2017 poa lecture [read-only] · elastin in the extracellular matrix connective tissue maintenance...

2/28/2017

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NEW TOPICS IN GLAUCOMA DIAGNOSIS AND TREATMENT

G. RICHARD BENNETT, M.S., O.D., F.A.A.O.

PROFESSOR AND CHIEF

THE GLAUCOMA SERVICE, THE EYE INSTITUTE, SALUS UNIVERSITY

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DISCLOSURES CONSULTANT/ADVISORY BOARD: ALLERGAN,

ALCON

LECTURE HONORARIA: ALCON

THE CONTENT AND FORMAT OF THIS COURSE IS PRESENTED WITHOUT COMMERCIAL BIAS AND DOES NOT CLAIM SUPERIORITY OF ANY COMMERCIAL PRODUCT OR SERVICE

New Diagnostic Approaches To Glaucoma

New Thoughts, Tools, and Techniques

Exfoliation Syndrome (aka “Glaucoma Capsulare,”

“Pseudoexfoliation Syndrome,” PXF, PEX, PXS, XFS)

Prevalence: Female > Male Scandinavian Countries (historically)

Incidence doubles with each decade of life over age 50

Genetics: (discovered in 2007) Principle genetic risk factor = single

nucleotide polymorphisms (SNPs) of the lysyl oxidase-like 1 (LOXL1) gene on chromosome 15q24.1 Within Nordic population, 2 of these SNPs

attribute to a 99% higher risk for PXS and PXG

Genetics LOXL1 Enzymes involved in the cross-linking of collagen and

elastin in the extracellular matrix Connective tissue maintenance

Actual role in the syndrome still unclear LOXL1 risk genotypes seen in 92% of XFS, but also seen in

74% of normal population

Contactin-associated protein-like 2 – found in German cohort Potassium channel trafficking

Others: lysosomal trafficking regulator, clusterin, adenosine receptors, matrix metalloproteinase (MMP1), glutathione transferase

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A Systemic Disorder Material: Grey-white, fibrillogranular, extracellular, matrix material

Protein core surrounded by glycosaminoglycans

FXS material deposits around blood vessels of connective tissue Lung, liver, kidney, gall bladder, cerebral meninges Potentially related to cardio, cerebrovascular disease,

hearing loss, and Alzheimer’s disease*

Strong literature evidence that this is an ischemicsystemic disorder

XFS in the Eye Deposition: anterior lens capsule,

zonules, ciliary body, iris, trabeculum, anterior vitreous face, conjunctiva

Ocular Signs of Exfoliative Syndrome Cornea:

FXS material on the endothelium Pigment deposition – Potential for

Krukenberg spindle

Anterior Chamber: Mild flare –breakdown of blood aqueous

barrier

Iris: FXS material on pupillary margin Sphincter atrophy – “moth eaten” TIDs Patchy iris neovascularization c

extensive capillary dropout

Ocular Signs of Exfoliative Syndrome

Anterior Lens: Central translucent disc c rolled edges

Clear mid-zone due to constant rubbing of the pupil

Peripheral granular band c multiple radial striations Only detected post-dilation

Lens Zonules Accumulation of PEX material

Zonular dehiscence Phacodonesis or lens subluxation

Pseudoexfoliation Syndrome and Cataracts Pre-op (Blue Mountain Eye Study 2013): Contributing to progression of cataracts Due to free radicals and oxidative damage

Zonulodialysis -> Phacodonesis

Post-op: Poorly dilating pupil Increased incidence of post-op capsular opacification and contraction Increased incidence of spontaneous dislocation of IOL Prolonged intraocular inflammation and corneal decompensation

Exfoliative Syndrome and the Retina

Correlation with ocular ischemia

XFM found in vortex veins and central retinal veins

[Ritch et al. 2010] found correlation with incidences of CRVO with XFS

CRVO (but not BRVO)

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Conversion into Glaucoma: XF Glaucoma

XFS is the most common cause of secondary open angle glaucoma

Males > Females Although Females > Males in XFS

Diagnosis usually in 7th decade of life

Usually unilateral in presentation

Risk factors: Cumulative risk for conversion 5% at 5 years 15% at 10 years

Unilateral XF GLC and XFS in fellow eye : 50% in 5 years Unilateral XF GLC and NO PEX in fellow eye : low risk

