While I don't regularly have to work after-hours or nights or weekends, there are exceptions. On Christmas Eve, I did a necropsy on a police K9. On MLK Day, my colleague and I did a necropsy on a racehorse that collapsed on the track that morning. These are high-profile cases that require us to provide a fairly immediate response. All after-hours cases come in via a dedicated phone that my colleague and I swap between us every few weeks. Right now, I have that phone. Last night, it rang at 2:17am.
I was asleep but jerked awake right away. I fumbled around a bit, and managed to answer the phone in time. It was a guy who told me that his dog had just died. He wanted us to do a necropsy so he could find out what happened.
I always try to manage expectations for these companion animal owners, because necropsies are not magic. Our track record is very good, but we don't always find a cause of death in every case. And for this kind of case, we wouldn't be doing the necropsy until Monday. We briefly talked about a few logistics (we have a dock cooler where companion animals can be dropped off after-hours).
But it turned out that what this guy really wanted was to talk to somebody about his dog. I was that somebody.
So I took a deep breath, sat up and rearranged my pillow and blankets. I spent about 20 minutes on the phone with this guy, talking about sharing our lives with dogs. Talking about seeing our dogs get old. Talking about grief. My eyes kept drifting across my pack--Archie curled up under the covers at my feet, Azza under her own blanket at the other end of the bed, Mimi tucked up next to me, belly in the air, and the cat curled up next to her. I kept this guy on the phone to make sure he heard the words he needed to hear.
Don't misread this. This story isn't about me. It's about being a caring human being. Life lessons.
Saturday, January 25, 2020
Sunday, January 19, 2020
A Love Letter To My Colleague
I've had a couple of long posts simmering in my brain for quite some time, and I thought I'd give one of them an airing. This post is about my colleague, JX. And no, I'm not really in love with him, but this is definitely a love letter.
JX and his wife, both Han Chinese from Xinjiang (that fact alone prompted me to write more than 1000 words on the current political situation in Xinjiang, which I subsequently deleted, as it's not the point of this post), have been in the US for close to 10+ years. He's got a good applied veterinary job with the state, she's got a good research job with the enormous medical research university here. Between them, they hold many degrees and accreditations.
Now I've got to loop in some old hair-raising tales from our lab. For years, the board-certified veterinary pathologists were stabbing each other in the back. They would sit on cases like they personally owned all data and test results. They would claw and scratch anyone who even dared to ask about the status of a case. They would literally close their office doors and refuse to communicate with lab techs, submitting veterinarians, farm managers, and especially co-workers. Cases would drag on for months.
My colleague JX was hired into this quagmire with the expectation that he would handle all veterinarian-submitted cases that didn't involve tissue or a body. And that's what he did for several years, until that toxic workplace imploded on itself.
I was told by the current lab director that the first time my colleague JX went onto the necropsy floor, the board-certified pathologists wasted no time showing up in the director's office to complain about the "contamination."
And here we are, at the heart of this post. Racism, egotism, white privilege. It all makes me sick to my stomach.
When the implosion occurred, and the racist, egoistic, privileged pathologists quit en masse, my colleague JX was left to hold down the fort in necropsy for months until I showed up in July of last year. Talk about trial by fire. He was certainly qualified but had limited necropsy experience to that point. JX was thrown into the deep end of the pool...and he excelled. He rose to the occasion, and he learned what he needed to learn despite the lack of supervision, guidance, and mentorship.
When I arrived, I met a seasoned gross pathologist, a solid veterinary diagnostician. He freely and generously offered his opinion...but only when asked. He acknowledged that our lab section was in desperate need of supervision...but he didn't want to be the person in charge. When I was made supervisor of our section, he told me, "I have your back. I will support all decisions that you make." How awesome is that? Any supervisor ever would be over the moon to hear that from a high-level report.
And here's the thing. JX might not be in charge, but I don't make very many decisions without consulting with him first. He and I talk about our active cases every day--we discuss what our differentials are, what ancillary tests we might want to run, what results have come in and how they are to be interpreted, and what is important and what is just of "academic" interest. Our discussion are loud, lively, and often involve citing references to each other. Our lab director told me privately that he often has no idea what we are arguing about most of the time, but that he loves overhearing us. In fact, JX and I work so closely that we do necropsies together, and even trade cases between ourselves. This drives Receiving crazy as they want to know "who has this case" but I tell them, JX and I will sort that out later.
