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Management of Complication of Cirrhosis and the Role of Albumin

Mar 30 | 1:30 PM

There are unmet medical needs in understanding the role of albumin in the management of cirrhosis complications. Multiple problems exist in such patients in terms of achieving optimal outcomes, recommendations adoption, and evidence-based care. Join us live to make the most of Dr. KT Shenoy's and Dr. Vaibhav Somani's rich clinical expertise in hepatology.

[Music] uh good evening everyone uh this is uh dr anosha connecti from the medical team uh takeda uh i welcome one and all for today's session on the management of complication of cirrhosis and the role of abdomen so today with us we have two important eminence speakers dr katie shinoyser who is the professor and uh head of the department of gastroenterology from gokula medical college and we also have doctor who is a consultant and gastroenterologist hospital in mumbai so before we head on to the discussion today i would like to flash in the agenda for today so for the first 20 minutes doctor vivo sumanisa would be set in the context and he would be discussing on the complications of cirrhosis uh and uh we have katy schneisser those that would be taking on a roll of albumin india competition and post which we have q and a i would be requesting all the audience to posting their questions in the comment box so that we can take up the questions so uh post the uh uh post the discussion by the two speakers so with this i shall welcome dr viber so many small about management of complications of services so as we all know liver disease is increasing all over the world and there are around 2 million deaths worldwide every year and most of them are due to complications of cirrhosis and cellular carcinoma it is one of the most common cause of death globally and almost account for 3.5 percent of all the deaths worldwide so around uh and the most common cause of zeros is being the alcohol and the rising trend of nfld over the last few years i think uh inspiration in the western world nfld has taken over the alcohol as the most uh around 75 million are at risk of developing and coming to nfnd as the diabetes and obesity are increasing the metabolic syndrome is increasing especially also in the pediatric age group the there is rising cases of nafld leading to syllosis even the global prevalence of viral epidemic still remains the high and also the autoimmune liver diseases still remains the eye and liver transplant is the second most common cause of solid solid organ transplantation throughout the world so there are a lot of unmet needs in this newer transplant programs worldwide especially in india where we have uh dearth of donors so being gastroenterologists and hepatologists we see this people uh cirrhosis daily in our clinical practice and it is one of the most challenging to manage them so if you go by epidemiology of ceres is in india this is the latest study which was done in around 2017 and we was found to be alcoholic liver disease and hepatitis b was the most common cause of non-serotic liver disease so cirrhosis was again alcoholic liver disease is the most common cause of cirrhosis in india till now but i think nfld will uh cross it in coming years maybe next five to ten years and if you go by the reason why is the north uh north uh hippity c as the most common cause while east and southern repetitive invested so as we all know the development of over a period of many years and most of the etiological factors start few years in advance like alcohol abuse viral infection especially chronic hepatitis b and c and fld and others so as the uh there is damage to the liver which is fibrosis and f1 3 fibrosis which eventually leads to cirrhosis of the liver this all takes around 15 to 20 years for me to develop coming to the stages of cirrhosis of liver as we all know very firmly compensated and decompensated are the two main stages of liver if we go by stage one two three four there are four stages and this uh stage one has no varieties no societies stage two patient has varieties but no societies and no variation building stage three where patient has varices with ascites and stage four is bleeding viruses with or without anxiety so why this is important it is important because if you see the death rate each year it increases as the stage of the disease increases especially [Music] so what is the nature history of cirrhosis of fever so as i said which uh civilizes of liver goes from starts with the chronic liver disease then compensated cirrhosis then decompensates the main factor behind the stage population of the stage is the portal hypertension so as the neurofibrosis increases there is increased total increase in the total pressure and once the total pressure goes about 10 minutes patient develops decompensation and decompensation usually in the form of variational images hypertension further increases above 16 to 20 mm the uh the complication uh even further increase in the form of recurrent bleed refractory syndrome and bacterial infections so this is the natural history of liver cirrhosis and why it is important because if you see the chart here uh compensate the median survival of compensated civilized versus decomposition is a wide difference and decompensated with patient median