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Nursing assessment and management of patients with hepatic disorders

Liver or Hepatic disorders are common and may result from a virus or exposure to toxic substances such as alcohol.
Another liver disorder is cancer: hepatocellular carcinoma is a highly malignant tumor that is difficult to treat and often fatal.
Liver function is complex, and liver dysfunction affects all body systems.
For this reason, the nurse must understand how the liver functions and must have expert assessment and clinical management skills to care for patients undergoing complex diagnostic and treatment procedures.
The liver plays additional roles in detoxification of chemicals and synthesis and storage of important nutrients and The liver is especially important in the regulation of glucose and protein metabolism .

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Nursing assessment and management of patients with hepatic disorders

  1. 1. 1. Jaundice 2. Hepatic cirrhosis 3. Portal hypertension 4. Ascites 5. Hepatic encephalopathy and coma 6. Liver cancer 7. Liver abscess
  2. 2. Liver or Hepatic disorders are common and may result from a virus or exposure to toxic substances such as alcohol. Another liver disorder is cancer: hepatocellular carcinoma is a highly malignant tumor that is difficult to treat and often fatal.
  3. 3. Liver function is complex, and liver dysfunction affects all body systems. For this reason, the nurse must understand how the liver functions and must have expert assessment and clinical management skills to care for patients undergoing complex diagnostic and treatment procedures. The liver plays additional roles in detoxification of chemicals and synthesis and storage of important nutrients and The liver is especially important in the regulation of glucose and protein metabolism .
  4. 4. Functions of the liver include: 1. Storage of vitamins A, B, D; iron; and copper. 2. Synthesis of plasma proteins, including albumin and globulins. 3. Synthesis of the clotting factors vitamin K and prothrombin. 4.Storage of glycogen and synthesis of glucose from other nutrients (gluconeogenesis). 5. Breakdown of fatty acids for energy. 6.Production of bile. 7. Detoxification and excretion of waste products.
  5. 5. FUNCTIONS OF THE LIVER 1. Glucose Metabolism : The liver plays a major role in the metabolism of glucose and the regulation of blood glucose concentration. After a meal, glucose is taken up from the portal venous blood by the liver and converted into glycogen, which is stored in the hepatocytes.
  6. 6. The liver also plays an important role in protein metabolism. It synthesizes almost all of the plasma proteins (except gamma globulin), including albumin, alpha and beta globulins, blood clotting factors, specific transport proteins, and most of the plasma lipoproteins. Vitamin K is required by the liver for synthesis of prothrombin and some of the other clotting factors.
  7. 7. The liver is also active in fat metabolism. Fatty acids can be broken down for the production of energy and the production of ketone bodies (acetoacetic acid, beta-hydroxybutyric acid, and acetone).
  8. 8. Vitamin and Iron Storage Vitamins A, B, and D and several of the B-complex vitamins are stored in large amounts in the liver. Certain substances, such as iron and copper, are also stored in the liver.
  9. 9. Drug Metabolism The liver metabolizes many medications, such as barbiturates, opioids, sedative agents, anesthetics, and amphetamines.
  10. 10. Bile Formation Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. It is composed mainly of water and electrolytes such as sodium, potassium, calcium, chloride, and bicarbonate, and it also contains significant amounts of lecithin, fatty acids, cholesterol, bilirubin, and bile salts.
  11. 11. Bilirubin Excretion Bilirubin is a pigment derived from the breakdown of hemoglobin by cells of the reticuloendothelial system, including the Kupffer cells of the liver.
  12. 12. ANATOMY OF THE LIVER The liver is located behind the ribs in the upper right portion of the abdominal cavity. It weighs about 1,500 g and is divided into four lobes.
  13. 13. ANATOMY OF THE LIVER
  14. 14. ANATOMY OF THE LIVER
  15. 15. ASSESSMENT 1. HEALTH HISTORY 1. If liver function test results are abnormal, the patient may need to be evaluated for liver disease. In such cases, the health history will focus on exposure of the patient to hepatotoxic substances or infectious agents. 2. The patient’s occupational, recreational, and travel history may assist in identifying exposure to hepatotoxins (e.g., industrial chemicals, other toxins) responsible for illness. The patient’s history of alcohol and drug use, including but not limited to the use of injectable drugs, provides additional information about exposure to toxins and infectious agents.
  16. 16. ASSESSMENT 1. HEALTH HISTORY 3. A careful medication history to assess hepatic dysfunction should address all prescribed and over-the counter medications, herbal remedies, and dietary supplements used by the patient currently and in the past. 4. Lifestyle behaviors that increase the risk for exposure to infectious agents are identified. 5. Injectable drug use, sexual practices, and a history of foreign travel are all potential risk factors for liver disease. The amount , duration and type of alcohol consumption.
  17. 17. ASSESSMENT 1. HEALTH HISTORY 5. The family history includes questions about familial liver disorders that may have their etiology in alcohol abuse or gallstone disease, as well as other familial or genetic diseases, such as hemochromatosis, Wilson’s disease, or alpha-1 antitrypsin disease.
  18. 18. ASSESSMENT 1. HEALTH HISTORY 6. The history also includes reviewing symptoms that suggest liver disease such as . 1.Jaundice 2.Malaise and weakness fatigue 3. Pruritus 4. Abdominal pain, fever and anorexia.
