Don’t kill old rolling…horses?

“Don’t kill old rolling…horses?”

Kate Connell

University of Pennsylvania

            When Sunny first presented to our emergency service, I thought that he would make an extraordinary case study. He had the stuff of an academic one-hit wonder: mystery, suspense, drama, and plot twists rivaled only by 1990s M. Night Shyamalan. The downfall of Sunny’s case was that it was lacking a definitive diagnosis or revolutionary treatment protocol. But the way I see it, even if Sunny didn’t turn out to be journal-worthy, he taught me many valuable lessons about veterinary medicine that I thought would be worth sharing. For the sake of sounding somewhat academic, I will start this story like any respectable vet student would:

            Sunny, a 4 year old fell pony gelding, and his herdmate Jenny, a 5 year old fell pony mare, were presented to the New Bolton Center Emergency Service with a 48 hour history of lethargy and inappetance. The owner reported that two other horses had exhibited similar symptoms earlier in the week. One of the affected horses died acutely two days prior, and the second was euthanized by the vet that morning. Several other horses on the property were exhibiting “suspicious symptoms.”   

            When the referring veterinarian was consulted, he informed us that the horses were not just “lethargic,” but were exhibiting neurologic signs.  He strongly suspected botulism after examining their new batch of hay, which was wet and pungent.

It sounded like we had a diagnosis before the ponies had even arrived.

            That was not the case.

            The trailer pulled up, and we set about examining the horses. We pulled out Sunny’s tongue, and he left it hanging. Slam-dunk for botulism.  Or, as it turns out, it is a sign that your pony is so neurologically impaired that it just doesn’t care that its tongue is hanging out in the world. As it turns out, Sunny was the latter of the two. As soon as we tried to move him, he staggered out of the trailer, legs crossing and trunk swaying. Not botulism.*  

            We started spouting out differentials. Hepatic encephalopathy! Normal liver values. Moldy corn toxicity! The owner doesn’t feed grain. Salt toxicity! The horses had plenty of access to water. One of the Equine Encephalopathies! EEE! WEE! VEE! Vaccinated against the first two. No fever. And the odds of us finding a VEE outbreak in PA right now? Nil. Meningitis! In a herd outbreak? Rabies! Now we were just getting desperate…what, did a rabid raccoon get into the barn and bite all of the horses at once, and they all presented at the same time?

            And so without a diagnosis, the ponies were put into the isolation unit and put on fluids, banamine, and thiamine. They were left with a generous amount of hay and water, and were observed to be quiet overnight.

            The next day was full of surprises.

Jenny, Day 2

I visited Jenny, who as you’ll recall, was Sunny’s herdmate. She had the same clinical signs as Sunny, but was affected to a lesser degree. The morning after initial presentation, she was bright, neurologically appropriate, and had eaten enough hay to satiate a Clydesdale. This will be the last you hear about dear, sweet Jenny in this story because from that morning forward, she was a perfectly uninteresting in the medical sense.

Sunny, on the other hand, only got stranger.

That morning, he was as dull as he had been on presentation, with no inclination to eat or drink for us. As I checked on him throughout the day, he didn’t move much; occasionally going to a corner to head-press, but mostly standing statue-still in the middle of the room.

And then six o’clock treatments rolled around. I started pulling on my layers of PPG (remember, these ponies were in our isolation ward, meaning that each visit meant a gown, plastic booties, gloves, cap, and mask), and I glanced through the window and noticed something odd. Sunny was standing quietly in the corner, as he had been for every other check, but there were dark smears across the walls.

I entered the anteroom with a knot in my stomach. Stepping through the bleach bath, I put on a brave face and opened the stall door. Sunny remained statue-like in his corner, non-responsive to the noise of my entry.

What I hadn’t been able to appreciate through the layers of glass was the fact that Sunny had mangled his face. He had deep abrasions over every bony prominence, and blood was streaming from both nostrils. The walls were painted with his blood, smeared in zig-zags around the entire circumference of the room. His water buckets had been pulled from their anchors, misshapen from being trampled.

I tried to call the pony to gauge his mental status without getting too close. Much to my surprise, his ears flicked to attention, and his head elevated. That was more of a response than I had ever received from Sunny. Emboldened, I entered the stall and said his name again. He turned his head towards the sound, and I froze mid-stride. There is probably a medical term for what I saw in his eyes, but all that I can say is that even though he was looking towards me, Sunny’s gaze was absent. He was seeing but not comprehending, a blank slate, whatever you want to call it. But my gut told me that there was something terribly wrong. As I backtracked to the door, Sunny charged, and slammed face-first into the wall next to me.

I evacuated the room, stripping from my PPG to reach the cell phone in my scrubs pocket. I called the clinician on the case, saying something along the lines of Dear God, please help me, I’m not qualified to deal with a psycho white-walker murder horse! Before the clinician could finish telling me to hang tight, there was movement in the stall.

Sunny, who had kept his footing after smashing into the wall, had glued his blank gaze on the window and hadn’t twitched a muscle since. The movement that caught my eye was slight, just a small sway. As I turned to face him, he toppled like a domino: legs straight, no stumble, just vertical to horizontal with a resounding thud.

I raced back into the anteroom and cracked the door to look in at him. His chest didn’t move. I ran back outside (I find that our clinical year involves a lot of running back and forth like a headless chicken), and collided with the clinician in the hallway.

