NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE

NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER Spring 2009

TOPICS TO BE REVIEWED • • HEPATITIS CIRRHOSIS STEATOHEPATITIS (FATTY LIVER) HEPATIC ABSCESS LIVER TRAUMA CANCER OF LIVER TRANSPLANT

NORMAL FUNCTION OF LIVER MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism • Maintains normal serum glucose levels • Ammonia conversion • Protein metabolism • Fat metabolism • Vitamin and Iron storage • Drug metabolism and detoxification

LIVER FUNCTION: GLUCOSE METABOLISM • • • What happens to glucose in the liver? Where is it stored? When is it released? What is gluconeogenesis? When does it take place?

LIVER FUNCTION: AMMONIA CONVERSION • When gluconeogenesis takes place what is the byproduct of the process? • What happens to the byproduct? • What do the bacteria in the intestines produce as a byproduct? • How is this byproduct removed?

LIVER FUNCTION: PROTEIN METABOLISM • What is the liver’s job in terms of synthesizing plasma proteins? • What does the liver need to complete it’s job?

LIVER FUNCTION: FAT METABOLISM • What is the liver’s job in terms of fat metabolism? • When does the liver do this? • What are the results of this metabolism used for?

LIVER FUNCTION: VITAMIN & IRON STORAGE • Stores which fat soluble vitamins? • What other vitamins are stored in the liver? • What are these vitamins responsible for? • Which minerals are stored in the liver?

LIVER FUNCTION: DRUG METABOLISM and DETOXIFICATION • THE FOLLOWING CLASSIFICATION OF DRUGS ARE METABOLIZED BY THE LIVER? • What else is metabolized by the liver? • What does the liver do in terms of detoxification?

NORMAL FUNCTION: bile secretion • • • What is the liver’s job with Bile? When is bile secreted? Where is Bile collected and stored? How is this related to Billirubin? When do Billirubin levels increase?

LIVER FUNCTION: PROTECTION • What does the liver’s protection function involve? • What do the cells do?

LIVER FUNCTION CONTINUED • Inactivates Hormones – Estrogen – Testoterone – Progesterone – Aldosterone – cortisol • Sinusoids store blood (about 200 -400 cc)

DISORDER OF THE LIVER HEPATITIS

Hepatitis Widespread viral inflammation of liver cells • Hepatitis A (HAV) • Hepatitis B (HBV) • Hepatitis C (HCV) • Hepatitis D (HDV) • Hepatitis E (HEV) • Hepatitis F and G are uncommon (HFV, HGV) • DRUG INDUCED HEPATITIS • Occurs as a secondary infection

Hepatitis A (HAV) • 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 (HAV)(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 (HBV) • 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 (HBV) (Continued) • Hepatitis carriers can infect others, even if they are without symptoms.

Hepatitis C (HCV) • Spread is by sharing needles, 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. • NOT TRANSMITTED BY CAUSUAL OR INTIMATE HOUSEHOLD CONTACT

Hepatitis D (HDV) • Transmitted primarily by parenteral routes • Incubation period 14 to 56 days • HDV coinfects with HBV and needs it presence to replicate

Hepatitis E (HEV) • Present in endemic areas where waterborne epidemics occur and in travelers to those areas (India, Asia, Africa, Middle East, Mexico, Central America & South America) • Also seen in travellers coming from these areas • Transmitted via fecal-oral route • Resembles hepatitis A • Incubation period 15 to 64 days

Clinical Manifestations of all Hepatitis • Abdominal pain • Changes in skin or eye color • Arthralgia (joint pain) • Myalgia (muscle pain) • Diarrhea/constipation • Wgt loss • Hepatomegaly • • Fever Lethargy/Malaise Nausea/vomiting Intolerance to fats/dyspepsia • Pruritus • CHANGES IN COLOR OF URINE AND STOOL

ASSESSMENT HEALTH HISTORY • Suspected exposure • Medical history SIGNS/SYMPTOMS • Pre-icteric stage • Icteric stage • Post-icteric stage

