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Cirrhosis: Difference between revisions
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Cirrhosis is a chronic liver disease characterised by replacement of normal liver tissue by scar tissue. It’s | '''Cirrhosis''' is a chronic liver disease characterised by replacement of normal liver tissue by scar tissue. It’s the irreversible end-stage of [[hepatitis]] which cause significant morbidity and mortality. There is continuous loss of functional liver tissue, which is initially compensated and asymptomatic as the remaining liver can compensate. However, acute insults precipitate decreases in liver function, causing hepatic decompensation and development of dramatic and life-threatening complications. Cirrhosis is also an important risk factor for [[hepatocellular carcinoma]]. | ||
Cirrhosis is a common condition worldwide. | Cirrhosis is a common condition worldwide. | ||
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== Etiology == | == Etiology == | ||
* Alcoholic liver disease | * [[Alcoholic liver disease]] | ||
* Metabolic associated fatty liver disease | * [[Metabolic associated fatty liver disease]] | ||
* Chronic viral hepatitis (C, B or D) | * Chronic [[viral hepatitis]] (C, B or D) | ||
* Haemochromatosis | * [[Haemochromatosis]] | ||
* Biliary obstruction (primary biliary cholangitis, primary sclerosing cholangitis) | * Biliary obstruction ([[primary biliary cholangitis]], [[primary sclerosing cholangitis]]) | ||
* Autoimmune hepatitis | * [[Autoimmune hepatitis]] | ||
* | * [[Wilson disease]] | ||
* Heart failure | * [[Heart failure]] | ||
* Alpha-1 antitrypsin deficiency | * [[Alpha-1 antitrypsin deficiency]] | ||
The most common causes in the Western world are alcoholic liver disease and metabolic associated fatty liver disease. | The most common causes in the Western world are alcoholic liver disease and metabolic associated fatty liver disease. | ||
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* Infection | * Infection | ||
* Alcohol use | * [[Alcohol]] use | ||
* Hypovolaemia (bleeding or dehydration) | * [[Hypovolaemia]] (bleeding or dehydration) | ||
== Classification == | == Classification == | ||
The liver function or cirrhosis severity can be classified according to the Child-Pugh or MELD scores. The latter is mostly used in the context of transplantation. The Child-Pugh score scores cirrhosis mortality based on: | The liver function or cirrhosis severity can be classified according to the Child-Pugh or MELD scores. The latter is mostly used in the context of transplantation. The [[Child-Pugh score]] scores cirrhosis mortality based on: | ||
* Bilirubin level | * [[Bilirubin]] level | ||
* Albumin level | * [[Albumin]] level | ||
* INR | * [[INR]] | ||
* Ascites | * [[Ascites]] | ||
* Encephalopathy | * Encephalopathy | ||
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Decompensation occurs when the liver function worsens due to an acute insult, or in end-stage cirrhosis where there is too little functional liver tissue left. This can cause a variety of symptoms and complications: | Decompensation occurs when the liver function worsens due to an acute insult, or in end-stage cirrhosis where there is too little functional liver tissue left. This can cause a variety of symptoms and complications: | ||
* Jaundice | * [[Jaundice]] | ||
* Pruritus | * Pruritus | ||
* Upper <abbr>GI</abbr> bleeding (from variceal bleeding) | * Upper [[Gastrointestinal bleeding|<abbr>GI</abbr> bleeding]] (from [[variceal bleeding]]) | ||
* Ascites | * [[Ascites]] | ||
* Hepatic encephalopathy | * [[Hepatic encephalopathy]] | ||
* Spontaneous bacterial peritonitis | * [[Spontaneous bacterial peritonitis]] | ||
* Hepatocellular carcinoma | * [[Hepatocellular carcinoma]] | ||
* Hepatorenal syndrome | * [[Hepatorenal syndrome]] | ||
* Hepatopulmonary syndrome | * [[Hepatopulmonary syndrome]] | ||
Physical examination may reveal: | Physical examination may reveal: | ||
* Telangiectasia | * [[Telangiectasia]] | ||
* Caput medusae | * [[Caput medusae]] | ||
* Hepatomegaly | * Hepatomegaly | ||
* Splenomegaly | * Splenomegaly | ||
* Features of hyperoestrogenism (gynaecomastia, hypogonadism) | * Features of hyperoestrogenism (gynaecomastia, hypogonadism) | ||
Complications not considered to | Complications not considered to be a sign of decompensation: | ||
* Portal vein thrombosis | * [[Portal vein thrombosis]] | ||
* Cardiomyopathy | * [[Cardiomyopathy]] | ||
* Coagulopathy -> excessive bleeding | * Coagulopathy -> excessive bleeding | ||
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== Diagnosis and evaluation == | == Diagnosis and evaluation == | ||
Diagnosis of cirrhosis can usually be made based on clinical features, ultrasound, and special non-invasive investigations like FibroScan, transient elastography (TE) and acoustic radiation force impulse (ARFI). Ultrasound shows a shrunk liver with nodular surface and loss of homogeneity. | Diagnosis of cirrhosis can usually be made based on clinical features, [[ultrasound]], and special non-invasive investigations like [[FibroScan]], [[transient elastography]] (TE) and [[acoustic radiation force impulse]] (ARFI). Ultrasound shows a shrunk liver with nodular surface and loss of homogeneity. | ||
