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BackTable / VI / Podcast / Transcript #127

Podcast Transcript: Portal Hypertension and Ascites Management

with Dr. Parvez Mantry

Interventional Radiologist Christopher Beck talks with Hepatologist Parvez Mantry about the management of Portal Hypertension and Ascites, and the importance of multi-disciplinary collaborative care for these patients. You can read the full transcript below and listen to this episode here on BackTable.com.

Table of Contents

(1) Overview of Chronic Liver Disease

(2) Chronic Liver Disease Workup

(3) Liver Biopsies for Detecting Fibrosis

(4) Complications of Chronic Liver Disease

(5) Diagnosing Hepatocellular Carcinoma (HCC)

(6) Managing Portal Hypertension and Ascites

(7) Modifying Diuretic Regimens

(8) Alternatives to Diuretics

(9) Prognostic Indicators for Liver Disease

(10) Advice for Providers and Patients Awaiting Transplant

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Portal Hypertension and Ascites Management with Dr. Parvez Mantry on the BackTable VI Podcast)
Ep 127 Portal Hypertension and Ascites Management with Dr. Parvez Mantry
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[Dr. Christopher Beck]
Ladies and gentlemen, welcome to the BackTable Podcast, your source for all things endovascular and minimally invasive. If you are a new listener, welcome. For all of our regular listeners, welcome back. Let's take a moment to thank our sponsor GI Supply. The RenovaRP Paracentesis Management System by GI supply offers a new option for your patients with recurrent ascites. This unique approach puts the focus on patient and staff satisfaction, providing a closed system alternative to vacuum bottles and wall suction that's fast and gentle. Learn more about RenovaRP by visiting www.rethinkparas.com

[Dr. Christopher Beck]
Today, we’ll be broadly talking about chronic liver disease and then drill down a bit further into those patients with portal hypertension. Our guest today is a gastroenterologist and hepatologist in Dallas, Dr. Parvez Mantry. Parvez, welcome to the show.

[Dr. Parvez Mantry]
Thank you very much, Chris. It's a pleasure to be here.

[Dr. Christopher Beck]
A pleasure to have you. All right. So let's just have our audience get to know you a little bit. Can you talk about your background, specifically what the hepatology/GI training looks like?

[Dr. Parvez Mantry]
Sure, Chris. I'm Parvez Mantry. I'm a transplant hepatologist. I currently serve as Executive Medical Director for the Methodist Health System Clinical Research Institute and a transplant hepatologist at the Methodist Dallas Medical Center. I've been in Dallas for the last 13 years and started my career in New York. I did my residency at New York Medical College and then my fellowship in Gastroenterology and Hepatology at the University of Rochester. I stayed back as faculty and Director of Transplant Hepatology in the University of Rochester from 2003 and then moved to Dallas in 2008.

[Dr. Christopher Beck]
As far as gastroenterology and hepatology, is that built into one fellowship, or are there two different fellowships? When you pick your fellowship, do you know that you want to do GI with a focus on hepatology?

[Dr. Parvez Mantry]
Sure, Chris. That’s a great question. Gastroenterology is the mother fellowship, and hepatology is a specialized fellowship within it. Typically, if people are interested in liver diseases and transplant medicine, they do three years of gastroenterology and an additional year of a hepatology fellowship. Since I did this 18 years ago, I was fortunate enough to have been grandfathered in the system where I did two years of gastroenterology fellowship. Then, in my final year, I just focused on hepatology.

(1) Overview of Chronic Liver Disease

[Dr. Christopher Beck]
Let's talk about chronic liver disease and the 3,000-foot view. Will you talk about how big of a problem this is and why this deserves so much of your attention?

[Dr. Parvez Mantry]
Yeah, absolutely. So chronic liver disease and cirrhosis are major public health problems in the United States and all over the world. This is because the causes of chronic liver disease are ubiquitous. They are built into our social lifestyle and pretty much no one is immune to it. The liver is the largest visceral organ in the body, and it's the most important digestive organ. Pretty much every food that we eat and every toxin that we ingest go directly into the liver. Therefore, from excessive consumption of alcohol, to excessive consumption of sugar or calories, to immunological conditions, to genetic conditions, the liver can be affected by pretty much anything and everything under the sun, which is why the burden of disease in the United States from chronic liver disease is extremely high. In 2021, maybe about 40 to 50 million Americans have some form of chronic liver disease.