SIGNS/SYMPTOMS • PRE-ICTERIC STAGE • Lasts about 1 week

SIGNS AND SYMPTOMS • ICTERIC STAGE • Lasts 2 -6 weeks • Jaundice appears • Yellow skin, sclera, mucous membranes • Dark amber urine • Clay colored stools

SIGNS AND SYMPTOMS • POST-ICTERIC STAGE • Lasts 2 -6 weeks • Jaundice subsides • Liver decreases in size • Good appetite

LABORATORY TESTS FOR HEPATITIS • There will be an increase of liver enzymes and serologic markers INDICATING A PRESENCE OF HEPATITIS A, B, C

LABORATORY TESTS FOR HEPATITIS A (HAV) • Presence of hepatitis A in client: when hepatitis A (HAV) antibodies (anti-HAV) are found in the blood • Presence of immunoglobulin M(Ig. M) antibodies means that ongoing inflammation of liver present (persisits for 4 -6 wks) • Previous infection indicated by presence of immunoglbulin G (Ig. G) antibodies which provides permanent immunity to disease

LABORATORY TESTS FOR HEPATITIS B (HBV) Serologic markers which indicate client has Hepatitis B (HBV) are: • HBs. Ag (Hepatitis B surface Antigen) • Anti-HBc Ig. M (Ig. M antibodies to hepatitis B core antigen) If these levels are elevated after 6 months: chronic or carrier state Presence of antibodies to HBs. Ab (hepatitis B surface antibody): indicates recovery and immunity to hepatitis B Someone immunized will have a positive HBs. Ab

LABORATORY TESTS FOR HEPATITIS C (HCV) • ELISA (enzyme linked immunosorbent assay ) SCREENS INITIALLY & for HCV antibodies (anti. HCV): can detect antibodies in 4 wks • RIBA: (recumbent immunoblot assay): used to confirm that client has been exposed and has developed antibody • HCV PCR (HCV polymerase chain reaction test): confirms presence of circulating active virus

LABORATORY TEST FOR HEPATITIS D (HDV) • Presence of virus confirmed by identification of intrahepatic delta antigen • Also by rise in hepatitis D virus antibodies (anti-HDV) titer • Found within a few days of infection

LBORATORY TESTS FOR HEPATITIS E (HEV) • VIRUS CANNOT BE DETECTED • Presence of hepatitis E antibodies (anti. HEV) is found in people infected with virus

LABORATORY TESTS CONTINUED • A person having a previous infection is indicated by immunoglobulin G (Ig. G) antibodies. They persist in blood and provide permanent immunity to HAV

LABORATORY TESTS INDICATING HEPATITIS TESTS WHICH ARE LOWERED: • Leukocytes (leukopenia) • Serum albumin • Serum glucose (hypoglycemia) • PT (prolonged) TESTS WHICH ARE ELEVATED: • serum bilirubin • Bilirubin in urine • ALT • AST • Alkaline phosphatase elevated or may be normal

Nonsurgical Management • Physical rest • Psychological rest • Drug therapy includes: – – Antiemetics Antiviral medications Immunomodulators Corticosteroids • DECREASE # MEDS TO ALLOW LIVER TO REST

DRUGS • ANTIVIRALS: – Lamivudine (Epivir-HBV) – Adefovir dipivoxil (Hepsera) • USED: to destroy Hepatitis B virus in chronic disease • SIDE EFFECTS: alters renal function; granulocytopenia

DRUGS IMMUNOMODULATING DRUGS: – Interferon(peginterferon alfa-2 a) (Pegasys) – Oral ribavirin (Virazole)

NURSING CARE Diet therapy • Hydration • No alcohol • Low fat, moderate protein, high CHO diet, high calorie • Small frequent meals • Vit B, C, K

PATIENT EDUCATION • Prevention to health care professionals • Knowledge of transmission routes • Proper personal hygiene and good sanitation • Gamma Globulin • Avoid sex until antibody results (negative) • Hepatitis A Vaccine • Hepatitis B vaccine • No vaccine for Hepatitis E • Hepatitis C mainly spread through blood transfusions: (screen blood products)

CIRRHOSIS DEFINED • • Chronic Degenerative Causes liver enlargement Causes loss of normal liver function

