Focus on Cirrhosis of the Liver Relates to

Focus on Cirrhosis of the Liver (Relates to Chapter 44, “Nursing Management: Liver, Pancreas, and Biliary Tract Problems” in the textbook) Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc.

Description • A chronic progressive disease of the liver § Extensive parenchymal cell degeneration § Destruction of parenchymal cells Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 2

Cirrhosis Fig. 44 -4. Cirrhosis that developed secondary to alcoholism. The characteristic diffuse nodularity of the surface is due to the combination of regeneration and scarring of the liver. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 3

Description • Liver cells attempt to regenerate. § Regenerative process is disorganized. • Abnormal blood vessel and bile duct formation • New fibrous connective tissue distorts liver’s normal structure, impedes blood flow. • Poor cellular nutrition and hypoxia result. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 4

Description • Insidious, prolonged course • Ninth leading cause of death in United States • Fourth leading cause of death in persons ages 35 to 54 • Twice as common in men Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 5

Etiology and Pathophysiology • Factors that can lead to cirrhosis § Chronic alcohol abuse • Excessive alcohol ingestion is the single most common cause of cirrhosis. • Alcohol has a direct hepatotoxic effect. • First change from excessive alcohol intake is fat accumulation in liver cells. • With continued abuse, scar formation occurs. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 6

Etiology and Pathophysiology § Nonalcohol fatty liver disease (NAFLD) § Malnutrition that occurs concurrently with excessive alcohol intake, extreme dieting, malabsorption, and obesity § Environmental factors, as well as a genetic predisposition § Postnecrotic cirrhosis • Complication of viral, toxic, or idiopathic hepatitis Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 7

Etiology and Pathophysiology § Biliary cirrhosis • Associated with chronic biliary obstruction • Diffuse fibrosis of liver with jaundice § Cardiac cirrhosis • From long-standing severe right-sided heart failure Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 8

Clinical Manifestations Early manifestations • Onset usually insidious • GI disturbances: § Anorexia § Dyspepsia § Flatulence § Nausea/vomiting § Change in bowel habits Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 9

Clinical Manifestations Early manifestations (cont’d) • Abdominal pain • Fever • Lassitude • Weight loss • Enlarged liver or spleen Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 10

Clinical Manifestations Late manifestations • Two causative mechanisms § Hepatocellular failure § Portal hypertension Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 11

Pathophysiology of Cirrhosis Fig. 44 -5. Continuum of liver dysfunction in cirrhosis and resulting manifestations. ADH, Antidiuretic hormone; ALT, alanine aminotransferase; AST, aspartate transaminase. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 12

Clinical Manifestations Fig. 44 -6. Systemic clinical manifestations of liver cirrhosis. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 13

Clinical Manifestations Late manifestations (cont’d) • Jaundice § Decreased ability of liver cells to conjugate and excrete bilirubin § Functional derangement of liver cells § Compression of bile ducts by overgrowth of connective tissue Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 14

Clinical Manifestations Jaundice (cont’d) § Minimal or severe, depending on liver damage § Late stages of cirrhosis • Patient usually will be jaundiced. § If biliary tract obstructed, pruritus can occur. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 15

Clinical Manifestations • Skin lesions § Due to increase in circulating estrogen caused by inability of liver to metabolize steroid hormones Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 16

Clinical Manifestations • Skin lesions (cont’d) § Spider angiomas • Small dilated blood vessels with bright red center and spiderlike branches • Nose, cheeks, upper trunk, neck, shoulders § Palmar erythema • Red area on palms of bands that blanches with pressure Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 17

Clinical Manifestations • Endocrine disorders § Steroid hormones of the adrenal cortex, testes, and ovaries are metabolized and inactivated by the normal liver. § Damaged liver is unable to metabolize these hormones, and various manifestations occur. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 18

Clinical Manifestations • Hematologic disorders § Splenomegaly • From backup of blood from portal vein § Bleeding tendencies • Decreased production of hepatic clotting factors Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 19

Clinical Manifestations • Peripheral neuropathy § Dietary deficiencies of thiamine, folic acid, and cobalamin (vitamin B 12) Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 20

Complications • Portal hypertension • Esophageal and gastric varices • Peripheral edema and ascites • Hepatic encephalopathy • Hepatorenal syndrome Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 21

Complications Portal hypertension • Characterized by § Increased venous pressure in portal circulation § Splenomegaly § Ascites § Large collateral veins § Esophageal varices § Systemic hypertension Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 22