  19. 19. ASSESSMENT 1. HEALTH HISTORY 5. Weight gain, edema and increasing abdominal girth. 6. Hematemesis, melena, hematochezia (passage of bloody stools). 7. Easy bruising, decreased libido in men and secondary amenorrhea in women, changes. 8. Changes in mental acuity, personality changes, and sleep disturbances.
  20. 20. PHYSICAL EXAMINATION 1. The nurse assesses the patient for physical signs that may occur with liver dysfunction, including pallor of chronic illness and jaundice. 2. The skin, mucosa, and sclerae are inspected for jaundice, and the extremities are assessed for muscle atrophy, edema, and skin excoriation secondary to scratching. 3. The nurse observes the skin for petechiae or ecchymotic areas (bruises), spider angiomas, and palmar erythema.
  21. 21. PHYSICAL EXAMINATION 1. The male patient is assessed for unilateral or bilateral gynecomastia and testicular atrophy due to endocrine changes. 2. The patient’s cognitive status (recall, memory, abstract thinking) and neurologic status are assessed. The nurse observes for general tremor, asterixis, weakness, and slurred speech.
  22. 22. PHYSICAL EXAMINATION 1. The nurse assesses the abdomen for dilated abdominal wall veins, ascites, and a fluid wave (discussed later). 2. The abdomen is palpated to assess liver size and to detect any tenderness over the liver.
  23. 23. Methods for Palpating the Liver
  24. 24. PHYSICAL EXAMINATION Tenderness of the liver implies recent acute enlargement with consequent stretching of the liver capsule. The absence of tenderness may imply that the enlargement is of long-standing duration.
  25. 25. Common clinical manifestations of Hepatic Dysfunction 1. Jaundice, resulting from increased bilirubin concentration in the blood 2. Portal hypertension, ascites, and varices, resulting from circulatory changes within the diseased liver and producing severe GI hemorrhages and marked sodium and fluid retention 3. 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 4. Hepatic encephalopathy or coma, reflecting accumulation of ammonia in the serum due to impaired protein metabolism by the diseased liver.
  26. 26. Diagnostic Evaluation 1. LIVER FUNCTION TESTS: More than 70% of the parenchyma of the liver may be damaged before liver function test results become abnormal. Function is generally measured in terms of serum enzyme activity (i.e., alkaline phosphatase, lactic dehydrogenase, serum aminotransferases) and serum concentrations of proteins (albumin and globulins), bilirubin, ammonia, clotting factors, and lipids.
  27. 27. LIVER FUNCTION TESTS 1. Serum aminotransferases (also called transaminases) are sensitive indicators of injury to the liver cells and are useful in detecting acute liver disease such as hepatitis. 2. Alanine aminotransferase (ALT) (formerly called serum glutamic- pyruvic transaminase [SGPT]), aspartate aminotransferase (AST) (formerly called serum glutamic-oxaloacetic transaminase [SGOT]), and gamma glutamyl transferase (GGT) (also called G-glutamyl transpeptidase) are the most frequently used tests of liver damage. 3. ALT levels increase primarily in liver disorders and may be used to monitor the course of hepatitis or cirrhosis or the effects of treatments that may be toxic to the liver.
  28. 28. LIVER BIOPSY
  29. 29. LIVER BIOPSY 1. Liver biopsy is the removal of a small amount of liver tissue, usually through needle aspiration. It permits examination of liver cells. 2. The most common indication is to evaluate diffuse disorders of the parenchyma and to diagnose space- occupying lesions. Liver biopsy is especially useful when clinical findings and laboratory tests are not diagnostic of liver disease.
  30. 30. Liver biopsy procedure
  31. 31. PRE PROCEDURE 1. Ascertain that results of coagulation tests (prothrombin time, partial thromboplastin time, and platelet count) are available and that compatible donor blood is available. 2. Check for signed consent; confirm that informed consent has been provided. 3. Measure and record the patient’s pulse, respirations, and blood pressure immediately before biopsy. 4. Describe to the patient in advance: steps of the procedure; sensations expected; after-effects anticipated; restrictions of activity and monitoring procedures to follow. 5. Bleeding and bile peritonitis after liver biopsy are the major complications; therefore, coagulation studies are obtained, their values are noted, and abnormal results are treated before liver biopsy is performed.
  32. 32. POST PROCEDURE 1. Immediately after the biopsy, assist the patient to turn onto the right side; place a pillow under the costal margin, and caution the patient to remain in this position, recumbent and immobile, for several hours. Instruct the patient to avoid coughing or straining. 2. Measure and record the patient’s pulse, respiratory rate, and blood pressure at 10- to 15-minute intervals for the first hour, then every 30 minutes for the next 1 to 2 hours or until the patient’s condition stabilizes. 3. If the patient is discharged after the procedure, instruct the patient to avoid heavy lifting and strenuous activity for 1 week.
  33. 33. OTHER DIAGNOSTIC TESTS 1. Ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) are used to identify normal structures and abnormalities of the liver and biliary tree. 2. A radioisotope liver scan may be performed to assess liver size and hepatic blood flow and obstruction. 3. Laparoscopy (insertion of a fiber-optic endoscope through a small abdominal incision) is used to examine the liver and other pelvic structures. It is also used to perform guided liver biopsy, to determine the etiology of ascites, and to diagnose and stage tumors of the liver and other abdominal organs.
  34. 34. OTHER DIAGNOSTIC TESTS 1. Endoscopic Retrograde Cholangiopancreatography (ERCP) : Endoscopic visualization of the common bile, pancreatic, and hepatic ducts with a flexible fiber-optic endoscope inserted into the esophagus, passed through the stomach and into the duodenum.
