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When your patient is in liver failure

WHITEMAN, KIM RN, CCRN, MSN; MCCORMICK, CRYSTAL RN, CCTN

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Find out what leads up to liver failure, how it's diagnosed, and how to care for your patient.

Each year, 1 in 10 Americans is diagnosed with liver disease. Here's what you need to know if one of those patients is yours.

EACH YEAR, 1 in 10 Americans is diagnosed with liver disease; 25,000 die of liver disease complications. Untreated or refractory liver disease can lead to liver failure, defined as the loss of 80% to 90% of liver function. Liver failure can come on quickly (for example, from fulminant hepatitis) or slowly (for example, from alcoholic cirrhosis). In this article, we'll look at the disorders that can lead up to liver failure (see Common liver diseases in adults) and discuss how to assess and manage liver disease. For more on the structure and function of the liver, see Liver lowdown.

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Liver disease: The beginning

Liver disease falls into two main categories: hepatocellular, such as viral hepatitis or alcohol- or drug-related liver disease, and cholestatic, or obstructive disease, such as that caused by gallstones, malignancy, or primary biliary cirrhosis. All can lead to liver failure.

Liver failure, also known as end-stage liver disease, can be caused by an acute injury (also called fulminant liver failure) or result from a chronic disease. Fulminant liver failure might follow an infection (hepatitis) or an acetaminophen overdose, or it could result from hepatic vein obstruction (Budd-Chiari syndrome). Fulminant liver failure is characterized by coagulopathy and encephalopathy that develop within 8 weeks of the injury or start of an illness. Prompt treatment based on the underlying problem is key.

Symptoms of liver failure occur later in patients with chronic liver disease. Alcohol abuse and viral hepatitis are among the diseases that can lead to cirrhosis, a nonuniform scarring and fibrosis of the liver that can lead to liver failure.

Some patients with well-compensated chronic liver disease may experience an acute decline in liver function after an infection or gastrointestinal (GI) bleeding. This is referred to as acute-on-chronic liver failure. These patients may return to baseline liver function with supportive treatment and not need an emergency liver transplant.

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Recognizing danger signs

Once the liver begins to fail, disorders of its various functions lead to characteristic signs and symptoms. Let's look at these by body system:

