Hepatic and Biliary Disorders PDF

Assessment and Management of Patients With Hepatic Disorders Assessment and Management of Patients With Biliary Disorders Chapter 49 Chapter 50  Describe causes, manifestations, method of transmission...

Assessment and Management of Patients With Hepatic Disorders Assessment and Management of Patients With Biliary Disorders Chapter 49 Chapter 50  Describe causes, manifestations, method of transmission, and management of hepatitis Identify causes, pathophysiology, manifestations, and the medical management of liver cirrhosis Use the nursing process to develop care plans Objectives for a patient with liver cirrhosis. Identify causes, manifestations, and medical management of cholelithiasis and cholecystitis. Develop a nursing care plan for a patient with gall bladder disorders. Hepatic Functions Glucose metabolism Ammonia conversion Protein metabolism Fat metabolism Vitamin and iron storage Bile formation Bilirubin excretion Drug metabolism VIRAL HEPATITIS  A systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms, and cellular and biochemical changes. Viral Hepatitis Hepatitis A, B, C, D, and E. Hepatitis A and E are similar in mode of transmission Hepatitis B, C, and D share many characteristics.  Hepatitis A (HAV) Transmission Fecal–oral Spread primarily by -Poor hygiene -Hand-to-mouth contact -Close contact, or through food and fluids Incubation: 2 - 6 weeks, approximately 4 weeks Illness last 4–8 weeks, No carrier state exists, and No chronic hepatitis Mortality 0.5% for younger than age 40 and 1–2% for older adults Manifestations: Many patients are anicteric (without Later jaundice and dark urine jaundice) and symptomless. Indigestion and epigastric distress Mild flu-like symptoms Strong aversion to the taste of Low-grade fever cigarettes and other strong odors Anorexia These symptoms tend to clear as soon as the jaundice reaches its peak, perhaps 10 days after its initial appearance. Hepatitis A (HAV) Assessment and Management Assessment The liver and spleen are often moderately enlarged for a few days after onset Hepatitis A antigen may be found in the stool 7 to 10 days before illness And for 2 to 3 weeks after symptoms appear HAV antibodies are detectable in the serum when S&S appear Prevention Good hand washing, safe water, and proper sewage disposal Vaccination Immunoglobulin for contacts to provide passive immunity within 2 weeks of exposure See page 3707 Chart 49-6 HEALTH PROMOTION Hepatitis A (HAV) Assessment and Management Medical Management Bed rest during the acute stage Scheduling activity and rest Nutritional support Nursing Management Assists the patient and family in coping with the disability and fatigue Patient education about t diet, rest, follow-up blood work, and the importance of avoiding alcohol, as well as sanitation and hygiene measures  Hepatitis B (HBV) - Blood: found in: * Blood, * Saliva, TRANSMISSION * Semen * Vaginal secretions, - Mucous membranes and breaks in the skin - Transmitted to infant at the time of birth Incubation: It replicates in the liver and remains in the serum for relatively long periods, allowing transmission of the virus (1 to 6 months) Illness - Most people develop antibodies and recover spontaneously in 6 months. - 10% progress to a carrier state or develop chronic hepatitis - A major worldwide cause of cirrhosis and liver cancer - The mortality rate from acute HBV has been reported to be as high as 1%. Manifestations: Insidious and variable. loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, weakness, and may or may not Jaundice. Liver may be tender and enlarged. Spleen and posterior cervical lymph nodes may also be enlarged  RISK FACTORS Close contact with carrier of hepatitis B virus Frequent exposure to blood, blood products, or other body fluids Health care workers: hemodialysis staff, oncology and chemotherapy nurses, personnel at risk for needlesticks, operating room staff, respiratory therapists, surgeons, dentists Hemodialysis IV/injection drug use Male homosexual and bisexual activity Mother-to-child transmission Multiple sexual partners Receipt of blood or blood products (e.g., clotting factor concentrate) Recent history of sexually transmitted infection Tattooing Travel to or residence in area with uncertain sanitary conditions  Assessment and diagnostic findings The virus has antigenic particles that elicit specific antibody markers during different stages of the disease Anti-HBc—antibody to core antigen or HBV; persists during the acute phase of illness; may indicate continuing HBV in the liver Anti-HBs—antibody to surface determinants on HBV; detected during late convalescence; usually indicates recovery and development of immunity Anti-HBe—antibody to hepatitis B e-antigen; usually signifies reduced infectivity Anti-HBxAg—antibody to the hepatitis B x-antigen; may indicate ongoing replication of HBV  Prevention Preventing transmission Hepatitis B Active immunization: Vaccines for persons at high risk, routine vaccination of infants (HBV) Passive immunization