Pancreatitis | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about pancreatitis that includes both acute and chronic pancreatitis this is part of our clinical medicine section if you guys like these videos they make sense they help you please support us you can do that in simple ways one hit the like button comment down the comment section and subscribe to help yourself though and I really think that you can do this by going down in the description box below clicking on the link that goes to our website there you'll find some amazing supportive features such as notes illustrations quiz questions and even exam prep courses that are coming soon so go check that out become a member and gain all those premium resources all right let's talk a little bit about pancreatitis this is a behemoth of a topic it's very very common for your Internal Medicine concept that you have to be able to get down pth what we're going to do is is we're going to talk about both acute and Chron but we're going to do it in a pathophysiological concept that I think will help you to make sense of it as well as help you with the complications as well as to help you with the diagnostic approach so first thing pancreatitis inflammation of the pancreas right an acute pancreatitis it's an acute inflammation an Abrupt onset with chronic pancreatitis it's repeated inflammation that leads to fibrosis and calcification of the pancreas leading to its subsequent failure and we'll talk about that as we go along when we talk about what causes the inflammation of the pancreas it's usually two particular things one is you've injured these little cells here you see these little guys here they're called the asinar cells these are the ones that make a lot of your pancreatic enzymes all right that's one way that we can kind of cause pancreatitis the second way is you inflame these ducks so you see these like long tubes with all these like little branches these are your pancreatic ducks and there's cells in there that help to make with pancreatic juice when we injure those two cells we precipitate inflammation and inadvertent inactiv inadvertent activation of pancreatic enzymes those pancreatic enzymes are harsh we don't want them to be activated in the pancreas we want them to be activated in the intestines when they're activated in the pancreas they cause inflammation digestion of the pancreas and then a plethora of complication so let's go through this first thing is what can cause the SNR cells to become really injured in the acute phase meaning that these would be causes of acute pancreatitis there's really only a couple that I think are high yield to remember one is going to be generally this is a pretty big one alcohol so alcohol use not to the point of where the patient is like alcohol abuse or dependent but a lot of alcohol use alcohol has been shown to naturally be in a senar Cell kind of like pathogenic effect so increasing alcohol use has definitely been tied to cause causing direct SNR cell injury so look how these puppies are going to directly injure the SNR cells the second one I'd say that's really important is going to be hypertriglyceridemia so whenever a patient has super super high triglycerides and this is to the point where I'm talking it's like really really high like it has to at least be greater than a th000 milligrams to really cause this type of effect on the pancreas and so whenever the triglycerides are profoundly High these have also been shown to cause direct injury to the asinar cells another one is called hyper calcemia okay and Hyper calcemia is when the calcium levels are just really high and they have to be pretty profoundly high at least approaching towards 14 milligrams to really start kind of having this effect on the pancreas calcium is a nice co- kind of like factor it's really helpful in being able to activate in enzymes and so when calcium is extremely high it's been able to been shown to not only injure these cells the asiner cells but activate these actual proteases in the in the pancreas so that's one particular problem I think what you really want to remember is a patient who has chronic alcohol use really big one for acute pancreatitis triglycerides whenever these are really high you want to be thinking about this in patients who are on like prolong propofol infusions or have very poor diets or so obesity metabolic syndrome types of things the third one is do they have some type of like inherited hyper triglyceridemia like a type one or type of like type four dyslipidemia of some sort calcium whenever this is high it's either hyper parathyroidism and malignancy we'll talk about that in the calcium lectures these I'd say would be the big ones the other ones is there's so many drugs and toxins that have been tied to this but these are kind of like hard to really kind of sus out because there is many and many and many of these and I don't I want you to get bogged down with these there's all these pneumonics and things that they use to help you to remember you know pancreatitis like the pneumonic I get smashed I think that's great but I think the most common causes are going to be these top three up here that I want you to remember for a Sinar cell injury now we've really jacked up these asinar cells cause them to become injured which will lead to a downstream effect that we'll talk about here in a second it'll lead to this kind of effect that we'll talk about the thing that I want you to understand is what can Chron Ally repeatedly repeatedly injure these kind of cells and that's a big one to remember alcohol use has been definitely linked to acute pancreatitis but often times alcohol use is very commonly very consistent trigger for repeated bouts of pancreatitis and so when a patient has chronic alcohol use to the point where we call them kind of like alcohol abuse then we're getting into the point where this is causing repeated repeated repeated kind of constant constant constant bouts of repeated pancreatic inflammation so alcohol abuse is a very common chronic cause of repeated pancreatic inflammation these are usually acute abrupt causes of pancreatic inflammation all right and we'll talk about this in a second of how whenever these asent our cells are injured what's the downstream effect the second cause to why the pancreas can become inflamed and injured is you injured the ductal cells so something within these cells now you have to remember a little bit of your Anatomy you have the liver the liver you also have what's called your common patic ducts you have your hepatic ducts which converge into What's called the common patic duct it fuses with was called the cystic duct which come from the gallbladder and makes the common bow duct which fuses with the main pancreatic duct and then right here we have What's called the apat pancreatic ampula what if I have a stone that's like here in the gallbladder and I flick it out and that stone goes and gets stuck right here where it's kind of like at the same point where the common duct and the pancreatic duct fuse so one would be like a gallstone right and I'd say out of the most common reasons are common causes of why patients develop pancreatitis this is going to be one and this is going to be two if you remember these it doesn't matter if you forget all the rest of them I'm not kidding it's the most common cause they