Intravitreal Therapy and IOP: Someone Get the Answers!

There’s a bit of a conundrum at hand in the ophthalmic world. To be clear, there’s certainly more than one conundrum, but the one we’re talking about is a large-scale and systemic one — specifically, the link between intravitreal treatments and concurrent increases in intraocular pressure (IOP). 

You likely don’t need us to tell you that this is a complex, multifactorial problem, but we’ll say it anyway: It’s just that. If anyone has the smoking gun link and the solution, we’d love it if they’d come forward and set us all straight. Until that time, the best we can do is explore the links and examine the impact on both doctor and patient. 

Let’s start with a simple assertion, put forward in this paper in the Indian Journal of Ophthalmology: “Most, if not all, intravitreal agents cause ocular hypertension, both in the short and long term. The functional consequences of these observations are not very clear.”

If nothing else, the practice of medicine explores problems until the solution is found. Considering the countless factors that go into IOP issues linked to intravitreal treatment, it’s unlikely we’ll track down one simple solution. However, we can start where most detectives would by investigating the scene of the crime(s). 

IOP and Anti-VEGF Therapy

It’s largely indisputable that a sustained IOP rise follows intravitreal anti-VEGF administration. However, this occurrence is still only known as a phenomenon, and many aren’t quite sure what to do about it.

One of the trickiest aspects of this relationship is all the other factors involved. These factors include age, glaucomatous condition, gender and more. Tellingly, the Indian Journal of Ophthalmology describes these various underlying conditions as “complex.” That’s med-speak for “we don’t really get it.”

And that’s okay. The American Academy of Ophthalmology (AAO) can help us boil this down a bit to its most salient points. First, anti-VEGF agents lead to an “immediate and transient” increase in IOP. However, a long-term increase in IOP may also be present — but we don’t quite know who’s at risk yet. 

Worth noting is that aflibercept and ranibizumab are both associated with a rise in IOP, though some studies don’t indicate any sustained IOP rise following their administration. Again, we’re back to a multifactorial problem without a clear culprit. 

Knowing that anti-VEGF agents can lead to increased IOP doesn’t mean that anti-VEGF treatments should be halted by any means. Indeed, doctors will have to weigh the benefits and drawbacks of the outcome based on the individual patient. And again, knowing how many factors are at play here means it’s impossible to make a blanket statement for suggestions. 

Some associations between sustained IOP rise and a number of conditions were reached by the Indian team, and they include the following:

IOP lowering meds before anti-VEGF? 

Some studies indicate that pre-treating patients with IOP-lowering medications or even ocular massage can prevent or lessen the effects of the short-term IOP spike following intravitreal anti-VEGF treatments. The long-term effects of these treatments are as yet unknown, but controlling IOP spikes is a good step. 

There appears to be a controversy in the correlation between pre-existing glaucoma and sustained IOP rise following anti-VEGF treatments. In short, more studies need to be done to verify any current beliefs, which are all over the map. One confounding concept, for example, is that AMD may represent a generalized degeneration of the eye, affecting the trabecular meshwork outflow and potentially leading to increased IOP. 

Those patients with worsening AMD would need more treatments, leading to potentially worse IOP, and, well … you see where this is going. It’s almost like a riddle, and we’d love for someone to find the answer. 

It Ain’t Just Anti-VEGF

Other intravitreal treatments have also been associated with increased IOP, including steroids, intravitreal dexamethasone and triamcinolone acetonide. The latter of those, for example, is well documented in leading to short-term IOP spikes, long-term ocular hypertension, and may also lead to cataracts. 

So, where do we stand with these relationships? Simply put, more studies need to be conducted to figure out just who the at-risk group is and just how at-risk they are. Is it worth it to stop intravitreal treatments for patients with a high risk of long-term ocular hypertension? We don’t know, and we won’t until solid data is there for us to sort through. 

But sort through it we will when it’s there, and we’ll be sure to let you know about it. In the meantime, we know for sure that intravitreal therapy is linked to ocular hypertension in both the short and long term — but for how much and how long and for whom is a situational issue we need to figure out. By “we” we mean the medical community, which we’re fortunate enough to play some role in. 

Be sure to check back with us on this, since we’ll be keeping a close eye on it — though we’ll make sure to keep our pressure down, since we don’t want IOP spikes either.