Cirrhosis is a condition defined by scarring of the liver, which can impede its function. When the damage becomes so extensive that the liver can no longer perform its necessary jobs, the condition is referred to as decompensated cirrhosis. This advanced stage of liver disease is characterized by noticeable symptoms, indicating the organ is failing. It represents a point in the progression of chronic liver disease where the body’s ability to cope with the damage has been overcome.
The Shift from Compensated to Decompensated Cirrhosis
The journey to decompensated cirrhosis begins with a phase known as compensated cirrhosis. In this initial stage, the liver has sustained scarring, but it can still perform most of its functions adequately. Many individuals with compensated cirrhosis experience few to no symptoms and may be unaware of their condition. This period can last for many years.
The transition to decompensated cirrhosis marks a turning point where the liver’s functional capacity is overwhelmed. This shift occurs as progressive scarring, or fibrosis, replaces healthy liver tissue, obstructing blood flow and impairing the organ’s ability to process toxins and produce proteins. The development of major complications signals that the body can no longer compensate for the loss of liver function.
This progression is not always a one-way street; with effective treatment of the underlying cause and complications, a state of decompensation can revert to a compensated one. This “recompensation” doesn’t mean the cirrhosis is cured, but that liver function has improved to a point where the most severe symptoms are controlled. The underlying scarring remains, and the risk of future decompensation persists.
Major Complications and Symptoms
Ascites
Ascites is the accumulation of fluid in the abdominal cavity, causing swelling, discomfort, and a feeling of fullness. This occurs due to increased pressure in the veins that supply the liver, a condition called portal hypertension. The scarred liver obstructs normal blood flow, causing pressure to build up and forcing fluid to leak into the abdomen. A failing liver also struggles to produce albumin, a protein that helps keep fluid within blood vessels, contributing to the leakage.
Variceal Bleeding
Portal hypertension also forces blood to find alternative routes around the congested liver, leading to the formation of enlarged veins called varices. These typically develop in the esophagus and stomach and have thin, fragile walls. The high pressure within these veins makes them prone to rupture, which can cause severe bleeding. Symptoms include vomiting large amounts of blood or passing black, tarry stools. Variceal bleeding is a medical emergency.
Hepatic Encephalopathy
When the liver fails, it can no longer effectively remove toxins from the blood. One such toxin, ammonia, is produced during the digestion of protein in the intestines. Normally, the liver converts ammonia into urea, which is then eliminated by the kidneys. In decompensated cirrhosis, ammonia and other toxins are not processed by it, allowing them to travel to the brain. This buildup can lead to a decline in brain function known as hepatic encephalopathy, with symptoms ranging from mild confusion and personality changes to severe drowsiness and coma.
Jaundice
Jaundice is the yellowing of the skin and the whites of the eyes. This discoloration is caused by a buildup of bilirubin, a yellow substance created when old red blood cells are broken down. A healthy liver processes bilirubin and excretes it into bile. In decompensated cirrhosis, the damaged liver cannot properly process bilirubin, causing its levels in the blood to rise and deposit in the skin and eyes.
Underlying Causes of Cirrhosis
The most frequent causes of cirrhosis are chronic alcohol abuse, chronic viral hepatitis infections, and a condition known as metabolic dysfunction-associated steatotic liver disease (MASLD), previously called non-alcoholic fatty liver disease (NAFLD). Long-term excessive alcohol consumption directly damages liver cells, leading to inflammation and scarring. Similarly, chronic infections with the hepatitis C or hepatitis B virus trigger persistent inflammation that gradually destroys liver tissue over decades.
MASLD and its more aggressive form, metabolic dysfunction-associated steatohepatitis (MASH), are increasingly common causes linked to obesity, type 2 diabetes, and high cholesterol. In these conditions, excess fat accumulates in the liver, causing inflammation and damage that can progress to cirrhosis. Less common causes include autoimmune diseases where the body’s own immune system attacks the liver, and genetic disorders such as hemochromatosis (iron buildup) and Wilson’s disease (copper buildup).
Medical Management and Treatment Approaches
The management of decompensated cirrhosis is complex, focusing on treating the specific complications, addressing the underlying cause of the liver disease, and evaluating the patient for a liver transplant. Treatment is tailored to each individual’s symptoms and overall health status. The primary goal is to manage symptoms, prevent further decompensation events, and improve the patient’s quality of life.
For ascites, medical treatment starts with a strict low-sodium diet to reduce fluid retention. Doctors often prescribe diuretics, such as spironolactone and furosemide, to help the kidneys excrete more salt and water. In cases of refractory ascites, where diuretics are no longer effective, a procedure called large-volume paracentesis may be performed to manually drain the fluid from the abdomen.
To manage the risk of variceal bleeding, physicians may prescribe medications known as non-selective beta-blockers, which lower the pressure in the portal vein system. For patients with large varices or those who cannot tolerate beta-blockers, a procedure called endoscopic variceal ligation is used. During an endoscopy, tiny elastic bands are placed around the varices to cut off their blood supply and prevent them from rupturing.
The treatment for hepatic encephalopathy aims to reduce the production and absorption of toxins like ammonia in the intestines. The primary medication used is lactulose, a synthetic sugar that works as a laxative, helping to flush ammonia-producing bacteria from the gut. The antibiotic rifaximin is often added to lactulose therapy to further reduce the amount of ammonia produced by intestinal bacteria. For all patients, treating the original cause of cirrhosis is a foundational part of the management strategy. Ultimately, the only definitive cure for end-stage liver disease is a liver transplant.
Prognosis and Lifestyle Adjustments
The long-term outlook for an individual with decompensated cirrhosis depends on the severity of the liver damage, the specific complications present, and the person’s overall health. Doctors often use scoring systems, such as the Model for End-Stage Liver Disease (MELD) score, to assess the severity of the illness and help predict 3-month survival. This score, which is based on lab tests for bilirubin, creatinine, and blood clotting (INR), helps prioritize patients on the liver transplant waiting list.
Lifestyle adjustments are a large part of managing the condition and can significantly impact quality of life and slow disease progression. Strict adherence to a low-sodium diet, typically limited to 2,000 milligrams per day, is a primary strategy for controlling ascites and fluid retention. Complete abstinence from alcohol is mandatory, as any amount can cause further liver injury and worsen complications.
Following the prescribed medication regimen without fail is also necessary for managing the various symptoms. This includes consistently taking diuretics for fluid control, beta-blockers for varices, and lactulose for hepatic encephalopathy to maintain its therapeutic effects. Regular exercise, as approved by a healthcare provider, can help combat the muscle wasting and frailty that often accompany advanced liver disease. These patient-led actions, in combination with medical care, are foundational to living with decompensated cirrhosis.