How'd I Do?

 The horse gut is an amazing and complex thing. They have a single stomach like us, although it's only partially glandular like ours. The real magic happens in their cecum and very long colons. They have a right ventral colon, a left dorsal colon, and a right dorsal colon, plus a regular colon called the descending colon. Their cecum is an enormous blind sac located between the small intestines and all of these colons. 

Depending on the particular pathologies involved, it can be kind of difficult to identify the various parts of the horse's gut during a necropsy. The best way is to remove the entire digestive tract from stomach down, cut all of the ligaments (thin sheets of tissue that hold it in a particular shape), and stretch it out. 

Yesterday I had a foal who died from not one but two intestinal ruptures. For accuracy in my report, I wanted to figure out exactly what parts were affected. Because everything in the foal's abdomen had been marinating in intestinal contents and bacteria for a couple of days, there was a lot of autolysis (post-mortem changes). And there was necrosis of various parts of his gut associated with ulcers and hemorrhage that preceded the two ruptures. Tissues were delicate and friable. Everything was coated in bits of partially digested feed and greenish, bloody fluid. 

We of course took pictures but those can be hard to interpret, and sometimes the techs don't get those loaded onto the server for a couple of days. After I had extricated his gut and stretched it out, I made a quick sketch, labeled some key bits, and marked the areas of the ruptures. Here's the result:

 

"Colon" is the descending colon, RDC is the right dorsal colon, PF is the pelvic flexure (a distinctive anatomical feature of the horse gut), "base cecum" is where the cecum opens into the right ventral colon, J is jejunum, D is duodenum, and "stom" is the stomach. That bit sticking off the stomach would be the esophagus. The heavy black bars are the two rupture sites.

Compare this to a diagram from one of my vet school textbooks:

 

I think I produced a real masterpiece!

Notice how I positioned the stomach to the right, descending colon to the left, the same way as in the picture. That's because we necropsy ruminants and horses from a left lateral position, meaning their left sides are down on the table. This creates the same right lateral view of the intestines as shown in the picture. I'm pretty sure I would struggle to identify things if I had to look at them from the left aspect. 

Consistency is important when doing necropsies. If we examine tissues in the same order every time, we are much less likely to miss problems.

Fun With Fungi

Rain. So much rain. Fungi with amazing colors and textures are popping up all over my property. Here's a sampling. 

Each One A Puzzle

Every necropsy case is a puzzle. To find the solutions, my colleague and I have considerable agency to select the tests that we want to apply. At one end of the spectrum is the shotgun approach: collect every type of sample (tissues, swabs, fluids) and run every test available. But where's the fun in that? Not only does this approach lack elegance and waste resources, it isn't intellectually pleasing. It's lazy diagnostics. It's more challenging by far to build a list of differentials based on signalment and history, modify that list based on gross findings from the necropsy, then thoughtfully select specific tests that will rule in or rule out your top differentials for the cause of death. 

Sometimes the necropsy itself is the only test we need. That is informally referred to as "grossing out" a case, meaning we are able to determine a definitive cause of death of an animal during the gross examination conducted during the necropsy, and the case is closed out with no further testing. Necropsies are meticulous and require a lot of careful examination, and the word "gross" in this context means we aren't using any special diagnostic tools beyond our eyes and fingers. For example, when we find heartworms in a dog who died suddenly or who had clinical signs like fainting, low energy, or coughing, and there are no other major findings such as pneumonia or masses in other organs, we gross that case out. 

While it can be satisfying to close a case based only on the necropsy, it is even more satisfying to identify a pathology during necropsy and verify it with just a handful of carefully chosen tests. Those cases give us a lot of validation. We've had several cases like this recently.

A beef cow-calf operator brought in a yearling cow. The cow was petite, quite pretty. She'd been sick for a couple of days and had not responded to his treatments. He'd lost several from his herd in the past few days, all with similar clinical signs. All of the sick or dead cows were yearlings or older--he hadn't lost any nursing calves. That was interesting. Based on my initial conversation with him, it sounded like a toxicity event and not infectious disease that was killing his cows, and he agreed. We went through the list of the usual suspects--paint cans, old batteries, sheds with old bags of fertilizer, rusting 50-gallon drums containing mystery liquids--cows are both curious and relatively indiscriminate eaters. Nothing really fit though. So into necropsy I went. 

Even if you think you know the answer, which I did not in this case, you still approach every necropsy systematically to make sure that you don't miss anything important. Heart, lungs, and spleen looked good. But the liver was moderately autolyzed. Autolysis refers to post-mortem changes that occur in tissues due to cell death and bacterial activity. The state of the liver didn't match the other tissues. I couldn't find anything wrong with the liver that would explain this, such as liver flukes or evidence of a bacterial infection in the liver. This was a symptom of something else, not the primary problem.