for those exposed (Hepatitis B Immune Globulin) Prevention See page 3708 Chart 49-6 HEALTH PROMOTION Medical Management and Bed rest: Activities are restricted until the hepatic enlargement and Management level of serum bilirubin and liver enzymes have decreased. Gradually, increased activity is then allowed. Nutritional support - Proteins are not restricted. Protein intake should be 1.2 to 1.5 g/kg/day. Medications for chronic hepatitis type B include alpha interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)  Hepatitis C (HCV) Transmission Blood and sexual contact Spread primarily by Needle sticks Sharing of needles Sexually transmitted Incubation: 15–160 days Average: 50 days Illness chronic carrier state occurs frequently, and there is an increased risk of chronic liver disease, including cirrhosis or liver cancer Manifestations: Similar to HBV but usually mild  RISK FACTORS Children born to women infected with hepatitis C virus Health care and public safety workers after needlestick injuries or mucosal exposure to blood Multiple contacts with a hepatitis C virus–infected person Multiple sex partners, history of sexually transmitted infection, unprotected sex Past/current illicit IV/injection drug use Recipient of blood products or organ transplant before 1992 or clotting factor concentrates before 1987  Prevention Screening of blood Prevention of needle sticks for health care workers Measures to reduce spread of infection as with Hepatitis C hepatitis B Alcohol encourages the progression of the Management disease, so alcohol and medications that effect the liver should be avoided See page 3708 Chart 49-6 HEALTH PROMOTION Medical management Antiviral agents  Hepatitis D and E Hepatitis D Hepatitis E Only persons with hepatitis B are at risk Transmitted by fecal–oral route, for hepatitis D. Incubation period 15–65 days, Transmission is through blood and sexual Resembles hepatitis A and is self-limited contact. with an abrupt onset. Jaundice is almost The incubation period varies between 30 always present and 150 days No chronic form. Symptoms and treatment are similar to hepatitis B but more likely to develop liver failure and chronic active hepatitis and cirrhosis.  It results from damage to the liver’s parenchymal cells – Directly from primary liver diseases – Indirectly from either obstruction of Hepatic bile flow or instabilities of hepatic circulation. Dysfunction Acute Chronic  Hepatic Cirrhosis Cirrhosis is a chronic disease characterized by replacing normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver. Types: – Alcoholic → chronic alcoholism – Post-necrotic → acute viral hepatitis – Biliary → chronic biliary obstruction and infection Clinical manifestation Compensated Decompensated Signs and symptoms of Abdominal pain Ascites Ankle edema Clubbing of fingers cirrhosis increase in Firm, enlarged liver Continuous mild fever severity as the disease Flatulent dyspepsia Epistaxis progresses. Intermittent mild fever Gonadal atrophy Palmar erythema (reddened Hypotension palms) Jaundice Splenomegaly Muscle wasting Unexplained epistaxis Purpura (due to decreased Vague morning indigestion platelet count) Vascular spiders Sparse body hair Spontaneous bruising Weakness Weight loss White nails  Clinical manifestation Among the most common and significant symptoms of liver disease are the following: Jaundice, resulting from increased bilirubin concentration in the blood Portal hypertension, ascites, and varices, resulting from circulatory changes within the diseased liver and producing severe GI hemorrhages and marked sodium and fluid retention (ascites) Nutritional deficiencies, which result from the inability of the damaged liver cells to metabolize certain vitamins; responsible for impaired functioning of the central and peripheral nervous systems and for abnormal bleeding tendencies Hepatic encephalopathy or coma, reflecting accumulation of ammonia in the serum due to impaired protein metabolism by the diseased liver  Hepatic Cirrhosis Manifestations Jaundice Yellow- or green-tinged body tissues; sclera and skin due to increased serum bilirubin levels Types – Hemolytic – Hepatocellular – Obstructive – Hereditary hyperbilirubinemia Note Hepatocellular and obstructive jaundice are most associated with liver disease  Signs and Symptoms Associated with Jaundice Hepatocellular – May appear mildly or severely ill – Lack of appetite, nausea, weight loss – Malaise, fatigue, weakness – Headache chills and fever if infectious in origin Obstructive – Dark orange-brown urine and light clay-colored stools – Dyspepsia and intolerance of fats, impaired digestion – Pruritis  Portal Hypertension Obstructed blood flow through the liver results in increased pressure throughout the portal venous system Ascites Esophageal varices Medical management of Ascites Bed rest Dietary Modification: The goal of treatment is a negative sodium balance to reduce fluid retention. – Instruct patient to take low sodium diet. – Avoid salty foods, salted butter, and all ordinary canned and frozen foods  Medical management of Ascites Diuretics: Spironolactone (Aldactone), an aldosterone- blocking agent, is the first-line therapy in patients with ascites from cirrhosis. – It can help prevent potassium loss. Oral diuretics such as furosemide (Lasix) may be added Ammonium chloride is contraindicated (may precipitate hepatic coma). Possible complications of diuretic therapy include: – Fluid and electrolyte disturbances (hypovolemia, hypokalemia, hyponatremia, and hypochloremic alkalosis), and encephalopathy.  