Ocular Disease Iv

Front 1

New COURSE: Ocular Disease IV

Front 2

ocular disease II, III and IV notecards were made from lecture recordings and lecture powerpoints. ocular disease I was made from only the lecture powerpoints and not the lecture recordings.

Front 3

New lecture: 1GlcAssessST2010

Front 4

deciding if a pt has glaucoma or not and WHEN to treat is much harder than deciding how to tx them (what drugs to start with etc.)

Front 5

you see what you look for, not what you look at.

Front 6

glaucoma is many different diseases and which one it is can have a large impact on the prognosis and tx.

Front 7

what is the definition of glaucoma

Back 7

"a group of ocular diseases with various causes that ultimately are associated with a progressive optic neuropathy leading to loss of vision function". -this implies that in order to say that a person has glaucoma they need to have optic nerve involvement and vision loss (including field loss). without both of those thing you are probably dealing with a glaucoma suspect or an ocular hypertensive.

Front 8

you do not have to have a diagnosis of glaucoma in order to tx. you can tx in a preventative manor.

Front 9

most people agree that what IOP is high enough to treat based on IOP alone

Back 9

30 mmHg or higher (between 30 and 24 there are a lot of different opinions; but most people agree that below 24, that is not high enough to tx based on IOP alone)

Front 10

at this point, IOP is the only risk factor for glaucoma that we know how to tx relatively effectively. it is the only risk factor that we can monitor on a fine enough scale to see changes in the short term (field loss and ONH changes occur too gradually for us to effectivly use to monitor glaucoma progression in the short term)

Front 11

how common is glaucoma in caucasians and african peoples

Back 11

about 2% of caucasians. 6% of individuals of african descent. -that's not that common, but not that rare either.

Front 12

consider baseline IOP when establishing a target IOP

Front 13

what are the traditionally accepted risk factors associated with glaucoma

Back 13

1. increasing age 2. geneder (male more likely to develop primary open-angle glaucoma; females more likely to develop narrow angle glaucoma) 3. race (africans; native americans and asians fall inbetween caucasians and africans in terms of their prevelance of glaucoma) 4. vascular conditions (migraine HAs, heart problems, vasculitis) 5. inflammatory conditions 6. medications (corticosteroids; oral and topical) 7. trauma 8. surgery (can change the aqueous flow) 9. refractive status (myopes deveop primary open-angle glaucoma more) 10. increased IOP 11. visual field status 12. ONH (larger cup)

Front 14

when was the OHTS study published

Back 14

2002

Front 15

the OHTS study is a multicenter randomized clinical trial. which tells you that it was controlled pretty well, and usually that there was a pretty high N (number of participants). the OHTS study has 1636 participants with ocular hypertension (one eye with an IOP between 24 and 32, and the other eye between 21 and 32). they were divided into two groups, treated and untreated; and they were followed for 5 years. then they evaluated the ones that did develop glaucoma and tries to determine which risk factors were associated with the development of glaucoma. risk factors evaluated by OHTS: age, self-identified race, gender, vertical CD ration, horizontal CD ratio, IOP, family history of glaucoma, visual field indices, myopia, heart disease, high blood pressure, low blood pressure, use of oral calcium channel, blockers, use of oral beta-blockers, cerebrovascular accident, diabetes mellitus, migraine, central corneal thickness.

Front 16

why is high blood pressure considered as risk factor for glaucoma? why is low blood pressure considered as risk factor for glaucoma?

Back 16

high BP: high blood pressure causes atherosclerosis. which causes poor perfusion to the tissue low BP: low blood pressure causes poor perfusion to the tissue (particularly if there is high IOP; arteries in the eye are a very low pressure system, so the pressure in the eye can actually be higher than the pressure in the artery, which leads to poor perfusion)

Front 17

to what range of IOP do the results of the OHTS study apply

Back 17

generally accepted to apply to IOPs in the range of 24-32.

Front 18

calcium channel blocker were looked at in the OHTS because they cause peripheral vasodilation. there was one study that claimed that calcium channel blockers actually reversed visual field loss due to glaucoma. this study is now believed to be false and that the improvements were actually due to a learning effect on the part of the participants.

Front 19

what was the most significant risk factor for glaucoma that they found in the OHTS

Back 19

central corneal thickness.

Front 20

to whom do the results of the OHTS study apply

Back 20

people with OCULAR HYPERTENSION. you CAN NOT apply the results of the OHTS study to people who do not have ocular hypertension. -it may be that they do apply, but that is not what the study showed, and we do not have any proof that they do apply to people without ocular hypertension.

Front 21

what is the difference between multivariant and univariant risk factors

Back 21

multivariant: means that you recognize that there are multiple variables that could be influencing it and you try to compensate for that univariant: looks at one variable at a time and does not consider wheather or not it is being influenced by another variable -you notice that the grass turns brown in the summer and you think that it is related to the amount of sun. then you do statistical analysis comparing the amount of sun to the amount of brownness in the grass. that is univariant analysis. if you think about it, increased sun means decreased rain, and decreased rain means borwnness of the grass. it's also possible that the sun its self is causing the brownness of the grass. figuring out how much is due to lack of rain and how much is due to sun exposure is multivariant analysis. -in the OHTS study we know that IOP increases with age, but both are a risk factor for glaucoma. how much is due to IOP and how much is due to age? it is possible that age is not a risk factor and that increasing IOP with age is the only reason that you get increased glaucoma with age. to isolate these factors you take people in many different age categories, but with the exact same IOP and see if there is a difference in the incidence of glaucoma. this is a mutivariant example. -multivariant is usually considered to be a stronger statistic than univariant.

Front 22

name the multivariant and the univariant risk factors found in the OHTS study

Back 22

multivariant: 1. age (1.22 per decade) 2. vertical CD ratio (1.32 per 0.1 larger) 3. horizontal CD ratio (1.27 per 0.1 larger) 4. IOP (1.10 per mmHg) 5. central corneal thickness (1.71 per 40 microns thinner) univariant: 1. male gender (1.87; probably because males have more of the other risk factors than females) 2. self-identified race: african american (1.59; if you have an african american and a caucasian with exactly the same IOP, CD, corneal thickness and other risk factors, then individuals of african american descent were no more likely to develop glaucoma than caucasians) 3. heart disease (2.11) -univariant risk factors were significan on univariant analysis AND not significan on multivariant analysis.

Front 23

what are the traditional risk factors that were NOT found to be significant in the OHTS study

Back 23

1. family history of glaucoma (still generally accepted as a risk factor OHTS admits that they didn't do this part of the study right, because they didn't do a background check and relied entirely on pt report. almost all other studies support family history as a risk factor for glaucoma) 2. vascular disease (diabetes and migraine) 3. diabetes mellitus (study actually found that diabetes was protective for glaucoma. this disagrees with every other study done. every other study has either found no association or that is was a risk factor. once again they did not conformation of wheather or not the subject had diabetes; they relyed entirely on pt report. they also excluded anyone with diabetic retinopathy from the study. Dr. Lingle doesn't know of anyone who thinks that diabetes is protective for glaucoma) 4. high OR low blood pressure (low blood pressure is probably not a risk factor for glaucoma, but one one thought that it was a risk factor for primary open-angle glaucoma, it is thought to be a risk factor for normotensive glaucoma) 5. cerebrovascular accident 6. oral calcium channel blockers 7. oral beta-blockers 8. myopia (there are a lot of studies that show high myopia as a risk factor for glaucoma. the OHTS study did not have many high myopes and most experts still consider it a risk factor)

Front 24

if your mother has glaucoma it is more of a risk factor than if your father has glaucoma. if a sibling has glaucoma it is more of a risk factor than if either of your parents have glaucoma.

Front 25

remember that the results of the OHTS study only apply to people with ocular hypertension (IOP between 24 and 32). be vary cautious about applying the results of this study to people with IOPs outside this range. they may well apply, but we don't know that they do.

Front 26

there is a calculator based on the results of the OHTS study that will tell you what your risk of developing glaucoma within the next five years with and without treatment. talks about this on slide 19 of powerpoint 1GlcAssessST2010. Dr. Lingle did an example and the risk was 15% with tx and 9% without tx. it is important to know this when deciding with the pt wheather to tx or not.

Front 27

why is it important to look at pupil size when evaluating a glaucoma suspect

Back 27

because pupil size will influence visual field results, and if we ignore pupil size we may misinterprate visual field results -anything else that will influence the amount of light getting in the eye (cataract, corneal/lenticular opacities, pterygium) will impace the visual field.

Front 28

what refractive error is most likely to have krukenberg's spindle

Back 28

high myopes.

Front 29

where does the pigment come from in krukenburg's spindle and why

Back 29

-pigment comes from the back of the iris from it rubbing on the zonules. the iris is often concave.

Front 30

how do you do iris transillumination

Back 30

magnification: 10X. if you mag. is too high you will lose your contrast. illumination: dark you: you should be dark adapted beam: it doesn't really matter what shape the beam is, it just needs to be inside the pupil -you should be looking in the mid-periphery (zonules rubing on iris)

Front 31

describe the prognosis of pseudoexfoliative glaucoma compared to other forms of glaucoma

Back 31

has a worse prognosis. response less to tx. usually requires surgery much faster and results in more field loss.

Front 32

how do you find pseudoexfoliative glaucoma

Back 32

you have to dilate the pt and THEN do biomicroscopy

Front 33

remember that there are several studies that indicate that beta-blockers increase cataracts. if you see worsening fields and don't consider that it may be from increasing cataracts, you might think that the therapy is not working.

Front 34

making a diagnosis of glaucoma is not urgent, because it is a slowly progressive disease. you can wait until you are more sure of the diagnosis before you decide. consider that studies show that just by telling someone that they have glaucoma, their quaility of life decreases because they worry about it. so you don't want to take the diagnosis of glaucoma lightly, but you don't want to ingore it either. also consider that once you diagnose someone with glaucoma there are not very many people that will "undiagnose" them. your diagnosis is pretty permanent, so if you're not sure it is a good idea to wait. Dr. Lingle has only removed the diagnosis of glaucoma on one pt in her entire carear

Front 35

studies have shown over and over again that visual fields are not very repeatable. if it were not for the human component, it would probably be a much more repetable test; so you really need to pay attention to what is going on during the visual field. (type A will wait until they are sure that they see the light)

Front 36

what is the sensitivity and specificity of diagnosing glaucoma based on using an IOP measurement of >24

Back 36

sensitivity: 34% specificity: 99%

Front 37

what is the sensitivity and specificity of diagnosing glaucoma based on a visual field SCREEING

Back 37

sensitivity: 52% specificity: 90% -you need to use several different findings to diagnose glaucoma

Front 38

what is the sensitivity and specificity of a GDX screen

Back 38

sensitivity: 80% specificity: 90%

Front 39

visual fields, tonometry and CD together with any one being abnormal yields 90% sensitivity and 90% specificity

Front 40

what is the sensitivity and specificity for early glaucoma of the FDT

Back 40

sensitivity: 80% specificity: 93% -appears to be excellent screening tool for glaucoma especially when used in the threshold mode. accurately predicted location and relative depth of scotomas found with humphrey visual field

Front 41

what are the advantage of FDT

Back 41

1. very fast 2. skill level required of technician much lower than other field tests 3. blur has a limited effect

Front 42

how do you interpret the FDT

Back 42

abnormal if any of the following: 1. any defect in central five locations 2. two or more mild defects in the outer twelve locations 3. one or more moderate or severe defects in the outer twelve locations 4. longer than 90 seconds to perform the test on one eye

Front 43

FDT is useful for as a glaucoma screening, but humphrey visual field is useful for glaucoma diagnosis and is often used as a test to prove diagnosis in studies.

Front 44

recognize that there is a learning effect to humphrey visual field. also remember that you need to compare your visual field results to the appearance of the optic nerve head. you need to do dilation on the same visit as a field, not 3 months later. if you can't, you need to at least look undilated.

Front 45

how do you determine if a visual field is reliable (specifically)

Back 45

1. fixation losses: gaze monitoring, blind spot testing (20% or less is reliable (up to 33% in older pts)), false positives (<33% is reliable), false negatives (<33% is reliable), short term fluctuation (flagged if outside of norm).

Front 46

what is a short-term fluctuation

Back 46

there are 10 predetermined points in a humphrey visual field that are always retested (if short-term fluctuations are turned on), then they use a mathmatical model to measure variability (check variablility on that test. short-term fluctuations are considered an indication of unreliability).

Front 47

how could short-term fluctuations be a very early sign of a visual field defect

Back 47

short term fluctuations could also be a very early sign of a visual field defect, because there is a certain angular distance between the closest areas that lights are presented in a visual field, if you have a very small visual field defect that is right inbetween the two closest spots that lights are presented if the pt were only slightly misaligned between the two presentations, they may see it one time and not another time. this is how short-term fluctuations could be a sign of a very early defect. if a pt has really good reliability in every other way except for short-term fluctuations, you should consider that it might be because of an early, shallow defect.

Front 48

how many degrees seperate two lights in a humphrey 30-2

Back 48

6 degrees

Front 49

what is a false negative

Back 49

false negative: present a stimulus in a spot that you have previously said that you could see that is much brighter. you should see it, if you say that you don't, it is a false negative.

Front 50

how does blind spot testing work

Back 50

the instrument places a stimulus where it thinks the blind spot should be and sees if you indicate that you see it.

Front 51

what do upward and downward spikes on gaze monitoring mean

Back 51

upward: true deviation downward: blink or unable to track (long downward stroke means the pt blinked. short downward stoke means the machine lost its ability to track) -downward strokes are better than upward strokes.

Front 52

how does a field machine accomplish gaze monitoring

Back 52

reflections off the cornea. as the pt keeps their eyes open for longer and longer periods of time the reflections off the cornea get worse, so it is common for us to see more downward spikes as the test goes on.

Front 53

what is the raw data display

Back 53

true threshold in dB (not adjusted for age)

Front 54

what is the function of the grayscale

Back 54

should be ignored by the practitioner. used for pt education only. -for one thing, lights are present a minimum of 6 degrees apart; the gray scale will make extrapolations in between these points that are not necessairly correct.

Front 55

what does the glaucoma hemifield test do

Back 55

compares similar points above and below the horizontal midline. (will say within normal limits, outside, or boarderline). even if it says they are outside normal limits, you should NOT say that the pt has glaucoma based soley on this. there are many other conditions that would cause the glaucoma hemifield test to be outside normal limits (anterior ischemic optic neuropathy for example (altitudinal defect))

Front 56

are high dBs brighter or dimmer than low dBs in visual fields

Back 56

higher dBs are more sensative areas, so they are dimmer stimuli

Front 57

what is an absolute scotoma and what would it measure in dBs

Back 57

an area where there is no light perception. zero decibels (really saying that the pt has no light perception at the brightest stimulus the instrument can present)

Front 58

what is the total deviation plot of a visual field test

Back 58

the difference between what is expected for age and the achieved.

Front 59

what does a negative number on a total deviation plot mean

Back 59

the pts performance was less sensitive than expected for their age

Front 60

is it more common to have a positive or negative number on the total deviation plot? why?

Back 60

more common to get negative numbers. you would expect that they would be positive half the time and negative half the time, but it is negative because of the learning curve. the average person in the humphrey database performed the test every 6 months and were more experienced than your average pt.

Front 61

what is the probability plot of the total deviation of a visual field

Back 61

how likely the total deviation is due to chance. also age adjusted, but based on a very well trained normal database.

Front 62

humphrey will not give us information about the demographic in their normalized data base because they say that it is proprietary information

Front 63

what is the pattern deviation of a visual field

Back 63

the instrument compensates for any overall depression or overall increase in sensitivity. if you look at the picture, all the points on this persons field (with the exception of one or two points) are far enough away from normal that they would be the darkest black on the total deviation probability plot. so the whole field would be black an you could miss the fact that there is a pattern indicitative of some disease process unless you adjust for an overall depression for the fild (look at the pattern deviation). (example: a cataract could prevent you from detecting glaucoma unless you look at the pattern deviation plot). -it is age adjusted because it is based on the total deviation

Front 64

name some things that could cause a person to have an overall depression in sensitivity of their visual field

Back 64

-anything that reduces light to the retina 1. cataract 2. tinted contact lenses 3. very small pupils 4. corneal scar 5. a pt who doesn't want to push the button until they are absolutely positivethey see the light -many other things

Front 65

after cataract surgery a person may have an overall increase in sensitivity of their visual field compared to their age.

Front 66

name the global indicies of a visual field

Back 66

1. mean deviation 2. pattern standard deviation 3. short term fluctuation 4. corrected pattern standard deviation

Front 67

what is the mean deviation of a visual field

Back 67

overall depression or elevation of visual sensitivity. not very specific, can be influenced by cataracts or very deep depressions (just like any other mean it can be significantly influenced by outliers). it is related to the total deviation and can be considered an average of the values in the total deviation plot. -it is calculated from age matched values

Front 68

what is the pattern standard deviation of a visual field

Back 68

look at how much the visual field has variations from the normal shape of the visual field (hill of vision; sesative in middle and drops off in the periphery). looks at the pattern to see how the points compare in terms of what is expected compared to its neighboring point. related to the pattern deviation plot; a single number that represents the variation from normal on the pattern deviation plot. -also calculated from age matched values

Front 69

what are short term fluctuations

Back 69

takes certain preassigned points and evaluates them to determine how much variation the pt is giving us on a single day

Front 70

what is the corrected pattern standard deviation

Back 70

number representing the pattern standard deviation corrected by short term fluctuations. adjusts for pt reliability. if pt variability was greater that day, it will accept more variability as normal.

Front 71

name the types of visual field defects found in glaucoma

Back 71

early (most to least common) 1. partial arcuate 2. paracentral 3. nasal step 4. temporal wedge later loss 5. arcuate 6. altitudinal

Front 72

what is a partial arcuate field defect

Back 72

visual field loss in the nerve fiber bundle that extends incompletely from the blind spot to the nasal meridian. generally they are contiguous with either the blind spot or the masal meridian. in order to be called a partial arcuate the field must have at least 1 abnormal spot in the temporal field. (picture is two different examples of partial arcuate, they are not the same pt)

Front 73

what are paracentral scotomas

Back 73

small isolated scotoma in the nerve fiber bundle region. they are generally NOT contiguous with either the blind spot or the nasal meridian (if they were they would probably be called an early arcuate). they do not involve points outside 15 degrees that are adjacent to the nasal meridian (that would be a nasal step). superior temporal portion most commonly involved.

Front 74

how do you determine how many degrees away from central fixation a defect is

Back 74

remember that each point is 6 degrees away from each other, but that the points closest to the center of fixation are only three degrees away from fixation (but they are still 6 degrees away from each other). in the picture the defect is 15 degrees away from central fixation.

Front 75

what is a nasal step field defect

Back 75

limited field loss adjacent to the nasal horizontal meridian. includes at least one abnormal spot at or outside 15 degrees on the meridian. they tend to develop more in the periphery first and move towards the center. can not include more than 1 significant point on either plot in the nerve fiber bundle region on the temporal side. also, it can't be from a neurologic cause.

Front 76

what is a temporal wedge defect

Back 76

small defect temporal to the blind spot from damage to the nasal disc fibers. they typically do not respect the horizontal midline.

Front 77

notice that glacoumatous field loss (partial arcuate, paracentral, nasal step, temporal wedge) tend to be in EITHER the superior or inferior field. this creates an asymmetry between superior and inferior fields (glaucoma hemifield test). why does this occur?

