Care of Patients with Liver Problems Chapter 61 Mrs. Kreisel MSN, RN NU130 Adult Health Summer 2011

Cirrhosis Cirrhosis is extensive scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis. Complications depend on the amount of damage sustained by the liver. In compensated cirrhosis, the liver has significant scarring but performs essential functions without causing significant symptoms.

Complications Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal-systemic encephalopathy with hepatic coma Hepatorenal syndrome Spontaneous bacterial peritonitis

Esophageal Varices

Etiology Known causes of liver disease include: Alcohol Viral hepatitis Autoimmune hepatitis Steatohepatitis Drugs and toxins Biliary disease Metabolic/genetic causes Cardiovascular disease

Clinical Manifestations In early stages, signs of liver disease include: Fatigue Significant change in weight GI symptoms Abdominal pain and liver tenderness Pruritus

Clinical Manifestations (Cont’d) In late stages, the signs vary: Jaundice and icterus (pigmentation of tissue, membranes and secreations with bile pigments) Dry skin Rashes Petechiae, or ecchymoses (lesions) Warm, bright red palms of the hands Spider angiomas: associated with cirrhosis of the liver, branched growth of dilated capillaries on the skin looking like a spider Peripheral dependent edema of the extremities and sacrum

Abdominal Assessment Massive ascites Umbilicus protrusion Caput medusae (dilated abdominal veins) Hepatomegaly (liver enlargement)

Liver Dysfunction

Other Physical Assessments Assess nasogastric drainage, vomitus, and stool for presence of blood Fetor hepaticus (breath odor) Amenorrhea Gynecomastia, testicular atrophy, impotence Bruising, petechiae, enlarged spleen Neurologic changes Asterixis ( also known as liver flap or liver tremors: abnormal involuntary jerking muscles)

Laboratory Assessment Aminotransferase serum levels and lactate dehydrogenase may be elevated. Alkaline phosphatase levels may increase. Total serum bilirubin and urobilinogen levels may rise. Total serum protein and albumin levels decrease.

Laboratory Assessment (Cont’d) 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.

Excess Fluid Volume Interventions: Nutrition therapy consists of low sodium diet, limited fluid intake, vitamin supplements. Drug therapy includes a diuretic like Lasix, electrolyte replacement. Paracentesis is the insertion of a trocar catheter into the abdomen to remove and drain ascitic fluid from the peritoneal cavity. Observe for possibility of impending shock.

Comfort Measures For dyspnea, elevate the head of the bed at least 30 degrees, or as high as the patient wishes to help minimize shortness of breath. Patient is encouraged to sit in a chair. Weigh patient in standing position, because supine position can aggravate dyspnea.

Fluid and Electrolyte Management Interventions: Fluid and electrolyte imbalances are common as a result of the disease or treatment; test for: Blood urea nitrogen level Serum protein level, if low may order albumin (protein) Hematocrit level Electrolytes

Surgical Interventions Peritoneovenous shunt & Portocaval shunt are rarely done today because of serious complications. They are shunts that divert fluid away from the diseased liver into the venous system. Transjugular intrahepatic portosystemic shunt is a nonsurgical procedure done in interventional radiology. Thread a balloon through the jugular to the liver into the portal vein. Enlarge it with a balloon and insert a stent to keep it open

Potential for Hemorrhage Interventions include: Identifying the source of bleeding and initiating measures to halt it Massive esophageal bleeding Esophageal varices

Potential for Hemorrhage (Cont’d) Nonsurgical management includes: Drug therapy—possibly nonselective beta blocker Gastric intubation Esophagogastric balloon tamponade: catheter surround3d by a balloon used in the esophagus to arrest bleeding from varices. 3 lumens, one for fluids, one balloon, control of the balloon

Esophageal Gastric Tamponade

Management of Hemorrhage Blood transfusions Esophagogastric balloon tamponade Vasoactive therapy Endoscopic procedures Transjugular intrahepatic portal-systemic shunt Surgical management

Potential for Portal-Systemic Encephalopathy Interventions include: Role of ammonia: it is converted into urea in the liver and along with CO2 it becomes the final product of protein metabolism Reduction of ammonia levels High levels indicate Liver Failure Nutrition therapy using simple and brief guidelines Drug therapy: Lactulose: Empty the bowel of ammonia Neomycin sulfate Metronidazole

Hepatitis Widespread viral inflammation of liver cells can lead to Hepatic Encephalopathy (brain dysfunction due to high ammonia levels or orther liver problems. Can lead to a coma. Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Hepatitis A Similar to that of a typical viral syndrome; often goes unrecognized Spread via the fecal-oral route by oral ingestion of fecal contaminants Contaminated water, shellfish from contaminated water, food contaminated by handlers infected with hepatitis A Also spread by oral-anal sexual activity Incubation period for hepatitis A is 15 to 50 days. Disease is usually not life threatening. Disease may be more severe in individuals older than 40 years. Many people who have hepatitis A do not know it; symptoms are similar to a GI illness.