Next, I examined her gastrointestinal system. The rumen was filled with 20-30 L of a thin liquid slurry of finely shopped feed. Her abomasum, her glandular stomach, was red-black inside and contained a couple of liters of cloudy red-brown liquid. The rest of her intestinal tract was empty. All three of these observations were a surprise. Her rumen should have contained layers of material--a mat of feed at the bottom, a slurry on top, and a gas cap on top of that. Sure, this stratification gets a bit mixed up when animals are moved and transported after death, but the basic components can be identified at necropsy. I only saw slurry, and far too much of it. Her abomasum should have normally contained feed. It shouldn't be bloody. And she should have had digesta scattered all along her gut and feces in her colon. All of this added up to an animal that had stopped eating and had developed ileus, or a cessation of the normal peristalsis of her gut. She had continued to drink water, thus the rumen was distended with liquid. Cows can develop ileus as a result of torsion or displacement of the abomasum, heavy parasite load, blockage of the rumen by a foreign object (baling twine and plastic bags in cow rumens are common incidental findings, but they can sometimes cause problems), chronic diarrheal disease, or something called vagal indigestion related to dysfunction of the vagal nerve and rumen function. There was no evidence of any of this, so the ileus was a symptom, not the primary problem.

Next, I examined her kidneys. Kidneys are often the first tissues in a cow to autolyze, which refers to the post-mortem changes in tissues due to bacterial activity and cell death. This cow was very fresh so I didn't expect to see autolyzed kidneys. Normal cow kidneys are not quite as dark as our own but they fall well into the range of what we might call "kidney colored." Her kidneys were golden brown and covered with bloody pinpoints. The same pinpoints were visible inside in the renal cortices. These distinctive lesions are textbook examples of oak toxicity. Leptospirosis, an infection caused by bacterial spirochetes, was definitely a differential. But my other observations fit oak toxicity better. Oak toxicity is caused by tannins in leaves and acorns. It can cause hemorrhage in the glandular stomach, which was likely the precipitating cause of the ileus (the cow didn't feel good so she stopped eating), and liver necrosis, which set the liver up to autolyze faster than surrounding tissues. And it causes pinpoint hemorrhages in the kidneys.

I called the owner back and surprised him by asking about oak trees that might be in or around the pasture. Turns out that during stormy weather a couple of weeks prior, wind had knocked down several branches from an oak tree in the middle of the field. The producer had observed several of his cows eating leaves from the fallen branches. He didn't think much of it because he thought oak toxicity was only caused by buds or acorns, and we are past the time for the first and not yet into the season for the second. He gave them new forage and cleaned up the branches. I told him that young leaves and their stems are toxic too, and that unfortunately the damage had already been done. Nursing calves didn't eat any leaves so they weren't affected. And the leaf-eating had occurred long enough ago that no leaf remnants were in the rumen of this cow. I told him to expect more mortalities in the handful of cows that were still sick.

There is no bench test for oak toxicity. Diagnosis is made by gross findings and distinctive microscopic changes to the kidneys. I had to wait a couple of days for the tissues to fix in formalin, another day for trimming, and another day to cut and stain the slides. But eventually, I had the slides in my hand. Textbook case. 

My colleague recently had a similar puzzle that he quickly solved. A breeder had submitted two French bulldog puppies, only 7 days old. She had already lost most of the litter. When this kind of thing happens in pure-bred dogs or cats, breed-specific genetic or congenital abnormalities top the differential list. That list is of course rather long for French Bulldogs and other brachycephalic breeds, especially since breeders are selecting for ever more extreme deformation of the faces of these dogs. I recently did a necropsy of an adult female Bulldog whose nasal openings were positioned so far back on her head that they were over her molars, not in front of her incisors. Selecting for extreme body deformities often comes with unanticipated deformities in critical things like hearts, skeleton, and brains. Oops.

But back to the puppies. For high litter mortality, you also have to consider canine parvovirus, which can be transmitted through the placenta. Ideally, the dam should have been vaccinated for parvovirus and she would have passed antibodies to her puppies when they nursed the first time or two, but the number of people who refuse to give vaccines to their dogs is growing. She could have been infected during pregnancy, and infected her puppies in utero. Canine herpesvirus is a bit more insidious. There is no vaccine. It can also be passed to the puppies in utero and often results in abortion in those cases, but the more common route is post-natal infection. It can result in high mortality in young puppies. Dogs older than about 8-12 weeks usually only get mild disease from herpesvirus, but they shed virus in all of their body secretions. Keeping it out of a kennel is a matter of biosecurity--wash hands and shoes, quarantine new additions, segregate animals of different ages, clean surfaces. 