account for about almost 70 to 80% of the cases sometimes if we can't figure it out it's often idiopathic as well now with that being said if a gallstone gets stuck here you get all this back pressure if you will and all that back pressure is tough on these um pancreatic ductal cells and that will cause injury that constant like back pressure will cause injury to these pancreatic ductal cells so that's one cause another one is we do this quite often and patients who have gall stones especially if the stone is somewhere andin the biliary tree we often do this kind of like test or therapeutic kind of like measure where we take this scope we run it down through the esophagus and we run it down via the stomach and into the dadum and then we try to take this thing retrograde all right and we try to generally run it up through through the actual bile duct but in order for us to get it through the bile duct we have to go through the pancreatic duct that area there and whenever you do that you can most certainly directly injure these pancreatic ductal cells so we get pancreatic Doyal injury from a stone or what's this test here called ercp so it's very common to see this with patients who get what's called ercps all right e CP which is like a retrograde cango pancreatography and it's an endoscopic procedure but that kind of endoscope can hit the pancreatic ductal cells and cause injury all right so we have iatrogenic cause and gallstone what's something chronically that have repeated repeated repeated bouts these patients will experience this Non-Stop and develop with repeat BS of inflammation that lead to fibros fibrosis and calcification this one that can cause repeated injury because it's causing pancreatic dual obstruction and injury is common in patients who are younger have frequent pulmonary infections have moonium aspiration have exocrine pancreatic in deficiency because they've destroyed the pancreas you know what this is it's a bunch of mucus that gets stuck within those pancreatic ducts it's called cystic fibrosis so cystic fibrosis is a very common cause of chronic pancreatitis so what I want you to remember is if I say acute pancreatitis you're thinking alcohol use you're thinking hyper triglyceridemia hypercalcemia drugs toxins ercp and a gallstone if I said chronic pancreatitis you're thinking about alcohol abuse causing repeated bouts it's just St fibrosis causing repeated obstruction of the pancreatic ducts causing chronic fibrosis and inflammation and calcifications now with this ductal injury what's the problem here well I have two things I've injured the ASR cells and I've injured these ductal cells when you injure these cells what happens is you have these different enzymes here you know what these enzymes are these are pancreatic enzymes let's say that there's just a couple of them you have what's called proteases which which I say is going to be the most important one for this process you have lipases and you have amales there's even nucleases as well but these are all these enzymes that are located kind of in the cell and also can be located in pancreatic ducts when these cells get injured they activate undesirably activate these enzymes these enzymes are not supposed to be activated in the pancreatic docs or activated in the pancreatic cells but when they become activated they start causing digestion proteases if you kind of increase the activation of proteases increase the activation of lipases they will literally start digesting they'll cause autodigestion of the cell and autodigestion of the ductal cells that's L what's going to happen I'm going to start having what's called Auto digestion of the pancreas that will start to occur because of inadvertent activation of pancreatic enzymes with the most important ones being the proteases once this happens and they injure they start autod digesting the pancreas you're injuring cells it's going to start causing alarm bells to go off and kind of trigger inflammation so then what happens is is you start getting a pancreas we look at it from the overall view of multiple cells and multiple ductors cells getting injur injured look at this sucker it's hot it's red it's angry it's super super super inflamed and this is kind of the process of how inflammation of the pancreas generally starts to occur so we're going to increase the inflammation of this pancreas now once we've kind of triggered this particular process to occur I think the big thing to remember is how does pancreatitis generally present whenever they're super inflamed well one way and I think that this is really important the classic finding is to remember where is the pancreas it's right behind the stomach so in the epigastric region so if you inflame that area it's going to cause pain in that particular region and so oft times these patients experience the classic finding what we refer to as epigastric pain all right and it's definitely even positional as well I'd say that this is one big classic finding that you have to watch out for but here's the other Downstream effect when the pancreas is inflamed it really kind of starts to alert your immune system and what you do is you start stimulating a bunch of white blood cells right I'm going to activate a ton of white blood cells to come to this area from injury I'll activate neutrophils since it's more of an acute process I'll activate macras since it's more of an acute process and these suckers man they pump out cyto kindes and this is where everything kind of goes wrong they pump out cyto kindes which I actually do think is kind of relevant here like interlan one interlan 6 and tnf Alpha they're going to be pumping all these things out now what happens is these cyto kindes when you pump out so many of them for some reason pancreatitis really really amplifies this this gets out into the systemic circulation you pump up your white blood cells you pump up all these cyto kindes and they get into the bloodstream and what happens is you get something called a c a systemic inflammatory response syndrome type of effect and we'll talk about what that looks like in the complication section it's really profound and scary these patients can get really really sick and have systemic complications all right but this is because of the massive systemic inflammation the other thing that's really kind of interesting is is that these cyto kindes will come in and they will just amplify the immune response which will cause more inflammation more types of local complications to the pancreas and so what are some of those local complications well some of the local complications that can occur here is that these patients may start to experience a lot of nasty things so we'll put Here Local complications that we'll discuss in more detail but some of these local complications that are pertaining to the pancreas from propagated inflammation includes what well one of them is you're going to amplify the edema so you're going to stimulate edema one is you'll start to cause necrosis of the tissue and lastly you're going to start causing hemorrhaging of the tissue and so this is kind of the Cascade of events that occurs here is edema necrosis and the worst case scenario is hemorrhage and these are all due to massive propagator inflammation now the last thing I think that's really really important is that if a patient experiences