survival is only 1.6 years while it is around 9 years for patients with compensated so there are many complications of uh cirrhosis of liver and the most common uh of them being the ascites complicating into some spontaneous bacterial peritonitis gibb in the so it is not possible to discuss everything in such a short period of time i will mainly focusing on the ascites it's complication and hepatorenal syndrome where uh because we are more concentrating on the uses of albumin which doctor signature will be taking after me so these two are the main complications uh which will be is one of the most common complications which developed in patients with cirrhosis of liver it is due to usually increased hepatic sinusoidal pressure and the the main pathophysiological process which occur here are systemic arterial vasodilation activation of sodium uh water retention and sinusoidal total hypertension so as we see in this initially the patient has compensated there is normal effective blood volume as the years passes by and total hypertension increases patients uh effective uh volume develops and that leads to uh stimulation of the uh remaining angiotensin aldosterone system sympathetic nervous system and uh adh activation so this all leads to uh strengthening constriction and decreasing so same thing in a simpler way this which initially leads to sodium retention followed by water and sodium retention and extreme type 2 hrs so this is the basic pathophysiology development of a site is an hrs if you go to the epidemiology of asides it's occurring around 50 so this is fifty percent of the compensated zero suspicions mortality is around forty percent at one year and fifty percent at two years the most reliable factors predicting the poor prognosis in patients with cirrhosis are hyponatremia low arterial pressure increased serum creatinine and low urinary sodium so these all as we i already told in the pathophysiology development uh the main thing uh here i would like to highlight is that uh every patient who has a scientist and cirrhosis does not mean that aside is only due to psychosis we have to rule out other causes of assets like uh the cardiac acids tuberculosis malignancies uh confirm the diagnosis that the scientists due to liver only there are sometimes also which we have seen then we have to treat accordingly which is quite subjective now the types of societies can be complicated or uncomplicated uncomplicated is one without any sbp or not again has two subtypes uh diuretical and diuretic resistant residues refractory society occurs in around 10 percent of these erotic patients and median survival is very poor of around six months once patient developed refractory and mortality is around 70 within a year of the diagnosis is because of the inability to provide effectiveness of diabetes as the patient develops adverse effects of the diabetes so coming to the management of the scientists so as i said diagnostic evaluation is very very important to confirm the diagnosis serotonin which establishes total hypertension neutrophilic count of more than 250 is diagnostic of sbp and even culture scientific culture should be done severity of societies [Music] further complications in these patients should have a diagnostic evaluation you should rule out in patients with syracuse's and because it needs further treatment in the form of anticoagulation therapy so it is very very important to reload from versus so coming to the management there are three main things one is sodium restriction and diuretics and followed by large volume parasympathetic [Music] and which is six to eight gram per liter of ascites about the five liters when it is given because it helps in preventing the post parasympathetic circulatory dysfunction so coming so how do we explain the sodium restriction to the patient you can't just tell that uh take low salt diet or salt restricted it has to be explained properly that the amount of sodium goes uh appropriately and in the fixed uh daily so what we usually do is we ask patient to avoid any salt in the diet and avoid all the bakery products etc which contain salt all soda containing items irrigated drinks and we ask them to have salt free make a salt free diet for them food and then add one teaspoon of salt which one teaspoon is around five grams so around four to five grams salt uh in whole day in all the means they can add from [Music] so that will be the exact amount of salt which patient consumes and along with uh usually mild as it is resolved with sodium restriction patients with moderate to severe assets will require diuretic therapy so the main proven diuretics which we use weight and weight loss is less than one kg in first week and less than two kg thereafter or we decrease the diabetes if the weight loss is more than 0.5 kg in a day in patients without more than one kg in a day impressions so we decrease the dose when there is excessive diabetes we monitor patients for renal dysfunction so once the patient is which does not improve the survival first in the foreign stream and it may lead to parasympathetic circulatory dysfunction and albumin has to be given unless the patient has major complications due to diabetic or the urinary sodium is less than 15 minutes per day another thing in the management of refractive sites is the tips this is or