Glaucoma Flashcards
Pilocarpine : Mechanism of Action
Parasympathomimetic - Pilocarpine directly stimulates cholinergic receptors, acting on a subtype of muscarinic receptor (M3) found on the iris sphincter muscle, causing the muscle to contract and produce miosis. timulates the sphincter pupillae in the iris and the ciliary muscle, resulting in displacement of the scleral spur, opening of the trabecular meshwork and/or Schlemm’s canal, and enhancement of conventional aqueous outflow.
Beta-Blockers: MOA
Beta-blockers decrease aqueous humor production by the ciliary body and hence reduce IOP.
Carbonic Anhydrase Inhibitors
Carbonic anhydrase is an enzyme that catalyzes the reaction of H2O and CO2 in equilibrium with H+ and HCO3−. The net effect of the enzyme on aqueous production is to generate bicarbonate ions, which are transported actively across the ciliary epithelial membrane into the posterior chamber (sodium is the primary cation); an osmotic gradient is established. Water passively follows because of the presence of the gradient, which results in aqueous production. Inhibition of this enzyme results in lower IOP because aqueous production is decreased approx 50% or more;aqueous outflow and episcleral venous pressure are affected little or not at all.
Alpha-Adrenergic Agonists
Apraclonidine decreases aqueous production but is also associated with an increase in outflow facility and a decrease in episcleral venous pressure. Brimonidine is 23 times more alpha-2 selective than apraclonidine and 12 times more selective than clonidine. Its mechanism of action includes a reduction in aqueous formation as well as an increase in uveoscleral outflow
Relate Ciliary Body Anatomy to demonstrate the difference between Angle Recession, cyclodialysis and irido-dialysis
Angle recession is a separation between the longitudnal and radial muscles of the ciliary body. (you see a wide CB band but otherwise N structures) Cyclodialysis is when the longitudnal muscles separate from the scleral spur and ca cause hypotony and haemorrhage. Irido dialysis is separation of the iris root and the ciliary body.
OHTS found 5 significant risk factors that increased the risk of POAG
- age
- higher iop
- CDR
- greater pattern standard deviation
- reduced CCT
What were the pressure lowering goals of OHTS and CNTGS
OHTS: 20% from baseline
CNTGS: 30% from baseline
What are the risk factors for steroid responders (5)
- known POAG
- family hx
- age
- DM
- myopia
DDx of arcuate defects
Glaucoma ONH drusen NAION, AAION Myelinated NFL Hemiretinal vein occlusions BRAO Optic nerve colobomas, pit Laser scars to one area of retina
DDx of enlarged blind spot
ONH drusen Papilledema Diabetic papillitis Hypertensive papillitis Optic neuritis MEWDS/IEBSS Megalopapilla High myopia (PPA)
Glaucomatous nerve features
High CDR Assymetric CDR Notch Loss of NFL Optic disc hg Bayonetting of vessels Nasalisation of vessels Vertical elongation of the cup Laminar dots (?)
