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118 Cards in this Set

  • Front
  • Back

Characteristics of CRVO

- usually UNILATERAL, but up to 7% may develop CRVO in fellow eye within 5yrs


- men = women


- elderly

3 major Risk Factors for CRVO

1) HTN (#1 RF)


2) Diabetes


3) POAG

Pathogenesis of CRVO

- physical blockage


- lumina of the CRA & CRV are narrower at the lamina cribosa


- vessels are bound by a common sheath


- lamina limits expansion of ON & vessels


- results in an obstruction to blood flow


- thrombotic/atherosclerotic phenomenon


- laminal constriction site for occlusion: nidis

CRVO Symptoms

- blurred vision


- scotoma


- sudden, painless loss of vision

CRVO Appearance

BLOOD & THUNDER! 

BLOOD & THUNDER!

CRVO Signs

- dilated, tortuous veins


- deep & superficial hemorrhages


- disc edema


- CWS (NOT exudates)


- collateral vessels


- macular edema (main cause for vision reduc.)


- anter/posterior segment neovascularization

Describe the retinochoroidal collaterals that develop with CRVO:

- "protective" effect


- develop 3-14 months after occlusion


- bypasses vascular bed occlusion


- do not leak


- in 5% CRVO w/ iris/angle NV


- in 58% CRVO w/o iris/angle NV (PROTECTIVE!)

Classification of CRVO

1) Perfused (non-ischemic)


2) Non-perfused (ischemic)

Perfused (non-ischemic) CRVO

- less than 50% capillary non-perfusion


- 70-80% of all CVO's


- acuity better than 20/200


- deep hemorrhage (dot/blot)


- should be treated as the TIP of the STYSTEMIC iceburg!


- 83% of "interdeterminate" CRVO converts to ischemic


- CWS are RARE!


- NO APD

Non-perfused (ischemic) CRVO

- greater than 50% non-perfusion


- 19-30% of all CVO's


- will have +APD


- poor VA


- CWS present


- 16% of all CRVO's develop NVI/NVA (CVOS)


(very high risk of NVI/NVA via VEGF)

What's the major complication (most serious) that can arise from CRVO? What is it correlated with?

Neovascularization; correlated with the degree of capillary non-perfusion

How is the amt of perfusion detemined with CRVO?

- FA!


- less than 10 DD of non-perfusion = perfused


- more than 10 DD of non-perfusion = non-perfused

What factors/signs differentiate Perfused (Non-ischemic) vs Non-perfusion (Ischemic)?

- VA (worse with ischemic)


- pupils (+APD with ischemic)


- DFE (orange appearance & CWS w/ ischemic)


- VF examination


- FA (>10 DD ischemia with ischemic)


- elctroretinogram

What's the #1 reason for vision loss with CRVO?

macular edema


(other causes include: RPE atrphy, macular ishemia, retinal hemorrhage, NVG)

What assessments should we do if we suspect CRVO?

- FA


- pupil testing


- retinal photo


- gonio (r/o NVA)


- measure IOP


- NVG evaluation

How do we manage/treat CRVO?

- systemic condition needs to be treated


- refer for PRP if NVD, NVI, NVG or macular edema develops


- f/u every 1-2 months for 6-8 months

CVOS study

- PRP only after NV is observed


- macular laser did NOT have a significant effect on VA, thus is NOT indicated


- SLE with gonio is mandatory


What is Papillophlebitis?
- CRVO in a young patient w/o systemic dz
- inflammatory etiology (unlike true CRVO)
- prognosis is great; majority non-ischemic
- disc swelling & disc edema
- symptoms: GOLD & PURPLE flashing lights
- do these tests: CVC w/ diff, lipid panel, BP, & tested for antiphospholipid AB syndrome
- same neo complications as true CRVO
- monitor 1 q mos until resolution
Young, healthy patient with complaints of gold & purple flashing lights. What is the diagnosis?

Young, healthy patient with complaints of gold & purple flashing lights. What is the diagnosis?

