Acute Pancreatitis | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment

what's up ninja nerds in this video we're going to be talking about acute pancreatitis so buckle up if you guys want to follow along though with some awesome notes some illustrations please do so down in the description box below there'll be a link to our website go check that out also you like these videos you benefit from it it truly helps if you have fun please support us by hitting that like button commenting down the comment section and please subscribe let's get into it all right ninja so let's talk about pancreatitis first off acute pancreatitis is an inflammation of the pancreas now that we know that the pancreas is a very special type of heterochronic gland right so it's an endocrine gland and an exocrine gland we're going to be kind of focusing more on the exocrine portion which is the secretory portion that makes different types of digestive juices right so we we take a look at the pancreas in general right you know that you have this little ductal system here so you have all these pancreatic ducts and the whole point of the pancreatic ducts is that from these pancreatic ducts it connects particularly the main pancreatic duct connects to our gi tract and that's where we dump a bunch of different things into the actual duodenum so this kind of tube here would be representing the duodenum and then this here is the pancreas now the pancreas makes a bunch of different types of things digestive juices which consists of pancreatic enzymes and a bicarbonate-rich fluid but in order for us to understand those two different things we have to really zoom in because there's two components of the pancreas so the pancreas is made up of a bunch of different portions right so the biggest part is that we have this ductile system and there's a bunch of different ducts right so you have the main pancreatic ducts you have all these different types of small little ducts as well then you have this portion here which is these like little sac-like structures here that we're going to zoom in on and these are called the acenar cells so let's kind of take a look at these kind of in a zoomed in view so again what i want you to remember is pancreatitis inflammation of the pancreas what's the big function of the pancreas it secretes different types of pancreatic juices digestive enzymes bicarbonate rich fluid into the gi tract particularly the duodenum now if we zoom in on kind of parts of that pancreatic structure we have here our ductal system so this is our duct and then we have these tiny little accessory ducts right these tiny little ducts that are coming off here and branching into these things called a senai now what i want you to remember is we're going to represent these as purple these little cells here that are lining these tiny little ducts this is called our ductal epithelium now what's the purpose of the ductal epithelium it's supposed to make a bicarbonate rich type of pancreatic fluid so that's the job of these little ductal cells the job of the ductal cells is to be able to secrete kind of a nice thin bicarbonate rich pancreatic fluid okay that's the job of it now these cells here which are called your acinar cells which are the ones in orange right so what are these cells here called these are called your acenar cells let's zoom in on them and see what particularly they do so we know that the little ductile epithelial cells make pancreatic secretions in fluid rich in bicarbonate the acenar cells these bad boys the ascent our cells are the secretory cells these are the ones that make all of those digestive enzymes okay and there's a bunch of different types of digestive enzymes that they make and we'll talk about some of these but what i want you to remember is here we have these ascendant cells we're zooming in on one of these little asyni okay these cenar cells have their nucleus right which contains their dna right the dna has to get transcribed when it gets transcribed it makes something called mrna mrna will then go to our rough endoplasmic reticulum which contains ribosomes it'll get translated into proteins those proteins will then get synthesized into vesicles those vesicles will then get taken to the golgi the golgi will then go ahead and form those modify them a little bit and package them into nice little vesicles so now we're going to have here a vesicle which is going to be containing a bunch of different types of proteins and enzymes and things of that nature okay so let's say that we take a look and kind of zoom in on these like vesicles that contain these very interesting types of digestive enzymes so here we're zooming in on this granule here so this is a granule located inside of the a cinar cell in this granule we have these things in here called zymogens so zymogens are basically the inactive form of the enzyme so i just want you to remember they're the in active enzyme so it's just the enzyme and it's in active form now there's different types of these enzymes let's imagine here these blue ones here these blue ones here these are called let's say lipases so you have different types of enzymes you may have what's called lipases you may have these ones here in maroon let's say these maroon ones here these are called amylases so what do lipases do they break down lipids they break down triglycerides amylases break down sugar what else could we have in here now the red ones is the one that i want you to remember these are your proteases and these are the ones that are going to be breaking down tons of proteins and then you have one thing in there because here's the thing these zymogens they're the inactive enzyme we don't want them to be activated unless there's a particular scenario where we need them which is we need them in the duodenum and then they get activated there to be able to chop up the different proteins that we consume in our diet to chop up the lipids in our diet to chop up the carbohydrates in our diet but when they're in our cells being stored we do not want them to be activated so we have a very very special enzyme that sits within these granules to keep the proteases inactivated very specifically the proteases what do you think we call this black enzyme here this is called the protease inhibitor real original right it's a simple thing so we have protease inhibitors which are present in these granules to keep them in the inactive state we don't want them to be activated when they're not in the duodenum okay so here's what i want you guys to remember how does pancreatitis develop inflammation of the pancreas but very very specifically damage of the pancreas that maybe alters the digestive enzyme secretion into the duodenum you know how this actually happens it happens by two ways one way is we have some type of negative effect here there's some type of obstruction within the ducts with in the ducts okay that's one particular thing if you have an obstruction so let's imagine here let's say that you have like some type of instruction whatever the reason is we'll go over the different causes let's say here that you have an obstruction in this duct you have an obstruction here at this part of the duct you have an obstruction at this part of the duct what's that going to do you're going to have all these secretions that are going to build up behind that that blockage and so that's going to cause the pressure to start rising and if the pressure starts rising in these ductal cells and in the assini guess what that pressure does it alters the normal movement of enzymes if you kind of alter this basic process where you want to kind of excrete out these different enzymes okay you know what happens you know what you have inside of your cells you have these things called lysosomes and whenever you have this back pressure due to some type of obstruction and the pressure builds up behind that obstruction this alters the normal excretion process of the zymogens and then the lysosomes will start fusing with these actual granules containing the zymogens you know what lysosomes can do lysosomes can activate specific types of proteases and you know what that leads to oh no then i'm able to release out these active proteases and these active proteases will start causing destructive damage to the pancreas auto digestion of the pancreas so that's one way one way that we can lead to pancreatitis is you develop an obstruction within the ducts causing a back pressure altering the normal movement of enzymes which should go mrna to ribosomes to package into vesicles to golgi to granules which should be excreted and then activated in the duodenum but because of the obstruction the back pressure alters this normal movement instead this obstruction of the ducts leads to lysosomes inadvertently fusing with the granules activating those proteases when they should not be activated in the pancreaticus in our cells in the ducts and it starts auto digesting the pancreas that's one way you know what the second way is the second way that we can cause this is you cause damage the ascendant cells directly if i damage the acinar cells directly i damage these this can also stimulate this process it can also lead to the release of these zymogens the release of the lysosomes they can then become activated within the pancreatic ducts or smaller ducts boom you lead to activation of pancreatic proteases they start causing auto digestion of the pancreas so now my question to you is what are the things the particular types of causes that lead to obstruction within the ducts or lead to direct destruction of the nsnr cells that leads to auto-digestion of the pancreas i'm so glad you asked so the first one that i want you guys to remember is gallstones this is by far the most common cause so gallstones how does this do it well you know you have your gallbladder here and then the gallbladder has what's called the cystic duct then the cystic duct will fuse with the common hepatic duct to make this thing called the common bile duct well you know the common bile duct will come down and fuse with this orange structure here what's this main duct of the pancreas called this is called the main pancreatic duct when they fuse they make this structure called the apatopancratic ambulant this portion here is where you spit the digestive juices the pancreatic enzymes the bicarbonate rich fluid and bile all into the duodenum this is all at that portion right there what if someone gets a stone they have a gallstone here that gallstone pops off pops out and it gets stuck right here at that apatopancratic ampulla now if it gets stuck here can you secrete all these digestive enzymes out no what happens you start developing an obstruction and a back pressure what does that back pressure do it alters the normal movement of the zymogens to be secreted they inadvertently combine with the lysosomes they lead to the fusion and inact and then lead to direct activation of those enzymes and they start causing destruction of the pancreatic tissue auto-digestion so this is one of the causes that i want you guys to remember the most common cause is going to be gallstones so the most common okay and specifically gallstones that form right at that hepatopancretic ampulla okay what's the second most common cause the second most common cause is ethanol so alcohol abuse right usually you see this particularly in patients with chronic pancreatitis so they have chronic pancreatitis because they're constantly drinking alcohol and then they develop an acute exacerbation of their chronic pancreatitis okay so how does ethanol do it ethanol is a son of a gun it does it by a bunch of different ways one it's weird is imagine here's kind of a glass right a glass of wine this actually can directly stimulate your center cells it's really weird they can take and work directly on the incentive cells and when they work directly on the ascendant cells they cause these zymogens to be released so they increase the release of these zymogens but whenever they do that because you're pushing so much of these zymogens out into the actual ductal system some of these can get undesirably activated and start causing pancreatic auto digestion you know what else it can do it's an interesting thing it can also tell the epithelial cells remember those ductile epithelial cells that we have right here these ones right here it tells these ductile epithelial cells to make a very thick type of bicarbonate rich secretion so it really makes it a super super thick kind of mucusy type of secretions here and as you start getting a lot of these thick and mucusy types of secretions because of the alcohol what does that do that plugs up the ducts it obstructs them causes back pressure