Retinal Vascular Occlusions

Front 1

What can RAO and RVO become?

Back 1

RAO/RVO --> ISCHEMIA --> leads to either

1) STRAIGHT to vision loss or
2) neovascularization --> GLAUCOMA --> vision loss

(use PRP laser to prevent the two steps above)

Front 2

What can happen to an untreated RAO?

Back 2

retinary artery feeds the ENTIRE eye, kill that off, kill the eye!

Front 3

What are the different types of RAO?

Back 3

-opthalmic artery
-central retinal artery (comes right off the optic nerve)
-branch retinal artery (comes off the central retinal artery)
-cilioretinal artery
-combined RAO-RVO
-cotton wool spots

Front 4

What's the incidence and demographics of CRAO?

Back 4

-60s, >men, OD=OS
-1 in 10,000 office visits (LOTS OF PEOPLE)
-57% = RAO
-1-2% bilateral (also think about cardiac valvular disease, giant cell arteritis, vascular inflammation)

(very uncommon, but when it does occur, must think of more systemic problems (plaques in the heart OR giant cell arteritis - scalp tingling, jaw claudification (hurts), vision LOSS in one eye! (scalp tenderness as well.) IF YOU MISS THIS, YOU KILL THEM!) (temporal arteritis) (condition that affects the medium arteries, vascular inflammation)

Front 5

If you miss what monocular loss of vision condition wilt you kill the patient?

Back 5

GIANT CELL ARTERITIS!

Front 6

Etiology of CRAO

Back 6

Most common: embolism! (45% from the carotid artery) (note a fib - with cardiac embolism)

-Vasculitic (giant cell arteritis)

Front 7

Symptoms of CRAO

Back 7

painless vision loss, several seconds

Front 8

What's the acute presentation of CRAO?

Back 8

-RAPD (relative afferent pupillary defect)
-retinal whitening (death)
-cherry red spot
-emboli
-"boxcarring"

Front 9

Late clinical findings of CRAO

Back 9

-retinal whitening resolves 4-6 weeks (resolves in a month)
-pale optic nerve*
-narrowed retinal vessels*

Front 10

What are the systemic associations of CRAO?

Back 10

HTN, DM, GCA (giant cell arteritis)

(do a cardiac echo if pt is younger, above conditions exist in older pts & check their coagulation)

Front 11

What are the recommended diagnostic ideas for CRAO?

Back 11

<50: cardiac echo, anticoagulation studies (prot c, s)

>50: ESR, CRP, CBC, Carotid doppler, cardiac echo

Front 12

For CRAO, what do most treatment options do?

Back 12

Most treatments cause vasodilation of the arteries...which means the emboli could get stuck somewhere else!

-Monkey study: must fix within 90 minutes or else PERMANENT vision loss

-LOWER IOP (always do first, lower their intraocular pressure!) (by OCULAR massage, topical meds, AC, paracentesis (anterior chamber tap, use a small needle to take stuff out)

-Hyperbaric Oxygen (HBO) - put them in a room and turn up the O2, doesn't usually work (produces pO2 at the retinal surface)

-Brown bag it (increase CO2, increases vasodilation)

Front 13

Is there a lot to do for people with CRAO?

Back 13

no not at all!!! the vision loss will be profound :( the mortality is terrible, they've gone blind and DIED earlier!

Front 14

CRAO prognosis?

Back 14

-Visual recovery is UNLIKELY (even worse if they develop neovacular glaucoma)

-Survival 5.5 years vs 15.4 years in age-matched controls

Front 15

What percentage of BRAO is RAO?

Back 15

38% are branch retinal arterial occlusions

90% involve the temporal branch retinal arteries (heads towards the ears - vision depends if you nicked the fovea/macula area)

Front 16

What's the etiology of BRAO?

Back 16

same as CRAO:
-Embolism (remember it's the most common) (most likely arteriosclerosis of the carotid artery)

-NO association w/giant cell arteritis!!

Front 17

What's the difference in etiology of CRAO and BRAO?

Back 17

It's the same: embolism, but

BRAO (branch related arterial occlusion is NOT associated w/giant cell arteritis!!!)

Front 18

What are the symptoms of BRAO?

Back 18

C.BP
-central acuity may be spared!
-blind spot
-painless vision loss

Front 19

What is the acute presentation of BRAO?

Back 19

BoRNE

-boxcarring on vessel affected
-retinal whitening along the distribution of a vessel
-emboli
-normal pupillary response, no marcus gunn pupil!

Front 20

LATE clinical findings of BRAO?

Back 20

-retinal whitening resolves 4-6 weeks
-narrowed retinal vessel
***-optic nerve may appear normal***

Front 21

What's the differences between BRAO and CRAO?

