7 HPB- edited
[00:00:00] Okay, behind the knife ab site review. Today we are reviewing a hepatobiliary. This is going to be a long one, so buckle up. Let's start with some anatomy. Kevin, what are the structures of the portal triad? So you got your common bile duct, which is anterior lateral. You have your proper hepatic artery, which is anterior medial.
And then posteriorly, you have your portal vein. Yeah, make sure you know what that looks like on an ultrasound, because sometimes you'll have a picture that just shows a cross section, and being able to identify those structures on an ultrasound is sometimes a question on the ab site. John, what separates the right and left lobes of the liver?
Yeah, that's Cantley's line. It's the line between the gallbladder fossa and the IVC. Right. Draw an imaginary line between the gallbladder IVC. It is not the fosiform ligament. Those will both be options, so Cantley's line separates the right and left lobes. Kevin, can you describe the venous drainage of the liver?
Yeah, so the liver has three hepatic veins [00:01:00] that drain directly into the IVC. And then the medial and left hepatic vein usually merge together before draining into the IVC. Perfect. John, let's talk a little bit about aberrance and hepatic vascular anatomy. What are the most common aberrance vessels?
The most common one is the replaced right hepatic. It normally branches from the proper hepatic artery, but alternatively it can branch off the SMA. It travels behind the pancreas and the common bowel duct. Additionally, you can have a replaced left hepatic. Which normally branches from the proper hepatic RE, but ultimately can branch from the left gastric traveling in the gastrohepatic ligament.
Sorry, I gotta add a little vascular tidbit here. The replaced left hepatic is what you can get into when you're trying to get a superceliac clamp. On a patient and you're in that gastric, dividing that gastropathic ligament. So something to be really careful of is not that infrequently encountered.
Yeah. And this is a, for myself as a foregut surgeon, this is something I also have to watch out for as it travels in that gastropathic ligament when I'm doing [00:02:00] my. anti reflux procedures or my parasophageal hernias. So both replace right and replace left are common. You can run into the replace right during cholecystectomies.
So these are very clinically relevant and they are frequently tested as well. So know those aberrant, those common aberrance anatomy permutations. Okay. So moving on to benign biliar disease. So, Kevin, treatment for asymptomatic gallstones? Observation. Okay. John, management of uncomplicated symptomatic cholelithiasis?
Elective cholecystectomy. Okay. What about in pregnancy? Symptomatic cholelithiasis, the patient's pregnant. You know, we used to say, let's wait and defer until after pregnancy. What's the current recommendations? So, they have a higher rate of spontaneous abortion with non operative management. So, ideally we'd perform the laparoscopic cholecystectomy during the second trimester.
Yeah, second trimester is probably the best, you know, the latest SAGE's guidelines say lap cholate [00:03:00] really during any trimester for symptomatic cholecystectomy is safe. There are a few things with pregnant women as far as positioning and those type of things. What are some pearls and tips there? So we want to make sure we are very careful when placing ports.
We usually would do this through the open Hasana technique. We want to keep the pneumoperitoneum as low as visually possible. And we also want to place a bump under the right side to offload the vena cava, especially late in pregnancy. Yeah, great. Those are good tips. So again symptomatic cholelithiasis during pregnancy, the recommendation, the official stages clinical practice guidelines say laparoscopic cholecystectomy during any trimester is, is safe.
And so that's been a recent change. So, be familiar with that. Okay, Kevin acute cholecystitis, what's, how do we time the cholecystectomy? Generally we recommend an early cholecystectomy. Yeah, great. So there's no benefit to waiting and cooling off the gallbladder prior to cholecystectomy. So early cholecystectomy for acute cholecystitis if [00:04:00] surgically a fit.
What about patients who aren't able to really tolerate surgery? So they can get a cholecystosomy tube if they're unable to tolerate surgery. Great. Cholecystostomy tube. What, what do we, how do we manage that? Is that, is that definitive treatment? No, they eventually need to have a definitive cholecystectomy once they have it improved.
Yeah. I'll say for patients who are poor surgical candidates who get a cholecystostomy tube in the setting of A calculus cholecystitis you can at about the six week mark, four to six weeks, you can perform a cholangiogram through that tube, and if they don't have stones and their cystic duct is open, they don't necessarily need an interval cholecystectomy, but certainly for patients with calculus cholecystitis, once you're able to optimize them the definitive cholecystectomy is recommended.
What about a prophylactic cholecystectomy John, what kind of patients would benefit from this? Yeah, these are the most common is sickle cell anemic patients also patients with porcelain [00:05:00] gallbladders. Those with large gallstones usually greater than two and a half centimeters. Those with large polyps greater than one centimeter and potentially patients with known gallstones undergoing a bariatric surgery.