Typical laboratory findings of cirrhosis include: | Typical laboratory findings of cirrhosis include: | ||
* Elevated AST, ALT | * Elevated [[AST]], [[ALT]] | ||
* Elevated INR – due to decreased production of coagulation factors | * Elevated [[INR]] – due to decreased production of coagulation factors | ||
* Hypoproteinaemia and hypoalbuminaemia | * [[Hypoproteinaemia]] and [[hypoalbuminaemia]] | ||
* Thrombocytopaenia | * [[Thrombocytopaenia]] | ||
* Macrocytic anaemia | * [[Macrocytic anaemia and megaloblastic anaemia|Macrocytic anaemia]] | ||
Determination of the etiology is based on patient history as well as laboratory examination: | Determination of the etiology is based on patient history as well as laboratory examination: | ||
* Viral hepatitis serology | * [[Viral hepatitis]] serology | ||
* Alpha-1 antitrypsin – for deficiency | * [[Alpha-1 antitrypsin]] – for deficiency | ||
* Autoantibodies and hypergammaglobulinaemia – for autoimmune hepatitis | * Autoantibodies and hypergammaglobulinaemia – for [[autoimmune hepatitis]] | ||
* Iron studies – for haemochromatosis | * Iron studies – for [[haemochromatosis]] | ||
* Copper studies – for Wilson disease | * Copper studies – for [[Wilson disease]] | ||
Histology is the gold standard for the evaluation of cirrhosis, but it’s not usually required for the diagnosis. | Histology is the gold standard for the evaluation of cirrhosis, but it’s not usually required for the diagnosis. | ||
== Treatment == | == Treatment == | ||
Management of cirrhosis involves preventing and treating complications. This also involves regular surveillance for worsening of the cirrhosis, and for development of hepatocellular carcinoma (by regular ultrasound (every 6 months) and monitoring of AFP). | Management of cirrhosis involves preventing and treating complications. This also involves regular surveillance for worsening of the cirrhosis, and for development of [[hepatocellular carcinoma]] (by regular [[ultrasound]] (every 6 months) and monitoring of [[AFP]]). | ||
To prevent triggers of decompensation, avoidance of hepatotoxic substances (including alcohol), as well as routine vaccinations, are important. Hepatic decompensation is usually self-limiting, but an episode of decompensation increases the risk for further episodes and complications later. | To prevent triggers of decompensation, avoidance of hepatotoxic substances (including [[alcohol]]), as well as routine vaccinations, are important. Hepatic decompensation is usually self-limiting, but an episode of decompensation increases the risk for further episodes and complications later. | ||
To avoid catabolic state, which could precipitate hepatic encephalopathy, it’s important to achieve sufficient energy and protein intake, ~80 – 100g protein and ~3000 Kcal/day, to avoid deficiency. Enteral nutrition should be added if patient cannot achieve this by regular foods. | To avoid catabolic state, which could precipitate [[hepatic encephalopathy]], it’s important to achieve sufficient energy and protein intake, ~80 – 100g protein and ~3000 Kcal/day, to avoid deficiency. Enteral nutrition should be added if patient cannot achieve this by regular foods. | ||
Other important treatments for complications of cirrhosis include: | Other important treatments for complications of cirrhosis include: | ||
* Propranolol – decreases portal hypertension and the risk of variceal bleeding | * [[Propranolol]] – decreases portal hypertension and the risk of variceal bleeding | ||
* Ligation – to decrease the risk of variceal bleeding | * Ligation – to decrease the risk of [[variceal bleeding]] | ||
* Transjugular intrahepatic portosystemic shunt (TIPS) – in case of persistent or recurrent upper GI bleeding due to portal hypertension, or ascites. | * [[Transjugular intrahepatic portosystemic shunt]] (TIPS) – in case of persistent or recurrent upper GI bleeding due to [[portal hypertension]], or [[ascites]]. | ||
* Sodium restriction, fluid restriction, diuretics (<abbr>MRA</abbr> or loop) – in case of ascites | * Sodium restriction, fluid restriction, diuretics (<abbr>[[MRA]]</abbr> or [[Loop diuretic|loop]]) – in case of ascites | ||
* | * Antibiotics – for [[spontaneous bacterial peritonitis]] | ||
* Lactulose ± rifaximin – for hepatic encephalopathy | * Lactulose ± rifaximin – for [[hepatic encephalopathy]] | ||
* Fresh frozen plasma – for coagulopathy | * [[Fresh frozen plasma]] – for coagulopathy | ||
Liver transplantation is the only curative treatment for cirrhosis. It’s indicated for all cases of cirrhosis where decompensation has developed. | [[Liver transplantation]] is the only curative treatment for cirrhosis. It’s indicated for all cases of cirrhosis where decompensation has developed. | ||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||