[Dr. Christopher Beck]
Wow. Will you talk about some of the most common causes that you see in the US and specifically in your practice in Dallas?

[Dr. Parvez Mantry]
In the US, the most common causes of liver disease, if I were to rank them in order, are: chronic hepatitis C, alcoholic liver disease, and nonalcoholic steatohepatitis (NASH). This list is followed by a bunch of other conditions like autoimmune liver diseases, primary biliary cholangitis, autoimmune hepatitis, primary sclerosing cholangitis, hemochromatosis, alpha-1 antitrypsin deficiency and so on and so forth. But the top three are hepatitis C, alcohol, and a fatty liver not caused by alcohol, which is due to diabetes and obesity.

[Dr. Christopher Beck]
Out of curiosity, have you seen, basically since you started practicing hepatology to where you are today, a meteoric rise in NASH?

[Dr. Parvez Mantry]
Yes, absolutely. In the last 20 years, NASH has been a relatively new diagnosis. We knew about fatty liver, but we did not know how serious it could get. It's only been in the last 15 to 20 years that we have painfully discovered how serious a medical issue this is and what a burden it imposes on society. It also gives us a really strong alert on trying to find it and fix it early. For example, in the '90s, about 19 out of 50 states were overweight, which means that more than 30% of their population was obese or had a BMI greater than 30. Well, in 2021, 47 out of 50 states are considered obese. And when you consider the phenomenon of obesity and diabetes, also called as diabesity, about a quarter of that population will have a form of progressive liver disease, which we refer to as NASH or nonalcoholic steatohepatitis. So it is pretty staggering.

[Dr. Christopher Beck]
Out of curiosity, do you have any idea what the three States that don't fall into the obesity category are? I would have to guess Hawaii, Colorado, and Oregon.

[Dr. Parvez Mantry]
You’re a little close, but actually Hawaii has a very high obesity population in the Native Americans. It is Connecticut and Massachusetts, and I do not know the third state. However, where we live (in Texas, Louisiana, Alabama, and Mississippi), our states considered the four most obese states in the country, and they have a very substantial burden of liver disease. In fact, they have the highest prevalence rates of liver cancer and in Texas, we have the highest mortality from liver cancer in the entire country.

(2) Chronic Liver Disease Workup

[Dr. Christopher Beck]
Wow. All right, well that hits home. I don't know if I mentioned this earlier, but I practice in New Orleans, which is located right in Louisiana. Let’s shift gears a little bit and talk about your practice specifically. Can you speak about the workup that you perform for chronic liver disease? And I know this is a loaded question. It's probably very dependent on etiology, but for either the trainees out there, or for interventional radiologists who don't do this on a day-to-day basis, can you give us a brief summary of what a good standard workup for CLD looks like?

[Dr. Parvez Mantry]
Absolutely. So, the first visit for somebody with suspected CLD is the most important because I want to take a detailed history and look at all the historical records. Sometimes these patients have been to other places or have had tests running for years, which gives me an idea of the chronicity of the illness. I ask for a detailed and granular history of what their weight was 5 and 10 years ago, how long they have been diabetic, or what their hemoglobin A1c has been over the years. I ask questions about how much they really drink or how much they drank in the past. Also, I take a family history, especially in certain ethnic groups like Hispanics. It is important to know if they have a strong family history of liver disease because NASH can have a genetic predisposition.

[Dr. Parvez Mantry]
Honing into examination features, I check if they have any sarcopenia, pedal edema, ascites, or evidence of encephalopathy. Looking at the basic labs, I can assess the Child-Pugh score and the MELD score. Also, cross-sectional imaging is supremely important. You're a radiologist, so you probably know that very well. I do an ultrasound and, in non-obese patients, a multiphasic MRI to assess their vasculature and their liver surface to rule out cancers. Also, the serological workup is extremely important. When we start from fresh, we never assume anything. If they're a Baby Boomer, I will double check that their hepatitis panel has been checked because they're still likely to have hepatitis C, even if they present with no risk factor.. Then, we check the autoimmune markers with muscle antibody and antinuclear antibody. If they are younger and if nothing else is evident; for example, let’s say a 40 year old patient comes to me with cirrhosis, then I will check his cellular plasma and alpha-1 antitrypsin. I will also check his iron studies and any other genetic markers to see if he has any genetic condition predisposing to cirrhosis.

