Classification of Findings Flashcards
Size and shape

2.1mm2 and 2.8mm2 with a range The average vertical disc diameter is 1.8mm with a horizontal disc diameter of 1.7mm.
Caucasians - Smaller
Mexicans < Asians < Africans
CDR is normally less than 0.60, relative to the size of the disc so that smaller cupping - small-sized disc and larger cupping - large discs
tends to enlarge in the vertical meridian in glaucoma
Size, How to classify
(could use bloodvessels as broad guide)
optic disc size as small (vertical diameter <1.5mm),
average or large (vertical diameter >2.2mm)
Use slit beam height to match vert - Using 90D
correction factor will be 1.0x for a 60 D lens, 1.1x for a 78 D and 1.3x for a 90 D lens.
Larger with Biomicroscope
ISN’T rule
Neural rim tissue THICKEST
Inferior of the disc, then the Superior and Nasal, being thinnest in the Temporal region
normal neural rim tissue
LAMINA CRIBROSA

It is a sieve-like structure of largely connective and glial tissue that is continuous,
although embryologically distinct, with the scleral coat
OPTIC NERVE DRUSEN

Bilateral
pseudopapilloedema. They are golden, autofluorescent, glowing, calcific globular deposits that sit in front of the lamina cribrosa
can shear blood vessels and/or nerve fibres, leading to haemorrhages (2-10%) and visual field loss (~75%),
Myelinated nerve fibres

Myelin sheathing of the optic nerve fibres that extends beyond the lamina cribrosa and presents a superficial, white, feathery opacification which hides any underlying retinal blood vessels.
Classification of Glaucoma
Normal

- Good rims
- Good IOP
- No Family Hx
- No Trauma related incidents that can increase risk
- No medications that can increase IOP
( Topical and Systemic Steroids / TOPAMAX (Weightloss / seizures / migraines)
Nerve fibre layer striations

brightest at the superior and inferior poles, where the nerve fibre layer is thickest and are best seen in young patients, particularly those with heavily pigmented fundi (Figure 9). The striations are caused by the tubes of astrocytes that surround the retinal ganglion cell axon
Peripapillary atrophy (PPA)

The RPE and choriocapillaris are lost and all that is visible are the large choroidal vessels and sclera
15% of normal eyes bordering the disc BETA zone
More prevelent in glaucoma
Tilted discs & optic disc malinsertion

the disc or discs are commonly tilted inferior nasally with a nasal staphyloma (bulging of the sclera) and situs inversus, where the temporal blood vessels first course towards the nasal retina before sharply changing course
staphyloma can produce a temporal visual field defect
Optic disc basic Examination
C x 3
VEINS &ARTERIES
CUP
CONTOUR
COLOUR
Veins - Darker
Arteries Lighter lumen
COLOUR of optic disc
Orange - Pink
What Causes Palor?
NIGHT TIC
- Neuritis
- Ischaemic
- Granulomatous
- Hereditory
- Traumatic
- Toxic
- Irradiation
- Compression
Goldman Perimetry
Advantages
Goldmann Perimetry
• Advantages
◦Can use both kinetic and static targets
◦Can test both central and peripheral fields
◦Can change both target luminance and size
◦A specific area of the field may be quickly isolated and tested
• Used mostly in low vision and neuro-ophthalm to map fields•
Goldman Perimetry
Disadvantages
Disadvantages
◦Testing the full field is time consuming and tedious
◦The exposure time, speed of movement, and point location are NOT set by the machine, so
there can be variability between users

Automated Fields
• HVF 3 - Has a liquid lens, just enter the Rx

Automated Perimeters
• HVF Analyzer 2
• Octopus
• Oculus Zeiss

Different Types of Stimulus Presentations
- Projection (ie: Humphrey)
- Movable LED (ie: Octopus 1-2-3)
Automated Perimetry
Advantages
• Advantages
◦Testing conditions are reproducible
◦Accurate
◦Numerical results (Not X or sqaures)
◦Most testing can be done by techs
◦Insurance carriers reimburse
Automated Peimetry
Disadvantages
• Disadvantages
◦Interpretation of results can be difficult
◦Variability between different manufacturers —> hard to compare
◦Length of time for threshold testing
◦Initial cost of instrument
Automated VF Luminace terminolegy
Apsotilb (Asb)
Decibels (Db)
and the comparison

• Apostilb(asb.)
◦Unit of light intensity
◦Apostilb = candela/pi m = lumens m
- *• Decibels (dB)**
- *target size** NOT considered or background illumination
◦0.1 log units = 1 dB
‣ 0 dB corresponds to brightest stimulus on a machine
‣ > 0 on a printout means pt cannot see the brightest stimulus
‣ 50 dB corresponds dim stimulus on a given machine
‣ highest you see is about 40 dB

Automated Perimetry
Background
For all automated perimeters, the background is in the mesopic range (between 1-100 asb)
◦This range stimulates both rods and cones
◦Humphrey: 31.5 asb
◦Regular Octopus: 4 asb
Octopus 1-2-3: 31.5 asb
Threshold vs. Sensitivity
• Automated machines are threshold tests
◦Higher dB = dimmer stimulus = the better vision = more sensitive
• ie: a threshold value of 10 dB has a lower sensitivity than a threshold value of 20 dB
◦10 dB is brighter than 20 dB, which means person is less sensitive if this is their threshold
How size of target influence Db and how calculated

Sizes:
◦Humphrey III target is 0.43 deg diameter, 4.00 mm
◦Humphrey V target is 1.72 deg diameter, 64.00 mm
◦Log(4) = 0.6 (6 dB), so going from a III to V would increase the dB by about 12 dB
◦Ie: Test patient in one location with III size and get 20 dB, if you repeat with V size you would
get about 32 dB
Gray Scale

◦Visual representation using varying shades of gray to represent sensitivity
◦Darker gray = greater reduction in sensitivity
◦NOT a substitute for numerical chart —> can be misleading at times
◦Skewed to recognize defects
◦Good tool for patient education
◦Gray scale is a simple representation (not an interpretation)
Fixation Monitoring
Fixation Monitoring
• Heijl-Krakau Fixation Quotient
◦A blind spot is mapped
◦A stimulus is placed at the center of the already mapped blind spot to ensure the pt is not
tracking the stimulus and to check for alignment changes ◦Expressed as a ratio
‣ Numerator = # times the pt lost fixation
‣ Denominator = # of trials
◦Greater than 0.20-0.25 is usually considered invalid or unreliable
Optical monitoring

• Optical monitoring
◦Humphrey system projects infrared light onto the cornea
◦Enables perimeter to calculate the eye rotation from the distance the corneal reflex moves
compared to a baseline measurement taken before VF begins ◦“Gaze tracking”
3 Ways to varify Fixation losses
Tech Tips
how to pause test by holding button
Run demo
Pause every 5mins for break - avoid fatigue artifact
• Monitor pt fixation manually through entire test especially if 10 degree
Fixation Losses
◦Blind spot check is easily fooled
‣ Slight tilting of head or anatomical variation
‣ Catch trials are skewed - more in the first few minutes and less as attention decreases
◦Gaze track can lose its lock
‣ Not all patients pass gaze track initialization
‣ Thrown off by head movement and dry eye
‣ Fair accuracy, 1-2 degrees
‣ Interpretation is subjective (no standards!)
◦Gaze track and fixation loss (FL) catch trials often disagree
◦Direct observation by tech is probably best - final arbitration of reliable fixation
Rx needed for visual Fields?

• Humphrey bowl is 30cm deep
◦Peripheral field —> No Rx needed , the ring of the lens will interfere with the test
◦Central field (30 deg) —> Rx is needed
• metal rimmed trail lenses
• Patient is dilated with anti-cholinergic (tropicamide) to wipe out accommodation, a +3.25 Add should be used
◦Phenylephrine is a sympathetic agonist,
tropicamide is a parasympathetic antagonist
• For Rx’s with 0.75 cyl or below, the spherical equivalent can be used
• For 1.50 cyl, you must use it in perimetry

How to read A Humphries test
+
Considerations.
How to read Humphrey Visual Field Printout
(1). Type of test
◦Threshold or screening?
(2). Name of Patient
◦Always enter the name the same way
(3). Strategy
◦Full Threshold, Fast Pac, SITA Standard, or SITA Fast or SITA Faster
(4). Rx used
(5). Pupil Diameter
◦If pupil is less than 2-3mm, pupil should be dilated
(6). Fixation Losses
◦Predicts validity or reliability, if greater than 20% need to repeat unless there are reasons
(7). False Positives
(8). False Negatives
◦If pt is thresholded at one stimulus, then a stimulus that is 9 dB brighter will be presented at the same point
‣ Ie: 20dB threshold, 9 dB brighter would be 11 dB
◦If the pt does not see this point, it is a false negative
◦May indicate that the pt is tired or no longer attentive to the test
Patient and Perimetrist factors to consider
Human Factors to Consider
• Fatigue
• Learning
• Fixation
• Distractions
• Anxiety
• Medical problems (ie: arthritis)
• Droopy lids
• Pupil size
• Long-term fluctuation
• Short-term fluctiation (indicator of pt reliability)
Perimetrist Factors to Consider
• Correct pt instructions
• Correct type of path
• Correct Rx
• Correct alignment of the patient
• Encouragement of pt
• Rx must be metal rimmed lens
• Lens holder must be close to the eye
• Lid must be held open or taped
• Perimetrist should be sensitive to the individual needs of the pt
Do not create Pseudo defects
• You lose 1 dB per diopter that you’re out of focus
- Dirty trial lens
- lenses instead of - lenses
- Not taking away the lens holder when testing periphery
- Using wrong cyl axis
- Noisy testing room
- Using plastic rims instead of metal
Evaluating a Field
WANDER
◦What was done?
◦Was the field accurate?
◦Was the field normal?
◦What defects are present?
◦Evaluation of visual defect?
◦Re-revaluation of visual field
Visual fields (How many points And location)
24-2
30-2
10-2
24-2C
Usually grid for glaucoma is (24) 54 pts or (30) 76 pts
Macula 10-2 tests 68 points in the central 10 deg
24-2C (new) takes all points of a 24-2 and adds 10 points from 10-2 for a total of 64 points
Full field test goes out to 60 deg —> very useful, but takes too long to threshold
How FULL threshold is determined
The threshold at any given point is determined by a staircase method
◦A 4-2-2 staircase with the last seen value taken as the pt’s threshold
◦Once it has crossed the line from seeing to non-seeing or vice versa, it goes in 2 dB steps
◦At each threshold location, a dB number is assigned
◦Can detect very shallow defects
◦Can take up to 18 mins per eye on some pts

FASTPAC 3-3
Threshold Strategy: FASTPAC 3-3
• Start with 4 seed points at 25 dB, then uses the FASTPAC strategy to get threshold
• FASTPAC then starts thresholding half the points 1 dB brighter and the other half 2 dB dimmer
• It only makes one transition from seeing to non-seeing or vice versa

SITA
SITA FAST
SITA FASTER
SITA (Swedish Interactive Threshold Algorithm)
theoretically better startingpoint
• Data constantly updates as more info is gathered during the test
• Uses frequency of seeing curves
• At the end of exam, threshold values are recomputed using all stimulus luminance with a 50%
probability fo being seen
• It does NOT directly test false positives - uses response time to estimate the false positive response
• It speeds up the rate of stimulus presentation in accordance to how quickly the pt can respond
• Response time is set by the patient
• The machine theoretically calculates when to stop testing points that are fluctuating a lot
• Other algorithms re-threshold if 7 dB off, but this algorithm only retests if 12 dB off 24dB seen
Threshold is 24 dB
SITA Fast
• SITA Faster —> no false negatives and no blindspot checks
◦Rationale: more fields are important and we need to do them quicker
SITA FASTER
◦Rather than using starting point of 25 dB for the 4 primary points, it uses a faster age- corrected normal value
SITA Faster uses only one staircase test reversal
◦The SITA tests use real time determination to stop testing based on full threshold program norms. SITA Faster uses norms from SITA Fast to stop testing a given point
◦Does not re-test absolute blind spots (ie: not seen at 0 dB), while older strategies do
◦Does not test for false negatives
◦Uses gaze tracker for monitoring fixation (does not place a point in the blind spot)
◦Eliminates delay after non-seen stimuli
‣ Older SITA programs had an extra 300ms delay after non-seen stimuli at the end of the response time window before a new stimulus was presented
SWAP
SWAP (Short Wavelength Automated Perimetry)
- Blue target, yellow background
- Do less of this now
- Hard to do with cataracts, hard to interpret the threshold testing
Interpreting Visual field testing
• Very deep defects are easily spotted
- lose a decibel a decade after age 20.
Hill of vision changes roughly 3 dB every
10 degrees throughout the field
Mirror Imaging and Defect Depth (Hirsch)
• If point is 9 dB less than its neighbours, it’s a defect
• If point is 6 dB less than its neighbours, it’s possibly a defect
• If 2 or more points are 6 dB less than neighbouring points, they are probably defects
• Often a collection of points will have a reduced sensitivity (ie: an arcuate or quadrant defect)
◦Comparing the values in different locations on the graph will help identify problems ◦Compare dB values in the same coordinates between eyes

MEAN Deviation
◦Mean elevation or depression of the pt’s overall field compared to normal reference field
◦Takes all points, averages them, compares to your age
◦Peripheral points do not weigh as much, central is more important (weighted average)
◦P<2 means less than 2% of the normal population shows an MD larger than the value found in this test
Total Deviation and
Patern Deviation
• Total Deviation
◦Point-by-point representation of the difference in dB between pt’s test and age-corrected normals
◦Translates into gray scale symbols
◦ie: 33 is what you should score, but you scored 29 —> -3
• Pattern Deviation
◦Similar to total deviation, except results are adjusted for the overall changes in height of PX’s
measured hill of vision
◦If the pt has overall depression, this is filtered out

