[Music] good evening everyone netflix team welcomes you today for a very important and management today we have with us an eminent faculty doctor ravindranath who has been a retired professor in department of medicine in km hospital mumbai and currently is working as a consultant physician with apollo hospital and also as a professor in diwa battle medical college and the most important thing about sir is that he has extraordinary videos on youtube i think i have cracked my neat pg exam watching his videos i've done my final exams watching his videos so his videos are extraordinarily amazing and it has taught us a lot regarding medicine it's examination and his uh his heart touching clinical skills so over to you sir we hope to have a very delightful session today sure so all right thank you very much yeah so last time we did a site test is a complication of cirrhosis so today i've been asked to take cirrhosis of liver okay so this is a common condition okay in day to day practice right so i have to just decide on the level that i will be telling you okay there each facet of cirrhosis has its own expanded understanding okay and details about each factor so i'll try to fit in within the time okay so that all of you get a hang of what actually cirrhosis is what you expect what problems can occur in the patient of cirrhosis okay how to diagnose it suspected all that okay so cirrhosis of liver is a chronic liver disease right it is different from other chronic liver chronic diseases as such in that the chronic chronicity includes destruction of the hepatocytes [Music] but simultaneous regeneration of the hepatocytes so this is a chronic liver disease cirrhosis in which there is fibrosis means necrosis of the hepatocytes but with simultaneous regeneration of the hepatocytes liver is an organ which has large number of functions for animal survival for individual survival therefore nature has imparted intense regenerative capacity to the liver if it was just fibrosis and destruction of the hepatocytes the features would have been different but because there is regenerative capacity the surrounding tissues which are not degenerated will regenerate okay this results in a disturbed architecture of the liver liver architecture is essential for its function okay this is the only organ one of the few organs which receive blood from two sources there is an arterial source there is a venous source right then there is system for drainage of the blood there is system for drainage of the secretions of the liver unlike the bile okay so there are multiple conduits passing through the liver which have to be in definite architectural design okay so this gets disrupted because of the degeneration and simultaneous regeneration so cirrhosis is a unique chronic liver disease okay characterized by degeneration and simultaneous regeneration of the hepatocytes now what consequences it causes because liver is degenerating so there is hepatic dysfunction [Music] okay because of the death of necrosis of the hepatocytes but because it is regenerating there is not a rapid destruction of hepatic function so a patient with cirrhosis can survive for very long okay it takes a very long time to realize that anything is wrong with the liver because of the regenerative hepatocytes but then because the architecture is getting disrupted so the blood flow to the liver okay that is affected and the blood flow is majorly from the portal vein right total vein drains major part much of the intestine right and blood from the intestine must go through the liver okay because it is called carrying lot of toxins it's carrying nutrition so all these cannot go directly into the systemic circulation it has to go through the liver and the liver selectively removes the toxins picks up the nutrients like metabolizes them and then pushes into the systemic circulation so this flow through the liver through the portal vein gets affected therefore it leads to what we commonly know as total hypertension therefore cirrhosis of liver is associated with two remarkable features one is a decrease in the hepatic function okay decrease in the hepatic function which we say science or liver cell failure or science of hepatic dysfunction but before that manifests there are features of total hypertension so these are the two remarkable clinical features of cirrhosis of liver before we go on what would be the clinical features of cirrhosis let me just give you an idea of what is the etiology of cirrhosis why cirrhosis would occur right so this is the common okay the most common is chronic alcoholism now we will request the organizers to have sessions on each of them each of the etiologies and cirrhosis of liver okay they are so good to understand because these etiologies that they could constitute one full session on them okay here i will just go through them okay if you need to ask you can so the most common is chronic alcoholism right and that also okay as i told you there are intricacies okay deep insights into this so for quick knowledge is a definite amount of alcohol quite sufficient amount of alcohol okay different books mentioned different amounts right so for male it is about 80 grams of alcohol for females 60 grams per day for 10 to 15 years okay so this would lead to cirrhosis now apart from chronic alcoholism other factors will lead to cirrhosis because the second one is post hepatitis post infective an infection with hepatic viruses okay most impressively hepatitis c okay those who get hepatitis c okay eighty percent will go to chronicity and about one fourth of them will develop