(3) Liver Biopsies for Detecting Fibrosis

[Dr. Christopher Beck]
At what point does a native liver biopsy come into the workup? Is that something that all patients with chronic liver disease will go through, or is it performed on a case by case basis?

[Dr. Parvez Mantry]
That's a great question. So I think one of the key distinctions here is chronic liver disease versus just cirrhosis and end-stage liver disease. I think that the conversation I was alluding to earlier was mostly about patients presenting with established cirrhosis and/or some signs of liver failure in which there's not really any role for a further assessment of fibrosis, like a liver biopsy. However, let's take a different scenario. I have a patient coming to me for evaluation of abnormal liver function tests. They had an ultrasound which shows a core psychogenic liver or a different echogenicity. In those patients, it is really important to assess their liver fibrosis, and we do it by one of four methods. One is a blood test, called a FibroSure, which is the least reliable, but it is readily available. Two, a FibroScan, also called transient elastography, which we use most commonly in order to assess the degree of liver fibrosis, and we can grade it from 0 to 4 (0 being normal and 4 being cirrhosis).

[Dr. Parvez Mantry]
Three, we now have the ability for MR elastography, which we had acquired at our center seven years ago. It's a really neat non-invasive tool that can tell us exactly how much damage the liver has. And then number four, the last but not the least important, is the liver biopsy, which a lot of us, myself included, perform ourselves. It's a 10 minute procedure, but it is slightly invasive. We give a patient some sedation and pick a spot, which is ultrasound-guided between the intercostal spaces. We take a 16 gauge needle and take a sample. That is still considered the gold standard for diagnosis of a chronic liver disease, especially in conditions like steatohepatitis, if we know that the patient does not already have full-fledged cirrhosis.

[Dr. Christopher Beck]
How often do patients get referred for a transjugular liver biopsy (instead of a percutaneous biopsy), with the additional diagnostic benefit of pressure measurements?

[Dr. Parvez Mantry]
There are a few conditions or situations where I would prefer a transjugular liver biopsy. Oftentimes, we will have a patient who does not have any obvious features of liver disease, and yet shows variceal bleeding or ascites. I look at the liver numbers, and they're all completely normal. Of all the risk factors I pointed out, the patient does not seem to have any. All the serological workup is negative. The ultrasound or CT or MRI shows a very smooth liver. I want to find out: What's wrong with the liver? Alternatively, are the ascites and bleeding coming from a different issue, like a vascular issue or an issue that is non-related to the liver?

[Dr. Parvez Mantry]
In those cases, I will always perform a transjugular biopsy because my radiologists can tell me the hepatic venous wedge gradient. And that is of course, an indirect measurement of the portal vein pressure. If it is more than 12, I know that this patient has portal hypertension and is most likely cirrhotic. Of course, a biopsy will corroborate as well. If it is low, then I know that this patient has extrahepatic portal hypertension or something else causing the ascites and bleeding.

(4) Complications of Chronic Liver Disease

[Dr. Christopher Beck]
I see. I want to dig into one of the complications related to CLD, specifically portal hypertension. If you want, can you just give us a brief overview of the most common complications or secondary issues that you run into on patients who suffer from chronic liver disease?

[Dr. Parvez Mantry]
Absolutely. When we look at the complications of chronic liver disease, we divide it into two areas. One is complications related to liver synthetic dysfunction because the liver is responsible for production of proteins, chemicals, and clotting factors. And two, are those complications related to portal hypertension. When the liver architecture is lost, it loses its ability to filter blood. The unfiltered blood backtracks into veins, which surround the stomach, esophagus, and spleen. This leads to varices, because the blood is trying to find a way to get back into the systemic circulation through the collaterals. Those are the two main ways we decipher the complications from liver disease. Ascites, which is the most ominous and the most common cause of chronic liver disease, needs a component of both.

[Dr. Parvez Mantry]
For ascites to happen, you need portal hypertension and liver synthetic dysfunction. Esophageal or gastric varices only require portal hypertension to be there. Sarcopenia (muscle wasting) requires liver synthetic dysfunction. For pedal edema to happen, there usually needs to be liver synthetic dysfunction. For hepatic encephalopathy to occur, there needs to be both portal hypertension, so that the unfiltered blood and toxins reach the brain, as well as a component of liver synthetic dysfunction. That's how we glean between the differences and determine exactly what is going on in the liver.

