Final Flashcards
How to reduce progression in glaucoma?
IOP control. No longer part of glaucoma definition.
GLT
Glaucoma Laser Trial. Argon laser trabeculoplasty vs. topical meds. Found that ALT is at least as efficacious as topical medical therapy.
Laser trabeculoplasty options
ALT, SLT, MLT.
MLT
Adjustable pulse diode laser. Allows for cooling affect. Multiple doses
AGIS. What did it ask
Advanced Glaucoma Intervention Studies. How to treat advanced glaucoma.
Groups in Agis
- ALT-trabeculectomy-trabeculectomy 2. Trabecultecomty-ALT-Travecultectomy
Result of AGIS
VF worsened in all groups except in the 100% <18. . Progression halted if IOP reduced by 38-46% and IOP kept below 18 with a mean of 12.
EMGT
Early manifest glaucoma trial. 1. ALT and topical betaxolol. 2. observations.
EMGT results
Less progression with treatment. CCT was risk factor for high IOP. Each 1 mm hg of higher IOP gaze a ratio of 1.13 for progression of POAG.
CIGTS
Collaborative Initial Glaucoma Treatment Study. Looked at filtration surgery vs. meds. Less progression with meds.
OHTS
Ocular hypertension treatment study.
OHTS outcome
more progression in observation. CCT is greatest risk factor.
CGS
Canadian Glaucoma Study. Look at risk factors for VF progression.
CGS results
1 mm HG increase in pressure has increased glaucoma risk. Female, abnormal baseline anticardiolipodiman, age.
DIGS
Diagnostiic Intervations in Glaucoma.
DIGS
Just followed the patient with no tx. 25% progression. CCT, age, IOP, C/D, and PSD were the risk factors.
EGPS
European Glaucoma Progression Study. Looked at dorzolamide vs. observation. No difference in progression between the two.
CNTGS
Collaborative Normotensive Glaucoma Study. 1. Topical meds or surgery 2. observation.
CNTGS results
Less progression with tx. Women, migraine suffers, and patient who present with disc hemorrhages are at greater risk of progression.
LoGTS
Low pressure glaucoma treatment study. Compare brimonidine to timolol.
LoGTS results
similar efficacy. Less progression with brimonidine.
NYGS
New York Glaucoma Study. Mean IOP and Peak IOP fluctuations associated with VF progression. 1mmHG increase glaucoma progression by 10%.
Key clinical points from landmark studies
- 1 mm hg increase is 10% risk. 2. Glaucoma progression decreased if 20-30 reduction. 3. Halted if below 18.
Causes of POAG and OHTN
50% have >21 mm HG
Why progress of glaucoma even with TX
Undetected IOP spikes, noncompliance, increased suspectiblity of the lamina cribosia, other processes outside of IOP that damage ganglion cells (premature apoptosis, insufficient ocular perfusion, neurodegenerative process)
Most important non ocular risk factors in glaucoma
Family history, Age, Race (black)
Most important ocular risk factors
Large C/D, Elevation IOP, Thin Corneas.
When is IOP highest
during the night
Corneal hysteresis
The pressure when bend cornea with puff and then bends back. 10. Lower is higher risk for glaucoma. Decreases with age. Lower in keratoconus, glaucoma, and fish’s corneal dystrophy.
What RE is most likely to get glaucoma
Myopia
Diastolic Perfusion Pressure
Lower is greater risk of glaucoma. <30? Decreases at night time as well as blood pressure.
Vascular risk factors and glaucoma
increased risk with migraine, low profusion to fingers, nocturnal hypotension.
40 micrometers decrease in CCT equal
71% glaucoma risk
When to tx for glaucoma
- change in VF or ON 2. wants it 3. vascular dz with dance or vascular occlusion 4. Iop above 30
CRVO
Twice as likely to occur in an eye with glacumotous cupping.
Guidelines for IOP target
decrease by 20%.
Early glaucoma
deficiencies in optic nerve that are char. of glaucoma but no VF changes or only changes with short wavelength or frequency doubling.
Moderate glaucoma
ON deficients and VF defect in 1 hemifield but not within 5 degrees of fixations.