antibiotic water system action as you all know so the main uh important part in the uh before doing the tips is the selection of the patient which is i think very very important uh we don't know how it it decreases the sinusoidal pressure and it also increases the survival rate especially in patients where the tips which is still controversial ideally it should only be used as a bridge to transplant the patient selection especially the main thing is if male and as the substrate says levels should be less than 1.5 or less than 1.5 milli less than 2 which that would be the ideal patient for selection of the tips another new modality in patients who cannot undergo it is a battery operated device which requires uh frequent change of batteries at least twice a day and mainly useful impressions are unsuitable for tips and but uh it decreases the frequency of the large volume parasympathetic that is how [Music] and coming if possible [Music] [Music] sodium restriction diuretics avoidance of the risk factors these patients increasing the frequency of large volume disease especially in patients who have hypotension we can use this agent and sometimes works very well and if it doesn't as we discussed so what is another complication which requires antibiotics so this was society's uh refractory ascites and its complications now we move into second most common uh complication in the form of hepatolinal syndrome so by definition it is uh cirrhosis with uh patients with cirrhosis with anxieties and presence of renal failure is more than 1.5 grams and lack of improvement of creatinine with volume expansion with aluminium absence of shopping no use of any natural toxic drug or any parent disease should be ruled out with by ruling out urinary protein india hematuria and urinary obstruction by imaging so this is the most commonly used definition of api in zerotics so any rising creatinine of more than three milligram per deciliter will be 48 hours or increasing more than 50 within prior to seven days so this is the definition of acquiring use and the staging of stage one two three according to that definition so what are the characteristics of the petroleum of synonyms follow the activation of uh [Music] sympathetic nervous system activation which leads to renal uh hypoperfusion which is the cause of reproductive renal syndrome as you can see this in the diagram so what are the types of hrs there are two types one and two so type one is more commonly seen it is rapidly progressing and it is usually triggered by sepsis or alpha indeed and it is untreated it is a high mortality if it is not treated and type 2 is more slowly progressing diabetic resistant societies whereas creatinine increases slowly and it has a better prognosis and [Music] because over a period of time patient will develop more complications and survival is drastically decreasing so once patient develop hrs all the suitable candidates should be uh explained about the need for liver transplant we have to exclude the is is have shown again it is controversial so the main thing is and ruling out other causes treatment of sepsis which is the most important thing in the management of the hrs [Music] is [Music] is [Music] [Music] blue be at high risk of rebreathing and should consider the prophylactic tips if needed if patient is having persistent bleeding then volume temporary strain which is used nowadays can be used for emergency tips can be used in these patients secondary profile access is very very important and starting learning beta blockers is also important primary prophylaxis depends on the patient's and local expertise if there are great rcs usually it is caused by brain dysfunction which is caused by liver insufficiency due to court of systemic chanting the most common agents implicating in this photosystemic change bypass or something which occurs after tips also sometimes where there are some natural large shunts then also it causes and type c is the most common what we see is seen in sibotics there are multiple sub classifications which i won't go into the details of but the main two are overtyped is the most common uh clinical practice in the form of bleed or stroke in these patients the most common predisposing factors for hepatic encephalopathy have to be addressed first that is infection hypokalemia or other disease options again are uh first and foremost is everywhere within circulation then lactose we uh followed by defects in these two are the main treatment options are available and they have shown to be very [Music] [Music] with repetitions they are all already malnourished so high proper nutrition and high protein intake is very very important in these patients so [Music] one of the most common diseases we see in our daily practice and these are the assigted and hypnotic uh original syndrome where i should read up the common complications we see in our clinical practice so this is the basic management and [Music] thank you very much team takeda dr anusha and the other organizers for this one-hour webinar on cirrhosis complications and the role of albumin in the next 20 minutes i shall touch upon what is the molecule albumin and what is its effect in the compensated cirrhosis next slide please i will try to put my topic under the following heads albumin has been in the use for the last 50 to 60 years ever