Hepatic Function Lecture

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Hepatic Function Lecture

  1. 1. Learning Objectives:At the end of this lecture, you will be able to:1. Identify the metabolic functions of the liver and thealterations in these functions that occur with liverdisease.2. Explain liver function tests and the clinicalmanifestations of liver dysfunction in relation topathophysiologic alterations of the liver.JOFRED M. MARTINEZ, RN
  2. 2. 3. Relate jaundice, portal hypertension, ascites, varices,nutritional deficiencies, and hepatic coma topathophysiologic alterations of the liver.4. Describe the medical, surgical, and nursingmanagement of patients with esophageal varices.5. Compare the various types of hepatitis and theircauses, prevention, clinical manifestations,management, prognosis, and home health careneeds.6. Use the nursing process as a framework for care ofthe patient with cirrhosis of the liver.Learning Objectives (Cont’d.):
  3. 3. 7. Compare the nonsurgical and surgical management ofpatients with cancer of the liver.8. Describe the postoperative nursing care of the patientundergoing liver transplantation.Learning Objectives (Cont’d.):
  4. 4. HEALTH HISTORY• The patient’s occupational, recreational, and travel historymay assist in identifying exposure to hepatotoxins (eg,industrial chemicals, other toxins) responsible for illness.• The patient’s history of alcohol and drug use, including butnot limited to the use of injectable drugs.• A careful medication history to assess hepatic dysfunctionshould address all prescribed and over-the countermedications, herbal remedies, and dietary supplementsused by the patient currently and in the past.• Many medications (including acetaminophen,ketoconazole, and valproic acid) are responsible forhepatic dysfunction and disease.Assessment
  5. 5. HEALTH HISTORY• Lifestyle behaviors that increase the risk for exposure toinfectious agents are identified. Injectable drug use,sexual practices, and a history of foreign travel are allpotential risk factors for liver disease.• The amount and type of alcohol consumption areidentified using screening tools (questionnaires) thathave been developed for this purpose.• The history also includes an evaluation of the patient’spast medical history to identify risk factors for thedevelopment of liver disease.• Current and past medical conditions, including those ofa psychological or psychiatric nature, are identified.Assessment
  6. 6. HEALTH HISTORY• The family history includes questions about familialliver disorders that may have their etiology in alcoholabuse or gallstone disease, as well as other familial orgenetic diseases, such as hemochromatosis, Wilson’sdisease, or alpha-1 antitrypsin disease.• The history also includes reviewing symptoms thatsuggest liver disease.• Symptoms that may have their etiology in liver diseasebut are not specific to hepatic dysfunction includejaundice, malaise, weakness, fatigue, pruritus,abdominal pain, fever, anorexia, weight gain, edema,Assessment
  7. 7. HEALTH HISTORY• increasing abdominal girth, hematemesis, melena,hematochezia (passage of bloody stools), easybruising, decreased libido in men and secondaryamenorrhea in women, changes in mental acuity,personality changes, and sleep disturbances.Assessment
  8. 8. PHYSICAL EXAMINATION• The skin, mucosa, and sclerae are inspected forjaundice, and the extremities are assessed for muscleatrophy, edema, and skin excoriation secondary toscratching.• The nurse observes the skin for petechiae orecchymotic areas (bruises), spider angiomas, andpalmar erythema. The male patient is assessed forunilateral or bilateral gynecomastia and testicularatrophy due to endocrine changes.• The patient’s cognitive status (recall, memory, abstractthinking) and neurologic status are assessed.Assessment
  9. 9. Assessment
  10. 10. Assessment
  11. 11. Assessment
  12. 12. Assessment
  13. 13. Assessment
  14. 14. Assessment
  15. 15. PHYSICAL EXAMINATION• The nurse observes for general tremor, asterixis,weakness, and slurred speech.• The nurse assesses the abdomen for dilatedabdominal wall veins, ascites, and a fluid wave.• The abdomen is palpated to assess liver size and todetect any tenderness over the liver.• The liver may be palpable in the right upper quadrant. Apalpable liver presents as a firm, sharp ridge with asmooth surface.• The nurse estimates liver size by percussing its upperand lower borders.Assessment
  16. 16. Assessment
  17. 17. PHYSICAL EXAMINATION• When the liver is not palpable but tenderness issuspected, tapping the lower right thorax briskly may elicittenderness.• If the liver is palpable, the examiner notes and records itssize and consistency, whether it is tender, and whether itsoutline is regular or irregular.• If the liver is enlarged, the degree to which it descendsbelow the right costal margin is recorded to provide someindication of its size.• The examiner determines whether the liver’s edge issharp and smooth or blunt, and whether the enlarged liveris nodular or smooth.Assessment
  18. 18. PHYSICAL EXAMINATION• Tenderness of the liver implies recent acuteenlargement with consequent stretching of the livercapsule.• The absence of tenderness may imply that theenlargement is of long-standing duration.• The liver of a patient with viral hepatitis is tender,whereas that of a patient with alcoholic hepatitis is not.• Enlargement of the liver is an abnormal findingrequiring evaluation.Assessment
  19. 19. LIVER FUNCTION TESTS• Function is generally measured in terms of serumenzyme activity.• Serum aminotransferases are sensitive indicators ofinjury to the liver cells and are useful in detecting acuteliver disease such as hepatitis. Alanineaminotransferase (ALT), aspartate aminotransferase(AST), and gamma glutamyl transferase (GGT) are themost frequently used tests of liver damage.• ALT levels increase primarily in liver disorders and maybe used to monitor the course of hepatitis or cirrhosis orthe effects of treatments that may be toxic to the liver.Assessment
  20. 20. LIVER FUNCTION TESTS• AST is present in tissues that have high metabolicactivity; thus, the level may be increased if there isdamage to or death of tissues of organs such as theheart, liver, skeletal muscle, and kidney. Although notspecific to liver disease, levels of AST may beincreased in cirrhosis, hepatitis, and liver cancer.• Increased GGT levels are associated with cholestasisbut can also be due to alcoholic liver disease.AssessmentNORMAL VALUES: AST 4.8 – 19 U/LALT 2.4 – 17 U/L
  21. 21. LIVER BIOPSY• Liver biopsy is the removal of a small amount of livertissue, usually through needle aspiration. It permitsexamination of liver cells.• The most common indication is to evaluate diffusedisorders of the parenchyma and to diagnose space-occupying lesions• Bleeding and bile peritonitis after liver biopsy are themajor complications; therefore, coagulation studies areobtained, their values are noted, and abnormal resultsare treated before liver biopsy is performed.Assessment
  22. 22. LIVER BIOPSY• A liver biopsy can be performed percutaneously underultrasound guidance or transvenously through the rightinternal jugular vein to right hepatic vein underfluoroscopic control.• Liver biopsy can also be performed laparoscopically.AssessmentImmediately after the biopsy, assist the patient toturn onto the right side; place a pillow under thecostal margin, and caution the patient to remain inthis position.