Late glaucoma
ON deficients and VF defects in both hemifields and/or within 5 degrees of fixations.
Target IOP guidelines
If >32 low 20s, if risk >21, VF loss >18 with glaucoma early, Moderate to advanced with VF loss >15, Advanced with central loss >12.
Glaucoma masqueriders
MOATVP MS, Optic nerve compression, AION, Tramatic ON, Vascular occlusion, pan retinal photocoagulation
2.5 ml
1gtt qd for 1 month
Trialing rxn
2-3 weeks.
How long to wait between gets?
5 minutes
Prostaglandin
First drug for glaucoma. Latanoprost typically. 20-30% decrease. QHS (every night at bed time) Increases uveosclearl output.
SE of prostaglandin
hyperemia, hyerchiasis (eyelashes), hyper pigmentation around lower lid and iris, and reduced periorbital fat
Very Rare SE of prostaglandin
CME
Prostaglandin and Cataract surgery
stop 7-10 days before and put on CAI or alpha agonist. Continue 4-6 weeks after.
what prostaglandins are CI
latanoprost and bimatoprost
what to do if not getting desired decrease in IOP with prostaglandin
There is no increase effect with increased dosing. Should do an in class switch before adding another (no L and B)
How many patients need another treatment within 1 year of starting prostaglandin tx
30%
Beta blockers
20-30%. Decrease aqueous humor production. qam or bid. work poor at night.
PGA bottle color
turqoise
BB bottle color
blue or yellow
CAI
amide. tid or bid. decrease aqueous production. 20-30%.
CAI bottle color
orange.
Sulfa allergy and CAI
Less concerned with CAI. More worried with adrenergic agonist.
CAI adverse rxn
Guttate with fuch’s can cause cornea to become opaque. Do not use with any patients with endothelial defects.
Alpha 2 Adrenergic Agonist
dine. 20-25%. bid or tid. decrease aqueous and increase uveosclera.
SE alpha 2 adrenergic agnoist
allergic response in 10-20 Brimonidine and 48 Apraclonine. Can also cause vasoconstriction, pupillary dilation, eyelid retraction.
CI of alpha 2 adrengerics
MAOIS and TCAs. Both for depression. Effect on perfusion pressure.
Miotic
Pilocarpine. 20-25%. Increase outflow by normal way. qid.
PGA peak effect
2 weeks, stabilize at 6 weeks
BB peak effect
4-6 weeks
CAI peak affect
3 days
A2 agonist peak affect
2 weeks, stabilize at 6 weeks
Mioticic peak affect
3 hours.
Glaucoma suspects follow up
Depends on severity by 6-12 months
Stable mild glaucoma
4-6 months
Stable moderate glaucoma
2-4 months
stable severe stage
1-3 months
unstable with progression
1-2 weeks
recently established stability
1-3 months
How often to do gonio on FU
2-5 years on all but poor controled
ON/RNFL photography on FU
Annual for all but unstable
VF FU
Annual for suspect nd mild. a6m for moderate. q3-4 months for sever. q1-2m for unstable.
OCT FU
Annual for suspect and mild. q6m for moderate, q3-4 months for severe. q1-2 months for unstable.
Deepening of scotoma
Two or more points 10 db or poorer in the same location as the baseline scotoma
Expansion of scotoma
2 or more points 10 db poorer adjacent to the baseline scotoma.
New Scotoma
2 or more adjacent points not within or adjacent to the baseline scotoma now showing a probability on pattern deviation of P<1% or worse. 1 Point within the central 10 degrees that decline by 10 db in a previously normal location.
Progression with previously normal VF
Abnormal glaucoma hemifield test, PSD abnormal at 5% level, single point P<0.5%, 2 clustered points with P<5% with one point worse than P<1%. 3 or more clusters worse than P<5%. Needs to be repeatable, 2 or more times.
When do you get floor effect
54-55 um. Later monitor with VF
which one to not add to prostaglanidn
Alpha 2 agonist.