Back 77

the area of the optic nerve head that tends to be damaged is the area furthest from the central retinal artery truck.

Front 78

what are arcuate scotomas

Back 78

significant field loss in nerve fiber bundle layer. extends across contiguous abnormal points from the blind spot to at least 1 poing outside 15 degrees that is adjacent to the nasal meridian. -you would be able to see the damage to the ONH by the time it gets to this stage.

Front 79

what is an altitudinal field defect

Back 79

severe field loss in one hemifield that respects the horizontal midline. most points in hemifield have P<.05 on total deviation. typically the entire horizontal midline is abnormal. -this is caused by other things besides glaucoma (AION)

Front 80

how would you tell if a longstanding altitudinal visual field loss was due to glaucoma or anterior ischemic optic neuropathy based on the appearance of the optic nerve head

Back 80

longstanding: in glaucoma there would extreme changes to the cup. in AION the nerve would be pale but there would not be changes to the cup.

Front 81

generalized depression in the visual field can be caused by glaucoma, but usually it is from other causes.

Front 82

this is not glaucoma. what is it

Back 82

this is a central defect. the fibers around the macula tend to be spared in glaucoma.

Front 83

this is not glaucoma. what is it

Back 83

quadranopsia

Front 84

this is not glaucoma. what is it?

Back 84

hemianopsia

Front 85

this is not glaucoma. what is it?

Back 85

defect from trial lens

Front 86

what type of defect is this

Back 86

double arcuate

Front 87

what type of defect is this

Back 87

temporal wedge

Front 88

what type of field defect is this

Back 88

nasal step

Front 89

what type of field defect is this

Back 89

partial arcuate

Front 90

how do you tell is a field is significant for glaucoma

Back 90

has to be repeatable AND consistant with a defect caused by glaucoma AND any of the following: 1. a single non-edge point worse than P<0.5% 2. 2 or more adjacent non-edge points that exist at P<5% level, with one of them at P<1% (adjacent is horizontal or verticle, not diagonal) 3. 3 or more adjacent non-edge points existing at P>5% level 4. 2 adjacent points that differ from points across the horizontal midline by at lead 10 dB (nasal step) 5. corrected pattern standard deviation in <5% of normal 6 glaucoma hemifield test not within normal limits -these are very stringent guidelines. they are from the OHTS study, which had very well trained participants. you might have to fudge them a little bit in clinical practice (particularly #1)

Front 91

at about what pupil size will we start to see an overall depression in the visual field

Back 91

3mm and below

Front 92

New lecture: 2GlcAssessST2010

Front 93

corneal thickness has an effect on IOP measurement. the thicker the cornea the higher the measured IOP, but exactly what that relationship is is still under debate.

Front 94

goldmann tonometry was created for corneas of thickness 520 microns. mean corneal thickness is 534 to 554. caucasians tend to have thicker corneas. there is a large amount of variability from individual to individual though.

Front 95

how does the average central corneal thickness compare to normal for pts with normotensive gluacoma and for pts with ocular hypertension

Back 95

normotensive: lower CCT than normal OHT: higher CCT than normal

Front 96

how does corneal size in pts with ocular hypertension effect their risk of developing primary open-angle glaucoma

Back 96

thinner corneas with ocular hypertension show an increased risk of developing POAG in OHTS -remember that this only applies to people with ocular hypertension, we don't know what effect central corneal thickness has on people who don't have ocular hypertension

Front 97

people used to think you needed 10 measurements for accuracy in pachymetry. but studies have shown that you only need to take three measurements to be accurate.

Front 98

it is hard to find any support in the literature that indicates that there is any kind of linear or repeatible effect of corneal thickness change on IOP. the belief is that a thicker cornea will result in higher IOP measurement, but to what extent and how to adjust for that we still up for grabs. picture has plotted measured IOP and corneal thickness. if there was a clear relationship between corneal thickness and IOP you would expect a tighter grouping in this graph. you notice that you do measure higher IOP with increasing corneal thickness, but notice the variability. as it is, it is hard to say exactly how corneal thickness affects IOP measurement.

Front 99

when you see charts for adjusting IOP based on corneal thickness you should take that with a grain of salt. also, there are multiple different methods of conversion. some say subtract 1 mmHg for every 50 microns of thickness. some say 10% change in thickness changes IOP 1-3.5 mmHg. some say change 1 mmHg for every 10 microns. you should realize that increasing corneal thickness does increase measured IOP, but we don't know the exact relationshiop. you are exchanging one false IOP for another flase IOP. the only way we can know the true IOP is by sticking a probe inside the eye.

Front 100

how does diurnal variability of IOP affect the risk of developing glaucoma

Back 100

studies have show that increased diurnal variability of intra-ocular pressure SIGNIFICANTLY increases the risk of developing glaucoma.

Front 101

you should consider measuring IOP at different times of day on glaucom suspects. also, as far a therapy it is importnant that if you rx a drop bid that they actually take it two times a day, because otherwise they are increasing their diurnal variability which is a significant risk factor for IOP

Front 102

what is normal diurnal variation in IOP

Back 102

about 4 mmHg. above 7 is abnormal.

Front 103

name some things that can influence your measured IOP besides corneal thickness

Back 103

1. exercise (increase) 2. repeated tonometry (decrease (pushing on the eye)) 3. apparel (tie can increase) 4. gonioscopy (decrease (same as tonometry)) 5. visual fields

Front 104

tonometry should be used more in the management of glaucoma than in the diagnosis

Front 105

gonioscopy should be performed on all glaucoma suspects when they become a suspect and then yearly. why does it need to be done yearly?

Back 105

because as the lens changes the appearance of the angle can change. you can have a glaucoma pt that you have been managing successfully for years and then all of a sudden they come in and their IOP is up and you change their meds around but that doesn't seem to help, then you check gonioscopy and realize that they now have a narrow angle glaucoma.

Front 106

during gonioscopy don't forget to look at the iris (including the pupillary ruff). how is the iris usually classified on gonioscopy

Back 106

1. concave (wide angle) 2. flat 3. convex (narrow angle)

Front 107

what colors do the ciliary body, scleral spur, trabecular meshwork, and schwalbe's line tend to be

Back 107

ciliary body: dark (usually), light tan scleral spur: white (glisens if you move your light around) trabecular meshwork: white, pink, brown, tan schalbe's line: white

Front 108

how can you tell clinically on gonioscopy where schwalbe's line is

Back 108

if you use a slit and look carefully, the beam will split into two and then join back into one when it hits schwalbe's line. one portion of the light is reflected off the endothelium and one poriton of the light is reflected off the epithelium

Front 109

how do you record for gonioscopy

Back 109

1. pt name 2. date 3. drops used 4. time 5. eye 6. make an X and write the deepest structures you could see in that meridian 7. PAS (peripheral anterior synechiae) 8. record iris approach 9. record the amount of pigment in the TM in all four quadrants

Front 110

good site for learing to recognize gonioscopy: http://www.gonioscopy.org/index.html

Front 111

when we rate the amount of pigment in the trabecualr meshwork it is important to recognize that we are not rating the darkness (color) of the TM, but how many granules of pigment there are in the TM.

Front 112

what structure can the iris processes help you distinguish

Back 112

they tend to point to the trabecular meshwork. not always the case, but can help you find it

Front 113

what is in this picture

Back 113

blood vessels from the major circle of the iris. it is very important to be able to distinguish them from neovasularization (rubeosis iridis) (how to distinguish them is next question)

Front 114

how do you distinguish normal blood vessels of the major circle of the iris (normal) from rubeosis (pathologic)

Back 114

normal blood vessels are large and ropy. neo can be pretty ropy, but along with the ropy blood vessels there is a fine net of blood vessels (net won't be there in normal blood vessels). vessels of the major circle will tend to be circumfrential around the iris; neovascularization tends to follow no pattern at all. normal vessels of the major circle tend to have a "lock ness" appearance meaning that they come up from the iris and then dive back down (like a bunch of half circles). neovascularization will tend to run along the surface of the iris and not dive down into the stroma. finally, with vessels of the major circle, if you look really closely, you will be able to see the glistening of the vessel wall. neovascularization tends to be fine enough vessels that you don't see the wall. neo of the iris can start at the pupil or in the angle. it is very important to be able to distingish between them.

Front 115

optic nerve head evaluation is one of the best tests for assessing glaucoma. even so, the more tests you do that support the diagnosis the better. in most cases tissue is lost in the ONH before there is field loss. the best view is with a goldman contact fundus lens. you need to take pictures though; think about putting a lobster into boiling water and it jumps out, but is you put it in room temp water in a pot and slowly turn up the heat you can boil it. the same is ture with ONH evaluation, changes are so slow that you WON'T see them over time. you need to take pictures so you can compare ONH changes over time.

Front 116

when does the rim tissue end and the cup begin

Back 116

when the contour changes (not the color)

Front 117

what is the normal shape of the optic nerve head

Back 117

oval. vertical greater than horizontal

Front 118

what is the normal shape of the cup

Back 118

round. if elongated it is usually horizontal greater than verticle.

Front 119

what color is the normal rim tissue

Back 119

pink

Front 120

what is the normal size of the ONH

Back 120

verticle: 1.88 mm horizontal: 1.77 mm -normal variation is quite large though.

Front 121

how does ONH size affect CD

Back 121

larger nerve head is associated with larger CD ratio

Front 122

describe the procedure of measuring the ONH with the slit lamp beam

Back 122

adjust the slit lamp beam to a known height and measure it to make sure the measurement device on the slit lamp is calabrated. measure horizontal and vertical disc diameters by adjusting slit beam height. apply the appropriate correction factor for your lens (1.33 for 90D ?)

Front 123

how do you calculate the disc area after you have measured it in the vertical and horizontal directions

Back 123

Horizontal disc diameter X vertical disc diameter X ?/4 = disc area

Front 124

what is an easy but accurate way of comparing the size of the ONH between the two eyes

Back 124

adjust the slit height to the size of one of the ONHs and then move over to the other side without adjusting the height of the beam at all and see if they are the same.

Front 125

how many fibers are there in each optic nerve

Back 125

1.2 million.

Front 126

in glaucoma you are looking for contour changes of the rim, cup and disc vessels and NOT pallor in the center of the disc (that is not important)

Front 127

is thinning of the neuroretinal rim the same thing as notching

Back 127

no. all notching is thinning, but not all thinning is notching

Front 128

what part of the ONH tends to lose ganglion cells first

Back 128

usually superior and inferior first (inferior temporal most frequently). nasal and temporal later in disease. results in vertical elongation (picture).

Front 129

the evaluation of rim tissue thickness is more important than the CD in glaucoma. what is the rim/disc ratio and how do you evaluate it in each quadrant

Back 129

-rim/disc: the distance between the edge of the cup and the edge of the disc Determined rim/disc ratio in each quadrant Needs to add up to 1.0 with C/D ratio in each meridian Allows increased sensitivity in noting change

Front 130

you can double check your CDs by estimating rim/disc ratios in each quadrant and seeing if they add up to 1 in each meridian

Front 131

can you use the rim/disc values to make an inference about wheather the ISNT rule is met or not

Back 131

no. the disc may have a total diameter that is different in the vertical and horizontal directions. since these values are a ratio you can't compare one meridian to the other.

Front 132

what is this graph telling us

Back 132

on the vertical axis we have the smalles rim/disc ratio and on the horizontal axis we have the diameter of the disc (in the meridian of the smallest rim/disc ratio). it indicated the likihood of glaucomatous damaged (as you can see the larger the diameter the smaller the rim/disc ratio that is considered normal). you should take graphs like these with a grain of salt, because most temporal rims are very thin if you look at contour and most of these graphs were made when they were looking at color. these graphs are not really useful, it should just remind us that as we have a larger disc diameter a smaller rim/disc ratio is acceptable. if you do try to use it clinically you should probably ignore the temporal rim.

Front 133

what value for the horizontal CD over the vertical CD is normal

Back 133

greater than 1 (1.15-1.19 typically). only 7% of normals have value of less than 1. usually if it is less than one you can find some reason for it like malinserted disc or odd shaped nerve head.

Front 134

careful evaluation of the vessels of the ONH can help you detect subtle glaucomatous changes.

Front 135

where is the central retinal artery trunk located in the majority of people

Back 135

superior nasal is the most common position

Front 136

what is the significance of the location of the central artery trunk

Back 136

the area of the ONH that is farthest from the CRA trunk is most likely to experience rim tissue loss first in glaucoma -2 theories as to why: mechanical support from the trunk prevents blockage of axoplasmic flow. or they could be getting nutrients from the CRA trunk

Front 137

when do you see diffuse arteriole narrowing

Back 137

found in most types of ONH damage, not just glaucoma

Front 138

look for shifts in vessel position on the ONH; the tissue that was once supporting them is no longer there. they can serve as a sensitive marker in photos.

Front 139

give two names for the hemorrhage near the ONH commonly associated with glaucoma

Back 139

splinter hemorrhage, drance hemorrhage

Front 140

name some causes of splinter hemorrhage

Back 140

glaucoma, posterior vitreous detachment, resolving branch retinal vein oclusion, diabetic retinopathy

Front 141

what shape are splinter (drance) hemorrhages

Back 141

flame-shaped when just off the ONH. blot-like when on the disc

Front 142

what location on the ONH are splinter (drance) hemorrages from glaucoma most likely to occur? why?

Back 142

inferior pole. central retinal artery trunk most likely in superior half

Front 143

example of a drance hemorrhage

Front 144

what other ONH sign is typically associated with drance hemorrhages DUE TO GLAUCOMA

Back 144

usually associated with an area of notching underneath them after they resolve. (if due to other conditions there is usually no such damage)

Front 145

how long does it typically take for a drance hemorrhage to resolve

Back 145

10 weeks (2-35 weeks; since they are asymptomatic there is not way to know how long they have been there when we first see them)

Front 146

do drance hemorrhages tend to recur

Back 146

it is farily common for them to recurr in the same spot after about 6 months. it is more common for this to happen in normotension glaucoma than primary open-angle

Front 147

what is the prognosis associated with drance hemorrhage

Back 147

poorer prognosis (if due to glaucoma and not some other factor like PVD). strong indication for intervention if you are not treating or increased intervention if you are.

Front 148

peripapillary pigmentary changes indicate an increased risk of glaucoma. this is atrophy (not scleral or choroidal crescent). cause a mottled appearance to the RPE seen around the disc.

Front 149

what is the peripheral alpha zone and the central beta zone

Back 149

-peripapillary pigmentary changes peripheral alpha zone: start of peripapillary pigmentary changes seen as a darkening and irregularity to the pigment (hyper and hypo pigmentation). it tends to touch or be in contact with normal retina central beta zone: as time progresses alpha peripapillary atrophy tends to get worse. if atrophy get so bad that we lose all pigmentation and we have a white coloration. beta is worse. -also known as alpha and beta peripapillary atrophy?

Front 150

how does beta peripapillary atrophy differ from a scleral crescent in appearance

Back 150

beta atrophy does NOT have smooth boarders; they are less well defined. (picture is beta). also color is not a nice clean white in beta atrophy as it is in a scleral crescent. also beta progresses from alpha atrophy.

Front 151

do you ever see alpha or beta peripapillary atrophy in normal eyes

Back 151

it is very common to see alpha peripapillary atrophy on the temporal side of ONH in normals. but it is quite UNcommon to find beta peripapillary atrophy in normal eyes.

Front 152

beta peripapillary atrophy is usually found in advanced damage and is often associated with rim loss in the same quadrant.

Front 153

what causes beta peripapillary atrophy

Back 153

we dont' know for sure, but we think it has to do with ischemia in the nerve fiber layers of the retina in that area. fluorescein angiography shows poor choriocapillaris perfusion in the area of beta atrophy.

Front 154

are acquired pits of the ONH due to glaucoma common or uncommon

Back 154

pretty uncommon

Front 155

in what type of glaucoma are acquired pits of the ONH most common

Back 155

more common in pts with normal tension glaucoma

Front 156

what are acquired pits of the ONH

Back 156

sharply localized depressions of lamina cribrosa due to loss of laminar architecture.

Front 157

do acquired pits of the ONH tend to be larger or smaller than congenital pits

Back 157

acquired pits tend to be smaller

Front 158

where do acquired pits of the ONH tend to be localized

Back 158

usually found in outer edge of disc. most likely in inferior temporal quadrant (farthest from central retinal artery trunk). -then tend to be white in appearence like in this picture.

Front 159

how can you tell the difference between an acquired and congenital ONH pit based on appearence

Back 159

acquired: white in color, smaller, rounder congenital: more grey in color, larger, not round

Front 160

is this a congenital or acquired optic pit

Back 160

looks more like a congenital (and it is)

Front 161

are congenital pits of the ONH relatively common or rare

Back 161

relatively common

Front 162

what is the white ring around the outside of this ONH

Back 162

a scleral ring (not called a scleral crescent). most people have it to some degree or another. you should NOT include it when you are measuring the CD ratio.

Front 163

this is definately notching inferiorly

Front 164

New lecture: 3GlcAssessST2010

Front 165

describe the normal appearance of the nerve fiber layer

Back 165

casts a whitis haze over underlying retinal structures. we are seeing reflections off the bundles of the NFL

Front 166

how can we get an idea of the thickness of the nerve fiber layer with high plus or BIO and why is that important

Back 166

the brighter the reflections the thicker the NFL. we expect the reflections to be equal between between the inferior and superior archades AND to be equal between the two eyes

Front 167

we expect nerve fiber layer to be thick enough that it covers smaller blood vessels when you are looking at it with high plus or BIO

Front 168

what is the best way to see the nerve fiber layer

Back 168

BIO with the red free filter. you have a larger field of view and that is important for seeing overall differences in brightness or any defects. BIO is preferable over high plus. -you need to use pretty high illumination which will be uncomfortable for the pt, but you need to do it to see the NFL otherwise you might as well not do the technique

Front 169

how does the color of the fundus affect your ability to see the nerve fiber layer

Back 169

the lighter the fundus the harder it is to see the nerve fiber layer.

Front 170

name the types of glaucomatous defects are you looking for when you examine the nerve fiber layer

Back 170

1. slit defect 2. wedge defect 3. diffuse atrophy

Front 171

what causes a slit defect

Back 171

retrograde degeneration of the ganglion cell axons back to the cell body in the retina

Front 172

what do slit defects look like

Back 172

dark slits about the size of an arteriole that travel back to the disc

Front 173

what type of nerve fiber defect is this

Back 173

superior is a slit defect. inferior is a wedge defect

Front 174

how common is it to see a slit defect in a normal person

Back 174

can be seen in up to 10% of normals (but raises level of suspicion of glaucoma)

Front 175

what is a wedge defect

Back 175

an expanding loss of ganglion axons in the same area of the optic nerve. wedge shaped, they are more narrow as they get toward the optic disc and widen out as they go away.

Front 176

what is the most common type of nerve fiber layer defect? what is the least common?

