All right, everybody, tonight is session five of the Zuku's NAVLE® Prep Accelerator Hoot Camp. Tonight we're covering a small animal topic, something absolutely classic and something you certainly are going to see in practice, whether you're a general practitioner or a specialist. My name is Dr. Steve McLaughlin. I'll be talking about study strategy. And as you can see there, we have the one and only Dr. Jen Mahon with us to talk about our canine topic tonight. 

Our structure is the same as each session. We'll have the weekly warm-up where we review the topic from the previous session. We'll do a clinical talk. Tonight it's about a canine classic case with some Q&A. If you have questions, put them in the Q& A box for Dr. Mahon to answer. I'll be speaking tonight about make it stick. How do you do independent study outside of practice testing in ways that helps information stick in your head and in ways and hope you approach those cases from a new direction than testing. Finally, as always, we'll end up class with a reinforcement low-stakes quiz on the topic of the night, and then we'll move on to a very, very short assignment, poultry for Sunday. Don't panic. 

All right, it's our weekly warmup, everybody. As you know, we're going to start with four or five questions that are based on stuff we've seen in previous sessions. What we're trying to do is get you to actively pull answers out of recent memory. This is the foundation of learning. And studies, peer-reviewed research studies, of how people learn, they call this retrieval practice. Retrieval practice, pulling information out of your head reinforces the knowledge you've been working on, and you're literally opening the doors between the information in your head and your fingertips. Okay, so without further ado, here we go. 

Remember we talked last Sunday about horses. A 12-year-old Morgan mare presents in the spring in Pennsylvania with a short strided gait, reluctance to turn, and increased digital pulses in the forelimbs. She alternates lifting her feet, but is not lame at the walk. Horse testers elicit pain at the toe, which diagnostic is the most appropriate to localize the lameness. Palmar Digital Nerve Block? Abaxial Nerve Block? Low four-point nerve block? Distal limb radiographs? Endocrine testing? So I'll let you sit with that for a moment. Remember our topic from Sunday. You're not likely to get a ton of lameness questions on the NAVLE®, but you're probably going to get couple. And so, you know, if you have a rough, rough idea of what nerve blocks you might want for the biggest of the biggest lamenesses, that will probably serve you pretty well. Chat room is lighting up. Okay, we've got, all right, excellent. Can you guys see my screen? I just got a message that people can't see my screen and it sounds like people can see it. Okay, they can see. I was panicking. Well, it may not matter what comes to you, Jen, because I'm going to hand off hosthood to you. All right, guys, you ready? I see a couple of different choices. Most people in chat are choosing A or B. I love that I see that. It means some people are probably right. Some people are not right. If you don't get it right, remember, mistakes are your best friend. You'll not forget it next time. So here comes our answer. I think I have to click something. There we go. So, the diagnostic most appropriate to localize the lameness we're worried about is the abaxial nerve block. Anybody there in chat want to tell me what they're worried about? What lameness condition are we thinking of here? Way down in the hoof. Yeah, there it is. Dr. Smith. Dr. Ernesto, yeah, Dr. Havel, very good. Dr. Strain, 100 percent. You guys are, everybody's getting it. Well done. Very well done. 

Okay, question number two. A six-year-old obese indoor neutered male cat presents with lethargy, vomiting, and a history of straining to urinate. You suspect urethral obstruction. You attempt catheterization. But the urethra remains obstructed after sedation. What is the most appropriate next step? Administer NSAIDs and attempt catheterization again? Immediate surgery to create a perineal urethrostomy? Recommend euthanasia due to poor prognosis? Administer furosemide and reattempt catheterization? Perform decompressive cystocentesis under sedation? So we're reaching back here to a week ago when we covered session, let's see, three, I believe it was. Very good. Irvin, Dr. Irvin, well done. I see Dr. Ramirez, what I like, what I see here. I'm the only person who can see everybody in chat, guys, so the reason we don't make it so you can see everyone is because it gets a little distracting. Let's see. I see somebody said A or E, which I love that. It means you narrowed it down to two and you're taking a guess. That means you've got one of the most fundamental, useful study habits in your head. If you don't know, narrow it down to two and then take a guess. All right. Here we go. If you have a question, send it to me in the Q&A, I'll be happy to have a look. Here's our answer. Perform decompressive cystocentesis under sedation. So these guys, you can rupture a bladder if you're blocked for too long and if you can decompress the bladder with cystocentesis you give yourself some time and you give the cat some time. 

Which choice is the most common cause of laminitis in adult horses? Sepsis secondary to retained placenta, colitis, and etc? Contralateral limb overload from a unilateral severe lameness on the other side? Black walnut bedding or ingestion? Endocrinopathic or insulin dysregulation? Repetitive trauma on hard ground? So what we're looking for is the most common cause of laminitis. It's possible that some of these choices, maybe even all of these choice, could predispose a horse to laminitis. We want to know what's the most common cause. All right, we're gonna check into the chat room here. I love it. So I see a few people going, I think it could be this or that. That's good, it means you're trying to guess, you're try to narrow it down, and that's good. Dr. Ernesto, right on it once again. Good job, everybody. Okay, here comes our answer. So in this case, the correct answer is D, endocrinopathic or insulin dysregulation, basically an endocrine problem. Now, if you missed it, remember, once you miss, you're going to get it right the next time you see it. It's a, mistakes sting a little bit and we remember them, okay? And in this, case I'm not an expert on horses, let alone lameness, but even I know like black walnut can be associated with laminitis. Trauma can be a problem. Sepsis secondary to other problems can, can contribute to it. And if you have one leg on one side, that's really in trouble, and so they're putting all the weight on the contralateral leg, boom you've got laminitis. Okay. It's just that endocrine is the big answer. 