Cosopt
Timolol and drozolamide
Combigan
Timolol and briminodine
Simbrinza
Brimonidine and brinzolamide
ALT vs SLT
SLT easier 180-360 and can perform in same spot. ALT is 180 and final
Pre-operative for laser trabeculoplasty
pilocarpine 10 minutes prior. 1 gtt. brimonodine or apracolodine during procedure.
Post-op for LT
Check pressure after 1 hour. If >8 add glaucoma drop. Check 1 day then 1-3 weeks. Takes 3 months for effect.
SE of LT
Pain, inflammation (topical steroid aid for 4-5 days) scaring of TM and PAS.
Possible mechanism of ALT
Mechanical: contract tissue and open up flow. Biological: increase cellular activity of TM
Possible mechanism of SLT
Biological: increase chemocatic and vasoactive agent which increase outflow.
MLT
Less damage than ALT
TSLT
No damage to TM.
Who to perform LTP
elderly, POAG, pigmentary, pseudo exfoliative.
LTP effectiveness
SLT and ALT equal
Pretreatment of SLT
360 pretreatment has 15% decrease. Can do over an ALT.
States with laser privledges
Louisiana, Kentucky, Oklahoma.
Trabeculectomy
create a passage for drainage.
PO for traveculectomy
AB qid for 2 weeks, steroid q2hours during waking hours for 2 weeks and then taper for 4-8 weeks, atropine qd-bid for 2 weeks. Close monitoring of pain and IOP.
IOP decrease in trabeculectomy
50%
Complications of trabeclectomy
uveitis, enophthamitis, hyphen, underdraining, overtraining, aqueous misdirection, reduced VAs.
Managing a leaking blob
Manage IOP with BB or CAI, pressure patch or CL, apply AB, make sure eye has moisture.
Later complication with trabeculectomy
cataract formation, blebitis, ptosis, persistent leak. . Bleb scaring so it won’t leak. Use antimetabolites.
Risk factors for failure with traveculectomy
Age <40, black, prior failed surgery, aphasia or psudophakia, neovascular glaucoma, inflammatory glaucoma.
Happy bleb
shallow, widespread, pale but not avascular, upper lid, has micro cysts, no side.
Choroidal Effusion
serous fluid in suprachoidal space. Myopic shift, scotoma, If hemorrhagic: onset pain with decreased VA, high IOP.
What causes choroidal effusion
Low IOP and inflammation.
TX for choroidal effusion
address the cause, cycloplegia if AC shallow, topical steroid for inflammation, with hemorrhagic IOP reduction needed with topical and oral IOP meds.
Vision loss with trabeculectomy
56% transient. 8% permanent.
bleb needling
when you want to increase flow with trabeculectomy.
Shunt.
similar to trabeculectomy. Bleb is still needed but no iridotmy. Less complications and failures.
Tube vs shunt
Tube: high risk glaucoma, uveitis, ICE syndrome, aphasia. Need for surgery in the future. Poor compliance (Fu not as important as with trap) TRAB: severe disease or phakic.
Canoloplasty
360 tubing of scheme’s canal.
Pros of canoloplasty
non pentrating, no bleb, less post operative mgmt
Cons of conoloplaty
cannot perform if any damage to scheme’s canal, not as significant of a decrease, CI in narrow angles, (SLT is okay),
CI of canoloplasty
angle closure, narrow angle, neovascularization, post traumatic glaucoma
Trabectome
abates TM with cataract surgery. CI with cloudy cornea, large drop will occur, narrow angles.
cycloablation
used as last resort. CB is damaged. 50 to 85% reduction. Controls post op inflame with prednisone acetate.
cycloablation SE
40% have vision loss.
Lattice degernation
Thinning of inner retinal layers. Overlying packet of liquefied vitreous. Condense vitreous fibers attached at edge. 10-12% of eyes. 40% had RD.
When to tx lattice degernation
flashing lights, fellow eye suffered RD.
Cystic Retinal Tufts
Congenital lessions. Discrete tuffs of tissue extending into the vitreous. If symptomatic treat. Can have tractional retinal flaps, adjacent atrophic holes, percolated tears.
Atrophic retinal holes
well defined hole in periphery. Scleral depression to diff. from hemorrhage. Any symptoms and treat.