since the research by professor late sheila the molecule has gone in a long distance and currently we have a number of clinical trials which have put the status of the drug albumin so today i will be discussing albumin as a drug with its structure and function what are the physiological role of albumin in the human body what is his role in decompensated liver disease the current status and my previous speaker has given a very elaborate account of the decompensated liver disease and he has mentioned that the survival benefit will be much more above the 12 to 15 months normally they survive for 12 to 15 months so the survival benefit by albumin should be anywhere more than the survival benefit currently available i will also touch upon the cost efficacy or the cost effectiveness ratio i will highlight the future directions and finally we will recap next slide please why we focus on albumin albumin is one of the most important pivotal molecule which is only synthesized by the body in the liver it is the plasma protein distributed with the 3.525 grams per kilowatt per deciliter the plasma albumin modulates the oncotic pressure the oncotic pressure is the pressure which retains the fluid within the vascular system and it also helps in the distribution of the fluid between the vascular and the non-vascular compartments the molecule is a pliotropic one which has got multiple actions both oncotic and non-oncotic it also regulates the systemic and the redox homeostasis this molecule by its non-oncological pro non oncotic properties has immunological properties and anti-inflammatory properties to adhere to the bacterial molecules which cause injury to the liver it also has an action on the pro-inflammatory cytokine release it also action on the drug pharmacokinetics and the delivery so this molecule with its ubiquitous oncotic and non-oncotic properties has a very important role in preventing the progression of chronic liver disease from a well-compensated cirrhosis to a totally decompensated cirrhosis with the progressive functional deterioration reducing the effective albumin level and thereby increases the chance of infection increasing the chance of morbidity and mortality the acute decompensation of the liver disease as seen in aclf is one new aspect which has been researched and albumin is one such molecule which has been researched widely by the indian team as well as the global team the albumin which is native will be altered in the pathophysiological conditions it may be oxidized or it may get into a form which is called as the pathological albumin which has the deleterious effects on the endothelial membrane and the tissues in the human body so this is the reason why we should focus on albumin as a unique molecule which is going to be an important molecule for the next few decades to be researched by pharmaceutical agencies and to be delivered for the benefit of the patients next slide please my previous speaker has given you that cirrhosis is a condition which can lead into complications such as bacterial infections as well as the various other mechanisms i will not go through the bc slide except to show that some of the molecules which are released from the liver as well as during inflammation these molecules damage many organs and albumin is one such molecule which can take control of these next one alterations of the albumin level structure and function in chronic liver disease a term which is called as albuminous oh i have taken this picture and i would like to thank a processor in steam which has published a paper in hepatology it has not been in print as of now this is a pre-print which i have gathered and this uh this is jagdish and two others including professor sari 2021 this picture describes the whole molecular biology of albumin where albumin can has to be replenished when there is a natural loss of albumin in a progressing liver disease or it has to be replenished so it has to be replenished when there is a multiple injuries in the body either in the form of an infection bacterial sepsis or in the form of a decompensation with a deteriorating liver function and a refractory ascites or an impairment of the renal function which we call as the hrs or the various types of the acute kidney injuries associated with the cirrhosis liver so whatever may be the pathology either it has to be replenished or it has to be taken care of next one albumin what is albumin this is a panel which this is an article which i have taken and this diagram has been taken from the article in 2021 a very interesting concept of the whole albumin this is what is the panel here in the diagram which is the molecular structure of the human albumin which has got the various sub domains the sub domain 1 a 1b the sub domain 2a and 2b the subdomain 3a and 3b and these are the domains which are mostly endogenous or exogenous compound binding sites and these sites help in the multi-metal binding sites you can see a number of molecules which i have mentioned they are too complex to be explained in detail but to me these are the sides which adhere to many of the molecules in the body including wild salts so this is the panel here we have two other panel next slide please the two other panels are the panel b and the panel c which is again the albumin molecule showing the panel b showing seven