Cram The Pance - S1E8 Acute Pancreatitis vs. Chronic Pancreatitis

Episode Date: January 21, 2021

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All right. So today we're going to be going over two pretty important topics for the pants, your panery, your ERs. And that's going to be acute pancreatitis and chronic pancreatitis. Real quick before we get started, I just wanted to say if you like my material with the podcast, I do have a YouTube channel as well under the same name, Cramed the pants. If you want to check out those videos, do have some pretty good visuals to go along with the audio. So let's start with acute pancreatitis. Essentially what acute pancreatitis is, there has been some sort of trauma to the pancreas, whether it's golf, stones, alcohol, whatever it is, that led to cellular injury in the pancreas, which is essentially causing the pancreas to digest itself, to put it pretty simple. So what happens is there was some sort of injury, whether it's, like I said, a gallstone, it can be from alcohol, that injured the pancreatic exocrine cells, which are known as acinar cells. It's A-C-I-N-A-R. So there's something that cause an injury to these cells. And these acin-ar cells are the functional unit of the exocryin pancreas. So they store, synthesize, secrete digestive enzymes. So there was an injury to these cells.

It could have been from a gallstone. It could be, you know, impaired blood flow, alcohol drugs. And what happens when these cells get injured, instead of releasing this, you know, the exocrine, the digestive enzymes, they get injured in a way that they're prematurely activating these enzymes within the cell. So the cell is actually the enzymes are actually activating within the cell, which is causing the pancreas to digest itself. So essentially, like I said, the pancreas is auto-digesting. These exocryne cells aren't able to put out the enzymes. They're actually activating within the cell. So you have this intracellular activation of enzymes.

Obviously, this can cause some problems. So as far as the etiologies of this, your most common, cause by far is going to be gallstones. That's about 40 to 70% of causes of acute pancreatitis. And the reason is the gallstones, when they get caught in the common bile duct, the common bile duct is shared at a certain point with the pancreatic duct. So the gallstones get caught in the common bile duct. So, you know, bile can back up. This can block the pancreatic duct. And this all leads to a CNR cell injury. And again, the same patho that I just went over, it's going to cause. that same type of problem. So that's the thought behind the reason gallstones cause it.

Your second most common cause for acute pancreatitis is going to be alcohol. Again, these are CNR cells. When they break down alcohol, it actually produces a toxic byproduct, which damages these cells. And again, just like I just went over, you can understand the process of that and what happens here. So your two ones that you should know really well, the two etiologies that you should know more than anything else because there's a lot of causes of acute pancreatitis, but no gallstones and no alcohol. Those are your really big ones. So let's go over a few other causes. Hydrochlorothiazide, as far as medications is a pretty big one. Protease inhibitors, those are the HIV medications like retonevere can cause it. Exenotide. If you remember,

those are your GLP 1 agonis, the diabetes medication. That can also cause acute pancreatitis. Valproic acid is another big one too. So those are some. the ones you should know also. And if you want to get really fancy, there's a mnemonic, so you can remember all of them. And it's, uh, the mnemonic is I get smashed. You've probably heard it. It's a pretty popular mnemonic for causes of acute pancreatitis. I don't know if I would waste my time memorizing it because I don't think you need to know every cause, but I'm going to go over real quick just for the, the podcast you guys can hear it. So I get smashed. Um, stands for idiopathic, which is one, the first one. G in get stands for gallstones. E. Ethanol.

so your alcohol. T, trauma. S stands for steroids. M stands for mumps and malignancies. A stands for autoimmune. S stands for scorpion bites or scorpion stings. H stands for hyper triglyceridemia and hypercalcemia. Hyper triglyceridemia is kind of rare. It really only happens if the triglycerizer elevated above a thousand. So it needs to be pretty significant for this to actually happen. E stands for ERCP and then D for drugs. And I went over some of those already, the hydrochor thysi and the protease inhibitors, GLP ones, all of those. So that's a way for you to remember if you wanted to go over all the different causes.

That's a pretty extensive way for you to know all of them. Another thing to know about Q pancreatitis, normally you're going to see this in middle to older age patients, but it can actually happen pretty commonly in cystic fibrosis patients or children who took aspirin leading to Ray syndrome. So remember this doesn't necessarily have to be an older person's disease. This can actually happen in children as well because those are a few different ways that children can get this as well. So as far as how the patient's going to present when they have acute pancreatitis,

they're going to have epigastric pain. Normally this pain is going to radiate to the back. So remember that. That's pretty important. That normally points to acute pancreatitis when you hear radiates to the back. So epigastric pain radiates to the back. Sometimes described as boring pain. And boring pain doesn't mean boring as in boring and like boring.