Back 176

most common: diffuse atrophy least common: wedge defect

Front 177

there is usually corresponding visual field loss with wedge defects; they are helpful to confirm glaucomatous damage, but they are often not the first sign. easiest to see, but the least common pattern

Front 178

what is the hardest type of glaucomatous damage to the NFL to see clinically

Back 178

diffuse atrophy

Front 179

in what type of glaucoma is diffuse atrophy more common

Back 179

high tension glaucoma

Front 180

what is diffuse atrophy

Back 180

atrophy to the NFL that occurs in the superior and inferior arcades. it appears as a decrease in the light intensity that is reflected back when we are looking at the NFL clinically. this is hard to recognize and is why it is important to know what normal brightness should be for differently pigmented retinas. sometimes you get an apperance like someone has drug a rake or a comb through the retina, but often times you don't. (picture is mild-moderate diffuse atrophy. notice that there is not a difference in light intensity between the superior and inferior arcades. also notice that you can see even the small blood vessels because the reflection is not too bright for you to see them).

Front 181

what is nerve fiber layer reversal

Back 181

in advanced diffuse atrophy you can have a pattern reversal (nerve fiber layer reversal) where the papillomacular area becomes brighter than the superior and inferior arcades.

Front 182

what other objective retinal signs are associated with diffuse atrophy

Back 182

1. thinning of corresponding neuroretinal rim 2. small, ordinarily indistinct vessels become visible 3. depressed level of green light reflection from the retina 4. diffuse depression or constrinction of corresponding field

Front 183

if you think you have diffuse atropy of the NFL you need to compair one eye to the other. you need to look at the NFL of one eye right after the other and go back and forth between the two eyes. (don't do BIO on the second eye before you look at the NFL if you have looked at the NFL last on the first eye)

Front 184

name four nerve fiber analyzers

Back 184

Stratus Optical Coherence Tomographer (OCT III) Heidelberg Engineerings Retinal Tomograph (HRT 3) Laser Diagnositic Technologies GDx Talia/Marco: Retinal thickness Analyzer (RTA) One study showed reproducibility highest in the following order (reproducibility doesn't necessarily mean that your findings are accurate, just that they are the same every time) GDX, HRT, OCT (RTA not tested) -each of them has grown to become more like the others over time.

Front 185

to become good with a nerve fiber analyzer you need to become very familiar with one type of instrument and work with that instrument exclusively

Front 186

most studies show that nerve fiber analyzers have similar sensitivities and specificities, but that they are all better at diagnosing moderate glaucoma than early glaucoma. the best reason to have a nerve fiber analyzer is to monitor the same pt over time. not useful for monitoring late glaucoma because there is not enough nerve fiber left to be useful. they are NOT to be used as a single test to diagnose glaucoma. they tend to match ONH findings more than visual fields. they provide objective information (observation with BIO is really subjective estimation). they cost $60,000-$100,000 each. you need repeatable tests for them to be considered reliable. some require operator skill to set ONH boarders.

Front 187

what is the reference plans (in reference to nerve fiber analyzers)

Back 187

how it determines where the cup is. it says that anything farther than a set distance (50 microns in the picture) from the top of the nerve fiber layer is part of the cup. -if you have a slowly sloping cup then you will estimatie it differently with high plus than the instrument will assess it (if there are steep boarders you and the instrument will agree, if there are very slowly sloping boarders you and the instrument will disagree)

Front 188

why is 50 microns used as the reference plane in many of the nerve fiber analyzers

Back 188

they did monkey studies and the average thickness of the papillomacular nerve fiber layer in monkeys was 50 microns.

Front 189

glaucoma decreases NFL thickness, so reference plane may change with time. so, as the fibers get thinner the reference plane drops; so even if the cup were getting larger the instrument might measure it as no change.

Front 190

how does the OCT set its reference plane

Back 190

it finds the level of the bottom of the NFL and sets the reference plane 150 microns up (inner). (this is a more stable baseline than measuring it from the top)

Front 191

how does the OCT measure the retina

Back 191

uses echo delay time of light returned from layers of the retina. similar to ultrasound but using near infrared light. then uses a computer to create a 2-D cross section of the ocular tissue.

Front 192

describe the normal database of the OCT

Back 192

has about 300 pts and about 80% of them are caucasian. it is age adjusted. showed glaucoma as decreased thickness in NFL usually in interotemporal and superotemporal

Front 193

what do the TSNIT graphs tell you in this OCT printout

Back 193

the black line is the pts NFL thickness. if the black line is within the green section then they are considered normal as compared to their database.

Front 194

what is the most useful way to use the OCT

Back 194

retinal nerve fiber layer thickness serial analysis report. compares the NFL thickness on a single pt over a period of more than one visit. allows you to monitor changes in the NFL thickness.

Front 195

OCT was origionally designed to look for elevations in the nerve fiber layer; but since glaucoma analysis is so important they adapted it to look at thinning as well.

Front 196

how does the HRT measure retinal nerve fiber thickness

Back 196

uses confocal scanning laser (makes light parallel before they send it into the eye) to measure ONH and NFL height. (because lihgt is parallel, they can measure through a very small pupil). multiple images at different depth are reconstructed by a computer which allows for a 3-D map to be made. allows manipulation of image

Front 197

what is the HRT's "claim to fame"

Back 197

how well it analyzes the optic nerve head.

Front 198

HRT depends on subjective placement of contour line for analysis that looks at the ONH. it has a whole pamphlet on how and where to place the line and it makes a big difference in the analysis where it is placed. however, it uses the same placement each time you do the test on an individual (this could be bad if the inital line was not place well, but allows you consistancy on serial analysis). -the newer HRT does NOT rely on subjective placement of the contour line. the instrument determines this on its own (this is considered to be an advantage).

Front 199

describe the database for the HRT

Back 199

excellent age matched norms: >700 caucasians >200 african origin >100 southeast asian -hispanic and asian database in process -it does consider ethnicity when doing analysis

Front 200

for the HRT what value is considered to be a good quality image

Back 200

anything below 30

Front 201

how does the GDx measure NFL thickness

Back 201

uses confocal scanning laser polarimeter. indirectly measures NFL thickness by measuring the slowing of light after it passes through the retinal nerve fiber layer twice. it uses a mathmatical model to calculte retinal thickness (indirect measurement, not direct; this does NOT use a reference plane)

Front 202

pts eyes can not be dilated for GDx

Front 203

describe the norm database for the GDx

Back 203

540 normal eyes, 271 abnormal eyes (does not correct for ethnicity)

Front 204

GDx comes up with a number which according to the manufacturer indicated risk of glaucoma Higher number indicates increased risk 0-30 = normal, 31 – 70 = suspect, 71 – 100 = glaucoma however, there is enough variability that you can only go by the category that a score places you in. for instance if you have a score of 26, you can infer that this is normal, but statistically you can NOT infer that they are at any more risk than a person with a score of 1. don't rely on the number, just analyze the data yourself (lots of normal variations can influence these numbers; tilted disc for example).

Front 205

if the vessels bifricate early it is possible for a nerve fiber analyzer to pick up the depression inbetween them as thinning.

Front 206

how do you assess quality of an image on GDx

Back 206

Q: equals quality value. range is from 1-10. 10 is the best.

Front 207

how does the RTA measure retinal thickness

Back 207

it is a scanning laser ophthalmoscope. it uses a helium neon laser beam bounding off the retina to determine the depth between the NFL and the RPE. considers this difference the NFL thickness. (values can be influenced by corneal curvature) -it can map the optic disc, the posterior pole and the peripapillary region.

Front 208

what is the major difference between the RTA and the other NFL analyzers

Back 208

advocates use of the macular fiber depth for early glaucoma detection.

Front 209

why does the RTA advocate looking at the macular for early glaucoma detection

Back 209

since the central 20 degrees of the macula contains 50% of the retinal ganglion cells, and because we know that the ganglion cells are affected early in glaucoma we should be looking at the macula for early detection (there is good support for this theory) -they look at the disc too

Front 210

OCT: needs dilation. norm data exists. there's no subjective countour line. HRT: small pupil is okay. better normal database. can do statistical analysis to compre to self (changes over time) GDx: no dilation. there is no reference plane. more intuitive to evaluate printout. RTA: looks at the macula. allows statistical analysis for change over time.

Front 211

recommendations on scanning lasers from Dr. Lingle: if you have a big co-management practice where you are doing a lot of surgical evaluation you might chose an OCT because it looks for glaucoma but it is also very good at looking for macular edema from cystoid macular edema after surgery. it would also be good if you had a big diabetes practice because it looks really nicely at retinal thickness. if you have a general practice that is not heavily into any of those areas you might want an GDx because it is simple and easy and your tech can do it without any formal training and no dilation is needed, so it is a good screening tool. if you were really big into glaucoma you might want an HRT because of the ethnic backgrounds diversity in the normal database. it is most important to get used to one and to know its nuances and evaluate the data it gives you, not just look at wheather the instrument tells you they have glaucoma or not.

Front 212

ocular blood flow analyzers analyze the blood flow to the ONH for evaluation of glaucoma. they are not mainstream yet and are only used in reasearch settings at this point.

Front 213

certain medicare pts do have the right to have a glaucoma screening every year at no charge to them. we need to be aware of this. it is a dilated eye exam with IOP measurement and either a direct ophthalmoscopy exam (not a good idea) or a slit lamp exam using high plus. people who are considered high risk are eligable for this. they are:

Back 213

1. diabetics 2. those with family history of glaucoma 3. african americans age 50 or older 4. hispanic americans age 65 or older -you have to be on medicare to be eligable for this

Front 214

New lecture: 4POAGMngmntst2010

Front 215

name some goals for the tx of glaucoma

Back 215

1. maintain usable vision for the rest of the pts life 2. maintain pts quality of life (psychological (just telling a pt they have glaucoma has been shown to decrease quality of life), physical, financial) 3. do no harm

Front 216

the decision of wheather or not to tx glaucoma is not cut and dry: 16% of POAG have normal IOP. furthermore, there are estimated to be 10 million ocular hypertensives and OHTS has shown that 9.5% develop nerve damage in 5 years.

Front 217

the effectriveness of treatment of glaucoma is not cut and dry either. studies vary in results. all tend to show that treatment helps SOME pts. some studies find a correlation between IOP and progression and some do not. IOP is the only risk factor that we can really treat at this time.

Front 218

what is the collaborative normal tension glaucoma study and what did it show

Back 218

140 eyes of 140 pts. 61 treated 79 untreated. these were people withOUT ocular hypertension who were already determined to have glaucoma for some reason. 35% of control eyes and 12% of treated eyes showed continuing glaucomatous damage (they already thought these people had glaucoma and it wasn't due to IOP; even in the people they chose not to treat 65% did not progress). they were pretty agressive in their treatment (30% IOP reduction for normotensive glaucom).

Front 219

what did the ocular HTN treatment study show about the treatment effectivness of glaucoma

Back 219

goals for treated pts were to decrease IOP by 20% or down to 24 mmHg, whichever was lower. 4.4% of the treated group developed POAG in 5 years and 9.5% of the non-treated group did. (the drug companies took this and said that treatment can prevent development of glaucoma in 50% of pts. realize that 90% of them would not have developed glaucoma anyway). we don't know what happens after 5 years. Proves that treatment helps, but that a lot of people aren't going to progress anyway.

Front 220

what did the Hattenhauer study published in 1998 show us

Back 220

attempted to determine probability of developing legal blindness in either one or both eyes from newly diagnosed and treated open angle glaucoma. it was retrospective and looked at 295 pts diagnosed between 1965 and 1980 with a mean follow up of 15 years. they were treated with either medical, surgical or both. these were all pts who were being treated: 27% went blind in one eye and 9% in both eyes. it is important to realize though that in 1955 we had one medication for treating glaucoma and it wasn't particularly effective or conducive to compliance. although we are more effective at treating IOP we are still only treating this one risk factor and it was shown to only be effective in some people.

Front 221

what did the Kwon study published in 2001 tell us

Back 221

take home on this one: for most patients on standard glaucoma therapy, rate of VF loss in open angle glaucoma is slow but unrelenting. looked at 40 eyes of 40 pts and followed them for at least 8 years (mean of 14). it showed 68% had decreased visual field. five eyes became legally blind. cumulative rate of blindness from glaucoma was 19% at 22 years. higher IOP was associated with an increased loss.

Front 222

what did the early manifest glaucom trian (EMGT) tell us about glaucoma treatment

Back 222

attempted to evaluate the effectiveness of reducing IOP in early previously untreated open angle glaucoma and understand the role of IOP and natural hx of glaucoma. 255 pts aged 50-80 with EARLY glaucoma. treated with trabeculoplasty plus topical betaxolol bid or not tx at all. results: average IOP reduction was 25%. progression found in 45% of treated and 62% of controls. progression occurred on average at 66 months for treated and 48 months for control. But they noted a significant side effect of increased incidence of cataracts in treated pts (what we would expect for either surgery or beta blocker). on average for every 1 mmHg drop in IOP there was a 10% reduction in risk of glaucoma progression. (one of the more positive studies in terms of IOP correlation to progression).

Front 223

what did the advanced glaucoma intervention study tell us about glaucoma treatment

Back 223

looked at 586 glaucomatous eyes separated into groups based on IOP after treatment with ALT or trabeculectomy. looked at worsening of visual fields. seperated into two groups eyes with IOP less than 18 at 100% of visits over 6 years and eyes with IOP less than 18 for 50% of visits. <18 100% of the time had almost completely stable visual fields. <18 50% of the time had definite worsening of visual fields. suppots idea that IOP level is related to loss of visual field -supports idea that stability of IOP is important

Front 224

summary of glaucoma treatment study outcomes: we know that it is a chronic disease. at best we can stabilize visual function. disease progression is variable among patients with some patients never progressing and some progressing even with treatment. our treatment of the risk factor of IOP MAY slow progression. the level of IOP reduction must be individualized for the pt

Front 225

when should you begin treatment for glaucoma

Back 225

1. when IOP exceeds 30 mmHg 2. changes in ONH, NFL or visual field (make sure they are consistent with each other, and that they are consistent with glaucoma) 3. possible if the pt requests initiation of therapy 4. if pt demonstrates vascular changes (vascular occlusion, drance hemorrhage) 5. when risk factors outweigh equivocal findings

Front 226

point system for determining the appropriatness of treatment in glaucoma. have to consider current meds available and side effects, cost, life expectancy is hard to estimate and system represents aggressive treatment. 7 points or more is appropriate to treat 3 points or fewer is inappropriate to treat. there are other point systems.

Front 227

the more initial glaucomatous damage you see the more aggressive therapy you should use. (it is like spraining an ankle; once there is damage there is more likely to be damage in the future)

Front 228

describe the stages of primary open angle glaucoma. -not the best classification system clinically because there is so much variability in glaucoma. but they are AOA guidelines and could hold up in court.

Back 228

1. mild if they have ANY of the following: mild concentric narrowing or partial localized narrowing of the neuroretinal rim, disc hemorrhage (from NO other cause), asymmetry between the two eyes in terms of ONH appearance, nerve fiber changes (less bright reflex, fine striations, large retinal blood vessels clear), visual field (isolated paracentral scotomas, nasal depression or step, diffuse depression (mean deviation)) 2. moderate if they have ANY of the following: concentric narrowing of the ONH rim, increased area of central disc pallor, loss of neuroretinal rim in one quadrant, focal notching of rim, vessel undermining, NFL changes (minimal reflex brightness, all vessels clear), visual field changes (complete arcuate scotoma in at least one hemifield) 3. severe if: complete absence of the neuroretinal rim in at least 3 quadrants, vessel bayonetting, markedly increased central disc pallor, NFL changes (all vessels clear, dark reflex), visual field changes (complete arcuate scotoma in both hemifields with 5-10 degree central island of vision)

Front 229

the AAO has different guidelines for staging of glaucoma

Front 230

what is vessel undermining

Back 230

the shape of a vessel on the ONH has changed because it has lost tissue underneath it.

Front 231

what is vessel bayonetting

Back 231

where there is a vessel that appears to go underneath the rim of the ONH

Front 232

general considerations for selection of target pressure

Back 232

Consider all risk factors Consider current level of damage and rate of progression Consider presenting IOP Consider patient age Consider medical history No set amount or "established" target Will need to be re-evaluated constantly Generally try to decrease IOP 20- 50%

Front 233

what is a target pressure

Back 233

your first best guess at what you think is going to be necessary to prevent progression of glaucoma -if you don't meet your target and they don't have progression that is fine. if they meet your target and do have progression you need to change it. (remember some pts will progress regardless of what target you set) -if you don't meet your target pressure you can't just say oh well, you need to do what it takes to lower them if you can

Front 234

what are the recommended target pressures from evidence based studies

Back 234

1. ocular hypertension with risk factors: decrease 20% (OHTS) 2. visual field loss or ONH notching: decrease 30-35% (collaborative normotension treatment study 3. extreme visual field loss or cupping: decrease 50% (AGIS) -AAO has guidelinse of it's own. they are pretty similar, but suggest that you lower 20% or <20mmHg, which ever is a larger reduction.

Front 235

true notching of the ONH is NOT an anatomical variation you would expect to see. it would almost always be due to pathological changes.

Front 236

what are is target IOP based on Cole/Lewis in review of opt.

Back 236

take the initial IOP and reduce it by the percent of whatever the raw IOP was in mmHg Original IOP of 20 mmHg: Decrease IOP by 20% Original IOP of 30 mmHg: Decrease IOP by 30% Generally considered minimum reduction Doesn’t consider severity of damage or other risk factors

Front 237

what are the target IOP guidelines base in Jampel

Back 237

Target IOP = Maximum IOP- Maximum IOP% (same as cole/lewis) -Z Z = optic nerve damage severity factor 0 = normal ONH and VF 1 = Abnormal disc and normal VF 2 = VF loss not threatening fixation 3 = VF loss threatening or involving fixation

Front 238

which method of estimating target IOP is the most aggressive

Back 238

Hartelben (by far)

Front 239

describe the hartelben method of target IOP estimation

Back 239

Target = IOP – IOP% - MD on visual field

Front 240

for setting target IOP most people do calculations using more than one method and then make adjustments based on other risk factors, level of damage, pts expected life span and clinical judgment. remember that you will constantly need to be re-evaluating your target IOP based on how it is controlling progression.

Front 241

calculate target IOP base on evdence based data, AAO, Cole/Lewis, Jampal, and Hartelben guidelines for the following case: 58 yo male with 28 mmHg IOP with possible thinning of inferior rim and possible but not statistically significant paracentral scotoma in superior visual field with a MD of -5 dB

Back 241

Evidence based: 22 AAO: 20 (everyone should be 20 or less) cole/lewis: 20 Jampal: 19 (cole/lewis - 1mmHg; this one is debatable) Hartelben: 15

Front 242

New lecture: 5POAGMngmnt2010stwpics

Front 243

how should you decide what treatmet to start with for management of glaucoma

Back 243

1. start with medications (in US; in europe they start with surgery) 2. start with safest drug (often pts have contraindications to all the drugs and you have to chose the least offensive one) 3. efficacy 4. factors influencing compliance (drops per day, price, side effects) 5 start with lower concentration (why use higer if lower will work) 6. as few medications as possible 7. uniocular trial

Front 244

target pressures should always be set for each eye individually

Front 245

what is the problem with uniocular trials

Back 245

a lot of drugs will lower IOP in both eyes some amount even if you only put the drop in one eye (particularly beta blockers).

Front 246

you should use a sample medication if one is available until you are convinced treatment is effective (usually 2-3 weeks). about 1/5 of people just won't respond to a particular drug, or class of drugs. so you don't want them to go and pay for the medication unless you know that it is going to work.

Front 247

you should rx the largest bottle available for glaucoma meds. studies show that pts waist about 1 out of 3 drops because they don't know how to instill them properly, so if you rx a small bottle they will run out before they are eligable to get another bottle.