  • Neurologic. Hepatic encephalopathy is the broad term for neurologic changes caused by liver failure. These changes, which can range from monotonous speech and drowsiness to profound coma, may be related to the liver's inability to break down ammonia, a by-product of protein (amino acid) catabolism. Asterixis, a sudden, brief, nonrhythmic flexion of the hands and fingers when you ask the patient to extend his arms and dorsiflex his wrists, is a clinical warning that warrants further investigation.
  • Cardiovascular. Patients in liver failure, especially those with cirrhosis, have dilated peripheral blood vessels and increased cardiac output. Assessment findings may include flushed extremities, tachycardia, bounding pulses, and hypotension.
  • Hematologic. Because the liver synthesizes coagulation factors, a patient in liver failure may have petechiae, occult bleeding, or other bleeding disorders. Vitamin K absorption also is impaired, exacerbating the liver's problems in synthesizing coagulation factors. The patient's lab results may show a prolonged prothrombin time and international normalized ratio.
  • Patients may appear malnourished because of dietary restrictions and the liver's inability to metabolize food. They're often anemic because of blood loss, impaired red blood cell (RBC) formation, and excess RBC destruction.
  • Poorly functioning Kupffer's cells (the phagocytic cells in the liver) and general debilitation make the patient susceptible to infection, including sepsis. Fluid retention as a result of low serum albumin levels may cause varying degrees of peripheral edema.
  • Pulmonary. Patients with liver failure have a tendency to develop pleural effusions, especially on the right side. This hepatic hydrothorax is believed to be caused by fluid transfer from the peritoneal cavity through the diaphragm. The patient may be asymptomatic when the effusion is small, but will become short of breath on exertion or at rest as the size of the effusion increases or if the effusion develops rapidly.
  • GI. Scarring and fibrosis of the liver from chronic liver disease and splenomegaly often result in portal hypertension. Pressure increases in the portal system, the veins that carry blood from the intestines and abdominal organs to the liver. Normal portal pressure is 5 to 10 mm Hg; portal pressure above 10 mm Hg is considered hypertension.
  • To compensate for this increased pressure, the body develops collateral circulation to and around the liver, but pressure causes enlarged, distended vessels (varices). Commonly occurring in the esophagus, rectum, and abdomen, these varices can rupture and cause life-threatening bleeding. Signs and symptoms of ruptured varices include large amounts of bright red blood from the patient's GI tract (mouth and nasogastric tube), hypotension and tachycardia, and cold, clammy skin. He may also have bloody or black, tarry stools (melena).
  • Many patients with liver failure develop ascites, or excessive fluid in the peritoneal cavity caused by portal hypertension, sodium retention, and hypoalbuminemia. The patient's abdomen may be distended or tense, and his breathing or movement may be restricted by the size of his abdomen. On percussion, you might find a fluid wave or shifting dullness as fluid moves from one area to another. (For more pointers, see “Assessing for Ascites” in the February issue of Nursing2005.) If your patient has ascites and develops a fever, suspect spontaneous bacterial peritonitis, an infection of the ascites fluid. Signs include fever, abdominal pain, and hypotension.
  • Another GI sign of liver failure is clay-colored stools, caused by the patient's inability to conjugate bilirubin in the GI tract. (Normal stools are brown because they contain conjugated bilirubin.) The patient's stool also may contain fats that couldn't be reabsorbed into the body, a condition called steatorrhea.
  • A distinct breath odor called fetor hepaticus often accompanies liver failure and tends to become more pronounced as liver failure progresses. This odor often is described as a “sweet, fecal” smell.
  • Genitourinary. A small amount of bilirubin is normally excreted in the urine in the form of urobilinogen. When the liver fails, excess bilirubin is excreted via the kidneys and the normally yellow urine becomes reddish brown in color. Patients may have decreased urine output and elevated blood urea nitrogen and serum creatinine levels. Some patients develop acute oliguric renal failure, called hepatorenal syndrome, from intrarenal vasoconstriction in otherwise normal kidneys.
  • Endocrine. A failing liver has trouble metabolizing endogenous steroids, including the sex hormones. Consequently, men in liver failure may experience breast enlargement, testicular atrophy, and loss of body hair. Women may develop more facial hair, smaller breasts, and amenorrhea. Both sexes experience decreased libido.
  • Skin. Jaundice, the yellow discoloration of skin and sclerae, is a classic sign of liver disease and has many causes.

If the body is producing bilirubin faster than the liver can conjugate it, as in hemolysis, the patient may exhibit prehepatic jaundice associated with elevated unconjugated bilirubin levels.

Someone with viral hepatitis or alcoholic cirrhosis may experience intrahepatic jaundice (also called parenchymal or hepatocellular jaundice), which reflects the liver's impaired ability to metabolize bilirubin at the cellular level. This patient will have elevated conjugated and unconjugated bilirubin levels.

A patient with cholestasis or bile duct obstruction may develop obstructive jaundice, characterized by elevated conjugated bilirubin levels.

Pruritus is associated with liver disease and may be caused by accumulation of bile acids under the skin. A patient with alcoholic cirrhosis may have red palms and feet. He may also have fiery red vascular spiders (spider angiomas) on the face, neck, arms, and upper trunk that blanch under pressure. Many people with primary biliary cirrhosis and high cholesterol levels have white fatty deposits around the eyes (xanthomas). Poor nutrition may lead to fragile, thin skin that tears easily, and coagulopathy may lead to bruises and petechiae.

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Diagnostic studies

Elevated liver enzymes are one of the first signs of liver disease. But because liver enzymes may be elevated for various reasons, consider the patient's history—including his medication history—when analyzing the values. Almost any medication, including over-the-counter drugs and herbal preparations, can cause a transient elevation in liver enzymes. (For more on liver enzymes, see Lab clues pointing to liver trouble.)