Complications Portal hypertension (cont’d) • Primary mechanism is increased resistance to blood flow through the liver. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 23

Complications Portal hypertension (cont’d) • Esophageal varices § Complex of tortuous veins at lower end of esophagus § Develop in areas where collateral and systemic circulations communicate Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 24

Complications • Esophageal varices (cont’d) § Contain little elastic tissue and are fragile § Bleeding esophageal varices • Most life-threatening complication of cirrhosis § 80% of variceal hemorrhages Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 25

Complications Portal hypertension (cont’d) • Gastric varices § Located in upper portion of stomach § 20% of variceal hemorrhages Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 26

Complications Portal hypertension (cont’d) • Internal hemorrhoids § Occur because of the dilation of the mesenteric veins and rectal veins • Caput medusae § Ring of varices around the umbilicus Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 27

Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 28

Complications Peripheral edema and ascites • Edema § ↓ Colloidal oncotic pressure from impaired liver synthesis of albumin § ↑ Portacaval pressure from portal hypertension § Occurs as ankle/presacral edema Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 29

Complications Peripheral edema and ascites (cont’d) • Ascites § Accumulation of serous fluid in peritoneal or abdominal cavity § Abdominal distention with weight gain § Common manifestation of cirrhosis Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 30

Ascites Fig. 44 -7. Mechanisms for development of ascites. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 31

Gross Ascites Fig. 44 -8. Gross ascites. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 32

Complications • Ascites (cont’d) § Factors involved in the pathogenesis • ↓ Serum colloidal oncotic pressure • ↑ Levels of aldosterone • Portal hypertension • ↑ Flow hepatic lymph • Impaired water excretion Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 33

Complications Hepatic encephalopathy • Neuropsychiatric manifestation • Terminal complication in liver disease Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 34

Complications Hepatic encephalopathy (cont’d) • Etiologic factors § Disorder of protein metabolism and excretion • Liver unable to convert ammonia to urea, or blood shunted past liver through, so ammonia stays in systemic circulation • Ammonia crosses blood-brain barrier and causes neurologic toxic manifestations. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 35

Complications Hepatic encephalopathy (cont’d) • Etiologic factors (cont’d) § Altered astrocyte function • Regulate blood-brain barrier and detoxification of ammonia Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 36

Complications Hepatic encephalopathy (cont’d) • Clinical manifestations § Changes in neurologic and mental responsiveness • Ranging from sleep disturbance to lethargy to deep coma Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 37

Complications Hepatic encephalopathy (cont’d) • Grading system used to classify stages § Stages 0 through 4 § 4 is most advanced. • Asterixis § Characteristic symptom § Flapping tremors involving arms and hands Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 38

Complications Hepatic encephalopathy (cont’d) • Fetor hepaticus § Musty, sweet odor on patient’s breath § Accumulation of digestive by-products that liver is unable to degrade Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 39

Complications Hepatorenal syndrome • Serious complication of cirrhosis • Functional renal failure with § Azotemia § Oliguria § Intractable ascites Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 40

Complications Hepatorenal syndrome (cont’d) • No structural abnormality of kidney • Splanchnic and systemic vasodilation and ↓ arterial blood volume § Renal vasoconstriction occurs with renal failure. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 41

Diagnostic Studies • History/physical examination • Laboratory tests § Liver function tests § Serum electrolytes § CBC Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 42

Diagnostic Studies • Laboratory tests (cont’d) § Prothrombin time § Serum albumin § Stool for occult blood § Analysis of ascitic fluid • Liver biopsy Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 43

Collaborative Care • Rest • Administration of B-complex vitamins • Avoidance of alcohol, aspirin, acetaminophen, and NSAIDs • Management of ascites Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 44

Collaborative Care • Prevention and management of esophageal variceal bleeding • Management of encephalopathy Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 45

Collaborative Care • Ascites § High-carbohydrate, low-Na+ diet (2 g/day) § Diuretics § Paracentesis • Removes fluid from abdominal cavity • Temporary measure Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 46

Collaborative Care • Ascites (cont’d) § Peritoneovenous shunt • Continuous reinfusion of ascitic fluid from the abdomen to the vena cava • Not first-line therapy • Complications : Thrombosis, infection, fluid overload, DIC Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 47

Collaborative Care • Esophageal and gastric varices § Goal: Avoid bleeding/hemorrhage § Avoid alcohol, aspirin, and irritating foods. § Respiratory infection promptly treated Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 48