  23. 23. Assessment
  24. 24. OTHER DIAGNOSTIC TESTS• Ultrasonography, computed tomography (CT), andmagnetic resonance imaging (MRI) are used to identifynormal structures and abnormalities of the liver andbiliary tree.• A radioisotope liver scan may be performed to assessliver size and hepatic blood flow and obstruction.• Laparoscopy is used to examine the liver and otherpelvic structures. It is also used to perform guided liverbiopsy, to determine the etiology of ascites, and todiagnose and stage tumors of the liver and otherabdominal organs.Assessment
  25. 25. • Hepatic dysfunction results from damage to the liver’sparenchymal cells, either directly from primary liverdiseases or indirectly from obstruction of bile flow orderangements of hepatic circulation.• Liver dysfunction may be acute or chronic; chronicdysfunction is far more common than acute.• The rate of chronic liver disease for men is twice that forwomen, and chronic liver disease is more common amongAfrican Americans than Caucasians.• Disease processes that lead to hepatocellular dysfunctionis caused by infectious agents such as bacteria,viruses,anoxia, metabolic disorders, toxins and medications,nutritional deficiencies, and hypersensitivity states.Hepatic Dysfunction
  26. 26. The most common and significant symptoms of liverdisease are the following:• Jaundice, resulting from increased bilirubinconcentration in the blood• Portal hypertension, ascites, and varices, resulting fromcirculatory changes within the diseased liver andproducing severe GI hemorrhages and marked sodiumand fluid retention• Nutritional deficiencies, which result from the inability ofthe damaged liver cells to metabolize certain vitamins;responsible for impaired functioning of the central andperipheral nervous systems and for abnormal bleedingtendenciesHepatic Dysfunction
  27. 27. • Hepatic encephalopathy or coma, reflectingaccumulation of ammonia in the serum due to impairedprotein metabolism by the diseased liverHepatic Dysfunction
  28. 28. JAUNDICE• When the bilirubin concentration in the blood is abnormallyelevated, all the body tissues, including the sclerae andthe skin, become yellow-tinged or greenish-yellow.• Jaundice becomes clinically evident when the serumbilirubin level exceeds 2.5 mg/dL. Increased serumbilirubin levels and jaundice may result from impairment ofhepatic uptake, conjugation of bilirubin, or excretion ofbilirubin into the biliary system.• There are several types of jaundice: hemolytic,hepatocellular,obstructive, or jaundice due to hereditaryhyperbilirubinemia.Jaundice
  29. 29. Jaundice
  30. 30. HEMOLYTIC JAUNDICE• Hemolytic jaundice is the result of an increaseddestruction of the red blood cells, the effect of which isto flood the plasma with bilirubin so rapidly that the liver,although functioning normally, cannot excrete thebilirubin as quickly as it is formed.• This type of jaundice is encountered in patients withhemolytic transfusion reactions and other hemolyticdisorders.• Prolonged jaundice, even if mild, predisposes to theformation of pigment stones in the gallbladder, andextremely severe jaundice poses a risk for brain stemdamage.Jaundice
  31. 31. HEPATOCELLULAR JAUNDICE• Hepatocellular jaundice is caused by the inability ofdamaged liver cells to clear normal amounts of bilirubinfrom the blood.• The cellular damage may be from infection, such as inviral hepatitis (eg, hepatitis A, B, C, D, or E) or otherviruses that affect the liver, from medication or chemicaltoxicity (eg, carbon tetrachloride, chloroform,phosphorus, arsenicals, certain medications), or fromalcohol.• Patients with hepatocellular jaundice may be mildly orseverely ill, with lack of appetite, nausea, malaise,fatigue, weakness, and possible weight loss.Jaundice
  32. 32. OBSTRUCTIVE JAUNDICE• Obstructive jaundice of the extrahepatic type may becaused by occlusion of the bile duct by a gallstone, aninflammatory process, a tumor, or pressure from anenlarged organ.• The obstruction may also involve the small bile ducts withinthe liver (ie, intrahepatic obstruction), caused, for example,by pressure on these channels from inflammatory swellingof the liver or by an inflammatory exudate within the ductsthemselves.• Intrahepatic obstruction resulting from stasis andinspissation of bile within the canaliculi may occur after theingestion of certain medications, which are referred to ascholestatic agents.Jaundice
  33. 33. OBSTRUCTIVE JAUNDICE• These include phenothiazines, antithyroid medications,sulfonylureas, tricyclic antidepressant agents,nitrofurantoin, androgens, and estrogens.• Because of the decreased amount of bile in theintestinal tract, the stools become light or clay-colored.• The skin may itch intensely, requiring repeated soothingbaths.• Dyspepsia and intolerance to fatty foods may developbecause of impaired fat digestion in the absence ofintestinal bile. AST, ALT, and GGT levels generally riseonly moderately, but bilirubin and alkaline phosphataselevels are elevated.Jaundice
  34. 34. HEREDITARY HYPERBILIRUBINEMIA• Increased serum bilirubin levels resulting from severalinherited disorders can also produce jaundice.• Gilbert’s syndrome is a familial disordercharacterized by an increased level of unconjugatedbilirubin that causes jaundice. Although serum bilirubinlevels are increased, liver histology and liver functiontest results are normal, and there is no hemolysis. Thissyndrome affects 2% to 5% of the population.Jaundice
  35. 35. HEREDITARY HYPERBILIRUBINEMIA• Other conditions that are probably caused by inbornerrors of biliary metabolism include Dubin–Johnsonsyndrome (chronic idiopathic jaundice, with pigment inthe liver) and Rotor’s syndrome (chronic familialconjugated hyperbilirubinemia without pigment in theliver); ―benign‖ cholestatic jaundice of pregnancy, withretention of conjugated bilirubin, probably secondary tounusual sensitivity to the hormones of pregnancy; andprobably also benign recurrent intrahepatic cholestasis.Jaundice
  36. 36. PORTAL HYPERTENSION• Obstructed blood flow through the damaged liver resultsin increased blood pressure throughout the portalvenous system.• Splenomegaly with possible hypersplenism is acommon manifestation of portal hypertension, two majorconsequences of portal hypertension are ascites andvarices.Hepatic Dysfunction
  37. 37. ASCITES• Portal hypertension and the resulting increase incapillary pressure and obstruction of venous blood flowthrough the damaged liver are contributing factors toascitis.Ascites
  38. 38. Ascites
  39. 39. Ascites
  40. 40. CLINICAL MANIFESTATIONS• Increased abdominal girth and rapid weight gain arecommon presenting symptoms of ascites.• The patient may be short of breath and uncomfortablefrom the enlarged abdomen, and striae and distendedveins may be visible over the abdominal wall.• Fluid and electrolyte imbalances are common.AscitesAlbumin is a very large protein that is responsiblefor holding fluid in the vascular space. If albuminis deficient then the fluid will shift.
  41. 41. ASSESSMENT AND DIAGNOSTIC EVALUATION• The presence and extent of ascites are assessed bypercussion of the abdomen.• When fluid has accumulated in the peritoneal cavity, theflanks bulge when the patient assumes a supineposition.• Daily measurement and recording of abdominal girthand body weight are essential to assess theprogression of ascites and its response to treatment.• A fluid wave is likely to be found only when a largeamount of fluid is present.Ascites
  42. 42. Ascites
  43. 43. MEDICAL MANAGEMENTDIETARY MODIFICATION• The goal of treatment for the patient with ascites is anegative sodium balance to reduce fluid retention.• Commercial salt substitutes need to be approved by thephysician because those containing ammonia couldprecipitate hepatic coma. Most salt substitutes containpotassium and should be avoided if the patient hasimpaired renal function.• The patient should make liberal use of powdered, low-sodium milk and milk products.Ascites
  44. 44. MEDICAL MANAGEMENTDIURETICS• Spironolactone (Aldactone), an aldosteroneblockingagent, is most often the first-line therapy in patients with• ascites from cirrhosis. When used with other diuretics,spironolactone helps prevent potassium loss.• Oral diuretics such as furosemide (Lasix) may be addedbut should be used cautiously because with long-termuse they may also induce severe sodium depletion.• Ammonium chloride and acetazolamide (Diamox) arecontraindicated because of the possibility ofprecipitating hepatic coma.Ascites
  45. 45. MEDICAL MANAGEMENTDIURETICS• Possible complications of diuretic therapy include fluidand electrolyte disturbances (including hypovolemia,hypokalemia, hyponatremia, and hypochloremicalkalosis) and encephalopathy.• Encephalopathy may be precipitated by dehydrationand hypovolemia.Ascites
  46. 46. MEDICAL MANAGEMENTBED REST• In patients with ascites, an upright posture is associatedwith activation of the renin-angiotensin-aldosteronesystem and sympathetic nervous system. This results inreduced renal glomerular filtration and sodium excretionand a decreased response to loop diuretics.• Bed rest may be a useful therapy, especially for patientswhose condition is refractory to diuretics.Ascites
  47. 47. MEDICAL MANAGEMENTPARACENTESIS• Paracentesis is the removal of fluid from the peritonealcavity through a small surgical incision or puncturemade through the abdominal wall under sterileconditions.• A sample of the ascitic fluid may be sent to thelaboratory for analysis. Cell count, albumin and totalprotein levels, culture, and occasionally other tests areperformed.Ascites
  48. 48. Ascites
  49. 49. MEDICAL MANAGEMENTOTHER METHODS OF TREATMENT• Insertion of a peritoneovenous shunt to redirect asciticfluid from the peritoneal cavity into the systemiccirculation is a treatment modality for ascites, but thisprocedure is seldom used because of the highcomplication rate and high incidence of shunt failure.• The shunt is reserved for those who are resistant todiuretic therapy, are not candidates for livertransplantation, have abdominal adhesions, or areineligible for other procedures because of severemedical conditions, such as cardiac disease.Ascites
  50. 50. Ascites
  51. 51. NURSING MANAGEMENT• If a patient with ascites from liver dysfunction ishospitalized, nursing measures include assessment anddocumentation of intake and output, abdominal girth,and daily weight to assess fluid status.• The nurse monitors serum ammonia and electrolytelevels to assess electrolyte balance, response totherapy, and indicators of encephalopathy.Ascites
  52. 52. ESOPHAGEAL VARICES• Esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus.• They are most often a consequence of portalhypertension, commonly due to cirrhosis; patients withesophageal varices have a strong tendency todevelop bleeding.Esophageal VaricesEsophageal varices may abruptly begin to bleed,leading to hemorrhage and death. This is amedical emergency!!!