Boring actually, the medical term means like a piercing deep within the body like pierced with an object. So that's what boring pain means. So if you hear that, that's actually what they're referring to. So it's sometimes described as boring pain like something boring into the body, like a sharp object. Then another important thing to know about the presentation is that a patient with pancreatitis is normally, the pain is normally going to be worse when they're laying flat, when they're laying superlaping. pine and it gets better when they lean forward or crouch forward. So a lot of times you'll see these patients sitting or kind of crouched up in a fetal position with their knees tucked up to their chest because when they're leaning forward, bringing the legs forward and crouching forward,

they actually feel better. It's going to be worse when they're laying down. They also may have nausea, vomiting fever, things like that. On physical exam, there's a couple of important things that you need to know. And there's two things called colon sign and gray turner sign. So these are not 100% specific to acute pancreatitis, really there are signs that are consistent with abdominal wall hemorrhage. So they can be from a number of different things. Actually, in fact, colon sign was invented by Thomas Colon in a long time ago, like in the early 1900s, and it was actually referring back then in a patient that had a ruptured ectopic pregnancy. So it doesn't have to be acute pancreatitis, but it is pretty common when you hear this,

especially on your exams, your boards. If you see colon sign or gray Turner sign, think acute pancreatitis. And what this is, so you have, colons, we'll start with that one. So it's echemosis, a hemorrhagic discoloration that's seen around the umbilicus. So colons is going to be around the umbilicus. So you'll have this bruising, this ekemosis seen around the um, and then gray turner is going to be ekemosis of the flank. So you'll see it on the sides of the abdomen there. So colins is going to be ekemosis around the umbilicus. Gray Turner around the flank. I always remember Gray Turner because I think about like turning when you turn your, you kind of turn like with your flank and that's just how I remembered. It doesn't really work

that well. I say it out loud, but it somehow made me remember that. So if you do see these signs, it's not very common. It's really only occurs in less than like 1% of people with acute pancreatitis, but if you do see it, there's a very high mortality rate. As you can imagine, this is basically an abdominal wall hemorrhage. So these are really, you know, serious. signs when you do see this. So colones, gray turners, colons around the umbilicus, gray turners, ectomosis around the flanks. Remember those for your physical exam findings. Um, and then as far as moving on to labs, the first thing that you're going to do really important is you're going to check their amylase and their lipase. So amylase and lipase, you'll see an elevation and a lot

of patients. Lipase is going to be your more, um, that's the more, uh, I don't know, they are both pretty sensitive and specific. But, that lipase is actually can remain elevated for up to 14 days after patient presentation, whereas amylase only stays elevated for about five days. So lipase is going to be the more important lab to get here. And it's better for a patient with a delayed presentation because maybe they came in five, six days after presentation. The amylase is back to normal, but the lipase will actually stay elevated for a couple of weeks.

So lipase over amylase when you're doing labs. But either one can be elevated. And then another thing that you may see in your labs is hypocalcemia. And the reason that you see hypokalcemia in an acute pancreatitis patient is something called calcium soaps. So what happens is when the pancreatic tissue dies, you have this necrotic fat around the pancreas, and this necrotic fat actually binds to free calcium that's floating around in the serum, which can lead to decreased serum level. So that's the reason you see hypokalcemia and acute pancreatitis.

Another lab finding that you may see is an increased ALT. If it's increased three times above the normal limit, this can indicate a gallstone pancreatitis. So ALT three times the normal limit, think gallstone pancreatitis. Some imaging that you can get done is your cat scan is going to be your best imaging study. That's going to be your first line when you go to imaging. You can also do an ultrasound, but ultrasound's really going to just be able to check for gallstones or checking for biolucut patency, seeing if there's any dilation of the bile ducts and things like that. Really, CT will be your first line.

And then if you do an x-ray, again, not going to be your best test. But if you do an x-ray, there's a couple different signs that you should know about that point to acute pancreatitis. So the first thing is known as a sentinel loop. And this is an ilias, which is a paralysis of the small bowel from nearby inflammation from the pancreas. So it can actually cause this paralysis of the small bowel in ilias. And it's known as a sentinel loop, if you see that, on x-ray. There's one other sign that you should know for x-ray as far as acute pancreatitis, and that's something called a colon cut-off. And that's something you'll look at the large bowel,

you'll look at the colon, and all of a sudden you'll see a gas pattern all normal, and then all of a sudden you'll see this cut-off, where it goes from gas pattern to nothing. So there's an abrupt termination of the gas pattern in the large bowel, and this can be another indicator of acute pancreatitis on an abdominal x-ray. So that's another important one to know. all right so those are the ways you can diagnose there's also criteria you should know because you can have all these positive labs but there's there's actually a criteria that will help you make the diagnosis it's known as Atlanta criteria and you do need to know this and the way you make the diagnosis for acute pancreatitis you need two out of the three of the following so I'm going to

