GEORGE T. BANYAS, OD, FAAO
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High pressures
Rim defects, typically
Pre- perimetric defects
Classic field defects
Typically no ocular or systemic history
Family history
Race
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Low pressures
Normal anatomy
Often good discs since slowly progressive
Masquerade syndrome?
No symptoms until late in disease
Is it really glaucoma?
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Africans
Elderly
High myopes/ large disc
Elevated IOP
Positive family history
Low systolic BP with reduced perfusion
Thinner central corneas
Autonomic dysregulation
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Untreated IOP typically < 21mm
Open , non-pigmented filtration angles
Acquired progressive “glaucomatous” injury
Progressive “glaucomatous” field loss
Females, autonomic dysregulation
A different type of optic neuropathy?
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1/3 of glaucoma patients possess NTG
1/3 of NTG patients have unilateral cupping
Progression is slow. No hasty decisions!
Chairside presentation will always include
IOP 21 or less
Systemic disorders not required
Systemic disease may be the cause
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Juvenile optic atrophy
Simple congenital optic atrophy
Recessive optic atrophy
Leber’s disease (through age 80)
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Burned out pigmentary glaucoma
Past history of steroid use
Severe blood loss/cardiac surgery
Post –traumatic optic neuropathy
Old BAO
Systemic beta blocker use
Past subdural hematoma
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Old ION
Posterior ciliary infarct
Intrasellar tumor
Syphilitic optic neuritis
RBON
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Subacute angle closure
Nocturnal hypotension
Systemic beta blocker use
Toxic optic neuropathy
Compression ( pituitary adenoma,
meningioma)
Sleep apnea (low O2 partial pressure)
Diurnal or nocturnal IOP swings
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Pachymetry under 550 um
Pigment dispersion or pseudoexfoliation
Compression by ICA or anterior cerebral
artery
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ICA and anterior cerebral disorders
- abnormal juxtaposition
- sclerosis
- aneurysms
- pituitary tumors, craniopharyngiomas,
meningiomas , sarcoidosis, Wegener’s
MRI with contrast is the imaging mode of
choice for sellar and chiasmal lesions
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Intracavernous sinus lesions
- thrombosis/ blood dyscrasias
-infection
- ICA aneurysm
- inflammation
Company kept includes III, IV, VI, V1, V2, and
oculosympathetic fibers. IF note a Horner’s in
unilateral “NTG” eye, must R/O cavernous s.
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Sarcoid, pseudotumor
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Acromegaly (pituitary hypersecretion of
HGH)
Paget’s disease – 1% of adults over 50, may
see angioid streaks
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Pial vessels, posterior ciliary and short
posterior ciliary vessels, CRA, ophthalmic a.
Thrombosis, inflammation, autonomic
dysregulation, infection , metabolic
syndrome resulting in ischemia
genuine ischemic optic neuropathy
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Sarcoid
Autoimmune disease
Anemia
Hypotension
Hypertension/diabetes
Vasospasm
Paraproteinemias
Hyperhomocysteinemia
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RETINA - perfusion
retinal arteries - retinal veins – CRV – cavernous s.
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UVEA/ciliary body – aqueous outflow
2 long posterior ciliary arteries - several anterior
ciliary arteries – short posterior ciliary arteries choroidal plexus – vortex veins – superior and
inferior orbital veins – cavernous s.
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Sclera/episclera/conjunctiva/canal of
Schlemm
anterior ciliary arteries – surface arterioles - venous
plexus of sclera/episclera/conjunctiva – anterior
ciliary veins – inferior/superior orbital vein –
cavernous sinus
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Wax and Associates found high titers of
antibodies against retinal proteins
- rhodopsin
- heat shock proteins
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C/D may be meaningless
Large disc has large cup
Small disc has small cup
Average size disc is consistent with 5 degree
spot size on direct
Disc size does not determine susceptibility to
glaucoma
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Normal disc shape is oval
Vertical diameter is 10 degrees greater than
horizontal
Optic disc shape does not increase
susceptibility
High astigmia may alter appearance
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Thickness – inferior -> superior-> nasal->
temporal ( ISNT rule )
Inferior and superior temporal rim effected
first
With advanced glaucoma, only nasal sector
remains
So, vertical margins effected first
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Various shades of pink and symmetric
Pseudophakes appear more pale
If advanced, pallor more an artifact due to
excavation
Pallor that exceeds cupping requires neuroophthalmic work up
Rarely, pallor may exceed cupping
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Cup is defined by contour , not color
Stereoscopic viewing
Disc shape is vertical, however cup shape is
usually horizontal
Place emphasis on the rim!
Glaucoma experts assess disc better than
OCT!