  53. 53. Esophageal Varices
  54. 54. Esophageal Varices
  55. 55. Esophageal Varices
  56. 56. ASSESSMENT AND DIAGNOSTIC FINDINGS• Endoscopy is used to identify the bleeding site, alongwith barium swallow, ultrasonography, CT, andangiography.PORTAL HYPERTENSION MEASUREMENTS• Portal hypertension may be suspected if dilatedabdominal veins and hemorrhoids are detected. Apalpable enlarged spleen and ascites may also bepresent.• Indirect measurement requires insertion of a fluid-filledballoon catheter into the antecubital or femoral vein.Esophageal Varices
  57. 57. ASSESSMENT AND DIAGNOSTIC FINDINGS• The catheter is advanced under fluoroscopy to ahepatic vein. A ―wedged‖ pressure is obtained byoccluding the blood flow in the blood vessel; pressure inthe unoccluded vessel is also measured.• Direct measurement of portal vein pressure can beobtained by several methods. During laparotomy, aneedle may be introduced into the spleen; a manometerreading of more than 20 mL saline is abnormal.• Another direct measurement requires insertion of acatheter into the portal vein or one of its branches.• Endoscopic measurement of pressure within varices isused only in conjunction with endoscopic sclerotherapy.Esophageal Varices
  58. 58. LABORATORY TESTS• Laboratory tests may include various liver function tests,such as serum aminotransferase, bilirubin, alkalinephosphatase, and serum proteins.• Splenoportography, which involves serial or segmentalx-rays, is used to detect extensive collateral circulationin esophageal vessels, which would indicate varices.• Other tests are hepatoportography and celiacangiography. These are usually performed in theoperating room or radiology department.Esophageal Varices
  59. 59. MEDICAL MANAGEMENT• Bleeding from esophageal varices can quickly lead tohemorrhagic shock and is an emergency.• The extent of bleeding is evaluated and vital signs aremonitored continuously when hematemesis and melenaare present.• Signs of potential hypovolemia are noted, such as coldclammy skin, tachycardia, a drop in blood pressure,decreased urine output, restlessness, and weakperipheral pulses.• Blood volume is monitored by a central venouspressure or arterial catheter.Esophageal Varices
  60. 60. MEDICAL MANAGEMENT• Oxygen is administered to prevent hypoxia and tomaintain adequate blood oxygenation.• Intravenous fluids with electrolytes and volumeexpanders are provided to restore fluid volume andreplace electrolytes.• Transfusion of blood components also may be required.• An indwelling urinary catheter is usually inserted topermit frequent monitoring of urine output.Esophageal Varices
  61. 61. MEDICAL MANAGEMENTPHARMACOLOGIC THERAPY• Vasopressin (Pitressin) may be the initial mode oftherapy because it produces constriction of thesplanchnic arterial bed and a resulting decrease inportal pressure.• Vital signs and the presence or absence of blood in thegastric aspirate indicate the effectiveness ofvasopressin.• Monitoring of fluid intake and output and electrolytelevels is necessary because hyponatremia may occurand vasopressin may have an antidiuretic effect.Esophageal Varices
  62. 62. PHARMACOLOGIC THERAPY• The combination of vasopressin and nitroglycerin hasbeen effective in reducing or preventing the side effectscaused by vasopressin alone.• Somatostatin and octreotide (Sandostatin) have beenreported to be more effective than vasopressin indecreasing bleeding from esophageal varices withoutthe vasoconstrictive effects of vasopressin.• These medications cause selective splanchnicvasoconstriction. Propranolol (Inderal) and nadolol(Corgard), beta-blocking agents that decrease portalpressure, have been shown to prevent bleeding fromesophageal varices in some patients.Esophageal Varices
  63. 63. PHARMACOLOGIC THERAPY• However, it is recommended that they be used only incombination with other treatment modalities such assclerotherapy, variceal banding, or balloon tamponade.• Nitrates such as isosorbide (Isordil) lower portalpressure by venodilation and decreased cardiac output.Esophageal Varices
  64. 64. BALLOON TAMPONADE• In this procedure, pressure is exerted on the cardia andagainst the bleeding varice by a double-balloontamponade (Sengstaken-Blakemore tube).• The tube has four openings, each with a specificpurpose: gastric aspiration, esophageal aspiration,inflation of the gastric balloon, and inflation of theesophageal balloon.• The balloon in the stomach is inflated with 100 to 200mL of air.• An x-ray confirms proper positioning of the gastricballoon.Esophageal Varices
  65. 65. Esophageal Varices
  66. 66. NURSING MANAGEMENT• Nursing measures include frequent mouth and nasalcare. For secretions that accumulate in the mouth,tissues should be within easy reach of the patient. Oralsuction may be necessary to remove oral secretions.• The patient with esophageal hemorrhage is usuallyextremely anxious and frightened. Knowing that thenurse is nearby and will respond immediately can helpalleviate some of this anxiety.• Explanations during the procedure and while the tube isin place may be reassuring to the patient.Esophageal Varices
  67. 67. ENDOSCOPIC SCLEROTHERAPY• In endoscopic sclerotherapy, a sclerosing agent isinjected through a fiberoptic endoscope into thebleeding esophageal varices to promote thrombosis andeventual sclerosis.• After treatment, the patient must be observed forbleeding, perforation of the esophagus, aspirationpneumonia, and esophageal stricture.• Antacids may be administered after the procedure tocounteract the effects of peptic reflux.Esophageal Varices
  68. 68. Esophageal Varices
  69. 69. ESOPHAGEAL BANDING THERAPY(VARICEAL BAND LIGATION)• In variceal banding, a modified endoscope loaded withan elastic rubber band is passed through an overtubedirectly onto the varix (or varices) to be banded.• After suctioning the bleeding varix into the tip of theendoscope, the rubber band is slipped over the tissue,causing necrosis, ulceration, and eventual sloughing ofthe varix.• Variceal banding is comparable to endoscopicsclerotherapy in the effective control of bleeding.Esophageal Varices
  70. 70. Esophageal Varices
  71. 71. Esophageal Varices
  72. 72. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNTING• Transjugular intrahepatic portosystemic shunting (TIPS)is a method of treating esophageal varices in which acannula is threaded into the portal vein by thetransjugular route.• An expandable stent is inserted and serves as anintrahepatic shunt between the portal circulation and thehepatic vein, reducing portal hypertension.• Creation of a TIPS is indicated for the treatment ofrecurrent variceal bleeding refractory to pharmacologicor endoscopic therapy.Esophageal Varices
  73. 73. Esophageal Varices
  74. 74. SURGICAL MANAGEMENT• Procedures that may be used for esophageal varicesare direct surgical ligation of varices; splenorenal,mesocaval, and portacaval venous shunts to relieveportal pressure; and esophageal transection withdevascularization.Esophageal Varices
  75. 75. Esophageal Varices
  76. 76. Esophageal Varices
  77. 77. Esophageal Varices
  78. 78. Esophageal Varices
  79. 79. SURGICAL MANAGEMENTDEVASCULARIZATION AND TRANSECTION• Devascularization and staplegun transectionprocedures to separate the bleeding site from the high-pressure portal system have been used in theemergency management of variceal bleeding.• The lower end of the esophagus is reached through asmall gastrostomy incision; a staple gun permitsanastomosis of the transected ends of the esophagus.Esophageal Varices
  80. 80. NURSING MANAGEMENT• Overall nursing assessment includes monitoring thepatient’s physical condition and evaluating emotionalresponses and cognitive status.• The nurse monitors and records vital signs andassesses the patient’s nutritional and neurologic status.• Complete rest of the esophagus may be indicated withbleeding, so parenteral nutrition is initiated.• Gastric suction usually is initiated to keep the stomachas empty as possible and to prevent straining andvomiting.Esophageal Varices
  81. 81. NURSING MANAGEMENT• The patient often complains of severe thirst, which may berelieved by frequent oral hygiene and moist sponges to thelips.• The nurse closely monitors the blood pressure.• Vitamin K therapy and multiple blood transfusions oftenare indicated because of blood loss.• A quiet environment and calm reassurance may help torelieve the patient’s anxiety and reduce agitation.• The nurse provides support and explanations regardingmedical and nursing interventions.• Monitoring the patient closely will help in detecting andmanaging complications.Esophageal Varices
  82. 82. • Hepatic encephalopathy, a life-threatening complicationof liver disease, occurs with profound liver failure andmay result from the accumulation of ammonia and othertoxic metabolites in the blood.• Hepatic coma represents the most advanced stage ofhepatic encephalopathy.Hepatic Encephalopathy
  83. 83. • Hepatic encephalopathy, a life-threatening complicationof liver disease, occurs with profound liver failure andmay result from the accumulation of ammonia and othertoxic metabolites in the blood.• Hepatic coma represents the most advanced stage ofhepatic encephalopathy.• Portal-systemic encephalopathy, the most common typeof hepatic encephalopathy, occurs primarily in patientswith cirrhosis with portal hypertension and portal-systemic shunting.Hepatic Encephalopathy
  84. 84. CLINICAL MANIFESTATIONS• The earliest symptoms of hepatic encephalopathyinclude minor mental changes and motor disturbances.• The patient appears slightly confused, has alterations inmood, becomes unkempt, and has altered sleeppatterns.• The patient tends to sleep during the day and haverestlessness and insomnia at night.• As hepatic encephalopathy progresses, the patient maybe difficult to awaken.• Asterixis may occur. Simple tasks, such as handwriting,become difficult.Hepatic Encephalopathy
  85. 85. Hepatic Encephalopathy
  86. 86. ASSESSMENT AND DIAGNOSTIC FINDINGS• The electroencephalogram (EEG) shows generalizedslowing, an increase in the amplitude of brain waves,and characteristic triphasic waves.• Occasionally, fetor hepaticus, a sweet, slightly fecalodor to the breath presumed to be of intestinal originmay be noticed.• In a more advanced stage, there are gross disturbancesof consciousness and the patient is completelydisoriented with respect to time and place.• With further progression of the disorder, the patientlapses into frank coma and may have seizures.Hepatic Encephalopathy
