataract, angle

closure, choroidal effusion

• “Wipe out” or “snuff out” syndrome – acute loss of central

acuity without obvious intraoperative complication

• Decreased visual acuity - Patient only knows that they

see much worse after surgery

Glaucoma drainage implant surgery

- Muscle imbalance – noncommitant diplopia

ADDITIONAL RISKS OF GLAUCOMA

SURGERY

Late postoperative period

- Posterior synechiae formation – poor dilation

- Cataract formation

- Bleb scarring and return of high IOP

Very late postoperative period

• Endophthalmitis and blebitis

• Remember “RSVP” • R – Redness

• S – Sensitivity to light

• V – Vision Change

• P – Pain

Edna

20/20 OD, OS

Age 37

10-2 SS OS 10-2 SS OD

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HAZEL AND JOSEPH

87 YOF; 95 YOM- managed for 16 years

Hazel: 20/20 OD; 20/30 OS; MMT; s/p SLT

- IOP; 17 mm OD; 20 mm OS

- CCT: 472 OD, 474 OS

Joseph: 20/25 OD, OS

- Cosopt, xalatan, and alphagan

- IOP 11 mm OD, 13 mm OS

- CCT 473 OD, 473 OS

HAZEL

JOSEPH

JOSEPH

HAZEL AND JOSEPH

For whom is surgery right and for whom is

surgery wrong?

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WHEN DO YOU SUSPECT

SOMETHING OTHER THAN

GLAUCOMA AND NEUROIMAGE?

IS IT ONLY GLAUCOMA?

53 YOBF- No complaints

BVA 20/20 OD, OS

Perrl (+) RAPD OS

IOP 30 mm Hg OD and 32 mm Hg OS

Unilateral sectorial disc pallor with minimal

rim damage

Color vision testing normal

SLE normal OU

Anterior chamber angles open

gonioscopically.

Is this glaucoma or something else like

a tumor?

Unilateral disc pallor? Glaucoma, something else, or both?

Neuroimage or not?

“THE CUPPED DISC: WHO NEEDS

NEUROIMAGING?”

Patients with glaucoma were:

- Older

- Better visual acuity

- Greater vertical loss of neuroretinal rim

- More frequent disc hemorrhages

- Less neuroretinal rim pallor

- Field defects along the horizontal

Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc: Who needs neuroimaging? Ophthalmology 1998; 105:1866-74.

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“THE CUPPED DISC: WHO NEEDS

NEUROIMAGING?”

Patients with mass lesions:

- Visual acuity less than 20/40

- Vertically aligned visual fields defects

- Optic disc pallor in excess of cupping

- Age younger than 50 years

Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc: Who needs neuroimaging? Ophthalmology 1998; 105:1866-74.

MORE INDICATIVE OF A COMPRESSIVE

MASS LESION THAN GLAUCOMA

Younger age

Lower levels of visual acuity

Vertically aligned visual field defects

Neuroretinal rim pallor

Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc: Who needs neuroimaging? Ophthalmology 1998; 105:1866-74.

BACK TO THE PATIENT…

Rim minimally notched

Disc pallor

Unilateral damage

No disc hemorrhage/ parapapillary atrophy

Age over 50

Arcuate defect- glaucomatous

Risk factor- IOP 30s

Acuity and color normal

CASE: 56 YOBF

Dx POAG OU 5 years ago

Slowly progressive vision loss

LP OD; 20/30 OS

Used combo med- ran out months ago

IOP: 19 mm OD, 18 mm OS

CCT: 560; 544

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45 YOM- KERATOCONUS

20/30- OD; 20/25- OS

17 mm Hg OU

PERRL (-) RAPD

No pachymetry yet

74 YOF

Diagnosed with glaucoma in Jamaica

Ran out of meds: IOP 20 mm OU

20/50 OD, 20/40 OS

NS 2+

PERRL(-)RAPD

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65 YOF- POAG OU; 20/40 OU

Peak IOP unknown; s/p SLT OU and on latanoprost at first visit.