Okay, there's many treatment options for laminitis, but what are the mainstays? What are the top, top things we think about when we're trying to address laminitis in a horse? Because remember, you don't always know the underlying etiology, you just know the horse has laminitis. Antibiotics, a heart bar shoe, and limit exercise? Corticosteroids, cryotherapy, deep digital flexor tenotomy? NSAIDs, hoof support, treatment of the underlying cause? Opioids, regional limb perfusions, and a hoof wall resection? Abaxial nerve block, frequent trimming, increased turnout time? So what I'm looking for are the mainstays, the foundations of basic treatment for basic laminitis. Okay chat room. Okay people are homing in on this one pretty well. I see basically people seem to be choosing C or E. So I loved I love that I see people narrowing it down and I love that I see people committing because that's good. You're making the decision as best you can with what you know in your head. Remember this is low stakes. Nothing is riding on this. We're using this as a learning exercise. Practice testing is a great way to learn. Here's your answer. The foundations of treatment for laminitis, no matter what the cause would be, NSAIDs, to decrease, address inflammation and pain, hoof support, and trying to treat the underlying cause, whatever that might be. 

[00:10:55] Okay, question number five. We're back to kitty cats. You are attempting to stabilize a hypothermic and bradycardic cat with urinary obstruction and you've started IV fluids and analgesia. Blood work confirms hyperkalemia. Which treatment is best to protect the myocardium? Remember that we know that hyperkalemia is bad, okay? Are we going to give a hypertonic saline bolus IV? Fentanyl, CRI? Dexmedetomidine, IM? Calcium gluconate IV? Albuterol nebulized? So we've got a cat who's in trouble, and we need to address the hyperkalemia. Okay, people seem to be homing in unanimously on one choice here. Let's see how people do. The answer is calcium gluconate IV. Remember, too much potassium causes fatal arrhythmias and that's why we wanna get that hyperkalemia addressed right away. Too little potassium, hypokalemia, can give you a cervical ventroflexion and that its own kind of problem. You see that maybe with chronic renal kitties. 

Okay, I think this is our final question for tonight unless I threw something strange in there. Question six. A 14-year-old pony with equine metabolic syndrome presents with a short stilted gait and a reluctance to turn. She has Obel grade two lameness with increased digital pulses and positive hoof tester response over the toe. You recommend immediate hoof support using padded boots and a soft frog insert. What is the primary goal of providing hoof support in this patient? So here are our answer options. To reduce the mechanical stress on the lamina and redistribute the weight? To stimulate the coronary band to promote new hoof wall growth? Offload the deep digital flexor tendon to reduce tension on the navicular bone? Improve blood flow, and protect sole from abscess causing bacteria? Correct medial lateral imbalance of the hoof capsule? All right, let's see how we do. All right, I'm seeing some A's, I am seeing some C's here, very good, very good. So some people, people are choosing different things, that's great. Remember, you can miss a question, it's not the end of the world. You don't need a hundred on this test. In this case, the correct answer is to A, reduce mechanical stress on the lamina and redistribute the weight in the hoof. Okay, you're trying to take the off that lamina inside the hoof and support that a bit. Okay? Great job everybody. Well done. 

Oh, look at that, I threw one more in. Remember we talked a little bit about reptiles last time, so I just threw this in for practice. We have a three-year-old female aquatic red-eared slider turtle. Presents with a one to two month, so chronic, history of poor appetite and sluggishness. The enclosure includes a water pool and sunning rocks, and it's cleaned at least once a month as needed. That's a red flag that it's probably a clean environment. The diet is primarily cooked chicken and lean beef. Two juvenile slider turtles of about four months of age in the same tank are reportedly normal. On physical exam, the turtle appears subdued with swelling OS. OS means the left eye. So what's your best course of action? This is a classic example of a what's-your-next-step format question in NAVLE®. It's a very common kind of question you can expect in NAVLE® and you'll definitely get these in Zuku. So let's just, before we dive into the answer options, let's look at that picture up close because in Zuku, if you click on the image you can make it big. So we're looking at this guy and sure enough the left eye definitely does seem swollen. So something's not right here. A swollen eye or bilateral swollen eyes, particularly in an aquatic reptile, but even some of the other ones, that's kind of a big red flag for a particular problem. So our question is, what's our best course of action, not what's our diagnosis. If you happen to have a diagnosis in your head, tell me in chat, because this is one of the biggies, okay? Here's your choices of action you can choose from. Are we going to change the diet to dark leafy greens and aquatic plants with some live prey? Are we gonna start a course of amikacin and ceftazidine and separate it from the other turtles? Are we gonna go with topical ophthalmic steroid OU and then test the younger sliders for salmonellosis? Are we are going to increase UVB exposure and ensure that the humidity is between 30 and 45 percent? Or are we going to go with dietary vitamin D supplementation? So I see the answers are piling up fast on this one. Right on. Excellent. Okay, so we've got got a mix of responses here and that's I love to see that. There will be some reptile questions on your NAVLE®, not very many. Maybe three or four that count at the very most. Probably three that count. That said this is one of the big conditions in reptiles we're looking here at vitamin A deficiency and so typically with these guys you're thinking about a dietary change, okay? So what's going on here is adult turtles, aquatic turtles like this, are usually not completely carnivorous, they need some leafy greens to supplement the vitamin A. So a big swollen eye is a big classic sign. They can get pneumonia, and so one of their lungs consolidates, and then they float at an angle in the water. Where if you look at a radiograph, you'll see like this big density where the lungs ought to be. So this is an example of an explanation in Zuku, but basically we're looking at a classic case of vitamin A deficiency, so you want to change the diet. Thinking about the environment and the diet in some of these exotic animals is often a good thing to have in the back of your mind. It's classic that it shows up as ocular swelling. You can see squamous metaplasia of the tongue. Sometimes it can't really eat. Don't forget about things like pneumonia. In a water turtle, the other thing you might see is foam coming out of their nose, which means they've probably got pneumonia, okay? And what's going on is the vitamin A is needed to keep your mucous membranes healthy, including all the ones where you breathe through. The reason that the young turtles didn't get this problem, they tend to be, they need more protein. Just like a puppy or a kitten, tends to eat a higher protein diet as they grow in their fast phase of growth. Same thing with turtles. 

So today we're going to talk about a very common canine condition. This is our patient. He is a four year old male castrated Irish setter. He comes in for retching and progressive abdominal distension, kind of a nervous dog in general. 