Radiographic tests can provide valuable information about the liver. An ultrasound can reveal the patency of blood vessels that supply the organ, the presence of gallstones, and obstructed bile ducts. Depending on the size and location, some cysts and tumors of the liver and pancreas may also be visible on ultrasound. Computed tomography scans can show liver size and detect small lesions or bile duct dilation.

In endoscopic retrograde cholangiopancreatography (ERCP), contrast media is injected into the biliary tree through a specialized endoscope. Besides examining the biliary tree, the clinician can perform biopsies and treatments via the endoscope. For example, if he sees that a stone is obstructing a bile duct, he can remove it during the procedure.

A newer technique, magnetic resonance cholangiopancreatography, is similar to ERCP, but doesn't require contrast media. However, it can't be used to perform biopsies and treatments.

The liver biopsy is the definitive test to assess the cause and severity of liver dysfunction. Although a biopsy can be done percutaneously at the bedside, it's more likely to be performed using image guidance, such as computed tomography scan. After administering a local anesthetic, the clinician inserts a specialized needle to obtain a sample of hepatic tissue. Procedure-related pain should be dull and mild and ease soon after the procedure.

Hemorrhage and bile leakage are the main complications. Monitor vital signs for 4 to 6 hours after the procedure and check his hematocrit level after 6 hours. Severe or ongoing pain may indicate bleeding, so report this to the patient's health care provider immediately.

Because a patient with coagulopathy associated with liver disease is particularly vulnerable to bleeding, a transjugular liver biopsy may be a better option than needle biopsy because it carries less bleeding risk. An interventional radiologist performs this procedure using fluoroscopy. To obtain a liver specimen, he places a catheter via the right internal jugular vein and threads it through the right atrium, inferior vena cava, and hepatic vein. In some cases, he may insert the catheter in the left internal jugular vein instead if the right internal jugular vein can't be used.

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Symptom management

Your interventions will be based on your patient's clinical condition, which may include the symptoms described below:

  • Hepatic encephalopathy can be exacerbated by electrolyte imbalances, GI bleeding, infection, constipation, diuretics, and medications that act on the central nervous system. To reduce the severity of hepatic encephalopathy, a patient in liver failure may be placed on a low-protein diet and medications that help reduce serum ammonia level.
  • Lactulose, the medication of choice, produces an osmotic effect in the colon, which stimulates peristalsis. Besides increasing GI motility, its effects include lowering intestinal pH and decreasing ammonia, probably because of bacterial degradation. If lactulose causes excessive diarrhea or abdominal bloating and cramping, the health care provider may order neomycin or metronidazole instead.
  • To help reduce the risk of bleeding from esophageal varices, the patient may be placed on a beta-adrenergic blocker such as propranolol, which lowers blood pressure.
  • If the patient experiences GI bleeding, your first priority is to support circulation by replacing lost fluid and blood. Monitor for tachycardia and hypotension, which are early signs of hypovolemic shock.
  • Typically, the clinician uses endoscopy to find and treat the bleeding site and sclerotherapy to seal the varices. This procedure involves injecting a strong, irritating agent into the area to cause scarring. Other options include:
    • endoscopic electrocautery, which uses thermal energy to coagulate the blood vessel
    • ligation or banding procedures, which ensnare the esopha-geal mucosa and submucosa containing the varices, stopping the bleeding and obliterating the varices
    • an intravenous (I.V.) infusion of octreotide or vasopressin, drugs that restrict portal inflow by vasoconstriction of splanchnic arteries. This helps control variceal bleeding.
    • balloon tamponade, if the patient is unstable.
  • Closely monitor the patient's central venous pressure, manage fluid intake as ordered, and document intake and output meticulously. Measure urine output via an indwelling urinary catheter.
  • To treat ascites, the patient may be placed on a low-sodium diet and potassium-sparing diuretics such as spironolactone. If he needs further treatment, administer additional diuretics or diuretics plus I.V. albumin as ordered.
  • For rapid relief of symptomatic ascites, the patient may undergo paracentesis to remove fluid from the abdomen. Be sure to replace intravascular fluid losses from paracentesis; hypovolemia from aggressive removal of ascites can lead to hepatorenal syndrome.
  • During paracentesis, note the appearance of the ascites fluid; it should be clear and yellow. Cloudy fluid indicates infection and possible spontaneous bacterial peritonitis, which should be treated with antibiotics.
  • A patient with ascites may develop a pleural effusion, which threatens respiratory function. Initial treatment, which aims to reduce the ascites, may include diuretics or a combination of I.V. albumin and diuretics. If this doesn't resolve the effusion, the patient may need thoracentesis to remove fluid from the pleural space. Use the smallest tube possible to prevent complications.
  • Patients with portal hypertension may be treated with a transjugular intrahepatic portosystemic shunt, which reduces portal pressure by diverting portal blood flow into the hepatic vein.
  • The key to managing hepatorenal syndrome is preventing it. Avoid excessive diuresis and closely monitor the patient for electrolyte imbalances, especially hyponatremia. If you suspect hepatorenal syndrome, rule out all other causes of renal dysfunction, including hypovolemia. Tell a patient with cirrhosis to avoid nonsteroidal anti-inflammatory drugs, which can precipitate renal failure.
  • Some patients with severely compromised renal function may require hemodialysis while awaiting liver transplantation. If a patient with hepatorenal syndrome receives a liver transplant, the kidneys usually return to adequate function.
  • Pruritus, a major source of discomfort for many patients with liver failure, can be treated with medications that bind with the bile acids and prevent them from accumulating under the skin. Cholestyramine, colestipol, and colesevelam are common choices. Diphenhydramine can help relieve symptoms at night, when its sedative effects aren't an issue.
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Treating liver failure