JX took in a racehorse today. He texted me to let me know. I replied, "When do you want to do the necropsy?"--it's his case, after all. It's a holiday on Monday and the lab is officially closed and our techs are not available. He said, "Your thinking?" and I replied, "Insured. We shouldn't wait. Tomorrow morning?". He replied, "9am". Perfect. He's in charge, I will be his tech, and it will be a fantastic morning in necropsy with my colleague.
I've had plenty of colleagues and mentors in my checkered career(s). But JX stands out. Professional. No drama. Amazing powers of observation (he found a PDA in a calf, super rare). Thorough but level-headed, so he isn't obsessive. He is kind. He is perfectly happy to indulge in black humor. He thinks outside of the box. He is willing to take risks. But he does not want to be in charge. And here I am, bossy-pants, ready to tell everyone what to do. Match made in heaven.
This is a love letter to my colleague. JX, because of you, I am a better veterinarian, a better gross pathologist, and a better manager.
JX and his wife, both Han Chinese from Xinjiang (that fact alone prompted me to write more than 1000 words on the current political situation in Xinjiang, which I subsequently deleted, as it's not the point of this post), have been in the US for close to 10+ years. He's got a good applied veterinary job with the state, she's got a good research job with the enormous medical research university here. Between them, they hold many degrees and accreditations.
Now I've got to loop in some old hair-raising tales from our lab. For years, the board-certified veterinary pathologists were stabbing each other in the back. They would sit on cases like they personally owned all data and test results. They would claw and scratch anyone who even dared to ask about the status of a case. They would literally close their office doors and refuse to communicate with lab techs, submitting veterinarians, farm managers, and especially co-workers. Cases would drag on for months.
My colleague JX was hired into this quagmire with the expectation that he would handle all veterinarian-submitted cases that didn't involve tissue or a body. And that's what he did for several years, until that toxic workplace imploded on itself.
I was told by the current lab director that the first time my colleague JX went onto the necropsy floor, the board-certified pathologists wasted no time showing up in the director's office to complain about the "contamination."
And here we are, at the heart of this post. Racism, egotism, white privilege. It all makes me sick to my stomach.
When the implosion occurred, and the racist, egoistic, privileged pathologists quit en masse, my colleague JX was left to hold down the fort in necropsy for months until I showed up in July of last year. Talk about trial by fire. He was certainly qualified but had limited necropsy experience to that point. JX was thrown into the deep end of the pool...and he excelled. He rose to the occasion, and he learned what he needed to learn despite the lack of supervision, guidance, and mentorship.
When I arrived, I met a seasoned gross pathologist, a solid veterinary diagnostician. He freely and generously offered his opinion...but only when asked. He acknowledged that our lab section was in desperate need of supervision...but he didn't want to be the person in charge. When I was made supervisor of our section, he told me, "I have your back. I will support all decisions that you make." How awesome is that? Any supervisor ever would be over the moon to hear that from a high-level report.
And here's the thing. JX might not be in charge, but I don't make very many decisions without consulting with him first. He and I talk about our active cases every day--we discuss what our differentials are, what ancillary tests we might want to run, what results have come in and how they are to be interpreted, and what is important and what is just of "academic" interest. Our discussion are loud, lively, and often involve citing references to each other. Our lab director told me privately that he often has no idea what we are arguing about most of the time, but that he loves overhearing us. In fact, JX and I work so closely that we do necropsies together, and even trade cases between ourselves. This drives Receiving crazy as they want to know "who has this case" but I tell them, JX and I will sort that out later.
JX took in a racehorse today. He texted me to let me know. I replied, "When do you want to do the necropsy?"--it's his case, after all. It's a holiday on Monday and the lab is officially closed and our techs are not available. He said, "Your thinking?" and I replied, "Insured. We shouldn't wait. Tomorrow morning?". He replied, "9am". Perfect. He's in charge, I will be his tech, and it will be a fantastic morning in necropsy with my colleague.
I've had plenty of colleagues and mentors in my checkered career(s). But JX stands out. Professional. No drama. Amazing powers of observation (he found a PDA in a calf, super rare). Thorough but level-headed, so he isn't obsessive. He is kind. He is perfectly happy to indulge in black humor. He thinks outside of the box. He is willing to take risks. But he does not want to be in charge. And here I am, bossy-pants, ready to tell everyone what to do. Match made in heaven.
This is a love letter to my colleague. JX, because of you, I am a better veterinarian, a better gross pathologist, and a better manager.