His physical exam, he's got a wicked tachycardia. So his heart rate's about 180. He's got pulse deficits. He's gotta distended tympanic abdomen, kind of groans when you press on it. And because of his tachycardia, you're a smart doc and you put him on an ECG. He very kindly shows you his ventricular tachycardia. So remember that ventricular tachycardia involves a widening and inversion of the QRS complex. And the QRS complex often kind of stomps on and obliterates the P wave. So what is your top differential diagnosis gonna be? 

It's gonna be GDV, right? The other rule out that you might have is gastric dilatation without volvulus, and you will see these cases in practice as well. And I'll be honest with you folks, they are just not quite as sick as your average GDV patients. GDV is common. It is a condition whereby gastric enlargement occurs and then there's 180 degree, sometimes 360, but 180 is way more common, 180 degree rotation on the mesenteric axis. And this is life-threatening. It leads to shock. And the true etiology is unknown, though lots and lots of risk factors have been described. Probably the money shot kind of risk factors that y'all need to know of for boards and in clinics are dogs with a deep narrow chest and large and giant breeds. So dogs like we have on the right, Shepherds, Labradors, Cane Corso's, Dog de Bordeaux, Huskies. I have seen GDV in a Dachshund once in 20, more than 20 years and it's been reported in guinea pigs but really it's a big dog disease by and large. So again think about what are the things that happen commonly? Common things happen commonly. 

The pathophysiology is that gas and fluid accumulates and this causes the stomach to swell and dilate and then the volvulus, that twist, prevents the release of gastric contents. So this is why these dogs are retching and they can't bring anything up. The caudal vena cava gets compressed and this is going to limit preload. And if you think back to your cardiovascular physiology without preload going into that right atrium, right ventricle, it's not going to get around to the left atrium left ventricle and that's going to cause hypotension. Meanwhile, blood is getting sequestered in the splanchnic and renal vascular beds. And these patients end up with ischemia and reperfusion injury. And sometimes this can get so bad that the stomach will actually necrose and burst and spill gastric contents into the abdominal cavity. That's what happened with the great dane that you all see on the right side of your screen. And she was treated as an open abdomen because there was kibble floating around in her belly. And no matter how hard we tried, we couldn't flush it all out. That dog actually lived despite a really, really terrible consequence of GDV. That rupture sort of situation, also pretty uncommon. So most dogs with GDV do not come in with ruptured stomachs. Those are uncommon presentations. 

So the thing about these is that these are gonna be dogs that have an acute history of retching on the order of hours. This is not gonna be a dog that's intermittently retching for days and days on end. They'll have gastric distension with tympani. So their stomach is gonna feel hard and taut like a drum. And you can even ballott the stomach sort of like you would with a cow. So making those kinds of associations across species can be helpful sometimes too. And that tympanic sound is gonna help you distinguish it from ascites and a fluid wave. These patients are gonna be shocky. They're all gonna have some degree of shock. That shock might be occult if it's super early, but these patients will be developing shock or in shock when you see them. So hallmarked by tachycardia and hypotension. Ventricular arrhythmias are super common because the myocardium gets robbed of perfusion. Pain is really common as well. 

So as you're stabilizing these dogs, you're gonna put two short, large bore IV catheters in the cephalic veins. You don't wanna use the saphenous veins because remember, the stomach is distended and compressing that cava, so any fluids that you put in a caudal limb isn't really gonna get where you need it to go, which is to the heart to help replenish that preload and improve that perfusion. You're gonna start with a half-shock dose of crystalloids and you're gonna give it fast. This is the patient that you're going to put those fluids on a slam bag, a compression bag. You're going get these patients their fluids fast. Put that ECG on, treat those ventricular arrhythmias with lidocaine. Lidocaine has actually been shown to have other benefits in these cases as well. Shortens hospitalization, reduces arrhythmias, treats any AKI, acute kidney injury that these patients can develop, and it's analgesic as well. Even though they're not actually vomiting, these patients do experience a fair bit of nausea. So treat them with an anti-emetic as well, usually Meropitent or Ondansetron, and give analgesics, and I like to reach for pure mu opioid in these cases, mainly because if I have to reverse it because the patient acutely decompensates, then I have that option and that opportunity. 

Radiographs, you're gonna start with a right-sided lateral abdominal view. You might take some dorsal ventral views if you have to. That can be helpful for diagnosing those rare, rare 360 degree torsions. But by and large, personally in practice, this is one of those cases where I'm not taking three view rads necessarily. I'm just gonna take that rad that's gonna get me the diagnostic that I need. And don't put these guys on their back because the aspiration risk is high. The thing that your rads are going to show you is severe gastric distension with the pylorus dorsal and cranial to the fundus. And people call this the reverse C shape, the double bubble, the boxing glove, Popeye's fist. Lots and lots of colloquialisms will help you remember what this looks like, but anatomically, that pyloris is going to be dorsal and cranial to the fundus. Splenic enlargement and malposition is common. And if the stomach wall has started to necrose, you might actually see some gas bubbles within the gastric wall as well. That's not common again, but it is something to look for.

Blood work, you're gonna reach for PCV total solids. These are usually like kind of normal, but sometimes when the stomach twists, you actually end up with tearing of the short gastric vessels, so they might have a small volume hemoperitoneum. Lactate is commonly elevated. And if it is, but the patient doesn't look quite as shocky as you would think, that helps you understand that there is some degree of occult shock. Remember that lactate is telling you that microvascular perfusion is compromised. Lactate helps you track the success of your resuscitation. And there's some degree of correlation with gastric necrosis and outcome as well. And I say some because there's been a lot of studies done on this, and sometimes they're a little bit mixed results, but if you were sitting there taking the NAVLE® and it said what biochemical parameter is most closely correlated with gastric necrosis in GDV, the answer is lactate. It's not glucose, it's not ALT, it's not anything else, it is lactate. CBC is usually gonna be normal. Your chemistry, you might see a little pre-renal azotemia. ALT and AST can be elevated due to hepatic hypoxia. Remember, compression of that caudal cava and pooling in the splenic and renal vascular beds will cause the liver to end up with some degree of hypoperfusion and hypoxic. And these patients will be hypoglycemic if they're septic as well.

