DIS - Secondary Glaucoma II - Week 4 Flashcards
What kind fo inflammatory condition can cause secondary glucoma?
Trabeculitis
What are the two associations for glaucomatous optic neuropathy with central retinal vein occlusion?
Increased IOP causes central retinal vein occlusion or is a complication of central retinal vein occlusion
What percentage of central retinal vein occlusions are caused by increased IOP in open angle glaucoma?
20%
Describe how increased IOP causes central retinal vein occlusion (4).
Increased IOP causes blood vessel diameter reduction
Results in damage to blood vessel wall
This causes venous stasis
Results thrombus formation
Describe how central retinal vein occlusion results in iris neovascularisation (2). What can happen following this and after how long?
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
Describe how iris neovascularisation can cause angle closure. What else can VEGF cause?
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
What percentage of central retinal vein occlusions are ischaemic? What about non-ischaemic? What is this condition referred to as?
20% - ischaemic
80% - venous stasis retinopathy (non-ischaemic)
What appearance does ischaemic central retinal vein occlusion have?
Very bloody
List four ocular signs of ischaemic central retinal vein occlusion.
Poor VA (worse than 6/24)
VF loss
RAPD
CWPs
What macula OCT thickness is a sign of ischaemic central retinal vein occlusion?
> 600um
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?
Internal carotid artery
Giant cell arteritis
Often in older debilitated people
What is the risk of secondary glaucoma like with ischaemic central retinal vein occlusion and within what time period?
Very high within 90-120 days
Is venous stasis retinopathy a high or low risk for secondary glaucoma?
Low risk
What percentage of venous stasis retinopathy will convert to the ischaemic form? Does this increase with age?
20%
Increased risk with age
List four objective signs of ischaemic central retinal vein occlusion. What about the non-ischaemic form?
Widespread haemorrhaging
Multiple (6+) and widespread CWPs
Progressive ON erosion
Macula OCT >600 microns
Non-ischaemic form - mild expression of the above
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.
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
What are the three objectives of central retinal vein occlusion management? Can treatment restore vision?
Treat the systemic cause (GP)
Prevent ischaemic complications (NVI)
Prevent vision loss from cystoid macular oedema
No treatment restores vision
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?
All patients should be referred
Ophthalmologist for eye therapy
What ophthalmic care is given to central retinal vein occlusion patients including both <600 and >600um (3)?
Anti-VEGF for cystoid macular oedema for <600um
FA to define ischaemia for >600um
Pan-retinal photocoagulation for ischaemia ± aVEGF/steroids
How should central retinal vein occlusion patients be monitored and why?
Monitor IOP monthly as 25% can progress to glaucoma
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?
Initial thickening is ischaemia related - treated with aVEGF ± NSAIDs
After 4-6 motnhs, an inflammatory overlay sets in ± ischaemia - hard to treat
With cystoid macula oedema, does VA improve following aVEGF? Explain.
Improves as thickness normalises, but response is variable
Where is iris neovascularisation most common in central retinal vein occlusion?
Pupillary margin
How common/rare is neovascularisation in the angle following central retinal vein occlusion? Explain why.
Rare
Concentrations of VEGF are greatest at the pupillary margin, and become increasingly diluted towards the angle
How long can venous stasis retinopathy last?
1 week to 4 months
When should you refer a case of venous stasis retinopathy? How should the review schedule be?
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
Should venous stasis retinopathy patients be referred for systemic workup?
Yes
What would be a good prognosis for venous stasis retinopathy with macula OCT thickness and digital test?
If macula thickness <300um and pass digital test at 4 months, then good prognosis
Should IOP be measured at each review for venous stasis retinopathy? What should you watch out for?
Yes
Watch for progressive cupping in either eye
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.
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
Is trabeculitis recurrent? Is it self-limiting or does it require treatment/referral?
Recurrent and self-limiting
What can trabeculitis lead to and after what (2)?
Can lead to glaucomatous optic neuropathy after multiple episodes and older age
What is the theory behind the cause of trabeculitis? What pathway is involved and how does this affect possible treatment?
High prostaglandin levels in the anterior chamber initiate TM inflammation
Shown to involve COX pathways - controlled by steroids and/or oral/topical NSAIDs