PSD

◦Pattern standard deviation is a measure of the degree to which the shape of the pt’s measured field departs from the normal age-corrected reference field
◦Low PSD = smooth hill - follows the shape
◦High PSD = irregular hill - all over the place
◦PSD < 3 is abnormal
Visual Field Index
VFI
“what % of the field is normal?”
An enhanced MD designed to be less affected by cataract, and more sensitive to changes near the center of the VF to correlate better with ganglion cell loss
Center >> periphery
Reduces cataract contribution to the measurement of VF loss
VFI plotted against age
◦Facilitates estimates of disability risk
Glaucoma Hemifield Test
GHT
• In glaucoma, inferior rim of the optic nerve is attacked first
• Glaucoma is known to affect one 1/2 of the field to a greater extent before involving the other half
• Compares one half of pt’s VF to mirror image of the other half
◦Looks for asymmetry
◦Can be fooled by symmetrical loss
• Pattern deviation scores in each of 5 zones in the upper hemifield are compared to findings in mirror-image zones in the inferior visual field
• Scoring differences between mirror image zones are compared to normative significance limits specific to each zone pair
• GHT findings are divided in the following categories:
◦Outside normal limits - whenever at least one zone pair differs by an amount found in fewer than 1% of normal subjects
◦Borderline - whenever at least one zone pair differs by an amount found in fewer than 3% but more than 1% of normal subjects
◦General depression or Abnormally high sensitivity - whenever even the best test point locations are either so low or so high as to be at levels seen in fewer than 0.5% of normal subjects
◦Within normal limits - whenever none of the above conditions are met
Which test to do for Gaucoma suspect
• Most doctors do a 24-2 (54 points, 6 deg apart)
• Some do a 30-2 (76 points, 6 deg apart)
• Newest theories on glaucoma: do a 24-2 and a 10-2 (76 points, 2 deg apart)
◦Idea of the 24-2C —> now have 64 points, and the 10 points in the central 10 deg are the ones thought to be the most commonly flagged if glaucoma develops
Which Test Strategy?
• SITA STANDARD vs. SITA Fast vs. SITA FASTER
◦Standard may be more accurate, but not clinically significant
◦Fatigue artifact wins over theoretical
◦SITA FASTER doesn’t do false negatives and doesn’t check fixation (just checks activity at
the bottom)
◦Hanley: SITA Standard >> Fast
‣ Fast misses defects but the data seems to point to not much difference
Which Test to Run: 30 vs. 24 vs. 10?
• For glaucoma, either 24 or 30 is effective, but 24 is faster and lessens fatigue artifacts
◦Eliminates edge points of limited value
◦not involved in early diagnosis, too variable
◦Lessening of fatigue artifact outweighs any theoretical advantage of 30
• For neuro: use 30 with SITA standard or SITA Fast
• For decrease vision and/or endstage glaucoma
◦Always use 10-2 for evaluation of decreased vision ◦2 degree spacing vs. 6 degree
◦24/30 suboptimal for testing decreased vision ◦Potential for detecting early glaucoma with 10-2
Evaluating Threshold Fields Over Time
VFI plotted against age (projected loss)
- ◦Healthy —> lose about 1 dB a decade
- ◦Glaucoma —> lose about 1 dB a year
Guided Progression Analysis (GPA)
• 2 baseline visual fields and compares the new field
• Possible progression - 3 or more points show deterioration in at least 2 consecutive fields (4 min fields)
• Likely progression - 3 or more points show deterioration on 3 consecutive fields (Min 5 fields)
• A simple linear projection is shown as a dashed line
• A regression line is drawn through the best fit to the VFI data
◦Projected out 5 years to help the pt and doctor understand the anticipated impact of glaucoma progression if things continue along the current course
• Cons of VFI:
◦Estimates are more optimistic than those of experts
◦Rates of change over time with both indices were closely related, but the reliance of the VFI
on pattern deviation probability maps have caused a ceiling effect that may have reduced its sensitivity to change in eyes with early damage
‣ In this group of pts, there’s no evidence to suggest that the VFI is either superior or inferior to the MD as a summary measure of visual field damage
• Pts get cataracts over time, so may have to create new base VFs
How many fields are needed to determine progression?
GPA
◦Minimum 5 years with annual testing using linear regression ◦Clinically, minimum of 2, or 3 if major therapeutic intervention planned
◦Suggest 2 in first 6 months, third 4-6 months later
Screening Modes/Tests on Humphries
- Two-zone strategy
- Three-zone strategy
- Quantify defects
• 2 different approaches
(1) Four primary points, one in each quadrant are thresholded
Second most sensitive value used to calculate the expected height of the hill of vision
(2) From the age-related norms, the machine will set the hill
Age related is the one most commonly used
Two-zone Strategy
Two-zone Strategy
- From expected height, theoretical hill of vision is calculated
- Targets then presented 6 dB brighter than theoretical hill
- If seen at 6 dB brighter, then it is tested a 2nd time
- Points missed twice at the 6 dB brighter level are recorded as defects, and a SOLID BLOCK is recorded
3 ZONE Strategy
Three-zone Strategy
• Begins same as threshold-related strategy
◦4 primary points, one in each quad, thresholded
◦Second most sensitive value used to calculate the expected height of the hill
◦From expected height, theoretical hill is calculated
◦Targets 6 dB brighter than the theoretical hill
• Points missed twice at the 6 dB level are retested with the brightest stimulus for the machine
• If see at brightest, an X is recorded
• If not seen at brightest level, a solid block is recorded
• Very useful strategy for patients who have had strokes
Qauntify Defects
• Begins same as two-zone strategy
◦Targets are presented 6 dB brighter than the theoretical hill
◦ If missed twice, the area is then thresholded
◦The number expressed is the depth of the defect from theoretical threshold, NOT THE
ACTUAL THRESHOLD
◦Ie: expect 33 dB point, but pt misses it twice. Thresholded to 10 dB, so 33 - 10 = 23 dB
‣ 23 dB is shown on the quantify defect graph
Quantify Defects
The higher the number, the deeper (worse) the defect
Do not confuse this with the numbers on the full thresholding tests where higher dB is better
If only one isolated point is missed and the defect depth is less than or equal to 8 dB, it probably
does not represent a defect if it is beyond 20 deg
If one point is missed and the defect depth is greater than 8 dB, it probably represents a defect
If two adjacent points are missed with a defect depth of 6 dB or higher, they probably represent a defect
FDP
• Frequency Doubling Perimetry (FDP)
◦Stimulus is a grating of low spatial frequency that is flickered at a high temporal frequency
◦Minimum contrast for each stimulus to be detected is used to determine threshold
◦At a certain frequency, the total number of bars appears to be double
◦When a low spatial frequency undergoes a high temporal frequency, the stimulus display appears to have twice as many light and dark bars than are actually present
• Frequency doubling is controlled by the magnocellular pathway
• The M cells are responsible for low-contrast, high temporal frequency (or motion) stimulus
detection
• They make up only 15% of the total number of axons in the eye
• There is a small subset of M cells called My cells that actually respond to frequency doubling
• My cells are thought to be affected in early glaucoma
• The My cells contribute about 5% of total axons in the eye
Anterior Causes of
Visual Field Defects
• Lids - ptosis
◦Superior defect secondary to location of nodal point
• Cornea
◦Dense scars can create VF defects
◦Corneal dystrophy —> MD decreased, total deviation decreased, pattern deviation looks normal, PSD normal
◦Fields are not usually done for corneal problems, however your glaucoma pt may also have a corneal dystrophy
• Cataracts
◦Usually associated with generalized overall depression, especially nuclear opacities
◦Can be associated with scotomas or localized depression depending on locaiton and density

4 Main terretories for defects after the Nodal point

• Territory I - retinal rods and cones
‣ Macular degeneration, retinal detachments, retinitis pigmentosa
• Territory II - retinal ganglion cells and axons, nerve fibre layer, optic nerve
‣ Nerve fibre pattern on the retina: papillomacular bundle, inferior arcuate fibres, superior arcuate fibres, horizontal raphe, nasal radial bundles
• Territory III - optic chiasm, usually caused by pituitary adenomas
• Territory IV - optic tract, LGN, optic radiations, visual cortex
Visual Field Loss with Glaucoma

• Paracentral scotomas (usually in Bjerrum’s Area 5-20 deg from fixation)
• Central and peripheral nasal steps
◦Inferior macula vulnerability zone

Progression of focal depths
◦Increase in depth (ie: one point goes from 20 dB to 15 dB)
◦Increase in size (ie: 2-3 points affected before, now 4-5 points affected)
◦New scotomas
- *◦Isolated paracentral scotomas merge to form arcuates**
- *• In end stage glaucoma, usually all that’s left is nasal rim**
- *• The last thing to go is 20/20 vision**
Terretory 2 Visual field Defects
• Most common is glaucoma
◦Paracentral —> 70%
◦Nasal step —> 5%
◦Both paracentral and nasal step (upon 1st exam) —>10% ◦Temporal wedge —> 5%
due to changes in rim tissue
• Myelinated nerve fibres
• Drusen on ONH
• Papilledema
• Optic neuritis
• Ischemic optic neuropathy
Direct Opthalmoscopy
General
• The dioptral power of the wheel should be the sum of your Rx (if you are uncorrected) and the pt’s Rx to get the retina in focus
◦Ie: you are a -2 D myope without correction on, your patient is a -4 D myope. The wheel on your oscope should be -6
◦Ie: you are + 4 D without correction on, your patient is pl. Wheel on your oscope is +4
• Angle your head at a 15 degree angle to view the optic nerve, move temporally to see nasal retina

Components to disc Diagraming
• Media - does the disc look clear or hazy
◦Anything along the visual pathway can fog up your view
• Look at disc margins - are they distinct or indistinct
• Crescents - around the disc margins
• Evaluating size of disc
• Evaluating each rim
• Evaluate the size of the cup compared to the disc
• Evaluate the cup rims sloping, undermined, indistinct, etc.
• Proper symbols to be used when drawing an optic nerve
Disc Edema

Ask yourself is it unilateral or bilateral?
• Is the vision decreased?
◦Did it come on quickly or gradually?
• Are there any other symptoms / headache, vomiting, electrical impulses, etc?

What causes indistinct Margins?
• Increased intracranial pressure - papilledema
• Papillitis - infiltration or inflammation of the optic nerve
• Ischemic optic neuropathy
• Pseudo disc edema
congenital tilted nerves in high myopic astigmatic

- *SIGNS**
- *• Hemorrhages**
- *• Dilated, twisted veins**
- *• Tilted discs**
- *• Glial veils** (do not make margins indistinct, because they hover above the retina at the disc)
- *• Crescents**

CRESENTS:
- *• Scleral crescents** - white semilunar patch of sclera adjacent to the optic disc due to the fact that the choroid and RPE do not extend to the optic disc
- *• Choroidal crescents** - occur because the RPE is not abutted to the optic nerve
- *• Pigment crescents** - in almost all eyes, the RPE shows some histological irregularities close to the tip of Bruch’s membrane at the border of the optic disc
- *• Peripapillary atrophy (PPA)** - thinning of the retina and RPE in the region immediately surrounding the optic nerve head
CD RATIO

- Average cup to disc is about 0.35-0.4
- Ilarge discs should have large physiological cups, and pts with smaller discs should have small C/D ratios
- above 0.6 C/D ratio should get VF done
How to evaluate disc size…
• mid-size oscope light target, that’s about equivalent to average disc size
• If you use a 90, 78, 60 DD lens,
◦Correcting factor:
60 is 1.0x
78 is 1.1x
90 is 1.3x

WHICH EYE

- If the vessels are not central, if anything, they move nasally
- Margins - usually the optic nerve slopes temporally
- Fovea will be temporally
- Straight vessels tend to go nasally
- Vessels arch going toward the fovea
Glaucoma Deffinition
New and Old
- Chronic neurodegenerative disease characterized by loss or retinal ganglion cells resulting in distinctive changes in the optic nerve head and retinal and nerve fiber layer
• Optic neuropathy that is consistent with remodeling of connective tissue elements of the optic nerve head and with loss of neural tissue associated with eventual development of distinctive patterns of visual dysfunction
Chronic Open Angle Glaucoma
POAG
- Bilateral with one eye preceding the other
- IOP was greater than or equal to 21 mm Hg and the filtration angle (trabecular meshwork) was open by gonioscopy
- Glaucoma is the leading cause of irreversible blindness in the US. and 2.7 million who are over 40 have POAG
- OAG most common form and affects 95% of individuals with glaucoma. It is more common in African Americans and Hispanics than other ethnic groups. OAG is up to 3-4x more common in African Americans than Caucasians and tends to occur at an earlier age
2 Types of Glaucoma:
- Open Angle Glaucoma – the aqueous appears to have open access to the trabecular meshwork. The iris does not appear to be blocking the trabeculum. Initially this condition has no symptoms. At some point, side (peripheral) vision is lost and without treatment, an individual can become totally blind.
2. Closed Angle Glaucoma – the trabeculum is blocked by the iris and aqueous cannot drain from the eye causing the IOP to rise
RISK Factors
POAG
Primary Open Angle Glaucoma
- Age
- African or Latino ethnicity
- Family history
- Increased IOP
- Myopia
- Decreased corneal thickness
- Diurnal intraocular pressure variation
- Long-term intraocular pressure variation
- Sleep apnea
- Migraine sufferers
Risk Factors
Angle closure Glaucoma
Angle Closure Glaucoma
- Age
- Female gender
- Asian ethnicity
- Shallow anterior chamber
- Short axial length
- Small corneal diameter
- Steep corneal curvature
- Shallow limbal chamber depth
- Thick or anteriorly positioned lens
Genetics - Inherited Glaucoma
Genetic loci linked to POAG
underlying genes Myocilin (MYOC),MYOC appears to affect protein unfolding in the trabecular meshwork Optineurin (OPTN) and WD repeat Domain 36, (WDR36) is well established
Glaucoma Prevelance based on RACE
POAG vs Angle Closure
Open angle glaucoma VS Narrow angle glaucoma dt race:
- Whites 11:1
- African American 150:1 (More OAG)
- Chinese 1:3 (More angle closure)
Prevalence of POAG Glaucoma based on race
European descent is about 2.5% for patients over 40
5.6% of African Americans have open angle glaucoma
Filipinos >>> Caucasions to normal tension glaucoma and POAG
Inuit’s over 40, 2-3% have angle closure glaucoma (opposite)
• Asians in general have more normal tension glaucoma and more angle closure (Highest) risk as a large amount of the population have narrow angles
Age as a risk factor
Increased risk of glaucoma as you get older. Age serves as a marker for metabolic and degenerative changes of the tissue.
Prevalence is about 0.25% at age 20 and doubles every 10 years.

