Cirrhosis of Liver Life Expectancy

Liver cirrhosis

Cirrhosis is a progressive disease, meaning it gets worse over time. Once you have cirrhosis, there’s no way to reverse it. Instead, treatment focuses on slowing down its progression.

Depending on how severe it is, cirrhosis can have an effect on life expectancy. If you have cirrhosis, there are several tools your doctor can use to give you a better understanding of your outlook.

The life expectancy for advanced cirrhosis is 6 months to 2 years depending on complications of cirrhosis, and if no donor is available for liver transplantation then the life expectancy for people with cirrhosis and acholic hepatitis can be as high as 50%.

During stage 1, cirrhosis is so mild it’s often difficult for physicians to detect. The most common symptom is fatigue. The cirrhosis is still reversible during this stage, but not enough liver tissue has been damaged to produce obvious symptoms of disease. Patients with stage 1 cirrhosis have a 99% 1-year survival rate.

During stage 2, scar tissue increasingly builds up within the liver, replacing liver cells. Portal hypertension appears in the liver, which is increased blood pressure in that particular region of the body in this case it makes cirrhosis easier to diagnose. At this stage, partial reversal of cirrhosis is still possible. The one-year survival rate for patients in stage 2 is 98%.

During stage 3, fluid accumulates in the abdominal cavity. Clinical symptoms become obvious, which include weight loss, yellowing skin, fatigue, and confusion. Cirrhosis has become irreversible. Diagnosed at stage 3, the 1-year survival rate is 80%. It’s during stage 3 that a liver transplant may be recommended. There’s always a risk a person’s body will reject the transplant, but if accepted, 80% of transplant patients survive more than 5 years past their operation.

During stage 4, an immense amount of scar tissue has built up. The structure of the scar tissue has created a risk of rupture within the liver. That can cause internal bleeding and become immediately life-threatening. With respect to stage 4 cirrhosis of the liver life expectancy, roughly 43% of patients survive past 1 year.

Table of Contents

How is life expectancy determined in cirrhosis of liver?

Fibro test

FibroTest, known as FibroSure in the US, is a biomarker test that uses the results of six blood serum tests to generate a score that is correlated with the degree of liver damage in people with a variety of liver diseases.

Alpha-2-macroglobin, Haptoglobin,Apolipoprotein A1, Gamma-glutamyl transpeptidase(GGT), Total bilirubin and Alanine transaminase(ALT).

ALT is used in a second assessment called ActiTest that is part of FibroTest.

FibroTest ScoreStageInterpretation
0.00-0.21*F0No fibrosis
0.21-0.27*F0-F1No fibrosis
0.27-0.31*F1Minimal fibrosis
0.31-0.48*F1-F2Minimal fibrosis
0.48-0.58*F2Moderate fibrosis
0.58-0.72*F3Advanced fibrosis
0.72-0.74*F3-F4Advanced fibrosis
0.74-1.00F4Severe fibrosis (Cirrhosis)
ActiTest ScoreGradeInterpretation
0.00-0.17*A0No activity
0.17-0.29*A0-A1No activity
0.29-0.36*A1Minimal activity
0.36-0.52*A1-A2Minimal activity
0.52-0.60*A2Significant activity
0.60-0.62*A2-A3Significant activity
0.62-0.100A3Severe activity

CHILD PUGH SCORE

The Child-Pugh score is a system for assessing the prognosis — including the required strength of treatment and necessity of liver transplant — of chronic liver disease, primarily cirhosis. Smililarly it provides a forecast of the increasing severity of your liver disease and your life expectancy.

It’s also referred to as the Child-Pugh classification, the Child-Turcotte-Pugh (CTP) calculator, and the Child Criteria.

Following are the five clinical measures:

  • total bilirubin: yellow compound in bile from hemoglobin breakdown
  • serum albumin: blood protein produced in the liver
  • prothrombin time, prolongation(s) or INR: time for blood to clot
  • ascites: fluid in peritoneal cavity
  • hepatic encephalopathy: brain disorder from liver disease

Further,the interpretation of the clinical measures is as follows:

Class A

  • 5 to 6 points
  • least severe liver disease
  • one- to five-year survival rate: 95%

Class B

  • 7 to 9 points
  • moderately severe liver disease
  • one- to five-year survival rate: 75%

Class C

  • 10 to 15 points
  • most severe liver disease
  • one- to five-year survival rate: 50%

MELD SCORE

The Model for End-Stage Liver Disease or MELD is a scoring system for assessing the severity of chronic liver disease and determining life expectancy in liver cirhosis.

