DIS - Secondary Glaucoma I - Week 4 Flashcards
List 5 common causes of secondary glaucoma.
Caused by trauma
Associated with ocular disease/degeneration
Associated with systemic disease/disorder
Iatrogenic secondary glaucoma
Caused by inflammation
What is the most common cause of secondary glaucoma? List three common mechanisms.
Restriction to aqueous circulation or trabecular outflow
-due to trauma
-pseudoexfoliation
-pigment dispersion
If IOP is <24mmHg in secondary glaucoma, what is often all thats required in management?
Treat the underlying disorder, this is often all thats needed for IOP <24mmHg
If IOP is elevated (≥24 for 7 days or ≥30mmHg for 24h) what is the course of action (2)? When should the review be and what is expected?
Apply aqueous suppressents aggressively depending on IOP
Apply outflow modulators as needed (q5min x2 then prn)
Review in 24h, if IOP remains high (30+) with therapy, consider prompt referral for surgical intervention
Consider elevated IOP (30+) on review even with therapy. what is the main concern (3)?
Retinal vein occlusion
Iris ischaemia
RGC loss
How does the urgency of referral for surgical intervention compare in IOP of 24-30 vs 30+ (assuming after therapy)?
24-30 can wait a week
Prompt referral for 30+ IOP
What are the two most likely causes of secondary glaucoma with high IOP (30+)?
Primary angle closure (iridocorneal endothelial syndrome)
Trabeculitis
Consider the course of action taken for secondary glaucoma with high IOP (30+). Explain the logic behind why it is done in this manner (2). Also name the condition this high IOP can potentially cause.
Apply aqueous suppressants aggressively
-dealing with sick tissue
-response is likely blunted at normal drug concentrations
-high IOP has potential for central retinal vein occlusion
If IOP is >30 in secondary glaucoma, must IOP be reduced quickly or is there no rush?
IOP must be reduced quickly
Describe the protocol for secondary glaucoma with high IOP (5).
Start with 1gtt pilocarpine 2% and timolol 0.5%
Repeat after 5 mins
Then timolol 0.5% QiD for 24h
Repeat above after 24h until IOP <30mmHg
Then maintain Rx prn
After what amount of time does timolol have maximal effect in healthy eyes?
By 1h after instilling
Consider the protocol for secondary glaucoma with high IOP. what does it tell you if it doesnt work (2)?
It should be enough for healthy tissue
-if it doesnt work, tissue is likely not healthy
Consider the protocol for secondary glaucoma with high IOP. What if IOP has not decreased sufficiently on review 24h later (2)? What should you check for?
Add acetazolamide 250mg po or CAI eyedrop TiD
Check for iridocorneal endothelial syndrome
Consider the protocol for secondary glaucoma with high IOP. What is an alternative to pilocarpine?
PGA (xalatan 0.005%)
What is the most likely cause of secondary glaucoma with moderate IOP (24-30mmHg for >1 week)? List four mechanisms for this.
Open angle with TM disorder
-dysfunctional trabecular cells
-dysfunctional schlemms canal endothelial cells
-blocked TM
-compromosed outflow
Consider secondary glaucoma due to compromised outflow. List two mechanisms of this.
Venous congestion
Scleral spur malfunction
What is the management of secondary glaucoma with moderate IOP (2)?
Aqueous suppressants
Increase uveo-vortex flow to bypass TM
Describe the protocol for secondary glaucoma with moderate IOP including eyedrops and review (3). Explain what to expect on review.
Timolol 0.5% BiD
Prosaglandin analogue (xalatan 0.005%) noce
Review in 24h
Expect 20-30% drop in IOP
Describe the two mechanisms of secondary glaucoma due to trauma (blunt trauma).
Blocked TM with debris following trauma
-pigment, blood, material
Break ciliary muscle insertions to scleral spur, reducing schlemms canal pmping, reducing outflow
What is the treatment for secondary glaucoma due to trauma (3)?
Aqueous suppressants
-timolol, PGAs
Surgery for iridodialysis
What are pseudoexfoliative syndrome and pigment dispersion manifestations of?
Age related manifestations of genetic weakness in anterior structures (iris)
What is pseudoexfoliative syndrome an abnormality of (2)?
Collar blood vessels of the iris and GAG synthesis