cirrhosis so post infective is the second common cause for cirrhosis in that hepatitis c and less commonly hepatitis b both would lead to chronicity and ultimately chronic liver disease how to pick them up as i told you okay we decided we'll have different sessions on viruses okay hepatic viruses how to detect okay how to predict that this may lead to chronicity all that okay for the time we understand viral infection of the liver especially with hepatitis c less commonly with hepatitis b will lead to chronicity cirrhosis and its complications now in the modern world what new changes new understand what is the cause of cirrhosis but the understanding as they are opening up okay factors included in them what we earlier was thought to be cryptogenic could be an even hitting the world now with india in india as well okay so obesity itself would lead to candy factor for causing contrasting to right there is non alkali fatty liver disease is a spectrum okay from the very minor okay it's being most basic and the most severe non-alcoholic tiato hepatitis the inflammation begins to occur because of the fat fat accumulation in the liver okay i have seen quite young people the last i saw the last patient is only 17 year old she's going to use for study okay but because of her weight she's having this hepatic dysfunction so it is what was thought no other practice easy ones okay but you don't get to see them so frequently are metabolic disorders which can lead to cirrhosis okay metabolic disorders like say hemachromatosis okay quite a common condition in fact we do not realize many patients with hemochromatosis where there is an iron load in one eyelid okay so it commonly design excess of iron gets deposited in the liver and other organs earlier it was popularly known as bronze diabetes because the excess iron would deposit in the liver the pancreas and the skin so fair skin people okay the europeans who pioneered the work okay their skin would get bronzed pancreas okay and apart from cirrhosis bronze diabetes right then you have wilson's disease again you take physicians you will get more physicians would encounter this any chronicity or the chronic disorder of the liver can lead to it so what is known as cardiac cirrhosis that there is a chronic right heart failure at one time used to be quite common now you don't get to see so many because the treatment of right hand theory cirrhosis okay wherever there is obstruction to bile flow like in primary biliary cirrhosis or primary sclerosing cholangitis so there is obstruction to bile flow and the reflux of bile into the liver bile is highly necrotic so it would cause a chronic destruction of the petrocytes okay because of chronic destruction the hepatocytes would regenerate okay and would lead to cirrhosis so cardiac cirrhosis okay biliary cirrhosis and one interesting one okay which has indian connection they're not seen anymore there's indian childhood cirrhosis okay it doesn't mean fine mentioned books anymore but one time it used to maybe it was reported by the british army in india okay they are fascinated how children can get in british indian army okay in the 1800s they have mentioned the right one line indian brahmins are afflicted by childhood services so this so much being of government the army doctors could find that this small indian kids are getting cirrhosis and they found that they are all brahmins so they thought it is something to do with being a brahmana okay therefore they concluded erroneously of course that it is because of being a vegetarian they couldn't imagine that any animal is used to be an interesting aspect as yes said 20 years ago the that was the outcome of the observation of the british army doctors in india so they thought that diamonds they don't eat meat therefore the chicken are getting cirrhosis okay but all these big studies okay after famines okay especially the african famine the quash yorker and marasmus when they were studied it was found that all the patients recovered from fossil fuel protein deficiency and none of them got cirrhosis they were very doubtful why indian brahmin children is getting they are getting then finally the observation milk is taken in copper vessels so brahmins were the ones who could afford corporations meat was boiled and children had fed that milk so it had excess of copper so indian challenge finally found out to be autoimmune cirrhosis due to excess copper just like wilson's disease so that was interesting fact historical fact okay but the rest that i mentioned okay in current context okay alcoholism alcoholism commonly cause of chronic liver disease okay in fact in developed worlds like in america okay is alcoholism only okay not hepatitis b or c like in asia the chronic alcoholism is positive i'm sorry i beg your pardon the communist cause worldwide in us develop developed countries is not alcohol but obesity okay so that so the interest in shifting to non-alcoholic fatty liver disease okay being obese is a major reason okay so it does not come up so much especially in india in our country but it is coming up okay so how to manage that and how to detect it right so these are all etiologies of cirrhosis of liver now if any of the risk factors are there then only you suspect okay otherwise because manifest cirrhosis okay clinically manifests and then one can see okay you can diagnose it so there should be ways of picking your feet up early so picking up cirrhosis early would be interesting in the sense that something can be done to reverse the process or stall the process okay it doesn't progress right so detection