Cirrhosis is the advanced stage of chronic liver disease, characterized by the replacement of healthy liver tissue with scar tissue (fibrosis). This scarring disrupts the liver’s normal structure, progressively impairing its function. The condition is categorized into two stages: compensated and decompensated. Compensated cirrhosis is the earlier, often asymptomatic stage where the liver can still perform its essential tasks, allowing patients to live for many years without major complications.
Decompensated cirrhosis marks a turning point, signifying liver failure where the organ can no longer sustain the body’s physiological needs. This shift is associated with the onset of severe, noticeable symptoms and a worse outlook for the patient. The transition is defined by the development of clinical complications like fluid accumulation, confusion, or internal bleeding. This advanced stage requires immediate medical intervention to manage the life-threatening manifestations of liver failure.
Defining the Decompensated State
The transition to decompensated cirrhosis is driven by two interrelated problems: portal hypertension and hepatocellular synthetic dysfunction. Portal hypertension is abnormally high blood pressure in the portal vein system, which carries blood from the digestive organs to the liver. The dense scar tissue within the cirrhotic liver creates resistance, impeding blood flow and causing pressure to back up into surrounding vessels.
This back-pressure causes circulatory dysfunction, including the dilation of blood vessels in the splanchnic circulation. Simultaneously, the damaged liver loses its ability to synthesize crucial proteins, such as albumin, and to detoxify waste products. The combination of increased pressure, shunting of blood around the liver, and diminished synthetic function leads directly to the clinical manifestations of decompensation.
Major Clinical Complications
Ascites
Ascites is the accumulation of fluid within the peritoneal cavity (the abdomen). This is the most common manifestation of decompensated cirrhosis, occurring in approximately half of all patients within ten years of diagnosis. The mechanism involves high pressure from portal hypertension combined with a reduction in the liver’s production of albumin.
The elevated pressure forces fluid out of the vessels, while low albumin (hypoalbuminemia) reduces the oncotic pressure needed to keep fluid in the bloodstream. The body senses a reduced effective blood volume, triggering the kidneys to retain excessive sodium and water. This fluid imbalance perpetuates the cycle of accumulation, often causing discomfort and abdominal distension.
Hepatic Encephalopathy
Hepatic encephalopathy (HE) is a potentially reversible disorder of brain function that occurs when the liver fails to clear neurotoxic substances from the bloodstream. The most significant substance is ammonia, a byproduct of protein breakdown generated by gut bacteria. Normally, the liver efficiently converts ammonia into urea for kidney excretion.
In decompensated cirrhosis, the scarred liver cannot perform this conversion effectively. Furthermore, portal hypertension causes blood to bypass the liver entirely through collateral vessels, a process called portosystemic shunting. This allows ammonia to enter the systemic circulation and travel to the brain, leading to neurological symptoms ranging from subtle personality changes and sleep disturbances to profound confusion and coma.
Variceal Bleeding
Variceal bleeding is a complication arising directly from portal hypertension. As blood flow through the liver is obstructed, the body forms collateral vessels to divert blood to the systemic circulation, bypassing the liver. These detours often occur in the submucosa of the esophagus and stomach, where the vessels, known as varices, become engorged and distended due to persistent high pressure.
When the pressure within these thin-walled varices reaches a threshold, they can rupture, leading to a life-threatening hemorrhage. Variceal bleeding carries a high risk of re-bleeding and is associated with mortality. This complication requires immediate endoscopic intervention to stop the bleeding and indicates advanced, unstable liver disease.
Assessing Disease Severity
Clinicians use standardized scoring systems to quantify the severity of decompensated cirrhosis, predict patient survival, and determine the urgency for definitive treatment. The two most common tools are the Child-Pugh score and the Model for End-Stage Liver Disease (MELD) score. The Child-Pugh score classifies the severity of cirrhosis into three classes (A, B, or C), using five variables.
These variables include total bilirubin and albumin levels, the International Normalized Ratio (INR) for blood clotting time, and the presence of ascites and hepatic encephalopathy. Although widely used, the Child-Pugh score has limitations because ascites and encephalopathy require subjective clinical assessment. Furthermore, it does not account for renal function, which is often compromised in advanced liver disease.
The MELD score is a more objective, continuous numerical scale, ranging from 6 to 40, that predicts a patient’s three-month survival. It incorporates three objective laboratory values: serum bilirubin, serum creatinine, and the INR. The MELD score is the standard system used to prioritize patients on the liver transplant waiting list, where a higher score indicates a more urgent need. A modified version, the MELD-Na score, also includes serum sodium, providing a more accurate prediction of mortality, especially in patients with severe fluid retention.
Treatment Approaches and Outlook
The management of decompensated cirrhosis focuses on treating specific complications and addressing the underlying cause of liver damage. Symptom management involves targeted therapies to improve patient comfort and prevent deterioration. For ascites, treatment includes a low-sodium diet and diuretics, which help the kidneys excrete excess fluid and salt.
Hepatic encephalopathy is treated with non-absorbable disaccharides like lactulose, which reduces ammonia production and absorption in the gut. Antibiotics such as rifaximin are often added to alter the gut flora and decrease ammonia production. Variceal bleeding is a medical emergency managed with medications to lower portal pressure and procedures like endoscopic band ligation to tie off the enlarged veins.
Liver transplantation remains the only definitive curative option for end-stage decompensated cirrhosis. The MELD score determines a patient’s place on the transplant list, ensuring those with the highest risk of short-term mortality are prioritized. The outlook for patients is guarded, with median survival estimated at approximately two years without transplantation. However, with effective management and access to a transplant, the quality of life and survival rates improve.