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Posterior Segment Disease > B14-1 Artery Occlusions & Ischemic Disease > Flashcards

B14-1 Artery Occlusions & Ischemic Disease Flashcards

1
Q

What causes Ocular Ischemic Syndrome (OIS)?

A

Ipsilateral carotid obstruction or ophthalmic artery obstruction

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2
Q

Name 3 symptoms of Ocular Ischemic Syndrome (OIS)

A
  • Gradual vision loss that develops over a period of weeks to months
  • Aching pain localized to the orbital area of the affected eye
  • Prolonged vision recovery after exposure to bright light
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3
Q

Name 2 anterior segment findings associated with Ocular Ischemic Syndrome (OIS)

A
  • NVI in 2/3 of cases

- Anterior chamer cellular response in 1/5 of eyes

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4
Q

Several vascular diseases can cause NVI/NVA, what is one scenario that is characteristic of Ocular Ischemic Syndrome (OIS)?

A

NVA & low IOP, doesn’t usually happen, most likely due to imparied aqueous production

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5
Q

Ocular ischemic syndrome can cause a retinopathy similar in appearance to a partial CRVO &/or Diabetic Retinopathy; what is one differentiator found on a fundus exam that is characteristic of OIS?

A

Mid-peripheral dot/blot hemorrhages, whereas Diabetes primarily effects the posterior pole only

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6
Q

Name a test that can be helpful in differentiation of Ocular Ischemic Sydrome from a CRVO/CRAO?

A

ERG:

  • demonstrates global amplitude reduction in OIS
  • an electronegative electroretinogram occurs in the case of a CRVO/CRAO since they largely affect only the inner-retinal structures, whereas OIS compromises the entire eye
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7
Q

Most common etiology of OIS? What are some other causes?

A
  • Atherosclerosis

- Carotid artery dissection or Giant Cell/Temporal arteritis

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8
Q

How much obstruction is necessary to cause OIS?

A

90%

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9
Q

What is the 5-year mortality rate of patients with OIS?

A

40%

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10
Q

What is the most definitive Tx for OIS?

A
  • Carotid artery stents

- Endarterectomy

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11
Q

Name 3 studies that should be performed with OIS

A
  • Carotid duplex
  • CTA/MRA of head and neck
  • Consult with cardiology and/or vascular surgery
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12
Q

What is the perioperative risk of death in a symptomatic OIS patient?

A

< 6%

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13
Q

What is the perioperative risk of death in an asymptomatic OIS patient?

A

< 3%

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14
Q

What is the most common type of emboli involved with an ocular artery occlusion? Describe it

A

Hollenhorst plaque, which is refractile yellow-white cholestrol from the carotid

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15
Q

Urgent specialist vascular evaluation is rapidy becoming the standard of care following a retinal arterial event. Why?

A

Because 25% of TIA patients will have a stroke within 3 years

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16
Q

What percentage of CRAO cases are caused by GCA? What age do these usually occur?

A

1-2%, extremely unlikely under the age of 55

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17
Q

Other than regular cardiac evaluation like BP, pulse, auscultation, etc., what systemic assessments do all artery occlusion patients typically have?

A

MRA/CTA for neuro assesment

ECG for arrhythmia and/or other cardiac disease

ESR/CRP for GCA

Carotid Duplex to check severety of stenosis

Other blood tests like CBC, glucose, lipids, urea and electrolytes

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18
Q

Characterized by a transient, painless, monocular loss of vision that is often described as a “curtain coming down over the eye”

A

Amaurosis Fugax

19
Q

Overall, how should you treat any artery occlusion, whether it be a TMVL/CRAO/BRAO? What were the numbers from the meta analysis to support this?

A

As an acute stroke, because roughly 20-30% of BRAO/CRAO patients and 8-11% of TMVL patients are having/will have a stroke

20
Q

What is the most common cause of Cotton-Wool Spots (CWS)? How do they form? What’s the usual course of action upon finding a CWS?

A
  • Diabetic Retinopathy
  • acute obstruction in the distribution of the radial peripapillary capillary net, NOT an artery or arteriole
  • not typicallly an urgent or emergent scenario, can usually be monitored and evaluated on an outpatient basis and they will typically fade in 5-7 weeeks.
  • HOWEVER, even 1 CWS in an otherwise apparently healthy eye should prompt the clinician to initiate a workup for underlying etiology
21
Q

What is the typical course of a BRAO?

A
  • sudden and painess unilateral visual field defect and/or reduction in VA (patient may complain of “blacking out”, flickering, or dimming of their vision)
  • an acute BRAO may be subtle and unapparent on initial fundus exam, but then can lead to edematous opacification within hours to days
  • in time, the occluded vessel recanalyzes, perfusion returns, and the edema resolves. HOWEVER, a permanent visual field defect remains.
22
Q

How is a BRAO confirmed?

