Ocular Disease III: Exam 2: Lecture 9: Retinal Arterial Occlusive Diseae

Question 1

1. WHAT is the HALLMARK of CRVO?

Answer 1

1. it’s DILATED, TORTUOUS VESSELS!!!! (you will see it ALL the TIME)

Question 2

1. There’s a trick question he likes to ask: Which one is more prone to Glaucoma: Shallow DIsk or Deep Disk?
   a. Which is more tough to spot?
2. What is one of the main risk factors in CRVO?
3. Gold Standard for Glaucoma?

Answer 2

1. NEITHER! A disc is a disc.
   a. Shallow Disc.
2. POAG
3. VF, Fundus Photo, Gonioscopy, and Pachymetry (OCT is becoming a 5th, but not there yet)

Question 3

Terminology

1. Laying down of cholesterol and lipid into tunica intima of medium and large arteries
2. Broad term: thickening of vascular walls
3. applies to arterioles
4. Aggregation of fibrin, platelets, etc. on vessel walls or ulcerated artery plaque.
5. solid parts of thrombotic plaque dislodge and travel freely thru the vascular system

Answer 3

1. Atherosclerosis
2. Arteriosclerosis
3. Arteriolosclerosis
4. Thrombus
5. Emboli

Question 4

3 Types of Plaques (KNOW them, and origin of them)

1. What are they.

Answer 4

1. Fischer
2. Hollenhorst
3. Calcific

Question 5

Fischer Plaque

1. What is it?
   a. ORIGIN?

b. What does it look like?
c. Readily migrates thru what?
d. WHAT DOES IT LOOK LIKE?

Answer 5

1. Fibrin/Platelet Aggregate
   a. CAROTID IN ORIGIN

b. Dull gray or white
c. thru Vascular System
d. LOOKS LONG, STRINGY, GRAY (like squeezed toothpaste) (Slide 32)

Question 6

Hollenhorst: CHOLESTEROL

1. ORIGIN?
2. What do they look like?
3. How Common?
4. Typically they do what?
   a. OCCUR AT what?
5. MALLEABLE: Allows for blood to pass thru the Artery may appear what?
6. Will readily break up and what?
7. THIS IS THE ONLY ONE THAT WILL HAVE NO EFFECT ON WHAT?
8. Most common underlying cause?

Answer 6

1. CAROTID
2. Reflective, Glistening, Yellow
3. MOST COMMON (87%) of all Emboli
4. DO not occlude artery.
   a. AT BIFURCATION
5. totally blocked
6. and move distally
7. on Retina (cuz it allows blood to go thru. circulation still happening) (No effect on VISION EITHER) (MALLEABLE!!! ONLY ONE).
8. Atherosclerosis-Related Thrombosis (80%): due to thickening and hardening of arteriole walls at level of lamina cribrosa and HAVE TO HAVE >50% STENOSIS of IPSILATERAL CAROTID ARTERY!

Question 7

Cardiac Embolism

1. Responsible for what % of Retinal Artery Occlusions?
2. Associated w/INCREASE risk of what disease?
3. First branch of Internal Carotid?
4. Emboli originate from where?

Answer 7

1. 20%
2. of Cerebrovascular Disease.
3. Ophthalmic Artery
4. from Heart and its Valves

Question 8

Types of Cardiac Emboli

1. CALCIFIC
2. Vegetations
3. Thrombus
4. Myxomatous Material

Answer 8

1. From AORTIC or MITRAL VALVES
2. from cardiac valves in Bacterial Endocarditis
3. From Myocardial Infarction, Mitral Stenosis, or Mitral Valve Prolapse
4. from Atrial Myxoma (RARE)

Question 9

Calcific

1. ORIGIN?
2. What does it look like?
3. is it MALLEABLE?
4. Usually from what?
5. MOST LIKELY TO CAUSE what 2 things?
6. SMALLER don’t move far…so close to what?
7. MOST come from what?
8. If you SEE THIS, WHAT DO YOU EXPECT WILL HAPPEN?

Answer 9

1. CARDIAC
2. Dull White and Non-Reflective
3. NO! HARD, NON-MALLEABLE
4. ARTERY OCCLUSION and STROKE
5. to Optic Disc-Around Lamina Cribrosa
6. from the Heart (bacterial Endocarditic @ risk for CARDIAC FATALITY)
7. PATIENT WILL DIE.

Question 10

Endocarditis

1. What is it?
2. Heart murmurs present in what % of cases?
3. MOST COMMON SOURCE of CAUSE?
   a. What is also possible?
4. So if you discover this and it’s diagnosed, what do you expect the outcome will be?

Answer 10

1. Inflammation of inside lining of heart chamber and/or heart valves
2. Over 90% of cases
3. Bacterial Infection (Most common is STREPTOCOCCI VIRIDANS)
   a. Fungal infection can also cause Endocarditis
4. CHANCES ARE THEY WILL LIVE if you get it diagnosed and they TREAT IT with BACTERIAL INFECTION

Question 11

Symptoms of Endocarditis

1. Some general ones…

Answer 11

1. Fatigue, malaise, Aches/pains, heart murmur, Shortness of breath, other things..
   * Nail ABNORMALITY, Blood in Urine

Question 12

Visible Retinal Emboli: Mortality

1. % w/in 1 YR?
2. % w/n 3 yrs?
3. % w/n 7 yrs?
4. What DEATH is MORE PREVALENT THAN STROKE?