Okay, perfect. Okay, what about choledocal lithiasis? How do you, what raises your suspicion that a patient might have choledocal lithiasis and and how do you manage those patients? Yeah, so generally you'll have a, an idea about choledocolithiasis based on the preoperative imaging. You can see clinical cholangitis, you can see the bilirubin elevated, you can see elevated LFTs, you can see the common bile duct greater than six millimeters.
And so if you're in this situation, you have a few options. You can do a preoperative ERCP if you have that available to you. You can do an IOC in the operating room and a possible laparoscopic common bile duct exploration through the transcystic route. Or you can do your lap coli and then get an ERCP afterwards.
Yeah, I would agree with that. I think those are all acceptable and a little bit institution specific. With the caveat that if the patient does present with cholangitis that's not the [00:06:00] patient you want to take to the operating room. So that's one you want to resuscitate IV fluids, antibiotics, and emergent biliary drainage.
You know, the preferred method is with ERCP so that, that should be your answer on the outside for those patients with clinical cholangitis. Don't take those ones to the operating room, but for other patients with choledocal lithiasis, all those things you mentioned are acceptable options. You know, for patients that you have a moderate suspicion, then maybe they have a few abnormalities on their LFTs.
you can obtain an MRCP for better visualization of the biliary system versus doing that IOC like, like you mentioned. So let's say John, that we do do an IOC and we see common ducts, stones during the IOC, what are our stepwise approach? So your first step would be attempting to flush the duct after a minute of seeing glucagon, usually one to two milligrams.
You can usually try this up to two times. If it's a small stone and you have a large enough cystic duct, you can try a trans cystic common [00:07:00] biodeck exploration using fluoroscopic guidance or a choledocuscope. If it's not amenable to a trans cystic approach and you can perform either a lap or open common biodeck exploration.
Or, I post operative ERCP depending on the resources available to you and your institution. Great, alright. Nice, nice stepwise approach. So, let's say you're doing your IOC Kevin, and you are, you don't visualize the hepatic ducts. What do you do? Yeah, I, I do love my fluoroscopic images. So, in this situation, I would pull the catheter back and try flushing again.
Okay, and you still don't see them. At this point I'm getting a little more concerned but I would start with a Trendelenburg to see if I can change.
Yeah. Okay. So it may just be a third head up and you want gravity to work in your favor, but you need to say, what are you concerned about if you don't see those hepatic ducts? Yeah. I'm concerned there's an injury to the paddock. Yeah, exactly. So at this point you probably want to call for help and get your most experienced hepatobiliary colleague.
And even consider [00:08:00] converting to open to investigate the injury of the paddock duct. And that might be the answer on the outside is what they're getting at is that you have an injury that you may need to address. So John, another common presentation is gallstone pancreatitis. So when is an ERCP indicated for gallstone pancreatitis?
Yeah, an ERCP would be indicated if there's clinical signs of cholangitis. Additionally, if you have a stone an obstruction that does not resolve with a little bit of watchful waiting, you'll have to perform an ERCP. Yeah, so, yeah, I agree. Most, most of the times with a gallstone pancreatitis, a stone's passed.
But yeah, if you have evidence of, and so those patients typically don't need an ERCP, but certainly if you have evidence of a persistent common duck stone or if you have cholangitis, then those patients would need an urgent ERCP. Okay. What about really severe? Like they get rip roar and gallstone pancreatitis.
What about the timing for that one? Yeah. So if they have significant peripancreatic fluid collections, you should wait until the collections mature or regress. Okay, what's the [00:09:00] role of ERCP in those patients? In, in that scenario, an ERCP and sphincterotomy should be performed during the waiting period.
Yeah. So the, the concern there is recurrent gallstone pancreatitis, which is a very high risk in these patients. So if you were forced to do an interval cholecystectomy an ERCP and sphincterotomy will reduce that recurrence rate. So those can be very challenging patients and difficult to, to, to time that just right.
John, what about gallstone ileus? What's a gallstone ileus? Yeah, gallstone ileus is a small bowel obstruction, small bowel obstruction caused by gallstone typically at the IC valve. It's resulting from a cystoenteric fistula. Which is usually a fistula to the duo. Yeah, okay, so there's kind of a clinical triad.
What's that clinical triad associated with a gallstone ileus? Yeah, when you look in the question stem, you'll see a bowel obstruction, a gallstone seen in the intestine. Usually maybe an x ray, you might see a gallstone sitting down the right lower quadrant. And Pneumobilia on imaging. Yeah, so this is a good image one that they may give you a patient [00:10:00] with a bowel obstruction and just show you the image like an abdominal series and see, you'll see that Pneumobilia and so you'll know that they're going for a gallstone ileus.
What's the treatment? The primary goal is to relieve the obstruction. This is how you perform this is doing enterotomy proximal to the obstruction. And then milking the stone back and remove it through the enterotomy. Okay, perfect. Yeah, what you get the
stone out. What are you going to do with the gallbladder? You want to leave the gallbladder at that time combined procedure has a higher morbidity and the recurrence rates of this are quite low. Yeah, so in general you don't want to perform the concurrent cholecystectomy after you relieve the obstruction.