  35. 35. JAUNDICE
  36. 36. JAUNDICE When the bilirubin concentration in the blood is abnormally elevated, all the body tissues, including the sclera and the skin, become yellow-tinged or greenish- yellow, a condition called jaundice. Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5 mg/dL (43 fmol/L).
  37. 37. Types of Jaundice There are several types of jaundice: hemolytic, hepatocellular, obstructive, or jaundice due to hereditary hyperbilirubinemia. Hepatocellular and obstructive jaundice are the two types commonly associated with liver disease.
  38. 38. Hemolytic Jaundice ( Prehepatic jaundice) Hemolytic jaundice is the result of an increased destruction of the red blood cells, the effect of which is to flood the plasma with bilirubin so rapidly that the liver, although functioning normally, cannot excrete the bilirubin as quickly as it is formed. This type of jaundice is encountered in patients with hemolytic transfusion reactions and other hemolytic disorders.
  39. 39. Hemolytic Jaundice ( Prehepatic jaundice) Hemolytic jaundice is due to excessive break down of Red blood cells. Causes 1. Sickle cell anemia 2. Malaria 3. Thalassemia 4.Auto immune disorders 5.Massive hemorrhage
  40. 40. Hepatocellular Jaundice ( Hepatic jaundice) Hepatocellular jaundice is caused by the inability of damaged liver cells to clear normal amounts of bilirubin from the blood. The causes of hepatocellular jaundice such as: 1. The cellular damage may be from infection, such as in viral hepatitis (e.g., hepatitis A, B, C, D, or E) or other viruses that affect the liver (e.g., yellow fever virus, Epstein-Barr virus). 2. Medication or chemical toxicity (e.g., carbon tetrachloride, chloroform, phosphorus, arsenicals, certain medications). 3. From alcohol consumption.
  41. 41. Hepatocellular Jaundice ( Hepatic jaundice) Patients with hepatocellular jaundice may be mildly or severely ill, with lack of appetite, nausea, malaise, fatigue, weakness, and possible weight loss. The serum bilirubin concentration and urine urobilinogen level may be elevated. In addition, AST and ALT levels may be increased, indicating cellular necrosis. The patient may report headache, chills, and fever if the cause is infectious. Depending on the cause and extent of the liver cell damage, hepatocellular jaundice may or may not be completely reversible.
  42. 42. Obstructive Jaundice Obstructive jaundice is a particular type of jaundice and occurs when the essential flow of bile to the intestine is blocked and remains in the bloodstream. Obstructive jaundice of the extra hepatic type may be caused by occlusion of the bile duct by a gallstone, an inflammatory process, a tumor, or pressure from an enlarged organ.
  43. 43. Hereditary Hyperbilirubinemia Hereditary Hyperbilirubinemia : Increased serum bilirubin levels (hyperbilirubinemia) resulting from several inherited disorders can also produce jaundice. Gilbert’s syndrome is a familial disorder characterized by an increased level of unconjugated bilirubin that causes jaundice. Although serum bilirubin levels are increased, liver histology and liver function test results are normal, and there is no hemolysis. This syndrome affects 2% to 5% of the population. Other conditions that are probably caused by inborn errors of biliary metabolism include Dubin–Johnson syndrome (chronic idiopathic jaundice, with pigment in the liver) and Rotor’s syndrome (chronic familial conjugated hyperbilirubinemia without pigment in the liver); “benign” cholestatic jaundice of pregnancy, with retention of conjugated bilirubin.
  44. 44. Cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver. There are three types of cirrhosis or scarring of the liver.
  45. 45. HEPATIC CIRRHOSIS OR LIVER CIRRHOSIS HEPATIC CIRRHOSIS or Cirrhosis of the liver is characterized by scarring. It is a chronic disease in which there has been diffuse destruction and fibrotic regeneration of hepatic cells.
  46. 46. Types of liver cirrhosis There are three types of cirrhosis or scarring of the liver: 1. Alcoholic cirrhosis, in which the scar tissue characteristically surrounds the portal areas. This is most frequently due to chronic alcoholism and is the most common type of cirrhosis. 2. Postnecrotic cirrhosis, in which there are broad bands of scar tissue as a late result of a previous bout of acute viral hepatitis. 3. Biliary cirrhosis, in which scarring occurs in the liver around the bile ducts. This type usually is the result of chronic biliary obstruction and infection (cholangitis); it is much less common than the other two types.
  47. 47. Clinical manifestations Onset is insidious; may take years to develop. Clinical manifestations include intermittent jaundice and fever. Initially the liver is enlarged, hard, and irregular, but eventually it atrophies. Early complaints include fatigue, anorexia, ankle edema in the evening, epistaxis and bleeding gums, and weight loss. A) Chronic dyspepsia, constipation, or diarrhea. B) Plasma albumin is reduced, leading to edema and contributing to ascites. C) Anemia and poor nutrition lead to fatigue and weakness, wasting, and depression.
  48. 48. Clinical manifestations D) Deterioration of mental function from lethargy to delirium to coma and eventual death.(Additional include deterioration of mental function with impending hepatic encephalopathy and hepatic coma) E) Estrogen-androgen imbalance causes spider angiomata and palmar erythema; menstrual irregularities in females; testicular and prostatic atrophy, gynecomastia, loss of libido, and impotence in males. F) VITAMIN DEFICIENCY AND ANEMIA (Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C, and K), signs of their deficiency are common, particularly hemorrhagic phenomena associated with vitamin K deficiency).