this inflammation goes into remission never has a problem again cool but it's the patients that have these repeated repeated bouts of pancreatitis remission pancreatitis remission that develop this nasty complication where the pancreas starts to become I'm going to represent this with this blue tissue it becomes fibrotic and it develops calcifications so now this is from repeated bouts of inflammation and from this repeated bouts of inflammation you kind of start laying down so much scar tissue and start causing so much calcification that then this patient has progressed into something else they've progressed into what's called chronic pancreatitis so chronic pancreatitis whereas this is more of a acute this is more of a acute pancreatitis right because it's just that one episode of inflammation which will present with that classic epigastric abdominal pain this one can also present with kind of a dull epigastric abdominal pain but we'll talk about some of the other scary complications some of the big complications that we'll get into in more detail is the pancreas has a exocrine portion which it makes pancreatic enzymes which helps in digestion it also has a endocrine portion which makes hormones and if you destroy the pancreas and cause it to become replaced with fibrous tissue and calcified tissue it's not going to be able to do that so it loses its pancreatic enzyme functions and you start to develop malabsorption syndromes or you don't make a particular protein which I'm kind of representing with the eye there insulin which can lead to secondary diabetes and so we'll talk about now what are these cers complications what are these local complications and what is some of the complications of chronic pancreatitis hi my friend so a patient comes in they have pancreatitis whether it's acute pancreatitis chronic pancreatitis they're going to present generally with the acute epigastric abdominal pain if it's acute pancreatitis maybe more kind of like a dull long-term epigastric pain if it's more the chronic pancreatitis I told you when a patient experienced pancreatitis due to a syar cell or ductal cell injury there's autoactivation of those pancreatic enzymes they cause autodigestion they start really inflaming the pancreas white blood cells infiltrate the area and you get a lot of systemic kind of spill over so what happens is when the pancreatitis gets super inflamed so here we have some acute pancreatitis all right so here we have some pancreatitis and I want you guys to understand that when we talk about s this is more it to the acute form of pancreatitis not really for The Chronic form of pancreatitis when a patient experiences acute pancreatitis I already told you that it'll kind of activate it'll really stimulate these white blood cells right and when I stimulate my macr phases I stimulate my neutrophils what are they going to do well we already told you that they're going to start pumping out a bunch of different cyto kindes and there's so many of these but I think some of the big cyto kindes to who remember is going to be things like interlukin one tumor necrotic Factor Alpha and there's some other ones but these are going to be the primary ones that I think are going to be very pertinent these are massive inflammatory cyto kindes and when they're produced in large amounts they produce a pretty nasty effect on your systemic system so when these get into the bloodstream is where it really reeks Havoc so let's say that some of these inflammatory cyto kindes leak into the bloodstream all right here's the other thing thing not only are these the things that are released into the systemic circulation you know those pancreatic enzymes that were autoactivated and we causing a lot of pancreatic digestion a lot of these pancreatic enzymes can spill into the actual systemic circulation as well so watch out for that because sometimes you can have a lot of these nasty little enzymes inside of the bloodstream such as lipases is a really really big one this is kind of like in pretty large amounts inside of the blood bloodstream and other proteases but lice is the really really big one either way when these things get into the bloodstream one of the profound effects that they have is that they cause increase permeability of multiple vessels they cause them to dilate a little bit um but they also will really really really make them super leaky so now if I increase the capillary permeability now what I'm going to do is I'm going to make these vessels they're going to have a bunch of holes the endothelial cells are going to start retracting and when they retract any kind of fluid which we're representing here in blue will start to kind of exude out and as this fluid starts to kind of exude out of the circulation it'll kind of exude into the interstitial spaces and what do we call that when it leaks out into the intertial spaces it's called third spacing and so this third spacing effect if you will is very very problematic and one of the things that we'll see here is that this increased per ability it induces what's called third spacing and third spacing will cause fluid to leak out of the vasculature and that will precipitate what's called hypo volia which is a low volume of blood within the circulatory system now when a patient has hypovolemia this can affect multiple multiple different organs the most profound effect is really going to be on the heart and the kidneys now this kind of effect here whenever they have intense intense hypovolemia one of the big things is that your cardiovascular system is dependent upon blood volume and whenever you have a low blood volume you're going to have a low blood pressure and so often times these patients will have a very low blood pressure that'll send them into a period of what we call shock so they can develop what's called hypovolemic shock hypo volic shock and so their blood pressure will be kind of profoundly low that they're not able to profuse particular organs and that's one really big way so look for these patients to be more on the hypotensive side low systolic blood pressure low diastolic blood pressures that they kind of develop shock the other thing is that when you're kind of like super hypotensive this kind of creates a reflex of kind of effect on the heart that it kind of tells the heart hey hey blood pressure is really low you better try to help me out out a little bit here and what will happen is this will kind of try to trigger the heart to kind of go into this increased catac colomine effect and what it may do is it may increase the heart rate and so I think often times it's really really important to watch for a patient who has a very significant tacac cardia in combination with a very low blood pressure because that could suggest shock we use that What's called the shock index to determine that that's one thing now the bad thing about shock is that shock worsens everything with local pancreatic complications we'll talk about it a little bit later but at least want to kind of introduce you to this that shock if you're not profusing the tissues they can increase I want to write this down they increase necrosis and infections I think this is super super important to remember whenever your blood pressure is low you don't peruse organs one of those is the actual pancreas itself if the pancreas doesn't get blood flow