MELD uses the patient’s values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival.

It ranges from 6 to 40, based on lab tests.

MELD uses the patient’s values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. It is calculated according to the following formula:

  • MELD = 3.78×ln[serum bilirubin (mg/dL)] + 11.2×ln[INR] + 9.57×ln[serum creatinine (mg/dL)] + 6.43
  • MELD scores are reported as whole numbers – the equation result is rounded

interpreting the MELD Score in hospitalized patients, the 3 month mortality was :

  • 40 or more – 71.3 % mortality
  • 30-39 – 52.6% mortality
  • 20-29 -19.6% mortality
  • 10-19 – 6.0% mortality
  • <9 – 1.9 % mortality

Understanding  Cirrhosis

Liver cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver.

It includes triad of pathlogical changes( i.e; degeneration of hepatocytes ,  regenerative (nodular)hyperplasia of remaining or surviving hepatocytes and fibrosis.)

Causes

Following are some of the causes of liver cirhosis which also affect life expectancy of people having cirrhosis:

Alcohol

The relative risk of cirrhosis rises significantly for alcohol intake above 60 g/day for men and 20 g/day for women over a decade.

Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates.                         

The liver is also responsible for cleaning our blood, producing bile for digestion and storing glycogen for energy.

Chronic alcohol abuse causes destruction of liver cells, which results in scarring of the liver (cirrhosis), alcoholic hepatitis and cellular mutation that may lead to liver cancer.

Viral hepatitis B and C

Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection.

Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis.

Autoimmune hepatitis

This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis.

Nonalcoholic steato hepatitis (NASH)

In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications.

This disorder is similar to that of alcoholic liver disease but patient does not have an alcohol history

Blocked bile ducts

Bile ducts are small tubes that carry bile (a fluid that aids digestion) from your liver to your small intestine.

If these ducts get blocked because of disease or injury, the bile backs up into the liver and can cause cirrhosis.

Cystic fibrosis

Cystic fibrosis is a hereditary disease that affects the lungs and digestive system. The body produces thick and sticky mucus that can clog the lungs and obstruct the pancreas.

In patients with CF, bile produced by the liver cells becomes stickier than normal and begins to block the small bile ducts. This causes damage and scarring to the surrounding liver tissue .

Genetic causes (Wilson’s disease, and alpha1 anti-trypsin deficiency)

Wilson Disease is an inherited condition that causes the body to retain excess copper. The liver of a person who has Wilson Disease does not release copper into bile as it should. As the copper builds up in the liver, it begins to damage the organ.

Alpha-1 antitrypsin protein usually travels from liver through blood to protect lungs and other organs.

But if the proteins aren’t the right shape, they can get stuck in liver. This can cause cirrhosis, severe liver damage and scarring, and liver cancer.

Venous outflow obstruction (Budd-Chiari syndrome, veno-occlusive disease)

Veno-occlusive disease (VOD), which is also called sinusoidal obstruction syndrome (SOS), happens when the small blood vessels that lead into the liver and are inside the liver become blocked.

VOD is caused by high doses of chemotherapy and radiation therapy given before an allogeneic stem cell transplant.

Liver histology demonstrates obstruction of sinusoids in central areas with hepatocyte necrosis and hemorrhage.

Budd–Chiari syndrome is a very rare condition, affecting one in a million adults.The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement.

Cardiac causes(Chronic right-sided heart failure,Tricuspid regurgitation)

Decompensated right ventricular or biventricular heart failure causes transmission of elevated right atrial pressure to the liver via the inferior vena cava and hepatic veins.

At a cellular level, venous congestion impedes efficient drainage of sinusoidal blood flow into terminal hepatic venules.

Sinusoidal stasis results in accumulation of deoxygenated blood, parenchymal atrophy, necrosis, collagen deposition, and, ultimately, fibrosis.

Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as hepatic congestion, peripheral edema, and ascites.