alters the normal movement of the zymogens leading to them combining with the lysosomes and then inadvertently leading them becoming activated pancreatic auto digestion okay so that's another way as we can lead to increase thick ductal secretions the next way that it actually can work is it can activate it can activate these things called neutrophils so one of the things that we see is that the alcohol can actually activate and stimulate neutrophils you know what neutrophils can do if you have lots of alcohol and you stimulate the neutrophils particularly to come to the area of the pancreas it increases the production of reactive oxygen species it increases the production of proteases and what do these do they lead to direct destruction of the ascent our cells if you destroy the essential cells you cause them to release tons of zymogens if they release out these zymogens and it leads to the proteases getting activated what are the proteases gonna do they're gonna cause auto digestion the pancreas lead to inflammation boom roasted so we got gallstones as the most common ethanol is the second most common let's come down to the third thing the third one that i want you guys to remember is trauma but again it's a simple concept any kind of trauma really it has to be more specific like a penetrating trauma because that's going to cause direct damage to the essential cells so we want to really think about this as a penetrating trauma so imagine someone running around with a meat cleaver or like a i don't know some type of like sickle and they're trying to cut you up right so some type of penetrating trauma is going to cause direct injury to the center cells if you directly injure the ascent our cells they increase their zymogen release and if you increase the release of the zymogens and you stimulate those proteases they're going to start causing destruction of the pancreas auto digestion okay the next one that i want you guys to think about here this one's actually a it's not super common but it definitely is something to be keeping on your deferential is hypertriglyceridemia triglyceride emia this basically elevated triglycerides within the blood but whenever you have hypertriglyceridemia you know triglycerides they're actually particularly absorbed across the gi tract and when they're absorbed across the gi tract they actually get packaged in our enterocytes and when they get packaged into our enterocytes they get packaged into these little thingies these tiny little like lipoproteins which are called chylomicrons you guys know those structures they're called chylomicrons we'll abbreviate it ch so you absorb the triglycerides across the gi tract and if somebody has some type of genetic disorder or they're just having a large consumption of triglycerides they're going to get lots of chylomicrons so anything that really increases your triglycerides whether it's a genetic cause whether it's because you have a high consumption whatever it is lots of these chylomicrons get actually taken up into r eventually they get into the lymphatic circulation then they get into our blood circulation once they get into the blood these tiny little guys they're tiny little ones they can get stuck in small capillaries that supply the pancreas so if these chylomicrons get stuck in these capillaries what happens to the oxygen supply to the pancreatic tissue there's a decrease so now there's a decrease in the oxygen supply what happens if you have less oxygen that you're supplying to tissues they can start to become ischemic and what happens if that ischemia isn't actually corrected it can lead to necrosis or death of the pancreatic tissue and that can therefore lead to pancreatitis so we have so far gall stones we have ethanol we have penetrating trauma hypertriglyceridemia let's come up and talk about more potential causes all right what's another common cause another one that you want to be thinking about is if someone is taking any kind of corticosteroid okay so this is technically a drug related one but it's a very specific one and it's going to help us out with our mnemonics so steroids can also do this and steroids are interesting because again they work on that ductal epithelial cells and you know what they do to the doctor epithelial cells they tell those ductal epithelial cells to increase their secretions to make them a little bit thicker and so as a result the secretions by the ductal epithelial cells become thicker if you have an increased thick secretions that's going to cause an obstruction within the ductal system and that obstruction is going to lead to eventually the higher pressures altering the normal cascade movement of the zymogens being secreted and then being activated in the gi tract instead they become activated in the cells and then released this can lead to destruction of the pancreas and that then can lead to pancreatitis okay what else the next one especially in children you want to think about this is the mumps virus so the mumps virus can also do it two ways one is that this virus has the ability to directly act on the ductal epithelial cells and destroy these epithelial cells but also they have an ability to act directly on the cinar cells and if they act on the essential cells they cause the release of the zymogens if the zymogens are released they have the ability to increase their activation by combining with different types of hydrolytic enzymes particularly from the lysosomes and increasing the activity of the proteases and those proteases will start causing destruction of the pancreatic tissue what else so not only did that let's come down and talk about another one another particular one that you want to be thinking about is autoimmune you know autoimmune diseases very very specific types like for example you know whenever you produce antibodies against your own tissues unfortunately in certain conditions you know uh for example like maybe produce these things called ig g4 antibodies that could be one or you're producing other different types of antibodies related to sle related to rheumatoid arthritis you know these different types of antibodies may go and actually directly destroy the epithelial cells that are actually secreting that bicarbonate rich fluid and they may go and actually destroy the asynar cells leading to the inadvertent release of the zymogens and their undesirable activation to form activated proteases and now that these activated proteases are formed they can start causing destruction of the pancreatic tissue boom so we kind of got a kind of similar kind of flow here right so mumps autoimmune guess what the this one here it's probably the most random one it's the most interesting but it's probably the most rare and it's scorpion bites so scorpion particularly the toxin that's released by the scorpion so whenever the scorpion stings it releases a toxin and that toxin that it actually releases causes destruction of the epithelial cells of the ducts which again alters the bicarbonate rich fluid secretion but it also causes direct destruction of the ascinar cells releasing out those zymogens those zymogens become undesirably activated and when they become activated and form those proteases these proteases then start causing destruction of the pancreatic tissue oh my gosh it's like a never-ending cycle here right the last particular cause that i want you guys to think about here well actually the getting close to the end here is drugs now drugs may do this by a bunch of different ways particularly kind of inside the cell we don't have a complete understanding of how exactly these drugs do this but we know that there is very specific drugs that seem to track along with this disease some of those that i want you guys to remember tend to be your sulfa drugs so any kind of sulfa drug whether that be like bactrum sulfasalazine which is kind of used as a particularly like ibd even like ferocimide like any of those loop diuretics those potentially can cause pancreatitis another thing that you want to remember is any kind of like hiv medication particularly like your um nrtis or your protease inhibitors those can do it and another one is certain types of diabetic medications particularly those of like the glip one uh diabetes meds okay diabetes uh diabetes mellitus medications there's a bunch of different medications that can cause this but i want you guys to be thinking about like any kind of sulfa drug hiv medications your glyph1 medications these potentially can cause pancreatitis okay over here we have another potential cause this one is a very interesting one it's another one that you definitely want to remember it's called an ercp okay it's an endoscopic retrograde cholangiopancreatography so ercp it's basically a procedure that we do in someone that we think has a gallstone type of cause for pancreatitis or they have some type of thing where we need to go up and remove some type of stone so you basically take this camera you go around here where that pain paddle pancreatic gamble is you make a little cut of the patel pancreatic sphincter this little muscle here you go through the duct and then you go up through the common bile duct and if someone has maybe like a gallstone right here it can utilize that to diagnose the particular stone and remove the stone so it's kind of a therapeutic process but if in the process maybe that causes damage to the pancreatic tissue that can then lead to the destruction of the cinar cells causing them to release the zymogens increase the proteas activity and then cause destruction of the pancreatic tissue the last particular cause that i want you guys to remember here is called hypercalcemia so hypercalcemia so hypercalcemia is a very interesting one it's also a very rare cause but what happens is let's say that somebody has hypercalcemia when they have hypercalcemia a lot of that you know calcium is distributed through the blood taken to different areas certain organs like the pancreatic tissue you know whenever calcium is in high concentration calcium can actually directly stimulate these enzymes it can act as a kind of like a precursor to these enzymes and stimulate that particular proteases so normally your proteases should be held inactive but in the presence of calcium calcium can actually stimulate those proteases so as a result you may have an increase in advertent activation of proteases and those proteases can therefore cause destruction of the pancreas now before we move on here what i want you guys to think about is how really the whole problem is is that the pancreas is supposed to be kind of doing what here's your pancreas all right so here's our pancreas and let's say here is going to be the gi tract alright so here is our gi tract normally what happens is the pancreas is supposed to secrete these digestive enzymes into what into the duodenum and then in the duodenum they're supposed to be very special enzymes let's just put this enzyme here in like pink here this is a very special type of enzyme we'll call it an enteropeptidase okay so this enzyme is called an entero peptidase and what this enzyme is supposed to do is those pancreatic enzymes they're supposed to be inactive when they're present in the pancreas once they're secreted they're still inactive but once they interact with that enteropetidase they go from inactive to active so they're not supposed to be active until they're present in the duodenum and all of the processes that we just mentioned above whether it be due to an obstruction of the ducts that's altering the normal movement like cellular processes and cellular trafficking which leads to the inadvertent activation by combining with lysosomes or you're destroying the ascendant cells causing the pancreatic enzymes to be released into the ductal system and then they become activated either way they're becoming activated in the pancreas rather than in the duodenum and that's the whole issue now my question to you is how do i remember all these causes because there's so many of them don't worry you can remember the mnemonic i get smashed alright so how do we remember all of the causes because there's so many of them you guys are like oh my gosh i can't tolerate all these things don't worry i got you so you can remember all of these causes by the mnemonic i get smashed so i for idiopathic meaning we don't have any idea how the heck this happened g for gallstones which is the most common one so don't forget this one please ethanol which is the second most common one and trauma penetrating trauma s for steroids m for the mumps virus a for autoimmune would you like to think about sle think about particularly rheumatoid arthritis scorpion bites which is probably one of the more rare