Systemic associations with drusen
Autosomal dominant
PXE
Sickle cell
DDx of glaucomatous nerve
Physiologic cupping
Tilted discs
Anything that causes nerve damage... Glaucoma (open or closed) Optic neuropathies compression toxic/metabolic vascular insults
Disc hg ddx
Glaucoma (esp NTG) Hemorrhagic PVD Papilledema NAION AAION Diabetes HTN Valsalva
Thickest rim
I>S>N>T
Most suspectible to glaucoma (parts of the rim)
I>S>T>N
Angle most open
Inferior
Angle most pigmented
Inferior
Deep AC in who
Myopes
Young
Male
(basically everyone who gets PDS)
Shallow AC in who
Old
female
hyperopes
Eskimo/Asians
Steroid responder risks (5)
POAG Family history Age Myopia DM
CDN guidelines for suspect, early, mod, and adv glaucoma (dx and management)
Class; CDR; VF; Tmax you want; lower by
Suspect; — ; — ; 24; 20%
Mild; 10deg from fixation; 20; 25%
Moderate; 10 deg from fixation; 17; 30%
Severe: >0.9, within 10 deg of fixation; 14; 30%
Dose of MMC for trab
0.01% for 2 min (in real life this varies but this is a reasonable exam answer)
Two types of VF testing
Static (Humphrey or Goldmann)
Kinetic (Goldmann)
DDx of hyphema in adult
Trauma Bleeding diathesis Leukemia Ocular surgery Fuch's Other NVI/NVA UGH
PXF cataract risks
Poor dilation Stiff pupil Zonular weakness Increased risk of phacodynesis and vitreous loss Capsular fragility Lower endothelial cell count Unstable IOP post-op (spikes) Post-op inflammation
Findings in PXF
Poor dilation Ring of pigment on anterior lens capsule PXF material on pupil margin Pupil margin TID Pigmented angle Sampolessi line
Membrane over angle
ICE
Epithelial ingrowth
PAS (uveitis, bad ALT, chronic ACG)
NVI
ICE clinical variants
Chandler - mostly cornea
Iris nevus - membrane on iris tents up normal stroma to look like nevi (not actually nevi)
Essential iris atrophy (correctopia/polycoria)
3 lytic glaucomas
Lytic = macrophages clog up TM with junk
Phacolytic - lens particles
Hemolytic - RBC from hyphema
Melanomalytic - pigmented melanocytes (or something) from melanoma cells floating around
Secondary glaucomas after IOL implantation
UGH
Pupil block angle closure
Secondary pigmentary glaucoma
Pigmented TM in who
Pigmented people Older people PXF PDS Melanomas
IOP formula
IOP = F/C + EVP
Types of tonometry
Indentation - Schiotz
Applanation - tonopen, Goldmann, Perkins, pneumotonometer (don’t let this last one throw you - unless they say AIR PUFF, it’s still a contact tonometer)
Non-contact - air puff
Glaucoma with pigment
PXF PDS Pigmented people with open angles Pigment on endothelium from old inflammation, cataract surgery, trauma, hyphema ICE Melanoma
Intermittent ACG findings
Hx of intermittent ACG \+/-Normal IOP PAS Glaucomflecken Signs of glaucmatous damage to ON
Risk of ACG in the fellow eye after AACG
75%. So always do prophylactic LPI
Segmental iris atrophy
Cataract surgery Trauma HSV, EBV, CMV, VZV ICE syndrome Axenfeld reiger PPMD
Iridodenesis
Separation of iris from CB
Usually result of trauma or surgery
Rx with coloured CL or surgically re-insert
Causes of ectropion uveae
ICE Axenfeld reiger Uveitis PPMD NF-1 Epithelial downgrowth NVG uveitis
How do you tell epithelial ingrowth vs fibrous downgrowth
Epithelial ingrowth turns white with YAG
Lens induced glaucomas
Phacomorphic - angle closure with pupil block
Phacolytic - lens particles leak through intact capsule. Minimal inflammation, but macrophages ingest the particles and obstruct. NO KP.
Phacoanaphylactic - broken capsule. Maybe after surgery. Some books call this the same as lens particle glaucoma. LOTS OF INFLAMMATION with KP’s.
Lens particle - basically the same thing. Maybe it’s more after cataract surgery with some lens left behind.
UGH - from IOL
Dislocated lens (if dislocates anteriorly, causes ACG)
Same with microspherophakia causing ACG
Cyclodialysis def’n and treatment
Separation of CB from SS
Result of either trauma or surgery
Gonio to confirm
Rx with cycloplegics, most will close on their own in 6/52
Cause hypotony in the meantime, +/- spike when its closing
Risks for OHTN progression
Age High IOP High CDR High pattern standard deviation Low CCT
CCT definition in OHTS
588 = thick
RF for OAG
Age High IOP Family history Race Other: HTN, DM, Myope, migraines?
