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Hello. Um Let me just set this up properly. So that should be the, the Sure. Yeah. Ok. Come on c Yeah. Ok. No, hello everyone. Uh My name is Martin and I'm one of the Sh Os here at Luton and uh at Luton Hospital. Um This is the second part of the gallstone disease um presentation which is part of the Bedfordshire um Surgical Academy also known as bed, which uh focuses on surgical teaching and preparation of um junior doctors within uh sort of knowledge, preparation and skills within the speciality. So, um the first part of the presentation was covered uh around two weeks ago, but essentially uh what I talked about was cholelithiasis, um biliary colic, acute and chronic cholecystitis. Um That presentation is also metal uh and future presentations will also be on there. Um And the metal is just the platform we use to upload recording, so you can refer back to them. Um And then in the upcoming weeks, we'll have more presentations covering various topics within general surgery, um covering some anatomic anatomy, um going into surgical management in a bit more detail and so on and so forth. Um It's very useful to attend these um and also look at them and watch them online as I'm recording now. Um Because uh all of us have done a job in F one the other presented as well. Um And there's a lot, we didn't know about speciality prior to starting rotation. And there's a lot you could, we learned during the speciality or rotation, which we still use to this day. So today I'll be going through choledochal lysis and I'll explain the term in a bit more detail in a little while. And uh cholangitis for a semi cholangitis. Um ok. So choledocolithiasis, choledocolithiasis is the presence of gallstones within the common bile duct. Uh Most of these are migratory, which means they sort of originate um in the gallbladder before moving, moving out into the um cystic duct and then uh tracking down into the common bile duct. Um So these are um secondary stones which are more common than primary stones, um which are also known as de novo stones. Uh de novo stones uh can occur due to parasitic infections, uh the precipitation of bile um and again, parasitic infections is not very common in the West. Um So it's more of the um sort of precipitation of sludge and debris within the common bile duct itself. Um The reason I mentioned this is because someone can have a stone in the CBD without having a gallbladder. So it's always good to have that in the back of your mind as in stones can form de novo, even after a gallbladder is removed. But regardless, uh in someone who does have stones in the common bile duct, it is uh good to remove the um gallbladder itself in terms of risk in reducing the risk of further development of choledochal nephrosis. The cause of primary stone formation. I touched on that a little bit. There is a combination of factors, um can be due to bile stasis chemical imbalances, um increased bilirubin excretion, sludge formation and sludge is just a precursor of gallstones. The sort of bowel components symptomatically. Uh it can be asymptomatic and found as an incidental finding on imaging, but often it will show up as an obstructive jaundice picture which I'll talk about in just a minute. Um And the reason for this obstructive jaundice picture is because bile is simply not passing uh flowing past the stone and you get build up of uh bilirubin or bile and that causes jaundice for sort of clinical manifestations of increased bile in the bloodstream. You get a back pressure of the bowel into your bloodstream and that will um not be also cause bowel, not going into the duodenum itself from the common bile duct. Um This will cause uh conjugated bilirubin build up uh which is water soluble. So from the blood, it will go into uh be processed by the kidneys, the bowel itself and then from the kidneys, the bilirubin will uh manifest as dark urine when you excrete the bilirubin and the lack of bilirubin in the stools itself will cause pale or also known as clay colored stools. Um So that's if you just think about it, sort of deductively, bowel doesn't go into the, there's a stone in the common bile duct can't pass, uh, uh, bowel can't, bilirubin can't flow past the stone, can't go into the duodenum. So it backs up, it goes into your bloodstream, all the connecting blood vessels and then uh it will be excreted by the kidneys and it will go out of the kidneys and cause dark and since it can't go into the um duodenum, small intestine and so on, it can't be excreted. So that will cause p stools. One thing to know is that sometimes um stones are small enough to cause intermittent symptoms because they lodge and dislodge again. So, uh they cause transient uh obstructions. Um So, uh in someone who does have transient symptoms, those treatments are still the same. You have to go in there and remove the stuff and we'll talk about that in just a minute signs and symptoms of choledocholithiasis, uncomplicated, choledocholithiasis. Uh which means you won't be paraxial, there won't be an infection. You'll just have stones in the common bile duct. You will have a normal white cells. You'll be, you'll have no fever, you'll experience biliary colic, which is the pain associated with gallstones similar to cholelithiasis. In the first presentation, you'll get the right upper quadrant, epigastric pain, moderate in severity, intermittent or recurrent. Um This can be in episodes or it can be more persistent depending on the degree of blockage. If completely blocked, there will be more persistent pain. Of course, if there's an intermittent blockage like we discussed uh before, uh this is called a floating stone, by the way, um uh there will be an intermittent symptoms as well. Um Yeah. And as we mentioned before, the other symptoms, apart from dark urine and pale stools are you can get yellowing of the skin and you can get pruritis. Both of these are due to the same reasons as prior. Um There's a buildup of bilirubin in the bloodstream, it manifests in different places. Um It will build up under your skin and that will cause yellowing also be very itchy as well and also build up in the yellows of your eyes, the sclera scleral icterus. Um Yes. Ok. Um On examination, you can get some tenderness in the right upper quadrant or it can be very unspecific abdominal tenderness or maybe little to numb. It's very, it's not following a sort of set pattern, blood wise and uncomplicated choledocholithiasis. You will see a raised um obstructive uh liver enzymes um which is posthepatic. Um and this will be an AP, which is a raised and it can be at as well. But uh we don't really look at that in our hospital, mostly the AP and it will be there. The ALP which is the post hepatic enzymes will be raised in a greater um uh uh in comparison to the hepatic enzymes, the AST A LT will be raised at a much greater level. So you look at the ratio between the two because the ast alt will be the range to an extent because