During this 20-25 minute pre-recorded lecture, Dr. Kamron Pourmand discusses the topic of vascular and infectious complications. This in-depth review will provide an update on this topic for your clinical practice as well as supplement your learning for the ABIM Gastroenterology and Hepatology boards. CME pre-requiste of live Q & A webinar, 8th Annual Mount Sinai Intensive Board Review in Gastroenterology & Hepatology on Oct 13. Hello. Everyone will be going over some vascular and infectious complications and liver disease as well as discussing liver biopsy and its application. I have no disclosures. Let's jump into our first question. This is a 62 year old female with chronic treatment, naive hepatitis C. Who is presenting to your office for an initial consultation for hep C. Treatment. She has not been seen by a physician for many years and only recently established primary care. She takes no medications on exam. She's thin, her lungs are clearer, her abdomen soft and non tender. She's very mild pedal edema and there are multiple multiple spider ngoma on her skin. She has no john destroy asterix is Her lives are listed here. Notable for a mile trans am in its elevation, normal billy Rubin and alkaline Foster taste wild I nr Elevation of 1.3 relatively normal creatinine albumin and some mild pants. I. Dapena as well. Her radical question Doppler shows a nausea, liver spent omega lee and the portal vein is not seen. What is the next best step in management Start? Warfarin send a hyper critical work up, perform an upper endoscopy, refer her for a liver transplant evaluation or obtain blood cultures. So the correct answer is upper endoscopy. So what we were trying to get out with question one was a portal vein thrombosis. So they come in two different flavors that can be acute or chronic and it's important to differentiate the two because they have different clinical presentations and management. So the in cute setting patients often present with fever abdominal pain. Um they can actually get intestinal ischemia if it extends into the present eric veins um which can lead to sepsis of severe um There's usually a lack of portal hypertension in the acute phase but it can happen. Um But you'll also see a lack of collateral circulation on imaging for chronic PVT s. Um It usually presents as portal hypertension in this setting and these can be referred to as a cavern oma colloquially. Um You here if you see that an imaging or notes. Um And this is due to the fact that there is um collateral ization in in the clot. The most common ideologies for portal vein thrombosis are cirrhosis. Um tumors like have had a cellular carcinoma and hyper critical states. Think of hyper critical states. And patients that don't have cirrhosis. The most common tumors involved are outside of the cell carcinoma are neuroendocrine tumors. Pancreatic cancer. Um And cancers of unknown primary. Um And how these clots occur is basically just direct extension of the tumor cells into the vein. The incidence of portal vein thrombosis varies so a nonce erotic patients or compensated Sirat IX. The incidences 0.6 to 16% But d compensated cirrhosis and since increases quite a bit to 35%. Doppler ultrasound is a diagnostic test. The diagnostic test of choice at a 98% negative predictive value. And then contrast enhanced ct or MRI um is often obtained especially if a tumor is suspected or to further clarify the Doppler findings if there if there um ambiguous usually if if a right upper quadrant ultrasound is positive and the patient is so erotic. That kind of gives you your answer. Um But if really if you're suspecting a tumor for any reason, you may want to get contrast enhanced imaging or consider a hyper critical investigation if they're not so erotic. This is a diagram that kind of outlines the portal vasculature pretty nicely. Um So we can kind of go over it very briefly to kind of show why some of this pathology occurs when when when these clots form. So here I've highlighted the portal vein right before it goes into the liver. Um And when the portal vein to also clot in it extends. Um You can get these, you know, not just a portal venous thrombosis or PVT, you can get a porto esoteric thrombosis or you know, in this smb or superior mezza terek vein or the inferior mezza tonic veins as well when the cloud propagates into the you know um to them esoteric veins. This is what leads to the intestinal ischemia. Um and which can lead to the sepsis especially if it's a cute, so um that's just kind of depicts why that can occur and why these clots can propagate and cause an issue also remember there's different forms of portal hypertension there's pretty sinusitis. Post minus total um and interest minus total portal hypertension. So this is a form of pre signal soto portal hypertension because you can see the portal vein yet hasn't yet reached the liver. Um And we'll talk about some other causes of portal hypertension coming up next as well. Mhm. So the management of PVT um kind of