White without pressure
bilateral and symmetric in most cases.
When to refer with lattice degenreation
flashing lights or pigment cells in viterous
When to refer with cystic retinal tufts
status of fellow eye, family history of RD.
Rhegmatogenous retinal detachment
Associated with a retinal tear. Myopic patient and lattice degernation.
Regmatogenous RD signs
pale or opaque, corrugated surface, loss of choroidal detail, retinal vessels appear darker due to ischemia and becoming engaged, lower IOP than fellow eye,
Cryotherapy or laser photcoagulation
Use with regmatogenous RD. Seals off spread. Chorioretinal scaring.
Scleral Buckling
Regmatogenous RD. Occurs with vicetromy. Silicone band around eye. Eye elongated. Inferior retinal detachments good.
Pneumatic Retinoplexy
in office procedure for regmatogenous RD. Injection of intraocular gas to flatten the retina. Cryotherapy to seal the RT. Limited to superior detachment or a single retinal break.
Primary Virectomy
Reg. RD. Most common procedure. Outpatient. Vitrectomy in conjunction with a fluid/gas exchange. High incidence of cataracts.
Silicone oil
Vitreous substitute. Remains in the eye long term. Change in RE. Removal of oil is necessary if complications. Avoid silicone implant lenses. Inferior peripheral iridectomy may have to occur. Complicated RD.
Etiologies of tractional RD
proliferative retinal vas. dz, proliferative vitreoretinopathy, penetrating ocular trauma.
Signs of tractional retinal detachment
opaque, absence of choroidal detail, immobile, overlying fibrosis obscures underlying retinal vessels.
tx for tractional RD
vitrectomy with stripping off of the overlying fibrotic tissue, silicone oil.
exudative RD
Fluid accumulated under the retina from a pathological lesion.No retinal break.
Etiologies of exudative RD
Retinal hemangioma, coat’s disease, choroidal tumors, posterior uveitis (toxo). Severe AMD.
SX of exudative RD
shadows relative to elevated area, fluid shift with head position
TX for exudative RD
directed at underlying pathology. Commonly laser or cryotherapy.
RD referal
Macular on same day.
Macula off
within 48 hours.
Retinoschisis
5% population, 70% hyperopic, IT most common, BILATERAL.
Signs of retinoschisis
smooth cantor, transparent, immobile, NO demarcation line.
Demarcation line
pigment line that forms on the posterior margins of RD signifying the chronic presence of sub retinal fluid.
TX for retinocschisi
Laser photocoagulation.
Choroidal detachment
Elevated retinal area, brown or dark in color, abrupt transition with attached retinal, lower intraocular pressure, post surgical.
tx for choroidal detachment
topical steroids, topical cylcoplegics, oral steroids, surgical drainage.
Patient presenting with angle closure
Mid dilated pupil not reactive to light, gimbal hyperemia, cloudy cornea, closed angles with gonio, IOP 40-90.
Signs Symptoms
blurred vision, photophobia, halos, pain, nausea, HA, eye redness.
Primary angle closure suspect (PACs)
Likely apposition between peripheral iris and posterior TM without elevation of IOP or PAS.
PAC
narrow angles and apposition to angle be peripheral apposition or synechial angle closure
PACG
PAC with ON changes.
Gonioscopy tips with ACG
Dark room, 4 mirror without flange for indention, narrow slit with reduced light intensity, with steep insertions you can tilt mirror to the angle.
Dark room infrared gonio
perform without light to see worst case scenario.
Anterior segment OCT
Can be utilized in the dark, only able to appreciate the general structures, education tool. No touching the eye
How common is angle closure glaucoma to POAG
1/3 but equal number blind.
Epidemiology of ACG
Asian and Intuit women!
Risk factors for ACG
Shallower ACA, thicker lens, shorter axial length.e. hyperopia. Women at higher risk. Greater risk at 55.
If presenting like ACG but under 55
likely it is plates iris syndrome. When AC is deep but the angle is narrow. Angle is open and narrow when pupil is small and closed wen pupil is dilated.