Collaborative Care § If bleeding occurs, stabilize patient, manage airway, provide IV therapy. § Drug therapy may include • Octreotide (Sandostatin) • Vasopressin (VP, Terlipressin) • Nitroglycerin (NTG) • β-adrenergic blockers Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 49

Collaborative Care • Endoscopic sclerotherapy § Treatment for acute/chronic bleeding varices § Agent (morrhuate [Scleromate]) • Thromboses and obliterates distended veins Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 50

Collaborative Care • Endoscopic ligation § Banding of varices § Fewer complications than sclerotherapy • Balloon tamponade § Controls hemorrhage by compression of varices § Uses Sengstaken-Blakemore tube Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 51

Sengstaken-Blakemore Tube Fig. 44 -9. A, Sengstaken-Blakemore tube. B, Tube inserted into esophagus and stomach. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 52

Collaborative Care • Supportive measures for acute bleed § Fresh frozen plasma § Packed RBCs § Vitamin K § Histamine receptor blockers § Proton pump inhibitors § Lactulose (Cephulac) § Neomycin Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 53

Collaborative Care • Long-term management § β-adrenergic blockers § Repeated sclerotherapy/band ligation § Portosystemic shunts § Propranolol (Inderal) Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 54

Collaborative Care • Shunting procedures § Used more after second major bleeding episode § Surgical vs. nonsurgical Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 55

Collaborative Care • Nonsurgical procedure § Transjugular intrahepatic portosystemic shunt (TIPS) • Tract (shunt) between systemic and portal venous system • Used to redirect portal blood flow • Decreases portal venous pressure and decompresses varices Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 56

Total Portal Division After TIPS Fig. 44 -10. Total portal diversion after transjugular intrahepatic portosystemic shunt (TIPS). A, Portal venogram before TIPS shows filling of large esophageal varices (arrows). B, After insertion of a TIPS, flow to varices is eliminated. Intrahepatic portal vein flow is now reversed, with the direction of intrahepatic flow toward the TIPS. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 57

Collaborative Care • Surgical procedures § Portacaval shunt • Decreases bleeding episodes • Does not prolong life; patient dies of hepatic encephalopathy Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 58

Portosystemic Shunts Fig. 44 -11. Portosystemic shunts. A, Portacaval shunt. The portal vein is anastomosed to the inferior vena cava, diverting blood from the portal vein to the systemic circulation. B, Distal splenorenal shunt. The splenic vein is anastomosed to the renal vein. The portal venous flow remains intact while esophageal varices are selectively decompressed. (The short gastric veins are decompressed. ) The spleen conducts blood from the high pressure of the esophageal and gastric varices to the low-pressure renal vein. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 59

Collaborative Care • Surgical procedures (cont’d) § Distal splenorenal shunt (Warren shunt) • Leaves portal venous flow intact • ↓ Incidence of hepatic encephalopathy • With time, blood flow to liver ↓ Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 60

Collaborative Care • Hepatic encephalopathy § Goal: Decrease ammonia formation • Sterilization of GI tract with antibiotics (e. g. , neomycin) • Lactulose (Cephulac) traps NH 3 in gut. • Cathartics/enemas § Treatment of precipitating cause Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 61

Collaborative Care • Drug therapy § No specific drug therapy § Drugs are used to treat symptoms and complications of advanced liver disease. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 62

Nutritional Therapy • Diet for patient without complications § High in calories (3000 kcal/day) § ↑ carbohydrate § Moderate to low fat § Protein restriction rarely justified Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 63

Nutritional Therapy • Protein supplements if proteincalorie malnutrition • Low-sodium diet for patient with ascites and edema Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 64

Nursing Management Nursing Assessment • Past health history • • § Chronic alcoholism § Viral hepatitis § Chronic biliary disease Physical examination Medications Weight loss Jaundice Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 65

Nursing Management Nursing Assessment • Abdominal distention • Nausea/vomiting • Altered mentation • RUQ pain • Abnormal laboratory values Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 66

Nursing Management Nursing Diagnoses • Imbalanced nutrition: Less than body requirements • Impaired skin integrity • Ineffective breathing pattern • Excess fluid volume • Dysfunctional family processes: Alcoholism Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 67

Nursing Management Planning • Overall goals § Relief of discomfort § Minimal to no complications § Return to as normal a lifestyle as possible Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 68

