3 Cirrhosis
Learn how cirrhosis develops, what can cause and signal it, how clinicians assess it, and how common severity tools are interpreted.
What is
is advanced, diffuse liver scarring that disrupts normal liver structure and function. It can develop after years of chronic liver injury. Early disease may cause few or no symptoms; as damage progresses, signs of impaired liver function or may appear.
Causes of
The most common broad causes are alcohol-associated liver disease, metabolic dysfunction–associated steatotic liver disease, and chronic hepatitis B or C. More than one cause may contribute in the same person.
Other causes include autoimmune hepatitis, diseases affecting the bile ducts, inherited conditions such as hemochromatosis or Wilson disease, and some medications. Examples of less-common causes include primary biliary cholangitis, primary sclerosing cholangitis, chronic heart-related liver congestion, and medication-related injury. Alpha-1 antitrypsin deficiency is another inherited example.
Signs and complications
Possible manifestations include fatigue, poor appetite, muscle loss, itching, jaundice, easy bruising or bleeding, and leg edema. and reduced liver function can lead to ascites, variceal bleeding, and hepatic encephalopathy. These complications may be the first indication of previously unrecognized .
A low serum albumin level is associated with reduced liver synthetic function because albumin is produced by the liver. However, other conditions can also lower albumin.
Compensated and decompensated disease
Clinicians often describe as compensated when there has been no overt decompensating event. Decompensated is marked by complications such as ascites, hepatic encephalopathy, or portal-hypertensive gastrointestinal bleeding.
New abdominal fluid accumulation in a person with suggests a decompensating event. It should prompt clinical evaluation of the person’s overall condition, possible precipitating or associated problems, and severity; the finding should not be treated as a score alone. The compensated–decompensated distinction helps describe disease course but does not replace an individual clinical assessment.
Clinical assessment
Assessment combines the patient’s history, physical examination, laboratory tests, and imaging. History-taking explores risk factors and possible causes, including alcohol use, metabolic conditions, viral hepatitis, medications and supplements, and family history.
Examination may look for jaundice, abdominal distension, leg swelling, an enlarged liver or spleen, and tremor or other signs of encephalopathy. Blood tests may assess liver injury and function, blood counts, clotting, and possible causes. Ultrasound and elastography can help assess liver structure and stiffness. Biopsy is used when noninvasive assessment does not resolve the diagnosis or cause.
No single normal or mildly abnormal liver enzyme result rules out . Assessment relies on the overall clinical picture, laboratory findings, and imaging.
Tools for describing severity
The uses bilirubin, albumin, INR or prothrombin time, ascites, and encephalopathy to classify disease as class A, B, or C. Because ascites and encephalopathy are graded clinically, applying the score involves judgment.
use laboratory measurements to estimate short-term mortality risk and help guide liver-transplant prioritization. The tools serve different purposes, and neither should be interpreted without the patient’s clinical context. A score supports, rather than replaces, clinical judgment.