Medical management of Ascites Paracentesis It is the removal of fluid (ascites) from the peritoneal cavity through a puncture or a small surgical incision through the abdominal wall under sterile conditions. Large-volume (5 to 6 L) paracentesis has been shown to be a safe method for treating patients with severe ascites. Medical management of Ascites Trans-jugular intrahepatic portosystemic shunt (TIPS). TIPS is a method of treating ascites in which a cannula is threaded into the portal vein by the trans-jugular route. To reduce portal hypertension, an expandable stent is inserted to serve as an intrahepatic shunt between the portal circulation and the hepatic vein.  Assessment and Diagnostic Findings – Because the functions of the liver are complex, there are many diagnostic tests that may provide information about liver function Medical Management – The management of the patient with cirrhosis is usually based on the presenting symptoms.  Nursing management Promoting rest Improving nutritional status Rest reduces the demands on the liver and Without ascites, edema, or signs of impending increases the liver’s blood supply hepatic coma Weight and I&O are measured and recorded high-protein diet, supplemented by vitamins daily Ascites present, small, frequent meals Adjusts the patient’s position in bed for Patients with fatty stools (steatorrhea) maximal respiratory efficiency water-soluble forms of fat-soluble vitamins Oxygen therapy may be required Encourages the patient to increase activity Folic and iron are prescribed to prevent anemia. gradually Sodium restriction is also indicated to prevent Activity and mild exercise, as well as rest, are ascites. planned Patients with prolonged or severe anorexia Receive nutrients by the enteral or parenteral route  Nursing management Providing skincare – Frequent changes in position are necessary to prevent pressure ulcers. – Irritating soaps and the use of adhesive tape are avoided to prevent trauma to the skin. – Lotion may be soothing to irritated skin; – Measures to minimize scratching by the patient Reducing risk of injury – Protects from falls and other injuries. – The side rails should be in place and pads used in case the patient becomes agitated or restless. – To minimize agitation, the nurse orients the patient to time and place and explains all procedures. – The nurse instructs the patient to ask for assistance to get out of bed. – The nurse carefully evaluates any injury because of the possibility of internal bleeding.  Nursing management Monitoring and managing potential complications – Bleeding and hemorrhage – Hepatic encephalopathy – Fluid volume excess Promoting home and community-based care – Educating Patients About Self-Care – Continuing and Transitional Care Page 3739 - 3741  Nursing Diagnosis Ineffective breathing pattern related to ascites and restriction of thoracic excursion secondary to ascites, abdominal distention, and fluid in the thoracic cavity Activity intolerance related to fatigue, lethargy, and malaise Fluid volume excess related to ascites and edema formation Imbalanced nutrition: less than body requirements, related to abdominal distention and discomfort and anorexia Impaired skin integrity related to pruritus from jaundice and edema Chronic pain and discomfort related to enlarged tender liver and ascites Chart 49 – 11 PLAN OF NURSING CARE The Patient With Impaired Liver Function (p. 3732 – 3739) Assessment and Management of Patients With Biliary Disorders  Biliary System Several disorders affect the biliary system and interfere with the normal drainage of bile into the duodenum. These disorders include: Inflammation of the biliary system and carcinoma that obstructs the biliary tree. Gallbladder disease with gallstones – Is the most common disorder of the biliary system. Cholecystitis: acute inflammation of the gallbladder – More than 90% of patients with acute cholecystitis have gallstones. Cholelithiasis (calculi in the gallbladder)  Cholecystitis Pain, tenderness, and rigidity of the upper right abdomen that may radiate to the midsternal area or right shoulder Associated with nausea, vomiting, Usual signs of acute inflammation. An empyema of the gallbladder develops if the gallbladder becomes filled with purulent fluid (pus).  