Liver Decompensation

Due to its large blood supply, the liver has some remarkable regenerative properties. The liver can compensate for a significant amount of damage, but eventually a threshold is reached and liver functions decline markedly, resulting in liver decompensation.

Signs of liver decompensation include:

• Abnormal clearance of proteins absorbed through the intestinal tract, leading to ammonia retention and hepatic encephalopathy
• Abnormal excretion, leading to an accumulation of bilirubin in the blood, producing jaundice.
• Ascites: increased sinusoidal pressure, as with severe inflammation or scarring of the liver, leads to fluid accumulation in the abdomen that becomes more difficult to control with progressive liver decompensation.
• Portal hypertension: scarred liver tissue acts as a barrier to blood flow and causes increased portal blood pressure. A major consequence is the rupture of esophageal varices, causing massive and potentially fatal bleeding.

Cirrhosis of the liver is defined as irreversible, diffuse fibrosis or scarring of the liver that is a common endpoint for many chronic liver diseases. Cirrhosis results from repeated liver injury. Common causes of cirrhosis include:

• Excessive alcohol consumption
• Chronic viral hepatitis
• Repeated exposure to toxic chemicals
• Chronic cholestatic diseases, such as primary biliary cirrhosis and sclerosing cholangitis
• Metabolic disorders such as hemachromatosis, Wilson's disease, and alpha-1 antitrypsin deficiency
• Malignancies, such as hepatocellular carcinoma

Alcoholic cirrhosis, also known as Laennec's cirrhosis, accounts for up to 50% of cases. The liver primarily metabolizes alcohol, and alcohol metabolites can cause severe liver damage over time. The risk of hepatic toxicity increases if more than 40 grams, or about 4 alcoholic drinks, are consumed per day. Primary biliary cirrhosis is a disease of unknown etiology that primarily affects middle-aged women. Chronic hepatitis, metabolic liver disease, or exposure to hepatotoxins or industrial chemicals also cause cirrhosis. Cirrhosis, regardless of its cause, increases the risk of primary hepatocellular carcinoma.

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Cirrhosis occurs as a result of repetitive injury to the liver.

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As the healthy liver becomes replaced with fibrous tissue due to cirrhosis, the liver becomes increasingly unable to perform its normal functions.

Complications of cirrhosis include:

• Elevated serum bilirubin levels, causing jaundice and itching
• Inability to metabolize fats or absorb fat-soluble vitamins, resulting in malnutrition, bleeding tendencies, and diarrhea
• Altered hormone levels, producing amenorrhea in women, gynecomastia in men, and other hormonal abnormalities
• Severe muscle wasting, excessive weight loss, and fatigue
• Portal hypertension and development of varices
• Ascites
• Hepatorenal syndrome
• Hepatic encephalopathy

Signs and symptoms of cirrhosis include weight loss, anorexia, abdominal pain, easy bruising, and jaundice. Jaundice occurs when excess bilirubin that cannot be excreted is deposited in areas containing elastin, such as the sclera of the eyes and the nail beds. A definitive diagnosis of cirrhosis requires histologic confirmation obtained from a liver biopsy. Most well established cases of cirrhosis are irreversible, but the progress of the disease may be halted by managing its cause and complications. For example, abstinence from alcohol slows down the progression of alcoholic cirrhosis. The prognosis is grave for cirrhotic patients with persistent jaundice, repetitive ascites, coagulopathy, bleeding esophageal varices, or hypoalbuminemia.

Portal hypertension occurs when liver blockage creates resistance to blood flow in the normally low-pressure portal system. As blood enters the liver through the portal vein, the cirrhotic changes compressing the blood vessels cause resistance, thereby forcing the blood back into collateral vessels that may be formed in the esophagus, umbilical area, duodenum, abdomen, or rectum, producing varices. Bleeding esophageal varices are associated with a high mortality rate. Measuring the portal vein pressure gradient is an effective way of assessing the extent of portal hypertension. Portal hypertension may be treated by surgery that diverts blood flow around the liver and away from collateral vessels, but allows some blood into the liver. Some of the pressure diverting shunts that are used are portal caval, splenorenal, or mesocaval shunts.

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Malnutrition and bleeding tendencies seen in cirrhosis are due to the liver's inability to metabolize fats and fat-soluble vitamins.

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The most serious consequences of portal hypertension are rupture of dilated esophageal blood varices, causing massive bleeding, and portosystemic shunting, in which substances from the intestine, including drugs, bacteria, and toxic substances such as ammonia, bypass the liver and thus have access to other body tissues where they can produce damage.

When fibrous tissues caused by cirrhosis prohibit blood from leaving the liver via the vena cava, the liver begins to expand beyond its normal capacity. When this occurs, plasma fluids leak outside of the liver into the peritoneal cavity, causing an accumulation of serous fluid called ascites. Patients with ascites are initially treated with sodium restriction, administration of diuretics, and bed rest. Paracentesis, or removal of the ascitic fluid is done only to relieve acute respiratory or abdominal distress or for diagnostic purposes.

In some situations, a shunt may be inserted to divert ascitic fluid from the abdominal cavity into the superior vena cava.

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The most serious consequence of portal hypertension is ascites.

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Hepato-renal syndrome is a progressive form of renal failure that occurs in patients with severe liver disease, in the absence of clinical or anatomic evidence of other causes to explain the degree or persistence of renal failure. Hepato-renal syndrome is characterized by progressive azotemia, or accumulation of nitrogenous substances in the blood, urine volume less that 500 ml per day, concentrated urine and a low urine sodium concentration. A high potassium level or hyperkalemia, hepatic encephalopathy, and coma frequently precede or accompany the renal deterioration. The prognosis for patients with hepatorenal syndrome is very poor, with a mortality rate of over 90%.

Hepatic encephalopathy is a major neuropsychiatric complication of chronic liver disease that occurs when large amounts of ammonia accumulate within brain tissues. Ammonia is normally produced by the breakdown of protein in the bowel, and in healthy individuals it is metabolized by the liver to form urea. In patients with significant portal hypertension, blood cannot pass into the liver and the ammonia enters the systemic circulation where it enters brain tissues. Hepatic encephalopathy and its final stage, hepatic coma, occur in 4 stages.

• In the first stage, the patient may exhibit mild confusion, mood changes, inability to concentrate, sleep disturbances, and mild asterixis: rapid involuntary flapping of the wrists, also known as "liver flap."
• In stage two, the patient experiences confusion, apathy, aberrant behavior, asterixis and apraxia: problems in carrying out familiar, purposeful movements.
• Stage three is characterized by severe confusion, incoherence, diminished responsiveness to verbal stimuli, and hyperactive deep tendon reflexes.
• Hepatic coma occurs in the last stage: the patient has no reaction to painful stimuli, no corneal reflex, dilated pupils, and assumes the flexion or extension posture characteristic of severe brain damage.

Correcting pH and electrolyte disturbances, restricting dietary protein, preventing constipation, and preventing gastrointestinal bleeding are methods used to treat hepatic encephalopathy in its early stages. When bleeding occurs in the gastrointestinal tract, bacterial action creates increased ammonia. Sterilizing the bowel by giving neomycin, a drug that is poorly absorbed from the gastrointestinal tract, may prevent ammonia formation by decreasing bacterial counts. Lactulose may also be given to help contain ammonia in the gastrointestinal tract where it can be excreted in the feces.

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Hepatic encephalopathy is caused by increased blood levels of ammonia.

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The American Liver Foundation has a lot of information at their website about the liver and liver disease.

Click here to read specifically about Alcohol and the Liver.

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