it doesn't get oxygen if it doesn't get oxygen it gets es schic if it gets esic it infar and starts to die if the bowel doesn't get oxygen becomes es schic if the bowel becomes es schic can it control bacteria translocating no bacteria can get into the bloodstream and can cause infections and that's really really really bad so we want to watch out for this with pertaining to the local complications the next thing is whenever patients are hypovolemic you have a decreased renal profusion so these guys also have very little blood flow moving in via the kidneys to peruse the kidneys and so when you have a low renal perfusion because of hypovolemia this can lead to acute kidney injury it's more of what we call a prerenal Aki but either way these patients will have an acute kidney injury which is usually classified by a drop in urine output and an increase in the creatinine and an increase in The Bu so watch out for drops in this increases in this due to a poor renal profusion from hypovolemia all right so if a patient's kidney function sucks their blood pressure is low their tartic that's some potential systemic complications from these massive inflammatory cyto mines the other thing is that this third spacing not only does it cause hypovolemia but it causes lung injury and so I want you to think about that leakage of fluid this happens pretty heavily in multiple alvioli and so now if fluid kind of leaks out here it can leak out into the alveoli and fill these alvioli with fluid it also can leak out into the inter spaces and when this leaks out into all these different types of spaces what's the particular problem with this well this happens in multiple alveoli and so this induces what's called a lot of alveolar edema or alveolar filling and if this causes diffuse alveolar filling to the point where these patients can't even perform gas exchange so now they're they're developing what's called shunt physiology they develop shunting is the big kind of feature here we talked about this in the respiratory system shunting is a really big feature here if they have diffuse alveolar filling with tons and tons of fluid this can cause the patient to present with ards and these patients can have profoundly low oxygen levels due to shunting and then because their oxygen is low they work really hard to breathe so they breathe fast and they use a lot of accessory muscles to induce that process so watch out for diff avolar filling stimulating ards stimulating a drop in oxygen increase in respiratory distress this is another potential complication so if a patient comes in with low blood pressure Tacho cardia not making good urine acute kidney injury and difficulty breathing with hypoxemia and the setting of epigastric abdominal pain definitely thinking about systemic complications from pancreatitis if that's not enough there's other things that happen these inflammatory cyto kindes they stimulate particular enzymes that are present inside of our bloodstreams uh bloodstream and this this kind of like nasty enzymes here are called tissue Factor now these are naturally kind of like coagulating kind of related enzymes now whenever this is massive inflammation inflamation always kinds of pro causes problems with coagulation Cascades and what it does is it stimulates an increase in the activity of tissue Factor now tissue Factor wants to induce clotting and so what happen is this will stimulate an increase in the clotting process it'll do it via the extrinsic pathway yeah and now once this happens you're going to start seeing an increase in the clotting process so now I'm going to throw clots everywhere I'm going to have clots all over the place because of this massive systemic inflammation it's causing diffuse clotting so let's actually write the time it's diffuse it's not just in one location because it's systemic it's kind of going throughout the bloodstream what happens is is this leads to what's called consumption and this is what's terrifying about it it consumes platelets to make the clots it consumes red blood cells to make the clots it also uses a bunch of coagulation proteins and so this affects what we call the PT INR the PT and then it causes a lot of like these little degradation products to also kind of be present in large amounts and so what happens is these patients will have weird lab values because of increased consumption of coagulation factors and things that I need to make clots and so what happens is their platelets get consumed so they drop so they develop thrombocytopenia their red blood cells drop they develop anemia but because this is the weird thing you consume so many of their clotting proteins that they don't have enough clotting proteins to be able to help them for any more clots and so what happens is their PTINR goes up which means that it takes longer for them to be able to clot which is it sounds paradoxical right PTT goes up meaning it takes longer time for them to clot and they have an increased amount of dher which means there's lots of clotting going on so the weird thing about this is that they're clotting diffusely but their labs are maybe concerning that they can't clot anymore and that they're at higher risk of bleeding this is a weird paradoxical thing of where these patients are clotting everywhere but they're also having a high risk of bleeding because of the pathophysiology we just discussed this disease whenever you see this is very suggestive of what we call uh what we call disseminated intravascular coagulation okay so I want you guys to watch out for diic DIC ARS Aki shock all in the setting of pancreatitis if that wasn't enough pancreatitis causes massive systemic inflammation but it also causes a lot of inflammation localized to the pancreas when this occurs same concept again stimulate white blood cells stimulate white blood cells these pump out what same thing they pumped out everything that we just talked about before Bunches of cyto and these cyto that we kind of elucidated here are interlan one tumor necrotic Factor Alpha there's even interlan 6 as well and again there's going to be lots of these nasty enzymes that are kind of being released that are really suggestive of pancreatic inflammation and that's all these like lipases and proteases so large amounts of these bad boys right now problem is is that these things not only cause capillary permeability of the systemic blood vessels they cause capillary per ability to increase for the pancreatic vessels so here's your pancreatic vessels so these are vessels that are found in or around the pancreas now these things get super leaky because of those cyto kindes if they get super leaky what happens fluid will leak out of these into the surrounding pancreatic spaces and into the pancreatic tissue and that is the potential complication that we'll see I'd say by far out of most of the complications local complications that you see within this it's primarily going to be this which is going to be aditus related pancreatitis so now you're going to get tons of this kind of like pancreatic edema that's going to start forming so you're going to get a lot of what's called pancreatic edema right now this happens and when this occurs and if it's less than usually less than 4 weeks since they've had the initial insult of pancreatitis this edema will accumulate in particular areas but it won't be like