You can consider it in very select circumstances. So if the patient is totally stable and they have a nasty gangrenous... In other words, you kind of need to do it for source control. So if the patient is stable and you really need to do it, you can do it. But in general, just relieve the [00:11:00] obstruction and leave that gallbladder behind.
What about, Kevin, let's go back to you. What is Maritzi syndrome and how do we manage it? Yeah, so this is when you have external compression of the common hepatic duct from a stone within the cystic duct. So an ERCP will demonstrate a normal appearing common bile duct with external compression of the common hepatic duct.
And I would manage this with a cholecystectomy. Yeah, these can, there can be a lot of inflammation and scar tissue in these, so they can be very challenging and sometimes you'll have to do a subtotal cholecystectomy. And that's okay in order to avoid damage to the common duct. John. So, sometimes we'll get patients in clinic with gallbladder polyps.
So, what's the most common etiology of gallbladder polyps and how do we manage these? The majority of these are benign hyperplastic polyps. The management depends on size as well as symptomology. So, if they're symptomatic you want to perform a cholecystectomy. If they're asymptomatic you [00:12:00] want to perform a cholecystectomy that's greater than 10 millimeters in size.
If it's over 18 millimeters, you want to treat it as a gallbladder cancer until proven otherwise. And polyps over 6 millimeters need serial imaging or consider surgery to avoid the need for surveillance. Yeah, so I'd say most of these are going to eventually end up taken out. So, if they're symptomatic, certainly.
If there's polyps and there's associated stones, those actually have an increased risk of gallbladder cancer long term. So you should take those out certainly over 10 millimeters of size as they get larger, there's a, a association with gallbladder cancer and sometimes patients just don't want to undergo that serial imaging.
So that'd be another indication to take it out. Okay. So Kevin what causes biliary strictures following cholecystectomy and how do you manage them? Yeah. Many times this can be iatrogenic, either a partial train section, a partial clip placement or a thermal injury to the common bile duct. Okay. And yeah, so a lot of times they can present late to those thermal injuries can even present [00:13:00] years down the road with the, with the biliary stricture.
So how about management? So it kind of depends on, on how symptomatic and what the symptoms are. If there's no biliary leakage, there's could be some endoscopic management of this with like a balloon dilation. If there's a stricture that's recurrent or unresponsive to dilation, you may need surgical intervention.
Okay, great. So, John, so just to wrap up our discussion of benign biliary pathology talk to me about sphincter OD dysfunction. This, this can be somewhat challenging. So how do we manage these? Yeah, typically nowadays we'll manage with the endoscopic sphincterotomy is the preferred method.
Historically, we do a transduodenal sphincteropathy. You'd perform a sphincterotomy at the 11 o'clock position and suture the wall of the common bowel duct to the duodenal mucosa. Yeah. The Speak for Bodies is often a diagnosis of exclusion. It's relatively rare. You know, definitive diagnosis is, is made with ERCP and manometry performed by gastroenterology.
Okay, so let's move [00:14:00] on to a different subject. We're going to talk about now about portal hypertension. So, John, what is the hepatic vein pressure gradient? It's the gradient between the wedged hepatic vein pressure and the free hepatic vein pressure. This requires passage of a balloon catheter into the hepatic vein under fluoroscopy.
And what's normal? Normal is less than six millimeters of mercury. And portal hypertension is greater than six millimeters of mercury. Okay, Kevin, what do we see clinically with portal hypertension? Yeah, so you're gonna see portosystemic venous collaterals. These patients will have ascites. When it gets towards the end stage, you get hepatic encephalopathy and hepatosplenomegaly.
Okay John, what's the relationship between the site of the increased portal resistance and it's, it's etiology. So I'm talking about, you know, that pre sinusoidal, sinusoidal, post sinusoidal, break that down for me. Yeah, this can give you some idea of what's going on. So pre sinusoidal the most [00:15:00] common cause of this is schistosomiasis.
Sinusoidal is alcoholic cirrhosis and viral hepatitis. And post sinusoidal the most common cause is budghiari syndrome. Yeah. And then there's also some mixed disorders. So, you know, like primary biliary cirrhosis has both a pre sinusoidal component and a sinusoidal component. Good job. How about the collateral circulation in the setting of portal hypertension?
Where do we see this? This is where the splenctic vetus system meets the systemic drainage. For example, the distal esophagus and proximal stomach. That's where you have your esophageal submucosal veins to the proximal gastric veins. Also in the rectum where you have the IMV to the pedundal vein the umbilicus or the vestigial umbilical vein meets the left portal vein.
And the retroperitoneum, where the mesenteric and ovarian veins meet. Great, perfect. Okay, so let's move on to management of portal hypertension. So Kevin, what are some ways that we manage portal hypertension? Yeah, so we'll start with our pharmacologic [00:16:00] methods. So you can use splanchnic vasoconstrictors in the acute settings, such as vasopressin and octreotide.