Cholecystitis Calculous cholecystitis Acalculous cholecystitis – Gallbladder stone obstructs bile – occurs after major surgical outflow. procedures, orthopedic – Bile remaining in the gallbladder procedures, severe trauma, or initiates a chemical reaction; burns. autolysis and edema occur; – The blood vessels in the – Other factors associated with gallbladder are compressed, this type of cholecystitis include compromising its vascular supply. torsion, cystic duct obstruction, – Gangrene of the gallbladder with primary bacterial infections of perforation may result. the gallbladder, and multiple blood transfusions  Cholelithiasis Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile. Pigment stones The risk of developing such stones is increased in patients with cirrhosis, hemolysis, and infections of the biliary tract. Pigment stones cannot be dissolved and must be removed surgically.  Cholelithiasis Cholesterol stones – There is decreased bile acid synthesis and increased cholesterol synthesis in the liver, resulting in bile supersaturated with cholesterol, which precipitates out of the bile to form stones  Cystic fibrosis (oral contraceptive) Diabetes Frequent changes in weight Ileal resection or bypass (GIT malabsorption) Risk Factors Low-dose estrogen therapy—carries a small for increase in the risk of gallstones Obesity Cholelithiasis Treatment with high-dose estrogen (e.g., in prostate cancer) Women (2-3 times > men), especially those who have had multiple pregnancies Age (older than 40)  Gallstones may be silent, producing no pain and only mild GI symptoms. Epigastric distress (may occur after eating a fatty meal). – Fullness, abdominal distention, – Vague upper right quadrant pain. Clinical Pain and Biliary Colic characteristics : Manifestations – Severe upper right abdominal pain that radiates to the back or right shoulder – Palpable abdominal tender mass – Associated with fever, nausea, and vomiting. – It occurs several hours after a heavy meal.  Jaundice The bile is absorbed by the blood and gives the skin and mucous membranes a yellow color. This may cause pruritus (itching) of the skin. Clinical Changes in Urine and Stool Color – The urine a very dark color. Manifestations – The feces, are grayish, clay-colored. (absence of bile pigments) Vitamin Deficiency because the obstruction of bile flow interferes with absorption of the fat- soluble vitamins A, D, E, and K.  Abdominal X-Ray Cholelithiasis Ultrasonography Assessment Radionuclide Imaging or Cholescintigraphy Cholecystography and Diagnostic Endoscopic retrograde cholangiopancreatography (ERCP) Findings Percutaneous Transhepatic Cholangiography  Nutritional and Supportive Therapy Medical Pharmacologic Therapy Management Nonsurgical stone removal Cholecystectomy – Laparoscopic cholecystectomy / surgical  The diet required immediately after an episode is usually: limited to low-fat liquids. Nutritional Cooked fruits, rice, lean meats, and mashed potatoes, non–gas-forming vegetables, bread, coffee, or tea may Supportive be added as tolerated. Therapy The patient should avoid: – eggs, cream, fried foods, cheese, gas- forming vegetables, and alcohol. Pharmacologic Therapy Ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (chenodiol) Used to dissolve small, radiolucent gallstones composed primarily of cholesterol.  Nonsurgical Removal of Gallstones Dissolving Gallstones – by infusion of a solvent (mono- octanoin or methyl tertiary butyl ether [MTBE]) into the gallbladder. Stone Removal by Instrumentation Intracorporeal Lithotripsy. A laser pulse is directed under fluoroscopic guidance with the use of devices that can distinguish between stones and tissue. Extracorporeal Shock Wave Lithotripsy  Laparoscopic Cholecystectomy The surgeon makes four small incisions in the abdomen and inserts a laparoscope with camera through the umbilical incision. The camera allowing the surgeon to visualize the sections of the organ for removal.  Acute pain and discomfort related to surgical incision Impaired gas exchange related to the high abdominal surgical incision (if traditional The Care of the surgical cholecystectomy is performed) Patient Undergoing Impaired skin integrity related to altered biliary drainage after surgical intervention (if a T-tube Surgery for is inserted because of retained stones in the Gallbladder Disease common bile duct or another drainage device is employed) Nursing diagnosis Imbalanced nutrition, less than body requirements, related to inadequate bile secretion Deficient knowledge about self-care activities related to incision care, dietary modifications (if needed), medications, reportable signs or symptoms (eg, fever, bleeding, vomiting) See Nursing Process: The patient undergoing surgery for gallbladder disease p. 3798 – 3805  Low Fowler’s position NPO until bowel sounds return, then a soft, low-fat, high-carbohydrate diet postoperatively Care of biliary drainage system Postoperative – Record the amount, color, and character of the drainage. – Record of fluid intake and output Care – Observes the color of stools daily and urine Administer analgesics as ordered and Interventions medicate to promote/permit ambulation and activities, including deep breathing Turn, and encourage coughing and deep breathing, splinting to reduce pain Early Ambulation Any Questions?