Answer 12

1. 15%
2. 29%
3. 54%
4. CARDIAC DEATH!
   * These %’s are WITH TREATMENT!

Question 13

Arterial Occlusive Disease

1. What 5 things?

Answer 13

CRAO

Ophthalmic Artery Occlusion

Cilioretinal Artery Occlusion

BRAO

CAD (Carotid Artery Disaease)

Question 14

CRAO (Central Retinal Artery Occlusion)

1. It’s an abrupt diminution of Blood flow thru CRA SEVERE ENOUGH to cause what?
2. Uni/BI?
   a. Type of VISION LOSS?
3. HOW MUCH VISION LOSS?
4. Men/Women?
5. Mean Age of Onset?

Answer 14

1. to cause ISCHEMIA of the INNER RETINA (very easy question to ask)
2. UNI (1-2% BILATERAL)
   a. SUDDEN, SEVERE, PAINLESS LOSS OF VISION
3. SEVERE (20/800 to Hand motion to Light Perception) (NLP is RARE)
4. MEN > Women 2:1
5. 60 years of age
   * By sudden, he means SECONDS then it’s lost.

Question 15

CRAO: Signs

1. What happens to the retina in the Posterior Pole?
   a. Why?
2. What is seen AT THE MACULA in 60% of cases?
3. Pupils?
4. What happens to the Arterioles?
5. Retinal Arteriolar Emboli: (Visible ONLY in what % of cases)
6. *He could ask a question like this: In CRAO, which is the LEAST LIKELY Plaque you will SEE?
7. Cherry Red Macula: 3 conditions…

Answer 15

1. Superficial Whitening of the Retina
   a. Due to ISCHEMIC BLOOD FLOW
2. “CHERRY-RED SPOT” AT MACULA
3. • APD!
4. Narrowed Retinal Arterioles
5. 20%
6. HOLLENHORST PLAQUE (Cholesterol). Why? BECAUSE it’s MALLEABLE!!!!! So it wouldn’t cause a CRAO.
7. First thing should go to CRAO!

Question 16

CRAO: Signs

1. If optic disc swelling is present: HAVE TO RULE OUT WHAT?
2. By 4-6 wks after obstruction, what happens to the retina?
3. What develops?
4. What may form on the disc?
5. NEO occurs in what %?
6. % develop NVD w/Vit heme to follow?
7. What other plaque other than a Calcific plaque can cause CRAO?

Answer 16

1. GIANT CELL ARTERITIS (if they have this, then chances are, the OTHER EYE WILL BE NEXT!)
2. Retinal whitening is usually resolved by then
3. Optic Disc Pallor
4. Arteriole Collateral
5. 18%
6. 2%
   * Here the eye is gone…we are simply just trying to prevent pain from occurring from NEO and having to remove the eye.
7. a Platelet FIBRIN EMBOLUS

Question 17

CRAO: Signs

1. Okay…so 2 BIG signs of CRAO?

Answer 17

1. CHERRY RED SPOT, and Pale Optic Nerve!

Question 18

CRAO Pathophysiology

1. Etiology
2. Emboli of what origin are more likely?
3. % of CRAO caused by Embolism?
4. % due to Thrombi?
   a. MOST SCARY one to worry about?

Answer 18

1. Emboli from Carotid Artery of heart lodging in CRA at Laminar constriction
2. of CARDIAC origin than carotid origin to cause Artery Occlusion
3. 90%
4. 10%
   a. GCA (Inflammation)

Question 19

Risk Factors (CRAO)

1. Cardiac issues?

Answer 19

1 Heart murmur

MALIGNANT HYPERTENSION (260/134)

Diabetes Mellitus (BS > 300 mg/dl)

Cigarette Smoking (1/2 pack for 40 years)

Hyperlipidemia

Question 20

Abnormalities Associated w/CRAO in pts under 30 yrs.

What are they?

Answer 20

1. Atherosclerosis (VERY RARE)
2. Migraine
3. Coagulation abnormalities
4. Cardiac Abnormalities
5. Trauma
6. Sickling Hemoglobinopathies
7. ONH Drusen can even cause it due to crowding…can crush it.

Question 21

1. CRAO: with cilioretinal sparing.

2. How much time from Loss of BF to the RETINA, the RETINA SUFFERS IRREVERSIBLE DAMAGE?

Answer 21

1. Slide 55 Lecture 9.

2. w/in 90 MINUTES!!! (for this reason, peeps will pretty much have severe vision loss)

Question 22

Treatment CRAO

Answer 22

1. Really nothing proven
   * increase retinal oxygenation, increase retinal arterial blood flow

reverse arterial obstruction

prevent hypoxic retinal damage

Question 23

Heroic Tx for CRAO

1. Has to be instituted w/in 24 hrs of event.
   a. Paracentesis: Does what?
   b. Carbogen
   c. Digital Massage
   d. Breathing in a Brown Paper Bag.
   e. 1-24 Hr window of opportunity
   f. Intravenous Acetazolomide
   g. Tx vs. NO TX: Difference in SNELLEN Acuity?
2. If caused by inflammatory Thrombosis from GCA, will this help?