You can also use non selective beta blockers for prophylaxis such as propranolol. And then for endoscopic management, there's variceal banding for bleeding. You can do this for the acute issue or you can prophylactically do it. What's the role of TIPS for portal hypertension? Yeah, TIPS is huge. This really helps decompress the portal system.
And so it's used for acute or recurrent variceal Or Bud Khari syndrome or hepatic hydro Thax. Yeah. I will say that it's, it's not the best for, for ascites, but certainly for those other things that you mentioned. It could be potential indications, but you, what, what's the concern with, with tips? What's the downside?
Yeah, it can certainly worsen the hepatic ence encephalopathy. Yeah. Yeah. Often that hepatic encephalopathy will, will get worse. So there, there is definitely a downside. John we, we mentioned these varices and [00:17:00] we can get acute esophageal variceal bleeding, which is a bad day for everybody. So how do, how do we manage these patients?
Yep. So we want to start in resuscitation immediately, and that includes your transfusion. You also want to start antibiotics. You may need to intubate for airway protection. And our next step is controlling the bleeding. The most definitive way of doing this is with endoscopy. But we can also place some type of balloon tamponade to say Blakemore tube as a temporizing measure.
We also want to make sure we start Octreotide during this time. If we can't control the bleeding with endoscopy we may have to perform an emergent tips. Yeah. Great. You know, TIPS has really kind of changed the game. There are some really more historical surgical options for these, you know, gastroesophageal devascularization procedures, but those are infrequently done if ever anymore.
And they're even more infrequently tested, so we're not going to go into that. But what is sometimes tested are some different options for [00:18:00] portosystemic shunts. So Kevin, I'm going to throw this to you. We have... Thank you. You know, selective shunts, we have non selective shunts, we have partial non selective shunts, so walk us through those because those do every once in a while show up.
Yeah, so for the selective shunts this only decompresses a part of the portal venous system. So the kind of classic one is the splenorenal shunt where you hook up this renal vein to the splenic vein. That can help decompress the portal system. Then you have your partial non selective shunts, and this is where you do like a PTFE graft, and you can choose the size of it to help kind of limit the flow through it.
And then you have your non selective shunts. So this is where you literally just do a portal cable shunt. So... the portal vein to the IVC. So you're completely, basically like an open tips sort of procedure. But this has high rates of encephalopathy and complicates liver transplant later. Great. Perfect.
Okay. So let's move out of portal hypertension and let's talk about some liver abscesses. So John, what types of abscesses can be found in the liver and how [00:19:00] are they managed? So your most common abscess is your pyogenic abscess. And it's usually secondary to a biliary tract infection or a GI source, such as diverticulitis or appendicitis.
We manage this with a percutaneous drain and antibiotics. Additionally, you can have an amoebic abscess. A typical presentation on the test is a patient with a liver abscess after travel to Mexico. We diagnose with, diagnose this with circulating anti amoebic antibodies. Management for this is metronidazole and it rarely needs drainage.
The last one is a conococcal cyst or adatid cyst. The diagnosis of this is a characteristic double walled cyst on CT. The labs you would see for this type is an ELISA test an indirect hemagglutination test an indirect immunofluorescence antibody test, a latex agglutination test. Those would be positive for a adapted cyst.
The management is albendazole followed by drainage. You want to drain these using the pair technique. Puncture, aspiration, [00:20:00] injection, and then re aspiration. And also consider surgical resection for very large cysts. Yeah, so, frequently what's asked on the outside is which is the most common liver abscess?
And again Kevin, which is the most common? Pyogenic. Yeah, pyogenic. So you'll have options of pyogenic versus parasitic so pyogenic most likely due to the GI sores, diverticulitis, appendicitis, E. coli is the most common pathogen so that is really the kind of the highest yield thing there for, for the app site.
Okay, so next up is cystic compatibility lesions. So let's talk about coelodocal cysts. John, what are coelodocal cysts? Corticosis there is an unknown etiology to it, but likely secondary to an anomalous biliary pancreatic duct junction with reflux of pancreatic enzymes it's a long common BP duct.
Most are identified and treated early in childhood it is a pediatric disease typically. It can cause pain biliary obstruction and cirrhosis, and they do carry [00:21:00] a malignant potential. Yeah, so we'll talk a little bit about management and specifically with that, you know, malignant potential, but there's a classification system that really everybody needs to know because it is frequently tested and it's the Todani classification system.
So let's just go through them. So Kevin, what's a type one coelodocal cyst? So that's the fusiform dilation of the extra hepatic biliary tree. Right. Fusiform dilation, extra hepatic biliary tree. How do you treat them? This is resection with hepatico jejunostomy. Type 1 resection, hepatico jejunostomy. John, a type 2 choledocal cyst.