  49. 49. Clinical manifestations Compensated Decompensated Intermittent mild fever Ascites Jaundice Vascular spiders Weakness, Muscle wasting and Weight loss Palmar erythema (reddened palms) and Unexplained epistaxis Continuous mild fever, Clubbing of fingers Ankle edema Purpura (due to decreased platelet count) Spontaneous bruising Vague morning indigestion ,Flatulent dyspepsia and abdominal pain Epistaxis Hypotension Firm, enlarged liver Sparse body hair and White nails Splenomegaly Gonadal atrophy
  50. 50. Assessment and Diagnostic Findings The extent of liver disease and the type of treatment are determined after reviewing the laboratory findings. 1. History collection . 2. Liver biopsy detects destruction and fibrosis of hepatic tissue. 3. Liver scan shows abnormal thickening and a liver mass. 4. CT scan determines the size of the liver and its irregular nodular surface. 5. Esophagoscopy to determine esophageal varices. 6. Paracentesis to examine ascitic fluid for cell, protein, and bacterial counts. 7. Laparoscopy and liver biopsy permit direct visualization of the liver. 8. Serum liver function test results are elevated.
  51. 51. Medical Management clients with liver cirrhosis The management of the patient with cirrhosis is usually based on the presenting symptoms. For example, antacids are prescribed to decrease gastric distress and minimize the possibility of GI bleeding. Vitamins and nutritional supplements promote healing of damaged liver cells and improve the general nutritional status. Minimize further deterioration of liver function through the withdrawal of toxic substances, alcohol, and drugs. Correction of nutritional deficiencies with vitamins and nutritional supplements and a high-calorie and moderate- to high-protein diet.
  52. 52. Medical Management clients with liver cirrhosis Treatment of ascites and fluid and electrolyte imbalances. ◦ Restrict sodium and water intake, depending on amount of fluid retention. ◦ Bed rest to aid in diuresis. ◦ Diuretic therapy, frequently with spironolactone (Aldactone), a potassium-sparing diuretic ◦ Abdominal paracentesis to remove fluid and relieve symptoms ◦ Administration of albumin to maintain osmotic pressure.
  53. 53. Medical Management clients with liver cirrhosis Preliminary studies indicate that colchicine, an anti-inflammatory agent used to treat the symptoms of gout, may increase the length of survival in patients with mild to moderate cirrhosis. Improved survival has been observed in patients with alcoholic cirrhosis. Colchicine is believed to reverse the fibrotic processes in cirrhosis, and this has improved survival.
  54. 54. Colchicine
  55. 55. NURSING PROCESS: THE PATIENT WITH HEPATIC CIRRHOSIS Assessment: Nursing assessment focuses on the onset of symptoms and the history of precipitating factors, particularly long-term alcohol abuse, as well as dietary intake and changes in the patient’s physical and mental status. The patient’s past and current patterns of alcohol use (duration and amount) are assessed and documented. It is also important to document any exposure to toxic agents encountered in the workplace or during recreational activities.
  56. 56. NURSING PROCESS: THE PATIENT WITH HEPATIC CIRRHOSIS 3. The nurse assesses the patient’s mental status through the interview and other interactions with the patient; orientation to person, place, and time is noted. 4. The nurse assesses nutritional status, which is of major importance in cirrhosis, by daily weights and monitoring of plasma proteins, transferrin, and creatinine levels.
  57. 57. Complications 1. Bleeding and hemorrhage 2. Hepatic encephalopathy (Hepatic encephalopathy and coma, possible complications of cirrhosis, may present as deteriorating mental status and dementia as well as physical signs such as abnormal voluntary and involuntary movements). 3. Fluid volume excess
  58. 58. NURSING DIAGNOSES 1. Activity intolerance related to fatigue, general debility, muscle wasting, and discomfort. 2. Imbalanced nutrition, less than body requirements, related to chronic gastritis, decreased GI motility, and anorexia. 3. Impaired skin integrity related to compromised immunologic status, edema, and poor nutrition. 4. Risk for injury and bleeding related to altered clotting mechanisms. 5. Disturbed Thought Processes related to deterioration of liver function and increased serum ammonia level. 6. Imbalanced Nutrition: Less Than Body Requirements related to anorexia and GI disturbances 7. Impaired Skin Integrity related to edema, jaundice, and compromised immunologic status
  59. 59. Nursing Interventions 1. PROMOTING REST 2. IMPROVING NUTRITIONAL STATUS 3. PROVIDING SKIN CARE (Providing careful skin care is important because of subcutaneous edema, the patient’s immobility, jaundice, and increased susceptibility to skin breakdown and infection. Frequent position changes are necessary to prevent pressure ulcers). 4. REDUCING RISK OF INJURY (The nurse protects the patient with cirrhosis from falls and other injuries. The side rails should be in place and padded with blankets in case the patient becomes agitated or restless. ) 5. MONITORING AND MANAGING POTENTIAL COMPLICATIONS
  60. 60. Patient Education and Health Maintenance 1. Stress the necessity of giving up alcohol completely. 2. Urge acceptance of assistance from a substance abuse program. 3. Provide written dietary instructions. 4. Encourage daily weighing for self-monitoring of fluid retention or depletion. 5. Discuss adverse effects of diuretic therapy. 6. Emphasize the importance of rest, a sensible lifestyle, and an adequate, well- balanced diet. 7. Involve the person closest to the patient because recovery usually is not easy and relapses are common. 8. Stress the importance of continued follow-up for laboratory tests and evaluation by a health care provider.