ones but it's the cool one and then h it's a double hypertriglyceridemia and hypercalcemia then we also have the ercp and the drugs the sulfa drugs the hiv medications some of the anti-diabetic medications of the glip one category so these are the particular causes that if you want a quick remembering of all of these causes and we can just move on to pathophys utilize this mnemonic now let's talk about the pathophysiology all right so let's talk a little bit about the pathophysiology of acute pancreatitis right so we have an understanding of the particular causes i get smashed right or the particular things that we just reviewed now once these particular causes lead to the damage of the pancreas the inflammation of the pancreas it'll lead to the very obvious clinical features and complications of pancreatitis what are those clinical features so think about it where is the pancreas located location wise it's located within the epigastric quadrant right so the epigastrium area right here okay now within that area if there's lots and lots of inflammation of the pancreas it should produce a referred pain localized to that area so what do we call that type of pain we call this a epi gastric abdominal pain okay abdominal pain now there's a couple things that we definitely need to talk about with respect to this pain that they may ping you on for the exam one of the things is that there's other things that are in that area that can also present with that kind of epigastric abdominal pain like a peptic ulcer disease so how do i differentiate that this isn't peptic ulcer related and it's actually pancreatitis-related well one of the big things is that the pain is constant and where peptic ulcer disease is kind of intermittent it depends upon what type of times we're eating food right so it's more dependent upon meal times so that's one big thing it's a constant pain the other thing is it radiates where does it radiate to well it radiates into the back peptic ulcer disease does that as well but it's different in the sense that it's constant whereas peptic ulcer disease is in different times that we're eating so it's radiates to the back that's another big thing here's the next thing that i need i need you guys to remember the other important type of piece of information is that there are certain positions that make it worse and certain positions that make it better when you're laying on your back you tend to stretch that area and cause a lot more pain so when you're laying supine laying down on your back it's actually much worse so the pain is much much more worse so that's one of the big things that you can remember is that laying supine it causes the pain to become worse whereas if you're leaning forward sometimes they'll kind of lean forward this will make the pain much much better and it just feels a little bit more comfortable less stretch on that area of the pancreas okay so that's the big things that i really want you guys to remember is very specifically epic gastric abdominal pain how do we opqr st it we know that it's constant we know it radiates to the back it's better whenever we're leaning forward and it's worse whenever we're actually laying down flat or supine okay the other thing that i want you guys to remember is respect that it has on our gi tract so imagine you have a lot of inflammation of the pancreas nearby what structures does it run nearby well here we're going to have the duodenum and then right above it we're going to have the stomach imagine causing so much inflammation that it causes the irritation and inflammation of the nearby structures enough so that if you have enough inflammation what could this potentially do to the lumen of the duodenum what could it potentially do to the lumen of the gastric outlet tract what could this do it could narrow it and all of that inflammation will alter the normal movement of food normally food wants to move from our stomach and then into the duodenum and then move from the duodenum into the jugenum so on and so forth but if you have so much inflammation because of the pancreas and the nearby inflammatory collections that it causes it may cause inflammatory compress it may cause inflammation of nearby structures or so much inflammation that's compressing on nearby structures if it's compressing near the duodenum are you gonna be able to get food past that no if you're compressing it near the gastric outlet are you gonna be able to get food past that no so as a result this may lead to abdominal distension because these areas are just going to balloon up like the michelin man and then if it gets so bad to where it distends it so much and you can't have food moving down guess where it's going to go it's going to come up and this may lead to the respective nausea and vomiting as well so these are big things to remember you know what else it can do because of all this inflammation nearby sometimes it can even hit nearby like small intestine areas they can affect their motility and if you have so much inflammation that it actually decreases the motility of the small intestine this can present with an alias so it can have decreased contraction of the smooth muscle so it can present somewhat like a bowel obstruction but it's not a mechanical bowel obstruction it's like a physiological one and so sometimes if you're actually auscultating their belly and they're having less motility what would you hear less of less bowel sounds so sometimes they may have decreased bowel sounds as well so that's a big thing to remember all right we got a good chunk of this down now epigastric abdominal pain constant radiates to the back worse when laying supine better when leaning forward if there's a lot of inflammation compressive symptoms abdominal distension nausea vomiting functional type of physiological illness with decreased bowel sounds boom yadda yadda what else can happen okay the next thing that you guys have to remember here is one more this is an interesting one what if i have a gallstone this is just kind of because gallstones seem to be the most common what if i have a gall stone somewhere along that ipad a pancreatic ampulla right a stone's getting stuck can bile get pushed down this normal gallbladder cystic duct common bile duct into the duodenum no and so as a result bile will start backing up and when bile backs up and gets into our circulation what's the primary pigment component of the bile bilirubin right so you get what's called bilirubin and if bilirubin gets into the bloodstream a lot of it what can this produce when it gets deposited into our skin tissues jaundice so another potential symptom that you guys want to be looking for especially as cueing you in on maybe the etiology or the cause of this person's pancreatitis is also jaundice okay beautiful now let's talk about some of the complications pancreatitis is just this massive inflammatory reaction man so whenever there's this significant inflammation of the pancreas because of the causes that we talked about so there's already been pancreatic destruction and damage when that happens it pulls in you know whenever the pancreas tissue is damaged it releases different types of chemokines and kind of inflammatory meters like prostaglandins and leukotrienes and bradykines all these different types of molecules that try to pull in white blood cells to the inflamed area because we want white blood cells to come in and clean up all of that debris when it comes to that area brings with it neutrophils and it brings with it macrophages and what happens is these guys unfortunately some of the more neutrophils that come to the area they try to release reactive oxygen species and proteases and unfortunately you know in an attempt to try to help like whatever is going on it may unfortunately lead to an increased destruction and propagate this process even more but what this may do is it may stimulate the macrophages very or the macrophages very specifically and cause these macrophages to lead to a ton of cytokine release you know very specifically interleukin 1 interleukin 6 tnf alpha these very very specific molecules get released and you know what these guys love to do they love to act on our vessels so you release tons of these molecules because of the massive pancreatic inflammation these love to act on our vasculature you know what they do to the vasculature they cause the blood vessels to undergo a vasodilatory response so that's the first thing that happens is they undergo a vasodilation response that's the first thing the second thing is they cause them to become very leaky and very permeable so they cause the endothelial cells to kind of contract near one another and as a result the endothelial cells start leading to a lot of leakiness so as a result we'll put this kind of here in brown now any of the fluid that's running through here can start leaking out of the vasculature and into the interstitial spaces what's the end result of all of this crap the end result of causing vasodilation increased capillary permeability there's a bunch of different things one is if you cause vasodilation that's going to lead to a decrease in the systemic vascular resistance and that's going to lower your blood pressure so it can cause hypotension right the other thing is that if you have an increase in the capillary permeability that's going to cause a lot of edema like interstitial edema so edema is going to fill up in different areas of the body so it can cause interstitial edema but also you're going to have a decreased effective arterial blood volume meaning that out of all the actual volume in your blood because you know blood is made up of plasma which is primarily like water fluid and it also has your formed elements your red blood cells your platelets your white blood cells all that stuff if you have an increased capillary permeability you're just leaking all of that fluid and you have less fluid within the vessel so these are things that i want you guys to think about that may happen as a response to this now here's the next thing so we know that we get this vasodilation we get this increased capillary permeability here's what i want you to remember this vasodilation is widespread and if you have this vasodilation it leads to a drop in the systemic vascular resistance a drop in the blood pressure right what's going to happen what's the heart going to do in response to a low systemic vascular resistance in a low blood pressure well it's going to activate those baroreceptors so what it does is it stimulates the bare receptors you know those receptors that are present like in the carotids and in the aorta it's going to activate those and it's going to increase the activity of your sympathetic nervous system you know what your sympathetic nervous system is going to do is going to act on those sa node it's going to act on the av node and it's going to try to increase the conduction through the heart i know what that's going to do that's going to try to increase your heart rate because you know if you try to increase your heart rate it's supposed to increase your cardiac output and increase your blood pressure so that's what's going to happen is as a result they develop a increase in heart rate the other thing is if you have less blood volume so if you have less blood volume like effective arterial blood volume because you're leaking it all over the dang place less blood is getting taken to the right heart less blood is going from the right heart to the left heart and less blood is getting pumped out of the left heart and into the systemic circulation and that is also dropping your cardiac output and dropping your blood pressure you get so you get kind of a double whammy effect here you get the vasodilation that causes your actual blood vessels to have become wider lower the resistance and lower the pressure that creates a reflexive tachycardia but if you're leaking all of your fluid into the interstitial spaces and less of it is actually in your vessels that means the venous return is less and you have less blood that's actually being pumped through your vasculature that also can lead to hypotension so we see hypotension and tachycardia as a potential complication man what else could we see another thing that we can see from this is these cytokines they're sons of guns man these cytokines these interleukin-1 the interleukin-6 the tnf alpha all of them can have multiple effects on other organs like peripheral organs and one of the things that we start to see out of this is that it can act on our coagulation system you know we have different types of coagulation enzymes we have what's called pro coagulants we'll put pro coag and then we'll put anti-coag proteins these cytokines