That's the saccular diverticulum of the common bile duct, and you treat it with the excision of the cyst. Okay, good. So type 2, saccular diverticulum, common bile duct, cyst excision is the treatment. Okay, Kevin, type 3 choledocal cyst. Yeah, so this is dilation of the intramural duct. Yeah, otherwise known as?
Coli docoseal. Yeah, so type 3 is coli docoseal. How do you manage those? So, you can approach these transduodenally and you can do a transduodenal excision or [00:22:00] sphincteroplasty. Yeah, yeah. The way it's typically worded is a sphincteroplasty so type three, choledoplasty, sphincteroplasty. John, so type four, there's a type four A and a type four B.
Break those down. Yeah. Type four A, multiple dilations of intra and extra hepatic ducts. You treat it with a hepatic reconstruction. Type 4b, multiple dilations of only extrahepatic ducts, excision and hepatic adrenostomy. Okay, perfect. And then, and then Kevin, type 5? So this is multiple dilations of intrahepatic ducts or Correli's disease.
Okay, and treatment? Transplant. Okay, okay. Yeah, you can have one attempt at a partial resection depending on the distribution, but typically the, you know, the thing to remember is multiple dilations of the intrahepatic ducts, Correli's disease, and the treatment is typically a liver transplantation.
Okay, so more commonly seen than colodocal cysts are simple hepatic cysts. So what's the management of a simple hepatic cyst, John? So no [00:23:00] treatment if these are asymptomatic. If they are symptomatic, you can do a laparoscopic cyst fenestration. And then you want to send the capsule to pathology. What about aspiration?
Can't you just IRR says, I got a great target, let me just aspirate it. Well, apparently it's a 100 percent recurrence rate with aspirational bone. Okay, and what if you're concerned for an abscess, a hidatid cyst, or a malignancy like we said before? You want to aspirate and send to cytology. Okay, great.
Okay, so now we're going to start working through some different hepatobiliary tumors. So let's start with the most common one, the hepatic hemangioma. So John, what can you tell me about a hepatic hemangioma? Yeah, it's the most common liver tumor. It's female predominance it's caused by congenital vascular malformations.
How does it present? Present generally asymptomatic. It can cause pain or compressive symptoms. Rarely where you have hemorrhage from these also rare would be inflammation or coagulopathy. So I've heard of this thing called the Casabach Merritt [00:24:00] syndrome. What is the Casabach Merritt syndrome? It's hemangioma plus consumptive Okay, so sometimes you'll see that.
They'll give you laboratory values in somebody with a large hemangioma. And they'll ask you what's going on. And again, it's a consumptive coagulopathy. Now, hemangiomas have some pretty characteristic imaging. And what I'll tell everybody who's listening is go to our ab site companion. There's an excellent image in there that has examples of how these different tumors look on imaging.
We're going to talk through it as you review that. But on the exam, you're going to be expected to be able to recognize these tumors on the actual images. So be sure to review that. So for hepatic hemangioma, what are the characteristic findings on CT and MRI, John? So CT, you'd have a hypodense lesion pre contrast.
It will enhance peripheral to central. In the arterial phase. And then you also have persistent contracts [00:25:00] on delayed series. Okay, so hypodense pre contrast peripheral to central enhancement in the arterial phase and persistent contrast on the delayed series. Okay, how about an MRI? MRI will be hypo intense on T1 and hyper intense on T2.
Okay, treatment? The treatment for these is just observation for asymptomatic lesions regardless of size. There's not really any risk of rupture. For symptomatic lesions, you want to resect these. Okay. All right. So that's hepatic mangioma. So moving on from there, let's talk about focal modular hyperplasia.
Kevin, what's the epidemiology of focal nodular hyperplasia? Yeah, so this is the second most common liver tumor and it's found in women around 30 to 50 years old. And how does it present? It's normally found incidentally on imaging. It's also normally asymptomatic. Yeah. And sometimes you'll even see these intraoperatively on the liver.
And so you kind of need to know how to recognize what they look like. What do you see on imaging with these? Yeah, so it's well demarcated and has rapid arterial enhancement with a [00:26:00] central stellate scar. Yeah, the central stellate scar That's the that's the the buzzword for focal nodular hyperplasia.
What about on MRI? On MRI? It'll be hypo intense with the central scar in t1 and it'll be iso intense with hyper intense scar in T2. So what, what, how do you treat these? Do we need to worry about these when we see them? Nope. There's no malignant potential and there's no bleeding risk. Perfect. Okay. So next is a hepatic adenoma.
So, John, epidemiology of a hepatic adenoma. These are also rare. They're associated with oral contraceptive use and androgen steroid use. They do have a malignant transformation rate, about 10%. And then risk of rupture increases with size. So there's about 30 percent risk of spontaneous bleeding and tumors greater than five centimeters.
Right, so in contrast to that FNH, the adenomas do have a malignant potential and they are at risk of rupturing. So how do they present? They can present with pain, abdominal fullness, abnormal LFTs, or bleeding from the rupture. Okay, and what do [00:27:00] these look like on imaging? So on CT you get arterial enhancement with washout on portal phase.