RF for AACG
Female Age Previous ACG Race - inuit or asian Hyperopic Nanophthalmos Family history
RF for NTG
Female Disc hg migraine vasospasm/raynauds smoking
DDx of NTG
IOP is high, but you’re not measuring it:
- uncalibrated equipment
- low CCT
- corneal edema
IOP is high sometimes but you’re missing it:
- diurnal fluctuations
- intermittent ACG
- Posner Schlossman episodes
IOP was high before but its ok now:
- burned out OAG (PDS, PXF)
- old AACG
It’s not glaucoma at all:
- ONH drusen
- old optic neuritis, NAION, AION, etc
- compressive lesion (do a CT - nerve to chiasm)
- infiltrative lesion of the nerve (sarcoid, TB, lyme, etc)
Only if you’ve ruled all that out can you call it NTG.
Acute IOP rise ddx
After laser (LPI, SLT, etc)
After surgery (retianed visco, retained lens particles)
Inflammatory (HSV, CMV, Posner Schlossman, Fuch’s)
Steroid responder
After hyphema
AACG
Characteristics of plateau iris and treatment
Deep central AC, shallow periphery
Flat iris
Bunched up iris in angle
No change in configuration despite LPI
Rx:
- always make sure they have an LPI first
- Argon iridoplasty to pull the iris out of the angle
- miotics
DDX of increased EVP
AV malformation: CCF, SWS, orbital varix
Lesion compressing SOV: thyroid, tumor, orbital vein thrombosis, cavernous sinus thrombosis, SVC syndrome
Idiopathic: posture (lying down), familial EVP
DDx of blood in Schlemm’s
High EVP (AV issues, something compressing SOV)
Hypotony (inflammation, hypotony, following trab)
Normal with compression gonioscopy (occludes episcleral veins)
DDx of axenfeld-reiger
ICE Aniridia Isolated posterior embryotoxin (N in 15%?) Peter's anomaly Ectopia lentis et pupillae (no glaucoma)
Systemic findings in axenfeld reiger
Microdontia
Redundant peri-umbilical skin
Schabel’s optic atrophy def’n and ddx
Hyaluronic acid infiltation of the nerve (stains with colloidal iron, alcian blue)
either from end-stage glaucoma or ischemic optic neuropathy (NAION, AION, etc)
Posterior pushing mechanisms of ACG
Choroidal effusions Vitreous overfill from gas Ciliary body mass Supra-choroidal hemorrhage Malignant glaucoma Contraction of retro-lental tissue (ROP, PHPV)
DDx of NVI/NVA
Fuch's heterochromic iridocyclitis DM, radiation retinopathy, OIS CRVO, BRVO, CRAO RB!!! Always think RB ROP/FEVR/Eales Sickle cell
Types of ONH analysers
Surface topography - HRT
Cross section - OCT
Types of setons
Valved (Ahmed)
Non-valved (Baerveldt, Molteno)
Pilocarpine for ACG - what types of ACG?
Really just for pupil block or plateau iris
Everything else you dilate (malignant, CACG, NVG, cyclodialysis)
Also, pilo won’t work in IOP > 40 because iris muscle is ischemic. Need to lower IOP first
Malignant glaucoma risks
Hyperopia Female Nanophthalmos Previous ACG Recent surgery (5d)
Malignant glaucoma rx
Always do an LPI first to resolve any component of pupil block
Dilate
Decrease IOP with aq suppressants or hyperosmotics
If pseudophake/aphake, can YAG anterior hyaloid face
If phakic, need vitrectomy
Injuries with anterior segment trauma
Conj laceration Scleral perforation Corneal perforation Hyphema Traumatic iritis Traumatic mydriasis Angle recession Cyclodialysis Iridodialysis PVD RT, GRT RD Retinal dialysis
Nanophthalmos - what do you get in the eye and how do you treat
- Large lens - gives phacomorphic ACG. LPI. Can dilate to pull the lens back a bit.
