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Life expectancy of cirrhosis?
My ex has hep c, ascities, cirrhosis, chronic leukemia and drinks daily. I can't imagine he has long? He also has neropathy.
You know your stuff!! I'm sorry you have this illness, may you stay well!
I have decided, due to the incredible emotional damage this person did to me, I do not feel comfortable supporting them in this. He has family and others. Ty
I have decided, due to the incredible emotional damage this person did to me, I do not feel comfortable supporting them in this. He has family and others. Ty
“Transition to a decompensated stage is marked by the development of any of the following complications: variceal haemorrhage, ascites, encephalopathy and jaundice“
Mild ascities like I have which are only noticible with ultrasound is still considered decompensated. Pronounced ascities with the patient appearing pregnant having difficulty breathing due to the retention of fluid pressing on the diaphragm or loss of appetite because of the fluid pressing on the stomach area making the patient feel full and so not hungry is a definite sign of decompensation and liver failure. A rush of having this fluid is it can suddenly become infected called SBP (spontaneous bacterial periodontitis) this can cause death from massive infection. Treatment for duretic resistant ascities is the person being drained periodically of the excess fluid or putting in a shunt bypassing the liver to reduce portal hypertension to prevent the ascities from forming.
However, having a shunt placed then increases the risk of HE (hepatic encephalopathy)
“Therapeutic paracentesis may be performed in patients who require rapid symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid are removed, saline alone is an effective plasma expander. The removal of 5 L of fluid or more is considered large-volume paracentesis.”
“Refractory ascites is defined by an inability to mobilize ascites despite maximal doses of diuretics [10] and has a significant morbidity [7]. Therapeutic options for refractory ascites include frequent paracentesis, transjugular intrahepatic portosystemic shunt (TIPS) placement, and liver transplant”
Mild ascities like I have which are only noticible with ultrasound is still considered decompensated. Pronounced ascities with the patient appearing pregnant having difficulty breathing due to the retention of fluid pressing on the diaphragm or loss of appetite because of the fluid pressing on the stomach area making the patient feel full and so not hungry is a definite sign of decompensation and liver failure. A rush of having this fluid is it can suddenly become infected called SBP (spontaneous bacterial periodontitis) this can cause death from massive infection. Treatment for duretic resistant ascities is the person being drained periodically of the excess fluid or putting in a shunt bypassing the liver to reduce portal hypertension to prevent the ascities from forming.
However, having a shunt placed then increases the risk of HE (hepatic encephalopathy)
“Therapeutic paracentesis may be performed in patients who require rapid symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid are removed, saline alone is an effective plasma expander. The removal of 5 L of fluid or more is considered large-volume paracentesis.”
“Refractory ascites is defined by an inability to mobilize ascites despite maximal doses of diuretics [10] and has a significant morbidity [7]. Therapeutic options for refractory ascites include frequent paracentesis, transjugular intrahepatic portosystemic shunt (TIPS) placement, and liver transplant”
Cirrhosis is ESLD in other words the is no higher level of liver damage above cirrhosis so cirrhosis is called end stage liver disease.
But then there is very advanced decompensated liver cirrhosis. Specifically, decompensated cirrhosis is defined by the development of jaundice, ascites, variceal hemorrhage, or hepatic encephalopathy.
The 1-year mortality is 20.2% in decompensated patients. So for those with decompensated cirrhosis the odds of dying within a year are about 20% so the odds of living a full year is about 80%
But then there is very advanced decompensated liver cirrhosis. Specifically, decompensated cirrhosis is defined by the development of jaundice, ascites, variceal hemorrhage, or hepatic encephalopathy.
The 1-year mortality is 20.2% in decompensated patients. So for those with decompensated cirrhosis the odds of dying within a year are about 20% so the odds of living a full year is about 80%
2 Comments
This is from:
Liver international journal
Prognostic indicators of survival in patients with compensated and decompensated cirrhosis
Patients with cirrhosis are classified in a compensated and a decompensated stage. Portal hypertension is responsible for most of the complications of cirrhosis that mark the transition from compensated to decompensated cirrhosis.
The natural course of cirrhosis is characterized by a compensated stage followed by a decompensated stage (1, 2). Transition to a decompensated stage is marked by the development of any of the following complications: variceal haemorrhage, ascites, encephalopathy and jaundice (1, 3). These complications result from portal hypertension and/or from liver insufficiency. The survival of both stages is markedly different with compensated patients having a median survival time of over 12 years compared to decompensated patients who survive less than 2 years (1, 3). It has also been shown that both stages have different predictors of death (1). Therefore, it was recently determined, by consensus, that compensated and decompensated cirrhosis should be considered separate disease entities (4).
Moreover, based on data from an Italian cohort of 1649 patients followed prospectively over 10 years, the 2005 Baveno consensus conference (5) and a recent published systematic review (1), two prognostic substages within compensated cirrhosis (stage 1 and 2) and decompensated cirrhosis (stages 3 and 4) have been identified. Stage 1 consists of compensated patients without varices with a low 1-year mortality of 1%. Stage 2 comprises compensated patients with varices (without variceal haemorrhage), with a low mortality of 3% per year, but significantly greater than at stage 1. Stage 3 comprises patients with ascites (with or without varices) but without variceal haemorrhage, in whom the 1-year mortality was 20%. Stage 4 was associated with the highest 1-year mortality of 57% and consists of patients presenting variceal haemorrhage (with or without ascites) (1). The Italian cohort's follow-up started 30 years ago, at a time when standards of care for variceal haemorrhage and other complications of cirrhosis were different from current standards. In a recent AASLD/EASL consensus conference, the recommendation was made to validate this substaging system of patients with cirrhosis (4).
