Chapter 49Assessment and Management of Patients With Hepatic Disorders

Question Which diuretic medication would most often be used for a patient with ascites?

Actazolamide (Diamox) Ammonium chloride Furosemide (Lasix) Spironolactone (Aldactone) Answer Spironolactone (Aldactone) Spironolactone (Aldactone) is most often the first-line therapy in patients with ascites from cirrhosis. Oral diuretics such as furosemide (Lasix) may be added but should be used cautiously. Ammonium chloride and acetazolamide (Diamox) are contraindicated because of the possibility of precipitating hepatic coma.

Etiology Known causes of liver disease include:

Alcohol Viral hepatitis Autoimmune hepatitis Steatohepatitis Drugs and toxins Biliary disease Metabolic/genetic causes Cardiovascular disease Progression of Liver Disease

Laboratory Assessment: Liver Dysfunction

Aminotransferase (ALT, AST) serum levels and lactate dehydrogenase (LDH) may be elevated. Alkaline phosphatase levels may increase. Total serum bilirubin and urobilinogen levels may rise. Total serum protein and albumin levels decrease. Prothrombin time is prolonged; platelet count is low. Hemoglobin and hematocrit values and white blood cell count are decreased. Ammonia levels are elevated. Serum creatinine level is possibly elevated. PTT PT and INR Liver Function Tests Alanine aminotranferase (ALT) Aspartate aminotransferase (AST) Alkaline phosphatase (ALP) Gamma-glutamyltransferase (GGT) Lactic dehydrogenase (LDH5) Serum bilirubin Total Conjugated - 0.3mg/dl Unconjugated - 0.9mg/dl Tests to determine Liver Function Tests for viral antigens CBC Coagulation studies Serum Albumin Serum ammonia Abdominal ultrasound Esophagoscopy Liver biopsy Ammonia Liver Biopsy Pre Prothrombin Time & platelet count May need to give Vitamin K Client voids prior to procedure Supine Position Local anesthetic Have client hold breath during needle insertion

Question Is the following statement true or false? The majority of blood supply to the liver, which is poor in nutrients, comes from the portal vein.

Answer False The majority of blood supply to the liver, which is rich in nutrients from the gastrointestinal tract, comes from the portal vein.

Question Is the following statement true or false? Only persons with hepatitis B are at risk for hepatitis D.

Answer True Only persons with hepatitis B are at risk for hepatitis D. Clinical Manifestations Abdominal pain Changes in skin or eye color Arthralgia (joint pain) Myalgia (muscle pain) Diarrhea/constipation Fever Lethargy Malaise Nausea/vomiting Pruritus Hepatitis Nonsurgical Management Physical rest Psychological rest Diet therapy Drug therapy includes: Antiemetics Serotonin (5HT3) Antagonists (granisetron - Kytril; ondansetron - Zofran) Dopamine Antagonists (prochlorperazine - Compazine; promethazine - Phenergan; metoclopramide - Reglan) Antiviral medications Oral ribavirin (Copegus, Rebetol) daily Immunomodulators Pegylated interferon alpha-2b (PEG-Intron) weekly Reduces replication of virus and increases immunity Hepatitis Vaccines Vaccines for hepatitis A & B Hepatitis A prophylaxis - immune globulin Hepatitis B prophylaxis - immune globulin Disease Process: Hepatitis Chronic Hepatitis Chronic infection Elevated liver enzymes Symptoms Causes cirrhosis and liver cancer

Question Is the following statement true or false?

Bleeding esophageal varices result in an increase in renal perfusion. Answer False Bleeding esophageal varices do not result in an increase in renal perfusion. Bleeding esophageal varices result in a decrease in renal perfusion. Endoscopic Sclerotherapy Esophageal Banding Balloon Tamponade: Sengstaken-Blakemore Tube Portal Systemic Shunts

Obstructive

Dark orange-brown urine, clay-colored stools Dyspepsia and intolerance of fats, impaired digestion Pruritus Signs and Symptoms - Hepatocellular and Obstructive Jaundice Hepatocellular Patient may appear mildly or severely ill. Lack of appetite, nausea, weight loss Headache, chills, and fever if infectious in origin Malaise, fatigue, weakness Obstructive Dark orange-brown urine and light clay-colored stools Pruritus Dyspepsia and intolerance of fats, impaired digestion Liver Dysfunction Portal Hypertension Obstructed blood flow through the liver results in increased pressure throughout the portal venous system Results in Ascites Esophageal varices Ascites: Fluid in Peritoneal Cavity—Causes Portal hypertension resulting in increased capillary pressure and obstruction of venous blood flow Vasodilatation of splanchnic circulation (blood flow to the major abdominal organs) Changes in the ability to metabolize aldosterone, increasing fluid retention Decreased synthesis of albumin, decreasing serum osmotic pressure Movement of albumin into the peritoneal cavity Ascites Assessment of Ascites Record abdominal girth and weight daily Patient may have striae, distended veins, and umbilical hernia Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave Monitor for potential fluid and electrolyte imbalances Abdominal Assessment Massive ascites Umbilicus protrusion Caput medusae dilated abdominal veins

NCLEX Question Which of the following is not considered an age-related change of the hepatobiliary system?