The way you treat them, trocharize them. So find the most tympanic region on the right abdominal wall. You clip and aseptically prepare the site and you put your large gauge needle or your catheter through the skin into the stomach to relieve the air. So you should hear kind of a whooshing sound when that happens and often someone will say, oh gosh, it stinks in here. So that means that you've done it right. The complications of trocharization is that that needle going in could lacerate the spleen. If you put the needle into the stomach and the stomach is really on the edge of starting to necrosis, you could end up with some gastric perforation and then gastric contents could also spill into the abdominal cavity and that could lead to septic peritonitis. The thing is, is that you're going to get these patients in the operating room and you can rectify all of that in the operating room. But what you can't rectify easily is if they die before you get them into the OR. So step up with your trocharization and do it pretty quickly and aggressively. These patients do not need to be sedated for trocharization. The technique is simple and easy and in my mind every GDV out there should be getting trocharized. It's going to help improve that preload because you're going to be pulling some pressure off that caudal cava too. And these are the types of catheters that you might want to reach for. These are pretty darn long, but honestly, a long 18 gage catheter will also get you where you need to go with these cases. 

Another option as stabilization preoperatively is you could pass an orogastric tube and lavage. You have to put these patients under general anesthesia unless they're moribund because you have to intubate them and protect that airway. You will probably go on YouTube or see pictures of people holding a dog and putting something in their mouth that's like round and hollow and then like taping the muzzle shut and then shoving a tube down there. Y'all, please don't do this, please. Because honestly, if somebody was doing that to you in a human ER and not explaining what was being done, you're gonna fight as well. And it's just not humane. The technique for doing this is well described in the literature, I'm not gonna get into that here. Just know that the risks are that you could perforate the esophagus. That being said, is if a soft tube is gonna perforate the esopagus, then honestly the tissue is pretty darn compromised anyway. The esophagus and really the stomach at that juncture is kind of a tough bit of tissue. You can have anesthesia associated risks. And the biggest problem I see is that this delays the operation. So if you've got a surgeon that's scrubbed and ready to roll, but you're not going to pet down and pass in an orogastric tube, don't do that. Just get them all the way to the OR. Pass the orogastro tube once the patient's situated on the operating room table. 

The surgery is an emergency, bar none. This is not a patient that you wanna sit on and wait in the middle of the night. The duration of clinical signs is really strongly correlated with death. Once you get in there, you reposition the stomach, you flip it back where it's supposed to be, and you pexy it, which is a surgical technique, to affix the stomach to the right body wall. You don't wanna do a left gastropexy, you wanna do right one. A variety of techniques have been described. The incisional gastropexy has the least number of complications, but there's a lot of other options out there. If the stomach is necrosed, you're gonna do a gastrectomy. And remember that when you're looking at the stomach and the intestine and trying to figure out, all right, is it dead or alive? Is it dead, or alive? You wanna think about your P's. Is it pink? Are there pulses? Is there perfusion? Is their peristalsis? And when you palpate the tissue, does it all kind of hold together? Or does it feel squishy and slimy and like it's coming apart within the lumen of the gastrointestinal tract? So remember your five P's when you're in the operating room. You definitely wanna lavage the abdominal cavity and suction. If you don't lavage and suction, you could be leaving some bacteria behind from your trocharization, and it doesn't take many bacteria to set up sepsis later down the line. 

Post-operative care, these patients are gonna get fluids, analgesics, antiemetics, ECG monitoring and arrhythmia management. Sometimes even if they don't have arrhythmias in the pre or intraoperative period, they will have arrhythmias in the post-operative period. So put these guys on a monitor, blood pressure monitor and nutritional support. Whenever you're going in and doing a GI surgery, you have to think about early nutrition for these patients. 

Our patient here, the four-year-old Irish setter that we started with, got trocharized preoperatively. He got an exploratory laparotomy. Stomach was repositioned and he got an incisional gastropexy. No splenectomy was needed. Some patients do need a splenectomy because the spleen gets all twisted up and hypoperfused as well, but he was lucky he got to keep his spleen. Interop, his ventricular tachycardia worsened. He got a lidocaine bolus and his CRI was increased. He had a positive response to that. And postoperatively, he got fluids, fentanyl and antiemetics, and he did quite well and went home. So how well do these dogs do? Is the surgery worth it? Like, should we go ahead and cut these patients? 

The answer is, in my mind, yeah. The prognosis is generally really good. Only about like 10 to 33%, again, it depends on what paper you read, only about 10 to 33% of these dogs will die. The things that are gonna increase the risk of death are greater than six hours duration of clinical signs. I doubt that the NAVLE® would ask you about that six hour number, but just know that the longer that stomach is twisted, the worse the prognosis will be. Needing a splenectomy or partial gastrectomy simply because those patients have usually been twisted for longer are in worst shock. Again, hyperlactatemia correlates with gastric necrosis by and large. Hypotension is a negative prognostic indicator. Peritonitis or sepsis, always a negative prognostic indicator with almost every disease out there, and developing disseminated intravascular coagulation is a terrible prognostic indicator. To be perfectly fair, I haven't seen a heck of a lot of GDVs develop DIC, Disseminated Intravascular Coagulation. I've seen a lot other diseases cause it though. So if your GDV patient does develop DIC, they're in a world of hurt, they're in a lot of trouble. Their prognosis is poor. I think that it's fair to discuss prophylactic gastropexy with at-risk breeds. So animals that are in that category of large or giant, have that deep, narrow chest tend to be a little bit more stressy and you can look up the other risk factors and make advisements when you're on the clinic floor. But also military working dogs and other service type animals, because if a dog out in the field when they're supposed to be helping fight a war or take down a criminal or something like that develops a GDV, that patient's gonna be out of work for a much longer period of time than the time that it takes for them to recover from a prophylactic gastropexy. 