Gender as a Risk Factor in Glaucoma
Gender – no significant difference for primary open angle glaucoma.
Females are more prone to angle closure glaucoma, the reason is
unknown. More women have open angle glaucoma mostly because women tend to outlive men
Sample set is larger.

Juvenile Glaucoma
Primary Pediatric Glaucomas are classified as follows:
- Congenital glaucoma (congenital open angle glaucoma)
- Juvenile open angle glaucoma
- Glaucoma associated with systemic disease
- Glaucoma associated with other ocular anomalies
Causes and Variations of Juvenile Glaucoma
Primary congenital glaucoma – about 20-40% of the cases are caused by increased IOP during life in the womb and the baby has ocular enlargement of the eye (buphthalmos).
Features include: enlarged corneas, Steamy corneas, elevated IOP, Haab striae may present at birth or prior to 1 month (newborn)
- Infantile PCG presents within the first 2 years
- Late diagnosed PCG may present after the age of 2
Congenital Glaucoma
Congenital Glaucoma is present at birth and bilateral in 2/ 3 of cases.
Males >> than females except in Japanese individuals. It is thought to be due to a developmental defect where the iris inserts more anteriorly than in normal eyes which prevents fluid from draining causing an increase in IOP. The prevalence is higher in cultures with consanguinity, particularly those with a high carrier rate of CYP1B1 gene (GLC3A locus on chromosome 2p21) and LTBP2 within GLC3C locus
Congenital/ infantile glaucoma presents with marked elevated IOP causing the sclera to enlarge and become thinner. The eye looks bluer than normal because the choroid is more easily visualized through the thinned sclera.
The common clinical triad is epiphora, blepharospasm and photophobia.
The cornea appears cloudy due to edema from the increased IOP, horizontal breaks in Descemet’s membrane occur called Haab striae and the scleral canal increases in size. The normal cornea of an infant is 10mm (adult is 11.8mm), > 13mm corneal diameter is suspect before the age of 1 and >14mm is typical of advanced buphthalmos.
Normal versus Abnormal angle presentation in an infant
The normal anterior chamber of an infant compared to an adult
- Less pigmented TM
- Less prominent Schwalbe line
- Less distinct junction between scleral spur and CBB
• In PCG (primary congenital glaucoma)
- There is high iris insertion
- The angle recess is absent
- The iris root appears as a scalloped line of glistening tissue. This glistening membrane is what is referred to as Barkan’s membrane and likely represents thickened and compacted trabecular meshwork.
Juvenile Glaucoma
- The disease becomes manifest after 2 years, but before 16 years of age.
- Most cases of juvenile appear be autosomal dominant with only minor sporadic cases occurring.
- These cases are linked to TIGR (trabecular meshwork inducible glucocorticoid response) / MYOC (myocillin ) gene locus GLC1A
Name 2 systemic diseases causing Juvenile Glaucoma
Axenfeld Riegers Syndrome
Sturge Weber syndrome.
Sturge Weber Syndrome
Congenital, It is characterized by a facial birthmark and neurological abnormalities.
Ocular manifestation is high IOP in eye with port wine stain. Glaucoma 70% , when birth mark close to eye / the hemangioma is
on the upper lid.
Patients can also have CNS angiomas which can produce seizures.
GLAUCOMA caused due to an isolated trabeculodysgenesis.
As the child ages, elevated IOP is due to elevated episcleral venous pressure that occurs as a result of arterioveonous shunts through the episcleral hemangiomas.
Patient have a marked increase in pigment in one eye and more pigment in TM about 10% have elevated IOP in the hyper pigmented eye.
Nevus of ota

Nevus of Ota presents as a blue or gray patch on the face, which is congenital, with onset at birth or around puberty and is within the distribution of the ophthalmic and maxillary branches of the trigeminal nerve. The nevus can be unilateral or bilateral, and, in addition to skin, it may involve ocular and oral mucosal surfaces
Types of field loss in Glaucoma
Focal loss

Increase in short term fluctuation on threshold fields
Paracentral scotomas (usually in Bjerrum’s Area 5-20 degrees
from fixation)
Central and peripheral nasal steps
Progression of focal depths
o Increase in depth (one point goes from 20 db to 15 db)
o Increase in size (2-3 points affected now 4-5 points affected
o New scotomas
o Isolated paracentral scotomas merge to form arcuates

Early glaucoma changes, predict field loss

Superior nasal
Paracentral scotoma

Predict the fisual field loss in moderate Glaucoma

Superior Arcuate Scotoma
Bjerrum’s Area 5-20 degrees
& Nasal Step

Predict the field loss in this Moderate advanced glaucoma Px

Superior arcuate scotoma
Inferior Paracentral scotoma, general depression

Predict the visual field defect in Advanced Glaucoma

Temporal island OD

Visual field defects in Glaucoma

Progression of visual field defects

Progression of glaucoma field defects


3 Phases of Glaucomatous field loss:
I / T / M

- Initial Phase - IOP is causing damage to the optic nerve head but the field is normal
- Threshold Phase - patient shows an increase influctuationand visualfields are inconsistent andvariable
- Manifest Phase - positively reproducible visual field loss
Causes of a generalized depression MISTAKEN for Glaucoma

Decreased MD / Also with Glaucoma
o Wrong Rx
o Cataracts
o Miosis
o Aging and other ocular conditions
Criteria for Minimal Abnormality in Glaucoma
Three or more adjacent points in an expected location of the central 24 field* that have P < 5% on the pattern deviation plot, one of which must have P < 1 % on at least 2 consecutive fields
OR
Glaucoma hemifield test“outside normal limits“ on at least 2 fields ‘(Upper and lower differ from each other by P<1% or 2 corresponding zones are both depressed relative to normal at a P< 0.5% level
OR
Corrected pattern standard deviation with PSD flagged at 5% on two consecutive fields
* Must be nonedge points in central 300 field

GRADING of defects in Glaucoma
EARLY DEFECT
Lower IOP 20-30%
T-Target
Mean deviation > -6 dB
or
On pattern deviation plot, depressed below the 5% level and fewer than 15% of
points depressed below 1% level
or
No point within central 5 below 15dB

Visual field defect GRADING
Moderate defect:
Mean deviation worse than -6 dB but not less than 12dB
or
On pattern deviation plot, < 50% of points
depressed below the 5% level and fewer than 25% of
points depressed below 1% level
or
No point within central 5 below 10dB
or
Only 1 hemifield containing a point less than 15 dB within 5 of fixation

Visual field defect GRADING
SEVERE Defect
40 - 50% IOP lowering
Mean deviation worse than -12dB
or
On pattern deviation plot, > 50% of points
depressed below the 5% level and more than 25% of
points depressed below 1% level
or
No point within central 5 less than or Eqaul to 0dB
or
Only 1 hemifield containing a point less than 15 dB within 5 of fixation

CAPRIIOLI’s Criteria for Abnormality
- Three contiguous points same side of horizontal
- One points p<1% or worse on Pattern Deviation Plot and two other points p<5 or worse
What causes Changes to the Optic nerve
with POAG
ISCHEMIC THEORY
The blood supply from the short
posterior ciliary artery and surface of nerve supplied
by retinal arterioles of the CRA
Increased IOP → decreased perfusion → lamina crushes axons → cupping
Perfusion pressure is insufficient to support adequate blood
flow through the nerve
Glaucoma patients do not have good autoregulatory control when their IOP goes up
Causes for Changes of Optic Nerve in
POAG
Lamina Distortion Theory

IOP causes compression of the lamina sheets →
mechanical compression of the axons and also
compresses the arteries cupping →
NFL drop out and death of the axons.
- Mean of 550 pores in lamina smaller temporally + nasally and bigger Superior and Inferior
Bigger Pores = Easier to crush

Causes for the change of ONH glaucoma
Interruption of Axoplasmic flow
Axonal transport at the level of lamina and organelles
within the NFL is stopped due to elevated IOP
long enough time, NFL death will occur
o 5 dB loss probably corresponds to a 20 % loss of axons
Y Axoplasmic flow also stops with ocular hypotony ( 4mmHg)
pressure difference across the ONH regardless of high or low IOP, causes
mechanical compression of the axonal bundles
Causes for the change of ONH glaucoma
NFL Death
Neurotrophin deprivation and Glutamate toxicity
- Neurtotrophin are peptides - development and maintenance retinal ganglion cells.
glaucoma there is an obstruction of neurotrophin
transport to the ONH which results in RCG apoptosis
neurotrophic deprivation
dt loss of neurons in the lateral geniculate nucleus
Y Glutamate is a normal neurotransmitter may accumulate to toxic levels secondary to release from apoptosis
Causes for the change of ONH glaucoma
Brain disease
CONCLUSIONS:
Y These results suggest that patients with glaucoma undergo widespread and complex changes in cortical brain structure and that the extent of these changes correlates with disease severity.
Y Considered together, these data suggest that patients with glaucoma may have volumetric gains in some structures early in disease, but that brain volumes decrease toward and in some cases below control volumes as the disease progresses
Y Also OCT seem to show Ganglion loss with Glaucoma but also
with Alzheimer Disease
Spontaneous venous Pulsation
In glaucoma
lack of SVP may be also more important when
we consider POAG
Y Possibly be due to the fact that Px’s
glaucoma have significantly lower CSF pressure than
patients without glaucoma

Optic nerve changes in
GLAUCOMA
- Generalized Enlargment of the cup
- Barring of Circumlinear Vessels
- Bean Potting
- Vertical Elongation ( 0.2 more than Hor cupping)
- Notching
- Drance Hemhorages (dt notch, inferior disc. Splinter hem dt stretching that it ruptures)
- Asymmetry of CD Ratio between eyes (Diff of 0.2 and more)
- Distorted Lamina Dots
- Aquired Optic pit
- PPA (Peripapillary Atrophy) BETA ZONE
- NFL Dropout
- Nasal cup - extendes past BV / Nasal shift of BV
Classification of Glaucoma
Ocular Hypertension
IOP >22 mm Hg
Optic nerve head is normal
Visual field is normal
4-10% of patients over 40 are ocular
hypertensive
IOP 24 to 32 in one eye and at
least 21 in the other eye
30-2 q(6) months and stereo
photos every year
Classification of Glaucoma
PACHYMETRY consideration

