Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, and end-stage liver disease, is the impaired liver function caused by the formation of scar tissue known as fibrosis, due to damage caused by liver disease. Damage causes tissue repair and subsequent formation of scar tissue, which over time can replace normal functioning tissue leading to the impaired liver function of cirrhosis. The disease typically develops slowly over months or years. Early symptoms may include tiredness, weakness, loss of appetite, unexplained weight loss, nausea and vomiting, and discomfort in the right upper quadrant of the abdomen. As the disease worsens, symptoms may include itchiness, swelling in the lower legs, fluid build-up in the abdomen, jaundice, bruising easily, and the development of spider-like blood vessels in the skin. The fluid build-up in the abdomen may become spontaneously infected. More serious complications include hepatic encephalopathy, bleeding from dilated veins in the esophagus, stomach or intestines, and liver cancer.
|Other names||Cirrhosis of the liver, hepatic cirrhosis|
|The abdomen of a person with cirrhosis showing massive fluid buildup and very visible veins|
|Symptoms||Tiredness, itchiness, swelling in the lower legs, jaundice, easily bruising, fluid build-up in the abdomen|
|Complications||Spontaneous bacterial peritonitis, hepatic encephalopathy, dilated veins in the esophagus, liver cancer|
|Usual onset||Over months or years|
|Causes||Alcoholic liver disease, hepatitis B, hepatitis C, non-alcoholic steatohepatitis|
|Diagnostic method||Blood tests, medical imaging, liver biopsy|
|Prevention||Vaccination (such as hepatitis B), avoiding alcohol|
|Treatment||Depends on underlying cause|
|Frequency||2.8 million (2015)|
|Deaths||1.3 million (2015)|
Cirrhosis is most commonly caused by alcoholic liver disease, non-alcoholic steatohepatitis (NASH) – (the progressive form of non-alcoholic fatty liver disease), chronic hepatitis B, and chronic hepatitis C. Heavy drinking over a number of years can cause alcoholic liver disease. NASH has a number of causes, including obesity, high blood pressure, abnormal levels of cholesterol, type 2 diabetes, and metabolic syndrome. Less common causes of cirrhosis include autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis that disrupt bile duct function, genetic disorders such as Wilson's disease and hereditary hemochromatosis, and chronic heart failure with liver congestion.
Hepatitis B vaccine can prevent hepatitis B and the development of cirrhosis, but there is no vaccination against hepatitis C. There is no specific treatment for cirrhosis but many of the underlying causes may be treated by a number of medications that may slow or prevent worsening of the condition. Avoiding alcohol is recommended in all cases. Hepatitis B and C may be treatable with antiviral medications. Autoimmune hepatitis may be treated with steroid medications. Ursodiol may be useful if the disease is due to blockage of the bile ducts. Other medications may be useful for complications such as abdominal or leg swelling, hepatic encephalopathy, and dilated esophageal veins. If cirrhosis leads to liver failure a liver transplant may be an option.
Cirrhosis affected about 2.8 million people and resulted in 1.3 million deaths in 2015. Of these deaths, alcohol caused 348,000, hepatitis C caused 326,000, and hepatitis B caused 371,000. In the United States, more men die of cirrhosis than women. The first known description of the condition is by Hippocrates in the 5th century BCE. The term cirrhosis was invented in 1819, from a Greek word for the yellowish color of a diseased liver.
Signs and symptoms
Cirrhosis can take quite a long time to develop, and symptoms may be slow to emerge. Early symptoms may include tiredness, weakness, loss of appetite, unexplained weight loss, nausea and sickness, and discomfort in the upper right abdomen. With declining liver function other signs and symptoms may develop such as cognitive impairments, confusion, memory loss, sleep disorders, and changes in personality. Further decline may result in a build-up of fluid in the lower legs and feet; severe bloating of the abdomen from a fluid build-up known as ascites; jaundice; severe itchy skin, and darkly colored urine. Some of these symptoms may be secondary to subsequent portal hypertension – increased blood pressure in the blood supply to the liver.
The following features are a direct consequence of liver cells not functioning.
- Spider angiomata or spider nevi are vascular lesions consisting of a central arteriole surrounded by many smaller vessels (hence the name "spider") and occur due to an increase in estradiol. One study found that spider angiomata occur in about one third of cases.