[Dr. Christopher Beck]
Is hepatocellular carcinoma also considered one of the complications, or is that a separate entity that gets rolled up in workup of all patients with CLD?

[Dr. Parvez Mantry]
Hepatocellular carcinoma is a very important complication of cirrhosis. It is directly tied to development of cirrhosis, and 9 out of 10 people presenting with liver cancer in the United States will have underlying cirrhosis. That's primarily linked to faulty regeneration in the liver because when the liver gets really badly damaged, it tries to regenerate. However, when the regeneration is defective, it causes dysplasia and predisposes to cancer. Also, there are certain agents which are directly carcinogenic to the liver: the Hepatitis C virus, Hepatitis B virus (especially because it gets integrated into the DNA of the cell), alcohol, diabetes, and obesity.

(5) Diagnosing Hepatocellular Carcinoma (HCC)

[Dr. Christopher Beck]
So just taking a slight left turn into HCC, I'm interested to know your institution diagnoses HCC, and specifically, if biopsy plays a role in the diagnosis.

[Dr. Parvez Mantry]
That's a great question. Let me answer the second part. Biopsy is not required for diagnosis of HCC. It is actually an imaging diagnosis. In fact, we discourage biopsy for a majority of the time for two reasons. One, HCC is a very vascular tumor and by biopsying, you can spread it by intraperitoneal spread through bleeding. Two, there is a high false negative rate. 95 to 98% of the time, multiphasic MRI, with all its sequences and restricted diffusion imaging, can diagnose an HCC. If the patient is not a good candidate for an MRI, for example, if there was an MRI-unfriendly pacemaker or they are severely claustrophobic, then we employ a quadruple-phase CT. Between the two, we can diagnose HCC 98% of the time.

[Dr. Christopher Beck]
I think that's one thing that gets lost in the community. Pathology can oftentimes be less specific than a clinical laboratory and imaging diagnosis of HCC. Can you speak a little bit about that? Do you have any idea exactly what the sensitivity and specificity of a percutaneous biopsy for HCC are? I'm imagining it can vary from institution to institution, but do you have a rough idea?

[Dr. Parvez Mantry]
A percutaneous biopsy for HCC is about 90% sensitive and specific. So it's up there. However, it is less accurate than an imaging study, and it is fraught with the risk of causing seeding of the tumor and bleeding complications, and therefore we avoid it. We have biomarkers. Most commonly we use the alpha-fetoprotein, but we have some new biomarkers like des-γ-carboxy prothrombin. Because we are a big research institute, we have a few biomarkers that are currently in development, which we are using in consult with imaging tests to improve accuracy. This is completely non-invasive. We also call it a liquid biopsy.

[Dr. Christopher Beck]
Interesting. What are some of those markers?

[Dr. Parvez Mantry]
There are some methylated genetic markers and tests that are still currently in development. Their composition is a little bit proprietary but you'll be hearing about them, hopefully in the next couple of years. The ones which are currently available are alpha-fetoprotein, and also a subcomponent of the AFP called the Lens culinaris fraction, or AFP-L3. If that is elevated, it is very specific for AFP. In patients who do not express an elevated AFP, we use a des-γ carboxy prothrombin, which was developed in Japan. It is also called “protein induced by vitamin K absence/antagonism” (PIVKA). That's a really useful marker and it's commercially available in the United States.

(6) Managing Portal Hypertension and Ascites

[Dr. Christopher Beck]
Excellent. I'll try and link to some of those because I can't speak for all the listeners, but some of those are very new to me and I'll just try and get a list from you and we'll post those in the show notes. That'll be interesting. Let's talk a little bit about portal hypertension and ascites management. How common are portal hypertension and ascites in your patient population?

[Dr. Parvez Mantry]
Pretty much every patient with cirrhosis, at some point in their lifespan, will develop portal hypertension if they already don't have it. So it is ubiquitous. As I mentioned earlier, ascites is the most common and the most ominous sign of cirrhosis and liver failure, primarily because it is a manifestation of both liver synthetic dysfunction and portal hypertension. It takes two of those underlying conditions for the patient to develop ascites.

[Dr. Christopher Beck]
Once you have a diagnosis of ascites, can you talk about what the workup looks like as far as diagnosing the underlying cause? If you have a patient who is new to you and presents with ascites, what does their specific workup look like? We'll move into treatment algorithms afterwards.