In a very professional, calm (hysterical, probably swearing) manner, I informed the clinician that Sunny was dead.

We entered the stall together and stared at the pony that was. After what felt like several minutes, he took a breath. Thirty seconds later, he took a second breath.

Despite his ability to produce a staggering respiratory rate of 2 breaths per minute, the clinician decided that Sunny’s time had come. She called the owner to get permission for euthanasia. No answer. She redialed the number for the next twenty minutes to no response.

And then, Sunny rolled into sternal. He blinked blearily. We watched him in dumbfounded silence for another ten minutes, and he stood up without so much as a wobble. I believe the clinician said something along the lines of, “huh.” I probably said something equally profound. What Sunny did next was probably the last thing that we had expected. He began to eat. His hay was mounded in the center of the stall from his circling frenzy, and blood still oozed from a nostril, but that pony acted like this was just his typical Friday night.

The owner finally did return our calls, but given Sunny’s sudden change of heart, we opted to continue the wait and see protocol.

The following morning, Sunny continued to look remarkably bright. His appetite was insatiable to the point of psychosis. If there weren’t two flakes of hay in his stall at all times, you would come back to find him gobbling up his straw. We began to feel tentative optimistic about his outcome.

Six o’clock treatment time came. I jauntily walked down the isolation hallway, but the spring in my step died when I saw Sunny. He was back in the corner with his neck was fully extended, his chest, neck, and mandibles shoved into the wall. It was the most uncomfortable position I think I’ve ever seen.

The owner was called again with concerns regarding our treatment options. At this point all diagnostic testing showed no abnormalities. A CSF tap had been turned down by the owner that morning because of his apparent improvement.

His regression made our earlier optimism feel foolhardy, but the owner wanted to push forward. More supportive care. Put a helmet on that pony in case he has a repeat performance of Drop it like its Hot. Wait and see.

            Fortunately, Sunny just did his head-pressing and circling the room routine without further excitement. He broke his third water bucket off the wall (he did not believe in detours from his circle), gave himself another bloody nose, but survived the night.

Sunny, Day 3

            I began to feel a crushing sense of déjà vu when I found Sunny eating straw the following morning. The sight failed to inspire any confidence. Especially when one of the nurses discovered pus running out of his front left fetlock.

As it turned out, in his enthusiasm for breaking buckets, Sunny had managed get a puncture wound. How the nurse had been able to spot the lesion amongst his crusty feathering, I’ll never know, because I made it a rule to not evaluate neurologic horse feet at risk of finding myself crushed beneath said neurologic horse.   

The discussion amongst the clinicians was grim. A septic joint seemed like the final strike for poor Sunny. He was too neurologic to get to the standing stocks. Anesthesia didn’t want to touch him.

But then, in what I still consider to be the ballsiest move that I’ve seen in an academic institution, one of the clinicians decided that she could flush the joint. With the magic of propofol, limited regard for personal safety, and a fast acting team of students in way over their heads, she dropped that pony, clipped and scrubbed, and flushed the bejesus out of the joint. He was down and up within fifteen minutes.

That quick and dirty approach was deemed the best that we could do for a neurologic pasture pony, and now we were back on the “wait and see” train.

And by some miracle, Sunny began to improve. He continued to have weird cyclic relapses in the evening, but each night they became less and less severe. In the following weeks they stopped altogether.

We never did discover the etiology of the outbreak. The rancid hay was discarded by the owner but never sent out for analysis. Necropsies were refused for the first ponies that fell victim to the neuropathy, and a CSF tap was never performed on Sunny in the end.

That was probably the most frustrating aspect of the case; to have such a bizarre presentation and to never learn the cause felt like an episode of House, M.D. that got interrupted. After all of that work that went into solving the mystery, it felt unfair to not get the answer at the end.

So that was the first lesson that Sunny taught me: medicine isn’t always fair. You won’t always get the answer, especially in veterinary medicine when owners don’t have the financial means to pursue that answer. You have to be satisfied with sending your patient home at the end of the day, hoping that your best guess was right.

The second lesson that Sunny taught me was a lesson that I didn’t anticipate: the value of giving an animal time to fight through something. My early years of exposure to vet medicine were in wildlife and conservative practices, where if an animal was statistically unlikely to recover, euthanasia was pursued earlier rather than later. This was always the humane option in my mind, so I struggled a great deal watching Sunny having his episodes when his prognosis seemed so grim. It seemed so obvious to me that he needed to be put out of his misery. That was a horse that I was certain needed to be euthanized. What were the clinicians thinking? And now thanks to that chance, Sunny has many years ahead of him. So while I don’t believe that I’ll be bold enough to see a horse like Frosty in the future and say, “we should definitely just wait and see,” I won’t be so quick to disregard the possibility. I’m happy to be proven wrong.  

* For those of you who haven’t learned about botulism yet, or for those of you (like myself) who need a brief refresher on why ataxia doesn’t fit with the disease process, allow me to enlighten you. The botulinum toxin acts at the level of the neuromuscular junction, which gives clinical signs such as profound muscle weakness. The ataxia that we saw looked like spinal proprioceptive deficits, which means that the neurologic abnormality could be localized to his spinal cord or his brain. Considering his profound mental dullness and inappropriate mentation, we felt confident that the pathology could be localized to the brain.