My colleague approached the necropsy with his usual care. Nothing significant turned up until he looked at the kidneys. The kidneys of both puppies had many small hemorrhages inside and out. Textbook example of canine herpesvirus infection. He was so excited by this finding that he called me down to necropsy to take a look. Definitive diagnosis of canine herpesvirus is available with a PCR test. It of course came back positive, and he closed the case with no further testing. We made slides of the kidneys for our own learning because they were such good examples of this disease. You could see inclusions comprised of many viral particles (far too small to see individually) in the nuclei of the cells lining the renal tubules.

Two interesting puzzles: cases of multifocal renal hemorrhage and nephritis identified at necropsy of two different species. When we combined our gross observations with signalment and history, we were able to land on diagnoses quickly. Two puzzles that we got a lot of satisfaction from solving!

Small Acts of Kindness

I got these flowers today at the lab. They were sent by a veterinarian out in the wilds of southwestern Arkansas whom I've never even met. She called the lab yesterday, almost in tears, worried that she had screwed up a case, second-guessing all of her decisions, and needing to talk to someone about necropsies. Receiving sent her to me.

I spent over 30 minutes on the phone with her. The clients were being difficult, accusing her of killing their dog. She did an in-clinic necropsy and found many dozens of heartworms in its heart and vessels of its lungs. She was worried that she did something wrong. I assured her that she did everything right. I told her that the outcome would have been the same if she had sent the dog to the lab for necropsy. I thanked her for trying to find the best answers for her patient and the owners. 

Today she sent me flowers and a short note.

It is these small acts of kindness that we give each other that get us through.

We Are All Partners In This

Despite being barely two years out of vet school, I apparently project an air of confidence and competence to my veterinary peers. I've been thinking about this ever since my conversation with Dr. M that I mentioned in my last post. It's absolutely true that I don't know everything about vet med. I've got a lot to learn. But I bring so much more to the table--years of experience with scientific writing, public speaking, and critical thinking. And my own personality contributes a lot as well--I have always had a habit of calling things like I see them.  

On Tuesday, one of the regional USDA-APHIS vets emailed me to see if I could help them out. They felt like they were not fully prepared to conduct poultry necropsies if there was an FAD event in Arkansas. 

FAD means Foreign Animal Disease. There is a very long list of FADs that are of concern to the USDA, but in the poultry world, we are mainly talking about HPAI (highly pathogenic avian influenza) and vNDV (virulent Newcastle Disease Virus). If either of those were to appear in Arkansas, it would be devastating to the poultry industry here. Containment and sampling are critical. It is far beyond the scope of my blog to talk about the training that USDA-APHIS and USDA-accredited veterinarians receive (I have Category II accreditation), but if there was a disease outbreak, USDA and other federal agencies would run the show. Their people would go into the poultry houses and conduct necropsies and collect samples which would then be sent off to the various national labs. 

So back to my vet colleagues, who reached out to me for help. The vet that emailed me asked if I could run a workshop for them, a wet lab with hands-on instruction in poultry necropsies. Sure, I said, that sounds like fun. I mean, what else would I say? I love teaching. I love working with poultry. I put in a lot of effort during vet school to gain knowledge and experience in poultry vet med. Only 2 or 3 vet schools teach about poultry, so most vets never even touch a chicken during school or during practice. 

The only problem was that I can't predict when poultry cases come into the lab. We needed birds for this workshop. Then I had an idea. We do a lot of serology testing for the big poultry companies in Arkansas. Most of them regularly send us necropsy cases too. But one of the bigger companies hasn't used us much for necropsies in the past. However, since I joined the lab, their regional rep has been sending me tough cases that really allow me to stretch my diagnostic skills. He never fills out the history on the submission form, instead preferring to call me up and chat for half an hour about what is going on at that particular farm. 

My idea? I emailed him, told him that USDA wanted a workshop, that I was happy to run it at the lab, and would he be willing to donate birds? He didn't hesitate. He immediately grasped the larger picture--if USDA vets are better prepared for a FAD event, his company would directly benefit. We are all partners in this. 

A flurry of emails ensued, and the workshop was arranged for Friday. I downloaded the training manuals that the USDA vets use so that I could see what they were being instructed to do, and I wrote a brief outline for the workshop to ensure that they would learn how to collect the samples they needed to collect.