[Dr. Parvez Mantry]
Absolutely. When I look at ascites, I divide this into two broad areas. One is a patient whom I already know and have diagnosed with cirrhosis and liver failure. Two is somebody I meet in the emergency room, or somebody who comes to my office, brand new, with just ascites and has no other evidence or predisposition for liver failure. Their workups are entirely different. In somebody who already has established cirrhosis and liver failure, we only do the basic labs. And then when we do a paracentesis, we will check their albumin and their cell count. And that's it. We do not check anything else because it is not really required.

[Dr. Parvez Mantry]
On the other hand, if I have an emergency room patient with sudden onset of large-volume ascites, I will look for many of the things. This could be from a gastrointestinal malignancy, meaning peritoneal carcinomatosis. These patients may have been hale and hearty two weeks ago, and then suddenly just develop ascites and they have no idea what's going on. They may find out that they have a colorectal, gallbladder, or pancreatic malignancy, which is usually quite ominous.

[Dr. Christopher Beck]
I like the idea of breaking it into two big broad categories, those who are known cirrhotics versus those with unknown ascites. And like you said, the workup is very different for both. So let's talk about some of the treatments for ascites. From an interventional radiologist's perspective, I always think of three things: things: diuretics (which is not something I typically manage), paracentesis, and TIPS procedure. Can you speak about how you approach the management of patients with ascites?

[Dr. Parvez Mantry]
When patients have mild or moderate ascites (which means that I can feel the ascites, but their belly is not tense) and they have a lot of pedal edema, I will usually start them with a combination of furosemide and spironolactone. With a loop diuretic, potassium-sparing diuretic, and salt restriction, we may be able to manage the ascites 70% to 80% of the time. In the other scenario where somebody comes with tense ascites, their abdominal wall is stretched, their umbilicus is everted, and they are usually very uncomfortable. In addition to starting them on diuretics, I will usually perform a paracentesis in the office and remove 8-10 liters of fluid and give intravenous albumin. Now, patients who require paracentesis on a weekly basis, with livers that are still salvageable (measured by MELD score), are suitable candidates for placement of a transjugular intrahepatic portosystemic shunt (TIPS). And then we have some experimental therapies that are coming up for management of ascites as well.

(7) Modifying Diuretic Regimens

[Dr. Christopher Beck]
I want to talk more about diuretics. Let’s assume renal function stays stable, and you want to increase diuretics. How often do you tweak the diuretics to get the level of ascites managed appropriately? How often are you seeing these patients to change their diuretics regimens?

[Dr. Parvez Mantry]
That's a good question. So initially, I see them every one or two weeks. Some patients are very sensitive to diuretics when we start them off. We want to make sure that their potassium, sodium and creatine are okay. Usually, we do not escalate diuretics by more than one week at a time, unless they're in-patients. If they are in-patients, we can make those changes on a daily basis because we are monitoring them so closely. Otherwise, it is one to two weeks. We look at their weight and pedal edema. For instance, if the pedal edema is gone but the ascites is still large, we are very wary of increasing diuretics because those patients are at a higher risk of developing hepatorenal syndrome. Those patients also tend to run a low borderline blood pressure. You have to be very alert and very mindful of everything that's going on around them, because diuretics are clearly a very double-edged sword. They are very helpful, but slight mismanagement of them can be very unforgiving.

[Dr. Christopher Beck]
How about patients who do not tolerate their original diuretic regime very well? If you see bumps in their creatinine and a decrease in their GFR, can you back off their diuretics? Are there opportunities to work back up to increasing those diuretics after you've had some time to establish a new equilibrium?

[Dr. Parvez Mantry]
Most certainly. We play this ping pong game with diuretics all the time. One week, I may scale them down, and in the next week, I may go back up. The kidney function is very, very critical in cirrhotic patients because once hepatorenal syndrome sets in, if we are not very mindful of making these adjustments, these patients can go downhill very, very rapidly. And so we make these changes all the time. Sometimes, if the creatinine has gone up rapidly, I will put them in the hospital and give them some intravenous albumin. This increases the colloid oncotic pressure. By doing that, it improves the renal perfusion and we are able to reset the diuretics to a point where these patients can effectively lose that extra amount of extracellular fluid.