is important but that for that there has to be suspicion so most chronic alcoholics or obese patients should undergo hepatic function test okay the hepatic enzymes are raised so that gives an indication that they may be heading towards chronicity okay an investigation for cirrhosis is with uh good sonologists can pick up by an ultrasound okay the changes that are occurring in the liver the nodularity seeing the nodularity of the liver these days people people have heavily bank on okay what is called as fibroscan the fibrous content of the liver increases okay so fibroscan is being used okay but once it is being suspected heavily okay uh biopsy hepatic biopsy okay you can confront the diagnosis but this is something which in where you're doing a procedure okay so it is an invasive procedure biopsy so best avoiding okay so with suspicion and investigation of hepatic function plus a scan one should try to diagnose the cirrhosis now clinically how it would manifest so as i told you in the mind okay you should have the cirrhosis of liver will have two aspects one is hepatic dysfunction and the other is total hypertension so these signs have to be looked for okay so that is there in the book okay all of us have encountered it signs of hepatic dysfunction okay so one major one is endocrine dysfunction liver is the organ which metabolizes the hormones right so in males the estrogen is not metabolized sufficiently therefore estrogenic manifestations okay that is the most common early feature okay like alopecia okay or gynecomastia flushing like palmer usual flushing over the body okay so these occur because of estrogenic effect at the same time there is increased production of nitric oxide in patients of cirrhosis therefore these biased dilatory features have parameters okay and flushing with the skin you shake hands with this erotic it is quite warm shaken okay because palms are flushed you can increase blood flow right then there is spider and humans spider nevi what is called okay dilated arterioles okay with surrounding dilated capillaries looking like spider especially in the front of the chest what is called necklace area yeah and the forearm so these are okay usual clinical features to be picked up patients some of them like chronic alcoholics will have features of chronic alcoholism like endocrine organ glandular tissue inflammation steroiditis increased size of the parotid gland or testicular atrophy okay this so these features would occur in females if surprisingly instead of alopecia they will get hazard okay you see beards sprouting okay that is because the testosterone is not getting them metabolized okay the estrogen cannot make its effect the testosterone excess that begins to manifest so in females you'll get breast atrophy menstrual amenorrhoea menstrual irregularities the histidism this would occur in females then you would have signs of total hypertension so easy so signs of portal hypertension actually are due to opening up of the photosystemic anastomosis because the bottle pressure has risen reason for total pressure to rise you can understand total vein opens into the liver blood cannot flow across the liver okay easily because of the fire okay so it is causing obstruction to blood flow across the liver at the same time there is vasodilation of this planting arteries because of the nitric oxide so increased blood flow into the gutter will decrease exit so there is intestinal pooling of blood all serotics okay will have excess blood in the splenic vessels congestive mesenteric vessels why because of arterial dilatation decreased venous outflow this contributes to blood pooling in the gutter it's called splank because of the splendid cooling of blood the intravascular volume decreases so that i we discussed in um ascites so there is decreased blood volume leads to the complications i'll come to them right so cirrhosis will have loaded intestine okay and because the blood cannot pass through the portal vein across the liver therefore this increased pressure in the portal vein causes the photosystemic anastomosis to open up plus congestion of the organs which is drained by the fluid the most remarkably the signs of portal hyphenation the most consistent sign is phenomenal because the spleen would enlarge they become palpable they are difficult to palpate because of that then it is increased in size one should look for splenomegaly in all serious the early signs with investigation and endoscopic examination the second way to diagnose portal hypertension is to do an endoscopy and see the distended esophageal varices at the lower end of the esophagus that's the other way to pick it up okay very obvious sign much but much opening of the photosystemic anastomosis around the amplicus commonly called caput head medusa of the medusa so medusa is supposed to be wearing a crown of snakes therefore it would look like okay that around the amplicus there are snakes there are distended veins around the implants that's captured medicine okay increased incidence of hemorrhoids that is the other place where there is an astonishes so by this one can pick up total hypertension okay splenomegaly verizon's capute medicine yeah right so these are signs of hepatic dysfunction and total hypertension but one most significant sign of cirrhosis is ascites which is a combination of both hepatic dysfunction as well as total hypertension right so because so both are there therefore site is in early future of cirrhosis yeah so that's it now this is how clinically you can suspect if you are suspecting the investigations okay you know what