comes down to the ideology um and the acuity of it. So and patients with cirrhosis who have a PVT you wanna screen first officer viruses and applied treatment as you would for anyone else. Um Coming in with viruses. So primary and secondary prophylaxis. According to guidelines the patient is a decompensate. It's erotic. You want to consider transplant evaluation in these patients. If the PVT propagates to the superior Mesen Terek vein becomes difficult to perform an isolated liver transplant in that setting. Often patients would need a multi visceral transplant. So if there'd be compensated. Um They have other indications for transplant. If they develop a PVT it's probably prudent to have them be evaluated just to make sure that's not an option for them in the acute setting. Um Consider anti regulation. If you have prior imaging that doesn't show this and you have repeat imaging that's um within a fairly short time period that shows um a clot. You can consider antique regulation of these patients that don't have an excessive risk of bleeding. Um And these patients that you want to consider antique regulation and especially if they're so erotic with various is you want to make sure their various is if they're large are you know abandoned eradicated or have appropriate primary prophylaxis before um starting anti regulation in order to prevent any bleeding in chronic PV TSR cavern Omagh's um In patients with cirrhosis, these do not requiring tabulation. It will not help alleviate the cloth in acute PVT in patients without cirrhosis. Um And these patients often again they can come in with you know fever, abdominal pain, some concern for intestinal ischemia, potentially see when a hospitalizes patients start anti coagulation, consul interventional radiology um And often they're able to you know deal with these especially if they clawed extends either via tips or thrown back to me. Um And surgery is also usually involve just you know as a backup as well. And chronic PVT s. Um and patients without cirrhosis. And these patients again, you know, anti regulation isn't as straightforward. So it would definitely investigate with a hyper questionable work up. And if there is another indication for for anti coagulation, I would definitely consider it in those patients. And if it's a tumor thrombosis. Um These patients you know, don't respond to anti coagulation. Um Sometimes tumor thrombosis can be identified if the clot enhances on the arterial phase on a contrast enhanced image. So let's go back to our first question and figure out why the other answer choices were incorrect. So in this patient who's presenting with a PVT with underlying cirrhosis. Um This patient you know, we wouldn't start coming in on because the patient is erotic and lacks acute symptoms. So it's most likely a chronic PVT. Um we wouldn't send a hyper equitable work out because the patient is erotic. So that's the that's the reason why they developed a clot. It probably wasn't due to a secondary thrombin, ophelia. So not necessary in a patient um like this who is well compensated with an otherwise low melts or refer for transplant evaluation, probably want to be the best next step. But something always to consider in the background, especially if they get worse and blood cultures. This is kind of getting at um some type of a form of pilot phlebitis, which is basically when you develop a clot that you worry super infected and can lead um to sepsis. So she has no fevers pain or anything like that suggests pilot phlebitis. So that one was not correct either. Moving on to Question # two. So this is a 19 year old male who's presenting to the hospital with abdominal pain. He'd been having right upper quadrant abdominal pain for four days and was referred to the emergency room by his pediatrician when they noted significant abdominal distention. He has no history of liver disease, alcohol use or smoking. His on has factor five leiden on exam. He has tenderness in the right upper quadrant without rebound regarding and a positive fluid wave, he does not have asterix is he does not have any stigmata of chronic liver disease such as spider angio meta or palmer erythema. On exam, his labs are notable for a trans am in its elevation lT nay str elevated to 1409 100 respectively. His billy Rubin is elevated at 2.8. His alkaline foster taste is normal. His hemoglobin is 18 relative policy. Thenia and his platelets are also elevated. 