Drug toxins and infection(methotrexate, alpha methyldopa, amiodarone)

Disruption of the hepatocyte

Disruption of the transport proteins

Apoptosis of hepatocytes

Mitochondrial disruption

Bile duct injury

Types

There are 4  types of cirrhosis of liver:

1.Alcoholic cirrhosis

In it the scar tissue characteristically surrounds the portal areas & is more frequently caused by chronic alcoholism .It is the most common type of  cirrhosis.

2.Postnecrotic cirrhosis

 In it there are broad bands of scar tissue. This is a result of a previous bout of acute viral hepatitis.

3.Billiary cirrhosis

 In it scarring occurs in the liver around the bile ducts.It usually occurs from chronic billiary obstruction & infection. It is much less common.

4.Cardiac cirrhosis

Associated with severe right sided long term heart failure, fairly rare.

Pathophysiology

Primary event is injury to hepatocellular elements.

Initiates inflammatory response with cytokine release which results in increase in toxic substances.

Destruction of hepatocytes, bile duct cells, vascular endothelial cells.

 Repair through cellular proliferation and regeneration.

 Finally, formation of fibrous scar.

Clinical Manifestations

  • Early symptoms are weakness and weight loss
  • Intermittent mild fever
  • Unexplained epistaxis
  • Abdominal pain
  • Firm enlarged liver
  • Splenomegaly
  • Muscle wasting
  • Ascites
  • Jaundice
  • Clubbing of nail
  • Purpura due to decreased platelet count
  • Spider vein
  • Shrinking testicles and breast growth in men(gynecomastia)
  • For women, absent or loss of periods not related to menopause

Diagnosis

  • History taking
  • Physical examination
  • Liver function tests: Serum albumin ,serum globulin, serum alkaline phosphatase , transaminases , serum bilirubin, ALT , AST,GGT , serum cholinesterase.
  • Haematological tests : to rule out anemia ,leucopenia. thrombocytopenia, prothrombin time
  • Ultrasound , MRI,CT scan: Cirrhotic liver shows nodular hepatic contour, changes in volume distribution, including an enlarged caudate lobe and left lobe lateral segment, atrophy of the right and left lobe medial segments, widening of the fissures and the porta hepatis, and regenerative nodules.
  • Liver biopsy: It is the gold standard for diagnosis that may be through a percutaneous , transjugular, laparoscopic, or fine- needle approach.
  • Ascitic fluid examination

Medical Managements to improve the cirrhosis of liver life expectancy

To increase cirrhosis of liver life expectancy medical management is mostly required. Medical treatment seeks to support liver regeneration and to treat the complications of liver failure. Following are some of the medical managements that help to increase cirrhosis of liver life expectancy:

For Ascites:

  • Use of diuretics specially potassium sparing diuretics such as spironolactone (100-200 mg/day).
  • Furosemide 20mg & spironolactone 50 mg gives rapid relief of symptoms in these cases and there is no need of potassium replacement.
  • For ascites, water restriction e. 1L/day & restriction of salt(1 gm /day) & high potency diuretic such as furosemide (40-160 mg/day).
  • Ascites may be treated by the nonsurgical placement of a shunt between the portal and systemic venous systems, which is called a transjugular intrahepatic portosystemic shunt (TIPS).

Treat the fluid volume deficit caused by the bleeding.

  • Maintain fluid and electrolyte balance.
  • Bleeding varices are treated with vasoconstrictors such as vasopressin, with temponade (direct pressure on the bleeding veins), or with emergency sclerotherapy to close the veins.
  • Vitamins and minerals are increased which promotes healing of damaged liver cells and improve patients general nutritional status.
  • Antacids or H2 antagonists are prescribed to decrease gastric distress & minimize possibility of GI bleeding.
  • Treating clotting disorders: Vitamin K supplementation helps in producing prothrombin a protein and clotting factor that is important in blood clotting which prevents low level of clotting factors.