No apparent association between angle characteristics and severity

In Scandanavia, this accounts for 50% of open angle glaucoma

Pseudophakic Exfoliative Glaucoma XF material can still deposit on an IOL Characteristic pattern as seen on a phakic lens Deposition in areas exposed to the highest aqueous humor flow

XF material can develop on the IOL surface 4-10 yrs post CE in patients with XFS

Pseudophakic Exfoliative Glaucoma

New Research: The Latitude Effect

[Stein, Pasquale, et al. 2011]

Purpose: Determine the risk of exfoliation syndrome based on geographic and climatic risk factors

Retrospective study of 626,901 patients spanning 47 states seen between the years of 2001 – 2007

Results: Northern tier residence (above 42°N) was associated

with increased hazard

Southern tier residence (below 37°N) was associated with decreased hazard

*** Excluding whites did not change these associations***

The Latitude Effect

The Latitude Effect Climate Findings:

Conclusion:

Ambient temperatures and sun exposure may be environmental triggers for XFS

Change in Temps Hazard of PXS

1° increase in July high temp

Decreased by 9%

1° increase in Jan low temp

Decreased by 3%

Addl sunny day annually Increased by 1.5%

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The Lattitude Effect

Possible Explanation Nucleation reaction is prone to

occur at lower temperatures. Anterior chamber and lens may

be susceptible to ambient temperatures.

Reaction also related to UV exposure Pasquale et al. current project: Solar Exposure Questionnaire

Lifeguards: 3x more risk

Ski Instructors: 8x more risk

Differential Diagnosis: Pigmentary Dispersion Syndrome

Confused because:

Both have material found in the angle and anterior chamber

Potential for Krukenberg spindle

Difference:

Age of onset: PDS usually in 30-40s

Transillumination defects

Pupillary border of iris

Appearance of anterior lens after dilation

Zonular changes

Pigment Dispersion Syndrome

GONIOSCOPY

Goniolens Options

Angle Documentation

GONIOSCOPYPosner 4-Mirror Lens

Sussman 4-Mirror Lens

Single Mirror Lens

Goldmann 3- Mirror Lens

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Spaeth SystemLevel of iris insertion:A – anterior to trabecular meshwork B – anterior to posterior limit of trabecular meshworkC – posterior to scleral spurD – into the mid‐ciliary body face (anterior CB band visible)E – posterior CB (wide band of CB band visible)

Angle width – estimate in degrees from line tangential to the trabecular meshwork to line tangential to the iris surface one third of the way from the periphery (ranges from 0 ‐ 40 degrees)

Curvature of iris: f – flat configuration, no significant forward or backward arching of iris b – bowed or forward bowing (convex) curvec – concave or posterior bowing curve P– plateau iris configuration

Pigmentation: 0 (no pigment) to 4 (heavy pigmentation)

Gonioscopy Perform when suspicious for narrow angle

Occludable angles:

posterior, usually pigmented TM is seen for less than 90° of the angle circumference

or if the angle width is less than 20°

Perform gonioscopy in a dark room

smallest square of light for a slit beam, so as to avoid stimulating the pupillary light reflex

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Neovascularization of the Angle

DYNAMIC (COMPRESSION OR APPOSITIONAL) GONIOSCOPY

Useful in differentiating pupillary block in angle-closure glaucoma

Appositional Gonioscopy

Differentiates appositional closure from synechial closure

Gentle pressure on the cornea with goniolens pushes back the iris and reveals whether the angle can be opened any further synechial closure is present if unable to

open can also help break acute attacks by

forcing fluid into the periphery and opening areas of appositional closure

Angle from synechial closure will not open

IMAGING MODALITIES supplement gonioscopy

detailed images of structures and quantitative measurements

useful in primary angle closure but can also help detect secondary cases of angle closure such as ciliary body masses or anterior rotation

no widely agreed upon quantitative measurement cutoffs

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Evaluating Anterior Chamber Depth

Average Depth: 3.15 mm

Shallows by 0.01 mm per year

Less than 2.5 mm is at risk for angle closure

Measuring: A ScanOCT UBM

A-SCAN ULTRASONOGRAPHY

Narrow anterior chamber angles may be measured with A-scan ultrasonography

Relative risk of angle-closure can be assessed

75% of ACG occurs in chambers < 1.5mm

ACG very rare in chambers > 2.5mm

Anterior segment OCT (AS-OCT)

• diode light source

• highly detailed images of the cornea, angle region, and anterior CB

• similar to those seen with UBM

• AS-OCT is unable to image structures posterior to the iris plane well because of posterior pigmented iris shadowing and scleral light scattering.