  87. 87. MEDICAL MANAGEMENT• Lactulose (Cephulac) is administered to reduce serumammonia levels. It acts by several mechanisms thatpromote the excretion of ammonia in the stool: (1)ammonia is kept in the ionized state, resulting in a fall incolon pH, reversing the normal passage of ammoniafrom the colon to the blood; (2) evacuation of the boweltakes place, which decreases the ammonia absorbedfrom the colon; and (3) the fecal flora are changed toorganisms that do not produce ammonia from urea.• Two or three soft stools per day are desirable; thisindicates that lactulose is performing as intended.Hepatic Encephalopathy
  88. 88. MEDICAL MANAGEMENTAdditional principles of management of hepaticencephalopathy include the following:• Therapy is directed toward treating or removing thecause.• Neurologic status is assessed frequently. A daily recordis kept of handwriting and performance in arithmetic tomonitor mental status.• Fluid intake and output and body weight are recordedeach day.• Vital signs are measured and recorded every 4 hours.Hepatic Encephalopathy
  89. 89. MEDICAL MANAGEMENT• Potential sites of infection (peritoneum, lungs) areassessed frequently, and abnormal findings arereported promptly.• Serum ammonia level is monitored daily.• Protein intake is restricted in patients who are comatoseor who have encephalopathy that is refractory tolactulose and antibiotic therapy.• Reduction in the absorption of ammonia from the GItract is accomplished by the use of gastric suction,enemas, or oral antibiotics.Hepatic Encephalopathy
  90. 90. MEDICAL MANAGEMENT• Electrolyte status is monitored and corrected ifabnormal.• Sedatives, tranquilizers, and analgesic medications arediscontinued.• Benzodiazepine antagonists (flumazenil [Romazicon])may be administered to improve encephalopathywhether or not the patient has previously takenbenzodiazepines.Hepatic Encephalopathy
  91. 91. NURSING MANAGEMENT• The nurse is responsible for maintaining a safeenvironment to prevent injury, bleeding, and infection.• The nurse administers the prescribed treatments andmonitors the patient for the many potentialcomplications.• The nurse also communicates with the pa tient’s familyto keep them informed about the patient’s status, andsupports them by explaining the procedures andtreatments that are part of the patient’s care.• If the patient recovers from hepatic encephalopathy andcoma, rehabilitation is likely to be prolonged.Hepatic Encephalopathy
  92. 92. OTHER MANIFESTATIONS OF LIVER DYSFUNCTIONEDEMA AND BLEEDING• Many patients with liver dysfunction developgeneralized edema from hypoalbuminemia that resultsfrom decreased hepatic production of albumin.• The production of blood clotting factors by the liver isalso reduced, leading to an increased incidence ofbruising, epistaxis, bleeding from wounds, and, asdescribed above, GI bleeding.Hepatic Encephalopathy
  93. 93. OTHER MANIFESTATIONS OF LIVER DYSFUNCTIONVITAMIN DEFICIENCY• Decreased production of several clotting factors may bedue, in part, to deficient absorption of vitamin K from theGI tract. This probably is caused by the inability of livercells to use vitamin K to make prothrombin.• Absorption of the other fat-soluble vitamins (vitamins A,D, and E) as well as dietary fats may also be impairedbecause of decreased secretion of bile salts into theintestine.Hepatic Encephalopathy
  94. 94. VITAMIN DEFICIENCY• Vitamin A deficiency, resulting in night blindness andeye and skin changes• Thiamine deficiency, leading to beriberi, polyneuritis,and Wernicke-Korsakoff psychosis• Riboflavin deficiency, resulting in characteristic skin andmucous membrane lesions• Pyridoxine deficiency, resulting in skin and mucousmembrane lesions and neurologic changes• Vitamin C deficiency, resulting in the hemorrhagiclesions of scurvyHepatic Encephalopathy
  95. 95. VITAMIN DEFICIENCY• Vitamin K deficiency, resulting in hypoprothrombinemia,characterized by spontaneous bleeding andecchymoses• Folic acid deficiency, resulting in macrocytic anemia• The threat of these avitaminoses provides the rationalefor supplementing the diet of every patient with chronicliver disease (especially if alcohol-related) with amplequantities of vitamins• A, B complex, C, and K and folic acid.Hepatic Encephalopathy
  96. 96. METABOLIC ABNORMALITIES• Abnormalities of glucose metabolism also occur; theblood glucose level may be abnormally high shortlyafter a meal (a diabetic type glucose tolerance testresult), but hypoglycemia may occur during fastingbecause of decreased hepatic glycogen reserves anddecreased gluconeogenesis.• Because the ability to metabolize medications isdecreased, medications must be used cautiously andusual medication dosages must be reduced for thepatient with liver failure.Hepatic Encephalopathy
  97. 97. METABOLIC ABNORMALITIES• Many endocrine abnormalities also occur with liverdysfunction because the liver cannot metabolizehormones normally, including androgens or sexhormones.• Gynecomastia, amenorrhea, testicular atrophy, loss ofpubic hair in the male, and menstrual irregularities in thefemale and other disturbances of sexual function andsex characteristics are thought to result from failure ofthe damaged liver to inactivate estrogens normally.Hepatic Encephalopathy
  98. 98. PRURITUS AND OTHER SKIN CHANGES• Patients with liver dysfunction resulting from biliaryobstruction commonly develop severe itching (pruritus)due to retention of bile salts. Patients may developvascular (or arterial) spider angiomas on the skin,generally above the waistline.• Patients may also develop reddened palms (―liverpalms‖ or palmar erythema).Hepatic Encephalopathy
  99. 99. Hepatic Encephalopathy
  100. 100. VIRAL HEPATITIS• Viral hepatitis is a systemic, viral infection in whichnecrosis and inflammation of liver cells produce acharacteristic cluster of clinical, biochemical, andcellular changes.• To date, five definitive types of viral hepatitis have beenidentified: hepatitis A, B, C, D, and E. Hepatitis A and Eare similar in mode of transmission (fecal–oral route),whereas hepatitis B, C, and D share manycharacteristics.Viral Hepatic Disorders
  101. 101. HEPATITIS A VIRUS (HAV)• Hepatitis A, formerly called infectious hepatitis, iscaused by an RNA virus of the Enterovirus family.• The mode of transmission of this disease is the fecal–oral route, primarily through the ingestion of food orliquids infected by the virus.• Typically, it is acquired by poor hygiene, hand-to-mouthcontact, or close contact.• It is more prevalent in developing countries or in areaswith overcrowding and poor sanitation.Viral Hepatic Disorders
  102. 102. HEPATITIS A VIRUS (HAV)• It is rarely, if ever, transmitted by blood transfusions.• Hepatitis A can be transmitted during sexual activity;this is more likely with oral–anal contact, analintercourse, and a greater number of sex partners.• The incubation period is estimated to be 15 to 50 days,with an average of 30 days. The illness may beprolonged, lasting 4 to 8 weeks. It generally lasts longerand is more severe in those older than 40 years of age.• Hepatitis A confers immunity against itself, but theperson may contract other forms of hepatitis.Viral Hepatic Disorders
  103. 103. CLINICAL MANIFESTATIONS• Many patients are anicteric and symptomless.• When symptoms appear, they are of a mild, flu-likeupper respiratory tract infection, with low-grade fever.• Anorexia, an early symptom, is often severe.• Later, jaundice and dark urine may become apparent.• Indigestion is present in varying degrees, marked byvague epigastric distress, nausea, heartburn, andflatulence.• The patient may also develop a strong aversion to thetaste of cigarettes or the presence of cigarette smokeand other strong odors.Viral Hepatic Disorders
  104. 104. ASSESSMENT AND DIAGNOSTIC FINDINGS• The liver and spleen are often moderately enlarged fora few days after onset; otherwise, apart from jaundice,there are few physical signs.• Hepatitis A antigen may be found in the stool a week to10 days before illness and for 2 to 3 weeks aftersymptoms appear.• HAV antibodies are detectable in the serum, but usuallynot until symptoms appear.• Analysis of subclasses of immunoglobulins can helpdetermine whether the antibody represents acute orpast infection.Viral Hepatic Disorders
  105. 105. PREVENTION• Proper community and home sanitation• Conscientious individual hygiene• Safe practices for preparing and dispensing food• Effective health supervision of schools, dormitories,extended care facilities, barracks, and camps• Community health education programs• Mandatory reporting of viral hepatitis to local healthdepartments• Vaccination for travelers to developing countries, illegaldrug users, men who have sex with men, and persons withchronic liver disease• Vaccination to interrupt community-wide outbreaksViral Hepatic Disorders
  106. 106. MEDICAL MANAGEMENT• Bed rest during the acute stage and a diet that is bothacceptable to the patient and nutritious are part of thetreatment and nursing care.• During the period of anorexia, the patient should receivefrequent small feedings, supplemented, if necessary, byIV fluids with glucose.• Because this patient often has an aversion to food,gentle persistence and creativity may be required tostimulate the appetite.• Optimal food and fluid levels are necessary tocounteract weight loss and slow recovery.Viral Hepatic Disorders
  107. 107. MEDICAL MANAGEMENT• The patient’s sense of well-being as well as laboratorytest results are generally appropriate guides to bed restand restriction of physical activity.• Gradual but progressive ambulation seems to hastenrecovery, provided the patient rests after activity anddoes not participate in activities to the point of fatigue.Viral Hepatic Disorders
  108. 108. DIETARY MANAGEMENT OF VIRAL HEPATITIS• Recommend small, frequent meals.• Provide intake of 2,000 to 3,000 kcal/day during acuteillness.• Although early studies indicate that a high-protein, high-calorie diet may be beneficial, advise patient not toforce food and to restrict fat intake.• Carefully monitor fluid balance.• If anorexia and nausea and vomiting persist, enteralfeedings may be necessary.• Instruct patient to abstain from alcohol during acuteillness and for 6 months after recovery.Viral Hepatic Disorders
  109. 109. DIETARY MANAGEMENT OF VIRAL HEPATITIS• Advise patient to avoid substances (medication, herbs,illicit drugs, and toxins) that may affect liver function.Viral Hepatic Disorders
  110. 110. NURSING MANAGEMENT• The patient is usually managed at home unlesssymptoms are severe.• The nurse assists the patient and family in coping withthe temporary disability and fatigue that are common inhepatitis and instructs them to seek additional healthcare if the symptoms persist or worsen.• The patient and family also need specific guidelinesabout diet, rest, follow-up blood work, and theimportance of avoiding alcohol, as well as sanitationand hygiene measures to prevent spread of the diseaseto other family members.Viral Hepatic Disorders