super encapsulated and really really large but it'll have these like these acute pancreatic fluid collections this is super characteristic and I'd say 85% of the complications related to local complications is this right here so super super common you're going to develop a lot fluid collections in and around the pancreas and we call this acute pancreatic fluid collection this literally accounts for probably 85% of the local complications of the pancreas all right it's just a lot of this edema because of capillary leakage what can happen and can bring about further complications is if this kind of like edema continu and then when the edema continues maybe you have some areas that are still showing a lot of like pancreatic fluid collections but then they started to become really really encapsulated en large in cystic appearing and usually this complication usually develops greater so over a period of more than four weeks if they move into this next period here where it starts to look a little bit more organized and large and cystic now we have a pancreatic pseudocyst now often times this is a super common complication and patients usually are relatively asymptomatic and they probably never even know that they have one of these dang things these are the pseudois what happens is if these pseudois potentially have a couple other things happen to them so let's see the pancreatic pseudois becomes infected so if I stimulate an infection of this pan ptic ptosis I already told you what the primary trigger and reason why they would develop infections of the ptosis what was it hypovolemia so low blood volume leading to low perfusion of the of particularly the bowel becomes es schic bacteria cross the bowel because it no longer has the good mucosal Integrity gets into the bloodstream and goes and infects these dang pseudois and then you get an infected ptosis so hypovolemia is a really really big trigger here and this can lead to what's called an infected pseudois how would I know the difference often times these are accompanied not just with pain but also systemic features maybe an increase in the white blood cell count maybe a fever that'll start to rise along with potentially increasing pain all right so watch out for that this is a big thing to watch out for a potential infected pancreatic pseudos saste the other thing is that these things can rupture or the the other thing is not only can they rupture they can compress bow so in this particular scenario let's say that I actually cause it to I stimulate a rupture and if I stimulate it to rupture it'll rupture right into the perenium and this could potentially ensue and lead to what's called to peritonitis okay peritonitis would lead to definitely a lot of systemic features like increasing white blood cell fever but you'll also have abdominal pain you'll have rigidity guarding rebound tenderness all right especially in the setting of pancreatitis and the last thing is it also can potentially cause um it can stimulate it can get large enough and bowels large a small intestine run around this area so small intestine usually the duodenum runs right around this area if these things are big enough they can Mash on the dadum and they can cause bow bowel compression and if they do they can lead to a small bow obstruction and so that's another thing that I would want you guys to watch out for is features of cramping abdominal pain abdominal distension vomiting obstipation due to a lot of massive pancreatic pseudois compressing on it pancreatitis does cause a little bit of a localized ilas but I don't want you to get too too complicated here the other thing is if these things get like super super huge if the if these things get really really really big in size they can potentially cause increasing pain but often times these are usually asymptomatic and you usually never know that they are causing any kind of issues and you just leave them alone here's the next concept so the next concept here is we talked about the emitus complication right so we said if we stimulate edema remember I told you how edema was a big complication here well the other complications here are going to be necrosis and then the most feared the Hemorrhage remember I wrote this down in the first aspect here this is the other complications that can arise out of these edema accounts for 85% of the local complications necrosis accounts for about the remaining 15% all right Hemorrhage doesn't really occur that often it's relatively rare but we'll talk about it because they like to ask this dang thing on the exam when patients experience necrosis they have all this pancreatic inflammation and tissue begins to Die Why does tissue begin to die well you get lots of what's called tissue necrosis and this tissue necrosis occurs for two particular reasons one is autodigestion you get autodigestion and inflammation that will cause tissue necrosis but what else can worsen and cause tissue necrosis hypovolemia so I think it's a really big Point here if you haven't gotten it already that low blood volume is a very profound stimulus for tissue necrosis and also autodigestion from the initial insult is also a profound stimulator of tissue necrosis so if a patient's hypovolemic they're not going to perfuse what their pancreas and if they don't peruse their pancreas that tissue will become es schic and it'll start to become necrotic now acute pancreatic necrosis can occur and if it does occur you can potentially see these patients have a little bit worsening abdominal pain maybe some slight systemic features but often times it's important to remember that this again usually develops in the first four weeks similar to acute pancreatic fluid collections these develops in the first four weeks what can potentially happen further is if this pancreatic necrosis continues to occur and what happens is this necrotic tissue over time over greater than a 4-we period gets walled off so now what I'm going to do is I'm going to wall this off wall this off wall this off wall this off you develop somewhat of a capsule around it and this is very very common and indicative of what's called wall off necrosis thus the name this is now a patient who's moved into what's called wal off necrosis once we've gotten to this point that's usually when you've gotten to greater than than four weeks so after greater than four weeks if you progress to this one that's when we'll see this complication why is this one scary wal off necrosis can become infected it can easily become infected and this is the terrifying thing if a patient develops an infected necrosis this usually the only thing that you can really do for this you can try to treat it with antibiotics but often times you have to go in and debride the infected necrotic tissue so infected necrosis is something that you don't want to see what would be a trigger of infected necrosis I've said it a million times hypovolemia so if patients have hypovolemia you're not profusing the tissues particularly the pancreas so it's wors in necrosis and if you don't have good blood volume you won't peruse the bowel if you don't peruse the bowel you won't allow for good delivery of oxygen to the bowel the bowel will become es schic if the bowel becomes es schic translocates back IA gets into the bloodstream causes an infection of that walop necrosis and these patients can