Once you've reached the acute phase of laminitis, you have a massive amount of inflammation with the presence of the various
mediators, including leukotrienes, cytokines, prostaglandin, Interleukin-B1, protein-C, NfkappaB, etc. These mediators are
appearing before the horse becomes lame, and so is the decreased blood flow. Which one comes first has not been determined.
Certainly with any horse at risk, because of the phenomenal inflammation, treatment includes the aggressive use of non-steroidal
"We've found an incredible amount of cytokine expression (up to 1,000-fold increase) COX-2, as well as numerous other cytokines,
As a treatment option, drugs that decrease leukocyte activation are being looked at; so is the use of more aggressive doses
"What am I going to do with a horse with early signs, whether one with metritis or colitis, or post-op colon torsion? I'm
going to do the physical things of padding its feet, and then give it a very aggressive regimen of NSAIDs," Belknap says.
"One thing that they've shown on the human side, which I'm sure is true for us too, is that when you use high doses of NSAIDs,
you actually block more than just COX-2. You also seem to block some of the other inflammatory cascades at a more basic level,
such as NF Kappa B," Belknap continues. "NF Kappa B is a basic protein that induces all the inflammatory cascades. These horses
have phenomenal inflammation, even though they're showing absolutely no clinical signs. They may have normal feeling feet,
have no digital pulse, and they're not lame. So I think the biggest thing we've got to really nail down is that there is incredible
inflammation going on early, both systemically and locally. If we hit that hard, as they are doing in human sepsis, I think
we may make a difference here, too."
They're focusing on some other products as well, such as the metallo-protease inhibitors.
"If you can block the systemic leukocyte activation, maybe we don't have to worry about it, though I don't think there is
going to be a silver bullet," Belknap says.
Is it manageable?
Treatment options haven't made much progress in the past 30 years, says Bill Moyer, DVM, director of Large Animal Medicine
at Texas A&M University College of Veterinary Medicine.
"The basic problem is that there is a lag time between the trigger point and when pain occurs," Moyer explains.
There typically is a certain amount of damage within the interface of the coffin bone and the hoof capsule before it's painful.
It might have started 72 hours ago, and yet the horse is not lame. Then there is an additional lag time, which sometimes is
more extraordinary then the first, when it starts to bother the horse and when an owner or a horseman is even aware of it.
"By the time the veterinarian is asked to examine the horse, it is not at all unlike calling the fire department after the
barn is already razed," Moyer says. "The problem in trying to manage them is that we're already too late by the time we get
there. Let's assume we're on time. What are we going to do about it? How are we going to stop it? Even the medications that
we've classically used for years don't seem to make a difference to the outcome. Down the line, we've got to figure out how
to prevent it. That's the solution. By the time you treat it, you're already dealing with a forest fire with just a balloon
full of water. What I attempt to do is to try to manage each foot as best I can. It's seldom I'm doing the same thing even
to each foot, much less on each horse," Moyer says.