- Palmar erythema is a reddening of palms at the thenar and hypothenar eminences seen in about 23% of cirrhosis cases as a result of increased estrogen.
- Gynecomastia, or benign increase in breast size in men, is caused by increased estradiol and can occur in up to 2/3 of cases. This is different from increase in breast fat in overweight people. A swollen scrotum may also be evident.
- Hypogonadism, a decrease in male sex hormones may manifest as impotence, infertility, loss of sexual drive, and testicular atrophy, and can result from primary gonadal injury or suppression of hypothalamic/pituitary function. Hypogonadism is associated with cirrhosis due to alcoholism or iron overload.
- Liver size can be enlarged, normal, or shrunken in people with cirrhosis.
- Ascites, accumulation of fluid in the peritoneal cavity in the abdomen, gives rise to bulging flanks.
- Jaundice, is yellow discoloration of the skin and mucous membranes notably of the white of the eyes due to increased levels of bilirubin which may also cause the urine to be dark colored.
Liver cirrhosis increases resistance to blood flow and leads to higher pressure in the portal venous system, resulting in portal hypertension. Effects of portal hypertension include:
- An enlarged spleen is found in 35% to 50% of cases.
- Esophageal varices result from collateral portal blood flow through vessels in the stomach and esophagus (a process called portacaval anastomosis). When these blood vessels become enlarged, they are called varices and are more likely to rupture. Variceal rupture often leads to severe bleeding, which can prove fatal.
- Caput medusae are dilated paraumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be shunted through the paraumbilical veins and ultimately to the abdominal wall veins, manifesting as a pattern that may resemble the head of Medusa.
- Cruveilhier-Baumgarten bruit is a venous hum heard in the epigastric region (on examination by stethoscope) due to collateral connections forming between the portal system and the paraumbilical veins as a result of portal hypertension.
Other non-specific signs
As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.
- Bruising and bleeding resulting from decreased production of clotting factors.
- Hepatic encephalopathy (HE) – occurs when ammonia and related substances build up in the blood and affect brain function when they are not cleared from the blood by the liver. This may result in neglect of personal appearance, unresponsiveness, forgetfulness, trouble concentrating, changes in sleep habits or psychosis. One classic physical exam findings is asterixis, bilateral asynchronous flapping of outstretched, dorsiflexed hands. Fetor hepaticus is a musty breath odor resulting from increased dimethyl sulfide and is a feature of HE.
- Sensitivity to medication caused by decreased metabolism of the active compounds.
- Acute kidney injury (particularly hepatorenal syndrome).
- Cachexia associated with muscle wasting and weakness.
Cirrhosis has many possible causes, and sometimes more than one cause may be present. History taking is of real importance in trying to determine the most likely cause. Globally, 57% of cirrhosis is attributable to either hepatitis B (30%) or hepatitis C (27%). Alcohol use disorder is another major cause, accounting for about 20-40% of the cases.
- Alcoholic liver disease (ALD). Alcoholic cirrhosis develops for 10–20% of individuals who drink heavily for a decade or more. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. This injury happens through the formation of acetaldehyde from alcohol which itself is reactive, but which also leads to the accumulation of other reactive products in the liver. People with ALD may also have concurrent alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT blood levels are both elevated, but at less than 300 IU/liter, with an AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. In the United States, 40% of cirrhosis-related deaths are due to alcohol.
- Non-alcoholic fatty liver disease (NAFLD). In NAFLD, fat builds up in the liver and eventually causes scar tissue. This type of disorder appears to be associated with obesity (40% of NAFLD cases) diabetes, protein malnutrition, coronary artery disease, and treatment with steroids. Though similar in signs to alcoholic liver disease, there is no history of notable alcohol use. Blood tests, and medical imaging are used to diagnose NAFLD and NASH and sometimes a liver biopsy is needed.
- Chronic hepatitis C. Infection with the hepatitis C virus causes inflammation of the liver and a variable grade of damage to the organ. Over several decades, this inflammation and damage can lead to cirrhosis. Among patients with chronic hepatitis C, 20–30% will develop cirrhosis. Cirrhosis caused by hepatitis C and alcoholic liver disease are the most common reasons for liver transplant.