Basically thin corneas are considered to be a risk for glaucoma
but one should not convert all IOPs with the chart is what we
do now
Classification of Glaucoma
Ocular Hypertension study
Summary
A 20% reduction in IOP resulted in a 50% reduction in the
development of primary open angle glaucoma in a 5 year
span.
o 4.4% progressed to glaucoma in treated group
o 9.5% progressed to glaucoma in untreated group
>90% of OHTS patients when left untreated did not progress
in 5 years
CCT should be measured
Glaucoma RISK calculator
5 inputs
The estimated risk of development of glaucoma in 5 years
- Age
- IOP 20-32 x3
- Central Corneal thickness (475-650) x3 could change DT LASIK SX
- Pattern standard deviation x2
- Vertical cup disc by contour
- *Low < 5%** Observe and monitor
- *Moderate 5-15%** Consider treatment
- *High >15%** treatment
Phase 2 Of Ocular Hypertension study
Summary
This showed that early IOP-lowering intervention reduces the
cumulative burden of disease,
The absolute effect was greatest in patients with the highest
risk as determined by a prediction model that was developed
and validated using OHTS data. It incorporates age, IOP,
central corneal thickness, cup–to-disc ratio and field pattern
standard deviation as significant risk factors.
POAG Glaucoma Suspect
Px classification
2 sibling with POAG
large cupping with normal visual fields and IOP
larger than usual diurnal variation on IOP
asymmetric c/d
large c/d but normal fields
AAO Def: following findings in at least 1 eye:
- Optic nerve or nerve fiber layer defect suggestive of glaucoma ( enlarged cup–disc ratio, asymmetric cup–disc ratio, notching or narrowing of the neuroretinal rim, a disc hemorrhage, or suspicious alteration in the nerve fiber layer)
- a visual field abnormality consistent with glaucoma
- an elevated IOP greater than 21 mm Hg
- Naturally the gonioscopy angle is normal and open
- An individual with a suspicious nerve or NFL appearance in the absence of a visual field loss
- A visual field defect suggestive of glaucoma in the absence of a corresponding glaucomatous optic nerve abnormality
POA Glaucoma Suspect
Open-angle glaucoma suspects
(based on the number of risk factors: family history, race,
elevated IOP, optic disc appearance and thin central corneal
thickness):
Open-angle suspect, low risk (one or two risk factors)
Open-angle suspect, high risk (three or more risk factors)
Classification Of Glaucoma
POAG
Primary open angle glaucoma
- Gonioscopy shows an open angle
- IOP is > 21 on at least one occasion
- Not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow or damage to the optic nerve(i.e. patient does not have PXE or steroid induced glaucoma)
- The optic nerve shows a characteristic optic neuropathy that is consistent with
- excavation and undermining of neural and connective elements of the optic disc and eventual
- development of distinctive patterns of visual dysfunction.
POAG
RISK FACTORS
- ISNT Rule
- Rim notching
- NFL dropout
- High IOP
- Distorted Lamina
- Drance Hemorrhages
- C/D asymmetry
- Greater than .6 cupping
- Thin corneas
- Abnormal gonioscopy
- Abnormal OCT of optic nerve
- Hx of hyphema
- Hx of ocular trauma
- Family Hx of glaucoma esp sibs
- Hx of PXE or PDS
- Migraine/Raynaud’s
- Race - African American
Goal of Treatment POAG
- To preserve visual function by lowering IOP to a level that is likely to prevent further optic nerve damage
- Therapy with the fewest adverse affects
- Least amount of disruption to patient’s life
- Cost consideration
Can only treat currently by lowering IOP
SX and Laser:
selective laser trabeculoplasty (SLT) in some patients may be a
first line
Injections / MGIS / ALT
Treatment Considerations
POAG
Principal factors:
Life expectancy
Stage of Disease
Rate of Progression
History
IOP since and multiple readings
Optic nerve evaluation
Visual fields
Pachymetry
Imaging OCT
Gonio (always do gonio before you treat glaucoma)
Classification of Glaucoma
MILD / MODERATE / SEVERE
Mild:
Definite optic disc, RNFL, or macular imaging
abnormalities consistent with glaucoma and a normal visual
field
Moderate:
- *Definite** optic disc, RNFL, or macular imaging
- *abnormalities** consistent with glaucoma
visual field abnormalities in one hemifield that are not within 5 degrees of fixation
Severe:
visual field abnormalities in both hemifields and/or loss
within 5 degrees of fixation in at least one hemifield
Guidelines for Glaucoma
- Establish baseline IOP 3x
- Obtain an OCT
- Classify amount of glaucoma damage as mild, moderate, severe
- Use the highest IOP (Tmax) and set target pressure based on the severity of the glaucoma
- Consider lowering target pressure an additional 10% if patient is
* *younger than 50 years, African American, monocular , or has a sibling with advanced glaucoma**
T-max
T- Target
Tmax
Highest the IOP ever been recorded in the eye
Importance of this number as the calculation of the
target pressure is based off of Tmax, not the IOP at the time of
diagnosis or starting treatment
T-Target
Classification of Glaucoma
severity of the glaucoma
IOP from baseline (Tmax) by different amounts
o Mild Severity – 20-30% IOP lowering
o Moderate Severity – 30-40% IOP lowering
o Severe Severity – 40-50% IOP lowering
o Though new guidelines from AAO recommend starting with a
minimal of 25% reduction
Ocular hypertension
o Lower the IOP by 20%-30%, or to 20 mm Hg or less.
Structure Vs Function evaluation
Glaucoma
Theoretically remember 20% loss of NFL(Structure) to get 5dB field loss(Function)
OCTs to monitoring structural
consistent with glaucoma however
Y Once the damage is significant,
- *visual fields** are probably best
- *to monitor progression**
- Stereoscopic viewing of the optic nerve still the way to diagnose glaucoma
- OCT have a lot of false positives and false negatives.
False Positives with OCT

- High myopes : fall outside of the
normal range, showing up as red.
- On the other hand, small focal areas of damage show up as green because the instrument averages the thickness
- The average is often within the normal range, despite the focal loss.
- impression that there is no damage present.

High Myopia, Suspicious Discs
(get more INFO!!!!!!!!!)

3 IOPs
2VF
Gonioscopy ****
Pachymetry (some recommend separate day readings)
OCT
Evaluate risk factors

INCREASED
OUTFLOW meds
Topical miotic – cholingeric agents
o Alpha adrenergic agonist
o Prostaglandin analogues mostly increase uveoscleral outflow but also affect some increase in trabecular meshwork outflow
Decrease Aqueous Production
Meds
o Beta Blockers
act on the [beta]-adrenergic receptors in the ciliary processes
o Carbonic Anhydrase Inhibitors
inhibit carbonic anhydrase in the ciliary
epitheliumand decrease aqueous humorsynthesis
o Alpha2-adrenergic Agonists
• Apraclonidine: Relative selective alpha 2 adrenergic agonist but does activate some
alpha - 1 receptors,
• Brimonidine: more alpha 2 selective
Glaucoma Meds
Mode of action

Increase Uveoscleral Outflow
o Prostaglandins analog: binds and activates receptors in the ciliary smooth muscle and improves uveoscleral outflow
o Selective alpha-adrenergic agonists: Brimonidine
Systemic
o CAI :Diamox (Sigma), Neptazane (Wyeth-Ayerst) and Daranide (Merck,Sharp, & Dohme)
Decrease Aqueous Production and
ORAL CAI reduce vitreous volume
o
Inhibit carbonic anhydrase in the ciliary epithelium and decrease aqueous humor synthesis
o Osmotic agents
Vyzulta 0.024%
(latanoprostene Bunod)
1gtt qhs OU

- *latanoprostene bunod 0.024% Vyzulta**
- *metabolizing** into two moieties:
- latanoprost acid - primarily uveoscleral pathway to increase aqueous humor outflow
- butanediol mononitrate, which releases nitric oxide (NO) to increase outflow through the trabecular meshwork and Schlemm’s canal.
nitric oxide-donating prostaglandin F2-alpha receptor agonist
One drop in the affected eye(s) once daily in the evening
- Unopened bottles should be refrigerated
- Open bottle can be stored at 2° to 25°C for 8 weeks
Vyzulta really only acts the trabeculum and not the retina
RHOPRESSA®0.02%

(netarsudil ophthalmic solution) 0.02%
1gtt qhs
netarsudil ophthalmic solution 0.02%
- Rho kinase inhibitor which is believed to reduce IOP byrelaxing the cells of the meshwork and inner walls of Schlemm’s canal, increasing outflow.
- also decreases inflow by inhibiting norepinephrinetransporter therefore reducing the production of aqueous humor. It has also been shown to lower episcleral venous pressure.
Y One drop daily in the evening.
20% will get Vertex Keratopathy (Corneal verticillata) after 4 weeks
- Unopened Store in refrigerator
- After opening, product may be stored in refrigerator or at room temperature for up to 6 weeks.

Monocular trails
use in cases where you want to determine the effectivity of the meds and risk is low for vision loss
Conclusion: The monocular trial of therapy is effective in
accurately predicting the response of an untreated eye to
monotherapywith aprostaglandin analogue at all daytime
time points measured
Side effects of glaucoma meds
Side Effects of Glaucoma Medications
- Prostaglandin Analogs: eye color change, darkening of eyelid skin, eyelash growth, droopy eyelids, sunken eyes, stinging, eye redness, and itching
- Beta Blockers: low blood pressure, reduced pulse rate, fatigue, shortness of breath; rarely: reduced libido, depression.
- Alpha Agonists: burning or stinging, fatigue, headache, drowsiness, dry mouth and nose, relatively higher likelihood of allergic reaction.
- Carbonic Anhydrase Inhibitors: in eye drop form: stinging, burning, eye discomfort;
- in pill form: tingling hands and feet, fatigue, stomach upset, memory problems, frequent urination.
- Rho Kinase Inhibitors: eye redness, corneal deposits, stinging, and small bleeds on the white of the eye.
Cholernergic agents
Glaucoma Gtt

Pilocarpine 1% 2% 4%

BETA Blockers


Carbonic Anhydrase Inhibitors


Alpha Agonist Clonodine derivatives


Prostaglandin Analogs


Prostaglandins
Often first drug of choice
Lower the IOP by approximately 30%
Mechanism
– Alter the function and the structure of the
uveoscleral pathway to increase aqueous outflow
Y less increase in trabecular outflow facility.
DOSE: 1gtt qhs
twice day dosing is less effective
Two weeks to 6 weeks for maximum overall effect
ALWAYS ASK PX WHEN LAST GTT WAS INSTILLED
Xalatan
latanoprost 0.005%
1 gtt qhs OU

Increases Uveal Scleral outflow
starts 3-4 hours after installation, maximum effect is
8-12 hours after administration
unopened bottle(s) - regfigerator (transport 8day up to 40C)
opened - room temperature up to 25°C
(77°F) for 6 weeks
ocular redness (worst 30min / better 1hr)
stinging - refrigerator to not sting
21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye
Travatan
tarvoprost 0.004%
1gtt qhs OU

Increase Uveal scleral Outflow
starts 2 hours after installation, maximum effect 12
hours
Un-opened - not need refrigeration shelf life of 18 months.
Opened - between 2° - 25°C disgard 6wks
ocular redness (worst 30min / better 1hr)
stinging - refrigerator to not sting
21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye
Lumigan

bimatoprost 0.03%
1gtt qhs OU
Increases Uveal scleral outflow
starts 4 hrs and maximum effect is 8-12 hrs
Opened Bottel - doesn’t require refrigeration.
Disgard Open container 6wks
ocular redness (worst 30min / better 1hr)
stinging - refrigerator to not sting
21% IOP drop in NTG
No crossover to fellow eye, as low strength and metabolized in
eye
Prostaglandin
Side Effects
- Conjunctival hyperemia up to 25%
- Foreign body sensation/irritation
- Superficial Punctate Keratopathy
- Hyperpigmentation of periocular skin
- Permanent darkening of the irises
- Darkening and increasing length of eyelashes
- Anterior Uveitis – rare
- Orbital fat atrophy
- Problem with Cystoid Macula Edema
- Possible herpes simplex activation
- Migraine like headaches
- Flu like symptoms

Prostaglandins
4.1% are non responders – defined as <15%
reduction
Then you add beta blocker AM
Adding another med from the same family will not show an additive effect on IOP decrease
- Switch in prostaglandins discontinuing one d/c and trying another
Side Effects
- Macular edema
- History of herpes simplex in eye
- Active uveitis
- Class C for pregnancy
Beta Blockers
2 types
The beta-blockers act on the beta-adrenergic receptors in the
ciliary processesandreduce aqueous humor production.
- selective (Block beta 1 receptors) or
- nonselective (block both beta-1 and B2 receptors equally)
however even the selective can cause pulmonary effects
Non-selective approximately 25% IOP decrease
Levobunolol(Betagan), Timolol(Timoptic)
Cartechol (Ocupress)
Selective approximately 20% decrease
Betaxolol (Betoptic S)
BB most effective when given in the morning
Timoptic
timolol maleate 0.25% / 0.5%
1gtt AM

Most common beta-blocker is
Non-selective B-blocker Lowers IOP by ~25%
IOP begins to fall in 30-60 minutes and peak in
reduction in 2-3 hours and back to baseline in 24 -48 hours
About 10-20% of patients do not respond with lower IOP
Best results AM
CONTRA Indications!!!!!!!
Problems
with Beta Blocker Gtt
Problems
Short term escape
o Loss of efficacy within 1 month
This is secondary to receptor saturation
Long term drift (tachyphylaxis)
o Extended use of B blockers may reduce their effectiveness because the response of B adrenergic receptors is affected by constant exposure to an agonist.
Need at least 4 weeks for washout from the receptors
Beta Blocker
Contraindications
Patients with or had asthma
Patients with COPD (Chronic obstructive Pulmanory disease)
Patients with Bradycardia
o Check pulse if below 55 – 60 BPM
Patients with myasthenia gravis
- *CHF** (Congestive Heart Failure)
- *Hypotension**
Controversial if already on a systemic beta blocker if you should also use it to treat glaucoma
Beta Blockers
Ocular Side Effects
Dry eye
Corneal anesthesia
Allergic blepharoconjunctivitis
Uveitis
Beta Blockers
Systemic Side Effects
- Systemic hypotension – left ventricular failure and atrioventricular conduction disturbances
- Bronchospasm
- Adverse CNS effects – fatigue, depression, amnesi
- Ocupress – less effect on bad cholesterol profile
- Mask clinical signs of hyperthyroidism (i.e. tachycardia) because of the thyroid storm
- Bradycardia – if they have a pace maker it is ok
- Mask hypoglycemic signs and symptoms, sometimes resulting in dangerously low blood sugar
- Impotence
Alpha Agonists
Used for short term activation
Angle closure
Iopadine
Could be used before Timoptic
A-2 receptors located on presynaptic adrenergic nerve terminal and postsynaptic terminal
- *o A2 presynaptic** activation inhibits NE release
- *o Postsynaptic A2** activation reduces cAMP levels
Overall these drugs reduce aqueous production as well as increase uveoscleral outflow
Lower IOP by ~20-25%
Brimonidine and Apraclonidine which are alpha 2 selective
Alphago”
o Brimonidine is more alpha 2 selective
Alpha Agonists
Brimonidine (Alphagan)
1gtt TID (used alone)
o Starts to work in 1 hour ,peak effect after 2 hours lasts for 12 hours
Apraclonidine (Iopidine)
post Sx / Angle closure / Risk procedures
o Starts first hour work peak 3 hours lowers and lasts _for 12 hours but large tachyphylaxis(_Toxic)
so not usually used for long term treatment used for short term ,i.e after and before ALT,LPI Acute Angle Closure
Alpha Agonists
Alphagan
Ipoidine
OCULAR Side Effects

