DIS - Secondary Glaucoma II - Week 4

Question 1

What kind fo inflammatory condition can cause secondary glucoma?

Answer 1

Trabeculitis

Question 2

What are the two associations for glaucomatous optic neuropathy with central retinal vein occlusion?

Answer 2

Increased IOP causes central retinal vein occlusion or is a complication of central retinal vein occlusion

Question 3

What percentage of central retinal vein occlusions are caused by increased IOP in open angle glaucoma?

Answer 3

20%

Question 4

Describe how increased IOP causes central retinal vein occlusion (4).

Answer 4

Increased IOP causes blood vessel diameter reduction
Results in damage to blood vessel wall
This causes venous stasis
Results thrombus formation

Question 5

Describe how central retinal vein occlusion results in iris neovascularisation (2). What can happen following this and after how long?

Answer 5

Retinal ischaemia after vein occlusion results in the release VEGF, resulting in iris neovascularisation
Angle closure glaucoma is caused by iris neovascularisation 90-120 days after vein occlusion

Question 6

Describe how iris neovascularisation can cause angle closure. What else can VEGF cause?

Answer 6

An initially open angle closes with time after the formation of a neovascular membrane, which shrinks with time, pulling on the angle and closing it
VEGF can also result in cystoid macular oedema

Question 7

What percentage of central retinal vein occlusions are ischaemic? What about non-ischaemic? What is this condition referred to as?

Answer 7

20% - ischaemic

80% - venous stasis retinopathy (non-ischaemic)

Question 8

What appearance does ischaemic central retinal vein occlusion have?

Answer 8

Very bloody

Question 9

List four ocular signs of ischaemic central retinal vein occlusion.

Answer 9

Poor VA (worse than 6/24)
VF loss
RAPD
CWPs

Question 10

What macula OCT thickness is a sign of ischaemic central retinal vein occlusion?

Answer 10

> 600um

Question 11

In which two arteries can cardiac or arterial deficiency or stenosis cause stagnant blood flow and what demographic does it often happen? What other vascular disease can cause this?

Answer 11

Internal carotid artery
Giant cell arteritis
Often in older debilitated people

Question 12

What is the risk of secondary glaucoma like with ischaemic central retinal vein occlusion and within what time period?

Answer 12

Very high within 90-120 days

Question 13

Is venous stasis retinopathy a high or low risk for secondary glaucoma?

Answer 13

Low risk

Question 14

What percentage of venous stasis retinopathy will convert to the ischaemic form? Does this increase with age?

Answer 14

20%

Increased risk with age

Question 15

List four objective signs of ischaemic central retinal vein occlusion. What about the non-ischaemic form?

Answer 15

Widespread haemorrhaging
Multiple (6+) and widespread CWPs
Progressive ON erosion
Macula OCT >600 microns
Non-ischaemic form - mild expression of the above

Question 16

Describe the digital test for blood flow patency, including the logic behind it and what you expect to happen vs in CVO, including which of the artery/vein you expect to collapse first and why and what this tells us.

Answer 16

Digital pressure on the eye will increase IOP. If the vein has high internal pressure (equaling the artery), the vein will collapse around the same time as the artery
Normally, the vein should collapse or pulse before the artery
If they pulse/collapse about the same time, this indicates for high venous pressure due to thrombus - poor prognosis

Question 17

What are the three objectives of central retinal vein occlusion management? Can treatment restore vision?

Answer 17

Treat the systemic cause (GP)
Prevent ischaemic complications (NVI)
Prevent vision loss from cystoid macular oedema
No treatment restores vision

Question 18

Should all ischaemic central retinal vein occlusion patients be referred for a systemic workup or is this unnecessary? What other referrals are made for ischaemic central retinal vein occlusion patients?

Answer 18

All patients should be referred

Ophthalmologist for eye therapy

Question 19

What ophthalmic care is given to central retinal vein occlusion patients including both <600 and >600um (3)?

Answer 19

Anti-VEGF for cystoid macular oedema for <600um
FA to define ischaemia for >600um
Pan-retinal photocoagulation for ischaemia ± aVEGF/steroids

Question 20

How should central retinal vein occlusion patients be monitored and why?

Answer 20

Monitor IOP monthly as 25% can progress to glaucoma

Question 21

What is the initial thickening of the macula after central retinal vein occlusion related to, how is it treated (2) and what happens after this (how long)? Is it easy to treat?

Answer 21

Initial thickening is ischaemia related - treated with aVEGF ± NSAIDs
After 4-6 motnhs, an inflammatory overlay sets in ± ischaemia - hard to treat

Question 22

With cystoid macula oedema, does VA improve following aVEGF? Explain.

Answer 22

Improves as thickness normalises, but response is variable

Question 23

Where is iris neovascularisation most common in central retinal vein occlusion?

Answer 23

Pupillary margin

Question 24

How common/rare is neovascularisation in the angle following central retinal vein occlusion? Explain why.

Answer 24

Rare

Concentrations of VEGF are greatest at the pupillary margin, and become increasingly diluted towards the angle

Question 25

How long can venous stasis retinopathy last?

Answer 25

1 week to 4 months

Question 26

When should you refer a case of venous stasis retinopathy? How should the review schedule be?

Answer 26

Refer if VA is worse than 6/12

Review 1 monthly for 4/12 then every 3/12 for 12/12 if VA better than 6/12

Question 27

Should venous stasis retinopathy patients be referred for systemic workup?

Answer 27

Yes

Question 28

What would be a good prognosis for venous stasis retinopathy with macula OCT thickness and digital test?

Answer 28

If macula thickness <300um and pass digital test at 4 months, then good prognosis

Question 29

Should IOP be measured at each review for venous stasis retinopathy? What should you watch out for?

Answer 29

Yes

Watch for progressive cupping in either eye

Question 30

What is trabeculitis, in what ages does it occur, what does it suppress, and what effect does it have on IOP? Is it chronic or acute and how long does it last? Explain.

Answer 30

Episodic inflammation of TM SC cells in 20-60 year olds
Suppression of formation of endothelial vacuoles
Gives very acute IOP elevation (40-60mmHg)
Short lived

Question 31

Is trabeculitis recurrent? Is it self-limiting or does it require treatment/referral?

Answer 31

Recurrent and self-limiting

Question 32

What can trabeculitis lead to and after what (2)?

Answer 32

Can lead to glaucomatous optic neuropathy after multiple episodes and older age

Question 33

What is the theory behind the cause of trabeculitis? What pathway is involved and how does this affect possible treatment?

Answer 33

High prostaglandin levels in the anterior chamber initiate TM inflammation
Shown to involve COX pathways - controlled by steroids and/or oral/topical NSAIDs