love to ramp up the activity of the pro coagulant enzymes and decrease the activity of the anticoagulant enzymes and you know what that leads to if you ramp up the activity of these imagine you're going to have these proteins running down here let's say that these start clotting up a bunch of different areas here along this vessel so now i'm going to be using up a bunch of these clotting proteins to lead to clots but then i use up so many of these clotting proteins that i actually consume so much of those clotting proteins so i consume the clotting proteins that guess what next time i get like a little nick in the vessel i'm not going to have the clotting proteins present because i've consumed all of them to make a bunch of clots so i got cloths all over the dang place because i've consumed these proteins and i consume so many of them that now when i need them they're not there and as a result blood can start leaking out and what's the end result of this this can also lead to bleeding seems paradoxical right this is a nasty disease whenever you develop widespread blood clots and then also bleeding what is this condition called this is a nasty disease this is called disseminated intravascular coagulation so that's another thing that you want to be thinking about you know what else this interleukin-1 interleukin-6 tnf alpha also does it's a son of a gun right it also can act on our hypothalamus stimulates our hypothalamus and tells our hypothalamus to start jacking up our body temperature because there's inflammation somewhere in our body and if we jack up the temperature it's a thought that like oh this inflammation is infection related if we increase the body temperature bacteria can't survive in a way and so what happens is this stimulates your hypothalamus and your hypothalamus increases your internal body temp and this can lead to a fever which is another common clinical manifestation of someone with pancreatitis all right so what do we got so far we know that we have hypotension tachycardia we got potential for dic we also know that we can have fever and what else is another potential complication these high amounts of the cytokine storms can also act on our bone marrow it can activate the bone marrow you know why it can tell the bone marrow hey man there's a lot of inflammation going on get a lot of neutrophils to this area because something something's funky is going on so it activates our red bone marrow and tells them to start pumping out white blood cells so pumping out white blood cells and what is this called when you increase the amount of white blood cells leukocytosis so there may be a leukocytosis so we have fever leukocytosis hypotension tachycardia potential for dic what else these cytokines can also act on our liver and it can tell the liver hey man lots of inflammation going on you need to go ahead and alert other parts of our body to let them know and so the liver releases a bunch of different types of protein called acute phase what are these called acute phase reactant proteins and there's some very very specific ones that i want you guys to remember the big one here is called crp and there's another thing where it actually can affect what's called our erythrocyte sedimentation rate not as specific but it's similar to this esr so this could be measures of acute phase reactant proteins or inflammation generalized inflammation in the body and so crp esr will be elevated there's one more protein i'm not going to get too crazy about it but sometimes there's another protein that can be very more like what may way more specific for kind of infection related things and we'll talk about a little bit later but it's called procalcitonin and it's a little bit more sensitive than crp is but we'll talk about that later with the diagnostics okay so what do we got so far we got the complications in the cardiovascular system we got dic we got fever we got leukocytosis increasing crp and esr let's come over here all right so the other really scary thing from here that we got to talk about is remember we said that very specifically there was a vasodilatory effect and there was an increased capillary permeability and this was widespread okay it's not just happening near the area of the pancreas this stuff is going all over this the actual circulation when it gets to the lungs and it increases the capillary permeability in the lungs this can become a very very nasty devastating effect like super scary you can increase the capillary permeability of those pulmonary vessels and now as they're more leaky you can have fluid leaking out of the blood vessels into the interstitial spaces and then worst case scenarios not only does it leak into the interstitial spaces but it also starts leaking into the lung parenchyma like near the alveoli what is this called this is pulmonary edema but it's so diffused because you have this massive increased capillary premium permeability that when this happens this occurs diffusely throughout multiple alveoli worst case scenario this can lead to what's called a r ds and this is the number one cause of mortality in patients with pancreatitis so you can't forget that another super rare complication i don't want to get too crazy but sometimes if you get lots and lots of inflammation of the pancreas sometimes the pancreas if it gets really really inflamed and sometimes necrotic it can actually fistulize through the diaphragm you know the diaphragm is a structure here that's supposed to kind of run underneath here sometimes in worst case scenarios this pancreatic inflammation can actually destroy through the diaphragm and form a fistula between the pancreas and the pleural cavity and that can cause fluid all that inflammatory molecules to leak into the area of the pleural cavity what's that called when you get fluid tons and tons of fluid within the pleural cavity a pleural effusion so another potential complication is what's called a pleural effusion okay so we know that's a particularly scene with a pancreatic fistula all right all right what else is happening here because of that increased capillary permeability this is going to affect lots of leakiness and fluid collections within the abdomen which is where the actual pancreas is kind of located it's within that retroperitoneal cavity and because it causes lots of fluid accumulation in the abdomen the abdomen starts getting all kinds of bulky and you start looking like the michelin man and what is this called when you start getting a lot of fluid accumulation within the abdomen this is called ascites and so another potential complication is that this can lead to ascites because of all of that massive fluid accumulation the last thing that i want you guys to think about here just quickly before we move on to the nasty complications besides these is if it couldn't get any worse you're probably going to get worse yeah one more thing is that if you have less effective arterial blood volume and less blood pressure particularly less of the blood is actually going to the kidneys what could that do to the kidneys if there's less blood pressure because of less effective arterial blood volume so less effective arterial blood volume leads to low blood pressure you're not perfusing the kidneys what can happen to the kidneys as a result the kidneys won't get their volume of blood that they need to make urine what would that do that'll reduce their gfr and that may lead to an acute kidney injury what kind of acute kidney injury let's see if you guys remember from the aki video a pre-renal aki so this would be a pre-renal acai because you have less blood volume so they may have a bump in their bu in and a little bump in their creatinine because they're not having enough volume that's going to the kidneys because they're third spacing it or they're just not having enough perfusion because they have less volume in general all right now that we covered that let's cover some really really scary nasty complications of pancreatitis all right what's some other potential complications that you guys want to be definitely aware of in someone with pancreatitis well remember i told you that whenever there's all of this inflammation right so sometimes the pancreas can get super super kind of inflamed and when it starts getting really really kind of inflamed you know what is it really interesting there's a bunch of different types of enzymes that we talked about that can be released so whenever the pancreas is damaged not only is it because of this kind of like massive inflammatory cascade from like the cytokines but also remember whenever the pancreas is damaged it was because of lots of maybe proteases that are being released and lots of lipases that were causing this massive destruction of that tissue okay now when the proteases and the lipases are causing this auto digestion of the pancreas you know very very interestingly what can happen let's say specifically with the lipase is what they start to do the lipases they start breaking down a lot of the fat the peripancreatic fat and when they start breaking down that peripancreatic fat these lipases they really start going ham and they start breaking down that peripancreatic fat tissue you know what that leads to this peripancreatic fat tissue when it starts becoming destroyed and damaged it leads to a process called liquefactive necrosis so it's called liquefactive necrosis and what's really interesting about this is you start damaging some of the actual pancreatic tissue and as it starts damaging some of the pancreatic tissue it starts releasing out some triglycerides as a response to this because you know whenever you're breaking down lipids you can actually start releasing some triglycerides as a response to this particularly triglycerides will actually get broken down to these things called free fatty acids so whenever we're breaking down the fat tissue within the pancreas we're really breaking it down more specifically into these molecules called free fatty acids so it's breaking down the fat of the pancreas the lipases these free fatty acids you know what they do they love to combine with something in the bloodstream they love to combine with calcium they really like to leech up all of that calcium and so normally calcium should be circulating in our bloodstream in kind of a free form but what happens is from all of this liquefactive necrosis process where you're destroying some of the peripancreatic fat tissue releasing from that area lots of free fatty acids they soak up the calcium and when they soak up that calcium it leads to a low calcium within the bloodstream and this is called hypocalcemia now this liquefactive necrosis when it leads to all this damage and this hypocalcemia we actually call it technically like a saponification reaction let's not get too crazy we just know that there's definitely a lot of liquefactive necrosis that liquefactive necrosis right you start getting a lot of inflammation and damage and fluid collections in that area so you start getting lots of fluid collections right in that area here's what can really interestingly happen all right so what can happen is you start getting this area here where all of this inflammation all of these fluid collections start forming you start getting a lot of fibrous tissue that surround those fluid collections so here we're going to have this fluid collection and then surrounding that area of fluid collection is going to be this fibrous tissue okay so you have all of this necrosis this liquefactive necrosis and then what happens is okay so here's all that liquefactive necrosis you start getting this area of a fluid collection that gets housed or walled off or encapsulated what is what is this called this encapsulated fluid collection it kind of looks like a cyst it's called a pseudocyst this is called a pseudocyst a pancreatic pseudocyst you know what can happen though in certain situations that pancreatic pseudocyst can sometimes very very significantly scary can actually sometimes get filled with e coli so e coli may actually infiltrate into this area of the pancreatic pseudocyst and when it does that if it gets in there and actually causes like nasty bacterial infection to this area of the pseudocyst now you have all this bacteria that's encapsulated what is this called here this encapsulated infection this right here is called a pancreatic abscess and so these are also potential complications you know what a pancreatic studies sometimes they can be completely asymptomatic but if they get big enough they can compress on things remember what i told you they could compress on the stomach near the gastric outlet maybe lead to an obstruction they can compress near the maybe the bile duct the