long chain fatty acid binding sites starting with the fa1 to fa seven you can see them clearly and these are the fatty acid binding sites which help in the transport and inactivation of the biologically active lipids involved in systemic inflammation including prostaglandins and various molecules which are called as the pams which are liposaccharides and lipotechnic acid so this is the panel b now we have a panel c the panel c is again the albumin is the most important regulator of the oxidative stress and it presents many of the binding sites where the reactive oxidase species bind and the important site here is cis34 residue where these molecules are converted into irreversible oxidized molecules so this is the important biological aspect of arbument which has binding sites for fatty acids as well as binding sites for the oxidative stress release substances which are in this panel b and panel c so biologically albumin is a very important moiety which has not only the oncotic properties it has the non oncotic properties of binding with various substances within the human host next slide please this diagram is again taken from jagdish and sarin's article 2021 and my thanks to them a beautiful diagram which shows what happens to the human albumin the human albumin once it has entered it binds to an important molecule within the endothelium the vascular endothelium is a very important site where molecule which is called as the alpha bonding the second part of the diagram you can see the alpha bonding within the vascular endothelium where albumin binds and diseases destroyed whenever there is a decompensation so the albumin cannot effectively address its functions when the vascular endothelium has been irreversibly damaged by the bacterial translocation and the lipopolysaccharides so this diagram gives you the molecular mechanisms of the albumin binding within the intravascular compartment where the all bonding receptors and this albumin is trans cytoside next diagram please this is where the albumin gets into the recycling process the recycling process of the albumin is a mechanism maintaining the high concentration of albumin in the systemic circulation albumin which is synthesized in the body 10 to 15 grams of albumin is synthesized in the body and released into the vascular compartment the total human albumin is about 360 grams and 160 gram of albumin is in the intravascular compartment and 240 grams of albumin is in the extravascular compartment so there is an exchange of albumin to the extent of four to five percent every hour in the endothelium and within the extravascular pool and this is mediated by the gp60 receptor which i already enumerated as all bond tin and this diagram does not contain the all-mountain i have shown you in the previous diagram so this is the recycling of the albumin by the endothelial cells which is a very important mechanism to keep the argument within the system for a period of 17 to 21 days which is the half-life of serum albumin in the human host next one please till now i have taken you to the step of what are the ubiquitous actions of albumin again this is the diagram which i have taken from the article by dr sarin many thanks to him to putting putting out a beautiful diagram this diagram i will summarize in my last slide what are the various actions of albumin in the oxidative stress bacterial toxins the various antimetabolites and replenishing the albumin how it takes care of the polysaccharides all these things i will put up in my recap slide because that will be a very important slide at the end of my talk next one so albumin we know that it is used in a decompensated cirrhosis but of late we have started researching on acute on chronic liver failure there are differences in the definitions between the asia pacific the canonic and the various organization nevertheless the entity itself is a very unique one which is a progressive liver injury it's a very short survival and this diagram gives the use of human albumin this is where the abdomen will be very useful in binding the various sites and the sites of binding in the albumin helps in detoxification of the various toxins which are important in the aclf next slide please now let me come to the current indications of albumin the current indications of albumin some of them have been enumerated by my previous speaker we can classify them as some of the compensat decompensation mechanisms and the most important will be decompensated liver disease the busy slide the next one will be the the use of albumin in renal failure the third will be in spontaneous bacterial peritonitis the fourth one will be in aclf and the fifth one will be the other important complications such as hepatic encephalopathy so these are the current indications and this has been taken from one of the recent publications which i have put in the right side of the slide in the vertical fashion i have put this article next one there are other indications for use of albumin in the non-bacterial infections you can use them this is again taken from jagdish and sarin's article it's a busy slide some of these indications are not really worked out they may be still controversial but this is a field which is progressing very rapidly now let me come to the topic in proper next slide please the next is six to seven minutes