Some things to keep in mind when you're thinking about this disease and the NAVLE®. So GDV is a surgical emergency. Medical treatment alone is ineffective. You cannot just pass a stomach tube, wake the dog up and send it on its way. That stomach will retwist in a matter of hours or days. You have to start treatment before you start diagnostics in these patients because you have to start addressing shock and hypotension. So this is not a patient that it rolls in the door and you immediately bring them into the radiology suite. This is a patient that rolls in the door, you use your clinical judgment, your best assessment possible, your hands, eyes, ears to diagnose presumptively and start treatment based on that and then start rolling with your diagnostics once treatment has been instituted. Gastric necrosis worsens your prognosis and hyperlactatemia correlates with outcome. Owner education is important and a prophylactic gastropexy should be considered in certain situations. And this is just a visual for, this is a nice, healthy stomach. It's pink, there's well-perfused blood vessels here, and this is an example of a completely necrosed unsalvageable stomach. Now be mindful, when you get in the OR, sometimes it looks like this, you de-rotate and it still looks like this necrosed, unsalvable stomach. That's okay. Give the stomach a minute, let that reperfusion come online, do the rest of your abdominal explore, take a good look around, make sure that the spleen is okay. If there's a small volume hemoperitoneum, you're probably going to suction some blood out. So give the stomach a min or six to kind of get its act together. And by and large, most of them are going to start looking more on the order of this. 

I'm happy to take any questions, but this is also a picture of what a stapler directed partial gastrectomy could look like. So this is a fancy, cool stapler device, um, will speed your operation up tremendously, but you don't need this in order to do a partial gastrectomy. You certainly don't this in your suite of, of tools in order do these surgeries. It's a pretty simple surgery and a pretty good outcome. Wow! That was a tour de force. Well done. Very impressive. Thank you. 

Well, hi everybody. This is Dr. Steve and I'm back to talk to you tonight about making it stick. A simple study habit that works. We talked a lot in a previous session about using strategic guessing as a way to get better at answering questions and also to learn from your mistakes. Tonight, we're going to talk about the other half of your study, which is independent study. How do you hit the books? How do study notes or make notes in ways that gets the information to stick and gives you an avenue, gives you a way into the information, which is different than multiple choice questions, because you need both. You need practice testing and you need independent study, so let's talk about making it stick when you hit the books. 

We saw this slide on the very first talk of the Hoot Camp sessions. The three most effective parts of any study plan are these three. Number one, spend about two thirds of your time in any given week doing practice questions, whether it's the practice questions with no clock ticking or the timed tests at the end. Either way, in any give week, give about two-thirds of your study time you've got available to testing. But give one-third to independent study. That means reviewing books on key diseases, reviewing your notes, writing notes, and quizzing yourself on those notes. That's our topic for today. Then don't forget the third foundation of a good study plan, and that is in the final seven or eight weeks, don't forgot to redo 100 percent of your tests in timed test mode. You'd be amazed how many people we've consulted with in the last 18, 19 years. They didn't do the last step, and that's important too. But tonight, we're here to talk about the middle one, independent study. 

The second biggest mistake we see people make, the first one was they don't leave enough time to complete the timed tests at the very end. But the second biggest mistakes we've seen people make over the years is they just don't do any independent study. They might memorize a whole bunch of questions, whether it's in Zuku or in the other service, but they never actually do anything else. And then they sort of cannot handle it when they are faced with the real NAVLE® and they're asked to do some clinical thinking. And clinical thinking needs to be a little more flexible than just, oh, I memorized a bunch of answers, okay? So we're gonna talk about how to do that. So sometimes we see people, they just don't do any independent study. They never open a book, they never review notes, so they never write anything down. Another thing we'll see they do is they read notes or they read a book but they're just passive. They just look at the page and go, oh yeah, I know that. They never actually quiz themselves. That's a problem. Quizzing yourself about something you just read is one of the most effective things you can do and one of your best habits to help make stuff stick. So I wanna encourage you, whatever you're thinking about in your study plan, whether it's today or this week or this month, try to prioritize a balance where there's about two thirds of your time practice testing and about one third independent study. 

Why do we not want to just casually read some notes and think we know what's going on? Well, the reason we don't want to do that is because of a condition called overconfidence bias. And this is how to do notes wrong. And this is just this very simple concept that we read something and we think we know it. We think we've got it in our heads, but we never actually use that information. We don't actually know it, so we think that we're a lion and we're little bitty kitty cat. 

Overconfidence and bias in notes. This is called, when they study this in adult learning studies, they call this the Dunning-Kruger effect. This is a cognitive bias where people with limited competence overestimate their knowledge or abilities. And so I have to have a cartoon in here because I like cartoons. This guy's sitting up on top of a file cabinet, he says, my IQ is higher than yours. And the lady is saying, just get down, Justin. Okay, so this idea that you think you know more than you do just because you read something and you don't know it yet because you haven't handled it. You haven't made it yours. You haven't t quizzed yourself and done some retrieval practice. So I'm gonna try to convince you that the single best habit you can use for independent study is to do the same thing we do with practice testing, retrieval practice. Um, it turns out that this bias is apparently more based on ignorance. It's not arrogance. And so the best solution is just accurate feedback. You hand the notes to a friend and then have them ask you questions where you walk around the room and you can't see the notes and you quiz yourself. Or maybe you make some flashcards on it, something like that, but quizzing yourself routinely. Stimulates that whole retrieval process. And that's how we get information to stick. 