list these in order so the first one would be an increase in either your serum amylase or lipase three times the upper limit of normal. So remember we talked about the amylase and lipase being elevated. So either the amylase or the lipase elevated three times above the upper limit of normal. So that's one. Remember, you need two out of three. The second one is going to be epigastric pain consistent with acute pancreatitis. So whether it's pain radiating to the back, worse one, there's supine, boring pain, something that kind of points to acute pancreatitis rather than some other cause of epigastric pain. The third one, again, if you get the first two, you don't need to do imaging. You already have the diagnosis per Atlanta criteria for acute pancreatitis. But if, you know, one of those was negative, the third criteria would be findings on imaging

consistent with acute pancreatitis. So whether it's that sentinel loop on the x-ray, the bowel cut off, positive CT, which would be, sometimes you can see pancreatic fat stranding, inflammatory tissue surrounding the pancreas, just a positive finding on one of your imaging. in addition to one other factor. So two out of the three for that Atlanta criteria to make that diagnosis. It's one criteria I think you should know. There's also something called Ransons criteria.

I don't know if I would waste my time memorizing this entire thing for the off chance that maybe you get one question on this. But I'm going to just review it real quick for the podcast. So Ransons criteria is something that you can use on admission. There's also one that you can use for two days out to check the mortality rate. I'm not even going to go over that because I do not think you're should. to waste your time with it. But I will go over the admission criteria for Rancis criteria. This is going to estimate the severity of the pancreatitis. So the way you're going to figure this one out, and you're going to go by five different factors. So on admission, you're going to get their

glucose, their age, their LDH level, their AST, and their white blood cells. So of glucose, you need three or more to diagnose severe pancreatitis and less than three will be, you know, as severe, maybe a mild or a moderate case of pancreatitis. So three or more is it going to indicate severe pancreatitis, obviously leading to a higher mortality rate. So let's go down the numbers for those. So glucose above 200, age over 55, LDH above 350, AST above 250, white blood cells above 16,000. Say that one more time, glucose above 200, age above 55, LDH above 350, AST above 250, AST above 250, 50 and white blood cell count above 16,000. Three or more indicates severe pancreatitis.

If you'd like to memorize that, you can. I don't recommend it. I just don't think it's worth the time for maybe one question. Maybe one question. So moving on to treatment. Treatment is mainly going to be supportive. There's not a specific thing that you need to know for treatment outside of two really important factors.

Most patients are going to get, you know, recover. They'd say about 90% from what up to date is stating. 90% will recover with just supportive measures. So the supportive measures that you're going to do, essentially, you want to rest the pancreas. You don't want the pancreas to be working, producing all of these exocrine enzymes and endocrine, like insulin and everything like that. You want to rest the pancreas. So how are you going to do that? You're going to have the patient NPO, and then you're also going to give them IV fluids.

Those are the two really important things. Just remember those two. There's not too much else you need to know. Remember NPO to rest the pancreas and IV fluids. you're going to give them lots of IV fluids. So two things for treatment, don't go crazy, NPO IV fluids. So one other thing that I'm going to just make a note of, not as important, but these patients are obviously going to be in a lot of pain. And it used to be stated that for pain in these patients, you wanted to give them meperdine, which is also known as Demerol. And the reason behind that was because some of the other narcotic pain medications like morphine could increase the sphincter of odi pressure.

it could cause sphincter of odai vasospasm. So it was thought that demoral does not do that. So they decided that Demerol will be the right medication to treat these patients' pain. Well, it turns out that the studies, there's studies lacking this information. It was kind of something that was always stated, but not necessarily true. And if you check up to date, it's not something that's commonly used anymore in practice. And now the medications they're typically using are fentanyl, hydromorphone, things like that because they work a lot better to treat the pain and there's just not any studies to back up the fact that that demoral was working any better or decreasing this sphincter vody pressure or anything like that so it used to be stated meperdean you know demoral was used more commonly but

that's not really true anymore fentanyl hydromorphone are there more common medications morphine can even be used as well for pain but that's just kind of like off topic remember just MPO and IV fluids as far as treatment. So that's acute pancreatitis. That's the one you need to know the most for. Chronic pancreatitis will go over next, but there's not as much to know for this. So chronic pancreatitis is really a result of somebody who's had multiple episodes of acute pancreatitis, and they have this continual injury to the pancreas. They've had all this chronic inflammation that's going to lead to both loss of endocrine and extracrine function of the pancreas. You're going to have all this scar tissue you built up this calcification. These are patients who have had many episodes of acute pancreatitis

and are getting to this point, which is a chronic condition. And as far as the etiology's with acute pancreatitis, gallstones was your most common cause. Alcohol was your second. In this case, alcohol by far is your most common cause. So alcohol use, ETOH, about 70% of causes of chronic pancreatitis are going to be from alcohol. Some other causes, sometimes it can be. videopathic, sometimes it can be due to trauma. Golf stones, not as common a cause in chronic pancreatitis very far down the list. Really, the one you should know is alcohol use. That's about 70% of the time.

