Diabetes and Glaucoma optometric pearls | Optometry | Student Doctor Network
I made a blog entry about different pearls for the management of glaucoma and diabetic retinopathy patients, and I thought that it would be nice to share them.
Here they are: Diabetics: Ask what the patient's last blood glucose (particularly fasting) and HbA1c were.
Ask if it has been under good control.
These numbers are super helpful with predicting the likelihood of diabetic retinopathy, or how bad it is if they have it.
Ask how long the patient has had diabetes.
It is well recorded in the literature that the longer the patient has had diabetes, the higher the risk for retinopathy.
According to the American Diabetes Association, 10% of those who had been diagnosed for less than 5 years had retinopathy, 39% for those diagnosed 5-14 yrs, and a whopping 70% for those diagnosed for more than 15 years.
Record the pertinent negatives.
What does this mean?
Basically, record the main things that we check for in the eye for diabetics: check carefully for neovascularization of the iris, disc, and elsewhere (NVI, NVD, and NVE, respectively).
Also, check for clinically significant macular edema (CSME).
In other words, if you didn't see any of these signs, record "no NVI, NVD, NVE, CSME" Glaucoma: For glaucoma patients on medication, it's important to ask specific questions about compliance;
Don't simply ask "are you good with taking your drops?".
Ask them when they last took their medication.
Also ask them how often they forget their drops, if they do at all.
These questions are important for you to determine if the IOP that you're taking is falsely high or not, or if you're wondering why there are more defects in the threshold visual field test you just took.
It is not uncommon for glaucoma patients to be poor with compliance, especially if their vision is good and there is no immediate risk to vision loss.
Remember that suspicions for glaucoma are raised with race (especially African Americans) and a history of glaucoma in the family (in addition to your optic nerve head evaluation, threshold visual fields result, etc).
Make sure to take note of these facts in your assessment.
For every diagnosis of glaucoma, it is important to do gonioscopy.
In order to truly diagnose an open angle glaucoma, you must rule out other causes of glaucoma e.g.
Pigmentary dispersion, etc.
I'd love to hear of your own optometric pearls, and they don't have to be about glaucoma or DR.
If this post gets enough replies, I'd like to make a web page full of selected pearls, with your permission and due credit of course!
Thanks in advance, your contribution would benefit many!
Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.
Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.
I forget the reason, someone here may know.
Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same. 2.
Lumigan tends to lower IOP better than Travatan, which lowers IOP better than Xalatan. 3.
Lumigan is usually associated with the most conjunctival hyperemia, so I don't usually start Lumigan as first line therapy.
If a patient is using another prostaglandin analogue (Travatan or Xalatan), this tends to "prep" the eye and it will not be as hyperemic after switching to Lumigan later on. 4.
Azopt tends to be the best secondary agent when combined with a Prostaglandin analogue.
This is when compared to other drops like Alphagan or a beta blocker. 5.
Alphagan (and Combigan) can cause systemic sedation.
Patients may feel "tired or sleepy" when using these eye drops.
Make sure you instruct them to do punctal occlusion after drop instillation. 6.
Pseudoexfoliative glaucoma responds best to a beta blocker, followed by Prostaglandin 7.
I've heard that IOP is highest at 2am, is this true?!? I'll update this post if I think of anything else.
This attached lecture is an excellent evidence based review of treatment options. Also, in my experience Alphagan is my preference as a secondary/additive agent.
Quote: : Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.
Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.
I forget the reason, someone here may know.
Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same.
Lumigan (bimatoprost) is a prostamide, and the other prostaglandin analogues are not.
A good way to remember that: bimatoprost isn't as potent, so this is why Lumigan's drug concentration is 0.03%, where the others are 0.004% (Travatan) and 0.005% (Xalatan).
Quote: : 7. I've heard that IOP is highest at 2am, is this true?!? We've been taught it is highest right before waking up, around 5-6 am for normal schedule sleepers.
So 2,5,6 am, whatever, sometime early morning Oh, and if someone for example works the night shift, their IOP peak won't be the same time, it will change based on their sleep schedule.
Quote: : Correct me if anyone disagrees, but this is what I've read and also have experienced regarding glaucoma therapy: 1.
Travatan and Xalatan fall under the same mechanism of action as prostaglandin analogues, versus Lumigan, which is a prostaglandin analogue that works slightly differently.
I forget the reason, someone here may know.
Therefore, if you are currently using Travatan but it is not working well, consider switching to Lumigan instead of Xalatan, since they work the same. 2.
Lumigan tends to lower IOP better than Travatan, which lowers IOP better than Xalatan. 3.