Saturday, January 04, 2020
Some Unusual Production Animal Necropsy Cases
This is the season for beef cows to be calving and sheeps to be lambing, so we are seeing a spike in those animals coming into the lab for necropsy. As a result, I've had four very interesting cases in the past couple of weeks. It's a good thing my professional interests in reproductive pathologies has expanded to include neonatal pathologies!
In case 1, a four-day old beef calf was brought in. Like nearly all of these cases, it was "fine the night before, dead the next morning." The calf had compelling evidence of infection with the bacterium Clostridium. Clostridium species are anaerobic, and live in the soil, so they are everywhere. You already know about two common Clostridium species because they cause botulism and tetanus, diseases that affect both humans and animals. In cattle, other species cause necrosis of skeletal muscle tissue, with a preference for muscle around the thigh and hip joint so the disease is referred to as "black leg." The bacteria also have a preference for heart muscle. In addition to making black patches in muscle, these bacteria produce gas that makes tissues "bubbly" (emphysematous is the doctor word), and they cause gelatinization of fat. Clostridium infections also have a very distinctive "sewer" smell that is usually strong enough to defeat face masks. A lot of the other clinical signs of Clostridial disease are caused by circulation of endotoxins that the bacteria secrete.
So this calf was infected with Clostridium but it wasn't clear at first why. Yes, it died from the clostridial infection and the endotoxemia, but there had to be some precipitating event. Neonatal calves don't have a fully functional rumen yet, and when they nurse, milk bypasses the rumen and goes straight into the abomasum, the glandular chamber of ruminant forestomachs. This calf had huge, greasy, white chunks filling its abomasum, which was itself larger than it should have been. Abomasal bloat has been linked to overgrowth of ... yes, Clostridium bacteria. And Clostridium bacteria have yet another special talent--they cause agglutination of milk proteins. We cultured the same species of Clostridium from the abomasal fluid, from affected skeletal muscle, and from heart muscle. Even though the dam had been vaccinated for Clostridium, a sequence of unfortunate events cascaded through this calf to cause its death.
In case 2, another 2 to 3 day old beef calf was brought in (actually, on the same day as the calf in case 1). This calf had nearly identical clostridial lesions in skeletal muscle and its heart. However, there was no evidence that this calf had ever nursed. The diagnosis in this case was something called failure of passive transfer. When neonatal mammals don't get colostrum from their dams, they become susceptible to many viral and bacterial diseases. This calf never got any antibodies from its dam. Although the first case makes it clear that colostrum is not the only factor for survival (necessary but not sufficient), a complete lack of it is nearly always fatal for these neonates. If it hadn't been Clostridium, it would have been some other virus or bacteria that would have killed this calf.
In case 3, a 10 day old beef calf was brought in. Good necropsy technique means you conduct it in a systematic manner, and try to do it the same way every time, no matter what species you are working on. The actual order of things can vary somewhat, but most pathologists lay the animal on its side, open the abdomen, remove one half of the rib cage, then fully examine all thoracic structures (more or less the lungs, heart, esophagus, trachea, larynx, oral cavity). When we opened the abdomen, it was obvious that the problem was somewhere in there, but I stuck to the program and examined the thorax first. No lesions at all. Everything looked fine.
When you work on the abdomen, you often remove the liver and spleen and kidneys on their own, then examine the intestinal tract from one end to the other. In this calf, the forestomachs looked okay but the small intestines were necrotic and bloody. I was gently tugging on the entire intestinal tract to pull it out to examine it in more detail when suddenly the colon just popped out. I stood there holding a blind sac in my hand for several seconds before it registered what I was seeing. Normally, the colon attaches to the rectum, and normally, you shouldn't be able to "pull out" the colon. This colon did not connect to anything. Normal colons are fairly muscular organs, but this one was distended and flabby. Then I noticed that the muscles lining the pelvic inlet were green and covered with shaggy bits of fibrin. And then I noticed that the two sets of anal sphincter muscles (one is skeletal muscle, the other is smooth muscle) were completely missing. There was no anus or rectum in this animal. There was a hole in the skin below the tail, so on my initial physical exam it looked normal from the outside.
This was an extremely rare and severe case of the congenital abnormality called atresia ani. This abnormality can vary from mild forms in which the anal opening is absent but all of the other organs are present (this can be corrected surgically if it is identified early) to cases like this one in which the colon doesn't reach all the way to the rectum/anus. This case was even more severe because of the additional absence of anal sphincter muscles.