Blepharits
Dry Eye
Conjuctival hyperemia
Dry mouth Dry Nose
Allery Conjuctivitis
Follicular Conjuctivitis
Miosis
Alpha Agonists
Alphagan
Ipoidine
Systemic Side Effects
AVOID IN CHILDREN - can cause CYANOSIS and SEIZURES
CONTRAINDICATED for PX taking Monoamine Oxidase Inhibitors
& Px with Severe CARDIOVASCULAR Disease
Hypotension
Vasovagal attack
Anxiety
MAOI Inhibitor
Uses to treat depression
rasagiline (Azilect),
selegiline (Eldepryl, Zelapar),
isocarboxazid (Marplan),
phenelzine (Nardil),
tranylcypromine (Parnate)
CAI
Carbonic Anhydrase Inhibitors
Bicarbonate formation is an essential component of aqueous. Inhibiting carbonic anhydrase activity in the ciliary processes decreases the amount of bicarbonate
Results in decreased aqueous production
Lower IOP ~ 20%
Azopt Trusopt
Appears to work at night thought not as good as prostaglandin
CAI
Carbonic Anhydrase Inhibitors
Trusopt
Azopt
1gtt TID OU
Ask when last taken
Azopt – peak 2 hrs trough is 12 hours .
Trusopt peak 2 hours trough is about 12 hours
Both TID
Some people get a metallic taste
Contra indicated
Carbonic Anhydrase Inhibitors
Trusopt
Azopt
1gtt TID OU

SULFA ALLERGY
Endothelium compromise
FUCHS ENDOTHELIAL DYSTROPHY
Colernergic Agonists Miotics
PILOCARPINE
Not used as much today as in the past secondary to ocular problems with miosis and ciliary spasm
- Direct acting – activate cholinergic receptors directly at the neuro-junctions of iris sphincter and CB
- Indirect acting – exert effect by inhibiting cholinesterase increasing Ach in synaptic cleft
- Increase in outflow likely due to stimulation of CB longitudinal muscle which widens scleral spur
Lowers IOP by 15-25%
PILOCARPINE
Most common pilocarpine 0.5%, 1%, 2% , 4%, 6%
Colernergic Agonists Miotics
PILOCARPINE
Problems
Elderly: Decrease in VA dt NS and cataract formation
Young Adults: Decreases the Acc available, unable to read
Which drugs can cause the following
Systemic or Topical

Drops:
Rhopressa
Meds:
Amioderone- Drug for Anarythmia
Plaquenil - Arthritis treatment
(Bulls eye retinopathy)
Combination Meds of
Glaucoma
Cosopt
Combigan
Simbrinza
Better compliance, better IOP lowering than with
monotherapy of the same components
.
ROCKLATAN® (netarsudil/latanoprost ophthalmic solution) 0.02%/0.005% about $300 for 2.5 ml
Cons: Dosing regime BID (insead of TID)
Timolol-dorzalimide (Cosopt)
Timolol-brimonidine (Combigan)
Brinzolamide-Brimonidine (Simbrinza)
When should Px return for follow up?
Try to measure at trough of the drug.
when effect is least
Usually at 4-6 weeks but the medication dependent
if someone has severe glaucoma you may need to have them back in a week.
Make sure they can show you how to use the medication.
Pilocarpine- immediate effect
Beta blocker may take several weeks to stabilize return 4-6 weeks
Alphagan can return as early as 2 weeks but usually 4-6 weeks
CAI’s can return as early as 2 weeks but usually 4-6 weeks
Prostaglandins 2 weeks to possibly 3 months before best results is lowest effect observed
Glaucoma px follow up, Px target pressure under control
Always ask what medications you are taking and at what time did you last take them
Depends on severity of disease.
Severe cases frequent follow up, mild cases q 6 months The greater damage, the greater the risk for further damage.
FU - Always IOP / Prelims / Field and OCT Yearly.
1st Year 2-3 fields
** Gonio should be done on all patients before starting a patient on glaucoma meds you need to determine what type of glaucoma they have
T X and plan example

Optic nerve coloboma

Freaquency of follow up for Diagnosed Px’s

See Table
Direct Gonioscopy
Koeppe
Pedeatric PX

direct method, angle observed directly
hand held focal illuminator
- patient in supine position
- highly convex Koeppe lens is placed on
- *anesthetized** cornea
- provides a broad view of chamber gives excellent impression of physiological iris contour
and width of angle inlet distorts the angle very slightly relatively low magnification special equipment
time consuming
Indirect Gonioscopy
Opposite Angle evaluated

The two most common methods are:
- Zeiss 4 mirror lens
- Goldmann mirror lens
- Sussman lens, Posner lens
Performed at the slit lamp PX seated in upright position
Opposite Qaudrant evaluated
Zeiss 4 Mirror

Central lens : Posterior pole (Primary gaze)
Evaluate inferior 1st (Largest angle)
1gtt Proparacane
PROS:
- Stereo view of Fundus
- Faster exam / No Rotation
- No need for Gel / Bubbles
- Smaller corneal contact
CONS:
- Unwanted compression (alter angle appearance)
- Need to be steady

Goldman tonometry
1/2/3 lens options
Requires viscous solution eg: methylcellulose
- Past gonio gel(very preserved SPK)
- USE- Teargel / Celuvisc
- Bubble free / anesthesia (Proparacaine)
Optically excellent views
Goldman Gonioscopy
1 lens

Better for deeper set eyes / Smaller appertures
Able to view posterior pole
Goldman Gonioscopy
2 lens

Smaller - Easier to handle
Less rotation
Central view of fundus
Goldman Gonioscopy
3 lens

Central Lens
clear fundus contact lens
allows view of posterior pole
provides stereopsis and magnification
Image is upright

Goldman 3 Mirror
Mid-periphery (eqautorial lens)

largest trapezoid shape mirror
Equatorial
Eye needs to be very dilated
Able to see vortex veins in periphery
Goldman 3 Mirror
Far -periphery
eqautor + ORA serata

rectangular in shape
Dilated pupil needed
Goldman 3 Mirror
Thumb nail lens
Angle + Far periphery

Used for viewing the angle UNDILATED
Able to view the extreme periphery in a very dilated eye

Gonioscopy Procedure

Steps
- Align slit lamp for patient and examiner
- Scan anterior portion of eye
- if corneas are intact, anesthetize cornea
- Clean mating surface Dakin’s solution(9:1) 10/10
- Rinse with saline
- Fill 3/4 CELLUVISC(less viscous) Genteal(More viscous) Gonio scopic(SPK)
- Set up slit lamp (low mag.,~ 0° illum. arm, narrow beam, low light intensity), position so the gonioscopy mirror is placed on the eye superiorly
- without excessive pressure, fingers not used to brace Px forehead
- Look outside the mirror and move the illumination beam into the gonio mirror
- identify the pupil edge. Focus on the edge of iris
- Focus on the iris and note the color of the iris
- Increase the magnification to 16x (medium)

DO NOT DO
Gonioscopy Procedure
Corneal abrasion
Penetration injury
Hyphema
Laceration
Recent lasik surgery, corneal transplant
Corneal ulcer, infection
Gonioscopy considerations
Always Tonometry first
Arteficially could lower pressure if done first
Check the pupillary/iris frill and iris surface before observe the other angle structures
(Signs of EXP exfoliation syndrome)

Gonioscopy IRIS
Considerations

- observe and note the flatness or convexity of the iris plane
- Iris inserted more posterior in Myopes and Hyperopes

Gonioscopy
Structures

CBB
SS
TM
SL / Sampolisi’s line

Gonioscopy observation:
Ciliary Body Band (CBB)

Ciliary Body Band (CBB)
- *Darker** in eyes with more iris pigmentation
- *Height varies** dependent on iris insertion
Peripheral anterior synechias are formed when peripheral iris adheres to the peripheral cornea

Gonioscopy observation:
Ciliary Body Band (CBB)

Ciliary Body Band

Gonioscopy observation
Iris Processes

Normal variant and remnant of embryological development
Histologically iris tissue at its base and uveal tissue at the apex
Most dense nasally
Does NOT interfere with outflow- it is not an iris adhesions
Typically stop at the trabecular meshwork

Peripheral Anterior Synechiae (PAS)

formed when peripheral iris
adheres to the peripheral cornea

Compression Gonioscopy

Avoid compressions when unwanted
Make slight lens excursions
Gonioscopy observations
Scleral spur (SS)

Most easily seen in wide angled eyes at the anterior end of the angle recess where the ciliary body inserts
narrow white line
Blood fills Schlemm’s canal, or pigment deposits are found in the Trabecular meshwork anteriorly;
it can be easily located

Schlemm’s Canal within Trabecular Meshwork

can be sometimes discussed as a gray zone just above scleral spur
if blood flows through the canal can stand out

Gonioscopy observation: Schlemm’s Canal
Blood in schemm’s
- *Causes:**
- Excessive external pressure on goniscopy
- Low intraocular pressure
- Increased episcleral pressure
Sturge Weber syndrome
Corotid Carniverous sinus

Gonioscopy observation:
Trabecular Meshwork

- Trabecular pigment band due to
- *deposition of pigment of** granules
- Denser in pigmentation in brown iris patients than blue eyed patients
- With age, band becomes less translucent
- Pigment Of TM should be less than CBB

Gonioscopy observation
Scwalbe’s Line (SL)

condensation of collagenous fibers which runs round the inner peripheral cornea
Marks the anterior insertion limit of the angle structures
Schwalbe’s line is also called
Sampolesi’s line (Pigmented)
Most anterior limit of angle Termination of Descemet’s membrane
White glistening line: sometimes thickened

Observe the Iris Insertion:
Focal line technique

Optical section slitlamp
Angle the illumination arm either temporally or nasally 5-10 degrees off center
Medium magnification
Note 2 linear reflection: one from the external surface of the cornea. The other from the internal surface of the cornea
Edge formed due to juncture in angle curvature of cornea and sclera in angle
The 2 reflections meet at Schwalbe’s line; identifying the anterior limit of the trabecular meshwork
Observe the location of the iris insertion onto angle wall when focal lines are aligned

Observation of Iris insertion

Parallax issues

Technique issue: alter tilt of lens, patient looking in different direction
Could be a narrow angle
Bowed Iris
Iris roll preventing observation of iris reces
Diagram for Focal line technique


Classification of angle

CBB
SS
TM
SL

Primary versus Secondary views
Gonioscopy

Primary views: when patient is looking straight ahead
Secondary views: when patient looks towards the direction of the mirror the examiner tilts lens towards the angle of observation
If the angle as the gonio- lens does not reach the depth then secondary views are helpfull

Illumination Variation
Gonioscopy

Change of external stimulus can alter the anterior chamber assessment depth
Recommendation: performing gonioscopy
Dark Room
1mm beam Slitlamp beam
Patient position: straight ahead Primary Gaze
Adequate illumination
Importance is a false OPEN angle dt Illumination
Recording gonio Findings

Location of iris insertion
- Note presence of iris processes
- Grade Trabecular meshwork pigmentation
NORM: CBB <= TM

Shadow Technique
(Iris Bow)

- penlight technique: temporally
- if iris is FLAT, total illumination
- if iris is BOWED, shadow forms

Gonioscopy: Observation of the iris and pupillary edge

Check the pupillary/iris frill and iris surface before observe the other angle structures

Exfoliation syndrome

- Age related
- Most predominant Scandenavia / Further away from eqautor(Angle of light reflection WATER ICE)
- Solar radiation / Outdoors / Geographical Location
- High Coffee Consumption
- Decr Folate / Incr Homosysteine levels
- Genetics LOXLI gene
- Amyloid buildup on lens and Surounding structures
- Krukenberg spindle

Ocular findings
EXO syndrome

Amyloid Material on lens surface - Dilation caused a Bull’s eye appearance
Weakening of Zonules and cilliary processes LENS SUBLAXATION
Cat sx EXO should be taken into consideration
Iris Transillumination at Pupil margin
Krukenberg Spindle

Ocular findings
EXO syndrome

Gonioscopy findings
Roughened lens surface abrades iris pigment during pupil movement
Pigment releases from iris and collects on TM and SL Obstruction of outflow through TM
Dysfunction of TM increase in IOP
Krukenberg spindle / endo deposition of pigment
Uneven pigment deposition in Trabecular meshwork
“Patchy” lack of homogenous appearance
Pigmented Schwalbe’s line
Rare to see exfoliated material

Pigment dispersion syndrome

30-40 Males 10yr before Females MYOPES
Peripheral contour of iris more Concave
Risk of PIGMENTARY GLAUCOMA
Zonular rubbing causes shedding of iris pigmentation into the aqueous humor and thus Trabecular Meshwork (TM)

Ocular findings of
Pigment Dispersion Syndrome

Iris Transillumination (Mid Peripheral)
Krukenburg spindle
Due to convection currents of aqueous, pigment rubbed off from iris
flows into anterior chamber, deposits endothelium
Pigment deposit in a linear fashion at the junction of the
zonules and the posterior lens capsule = called Scheie’s stripe

Scheie’s stripe

DDX
Krukenburg spindle

Ocular findings related to
Pigment Dispersion Syndrome
Gonioscopy

According to Spaeth grade the amount of pigmentation the posterior portion TM at the 12 o’clock position

Comparison between
EXO & PDS


Angle Recession
Risk factor Glaucoma HX of injuries

Trauma create tears in locations between the sclera and uvea at the corneoscleral junction
Hx of injuries blunt TRAUMA
history or presence of hyphema(Blood in eye) may be an indication of ocular trauma
Leads disruption of uveal meshwork and
tears in the Trabecular meshwork (TM), ciliary muscle, iris root
SCARRING causes Glaucoma Years later