Papillophlebitis

Characteristics of BRVO

- elderly


- males = females


- more common than CRVO


- less visually disabling than CRVO


- involves one of the branch retinal veins


- small, localized area of the retina or as much as a quadrant


- most involve veins located temporal & superior to the disc

BRVO Pathogenesis

- venous compression at A/V crossing (75% of all BVO)


- arteriolosclerotic etiology


- sclerotic arteriole compreses on underlying venule leadint to leakage from capillary beds


- VEINS/VENULES DO NOT LEAK


- ALL leakage is from the CAPILLARIES

BRVO Symptoms

- reduced VA &/or VF may be present


- often is ASYMPTOMATIC

BRVO Classification

1) Ischemic vs Non-ischemic


2) based on LOCATION

BRVO appearance

3 location classifications for BRVO:

1) Hemispheric: before 1st bifurcation (aka: HRVO)


2) Intermediate: after 1st bifurcation, typical BRVO appearance (MAJORITY OF BRVO CASES)


3) Twig: macular area only

RFs for BRVO

#1: HTN (70% of cases)



- systemic associations


- DM


- atherosclerosis


- hyperlipidemia


ETC

Non-ischemic BRVO

- 70-80% of cases


- VA >20/200


- blot, flame shaped hemes


- RARE to see CWS


- mild macular edema


- collateral vessel formation

Ischemic BRVO
- defined as 5 DD of retinal capillary NON-perfusion on FA
- CWS
- macular edema (most common cause of vision loss)
- NVD/NVE/vitreous hemorrhage, tractional RD COMMON
- NVI/NVG are RARE
What's the most common cause of (irreversible) vision loss with BRVO?
macular edema

others: vitreous hemorrhage, tractional RD
BRVO management
- refer for directed W/U
- monitor q1mo until resolution of hemorrhages
- monitor every 4 months for next 3 yrs
- possible FA at 3 mos
- retinal pics at every visit
- retinologist ONLY if complications develop

HRVO

- "hemi-retinal vein occlusion"


- major branch occlusion at or near OD


- occlusion of one of the trunks of central retinal vein


- involves superior OR inferior drainage only


- develops like CRVO, behaves like BRVO


RFs for HRVO

1) HTN


2) Diabetes


3) Glaucoma

What is OIS?

Ocular Ischemic Syndrome is hypoperfusion of the anterior & posterior segments of the eye due to carotid obstructive disease.

OIS Etiology

- usually unilateral


- internal carotid artery atheromatous ulceration & stenosis at bifurcation of common carotid artery


- only occurs if stenosis >90% = NO BF in eye


- males > females


- 50-80 y/o


What's the 70-70 Rule with OIS?

- 70% of BF to brain is thru internal carotid artery


- don't start to get in trouble until you have at least 70% occlusion


- with 90% stenosis, you only drop down to 50% perfusion in CRA

Chronic signs of OIS

- diminished vision in bright light


- PAIN


- progressive vision loss

Systemic correlations with OIS

- systemic mobidity (arterial HTN, DM, ischemic heart dz, stroke, peripheral vasc. dz, etc)


- less common causes include: GCA


What is the #1 cause of mortality in OIS pts?

- CARDIAC DEATH is #1 cause of mortality

OIS posterior findings

- dilated, NOT tortuous veins


- dot/blot hemes in MIDPERIPHERY


- hemorrhages are usually more scattered (unlike with CRVO, more confluent)


- macular edema


- CWS


- spontaneous arterial pulsation


(IOP exceeds pressure w/in CRA)

OIS anterior segment findings

- diffuse episcleral injection & corneal edema


- aq. flare with few cells (ischemic pseudo-iritis); where the pain comes from!


**may appear like uveitis (dilate your pts!)


- iris atrophy & a mid-dilated/poorly reacting pupil


- RUBEOSIS IRIDIS is common & often progresses to NVG


- cataract in very advanced cases (prolonged ischemia)

What should you expect on FA with OIS patient?

1) early phase shows delayed choroidal filling & prolonged arteriovenous transit time


2) late phase shows disc & perivascular hyper-fluorescence & leakage at post. pole

OIS management

- r/o HTN, DM, cardiac dz, etc


- carotid ultrasound or doppler


( >70% w/o symp or >50% w/ symp --> carotid endartectomy or stenting)


- anterior segment treat with topical steroid & mydriatis


- NVG treated medically & surgically


- proliferation requires PRP

What are some differences between CRVO, DR, HTN, and OIS?

Mid-peripheral hemes, dilated (not tortuous) vessels - what is most probably diagnosis?

Mid-peripheral hemes, dilated (not tortuous) vessels - what is most probably diagnosis?