Do not usually demonstrate a delayed washout. You'll have, see a smooth surface with a tumor capsule and no central, central scar. On MRI, you have a mildly hyper intense on T1 and T2. Okay, great. Yeah, so again, no central scar with this. Arterial enhancement and washout on the portal face. That's what you're looking for.
What do you want to do with these? How do we treat them? So in small lesions, less than five centimeters, you want to discontinue. Oral contraceptives and then it may regress. Larger lesions, lesions greater than 5 centimeters, or no regression after stopping the oral contraceptives you want to resect.
Obviously, if they're ruptured, IR embolization would be your first go to. And then resect in an elective setting. Okay. Yeah. And again, a lot of that has to do with that malignant potential and the risk of rupture. So you, you, you want to resect these and it frequently shows up on the test that they'll have a [00:28:00] small, you know, two to three centimeter adenoma in a female on OCPs.
And the first step, as John mentioned, is to discontinue those OCPs and it may spontaneously regress after that. Okay. So now let's talk a little bit about hepatocellular carcinoma. So Kevin, what, what are some risk factors? For hepatocellular carcinoma. Yeah, so, Hepatitis B, Hepatitis C, cirrhosis of any cause, inherited errors of metabolism such as hemochromatosis or alpha 1 antitrypsin deficiency.
and aflatoxin. Yeah. And I think what all those things have in common is those are things that cause liver inflammation. So yeah, those are all great risk factors. Now these also have characteristic image and findings. So what are those? Yeah. So in CT scan, you're going to have hypervascular lesions that are hyper intense during the arterial phase.
And then hypodense during the delayed phase. Okay, so let's say that we, we have a tumor that has those characteristic findings and then we also have an elevated AFP so do those patients need a biopsy? [00:29:00] No. Okay, great. So characteristic on imaging and elevated AFP don't necessarily need a biopsy for diagnosis.
Is there any role for PET CT in hepatocellular carcinoma? Yeah, PET CT doesn't add anything to the workup here. Okay. Yeah. So no role for PET with in hepatocellular carcinoma. How about, where do these, how do these metastasize, where, where is the most common site for them to go? I believe it's hematogenous and it goes to the lung, right?
Yeah. So the most common site of a metastasis is, is a lung, is the lung. So, you certainly need to include that in your staging workup. So Ken, what's the management of hepatocellular carcinoma? So if you have a solitary mass without major vascular invasion and if you resect it and there'll be adequate liver function, resection is the best treatment.
Okay. Yeah. And resection is possible, but controversial for limited major vascular invasion or with multifocal disease that is still resectable. But that's a little bit more controversial. Now you mentioned Leaving [00:30:00] enough normal liver, so how much functional liver remnant is needed? Yeah, the liver is pretty remarkable.
If there's no evidence of cirrhosis, you only need to leave 20 25 percent of the liver. If they have child's class A cirrhosis, you need to leave 30 40 percent of the liver. How do you, how do you, what's the best way of, you know, determining what that CT and MRI and 3D reconstructions, they're able to determine this.
Okay, so what, what would you do if you do that and it turns out you're going to have less than that, you know, 20 to 25 percent in no cirrhosis or 30 to 40 percent with child's a cirrhosis. So what you can actually do is you can do a preoperative portal vein embolization of the disease size to cause hypertrophy of the other part of the liver.
Perfect. Yep. Exactly. So again, so no cirrhosis or child class A and it's early stage, you want to do a resection. So, how about for those with moderate to severe cirrhosis and still early stage hepatocellular [00:31:00] carcinoma? What are we, should we consider then? So this would be a good patient for transplant.
And is there any criteria that we, we look to when determining if if the patient is a candidate for transplant and hepatocellular carcinoma? Absolutely. There's the Milan criteria. And what this States is that if you have one lesion under five centimeters, Or you have three or fewer lesions that are all less than three centimeters with no gross vascular or extropedic spread.
You can do a liver transplant. You usually perform neoadjuvant chemotherapy prior to the transplant. Beat me to it. That was the exact point I was about to make. So yeah, these patients will get neoadjuvant chemotherapy prior to the transplant. How about like some local regional therapies? I've heard of things like TACE and, you know, there's these chemoembolization.
What, who are candidates for, for that therapy? Yeah. So these patients generally cannot tolerate a curative surgical treatment. And so this can be a bridge to curative therapy for them. Okay. And what are the different options? So kind of in broad strokes, you have the [00:32:00] ablative therapies, you have the arterially directed therapies and you have external green radiation therapy.
Okay. So who what lesions are best for ablations? You have radio frequency, cryo ablation, microwave. Yeah, so these are better for small lesions, less than five centimeters. Okay, well how about the taste, the trans arterial chemoembolization taste? Yeah, when you have a bigger lesion, like greater than five centimeters, they don't qualify for the ablation anymore.