Decreased drug metabolism Increased blood flow Decreased liver weight Increased prevalence of gallstones Review of Anatomy and Physiology Largest gland of the body Located in the upper right abdomen A very vascular organ that receives blood from GI tract via the portal vein and from the hepatic artery

Liver and Biliary System Section of a Liver Lobule Assessment and Metabolic Function Studies

Glucose metabolism Ammonia conversion Protein metabolism Fat metabolism Vitamin and iron storage Bile formation, Bilirubin excretion Drug metabolism Health history, gerontologic changes, refer to Chart 49-1 OTC medications Pallor, jaundice Petechiae, erythema, angiomas Gynecomastia Neurologic status

NCLEX Question Which of the following types of hepatitis is spread by poor sanitation?

Hepatitis C Hepatitis B Hepatitis A Hepatitis D

Signs and Symptoms Associated With Hepatocellular and Obstructive Jaundice

Hepatocellular Mild or severely ill Lack of appetite, nausea or vomiting, weight loss Malaise, fatigue, weakness Headache, chills, fever, infection

NCLEX Question These laboratory results are expected with which type of jaundice?

Indirect serum bilirubin: Increased Direct serum bilirubin: Normal Stool urobilinogen: Increased Urine urobilinogen: Increased Intrahepatic Hemolytic Obstructive Hepatocellular

NCLEX Question Which of the following treatment modalities exert pressure directly to bleeding sites in the esophagus and stomach?

Injection sclerotherapy Portal-systemic shunt Pitressin Balloon tamponade Balloon tamponade Nursing Management Monitor frequently for aspiration, changes in vital signs, emotional responses, and cognitive status Monitor for associated complications: hepatic encephalopathy resulting from blood breakdown in the GI tract and delirium related to alcohol withdrawal Oral care, tube care, and GI suctioning Implement measures to reduce anxiety and agitation Education and support of patient and family

Hepatic Encephalopathy and Coma

Life-threatening complications: accumulation of ammonia and other toxic metabolites in the blood Stages: refer to Table 49-3 Assessment EEG Changes in LOC Potential seizures Fetor hepaticus Monitor fluid, electrolyte, and ammonia levels Hepatic Encephalopathy and Coma A life-threatening complication of liver disease. May result from the accumulation of ammonia and other toxic metabolites in the blood. Late Signs and Symptoms: Constructional Apraxia Babinski's response Hypereflexia Lethargy Seizures Agitation Stupor leading to coma Effects of Constructional Apraxia Asterixis When the arms and hands are outstretched, the hands suddenly drop, then resume their original position The movements are repetitive, coarse, slow, and not rhythmic Hepatic Encephalopathy and Coma Assessment EEG Changes in level of consciousness; assess neurologic status frequently Potential seizures Fetor hepaticus Monitor fluid, electrolyte, and ammonia levels. Medical Management Eliminate precipitating cause Lactulose to reduce serum ammonia levels IV glucose to minimize protein catabolism Protein restriction Reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics Discontinue sedatives analgesics and tranquilizers Monitor or treat complications and infections Medications Avoid liver toxic drugs Diuretics Lactulose & Neomycin Beta blockers Ferrous sulfate Vitamin K Antacids

Additional Diagnostic Studies

Liver biopsy Ultrasonography CT MRI Other

Functions of the Liver

Metabolism & elimination of bilirubin Metabolism of carbohydrates, protein, and fat Metabolizes steroid hormones Metabolizes drugs Detoxifies alcohol & drugs Functions of the Liver (cont) Synthesizes blood proteins Converts ammonia to urea Produces bile Stores minerals and fat soluble vitamins Stores glycogen