Encepalopathy:

  • If symptoms of encephalopathy persist, oral antibiotics such as neomycin or metronidazole (Flagyl), can be added to the treatment regimen. Antibiotics work by blocking the production of the toxic compounds by the bacteria in the colon.
  • Avoid drugs (including alcohol) that cause liver damage. All patients with cirrhosis should avoid alcohol. Most patients with alcohol induced cirrhosis experience an improvement in liver function with abstinence from alcohol.Likewise patients with chronic hepatitis B and C can substantially reduce liver damage and slow the progression towards cirrhosis with abstinence from alcohol.
  • Laxatives, such as lactulose, decrease risk of constipation; their role in preventing encephalopathy is limited.
  • Lactulose, which is a liquid, traps the toxic compounds in the colon. Consequently, they cannot be absorbed into the blood stream and cause encephalopathy.

Pruritis:

  • Bile salt resins such as cholestyramine are usually the first line treatment for pruritus in cholestatic disease. Several studies have shown the efficacy of bile salt resins in symptom control of pruritus
  • Other medications that may provide relief against pruritus in addition to antihistamines (eg, diphenhydramine, hydroxyzine) and ammonium lactate 12% skin cream (Lac-Hydrin), include ursodeoxycholic acid, doxepin, and rifampin.

Treatment of Hepatitis:

  • Interferon is the drug of choice for treating several chronic forms of viral hepatitis, including hepatitis B and C.
  • Interferon alpha-2b is the form of the drug that works against chronic viral hepatitis B infection.
  • Likewise PEGylated interferon, PEGylated interferon alpha-2b (PEG-intron), interferon alpha-2b (Intron A, Rebetol), interferon alpha-2a (Roferon), and interferon aphacon-1 (Infergen) are used in hepatitis C.

Nutritional Managements to improve the cirrhosis of liver life expectancy

Nutrition is most important to keep liver helthy and well functioning so nutritional management is required to improve the cirrhosis of liver life expectancy.

  • A registered dietitian may modify the diet daily for patients with liver disease.
  • Usually these patients suffer from severe anorexia.For early or mild disease, protein is encouraged to support healing; later in liver disease, protein may be restricted.
  • For esophageal varices, soft foods are given, in addition to other restrictions.
  • Protein is restricted according to the individual’s ability to metabolize it.
  • Complete protein foods are selected to provide all the essential amino acids. Homogenized milk and eggs are offered because the fat is already emulsified, requiring less bile for digestion
  • Adequate carbohydrates are given to prevent the use of tissue protein for energy. Fluid and sodium are likely to be restricted if ascites is present.
  • Foods producing high ammonia levels may be restricted (e.g., chicken, ground beef, ham, peanut butter, potatoes, onions, , egg yolk, buttermilk ).

Surgical Managements to improve the cirrhosis of liver life expectancy

Surgical managements help to improve cirrhosis of liver life expectancy. These are some of the surgical managements of  liver cirrhosis:

  • Liver transplantation:

The indications for transplantation are fluminant hepatic failure due to any cause:

                            -end stage cirrhosis

                           -Alcoholic liver disease

                            -Wilsons disease 

  • Ligation of varices:

Esophageal varices are ligated which mainly occurs due to portal hypertension .

Nursing Managements to improve the cirrhosis of liver life expectancy

For improving life expectancy of people with cirrhosis of liver nursing management is required. Following are some of the nursing diagnosis with goals and nursing interventions:

1)  Activity intolerance related to fatigue, lethargy and malaise

Goals :patient reports decrease in fatigue and increase ability to participate in activities.

Nursing intervention:

  • Assess the level of activity intolerance and degree of fatigue, lethargy and malaise when performing routine activities of daily living.
  • Assist with activities and hygiene when fatigued.
  • Encourage the patient to take frequent rest when fatigued or in case of abdominal pain or any discomfort.
  • Provide diet high in carbohydrates with protein intake consistent with liver function.

2)  Imbalanced nutrition :less than body requirements related to abdominal distension and discomfort secondary to anorexia

Nursing intervention

  • Assess dietary intake, nutrition status through diet history and daily weight measurement and laboratory data.
  • Provide diet high in carbohydrate with protein intake consistent with liver function
  • Elevate head of bed during meals.
  • Offer smaller, more frequent meals
  • Provide attractive meals and an aesthetically pleasing setting at mealtime.