  61. 61. PORTAL HYPERTENSION Portal hypertension is abnormally high blood pressure in the portal vein (the large vein that brings blood from the intestine to the liver) and its branches. Obstructed blood flow through the damaged liver results in increased blood pressure (portal hypertension) throughout the portal venous system. Although portal hypertension is commonly associated with hepatic cirrhosis, it can also occur with non cirrhotic liver disease.
  62. 62. Portal hypertension is defined as the elevation of the hepatic venous pressure gradient to > 5 mmhg.
  63. 63. ASCITES
  64. 64. ASCITES Ascites is of Greek derivation ("askos") and refers to a bag or sack and describes pathologic fluid accumulation within the peritoneal cavity. Most patients (85%) with ascites have cirrhosis.
  65. 65. Peritoneal cavity It is a potential space between the parietal peritoneum and visceral peritoneum, the two membranes separate the organs in the abdominal cavity from the abdominal wall.
  66. 66. Peritoneal fluid It is a normal, lubricating fluid found in the peritoneal cavity. The fluid is mostly water with electrolytes, antibodies, white blood cells, albumin, glucose and other biochemical. Reduce the friction between the abdominal organs as they move around during digestion.
  67. 67. Ascites is defined as the accumulation fluid in the peritoneal cavity ( abdominal cavity).
  68. 68. Pathophysiology The mechanisms responsible for the development of ascites are not completely understood. Portal hypertension and the resulting increase in capillary pressure and obstruction of venous blood flow through the damaged liver are contributing factors. The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney. Sodium and water retention, increased intravascular fluid volume, and decreased synthesis of albumin by the damaged liver all contribute to fluid moving from the vascular system into the peritoneal space.
  69. 69. Clinical Manifestations 1. Increased abdominal girth and rapid weight gain are common presenting symptoms of ascites. 2. The patient may be short of breath and uncomfortable from the enlarged abdomen, and striae and distended veins may be visible over the abdominal wall. 3. Fluid and electrolyte imbalances are common.
  70. 70. Assessment and Diagnostic Evaluation The presence and extent of ascites are assessed by percussion of the abdomen. When fluid has accumulated in the peritoneal cavity, the flanks bulge when the patient assumes a supine position. The presence of fluid can be confirmed either by percussing for shifting dullness or by detecting a fluid wave.
  71. 71. Medical Management 1. DIETARY MODIFICATION : The goal of treatment for the patient with ascites is a negative sodium balance to reduce fluid retention. Table salt, salty foods, salted butter and margarine, and all ordinary canned and frozen foods (foods that are not specifically prepared for low-sodium diets) should be avoided.
  72. 72. Medical Management 2. DIURETICS: Use of diuretics along with sodium restriction is successful in 90% of patients with ascites. Spironolactone (Aldactone), an aldosteroneblocking agent, is most often the first-line therapy in patients with ascites from cirrhosis. Possible complications of diuretic therapy include fluid and electrolyte disturbances (including hypovolemia, hypokalemia, hyponatremia, and hypochloremic alkalosis) and encephalopathy.
  73. 73. Medical Management PARACENTESIS : Paracentesis is the removal of fluid (ascites) from the peritoneal cavity through a small surgical incision or puncture made through the abdominal wall under sterile conditions.
  74. 74. PARACENTESIS Paracentesis was once considered a routine form of treatment for ascites but is now performed primarily for diagnostic examination of ascitic fluid, for treatment of massive ascites that is resistant to nutritional and diuretic therapy.
  75. 75. Abdominal Paracentesis
  76. 76. Abdominal Paracentesis
  77. 77. PREPROCEDURE 1. Prepare the patient by providing the necessary information and instructions about the procedure and by offering reassurance. 2. Instruct the patient to void. 3. Gather appropriate sterile equipment and collection receptacles. 4. Place patient in upright position on edge of bed with feet supported on stool, or place in chair. Fowler’s position should be used for the patient confined to bed. 5. Place sphygmomanometer cuff around patient’s arm to allow monitoring of blood pressure during the procedure.
  78. 78. PROCEDURE 1. The physician, using aseptic technique, inserts the trocar through a puncture wound below the umbilicus. 2. Help the patient maintain position throughout procedure. 3. Measure and record blood pressure at frequent intervals from the beginning of the procedure. 4. Monitor the patient closely for signs of vascular collapse: pallor, increased pulse rate, or decreased blood pressure.
  79. 79. POST PROCEDURE 1. Return patient to bed or to a comfortable sitting position. 2. Measure, describe, and record the fluid collected. 3. Label samples of fluid and send to laboratory. 4. Continue to monitor vital signs every 15 minutes for 1 hour, every 30 minutes over 2 hours, then every hour over 2 hours and then every 4 hours. Monitor temperature after procedure and every 4 hours.
  80. 80. POST PROCEDURE 5. Assess for hypovolemia, electrolyte loss, changes in mental status, and encephalopathy. 6. Check puncture site when taking vital signs for bleeding and leakage. 7. Provide patient education (especially if patient is discharged after procedure) regarding monitoring for bleeding or excess drainage from puncture site, avoiding heavy lifting or straining, changing position slowly, and monitoring for fever.
