Classification of Findings Flashcards

Question

Optical monitoring

Answer 1

• 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”**

Answer 2

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**

Answer 3

• 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

Answer 4

## Footnote 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

Answer 5

## Footnote **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

Answer 6

• **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

Answer 7

◦**What** was done? ◦Was the field **accurate?** ◦Was the field **normal?** ◦What **defects** are present? ◦**Evaluation** of visual defect? ◦**Re-revaluation** of visual field

Answer 8

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

Answer 9

**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 f**rom 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

Answer 10

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**

Answer 11

**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

Answer 12

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

Answer 13

• 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 c**ollection 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

Answer 14

◦**Mean elevation or depression** of the pt’s overall field **compared** to **normal reference field** ◦**Takes all points**, a**verages** them, compares to **your age** ◦**Peripheral point**s do **not weigh as much**, c**entral** is more i**mportant** (weighted average) ◦**P\<2** means **less than 2% of the normal population shows an MD larger than the value found** in this test

Answer 15

**• 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**

Answer 16

## Footnote ◦**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**

Answer 17

**“what % of the field is normal?”** An **enhanced MD** designed to be l**ess 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

Answer 18

• 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

Answer 19

• 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

Answer 20

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**

Answer 21

◦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

Answer 22

* **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) F**rom the age-related norms**, the machine will set the hill Age related is the one most commonly used

Answer 23

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

Answer 24

Three-zone Strategy • Begins s**ame 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

Answer 25

• 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 ## Footnote 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

Answer 26

• **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

Answer 27

**• 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**

Answer 28

**• 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_

Answer 29

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

Answer 30

**• 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**

Answer 31

• **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

Answer 32

**• 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

Answer 33

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?

Answer 34

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

Answer 35

* *• 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

Answer 36

* Average cup to disc is about **0.35-0.4** * I**large 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

Answer 37

* If the vessels are not central, if anything, t**hey move nasally** * **Margins** - usually the o**ptic nerve slopes temporally** * **Fovea will be temporally** * **Straight vessels tend to go nasally** * Vessels arch going toward the fovea

Answer 38

* **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** • O**ptic 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

Answer 39

* **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**

Answer 40

1. **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 a**queous cannot drain** from the eye **causing the IOP to rise**

Answer 41

**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

Answer 42

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**

Answer 43

**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

Answer 44

**Open angle** glaucoma VS N**arrow 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**

Answer 45

**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.**

Answer 46

**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.

Answer 47

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

Answer 48

**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**

Answer 49

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 **blue**r 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.**

Answer 50

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.**

Answer 51

* 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**

Answer 52

Axenfeld Riegers Syndrome Sturge Weber syndrome.

Answer 53

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 i**ncrease in pigment in one eye and more pigment in TM** about 10% have elevated IOP in the hyper pigmented eye.

Answer 54

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 i**nvolve ocular and oral mucosal surface**s

Answer 55

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 I**ncrease 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**

Answer 56

Superior nasal Paracentral scotoma

Answer 57

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

Answer 58

Superior arcuate scotoma Inferior Paracentral scotoma, general depression

Answer 59

Temporal island OD

Answer 60

Progression of visual field defects

Answer 61

* I**nitial Phase** - IOP is causing damage to the optic nerve head but the **field is normal** * **Threshold Phase** - patient shows an i**ncrease in****fluctuation**and visual**fields are inconsistent and****variable** * **Manifest Phase** - **positively reproducible visual field loss**

Answer 62

**Decreased MD / Also with Glaucoma** o Wrong Rx o Cataracts o Miosis o Aging and other ocular conditions

Answer 63

**Three or more adjacent points** in an expected location of the central 24 field\* that have **P \< 5% on the pattern deviation plo**t, **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**

Answer 64

**Mean deviation** \> **-6 dB** or On **pattern deviation plo**t, **depressed below the 5% l**evel and fewer than 15% of points depressed below 1% level or **No point** within central 5 below 15dB

Answer 65

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

Answer 66

**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

Answer 67

* 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

Answer 68

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

Answer 69

**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_

Answer 70

**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**

Answer 71

**Neurotrophin deprivation** and **Glutamate toxicity** * **Neurtotrophin** are **peptides** - development and maintenance r**etinal ganglion cells.** **glaucoma** there is an **obstruction of neurotrophin** transport **to the ONH** which results i**n 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

Answer 72

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**

Answer 73

**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

Answer 74

1. Generalized Enlargment of the cup 2. Barring of Circumlinear Vessels 3. Bean Potting 4. Vertical Elongation ( **0.2 more than Hor cupping**) 5. Notching 6. Drance Hemhorages (dt notch, inferior disc. Splinter hem dt stretching that it ruptures) 7. Asymmetry of CD Ratio between eyes (**Diff of 0.2 and more**) 8. Distorted Lamina Dots 9. Aquired Optic pit 10. PPA (Peripapillary Atrophy) **BETA ZONE** 11. NFL Dropout 12. Nasal cup - extendes past BV / Nasal shift of BV