Hyphema
Blood in AC

Dt: Trauma 80%
Rubeosis 20% (Caused by Hypoxia at the retina)
Diabetes ALWAYS RECORD -NVI / Rubeiosis
Chec IOP / NO Gonio
***Bed Rest / Head Elevated ***

Px example
Glaucoma dt Angle recession

Compare CBB width in all Qauds
Small areas of iridodialysis, iris tears
Angle recession: CBB >>> SS + TM
Altered anatomical structure that can affect aqueous
outflow and cause angle recession glaucoma many years later

Ocular findings related to Angle Recession


Age related Lens changes – Mature cataract

- Thickening of lens
- Shallow AC
- IOP outflow Obstruction
- Could develop Hypermature Cataract

Hypermature cataract

- Hypermature cataract can cause Phacolytic glaucoma
- Ruptured capsule of mature lens evoking macrophage proliferation into anterior chamber
- Cloggs up TM dt hypersensitivety to Protein in AC

Neovascularization of the Iris

Rubeosis irides = Iris neovascularization
Hypoxic/ischemic changes in the retina
Diabetics, Vein occlusion, Ocular Ischemic Syndrome
Hyphema

Angle Closure Glaucoma
Epidermiology
Prevelance
PACG is the leading cause of blindness worldwide
80% of PACG Asia 1/6th of Asian pop Narrow ANGLE
- *Prevalence** of PACG
1. 5% of Asians over 40yo
0. 1-0.5% of patients over 40yo of European decent
0. 75% in adult Asians
0. 97% in Middle East group
1. 10% in China
1. 19% in Japan group
Angle closure

Definition
Related Structures
apposition of peripheral iris against the pigmented TM resulting in obstruction of aqueous outflow
- relationship between iris and lens regulates the flow of aqueous from the posterior to anterior
- 5micron space between iris and lens
- One way valve to maintain higher pressure in the posterior chamber prevents back flow
- relative pupillary block
increase in resistance flow of aqueous
pressure in posterior chamber rises and bows the iris forward
- *Iris bombe**
- *blocks the TM**, IOP inc

Risk Factors for PACG
older age
- 6th/7th decade . Iris thickens anteriorly
Gender
- 2-3x more women / dt anatolmical shallower AC
Family Hx
- autosomal dominant and autosomal recessive patterns for anatomy
Hyperopia
Prolonged dark states / Winter - Dilation
Eye anatomy
- small corneal diameters
- short axial length of globe
- anterior displaced lens
- increased curvature of the anterior lens
- increased thickness of the lens
- anterior insertion of iris into ciliary body
- *Emotional stress** - Dilates Pupil
- *Anterior displacement of the lens** - Accomodation

PASG anterior chamber
Physical Risk Factor parameters
shallow anterior chamber both centrally and peripherally
average depth = 3.15mm
expect 6:1 anterior chamber depth (Van Herrick)
RISK
central depth of <2.2mm risk for angle closure
4:1 anterior chamber depth
Plateau irises
Exeption to the rule
2.4mm -2.0mm Sometimes
much higher risk if = 1.8mm
75% of PACG patients are <1.5mm

Medications
that Affect PACG
sympathomimetic and anticholinergic drugs dilate pupils
- *medications that causes Dilation or Constriction**
ex. bronchodilators, nasal decongestants, antinausea, antispasmodics, antihistamines, adrenergic agonists, cholinergics, anticholinergics, sulfa-based drugs, SSRIs, TCAs and tetracyclic antidepressants, anticoagulants
Miotics
Pull the peripheral iris away from the anterior chamber angle
strong miotics may also cause the zonular fibers of the lens to relax, allowing the lens-iris interface to move forward results in greater iris-lens contact, potentially increasing pupillary block
General anesthesia
parenteral atropine sulfate during induction of anesthesia or muscle relaxants induce mydriasis
PACG
Dilation In office
Moderate Pupil Dilation
Caused By pharma
Moderate pupillary dilation increases risk for angle closure
posterior vector of force is at a maximum when the pupil is between 3-4.5mm dilated
Moderately dilated, the peripheral iris is under less tension and is easily pushed forward into contact with the TM
thicken the iris and bunch it into the TM
Risk of Relative Pupilary Block with in office
DILATION
Angle closure occurs after the patient leaves the office
Quick - no time to develop
Dilator muscle moves the iris peripherally (slower) and posteriorly (faster)
pulls the sphincter back posteriorly as well maximally dilated
little to no contact between the lens and the iris
Dilation wearing off
occurs slowly, pupillary block can develop as dilation comes down and pupil is mid-dilated
Eye that is at risk For Pupil Block
In office
0.5% tropicamide
(won’t dialate dark eyes + Diabetics as well
Do early in day for safety net)
NO phenylephrine or iris dilator stimulating agents
forces the iris posteriorly, increasing the pupillary block
0.5% tropicamide is preferred if need to dilate
fast acting
- *not safe** to dilate, send for LPI
- *1/2 of TM** –> refer
- *posterior TM in at least 180** –> refer
CASE (how would you Dilate this PX?)
Hx
flashes of light in left eye, started yesterday
two very large floaters
f
indings
1/8-1/4:1 Van Herick
open to mid-TM with gonio on secondary gaze
narrow angle
0.5% tropicamide
Gonioscopy
Misdiagnosis caused By:
- Need scotopic conditions
- different grading systems used
- dynamic or static
- no clear definition of at risk eyes/occludable angles
- ex. 1/4:1 or less
- ex. pigmented TM was not visible in 3/4 quadrants in primary gaze without manipulation or indentation
- failure to assess the anterior chamber depth
Theories for
Angle closure Glaucoma
Autonomic imbalance with increased sympathetic tone
iris dilator muscles are more developed and stronger
incr sympathetic - emotional distress, low light conditions, sympathomimetic drugs use
contraction - leads thickening of the middle-peripheral iris = AC
Water volume in iris - Some irises stiffer than others Don’t move anterior.
Peripheral iris attached to Trabicular wall.
Peripheral Anterior Synechiae (PAS)

characteristics
peripheral iris attached to TM (Superior narrowest angle)
iris won’t look irregular
can still react normally
Angle Closure
can start narrow but become broad and/or high as time progresses
Chronic angle closure - PAS are more basal and broad based
Larger PAS, the less likely LPI will be effective
PAS is more common in occludable angles
PAS is more extensive the longer the duration of the angle closure attack

Possible Angle closure
GONIOSCOPY

Gonioscopy should be performed:
- dim to dark room
- small 1mm slit beam
- patient looks straight ahead
- only modestly tilt the lens
Angle Closure Catagories
All present with
iridotrabecular contact (ITC)
Glaucoma if Neuropathy and VF loss
Primary angle closure suspect
iris touch the anterior chamber angle at the TM on non-comp gonioscopy
ITC 180deg or more
NO PAS, normal IOP, normal nerve and VF
Primary angle closure
ITC 180deg or more
PAS and/or elevated IOP
with no secondary cause for the PAS Trauma
Normal nerve and VF
refer for LPI
Primary angle closure glaucoma
80% is chronic
ITC 180deg or more
PAS and/or elevated IOP
with no secondary cause for the PAS
glaucomatous optic neuropathy and VF loss
Acute angle crisis glaucoma
Angle is occluded suddenly
20% of angle closure glaucoma
Identify

BOWED IRIS
Narrow angle
Laser Peripheral Iridotomy LPI
for
Primary Angle Closure PAC
Further treatment / interventionm
AAO
Progression and further intervention
- PAC’S eyes do not receive further intervention after LPI
-
PAC and APAC and most PACG eyes receive further treatment damaged optic nerve fragile
- GTT(Medication) , cataract surgery, or trabeculectomy
- progression to PACG is uncommon in PACS and PAC
LPI efficacy
LPI increases angle width in all stages of PAC
good safety profile
Angle closure Crisis
Charactaristices and Findings
ischemic sphincter –> dilates
ischemic dilator –> constricts

Characteristics
- angle is occluded suddenly
- can be self-limited and resolve spontaneously
- can have mini-attacks when in the dark for prolonged periods
- can occur repeatedly
- can cause permanent vision loss or blindness
Findings
- quickly elevated IOP
- ciliary flush/vascular congestion
- corneal epithelial edema/steamy
- causes intermittent blurring of vision and haloes
- ocular pain and/or headache
- nausea/vomiting
- mid-dilated pupil
- ischemia to iris muscles due to high IOP
- sphincter is stronger than dilator

PAS
Peripheral Anterior Synechia

Acute Angle closure Glaucoma

MX & TX
Acute angle closure Crisis
Management
- lower IOP (first) and provide comfort (second)
- Open the angle and break the attack
- Depends on pressure and length of attack most resolve in 4-6hrs if treated
medical treatment
- Start with drops GTT, if the IOP does not lower in 1hr start ORALS
aqueous suppressors may be ineffective due to decreased ability to reduce aqueous formation if the ciliary body is ischemic
Medications
MX TX
Angle closure Crisis
- *Beta Blocker**
- *1gtt timolol** or levobunolol followed by 2nd drop 10min later
- *takes effect within 20min**
Alpha Agonists
0.5-1% iopidine 1gtt followed by second drop 10min later
or 1gtt brimonidine works quickly
Steroid
1gtt 1% prednisolone acetate hourly
decreases inflammation
(raises pressure after 2-3weeks of use )
CAI’S
1gtt dorzolamide
500mg acetazolamide/Diamox orally or IV if nauseous
(not the time release capsule)
hyperosmotic agents
glycerine 50%, isosorbide 45% or mannitol 20%
cause rapid decrease in IOP
anti-cholinergics
controversial, may get more pupillary block
Only use if < 50mmHg
sphincter is ischemic when pressure is too high
1gtt 2% pilocarpine every 15min for 1hr
NON - Medications
MX TX
Angle closure Crisis
-
Compression for 30sec on and 30sec off
- 4 mirror gonio lens
- Q-tip perpendicular to the vertical axis
- push on eye with palm of hand
- Have patient lay on their back / Moves lens Back
-
Anterior chamber paracentesis
- apply anesthetic drops (ex. oxybupricaine) and clean eye with povidone iodine 5%
- insert a syringe 9 o’clock at the limbus aiming for the center of the anterior chamber
IOP is lowered too quickly,
retinal hemorrhaging can occur decompression retinopathy
-
laser iridotomy
- preferred surgical treatment
- favorable risk-benefit ratio
- can’t Dt corneal edema, cornea may be cleared with topical hyperosmotic agents or anterior chamber paracentesis
Evidence of previous angle closure attacks

PAS
- *Glaucomflecken**
- *infarction** of anterior lens epithelium from high IOP
- *white deposits** more irregular and no fluff on frill like in exfoliative
iris atrophy

Laser Iridotomy
Relieves pupillary block
prevent or slow the formation of PAS
timely treatment may prevent damage to the optic nerve, TM, iris, lens and cornea
2 TYPES

YAG (cutting of hole)
Effective alone in thin blue iris
far less effective in thick brown iris more of a cutting laser
Argon Laser (Burning laser)
Used to thin darker irises, then YAG laser is used to create the hole
Argon is more of a burning laser takes longer

Laser Iridotomy
Procedure
Preparation
- Topical proparacaine (Anestetic)
- 1% pilocarpine - stretches the iris to reveal the crypts/thinnest areas
- 0.5% or 1% apraclonidine due to post-laser IOP spike
Procedure
laser at a crypt until bubbles of fluid are seen coming through the iris. 3 or 9 o’clock prevents diplopia, photopsia, and diplopia
Post-LPI
1% prednisolone acetate 4x/day for 5-7days
glaucoma medications
Efficacy
need further treatment (drops, surgery)
0-8% PACS
42-67% with PAC
21-47% with APAC
83-100% with PACG
if the nerve is damaged, have to treat like POAG to keep pressure low and prevent further damage
Risks
6-10% 8-17mmHg IOP spike
2-11% dysphotopsia
30-41% anterior chamber bleeding (hyphema)
23-39% cataract progression
Dilation of Px with LPI
IOP Spike causes

Examination:
Sure it is patent before dilating / Thin membrane visible?
check with retro-illumination
can also use OCT to determine
if not sure, check with gonioscopy - Angle should be larger than Pre
check the IOP post dilating a patient with a LPI
Causes for IOP with dilation after LPI
LPI is not patent
incomplete LPI not able to view lens capsule
response to dilating agents
other causes ruled out
pigment liberation will observe anterior chamber shower
PI is patient but patient has plateau iris angle closure
malignant glaucoma
lens causing angle narrowing
phacomorphic, subluxated or abnormally anterior lens

Angle Closure Glaucoma Classification
ACUTE
Subacute (Intermittent)
CHRONIC
- recurrent and self-limiting episodes of closure with elevated IOP
- DARK lighting leads to pupil dilation and block
- Issues going from dim to bright - light like those with AMD and carotid artery disease
- bright light and sleep open angle as pupil becomes miotic
Hx
- episodic symptoms
- blurred vision, haloes, eye pain, headache, eye redness
- relatives with acute angle closure glaucoma
Findings
- PAS, esp. superiorly superior angle is narrowest
- IOP often normal in office can be misdiagnosed as NTG
- ONH cupping and VF loss are often the first indications
- *Management**
- *LPI first**
use medications after LPI
if LPI is not sufficient filtering surgery if needed
Angle Closure Glaucoma Classification
ACUTE
Subacute (Intermittent)
CHRONIC
Most common 80%
Findings
- asymptomatic
- more PAS zippering shut of angle, esp. superior angle
- iris atrophy
- Mistaken for POAG
- perform gonioscopy
Management
iridotomy first / CAT Sx if lens is part of the Cause
require medications after LPI to control IOP due to chronic trabecular damage
prostaglandin analogs are preferred
filtering surgery if not controlled