i will touch upon the molecule of albumin in d compensate cirrhosis as you see here there are now eight important studies which have been enumerated here we still don't have the answer so that is the answer trial in 20 to 2018 the second one is the match trial the third one and fourth one the fourth one is the incipa the fifth one is the attire the uk trial 2021 so whatever the trials are they are important one concept you have to start building up a larger dose of albumin to the extent of 1 to 1.5 gram per kilogram body weight you have to maintain the dose of albumin to the extent of 20 to 40 grams every day or maybe once in a week and then you have to follow these patients prospectively for a period of 10 to 12 months ultimately what is the outcome which we are measuring it we are trying to measure three important outcomes what is the progression of the disease in terms of the decompensated liver disease going into mortality which is the survival benefit what is the progression of decompensation to develop other complications like hepatic encephalopathy or sepsis or death so all these decompensated liver disease will have the ultimate end of the death so the survival benefit which is beyond 12 to 15 months is what we are trying to achieve from any of these trials but some trials have given a negative result though answer trial was positive the entire trial did not give much positive that is a european trial there is a trial from the indian group the aclf that acl of the asia pacific consortium the trial is not yet complete so i have put in the acl trial which is still a trial in evolution and continues to develop the results so let us wait for a couple of months so the summary of this important slide giving albumin at 1 to 1.5 kilogram per body weight in day one and then maintaining the levels of albumin by giving albumin so that we maintain an albumin we do not know at what level we have to maintain three or three point five and then we do not know what happens to these albumin which we have infused because albumin undergoes a degradation process and this degraded albumin may not be very active so we do not know what is the functional aspect of the infused albumin because studies have to be really carried out to find out the exogenously administered albumin compared to the endogenous albumin how this molecule will fare functionally within the human system next slide please [Music] these are the two important trials which i have given here a busy slide to compare between the answer trial and the match trial there is these are all various parameters which we take the survival benefit complication rates and what is the number of proportion of people developing into complications i do not like to describe each one of them between the two trials but the fact remains that inexpensive treatment which will be approximately 8 to 10 lakh rupees every year by giving intravenous albumin calculated that the rate of 3500 rupees for a 20 percent albumin 100 ml a modest estimate and i have seen this in one of my patients with the decompensated cirrhosis similar to the answer trial it came approximately 10 lakhs to keep him surviving for a period of 15 months so i do not know whether the answer is the answer trial whether the answer is the entire trial or the answer is the match trial but whatever may be the trial we are not at perfect in the use of albumin next slide please so these are some of the important papers which i have taken here human albumin infusion strategy liberal or restrictive you can think about liberal such as the answer trial or you can be restrictive depending upon the need and whenever they have severe hypoalbanemia next one this is again albumin indications in chronic liver disease again the summary of whatever i have told you the use of albumin in a decompensated cirrhosis that is the big arrow which i have shown the second is the decompensated liver disease with various complications like hrs spontaneous bacterial peritonitis people outright this and my previous speaker has mentioned hrs along with midodrine or with the turly proceed albumin has been tried again from the indian group by dr virinder singh and others there has been a study from delhi there has been studies from chandigarh but whatever it is these are only temporary measures which will improve the survival by a few months ultimately the proof of the pudding is the liver transplantation so i would like you to read these articles albumin indications in chronic liver disease again in the european journal of european uh united european gastroenterology journal next one i am coming to the last part of my of lecture albumin can be used in decompensated cirrhosis what is the mechanistic basis again quoting from jagdish and serene the mechanistic basis is binding of with the various sites the nitric oxide synthetic pathways and then the neutrophils are important you have to improve the neutrophil function it is a complex diagram but nevertheless this use of albumin will stabilize the lysosomal membrane it will stabilize the neutrophils it will remove the various molecular pathogens within the intracellular compartment which are the plants and the dam and my last slide next one please so this is the mechanism of albumin aclf a bc slide i will not discuss in detail i hope the organizers can transmit