So why do we do it? Because number one, if all you do is memorize questions, literally this is a metaphor, but it's like your mind is as stiff as a calf with tetanus. You might have memorized a bunch of answers on some questions you saw, but you're going to be in trouble when you get asked questions about things you haven't seen, or you get ask about a disease where you're not so sure, or you get asked about a diseases where they don't ask you what's the diagnosis, they ask you what tests you do, how you're going to treat it, what do you tell the owner. So what we want to encourage you to do is to train your mind the same way a person trains to train for a marathon, to train, for a race, or to get ready and go to yoga. We want you to limber up your mind, okay? Clinical thinking is flexible thinking. Clinical thinking is what we do in real life with real animals and clinical thinking is what works on the NAVLE®, okay? You will not know everything on the day you sit down to take your test, but if you can walk in with a pretty good foundation of all the stuff you've studied and a flexible mind to cope with the questions where you're not sure of the answer, but you can guess strategically, you're gonna do great. So coming at information from a different direction than just doing testing is going to help build your mental resilience, and it's going to stimulate some creativity, OK? You want a certain, there's a saying for people that ride horses, keep a loose hand. What is it? Keep a firm hand on a loose rein, OK. So you're holding the reins of the horse that are going to the bit in his mouth, and you're not yanking on the reins. So the reins are loose but your grip is firm. You want to go in with a reasonably firm grip on the information you do know, but you want to be a little loose, okay? You don't need to know everything to pass this test, you absolutely don't, but, you do need to be able to try to be better at thinking clinically, okay? We adapt to what's put in front of us. Whether you're a kitty that needs a cone or a dog that's had a intravenous disk disease problem. 

Alright, so fine. Steve, how do I start this? If you don't have notes, I would encourage you, at least maybe for the big four species, go to the trouble of writing down some half-page notes of your own, just for the physical practice of putting it on paper, okay? And in your own mind, homing in on what the main things are that you want to know. If you've heard me speak, you know it's always the same three things we want for any case. I want at least one good image. I'd like to be able to recognize what a classic case looks like and describe it. How do I test for it? How do i treat it? You could put a little more in there if you want, but this is not about too much detail, it's about enough detail, okay? And then what you do with those notes is you review by quizzing yourself. You can do it with notes that we've made in Zuku, and you can do with your own notes, okay. The ones you write yourself are the best, but it does take time to write notes, so it's a balance, okay, but if you pick 10 of the biggest diseases for dogs, cats, horses, and cows, and wrote your own notes, and you're really knew to those diseases, not bad. You want to be getting some extra credit, give me the same thing for five pig diseases and four chicken diseases, and five or six small ruminants. Now you're smoking. Now you're really doing well. 

All right, so let's try some questions and some notes. We have an adult dairy cow off feed, decreased milk production, no fever, swollen lymph nodes, somewhere, okay? So here we see a cow with a swollen pre-femoral lymph node, really big, no fever, off feed, no milk. Here we see a cow, with a big subbandibular lymph node. Here, we see a cow ,with a super mammary lymph node astoundingly big. Here we see it cow that looks like it's got a retrobulbar lymph node swelling. And here we see a cow with what looks like a parotid, parotid lymph nodes swelling. What are we thinking about? What what one big disease are you thinking about in an adult dairy cow with a big old lymph node somewhere, could be anywhere, and no fever? All right chat room, tell me what you got. Oh yeah, 100%. Very good. Very good, everybody. Yeah, everybody's saying it. Bovine BLV, bovine leukosis, lymphosarcoma, same thing. Yeah. Well done. You really are only going to see this in the adult animals, okay? So the disease that tops your differential list, bovine leukosis, lymphosocoma, okay. So that's great. That's what a quiz could look like. You can make a flashcard with this, right, and that's a great way to quiz yourself.

What do the notes look like? This is what notes could look like. They don't have to be long, a half page, OK? The exercise of you choosing what you thought are the 10 big diseases and you writing down, what's a classic case look like, how do I test for it, how do treat, that exercise is one of the things that helps engrave it in your brain. And then the thing that really fixes it, where you can get to it later, is that later that active quizzing yourself. Classic cases, we think of adult dairy cows, they're just not right. They're losing weight, they're off feed. Maybe the milk has dropped in their dairy animals. You may see these masses, the big swollen lymph nodes, and these animals tend to be bovine leukemia virus positive, BLV positive, okay? That's what they call enzootic leukosis, lymphosarcoma, people call it leukemia. That's the common one, okay? And you can test for it. Typically, we're doing serology. So it's AGID or ELISA. There are some rare sporadic forms. I'm not going to bother you with those. They do exist. If you want to study them, they're right there. But think about the biggies for your NAVLE®. In the same way that we just heard about gastric dilatation and torsion in dogs, and we heard the big stuff first, think that way for these diseases. Once you have clinical signs in these enzootic cows, survival is short, and there's no cure. There's no treatment. There's nothing you can do. This is a retroviral infection. You're never getting rid of it. You're going to cull or slaughter those animals. What do we do to prevent it? This is usually a good thing for these diseases where there's no treatment. We want to use colostrum from BLV negative cows in calves. Make sure you feed calves pasteurized milk or milk replacer, if that's what you use. Make sure you ID infected cows and calves and just get them out of the herd. That's it. Okay, three big things, one big disease, and some good pictures you just saw. 

So here's some just examples of the kinds of questions you might quiz yourself. What's your treatment of choice, everybody, for a cow that's positive for BLV? Just tell me in the chat. Treatment of choice is nothing. Cull, go to slaughter. You're correct, that is unfortunately the case. There's no treatment. What percentage of BLV-positive cows go on to develop clinical disease due to BLV infection? Now, during this talk, I actually didn't cover that, but that's in the notes. Think of it this way, if you're in a multiple choice test, they're either gonna show you some numbers, there's gonna be a big number and a little number and something in the middle, okay? So you just, best you can do is narrow it down and guess. Is it most cows that are BLV positive become symptomatic, or is it not very many? If all you did was that, that's not a bad way to narrow it down. It's not very many. It's a small percentage of cows that actually develop these clinical signs. That means that 95% of the cows that are BLV positive are walking around as carriers. 