- Thick sclera - get uveal effusions. Can do sclerectomies
- Malignant glaucoma - LPI, dilate, YAG hyaloid/vitrectomy
- Can also get high EVP from outflow obstruction through thick sclera - aq suppressants
Why cycloplege in uveitis
Reduces pain
Reduces PS
Reduces PAS by deepening the AC
Stabilise blood-aq barrier
Deadly effects of atropine
Red as a beet, dry as bone, mad as hatter, hot as hades, blind as a bat
Red - vasodilation, flushing, tachycardia Dry - dry eyes, dry mouth, constipation Mad - delerium Hot - fever Blind - cycloplegia
Rx with acetylcholinesterase inhibitor - e.g. physostigmine
Side effects of phospholine iodide
Iris cysts and ASC cataracts
Side effects of b-blockers
ASTHMA AND DECREASED HR/heart block
- always ask about asthma and check HR before giving BB
Side effects of brimonidine (and C/I)
NEVER GIVE TO CHILDREN - causes respiratory distress/apnoea, CNS depression, hypotension
Adult s/e:
- allergy
- increased HR
- HTN
- vasodilation/flushing
Side effects of CAI (and C/I)
Know this cold.
- SJS
- metallic taste
- tingling in hands/feet
- APLASTIC ANEMIA
- renal failure
- metabolic acidosis
- renal stones
- SICKLE CELL CRISIS
Don’t give to sickle cell ppl or kidney failure
Cloudy cornea infant ddx
G-STUMPED
Congenital ocular anomalies with assoc glaucoma
Anterior segment anomalies:
- ICE
- axenfeld reiger
- aniridia
- nanophthalmos, high hyperopia
- microspherophakia
Cornea:
- sclerocornea, megalocornea
Retina:
- PHPV, ROP
Systemic things:
- Lowe’s (cataract + glaucoma)
- Rubella (cataract OR glaucoma, never both)
Schwartz syndrome
Photoreceptor OS’s from old RD clog the TM and cause glaucoma. Resolves after RD repaired.
Hemosiderotic glaucoma
Hemosiderin from hyphema/vit hx clog TM
Thymoxamine - whats it used for
Causes pupil constriction without shifting iris-lens diaphragm forward. So you can see the effect of un-bunching iris from the angle without changing the position.
Helps you decide if prophylactic LPI would actually be helpful
(never actually used, i don’t think)
Photophobia/tearing child
Glaucoma
Lid/eyelash malposition
Corneal irritation, trauma, abrasion, infection
Dacryocystitis, congenital NLDO, canalliculitis, etc
Congenital glaucoma triad and signs
Tearing, blepharospam, photophobia
enlarged K diam cloud K Haab striae (horizontal) high IOP high CDR increasing myopia
Definition of congenital vs infantile vs juvenile glaucoma
Congenital = 0-3 mos Infantile = 3 mos - 3 years Juvenile = 3 yrs+
Descemet tears - diff types
Forceps trauma - vertical
Haab striae (glaucoma) - horizontal
Vogt’s striae (KC) - concentric to cone
Hydrops, PBK
Options for painful blind eye
Always do yearly B-scan to rule out mass if there’s no view
- atropine/PF
- cyclophotocoagulation
- retro-bulbar alcohol or chlorpromazine
- enucleation/evisceration
GA effects on IOP measurement
Ketamine and succinylcholine increase IOP
(KISS of high IOP)
Others lower it
Glaucoma surgery in kids - when to do what
Medical management is just temporizing in kids. Start with CAI. Never give brimonidine.