investigations have to be done okay imaging of the liver okay the gold standard is liver biopsy but may not be necessary by scanning without intervening non-invasive investigation can pick up cirrhosis why it is insignificant to pick up cirrhosis early is to intervene early so that the process can be stopped if not reversed right so this is it i'll tell you the how you one should attend attempt to manage cirrhosis and then we can talk a little bit about the complications of cirrhosis of liver the diagnosing as a tool through the investigations and to major treatment is prevention of progression of the disease in cirrhosis if if the question is how to manage okay so management consists of arresting the progress of the disease and number two is management of the complications therefore how to prevent progression of cirrhosis is to tackle the etiology okay as alcoholism is the most significant one okay therefore abstinence from alcohol would be the first step okay if it is we are suspecting an alcoholic cirrhosis but is easier said than done okay to abstain from alcohol foreign is almost impossible not impossible but very difficult okay it will require too much of self-confidence okay and application plus therefore it also has to be supported so there is some ways of supporting okay somebody to give up alcohol okay so actually there are experts for this only who will handle how to okay clean off a person from alcohol okay not easy thing okay people make use of drugs drag like at one time uh ant abuse was used okay and abused so that would cause increase in it actually contributes okay on the liver is because the aldehyde formation so the breakdown of aldehyde is reduced therefore it accumulates in the blood right but nowadays i think it's not used right so not you take one drink and it gives a very bad feeling okay so it discourages person from taking alcohol in the sense it causes the ill effects okay that bad feeling of having taken alpha so what is used now is something called a calcium okay so these are these work on the neurotransmitters in the brain right so a comprosate calcium that is okay commonly used in at least in the developed places okay where there is a group supportive group alcoholic anonymous though there okay they work with these agencies okay so a composite would work on the neurotransmitters in the brain and decrease the urge to take alcohol like it is you some similar substance is used for nicotine okay so this is what is being tried okay what else once patient is getting these stages of alcoholic has also got it so this is in to help patient to give up alcohol but if alcoholic if there is an alcoholic and alcoholic liver disease begins to setting the earlier sign is fatty infiltration but the liver will enlarge and become firm okay so in an alcoholic if the liver is enlarged and firm so the fatty is in that stage of fatty infiltration the next day would be a chronic inflammation so that's alcoholic hepatitis if pick up patient here okay this is quite common patient with having features of early cirrhosis with hepatic inflammation okay alcoholic hepatitis so here okay intervention is significant to prevent further damage okay and there is something called so you develop a mood for this how to pick up patients who can benefit the discriminant factor in alcoholics okay so a discriminant factor of every admitted patient of alcoholics okay hepatitis means alcoholic liver disease okay should be assessed on this model okay so a discriminant factor is calculated it is to do with the rise in the serum buildup in the formula is the serum bilirubin plus the difference in the prothrombin time of the patient okay from that of the control okay so serum will ruben plus the difference of prothrombin time as compared to that of a normal person which is called a control and multiplied by 4.6 okay so if the discriminant factor is 32 or more okay so they will benefit by intervention of an anti-inflammatory drug here okay so what is this the drug of choice is corticosteroid so alcoholics liver disease okay this is the spectrum you pick up whether it is fatty infiltration stage or hepatitis hepatitis only that will progress into cirrhosis so you can intervene here and give steroid and prevent for the fibrosis but all these patients have to ultimately stop alcohol otherwise it is not of use and it is all trials have shown that one month survival is improved with the use of steroids and so that's it corticosteroid use in chronic hepatitis due to alcoholism so i think even is used right even pentoxiphylline can be used instead of steroid so steroid is the drug of choice now this the inflammation is mediated through okay the mediators of inflammation tumor necrosis factor being the major one so drugs which inhibit tnf alpha okay when toxifying overall okay that is used so if you are you have difficulty using steroid because of its side effect this drug comes with its own side effect okay beyond six weeks you are using all of them will develop side effects of the steroid the dose in which it is to be used so the corticosteroid oral prednisone has to be used in anti-inflammatory dose because it's the point it was so after between four to six weeks it will start causing its side effects therefore pentoxophiline can be used okay so pentax falling is a human necrosis factor inhibitor okay an oral pentoxophiline this also has is being tried okay but the findings with the outcome not as encouraging as with corticosteroid okay now there are other tnf alpha inhibitors like pentoxide filing dr so okay all these okay whatever is there