• noncontact exam

• the patient can be imaged in an upright position avoiding positional lens changes

• all four quadrants can be scanned at once

• get undisturbed images in the dark

Ultrasound biomicroscopy (UBM) • B scan ultrasound

• high-resolution cross-sectional images of the anterior segment of the eye to the anterior vitreous

• helpful for evaluating plateau iris and other CB pathology

• Disadvantages

water bath immersion

specialized equipment

skilled technician to operate

relatively costly and time consuming

That Very Closed Open Angle

The Gonioscopically Challenged Doctor

CASE Patient treated for years for “Chronic

Open-Angle Glaucoma”

IOPs elevated to the low 30’s

Progressive visual field loss

Never evaluated with a gonioprism!

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Angle ClosureHigh Resolution Image

Pachymetry

Measurement of Central Corneal Thickness (CCT) found to be important in OHTS

Average CCT among OHT patients was found to be 570 microns: >588 microns was considered thick

Thin corneas (< 555 microns) were a significant risk factor in conversion

Thin corneas give a low Goldmann measurement- underestimates true IOP

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CCT ASSESSMENT Has become standard

Equipment has become widely available

DGH was used in OHTS

Consider potential effect of LASIK on IOP findings

Anterior Segment Imaging

560 μm in cornea

Cirrus HD-OCT anterior segment image of the cornea provides pachymetry readings using a caliper tool to measure central corneal thickness.

Corneal Hysteresis

•Corneal biomechanical and physical properties, such as corneal hysteresis and CCT, are highly correlated and associated with VF progression. •As corneal hysteresis may describe corneal properties more completely than thickness alone, it may be a parameter that is better associated with progression

Reichert ocular response analyser (ORA)

The Ocular Response Analyzer (ORA) is a new instrument that

measures the corneal biomechanical

response (corneal hysteresis, CH) to

rapid indentation by an air jet.

Goldmann Tonometry: The Gold Standard

Goldmann Tonometry

•Remains the standard of care

•Consider corneal hysteresis and CCT

•Other modalities may be less influenced by CH

and CCT

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Pascal Dynamic Contour Tonometer

The dynamic contour tonometer (DCT; Pascal tonometer) is a novel tonometer

designed to measure intraocular pressure (IOP) independent of corneal properties.

Pascal dynamic contour tonometer•A concave contact surface with a radius of curvature of 10.5 mm creates a distribution of forces between the central contour matching area of the tip and the cornea that equals the forces generated by the internal pressure of the eye.

•Readings are higher than with Goldmann applanation tonometry

•Appears to be less influenced by CCT

•May be useful S/P LASIK

Tono-Pen XL

The Tono-Pen XL cannot be used as a substitute for GAT in the

management of patients with glaucoma or

OHT.

Tono-Pen XL

Tono-Pen XL

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Cirrus™ HD-OCT Spectral domain OCT technology

Capable of volumetric (3D) & high definition line scanning of the retina

Similar to NFL polarimetry, OCT is used to determine the NFL thickness in the peripapillary region

Compared to ultrasonography using laser light instead of acoustic waves

How Does OCT Work?

Light Source

Beam Splitter

Reference Mirror

Detector

Cirrus RNFL Analysis

CALCULATION CIRCLEAutoCenter™ function automatically centers the 1.73mm radius peripapillary calculation circle around the disc for precise placement and repeatable registration.

OPTIC DISC CUBE SCANThe 6mm x 6mm cube is captured with 200 A-scans per B-scan, 200 B-scans.

Cirrus Optic Nerve Head Analysis

Automatically identifies the optic disc and cup boundaries.

Is generated using the dense data in the Optic Disc 200x200 data cube and a proprietary ZEISS algorithm.

Is designed to precisely measure the neuro-retinal rim while accounting for tilted discs, disruptions to the RPE and other challenging pathology.