Hepatic Dysfunction Acute or chronic, cirrhosis of the liver

Most common cause is malnutrition related to alcoholism Infection Anoxia Metabolic disorders Nutritional deficiencies Hypersensitivity states Manifestations Jaundice Portal hypertension, ascites, and varices Hepatic encephalopathy or coma Nutritional deficiencies Clinical Manifestations: Early Stages Fatigue Significant change in weight GI symptoms Abdominal pain and liver tenderness Pruritus Clinical Manifestations: Late Stages Jaundice (skin yellowing) and icterus (sclera) Dry skin Rashes Petechiae (pinpoint) or ecchymoses (large) Warm, bright red palms of the hands (palmar erythema) Clinical Manifestations: Late Stages Spider angiomas (nose, cheeks, upper thorax) Peripheral dependent edema of the extremities and sacrum Clubbing of nails Fixed flexion of fingers Jaundice Yellow- or green-tinged sclera and skin caused by increased serum bilirubin levels Hemolytic, hepatocellular, obstructive Hereditary hyperbilirubinemia Hepatocellular and obstructive jaundice are most associated with liver disease

Other Liver Disorders

Nonviral hepatitis Toxic hepatitis Drug-induced hepatitis Fulminant hepatic failure Hepatic Cirrhosis Types Alcoholic Postnecrotic Biliary Pathophysiology: refer to Table 49-5 Manifestations: liver enlargement, portal obstruction, ascites, GI varices, edema, vitamin deficiency, anemia, mental deterioration; refer to Chart 49-11

Bleeding of Esophageal Varices

Occurs in about one third of patients with cirrhosis and varices First bleeding episode has a mortality rate of 30% to 50% Manifestations include hematemesis, melena, general deterioration, and shock Patients with cirrhosis should undergo screening endoscopy every 2 years Esophageal Varices Thin walled dilated veins in esophagus Bleeding Esophageal Varices Treatment of Bleeding Varices  Treat for shock; administer oxygen IV fluids, electrolytes, volume expanders, blood and blood products Vasopressin, somatostatin, octreotide to decease bleeding Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction Propranolol and nadolol to decrease portal pressure; used in combination with other treatment Treat Bleeding Varices Avoid irritating substances Avoid straining Blood transfusion Vasoconstrictive medications Endoscopic banding Endoscopy sclerosing Balloon tamponade

Hepatitis D

Only persons with hepatitis B are at risk Blood and sexual contact transmission Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis

Hepatomegaly liver enlargement

Other Physical Assessments Assess nasogastric drainage, vomitus, and stool for presence of blood Fetor hepaticus (fruity or musty breath odor) Amenorrhea Gynecomastia, testicular atrophy, impotence Bruising, petechiae, enlarged spleen Neurologic changes Asterixis (liver flap) Treatment of Ascites Low-sodium diet Diuretics Bed rest Paracentesis Administration of salt-poor albumin Transjugular intrahepatic portosystemic shunt (TIPS) TIPS Paracentesis Insertion of trochar into the abdomen to drain fluid Empty bladder prior to procedure May cause hypovolemia Depletes protein and potassium

Liver Biopsy

Post Direct pressure Right side x 2-3 hours Monitor VS Q15"x4, Q30"x2, Q1'x4, then QS Avoid coughing, lifting, straining For 6 weeks

Cancer of the Liver

Primary liver tumors Associated with hepatitis B and C Hepatocellular carcinoma (HCC) Liver metastasis Few cancers originate in the liver Frequent site of metastatic cancer Manifestations Dull persistent pain, RUQ, back or epigastrium Weight loss, anemia, anorexia, weakness Jaundice, bile ducts occluded, ascites or obstructed portal veins Nonsurgical Management of Liver Cancer Underlying cirrhosis, which is prevalent in patients with liver cancer, increases risks of surgery Major effect of nonsurgical therapy may be palliative Radiation therapy Chemotherapy Percutaneous biliary drainage Other nonsurgical treatments Surgical Management of Liver Cancer Treatment of choice for HCC if confined to one lobe and liver function is adequate Liver has regenerative capacity Types of surgery Lobectomy Cryosurgery Liver transplant Liver Transplant Nursing Care of the Patient Undergoing a Liver Transplantation Preoperative nursing interventions Postoperative nursing interventions Patient teaching Ethical dilemma: refer to Chart 49-13 Caregiver stress: refer to Chart 49-14

Liver Function Studies

Serum aminotransferase: AST, ALT, GGT, GGTP, LDH Serum protein studies Direct and indirect serum bilirubin, urine bilirubin, and urine bilirubin and urobilinogen Prothrombin time Serum alkaline phosphatase Serum ammonia Cholesterol

NCLEX Question Which assessment parameter requires immediate intervention in a patient with severe ascites?