800 with an iron are of 2.7, both of which are elevated. His Doppler ultrasound shows happen omega lee besides and a large hepatic vein with absent flow signal, which of the following tests is most likely to be diagnostic a Jack to mutation analysis. An alfa feta protein, a diagnostic paris in texas, a liver biopsy or a smooth muscle antibody with serum immunoglobulins. So the correct answer here was a Jack to mutation analysis and this question. Um The patient has but chiari syndrome. So this is a vascular disorder of the venus outflow tract. So looking at the hepatic veins here signs include right upper quadrant pain in the sides. So in the setting of cloths, just like the portal venous thrombosis, there's like an acute and a chronic presentation. So the acute presentation causes dramatic congestion and hippolyta site hypoxia and this can actually lead to film that liver failure in patients if it's not resolved and chronic but chiari can lead to complications of portal hypertension. So again, acuity matters in terms of um uh you know how sick the patient can present ideologies and risk factors. So for Budd chiari um milo proliferate disorders are the most common um risk factor for this. So 50 almost half of patients that present with this have a Jack to mutation which is the reason why this answer choice Jack two mutation analysis was the correct answer here. Um Also with factors include anti fossil lipid syndrome, malignancy or all contraceptives and other inherited hypercritical states that are listed there. The incidence is um 1.2.1 and 2.5 million per year. And similar to P. V. T. S. A Doppler ultrasound is the initial diagnostic test of choice. Back to our picture of the venus um system here related to the liver. Um What we're looking at with Budd chiari is here this is these are post sinus or middle causes of portal hypertension. So after the blood flow um exit the liver going to the I. V. C. The right and left. The paddock veins are circled here. So this is where we're looking at obstruction occurring um For for but chiari. So as PVT was was the cause of pre sinus it'll portal hypertension. But chiari is a form of post minus total portal hypertension. Whereas cirrhosis on its own is a type of sinus oil, portal hypertension within the liver the management of the chiari. Um So the cornerstone is to relieve the obstruction. Um and identify the underlying cause as well as treating symptoms of portal hypertension. So um diagnostic evaluation. So usually if you know if the Doppler is suggestive but not completely diagnostic, you can get an MRI or ct with contrast. Um to really delineate the vasculature and you want to send a hyper quiet will work up in these patients. Um The acute presentation. Again the management is you know anti regulation and and dealing with the clot itself. Um And this can be done with medically or or uh with decompression either via interventional radiology or surgery if needed. And then again if the patient develops form and hepatic failure which can happen in these patients especially if it's a cute um You want to consider liver transplantation of these patients so they should be evaluated in a center that performs that. Moving on to Question # three. So switching gears a little bit here And this question we have a 35 year old male who presents to the emergency room with fever and abdominal pain. He had briefly traveled to Mexico two months prior for a bachelor party remembers having some self limited diarrhea. When he returned. He has no known past medical history on exam. His blood pressure is a little bit soft, 100 over 70. His heart rate's elevated at 1 10 and he's febrile to 11.9 he's mildly tender in the right upper quadrant without any peritoneal signs and he has no john this or stigmata of chronic liver disease. His labs are notable um for mile trans am in its elevation Billy Rubin of 1.5 and all faucets also elevated at 1190. Um and I and our of 1.1 relatively normal. In a white count, mild Lucas psychosis of 13.8. On a cat scan. With contrast, you see a small low density lesion in the right lobe of the liver with some peripheral enhancement, a smooth liver contour and a normal small intestine and colon. The next best step of management is obtaining stool studies starting stuff. Track zone and Metro Night is all colonoscopy, starting up benches all or a biopsy um respiration of the liver lesion. So the correct answer here was starting antibiotics um with subtract zone and Metro Night is all. So this question was getting an amoebic liver abscess. These are caused by anti amoeba histological which is endemic to India africa, central and south America. And the organism, you know, does its damage by, you know, boring into the colon is usually the right side of the colon. Um And you can actually see ulcers when this happens. And if you get aboard question where this pathology of a colonic ulcer and it has flask shaped um organisms that those are the you know, that's suggestive of geneva his politica, if you do see that. And so the organism kind of burrows through and injures the portal circulation and then, you know reaches the liver and then causes an abscess to form and you can get abdominal pain, fever. It's less um common to present with both an abscess and the diarrhea. So you're the diarrhea happens in this catalytic phase. Um and by the time the abscess forms that's kind of resolved um and you're left with like kind of just the right upper quadrant pain and fever at that point. Antibody testing for diagnosis is highly accurate but it may not be positive in the