Van herick
Chamber depth to corneal thickness: >cornea: 4 1/4-1/2: 3 1/4:2 <1/4:1 slit: very narrow.
oblique flashlight
If there is a shadow the angle is narrow. If there is no shadow it is open.
Meds to avoid with narrow angles
Anticholingerics (antihistamine, motion sickness, bladder control), Adrenergic agonists (decongestants), TAD, antipsychotics, antiparkinson.
Acute ACG
25%. May occur with dark illumination or drugs. Abrupt increase in IOP. ocular pain. Unilateral. At least 3 of the signs. Microcytic edema on cornea. Ischemia can produce sector atrophy that release pigment, bombe appearance, posterior synechiae. On may be hyperemic and edematous. CRVO may occur. Lens will have glakomflecken.
Intermittent ACG
Repeated brief episodes of angle closure. Attacks often resolve by going to sleep (mitosis helps with pupil block)
Chronic ACG
Gradual, asymptomatic closure of angle via formation of PAS. Often appear with VF loss. STNI (most common to least) Asian eyes common.
Plateau iris
AC appears deep with slit lamp but narrow with gonio. Indentation gonio creates double hump appearance. Less than 50. Still occludable after LPI.
Acute angle closure TX
Indention gonio may help break attachment. Can break with alpha 2 agonist, Beta Blocker (betaxolol for pulmonary issues), Pilocarpine. Acetazolamide.
Who do you not give acetazolamide to
sulfa allergy.
Oral osmotic agents for AAC
If not broken in 1 hour. Glycerol 50% solution. Isosorbide 45% solution. HA diarrhea, Nausea, vomiting. Serve over crushed ice. No water within first 2 hours of drinking.
Glycerol 50%.
1/5 ml/kg body weight. 5-7.5 per adult. Peak in 45-120 minutes. Careful for ketoacidosis in DM.
Isosorbide 45% solution.
1/5 ml/kg body weight. Peak in 45-120 minutes. Safe in diabetics.
Mannitol
diuretic. .5-1.5 g/kg body weight. IV dose. IOP may fall 30 or more. Ci with cardiac or renal DZZ. SE: HA, back pain, diuresis.
Indention gonioscopy
Indent central cornea for 30 seconds, rest for 30 second then repeat over 10-15 minutes
What to do if patient still in closure after 2 hours
Laser iridoplasty
If patient still has angle closure after 4-6 hours
emergency Laser Iridoplasty or surgical iridectomy.
Paracentesis
Symptoms relief is immediate and resolves quickly. Shallow AC which increase risk as blue enters eye. Choroidal hemorrhage from rapid pressure drop. LPI is still needed.
What to do after you control ACG
Check IOP q 15-30 minutes. If IOP <20 make sure angle is open. If open maintain patient on 2% pilocarpine and prednisolone acetate 1% until LPI performed.
PreOp for LPI
Pilocarpine, apraclonidine/bromonodine 1 hour before to control IOP spike, Topical anesthesia. Glycerol if cornea is edematous.
Post Op for LPI
Measure IOP 1-3 hours, Steroid 1 get qid for 4-7 days, FU in 1 week for gonio. Check at 1,2, and 6 months. Most LPI close in 6-8 weeks.
complications with LPI
corneal burn, transient IOP increase, cataract progression, post-op inflammation, late closure, hemorrhage, ghost image.
Prophylactic LPI
Closed in at least 270 degrees or 180 degrees
How many PAC patients have another closure in 5-10 years in other eye
40-80%
Argon laser peripheral iridoplasty
Useful in short term IOP lowering. Causes iris to shrink and pull away from angle. Works when IOP still high after LPI. Works for plateau iris.
Incisional Perihal iridoectomy
Small section of peripheral iris is excised through gimbal incision. When cornea too cloud for LPI. or AC too flat. Also good when ACG persists with LPI and iridoplasty.
Goniosynechialysis
Can combine with cataract. Replacement of lens stops formation. GO in a break up PAS. 80% success rate if PAS present for less than 1 year.
Glaucomatocyclit crisis (posner-Schlossman Syndrome)
20-50. Unilateral, recurrent. Ocular hypertension with uveitis (fine keratin precipitates). Blurred vision with haloes, minimal discomfort. ONH damage and VF defects may occur after many.