the slides to you any of the listeners so that they can make use of it next one so human albumin is used in chronic liver disease an albumin currently is a drug it can be used in spontaneous bacterial peritonitis epidermal syndrome it can be used in acute kidney injuries it can be used in aclf it can be used in hepatic encephalopathy it can be used in serotic cardiomyopathy so this is a very important molecule a drug which can be used in a number of decompensated liver conditions which includes even serotic cardiomyopathy next one next one so what are the prospects of albumin just go to the previous one the okay what are the prospects of albumin today albumin has to be functionally effective the given albumin as the exogenous albumin has to be very effective we should try to see the newer mechanisms of delivery including the transnasal albumin which may be a potentially more beneficial so we have to find out whether the album in which we are infusing what it have what happens to it in the human body how much of it is retained what is the mechanisms of retaining this albumin for a longer period of time or keeping it biologically active so to recap albumin is a very unique molecule currently it is not an infusion it is given as a drug the drug is widely used in a gastroenterology forum i am not discussing about the use of albamin in other indications like hypovolemia where the surgeons or the anaesthetist may use it i am restricting my discussion to the important molecule of albumin which is within the liver paradigm so this is the recap of whatever i told you the functions of albumin both oncotic as well as the non-oncotic functions have been used very critically in managing a very complex condition of a decompensated cirrhosis let me thank each and every one of you including the organizers the team takeda the team which is helping us in uh in digitizing this and giving and taking it to every one of you and my thanks to all of you for listening to the use of albumin asset drug thank you very much uh thank you dr shino isa uh sir hello [Music] it seems to be around 7 58 no problem i am available for you thank you so we'll have like five to eight more minutes so that the questions will start coming in if there are any so by the way i would start taking up the questions from my side uh sir you uh have i think we had a very good discussion first on the complications part and the management of liver cirrhosis by touching upon the role of albumin touched upon the trials basically the answer in the man's trials but sir how far are we practicing currently in your practice is it like are you starting with the higher doses of albumin or because the current evidence is state that 40 grams twice a week and then you know go back to 40 grams once a week so what is your current uh day of using it my goal my take in this will be the use of albumin mostly for refractory ascites in a site is where we have reached an end point of medical therapy by diuretics the maximum dose and keeping the patient alive so when there is a refractory ascites and as i mentioned the patient a six-year-old male who has refractory ascites requiring large organ parasympathies to the extent of five to seven liters and normally we have to give eight grams of albumin for every liter of fluid transfused which means seven liters into eight fifty six grams of and albumin about 2.5 bottles of 20 albumin or 25 percent two bottles okay i send him back after giving this infusion he comes back to me after three days with respiratory distress again the same refractory ascites the patient which i mentioned to you had 52 times i had to tap him the refractory ascites here two episodes of covid in between he was not willing for a transplant the support for him has come from the echs he was an ex-army person maybe alcoholic so the total cost of albumin i have calculated calculation a million rupee 10 lakh rupees spent on albumin but i have not improved his survival to a patient who cannot have the same albumin the survival benefit i found was only two to three months so a survival benefit of three months the use of albumin has 10 lakhs which means for every one month of survival i wanted to take the cost effectiveness during discussion because it's a very important topic to keep a person surviving for one month we have to spend approximately four to five lakhs if there is an option for transplantation which will be 30 to 35 lakhs if he gets a category or if he gets a live liver transplant there is nothing called as a transplant occurring in a live liver by a relative 90 percent of them are bogus they are all paid donors they're all paid donors i repeat this when the payment will be out of pocket about 25 to 30 lakhs so totally you spend about 50 to 55 lakhs the use of albumin in these patients will be very little post transplant again one area which i have not discussed really an area for research post transplant use of albumin but if you have a liver and get a liver transplant with the 55 lakhs and keep you surviving for a period of five to seven years i think that is the most cost effective strategy very true yes at the end i think that is where we uh lead into because patient is looking for the liver transplant uh obviously i would like to have the views of my previous speaker i think it is very important uh i think can