  111. 111. NURSING MANAGEMENT• Specific teaching to patients and families aboutreducing the risk of contracting hepatitis A includesgood personal hygiene, stressing careful hand washing,and environmental sanitation.Viral Hepatic Disorders
  112. 112. HEPATITIS B VIRUS (HBV)• Hepatitis B is transmitted primarily through blood(percutaneous and permucosal routes). HBV has beenfound in blood, saliva, semen, and vaginal secretionsand can be transmitted through mucous membranesand breaks in the skin.• HBV is also transferred from carrier mothers to theirbabies, especially in areas with a high incidence (ie,Southeast Asia).• HBV has a long incubation period. It replicates in theliver and remains in the serum for relatively longperiods, allowing transmission of the virus.Viral Hepatic Disorders
  113. 113. HEPATITIS B VIRUS (HBV)• Those at risk for developing hepatitis B includesurgeons, clinical laboratory workers, dentists, nurses,and respiratory therapists. Staff and patients inhemodialysis and oncology units and sexually activehomosexual and bisexual men and injection drug usersare also at increased risk.• Most people who contract hepatitis B infections willdevelop antibodies and recover spontaneously in 6months.• The mortality rate from hepatitis B has been reported tobe as high as 10%.Viral Hepatic Disorders
  114. 114. HEPATITIS B VIRUS (HBV)• Another 10% of patients who have hepatitis B progressto a carrier state or develop chronic hepatitis withpersistent HBV infection and hepatocellular injury andinflammation.• It remains a major cause of cirrhosis and hepatocellularcarcinoma worldwide.Viral Hepatic Disorders
  115. 115. RISK FACTORS FOR HEPATITIS B• Frequent exposure to blood, blood products, or otherbody fluids• Health care workers: hemodialysis staff, oncology andchemotherapy nurses, personnel at risk forneedlesticks, operating room staff, respiratorytherapists, surgeons, dentists• Hemodialysis• Male homosexual and bisexual activity• IV/injection drug use• Close contact with carrier of HBVViral Hepatic Disorders
  116. 116. RISK FACTORS FOR HEPATITIS B• Travel to or residence in area with uncertain sanitaryconditions• Multiple sexual partners• Recent history of sexually transmitted disease• Receipt of blood or blood products (eg, clotting factorconcentrate)Viral Hepatic Disorders
  117. 117. CLINICAL MANIFESTATIONS• Clinically, the disease closely resembles hepatitis A, butthe incubation period is much longer (1 to 6 months).• Fever and respiratory symptoms are rare; somepatients have arthralgias and rashes.• The patient may have loss of appetite, dyspepsia,abdominal pain, generalized aching, malaise, andweakness.• Jaundice may or may not be evident. If jaundice occurs,light-colored stools and dark urine accompany it.• The liver may be tender and enlarged to 12 to 14 cmvertically.Viral Hepatic Disorders
  118. 118. CLINICAL MANIFESTATIONS• The spleen is enlarged and palpable in a few patients;the posterior cervical lymph nodes may also beenlarged.Viral Hepatic Disorders
  119. 119. ASSESSMENT AND DIAGNOSTIC FINDINGSHBV is a DNA virus composed of the following antigenicparticles:• HBcAg—hepatitis B core antigen (antigenic material inan inner core)• HBsAg—hepatitis B surface antigen (antigenic materialon surface of HBV)• HBeAg—an independent protein circulating in the blood• HBxAg—gene product of X gene of HBV/DNAViral Hepatic Disorders
  120. 120. ASSESSMENT AND DIAGNOSTIC FINDINGSEach antigen elicits its specific antibody and is a markerfor different stages of the disease process:• anti-HBc—antibody to core antigen or HBV; persistsduring the acute phase of illness; may indicatecontinuing HBV in the liver• anti-HBs—antibody to surface determinants on HBV;detected during late convalescence; usually indicatesrecovery and development of immunity• anti-HBe—antibody to hepatitis B e-antigen; usuallysignifies reduced infectivityViral Hepatic Disorders
  121. 121. ASSESSMENT AND DIAGNOSTIC FINDINGS• anti-HBxAg—antibody to the hepatitis B x-antigen; mayindicate ongoing replication of HBVViral Hepatic Disorders
  122. 122. PREVENTION• The goals of prevention are to interrupt the chain oftransmission, to protect people at high risk with activeimmunization through the use of hepatitis B vaccine,and to use passive immunization for unprotected peopleexposed to HBV.Viral Hepatic Disorders
  123. 123. PREVENTING TRANSMISSION• Continued screening of blood donors for the presenceof hepatitis B antigens will further decrease the risk oftransmission by blood transfusion.• The use of disposable syringes, needles, and lancetsand the introduction of needleless IV administrationsystems reduce the risk of spreading this infection fromone patient to another or to health care personnelduring the collection of blood samples or theadministration of parenteral therapy.• Good personal hygiene is fundamental to infectioncontrol.Viral Hepatic Disorders
  124. 124. PREVENTING TRANSMISSION• Gloves are worn when handling all blood and bodyfluids as well as HBAgpositive specimens, or whenthere is potential exposure to blood or to patients’secretions.• Eating and smoking are prohibited in the laboratory andin other areas exposed to secretions, blood, or bloodproducts.• Patient education regarding the nature of the disease,its infectiousness, and prognosis is a critical factor inpreventing transmission and protecting contacts.Viral Hepatic Disorders
  125. 125. ACTIVE IMMUNIZATION: HEPATITIS B VACCINE• Active immunization is recommended for individuals athigh risk for hepatitis B. In addition, individuals withhepatitis C and other chronic liver diseases shouldreceive the vaccine.• The need for booster doses may be revisited if reportsof hepatitis B increase or an increased prevalence ofthe carrier state develops, indicating that protection isdeclining.Viral Hepatic Disorders
  126. 126. ACTIVE IMMUNIZATION: HEPATITIS B VACCINE• Both forms of the hepatitis B vaccine are administeredintramuscularly in three doses, the second and thirddoses 1 and 6 months after the first dose. The thirddose is very important in producing prolonged immunity.• Hepatitis B vaccination should be administered to adultsin the deltoid muscle.• Antibody response may be measured by anti-HBs levels1 to 3 months after completing the basic course ofvaccine, but this testing is not routine and not currentlyrecommended.Viral Hepatic Disorders
  127. 127. PASSIVE IMMUNITY: HEPATITIS B IMMUNE GLOBULIN• Hepatitis B immune globulin (HBIG) provides passiveimmunity to hepatitis B and is indicated for peopleexposed to HBV who have never had hepatitis B andhave never received hepatitis B vaccine.Specific indications for postexposure vaccine with HBIGinclude:(1) inadvertent exposure to HBAg-positive blood throughpercutaneous (needlestick) or transmucosal (splashesin contact with mucous membrane) routes,(2) sexual contact with people positive for HBAg, andViral Hepatic Disorders
  128. 128. PASSIVE IMMUNITY: HEPATITIS B IMMUNE GLOBULIN(3) perinatal exposure (babies born to HBV-infectedmothers should receive HBIG within 12 hours ofdelivery).Viral Hepatic Disorders
  129. 129. MEDICAL MANAGEMENT• The goals of treatment are to minimize infectivity,normalize liver inflammation, and decrease symptoms.• Of all the agents that have been used to treat chronictype B viral hepatitis, alpha interferon as the singlemodality of therapy offers the most promise.• This regimen of 5 million units daily or 10 million unitsthree times weekly for 4 to 6 months results inremission of disease in approximately one third ofpatients.• Interferon must be administered by injection and hassignificant side effects, including fever, chills, anorexia,nausea, myalgias, and fatigue.Viral Hepatic Disorders
  130. 130. MEDICAL MANAGEMENT• Late side effects are more serious and may necessitatedosage reduction or discontinuation.• Two antiviral agents (lamivudine [Epvir] and adefovir[Hepsera]) oral nucleoside analogs, have beenapproved for use in chronic hepatitis B.• Bed rest may be recommended, regardless of othertreatment, until the symptoms of hepatitis havesubsided.• Activities are restricted until the hepatic enlargementand elevated levels of serum bilirubin and liver enzymeshave disappeared.Viral Hepatic Disorders
  131. 131. MEDICAL MANAGEMENT• Gradually increased activity is then allowed.• Adequate nutrition should be maintained; proteins arerestricted when the liver’s ability to metabolize proteinbyproducts is impaired, as demonstrated by symptoms.• Measures to control the dyspeptic symptoms andgeneral malaise include the use of antacids andantiemetics, but all medications should be avoided ifvomiting occurs. If vomiting persists, the patient mayrequire hospitalization and fluid therapy.Viral Hepatic Disorders
  132. 132. NURSING MANAGEMENT• Convalescence may be prolonged, with completesymptomatic recovery sometimes requiring 3 to 4months or longer. During this stage, gradual resumptionof physical activity is encouraged after the jaundice hasresolved.• The nurse identifies psychosocial issues and concerns,particularly the effects of separation from family andfriends if the patient is hospitalized during the acute andinfective stages.• Planning that includes the family helps to decrease theirfears and anxieties about the spread of the disease.Viral Hepatic Disorders
  133. 133. HEPATITIS C VIRUS (HCV)• A significant proportion of cases of viral hepatitis areneither hepatitis A, hepatitis B, nor hepatitis D; as aresult, they are classified as hepatitis C (formerlyreferred to as non-A, non-B hepatitis, or NANBhepatitis).• Whereas blood transfusions and sexual contact onceaccounted for most cases of hepatitis C, otherparenteral means, such as sharing contaminatedneedles by IV/injection drug users and unintentionalneedlesticks and other injuries in health care workers,now account for a significant number of cases.Viral Hepatic Disorders
  134. 134. HEPATITIS C VIRUS (HCV)• The highest prevalence of hepatitis C is in adults 40 to59 years of age, and in this age group its prevalance ishighest in African Americans.• HCV is the underlying cause of about one-third of casesof hepatocellular carcinoma, and it is the most commonreason for liver transplantation.• Individuals at special risk for hepatitis C includeIV/injection drug users, sexually active people withmultiple partners, patients receiving frequenttransfusions or those who require large volumes ofblood, and health care personnel.Viral Hepatic Disorders
  135. 135. HEPATITIS C VIRUS (HCV)• The incubation period is variable and may range from15 to 160 days. The clinical course of acute hepatitis Cis similar to that of hepatitis B; symptoms are usuallymild.Viral Hepatic Disorders