Shallow respirations, rate 36 breaths/min Low-grade fever Confusion Tachycardia, rate 110 beats/min

Hepatitis A

Spread by poor hand hygiene; fecal-oral Incubation: 15 to 50 days Illness may last 4 to 8 weeks Mortality rate is 0.5% for those younger than age 40 years and 1% to 2% for those older than age 40 years Manifestations: mild flulike symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen Management of Hepatitis A Prevention Good handwashing, safe water, and proper sewage disposal Vaccine Refer to Chart 49-7 Immunoglobulin for contacts to provide passive immunity Bed rest during acute stage Nutritional support

Cirrhosis

The end stage of chronic liver disease Causes Alcoholism Chronic hepatitis B or C Prolonged biliary obstruction Manifestations of Cirrhosis Early Hepatomegaly Dull RUQ ache Weight loss Weakness Anorexia Change in bowel habits Manifestations (cont) Increasingly impaired metabolism Bleeding & low platelets Ascites & edema Hormonal changes Jaundice Neurologic changes Anemia - low RBC's Low WBC's Pathophysiology Hepatocytes are damaged and replaced by fibrous scar tissue Liver looses metabolic functions Fibrous tissue forms constrictive bands cutting off blood flow and bile flow Portal hypertension develops Nursing Process: The Care of the Patient With Cirrhosis of the Liver—Assessment Focus: onset of symptoms, history of precipitating factors Alcohol use or abuse Dietary intake and nutritional status Exposure to toxic agents and drugs Assess changes in mental status, ADL and IADLs, job and social relationships Monitor signs and symptoms related to bleeding; changes in fluid volume and laboratory data Nursing Process: The Care of the Patient With Cirrhosis of the Liver—Diagnosis Activity intolerance Imbalanced nutrition Impaired skin integrity Risk for injury and bleeding Collaborative Problems and Complications of Cirrhosis of the Liver Bleeding and hemorrhage Hepatic encephalopathy Fluid volume excess Complications Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal-systemic encephalopathy with hepatic coma Hepatorenal syndrome Spontaneous bacterial peritonitis Nursing Process: The Care of the Patient With Cirrhosis of the Liver—Planning Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications Activity Intolerance Rest and supportive measures Positioning for respiratory efficiency Oxygen Planned mild exercise and rest periods Address nutritional status to improve strength Measures to prevent hazards of immobility Imbalanced Nutrition I&O Encourage small frequent meals High-calorie diet, sodium restriction Protein modified or restricted if patient is at risk for encephalopathy Supplemental vitamins, minerals, B complex, provide water-soluble forms of fat-soluble vitamins if patient has steatorrhea Consider patient preferences Other Interventions Impaired skin integrity Frequent position changes Gentle skin care Reduce scratching related to pruritus Risk for injury Prevent falls, trauma related to risk for bleeding

Hepatitis C

Transmitted by blood and sexual contract, including needle sticks and sharing of needles The most common bloodborne infection A cause of one third of cases of liver cancer and the most common reason for liver transplant Risk factors: refer to Chart 49-10 Incubation period is variable Symptoms are usually mild Chronic carrier state frequently occurs Management of Hepatitis C Antiviral medications: interferon, ribavirin (Rebetol) Measures to reduce spread of infection as with hepatitis B Alcohol potentiates disease; medications that effect the liver should be avoided Prevention: public health programs to decrease needle sharing among drug users Screening of blood supply Safety needles for health care workers

Hepatitis E

Transmitted by fecal-oral route, Incubation period. 15 to 65 days Resembles hepatitis A; self-limiting, abrupt onset, not chronic

Hepatitis B

Transmitted through blood, saliva, semen, and vaginal secretions; sexually transmitted; transmitted to infant at the time of birth A major worldwide cause of cirrhosis and liver cancer Risk factors: refer to Chart 49-9 Long incubation period: 1 to 6 months Manifestations: insidious and variable; similar to hepatitis A Hepatitis B Most common Transmission by exposure to blood or body fluids Onset acute, symptoms more severe Most recover Can be fulminant (occurs suddenly and quickly, and is intense and severe to the point of lethality) and become chronic Spread is via: unprotected sexual intercourse with an infected partner sharing needles accidental needle sticks blood transfusions Hemodialysis maternal-fetal route Symptoms occur in 25 to 180 days after exposure and include: Anorexia Nausea and vomiting Fever Fatigue RUQ pain dark urine light stool joint pain Jaundice Hepatitis carriers can infect others, even if they are without symptoms. Management of Hepatitis B Medications for chronic hepatitis type B include alpha interferon and antiviral agents: lamivudine (Epivir), adefovir (Hepsera) Bed rest and nutritional support Vaccine: for persons at high risk, routine vaccination of infants Passive immunization for those exposed Standard precautions and infection control measures Screening of blood and blood products

Hepatitis

Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes. A and E: fecal-oral route B and C: bloodborne D: only people with hepatitis B are at risk Hepatitis G and GB virus-C Nonviral hepatitis: toxic and drug induced Refer to Table 49-4

Hepatitis Widespread viral inflammation of liver cells

Widespread viral inflammation of liver cells Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E