initial stages of the disease because it takes about a week for the antibodies to form fragile or Metro night is all is a highly effective antibiotic for this. Um And usually give it for about 7-10 days. You also want to give a Luminal agent. So para my son or die Oto hydroxy quint afterwards to destroy the Luminal system. You give that for about an additional week. Um to make sure the organism doesn't come back. It's important to realize that there are other types of infectious liver cysts. So a common one is a pie. A genic liver abscess is the most common. Um And these are poly microbial if for some reason you have an aspirate available to and in our patient, you know, we couldn't really discern between just a regular pie eugenic liver abscess or and to me of a given the demographic. Um So it's reasonable to cover with self tracks on as well as the Metronet is all just to kind of be a little bit broader to cover our bases. And that's why that was also in the answer choice had that insists are caused by a kind of Caucus. This is a different one. Um and that's carried by dogs and wolves. Um and if you have imaging you may see a internal sub stated cyst. Um that's kind of like a classic characterization of it and for this, you treat it without Ben Diesel. So going back to our questions them and why the other answers were incorrect. Um, stool studies. Um you know, may not be sensitive, especially if the kinetic phase has resolved colonoscopy. You can see these rights that ulcers apparently. Um but these are usually antecedent to the liver abscess. So and then the CT scan and this question, some didn't show any signs of colitis, at least for what it's worth on the imaging. So that wouldn't be too too helpful. Albin Diesel, like I mentioned just previously, is used to treat a kind of Caucus. Hi dad. It's is different from a music liver abscess and biopsy your aspiration of liver liver lesion would only occur if the if the legion was at risk for rupture. Um and this is if it's uh you know if the patient isn't responding to antimicrobial therapy remain septic, especially left sided abscess, which are a little bit more prone to rupture or if the diagnosis of what the lesion is is in question. Still Moving on to Question # four. So this is a 59 year old female with coronary heart disease on dual anti platelet therapy and stage renal disease on dialysis and diabetes who was referred by her transplant nephrologist Due to concerns for cirrhosis, she's been experiencing increasing increasing abdominal girth and dyspepsia on exam. She appears well with the functioning of the fistula and the left arm has a solid murmur and also as shifting dullness in the abdomen. No spider ngoma to Jonathan palmer erythema to kind of suggest chronic liver disease. Her labs are notable for a mile trans am. Its elevation. Billy Rubin is normal octopus. Maybe just a touch above Einars relatively normal and her virus, viral hepatitis viral hepatitis serology. These are negative. Her Doppler ultrasound shows an academic liver with a smooth contour, Peyton vessels and moderate societies. A diagnostic Paris and pieces is performed with a sag of 1.4. Total protein of 3.8 and a white blood cell count total of 120. What is the next best step in management? Clear her for a kidney transplant. Start Lasix and old Acton perform a per cutaneous liver biopsy. Perform a trans jugular liver biopsy. So the answer here was perform a trans jugular liver biopsy. So it's reviewed the wrong answer choices. So you wouldn't want to clear this patient for a kidney transplant without really determining what the ideology of our cities is and making sure she doesn't have significant portal hypertension. Mhm. You also don't want to start diuretics as you know they probably wouldn't be clinically as effective because she's dialysis dependent as as it turns out already. And then it also won't give you the answer as to why the societies is there to begin with pertains liver biopsy. Um A relative contraindications that would be having a societies or taking end sets. And it also wouldn't provide you a portal pressure assessment to really quantify the portal hypertension if it exists. So wouldn't be as helpful compared to a trans jugular liver biopsy as well. So let's continue this patient's case. So the same patient we just had before um she undergoes a transgender liver biopsy And the i. r. um provider provides these measurements. So the free hepatic venous pressure was 15 and the wedge hepatic venous pressure was 18. A liver biopsy is being processed by pathology as we speak. What is the next best step in management pursue a combined liver kidney transplantation since she has cirrhosis. Start a non selective beta blocker, obtain a trans thoracic echocardiogram or place the tips. The correct answer is to obtain a trans thoracic echocardiogram. So the key to understand this question is being able to interpret the pressure is obtained during the trans jugular liver biopsy. Uh the portal pressure. So you