- Chronic hepatitis B. The hepatitis B virus causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B and accelerates cirrhosis in co-infection.
Less common causes
- Primary biliary cholangitis (previously known as primary biliary cirrhosis). The bile ducts become damaged by an autoimmune process, leading to secondary liver damage. Patients may be asymptomatic or have fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin and usually positive anti-mitochondrial antibodies.
- Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis.
- Autoimmune hepatitis. This disease is caused by an attack of the liver by lymphocytes, causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins.
- Hereditary hemochromatosis. Usually presents with a family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, or cardiomyopathy, all due to signs of iron overload.
- Wilson's disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy and elevated 24-hour urine copper. May also have Kayser-Fleischer rings in the cornea and altered mental status.
- Indian childhood cirrhosis is a form of neonatal cholestasis characterized by deposition of copper in the liver.
- Alpha 1-antitrypsin deficiency (A1AD). Autosomal recessive disorder of decreased levels of the enzyme alpha 1—antitrypsin.
- Cardiac cirrhosis. Due to chronic right sided heart failure, which leads to liver congestion.
- Glycogen storage disease type IV
- Cystic fibrosis
- Hepatotoxic drugs or toxins, such as acetaminophen, methotrexate, or amiodarone
The liver plays a vital role in the synthesis of proteins (for example, albumin, clotting factors and complement), detoxification, and storage (for example, of vitamin A and glycogen). In addition, it participates in the metabolism of lipids and carbohydrates.
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal tissue. This scar tissue blocks the portal flow of blood through the organ, raising the blood pressure and disturbing normal function. Research has shown the pivotal role of the stellate cell, that normally stores vitamin A, in the development of cirrhosis. Damage to the liver tissue from inflammation, leads to the activation of stellate cells, which increases fibrosis through the production of myofibroblasts, and obstructs hepatic blood flow. In addition, stellate cells secrete TGF beta 1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it secretes TIMP1 and TIMP2, naturally occurring inhibitors of matrix metalloproteinases, which prevents them from breaking down the fibrotic material in the extracellular matrix.
As this cascade of processes continues, fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, and enlarged resulting in its retention of platelets, which are needed for normal blood clotting. Portal hypertension is responsible for the most severe complications of cirrhosis.
The gold standard for diagnosis of cirrhosis is a liver biopsy. This is usually carried out as a fine-needle approach, through the skin (percutaneous), or internal jugular vein (transjugular). Endoscopic ultrasound (EUS)-guided liver biopsy, using the percutaneous or transjugular route has become a good alternative to use. EUS can target liver areas that are widely separated, and can deliver bi-lobar biopsies. A biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk of complications from liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.
|Score||Platelet count x109||ALT/AST ratio||INR|
The best predictors of cirrhosis are ascites, platelet count < 160,000/mm3, spider angiomata, and a Bonacini cirrhosis discriminant score greater than 7 (as the sum of scores for platelet count, ALT/AST ratio and INR as per table).
The following findings are typical in cirrhosis:
- Thrombocytopenia – typically multifactorial. Due to alcoholic marrow suppression, sepsis, lack of folate, platelet sequestering in the spleen as well as decreased thrombopoietin. However, this rarely results in a platelet count < 50 000/mL.
- Aminotransferases – AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferase levels do not preclude cirrhosis.
- Alkaline phosphatase – slightly elevated but less than 2–3 times the upper limit of normal.
- Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
- Bilirubin – levels normal when compensated but may elevate as cirrhosis progresses.
- Albumin – levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
- Prothrombin time – increases, since the liver synthesizes clotting factors.
- Globulins – increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
- Serum sodium – hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
- Leukopenia and neutropenia – due to splenomegaly with splenic margination.