A

Visual Field Defect, since it is usually permanent

23
Q

What are the 3 main varieties of emboli that form Branch Retinal Artery Occlusions (BRAO)

A
  1. Cholestrol emboli - Hollenhorst plaques (from carotid arteries)
  2. Platelet-fibrin emboli (from large-vessel arteriosclerosis)
  3. Calcific emoli (from cardiac valves)
24
Q

Patient presents completely assymptomatic (ocularly and systemically) but you find what appears to be a Hollenhorst Plaque on the fundus exam. What do you do?

A
  • Do NOT assume it is a BRAO, but DO assume that it is new
  • Obtain records and order or recommend fairly urgent studies/evaluations (like a bilateral carotid duplex)
  • If the plaque has been present for some determined amount of time (many months/years), make sure they are following up with their other Doctor’s recommendations
25
Q

What are the 3 types of cilioretinal artery occlusion? Which is the most common?

A
  • Isolated Non-arteritic CLRAO
  • Isolated arteritic CLRAO (GCA)
  • Combined CLRAO (with CRVO/HRVO) is the most common; thought that the increased hydrostatic pressure associated with the CRVO can reduce blood flow in the cilioretinal artery to the point of stagnation.
26
Q

What should always be considered with any cilioretinal artery occlusion, but especially with an isolated CLRAO?

A

GCA

27
Q

What is a Paracentral Acute Middle Maculopathy (PAMM)?

A

Acute ischemic events that affect the deep macular capilllary layers (ICP and DCP)

28
Q

How does a PAMM present? How will it appear on OCT?

A
  • Patient will present with acute onset of negative scotoma
  • Hyperreflective band-like, multiple or isolated, focal or diffuse, lesions visible at the level of the inner nuclear layer (INL), often affecting from the IPL to potentially the ONL
29
Q

What level(s) of the retina does Type 1 PAMM affect?

A

Intermediate/middle capillary plexus (IPL/INL) region

30
Q

What level(s) of the retina does Type 2 PAMM affect

A

The deep capillary plexus in the INL/OPL/ and even the ONL region

31
Q

What is the primary differential for a PAMM? How are they different?

A
  • Acute Macular Neuroretinopathy
  • Paracentral Acute Middle Maculopathy (PAMM) patients are most often in their 50’s and 60’s (even though it can occur in young heathy patients), whereas Acute Macular Neuroretinopathy (AMN) patients are typicaly young healthy women in their teens-30’s and the lesions appear slightly lower on OCT (junction of the OPL and ONL)
32
Q

Diffuse PAMM lesions can harbour what kind of occlusions?

A

An occult central retinal artery occlusion

33
Q

This condition has been seen anecdotally with excessive caffiene intake

A

Paracentral Acute Middle Maculopathy (PAMM)

34
Q

Describe the classic fundus appearance of a CRAO

A

Retina becomes edematous and opaque (especially in the posterior pole) with a red/orange reflex from the intact choroidal vasculature beneath the foveola, called a “cherry red spot”

35
Q

Prognosis of a CRAO?

A
  • Overtime the retinal artery reopens and the edema clears, but VA loss is permanent since the inner retina has been infarcted
  • in one study 66% of eyes had VA’s worse than 20/400
  • 18% of eyes were 20/40 or better, and most often due to the presence of a cilioretinal artery
36
Q

What’s typicallly the cuplrit of vasoocclusive vision loss to the level of light perception/no light perception?

A

Ophthalmic artery occlusion

37
Q

If GCA is suspected, what should you do?

A
  • Start systemic corticosteroid therapy immediately since the other eye can becomme involved within hours to days after the first
  • Temporal artery biopsy shortly thereafter to confirm
38
Q

NVI may develop in what percentage of CRAO/BRAO cases?

A

1-20%

39
Q

List 4 potential causes of ophthalmic artery occlusion

A

Dissection of the internal carotid, orbital mucormycosis, embolization, cosmetic facial filler injections

40
Q

What percentage of Retinal Macroaneurysms are associated with HTN?

A

66%

41
Q

Where are retinal macroaneurysms most likely occur?

A

Superior temporal, same as BRVO’s

42
Q

What layers of the retina can be affected by a macroaneurysm?

A

Any level, often takes on an hour-glass shape if it transverses the entire retina

43
Q

How are Macroaneurysms treated in most cases?

A

Moderate intensity laser treatment of the retina

Posterior Segment Disease (5 decks)

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