in the armamentarium as a as the understanding improves okay the treatment is being added observed and studied so apart from oral dnf alpha inhibitor which is pentoxide you're telling so there are parental tnf alpha inhibitors okay in the monoclonal antibody infliximab okay and it under sept and beta intercept is a new drug which is all these are being tried but still benefit outcome is not shown as yet as with corticosteroid so at the point of time corticosteroid okay if you cannot use corticosteroid oral pentoxide you are right in that okay so this is being used so management of alcoholic cirrhosis is to be like this okay beyond this there is no management okay so a comprosite calcium okay this is to [Music] reduce the urge for alcohol and use of okay these drugs to reduce the inflammation okay these are the only treatment okay finally there is no treatment for there is has to be an hepatic transplantation okay so that's it so these at the moment these are the things that needs understanding okay should be more commonly used the use of discriminant factor would be a calculation absolutely essential okay and then that because that is the only modality of treatment that is there okay now for other treatments okay like if it is post viral infection okay post infective cirrhosis so you have to treat with antiviral drugs okay lamivudine adiphobia [Music] a lot of okay all these this would we will do this okay we do this session on anti-how to manage viral okay hepatic viruses with quite interesting okay how to predict which viral infection which viral hepatitis will progress to cirrhosis okay so interesting so therefore viral if it is viral hepatitis okay if the patient is in state of hepatitis they are likely to progress to cirrhosis so before cirrhosis sets in they all should be treated with antivirals okay so like um metabolic disorders as well hemochromatosis or wilson's disease so use of generating agents there okay so that's it so the underlying cause of cirrhosis has to be okay treated and then only progression can be stopped right many other drugs are used okay some fibrosis reversal drugs like calcium so they are all in state of okay trials there aren't still evidences that these drugs show benefit but then in due course of time okay in this platform only i hope you can have a discussion okay as things progress so these are when sometimes people think what to research on those who are in academics and in hospitals cirrhosis of liver is one such topic yeah wonderful to have okay study on means to prevent okay and whether fibrosis can be reversed and the one characteristic of liver of regeneration can be used okay to correct the condition so this is okay this is on the treatment modality that is available so now lastly let's focus on what complications can occur you should expect presently like in india we generally focus on management of the complication to prolong survival okay so that is it that is being done okay in america now there is a liver transplant registry okay so all those with chronic liver disease they are enrolled in that and they are waiting as the turn comes okay okay and depending on your requirement okay you can jump the gun means jump the queue so that is decided by the registry okay so that meticulous registry is maintained it is yet to come into india okay so hepatic transplant of course this is the way that okay at the moment it looks like by doing a hepatic transplant only there is a definite management for cirrhosis otherwise it's just alleviation of features and prevention of complications so what complications to expect okay and that which can be managed so one of them we did last time was ascitus okay so that okay that is that story is done okay so ascites must be managed right now other complications okay what kills the patient okay adds to the mortality his varicell bleed the the rises okay the rupture okay once each episode of varisil bleed has about 30 percent mortality so 10 patients getting very silly bleed three would succumb okay in the next episode of bleed another thirty percent good succumb okay so the percentage is quite high so all cirrhotics okay when it is picked up must undergo endoscopic examination and the varieties have to be picked up and viruses have to be either closed endoscopically sclerotherapy or banding bending is preferred now okay and medical management given to reduce the total pressure so that the episode is less okay all these we talked last time how to reduce total pressure okay so that has to be done now the next one which has mortality is hepatic encephalopathy okay patients with cirrhosis of liver tend to develop brain cerebral edema that is because of the photosystemic shunting mainly so photosystemic shunting and hepatic dysfunction so again total hypertension and hepatic dysfunction okay together they would lead to encephalopathy blood from the intestine must go into the systemic circulation through the liver where it is adequately dealt with because of photosystemic anastomosis much of the blood is getting shunted directly into the systemic circulation okay and those that are passing through the liver are not getting metabolized properly because of the decrease in the hepatic mass so therefore both add to encephalopathy okay so the factors which arise in the gut okay they get shunted into the systemic circulation like ammonia mercaptans okay so if they go into the brain they begin to form one false neurotransmitters okay so for the the presence of false neurotransmitters okay causes cerebral dysfunction plus they it adds to the cerebral edema so