Liver transplantation is the only definitive treatment for end-stage liver disease, so the patient should be referred to a transplant center as soon as possible. Organs for transplant are scarce, and many patients die waiting for a match. Several experimental treatments, including extracorporeal albumin dialysis and cell-based liver systems, may someday be used as a bridge to sustain life until a suitable organ is found.

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Living with liver disease

A patient with liver disease may experience chronic fatigue long before a diagnosis is made. Some of the physical changes associated with liver disease—such as the characteristic breath odor (fetor hepaticus), jaundice, and gynecomastia in men—can be embarrassing and difficult to accept. Patients may isolate themselves from social situations to avoid questions or stares. Refer your patient to a local or national support group for people with liver disease to help him deal with the issues surrounding this disorder.

Encourage good nutrition to help healing and to increase his energy. Tell the patient to maintain his prescribed diet (which may restrict dietary protein) and explain to him how his diet and medications control his symptoms.

If he abuses alcohol, refer him to an alcohol rehabilitation program.

By understanding what leads to liver failure and how to manage it, you may be able to help your patient avoid complications and get the treatment he needs.

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Liver lowdown

The jack-of-all-trades among organs, the liver has synthesis, storage, metabolic, and excretory functions. Let's look at the liver's anatomy before investigating what it does.

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Interesting setup

The liver has a dual blood supply. The hepatic artery, which carries oxygen-rich blood, contributes about 25% of blood delivered to the liver; the portal vein contributes the rest. The portal vein carries blood drained from the gastrointestinal tract that's rich in nutrients and metabolic by-products of digestion. Blood from the hepatic artery and portal vein mix in specialized capillary beds called sinusoids. There powerful cells of the reticuloendothelial system called Kupffer's cells clean the blood of bacteria or foreign material before it exits the liver.

Blood drains from the liver through the hepatic vein and flows into the inferior vena cava.