Because the animal couldn't defecate, the intestines became necrotic. Bacteria and dead cell contents leaked out (there may also have been a small rupture, hard to tell when the tissues are so altered), causing septic peritonitis. Circulation of dead cell contents caused septicemia and shock and death. I shared details of this case with a few colleagues and was told that I may never see this rare abnormality in my career again.
The fourth case was a pregnant ewe. Like the calves, she was "fine the day before, dead this morning." I spoke to the owner when he dropped her off, and I learned that she was late term and that he didn't have very good management practices. Sheep and goats that aren't dewormed regularly get a nasty abomasal worm called Haemonchus that makes them anemic and can kill both young and adult animals if not treated. Haemonchus was high on my differential list--present until proven otherwise. But sheep and goats are also quite susceptible to something called pregnancy toxemia, especially if they have multiple fetuses.
This ewe was small, 120 pounds, and extremely overconditioned (fat). A quick physical exam eliminated anemia even before we opened her up. Now Haemonchus was off the list (and in fact, we found no parasites in her intestinal tract). She had three nearly full-term fetuses, all about the same size and without gross defects or evidence of early death. No evidence of viral or bacterial placental infections. Her uterus was enormous, and had squashed her rumen up next to her spine and forward towards her lungs. The papillae that line her rumen were hard and shrunken. Her liver was huge and yellow. All of this, sadly, pointed to pregnancy toxemia.
It affects ewes who are either super skinny or super fat when they are in late gestation, and who have multiple fetuses. The energy demands of those fetuses cause the ewe to first use up her liver glycogen stores, then to begin to use her body fat stores to keep the fetuses alive. In the case of the skinny ewe, there is no body fat and she dies. In the case of the fat ewe, the amount of fat sent to the liver overwhelms it completely, and she begins to pump out ketone bodies and develops rumen acidosis. The papillae respond to the rumen acidosis by becoming keratinized. The liver cells become stuffed with fat and stop working. And she dies.
Pregnancy toxemia is preventable but it requires fairly close monitoring of the ewes before and during pregnancy, and adjustment of their diet to keep them in good condition before they become pregnant. It's also important to identify ewes who have multiple fetuses, usually via ultrasound, so they can be separated and fed separately.
These were not my only cases in the past two weeks (the intake of dog and cat cases is fairly regular), but I thought it was cool that all four of these production animal cases came in so close together. I also appreciated these cases because they really stretched my diagnostic skills.
In case 1, a four-day old beef calf was brought in. Like nearly all of these cases, it was "fine the night before, dead the next morning." The calf had compelling evidence of infection with the bacterium Clostridium. Clostridium species are anaerobic, and live in the soil, so they are everywhere. You already know about two common Clostridium species because they cause botulism and tetanus, diseases that affect both humans and animals. In cattle, other species cause necrosis of skeletal muscle tissue, with a preference for muscle around the thigh and hip joint so the disease is referred to as "black leg." The bacteria also have a preference for heart muscle. In addition to making black patches in muscle, these bacteria produce gas that makes tissues "bubbly" (emphysematous is the doctor word), and they cause gelatinization of fat. Clostridium infections also have a very distinctive "sewer" smell that is usually strong enough to defeat face masks. A lot of the other clinical signs of Clostridial disease are caused by circulation of endotoxins that the bacteria secrete.
So this calf was infected with Clostridium but it wasn't clear at first why. Yes, it died from the clostridial infection and the endotoxemia, but there had to be some precipitating event. Neonatal calves don't have a fully functional rumen yet, and when they nurse, milk bypasses the rumen and goes straight into the abomasum, the glandular chamber of ruminant forestomachs. This calf had huge, greasy, white chunks filling its abomasum, which was itself larger than it should have been. Abomasal bloat has been linked to overgrowth of ... yes, Clostridium bacteria. And Clostridium bacteria have yet another special talent--they cause agglutination of milk proteins. We cultured the same species of Clostridium from the abomasal fluid, from affected skeletal muscle, and from heart muscle. Even though the dam had been vaccinated for Clostridium, a sequence of unfortunate events cascaded through this calf to cause its death.
In case 2, another 2 to 3 day old beef calf was brought in (actually, on the same day as the calf in case 1). This calf had nearly identical clostridial lesions in skeletal muscle and its heart. However, there was no evidence that this calf had ever nursed. The diagnosis in this case was something called failure of passive transfer. When neonatal mammals don't get colostrum from their dams, they become susceptible to many viral and bacterial diseases. This calf never got any antibodies from its dam. Although the first case makes it clear that colostrum is not the only factor for survival (necessary but not sufficient), a complete lack of it is nearly always fatal for these neonates. If it hadn't been Clostridium, it would have been some other virus or bacteria that would have killed this calf.