  136. 136. RISK FACTORS FOR HEPATITIS C• Recipient of blood products or organ transplant prior to1992 or clotting factor concentrates before 1987• Health care and public safety workers after needlestickinjuries or mucosal exposure to blood• Children born to women infected with hepatitis C virus• Past/current illicit IV/injection drug use• Past treatment with chronic hemodialysis• Sex with infected partner, having multiple sex partners,history of STD, unprotected sexViral Hepatic Disorders
  137. 137. HEPATITIS D VIRUS (HDV)• Hepatitis D (delta agent) occurs in some cases ofhepatitis B. Because the virus requires hepatitis Bsurface antigen for its replication, only individuals withhepatitis B are at risk for hepatitis D.• Anti-delta antibodies in the presence of HBAg on testingconfirm the diagnosis.• It is also common among IV/injection drug users,hemodialysis patients, and recipients of multiple bloodtransfusions. Sexual contact with those with hepatitis Bis considered to be an important mode of transmissionof hepatitis B and D.Viral Hepatic Disorders
  138. 138. HEPATITIS D VIRUS (HDV)• The incubation period varies between 21 and 140 days.• The symptoms of hepatitis D are similar to those ofhepatitis B, except that patients are more likely todevelop fulminant hepatitis and to progress to chronicactive hepatitis and cirrhosis.• Treatment is similar to that of other forms of hepatitis;interferon as a specific treatment for hepatitis D is underinvestigation.Viral Hepatic Disorders
  139. 139. HEPATITIS E VIRUS (HEV)• Hepatitis E is believed to be transmitted by the fecal–oral route, principally through contaminated water inareas with poor sanitation.• The incubation period is variable, estimated to rangebetween 15 and 65 days.• In general, hepatitis E resembles hepatitis A. It has aself-limiting course with an abrupt onset.• Jaundice is nearly always present. Chronic forms do notdevelop.Viral Hepatic Disorders
  140. 140. HEPATITIS E VIRUS (HEV)• Avoiding contact with the virus through good hygiene,including hand washing, is the major method ofprevention of hepatitis E.• The effectiveness of immune globulin in protectingagainst hepatitis E virus is uncertain.Viral Hepatic Disorders
  141. 141. HEPATITIS G (HGV) AND GB VIRUS-C• It has long been believed that there is another non-A,non-B, non- C agent causing hepatitis in humans.• The incubation period for post-transfusion hepatitis is 14to 145 days, too long for hepatitis B or C.• Autoantibodies are absent. The clinical significance ofthis virus remains uncertain.• Risk factors are similar to those for hepatitis C. There isno clear relationship between GBV-C/HGV infection andprogressive liver disease.• Persistent infection does occur but does not affect theclinical course.Viral Hepatic Disorders
  142. 142. FULMINANT HEPATIC FAILURE• Fulminant hepatic failure is the clinical syndrome ofsudden and severely impaired liver function in apreviously healthy person.• According to the original and generally accepteddefinition, fulminant hepatic failure develops within 8weeks of the first symptoms of jaundice.Three categories are frequently cited: hyperacute, acute,and subacute liver failure.• In hyperacute liver failure, the duration of jaundicebefore the onset of encephalopathy is 0 to 7 days;• In acute liver failure, it is 8 to 28 days; andNon-Viral Hepatic Disorders
  143. 143. FULMINANT HEPATIC FAILURE• In subacute liver failure, it is 28 to 72 days.• The prognosis for fulminant hepatic failure is much worsethan for chronic liver failure.• However, in fulminant failure, the hepatic lesion ispotentially reversible, with survival rates of approximately50% to 85%. Those who do not survive die of massivehepatocellular injury and necrosis.• Viral hepatitis is a common cause of fulminant hepaticfailure; other causes include toxic medications (eg,acetaminophen) and chemicals (eg, carbon tetrachloride),metabolic disturbances (Wilson’s disease), and structuralchanges (Budd-Chiari syndrome).Non-Viral Hepatic Disorders
  144. 144. FULMINANT HEPATIC FAILURE• Jaundice and profound anorexia may be the initialreasons the patient seeks health care.• Fulminant hepatic failure is often accompanied bycoagulation defects, renal failure and electrolytedisturbances, infection, hypoglycemia, encephalopathy,and cerebral edema.Non-Viral Hepatic Disorders
  145. 145. MANAGEMENT• The key to optimizing treatment is rapid recognition ofacute liver failure and intensive interventions.• Treatment modalities may include plasma exchanges(plasmapheresis) or charcoal hemoperfusion for theremoval of potentially harmful metabolites.• Hepatocytes within synthetic fiber columns have beentested as liver support systems (liver assist devices)and a bridge to transplantation.• The acronyms ELAD (extracorporeal liver assistdevices) and BAL (bioartificial liver) have been used todescribe these hybrid devices.• These temporary devices help patients to survive untilNon-Viral Hepatic Disorders
  146. 146. MANAGEMENT• These temporary devices help patients to survive untiltransplantation is possible.• The BAL exposes separated plasma to a cartridgecontaining porcine liver cells after the plasma hasflowed through a charcoal column that removessubstances toxic to hepatocytes.• The ELAD device exposes whole blood to cartridgescontaining human hepatoblastoma cells, resulting inremoval of toxic substances.Non-Viral Hepatic Disorders
  147. 147. HEPATIC CIRRHOSIS• Cirrhosis is a chronic disease characterized byreplacement of normal liver tissue with diffuse fibrosisthat disrupts the structure and function of the liver.There are three types of cirrhosis or scarring of the liver:• Alcoholic cirrhosis, in which the scar tissuecharacteristically surrounds the portal areas. This ismost frequently due to chronic alcoholism and is themost common type of cirrhosis.• Postnecrotic cirrhosis, in which there are broad bandsof scar tissue as a late result of a previous bout of acuteviral hepatitis.Non-Viral Hepatic Disorders
  148. 148. HEPATIC CIRRHOSIS• Biliary cirrhosis, in which scarring occurs in the liveraround the bile ducts. This type usually is the result ofchronic biliary obstruction and infection (cholangitis); itis much less common than the other two types.Non-Viral Hepatic Disorders
  149. 149. CLINICAL MANIFESTATIONS OF CIRRHOSISCOMPENSATEDNon-Viral Hepatic Disorders• Intermittent mild fever• Vascular spiders• Palmar erythema• Unexplained epistaxis• Ankle edema• Vague morning indigestion• Flatulent dyspepsia• Abdominal pain• Firm, enlarged liver• Splenomegaly
  150. 150. CLINICAL MANIFESTATIONS OF CIRRHOSISDECOMPENSATEDNon-Viral Hepatic Disorders• Ascites• Jaundice• Weakness• Muscle wasting• Weight loss• Continuous mild fever• Clubbing of fingers• Purpura• Spontaneous bruising• Epistaxis• Hypotension• Sparse body hair• White nails• Gonadal atrophy
  151. 151. ASSESSMENT AND DIAGNOSTIC FINDINGS• Enzyme tests indicate liver cell damage: serum alkalinephosphatase, AST, ALT, and GGT levels increase, andthe serum cholinesterase level may decrease.• Bilirubin tests are performed to measure bile excretionor bile retention; elevated levels can occur with cirrhosisand other liver disorders.• Prothrombin time is prolonged.• Ultrasound scanning is used to measure the differencein density of parenchymal cells and scar tissue.• CT, MRI, and radioisotope liver scans give informationabout liver size and hepatic blood flow and obstruction.Non-Viral Hepatic Disorders
  152. 152. ASSESSMENT AND DIAGNOSTIC FINDINGS• Diagnosis is confirmed by liver biopsy.• Arterial blood gas analysis may reveal a ventilation–perfusion imbalance and hypoxia.Non-Viral Hepatic Disorders
  153. 153. MEDICAL MANAGEMENT• The management of the patient with cirrhosis is usuallybased on the presenting symptoms. For example,antacids are prescribed to decrease gastric distress andminimize the possibility of GI bleeding.• Vitamins and nutritional supplements promote healingof damaged liver cells and improve the generalnutritional status.• Potassium-sparing diuretics (spironolactone[Aldactone], triamterene [Dyrenium]) may be indicatedto decrease ascites, if present.• An adequate diet and avoidance of alcohol areessential.Non-Viral Hepatic Disorders
  154. 154. MEDICAL MANAGEMENT• Colchicine is believed to reverse the fibrotic processesin cirrhosis, and this has improved survival.Non-Viral Hepatic Disorders
  155. 155. MEDICAL MANAGEMENT• Colchicine is believed to reverse the fibrotic processesin cirrhosis, and this has improved survival.Non-Viral Hepatic Disorders
  156. 156. The Patient with Liver CirrhosisASSESSMENT• Nursing assessment focuses on the onset of symptomsand the history of precipitating factors, particularly long-term alcohol abuse, as well as dietary intake andchanges 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 toxicagents encountered in the workplace or duringrecreational activities.NURSING PROCESS:
  157. 157. The Patient with Liver CirrhosisASSESSMENT• The nurse documents and reports exposure topotentially hepatotoxic substances (medications, illicitIV/injection drugs, inhalants) or general anestheticagents.• The nurse assesses the patient’s mental status throughthe interview and other interactions with the patient;orientation to person, place, and time is noted.• The patient’s ability to carry out a job or householdactivities provides some information about physical andmental status.NURSING PROCESS:
  158. 158. The Patient with Liver CirrhosisASSESSMENT• The patient’s relationships with family, friends, andcoworkers may give some indication aboutincapacitation secondary to alcohol abuse and cirrhosis.• Abdominal distention and bloating, GI bleeding,bruising, and weight changes are noted.• The nurse assesses nutritional status, which is of majorimportance in cirrhosis, by daily weights and monitoringof plasma proteins, transferrin, and creatinine levels.NURSING PROCESS:
  159. 159. The Patient with Liver CirrhosisNURSING DIAGNOSES• Activity intolerance related to fatigue, general debility,muscle wasting, and discomfort• Imbalanced nutrition, less than body requirements,related to chronic gastritis, decreased GI motility, andanorexia• Impaired skin integrity related to compromisedimmunologic status, edema, and poor nutrition• Risk for injury and bleeding related to altered clottingmechanisms
  160. 160. The Patient with Liver CirrhosisCOMPLICATIONS• Bleeding and hemorrhage• Hepatic encephalopathy• Fluid volume excess
  161. 161. The Patient with Liver CirrhosisPLANNING AND GOALS• The goals for the patient may include increasedparticipation in activities, improvement of nutritionalstatus, improvement of skin integrity, decreasedpotential for injury, improvement of mental status, andabsence of complications.