Front 248

you should tell the pt about side effect that are either very common or very severe because they need to know about these. but realize that when you mention a side effect to a pt they are more likely to think that they have it.

Front 249

do oral beta blockers used for some other systemic condition lower IOP

Back 249

yes. it is considered inappropriate to rx topical beta blockers if a pt is on oral beta blockers because you will not get much effect out of them.

Front 250

there is a program on word that will tell you what grade level whatever you have typed is at. realize that the average person in the US is at a 5-6th grade reading level and that even the simplist medical literature is at a 12th grade level. when we are writing out medication instructions we need to make sure that it is simple enough for the average pt to understand.

Front 251

the glaucoma research foundation makes excellent pamphlets to give to pts for education on glaucoma

Front 252

it is a good idea to attach eye drop schedule to something that the pt does in their dialy routine: one in the when get up in the morning and one when you bruch your teeth at night.

Front 253

can pts put more than one glaucoma drop in there eyes back to back

Back 253

no, they need to space them out by at least 5 minuets.

Front 254

you should teach your pts how to put drops in their eyes if you are rxing glaucoma drops. also, punctal occlusion has been shown in the literature to significantly reduce systemic side effects even if it is just for 1 minute (2 is better) and to increase increases amount of medication that gets to the eye.

Front 255

you should always have your glaucoma pts bring their drops in with them for their exam. you need to make sure that they are taking the right drop on the right dosing schedule and they won't remember the names, so you won't know if they are doing it right unless they bring in the bottles so they can show you.

Front 256

it is important how you word things when warning the pt about taking medications. if you tell them that if they don't take the med the will lose their sight, then every time they take the drop they will think about going blind. but if you say if more positively, like these drops will help you keep their sight, then they will think about keeping their sight when they are taking their drops.

Front 257

what are the AOA guidelines for glaucoma follow up for mild, moderate and severe cases

Back 257

mild/moderate: follow every 2 weeks until target pressure reached severe: follow every 1 week until target pressure reached -follow up is less often after target pressure is reached (look it up) -AOA guidelines are pretty strict. after you get more experienced you can decide for yourself; but if you follow them you definitely won't get sued

Front 258

what do you do at a glaucoma follow up

Back 258

IOP (evaluate target), fields, and lot of education, history (compliance, side effects, changes in meds or general health), VA, blood pressure, pulse and lung copacity, Biomicroscopy (glaucoma meds are suggested to cause ocular surface disease and allergy), gonioscopy (yearly) -won't be doing dilation or GDx on every follow up visit

Front 259

we tend to have pts put prostaglandins in at night because they have their peak effect about 8 hours after instillation and we want the peak effect in the morning. so it would make sense to have them come in late in the day and not early in the morning because you want to see what IOP is when the drop is not working its best, not when it is.

Front 260

if you rx lotanoprost you can look for thinkening of the lashes as a sign of compliance

Front 261

for glaucoma follow ups you want to get an idea of the stability of IOP, so it makes sense to have them back at different times of the day to get an idea of diurnal variation of IOP

Front 262

all glaucoma drugs have a "honeymoon" period where they lower IOP a certian amount initially, but then there effectiveness goes down slightly over time (very slowly). it is a good idea to have a graph or a chart that looks at their change in IOP over time.

Front 263

what is a reverse uniocular trial

Back 263

you take a pt off drops on only one eye and see if the pressure in that eye is worse than baseline (to look for progression).

Front 264

for glaucoma follow up you need to do the same type of visual field each time (if you start with SITA standard, you need to do SITA standard on each of the follow ups)

Front 265

how often should you dilate a person you are following for glaucoma

Back 265

yearly unless unstable.

Front 266

name some indications of a need to change glaucoma treatment

Back 266

1. poor medication tolerance 2. optic nerve head changes 3. higher than desired IOP 4. visual field changes

Front 267

what are you looking for in a visual field to indicate that the pt is progressing (general)

Back 267

1. a new defect in a previously normal area 2. deepening of a pre-existing defect 3. expansion of a pre-existing scotoma into contiguous points 4. generalized depression (could be caused by other things) -make sure that changes are consistant with what you would expect from glaucoma

Front 268

STATPAC have a couple different ways of comparing serial visual fields

Front 269

every computer system that looks for progression tends to use the same guidelines to determine progression. what are the guidelines for a new defect in a previously normal area

Back 269

1. a cluster of 3 or more nonedge points, each of which declines greater than or equal to 5 dB compared to baseline on two consecutive fields OR . . . 2. a single non edge point that declines greater than or equal to 10 dB compared to baseline on two consecutive fields OR . . . 3. a cluster of 3 or more nonedge points, each of which declines p <5% level compared to baseline on two consecutive fields.

Front 270

what are the guidelines for deepening of a pre-existing defect to determine progression of a visual field

Back 270

1. a cluster of 3 nonedge points, each of which declines greater than or equal to 10 dB compared to baseline on two consecutive fields. the confirming points may differ if they are part of contiguous cluster OR . . . 2. a cluster of 3 nonedge points, or 3 point that are part of the same scotoma, each of which declines at least 5 dB and is compared to baseline at p<5% level on two consecutive fields. the confirming points may differ if they are part of a contiguous cluster.

Front 271

what are the guidelines for expansion of a pre-existing scotoma to determine progression of a visual field

Back 271

1. at least 2 previously normal points withing the central 15 degrees or three additional previously normal points outside 15 degrees, each of which declines greater than or equal to 10 dB each on two consecutive fields OR . . . 2. at least 2 previously normal points withing the central 15 degrees or three previously normal points outside 15 degrees, each of which is depressed at a p<0.5 level compared to baseline on two consecutive fields.

Front 272

what are the guidelines for generalized depression to determine progression of a visual field

Back 272

1. a decline in the mean deviation that is significant at the p<1% level and is not explained by media opacity or pupil size 2. a CPSD that shows an obvious trend based on at least five consecutive fields OR . . . 3. a decline of greater than or equal to 3 dB at all points on two consecutive fields that is not explained by media opacity or pupil size

Front 273

if your treatment is not effective the first thing you should consider is that the pts was not compliant. it is very difficult to predict who will and who will not be compliant

Front 274

New lecture: 6POAGMngmnSTt32010

Front 275

there is a word document titled "Glaucoma Meds Side Effects" in the ocular disease IV folder that has a chart with the important side effect and contraindications to the glaucoma medications. this is very important.

Front 276

if you are going to rx a medication that has as one of the side effects or contraindications anything to do with heart or lungs you need to check blood pressure, pluse rate and evaluate the lungs (forced expiratory volume) before you rx the medication.

Front 277

what types of allergies tend to react with cardonic anhydrase inhibitors

Back 277

sulfa allergies

Front 278

a lot of times older pts will have contraindications to all the glaucoma meds. so we need to determine which one will have the least negative impact or if the risks outweigh the benefits.

Front 279

what drugs do we typically rx first for glaucoma

Back 279

a prostaglandin analog, or a beta blocker

Front 280

what is the dosing schedule (and timing) for prostaglandins

Back 280

given once a day at bedtime

Front 281

what is the dosing schedule (and timing) for beta blockers

Back 281

either once a day in the morning, or bid

Front 282

how would you decide if you want to start out a glaucoma pt on a prostaglandin analog or a beta blocker

Back 282

consider things like which is covered by their insurance. if they are using it in only one eye prostaglandins tend to change the color of the iris and most people don't like having each eye a seperate color. also consider contraindications

Front 283

which is more expensive prostaglandins or beta blockers

Back 283

prostaglandins are definately more expensive (however one of the prostaglandins is going to become a generic in march of 2011)

Front 284

if you are rxing a beta blocker for first line care of normotensive glaucoma which drug do you need to use and why

Back 284

betaxolol; it is a selective beta blocker and selective beta blockers don't reduce blood flow to the ONH like non-selective beta blockers do

Front 285

what should your next move be if your target pressure is not met after rxing a first line drug (prostaglandin, beta blocker) for glaucoma treatment

Back 285

increase the concentration if available (prostaglandins often only come in one concentration because they are not more effective if you increase concentration)

Front 286

are there any circumstances where it is okay to give a prostaglandin analog twice a day

Back 286

no, there effectiveness actually decreases if you give them too high a concentration. since they are give qd you don't EVER want to rx them more often than that.

Front 287

what should your next move be if your target pressure is not met and you have already tried increasing the concentration of the medication

Back 287

try switching to a different medication. you could change classes, but sometimes switching to a different drug in the same class will cause the pt to respond better.

Front 288

what is your next move if you've tried increasing the concentration of your first line drug (prostaglandin, beta blocker) and you've tried switching to another drug or the other class (or both are contraindicated)

Back 288

consider switching to a combo med or brimonidine

Front 289

combination glaucoma drugs are good for compliance, but they are more expensive

Front 290

what is your next move in glaucoma tx if you have tried all your options and can't reach target IOP with a single medication

Back 290

some recommend last tx at this point. some suggest going to a 2nd drug before surgery. -the concern is that laser therapy can diminish efficacy of future meds and become less effective with time.

Front 291

describe the process of chosing a second drug for glaucoma therapy

Back 291

prostaglandins and beta blockers tend to work well together because beta blockers decrease production and prostaglandins increase outflow (different mechanisms). you could also go with a combo drug (usually have two different mechanisms). if prostaglandin is used and beta blockers are contraindicated you could add brimonidine or dorzolamide or brinzolamide.

Front 292

if you add a second glaucoma medication WILL you get and additional drop in IOP that is equal to what it would be if the drop was used alone?

Back 292

no; you will get less and less of an effect with each additional drop you add.

Front 293

name the surgical options for tx of glaucoma

Back 293

1. laser: SLT and ALT 2. microsurgery: trabeculetomy with bleb, canaloplasty, filtration devices, trabectome 3. cyclo-destructive procedures (destroyes part of the ciliary body)

Front 294

what did the advance glaucoma intervention study show us about which surgery was the best first surgery for glaucoma and why

Back 294

in african americans ALT best surgery. in caucasians trabeculectomy best 1st surgery. darker pigmentation increases the effectiveness of the laser and that is why ALT worked better in african americans than caucasians. -there are a lot of pt characteristics on which the surgen will decide which surgery will be best for the pt

Front 295

what two surgeries fall into the category of a laser trabeculoplasty (LTP)

Back 295

1. ALT 2. SLT

Front 296

what is a laser trabeculoplasty

Back 296

reshaping the trabecular meshwork with laser to enhance outflow; exach mechanism is unknown.

Front 297

what do we think is the mechanism for ALT

Back 297

mechanical from thermal burn causing contraction of tissue and opening adjacent areas of trabecular meshwork. (if I pull in in one area, you are going to be stretching the surrounding areas). there is also some evidence that phagocytotic cells in the area of the trabecular meshwork become active because of excitation.

Front 298

why do we think that ALT loses its effectiveness over time

Back 298

scarring caused by laser continues with time

Front 299

what does ALT stand for

Back 299

argon laser trabeculoplasty

Front 300

what does SLT stand for

Back 300

selective laser trabeculoplasty

Front 301

what do we believe is the mechanism of SLT

Back 301

has effect on pigmented trabecular meschwork cells only. there is not scarring, but activation of biological cells which causes chemotactic and vasoactive agents to be released which increase outflow

Front 302

which are larder the ALT or the SLT laser burns

Back 302

ALT: 50 microns SLT 400 microns

Front 303

can you repeat ALT

Back 303

no. it is generally believed that if you treat ALT in a previously treated area it causes so much scarring that IOP actually goes up. -wait untill you really need it

Front 304

can you repeat a SLT proceedure

Back 304

most of the literature supports the fact that you can repeat this proceedure. -treatment of choice for many because of this fact.

Front 305

is SLT or ALT believed to be more effective

Back 305

we believe they are about equally effective

Front 306

why is laser trabeculoplasty used more in open angle glaucoma than normotension glaucoma

Back 306

because the higher the IOP the more reduction in IOP you get

Front 307

in what percent of eyes treated with laser trabeculoplasty will there actually be a reduction in IOP (for at least 1 year)

Back 307

reduces IOP in 85% of treated eyes

Front 308

when it is effective, by how much does laser trabeculoplasty lower IOP

Back 308

25-30% when effective -may help flatten diurnal variation in IOP

Front 309

how long do we think laser trabeculoplasty usually works

Back 309

1-5 years.

Front 310

how does ALT compare to medication at controlling IOP (according to glaucoma laser trial)

Back 310

ALT as initial therapy alone controlled IOP in 44% of eyes ALT combined with a beta-blocker controlled IOP in 70% ALT combined with 2 meds controlled IOP in 89% In comparison: Single drug controlled IOP in 30% Two medications controlled IOP in 66% At 7 years: ALT first showed lower IOP and less VF loss -note that none of the studies that are published at this point are large sclae studies, but small case based studies. there are currently larger studies that are being conducted right now so we should have better information in the future.

Front 311

what are the complications associated with laser trabeculoplasty

Back 311

1. pain 2. spike in IOP first few hours after proceedure (tx w/ alpha-agonist) 3. mild iritis (topical steroids) 4. ALT may worsen glaucoma by scarring the TM and development of peripheral anterior synechia in some cases

Front 312

describe your followup for post-operative care for laser trabeculoplasty if you are co-managing the pt

Back 312

1. follow in 3-10 days to assess IOP and inflammation 2. follow in 4 weeks: if significant drop in IOP consider dropping one med. if IOP drop not significant consider treating the remaining 180 degrees or filtering proceedure.

Front 313

why is laser trabeculoplasty only done 180 degrees at a time

Back 313

becuase when you put a laser in the eye you get a spike in IOP because of inflammation. that is why you only do half at a time.

Front 314

what is the oldest glaucoma surgery

Back 314

trabeculectomy. it has been around the longest.

Front 315

what is a trabeculectomy

Back 315

you take out a piece of the trabecular meshwork, which creates a pathway from the anterior chamber to the sub-tenon's space underneath the conj

Front 316

at what position on the iris is trabeculectomy usually performed (360 degrees) and why

Back 316

superionasally. because very commonly we get this bulg that forms under the conj (bleb) and it is nice cosmetically if the bleb is hidden by the upper lid.

Front 317

why are sub-conjunctival injections given inferiorly

Back 317

to save the superior area from scarring in case they ever need a glaucoma surgery (trabeculectomy) any time in the future.

Front 318

what is the difference between a partial-thickness and a full-thickness trabeculectomy

Back 318

with a partial, you leave a scleral flap to cover the pathway. this provides some resistance to fluid leaving the anterior chamber. in a full-thickness proceedure only tenon's capsule and conjunctiva are left on top of the hole created by the sclerotomy.

Front 319

describe the procedure of a partial-thickness trabeculectomy

Back 319

flap of slcera is removed. hole is made through the trabecular meshwork into the anterior chamber. a peripheral iridectomy is performed to prevent iris from closing the channel. then the slcera is losely sutured back on (not a water tight seal, aqueous is allowed to flow through it). antimetabolites are then administered (5-fluorouracil) to inhibit fibroblastic activity. the procedure results in a balloon-like filtering bleb.

Front 320

when is a full thickness trabeculectomy indicated

Back 320

only in very severe cases where very low IOP levels are desired (<10 mmHg)

Front 321

canaloplasty is a new proceedure. by how much does it lower IOP

Back 321

30-35%

Front 322

what happens during a canaloplasty

Back 322

they inserta a small tube through schlemm's canal 360 degrees, which increases the size of the schleamms canal. then the tube is removed and a suture is placed in the same area where the tube was to maintain tenstion on the canal. hope to reduce IOP by 30-35%. (there is not bleb)

Front 323

why is not having a bleb an advantage (canaloplasty)

Back 323

because the bleb can perforate and result in infection. it can also result in a dellen on the cornea because the lid is lifted off the surface of the eye and so tears and mucin are not spread evenly across the cornea.

Front 324

how do filtration devices work as a glaucoma surgery and how is it implanted

Back 324

a flap of tissue just outside the limbal area is removed and a tube is inserted parallel to the iris and creates a duct for aqueous to flow out of the anterior chamber underneath the conj and sub-tenon's space where it is absorbed by the venous system. allow for more control of aqueous outflow. there is no way that the iris is going to block the tube, so iridectomy is not needed.

Front 325

by how much is a filtration device surgery able to reduce IOP

Back 325

greater than or equal to 40%. there is acutally less chance of hypotony though because we are able to control the diameter of the tube.

Front 326

what does ab interno mean

Back 326

from inside

Front 327

how does a surgeon perform an ab interno trabeculectomy

Back 327

make a small incision in the cornea similar to when doing cataract extraction. then a small hand held unit is inserted into that corneal incision, then electrocautery is done (run along schlemm's canal and we ablate or remove a front portion of schlemm's canal around the eye)

Front 328

by how much does an ab interno trabeculectomy reduce IOP

Back 328

30-40%

Front 329

is a bleb formed in an ab interno trabeculectomy

Back 329

no bleb

Front 330

what are cyclo-destructive procedures and why do you perform them

Back 330

destroy part of the ciliary body tissue in oder decrease aqueous production.

Front 331

when are cyclo-destructive procedures indicated

Back 331

used in blind painful eyes or eyes with neovascular glaucoma where the aqueous can't get out. typically used as an end-stage procedure.

Front 332

what are the two ways you can do a cyclo-destructive procedure

Back 332

transscleral: diode laser outside the globe endoscopic: performed through a limbal incision with direct application of laser to ciliary body.

Front 333

do optometrists generally do follow up for glaucoma surgery

Back 333

usually done by the surgeon (but that used to be the case with cataract surgery too, so this may change in the future).

Front 334

how do you check for a bleb leak

Back 334

look for siedel's sign just as in any other traumatic injury to the eye.

Front 335

what would help on follow up of glaucoma surgery if the eye is hypotenous

Back 335

discontinue steroids to allow scar formation and allow healing (fine line)

Front 336

what could you do (or the surgeon) on a glaucoma surgery follow up if there is not bleb when one is expected

Back 336

1. apply digital massage (pts are often told to do digital message daily to keep the bled open) 2. increase steroid (if they are in the healing stage to decrease healing and scar formation) 3. administer 5-FU 4. can also lyse the flap suture.

Front 337

they are trying to develop a contact lens that will deliver medications for 1 month. they are also working on a device that is basically like a punctal plug that releases medication over a 3 month period.

Front 338

New lecture: 7ACG2010wpicst

Front 339

what is the most common type of angle closure glaucoma

Back 339

relative pupillary block angle closeure glaucoma (RPB ACG). (if someone says angle closure glaucoma, unless they say differnetly you should assume that they are talking about relative pupillary block angle closure glaucoma)

Front 340

what are the risk factors for RPB angle closure glaucoma

Back 340

1. family history 2. age (as we age the lens increases in size) 3. female (they have smaller eyes) 4. hyperopia (smaller eyes) 5. ethnicity (rare in african americans, more common in inuit and asian)

Front 341

ethnicities that are more at risk for developing angle closure glaucoma tend to develop a more acute form (more easily recognizable), and ethnicities that are less likely to develop angle closure glaucoma (african americans) tend to develop a more chronic and smolering form (easier to mistake for another kind of glaucoma)

Front 342

what are the subjective symptoms associated with angle closure glaucoma

Back 342

1. blurred vision 2. halos 3. HA (very common) 4. pain (very common, not limited to the globe, follows the course of the trigiminal nerve (jaw, ear, cheak) 5. photophobia (common) 6 eye redness (common) -if you cause the angle closure with drops then it happens quickly enough to cause nausea and vommitting, but usually if it occurs on its own you will NOT have this symptom. drug you use to treat it can cause nausea and vommitting.