Cirrus RNFL and ONH

Report shows RNFL and ONH for both eyes, using the Optic Disc Cube 200x200 scan

Cirrus RNFL and ONH Analysis ElementsOCT en face fundus image shows boundaries of the cup and disc and the RNFL calculation circle.

The integrated RNFL thickness deviation map shows deviation from normal

RNFL thickness map also displays cup and disc mask

Optic Nerve Head calculations are presented in a combined report with RNFL thickness data. Key parameters are compared to normative data and displayed in table format

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Cirrus RNFL and ONH Analysis Elements

RNFL Peripapillary Thickness profile, OU compared to normative data

Neuro-retinal Rim Thickness profile, OU- compared to normative data

RNFL Quadrant and Clock Hour average thickness, OD and OS

- compared to normative data

Using the Cirrus HD-OCT, we can identify progression in RNFL loss through event analysis and trend analysis.

Event analysis assesses changes that are beyond an expected variability at certain points compared to normative data. If a patient falls outside this area, it is identified as progression.

Trend analysis looks at the rate of change over time, using linear regression to determine whether or not the trend is outside the expected rate of RNFL loss.

Cirrus GPA™ Analysis

GLANGLION CELL INJURY

GANGLION CELL ANALYSIS



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Cirrus GPA™ Analysis

RNFL Thickness Change Maps demonstrate change in RNFL between exams. Up to 6 progression maps are compared to baseline. Areas of statistically significant change are color-coded yellow when first noted and then red when the change is sustained over consecutive visits.

RNFL Thickness Maps provide a topographical display of RNFL for each exam.

Guided Progression Analysis (GPA)

GUIDED PROGRESSION ANALYSIS (GPA)

THE FUTURE OF LASER IMAGING

Broad applications in measurement of enlargement of the cup and change in the thickness of RNFL

DRANCE HEMORRHAGES

Optic Disc Hemorrhages observed in glaucoma perhaps noticed particularly in

NTG linked to progression of disease

not adequately controlled

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Drance Hemorrhage ?

Definition of “Glaucomatous” ODH

Flame- or splinter-shaped hemorrhage

– radially oriented and

– perpendicular to disc margin

Definition of “Glaucomatous” ODH

X Not associated with

disease other than glaucoma Vascular occlusive

disease Diabetic retinopathy Ischemic optic

neuropathy

Flame- or splinter-shaped hemorrhage

Drance Hemorrhages

Glaucomatous Optic Disc Hemorrhages characteristically in the axon bundles therefore, splinter-shaped and

superficial crossing the disc boundary, or over a peripapillary crescent or halo

or within the disc, not flame-shaped

OHTS DATA

Data from the Ocular Hypertension Treatment Study (OHTS) used to see:

what makes disc hemorrhage likely?

how predictive are they of the future course (conversion to glaucoma) in OHT?

Results: Cumulative Incidence of Disc Hemorrhage prior to POAG

96847260483624120

0.15

0.10

0.05

0.00

Months Since Randomization

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Cumulative Incidence of Disc Hemorrhage prior to POAG endpoint

12 months between disc photos

Disc hemorrhages may come and disappear between photographs

Therefore previous graph almost certainly underestimates the true incidence of ODH

Drance Hemorrhages

To our surprise Tx IOP lowering medicine did not reduce risk of ODH.

Q: What does this mean?

A: We don’t know ODH marks inadequate IOP lowering ODH marks pathogenic mechanism mechanism is still there but it no longer causes harm

ODH had lower incidence than POAG and analysis has insufficient power

ODH prediction of POAGin multivariate analysis

After adjusted for:

– Treatment Group

– Age

– Vertical cup/disc ratio

– Pattern standard deviation (visual field)

– Baseline IOP

– Central corneal thickness

Hazard ratio 3.7 [2.1 – 6.6]

Summary: Why do you get Drance Hemorrhages?

OHTS participants who developed ODHs

Similar to those who develop POAG

including older age, thinner corneas, and larger vertical C/D, higher PSD

EXCEPT THAT.. ODH not less frequent with

lower baseline IOP

assignment to treatment

Summary: What if you get ODH? ODH is an additional independent risk factor

for developing POAG

But ODH is not synonymous with developing POAG

87% of OHT participants with ODH did NOT develop POAG endpoint during follow-up period

153 eyes of 168 who developed POAG did so without prior ODH

Conclusions

ODH are difficult to find,

but a diligent search is worthwhile, because they represent one of the risk factors to be taken into account when making clinical decisions.

