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Cynthia A. Moylan, MD, discusses the clinical examination for liver disease and cirrhosis.
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Cynthia A. Moylan, MD, discusses the clinical examination for liver disease and cirrhosis.
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>> Hello, and welcome to JAMAevidence, our monthly podcast focused on core issues in evidence-based medicine. I'm David Simel, the Editor of The Rational Clinical Exam Series and Professor of Medicine at the Durham Veterans Affairs Medical Center in Duke University. Today we're discussing the clinical evidence for cirrhosis. Joining me to talk about this topic is my colleague Dr. Cynthia Moylan, Assistant Professor of Medicine in the Division of Gastroenterology at Duke University and the Durham Veterans Affairs Medical Center.
Cynthia, let's start with making sure we understand cirrhosis. When a liver is cirrhotic, what has happened that affects its structure and function? >> Dr. Simel, that's a great question, and I'm very happy to be here today talking about this important topic. So understanding cirrhosis is actually quite complicated. And we've learned a lot more about a liver's multiple functions and its regenerative capacity. But, in essence, once the liver becomes cirrhotic, that's really the pathologic endpoint of chronic liver injury for many, many different ideologies.
What happens is the ongoing liver injury, the liver develops fibrosis. And as the liver develops more and more fibrosis, the liver parenchyma becomes replaced by excess extracellular matrix. And this matrix is produced by special cells called hepatic stellate cells. The stellate cells become activated, and myofibroblasts then results in the formation of fibrotic bands. And this distorts the actual liver architecture.
So histologically, when the liver becomes cirrhotic, you have fibrotic bands that surround hepatocytes. And this is what's known as regenerative or cirrhotic nodules. And as you can imagine, as these cirrhotic nodules form and the architecture of the normal liver becomes distorted, you get progressive functional decline of the liver. What's really important to understand is that, even though the structure of the liver can be affected, the function of the liver may not be.
The function can actually be quite preserved even in cirrhosis. So even though cirrhosis is one diagnosis, we think of it as sort of a spectrum of severity. And this can basically be classified as compensated cirrhosis or decompensated cirrhosis, depending on whether the liver's able to maintain its normal function. So in compensated cirrhosis, many of these patients will look like me and you, and the liver function will be normal despite having fibrotic bands and regenerative nodules.
Whereas, in decompensated cirrhosis, the liver, then, can no longer then perform its normal functions. And it's at this stage that patients typically experience symptoms. And it's at this stage that those symptoms really are manifested by portal hypertension, where there's now changes in the blood flow through the liver. And that's when patients start having complications. >> So it sounds like the endstage of this liver damage is what we call cirrhosis. But there are lots of different conditions that can lead to cirrhosis.
Is the pathophysiology the same for all those diseases? >> So, again, it's quite complicated. But the pathophysiology at the end, when fibrosis is developed, yes, that's the same. It's really, cirrhosis is the final common pathologic pathway. But the injury, the chronic injury that leads to fibrosis and cirrhosis can be quite different, depending on the different ideologies of cirrhosis. So it might be good to talk about this in context of different examples.
So, for example, in alcoholic cirrhosis, the initial liver injury results from fat deposition in hepatocytes. You get reactive oxygen species in the liver and inflammation. This leads to more and more fibrosis and eventually cirrhosis. Whereas, in something like primary biliary cholangitis, the initial injury is quite different, and this is from inflammatory infiltrates and necrosis around the bile ducts. This progresses and, again, it forms fibrosis. You get bile duct loss and eventually cirrhosis, which is the same.
From viral liver injury, such as from chronic hepatitis B and C, you get necrosis of hepatocytes and inflammation, but in the end you still get fibrosis cirrhotic nodules that look the same. And that's why often times a liver biopsy may not be that informative as to the ideology of liver disease once a patient already has cirrhosis, because it basically looks the same histologically. >> So what would the leading causes of cirrhosis in the United States be?