Back 21

in the late clinical findings, the optic nerve may appear normal in BRAO, whereas it's pale in CRAO.

there's an APD in CRAO, but not in BRAO.

boxcarring in both, emboli caused in both

retinal whitening in both (and both resolve in 4-6 weeks!)

both have painless vision loss!!!!

Front 22

What are the diagnostic considerations for BRAO?

Back 22

only thing that's really different from CRAO, is that you don't have to check for giant cell arteritis!
-Systemic associations: HTN, DM
-Ancilliary studies:
<50: cardiac echo, anticoagulation studies (prot c, s)
>50: carotid doppler, cardiac echo

Front 23

Prognosis of BRAO?

Back 23

great if fovea is spared!

80% will spontaneously improve
BUT the visual field defect may persist (

Front 24

What are the BRAO treatment options?

Back 24

aggressive ocular tx is NOT pursued! (you really don't want to be too aggressive!)

Front 25

What's the incidence and demographics of CRVO?

Back 25

>65 years
men=women
OD=OS

UNILATERAL!!! (most of the time you won't get it in the other eye!) (same with the other conditions except giant cell arteritis which will most likely affect the other eye)

Front 26

What causes a CRVO?

Back 26

not really known!

could be: thombus, compression by atherosclerotic central retinal artery, hypercoacuable states, OPEN angle glaucoma (more predisposed to getting CRVO)

Front 27

Boy, are there a lot of etiologies for CRVO, name a few.

Back 27

HH OVOIDS

-hematalogic alterations (hyperviscosity syndroms)

-infectious vasculitis- HIV

-ocular disease - open angle glaucoma

- vascular (systemic) disease - **hypertension**, DM, carotid insufficiency

6) Medications - OCD's!!!!! (HUGE!) (also if they smoke= BAD (pro-thrombotic state)...but ALWAYS REMEMBER CANCER), hep B vaccine...5) Other - pregnancy, dehydration

-inflammatory conditions (SLE- systemic lupus)

-dehydration

-infectious vasculitis- syphillis

Front 28

What are the ssx of CRVO?

Back 28

-painless vision loss
-several seconds

(same as the others)

Front 29

Acute presentation of CRVO

Back 29

FROM. bc
-4 quadrants w/retinal hemorrhages
-RAPD (marcus gunn pupil!)
-Optic nerve edema,
macular edema
-BLOOD + thunder
cotton-wool spots

Front 30

What are the late findings of CRVO?

Back 30

-Shunt vessels
-neovascularization (bc eye is SO ischemia)
-neovascular glaucoma (happens 3 months after the initial CRVO)

Front 31

What are the diagnostic considerations you need to make for CRVO?

Back 31

1) Systemic associations (HTN, DM)
2) Ocular associations (glaucoma)
3) Young pts (hypercoaguable states)

Front 32

How's the prognosis of CRVO?

Back 32

-INITIAL Visual acuity prognostic
.....20/40, majority maintain
.....20/200, 20% improvement

-Neovascularization angle 6-12% (fairly large # - really can do a job on pt) --> can lead to glaucoma!!!

(aka may worsen w/development of neovascular glaucoma) (increase in pressure since the blood spews out of the leaky veins, breaks the pipes!) REMEMBER USUALLY UNILATERAL!

Front 33

What are the tx options for CRVO?

Back 33

-medical therapy (control systemic risk factors)
-surgical (macular edema: intravitreal bevacizumab) + (neovascular disease: PRP laser (KNOW THIS!!)

Front 34

What's the incidence of BRVO?

Back 34

*60-70 yo
*men=women
*unilateral!

Front 35

How does a BRVO occur?

Back 35

no one really knows ...if we see that they have an artery/vein crossing then it's probably going to be bad! (occurs distal to the av crossing usually!)

How?
-a+v share a common adventitial sheath
-a+v share common medium
-focal endothelial swelling @ crossing site
-venous thrombus formation

Front 36

What's the BRVO etiology? Include risk factors and a modifiable one.

Back 36

-Systemic vascular disease (HTN, DM, and hyperlipidmia)

-Ocular disease (open angle glaucoma)

-Modifiable RF (smoking!!!)

-Risk factors (alcohol consumption, high levels of HDL)

Front 37

As usual what are the ssx of BRVO? How does it present? late clinical findings?

Back 37

painless vision loss, several seconds

A quadrant of retinal hemorrhages, cotton wool spots, and macular edema

Late: shunt vessels, neovasularization, neovascular glaucoma

Front 38

How do you treat BRVO? (omgg so similar!)

Back 38

Medical therapy - control systemic risk factors, manage vision-threatening complications

Surgical-
macular edema (focal laser)
neovascular disease (PRP laser)

Front 39

Retinal venous occlusion is mostly associated with what...

Back 39

hypertension and glaucoma!! (open angle)