get super super sick they will look septic and again worsening abdominal pain pretty classic here one of the big things that you'll also see is systemic features right and so you may see an increase in their white blood cell count and a worsening fever and these are the things that you'll have to watch out for often times these kind of findings are often CT findings they're radiographic findings that we can see and we try to clinically correlate but you have to remember these timelines less than four weeks is acute pancreatic fluid Collections and acute pancreatic necrosis no problem here not infections over four weeks you go into pseudois don't really cause problems wal off necrosis doesn't really cause a ton of problems but if the pseudois become infected terrifying wal off necrosis becomes infected terrifying I'd say the most terrifying complication that can occur here is if the necrosis continues to occur so let's say that you develop an acute pancreatic necrosis and it actually starts to necrose and it erods into a blood vessel so it erods into a vessel that's kind of like around the pancreas that's terrifying you have the gastroepiploic arteries the gastroduodenal arteries that are nearby if these things start to erode and they chip away at these arteries what happens is most of the pancreas is retrop paranal parts of it some parts of it are intrarenal but when it leaks blood it'll leak it into the retrop parital space and these patients will start to experience what's called that's the name retr peraonal bleeding now these patients can become hemodynamically unstable but often times what what we look for is these classic hematoma findings so what are some of these hematoma findings that I think are super important to remember if you see a c so kind of make like this little little half C's here around the belly button that's called colon sign so this is called the cins too many L's Colin's sign all right so make some C's around the Bell button that's bleeding on the actual skin that you'll see from that retrop parital space if they bleed on the flanks all right here on the flanks that's gray Turner sign and these are often times commonly associated with again a patient having pancreatitis but more particularly the worst case scenario of pancreatitis where the inflammation has caused necrosis and the necrosis has spread all the way to the nearby blood vessels and eroded them away causing bleeding to occur the last thing that I want to briefly briefly talk about here because it's annoying and I think often times we get so focused on the fact that okay they're hypo I better give them enough fluid that is the case you want to give them an adequate amount of fluid and resuscitate them but you don't want to over resuscitate them here's why whenever a patient develops pancreatitis pancreatitis causes third spacing and this is via that capillary leakage process that we already talked about so these things will exude and leak fluid out what's one area that they will leak fluid out the parium and when they leak this fluid out it's called an exudative aites and so these patients will often develop what's called aites right their sag ratio will be less than 1.1 because it's an exuded process then what we'll do is will give them oh man if I let them get hypo liate they can get walled off necrosis they can cause a potentially p ptic infected necrosis and pancreatic infected pseudois oh I better I better give them like 20 L of fluid and we over resuscitate them and that excessive IV fluids causes all of this pancreatic this all this AES to get worse and what happens is this causes a patient to develop something called where they're uh intra they're they develop an increase in their abdominal pressure so they develop an increase in what's called intraabdominal pressure pressure when that pressure pumps up above 20 it starts choking off organs and we call that abdominal compartment syndrome and this is a terrifying complication and it's hard to identify because it seems like it's just pancreatitis on its own but abdominal compartment syndrome is when the pressure in the abdomen is so high that what it does is it compresses on a couple different organs three that I want you to remember one is it compresses on the diaphragm they can't take a deep breath in because their diaphragm is getting smashed they get to kipic second it compresses the venne Hava they don't get blood return back to their heart they get drop and Venus return their blood pressure drops hypotension third it compresses the kidney vessels and they develop acute kidney injury so if a patient develops worsening acute kidney injury worsening hypotension and respiratory distress you definitely want to go thinking about checking a bladder pressure and thinking do they have abdominal compartment syndrome I think the big thing to remember is all of these that we just talked about is only related to acute we didn't talk about chronic so for chronic pancreatitis there's three particular complications that I want you to watch out for malabsorption diabetes and uh pancreatic cancer whereas with acute I want you to think about sers and local pancreatic complications now with chronic pancreatitis the pancreatic function is down so you what's called a decrease in the exocrine function so the exocrine function goes down there's also an indoc crine function of the pancreas the endocrine function goes down the combination of these is what really will help you to set in and the patient who has chronic alcohol abuse or has cystic fibrosis to really think about chronic pancreatitis what happens is if I don't produce these enzymes such as proteas I'm not going to write them down we talked about them a lot in the malabsorptive section if I don't have good pancreatic function I can't make proteases to put into the Lumin of the intestine I can't make lipases and I can't make amales and there'll be a drop in the lipases proteases and amasis I'm not going to be able to absorb nutrients so what happens these patients won't be able to absorb proteins and because they can't absorb proteins they'll have muscle wasting and weight loss if I can't absorb car hydrates they'll have diarrhea flatulant and abdominal pain if I can't absorb fats they'll have like nasty fat containing stools called statera and vitamin A d e k malabsorption so these are big things to remember in these patients the second thing is that in these patients they have decreased endocrine function so if they have decreased endocrine function these eyelet cells of Langer hand can't make a particular hormone called insulin and insulin is really important because it's supposed to activate what's called pancreatic beta cells and if there's decreased insulin there's decreased stimulation of the pancreatic beta cells and if I don't stimulate these cells because I have no insulin signal here to work guess what happens do I bring glucose which I'll represent here in G can I bring this glucose into the cell no this is inhibited and so what happens is these patients build up glucose within the bloodstream what's that called hyperglycemia what are the features of hyperglycemia usually in a patient who has diabetes polyphasia polyurea polydipsia the last one and probably the most unfortunate complication of chronic pancreatitis is pancreatic cancer pancreatic carcinoma usually what happens