I told them, if there is a FAD event, you will be working in some seriously adverse conditions--taped into PPE head to toe, kneeling in hot, dusty poultry houses surrounded by dead and dying birds. I told them I was going to show them tricks and efficiencies to quickly collect the samples they needed, and to make sure they were diagnostic. And then I proceeded to do just that. 

 

Me on the left. These are broiler breeder hens. They lay eggs that are hatched to become broilers, which become chicken nuggets.

It was a great workshop. I can assure you those vets know a hell of a lot more about poultry anatomy now than they did when they woke up on Friday morning. They know how to hold and use scalpel blades without cutting themselves. They know how to get blood samples my way (my way is heresy, to be sure, but it works, it's amazingly fast, and the samples are just as diagnostic as those obtained the traditional way). They know how to perform tracheal swabs on live and dead birds. All of this delivered in less than 3 hours. It was so successful that I will run another one in May for the four vets that couldn't make this one.

To be sure, this was quite a professional accomplishment for me. My USDA colleagues valued my expertise enough to ask me to share it with them. I am empowered in my own job such that I can use state resources for this kind of activity without seeking permission (although I let the upper levels know what I was up to). I really value my personal relationships with lab stakeholders, and the effort I put into them paid off nicely.

We are indeed all partners in this.

Absurdly Alice

Here are some (slightly edited) conversations I've had at work in the past few days.

Backstory: One of my favorite vets called me up to get my opinion on a recent case he submitted last week. He knows now that our reports are strictly factual--we observed this, we measured that. But on the phone or in person, he is also aware that I will share any and all theories that my colleagues and I might have about the cause of death of the animals in his cases. That's what he called me to get--the crazy theories and speculations. 

Many of his clients are cow-calf operators in the southwest part of the state. It's a long haul for those producers to bring a cow or calf into the lab so he often does field necropsies and sends us what we call "a box of parts." After a fair bit of coaching from me, he sets the bar pretty high with his submissions, generally collecting diagnostic samples for most of his cases. He sends fresh tissues and feces and rumen contents knotted up in disposable obstetric sleeves, and cuts off pieces of affected tissues and drops them into a container of formalin. Pretty much every time he sends us a BOP, the container he uses is a large bottle that used to contain 500 tablets of cephalexin, an antibiotic that can be used in food animals. Since he submits cases almost weekly, well, that's a lot of cephalexin. 

Me: So, another fabulous field submission from Dr. M. I have to know, what's up with the cephalexin bottles? 

Dr. M: Well, it's a big bottle.

Me: I know, but why do you have so many empty ones? What do you do, give them out like M&Ms?

Dr. M: Yes, exactly, everyone that comes into the clinic gets some!

Me: Like Oprah! Cephalexin for you! And cephalexin for you too! Cephalexin for everybody!

This same vet submitted the headless, legless torso that I mentioned in my previous post. That came up in today's phone call too.

Me: Um, so why did you cut the head off? Why?

Dr. M: The calf wouldn't fit in the container and...

Me (interrupting): ...hahaha!

Dr. M: ...it wouldn't fit and the courier was getting upset, needed to leave...

Me: ...so you cut off the head but you so thoughtfully left the tail! You left us a handle!

(Me and Dr. M cackling like chickens)

Backstory: I'm on a committee at the lab that handles quality management issues. We are only a committee of three. We had an event that needed to be assigned to one of us. 

Committee leader: Which one of you will take this?

MBF and I look at each other. 

Me: Rock paper scissors?

MBF: Sure. But I'm terrible at this. My wife always wins.

Me: I'm glad to hear you and your wife have a healthy process for conflict resolution.

MBF: So, on 1-2-3-go?

Me: Yes.

MBF: 1-2-3...

And on "go", I throw out paper. 

MBF: No! After I say go!

Me: Oh. Okay.

MBF: 1-2-3-go...

And I throw rock as he throws scissors.

Me: I win!

Always setting a high bar for professionalism! 

Backstory: I was approached by our local colleagues in USDA APHIS about leading a wet lab for them in poultry necropsy and diagnostics. They wanted to be better prepared in case of a disease outbreak. Sure, I said, I can do that. But we need some birds, and waiting for a regular submission is not really a workable solution. I have developed a good relationship with a high level guy in one of the broiler breeder companies in Arkansas. He submits crazy cases that keep me on my toes. I decided to ask him to donate birds for the wet lab, either spent hens scheduled for slaughter or birds from a problem farm. He'd get a full report and diagnostics at no cost.