bile duct runs through here it could compress on that leading to jaundice it could compress on the duodenum which runs right here which can cause again an obstructive type of symptoms so these are things that can happen abscesses they're going to be very painful they're going to have fevers they're going to have severe abdominal pain they're even going to have an intense leukocytosis and this is going to be something that stays around usually these complications usually develop over a process of greater than or equal to four weeks after the initial pancreatitis event this is something that happens a little bit later the last thing that can happen with respect to this liquefactive necrosis is that you get these fluid collections here that aren't encapsulated sometimes okay if these fluid collections become infected then it's called a infective liquefactive necrosis so you can get two types of liquefactive necrosis you can have an infected liquefactive necrosis or you can have it where it's just this fluid collection where there's no bacteria that infiltrated into it and this is called a sterile liquefactive necrosis okay so now we have an idea here of all the potential complications with the liquefactive processes which is really kind of related to a lot of these lipases now let's say that it gets even worse let's say it gets even scarier really where again this pancreas is getting inflamed right because of all of the pancreatic proteases all the pancreatic lipases and again what starts happening here is you start again releasing all of these there's all of these proteases that are being released that are causing auto digestion there's lots of lipases that are getting released that's causing a lot of auto digestion we already talked about the effect of the lipases but what if these proteases and lipases start extending beyond the actual area of the pancreas you know the pancreas has vascular supply as well so proteases might start destroying some of the proteins the lipids might start destroying some of the lipids that are associated with nearby blood vessels if i start destroying some of these nearby blood vessels that are in the pancreas or near the pancreas then i'm going to start having blood that's going to be accumulating around the pancreas what is this called this is destruction of nearby pancreatic tissue and pancreatic tissue in general but now there's blood this type of necrosis here is called a hemorrhagic necrosis and the worst case scenario is maybe it's just like blood collections that accumulate near the pancreas from nearby pancreatic vessels but what if this actually invades into a gastroduodenal artery a gastropolic artery worst case scenario it erodes into nearby aortic vessel this could lead to hypovolemic shock because of a massive rupture okay because of massive rupture of a large blood vessel so that's another scary complication that can happen so you can get this hemorrhagic necrosis and this can lead to hypovolemic shock and bleeding and this bleeding is what can really kind of be scary because it loves to bleed you know where the pancreas is actually located it's actually located within the retroperitoneum right so you have the peritoneum which is having that you have the visceral peritoneum the parietal peritoneum and it kind of helps to keep all the organs located in that kind of like imagine like a trash bag right you have all of that sitting inside of it well behind that trash bag is the retroperitoneum that's where the pancreas is located and that blood can accumulate okay and it can accumulate in the retroperitoneum and that can lead to very very interesting types of signs that you may see in a patient it's rare and if you do see it it's kind of an ominous finding sometimes you can see blood like this like what looks like echomosis that kind of forms around the belly button this kind of echomosis or hemorrhage which is indicative of retroperitoneal bleeding so you're kind of invading what happens is all that proteases and light places are invading and destroying nearby blood vessels and it's causing retroperitoneal hemorrhage this is called the cullens sign okay i like to think about a scene a sea near the actual umbilicus and then if you get a lot of hemorrhage that occurs near the flanks you know you've got to turn on your side this is called a gray turner sign and these are indicative of retroperitoneal hemorrhage from hemorrhagic necrosis these are also some scary things that you want to be very very careful of in a patient that has acute pancreatitis now that we've covered that let's talk about the diagnosis all right so how do we diagnose pancreatitis okay well obviously they have to have that classic like signs and symptoms right so the epigastric abdominal pain constant radiating to the back it's again worse particularly when they're laying supine feels better whenever they're laying forward and again they may have that associated nausea vomiting those are the classic kind of signs of pancreatitis so if you hear those things then the next thing is to say okay we have that let's do they have any risk factors for pancreatitis oh they had a history of gallstones oh they're an alcoholic or they have particularly hypertriglycemia again go through all the causes think about those things if they fit the bill test the light passes remember whenever there's destruction of the pancreas all right you start releasing out these lipases and that light paste causes the liquefactive necrosis the saponification reactions and so whenever somebody has pancreatitis they should have the lipases that are being destroyed and released into nearby vasculature so what you do is you check their lipases and if the lipases that you check with inside of the blood is three times the upper limit of normal this is indicative of pancreatitis there is another enzyme that you could check but i think it's on the way out again what is the other enzymes that were present not just the proteases so there was proteases lipases and amylases this one is not as good but amylases if they are also three times the upper limit of normal and you find these higher up in the blood again that may be helpful in pancreatitis but really the best one is just lipases because they're way more specific for the pancreas amylase can be released from multiple different areas remember it's released by the salivary glands so again in some kind of situation where you tickle the salivary glands if you're trying to intubate a patient who has pancreatitis they may have an elevated amylase so stick with the lipase and you can't go wrong so clinical symptoms that we talked about plus lipases that are three times the upper limit of normal is diagnostic you can also get imaging to aid in that diagnosis as well what are some other things that you might want to throw on uh in order to make sure that you also kind of look at the pancreatitis like grading its severity looking for any complications or figuring out the cause the other thing that i like to look at here is i like to get a cbc now remember in a patient with pancreatitis what happens to their vessels they're super leaky right and so they're leaking out all of their plasma a lot of lots and lots of their plasma so if you were to get a cbc all right particularly to look at their hematocrit i like to look at their hematocrit and when i look at this i'm going to see let's say here about 45 percent of that hematocrit should be red blood cells then you should have a tiny bit of it like less than one percent that's a part of your buffy coat and then the last part should be your plasma but what's happening to these patients with pancreatitis in severe cases they're third spacing a lot of that fluid and so their actual plasma may be very low normally this is supposed to be 55 but if you take and try to calculate the hematocrit what is it the hematocrit is basically taking the red blood cell layer over the total blood which includes the buffy coat and the plasma layer well if the plasma layer is really low what's going to happen to your total hematocrit the hematocrit may be higher so this could be indicative of something called hemoconcentration now what's another thing though to think about that maybe it's not just this what if the pancreatic inflammation actually caused the necrosis or destruction of nearby vessels and you started actually leaking tons of blood into the retroperitoneum what may be another sign that you would see in these patients not just a high hematocrit from hemoconcentration but you may see a low hemoglobin if there was any kind of retroperitoneal hemorrhage or bleeding so this may be indicative of bleeding so that's something i would think about is there any hemo concentration maybe the third spacing a lot of the fluid is their hemoglobin law maybe they're bleeding from a retroperitoneal hemorrhage i can get a lot of that from a cbc what else could a cbc tell me what happens to our white blood cells again you make more of them so another thing that we may pick up from the cbc besides a drop in hemoglobin indicating indicative of bleeding a high hematocrine indicative of hemoconcentration but i may have more of these neutrophils and what is this here called my white cell count would be going up and this is a leukocytosis maybe more specifically i'd see a lot more neutrophils within my white blood cell my cbc particularly within the white blood cell component okay so right now i can tell from my cbc if there's any hemo concentration bleeding or a leukocytosis pretty good stuff right there right what else could i do the other thing i could do is i could just check a lipid panel right why why would i check a lipid panel particularly the more specific one let's actually be more specific i can check a lip panel but really i'm only looking for one component in that lipid panel the triglycerides so i could quickly order someone's triglyceride level now this is actually high yield i do want you guys to know this i don't want you to remember numbers too often but this is one that you need to remember the triglyceride levels it actually has to be greater than or equal to a thousand milligrams per deal to actually be significant enough to cause pancreatitis you have a pretty good hypertriglyceridemia you see this greater than that it's probably cause of their pancreatitis so that's another thing i'll do i'll check their triglyceride level so i'll send off for a cbc i'll check their amylase and lipase i'll check their triglyceride levels and then another thing i'll do is what's another potential cause it's an easy one i can quickly order it i can order a calcium level right so i could check their calcium and the calcium could be two things right if the hypercalcemia is there that might have been their cause of the pancreatitis but what did i tell you may happen as a result of the liquefactive necrosis remember the free fatty acids get released they combine and complex with the calcium what also could be a complication you may also have hypocalcemia but this is a complication this may be a result of that saponification or liquefactive necrosis so if it's super high oh that might be their cause if it's low oh that could be a result of that liquefactive necrosis process all right what else would i check obviously i would check all their vitals do they have hypotension do they have tachycardia all of those things what was another thing i said if they have a lot of this third spacing of fluid and they have a low blood volume particularly what we've got to be specific a low effective arterial blood volume that's less perfusion to the kidneys less perfusion to the kidneys means less urine output but what did i say would happen if you're not perfusing the kidneys they have a low gfr they're not excreting urea and what happens to their bun it goes up so what could i do to check the person's bun a b and p so i could check a b m p and that may give me their bu in it also may give me their crack and they may also have a small bump in there creatinine as well but this is the more important one the bun okay all right so that's one thing what's another thing i do remember i told you this also is a very interesting thing where is my maroon marker here it is okay with all of this things that we were talking about right especially with the inflammation so remember those uh macrophages they were releasing tons of interleukin-1 they're releasing tons of interleukin-6 and that was acting on the liver and it was telling the liver to make a lot of acute phase reactive proteins what were the particular ones that i wanted you to remember crp so another thing i could check if i really wanted to is i could check a patient's crp if their crp is really high and i have a