Now I want to be thinking about some herd testing. What age group represents the thymic form of lymphosarcoma? You may remember I said ignore all that because it's not common. So, we're going to talk about what they call prior knowledge in a talk that's coming up. When I say the word thymus to you, what age of animal even has a thymus? A young animal, right? So I'm guessing that the thymic form is something in younger animals, calves, okay? I had no idea, I guessed. That's what we do in real life too. I think it's our last question. What is the most common clinical sign in cows with clinical lymphosarcoma. So they're clinical, there's something to see. What are we thinking? Swollen peripheral lymph nodes in most, but not all. Okay, so the big lymph nodes, that's your picture that you stick in your notes. You've can have these vague, ain't doing right signs, they call that ADR, maybe some weight loss, decreased production, lack of fever and a big swollen lymph node, that's a big red flag. Okay, good job everybody, well done. Oh wait, we have one more. What are your tests of choice for bovine leukosis? This may evolve, but remember what they were? It was serology, right? So you're thinking about ELISAs and AGIDs, things like that. It's not that there aren't other tests. We just need something basic. 

We have time for one more notes example tonight. I on purpose picked a species we've already covered but not a disease we've already covered and we're just going to do the same thing we did with the cows. What do we want to know? I want to see a picture. I want to be able to identify a classic case if I hear about it. How do I test? How do i treat? So let's start with a question. I have a 10-year-old mare. Repeated bouts of fever and ventral edema. I think, yeah, it's circled there. So there's sort of this ventral edema in the bottom of the horse there. Okay, you can sort of see it's swollen up. On physical exams, she has petechial hemorrhages of the gums. Okay. So that's those little spots on the gums. This is a big red flag for something's going on hematologically. Ventral edema suggests low protein, petechial hemorrhages suggests a bleeding diathesis. Sure enough, our PCV is low, 25%. Remember, on your NAVLE® and on any of the licensure tests, if they give you a value, they will also give you the normal range. There's a marked thrombocytopenia, so low platelets. Total protein is also low. Low protein, that gives you the ventral edema. Thrombocytopenia that gives you the petechial hemorrhages. Low PCV is secondary probably to the thrombocytopenia. What do we got here? We have an anemic horse. Big clue. I'm not asking you what the disease is, just like in real life and just like on the NAVLE®, we're going to ask you about the clinical scenario. What test do you want to do for the disease you worry about the most? All right. The chat room is blowing up. Excellent, excellent work here, people. Okay, now I see a really nice diversity of answers. And this is great because this is not multiple choice, so it's a little harder. So I see some really good diagnostic options. What disease are we worried about though? Throw some ideas out to me. What are we worry about in an anemic adult horse with a severe problem like this? I'll give you a hint. We're thinking infectious. Bingo, there it is. Yes, we're thinking about equine infectious anemia. Very good, that is what it is, so the test of choice for this, I don't remember off the top of my head, but I'm pretty sure it's gonna be a Coggins or one of those serologic tests that you have to send to the lab. Yeah, so it's an AGID or ELISA once again, and there's probably more sophisticated tests that the lab can do. But the big red flag in your head is, uh-oh, I might have an EIA horse, okay? These are not common. In my career, I've only seen one. Dr. Grenager has probably seen more. Not a good diagnosis, okay. But this is the reason we do Coggins tests. It's one of the big things you have to verify the horse is negative for before you will sign an interstate health certificate. Okay, what's your treatment? Just asking you for a guess. You may not know, okay? And if you don't know, it's okay. Take a wild guess. How am I going to treat this severe disease? Yeah, very good. Dr. Roscoe, muy bien. Dr. Alfonso, si, como no. Yeah, good job. Yeah, Dr. Bulle, right on. Dr. Hidalgo, muy bién. Yeah, this is very well done, everybody. So what people are saying on chat is there's no treatment. You're either going to cull or perform euthanasia or you're going to isolate the horse for life somewhere far away from other horses, only with horses that also have this problem. 

So what we're talking about here is equine infectious anemia, not common in the United States or Canada these days, but it is something we try to prevent. It's reportable. And what you're going to see in a classic case is a horse with recurrent fever, petechia, anemia and edema, okay? That's a huge simplification of a clinical case because they can show up acutely. They can be chronic. You can have inapparent carriers, but a clinical will have the signs of this horse, okay? That's the acute EIA right there. Chronic, you get these recurrent fevers, this hemolytic anemia presentation. Remember what we see with other hemoolytic anemias like AIHI in puppies? You know, the thrombocytopenia, There's not a lot that's going to do that. Um, dependent edema, that's a pretty big clue you've got a problem going on. Um, it can look like a lot of other things, so you're probably going to have to do some diagnostics, but if in doubt, definitely throw a Coggins in there or the ELISA that goes with it. 

Treatment, there is none. The one horse I saw, the owner elected euthanasia. If they're not euthanized, you have to quarantine them in a fly proof area that's at least 200 meters, two football fields away from other horses. These pictures are healthy horses that have been tested positive and they've been kept together on a farm where they can't hurt each other. What do you, how did they get it? It's spread by biting insects like horseflies and deerflies. And so basically it's a bloodborne infection transmitted between horses. And that's why these lifelong carriers are a risk to other horses. You don't wanna be anywhere near horses that are clean. It's a reportable disease. God job. 

Here's a couple of EIA questions, just to quiz ourselves, to wrap up. What are four clinical signs of EIA? We're talking about clinical EIA now. What are you thinking? Chat room says petechiation, good. Ventral edema, fever, good, anemia, thrombocytopenia, good. Yeah, good job. Good job. You can also have horses with no clinical signs, but as I said, I asked for a clinical one, okay? But you can have inapparent carriers. How is EIA commonly transmitted? Very good. 100%. Biting flies. Good job. 

All right, everybody. Well done. You did stellar on that. Take home message about making your independent study active is simply when you read notes, when you write notes, quiz yourself after and then come back a couple days later, skim them again and quiz yourself again. It's that back and forth. Study, quiz yourself. Study, quiz yourself. That helps a lot, and the reason independent study matters, hitting the books, hitting the notes, writing notes, is because it strengthens what we're learning, pardon me, in the practice testing. It is low stakes quiz time. It is the end of our session tonight. We're going to be doing some sample NAVLE® style questions based on tonight's big topic. So here we go. 