OIS

What should you do if your CRVO pt has signs of NVD, NVE, NVI?

refer to retinal specialist for PRP!
(CVOS study: PRP ONLY after NV is observed!)

What's the hallmark of CRVO?

sudden, painless loss of vision

According to the BVOS study, can photocoagulation (grid laser) improve VA in eyes with macular edema?

YES! Grid laser is STD of care for macular edema in BRVO! 65% incr. VA by 2 lines!
(this is similar to Diabetic Retinopathy; unlike CRVO, which does not indicate grid laser according to CVOS)
Note: grid laser more beneficial for HTN pts than non-HTN patients with BRVO

According to the BVOS study, can PRP prevent VH in eyes with NV?

32% absolute risk reduction
conclusion: PRP once retinal NV has appeared (just like with CRVO/CVOS study!)

Describe the classifications of MACULAR EDEMA in BRVO (perfused & ischemic).

Perfused: most common, leakage (FA), 1/3 spontaneously resolve, frequently has persistent decr. in VA
Ischemic: CYTOTOXIC/VASOGENIC SWELLING, NO leakage of FA, 90% spontaneous resolution, appears to be a transient phenomenon with visual improvement as edema resolves

What does the BVOS study have to say about treating macular edema?

1) 3-18 mo window of opportunity to tx
2) do NOT treat macular HEMORRHAGE
3) grid laser should NOT be considered if MACULAR ISCHEMIA is present with macular edema (...unless VA isn't improving)
4) tx only if VA <20/40 & due to macular edema
5) grid lair does work for macular edema due to BRVO

How should you manage a BRVO patient?

1) refer to internist for w/u
2) monitor every month until hemorr. resolve
3) monitor every 4 mos x 3 yrs
4) possible FA/3 months
5) retinal photography at every visit
6) retinal specialist referral ONLY IF COMPLICATIONS develop

Is macular grid laser tx effective in improving the vision in eyes with CRVO & VA 20/50 or worse due to macular edema?

NO!
CVOS study: macular laser did NOT have a significant effect on VA, thus not indicated!

T or F: NVD/NVE, VH, Tracitonal RD may cause permanent severe vision loss in BRVO?

True.
Same goes for Diabetic Retinopathy. (CRVO perm. vision loss is more likely due to NVG.)

What is common in CRVO, but rare in BRVO?

NVI/NVG

What's the "50% Rule"? (Hint: BRVO)

1) If the BRVO involves at least 1 quadrant, there's a 50% chance of developing 5DD+ of retinal non-perfusion.
2) If the BRVO is associated with 5DD+ of non-perfusion, there is a 50% change of developing NVD or NVE.
3) If the BRVO is associated with NVD or NVE, there's a 50% change of developing vitreous hemorrhage.

Name at least 2 ways that BRVO differs from CRVO.

1) ischemic classification (>10DD for CRVO; 5DD for BRVO)
2) NVI/NVG (more common in CRVO; rare in BRVO)
3) their general classifications (CRVO is based on amt of non-perfusion; BRVO is based on location)
4) symptoms (CRVO often the pt has sudden severe vision loss; BRVO is often asymptomatic)
**there are more than what's listed here, I only named a few

HRVO develops like _____(CRVO, BRVO), but behaves most like _____ (CRVO, BRVO).

CRVO; BRVO
"HRVO develops like CRVO, but behaves most like BRVO"

Conclusion of SCORE study regarding BRVO.

NO significant differences among the 3 tx groups.
= so, STD of CARE is STILL grid laser for BRVO

HRVO involves what kind of drainage?

superior or inferior ONLY
(side note: in BRVO, most veins involved are temporal & superior to disc)

This study focused on Triamcinolone for CRVO.

SCORE (std care vs corticosteroids for retinal vein occlusion)


= std of care for CRVO is NO longer just "watching it until neo"; now it is INJECTIONS if CRVO pt has macular edema (no grid laser, but yes to injectables)
**however, if no neo OR macular edema, just WATCH CRVO

What's the most common cause of vision reduction in BRVO?

Macular edema
(same as CRVO & Diabetic Retinopathy!)

What conclusion was made about SLE in the CVOS study?

SLE with GONIO is MANDATORY! (need to rule out NVI/NVA!)