you be louder can you be louder so there is no discussion there is no need of any discussion on the uh role of aluminium treatment is very clear and it is absolutely fantastic to have there is no doubt about it so as you rightly say the only issue here is the cost and that is the major problem we also face daily in our practice any patient who is admitted civilizations if we calculate the dose of one milligram per kg it is very difficult to give that those two three one gram per kilogram one gram per kilogram which will be about 70 grams of albumin yes practically i have never given that those in my clinical practice you try to titrate the roses but what one bottle of five thousand rupees or two bottles a day ten thousand it [Music] album with a new strength coming in how do you see uh 25 percent uh coming to the rescue in such cases because i think you see the problem here is i will answer this question a 20 albumin to me it comes at about 3 700 rupees a 25 albumin comes to me from the from takeda at about 4 600 rupees so i spend about 900 rupees for an extra five percent can you get my point we all calculate what is called the incremental cost the extra cost for five percent between twenty to twenty five percent the hyper oncotic albumin preparation there is no difference it is only that five grams of extra albumin you are giving i think what we need is a strategy to decrease the cost which is very difficult [Music] do we have a strategy to reduce the sir i think uh we we can have a discussion separately on this since we are having a scientific discussion and we have lot of spectators on this but i think we had a very uh good discussion specifically when it comes to the trials because this is where the most of the enlightenment is needed in terms of specifically uh you know their role of albumin please and i think uh vibosa has beautifully brought up the concept of different complications of cirrhosis and you are touching upon mirotrain and thirly protein of the combination with albumin i think with evidences because that is mostly the important part and i think we had a wonderful discussion uh i would request the participants to post in these questions because this session will go live uh on the platform and uh so there's one more question how we calculate albumin therapy and life expectancy any patho mechanisms which affect the iv albumin function with the time see the problem is whatever albumin we give suppose we give 50 grams of albumin within uh four hours sixty percent of this will be destroyed i will give you if you take a volunteer and give them 50 grams of albumin 50 of death will disappear from the system within 240 minutes if you give a 60 grams of aluminium 60 percent of this will disappear into 40 minutes the half-life of albumin will never be prolonged about 21 days come what may be it is 70 to 71 days so retaining albumin in the human system there is no other mechanism other than this albumin going through the cycle of what i have shown you getting into the system and then remaining but because of the endothelial damage the albumin cannot be retained in the system because the algondine doesn't function because there is endothelial damage so this recycling is very defective so the half-life has been much more shorter compared to the natural albumin or the endogenous argument to summarize 50 percent to 60 percent of the given albumin will be out of the system from the intravascular compartment to the other sides in 240 minutes okay so so uh vibration we have one last question to take uh sir are your thoughts on the role of injection on vitamin k in alcoholics there is no role of vitamin k in not only in alcoholic varieties but any prolonged iron in any patient [Music] there has been enough evidence now and [Music] stresses in this patient so prolonged inr you don't need to treat it by giving vitamin k it is just a prognostic marker which we calculated [Music] all the participants if you have any questions the session would be live you can question those questions and they will uh connect to viber and chinoy surfer for any of their discussion for those questions and i would personally thank all the participants and that was an excellent discussion we look forward to your you know uh sessions for the near future because everyone is saying we had a very nice talk um thank you so much dr neuser and vibrowser

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Dr. Murtuza Zozwala & 616 others

SPEAKERS

dr. KT Shenoy

Dr. KT Shenoy

Professor and Head, Department of Gastroenterology, SreeGokulam Medical College and Research Foundation, Trivandrum

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dr. Vaibhav Somani

Dr. Vaibhav Somani

Consultant in Department Of Gastroenterology, Bombay Hospital, Mumbai

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dr. Koneti Anusha

Dr. Koneti Anusha

Consultant Physician

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dr. KT Shenoy

Dr. KT Shenoy

Professor and Head, Department of Gastroenter...

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dr. Vaibhav Somani

Dr. Vaibhav Somani

Consultant in Department Of Gastroenterology,...

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dr. Koneti Anusha

Dr. Koneti Anusha

Consultant Physician

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