Answer 75

**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**

Answer 76

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

Answer 77

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**

Answer 78

1. **Age** 2. IOP 20-32 **x3** 3. Central Corneal thickness (475-650) **x3** could change DT LASIK SX 4. **Pattern standard deviation x2** 5. Vertical cup disc by contour * *Low \< 5%** Observe and monitor * *Moderate 5-15%** Consider treatment * *High \>15%** treatment

Answer 79

This showed that **early IOP-lowering intervention** reduces the **cumulative burden of disease**, The **absolute effect** was **greates**t 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.

Answer 80

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

Answer 81

**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)

Answer 82

**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.**

Answer 83

* 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

Answer 84

* 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

Answer 85

History IOP since and **multiple** readings Optic nerve evaluation Visual fields Pachymetry Imaging OCT **Gonio (always do gonio before you treat glaucoma)**

Answer 86

**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**

Answer 87

1. Establish **baseline IOP** 3x 2. Obtain an OCT 3. **Classify** amount of glaucoma damage as **mild, moderate,** **severe** 4. Use the **highest IOP (Tmax)** and set **target pressure based on the severity of the glaucoma** 5. Consider lowering target pressure an **additional 10%** if patient is * *younger than 50 years, African American, monocular , or has a sibling with advanced glaucoma**

Answer 88

Tmax Highest the **IOP** e**ver 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

Answer 89

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.**

Answer 90

**OCTs** to monitoring **structural consistent with glaucoma** however Y Once the **damage is significant**, ## Footnote * *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.

Answer 91

* **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.

Answer 92

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

Answer 93

**Topical miotic** – cholingeric agents ## Footnote o **Alpha adrenergic agonist** o **Prostaglandin analogues** mostly **increase uveoscleral outflow** but also affect some **increase in trabecular meshwork** outflow

Answer 94

o Beta Blockers act on the **[beta]-adrenergic receptors** in the ciliary processes o Carbonic Anhydrase Inhibitors **inhibit carbonic anhydrase** in the **ciliary epithelium**and decrease aqueous humor**synthesis** ## Footnote o Alpha2-adrenergic Agonists • Apraclonidine: Relative **selective alpha 2 adrenergic agonist** but does activate some alpha - 1 receptors, • Brimonidine: **more alpha 2 selective**

Answer 95

**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

Answer 96

* *latanoprostene bunod 0.024% Vyzulta** * *metabolizing** into **two moieties**: 1. **latanoprost acid -** primarily **uveoscleral pathway** to increase aqueous humor outflow 2. **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**

Answer 97

**netarsudil ophthalmic solution 0.02%** * **Rho kinase** **inhibitor** which is believed to reduce IOP by**relaxing the cells of the meshwork** and **inner walls of Schlemm’s canal**, **increasing outflow**. * **also decreases inflow** by inhibiting norepinephrine**transporter** 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.

Answer 98

Conclusion: The **monocular trial of therapy is effective** in **accurately predicting the response of an untreated eye to monotherapy**with a**prostaglandin analogue** at all daytime time points measured

Answer 99

**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.

Answer 100

Pilocarpine 1% 2% 4%

Answer 101

**Mechanism** ## Footnote – 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**

Answer 102

**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

Answer 103

Increase Uveal scleral Outflow starts **2 hours** after installation, **maximum effect 12 hours** Un-opened - **not need refrigeratio**n **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

Answer 104

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

Answer 105

* 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

Answer 106

**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** 1. Macular edema 2. History of herpes simplex in eye 3. Active uveitis 4. Class C for pregnancy

Answer 107

The beta-blockers act on the **beta-adrenergic receptors in the ciliary processes**and**reduce aqueous humor production.** 1. selective (Block beta 1 receptors) or 2. 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**

Answer 108

Most common beta-blocker is N**on-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!!!!!!!

Answer 109

Problems **Short term escape** o Loss of efficacy within 1 month This is **secondary to receptor saturation** ## Footnote **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**

Answer 110

Patients **with or had asthma** Patients with **COPD (**Chronic obstructive Pulmanory disease) Patients with B**radycardia** 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

Answer 111

Dry eye Corneal anesthesia Allergic blepharoconjunctivitis Uveitis

Answer 112

1. **Systemic hypotension** – left ventricular failure and atrioventricular conduction disturbances 2. **Bronchospasm** 3. Adverse CNS effects – f**atigue, depression, amnesi** 4. **Ocupress – less effect on bad cholesterol profile** 5. **Mask clinical signs of hyperthyroidism** (i.e. tachycardia) because of the thyroid storm 6. **Bradycardia** – if they have a pace maker it is ok 7. **Mask hypoglycemic signs and symptoms**, sometimes resulting in dangerously low blood sugar 8. Impotence

