Cirrhosis is a chronic liver disease characterized by scar tissue replacing healthy liver cells. This scarring interferes with the liver’s ability to perform vital functions, such as filtering toxins, producing essential proteins, and regulating blood clotting. Decompensated cirrhosis represents an advanced stage where the liver can no longer adequately perform these tasks. This leads to various health complications.
What Decompensated Cirrhosis Means
Cirrhosis exists in two main stages: compensated and decompensated. In compensated cirrhosis, the liver, despite scarring, functions sufficiently, and individuals may not experience significant symptoms. This stage can persist for years, with some patients having a median survival time exceeding 12 years. If the underlying cause of liver damage is not addressed, compensated cirrhosis can progress to the decompensated form.
Decompensation occurs when liver damage becomes so profound that the organ loses its capacity to perform its functions. This failure leads to noticeable and serious symptoms. The transition to decompensated cirrhosis is a turning point, often signaling a decline in the median survival rate to about 1 to 2 years. It is characterized by complications indicating the liver’s inability to maintain the body’s balance.
Key Signs and Symptoms
The liver’s inability to function properly in decompensated cirrhosis leads to several signs and symptoms. Jaundice, a common symptom, manifests as yellowing of the skin and whites of the eyes. This occurs because the damaged liver cannot effectively process bilirubin, a yellow pigment from red blood cell breakdown, causing it to accumulate.
Ascites, another frequent sign, is marked by fluid accumulation in the abdominal cavity, leading to noticeable swelling. Portal hypertension, increased blood pressure within veins leading to the liver, contributes to this fluid buildup by causing fluid to leak from blood vessels. Fluid retention can also lead to peripheral edema in the legs and ankles.
Individuals may also experience easy bruising and bleeding. The liver produces proteins necessary for blood clotting, and its impaired function means these are not made in sufficient quantities, increasing hemorrhage risk. Persistent fatigue is also common, reflecting the liver’s diminished capacity and toxin accumulation.
Serious Complications
Decompensated cirrhosis is defined by the emergence of complications arising from the liver’s extensive damage. These complications directly reflect the liver’s failure to perform its roles.
One complication is hepatic encephalopathy, involving impaired brain function due to toxin buildup, particularly ammonia. Ammonia, a byproduct of protein breakdown, normally converts into urea for excretion by the liver. When the liver is damaged, ammonia bypasses this process, accumulating in the bloodstream and crossing the blood-brain barrier. This accumulation can lead to neurological symptoms, from confusion and disorientation to coma.
Variceal bleeding, another complication, occurs from enlarged, fragile veins in the esophagus or stomach. These varices develop due to portal hypertension, where increased pressure in the portal vein system causes blood to back up and seek alternative routes, leading to vein wall swelling and thinning. Rupture can result in sudden internal bleeding, a medical emergency.
Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid that develops in individuals with ascites. Fluid accumulation in the abdomen provides a favorable environment for bacterial growth, often without an obvious infection source. SBP is a serious condition that can worsen liver function and increase other complication risks.
Hepatorenal syndrome (HRS) is a form of kidney failure occurring in advanced liver disease. This condition involves a rapid decline in kidney function due to changes in blood flow to the kidneys, rather than direct kidney damage. Liver dysfunction leads to widespread circulatory changes, including kidney blood vessel constriction, impairing waste filtration. HRS is a challenging complication with a high mortality rate.
Diagnosis and Management Approaches
Diagnosing decompensated cirrhosis involves clinical assessment and medical tests. Healthcare providers evaluate symptoms and conduct blood tests, including liver function tests, complete blood counts, and coagulation studies, to assess liver damage. Imaging techniques such as ultrasound, CT scans, and MRI provide views of the liver’s structure and identify nodules, an enlarged spleen, or fluid accumulation. Endoscopy may also visualize varices in the esophagus or stomach.
Management focuses on addressing specific complications and improving quality of life. For ascites, diuretics like spironolactone and furosemide are commonly used to remove excess fluid. Dietary sodium restriction is also recommended to reduce fluid retention. In cases of large fluid buildup, therapeutic paracentesis, draining the fluid, may be necessary.
Hepatic encephalopathy is managed with medications like lactulose, a synthetic sugar that reduces ammonia by promoting bowel excretion. Rifaximin, a non-absorbable antibiotic, may be added to lactulose therapy to reduce ammonia-producing bacteria and prevent recurrence.
For variceal bleeding, endoscopic procedures such as variceal band ligation stop acute bleeding and prevent future episodes. This involves placing small elastic bands around varices to cut off their blood supply. Non-selective beta-blockers also reduce portal hypertension and bleeding risk.
Lifestyle modifications, including strict alcohol abstinence and dietary changes, are important to prevent further liver damage. For eligible individuals, liver transplantation offers a definitive treatment, replacing the damaged liver with a healthy one. Transplantation is considered when other treatments are no longer effective and benefits outweigh risks.