Atypical Angle Closure Glaucoma
asymptomatic until closure attack
Plateau Iris
Plateau iris Configuration
Plateau Iris Syndrome

Plateau iris configuration
iris is flat centrally then peripherally then becomes very steep
ciliary body is abnormally anteriorly displaced,

pushing the iris forward gonioscopically,
steep peripheral iris that it is closely apposed to the angle
not be detected on Van Herick - narrow until far periphery
Plateau iris syndrome
angle closure either spontaneously or after pharmacological dilation in an eye with a patent LPI
iris pulls back directly into the angle causing an IOP spike
Plateau Iris Variations
Diagnostic signs
perform LPI because you think there is pupillary block ACG and after LPI when pupil dilates the IOP still goes up
S shaped hump or double trough sign
- *Subtypes**
- *Complete plateau iris syndrome**
- *IOP rises** when the angle closes with pupillary dilation
Incomplete plateau iris syndrome
height of the plateau is less and leaves the filtering meshwork either partially or all open covers the SS but not the TM
Primary angle closure
demographics
female younger than with pupil block (45-50yo)
less hyperopia than pupil block
bilateral
wide dilation is a risk
often retrospective diagnosis
perform LPI because you think there is pupillary block ACG and after LPI when pupil dilates the IOP still goes up
must perform compression gonioscopy
won’t pick this up with Van Herick
S shaped hump or double trough sign
results from the iris following the curvature of the lens then drops when the iris reaches the deepest point at the lens equator and then rises again over the ciliary processes before dropping peripherally
normal iris has one hump

Plateau Iris

MX & TX
pilogel at night or 1-2% pilocarpine 2-4x/day
gonioplasty/iridoplasty
treat eyes with recurrent high IOP after dilation or if IOP is high after LPI
treat syndrome, not just configuration
if only SS is covered, no need to treat
- *Miotics**
- *pilogel at night or 1-2% pilocarpine 2-4x/day**
gonioplasty/iridoplasty
evenly spaced burns around peripheral iris
argon laser burn to the stroma
constricts the peripheral iris by pulling it away from the angle
Complications
marked anterior chamber inflammation
corneal endothelial cell damage
Pseudoplateau Iris
MX TX

primary cysts of iris and ciliary body
stationary / no harm
clinically identical to plateau iris, but different cause
anterior chamber is uneven in depth and the angle is variable in width
Van Herick
Management and Treatment
confirmed by UBM (ultrasound)
monitored or puncture cysts with argon or YAG laser
Malignant Glaucoma
also known as ciliary body or aqueous misdirected glaucoma
Topamax
Incr minus, 7 days, 85 cases bilateral

- *shallow angle chamber** both peripherally and centrally
- *high IOP**
- *no pupillary block**
- *aqueous is misdirected into vitreous** causing rotation of ciliary body causing anterior lens displacement and angle closure
- Caused by choroidal expansion with fluid
- after ocular or cataract surgery
- after CRVO
- edema in uveal tract can cause angle closure
- can also cause 100day neovascular glaucoma
- Scleritis
- allergy to sulfa drugs (acetazolamide, sulfamethoxazole, hydrochlorothiazide)
- HIV, AIDs, HZ
topirimate/Topamax (rare)
indicated for migraines, seizures, weight loss
swells ciliary body with anterior displacement of the lens-iris diaphragm
increase in minus dt lens moving anteriorly
most attacks happen within 7days of starting the medication
tell patient if there is eye pain or a change in vision to come in that day
85% of cases are bilateral
Malignant Glaucoma
MX, TX
Atropine, Steroids, LPI(Vitrectomy and CAT sx)
Management
if medication induced d/c medication
MX medications
cycloplegic
atropine may be drug of choice to relax ciliary body
deepens the anterior chamber
Steroids
topical aqueous suppressors
Narrow Anterior Chamber Ddx


Neovascular Glaucoma

- *Retinal ischemia** triggers angiogenesis factors to be released
- *secondary to variety of ocular and systemic diseases**
- *fibrovascula**r membrane grows over the TM leading to increased IOP and glaucoma
Causes
Ocular
post-CRVO 100 day glaucoma, ocular ischemic syndrome, proliferative diabetic retinopathy, BRVO, CRAO, tumor, retinopathy of prematurity, chronic RD
Systemic
sickle cell retinopathy, GCA, lupus, Marfan’s, Sturge Weber Syndrome, syphilis, endophthalmitis, carotid artery occlusive disease

Neovascular glaucoma
MX TX
PRP (Panretinal Photocoagulation)
Anti - VEGF

treatment
refer NVI in 24-48hrs
despite being blind in that eye because angle closure is very painful
PRP
anti-VEGF
stages
stage 1: pre-glaucoma with abnormal blood vessels at the pupillary margin
want to eliminate neo before pressure goes up
inject anti-VEGF or PRP if there is retinal ischemia
treat inflammation
stage 2: angle is open but IOP is elevated because of the abnormal blood vessels in the angle
PRP and inject anti-VEGF to decrease pain and complications
standard glaucoma treatments to address high IOP
glaucoma surgery if drugs are insufficient
stage 3: angle is closed and IOP is elevated
PRP and inject anti-VEGF
reduce inflammation
treat glaucoma with drugs and surgery
glaucoma drainage implant is needed

Ectropian uvea

portion of the posterior pigment epithelium of the iris is drawn around the pupillary margin onto the anterior iris surface by the fibrovascular membrane
may be acquired following NVI or congenital

Phacolytic Glaucoma

leakage of proteins from an intact but permeable lens capsule
associated with hyper-mature lens with liquified cortex
non-allergic cellular response
high molecular weight proteins block the TM
glaucoma is very acute and slit lamp shows a very heavy flare and cellular reaction
inflamed, painful, red eye
high IOP
blurry vision
can see the material blocking the angle
Phacotoxic Glaucoma
lens particle glaucoma
treatment
medically
remove cortical fragments surgically and washout anterior chamber
process
associated with cataract extraction
cortical material is left behind
occurs days to years after cataract extraction
marked uveitis
treatment
medically
remove cortical fragments surgically and washout anterior chamber
Identify
Lisch nodules
Neurofribromatosis

Krukenberg Spindle
Pigment dispersion syndrome


Angle Resession


Hyphema

Angle resession

Pigment Dispersion Syndrome
Normal VF, No Optice nerve Changes, IOP < 21
Monitor.

- Concave bowing peripheral iris / posterior iris rubs on zonules
- Bilateral
- Young myopic males 20-40yo
Ocular Findings
- liberation of pigment from posterior iris
- iris transillumination defects Mid peripheral Iris
- moth-eaten appearance
- Krukenberg’s spindle
- pigment deposition on zonules and posterior lens capsule
- zonules attach to the capsule, forming Scheie’s stripe
- TM hyperpigmentation
Complications
- large diurnal variations in IOP as well as spikes in IOP
- strenuous exercise activates pigment dispersion

Pigmentary Glacoma

IOP > 21 / glaucomatous changes to optic nerve / Decr VFin those with PDS
Px 60+ Selflimiting - lens pushes iris forward
Scheie Stripe
Treatment (Aggessive Px younger)
LP Iridotomy
pilocarpine - constricts iris to get the iris off the zonules
causes 3D of myopic fluctuations throughout the day
ALT (argon laser trabeculoplasty)
laser TM to clean it out
SLT (selective laser trabeculoplasty)
laser TM to clean it out
long-term effect is low
success rate decreases over time
AAO study
10% risk at 5yrs and 15% risk at 15yrs
mean age at diagnosis of pigmentary glaucoma was 42 +/- 12yrs
78% of patients were male
58% of patients with PDS were male
other studies don’t show gender bias
underdiagnosed in black patients
hard to transilluminate the iris
most significant risk factor = IOP > 21mmHg at initial exam
most studies say 10-20% convert to glaucoma
some studies report at high as 35% conversion over 17yrs

Pseudoexfoliation Syndrome
Systemic condition

Unilateral - 5yrs bilateral
LOXL1 (lysyl oxidase-like 1) gene
apraclonidine/iopidine before dilation for pos SPIKE
phenylephrine causes more amyloid release
Risk CAT sx lens dislocation
- exfoliative material is released AMYLOID - elastic fibers (fibrillin and alpha-elastin) and non-collagenous basement membrane material (laminin) that forms fibrils
- Iris rubs on amyloid material
- unilateral and becomes bilateral in 5yrs
- Older patients 50-70
- Geographic away form Eqautor / UV at angle during youth
Findings
- white, flaky, dandruff-like deposits at pupillary border, anterior lens, posterior iris and ciliary processes
- Bull’s eye appearance scalloped border appearance around area of mid-peripheral clearance on anterior lens
-
pigment deposition
- patchy hyperpigmentation of the TM
- SL pigmentation Sampolisis LINE Wavy
- Krukenberg’s spindle
- must be seen every 6months at minimum
IOP > 21mmHg, lower IOP with glaucoma medications
even if optic nerve, OCT and VF are normal

Exfoliative Glaucoma (XFG)

Elevated IOP due to closure of angle accompanied by forward displacement of the lens due to zonular weakness
one of the most common secondary open angle glaucomas
Angle Open - POAG
- elevated IOP impairment of aqueous humor outflow due to deposition of pigment and exfoliation material in TM
- Fluctuations in IOP of 15mmHg or greater in 35% of patients
- increased vulnerability of the lamina cribosa toward elevated IOP, facilitating progression of glaucomatous optic neuropathy
CAT sx - Indication - possible sublazation due to weekened Zonules
post-cataract surgery
TM is aspirated intraoperatively
exfoliative material is lavaged out and vacuumed up
ALT and SLT lower IOP
SLT has greater lowering effect in XFG
Angle Recession Glaucoma
months to years after blunt trauma to the eye

results from a contusion to the TM and tears in the uveal meshwork and ciliary muscle
- Posterior recessed insertion of the iris onto the CBB
- diagnose with gonioscopy
- main feature = widening of the CBB in part or all of the angle
- Dense large pigment deposits TM and CBB
- CBB > TM+SS
- wide diurnal IOP curves
Aqueous suppressor drugs work best
TM outflow is impaired, best to decrease inflow
beta blockers, alpha agonists, carbonic anhydrase inhibitors
use whatever works
sometimes prostaglandins can work

Low/Normal Tension Glaucoma
signs of glaucomatous optic disc changes and glaucomatous field loss
IOP < 21mmHg
Japanese
Shallow Cupping

Multiple IOP readings to Ddx POAG
mutations in GCL1G gene for optineurin
related to ischemic theory
HX: carotid artery disease, cardiovascular disease, major blood loss, systemic hypotension, severe anemia, migraines, Raynaud’s, sleep apnea, hyperviscosity
Findings
splinter/Drance hemes at the disc more than norn
shallower cupping
more peripapillary atrophy
arcuate field loss closer to fixation
should consider a 10-2 or 24-2C

Normal tension Glaucoma
complete systemic workup
esp. if under 65yo
blood tests for hyperviscosity, anemia, lipids, and ESR, test carotid flow, neuroimaging
Ddx:post-ischemic optic neuropathies
past massive systemic blood loss
previous steroid use
steroid responder
Management and treatment
Beta blockers
SLT
filtering surgery
NTG vs. neurological problem
think neurological problem if:
unilateral or marked asymmetry
color vision loss without VF loss
VF loss that is atypical or not proportional to the optic nerve damage
Posner Schlossman
Glaucomatocyclitic Crisis (GCC)
unilateral
mild inflammation in anterior chamber but large increase in IOP
locus of inflammation may be the TM (trabeculitis)
Heterochromia
1% Prednisone Acetate QID (taper)
NO - Prostaglandins
- 20-60yo
- unilateral
- Mild inflammation AC (few cells)- large increase in IOP (40-70)
Findings
asymptomatic - dull ache in the eye
mild haze from edema if IOP is very high
KP in AC
angles are open
no synechia
40% heterochromia
inflammation may be the TM (trabeculitis) decr Outflow
HSV, VZV, CMV could be triggers
- *Treatment**
- *first line therapy:**
- *steroid and aqueous suppressors**
1% prednisone acetate QID
second line therapy:
oral CAis for IOP
topical or oral NSAIDs for inflammation
NOT
cycloplegics
prostaglandin analogues and miotics
Fuch’s Heterochromic Iridocyclitis

featureless iris
no crypts or furrows (Looks ironed)
Low grade chronic anterior uveitis
lighter eye has the issue
but in very blue eyes it can be the opposite
reverse heterochromia
No Steroids
Characteristics
very rare chronic form of iridocyclitis
85% unilateral
presents at middle age
Findings
- relatively asymptomatic
- 80% iris heterochromia Lighter affected
- small diffuse stellate keratic precipitates
- featureless iris no crypts or furrows
- can develop PSCs
10-30% have small blood vessels go up the gonio angle
does not come with fibrotic tissue so no peripheral anterior synechiae
60% get anterior vitritis
may be associated with Rubella, toxoplasmosis, herpes
those immunized against Rubella do not develop this condition
Treatment
Aqueous suppressors

Iridocorneal Endothelial (ICE) Syndromes
Middle aged women
Abnormal corneal endothelium progressive iris and angle changes

- rare group of disorders characterized by abnormal corneal endothelium progressive iris and angle changes
- epithelial-like corneal endothelium grows as a membrane over the angle
- leads to peripheral anterior synechiae that usually extend to SL
Forms
Chandler syndrome
predominantly corneal changes
corneal edema = primary feature
essential iris atrophy
iris changes predominate
causes corectopia and polycoria
treatment
difficult to treat
endothelium grows into blebs and shunts
no cholinergics or trabeculoplasty
prostaglandins are not likely very effective
anterior face of ciliary body is covered by synechia
may need penetrative keratoplasty to treat corneal decompensation
Argon Laser Trabeculoplasty
POAG, exfoliative glaucoma
5yr limit, less effective