Answer 113

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

Answer 114

Brimonidine (**Alphagan)** **1gtt TID (used alone)** o **Starts** to work in **1 hour** ,**peak** effect after **2 hours** **lasts for 12 hours** ## Footnote Apraclonidine (**Iopidine)** post Sx / Angle closure / Risk procedures o Starts **first hour** work **peak 3 hours** lowers and lasts _for 12 hours but l**arge tachyphylaxis(**_Toxic) so **not usually used for long term treatment** used for short term ,i.e after and before ALT,LPI Acute Angle Closure

Answer 115

Blepharits **Dry Eye** Conjuctival hyperemia Dry mouth Dry Nose **Allery Conjuctivitis** **Follicular Conjuctivitis** **Miosis**

Answer 116

**AVOID IN CHILDREN - can cause CYANOSIS and SEIZURES** CONTRAINDICATED for PX taking **Monoamine Oxidase Inhibitors** **& Px with Severe CARDIOVASCULAR Disease** Hypotension Vasovagal attack Anxiety

Answer 117

rasagiline **(Azilect)**, 􏰀 selegiline **(Eldepryl, Zelapar)**, 􏰀 isocarboxazid (**Marplan),** 􏰀 phenelzine **(Nardil),** 􏰀 tranylcypromine **(Parnate)**

Answer 118

**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

Answer 119

**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

Answer 120

**SULFA ALLERGY** **Endothelium compromise** **FUCHS ENDOTHELIAL DYSTROPHY**

Answer 121

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%

Answer 122

Elderly: Decrease in VA dt NS and cataract formation Young Adults: Decreases the Acc available, unable to read

Answer 123

Drops: **Rhopressa** Meds: **Amioderone-** Drug for Anarythmia **Plaquenil -** Arthritis treatment (Bulls eye retinopathy)

Answer 124

􏰀 **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**)

Answer 125

􏰀 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** 􏰀 **Prostaglandin**s 2 weeks to possibly 3 months before best results is lowest effect observed

Answer 126

􏰀 Depends on severity of disease. ## Footnote 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**

Answer 127

Optic nerve coloboma

Answer 128

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

Answer 129

The two most common methods are: 1. Zeiss 4 mirror lens 2. Goldmann mirror lens 3. Sussman lens, Posner lens Performed at the **slit lamp** PX **seated in upright position** Opposite Qaudrant evaluated

Answer 130

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

Answer 131

Requires viscous solution eg: **methylcellulose** * Past gonio **gel(very preserved SPK)** * USE- Teargel / Celuvisc * Bubble free / anesthesia (Proparacaine) Optically excellent views

Answer 132

Better for deeper set eyes / Smaller appertures Able to view posterior pole

Answer 133

Smaller - Easier to handle Less rotation Central view of fundus

Answer 134

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

Answer 135

**largest trapezoid shape mirror** Equatorial Eye needs to be very dilated Able to see vortex veins in periphery

Answer 136

**rectangula**r in shape Dilated pupil needed

Answer 137

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

Answer 138

Steps 1. Align slit lamp for patient and examiner 2. Scan anterior portion of eye 3. if **corneas are intact**, anesthetize cornea 4. Clean mating surface Dakin’s solution(9:1) 10/10 5. Rinse with saline 6. Fill 3/4 CELLUVISC(less viscous) Genteal(More viscous) Gonio scopic(SPK) 7. 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 8. without excessive pressure, fingers not used to brace Px forehead 9. Look outside the mirror and move the illumination beam into the gonio mirror 10. identify the pupil edge. Focus on the edge of iris 11. Focus on the iris and note the color of the iris 12. Increase the magnification to 16x (medium)

Answer 139

Corneal abrasion 􏰁 Penetration injury 􏰁 Hyphema 􏰁 Laceration 􏰁 Recent lasik surgery, corneal transplant 􏰁 Corneal ulcer, infection

Answer 140

**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)

Answer 141

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

Answer 142

CBB SS TM SL / Sampolisi's line

Answer 143

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**

Answer 144

Ciliary Body Band

Answer 145

**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**

Answer 146

formed when **peripheral iris** adheres to the **peripheral cornea**

Answer 147

Avoid compressions when unwanted Make slight lens excursions

Answer 148

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 cana**l, or **pigment deposits** are found in the **Trabecular meshwork anteriorly**; it can be easily located

Answer 149

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

Answer 150

* *Causes:** - Excessive external pressure on goniscopy - Low intraocular pressure - Increased episcleral pressure _Sturge Weber syndrome_ _Corotid Carniverous sinus_

Answer 151

* 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**

Answer 152

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

Answer 153

Optical section slitlamp Angle the illumination arm either t**emporally 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

