Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics > Central Retinal Vascular Disorders > Flashcards

Central Retinal Vascular Disorders Flashcards

1
Q

What are the clinical signs for OAO?

A

Retinal whitening, cherry spot (in 1/3 cases), optic atropy, and afferent pupil defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the symptoms for CRAO?

A

Unilateral, painless, acute vision loss (counting fingers to light
perception in 94% of eyes) occurring over seconds; may have a history
of transient visual loss (amaurosis fugax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do you differential CRAO and OAO?

A

Acute ophthalmic artery occlusion: Usually no cherry-red spot;
the entire retina appears whitened. Increased concern for GCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the work up/diagnosis for Retinal Vascular conditions

A
  1. Standard exam
  2. OCT (possible inner retinal oedema)
  3. Referral for FA (not in acute cases)
  4. CBC, ESR (exclude GCA), fasting blood sugar
  5. Refer to stroke centre to assess risk of cardiovascular event
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for OAO, CRAO, BRAO?

A
  1. Ocular massage
  2. Refer to ophthalmologist for YAG laser or intra - arterial tPA (OAO)
  3. IOP reduction with beta blocker (e.g. timolol 0.5% daily) or acetazolamide 500mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When should you review a OAO, CRAO, BRAO patient and why?

A

1 - 4 weeks to check to neovascularisation on any ocular structures, VA and VF for improvement

Refer if there is neovascularisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk factors for Arterial Occlusive disease?

A
  • Risk factors: vascular conditions i.e. hypertension, hypertensive crisis, diabetes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Differentials for CRAO

A

Acute OAO, commotio retinae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for BRVO?

A

: diabetes, glaucoma (increased IOP can displace lamina cribosa), increase CD ratio, article narrowing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Symptoms of CRVO?

A

Painless loss of vision, usually unilateral.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical signs of CRVO?

A

Critical. Diffuse retinal hemorrhages in all four quadrants of the
retina; dilated, tortuous retinal veins.

Other. CWSs; disc edema and hemorrhages; macular edema (ME);
optociliary collateral vessels on the disc (later finding); NVD, NVI,
NVA, and NVE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differentials for CRVO

A

OIS - no vein tortuosity, may have pain, decreased IOP, may have ocular inflammation

DR - hb and vascular tortuosity should not be as intense

Papilledema - Would not expect as
extensive and diffuse retinal hemorrhage and vascular tortuosity.

Radiation retinopathy: History of irradiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Possible etiology of CRVO

A

HTN, optic disc oedeam, glacuoma, disc drusen, vasculitis, drugs, orbital disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classification of CRVO

A

Nonischemic CRVO: Vision often better than 6/60, mild or no
RAPD, mild fundus changes. Lower risk of neovascularization.

Ischemic CRVO: Vision typically worse (<20/200) with RAPD and
visual field defects. Extensive retinal hemorrhage, CWSs, venous
tortuosity, and widespread capillary nonperfusion on IVFA (often
>10 disc diameters)

Papillophlebitis (inflammatory occlusion)
Type 1 – disc odema + minor retinal changes
Type 2 – resembles classic CRVO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Work up for CRVO

A
  1. Standard Dilated Fundus examination (VA, IOP, pupil reactions, CV, VF, motilies, Amsler, gonioscopy) + OCT
  2. Consider referral to retinal ophthalmologist for fluorescein angiography (NOT IN ACUTE CASES – too time consuming)
  3. Refer for comprehensive blood test to identify the case.
    a. ESR if >55 to exclude GCA.
    b. CBC
    c. Fasting blood sugar
    d. BP
    e. Vascular work up (if you suspect cardiovascular disease or hypercoagulability)
  4. Refer to stroke centre to assess and manage risk of subsequent stroke: blood pressure or cardiac evaluation (especially in high-risk cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for CRVO

A
  1. Control the underlying medical conditions (check if medication exacerbate ocular condition) – Papillophlebitis (is generally self-limiting)
  2. Cease smoking (consult with GP to assist patient to quit)
  3. Reduce IOP if elevated
  4. Referral to ophthalmologist for Anti-VEGF, Steroids or Laser treatment
17
Q

What are the relevent studies for CRVO/BRVO treatment? (Anti VEGF)

A

a. CRUISE study supports using ranibizumab injections 6 monthly then PRN rather than sham injections. Delayed treatment affected patients’ vision adversely.
b. HORIZON study (follow up of CRUISE trial) supports 0.5mg ranibizumab injection with the best mean change from baseline VA. Fewer injections = reduced vision in CRVO but no BRVO (may require more treatment)
c. RETAIN study (follow up form HORIZON) ranibizumab and laser photocoagulation (scatter) had better BCVA improvement after 50 months in responsive patients. Nonresponsive patients require more injections and low visual gains.
d. COPERNICUS (PRN aflibercept vs 4 weekly sham) – 16% VA improvement at 100 weeks, most patients were ischaemic CRVO.
e. GALILEO >10% of patients improved VA, however VA improvement decreased over time.
f. INSUFFICIENT data to say aflibercept is better than ranibizumab – similar resolution of macula oedema.

18
Q

What are the relevent studies for CRVO/BRVO treatment? (Steriods)

A

a. SCORE (1mg vs 4mg of triamcinolone vs observation). >25% of px improved VA by 3 lines compared to observation, however no change in OCT thickness. 1mg better safety profile, less IOP increases and less cataract development.
b. GENEVA study (0.35mg vs 0.7mg dexamethasone intravitreal implant) Px baseline VA was 6/24 and improved by 15 letters in 41% (0.7mg), 40% (0.35mg) and 23% (sham). No statistically significant difference between the groups. Better for recent onset oedema than chronic oedema

19
Q

What is the follow up routine for CRVO/BRVO?