Oh, by the way, she remembered waking up 10 years ago

unable to speak for several hours.

NOW HOW WOULD YOU HANDLE

THESE? DON’T WORRY…

JP: 38 YOF

Referred for glaucoma eval in 2002 after

failing LASIK screening

Had been treated since mid 20s for glaucoma

IOP in mid-upper teens off meds

CCT: 459 OD; 469 OS

Anomalous nerves with mild field loss

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JP: NOW 49 YOF

Congenitally anomalous nerves with field

loss

Monitored for 11+ years

Field changes late

Pt now treated with IOP 09 mm OD; 10 mm OS

Pt had/had congenitaloma and now has

glaucoma

- Doubloma

SIMILAR…YET DIFFERENT

45 YOF

Referred for glaucoma evaluation

IOP never exceeds mid-teens

CCT: 554 OU

Marginal effect of meds

CONUNDRUMS

Field loss due to anomaly, glaucoma, or

both?

Progressive or congenital?

Mid-teen IOP and poor medical response

Treatment or observation?

WHAT CAUSES A DISC

HEMORRHAGE AND IS IT

PROGRESSION OR A RISK OF

PROGRESSION?

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WHAT DO YOU DO WHEN YOU

SEE A DISC HEMORRHAGE?

Not all hemorrhages of the

disc are disc hemorrhages.

RISK FACTORS: DISC

HEMORRHAGES

Inferior, inferior temporal,

superior, and superior

temporal regions of the disc

are most susceptible and

account for virtually all true

glaucomatous disc

hemorrhages

Typically occurs where notches

and RNFL defects occur

Hemorrhages at other areas of the disc (nasal and temporal)

tend to not be associated with glaucoma.

OTHER CAUSES OF ‘DISC’HEMORRHAGES

PVD

HTN

Anemia

Diabetes

Vascular occlusion

Subarachnoid bleed

- Terson’s syndrome

• Subretinal and intraretinal

• May be juxtapapillary

BRVO PVD

Terson’s

Not all hemorrhages of the disc are disc hemorrhages.

Make sure that the glaucomatous characteristics

are there.

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EARLY MANIFEST GLAUCOMA

TRIAL

Disc hemorrhages- predictive of progression

Treatment was unrelated to the presence or

frequency of disc hemorrhages.

- Disc hemorrhages were equally common in both the

treated and untreated groups of patients.

- Disc hemorrhages don’t occur in all glaucoma pts.

Disc hemorrhages cannot be considered an

indication of insufficient IOP-lowering

treatment,

- Glaucoma progression in eyes with disc hemorrhages

cannot be totally halted by IOP reduction.

OCULAR HYPERTENSION

TREATMENT STUDY

The occurrence of a disc hemorrhage

increased the risk of developing POAG 6-fold

in a univariate analysis and 3.7-fold in a

multivariate analysis that included baseline

factors predictive of POAG

Occurrence of an optic disc hemorrhage was

associated with an increased risk of

developing a POAG end point in participants

in the OHTS

- However, most eyes (86.7%) in which a disc

hemorrhage developed have not experienced a POAG

end point to date

55 YOM

2012 presents without complaints

BCVA 6/6 OD, OS

IOP:

- OD: 27 mm; 30 mm

- OS: 15mm; 15 mm

CCT: 536; 531

55 YOM

Treatment initiated

- IOP drops to mid teens OU

Optic disc change OS noted 4/14

Therapy amplified

7/15: latanoprost and dorzolamide/timolol FC

OU

IOP: 10 mm OU

CCT: 536; 531

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2016

2012SO WHAT DO I DO WHEN I SEE A

DISC HEMORRHAGE?

(Treated) IOP high teens:

- Progression documented- increase therapy

- Risk of visual disability- increase therapy

- None of the above: increase therapy or monitor for

progression then increase therapy

(Treated) IOP low teens

- Monitor for progression (if safe)- no change

- Progression documented or risk visual disability

• ? Therapy increase

• Equal risk of blindness from disease or treatment

HOW DO YOU MANAGE

GLAUCOMA SUSPECTS?