Lumigan is usually associated with the most conjunctival hyperemia, so I don't usually start Lumigan as first line therapy.
If a patient is using another prostaglandin analogue (Travatan or Xalatan), this tends to "prep" the eye and it will not be as hyperemic after switching to Lumigan later on. 4.
Azopt tends to be the best secondary agent when combined with a Prostaglandin analogue.
This is when compared to other drops like Alphagan or a beta blocker. 5.
Alphagan (and Combigan) can cause systemic sedation.
Patients may feel "tired or sleepy" when using these eye drops.
Make sure you instruct them to do punctal occlusion after drop instillation. 6.
Pseudoexfoliative glaucoma responds best to a beta blocker, followed by Prostaglandin 7.
I've heard that IOP is highest at 2am, is this true?!? I'll update this post if I think of anything else.
A couple of thoughts: On the prostaglandins: don't go straight for the "if the Xalatan doesn't work well, go with Travatan" try to know the reasons.
Studies are showing that Travatan works better in black patients than Xalatan. Lumigan causes less of the hyperpigmentation problems with the other 2, less headaches (as symptoms ) but will give more conj hyperemia. Also, recent, recent studies and discussions in glaucoma are moving away from "whichever lowers IOP best" when you can have a low IOP but still have NFL loss.
Some studies are recommending for newly diagnosis, use a prostaglandin to get the IOP controlled, then transfer to a Alphagan- as it is a neuroprotectant.
I encourage everyone to read new literature on neuroprotectants. Jack Kanski (love him) has listed several items of interest to prescribe: Betaxolol, Alphagan, Vit E, and Ginko Biloba.
These items have nueroprotective qualities to them, with the drugs having proved VF saving results. This explains renewed interest in some poly glaucoma drugs as they are incorporating a proven IOP lowering substane with a paired nueroprotectant. Please research this! Good luck everybody!
Quote: : courage everyone to read new literature on neuroprotectants. Jack Kanski (love him) has listed several items of interest to prescribe: Betaxolol, Alphagan, Vit E, and Ginko Biloba.
These items have nueroprotective qualities to them, with the drugs having proved VF saving results. This explains renewed interest in some poly glaucoma drugs as they are incorporating a proven IOP lowering substane with a paired nueroprotectant.
Any relevant articles on this?
My understanding is that the whole "neuroprotection" thing is still very much just speculation without any solid research behind it...
Quote: : Any relevant articles on this?
My understanding is that the whole "neuroprotection" thing is still very much just speculation without any solid research behind it...
There are about 10 years of studies done on Timolol vs Brimonidine showing that Timolol does keep the IOP lower, but visual field continues to restrict over the years, while Brimonidine does not lower IOP as much, yet visual field is preserved.
Betaxolol is also showing this preservation of the VF. This is why I said Alphagan is quickly becoming a preferred polypharmacy with a Beta Blocker or Prostaglandin. Its not a bunch of hocus pocus--- unless someone claims to know HOW this works.
That is not yet certain. I'll repost tomorrow concerning the articles for those wanting to read this info for themselves.
Quote: : There are about 10 years of studies done on Timolol vs Brimonidine showing that Timolol does keep the IOP lower, but visual field continues to restrict over the years, while Brimonidine does not lower IOP as much, yet visual field is preserved.
Betaxolol is also showing this preservation of the VF. This is why I said Alphagan is quickly becoming a preferred polypharmacy with a Beta Blocker or Prostaglandin. Its not a bunch of hocus pocus--- unless someone claims to know HOW this works.
That is not yet certain. I'll repost tomorrow concerning the articles for those wanting to read this info for themselves.
I agree, brimonidine is my preferred agent for adjunctive therapy, but I think they're still plenty of work left to prove this neuroprotection thing.
Info can be found in: Glaucoma, by Jack Kanski: http://www.amazon.com/Glaucoma-Jack-...4873501&sr=8-1 articles: http://www.pubmedcentral.nih.gov/art...?artid=1936355 I have two more, but cannot find them for some reason. The research started about 1999, and is continuing.
Also, this nuero-protection stuff seems to be hocus-pocus when discussed regarding Parkingsons, but the glaucoma test-trails are promising. thanks for the interest.
Quote: : I agree, brimonidine is my preferred agent for adjunctive therapy, but I think they're still plenty of work left to prove this neuroprotection thing.
I just returned from vision expo and the consensus was that the whole "neuro protection" thing was such a titanic failure that Allergan shelved the entire thing after spending $65 million.