  81. 81. Nursing Management If a patient with ascites from liver dysfunction is hospitalized, nursing measures include assessment and documentation of intake and output, abdominal girth, and daily weight to assess fluid status. The nurse monitors serum ammonia and electrolyte levels to assess electrolyte balance, response to therapy, and indicators of encephalopathy.
  82. 82. HEPATIC ENCEPHALOPATHY & COMA The loss of brain function when a damaged liver doesn't remove toxins from the blood. Hepatic encephalopathy, a life-threatening complication of liver disease, occurs with profound liver failure and may result from the accumulation of ammonia and other toxic metabolites in the blood.
  83. 83. HEPATIC ENCEPHALOPATHY & COMA Hepatic coma represents the most advanced stage of hepatic encephalopathy. Some researchers describe a false or weak neurotransmitter as a cause, but the exact mechanism is not fully understood.
  84. 84. Pathophysiology 1. Ammonia accumulates because damaged liver cells fail to detoxify and convert to urea the ammonia that is constantly entering the bloodstream. 2. Ammonia enters the bloodstream as a result of its absorption from the GI tract and its liberation from kidney and muscle cells. The increased ammonia concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy
  85. 85. Pathophysiology 1. Other factors unrelated to increased serum ammonia levels that may cause hepatic encephalopathy in susceptible patients include excessive diuresis, dehydration, infections, surgery, fever, and some medications (sedative agents, tranquilizers, analgesic agents, and diuretic medications that cause potassium loss).
  86. 86. Clinical Manifestations 1. The earliest symptoms of hepatic encephalopathy include minor mental changes and motor disturbances. 2. The patient appears slightly confused, has alterations in mood, becomes unkempt, and has altered sleep patterns. 3. The patient tends to sleep during the day and have restlessness and insomnia at night. As hepatic encephalopathy progresses, the patient may be difficult to awaken.
  87. 87. Clinical Manifestations 1. Asterixis ( flapping tremor of the hands) (Asterixis (also called the flapping tremor, or liver flap) is a tremor of the hand when the wrist is extended, sometimes said to resemble a bird flapping its wings.) may occur. Simple tasks, such as handwriting, become difficult. A handwriting or drawing sample (e.g., star figure), taken daily, may provide graphic evidence of progression or reversal of hepatic encephalopathy. Inability to reproduce a simple is referred to asconstructional apraxia
  88. 88. Asterixis ( flapping tremor of the hands
  89. 89. Assessment and Diagnostic Findings 1. The electroencephalogram (EEG) 2. Occasionally, fetor hepaticus, a sweet, slightly fecal odor to the breath presumed to be of intestinal origin may be noticed. Approximately 35% of all patients with cirrhosis of the liver die in hepatic coma.
  90. 90. Medical Management Lactulose (Cephulac) is administered to reduce serum ammonia levels. It acts by several mechanisms that promote the excretion of ammonia in the stool:
  91. 91. Medical Management Possible side effects include intestinal bloating and cramps, which usually disappear within a week. To mask the sweet taste, to which some patients object, lactulose can be diluted with fruit juice. The patient is closely monitored for hypokalemia and dehydration. Other laxatives are not prescribed during lactulose administration because their effects would disturb dosage regulation. Lactulose can be administered by nasogastric tube or enema for patients who are comatose or in whom oral administration is contraindicated or impossible.
  92. 92. Medical Management Other aspects of management include intravenous administration of glucose to minimize protein breakdown, administration of vitamins to correct deficiencies, and correction of electrolyte imbalances (especially potassium). NURSING ALERT (The patient receiving lactulose is monitored closely for the development of watery diarrheal stools, because they ! indicate a medication overdose)
  93. 93. Additional principles of management of hepatic encephalopathy include the following 1. Therapy is directed toward treating or removing the cause. 2. Neurologic status is assessed frequently. A daily record is kept of handwriting and performance in arithmetic to monitor mental status. 3. Fluid intake and output and body weight are recorded each day. 4. Vital signs are measured and recorded every 4 hours. 5. Potential sites of infection (peritoneum, lungs) are assessed frequently, and abnormal findings are reported promptly. 6. Serum ammonia level is monitored daily.
  94. 94. 7. Protein intake is restricted in patients who are comatose or who have encephalopathy that is refractory to lactulose and antibiotic therapy. 8. Reduction in the absorption of ammonia from the GI tract is accomplished by the use of gastric suction, enemas, or oral antibiotics. 9. Electrolyte status is monitored and corrected if abnormal. 10. Sedatives, tranquilizers, and analgesic medications are discontinued. 11. Benzodiazepine antagonists (flumazenil [Romazicon]) may be administered to improve encephalopathy whether or not the patient has previously taken benzodiazepines.
  95. 95. Nutritional Management of Hepatic Encephalopathy 1. Prevent the formation and absorption of toxins, principally ammonia, from the intestine. 2. Keep daily protein intake between 1.0 and 1.5 g/kg, depending on the degree of decompensation. 3. Avoid protein restriction if possible, even in those with encephalopathy. If necessary, implement temporary restriction of 0.5 g/kg. 4. For patients who are truly protein-intolerant, provide additional nitrogen in the form of an amino acid supplement. Use of branched-chain amino acids is still controversial. 5. Provide small, frequent meals and an evening snack of complex carbohydrates to avoid protein loading. 6. Substitute vegetable protein for animal protein in as high a percentage as possible.
