Intraocular Pressure and It’s Role in Open-Angle Glaucoma

January 17, 2020

Transcript:

 

Transcript:

Joseph F. Panarelli, MD: Hello and welcome to this discussion presented by Ophthalmology Times, titled “Updates on Pharmacologic Treatment of Open-Angle Glaucoma.”

I am Dr. Joseph Panarelli, Associate Professor in the Department of Ophthalmology at NYU Langone Medical Center in New York.  Please join me in welcoming my colleague, Dr. Sahar Bedrood, a glaucoma specialist at Acuity Eye Group and Assistant Professor of Clinical Ophthalmology at the USC Roski Eye Institute in Pasadena, California.

In today’s discussion, we’ll talk about available therapies and practical considerations in treatment of open-angle glaucoma.

Let’s start by talking about intraocular pressure, which is the only known modifiable risk factor for open-angle glaucoma progression. Numerous studies indicate that patients continue to go blind and/or progress despite maximal topical medical therapy.

Dr. Bedrood, what are your theories on the role of IOP in glaucoma, and IOP-dependent vs IOP-independent variables associated with visual field (VF) progression in glaucoma?

Sahar Bedrood, MD, PhD: There are a number of theories about how IOP plays a role in visual field loss. One of them is the classical mechanical stress/strain model. What that means is really the intraocular pressure places a little bit of strain onto the sclera and the optic nerve, thereby causing apoptosis and retinal ganglion cell loss. And that’s kind of one of the major theories for the stress/strain model.

The other one which relies a little bit less on IOP is the vascular theory. That is when the optic nerve is supplied by a number of blood vessels and those little blood vessels don’t get enough oxygen, and so what happens over time is you get apoptosis and nerve fiber layer loss, which leads to visual field loss.

Dr. Panarelli: With patients living 10+ years after OAG diagnosis, describe how that impacts disease progression/treatments.

Dr. Bedrood: The rate of glaucoma progression is different in a lot of different people. Some patients who have a very strong genetic component are going to progress very quickly, and some, not so much. What we do know is after 10-plus years of treatment some of those treatments that initially worked may not work as well. SLT (selective laser trabeculoplasty) will wear off, or it may need a touchup or a second round. The glaucoma drops we use, patients sometimes develop an intolerance, either an allergy or the drugs simply don’t work as well. So over a course of 10 years a lot can change. Their rate of progression can fluctuate. Their tolerance of drugs can fluctuate. And oftentimes at 10, or 15, or 20 years we’re looking at other modalities of treatment like surgery, or something that can regulate their pressure a little bit better - other additional drugs for instance.

Dr. Panarelli: With the growth of microinvasive glaucoma surgery (MIGS), are you performing surgery earlier on some of these patients you are expecting to live longer?

Dr. Bedrood: Actually I am. With the advent of all these new technologies and surgical techniques, we have the benefit of being able to do surgery for them earlier. So, frankly speaking, I don’t put on three or four different drops if it’s not working for the patient. I will move forward with a MIGS device of some sort so that we really get them to lower their pressure in a more effective way.

Dr. Panarelli: Comment on the importance of knowing about patients’ IOP fluctuation.

Dr. Bedrood: What’s interesting is when we see a patient in our clinic, it’s a snapshot in time. We see the patients, we see one pressure. But in reality patients’ pressures do fluctuate throughout the day. And studies have shown that these fluctuations of greater than 8 to 10 mm Hg can actually lead to visual field progression, and progression of their glaucoma as well. So monitoring their fluctuations in certain patients, especially ones that are progressing faster than we had suspected, or expected, is really important I think. And trying to maintain a steady IOP all day every day is even more important than we had previously thought.

Dr. Panarelli: Describe the parameters that contribute to IOP and which classes of medicines address which parameter.

Dr. Bedrood: There are a number of parameters that play a role in IOP. One of them is called EVP, Episcleral Venous Pressure. You see that increased in diseases like Sturge-Weber, thyroid eye disease, scleral buckles.

The EVP is usually between 8 and 10 in a normal person, and in patients who have this increased EVP, what happens is it collapses their Schlemm’s canal and it increases a resistance, so they end up having higher pressure in their eyes than a normal person.

And one of the new classes of drugs that can actually reduce the EVP are the Rho-kinase inhibitors. It relaxes the musculature, the smooth muscle around the trabecular meshwork (TM), and basically helps with not just TM outflow, but episcleral venous outflow and reduces that resistance. So that’s one way.

Another parameter that we use for IOP lowering is the aqueous production. We can actually lower that with beta blockers, as we know, and the Rho-kinase inhibitors can reduce that as well.

Next is the uveoscleral pathway. The uveoscleral pathway, classically, we use the prostaglandins to increase the flow out of there, and that is one of the most potent and one of the most popular first-line treatments is to use the prostaglandins.

And then, not to mention, we, of course, have the conventional pathway, which is flow through the trabecular meshwork. And that includes drugs such as the Rho-kinase inhibitors, the alpha agonists. We have all these different ways in this tiny little space where pressure is reduced somehow, either through aqueous production reduction, or through increased outflow. And with all the different classes we are able to use the different medications in different ways to get those patients as low of an IOP as possible.

 

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