What's the most significant RF for predicting NVI/NVA?

amount of non-perfused retina (remember that with ischemic CRVO, you have >10DD of non-perfusion; high risk of NVI/NVA with ischemic CRVO)

When should you follow up with your CRVO pt?


20/40 or better: q1-2 mos x6mo
20/200 or worse: month x6-8mo
(side note: for Papillophlebitis, f/u q month until its resolved!)

T or F: Of "inteterminate" CRVO cases, roughly 80% will progress to ischemic CRVO.

True.

What did the CVOS declare about doing macular laser? (Hint: CRVO study)

Macular laser did NOT have a significant effect on VA, thus is NOT indicated. In CRVO, just WATCH macular edema until NEO develops.
(In BRVO, grid laser is std of care (just like with DR))

T or F: Papillophlebitis' etiology is different than that of CRVO.

True.
Papillophlebitis is more likely from inflammatory etiology (HOWEVER, make note that steroids do NOT help..)

What's a unique symptom of Papillophlebitis?

Gold & Purple flashing lights

T or F: Sclerotic arteries leads to compression on underlying venule, which causes the venue to leak. (Hint: BRVO)

FALSE.
As the arteriole becomes sclerotic, it compresses the underlying venule, leading to leakage from CAPILLARIES/CAPILLARY BED draining into the venule. (VENULES NEVER LEAK - all leakage is from capillaries!)

T or F: BRVO is often asymptomatic.

True. (Often, but not always..may present with loss of VA or VF.)

"Define" Ischemic BRVO.

5DD of retinal capillary NON-perfusion on FA
**notice that it is 5 DD & NOT 10 DD (10 DD --> CRVO classification)

CRVO or BRVO: Which one is more visually disabling? Which is more common?

CRVO; BRVO (3x's more common)

Characteristics of Macular Holes

- usually 6th or 7th decade of life


- more common in females (2:1)


- usually uniliateral (10-20% bilateral)


Macular Hole symptoms

- painless, central vision loss


- early: central metamorphopia or blue, micropsia


- late: severe decr. in central vision


- symptoms noticed with other eye closed

Macular Hole Pathophysiology

- shrinkage of the perifoveal vitreous cortex (perifoveal vitreous "shrinks up")


- incomplete perifoveal PVD


- foveal adherance of posterior hyaloid --> vitreous traction on the fovea

How many stages of macular holes are there?

4

Describe Stage 1a (impending) of macular holes:

- split in inner retina


- cystic space (pseduocyst)


- vitreous pulls at the fovea


- photoreceptor layer intact


- loss of foveal light reflex


- yellow spot


- 50% resolve spontaneously

Describe Stage 1b of macular holes:

- pseudocyst enlargement


- extension to the outer retina, disrupting photoreceptor layer


- small central yellow ring


- loss of foveal depression

Describe Stage 2 of macular holes:

- roof of cyst opens ("can opener")


- full thickness defect less than 400um in diamter


- small retinal defect (hole) seen within yellow ring

Describe Stage 3 of macular holes:

- full thickness defect more than 400um in diameter


- thickened edges due to intraretinal cystoid spaces


- central, RED round full thickness retinal defect


- surrounding, subretinal fluid cuff

Describe Stage 4 of macular holes:

- Stage 3 + PVD (possible Weiss ring)

Describe VA of each stage of macular holes:

Stage 1a/b --> 20/20-20/50


Stage 2 --> 20/50-20/200


Stage 3 --> 20/200-20/800


Stage 4 --> 20/200-20/800

What are some diagnostic tests to run for macular holes?

- OCT (useful for staging)


- Watzke-Allen Test

What is the Watzke-Allen test?

- put narrow beam over center of hole


- w/ macular hole, pt reports beam broken or thinned


- w/ pseudohole or cyst, pt reports beam distorted

Determine the stage of this macular hole:

Determine the stage of this macular hole:

Stage 1a (impending)

Determine the stage of this macular hole:

Determine the stage of this macular hole:

Stage 1b

Determine the stage of this macular hole:

Determine the stage of this macular hole:

Stage 2

Determine the stage of this macular hole:

Determine the stage of this macular hole:

Stage 3

Determine the stage of this macular hole:

Determine the stage of this macular hole:

Stage 4

How you do manage each stage of macular hole?

Stage 1: monitor; 50% spontaneously resolve



Stages 2-4 (full thickness): treatment required IF 20/40 or worse for VA

What's the treatment for Stages 2-4 Macular Holes?