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SURGICAL MANAGEMENT OF GLAUCOMA

ALT

SLT

LPI

MIGS

FILTRATION SURGERY

SETONS

Selective Laser Trabeculoplasty(SLT)

• Q-Switched frequency doubled (532 nm) Nd:YAG Laser

• Selective targeting of pigmented (TM) cells

• No structural or coagulative damage to the TM-less destructive than ALT

• Cytokines released that attract macrophages

360o with 90-100 non-overlapping spots

ALT Spot vs. SLT Spot Size

Courtesy M. Berlin, M.D.

SLT vs. ALT

Courtesy M. Berlin, M.D.

Human TM (organ system) ALT 50 um spot

R. Noecker, T. Kamm

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Human TM (organ system) SLT 400 um spot, 0.8 mJ/pulse

R. Noecker, T. Kamm

Laser Iridotomy

Laser Iridotomy: Indications

Primary angle closure glaucoma

Secondary pupil block glaucoma

Fellow eye in primary angle closure

High risk asymptomatic narrow angles

Nanophthalmos

Long term miotic therapy with narrow angles

Pigmentary glaucoma (controversial)

IRIDOTOMIES

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MIGS: MICROINVASIVE GLAUCOMA SURGERY

GLAUCOMA FILTRATION SURGERYTrabeculectomy involves 8 separate incisions

ConjunctivaSub-Tenon’s spaceTension insertion at limbusEpiscleraScleral flap edgesScleral flap baseSclerectomy Iridectomy

Penetrating Filtering Surgery - Trabeculectomy

BLEB-RELATED ENDOPHTHALMITIS

Hypopyon, Vitritis

MIGS: MICROINVASIVE GLAUCOMA SURGERYMIGS

ViscocanalostomyCanaloplastyTransciliary Filtration (Fistulization)Trabectome iStentXEN Gel Stent Glaucoma Implant Hydrus Microstent (Investigational)CyPass Micro-Stent (Investigational)

iStent Trabecular Micro- Bypass Stent

Micro stent implanted in

Schlemm’s canal

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iStent: Heparin-Coated Nonferromagnetic Surgical Grade Titanium

iStent: Placed in Schlemm’s Canal at Lower Nasal Quadrant

Visible on Gonioscopy

The stent is a soft, permanent, subconjunctival implant that shunts fluid from the anterior chamber to the subconjunctival space.

XEN Gel Stent for Glaucoma

Approximately 6-mm long and the width of a human hair, the stent comes preloaded in a disposable Xen injector and is implanted

through a small, self-sealing corneal incision.

GLAUCOMA GRAND ROUNDS

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CASE 1

57-YEAR OLD ASIAN MALE

No visual complaintsS/P repair herniated discOther review of systems negativeNo allergies to medicationsNegative family historyNegative social historyPresented taking 0.5% Timolol b.i.d. O.U.

PHYSICAL EXAMINATION

Entering Visual Acuity: O.D. 20/25 O.S. 20/20

No improvement with manifest refractionPupils: 1+ RAPD O.D.SLE: Unremarkable O.U.Gonioscopy: D-40-f configuration with

1+ pigment observed O.U.


Color vision normal with AO-HRR pseudo-isochromatic plates O.U.

Desaturation to color targets O.D.Exophthalmometry normal O.U.Positive maintenance, pursuit, saccadic,

vergence, oculocephalic, and ocular kinetic nystagmus (OKN) systems were intact


Tonometry: O.D. 10 mm Hg O.S. 11 mm Hg

Review of prior records and subsequent diurnal examination show IOPs have consistently been measured from 10 to 15 mm Hg

OPHTHALMOSCOPY AND FUNDUS EVALUATION

Clear media O.U.Sharp disc margins+ Foveal reflexHealthy peripheral retinaIntact retinal nerve fiber layer O.U.

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OPHTHALMOSCOPY

Right nerve showed a large cup with shelving of the superior neuroretinal rim

Left cup was smaller with an intact neuroretinal rim

OPHTHALMOSCOPY

THRESHOLD VISUAL FIELDS

30-2 Humphrey Visual Fields showed a dense inferior arcuate bundle defect breaking out of the blind spot O.D.

