Interventions for Clients with Liver Problems

Cirrhosis Cirrhosis is extensive scarring of the liver, usually caused by a chronic irreversible reaction to hepatic inflammation and necrosis. Complications depend on the amount of damage sustained by the liver. In compensated cirrhosis, 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

Etiology Known causes of liver disease include: –Alcohol –Viral hepatitis –Autoimmune hepatitis –Steatohepatitis –Drugs and toxins –Biliary disease (Continued)

Etiology (Continued) –Metabolic/genetic causes –Cardiovascular disease

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

Clinical Manifestations In late stages, the signs vary: –Jaundice and icterus –Dry skin –Rashes –Petechiae, or ecchymoses (lesions) –Warm, bright red palms of the hands –Spider angiomas –Peripheral dependent edema of the extremities and sacrum

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

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

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. (Continued)

Laboratory Assessment (Continued) Prothrombin time prolonged; platelet count low Decreased hemoglobin and hematocrit values and white blood cell count Elevated ammonia levels Serum creatinine level possibly elevated

Surgical Interventions Peritoneovenous shunt Portocaval shunt Transjugular intrahepatic portosystemic shunt

Potential for Hemorrhage Interventions include: –Identifying the source of bleeding and initiating measures to halt it –Massive esophageal bleeding –Esophageal varices –Nonsurgical management includes: Drug therapy: possibly nonselective beta blocker Gastric intubation Esophagogastric balloon tamponade

Management of Hemorrhage Blood transfusions Endoscopic procedures Transjugular intrahepatic portal- systemic shunt Surgical management

Potential for Portal-Systemic Encephalopathy Interventions include: –Role of ammonia –Reduction of ammonia levels –Diet therapy using simple and brief guidelines –Drug therapy: Lactulose Neomycin sulfate Metronidazole

Hepatitis Widespread viral inflammation of liver cells Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis F and G are uncommon

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 (Continued)

Hepatitis A (Continued) 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 of age. Many people who have hepatitis A don’t know it; symptoms are similar to a gastrointestinal 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. (Continued)

Hepatitis B (Continued) Hepatitis carriers can infect others, even if they are without symptoms.

Hepatitis C Spread is by sharing needles, blood, blood products, or organ transplants (prior to 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 U.S.

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 Arthralgia (joint pain) Myalgia (muscle pain) Diarrhea/constipation Fever Lethargy Malaise Nausea/vomiting Pruritus

Nonsurgical Management Physical rest Psychological rest Diet therapy Drug therapy includes: –Antiemetics –Antiviral medications –Immunomodulators

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 Many clients 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

Cancer of the Liver One of the most common tumors in the world Most common complaint: abdominal discomfort Treatment includes: –Chemotherapy –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