WHO IS A GLAUCOMA SUSPECT?

Elevated IOP/ OHTN

Suspicious disc appearance

- Thin rim tissue; Disc asymmetry

Suspicious RNFL/ OCT

Disc hemorrhage

Suspicious visual field loss

Family history of glaucoma

Age

Race

Phakic hyperopia- angle closure suspect

DISC EVALUATION

Size

Rim color

Focal rim defects (notching)

Hemorrhages

RNFL defects

Parapapillary atrophy

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WHICH OF THESE 3

PATIENTS DO YOU MOST

SUSPECT HAS

GLAUCOMA?

• IOP: 11 mm

• CCT: 610

PATIENT 1: 28 YOF

PATIENT 2: 56 YOM

• IOP: 22 mm

• CCT: 598

• IOP: 31 mm

• CCT: 490

PATIENT 3: 64 YOF

WHICH PATIENT HAS

GLAUCOMA? 1? 2? 3?

WHICH PATIENT HAS

GLAUCOMA? 1? 2? 3?

• IOP: 11 mm

• CCT: 610

• IOP: 22 mm

• CCT: 598• IOP: 31 mm

• CCT: 490

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RULE: WHEN

DIAGNOSING

GLAUCOMA, TAKE IOP

OUT OF THE EQUATION

(When managing glaucoma, put IOP back into the

equation…but that’s another lecture.)

WHO ARE THE GLAUCOMA

SUSPECTS?

Large cupping- normal IOP

Large cupping- high IOP

Normal cupping- high IOP

IS THIS GLAUCOMA?

34 YOHF

“Highly suspicious” ONH OU

IOP statistically normal

• 13 mm Hg OU

Average CCT

Previously treated for NTG

My advice to patients: If you insist on having a suspicious optic

disc, you had better be a good field taker.

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IS THIS GLAUCOMA?

78 YOWM

Annual exams with multiple doctors

IOP ranges from 17 – 21 mm Hg

CCT 570

Ocular health always “normal”

Small discs with indistinguishable cupping

• 0.2/0.2 – 0.3/0.3

Color

Contour

DON’T OVER-TEST

“When you get the answer

you want, hang up”

BUT DON’T UNDER-

TEST, EITHER

WHO ARE THE GLAUCOMA

SUSPECTS AND WHAT DO I DO?

Large cupping- normal IOP

- Does the nerve look glaucomatous?

• Yes- photos, fields, pachymetry, gonio, OCT

• No- OCT- if normal-done; if abnormal- fields- if normal- done,

if abnormal- monitor

Large cupping- high IOP

- Does the nerve look glaucomatous?

• Yes- photos, fields, pachymetry, gonio, OCT

• No- OCT, photos, pachymetry, fields, gonio

Normal cupping- high IOP

- OCT, photos, pachymetry, fields, gonio

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LARGE CUPPING-

NORMAL IOP

Annual exams

LARGE CUPPING- UNKNOWN IOP-

DIAGNOSED WITH GLAUCOMA

46 YOF

Diagnosed and treated for glaucoma in

Jamaica

Brimonidine 0.1%; latanoprost/timolol FC OU

IOP: 14 mm OD, 16 mm OS

CCT: 530; 528

0.75/0.75 OU

Fields unreliable- high FP

D/C all meds:

IOP: 17 mm

OD, 18 mm OS

LARGE CUPPING-

HIGH IOP56 YOF

IOP: 24 mm OH

CCT: 550 OD, 539

OS

RTC 6 mos fields

Follow w/o

treatment Q 6

mos

NORMAL CUPPING-

HIGH IOP IOP: 30 mm OD,

32 mm OS

Mother +

glaucoma

(10-2 field)

Rx: Latanoprost

OU

56 YOM: mother had glaucoma

CCT: 548 OU

Peak IOP: 29 mm

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Make a decision! Patients shouldn’t be

‘glaucoma suspects’ for ten years. Either

they have the disease or they don’t.