lot of these other things oh it could be a pancreatitis but remember it's not super super specific remember i told you you could check another thing which is a little bit better but it's only really particularly seeing if the patient has pancreatitis with infection like an infected necrosis that's called procalcitonin so another thing that you could add is what's called a pro calcitonin if there is question of infection so sometimes people have pancreatitis it can look like they have an infection right they have a fever they have hypotension they have tachycardia they have a they have a leukocytosis and you're like dang i don't know maybe they have an infection sometimes procalcitonin may help to guide you to say is the pancreatitis all that necrosis that they have becoming infected do they have an abscess that may be helpful in these scenarios the next thing that i want you guys to remember is what if a patient's cause was a gallstone right they have a gallstone that stuck it that apatopancratic ampulla right we know that that could cause the pancreatitis but we know that some of that other stuff can back up into the liver it can back up into the gallbladder all right and what is some of the things that can actually back up well we know that they can have an increase in bilirubin and if there's enough that it actually enough of the bile starts backing up and it actually causes liver injury from all of the pressure from all of this kind of blockage here that could lead to an increase in what other things liver enzymes what are the liver enzymes that could be indicative of liver injury ast and alt so another thing that i could do to see is this maybe related to the gallstones is i could check a bilirubin and i could also check there ast and alt to see if the liver has any kind of relationship involvement here okay so we kind of got a good idea of what i can check here to see what's going on with this patient so now that we've gone through the clinical features the labs what are some particular images that we could add on to aid in our diagnosis or figure out the cause all right so what kind of imaging would we order for this patient who we think has pancreatitis let's say that they have the classic features their labs particularly what was the most important one if you forget all that stuff up there that's fine but only one lab i need you guys to remember it's the lipases has to be three times the upper limit of normal epigastric abdominal pain and the classic kind of presentation what else is another thing that helps us to diagnose it the other thing is particular imaging so one of the first things you should do is obviously order a light paste order some of the other stuff that we talked about but i would automatically i would get a right upper quadrant ultrasound the reason why is a right upper quadrant ultrasound may tell you the exact cause of the person's pancreatitis if i get the right upper quadrant ultrasound and i see any type of stone so i see the evidence of the actual gallstone or i see any ductal dilation that might right away tell me oh there's their particular cause of pancreatitis it's not super great if they have a lot of like uh like uh particularly like enlargement of their abdomen like a distention lots of bowel gas it may have struck the pancreas if you're really good at ultrasound sometimes you can pick up particularly like fluid collections like pseudocyst and walled off necrosis but i think the right upper quadrant ultrasound is kind of like the quick thing that you should do to see is there a stone is there any ductile dilation let's take a look at an ultrasound and see what that could look like all right ninja so we talked about the ultrasound let's take a look at what we would really kind of be looking for if we did a right upper quadrant ultrasound we see here we have this big kind of structure here the gallbladder and the gallbladder should eventually kind of connect particularly has the cystic duct that fuses with the common hepatic duct and then you get the common bile duct what happens is when your common bile duct is approaching anywhere near like 10 millimeters or greater that's some pretty significant dilation of the common bile duct and what we might want to suspect is that there's something downstream that's plugging up that biliary duct and that in my friends is actually a gallstone and so this patient had gallstone pancreatitis and when we did a right upper quadrant ultrasound they had a very dilated common bile duct due to a downstream gallstone so again that's one of the quick ways that you can see is their gallstone is there any ductal dilation that may be suggestive of gallstone pancreatitis all right what's another potential test that i could do all right so let's say that i know a patient has pancreatitis and i think that their cause of pancreatitis has something to do with a stone maybe their ultrasound was kind of inconclusive so maybe it was inconclusive i still don't know if there was any ductal dilation if there was any stone i saw some non-specific stuff maybe related to pancreatitis potentially what i may do is i may do something called an mrcp it's basically an mri and it looks at particularly that entire kind of pancreatic pancreatic and biliary system to look to see is there any kind of filling defect or any point where there's a stone or something blocking some part of that hepatopancreatic ampulla biliary system pancreatic system so that's a good thing the other thing that you may do is if you have a very high suspicion and the patient is kind of like not super stable you may go straight to a ercp because this is both diagnostic and therapeutic so with this one you actually take and run the camera down or you actually run the catheter down through the duodenum up through the pancreatic duct up into the actual biliary system and then you kind of shoot some contrast up there to see is there any kind of gallstone or issue there and then from there if you find it in real time you can actually extract and remove that stone in the process so that's another thing that you could do so we'll take a look at an mrcp here in a second then we'll take a look at a video of an ercp so let's take a look here in mrcp that maybe we're going to take the extra step here as we move through an mrcp which is just a magnetic resonance calandrio pancreatography what i really want you to focus on is this area here this right here is going to be the area of the gallbladder okay so we're kind of filling up the biliary tract with any kind of like contrast and we're getting down to the area of like the where the cystic duct and the common hepatic duct should fuse and form what's called the common bile duct so i want you to kind of follow this down anytime you see kind of any dark areas it may be identifiable of something that's causing a defect or something that's blocking contrast moving down there so let's move through there and you can already see something dark right here so there's some signs here of some gallstones that are kind of clogging up this common bile duct right there you see definitely some stones something that's kind of clogging that up and then right around here is our pancreas the main pancreatic duct should fuse with that common bile duct so if we continue to follow it down it would eventually kind of fuse around this area of the head of the pancreas with the common impact the common bile duct will fuse the main pancreatic duct into the area the apatopancratic ampulla okay so this right here could definitely be an evidence of some type of gallstone pancreatitis or maybe like some mild ductal dilation here that you can see on the mrcp okay let's take a look now at an ercp but before we do that let's take a look at kind of the overall concept that i want you guys to get from this boom we've got a big old gallstone smack dab within that bile duct and a little bit of ductal dilation all right let's take a look at an ercp now all right so let's take a look here in ercp so again we can kind of see that we're coming down endoscopically and we're kind of running through the pato pancreatic ampulla and near the area of the main pancreatic duct and then up through the common bile duct and as you can see here we have a suspicion that this person has some type of gallstone related pancreatitis and as you can see you can kind of see that this common bioduct is a little dilated and there may be some stones a couple stones kind of lodged within this area of the biliary duct and maybe even downstream near the apa where the apatopancretic ampulla is and so again this may be something that's interesting with the ercp where you may be able to diagnose the person has it having gallstone pancreatitis or some type of choledocolophiasis or maybe complications like ascending cholangitis and then therapeutically you might be able to treat and remove those stones at the same time in real time so this is kind of an interesting ercp that we are going to be talking about here all right what's another potential thing that i could look for okay the other thing that you could do is you could get a ct scan now a ct scan is relatively good okay so ct of the abdomen again i would try to hold off so like the first test i would advocate to do is the right upper quadrant ultrasounds a super quick easy test mrcp ercp if the ultrasound is somewhat inconclusive if you're concerned about complications of pancreatitis what do i mean so it's been a couple weeks and they're still having some kind of weird symptoms of pancreatitis or some non-specific symptoms you may be able to pick up that pancreatic pseudocyst remember that's that fluid collection that's kind of encapsulated the other thing it may help to pick up is is there a fluid collection that looks like it's kind of loculated and has infectious material in it in other words is there any abscess and it also helps to pick up on if there's any kind of necrosis so necrosis particularly is it infected necrosis is there any hemorrhagic necrosis is there any bleeding as well which again can be a complication as well so these are good things for the ct so a ct of the abdomen really shouldn't be like a first line test it's very good but a ct of the abdomen it may show a lot of peripancreatic fat stranding which could be obvious but usually in the acute phase it may be hard to see because of so much inflammation going on that it may be difficult to demarcate a lot of the margins of the pancreas but one of the things that this is best for is it's best for an unclear diagnosis of pancreatitis or you have fears that there's some type of complication of the pancreatitis as we mentioned here on the side such as do they have a pancreatic pseudocyst do they have an abscess do they have an infected necrosis like an area of kind of infection necrosis is there any signs of bleeding due to the hemorrhagic necrosis those are things that you would definitely want to get a ct for all right ninjas let's take a look here at a ct of a patient with pancreatitis so we're looking at a ct this is a axial section here this is the right side of the body this is the left side of the body you see remember we got the heart here smacked up in the middle as we start working our way down we're going to get into the abdomen so now we're in the abdomen you can obviously see the liver here you can see a lot of fluid behind here so obvious evidence of ascites but as we continue to go down we see the stomach and we're looking for the pancreas to be right behind the stomach right in this vicinity about right here so let's see if we start to see it pop up and there is our pancreas right here best way to kind of identify the pancreas is you see this vessel here this is one of the splenic vessels it usually kind of curls around that posterior edge of the pancreas so here we have the pancreas and what you're noticing is just a lot of like this like white stranding type of like matter all around it all of that is kind of edema but it's indicative of what's called peri pancreatic fat stranding which is pretty indicative of pancreatitis so we definitely see a lot of inflammation around the area of the pancreas thus indicating again pancreatitis especially in the clinical context of this patient who presented with abdominal pain they presented with fatigue nausea vomiting so these are constant things as well as a elevated lipase level that was three times the upper limit of normal okay that's our image here so if we take a look at what's the overall thing we see here is our pancreas right behind that splenic vessel you can see that kind of structure there and all of this fat stranding around there is the peripancreatic batch training from the liquefactive