PATHOPHYSIOLOGY • Fibrotic bands of connective tissue change the structure of the liver • Inflammation causes degeneration and destruction of liver cells • Tissue becomes nodular • Nodules block bile ducts and normal blood flow throughout the liver • Blood flow changes occur from compression by the fibrous tissue

TYPES OF CIRRHOSIS • Laennec’s cirrhosis: chronic ETOH, nutritional deficiencies • Biliary • Postnecrotic cirrhosis: hepatic necrosis • Cardiac: congestion and tissue damage due to heart failure

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

EARLY SIGNS AND SYMPTOMS CIRRHOSIS • • • Same for all types regardless of the cause Start out vague, like flu General weakness, Fatigue Anorexia, Indigestion Abnormal bowel function (constipation, or diarrhea) Abdominal pain/liver tenderness

LATE S & S • Jaundice, pruritus, dry skin, warm bright red palms of hands (palmar erythema), rashes • Edema, ascites, significant wgt change, peripheral dependent edema extremities and sacrum • Bleeding tendencies/Anemia/petecchiae, echymosis • Infections • Menstrual irreg/gynecomastia/impotence • Renal failure/dark amber urine • Clay colored stools

ASSESSMENT INSPECTION: • Jaundice • Caput medusae: dilated abd veins, • striae, • spider angiomas • Contour of abdomen: Distension: massive ascites • Everted umbilicus (umbilicus protrusion) • HEPATOMEGALY, SPLENOMEGALY

Other Physical Assessments • Assess nasogastric drainage, vomitus, and stool for presence of blood • Fetor hepaticus (breath odor) • Amenorrhea • Gynecomastia, testicular atrophy, impotence • Neurologic changes: changes in LOC, leading to coma, Asterixis

HOW TO ELICIT ASTERIXIS • • Have client extend the arm, dorsiflex the wrist Extend the fingers OBSERVE rapid non-rhythmic extensions and flexions

Laboratory Assessment • AST: Aminotransferase serum levels and LDH: lactate dehydrogenase may be elevated from hepatic cell destruction. • Alkaline phosphatase levels may increase from obstructive jaundice. • Total serum bilirubin from hepatic disease and urobilinogen levels may rise from hepatocellular obstruction or liver disease. • decrease. (Continued)

Laboratory Assessment (Continued) • Fecal urobilinogen is decreased due to obstructive liver disease • Total serum protein and albumin levels decreased • Prothrombin time prolonged; platelet count low • Decreased hemoglobin and hematocrit values due to anemia and white blood cell count

LABORATORY ASSESSMENT CONTINUED • Elevated ammonia levels: liver cannot excrete ammonia • BUN and Serum creatinine level possibly elevated due to decreased renal function

COMPLICATIONS: PORTAL HYPERTENSION • Increase pressure in portal vein • Comes from obstruction of blood flow from pressure by CT bands (see patho) • New channels looked for • Blood flows back to spleen (splenomegaly) • Veins become dilated (esophagus, stomach, intestines, abdomen, rectum)

PORTAL HYPERTENSION (CONTINUED) • Results in: – Ascites – Esophageal varices – Prominent abdominal veins (caput medusae) – hemorroids

COMPLICATION: ASCITES DEFINED AS: • Accumulation of free fluid within the peritoneal cavity • With increased hydrostatic pressure from portal hypertension fluid leaks into peritoneal cavity • Albumin in fluid hypoalbuminemia

ASCITES CONTINUED • • • Hypovolemia renal vasoconstriction Renin-angiotensin system triggered Sodium and water retention Leads to increased hydrostatic pressure Perpetuates the cycle of ASCITES

COMPLICATIONS ASCITES: • Bed rest, HOB up 30 degrees or higher; or sitting in chair • Abdominal girth measurements • bid wgts standing • Strict fluid restriction; strict I & O, vitamin supplements • Salt free diet/diuretics/electrolyte replacement

Excess Fluid Volume (Continued) Paracentesis is insertion of trocar catheter into abdomen to remove & drain fluid from the peritoneal cavity. – Observe for possibility of impending shock, electrolyte imbalances: albumin IV.