  96. 96. Nursing Management The nurse is responsible for maintaining a safe environment to prevent injury, bleeding, and infection. The nurse administers the prescribed treatments and monitors the patient for the many potential complications. The nurse also communicates with the patient’s family to keep them informed about the patient’s status, and supports them by explaining the procedures and treatments that are part of the patient’s care.
  97. 97. Hepatocellular Carcinoma (Liver Cancer) Hepatic tumors may be malignant or benign. Benign liver tumors.
  98. 98. What is Hepatocellular Carcinoma? 1. Most primary liver cancers are classified as hepatocellular carcinoma. 2. Hepatocellular carcinoma is a malignant tumor composed of cells resembling hepatocytes ; however, the resemblance varies with the degree of differentiation . 3. Hepatocellular carcinoma is commonly associated with cirrhosis This type of liver cancer is potentially curable by surgical resection. However, only those patients with localized disease are surgical candidates.
  99. 99. Most primary liver tumours (90%) originate in the parenchymal cells and are hepatomas ( also called hepatocellular carcinomas).
  100. 100. Pathophysiology and Etiology 1. Incidence of primary cancer of the liver is increasing in the United States in the younger population and in females. 2. Cirrhosis, HBV, and HCV have been implicated in its etiology. 3. Rarer associated causes are hemachromatosis; alpha1-antitrypsin deficiency; aflatoxins; chemical toxins, such as vinyl chloride and Thorotrast; carcinogens in herbal medicines; nitrosamines; and ingestion of hormones, as in oral contraceptives. 4. Few cancers originate in the liver. Primary liver tumors usually are associated with chronic liver disease, hepatitis B and C infections, and cirrhosis.
  101. 101. LIVER METASTASES Metastases from other primary sites are found in the liver in about half of all advanced cancer cases (Bacon & Di Bisceglie, 2000). Malignant tumors are likely to reach the liver eventually, by way of the portal system or lymphatic channels, or by direct extension from an abdominal tumor.
  102. 102. Clinical Manifestations 1. The early manifestations of malignancy of the liver include pain, a continuous dull ache in the right upper quadrant, epigastrium, or back. 2. Weight loss, loss of strength, anorexia, and anemia may also occur. The liver may be enlarged and irregular on palpation. 3. With portal vein obstruction, ascites and esophageal varices occurs.
  103. 103. Assessment and Diagnostic Findings 1. The liver cancer diagnosis is based on clinical signs and symptoms, the history and physical examination, and the results of laboratory and x-ray studies. 2. Increased serum levels of bilirubin, alkaline phosphatase, AST, GGT, and lactic dehydrogenase may occur. 3. AFP (alpha-fetoprotein) is the principal tumor marker for hepatocellular carcinoma and is elevated in 70% to 95% of patients with primary liver cancer. 4. Ultrasonography and CT along with MRI are the most useful noninvasive tests to detect liver cancer and assess if the tumor can be surgically removed. 5. Percutaneous liver needle biopsy or biopsy assisted by ultrasonography or CT scan may be done. 6. Laparoscopy with liver biopsy may be performed.
  104. 104. 1. Liver function test 2. Laboratory investigation of Alpha- fetoprotein levels increase above 500 mcg/ml.
  105. 105. Medical Management Although surgical resection of the liver tumor is possible in some patients, the underlying cirrhosis, so prevalent in cancer of the liver, increases the risks associated with surgery. Radiation therapy and chemotherapy have been used in treating cancer of the liver with varying degrees of success. Although these therapies may prolong survival and improve quality of life by reducing pain and discomfort, their major effect is palliative.
  106. 106. Medical Management PERCUTANEOUS BILIARY DRAINAGE (PBD) : Percutaneous biliary or transhepatic drainage is used to bypass biliary ducts obstructed by liver, pancreatic, or bile duct tumors in patients with inoperable tumors or in those considered poor surgical risks.
  107. 107. PERCUTANEOUS BILIARY DRAINAGE (PBD)
  108. 108. OTHER NONSURGICAL TREATMENTS Laser hyperthermia has been used to treat hepatic metastases. Heat has been directed to tumors through several methods to cause necrosis of the tumor cells while sparing normal tissue.
  109. 109. SURGICAL MANAGEMENT 1. Surgical resection is the treatment of choice when HCC is con- fined to one lobe of the liver and the function of the remaining liver is considered adequate for postoperative recovery. 2. In preparation for surgery, the patient’s nutritional, fluid, and general physical status is assessed and efforts are undertaken to ensure the best physical condition possible. Support, explanation, and encouragement are provided to help the patient prepare psychologically for the surgery. 3. Extensive diagnostic studies may be performed. Specific studies may include liver scan, liver biopsy, cholangiography, selective hepatic angiography, percutaneous needle biopsy, peritoneoscopy, laparoscopy, ultrasound, CT scans, MRI, and blood tests, particularly determinations of serum alkaline phosphatase, AST, and GGT and its isoenzymes.
  110. 110. Lobectomy (Removal of a lobe of the liver is the most common surgical procedure for excising a liver tumor.
  111. 111. Cryosurgery In cryosurgery (cryoablation), tumors are destroyed by liquid nitrogen at −196° C. To destroy the diseased tissue, two or three freeze-and-thaw cycles are administered via probes during open laparotomy.
  112. 112. Liver transplantation (LT) is a life saving procedure for patients with end stage liver disease and its complications, and for liver failure. LT is also curative for some hereditary metabolic disorders like familial hypercholesterolemia and for selected cases of malignancies involving the liver, such as hepatocellular carcinoma (HCC) and hepatoblastoma.