So really know that one. The other ones are not as important, idiopathic trauma, but alcohol by far. As far as the patient presentation, there's a triad that you should know. It's really only present in about maybe 25% of patients, maybe 35 around there. but if you do see it, it's a hallmark kind of pathonomonic for chronic pancreatitis. So what this triad is is calcification seen on imaging. So that's going to be a sign of chronic inflammation. So you're going to see calcifications in the pancreas.

The second thing in the triad is going to be steatorea. So that's going to be oily or fatty stools. They often float because of the high fat content. And this is because the endocrine function is shutting down in the pancreas. So you're going to have these decreased enzymes, which you're going to have these decreased enzymes, which leads to malnutrition and the fat not being able to be absorbed because you're not getting these enzymes that are necessary to break down the fat. So these patients have steatorrhea. The third thing in the triad is going to be diabetes malitis because remember this is an endocrine and exocrine problem. So your

endocrine is also shutting down, which is your insulin production. So these patients also may be diabetic. So the triad again is going to be diabetes malitis, steatorrhea. And then the first one is calcifications that you'll see on imaging. These patients also may have, you know, just like an acute pancreatitis, the epigastric pain that radiates to the back. Some patients are actually going to be asymptomatic, and it may just be an incidental finding on maybe an abdominal x-ray or a cat scan that they find out. Diagnosis with these patients, amylase and lipase is not really important, and a lot of times it can be completely normal. In some advanced chronic pancreatitis, sometimes these levels can actually be low, but overall amylase and lipase and chronic pancreatitis has very little diagnostic value really no

diagnostic value if you do a ct or an x-ray you're going to see calcified pancreas and that's the really important one remember that's in the triad so you see calcifications in the pancreas in either a cat scan or an x-ray and another important test that you can do is you can test the pancreatic function and you do this by testing something called fecal elastase so um Elastase is an enzyme that's made in the pancreas in a normal functioning pancreas. And what this test does is it tests the amount of elastase in the stool. In a normal person, there should be around 2 to 500 of this elastase found in the stool. And patients with chronic pancreatitis, remember, again, their exocrine function is shutting down.

So you're not going to see as much of this elastase in the stool. You're going to normally see less than 200. Those figures aren't too important. I just wanted to let you know that. But this is another test you can do, which is pancreatic function. testing for chronic pancreatitis patients. So as far as the diagnosis, this is a good thing for the boards because when the diagnosis isn't an easy one to make, they can't really test you on it because establishing a diagnosis in chronic pancreatitis can be really challenging.

There's many different diagnostic criteria available, but none of them are universally accepted. And the diagnosis is really just made with a combination of, you know, positive patient symptoms along with some positive diagnostic findings. not one specific criteria that's agreed upon, so they really can't test you on this. You should know a lot of those things to pick it out in a vignette, but they really can't test you on one specific thing to diagnose chronic pancreatitis because it's a combination of many different things. And as far as treatment, again, this is going to be another thing where it's just a number of different factors. One of the most important things as far as treatment is going to be to discontinue all alcohol use.

You don't want to be, you don't want to have these patients drinking anymore because they're going to continue to destroy their pancreas. So discontinuing alcohol is really important. These patients are going to need pancreatic enzyme replacement because remember again, this exocrine function shutting down. They may need pain control for some of the abdominal pain they're having. Low-fat diet is important because they're not going to be able to digest fat as well because of the decreased enzymes that are being produced.

And they also may need vitamin replacement. And in some cases, these patients that have real severe cases due to pain and other GI problems, they may even need anterioral feeding, like a feeding tube to bypass to go straight into the stomach into the small bowel, which sometimes help with some of their symptoms. So overall, the treatment, not one specific thing. It's really a combination of a lot of different lifestyle changes, you know, enzymes and vitamins and things like that. So nothing real specific to point to there.

And that's chronic pancreatitis and acute pancreatitis in a nutshell. Hopefully that helps you guys. again please leave me some comments alike and let me know how this is helping you and as always good luck on your exams your pants your panor your u rs and good luck in pa school