- Coagulation defects – the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
- Glucagon – increased in cirrhosis
- Vasoactive intestinal peptide – increased as blood is shunted in the intestinal system because of portal hypertension
- Vasodilators – increased (such as nitric oxide and carbon monoxide) reducing afterload with compensatory increase in cardiac output, mixed venous oxygen saturation
- Renin – increased (as well as sodium retention in kidneys) secondary to fall in systemic vascular resistance
Other laboratory studies performed in newly diagnosed cirrhosis may include:
- Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle, anti-mitochondria, anti-LKM)
- Ferritin and transferrin saturation: markers of iron overload as in hemochromatosis, copper and ceruloplasmin: markers of copper overload as in Wilson's disease
- Immunoglobulin levels (IgG, IgM, IgA) – these immunoglobins are non-specific but may help in distinguishing various causes
- Cholesterol and glucose
- Alpha 1-antitrypsin
Markers of inflammation and immune cell activation are typically elevated in cirrhotic patients especially in the decompensated disease stage:
- C-reactive protein (CRP)
- Procalcitonin (PCT)
- soluble CD14
- soluble CD163
- soluble CD206 (mannose receptor)
- soluble TREM-1
Ultrasound is routinely used in the evaluation of cirrhosis. It may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas. Other liver findings suggestive of cirrhosis in imaging are an enlarged caudate lobe, widening of the fissures and enlargement of the spleen. An enlarged spleen, which normally measures less than 11–12 cm in adults, may suggest underlying portal hypertension. Ultrasound may also screen for hepatocellular carcinoma, and portal hypertension, by assessing flow in the hepatic vein. An increased portal vein pulsatility is an indicator of cirrhosis, but may also be caused by an increased right atrial pressure. Portal vein pulsatility can be quantified by pulsatility indices (PI), where an index above a certain cutoff indicates pathology:
|Average-based||(Max – Min) / Average||0.5|
|Max-relative||(Max – Min) / Max||0.5–0.54|
Cirrhosis is diagnosed with a variety of elastography techniques. Because a cirrhotic liver is generally stiffer than a healthy one, imaging the liver's stiffness can give diagnostic information about the location and severity of cirrhosis. Techniques used include transient elastography, acoustic radiation force impulse imaging, supersonic shear imaging and magnetic resonance elastography. Vibration-controlled transient elastography and magnetic resonance elastography can give an indication of the stage of advanced fibrosis. Compared to a biopsy, elastography can sample a much larger area and is painless. It shows a reasonable correlation with the severity of cirrhosis. Other modalities have been introduced which are incorporated into ultrasonagraphy systems. These include point shear wave elastography using an added acoustic radiation force impulse imaging, or 2-dimensional shear wave elastography.
- Liver cirrhosis with ascites
- caudate lobe hypertrophy in ultrasound due to cirrhosis
- Hepatofugal flow in portal vein in ultrasound
Gastroscopy (endoscopic examination of the esophagus, stomach, and duodenum) is performed in cases of established cirrhosis. If esophageal varices are found, prophylactic local therapy may be applied such as sclerotherapy or banding, and beta blockers may be used.
Rarely are diseases of the bile ducts, such as primary sclerosing cholangitis, causes of cirrhosis. Imaging of the bile ducts, such as ERCP or MRCP (MRI of biliary tract and pancreas) may aid in the diagnosis.
Macroscopically, the liver is initially enlarged, but with the progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and if associated with steatosis the color is yellow. Depending on the size of the nodules, there are three macroscopic types: micronodular, macronodular, and mixed cirrhosis. In the micronodular form (Laennec's cirrhosis or portal cirrhosis), regenerating nodules are under 3 mm. In macronodular cirrhosis (post-necrotic cirrhosis), the nodules are larger than 3 mm. Mixed cirrhosis consists of nodules of different sizes.
- Micronodular cirrhosis, with diffuse areas of pallor.
- Pale macronodules of cirrhosis.
- Cirrhosis leading to hepatocellular carcinoma (autopsy specimen)
However, cirrhosis is defined by its pathological features on microscopy: (1) the presence of regenerating nodules of hepatocytes and (2) the presence of fibrosis, or the deposition of connective tissue between these nodules. The pattern of fibrosis seen can depend on the underlying insult that led to cirrhosis. Fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: including the sinusoids, the space of Disse, and other vascular structures, which leads to altered resistance to blood flow in the liver, and portal hypertension.
- Trichrome stain, showing cirrhosis as a nodular texture surrounded by fibrosis (wherein collagen is stained blue).