Front 343

chronic smoldering forms of angle closure glaucoma can cause no symptoms other than blurred vision

Front 344

decongestants list on the medication glaucoma as a contraindication. really they are only at risk for angle closure. open angle glaucoma is NOT a contraindication, but the packaging is not specific enough.

Front 345

how much is vision reduced in angle closure glaucoma

Back 345

can be any where from 20/25 to light perception depending on how badly the nerve fiber layer is damaged. most of the time they are in the 20/30 to 20/40 range though.

Front 346

how fast can the IOP increase in angle closure glaucoma

Back 346

IOP can increase 1 mmHg/min

Front 347

how high does the IOP generally have to be in order for the pt to see halos

Back 347

in the 50s

Front 348

how do the pupils appear in angle closure glaucoma and why

Back 348

almost always mid-dilated and fixed. the reason is that increased IOP causes ischemia of the iris (pressure in the eye is greater than pressure in the iris blood vessels), and the ischemia causes the iris muscles to work poorly (think of claudication)

Front 349

what signs on the iris indicate previous angle closure episodes

Back 349

1. iridectomy 2. scarring and fibrosis of the iris 3. irregularly shaped pupil 4. generalized cataract -all are in the picture

Front 350

you HAVE to do gonioscopy to diagnose angle closure glaucoma. you can't diagnose it unless you look at the angle (it is the one test that you absolutely have to do to diagnose ACG). both fundoscopy and gonioscopy can be hard to do in an acute angle closure attack, because the eye is edematous and is hard to see through. what can you do to see through it.

Back 350

-place a drop of glycerine in the bowl of the gonio lens and place it on the eye. the glycerine is hyperosmotic and will draw fluid out of the cornea and at least allow you a view.

Front 351

why would you want to consider doing a refraction if you have an angle closure glaucoma that is not acute

Back 351

to differentiate from uveal effusion glaucoma

Front 352

how does uveal effusion glaucoma affect the refractive error

Back 352

can shift refractive error by 6-8 diopters (pretty gross refraction would help to differentiate)

Front 353

what does the depth of the lesion in glaucomfleken tell you

Back 353

the deeper in the len the longer ago the previous episode of angle closure glaucoma occured

Front 354

name the objective signs associated with angle closure glaucoma (including signs of previous attacks)

Back 354

1. fixed mid-dilated pupils 2. iridectomy 3. iris fibrosis and scarring 4. irregularly shaped pupil (current and past) 5. anterior peripheral synechia 6. posterior synechia 7. glaucomflecken 8. optic nerve head edema 9. optic nerve atrophy 10. circumlimbal injection 11. IOP 40-90 mmHg 12. corneal edema 13. gonioscopically closed angles

Front 355

why is this a common appearance for the iris in angle closure glaucoma

Back 355

the iris is twisted. this is because the muscles are ischemic and working unevenly causing the iris to appear twisted.

Front 356

how much of the eye do you expect to be closed (of 360 degrees) before you experience the symptoms of angle closure galucoma

Back 356

about 75% or more

Front 357

describe the mechanism associated with relative pupillary block angle closure glaucoma

Back 357

the iris comes into contact with the lens. they are not attached to each other they are just touching each other. but by touching each other they make it harder for the aqueous to get to the anterior chamber. as aqueous is produced, pressure in the posterior chamber increases and that pressure causes the iris to balloon forward (typically in the mid-peripheral area). that ballooning forward of the iris ends up blocking the angle.

Front 358

why does relative pupillary block angle closure glaucoma tend to happen most commonly when the iris is in the mid-dilated state

Back 358

because when it is only mid-dilated the iris is most "floppy" and the tissue is more able to balloon forward.

Front 359

if you have an angle closure glaucoma that you think is relative pupillary block, you have better make sure that that is what it actually is before you start treating, because some of the differentials are actually treated in exactly the opposite way from the way you would tx relative pupillary block. name all the differentials

Back 359

1. glaucomatocyclitic crisis 2. pseudoexfoliative glaucoma 3. glaucoma associated with ICE 4. plateau iris 5. malignant glaucoma 6. mobile lens 7. uveal effusion 8. neovascular

Front 360

how does treatment for relative pupillary block angle closure glaucoma differ if it is acute vs. chronic

Back 360

if it is acute then you want to break the attack using medical therapy. then you will have a peripheral iridotomy or surgical iridectomy performed. and allways evaluate the fellow eye for consideration of tx if it si at risk. -if they are chronic or at risk, then we perform a peripheral iridotomy or lensectomy (IOL implant is thinner than crystaline lens). then evaluation fellow eye for consideration of tx. medical tx is the same as with acute forms, but it tends to be less responseive to tx and is less of an emergency because pressure is not raising as quickly.

Front 361

describe in detail the tx of angle closure glaucoma

Back 361

-in order of steps: 1. oral acetazolamide (two 250 mg tablets) -not to be used in pts with sulfa allergy or in pts with severe kidney disease 2. apraclonidine 1% (Iopidine): one to two drops 3. timolol 0.5% (timoptic): one drop at time of diagnosis -betaxolol 0.25% in pts with pulmonary problems (use as with timolol) 4. pilocarpine 2%: one to two drops every 15-60 minuets (not to exceed more than 4 drops in a 2-3 hour time frame) 5. check IOP every 15 minuets: if IOP < 20 mmHg, perform gonioscopy to confirm angle is open. 5a. if angle is open, maintain pt on 2% pilocarpine OU qid and rx prednisolone acetate 1% qid until laser peripheral iridotomy is performed (2-7 days later). 5b. if IOP is still elevated or angle closed after one hour, repeat all topical medications, and add oral hyperosmotics if available 6. oral hyperosmotics: glycerine 50% solution (caution for diabetics), or isosorbide 50% (safe for diabetics). use 1-2 ml/lb (220 ml bottle for adults) served over crushed ice. drink within 5 minuets, NO water within first 2 hours 7. at this point you can do corneal indentation: 30 seconds on 30 seconds off for 10-15 minuets (pt may be too uncomfortable to tolerate) 8. if IOP is still elevated and angle closed after 2 hours, pt shoudl have laser gonioplasty

Front 362

what is the first drug that you will give if you have angle closure glaucoma (and specific dosage)

Back 362

oral carbonic anhydrase inhibitors. two 250 mg tablets. (500 mg total; but recongnize that the single 500 mg tablets are slow release and you DON'T want to use that)

Front 363

what are the contra indications to giving oral carbonic anhydrase inhibitors for angle closure glaucoma

Back 363

1. allergy to sulfa 2. severe kidney disease (you are drawing fluid out of the body which can put stress on the kidney)

Front 364

why is Iopidine typically reserved for use in acute angle closure

Back 364

because if it is used long term, pts tend to develop allergies to it

Front 365

what alpha-agonist is used in angle closure glaucoma (specific dosing)

Back 365

apraclonidine 1% (Iopidine). one to two drops at time of diagnosis. repeat once in one hour if needed.

Front 366

what beta blocker is used in angle closure glaucoma (specific dosage)

Back 366

timolol 0.5% (timoptic). one drop at time of diagnosis, repeat once in one hour if needed. if they have pulmonary disease use betaxolol 0.25% (Betoptic S) (used the same as timolol)

Front 367

some people urge the use of timolol, 1 drop q 12 h until laser peripheral iridotomy can be performed.

Front 368

what miotic is used for angle closure and the specific dosage?

Back 368

pilocarpine 2% one to two drops every 15-60 minuets. don't exceed more than 4 drops in any 2-3 hour time frame. it is important that you use the 2% formulation and NOT the 4% formulation because 4% has been shown to thicken the iris, which would be very bad.

Front 369

when do you expect pilocarpine to be effective in angle closure glaucoma

Back 369

-iris ischemia tends to occur at 40 mmHg; when we use pilocarpine we are stimulating the iris sphincter to contract; if the pressure is higher than 40 mmHg, we don't expect to get much of an effect from pilocarpine because the tissue is ischemic. you could instill the drops and then when the pressure drops below 40 you will start to see an effect (takes 15-20 minuets after instillation to get full effect), or you could wait until you measure the IOP at 40 or less to instil the drops; opinions on this vary.

Front 370

some people recommend treating the fellow eye with pilocarpine in angle closure if it is predisponsed to prevent an angle closure attack.

Front 371

in angle closure the pts eye will be painful and they will not like having gonio done. when the pressure drops below 20 why do we still need to check with gonio to see if the angle is open

Back 371

because we have stoped aqueous production and fulled fluid out of the eye with diamox. so the angle could still be closed even though the pressure is less than 20 mmHg. the last thing you would EVER want to do is to get the pressure below 20 and release them to see the ophthalmologist the next day and the angle is actually still closed. because their pressure will go right back up where it was and YOU will be liable. we typically don't perform gonio until the pressure is below 20 because their eye is painful and you don't want to do it more than necessary, but you HAVE to check to make sure that the angle is actually open before you release them.

Front 372

why do you wait 2-7 days after an angle closure attack to schedule them for laser peripheral iridotomy

Back 372

because they eye is going to be swollen from the attack and it is hard for a laser to punch through swollen tissue. also the laser is going to contribute to inflammation. also, the cornea is typically not very clear. LPI is better if we wait until the eye is quiet.

Front 373

oral hyperosmotic solutions will make the pt thursty, but they CAN'T drink water because this will eliminate the effect of the solution. they tast very bad and they can make the pt sick.

Front 374

if the pt gets sick and vommits after you give them an oral hyperosmotic, do you need to redose them?

Back 374

no, it is absorbed very quickly and typically you don't redose them. if it is immediate you might consider it, but if it is in there for even a couple minuets then you should be fine.

Front 375

how long does it take for the IOP drop if you give an oral hyperosmotic

Back 375

30-60 minuets.

Front 376

remember that if you do corneal indentation with a gonio lens on an angle closure pt, the surface of the lens touching the eye needs to be smaller than the size of the corne, otherwise you are just forcing the angle closed.

Front 377

remember that if you have an angle closure pt late on a friday afternoon, that you need to call the specialist righ away as you start treatment, because you don't want to start all your treatment only to realize that they have all left for the day.

Front 378

what is laser gonioplasty

Back 378

we are trying to alter the shape of the angle by altering the shape of the iris as it enters the angle. large argon spot is put onto the tissue, which causes it to contract and may open portions of the angle. this is not a cure, LPI still must be performed. if IOP is still elevated and angle closed after 4-6 hours, pt should have emergency LPI performed (this is very difficult to do on an inflammed and angry eye).

Front 379

what type of laser is used in a peripheral iridotomy

Back 379

YAG laser

Front 380

what position 360 degrees is a laer peripheral iridotomy typically done and why?

Back 380

around the 12 o'clock position. you want it very superior because it will be covered by the upper lid, this will prevent any ghost images or monocular diplopia.

Front 381

why does a laser peripheral iridotomy help in relative pupillary block angle closure glaucoma

Back 381

because of the increased pressure in the posterior chamber causes the iris to bulge forward and block the angle, when we punch a hole in the iris is allows aqueous to move from the posterior chamber to the anterior chamber and this prevents pressure from buildin up in the posterior chamber and causing the iris to bulge forward, blocking the angle.

Front 382

describe the medical therapy that is required related to laser peripheral iridotomy

Back 382

1. Iopidine 1-2 hrs pre iridotomy (laser energy in the eye causes raise in IOP) 2. prednisolone acetate 1% qid to treat and try to prevent any transient uveitis.

Front 383

what proceedure does the surgen do if you weren't not able to break an angle closure glaucoma with medical therapy and they tried laser gonioplasty and emergency laser peripheral iridotomy, but they were ineffective?

Back 383

surgery: peripheral iridectomy. -you don't want to do this unless you really have to.

Front 384

what is a peripheral iridectomy

Back 384

a corneal incision is made in the superior quadrant and a section of prolapsed iris is then excised (they pull the iris out of the cornea with forceps and cut it). the anterior chamber is then reformed with saline if necessary.

Front 385

when you see a superior peripheral iridectomy in a pt who has their natural crystaline lens, it is vertually always because they have had angle closure glaucoma. if the peripheral iridectomy is inferior you have to worry more about retinal detachment being the cause for the surgery.

Front 386

describe the prognosis for angle closure glaucoma

Back 386

guarded. they are considered glaucoma suspects for the rest of their life (open as well as closed angle: remember that once damage to the NFL start the more likely further damage is to occur (ankle sprain analogy))

Front 387

can you rely on transillumination as a sign that a peripheral iridotomy is patent? why or why not?

Back 387

no, when you plut the gonio lens on you need to be able to see through it. you can't rely on transillumination because you can have things blocking it and still have transillumination.

Front 388

what is another name for glaucomatocyclitic crisis

Back 388

Posner-Schlossman Syndrome

Front 389

in what age range do you expect to see claucomatocyclitic crisis and is that different from relative pupillary block angle closure glaucoma

Back 389

glaucomatocyclitic crisis is usually seen in young pts. RPB ACG is seen in older pts.

Front 390

how do they symptoms for glaucomatocyclitic crisis differen from relative pupillary block angle closure glaucoma

Back 390

GC: no pain, subtle uveitis, minimal conjunctivitis RPB ACG: painful, extreme conjunctival injection -both are usually unilateral and IOP is in a similar range of IOP

Front 391

describe the tx of glaucomatocyclitic crisis

Back 391

1. most important part of the therapy is STEROID (to decrease inflammation) 2. ocular hypotensives (not as emergent as angle closure; usually just one drop) 3. oral indomethacin 4. no cycloplegia necessary (unlike other inflammatory ocular conditions)

Front 392

what type of ocular hypotensive drug do you NOT want to use in glaucomatocyclitic crisis

Back 392

prostaglandins (inflammation)

Front 393

is pseudoexfoliative glaucoma usually unilateral or bilateral

Back 393

starts unilateral and becomes bilateral with time

Front 394

is the angle open or closed in glaucomatocyclitic crisis? how about pseudoexfoliative glaucoma

Back 394

open in both

Front 395

what are the objective signs associated with pseudoexfoliative glaucoma

Back 395

1. anterior lens and pupillary border deposits 2. defects in the pupillary ruff 3. increased pigment in the TM 4. high IOP (not uncommon to see IOP in the 50s)

Front 396

describe the management of pseudoexfoliative glaucoma

Back 396

managed like primary open angle glaucoma, but less responsive. treat agressively including filtration surgery.

Front 397

in what age ranges do you tend to see glaucoma related to ICE syndromes

Back 397

20-40 years old

Front 398

describe the pathophysiology associated with glaucoma related to ICE syndromes

Back 398

proliferation of corneal endothelium and basement membrane; growth over the trabecular meshwork. broad peripheral anterior synechia formation.

Front 399

describe the management of glaucoma ralated to ICE syndromes

Back 399

1. early on can be controlled with meds -used meds that decrease aqueous production (not drugs that increase outflow) 2. filtering surgery often required 3. hypertonics for corneal edema 4. DSEK or PK if significant corneal edema

Front 400

what is plateau iris configuration angle closure glaucoma

Back 400

it is a type of angle closure glaucoma (rare). the iris is very close to the angle in periphery but the angle appears deep. dilation causes pleating of the iris and angle closure. -when you do von herick on these pts the angle will look open and then you will dilate and the angle will close -indentation gonioscopy increases peripheral pleating (which differs from relative pupillary block in which the iris flattens with indentation gonioscopy; so it is important to look while you are doing indentation to see the angle close more instead of open)

Front 401

descirbe tx associated with plateau iris configuration

Back 401

1. miotic drops short term and chronically 2. laser iridotomy to eliminate any pupillary block 3. main tx is laser gonioplasty, which scars and changes the shape of the iris

Front 402

what is another name for malignant glaucoma

Back 402

aqueous misdirection syndrome

Front 403

what is malignant glaucoma and describe the pathophysiology involved

Back 403

the iris is pushed all the way up agains the corneal endothelium. classically follows intraocular surgery (often for angle closure glaucoma), it can occur as long as one year after surgery. what is happening is that due to the malipulation of the eye during surgery there was a pathway formed where aqueous formed in the posterior chamber is allowed to move behind the vitrious, which pushed the vitreous and the lens forward whcih pushes the iris all the way up against the cornea.

Front 404

describe the prognosis associated with malignant glaucoma

Back 404

one of the most seious forms of glaucoma. named for it poor response to treatment.

Front 405

describe the tx associated with malignant glaucoma

Back 405

-this is one where you want to get it out of your chair ASAP! you can put the meds in if you want (optional), but you need to send it off right away 2.5% Phenylephrine, 1 drop qid Plus 1% Atropine, 1 drop qid Beta-blocker, 1 drop bid Alpha2 agonists: 1/2% Apraclonidine, 1 drop tid Topical 2% Dorzolamide, 1 drop tid And/or Oral Acetazolamide, 250 mg, orally, qid Hyperosmotic agents: 50% Isosorbide solution Or 50% Glycerin solution, as for RPB ACG, po, bid if tolerated or maximum tolerated frequency then extensive surgical management is required -notice that we are using atropine instead of pilocarpine, that is because we want to tighten the zonules up to help move the lens away from the cornea. pilocarpine would losen the zonules, which is not what you want.

Front 406

what is mobile lens (lens forward) glaucoma

Back 406

similar to malignant glaucoma, but occurs without surgical intervention. the zonules are lax and the lens moves forward due to vitreous pressure.

Front 407

do you want to use a miotic or a cycloplegic if you have mobile lens glaucoma

Back 407

cycloplegics will tighten up the zonules (do NOT use miotics because they will make it worse)

Front 408

what is uvel effusion glaucoma

Back 408

similar to mibile lens glaucoma, but instead of having lax zonules the problem is acutally an anterior rotation of the ciliary body. this causes relaxation of the zonules, which causes thickening of the lens and myopia. it is often associated with medication use (topiramate (well known side effect of topiramate), sulfonamides etc.). it is a bilateral presentation. -the myopia is the significant finding. they will have a SIGNIFICANT myopic shift in their refractive error.

Front 409

describe the management fo uveal effusion glaucoma

Back 409

1. agent to stop aqueous production (beta-blocker (bid), alpha-agonist (tid)) 2. 1% atropine qid 3. oral acetazolamide 250 mg capsules (2) po 4. stop causative medication with permission of the PCP

Front 410

how long does uveal effusion tend to last

Back 410

1-2 weeks after discontinuation of the medication

Front 411

is uveal effusion a primary or a secondary glaucoma? what about neovascular glaucoma

Back 411

uveal effusion: secondary neovascular: secondary

Front 412

what is neovascular glaucoma

Back 412

blood vessels have fibrovascular tissue with them and tissue blocks the angle

Front 413

what is the treatment for neovascular glaucoma

Back 413

1. agents to decrease aqueous production (short-term) 2. hyperosmotic agents (short-term) 3. surgery (surgery is really the only effective option long-term)

Front 414

New lecture: 8OcVascslidest2010

Front 415

describe the arteriol pathway from the heart to the retina

Back 415

heart-aorta-common carotid-internal carotid-ophthalmic artery-central retinal artery

Front 416

the ophthalmic artery makes a very sharp angle with the internal carotid artery (not a Y shape)

Front 417

why would poor blood flow through the central retinal artery cause optic nerve head edema

Back 417

because it supplies blood to the inner retina AND to the surface of the optic nerve head

Front 418

the central retinal artery is primarily autoregulated. this means that it is less effected by the sympathetic and the parasympathetic system and more effected by the amount of oxygena and carbin dioxide in the blood and other neuro factors that are trying to maintain a balance between IOP and pressure in the retinal vessels

Front 419

what is ocular ischemic syndrome

Back 419

ocular signs and symptoms secondary to severe carotid artery obstruction

Front 420

describe the epidemiology associated with ocular ischemic syndrome

Back 420

men (67%). mean age is 65 years old.