need to calculate a hepatic venous pressure gradient. This is a period of H. V. P. G. So it's the wedge pressure minus the free hip added pressure. And in our patients 18 -15 equals three. Now how do you interpret these numbers? A normal H. P. P. G. Is 1 to 5. And if you have portal hypertension from cirrhosis it will be equal to or greater than six. And there's a direct correlation with you know the elevation of the of the gradient and your risk of developing complications from public attention. So the higher the number the more risk of developing um significant societies as well as very still bleeding. So in our patient um you know the gradients actually within the normal range. But they do have findings consistent with portal hypertension in in lieu of the you know societies that they have. So these findings are actually consistent with non so erotic hypertension because remember this gradient if it's elevated greater than six is telling you someone has portal hypertension from cirrhosis. So non psoriatic causes a lot of attention will show. Can show a normal gradient actually. So it's a large differential diagnosis here including pre hepatic, post hepatic and intra patrick causes and in post a paddock, portal hypertension usually see elevated wedge pressures and elevated free paddock pressures with a normal HPpD. So both 18 and 15 are actually elevated pressures but they're the actual gradient is normal. So in these settings we think of post hepatic portal hypertension and this can be seen in both chiari as we kind of talked about earlier in the session as well as right heart failure or constrictive pericarditis. So given this patient's risk factors um and you know in terms of their cardiac history as well as this pressure assessment that we've now obtained trans thoracic echocardiogram is the next best step. Let's go back to the other answer choices and figure out why they were incorrect. So her choice a you won't want to pursue a combined liver kidney transplantation since she has cirrhosis because her normal H. V. P. G. Argues against cirrhosis of the ideology as we just described. You wouldn't want to start a non selective beta blocker either for primary very still bleeding prophylaxis. If you haven't performed an A. G. D. First to see if they actually have viruses that are at risk for bleeding. And the tips placement in this patient would be contraindicated if she has significant right heart failure which were worried maybe the case given the pressure assessment that we have. So you wouldn't want to pursue that without a thorough cardiac work up. Here's the final question and it's a continuation of the same patient. The patient calls you overnight as the covering physician for abdominal pain and black stools after her liver biopsies just 12 hours before. And she she comes to the er on your guidance in the er she's hypotensive and tachycardic a federal. Her exam is notable for right upper quadrant tenderness without any parent Neil signs. She has no and she also has jaundice. Her labs are notable for a Billy Rubin of 4.2. It was one before the biopsy. Her hemoglobin is 92 points down and a non contrast ct abdomen pelvis is unremarkable. She's admitted and you perform an urgent endoscopy. The findings are listed here in the picture which of the following is the most likely cause of the patient's symptoms salvage of viruses do wanna ulcer. He must suck us pantry atticus hemophilia or an intraperitoneal hemorrhage. So the answer here is hemophilia and this is looking at the duodenum. Um And that's the M. P. L. A. With uh blood coming out of it. So hemophilia this is bleeding into the billiard track from a fistula formed with liver vasculature you get a tried of abdominal pain, obstructive jaundice and gi bleeding. It can be diagnosed with endoscopic visuals like visualization of blood coming from the impala. The most common cause of this is trauma such as the liver biopsy. Other ideologies include tips placement. Hepatic or biliary tumors, chemo embolization and gallstone Disease management includes resuscitation and often angiography in our patient, they went under one a non contrast ct abdomen pelvis. So if they got a C. T angiogram. If the questions have said that you may have been able to diagnose this. Um And management with interventional radiology. Um Instead of having to do an endoscopy First contrast this with another different item on the differential diagnosis, which is him, Osaka's pancreatic. A. So this is bleeding from a perry pancreatic blood vessel into the pancreatic duct. Um And this also communicates with the impala, so blood coming out of the ampule look and can come from different sources. So this is due to rupture of aneurysms that are usually associate with pseudo cysts or pancreatitis. So different pathology that can lead to significant bleeding from the impala, but a different ideology here that you may get tested on the boards as well, very rare and that concludes this session. Um Thank you for your time.