Figure

Figure

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What the liver does

  • Cleaning: The liver is responsible for ridding the blood of bacteria from the intestinal tract and for detoxification or excretion of drugs (including alcohol) and endogenous steroids and hormones.
  • Storage: It stores fat-soluble vitamins (A, D, E, K), water-soluble vitamin B12, and trace minerals including iron and copper. The liver can also store blood and release it into the circulation if needed after trauma or hypovolemia. Carbohydrates are stored in the liver in the form of glycogen. When needed, the liver converts glycogen into glucose and releases it into the circulation. In times of low carbohydrate intake or starvation, the liver can convert fats and protein into glucose.
  • Manufacturing: The liver makes or synthesizes many compounds needed in the body, including bile, whose two major components are conjugated bile acids and conjugated bilirubin. Other substances synthesized in the liver are albumin, a major source of oncotic pressure in the blood vessels, and all coagulation factors except von Willebrand's factor.
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Common liver diseases in adults

  • Autoimmune hepatitis, in which the body's immune system attacks and destroys the liver, is more common in women.
  • Budd-Chiari syndrome is liver failure related to obstruction of the hepatic venous system, usually at the level of the hepatic veins. This syndrome can lead to fulminant hepatitis or cirrhosis.
  • Cancer can occur in the bile ducts (cholangiocarcinoma) or the liver itself (hepatocellular carcinoma). Patients who abuse alcohol and those who've had viral hepatitis are at high risk for hepatic cancer.
  • Acute fatty liver is a complication of alcohol abuse, pregnancy, and long-term total parenteral nutrition.
  • Primary sclerosing cholangitis is a chronic, progressive inflammatory disease characterized by fibrosis of the bile ducts. This disease is more common in men and probably has an autoimmune component: It's associated with inflammatory bowel disease.
  • Cirrhosis is a pattern of diffuse nodules and nonuniform scarring caused by alcohol abuse, hepatitis, biliary obstruction, toxic reaction to drugs or chemicals, or hereditary diseases.
  • Figure

    Figure

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Lab clues pointing to liver trouble

  • Total bilirubin (normal, 0.3 to1.5 mg/dl). This level is elevated in jaundice, hepatitis, liver cell damage, and bile duct problems.
  • Alkaline phosphatase (normal, 40 to 125 units/liter). Elevations usually indicate bile duct damage or obstruction, but the level may be elevated in pregnancy, during periods of rapid bone growth, or with bone disease or tumors.
  • Aspartate aminotransferase (AST—normal, less than 40 units/liter). An elevated level may indicate liver cell damage.
  • Alanine aminotransferase (normal, less than 40 units/liter). An elevated level may indicate liver cell damage. This enzyme is more specific for the liver than AST.
  • Gamma-glutamyltransferase (normal for men, less than 65 units/liter; for women, less than 40 units/liter). Levels tend to rise with all forms of liver damage, exposure to drugs or alcohol, pancreatic and cardiac disease, and diabetes.
  • Figure

    Figure

At the University of Pittsburgh (Pa.) Medical Center, Kim Whiteman is a nurse-educator and Crystal McCormick is primary nurse care coordinator in the transplant intensive care unit.

The authors have disclosed that they have no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

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SELECTED WEB SITES

American Liver Foundation http://www.liverfoundation.org

Centers for Disease Control and PreventionChronic Liver Diseases

http://www.cdc.gov/nchs/fastats/liverdis.htm

Last accessed on March 2, 2005.

To take this test online, visit http://www.nursingcenter.com/ce/nursing

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SELECTED REFERENCES

Dallal H, Palmer K. ABC of the upper gastrointestinal tract: Upper gastrointestinal haemorrhage. British Medical Journal. 323(7321):1115–1117, November 10, 2001.
Krige J, Beckingham I. ABC of diseases of liver, pancreas, and biliary system: Portal hypertension–2. Ascites, encephalopathy, and other conditions. British Medical Journal. 322(7283):416–418, February 17, 2001.
Sen S, et al. The pathophysiological basis of acute-on-chronic liver failure. Liver. 22(Suppl. 2):5–13, 2002.
Urden L, et al. Thelan's Critical Care Nursing, 4th edition. St. Louis, Mo., Mosby, 2001.
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    When your patient is in liver failure

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