Answer 23

1. a. reduce iOP and allow less compression on CRA to allow Emboli to pass further
   b. Pt hospitalized and breathes this stuff 5-10 min every hour for 24 hrs. Using pure O2 is WORSE cuz there will be reflex constriction of the BVs. it increases CO2 levels causing a rebound vasodilation
   c. with 3 mirror CL and compression of globe for 10 seconds, followed by 5 seconds of release for 20 min
   d. Increase blood CO2 Levels
   e. Anti-Fibrinolytic Agents (Urokinase, Streptokinase)
   f. Prolonged lowering of intraocular pressure than with repeated paracentesis
   g. 1/4 line difference…so, OVERALL, HEROIC MEASURES DO NOT AFFECT FINAL VA! (basically it’s gone)
2. the heroic measures will DO NOTHING cuz there’s NO embolus to DISLODGE!

Question 24

CRAO: Tx: What you really do: Work-up and Follow-Up of CRAO

1. WORK UP
2. Follow-up
3. REFERRAL to what ***

Answer 24

1. ALL PTs. STAT (ESR, CRP if pt. over 60).
   a. Blood work up: CBC w/diff
   b. Pulse
   c. Auscultation (but better to order Carotid Doppler)
   d. Echocardiogram
   e. Consider IVFA to CONFIRM DIAGNOSIS (but maybe not worth it…) (most peeps won’t order an FA on these patients)
2. WEEKLY for first month to check for NVI/NVA. If NEO develops: CONSIDER PRP (this is DONE for QUALITY OF LIFE and Prevent/Improve PAIN).
3. CARDIOLOGY REFERRAL (MOST IMPORTANT. SOC)

Question 25

Ophthalmic Artery Occlusion 1. Vision? 2. Cherry red spot? 3. MORE severe what? 4. *KNOW: Systemic Association SIMILAR to what?

Answer 25

1. NLP Vision (Compare to CRAO: not as common...CRAO: get light perception, hand motion) 2. NO! 3. More severe RETINAL WHITENING 4. to CRAO, but much HIGHER INCIDENCE OF GCA!!!!

Question 26

Ciliary Artery Occlusion 1. HIGHEST INCIDENCE with what? 2. What is it?

Answer 26

1. with GCA (esp. if concurrent AION exists) 2. Local infarcted area, severe loss of Central Acuity w/preservation of Peripheral FIELD! * Systemic like CRAO

Question 27

Cilioretinal Artery 1. % of pop that have this artery? a. Comes from what? b. Supplies what? 2. Occlusion a. Presents with what kind of vision loss? b. Cloudiness localized to the part of the retina normally perfused by what? c. FA shows what?

Answer 27

1. 20-30% a. Posterior Ciliary Circulation b. Macula and Papillomacula Bundle 2. a. Acute Severe Loss of Central Vision b. by the Vessel c. Filling Defect

Question 28

Branch Retinal Artery Occlusion 1. Visible Retinal Emboli Lodged in arteriole a. 4 of them? 2. MOST COMMON CAUSE by what PLAQUE? 3. Caused by GCA? 4. Acuity? a. Is this important?

Answer 28

1. Cholesterol, Calcific, Fibrin-Platelet, Infectious 2. CALCIFIC PLAQUE (cause central big one)... but the one that travels far...would be the Hollenhorst. 3. RARELY. LEAST CAUSED by GCA. (There will be a QUESTION on THIS Association) 4. 20/20 to Hand motion. Depends on DEGREE of MACULA INVOLVED a. No. SYSTEMIC IS MOST IMPORTANT!

Question 29

Branch Retinal Artery Occlusion 1. Retina looks like? 2. NEO common? 3. Systemic Associations same as CRAO, but...? 4. Referral to whom?

Answer 29

1. Whitened retina in distribution of arteriole. w/resolution, retina becomes more normal in appearance, BUT NOT FUNCTION 2. RARE 3. LOWER SURVIVORSHIP (why? Because they're SMALLER...get to the brain --> Death) 4. CARDIOLOGY

Question 30

Branch Retinal Artery Occlusion 1. Presents with what? a. VA? 2. VA's good to worse...for occlusions? * Same: Fundus: narrowing arteries and veins, cloudy white retina from edema, emboli may be present (ITS JUST SMALLER) or Less affected area

Answer 30

1. Sudden and profound altitudinal or sectoral VF Loss (CAN DO A VF!!) a. VARIABLE (ONLY ONE!) 2. WORSE: Ophthalmic, then CRAO, then Macula Ciliary one, then BRAO (WORSE to BEST for VA)

Question 31

Branch Retinal Artery Occlusion Work Up: Same as the other CRAO

Answer 31

1. STAT: ESR and CRP if pt over 60. Same...as CRAO... Follow up every week for first month to check for NVI/NVA. If NEO develops, consider PRP **CARDIOLOGY REFERRAL!!!