Front 421

name three causes of ocular ischemic syndrome. which is most common?

Back 421

1. atherosclerosis (most common by far) 2. giant cell arteritis 3. diffuse systemic ischemia

Front 422

if atherosclerosis is the cause of ocular ischemic syndrome what percent ipsilateral obstruction of the carotid can we expect

Back 422

greater than or equal to 90% -there is probably at least some obstruction in both sides by this stage

Front 423

describe the vision loss associated with ocular ischemic syndrome

Back 423

gradual vision loss over a week or two (note that this is different from central retinal artery occlusion or AION). unilateral in 80% of cases. abrupt loss can occur in 12% of cases. 33% have VA of 20/20 to 20/40 at discovery and 33% have counting fingers or worse at time of discovery.

Front 424

what are the objective signs associated with ocular ischemic syndrome

Back 424

1. gradual loss in VA over a week or two 2. light-induced amaurosis fugax 3. dull, aching pain to orbital area of involved eye "ocular angina" (40%) 4. sluggish pupil (same mechanism as angle closure: ischemia) 5. ischemic uveitis (flare in majority of cases, cells in 20%) 6. neovascularization of the iris (67%) 7. elevated IOP (secondary to NVI) 8. retinal artery narrowing 9. retinal veins dilated and may be beaded 10. retinal hemorrhages in the MID-periphery(80%) 11. macroaneurysms 12. neovascularization of the disc 13. spontaneous ARTERY pulsation

Front 425

name and describe the pathopneumonic finding associated with ocular ischemic syndrome

Back 425

light-induced amaurosis fugas (LIA): when they are exposed to a bright light they experince a fuzzyness or hazyness in their central vision that lasts for several minutes

Front 426

how do you differentiate between TIA and light-induced anaurosis fugax

Back 426

-it is very important to be able to differentiate this from TIA. TIAs are also traisient and also last for minutes, but the pt will complains of more of a peripheral greying out of vision down to central. LIA tends to have the central vision effected and the periphery uneffected. additionally LIA is almost always described as a fuzzy cloud of white central area, it is not greying of the vision like TIA is.

Front 427

why do only 50% of the pts with neovascualrization fo the iris in ocular ischemic syndrome have elevated IOP

Back 427

the ciliary body is producing less aqueous because it is ischemic too -when you send them out for endarterectomy the ocular perfusion goes way up and then you can get a large increase in IOP in these pts.

Front 428

hemorrhaging in the mid peripheray occurs in 80% of pts with ocular ischemic syndrome. this is significant because there just aren't that many other things that cause hemorrhaging in the mid-periphery. so, if you see it you really need to rule out OIS

Front 429

in ocular ischemic syndrome veins are dilated and may be deaded, but they are NOT tortuous. tortuosity indicates that there is high pressure in the veins and there is definately not high pressure in the veins here because there is low blood flow in this condition.

Front 430

anytime you see a macroaneurism you should be asking about light-induce amaurosis fugax

Front 431

what does spontaneous artery pulsation indicate

Back 431

the IOP is greater than the pressure inside the artery when the hart is not pushing blood through the arteries. this should not normally be the case, the pressure inside the central retinal artery is normally about 70 mmHg. so, either there is really high pressure inside the eye, or there is decrease pressure in the artery. -in ocular ischemic syndrome you can see spontaneous artery pulsation because there is decreased blood flow to the retina and decreased pressure inside the arteries. it is very rare, but if you do see it, it should raise huge red flags.

Front 432

ocular ischemic syndrome has a pretty poor systemic prognosis. high mortality rate due to heart attack etc.

Front 433

how do you differentially diagnose between ocular ischemic syndrome and diabetic retinopathy

Back 433

diabetic retinopathy: usually bilateral (not always), if you see hard exudates you should really think diabetic retinopathy and not ocular ischemic syndrome, retinopathy is more in the posterior pole (mid-periphery in OIS)

Front 434

how do you differentially diagnose between ocular ischemic syndrome and a mild central retinal vein occlusion

Back 434

CRVO: has venous tortuosity, significant retinal edema

Front 435

carotid evaluation should be performed on every pt with ocular ischemic syndrome symptoms. how do you do that in the exam room

Back 435

listen for a carotic bruit and THEN feel for the carotid pulse (you don't want to feel around there if you hear a bruit because you don't want to dislodge a thrombis and cause a stoke; but you need to feel if you don't hear one because it could be that you are not hearing it because it is completely blocked (if it is completely blocked there is very little risk of causing a stroke because there is no blood flow))

Front 436

describe the management associated with ocular ischemic syndrome

Back 436

1. carotid endarterectomy to prevent stoke in pts with 70-99% occlusion (evidenced based) 2. ASA for symptomatic pts between 0-60% obstruction 3. pan-retinal photocoagulation if neovascularization of the iris

Front 437

what is an endarterectomy

Back 437

they open up the neck and remove the atherosclerotic plaque from the carotid artery (they will have a big scar on their neck)

Front 438

describe the epidemiology associated with retinal artery occlusion

Back 438

mean age is 65; males>females

Front 439

describe the signs and symptoms assocaited with retinal artery occlusion

Back 439

1. sudden, painless, profound loss of VA 2. APD (if unilateral; which is usually the case) 3. retina appears white and edematous within a few hours 4. foveola stands out as "cherry red spot" (happens because there a less layers of the retina in this area and so there is less edema to look through to see the choroid) 5. venules distended and segmented (boxcarring)

Front 440

what is this

Back 440

macula is spared in a central retinal artery occlusion because of a cilioretinal artery

Front 441

if the macular was spared in a central retinal artery occlusion, whould there still be an APD

Back 441

yes, most of the fibers in that eye are still affected even though they still have 20/20 acuity

Front 442

describe the objective signs associated with branch retinal artery occlusion

Back 442

1. looks similar to CRAO in area supplied by artery. 2. most often the superior temporal region is affected 3. normal VA is common 4. visual field loss is very respectfull of the horizontal midline because of the horizontal raphe

Front 443

in what percent of cases of retinal artery occlusion can emboli be seen within the arterial system

Back 443

11-40% (much higher in branch than central artery occlusion)

Front 444

name and describe the different types of plaques that can be seen in retinal artery occlusion

Back 444

1. cholesterol emboli (hollenhorst plaque): small and yellow; often seen at a bifrication; look like they fit within the vessel (even though they look like they are as wide as the vessel, they are often very flat and so blood flow is able to go around them even thought it doesn't look like it should be able to) (carotid is the most likely source of this type of emboli) 2. calcific emboli: large and white; they tend to look like they are bigger than the blood vessel (just has to do with the way they reflect light). they are round and do block the blood vessel. most likely location is from the hear (valvular disease) 3. platelet/fibrin emboli: typically not at a bifrication; usually a sign of some kind of hematologic disorder (tend to be the type you see in younger people)

Front 445

what type of emboli is this (slide 22 of this lecture)

Back 445

cholesterol

Front 446

what type of emboli is this (slide 22)

Back 446

calcific

Front 447

what type of emboli is this (slide 22)

Back 447

platelet/fibrin

Front 448

describe the management associated with central retinal artery occlusion

Back 448

acute management: treat all cases seen withing 24 hours of onset (this is the standard of care; the truth is that it is not likely to do any good if it has been more than 2-4 hours) 1. firm massage of globe for 15 min. (10 sec. on 10 soc. off) 2. anterior chamber paracentesis 3. acetazolamide 500 mg iv or 250 mg X 2 po with topical antiglaucoma agent to lowe IOP. then 250 mg q 6h for several days 4. carbogen (5% CO2 and 95% O2) (basically the same as breathing in a paper bag) -remember that the vessels are autoregulatory, so we are trying to get the vessels to kick in and cause dilation -intra-arterial thrombolytic therapy is a possibility for young people with a fibrin clot (new technique; there are significant risks associated with this therapy)

Front 449

describe the long-term prognosis and consequences associated with central retinal artery occlusion

Back 449

1. VA typically poor 2. retinal tissue replaced with glial tissue in weeks 3. ONH becomes atrophic and pale 4. neovascularization of the retina or the iris is possible

Front 450

what will an OCT show if the retinal tissue has been replaced with glial tissue as a result of a central retinal artery occlusion

Back 450

thinning

Front 451

describe the epidemiology associated with central retinal vein occlusion

Back 451

90% are males>50; but can occur at any age

Front 452

how does IOP effect the likelyhood of developing central retinal vein occlusion

Back 452

high IOP increases risk, because veins are low pressure and thin walled.

Front 453

name the two types of central retinal vein occlusion

Back 453

ischemic (non-perfused) and non-ischemic (perfused) -it is important to be able to differentiate because it influences that management

Front 454

describe the incidence and prognosis associated with ischemic and non-ischemic central retinal vein occlusion

Back 454

ischemic: 20%; permanent poor VA with VF defects common and NVI and neovascular glaucoma in 45% non-ischemic: 80%; good VA common long-term, blinding complications rare, central scotoma possible

Front 455

what is the most reliable test to determine if a central retinal vein occlusion is ischemic or non-ischemic

Back 455

severity of the APD (appearance on ophthalmoscopy is actually the least reliable way)

Front 456

name the different ways you can differentiate between ischemic and non-ischemic CRVO

Back 456

1. VA (20/400 or worse indicates ischemic) 2. RAPD as measured with neutral density filter 3. visual field (really shold be goldmann, because it measures further out in the peripher) 4. fluorescein angiography

Front 457

what percent of pts present with VA of 20/400 or worse in both the ischemic and the non-ischemic form of central retinal vein occlusion

Back 457

non-ischemic: 20% ischemic: 93%

Front 458

how do you most easily measure an APD with a neutral density filter

Back 458

place the filter in front of the light when it is shining in the "good" eye (so you can see the pupil; it is hard to see through the filter). what you are looking for is when the filter is in front of the good eye and you move the light to the bad eye and see contriction that is the level of the APD

Front 459

how does the level of APD (as measured with neutral density filter) vary btwn ischemic and non-ischemic types of CRVO

Back 459

non-ischemic: 97% have RAPD < 0.6 log units ischemic: 94% have RAPD > 0.9 log units

Front 460

if you do fluorescein angiography how would you use it to tell if CRVO is ischemic or not

Back 460

capillary non-perfusion is required for diagnosis of ischemic CRVO (lack of filling of the capillary system) -could be difficult to tell because hemorrhages are often blocking the view. also small pupils and cloudy media may limit view. also it is hard to see the periphery with fluorescein angiongraphy and that is where most nonperfusion starts. -in the picture the top is perfused and the bottom of the picture is not perfused

Front 461

you really can't differentiate ischemic and non-ischemic CRVO based of appearance with ophthalmoscopy

Front 462

what causes central scotoma in CRVO

Back 462

chronic macular edema, caused by poor blood flow

Front 463

describe the long-term complications associated with perfused CRVO

Back 463

1. transition from perfused to non-perfused possible 2. chronic macular edema, leading to central scotoma

Front 464

what are the long-term complications associated with non-perfused CRVO

Back 464

1. ocular neovascularization of anterior seg. (2/3 to 3/4 develop neovascular glaucoma) 2. vitreous hemorrhages 3. macular degeneration 4. optic atrophy 5. loss of eye -this is why non-perfused cases need to be followed much more closely

Front 465

describe the management of ischemic and non-ischemic CRVO

Back 465

controversial: -generally just wait and watch. follow ischemic every 2-3 weeks and non-ischemic every 2 months.

Front 466

what did the SCORE study look at

Back 466

CRVO. only non-ischemic with VA 20/40 to 20/400. looked to see if treating with intra-vitreal steroids helped macular edema from CRVO

Front 467

what were the results of the SCORE study

Back 467

intra-vitreal steroids did help macular edema and resulted in significant improvement in VA. but came with many risks.

Front 468

if diabetic retinopathy is unilateral or asymmetric is it better or worse on the side with good blood flow

Back 468

worse on the side with good blood flow; because it is caused by leaky pericytes. -if you see unilateral diabetic retinopathy you are usually more concerned about the carotid artery on the side with less retinopathy.

Front 469

New lecture: 9OPT 733 Macular Diseases Yudcovitch 2010 NOTES

Front 470

how big is the macula

Back 470

1.5 mm. about the same size as the optic nerve head

Front 471

name the layers of the retina

Back 471

Internal limiting membrane Retinal nerve fiber layer (RNFL) Ganglion cell layer Inner plexiform layer Inner nuclear layer Outer plexiform layer Outer nuclear layer External limiting membrane Photoreceptor layer (PRL) Retinal pigmented epithelium (RPE)

Front 472

some other names for epiretinal membrane

Back 472

Premacular gliosis Cellophane maculopathy Surface-wrinkling retinopathy Preretinal fibrosis Macular pucker (more severe)

Front 473

describe the pathophysiology associated with epiretinal membrane

Back 473

internal limiting membrane breaks allowing glial cells to proliferate. postulated that these breaks may be created when the posterior vitreous detaches from the macula.

Front 474

is epiretinal membrane unilateral or bilateral

Back 474

usually unilateral. bilateral in 5% of cases

Front 475

what is this

Back 475

vitreoretinal traction (V shaped)

Front 476

what is this

Back 476

epiretinal membrane

Front 477

describe the objective and subjective indications of epiretinal membrane

Back 477

1. translucent membrane causes irregular light reflex or sheen 2. fine surface striae as it thickens and contracts 3. tortuous superoinferotemporal vessels (contracting membrane pulls vessels) 4. posterior vitreous usually detached from macula 5. metamorphopsia 6. VA normal to slightly reduced (rarely worse than 20/40)

Front 478

what is the best way to see macular pucker

Back 478

with the red-free filter

Front 479

what is macular pucker

Back 479

more sever form of epiretinal membrane. more sever blood vessel distortion. metamorphopsia and reduced VAs (20/40 to 20/60). pseudohole or CME may form at the macula.

Front 480

what is the surgery for epiretinal membrane called

Back 480

membrane peal. it is an extremely delicate procedure and only done in very severe cases.

Front 481

describe the epidemiology associated with macular hole. is it usually unilateral or bilateral?

Back 481

usually older women. bilateral in only 10% of cases.

Front 482

name some causes of macular hole

Back 482

1. idiopathic 2. severe myopia 3. trauma (vitreous traction or commotio retinae) 4. solar retinopathy

Front 483

name and describe the stages of macular hole

Back 483

stage 1: impending macular hole (cyst). decreased or absent foveal depression, small round yellow spot in fovea. stage 2: early macular hole (tear). tear at one edge of fovea. stage 3: full thickness hole. round punched-out area (about 1/3 DD). may have yellow deposits within the hole at RPE level. translucent operculum may be seen. VA usually 20/200 or worse. stage 4: vintage macular hole. edematous "cuff" at margins. complete PVD.

Front 484

name and describe the clinical test you can do for macular hole in the slit lamp

Back 484

watzke-allen technique. narrow your beam with a high plus lens and move it back and forth over the macula. if the beam is straight up and down the macula is normal and there is no hole. if there are distortions in the beam that indicates early changes. if there is a part of the beam completely missing, then there is a full thickness hole.

Front 485

what is the treatment for a macular hole

Back 485

internal limiting membrane peel and vitrectomy. goal is to stimulate glial cell proliferation/migration and relieve vitreo-retinal traction. followed with gas or oil tamponade (face-down for at least 1 week) -our ability to improve VA with these techniques is improving, so if you have someone with a macular hole that developed within the last year you should consider sending them for a consult.

Front 486

macular hole surgery outcome: Closure expected in > 90% of macular holes after one operation Closure approaches 100% of stage II or early stage III holes 25 to 50% of closed macular holes fail to achieve better than 20/50 About 20% risk of cataracts and retinal tears Despite this, surgery usually has beneficial effect on patients’ quality of life Currently no large randomized clinical trials to establish the risks and benefits of surgery Reference: Williams GA. Macular Holes: The Latest in Current Management. Retina. Volume 26(6) supplement, July/August 2006, pp S9-S12

Front 487

what is a macular pseudohole

Back 487

looks like a macular hole on ophthalmoscopy. due to epiretinal membrane. visual acuity is usually good (possible metamorphopsia)

Front 488

what is a foveal pseudocyst

Back 488

thin layer (lamella) of macular tissue. may be a pre-macular hole, may be a "self-healed" full-thickness macular hole, may also result from macular hole surgery

Front 489

what is cystoid macular edema, and what causes it

Back 489

accumulation of fluid within the macula. accumulation is centered around the foveola and is loss of foveal depression. causes a petaloid (flower petal-shaped) pattern. caused by a breakdown of the inner blood-retinal barrier.

Front 490

what is the prognosis associated with cystoid macular edema

Back 490

usually benign in the short-term (hours-days). long-standing causes (weeks to months) result in coalescence of the fluid filled microsysts and can result in large lamellar hole formation and premanent loss of VA.

Front 491

what is the treatment for cystoid macular edema

Back 491

1. laser photocoagulation/vitrectomy 2. systemic carbonic anhydrase inhibitors 3. steroids/NSAIDs

Front 492

what is clinically significant macular edema

Back 492

macular edema associated with diabetes. the most common cause of VA loss with DM

Front 493

how do you diagnose clinically significant macular edema

Back 493

one or more of the following: -retinal edema withing 500 microns of the fovea -hard exudates within 500 micronse of the fovea with adjacent retinal thickening -retinal edema 1 DD (1500 microns) or larger, any part of which is withing 1 DD of the fovea.

Front 494

what is the treatment for clinically significant macular edema

Back 494

1. focal treatment 2. grid treatment 3. pan-retinal treatment

Front 495

what is cental serous retinopathy

Back 495

also called central serous chroioretinopathy. typically sporadic and self-limiting. usually occurs in yound to middle-aged males (type A personality (stress)). there is localized sensory retinal detachment due to a focal break or gap in the RPE. sub-retinal fluid leaks through this gap.

Front 496

what is this

Back 496

"smokestack" or "umbrella" appearance on fluorescein angiography. associated with central serous retinopathy.

Front 497

how do you diagnose centra serous retinopathy

Back 497

1. fairly sudden VA reduction in one eye (20/30-20/40) 2. hyperopic refractive shift (VA improves to 20/20 with low plus) 3. relative scotoma 4. metamorphopsia 5. micropsia 6. shallow, round or oval elevation 7. associated retinal vessels will cast shadows 8. possible RPE detachment (picture)

Front 498

what is the prognosis assocaited with central serous retinopathy

Back 498

80% will spontaneously resolve in 1-6 months. 20% resolve in 1 year. some mild metamorphopsia can remain. a small number have permanent VA reduction (usually due to prolonged detachment or multiple reccurent attacks)

Front 499

what is the tx for central serous retinopathy

Back 499

focal laser photocoagulation to obliterate leakage site of RPE. may speed up resolution by a few months, but does not improve visual outcome.