necrosis which is indicative of pancreatitis all right let's take a look at another thing that we can see in the ct all right so remember i told you guys that when we're taking a get a ct of a patient with pancreatitis it's important to remember that we're doing it to look for any complications of someone who may have pancreatitis so we do try to do it a little bit later within the stages of pancreatitis and one of the reasons why is one of the things that you might start seeing signs of is again we have to find the pancreas so the pancreas i kind of look for that splenic vessel right splenic vessel here's your spleen so there should be the pancreatitis here the pancreas is so inflamed that it is almost so difficult to be able to make out and demarcate all of the margins of the pancreas in this guy right it's around this vicinity right here but you're seeing all of these like fluid collections and necrosis all around the vicinity of the pancreas all of this is kind of this necrotic tissue around the area of the pancreas with lots of fluid collections so those fluid collections are becoming infected or necrotic and so that could be indicative of particularly a necrotizing pancreatitis in this patient okay so let's take a look here what we kind of highlighted again we have some necrotizing tissue here again this could have been from a lot of the necrosis of the tissue liquefactive necrosis as well all right so that is necrotizing pancreatitis look at another complication that we can see from pancreatitis all right so let's take a look at another ct of a patient who we suspect has pancreatitis or we're trying to exclude some other complications or particularly we think that maybe there's something else going on and as we start scrolling through these patients oh my gosh oh my gosh look at this big beast in here in their abdomen this is a massive pancreatic pseudocyst it's so big that it's actually compressing the nearby ureter and causing hydronephrosis of this kidney here so this is a big beasty boy here and it's a pretty significant complication that you can see like four weeks after a person who had pancreatitis acute pancreatitis and this is definitely one of the reasons why we would get a ct for a patient okay so again that would be an identifier of what again this would be a pancreatic pseudocyst that we would see in a patient usually a little bit later in the initial after the initial stages of pancreatitis and this is definitely important the other test that you can order is you can get an abdominal x-ray an abdominal x-ray is also a really quick easy test because it can help to rule out any kind of signs of bowel obstruction as well but an abdominal x-ray what you're looking for is whenever there's lots of inflammation of the pancreas one of the things that it can do is it can really cause some dilation of the nearby small bowel and it can kind of really make it look a little dilated and this dilation of the small bowel is called a sentinel loop okay we'll take a look at not only just a abdominal x-ray but also take a look at some ct scans to look at some of these abnormalities and complications but that's one thing is you may see some dilation of the nearby small bowel you know what else is interesting if there's lots of inflammation near the tail of the pancreas you know the tail of the pancreas is near this area called the splenic flexure the splenic flexure can get lots of inflammation and fluid collections that can compress down on that splenic flexure and if you can compress down on it that causes an increase in the back pressure proximal to that and that causes some dilation of the bowels that are proximal to the splenic flexure what's proximals of the splenic flexure well then you have your ascending colon and you have your transverse colon they can actually be super dilated and kind of like large so sometimes if you also see this dilation of the ascending colon transverse colon and then a cut off near the splenic flexure that may also be a sign of pancreatitis and this is called the colon cut off sign so something on abdominal x-ray that you may ask you is kind of like those buzzword terms not super super common to think about but definitely something to remember is is there a sentinel loop nearby dilatation of the duodenum or nearby compression of the splenic flexure that causes bowel gas appearance of the transverse colon and ascending colon let's take a look at some of these images and then let's talk about the treatment of pancreatitis all right so let's take a look at an abdominal x-ray again these aren't like super diagnostic of a patient with we suspect as pancreatitis it's just something that if you see it hey maybe they could have pancreatitis if their symptoms and some of their labs are kind of indicative of that but again something that you may see on your exam as a very important thing is what's called a sentinel loop so what happens is because of all that pancreatic inflammation you get kind of a localized alias and you kind of see this bowel gas pattern that almost looks like an obstruction but it's a non-obstructive type of biogas pattern and this is called a sentinel loop so this may be something that you can see whether it be nearby the pancreas maybe it's a little bit more downstream seeing these kind of dilated bowel gas patterns without an obvious form of obstruction is indicative of potentially an acute pancreatitis all right let's take a look at another one called a colon cut off sign alright so let's take a look here at the last image that i want you guys to be thinking about particularly with acute pancreatitis especially on your exams but again the patient has some symptoms of acute pancreatitis potentially concerning on some of their labs like the lipase and you get an abdominal x-ray because they're having abdominal pain and in this part here you kind of see what's interesting you kind of see this bowel gas pattern so it kind of looks like there's some bow gas uh pattern here particularly within like the area right around the splenic flexure transverse colon then you can't see it but it would go down it's like the ascending colon so this is interesting there's some definitely some bow gas patterns and what looks like a cut just around the area where the splenic flexure ends and we go down into the descending colon what happens is whenever there's pancreatitis near the tail end of the pancreas that inflammation can cause again somewhat of a nearby kind of obstruction kind of pattern here it's not a complete obstruction but there's enough inflammation here that it causes this cutoff sign near the area of the splenic flexure and then causes this dilated bowel gas pattern proximal to that this is indicative potentially of an acute pancreatitis and we call this a colon cut off sign all right that covers our images that we're talking about with the diagnostic section let's now move into the treatment section what i want you guys to understand is kind of like the hallmark the backbone behind treating pancreatitis and the first one is your fluid administration so we're giving fluid to these patients why well because they're they're having a vasodilatory effect right and what that vasodilation is doing is is there's a drop in blood pressure right so there's hypotension the second thing is it's causing a lot of edema our third spacing of fluid right so we call that third space is when it's kind of sp the fluid is accumulating in interstitial space whether that be within the uh the lungs pulmonary edema and lower extremities peripheral edema whether that be in the abdomen causing ascites and things of that nature that's some of the complications or fears and so what we want to do is we want to give fluids and there's two types of fluids you can give normal saline you can give lactated ringers i'm more of the lactated ringers one because some of the literature actually shows that it may be superior to normal saline in these patients but one of the things that you have to be giving fluid for because one of the things that they say is you got to push in like 10 to 12 liters of fluid to these patients within the first couple hours no my gosh please don't be pushing this much fluid into your patients the reason why is is if you're giving too much iv fluids excessively large volumes of fluid they're just going to keep third spacing that fluid that's the problem with these patients and you increase the risk of fluid overload particularly what's one of the complications associated with patients particularly developing a very severe pancreatitis ards right from the increased capillary permeability if they have increased capillary permeability you just flush them with tons of fluid you're just going to push all that fluid into their interstitial spaces into the lungs worsen their potential arts or put them into arts the other thing is if you give them tons and tons of fluid and they just keep third spacing it into the retroperitoneal cavity and all their abdomen then they're gonna cause the pressure in their abdomen to rise so much that you're gonna lead to what's called abdominal compartment syndrome abdominal compartment syndrome and these are just negative negative things man so what i try to say is give them fluids particularly lactated ringers and target particularly have targets target their blood pressure like maybe their map is one target maybe you target their urine output as another target maybe you're looking at their bun and looking to see if that's improving maybe you're looking at their hematocrit to see if that's improving right so if you're giving them fluid hopefully their map goes up hopefully their urine output increases hopefully their bun goes down hopefully their hematocrit goes down because they're having less hemo concentration these are kind of parameters to be looking at when you're giving fluid don't just blindly give someone 10 to 12 liters of fluid in the first 24 hours and then not pay attention to them they might put them into r's or abdominal compartment syndrome okay so first thing is fluid administration the next thing is this disease is very very very painful so analgesia is a very important thing and so one of the things that we try to go with is obviously when you're giving analgesia you can start off with something like tylenol that might not be enough and that's when you go to the next step so maybe the tylenol isn't working the next thing you go to is prn opioids okay so you may try things like fentanyl and see if that works you may try things like particularly like hydromorphone and see if that works and usually if these don't work maybe you have to go to the next step which is things of particularly like they say that morphine may cause spasm of the sphincter of odi there's that's kind of not like that some of the literature is actually kind of going against that they say like my parody may be a good option for that um but again i think that's kind of like they're changing a little bit in the literature but yeah there is like with a questionable concern of whether morphine can cause spasm of the sphincter of odi i don't think that that's super true based upon kind of like the literature but pr and opioids may be an option um and another thing that you may want to consider that i'm a big fan of um especially in these patients is maybe a low dose ketamine infusion the reason why is here's the thing whenever you're giving patients who have this pain opioids what can opioids do to the actual bowels it can decrease the contractility of the bowels and so if you're giving all of these tons of opioids what can that do that can actually lead to an ileus and if you lead to an ileus you're just going to worsen their condition that they already have with pancreatitis so i'd be very very careful yes you have to treat their pain but try things like tylenol try things like low dose ketamine and then if you have to go to your pra and opioids and sometimes you may have to get it pretty scheduled okay all right what's the next important thing this is actually a super important one so whenever patients who develop pancreatitis what we found is is that yay let's let's make them mpo let's give them some bowel rest maybe we have to put in an ng tube if they're having lots of inflammation they're vomiting all the time if that's the case yeah i think it's a good idea if they're having lots of pain they're having lots of nausea they're vomiting a lot they have a lot of inflammation and gastric outlet obstruction sure make the mpo put an ng tube in to decompress the bowels i think it's a good idea but once they're pain-free the literature actually is showing that you should try to feed them early so maybe you feed them early via