  162. 162. The Patient with Liver CirrhosisNURSING INTERVENTIONS• PROMOTING REST• IMPROVING NUTRITIONAL STATUS• PROVIDING SKIN CARE• REDUCING RISK OF INJURY• PROMOTING HOME AND COMMUNITY-BASEDCARE
  163. 163. The Patient with Liver CirrhosisMONITORING AND MANAGINGPOTENTIAL COMPLICATIONSBLEEDING AND HEMORRHAGE• Precautionary measures include protecting the patientwith padded side rails, applying pressure to injectionsites, and avoiding injury from sharp objects.• The nurse observes for melena and assesses stools forblood.• Vital signs are monitored regularly.• Precautions are taken to minimize rupture ofesophageal varices by avoiding further increases inportal pressure .
  164. 164. The Patient with Liver CirrhosisBLEEDING AND HEMORRHAGE• Dietary modification and appropriate use of stoolsofteners may help prevent straining during defecation.• The nurse closely monitors the patient for GI bleedingand keeps readily available equipment (Sengstaken–Blakemore tube), IV fluids, and medications needed totreat hemorrhage from esophageal and gastric varices.• If hemorrhage occurs, the nurse assists the physician ininitiating measures to halt the bleeding, administeringfluid and blood component therapy and medications.
  165. 165. The Patient with Liver CirrhosisHEPATIC ENCEPHALOPATHY• Hepatic encephalopathy is mainly caused by theaccumulation of ammonia in the blood and its effect oncerebral metabolism.• Treatment may include the use of lactulose andnonabsorbable intestinal tract antibiotics to decreaseammonia levels, modification in medications toeliminate those that may precipitate or worsen hepaticencephalopathy, and bed rest to minimize energyexpenditure.• Monitoring is an essential nursing function to identifyearly deterioration in mental status.
  166. 166. The Patient with Liver CirrhosisHEPATIC ENCEPHALOPATHY• The nurse monitors the patient’s mental status closelyand reports changes so that treatment ofencephalopathy can be initiated promptly.• Because electrolyte disturbances can contribute toencephalopathy, serum electrolyte levels are carefullymonitored and corrected if abnormal.• Oxygen is administered if oxygen desaturation occurs.• The nurse monitors for fever or abdominal pain, whichmay signal the onset of bacterial peritonitis or otherinfection.
  167. 167. The Patient with Liver CirrhosisFLUID VOLUME EXCESS• A hyperdynamic circulatory state develops in patientswith cirrhosis, and plasma volume increases. Thisincrease in circulating plasma volume may be due inpart to splanchnic venous congestion.• Close assessment of the cardiovascular and respiratorystatus is key for the nurse caring for patients with thisdisorder.• Administering diuretics, implementing fluid restrictions,and enhancing patient positioning can optimizepulmonary function.• Fluid retention may be noted in the development ofascites and lower extremity swelling and dyspnea.
  168. 168. The Patient with Liver CirrhosisFLUID VOLUME EXCESS• Monitoring intake and output, daily weight changes,changes in abdominal girth, and edema formation ispart of nursing assessment in the hospital or in thehome setting.• Patients are also monitored for nocturia and, later,oliguria as these states indicate increasing severity ofliver function.
  169. 169. The Patient with Liver CirrhosisEVALUATIONEXPECTED PATIENT OUTCOMES1. Participates in activitiesa. Plans activities and exercises to allow alternatingperiods of rest and activityb. Reports increased strength and well-beingc. Participates in hygiene care2. Increases nutritional intakea. Demonstrates intake of appropriate nutrients andavoidance of alcohol as reflected by diet logb. Gains weight without increased edema and ascitesformation
  170. 170. The Patient with Liver CirrhosisEVALUATIONEXPECTED PATIENT OUTCOMESc. Reports decrease in GI disturbances and anorexiad. Identifies foods and fluids that are nutritious andallowed on diet or restricted from diete. Adheres to vitamin therapy regimenf. Describes the rationale for small, frequent meals3. Exhibits improved skin integritya. Has intact skin without evidence of breakdown,infection or traumab. Demonstrates normal turgor of skin of extremitiesand trunk, without edema
  171. 171. The Patient with Liver CirrhosisEVALUATIONEXPECTED PATIENT OUTCOMESc. Changes position frequently and inspects bonyprominences dailyd. Uses lotions to decrease pruritus4. Avoids injurya. Is free of ecchymotic areas or hematoma formationb. States rationale for side rails and asks for assistanceto get out of bedc. Uses measures to prevent trauma (eg, uses electricrazor and soft toothbrush, blows nose gently,arranges furniture to prevent bumps and falls, avoidsstraining during defecation)
  172. 172. The Patient with Liver CirrhosisEVALUATIONEXPECTED PATIENT OUTCOMES5. Is free of complicationsa. Reports absence of frank bleeding from GI tract (ie,absence of melena and hematemesis)b. Is oriented to time, place, and person anddemonstrates normal attention spanc. Has serum ammonia level within normal limitsd. Identifies early, reportable signs of impaired thought
  173. 173. • Hepatic tumors may be malignant or benign. Benignliver tumor were uncommon until the widespread use oforal contraceptives.• With the use of oral contraceptives, benign tumors ofthe liver occur most frequently in women in theirreproductive years.PRIMARY LIVER TUMORS• Primary liver tumors usually are associated with chronicliver disease, hepatitis B and C infections, and cirrhosis.• Hepatocellular carcinoma (HCC) is by far the mostcommon type of primary liver cancer.Cancer of the Liver
  174. 174. • HCC is usually nonresectable because of rapid growthand metastasis.• Other types of primary liver cancer includecholangiocellular carcinoma and combinedhepatocellular and cholangiocellular carcinoma.• Cirrhosis, chronic infection with hepatitis B and C, andexposure to certain chemical toxins (eg, vinyl chloride,arsenic) have been implicated as causes of HCC.• Cigarette smoking has also been identified as a riskfactor, especially when combined with alcohol use.• Some evidence suggests that aflatoxin, a metabolite ofthe fungus Aspergillus flavus, may be a risk factor forHCC.Cancer of the Liver
  175. 175. LIVER METASTASES• Metastases from other primary sites are found in theliver in about half of all advanced cancer cases.• Malignant tumors are likely to reach the liver eventually,by way of the portal system or lymphatic channels, or bydirect extension from an abdominal tumor.Cancer of the Liver
  176. 176. CLINICAL MANIFESTATIONS• The early manifestations of malignancy of the liverinclude pain, a continuous dull ache in the right upperquadrant, epigastrium, or back.• Weight loss, loss of strength, anorexia, and anemia mayalso occur.• The liver may be enlarged and irregular on palpation.• Jaundice is present only if the larger bile ducts areoccluded by the pressure of malignant nodules in thehilum of the liver.• Ascites develops if such nodules obstruct the portalveins or if tumor tissue is seeded in the peritonealcavity.Cancer of the Liver
  177. 177. ASSESSMENT AND DIAGNOSTIC FINDINGS• The liver cancer diagnosis is based on clinical signs andsymptoms, the history and physical examination, andthe results of laboratory and x-ray studies.• Increased serum levels of bilirubin, alkalinephosphatase, AST, GGT, and lactic dehydrogenase mayoccur.• Leukocytosis, erythrocytosis, hypercalcemia,hypoglycemia, and hypocholesterolemia may also beseen on laboratory assessment.• The serum level of alpha-fetoprotein (AFP), whichserves as a tumor marker, is elevated in 30% to 40% ofpatients with primary liver cancer.Cancer of the Liver
  178. 178. ASSESSMENT AND DIAGNOSTIC FINDINGS• Levels of carcinoembryonic antigen (CEA), a marker ofadvanced cancer of the digestive tract, may beelevated.• X-rays, liver scans, CT scans, ultrasound studies, MRI,arteriography, and laparoscopy may be part of thediagnostic workup and may be performed to determinethe extent of the cancer.• Positive emission tomograms (PET scans) are used toevaluate a wide range of metastatic tumors of the liver.• Confirmation of a tumor’s histology can be made bybiopsy under imaging guidance (CT scan or ultrasound)or laparoscopically.Cancer of the Liver
  179. 179. ASSESSMENT AND DIAGNOSTIC FINDINGS• Local or systemic dissemination of the tumor by needlebiopsy or fine-needle biopsy can occur but is rare.Cancer of the Liver
  180. 180. MEDICAL MANAGEMENT• Radiation therapy and chemotherapy have been used intreating cancer of the liver with varying degrees ofsuccess.• Although these therapies may prolong survival andimprove quality of life by reducing pain and discomfort,their major effect is palliative.Cancer of the Liver
  181. 181. RADIATION THERAPYEffective methods of delivering radiation to tumors of theliver include:(1) intravenous or intraarterial injection of antibodies thatare tagged with radioactive isotopes and specificallyattack tumor-associated antigens and(2) percutaneous placement of a high-intensity source forinterstitial radiation therapy (delivering radiationdirectly to the tumor cells)Cancer of the Liver
  182. 182. CHEMOTHERAPY• Systemic chemotherapy and regional infusionchemotherapy are two methods used to administerantineoplastic agents to patients with primary andmetastatic hepatic tumors.• An implantable pump has been used to deliver a highconcentration of chemotherapy to the liver through thehepatic artery. This method provides a reliable,controlled, and continuous infusion of medication thatcan be carried out in the patient’s home.Cancer of the Liver