As cirrhosis can be caused by many different entities which injure the liver in different ways, cause-specific abnormalities may be seen. For example, in chronic hepatitis B, there is infiltration of the liver parenchyma with lymphocytes. In congestive hepatopathy there are erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins. In primary biliary cholangitis, there is fibrosis around the bile duct, the presence of granulomas and pooling of bile. Lastly in alcoholic cirrhosis, there is infiltration of the liver with neutrophils.
The severity of cirrhosis is commonly classified with the Child–Pugh score. This scoring system uses bilirubin, albumin, INR, the presence and severity of ascites, and encephalopathy to classify patients into class A, B, or C. Class A has a favourable prognosis, while class C is at high risk of death. This system was devised in 1964 by Child and Turcotte, and modified in 1973 by Pugh and others.
A later introduction, the Model for End-Stage Liver Disease (MELD) score, uses three laboratory values (total bilirubin, creatinine, and INR) and is primarily used to determine the allocation of liver transplants.
MELD-Plus is an even later risk score to assess severity of chronic liver disease. The score includes nine variables as effective predictors for 90-day mortality after a discharge from a cirrhosis-related admission. The variables include all Model for End-Stage Liver Disease (MELD)'s components, as well as sodium, albumin, total cholesterol, white blood cell count, age, and length of stay. MELD-Plus was created as a result of a collaboration between Massachusetts General Hospital and IBM.
The hepatic venous pressure gradient, (difference in venous pressure between afferent and efferent blood to the liver) also determines the severity of cirrhosis, although it is hard to measure. A value of 16 mm or more means a greatly increased risk of death.
Key prevention strategies for cirrhosis are population-wide interventions to reduce alcohol intake (through pricing strategies, public health campaigns, and personal counseling), programs to reduce the transmission of viral hepatitis, and screening of relatives of people with hereditary liver diseases.
Little is known about factors affecting cirrhosis risk and progression. However, many studies have provided increasing evidence for the protective effects of coffee consumption against the progression of liver disease. These effects are more noticeable in liver disease that is associated with alcohol use disorder. Coffee has antioxidant and antifibrotic effects. Caffeine may not be the important component; polyphenols may be more important. Drinking two or more cups of coffee a day is associated with improvements in the liver enzymes ALT, AST, and GGTP. Even in those with liver disease, coffee consumption can lower fibrosis and cirrhosis.
Generally, liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process. Close follow-up is often necessary. Antibiotics are prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose, decrease the risk of constipation; their role in preventing encephalopathy is limited.
Alcoholic cirrhosis caused by alcohol use disorder is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.
Cirrhosis caused by Wilson's disease, is treated by removing the copper which builds up in organs. This is carried out using chelation therapy such as penicillamine. When the cause is an iron overload then the iron is removed using a chelation agent such as deferoxamine.
Preventing further liver damage
Regardless of the underlying cause of cirrhosis, consumption of alcohol, as well as other potentially damaging substances, are discouraged. There is no evidence that supports the avoidance or dose reduction of paracetamol in people with compensated cirrhosis; it is thus considered a safe analgesic for said individuals.
Vaccination of susceptible patients should be considered for hepatitis A and hepatitis B. Treating the cause of cirrhosis prevents further damage; for example, giving oral antivirals such as entecavir and tenofovir where cirrhosis is due to hepatitis B prevents progression of cirrhosis. Similarly, control of weight and diabetes prevents deterioration in cirrhosis due to non-alcoholic fatty liver disease.
If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary. Survival from liver transplantation has been improving over the 1990s, and the five-year survival rate is now around 80%. The survival rate depends largely on the severity of disease and other medical risk factors in the recipient. In the United States, the MELD score is used to prioritize patients for transplantation. Transplantation necessitates the use of immune suppressants (ciclosporin or tacrolimus).
Manifestations of decompensation in cirrhosis include gastrointestinal bleeding, hepatic encephalopathy (HE), jaundice or ascites. In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation, infection (of any source), increased alcohol intake, medication, bleeding from esophageal varices or dehydration. It may take the form of any of the complications of cirrhosis listed below.