Hepatitis B 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; symptoms include anorexia, nausea and vomiting, fever, fatigue, right upper quadrant pain, dark urine, light stool, joint pain, and jaundice. Hepatitis carriers can infect others, even if they are without symptoms.

Hepatitis C Spread is by sharing needles, blood, blood products, or organ transplants (before 1992), needle stick injury, tattoos, intranasal cocaine use. Incubation period is 21 to 140 days. Most individuals are asymptomatic; damage occurs over decades. Hepatitis C is the leading indication for liver transplantation in the United States.

Hepatitis D Transmitted primarily by parenteral routes Incubation period 14 to 56 days

Hepatitis E Present in endemic areas where waterborne epidemics occur and in travelers to those areas Transmitted via fecal-oral route Resembles hepatitis A Incubation period 15 to 64 days

Clinical Manifestations Abdominal pain Changes in skin or eye color (Jaundice) Arthralgia (joint pain) Myalgia (muscle pain) Diarrhea/constipation Fever Lethargy Malaise Nausea/vomiting Pruritus (itching)

Nonsurgical Management Physical rest Psychological rest Diet therapy Drug therapy includes: Antiemetics Antiviral medications Immunomodulators AVOID DRUGS METABOLISED BY THE LIVER SUCH AS TYLENOL

Fatty Liver (Steatohepatitis) Fatty liver is caused by the accumulation of fats in and around the hepatic cells. Causes include: Diabetes mellitus Obesity Elevated lipid profile Alcohol abuse Many patients are asymptomatic.

Hepatic Abscess Liver invaded by bacteria or protozoa causing abscess Pyrogenic liver abscess; amebic hepatic abscess Treatment usually involves: Drainage with ultrasound guidance Antibiotic therapy

Liver Trauma The liver is one of the most common organs to be injured in patients with abdominal trauma. Clinical manifestations include abdominal tenderness, distention, guarding, rigidity. Treatment involves surgery, multiple blood products.

Cancer of the Liver One of the most common tumors in the world Most common complaint—abdominal discomfort Treatment includes: Chemotherapy Hepatic artery embolization Hepatic arterial infusion (HAI) Surgery

Liver Transplantation Used in the treatment of end-stage liver disease, primary malignant neoplasm of the liver Donor livers obtained primarily from trauma victims who have not had liver damage Donor liver transported to the surgery center in a cooled saline solution that preserves the organ for up to 8 hours

Complications Acute, chronic graft rejection Infection Hemorrhage Hepatic artery thrombosis Fluid and electrolyte imbalances Pulmonary atelectasis Acute renal failure Psychological maladjustment

NCLEX TIME

Question 1 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 Answer: B Rationale: These laboratory values are congruent with hemolytic jaundice. Jaundice may be caused by intrahepatic obstruction but is not referred to as intrahepatic jaundice. In obstructive jaundice, neither stool nor urine urobilinogen are present. In hepatocellular jaundice, both stool and urine urobilinogen are either normal or increased.

Question 2 A possible outcome for the patient receiving a liver transplant because of hepatitis C–induced cirrhosis is that the newly transplanted liver may Be a likely site for cancer growth in the future Make the patient more likely to develop obstructive jaundice in the future Become re-infected with the hepatitis C virus Make the patient more susceptible to develop other forms of hepatitis Answer: C Rationale: Hepatitis C–induced cirrhosis is the leading indication for liver transplantation in the United States. However, the newly transplanted liver often becomes re-infected with the virus. There is no evidence provided to indicate that the newly transplanted liver would make the patient more likely to develop other conditions such as obstructive jaundice or other forms of hepatitis.

Question 3 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 Answer: A Rationale: Ascites can increase abdominal distention, which interferes with lung expansion and compromises ventilation and oxygenation. Risk for infection, fluid displacement, and confusion are also assessment variables requiring monitoring in a patient with ascites.

Question 4 A priority intervention in the management of a patient with decompensated cirrhosis would be: Limit protein intake. Monitor fluid intake and output. Manage nausea and vomiting Elevate head of bed >30 degrees Answer: C Rationale: Decompensated cirrhosis has multiple complications. However, bleeding esophageal varies can present a life-threatening emergency. Preventing nausea and vomiting is an important intervention in the management of esophageal varices. Monitoring protein, fluid balance, and patient positioning are also important interventions in the care of the patient with end-stage liver disease.

Question 5 Which racial group is at the highest risk for developing liver cancer? Caucasian African American Asian Hispanic/Latino Answer: C Rationale: Liver cancer is most often seen in regions of Asia and the Mediterranean area. Worldwide, it kills about 1 million people each year, with the highest prevalence in Asian individuals. Black and Hispanic populations have twice the rate of the disease as Euro-Americans, and older adults are affected more than other age-groups. Source: www.nci.nih.gov/cancer