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Complications of Cirrhosis

Cirrhosis can be the end stage of any chronic liver disease (Garcia-Tsao 2009). It begins with chronic inflammation, triggering the wound healing process and initiating tissue destruction and its replacement with new fibrous tissue. As the chronic disease persists, low level “wound healing“ and deposition of fibrous tissue continues, eventually building scar tissue with decreasing probability of being reversed and remodeled into functional tissue (Schuppan 2013).

Cirrhosis can be classified as compensated or decompensated. Compensated (where liver function is maintained) cirrhosis can remain asymptomatic for many years. Decompensated (marked by deteriorating liver function) cirrhosis is characterized by the development of a serious complication; once a complication of cirrhosis develops, the 5-year survival rate decreases to less than 20% (Liou 2014; Schuppan 2013; Garcia-Tsao 2009; D'Amico 2006).

There are many possible complications of cirrhosis:

Portal hypertension (high blood pressure in the liver). During cirrhosis, deposition of fibrous tissue increases resistance to the flow of blood through the portal vein of the liver; this increases portal blood pressure and causes portal hypertension. To alleviate the excessive pressure, new collateral blood vessels are generated, which bypass the liver and deliver intestinal blood to the other organs. Portal hypertension leads to dramatic changes in circulation, with detrimental consequences for kidney, lung, gastrointestinal, and cardiovascular function (Iwakiri 2014; Busk 2013; Biecker 2013; Aprile 2002). Portal hypertension is the cause of a majority of complications associated with cirrhosis (Tsochatzis 2014; Procopet 2013).

Ascites. Ascites is the the most common complication of cirrhosis; 50% of patients will develop ascites within 10 years (Liou 2014). Ascites is associated with a 50% increased risk of mortality over two years (Moore 2006). Ascites, an increase in free fluid in the abdomen, is due to increased pressure of hepatic circulation that forces blood plasma (the clear, fluid portion of the blood) out of blood vessels and into the body cavity (Chung 2013; Gatta 2012; Moore 2006).

Bacterial peritonitis. Infection of the ascitic fluid in the abdominal cavity occurs in about 30% of patients with cirrhosis and ascites; it has an in-hospital mortality rate of about 20% (Liou 2014; A.D.A.M. 2014). Decompensated liver cirrhosis delays intestinal motility and increases intestinal permeability, both of which facilitate the translocation of harmful bacteria out of the intestines (Bruns 2014).

Coagulopathy. The majority of protein factors responsible for blood clotting, as well as those that prevent clotting, are synthesized in the liver. In patients with severe liver disease, the ability to synthesize these factors is reduced, and clotting disorders (coagulopathies) are possible. These often manifest as increased bleeding (hemorrhagic coagulopathies), although increased clotting (thrombosis) is also possible. The liver also manufactures protein factors that stimulate blood platelet production, and cirrhotic patients can have low platelet counts (thrombocytopenia) that further increase bleeding risk. Additionally, liver disease can result in malabsorption of fat-soluble vitamin K, a cofactor for the activity of multiple enzymes in the clotting cascade. A variety of tests can be used to monitor changes in clotting in patients with cirrhosis-related coagulopathies (see Life Extension’s Blood Clot Prevention protocol for detailed descriptions of these tests). Severe bleeding episodes are treated by a number of methods, including vitamin K injection, plasma or platelet transfusion, blood protein transfusion (cryoprecipitate), or clot-forming drugs; thromboses and embolisms are treated with injectable anticoagulants (Amarapurkar 2011).

Gastroesophageal varices. Esophageal varices are abnormal, enlarged veins in the lower part of the esophagus. Gastric varices are enlarged veins in the stomach. Both result from portal hypertension (Garcia-Tsao 2007). Rupture and hemorrhage is a major complication of varices, with a 15-20% risk of mortality from each bleeding episode (Albillos 2014). Varices are present in 30-40% of patients with compensated cirrhosis and about 60% of patients with decompensated cirrhosis at the time of diagnosis (Liou 2014; Henry 2014).

Hepatocellular carcinoma. As of 2013, hepatocellular carcinoma was the fifth most common cancer in men and the seventh in women worldwide (Kmiec 2001). The chronic inflammatory environment of cirrhosis plays an essential role in the development of hepatocellular carcinoma (Ding 2014; Berasain 2009).