Answer 154

**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

Answer 155

CBB SS TM SL

Answer 156

**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

Answer 157

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

Answer 158

Location of iris insertion 3. Note presence of **iris processes** 4. **Grade T**rabecular meshwork **pigmentation** **NORM: CBB \<= TM**

Answer 159

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

Answer 160

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

Answer 161

1. Age related 2. Most predominant Scandenavia / Further away from eqautor(Angle of light reflection WATER ICE) 3. Solar radiation / Outdoors / Geographical Location 4. High Coffee Consumption 5. **Decr Folate / Incr Homosysteine levels** 6. **Genetics LOXLI gene** 7. **Amyloid buildup** on lens and Surounding structures 8. Krukenberg spindle

Answer 162

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 K**rukenberg Spindle**

Answer 163

**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

Answer 164

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 T**rabecular Meshwork** (TM)

Answer 165

**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**

Answer 166

DDX Krukenburg spindle

Answer 167

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

Answer 168

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

Answer 169

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

Answer 170

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**

Answer 171

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

Answer 172

* 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

Answer 173

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

Answer 174

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

Answer 175

apposition of **peripheral iris** against the **pigmented TM** resulting in **obstruction of aqueous outflow** * relationship between iris and lens r**egulates 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

Answer 176

**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

Answer 177

**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**

Answer 178

* *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

Answer 179

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**

Answer 180

**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**

Answer 181

NO **phenylephrine** or i**ris 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, s**end for LPI** * *1/2 of TM** --\> refer * *posterior TM in at least 180** --\> refer

Answer 182

0.5% tropicamide

Answer 183

* 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**

Answer 184

**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 **t****hickening 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.**

Answer 185

**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**

Answer 186

**Gonioscopy** should be performed: * dim to **dark** room * small **1mm slit beam** * patient looks **straight ahead** * only **modestly tilt** the lens

Answer 187

**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 IO**P 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

Answer 188

BOWED IRIS Narrow angle

Answer 189

**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

Answer 190

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

Answer 191

Acute Angle closure Glaucoma

Answer 192

**Management** 1. **lower IOP (first)** and provide comfort (second) 2. **Open the angle** and break the attack 3. Depends on **pressure and length of attack** most **resolve in 4-6hr**s if treated medical treatment 1. 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**

Answer 193

* *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**

Answer 194

* **Compression** for **30sec on and 30sec off** * **4 mirror gonio len**s * **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**

Answer 195

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

Answer 196

**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

Answer 197

**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**

Answer 198

**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

Answer 199

* **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 o**pen 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

Answer 200

**Findings** * asymptomatic * more **PAS zippering shut of angle**, esp. s**uperior 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

Answer 201

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

Answer 202

* *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

Answer 203

**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

Answer 204

**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 c**onfirmed by UBM (ultrasound)** monitored or puncture cysts with argon or YAG laser

Answer 205

* *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 trac**t 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

Answer 206

**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**

Answer 207

* *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

Answer 208

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 complication**s **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**

Answer 209

**leakage of proteins** from an **intact but permeable lens capsule** associated with **hyper-mature len**s 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

Answer 210

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**

Answer 211

**Lisch nodules** **Neurofribromatosis**

Answer 212

Angle resession

Answer 213

* 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**

Answer 214

**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

Answer 215

* 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, p**osterior 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

Answer 216

* **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

Answer 217

* 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

Answer 218

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

Answer 219

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**

Answer 220

* 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**

Answer 221

**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 n**o 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**

Answer 222

* rare group of disorders characterized by **abnormal corneal endothelium progressive iris and angle changes** * epithelial-like corneal endothelium g**rows as a membrane over the ang**le * 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

Answer 223

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

Answer 224

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**

Answer 225

**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

Answer 226

**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

Answer 227

* **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 i**s 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

Answer 228

**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

Answer 229

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

Answer 230

**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

Answer 231

BRAO r**etro-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 gri**d more so inferior because edema is worse superior refer for anti-VEGF injections flame hemes superiorly

Answer 232

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

Answer 233

Retinitis Pigmentosa ## Footnote 20-50 from fixation Develop PSC earlier Bone Specules

Answer 234

**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.)

Answer 235

**Optic nerve drusen** **field loss can be anywhere** can mimic glaucoma hard to predict VF defects due to potential impact of buried drusen

Answer 236

**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

Answer 237

**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 - T**emporal VF **inferior nasa**l 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**

Answer 238

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

Answer 239

**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_***

Answer 240

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

Answer 241

**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**

Answer 242

**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_***

Answer 243

**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_***

Answer 244

**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 quadrantopsia_***Effects 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

Answer 245

**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**

Answer 246

**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

Answer 247

**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_***

Answer 248

Treatment PLAN

Answer 249

Glaucoma MEDS

Classification of Findings Flashcards

(289 cards)