  183. 183. PERCUTANEOUS BILIARY DRAINAGE• Percutaneous biliary or transhepatic drainage is used tobypass biliary ducts obstructed by liver, pancreatic, or bileduct tumors in patients with inoperable tumors or in thoseconsidered poor surgical risks.• Complications of percutaneous biliary drainage includesepsis, leakage of bile, hemorrhage, and reobstruction ofthe biliary system by debris in the catheter or fromencroaching tumor.• Therefore, the patient is observed for fever and chills, biledrainage around the catheter, changes in vital signs, andevidence of biliary obstruction, including increased pain orpressure, pruritus, and recurrence of jaundice.Cancer of the Liver
  184. 184. OTHER NONSURGICAL TREATMENTS• Laser hyperthermia has been used to treat hepaticmetastases.• In radiofrequency thermal ablation, a needle electrode isinserted into the liver tumor under imaging guidance.• In immunotherapy, lymphocytes with antitumor reactivityare administered to the patient with hepatic cancer.• Transcatheter arterial embolization interrupts the arterialblood flow to small tumors by injecting small particulateembolic or chemotherapeutic agents into the arterysupplying the tumor.• For multiple small lesions, ultrasound-guided injection ofalcohol promotes dehydration of tumor cells and tumornecrosis.Cancer of the Liver
  185. 185. SURGICAL MANAGEMENTLOBECTOMY• Removal of a lobe of the liver is the most commonsurgical procedure for excising a liver tumor.CRYOSURGERY• In cryosurgery (cryoablation), tumors are destroyed byliquid nitrogen at −196° C. To destroy the diseasedtissue, two or three freeze-and-thaw cycles areadministered via probes during open laparotomy.LIVER TRANSPLANTATION• Removing the liver and replacing it with a healthy donororgan is another way to treat liver cancer.Cancer of the Liver
  186. 186. NURSING MANAGEMENT• If the patient has had surgery to treat liver cancer,potential problems related to cardiopulmonaryinvolvement include vascular complications andrespiratory and liver dysfunction.• Metabolic abnormalities require careful attention. Aconstant infusion of 10% glucose may be required in thefirst 48 hours to prevent a precipitous fall in the bloodglucose level resulting from decreasedgluconeogenesis.• Because extensive blood loss may occur as well, thepatient will receive infusions of blood and IV fluids.Cancer of the Liver
  187. 187. NURSING MANAGEMENT• The patient requires constant, close monitoring andcare for the first 2 or 3 days, similar to postsurgicalabdominal and thoracic nursing care.• The patient undergoing cryosurgery is monitored closelyfor hypothermia, hemorrhage, or bile leak;myoglobinuria can occur as a result of tissue necrosisand is minimized by hydration, diuresis, and at timesmedications (allopurinol) to bind to and aid in theexcretion of toxic products.Cancer of the Liver
  188. 188. NURSING MANAGEMENT• If the patient will receive chemotherapy or radiationtherapy in an effort to relieve symptoms, he or she maybe discharged home while still receiving one or both ofthese therapies.• The patient may also go home with a biliary drainagesystem in place.• The need for teaching is great because of the need forthe patient to participate in care and the family’s role incare at home.Cancer of the Liver
  189. 189. • Liver transplantation is used to treat life-threatening,end-stage liver disease for which no other form oftreatment is available.• The transplantation procedure involves total removal ofthe diseased liver and its replacement with a healthyliver in the same anatomic location (orthotopic livertransplantation [OLT]).• The success of liver transplantation depends onsuccessful immunosuppression.• Immunosuppressants currently in use includecyclosporine (Neoral), corticosteroids, azathioprine(Imuran), mycophenolate mofetil (CellCept), OKT3 (amonoclonal antibody), tacrolimus (FK506, Prograf),Liver Transplant
  190. 190. sirolimus (formerly known as rapamycin [Rapamune]),and antithymocyte globulin.• General indications for liver transplantation includeirreversible advanced chronic liver disease, fulminanthepatic failure, metabolic liver diseases, and somehepatic malignancies.• Examples of disorders that are indications for livertransplantation include hepatocellular liver disease (eg,viral hepatitis, drug- and alcohol-induced liver disease,and Wilson’s disease) and cholestatic diseases (primarybiliary cirrhosis, sclerosing cholangitis, and biliaryatresia).Liver Transplant
  191. 191. Liver Transplant
  192. 192. Liver Transplant
  193. 193. COMPLICATIONS• Immediate postoperative complications may includebleeding, infection, and rejection.• Disruption, infection, or obstruction of the biliaryanastomosis and impaired biliary drainage may occur.• Vascular thrombosis and stenosis are other potentialcomplications.BLEEDING• Bleeding is common in the postoperative period andmay result from coagulopathy, portal hypertension, andfibrinolysis caused by ischemic injury to the donor liver.Liver Transplant
  194. 194. COMPLICATIONSBLEEDING• Administration of platelets, fresh-frozen plasma, andother blood products may be necessary.INFECTION• Infection is the leading cause of death after livertransplantation.• Pulmonary and fungal infections are common;susceptibility to infection is increased by theimmunosuppression needed to prevent rejection.Liver Transplant
  195. 195. COMPLICATIONSINFECTION• Precautions must be taken to prevent nosocomialinfections by strict asepsis when manipulating arteriallines and urine, bile, and other drainage systems;obtaining specimens; and changing dressings.Meticulous hand hygiene is crucial.REJECTION• A transplanted liver is perceived by the immune systemas a foreign antigen. This triggers an immune response,leading to the activation of T lymphocytes that attackand destroy the transplanted liver.Liver Transplant
  196. 196. COMPLICATIONSREJECTION• Immunosuppressive agents are used long term toprevent this response and rejection of the transplantedliver.• Corticosteroids, azathioprine, mycophenolate mofetil,rapamycin, antithymocyte globulin, and OKT3 are alsoelements of the various regimens ofimmunosuppression and may be used as the initialtherapy to prevent rejection, or later to treat rejection.• Liver biopsy and ultrasound may be required toevaluate suspected episodes of rejection.Liver Transplant
  197. 197. COMPLICATIONSREJECTION• Retransplantation is usually attempted if thetransplanted liver fails, but the success rate ofretransplantation does not approach that of initialtransplantation.Liver Transplant
  198. 198. NURSING MANAGEMENT• The nurse must be aware of these issues and attunedto the emotional and psychological status of the patientand family.• Referral of the patient and family to a psychiatric liaisonnurse, psychologist, psychiatrist, or spiritual advisormay be helpful to them as they deal with the stressorsassociated with end-stage liver disease and livertransplantation.Liver Transplant
  199. 199. • Two categories of liver abscess have been identified:amebic and pyogenic.• Amebic liver abscesses are most commonly causedby Entamoeba histolytica. Most amebic liver abscessesoccur in the developing countries of the tropics andsubtropics because of poor sanitation and hygiene.• Pyogenic liver abscesses are much less common butare more common in developed countries than theamebic type.Liver Abscesses
  200. 200. CLINICAL MANIFESTATIONS• Fever with chills and diaphoresis, malaise, anorexia,nausea, vomiting, and weight loss may occur.• The patient may complain of dull abdominal pain andtenderness in the right upper quadrant of the abdomen.• Hepatomegaly, jaundice, anemia, and pleural effusionmay develop.• Sepsis and shock may be severe and life-threatening.Liver Abscesses
  201. 201. ASSESSMENT AND DIAGNOSTIC FINDINGS• Blood cultures are obtained but may not identify theorganism.• Aspiration of the liver abscess, guided by ultrasound,CT, or MRI, may be performed to assist in diagnosisand to obtain cultures of the organism.• Percutaneous drainage of pyogenic abscesses iscarried out to evacuate the abscess material andpromote healing.• A catheter may be left in place for continuous drainage;the patient must be instructed about its management.Liver Abscesses
  202. 202. MEDICAL MANAGEMENT• Treatment includes IV antibiotic therapy; the specificantibiotic used in treatment depends on the organismidentified.• Continuous supportive care is indicated because of theserious condition of the patient.• Open surgical drainage may be required if antibiotictherapy and percutaneous drainage are ineffective.Liver Abscesses
  203. 203. NURSING MANAGEMENT• The nursing management depends on the patient’sphysical status and the medical management that isindicated.• For patients who undergo evacuation and drainage ofthe abscess, monitoring of the drainage and skin careare imperative.• Strategies must be implemented to contain the drainageand to protect the patient from other sources ofinfection.• Vital signs are monitored to detect changes in thepatient’s physical status.Liver Abscesses
  204. 204. NURSING MANAGEMENT• Deterioration in vital signs or the onset of newsymptoms such as increasing pain, which may indicaterupture or extension of the abscess, is reportedpromptly.• The nurse administers IV antibiotic therapy asprescribed.• The white blood cell count and other laboratory testresults are monitored closely for changes consistentwith worsening infection.Liver Abscesses
  205. 205. NURSING MANAGEMENT• The nurse prepares the patient for discharge byproviding instruction about symptom management,signs and symptoms that should be reported to thephysician, management of drainage, and theimportance of taking antibiotics as prescribed.Liver Abscesses

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