Surgical Tx:


1) Vitrectomy (PPV)


2) Peeling of ILM


3) Fluid-gas exchange


4) Post-op face-down positioning

Describe the post-op of macular hole repair:

- after surgery to repair the macular hole, the pt should be positioned face down for 24 hrs for 5-10 days

What's the #1 complication of macular hole surgery?

CATARACT! (75%)

What does ERM stand for?

Epi-retinal membrane

Characteristics of ERM

- aka: mucular pucker, cellophane maculopathy


- fairly common in pts over 40 y/o


- bilateral involvement in 20-30% of cases

What are the causes of an ERM?

- idiopathic (most common!)


- following intraocular sx


- retinal vasc. dz


- intraocular inflamm.


- trauma

What are symptoms of an ERM?

- blurred vison


- metamorphopsia


- macropsia due to crowding of the photoreceptors



(mild, transparent ERM are often asymptomatic)

What are the clinical signs of an ERM?

- presents as a translucent, shimmering or whitish gray membrane along inner retina


- retinal traction can cause: distortion/tortuosity of BVs, retinal striae, & CME


- OCT is great test to view ERM

What is the shimmering membrane in this OCT photo?

What is the shimmering membrane in this OCT photo?

ERM

Complications of ERM

- contraction of ERM can cause distortion/folds of inner retina


- in some cases, there may be edema visible as black spaces (OCT) in the outer retina

ERM Pathophysiology

- ERM are due to proliferation of retinal GLIAL cells (as well as other cells) at the vitreoretinal interface


- the cells gain access to the retinal surface through breaks in the ILM


- PVD is believed to play a role in development of ERM

How do you manage ERMs?

- surgery is typically recommended in pts with BCVA of 20/40 or worse (or severe metamophopsia)

What's the treatment for ERMs that need it?

1) Vitrectomy (remove vitreous)


2) Membranectomy (ERM peeled off)

What's the expected outcome after ERM tx?

- VA usually improves 50%


- most pts have decr. in metamorphopsia

What's the #1 complication of ERM tx?

CATARACTS! (just like macular hole tx!)

What does VMT stand for?

Vitreomacular Traction

What is VMT?

- condition in which the vitreous gel has an abnormally strong adhesion to the retina


- complication of incomplete PVD


- exerts anterior-posterior traction on the fovea

Clinical signs of VMT

- early stages may be hard to see


- may see glistening of the posterior hyaloid


- partial PVD usually present


- center of fovea may show reddish or yellowish spot


- macula may appear thickecned due to edema

What does VMT look like on an OCT?

- bright posterior hyaloid tenting up the fovea & surrounding area


- perifoveal vitreous detachment

- bright posterior hyaloid tenting up the fovea & surrounding area


- perifoveal vitreous detachment

What are the threats to vison from VMT?
- CME or macular hole formation
- the narrower the VM attachment, the greater the force exterted upon the macula in that area, the greater the risk of macular hole formation
- VMT & EMR can occur simutaneously

How do we manage/tx VMT?

- early, asymptomatic VMT observed for progression w/o tx


- previously, vitrectomy was the only tx


- intravitreal injections of an enzymatic agent is a new treatment approach that was FDA approved

What's the name of the intravitreal injection used to treat VMT?

Ocriplasmin (Jetrea)



- side effects: floaters (NOT cataracts!)

What are the differences between an ERM & VMT?

What is a Pseudohole?

- have intact photoreceptor layer


- commonly retain near normal VA


- caused by ERM contraction


- ERM that have a central opening in the foveal area


- normal central foveal thickness


- incr. parafoveal thickness

How do we manage/tx Pseudoholes?

- surgical peeling of the ERM is indicated when vision is reduced (worse than 20/40)

What is a Lamellar Hole?

- result of an abortive process of macular hole formation


- VA is usually preseverd


- macular shoes a stable, round, well circumscribed REDDISH lesion


- irregular foveal contour


- split b/w the layers


- photorectpor layer intact


- bi-lobed or anvil-shaped

How do we manage/tx Lamellar Holes?

- typcally stable condition


- tx usually not necessarily (acuity preserved)

What is the finding on the left? On the right?

What is the finding on the left? On the right?

Left: pesudohole


Right: lamellar hole