  113. 113. Liver Transplantation Removing the liver and replacing it with a healthy donor organ is another way to treat liver cancer. Recurrence of the primary liver malignancy after transplantation, however, has been reported to occur in 70% to 85% of cases, and the survival time after recurrence is brief. But transplant surgery is performed infrequently because of its risks, its high cost, and the difficulty procuring organs.
  114. 114. Liver transplantation is used to treat life-threatening, end-stage liver disease for which no other form of treatment is available. The transplantation procedure involves total removal of the diseased liver and its replacement with a healthy liver in the same anatomic location (orthotopic liver transplantation [OLT]).
  115. 115. Liver Transplantation
  116. 116. Liver transplantation
  117. 117. Indications for Liver transplantation General indications for liver transplantation include: 1. irreversible advanced chronic liver disease 2. fulminant hepatic failure 3. metabolic liver diseases, and some hepatic malignancies. Examples of disorders that are indications for liver transplantation include hepatocellular liver disease (e.g., viral hepatitis, drug- and alcohol-induced liver disease, and Wilson’s disease) and cholestatic diseases (primary biliary cirrhosis, sclerosing cholangitis, and biliary atresia).
  118. 118. COMPLICATIONS  The postoperative complication rate is high, primarily because of technical complications or infection.  Immediate postoperative complications may include bleeding, infection, and rejection.  Disruption, infection, or obstruction of the biliary anastomosis and impaired biliary drainage may occur. Vascular thrombosis and stenosis are other potential complications.
  119. 119. Pre- Operative Nursing interventions Care of the client undergoing liver transplantation involves initiation of immunosuppression therapy (The definition of induction therapy is intensive peri-operative prophylactic immunosuppression used to prevent acute cellular rejection in the first months following transplantation) and pre – and post operative emotional support of patient and family.
  120. 120. Pre-operative preparation 1. As ordered , begin immunosuppressant therapy to decrease the risk of tissue rejection, using such drugs as cyclosporine, tacrolimus and corticosteroids. 2. Explain the need for lifelong therapy to prevent rejection. 3. Before transplant surgery, address the patients ( and family members) emotional needs. 4. The nurse and other health care team members provide the patient and family with full explanations about the procedure, the chances of success, and the risks, rejection of organ including the side effects of long-term immunosuppression. 5. Malnutrition, massive ascites, and fluid and electrolyte disturbances are treated before surgery to increase the chance of a successful outcome.
  121. 121. POSTOPERATIVE NURSING INTERVENTIONS 1. The patient is maintained in an environment as free from bacteria, viruses, and fungi as possible, because immunosuppressive medications reduce the body’s natural defenses. 2. In the immediate postoperative period, cardiovascular, pulmonary, renal, neurologic, and metabolic functions are monitored continuously. 3. Mean arterial and pulmonary artery pressures are monitored continuously.
  122. 122. 4. Cardiac output, central venous pressure, pulmonary capillary wedge pressure, arterial and mixed venous blood gases, oxygen saturation, oxygen demand and delivery, urine output, heart rate, and blood pressure are used to evaluate the patient’s hemodynamic status and intravascular fluid volume. 5. Liver function tests, electrolyte levels, the coagulation profile, chest x-ray, electrocardiogram, and fluid output, including urine, bile, and drainage from Jackson-Pratt tubes, are monitored closely.
  123. 123. Post operative care 1. Maintaining immunosuppressant therapy. 2. Monitoring for early signs of rejection and other complications. 3. Prevent opportunistic infections, which can lead to rejection and providing emotional support and reassurance throughout the prolonged recovery period. 4. Monitor vital signs every 15 minutes until stable, and monitor for haemorrhage and rejection. 5. Perform hourly assessments of fluid volume and vital signs required to detect bleeding and hypovolemic shock, along with pulses, urine output, LOC. 6. Assess incision site for signs symptoms of wound infection or abscess. 7. If the patient complains of acute pain in the right upper quadrant ( RUQ), cramping pain or tenderness, N &V , he or she may be experiencing vascular obstruction and need emergency thrombectomy.
  124. 124. 1. Assess the daily weight. 2. After removal of the endotracheal tube, the nurse encourages the patient to use an incentive spirometer, pulmonary hygiene protocol to decrease the risk for atelectasis. 3. Once the arterial lines and the urinary catheter are removed, the patient is assisted to get out of bed, to ambulates tolerated, and to participate in self-care to prevent the complications associated with immobility.
  125. 125. Patient Teaching 1. Before discharge the client teach the patient and family members to recognize the early indicators of tissue rejection ( pain and tenderness in the RUQ or centre of the back, fever tachycardia, jaundice and changes in colour in urine and stool ) 2. The nurse provides written as well as verbal instructions about how and when to take the medications. To avoid running out of medication or skipping a dose, the patient must make sure that an adequate supply of medication is available.
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Liver or Hepatic disorders are common and may result from a virus or exposure to toxic substances such as alcohol. Another liver disorder is cancer: hepatocellular carcinoma is a highly malignant tumor that is difficult to treat and often fatal. Liver function is complex, and liver dysfunction affects all body systems. For this reason, the nurse must understand how the liver functions and must have expert assessment and clinical management skills to care for patients undergoing complex diagnostic and treatment procedures. The liver plays additional roles in detoxification of chemicals and synthesis and storage of important nutrients and The liver is especially important in the regulation of glucose and protein metabolism .

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