- goniotomy - needs clear K
- trabeculotomy - don’t need clear K
- trabeculectomy - if the others fail
6 reasons to do an LPI
- acute ACG
- prophylactic if other eye has ACG
- occludable angles
- malignant glaucoma
- plateau iris
- if silicone oil in an aphakic eye (do it inferiorly. SO rises so a superior one will get plugged with SO)
- with ACIOL
Define false positive
Patient presses the button when there is no stimulus provided
Max acceptable = 30%
Define false negative
Patient doesn’t press the button despite it being suprathreshold and in the same area as where they previously saw it
Max acceptable = 30%
Define fixation loss (2 ways)
- There’s a pupil tracker on most machines that follows where the patients eye is moving
- Patient sees a spot that’s in the blind spot that was already mapped out
Max acceptable = 1/3
What is short term fluctuation on VF
10 points are re-tested 2x each
It measures the difference in brightness that the patient responds to
Can reflect inattention or advanced dz
What is MD on visual field
Average of the deviation of all the patient’s spots from age-matched control. Measure of the total drop in VF (could be due to glaucoma or cataract/etc)
What is PSD on visual field
Measure of the standard deviation of the difference in the patient vs age-matched control. An estimate of the depression in the hill of vision
How would a scotoma look if BCVA is
Wider and deeper
What happens to the VF if pupil
Globally depressed
How do you define a scotoma on VF
Area of vision >3 degrees that is depressed >6 db
Or 1 pt on Humphrey > 10 db depressed
or 2 adj points > 5 db each
What is the definition of legal blindness
BCVA in the BETTER eye
what doubles in FDT
It’s basically a bunch of wide stripes that they flicker really fast in different areas of the VF
So it’s high temporal frequency, low spatial frequency
What doubles is the temporal frequency
What cells do FDT preferrentially test for
M cells (may be affected first in glaucoma so it may be more sensitive as a screening tool than humphrey)
What are the 4 types of VF testing algorithms
Acronym - STER (like a STER-case that we know is used in VF testing)
- Threshold: staircase of up 4 db, then down 2 db until it reverses again
- Supra threshold: screening test that shows bright spots higher than threshold. Only picks up severe defects as a screening tool.
- Efficient threshold: estimates threshold for age-matched and tests those first. Subsequent spots up/down based on what was seen. Only one reversal @ each spot (=SITA)
- Threshold-related: Threshold determined for a few points then hill of vision determined from those. Then shows 6 db brighter at all spots than threshold - i.e. again just a screening tool for mod/adv dz.
How do you classify ACG
Primary or secondry, pupil block or not
Primary pupil block: AACG
Primary non pupil block: chronic ACG, plateau iris
Secondary pupil block: phacomorphic, PS, bombe, lens dislocation/microspherophakia, IOL pupil block
Secondary non-pupil block:
- Anterior pulling: PAS, NVG, ICE, PPMD, epithelial downgrowth
- Posterior pushing: choroid (effusion or anterior rotation), vitreous pressure (silicone oil, gas, tumors, aq misdirection), retro-lental membranes (ROP, PHPV)
What did GLT show
L = laser, T = timolol
Laser (ALT) vs drops as first line therapy. Both are ok.
What did CIGTS show
T = timolol, S = surgery
For initial glaucoma, is medical therapy better or surgery?
Surgery was worse initially but both had equal Va and IOP control and VF changes at 5 years
What did EMGT show
T = timolol (vs nothing)
Is lowering IOP even helpful for glaucoma?
Used timolol +/- ALT needed
Answer is yes, obviously.
53% progressed (62% with no rx, 45% with rx)
What did AGIS show
S = surgery
This was primarly a surgical trial looking at ALT vs trab in advanced glaucoma that had failed medical therapy.
Results based on race:
- Blacks: ALT is better initially (because they scar a lot - think keloids - so trab is not going to be good)
- Whites: trab is better initially
ALT failure assoc with young age, high IOP
Trab failure: young age, higher IOP, DM, post-op complications (IOP, inflammation, etc)
What did TVT show
Looked at people with glaucoma who either had prev cataract or prev trab surgery
Randomized to get a trab (with MMC) or tube as the next step
Both groups did well. Therefore, tubes can be used earlier than previously thought.