there will be a backflow of bilirubin and there will be some damage to the hepatic cells themselves. So you will still see an ast alt rise to an extent, but the AP will be raise rise um increased at a much greater level than the AST at. And the reason that you get a rise in AP just a bit of pathogenesis is there will be um when there's bile uh lining the hepatocytes that will cause a spillover of AP and it will cause a rise in the production of AP and a spillover into the bloodstream. Therefore, prothrombin time uh will be increased. Uh This is due to the lack of um bowel reaching the intestine leading to a fat soluble vitamin deficiency um including this m which increases the risk of bleeding. So, management does involve um correcting coagulation. So don't always uh do a coagulation screen when you have a patient with suspected um obstructive jaundice. Uh Do we use knees do assess for hydration as well? Always a good idea. And of course, you will see a raised bilirubin, which if you do a separate screen, you will find it's mostly a conjugated rise because the liver does ally process that prehepatic bilirubin. There's not an issue that with the processing of bilirubin itself. First line investigation for um any sort of uh suspected bilirubin disease. Oh, and just to mention before we get into that, always check a light base as well. Make sure that there's no pancreatic involvement. Um We'll discuss gallstone pancreatitis in a future presentation. And uh yeah, so first line for any suspected biliary disease is we do an ultrasound abdomen. This will show presence of stones in the common bile duct or um a dilated bile duct itself. But uh because of the presence of gas in the duodenum. Um and also because of lots of subcutaneous in people who have more subcutaneous fat um that might obstruct the view and there's low sensitivity to this. So interpretation is very limited. The gold standard uh is in essence an M RCP. This is because if you're in doubt that there are CBD stones, but you don't see it on the ultrasound, then you do an M RCP. An M RCP is an MRI of the biliary sys biliary system and pancreatic ducts. So, treatments even if you're asymptomatic with these stones are to remove the stones and this can be done in several ways. Um depending on the circumstances, but mostly it's commonly done via an E RCP. Um Endoscopic retrograde cholangiopancreatography which involves sort of removing the stone. Um putting, putting a nick in the um just to get in there and also um possibly putting a stent in there. If there's a biliary stricture, if there's malignancy, there's different things that can be done for different indications, which will go into that in later lectures, but just know that the management of A CBD stone is most commonly an CP. Um and then later on, um if the, if they haven't had one A LA co is indicated as well after the E RCP to prevent reoccurrence of uh asto the risks of an E RCP are well noted. You can get post E RCP pancreatitis, which can be due to the hydrostatic injury of injecting a dye into the um sort of the uh where the pancreatic ducts meet the common bile duct or um due to mechanical instrumental injury itself. You can also do a PTC. Um Let me just try to show that there. So PTC is a um percutaneous transhepatic cholangiography, which essence is where you put a sort of um guide wire and you place it through the skin place through the liver, put it into the uh common bile duct. And uh it will help, first of all visualize the uh bar ducts and then also you leave a tube there which will be allowed to train externally or if you can get past the obstruction, you can do an internal train as well, um, and then you can nick this sort of ball back there. And that is an image of a percutaneous transhepatic biliary drainage, which, um, if there's a failed E RCP, you can do that instead as the management which will drain all the bowel through that back, the, um, from the guide wire and tube insertion. And if everything's uncomplicated, you can go home the next day or the same day. A right. So, uh just before to mention, if there's no sort of infection, you wouldn't really give antibiotics. Um You can top up on our analgesia post procedure monitor for any complications. The monitor, you mentioned pancreatitis, bleeding, infection, et cetera, et cetera. And then uh yeah, send them no. Um we go into asemic cholangitis which is infection of the biliary tree itself. Um There's something called charcots triad which is a triad of symptoms, symptoms, uh right upper corner of pain fever and jaundice, which is very common in people who have um uh infection of the common bile duck of the biliary tree. Um And then you can get something called renal renal spent out, which is again, is another sign of asemic cholangitis, which is shock who triad by fever and jaundice plus two other uh signs and symptoms. Um You get confusion and then you also get signs of shock. You get that hypertension, hypertension plus high heart rate or uh yeah. So, uh these patients are at high risk of mortality. So you really need to get on top of this quickly. Uh You will get the obstructive jaundice symptoms we mentioned before, due the blood cultures because they will have a fever, most likely have a fever. Uh and the white cells will be raised and the liver function will be uh deranged as prior, look at the post hepatic enzymes. Um and yeah, management similar to as previous you, but you need to make sure that they're somewhat stable before you're sending, sending, trying to send them off to E RCP. You give them some IV, antibiotics, IV, fluid resuscitation, analgesia and then you do the E RCP. Um and er, if they are still not getting better and you can't wait for them to sort of stabilize a bit more, you might need to do an emergency, er, sleeping. Um, and we discuss the PTC. If there's a, a failed uh E RCP, there's also other causes of ascending cholangitis and thus anything that can essentially cause a bacter bilia, which is a bacteria in the bile duct. Um, it can be things like cholangiocarcinoma, um which can cause uh which we would treat with a stent. Um, and there's other treatments as well. Um I, so, but uh sorry about that. Uh let me just bring that back there and then, yeah, there. Ok. Oh, sorry, just gonna set back and then the other course. Um Yeah. Ok. So where were we? Yeah. So, um, yeah, So patients have cho patients with uh choledocholithiasis are at more risk of sepsis and cholangitis because of the bacteria producing a bowel film over the stones, um which um make the bacteria aggregate and they produce a slight matrix, making them less resistance to the penetrance of um antibiotics. So you need to um be really on top of people who are coming in with a 70 cholangitis or choledocholithiasis, you need to really get on top of that. Um And also just one more thing is to always remember to give Vitamin K if the PT or I NR is raised or PT is prolonged or I NR is above 1.5. Ok. Here are some sources and thank you very much.