This is where the arterial directive of the taste... Okay. So yeah, considered for larger tumors, unresectable greater than five centimeters. Okay. And you said something about external beam radiation therapy. Yeah. So if this is a patient that has unresectable disease or not amenable to ablation or case.
Okay, perfect. So John, back to you. So let's talk about cholangiocarcinoma. So moving on from hepatocellular carcinoma now into cholangiocarcinoma. What are the features of cholangiocarcinoma? Yeah, we classify cholangiocarcinoma as intra hepatic or extra hepatic disease. Okay, and what are some risk [00:33:00] factors?
So just like the liver inflammation of the bowel ducts is the main risk factor, including primary sclerosin cholangitis, bowel duct stones, caudal cysts, liver fluke infections, and HBV and HCV. Okay, so let's first tackle intrahepatic cholangiocarcinoma. What are some management principles for intrahepatic cholangiocarcinoma?
So the first thing is that we don't have to biopsy these if they're concerning radiographically and clinically suggesting malignancy. You can do a diagnostic laparoscopy to rule out disseminated disease and that is most common. Lymph node metastases pass portal hepatitis and distant metastases contraindicate resection.
A multifocal liver disease is generally not amenable to resection as well. Hepatic resection with negative margin is the goal. Usually through a formal anatomic resection, but you can also do a wedge resection or segmental resection. Now what's the role for, you know, like [00:34:00] hepatocellular carcinoma, we could do a a transplant for, you know, sometimes that multifocal disease.
Is that an option for cholangiocarcinoma? No, not in multifocal. hepatocellular carcinoma,
you know, you can Transplant as long as you meet the Milan criteria, but for cholangiocarcinoma, that is not an option. Okay now Kevin Let's talk about extra hepatic cholangiocarcinoma. So what are some basic principles for management of extra hepatic cholangiocarcinoma? Yeah. So it's kind of the standard oncologic principles of, you need to do a complete resection with negative margins with a regional lymphadenectomy.
Okay. Well, how about Hylar? Let's talk about Hylar cholangiocarcinoma. Yes. In order for this to be resectable, the contralateral hemiliver must be intact as far as arterial and portal flow and biliary drainage uninvolved with the tumor. Okay. Okay. And what's involved with that resection here at the hylum?
So you're gonna have to do I would imagine some [00:35:00] type of reconstruction, right? Exactly. Generally, you're gonna end up doing a Roux en Y hepatico jejunostomy. Yep. That's right resection with Roux en Y hepatico jejunostomy. Okay, one more Kevin. How about the surgical management of a distal cholangiocarcinoma?
So it's very distal on the duct, right? So at this point now you're doing a Whipple. Yep, pancreaticoduonectomy. Perfect. Okay John let's move on. Out of the liver and into the gallbladder. So gallbladder cancer. Very rare, but what are some risk factors? Yeah, there's lots of risk factors here. Some Mexican Americans, Native Americans, females, obesity, large gallstones greater than three centimeters, going back to that inflammation thing, chronic inflammation porcelain gallbladder, which is a much lower risk than previously thought, polyps greater than one centimeter, Typhoid infection, primary sclerosing cholangitis segmental mucosal calcifications, and finally anomalous pancreabiliary junction.
Yeah. So yeah, a lot of risk factors there. A lot of things that increase [00:36:00] inflammation. The porcelain gall bladder was previously thought to be a very high risk. Now it's probably a very low risk. That's been overblown, but absolutely. So, and I think probably the, the, the, the, These are most often discovered incidentally at the time of cholecystectomy for symptomatic gallbladder disease.
It is the way you'll see this both clinically and actually on the test. That's what will happen. You'll have a patient that underwent a cholecystectomy and on pathology, lo and behold, it's gallbladder cancer. So, how do we, what do we do in that situation John? So, this guides our next surgical management.
So, we found a tumor, a T1A tumor that just invades the lamina propria. then we're okay with cholecystectomy alone. If we have a T1B and greater, which invades the muscle layer of the gallbladder, then we need to do, we've already done the cholecystectomy, but we also do a limited hepatic resection, typically just segments 4B and 5A.
And also a [00:37:00] portal lymphadenectomy. Yeah, and you know, more extensive resection might be required for advanced and larger tumors to obtain negative margins. But the way you're going to see on the outside, it's going to be that you're going to make that distinction between the T1A and 1B, so you need to know that.
So, essentially, if it's invading the muscle layer, you know you have to do more, which is a segment 4B5 resection, 4B5, and that's the way it'll be listed on the exam. And don't forget that portal lymphadenectomy along with that. Okay, well, that's a great review of hepatobiliary, so let's end it off with some quick hits.
You guys ready? Absolutely. Let's go. All right. So Kevin what hepatic vein pressure gradient is typically required for a variceal rupture? Yeah, I think about around 12 is when you have that risk. Yep. That's when you get concerned at 12. John, what is the actual definition of portal hypertension?
