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

1
Q
  1. WHAT is the HALLMARK of CRVO?
A
  1. it’s DILATED, TORTUOUS VESSELS!!!! (you will see it ALL the TIME)
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2
Q
  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?
A
  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)
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3
Q

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

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

  1. What are they.
A
  1. Fischer
  2. Hollenhorst
  3. Calcific
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5
Q

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?

A
  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)

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6
Q

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?
A
  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!
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7
Q

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?
A
  1. 20%
  2. of Cerebrovascular Disease.
  3. Ophthalmic Artery
  4. from Heart and its Valves
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8
Q

Types of Cardiac Emboli

  1. CALCIFIC
  2. Vegetations
  3. Thrombus
  4. Myxomatous Material
A
  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)
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9
Q

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?
A
  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.
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10
Q

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?
A
  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
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11
Q

Symptoms of Endocarditis

  1. Some general ones…
A
  1. Fatigue, malaise, Aches/pains, heart murmur, Shortness of breath, other things..
    * Nail ABNORMALITY, Blood in Urine
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12
Q

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?
A
  1. 15%
  2. 29%
  3. 54%
  4. CARDIAC DEATH!
    * These %’s are WITH TREATMENT!
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13
Q

Arterial Occlusive Disease

  1. What 5 things?
A

CRAO

Ophthalmic Artery Occlusion

Cilioretinal Artery Occlusion

BRAO

CAD (Carotid Artery Disaease)

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14
Q

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?
A
  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.
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15
Q

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…
A
  1. Superficial Whitening of the Retina
    a. Due to ISCHEMIC BLOOD FLOW
  2. “CHERRY-RED SPOT” AT MACULA
    • APD!
  3. Narrowed Retinal Arterioles
  4. 20%
  5. HOLLENHORST PLAQUE (Cholesterol). Why? BECAUSE it’s MALLEABLE!!!!! So it wouldn’t cause a CRAO.
  6. First thing should go to CRAO!
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16
Q

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?
A
  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
17
Q

CRAO: Signs

  1. Okay…so 2 BIG signs of CRAO?
A
  1. CHERRY RED SPOT, and Pale Optic Nerve!
18
Q

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?
A
  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)
19
Q

Risk Factors (CRAO)

  1. Cardiac issues?
A

1 Heart murmur

MALIGNANT HYPERTENSION (260/134)

Diabetes Mellitus (BS > 300 mg/dl)

Cigarette Smoking (1/2 pack for 40 years)

Hyperlipidemia

20
Q

Abnormalities Associated w/CRAO in pts under 30 yrs.

What are they?

A
  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.
21
Q
  1. CRAO: with cilioretinal sparing.

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

A
  1. Slide 55 Lecture 9.

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

22
Q

Treatment CRAO

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

reverse arterial obstruction

prevent hypoxic retinal damage

23
Q

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?
A
  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!
24
Q

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

  1. WORK UP
  2. Follow-up
  3. REFERRAL to what ***
A
  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)
25
Q

Ophthalmic Artery Occlusion

  1. Vision?
  2. Cherry red spot?
  3. MORE severe what?
  4. *KNOW: Systemic Association SIMILAR to what?
A
  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!!!!
26
Q

Ciliary Artery Occlusion

  1. HIGHEST INCIDENCE with what?
  2. What is it?
A
  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
27
Q

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?
A
  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
28
Q

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?
A
  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!
29
Q

Branch Retinal Artery Occlusion

  1. Retina looks like?
  2. NEO common?
  3. Systemic Associations same as CRAO, but…?
  4. Referral to whom?
A
  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
30
Q

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
A
  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)
31
Q

Branch Retinal Artery Occlusion

Work Up: Same as the other CRAO

A
  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!!!