People with decompensated cirrhosis generally require admission to a hospital, with close monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical treatment – often with diuretics, antibiotics, laxatives or enemas, thiamine and occasionally steroids, acetylcysteine and pentoxifylline. Administration of saline is avoided, as it would add to the already high total body sodium content that typically occurs in cirrhosis. Life expectancy without liver transplant is low, at most 3 years.
Palliative care is specialized medical care that focuses on providing patients with relief from the symptoms, pain, and stress of a serious illness, such as cirrhosis. The goal of palliative care is to improve quality of life for both the patient and the patient's family and it is appropriate at any stage and for any type of cirrhosis.
Especially in the later stages, people with cirrhosis experience significant symptoms such as abdominal swelling, itching, leg edema, and chronic abdominal pain which would be amenable for treatment through palliative care. Because the disease is not curable without a transplant, palliative care can also help with discussions regarding the person's wishes concerning health care power of attorney, Do Not Resuscitate decisions and life support, and potentially hospice. Despite proven benefit, people with cirrhosis are rarely referred to palliative care.
Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). Diuretics may be necessary to suppress ascites. Diuretic options for inpatient treatment include aldosterone antagonists (spironolactone) and loop diuretics. Aldosterone antagonists are preferred for people who can take oral medications and are not in need of an urgent volume reduction. Loop diuretics can be added as additional therapy.
Where salt restriction and the use of diuretics are ineffective then paracentesis may be the preferred option. This procedure requires the insertion of a plastic tube into the peritoneal cavity. Human serum albumin solution is usually given to prevent complications from the rapid volume reduction. In addition to being more rapid than diuretics, 4–5 liters of paracentesis is more successful in comparison to diuretic therapy.
Esophageal variceal bleeding
For portal hypertension, nonselective beta blockers such as propranolol or nadolol are commonly used to lower blood pressure over the portal system. In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting (TIPS) is occasionally indicated to relieve pressure on the portal vein. As this shunting can worsen hepatic encephalopathy, it is reserved for those patients at low risk of encephalopathy. TIPS is generally regarded only as a bridge to liver transplantation or as a palliative measure.
Hepatic encephalopathy is a potential complication of cirrhosis that may lead to functional neuronal impairment, ranging from mild confusion to coma. Common first line treatment may include lactulose, or the antibiotic rifaximin. Protein uptake is encouraged to at least match general recommendations for cirrhosis. A low protein diet may be recommended for short term use in severe cases with gastrointestinal bleeding.
Hepatorenal syndrome is a serious complication of end-stage cirrhosis when kidney damage is also involved.
Spontaneous bacterial peritonitis
People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis.
Portal hypertensive gastropathy
Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize (for example, worsening encephalopathy but no fever). Moreover infections in cirrhosis are major triggers for other complications (ascites, variceal bleading, hepatic enecphalopathy, organ failures, death).
Each year, approximately one million deaths are due to complications of cirrhosis, making cirrhosis the 11th most common cause of death globally. Cirrhosis and chronic liver disease were the tenth leading cause of death for men and the twelfth for women in the United States in 2001, killing about 27,000 people each year.
The cause of cirrhosis can vary; alcohol and non-alcoholic fatty liver disease are main causes in western and industrialized countries, whereas viral hepatitis is the predominant cause in low and middle-income countries. Cirrhosis is more common in men than in women. The cost of cirrhosis in terms of human suffering, hospital costs, and lost productivity is high.
Globally, age-standardized disability-adjusted life year (DALY) rates have decreased from 1990 to 2017, with the values going from 656.4 years per 100,000 people to 510.7 years per 100,000 people. In males DALY rates have decreased from 903.1 years per 100,000 population in 1990, to 719.3 years per 100,000 population in 2017; in females the DALY rates have decreased from 415.5 years per 100,000 population in 1990, to 307.6 years per 100,000 population in 2017. However, globally the total number of DALYs have increased by 10.9 million from 1990 to 2017, reaching the value of 41.4 million DALYs.
The word "cirrhosis" is a neologism derived from Greek: κίρρωσις; kirrhos κιρρός, meaning "yellowish, tawny" (the orange-yellow colour of the diseased liver) and the suffix -osis, i.e. "condition" in medical terminology. While the clinical entity was known before, René Laennec gave it this name in an 1819 paper.
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