Front 500

describe the retinal changes associated with myopic degeneration

Back 500

1. posterior staphyloma 2. lacquer cracks (4% of highly myopic eyes) 3. fuch's spot (secondary pigmentary proliferatino from choroidal vessel growth)

Front 501

name some drugs that can cause toxic maculopathies

Back 501

1. antimalarials (chlooquine/hydroxychloroquine (plaquenil)) 2. phenothiazines 3. tamoxifen 4. canthanxanthin 5. talc

Front 502

you know the pt has a good primary care provider if they refer to you before they start the pt on plaquenil, because you need to do baseline testing before they initiate therapy

Front 503

what diseases does plaquenil treat

Back 503

malaria and rheumatologic disorders (arthritis, lupus)

Front 504

severe blindness can result from antimalarial use. hydroxychloroquine has less maculopathy risk than chloroquine

Front 505

what should you do as baseline testing if you have a pt come in that is about to start an antimalarial drug

Back 505

1. visual acuities 2. amsler grid 3. color vision 4. visual fields 5. dilated retinal examination 6. fundus photos -follow every 6 months after

Front 506

what is cinchonism

Back 506

ocular toxicity due to antimalarial quinine: 1. VA loss 2. fixed dilated pupils 3. retinal edema 4. constricted visual fields 5. optic atrophy

Front 507

what are the phenothiazine drugs used for

Back 507

antipsychotic drugs

Front 508

what ocular problem typically is associated with phenothiazine

Back 508

salt and pepper maculopthy

Front 509

be careful about telling pts that their medication is causing their reduced vision because they might stop taking drugs that they really need for their systemic health. if you think a drug is causing maculopathy, you need to consult with their primary care provider.

Front 510

what is tamoxifen used for

Back 510

treats breast cancer. they used to think that you needed a larger dose than they do now, so tamoxifen maculopathy was more common in the past that it is now

Front 511

name some drugs that can cause vortex keratopathy

Back 511

amiodarone, plaquinil, tamoxifen

Front 512

describe the retinal appearance associated with tamoxifen retinotoxicity

Back 512

multiple superficial yellow crystalline ring-like deposits that encircle the macula. distince appearance.

Front 513

what causes the deposits assocaited with tamoxifen retinopathy

Back 513

they are deposits of the drug its self

Front 514

what is canthaxanthin used for

Back 514

oral agen that enhances suntanning

Front 515

what types of ocular side effects are associated with canthaxanthin

Back 515

prolonged used can cause maculopathy. thiny glistening yellow dots in a donut-shaped ring around both of the maculae. these deposits are in superficial retina and are generally benign.

Front 516

what is talc

Back 516

inert filler material for tablets. drug users crush tablets and boil it before IV injection of narcotics. talc particles enter circulation and embolized most parts of the bloodstream including the retina.

Front 517

how do you differentiate between talc and hard drusen or exudates

Back 517

1. case history 2. talc will glisten on ophthalmoscopy 3. talc is very superficial (anterior to retinal blood vessels)

Front 518

name some of the complications that can be associated with talc deptosits in the retina

Back 518

macular edema, venous engorgement, punctate or flame hemorrhages, and arterial occlusion, blur/blind spots in VF can occur

Front 519

talc deposits on the retinal are typically seen after injection of over 12,000 tablets

Front 520

what is solar maculopathy

Back 520

occurs 2 weeks after exposure to short wave length light (sun-gazing, eclipse viewing, arc welding). causes a very small, circumsribed lamellar hole or cyst on the foveola.

Front 521

what is foveomacular retinitis

Back 521

solar maculopathy when no cause is found

Front 522

what do we think of when we think of the ohio-missippi river valley

Back 522

histoplasmosis

Front 523

what causes histoplasmosis

Back 523

inhalation of spores from feces of chickens

Front 524

why is it called presumed ocular histoplasmosis syndrome

Back 524

because they have never actually isolated the organism in ocular tissues, only found antibodies for it

Front 525

what is the classic retinal triad for histoplasmosis

Back 525

1. histo spots 2. peripapillary atrophy 3. choroidal neovascular membrane

Front 526

clinical pearl: if the lesions have a greenish tinge, think histoplasmosis

Front 527

what is toxoplasma gondii and toxocara canis

Back 527

toxoplasma: protozoan contracted from cats toxocara: roundworm contracted from dogs

Front 528

what ocular consequence is seen during active toxoplasma infection

Back 528

"headlights in the fog"

Front 529

what are the retinal signs associated with toxocara

Back 529

1. central granulomas 2. optic nerve/peripheral granulamas 3. contraction of granulomatous bands between nerve and macula

Front 530

what are angioid streaks

Back 530

crack-like dehiscences in collagenous and elastic portions of bruch's membrane. secondary RPE and choriocapillaris changes. linear grey or dark red linear lesions with irregular serrated edges. streaks link in ring-like fashion around ONH.

Front 531

what retinal findings are associated with angioid streaks

Back 531

1. peau d'organe or lepard skin spotting 2. salmon spots 3. optic nerve drusen 4. choroidal neovascularizatin 5. choroidal rupture (fragile eyes, no contact sports) 6. foveal involvement

Front 532

name some common systemic diseases that are assocaited with angioid streaks

Back 532

1. pseudoxanthoma elasticum (PXE) 2. paget's disease 3. ehlers-danlos syndrome

Front 533

what is pseudoxanthoma elasticum

Back 533

inheritable connective tissue disorder that effects the dermis elastin, arterial walls and bruch membrane. 85% develope angioid streaks.

Front 534

what is paget's disease

Back 534

chronic progressive bone deformity that may result in skull enlargement, long bone deformities and kyphoscoliosis. deafness is common. angioid streaks in 2% of cases.

Front 535

what is ehlers-danlos syndrome

Back 535

rare inherited collagen disorder. hyperelastic skin and hyperextensible joints.

Front 536

what are the ocular complicatinos associated with ehler's-danlos syndrome

Back 536

1. epicanthal folds 2. keratoconus (stroma is made of collagen) 3. high myopia 4. retinal detachment 5. blue sclera 6. lens subluxation

Front 537

what is often the cause of choroidal rupture

Back 537

trauma (usually blunt trauma)

Front 538

what complication may occur after choroidal rupture

Back 538

choroidal neovascular membrane

Front 539

what is this

Back 539

choroidal folds

Front 540

what are the causes of choroidal folds

Back 540

1. idiopathic (more common in hyperopes bc of smaller eye) 2. orbital disease (retrobulbar mass) 3. choroidal tumor 4. posterior scleritis 5. ocular hypotony

Front 541

New lecture: 10Goldmann Visual Fields

Front 542

New lecture: 11DRcarewimagestu2010

Front 543

what percent of diabetic pts have some manifestation of diabetic eye disease

Back 543

61%

Front 544

risk of blindness is about 25 times greater in pts with diabetes. early intervention lessens risk and severity of vision loss. this area is our "bread and butter" in the profession

Front 545

vision loss in diabetics is most frequently caused by diabetic retinopathy, but there are many other ocular manifestations that can severely impact the pt. what are they?

Back 545

1. tritan color vision deficiencies 2. refractive error changes 3. accommodative dysfunction 4. visual field defects 5. EOM anamolies (3rd, 4th and 6th cranial nerves affected due to ischemia) -pupils spared (not blown) in third nerve palsy 6. slugish pupillary reflexes (ischemia of iris tissue, not nerve dysfunction)(stronger meds are required for dilation) 7. conj. microaneurysms 8. dry eye (often severe and overlooked) 9. cornea: reduced sensitivity, reduced wound healing ability, basement membrane abnormalities, endothelial cell morphology changes, increased corneal thickness (edema) 10. iris: depegmentation, rubeosis iridis, peripheral anterior synechia, neovascular glaucoma 11. higher prevalence of cataracts 12. vitreous hemorrhages 13. macular edema 14. ischemic optic neuropathy 15. disc edema

Front 546

there is controversy over whether it is appropriate to treat diabetics with contact lenses

Front 547

it is standard of care to do gonioscopy on diabetics before you dilate to look for neovascularization of the iris and angle

Front 548

vitreous hemorrhage is difficult to diagnose based on observation for the first time observer. it just may look like your view is blurry because the light is being scattered off the blood in the vitreous (picture)

Front 549

when do type 1 and type 2 diabetics need retinal exams

Back 549

type 1: 3-5 years after diagnosis, then annually type 2: at initial diagnosis, then annually -type 1s will generally not have the disease long before diagnosis because it is so acute (that is why they don't need it at the time of diagnosis. types 2s often have had the disease for a long time at the time of diagnosis (20% have retinopathy at time of diagnosis) -more often if poorly controled. -there is controversy in this topic

Front 550

what should you educate pts who are diabetic and of child bearing age

Back 550

it is very important to have more frequent eye exams if they are planning pregnancy or become pregnant.

Front 551

how often should pregnant women with diabetis get a retinal exam

Back 551

in the first trimester and then every 1-3 months through the pregnancy and for 1 year postpartum. (due to the remping up of metabolism)

Front 552

can you dilate a pregnant woman

Back 552

if there is a medical reason it is totally appropriate. for routine exam you might want to put it off if there is no reason to dilate.

Front 553

you need to get the name and address of primary care physician for diabetics so you can write them a letter of evaluation for the pt. it is very common for them to have been told in school that they need to send diabetics to an ophthalmologist, so they need to know that we know what we are doing. also, ophthalmologists are less likely to send a report so they will send more pts to you. (send a report to primary care even if they did'nt refer the pt to you for a diabetic eye exam)

Front 554

most all of the home based blood glucose measuring instruments have a way to keep a running average for their readings.

Front 555

what tests do you need to due during a diabetic examination

Back 555

1. BVA 2. pupillary reflexes 3. motility 4. refraction (may or may not want to rx it if it is fluctuating) 5. visual fields (you need a baseline, so do it if they have not have one before) 6. biomicroscopy 7. gonioscopy 8. tonometry 9. stereo retinal examinatino with dilation 10. photography

Front 556

what is the level we want a diabetics HbA1C to be

Back 556

less than 7%

Front 557

what do we want the blood pressure for a diabetic to be

Back 557

lower than for a non-diabetic. less than 130/80. should be measured at each visit.

Front 558

what do you want the cholesterol levels to be for a diabetic

Back 558

LDL less than 100 mg/dL. less than 70 if they have cardiovascular disease. -send them to lab if they don't know it. if they don't know their sugar levels you should do an in-office finger stick.

Front 559

what percent of diabetics if tested would have diabetic retinopathy. what percent would have proliferative diabetic retinopathy?

Back 559

DR: 25% PDR: 5%

Front 560

describe the pathophysiology associated with diabetes

Back 560

not fully understood. loss of function of intramural pericytes of retinal capillaries (due to glucose causing damage to blood vessel walls). because capillaries don't function well, we end up with non-perfusion.

Front 561

what are the pertinent negatives for diabetic retinopathy

Back 561

1. microaneurysms 2. hemorrhages 3. cotton wool spots 4. hard exudates 5. clinically significant macular edema 6. intraretinal microvascular abnormalities 7. venous beeding 8. neovascualrization of the disc 9. neovascularization elsewhere 10. neovascularization of the iris

Front 562

what is the first clinically detectable sign of diabetic retinopathy

Back 562

microaneurysms

Front 563

what is the best way to see microaneurysms

Back 563

direct ophthalmoscope. you can miss them with a 90 because they are so small. 90 causes minification, direct causes magnification.

Front 564

what are microaneurysms

Back 564

areas of capillaries where the walls have become so thin that they ballon out even though the capillaries are a low pressure system.

Front 565

how do you differentiate between microaneurysms and dot hemorrhages

Back 565

microaneurysms are smaller than 12 disc diameter (average size of a vien at the disc margin). if they are smaller than that consider them microaneurysms. it really doesn't change our tx of diabetic retinopathy, so it is really not that important.

Front 566

fluid does leak from the walls of microaneurysms, so they light up on fluorescein angiography

Front 567

what is the next step in diabetic retinopathy after microaneurysms

Back 567

hemorrhages

Front 568

what does the presence of hard exudates tell us

Back 568

that there is long-standing retinal edema -they are lipid deposits

Front 569

how do you differentiate between hard exudates and drusen

Back 569

hard exuadates are hard looking and have sharp boarders. if you look with stereo, you should be able to appreciate that they are in the anterior layer of the retina (hard exudates). drusen are deeper in the retina.

Front 570

why do hard exudates form

Back 570

because damaged blood vellels leak protein and serum. when it leaks into an area of healthy blood vessels, the serum is absorbed back into the vessel, but since the cell walls of the blood vessel are healthy the protein can not enter back into them and are left in the retina.

Front 571

describe the pathophysiology associated with cotton wool spots

Back 571

they are due to retinal hypoxia. they are due to capillary occlusion in the retinal NFL which causes interruption in axoplasmic flow and swelling in the NFL, which results in death of the NFL. so even after the cotton wool spot is gone, the cells that were swollen are still dead.

Front 572

what is a soft exudate

Back 572

cotton wool spot

Front 573

how do you tell the difference between a hard exudate and a soft exudate

Back 573

soft: irregular boarders, larger size, if they are near a blood vessel they will mask the blood vessel so you can't see it, yellowish in appearance and "soft" looking

Front 574

why is it important to differentiate between IRMA and neovascularization

Back 574

because the management is different. one requires watching and one requires treatment.

Front 575

how do you differentiate between IRMA and neovascularization

Back 575

IRMA: looks flat (neo looks like it is comming out into the vitreous), less disorganized than neo, looks like a curvy road that is a detour around something (neo is completely disorganized; IRMA will often loop around and connect back to the same blood vessel). also IRMA is not new blood vessels and they won't leak like neo would on fluorescein angiography. -picture is IRMA -if you have doubts about whether it is flat or elevated the center lens of the gonio lens gives you the best stereo view.

Front 576

can IRMA progress to neovascularization

Back 576

yes. IRMA is the area where neo is most likely to occur; so in future visits that is the area you would want to watch most closely.

Front 577

what is the difference between IRMA and collateral vessels

Back 577

IRMA is a form of collateral. IRMA usually goes from one blood vessel back to that same blood vessel. collaterals usually go from one blood vessel to another blood vessel.

Front 578

what retinal sign indicates that the pt is at the most significant risk of developing neovascualarization in diabetic retinopathy

Back 578

venous beading. IRMA is the site where it is most likely to occur, but venous beading indicates the most significant risk.

Front 579

what is another name for venous beading

Back 579

boxcarring.

Front 580

describe the pathophysiology associated with venous beading

Back 580

it is caused by hypoxia. hypoxia causes damage to the basement membrane and pericytes of the cell walls. damage to the walls of the blood vessels along with pressure on the vessel from the inside of the eye causes the beading appearance.

Front 581

why is beading more likely to occur in the venous system than the arterial system

Back 581

because the venous system has thinner walls and so will be a lot more influenced by pressure and damage to the wall. there is probably damage to the basement membrane and the pericytes of the arteries too, but since the walls of the arteries are thicker and better able to withstand pressure from the vitreous in the presence of damage to the walls we are less likely to see it in the arterial system

Front 582

retinal edema is tough to see and you need to train yourself to look for it.

Front 583

at what layer in the retina do cotton wool spots, flame shaped hemorrhages, IRMA, dot/blot hemorrhages, hard exuates and drusen occur

Back 583

cotton wool spots: nerve fiber layer flame-shaped hemorrhages: nerve fiber layer IRMA: cappilary bed of ganglion cell layer dot/blot: boarder of inner nuclear layer/outer plexiform layer microaneurysms: boarder of inner nuclear layer/outer plexiform layer hard exudates: boarder of inner nuclear layer/outer plexiform layer drusen: RPE -hard exudates and edema are more anterior than drusen, but less anterior than cotton wool spots

Front 584

how do you define neovascularization of the disc (NVD)

Back 584

neovascularization at or within 1-2 disc diameters from the disc

Front 585

where does neovascularization elsewhere (NVE) tend to occur

Back 585

along the major arcades (often sprouts from IRMA)

Front 586

which is more concerning neovascularization of the disc or elsewhere

Back 586

NVD bleeds more easily and is more concerning

Front 587

translucent fibrous tissue adjacent to neovascularization of the fundus adhere to the vietrous and be pulled when the pt moves around causing bleeding

Front 588

name the MAJOR classifications of diabetic retinopathy

Back 588

1. no diabetic retinopathy (non what so ever; not even any microaneurysms) 2. nonproliferative diabetic retinopathy 3. proliferative diabetic retinopathy 4. clinically significant macular edema

Front 589

name the pertinent negatives for diabetic retinopathy

Back 589

1. microaneurysms 2. hemorrhages 3. cotton wool spots 4. hard exudates 5. IRMA 6. venous beading 7. NVD 8. NVE 9. NVI 10. CSME

Front 590

name the sub-classifications for non-proliferative diabetic retinopathy

Back 590

1. mild 2. moderate 3. severe 4. very severe

Front 591

describe the mild classification of nonproliferative diabetic retinopathy

Back 591

1. at least one microaneurysm (people can get hemorrhages for reasons other than diabetic retinopathy) 2. one or more of the following: retinal hemorrhaging less than standard photo 2A (picture), hard exudate, cotton wool spots 3. definition not met for more severe grades (clinically you should start at the worst category and work your way back because of this point)

Front 592

when we say less hemorrhaging than the standard photo, for example, is that referring to the number or hemorrhages (or whatever it may be) or the severity

Back 592

the guidelines are not clear on that, so clinically you should combine number and severity when making your comparison

Front 593

if you are boarderline in what grading you think the fundus of a nonproliferative diabetic retinopathy pt is, it is more conservative to put them in the more severe category because the guidelines are such that you will see them back more often if they are in the more severe category and you will refer them more quickly if they are in the more severe category.

Front 594

are microaneurysms on blood vessels that you can see on ophthalmoscopy

Back 594

no they are capillaries, which are too small for us to see clinically

Front 595

what is the moderate classification of nonproliferative diabetic retinopathy

Back 595

any of the following: 1. hemes or microaneurysms greater than standard photo 2A 2. soft exudates, venous beading, and IRMA definitely present 3. definition not met for more severe grades -the problem is with line number 2 above. in the severe category they talk about IRMA OR venous beading greater than a standard photo. this implies that you can have IRMA and no venous beading in the severe category, but you have to have both in the moderate category. so what most clinicians do is the following: any of the following: 1. hemes or microaneurysms greater than standard photo 2A 2. venous beading OR IRMA definitely present

Front 596

describe the severe category of nonproliferative diabetic retinopathy

Back 596

4-2-1 rule: -retinal quadrants are divided through the macula, not the nerve head any one of the following: 1. hemes or microaneurysms greater than standard photo 2A in all 4 quadrants 2. venous beading definitely present in at least 2 quadrants worse than standard photo 6B 3. IRMA greater than standrad photo 8A in at least 1 quadrant (clinically most people put it into this category if they are sure that they are seeing IRMA because the standard photo is not very severe) -must be no frank neovascularization and definition for more severe grades not met

Front 597

what is this

Back 597

standard photo 8A

Front 598

what is this

Back 598

standard photo 6B

Front 599

describe the categorization of very severe nonproliferative diabetic retinopathy

Back 599

-two or more features of severe nonproliferative diabetic retinopathy (IRMA in two quadrants for example would count) -definition not met for more severe grades

Front 600

name the categories of proliferative diabetic retinopathy

Back 600

1. early PDR 2. high-risk PDR -there used to be three categories, so don't be confused if you see that in older literature.

