One of the things I did at ACVIM was just to walk around and talk to veterinarians about their experiences at the conference and what they’d be taking back with them. Most were between sessions and hurrying to the next, but I was fortunate to spend quite a bit of time talking to Michael Davis, professor and endowed chair in equine sports medicine at Oklahoma State University in Stillwater. He’s also chair of ACVIM’s scientific review board and president-elect of the ACVIM Foundation. Unfortunately, I didn’t get all of our conversation on tape, but here are portions of it, starting after a little banter about the OU (my alma mater)/OSU rivalry.
Kim Thornton: So tell me what the Foundation does.
Michael Davis: The Foundation is basically an arm of the college that is responsible for advancing through research grants and awarding dollars to advance veterinary internal medicine both through specific scientific studies on disease but also to help train new clinician scientists so that we have a larger team of investigators who are doing research, whether it’s funded by us or anybody else to advance the health and wellbeing of animals domesticated as pets. The Foundation has been working with ACVIM for a number of years on the concept of what we refer to as “one medicine.”
In a nutshell, the one-medicine idea draws on the fact that although a Chihuahua does not look like a Great Dane, does not look like a Persian cat, does not look like a human, so much of what we do, whether we’re veterinarians, whether we’re physicians, is very similar, and the similarities are just as valuable in the learning process as the differences. We’ve made it our mission to draw everybody’s attention to that and get folks to understand that the basic principles of medicine are very similar, no matter what species you’re dealing with. In many respects, the knowledge base that you have to draw from is not anywhere close to similar, but that’s what we’re trying to address. We don’t have to learn every single thing about every single species on an individual basis. There are generalizations that we make every day. We recognize those and build on them so that once we’ve got a general picture of what causes heart failure or what causes chronic renal disease, any number of diseases, we can then start addressing the specifics that, compared to the generalizations, are important ultimately in the outcome of what you do to diagnose and treat the disease. But those specifics are far easier to get ahold of once you’ve got a generalized picture that spans all medicines.
Kim Thornton [having heard the words "equine sports medicine]: Can we talk racehorses?
Michael Davis: We can talk racehorses.
Kim Thornton: What can or should owners and trainers and racetracks be doing to help prevent these injuries that we’ve been seeing so much of lately?
Michael Davis: The researcher in me says ‘Well, we need to do more research, so everybody fund more research,’ but beyond that sort of glib answer, again, we’re talking about things that are very similar to conditions that are well known in human sports medicine, for example. A horse that through repeated concussion on the racetrack is gradually creating microfractures in its leg is only quantitatively different, not qualitatively different, from a human that develops shin splints. The basic pathophysiologic process is identical. It’s just more catastrophic when a horse does it, and it’s because the human is not loading the bone to the magnitude that the horse is. But other than that, it’s a very comparable process. We are drawing information from studies performed in human biomedical science to try to figure out how we can intervene in a racehorse. But ultimately we do have to get to the specifics and that is more or less where we are right now: how can we identify the horse that’s at risk?
One thing that we keep coming back to over and over in veterinary medicine is that our patients can’t talk. 
At least, they can’t talk to us. When a human starts to develop sore shins, they can simply articulate that fact. A racehorse can’t articulate that as easily, so we have to become much, much better diagnosticians than comparable sports medicine physicians, who have the luxury of their patients being able to tell them where they hurt. Once we start being able to identify the horses at risk, those techniques are going to be widely embraced because the bottom line is whether you’re the racehorse owner or the trainer or the spectator, nobody likes it, and there’s really not any level of ambivalence to those sorts of catastrophic injuries. I think we’re working in that direction, we are making progress, we have some of the unique challenges that are a facet of veterinary medicine; we also have the ability to draw quite a bit of information from our physician counterparts so that we don’t have to repeat all the work they’ve done in the last couple of centuries.
Kim Thornton: Should we not be racing them so young? We tell dog owners not to jump or run their dogs on hard surfaces until they’re 2 years old.
Michael Davis: Well, from a scientific standpoint, it’s impossible to answer that question. We don’t have as solid a dataset as we would like to be able to make that assessment with confidence. I will say that the data we do have would suggest that campaigning at the younger age does not have an effect on the breakdown rate, but given the gravity of the consequences for being wrong in that conclusion, I think most equine researchers would suggest that while the data are pointing in that direction, they’re not solid enough to be able to say absolutely that it’s not an issue, we’ve had the final word, we don’t need to study it anymore. I guess the take-home point is that from a scientific basis, I don’t think we can conclude that it’s bad, but by the same token, even though what data are available suggest that it’s okay, those data are not solid enough to be the end of the story.