A six-year-old Great Dane, pardon me, presents with acute non-productive retching, abdominal distension, signs of hypovolemic shock. On physical exam, the abdomen is tympanic and firm. Pardon me, I'm getting dry. What's the most appropriate next diagnostic step to confirm your leading diagnosis? Is it CT of the abdomen? AFAST scan? Abdominal radiographs? Exploratory surgery? Or abdominocentesis and fluid cytology? Oh, Dr. Mahon, you taught them well. People are knocking it out of the park 100%. Good job. The answer is abdominal radiographs. You're in a hurry. We're not going to be doing CT scans on this guy. 

Which clinical finding most strongly supports a diagnosis of GDV over other causes of an acute abdomen. Retching with a firm tympanic abdomen? Hyperdynamic pulses with abdominal pain? A fluid wave on abdominal palpation? Hypotension plus pale mucous membranes? Vomiting and abdominal pain? All right, let's check the chat room. There you go. Oh man, everybody's picking the correct answer. This is great. Dr. Mahon, you taught them well. All right, retching with a firm tympanic abdomen. Remember, I really loved what Dr. Mahon did there when she compared these guys to a cow with a displaced abomasum, because you can hear a ping on a dog just the same way as you can a ping a cow, and you'll never forget it once you've heard one. 

And the technique is exactly the same. 

Ballotment. Okay, question three, seven-year-old male-neutered Doberman Pinscher presents after collapsing at home. The owner reports non-productive retching and progressive abdominal bloating over the past few hours. On exam, the dog is tachycardic. I'd be tachycardic too. The dog is tachycardic hypotensive has a distended tympanic abdomen, you suspect GDV and prepare for fluid resuscitation. Which vein is the most appropriate for IV catheter placement in this patient? Lateral saphenous? Cephalic? Dorsal pedal? Jugular? Or one I cannot see, femoral? Boy, Jennifer, you nailed it. Everybody's getting it right there in the chat room. And the correct answer is the cephalic vein. Well done. And remember, as she said, we don't pick the saphenous because that may be occluded by the distension and the twisting of the stomach. Did I get that right? 

Yeah, basically, the saphenous is going to ultimately feed up into the caudal cava, but the caudal cava is compressed. Think about a traffic jam on your local major highway. Like cars ain't going to go through if there's a big old wreck. The GDV is that wreck. So you want to make sure that you're choosing the fastest route. And that's going to be your cephalic vein. In the event that the patient was profoundly collapsed and moribund, I would use a jugular instead. But like for like 99% of the GDVs use the cephalic vein. And you want to do both of them and you want short catheters. 

Why do you want short catheters? 

There is some sort of law by some physicist that says that the radius and the length and the tube and the flow and the pressure, one of those things that I don't remember the details of, but you don't want a long catheter because then the fluid is going to have to go through a more compressed area for a longer time. You want a fire hose of fluids, not a truck.

Got it, excellent. Yeah, cause these guys are like great candidates for shock, right? Okay, lo and behold, here we are at shock. You were treating a shocky, painful dog with GDV and you choose to trocarize to quickly reduce abdominal distension and improve preload. How do you decide where to insert the catheter? Always on the left side to avoid the spleen? Midline cranial to the umbilicus? Right side caudal to the last rib? The dog is too sick to trocarize? And the most tympanic area? Some people were answering this one even before I got it out there. Okay, great. So we see a little bit of diversity here. I see some people saying, people saying well it's either this one or that one. You know I love to see that because that means you're strategically guessing. You're eliminating the choices you don't feel good about, narrow it down to two, take a guess. Even if you miss it, you're going to remember it next time. Okay, good job everybody. And the answer is is Dr. Mahon, what is the answer? 

The most tympanic area. And frankly it doesn't matter where on the dog it is if it's the left side the right side the upside the downside it doesn t matter you're going where the most tympatic sound is because that's the area where the gas is in the stomach and pressing up against that body wall that's going to be your safest area to put that needle in or that catheter in and I would like to emphasize that there is not a single dog that is too sick to be trocarized and I have definitely trocarized or performed micro gastrectomies on these dogs while CPR is being performed. So do not be afraid to trocarize these dogs, seriously. And if you're like, I don't really remember like, you know, the most tympanic area, you know start just start ballotting and pinging that dog and trying to find where that is, especially for the 360 ones, again, rare, but they can trick you. So, in fact, you might be actually, like, trocarizing on a side that you wouldn't expect. 

Um, and what's nice about this, guys, it's not rocket science. It's really clear what kind of a problem you're dealing with. Um, And there's a lot you can do that'll help, uh, really nice corollary to what we just heard about going for, you know, uh getting the trocar in there, even if they're, you know, getting ready to have other things done to them. Remember what Dr. Reiss said about a blocked cat when you can't get the catheter in, at least get a cystosyntesis going to relieve pressure on that bladder. Same reason, you're going to make them less critical and you've given yourself the gift of time. Okay, so one of the best things you can do is you learn about these clinical cases to think flexibly is find connections. Yeah, okay, I think I might have one more, I might've thrown a curveball in here. Let's see. I did not. I thought I was going to throw another reptile question. I like reptiles. What can I say? 

Folks, we are at the end of tonight's session. Dr. Mahon, thank you. That was amazing. Really, really well done. Our assignment for Sunday's session is to do a very quick review of GDV. Just literally pop over to the Merck, give it a skim, just remind yourself of the high points, okay? We're going to need about a week to 10 days at least to format this video and then post it under useful tools, but it will be up there. But it's always good to do some independent studies, so pop over to the Merck. Your tune-up topics for Sunday... Don't overdo it, give it 15 minutes max, is we're gonna cover with Dr. Alenia Tracy, avian influenza and Marek's disease. And all I want you to tune up on is what's a classic case look like, what's my test of choice for these bugs, and if there's a treatment, what is it, okay? And that would be a great way, just 20 minutes of tune up on GDV and those two diseases, so that you're a little bit prepared with your prepared mind when you show up. I'm going to put this in the chat room, but I believe we made it to the end. Thank you very much, everybody, for coming. Dr. Mahon, thank you. That was Tour de Force, 100 out of 100. 

Glad you enjoyed it.