EXCESS FLUID SURGICAL MANAGEMENT CONTINUED – LAVEEN SHUNT (peritoneovenous shunt): surgical procedure, tube placed in peritoneal cavity, drain fluid into superior vena cava – PORTACAVAL SHUNT: (See p 1378 fig 62. 4) surgical shunting diverts portal venous blood flow from the liver TIPS (transjugular intrahepatic portalsystemic shunt): non surgical procedure creating a connection within the liver between the portal and systemic circulation to reduce portal pressure

COMPLICATION: BLEEDING ESOPHAGEAL VARICES DEFINED: fragile thin walled esophageal veins become distended from pressure Portal hypertension blood backs up from liver to esophageal and gastric vessels

COMPLICATIONS ESOPHAGEAL VARICES MEDICAL EMERGENCY LIFE THREATENING S&S: hematemesis, melena, shock Can occur spontaneously Can be caused by any activity that Abdominal pressure

TREATMENT OF BLEEDING ESOPHAGEAL VARICES • IV fluids/electrolytes/volume expander/ transfuse • ESOPHAGOGASTRIC BALLOON TAMPONADE: via Sengstaken. Blakemore tube – Compressing bleeding vessels with this tube

SENGSTAKEN-BLAKEMORE TUBE Used to control bleeding • Esophageal balloon • Gastric balloon • 3 lumens – 1 for gastric lavage – 1 for inflating the esophageal balloon – 1 for inflating the gastric balloon

SENGSTAKEN-BLAKEMORE TUBE: NRSG CARE • MD inserts tube with HOB 30 -45 degrees MOST SERIOUS COMPLICATION: ASPIRATION AND AIRWAY OCCLUSION SURGICAL SCISSORS AT BEDSIDE • Monitor for respiratory distress • Suction saliva from upper esophagus, nasopharynx • Check nostrils frequently, cleanse and lubricate to prevent ulceration • Removed after bldg controlled

RUPTURE OF ESOPHAGEAL VARICIES • Vasopressin: constriction arterial bed • Somatostatin: decreases bldg without vasoconstrictive effects of Vasopressin • Propranolol: beta blocker to decrease portal pressure

COMPLICATION: COAGULATION DEFECTS • synthesis of bile in liver • Prevents absorption of fat soluble vitamins (vit K) • Without vit K clotting factors are not produced • susceptible to bleeding • Abnormal PT (prolonged or )

COMPLICATION: SPLENOMEGALY • Backup of blood into spleen • Spleen destroys platelets • thrombocytopenia (first sign of liver dysfunction)

COMPLICATION: JAUNDICE • Liver cells cannot excrete bilirubin • circulating bilirubin levels LABORATORY TESTS: changes with hepatocellular jaundice Serum bilirubin (indirect and direct) Urine bilirubin Urobilinogen stool: normal to Urobilinogen urine: normal to

COMPLICATIONS: PORTAL SYSTEMIC ENCEPHALOPATHY (PSE) • Also called HEPATIC ENCEPHALOPATHY AND HEPATIC COMA SEE: neurologic symptoms Impaired LOC Impaired thinking Impaired neuromuscular disturbances ACUTE AND REVERSIBLE with early intervention CAUSED BY: elevated ammonia levels

NURSING DIAGNOSIS • • • Activity intolerance Fluid volume deficit Fluid volume excess Ineffective breathing patterns Risk for hemorrhage Risk for infection Altered nutrition Pain Sexual dysfunction

NURSING DIAGNOSIS CONTINUED • Altered thought processes • Risk for violence

NURSING CARE • • Bed rest with controlled activity, prevent clots Prevent infection (pneumonia) Assess for bleeding Treat dry itching skin: no soap, soft linens, lotions, antihistamines • Assess F & E status, bid wgts, abd girth once shift, I&O, fluid restriction, amt of dietary protein • Assess neuro status q 2 hr • Psychological support/abstinence of alcohol

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

Liver Trauma • The liver is the most common organ injured in clients with penetrating trauma of the abdomen, such as gunshot wounds and stab wounds. • 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 • LIVER BX: done in same day surgery, local anesthetic, done through skin. CRITICAL THAT COAGULATION TESTING BE DONE. MAJOR SE: hemorrhage • Most common c/o: abd discomfort • Tx 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