Argon laser and a gonioscope mirror and delivering approximately 100 burns usually in two treatments of 50 burns usually do ½ the TM first
The laser burns are placed at boarder between the nonpigment and pigmented TM
Pretreat
Pilocarpine to stretch the iris
Iopidine to lower IOP
Post treat
prednisolone acetate 4 times a day for 4-7 days
Glaucoma medication

Different Laser treatments
ALT
SLT

SLT (Non Scarring)
does not cause thermal damage like ALT
delivers just enough energy to target specific melanin-rich cells in pigmented TM
ALT
Pilocarpine to stretch the iris
Iopidine to lower IOP
Argon laser delivers 100 burns over 180deg of the TM
performed in two treatments of 50 burns
laser burns are placed at boarder between non-pigmented and pigmented TM
- *Post-treatment**
- *prendisolone acetate 4x/day for 4-7days**

MGIS
Minimally Invasive Glaucoma Surgery
Microinvasive Glaucoma Surgery

I-Stent
insert 2-3 during cataract surgery
directs aqueous directly to SC from anterior chamber
Removal of TM
improves aqueous outflow
can perform with or without cataract surgery
TRrabectome
burns off the TM
Kahook
cuts the TM out with a blade

MIGS
iStent vs. Hydrus
mild glaucoma and cataract surgery –> iStent
moderate glaucoma and cataract surgery –> Hydrus

XEN Stent
creates a filtering bleb
cylindrical implant made of porcine gelatin that has been cross-linked with glutaraldehyde
small corneal incision - inserted with an injector
CyPass
voluntarily recalled
causes endothelial cell density loss over 5yrs
very good at lowering IOP
Hydrus microstent
inserted into SC to hold it open over 3 clock hours
partial bypass of the TM

Trabeculectomy
Remove a block of peripheral corneoscleral tissue to create an opening under the conjunctiva to the anterior chamber
aqueous is filtered under the conjunctiva into a filtering bleb
ketones and scarring (African Americans), can scar up and close

- mitomcyin to prevent scarring
- Create a scleral flap
- remove a block of peripheral corneoscleral tissue to create an opening under the conjunctiva to the anterior chamber
- aqueous is filtered under the conjunctiva into a filtering bleb
- peripheral iridectomy is performed so iris doesn’t clog the opening
Complications
choroid effusion
CME
dellen formation
hyphema
hypotony
causes shallow or flat anterior chamber
prone to infection
blebitis can lead to endophthalmitis
malignant glaucoma
wound leak
cataract formation
ptosis

Tube Shunts

body and a tube extending from it that enters the anterior chamber drains fluid from anterior chamber and allows it to be absorbed into surrounding tissues
Express shunts
Ahmed glaucoma valve
Express shunts
stainless steel shunt placed under scleral flap
compared to filtering bleb less risk of hypotony
Ahmed glaucoma valve
large decrease in pressure
can laser in more holes later if more outflow is needed

Loose ends collaterals
Collaterals
collaterals can form in advanced glaucoma
like those seen with CRVO, BRVO, tumor behind the eye

Pseudo-defects

- Lens holder in the way
- Wrong Rx lose 1 dB per diopter
- Lids - ptosis, Dermatochalysis - superior depression
- Cornea
- central dystrophies, central scars, keratoconus ex. Band keratopathy
- Juvenile RA with lots of uveitis may want to evaluate VF for uveitic glaucoma or steroid induced glaucoma
Cataracts (ACC, NS, PSC, PCC)
ex. NS - diffuse overall field loss
decreased MD and total deviation
pattern deviation and PSD are normal
ex. PSC
VF defect closer to fixation, likely a relative scotoma
decreased MD,increased PSD
if defect is right near the nodal point, Affect visual field more

Territory 1: Rods and Cones
retinoschisis
retinal detachment
pre-retinal hemorrhage
macular holes

BRAO
retro-atrophy of the nerve
ex. inferior arcuate defect
vessels respect the horizontal raphe
could confuse with a glaucomatous defect once retina regains normal coloration
BRVO systemic HTN
example:
macula edema with exudates
will have distorted Amsler grid
more so inferior because edema is worse superior
refer for anti-VEGF injections
flame hemes superiorly

Myelinated NFL

BRAO
Hx very important. Won’t be able to see in 3 yrs
Papliomacular bundle spared

BRVO
with CME

Retinitis Pigmentosa

20-50 from fixation
Develop PSC earlier
Bone Specules
Geographic Atrophy

Territory 2: Ganglion Cells and Axons within RNFL and Optic Nerve
disc edema
grade 4 HTN
tilted disc
optic neuritis
example: papillitis
25yo, decreased vision x 3days OD
VA = 20/50 OD
RAPD OD
can get any VF defects
central scotoma, arcuates, altitudinal
have to determine cause (demyelination, sarcoid, etc.)

Ischemic optic neuropathy

inferior altitudinal or nasal defects
due to blood supply cut off to superior retina
inferior altitudinal defects are blanket defects inferior to horizontal raphe
arteritic comes with worse VA (20/200-20/400) than non-arteritic
NAAION
Optic nerve drusen
field loss can be anywhere
can mimic glaucoma
hard to predict VF defects due to potential impact of buried drusen

Optic Pit
Pistol Grip Scotoma

Optic atrophy
pale optic nerve
can occur post-CRAO or post-ION
suspect tumor behind the eye
example:
73yo
VA = 20/80 OD, 20/30 OS
IOP = 24 OU
RAPD OD
has rim tissue but it has atrophied
PPA around the disc

Territory III: Optic Chiasm
axons organization

Temporal fibers - nasal VF
remain ipsilateral
Macula fibers
travel in center of optic tract
temporal macular fibers remain ipsilateral
macular fibers cross at posterior chiasm to the contralateral optic tract
Nasal fibers - Temporal VF
inferior nasal cross in anterior chiasm and loop into the contralateral optic nerve before joining the optic tract
loop = knee of Willibrand
superior nasal loop into ipsilateral optic tract then cross in posterior chiasm before joining contralateral optic tract
- *Inferior fibers** pass inferiorly
- *superior VF**
- *Superior fibers** pass superiorly
- *inferior VF**

Optic Chiasm

Generalities
pressure from below and anterior –> superior bitemporal
pressure from above and posterior–> inferior bitemporal
pressure from both sides –> binasal
Field defects that respect the midline
large tumors or lesions may not respect the vertical meridian
not all junctional defects cause superior temporal defect, can cause a whole temporal field defect
nuance
can have many different presentations in chiasmal lesions
many times it is not clear whether VF defects are secondary to direct compression of the axons or secondary to interference of the vascular component
25% of all chiasmal lesions will affect the junction
important to do fields in both eyes when you have a patient with unexplained VA loss in one eye
example:
20/20 OD, 20/25- OS
nerve and macula look fine, OCT is fine
BIO light looked dimmer OS, red desaturation OS
perform VFs –> bitemporal defects
diagnosed with pituitary tumor

Junctional Visual Defects
Chiasm
cut OS optic nerve right before the chiasm
loss all of OS VF
lose OD knee of Willebrand –> inferior nasal fibers
superior temporal VF defect
Case ex and insert
Tumor compressing OS optic nerve near chiasm
bitemporal heteronymous hemianopsia
all of temporal VF OS is gone
part of superior temporal VF OD is gone
knee of Willebrand/inferior nasal fibers OD are compressed
defect gets more pronounced with the smaller target size

Pressure anterior and inferior on OD optic nerve before chiasm
lose OS knee of Willebrand (inferior nasal fibers)
superior temporal defect
lose OD inferior nasal fibers
superior temporal defect
superior bitemporal heteronymous quadrinopsia
Pressure from below the chiasm (pituitary)
fovea is usually preserved
lose inferior nasal fibers from both eyes
superior bitemporal VF defect

Pituitary Tumors
Chromophobe adenoma (most common) 80% have symptoms headache, fatigue, impotence, sexual hair changes, amenorrhea

- radiation
- external beam radiation
- gamma knife stereotactic radiosurgery
- surgery
- endoscopic trans-nasal trans-sphenoidal approach
pituitary adenoma compressing or invading the cavernous sinus can produce unilateral or bilateral ophthalmoplegia
cavernous sinus lies lateral to the sellae turcica such that a laterally expanding pituitary tumor can involve the 3rd, 4th or 6th nerve

Lesions
Causing Pressure from Above the Chiasm
2 main groups
hard and slow growing vascular tumors occurring along meningeal vessels
more common in adults
aneurysms of the anterior cerebral and anterior communicating artery
impinge on chiasm from the posterosuperior direction
Rathke pouch tumors/craniopharyngioma and lesions which cause a dilation of the third ventricle are most common
craniopharyngiomas are more common in children
VF loss
lose superior nasal fibers –> inferior bitemporal defects

Aneurysms of Internal Carotid Arteries
aneurysm of one carotid shifts chiasm against the other carotid
compresses chiasm from the sides
produces binasal defects

HOMONYMOUS
CONGROUS

homonymous
symmetric halves or parts of VF
occupy the same side of the VF in both eyes
respect vertical meridian
defects are either “right” or “left”
labeled in terms of defective side
do not have to be congruous
example: right homonymous congruous hemianopsia
congruous
equal in size, shape and intensity in both eyes
have to be homonymous to be congruous

Optic Tract Visual Field Defects
Right optic tract carries information from left VF
Findings seen with a lesion of the left optic tract: (A) Goldmann visual field showing a partial right homonymous hemianopia from a left optic tract lesion; (B) fundi showing “bow-tie” atrophy of the right optic disc and temporal pallor of the left optic disc;
The RAPD seen with a complete optic tract lesion is found in the contralateral eye. This reflects the larger size of the contralateral eye’s temporal visual field compared to the ipsilateral eye’s nasal visual field, and is consistent with the slight preponderance of crossed fibers over uncrossed fibers

Right optic tract carries information from left VF and vice versa
most defects present as homonymous and usually incongruous
fibers from the two eyes are not perfectly aligned in the tract
create incongruous homonymous hemianopsias on left or right
defects usually occur medial or lateral to the tract
- *medial lesion** usually affects the contralateral eye more
example: left medial optic tract lesion - right incongruous homonymous hemianopsia*
- *lateral lesion** usually affects the ipsilateral eye more
example: left lateral optic tract lesion - right incongruous homonymous hemianopsia*

Visual fields
Post Chiasm

LGN
very complicated
not many patients have LGN lesions, fairly protected
creates half of an hourglass shaped defect
example: right LGN lesion
left homonymous incongruous hemianopsia

Optic Radiations
- fibers from inferior retina travel temporally in the temporal lobe (Meyers loop) SUPERIOR VF DEFECT
- fibers from superior retina travel medially in the parietal lobe INFERIOR VF DEFECT
lesions do not produce optic atrophy

Temporal lobe lesions
produce an incongruous superior homonymous quadrantopsia with sloping margins
pie in the sky
example: left temporal lobe lesion
right incongruous superior homonymous quadrantopsiaEffects
behavioral disorders, aphasia (defect or loss of power or expression or speech and writing) and/or amnesia (lack or loss of memory)
formed and unformed hallucinations are possible
formed = see a rat
unformed = see flashes of lights

Optic Radiations
fibers from inferior retina travel temporally in the temporal lobe (Meyers loop) SUPERIOR VF DEFECT
fibers from superior retina travel medially in the parietal lobe INFERIOR VF DEFECT
lesions do not produce optic atrophy

Parietal lesions
produce an incongruous inferior homonymous quadrantopsia with sloping margins
pie on the floor
example: left parietal lobe lesion
right incongruous inferior homonymous quadrantopsia
somatic perceptual disorders
extinction phenomenon
neglect on one side of VF
can see stimuli when presented on the defective side of VF alone, but cannot see the stimuli on the defective side if stimuli are presented on both sides of the VF

Causes of Lesions
80% of lesions at the chiasm and anterior are caused by a tumor
20% of lesions after the chiasm are caused by a tumor
80% are vascular (strokes)

Occipital Striate Cortex
lesions usually produce defects which are:
- complete or incomplete congruous homonymous hemianopsia
- macular sparing - More POSTERIOR
- Macular Splitting - Anterior lesion
- produce discrete VF defects
vascular lesions
Thrombosis of posterior cerebral or calcarine artery
produce complete homonymous hemianopsia
vascular lesions of the small vessels quadrantopsia, hemianopic scotomas
symptoms of lesions
alexia (understands what they seen but cannot read out loud)
headaches
failing VA
sometimes cannot read Snellen letters, have them write what they see instead
macular sparing

MONOCULAR Visual field defect in Visual CORTEX
- *nasal field extends 60deg** from fixation as compared to 100deg for temporal VF
- *40deg of unpaired field forms an unpaired temporal crescent in the VF**
the most anterior portion of the visual cortex receives fibers only from the peripheral nasal retina in the contralateral eye

The most anterior portion of the visual cortex receives fibers only from the peripheral nasal retina in the contralateral eye
some lesions spare this anterior portion of the cortex and leave an intact crescent in temporal VF
can get a lesion only in this area and get a monocular crescent defect in temporal VF
example: left posterior occipital lobe lesions
right homonymous congruous hemianopsia with macula sparing
congruous despite temporal crescent

CASE
Pappiladema
Hyperope RISK
NAION (Non-Arthritic Ischemic Optic Neuropathy)

CASE

Case
Posterior Communicating Art hemanoma.
Causes 3rd Nerve Palsy
Look at Script RX

Treatment PLAN

Glaucoma MEDS

Glaucoma MEDS