all hepatic encephalopathies would have false neurotransmitters in the brain and edema so once it is suspected the patient is developing encephalopathy okay mainly there are precipitating factors for this like excess protein in the gut okay the excess protein in the gut is acted upon by the bacteria okay and ammonia is released so increased ammonia and that is getting shunted in the systemic circulation okay so that has to be treated so we i promise that we'll have a session on management of the complications okay like encephalopathy it is quite interesting to know a little bit i'm telling you we can discuss you can ask also okay so once the patient is how to pick it up early are by the signs that this orientation the patient of cirrhosis is getting disoriented the first thought should be that patient is developing encephalopathy his sleep pattern would get altered okay most of time daytime when you get to see the patient patient would be sleeping and in the night when you're not there patient is remains awake so this alteration in the sleep pattern removes the early one right then on examination if the encephalopathy sets in the patient will develop flapping tremors you will be asked to extend the elbow okay patient flaps okay so this is this is postural apraxia difficulty in because the brain is not functioning so a different posture is difficult to maintain okay this extension of the wrist on an extended elbow is a difficult posture to maintain therefore patient is unable to maintain this posture so there is a lapse in the posture which patient tries to control because the patient should be conscious to be able to demonstrate the sign okay so correction in the lapse posture looks like his depression is flapping okay so flapping tremor early sign or feet of hepatic is standing next to a patient you can smell encephalopathy these are mercations in the brain in the breath which are coming into the systemic circulation being organic volatile compound they're released in the breath so this fetal hepatics would occur okay and then abnormality of meditation the mental function deteriorates yeah the patient will have like i told you postural apraxia difficult to maintain posture so similarly they will have constructional apraxia inability to form simple figures they won't be able to draw circles so these are bedside tests how you decide okay in laboratory people do ammonia level but in u.s and all the people don't bank with on the ammonia level because the level of encephalopathy does not match the hyperammonium okay but then yes ammonia will be definitely raised in all encephalopathies many people do eeg to demonstrate cerebral dysfunction means the presence of false neurotransmitters so to cut it short okay as i said we will have it on some other day about all these complications so if you your pet against a floppy man develop okay and then it has to be taken care of the drug of choice is like to lose okay so again later how lactose acts yeah and all those okay so there is still bleed where you have to do reduction of total pressure and glue physical closure of the viruses encephalopathy okay where if once it sets in the patient has to be given like to lose patient can adjust his own goals like to lose and gut sterilizers like antibiotics earlier time with metal disorder and neomycin was used now rifaximin is used and non-observable antibiotic so these are used so two major things that you have complications that you have to suspect always be on the lookout in your serious this varicel bleed must be tackled you always suspect that patient is going to get it and hepatic encephalopathy and on the management of cirrhosis is prevention of complications so you have to handle this and the third complication which also should be suspected high chances of getting it is hepato renal syndrome renal failure as a cause of cirrhosis but all these cirrhotics should have some impressive ascites to cause the better renal syndrome when we are discussing the scientists last time okay we talked about that the intravascular volume is low okay the low intravascular volume sets up the running and utensil and the strong mechanism okay so this angiotensin two acts on the efferent arteriole on the kidney okay so these people would develop tubular necrosis okay and that usually would lead to renal dysfunction so serotonins are very prone to it because of the low intravascular volume sir this has to be kept in mind then when you're handling cirrhotics you should not deplete the intravascular volume all cirrhotics okay we would have a scientist an impressive edema in the legs so the first response is to reduce these and people tend to use potent diuretics which actually is contraindicated in the cirrhotic the diuretic of choice for ascites and the edema is not flucemide because through semi potent diuretics they will deplete the intravascular volume which already is low in acidotic okay so that we discussed in the management of societies that we use paranormal electron this is hardly a diuretic is aldosterone antagonist okay so therefore care in all cirrhotics to be taken is not to deplete the intravascular volume so they should not be given potent diuretics step number one number two seeing a huge ascites in a cirrhotic the tendency to drain again parasynthesis is contraindicated if you do just like that in ascerotic because it depletes you remove the acidic fluid the sciatic fluid the peritoneal space is in equilibrium with the intravascular compartment so fluid will shift rapidly from the intravascular compartment in the peritoneal cavity so you