What did OHTS show
Inclusion: IOP 24-32, normal field, normal nerve
Lowering IOP by 20% reduces progression from 9.5% to 4.5% over 5 years
Risks for progression:
- age
- lower cct (
What did NTGS show
Lowering IOP by 30% is helpful in reducing progression
Risks of progression:
- female
- disc hg
- migraine
What are the laser settings for ALT
Argon Spot size 50um Power 400 mw Time 0.1 s 50 spots x 180 deg
What are the laser settings for SLT
YAG laser on SLT setting
400 um size
power - start at 0.6-0.9 mJ, want champagne bubbles on some shots
50 spots / 180 deg
What are the laser settings for iridoplasty
Argon
500 um size
400 mw power
0.5 - 1.0 seconds (whoa, long)
Think of iridoplasty as 10x argon... same power (400 mw) 10x spot size (500 vs 50) 10x time (1 sec vs 0.1 sec)
What is total deviation on VF
Map of deviation of each point from an age-matched control
What is pattern deviation on VF
Take the total deviation, subtract the 7th BEST point and apply that subtraction to all points
Should remove media opacities or general depressions and help you see the hill of glaucoma defects
Gene for PXF
LOXL-1
2 types of outflow and relative contributions
Trabecular = 90%
UVS = 10%
(% vary depending on source)
What drops have an effect on which outflows
PG’s: increase UVS
Alpha ag: increase UVS
Cycloplegics: increase UVS
Miotics: increase TM outflow
Greatest site of resistance to outflow
Juxta-canalicular meshwork (part of UVS pathway)
Outflow measurement called what
Tonography
Outflow rate normally
0.22-0.28 ul/min/mmHg
GAT size
3.06 diam
Ideal cct for GAT
520 um
How to clean GAT
alcohol wipe
or 5 min soak with:
- 70% etoh
- 1:10 bleach
- 3% hydrogen peroxide
Schaeffer grading system for narrow angle
I = narrow IV = open
What supplies ONH
short posterior ciliary arteries
NFL supplied by what
recurrent branches from CRA
everything OPL and forward is from CRA
2 theories of glaucoma damage
- mechanical: compression of NFL axons from high IOP causes damage
- ischemic: poor blood flow to NFL axons causes them to die
% normals with CDR > 0.6
5%
% normals with assym CDR > 0.2
1%
Hemifield assymetry on VF
compares top half of VF to bottom half
sup is normally 1-2 db less than inferior
(see better inferiorly)
anything different is suspicious
Narrow angle provocative tests
Prone-dark test (30-60 min lying prone in the dark)
SLT best for who
Pigmented glaucoma and angles
PXF and PDS
PDS - risk of glaucoma
25-50%
Who gets PDS
young, myopic, males
Compare Fuch’s vs Posner Schlossman
Fuch’s:
- presents with blurred vision
- fine stellate KP
- min AC rxn
- iris heterochromia
- fine angle vessels that bleed easily
- treat IOP, steroids don’t really help
PS:
- mild AC rxn
- no KP
- no heterochromia
- episodic unilateral pain
- rx with steroid (IOP should come down on its own)
Sickle cell - how to treat IOP
avoid CAI
avoid alpha-1 ag (apraclonidine). alpha-2 ok (brimonidine)
Abx in kids - whats not ok
Tetracyclines def not ok
When do you get ghost cell glaucoma
1-3 months after vit hx
How do you treat ACG from microspherophakia
DILATE the pupil (flattens the lens and pulls it back)
How to treat fibrous ingrowth/epi downgrowth over the angle
If blocks the angle, treat with meds first
Can’t do laser
Rx for topamax induced ACG
dilate the pupil (rotate CB backwards)
how to treat glaucoma in pregnancy
All drugs class C except brimonidine (class B) better to do laser first if you can
Stop brimonidine once she starts nursing
ALT stats
Decreases IOP by 20-25%
80% ppl respond
50% success at 5 years (10% per year drop off)
Bleb endopht risks
young age
male
blepharitis
dacryocystitis, NLDO
Bleb endopht bugs
Strep pneumo, H flu
How to treat bleb endophth
tap and inject + fortified topicals
EVS PPV results don’t really apply. So might do PPV earlier I think?
Rate of aq production
2-3 ul/min = 3 ml/day
AC vol
250 ul
Fluorophytometry is what
Measures rate of aq production
Decreased aq production with:
age
sleep (45% less!)
inflammation, surgery, trauma, meds
Aq humor compared to plasma
15X more ascorbate (remember this one)
Less protein, less ca, less phosphorous
everything else the same
Blood:CB barrier is…
fenestrated
CB = what layers
Inner non-pigmented epithelium (equiv to retina - inner and non-pig)
Outer pigmented epithelium (continuous with RPE - think outer, pigmented)