is with chronic inflammation this is a recipe for dysplasia so there's an increase in dysplasia because inflammation causes cells to have to adapt and whenever they adapt Unfortunately they can become cancerous and one of the cancer is usually pancreatic adnoc carcinoma and this usually forms near the head of the pancreas most commonly so pancreatic adoc carcinoma is by far going to be a very common complication from repeated bouts of inflammation to the pancreas how would this one generally present often times it causes persistent abdominal pain from compression of nearby structures second it causes hypercoagulation these patients clot like crazy and third it compresses the biliary duct and the the flow of bile so they often sometimes develop jaundice and so it's important to remember that but we'll talk about that in its own section on GI cancers all right my friends that covers the complications of pancreatitis now let's move into diagnostic approach the last thing here is going to be how do we diagnostically approach these diseases especially acute pancreatitis and we'll talk about chronic pancreatitis really briefly both of these patients is going to come in with epigastric abdominal pain right and it's usually going to feel like it's wearing its way into the back they may have some Associated nausea and vomiting what I want to do is I have to remember the most important enzyme that is leaked out of the pancreas during the initial injury is light Pace if it is elevated at least three times the upper limit of normal it has to be acute pancreatitis in patients who have you know chronic pancreatitis their lipce is not usually elevated it's usually normal so if I see a normal life Pace it's not acute pancreatitis it could be chronic pancreatitis though so how do I kind to really think about chronic pancreatitis I have to remember this is a person who maybe comes in with epigastric pain maybe they have some malabsorptive features maybe they also have um you know some other issues that make me think that they could have chronic pancreatitis well if that's the case I should obtain a fecal elastase the reason why is this is another pancreatic enzyme that's released and if it's in low amounts in the feces it really suggests that the pancreas is just not working its exocrine function is really declin mind and that would then take me to The Next Step which is let's look for the calcifications and let's look for the fibrosis of the pancreas here in the CT of the abdomen so get the light Pace if it's normal it's not a cute pancreatitis unlikely then from there if you really have a strong suspicion they have epigastric abdominal pain chronic alcohol use cystic fibrosis malabsorption then I would start thinking could they have a chronic pancreatitis especially if they have diabetes too check the fecal last days if it's low get the CT the abdomen find the calcifications and fibrosis and then from there you should have a pretty good idea that they probably have chronic pancreatitis on the other hand though if that light pace is three times the upper Lim normal that's high that's an acute injury and that's really suspicious of acute pancreatitis now technically I could make the diagnosis and I'm done if I have a patient with the classic epigastric abdominal pain and a light paast three times the upper limit of normal there's not many diseases that do this I'm prettyy much done I got I got a q pancreatitis but if I'm uncertain maybe I'm not completely sure if they have pancreatitis I could go an extra step and I could get a CT of the abdom but it's really important to remember that the CT of the abdomen is not needed to be able to diagnose acute pancreatitis if I have an elevated life pace and epigastric pain what it's really more beneficial for is identifying complications especially in that four- week or greater than four-week frame so in the less than four weeks what were the two big complications that I want you guys to remember one's edema so acute pancreatic fluid collections the other one's acute pancreatic necrosis so here I can see that there's areas of dead tissue here in the pancreas and good amount of edma as well the other thing is if it's greater than four weeks if it's greater than four weeks there were two things one is a pseudocyst so you see here is a pancreatic pseudois that's taking place there's a walled off encapsulated area of fluid collection the other one would be a walled off necrosis and so I can see here that I have areas that are walled off in this necrotic tissue and so that's definitely going to be indicative of complications that we can see in the patient having aute pancreatitis but let's say that maybe I have a patient here they only have a lipace elevation they don't really have any epigastric abdominal pain I get a CT of the abdomen and it definitely shows oh wow the pancreas is kind of got this fat stranding here it's definitely a Demus okay they they definitely got a C pancreatitis because there's only a couple things there's really not many things that will elevate your life Pace to three times the Lev of normal and if I have a CT that shows me that the pancreas is inflamed I have the diagnosis so the next thing I think that's really really important to determine is when a patient has acute pancreatitis we said there's ductal cell injury like gallstones ercp and then we said that there's a Sinar cell injury alcohol use hyper triglyceridemia hypercalcemia and drugs the big one that you can't miss that you have to find quickly because it can become really bad if you miss it is gallstone pancreatitis and so what I think is best is if you think that there is any evidence of G Stone maybe they have some rer quadron abdominal pain maybe they have some jaundice they have some elevation in their Al fos or their ggt then I should go ahead and get a right upper quadron ultrasound and look to see hey what's their their bile duck like like oh it's crazy dilated oh do I also see a stone that's maybe present here then if that's the case I probably have a patient who has a gallstone pancreatitis and that's their cause and I need to send them to get an ercp potentially all right so with that being said that's a lot to talk about I think the biggest thing to remember here is that sometimes what we try to do in these patients who come in with a Q pancreatitis is we try to First find do they have an elevated light Pace epigastric abdominal pain cool I got the diagnosis if maybe they only have one of these two then I would go to a CT abdomen to look for evidence of inflammation really the CT abdom is better to identify complications though and then again light Pace if it's normal run down this list and think about chronic pancreatitis let's talk about one more quick thing this is called the Ranson criteria the Ranson criteria is actually something that we use to determine the chance of mortality for the patient helps me to guide like what level of care should I give them and what we do is on admission we look at a couple different things we look at what's called a ga law so glucose is it really elevated greater than 200 this is usually a reactive process to inflammation is the a greater than 250 is the LDH greater than 350 is the age greater than 55 and is the white blood cell count greater than 16k so just remember GA law this helps in basic basically we