oral if they can tolerate it or maybe you do this via some type of ng tube regardless internal feeding early has been shown to be able to actually change the gastric permeability because whenever there's lots of inflammation with the pancreas it can cause the gut to become super permeable and imagine if the gut is super permeable what can actually pass across the gut that's a part of our natural flora bacteria and so bacteria can actually translocate when there's all this permeability they found that whenever you do oral feeding early or in g tube feeding early this was shown particularly to inhibit this process to inhibit the gut permeability inhibit bacterial translocation and reduce the risk of infection associated with pancreatitis so that's another important thing fluid don't crush them with fluids though pain control try to avoid tons of opioids third thing nutrition if they need some virus because they're vomiting they're in lots of pain make them mpo put an energy tube to decompress the valve need be once they're pain-free get them eating if they can orally tolerate it good if they need an ng2 and you have to feed them that way good just do it early so you reduce the risk of infections what's the next thing okay so we've done kind of our conservative measures now we're kind of getting into the particular cause cause-related things for pancreatitis as well as complications so the next thing that i want you guys to be thinking about here is what if somebody's cause oh my gosh so loud they have a stone they have a stone there stuck within the hepatopancreatic ampulla and we know that the cause of that stone is because they have some type of gallbladder disease you know they're they have what's called cholethiasis and they're constantly popping out these stones that are getting stuck down in the actual patopancratic ampulla what can i do to remove that stone and then reduce the risk of reoccurrence of them developing gallstone pancreatitis i can go in utilizing this type of tool here coming down the duodenum cutting open the sphincter of od and then sucking out that that actual stone what is that called it's called an er cp so that would be one way one way is we're removing the stone via an ercp or what's another thing that we can do besides this plus or minus if they have a high risk of recurrence and we want to reduce that risk of recurrence what could i do i could just cut this bad boy out reduce the risk of forming any types of gallstones reducing them actually being dislodged into the ductal system and causing obstruction of the pancreatic ampulla there and so this would lead to a chole cystectomy which will abbreviate a ccy okay so this is another potential thing that you have to be thinking about if the patient has gallstone pancreatitis ercp plus or minus cholecystectomy to reduce the risk of recurrence okay the next one i really want to mention this one because it's actually super cool i've seen it once i've seen a patient who was um on tons and tons and tons of propofol and they developed a super crazy high hypertriglyceridemia it was in like the almost near the 2000s and that hypertriglyceridemia had actually induced pancreatitis and so what happens is you know what's actually really interesting with this is obviously you want to discontinue the offending agent whatever the cause is in this case if it's propofol or if they have some type of like genetic condition sometimes um a did an alternative like a mutation or deficiency in an enzyme called the lipoprotein lipase enzyme that can actually cause this so there is genetic conditions that can increase your risk of hypertriglyceridemia but whatever the cause of it is you have to reverse that but then we got to treat it so there's uh insulin you know you give a patient insulin you put them on an insulin infusion and we'll put it as a drip gtt right so you put them on an insulin infusion what the insulin infusion does is it actually stimulates a very special enzyme called lipo protein lipase and what lipoprotein lipase does is is it actually helps to break down these triglycerides so if you have tons and tons of triglycerides within the blood it breaks down the triglycerides into free fatty acids and into glycerol effectively lowering the triglyceride concentration because this will get taken up by muscle cells and cardiac cells and different tissues so that's one particular thing that we may do now if that doesn't work you know what else we can do you can actually give them another drug that actually helps to inhibit triglyceride formation another drug that you can give besides insulin drip is you can give something called fibrates fibrates have been shown to be able to kind of reduce triglyceride production and the third thing that you may do is if the refractory to all of these things is you may actually have to pull you actually take their blood out and then through kind of a machine that sifts all of the actual fat out and then sends their blood back in and that's called an apheresis so these are interesting things that you might have to do as well so lipoprotein lipase can be stimulated by insulin fibrates and then plus or minus apheresis if they're very severe hypertriglyceridemia okay now we're on to the next thing so fluid collections so we know that with all of that necrosis and inflammation you can start developing lots and lots of fluid collections around the pancreas and now here's the thing though these fluid collections that you can get that can be completely sterile so you can get all of these fluid collections and they can be a completely sterile type of fluid collection you don't do anything about these you just observe there's no particular type of treatment for these fluid collections now the question is is what happens if the sterile fluid collections that you get because of all of the type of liquefactive necrosis all of the inflammation all the hemorrhagic necrosis occurs what do i do if you start actually getting some fibrous tissue so you know you start getting like fibroblasts they start coming to the area and these fibroblasts in response to all of this inflammation they start making lots of fibrous tissue and that fibrous tissue starts walling off these fluid collections what is this called this is called a pancreatic pseudocyst now pancreatic pseudocyst guess what you do well remember when do these actually form there's a complications that come down the line usually greater than or equal to four weeks after the initial event of pancreatitis you can develop these you know what you do with these if you're asymptomatic if asymptomatic you just observe and you just hold on and usually these will resolve and they won't cause any problems now if they develop symptoms what the heck does that mean if they develop symptoms well think about it what is that actual so let's say here for example let's say here we put the pancreas and let's say here we have a big pseudocyst here's a big pseudocyst what are the things that it could compress nearby what would be right above the pancreas what's right here stomach what's coming around the pancreas duodenum what's a structure that runs down from the gallbladder and fuses with the pancreatic duct the bile duct if the pancreatic pseudocyst is getting so large that it's causing persistent pain and it's compressing the gallbladder causing jaundice i mean sorry the bile duct causing jaundice it's compressing the gastric outlet causing vomiting nausea as well as bowel obstruction it's compressing the duodenum causing bowel obstructive symptoms and malabsorption then you would go in and drain the actual abscess you may do what's called a percutaneous drainage okay so you stick a thing in there and they'll needle in there and suck that little out suck all that fluid up okay that may be something that you go to you try to be able to avoid this at all possible but if the symptoms become very persistent and problematic then you may have to percutaneously drain that pseudocyst okay the next question okay what if that pancreatic pseudocyst was not problematic right so here's my pancreatic pseudocyst and it's got some sterile fluid in there but all of a sudden some e coli some nasty little bugger e coli start saying i like my pseudocyst and it starts infiltrating into that pancreatic pseudocyst and now that pancreatic pseudocyst starts getting tons and tons of bacteria that is now walled off by this fibrous tissue that was persistently there with the pancreatic pseudocyst now what do i have now i have a pancreatic abscess a pancreatic abscess is going to cause persistent abdominal pain persistent fevers leukocytosis a palpable mass and they can really look septic appearing and these patients you get that ct you find the abscess what do you do well you may start off with antibiotics what antibiotics is actually preferred in a patient with pancreatitis but is an abscess related they have an infected necrosis remember pancreatitis in general you do not start antibiotics you only start the antibiotics if they have evidence of an abscess or some type of walled off infective necrosis not in general the antibiotics that you start with are your carbapenems karba penums so maripenum emmapenum these are the general ones that you're going to start with so carbapenums would be kind of your first go-to now if you start the carbopenems and they're still maybe not getting any better you may actually have to suck some of that pus material out and so you may also have to do a particularly a drainage you may have to do what's called a ct guided drainage of that area okay now the question is how the heck do i figure out if this is actually infection versus just a pancreatic pseudo-cyst the only way that you may figure that out is you may kind of go based upon their clinical features but you may have to do what's called a fine needle aspiration so you may have to take and suck out some of that material from what you think is either an abscess or a pancreatic pseudocyst take it out send it out for culture all the gram staining process and if it comes back positive then you treat them with antibiotics and then you suck all the actual pus out of there okay now here's the next question okay so we have a patient with that sterile necrosis right so let's go back to that you have a patient with these fluid collections here right so these fluid collections and it's sterile okay so here there's their sterile fluid collections that they have it's not infected so it's sterile do you give these patients antibiotics no no antibiotics you just observe if over time these fluid collections that you have start getting walled off so maybe you start getting some fibrous tissue around that area that start walling off these fluid collections and then on top of that not only do you have the necrosis with the fluid collections and the fibrosis but now bacteria start invading into that necrotic area the bacteria start invading into that necrotic area what is this called this is called infection necrosis so this is called a infected necrosis in this situation you may start antibiotics what type carbopenums like maripenum or imipenem how do i determine though that this is a sterile necrosis versus an infected necrosis what may i have to do a fine needle aspiration right so i may have to suck some of this actual material out va fine needle aspiration send it off for a gram stain send it off for cultures and if it comes back positive oh it's infection treated with antibiotics like emma penum or meropenem and then you know what i may have to do let me have to cut that necrotic tissue out so in this one i just drained it in the abscess but in this one i may actually have to cut the necrotic tissue out and so sometimes we may have to do what's called a uh you may have to you may be able to do it percutaneously but generally you have to do what's called a debridement so you may have to debride this area now you can do this endoscopically where you actually go in kind of percutaneous like you may do endoscopically percutaneously or you may open them up and then cut out some of that necrotic tissue but generally we have to debride this area and so we may do a again an endoscopic type of procedure debridement maybe a percutaneous or an open necrosectomy so these are things that we may have to go to if there's an infection necrosis as well and ninja nerds this covers pancreatitis i hope this made sense i hope that you guys enjoyed and as always until next time [Music] you

Channel: Ninja Nerd

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Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

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Length: 102min 36sec (6156 seconds)

Published: Fri Nov 19 2021