Jaundice (yellow skin) may appear as a symptom occasionally, but is most common during an acute attack. Jaundice is caused by the buildup of bile pigment that is passed by the liver into the intestines. This same bile buildup can also cause intense itching.
Some people experience a swelling of the liver (hepatomegaly) or the spleen (splenomegaly) as a result of
Spider nevi are small capillaries that are seen on the surface of your skin. Branches form (grow) from the
one capillary and it can either look like a small red spider or a splat (kind of like a squashed spider). They are also referred to as spider angiomas. If you have less than 10 it can be considered normal, but more than that and it’s an indication of chronic liver disease. They can be found only above the waist, usually on the chest, upper arms, shoulders, face, neck and upper back.
Occurring in cirrhosis, the accumulation of fluid in the abdominal cavity, or ascites, is related to portal hypertension, significant reduction in serum albumin, and renal retention of sodium. The volume of abdominal ascites in adults with cirrhosis may reach levels as great as 10 to 12 litres (10.6 to 12.7 quarts).
Ascitic fluid may accumulate in the scrotum and in the chest cavity, where its presence, combined with the upward pressure on the diaphragm from the abdominal fluid, may severely affect breathing. Appetite also is often reduced by the abdominal distension. Ascites is treated by the removal of enough fluid directly from the abdomen by needle puncture to ease discomfort and breathing.
Patients are placed on diets low in salt, and they are given diuretic drugs to increase the output of water by the kidneys. If these measures do not control massive ascites, ascites can be drained internally into the general venous blood system by running a plastic tube from the abdominal cavity, under the skin of the chest, into the right internal jugular vein of the neck (peritoneovenous shunt of LeVeen).
Sometimes occurring in cirrhosis, portal hypertension is the increased pressure in the portal vein and its tributaries resulting from blockages to the blood flow into the liver. It is usually caused by the scarring processes of cirrhosis. The increased pressure causes varices, or dilations of the veins leading into the portal vein. When varices are located in superficial tissues, they may rupture and bleed profusely. Two such locations are the lower esophagus and the perianal region.
Esophageal varices are likely to bleed most heavily, and this bleeding is frequently associated with the onset of hepatic encephalopathy or coma. Because of their location at the lower end of the esophagus, or the upper portion of the stomach, bleeding from varices is often difficult to control. If variceal bleeding persists, surgical formation of a shunt, or artificial passageway, from the portal vein to an abdominal vein may be done.
Hepatic encephalopathy refers to the changes in the brain that occur in patients with advanced acute or chronic liver disease. If liver cells are damaged, certain substances that are normally cleansed from the blood by the healthy liver are not removed (mainly ammonia, or possibly certain fatty acids). A patient with chronic hepatic encephalopathy may develop progressive loss of memory, disorientation, untidiness, and muscular tremors, leading to a form of chronic dementia. The ingestion of protein invariably aggravates these symptoms.
The treatment of hepatic encephalopathy involves, first, the removal of all drugs that require detoxification in the liver and, second, the reduction of the intake of protein. Restricting the amount of protein in the diet will generally lower the levels of amino acids and ammonia in the bloodstream and brain. Most physicians advise their patients with this condition to eat only about 40 grams of protein a day, and will prescribe lactulose or neomycin to lower amino acid production. Non-meat proteins, such as those found in vegetables and milk, are also recommended. Certain amino acids are used in treatment, since they are considered less likely to cause mental impairment. A dietary supplement rich in these amino acids is used at many liver treatment centers.
When chronic diseases cause the liver to become permanently injured and scarred, the condition is called cirrhosis. The scar tissue that forms in cirrhosis harms the structure of the liver, blocking the flow of blood through the organ. The loss of normal liver tissue slows the processing of nutrients, hormones, drugs, and toxins by the liver. Also slowed is production of proteins and other substances made by the liver.
People with liver cirrhosis may develop many problems beyond the liver. When the liver is scarred the blood cannot easily get through, and backs up under higher than normal pressure (portal hypertension). This often causes ascites, which is yellow fluid that leaks out of the bloodstream into the abdominal cavity.
If the ascites becomes tense, it can cause an umbilical hernia (a protruding belly button). The backed-up blood also often creates varices, in which the pressure causes the blood vessels around the esophagus to burst causing significant blood loss. Varices can be treated with beta blockers, using endoscopically-placed rubber bands to obliterate them, or by injections of liquid that cause the varices to scar. If endoscopy fails to stop bleeding, TIPS (transjugular intrahepatic portosystemic shunt) can be created by inserting a short metal mesh tube through a neck vein into the liver and connecting the portal vein in the liver to a regular vein in the liver. Another alternative is to surgically redirect some of the blood flow around the liver.
People with cirrhosis sometimes may develop jaundice (a yellowing of the whites of the eyes or the skin) due to an accumulation of bilirubin in the blood. If the bilirubin is excreted in the urine, the urine may turn dark.
People with cirrhosis are also at risk for hepatic encephalopathy, which is fatigue or confusion caused by ammonia and other products of protein digestion which are inadequately cleared from the bloodstream by the liver.
People with cirrhosis often bruise easily because the liver manufactures reduced amounts of clotting factors.
Additionally, platelets may be lower than normal in the circulation if the spleen is enlarged.
A spleen enlarged from portal hypertension may hold onto too many platelets.
Chronic HCV infection leads to cirrhosis in at least 20 percent of patients within 2 decades of the onset of infection. Cirrhosis and end-stage liver disease may occasionally develop rapidly, especially among patients with concomitant alcohol use. (National Institutes of Health Consensus Statement on Hepatitis C 1997)
“Nearly 80 percent of chronic hepatitis C sufferers who have the disease for several decades will develop cirrhosis or end-stage liver disease later in life,” according to a trial done on Asian patients infected for probably more than 60 years. (Clin Gastroenterol Hepatology 2005;3:910-917.)
In very rare cases hepatitis symptoms develop quickly and become very severe. This less common form of hepatitis is called fulminant hepatitis, or fast-progressing hepatitis, and it requires prompt medical attention. It can be fatal in up to 80% of cases. The kidneys may fail, and the liver shrinks as cells are killed. The person may fall into a coma and die. Fulminant liver failure following HCV infection has been reported but is a rare occurrence.
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