plug this into a calculator and determine their number gives us an idea of what their mortality and what their chances of dying are and helps us determine how aggressive we need to be in their care after them being in the hospital for 48 hours we can also then extend this prognostic indicator to look at what's called cah hob so what's the calcium level the next thing is uh the hematocrite has a drop by greater than 10% is the oxygen less than 60 is The Bu increased by greater than five is the base deficit greater than five and is their sequestration of fluid that's greater than six liters if I had to give them a ton of fluid to maintain normal volume and again this is something that we would look at to determine their chance of mortality prognosticating and determine their level of care it's not something that I want you guys to go cam on memorizing everything for but try to know that this is a tool that we use to determine the prognosis the mortality of these patients and what level of care they require now let's go and finish this off with again how do I diagnose a c pancreatitis because this is really important one is I need at least two of the three I need epigastric abdominal pain I need a liace three times the upper limit of normal and if I have a CT abdomen that shows pancreatic edema fat straining maybe some of these complications potentially I have the diagnosis of acute pancreatitis all right we have a patient who comes in they have epigastric abdominal pain they have a light Pace three times they have limit of normal they have a CT skin that shows that they have evidence of pancreatic edema and fat stranding they got aute pancreatitis how do we treat these patients well first thing I told you is that if it's a stone and you find it on the right upper quadrant ultrasound you have to get that thing out so usually an ercp is usually going to be the thing that we'll do now often times if they have severe pain we will go and do this but the other thing that you want to watch out for is that ercps they do have the complication of wors in pancreatitis and so often times the one of the reasons why we'll maybe hold off a little bit and give them some time is to not worse in the pancreatic injury but if they have a gall stone that's causing jaundice it's causing Fe fever as causing right upper quadrant abdominal pain and maybe even a lucyisanerd in colangitis the other thing is I really don't want these patients to have hypovolemia and develop shock I don't want them to have an acute kidney inury so often times we need to give them good amount of fluids because they're third spacing the fluid and so you need to give them fluids intravascularly replete them to improve their blood pressure improve their tack of cardia and improve their profusion to the kidneys it's just important to make sure that you monitor their heart rate their blood pressure their urine output to make sure that you're not over resuscitating them and pushing them into abdominal compartment Centum or that their heart rate and blood pressure is still altered they're not making much urine and you need to again give them more fluids so monitor those things closely the other thing is that the pancreas is pretty close to the dadum it can compress it some of that local edema can cause some compression of the the small intestine and make it harder for the patient to be able to want to eat the other thing is that pancreatic enzymes are needed in order for you to digest food so it can make it harder to digest food if the pancreas is super inflamed and so sometimes we will give a small amount of time maybe 24 48 hours and then we'll start slowly introducing food back into them but often times initially make them n and then over time you can start pushing them into giving them food whether that be through an NG tube or whe whether that maybe be through just them eating on their own if they have the ability to remember I told you pseudo cyst we really won't do anything for but if a patient develops a ballop struction they develop a rupture they develop an infected pseudocyst or they develop an enlargement to the point where it's causing compression and pain we should actually go in and endoscopically drain that pseudocyst so we'll take this kind of like a little Contraption down here we'll go through the stomach because right behind the stomach is the pancreas we'll go right there and then we'll suck the actual fluid out of that pancreatic ptoy reducing its size reducing its compression of nearby structures reducing the risk of it rupturing reducing the risk of it compressing on the small bowel Etc the other thing is infected necrosis so often times if patient has a pancreatic necrosis like a normal pancreatic necrosis that's walled off or it's a q pancreatic flu necrotic tissue we will not do anything about it just make sure that we're trying to supportive care of that patient no need for antibiotics but if they start to develop worsening pain they start develop worsening Luc cytosis they start developing a really high fever and they're just not getting better and their CT scan shows that they may have areas of infected necrosis you have to put these patients on antibiotics but again we won't put patients on antibiotics with acute pancreatitis unless they have concerning evidence for infected necrosis the other thing that we could consider is if it's really bad there's a lot of infected tissue you may have to go and debride that tissue so sometimes they may do a debridment of that area of infection another thing that's really important to remember is identifying abdominal compartment syndrome so sometimes in patients who have really bad pancreatitis with the pancreatic AES and also they're getting a ton of O IV fluids and maybe they're getting a little bit more tnic maybe they're getting a little bit more hypotensive maybe their kidney injuries are getting a little bit worse and if they're on the ventilator maybe their Peak pressures are going up I should definitely check a bladder pressure and see if they have a high intraabdominal pressure and if they do and it's greater than 20 then I need to go ahead and I need to decompress them right away and often times that could be going in and doing like a fasciotomy to do that process now in patients who have chronic pancreatitis it's important to remember these patients have done a lot of damage to their their pancreas and more it's just trying to prevent them from having further malabsorption and prevent them from deing further injury so often times the goal of treatment is just treating their cause alcoholism try to abstain from alcohol but often times it's just treating their pain these patients can have a significant amount of pain so it may start off with they may go to nerve blocks sometimes they even require surgical reection of the pancreatic areas but I think the biggest thing to remember for chronic pancreatitis here the most important point is that these patients will develop malabsorption and so you may have to supplement them with pancreatic enzymes because it's not making them you may have to give them the pancreatic enzymes so that they get an optimal amount of absorption of proteins fats and carbohydrates all right my friends that was a lot with pancreatitis I hope it made sense I hope that you guys did enjoy it and as always until next time [Music]