Given that portal hypertension is one of the main factors responsible for the complications of cirrhosis, the importance of measurements of hepatic venous pressure gradient (HVPG) (an estimation of portal hypertension) at the time of diagnosis of cirrhosis in predicting mortality in cirrhosis is important and has not been sufficiently analysed, particularly in the setting of other recognized predictors of death in cirrhosis (1).
Liver international journal
Prognostic indicators of survival in patients with compensated and decompensated cirrhosis
Patients with cirrhosis are classified in a compensated and a decompensated stage. Portal hypertension is responsible for most of the complications of cirrhosis that mark the transition from compensated to decompensated cirrhosis.
The natural course of cirrhosis is characterized by a compensated stage followed by a decompensated stage (1, 2). Transition to a decompensated stage is marked by the development of any of the following complications: variceal haemorrhage, ascites, encephalopathy and jaundice (1, 3). These complications result from portal hypertension and/or from liver insufficiency. The survival of both stages is markedly different with compensated patients having a median survival time of over 12 years compared to decompensated patients who survive less than 2 years (1, 3). It has also been shown that both stages have different predictors of death (1). Therefore, it was recently determined, by consensus, that compensated and decompensated cirrhosis should be considered separate disease entities (4).
Moreover, based on data from an Italian cohort of 1649 patients followed prospectively over 10 years, the 2005 Baveno consensus conference (5) and a recent published systematic review (1), two prognostic substages within compensated cirrhosis (stage 1 and 2) and decompensated cirrhosis (stages 3 and 4) have been identified. Stage 1 consists of compensated patients without varices with a low 1-year mortality of 1%. Stage 2 comprises compensated patients with varices (without variceal haemorrhage), with a low mortality of 3% per year, but significantly greater than at stage 1. Stage 3 comprises patients with ascites (with or without varices) but without variceal haemorrhage, in whom the 1-year mortality was 20%. Stage 4 was associated with the highest 1-year mortality of 57% and consists of patients presenting variceal haemorrhage (with or without ascites) (1). The Italian cohort's follow-up started 30 years ago, at a time when standards of care for variceal haemorrhage and other complications of cirrhosis were different from current standards. In a recent AASLD/EASL consensus conference, the recommendation was made to validate this substaging system of patients with cirrhosis (4).
Given that portal hypertension is one of the main factors responsible for the complications of cirrhosis, the importance of measurements of hepatic venous pressure gradient (HVPG) (an estimation of portal hypertension) at the time of diagnosis of cirrhosis in predicting mortality in cirrhosis is important and has not been sufficiently analysed, particularly in the setting of other recognized predictors of death in cirrhosis (1).
Thank you fly. This is exactly what I was looking for. To understand where he's at and what's happening. My best to you. If ppl need information, this is the place. God bless
Until a patient is at late end stage in liver failure there really is no way to know. Once in very late endstage it might be 6 months to a year.
But, for example if he has untreated esophageal varicies the could burst and he could bleed out and be gone tomorrow. Or the ascities could become infected called SBP and he could pass away from bacterial infection of the ascitic fluid.
But, for example if he has untreated esophageal varicies the could burst and he could bleed out and be gone tomorrow. Or the ascities could become infected called SBP and he could pass away from bacterial infection of the ascitic fluid.
1 Comments
Ascities is end stage though, right? Or no...
I never heard of chronic leukemia so I googled this.
“Survival rate for chronic lymphocytic leukemia. CLL has a higher survival rate than many other cancers. The five-year survival rate is around 83 percent. This means that 83 percent of people with the condition are alive five years after diagnosis”
As far as cirrhosis it is really impossible to say. I have had cirrhosis for over 10 years. But I stopped any alcohol when I was told I had cirrhosis because I was infected with hep c for 30 years at that time. I was treated for esophageal varicies in 2012 and have some small amount of ascities.
My prognosis is greatly improved since I was cured of hep c 3 years ago with Harvoni.
People with cirrhosis even if they continue to drink can still hang on for a while. Does have advanced ascities to the point he looks pregnant? Has he been checked for esophageal varicies? Does he have any hepatic encephalopathy symptoms? Do you have any idea what is his MELD score? Patients need a MELD score of at least 15 to be on the transplant list with most being transplanted at about 30. The max MELD score is 40. However, he is not eligible to be on the transplant list because of his drinking.
The best person with insight on his prognosis would be his hepatologist.
“Survival rate for chronic lymphocytic leukemia. CLL has a higher survival rate than many other cancers. The five-year survival rate is around 83 percent. This means that 83 percent of people with the condition are alive five years after diagnosis”
As far as cirrhosis it is really impossible to say. I have had cirrhosis for over 10 years. But I stopped any alcohol when I was told I had cirrhosis because I was infected with hep c for 30 years at that time. I was treated for esophageal varicies in 2012 and have some small amount of ascities.
My prognosis is greatly improved since I was cured of hep c 3 years ago with Harvoni.
People with cirrhosis even if they continue to drink can still hang on for a while. Does have advanced ascities to the point he looks pregnant? Has he been checked for esophageal varicies? Does he have any hepatic encephalopathy symptoms? Do you have any idea what is his MELD score? Patients need a MELD score of at least 15 to be on the transplant list with most being transplanted at about 30. The max MELD score is 40. However, he is not eligible to be on the transplant list because of his drinking.
The best person with insight on his prognosis would be his hepatologist.
1 Comments
Ty, but I do not have contact. I'm glad you're well! I figured the cll, would affect the liver and he's a goner. I do know of approx 3 times, ascities was like a pregnancy. His cancer Dr said 5 years, but I don't think he's aware of the drinking. I have no other information, than for about 8 years, dark pee. Tc
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