The left visual field was normal and reliable

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Statistical analysis of subsequent visual fields (overview and change analysis) showed stable visual fields O.U.

TREATMENT PLAN

D/C timolol (which he had been taking for several years without effect on IOPs)

IOPs remained low and stableCurrently being followed with serial visual

fields, stereo disc photography, IOPs, and OCT imaging

Currently on no medications



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Follow-Up Evaluation 01/2017

IOPS: OD 11 OS 10

This patient has remained stable for 25 years off topical medication

Careful observation is still required

Monitor with visual fields, OCT, tonometry, fundus photography and IOPS x 6 months

CASE 2

49-YEAR OLD WHITE MALE

Longstanding history of right hyper deviation

HypercholesterolemiaOther review of systems negativeNo allergies to medicationsNegative family historyNegative social historyPresented with CC of “things sometimes

being more out of focus”


Visual Acuity: OD 20/20 OS 20/20

Refraction: OD -5.50-3.50x174 OS -6.50-3.00x174

Pupils: Reactive with trace RAPD OS

Bright Illumination: OD 4.25 OS 3.75

Dim Illumination OD 5.75 OS 4.75

Lids demonstrate a 2 mm ptosis OS


+ Aproclonidine test

Anhidrosis left side of face

Horner (Horner’s) Syndrome: Interruption of sympathetic nerve supply

Anhidrosis, miosis and partial ptosis

THRESHOLD VISUAL FIELDS 2/2011

Threshold Visual Fields (24-2 Program):

OD Superior Nasal Step

OS Superior Arcuate Defect With Superior Nasal Step

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THRESHOLD VISUAL FIELDS 2/2011

PHYSICAL EXAMINATION 2/2011

OD 551 microns OS 556 microns

IOPs: OD 16 OS 17 Note: IOPs never higher than 18 OD and 17 OS with multiple readings over 18 years

Color Vision: OD 6/14 OS 5/14 using Ishihara Plates

Fundus: OD .55/.6 OS .6/.65 with pallor of the neuroretinal rims. Pallor and cupping increased from photos taken in 1993

ONH Photographs 2/2011

FOLLOW-UP EVALUATION

Neuro-eye Group ordered extensive testing including imaging, carotid duplex test, cardiac work-up, and comprehensive laboratory testing

MRI of brain, orbits and neck were all normal including lung apices

Carotid ultrasound normal

All other testing was unremarkable and the patient referred for treatment of presumed normal tension glaucoma (NTG)

FOLLOW-UP EVALUATION 2012

Neuro-eye group ruled/out non-glaucomatous optic neuropathy and referred for glaucoma management

Treatment was initiated with Travatan-Z qhs OU with a target IOP of 10 mmHg OU

Treatment was increased by adding Simbrinza tid OU and target IOPs were achieved

OCT showed significant RNFL thinning OS>OD

ONH examination showed progressive pallor and cupping OS>OD

OCT RNFL ANALYSIS 10/2012

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ONH PHOTOGRAPHS 10/2012

FOLLOW-UP EVALUATION

Although target IOPs were achieved, there appeared to be progressive ONH and visual field changes observed

OCT RNFL Analysis showed thin RNFL OS>OD

Pupils were reactive but appeared to demonstrate a reversal of Horner Syndrome and fundus examination showed progressive ONH cupping OS>OD

Blood pressure was very low at 110/60 and pulse was low at 40 bpm

SLT laser treatment was performed to attempt to maintain IOPs as low as possible in addition to maximum medical therapy

OCT RNFL Analysis 3/14

WHY NO BETA-BLOCKERS?

Significant concerns re: very low pulse and blood pressure

In addition, there are theoretical concerns with respect to beta-blockers such as timolol and perfusion to the ONH

The patient was maintained on TravatanZ and Simbrinza S/P SLTs

IOPs were found to be OD 08 and OS 09 in 8/2015

The patient was again referred to Neuro-eye Services to R/O non-glaucomatous optic neuropathy


Neuro-eye found no new complaints and reports excellent compliance with his topical medication

Currently taking Lipitor for hypercholesterolemia

Runs regularly and reports excellent health

Blood Pressure 115/64 ras and Pulse 44 bpm

Visual Acuity: OD 20/20- OS 20/20-

IOPs: OD 11 OS 10


Pupils: Reactive but + RAPD OS

Bright Illumination: OD 4.0 OS 4.5

Dim Illumination: OD 4.5 OS 5.0

+ Aproclonidine test

Horner Syndrome reversal!! What does that mean???