TX for glacumomatocylit crisis
topical steroids, topical glaucoma gets (NO PGA). No cycloplegia.
Pseudo exfoliative glaucoma
Increases with age. Unilateral to bilateral. Find PXE material on pupil margin and on lines, increased pigment inferiorly on gonio. Treat like POAG. Often filtering surgery.
Iridocorneal Endothelial Syndromrome (ICE)
20-50. F>M. Unilateral. Abnormal corneal endothelium (bronze), iris changes, corneal edema, PAS extending above schwalbe’s line, secondary angle closure glaucoma. Corneal endothelial cells go to TM.
TX for ice.
OHTN meds, filtering surgery, hyportonic for corneal edema.
Malignant glaucoma
rare form of glaucoma, typically following glaucoma surgery. High IOP with shallow AC following surgery. Pain and hyperemia. Need to confirm no pupillary block, may occur as long as 1 year after surgery. That that vitreous pushes and moves forward.
TX for Malignant Glaucoma
Cycloplegia (phenyl and atropine aid), decrease IOP with acetazolamide, BB, AA< CAI. Reduce vitreous volume with mannitol, glycerol, isosorbide, anti-inflammatory.
Prognosis of malignant glaucoma
50% fix in 5 days.
Mobile Lens
zones are lax and lens moves forward to to vitreous pressure. TX is lens removal.
Uveal Effusion (choroidal effusion)
Mobile lens but with anterior rotation of ciliary body. Bilateral. Choroidal effusion often associated with medications (topirmate, sulfonamides, SSRI). TX: cycloplegia, lower IOP, stop causative meds.
Steroid Induced Glaucoma
Degrade outflow of TM by inhibiting degration of ECMin the TM. Baseline IOP then 2 weeks, then months for 2-3 months and hen 6 months. Steroid response resolves in 1-4 weeks for responds and a few days for acute responders.
What percentage of the population is steroid responders.
18-36%
Are patient with POAG more likely to be steroid responders
YES.
Neovascular glaucoma
Most common causes: CRVO, DR, OIS. Need to have a high index of suspicion. Treat with PRP, IOP lowering meds.
Control of Diabetic AC1
DCCT: reduces risk of Diabetic retinopathy and slower progression,
United Kingdom Prospective Diabetes study (UKPDS)
For every percentage of reduction of A1C there was a 35% reduction of risk of microvascular complications.
If you decrease you average blood sugar by 30 the AIC goes don by
1%
How soon should someone with DM I have an eye exam
5 years.
How soon should someone with DM II have an eye exam
Soon. Takes a long time to dx.
DMI retinopathy rates
After 5 years 25% will have tetonpathy, After 19 years, 60%, after 15, 80%.
Is there increased risk of DR with gestational DM
No. Ret takes a long time. Greater chance they will get DM later in life though.
Is there increased risk of DR if insulin dependent and DM II
Yes. Basal levels are poor.
Type II DR
After 5 years 24% not on insulin and 40% on. After 19 53% not on and 84% on insulin.
Pt with DM but no DR
FU in 1 year. 5-10% will develop DR in 1 year.
Mild NPDR
At least one MA. FU in 1 year. DMI: 16% of patient with mild NPDR will progress to PDR in 4 years.
Can an MA go away.
Yes but this is bad. MeMean that blood flow is stopped at that area.
Moderate NPDR
Hemmorrhages/microaneurysms worse than 2a and or cotton wool spots. FU in 6 months.
Severe NPDR
- 4 quads of hemorrhages worse than standard photo 2a. 2 quadrants of venous beading worse than standard photo 6b. 1 quadrant of IRMA.
High risk for PDR
NVD greater than 1/3 disc area, any NVD with vitreous hemorrhage, NVE greater than 1/2 disc area with vitreous hemorrhage,
In 4 years, _____ patient with high risk PDR develop severe vision loss
44%.
PRP
Decrease in number of hypoxic cells producing VEGF. Complications are decreases VF, decreased night vision, transient increase in DME, impaired color vision, impaired dark adaption, vitreous hemorrhage.e
Gold standard for PDR
PRP. Ranizamaub is not bad alternative.