>> It really depends on the ethnicity and the specific patient populations that you're looking at. That can be quite different. But overall, the two main or most common causes of cirrhosis in the United States remain chronic hepatitis C virus infection as well as alcohol-related liver disease. This may change soon as the prevalence of nonalcoholic steatohepatitis is really increasing in the United States. And NAFLD or nonalcoholic fatty liver disease or NASH, nonalcoholic steatohepatitis is the third most common cause of cirrhosis.
And given the increasing prevalence of diabetes and obesity in the United States, as well as our ability to treat and cure hepatitis C, I think that NAFLD or NASH may soon overtake hep-C in the United States as one of the leading causes of cirrhosis. >> Okay. Well, I think we have a lot of listeners from around the world. How does the ideology of cirrhosis vary in other areas? >> That's a great question. So, again, it can vary by ethnicity, by geography, but there's probably some overarching themes.
Chronic hepatitis B virus is the most common cause in the Asia Pacific region as well as in sub-Saharan Africa. In Western countries, again, like the United States, the most common causes are alcoholic liver disease, chronic hepatitis C virus infection and nonalcoholic fatty liver disease. And alcohol is fairly predominant as a leading cause in most Western countries, including Europe as well as in South America. >> All right. So is it important for clinicians to be able to recognize cirrhosis early in the course of disease?
Or do I just wait until it becomes more obvious? >> I personally think it is very important to recognize this early in the course of disease. It can be very difficult. But if we get patients in to the appropriate care, it can really reduce the associated morbidity and mortality with cirrhosis. So I think it is really important to be able to recognize this condition early. And that may actually reduce patients' future morbidity and mortality.
So if you can identify patients with cirrhosis early, they can get put into effective screening and surveillance programs, because we know patients with cirrhosis are at increased risk for various complications. Some of these include liver-related morbidity and mortality, such as things you would think of as complications from portal hypertension, including esophogeal varices. So if patients are diagnosed with cirrhosis, they can be put into surveillance programs and undergo periodic endoscopic evaluation.
And they could even start treatment to prevent bleeding esophogeal varices. Patients with cirrhosis are also at increased risk for developing hepatocellular carcinoma and should be entered into surveillance programs with periodic ultrasound imaging of the liver every six months. So that's an important thing that may reduce future morbidity and mortality. Further cirrhotics can develop other complications, like encephalopathy or ascites. And if one is able to diagnosis cirrhosis early, we may be able to actually treat the underlying cause of cirrhosis and prevent those types of complications from ever happening.
More generally, patients with cirrhosis might be at increased risk for having complications while taking certain drugs that are metabolized through the liver, and it's important to know if they have cirrhosis. And they could be at increased risks for complications from surgery. So I think it is very important to identify these patients early. >> Well, in my clinical practice, whenever I've identified it early, it's always been before the presence of symptoms and signs. And I wind up relying on laboratory findings as subtle clues.
Which of the laboratory findings are most useful when trying to diagnosis cirrhosis early? >> I think you've hit the nail on the head. I think a lot of providers feel the same way, that the presence of cirrhosis can often be independent of signs or symptoms. And it is often that laboratory results can trigger a clinician's suspicion for cirrhosis. A lot of times providers feel that, oh, a patient has abnormal liver enzymes, and that may mean that the patient has cirrhosis.
And, in fact, liver enzymes are not very sensitive or specific for cirrhosis. They may identify liver injury, but they are not good at identifying patients with cirrhosis. More useful, and things that I use and potentially you use in your clinical practice, are those laboratory tests that reflect the liver's actual function or something that may happen as sequelae of cirrhosis. And these include the platelet count, the international normalized ratio or INR, and sometimes the serum albumin can also be helpful.
Often times thrombocytopenia or a low platelet count can be the first signal. And, in fact, you're a coauthor on a meta analysis that was published in JAMA in 2012, as part of The Rational Clinical Examination Series. And this meta analysis was geared towards looking at useful clinical and laboratory data to detect or exclude the presence of cirrhosis. And what the authors, including yourself, found in this meta analysis was that the presence of thrombocytopenia was the single most useful laboratory investigation to detect cirrhosis.