ONH evaluation showed a C/D ratio of

OD .75/.8 and OS .9/.95

OCT shows marked RNFL thinning OS>OD

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OCT RNFL ANALYSIS 8/2015

Threshold Visual Fields 10/2015

Guided Progression Analysis GPA) 10/2015

TREATMENT PLAN Neuro-eye work-up was unremarkable except for very

low blood pressure and pulse.

Second opinion Neuro-eye opinion at Wills Eye Hospital was in agreement with our findings and treatment plan

Two cardiology opinions were obtained with our suggestion of implanting a pacemaker

Low perfusion pressure seems to be the only remaining modifiable risk factor

Maximum medical therapy was maintained and IOPs (8/2016) were OD 10 OS 09

Follow-Up Evaluation 02/2017 IOPs increased to OD 18 and OS 17 (Repeatable)

Surgical Trabeculectomy with MMC scheduled for 03/2017

Sleep study in New York- still considering pacemaker

To be continued!

CASE 3

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67-YEAR-OLD WHITE MALE

Hx: Referred from Primary Care Module for elevated IOP OS

Originally from Canada and worked as a ski instructor

No ocular or visual complaintsNegative family Hx

PHYSICAL EXAMINATIONEntering VA: OD 20/20-3

OS 20/25-1Pupils: PERRL but sluggish with + RAPD OSEOMs: Smooth and FullGonioscopy (Sussman): OD D-40-f

OS D-40-f Marked pigment deposition on the trabecular

meshwork and Schwalbe’s Line OS>OD

PHYSICAL EXAMINATIONTA: OD 22 mmHg

OS 38 mmHgOphthalmoscopy:

OD .45/.45 with intact rim 360°OS .85/.85 with loss of the inferior

neuroretinal rimCCT: OD 570 microns

OS 565 microns


Slit-Lamp Examination: White, flaky material on the anterior border of the iris and on the anterior surface of the anterior lens capsule OS>>OD. Only a few flakes were present OD

A clear middle zone was present OS with material present centrally and in the periphery

Positive iris transillumination defects were present OS>>OD giving a “moth eaten” appearance to the pupillary margin.

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Threshold Visual Field testing revealed essentially normal fields in the OD (borderline GHT)

The OS showed profound loss of the superior hemifield

DIAGNOSIS

Advanced Exfoliation Glaucoma OS (PXG)with borderline IOPs OD

MEDICAL MANAGEMENT

Rx: TravatanZ qhs OS monocular trial

FOLLOW-UP

Follow-up at 3 weeks showed IOP decreased to 17 mmHg OS

OD increased to 23 mmHgRx: Travatan qhs OUFollow-up at 4 weeks

demonstrated IOPs of : OD 14 mmHg

OS 15 mmHgCareful observation x 3 months

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FOLLOW-UP 2/2015

Regular follow-up evaluations have demonstrated stable visual fields and optic nerve head appearance.

IOPs were elevated to OD 18 mmHg OS 24 mmHg

on current regimen of Travatan Z and AzoptCombigan bid OU was added 2/2015

FOLLOW-UP 6/2015

Reports excellent compliance with medications IOPs were improved at

OD 13 mmHg OS 17 mmHg

on current regimen of Travatan Z, Azopt, and Combiganbut target IOPs were not achieved OSSLT laser was performed 7/2015 OS and 8/2015 OD

FOLLOW-UPRegular follow-up evaluations have

demonstrated stable IOPs, OCT, visual fields, and optic nerve head appearance. Normal corneal hysteresis OU (OD 11.1 OS 10.9)

Last examination (02/17) showed IOPs of:OD 09 mmHg OS 12 mmHg

on current regimen of Travatan Z, Combigan and Azopt S/P SLT OUDo we need incisional surgery??

CHANDLER AND GRANT

“It does not require any genius to treat this disease. All one needs is a knowledge of the basic principles of diagnosis and treatment and of their correct application to the individual case.”

THANK YOU!!

2017 poa lecture [read-only] · elastin in the extracellular matrix connective tissue maintenance...

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