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Disc hemorrhages are not typically normal
Detected in less than 8% of glaucoma
patients
Greater association with NTG than other
glaucomas
Indication of progression
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Peripapillary chorioretinal atrophy may be
associated with glaucoma
Central beta (RPE atrophy and visible
choroidal vessels)
Peripheral alpha (pigmentary changes and CR
atrophy)
Greater with damage?
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A.D. disc drusen may result in NFL loss and
field defects identical to glaucoma
Disc drusen might mask cupping
Single most common cause of glaucoma
without cupping
B scan or auto fluorescence to diagnose
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Crescents
Tilts
Physiologic differences
Very slow progression
Disc drusen
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Most early cases will be missed!
Add FDT screening fields and may capture a
few
Perform routine pachymetry and may
capture some
Add threshold perimetry and may capture a
few more
Discs that do not respect ISNT caught
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Managing a condition with unknown
pathogenesis
May be secondary to systemic disease
Systemic disease may result in
morbidity/mortality if not managed
Disorder may progress regardless of your
intervention
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Very good history
- previous history of any IOP elevation
- ocular trauma/ inflammation/ steroid use
-sleep apnea (may need to ask spouse)
-nocturnal BP dips
- erectile dysfunction drugs
-hemodynamic crisis (blood loss,
hypotension, anemia, syncope, blood
transfusions, surgery (usually open chest)
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Weakness in extremities, dizziness,
headache, loss of consciousness, diplopia
Color vision testing, ruling out
dyschromatopsia, particularly if asymmetric
cupping
Pupil testing
Systemic medications
Gonioscopy
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CBC to rule out anemia
ESR – rarely elevated, but more to R/O ION
RPR, if positive then FTA-ABS
ANA to rule out collagen vascular
AP Abs, rhodopsin Abs, HSP Abs
Serum immunofixation for monoclonal
gammopathy….10% of NTG patients
C reactive protein…. Often high in NTG
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Chest X-ray to rule out sarcoidosis, superior
vena cava obstruction
Carotid Doppler to rule out carotid
insufficiency
Scanning
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Which one?
- the anatomic site
- the pathophysiology
- the cost
Who should order?
- the person treating
- suggestions are welcomed
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Disc drusen – CT
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CT for Grave’s – axial and coronal views with
contrast
CT for vascular abnormalities – varices,
hemangiomas, and lymphomas
Pseudotumor – CT or MRI
Optic nerve tumor – MRI with fat suppression
and contrast
* Contrast presumed in all instance of CT
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MRI is choice for sellar and chiasmal lesions
Craniopharyngiomas, pituitary adenomas,
and meningiomas
Intracavernous lesions – look for constriction
of the carotid arteries
ICA or anterior cerebral artery abnormalities
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MR angiography – evaluates flow
CT angiography – evaluates blood volume
Either good for aneurysms
Can not definitively R/O aneurysm
Not good for lesions < 5mm
Catheter angiography is still the gold
standard
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Done before gonioscopy
Preferably before dilation
At least two hours after awakening
Stability following contact lens wear?
Normal population 544+ 34um
2.5-3.5mm per 50um
3 readings with SD of 5um or less
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37 published studies have demonstrated CCT
is a risk factor for progression to glaucoma
German study determined relationship
between CCT and field loss
NTG patients tend to have thinner CCT
“thin” cornea may be masking POAG
Optic nerve photos before LASIK?
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Structural changes before functional changes
OHTS demonstrated 93% chance of not
developing glaucoma with normals
Greatly expanded database heightens
sensitivity
May identify changes in visual fields up to 8
years earlier
Disc and nerve fiber layer
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Baseline images to compare patients to
norms
Detection of progression may disagree with
perimetry
Irregularities, even before field change may
be predictors
Still possible to have field loss before
structural changes!
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Functional changes may precede structural
Diagnostic ability demonstrated to be less
accurate than disc assessments by a
glaucoma specialist
Tells how much tissue is there, but is it
healthy
5,000 axons lost on average per year
Variable normal disc topography
Specificity not 100% for glaucoma
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Required! Possible to have field loss before
structural changes
C30-2 SAP
SWAP may provide earlier diagnosis –
stimulus V blue (440 nm) on yellow, that’s
about all
FDT matrix may provide earlier diagnosis
than SWAP and SAP. That’s about all
Right field is WNL. Left finds correlation between the two
Not looking for:
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Focal defects are not uncommon
Defects are closer to fixation often
Defects are deeper
Less slope from seeing to non-seeing
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Collaborative NTG Group Study showed slow
or non-progression in NTG
Risk factors such as migraine or disc
hemorrhage should be followed closely
With conclusive demonstration of
progression consider treatment
50% of eyes without progression showed no
progression by 7 years
Reduce IOP 30%
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Assess ocular environment
Most common comorbidity in glaucoma
patients is dysfunctional tear syndrome
DTS present in 8-20% of population
Topical glaucoma therapy daily, for years,
may further compromise the surface
48% of glaucoma patients report mild to
severe symptoms
Would you give a pill
to someone that
can’t swallow?