They looked at several thresholds and found that a platelet count of less than 160,000 had the highest diagnostic accuracy. And in that same study, they also found that a prolonged prothrombin time or INR or a serum albumin less than 3.5 grams per deciliter were also quite useful for diagnosing cirrhosis. There are also several noninvasive biomarkers that I use in my practice if I have a suspicion of cirrhosis but don't feel comfortable or cannot perform a liver biopsy.
And these include a diagnostic test called the FIB-4, which combines four variables -- including the aspartate aminotransferase or AST value, the alanine aminotransferase or ALT value, a patient's age and platelet count -- to give you a number that associates with cirrhosis or not. Another useful index is called the AST platelet ratio index or APRI, which is a formula that contains the AST and platelet count again. And if you use these in combination with other laboratory tests, you have a fairly high diagnostic likelihood of being able to rule in or out cirrhosis.
>> Okay, so sometimes I'm actually thinking about cirrhosis if my patient has risk factors. So, for example, maybe they've been a heavy drinker or maybe they have hepatitis C. Are there a set of normal findings that makes cirrhosis unlikely in those patients? >> Yeah, that's a great question. Unfortunately, as you've probably noticed there isn't one good diagnostic test or normal physical finding that can completely rule out cirrhosis.
But I think there are several predictors, if you look at them as a whole, that can work in your advantage. So, again, in that JAMA article, they found that thrombocytopenia or a platelet count greater than 160,000 had performed well in ruling out cirrhosis. They also found that a normal INR, a normal albumin were good indicators to rule out cirrhosis as well. And the physical exam is often less helpful. Unfortunately, physical exam signs are typically better at ruling in cirrhosis than ruling out cirrhosis.
But that being said, it's usually fairly uncommon to have cirrhosis in the absence of the hepatomegaly or splenomegaly. Although, these can be often difficult to diagnosis or assess given the patient's body habitus. Sort of more subtle signs, if a patient lacks [inaudible], palmar erythema, those can also be helpful finds rule out cirrhosis, but it's not perfect. >> When we published our article in The Rational Clinical Examination Series on cirrhosis, the FibroScan was emerging as a possible useful noninvasive way of assessing patients for the likelihood of cirrhosis.
Since then it's become rapidly adopted and widely used. Can you describe for our listeners what the patient experience is like during a scan? And how the results are interpreted? >> Sure, I would be happy to. We have incorporated FibroScan, which really is the trade name of a diagnostic test called transient elastography. And we've incorporated this into our practice more and more. So I think it is important that providers and patients understand how it works and how to interpret the findings.
Basically transient elastography or FibroScan works by measuring the shear wave velocity across the liver. The shear wave velocity is converted into a number expressed as kilopascals, and that associates with liver stiffness. So what the patients are asked to do is, prior to the test, they're asked to not eat or drink anything three hours prior to testing, as some results have found that eating a meal can interfere with the reliability of the results. So we do ask them to fast.
And then the procedure itself can really be performed almost anywhere where there's a flat bed. Providers have to be trained in the technique. So patients are asked to lie on their back. They put their right arm raised behind their head so that the right abdominal area is exposed. And then the person performing the procedure will apply a small amount of water-based gel, kind of like ultrasound gel, to the skin on the right side. And the noninvasive probe is placed over this area, right at the right lobe of the liver.
So typically between two of the rib spaces, similar to where we would do a liver biopsy. And then during the exam, the patient may feel a slight vibration on the skin as the tip of the probe delivers the ultrasound wave to the area across the liver that it's measuring. It feels sort of like a thump on the liver. It doesn't hurt. It's noninvasive, but some patients can be tickled by the probe something, sometimes. And you need 10 high-quality measurements to get a good median value.
And the whole test typically takes less than 20 minutes. There's really no side effects, and we dent use any anesthesia for the test. Most patients are candidates for FibroScan. There are some patients in which it's less reliable, so we don't often perform it in those patients. Patients with ascites, patients who are pregnant, we can't do the test. And obesity can be a problem. But now the company has developed larger probes so we can use it more effectively in patients with obesity.
Patients with implanted cardiac devices, like pacemakers or ICDs, really can't get FibroScanned either, because the results may be unreliable. And then the results may be inaccurate in some patients who have severe liver inflammation, liver congestion from heart failure or bile duct obstruction. So it's important to keep those things in mind as providers and patients interpret their findings. So the main goal of interpreting the FibroScan or transient elastography result is really to rule in or out cirrhosis alone.
And the test results range from 2.5 kilopascals to 75 kilopascals, with higher numbers being associated with a stiffer liver or fibrosis and cirrhosis. And a good way to think about it is that about 90 to 95 percent of patients without liver disease will have liver stiffness value measurements less than 7 kilopascals. For cirrhosis, the threshold values can differ depending on the ideology of liver disease. But for the most part a diagnosis of cirrhosis, the threshold values typically are over 10 and between 10 and 17 kilopascals.
So, for example, if a patient has chronic hepatitis C and you want to see if they have cirrhosis, if they have a high quality test and the result is over 12.5 kilopascals, that has a pretty good reliability for the diagnosis of cirrhosis. If the value's greater than 14 kilopascals, that's associated with a 90 percent probability of having cirrhosis. >> Well, it's great to get an update on things that have happened since our publication. Does the transient elastography avoid the need for liver biopsy?
>> It can in many patients. If you are just interested in making the diagnosis of advanced fibrosis or cirrhosis, then I think using these various laboratory tests and algorithms and FibroScan may be sufficient to diagnosis cirrhosis. If you're more interested in the ideology of liver disease, say you want to rule in or out nonalcoholic steatohepatitis or complications from drug-induced liver injury or diagnose autoimmune hepatitis, then liver biopsy, in my opinion, still has a place.
But for cirrhosis, liver biopsy may not be the best test. And FibroScan and other laboratory findings and physical exam findings may actually be better. >> So this has been a very informative discussion for me. Is there anything else you would like to tell our listeners about the clinical examination for cirrhosis in patients with liver disease? >> First, I'd like to thank you for picking this topic and giving me the chance to discuss it today. But I think overall, like yourself, if clinicians have a very strong clinical suspicion for cirrhosis, that really goes a long way in making the right diagnosis.
And I would urge them to act on that suspicion. And that's becoming more and more important as our population ages and patients are developing nonalcoholic fatty liver disease, and they may develop cirrhosis with no signs or symptoms at all. And in order to avert future morbidity and mortality associated with disease, clinicians really need to have a high index of suspicion and get them into care. So I would urge them to continue to use their clinical acumen and diagnostic tools to make the diagnosis of cirrhosis.
And then get them into the appropriate liver care when they can. >> Well, thank you very much for talking to me today. More information about this topic is available in The Rational Clinical Examination Series and on our website jamaevidence.com, where you can listen to our entire roster of podcasts. I'm David Simel, and I'll be back with you soon for another edition of JAMAevidence. [ Music ]
Segment:0 .
>> Hello, and welcome to JAMAevidence, our monthly podcast focused on core issues in evidence-based medicine. I'm David Simel, the Editor of The Rational Clinical Exam Series and Professor of Medicine at the Durham Veterans Affairs Medical Center in Duke University. Today we're discussing the clinical evidence for cirrhosis. Joining me to talk about this topic is my colleague Dr. Cynthia Moylan, Assistant Professor of Medicine in the Division of Gastroenterology at Duke University and the Durham Veterans Affairs Medical Center.
Cynthia, let's start with making sure we understand cirrhosis. When a liver is cirrhotic, what has happened that affects its structure and function? >> Dr. Simel, that's a great question, and I'm very happy to be here today talking about this important topic. So understanding cirrhosis is actually quite complicated. And we've learned a lot more about a liver's multiple functions and its regenerative capacity. But, in essence, once the liver becomes cirrhotic, that's really the pathologic endpoint of chronic liver injury for many, many different ideologies.
What happens is the ongoing liver injury, the liver develops fibrosis. And as the liver develops more and more fibrosis, the liver parenchyma becomes replaced by excess extracellular matrix. And this matrix is produced by special cells called hepatic stellate cells. The stellate cells become activated, and myofibroblasts then results in the formation of fibrotic bands. And this distorts the actual liver architecture.
So histologically, when the liver becomes cirrhotic, you have fibrotic bands that surround hepatocytes. And this is what's known as regenerative or cirrhotic nodules. And as you can imagine, as these cirrhotic nodules form and the architecture of the normal liver becomes distorted, you get progressive functional decline of the liver. What's really important to understand is that, even though the structure of the liver can be affected, the function of the liver may not be.
The function can actually be quite preserved even in cirrhosis. So even though cirrhosis is one diagnosis, we think of it as sort of a spectrum of severity. And this can basically be classified as compensated cirrhosis or decompensated cirrhosis, depending on whether the liver's able to maintain its normal function. So in compensated cirrhosis, many of these patients will look like me and you, and the liver function will be normal despite having fibrotic bands and regenerative nodules.
Whereas, in decompensated cirrhosis, the liver, then, can no longer then perform its normal functions. And it's at this stage that patients typically experience symptoms. And it's at this stage that those symptoms really are manifested by portal hypertension, where there's now changes in the blood flow through the liver. And that's when patients start having complications. >> So it sounds like the endstage of this liver damage is what we call cirrhosis. But there are lots of different conditions that can lead to cirrhosis.
Is the pathophysiology the same for all those diseases? >> So, again, it's quite complicated. But the pathophysiology at the end, when fibrosis is developed, yes, that's the same. It's really, cirrhosis is the final common pathologic pathway. But the injury, the chronic injury that leads to fibrosis and cirrhosis can be quite different, depending on the different ideologies of cirrhosis. So it might be good to talk about this in context of different examples.
So, for example, in alcoholic cirrhosis, the initial liver injury results from fat deposition in hepatocytes. You get reactive oxygen species in the liver and inflammation. This leads to more and more fibrosis and eventually cirrhosis. Whereas, in something like primary biliary cholangitis, the initial injury is quite different, and this is from inflammatory infiltrates and necrosis around the bile ducts. This progresses and, again, it forms fibrosis. You get bile duct loss and eventually cirrhosis, which is the same.
From viral liver injury, such as from chronic hepatitis B and C, you get necrosis of hepatocytes and inflammation, but in the end you still get fibrosis cirrhotic nodules that look the same. And that's why often times a liver biopsy may not be that informative as to the ideology of liver disease once a patient already has cirrhosis, because it basically looks the same histologically. >> So what would the leading causes of cirrhosis in the United States be?
>> It really depends on the ethnicity and the specific patient populations that you're looking at. That can be quite different. But overall, the two main or most common causes of cirrhosis in the United States remain chronic hepatitis C virus infection as well as alcohol-related liver disease. This may change soon as the prevalence of nonalcoholic steatohepatitis is really increasing in the United States. And NAFLD or nonalcoholic fatty liver disease or NASH, nonalcoholic steatohepatitis is the third most common cause of cirrhosis.
And given the increasing prevalence of diabetes and obesity in the United States, as well as our ability to treat and cure hepatitis C, I think that NAFLD or NASH may soon overtake hep-C in the United States as one of the leading causes of cirrhosis. >> Okay. Well, I think we have a lot of listeners from around the world. How does the ideology of cirrhosis vary in other areas? >> That's a great question. So, again, it can vary by ethnicity, by geography, but there's probably some overarching themes.
Chronic hepatitis B virus is the most common cause in the Asia Pacific region as well as in sub-Saharan Africa. In Western countries, again, like the United States, the most common causes are alcoholic liver disease, chronic hepatitis C virus infection and nonalcoholic fatty liver disease. And alcohol is fairly predominant as a leading cause in most Western countries, including Europe as well as in South America. >> All right. So is it important for clinicians to be able to recognize cirrhosis early in the course of disease?
Or do I just wait until it becomes more obvious? >> I personally think it is very important to recognize this early in the course of disease. It can be very difficult. But if we get patients in to the appropriate care, it can really reduce the associated morbidity and mortality with cirrhosis. So I think it is really important to be able to recognize this condition early. And that may actually reduce patients' future morbidity and mortality.
So if you can identify patients with cirrhosis early, they can get put into effective screening and surveillance programs, because we know patients with cirrhosis are at increased risk for various complications. Some of these include liver-related morbidity and mortality, such as things you would think of as complications from portal hypertension, including esophogeal varices. So if patients are diagnosed with cirrhosis, they can be put into surveillance programs and undergo periodic endoscopic evaluation.
And they could even start treatment to prevent bleeding esophogeal varices. Patients with cirrhosis are also at increased risk for developing hepatocellular carcinoma and should be entered into surveillance programs with periodic ultrasound imaging of the liver every six months. So that's an important thing that may reduce future morbidity and mortality. Further cirrhotics can develop other complications, like encephalopathy or ascites. And if one is able to diagnosis cirrhosis early, we may be able to actually treat the underlying cause of cirrhosis and prevent those types of complications from ever happening.
More generally, patients with cirrhosis might be at increased risk for having complications while taking certain drugs that are metabolized through the liver, and it's important to know if they have cirrhosis. And they could be at increased risks for complications from surgery. So I think it is very important to identify these patients early. >> Well, in my clinical practice, whenever I've identified it early, it's always been before the presence of symptoms and signs. And I wind up relying on laboratory findings as subtle clues.
Which of the laboratory findings are most useful when trying to diagnosis cirrhosis early? >> I think you've hit the nail on the head. I think a lot of providers feel the same way, that the presence of cirrhosis can often be independent of signs or symptoms. And it is often that laboratory results can trigger a clinician's suspicion for cirrhosis. A lot of times providers feel that, oh, a patient has abnormal liver enzymes, and that may mean that the patient has cirrhosis.
And, in fact, liver enzymes are not very sensitive or specific for cirrhosis. They may identify liver injury, but they are not good at identifying patients with cirrhosis. More useful, and things that I use and potentially you use in your clinical practice, are those laboratory tests that reflect the liver's actual function or something that may happen as sequelae of cirrhosis. And these include the platelet count, the international normalized ratio or INR, and sometimes the serum albumin can also be helpful.
Often times thrombocytopenia or a low platelet count can be the first signal. And, in fact, you're a coauthor on a meta analysis that was published in JAMA in 2012, as part of The Rational Clinical Examination Series. And this meta analysis was geared towards looking at useful clinical and laboratory data to detect or exclude the presence of cirrhosis. And what the authors, including yourself, found in this meta analysis was that the presence of thrombocytopenia was the single most useful laboratory investigation to detect cirrhosis.
They looked at several thresholds and found that a platelet count of less than 160,000 had the highest diagnostic accuracy. And in that same study, they also found that a prolonged prothrombin time or INR or a serum albumin less than 3.5 grams per deciliter were also quite useful for diagnosing cirrhosis. There are also several noninvasive biomarkers that I use in my practice if I have a suspicion of cirrhosis but don't feel comfortable or cannot perform a liver biopsy.
And these include a diagnostic test called the FIB-4, which combines four variables -- including the aspartate aminotransferase or AST value, the alanine aminotransferase or ALT value, a patient's age and platelet count -- to give you a number that associates with cirrhosis or not. Another useful index is called the AST platelet ratio index or APRI, which is a formula that contains the AST and platelet count again. And if you use these in combination with other laboratory tests, you have a fairly high diagnostic likelihood of being able to rule in or out cirrhosis.
>> Okay, so sometimes I'm actually thinking about cirrhosis if my patient has risk factors. So, for example, maybe they've been a heavy drinker or maybe they have hepatitis C. Are there a set of normal findings that makes cirrhosis unlikely in those patients? >> Yeah, that's a great question. Unfortunately, as you've probably noticed there isn't one good diagnostic test or normal physical finding that can completely rule out cirrhosis.
But I think there are several predictors, if you look at them as a whole, that can work in your advantage. So, again, in that JAMA article, they found that thrombocytopenia or a platelet count greater than 160,000 had performed well in ruling out cirrhosis. They also found that a normal INR, a normal albumin were good indicators to rule out cirrhosis as well. And the physical exam is often less helpful. Unfortunately, physical exam signs are typically better at ruling in cirrhosis than ruling out cirrhosis.
But that being said, it's usually fairly uncommon to have cirrhosis in the absence of the hepatomegaly or splenomegaly. Although, these can be often difficult to diagnosis or assess given the patient's body habitus. Sort of more subtle signs, if a patient lacks [inaudible], palmar erythema, those can also be helpful finds rule out cirrhosis, but it's not perfect. >> When we published our article in The Rational Clinical Examination Series on cirrhosis, the FibroScan was emerging as a possible useful noninvasive way of assessing patients for the likelihood of cirrhosis.
Since then it's become rapidly adopted and widely used. Can you describe for our listeners what the patient experience is like during a scan? And how the results are interpreted? >> Sure, I would be happy to. We have incorporated FibroScan, which really is the trade name of a diagnostic test called transient elastography. And we've incorporated this into our practice more and more. So I think it is important that providers and patients understand how it works and how to interpret the findings.
Basically transient elastography or FibroScan works by measuring the shear wave velocity across the liver. The shear wave velocity is converted into a number expressed as kilopascals, and that associates with liver stiffness. So what the patients are asked to do is, prior to the test, they're asked to not eat or drink anything three hours prior to testing, as some results have found that eating a meal can interfere with the reliability of the results. So we do ask them to fast.
And then the procedure itself can really be performed almost anywhere where there's a flat bed. Providers have to be trained in the technique. So patients are asked to lie on their back. They put their right arm raised behind their head so that the right abdominal area is exposed. And then the person performing the procedure will apply a small amount of water-based gel, kind of like ultrasound gel, to the skin on the right side. And the noninvasive probe is placed over this area, right at the right lobe of the liver.
So typically between two of the rib spaces, similar to where we would do a liver biopsy. And then during the exam, the patient may feel a slight vibration on the skin as the tip of the probe delivers the ultrasound wave to the area across the liver that it's measuring. It feels sort of like a thump on the liver. It doesn't hurt. It's noninvasive, but some patients can be tickled by the probe something, sometimes. And you need 10 high-quality measurements to get a good median value.
And the whole test typically takes less than 20 minutes. There's really no side effects, and we dent use any anesthesia for the test. Most patients are candidates for FibroScan. There are some patients in which it's less reliable, so we don't often perform it in those patients. Patients with ascites, patients who are pregnant, we can't do the test. And obesity can be a problem. But now the company has developed larger probes so we can use it more effectively in patients with obesity.
Patients with implanted cardiac devices, like pacemakers or ICDs, really can't get FibroScanned either, because the results may be unreliable. And then the results may be inaccurate in some patients who have severe liver inflammation, liver congestion from heart failure or bile duct obstruction. So it's important to keep those things in mind as providers and patients interpret their findings. So the main goal of interpreting the FibroScan or transient elastography result is really to rule in or out cirrhosis alone.
And the test results range from 2.5 kilopascals to 75 kilopascals, with higher numbers being associated with a stiffer liver or fibrosis and cirrhosis. And a good way to think about it is that about 90 to 95 percent of patients without liver disease will have liver stiffness value measurements less than 7 kilopascals. For cirrhosis, the threshold values can differ depending on the ideology of liver disease. But for the most part a diagnosis of cirrhosis, the threshold values typically are over 10 and between 10 and 17 kilopascals.
So, for example, if a patient has chronic hepatitis C and you want to see if they have cirrhosis, if they have a high quality test and the result is over 12.5 kilopascals, that has a pretty good reliability for the diagnosis of cirrhosis. If the value's greater than 14 kilopascals, that's associated with a 90 percent probability of having cirrhosis. >> Well, it's great to get an update on things that have happened since our publication. Does the transient elastography avoid the need for liver biopsy?
>> It can in many patients. If you are just interested in making the diagnosis of advanced fibrosis or cirrhosis, then I think using these various laboratory tests and algorithms and FibroScan may be sufficient to diagnosis cirrhosis. If you're more interested in the ideology of liver disease, say you want to rule in or out nonalcoholic steatohepatitis or complications from drug-induced liver injury or diagnose autoimmune hepatitis, then liver biopsy, in my opinion, still has a place.
But for cirrhosis, liver biopsy may not be the best test. And FibroScan and other laboratory findings and physical exam findings may actually be better. >> So this has been a very informative discussion for me. Is there anything else you would like to tell our listeners about the clinical examination for cirrhosis in patients with liver disease? >> First, I'd like to thank you for picking this topic and giving me the chance to discuss it today. But I think overall, like yourself, if clinicians have a very strong clinical suspicion for cirrhosis, that really goes a long way in making the right diagnosis.
And I would urge them to act on that suspicion. And that's becoming more and more important as our population ages and patients are developing nonalcoholic fatty liver disease, and they may develop cirrhosis with no signs or symptoms at all. And in order to avert future morbidity and mortality associated with disease, clinicians really need to have a high index of suspicion and get them into care. So I would urge them to continue to use their clinical acumen and diagnostic tools to make the diagnosis of cirrhosis.
And then get them into the appropriate liver care when they can. >> Well, thank you very much for talking to me today. More information about this topic is available in The Rational Clinical Examination Series and on our website jamaevidence.com, where you can listen to our entire roster of podcasts. I'm David Simel, and I'll be back with you soon for another edition of JAMAevidence. [ Music ]
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Form Title Accessibility
The cadmore media player is a professional video and audio player experience designed to deliver media as well as relevant transcript, segmentation, and metadata. On the screen is a traditional html audio player with buttons such as play, pause, forward, captioning, language and play speed selection and more. Adjacent to the audio player are generally tabs, one of which shows a scrolling transcript of the audio and the other shows any segmentation of the media, sometimes referred to as chapters. At the top of the audio player is a menu bar containing an Explore button and Tools button. The Explore button allows you to dig deeper into the audio by opening up an explore dialog which contains an about tab which contains rich metadata about the media, a segments tab which contains further information about the audio, and a related tab which contains links to other media related to this media. The tools button opens a menu with options for sharing the media on social media, creating bookmarking links, creating embed codes for your website, generating citations, and more.
Keyboard Shortcuts
Keyboard shortcuts only work while you are in forms mode. By entering forms mode, you will be able to quickly access portions of the media player with single key commands.
Spacebar: Play/Pause Toggle
E: Explore Menu,
O: Tools Menu
T: Transcript Tab,
S: Segments Tab
F: Forward 15,
R: Rewind 15
L: Languages,
P: Playspeed
M: Mute Toggle,
V: Volume Bar
N: Video Only Toggle,
B: Full Screen Toggle
C: Captions Toggle
Escape: Closes dialogs and menus
Z: Next Transcript Chapter
X: Previous Transcript Chapter
Q: Next Transcript Paragraph
W: Previous Transcript Paragraph
Form Title Embed Media
Entire Media
Segment(s)
Custom Clip
Start At:
End At:
Embed Size
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You Size - Responsive
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We Size - Responsive
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Picture Overlay Popup
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400 x 225
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512 x 288
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400 x 700
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768 x 1024
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1024 x 512
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1280 x 608
Form Title Cite
No citation provided.
Info
Segments
Related
Thumbnails
Accessibility
Using forms mode, you can utilize keyboard shortcuts to make usability more efficient.
Space bar will play and pause the media.
You can press A to open the Accessibility Dialog.
This describes many other keyboard shortcuts for media controls.
Exit Clip Mode
The video is currently set-up to show just a clip from 0:00 to video end. You have requested to see a portion of the media outside of the clip.
Click OK to switch to the full media or click if you would like to stay inside the clip. You can always go back to the clip with Tools and Clip Mode