[Dr. Christopher Beck]
I think there's always a patient that we struggle with, and it's the patient who doesn't tolerate diuretics particularly well. You're seeing them in the office once or twice a week for repeat paracentesis. Can you talk a little bit about why these patients pose such a challenge to us, and ways that we can better manage treatment for these patients?

[Dr. Parvez Mantry]
The patient population you're talking about is at least a third of all the cirrhotics with ascites that we manage. So it is a very, very common problem. There are a few things that we have to be very mindful of. The most important thing is if the patient keeps developing rapid accumulation of ascites (despite diuretics) and we look at their feet and they are not swollen (meaning the edema is gone). Those patients almost invariably need something more than diuretics, meaning consideration of a shunt or transplant. Hopefully they've already prepared for that. Another second issue is the patients with the borderline low blood pressure. In those patients, the renal arteries are vasoconstricted. The diuretics will not work as well and those patients are also at risk of going into renal failure.

[Dr. Parvez Mantry]
The third issue is the patients with severe muscle wasting. Because they have a lot of muscle wasting, it's an indirect assessment that they have very poor colloid oncotic pressure. When you have poor colloid oncotic pressure, the diuretics are not able to extrapolate all that extracellular fluid volume. So if you imagine a patient who is muscle-wasted, has a creatinine of 1.6, has a blood pressure of 95/ 60, and a zero for the second paracentesis, I know that this person is invariably going to need something more than the regular diuretic management. We'll have to go over and beyond to figure out what else we can do for this patient.

(8) Alternatives to Diuretics

[Dr. Christopher Beck]
Without having too many specifics about the patient, what else is there to do? I'm sure it can vary between patients, but how do you approach that and begin to troubleshoot it?

[Dr. Parvez Mantry]
Initially we make the assessment of whether the patient is a transplant candidate. If they are, and they are eligible, we put them on the list. So sometimes it would be waitlist management. If they are not transplant candidates, we look at the initial cause, make sure that they are abstinent from alcohol, and control their diabetes. When we go to the granular details on how to manage the ascites, there are basically two options. One is placement of a TIPS. The other is that we can just tap them on a weekly basis using machines or equipment like RenovaRP, where we can get a lot of fluid out of their abdomen fairly rapidly and safely. This is an alternative to TIPS while they're either waiting for transplant or other things.

[Dr. Christopher Beck]
Is a Denver shunt in the algorithm for the treatment of these patients? Do you have any experience with patients being referred for these shunts?

[Dr. Parvez Mantry]
Denver shunts are almost obsolete because of their very high risk of infections and DIC. We do have a research protocol using an alfapump, where there's a catheter placed into the bladder from the peritoneal cavity, and that has some promise. In patients who are very terminally ill and who are not transplant candidates, we do put a PleurX catheter in them. They can just drain this at home. Usually, those are patients who have a life expectancy of three months or so. But for all practical purposes, the only shunt we would use is a transjugular intrahepatic portosystemic shunt.

[Dr. Christopher Beck]
I haven't heard of the alfapump. Is this relatively new? Is this something that urologists do?

[Dr. Parvez Mantry]
This is done by our surgeons and radiologists. It has been in Europe for the last year or so. I started a clinical trial with it about six months ago. There are a few sites in the US doing it.

[Dr. Christopher Beck]
Going back to the paracentesis, is there a limit to how much volume you will take off for a patient, either who is new to you, or a patient that you see for recurrent ascites on a weekly or a biweekly basis?

[Dr. Parvez Mantry]
That's a great question. It totally depends. The most important determinant is kidney function. If the GFR is less than 30, then we typically do not want to remove more than 6 liters of fluid, and we will always give them intravenous albumin. In our practice, as well as that of our IR colleagues, if anybody requires more than 4 liters of paracentesis, we give them intravenous albumin: 10 gram per liter of fluid removed. This is to avoid a condition called post-paracentesis circulatory dysfunction, which leads to kidney failure and can be very catastrophic. So that's the rule of thumb. In patients who have normal kidney function and have a normal blood pressure, I could potentially remove up to 15 liters of fluid, as long as I'm very particular and diligent about the albumin. If I remove 15 liters of fluid, I give them 150 grams of IV albumin.