CSME
Any retinal thickening with 500 of macula, exudates within 500 macula with associated thickening, 1500 of thickening with 1DD of macula.
When to think macula thickening on OCT
When foveal thickness is greater than 252.
Focal on FA
Leakage from MA
Diffuse on FA
MA, retinal capillaries, arterioles.
Grid laser
Used to treat diffuse. Avoid fovea. RPE cells broken so better can replace
Focal laser
for focal leakage. Must be 300-500 from macula. Closure with thermal coagulation.
Early treatment diabetic retinopathy study
Use lasers with 20/40 or worse.
Resolve Study
CSME fixed with ranizamabut compared to sham.
Which anti-VEGF meds is most effective for DME
Lucent is (ran)
Risk of VEGF
Cataract progression, endopthlamos, inflammation,, retinal tracking, stroke.
Steroid with DME
Works well if you don’t factor in cataracts.
Ozurdex
Intraviteral implant with dexamethasone. Works 3-6 months and biodegradable.
Iluvien
intraviteral fluocinolone acetonic. 36 months. not biodegradable. Must check if steroid responder.
FAME study
FLuroquinole acetate good for DME. Need cataract surgery though.
Venous loops and beading
Occur next to areas of non profusion. Big predictor of ischemia.
IRMA
Found near areas of non profusion.
Cause of pre retinal hemorrhage in diabetics
neovascularization.
Pre-retinal hemorrhage
If dense and persistent think of vitrectomy. Can also use Yag. Can have traction.
Yag and pre-retinal hemorrhage
very effective.
Diabetic retinopathy vitrectomy study (DRVS)
Better if do vitrectomy sooner.
Timings for vitrectomy
DMI: 1 month. DMII: 2-3 months. Pre-retinal hemorrhage: 1 month.
Does aspirin increase hemorrhages in DR
NO!
Diabetic papillopathy
Variant of AION. More commonly bilateral, younger Diabetic pt, minimal to no VA loss, mild to no APD, minimal to no VF defect, insidious onset.
Tx for diabetic papillopathy
better diabetic control. A dx of occlusion.
Why does AV ratio get smaller with atherosclerosis?
The walls are thicker so lumen is smaller.
What vasculature is tortuous with hypertension
arterioles.
Artery and vein changes with hypertension
Split off at 90 degrees.
Stage one of hypertension
Decrease in A/V and increased light reflex with atherosclerosis
Stage two of hypertension
moderate to severe retinal changes. AV nicking
stage 3 of hypertension
retinal edema, cotton wool spots, hemorrhages.
Most common area for BRVO
ST.
Risk factors for BRVO
old age, HTN, DM, Hyperlipedima, oral contraceptive, smoking, inflammatory dz.
Acute signs of BRVO
dilated and tortuosity of the venous segment of the occlusion. Flame and dot blot hemorrhages, retinal edema, CWS. HypoF due to blockage and capillary drop out, staining of vessel wall.
Chronic signs of BRVO
Hard exudates, venous sheathing, and sclerosis. Collaterals. Chronic macular edema, neovascarization.
Prognosis with BRVO
within 6 months 50% have VA of 20/40 or better
Ischemic BRVO
5DD or greater non perfusion on FA. 40% will develop neovascularization.
Tx for neovascularization with BRVO
sector PRP.
Macular edema with BRVO
Grid laser if VA 20/40 or worse after3-6 months or ranibizumab.
CRVO non-ischmic
Non-ischemic is sudden painless decrease in acuity. Capillary perfusion in FA.
CRVO ischemic
Sudden decrease in vision, CF or worse. 10DD of capillary non perfusion.
What will you see with CRVO
Blood and Thunder.
Signs of non-ischemic acute CRVO
tortuosity and elation of all branches of CRV. Dot blot and flame hemorrhages, macular edema, CWS. FA blockages by hemorrhages, Good retinal capillary perfusion and late leakage.
Chronic non-ischemic CRVO
Disc collateterals, macular epiretinal gliosis, pigmentary changes, chronic macular edema. Can cover to to ischemic.