Me: I have an unusual request. blah blah wet lab blah blah USDA blah blah warm fuzzies all around. I only need about 10 live birds.

SL: Sure! But how will we get them to the lab? 

Me: I'll bet we can get one of those USDA folks to pick them up from your folks. And I almost forgot, they wanted some deceased birds too. Can we get a few of those? 

SL: How many dead ones do you want?

Me, reading the email asking me how many dead ones I wanted: This is a strange email conversation. I want five dead ones.

SL: It's always a strange email conversation in this business. Done!

My job challenges me in many ways. I would never have expected days that leave me feeling like Alice in Wonderland.

Surprise!

I've discussed before about how we approach each necropsy case with a list of differentials for the cause of death. Before you even see the animal's remains, you can posit a decent list just on signalment (age, sex, breed) and clinical history, if one is provided. The time of year and the weather can suggest a few differentials too. And I'd say that, for most cases, our differential lists don't change much, other than to usually get a lot shorter. 

Then there are the surprises. 

Oh, a calf was sent in for necropsy? It's wrapped up and packed in a styrofoam box, and Receiving won't open it up, of course. They leave that for us in Necropsy. The box seems small but maybe it was a neonate? Surprise! We opened the box to find a single, long-ago melted ice pack and a trash bag. Inside the trash bag was a torso. A calf torso, minus the head and four legs, removed to reduce weight and thus reduce the shipping cost. They thoughtfully left the tail, however. But because the torso was shipped without enough ice, and because they had removed the head and didn't take quite enough care when removing the legs, fluids produced by rotting tissues had mixed during shipping with the diarrhea that had oozed out of the anus and blood that seeped from everywhere else to create a foul ichor, a marinade that penetrated all crevices of the torso. Except for a PCR test for mycoplasma pneumonia, the tissues were not usable for anything else. 

We see many dogs who died from heartworm infections. These cases make me angry because it was a completely preventable death. And we can often predict which cases these will be: owner-submitted, large breed, intact male dogs are vastly over-represented. Even if you are expecting to find heartworms in the heart, there are always the surprises, in which you find literally hundreds of worms packed into the heart, worms in the pulmonary arteries and even in the smaller vessels deep in the lungs. By far the worst are the dogs who died of caval syndrome in which the worms migrated upstream, back out of the heart into the caudal vena cava. Surprise! It's a plug of worms thicker than a broom handle blocking the largest vein in the dog's body. 

We handle about a dozen legal cases per year. They are always difficult since most involve animal abuse of one form or another. But we have a process that we follow, and focusing on the process helps us get through them. But there are the cases that take unexpected turns and become legal cases based on our findings at necropsy. Last year, I had a medium sized, mixed breed dog submitted for necropsy. I started by conducting a thorough physical examination. Surprise! That looks like a projectile entry wound! I ripped off my gloves and called the vet listed on the submission form and asked her, why didn't you mention that the dog had been shot? Turns out she never even saw the dog, just directed the owners to take it to the lab when it died suddenly. I took the dog over to the Crime Lab for radiographs, identified the location of the projectile, and retrieved it later during necropsy--a 9 mm slug.

And of course there are always rare congenital anomaly cases that you really just can't predict at all. The animals may have died as fetuses, or lived for a few days or even years. But they did die eventually and ended up on our necropsy table. Surprise! This Hereford calf fetus is missing most of its brain. Skull is normal, brain, not so much. Surprise! This 10-day old Angus calf doesn't have a rectum or anus! Its colon ended about 6 cm too early. Surprise! This obese 6 year old cat that died after a vet visit had two tracheas! Two tracheas all the way down, one going to the left lung lobes and the other to the right lung lobes. It also had feline cardiomyopathy, which was not a surprise. Surprise! This pure bred cat that has been genetically selected to have defects in how it makes collagen so that it will have folded back ears has malformed collagen everywhere else too, including the heart, blood vessels, skin, liver, kidneys, ligaments holding vessels in place. Nothing was normal in that cat. It was like working with a Picasso vision of a cat necropsy. A 10 month old German Shepherd pup, purchased at great expense by a breeder hoping to use him for stud work, was a "poor doer" from the start with vomiting, diarrhea, and poor growth. Surprise! The poor pup had two kidneys but they were very small. Under the microscope we could see that the usual renal structures had not formed, and the kidneys were mostly not functional. He had full thickness, bleeding ulcers in his stomach from the uremia, because the non-functional kidneys were unable to remove urea from his blood.

We approach every necropsy case with a plan, a list of differentials and tests we might want to run. We also need the flexibility and knowledge to modify that plan on the fly based on what we find, whether we expect it or not.