Cirrhosis is the result of long-term damage to the liver, where healthy tissue is progressively replaced by scar tissue, impairing the organ’s ability to function. End-stage cirrhosis, also referred to as decompensated cirrhosis, marks the point where the liver has sustained so much damage that it can no longer perform its necessary filtering and synthesizing roles. This transition is characterized by the onset of severe symptoms and complications that profoundly affect nearly every major organ system. The body begins to display a cascade of failures, moving beyond the liver itself and leading to systemic collapse.
External Physical Manifestations
The failure of the liver to properly process waste products leads to several noticeable changes in a person’s physical appearance. Jaundice is one of the most visible signs, causing the skin and the whites of the eyes to take on a distinct yellow discoloration. This yellowing is caused by the liver’s inability to clear bilirubin, a yellowish compound that remains after the breakdown of old red blood cells.
The severe metabolic strain and poor nutritional absorption often result in marked muscle wasting, known as cachexia. This generalized frailty and loss of muscle mass, particularly noticeable in the limbs and face, reflects the body’s inability to synthesize proteins. The advanced stage of the disease also impacts the small blood vessels close to the surface of the skin.
Two common dermatological signs emerge: palmar erythema and spider angiomas. Palmar erythema appears as a blotchy redness on the palms, due to increased levels of circulating hormones that the damaged liver cannot metabolize. Spider angiomas are tiny, visible blood vessels that branch out from a central red spot, typically appearing on the upper torso, face, and arms.
Complications Stemming from Portal Hypertension
A major consequence of the extensive scarring in end-stage cirrhosis is portal hypertension, which is abnormally high blood pressure in the portal vein. The dense scar tissue obstructs the normal flow of blood through the liver, forcing the blood to back up and seek alternative routes. This increased pressure is responsible for many serious complications of decompensated cirrhosis.
The pressure forces fluid to leak out of the blood vessels and into the abdominal cavity, leading to ascites, the accumulation of fluid in the abdomen. Ascites causes significant abdominal swelling, discomfort, and bloating, often representing the first sign of decompensation. The mechanism involves both the mechanical pressure from the portal vein and the liver’s decreased production of albumin, a protein that helps keep fluid within the vessels.
Fluid retention also occurs in the lower extremities, known as peripheral edema, causing swelling in the ankles and legs. The redirection of blood flow bypasses the liver and creates new, enlarged veins, particularly in the esophagus and stomach, called esophageal varices. These varices are fragile and prone to rupture because they are not meant to handle the high pressure.
Bleeding from ruptured esophageal varices is a medical emergency and a major cause of death in end-stage cirrhosis. The blood loss can be massive and sudden, often presenting as vomiting blood or passing black, tarry stools. The risk of rupture increases as the pressure within the portal system rises.
Neurological and Cognitive Deterioration
The failing liver’s inability to filter toxins from the blood directly impacts the brain, leading to hepatic encephalopathy (HE). The liver typically converts neurotoxins, such as ammonia, into harmless compounds for excretion, but in cirrhosis, these substances build up in the bloodstream and travel to the brain. The accumulation of these toxins interferes with normal brain function, causing neuropsychiatric abnormalities.
Symptoms of HE range from subtle cognitive deficits to profound consciousness changes. Early signs include difficulty concentrating, forgetfulness, and minor personality changes. As the condition progresses, a person may experience slurred speech, severe disorientation, and sleep cycle disturbances.
A specific physical manifestation is asterixis, often described as a “flapping tremor,” which is an involuntary, jerky movement of the hands when the arms are outstretched. In the most severe stages, HE can lead to stupor and eventually a coma, representing a decline in neurological function.
Systemic Organ Failure and Infection Vulnerability
End-stage cirrhosis triggers a systemic inflammatory state and weakens the body’s immune defenses, termed cirrhosis-associated immune dysfunction. This compromised immune system makes patients highly vulnerable to bacterial infections, which are a common cause of acute decompensation and high mortality. Infections can occur in any part of the body, but are often aggressive due to the underlying immune impairment.
A major concern is spontaneous bacterial peritonitis (SBP), an infection of the ascitic fluid that develops without any apparent source. SBP is a serious complication that requires immediate medical attention, as it can rapidly progress to sepsis. The presence of infection triggers an exaggerated inflammatory response that can lead to multi-organ failure.
The functional decline of the liver also precipitates the failure of other non-liver organs, notably the kidneys, a complication known as Hepatorenal Syndrome (HRS). HRS is a severe form of acute kidney injury characterized by the progressive constriction of blood vessels leading to the kidneys, secondary to the systemic circulatory changes driven by the advanced liver disease. Bacterial infections are often the most common trigger for the development of renal failure. The combined failure of multiple organ systems characterizes the final stages of the disease.