[Dr. Christopher Beck]
Actually, I did want to drill down on your protocol for albumin. You gave a good example with removing 15 liters, but I just want to repeat it with some numbers that might be a little more reasonable for people to follow. If you remove 6 liters, you're going to give 60 grams of albumin?

[Dr. Parvez Mantry]
Correct.

[Dr. Christopher Beck]
Okay. And then anything below 4 liters doesn't warrant albumin?

[Dr. Parvez Mantry]
Anything below 4 liters, you can get away without use of IV albumin. You won't go wrong with IV albumin, but there are logistics that have to be taken into consideration: Does the patient have an IV? What would the albumin cost? However, for the overwhelming majority of the time, we will give IV albumin during the paracentesis.

[Dr. Christopher Beck]
One thing that I wanted to go back to, for listeners who are trainees, can you talk a little bit about why a PleurX or a tunneled peritoneal drain is not a great idea for someone who is not end-of-life?

[Dr. Parvez Mantry]
I'm glad you asked that. Well, there are two reasons. One is that the risk of infection is almost 100% because the fluid inside the abdominal cavity in patients with ascites is very, very prone to infections. It has low albumin and it is low on opsonization. There is also a portal from the skin which can cause severe infections. The second thing is, when patients go home with the PleurX catheter, they are not able to receive intravenous albumin. They eventually succumb to severe circulatory dysfunction and kidney failure, which eventually lead to death.

[Dr. Christopher Beck]
Do you have any troubleshooting tips for patients who have a lot of leakage from the stick site, after they undergo paracentesis?

[Dr. Parvez Mantry]
That's a great question. In fact, just yesterday, I was writing a new research project on this issue. It is a very common problem. There are four ways to mitigate it. First, we use Dermabond, which we found is very helpful. It is very minimally irritating to the skin. Second, we can actually do a cerclage stitch, if it is a really big opening and our interventional radiologists do that a lot. Third, if these patients are not in a tertiary referral center, they can be sent to one. But until they can come and see me at the tertiary center, I'll just ask them to put a colostomy bag. Fourth, the best treatment when these patients have a large amount of ascites and leakage is to do another paracentesis because the leakage is due to excessive pressure in the abdomen. If you can tap them dry, then the leakage will automatically go away.

(9) Prognostic Indicators for Liver Disease

[Dr. Christopher Beck]
If you can just dry it up, then that will allow it a chance to crust over and get a scab over it. That's helpful. Alright, so I think we tackled a lot. One of the things that I wanted to discuss was prognostic indicators. You mentioned earlier that you use the MELD score and the Child-Pugh score for diagnosing, but is this something you track regularly, or is it something that once you have their baseline score, then it's more of clinical surveillance (rather than tracking these scores)?

[Dr. Parvez Mantry]
So we usually track the Child-Pugh score when we are managing a liver cancer or the patient requires a non-hepatic surgery. For example, if a cirrhotic patient needs a hip surgery, then I will need to know whether they are Child-Pugh A, B or C. Other than that, we don't use it that often. The MELD score is supremely important because it has a direct correlation with mortality. And it has a direct correlation with the need and assessment for transplant, as well as the ability to undergo TIPS, for example, in patients with refractory ascites. We typically will perform a transplant evaluation on somebody whose MELD score is greater than 15. And that is also the norm that is used by insurance companies, because at that point, the mortality from liver disease exceeds the mortality from a transplant.

[Dr. Parvez Mantry]
If the MELD score is greater than 20, then we check that every couple of weeks. If it is more than 25, we check it every week if they are on the list, because that's how they are ranked on the list. It also helps us determine the ability to do a TIPS on somebody. So if the MELD score is more than 15, I would be very reluctant to do a TIPS, unless the patient is already listed for a liver transplant. If the MELD is more than 20, I would not do it at all.

(10) Advice for Providers and Patients Awaiting Transplant

[Dr. Christopher Beck]
Switching gears a little bit from these prognostic indicators and more to transplant, is there any advice you can give to physicians in the community or people who aren't at transplant centers? First, can you talk about a way to plug patients in with a local referring transplant center? And then I'm going to ask you some follow-up questions about just some transplant basics.