Front 601

describe the two categories of proliferative diabetic retinopathy

Back 601

-early PDR (non high-risk): neovascularization of the disc or elsewhere that does not meet the difinition for the more severe grade. -high-risk PDR: one or more of the follwoing: 1. NVD greater than or equal to 1/4 of the disc area (standard photo 10A) 2. NVD with vitreous hemorrhage or pre-retinal hemorrhage 3. NVE greater than 1/2 disc area WITH vitreous hemorrhaging or pre-retinal hemorrhaging

Front 602

what is the definition of macular edema

Back 602

any edema that occurs within 1 DD from the center of the macula -not all macular edema is clinically significant macular edema

Front 603

what is the definition of clinically significant macular edema

Back 603

one or more of the following: 1. thickening of the retina 500 microns (1/3 disc diameter) 2. hard exudates 500 microns from the center of the macula with thickening of the adjacent retina 3. a zone or zones of retinal thickening greater than or equal to 1 disc area in size, any part of which is less than or equal to 1 disc diameter from the center of the macula.

Front 604

does controlling your blood sugar effect the level of diabetic retinopathy

Back 604

yes! stable blood glucose levels may prevent, retard or reverse some complications.

Front 605

what are the referral guidelines for the different categories of diabetic retinopathy

Back 605

refer within 2-4 weeks: macular edema, early (non-high-risk) proliferative diabetic retinopathy, very severe nonproliferative diabetic retinopathy refer within 24-48 hours: high risk proliferative diabetic retinopathy, vitreous hemorrhage.

Front 606

with vitreous hemorrhage there is almost always proliferative diabetic retinopathy

Front 607

New lecture: 12Opt 733 - ARMD Review 2010

Front 608

when was AREDS published and what did it look at

Back 608

2001. first large-scale trial to investigate if supplementation with antioxidants nutrients can help slow the progression of AMD and it's associated vision loss

Front 609

what categories of AMD did the AREDS study look at

Back 609

category 2, 3, 4 and "wet" AMD

Front 610

what were the groups of suppliments that they studies in the AREDS study

Back 610

1. antioxidants (A, C, E) plus zinc 2. antioxidants (A, C, E) alone 3. zine alone 4. placebo

Front 611

describe the AREDS category 1 AMD

Back 611

-total area of less than 5 small (less than 63 micron diameter) drusen -20/32 or better in both eyes

Front 612

describe category 2 AMD

Back 612

-multiple small drusen, nonextensive (less than 20 in number) intermediate (63-124 micron diameter) drusen, pigment abnormalities, or any combination thereof -20/32 or better in both eyes

Front 613

what is category 3 AMD

Back 613

-at least 1 large (greater than 125 micron diameter) drusen, extensive intermediate drusen, and/or geographic atrophy not in macula center -at least 1 eye 20/32 or better

Front 614

what is category 4 AMD

Back 614

-no advanced AMD (geographic atrophy in macula center or choroidal neovascularization) in the study eye, fellow eye either category 4a or 4b category 4a: advanced AMD (geographic atrophy in macula center or choroidal neovascularization) category 4b: VA worse than 20/32 with AMD explaining the VA loss

Front 615

in the AREDS study, for what categories of AMD where there no significant improvement in acuity with any of the therapy options studied

Back 615

category 1 and 2

Front 616

which of the suppliments studied in the AREDS study showed no significant benefits in any AMD category

Back 616

zinc alone or antioxidants alone

Front 617

which AREDS categories showed improvement in visual outcome with antioxidants + zinc

Back 617

categories 3 and 4

Front 618

by what percent does the use of antioxidants plus zinc reduce the risk of progression to advanced AMD in 5 years for category 3 and 4

Back 618

25% (from 28% in placebo to 20% with therapy)

Front 619

what is the contraindication to AREDS vitamins that you have to remember to ask about

Back 619

beta-carotene increases the risk of lung cancer in smokers.

Front 620

what did the blue mountian eye study tell us

Back 620

40-50% reduction in the risk of advanced AMD with high consumption of fish with omega 3 fatty acids

Front 621

what can people do to prevent AMD

Back 621

1. wear UV protection in bright sunlight 2. do not smoke 3. balanced diet rich in green, leafy vegtables and plenty of fruit 4. treat high blood pressure 5. omega 3 fatty acids 6. consider antioxidant and zinc supplements after duscussing with your doctor

Front 622

should you rx AREDS antioxidants

Back 622

you should give them a sample and tell them to take them to their primary care physician because there is always a possibility that they may react negatively with the medications they are on

Front 623

what is AREDS 2 looking at

Back 623

protective effects of xanthophylls (lutein and zeaxanthin) and omega-3 fatty acids on the development of advanced AMd

Front 624

AREDS 2 is currently ongoing

Front 625

what were the results of the LAST study

Back 625

subjects who took the lutein and lutein plus antioxidants showed 50% increase in average macular pigment optical density over 12 months compared to placebo.

Front 626

why is lutein good for the eyes

Back 626

thought to be protective against damage from untraviolet light

Front 627

name the validated treatments for AMD

Back 627

1. laser photocoagulation 2. photodynamic therapy (verteporfin (visudyne)) 3. intravitreat therapy (macugen, lucentis) (avastin is used off-label)

Front 628

what did the macular photocoagulation study look at

Back 628

evaluated laser treatment of choroidal neovascularization through randomized, controlled clinical trials.

Front 629

name and describe the 4 neovascular categories in the macular photocoagulation study

Back 629

1. extrafoveal CNV: 200-2500 microns from fovea 2. juxtafoveal CNV: 1-199 microns from fovea 3. subfoveal new CNV: under the fovea 4. subfoveal recurrent CNV: previously treated with laser and came back

Front 630

what were the visual acuity outcomes found in the macular photocoagulation study for extrafoveal, juxtafoveal, subfoveal new and subfoveal recurrent choroidal neovascular membranes for the treated vs. control groups

Back 630

extrafoveal: 20/125 vs. 20/200 (laser vs. control) juxtafoveal: 20/200 vs. 20/250 (laser vs. control) subfoveal new: 20/320 vs. 20/500 (laser vs. control) (this one at 4 years) subfoveal recurrent: 20/250 vs. 20/320 (laser vs. control) (this one was at 3 years)

Front 631

what is the summery of the macular photocoagulation study

Back 631

eyes with AMD and subfoveal choroidal neovascularizatino benefited from laser treatment vs. observation. eyes recieving direct laser treatment to the fovea for new CNV immediately lost more visual acuity than observed eyes, however, the amount of visual acuity loss in observed eyes exceeded the level of treated eyes after 12 months. eyes with smaller lesion s and worse inital visual acuity had greater and earlier benefits of laser treatment. eyes with large subfoveal neovascular lesions and good initial visual acuity are not good candidates for focal laser photocoagulation.

Front 632

left off at 28:00 on 11-16 part A and slide 39

Front 633

New lecture: 13Management of Vitreoretinal Disorders

Front 634

you need to look at critical landmarks so that you know where you are in the retina when you do BIO (vortex veins, long and short ciliary nerves)

Front 635

many of the retinal diseases are a result of changes in the vitreous

Front 636

name the parts of the vitreous

Back 636

1. posterior hyaloid face 2. anterior hyaloid face 3. cortical gel 4. central gel

Front 637

why is it important to look at the anterior vitreous before you move to the back of the eye when the pt is dilated

Back 637

that is where you will find shaefer's sign; a very important indicator of retinal detachment

Front 638

what are the three most common conditions that put an individual at an increased risk of developing an retinal break or a retinal detachment

Back 638

1. lattice degeneration 2. atrophic retinal holes 3. cystic retinal tufts

Front 639

white without pressure can look like a retinal detachment clinically

Front 640

describe the pathophysiology of lattice degeneration

Back 640

there is a thinning of inner retinal layers with an overlying pocket of liquefied vitreous and attachment of condense vitreous fibrils at the edge of the lesion. this is a setup for a retinal break during a posterior vitreal detachment.

Front 641

where is lattice degeneration most commonly seen

Back 641

you can see it anywhere in the eye, but it is far more common to see it at the equator than anywhere else. typically runs circumfrential. also typically symmetric btwn the two eyes (if you see it superior temporal in one eye you will often see it superior temporal in the other eye)

Front 642

what percent of eyes that come in with a retinal detachment will have lattice degeneration

Back 642

40%. (10-12% of the general population)

Front 643

what are Dr. Jay Haynie's recommendations for the treatment criteria of lattice degeneration

Back 643

treat if: 1. chronic persistant flashing lights (photopsia is caused by vitreous traction) 2. if the fellow eye has suffered a retinal detachment (100% of the time; this is very important and considered standard of care across the nation) 3. consider treatment pre-cataract surgery

Front 644

what is the age of onset of cystic retinal tufts

Back 644

congential lesions

Front 645

what is the best way to see a cystic retinal tuft

Back 645

scleral depression. without scleral depression they look like a little white dot, but with scleral depression they stand out.

Front 646

in what part of the retina are cystic retinal tufts most common

Back 646

superior nasal

Front 647

name three potential negitive retinal outcomes resulted with cystic retinal tufts

Back 647

1. tractional retinal flaps 2. adjacent atrophic holes 3. operculated tears

Front 648

if you have a pigmented lesion in the retinal periphery and the edges of it turn white, what does that tell you?

Back 648

that is most likely a region of lattice degeneration

Front 649

how does scleral depression help you differentiate between atropic hole and a hemorrhage

Back 649

if it is an atropic hole the area of degeneration around the edges will turn white. if you depress a hemorrhage the surrounding tissue will stay its normal color.

Front 650

how do you differentiate between a retinal detachment and whie without pressure if they are similar in appearance

Back 650

1. retinal detachment will be symptomatic (flashes and floaters) 2. retinal detachment will have cells in the vitreous nearly 100% of the time 3. white without pressure will be flat on scleral depression

Front 651

when should you refer lettice degeneration, cystic retinal tufts and atrophic holes for a second opinion

Back 651

1. flashing lights 2. pigment cells in the vitreous 3. family history or RD

Front 652

remember to always make a follow up on pts who are symptomatic. otherwise you will be legally liable.

Front 653

can you see a retinal tear without cells in the vitreous? can you see pigment cells in the vitreous without a retinal tear?

Back 653

you will never see a retinal tear without pigment cells in the vitreous. but you can see pigment cells in the vitreous without there being a retinal tear.

Front 654

if you refer for a second opinion your chances of losing a law suit are extremely rare

Front 655

name the types of retinal detachments. which is the most common

Back 655

1. rhegmatogeneous (by far the most common) 2. tractional 3. exudative 4. secondary to a mass

Front 656

what is a rhegmatonenous retinal detachment

Back 656

associated with a retinal tear

Front 657

what is the incidence of rhegmatogenous retinal detachment

Back 657

1 in 10,000

Front 658

why does the retinal turn pale and opaque when it detaches

Back 658

it has lost its source of oxygen and has become hypoxic. when the retina becomes hypoxic it turns white.

Front 659

why do you have a loss of choroidal detail in the area of a retinal detachment

Back 659

because the retinal is normally transparent. when it becomes detached, it becomes opaque and you lose you ability to see the choroidal detail.

Front 660

how does a retinal detachment affect the IOP

Back 660

lower IOP in the eye with the retinal detachment. this is because the ciliary body shuts down. low IOP is not always seen, so you should not rely on it to diagnose. pressures tend to normalize with time. -the degree of drop in IOP is dependant on the baseline level of IOP. higher baseline equal higher drop in IOP

Front 661

name the 5 different ways of reparing a retinal detachment

Back 661

1. cryotherapy or laser photocoagulation 2. scleral buckling 3. pneumatic retinopexy 4. primary vitrectomy 5. silicone oil tamponade

Front 662

what determines whether you will use cryotherapy or laser photocoagulation

Back 662

the location of the retinal break. if you have a lesion that is anterior to the equator it is very difficult to get a laser back there. if it is posterior to the equator it is harder to get the cryo probe back there.

Front 663

when is cryotherapy or laser photocoagulation indicated

Back 663

cryo and laser are used on very small retinal detachments

Front 664

how does cryotherapy and laser photocoagulation help a retinal detachment

Back 664

seals off spread of sub-retinal fluid and prevent the tear from progressing

Front 665

how does cryotherapy work

Back 665

the cryo probe is basically like a scleral indenter. when the surgen indents the area of the lesion, he steps on a pedal and the probe (which is hooked up to a tank of nitrous oxide) feezes the outer eyewall and the cold creates chorioretinal scar in the area of the retinal break.

Front 666

you can not do laser photocoagulation through sub-retinal fluid. so if there is serous fluid under a retinal tear they have to laser all the way out at the attached retina.

Front 667

describe the scleral buckel procedure

Back 667

scleral buckel requires the pt to be put under general anesthesia. it is done in conjunction with vitrectomy. then a silicone band is place around the eye underneath the extraocular muscles. the band is then tightened, resulting in increasing of the axial length of the eye and significant increase in refractive error (myopic direction) -think of a rubber band that you have stretched out. there are two ways to relieve the tension on the rubber band. you can either bring the ends of the rubber band closer together (scleral buckle) or you can cut the rubber band (vitrectomy)

Front 668

name some of the complications that can result from scleral buckle

Back 668

1. if they tighten it too tight it is uncomfortable 2. if they place the band over a vortex ampule they can block circulation resulting in chronic choroidal edema 3. if they place it on the eye crooked, they can end up with a tropia (diplopia is common)

Front 669

when is a scleral buckeling proceedure done

Back 669

the only time it is done is when there is an inferior retinal detachment (between 5 and 7 o'clock). this is the only option when the break is in that location (because gas bubbles don't work on inferior detachments; because they would have to stand on their head to get the bubble in the right position)

Front 670

describe the procedure of pneumatic retinopexy

Back 670

injection of gas to flatten retina and force the subretinal fluid back into the vitreous cavity. then cyrotherapy to seal the tear (laser is possible, but you can't do laser through a gas bubble). gas bubble stays in the eye for 10-12 days. the amount of fluid that is displaced with the gas bubble is then removed with paracentesis. then the pt must be instructed on how to hold their head in a position where the gas bubble is over the tear.

Front 671

how long does it take a retinal tear to begin to seal and to completely seal after cryotherapy or laser photocoagulation

Back 671

it takes a tear 5 days to start and 3 weeks to finish sealing after laser or cryo therapy.

Front 672

what is the success rate with pneumatic retinopexy

Back 672

about 50%. most common reason for failure is that the patient didn't position themselves in the position they were instructed to. second most common reason for failure is that the surgen didn't find all the retinal breaks.

Front 673

why do they never do pneumatic retinopexy on a pseudophakic eye

Back 673

pseudophakes are very well known for having multiple small breaks in the retina that were created at the time of the surgery and never developed into retinal detachment until the big one came. if you don't seall ALL of the breaks the procedure is going to fail and they are known for having many breaks that are difficult to see clinically.

Front 674

what is the most common method of reparing a retinal detachment

Back 674

primary vitrectomy

Front 675

what is a primary vitrectomy

Back 675

vitrectomy with fluid exchange/gas bubble.

Front 676

what is the advantage of a primary vitrectomy over a pneumatic retinopexy

Back 676

the difference between primary vitrectomy and a pneumatic retinopexy is that the vitrectomy is done in primary vitrectomy. if you don't remove the vitreous and they have an unnoticed break in the retina they can have more breaks down the road. if you do a vitrectomy it is very rare to have a break later down the road, because you have "cut the rubber band" and relieved the tension on the retina. also with primary vitrectomy you can fill the eye 100% with gas, and so the positioning of the pt is not as critical.

Front 677

name the three types of gas that can be use in primary vitrectomy and how long they last in the eye before they are reabsorbed.

Back 677

atmospheric air: 2-3 weeks FS6: 2-3 weeks C3F8: 3 months -less if pneumatic retinopexy because there is less volume of gas in that procedure. -there are things that pts can not do with a gas bubble in their eye. they can't lay flat on their back. they can't travel over a pass or fly in an airplane (because the gas will expand)

Front 678

is silicone oil as a viteous placement temporary or permanent

Back 678

they are permanent. thety are only removed if there are complications.

Front 679

when is silicone oil used for a treatment of retinal detachment

Back 679

when other therapy options have failed.

Front 680

what is the most common location for a peripheral iridectomy? when would you see it in the inferior position?

Back 680

most common is at 10 and 2 o'clock. the only reason they would have one in the interior position is if they have or have had silicone oil in the eye. the reason is that if you have oil in the eye you are likely to create a pupillary block situation (if there is a lens in the eye) and there is no where for the aqueous to go.

Front 681

if you have to put silicone oil in the eye, what type of IOL do you need to avoid or remove and why?

Back 681

silicone IOL. the IOL and the oil will lock together and completely fog up the lens

Front 682

what can cause a tractional retinal detachement

Back 682

1. proliferative retinal vascular disease (diabetic retinopathy being the most common type) 2. proliferative vitreoretinopathy 3. penetrating ocular trauma

Front 683

tractional retinal detachments are a slow moving process and they are immoble

Front 684

what are the therapy options for a tractional retinal detachment

Back 684

vitrectomy is the only option. -you have to mechanically peal the retinal fibrosis off so that the retinal can lay back down. they often end up with silicon oil in the eye.

Front 685

what is an exudative retinal detachment

Back 685

fluid accumulates under the retina from a pathologic lesion. there is not tear in the retinal and there is not uverlying fibrosis.

Front 686

name some of the potential etiologies of exudative retinal detachment

Back 686

1. retinal hemangioma 2. coat's disease 3. choroidal tumor 4. posterior uveitis 5. severe macular degeneration 6.

Front 687

with an exudative retinal detachment is the area of the fluid accumulation fixed or mobile

Back 687

fluid shifts with pts head position

Front 688

how do you treat an exudative retinal detachment

Back 688

laser or cryo is applied to the area where the leak is occuring. the RPE then pumps out the accumulated fluid over time and the detachment will reattach

Front 689

what is the time frame for retinal detachment with macula on and off

Back 689

macula on: same day referral! macula off: within 48 hours (permanent vision loss regardless of treatment)

Front 690

what are the two major differentials with retinal detachment

Back 690

1. retinoschisis 2. choroidal detachment

Front 691

what is the refractive error associated with retinoschisis?

Back 691

over 70% hyperopic

Front 692

what location is most common for retinoschisis? are they unilateral or bilateral

Back 692

inferior temporal. BILATERAL 99% of the time.

Front 693

you can fairly well differentiate between retinal detachment and retinoschisis based on history and presentation. RDs are usualy in myopes, retinoschisis in hyperopes. RDs are unilateral, retinoschisis is almost always bilateral.

Front 694

what pertinent negatives do you need to document if you have a retinoschisis

Back 694

1. absence of a demarcation line 2. inner wall holes 3. outer wall breaks a demarcation line is a line of pigment that forms on the posterior margin of a retinal detachment (signifies the chronic presence of sub-retinal fluid). -if you see a line of pigment it is NOT a retinoschisis.

Front 695

can a retinoschisis progress to a retinal detachment

Back 695

yes

Front 697

is retinoschisis stable or progressive

Back 697

stable. if it is progressing it is probably a retinal detachment.

Front 698

what is the most common cause of choroidal detachment

Back 698

surgery. it is caused by low IOP

Front 699

what is the treatment for choroidal detachment

Back 699

lots of steroids. this raises the IOP and they usually resolve on their own. rarely they will need to be drained.