A
  1. 6/12 or better – every 1- 2 month for 6 months
  2. <6/60 (if under treatment – review as required), monthly for 6 months then taper.
    Monitor for
    * BRVO/CRVO in fellow eye – 8 – 10% risk.
    * IOP
    * Develop of CMO or neovascularisation
20
Q

BRVO symptpms?

A

Blind spot in the visual field or loss of vision, usually unilateral.

21
Q

Clinical signs for BRVO

A

Critical. Superficial hemorrhages in a sector of the retina along a
retinal vein. The hemorrhages usually do not cross the horizontal
raphe (midline).
Other. CWSs, retinal edema, a dilated and tortuous retinal vein,
narrowing and sheathing of the adjacent artery, retinal
neovascularization, VH.

22
Q

BRVO differentials

A

DR - Hb cross the horizontal midline, usually bilateral

Hypertensive Retinopathy - Narrowed retinal arterioles.
Hemorrhages are not confined to a sector of the retina and
usually cross the horizontal raphe. Bilateral in most

23
Q

BRVO classifications?

A

Major BRVO - * 1st order temporal branch at optic disc
* 1st order temporal branch away from the disc, involving macula branches

Minor - * Involving macula branches

Peripheral - * Not involving macular branches

24
Q

Symptoms of HTN retinopathy

A

Usually asymptomatic, although may have decreased vision.

25
Q

Retina signs of mild HTN retinopathy?

A

Generalized or localized retinal arteriolar narrowing, almost
always bilateral.

Modest risk of stroke, coronary heart disease or death

26
Q

Retina signs of moderate HTN retinopathy?

A

Generalized or localized retinal arteriolar narrowing, almost
always bilateral. + hb, MA, CWS, Hex or any combination of these

Strong risk of stroke, coronary heart disease or death

27
Q

Retina signs of malignant HTN retinopathy?

A

Signs of retinopathy + optic disc swelling

Strong association with death

28
Q

Work up of HTN retinopathy

A
  1. Standard DFE (IOP + gonioscopy)
  2. Systemic work up:
    a. Check BP
    b. Fasting blood sugar
    c. Cholesterol
    d. ESR
    e. CBC
    f. Vascular work up
  3. MRI brain and orbit
    a. 18% stroke risk if hypertensive retinopathy and cerebral lesion are present.
    b. Generalised retinal arteriolar narrowing (70% 3 – year survival) and arteriolar wall (6% 3 – year survival)
29
Q

Treatment for HTN retinopathy

A
  1. Consider getting better BP control with GP assistance (limited evidence)
  2. No retinopathy – review 1 – 2 yearly
  3. Mild to moderate retinopathy: aggressive approach to reduce risk (manage HTN)
  4. Malignant retinopathy:
    a. Urgent antihypertensive treatment
    b. Rule out anterior ischemic optic neuropathy (disc oedema + VF loss)
  5. Refer to ophthalmologist if
    a. Retinal oedema
    b. Optic nerve swelling
    c. Presence of exudative retinal detachment
30
Q

Review period for HTN retinopathy

A

Every 2 – 3 months at first then every 6/12 months

31
Q

Differentials for HTN retinopathy

A

CRVO or BRVO: Unilateral, multiple hemorrhages, venous
dilation, and tortuosity. May be the result of HTN.

Diabetic retinopathy: Hemorrhages are usually dot-blot and
microaneurysms are common; vessel attenuation is less common.

Radiation retinopathy: History of irradiation. Most commonly
occurs within a few years, but can develop at any time

32
Q

OIS symptoms

A

Decreased vision, ocular or periorbital pain, , may have a history of
transient monocular visual loss (amaurosis fugax). Usually unilateral,
although up to 20% of cases can be bilateral. Typically occurs in
patients aged 50 to 80 years. Men outnumber women 2:1.

33
Q

Clinical signs of OIS

A

Critical. Although retinal veins are dilated and irregular in caliber,
they are typically not tortuous. The retinal arterioles are narrowed.
Associated findings include midperipheral retinal hemorrhages (80%),
iris neovascularization (66%), neovascularization of the disc (35%),
and neovascularization of the retina (8%).

34
Q

Differentials for OIS

A

CRVO: Diffuse retinal hemorrhages. Dilated and tortuous retinal
veins. Ophthalmodynamometry and IVFA may
aid in differentiating OIS from CRVO.

Diabetic retinopathy: Bilateral, usually symmetric. Hard exudates
are often present

35
Q

Work up and management for OIS

A

Work up.
1. Standard eye exam (gonioscopy, DFE)
2. Consider referral to retinal ophthalmologist for fluorescein angiography (NOT IN ACUTE CASES – too time consuming)
3. Systemic work up
a. BP, pulse
b. Fasting blood sugar, CBC – attention to cardiovascular disease
c. Carotid artery evaluation (carotid duplex ultrasonography)
4. Referral to ophthalmologist for PRP/Anti – VEGF if NVC
5. Report to GP to recommend control of HTN, diabetes and cholesterol.
6. Referral to stroke unit for carotid endarterectomy within 2 weeks

35
Q

Follow up for OIS

A
  • Review based on age, general health and symptoms and signs.
  • 3 – 12 monthly

Therapeutics (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions