Decompensated Cirrhosis (28 Apr 2025)

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Dr Emma Spencer (ES): So, hello and welcome to this episode of Clinical Conversations brought to you by the Royal College of Physicians of Edinburgh and the Trainees and Members Committee. My name is Emma and I'm a member of the Trainees and Members Committee and today I'm delighted to be joined by Dr Michael Williams. He's a hepatologist at the Royal Infirmary of Edinburgh and we're going to talk a little about decompensated cirrhosis today. Welcome Dr Williams.

Dr Mike Williams (MW): Hi Emma, thanks for having me.

ES: No problem. So, I thought we could start off today talking about the definition of decompensated cirrhosis and what you as a herpetologist might mean by that.

MW: Yes, so it's a term that's used a lot by hepatologists and by medics, and surprisingly for such an important term, there is Not an absolutely clear agreement on what is meant. So, in general, it's a description of the development of complications of cirrhosis that reflects impaired liver function. And traditionally, the things that would make us think of that would be the development of jaundice, ascites, encephalopathy, and variceal bleeding. So those are definitely decompensating events. It can also sometimes be used to describe This situation where people's blood results are deteriorating, so they have evidence of impaired synthetic function biochemically. And increasingly it's used to include the development of sepsis due to bacterial infections or the development of acute kidney injury in cirrhosis. Though it's a little bit less clear cut as to whether those are truly decompensating events. The other thing to be aware of is that we often describe it as an event, but sometimes these things can come on A bit more insidiously, so often the first decompensation of cirrhosis can often be quite a sub-acute onset, so the most common first decompensation is the development of ascites. And so usually that's something that people notice over a period of weeks or even months. And similarly, sometimes low-grade encephalopathy can just be something that has come on gradually. Whereas there are some that are very acute episodes, so people who have variceal bleeding or sepsis will present with a very sudden change. But all of those things are often grouped together as decompensated cirrhosis.

ES: Yeah, and I think what I initially found a bit tricky when I was kind of getting my head around this and seeing more of these conditions on the take is sometimes I would see people present with jaundice or ascites or a variceal bleed or encephalopathy, so one of those kind of more defining conditions, without necessarily a diagnosis of Liver failure or cirrhosis in the background, so sometimes a decompensation can be the first time you might pick up liver disease.

MW: Absolutely. So, we definitely do see patients where their first contact with medical services and their first diagnosis is with a decompensation. So, it's always important if people are presenting with Any of those presentations to think about do they have risk factors for chronic liver disease. And often quite a good clue is do they have physical stigmata of cirrhosis. And I know there are lots of elements of physical examination that have been largely superseded by increased diagnostic testing, but in the emergency department or the acute receiving unit, Actually looking for spider nevi and palm erythema can be really useful to give you an indication that patients do have underlying chronic liver disease if they come in with one of these presentations. Yeah, absolutely. So those can be clues of, I guess, more chronic liver disease that just hasn't been yet diagnosed.

ES: Yes. Brilliant. And then a question that I wanted to ask as well is I think I maybe continue to find some of the terminology around these decompensations with liver failure. A bit confusing because I think decompensated cirrhosis, as you mentioned, is something that is used fairly widely. And I've started to hear terms such as acute or chronic liver failure. Is that the same thing or are there subtle differences there that we need to be aware of?

MW: So, you're right, that's a term that has really gained a lot of prominence over the last five or ten years, and it is even less clearly defined than acute decompensation. There are different European, American, and Asian definitions of acute and chronic liver failure, but they broadly come down to the same thing. So, ACLF, which is acute on chronic liver failure, describes those patients who have an acute decompensation, but that that then triggers increasing extra-hepatic organ failures. They often do present with those same problems of jaundice or ascites or encephalopathy, but they go on to develop renal failure or respiratory failure, cardiovascular failure. So ACLF is an acute decompensation with accompanying extra hepatic organ failures. And there is debate as to whether that really represents a discrete pathophysiological entity or there is definitely crossover between the ways that these people present. But the reason it's gained such prominence is that there's very good evidence that if you have ACLF with the increasing numbers of organ failure comes an increasingly poor prognosis. So, it is helpful in recognizing patients that need critical care support but also is important in starting to recognize futility of patients who have so many organ failures. That survival is unlikely even with intensive care support. So, there are now Calculators available online that can help you to work out if somebody meets the criteria for diagnosing acute and chronic liver failure and to give you a predicted prognosis depending on how many organs are affected. But broadly speaking, if you have one or two extra hepatic organ failures, you definitely have a higher short-term mortality, but that definitely can be reversed with Active supportive care. Once you start getting three or more organ failures, the prognosis is often very poor.

ES: Yeah, understandably. And that's useful to know a bit more about that term and actually the implications on where you might manage your patient Obviously, you think recognising decompensated cirrhosis is important as a hepatologist, but would you just be able to explain a little bit of why you'd want the general medic in an acute receiving unit to be able to Watch out for these, the conversation events.

MW: Absolutely. So, this, any of these events really are a major watershed for these patients in terms of their prognosis. So often when we see medical textbooks, they list signs of cirrhosis, and they cheerfully intermingle spider nevi and jaundice. Without really necessarily highlighting that some of these carry a much worse prognostic significance. So, patients who have compensated cirrhosis Have overall, the median overall survival is over a decade. So, if you have well compensated disease, often the prognosis is still, it is a life-limiting diagnosis for a lot of these patients, but they have a good short and medium-term survival with that. Once you develop decompensated cirrhosis, that overall median saliva drops to between one and three years. And that depends a little bit on which complications you have and the aetiology of the liver disease and whether there are specific treatments that can reverse that. So, if you develop encephalopathy in general, that's associated with about a one-year median survival period. And the onset of refractory ascites is, again, around two-year overall survival. So, these are very significant events for these patients and it's important to recognize that that is a major change in what they're going to expect. And there are some that have really very high immediate short-term mortality, so conditions like spontaneous bacterial peritonitis. Sepsis, variceal bleeding has a significant in-hospital mortality associated with them. So, it's important to actively look for these conditions and treat them aggressively, and it's also important to start the thought process about longer term planning. Is there anything else that can be offered for these patients? And trying to make sure that they are aware that this is often the beginning of a cycle of repeated hospital admissions unless we can change their trajectory.

ES: Yeah, I think that's interesting. I think I was always aware of how sick some of these decompensated liver patients were but actually thinking about how this might be a significant event at the start of quite a rapid decline for some of these patients is really useful as in terms of thinking why these decompensation events happen, there are obviously multiple triggers. What would the main ones you would say that we should be investigating for at the front door?

MW: Yeah. So again, that depends a little bit on how they're presenting. So sometimes it can just be a reflection of a progression of their underlying liver injury. So, Patients who are coming in with a gradual development of ascites may just be if they have alcohol-related cirrhosis and they're continuing to drink If they have MASLD cirrhosis and continue to be overweight with diabetes or if they have what we know are often progressive autoimmune liver diseases like PBC or PSC. So sometimes it is just that their underlying liver disease is progressing, but equally there may be specific triggers that lead to that presentation. So, if you think about patients coming in with acute onset jaundice, if you rapidly become very jaundiced, that is certainly typical for alcoholic hepatitis. So, patients who have been drinking up until relatively recently who get a really rapid onset of jaundice, that is often the explanation. Equally, we sometimes see jaundice as a result of a drug-induced liver injury, so it's worth looking at have they had any antibiotics, any antipsychotics, drugs that are known to be associated with an injury in their own right. Or if they have a very high ALT, is there an additional injury like a viral hepatitis? So, Hepatitis E virus now, again, is increasingly common as a cause of an acute hepatic illness and in patients who have underlying cirrhosis that can often be clinically much more severe than it would be in a health So, think about those triggers for jaundice. Encephalopathy is the condition that classically has a number of triggers So again, whilst it can sometimes occur spontaneously, very often we do find an underlying cause. So common ones would be constipation or dehydration. Either because of poor intake or because we have given them diuretics to intentionally dehydrate them or infections of any sort trigger off encephalopathy. GI bleeding can certainly make encephalopathy worse, but usually that is obvious in its own right rather than needing to be looked for specifically. And then the other thing that we often see is patients who come into hospital with another presentation and end up undergoing surgery and that in itself can sometimes Cause their liver disease to decompensate just from that additional stress. So, it's not uncommon for patients who have cirrhosis and undergo surgery to then develop problems. With jaundice or ascites or encephalopathy in that early post-operative period.

ES: Yeah, that's interesting having like a surgical intervention as a stressor event in and of itself and perhaps one we maybe think of a little less. One other question I just wanted to ask you there, you talked about MASLD liver disease there, is that now the preferred terminology that was NAFLD?

MW: Yes. So, there was an intentional name change globally to move away from NAFLD. For a couple of reasons, the diagnosis of being non-alcoholic stressed something that wasn't felt to be important. And at the same time caused confusion if patients did drink alcohol and also had other risk factors. So, it was changed to metabolic dysfunction associated steatotic liver disease to stress the positive the fact that this is triggered by metabolic disease, usually obesity and or type two diabetes, but with input from the other features of the metabolic syndrome. And at the same time as that aetiology focus, they also wanted to move away from the word fatty as that could be perceived as pejorative. In reality, telling a patient that they have metabolic dysfunction associated steatotic liver disease is often met with a slightly Blank look and you often end up having to use the word fat and fatty to try and explain it. But I think it is a shift that we are encouraging people to move towards using the term MASLD.

ES: Yeah, totally, and I don't want to deviate too much away from our acute decompensations, but I did want to ask that because I think that's a change that I've also noticed in terminology in recent years, and it's just interesting to hear the reasons behind that as well. So back to talking about more acute decompensation events. So obviously you've really nicely explained some of the different causes to look for there, especially pertaining to what particular symptoms are presenting. I remember when I was in IMT1 when I was first introduced to what they call the BASL Liver Bundle and I've never come across it before and I've since found it very And I know that's been brought in by the British Association of the Liver, is that right? I just wondered whether you wanted to talk through any elements of that that you think Are particularly important or sometimes you find the hepatologist less commonly or less well done in the acute receiving unit?

MW: Yeah, so if people haven't come across it, I would strongly recommend them to look that out. So, this was a care bundle that was put together by... BASL, the British Association for the Study of the Liver, and BSG, the British Society of Gastroenterology. And it was developed specifically for general medics who are dealing with these patients at the front door. As an aid memoir and checklist for all the things to think about in patients presenting with decompensated cirrhosis in that first period - twenty-four hours – and particularly the first six hours where we know that early diagnosis and early treatment can make a big difference. So, it nicely breaks it down into the different aspects of decompensation to give you specific pointers to look for. And so, we can talk through briefly. So, there are generic tests, including infection screening, because often these patients are at higher risk of sepsis. Looking at their alcohol consumption, because that is still the leading cause of liver related deaths in the UK, unfortunately. So, trying to make sure that we get clear documentation of that at the front door and thinking about the risk of withdrawal and giving addiction support. Looking specifically for infections and treating us aggressively. Looking for kidney dysfunction. And again, there's been a lot more emphasis on that in recent years. As there has been in non-cirrhotic patients of recognising the early acute kidney injury. And for patients with cirrhosis, that's important because often their baseline creatinines are very low. Sometimes because they have low muscle mass. And so, a creatinine of seventy-five or eighty might be double their normal baseline. So, encouraging people to look back at previous blood results. Detect any kidney injury early and intervene for that. And GI bleeding, again, I think there is definitely Much more awareness now of the importance of things like prophylactic antibiotics for GI bleeding, a restrictive transfusion policy so that we don't overload these patients. So, there are clear step-by-step guidelines. And again, just prompts to look for triggers for encephalopathy and treat that. And I would say certainly in our area, the things that tend to get left are the acidic tap. And I think there is anxiety in people who aren't doing that regularly about Whether they're at risk of bleeding, these patients often do have an abnormal prothrombin time. They often have a low platelet count. And so, the tendency, if people Aren't confident with that procedure is to try and defer it until the shift change over and the next team come on. But as I said earlier, SBP is one of the ones that we worry about most in terms of its short-term mortality. So, if somebody comes in with ascites and is unwell for any reason, that should be tapped as soon as possible, certainly within six hours of admission to hospital. If their abnormal prothrombin time in liver disease does not reflect an increased bleeding risk, so there's very good evidence that there's Poor correlation between prothrombin time and bleeding risk in patients with chronic liver disease. So, if their PT is raised, I would ignore it and still do an acidic tap. And the platelet count really has to be pretty low before they start being at a significantly increased risk of bleeding. So certainly, a platelet count of over fifty is definitely safe and a lot of guidelines would suggest that a platelet count of over twenty is adequate for doing a diagnostic acidic tap. So, I'd encourage people to just refresh their knowledge of the landmarks of where it's safe to do that. And to use a sterile technique, but to do that at the front door when these patients come in, because if they have a high Polymorph or neutrophil count in their acidic fluid, they need to start antibiotics and get albumin supplementation as soon as possible.

ES: Yeah, absolutely. I think that's something that people are always a bit shy about doing in the acute receiving unit and sometimes understandably, but it's really useful to hear how important it is and actually to allay some of the worries around bleeding and platelets with that procedure. In terms of management of these patients, so obviously the liver bundle has come in because we recognize that first twenty-four hours is key in recognizing and managing these patients. What are the main steps that you'd want to be seen done in that first kind of twenty-four hours to support these patients?

MW: Yeah, so I think screening for infection and treating it, ensuring that patients are adequately hydrated. And again, I know there's a lot of angst around the choice of fluids in patients with cirrhosis. And on the whole, if they have oedema or ascites, it's likely that their total body sodium is high and we try to avoid giving High sodium fluids where possible, just because that will worsen their fluid retention the longer term. So, if you can give these patients Albumin rather than a saline infusion, that is preferable. But at the end of the day, if you have sick hypotensive patients, they are better getting Any fluid than no fluid, so just thinking about what fluid resuscitation they might need. I guess in terms of that initial assessment, a lot of patients with cirrhosis run a relatively low blood pressure, particularly when they are approaching the stage where they might be coming in with decompensating events. So, we then need to think, is that blood pressure too low? So, it's really important to assess perfusion as you would in any other patient. So, thinking about their cognition, if they are drowsy or confused with a low blood pressure, is it encephalopathy or do they actually just need a better blood pressure to perfuse their brain? What are their kidneys like? Is their creatinine genuinely normal? Are they passing urine? Looking at their lactate to see, are they perfusing their tissues adequately? And thinking about escalating to critical care if there is concern around any of those features. Fluid resuscitation is difficult to assess in some of these patients because often they have ascites, they have a lot of peripheral oedema. But if they are becoming septic or having a variceal bleed, equally they can be intravascularly depleted. And again, sometimes if there are concerns around that, then having central monitoring can be helpful to guide that. And thinking again in the short term, do they need airway protection if you have somebody who's encephalopathic and is at risk of aspirating. Do they need critical care just to stop them for aspirating whilst you wait for treatments to improve their conscious level? And if they come in with variceal bleeding, again, often we protect their airway with a general anaesthetic and endotracheal intubation around the time of endoscopy so that they don't aspirate during that.

ES: Yeah, I think my experience has always been these patients, their fluid balances is tricky to manage, and I think probably just comes with lots of experience. So, another question we wanted to pose to you was obviously these patients prevent with their acute decompensations which with supportive care you hope there'll be an element of recovery from, but we understand there's ongoing underlying Liver failure in all of these patients. So just wondering if there's any things that we would think about with the ongoing care that you'd want to consider.

MW: Absolutely. So, I've already said that these patients often are at risk of getting recurrent admissions and recurrent problems once they've had a first decompensating event. So, there are a few things to think about really for quite early on. The first thing is, have we definitely assessed the cause of their liver disease fully to look for any other treatable elements and put that support in place? So, people who drink heavily can have additional co-existent liver pathology, particularly things like hepatitis C infection or hemochromatosis. So, it's important not to assume that just because somebody drinks heavily or is overweight that it is alcohol or MASLD as the cause. So, we should be screening for Chronic viral hepatitis, B and C. Inherited causes such as hemochromatosis and in younger patients, thinking about Wilson's disease. And depending on the pattern of their liver disease, thinking about autoimmune liver disease as a co-existent cause and making sure that we address those. It's also important to think if this is the first event that marks a prognostic change, is this a patient who's suitable for liver transplant assessment? And that can be difficult at the front door, but it's important to start that thought process because A number of patients coming in with liver disease won't be suitable at that stage. So, if you, as I said, the most common cause is alcohol, and if you are still drinking, then we would not be considering transit at that point. But sometimes it can be helpful for patients to know that their liver disease is bad enough to be thinking about that and that they really do need to abstain firstly to see if that will help. Allow things to recover spontaneously. But secondly, because if things don't recover, transplantation would be an option further down the line. And certainly, for non-alcohol related aetiology, so things like MASLD, trying to think is this somebody who actually their liver disease is their main problem and that would be a suitable intervention. So, it can be difficult to assess their comorbidities. Clearly, if people have got severe ischemic heart disease as a consequence of their metabolic syndrome, it may not be appropriate. But if there's any doubt, discuss with the liver transplant team, we're always happy to discuss these patients at an early stage to think about their suitability and certainly for Younger and otherwise fit patients. It's a really important intervention that we don't want to miss a window for opportunity and get referred patients on their Fifth or sixth admission at a point where they're becoming very deconditioned and can sometimes be too ill to offer transplant to.

ES: Yeah, I think that's a really good point actually, isn't it? Because these recurrent admissions start to occur, the deconditioning and that downward spiral that you see, it's nice to think about this early to break that spiral almost. Perfect. So, thank you so much for your time, Dr. Williams. That's been a really informative podcast and certainly answered a lot of my questions around decompensated cirrhosis. So, thank you so much. And just to let the audience know that we've got lots of other podcasts available from RCP, those clinical conversation ones, particularly pertaining to lots of different conditions that you may see in the acute receiving unit. So, thank you.

MW: Thank you.

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