need not drain the static fluid right unless you are raising the intravascular osmotic pressure so use of albumin okay is absolutely essential and in the those which is been prescribed prescribed means out of observation it is known at what level the intravascular osmotic pressure is to be maintained with the albumin so how much albumin to be used for the amount of fluid being drained if this is matched then only one should attempt to decrease the i mean remove the acidic fluid by parasynthesis okay so therapeutic parasymptosis should always be accompanied by intra vascular intravenous albumin replacement in the prescribed dose okay for each liter eight to ten gram of albumin has to be given so this has to be prevented if at all any para synthesis being done is just to relieve the respiratory dysfunction or distress which is which is the large volume of ascites is causing okay not beyond one liter okay because we are going to precipitate hepatograms syndrome by depleting the endovascular volume so take care of the flucimide that people tend to use in cirrhotics because of the edema and parasynthesis okay all these these two okay frustrating is this kind of potent diuretics have multiple problems in ascerotic like they also deplete the potassium okay so if you deplete the potassium hypokine because of fructomide it will induce encephalopathy okay it will cause hypokalemic alkalosis okay so any alkalosis and hypokalemia is likely to induce encephalopathy okay so flucimide one has to be very careful actually not to be used in fact bird is contraindicated right so this is the third complication the rest of the complications are difficult to manage but then in the next episode they are subsequent okay we'll use we'll do complications of cirrhosis in their details yeah if it occurs you are all of those all physicians okay who are managing cirrhosis or scientists are likely to encounter their complications the next complication is hepatocellular carcinoma okay so not preventable patient gets chronic liver disease okay the progress to malignancy is a natural fallout of that okay so you always have to be on the lookout the future of malignant change okay is that a pseudotic liver will become palpable because serotonin levels are not palpable because by the time they manifest they are all shrunken so serotonin liver getting palpable one first thing you should suspect is whether hepatocellular carcinomas or sudden increase in level of ascites so these are the two features okay so hepatocellular carcinomas right many patients get what is called as hepatopulmonary syndrome and another interesting thing to know is just like hepato renal so because of the vasodilatory effect that occurs in cirrhosis because of the estrogen and the nitric oxide the pulmonary artery venous communications they open up okay and there is shunting of pulmonary artery blood straight into the pulmonary vein by passing the lung right so pulmonary arterial blood is venous as a deoxygenated blood okay that gets shunted into the pulmonary vein which contains oxygenated okay so another feature is that patient may develop ultimately cyanosis okay it is mainly postural in the sitting up position okay the shunts open up maximally so the battery culinary syndrome this symptoms features will manifest in the sitting position so it causes begins to cause breathlessness okay because of hypoxia shunting of blood so patient tends to lie down is the reverse of cardiac breathlessness here breathlessness occurs in the sitting position and relieved in lying down position okay so these are complications one should suspect in a serious and they have to be taken care of okay i think we stop at this again there is you can take this over next we will ask the organizers to have for you the complications because all the complications in detail what is interesting take which you suspect in alcoholics in the present circumstances that nash is what fatty liver cantilever is actually an entity okay and its management is interesting just like diabetes this is occurring those who have insulin resistance metabolic syndrome one manifestation of the metabolic syndrome in coming years would be one fatty liver and ultimately cirrhosis dysfunction and cirrhosis okay so all this next time right right okay thank you so much it was a wonderful session so uh yeah we had a very enlightening and very informative session on citosis it's such a vast topic that it cannot be everything cannot be discussed in just one meeting itself so uh we'll just take a few questions so uh yeah so uh first question liver cirrhosis with pregnancy how is it managed there's not nothing new [Music] getting pregnant [Music] so during pregnancy the early features of primary biliary cirrhosis appear many people think this is called status of pregnancy lady during pregnancy is developing this kind of static feature especially is marked by through rightist okay reaching all over the body okay an increase in alkaline phosphatase and bilirubin level okay through right is ma preceding right is preceding development of jaundice so this likely to be primary biliary cirrhosis or cholestasis of pregnancy okay to develop cirrhosis is very unlikely during that period so yes will develop in the 50s but it will give its indication during pregnancy in ladies it is a disease of women [Music] or acute fatty liver of pregnancy or health i think these are the three most common things associated with pregnancy and liver they are not serotonin that's true then when to use steroids in alcoholic liver disease just i think that's already answered and