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Nafl tear BUT
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Corneal/conjunctival
staining
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Meibomian gland
inspissation
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Anterior blepharitis
- Steri-lid HS
- warm compresses/massage
- antibiotic or antibiotic/steroid ung HS
- soft preserved tears daytime
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Posterior blepharitis
- Steri-lid HS
- warm compresses/massage
- steroid/antibiotic ointment HS x 1-2 weeks
- cyclosporin BID if MGD appears primary
- doxycycline 100mg QD
- omega 3’s ( fish oil/flax), good hydration
- soft preserved lubrication daily
60 times better penetration
than other topical antibiotics
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Topical 1% solution (Azasite, Inspire Pharma)
Warm compresses/massage with 1% Azasite
BID x2days, then QD x 12 days
Well documented anti-inflammatory activity
75% of patients
Macrolides have demonstrated antiinflammatory properties by inhibiting MMPs
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Lacrimal gland disease
- soft preserved tears daily such as Systane
- gels HS
- consider cyclosporin
- omega 3’s, good hydration
- question systemic medications
- plugs
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Canthal tendon laxity
- poor tear ejection
- ectropion
- floppy eyelid syndrome
Conjunctivalchalasis
Pinguecula
EBMD – muro 128 drops/ung/debridement
Allergies - Patanol
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BAK – a detergent that disrupts cell
membranes
- reduced TBUT
-conjunctival fibrosis
- concentration-dependent cell mortality
- goblet cell reduction/loss of microvilli
- basement membrane damage
- not all patients suffer
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Benzododecium bromide – timolol gel
Purite – brimonidine
Sofzia – travoprost
Newer reduced concentration
- Lumigan 0.1%
Unit doses
- Timoptic
- Zioptan
- Cosopt PF
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Shown to lower IOP 15-30% in NTG
Interestingly, not utilized in the CNTGS
Little circadian variation in IOP
Some work better than others in some
patients
non-BAK option – Travoprost/Zioptan
Could exacerbate inflammation with OSD
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Travoprost has shown efficacy beyond 24
hours
DuBiner et.al. observed IOP significantly
reduced out to 84 hours.
Sit et.al. showed efficacy 41-63 hours
Peace et.al. showed travoprost with and
without BAK effectively lowered IOP at all
times out to 60 hours
Partially reversible after a few months
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Safe systemically, really, but use Betoptic
QD dosing usually enough
Should be reconsidered for NTG. Possible
reduction in perfusion to disc, where Betoptic
shown to possibly enhance optic nerve
perfusion
OK for patients with asthma. Clear with their
physician first.
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May be neuroprotective (increased ganglion
cell survival in rat optic nerve crush injury)
Concern about reduced perfusion
Good peak effect, reduced trough effect with
short duration of action
Less effect between midnight and 6 a.m.
Tachyphylaxis / allergy
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Dorzolamide – increased retinal blood flow in
humans
Brinzolamide (Azopt, Alcon)
Better 24 hour efficacy vs. B blockers or alpha
agonists
Diamox – may be necessary when intervening
in surface disease
May be better adjunctive drug to use with
prostaglandins
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Prostaglandins and……
CAI> alpha agonists> beta blockers
Prostaglandins + CAB
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Cosopt – dorzolamide /timolol maleate
Xalacom – latanoprost / timolol (not here)
Combigan – brimonidine / timolol (adjunct)
travoprost/timolol - (not here)
the presence of beta blockers might
contraindicate use with NTG
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Antihypertensives in AM
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Seek to maintain diastolic no less than 80mm
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Tell MD to change their regimen or else
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Non-adherence to medications
Inability to lower IOP 30%
Impression of greater diurnal shift
Surface disease
Progression
Cognitive impairment
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Patient characteristics
Provider characteristics
Characteristics of the medical regimen
Situational/logistical factors, including cost
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Difficulty detecting non-compliance
Non-compliance increases with increasing
meds, dosages
Tsai and colleagues identified 20 specific
barriers that patients reported interfered with
using glaucoma meds
Provider communication and concern about
future consequences drive adherence
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13,956 patients
89% claimed taking meds daily
Medication possession ratio revealed an
average of drug taken 64% of time
Drug taking ranged from 36% of time to
100% of time
Only 10% fit the 100% category
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Google OHTS risk calculator
I phone app for glaucoma risk calculator
LET’S EAT!