Nursing Management Nursing Implementation • Health promotion § Treat alcoholism. § Identify hepatitis early and treat. § Stress importance of adequate nutrition. § Identify biliary disease early and treat. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 69

Nursing Management Nursing Implementation • Acute intervention § Rest § Oral hygiene § Between-meal nourishment § Explanation of dietary restrictions Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 70

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Accurate I/O § Daily weights § Abdominal girth • Kneeling position, if possible § Extremities measurement Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 71

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Paracentesis • Patient void immediately before • High Fowler’s or side of bed • Monitor for electrolyte imbalances. • Monitor dressing for bleeding/leakage. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 72

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Check respiratory status frequently. • Semi- or high Fowler’s § Skin care • Turning schedule, at least every 2 hours § ROM exercises § Coughing/deep breathing exercises Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 73

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Monitor for electrolyte disturbances. • Diuretic therapy alters electrolytes. • Hypokalemia • Cardiac dysrhythmias, hypotension, tachycardia, muscle weakness § Observe for bleeding disorders. § Always be a supportive listener. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 74

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Bleeding varices • Close observation for signs of bleeding • Balloon tamponade care • Explanation of procedure • Check for patency. • Position of balloon verified by x-ray Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 75

Nursing Management Nursing Implementation • Acute intervention (cont’d) • Balloon tamponade (cont’d) • Saline lavage/NG suction to remove blood • Monitor for complications (i. e. , aspiration pneumonia). • Scissors at bedside • Semi-Fowler’s position • Oral/nasal care Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 76

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Hepatic encephalopathy • Maintain safe environment. • Assess carefully. • Level of responsiveness • Sensory and motor abnormalities • Fluid/electrolyte imbalances • Acid-base balance • Effects of treatment measures Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 77

Nursing Management Nursing Implementation • Acute intervention (cont’d) § Hepatic encephalopathy (cont’d) • Neurologic assessment every 2 hours • Prevention of constipation • Limited physical activity • Control of hypokalemia • Ensuring proper nutrition Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 78

Nursing Management Nursing Implementation • Ambulatory and home care § Symptoms of complications § Written instructions with adequate explanations for patient/family § When to seek medical attention § Remission maintenance § Abstinence from alcohol § Caring attitude always Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 79

Nursing Management Evaluation • Maintenance of food/fluid intake to meet needs • Maintenance of muscle tone and energy • Maintenance of skin integrity • Normalization of fluid balance Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 80

Nursing Management Evaluation • Maintenance of blood pressure and urinary output • Reports increased ease of breathing • Experiences normal respiratory rate/rhythm Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 81

Audience Response Question A patient with advanced cirrhosis with ascites is short of breath and has an increased respiratory rate. The nurse should: 1. Initiate oxygen therapy at 2 L/min to increase gas exchange. 2. Notify the health care provider so a paracentesis can be performed. 3. Ask patient to cough and deep breathe to clear respiratory secretions. 4. Place the patient in Fowler’s position to relieve pressure on the diaphragm. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 82

Case Study Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 83

Case Study • 35 -year-old woman was admitted with hepatic coma. • History of numerous hospitalizations since age 19 § Usually for psychosomatic and nervous disorders Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 84

Case Study • Denies alcoholism and having more than 3 oz of alcohol per day § States “the girls and I have social drinks” Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 85

Case Study • Review of old medical records shows progressive weakness, weight loss, anorexia, jaundice, edema, ascites, and mental disorientation. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 86

Case Study • Accepts treatment only during crises • Upon admission, she is stuporous and hypotensive, and has twitching and asterixis. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 87

Case Study • She is thin and malnourished with marked edema on lower extremities and ascites. • Liver and spleen are both palpable. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 88

Case Study • Jaundice and spider angiomas are present. • Evidence of bruising throughout body Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 89

Case Study • Previous liver biopsies indicated § At age 29, fatty liver § At age 31, cirrhosis with hyaline necrosis Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 90

Case Study • Laboratory values § Total bilirubin 11 mg/d. L § AST 80 U/m. L § ALT 70 U/m. L § LDH 700 U/m. L § Serum ammonia 220 mg/d. L § WBC 21, 450/u. L § Hematocrit 24% Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 91

Discussion Questions 1. What clinical manifestations of cirrhosis does she have? 2. Explain the results of her diagnostic findings. Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 92

Discussion Questions 3. What is the priority of care for her? 4. What patient and family teaching is essential? Copyright © 2011, 2007 by Mosby, Inc. , an affiliate of Elsevier Inc. 93