covered so i'm going to tell that again somebody else okay so i think it's based on discrimination factor calculate discriminant factor with more than 32 you three right and then stewards of the transactions yes uh so yeah do prophylactic antibiotics like extended release quinolones like non-phloxacin uh should it be given uh to prevent spontaneous bacterial peritonitis in hypoalbuminemia so alpha hypothyroidism this we discussed last time when we talked on a scientist the spontaneous bacterial peritonitis is a complication of transitive ascites which occurs in cirrhosis if a patient has developed spontaneous bacterial paragonitis okay once they have developed and successfully managed all of them should be put on prophylactic antibody using human alone you know the drug so the question is correct once patient develops the spontaneous bacterial parathynitis it has been managed so all such patients should be put on prophylaxis then uh when to start propranolol lactulose refractive in when and what dose and for how long to use a natural course of cirrhosis so propanol is used for primary prophylaxis as well as secondary prophylaxis in patients with blood so in order to prevent okay prevent viruses bleed in serotonin okay so that's why i said the workup of the cirrhotic we are suspecting is always an endoscopic examination and detection of the rises if they are the rises are present all of them must be given prophylaxis and the easiest of the prophylaxis okay the question is good easy the prophylaxis and that must be followed non-invasive is to give non-selective beaters okay but the dose is significant okay how you what is the dose at which it should be given even if not such a degree that it does not require sclerotherapy or binding then also propanol should be given so beta blocker non-selected those given is that you should have manifestation of visa okay the best parameter to know this is to take care of or to take into account so when propanol is used okay as a prophylaxis it should be used in a dose that causes 25 percent reduction in the policy say somebody has got 80 per minute pulse rate okay so 25 percent so you bring it down to 60 100 bring it down to it like that 25 percent reduction in pulse rate that is [Music] it is important to have bacteria in the world right so once encephalopathy is occurred you are suspecting encephalopathy then only got sterilization at any point and once gut sterilization is done okay it need not be continued okay therefore the faximin it is format industry [Music] okay so it doesn't disturb the gut bacteria okay if at all somebody has developed encephalopathy you want to use it for long term okay so only computing active so there's one common question which has been asked me so i think that's because uh majority of the clinicians usually see it that whenever a patient comes they get a scan done all the scan reports will show fatty liver so when to treat but not to treat and yeah will have fatty infiltration fatty liver okay so when to treat what so therefore the markers of hepatic dysfunction that is very important okay so we will have a session on what is what are the markers okay okay we use enzymes hepatic enzymes as a marker okay so any increase in the markers okay that is significant especially the asd rise and if the emphatic this option is hitting it that means fat accumulation is causing there are markers for that okay so that is important so it is requested of the organizers to have a whole session on fatty loads but all fatty livers okay the easiest of the investigation okay to do significant is sjot they fall rise if there is a three-fold rise okay then only okay it needs to be intervened what is fantastic is what is the intervention okay all that okay the fatty influence what can you do so modalities for fatty infiltration surely next time but then yes all foreign infiltrates every any obese person will have it when it is significant at the moment when the hepatic enzymes rise only then like in alcoholic hepatitis when alcohol is causing a injury so you make use of enzyme okay and as as you derive more than as gpt twice same another condition so that rise in the enzymes at the moment you take it like that so i think uh that's it's a majority of the questions are covered which are related to it and rest of the questions they are comprise a different section all together for different sub topics so i think we can next time we'll have complications or encephalopathy or hepatorenal syndrome okay so what is encouraged to panic and depending on what facility is available you give a fight to it okay you can do that if you know how to do it so anybody it can be learned how to manage this okay so thank you so much for joining with us it was great time to have you here with us yeah thanks a lot sir thank you dr jacob for wonderfully motivating it thanks a lot and you have given a lot of many topics for future sessions we'll definitely have those yes we shall thanks a lot so again yes thank you so much you
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Cirrhosis is a consequence of chronic liver inflammation characterized by diffuse hepatic fibrosis and regenerative nodules.Progressive portal hypertension,systemic inflammation,and liver failure drive disease outcomes. Dr. Ravindra Nath Sahay, a prominent Physician and Professor of Internal Medicine (Retired), joins us LIVE on Medflix as we comprehend the disease burden, pathophysiology, and recommendations for the diagnosis and management of cirrhosis and its complications.
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