Lewis: Medical-Surgical Nursing, 8th Edition

Chapter 44: Nursing Management: Liver, Pancreas, and Biliary Tract Problems Answer Key - Guidelines for Case Studies in Text 1. What are possible causes of cirrhosis? What type of cirrhosis does M.B. probably have? Possible causes of cirrhosis include alcohol abuse, complication of hepatitis, chronic biliary obstruction and infection, and long-standing severe, right-sided heart failure. M.B.s cirrhosis is likely the result of his 20-year history of heavy drinking. Based on this history, M.B.s cirrhosis is alcoholic cirrhosis. 2. Describe the pathophysiologic changes that occur in the liver as cirrhosis develops. The first change in the liver from excessive alcohol intake is an accumulation of fat in the liver cells. The liver cells attempt to regenerate, but the regenerative process is disorganized, resulting in abnormal blood vessel and bile duct architecture. The overgrowth of new and fibrous connective tissue distorts the livers normal lobular structure, resulting in lobules of irregular size and shape with impeded blood flow. Eventually, irregular, disorganized regeneration; poor cellular nutrition; and hypoxia caused by inadequate blood flow and scar tissue result in decreased functioning of the liver. Uncomplicated fatty changes in the liver are potentially reversible if the person stops drinking alcohol. If the alcohol abuse continues, widespread scar tissue formation occurs throughout the liver. 3. List M.B.s clinical manifestations of liver failure. For each manifestation, explain the pathophysiologic basis. A thin and malnourished state in liver failure results from the anorexia, dyspepsia, and nausea and vomiting caused by altered metabolism of carbohydrates, fats, and protein by the liver. Ascites and peripheral edema develop as a result of several mechanisms. Portal hypertension causes leakage of proteins from the blood vessels into the lymph spaces in the liver tissue. When the lymphatic system is unable to carry off the excess proteins and water, they leak through the liver capsule into the peritoneal cavity. The osmotic pressure of the proteins pulls additional fluid into the peritoneal cavity, creating ascites. Hypoalbuminemia resulting from impaired liver synthesis of albumin also contributes to ascites and peripheral edema by decreasing colloidal osmotic pressure. Hyperaldosteronism resulting from impaired liver metabolism of aldosterone also contributes to ascites and edema by causing increased sodium reabsorption by the renal tubules. The retention of sodium, as well as an increase in antidiuretic hormone (ADH), causes additional water retention in the patient with liver failure. Jaundice of the sclera and skin results from functional derangement of liver cells and compression of bile ducts by connective tissue growth that impairs the ability of the liver to conjugate and excrete bilirubin. Hepatomegaly occurs from the fatty infiltration, inflammatory reactions, and scarring of the liver that occurs with cirrhosis, whereas splenomegaly occurs as a result of portal hypertension and congestion of the spleen. 4. Explain the significance of the results of his laboratory values.
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Answer Key - Guidelines for Case Studies in Text

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M.B.s total bilirubin is 15 mg/dL (257 mmol/L). Total (conjugated and unconjugated) bilirubin increases as a result of the livers altered ability to take up bilirubin from the blood or to conjugate or excrete it. His serum ammonia level is 220 mcg/dL (122 mmol/L). A major source of ammonia is the bacterial and enzymatic deamination of amino acids in the intestines. The ammonia that results from this deamination process normally goes to the liver via the portal circulation and is converted to urea, which is then excreted by the kidneys. When the blood is shunted past the liver via the collateral anastomoses or the liver is unable to convert ammonia to urea, large quantities of ammonia remain in the systemic circulation. The laboratory value for his AST is 190 U/L (3.2 kat/L) and his ALT is 210 U/L (3.5 kat/L). Enzyme levels, including alkaline phosphatase, AST, ALT, and GGT are elevated because of the release of these enzymes from damaged liver cells. 5. If M.B. begins to manifest signs and symptoms of hepatic encephalopathy, what would you monitor? What measures should be instituted to control or decrease the encephalopathy? Clinical manifestations of encephalopathy are changes in neurologic and mental responsiveness, ranging from lethargy to deep coma. Changes may occur suddenly because of an increase in ammonia in response to bleeding varices or gradually as blood ammonia levels slowly increase. In the early stages, manifestations include euphoria, depression, apathy, irritability, memory loss, confusion, yawning, drowsiness, insomnia, agitation, slow and slurred speech, emotional lability, impaired judgment, hiccups, slow and deep respirations, hyperactive reflexes, and a positive Babinski reflex. Clinical manifestations of impending coma include disorientation as to time, place, or person. A characteristic symptom is asterixis, or flapping tremors (liver flap). This may take several forms, the most common involving the arms and hands. Other signs include hyperventilation, hypothermia, grimacing, and grasping reflexes. The goal in managing hepatic encephalopathy is to reduce ammonia formation. Several measures to reduce ammonia formation in the intestines are used. Lactulose (Cephulac) may also be used to treat hepatic encephalopathy. In the colon, it is split into lactic acid and acetic acid, which decreases the pH from 7.0 to 5.0. The acidic environment discourages bacterial growth. The lactulose traps the ammonia in the gut, and the laxative effect of the drug expels the ammonia from the colon. It is usually given orally but may be given as a retention enema or via NG tube. Sterilization of the intestines with antibiotics such as neomycin sulfate, which are poorly absorbed from the GI tract, is another method. Neomycin can be given orally or rectally. This reduces the bacterial flora of the colon. Bacterial action on protein in the feces results in ammonia production. Cathartics and enemas are also used to decrease bacterial action. Constipation should be prevented. Control of hepatic encephalopathy also involves treatment of precipitating causes. This involves controlling GI hemorrhage and removing the blood from the GI tract to decrease the protein in the intestine. Electrolyte and acid-base imbalances and infections should also be treated. 6. What are possible causes of his gastrointestinal bleeding? Esophageal varices are a common complication, occurring in 66% to 75% of patients with cirrhosis. These collateral vessels contain little elastic tissue and are quite fragile. They have

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Answer Key - Guidelines for Case Studies in Text

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poor tolerance for the high pressure, and the result is distended, tortuous veins that bleed easily. Large varices are more likely to bleed. In addition, because of compromised liver function, there are alterations in normal blood clotting mechanisms. 7. Priority Decision: Based on the assessment data, what are the priority nursing diagnoses? Are there any collaborative problems? Nursing diagnoses: nausea, imbalanced nutrition: less than body requirements, impaired skin integrity, disturbed sensory perception Collaborative problems: anorexia, malnourishment, esophageal varices, hepatic encephalopathy 8. Priority Decision: What are the priority nursing interventions for the patient at this stage of his illness? Health promotion for cirrhosis depends on the cause of the cirrhosis. Patients need to be urged to avoid alcohol ingestion and their efforts must be supported. Adequate nutrition, especially for alcoholics and other individuals at risk for cirrhosis, is essential to promote liver regeneration. Hepatitis must be identified and treated early so that it does not progress to chronic hepatitis. Drugs that are potentially toxic to liver cells should also be avoided. Biliary disease must be treated so that the stones do not cause obstruction and infection. The underlying cause (e.g., chronic lung disease) of right-sided heart failure must be treated so that the heart failure does not lead to cirrhosis.

Mosby items and derived items 2011, 2007 by Mosby, Inc., an affiliate of Elsevier, Inc.