That's when your hepatic vein pressure gradient [00:38:00] is six millimeters of mercury or higher. Okay, great. Kevin, what are the components of the, the child's pew score. So that'll be your bilirubin, your albumin, your prothrombin time and your encephalopathy and ascites. Bilirubin, albumin, prothrombin, the presence of encephalopathy then the presence of ascites.
John what are the components of the MELD score? That's bilirubin, INR. Creatinine and sodium. Yup, bilirubin, iron, arcanine, and sodium. Perfect. At what MELD score do, has it been shown that patients have a survival benefit with transplantation? Once you get to 15. Yup, 15. Okay, John. So you have a patient with colorectal cancer and an isolated liver met.
He receives neoadjuvant full FOX therapy, and then he's restaged, which showed a complete radiologic response. What's your next step? You'd still perform the hepatic resection as complete pathologic responses is rare. Yeah. So that's kind of the same principle as rectal cancer that is clinically resolved after neoadjuvant therapy.
[00:39:00] So Kevin, patient with an asymptomatic cholelithiasis and a five millimeter gallbladder polyp. What do you do? You'd do a cholecystectomy in this situation. Yeah, so why is that? I thought we said that you know, polyps under a centimeter don't need cholecystectomy and those under six millimeters don't even need surveillance.
So why are you doing it in this situation? Well, there is a little bit of a risk of malignant transformation within the gallbladder polyps has been linked when they have concurrent cholelithiasis. Good, great. Okay, so John what's the highest negative predictive value test for choledocholithiasis?
that's your GGTA normal GGT has 97% negative predictive value. Great. Okay. Okay, Kevin. So, you have a patient with a prior RU and y gastric bypass, and now they come in with Choli. Dosis. What's the problem and what do you gotta do? Well, now you've bypassed their stomachs. You can't easily get there with an ERCP.
So you do a transgastric ERCP or an advanced double balloon [00:40:00] endoscopy. Cool. Yep. Transgastric ERCP. They're actually fun cases. So John what is the significance of hepatocellular cancer found in a young patient without cirrhosis? All right. So this is the fibrolamellar variant of hepatocellular carcinoma.
It has a better prognosis but recurrence is common. The marker we use for this, Jason? Oh, that's Neurotensin. And that's very testable. So, Fibromyalgia variant, young patients, hepatocellular cancer, Neurotensin is a marker. You will see that. So, Kevin, you have an incidentally found adenocarcinoma invading the lamina propria layer of the gallbladder following cholecystectomy.
What's your next step? No further treatment. Cholecystectomies alone is enough in this scenario. Okay, and just to revisit, let's say it invaded the muscularis. What do you do then? Well, then you need to do your concomitant liver section. Yeah, segment 4B, 5, and? portal lymphadenectomy. Yep. Absolutely. Yeah. To add that lymphadenectomy and also don't forget to [00:41:00] stage the patient too.
So CT chest out of the pelvis, tumor markers, CA 19, nine CEA. So don't forget your staging. So let's say Johnny, we're in that same situation or we've gone back, we've done our, our resection. What about I've heard people say you should excise the port sites from your lap Coley in the setting. Do we need to do that?
No, it's not been demonstrated to be an oncologic benefit. Yeah, so don't need to do that. Okay, back to you Kevin. What is the significance of isolated gastric parencies? So this is most commonly caused by splenic vein thrombosis, secondary to pancreatitis. Yeah, okay, right, okay, and what's the treatment?
Splenectomy. Splenectomy, perfect. John you have a patient that's four weeks after hospitalization for a car accident that had a liver laceration was managed non operatively, but now presents with an upper GI bleed. What's your first step and what do you want to do? So the first step just like mostly all upper GI bleeds is an EGD.
If you see blood coming from [00:42:00] the duodenal papilla you have to be concerned about hepatic artery biliary duct fistula, and the treatment for this would be angioembolization. Perfect. Yep, EGD, make the diagnosis hemobilia, treat with angioembolization. Okay, so let's go over some different segmental resections of the liver.
And I want you to tell me, Which segments you take out with these particular resections. It's a little confusing, but it'll make sense. So, so Kevin, let's say you're doing a right liver resection. What liver segments do you take out with a right liver resection? Five through eight. Yeah, five through eight.
Okay John, a left liver resection. This is two through four plus or minus the caudate. Okay, okay. Kevin, a left lateral segmentectomy. What segments are involved in that? Two and three. Okay. John, an extended right, which is also known as a right trisectionectomy? That's five through eight plus the four segment.
Okay, what about an extended left? That's 2 through 4 plus 5 and 8. Yeah, so it's a [00:43:00] good idea just to have a map in your head of the liver because sometimes you will have to identify these liver segments based on a description. We do have a good image inside the companion, so memorize that image and have that liver map in your head and know where those segments are.
Okay, that does it for hepatobiliary. Hope everybody found it helpful. Thanks for listening.