Interlude: I had not expected to spend more than a few minutes talking to Davis, so at this point I switched off my recorder (bad Kim, bad, bad Kim), but we ended up continuing our conversation–including a discussion about last year’s Eight Belles tragedy–and eventually I turned it back on.
Michael Davis: We were some of the first folks to start using mechanical ventilation on foals; we were one of the first teams to use exogenous surfactant on premature foals. This neonatal foal was premature because the mare had colicked. We took her to surgery and fixed the displacement–she was about 300 days–took her back to recovery and there’s this cannon shot sound as she snaps her femur during recovery. I so distinctly remember this because we were all just sitting there in shock. The anesthesiologist is in the process of euthanizing the mare and turns to us and says ‘What do you want to do with the foal?’ We’re like ‘Huh?’ She said, ‘You’d better decide in the next couple of minutes because it’s coming out,’ and we looked down and here’s this premature foal squirting out. So we go rushing in there and we hook it up to a ventilator and it’s like trying to ventilate a sirloin steak. It’s just not happening. So we get this brilliant idea to use some exogenous surfactant. We were able to keep the foal alive for 36 hours while we’re rounding up the surfactant and we poured it in the foal’s trachea. It’s in intensive care, we’ve gotten every monitor we could possibly come up with, numbers and dials and beeping alarms, and right before our eyes, everything normalizes within minutes and everybody in the room had goose bumps. It was as close to a veterinary miracle as we’ve ever seen.
And then the foal died of something else.
Kim Thornton: Oh, I was waiting for the happy ending.
Michael Davis: Well, we were too. It was so frustrating to realize that what we perceived to be the hurdle–if we can get over this, the foals live–was really ‘If you get over this, nature will disclose its next hurdle.’
Kim Thornton: Is that a common thing now, to use the surfactant?
Michael Davis: It’s not, because when it comes right down to it, it’s expensive. It’s really not a practical option for the vast majority of situations. The mechanical ventilation, for example: you’ve basically got to have somebody who is at least a veterinarian and probably has a couple of years of experience in a residency program parked there 24/7 because all of this stuff is constantly being adjusted and fine-tuned on a minute-by-minute basis. It’s not like a fluid pump that you can set and come back six hours later. Most places don’t have that depth of resource, and in our particular case, the first one that we did, we were running around looking for synthetic surfactant. We had a very deep-pocketed owner, but the problem that we ran into–it was almost surreal–we were calling around to area hospitals and nobody had more than two or three doses of the synthetic surfactant on hand and they wouldn’t sell us all of what they had because the next premature human that came in, they’d be empty-handed. We wound up, in order to get a comparable dose for a 120-pound foal, we had to raid 18 different hospitals. That treatment alone, we dumped about $30,000 of surfactant into the foal in about five minutes.
What is more common, and it’s pretty crude, but to a certain extent, surfactant is surfactant is surfactant. You could never do this in humans, but you can run down to the local slaughterhouse, grab the next cow off the line that gets slaughtered, grab the lungs, dump a bunch of chloroform into the lungs and then pour it all out into a vial and put in a fume hood or something and evaporate the chloroform and you have surfactant. It’s not sterile, it’s not purified, there’s no telling what’s in there, but it’s surfactant and if you don’t have $30,000 to get the synthetic stuff…a lot of the problems that might create can be overcome with just a few more doses of antibiotics. It’ll get you over the hurdle of not being able to oxygenate the little bugger. The approach we started taking was just ‘We’ll worry about the problem when it occurs. Right now we have a foal that can’t breathe. We’ll make it breathe and then see what happens, but we know if we don’t make it breathe in next little bit, it’s going to die. What do we have to lose?’
Kim Thornton: I heard something similar recently from a shelter director who had the same attitude about a particular issue: ‘Yes, this thing is a problem, but we’ll worry about that later.’
Michael Davis: A lot of the things that we do, we talk about it around the clinic a lot when we’re dealing with a horse with pleural pneumonia–there’s sort of the general impression among internists that there’s some theoretical level or point where it’s not the infection that’s killing the horse, it’s the immune response to the infection that’s killing the horse. None of us can agree on how to define that sort of breakpoint, but we all sort of agree that it’s there and we all agree that even though this is an infectious disease, there’s some point where in order to buy the time to actually treat the infection, you’re going to have to immunosuppress the horse a little bit with some steroids. You sit in front of the stall during rounds and you’re looking at all the lab work and you’re going ‘Which side of the line are we on? Can we come to a consensus?’ We recognize that when we give this dose of dexamethasone that we’re shutting down parts of the immune system and potentially giving the bacteria a leg up, but there’s a general agreement that if we don’t do something about the inflammatory response in the next six hours, we’re not going to have a patient to worry about in 12 hours.
At this point, I actually did run out of tape, which is too bad, because we went on to talk about his sled-dog research, so that will have to wait for another day.
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