[Dr. Parvez Mantry]
Absolutely. So for the listeners in the community, I think it's really important to have a relationship with your transplant center because patients with liver disease can deteriorate very rapidly and the deterioration can often be catastrophic. And folks at transplant centers like ours usually want to have very close community liaisons with these providers, so we can bring them at the drop of a hat, either inpatient or outpatient. Our information is usually on websites. We have the https://www.theliverinstitutetx.com/ and depending on where you are, we have satellite locations, which are all over the metroplex to help us serve these patients. And so the key thing is if your patient has started showing signs of hepatic decompensation, which is ascites, pedal edema, had one episode of bleeding from varices, hepatic, encephalopathy, muscle wasting, or jaundice, those are the signs that should alert you to get them plugged in into your closest liver transplant center.

[Dr. Christopher Beck]
I'm happy that you mentioned the satellite locations, because I think one of the barriers for people in the community and oftentimes rural communities are that these patients have to come from really far away and they may have limited means. Taking a day off of work or just taking the resources needed to get to a transplant center, it can be very taxing. Sometimes there are satellite locations where you don't have to go to the mothership to actually get worked up. Moving to a transplant assessment, are there any tips that you could give patients in the community? Are there any patients who should not go to a transplant center because there's no way they would be a transplant candidate?

[Dr. Parvez Mantry]
My tips to the patients will be twofold. One is, oftentimes, I've had patients who felt that they were not transplant candidates because of their age or something like that, and they were excellent transplant candidates. My advice to patients would be to let your liver team decide and make those judgements on your behalf because we do an extensive workup and make those determinations. But in order to prep patients best for consideration of transplant, there are three or four things that are supremely important that will help them become better transplant candidates. This is of course apart from the obvious, which is staying away from any toxins like alcohol, and taking good care of their health, especially diabetes control. But really in liver failure, food is medicine. I advise patients to eat multiple meals a day, maintain a high protein diet up to 100 grams a day, and eat a bedtime snack. This will maintain that anabolic rate and prevent muscle loss. I encourage them to do physical activity and walk as much as possible, maybe 20-30 minutes, two or three times a week. Having a family support system is very important. Transplant is something that cannot be done by the patients themselves. They need help. I tell my patients, don't fight this battle on your own, inform your close family members and see what help you can mobilize from them. And then finally, I advise them to keep a close network of doctors, to be in touch with their primary care physician, gastroenterologist, hepatologist, and transplant center. This helps us communicate and tie all the loose ends well.

[Dr. Christopher Beck]
Okay, excellent. Parvez, I think that we've done a really good job. I really think that it was a broad topic and you did a good job, diving into what can be a pretty daunting overview of chronic liver disease and specifically portal hypertension. Are there any favorite papers or references that you can recommend to our trainee audience or people who are just interested in knowing more about chronic liver disease and portal hypertension management?

[Dr. Parvez Mantry]
Absolutely. Well, and there's tons of papers. The SLD practice guidelines, which are published in Hepatology. I think the last publication was in 2019. And then the white paper on the management of hepatocellular carcinoma from Hepatology are some of the best papers. There is also a paper on the management of ascites, the guidelines set by the International Ascites Club. So those would be the three top papers I would recommend for both the trainees, as well as curious patients, primary care physicians, or even radiologists if you'd like to take a deeper dive into the disease.

[Dr. Christopher Beck]
Excellent. Well, I appreciate you coming on the podcast. We’ve loved having you. Thank you for your time.

[Dr. Parvez Mantry]
It was my pleasure, Chris, and thank you for having me on the show. I really enjoyed it.

Podcast Contributors

Dr. Parvez Mantry discusses Portal Hypertension and Ascites Management on the BackTable 127 Podcast

Dr. Parvez Mantry

Dr. Parvez Mantry is the Medical Director of the Liver Institute Research and the Hepatobiliary Tumor Program at the Methodist Health System in Dallas, Texas.

Dr. Christopher Beck discusses Portal Hypertension and Ascites Management on the BackTable 127 Podcast

Dr. Christopher Beck

Dr. Chris Beck is a practicing interventional radiologist with Regional Radiology Group in New Orleans.

Cite This Podcast

BackTable, LLC (Producer). (2021, May 17). Ep. 127 – Portal Hypertension and Ascites Management [Audio podcast]. Retrieved from https://www.backtable.com

Disclaimer: The Materials available on BackTable.com are for informational and educational purposes only and are not a substitute for the professional judgment of a healthcare professional in diagnosing and treating patients. The opinions expressed by participants of the BackTable Podcast belong solely to the participants, and do not necessarily reflect the views of BackTable.

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