Hepatopulmonary syndrome. Hepatopulmonary syndrome, a serious complication of liver cirrhosis, is present in 10-17% of patients with liver cirrhosis and is associated with a poor prognosis (Nusrat 2014). In hepatopulmonary syndrome, portal hypertension causes bacteria to cross from the intestines into the bloodstream. The body responds by secreting a vast number of different cellular messengers, which cause blood vessels, particularly those of the lungs, to dilate, which then causes inadequate blood oxygenation. Thus, a symptom of hepatopulmonary syndrome is dyspnea, or breathing difficulty (Tumgor 2014).

Hepatic encephalopathy. A failing or cirrhotic liver is not able to effectively metabolize ammonia into urea, which results in a buildup of this toxin in the blood and in the brain, causing hepatic encephalopathy (Siegel 2006; Garcia-Tsao 2012; Rivera-Mancia 2012; Krieger 1995). Patients can exhibit various neuropsychiatric signs and symptoms: confusion, sleep disruption, cognitive and intellectual dysfunction, impaired motor activity, slowed or slurred speech, and incoordination. Coma and even death are possible in severe cases.

Hepatorenal syndrome. Approximately 20% of hospitalized cirrhosis patients with ascites will develop kidney dysfunction (Liou 2014). Hepatorenal syndrome is a functional renal failure that develops as less blood is available to circulate to the kidneys (Angeli 2012). This is a result of alterations in systemic circulation that accompany portal hypertension. Hepatorenal syndrome is almost always accompanied by ascites and can lead to rapid (type I hepatorenal syndrome) or slowly progressing (type II hepatorenal syndrome) kidney failure (Lata 2012). Signs and symptoms can be non-specific and may parallel those of liver disease (nausea, weight gain, dark urine), although low blood pressure, increased heart rate, low blood sodium, and sustained increases of nitrogenous compounds such as creatinine and urea in the blood (azotemia) are warning signs for the disease (Ng 2007; A.D.A.M. 2012; Lata 2012).

Immune dysfunction. Cirrhosis is associated with various levels of immune dysfunction, referred to as cirrhosis-associated immune dysfunction syndrome. Cirrhosis reduces production of immune-signaling molecules in the liver, depresses activity and abundance of innate immune cells, and increases production of antibacterial antibodies that may also have autoimmune activity (Sipeki 2014).

Malnutrition and hepatic cachexia. Malnutrition in cirrhotic patients is characterized by the loss of skeletal muscle and lean body mass (sarcopenia), adipose (fat) tissue (adipopenia), or both (hepatic cachexia), and does not respond to adequate dietary intake of fats or protein. Malnutrition, especially protein malnutrition, is associated with an increased incidence of several major complications of cirrhosis (including sepsis, ascites, and hepatic encephalopathy), increased mortality, and reduced quality of life (Periyalwar 2012). Malnutrition in cirrhosis patients may also include micronutrient deficiencies (Periyalwar 2012); cirrhotic patients are often deficient in water-soluble vitamins (especially thiamine) and minerals (Amodio 2013), and those with cholestatic liver disease (a disease that affects bile flow) may have difficulty absorbing fat-soluble vitamins (A, D, E and K) (Purnak 2013; Jaurigue 2014).

Other complications of cirrhosis include:

  • Hepatic hydrothorax. Hepatic hydrothorax is a relatively uncommon complication (5-10% of patients with cirrhosis and ascites) in which fluid accumulates in the compartment around the lungs, potentially leading to breathing difficulties (Liou 2014; Norvell 2014).
  • Endocrine disorders. Testicular atrophy and low testosterone levels are frequent in men with cirrhosis, and this can be associated with signs of feminization and gynecomastia. The liver and adrenal glands have a complex interrelationship, and adrenal insufficiency is common in patients with stable and decompensated cirrhosis (Burra 2013; Trifan 2013).
  • Hepatic osteodystrophy. A metabolic bone disease that can occur in patients with chronic liver disease, hepatic osteodystrophy can result in osteoporosis (loss of bone density and mass) and/or osteomalacia (softening of bones).