In case 3, a 10 day old beef calf was brought in. Good necropsy technique means you conduct it in a systematic manner, and try to do it the same way every time, no matter what species you are working on. The actual order of things can vary somewhat, but most pathologists lay the animal on its side, open the abdomen, remove one half of the rib cage, then fully examine all thoracic structures (more or less the lungs, heart, esophagus, trachea, larynx, oral cavity). When we opened the abdomen, it was obvious that the problem was somewhere in there, but I stuck to the program and examined the thorax first. No lesions at all. Everything looked fine.
When you work on the abdomen, you often remove the liver and spleen and kidneys on their own, then examine the intestinal tract from one end to the other. In this calf, the forestomachs looked okay but the small intestines were necrotic and bloody. I was gently tugging on the entire intestinal tract to pull it out to examine it in more detail when suddenly the colon just popped out. I stood there holding a blind sac in my hand for several seconds before it registered what I was seeing. Normally, the colon attaches to the rectum, and normally, you shouldn't be able to "pull out" the colon. This colon did not connect to anything. Normal colons are fairly muscular organs, but this one was distended and flabby. Then I noticed that the muscles lining the pelvic inlet were green and covered with shaggy bits of fibrin. And then I noticed that the two sets of anal sphincter muscles (one is skeletal muscle, the other is smooth muscle) were completely missing. There was no anus or rectum in this animal. There was a hole in the skin below the tail, so on my initial physical exam it looked normal from the outside.
This was an extremely rare and severe case of the congenital abnormality called atresia ani. This abnormality can vary from mild forms in which the anal opening is absent but all of the other organs are present (this can be corrected surgically if it is identified early) to cases like this one in which the colon doesn't reach all the way to the rectum/anus. This case was even more severe because of the additional absence of anal sphincter muscles.
Because the animal couldn't defecate, the intestines became necrotic. Bacteria and dead cell contents leaked out (there may also have been a small rupture, hard to tell when the tissues are so altered), causing septic peritonitis. Circulation of dead cell contents caused septicemia and shock and death. I shared details of this case with a few colleagues and was told that I may never see this rare abnormality in my career again.
The fourth case was a pregnant ewe. Like the calves, she was "fine the day before, dead this morning." I spoke to the owner when he dropped her off, and I learned that she was late term and that he didn't have very good management practices. Sheep and goats that aren't dewormed regularly get a nasty abomasal worm called Haemonchus that makes them anemic and can kill both young and adult animals if not treated. Haemonchus was high on my differential list--present until proven otherwise. But sheep and goats are also quite susceptible to something called pregnancy toxemia, especially if they have multiple fetuses.
This ewe was small, 120 pounds, and extremely overconditioned (fat). A quick physical exam eliminated anemia even before we opened her up. Now Haemonchus was off the list (and in fact, we found no parasites in her intestinal tract). She had three nearly full-term fetuses, all about the same size and without gross defects or evidence of early death. No evidence of viral or bacterial placental infections. Her uterus was enormous, and had squashed her rumen up next to her spine and forward towards her lungs. The papillae that line her rumen were hard and shrunken. Her liver was huge and yellow. All of this, sadly, pointed to pregnancy toxemia.
It affects ewes who are either super skinny or super fat when they are in late gestation, and who have multiple fetuses. The energy demands of those fetuses cause the ewe to first use up her liver glycogen stores, then to begin to use her body fat stores to keep the fetuses alive. In the case of the skinny ewe, there is no body fat and she dies. In the case of the fat ewe, the amount of fat sent to the liver overwhelms it completely, and she begins to pump out ketone bodies and develops rumen acidosis. The papillae respond to the rumen acidosis by becoming keratinized. The liver cells become stuffed with fat and stop working. And she dies.
Pregnancy toxemia is preventable but it requires fairly close monitoring of the ewes before and during pregnancy, and adjustment of their diet to keep them in good condition before they become pregnant. It's also important to identify ewes who have multiple fetuses, usually via ultrasound, so they can be separated and fed separately.
These were not my only cases in the past two weeks (the intake of dog and cat cases is fairly regular), but I thought it was cool that all four of these production animal cases came in so close together. I also appreciated these cases because they really stretched my diagnostic skills.
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