3) Impaired skin integrity related to pruritus from jaundice and edema

Goals: decrease potential for pressure ulcers

Nursing intervention

  • Assess the degree of discomfort related to pruritus and edema
  • Then note and record degree of jaundice and extent of edema
  • Keep patient’s fingernail short and smooth
  • Provide frequent skin care, avoid use of soaps and alcohol based lotions
  • Massage every 2 hours with emollient; turn every 2 hours.
  • Initiate use of alternating pressure mattress or low air loss bed.
  • Also assess skin integrity every 4-8 hours. Instruct patient and family in this activity.

4)  Excess fluid volume related to ascites and edema formation

Goal: restoration of normal fluid volume

Nursing intervention

  • Administer diuretic agent, potassium and protein supplements as prescribed.
  • Record intake and output every 1-8 hours depending on response to intervention.
  • Likewise measure and record abdominal girth and weight daily.
  • Explain rationale for sodium and fluid retention.

5)  Risk for injury related to altered clotting mechanisms secondary to altered level of consciousness

Goal : reduced risk of injury

Nursing intervention:

  • Assess the level of consciousness and cognitive levels.
  • Provide safe environment(side rails, remove obstacles)
  • Observe each stool for color , consistency and amount.
  • Be alert to symptoms of anxiety, epigastric fullness, weakness and restlessness.
  • Also observe for hemorrhagic manifestation: ecchymosis, epistaxis, petechiae and bleeding gums.

6) Ineffective breathing pattern related to ascites and restriction of thoracic excursion secondary to ascites, abdominal distention, and fluid in the thoracic cavity.

Goal: Maintain effective respiratory pattern; be free of dyspnea and cyanosis, with ABGs and vital capacity within acceptable range.

Nursing interventions:

  • Monitor respiratory rate ,depth and effort.
  • Auscultate breath sounds, noting crackles, wheezes, rhonchi.
  • Investigate level of change in consciousness.
  • Keep head of bed elevated. Position on sides.
  • Encourage frequent repositioning and deep breathing exercises and coughing exercises.
  • Monitor temperature. Note presence of chills, increased coughing, changes in color and character of sputum.
  • Monitor serial ABG ,pulse oximetry and chest x-ray.
  • Provide supplemental O2as indicated.

Complications

1.Portal hypertension

It is a persistent blood pressure elevation in the portal circulation of the abdomen.

2.Ascites

Ascites is an accumulation of serous fluid in the abdominal cavity(more than 500ml).

–   The fluid accumulates primarily because of low prodution of albumin by the failing liver.

–  An insufficient amount of protein in the capillaries causes plasma to seep into the abdominal cavity.

-The accumulated fluid causes a markely enlarged abdomen. The fluid may cause severe respiratory distress as a result of elevation of the diaphragm.

3.Clotting defects

It may develop because of impaired prothrombin and fibrinogen production in the liver.

 -Further the absence of bile salts prevents the absorption of fat soluble Vitamin-K,which is essential for some blood clotting factors.

 -Patients with chronic liver disease have a tendency to bruise easily and may progress to dissemianated intravascular coagulation or hemorrhage

4.Hepatic encephalopathy

It is caused by the accumulation of noxious substances in the circulation.

 – The failing liver is unable to make the toxic substances water soluble for excretion in the urine.

– Ammonia a by product of protein metabolism is most commonly the substance causing signs and symptoms of  HE

-Includes progressive confusion, asterexis, flapping tremors in the hands caused  by toxins at peripheral nerves,and fetor hepaticus,or foul breath caused by metabolic end products related to sulfur.

Health Teaching

  • Avoid alcohol.
  • Weigh daily and keep a weight log. If there is sudden change in weight, should inform healthcare provider.
  • Cut back on salt and also don’t add salt to your food at the table.
  • Limit canned, dried, packaged and fast foods.
  • Season foods with herbs instead of salt when you cook.
  • Take medicines exactly as directed and avoid aspirin and other blood-thinning medicines.
  • Talk with provider before taking vitamins, over-the-counter medicines, or herbal supplements. Similarly Some herbal supplements may be toxic to the liver. Pain killers called NSAIDs (nonsteroidal anti-inflammatory drugs) such as ibuprofen can harm the liver.
  • Proper skin care must be provided,

Also visit: Medication Adherence

Cirrhosis icd 10

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