Ischemic CRVO
sudden very bad CF. APD. 10 DD of capillary nonperfusion
Signs of acute ischemic CRVO
Sever tortuosity of all branches of CRV, extensive dot blot and flame, CWS, ONH swelling and hyperemia.
Chronic CRVO
disc collaterals, macular epiretinal gliosis, macular pigmentary changes. Chronic macular edema. Iris rubeosis, angle neovascularization. Neovascular glaucoma. Retinal neovasclulzation.
Hemiretinal Vein Occlusion
Variant of CRVO. ischemic or non. Sudden onset of altitudinal defect. VA reduction variable. Not as common as CRVO but les common than in BRVO.
Fern like appearance around macula
Ischemic edema.
Central Vein Occlusion Study
Greater NVI with worse initial VA and less perfusion.
Should you treat macular edema from CRVO with grid laser
NO!
Geneva Study for macular edema
Better to start treatment early.
Gold standard tx for neovascularization with CRVO
PRP.
Gold standard for neovascarization with BRVO
sector PRP.
When to do vitrectomy with BRVO
Virtual hemorrhage.
FU for nonischemic CRVO
FU in 3 months for first 6 months. RTC with problems. Closely monitor for 24 months.
FU for ischemic CRVO
FU monthly for 6 months, closely monitor for 24 months.
Recombinant Tissue plasminogen actibator
Breaks up clots
Choriorteinal venous anastomosis
Allows transretinal retrograde flow of venous blood.
Radial optic neuotomy
combined vitrectomy and transvitreal incision of nasal scleral ring. Not very often.
RAO
Atherosclerosis most common with emboli (cholesterol-hollenhorse, fibrin, calcific)
BRAO
Embolus is main cause. M?F. Older. Sudden a painless altitudinal or sectoral field loss. +RAPD.
Where is BRAO most commonly
temporal side.
BRAO acute
attenuation of arteries and veins. Cloudy which edematous retina like triangle, one or more emboli, OCT inner retinal thickening. VF defect that doesn’t recovery
Chronic BRAO
Retina appears normal, collateral may form, sheathing of arteriole common.
BRAO TX
no treatment. VA better than CRAO so no maneuvers. Look for emboli cause. 80% to 20/40 or better.
CRAO
M>F. Unilateral. Sudden profound loss of vision with no pain. Amaurosis fugal can cause. +RAPD.
Acute CRAO signs
Sliding and segmentation of blood column, cloudy which retina, cherry red spot, peripaillary retina may appear swollen, emboli, OCT shows inner retinal thickening.
Chronic CRAO
Optic nerve pallor, arterial attenuation, vessel sheathing, patchy inner veinal atrophy, rep changes, NVI, Inner retinal thinning.
CRAO TX
Attempt within 24 hours. 911. Spin position. Ocular massage. Paracentesis. Aproclinodine, timolol, acetazolamide. Breathing into a paper bag,
Prognosis for CRAO
Poor.
CIRAO
Rare. Cilioretinal artery occlusion. Can be alone or with CRVO. Good prognosis.
Ocular Ischemic Syndrome
Chronic ocular hypo perfusion usually secondary to severe carotid artery obstruction. M. unilateral.
Signs of Ocular Ischemic Syndrome
Decreased VA, dull ache over brow, variable VF loss. . Neovascarization of iris, neovascular glaucoma, mild iritis, anterior segment reaction and flare. Retinal arterial narrowing, retinal venous dilation without tortuoaisity, neovascularization of the topic disc, cherry read spot, cotton wool spot, macular edema.
Tx for OIS
Carotid Endarterectomy (stenosis of >70 or AF, TIA, non disabling stroke). PRP or anti-VEGF.
OIS prognosis
POOR.
OIS vs. CRVO
Venous dilated only in OIS but tortousity in CRVO. Hemorrhages in NFL pole in CRVO. Peripheral in D&B in OIS. Delayed choroidal fillingOIS Normal in CRVO. Arterial staining more than vein with OIS. Vein more than artery in CRVO. Normal ON in OIS. Swollen ON in CRVO.
